ACUTE ABDOMINAL PAIN By Glen E.

Hastings MD July 24, 2005 History: Nowhere is the medical history more important than with the complaint of abdominal pain. The possible causes of abdominal pain are so numerous as to preclude systemically excluding them all, but a meticulously detailed history of the present illness at the very least tells the skilled clinician where to start. Table 1: Symptom Descriptors It is exquisitely important to obtain as specific a description of the pain Quality Location as the patient is able to give as well as its exact location, whether or not Radiation it radiates & if so where, any associated symptoms (See Table 1) such Associated Symptoms as nausea or vomiting, factors thought to incite the pain or relieve it & Precipitating Factors factors about the timing of the pain (eg. Is it continuous or intermittent, Ameliorating Factors Abrupt or Gradual Onset gradual or abrupt in onset, or recurrent?). Continuous or Intermittent II Varieties of Abdominal Pain 1,2 : Has It Happened Before? o Visceral Pain is poorly localized. It is frequently described as Pattern of Prior Occurrences deep & dull & aching or pressure-like. Visceral pain is caused by over-distention or spastic contraction of a hollow viscus or by stretching of the capsule of a solid organ or a metabolic cause (Arterial injection of lactate, hypertonic, acidic or alkaline IV solutions, or bradykinin as well as black widow spider bites, porphyrea or diabetic ketoacidosis all produce visceral abdominal pain). Severe episodes may be accompanied by sensitization to painful stimuli along with autonomic activation (i.e. sweating, nausea or vomiting, tachycardia or bradycardia followed later by deteriorating blood pressure, skin pallor & hyperesthesia). o Somatic Pain is caused by inflammation of the parietal peritoneum following contact with blood, bile, gastric acid or inflammatory exudates. It is sharper & more discrete than visceral pain & is localized to the site of inflammation. It is exacerbated by pressure, both from the examining fingers & from within the inflamed viscus (eg. "tenderness to palpation). Involuntary muscular contraction over the area of inflammation (involuntary guarding) & rebound tenderness (caused by any sudden movement of the inflamed peritoneum) are characteristic findings. o Referred Pain may occur because of two discrete mechanisms: The first & most commonly recognized is when the pain from a diseased visceral source is perceived to be localized over a somatic area of the body not obviously related to the source of the pain. Such pains are said to be referred to an area on the surface of the body enervated by nerve fibers from the same dermatome as the viscus. The usual explanation for this phenomenon is that the hypothalamic or cortical centers that process sensory input from viscera are too sparsely enervated to discretely localize visceral sensations so, lacking that capacity, they refer it to a more familiar source of noxious stimuli, the skin overlying the same dermatome as that servicing the viscus. Similarly, visceral pain may be referred to a site of previous trauma or painful surgery & in this case is referred to as habit reference. Similar to habit reference, both physical & psychological trauma may induce continuous chronic defensive tightening of specific muscle groups throughout the body. When these defensive posturings become habitual & chronic they may also become the source of a 3rd type of persisting long-term referred pain, even though the original inciting event(s) are usually repressed & thereby not available to conscious memory. In the language of massage therapist & others involved in the treatment of these disorders these chronic persisting musculoskeletal tensions are termed body armor. Among non-psychiatrist medical practitioners they are usually referred to as psychosomatic or psychological overlay. III Etiologies: The formidable list of diagnostic possibilities shown in Table 2 illustrates why meticulous attention to the medical history & physical findings is essential before diagnostic testing begins, for each of these conditions has its own cluster of unique & diagnostically significant symptoms & signs. The challenge of clinical medicine is to discern from the patients story which are most likely. Below we will discuss some of those features for some of the more familiar causes. I

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Table 2: Causes of Acute Abdominal Pain: Acute Gastroenteritis1 Common Intra-abdominal Causes: Less Common Intra-abdominal Causes Primary care clinicians Gastroenteritis Muscle Trauma or Strain usually get the first clue Appendicitis Meckels Diverticulum for the diagnosis of Cholecystitis or Choledocholithiasis Ruptured Solid Organ: Peptic Ulcer (Liver, Spleen, Mesentery) acute gastroenteritis by Diverticulitis Ruptured Blood Vessel the presence of similar Pancreatitis (Aortic, Splenic or Live r Aneurism) cases being present in Hepatitis Acute Bacterial Peritonitis: o o the local community. Bowel Obstruction or intussusception (1 : Strep or Staph, 2 : viscus rupture) Acute Splenomegally or Hepatomegally Inflammatory Bowel Disease: The onset is abrupt: the (CHF or Budd-Chiari syndrome) (Crohns Disease, Ulcerative Colitis) pain is cramping & Omental Torsion Perforated or Ruptured Hollow Viscus: poorly localized & (Peptic Ulcer, Gallbladder, Ovarian Cyst) Hepatic or Splenic Abscess usually accompanied by Hepatic Infarction: Mesenteric Lymphadenitis (Toxemia of pregnancy or HELLP) Constipation watery diarrhea, nausea Splenic or Omental Infarction Mesenteric Artery Occlusion or Ischemia & vomiting. The abdomen may be Common Pelvic Causes: Mittelschmertz Less Common Pelvic Causes: diffusely tender but Large or Ruptured Ovarian Cyst Tuboovarian Abscess without localization or Pelvic Inflammatory Disease Torsion or Degeneration of a Fibroid rebound tenderness. Endometritis Prostatitis, Epididymitis Between cramps the Ectopic Pregnancy with/without rupture Endometriosis abdomen is usually soft Less Common Extraperitoneal Causes: & nontender. WBCs Common Extraperitoneal Causes: Acute Pyelonephritis may be decreased Psychogenic Hereditary Angioedema Drugs & Drug Withdrawal normal or elevated with Abdominal Epilepsy Acute Myocardial Ischemia/Infarction. either a right or left shift Porphyrea Pneumonia or Pulmonary Embolus Tabes dorsalis depending on the Sickle Cell Crisis Black Spider Bites & other toxins causal organism. Low Herpes Zoster Rectus Sheath Hematoma Diabetic Neuropathy or Ketoacidosis grade fever may also be Lead Poisoning Ureteral Stone present. Abdominal Addisonian Crisis upright x-rays usually show small & large bowel gas without air-fluid levels. Treatment is symptomatic & supportive. Acute Appendicitis 3 in its early stages is usually as a dull poorly localized discomfort in the periumbical region (i.e. like visceral pain). Anorexia is almost always present; & hunger virtually excludes the diagnosis. Vomiting may occur several hours the pain starts. Four to 6 hours later the pain becomes sharper & more discretely localized to the right lower quadrant as inflammatory exudates activate somatic pain receptors in the parietal peritoneum adjacent to the appendix. About 50% of patients report this typical progression of events. Sometimes the patient lies quietly on the right side with the knee flexed in order to avoid sudden movements. Tenderness to palpation at Mc Burneys point in the right lower quadrant along with involuntary guarding & rebound tenderness are characteristic except when the inflamed appendix is retrocecal or pelvic in location. In these cases deep rectal examination reveals tenderness toward the right lower quadrant. There may be low grade fever up to 100o F & a mildly elevated WBC with a left shift. Fever >101o & WBC > 20,000 suggest that perforation may have occurred. The diagnosis must be differentiated from mesenteric adenitis & Crohns disease, acute gastroenteritis, PID, or a ruptured graffian follicle. The diagnosis may sometimes be made by abdominal CT with GI contrast of the right lower quadrant, but sometimes laparoscopy or laparotomy are required. The treatment is surgical. Choledocholithiasis4 occurs when a gallstone abruptly obstructs the cystic or common bile duct (CBD), thereby increasing intraluminal pressure in the gall bladder unrelieved by repeated contractions & producing a steady, poorly localized (visceral) right upper quadrant pain which may radiate to the right infrascapular or intrascapular area or to the right shoulder. In common duct obstruction the pain is usually epigastric & may radiate to the lumbar area. The pain is continuous aching & pressure-like (so the term gallbladder colic is a misnomer); centered in the right upper quadrant or the epigastrium & unrelieved by antacids. It may occur 30 minutes to 2 hours after eating fatty foods or after eating a large meal following a fast or rigorous diet & may occur at night. It persists for 30 minutes to 5 hours. Pain persisting longer than 5 hours suggests

Abdominal Pain: Page 3 of 10 acute cholecystitis. About 10% of such patients do not have gallstones. The same symptoms may be caused by bile sludge in a poorly contractile gallbladder. In such patients a HIDA scan following cystokinin administration will reveal a gallbladder ejection fraction < 40% at 45 minutes. As in the presence of gallstones, cholecystectomy may relieve the symptoms. The 10 year risk of any kind of clinical complication from asymptomatic gallstones is about 15% & the mortality rate virtually nil, so prophylactic cholecystectomy for asymptomatic gallstones is rarely recommended. Acute Cholecystitis 4 , in 50 to 60% of cases starts like a typical episode of choledocholithiasis except that it stays & gets worse. Anorexia & vomiting are common as is low grade fever & a modestly elevated WBCs with a left shift. Peritoneal signs develop, producing pain with deep respiration or sudden movement, as phospholipidases in the confined bile catalyse the production of the inflammatory agent lysolethicin via their action on bile lethicin. In the majority of patients, inflammatory exudates related to bacterial infection with E coli, Klebsiella, Streptococcal or Clostridium spp, are also present. The distended gallbladder may be palpable in patients with lean abdomens. Murphys sign is present if deep palpation of the right upper abdomen produces exquisite tenderness as the patient inhales deeply or coughs. Ultrasound reveals gallstones in 90 to 95% of cases. Serum bilirubin or liver enzymes may sometimes be elevated but not consistently enough to be used to exclude the diagnosis. 75% of patients recover spontaneously with 2 to 7 days of supportive treatment. The 25% who do not respond require prompt surgical intervention. Those who do respond to treatment or have poor ejection fractions & bile sludge should usually undergo elective cholecystectomy as the recurrence rate is about 60% in 6 years. Peptic Ulcer Disease (PUD) 5 usually presents with gnawing or burning epigastric pain 2 to 3 hours after meals & in of cases may awaken the patient between midnight & 2am. Unfortunately about of patients with non-ulcer dyspepsia have similar symptoms. At first, when peptic ulcer is present, the pain is relieved by antacids or food, except in the case of gastric ulcer, where eating may precipitate the pain. Concomitant weight loss or nausea also suggest gastric ulcer or gastric outlet obstruction. Sudden onset of severe generalized abdominal pain, unrelieved by antacids & accompanied by physical signs of peritoneal inflammation (tenderness, involuntary guarding & rebound tenderness) suggest perforation of the ulcer into the abdominal cavity. Posterior perforations go into the pancreas so they may present without peritoneal signs but with radiation of pain to the lower thoracic or upper lumbar mid-back. Physical findings may be non-existent & are more often limited to epigastric point-tenderness in uncomplicated PUD. The most frequent first diagnostic tool used by most primary care clinicians in patients below age 45 is an empirical trial of a proton pump inhibitor. The most sensitive & specific is upper endoscopy. Less frequently double-contrast upper GI x-ray is used. The sensitivity of x-ray approaches 80% only if double contrast technique is used. Gastric ulceration by x-ray requires followup endoscopy & biopsy to exclude gastric carcinoma. About 15% of patients have at least one episode of UGI bleeding, 6 to 7% experience a perforation (see above) & 1 to 2% develop gastric outlet obstruction. Early satiety, nausea, vomiting, weight loss & increasing postprandial pain suggest outlet obstruction or gastric cancer. The majority of peptic ulcers are related to H pylori infection, about 20% to NSAIDs & 0.5 to 1% to Zollinger-Ellison (ZE) syndrome. Patients with multiple DUs, refractory disease or DU below the duodenal bulb should be screened by serum gastrin level (< 200pg/dL) to exclude ZE syndrome. Acute Pancreatitis 6 presents with steady boring upper abdominal pain of variable intensity radiating to the back, flanks or lower abdomen. The patient is distressed & anxious; the abdomen tender & guarded but the bowel sounds are faint or absent. In severe cases there may be 3rd spacing of fluids & inflammatory exudates within the abdominal cavity of sufficient magnitude to produce hemodynamic shock. Diffuse symmetrical Velcro crackles throughout both lung fields occurring during the first week accompanied by deteriorating O2 saturation suggests ARDS. Cullins sign (periumbilical discoloration) & Turners sign (discoloration of the flank) may occur in necrotizing pancreatitis. Sudden vision loss during the first week suggests Purtchers retinopathy. The optimal diagnostic test for acute pancreatitis is serum lipase which is 91% sensitive & 98% specific when > 3x the upper limits of normal of the lab performing the test. At best (3x normal) serum amylase is 80% sensitive & 70% specific. Abdominal CT without contrast is almost 100% specific & sensitive but is more costly & unnecessary unless lipase is normal. Most patients have only edematous pancreatitis & require only supportive care, fluid/electrolyte & pain management

Abdominal Pain: Page 4 of 10 & bowel & for recover in 3 to 5 days. Those less likely to recover may be predicted by the presence of more than 2 of the prognostic criteria of Ranson or Glascow (See below).
Ransons Criteria
Non-gallstone Pancreatitis On Admission: Age > 55 WBC > 16,000 Blood glucose>200 mg/dL Serum LDH > 350 IU/L AST (SGOT) > 250 IU/L Within 48 hours: Hematocrit decrease > 10% BUN increase > 5 mg/dL Serum calcium < 8 mg/dL Arterial pO2 < 60 mm Hg Base deficit > 4 Fluid deficit > 6L Gallstone Pancreatitis On Admission: Age > 70 WBC > 18.5 K Blood glucose> 180 mg/dL LDH > 400 U/dL AST >250 U/dL Within 48 Hours: Hematocrit decrease > 10% BUN increase > 2 mg/dl Serum Calcium < 8 mg/dl Base deficit > 5 mmol/L Fluid deficit > 4 liters

Modified Glasgow Criteria

Age >55 WBC > 15,000 Blood glucose> 180 mg/dL BUN > 45 (after rehydration) pO2 < 60 mm Hg Ca < 8 mg/dL Albumin < 3.4 gm/dL LHD > 600 IU AST or ALT > 200 IU

Interpretation: 3 or more at any time during the first 48 hours indicates severe pancreatitis.

Interpretation: mild attack: < 0-2 sign (<1% mortality) moderate attack: 3-4 signs (16% mortality) severe attack: 5 or more signs (>40% mortality)

Looking for & finding 3 or more prognostic criteria is not simply an interesting academic exercise because it calls for other actions: First of all it calls for the administration of prophylactic antibiotics (they are otherwise not indicated). Most patients who die of pancreatitis die after the 3rd week of sepsis. Antibiotic prophylaxis in high risk patients has been shown to reduce mortality. Since patients who die of pancreatitis first have pancreatic necrosis as the culture medium for translocated bowel flora, one would like to know if necrosis is present. This can be assessed by doing a rapid-bolus contrast CT 3 to 5 days after the onset of pain. If necrosis is demonstrated, a needle aspiration of the necrotic area using CT guidance is indicated if warranted by the clinical picture (about 40% of necrotic areas will be infected at the time of 1st aspiration). Culture will allow bacteria sensitivity driven therapy. Acute Hepatitis may present with abdominal pain as part of the clinical picture, which may also include nausea, vomiting, malaise & eventually jaundice. The abdominal pain of hepatitis occurs because of stretching of the capsule of the liver hence it is aching or pressure-like & diffusely localized to the right upper quadrant. The timing of the appearance of pain depends on the severity of the insult to the liver. Non-Viral Hepatitis: Acetaminophen 7 , Amanita phalloides, carbon tetrachloride, halothane & other hepato-toxins, at toxic levels may cause abdominal pain along with nausea, vomiting & diarrhea within 4 to 12 hours after exposure. In acetaminophen toxicity it takes 24 hours before laboratory evidence of severe hepatocellular damage reflects a prolonged INR, & 48 hours before jaundice & aminotransferase elevations make the diagnosis obvious. By that time its too late for treatment! Hence, systematic inquiry about possible toxic drug exposure is an essential feature of the workup for acute abdominal pain. Acute hepatic necrosis usually means >25 grams of acetaminophen have been ingested. The Rumack-Mathew Acetaminophen nomogram shown on the right indicates the serum levels at 4 hours after ingestion of acetaminophen that are likely to cause clinically significant toxicity. Levels >300mg/dL may cause fulminant hepatic failure. The treatment for acetaminophen overdose is acetyl-cysteine administered orally or IV as soon as the diagnosis is made. There is no evidence of treatment benefit after 52 hours.

Abdominal Pain: Page 5 of 10 Viral Hepatitis 8 : Fulminant hepatitis is an unusual presentation of viral hepatitis, which usually presents with prodromal phase symptoms which may consist of various combinations of fatigue & malaise, anorexia, nausea, arthralgias, headache, myalgias, alterations of the senses of taste & smell or upper respiratory symptoms. Liver enlargement, accompanied by right upper quadrant visceral pain, clinically apparent jaundice & characteristic aminotransferase elevations are features of the clinical phase & resolve during the recovery phase of the illness. Acute Fatty Liver of Pregnancy 9 is a cause of fulminant hepatitis, starting as a flu-like syndrome in the 3rd trimester of a first pregnancy & rapidly progressing to abdominal pain caused by swelling of the inflamed liver confined within its capsule followed by jaundice & hepatic encephalopathy. The treatment is immediate delivery. The mortality is 20 to 30%. Severe Preeclampsia9 may present with excruciating right upper abdominal pain caused by subcapsular hemorrhage of the liver stretching the liver capsule. The treatment is immediate delivery. HELLP Syndrome is severe preeclampsia with hemolysis, elevated liver enzymes, & thrombocytopenia. Preeclampsia can occur at any time beyond the 20th week of gestation & can be recognized by the presence of hypertension, proteinurea & thrombocytopenia. Intestinal Obstruction 10 begins with abdominal distention; greater if the obstruction is in the colon & progressively less, the higher the obstruction. Intestinal obstruction may be mechanical or functional (termed adynamic ileus). Although adynamic ileus is the most common cause of intestinal obstruction, a presenting complaint of pain suggests the presence of a mechanical obstruction. Pain originating in the duodenium tends to be felt in the epigastrium, the rest of the small bowel in the periumbilical & flank areas; pain from the colon in the lower abdomen & suprapubic areas. Absent bowel sounds do not exclude a mechanical obstruction or favor the diagnosis of adynamic ileus. Adynamic Ileus can be caused by many adverse intra-abdominal or thoracic events, drugs, pathological conditions of the lumbar or thoracic spine, & various metabolic abnormalities, most frequently hypokalemia or diabetic ketoacidosis. The only discomfort in adynamic ileus is a vague generalized visceral pressure-like discomfort. Cramping pain is not present. Abdominal distention may be marked & vomiting is common but not profuse. Hiccups are common. Upright x-rays of the abdomen show both small & large bowel gas & may show airfluid levels. Nasogastric tube aspiration, supportive care & correction of the precipitating condition are the treatments. Mechanical Small Bowel Obstructions (SBOs) present with cramping, paroxysmal midabdominal pain which becomes less severe as the abdomen becomes more distended & quiet. Borborygimous bowel sounds may be heard that are synchronistic with the cramping paroxysms. When a strangulated loop of small bowel is the cause, the pain will be more constant, more localized & devoid of the colicky quality. Vomiting is almost always present & may be feculent if the obstruction is ileal. A palpable abdominal mass usually is a tense fluid filled closed loop of strangulated small bowel. An upright abdominal x-ray that shows dilated loops of small bowel arranged in a stair step pattern with no evidence of colon gas almost always indicates a complete small bowel obstruction with or without early strangulation. Later, strangulation may cause exudation of fluid into the peritoneal space causing a hazy ground glass appearance accompanied occasionally by a coffee-bean shaped mass (made by a fluid filled bowel loop) but the x-ray may also be normal. A normal KUB film suggests strangulation & indicates the need for a CT of the abdomen. An incomplete obstruction may not be differentiated from adynamic ileus because colon gas is present in both. About 75% of SBOs are caused by adhesions or incarcerated internal or external hernias. The remainder by a variety of conditions including Crohns disease, carcinoids, adenocarcinomas, leiomyomas & intussusceptions. Although nasogastric decompression & supportive care will many times relieve the presenting symptoms, non-operative management alone is safe only when the obstruction is incomplete & the patient is known to have had a recent episode or repeated episodes of SBO or has recently had peritonitis.

Abdominal Pain: Page 6 of 10 Mechanical Colon Obstructions produces a less intense colicky lower abdominal pain similar to but milder than SBO. Vomiting is rare. Marked abdominal distention which may have progressed over several weeks is not uncommon. Upright abdominal x-ray shows air in the colon & is easy to recognize by x-ray if the ileocecal valve is competent because the trapped air is distributed only in the colon. The location to which the air extends may indicate the site of the obstruction & a fecal impaction or intussusception may also be seen. When the ileocecal valve is competent & the obstruction is complete, early operative management is important because the colon gas will eventually pool in the cecum because of its larger surface, distending its walls & eventually the pressure of the gas will cause cecal gangrene. Adhesions are rarely the cause of colon obstruction. More common causes include adenocarcinoma, diverticulitis, cecal or sigmoid volvulus. Surgical intervention is almost always required although patients with incomplete obstruction can usually be supported long enough for appropriate diagnostic tests to be performed. Acute Diverticulitis 11 is a clinical diagnosis that presents with new onset left lower quadrant abdominal pain, fever & diarrhea or obstipation & if perforation has occurred, peritonitis. The inflammation is limited to the sigmoid bowel in more than half of the cases. Isolated diverticulitis of the right colon is unusual (2% of cases). The abdomen may or may not be distended. There is tenderness & sometimes a tender palpable mass in the left lower quadrant. Deep pressure over the right side of the abdomen may increase the discomfort in the left lower quadrant. The diagnosis can be confirmed by CT findings of a thickened colonic wall >4mm & inflammatory changes in the surrounding fat tissue. Leukocytosis with a left shift is so common that its absence makes the diagnosis suspect. Bowel rest, fluids, pain control & IV antibiotics resolve these symptoms in 85% of cases within 3 days, after which colonoscopy or sigmoidoscopy with an air contrast barium enema should be electively planned. Neither study should be performed during the acute phase because of the danger of perforation through one of the inflamed diverticulae. Patients who do not respond promptly, those with complications or those who present with the first attack before age 40 should be offered a surgical option. Inflammatory Bowel Disease 12 : Ulcerative Colitis (UC) patients with Moderate to Severe UC disease present with more than 6 loose stools/day usually with severe abdominal pain, & sometimes with weight loss, fever &/or obstructive symptoms. Up to 3% present with toxic megacolon as the first manifestation. The rectal mucosa is involved in 95% of cases. Crohns Disease (CD) is more likely to present with the insidious onset of right lower quadrant pain & localized tenderness along with diarrhea that may or may not be bloody. Constitutional symptoms such as low-grade fever, night sweats or weight loss are common. CD may also present initially as perirectal disease, so the perirectal area should be inspected in suspected CD. Aphthus ulcers of the mouth may often be the earliest manifestation of CD in children. About 40% of younger children with CD present initially with failure to thrive. Diagnosis: In 10-20% the differential diagnosis between UC & CD may not be discernible but colonoscopy with biopsies usually establishes the type of disease. Management depends on the disease diagnosis, the acuity of its presentation & the extent of disease & is beyond the scope of this inventory of causes of abdominal pain. Mesenteric Vascular Insufficiency11 is caused by acute vascular thrombosis or embolization, mesenteric arterial vasospasm or venous occlusion of the mesenteric veins. Arterial insufficiency is the most common cause. Not surprisingly the incidence of these disorders increases with age in parallel with the incidence of coronary artery disease. Acute Total Occlusion by Arterial Embolism or Thrombosis of a major mesenteric artery is a catastrophic event that presents with acute, severe & unremitting abdominal pain, while the early abdominal findings are limited to mild distention & decreased bowel sounds. Signs of peritonitis & hemodynamic instability develop later as bowel necrosis & perforation occur. Comorbidities that predispose to embolic events include atrial fibrillation, acute myocardial infarction, CABG or aortic catheterization or aneurism repair. Early upright abdominal films may identify free air & the bowel wall becomes edematous producing a thumbprint pattern. When acute total arterial occlusion is suspected, after the patient is medically stable, the optimal diagnostic tool is laparotomy with direct inspection of the entire small bowel followed

Abdominal Pain: Page 7 of 10 by restoration of blood flow to segments that seem viable & resection of gangrenous segments. Mortality approaches 50%. Ischemic Colitis (eg. Incomplete Arterial Occlusion) presents with poorly localized abdominal pain, bloody stools, anorexia & abdominal distention. If LLQ guarding & rebound tenderness are present, perforation has likely occurred & laparotomy is indicated. If not, bowel rest, IV fluid management, sometimes blood transfusion & antibiotic coverage for gram negative, gram positive & anaerobic organisms is the initial treatment of choice. KUB upright films will usually show thickening of the bowel wall with thumb printing in the territory of the ischemic bowel. Colonoscopy should be performed when ischemic colitis is suspected in order to assess the severity of the ischemic insult on the bowel mucosa. Mild ischemic colitis is present if the mucosa is erythematous moderate when pale with mucosal ulcerations revealing the muscularis mucosa & severe in ulcerated areas of black or green discoloration.. Abdominal Angina produces cramping, pressure-like abdominal pain that occurs after eating because of increased postprandial demand for intestinal blood flow. Weight loss & diarrhea are common. Abdominal pain without weight loss is not abdominal angina. Physical examination sometimes reveals an abdominal bruit & other stigmata of atherogenic disease. In general, treatment consists of lipid & blood pressure management & smoking cession. MRA may be used to identify areas of flow disturbance which may often be ameliorated by endovascular stenting with a long term success rate of about 80%. Mesenteric Venous Thrombosis presents with vague abdominal pain, nausea & vomiting in a patient predisposed by the presence of some type of major hypercoagulablopathy: cancer, antithrombin III deficiency, protein C or protein S deficiency, or a combination of minor thrombogenic traits. The diagnosis is made with spiral CT with IV & GI contrast. Treatment is massive fluid resuscitation & nomogram administered unfractionated heparin unless bowel necrosis is suspected, in which case surgical exploration is mandatory. Pelvic Inflammatory Disease 13 is easily diagnosed when patients present with classically signs & symptoms: menstrual disturbances, lower abdominal pain, chills & fever > 38.3o, cervical motion tenderness & adnexal tenderness & a purulent vaginal or endocervical discharge. Right upper quadrant pain may indicate an associated perihepatitis (Fitz-Hugh Curtis syndrome). The major problem in the diagnosis of PID is that many patients present with much more subtle symptoms or none at all. Pelvic examination is a routine part of the workup for abdominal pain in women, especially when fever is present. Tenderness guarding & rebound tenderness may be found upon palpating the lower abdomen. Cervical motion tenderness indicates the presence of peritonitis in the area adjacent to the cervical fundus. However cervical motion tenderness is not specific for PID; it may be caused by appendicitis or other intra-abdominal infections. PID is usually related to N gonorrhea or C trachomatis. Transvaginal sonography or MRI confirms the diagnosis, showing thickened, fluid filled Fallopian tubes with or without free fluid in the pelvis or tubo-ovarian abscess. PID patients should be admitted for inpatient care when appendicitis cannot be ruled out, tubo-ovarian abscess is present, the patient is pregnant, when out patient management has failed or when the patient is extremely ill. Many women with PID have no subjective symptoms at all & those can be safely treated as outpatients. Ectopic Pregnancy9 is a diagnosis that must not be missed. Undiagnosed ectopic pregnancy is the most common cause of maternal death in the first trimester. In about 40% of cases it presents with sudden onset of severe lancing intermittent lower abdominal pain as the sac ruptures into the peritoneal cavity. Backache is also present during paroxysms of pain. Shock may be present in as many as 10% of cases. Most give a history of menstrual irregularities & many report one of the known risk factors for ectopic pregnancy: previous ectopic pregnancy, current IUD use, previous PID or tubal surgery. In 60% the onset is more insidious, presenting with abdominal distention & ileus with vague abdominal discomfort, as blood leaks slowly from the tubal ampulla into the peritoneal cavity. These patients too will likely report menstrual irregularities & vaginal spotting & possibly suspect pregnancy. Pelvic examination usually reveals an adnexal mass. Cervical motion tenderness will be present if rupture has occurred & may or may not be present before. Before rupture, the diagnosis can be made with certainty if the -hCG level is > 6500 & the uterine cavity is empty by transabdominal ultrasound. A -hCG level of 2000mU/mL is suspicious for ectopic pregnancy if transvaginal ultrasound reveals no evidence of intrauterine pregnancy. The -hCG level in ectopic pregnancy is always lower than with an

Abdominal Pain: Page 8 of 10 intrauterine pregnancy of the same duration. Laparoscopy is the diagnostic gold standard & also the usual means of definitive treatment. Stable patients with early ectopic pregnancies may sometimes be candidates for medical treatment with methotrexate or another abortifactant when the diagnosis & the patient otherwise at low risk. Ectopic pregnancy recurs in about 12% of cases. Psychogenic Abdominal Pain is very common & not innocuous, for when misdiagnosed it may & frequently does lead to one or more unnecessary surgical procedures. Irritable Bowel Syndrome (IBS) 14 is a very frequent & very troublesome cause of chronic, recurrent abdominal pain that is associated with alterations of bowel habits without detectable structural abnormalities (See Rome II Criteria; Table 3). Its onset is almost always before age 45 & of IBS patients are women. The pain is quite variable in intensity & location. It is most frequently described as cramping but cramps may sometimes be superimposed on a dull poorly localized continuous ache. Most commonly the alteration of bowel habit is dominantly constipation, the second most common is constipation alternating with diarrhea & a few with diarrhea alone. Except in the most severe of cases, the symptoms do not disturb sleep & are limited to the daylight hours. They are made worse by eating or by emotional stress & relieved by defecation. One third of IBS patients also have dyspepsia. The etiology is uncertain but pathogenetically, IBS patients exhibit increased GI reactivity to a variety of GI stimuli. They have increased numbers of serotonin containing cells in the colonic mucosa & stimulation of the GI mucosa shows increased frontal lobe activity in an area thought to be related to visceral sensation Table 3: Rome II Criteria for IBS perception. There is no definitive test for IBS so it At least 12 weeks of the last 12 months with abdominal pain & 2 of the following: remains a diagnosis of exclusion. There is no gold Relieved by defecation standard treatment. A careful dietary history or a Onset with changes of Bowel Frequency rotational exclusion diet may help to identify & permit Onset with changes in Stool Form exclusion of foods that produce symptoms. Stool bulking agents such as psyllium may be of benefit & a variety of other agents are sometimes useful for symptom relief. They include anticholinergic antispasmodics, antidiarrheal agents such as loperimide, antidepressants antiflatulant drugs such as simethicone. Tegaserod a serotonin agonist is prokinetic & FDA approved for treating women with dominantly constipation related IBS. Alosetron is a serotonin antagonist that also inhibits GI cholinergic neurons thereby slowing colon motility & reducing sensitivity to visceral pain. It is an FDA approved treatment for women with diarrhea dominant IBS. Alosetron should be reserved only for the most severe of cases as it is known to cause ischemic colitis in 4:1000 patients. Somatization Disorder (Briquets Syndrome) 15 often presents with abdominal pain, all too frequently leading to unnecessary surgery. Polysurgery is one feature of this condition. Patients with somatization disorder have poor self esteem & poorly developed mechanisms for coping with anxiety. When an anxiety provoking event occurs, they repress the anxiety & split it from the memory of the event, then express the anxiety as a symbolically related somatic symptom. This is not a conscious process (eg. These patients arent consciously doing it) & they truly experience somatic pain! At the same time, they cannot give up the somatic symptom, for that would release the repressed anxiety. It does no good to try to talk them out of the symptom; the best approach is to explore all reasonable biological explanations & then reassure the patient. Avoid surgery & other hazardous interventions unless strongly indicated. Also, because of their low self esteem & poor coping skills these patients depend inordinately on any authority figure (eg. the doctor) who seems willing to solve their problems for them. Indeed, preoccupation with medical & surgical therapies frequently excludes their interest in healthier social & interpersonal outlets. It is extremely important to avoid leading such patients when interviewing them, because many are inordinately eager to please authority figures & unsure in their own minds about the nature of their symptoms. It is essential to employ non-directive interview techniques with these patients. The doctor who prescribes an intervention that goes wrong for such a patient must have carefully documented records because these patients will recall the events leading up to the intervention quite differently, because it is quite painful for them to accept even a hint of blame of any kind, or to accept personal responsibility for their own health. These personality traits usually appear first during late teen age years or the second decade. They are ten

Abdominal Pain: Page 9 of 10 times more frequent in women than men & more frequent in the lower socioeconomic groups. There is invariably a prior history of multiple long term somatic symptoms: lump-in-thethroat, dysmenorrhea, shortness of breath, amnesia or pain in the extremities. Usually other members of the patients family exhibit similar multisystem complaints. Failure of 3 or more clinicians to make the diagnosis is a strong clue to the problem. There is no silver bullet to cure these patients. The best that can be done is to try to shield the patient from therapeutic misadventure by nurturing a close doctor-patient relationship & by systematically listening to & evaluating each new complaint. The prognosis for avoiding harm is better if the primary physician intervenes early, before a new complaint becomes a part of life. Munchausen Syndrome15 often presents in the ER with abdominal pain with a textbook history for some intra-abdominal condition. It differs from somatization disorder in that these patients fabricate the symptoms they present, as well as laboratory abnormalities & physical examination findings. The deception may involve self mutilation, induction of fever, seizures, hemorrhage or hypoglycemia & is usually presented in a dramatic manner that mandates hospitalization. These patients are frequently associated in some way with the health professions & many are migratory, moving from emergency room to emergency room from town to town with the apparent goal of simply enjoying the sick role. Munchausens-byproxy is the term used when a parent creates an illness in a child, usually as a means of maintaining a relationship with the doctor. Table 4: Precipitating Drugs Acute Intermittent Porphyria 16 is a rare cause of abdominal pain Ethanol Sulfa Drugs that is quite varied in its severity. It is poorly localized & sometimes Barbiturates cramping in character & is usually precipitated by exposure to Synthetic Estrogens & Progestins ethanol, barbiturates, an infection or another precipitating factor Most Anticonvulsants (See Table 4 for a partial listing of hazardous drugs.) The disease Alkylating agents Food additives can be disabling but is rarely fatal. It is inherited as an autosomal Theophylline dominant with poor penetrance. Women are most likely to develop Antifungal agents clinical disease & it usually starts in the teens or early 20s. Rifampin Abdominal tenderness, fever & leukocytosis are usually absent but Macrolide antibiotics Ergot amines nausea, vomiting, constipation, muscle weakness, tachycardia, Clonidine, Hydralazine, hypertension, mental symptoms & urinary retention are common. -methyl DOPA, Gluthimide Attacks do not occur before puberty & can be avoided by avoiding exposure to a known precipitating conditions. The diagnosis is made by demonstrating elevated porphobilinogens & -aminolevulinic acid levels in the urine. The diagnosis is frequently missed because it isnt considered & sought. Treatment of acute attacks with IV glucose is usually sufficient, although IV infusions of heme are more effective in relieving the acute symptoms Familial Angioedema 17 is another inherited zebra that frequently presents as cramping abdominal pain. It is inherited as an autosomal dominant condition & may present with cervical or laryngeal edema without evidence of pruritis or urticaria. The pathogenetic abnormality in familial angioedema is deficiency of C1 inhibitor (Type 1) or a dysfunctional C1 inhibitor molecule (Type 2). The reason for the abdominal colic is frequent episodes of angioedema within the bowel. The angioedema occurs because of the accumulation of excessive tissue bradykinins that accumulate because of the inability of the available C1 inhibitor to adequately control C1 activity. Diagnosis hinges on demonstrating reduced levels or deficient C1 inhibitor & depleted C2 & C4.

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Silen W, Abdominal Pain. Chapter 13 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 82-84. Pasricha PJ Approach to the patient with abdominal pain. Chapter 38 in Textbook of Gastroenterology 4 Edition. Editors: Yamada T Alpers DH, Kaplowitz N, Laine L, Owyang C, Powell DW. Lippincott, Williams & Wilkins. Philadelphia, PA. 2003 Pages 781-801. McQuaid KR Alimentary Tract. Chapter 14 in 2004 Current Medical Diagnosis & Treatment. Editors: Tierney LM, McPhee SJ, Papadakis MA. Lange Medical Books/McGraw-Hill. NY, NY 2004. Pages 590-91. Greenberger NJ, Paumgartner G. Diseases of the gallbladder & bile ducts. Chapter 292 in Harrisons Principles of th Internal Medicine 16 Edition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGrawHill NY,NY 2005 Pages 1880-91. Del Valle J Peptic Ulcer Disease & Related Disorders. Chapter 274 in Harrisons Principles of Internal Medicine 16 Edition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 1880-91. Banks PA: Practice guidelines in acute pancreatitis. Am J Gastroenterol 1997;92:377-86. OGrady JG: Paracetamol-induced acute liver failure: prevention and management. J Hepatol 1997;26(Suppl 1):41-46. Dienstag JL, Isselbacher KJ Acute viral hepatitis. Chapter 285 in Harrisons Principles of Internal Medicine 16 Edition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 182238. Crombleholm WR. Obstetrics. Chapter 18 in 2004 Current Medical Diagnosis & Treatment. Editors: Tierney LM, McPhee SJ, Papadakis MA. Lange Medical Books/McGraw-Hill. NY, NY 2004. Pages 734-38. Silen W, Abdominal Pain. Chapter 280 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 1802-5. Gearhart SL, Bulkley G, Common Diseases of the colon & rectum & mesenteric vascular insufficiency. Chapter 279 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 1795-1803. Friedman S , Blumberg RS. Inflammatory bowel disease. Chapter 276 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 1776-89. Mac Kay HT. Gynecology. Chapter 117 in 2004 Current Medical Diagnosis & Treatment. Editors: Tierney LM, McPhee SJ, Papadakis MA. Lange Medical Books/McGraw-Hill. NY, NY 2004. Pages 707-8. Owang C. Irritable bowel syndrome. Chapter 277 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 1789-93. Eisendraath SJ, Lichtmacher JE. Psychiatric disorders. Chapter 25 in 2004 Current Medical Diagnosis & Treatment. Editors: Tierney LM, McPhee SJ, Papadakis MA. Lange Medical Books/McGraw-Hill. NY, NY 2004. Pages 1012. Desnick RJ. The porphyreas Chapter 337 in Harrisons Principles of Internal Medicine 16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 2303-8. Austen KF. Allergies, anaphylaxis & systemic mastocytosis. Chapter 288 in Harrisons Principles of Internal Medicine th 16 Edition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Page 1951.
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