History of Present Illness (HPI)

Obtaining an accurate history is the critical first step in determining the etiology of a patient's problem. A large percentage of the time, you will actually be able to make a diagnosis based on the history alone. The value of the history, of course, will depend on your ability to elicit relevant information. Your sense of what constitutes important data will grow exponentially in the coming years as you gain a greater understanding of the pathophysiology of disease through increased exposure to patients and illness. However, you are already in possession of the tools that will enable you to obtain a good history. That is, an ability to listen and ask common-sense questions that help define the nature of a particular problem. It does not take a vast, sophisticated fund of knowledge to successfully interview a patient. In fact seasoned physicians often lose site of this important point, placing too much emphasis on the use of testing while failing to take the time to listen to their patients. Successful interviewing is for the most part dependent upon your already well developed communication skills. What follows is a framework for approaching patient complaints in a problem oriented fashion. The patient initiates this process by describing a symptom. It falls to you to take that information and use it as a springboard for additional questioning that will help to identify the root cause of the problem. Note that this is different from trying to identify disease states which might exist yet do not generate overt symptoms. To uncover these issues requires an extensive "Review Of Systems" (a.k.a. ROS). Generally, this consists of a list of questions grouped according to organ system and designed to identify disease within that area. For example, a review of systems for respiratory illnesses would include: Do you have a cough? If so, is it productive of sputum? Do you feel short of breath when you walk? etc. In a practical sense, it is not necessary to memorize an extensive ROS question list. Rather, you will have an opportunity to learn the relevant questions that uncover organ dysfunction when you review the physical exam for each system individually. In this way, the ROS will be given some context, increasing the likelihood that you will actually remember the relevant questions. The patient's reason for presenting to the clinician is usually referred to as the "Chief Complaint." Perhaps a less pejorative/more accurate nomenclature would be to identify this as their area of "Chief Concern." Getting Started: Always introduce yourself to the patient. Then try to make the environment as private and free of distractions as possible. This may be difficult depending on where the interview is taking place. The emergency room or a non-private patient room are notoriously difficult spots. Do the best that you can and feel free to be creative. If the room is crowded, it's OK to try and find alternate sites for the interview. It's also acceptable to politely ask visitors to leave so that you can have some privacy. If possible, sit down next to the patient while conducting the interview. Remove any physical barriers that stand between yourself and the interviewee (e.g. put down the side rail so that your view of one another is unimpeded... though make sure to put it back up at the conclusion of the interview). These simple maneuvers help to put you and the patient

on equal footing. Furthermore, they enhance the notion that you are completely focused on them. You can either disarm or build walls through the speech, posture and body languarge that you adopt. Recognize the power of these cues and the impact that they can have on the interview. While there is no way of creating instant intimacy and rapport, paying attention to what may seem like rather small details as well as always showing kindness and respect can go a long way towards creating an environment that will facilitate the exchange of useful information. If the interview is being conducted in an outpatient setting, it is probably better to allow the patient to wear their own clothing while you chat with them. At the conclusion of your discussion, provide them with a gown and leave the room while they undress in preparation for the physical exam. Initial Question(s): Ideally, you would like to hear the patient describe the problem in their own words. Open ended questions are a good way to get the ball rolling. These include: "What brings your here? How can I help you? What seems to be the problem?" Push them to be as descriptive as possible. While it's simplest to focus on a single, dominant problem, patients occasionally identify more then one issue that they wish to address. When this occurs, explore each one individually using the strategy described below. Follow-up Questions: There is no single best way to question a patient. Successful interviewing requires that you avoid medical terminology and make use of a descriptive language that is familiar to them. There are several broad questions which are applicable to any complaint. These include: 1. Duration: How long has this condition lasted? Is it similar to a past problem? If so, what was done at that time? 2. Severity/Character: How bothersome is this problem? Does it interfere with your daily activities? Does it keep you up at night? Try to have them objectively rate the problem. If they are describing pain, ask them to rate it from 1 to 10 with 10 being the worse pain of their life, though first find out what that was so you know what they are using for comparison (e.g. childbirth, a broken limb, etc.). Furthermore, ask them to describe the symptom in terms with which they are already familiar. When describing pain, ask if it's like anything else that they've felt in the past. Knife-like? A sensation of pressure? A toothache? If it affects their activity level, determine to what degree this occurs. For example, if they complain of shortness of breath with walking, how many blocks can they walk? How does this compare with 6 months ago? 3. Location/Radiation: Is the symptom (e.g. pain) located in a specific place? Has this changed over time? If the symptom is not focal, does it radiate to a specific area of the body? 4. Have they tried any therapeutic maneuvers?: If so, what's made it better (or worse)? 5. Pace of illness: Is the problem getting better, worse, or staying the same? If it is changing, what has been the rate of change?

6. Are there any associated symptoms? Often times the patient notices other things that have popped up around the same time as the dominant problem. These tend to be related. 7. What do they think the problem is and/or what are they worried it might be? 8. Why today?: This is particularly relevant when a patient chooses to make mention of symptoms/complaints that appear to be long standing. Is there something new/different today as opposed to every other day when this problem has been present? Does this relate to a gradual worsening of the symptom itself? Has the patient developed a new perception of its relative importance (e.g. a friend told them they should get it checked out)? Do they have a specific agenda for the patient-provider encounter? The content of subsequent questions will depend both on what you uncover and your knowledge base/understanding of patients and their illnesses. If, for example, the patient's initial complaint was chest pain you might have uncovered the following by using the above questions: The pain began 1 month ago and only occurs with activity. It rapidly goes away with rest. When it does occur, it is a steady pressure focused on the center of the chest that is roughly a 5 (on a scale of 1 to 10). Over the last week, it has happened 6 times while in the first week it happened only once. The patient has never experienced anything like this previously and has not mentioned this problem to anyone else prior to meeting with you. As yet, they have employed no specific therapy. This is quite a lot of information. However, if you were not aware that coronary-based ischemia causes a symptom complex identical to what the patient is describing, you would have no idea what further questions to ask. That's OK. With additional experience, exposure, and knowledge you will learn the appropriate settings for particular lines of questioning. When clinicians obtain a history, they are continually generating differential diagnoses in their minds, allowing the patient's answers to direct the logical use of additional questions. With each step, the list of probable diagnoses is pared down until a few likely choices are left from what was once a long list of possibilities. Perhaps an easy way to understand this would be to think of the patient problem as a Windows-Based computer program. The patient tells you a symptom. You click on this symptom and a list of general questions appears. The patient then responds to these questions. You click on these responses and... blank screen. No problem. As yet, you do not have the clinical knowledge base to know what questions to ask next. With time and experience you will be able to click on the patient's response and generate a list of additional appropriate questions. In the previous patient with chest pain, you will learn that this patient's story is very consistent with significant, symptomatic coronary artery disease. As such, you would ask follow-up questions that help to define a cardiac basis for this complaint (e.g. history of past myocardial infarctions, risk factors for coronary disease, etc.). You'd also be aware that other disease states (e.g. emphysema) might cause similar symptoms and would therefore ask questions that could lend support to these possible diagnoses (e.g. history of smoking or wheezing). At the completion of the HPI, you should have a pretty good idea as to the likely cause of a patient's problem. You may then focus your exam on the search for physical signs that would lend support to your working diagnosis and help direct you in the rational use of adjuvant testing.

Recognizing symptoms/responses that demand an urgent assessment (e.g. crushing chest pain) vs. those that can be handled in a more leisurely fashion (e.g. fatigue) will come with time and experience. All patient complaints merit careful consideration. Some, however, require time to play out, allowing them to either become "a something" (a recognizable clinical entity) or "a nothing," and simply fade away. Clinicians are constantly on the look-out for markers of underlying illness, historical points which might increase their suspicion for the existence of an underlying disease process. For example, a patient who does not usually seek medical attention yet presents with a new, specific complaint merits a particularly careful evaluation. More often, however, the challenge lies in having the discipline to continually re-consider the diagnostic possibilities in a patient with multiple, chronic complaints who presents with a variation of his/her "usual" symptom complex. You will undoubtedly forget to ask certain questions, requiring a return visit to the patient's bedside to ask, "Just one more thing." Don't worry, this happens to everyone! You'll get more efficient with practice. Dealing With Your Own Discomfort: Many of you will feel uncomfortable with the patient interview. This process is, by its very nature, highly intrusive. The patient has been stripped, both literally and figuratively, of the layers that protect them from the physical and psychological probes of the outside world. Furthermore, in order to be successful, you must ask in-depth, intimate questions of a person with whom you essentially have no relationship. This is completely at odds with your normal day to day interactions. There is no way to proceed without asking questions, peering into the life of an otherwise complete stranger. This can, however, be done in a way that maintains respect for the patient's dignity and privacy. In fact, at this stage of your careers, you perhaps have an advantage over more experienced providers as you are hyper-aware that this is not a natural environment. Many physicians become immune to the sense that they are violating a patient's personal space and can thoughtlessly over step boundaries. Avoiding this is not an easy task. Listen and respond appropriately to the internal warnings that help to sculpt your normal interactions.

The Rest Of The History

The remainder of the history is obtained after completing the HPI. As such, the previously discussed techniques for facilitating the exchange of information still apply. Past Medical History: Start by asking the patient if they have any medical problems. If you receive little/no response, the following questions can help uncover important past events: Have they ever received medical care? If so, what problems/issues were addressed? Was the care continuous (i.e. provided on a regular basis by a single person) or episodic? Have they ever undergone any procedures, X-Rays, CAT scans, MRIs or other special testing? Ever been hospitalized? If so, for what? It's quite amazing how many patients forget what would seem to be important medical events. You will all encounter the patient who reports little past history during your interview yet reveals a complex series of illnesses to your resident or attending! These patients are generally not

purposefully concealing information. They simply need to be prompted by the right questions! Past Surgical History: Were they ever operated on, even as a child? What year did this occur? Were there any complications? If they don't know the name of the operation, try to at least determine why it was performed. Encourage them to be as specific as possible. Medications: Do they take any prescription medicines? If so, what is the dose and frequency? Do they know why they are being treated?* Medication noncompliance/confusion is a major clinical problem, particularly when regimens are complex, patients older, cognitively impaired or simply disinterested. It's important to ascertain if they are actually taking the medication as prescribed. This can provide critical information as frequently what appears to be a failure to respond to a particular therapy is actually non-compliance with a prescribed regimen. Identifying these situations requires some tact, as you'd like to encourage honesty without sounding accusatory. It helps to clearly explain that without this information your ability to assess treatment efficacy and make therapeutic adjustments becomes difficult/potentially dangerous. If patients are, in fact, missing doses or not taking medications altogether, ask them why this is happening. Perhaps there is an important side effect that they are experiencing, a reasonable fear that can be addressed, or a more acceptable substitute regimen which might be implemented. Don't forget to ask about over the counter or "non-traditional" medications. How much are they taking and what are they treating? Has it been effective? Are these medicines being prescribed by a practitioner? Self administered? * You'll be surprised to learn how many patients don't know the answers to these questions. Encourage them to keep an up to date medication list and/or write one out for them. When all else fails, ask the patient to bring their meds with them when they return or, if they are in-patients, see if a family member/friend can do so for them. Allergies/Reactions: Have they experienced any adverse reactions to medications? The exact nature of the reaction should be clearly identified as it can have important clinical implications. Anaphylaxis, for example, is a life threatening reaction and an absolute contraindication to re-exposure to the drug. A rash, however, does not raise the same level of concern, particularly if the agent in question is clearly the treatment of choice. Smoking History: Have they ever smoked cigarettes? If so, how many packs per day and for how many years? If they quit, when did this occur? The packs per day multiplied by the number of years gives the pack-years, a widely accepted method for smoking quantification. Pipe, cigar and chewing tobacco use should also be noted. Alcohol: Do they drink alcohol? If so, how much per day and what type of drink? Encourage them to be as specific as possible. One drink may mean a beer or a 12 oz glass of whiskey, each with different implications. If they don't drink on a daily basis, how much do they consume over a week or month? Other Drug Use: Any drug use, past or present, should be noted. Get in the habit of asking all your patients these questions as it can be surprisingly difficult to accurately determine who is at risk strictly on the basis of appearance. Remind them that these 5

questions are not meant to judge but rather to assist you in identifying risk factors for particular illnesses (e.g. HIV, hepatitis). In some cases, however, a patient will clearly indicate that they do not wish to discuss these issues. Respect their right to privacy and move on. Perhaps they will be more forthcoming at a later date. Obstetric (where appropriate): Have they ever been pregnant? If so, how many times? What was the outcome of each pregnancy (e.g. full term delivery; spontaneous abortion; therapeutic abortion). Sexual Activity: This is an uncomfortable line of questioning for many practitioners. However, it can provide important information and should be pursued. As with questions about substance abuse, your ability to determine on sight who is sexually active (and in what type of activity) is rather limited. By asking all of your patients these questions, the process will become less awkward. Do they participate in intercourse? With persons of the same or opposite sex? Are they involved in a stable relationship? Do they use condoms or other means of birth control? Married? Health of spouse? Divorced? Past sexually transmitted diseases? Do they have children? If so, are they healthy? Do they live with the patient? Family History: In particular, you are searching for heritable illnesses among first or second degree relatives. Most common, at least in America, are coronary artery disease, diabetes and certain malignancies. Patients should be as specific as possible. "Heart disease," for example, includes valvular disorders, coronary artery disease and congenital abnormalities, of which only coronary disease has genetic implications. Find out the age of onset of the illnesses, as this has prognostic importance for the patient. For example, a father who had an MI at age 70 is not a marker of genetic predisposition while one who had a similar event at age 40 certainly would be. Also ask about any unusual illnesses among relatives, perhaps revealing evidence for rare genetic conditions. Work/Hobbies/Other: What sort of work does the patient do? Have they always done the same thing? Do they enjoy it? If retired, what do they do to stay busy? Any hobbies? Participation in sports or other physical activity? Where are they from originally? These questions do not necessarily reveal information directly related to the patient's health. However, it is nice to know something non-medical about them. This may help improve the patient-physician bond and relay the sense that you care about them as a person. It also gives you something to refer back to during later visits, letting the patient know that you paid attention and really remember them. In recounting their history, patient's frequently drop clues that suggest issues meriting further exploration. If, for example, they are taking anti-hypertensive or anti-anginal medications yet made no mention of cardiac disease, additional history taking would be in order. Furthermore, if at any time you uncover information relevant to the chief complaint don't be afraid to revisit the HPI.

Vital Signs
Vital signs include the measurement of: temperature, respiratory rate, pulse, blood pressure and, where appropriate, blood oxygen saturation. These numbers provide critical information (hence the name "vital") about a patient's state of health. In particular, they: 1. Can identify the existence of an acute medical problem. 2. Are a means of rapidly quantifying the magnitude of an illness and how well the body is coping with the resultant physiologic stress. The more deranged the vitals, the sicker the patient. 3. Are a marker of chronic disease states (e.g. hypertension is defined as chronically elevated blood pressure). Most patients will have had their vital signs measured by an RN or health care assistant before you have a chance to see them. However, these values are of such great importance that you should get in the habit of repeating them yourself, particularly if you are going to use these values as the basis for management decisions. This not only allows you to practice obtaining vital signs but provides an opportunity to verify their accuracy. As noted below, there is significant potential for measurement error, so repeat determinations can provide critical information. Getting Started: The examination room should be quiet, warm and well lit. After you have finished interviewing the patient, provide them with a gown (a.k.a. "Johnny") and leave the room (or draw a separating curtain) while they change. Instruct them to remove all of their clothing (except for briefs) and put on the gown so that the opening is in the rear. Occasionally, patient's will end up using them as ponchos, capes or in other creative ways. While this may make for a more attractive ensemble it will also, unfortunately, interfere with your ability to perform an examination! Prior to measuring vital signs, the patient should have had the opportunity to sit for approximately five minutes so that the values are not affected by the exertion required to walk to the exam room. All measurements are made while the patient is seated. Observation: Before diving in, take a minute or so to look at the patient in their entirety, making your observations, if possible, from an out-of-the way perch. Does the patient seem anxious, in pain, upset? What about their dress and hygiene? Remember, the exam begins as soon as you lay eyes on the patient. Temperature: This is generally obtained using an oral thermometer that provides a digital reading when the sensor is placed under the patient's tongue. As most exam rooms do not have thermometers, it is not necessary to repeat this measurement unless, of course, the recorded value seems discordant with the patient's clinical condition (e.g. they feel hot but reportedly have no fever or vice versa). Depending on the bias of a particular institution, temperature is measured in either Celcius or Farenheit, with a fever defined as greater than 38-38.5 C or 101-101.5 F. Rectal temperatures, which most closely reflect internal or core values, are approximately 1 degree F higher than those obtained orally.

Respiratory Rate: Respirations are recorded as breaths per minute. They should be counted for at least 30 seconds as the total number of breaths in a 15 second period is rather small and any miscounting can result in rather large errors when multiplied by 4. Try to do this as surreptitiously as possible so that the patient does not consciously alter their rate of breathing. This can be done by observing the rise and fall of the patient's hospital gown while you appear to be taking their pulse. Normal is between 12 and 20. In general, this measurement offers no relevant information for the routine examination. However, particularly in the setting of cardio-pulmonary illness, it can be a very reliable marker of disease activity. Pulse: This can be measured at any place where there is a large artery (e.g. carotid, femoral, or simply by listening over the heart), though for the sake of convenience it is generally done by palpating the radial impulse. You may find it helpful to feel both radial arteries simultaneously, doubling the sensory input and helping to insure the accuracy of your measurements. Place the tips of your index and middle fingers just proximal to the patients wrist on the thumb side, orienting them so that they are both over the length of the vessel. Technique for Measuring the Radial Pulse The pictures below demonstrate the location of the radial artery (surface anatomy on the left, gross anatomy on the right).

Frequently, you can see transmitted pulsations on careful visual inspection of this region, which may help in locating this artery. Upper extremity peripheral vascular disease is relatively uncommon, so the radial artery should be readily palpable in most patients. Push lightly at first, adding pressure if there is a lot of subcutaneous fat or you are unable to detect a pulse. If you push too hard, you might occlude the vessel and mistake your own pulse for that of the patient. During palpation, note the following: 1. Quantity: Measure the rate of the pulse (recorded in beats per minute). Count for 30 seconds and multiply by 2 (or 15 seconds x 4). If the rate is particularly slow

or fast, it is probably best to measure for a full 60 seconds in order to minimize the impact of any error in recording over shorter periods of time. Normal is between 60 and 100. 2. Regularity: Is the time between beats constant? In the normal setting, the heart rate should appear metronomic. Irregular rhythms, however, are quite common. If the pattern is entirely chaotic with no discernable pattern, it is referred to as irregularly irregular and likely represents atrial fibrillation. Extra beats can also be added into the normal pattern, in which case the rhythm is described as regularly irregular. This may occur, for example, when impulses originating from the ventricle are interposed at regular junctures on the normal rhythm. If the pulse is irregular, it's a good idea to verify the rate by listening over the heart (see cardiac exam section). This is because certain rhythm disturbances do not allow adequate ventricular filling with each beat. The resultant systole may generate a rather small stroke volume whose impulse is not palpable in the periphery. 3. Volume: Does the pulse volume (i.e. the subjective sense of fullness) feel normal? This reflects changes in stroke volume. In the setting of hypovolemia, for example, the pulse volume is relatively low (aka weak or thready). There may even be beat to beat variation in the volume, occurring occasionally with systolic heart failure. Blood Pressure: Blood pressure (BP) is measured using mercury based manometers, with readings reported in millimeters of mercury (mm Hg). The size of the BP cuff will affect the accuracy of these readings. The inflatable bladder, which can be felt through the vinyl covering of the cuff, should reach roughly 80% around the circumference of the arm while its width should cover roughly 40%. If it is too small, the readings will be artificially elevated. The opposite occurs if the cuff is too large. Clinics should have at least 2 cuff sizes available, normal and large. Try to use the one that is most appropriate, recognizing that there will rarely be a perfect fit. Blood Pressure Cuffs

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In order to measure the BP, proceed as follows: 1. Wrap the cuff around the patient's upper arm so that the line marked "artery" is roughly over the brachial artery, located towards the medial aspect of the antecubital fossa (i.e. the crook on the inside of their elbow). The placement does not have to be exact nor do you actually need to identify this artery by palpation. Antecubital Fossa The pictures below demonstrate the antecubital fossa anatomy (surface anatomy on the left, gross anatomy on the right).

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2. Put on your stethescope so that the ear pieces are angled away from your head. Twist the head piece so that the diaphragm is engaged. This can be verified by gently tapping on the end, which should produce a sound. With your left hand, place the diaphragm over the area of the brachial artery. While most practitioners use the diaphragm of the stethescope, the bell may actually be superior for picking up the low pitched sounds used for measuring BP. Experiment with both and see if this makes a difference. It's worth mentioning that a number of different models of stethescops are available on the market, each with its own variation on the structure of the diaphragm and bell. Read the instruction manual accompanying your stethoscope in order to determine how your device works. 3. Grasp the patient's right elbow with your right hand and raise their arm so that the brachial artery is roughly at the same height as the heart. The arm should remain somewhat bent and completely relaxed. You can provide additional support by gently trapping their hand and forearm between your body and right elbow. If the arm is held too high, the reading will be artifactually lowered, and vice versa. 4. Turn the valve on the pumping bulb clockwise (may be counter clockwise in some cuffs) until it no longer moves. This is the position which allows air to enter and remain in the bladder. 5. Hold the diaphragm in place with your left hand. Use your right hand to pump the bulb until you have generated 150 mmHg on the manometer. This is a bit above the top end of normal for systolic blood pressure (SBP). Then listen. If you immediately hear sound, you have underestimated the SBP. Pump up an additional 20 mmHg and repeat. Now slowly deflate the blood pressure cuff (i.e. a few mm Hg per second) by turning the valve in a counter-clockwise direction while listening over the brachial artery and watching the pressure gauge. The first sound that you hear reflects the flow of blood through the no longer completely occluded brachial artery. The value on the manometer at this moment is the SBP. Note that although the needle may oscillate prior to this time, it is the sound of blood flow that indicates the SBP. 6. Continue listening while you slowly deflate the cuff. The diastolic blood pressure (DBP) is measured when the sound completely disappears. This is the point when the pressure within the vessel is greater then that supplied by the cuff, allowing the free flow of blood without turbulence and thus no audible sound. These are known as the Sounds of Koratkoff. Technique for Measuring Blood Pressure

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7. Repeat the measurement on the patient's other arm, reversing the position of your hands. The two readings should be within 10-15 mm Hg of each other. Differences greater then this imply that there is differential blood flow to each arm, which most frequently occurs in the setting of subclavian artery atherosclerosis. 8. Occasionally you will be unsure as to the point where systole or diastole occurred and wish to repeat the measurement. Ideally, you should allow the cuff to completely deflate, permit any venous congestion in the arm to resolve (which otherwise may lead to inaccurate measurements), and then repeat a minute or so later. Furthermore, while no one has ever lost a limb secondary to BP cuff induced ischemia, repeated measurement can be uncomfortable for the patient, another good reason for giving the arm a break. 9. Avoid moving your hands or the head of the stethescope while you are taking readings as this may produce noise that can obscure the Sounds of Koratkoff. 10. You can verify the SBP by palpation. To do this, position the patient's right arm as described above. Place the index and middle fingers of your right hand over the radial artery. Inflate the cuff until you can no longer feel the pulse, or simply to a value 10 points above the SBP as determined by auscultation. Slowly deflate the cuff until you can again detect a radial pulse and note the reading on the manometer. This is the SBP and should be the same as the value determined with the use of your stethescope. Normal is between 100/60 and 140/90. Hypertension is thus defined as either SBP greater then 140 or DBP greater than 90. It is important to recognize that blood pressure is rarely elevated to a level that causes acute symptoms. That is, while hypertension in general is common, emergencies resulting from extremely high values and subsequent acute end organ dysfunction are quite rare. Rather, it is the chronically elevated values which lead to target organ damage, though in a slow and relatively silent fashion. At the other end of the spectrum, the minimal SBP required to maintain perfusion varies with the individual. Therefore, interpretation of low values must take into account the clinical situation. Those with poorly functioning hearts, for example, can adjust to a chronically low SBP (e.g. 80-90) and live without symptoms of hypoperfusion. However others, used to higher baseline values, might become quite ill if their SBPs were suddenly decreased to these same levels. Many things can alter the accuracy of your readings. In order to limit their impact, remember the following: 1. Do not place the blood pressure cuff over a patients clothing or roll a tight fitting sleeve above their biceps when determining blood pressure as either can cause elevated readings. 2. Make sure the patient has had an opportunity to rest before measuring their BP. Try the following experiment to assess the impact that this can have. Take a patient's BP after they've rested. Then repeat after they've walked briskly in place for several minutes. Patients who are not too physically active (i.e. relatively deconditioned) will develop an elevation in both their SBP and DBP. Also, see what effect raising or lowering the arm, and thus the position of the brachial artery relative to the heart, has on BP. If you have a chance, obtain measurements 13

3. 4. 5.

6.

on the same patient with both a large and small cuff. These exercises should give you an appreciation for the magnitude of error that can be introduced when improper technique is utilized. If the reading is surprisingly high or low, repeat the measurement towards the end of your exam. Instruct your patients to avoid coffee, smoking or any other unprescribed drug with sympathomimetic activity on the day of the measurement. Orthostatic (a.k.a. postural) measurements of pulse and blood pressure are part of the assessment for hypovolemia. This requires first measuring these values when the patient is supine and then repeating them after they have stood for 2 minutes, which allows for equilibration. Normally, SBP does not vary by more then 20 points when a patient moves from lying to standing. In the setting of significant volume depletion, a greater then 20 point drop may be seen. Changes of lesser magnitude occur when moving from lying to sitting or sitting to standing. This is frequently associated with symptoms of cerebral hypoperfusion (e.g.. light headedness). Heart rate should increase by more then 20 points in a normal physiologic attempt to augment cardiac output by providing chronotropic compensation. In the setting of GI bleeding, for example, a drop in blood pressure and/or rise in heart rate after this maneuver is a marker of significant blood loss and has important prognostic implications. Orthostatic measurements may also be used to determine if postural dizziness, a common complaint with multiple possible explanations, is the result of a fall in blood pressure. For example, patients who suffer from diabetes frequently have autonomic nervous system dysfunction and cannot generate appropriate arteriolar vaosconstriction when changing positions. This results in postural vital sign changes and symptoms. The 20 point value is a rough guideline. In general, the greater the change, the more likely it is to cause symptoms and be of clinical relevance. If possible, measure the blood pressure of a patient who has an indwelling arterial catheter (these patients can be found in the ICU with the help of a preceptor). Arterial transducers are an extremely accurate tool for assessing blood pressure and therefore provide a method for checking your non-invasive technique.

Oxygen Saturation: Over the past decade, this non-invasive measurement of gas exchange and red blood cell oxygen carrying capacity has become available in all hospitals and many clinics. While imperfect, it can provide important information about cardio-pulmonary dysfunction and is considered by many to be a fifth vital sign. In particular, for those suffering from either acute or chronic cardio-pulmonary disorders, it can help quantify the degree of impairment.

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Head and Neck Exam

Lymph Nodes: The major lymph node groups are located along the anterior and posterior aspects of the neck and on the underside of the jaw. If the nodes are quite big, you may be able to see them bulging under the skin, particularly if the enlargement is asymmetric (i.e. it will be more obvious if one side is larger then the other). To palpate, use the pads of all four fingertips as these are the most sensitive parts of your hands. Examine both sides of the head simultaneously, walking your fingers down the area in question while applying steady, gentle pressure. The major groups of lymph nodes as well as the structures that they drain, are listed below. The description of drainage pathways are rough approximations as there is frequently a fair amount of variability and overlap. Nodes are generally examined in the following order: Palpating Anterior Cervical Lymph 1. Anterior Cervical (both superficial and Nodes deep): Nodes that lie both on top of and beneath the sternocleidomastoid muscles (SCM) on either side of the neck, from the angle of the jaw to the top of the clavicle. This muscle allows the head to turn to the right and left. The right SCM turns the head to the left and vice versa. They can be easily identified by asking the patient to turn their head into your hand while you provide resistance. Drainage: The internal structures of the throat as well as part of the posterior pharynx, tonsils, and thyroid gland. 2. Posterior Cervical: Extend in a line posterior to the SCMs but in front of the trapezius, from the level of the mastoid bone to the clavicle. Drainage: The skin on the back of the head. Also frequently enlarged during upper respiratory infections (e.g. mononucleosis). 3. Tonsillar: Located just below the angle of the mandible. Drainage: The tonsilar and posterior pharyngeal regions. 4. Sub-Mandibular: Along the underside of the jaw on either side. Drainage: The structures in the floor of the mouth. 5. Sub-Mental: Just below the chin. Drainage: The teeth and intra-oral cavity. 6. Supra-clavicular: In the hollow above the clavicle, just lateral to where it joins the sternum. Drainage: Part of the throacic cavity, abdomen. A number of other lymph node groups exist. However, palpation of these areas is limited to those situations when a problem is identified in that specific region (e.g. the preauricular nodes, located in front of the ears, may become inflamed during infections of the external canal of the ear). Lymph nodes of the head and neck

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A number of other lymph node groups exist. However, palpation of these areas is limited to those situations when a problem is identified in that specific region (e.g. the preauricular nodes, located in front of the ears, may become inflamed during infections of the external canal of the ear). What are you feeling for? Lymph nodes are part of the immune system. As such, they are most readily palpable when fighting infections. Infections can either originate from the organs that they drain or primarily within the lymph node itself, referred to as lymphadenitis. Infected lymph nodes tend to be:

Firm, tender, enlarged and warm. Inflammation can spread to the overlying skin, causing it to appear reddened.

If an infection remains untreated, the center of the node may become necrotic, resulting in the accumulation of fluid and debris within the structure. This is known as an abscess and feels a bit like a tensely filled balloon or grape (a.k.a. fluctuance). Knowledge of which nodes drain specific areas will help you search efficiently. Following infection, lymph nodes occasionally remain permanently enlarged, though they should be nontender, small (less the 1 cm), have a rubbery consistency and none of the characteristics described above or below. It is common, for example, to find small, palpable nodes in the submandibular/tonsilar region of otherwise healthy individuals. This likely represents sequelae of past pharyngitis or dental infections. Malignancies may also involve the lymph nodes, either primarily (e.g. lymphoma) or as a site of metastasis. In either case, these nodes are generally:

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Firm, non-tender, matted (i.e. stuck to each other), fixed (i.e. not freely mobile but rather stuck down to underlying tissue), and increase in size over time.

The location of the lymph node may help to determine the site of malignancy. Diffuse, bilateral involvement suggests a systemic malignancy (e.g. lymphoma) while those limited to a specific anatomic region are more likely associated with a local problem. Enlargement of nodes located only on the right side of the neck in the anterior cervical chain, for example, would be consistent with a squamous cell carcinoma, frequently associated with an intra-oral primary cancer.

Cervical Adenopathy: Massive right side cervical adenopathy secondary to metastatic squamous cell cancer originating from this patient's oropharynx.

Cervical Adenopathy: Right anterior cervical adenopathy secondary to metastatic cancer.

Diffuse upper airway infections (e.g. mononucleosis), systemic infections (e.g. tuberculosis) and inflammatory processes (e.g. sarcoidosis) can also cause lymphadenopathy (i.e. lymph node enlargement). This can be either symmetric or asymmetric. Historical information as well findings elsewhere in the body are critical to making these diagnoses. Furthermore, it may take serial examinations over the course of weeks to determine whether a node is truly enlarging, suggestive of malignancy, or responding to therapy/the passage of time and regressing in size, as might occur with other inflammatory processes. The Ear External structures: Briefly examine the outer structures, paying particular attention to any skin changes suggestive of cancer (e.g basal cell, melanoma, squamous cell), a common asymptomatic abnormality affecting this sun exposed area. If the patient has pain, try to identify its precise location. Infection within the external canal, for example,

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may cause discharge from the ear as well as pain on manipulation of any of the external structures. Otoscope

Otoscopy: The otoscope allows you to examine the external canal, the structure that connects the outside world with the middle ear, as well as the ear drum and a few inner ear structures. Proceed as follows: 1. Put the otoscopic head on your oto-opthalmoscopic. It should easily twist into position. 2. Turn on the light source. 3. Place one of the disposable specula on the end of the scope. 4. Grasp the scope so that the handle is either pointed directly downward or angled up and towards the patient's forehead. Either technique is acceptable. The scope should be in your right hand if you are examining the right ear. 5. Place the tip of the specula in the opening of the external canal. Do this under direct vision (i.e. not while looking through the scope). 6. Gently grasp the top of the left ear with your left hand and pull up and backwards. This straightens out the canal, allowing easier passage of the scope. 7. Look through the viewing window with either eye. Slowly advance the scope, heading a bit towards the patient's nose but without any up or down angle. Move in small increments. Try not to wiggle the scope too much as the external canal is quite sensitive. I find it helpful to extend the pinky and fourth fingers of my right hand and place them on the side of the patient's head, which has a stabilizing effect. As you advance, pay attention to the appearance of the external canal. In the setting of infection, called otitis externa, the walls becomes red, swollen and may not accommodate the speculum. In the normal state there should be plenty of room. If wax, which appears brownish, irregular and mushy, obscures your view, stop and go to the other side. Do not try to extract it until/unless you have had

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specific training in this area! There are pharmacologic means of softening wax, which may then be easily irrigated from the canal.

Otitis Externa: Swelling due to infection in the external canal of the left ear (picture on right) limits the space around the Q-Tip. Picture on left is of normal ear for comparison. After moving ahead a few centimeters, you should see the tympanic membrane (a.k.a. ear drum). Pay particular attention to: Otoscopic Examination a. The color: When healthy, it has a grayish, translucent appearance. b. The structures behind it: The malleous, one of the bones of the middle ear, touches the drum. The drum is draped over this bone, which is visible through its top half, angled down and backwards. The part that is closest to the top of the drum is called the lateral process, and is generally most prominent. The tip at the bottommost aspect is the umbo.

c. The light reflex: Light originating from your scope will be reflected off the surface of the drum, making a triangle that is visible below the malleous. d. In the setting of infection within the middle ear (known as otitis media, the most common pathologic process affecting this area), the drum becomes diffusely red and the light reflex is lost. The malleous also appears less prominent and you may be able to see a line caused by fluid collecting behind the drum. This is called a middle ear effusion and can cause the drum to bulge outwards. e. There is a valve on your scope that allows the attachment of a small, compressible bulb. Place the bulb in the palm of the hand which is not holding the scope. With this device, you can squirt small puffs of air 19

(known as pneumatic otoscopy) at the tympanic membrane. The normal membrane moves, which can be appreciated by the examiner. Effusions prevent this from occurring. Ask an experienced examiner to demonstrate as this is quite awkward at first and it's difficult to appreciate the movement. 8. Move to the other side of the body and examine the left ear. Hand position is reversed. Auditory Acuity: If the patient does not complain of hearing loss, this part of the exam is omitted. A crude assessment can be performed by asking the patient to close their eyes while you place your fingers a few centimeters from either ear. Rub the finger tips of first one hand and then the other. Make note of any obvious differences in hearing. Alternatively, you can stand behind the patient and whisper a few words in first one ear and then the other. Are they able to repeat the phrases back correctly? Does this seem to be equal on either side? These tests obviously are not very objective. Precise quantification requires sensitive equipment and is usually done by a trained audiologist. Detecting Conductive v. Sensorineural Deficits: As with acuity, these tests would only be performed if the patient complained of hearing loss. Transmission of sound can be broken into two components: 1. Conduction: The passage of sound from outside to the level of the 8th cranial nerve. This includes transmission of sound through the external canal and middle ears. 2. Sensorineural: The transmission of sound through the 8th nerve to the brain. Hearing loss can occur at either level. To determine which is affected, the following tests are performed: Weber: Grasp the 512 Hz tuning fork by its stem and get it to vibrate by either striking the tines against your hand or by "snapping" the ends between your thumb and middle finger. Then place the stem towards the back of the patient's head, on an imaginary line equidistant from either ear. The bones of the skull will transmit this sound to the 8th nerve, which should then be appreciated in both ears equally. Remind the patient that they are trying to detect sound, not the buzzing vibratory sensation from the fork. If there is a conductive deficit (e.g. wax in the external canal), the sound will be heard better in that ear. This is because impaired conduction has prevented any competing sounds from entering the ear via the normal route. You can create a transient conductive hearing loss by putting a finger in one ear. Sound transmitted from the tuning fork will then be heard louder on that side. In the setting of a sensorineural abnormality (e.g. an acoustic neuroma, a tumor arising from the 8th CN), the sound will be best heard in the normal ear. If sound is heard better in one ear it is described as lateralizing to that side. Otherwise, the Weber test is said to be mid-line.

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Weber Test

Rinne: Strike the same tuning fork and place the stem on the mastoid bone, a bony prominence located just behind and below the ear. Bone conduction will allow the sound to be transmitted and appreciated. Instruct the patient to let you know as soon as they can no longer hear the sound. Then place the tines of the still vibrating fork right next to, but not touching, the external canal. They should again be able to hear the sound. This is because, when everything is functioning normally, transmission of sound through air is always better then through bone. This will not be the case if there is a conductive hearing loss (e.g. fluid associated with an infection in the middle ear), which causes bone conduction to be greater then or equal to air. If there is a sensorineural abnormality (e.g. medication induced toxicity to the 8th CN), air conduction should still be better then bone as they will both be equally affected by the deficit. Rinne Test

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The Nose In the absence of symptoms, this exam is generally omitted. First check to see if the patient is able to breathe through either nostril effectively. Push on one nostril until it is occluded and have them inhale. Then repeat on the other side. Air should move equally well through each nares. To look in the nose, have the patient tilt their head back. Push up slightly on the tip of the nose with the thumb of your left hand. Place the end of the speculum (it's OK to use the same one from the ear exam) into the nares under direct vision. Now look through the viewing window, noting: 1. The color of the mucosa. It can become quite reddened in the setting of infection. 2. The presence of any discharge as well as its color (clear with allergic reactions; yellowish with infection). 3. The middle and inferior turbinates, which are shelf-like projections along the lateral wall. Any polypoid growths, which may be associated with allergies and obstructive symptoms? 4. The other nostril is examined in a similar manner. 5. Loss of smell (anosmia) is a relatively common problem, though often undiagnosed. In patients who make mention of this problem, olfaction can be crudely assessed using an alcohol pad sniff test as follows: a. Ask the patient to close their eyes so that they don't get any visual cues. b. Occlude each nostril seqeuentially, making sure that they can move air adequately thru both. c. Occlude one nostril and then present an alcohol pad to the other side, asking the patient to inform you when they are able to detect its smell. A patient should be able to detect the odor of the alcohol pad at a distance of 10 cm. Alcohol is used for convenience, as most exam rooms have these pads. More sophisticated testing can be done using vials containing very distinctive odors (e.g. coffee grounds, wintergreen oil, etc).

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Alcohol Pad Smell Test Evaluation of Frontal and Maxillary Sinuses

Maxillary and Frontal Sinuses The head and face contain a number of sinuses, open cavities that communicate with the upper airway. They function to warm and cleanse air before it travels down to the lungs. They may also help to reduce the total weight of the skull. In normal health, these sinuses cannot be appreciated on examination and cause no symptoms. Inflammatory states, in particular those caused by allergy or infection, produce symptoms and findings that may 23

be detected during examination. Symptoms associated with sinusitis include: nasal congestion, nasal discharge, facial pain, fever, and pain on palpation of the maxillary teeth. The frontal and maxillary sinuses are the two that can be indirectly examined. Examination for sinusitis should include the following: 1. Examination of the nasal mucosa for colored discharge as described above. This is due to the fact that the maxillary sinuses drain into the nose via a passageway located under the middle turbinate. 2. Directly palpate and percuss the skin overlying the frontal and maxillary sinuses. Pain suggests underlying inflammation. 3. Dim the room lights. Place the lighted otoscope directly on the infraorbital rim (bone just below the eye). Ask the patient to open their mouth and look for light glowing through the mucosa of the upper mouth. In the setting of inflammation, the maxillary sinus becomes fluid filled and will not allow this transillumination. There are specially designed transilluminators that may work better for this task, but are not readily available.

4. Transillumination of the right maxillary sinus 5. Using a tongue depessor, tap on the teeth which sit in the floor of the maxillary sinus. This may cause discomfort if the sinus is inflamed. The Oro-Pharynx Exposure and good lighting are critical. Head and Neck specialists have head lamps that provide excellent illumination and allow them to use both hands to explore the oral cavity. Most other physicians, however, use an otoscope or flashlight for illumination. A tongue depressor assists with the exploration. The exam should be performed in an orderly fashion as follows:

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1. Have the patient stick out their tongue so that you can examine the posterior pharynx (i.e. the back of the throat). Ask the patient to say "Ah", which elevates the soft palate, giving you a better view. If you are still unable to see, place the tongue blade way back on the tongue and press down while the patient again says "Ah," hopefully improving your view. This causes some people to gag, particularly when the blade is pushed onto the more proximal aspects of the tongue. It may occasionally be important to determine whether the gag reflex is functional (e.g. after a stroke that impairs CNs 9 or 10; or to determine if a patient with depressed level of consciousness is able to protect their airway from aspiration). This is done by touching a q-tip against the posterior pharynx, uvula or tongue. It is not necessary to do this during your routine exam as it can be quite noxious! 2. Note that the uvula hangs down from the roof of the mouth, directly in the midline. With an "Ah," the uvula rises up. Deviation to one side may be caused by CN 9 palsy (the uvula deviates away from the affected side), a tumor or an infection.

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Cranial Nerve 9 Dysfunction: Patient has suffered stroke, causing loss of function of left CN 9. As a result, uvula is pulled towards the normally functioning (ie right) side. 3. The normal pharynx has a dull red color. In the setting of infection, it can become quite red, frequently covered with a yellow or white exudate (e.g. with Strep. Throat or other types of pharyngitis). 4. The tonsils lie in an alcove created by arches on either side of the mouth. The apex of these arches are located lateral to and on a line with the uvula. Normal tonsils range from barely apparent to quite prominent. When infected, they become red, are frequently covered by whitish/yellow discharge. In the setting of a peritonsilar abscess, the tonsils appear asymmetric and the uvula may be pushed away from the affected side. When this occurs, the tonsil may actually compromise the size of the oral cavity, making breathing quite difficult.

Left Peritonsilar Abscess. Note deveiation of uvula towards right.

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5. Look carefully along the upper and lower gum lines and at the mucosa in general, which can appear quite dry if the patient is dehydrated. 6. Examine the teeth to get a sense of general dentition, particularly if the patient has a dental complaint. Pain produced by tapping on a tooth is commonly caused by a root abscess.

Tooth Abscess: Tooth abscess involving left molar region. Associated inflammation of left face can clearly be seen. 7. Have the patient stick their tongue outside their mouth, which allows evaluation of CN 12. If there is nerve impairment, the tongue will deviate towards the affected side. Any obvious growths or abnormalities? Ask them to flip their tongue up so that you can look at the underside. If you see something abnormal, grasp the tongue with gauze so that you can get a better look.

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Left CN 12 Dysfunction: Stroke has resulted in L CN 12 Palsy. Tongue therefore deviates to the left. 8. Make note of any growths along the cheeks, hard palate (the roof of the mouth between the teeth), soft palate, or anywhere else. In particular, patients who smoke or chew tobacco are at risk for oral squamous cell cancer. Any areas which are painful or appear abnormal should also be palpated. Put on a pair of gloves to better explore these regions. What do they feel like? Are they hard? To what extent does a growth involve deeper structures? If the patient feels something that you cannot see, try to get someone else to hold the light source, freeing both your hands to explore the oral cavity with two tongue depressors. 9. The parotid glands are located in either cheek. Infection will cause pain and swelling in this area, which can be confirmed on palpation. The ducts which drain the parotids enter the mouth in line with the lower molars and are readily visible. When infected, you may be able to express pus from the ducts by gently palpating the gland.

Right parotid mass. Note enlargement on right compared with left.

The Thyroid Exam Prior to palpation, look at the thyroid region. If the gland is quite enlarged, you may 28

actually notice it protruding underneath the skin. To find the thyroid gland, first locate the thyroid cartilage (a.k.a the Adams Apple), which is a mid-line bulge towards the top of the anterior surface of the neck. It's particularly prominent in thin males, sits atop the tracheal rings, and can be seen best when the patient tilts their head backwards. Deviation to one side or the other is usually associated with intra-thoracic pathology. For example, air trapped in one pleural space (known as a pneumothorax) can generate enough pressure so that it collapses the lung on that side, causing mediastinal structures, along with the trachea, to be pushed towards the opposite chest. This deviation may be visible on inspection and can be accentuated by gently placing your finger in the top of the thyroid cartilage and noting its position relative to the midline. The thyroid gland lies approximately 2-3 cm below the thyroid cartilage, on either side of the tracheal rings, which may or may not be apparent on visual inspection. If you're unsure, give the patient a glass of water and have them swallow as you watch this region. Thyroid tissue, along with all of the adjacent structures, will move up and down with swallowing. The normal thyroid is not visible, so it's not worth going through this swallowing exercise if you don't see anything on gross inspection. Location of the Thyroid

Palpation: The thyroid can be examined while you stand in front of or behind the patient. Exam from behind the patient is described below: 1. Stand behind the patient and place the middle three fingers of either hand along the mid-line of the neck, just below the chin. Gently walk them down until you reach the top of the thyroid cartilage, the first firm structure with which you come into contact. Use gentle pressure, otherwise this can be uncomfortable. Make sure that you tell your patients what you're doing so they know you're not trying to choke them! The cartilage has a small notch in its top and is approximately 1.5-2 cm in length. As you cannot actually see the area that you're examining, it may be helpful to practice in front of a mirror. You can also try to identify and feel the

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structures from the front while looking at the area in question before performing the exam from behind. 2. Walk down the thyroid cartilage with your fingers until you come to the horizontal groove which separates it from the cricoid cartilage (the first tracheal ring). You should be able to feel a small indentation (it barely accepts the tip of your finger) between these 2 structures, directly in the mid-line. This is the cricothyroid membrane, the site for emergent tracheal access in the event of upper airway obstruction. 3. Continue walking down until you reach the next well defined tracheal ring. Now slide the three fingers of both hands to either side of the rings. The thyroid gland extends from this point downwards for approximately 2-3 cm along each side. The two main lobes are connected by a small isthmus that reaches across mid-line and is almost never palpable. Apply very gentle pressure when you palpate as the normal thyroid tissue is not very prominent and easily compressible. If you're unsure or wish confirmation, have the patient drink water as you palpate. The gland should slide beneath your fingers while it moves upward along with the cartilagenous rings. It takes a very soft, experienced touch in order to actually feel this structure, so don't be disappointed if you can't identify anything. Thyroid Examination

4. Pay attention to several things as you try to identify the thyroid: If enlarged (and this is a subjective sense that you will develop after many exams), is it symmetrically so? Unilateral vs. bilateral? Are there discrete nodules within either lobe? If the gland feels firm, is it attached to the adjacent structures (i.e. fixed to underlying tissue.. consistent with malignancy) or freely mobile (i.e. moves up and down with swallowing)? If there is concern re: malignancy, a careful lymph node exam (described above) is important as this is the most common site of spread

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The Lung Exam

The 4 major components of the lung exam (inspection, palpation, percussion and auscultation) are also used to examine the heart and abdomen. Learning the appropriate techniques at this juncture will therefore enhance your ability to perform these other examinations as well. Vital signs, an important source of information, are discussed elsewhere. Inspection/Observation: A great deal of information can be gathered from simply watching a patient breathe. Pay particular attention to: 1. General comfort and breathing pattern of the patient. Do they appear distressed, diaphoretic, labored? Are the breaths regular and deep? 2. Use of accessory muscles of breathing (e.g. scalenes, sternocleidomastoids). Their use signifies some element of respiratory difficulty. 3. Color of the patient, in particular around the lips and nail beds. Obviously, blue is bad!

Cyanosis of nail beds 4. The position of the patient. Those with extreme pulmonary dysfunction will often sit up-right. In cases of real distress, they will lean forward, resting their hands on their knees in what is known as the tri-pod position. Patient with emphysema bending over in Tri-Pod Position

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5. Breathing through pursed lips, often seen in cases of emphysema. 6. Ability to speak. At times, respiratory rates can be so high and/or work of breathing so great that patients are unable to speak in complete sentences. If this occurs, note how many words they can speak (i.e. the fewer words per breath, the worse the problem!). 7. Any audible noises associated with breathing as occasionally, wheezing or the gurgling caused by secretions in large airways are audible to the "naked" ear. 8. The direction of abdominal wall movement during inspiration. Normally, the descent of the diaphragm pushes intra-abdominal contents down and the wall outward. In cases of severe diaphragmatic flattening (e.g. emphysema) or paralysis, the abdominal wall may move inward during inspiration, referred to as paradoxical breathing. If you suspect this to be the case, place your hand on the patient's abdomen as they breathe, which should accentuate its movement. 9. Any obvious chest or spine deformities. These may arise as a result of chronic lung disease (e.g. emphysema), occur congenitally, or be otherwise acquired. In any case, they can impair a patient's ability to breathe normally. A few common variants include: o Pectus excavatum: Congenital posterior displacement of lower aspect of sternum. This gives the chest a somewhat "hollowed-out" appearance. The x-ray shows a subtle concave appearance of the lower sternum.

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Barrel chest: Associated with emphysema and lung hyperinflation. Accompanying xray also demonstrates increased anterior-posterior diameter as well as diaphragmatic flattening.

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Spine abnormalities: Kyphosis: Causes the patient to be bent forward. Accompanying X-Ray of same patient clearly demonstrates extreme curvature of the spine.

Scoliosis: Condition where the spine is curved to either the left or right. In the pictures below, scoliosis of the spine causes right shoulder area to appear somewhat higher than the left. Curvature is more pronounced on x-ray.

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Review of Lung Anatomy: Understanding the pulmonary exam is greatly enhanced by recognizing the relationships between surface structures, the skeleton, and the main lobes of the lung. Realize that this can be difficult as some surface landmarks (eg nipples of the breast) do not always maintain their precise relationship to underlying structures. Nevertheless, surface markers will give you a rough guide to what lies beneath the skin. The pictures below demonstrate these relationships. The multi-colored areas of the lung 35

model identify precise anatomic segments of the various lobes, which cannot be appreciated on examination. Main lobes are outlined in black. The following abbreviations are used: RUL = Right Upper Lobe; LUL = Left Upper Lobe; RML = Right Middle Lobe; RLL = Right Lower Lobe; LLL = Left Lower Lobe.

Anterior View

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Posterior View

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Right Lateral View

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Left Lateral View

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Palpation: Palpation plays a relatively minor role in the examination of the normal chest as the structure of interest (the lung) is covered by the ribs and therefore not palpable. Specific situations where it may be helpful include: 1. Accentuating normal chest excursion: Place your hands on the patient's back with thumbs pointed towards the spine. Remember to first rub your hands together so that they are not too cold prior to touching the patient. Your hands should lift symmetrically outward when the patient takes a deep breath. Processes that lead to asymmetric lung expansion, as might occur when anything fills the pleural space (e.g. air or fluid), may then be detected as the hand on the affected side will move outward to a lesser degree. There has to be a lot of plerual disease before this asymmetry can be identified on exam. Detecting Chest Excursion

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2. Tactile Fremitus: Normal lung transmits a palpable vibratory sensation to the chest wall. This is referred to as fremitus and can be detected by placing the ulnar aspects of both hands firmly against either side of the chest while the patient says the words "Ninety-Nine." This maneuver is repeated until the entire posterior thorax is covered. The bony aspects of the hands are used as they are particularly sensitive for detecting these vibrations.

Assessing Fremitus Pathologic conditions will alter fremitus. In particular: A. Lung consolidation: Consolidation occurs when the normally air filled lung parenchyma becomes engorged with fluid or tissue, most commonly in the setting of pneumonia. If a large enough segment of parenchyma is involved, it can alter the transmission of air and sound. In the presence of consolidation, fremitus becomes more pronounced. B. Pleural fluid: Fluid, known as a pleural effusion, can collect in the potential space that exists between the lung and the chest wall, displacing the lung upwards. Fremitus over an effusion will be decreased. In general, fremitus is a pretty subtle finding and should not be thought of as the primary means of identifying either consolidation or pleural fluid. It can, however, lend supporting evidence if other findings (see below) suggest the presence of either of these processes.

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Effusions and infiltrates can perhaps be more easily understood using a sponge to represent the lung. In this model, an infiltrate is depicted by the blue coloration that has invaded the sponge itself (sponge on left). An effusion is depicted by the blue fluid upon which the lung is floating (sponge on right).

3. Investigating painful areas: If the patient complains of pain at a particular site it is obviously important to carefully palpate around that area. In addition, special situations (e.g. trauma) mandate careful palpation to look for evidence of rib

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fracture, subcutaneous air (feels like your pushing on Rice Krispies or bubble paper), etc. Percussion: This technique makes use of the fact that striking a surface which covers an air-filled structure (e.g. normal lung) will produce a resonant note while repeating the same maneuver over a fluid or tissue filled cavity generates a relatively dull sound. If the normal, air-filled tissue has been displaced by fluid (e.g. pleural effusion) or infiltrated with white cells and bacteria (e.g. pneumonia), percussion will generate a deadened tone. Alternatively, processes that lead to chronic (e.g. emphysema) or acute (e.g. pneumothorax) air trapping in the lung or pleural space, respectively, will produce hyperresonant (i.e. more drum-like) notes on percussion. Initially, you will find that this skill is a bit awkward to perform. Allow your hand to swing freely at the wrist, hammering your finger onto the target at the bottom of the down stroke. A stiff wrist forces you to push your finger into the target which will not elicit the correct sound. In addition, it takes a while to develop an ear for what is resonant and what is not. A few things to remember: 1. If you're percussing with your right hand, stand a bit to the left side of the patient's back. 2. Ask the patient to cross their hands in front of their chest, grasping the opposite shoulder with each hand. This will help to pull the scapulae laterally, away from the percussion field. 3. Work down the "alley" that exists between the scapula and vertebral column, which should help you avoid percussing over bone. 4. Try to focus on striking the distal inter-phalangeal joint (i.e. the last joint) of your left middle finger with the tip of the right middle finger. The impact should be crisp so you may want to cut your nails to keep blood-letting to a minimum!

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5. If you're percussing with your right hand, stand a bit to the left side of the patient's back. 6. Ask the patient to cross their hands in front of their chest, grasping the opposite shoulder with each hand. This will help to pull the scapulae laterally, away from the percussion field. 7. Work down the "alley" that exists between the scapula and vertebral column, which should help you avoid percussing over bone. 8. Try to focus on striking the distal inter-phalangeal joint (i.e. the last joint) of your left middle finger with the tip of the right middle finger. The impact should be crisp so you may want to cut your nails to keep blood-letting to a minimum! 9. The last 2 phalanges of your left middle finger should rest firmly on the patient's back. Try to keep the remainder of your fingers from touching the patient, or rest only the tips on them if this is otherwise too awkward, in order to minimize any dampening of the perucssion notes. 10. When percussing any one spot, 2 or 3 sharp taps should suffice, though feel free to do more if you'd like. Then move your hand down several inter-spaces and repeat the maneuver. In general, percussion in 5 or so different locations should cover one hemi-thorax. After you have percussed the left chest, move yours hands across and repeat the same procedure on the right side. If you detect any abnormality on one side, it's a good idea to slide your hands across to the other for comparison. In this way, one thorax serves as a control for the other. In general, percussion is limited to the posterior lung fields. However, if auscultation (see below) reveals an abnormality in the anterior or lateral fields, percussion over these areas can help identify its cause.

Percussion Technique

11. The goal is to recognize that at some point as you move down towards the base of the lungs, the quality of the sound changes. This normally occurs when you leave 44

the thorax. It is not particularly important to identify the exact location of the diaphragm, though if you are able to note a difference in level between maximum inspiration and expiration, all the better. Ultimately, you will develop a sense of where the normal lung should end by simply looking at the chest. The exact vertebral level at which this occurs is not really relevant. 12. "Speed percussion" may help to accentuate the difference between dull and resonant areas. During this technique, the examiner moves their left (i.e. the nonpercussing) hand at a constant rate down the patient's back, tapping on it continuously as it progresses towards the bottom of the thorax. This tends to make the point of inflection (i.e. change from resonant to dull) more pronounced. Practice percussion! Try finding your own stomach bubble, which should be around the left costal margin. Note that due to the location of the heart, tapping over your left chest will produce a different sound then when performed over your right. Percuss your walls (if they're sheet rock) and try to locate the studs. Tap on tupperware filled with various amounts of water. This not only helps you develop a sense of the different tones that may be produced but also allows you to practice the technique. Auscultation: Prior to listening over any one area of the chest, remind yourself which lobe of the lung is heard best in that region: lower lobes occupy the bottom 3/4 of the posterior fields; right middle lobe heard in right axilla; lingula in left axilla; upper lobes in the anterior chest and at the top 1/4 of the posterior fields. This can be quite helpful in trying to pin down the location of pathologic processes that may be restricted by anatomic boundaries (e.g. pneumonia). Many disease processes (e.g. pulmonary edema, bronchoconstriction) are diffuse, producing abnormal findings in multiple fields.

1. Put on your stethoscope so that the ear pieces are directed away from you. Adjust the head of the scope so that the diaphragm is engaged. If you're not sure, scratch lightly on the diaphragm, which should produce a noise. If not, twist the head and

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try again. Gently rub the head of the stethoscope on your shirt so that it is not too cold prior to placing it on the patient's skin. 2. The upper aspect of the posterior fields (i.e. towards the top of the patient's back) are examined first. Listen over one spot and then move the stethoscope to the same position on the opposite side and repeat. This again makes use of one lung as a source of comparison for the other. The entire posterior chest can be covered by listening in roughly 4 places on each side. Of course, if you hear something abnormal, you'll need to listen in more places. Lung Auscultation

3. The lingula and right middle lobes can be examined while you are still standing behind the patient. 4. Then, move around to the front and listen to the anterior fields in the same fashion. This is generally done while the patient is still sitting upright. Asking female patients to lie down will allow their breasts to fall away laterally, which may make this part of the examination easier. A few additional things worth noting. 1. Don't get in the habit of performing auscultation through clothing. 2. Ask the patient to take slow, deep breaths through their mouths while you are performing your exam. This forces the patient to move greater volumes of air with each breath, increasing the duration, intensity, and thus detectability of any abnormal breath sounds that might be present. 3. Sometimes it's helpful to have the patient cough a few times prior to beginning auscultation. This clears airway secretions and opens small atelectatic (i.e. collapsed) areas at the lung bases. 4. If the patient cannot sit up (e.g. in cases of neurologic disease, post-operative states, etc.), auscultation can be performed while the patient is lying on their side. Get help if the patient is unable to move on their own. In cases where even this 46

cannot be accomplished, a minimal examination can be performed by listening laterally/posteriorly as the patient remains supine. Requesting that the patient exhale forcibly will occasionally help to accentuate abnormal breath sounds (in particular, wheezing) that might not be heard when they are breathing at normal flow rates.. What can you expect to hear? A few basic sounds to listen for: 1. A healthy individual breathing through their mouth at normal tidal volumes produces a soft inspiratory sound as air rushes into the lungs, with little noise produced on expiration. These are referred to as vessicular breath sounds. 2. Wheezes are whistling-type noises produced during expiration (and sometimes inspiration) when air is forced through airways narrowed by bronchoconstriction, secretions, and/or associated mucosal edema. As this most commonly occurs in association with diffuse processes that affect all lobes of the lung (e.g. asthma and emphysema) it is frequently audible in all fields. In cases of significant bronchoconstriction, the expiratory phase of respiration (relative to inspiration) becomes noticeably prolonged. Clinicians refer to this as an increased I to E ratio. Normal is approximatley 1:2 (i.e. expiration twice as long as inspiration) though actual timed measurements are neither practical nor reliable. Focus instead on simple observation, noting whether E seems >> I. The greater the difference, the worse the obstruction. Occasionally, focal wheezing can occur when airway narrowing if restricted to a single anatomic area, as might occur with an obstructing tumor or bronchoconstriction induced by pneumonia. Wheezing heard only on inspiration is referred to as stridor and is associated with mechanical obstruction at the level of the trachea/upper airway. This may be best appreciated by placing your stethescope directly on top of the trachea. 3. Rales (a.k.a. crackles) are scratchy sounds that occur in association with processes that cause fluid to accumulate within the alveolar and interstitial spaces. The sound is similar to that produced by rubbing strands of hair together close to your ear. Pulmonary edema is probably the most common cause, at least in the older adult population, and results in symmetric findings. This tends to occur first in the most dependent portions of the lower lobes and extend from the bases towards the apices as disease progresses. Pneumonia, on the other hand, can result in discrete areas of alveolar filling, and therefore produce crackles restricted to a specific region of the lung. Very distinct, diffuse, dry-sounding crackles, similar to the noise produced when separating pieces of velcro, are caused by pulmonary fibrosis, a relatively uncommon condition. 4. Dense consolidation of the lung parenchyma, as can occur with pneumonia, results in the transmission of large airway noises (i.e. those normally heard on auscultation over the trachea known as tubular or bronchial breath sounds) to the periphery. In this setting, the consolidated lung acts as a terrific conducting medium, transferring central sounds directly to the edges. It's very similar to the noise produced when breathing through a snorkel. Furthermore, if you direct the patient to say the letter 'eee' it is detected during auscultation over the involved lobe as a nasal-sounding 'aaa'. These 'eee' to 'aaa' changes are referred to as egophony. The first time you detect it, you'll think that the patient is actually 47

saying 'aaa' have them repeat it several times to assure yourself that they are really following your directions! 5. Secretions that form/collect in larger airways, as might occur with bronchitis or other mucous creating process, can produce a gurgling-type noise, similar to the sound produced when you suck the last bits of a milk shake through a straw. These noises are referred to as ronchi. 6. Auscultation over a pleural effusion will produce a very muffled sound. If, however, you listen carefully to the region on top of the effusion, you may hear sounds suggestive of consolidation, originating from lung which is compressed by the fluid pushing up from below. Asymmetric effusions are probably easier to detect as they will produce different findings on examination of either side of the chest. 7. Auscultation of patients with severe, stable emphysema will produce very little sound. These patients suffer from significant lung destruction and air trapping, resulting in their breathing at small tidal volumes that generate almost no noise. Wheezing occurs when there is a superimposed acute inflammatory process (see above). Most of the above techniques are complimentary. Dullness detected on percussion, for example, may represent either lung consolidation or a pleural effusion. Auscultation over the same region should help to distinguish between these possibilities, as consolidation generates bronchial breath sounds while an effusion is associated with a relative absence of sound. Similarly, fremitus will be increased over consolidation and decreased over an effusion. As such, it may be necessary to repeat certain aspects of the exam, using one finding to confirm the significance of another. Few findings are pathognomonic. They have their greatest meaning when used together to paint the most informative picture.

The Dynamic Lung Exam: Pulse Oxymeter

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Oftentimes, a patient will complain of a symptom that is induced by activity or movement. Shortness of breath on exertion, one such example, can be a marker of significant cardiac or pulmonary dysfunction. The initial examination may be relatively unrevealing. In such cases, consider observed ambulation (with the use of a pulse oxymeter, a device that continuously measures heart rate and oxygen saturation, if available) as a dynamic extension of the cardiac and pulmonary examinations. Quantifying a patient's exercise tolerance in terms of distance and/or time walked can provide information critical to the assessment of activity induced symptoms. It may also help unmask illness that would be inapparent unless the patient was asked to perform a task that challenged their impaired reserves. Pay particular attention to the rate at which the patient walks, duration of activity, distance covered, development of dyspnea, changes in heart rate and oxygen saturation, ability to talk during exercise and anything else that the patient identifies as limiting their activity. The objective data derived from this low tech test can aid you in determining disease and symptom severity, helping to create a list of possible diagnoses and assisting you in the rational use of additional tests to further delineate the nature of the problem. This can be particularly helpful in providing objective information when symptoms seem out of proportion to findings. Or when patients report few complaints yet seem to have a cosiderable amount of disease. It will also generate a measurement that you can refer back to during subsequent evaluations in order to determine if there has been any real change in functional status.

Exam of the Heart

The major elements of the cardiac exam include observation, palpation and, most importantly, auscultation (percussion is omitted). As with all other areas of the physical exam, establishing adequate exposure and a quiet environment are critical. Initially, the patient should rest supine with the upper body elevated 30 to 45 degrees. Most exam tables have an adjustable top. If not, use 2 or 3 pillows. Remember that although assessment of pulse and blood pressure are discussed in the vital signs section they are actually important elements of the cardiac exam. Observation: Assessment for distention of the right Internal Jugular vein (IJ) is a difficult skill. Its importance lies in the fact that the IJ is in straight-line communication with the right atrium. The IJ can therefore function as a manometer, with distention indicating elevation of Central Venous Pressure (CVP). This in turn is an important marker of intravascular volume status and related cardiac function. The focus here is on simply determining whether or not Jugular Venous Distention (JVD) is present. A discussion of the a, c and v waves that make up the jugular venous pulsations can be found elsewhere. These are quite difficult to detect for even the most seasoned physician. Why is JVD so hard to assess? The IJ lies deep to skin and soft tissues, which can provide quite a bit of cover. Additionally, this blood vessel is under much lower pressure

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then the adjacent, pulsating carotid artery. It therefore takes a sharp eye to identify the relatively weak, transmitted venous impulses. A few things to remember: 1. Think anatomically. The right IJ runs between the two heads (sternal and clavicular) of the sternocleidomastoid muscle (SCM) and up in front of the ear. This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement. The two heads form the sides of a small triangle, with the clavicle making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks. Note, you are trying to identify impulses originating from the IJ and transmitted to the overlying skin in this area. You can't actually see the IJ. The External Jugular (EJ) runs in an oblique direction across the sternocleidomastoid and, in contrast to the IJ, can usually be directly visualized. If the EJ is not readily apparent, have the patient look to the left and valsalva. This usually makes it quite obvious. EJ distention is not always a reliable indicator of elevated CVP as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when CVP is normal. It also makes several turns prior to connecting with the central venous system and is thus not in a direct line with the right atrium.

2. Take your time. Look at the area in question for several minutes while the patient's head is turned to the left. The carotid artery is adjacent to the IJ, lying just medial to it. If you are unsure whether a pulsation is caused by the carotid or the IJ, place your hand on the patient's radial artery and use this as a reference. The carotid impulse coincides with the palpated radial artery pulsation and is characterized by a single upstroke timed with systole. The venous impulse (at

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3.

4. 5.

6.

least when the patient is in sinus rhythm and there is no tricuspid regurgitation) has three components, each associated with the aforementioned a, c and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin. In contrast, the carotid causes a single up and down pulsation. Furthermore, the carotid is palpable. The IJ is not and can, in fact, be obliterated by applying pressure in the area where it emerges above the clavicle. Search along the entire projected course of the IJ as the top of the pressure wave (which is the point that you are trying to identify) may be higher then where you are looking. In fact, if the patient's CVP is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else their will be no identifiable "top" of the column as the entire IJ will be engorged). After you've found the top of the wave, see what effect sitting straight up and lying down flat have on the height of the column. Sitting should cause it to appear at a lower point in the neck, while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest. Shine a pen light tangentially across the neck. This sometimes helps to accentuate the pulsations. If you are still uncertain, apply gentle pressure to the right upper quadrant of the abdomen for 5 to 10 seconds. This elicits Hepato-Jugular Reflux which, in pathologic states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the IJ, making the transmitted pulsations more apparent. Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure. Once you identify JVD, try to estimate how high in cm the top of the column is above the Angle of Louis. The angle is the site of the joint which connects the manubrium with the rest of the sternum. First identify the supra-sternal notch, a concavity at the top of the manubrium. Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch. This is roughly at the level of the 2nd intercostal space. The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the right atrium with the patient lying at a 45 degree angle. The sum is an estimate of the CVP. However, if you can simply determine with some accuracy whether JVD is present or not, you will be way ahead of he game! Normal is 7-9 cm.

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Bony Structures of the Chest

Finding the Angle of Louis:The wooden Q-tips highlight the different slopes of the sternum and manubrium. The point at which the Q-tips cross is the Angle of Louis.

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Determining the CVP Take some time to look across the left chest and try to identify the transmitted impulse caused by ventricular contraction, which may be apparent when contractions are particularly vigorous. Palpation: The palm of your right hand is placed across the patient's left chest so that it covers the area over the heart. The heel should rest along the sternal border with the extended fingers lying below the left nipple. Focus on several things: Palpation of the Precordium to Determine the Location of the PMI

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1. Can you feel a Point of Maximum Impulse (PMI) related to contraction at the apex of the underlying left ventricle? If so, where is it located? After identifying the rough position with the palm of your hand, try to pin down the precise location with the tip of your index finger. The normal sized and functioning ventricle will generate a penny sized impulse that is best felt in the mid-clavicular line, roughly at the 5th intercostal space. If the ventricle becomes dilated, most commonly as the result of past infarcts and always associated with ventricular dysfunction, the PMI is displaced laterally. In cases of significant enlargement, the PMI will be located near the axilla. Occasionally, the PMI will not localize to any one area, which does not necessarily indicate ventricular enlargement or dysfunction. Obesity and COPD may also limit your ability to identify its precise location. Palpating while the patient is in the left lateral decubitus position can make the PMI more obvious. 2. What is the duration of the impulse? In the setting of hypertension or any other state of chronic pressure overload, the ventricle hypertrophies and the PMI becomes sustained (i.e. you feel the impulse for a longer period of time). This is actually pretty subjective and can be tough to detect. Note that hypertrophy and dilatation are not synonymous. They can exist separately or in conjunction with one another. 3. How vigorous is the transmitted impulse? Processes associated with ventricular hypercontractility (e.g. compensated mitral regurgitation or aortic insufficiency that result in exceptionally large stroke volumes) generate an impulse of unusual vigor. 4. Do you feel a thrill, a vibratory sensation produced by turbulent blood flow that is usually secondary to valvular abnormalities? The feeling is similar to that produced when you squeeze on a garden hose, partially obstructing the flow of water. The location of the thrill will depend on the involved valve (e.g. thrills caused by aortic stenosis are best felt toward the right upper sternal border). If a loud murmur is detected during auscultation, you may then go back and reassess for the presence of a thrill. In general, thrills are an uncommon finding. *Palpation of the precordium of a female patient is best done by placing the palm of your right hand directly beneath the patient's left breast such that the edge of your index finger rests against the inferior surface of the breast. Make sure that you tell that patient what you are about to do (and why) before actually performing this maneuver. Remember that with age tissue turgor often declines, causing the breasts to hang below the level of the heart. 5. Carotid Artery Palpation: This is of greatest value during the assessment of aortic valvular and out flow tract disease (see below) and should thus be performed after auscultation so that you know whether or not these problems exist prior to palpation. However, for the sake of completeness it will be described here. The carotids can be located by sliding the second and third finger of either hand along the side of the trachea at the level of the thyroid cartilage (i.e. adams apple). The carotid pulsation is palpable just lateral to the groove formed by the trachea and the surrounding soft tissue. The quantity of subcutaneous fat will dictate how firmly you need to push. The pulsations should be easily palpable. Diminution may be caused by atherosclerosis, aortic stenosis, or severely impaired ventricular 54

performance. Do not push on both sides simultaneously as this may compromise cerebral blood flow.

Auscultation: The following anatomic pictures will aid you in understanding the principles of cardiac auscultation.

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1. Become comfortable with your stethescope. There are multiple brands on the market, each of which incorporates its own version of a bell (low pitched sounds) and diaphragm (higher pitched sounds). Some have the diaphragm and bell on opposite sides of the head piece. Others have the bell and diaprhragm built into a single side, with the bell engaged by applying light pressure and the diaphragm engaged by pushing more firmly. Adult, pediatric, and newborn sizes also exist. And some combine adult and pediatric scopes into a single unit. Take the time to read the instructions for your particular model so that you are familiar with how to use it correctly. Several sample stethescopes are pictured below. It's worth mentioning that almost any commercially available scope will do the job. The most important "part" is what sits betwen the ear pieces!

Adult Stethoscope

Adult Stethoscope: Diaphragm and Bell Incorporated Into Single Side.

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Combination Adult & Pediatric Stethoscope

Newborn Stethoscope

2. Engage the diaphragm of your stethescope and place it firmly over the 2nd right intercostal space, the region of the aortic valve. Then move it to the other side of the sternum and listen in the 2nd left intercostal space, the location of the pulmonic valve. Move down along the sternum and listen over the left 4th intercostal space, the region of the tricuspid valve. And finally, position the diaphragm over the 4th intercostal space, left midclavicular line to examine the mitral area. These locations are rough approximations and are generally determined by visual estimation. In each area, listen specifically for S1 and then S2. S1 will be loudest over the left 4th intercostal space (mitral/tricuspid valve areas) and S2 along the 2nd R and L intercostal spaces (aortic/pulomonic valve regions). Note that the time between S1 and S2 is shorter then that between S2 and S1. This should help you to decide which sound is produced by the closure of the mitral/tricuspid and which by the aortic/pulmonic valves and therefore when systole and diastole occur. Compare the relative intensities of S1 and S2 in these different areas. Auscultation of the Heart

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3. In younger patients, you should also be able to detect physiologic splitting of S2. That is, S2 is made up of 2 components, aortic (A2) and pulmonic (P2) valve closure. On inspiration, venous return to the heart is augmented and pulmonic valve closure is delayed, allowing you to hear first A2 and then P2. On expiration, the two sounds occur closer together and are detected as a single S2. Ask the patient to take a deep breath and hold it, giving you a bit more time to identify this phenomenon. The two components of S1 (mitral and tricuspid valve closure) occur so close together that splitting is not appreciated.

4. You may find it helpful to tap out S1 and S2 with your fingers as you listen, accentuating the location of systole and diastole and lending a visual component to this exercise. While most clinicians begin asucultation in the aortic area and then move across the precordium, it may actually make more sense to begin laterally (i.e. in the mitral area) and then progress towards the right and up as this follows the direction of blood flow. Try both ways and see which feels more comfortable. 5. Listen for extra heart sounds (a.k.a. gallops). While present in normal subjects up to the ages of 20-30, they represent pathology in older patients. An S3 is most commonly associated with left ventricular failure and is caused by blood from the left atrium slamming into an already overfilled ventricle during early diastolic filling. The S4 is a sound created by blood trying to enter a stiff, non-compliant left ventricle during atrial contraction. It's most frequently associated with left ventricular hypertrophy that is the result of long standing hypertension. Either sound can be detected by gently laying the bell of the stethoscope over the apex of the left ventricle (roughly at the 4th intercostal space, mid-clavicular line) and 58

listening for low pitched "extra sounds" that either follow S2 (i.e. an S3) or precede S1 (i.e. an S4). These sounds are quite soft, so it may take a while before you're able to detect them. Positioning the patient on their left side while you listen may improve the yield of this exam. The presence of both an S3 and S4 simultaneously is referred to as a summation gallop. Listening for Extra Heart Sounds

6. Murmurs: These are sounds that occur during systole or diastole as a result of turbulent blood flow. Traditionally, students are taught that auscultation is

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performed over the 4 areas of the precordium that roughly correspond to the "location" of the 4 valves of the heart (i.e. aortic valve area ='s the 2nd Right Intercostal Space, pulmonic valve area ='s the 2nd LICS, tricuspid valve area ='s 4th LICS, and mitral valve area ='s 4th LICS in the midclavicular line). This leads to some misperceptions. Valves are not strictly located in these areas nor are the sounds created by valvular pathology restricted to those spaces. So, while it might be OK to listen in only 4 places when conducting the normal exam, it is actually quite helpful to listen in many more when any abnormal sounds are detected. If you hear a murmur, ask yourself: a. Does it occur during systole or diastole? b. What is the quality of the sound (i.e. does it get louder and then softer; does it maintain the same intensity throughout; does it start loud and become soft)? It sometimes helps to draw a pictoral representation of the sound. c. What is the quantity of the sound? The rating system for murmurs is as follows: 1/6 Can only be heard with careful listening 2/6 Readily audible as soon as the stethescope is applied to the chest 3/6 Louder then 2/6 4/6 As loud as 3/6 but accompanied by a thrill 5/6 Audible even when only the edge of the stethescope touches the chest 6/6 Audible to the naked ear Most murmurs are between 1/6 and 3/6. Louder generally (but not always) indicates greater pathology. d. What is the relationship of the murmur to S1 and S2 (i.e. when does it start and stop)? e. What happens when you march your stethescope from the 2nd RICS (the aortic area) out towards the axilla (the mitral area)? Where is it loudest and in what directions does it radiate? By moving in small increments (i.e. listening in 8 or 10 places along the chest wall) you will be more likely to detect changes in the character of a particular murmur and thus have a better chance of determining which valve is affected and by what type of lesion. 7. Auscultation over the carotid arteries (see under aortic stenosis for additional information): In the absence of murmurs suggestive of aortic valvular disease, you can listen for carotid bruits (sounds created by turbulent flow within the blood vessel) at this point in the exam. Place the diaphragm gently over each carotid and listen for a soft, high pitched "shshing" sound. It's helpful if the patient can hold their breath as you listen so that you are not distracted by transmitted tracheal sounds. The meaning of a bruit remains somewhat controversial. I was taught that bruits represented turbulent flow associated with intrinsic atherosclerotic disease and that the disappearance of a bruit which was previously present was a sign that the lesion was progressing (i.e. further encroachment on the lumen of the vessel). However, a number of studies provide evidence that atherosclerotic disease is frequently absent when a bruit is present as well as the reverse situation. This is actually of clinical importance because recent data suggest that it may be 60

beneficial to surgically repair carotid disease in patients who have significant stenosis yet have not experienced any symptoms (e.g. Transient ischemic attacks or strokes. Surgery in these settings has already proven to be beneficial). Thus, it is becoming increasingly important to determine the best way of identifying asymptomatic carotid artery disease... and carotid auscultation may, in fact, not be the mechanism of choice! 8. Identifying the Most Common Murmurs: 9. 1. Systolic Murmurs: In the adult population, these generally represent either aortic stenosis or mitral regurgitation. To distinguish between them, remember the following: 10. Murmurs of Aortic Stenosis (AS): a. Tend to be loudest along the upper sternal borders and get softer as you move down and out towards the axilla. There is, however, a phenomenon referred to at the Gallavardin Effect which can cause murmurs of AS to sound as loud towards the axilla as they do over the aortic region. When this occurs, the shape of the sound should be similar in both regions, helping you to distinguish it from MR (see below). b. Have a growling, harsh quality (i.e. get louder and then softer.. also referred to as a crescendo decrescendo, systolic ejection, or diamond shaped murmur). When the stenosis becomes more severe, the point at which the murmur is loudest (i.e. its peak intensity) occurs later in systole, as it takes longer to generate the higher ventricular pressure required to push blood through the tight orifice.

c. Are better heard when the patient sits up and exhales. d. Are heard in the carotid arteries and over the right clavicle. Radiation to the clavicle can be appreciated by simply resting the diaphragm on the right clavicle. To assess for transmission to the carotids, have the patient hold their breath while you listen over each artery using the diaphragm of your stethescope. Carotid bruits can be confused with the radiating murmur of aortic stenosis. In general, carotid bruits are softer. Also, murmurs associated with aortic pathology should be audible in both carotids and get louder as you move down the vessel, towards the chest. In settings where carotid pathology coexists with aortic stenosis, a loud transmitted murmur associated with a valvular lesion may overwhelm any sound caused by intrinsic carotid disease, masking it completely. e. Carotid upstrokes refer to the quantity and timing of blood flow into the carotids from the left ventricle. They can be affected by aortic stenosis and must be assessed whenever you hear a murmur that could be consistent with AS. This is done by placing your fingers on the carotid artery as 61

described above while you simultaneously listen over the chest. There should be no delay between the onset of the murmur, which marks the beginning of systole, and when you feel the pulsation in the carotid. In the setting of critical (i.e. very severe) aortic stenosis, small amounts of blood will be ejected into the carotid and there will be a lag between when you hear the murmur and feel the impulse. This is referred to as diminished and delayed upstrokes (a.k.a. parvus et tardus), as opposed to the full and prompt inflow which occurs in the absence of disease. Mild or moderate stenosis does not alter the character of carotid in-flow. f. Sub-Aortic stenosis is a relatively rare condition where the obstruction of flow from the left ventricle into the aorta is caused by an in-growth of septal tissue in the region below the aortic valve known as the aortic outflow tract. It causes a crescendo-decrescendo murmur that sounds just like aortic stenosis. As opposed to AS, however, the murmur is louder along the left lower sternal border and out towards the apex. This makes anatomic sense as the obstruction is located near this region. It also does not radiate loudly to the carotids as the point of obstruction is further from these vessels in comparison with the aortic valve. You may also be able to palpate a bisferiens pulse in the carotid artery (see under aortic insufficiency). Furthermore, the murmur will get softer if the ventricle is filled with more blood as filling pushes the abnormal septum away from the opposite wall, decreasing the amount of obstruction. Conversely, it gets louder if filling is decreased. This phenomenon can actually be detected on physical exam and is a useful way of distinguishing between AS and sub-aortic obstruction. Ask the patient to valsalva while you listen. This decreases venous return and makes the murmur louder (and will have the opposite effect on a murmur of AS). Then, again while listening, squat down with the patient. This maneuver increases venous return, causing the murmur to become softer. Standing will cause the opposite to occur. You need to listen for 20 seconds or so after each change in position to really appreciate any difference. Because the degree of obstruction can vary with ventricular filling, sub-aortic stenosis is referred to as a dynamic outflow tract obstruction. In aortic stenosis, the degree of obstruction that exists at any given point in time is fixed. Murmurs of Mitral Regurgitation (MR): g. Sound the same throughout systole. h. Generally do not have the harsh quality associated with aortic stenosis. In fact, they sound a bit like the "shshing" noise produced when you pucker your lips and blow through clenched teeth. i. Get louder as you move your stethescope towards the axilla. j. Will get even louder if you roll the patient onto their left side while keeping your stethescope over the mitral area of the chest wall and listening as they move. This maneuver brings the chamber receiving the regurgitant volume, the left atrium, closer to your stethescope, accentuating the murmur.

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k. Get louder if afterload is suddenly increased, which can be accomplished by having the patient close their hands tightly. MR is also affected by the volume of blood returning to the heart. Squatting increases venous return, causing a louder sound. Standing decreases venous return, thereby diminishing the intensity of the murmur.

Sometimes murmurs of aortic stenosis and mitral regurgitation co-exist, which can be difficult to sort out on exam. Moving your stethescope back and forth between the mitral and aortic areas will allow for direct comparison, which may help you decide if more then one type of lesion is present or if the quality of the murmur is the same in both locations, changing only in intensity (i.e. consistent with a one valve problem). 2. Diastolic Murmurs: Tend to be softer and therefore much more difficult to hear then those occurring during systole. This makes physiologic sense as diastolic murmurs are not generated by high pressure ventricular contractions. In adults they may represent either aortic regurgitation or mitral stenosis, neither of which is too common. While systolic murmurs are often obvious, you will probably not be able to detect diastolic murmurs on your own until you have had them pointed out by a more experienced examiner. Aortic Regurgitation (AR); a.k.a. Aortic Insufficiency (AI):

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l. Is best heard along the left para-sternal border, as this is the direction of the regurgitant flow. m. Becomes softer towards the end of diastole (a.k.a. decrescendo). n. Can be accentuated by having the patient sit up, lean forward and exhale while you listen. o. Occasionally accompanies aortic stenosis, so listen carefully for regurgitation in patients with AS. p. Will cause the carotid upstrokes to feel extraordinarily full as significant regurgitation increases ventricular pre-load, resulting in ejection of an augmented stroke volume. AI can also produce a double peaked pulsation in the carotids known as a bisferiens pulse, which is quite difficult to appreciate. Feeling your own carotid impulse at the same time that you're palpating the patient's may accentuate this finding. In cases of co-existent AS and AI, a bisferiens pulse suggests that the AI is the dominant problem. It may also be present with sub-aortic stenosis (see above), helping to distinguish it from AS. Mitral Stenosis (MS): q. Heard best towards the axilla r. Can be accentuated by having the patient role onto their left side while you listen with the bell of your sthethescope. s. Associated with a soft, low pitched sound preceding the murmur, called the opening snap. This is the noise caused by the calcified valve "snapping" open. It can, however, be pretty hard to detect. Auscultation, an ordered approach: Try to focus on each sound individually and in a systematic fashion. Ask yourself: Do I hear S1? Do I hear S2? What is their relative intensities in each of the major valvular areas? Is S2 split physiologically? Are there extra sounds before S1or after S2 (i.e. an S4 or S3)? Is there a murmur during systole? Is there a murmur during diastole? If a murmur is present, how loud is it? What is its character? Where does it radiate? Are there any maneuvers which affect its intensity? Remember that these sounds are created by mechanical events in the heart. As you listen, remind yourself what is happening to produce each of them. By linking auscultatory findings with physiology, you can build a case in your mind for a particular lesion. Interrelationship of Cardiac Events & Sounds

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This diagram courtesy of Dr. Wilbur Lew, Department of Medicine, San Diego VA Medical Center.

A few final comments about auscultation: 1. Pulmonic valve murmurs are rare in the adult population and, even when present, are difficult to hear due to the relatively low pressures generated by the right side of the heart. 2. Tricuspid regurgitation (TR) is relatively common, most frequently associated with elevated left sided pressures which are then transmitted to the right side of the heart (though a number of other processes can cause TR as well). In this setting, both mitral and tricuspid regurgitation often co-exist. The murmur of MR is generally louder then that of TR, again due to the higher pressures on the left side of the heart. It can therefore be difficult to sort out if there is co-existent TR when MR is present. Try to listen along both the low left and right sternal borders (areas where the 65

3.

4.

5.

6.

tricuspid valve is best assessed) and compare this to the mitral area. Move your stethoscope slowly across the precordium and note if there is any change in the character/intensity of the murmur. TR murmurs are also accentuated by inhalation, which increases venous return and therefore flow across the valve. Patients with COPD (emphysema) often have very soft heart sounds. Air trapping and subsequent lung hyperinflation results in a posterior-inferior rotation of the heart away from the chest wall and causes the interposition of lung between the chest wall and heart. In this setting, heart sounds can be accentuated by having the patient lean forward and fully exhale prior to listening. Furthermore, in any patient with particularly "noisy" breath sounds, it may be helpful to ask them to hold their breath (if they're able) while you examine the heart. Rubs: These are uncommon sounds produced when the parietal and visceral pericardium become inflamed, generating a creaky-scratchy noise as they rub together. The classic rub is actually made up of three sounds, associated with atrial contraction, ventricular contraction, and ventricular filling. In reality, its rare to hear all 3 components (more commonly, 2 are apparent). They can be accentuated by listening when the patient sits up, leans forward and exhales, bringing the two layers in closer communication. I feel compelled to mention this finding only because a common short hand for reporting the results of the cardiac exam comments on the absence of "Gallops, murmurs, or rubs," implying (incorrectly) that rubs are a frequent finding. If a patient has an abnormal heart sound due to a structural defect that has been quantified by echocardiography, make sure that you compare your findings to those identified during the study. This is a great way of learning! Don't get frustrated! Auscultation is a difficult skill to "master" and we are all continually refining our techniques. Take your time. Make sure the room is quiet. Be patient. Ask for help frequently. Read about particular murmurs and their pathophysiology when you encounter them. A number of the more subtle findings (e.g. an S3 or S4) can be very difficult

2. 1. to identify when the patient is tachycardic, a not uncommon scenario as this is one of the compensatory mechanisms for dealing with the dysfunction that has generated these findings in the first place. Re-examination after the patient has made clinical improvement may be more revealing. In general, many of the above techniques are not used when examining every patient. If the exam is normal, it would be neither efficient nor revealing to put a patient through all of these maneuvers. The goal is to have a "bag of skills" at your disposal that you can reach into and employ to better define abnormalities when they present themselves.

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Exam of the Abdomen

The major components of the abdominal exam include: observation, auscultation, percussion, and palpation. While these are the same elements which make up the pulmonary and cardiac exams, they are performed here in a slightly different order (i.e. auscultation before percussion) and carry different degrees of importance. Pelvic, genital, and rectal exams, all part of the abdominal evaluation, are discussed elsewhere. Think Anatomically: When looking, listening, feeling and percussing imagine what organs live in the area that you are examining. The abdomen is roughly divided into four quadrants: right upper, right lower, left upper and left lower. By thinking in anatomic terms, you will remind yourself of what resides in a particular quadrant and therefore what might be identifiable during both normal and pathologic states.

Topical Anatomy of the Abdomen

Quadrants of the Abdomen

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By convention, the abdominal exam is performed with the provider standing on the patient's right side. Observation: Much information can be gathered from simply watching the patient and looking at the abdomen. This requires complete exposure of the region in question, which is accomplished as follows: 1. Ask the patient to lie on a level examination table that is at a comfortable height for both of you. At this point, the patient should be dressed in a gown and, if they wish, underwear. 2. Take a spare bed sheet and drape it over their lower body such that it just covers the upper edge of their underwear (or so that it crosses the top of the pubic region if they are completely undressed). This will allow you to fully expose the abdomen while at the same time permitting the patient to remain somewhat covered. The gown can then be withdrawn so that the area extending from just below the breasts to the pelvic brim is entirely uncovered, remembering that the superior margin of the abdomen extends beneath the rib cage. 3. The patient's hands should remain at their sides with their heads resting on a pillow. If the head is flexed, the abdominal musculature becomes tensed and the examination made more difficult. Allowing the patient to bend their knees so that the soles of their feet rest on the table will also relax the abdomen. Draping the Abdomen

4. The patient's hands should remain at their sides with their heads resting on a pillow. If the head is flexed, the abdominal musculature becomes tensed and the examination made more difficult. Allowing the patient to bend their knees so that the soles of their feet rest on the table will also relax the abdomen. 5. Keep the room as warm as possible and make sure that the lighting is adequate. By paying attention to these seemingly small details, you create an environment that gives you the best possible chance of performing an accurate examination. This is particularly important early in your careers, when your skills are relatively

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unrefined. However, it will also stand you in good stead when examining obese, anxious, distressed or otherwise challenging patients. While observing the patient, pay particular attention to: 1. Appearance of the abdomen. Is it flat? Distended? If enlarged, does this appear symmetric or are there distinct protrusions, perhaps linked to underlying organomegaly? The contours of the abdomen can be best appreciated by standing at the foot of the table and looking up towards the patient's head. Global abdominal enlargement is usually caused by air, fluid, or fat. It is frequently impossible to distinguish between these entities on the basis of observation alone (see below for helpful maneuvers). Areas which become more pronounced when the patient valsalvas are often associated with ventral hernias. These are points of weakening in the abdominal wall, frequently due to previous surgery, through which omentum/intestines/peritoneal fluid can pass when intra-abdominal pressure is increased. 2. Presence of surgical scars or other skin abnormalities. 3. Presence of surgical scars or other skin abnormalities. 4. Patient's movement (or lack thereof). Those with peritonitis (e.g. appendicitis) prefer to lie very still as any motion causes further peritoneal irritation and pain. Contrary to this, patients with kidney stones will frequently writhe on the examination table, unable to find a comfortable position.

Various Causes of Abdominal Distension

Obese abdomen

Hepatomegaly

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Ascites

Markedly enlarged gall bladder (labeled "GB")

Umbilical Hernia

Same umbilical hernia while patient performs valsalva maneuver.

5. Presence of surgical scars or other skin abnormalities. 6. Patient's movement (or lack thereof). Those with peritonitis (e.g. appendicitis) prefer to lie very still as any motion causes further peritoneal irritation and pain. Contrary to this, patients with kidney stones will frequently writhe on the examination table, unable to find a comfortable position. Auscultation: Compared to the cardiac and pulmonary exams, auscultation of the abdomen has a relatively minor role. It is performed before percussion or palpation as vigorously touching the abdomen may disturb the intestines, perhaps artificially altering their activity and thus bowel sounds. Exam is made by gently placing the pre-warmed (accomplished by rubbing the stethoscope against the front of your shirt) diaphragm on the abdomen and listening for 15 or 20 seconds. There is no magic time frame. The stethoscope can be placed over any area of the abdomen as there is no true compartmentalization and sounds produced in one area can probably be heard throughout. How many places should you listen in? Again, there is no magic answer. At this stage, practice listening in each of the four quadrants and see if you can detect any "regional variations."

Abdominal Auscultation

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What exactly are you listening for and what is its significance? Three things should be noted: 1. Are bowel sounds present? 2. If present, are they frequent or sparse (i.e. quantity)? 3. What is the nature of the sounds (i.e. quality)? As food and liquid course through the intestines by means of peristalsis noise, referred to as bowel sounds, is generated. These sounds occur quite frequently, on the order of every 2 to 5 seconds, although there is a lot of variability. Bowel sounds in and of themselves do not carry great significance. That is, in the normal person who has no complaints and an otherwise normal exam, the presence or absence of bowel sounds is essentially irrelevant (i.e. whatever pattern they have will be normal for them). In fact, most physicians will omit abdominal auscultation unless there is a symptom or finding suggestive of abdominal pathology. However, you should still practice listening to all the patients that you examine so that you develop a sense of what constitutes the range of normal. Bowel sounds can, however, add important supporting information in the right clinical setting. In general, inflammatory processes of the serosa (i.e. any of the surfaces which cover the abdominal organs....as with peritonitis) will cause the abdomen to be quiet (i.e. bowel sounds will be infrequent or altogether absent). Inflammation of the intestinal mucosa (i.e. the insides of the intestine, as might occur with infections that cause diarrhea) will cause hyperactive bowel sounds. Processes which lead to intestinal obstruction initially cause frequent bowel sounds, referred to as "rushes." Think of this as the intestines trying to force their contents through a tight opening. This is followed by decreased sound, called "tinkles," and then silence. Alternatively, the reappearance of bowel sounds heralds the return of normal gut function following an injury. After abdominal surgery, for example, there is a period of several days when the intestines lie dormant. The appearance of bowel sounds marks the return of intestinal activity, an important phase of the patient's recovery. Bowel sounds, then, must be interpreted within the context of the particular clinical situation. They lend supporting information to other findings but are not in and of themselves pathognomonic for any particular process.

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After you have finished noting bowel sounds, use the diaphragm of your stethoscope to check for renal artery bruits, a high pitched sound (analogous to a murmur) caused by turbulent blood flow through a vessel narrowed by atherosclerosis. The place to listen is a few cm above the umbilicus, along the lateral edge of either rectus muscles. Most providers will not routinely check for bruits. However, in the right clinical setting (e.g. a patient with some combination of renal insufficiency, difficult to control hypertension and known vascular disease), the presence of a bruit would lend supporting evidence for the existence of renal artery stenosis. When listening for bruits, you will need to press down quite firmly as the renal arteries are retroperitoneal structures. Atherosclerosis distal to the aorta (i.e. at the take off of the Iliac Arteries) can also generate bruits. Blood flow through the aorta itself does not generate any appreciable sound. Thus, auscultation over this structure is not a good screening test for the presence of aneurysmal dilatation. Percussion: The technique for percussion is the same as that used for the lung exam. First, remember to rub your hands together and warm them up before placing them on the patient. Then, place your left hand firmly against the abdominal wall such that only your middle finger is resting on the skin. Strike the distal interphalangeal joint of your left middle finger 2 or 3 times with the tip of your right middle finger, using the previously described floppy wrist action (see under lung exam). There are two basic sounds which can be elicited: 1. Tympanitic (drum-like) sounds produced by percussing over air filled structures. 2. Dull sounds that occur when a solid structure (e.g. liver) or fluid (e.g. ascites) lies beneath the region being examined. *Special note should be made if percussion produces pain, which may occur if there is underlying inflammation, as in peritonitis. This would certainly be supported by other historical and exam findings. Abdominal Percussion

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What can you really expect to hear when percussing the normal abdomen? The two solid organs which are percussable in the normal patient are the liver and spleen. In most cases, the liver will be entirely covered by the ribs. Occasionally, an edge may protrude a centimeter or two below the costal margin. The spleen is smaller and is entirely protected by the ribs. To determine the size of the liver, proceed as follows: 1. Start just below the right breast in a line with the middle of the clavicle, a point that you are reasonably certain is over the lungs. Percussion in this area should produce a relatively resonant note. 2. Move your hand down a few centimeters and repeat. After doing this several times, you will be over the liver, which will produce a duller sounding tone. 3. Continue your march downward until the sound changes once again. This may occur while you are still over the ribs or perhaps just as you pass over the costal margin. At this point, you will have reached the inferior margin of the liver. The total span of the normal liver is quite variable, depending on the size of the patient (between 6 and 12 cm). Don't get discouraged if you have a hard time picking up the different sounds as the changes can be quite subtle, particularly if there is a lot of subcutaneous fat. 4. The resonant tone produced by percussion over the anterior chest wall will be somewhat less drum like then that generated over the intestines. While they are both caused by tapping over air filled structures, the ribs and pectoralis muscle tend to dampen the sound. 5. Speed percussion, as described in the pulmonary section, may also be useful. Orient your left hand so that the fingers are pointing towards the patients head. Percuss as you move the hand at a slow and steady rate from the region of the right chest, down over the liver and towards the pelvis. This maneuver helps to accentuate different percussion notes, perhaps making the identification of the liver's borders a bit more obvious. Percussion of the spleen is more difficult as this structure is smaller and lies quite laterally, resting in a hollow created by the left ribs. When significantly enlarged, percussion in the left upper quadrant will produce a dull tone. Splenomegaly suggested by percussion should then be verified by palpation (see below). The remainder of the normal abdomen is, for the most part, filled with the small and large intestines. Try percussing each of the four quadrants to get a sense of the normal variations in sound that are produced. These will be variably tympanitic, dull or some combination of the above, depending on whether the underlying intestines are gas or liquid filled. The stomach "bubble" should produce a very tympanitic sound upon percussion over the left lower rib cage, close to the sternum. Percussion can be quite helpful in determining the cause of abdominal distention, particularly in distinguishing between fluid (a.k.a. ascites) and gas. Of the techniques used to detect ascites, assessment for shifting dullness is perhaps the most reliable and reproducible. This method depends on the fact that air filled intestines will float on top of any fluid that is present. Proceed as follows: 1. With the patient supine, begin percussion at the level of the umbilicus and proceed down laterally. In the presence of ascites, you will reach a point where 73

the sound changes from tympanitic to dull. This is the intestine-fluid interface and should be roughly equidistant from the umbillicus on the right and left sides as the fluid layers out in a gravity-dependent fashion, distributing evenly across the posterior aspect of the abdomen. It should also cause a symmetric bulging of the patient's flanks. 2. Mark this point on both the right and left sides of the abdomen and then have the patient roll into a lateral decubitus position (i.e. onto either their right or left sides). 3. Repeat percussion, beginning at the top of the patient's now up-turned side and moving down towards the umbilicus. If there is ascites, fluid will flow to the most dependent portion of the abdomen. The place at which sound changes from tympanitic to dull will therefore have shifted upwards (towards the umbillicus) and be above the line which you drew previously. Speed percussion (described above) may also be used to identify the location of the air-fluid interface. If the distention is not caused by fluid (e.g. secondary to obesity or gas alone), no shifting will be identifiable. The models below should help to clarify the concept of shifting dullness. With the "patient" lying flat on their back balloons (representing the intestines) float on the water (representing ascites). When the "patient" turns on their right side, a new air fluid level is established.

Shifting Dullness (real patient)

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Realize that there has to be a lot of ascites present for this method to be successful as the abdomen and pelvis can hide several hundred cc's of fluid that would be undetectable on physical exam. Also, shifting dullness is based on the assumption that fluid can flow freely throughout the abdomen. Thus, in cases of prior surgery or infection with resultant adhesion formation, this may not be a very useful technique. Palpation can also be used to check for ascites (see below). Palpation: First warm your hands by rubbing them together before placing them on the patient. The pads and tips (the most sensitive areas) of the index, middle, and ring fingers are the examining surfaces used to locate the edges of the liver and spleen as well as the deeper structures. You may use either your right hand alone or both hands, with the left resting on top of the right. Apply slow, steady pressure, avoiding any rapid/sharp movements that are likely to startle the patient or cause discomfort. Examine each quadrant separately, imagining what structures lie beneath your hands and what you might expect to feel. 1. Start in the right upper quadrant, 10 centimeters below the rib margin in the midclavicular line. This should insure that you are below the liver edge. In general, it is easier to detect abnormal if you start in an area that you're sure is normal. Gently push down (posterior) and towards the patient's head with your hand oriented roughly parallel to the rectus muscle, allowing the greatest number of fingers to be involved in the exam as you try to feel the edge of the liver. Advance your hands a few cm cephelad and repeat until ultimately you are at the bottom margin of the ribs. Initial palpation is done lightly. Abdominal Palpation

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2. Following this, repeat the examination of the same region but push a bit more firmly so that you are interrogating the deeper aspects of the right upper quadrant, particularly if the patient has a lot of subcutaneous fat. Pushing up and in while the patient takes a deep breath may make it easier to feel the liver edge as the downward movement of the diaphragm will bring the liver towards your hand. The tip of the xyphoid process, the bony structure at the bottom end of the sternum, may be directed outward or inward and can be mistaken for an abdominal mass. You should be able to distinguish it by noting its location relative to the rib cage (i.e. in the mid-line where the right and left sides meet). 3. You can also try to "hook" the edge of the liver with your fingers. To utilize this technique, flex the tips of the fingers of your right hand (claw-like). Then push down in the right upper quadrant and pull upwards (towards the patient's head) as you try to rake-up on the edge of the liver. This is a nice way of confirming the presence of a palpable liver edge felt during conventional examination Rib Cage

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4. You can also try to "hook" the edge of the liver with your fingers. To utilize this technique, flex the tips of the fingers of your right hand (claw-like). Then push down in the right upper quadrant and pull upwards (towards the patient's head) as you try to rake-up on the edge of the liver. This is a nice way of confirming the presence of a palpable liver edge felt during conventional examination. Hooking Edge of the Liver

5. Place your right hand at the inferior and lateral border of the ribs, pushing down as you push up from behind with your left hand. If the right kidney is massively enlarged, you may be able to feel it between your hands. 6. Now examine the left upper quadrant. The normal spleen in not palpable. When enlarged, it tends to grow towards the pelvis and the umbilicus (i.e. both down and across). Begin palpating near the belly button and move slowly towards the ribs. Examine superficially and then more deeply. Then start 8-10 cm below the rib margin and move upwards. In this way, you will be able to feel enlargement in either direction. You can use your left hand to push in from the patient's left flank, directing an enlarged spleen towards your right hand. If the spleen is very big, you may even be able to "bounce" it back and forth between your hands. Splenomegaly is probably more difficult to appreciate then hepatomegaly. The liver is bordered by the diaphragm and can't move away from an examining hand. The spleen, on the other hand, is not so definitively bordered and thus has a tendency to float away from you as you palpate. So, examine in a slow, gentle fashion. The edge, when palpable, is soft, rounded, and rather superficial. Repeat the exam with the patient turned onto their right side, which will drop the spleen down towards your examining hand. 7. Exploration for the left kidney is performed in the same fashion as described for the right. Kidney pain, most commonly associated with infection, can be elicited on direct examination if the entire structure becomes palpable as a result of associated edema. This is generally not the case. However, as the kidney lies in

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the retroperitoneum, pounding gently with the bottom of your fist on the costovertebral angle (i.e. where the bottom-most ribs articulate with the vertebral column) will cause pain if the underlying kidney is inflamed. Known as costovertebral angle tenderness (CVAT), it should be pursued when the patient's history is suggestive of a kidney infection (e.g. fever, back pain and urinary tract symptoms). Posterior View: Location of the Kidneys

Gross Retroperitoneum Anatomy

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8. Examine the left and right lower quadrants, palpating first superficially and then deeper. A stool filled sigmoid colon or cecum are the most commonly identified structures on the left and right side respectively. The smooth dome of the bladder may rise above the pelvic brim and become palpable in the mid-line, though it needs to be quite full of urine for this to occur. Other pelvic organs can also occasionally be identified, most commonly the pregnant uterus, which is a firm structure that grows up and towards the umbillicus. The ovaries and fallopian tubes are not identifiable unless pathologically enlarged. 9. Finally, try to feel the abdominal aorta. First push down with a single hand in the area just above the umbillicus. If you are able to identify this pulsating structure with one hand, try to estimate its size. To do this, orient your hands so that the thumbs are pointed towards the patient's head. Then push deeply and try to position them so that they are on either side of the blood vessel. Estimate the distance between the palms (it should be no greater then roughly 3 cm). This is, admittedly, a crude technique. Remember also that the aorta is a retorperitoneal structure and can be very hard to appreciate in obese patients. There have been no reports of anyone actually causing the aorta to rupture using this maneuver, so don't be afraid to push vigorously. What can you expect to feel? In general, don't be discouraged if you are unable to identify anything. Remember that the body is designed to protect critically important organs (e.g. liver and spleen beneath the ribs; kidneys and pancreas deep in the retroperitoneum; etc.). It is, for the most part, during pathologic states that these organs become identifiable to the careful examiner. However, you will not be able to recognize abnormal until you become comfortable identifying variants of normal, a theme common to the examination of any part of the body. It is therefore important to practice all of these maneuvers on every patient that you examine. It's also quite easy to miss abnormalities if you rush or push too vigorously, so take your time and focus on the tips/pads of your fingers. Examining for a fluid wave: When observation and/or percussion are suggestive of ascites, palpation can be used as a confirmatory test. Ask the patient or an observer to place their hand so that it is oriented longitudinally over the center of the abdomen. They should press firmly so that the subcutaneous tissue and fat do not jiggle. Place your right hand on the left side of the abdomen and your left hand opposite, so that both are equidistant from the umbillicus. Now, firmly tap on the abdomen with your right hand while your left remains against the abdominal wall. If there is a lot of ascites present, you may be able to feel a fluid wave (generated in the ascites by the tapping maneuver) strike against the abdominal wall under your left hand. This test is quite subjective and it can be difficult to say with assurance whether you have truly felt a wave-like impulse.

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Assessing for a fluid wave

The abdominal examination, like all other aspects of the physical, is not done randomly. Every maneuver has a purpose. Think about what you're expecting to see, hear, or feel. Use information that you've gathered during earlier parts of the exam and apply it in a rational fashion to the rest of your evaluation. If, for example, a certain area of the abdomen was tympanitic during percussion, feel the same region and assure yourself that there is nothing solid in this location. Go back and repeat maneuvers to either confirm or refute your suspicions. In the event that a patient presents complaining of pain in any region of the abdomen, have them first localize the affected area, if possible with a single finger, pointing you towards the cause of the problem. Then, examine each of the other abdominal quadrants first before turning your attention to the area in question. This should help to keep the patient as relaxed as possible and limit voluntary and involuntary guarding (i.e. superficial muscle tightening which protects intra-abdominal organs from being poked), allowing you to gather the greatest amount of clinical data. Make sure you glance at the patient's face while examining a suspected tender area. This can be particularly revealing when evaluating otherwise stoic individuals (i.e. even these patients will grimace if the area is painful to the touch). The goal, of course, is to obtain relevant information while generating a minimal amount of discomfort. Findings Commonly Associated With Advanced Liver Disease: Chronic liver disease usually results from years of inflamation, which ultimately leads to fibrosis and decline in function. Histologically, this is referred to as Cirrhosis. This can be driven by a number of different processes, most commonly chronic alcohol use, viral hepatitis (B or C) or hemachromatosis (the complete list is much longer). It's important to realize that a cirrhotic liver can be markedly enlarged (in which case it may be palpable) or shrunken and fibrotic (non-palpable). After many years (generally greater then 20) of chronic insult, the liver may become unable to perform some or all of its normal functions. There are several clinical manifestations of this dysfunction. While none are pathonomonic for liver disease, in the

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right historical context they are very suggestive of underlying pathology. Some of the most common findings are described and/or pictured below. 1. Hyperbilirubinemia: The diseased liver may be unable to conjugate or secrete bilirubin appropriately. This can lead to a. Icterus - Yellow discoloration of the sclera. b. Jaundice - Yellow discoloration of the skin. c. Bilirubinuria - Golden-brown coloration of the urine. 2. Ascites: Portal vein hypertension results from increased resistance to blood flow through an inflamed and fibrotic liver. This can lead to ascites, accumulation of fluid in the peritoneal cavity. 3. Increased Systemic Estrogen Levels: The liver may become unable to process particular hormones, leading to their peripheral conversion into estrogen. High levels promote: a. Breast development (gynecomastia). b. Spider Angiomata - dilated arterioles most often visible on the skin of the upper chest. c. Testicular atrophy. 4. Lower Extremity Edema: Impaired synthesis of the protein alburmin leads to lower intravascular oncotic pressure and resultant leakage of fluid into soft tissues. This is particularly evident in the lower extremities. 5. Varices: In the setting of portal hypertension, blood "finds" alternative pathways back to the heart that do not pass through the liver. The most common is via the splenic and short gastric veins, which pass through the esophageal venous plexus enroute to the SVC. This causes esophageal varices which can bleed profoundly, though these are not apparent on physical examination. A much less common path utilizes the recanalized umbilical vein, which directs blood through dilated superficial veins in the abdominal wall. These are visible on inspection of the abdomen and are known as Caput Medusae.

Icterus

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Caput Medusae

Ascites

Jaundice

Edema

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The Upper Extremities

Exam of the hands and arms is usually quite brief in the asymptomatic patient. Pay particular attention to the following:

The Hands:
a. Appearance of hand and fingers: Any obvious deformity or discoloration? Do they appear relatively red and well perfused or white/mottled? b. Nail shape and color (see below for discussion of cyanosis): Several examples of common nail pathology are shown below.

Onycholysis: Onychomycosis: Separation of Nail Paronychia: Nicotine Staining Fungal Infection of from Underlying Infection of skin the Nail Bed, often due to adjacent to nail of onychomycosis. middle finger. c. Capillary refill: This is a mechanism for gauging arterial perfusion. Press the nail bed or tip of any finger for several seconds, causing the underlying skin to whiten. After releasing pressure, the normal pink color should return in 2-3 seconds. Delay implies under perfusion. Interestingly, while atherosclerotic vascular disease is a common cause of arterial insufficiency in the lower extremity, it rarely occurs in the arms or hands. Thus, delayed capillary refill in the hands more likely reflects vasospasm or hypovolemia then it does intraluminal arterial obstruction. Severe vasospasm, referred to as Raynaud's Phenomenon, occurs most frequently in women after exposure to cool temperatures, causing both hands to become white and painful.

Tissue death (i.e. gangrene) Peripheral Vascular Disease, Hand of the fingers secondary to severe peripheral vascular disease.

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d. Temperature: Cool hands occur most commonly as a result of exposure to a cold environment. However, this can also reflect vascular insufficiency, vasospasm, or hypovolemia. e. Obvious joint abnormalities, noting particularly if there is a specific pattern or distribution. For example, deformity of the metacarpal-phalyngeal joints on every finger of both hands is consistent with a systemic inflammatory process like Rheumatoid Arthritis. An isolated abnormality of a single, distal joint, however, is more likely secondary to local trauma or degenerative arthritis. Joint deformities secondary to rheumatoid arthritis

And a few words about uncommonly encountered abnormalities The presence or absence of these findings are frequently mentioned in clinical medicine, giving 84

the impression that they are common and/or of great importance. This is more myth then fact as most patients with the disease states in question do not have these findings. Their clinical utility tends to be over emphasized. a. Clubbing: Bulbous appearance of the distal phalanges of all fingers along with concurrent loss of the normal angle between the nail base and adjacent skin. This is most commonly associated with conditions that cause chronic hypoxemia (e.g. severe emphysema), though it is also associated with a number of other conditions. However, in general it is neither common nor particularly sensitive for hypoxia, as most hypoxic patients do not have clubbing. b. Cyanosis: A bluish discoloration visible at the nail bases in select patient with severe hypoxemia or hypoperfusion. As with clubbing, it is not at all sensitive for either of these conditions.

c. Splinter Hemmorrhages: Short, thin, brown, linear streaks in the nails of some patients (the minority) with endocarditis. d. Edema: While edema is a relatively common finding in the lower extremity, it rarely occurs in the arms and hands. This is because the lower extremities are exposed to greater hydrostatic pressure due to their dependent position. Upper extremity edema, when present, usually occurs focally over an area of local

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inflammation (e.g. cellulitis). Diffuse arm edema can occur if drainage is compromised, as when the lymphatics are disrupted following axillary lymph node surgery for staging and treatment of breast cancer. Upper extremity venous obstruction can also cause edema, though blood clots in this region are much less common then in the lower extremity.

Note divit left (pitting) after application of pressure. Edema in this case is due to lymphatic obstruction.

Right upper extremity DVT. Note diffuse swelling. In the setting of injury or infection, the affected area should be examined in greater detail. For example, acute inflammation secondary to cellulitis of the upper extremity is demonstrated in the image below. 86

Lymph Nodes of the Upper Extremity: Epitrochlear Nodes: Found on the inside of the upper arm, just above the elbow. These are rarely the site of pathology and thus not routinely examined. If there is clinical evidence of an infection distal to the elbow, it makes sense to feel for these nodes as they are part of the drainage pathway. To examine, cup the patient's elbow in your hand (left elbow with right hand and vice versa) and palpate just above the elbow, along the inside of the upper arm. When inflamed, the nodes become large and tender. Palpation of Epitrochlear Lymph Nodes

Axillary Nodes: Pathologic enlargement occurs most commonly in the following settings: a. Infection: o systemic (e.g. TB, HIV) 87

o local (e.g. cellulitis of the hand/arm) b. Malignancy: o lymphoma, where the malignacy is based in lymph nodes o metastases, in particular breast, though could be from any site c. Other: o various systemic inflammatory illnesses (e.g sarcoidosis)

When examining healthy individuals, both axilla can be examined simultaneously. To do this, ask the patient to lift both arms away from the sides of their body. Then extend the fingers of both your hands and gently direct them towards the apices of the arm pits. You can do this through the patients gown if you don't want to place your fingers in direct contact with the axilla. Now press your hands towards the patient's body and move them slowly down the lateral chest wall. This allows you to explore the axillary regions in their entirety. Palpation of the Axilla

If you feel any abnormalities, repeat the exam of each axilla separately. When examining the left axilla, grasp the patient's left wrist or elbow with your left hand and lift their arm up and out laterally. Then use your right hand to examine the axillary region as described above. This technique permits the patient's arm to remain completely relaxed, minimizing tension in the surrounding tissues that can mask otherwise enlarged lymph nodes. The right axilla is examined in a similar fashion, though hand positioning is reversed. This examination may also be performed while the patient is supine, as would be done if you were to couple it with the female breast exam. Most patients do not have palpable axillary nodes. If you are able to feel adenopathy, make note of the following characteristics:

Size: Pathologic nodes are generally greater than 1 cm Firmness: Malignancy makes nodes feel harder Quantity: The greater the number of nodes, the more likely true pathology exists Pain: Often associated with inflammation (e.g. infection) 88

Relation to other nodes and surrounding tissue: Nodes fixed to each other or adjacent structures are worrisome for malignancy Changes over time: Nodes which regress spontaneously are obviously of less concern then those that increase in size, number, or appear to be growing in new locations. Making these determinations requires multiple evaluations over time.

Left Axillary Adenopathy

Exam of the Lower Extremities

The discussion which follows focuses on the search for evidence of arterial and venous insufficiency as well as edema. These are the most common serious ailments which affect the lower extremities and therefore merit the greatest attention. Joint and neurologic examinations are covered elsewhere. The Femoral Region: As with examination of any other area of the body, exposure is key. Socks, stockings, pants and skirts should all be removed. 1. Begin by simply looking at the area in question, which is on either side of the crease separating the leg from the groin region. Make note of any discrete swellings, which might represent adenopathy or a femoral hernia. 2. Palpate the area, feeling carefully for the femoral pulses as well as for inguinal/femoral adenopathy (nodes which surround the femoral artery and vein.... up to one cm in size are considered non-pathologic). If you feel any lymph nodes, note if they are firm or soft, fixed in position or freely mobile (fixed, firm nodes are more worrisome for pathologic states).

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3. The femoral pulse should be easily identifiable, located along the crease midway between the pubic bone and the anterior iliac crest. Use the tips of your 2nd, 3rd and 4th fingers. If there is a lot of subcutaneous fat, you will need to push firmly. 4. A femoral hernia, if present, is located on the anterior thigh, medial to the femoral artery. As it can be transient (i.e. the patient reports its presence yet you find nothing on examination), investigation should include observation as well as palpation while the patient performs a valsalva maneuver, which may make a hernia more prominent.

The Popliteal Region: 90

1. Move down to the level of the knee allowing it to remain slightly bent. 2. Place your hands around the knee and push the tips of your fingers into the popliteal fossa in an effort to feel the popliteal pulse. Note whether it feels simply pulsatile (normal) or enlarged and aneurysmal (uncommon). This artery is covered by a lot of tissue and can be difficult to identify, so you may need to push pretty hard. Even then, it may not be palpable, which is not clinically important if you can still identify the more distal pulses (see below).

Below The Knee: Now, turn your attention to the lower leg (i.e. from the knee to the foot). First, examine with your eyes, paying attention to: 1. Color: Venous insufficiency is characterized by a dark bluish/purple discoloration. Over time, long standing stasis of blood leads to the deposition of hemosiderin, giving the skin a dark, speckled appearance. If the leg is placed in a dependent position, the bluish/purple discoloration may darken dramatically, further suggestive of venous insufficiency. This occurs as a result of gravity working against an already ineffective blood return system. Patients with severe arterial insufficiency, on the other hand, may have relatively pale skin as a result of under perfusion. When their legs are placed in a dependent position, gravity enhances arterial inflow and the skin may become more red as maximally dilated arterioles attempt to bring blood to otherwise starved tissues. In cases of severe ischemia, the affected areas (usually involving the most distal aspect of the foot), can appear whitish or mottled, giving the leg a marbleized appearance. Dead tissue turns black (a.k.a. gangrene). Cellulitis (infection in the skin) will cause the skin to appear bright red. These changes can be difficult to detect in people of color.

Acute Arterial Insufficiency: Note Mottled Appearance of Skin

Chronic Arterial Insufficiency with Ulcers

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Gangrene of Toes

Venous Insufficiency

3. Cellulitis

4. 2. Obvious swelling of the leg: If present, is it symmetric? To what level does the swelling exist (i.e. ankle, calf, knee etc.)?

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Assymetric Leg, Swelling secondary to Deep Venous Thrombosis in Right Leg.

3. Nail growth: Nail thickening and deformity often occurs with arterial insufficicency; also with fungal infections. Onychomycosis

4. Skin: Any obvious growths? Shiny, hairless appearance (seen with arterial insufficiency)? Dilated or varicose superficial veins? Ulceration of the skin can occur in the setting of either venous or arterial disease.

Venous Stasis Ulcer

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5. The bottom of the foot and between the toes: These are common "problem areas," particularly in patients with diabetes who are predisposed as a result of sensory impairment, arterial insufficiency, or both.

Neuropathic Ulcer in Patient with Diabetic Neuropathy

6. Probing the depth of an ulcer: Ulcers can extend rather deeply. This can be explored with the use of a Q-tip. If the bone is visible or can be reached with the Q-tip, the infection is assumed to involve the underlying structure. This is referred to as clinical osteomyelitis. It's worth noting that if the ulcer developes in a patient with neuropathy (as is the case here), then the act of probing does not cause pain because the area is insensate.

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Clinical Osteomyelitis: Deep ulcer which permits passage of Q-tip to underlying level of bone.

Feel the skin, noting in particular: 1. Temperature: Arterial insufficiency will often cause the skin to feel cool. Infection, on the other hand, causes hyperemia and relative warmth. The back of your hand may be the most sensitive surface for detecting subtle temperature difference. Compare one leg to the other. It's also OK to use your own skin (e.g. face) as a reference point. Note that in cases where arterial insufficiency and infection occur simultaneously (which is quite common), impaired inflow of blood may generate less warmth (and also less redness) then might otherwise be expected. 2. Edema: Fluid frequently collects in the feet and ankles due to the effects of gravity. This is related to some perturbation in the Startling forces. Thinking in broad strokes, it's usually the result of: Low oncotic pressure: Either failure to synthesize albumin (as with malnutrition or liver disease) or increased loss of albumin (via the kidney or local leakage due to altered capillary permeability). Increased hydrostatic pressure: Transmitted back from the level of the heart (right heart failure), liver (portal hypertension), local venous insufficiency (e.g. venous valvular incomepetence with impaired flow of blood back to the heart from the legs), lymphatic obstruction (e.g. retroperitoneal adenopathy secondary to malignancy), or obesity (which may impair both venous and lymphatic drainage). Realize that all "circulation" problems are not the same. Disorders of blood inflow (arterial) and outflow (venous) have different associated signs and symptoms based on their varying pathophysiology (see above). Edema is commonly associated with venous insufficiency, a blood return problem. This disorder tends to get worse when the legs are allowed to dangle for prolonged periods below the level of the heart (e.g. towards the end of the day if the patient has been standinag for long periods of time). The fluid builds up preferentially in the most distal aspects of the leg and progress up towards the knee as the process worsens. Arterial insufficiency, on the other hand, rarely causes edema, which makes perfect sense as the problem lies in the delivery of blood to the extremity, not the return from it. On occasion, the conditions may coexist.

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It may be difficult to detect small amounts of fluid. Look around the malleoli, as fluid will cause a loss of the normally distinct appearing edges of the bone. Similarly, fluid will tend to "fill in" the spaces between the extensor tendons on the top of the foot, causing them to appear less defined. If you're not sure whether fluid is present, push on the area for several seconds, release, and then gently rub your finger over that same spot, feeling for the presence of a "divot," referred to as pitting. Much is said about pitting edema being associated with some disease states and non-pitting with others; however, the actual importance of this distinction is probably over stated. Also note the proximal extent of the edema and if it is present to the same degree in both legs. Edema may either be diffuse, involving all of the surrounding tissue symmetrically, as is frequently the case in disorders of low oncotic or elevated hydrostatic pressure. If, however, there is a local inflammatory process, as might occur with cellulitis, the area of edema can be quite focal. There is a very subjective scale for rating edema which ranges from "trace at the ankles" to "4+ to the level of the knees." After examining many patients, you'll develop a sense of what is a lot and what is not.

Edema of Right Foot. Note Loss of Distinct Edges of Malleolous and Extensor Tendons on Top of Foot

Massive edema. Note: Remaining imprint of fingers.

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Lymphedema, Left Leg

3. Capillary Refill: Push on the tip of the great toe or the nail bed until blanching occurs. Then release and note how long it takes for the red color to return, a reflection of blood inflow to the distal aspect of the lower extremity. Longer then 2-3 seconds is considered abnormal and consistent with arterial insufficiency. Refill may also be delayed in the setting of significant hypovolemia, as decreased blood volume available for perfusion is shunted away from the extremities to feed more vital organs. 4. Skin that is discolored from venous insufficiency blanches when pushed and it generally takes more then a few seconds for the bluish hue to return. Cellulitic areas, however, blanch and then very rapidly return to their bright red coloration. This can be helpful as it will occasionally be difficult to determine if infection and venous insufficiency are both present. 5. Pain: Cellulitic skin, for example, is often tender when touched. Remember that certain disease states (diabetes in particular) cause a peripheral neuropathy that predisposes these patients to the development of skin breakdown and subsequent infection precisely because they have abnormal sensation in their distal extremities. In these cases, then, infection may occur in the absence of pain.

Paronychia Great Toe. Note: Swelling and redness along lateral edge of nail.

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6. Note the character of any swollen area: Does it feel full of edema fluid? Is there a suggestion of a solid mass (uncommon)? Is there focal fluctuance, as would occur in an abscess? The Distal Pulses: Pulses are assessed to identify the presence of arterial vascular disease. In general, the less prominent the pulses, the greater the chance that there is occlusive arterial disease. This is not a perfect correlation, however, as pulses may be palpable even when significant disease is present (e.g. may be affecting predominantly smaller, more distal blood vessels). A history of pain/cramps with activity suggestive of arterial insufficiency is also of great importance. The location of the blockage(s) will dictate the symptoms and findings. Aorto-iliac disease, for example, will cause symptoms in the hips/buttocks and a loss of the femoral pulse while disease affecting the more distal vessels will cause symptoms in the calves and feet. 1. The Dorsalis Pedis (DP) Artery: Located just lateral to the extensor tendon of the big toe, which can be identified by asking the patient to flex their toe while you provide resistance to this movement. Gently place the tips of your 2nd, 3rd and 4th fingers adjacent to the tendon and try to feel the pulse. If you can't feel it, try moving your hand either proximally/distally or more laterally and repeat. Common pitfalls include pushing too hard and/or mistaking your own pulse for that of the patient. Palpating the patients radial artery or your own carotid simultaneously with your free hand can help sort this out. Location of Dorsalis Pedis Artery The pictures below demonstrate the location of the dorsalis pedis artery in relation to surrounding structures

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Palpating Dorsalis Pedis Artery 2. The Posterior Tibial (PT) Artery: Located just behind the medial malleolous. It can be palpated by scooping the patient's heel in your hand and wrapping your fingers around so that the tips come to rest on the appropriate area. Alternatively, you can reach your fingers over the top of the medial malleolous and approach the artery from this direction. In either case, you are attempting to locate the artery using the tips of your fingers. Pitfalls mentioned with the DP also apply here. Location of Posterior Tibial Artery The pictures below demonstrate the location of the posterior tibial artery in relation to surrounding structures (surface anatomy on left, gross anatomy on right).

Palpating Posterior Tibial Artery

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Palpating Posterior Tibial Artery 3. If there is a lot of edema, you will have to push your way through the fluid-filled tissue to get down to the level of the artery. 4. If you are unable to palpate a pulse, find a doppler machine, which should be present on any inpatient floor or ER, and use it to identify the location of the artery. Mark the place with a pen and then go back and again try to feel it with your fingers. In this way, you will be able to determine if the vessel was not palpable on the basis of limited blood flow or if you are simply having a "technical" problem. Using Doppler Device to Identify Posterior Tibial Artery

5.Pulses are rated on a scale ranging from 0 (not palpable) to 2+ (normal). As with edema, this is very subjective and it will take you a while to develop a sense of relative values. In the event that the pulse is not palpable, the doppler signal generated is also rated, ranging again from 0 to 2+. 100

Musculo-Skeletal Examination
Detailed examination of the joints is usually not included in the routine medical examination. However, joint related complaints are rather common, and understanding anatomy and physiology of both normal function and pathologic conditions is critically important when evaluating the symptomatic patient. By gaining an appreciation for the basic structures and functioning of the joint, you'll be able to "logic" your way thru the exam, even if you can't remember the eponym attached to each specific test! I have included detailed descriptions of the shoulder, knee, and low back examinations as these are the most commonly affected areas. In addition, a review of relevant anatomy, function, and common disorders are described for most of the other major joints. This is not meant to be an all-inclusive list. A few general comments about the musculoskeletal exam Historical clues when evaluating any joint related complaint:

What is the functional limitation? Symptoms within a single region or affecting multiple joints? Acute or slowly progressive? If injury, what was the mechanism? Prior problems with the affected area? Systemic symptoms?

Common approach to the examination of all joints:

Make sure the area is well exposed - no shirts, pants, etc covering either side gowns come in handy Carefully inspect the joint(s) in question. Are there signs of inflammation or injury (swelling, redness, warmth)? Deformity? As many joints are symmetric, compare with the opposite side Must understand normal functional anatomy - what does this joint normally do? Observe the joint while patient attempts to perform normal activity - what can't they do? What specifically limits them? Was there a discrete event (e.g. trauma) that caused this? If so, what was the mechanism of injury? Palpate the joint in question. Is there warmth? Point tenderness? If so, over what anatomic strucutres? Assess the range of motion, both active (patient moves it) and passive (you move it) if active is limited/causes pain. Strength, neuro-vascular assessment. Specific provocative maneuvers related to pathology occurring in that joint (see descriptions under each joint). In the setting of acute injury and pain, it's often very difficult to assess a joint as patient "protects" the affected area, limiting movement and thus your examination. It helps to examine the unaffected side first (gain patient's confidence, develop sense of their normal).

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The Knee Exam Observation: 1. Make sure that both knees are fully exposed. The patient should be in either a gown or shorts. Rolled up pant legs do not provide good exposure! 2. Watch the patient walk. Do they limp or appear to be in pain? When standing, is there evidence of bowing (verus) or knock-kneed (valgus) deformity? There is a predilection for degenerative joint disease to affect the medical aspect of the knee, a common cause of bowing.

Verus Knee Deformity, more marked on the left leg. 3. Make note of any scars or asymmetry. Chronic/progressive damage, as in degenerative joint disease, may lead to abnormal contours and appearance. Is there obvious swelling as would occur in an effusion? Redness suggesting inflammation? 4. Is there evidence of atrophy of the quadriceps, hamstring, or calf muscle groups? Knee problems/pain can limit the use of the affected leg, leading to wasting of the muscles.

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While both legs have well developed musculature, the left calf and hamstring are bulkier than the right. 5. Look at the external anatomy, noting structures above and below the knee itself: a. Patella b. Patellar tendon c. Quadriceps/Hamstring/Calf muscles d. Medial and lateral joint lines. e. Femur and Tibia f. Tibial tuberosity

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Palpation and Examination for Degenerative Joint Disease: 1. If the knee is injured, start by examining the unaffected side. This allows for comparison and relaxes the patient as you are not performing maneuvers that cause discomfort from the outset. 2. Ask the patient to bend the knee, gauging whether they can fully extend and flex. This is referred to as their active range of motion. Full extension is 0 degrees, full flexion ~ 140.

3. Knee Flexion (Left) and Extension (Right) 4. Place one hand on the patella. Note any warmth, which if present, would suggest inflammation. Grasp the ankle or calf with your other hand and gently flex the knee. Note the extent to which you can flex and extend the knee, referred to as its passive range of motion. Also, using the hand on the patella, feel for crepitus. This is a crackling/grinding sensation that occurs with movement. If present, it's suggestive, but not diagnostic, of degenerative joint disease (DJD). It reflects a loss of the normal smooth movement between the articulating structures (femur, tibia, and patella). DJD is suggested by the presence of pain with activity that gets progressively more limiting over time. There may be a history of antecedent injury, which caused the inciting damage to the articulating surface. And coexistent damage to ligaments or menisci may also be present (see below). When defining the extent of DJD, the knee is broken into 3 compartments: Medial, central, and lateral. DJD can occur in any or all regions. The precise location of the DJD can be hard to determine on examination and is more accurately defined via x-rays.

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5. X-Ray of Normal Knee (Left) and Knee With DJD (Right) 6. If any of the above maneuvers elicits pain, stop and note at what point in the range of motion this occurs. 7. It's important to note that many patients report noises (e.g., creaking, popping, cracking) associated with joint movement. The vast majority of these sounds are not clinically significant. Rather, pain or functional limitation are the subjective complaints which carry clinical relevance. Tests for an effusion: An effusion is the accumulation of fluid within the joint space. If there is a large collection, the knee will look swollen. Lesser amounts of fluid can be a bit more subtle. Patient's symptoms are often related to whatever caused the fluid to accumulate in the first place. The effusion itself makes the knee feel as if it's somewhat unstable or floating and may limit range of motion. Effusions resulting from inflammatory arthritis (e.g. infection, gout, rheumatoid arthritis) are associated with other signs of inflammation, including: warmth, redness, pain with any movement.

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Large Effusion, Right Knee. Ballotment (helpful if the effusion is large) 1. Slightly flex the knee which is to be examined. 2. Place one hand on the supra-pateallar pouch, which is above the patella and communicates with the joint space. Gently push down and towards the patella, forcing any fluid to accumulate in the central part of the joint. 3. Gently push down on the patella with your thumb. 4. If there is a sizable effusion, the patella will feel as if it's floating and "bounce" back up when pushed down.

Balloting the Left Knee. Milking (helpful for detecting small effusions) 1. Gently stroke upwards along the medial aspect of the patella, pushing fluid towards the top and lateral aspects of the joint. 2. Gently push on the lateral aspect of the joint. If there's a small effusion, the fluid which was milked to the lateral aspect will be pushed back towards the medial area of the joint, causing the medial skin to bulge out slightly. Inflammatory Arthritis and Effusions: Intense inflammatory processes within the joint space can also cause an effusion. Infection, gout, and rheumatoid arthritis are a few of the conditions that can lead to an inflammatory arthritis (IA) and effusion. The joint and overlying skin is usually warm and red. In addition, there is significant pain with any active or passive movement. The more intense the inflammation, the more severe the pain and the more limited the range of motion. Identifying the precise cause of IA is critical as it directs the clinician towards the best treatment, limiting permanent damage to the joint. This usually requires 106

aspiration and examination of the joint fluid. Inflammatory fluid has a high white cell count and should contain other clues as to its origin (e.g. gout --> crystals on microscopy; infection --> bacteria on gram stain and culture; etc). Fluid from those with degenerative effusions has relatively few white cells. Clinically, patients with DJD have few signs of inflammation and some degree of preserved range of motion (ROM). Historical information also helps distinguish DJD from IA. DJD is usually slowly progressive while those with IA more often have an acute presentation. Additionally, those with IA may have characteristic patterns of recurrence (e.g. great toe MTP in gout, MCPs of hands in RA), systemic symptoms, suggestive joint deformities (e.g. ulnar deviation of the hands in RA), and particular radiographic changes. Of course, it's possible to have element of both IA and DJD. DJD, for example, can result from joint damage that occurred secondary to past episodes of gout or infection.

Gouty Inflammation of Metatarsal-Phalangeal Joint, Left Great Toe Specific Maneuvers for the Knee Exam Tests for Meniscal Injury Normal anatomy and function: The menisci sit on top of the tibia and provide a cushioned articulating surface between the femur and tibia. Symptoms occur when a torn piece interrupts normal smooth movement of the joint. This can cause a sensation of pain, instability ("giving out") or locking in position. Injury may also cause swelling. If the meniscus has been injured and no longer adequately covers the tibia, damage can occur to the underlying bone, leading to degenerative arthritis.

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Anatomy of Menisci, Right Knee (patella has been removed). Joint Line Tenderness: 1. Have the patient slightly flex their knee. The knee is slightly flexed when performing all of the functional tests that are described below. This positions the joint such that other stabilizing elements do not interfere with the structure that is being tested. 2. Define the joint space along its lateral and medial margins. The joint line is perpendicular to the long axis of the tibia. 3. Gently palpate along first the medial and then the lateral margins. Pain suggests that the underlying meniscus is damaged. Osteoarthritis can also cause joint line tenderness

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4. Palpation Along Lateral (picture on left) and Medial (picture on right) Joint Lines. The Joint Line is Marked by Purple Line. 5. Note that only a portion of the meniscus lies near the joint line. The remainder of the meniscus cannot be assessed with this technique. McMurray's Test 1. When examining the right knee, place your left hand so that your middle, index, and ring fingers are aligned along the medial joint line. 2. Grasp the foot with your right hand and fully flex the knee. 3. Gently turn the ankle so that the foot is pointed outward (everted). Then direct the knee so that it is pointed outward as well (valgus stress). 4. While holding the foot in this everted position, gently extend and flex the knee. If there is medial meniscal injury, you will feel a "click" with the hand on the knee as it is extended. This may also elicit pain.

5. Simulated McMurray's Test With Foot Everted (picture on left). Close-up (picture on right) Reveals How This Maneuver Streeses The Medial Meniscus.

6.

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7. McMurray's Test: Assessment Of Medial Meniscus Demonstrated In Picture On Left, Lateral Meniscus In Picture On Right. 8. Now, return the knee to the fully flexed position, and turn the foot inwards (inversion). Then direct the knee so that it is pointed inward as well (varus stress). 9. Place the index, middle, and ring fingers of your left hand along the lateral joint line. 10. Gently extend and flex the knee. If the lateral meniscus has been injured, you may feel a "click" with the hand palpating the joint line. You may also elicit pain. Appley Grind Test 1. Have the patient lie on their stomach. 2. Grasp one ankle and foot with both of your hands and gently flex the knee to ninety degrees. Hold the patients leg down by gently placing your leg over the back of their thigh.

3. Appley Grind Test 4. Push down gently while rotating the ankle back and forth. 5. This maneuver places direct pressure on the menisci. If injured, it will cause pain. 6. Test the opposite leg in the same fashion. Tests for Injury to the Ligaments Normal anatomy and function The ligaments are very strong tissues that connect bone to bone. In the knee, they assure stability and correct alignment. There are 4 main ligaments in the knee: Medial collateral (MCL), lateral collateral (LCL), anterior cruciate (ACL) and posterior cruciate (PCL). The medial and lateral ligaments provide stability in response to medial and lateral joint stress. The cruciate ligaments limit anterior and posterior movement of the femur on the tibia and limit the degree to which the knee can rotate. Injury usually requires significant force. Following a ligamentous injury, there is generally acute pain, swelling and the injured person will often report hearing a "pop" (the sound of the ligament tearing). After the acute swelling and pain have dissipated, the patient may report pain and instability 110

(sensation of the knee giving out) during any maneuver that would expose the deficiency created by the damaged ligament (e.g. rotation, during which there is nothing to "check" the movement of the femur on the tibia).

Anatomy of Ligaments, Right Knee (Patella Has Been Removed). The following are common mechanisms of injury for each of the major ligaments: 1. ACL: Most commonly injured when the foot is planted while extreme rotational force is applied (e.g. a cleated foot caught in the turf while an athlete attempts to rotate towards that side). The ACL may also be injured from a direct force on the lateral knee while the foot is planted. 2. PCL: Much less commonly injured then the ACL. Posterior force on the tibia (e.g. the tibia striking against the dashboard in a motor vehicle accident) can lead to disruption. 3. LCL: Direct force on the medial aspect of the knee while the foot is planted. 4. MCL: Direct force on the lateral aspect of the knee while the foot is planted. Given the forces required to tear a ligament, menisci are often damaged at the same time. It is also possible to tear more then one ligament at once. When testing any ligament, remember the following: 1. Always begin your exam with the asymptomatic knee. This gives you some sense of the individual normal degree of laxity. That is, the "tightness" of everyone's ligaments varies somewhat. By working on their unaffected side, you will define "normal." It also helps to generate a sense of trust between you and the patient. 2. If you're unsure as to whether there is really an abnormality, check back and forth between the normal and abnormal sides. This will enhance your ability to identify differences.

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3. It can be difficult to examine patients with large joints, particularly if you have small hands! 4. Detecting subtle abnormalities takes lots of practice, particularly if you don't have a great sense for the range of normal. 5. It can be extremely difficult to examine the acutely injured knee. Movement often causes significant pain. The patient is understandably apprehensive and will use surrounding muscles to prevent movement. This inability to relax is a normal response and may limit the extent of your exam. It may be necessary to simply wait until the acute inflammation resolves (with rest, elevation, anti-inflammatory medications, and time) before being able to perform an accurate exam. Specifics of Ligament Testing Medial Collateral Ligament 1. 2. 3. 4. Slightly flex the right knee (~30 degrees). Place your left hand along the lateral aspect of the knee. Place your right hand on the ankle or calf. Push steadily inward with your left hand while supplying an opposite force with the right.

5. Stressing the MCL 6. If the MCL is completely torn, the joint will "open up" along the medial aspect.

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Simmulated Torn MCL--Note How Joint Line Opens Up Along Medial Aspect 7. Reverse hand position to assess the left knee. 8. Additionally, palpation along the course of the ligament may also elicit pain if it has been injured. Lateral Collateral Ligament 1. 2. 3. 4. Slightly flex the right knee (~30 degrees). Place your right hand along the medial aspect of the knee. Place your left hand on the ankle or calf. Push steadily outward with your right hand while supplying an opposite force with the left.

5. Stressing the LCL 6. If the LCL is completely torn, the joint will "open up" along the lateral aspect.

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Simmulated Torn LCL--Note How Joint Line Opens Up Along Lateral Aspect 7. Reverse hand position to assess the left knee. 8. Additionally, palpation along the course of the ligament may also elicit pain if it has been injured. Alternative method for stressing the medial lateral collateral ligaments: 1. Extend the patient's knee and cradle the heel between your arm and body. The knee should be slightly flexed. 2. Place your index fingers across the medial and lateral joint lines. 3. Using your body and index fingers, gently provide first medial and then lateral stress to the joint.

Stressing the MCL and LCL 114

Anterior Cruciate Ligament Lachman's Test 1. For testing the right leg, grasp the femur just above the knee with your left hand and the tibia with your right. 2. Flex the knee slightly. 3. Pull up sharply (towards your belly button) with your right hand while stabilizing the femur with the left. The intact ACL will limit the amount of distraction that you can achieve. The intact ACL is described as providing a firm end point during Lachman testing.

4. Stressing the ACL 5. If the ACL is completely torn, the tibia will feel unrestrained in the degree to which it can move forward (see above for image of simulated ACL tear). 6. Compare this to the other leg, reversing your hand position. 7. The patient must be able to relax their leg for this test to work. If they cant, then compensatory muscles will limit the degree of motion, making it very difficult to assess the integrity of the ACL. 8. If the thigh is too big in circumference (or your hand too small) to stabilize, you can perform the Lachman's test with the leg hanging off the side of the table (see picture below). It may also help to further stabilize the leg by holding their ankle between your legs.

Variation On Lachman's Test For Patients With Large Legs.

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Anterior Drawer Test (Note: This test has largely fallen out of favor. It is included for the sake of completeness). 1. Have the patient lie down, with the right knee flexed such that their foot is flat on the table. 2. Gently sit on the foot. Grasp below the knee with both hands, with your thumbs meeting along the front of the tibia. 3. Gently pull forward, gauging how much the tibia moves forward in relation to the femur. The ACL, if intact, will provide a discrete end point.

4. Stressing the ACL 5. If the ACL is completely torn, the tibia will feel unrestrained in the degree to which it can move forward.

Simmulated Torn ACL--Note How Far The Tibia Is Distracted Relative To The Femur

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6. Compare this to the other side by simply shifting your hands to the same position on the opposite leg and repeating. Posterior Cruciate (PCL) Posterior Drawer Test 1. Have the patient lie down, the right knee flexed to 90 degrees, foot flat on the table. 2. Gently sit on the foot. Grasp below the knee with both hands, with your thumbs meeting along the front of the tibia. 3. Gently push backward, gauging how much the tibia moves in that direction in relation to the femur. The intact PCL will give a discrete end point.

4. Stressing the PCL (Because Of Its Posterior Location, The Actual Ligament Cannot Be Seen In Picture On Right) 5. Compare this to the other side by simply shifting your hands to the same position on the opposite leg and repeating. 6. If the PCL is completely torn, the tibia will feel unrestrained in the degree to which it moves backwards.

Simmulated Torn PCL--Note How Far Back The Tibia Moves Relative To The Femur 117

7. If the PCL is completely torn, the tibia may appear to "sag" backwards even before you apply any force. Assorted Other Testing Patello-Femoral Syndrome: A problem with the way in which the patellar articulates with the femur and moves (tracks) during flexion and extension. As a result, cartilage lining the undersurface of the patella becomes irritated and worn down. Known as Chondromalacia, this process causes anterior knee pain with activity and often after prolonged sitting. Several ways of assessing for this condition are described below: 1. Have the patient slightly flex the leg to be tested. 2. Gently push down on the patella with both thumbs, which may elicit pain in the setting of Chondromalacia. 3. Now, gently move the patella from side to side and try to palpate its undersurface. This may elicit pain in the setting of Chondromalacia. 4. Hold the patella in place with your hand and ask the patient to contract their quadriceps muscle. This will force the inferior surface of the patella onto the femur, eliciting pain in the setting of Chondromalacia.

5. Assessing For Chondromalacia Bursitis Bursa are small pouches of fluid that lie between bony prominences and the tendons that surround joints. Their presence allows the tendons to move without generating a lot of friction. The bursa do not communicate with the joint space itself. Inflammation of the bursa, most commonly due to overuse of the tendon or direct trauma, can cause pain and swelling. Examination of the affected area reveals focal pain. Swelling, warmth, and redness may be prominent if there is concurrent infection, another cause of bursitis. Bursitis can be distinguished from an intra-articular process because of the location of the pain and the fact that movement of the joint itself does not cause discomfort. The major bursa surrounding the knee include:

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1. Pre-patella: Located directly on top of the patella. Most frequently affected due to direct trauma, as may occur with people who spend a lot of time on their knees (e.g. carpet layers, carepenters). 2. Infrapatella (a.k.a. anserine): Below the knee. Also affected by direct trauma, as with the prepatella bursa.

Location Of Bursa Is Shown On Model (Top). Picture On Right Demonstrates Septic Prepatellar Bursitis Of The Left Knee. Picture on Left Demonstrates Septic Infrapatellar Bursitis, Left Knee

Shoulder Exam
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I think that the most daunting aspect of the shoulder exam is appreciating the functional anatomy of this incredibly mobile joint. The primary benefit of the ball and socket arrangement is that it allows the hand to be positioned precisely in space, maximizing our ability to function. In terms of functionality, the shoulder might be best described as having a golf ball-on-a-tee design. Observation The shoulder joint is created by the confluence of 3 bony structures: the scapula, humerus and clavicle. These are held together by ligaments and an intricate web of muscles. Critical external landmarks include the following: 1. 2. 3. 4. 5. 6. 7. Acromion Clavicle Scapula Deltoid muscle Supraspinatus Infraspinatus Teres Minor

Anterior View On Left, Posterior On Right.

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Location Of The Muscle Groups Is Approximated In The Pictures Above. Start by looking at the normal (or more normal) side. Note any scars, obvious asymmetry, discoloration, swelling, or muscle asymmetry. Palpation Gently palpate around the shoulder, touching each of the landmarks noted above. Make note of pain. Range of Motion (ROM) If there are no symptoms, test both sides simultaneously. Otherwise, start with the normal side. Active ROM: 1. Abduction: Determine the extent to which the patient can abduct their arm. The patient should be able to lift their arm in a smooth, painless arc to a position with hand above their head. Normal range is from 0 to 180 degrees.

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2. Adduction and Internal rotation (Appley Scratch Test): Ask the patient to place their hand behind their back, and instruct them to reach as high up their spine as possible. Note the extent of their reach in relation to the scapula or thoracic spine. They should be able to reach the lower border of the scapula (~ T 7 level).

3. Abduction and External rotation: Ask the patient to place their hand behind their head and instruct them to reach as far down their spine as possible. Note the extent of their reach in relation to the cervical spine, with most being able to reach ~C 7 level.

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4. Forward flexion: Ask the patient to trace out an arc while reaching forward (elbow straight). They should be able to move their hand to a position over their head. Normal range is 0 to 180 degrees.

5. Extension: Ask the patient to reverse direction and trace an arc backwards (elbow straight). They should be able to position their hand behind their back.

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Passive ROM If there is pain with active ROM, assess the same movements with passive ROM. Have the patient relax and place one of your hands on their shoulder. Gently grasp the humerus in your other hand and move the shoulder through the range of motions described above. Note if there is pain, and if so which movement(s) precipitates it. Also note if you feel crepitus with the hand resting on the shoulder. Pain/limitation on active ROM but not present with passive suggests a structural problem with the muscles/tendons, as they are firing with active ROM but not passive. Crepitus suggests DJD. Limitations in movement in any of the directions should be noted. Where exactly in the arc does this occur? Is it due to pain or weakness? How does it compare with the other side? Determining the precise etiology can be defined using the tests below, though realize that there is often a significant amount of overlap between several conditions. Impingement, Rotator Cuff Tendonitis and Sub-Acromial Bursitis Anatomy and Function: I have placed these processes under one heading as they are all linked. Impingement is a dynamic condition that can lead to tendonitis and bursitis. Shoulder pain in general is very common, with impingement as the root cause in a large number of cases. The 4 tendons of the rotator cuff all pass underneath the acromion en route to their insertions on the humerus. The space between the acromion/coracoacromial ligament and the tendons (in particular, the supraspinatus) can become relatively narrowed for any number of reasons (e.g. the growth of an oteophyte on the under surface of the bone). This causes the tendons to become "impinged upon." The resulting friction inflames the tendons as well as the subacromial bursa, which lies between the tendons and the acromion. The net result is shoulder pain, particularly when raising the arm over 124

head (e.g. swimming, reaching for something on a top shelf, arm positioning during sleep). Over time, chronic irritation to the tendons can lead to fraying, tears, and even complete disruption.

Right Shoulder Anatomy (anterior view) Several tests can be done to localize the problem: Sub-acromial Palpation: First, identify the acromium by walking your fingers along the spine of the scapula until you reach its lateral endpoint, which is the acromium. Then gently palpate in the region of the sub-acromial space (see picture below). Palpation may cause pain if the tendons/bursa are inflamed.

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The following two tests passively maneuver the tendons so that they are most likely to rub against the acromion, generating symptoms related to impingement if it is in fact present. Neers Test: 1. Place one of your hands on the patient's scapula, and grasp their forearm with your other. The arm should be internally rotated such that the thumb is pointing downward. 2. Gently foreard flex the arm, positioning the hand over the head. 3. Pain suggests impingement.

Hawkin's (for more subtle impingement) 1. Raise the patient's arm to 90 degrees forward flexion. Then rotate it internally (i.e. thumb pointed down). This places the greater tubercle of the humerus in a position to further compromise the space beneath the acromion. 2. Pain with this maneuver suggests impingement.

Hawkins Test For Impingement 126

It's worth noting that defining the precise location of the problem (ie. bursitis, tendonitis or even partial rotator cuff tears) can be difficult to make on clinical grounds. One helpful adjunct is the diagnostic subacromial bursa injection. Local anesthetic and steroids are injected into the bursa. If the symptoms are due to bursitis, this provides significant relief. However, if the symptoms are predominantly caused by tendonitis or a partial rotator cuff tear, this will have little effect. MRI can also be extremely helpful in defining the precise nature of the pathology. Evaluation of the Muscles of the Rotator Cuff

Anterior View On Left, Posterior On Right.

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Anatomy and Function: There are 4 major muscles that allow shoulder movement. As mentioned above, symptoms caused by rotator cuff tears or tendonitis are often related to impingement. Acute shoulder trauma can also result in injury. Each of the 4 muscles can be tested individually as follows: Supraspinatus: Connects the top of the scapula to the humerus. Contraction allows the shoulder to abduct. This is the most commonly damaged of the rotator cuff muscles. Testing (aka "empty can test): 1. Have the patient abduct their shoulder to 90 degrees, with 30 degrees forward flexion and full internal rotation (i.e. turned so that the thumb is pointing downward). 2. Direct them to forward flex the shoulder, without resistance. 3. Repeat while you offer resistance.

Supraspinatus (Empty Can)Test

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Interpretation: If there is a partial tear of the muscle or tendon, the patient will experience pain and perhaps some element of weakness with the above maneuver. Complete disruption of the muscle will prevent the patient from achieving any forward flexion. These patients will also be unable to abduct their arm, and instead try to "shrug" it up using their deltoids to compensate. Infraspinatus: Connects the scapula to the humerus. Contraction allows the arm to rotate externally. Specifics of testing: 1. Have the patient slightly abduct (20-30 degrees) their shoulders, keeping both elbows bent at 90 degrees. 2. Place your hands on the outside of their forearms. 3. Direct them to push their arms outward (externally rotate) while you resist. Interpretation: Tears in the muscle will cause weakness and/or pain.

Testing Infraspinatus And Teres Minor (External Rotators) Teres Minor: Connects the scapula to the humerus. Provides the same function as the infraspinatus (external rotation). Testing is done as described for the Infraspinatus. Subscapularis: Connects the scapula to the humerus, though the origin is on the anterior surface of the scapula (i.e. on the side opposite the origin of the other 3 muscles of the RC). Contraction causes internal rotation. Function can be tested using "Gerber's lift off test:" 1. Have the patient place their hand behind their back, with the palm facing out. 2. Direct them to lift their hand away from their back. If the muscle is partially torn, movement will be limited or cause pain. Complete tears will prevent movement in this direction entirely.

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Gerbers Liftoff Test (Subscapularis) Drop Arm Test for Supraspinatus Tears: Adducting the arm depends upon both the deltoid and supraspinatus muscles. When all is working normally, there is a seamless transition of function as the shoulder is lowered, allowing for smooth movement. This is lost if the rotator cuff as been torn. Specifics of testing: 1. Fully abduct the patient's arm, so that their hand is over their head. 2. Now ask them to slowly lower it to their side. 3. If the suprapinatus is torn, at ~ 90 degrees the arm will seem to suddenly drop towards the body. This is because the torn muscle cant adequately support movement thru the remainder of the arc of adduction. Deltoid: Not a muscle of the rotator cuff, but important for the later aspects of abduction and flexion. The supraspinatus is responsible for the early component of abduction. The deltoid is readily visible on exam and not commonly injured.

Acromioclaviular Arthritis Anatomy and Function: The A-C joint is minimally mobile. However, inflammation and degeneration can occur, causing pain. Specifics of Testing: 130

1. Identify by palpation the point at which the end of the clavicle articulates with the acromion. 2. Gently push on the area, noting if it causes pain similar to what the patient was describing.

3. Ask the patient to move their arm across their chest. This stresses the a-c joint and will cause pain in the setting of DJD.

AC Disruption: Trauma can cause disruption of the ac joint, also known as AC separation. Specifics of testing: 1. Look at the area in question. If there has been significant disruption (or a fracture to the clavicle itself), the area will appear swollen and deformed compared with the other side. The patient will avoid movement, as this causes pain.

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Acromio-clavicular Joint Separation: Disruption of the right A-C joint, in this case caused by trauma. 2. Gently have the patient move their arm across their chest while you palpate in the AC region. This will cause pain specifically at the AC joint if there is separation. Biceps Tendonitis: The long head of the biceps tendon inserts on the top of the glenoid. The biceps muscle flexes and supinates the forearm and assists with forward flexion of the shoulder. Inflammation can therefore cause pain in the anterior shoulder area with any of these movements. Specifics of testing: 1. Palpate the biceps tendon where it sits in the bicipital groove, which is formed by the greater and lesser tubercles of the humeral head. Pain suggests tendonitis. It helps to have the patient externally rotate their shoulder. You can confirm the location of the tendon by asking the patient to flex and supinate their forearm while you palpate, which should cause it to move.

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Biceps Tendon Palpation Resisted Supination (Yergason's Test): 1. Elbow should be flexed to 90 degrees, shoulder adducted (ie elbow bent at right angle, arm against body). 2. Grasp the patient's hand and direct them to try and rotate their arm such that the hand is palm up (supinate) while you provide resistance. Pain suggests tendonitis of the biceps.

Resisted Supination (Yergason's Test) Speed's Maneuver for Bicipital Tendonitis: 1. Ask the patients to position the affected arm such that the elbow is flexed to ~30 degrees and the forearm supinated (palm up). 2. Direct the patient to flex their arm as you provide resistance. In the setting of tendonitis, this will produce pain. Biceps Tendon Rupture: As a result of chronic tendonitis or truama, the long head of the biceps may rupture. When this occurs, the biceps muscle appears as a ball of tissue and there is a loss of function.

Balled Up Biceps Secondary to Tendon Rupture 133

The Glenohumeral Joint Anatomy and Function: This joint is the actual place where the humerus articulates with the scapula (i.e. where the ball meets the socket). The cavity is lined by the labrum, which functions like the menisci of the knee, assuring smooth/cushioned contact between the bones. The joint is held together by the muscles of the rotator cuff as well as a tough capsule that surrounds the muscles. Glenohumeral DJD: DJD usually results from an injury that has disrupted the normal articulating surfaces. Over time, movement of the shoulder causes additional wear and tear, leading to DJD. Patients experience pain and gradual limitation in movement. This is particularly noticeable on external rotation and abduction. Palpation of the joint with a hand placed on the shoulder during movement may reveal crepitus. Assessment is done as follows: 1. Perform active ROM maneuvers as described previously, noting degree to which movement is limited. 2. Perform passive ROM, again noting limitations and degree of pain. 3. You may feel crepitus by placing your hand on the patient's shoulder during passive ROM.

Glenohumeral Joint Anatomy-Humerus has been removed from its normal position of articulation. Glenohumeral Instability: The rotator cuff, along with the outer joint capsule and the labrum, stabilize the joint. The labrum is a tough tissue that lines the cup formed by the scapular component of the glenohumeral joint. The rotator cuff and capsule surround the outside of the joint. Together, they allow the humerus enough freedom so that the shoulder maintains its full range of motion and function. Tears of the capsule or labrum can generate feelings of pain, instability, or a "dead arm" sensation. The patient may have a history of trauma or recurrent dislocation, where the humerus actually pops out of joint. Specifics of testing (The Apprehension Test): 134

1. Have the patient lie on their back with the arm hanging off the bed. 2. Grasp their elbow in your hand and abduct the humerus to 90 degrees. 3. Gently externally rotate their arm while pushing anteriorly on the head of the humerus with your other hand. 4. Instability will give the sense that the arm is about to pop out of joint.

Testing Glenohumeral Stability Relocation Test (to be done if + apprehension test) 1. Patient supine. 2. Push on the humerus in posterior direction while externally rotating the arm. 3. This maneuver should relieve any feeling of pain and/or sense that the shoulder is going to dislocate. Note, this technique is essentially the opposite of that used for the aprehension test. Acute Inflammatory Arthritis: Inflammatory processes within the joint can be caused by a number of processes, including infection (septic) or autoimmune (e.g RA). When this occurs, the shoulder may appear swollen, red, and will be painful to the touch. Any movement will be limited by pain. Sampling of fluid from within the joint space allows definitive diagnosis.

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Septic Shoulder: Intense Inflammation Over Shoulder Area As Seen In Picture On Left, Due To Intra-Articular Infection. Picture On Right Is Normal For Comparison. Adhesive Capsulitis: Also called a frozen shoulder, this is caused by idiopathic inflammation of the capspule around the shoulder. The net result is severe limitation of motion in any direction (active or passive). Pain is present with movement, and oftentimes when the shoulder is at rest. The etiology is unclear and it can be difficult to distinguish from a number of the above conditions. Referred Pain to the Shoulder Area It's important to recognize that not all shoulder pain is cause by shoulder pathology. A few sites that can cause referred symptoms: 1. Intra-abdominal inflammation can cause pain to be referred to the shoulder. In particular, inflammation that takes place just below the diaphragm (e.g. splenic abscess) may be referred to the shoulder. Examination and history would suggest that the pathology lies outside the shoulder. 2. Intrathoracic processes can also cause referred symptoms. MI, for example, can generate pain that radiates to the shoulder. As above, H&P should be revealing. 3. Cervical spine pathology can cause irritation of the cervical nerve roots, in particular C5 and C6. This causes a burning or tingling type pain to be referred to the deltoid area. Appropriately directed history and neuro examinations help to pin down the cervical spine as the location of the pathology.

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Hand and Wrist

Normal function of the hand and wrist is obviously of great importance. A cursory review of this area is included in the Upper Extremity Examination. What follows is a description of commonly occurring pain syndromes and pathologic processes involving this region. 1. Carpal Tunnel Syndrome Presentation and Anatomy: The median nerve travels through a narrow space when it crosses the wrist en route to the hand. Occasionally, this space becomes inadequate to accommodate the nerve, placing it under increased pressure. The precise reason why this occurs is not clear. Patients usually report some combination of the following:
o o o

o o

Numbness and tingling (ie neuropathic pain symptoms) in the distribution of the median nerve (thumb, index, middle and lateral of ring finger) Symptoms are often worse at night, presumably due to tendency to flex wrist during sleep. Flexing puts additional pressure on the nerve. Patients will often try to "shake out" their hands in an effort to reduce pain and "increase blood flow" (based on the patient's assumption that decreased perfusion caused the symptoms). With increased severity, pain can be present at all times during the day. In severe cases, there may be loss of motor strength of the thumb (see below).

Examination:
o o

The hand and wrist usually appear normal Pain may some times be reproducible by tapping over the nerve (Tinnel's sign). It may also occasionally be reproducible if the wrist is held in forced flexion x 1 minute (Phelan's sign). Neither of these signs is particularly sensitive.

Tinnel's Test

Phelan's Test

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In advanced carpal tunnel, there may be atrophy of the thenar eminence (due to denervation of the muscle as well as disuse atrophy) and associated decrease in motor strength. The Abductor Pollicis Brevis (APB) muscle receives sole innervation from the median nerve. Function can be tested by providing resistance to abduction up and away from the plane of the palm.

Resistance to movement of APB

o

Prolonged compression will lead to impaired 2 point discrimination on sensory testing. That is, the patient can't discern whether being touched with one object or 2 when separated by 5mm (can check using a bent paper clip). Carpal Tunnel Induced Atrophy: Chronic, severe compression of the median nerve within the carpal tunnel has led to atrophy of the Thenar muscles (hand on right). A normal appearing Thenar Eminence is demonstrated on left.

2. Ganglion Cyst Presentation and Anatomy: Idiopathic, spontaneous protrusion of joint fluid outside of the articular space. The cyst is painless and usually located on the dorsal aspect of the wrist.

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Examination:
o o o o

Patients often present noting the abrupt development of a focally swollen area. There is usually no associated pain or inflammation. On palpation, the structure has a fluid filled consistency and is non-tender. The structure should trans-illuminate when a light is placed upon it (as it's fluid filled).

3. Dupuytren's Contracture Presentation and Anatomy: Thickening of the palmar fascia, which is usually painless and develops slowly over time. If pronounced, it may prevent the hand from being able to fully open. Examination:
o o o

Obvious focal thickening on palmar aspect hand. On palpation, feels tough and thick, though non-tender and without signs of inflammation. May interfere with ability to fully open hand

Dupuytren's Contracture

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4. Heberden's Nodes Presentation and Anatomy: Bony excresences that cause deformity at the DIP joints of the fingers. Occurs slowly over time and is associated with Osteoarthritis. May affect many joints or only a few, though not usually symmetric. Similar protrusions at the PIP joints are called Bouchard's nodes. Examination:
o o o

Obvious bony protrusions at DIP joints Non-tender on palpation with an absence of inflammation Some times interfere with joint movement and function

Heberden's Nodes 5. Trigger Finger Presentation and Anatomy: Flexor tendons connect muscles proximal to the wrist to the fingers. When the muscles shorten, they pull on the tendons, causing the fingers to flex. Occasionally, nodules/irregularities develop along the tendons, which then interfere with their smooth movement thru "pulleys" on the palm. Patients note difficulty flexing and extending the affected finger and lack of smooth movement. This is associated with a sensation of sudden freeing of the tendon ("triggering") when the irregularity slips through the pulley. Examination:
o o

The palm and fingers usually appear normal. The affected tendon is not visible. Ask the patient to fully flex the affected finger. When they attempt to extend and flex it, the movement will be impaired. It's worth noting that sometimes the triggering does not occur with every movement. If you place one of your fingers over the affected tendon, you may feel the "pop" when it finally pulls thru. There is usually no associated pain or inflammation. 140

6. Tenosynovitis of the Thumb (DeQuervain's type) Presentation and Anatomy: Repetitive abduction and adduction of the thumb can irritate the tendons of the extensor policis brevis and abductor policis longus muscles. When this occurs, any movement of the thumb (in particular, gripping) may cause pain at its base.

Examination:
o o

The thumb usually appears normal. In cases of severe tendonitis, there may be swelling overlying the tendons. Tenderness at the point where the tendons of the extensor pollicis brevis and longus cross the radial styloid (distal end of the radius)

Pain with passive stretching of the tendons (a.k.a. Finklestein Test):

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a. Direct the patient to place the thumb in their palm. b. Have them cover the thumb with the fingers of the same hand, forming a fist. c. Gently deviate the wrist towards the ulna. This stretches the inflamed tendons over the radial styloid, reproducing the patient's pain.

Finkelstein's Test Selected Traumatic Injuries To The Hand (not in any way inclusive!) 1. Boxer's Fracture Presentation: When a closed fist strikes a solid surface, the force may cause a break in the 5th metacarpal. Examination:
o

Pain and swelling over the 5th metacarpal

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Boxer's Fracture. Note swelling over dorsal aspect of right hand, most pronounced below the small finger. It is the result of a fracture to the fifth metacarpal (bone below small finger), usually associated with striking an object with a closed fist. X-ray demonstrates fracture of distal right metacarpal.

2. Ulnar Collateral Ligament Disruption (Gamekeeper's Thumb)

Ulnar Collateral Ligament Anatomy

Gamekeeper Technique That Lead To UCL Injury (Don't Worry, Bunny Used In Photo Is Not Real!)

The ulnar collateral ligament (UCL) is a strong band of tissue that connects the first phalanx of the thumb to the metacarpal bone along the ulnar side. Injury to this structure was first described in Scottish Gamekeepers, who damaged the ligament as a result of the manner in which they killed rabbits. The head of the rabbit was grasped between thumb

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and first finger of one hand while they pulled on the rabbit's hind quarters with their other. This force chronically stressed the UCL, leading to weakening or frank rupture. After its initial description, it was quickly recognized that the ligament could be torn by any strong force that acutely abducts the extended thumb. Patient's are usually immediately aware that something is wrong, developing swelling, pain and instability at the metacarpal-phalangeal (MCP) joint . It has become a relatively common ski injury, occurring when a person falls on a hand that has a ski pole gripped between the thumb and forefinger.

Mechanism Of UCL Injury In Skiers Examination is remarkable for swelling and pain at the MCP. The key maneuver assesses the degree of laxity at the joint. Place the thumb in extension (see picture below for positioning). Gently grasp the end of the thumb and apply an abducting force. If the UCL has been disrupted, you will be able to distract the thumb to a much larger degree then when compared to the normal side.

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Picture on Left Demonstrates Normal Degree Of Laxity At The MCP Joint. Picture On The Right Demonstrates Markedly Increased Laxity Resulting From Disrupted UCL.

X-Ray Demonstrating Gamekeeper's Fracture (Fragment At Proximal End Phalnax). The ligament may become disrupted at it's insertion on the proximal phalanx, pulling away a small piece of bone that can be seen on x-ray.

Elbow
Function and Anatomy: Hinge type joint formed by the articulation of the Ulna and Radius (bones of the forearm), and Humerus (upper arm). Full extension is equal to 0 degrees, full flexion to ~ 150 degrees. Maximum supination (turning hand palm up so that it can hold a bowl of "soup") and pronation (palm down) are both 90 degrees.

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Elbow Pain and Symptom Syndromes 1. Lateral Epicondylitis (tennis elbow): Presentation and Anatomy: Extensors and supinators of the wrist insert on the lateral epicondyle of the humerus. Repetitive extension (e.g. back hand motion in tennis, though could be any activity with similar movement) of the wrist can cause inflammation and pain around this bony prominence. Examination is usually remarkable for: o Pain on palpation around the lateral epicondyle. o Reproducibility of pain with resisted wrist extension and supination. o Absence of warmth, erythema, or other findings of acute inflammation.

Palpation of lateral epicondyle

Resisted Wrist Extension

2. Anatomy of wrist extensors, University of Washington Lateral Epicondylitis, University of Washington, Click on Case 5 3. Medial Epicondylitis (golfer's elbow): Presentation: Flexors and pronators of the wrist insert on the medial epicondyle. Repetitive flexion of the wrist can cause inflammation and pain around this bony prominence. Examination is usually remarkable for: o Pain on palpation around the medial epicondyle. o Reproducibility of pain with resisted wrist flexion. o Absence of warmth, erythema, or other findings of acute inflammation.

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Palpation Medial Epicondyle

Resisted Wrist Flexion

4. University of Washington Anatomy Flexors 1 University of Washington Anatomy Flexors 2 5. Helpful Hint: If you forget where the flexors and extensor insert, extend and flex your own wrist while palpating both epicondyles with the other hand. It will become clear that your extensors attach laterally and flexors medially. 6. Olecranon Bursitis Anatomy: The olecranon process is formed by the proximal aspect of the Ulna and is the bony prominence that forms the tip of the elbow. The olecranon bursa is a fluid filled pouch that is located directly on top of the olecranon process. It provides a lubricating pad that minimizes direct trauma to the underlying bone during usual activity. Normally, the bursa is not apparent on examination. There are several situations when it becomes clinically prominent:

A.

Non-Inflammatory Bursitis Presentation: As a result of repeated trauma (e.g. persistent leaning on elbows), excess fluid can develop within the bursa, causing it to become very apparent on direct observation. Examination is remarkable for: Obvious swelling at the tip of the elbow. Absence of pain, redness or warmth, as there is usually a minimum of inflammation. Full, painless range of motion of the elbow.

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Normal Elbow
B.

Minimally Inflammatory Olecranon Bursit

Inflammatory Bursitis Presentation and Anatomy: As a result of infection (via abrasion to overlying skin) or any other intensely inflammatory process (e.g. gout, rheumatoid arthritis), the bursa can become very inflamed. Examination in this case is remarkable for:
1 1 1 1

Obvious swelling at the tip of the elbow Marked warmth, redness, and pain on palpation of the bursa. Range of motion of the elbow is usually preserved. This is one way of distinguishing inflammatory bursitis from inflammatory arthritis. Infection within the elbow joint (inflammatory arthritis) is rather rare. When it occurs, the elbow area is diffusely swollen (ie not limited to the area of the bursa) and there is pain with any flexion or extension of the elbow. Rarely, bursitis and/or cellulitis can be so severe that ROM is compromised, making it difficult to distinguish these entities from intra-articular inflammation.

1 1

Normal Elbow

Septic Olecranon Bursitis

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Elbow Effusion Cause articularInflammator 4. Ulnar Nerve Entrapment Presentation and Anatomy: The ulnar nerve runs in the groove between the medial epicondyle and olecranon process. When inadvertently struck, it causes the "funny bone" sensation of pins and needles/electric shock traveling down towards your hand. The ulnar nerve provides sensation to the pinky and medial half of the ring finger. It also provides motor function that allows wrist flexion (along with the median nerve), finger flexion (grip), finger adduction and finger abduction. Occasionally, pressure can develop on the nerve due to entrapment as it travels around the elbow through Guyon's canal. When this occurs, patients report neuropathic type pain (pins and needles, electric shock) along the nerve's distribution (i.e. from elbow down to the hand; sometimes also migrating proximal to the elbow). Examination in the setting of ulnar entrapment:
o o

o o

Normal external appearance Usually normal motor strength: wrist flexion, finger flexion (grip), finger adduction/abdution. May be compromised if nerve compression is severe and of long duration. Usually normal sensation in the pinky and medial half of the ring finger (assess by checking 2 point discrimination). Pain reproducible with tapping over nerve, referred to as ulnar Tinnel's sign.

Ulnar Tinnel Test

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Hip
Function and Anatomy: The hip is a ball and socket type joint, formed by the articulation of the head of the femur with the pelvis. Normal range of motion includes: abduction 45 degrees, adduction 20-30 degrees, flexion 135 degrees, extension 30 degrees, internal and external rotation. Hip pathology can cause symptoms anywhere around the joint, though frequently pain is anterior and radiates to the groin region. Additionally, pathology outside of the hip can be referred to this region. History and exam obviously help in making these distinctions.

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A few common problems are described below: 1. Degenerative Joint Disease and Osteoarthritis Presentation and anatomy: Patients usually report pain with weight bearing and ambulation. Symptoms progress slowly over time (ie years) with pain precipitated by less activity (ie shorter distances walked) as the disease worsens. This tends to occur in patients > 50, as age increases the risk of wear and tear on the joint. Obesity, which chronically increases the load and stress that the joint must bear, is a major risk factor. There may also be a history of significant antecedent trauma that damaged the joint, "setting it up" for degenerative changes over time.

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Examination:
o

Pain with walking, perhaps even with limping. Patient's may develop an Antalgic gait, characterized by trying to minimize the amount of time spent with weight bearing on the affected joint. Range of motion reduced as degeneration progresses. Early on, internal rotation may elicit more pain then movement in other directions.

2. Trochanteric Bursitis: Anatomy and function: The troachanteric bursa overlies the greater trochanter of the femur. When it becomes inflamed, patient's report vague hip pain, focused on the lateral area of the joint. Symptoms tend to get worse with walking. Examination:
o o o

Range of motion is generally preserved Pain on direct palpation over the bursa Pain with resisted abduction. This can be assessed by having patient lie on unaffected side and asking them to abduct the affected hip as you provide resistance.

Low Back Pain Low back pain is a very common condition. Examination and history provide important clues as to its etiology. Function and Anatomy: The lumbar spine must support a tremendous amount of weight, protect the spinal cord and yet still maintain flexibility that maintains range of motion. The low back is formed by 5 lumbar vertebrae and the sacrum. Each vertebrae articulates with the one above and below it in a precise fashion that helps to maximize function. The bones are covered by periosteum, which is innervated and thus generates pain if inflamed (see below). The vertebrae are separated by discs, which allow for smooth, cushioned articulation. The outer aspect of the disc is made of a tough fibrous tissue called the annulus fibrosis, while the inner aspect is gelatinous and known as the nucleus propulsus. Powerful ligaments connect the verterbrae to each other along their anterior and posterior aspects. The spinal cord runs in a bony canal, just posterior to the main body of the vertebrae. This space is well designed to protect the delicate nervous tissue of the cord. The vertebral column has regularly spaced lateral openings known as neuroforamina, through which nerve roots exit and travel to the target organs which they innervate. The actual cord ends at about the L1 level. Below this point, nerve roots (known as the cauda equine) drape down and fill the lower aspect of the spinal canal. The neuro formaina are identified by the vertebrae that are above and below it (e.g L5-S1 neuro foramen sits between the L5 and

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S1 vertebrae). Spinous processes make up the most posterior aspect of the spinal column and are palpable on exam. The rest of the structures (e.g. discs, spinal cord, nerve roots) are not palpable. In terms of surface landmarks, it's helpful to identify the posterior superior iliac crest. This point is roughly on line with the L4-5 intervertebral space.

Overview of Spine

Representative Segment of Spinal Column (Lateral View)

Common Benign Pain Syndromes--Symptoms and Etiology: 1. Non-specific musculoskeletal pain: This is the most common cause of back pain. Patients present with lumbar area pain that does not radiate, is worse with activity, and improves with rest. There may or may not be a clear history of antecedent over use or increased activity. The pain is presumably caused by irritation of the paraspinal muscles, ligaments or vertebral body articulations. However, a precise etiology is difficulty to identify. 2. Radicular Symptoms: Often referred to as "sciatica," this is a pain syndrome caused by irritation of one of the nerve roots as it exits the spinal column. The root can become inflamed as a result of a compromised neuroforamina (e.g. bony osteophyte that limits size of the opening) or a herniated disc (the fibrosis tears, allowing the propulsus to squeeze out and push on the adjacent root). Sometimes, it's not precisely clear what has lead to the irritation. In any case, patient's report a burning/electric shock type pain that starts in the low back, traveling down the buttocks and along the back of the leg, radiating below the knee. The most commonly affected nerve roots are L5 and S1. 3. Spinal Stenosis: Pain starts in the low back and radiates down the buttocks bilaterally, continuing along the backs of both legs. Symptoms are usually worse with walking and improve when the patient bends forward. Patient's may describe that they relieve symptoms by leaning forward on their shopping carts when walking in a super market. This is caused by spinal stenosis, a narrowing of the

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central canal that holds the spinal cord. The limited amount of space puts pressure on the nerve roots when the patient walks, causing the symptoms (referred to as neurogenic claudication). Spinal stenosis can be congenital or develop over years as a result of djd of the spine. As opposed to true claudication (pain in calfs/lower legs due to arterial insufficiency), pain resolves very quickly when person stops walking and assumes upright position. Also, peripheral pulses should be normal. 4. Mixed symptoms: In some patients, more then one process may co-exist, causing elements of more then one symptom syndrome to co-exist. Red Flags: There are a variety of ominous processes that cause low back pain, particularly in older patients (> 50). These problems carry significant morbidity and mortality and mandate a focused and rapid evaluation (including lab and imaging studies) different from what is required for the relatively benign processes described above. Careful history taking and examination can help distinguish these problems. Historical keys include: 1. Pain that doesn't get better when lying down/resting. 2. Pain associated by systemic symptoms of inflammation (e.g. fever, chills), in particular in those at risk for systemic infection that could seed the spinal area (e.g. IV drug users, patients with bacteremia). 3. Known history of cancer, in particular malignancies that metastasize to bone (e.g. prostate, breast, lung). 4. Trauma, particularly if of substantial force. 5. Osteoporosis, which increases risk of compression fracture (vertebrae collapsing under the weight they must bear). More common as people age, women > men. 6. Anything suggesting neurological compromise. In particular, weakness in legs suggesting motor dysfunction. Also, bowel or bladder incontinence, implying diffuse sacral root dysfunction. Note: it can sometimes be difficult to distinguish true weakness from motor limitation caused by pain. 7. Pain referred to the back from other areas of the body (e.g. intra-abdominal or retroperitoneal processes). Could include: Pyelonephritis, leaking/rupturing abdominal aortic aneurysm, posterior duodenal ulcer, pancreatitis, etc. Examination Keys: 1. Vital signs. In particular, pain may be reflected by increase pulse, BP or pain score (if asked). Also, temperature if concern re an infectious process. 2. Observe gait. Is it slow, limited by pain? 3. Look at the lumbar spine area. Any skin abnormalities suggesting underlying inflammation? Normal curvature is as follows: Cervical spine sweeps anteriorly, thoracic spine sweeps posteriorly, and lumbro-sacral spine sweeps anteriorly. 4. Range of motion testing should include forward flexion, hyperextension, lateral flexion, and rotation.

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5. Can the patient point to the precise area of the pain? Is it along the vertebral column? Para-spinal, as might occur with spasm? Radiating down the legs as would occur with nerve root irritation? 6. Palpate the spine. Processes that inflame the bone (e.g. compression fracture, osteomyelitis, metastatic disease) will generate pain when the affected vertebrae is palpated or percussed.

Spine Percussion

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7. Is the pain in the costo-vertebral angle area, suggestive of a kidney infection?

Location of kidneys drawn on back. In the setting of kidney infection (pyelonephritis), percussion over this area will cause pain. 8. If the patient's complains of a radiating type pain down one leg, suggestive of nerve root irritation, proceed as follows: a. Ask the patient to lie down on their back. b. Have the patient completely relax the affected leg. c. Cup the heel of their foot and gently raise the leg. If there is nerve root irritation, the patient will experience their typical pain when the leg is elevated between 30 and 60 degrees. This is referred to at the "straight leg raise test" and is sensitive for identifying root pathology (i.e. if it does not reproduce pain, root irritation unlikely). Sensitive (75-90%), but not specific. Therefore, negative test helps rule out nerve root irritation as cause of pain. d. If the straight leg test is positive, repeat the same test on the opposite leg. This is called the crossed straight leg raised test and is 85-95% specific for root irritation, but not sensitive. Therefore, positive test makes root irritation the likely etiology of the symptoms.

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Leg Raise Test 9. Assess bilateral lower extremity strength. In particular, if concern that nerve root pathology has lead to motor dysfunction (quite uncommon) check the following: a. Resisted great toe extension (extensor hallicis longus), mediated by the L5 nerve root. b. Walking on toes, as plantar flexion is mediated by the S1 root. 10. Reflexes, in particular the Achilles, which is a function of the S1 root. 11. Distal sensation, paying attention to the L5 and S1 d

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12. If patient's note any bowel or bladder symptoms, assess sacral nerve root function as follows: a. Rectal tone: Patient should be able to contract anal sphincter around examining finger when directed to do so. b. Saddle area anesthesia: This is the region around the rectum, genitalia and inner thighs. Patients should be able to easily distinguish light touch and pin prick. c. Post Void Residual: Patient's should normally be able to completely empty their bladders. In acute sacral root dysfunction, this may be compromised. This can be assessed by using either a bedside bladder scan or placement of a foley catheter. While not part of the typical exam, it is important is this setting. 13. Gently internally and externally rotate the hip. In pyriformis syndrome internal rotation will stretch an already tight external rotator, causing further compression of the underlying nerve. This should reproduce the patient's symptoms. Straight and crossed leg raising will not reproduce symptoms. 14. Check pulses in feet to assure that symptoms not related to peripheral vascular disease. Detailed review of lower extremity examination. 158

15. If any concern that symptoms are referred from the abdomen, a detailed exam of this area is performed. Also, if concern that back pain is a manifestation of systemic illness, appropriate detailed general exam should be performed.

The Mental Status Exam (MSE)

In actual practice, providers (with the exception of a psychiatrist or neurologist) do not regularly perform an examination explicitly designed to assess a patient's mental status. During the course of the normal interview, most of the information relevant to this assessment is obtained indirectly. This review provides an opportunity to consciously think of the elements contained within the MSE. In the day to day practice of medicine (and, in fact, throughout all of our interactions) we continually come into contact with persons who have significantly impaired cognitive abilities, altered capacity for memory, disordered thought processes and otherwise abnormal mental status. First and foremost, the goal is to be able to note when these abnormalities exist (you'd be surprised at how frequently they can be missed) and then to categorize them as specifically as possible. If a person seems "odd, confused or not quite right" what do we mean by this? What about their behavior, appearance, speech, etc. has lead us to these conclusions? In some instances, the patient's condition (e.g. markedly depressed level of consciousness, intoxication) will preclude a complete, ordered evaluation of mental status, so flexibility is important. Knowing when to "cut your losses" and abandon a more detailed examination obviously takes a bit of experience! The formulation of actual diagnoses, the final step in this process is, for the most part, beyond the scope of this discussion (I've included two of the most commonly encountered ones at the end of this section as examples). In fact, even if you had the experience and knowledge to generate diagnoses, this still may not be possible after a single patient encounter. The interview provides a "snap shot" of the patient, a picture of them as they exist at one point in time. Frequently, and this applies to the physical examination as well, several interactions are required along with information about the patient's usual level of function before you can come to any meaningful conclusions about their current condition. The components of the MSE are as follows: 1. Appearance: How does the patient look? Neatly dressed with clear attention to detail? Well groomed? 2. Level of alertness: Is the patient conscious? If not, can they be aroused? Can they remain focused on your questions and conversation? What is their attention span? 3. Speech: Is it normal in tone, volume and quantity? 4. Behavior: Pleasant? Cooperative? Agitated? Appropriate for the particular situation? 5. Awareness of environment, also referred to as orientation: Do they know where they are and what they are doing here? Do they know who you are? Can they tell you the day, date and year?

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6. Mood: How do they feel? You may ask this directly (e.g. "Are you happy, sad, depressed, angry?"). Is it appropriate for their current situation? 7. Affect: How do they appear to you? This interpretation is based on your observation of their interactions during the interview. Do they make eye contact? Are they excitable? Does the tone of their voice change? Common assessments include: flat (unchanging throughout), excitable, appropriate. 8. Thought Process: This is a description of the way in which they think. Are their comments logical and presented in an organized fashion? If not, how off base are they? Do they tend to stray quickly to related topics? Are their thoughts appropriately linked or simply all over the map? 9. Thought Content: A description of what the patient is thinking about. Are they paranoid? Delusional (i.e. hold beliefs that are untrue)? If so, about what? Phobic? Hallucinating (you need to ask if they see or hear things that others do not)? Fixated on a single idea? If so, about what. Is the thought content consistent with their affect? If there is any concern regarding possible interest in committing suicide or homicide, the patient should be asked this directly, including a search for details (e.g. specific plan, time etc.). Note: These questions have never been shown to plant the seeds for an otherwise unplanned event and may provide critical information, so they should be asked! 10. Memory: Short term memory is assessed by listing three objects, asking the patient to repeat them to you to insure that they were heard correctly, and then checking recall at 5 minutes. Long term memory can be evaluated by asking about the patients job history, where they were born and raised, family history, etc. 11. Ability to perform calculations: Can they perform simple addition, multiplication? Are the responses appropriate for their level of education? Have they noticed any problems balancing their check books or calculating correct change when making purchases? This is also a test of the patient's attention span/ability to focus on a task. 12. Judgment: Provide a common scenario and ask what they would do (e.g. "If you found a letter on the ground in front of a mailbox, what would you do with it?"). 13. Higher cortical functioning and reasoning: Involves interpretation of complex ideas. For example, you may ask them the meaning of the phrase, "People in glass houses should not throw stones." A few common interpretations include: concrete (e.g. "Don't throw stones because it will break the glass"); abstract (e.g. "Don't judge others"); or bizarre. Diagnoses are made on the basis of a pattern of responses to the above evaluation. Two commonly occurring disorders are described below: 1. Delirium: Also referred to as Altered Mental Status, Delta MS, Acute Confusional State, or Toxic Metabolic State. This is a very common condition (particularly among hospitalized patients) notable for an acute, global change in mental status that can be the result of physiologic derangement anywhere within the body. Causes include: infection, hypoxia, toxic ingestion, impaired ability of the body to handle endogenously produced toxins (e.g. liver or kidney failure), etc. There is a wide spectrum of presentations, ranging from unarousable to extremely agitated. Patients may appear quite ill, with markedly abnormal vital signs that in themselves can suggest the cause of the delirium (e.g. hypotension, infection). 160

They are frequently confused, disoriented, agitated and uncooperative. Formal evaluation of mood, affect, memory, judgment or insight can be hopeless. Thought process is disordered and content notable for delusions, paranoia and hallucinations. In general, the diagnosis is suggested by the time course of the illness (i.e. the change is acute). Treatment is dictated by the underlying insult, which can generally be determined after a detailed history (usually with the help of others who are familiar with the patient), review of medications, thorough examination, and appropriate use of lab and radiologic testing. The elderly as well as those with multiple medical problems (conditions which frequently coexist) are at the highest risk for developing this condition. Delirium in this patient sub-set can be provoked by seemingly minor precipitants. Initial presentation of psychotic disorders as well as dementia can be mistaken for delirium (and vice versa). This can only be sorted out with time and appropriate testing, though these distinctions are extremely important. 2. Dementia: A final common pathway for multiple disorders characterized by its slow, progressive nature, taking months to years to develop. While quite uncommon under 50, the incidence increases markedly with age. Patient's appearance and behavior vary with the extent of involvement. This ranges from well groomed, alert and cooperative to agitated, unable to care for themselves and incapable of answering even simple questions. Mood and affect can range widely, and may or may not be appropriate for the given situation. Thought process and content have similar variability. Memory, judgment and higher cortical function deteriorate with time. As this is a progressive disease, presentation will depend on the level of advancement. Contributions from other acute, reversible medical problems must be ruled out on the basis of history, examination and laboratory testing. The Mini Mental Status Examination (MMSE) is a brief bedside test that is an excellent means of quantifying cognitive function and decline. The following article from The American Journal of Family Practice- Early Diagnosis of Dementia, by KAREN S. SANTACRUZ, M.D., and DANIEL SWAGERTY, M.D., M.P.H. University of Kansas Medical Center, Kansas City, Kansas provides a copy of this test along with assorted supporting information. MMSE can also be accessed via Alzheimer's Society, UK. Many aspects of the MSE are extremely subjective. There is tremendous potential for our own cultural exposure and background to color these assessments. Realize that there is a major distinction between "different" and "abnormal." Proverbs, for example, are not necessarily a part of any communal experience. Thus, a "failure" to provide a correct interpretation may in fact have nothing to do with an individual's intellectual function but rather may simply reflect a different upbringing or background. Similarly, tests of memory which require the subject to recite past U.S. Presidents may not be an appropriate measuring tool depending on a person's country of origin, language skills, educational level, etc. These situations are unavoidable in the extremely diverse community in which we live. Quantifying and defining the nature of a specific abnormality is an important part of the practice of medicine. While it is reasonable to expect that people be aware of certain basic facts (e.g. their name, the year, the purpose of their visit to the hospital, etc.) it is also important to recognize that our observation and interpretation of patient behavior and responses is colored by our own life experiences. 161

Many aspects of the MSE are extremely subjective. There is tremendous potential for our own cultural exposure and background to color these assessments. Realize that there is a major distinction between "different" and "abnormal." Proverbs, for example, are not necessarily a part of any communal experience. Thus, a "failure" to provide a correct interpretation may in fact have nothing to do with an individual's intellectual function but rather may simply reflect a different upbringing or background. Similarly, tests of memory which require the subject to recite past U.S. Presidents may not be an appropriate measuring tool depending on a person's country of origin, language skills, educational level, etc. These situations are unavoidable in the extremely diverse community in which we live. Quantifying and defining the nature of a specific abnormality is an important part of the practice of medicine. While it is reasonable to expect that people be aware of certain basic facts (e.g. their name, the year, the purpose of their visit to the hospital, etc.) it is also important to recognize that our observation and interpretation of patient behavior and responses is colored by our own life experiences.

The Neurological Examination

Cranial Sensory and Motor Nerves Examinations Introduction The goals of the neurological examination are several: 1. For patients presenting with symptoms suggestive of a neurological problem, the examination should: a. Determine, on the basis of an organized and thorough examination, whether in fact neurological dysfunction exists. b. Identify which component(s) of the neurological system are affected (e.g. motor, sensory, cranial nerves, or possibly several systems simultaneously). c. If possible, determine the precise location of the problem (e.g. peripheral v central nervous system; region and side of the brain affected etc.). d. On the basis of these findings, generate a list of possible etiologies. Unlikely diagnoses can be excluded and appropriate testing (e.g. brain and spinal cord imaging) then applied in an orderly and logical fashion. 2. Screening for the presence of discrete abnormalities in patients at risk for the development of neurological disorders. This is appropriate for individuals who have no particular subjective symptoms suggestive of a neurological problem, yet have systemic illnesses that might put them at risk for subtle dysfunction. Diabetic patients, for example (particularly those with long standing poor control), may develop peripheral nerve dysfunction. This may only be detected
Reflex Testing Cerebellar Gait Testing Testing Making Sense of Neurological Findings

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through careful sensory testing (see below under Sensory Testing), which would have important clinical implications. 3. Cursory screening/documentation of baseline function for those who are otherwise healthy. In patients with neither signs nor risk factors for neurological disease, its unlikely that the detailed exam would uncover occult problems. Simply observing the patient during the course of the usual H&P (i.e. watching them walk, get up and down from the exam table, etc.) may well suffice. Many examiners incorporate some aspects of the neuro exam into their standard evaluations. Cranial Nerve testing, for example, can be easily blended into the Head and Neck evaluation. Deciding what other aspects to routinely include is based on judgment and experience. The major areas of the exam, covering the most testable components of the neurological system, include: 1. 2. 3. 4. 5. 6. 7. Mental status testing (covered in a separate section of this web site) Cranial Nerves Muscle strength, tone and bulk Reflexes Cerbellar Function Sensory Function Gait

Real and imagined problems with the neurological examination: The neurological examination is one of the least popular and (perhaps) most poorly performed aspects of the complete physical. I suspect that this situation exists for several reasons: 1. This exam is perceived as being time and labor intensive. 2. Students and house staff never develop an adequate level of confidence in their ability to perform the exam, nor in the accuracy of their findings. This, in turn, probably translates into poor performance later in their careers. 3. Exam findings are often quite subjective.Thus, particularly when the examiner does not have confidence in their abilities (see above), interpretation of the results can be problematic. 4. Understanding/Interpretation of some neurological findings requires an in depth understanding of neuroanatomy and pathophysiology. As many clinicians do not see a large number of patients with neurological disorders, they likely maintain a limited working understanding of this information. 5. There is an over reliance on the utility of neuro-imaging (e.g. CT, MRI). These studies provide an evaluation of anatomy but not function. Thus, while extremely helpful, they must be interpreted within the context of exam findings. Careful examination may make imaging unnecessary. Also, exam findings can make a strong case for the presence of a pathologic process, even if it is not seen on a particular radiological study (i.e. there are limits to what can be seen on even the most high tech imaging).

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The above are not meant to lower expectations with regards to how well a physician should be expected to learn and perform the neurological examination. Rather, I mention these points to highlight some of the real and imagined obstacles to clinical performance. Like all other aspects of the physical exam, there is a wealth of information that can be obtained from the neurological examination, provided that it is done carefully and accurately.This is, of course, predicated on learning how to do it correctly. A few practical considerations/suggestions: 1. In general, the neurological examination is not applied in its entirety to asymptomatic, otherwise healthy people as the yield (i.e. likelihood of identifying occult disease) would be quite low. It is, however, a good idea to practice the exam early in your careers, even when working with normal patients.This will improve the facility with which you perform the exam, provide you with a better sense of the range of normal, increase the accuracy of the results generated, and give you confidence in the meaning of findings identified when evaluating other patients. 2. It is sometimes appropriate to perform only certain parts of the neurological examination (e.g. just cranial nerves; or only motor testing)These situations will become apparent with experience. 3. The testing described below is still rather basic. There are many additional aspects of the exam that should be applied in specific settings. They are beyond the scope of this text, but can be found in other references. 4. Take advantage of those opportunities when a more experienced clinician examines one of your patients. When possible, watch them perform their exam. Then go back alone and verify the findings. Like any other aspect of the exam, the neurological assessment has limits. Testing of one system is often predicated on the normal function of other organ systems. If, for example, a patient is visually impaired, they may not be able to perform finger to nose testing, a part of the assessment of cerebellar function (see below). Or, a patients severe degenerative hip disease will prevent them from walking, making that aspect of the exam impossible to assess. The interpretation of findings must therefore take these things into account. Only in this way can you generate an accurate picture. Doing this, of course, takes practice and experience. Cranial Nerve (CN) Testing CN2 CN3, 4, 5 CN6

CN7

CN8

CN9, 10

CN11

CN12

Many practitioners incorporate cranial nerve testing with their complete examination of the head and neck (see the Head and Neck section of this web site for details). A detailed description of the CN assessment is provided below. As each half of the body has its own cranial nerve, both right and left sides must be checked independently. Cranial Nerve 1 (Olfactory): Formal assessment of ability to smell is generally omitted, unless there is a specific complaint. If it is to be tested:

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1. Each nostril should be checked separately. Push on the outside of the nares, occluding the side that is not to be tested. 2. Have the patient close their eyes. Make sure that the patient is able to inhale and exhale through the open nostril. 3. Present a small test tube filled with something that has a distinct, common odor (e.g. ground coffee) to the open nostril. The patient should be able to correctly identify the smell. If you wish to test olfaction and dont have any substance filled tubes use an alcohol pad as a screening test. Patients should be able to identify its distinctive odor from approximately 10 cm .

Alcohol Pad Sniff Test For more information about CN1, see the following links: Cranial Nerve 2 (Optic): This nerve carries visual impulses from the eye to the optical cortex of the brain by means of the optic tracts. Testing involves 3 phases (also covered in the section of this site dedicated to the Eye Exam): 1. Acuity: a. Each eye is tested separately. If the patient uses glasses to view distant objects, they should be permitted to wear them (referred to as best corrected vision). b. A Snellen Chart is the standard, wall mounted device used for this assessment. Patients are asked to read the letters or numbers on successively lower lines (each with smaller images) until you identify the last line which can be read with 100% accuracy. Each line has a fraction written next to it. 20/20 indicates normal vision. 20/400 means that the patient's vision 20 feet from an object is equivalent to that of a normal person viewing the same object from 400 feet. In other words, the larger the denominator, the worse the vision. 165

Snellen chart for measuring visual acuity c. There are hand held cards that look like Snellen Charts but are positioned 14 inches from the patient. These are used simply for convenience. Testing and interpretation are as described for the Snellen.

Hand held visual acuity card

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d. If neither chart is available and the patient has visual complaints, some attempt should be made to objectively measure visual acuity. This is a critically important reference point, particularly when trying to communicate the magnitude of a visual disturbance to a consulting physician. Can the patient read news print? The headline of a newspaper? Distinguish fingers or hand movement in front of their face? Detect light? Failure at each level correlates with a more severe problem. 2. Visual Field Testing: Specific areas of the retina receive input from precise areas of the visual field. This information is carried to the brain along well defined anatomic pathways. Holes in vision (referred to as visual field cuts) are caused by a disruption along any point in the path from the eyeball to the visual cortex of the brain. Visual fields can be crudely assessed as follows: a. The examiner should be nose to nose with the patient, separated by approximately 8 to 12 inches. b. Each eye is checked separately. The examiner closes one eye and the patient closes the one opposite. The open eyes should then be staring directly at one another. c. The examiner should move their hand out towards the periphery of his/her visual field on the side where the eyes are open. The finger should be equidistant from both persons. d. The examiner should then move the wiggling finger in towards them, along an imaginary line drawn between the two persons.The patient and examiner should detect the finger at more or less the same time. e. The finger is then moved out to the diagonal corners of the field and moved inwards from each of these directions. Testing is then done starting at a point in front of the closed eyes. The wiggling finger is moved towards the open eyes. f. The other eye is then tested. Meaningful interpretation is predicated upon the examiner having normal fields, as they are using themselves for comparison. If the examiner cannot seem to move their finger to a point that is outside the patients field dont worry, as it simply means that their fields are normal. Interpretation: This test is rather crude, and it is quite possible to have small visual field defects that would not be apparent on this type of testing. Prior to interpreting abnormal findings, the examiner must understand the normal pathways by which visual impulses travel from the eye to the brain. For more information about visual field testing, see the following links: 3. Pupils: The pupil has afferent (sensory) nerves that travel with CN2. These nerves carry the impulse generated by the light back towards the brain. They function in concert with efferent (motor) nerves that travel with CN 3 and cause pupillary constriction. Seen under CN 3 for specifics of testing.

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For more information about CN 2, see the following links: CN 3 (Occulomotor): This nerve is responsible for most of the eyeballs mobility, referred to as extra-occular movement. CN 3 function is assessed in concert with CNs 4 and 6, the other nerves responsible for controlling eyeball movement. CN 4 controls the Superior Oblique muscle, which allows each eye to look down and medially. CN 6 controls the Lateral Rectus muscle, which allows each eye to move laterally. CN 3 controls the muscles which allow motion in all other directions. The pneumonic S O 4 L R 6 All The Rest 3 may help remind you which CN does what (Superior Oblique CN 4 LateralRectus CN 6 All The Rest of the muscles innervated by CN 3). Testing is done as follows: 1. Ask the patient to keep their head in one place. Then direct them to follow your finger while moving only their eyes. 2. Move your finger out laterally, then up and down. 3. Then move your finger across the patients face to the other side of their head. When it is out laterally, move it again up and down. You will roughly trace out the letter H, which takes both eyeballs through the complete range of movements. At the end, bring your finger directly in towards the patient's nose. This will cause the patient to look cross-eyed and the pupils should constrict, a response referred to as accommodation.

CN 3 also innervates the muscle which raises the upper eye lid. This can first be assessed by simply looking at the patient. If there is CN 3 dysfuntion, the eyelid on that side will cover more of the iris and pupil compared with the other eye. This is referred to as ptosis.

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Right CN3 Lesion: Note patient's right eye is deviated laterally and there is ptosis of the lid (picture on left), and the right pupil (middle picture) is more dilated than the left pupil (picture on far right).

CN6 Palsy: This patient is unable to move left eye lateral of midline due to left CN6 lesion. Its also worth noting that disorders of the extra ocular muscles themselves (and not the CN which innervate them) can also lead to impaired eye movement. For example, pictured below is a patient who has suffered a traumatic left orbital injury. The inferior rectus muscle has become entrapped within the resulting fracture, preventing the left eye from being able to look downward.

Entrapment of Left Inferior Rectus Muscle The response of pupils to light is controlled by afferent (sensory) nerves that travel with CN 2 and efferent (motor) nerves that travel with CN 3. These innervate the ciliary muscle, which controls the size of the pupil. Testing is performed as follows: 1. It helps if the room is a bit dim, as this will cause the pupil to become more dilated. 2. Using any light source (flashlight, oto-ophtahlmoscope, etc), shine the light into one eye. This will cause that pupil to constrict, referred to as the direct response. 3. Remove the light and then re-expose it to the same eye, though this time observe the other pupil. It should also constrict, referred to as the consensual response.

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This occurs because afferent impulses from one eye generate an efferent response (i.e. signal to constrict) that is sent to both pupils. 4. If the patients pupils are small at baseline or you are otherwise having difficulty seeing the changes, take your free hand and place it above the eyes so as to provide some shade. This should cause the pupils to dilate additionally, making the change when they are exposed to light more dramatic. If you are still unable to appreciate a response, ask the patient to close their eye, generating maximum darkness and thus dilatation. Then ask the patient to open the eye and immediately expose it to the light. This will (hopefully) make the change from dilated to constricted very apparent. Interpretation: 1. Under normal conditions, both pupils will appear symmetric. Direct and consensual response should be equal for both. 2. Asymmetry of the pupils is referred to as aniosocoria. Some people with anisocoria have no underlying neuropathology. In this setting, the asymmetry will have been present for a long time without change and the patient will have no other neurological signs or symptoms. The direct and consensual responses should be preserved. 3. A number of conditions can also affect the size of the pupils. Medications/intoxications which cause generalized sympathetic activation will result in dilatation of both pupils. Other drugs (e.g. narcotics) cause symmetric constrictionof the pupils. These findings can provide important clues when dealing with an agitated or comatose patient suffering from medication overdose. Eye drops known as mydriatic agents are used to paralyze the muscles, resulting marked dilatation of the pupils. They are used during a detailed eye examination, allowing a clear view of the retina. Addiitonally, any process which causes increased intracranial pressure can result in a dilated pupil that does not respond to light. 4. If the afferent nerve is not working, neither pupil will respond when light is shined in the affected eye. Light shined in the normal eye, however, will cause the affected pupil to constrict. Thats because the efferent (signal to constrict) response in this case is generated by the afferent impulse received by the normally functioning eye. This is referred to as an afferent pupil defect. 5. If the efferent nerve is not working, the pupil will appear dilated at baseline and will have neither direct nor consensual pupillary responses. For more information about pupillary response and CN 3, see the following links: CN 4 (Trochlear): Seen under CN 3. CN 5 (Trigeminal): This nerve has both motor and sensory components. Assessment of CN 5 Sensory Function: The sensory limb has 3 major branches, each covering roughly 1/3 of the face. They are: the Ophthlamic, Maxillary, and Mandibular. Assessment is performed as follows:

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1. Use a sharp implement (e.g. broken wooden handle of a cotton tipped applicator). 2. Ask the patient to close their eyes so that they receive no visual cues. 3. Touch the sharp tip of the stick to the right and left side of the forehead, assessing the Ophthalmic branch. 4. Touch the tip to the right and left side of the cheek area, assessing the Maxillary branch. 5. Touch the tip to the right and left side of the jaw area, assessing the Mandibular branch. The patient should be able to clearly identify when the sharp end touches their face. Of course, make sure that you do not push too hard as the face is normally quite sensitive. The Ophthalmic branch of CN 5 also receives sensory input from the surface of the eye. To assess this component:

1. Pull out a wisp of cotton. 2. While the patient is looking straight ahead, gently brush the wisp against the lateral aspect of the sclera (outer white area of the eye ball). 3. This should cause the patient to blink. Blinking also requires that CN 7 function normally, as it controls eye lid closure. Assessment of CN 5 Motor Function: The motor limb of CN 5 innervates the Temporalis and Masseter muscles, both important for closing the jaw. Assessment is performed as follows: 1. Place your hand on both Temporalis muscles, located on the lateral aspects of the forehead. 2. Ask the patient to tightly close their jaw, causing the muscles beneath your fingers to become taught. 3. Then place your hands on both Masseter muscles, located just in from of the Tempero-Mandibular joints (point where lower jaw articulates with skull). 4. Ask the patient to tightly close their jaw, which should again cause the muscles beneath your fingers to become taught. Then ask them to move their jaw from side to side, another function of the Massester.

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CN6 (Abducens): See under CN 3. CN7 (Facial): This nerve innervates many of the muscles of facial expression. Assessment is performed as follows: 1. First look at the patients face. It should appear symmetric. That is: a. There should be the same amount of wrinkles apparent on either side of the forehead barring asymmetric Bo-Tox injection! b. The nasolabial folds (lines coming down from either side of the nose towards the corners of the mouth) should be equal c. The corners of the mouth should be at the same height If there is any question as to whether an apparent asymmetry if new or old, ask the patient for a picture (often found on a drivers license) for comparison. 2. Ask the patient to wrinkle their eyebrows and then close their eyes tightly. CN 7 controls the muscles that close the eye lids (as opposed to CN 3, which controls the muscles which open the lid). You should not be able to open the patients eyelids with the application of gentle upwards pressure. 3. Ask the patient to smile. The corners of the mouth should rise to the same height and equal amounts of teeth should be visible on either side. 4. Ask the patient to puff out their cheeks. Both sides should puff equally and air should not leak from the mouth. Interpretation: CN 7 has a precise pattern of inervation, which has important clinical implications. The right and left upper motor neurons (UMNs) each innervate both the right and left lower motor neurons (LMNs) that allow the forehead to move up and down.

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However, the LMNs that control the muscles of the lower face are only innervated by the UMN from the opposite side of the face. CN7 - Facial Nerve Precise Pattern of Innervation

Thus, in the setting of CN 7 dysfunction, the pattern of weakness or paralysis observed will differ depending on whether the UMN or LMN is affected. Specifically: 1. UMN dysfunction: This might occur with a central nervous system event, such as a stroke. In the setting of R UMN CN 7 dysfunction, the patient would be able to wrinkle their forehead on both sides of their face, as the left CN 7 UMN cross innervates the R CN 7 LMN that controls this movement. However, the patient would be unable to effectively close their left eye or raise the left corner of their mouth.

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Right central CN7 dysfunction: Note preserved abiltiy to wrinkle forehead. Left corner of mouth, however, is slightly lower than right. Left naso-labial fold is slightly less pronounced compared with right. 2. LMN dysfunction: This occurs most commonly in the setting of Bells Palsy, an idiopathic, acute CN 7 peripheral nerve palsy. In the setting of R CN 7 peripheral (i.e. LMN) dysfunction, the patient would not be able to wrinkle their forehead, close their eye or raise the corner of their mouth on the right side. Left sided function would be normal.

Left peripheral CN7 dysfunction: Note loss of forehead wrinkle, ability to close eye, ability to raise corner of mouth, and decreased naso-labial fold prominence on left. This clinical distinction is very important, as central vs peripheral dysfunction carry different prognostic and treatment implications. Bells Palsy (peripheral CN 7 dysfunction)tends to happen in patients over 50 and often responds to treatment with Acyclovir (an anti-viral agent) and Prednisone (a corticosteroid). Over the course of weeks or months there is usually improvement and often complete resolution of symptoms. Assessment of acute central (UMN) CN 7 dysfunction would require quite a different approach (e.g. neuroimaging to determine etiology). CN 7 is also responsible for carrying taste sensations from the anterior 2/3 of the tongue. However as this is rarely of clinical import, further discussion is not included. CN8 (Acoustic): CN 8 carries sound impulses from the cochlea to the brain. Prior to reaching the cochlea, the sound must first traverse the external canal and middle ear. Auditory acuity can be assessed very crudely on physical exam as follows: 1. Stand behind the patient and ask them to close their eyes.

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2. Whisper a few words from just behind one ear. The patient should be able to repeat these back accurately. Then perform the same test for the other ear. 3. Alternatively, place your fingers approximately 5 cm from one ear and rub them together. The patient should be able to hear the sound generated. Repeat for the other ear. These tests are rather crude. Precise quantification, generally necessary whenever there is a subjective decline in acuity, requires special equipment and training. The cause of subjective hearing loss can be assessed with bedside testing. Hearing is broken into 2 phases: conductive and sensorineural. The conductive phase refers to the passage of sound from the outside to the level of CN 8. This includes the transmission of sound through the external canal and middle ear. Sensorineural refers to the transmission of sound via CN 8 to the brain. Identification of conductive (a much more common problem in the general population) defects is determined as follows: Weber Test: 1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone. Alternatively you can get the fork to vibrate by "snapping" the ends between your thumb and index finger. 512 Hz Tuning Fork

2. Hold the stem against the patients skull, along an imaginary line that is equidistant from either ear. 3. The bones of the skull will carry the sound equally to both the right and left CN 8. Both CN 8s, in turn, will transmit the impulse to the brain. 4. The patient should report whether the sound was heard equally in both ears or better on one side then the other (referred to as lateralizing to a side).

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Weber Test Rinne Test: 1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone. 2. Place the stem of the tuning fork on the mastoid bone, the bony prominence located immediately behind the lower part of the ear. 3. The vibrations travel via the bones of the skull to CN 8, allowing the patient to hear the sound. 4. Ask the patient to inform you when they can no longer appreciate the sound. When this occurs, move the tuning fork such that the tines are placed right next to (but not touching) the opening of the ear. At this point, the patient should be able to again hear the sound. This is because air is a better conducting medium then bone.

Rinne Test Interpretation: 1. The above testing is reserved for those instances when a patient complains of a deficit in hearing. Thus, on the basis of history, there should be a complaint of hearing decline in one or both ears.

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2. In the setting of a conductive hearing loss (e.g. wax in the external canal), the Webber test will lateralize (i.e. sound will be heard better)in the ear that has the subjective decline in hearing. This is because when there is a problem with conduction, competing sounds from the outside cannot reach CN 8 via the external canal. Thus, sound generated by the vibrating tuning fork and traveling to CN 8 by means of bony conduction is better heard as it has no outside competition. You can transiently create a conductive hearing loss by putting the tip of your index finger in the external canal of one ear. If you do this while performing the Webber test, the sound will be heard on that side. 3. In the setting of a sensorineural hearing loss (e.g. a tumor of CN 8), the Webber test will lateralize to the ear which does not have the subjective decline in hearing. This is because CN 8 is the final pathway through which sound is carried to the brain. Thus, even though the bones of the skull will successfully transmit the sound to CN 8, it cannot then be carried to the brain due to the underlying nerve dysfunction. 4. In the setting of conductive hearing loss, bone conduction (BC) will be better then air conduction (AC) when assessed by the Rinne Test. If there is a blockage in the passageway (e.g. wax) that carries sound from the outside to CN 8, then sound will be better heard when it travels via the bones of the skull. Thus, the patient will note BC to be better then or equal to AC in the ear with the subjective decline in hearing. 5. In the setting of a sensorineural hearing loss, air conduction will still be better then bone conduction (i.e. the normal pattern will be retained). This is because the problem is at the level of CN 8. Thus, regardless of the means (bone or air) by which the impulse gets to CN 8, there will still be a marked hearing decrement in the affected ear. As AC is normally better then BC, this will still be the case. Summary: Identifying conductive v sensorineural hearing deficits requires historical information as well as the results of Webber and Rinne testing. In summary, this data is interpreted as follows: 1. First determine by history and crude acuity testing which ear has the hearing problem. 2. Perform the Webber test. If there is a conductive hearing deficit, the Webber will lateralize to the affected ear. If there is a sensorineural deficit, the Webber will lateralize to the normal ear. 3. Perform the Rinne test. If there is a conductive hearing deficit, BC will be greater then or equal to AC in the affected ear. If there is a sensorineural hearing deficit, AC will be greater then BC in the affected ear. For more information about CN 8, see the following links: CN9 (Glosopharyngeal) and CN 10 (Vagus): These nerves are responsible for raising the soft palate of the mouth and the gag reflex, a protective mechanism which prevents food or liquid from traveling into the lungs As both CNs contribute to these functions, they are tested together. 177

Testing Elevation of the soft palate: 1. Ask the patient to open their mouth and say, ahhhh, causing the soft palate to rise upward. 2. Look at the uvula, a midline structure hanging down from the palate. If the tongue obscures your view, take a tongue depressor and gently push it down and out of the way. 3. The Uvula should rise up straight and in the midline.

Normal Oropharynx Interpretation: If CN 9 on the right is not functioning (e.g. in the setting of a stroke), the uvula will be pulled to the left. The opposite occurs in the setting of left CN 9 dysfunction.

Left CN9 Dysfunction: Patient status post stroke affecting left CN9. Uvula therefore pulled over towards right. Be aware that other processes can cause deviation of the uvula.A peritonsilar abscess, for example, will push the uvula towards the opposite (i.e. normal) tonsil.

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Left peritonsillar abscess: infection within left tonsil has pushed uvula towards the right. Testing the Gag Reflex: 1. Ask the patient to widely open their mouth. If you are unable to see the posterior pharynx (i.e. the back of their throat), gently push down with a tongue depressor. 2. In some patients, the tongue depressor alone will elicit a gag. In most others, additional stimulation is required. Take a cotton tipped applicator and gently brush it against the posterior pharynx or uvula. This should generate a gag in most patients. 3. A small but measurable percent of the normal population has either a minimal or non-existent gag reflex. Presumably, they make use of other mechanisms to prevent aspiration. Gag testing is rather noxious. Some people are particularly sensitive to even minimal stimulation. As such, I would suggest that you only perform this test when there is reasonable suspicion that pathology exists. This would include two major clinical situations: 1. If you suspect that the patient has suffered acute dysfunction, most commonly in the setting of a stroke. These patients may complain of/be noted to cough when they swallow. Or, they may suffer from recurrent pneumonia. Both of these events are signs of aspiration of food contents into the passageways of the lungs. These patients may also have other cranial nerve abnormalities as lesions affecting CN 9 and 10 often affect CNs 11 and 12, which are anatomically nearby. 2. Patients suffering from sudden decreased level of consciousness. In this setting, the absence of a gag might indicate that the patient is no longer able to reflexively protect their airway from aspiration. Strong consideration should be given to intubating the patient, providing them with a secure mechanical airway until their general condition improves. CN 9 is also responsible for taste originating on the posterior 1/3 of the tongue. As this is rarely a clinically important problem, further discussion is not included.

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CN 10 also provides parasympathetic innervation to the heart, though this cannot be easily tested on physical examination. CN11 (Spinal Accessory): CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius) and turning the head laterally (Sternocleidomastoid). 1. Place your hands on top of either shoulder and ask the patient to shrug while you provide resistance. Dysfunction will cause weakness/absence of movement on the affected side.

2. Place your open left hand against the patients right cheek and ask them to turn into your hand while you provide resistance. Then repeat on the other side. The right Sternocleidomasoid muscle (and thus right CN 11) causes the head to turn to the left, and vice versa.

CN12 (Hypoglossal): CN 12 is responsible for tongue movement. Each CN 12 innervates one-half of the tongue. Testing: 1. Ask the patient to stick their tongue straight out of their mouth.

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2. If there is any suggestion of deviation to one side/weakness, direct them to push the tip of their tongue into either cheek while you provide counter pressure from the outside.

Interpretation: If the right CN 12 is dysfunctional, the tongue will deviate to the right. This is because the normally functioning left half will dominate as it no longer has opposition from the right. Similarly, the tongue would have limited or absent ability to resist against pressure applied from outside the left cheek.

Left CN 12 Dysfunction: Stroke has resulted in L CN 12 Palsy. Tongue therefore deviates to the left. Sensory and Motor Examinations A Brief Review of Anatomy and Physiology: Testing of motor and sensory function requires a basic understanding of normal anatomy and physiology. In brief: 1. Voluntary movement begins with an impulse generated by cell bodies located in the brain.

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2. Signals travel from these cells down their respective axons, forming the Cortiospinal (a.k.a. Pyramidal) tract. At the level of the brain stem, this motor pathway crosses over to the opposite side of the body and continue downward on that side of the spinal cord. The nerves which comprise this motor pathway are collectively referred to as Upper Motor Neurons (UMNs). Its important to note that there are other motor pathways that carry impulses from the brain to the periphery and help modulate movement. A discussion of these tracts can be found in other Neurology reference texts. 3. At a specific point in the spinal cord the axon synapses with a 2nd nerve, referred to as a Lower Motor Neuron (LMN). The precise location of the synapse depends upon where the lower motor neuron is destined to travel. If, for example, the LMN terminates in the hand, the synapse occurs in the cervical spine (i.e. neck area). However, if its headed for the foot, the synapse occurs in the lumbar spine (i.e. lower back). 4. The UMNs are part of the Central Nervous System (CNS), which is composed of neurons whose cell bodies are located in the brain or spinal cord. The LMNs are part of the Peripheral Nervous System (PNS), made up of motor and sensory neurons with cell bodies located outside of the brain and spinal cord. The axons of the PNS travel to and from the periphery, connecting the organs of action (e.g. muscles, sensory receptors) with the CNS. 5. Nerves which carry impulses away from the CNS are referred to Efferents (i.e. motor) while those that bring signals back are called Afferents (i.e. sensory). 6. Axons that exit and enter the spine at any given level generally connect to the same distal anatomic area. These bundles of axons, referred to as spinal nerve roots, contain both afferent and efferent nerves. The roots exit/enter the spinal cord through neruoforamina in the spine, paired openings that allow for their passage out of the bony protection provided by the vertebral column. 7. As the efferent neurons travels peripherally, components from different roots commingle and branch, following a highly programmed pattern. Ultimately, contributions from several roots may combine to form a named peripheral nerve, which then follows a precise anatomic route on its way to innervating a specific muscle. The Radial Nerve, for example, travels around the Humerus (bone of the upper arm), contains contributions from Cervical Nerve Roots 6, 7 and 8 and innervates muscles that extend the wrist and supinate the forearm. It may help to think of a nerve root as an electrical cable composed of many different colored wires, each wire representing an axon. As the cable moves away from the spinal cord, wires split off and head to different destinations. Prior to reaching their targets, they combine with wires originating from other cables. The group of wires that ultimately ends at a target muscle group may therefore have contributions from several different roots. For more information about radial nerve anatomy and function, see below. 8. Afferents carry impulses in the opposite direction of the motor nerves. That is, they bring information from the periphery to the spinal cord and brain. 9. Sensory nerves begin in the periphery, receiving input from specialized receptor organs. The axons then move proximally, joining in a precise fashion with other axons to form the afferent component of a named peripheral nerve. The Radial 182

Nerve, for example, not only has a motor function (described previously) but also carries sensory information from discrete parts of the hand and forearm. 10. As the sensory neurons approach the spinal cord, they join specific spinal nerve roots. Each root carries sensory information from a discrete area of the body. The area of skin innervated by a particular nerve root is referred to as a dermatome. Dermatome maps describe the precise areas of the body innervated by each nerve root. These distributions are more or less the same for all people, which is clinically important. In the setting of nerve root dysfunction, the specific area supplied by that root will be affected. This can be mapped out during a careful exam (see below), identifying which root(s) is dysfunctional. view a dermatomal map, Sensory input travels up through the spinal cord along specific paths, with the precise route defined by the type of sensation being transmitted. Nerves carrying pain impulses, for example, cross to the opposite side of the spinal cord soon after entering, and travel up to the brain on that side of the cord. Vibratory sensations, on the other hand, enter the cord and travel up the same side, crossing over only when they reach the brain stem (see following sections for detailed descriptions). For more information about sensory pathways, see the following link: 11. Ultimately, the sensory nerves terminate in the brain, where the impulses are integrated and perception occurs. Understanding the above neruo-anatomic relationships and patterns of innervation has important clinical implications when trying to determine the precise site of neurological dysfunction. Injury at the spinal nerve root level, for example, will produce a characteristic loss of sensory and motor function. This will differ from that caused by a problem at the level of the peripheral nerve. An approach to localizing lesions on the basis of motor and sensory findings is described in the sections which follow. Realize that there is a fair amount of inter-individual variation with regards to the specifics of innervation. Also, recognize that often only parts of nerves may become dysfunctional, leading to partial motor or sensory deficits. As such, the patterns of loss are rarely as pure as might be suggested by the precise descriptions of nerves and their innervations. Sensory Testing Sensory testing of the face is discussed in the section on Cranial Nerves. Testing of the extremities focuses on the two main afferent pathways: Spinothalamics and Dorsal Columns. 1. Spinothalamics: These nerves detect pain, temperature and crude touch. They travel from the periphery, enter the spinal cord and then cross to the other side of the cord within one or two vertebral levels of their entry point They then continue up that side to the brain, terminating in the cerebral hemisphere on the opposite side of the body from where they began.

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2. Dorsal Columns: These nerves detect position (a.k.a. proprioception), vibratory sensation and light touch. They travel from the periphery, entering the spinal cord and then moving up to the base of the brain on the same side of the cord as where they started. Upon reaching the brain stem they cross to the opposite side, terminating in the cerebral hemisphere on the opposite side of the body from where they began. A screening evaluation of these pathways can be performed as follows: Spinothalamics 1. The patient's ability to perceive the touch of a sharp object is used to assess the pain pathway of the Spinothalamics. To do this, break a Q-tip or tongue depressor in half, such that you create a sharp, pointy end. Alternatively, you can use a disposable needle as the sharp-ended probe. I would discourage the use of the pointy, metal spikes that accompany some reflex hammers. If, for example, you used this and caused bleeding, its possible (if the tip were not well cleaned) to transmit blood borne infections from one patient to another. Better to use a disposable implement. 2. Ask the patient to close their eyes so that they are not able to get visual clues. 3. Start at the top of the foot. Orient the patient by informing them that you are going to first touch them with the sharp implement. Then do the same with a nonsharp object (e.g. the soft end of a q-tip). This clarifies for the patient what you are defining as sharp and dull.

4. Now, touch the lateral aspect of the foot with either the sharp or dull tool, asking them to report their response. Move medially across the top of the foot, noting their response to each touch. 5. If they give accurate responses, do the same on the other foot. The same test can be repeated for the upper extremities (i.e. on the hand), though this would only be of utility if the patient complained of numbness/impaired sensation in that area.

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Dorsal Columns Proprioception: This refers to the bodys ability to know where it is in space. As such, it contributes to balance. Similar to the Spinothalamic tracts, disorders which affect this system tend to first occur at the most distal aspects of the body. Thus, proprioception is checked first in the feet and then, if abnormal, more proximally (e.g. the hands). Technique: 1. Ask the patient to close their eyes so that they do not receive any visual cues. 2. Grasp either side of the great toe. Orient the patient as to up and down. Flex the toe (pull it upwards) while telling the patient what you are doing. Then extend the toe (pull it downwards) while again informing them of which direction you are moving it.

Testing Proprioception 3. Alternately deflect the toe up or down without telling the patient in which direction you are moving it. They should be able to correctly identify the movement and direction. 4. Both great toes should be checked in the same fashion. If normal, no further testing need be done in the screening exam. 5. If the patient is unable to correctly identify the movement/direction, move more proximally (e.g. to the ankle joint) and repeat (e.g. test whether they can determine whether the foot is moved up or down at the ankle). Similar testing can be done on the fingers. This is usually reserved for those settings when patients have distal findings and/or symptoms in the upper extremities. Vibratory Sensation: Vibratory sensation travels to the brain via the dorsal columns. Thus, the findings generated from testing this system should corroborate those of proprioception (see above).

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Technique: 1. Start at the toes with the patient seated. You will need a 128 hz tuning fork.

128 Hz tuning fork 2. Ask the patient to close their eyes so that they do not receive any visual cues. 3. Grasp the tuning fork by the stem and strike the forked ends against the heel of your hand, causing it to vibrate. 4. Place the stem on top of the interphalangeal joint of the great toe. Put a few fingers of your other hand on the bottom-side of this joint.

Testing vibratory sensation 5. Ask the patient if they can feel the vibration. You should be able to feel the same sensation with your fingers on the bottom side of the joint. 6. The patient should be able to determine when the vibration stops, which will correlate with when you are no longer able to feel it transmitted through the joint. It sometimes takes a while before the fork stops vibrating. If you want to move

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things along, rub the index finger of the hand holding the fork along the tines, rapidly dampening the vibration. Repeat testing on the other foot. Additional/Special Testing for Dorsal Column Dysfunction Testing Two Point Discrimination: Patients should normally be able to distinguish simultaneous touch with 2 objects which are separated by at least 5mm. These stimuli are carried via the Dorsal Columns. While not checked routinely, it is useful test if a discrete peripheral neruropathy is suspected (e.g. injury to the radial nerve). Technique: 1. Testing can be done with a paperclip, opened such that the ends are 5mm apart. 2. The patient should be able to correctly identify whether you are touching them with one or both ends simultaneously, along the entire distribution of the specific nerve which is being assessed. Special Testing for Early Diabetic Neuropathy: A careful foot examination should be performed on all patients with symptoms suggestive of sensory neuropathy or at particular risk for this disorder (e.g. anyone with Diabetes). Loss of sensation in this area can be particularly problematic as the feet are a difficult area for the patient to evaluate on their own. Small wounds can become large and infected, unbeknownst to the insensate patient. Sensory testing as described above can detect this type of problem. Disposable monofilaments (known as the Semmes-Weinstein Aethesiometer) are specially designed for a screening evaluation. These small nylon fibers are designed such that the normal patient should be able to feel the ends when they are gently pressed against the soles of their feet.

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Technique: 1. Have the patient close their eyes so that they do not receive any visual cues. 2. Touch the monofilament to 5-7 areas on the bottom of the patient's foot. Pick locations so that all of the major areas of the sole are assessed. Avoid calluses, which are relatively insensate. 3. The patient should be able to detect the filament when the tip is lightly applied to the skin.

Monofiliment testing: Patients with normal sensation should be able to detect the monofiliment when it is lightly applied (picture on left). If the force required to provoke a sensory response is strong enough to bend the monofiliment (picture on right), then sensation is impaired. Interpretation: If the examiner has to supply enough pressure such that the filament bends prior to the patient being able to detect it, they likely suffer from sensory neuropathy. Testing should be done in multiple spots to verify the results. Patients with distal sensory neuropathy should carefully examine their feet and wear good fitting shoes to assure that skin breakdown and infections dont develop. Efforts should also be made to closely control their diabetes so that the neuropathy does not progress.

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Neuropathic Ulcer: Large ulcer has developed in this patient with severe diabetic neuropathy. Interpreting Results of Sensory Testing Patterns of Impairment for the Spinothalamic Tracts: 1. Patients should be able to correctly distinguish sharp sensation, indicating normal function of the spinothalamic pathway. 2. Mapping out regions of impaired sensation: The examination described above is a screening evaluation for evidence of sensory loss. This is perfectly adequate in most clinical settings. Occasionally, the history or screening examination will suggest a discrete anatomic region that has sensory impairment. When this occurs, it is important to try and map out the territory involved, using careful pin testing to define the medial/lateral and proximal/distal boundaries of the affected region. You may even make pen marks on the skin to clearly identify where the changes occur. As most clinicians have not memorized the distributions of all peripheral nerves or spinal nerve roots, you can simultaneously consult a reference book to see if the mapped territory matches a specific nerve distribution. This type of mapping is somewhat tedious and should only be done in appropriate situations. 3. Diffuse Distal Sensory Loss: A number of chronic systemic diseases affect nerve function. The most commonly occurring of these, at least in Western countries, is Diabetes. When control has been poor over many years, the sensory nerves become dysfunctional. This first affects the most distal aspects of the nerves and then moves proximally. Thus, the feet are the first area to be affected. As it is a systemic disease, it occurs simultaneously in both limbs. Exam reveals loss of ability to detect the sharp stimulus across the entire foot. Thus, the sensory loss does not follow a dermatomal (i.e. spinal nerve root) or peripheral nerve distribution. As the examiner tests more proximally, he/she will ultimately reach a point where sensation is again normal. The more advanced the disease, the higher up the leg this will occur. Hands can be affected, though much less commonly then feet as the nerves traveling to the legs are longer and thus at much greater risk. This pattern of loss is referred to as a Stocking or Glove distribution impairment, as the area involved covers an entire distal region, much as a sock or glove would cover a foot or hand. Such deficits may be associated with neuropathic pain, a continuous burning sensation affecting the distal extremity. 4. Peripheral Nerve Distribution: A specific peripheral nerve can become dysfunctional. This might, for example, occur as the result of trauma or infarction (another complication of diabetes). In this setting, there will be a pattern of sensory impairment that follows the distribution of the nerve. Radial nerve palsy, for example, can occur if an intoxicated person falls asleep in a position that puts pressure on the nerve as it travels around the Humerus (bone of the upper arm). Intoxication induced loss of consciousness then prevents the patient from reflexively changing position, the normal means by which we prevent nerves from being exposed to constant direct pressure. The resultant sensory loss would involve the back of the hand and forearm. Motor function would also be affected (see under motor exam). Pinning down the culprit nerve requires knowledge of nerve anatomy and innervation. On a practical level, most clinicians dont commit 189

this to memory. Rather, they gather a history suggestive of a discrete nerve deficit, verify the territory of loss on exam, and then look it up in a reference book. 5. Nerve Root Impairment: A nerve root (or roots) can be damaged as it leaves the cord. This will result in a sensory deficit along its specific distribution, which can in turn be identified on examination. The S1 nerve root, for example, can be compressed by herniated disc material in the lumbar spine. This would cause sensory loss along the lateral aspect of the lower leg and the bottom of the foot. Only the leg on the affected side would have this deficit. As mentioned under peripheral nerve dysfunction, most clinicians do not memorize the dermatomes related to each nerve root. Rather, they gather a history suggestive of a discrete nerve deficit, verify a dermatomal distribution of loss on exam, and then look it up in a reference book. 6. The Spinothalamics are also responsible for temperature discrimination. For practical reasons (i.e. its often hard to find test tubes, fill them with the requisite temperature water, etc) this is omitted in the screening exam. The information from sharp stimulus testing as described above should suffice. Temperature discrimination could be assessed as a means of verifying any abnormality detected on sharp/dull testing. 7. Testing of the sacral nerve roots, serving the anus and rectum, is important if patients complain of incontinence, inability to defecate/urinate, or there is otherwise reason to suspect that these roots may be compromised. In the setting of Cauda Equina syndrome, for example, multiple sacral and lumbar roots become compressed bilaterally (e.g. by posteriorly herniated disc material or a tumor). When this occurs, the patient is unable to urinate, as the lower motor neurons carried in these sacral nerve roots no longer function. Thus there is no way to send an impulse to the bladder instructing it to contract. Nor will they be aware that there bladders are full. There will also be loss of anal spincter tone, which can be appreciated on rectal exam. Ability to detect pin pricks in the perineal area (a.k.a. saddle distribution) is also diminished. Patterns of Impairment for Dorsal Column Dysfunction: Proprioception: Patients should be able to correctly identify the motion and direction of the toe. In the setting of Dorsal Column dysfunction (a common complication of diabetes, for example), distal testing will be abnormal. This is similar to the pattern of injury which affects the Spinothalamic tracts described above. Vibratory Sensation: 1. Patients should be able to detect the initial vibration and accurately determine when it has stopped. 2. As described under testing of proprioception, dorsal column dysfunction tends to first affect the most distal aspects of the system. When this occurs, the patient is either unable to detect the vibration or they perceive that the sensation

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extinguishes too early (i.e. they stop feeling it even though you can still appreciate the sensation with your fingers on the underside of the joint). 3. The findings on vibratory testing should parallel those obtained when assessing proprioception, as both sensations travel via the same pathway. Motor Testing The muscle is the unit of action that causes movement. Normal motor function depends on intact upper and lower motor neurons, sensory pathways and input from a number of other neurological systems. Disorders of movement can be caused by problems at any point within this interconnected system. Muscle Bulk and Appearance: This assessment is somewhat subjective and quite dependent on the age, sex and the activity/fitness level of the individual. A frail elderly person, for example, will have less muscle bulk then a 25 year old body builder. With experience, you will get a sense of the normal range for given age groups, factoring in their particular activity levels and overall states of health. Things to look for: 1. Using your eyes and hands, carefully examine the major muscle groups of the upper and lower extremities. Palpation of the muscles will give you a sense of underlying mass. The largest and most powerful groups are those of the quadriceps and hamstrings of the upper leg (i.e. front and back of the thighs). The patient should be in a gown so that the areas of interest are exposed. 2. Muscle groups should appear symmetrically developed when compared with their counterparts on the other side of the body. They should also be appropriately developed, after making allowances for the patients age, sex, and activity level.

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Muscle Assymetry While both legs have well developed musculature, the left has greater bulk. There should be no muscle movement when the limb is at rest. Rare disorders (e.g. Amyotrophic Lateral Sclerosis) result in death of the lower motor neuron and subsequent denervation of the muscle. This causes twitching of the fibers known as fasciculations,which can be seen on gross inspection of affected muscles. 3. Tremors are a specific type of continuous, involuntary muscle activity that results in limb movement. Parkinsons Disease (PD), for example, can cause a very characteristic resting tremor of the hand (the head and other body parts can also be affected) that diminishes when the patient voluntarily moves the affected limb. Benign Essential Tremor, on the other hand, persists throughout movement and is not associated with any other neurological findings, easily distinguishing it from PD. 4. For more information about Parkinson's Disease, see the following link: 5. NIH Sponsored Site About Parkinson's Disease 6. The major muscle groups to be palpated include: biceps, triceps, deltoids, quadriceps and hamstrings. Palpation should not elicit pain. Interestingly, myositis (a rare condition characterized by idiopathic muscle inflammation) causes the patient to experience weakness but not pain. 7. If there is asymmetry, note if it follows a particular pattern. Remember that some allowance must be made for handedness (i.e. right v left hand dominance). Does the asymmetry follow a particular nerve distribution, suggesting a peripheral motor neuron injury? For example, muscles which lose their LMN inervation become very atrophic. Is the bulk in the upper and lower extremities similar? Spinal cord transection at the Thoracic level will cause upper extremity muscle bulk to be normal or even increased due to increased dependence on arms for activity, mobility, etc. However, the muscles of the lower extremity will atrophy due to loss of innervation and subsequent disuse. Is there another process (suggested by history or other aspects of the exam) that has resulted in limited movement of a particular limb? For example, a broken leg that has recently been liberated from a cast will appear markedly atrophic.

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Diffuse Muscle Wasting: Note loss muscle bulk in left hand due to peripheral denervation. In particular, compare left and right thenar eminences. Tone: When a muscle group is relaxed, the examiner should be able to easily manipulate the joint through its normal range of motion. This movement should feel fluid. A number of disease states may alter this sensation. For the screening examination, it is reasonable to limit this assessment to only the major joints, including: wrist, elbow, shoulder, hips and knees. Technique: 1. Ask the patient to relax the joint that is to be tested. 2. Carefully move the limb through its normal range of motion, being careful not to maneuver it in any way that is uncomfortable or generates pain. 3. Be aware that many patients, particularly the elderly, often have other medical conditions that limit joint movement. Degenerative joint disease of the knee, for example, might cause limited range of motion, though tone should still be normal. If the patient has recently injured the area or are in pain, do not perform this aspect of the exam. Things to look for: 1. Normal muscle generates some resistance to movement when a limb is moved passively by an examiner. After performing this exam on a number of patients,youll develop an appreciation for the range of normal tone. 2. Increased tone (hypertonicity) results from muscle contraction. At the extreme end is spasticity, which occurs when the upper motor neuron no longer functions. In this setting, the affected limb is held in a flexed position and the examiner may be unable to move the joint. This is seen most commonly following a stroke, which results in the death of the upper motor neuron cell body in the brain. 3. Flaccidness is the complete absence of tone. This occurs when the lower motor neuron is cut off from the muscles that it normally innervates. 4. Disorders that do not directly affect the muscles, upper or lower motor neurons can still alter tone. Perhaps the most common of these is Parkinsons Disease (PD). This is a disorder of the Extra Pyramidal System (EPS). The EPS normally contributes to initiation and smoothness of movement. PD causes increased tone, generating a ratchet-like sensation (known as cog wheeling) when the affected limbs are passively moved by the examiner. Strength: As with muscle bulk (described above), strength testing must take into account the age, sex and fitness level of the patient. For example, a frail, elderly, bed bound patient may have muscle weakness due to severe deconditioning and not to intrinsic neurological disease. Interpretation must also consider the expected strength of the muscle group being tested. The quadriceps group, for example, should be much more powerful then the Biceps.

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There is a 0 to 5 rating scale for muscle strength: 0/5 1/5 2/5 No movement Barest flicker of movement of the muscle, though not enough to move the structure to which its attached. Voluntary movement which is not sufficient to overcome the force of gravity. For example, the patient would be able to slide their hand across a table but not lift it from the surface. Voluntary movement capable of overcoming gravity, but not any applied resistance. For example, the patient could raise their hand off a table, but not if any additional resistance were applied. Voluntary movement capable of overcoming some resistance Normal strength

3/5

4/5 5/5

+ and - can be added to these values, providing further gradations of strength. Thus, a patient who can overcome moderate but not full resistance might be graded 4+ or 5- . This is quite subjective, with a fair amount of variability amongst clinicians. Ultimately, its most important that you develop your own sense of what these gradations mean, allowing for internal consistency and interpretability of serial measurements. Specifics of Strength Testing - Major Muscle Groups: In the screening examination, it is reasonable to check only the major muscles/muscle groups. More detailed testing can be performed in the setting of discrete/unexplained weakness. The names of the major muscles/muscle groups along with the spinal roots and peripheral nerves that provide their innervation are provided below. Nerve roots providing the greatest contribution are printed in bold. More extensive descriptions of individual muscles and their functions, along with their precise innervations can be found in a Neurology reference text. 1. Intrinsic muscles of the hand (C 8, T 1): Ask the patient to spread their fingers apart against resistance (abduction). Then squeeze them together, with your fingers placed in between each of their digits (adduction). Test each hand separately. The muscles which control adduction and abduction of the fingers are called the Interossei, innervated by the Ulnar Nerve.

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2. 3. For more information about finger abductors and adductors, see the following link: 4. University of Washington, Anatomy of finger abductors and adductors 5. Flexors of the fingers (C 7, 8, T1): Ask the patient to make a fist, squeezing their hand around two of your fingers. If the grip is normal, you will not be able to pull your fingers out. Test each hand separately. The Flexor Digitorum Profundus controls finger flexion and is innervated by the Median (radial ) and Ulnar (medial ) Nerves.

6. Wrist flexion (C 7, 8, T 1): Have the patient try to flex their wrist as you provide resistance. Test each hand separately. The muscle groups which control flexion are innervated by the Median and Ulnar Nerves.

For more information about wrist flexors, see the following links: http://www.rad.washington.edu/atlas/abddigminimi.html (important, are toti muschii) Wrist extension (C 6, 7, 8): Have the patient try to extend their wrist as you provide resistance. Test each hand separately. The Extensor Radialis muscles 195

control extension and are innervated by the Radial Nerve. Clinical Correlate: Damage to the radial nerve results in wrist drop (loss of ability to extend the hand at the wrist). This can occur via any one of a number of mechanisms. For example, the nerve can be compressed against the humerus for a prolonged period of time when an intoxicated person loses consciousness with the inside aspect of the upper arm resting against a solid object (known as a Saturday Night Palsy).

7. Elbow Flexion (C 5, 6): The main flexor (and supinator) of the forearm is the Brachialis Muscle (along with the Biceps Muscle). Have the patient bend their elbow to ninety degrees while keeping their palm directed upwards. Then direct them to flex their forearm while you provide resistance. Test each arm separately. These muscles are innervated by the Musculocutaneous Nerve.

8. Elbow Extension (C 7, 8): The main extensor of the forearm is the triceps muscle. Have the patient extend their elbow against resistance while the arm is held out (abducted at the shoulder) from the body at ninety degrees. Test each arm separately. The Triceps is innervated by the Radial Nerve.

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9. Shoulder Adduction (C 5 thru T1): The main muscle of adduction is the Pectoralis Major, though the Latissiumus and others contribute as well. Have the patient flex at the elbow while the arm is held out from the body at forty-five degrees. Then provide resistance as they try to further adduct at the shoulder. Test each shoulder separately.

10. Shoulder Abduction (C 5, 6): The deltoid muscle, innervated by the axillary nerve, is the main muscle of abduction. Have the patient flex at the elbow while the arms is held out from the body at forty-five degress. Then provide resistance as they try to further abduct at the shoulder. Test each shoulder separately.

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11. Hip Flexion (L 2, 3, 4): With the patient seated, place your hand on top of one thigh and instruct the patient to lift the leg up from the table. The main hip flexor is the Iliopsoas muscle, innervated by the femoral nerve.

12. Hip Extension (L5, S1): With the patient lying prone, direct the patient to lift their leg off the table against resistance. Test each leg separately. The main hip extensor is the gluteus maximus, innervated by inferior gluteal nerve.

13. Hip Abduction (L 4, 5, S1): Place your hands on the outside of either thigh and direct the patient to separate their legs against resistance. This movement is mediated by a number of muscles.

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14. Hip Adduction (L 2, 3, 4): Place your hands on the inner aspects of the thighs and repeat the maneuver. A number of muscles are responsible for adduction. They are innervated by the obturator nerve.

15. Knee Extension (L 2, 3, 4): Have the seated patient steadily press their lower extremity into your hand against resistance. Test each leg separately. Extension is mediated by the quadriceps muscle group, which is innervated by the femoral nerve.

16. Knee flexion (L 5; S 1, 2): Have the patient rest prone. Then have them pull their heel up and off the table against resistance. Each leg is tested separately. Flexion is mediated by the hamstring muscle group, via branches of the sciatic nerve.

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17. Ankle Dorsiflexion (L 4, 5): Direct the patient to pull their toes upwards while you provide resistance with your hand. Each foot is tested separately. The muscles which mediate dorsiflexion are innervated by the deep peroneal nerve. Clinical Correlate: The peroneal nerve is susceptible to injury at the point where it crosses the head of the fibula (laterally, below the knee). If injured, the patient develops Foot Drop, an inability to dorsiflex the foot.

18. Ankle Plantar Flexion (S 1, S 2). Have the patient step on the gas while providing resistance with your hand. Test each foot separately. The gastrocnemius and soleus, the muscles which mediate this movement, are innervated by a branch of the sciatic nerve. Plantar flexion and dorsiflexion can also be assessed by asking the patient to walk on their toes (plantar flexion) and heels (dorsiflexion).

It is generally quite helpful to directly compare right v left sided strength, as they should more or less be equivalent (taking into account the handedness of the patient). If there is weakness, try to identify a pattern, which might provide a clue as to the etiology of the observed decrease in strength. In particular, make note of differences between: 1. 2. 3. 4. Right v Left Proximal muscles v distal Upper extremities v lower Or is the weakness generalized, suggestive of a systemic neurological disorder or global deconditioning 200

Special Testing for subtle weakness: Subtle weakness can be hard to detect. Pay attention to how the patient walks, uses and holds their arms and hands as they enter the room, get up and down from a seated position, move onto the examination table, etc. Pronator drift is a test for slight weakness of the upper extremities. The patient should sit with both arms extended, palms directed upward. Subtle weakness in either arm will cause slight downward drift and pronation of that limb (i.e. the arm will rotate slightly inward and down). Common peripheral nerves, territories of innervation, and clinical correlates. Peripheral Sensory Nerve Innervation Back of thumb, index, middle, and ring finger; back of forearm Motor Innervation Contributing Spinal Nerve Roots

Clinical

Radial Nerve

Wrist extension and abduction of thumb in palmer plane

C6, 7, 8

At risk for compression at humerus, known as "Saturday Night Palsy" At risk for injury with elbow fracture. Can get transient symptoms when inside of elbow is struck ("funny bone" distribution)

Ulnar Nerve

Palmar and dorsal aspects of pinky and of ring finger

Abduction of fingers (intrinsic muscles of hand)

C7, 8 and T1

Median Nerve

Palmar aspect of the thumb, index, middle and ring finger; palm below these fingers.

Abduction of thumb perpendicular C8, T1 to palm (thenar muscles).

Compression at carpal tunnel causes carpal tunnel syndrome

Lateral Cutaneous Nerve of Thigh

Lateral aspect thigh

L1, 2

Can become compressed in obese patients, causing numbness over its distribution

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Peroneal

Dorsiflexion of Lateral leg, top foot (tibialis of foot L4, 5; S1 anterior muscle)

Can be injured with proximal fibula fracture, leading to foot drop (inability to dorsiflex foot)

This table provides information about usual patterns of innervations. There is occasionally interindividual variation. In the setting of peripheral nerve dysfunction, the level of the lesion will determine the extent of the deficit. That is, proximal insults will cause the entire nerve distribution to be affected while more distal lesions will only impact function beyond the site of the injury. More on carpal tunnel syndrome... Video of findings in advanced carpal tunnel syndrome.

Carpal Tunnel Induced Atrophy: Chronic, severe compression of the median nerve within the carpal tunnel has led to atrophy of the Thenar muscles (hand on right). A normal appearing Thenar Eminence is demonstrated on left. Cranial Sensory and Motor Nerves Examinations
Reflex Testing Cerebellar Gait Testing Testing Making Sense of Neurological Findings

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Reflex Testing Reflex testing incorporates an assessment of the function and interplay of both sensory and motor pathways. It is simple yet informative and can give important insights into the integrity of the nervous system at many different levels. Physiology of Reflexes

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Assessment of reflexes is based on a clear understanding of the following principles and relationships: 1. Tendons connect muscles to bones, usually crossing a joint. When the muscle contracts, the tendon pulls on the bone, causing the attached structure to move. 2. When the tendon is struck by the reflex hammer, stretch receptors contained within it generate an impulse that is carried via sensory nerves to the spinal cord. At this juncture, the message is transmitted across a synapse to an appropriate lower motor neuron. An upper motor neuron, whose cell body resides in the brain, also provides input to this synapse. 3. The signal then travels down the lower motor neuron to the target muscle. 4. The sensory and motor signals that comprise a reflex arc travel over anatomically well characterized pathways. Pathologic processes affecting discrete roots or named peripheral nerves will cause the reflex to be diminished or absent. This can obviously be of great clinical significance. The Achilles Reflex (see below) is dependent on the S1 and S2 nerve roots. Herniated disc material (a relatively common process) can put pressure on the S1 nerve root, causing pain along its entire distribution (i.e. the lateral aspect of the lower leg). If enough pressure if placed on the nerve, it may no longer function, causing a loss of the Achilles reflex. In extreme cases, the patient may develop weakness or even complete loss of function of the muscles innervated by the nerve root, a medical emergency mandating surgical decompression. The specific nerve roots that comprise the arcs are listed for each of the major reflexes described below. 5. A normal response generates an easily observed shortening of the muscle. This, in turn, causes the attached structure to move. 6. The vigor of contraction is graded on the following scale: 0 1+ 2+ 3+ 4+ No evidence of contraction Decreased, but still present (hypo-reflexic) Normal Super-normal (hyper-reflexic) Clonus: Repetitive shortening of the muscle after a single stimulation

For more information about anatomy and physiology of reflexes, see the following link: Technique The Reflex Hammer You will need to use a reflex hammer when performing this aspect of the exam. A number of the most commonly used models are pictured below. Regardless of the hammer type, proper technique is critical. The larger hammers have weighted heads, such that if you raise them approximately 10 cm from the target and then release, they will 203

swing into the tendon with adequate force. The smaller hammers should be swung loosely between thumb and forefinger. Technique: 1. The muscle group to be tested must be in a neutral position (i.e. neither stretched nor contracted). 2. The tendon attached to the muscle(s) which is/are to be tested must be clearly identified. The extremity should be positioned such that the tendon can be easily struck with the reflex hammer. 3. If you are having trouble locating the tendon, ask the patient to contract the muscle to which it is attached. When the muscle shortens, you should be able to both see and feel the cord like tendon, confirming its precise location. You may, for example, have some difficulty identifying the Biceps tendon within the Antecubital Fossa. Ask the patient to flex their forearm (i.e. contract their Biceps muscle) while you simultaneously palpate the fossa. The Biceps tendon should become taut and thus readily apparent. 4. Strike the tendon with a single, brisk, stroke. While this is done firmly, it should not elicit pain. Occasionally, due to other medical problems (e.g. severe arthritis), you will not be able to position the patients arm in such a way that you are able to strike the tendon. If this occurs, do not cause the patient discomfort. Simply move on to another aspect of the exam. This grading system is rather subjective. Additional levels of response can be included by omitting the + or adding a - to any of the numbers. As you gain more experience, youll have a greater sense of how to arrange your own scale. Specifics of Reflex Testing The peripheral nerves and contributing spinal nerve roots that form each reflex arc are listed in parentheses: Achilles (S1, S2 Sciatic Nerve): 1. This is most easily done with the patient seated, feet dangling over the edge of the exam table. If they cannot maintain this position, have them lie supine, crossing one leg over the other in a figure 4. Or, failing that, arrange the legs in a frog-type position. 2. Identify the Achilles tendon, a taut, discrete, cord-like structure running from the heel to the muscles of the calf. If you are unsure, ask the patient to plantar flex (i.e. step on the gas), which will cause the calf to contract and the Achilles to become taut.

Achilles Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right. 3. Position the foot so that it forms a right angle with the rest of the lower leg. You will probably need to support the bottom of the foot with your hand. 204

4. Strike the tendon directly with your reflex hammer. Be sure that the calf if exposed so that you can see the muscle contract. A normal reflex will cause the foot to plantar flex (i.e. move into your supporting hand).

Positions for Checking Achilles Reflex Patellar (L3, L4 Femoral Nerve):

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1. This is most easily done with the patient seated, feet dangling over the edge the exam table. If they cannot maintain this position, have them lie supine (i.e. on their backs). 2. Identify the patellar tendon, a thick, broad band of tissue extending down from the lower aspect of the patella (knee cap). If you are not certain where its located, ask the patient to extend their knee. This causes the quadriceps (thigh muscles) to contract and makes the attached tendon more apparent.

Patellar Tendon: Outlined in pen on left, (gross dissection)on right. 3. Strike the tendon directly with your reflex hammer. If you are having trouble identifying the exact location of the tendon (e.g. if there is a lot of subcutaneous fat), place your index finger firmly on top of it. Strike your finger, which should then transmit the impulse.

Patellar Reflex Testing, seated patient 206

4. For the supine patient, support the back of their thigh with your hands such that the knee is flexed and the quadriceps muscles relaxed. Then strike the tendon as described above.

Patellar Reflex, supine patient 5. Make sure that the quadriceps are exposed so that you can see muscle contraction. In the normal reflex, the lower leg will extend at the knee. Biceps (C5, C6 Musculocutaneous Nerve): 1. This is most easily done with the patient seated. 2. Identify the location of the biceps tendon. To do this, have the patient flex at the elbow while you observe and palpate the antecubital fossa. The tendon will look and feel like a thick cord.

Biceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right. 207

3. The patients arm can be positioned in one of two ways: a. Allow the arm to rest in the patients lap, forming an angle of slightly more then 90 degrees at the elbow.

Biceps Reflex Testing b. Support the arm in yours, such that your thumb is resting directly over the biceps tendon (hold their right arm with your right; and vice versa).

Biceps Reflex Testing,arm supported 4. Make sure that the biceps muscle is completely relaxed. 5. It may be difficult to direct your hammer strike such that the force is transmitted directly on to the biceps tendon, and not dissipated amongst the rest of the soft tissue in the area. If you are supporting the patients arm, place your thumb on the tendon and strike this digit. If the arm is unsupported, place your index or middle fingers firmly against the tendon and strike them with the hammer. 6. Make sure that the patients sleeve is rolled up so that you can directly observe the muscle as well as watch the lower arm for movement. A normal response will cause the biceps to contract, drawing the lower arm upwards.

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Brachioradialis (C5, C6 Radial Nerve): 1. This is most easily done with the patient seated. The lower arm should be resting loosely on the patients lap. 2. The tendon of the Brachioradialis muscle cannot be seen or well palpated, which makes this reflex a bit tricky to elicit. The tendon crosses the radius (thumb side of the lower arm) approximately 10 cm proximal to the wrist.

Brachioradialis Tendon: Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right. 3. Strike this area with your reflex hammer. Usually, hitting anywhere in the right vicinity will generate the reflex.

Brachioradialis Reflex

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4. Observe the lower arm and body of the Brachioradialis for a response. A normal reflex will cause the lower arm to flex at the elbow and the hand to supinate (turn palm upward). Triceps (C7, C8 Radial Nerve): 1. This is most easily done with the patient seated. 2. Identify the triceps tendon, a discrete, broad structure that can be palpated (and often seen) as it extends across the elbow to the body of the muscle, located on the back of the upper arm. If you are having trouble clearly identifying the tendon, ask the patient to extend their lower arm at the elbow while you observe and palpate in the appropriate region.

Triceps Tendon:Tendon is outlined in pen on left, (gross dissection) on right. 3. The arm can be placed in either of 2 positions: a. Gently pull the arm out from the patients body, such that it roughly forms a right angle at the shoulder. The lower arm should dangle directly downward at the elbow.

Triceps Reflex, arm supported 210

b. Have the patient place their hands on their hips.

Triceps Reflex, arm unsupported 4. Either of these techniques will allow the triceps to completely relax. 5. If you are certain as to the precise location of the tendon, strike this area directly with your hammer. If the target is not clearly apparent or the tendon is surrounded by an excessive amount of subcutaneous fat (which might dissipate the force of your strike), place your index or middle finger firmly against the structure. Then strike your finger. 6. Make sure that the triceps is uncovered, so that you can observe the response. The normal reflex will cause the lower arm to extend at the elbow and swing away from the body. If the patients hands are on their hips, the arm will not move but the muscle should shorten vigorously . Making Clinical Sense of Reflexes: Normal reflexes require that every aspect of the system function normally. Breakdowns cause specific patterns of dysfunction. These are interpreted as follows: 1. Disorders in the sensory limb will prevent or delay the transmission of the impulse to the spinal cord. This causes the resulting reflex to be diminished or completely absent. Diabetes induced peripheral neuropathy (the most common sensory neuropathy seen in developed countries), for example, is a relatively common reason for loss of reflexes. 2. Abnormal lower motor neuron (LMN) function will result in decreased or absent reflexes. If, for example, a peripheral motor neuron is transected as a result of trauma, the reflex dependent on this nerve will be absent. 3. If the upper motor neuron (UMN)is completely transected, as might occur in traumatic spinal cord injury, the arc receiving input from this nerve becomes disinhibited, resulting in hyperactive reflexes. Of note, immediately following such an injury, the reflexes are actually diminished, with hyper-reflexia developing several weeks later. A similar pattern is seen with the death of the cell 211

body of the UMN (located in the brain), as occurs with a stroke affecting the motor cortex of the brain. 4. Primary disease of the neuro-muscular junction or the muscle itself will result in a loss of reflexes, as disease at the target organ (i.e. the muscle) precludes movement. 5. A number of systemic disease states can affect reflexes. Some have their impact through direct toxicity to a specific limb of the system. Poorly controlled diabetes, as described above, can result in a peripheral sensory neuropathy. Extremes of thyroid disorder can also affect reflexes, though the precise mechanisms through which this occurs are not clear. Hyperthyroidisim is associated with hyperreflexia, and hypothyroidism with hyporeflexia. 6. Detection of abnormal reflexes (either increased or decreased) does not necessarily tell you which limb of the system is broken, nor what might be causing the dysfunction. Decreased reflexes could be due to impaired sensory input or abnormal motor nerve function. Only by considering all of the findings, together with their rate of progression, pattern of distribution (bilateral v unilateral, etc.) and other medical conditions can the clinician make educated diagnostic inferences about the results generated during reflex testing. Trouble Shooting 1. If you are unable to elicit a reflex, stop and consider the following: a. Are you striking in the correct place? Confirm the location of the tendon by observing and palpating the appropriate region while asking the patient to perform an activity that causes the muscle to shorten, making the attached tendon more apparent. b. Make sure that your hammer strike is falling directly on the appropriate tendon. If there is a lot of surrounding soft tissue that could dampen the force of the strike, place a finger firmly on the correct tendon and use that as your target. c. Make sure that the muscle is uncovered so that you can see any contraction (occasionally the force of the reflex will not be sufficient to cause the limb to move). d. Sometimes the patient is unable to relax, which can inhibit the reflex even when all is neurologically intact. If this occurs during your assessment of lower extremity reflexes, ask the patient to interlock their hands and direct them to pull, while you simultaneously strike the tendon. This sometimes provides enough distraction so that the reflex arc is no longer inhibited. 2. Occasionally, it will not be possible to elicit reflexes, even when no neurological disease exists. This is most commonly due to a patient's inability to relax. In these settings, the absence of reflexes are of no clinical consequence. This assumes that you were otherwise thorough in your history taking, used appropriate examination techniques, and otherwise identified no evidence of disease.

Babinski Response

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The Babinski response is a test used to assess upper motor neuron dysfunction and is performed as follows: 1. Use the handle end of your reflex hammer, which is solid and comes to a point. 2. The patient may either sit or lie supine. 3. Start at the lateral aspect of the foot, near the heel. Apply steady pressure with the end of the hammer as you move up towards the ball (area of the metatarsal heads) of the foot. 4. When you reach the ball of the foot, move medially, stroking across this area. 5. Then test the other foot. 6. Some patients find this test to be particularly noxious/uncomfortable. Tell them what you are going to do and why. If its unlikely to contribute important information (e.g. screening exam of the normal patient) and they are quite averse, simply skip it. Interpretation: In the normal patient, the first movement of the great toe should be downwards (i.e. plantar flexion). If there is an upper motor neuron injury (e.g. spinal cord injury, stroke), then the great toe will dorsiflex and the remainder of the other toes will fan out. A few additional things to remember:

Babinski Response Present 1. Newborns normally have a positive Babinksi. It usually goes away after about 6 months. 2. Sometimes you will be unable to generate any response, even in the absence of disease. Responses must therefore be interpreted in the context of the rest of the exam. 3. If the great toe flexes and the other toes flair, the Babinski Response is said to be present. If not (i.e. normal), it is recorded as absent. For reasons of semantics, the Babinski is not recorded as + or -. 4. Withdrawal of the entire foot (due to unpleasant stimulation), is not interpreted as a positive response.

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Cerebellar Testing The cerebellum fine tunes motor activity and assists with balance. Dysfunction results in a loss of coordination and problems with gait. The left cerebellar hemisphere controls the left side of the body and vice versa. Specifics of Testing: There are several ways of testing cerebellar function. For the screening exam, using one modality will suffice. If an abnormality is suspected or identified, multiple tests should be done to determine whether the finding is durable. That is, if the abnormality on one test is truly due to cerebellar dysfunction, other tests should identify the same problem. Gait testing, an important part of the cerebellar exam, is discussed separately (see next section). 1. Finger to nose testing: a. With the patient seated, position your index finger at a point in space in front of the patient. b. Instruct the patient to move their index finger between your finger and their nose. c. Reposition your finger after each touch. d. Then test the other hand. Interpretation: The patient should be able to do this at a reasonable rate of speed, trace a straight path, and hit the end points accurately. Missing the mark, known as dysmetria, may be indicative of disease. 2. Rapid Alternating Finger Movements: a. Ask the patient to touch the tips of each finger to the thumb of the same hand. b. Test both hands. Interpretation: The movement should be fluid and accurate. Inability to do this, known as dysdiadokinesia, may be indicative of cerebellar disease. 3. Rapid Alternating Hand Movements: a. Direct the patient to touch first the palm and then the dorsal side of one hand repeatedly against their thigh. b. Then test the other hand. Interpretation: The movement should be performed with speed and accuracy. Inability to do this, known as dysdiadokinesia, may be indicative of cerebellar disease. 4. Heel to Shin Testing: a. Direct the patient to move the heel of one foot up and down along the top of the other shin. b. Then test the other foot. Intepretation: The movement should trace a straight line along the top of the shin and be done with reasonable speed. 214

Realize that other organ system problems can affect performance of any of these tests. If, for example, the patient is visually impaired, they may not be able to see the target during finger to nose pointing. Alternatively, weakness due to a primary muscle disorder might limit the patients ability to move a limb in the fashion required for some of the above testing. Thus, other medical and neurological conditions must be taken into account when interpreting cerebellar test results. Gait Testing Ability to stand and walk normally is dependent on input from several systems, including: visual, vestibular, cerebellar, motor, and sensory. The precise cause(s) of the dysfunction can be determined by identifying which aspect of gait is abnormal and incorporating this information with that obtained during the rest of the exam. Difficulty getting out a chair and initiating movement, for example, would be consistent with Parkinsons Disease. On the other hand, lack of balance and a wide based gait would suggest a cerebellar disorder. In each case, finding elsewhere in the exam should help point you in the right direction. A lot of information about neurological (and other) disorders can be gained from simply watching a patient stand and then walk. For the screening exam, simply observing while the patient walks into your office and gets up and down from the exam table will provide all of the relevant information. If there is suspicion of neurological disease (based on history, other exam findings, observation of gait) then more detailed testing should be performed. Proceed as follows: 1. Ask the patient to stand. If they are very weak or unsteady, make sure that you are in a position and capable of catching and supporting them if they fall. Enlist the help of a colleague if you need an extra pair of hands. If you are still unsure as to whether standing/walking can be performed safely, skip this area of testing. No test result is worth a broken hip! 2. Have the patient stand in one place. As mentioned above, make sure that you are capable/in position to catch and support them if they fall. This is a test of balance, incorporating input from the visual, cerebellar, proprioceptive, and vestibular systems. If they are able to do this, have them close their eyes, removing visual input. This is referred to as the Romberg test. Loss of balance suggests impaired proprioception, as it is this pathway which should provide input that allows the patient to remain stably upright. 3. Ask the patient to stand from a chair, walk across the room, turn, and come back towards you. Pay particular attention to: a. Difficulty getting up from a chair: Can the patient easily arise from a sitting position? Problems with this activity might suggest proximal muscle weakness, a balance problem, or difficulty initiating movements. b. Balance: Do they veer off to one side or the other as might occur with cerebellar dysfunction? Disorders affecting the left cerebellar hemisphere (as might occur with a stroke or tumor) will cause patients to fall to the left. Right sided lesions will cause the patient to fall to the right. Diffuse disease affecting both cerebellar hemispheres will cause a generalized loss of balance. 215

c. Rate of walking: Do they start off slow and then accelerate, perhaps losing control of their balance or speed (e.g. as might occur with Parkinsons Disease)? Are they simply slow moving secondary to pain/limited range of motion in their joints, as might occur with degenerative joint disease? etc. d. Atttitude of Arms and Legs: How do they hold their arms and legs? Is there loss of movement and evidence of contractures (e.g. as might occur after a stroke)? 4. Heel to Toe Walking: Ask the patient to walk in a straight line, putting the heel of one foot directly in front of the toe of the other. This is referred to as tandem gait and is a test of balance. Realize that this may be difficult for older patients (due to the frequent coexistence of other medical conditions) even in the absence of neurological disease. Making Sense of Neurological Findings While compiling information generated from the motor and sensory examinations, the clinician tries to identify patterns of dysfunction that will allow him/her to determine the location of the lesion(s). What follows is one way of making clinical sense of neurological findings. 1. Is there evidence of motor dysfunction (e.g. weakness, spasticity, tremor)? 2. If so, does the pattern follow an upper motor neuron or lower motor neuron pattern? a. If its consistent with a UMN process (e.g. weakness with spasticity), does this appear to occur at the level of the spinal cord or the brain? Complete cord lesions will affect both sides of the body. Brain level problems tend to affect one side or the other. It is, of course, possible for a lesion to affect only part of the cord, leading to findings that lateralize to one side (see below, under description of Brown Sequard lesion). b. Is it consistent with an LMN process (e.g. weakness with flaccidity)? Does the weakness follow a specific distribution (e.g. following a spinal nerve root or peripheral nerve distribution)? Bilateral? Distal? 3. Do the findings on reflex examination support a UMN or LMN process (e.g. hyper-reflexic in UMN disorders; hyporeflexic in LMN disorders)? 4. Do the findings on Babinski testing (assuming the symptoms involve the lower extremities) support the presence of a UMN lesion? 5. Is there impaired sensation? Some disorders, for example, affect only the Upper or Lower motor pathways, sparing sensation. 6. Which aspects of sensation are impaired? Are all of the ascending pathways (e.g. spinothalamic and dorsal columns) affected equally, as might occur with diffuse/systemic disease? 7. Does the loss in sensation follow a pattern suggestive of dysfunction at a specific anatomic level? For example, is it at the level of a Spinal nerve root? Or more distally, as would occur with a peripheral nerve problem? 8. Does the distribution of the sensory deficit correlate with the correct motor deficit, assuming one is present? Radial nerve compression, for example, would lead to characteristic motor and sensory findings.

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Information from the sensory, motor and reflex examinations should correlate with one another, painting the best picture of where the level of dysfunction is likely to exist. A few examples of injuries resulting in characteristic patterns of motor and sensory loss are described below: Example 1 In the setting of a suspected acute spinal cord injury at the T 10 vertebral level, for example, the following might be identified on detailed neurological examination: Sensation: Strength: Tone: Absence of ability to sense pin prick, vibration or propriocetion below the level of the umbilicus. No movement of the lower extremities (e.g. paralysis). Initially, decreased. Over weeks, tone increases with progression to spasticity and contractures of the lower extremities. Initially, absent Achilles and Patellar reflexes. After a few weeks, these will become hyperreflexic and demonstrate clonus. Toes will be up-going bilaterally (i.e. Babinski response will be present).

Reflexes:

Babinksi Example 2

Partial Cord Transection - The Brown-Sequard Lesion: A knife injury, for example, might damage only the right half of the cord at the T 10 level. This would result in the following findings on detailed exam: The patient would be unable to identify the pin stimulus on the left side of his body (remember that the spinothalamacs cross soon after entering the cord) below the level of the injury. Vibratory sensation would be impaired on the right side of the body below the level of the injury, as these paths do not cross over until they reach the base of the brain. The patient would be unable to move their right leg. Initially, decreased in the right leg. Over weeks, tone increases, with progression to spasticity. Initially, absent at the right Patellar and Achilles. After a few weeks becoming hyper-reflexic.

Sensation:

Strength: Tone: Reflexes:

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Babinksi

Up-going toe on the right

A few final comments about diagnosing neurologic disorders: It is also important to note that the pace at which a particular disorder develops will have a dramatic effect on symptoms and exam findings. Acute dysfunction (as might occur with a stroke) generally causes obvious symptoms as the loss of function is abrupt, allowing the patient no time to develop compensatory mechanisms. Patient presentation will also be affected by the size and location of the lesion. Larger lesions or those affecting critical areas of function tend to generate more overt problems. Additionally, patients with pre-existing medical or neurological dysfunction may well tolerate new lesions poorly. In contrast, disorders which occur more slowly tend to cause relatively subtle symptoms. For example, toxin induced damage to the cerebellum can result in profound atrophy of this region of the brain. While imaging may reveal significant volumetric loss, exam findings can remain relatively minimal. These same principles apply to most other aspects of the physical examination.

Putting It All Together

How do you perform the examination in a way that is complete, makes sense and yet is not awkward or prolonged? Is it OK to mix together different areas of the exam or should each system be explored as a block? As I am sure you've already recognized, these and many other related questions are not easy to answer. Putting together a smooth exam is, in fact, quite challenging. There is no single right way to perform a complete physical. The goal is to generate a method that works for you. Any technique, however, should: 1. Cover all aspects of the examination such that you have a reasonable chance of identifying any pathology that might in fact be present. 2. Be readily reproducible, allowing you to perform the exam the same way all the time. 3. Keep patient gymnastics to a minimum (i.e. limit the number of times that the patient has to get up and down). 4. Link together sections which, although disconnected physiologically, are connected spatially. It makes sense, for example, to integrate the cranial nerve and head and neck examinations as both involve the same region of the body. 5. Allow you to be efficient and perform the exam with an economy of movement (i.e. minimize the number of times that you pick up and put down instruments, move from one side of the patient to the other, etc.). It may take a fair amount of time, thought and practice before you come up with a system that works for you. I encourage you to experiment while choreographing your own moves.

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What follows is not an in-depth review detailing the specifics of each area of the exam. Rather, it is simply an outline of the "mechanical events" that make up a complete physical. 1. Wash your hands. 2. Have the patient change into a hospital gown and take a seat at the end of the examining table. If possible, spend a few minutes simply watching them. 3. Determine the blood pressure in both arms. 4. Count the pulse. Measure this at both radial arteries simultaneously. Following this, examine the hands and fingers. 5. Respiratory rate is noted while counting the pulse. Temperature is measured at the same time. 6. Feel for axillary lymph nodes. 7. Examine the scalp and head for any superficial abnormalities. 8. Feel for lymph nodes in the head and neck. 9. Have patient raise eyebrows, wrinkle forehead, close their eyes and smile (CN 7). 10. Check sensation to touch on face; Feel temporal and masseter muscles when jaw clenched (CN 5). 11. Assess extra occular movements (cranial nerves 3, 4, & 6). Check visual fields and acuity (CN 2) if appropriate. 12. Using ophthalmoscope, check pupillary response to light (direct and indirect). Look for red reflex. Examine external structures of the eye. 13. Perform fundoscopy. When examining the left eye you will have to walk to the left side of the body. 14. Examine the nose. 15. Ask the patient to show their teeth and stick out their tongue. Using the otoscope, examine the oral cavity. (CN 9, 10, 12). 16. Examine the outer and inner ears. You will again have to walk to the left side of the body to look at the left ear. Check hearing acuity, Weber, and Rinne (CN 8) if appropriate. 17. Have the patient shrug their shoulders and turn their head from side to side (CN 11). 18. Walk behind the patient and feel the thyroid gland. 19. Palpate the spine. 20. Observe, palpate, percuss and auscultate the posterior lung fields as well the right middle lobe and the lingula. 21. Walk around to the front, ask the patient to lie down, and listen to the anterior lung fields. 22. Look at the cardiac area of the chest. Then feel for the point of maximal cardiac impulse. 23. Auscultate the heart. 24. Have the patient turn their head to the left and assess for jugular venous distention. 25. Palpate the carotids. 26. Listen over the carotids. *Note....Steps 19 thru 25 can be performed without ever removing your stethoscope from your ears. 27. Observe, auscultate, percuss and palpate the abdomen. 219

28. Feel for inguinal adenopathy and asses femoral and then popliteal pulses. 29. Examine the feet, looking for edema, ulcers, discoloration, etc. Check for dorsalis pedis and posterior tibial pulses. 30. Ask patient to sit up. 31. Assess for Babinski. 32. Check achilles and patellar reflexes. 33. Assess muscle bulk, tone and strength in lower extremities. Check sensation to pin prick, light touch, vibration, and position sense in feet and lower extremities if appropriate. 34. Check biceps, triceps and brachioradialis reflexes. 35. Assess muscle bulk, tone and strength in upper extremities. Check sensation in upper extremities, as described for lower extremities, if appropriate. 36. Assess cerebellar function with finger to nose and heel to shin testing. 37. Have patient stand and then walk. Observe gait. Check for Romberg's Sign. 38. For male patients, perform genital and rectal exam while they are standing. 39. For female patients, perform pelvic exam. 40. Wash your hands. I have omitted the formal joint examination. If indicated, this can be done in concert with assessment of extremity strength towards the end of the exam. This approach keeps the movement of the examiner to a minimum, limits the frequency with which the patient has to get up and down, allows exploration of neighboring areas of the body even if they are part of different organ systems, and is reasonably logical, thorough and efficient. There is a lot of room for flexibility.

The Oral Presentation

The purpose of the oral presentation is to provide other clinicians with patient information. This must be done in such a way that it tells the patient's story in a logical, clear and complete fashion yet is neither cumbersome nor too long. It is a difficult skill to master and is made more complicated by the fact that different clinical situations demand different types of presentations. For example, presentations given during morning work rounds (the time when the medical team briefly visits with each patient to review their clinical course and determine the plan for the day), are not the same as those given at formal patient management conferences. The first situation requires a focused presentation, with emphasis placed on reviewing new facts and data (e.g. test results, vital signs, changes in clinical course, etc.) and outlining the care plan. The second example calls for a much more detailed discussion. The presenter, then, must take into account the "environmental" factors which determine the type of presentation that is required. These include:

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1. The audience to which you are presenting. A group of cardiologists, for example, are going to be most interested in the cardiac history. 2. The purpose of the presentation (e.g. is it for work rounds, teaching conference, clinic etc.?). 3. Time available to give the presentation. The longest, most complete presentation should take no longer then 5-7 minutes while shortened versions can be given in as little as 15 to 30 seconds. 4. Your familiarity with the case as well as associated pathophysiology. For the purposes of this discussion, we will focus on the formal/complete presentation as it is probably the form which is most complicated and intimidating. You will find, however, that once you grasp the logic and organization of this process and have an opportunity to practice, your presentations will become both more effective and less anxiety provoking. Tips for presenting during work rounds are provided in the "Inpatient Medicine" section of the Clinical Guide. In the discussion that follows, illustrative examples are frequently included and have been set off from the text by means of quotation marks and italics. The Formal Presentation Chief Complaint/Chief Concern: The presentation begins with a one sentence description of the patient and the reason prompting their evaluation (i.e. the Chief Complaint). This is a teaser that sets the tone for the information to follow. It should not be too inclusive. "Mr. H is a 50 year old male with AIDS who presents for the evaluation of fever, chills and a cough over the past 3 days." History of Present Illness (HPI): The HPI is presented in both a problem based and chronological fashion. That is, the dominant problem/complaint serves as the centerpiece of the history. If there is more then one problem, the presenter may try to link them together when appropriate. Information related to this main theme is presented in chronological order. This requires that the presenter go back far enough in time to cover any historical data that is relevant to the patient's main complaint. Your ability as a presenter to know which past information is important and which superfluous will be based on both your clinical experience and understanding of pathophysiology. At the current time, this might be quite limited. For the above patient, a thorough description would include: "Mr. H has been HIV + since 1987; his CD4 count in June of '97was 150 and viral load approximately 50,000. Past opportunistic infections have included: PCP pneumonia 12/95; CMV retinitis 1/96; and Kaposi's Sarcoma first noted on his skin 1/96. He currently takes 3TC, AZT, and Indinavir, all of which he has been receiving for approximately one year. He also takes Bactrim Single Strength tablets on a daily basis, along with Fluconazole troches PRN for thrush. He claims to be 100% compliant with all of his medication. He is homosexual though he is currently not sexually active. He has never used intravenous drugs." This information is not, in a strict sense, part of the present illness. However, it providescritical information that will have a direct bearing on the listener's interpretation 221

of this patient's active problem. Your ability to determine which background to incorporate into your HPI will improve with time and exposure. The details of the patient's acute problem are then presented: "Until 1 week ago, Mr. H had been quite active, walking up to 2 miles a day without feeling short of breath. Approximately 1 week ago, he began to feel dyspneic with moderate activity. This progressed to the point that, 1 day ago, he was breathless after walking up a single flight of stairs. 3 days ago, he began to develop subjective fevers and chills along with a cough productive of rust-colored sputum. There was associated nausea but no vomiting. He has spent most of the last 24 hours in bed. He denies head ache, photophobia, stiff neck, focal weakness, chest pain, hemoptysis, abdominal pain, diarrhea or other complaints. There is no know history of asthma, COPD or chronic pulmonary condition. His current problem seems different to him then his past episode of PCP." This section documents the course of the patient's most active problem. It concludes with a list of "pertinent negatives" that are meant to exclude, on the basis of history, other possible diagnoses that are known to have a similar symptom complex. In a patient with an HIV related illness, this review might actually be much more extensive than that provided above due to the diffuse, multi-organ system involvement that occurs with this disease. Note that the patient's baseline functional status is described, allowing the listener to gain some sense of the degree of impairment caused by the acute medical problem. If a patient is a poor historian, confused or simply unaware of all the details related to their illness, state this and move on. Historical information can be obtained from family, friends, etc. If this is the case, make sure that you note the source. If, for example, a patient complains of both chest pain and shortness of breath, they may well be secondary to a single underlying process such as myocardial ischemia resulting in heart failure. When the problems are completely unrelated, the "dominant issue" (as determined by the presenter) is treated first, followed by a discussion of the secondary complaint. This can get quite complicated when multiple problems exist in parallel. Review of Systems: The critical positive and negative findings discovered during a review of systems are generally incorporated at the end of the patient's history, as was done above. These questions are designed to uncover illnesses which might "travel with" the main problem and attempt to identify commonly occurring complications (e.g. hemoptysis can be a sequelae of pulmonary infection). The listener needs this information to help them put the remainder of the history in appropriate perspective. Any positive responses to a more inclusive ROS that covers all of the other various organ systems are then noted. The extent to which this is repeated is left to the discretion of the presenter. If it is completely negative, it is generally acceptable to simply state, "ROS negative." Past Medical History: Note is made of any other past medical problems which the patient has that are not related to the current complaint. Those items mentioned above are not repeated. "The patient's past medical history includes:

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1. Hypertension x 10 years 2. Gastro-Esophageal Reflux Disease 3. Degenerative Joint Disease of the Right Knee" Past Surgical History: Any prior surgeries (along with the year in which they occurred) are noted. "Past surgical history is remarkable for: 1. Status Post Cholycystectomy 1990 2. Status Post Appendectomy 1985 3. Status Post open repair and internal fixation of left femur fracture, 1983" Medications/Allergies: All current medications (along with dose, route and frequency) are mentioned: "The patient takes the following medications: AZT 300 mg, 1 PO, BID Indinavir 750 mg, 2 PO, TID 3TC 150 mg, 1 PO, BID Lansoprazole 20 mg, 1 PO, BID Lopressor 50 mg, 2 PO, BID Clotrimazole Troches 100 mg, 1 PO TID PRN Naprosyn 250 mg, 1-2, PO, BID PRN He has no allergies" Smoking and Alcohol (and any other substance abuse): Cigarettes and alcohol are highlighted because their use is so widespread and the deleterious effects associated with prolonged exposure well documented. Any additional substance abuse (e.g. cocaine use, intravenous drugs, etc.) should also be mentioned. "Mr. H smokes 1 pack of cigarettes per day and has done so for 20 years. He drinks approximately 1 glass of wine per week. He denies any other drug use." Social/Work History: This includes a brief description of the patient's work and home environments. Sexual history, if relevant to the oral presentation would also be presented here. Any unusual work-related exposures should be noted. "Mr. H works as an accountant for a large firm in Boston. He lives alone in an apartment in the city." Family History: Emphasis is placed on the identification of illnesses within the family (particularly among first degree relatives) that are known to be genetically based and therefore potentially inherited by the patient. This would include: history of coronary artery disease, diabetes, certain neoplasms, etc. "Both of the patient's parents are alive and well (his mother is 78 and father 80). He has 2 brothers, one 45 and the other 55, who are also healthy. There is no family history of heart disease or cancer." Physical Exam: This begins with a one sentence description of the patient's appearance along with their vital signs. In general, only '+' findings are noted. It is also reasonable to mention the absence of certain things that the listener will find helpful in excluding particular diagnoses. If, for example, a patient has shortness of breath secondary to asthma, the presenter might mention that rales, elevated jugular venous pressure and an S3 were not present, indicating that congestive heart failure is an unlikely diagnosis. 223

Some listeners expect the entire physical examination to be recounted, including "normal findings," particularly if the presenter is a student. The following exam is listed in more detail then is necessary. However, it should give you an idea of how abnormalities as well as "normal findings" are reported. "Mr. H was seated on a gurney in the ER, breathing comfortably through a face mask oxygen delivery system. Breathing was unlabored and accessory muscles were not in use.

Vital signs were: Temp 102 Pulse 90 BP 150/90 Respiratory Rate 20 O2 Sat (on 40% Face Mask) 95% Head, Eyes, Ears, Nose, Throat: Pupils equal, round and reactive to light; Tympanic membranes pearly gray with cone of light well seen; Sclera anicteric; No thrush was noted; Mucosa was dry and without lesions; There was no appreciable adenopathy; Thyroid non-palpable; JVP was less then 5 cm. Lungs: Crackles and Bronchial breath sounds noted at right base. E to A changes present. No wheezing or other abnormal sounds noted over any other area of the lung. Dullness to percussion and increased fremitus was also appreciated at the right base. Cardiac: Rhythm was Regular. Normal S1 and S2. No murmurs or extra heart sounds noted. Abdomen: Symmetric appearing; soft, flat, non-tender; no palpable masses; well healed Right upper and lower quadrant incisions at sites of prior apppendectomy and cholycystectomy. Rectal Exam: Brown stool in rectal vault, guiac negative; no masses; prostate small, smooth and non-tender. GU: Testes descended bilaterally; no masses; no hernia; penis without lesions. Extremities: No evidence of clubbing, cyanosis or edema; Dorsalis Pedis and Posterior Tibial pulses 2+ and equal bilaterally. Skin: a 2x3 cm raised, purplish, non-tender, non-blanching area noted on left mid-shin; no other skin abnormalities identified. Neurologic Exam: Mental Status: Awake, alert, appropriate and completely oriented. Cranial Nerves: 2 thru 12 tested and intact. Motor: Strength 5/5 all extremities. Cerebellar: Finger to nose well done. Reflexes: 2+ at ankles, knees, biceps and triceps Sensation: Intact to light touch and pin prick bilaterally; proprioception normal; vibration normal. Ambulation: Normal gait; negative Romberg."

Lab results, Radiological Studies, EKGs: In general, only lab values which are abnormal are mentioned. Similarly, if the interpretation of radiological studies and EKGs are directly relevant to the case, they are discussed. "Mr. H's lab work was remarkable for: White count of 18 thousand with 10% bands; Normal Chem 7 and LFTs. Room air blood gas: pH of 7.45/ PO2 of 55/PCO2 of 30. Sputum gram stain remarkable for an abundance of polys along with gram positive diplococci. CXR showed a dense right lower lobe infiltrate without effusion."

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Impression and Plan: This is your opportunity to summarize the important aspects of the history, physical exam and supporting lab tests and formulate a differential diagnosis as well as a plan of action that addresses both the diagnostic and therapeutic approach to the patient's problems. "Mr. H is an HIV + male with a low CD 4 count and high viral load who presents with an acute pulmonary process. The rapid progression, focality of findings on lung exam and radiography, along with the sputum gram stain suggest a bacterial infection, in particular Streptococcal pneumonia. Other pathogens to consider include H Flu and, less commonly, Legionella. While he is certainly at risk for PCP, his presentation, compliance with PCP prophylaxis and statement that his current illness seems different then past PCP infection would argue against this as the etiologic agent. Mycobacterial infection also seems unlikely. Viral infections and neoplastic processes like CMV or Kaposi's Sarcoma of the lung do not generally give this clinical presentation. Furthermore, the data does not support the existence of either a primary cardiac or noninfectious pulmonary process. The Current plan then is: 1. 2. 3. 4. 5. Follow up on cultures of sputum and blood. Obtain sputum for silver staining to r/o PCP Begin treatment with IV cefuroxime; Hold off on empiric treatment for PCP. Continue O2,with goal to keep sats greater then 92% IV fluid replacement with Normal Saline at 125cc/H for next 24 hours to correct mild hypovolemia, with plan to reassess volume status at that time 6. If patient does not show improvement (or worsens) and cultures are unrevealing, consider bronchoscopy as a means of making more definitive diagnosis."

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