CHAPTER 21  
Surgical Critical Care
Andrew H. Stephen, Charles A. Adams, Jr., William G. Cioffi
OUTLINE
Neurologic System Hematologic System
Cardiovascular System Endocrine System
Respiratory System Infection in the Intensive Care Unit
Gastrointestinal System Prophylaxis in the Intensive Care Unit
Renal System Special Issues
Hepatic System
The demand for quality surgical critical care is expected to increase
as the population of the United States ages, and care of these
patients will be increasingly more complex because of their more
numerous comorbidities. Surgical intensivists will need to stay
abreast of advances in medical treatments across multiple disci-
plines to continue to deliver quality critical care. Approximately
half of patients who require general surgical operations are taking
medications unrelated to the surgical condition, and this rate is
typically higher in patients destined for the intensive care unit
(ICU). Although many tertiary care facilities treat surgical critical
care patients in closed model ICUs, where care is directed by
specially trained teams led by specialty boarded surgical intensiv-
ists, it is imperative that surgeons understand the concepts and
thought processes involved in caring for these patients, particu-
larly for patients cared for in open model or mixed ICUs lead by
nonsurgical intensivists.
One of the greatest challenges for a critical care provider is to
be cognizant of and to integrate fully advances in technology into
clinical care for maximal benefit to critically ill patients. Each year
brings an array of new devices, diagnostic tools, and complex
therapies that pose a challenge to the intensivist. However, perhaps
the greatest challenge of all is to deliver quality, cost-efficient
care, especially in the present atmosphere of health care reform
and dwindling financial resources. As a corollary of the so-called
quality movement, awareness is increasing among health care
providers of the long-term ramifications of critical illness and its
devastating effects on quality of life after ICU discharge. With the
advent of each new technology or therapy, one must remember
that “more” in terms of volume, intensity, or complexity of care
does not always translate into better results and that a critically ill
surgical patient requires a measured and thoughtful systems-based
approach that optimizes outcomes in the most efficient and cost-
effective way. Surgical intensivists are critical care specialists, but
in contrast to their medical colleagues, they have the unique
ability to understand the impact of surgical disease and operative
procedures on physiology in the ICU, and this distinctive knowl-
edge base is thought to lead to better outcomes for critically ill
surgical patients.
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NEUROLOGIC SYSTEM
Dysfunction
Alterations in mental status in a critically ill surgical patient are
commonplace. For example, in a review of mechanically venti-
lated ICU patients, delirium was identified in 60% to 80%;
evidence has shown this increases costs, length of stay, risk of
infections, and mortality.1 It is unclear whether delirium causes
these worsened outcomes or is a general marker of critical illness,
but its impact on poor outcomes and complications is not debat-
able. The surgical ICU, with its goal to provide continuous care
around-the-clock, does not afford patients a calming environment
and rapidly disrupts circadian rhythms, particularly in elderly
patients. The level of heightened stimulation in the ICU is due
to many factors, including the need for frequent monitoring,
procedures, and bedside care; patient spacing issues; and a multi-
tude of tubes, lines, drains, and machinery typically required in
care of a critically ill surgical patient. However, the diagnosis of
“ICU delirium” is one of exclusion, and any alteration in mental
status should lead the clinician to seek out organic causes, such
as cerebrovascular accident (stroke), changes in intracranial pres-
sure, medications, hypoxia or hypercapnia, sepsis, and metabolic
causes.
The term altered mental status in the ICU encompasses a broad
number of clinical entities on the continuum from confusion to
delirium to encephalopathy and brain death. Confusion is one of
the typical terms used to describe neurologic function in an ICU
patient. Confusion is one of the least severe yet most common
disturbances of neurologic function. It is defined by any type of
disorientation to person, time, or place; inability to follow simple
commands; or excess drowsiness. Confusion often exists before
progression to more dangerous and difficult-to-treat alterations
such as delirium, so any episode of confusion should prompt
evaluation for possible organic causes. Delirium refers to a distur-
bance of attention, focus, or awareness to one’s environment that
occurs over a short time and is disparate from the patient’s baseline
level of function. Cognitive deficits such as memory loss and dif-
ficulty with language or visuospatial skills and a fluctuating course
547
548 SECTION III  Trauma and Critical Care
are the hallmarks of delirium. Active delirium, which is denoted
by agitation, is often detected by critical care providers. However,
negative delirium, which is denoted by lethargy and quiet inat-
tentiveness, is often not recognized, and defined assessment mea-
sures for delirium have been advocated by the Society of Critical
Care Medicine and the American Psychiatric Association to
increase recognition of this entity.2 The two most commonly used
and well-known delirium assessment tools are the Confusion
Assessment Method for the ICU (CAM-ICU) and the Intensive
Care Delirium Screening Checklist. These tools are highly sensi-
tive and specific for delirium in the ICU, and both have been
validated in patients on ventilation and patients without ventila-
tion assistance. Regardless of which tool is employed, it is impor-
tant to use a regularly scheduled, objective measure for detection
of delirium in the ICU. Elderly patients are particularly suscep-
tible to hypoactive delirium, and detecting this condition can be
difficult despite the application of tools such as CAM-ICU.
The term encephalopathy broadly describes any global brain
dysfunction. It can result from organic and nonorganic causes and
is often the result of direct effects on the brain, such as trauma,
ischemia, or toxins. Encephalopathy also may be caused by things
far removed from the central nervous system, as illustrated by the
classic example of hepatic encephalopathy, which is caused by liver
dysfunction resulting from impaired clearance of gut-derived
compounds. The grading system for encephalopathy ranges from
confusion to obtundation, stupor, and coma. Obtundation is a
mental blunting or reduced interest in the surrounding environ-
ment, slowed response to stimuli, and increased periods of sleep
even during the daytime. Stupor is one step further on the con-
tinuum and implies a severe lack of cognitive function in which
one is almost unconscious and responds only to the most noxious
stimuli. Coma is a state where the patient no longer is capable of
responding to verbal or physical stimuli and has no understanding
or awareness of his or her surroundings. Comatose patients have
such an advanced state of neurologic dysfunction that they cannot
protect their airway and should be intubated and placed on
mechanical ventilation.
Catatonia, which is often associated with schizophrenia, is
increasingly being recognized as a state of neurologic dysfunction
in critically ill patients.3 Classically, catatonia includes psychomo-
tor disturbances such as mutism, rigidity, hyperactivity, and com-
bativeness; it is actually more common in patients with medical
and surgical illnesses than in patients with psychiatric disorders,
and the ICU is one of the most common settings for its occurrence.
Similar to delirium, there are excited and withdrawn subtypes of
catatonia; also, similar to hypoactive delirium in elderly patients,
the withdrawn subtype is typically under-recognized in ICU
patients. Risk factors for catatonia include the use of dopamine
antagonists for agitation (e.g., haloperidol), atypical antipsychotics
(e.g., risperidone, quetiapine), and antiemetics (e.g., metaclo-
pramide, promethazine). Again similar to delirium, catatonia is
associated with negative outcomes, including myocardial infarc-
tion, pneumonia, venous thrombosis and pulmonary embolism,
pressure ulceration, prolonged catheterization, infections, decon-
ditioning, contractures, and death. Scales and measuring systems
are available to grade catatonia; however, they are beyond the scope
of this chapter. Basic treatment includes withholding the offending
agents and judicious use of small doses of benzodiazepines. To
distinguish catatonia from sedation or delirium, the clinician must
look for the more subtle signs, such as active but motiveless resis-
tance to movement, mimicking, mutism, and excessive continua-
tion or cooperation to a command from the examiner.
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It is crucial for the intensivist to understand and recognize each
of the entities described so far because confusion, catatonia, and
delirium all render the patient unable to participate in his or her
care and contribute to bad outcomes. There is often an opportu-
nity early on in the progression of any type of neurologic dysfunc-
tion to recognize and treat it so that the risk of negative outcomes
can be mitigated. A daily neurologic examination is mandatory
for all patients, and more frequent examinations are indicated if
a change in neurologic function is detected. All patients, whether
intubated or not, should be assessed for alertness; level of partici-
pation with the examination; orientation to person, time, and
place; and motor strength in all four extremities. Any deficits in
this examination should prompt a more thorough and detailed
examination searching for subtle lateralizing findings such as
asymmetry of sensation or strength. The physical examination
findings should be coupled with a comprehensive review of vital
signs, laboratory values, and medication adjustments or additions
as well as a search for infectious sources. Any lateralizing signs
warrant urgent computed tomography (CT) scan of the head, but
scans performed for global (nonlateralizing) findings are often
unrevealing. CT scans done in patients with obvious metabolic,
infectious, or recent medication adjustments have an even lower
yield.
The decision to send an ICU patient on a “diagnostic journey”
should not be made lightly because there are numerous risks
associated with transporting critically ill patients. The literature is
replete with examples of significant mishaps, such as endotracheal
tube dislodgment, worsening hypoxia, or hemodynamic compro-
mise, during transport of ICU patients; a careful risk-benefit
analysis must be performed before transport. Lastly, one of the
most important aspects of the neurologic examination and assess-
ment that is overlooked is discussion with the bedside nurse.
Because of frequent bedside interactions with the patient and
charting of objective data such as CAM-ICU, Glasgow Coma
Scale, or Richmond Agitation and Sedation Scores (RASS), the
bedside nurse is a crucial source of information and can facilitate
early diagnosis of the patient’s neurologic decline.
Specific treatment for the neurologic dysfunctions discussed so
far is too broad to review, but the principles are to determine the
underlying cause of the alteration, correct the problem in cases of
encephalopathy, and withdraw the agent contributing to delirium
or confusion whenever possible. In general, benzodiazepines
should be avoided in the ICU, particularly in elderly patients,
because they contribute to the development of delirium. However,
once delirium manifests, it is typically treated with haloperidol
or other antipsychotic agents. Providers should engage family
members in reorienting patients, physical therapy should con-
tinue for mobilization and exercise, and restoration of normal
sleep-wake cycles should be attempted. Daily routines, providing
the patient with his or her eyeglasses or hearing aid or both,
daytime stimulation, and nighttime quiet all are effective non-
pharmacologic methods of preventing and treating delirium.
Analgesia, Sedation, and Neuromuscular Blockade
Pain and discomfort in ICU patients is a constant problem
because of intubation and mechanical ventilation, invasive proce-
dures and equipment, wounds, burns, and surgical incisions. In
addition, the ICU environment is often hectic, unpredictable, and
very stimulating, leading to increased anxiety, which itself is often
a manifestation of inadequately treated pain. Nurse-driven anal-
gesia and sedation protocols have grown in popularity as a means
to facilitate early extubation for ventilated ICU patients, and

although they have been successful in this regard, there is some
concern because a large percentage of these patients recall feeling
pain, anxiety, and fear when surveyed shortly after ICU discharge.
The long-term consequences of these noxious memories is
unknown, but inadequately treated pain and anxiety can lead to
unplanned extubation and removal of important devices, increased
physiologic demand from high sympathetic output states, cardiac
decompensation, and prolonged pulmonary recovery. However,
excessive use of analgesia and sedation agents is associated with
many problems, including respiratory depression, hypotension,
prolonged mechanical ventilation, increased rates of ventilator-
associated events and pneumonia, prolonged lengths of stay,
venous thrombosis, and increased costs. Accumulation of analge-
sic and sedative agents and their metabolites in adipose tissue is
especially problematic when continuous infusions are used. The
proper balance of analgesics and sedatives in ICU patients is criti-
cal if good outcomes are to be maximized and complications are
to be minimized. In recent years, numerous randomized investiga-
tions have shown improved outcomes in mechanically ventilated
patients through use of analgesia and sedation protocols.4 Typi-
cally, these protocols are nurse-driven and incorporate daily awak-
ening, which encourages spontaneous breathing trials (SBTs) and
early liberation from mechanical ventilation. Additional benefits
are shorter ICU and hospital stays, reduced pneumonia rates, less
venous thromboembolism (VTE), and presumed reductions in
overall health care costs.
Pain should be monitored and charted on an hourly basis in
the ICU using one of numerous scoring systems and scales to
measure pain; the most notable scales are the visual analog scale
and Numeric Rating Scale. Awake patients who are able to self-
report their pain level are the most easily treated; however, most
critically ill patients cannot self-report because of intubation and
other obstacles to communication, neurologic dysfunction, and
medication effects. These patients are best assessed using objective
assessments via the Critical Care Pain Observation Tool or RASS,
and their pain is treated according to these objective measures.
Opioids are first-line agents for treating pain in the ICU
because they have a rapid onset of action, are easily titrated, are
inexpensive, and generally lack an accumulation of parent drug
or active metabolites. The most commonly used opiates are mor-
phine, fentanyl, and hydromorphone. Fentanyl has a rapid onset
of action, has a short half-life, generates no active metabolites, and
creates minimal cardiovascular depression. It is highly lipophilic,
so continuous infusions are associated with accumulation in lipid
stores resulting in a prolonged effect, and large doses have been
associated with muscle rigidity syndromes. Morphine has a slower
onset of action and longer half-life and is not suitable for hemo-
dynamically unstable patients because of its potential to cause
histamine release and vasodilation, which is also the reason for
associated pruritus. Morphine is contraindicated in renal failure
because an active metabolite, morphine-6-glucuronide, can accu-
mulate and lead to undesirable long-term effects. Hydromor-
phone is a synthetic opioid that has a half-life similar to morphine
but generates no active metabolites and does not cause histamine
release. It seems to be better tolerated in some patients who experi-
ence nausea with morphine, but all opioid analgesics are associ-
ated to some extent with varying degrees of respiratory depression,
hypotension, ileus, and nausea.
Pain may be treated with nonopioid agents such as non­
steroidal anti-inflammatory drugs (NSAIDs) including intrave-
nous ketorolac or oral ibuprofen. NSAIDs, which block the
production of prostaglandins, do not cause any adverse effects on
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CHAPTER 21  Surgical Critical Care 549
hemodynamics or gut motility and work synergistically with
opioid agents to treat pain effectively with lower opioid doses.
NSAIDs have many undesirable effects, and their greatest toxici-
ties are gastrointestinal bleeding and renal failure. Care should be
exercised in elderly patients and patients with marginal creatinine
clearance because these drugs may precipitate renal failure. All
patients receiving these drugs are at risk for gastrointestinal bleed-
ing. The mechanism of renal toxicity of NSAIDs is thought to be
due to direct injury to renal tubular cells by vasoconstriction
caused by decreased vasodilatory prostaglandins.
Acetaminophen is another pain reliever that can be used in
conjunction with opioid agents or alone in elderly patients or
patients with mild to moderate pain. In 2010, the U.S. Food and
Drug Administration approved intravenous acetaminophen, and
its use in ICU patients has expanded greatly. Some research has
shown an opioid-sparing effect with intravenous acetaminophen,
but evidence that it reduces opioid-related complications such as
nausea and emesis is limited. Intravenous acetaminophen is theo-
rized to be more efficacious than oral acetaminophen as a result
of avoidance of the first-pass effect, but the cost of intravenous
acetaminophen is many times that of the oral or rectal forms. It
also requires delivery in 100 mL of fluid over 15 minutes, so
administration can be cumbersome. However, in contrast to intra-
venous NSAIDs, the side-effect profile is very favorable, particu-
larly in elderly patients.
Pain medication can be delivered in many ways, but in general
continuous infusions should be avoided whenever possible. If the
patient’s gastrointestinal tract is functioning, oral agents can be
used, but this route can be problematic in the setting of ileus,
hemodynamic instability, or bowel discontinuity. Awake patients
may be able to administer their own agents via patient-controlled
analgesia devices. These devices deliver narcotics in a more timely
fashion, provide better patient satisfaction, and diminish anxiety
because the patient has some control over his or her medication
administration; however, some studies suggest that patients using
patient-controlled analgesia receive greater total doses than patients
on intermittent or scheduled regimens. Epidural analgesia given
through a catheter in the epidural space has been shown to provide
many benefits in patients who undergo major thoracic or abdomi-
nal surgery. Patient-controlled epidural analgesia is becoming more
prevalent and incorporates many of the benefits of patient-
controlled analgesia compared with continuous epidural infusions.
A meta-analysis of randomized trials found that patients who
received epidural analgesia had lower rates of mortality, atrial
arrhythmias, deep venous thrombosis (DVT), respiratory depres-
sion, and postoperative nausea and vomiting compared with
patients who received systemic analgesics. Patients who received
epidural analgesia also had earlier return of bowel function but
more episodes of hypotension owing to sympatholytic activity.5
Similar to administration of pain and analgesic agents, nurse-
driven protocols may be applied to the management of sedation.
Much of the more recent literature regarding pain and sedation
protocols overlaps, and there is good evidence that nurses can use
such protocols to assess and manage patients’ sedation needs when
they are properly trained and educated on protocol use. Most of
these protocols aim to keep patients calm but arousable, which
corresponds to a level of −1 to −2 on the RASS. Benzodiazepines
and propofol have long been the key agents used for sedation, but
they provide no analgesia, so narcotics are still necessary. More
recently, the concept of separate sedative-hypnotic approaches has
been replaced at many institutions by an analgosedation approach
where pain is treated first with the added benefit that the analgesic
550 SECTION III  Trauma and Critical Care
medication provides some sedation effect. Treating pain and dis-
comfort first and using this concept of an analgesia-based sedation
strategy has been shown to result in less time on mechanical
ventilation, to shorten ICU length of stay, and to reduce dosing
of benzodiazepines and other hypnotics.6
Midazolam and lorazepam are the most commonly used ben-
zodiazepines for sedation in the ICU. Diazepam is a longer acting
agent that is rarely used in this setting, but it may be beneficial
in treating severe muscle spasms, especially muscle spasms associ-
ated with fractures. Benzodiazepines, which are γ-aminobutyric
acid (GABA) agonists, induce a calming mood and can potentiate
opioids, but, as mentioned previously, they may cause or worsen
delirium. Midazolam is an agent with a short half-life that has
significant amnestic properties and is often given by continuous
infusion. It is metabolized by the liver but cleared renally, and so
its active metabolites, hydroxymidazolams, can cause continued
sedation in patients with renal failure. Lorazepam is a longer
acting agent, which makes it useful for intermittent dosing. Pro-
pofol, also a GABA agonist, has rapid onset and clearance making
it ideal for frequent neurologic examinations as required in
patients with traumatic brain injury, but it can cause marked
cardiovascular suppression and hypotension and unmask hypovo-
lemia. Propofol is lipid based and can lead to hypertriglyceride-
mia, pancreatitis, and the rare propofol infusion syndrome. The
propofol infusion syndrome must be recognized early because it
has a very high mortality; patients typically present with severe
metabolic derangements, including rhabdomyolysis, acute kidney
injury (AKI), metabolic acidosis, and shock. The α2-adrenergic
agent dexmedetomidine has increased in popularity in recent
years; its major advantage is that it does not cause respiratory
depression or delirium. It is approved by the Food and Drug
Administration to facilitate weaning ventilated patients, and it has
been shown to result in reduced ventilator times compared with
benzodiazepines. There is some evidence showing decreased
opioid requirements with dexmedetomidine as well as decreased
need for benzodiazepines in patients being treated for alcohol
withdrawal, but these data are limited.
Although neuromuscular blocking agents were used exten-
sively in ICU patients needing mechanical ventilation, most
patients do not need neuromuscular blockade to tolerate mechan-
ical ventilation. Indications for neuromuscular blockade include
managing difficult-to-control intracranial pressure, ventilator dys-
synchrony, profound hypoxemia, and reduction of oxygen con-
sumption in certain patient populations. In cases of ventilator
dyssynchrony, attempts should first be made to sedate patients
adequately, and neuromuscular blockade should be viewed as an
agent of last choice. Paralytics are useful adjuncts and provide
enhanced safety for certain procedures, especially procedures
involving the airway, such as intubation, tracheostomy, bronchos-
copy, or endotracheal tube exchange. Because neuromuscular
blocking agents provide no sedation or analgesia, it is crucial that
providers ensure that paralyzed patients are well sedated and that
adequate analgesia has been provided. Paralysis without analgesia
and sedation is cruel and is associated with debilitating memories
of the event and may contribute to post-traumatic stress disorder.
There are two classes of neuromuscular blocking agents—
depolarizing and nondepolarizing agents. Depolarizing agents are
similar in structure to acetylcholine and bind to their receptors at
the motor end plates, initially causing depolarization of the muscle
while blocking repolarization. Nondepolarizing agents competi-
tively block the acetylcholine binding sites in an antagonist
fashion. Succinylcholine, the only depolarizing neuromuscular
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blocking agent, has a rapid onset of action, has a short half-life of
about 15 seconds, and is often the paralytic used for rapid-
sequence intubation and short invasive procedures but never as a
continuous infusion. Succinylcholine is degraded by plasma pseu-
docholinesterases, and prolonged action may occur in patients
with a genetic deficiency of this enzyme. Because succinylcholine
causes intracellular potassium release, patients can develop tran-
sient hyperkalemia, which can be significant in patients with AKI,
burns, crush injury, rhabdomyolysis, and spinal cord injury or
prolonged immobility.
The nondepolarizing neuromuscular blocking agents are the
steroidal agents pancuronium, vecuronium, and rocuronium in
decreasing order of half-life, and they are metabolized and cleared
by the liver and kidneys. The duration of action of pancuronium
is approximately 90 minutes, and it has a significant vagolytic effect
and so should not be used in patients with coronary artery disease
or atrial fibrillation with rapid ventricular response because it
causes marked tachycardia. Vecuronium and rocuronium are used
as infusions or for short procedures but can accumulate in patients
with renal dysfunction. Atracurium and cisatracurium cause
minimal cardiovascular effects and have an almost immediate onset
of action. Cisatracurium causes less histamine release than atracu-
rium, and both agents are eliminated by plasma ester hydrolysis,
known as Hoffmann elimination. Atracurium and cisatracurium
are preferred in patients with renal or hepatic failure.
Patients receiving paralytic agents should be monitored for
depth of neuromuscular blockade with train-of-four testing, and
the goal should be to maintain a patient with one to two twitches.
If patients are paralyzed too deeply, this may indicate a drug
accumulation, which can be associated with increased risk of
complications such as critical illness myopathy and critical illness
polyneuropathy. Critical illness myopathy and critical illness poly-
neuropathy are now more recognized entities, and their occur-
rence should be minimized by stopping neuromuscular blocking
agents as early as possible or by observing occasional periods off
neuromuscular blockade, or “paralysis holidays.” Corticosteroid
use, prolonged mechanical ventilation, sepsis, and aminoglycoside
use all have been identified as contributors to development of
critical illness myopathy and critical illness polyneuropathy; both
conditions dramatically extend a patient’s recovery and are associ-
ated with long-term disabilities.
Alcohol Withdrawal and Opioid Dependence
An increasing number of patients who require critical care in the
perioperative period have a history of alcohol or opioid abuse or
opioid dependency. A history of alcohol abuse is present in 40%
of admitted patients, and a significant number of these patients
subsequently develop alcohol withdrawal syndrome. Alcohol
withdrawal syndrome causes autonomic instability and increased
metabolic demand resulting from tachycardia, hypertension,
tremors, and agitation. Patients progressing to delirium tremens
or alcohol-related seizures have a significantly increased risk of
dying. The goal in caring for patients with a history of alcohol
abuse should be to treat them early to prevent symptoms of
withdrawal. Benzodiazepines are the mainstay for prevention
and treatment of alcohol withdrawal syndrome, and they have
been shown to reduce seizure risk markedly in these patients
compared with neuroleptics such as haloperidol. Benzodiazepines
calm patients and control the autonomic instability associated
with alcohol withdrawal syndrome through GABAergic effects.
The main drawback of benzodiazepines is their tendency to
cause respiratory and cardiovascular depression. Propofol and

barbiturates are also GABAergic, but these agents cause more
severe respiratory and cardiovascular suppression, which greatly
limits their use in the treatment of alcohol withdrawal syndrome.
A few small studies examined dexmedetomidine, an α2-adrenergic
agonist, as an adjunct for treating alcohol withdrawal syndrome,
and although there have been some encouraging results, it lacks
GABA activity and is ineffective at preventing seizures. This agent
is given as an infusion and leads to minimal respiratory depression
but can cause bradycardia and hypotension. Dexmedetomidine is
not approved for treating alcohol withdrawal syndrome; because
this is considered an off-label use, it is associated with much
higher medication costs. However, dexmedetomidine is effective
as an adjunct to treat alcohol withdrawal syndrome effectively
with much smaller amounts of benzodiazepines.
Alcohol withdrawal syndrome encompasses many subjective
findings, and objective scoring systems such as the Clinical Insti-
tute Withdrawal Assessment (CIWA) are helpful in guiding the
treatment of alcohol withdrawal syndrome. Use of CIWA results
in reduced benzodiazepine dosing compared with fixed dosing.
Although CIWA is an effective tool for managing alcohol with-
drawal syndrome, its role in the ICU must be viewed with caution
because the differential diagnosis of agitation and restlessness is
broad and includes life-threatening entities such as hypoxia,
sepsis, shock, and stroke. Agents such as clonidine and beta block-
ers blunt autonomic hyperactivity in alcohol withdrawal syn-
drome, whereas atypical antipsychotics such as olanzapine and
quetiapine may control agitation but must be combined with
benzodiazepines because they often lower the seizure threshold.
Opioid dependency is a burgeoning problem in the United
States, and an increasing number of patients with opioid depen-
dency present to surgical ICUs. Opioid dependency and treat-
ment of this condition with methadone taper or mixed receptor
agonists such as buprenorphine add layers of complexity to treat-
ing acute pain. Buprenorphine is commonly used to taper patients
from opioid addiction or to treat chronic pain, and ICU providers
should be familiar with its mechanism and use, as it is anticipated
that the number of patients receiving this agent will increase.
There are very few protocols and little randomized evidence to
guide the administration of analgesics in this patient population,
but key themes have emerged. Patients with opioid dependency
who have undergone major surgery or have sustained significant
traumatic injury require narcotic quantities in excess of their
baseline dosing. If these patients are able to take oral medications,
starting them on their baseline doses of buprenorphine or metha-
done will result in inadequate pain control, and they will require
additional shorter acting agents for optimal pain control. Mixed
agents such as buprenorphine limit the effectiveness of other
opioids with the resultant need for escalating doses of opioids, so
providers need to be on guard for respiratory depression, ileus,
and other narcotic-related complications. It may be advisable to
suspend use of this agent in the acute setting and reinitiate it after
the patient’s acute pain has lessened. Patients who are dependent
on narcotics should have their pain addressed via a multifaceted
approach, including the use of nonsteroidal agents and epidural
and regional blocks as well as the added input of pain manage-
ment specialists, clinical pharmacists, and social workers.
CARDIOVASCULAR SYSTEM
Comorbidities, Events, and Risk Mitigation
Elderly adults (≥65 years old) comprise the fastest growing
segment of the U.S. population; by 2030, this subgroup will
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CHAPTER 21  Surgical Critical Care 551
comprise almost 20% of the population. This age group tends to
have more complex medical comorbidities, but if these chronic
health conditions are managed effectively, older adults are able to
live longer and more productive lives. Although previously elderly
patients were denied open surgical care because of concerns of
excess mortality, newer treatment options such as stent placement
and endovascular surgery and minimally invasive techniques have
allowed more elderly patients to have their health conditions
addressed surgically. As a result, more elderly patients with
complex cardiovascular issues undergo noncardiac surgery. In the
past, these types of patients were often admitted to the ICU or
surgical ward preoperatively to optimize their hemodynamic and
fluid volume status, but a lack of evidence to support this in terms
of better outcomes coupled with prohibitive costs of such an
approach rendered this an unsustainable approach. At the present
time, these patients are often admitted to the ICU with little or
no advance warning, and the opportunity for approaches to mini-
mize cardiovascular risk is extremely limited.
The most common perioperative events are arrhythmias, myo-
cardial infarction, and nonfatal and fatal cardiac arrest. These
events typically occur in the first 3 days after surgery and are likely
due to the convergence of the patient’s high sympathetic output
and myocardial metabolic demand in the midst of the greatest
intravascular volume shifts. Patient complaints of cardiac ischemia
during this time are frequently lost in the background of postop-
erative complaints of pain and nausea, and intubated patients are
extremely limited in their ability to relay cardiac distress. Cardiac
events in the noncardiac surgery perioperative period are associ-
ated with an in-hospital mortality of 15% to 25% and increased
risk of another myocardial infarction or cardiac death extending
6 months into the postoperative period. In a large review of
patients at a tertiary care center, nonfatal cardiac arrest was associ-
ated with in-hospital mortality of 65%, and increased risk of
cardiac death extended 5 years after the event. Historically, major
cardiac events occur in 1% to 2% of patients older than age 50
undergoing elective noncardiac surgery; however, most of these
retrospective reviews were conducted in the past, and it is likely
that the present rate is much higher given the aging population.
The rate of adverse cardiac events is even higher in emergency
operations.
The combination of events in the perioperative period includ-
ing intubation and extubation, bleeding and anemia, and immune-
inflammatory activation is analogous to one long cardiac stress
test. On ICU admission, the patient’s cardiovascular comorbidi-
ties, such as coronary stents or bypasses, peripheral vascular
disease, arrhythmias, valvular abnormalities (e.g., aortic stenosis),
hypertension, and ischemic stroke, should be thoroughly explored
so that risks of further cardiac events might be mitigated. The
patient’s medication history should be considered, and a plan
should be made for continuing or reintroducing critical agents
during the postoperative period, particularly if the patient will be
NPO. Generally, anticoagulants and antiplatelet agents are held
during the perioperative period because of concerns for bleeding.
Most antihypertensives and diuretics can be held until the patient
resumes oral intake and their volume status and hemodynamic
abnormalities have normalized. Beta blockers and clonidine
should not be abruptly discontinued because significant rebound
effects may occur with disastrous consequences. The decision to
start or stop antiplatelet agents in patients with coronary stents is
a highly nuanced decision; although it is too complex to be dis-
cussed here in depth, the type of stent and duration it has been
indwelling are critical components of this decision. The highest
552 SECTION III  Trauma and Critical Care
rates of stent thrombosis occur when antiplatelet agents are dis-
continued within 6 months of stent placement or with drug-
eluting stents.
Surgery and traumatic injury cause immune-inflammatory
activation marked by endothelial injury, capillary leak, hyperco-
agulability, and hormonal alterations that dramatically increase
myocardial oxygen demand and place the coronary arteries and
plaques under sheer stress. This is fertile ground for myocardial
oxygen demand and supply imbalances leading to non–ST-
segment elevation myocardial infarction (NSTEMI) and plaque
rupture and thrombosis (ST-segment elevation myocardial infarc-
tion [STEMI]). Patients who have preexisting coronary artery
stenosis are at greatest risk for perioperative coronary events. In
these patients, beta blockers and 3-hydroxy-3-methylglutaryl-
coenzyme A (HMG-CoA) reductase inhibitors are indicated and
can reduce the risk of cardiac events in this stressful perioperative
period. Beta blockers decrease heart rate, sympathetic output, and
myocardial contraction leading to reduced metabolic and oxygen
demand of the body and the myocardium, and there is some
evidence to suggest that they reduce levels of inflammatory cyto-
kines and may have an anti-inflammatory effect. Several investiga-
tions of beta blockers in noncardiac surgery showed improved
outcomes from a cardiac viewpoint, but this is controversial
because other studies showed that these benefits are offset by
increased complications such as stroke. A randomized investiga-
tion exploring the benefit of beta blockers and HMG-CoA reduc-
tase inhibitors in patients undergoing noncardiac surgery showed
that this group had a lower rate of myocardial infarction and
cardiac death.7 There was a trend toward improved outcomes in
patients given fluvastatin versus the control group, but these
results did not reach statistical significance. Many older trials
showed a protective benefit of perioperative beta blockers, and
evidence is mounting that HMG-CoA reductase inhibitors
(statins) have a favorable effect on outcomes after trauma, sepsis,
and other inflammatory conditions because of their global anti-
inflammatory effects. Statins were shown to lower the risk of
postoperative atrial fibrillation risk, an important and costly
cardiac event that results in increased length of stay and health
care expenses.8
The role of beta blockers in the ICU for patients who have
not been on them previously is controversial. The only Class I
recommendation the American Heart Association and American
College of Cardiology have been able to make is that beta block-
ers should be resumed in patients who have been on them as
early as possible because failure to do so results in increased
mortality. The Cardiac Risk Index (CRI) system was designed to
guide clinicians through the clinical decision process regarding
beta blocker use in the perioperative period. The CRI is com-
posed of six components: high-risk surgery, ischemic coronary
disease, congestive heart failure, diabetes, cerebrovascular disease,
and renal insufficiency (Box 21-1). Patients with two or more
of these CRI components should be started on beta blocker
therapy because 30-day mortality has been shown to be reduced
in these patients with this approach.9 The use and benefit of
beta blockers in the perioperative period, particularly in the
ICU, remain controversial, and the controversy is likely to persist
until there are more randomized investigations. Patients with
cardiac risk factors who are undergoing emergency surgery often
have contraindications to beta blockers, such as shock or hypo-
tension, but it may be prudent to use small doses of an intrave-
nous agent such as metoprolol as soon as feasible in the
postoperative period.
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BOX 21-1  Cardiac Risk Factor Indicators
for Beta Blocker Therapy
Consider beta blocker therapy if two or more of the following are present:
High-risk surgery (chest, abdomen, major vascular)
History of ischemic coronary disease (myocardial infarction, nitrate therapy,
positive exercise stress test, Q waves)
Congestive heart failure (pulmonary congestion, S3 gallop, bilateral rales)
Cerebrovascular disease (prior transient ischemic attack or stroke)
Diabetes
Renal insufficiency (baseline creatinine >2 mg/dL)
TABLE 21-1  Benefits of Early
Postoperative Beta Blockers and 3-Hydroxy-
3-Methylglutaryl-Coenzyme A Inhibitors
BETA BLOCKERS HMG-CoA INHIBITORS
Decrease global and cardiac oxygen Stabilize coronary plaques
demand
Reduce shear stress on coronary plaque Reduce incidence of atrial
fibrillation
Anti-inflammatory Anti-inflammatory
HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme A.
Dysfunction: Ischemic Disease, Non–ST-Segment
Elevation Myocardial Infarction, and Arrhythmias
Cardiac risk factor assessment in the preoperative period is con-
troversial, but there are certain straightforward approaches that
should be taken with these patients when they arrive in the surgi-
cal ICU. If the patient is to undergo acute emergency surgery, the
cardiac risk assessment is limited to vital signs, estimations of
volume status, and electrocardiogram (ECG). The ECG should
be examined for ST-segment elevations or depressions, T-wave
inversions, P–R interval, and rhythm. Awake patients should be
queried about chest pain or pressure, jaw pain, and nausea, while
recognizing that some of these complaints may be attributable to
a laparotomy. ST-segment changes or ischemic symptoms should
trigger assessment of troponin biomarkers looking for confirma-
tion of myocardial infarction. A perioperative myocardial infarc-
tion has significant prognostic value in predicting 30-day
postoperative mortality and mandates treatment to minimize
further myocardial damage. A newer entity, myocardial injury
after noncardiac surgery (MINS), likely represents a new under-
standing of NSTEMI.10 MINS results in injury to the myocar-
dium from ischemia that does not result in necrosis and typically
occurs in the first 30 days postoperatively. Elevation of troponin,
a biomarker of myocardial injury, is a predictor of postoperative
mortality, but it is unclear if this is a cause-and-effect relationship
or a marker of global illness because troponin may be elevated in
nonischemic entities such as sepsis, pulmonary embolism, and
cardioversion. Patients with MINS benefit from many of the same
treatments that benefit patients with actual myocardial infarction—
beta blockers, aspirin, and statins (Table 21-1). Patients who have
ST-segment elevations or depressions (i.e., STEMI) that are per-
sistent and accompanied by symptoms may benefit from attempts
at revascularization by percutaneous techniques or by coronary
artery bypass grafting. Percutaneous techniques usually mandate
powerful platelet inhibitors, and this may not be feasible or safe

in the immediate postoperative period. Alternatively, heparin
infusion is typically started for STEMI to arrest propagation of
coronary clots.
Dysrhythmias are common in the ICU because of increased
levels of catecholamines and other circulating inflammatory medi-
ators, but cardiac arrest is rare. The initial goal in the management
of cardiac arrest is to deliver quality cardiopulmonary resuscitation
(CPR) with a rate of 100 chest compressions per minute to main-
tain cerebral perfusion. The patient should be promptly attached
to a monitor and the rhythm analyzed. Pulseless electrical activity
and asystole are not amenable to cardioversion, but cardioversion
is indicated in ventricular fibrillation and pulseless ventricular
tachycardia. A definitive airway should be obtained, and 40 U of
vasopressin can be given one time while CPR is underway; alter-
natively, 1 mg of epinephrine repeated every 3 to 5 minutes may
be given. Throughout the resuscitative efforts, a search for the
underlying cause (e.g., hemorrhage, hyperkalemia, hypovolemia,
tension pneumothorax) of the arrest should be sought and treated
if found. CPR should be stopped every 2 minutes to assess the
patient’s rhythm and pulse, and if a pulse has returned, more
standard ICU resuscitation plans should continue, and the antiar-
rhythmic amiodarone should be given. Amiodarone is also indi-
cated for all unstable tachyarrhythmias including ventricular
tachycardia with and without a pulse. Calcium chloride is used
in an attempt to stabilize the myocardium, especially if a hyper-
kalemic arrest is suspected, whereas magnesium sulfate is indi-
cated in cases of torsades de pointes. Advanced cardiac life support
guidelines stress the importance of maintaining adequate CPR
throughout resuscitation efforts with as few interruptions for
therapeutic interventions as possible.
Bradycardia, defined as a heart rate less than 60 beats/min, is
evaluated first with an ECG, but if the patient has symptoms such
as shortness of breath, chest pain, or dizziness or is hypotensive,
atropine 0.5 or 1 mg should be given. Other β2 agonists (e.g.,
epinephrine or dopamine) may be required to increase the heart
rate and blood pressure while a workup for the cause of the bra-
dycardia is sought. If these approaches fail, percutaneous pacing
may be needed, but this modality is ineffective for long-term use,
and transvenous methods may be required. Bradycardia may be a
sign of profound myocardial ischemia, especially in patients with
advanced coronary artery disease, so efforts to increase myocardial
oxygen delivery should be started. Patients with wide QRS com-
plexes and tachycardia should be given amiodarone and undergo
cardioversion because this dysrhythmia is most likely ventricular
in origin; however, the ECG should be evaluated to rule out aber-
rant conduction as a cause of the wide QRS complexes. If the
QRS complex is narrow, and the patient is hemodynamically
unstable from tachycardia, synchronized cardioversion is war-
ranted. Sinus tachycardia is the most common tachycardia in the
ICU. It is often an appropriate response to fever, pain, sympa-
thetic stimulation, bleeding, hypotension, sepsis, or inflamma-
tion, and therapies should be directed at the underlying cause. If
the width of the QRS complex is unclear, intravenous adenosine
(6 mg, repeated once) may be administered and typically facili-
tates identification of the underlying rhythm. If the rate does
not slow, it should be treated as a wide-complex tachycardia; if
it slows, it should be treated as a narrow-complex tachycardia.
The differential diagnosis includes supraventricular tachycardias,
atrial fibrillation, atrial flutter, multifocal atrial tachycardia,
and uncertain tachycardias, all of which require different treat-
ments. A detailed discussion of the management of these rhythm
abnormalities is beyond the scope of this chapter, and expert
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CHAPTER 21  Surgical Critical Care 553
consultation may be necessary. Atrial fibrillation is the most
common sustained dysrhythmia in the ICU and its occurrence is
an indicator of the stresses and overall status of a patient. Etiolo-
gies of atrial fibrillation abound and include any condition associ-
ated with catecholamine release, increased sympathetic tone, or
generalized inflammation. New-onset postoperative atrial fibrilla-
tion develops in 7% to 8% of patients undergoing noncardiac
surgery and is associated with increased mortality and length of
stay and other cardiac events such as stroke and myocardial infarc-
tion. Greater than 80% of patients with new-onset atrial fibrilla-
tion are able to be discharged in sinus rhythm without the need
for anticoagulation or advanced antiarrhythmic agents. The most
successful initial pharmacologic approach is to attempt rate
control with beta blockers or calcium channel blockers to block
the atrioventricular node and promote conversion back to sinus
rhythm. Beta blockers have been shown to result in higher rates
of conversion to sinus rhythm than calcium channel blockers at
2 and 12 hours after onset of atrial fibrillation. Amiodarone is also
an effective therapy in atrial fibrillation and is preferred in patients
with systolic heart failure. Patients who fail to convert to sinus
rhythm within 48 hours of onset of atrial fibrillation typically
require therapeutic anticoagulation, which is a challenging deci-
sion in the newly postoperative patient.
Shock and Hemodynamic Monitoring
The definition of shock has evolved significantly from the descrip-
tions more than 100 years ago of a “peculiar effect on the animal
system produced by violent injuries” to our current understanding
that it is a condition in which tissue perfusion is inadequate to
meet oxygen needs. This simple definition overcomes some of
the disagreement about whether a patient is in shock resulting
from the multitude of available definitions and avoids the pitfalls
associated with embracing absolute values. There is no set blood
pressure that defines the shock state, and patients can be hypo-
tensive or hypertensive and be in shock. The etiologies of shock
are numerous and include hypovolemia and hemorrhage, sepsis,
cardiac pump failure, neurologic injury, and obstructive entities,
but regardless of the cause, all shock states should begin with
restoration of an adequate circulating volume. Even cardiac pump
failure initially responds to crystalloid administration, but the
challenge in resuscitation from shock lies in gauging when the
ideal amount of fluid has been given. The process of administering
intravenous crystalloids, blood, and blood products to restore
an effective circulating volume is referred to as resuscitation and
after resuscitation; vasopressor and inotropic agents are given
based on data obtained from invasive means of hemodynamic
monitoring.
Hypovolemic shock is the most common form of shock and
results from loss of plasma volume as seen in gastrointestinal losses
from diarrhea, fistulas, and vomiting; inadequate intake from
short gut syndrome, malnutrition, and dehydration; or conditions
such as epidermolysis and burns. The most dramatic form of
hypovolemic shock is hemorrhagic shock, which typically has a
more sudden onset and is due to surgery, trauma, or losses from
gastrointestinal sources. Patients in hemorrhagic shock should
initially be given blood and blood products instead of crystalloid.
Patients in hypovolemic or hemorrhagic shock initially compen-
sate for loss of intravascular volume with increased sympathetic
output, which increases systemic vascular resistance and heart
rate. Initially, such compensation may maintain blood pressure,
but as the circulating volume decreases and the systemic vascular
resistance reaches its maximum, end organ perfusion becomes
554 SECTION III  Trauma and Critical Care
inadequate, and the patient enters a shock state. Inadequate end
organ perfusion is the basis for the physical findings of shock,
such as tachycardia, dry mucous membranes, mottled skin,
decreased mental status, and oliguria.
Cardiogenic shock is due to significantly decreased cardiac
output as a result of diminished myocardial contractility or pro-
found bradycardia. In the ICU, the most common etiologies are
acute myocardial infarction, massive pulmonary embolism, or
advanced heart block. Patients in cardiogenic shock develop
increased ventricular filling pressures and significantly decreased
cardiac output, and, similar to patients with hypovolemic shock,
they compensate with increased systemic vascular resistance
setting the stage for a cycle of cardiac decompensation, volume
overload, and decreased coronary perfusion causing further myo-
cardial injury. The key aspect of treating cardiogenic shock is
inotropic and chronotropic support and for severe cases advanced
modalities such as intra-aortic balloon pumps or ventricular assist
devices. The physical findings of cardiogenic shock that help dif-
ferentiate it from hypovolemic shock are the presence of pulmo-
nary congestion, jugular venous distention, and other signs of
marked volume overload.
Septic shock is often placed into a broader category known as
distributive shock and is a result of loss of vasomotor tone and
decreased systemic vascular resistance along with hypovolemia.
Neurogenic shock is a form of distributive shock caused by inter-
ruption of the sympathetic nervous system, typically secondary to
trauma, with a striking reduction of systemic vascular resistance.
Septic shock is a far more common entity in the ICU and repre-
sents a host of physiologic derangements resulting from whole
body immune-inflammatory activation. Bacterial endotoxin,
cytokines, and nitric oxide result in loss of capillary gap junction
and endothelial integrity, which promotes fluid loss from the
intravascular space—hence septic shock always involves a degree
of hypovolemia. Compounding the hypovolemia is a disruption
in vasomotor tone decreasing the systemic vascular resistance and
myocardial suppression, which diminishes the cardiac output.
Although many clinicians associate sepsis with a hyperdynamic
cardiac response, most patients subsequently develop ventricular
systolic and diastolic dysfunction from mediators such as tumor
necrosis factor and interleukin-1; however, most patients recover
pump function when sepsis resolves.
Following the diagnosis of a shock state, it is desirable to obtain
some type of hemodynamic monitoring keeping in mind that
there is no single vital sign, physiologic variable, laboratory
marker, or measurement that can tell a provider what is occurring
at the tissue or organ level. An arterial catheter should be placed
in the radial artery using full barrier sterile precautions because
the risk of infection with arterial catheters is similar to the risk
with central venous catheters. Femoral placement is the next
preferred location for arterial cannulation, and this may be facili-
tated through the use of bedside ultrasound. The most reliable
data obtained from an arterial line is the mean arterial pressure
(MAP) because the MAP is not affected by systems issues such as
stiffness and resistance of the catheter or the measuring system,
which can result in overdamping or underdamping of the pressure
tracing.
Laboratory markers may be helpful in monitoring resuscitation
from the shock state and offer additional data to supplement
invasive parameters. Lactic acid, arterial blood gases (ABG), and
base deficit are global indicators of end organ perfusion and can
help guide responses to therapy because early normalization of
elevated lactic acid levels has been linked to increased survival in
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injured and critically ill patients. These laboratory measurements
are static in nature, and although following their trends can yield
valuable data, the quest to obtain minute-to-minute guidance
inspired cardiologists in the 1960s to seek a more advanced means
of monitoring. The landmark article by Swan and Ganz describing
the pulmonary artery catheter (PAC) in 1970 started an era of
more invasive and complex hemodynamic monitoring that has
continued to the present day. There are several invasive means for
guiding fluid resuscitation and gauging intravascular volume
status; however, no one device or modality has emerged superior,
and at best almost all claim equivalency to the PAC.
Central venous catheters have dual utility in that they provide
intravenous access while measuring central venous pressure
(CVP). CVP is a surrogate for end-diastolic pressure and volume
in the right ventricle, but this is dependent on right ventricular
compliance, cardiac valvular function, intrathoracic pressure, and
several other variables. CVP is an even poorer and more unreliable
marker for left-sided filling pressures because any pulmonary or
valvular abnormalities significantly degrade the assumption that
CVP correlates with the end-diastolic filling pressure of the left
ventricle. Measuring central venous oxygen saturation (ScvO2) in
addition to CVP yields better detection of tissue and organ hypo-
perfusion and allows clinicians to estimate global oxygen param-
eters better. These catheters, coined “sepsis catheters,” have been
associated with improved outcomes in patients with sepsis, injury,
and certain high-risk surgical procedures.
Central venous catheters are associated with two types of mor-
bidity: immediate technical complications and long-term compli-
cations. Immediate complications are usually related to procedural
mishaps and include pneumothorax, hemothorax, arteriovenous
fistula, air embolus, dysrhythmia, and death. Pneumothorax
occurs in about 1% to 5% of cases of subclavian vein cannulation,
whereas arterial injury is more common when the internal jugular
or femoral approach is used, but this risk has been significantly
reduced with the advent of real-time bedside ultrasound. Long-
term complications of central catheters are venous thrombosis and
infection. Subclavian catheters are the least likely to become
infected, and femoral catheters have the highest thrombosis and
infectious risk as a result of their contaminated local environment.
The femoral access site should be used as a last resort or in emer-
gency situations when other venous access cannot be established.
Patients admitted to the ICU from the emergency department or
the field should have their venous access changed because breaks
in sterile technique tend to occur when venous access is placed in
a patient in extremis. Patients undergoing tracheostomy should
have their internal jugular central access converted to the subcla-
vian site because tracheal secretions have been shown to increase
line infection rates significantly.
Although use of the PAC has declined significantly over the
last 2 decades, it is still a valuable tool and should not be over-
looked in critically ill patients. The PAC yields direct measure-
ments of CVP, right atrial pressure, pulmonary arterial pressure,
pulmonary artery wedge pressure, and mixed venous oxygen
saturation (SvO2) and calculations of cardiac output, oxygen
consumption, and other parameters such as systemic vascular
resistance and left ventricular stroke work. In contrast to the older
devices that relied on one-time injections of chilled saline, newer
PACs allow for continuous cardiac output. In more than 40 years,
very few studies have clearly shown a mortality benefit when PACs
are used in the management of critically ill patients; some data
indicate that PACs may contribute to worse outcomes. However,
in the right hands, the PAC is extremely useful in guiding fluid

resuscitation and vasopressor and inotropic support. Some litera-
ture suggests that the ability of critical care providers to interpret
the data yielded by the PAC accurately may be the true issue
and not the catheters—that is, there is a knowledge gap of clini-
cians interpreting PAC data. The newest PACs monitor right
ventricular end-diastolic pressure and calculate a right ventricular
ejection fraction on a continuous basis, which may circumvent
some of the problems presented by pulmonary and valvular
abnormalities.
As stated previously, there is no single vital sign, physiologic
variable, laboratory marker, or measurement that can tell a pro-
vider what is occurring at the tissue or organ level, but the trends
and responses to management interventions are significant. The
more derivations and calculations involved in modifying PAC
data, the more likely that data might be skewed by unseen vari-
ables. Thus, systemic vascular resistance, which is expressed as
dyne • sec/cm5 is more contrived and less helpful to managing
ICU patients than SvO2, which is directly measured and is
expressed as a percent (%). To some degree, PACs have been
slighted as a hemodynamic monitoring tool because study designs
evaluating their use have often been flawed, especially in terms of
patient selection and the rationale behind PAC data guiding inter-
ventions. In a large National Trauma Data Bank review by Friese
and colleagues,11 outcomes, including mortality, were shown to
be improved in severely injured elderly patients who received a
PAC as part of their ICU management.
Complications associated with PAC use should not be under-
estimated. In addition to those attributable to central venous
access, complications specific to PAC use such as heart block,
ventricular tachycardia, valvular damage, pulmonary infarction,
and the uniformly fatal event of pulmonary artery rupture have
been described. Left bundle branch block is a relatively strong
contraindication to PAC placement because complete heart block
may result. It is crucial that all clinicians caring for patients with
a PAC understand the waveforms, interpretations, and pitfalls
associated with their use, but a detailed review of all the data is
beyond the scope of this chapter.
There has been a focus more recently on bedside echocardiog-
raphy performed by trained intensivists as a rapid, noninvasive,
repeatable way to assess intravascular volume status and cardiac
performance in critically ill surgical patients. Echocardiography is
finally being recognized as a valuable tool in surgical ICU patients
after being used for decades to assess high-risk surgical patients in
the preoperative and intraoperative settings. Echocardiography
can rapidly assess cardiac function and hemodynamics by looking
at right ventricular and left ventricular systolic and diastolic func-
tion, valvular function, cardiac wall motion, and volume status
by assessing inferior vena cava changes in response to fluid chal-
lenge. Additional information, such as the presence of pericardial
fluid or collapse of the right ventricle signifying cardiac tampon-
ade, are among the many other uses of this modality. Evidence
suggests that echocardiography may be more accurate in deter-
mining left ventricular volume status than a PAC, but further
study is necessary. As is the case with any new technology, there
is skepticism regarding the true benefit of echocardiography
because there is a paucity of randomized evidence showing that
it leads to better outcomes. Over time and as evidence mounts,
it is likely that echocardiography in surgical ICUs will become the
norm, and the PAC may become a thing of the past.
Many less invasive hemodynamic monitoring tools, such as
cardiac contour output analysis, lithium dilution, and peripheral
catheter transpulmonary thermodilution, have emerged, but there
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CHAPTER 21  Surgical Critical Care 555
are no significant data demonstrating superior outcomes with
these new technologies compared with the PAC. Although it is
hoped that these modalities will afford the ICU clinician addi-
tional, less invasive options for hemodynamic monitoring, many
of these modalities require specialized proprietary equipment that
render them not cost-effective. Techniques such as thenar emi-
nence and gastric mucosal monitoring, near-infrared spectros-
copy, and other technologies extrapolate regional tissue bed data
into global indices of oxygen delivery and consumption with
varying degrees of success. As technology progresses, miniaturiza-
tion advances, and artificial intelligence emerges, it is likely that
revolutionary improvements in critical care will continue to
unfold, but at the present time, echocardiography, PACs, and a
dedicated and thoughtful clinician still represent the most effec-
tive options for optimizing hemodynamics and improving out-
comes for surgical ICU patients.
Resuscitation
Most patients in shock, regardless of the cause, benefit from a trial
of fluid resuscitation given in the form of a crystalloid bolus.
Interpretation of the response to this initial bolus can offer insight
into the cause of the patient’s shock and should be used to guide
the fluid resuscitation strategy. A patient in hypovolemic shock
should begin to show improvements in mentation, skin turgor
and color, heart rate, blood pressure, and urine output after one
or two boluses of crystalloid fluid, but it can be confusing because
similar initial improvements are seen in cases of septic and hemor-
rhagic shock. Although the initial response to fluid is typically
favorable in cardiogenic shock, this positive response is quickly
lost as filling pressures rise even higher and cardiac output falls
further on the Starling curve. Hemorrhagic shock responds favor-
ably to fluid as well; although there are some improvements in
hemodynamic parameters, markers of oxygen delivery worsen.
Despite a growing body of literature confirming the benefits of
restrictive transfusion strategies, none of these benefits apply to
actively bleeding patients, and blood and blood products should
remain the first-line therapy in resuscitating bleeding patients.
Recognizing when volume resuscitation is adequate is one of
the most complex and challenging decisions in critical care, and
this has remained controversial for decades. Over this time, a host
of parameters, known as end points of resuscitation, have been
touted as the ideal marker of volume resuscitation, and many
patients have paid the price for clinicians wedded to one number
instead of considering all the available data. The days of supra-
normal resuscitation originally promulgated by Shoemaker are
long behind us, having been disproven by subsequent trials. For
example, resuscitating burn patients with lower rates of fluid,
as denoted by the Brooke formula, has decreased the rate of
abdominal compartment syndrome (ACS) compared with the
Parkland formula, which mandates more aggressive resuscitation,
without incurring more renal failure.12 Hyper-resuscitation, intra-
abdominal hemorrhage, and catastrophes can lead to the develop-
ment of ACS, which occurs when blood, ascetic edema fluid, or
tissue swelling drives intra-abdominal pressure up as the limit of
abdominal fascial compliance is exceeded. ACS progresses from
intra-abdominal hypertension to the full-blown syndrome, which
is marked by multisystem organ failure (MSOF). Treatment of
this condition includes neuromuscular blockade and drainage of
ascites as temporizing maneuvers, but decompressive laparotomy
and temporary abdominal closure is usually required. Inadequate
resuscitation leads to persistence of end organ ischemia and the
shock state, which causes irreparable harm to the patient. The
556 SECTION III  Trauma and Critical Care
Fluid and Catheter Treatment Trial (FACTT) in 2006 showed
that surgical patients with lung injury and acute respiratory dis-
tress syndrome (ARDS) managed with a conservative fluid strat-
egy guided by lower CVP and pulmonary capillary wedge pressure
had significantly fewer days of mechanical ventilation compared
with patients managed with liberal fluid practices without any
increase in mortality or renal failure.13
Akin to the controversy surrounding how much fluid to give,
debates centered on which fluid to give have raged on for more
than a century. Lactated Ringer solution and normal saline are
the two crystalloid fluids most commonly used, and each has its
own subtle advantages and disadvantages. In large volumes,
normal saline can cause a hyperchloremic metabolic acidosis,
whereas lactated Ringer solution has been implicated as a cause
of metabolic alkalosis when used for prolonged periods. Because
lactate exists as a racemic mixture in solution, and the D-isomer
of lactate is a known neurotoxin, there are some concerns that
large volumes of lactated Ringer solution may result in encepha-
lopathy; however, clear-cut proof of this concern is lacking.
Because only one third of each liter of crystalloid remains in the
intravascular space, whereas the rest occupies the interstitial or
intracellular spaces, clinicians have sought colloids as resuscitative
fluids under the premise that they would be more inclined to stay
intravascularly. This notion fails to recognize that shock is associ-
ated with capillary leak and expansion of the intercellular com-
partment and that the breakdown of tight junctions results in
pores far larger than the size of most colloids. Albumin, which
can be given as a human derived colloid, normally provides 80%
of intravascular oncotic pressure, and it has been used extensively
as a resuscitative fluid. The debate about the ideal resuscitative
fluid, crystalloid versus colloids, continues at the present time,
and colloids have swung in and out of favor repeatedly.
The Saline Albumin Fluid Evaluation (SAFE) trial showed no
significant differences in mortality, ICU length of stay, need for
renal replacement therapy (RRT), or organ failure when patients
were resuscitated with 4% albumin compared with normal saline,
although albumin is much more expensive.14 The SAFE trial
looked at a very heterogeneous group of patients, whereas subse-
quent studies focused more on the role of albumin in resuscitating
patients with severe sepsis or septic shock. Although albumin
administration can reduce overall fluid requirements, there has
been no short-term or long-term benefit compared with crystal-
loids alone. Synthetic colloids such as hydroxyethyl starch initially
generated a lot of enthusiasm as a resuscitative fluid, but this has
waned. Because these agents cause renal failure in septic patients
and contribute to bleeding via platelet dysfunction, they have
largely been abandoned as a resuscitative fluid. An area of avid
investigation is centered on hemoglobin-based oxygen carriers,
particularly for military and field usage, but after some initially
encouraging results, these agents have not lived up to that
enthusiasm.
Hemodynamic Support
After the initiation of fluid resuscitation, subsequent therapies
designed to improve hemodynamics are largely pharmacologic
and involve the use of vasopressor or inotropic agents. Vasopres-
sors augment MAP and systemic perfusion by a direct constric-
tive action on blood vessels, but this does not lead to improved
perfusion at the tissue level. Vasopressors may be harmful to
tissue perfusion and may lead to a false sense of security because
an elevated MAP generally implies good tissue perfusion. Vaso-
pressor therapy should be guided by MAP and other physiologic
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parameters, such as mental status, urine output, lactate clearance,
and resolution of acidosis. Ideally, clinicians should seek to
actively wean patients off vasopressors, but this should not be
done at the expense of excessive fluid administration. In cases of
septic or distributive shock in which increased intravascular
capacitance plays a significant role in the shock state, the goals
should be first to restore an effective circulating volume and then
to add vasopressors to augment alpha-adrenergic mediated vaso-
motor tone.
The terms catecholamines and sympathomimetics are synony-
mous and denote endogenous and synthetically derived agents
that act directly on alpha- and beta-adrenergic receptors enhanc-
ing the sympathetic response of the individual. Phenylephrine is
a selective α1 agonist that works on receptors in the smooth
muscle cells of vessels rendering it a potent vasoconstrictor. It is
most useful in shock states in which intravascular volume is
deemed to be adequate but systemic vascular resistance is exceed-
ingly low, such as in neurogenic shock, epidural anesthesia–
induced hypotension, or transient hypotension associated with
inhaled anesthetics. Pure α1 agonists have little role in treating
septic or other forms of distributive shock because they lack any
direct effect on the heart. Norepinephrine, by virtue of its alpha
and beta effects, causes increased cardiac output by chronotropic
and inotropic activities as well as vasoconstriction via a potent α1
effect. Norepinephrine is the predominant agent used in septic
shock because of its favorable mix of alpha and beta actions, and
there is some evidence that it may attenuate the systemic inflam-
matory response. Although norepinephrine is the preferred pressor
for septic shock because of its lack of adverse effects compared
with dopamine, two large randomized controlled trials failed to
show benefits related to mortality and organ failure when norepi-
nephrine was compared with dopamine or vasopressin. Epineph-
rine is an endogenous catecholamine that has far more beta
activity than alpha activity, rendering it the preferred agent for
cardiac arrest, anaphylaxis, and cardiogenic shock and a second-
line agent for septic shock. Similar to dopamine, epinephrine is
associated with severe arrhythmias, and this is theorized to be due
to increasing myocardial workload and oxygen demand. Vasopres-
sin is an endogenous peptide, not an adrenergic agent, and its
mechanism of action is different from the previously mentioned
catecholamines. It works via a G protein–coupled receptor that
appears to be less denatured by acidemia, increasing its effective-
ness in severe septic shock. In many shock states, endogenous
vasopressin may be depleted, and so it is usually administered at
physiologic replacement doses. To date, no study has shown a
benefit to monitoring vasopressin levels, and dosing this drug
based on serum levels is not indicated; pharmacologic doses are
associated with splanchnic vasoconstriction and bowel ischemia.
The synthetic catecholamine dopamine is no longer a preferred
agent in the ICU because it is an unpredictable agent with numer-
ous negative side effects.
The management of acute heart failure and cardiogenic shock
in the ICU is very challenging because these patients typically
have a wide range of comorbidities as well as the usual confound-
ing perioperative factors. The goals of managing acute heart failure
are to optimize preload and intravascular volume, maximize con-
tractility, and decrease myocardial demand and oxygen consump-
tion. The synthetic catecholamine dobutamine is a useful to
augment heart rate and contractility via its β1 actions, while
decreasing left ventricular preload through its β2 vasodilatory
effects. Owing to its β2 effect, dobutamine should be avoided in
hypovolemic states and septic shock because it can cause profound

hypotension. Phosphodiesterase inhibitors milrinone and amri-
none act via intracellular second messengers to prevent the break-
down of cyclic adenosine monophosphate, which essentially
extends the time period of contraction and contractility of the
myocardium. Although these agents are not adrenergic agonists,
they behave similarly to dubutamine and increase contractility but
also promote vasodilation resulting in hypotension and significant
arrythymias. Afterload reducers and diuretics may have a role in
management of heart failure and cardiogenic shock, but their use
is too complex to be adequately discussed here. Similarly, mechan-
ical assist devices, such as left ventricular assist devices, biventricu-
lar assist devices, and right ventricular assist devices, have become
much more effective and portable allowing some patients to be
discharged with them in place. Intra-aortic balloon pumps are
useful tools as a bridge to cardiac recovery in patients with heart
failure or cardiogenic shock refractory to pharmacologic therapy,
patients awaiting cardiac transplant, and patients with post–
coronary bypass heart failure.
RESPIRATORY SYSTEM
Respiratory Failure
Respiratory failure is one of the most frequent reasons surgical
patients require ICU admission and may be due to diverse causes,
such as blunt chest trauma, altered mental status, cardiothoracic
surgery, sepsis, medical comorbidities, and shock. Even simple
abdominal operations may cause splinting, hypoventilation, atel-
ectasis, and hypoxemia leading to respiratory failure. Hypoxemia
is the hallmark of type I respiratory failure, and hypercapnia and
hypoxemia are associated with type II respiratory failure. Hypoven-
tilation from pain, narcotics, and mental status changes can result
in respiratory acidosis, whereas inadequate pulmonary toilet can
lead to pooling of secretions, atelectasis, and pneumonia. Most
surgical patients have type II respiratory failure because of mul-
tiple overlapping factors. Ideally, patients at high risk for respira-
tory failure are identified before they worsen to the point where
they require intubation to allow for measures to treat or mitigate
the underlying cause of the respiratory failure. Examples of these
measures are adequately treating pain to avoid splinting and atel-
ectasis, inducing diuresis in patients with volume overload, or
adjusting narcotics and sedatives in overmedicated patients.
Assessing a patient with respiratory failure is an urgent and
challenging endeavor for all clinicians, and a structured and sys-
tematic approach is indicated. Similar to the primary survey of
the Advanced Trauma Life Support course, asking the patient a
question and assessing his or her phonation, degree of breathless-
ness, and comfort in responding gives clues to airway patency,
pulmonary reserve, work of breathing, and mental status. Stridor,
or high-pitched upper airway obstructive sounds, is ominous,
and arrangements should be made for prompt intubation of the
patient. Prompt intubation is also indicated for unresponsive or
comatose patients. If the patient’s condition allows, supplemental
oxygen should be delivered by a high-flow face mask, and a
thorough chest examination should be done assessing chest
rise, accessory muscle use, and retractions followed by careful
auscultation of the type and quality of breath sounds. Physical
examination findings and a brief history are critical in rapidly
working through the vast differential diagnosis of acute respira-
tory failure. If the cause of the respiratory distress is not found
after assessing the airway, breathing, and circulation, a more
in-depth review of the patient’s recent ICU course should be
done with the patient’s nurse. Clues to the patient’s distress (e.g.,
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CHAPTER 21  Surgical Critical Care 557
aspiration, recent medications, procedures) likely can be learned
from this discussion.
Chest x-ray (CXR) and ABG analysis are sensible components
of the workup of a patient in respiratory distress. The CXR should
be reviewed for pathology paying special attention to the location
of the endotracheal tube in intubated patients. An ABG analysis
is key to assessing oxygenation and ventilation as well as data
about the patient’s acid-base balance. Analysis of the ABGs can
determine the alveolar-arterial (A-a) oxygen gradient, which is a
comparison of the fractional inspired oxygen (FIO2) to partial
pressure of oxygen in the ABGs. A large A-a gradient without
signs of abnormality on the CXR should raise suspicion for pul-
monary embolism. Although CXR and ABGs are useful adjuncts,
they are not necessary to make the decision to intubate a patient
struggling to breathe. In less critical situations, the SOAP mne-
monic can be used to guide the decision whether to intubate
patients:
Secretions that are excessive and cannot be cleared by the patient
Oxygenation that is inadequate
Airway compromise or obstruction
Pulmonary function not meeting ventilatory needs
Intubation in the ICU is generally a risky undertaking because
most patients have cardiopulmonary disturbances that do not
allow for adequate preoxygenation coupled with a hyperdynamic
state of very high oxygen consumption. There is little margin for
error, and only one attempt is possible before cardiac arrest in
many patients. For these reasons, clinicians in the ICU should
have extensive training in intubating these patients; otherwise, it
is imperative to seek assistance from someone more skilled. If
time allows, the anesthesia record of postoperative patients
should be reviewed to learn the airway findings, type of laryngo-
scope blade used, and any other difficulties previously encoun-
tered. Given the high degree of intra-abdominal processes in the
surgical ICU, all patients should be treated as if they are at high
risk for aspiration, and rapid-sequence intubation (RSI) should
be considered the norm. The key principles of RSI are preoxy-
genation with 100% oxygen via a face mask, avoidance of bag-
mask ventilation to reduce gastric distention, brisk induction
with hypnotic agents, and short-onset paralytic agents followed
by placement of an oral endotracheal tube by direct laryngos-
copy. Patients who are in extremis and cannot be intubated or
ventilated by bag-mask ventilation should undergo emergent
cricothyroidotomy.
Although there are many pharmacologic options for RSI, a few
standout as uniquely suited to for this purpose. Benzodiazepines,
narcotics, and sedative-hypnotics all are suitable induction agents.
Etomidate is a quick-onset and ultra-short-acting sedative-
hypnotic agent that has minimal adverse effects on hemodynam-
ics, which is a problem associated with many other sedating
agents. Propofol, another ultra-short-acting hypnotic agent, and
midazolam, a short-acting benzodiazepine, can be used for intuba-
tion but cause more hypotension, which is an undesirable com-
plicating factor in urgent intubations. Ketamine is a dissociative
agent that is chemically related to the street drug PCP (phenyl-
cyclohexyl piperidine) and is a useful agent for RSI because it can
provide sedation and hypnosis without causing hemodynamic
compromise. Compared with etomidate, ketamine was shown to
result in lower rates of adrenal insufficiency in a randomized trial
of critically ill patients requiring intubation because etomidate
directly inhibits cortisol production by blocking 11β-hydroxylase
in the adrenal cortex. The anticortisol effect of etomidate is worth
considering in patients with distributive shock of unclear cause
558 SECTION III  Trauma and Critical Care
because this effect may persist 12 to 24 hours after administration.
Paralytics are part of the RSI algorithm, and the two most
commonly used drugs are succinylcholine and rocuronium. As
previously mentioned, succinylcholine is a short-acting depolar-
izing paralytic agent with a half-life of approximately 15 seconds
that is useful in RSI because it wears off fairly quickly, which may
be lifesaving in patients who cannot be intubated. Rocuronium
is the most rapidly acting of all the nondepolarizing paralytic
agents and is indicated in cases where succinylcholine is contra-
indicated (see “Analgesia, Sedation, and Neuromuscular Block-
ade” for these contraindications). Few clinical trials comparing the
safety and effectiveness of paralytic agents have been performed
in the ICU setting, but a randomized investigation did not show
any difference in intubation failure rates, desaturation events, or
intubation conditions when succinylcholine was compared with
rocuronium.
Noninvasive and Mechanical Ventilation
In some special circumstances, it may be possible to avoid intuba-
tion and full mechanical ventilation, particularly if the cause of
the respiratory failure is identified and can be readily reversed.
Patients with hypoxemia and increased work of breathing may be
temporarily supported with noninvasive means until intravenous
diuretics can treat their volume overload. Similarly, hypoventilat-
ing patients who are overnarcotized may be supported with these
devices while they are given narcotic reversal agents such as nal-
oxone or their epidural infusion is turned down. Noninvasive
ventilatory support is a bridging therapy and should not be con-
sidered as a definitive treatment; if the underlying cause of hypoxia
or inadequate ventilation cannot be treated in a timely fashion,
formal intubation is mandatory. Options for noninvasive ventila-
tion include continuous positive airway pressure (CPAP), bilevel
positive airway pressure (BiPAP), and high-flow humidified
oxygen systems. CPAP acts by providing a continuous level of
positive pressure through a tight-fitting mask maintaining a
patient’s functional residual capacity (FRC) and is more effective
for treating type I respiratory failure. CPAP does not aid ventila-
tion and should be used with caution in patients with an altered
sensorium because they may vomit into the mask and aspirate and
die. BiPAP, similar to CPAP, provides a continuous level of posi-
tive airway pressure to augment FRC but also adds a driving
pressure when patients initiate a breath, which can augment ven-
tilation. Through its support of oxygenation and ventilation,
BiPAP is effective in treating type II respiratory failure. Patients
on CPAP and BiPAP require careful monitoring, and plans should
always be in place denoting the duration of the noninvasive trial,
end points of therapy, and action plans should the respiratory
failure worsen. High-flow oxygen humidification systems are a
more recent addition to the respiratory support armamentarium
and are effective in augmenting a patient’s oxygenation without
desiccating the upper airways and nasal passages. Literature has
shown that postoperative surgical patients who develop recurrent
respiratory failure after extubation should be promptly intubated
except in certain rare circumstances, the most notable exception
being antecedent chronic obstructive respiratory disease, where
BiPAP may be effective in overcoming recurrent respiratory
failure.
Many terms and management concepts are similar whether a
patient is on CPAP, BiPAP, or standard mechanical ventilation.
The FIO2 is the concentration of oxygen in the inspiratory flow
delivered to the patient. Positive end expiratory pressure (PEEP)
is delivered at the end of exhalation and prevents small airway
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closure, which maintains or increases the FRC. PEEP and FIO2
are the main determinants of oxygenation, but there are limits to
how much they may be increased before the patient starts expe-
riencing negative sequelae. High PEEP may adversely affect
hemodynamics by decreasing venous return to the heart, where
high FIO2 can lead to the generation of oxygen free radicals, which
may damage many cell types in the lungs. It is often easier to
conceptualize oxygenation and ventilation as two separate and
unrelated entities, each affected by different parameters. Although
this conceptualization is helpful, it is not accurate because there
is significant overlap and interplay between the determinants of
each. Ventilation is governed by the minute volume, which is a
product of the respiratory rate and tidal volume. Increasing the
driving pressure increases the tidal volume but may result in
barotrauma as pressures rise, whereas increasing the respiratory
rate also increases the minute volume, but at higher rates the lungs
may become hyperinflated because there is inadequate time for
complete exhalation.
In general, the more ill the patient, the more controlled his or
her ventilatory support should be. The clinician should set the
ventilator so that most components of the respiratory cycle are
governed by the machine, so the patient will get the desired
minute and tidal volumes to ensure ventilation and oxygenation.
Assist or support modes augment patient-initiated breaths by
adding defined amounts of positive pressure to each breath and
adding PEEP to maintain FRC. Patients placed on controlled
modes of ventilation are usually cycled according to preset tidal
volume and peak airway pressure goals; these are termed volume
control ventilation and pressure control ventilation, respectively.
When volume control ventilation is employed, decreases in airway,
lung, or chest wall compliance alter the delivered tidal volume,
and the ventilator’s processors alter the pressure until the desired
volume is delivered, but this mode may result in barotrauma.
Most modern ventilators have a setting termed pressure regulated
volume control, where a targeted tidal volume is delivered but the
delineated peak pressure is not exceeded. Older modes such as
assist control have limited utility and should be used only in
patients who are deeply sedated or receiving neuromuscular block-
ade. Spontaneously breathing patients should not be on assist
control because this typically results in overventilation and severe
respiratory alkalosis.
Pressure control modes are best suited to situations in which
the clinician is concerned about changing airway and lung com-
pliance. In these modes, the driving pressure, respiratory rate,
PEEP, and FIO2 are set by the clinician, but the tidal volume
delivered depends on the patient’s thoracic compliance. Pressure
control modes are more labor intensive because minute ventila-
tion can vary as compliance changes. Investigations are often
necessary to identify the causes of the changing compliance, but
these modes may protect against barotrauma. In this mode,
decreasing tidal volumes should prompt an evaluation for causes
of decreased compliance, such as pneumothorax, mucous plug-
ging, endotracheal tube obstruction, bronchospasm, worsening
abdominal distention, and ACS. Pressure control modes can also
be mandatory, assisted, or entirely patient initiated. The pressure
control mode where all breaths are patient initiated is termed
pressure support ventilation (PSV). In PSV modes, the driving
pressure, PEEP, and FIO2 are set, but the respiratory rate and tidal
volume are determined by the patient, and it is generally more
comfortable for patients. PSV typically results in less need for
sedation, which renders it an excellent choice for weaning from
mechanical ventilation.

Weaning and Extubation
From the very first moments an intubated patient arrives in
the surgical ICU or shortly after an ICU patient is intubated,
providers should be considering the possible duration of ventila-
tion and formulating a plan to wean and extubate the patient.
Prolonged mechanical ventilation is associated with ventilator-
induced lung injury, pneumonia, deconditioning, and other
adverse outcomes. Although there are several important benefits
from liberation from mechanical ventilation, inappropriate or
overzealous attempts at weaning should be avoided because they
can result in extubation failure and the need for emergent reintu-
bation with its attendant risks. Generally, one of the first questions
that must be answered when considering extubating a patient is:
Has the process that created the initial conditions requiring
mechanical ventilation still present? When this question is
answered, the clinician should review the response to daily awak-
ening and SBTs, the patient’s mental status and hemodynamics,
anticipated procedures, and impending travel out of the ICU for
diagnostic or therapeutic interventions. Despite large numbers of
investigations over the last 2 decades, there is no one set of criteria
or objective measures that can guide patient selection for weaning
and extubation, and the decision-making process must combine
objective elements with clinical judgment.
The decision to extubate an awake and oriented patient is far
easier than deciding to extubate a patient with encephalopathy,
traumatic brain injury (TBI), delirium, or other causes of altered
mental status. An adequate mental status is an important determi-
nant not only of a patient’s ability to protect his or her airway but
also whether they will participate in pulmonary toileting measures
that are critical to staving off the need for reintubation. Informa-
tion gathered during “sedation holidays” can greatly simplify this
determination. After assessing the patient’s mental status, focus
should shift to an assessment of the patient’s oxygenation, and the
most recent ABG analysis should be reviewed. The partial pressure
of oxygen from the ABG analysis can be divided by the FIO2 to
calculate a P : F ratio, which is an objective measure of the patient’s
oxygenation and is used in the Berlin definition of ARDS. Patients
who have acute lung injury (P : F <300) or ARDS (P : F <200) are
rarely successfully extubated, and efforts should be focused instead
on optimizing their oxygenation rather than extubation. Another
useful calculation is the rapid shallow breathing index (RSBI),
which was developed in the early 1990s as a measure to predict
suitability for extubation and has been successfully validated in
several large clinical trials. RSBI is defined as the ratio of respiratory
rate (breaths per minute) to tidal volume (liters) while a patient is
on zero driving pressure and PEEP. Patients with an RSBI of 105
or greater are highly unlikely to be successfully extubated; patients
scoring lower have higher chances of a successful extubation.15 As
stated earlier, SBTs are useful in predicting successful extubation,
but there is no uniform definition of the technique for a SBT. Some
techniques described include low-level PEEP (5 cm H2O) without
additional driving pressure, PSV with low-level settings of PEEP,
and driving pressure or T-piece trials in which the patient is
removed from positive pressure and is given supplemental oxygen
only but remains intubated. It is likely that the lack of positive
pressure and PEEP coupled with the airway resistance of the endo-
tracheal tube is the real test of the patient’s reserve and is the reason
behind the predictive value of the SBT. Randomized studies com-
paring SBT strategies of PSV versus T-tube have not shown signifi-
cant differences in percentages of patients who have remained
extubated after 48 hours, but both of these measures are useful in
formulating a decision to extubate a patient.
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CHAPTER 21  Surgical Critical Care 559
Pneumonia, Acute Respiratory Distress Syndrome,
Salvage Modes of Ventilation, and Extracorporeal
Membrane Oxygenation
Although pneumonia is not thought of as a surgical disease,
the highest rates of ventilator-associated pneumonia (VAP) are
observed in surgical critical care units, with the top rates of VAP
occurring in trauma and neurosurgical ICUs. It is important to
make this distinction because understanding the processes that
increase the risk of patients developing VAP allows providers to
embrace strategies to lessen its occurrence. Factors such as poor
postoperative pain control, inadequate pulmonary toilet, immo-
bilization, and prolonged mechanical ventilation all should be
addressed to reduce the risk of VAP. Upper midline abdominal
and thoracic incisions result in significant pain causing splinting,
shallow respirations, atelectasis, and poor clearance of secretions;
it is theorized that advancements in minimally invasive techniques
such as video-assisted thoracic surgery, laparoscopic surgical
approaches, and endovascular surgical approaches will lead to
lower pneumonia rates. VAP is one of the leading nosocomial
infections causing death in surgical ICUs. Although it may be an
oversimplification, it is impossible to get VAP without a ventila-
tor, and so the most effective preventive measure is timely extuba-
tion. The concept of combining several associated interventions
to reduce VAP led to the development of the “VAP bundle,”
which seeks to improve the care of ventilated patients and to
reduce the occurrence of VAP. The components of this bundle are
head of bed elevation to 30 degrees, oral care with chlorhexidine
solution, sedation interruption, and SBTs. Additional elements
such as venous thromboembolic prophylaxis and preventive
agents for stress ulcer bleeding have been added to this bundle as
well, which is ironic because more recent evidence shows that
proton pump inhibitors (PPIs) are associated with an increased
risk of VAP. Many ICUs have adopted “VAP prevention” teams
that make rounds multiple times a week with checklists to follow
bundle compliance and have resulted in lower VAP rates.
Despite the severity of the problem, there is still no universally
accepted definition of VAP. The U.S. Centers for Disease
Control and Prevention (CDC) has introduced the concept of
ventilator-associated events to include other conditions contri­
buting to prolonged mechanical ventilation. The diagnosis of
ventilator-associated events according to the CDC criteria is
objective and systematic, but this is not the case with VAP, the
diagnosis of which remains highly controversial. CXR findings
have been shown to be highly subjective rendering them ill-suited
for the diagnosis of VAP. Scoring systems such as the Clinical
Pulmonary Infection Score may not be valid in certain patient
populations as it has limited utility in surgical patients because of
the presence of many factors consistent with the systemic inflam-
matory response syndrome (SIRS). In particular, the Clinical
Pulmonary Infection Score is not helpful in diagnosing VAP in
trauma patients because these patients tend to have the most
pronounced SIRS response mimicking infections.16 The most
consistent finding in patients with VAP is hypoxemia, worsening
oxygenation, and the inability to wean, so VAP should be high
on the differential diagnosis list anytime these problems arise.
It has been well documented that ineffective or delayed therapy
for VAP leads to higher mortality, and clinicians treating
ICU patients with suspected VAP face the dual challenge of diag-
nosing this entity and initiating the correct therapy. The most
effective strategy for treating patients with suspected VAP may
center around the use of either blind or bronchoscopically directed
560 SECTION III  Trauma and Critical Care
quantitative cultures followed by administration of empirical anti-
biotics. The choice of the antibiotic is determined by several
factors, including the antibiogram of the ICU, the time from
hospital admission, and previous antibiotic therapy. Quantitative
cultures do not increase the sensitivity of detecting pneumonia,
but they dramatically increase diagnostic specificity, which allows
de-escalation from broad-spectrum empirical agents to narrow-
spectrum agents. Sputum culture is an inaccurate diagnostic
modality that typically results in the growth of multiple organ-
isms, which severely limits de-escalation.
Significant progress has been made in treating and preventing
ARDS since Ashbaugh’s first descriptions in the Lancet of a het-
erogeneous group of patients including patients with severe inju-
ries, pneumonia, pancreatitis, burns, ventilator-induced injury,
blood product transfusions, and infections who all manifested
ARDS. The mortality of ARDS remains quite high; the cause of
death is rarely profound hypoxia and more commonly multiorgan
failure or infection. Terms such as “shock lung” or “white lung”
are no longer used, and the Berlin definition is replacing the
criteria put forth in 1994 by the American European Consensus
Conference (AECC) that defined and categorized ARDS. The
AECC criteria for ARDS stated that the following elements were
required for a diagnosis: P : F 200 or less, bilateral and diffuse
CXR infiltrates, and noncardiogenic pulmonary edema with pul-
monary artery wedge pressure less than 18 if available. Acute lung
injury was a precursor of ARDS and was defined as a P : F between
200 and 300. The main criticisms of the AECC criteria have been
that they underestimate the prevalence of ARDS, have limited
prognostic value, and are misleading because higher levels of
PEEP may raise the P : F above 200. In 2012, the European
Society of Intensive Care Medicine put forth the Berlin definition
to broaden the hypoxemic categorization of ARDS to capture
more patients with the syndrome. A P : F of 201 to 300 was con-
sistent with mild ARDS, 101 to 200 was consistent with moderate
ARDS, and less than 100 was consistent with severe life-
threatening ARDS.17
The classic pathologic findings of ARDS are generalized lung
inflammation and neutrophil infiltration caused by parenchymal
cytokine release leading to diffuse alveolar and capillary damage.
Endothelial injury results in leakage of protein-rich edema fluid
into the alveoli and the formation of hyaline membranes. Efforts
to modify the disease process using corticosteroids, dietary supple-
ments, antioxidants, and surfactants have met with limited
success; thus, prevention of ARDS is paramount. A landmark
multicenter randomized trial found that ventilation using low
tidal volumes (6 mL/kg of ideal body weight) compared with
traditional tidal volumes (12 mL/kg) in patients with ARDS was
associated with lower plateau pressures, more ventilator-free days,
and overall reduced mortality.18 No other investigation of ARDS
has affected outcomes, management, and prevention of ARDS
more than this one, and it ushered in a new era recognizing that
excessive tidal volumes and airway pressures result in alveolar
stretch, shear stresses, and damage to the pulmonary epithelium
and endothelium. Patients ventilated with lower tidal volumes
were found to have lower levels of interleukin-6 suggesting that
this strategy causes less lung and systemic inflammation. The
lower tidal volume group required higher levels of PEEP compa-
rable to the higher tidal volume group, and it is theorized that
higher mean and plateau pressures reduced alveolar shear and
stretch, forces termed volutrauma. This appreciation of volu-
trauma led to ventilator management strategies that have lessened
the incidence of ARDS and reduced systemic inflammation.
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When patients develop hypoxemia that is refractory to maneu-
vers such as increasing FIO2, PEEP, and driving pressure, salvage
modes of mechanical ventilation should be considered. Two of
these modes are airway pressure release ventilation (APRV) and
high-frequency percussive ventilation (HFPV) via a volumetric
diffusive respirator (VDR). The goals of APRV are to minimize
alveolar phasic opening and closing, limiting shear stresses and
maintaining a high mean airway pressure. In APRV, the patient
is maintained at a pressure high (P-high) for a period of time
(T-high) during which the patient can take spontaneous breaths
followed by a brief period of release of pressure (T-low), at which
time the airway pressure decreases down to a baseline level (P-low)
that is akin to PEEP. The amount of time spent at T-low is less
than the time it takes for the small airway to close; APRV main-
tains a high MAP and promotes oxygenation. It is typical for the
ratio of time at P-high to P-low to be in the range of 4 or 5
seconds to 1 second, and this is probably why this mode was
initially called “continuous positive airway pressure with an inter-
mittent release phase.” APRV mainly improves oxygenation but
can cause problems in patients with chronic obstructive pulmo-
nary disease because of the short pressure release times and air
trapping.
HFPV is essentially a pressure-controlled mode of ventilation
that requires a specialized machine, the VDR, to deliver subphysi-
ologic tidal volumes at high frequencies superimposed on typical
ventilator flow. The VDR uses lower peak pressures and PEEP
than conventional settings because it maintains a higher mean
airway pressure. It can mobilize secretions in patients with inhala-
tion injury or pneumonia owing to eddy currents that form
around the aliquots of air as the subphysiologic tidal volumes are
delivered in a percussive fashion. Numerous investigations involv-
ing patients with inhalation injury and ARDS have shown
improved P : F ratios and lower peak pressures with HFPV com-
pared with conventional modes, but there are no significant ran-
domized data to show mortality benefit with HFPV. APRV and
HFPV are similar in that both use higher mean airway pressures
and smaller tidal volumes; this likely minimizes volutrauma,
although comparative studies are lacking.
The H1N1 influenza outbreak resulted in an increase in inter-
est in extracorporeal membrane oxygenation (ECMO) as a salvage
therapy for patients with florid ARDS. ECMO facilitates lung rest
and healing and can break the cycle of ongoing lung injury
because it can take over most of the patient’s ventilation and
oxygenation needs and avoids the high airway pressures and volu-
trauma that occur as part of ventilator management for patients
with ARDS. The CESAR study in 2009 was one of the first ran-
domized trials that assessed the benefits of ECMO for ARDS in
180 patients with severe respiratory failure.19 These patients were
randomly assigned to conventional ventilator versus ECMO, and
the study found less disability and fatalities in the ECMO group
6 months after ICU discharge. The CESAR study demonstrated
that ECMO therapy was approximately twice as expensive as
conventional therapy, but that this cost was offset in gained
quality-adjusted life-years.19 The CESAR study findings have been
echoed in more recent observational studies, and the concept of
transferring patients with ARDS to ECMO centers is gaining
popularity, even if it requires a mobile ECMO treatment team to
transport these critically ill patients.
Prone positioning is useful for treating patients with severe
ARDS. Similar to ECMO, there is some resistance to embrace
this therapy because of the logistical challenges it presents.
Prone positioning results in improved ventilation and perfusion

matching as well as alveolar recruitment to improve oxygenation
and reduce volutrauma. Multiple randomized trials have shown
improved oxygenation with prone positioning, but until more
recently few have shown a survival benefit. Although most ICU
providers view prone positioning as a salvage therapy for patients
with severe ARDS, emerging data show that this modality is an
effective adjunct for treating ARDS, especially if used early in the
disease process. Caring for patients in the prone position requires
significant nursing resources, and there is always a concern about
endotracheal or other tube dislodgments, skin breakdown, and
limited access to the patient in emergent situations. Surgical
patients in particular have unique challenges to prone positioning
because of abdominal incisions, open abdomens, and unstable
spine injuries.20
Special Issues: Tracheostomy and Obesity
Tracheostomy often conjures up negative images for patients,
families, and providers, who sometimes equate it with signs of
futility; however, numerous studies have shown it to be beneficial
in critically ill patients. Placement of a tracheostomy can facilitate
ventilator weaning in patients with chronic obstructive pulmo-
nary disease or cardiomyopathy because of its ability to reduce
dead space ventilation and work of breathing. It can improve
clearance of secretions in patients with altered mental status, TBI,
or neuromuscular weakness and provides a stable airway for coma-
tose patients. Discontinuing an endotracheal tube results in a
marked reduction in the patient’s sedation requirements, which
promotes wakefulness, spontaneous respiration, and ventilator
weaning and increases liberation from mechanical ventilation.
Tracheostomy can prevent airway narrowing and obstruction,
which often plagues patients with long-term endotracheal intuba-
tion secondary to buildup of biofilm and debris on the inner wall
of the tube because the inner cannula of the tracheostomy is easily
changed.
The timing of tracheostomy in patients with prolonged respira-
tory failure is controversial; previously, patients commonly
remained orally intubated for 14 or more days before the proce-
dure was considered. More recent data show decreased ICU
lengths of stay and duration of mechanical ventilation, without
increased complication rates, when tracheostomy is performed
within 7 days of the institution of mechanical ventilation. The
benefits of early tracheostomy has been further supported by
investigations showing similar results in a mixed population of
medical, surgical, and trauma patients who underwent tracheos-
tomy within 3 days of the initiation of mechanical ventilation.
Bedside bronchoscopic-guided percutaneous tracheostomy in the
ICU has become standard in most institutions and is associated
with lower costs and less transport complications, delays, postop-
erative hemorrhage, and infections compared with open trache-
ostomy done in the operating room.21 There are relatively few
contraindications to percutaneous tracheostomy, and many of the
previously identified contraindications, such as coagulopathy and
obesity, have been disproven as evidence and experience with the
procedure mount.
Obesity is a growing epidemic in the United States and the
developed world and presents significant challenges to the entire
critical care team. One in three Americans and one in four
ICU patients has a body mass index greater than 30, which is
the defining number for class I obesity. Almost every aspect of
the respiratory system in an obese patient is more difficult,
including bag-mask ventilations, intubation, emergency surgical
airway placement, ventilator management and weaning, and
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CHAPTER 21  Surgical Critical Care 561
tracheostomy. The anatomic effects of obesity on pulmonary
physiology are too many to list but include increased airway
resistance from parapharyngeal fat, collapsible airways from tra-
cheomalacia, and decreased compliance from weight of the chest
wall and pressure from abdominal girth. The most significant
pulmonary problem from obesity is a consistent decrease in
FRC, especially in dependent lung areas, that causes a marked
ventilation/perfusion mismatch. At rest, obese patients have been
shown to have a 60% increase in oxygen consumption compared
with nonobese patients, and half of this extra oxygen consump-
tion in the obese is energy required for the act of breathing.22
These patients can have obesity hypoventilation syndrome, which
has a neurally mediated mechanism that decreases respiratory
drive leading to hypoxia and hypercarbia. Obstructive sleep apnea
is much more common as body mass index increases, and this can
be a particularly dangerous problem in a postoperative patient
who has residual anesthetic and narcotics in his or her system. It
is important for surgeons to consider obstructive sleep apnea as
they formulate their postoperative care plans not only for patients
with known obstructive sleep apnea but also for patients with
obesity.
Obese patients are particularly subject to becoming hypoxemic
during intubation because of their limited pulmonary reserve,
increased oxygen demand, and anatomic obstacles such as a short
stout neck and airway abnormalities. Once intubated, obese
patients should be ventilated with tidal volumes based on their
ideal body weight and not their actual body weight because the
latter would lead to potentially injurious barotrauma. Ideal body
weight for men is calculated as 50 ± 2.3 kg for each inch over 5
feet and for women is calculated as 45.5 ± 2.3 kg for each inch
over 5 feet. Obese patients have diminished FRC, and slightly
increased levels of PEEP may be helpful in reducing alveolar col-
lapse and improving lung and chest wall compliance.
GASTROINTESTINAL SYSTEM
Background, Malnutrition, and Catabolism
of Critical Illness
Major surgery, injury, and critical illness all induce a stress response
that quickly leads to loss of lean body mass and an ongoing cata-
bolic state; this remains an area of prime focus for many research-
ers interested in inflammation. Several converging factors align to
contribute to this catabolic state, including decreased oral intake
because of NPO states, anorexia secondary to injury and inflam-
mation, and anatomic obstacles to enteral nutrition such as intes-
tinal surgery. Many surgical diseases are treated with bowel rest
including ileus, pancreatitis, intestinal ischemia, and intra-
abdominal infections, which greatly limits the intake of substrate
at a time of elevated catabolism. For most clinicians, nutritional
issues are often secondary in terms of acuity or urgency compared
with problems affecting the cardiovascular or respiratory systems,
leading to the insidious nature of malnutrition and catabolism.
The important contribution of nutrition and metabolism to out-
comes has been recognized only more recently by many ICU
providers. Although nutrition in the ICU is usually thought to be
a way of preserving lean body mass to promote mobilization,
weaning from mechanical ventilation, and overall recovery, it is
now recognized that nutrition has a direct effect on infectious
outcomes and complications.23
The catabolism associated with critically ill surgical patients
appears to be multifactorial and is likely the result of a complex
interplay among direct tissue injury, pain, immune-inflammatory
562 SECTION III  Trauma and Critical Care
activation, and ischemia-reperfusion injury leading to negative
nitrogen balance and increased energy consumption. As part of
the normal stress response, relative insulin resistance develops, and
glucose is not as readily used by tissues leading to increased break-
down of protein and fat stores. The so-called protein-sparing effect
of intravenous glucose solutions in critically ill patients is incon-
sequential, and this should never be thought of as addressing
nutritional needs for the sickest patients. Not only are protein
stores broken down during critical illness, but also there is a shift
in protein synthesis to proteins necessary for creating and main-
taining the inflammatory state; this is illustrated by the classic
concept that serum albumin falls in response to illness because it
is a “negative acute phase reactant,” whereas C-reactive protein
and other inflammatory mediators are greatly increased. In addi-
tion to protein and fat stores, the body’s stores of vitamins and
trace elements are consumed rapidly during this time. Many of
these vitamins and trace elements have critical roles in organ func-
tion, immune competence, and wound healing, and deficiencies
in these contribute to complications.
Muscle weakness and functional limitations may persist for
years after ICU discharge. Although this prolonged period of
weakness commences during the catabolic phase, the exact mecha-
nisms have not been elucidated. It is known that for muscle stores
to become depleted, the consumption of amino acids, especially
the branched chain varieties—leucine, isoleucine, and valine—
must exceed their intake because these are essential amino acids.
A study from the United Kingdom looked at acute skeletal muscle
wasting in critically ill patients who were in the ICU more than
7 days and on mechanical ventilation for at least 2 days and found
that there were significant declines in the cross-sectional area of
the quadriceps muscle, measured by ultrasound, and increased
muscle breakdown. These negative effects were seen day 1 to day
7 of study enrollment and were greater in patients with multior-
gan failure compared with patients with single-system failure,
which suggests that the catabolic effects of critical illness are pro-
portional to the “dose” of the illness. Furthermore, the degree of
muscle loss correlated with increases in C-reactive protein levels
and decreases in oxygenation, supporting the concept that muscle
wasting is a product of critical illness and organ failure.24 Although
muscle loss and functional deficits are known to occur in healthy,
well-fed individuals when placed on bed rest, these declines occur
surprisingly quickly in critically ill patients, despite adequate
delivery of calories and protein.
Assessment of Malnutrition and Energy Requirements
Regardless of the high prevalence of malnutrition and catabolism
in the surgical ICU and years of research focusing on this problem,
there is no uniform assessment method, laboratory value, or metric
to identify the patients at greatest risk for nutrition-related poor
outcomes. In the past, weight loss of a certain percentage of body
weight coupled with physical examination findings in the setting
of decreased caloric intake defined malnutrition. Although weight
loss of greater than 10% to 15% of body weight before ICU
admission has been shown to be associated with increased mortality
in surgical patients, this is a very crude assessment of malnutrition.
In 2010, the American Society for Parenteral and Enteral Nutri-
tion (ASPEN) and the European Society for Clinical Nutrition
and Metabolism proposed three distinct types of malnutrition:
chronic starvation without inflammation, chronic disease-related
malnutrition with mild to moderate chronic inflammation,
and acute disease-related malnutrition with acute and severe
inflammation. The incorporation of inflammation takes into
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consideration the “dose” of critical illness and alerts providers to
patients, such as obese patients, who are more likely to develop
malnutrition despite the perception of them being “overfed.”25
ASPEN and the Academy of Nutrition and Dietetics modified
the 2010 definitions by including the presence of two or more of
the following: inadequate energy intake, unintentional weight
loss, wasting on physical examination, and decreased grip strength
or functional loss.26 The Subjective Global Assessment and the
Malnutrition Universal Screening Tool look at similar factors as
the ASPEN screening guidelines, but both of these tools are
limited in their ability to assess malnutrition in different hospital
acuity levels, particularly the ICU. Obese patients are very diffi-
cult to assess because their body habitus often masks some of the
physical examination findings on which many of these tools focus.
Laboratory values are equally limited in their ability to define
malnutrition. The often cited serum markers (e.g., albumin, pre-
albumin, retinol binding protein) are more indicative of inflam-
mation or illness rather than a measure of how well the patient’s
nutritional needs are being met. Indirect calorimetry is a preferred
modality that determines a patient’s oxygen consumption and
carbon dioxide production to provide accurate and objective guid-
ance for nutritional delivery; however, it is expensive, not readily
available in all institutions, and impractical in patients on high
FIO2. Indirect calorimetry is a static measurement, and its utility
in identifying the nutritional needs of metabolic active and ever-
changing ICU patients is limited. In the absence of good objective
measurements or in difficult-to-assess patients, the standard rec-
ommendations of 25 kcal/kg/day and 1 to 2 g/kg of protein are
a good fallback option; however, “one size does not fit all,” and
adjustments should be made based on premorbid nutritional
status, functional status, medications, comorbidities, and the
degree of injury or inflammation.
Body weight, physical examination, and to a lesser degree labo-
ratory markers are subject to significant fluctuations in ICU
patients as a result of fluid shifts between intravascular and extra-
vascular compartments, which masks loss of muscle or adipose
mass. Tissue imaging techniques to estimate lean body mass and
nutritional status and body composition analysis have progressed
rapidly from anthropometric measurements to x-ray absorptio-
metric techniques to present-day CT scan–dependent methods.
CT is now recognized as the most accurate means of body com-
position analysis. With CT scanning, tissue densities and cross-
sectional area of muscle groups can be assessed. The third lumbar
vertebra has been identified as the conventional CT landmark
where cross-sectional analysis of tissue best reflects total body
muscle volume and lean body mass. Alternatively, psoas muscle
cross-sectional area can be used as a marker of cachexia and mal-
nutrition and may have some prognostic value based on more
recent data. The shortcomings of using CT to assess nutritional
status are cost, ionizing radiation, and need for transport; bedside
tools such as ultrasound are gaining popularity and may become
the standard way we monitor how effectively we are delivering
nutrition to critically ill patients.
Enteral Feeding
Critically ill patients have multiple factors adversely affecting their
ability to eat or take in substrate to meet their nutritional needs,
but there is often hesitancy among providers to address this
problem. Analogous to the prior discussion about a plan for
ventilator weaning being established immediately after the initia-
tion of mechanical ventilation, so too should a complete, indi-
vidualized nutritional plan be established for ICU patients on

admission. All intubated patients should have an oral or nasogas-
tric tube placed for administration of medications and liquid food
or “tube feeds,” and the position of these tubes must be confirmed
radiographically before anything is given through them. Patients
who are not intubated and who are unable to eat because of an
altered sensorium, sedatives, narcotics, or anorexia should have a
small-bore nasogastric tube placed as well. These tubes are readily
tolerated and are not as prone to clogging as pure feeding tubes;
they also allow for gastric suctioning and decompression should
that be required. The nutritional plan should never be “the patient
will start eating tomorrow” because more often than not tomor-
row never comes, and the patient’s nutritional deficits become
even greater. The advantages of enteral nutrition continue to
accrue in the literature and include maintaining gut integrity,
trophic effects on the liver, increased intestinal immunoglobulin
production, decreased infection rates, and more stable glycemic
profiles. In some patients, such as patients with burn injuries and
patients with TBI, enteral nutrition has been shown not only to
reduce the rates of ileus and gastroparesis but also to reduce septic
complications and promote better neurologic outcomes.
Several barriers to the effective delivery of enteral nutrition
exist, but one of the most common and troubling reasons that
patient’s needs are not met is frequent interruptions for various
reasons, such as turning the patient for care, washing or bedding
changes, diagnostic imaging studies, bedside procedures, and ill-
conceived NPO orders. Patients undergoing elective surgery are
kept NPO for 8 hours before intubation for fear of gastric aspira-
tion; however, this reason does not make sense in an ICU patient
with a critical need for nutrition who has a cuffed tube in the
airway as well as a gastric tube for decompression. These patients
should have their tube feeding stopped immediately before leaving
the ICU for the operating room, their nasogastric tube or feeding
tube flushed, and the stomach decompressed via suctioning.
Perhaps the most vexing reason tube feedings are stopped centers
around gastric residual volume (GRV) measurements. Trials have
shown that GRV measurements of 500 mL should be tolerated
so that the patient’s nutritional needs are met, without fear of
increased aspiration events.27 Most clinicians picture the pylorus
as a patent drain that allows unfettered egress of tube feeding from
the stomach into the duodenum, but this is in direct opposition
to gastric physiology, which mandates that receptive relaxation of
the stomach must occur before gastric emptying ensues. Although
feeding intolerance can result from gastroparesis and ileus, which
are common entities in ICU patients, clinicians should have a
higher tolerance for GRV without undue fear of aspiration.
Patients with ongoing elevated GRV and feeding intolerance
require a thoughtful evaluation because new-onset feeding intoler-
ance is often a harbinger of impending sepsis or infectious com-
plications. The medical record and bedside nurse should be
queried to determine when the patient last had a bowel move-
ment, and a digital rectal examination should be performed
looking for fecal impaction. The feeding tube should be checked
for patency and proper location on radiographs, which may also
yield data on the presence of ileus, pseudo-obstruction, or
suspected pneumonia, all of which are associated with feeding
intolerance. Some patients, especially patients with extensive
intra-abdominal surgery or injury, may require a CT scan to rule
out intra-abdominal abscess as a cause of the intolerance. Patients
who continue to fail attempts at gastric feeding can be treated
with prokinetic agents such as erythromycin or metoclopramide
or receive a postpyloric feeding tube. Postpyloric tubes are effec-
tive in circumventing gastroparesis but offer no advantage to
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CHAPTER 21  Surgical Critical Care 563
patients with ileus and are not associated with lower rates of
aspiration or pneumonia. Lastly, patients on moderate to high
doses of vasopressors should not receive enteral nutrition because
of the rare complication of bowel necrosis from the increased
intestinal oxygen demand induced by feeding in the setting of
splanchnic ischemia.
The concept of feeding to meet a 24-hour total nutritional goal
has emerged more recently and shows promise in overcoming
some of the previously discussed challenges to delivering enteral
nutrition. Because any interruption in tube feeding hinders the
delivery of the patient’s required calories and yet some interrup-
tions in tube feeding are unavoidable, the new strategy empowers
the bedside nurse to alter the rate of continuous tube feeding drips
or intervals between bolus tube feedings to compensate for any
interruptions so that the patient’s total caloric goal is met.
Although this strategy has resulted in better and more complete
delivery of enteral nutrition, it remains to be shown whether this
has any direct effect on outcomes. Similarly, bolus tube feeding
may be more effective in delivering nutrition because it is more
physiologic and mirrors how patients eat normally. Bolus tube
feeding has been shown to be a more effective method of deliver-
ing tube feeding in some patient populations, such as adult and
pediatric burn patients, but experience in broader ICU popula-
tions is limited.
Parenteral Nutrition
One of the oldest adages in the ICU is “if the patient has a gut,
use it,” which reinforces the importance of good nutrition in
critically ill patients and the benefits associated with enteral nutri-
tion, but circumstances arise where patients cannot be fed enter-
ally or the delivery of enteral nutrition has been inadequate
despite aggressive measures. Bowel obstruction, enterocutaneous
fistula, peritonitis, and active gastrointestinal bleeding all are con-
traindications to enteral nutrition, and in patients with these
problems parenteral nutrition is an effective way to meet nutri-
tional needs. The more difficult questions are: When will the
patient regain gastrointestinal function? When should parenteral
nutrition begin? How long can nutrition be withheld? In
the United States, the typical approach is to wait 1 week for
a patient who was previously well nourished to recover gastroin-
testinal function before starting parenteral nutrition. The Society
for Critical Care Medicine and ASPEN support this approach in
their guidelines because of concerns about complications of par-
enteral nutrition, including hypertriglyceridemia, hyperglycemia,
cholestasis, and central line–associated bloodstream infections
(CLABSI). Subsequent to these guidelines, randomized trials
evaluated the effect of starting parenteral nutrition on the first day
of ICU admission, but results of these studies have been mixed,
and the only reproducible benefit has been reduced costs of enteral
nutrition compared with parenteral nutrition. Some trials have
shown decreased ICU length of stay and infections when patients
received no nutrition compared with patients who received early
parenteral nutrition; the optimal time to wait before starting
parenteral nutrition remains unclear.
The risks and benefits of enteral nutrition and parenteral nutri-
tion remain contentious and confusing because parenteral nutri-
tion has received overly negative attention, and it is likely that
the obstacles to delivering enteral nutrition have been under-
stated. A randomized trial comparing enteral nutrition and par-
enteral nutrition within 36 hours of ICU admission demonstrated
no differences in 90-day mortality, infectious complications, or
several other secondary issues including the adequacy of caloric
564 SECTION III  Trauma and Critical Care
delivery between the two groups.28 Previous investigations that
demonstrated advantages of enteral nutrition over parenteral
nutrition, especially in infectious outcomes, were limited by small
sample sizes and confounding variables such as poor glycemic
control. Parenteral nutrition tends to be far more reliable in its
ability to meet nutritional needs because there are far fewer inter-
ruptions compared with enteral nutrition, and these needs are
typically met sooner as well. Parenteral nutrition is usually ordered
in a customized fashion with caloric needs established by weight-
based calculations or indirect calorimetry. Amino acids, lipids,
and dextrose are the key components along with electrolytes,
vitamins, and trace elements. It is thought that the catabolism of
critical illness that results in loss of lean body mass may be cur-
tailed by increasing the protein content of parenteral formulas,
but this is unsupported by evidence. Glutamine, the main fuel for
enterocytes and leukocytes, has been added to parenteral nutrition
in the hopes of maintaining immune competency as well as intes-
tinal function, but insufficient evidence supports this practice.
Customizing lipid preparations such that there are greater amounts
of anti-inflammatory omega-3 fatty acids instead of proinflamma-
tory omega-6 fatty acids has shown encouraging results, particu-
larly in patients with ARDS. Patients on parenteral nutrition
should receive balanced electrolytes in their formulas, and these
should be adjusted daily as abnormalities emerge. Delivering
nutrition after a prolonged period of starvation can result in life-
threatening electrolyte imbalances termed refeeding syndrome,
which is due to intracellular shift of potassium, magnesium, and
phosphate leading to arrhythmias, respiratory failure, neurologic
dysfunction, and possibly death, so permissive underfeeding is
reasonable in these patients.
RENAL SYSTEM
AKI, one of the most common forms of organ failure, affects
about one third of patients admitted to the surgical ICU within
24 hours of admission and is associated with increased mortality
and a markedly diminished quality of life in patients requiring
long-term RRT. AKI occurring in the ICU tends to recur more
often than AKI occurring in other settings and greatly complicates
the ICU management of patients because of its effects on fluid
balance, acid-base status, electrolytes, arrhythmias, clearance of
toxins and drug metabolites, encephalopathy, platelet function,
and erythropoiesis. Because all organ systems are inter-related,
AKI sometimes serves as the trigger in a cascade of organ systems
leading to MSOF. AKI results in tremendous resource utilization
and significantly increases ICU costs.
The Second International Consensus Conference of the Acute
Dialysis Quality Initiative Group met and developed the AKI
definition and subclassifications we know as the RIFLE criteria.
RIFLE criteria consist of risk, injury, failure, loss, and end-stage
renal disease. In the past, the definition of renal dysfunction was
not uniform, and at one point there were more than 30 definitions
of this condition. RIFLE has been shown to be the most sensitive
method for detecting AKI early in its course and is useful for
prognostic purposes (Table 21-2).29 The first sign of impending
renal failure is oliguria, defined in adults as less than 0.5 mL/kg/
hr or less than 400 mL per day or, less commonly, a sudden
increase in serum creatinine. Oliguria is a common occurrence in
the ICU and should prompt a thorough review of the patient’s
fluid balance, intake and output, and hemodynamics as well as a
physical examination to assess the patient’s volume status. Patients
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TABLE 21-2  RIFLE Criteria (Creatinine and
Urine Output Indicators)
Risk Increased serum creatinine × 1.5 UOP <0.5 mL/kg/hr × 6 hr
or GFR decrease >25%
Injury Increased serum creatinine × 2 UOP <0.5 mL/kg/hr ×
or GFR decrease >50% 12 hr
Failure Increased serum creatinine × 3 UOP <0.3 mL/kg/hr ×
or GFR decrease >75% 24 hr or anuria × 12 hr
Loss Persistent ARF, complete loss of
kidney function >4 wk
ESRD ESRD, complete loss of kidney
function >3 mo
ARF, acute renal failure; ESRD, end-stage renal disease;
GFR, glomerular filtration rate; UOP, urine output.
who have recently undergone a procedure should be carefully
examined to ensure that bleeding is not the cause of oliguria, and
a discussion with the bedside nurse should occur to determine if
any new or recent medications have been administered. The causes
of AKI fall broadly into three categories: prerenal causes secondary
to diminished renal perfusion, intrinsic or parenchymal causes,
and postrenal obstructive causes. Prerenal causes of AKI predomi-
nate in surgical patients, and the factors contributing to this are
too numerous to list here. Often an initial appropriate first step
is to administer a small bolus of isotonic crystalloid and observe
the response while a diligent evaluation of the patient is under-
taken. From the viewpoint of the kidney, systolic heart failure will
appear to be a prerenal cause of oliguria because renal perfusion
is diminished, but congestive failure ought to be easily discerned
from dehydration on physical examination. A quick and relatively
inexpensive way to confirm prerenal causes of oliguria involves
checking urine electrolytes and calculating a fractional excretion
of sodium (FeNa). A FeNa less than 1% is usually indicative of a
prerenal cause, whereas FeNa greater than 3% indicates an intrin-
sic problem such as acute tubular necrosis (ATN). As already
mentioned, there are caveats to a FeNa less than 1% because other
conditions such as hepatorenal syndrome or congestive failure
manifest this way, and recent diuretic administration tends to
invalidate interpretation of the FeNa. Simple urinalysis contains
a wealth of information to guide the workup of AKI because a
high urine specific gravity and low pH are consistent with prerenal
causes of AKI, whereas the presence of tubular or muddy brown
casts is indicative of renal parenchymal disease such as ATN. The
presence of eosinophils is associated with interstitial nephritis,
whereas “large blood” with no red blood cells is indicative of
muscle breakdown or intravascular hemolysis. ATN in the surgical
ICU is often a progression from a prerenal condition that results
from oxidative or ischemic injury to renal tubular cells, but similar
to AKI itself, the causes of ATN are legion.
Restoring an effective circulating volume usually treats AKI
resulting from prerenal hypovolemia, but there is no role for
supranormal fluid resuscitation to encourage renal recovery. Once
AKI is established, there are no interventions clinicians can
employ to promote renal recovery, and the goals of management
are to avoid further injury from nephrotoxins and recurrent hypo-
perfusion from hypovolemia and to adjust the dosing of renally
cleared agents. Failure to adjust dosages of medications can have
disastrous consequences, which is borne out by the example of
enoxaparin, which can result in severe bleeding if administration

is not adjusted for a decreasing creatinine clearance (CCr). The
medications that require dosing adjustments or discontinuation
are too numerous to list but include antibiotics, NSAIDs, anti-
hypertensives, narcotics, and many others; it is a good idea to
confer with a clinical pharmacist if available. An estimated CCr
can be calculated by collecting a 24-hour urine collection and
using the formula CCr = (UCr × V)/PCr, where UCr = urine creati-
nine concentration (mg/dL), V = urine volume (mL/min), and
PCr = plasma creatinine concentration (mg/dL), which yields the
Cockcroft-Gault formula, CCr = [(140 − age) × weight]/(PCr ×
72). Weight is measured in kilograms, and in women the final
value is multiplied by 0.85; normal CCr is about 95 mL/min in
women and 120 mL/min in men. Because 24-hour urine collec-
tion is a lengthy process, many clinicians collect urine for shorter
time periods and adjust the equation accordingly to extrapolate
CCr. Lastly, diuretics should be held in patients with worsening
AKI, and attempts to convert oliguric AKI to nonoliguric AKI do
not affect the need for RRT or mortality.
One of the most common electrolyte disturbances in patients
with AKI is hyperkalemia, which may result in arrhythmia and
sudden cardiac death. New-onset hyperkalemia in the ICU should
prompt a quick response from providers; the initial step is to
repeat the laboratory test to confirm the first value. A plasma
potassium level may be helpful in avoiding pseudohyperkalemia,
which is common in postsplenectomy states and other thrombo-
cytotic states. An ECG should also be assessed looking for peaked
T waves and widening of the QRS complex, but literature shows
that the detection of these findings in hyperkalemia is poor, even
by trained cardiologists, so treatment should not be deferred in
true cases of hyperkalemia based on ECG interpretation. Insulin,
dextrose, sodium bicarbonate, and β2 agonists all are effective at
shifting potassium intracellularly and are effective temporizing
measures, as is intravenous calcium, which stabilizes myocyte
membranes. At higher levels of hyperkalemia, urgent hemodialysis
should also be considered because it is the only effective way to
reduce total body potassium. Diuretics and resins such as sodium
polystyrene that pull electrolytes from the gastrointestinal tract
have a limited role in the treatment of hyperkalemia because
diuretics may worsen AKI, whereas resins with sorbitol have been
associated with colonic ischemia and necrosis.
The need for RRT is often a critical branch point in the care
of critically ill patients, and it is incumbent on providers to discuss
goals of care with the patient’s family and if possible the patient.
Long-term outcomes for patients requiring RRT during critical
illness are not favorable, and this needs to be discussed as part of
a goal of therapy discussion. Indications for RRT are hyperkale-
mia, metabolic acidosis, severe volume overload, uremia causing
encephalopathy or platelet-related bleeding, and some drug
overdoses. Options for RRT included intermittent hemodialysis
or continuous RRT. Hemodialysis works via a countercurrent
exchange mechanism to remove solutes and ultrafiltration to
remove volume and uses high flow rates, approaching 350 mL/
min, which often results in tachycardia and hypotension. Hemo-
dynamic instability and need for vasopressor support are relative
contraindications for hemodialysis. Continuous venous hemofil-
tration, continuous venovenous hemodialysis, and continuous
venovenous hemodiafiltration are the three most common forms
of continuous RRT in the ICU, with the last-mentioned being
the predominant mode. These continuous modes use low flow
rates, which are better tolerated in hemodynamically unstable
patients but at the expense of efficiency mandating their continu-
ous usage. This slow rate is also associated with blood clotting in
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CHAPTER 21  Surgical Critical Care 565
the dialysis circuit, so anticoagulants, heparin or citrates, are typi-
cally required, which may present problems for many patients in
the surgical ICU. It remains to be seen whether the timing of
RRT or the type of RRT (hemodialysis versus continuous RRT)
improves outcomes such as mortality and renal recovery. A trial
comparing hemodialysis with continuous RRT failed to show any
appreciable differences in critically ill patients.30
HEPATIC SYSTEM
Cirrhosis and Perioperative Liver Decompensation
Few comorbidities present as daunting a challenge to intensivists
as the management of cirrhosis in a surgical ICU patient. Similar
to renal failure, liver failure is a complex and far-reaching condi-
tion because it entails management of diverse problems such as
fluid shifts, coagulopathy, portal hypertension, hepatic encepha-
lopathy, and hepatorenal syndrome, but in contrast to renal
failure, there is no “liver dialysis” to support the patient. More
patients with liver failure will present to the ICU in the future
because the prevalence of infectious hepatitides and obesity-
related nonalcoholic hepatic steatosis is expected to rise. More
than 30 years ago, a landmark article examining the relationship
between cirrhosis, abdominal surgery, and outcomes demon-
strated mortality rates approaching 80% in patients with cirrhosis
and a prothrombin time more than 2.5 seconds longer than in
control subjects who underwent cholecystectomy. These fatalities
were attributable to intra-abdominal hemorrhage, progressive
hepatic and renal failure, and upper gastrointestinal hemorrhage
resulting from portal hypertension. Prothrombin time was identi-
fied as a better marker of hepatocellular function than albumin
because prothrombin more accurately estimates biosynthetic
function of the liver. More recently, the Model for End-Stage Liver
Disease score has been used to guide patient selection and prog-
nosticate morbidity and mortality in patients with chronic liver
disease undergoing major operations. The score is determined
through calculations incorporating serum bilirubin, prothrombin
time/international normalized ratio, and creatinine and has been
predictive in several studies looking at outcomes. The Model for
End-Stage Liver Disease has largely supplanted older subjective
predictive models of outcomes such as Child-Pugh. However in
contrast to renal failure, which is well defined by the RIFLE cri-
teria, there is no true formal definition or grading of postoperative
liver failure.
Multiple factors contribute to postoperative liver failure, but
the basic physiology is driven by ischemia of the hepatocytes.
Hypotension secondary to hypovolemia, hemorrhage, and vaso-
dilation all result in a decreased MAP, which diminishes nutritive
hepatic artery and portal vein flow. This mechanism is also
involved in some cases of liver failure observed after general anes-
thesia or laparoscopic procedures in which hepatocyte hypoperfu-
sion may not be as readily evident. Because the cirrhotic liver
already has significantly reduced numbers of hepatocytes, the
ischemic injury to the remaining hepatocytes is manifested in
decreased synthetic function with insufficient generation of criti-
cal proteins such as clotting factors and albumin. In addition, the
decrease in hepatocytes limits the ability of the liver to perform
normal metabolic functions, and toxins such as ammonia and
drug metabolites may build up. Many of the complications of
liver failure (e.g., bleeding, encephalopathy, ascites) are in some
way attributable to hepatocyte death. Patients with liver failure
also have generalized immune dysfunction caused by loss of
Kupffer cells as well as decreased production of critical elements
566 SECTION III  Trauma and Critical Care
of the inflammatory response, such as C-reactive protein, inter-
leukins, complement, and many other cytokines.
Perioperative fluid management in patients with liver disease
requires special attention to minimize delivery of sodium-
containing solutions, which in the setting of a low intravascular
oncotic pressure cause increased ascites and interstitial edema.
Patients with cirrhosis have activation of the renin-angiotensin
axis and can be intravascularly contracted, even though they have
total body fluid overload. In addition, dysregulation in nitric
oxide and many other vasoactive substances can lead to differing
degrees of vasoconstriction or dilation at the level of the tissue. In
extreme cases of liver failure, portal hypertension can inexplicably
result in splanchnic vasodilation, which may activate the juxtaglo-
merular apparatus of the kidney resulting in significant afferent
arteriole vasoconstriction and may lead to the development of
hepatorenal syndrome. This condition is difficult to treat, and it
is irreversible in most cases unless the patient undergoes liver
transplantation. The mortality of patients with cirrhosis who
develop AKI (with creatinine >2 mg/dL) in the ICU was shown
to be more than 80%.31 The classic finding in hepatorenal syn-
drome is FeNa less than 1% and very low urine sodium, indicating
the kidney senses hypovolemia and attempts to conserve sodium.
Albumin-containing solutions, which are low in sodium, are char-
acteristically used to volume resuscitate patients with cirrhosis
because they tend to minimize ascites and peripheral edema.
Patients who have suffered significant blood loss should be resus-
citated with blood and blood products and a minimal amount of
crystalloid solutions—so-called all product resuscitation. Even
albumin and other blood product colloids will leak from the
intravascular space, especially in sepsis, and the cycle of ascites
continues particularly if liver failure worsens. Patients who are not
critically ill and taking oral nutrition should be on sodium and
free water restriction as part of the management of ascites. Decom-
pensated liver failure and worsening ascites can lead to respiratory
failure as a result of increased intra-abdominal pressure, and diure-
sis, paracentesis, and transjugular intrahepatic portosystemic
shunt may be required in extreme cases.
Hepatic encephalopathy is another manifestation of advanced
liver failure and is due to impaired hepatic clearance of gut-
derived substances such as mercaptans and ammonia. These com-
pounds, which are normally produced by intestinal flora, have
sedating effects mediated by GABA receptors in the brain.
Ammonia, produced by the breakdown of urea in the gut, is a
neurotoxin that readily crosses the blood-brain barrier and is
normally metabolized by the liver to urea by a series of enzymes.
Hepatic encephalopathy is the result of numerous hepatic insults
(e.g., dehydration, infections, gastrointestinal bleeding, hepati-
cally metabolized medications) and may be seen in chronic and
acute liver failure. The degree of hepatic encephalopathy can be
graded by the West Haven scale (Table 21-3). Management of
TABLE 21-3  West Haven Criteria of
Hepatic Encephalopathy
LEVEL OF
GRADE CONSCIOUSNESS SYMPTOMS
0 Normal None
1 Minor mental slowing Diminished fine motor skills
2 Lethargic or apathetic Slurred speech, ataxia
3 Somnolent Clonus, asterixis
4 Coma Signs of intracranial hypertension
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hepatic encephalopathy centers on addressing the underlying
cause of the hepatic decompensation and reducing excess intake
of dietary protein and aromatic amino acids, but care must be
taken to avoid malnutrition. Lactulose, a nonabsorbable disac-
charide, creates an osmotic and cathartic effect that promotes the
elimination of ammonia and mercaptans from the gut. It is usually
given in 15- to 30-mL aliquots until the patient has three soft
bowel movements a day; overzealous titration should be avoided
because this can cause voluminous diarrhea, dehydration, and
worsening liver failure. Rifaximin and other enteral antibiotics can
treat hepatic encephalopathy by reducing the gut flora and the
production of the compounds that cause hepatic encephalopathy.
Studies have shown comparable results in terms of mental status
improvements in patients with hepatic encephalopathy treated
with lactulose versus rifaximin, and some literature suggests that
osmotic laxatives alone may be equally effective. Special enteral
formulas with varying amounts of aliphatic and branched chain
amino acids have been evaluated in liver and hepatic encephalopa-
thy with disappointing results.
HEMATOLOGIC SYSTEM
Review of Clotting Mechanisms and Thromboembolism
ICU patients are affected with coagulopathies and thrombophil-
ias, and both conditions may occur in the same patient during
the span of their ICU care. Coagulopathy tends to be more
common and can be the result of nutritional deficiencies, liver
dysfunction, congenital diseases such as hemophilia and von Wil-
lebrand disease, hemodilution, consumption, and many other
surgical causes. Sepsis, trauma, and almost every medication given
to ICU patients has been associated at some point with throm-
bocytopenia. Hypothermia, the scourge of trauma care, can
magnify coagulopathy through its negative effects on clotting
factors. Critical illness and inflammation cause activation of the
coagulation cascade leading to microvascular clotting and organ
dysfunction and is one theory behind the development of MSOF.
Even after major injury with bleeding and coagulopathy, patients
develop an increased risk of thrombosis as a result of endothelial
injury, venous stasis, and immobility. On the surface, these
dichotomies seem confusing, but when one considers that normal
homeostasis is maintained by simultaneous activation of the clot-
ting and fibrinolytic system, these conflicting conditions make
more sense. Scant evidence exists on the relationships between
coagulation abnormalities in the ICU and patient outcomes, and
good data to guide the management of the complex interplay
between these two competing systems are lacking.
The process of clotting is initiated when there is endothelial
injury, which exposes vascular wall elements that activate platelets.
Platelet activation draws in and activates more platelets leading to
the creation of a platelet plug, which is known as primary hemo-
stasis. Circulating clotting factors undergo a cascading activation
that eventually leads to the activation of thrombin that converts
fibrinogen to fibrin. Cross linking of fibrin monomers forms a
strengthening lattice, reinforcing the platelet plug. Thrombin is
one of the most important proteins in the coagulation cascade
because it activates numerous other clotting factors; increases
platelet activation and aggregation; and activates protein C, which
is a modulating inhibitor of the cascade. There are two coagula-
tion pathways, intrinsic and extrinsic, that coalesce into a common
pathway where factor X is activated and converts prothrombin to
thrombin and ultimately to deposition of fibrin. The effectiveness
of the intrinsic pathway is typically measured by the partial

thromboplastin time, and the extrinsic pathway, initiated by tissue
injury and release of tissue factor, is measured by the prothrombin
time. Prothrombin time and partial thromboplastin time are not
functional tests of clotting and are limited in assessing clot
strength, durability, or the quality of the clot formed by the inter-
play of platelets, von Willebrand factor, and fibrin. As previously
stated, activation of clotting factors is coupled to the simultaneous
activation of clotting inhibitors so that clotting is carefully coun-
tered by fibrinolysis. Disturbances in this delicate balance can lead
to uncontrolled thrombosis, as is seen in disseminated intravascu-
lar coagulation, a complication of sepsis, major surgery, severe
trauma, obstetric procedures, transfusion reactions, and malig-
nancies. Hyperfibrinolysis, as seen in liver failure, may result in
profound coagulopathy. The major regulators of clotting are
protein C, which breaks down factors Va and VIIIa; antithrom-
bin, which inactivates thrombin and factors Xa and IXa; and
plasmin, which cleaves fibrin. Recombinant plasminogen activa-
tors are widely available and are used to treat myocardial infarc-
tion, ischemic stroke, and pulmonary embolism.
The most frequently used tests of the clotting system, such as
prothrombin time, partial thromboplastin time, and the interna-
tional normalized ratio (which is a standardized modification of
the prothrombin time), are not functional assays of clotting. The
addition of data from checking bleeding time, platelet counts,
fibrinogen, or the concentration of individual clotting factors does
little to improve the assessment of this important system. Throm-
boelastometry is based on an assay that was initially used more
than 60 years ago and is a functional assay of clotting and clot
lysis. This test is performed with a small amount of sampled blood
(300 µL) to which a rotational force is applied, and a filament
yields real-time data such as time to clot formation, clot strength,
and clot breakdown. The first component of the thromboelastog-
raphy tracing is the reaction or “R” time, which is analogous to
the data gleaned from checking partial thromboplastin time and
prothrombin time. The kinetic time measures the time it takes for
clot strength amplitude to increase from 2 mm to 20 mm and is
a measure of fibrin and platelet function. Maximum amplitude
assesses the maximum strength of clot, and the lysis index mea-
sures the dissolution of clot over time with a low lysis index
indicating hyperfibrinolysis.32 The clinical benefits of functional
clotting assays, especially from point-of-care testing in the ICU,
are numerous and may lead to more effective use of blood, blood
products, and other agents, which, it is hoped, will lead to fewer
complications, lower costs, and better outcomes.
As previously stated, ICU patients have multiple factors that
leave them susceptible to clotting complications such as DVT,
pulmonary embolism, and heparin-induced thrombocytopenia
(HIT). ICU patients do not present with typical symptoms of
DVT, such as thigh or calf pain, and physical findings are often
obscured by anasarca, but they are at high risk because of the
presence of Virchow triad: endothelial injury, venous stasis, and
a hypercoagulable state. Surveillance ultrasonography and venog-
raphy studies in ICUs have shown rates approaching 40%, and
of cases that extend to the thigh, approximately 50% result in
pulmonary embolism. Ultrasound is the diagnostic study of
choice to detect DVT because it is portable, quick, and relatively
inexpensive. Because of the high rate of DVT in the ICU,
prophylaxis is crucial, and all patients should have sequential
compression devices, stockings, and a pharmacologic agent such
as heparin or low-molecular-weight heparin unless otherwise con-
traindicated. Risk for DVT is highest in patients with major
thoracic or abdominal operations lasting 30 minutes or longer,
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CHAPTER 21  Surgical Critical Care 567
neurosurgical procedures, coronary artery bypass grafting, severe
trauma, hip fracture, spinal cord injury, surgery or chemotherapy
for malignancy, and congestive heart or respiratory failure. In
high-risk patients with an absolute contraindication for pharma-
cologic DVT prophylaxis, an inferior vena cava filter is indicated,
and most of these are now removable. Pulmonary embolisms can
range from clinically insignificant subsegmental clots found inci-
dentally on a CT scan to a main pulmonary trunk embolus that
causes hypoxia, hemodynamic instability, and death. With increas-
ing resolution of CT scans, more incidental subsegmental emboli
are being found, but it appears that anticoagulation is not indi-
cated for these patients. Patients with larger pulmonary embo-
lisms should receive systemic anticoagulation with subsequent
conversion to oral agents. Patients with marked hypoxia or hemo-
dynamic instability typically require systemic thrombolytic
therapy with tissue plasminogen activator unless otherwise con-
traindicated. Large symptomatic pulmonary embolisms also may
be treated by interventional radiologic procedures and in rare cases
surgical thrombectomy. The decision to use systemic anticoagula-
tion or tissue plasminogen activator should not be made lightly
because of bleeding risks. A careful appraisal of risks and benefits
and a discussion with consultants and the surgeon of record
should be undertaken and documented in the medical record.
Heparin-Induced Thrombocytopenia
HIT is a serious complication that can result from exposure to
heparin products with unfractionated heparin having the highest
risk and low-molecular-weight heparins having the least risk.
There are two types of HIT. Type 1 HIT is a less serious, non–
immune-mediated form that causes clumping of platelets, but the
effects appear to be more transient and self-limited. Type 2 HIT
involves the development of heparin-associated antiplatelet anti-
bodies and occurs within a few days of heparin exposure or sooner
if the patient has been sensitized from prior exposure. The mani-
festations of type 2 HIT can be severe and include venous and
arterial thromboembolism. Because thrombocytopenia is common
in the ICU but may portend dangerous type 2 HIT, many clini-
cians use the 4T score, which combines the timing and severity
of the thrombocytopenia, occurrence of new thrombosis, and the
presence of alternative explanations for thrombocytopenia to
guide the workup and management of HIT. In one review, despite
use of the 4T score, the diagnosis of HIT was considered in 15%
of ICU patients but confirmed in less than 1%. Patients with a
platelet count less than 50,000 µL or whose platelet count
decreases 50% or more of baseline are usually evaluated for HIT
with an enzyme-linked immunosorbent assay (ELISA) or sero-
tonin release assay (SRA). ELISA testing is usually immediately
available, but the confirmatory SRA typically requires reference
laboratory testing; thus, for most patients, an ELISA screen can
be performed as a screening test. If the ELISA is positive and the
patient’s pretest probability of HIT is high, a direct thrombin
inhibitor such as argatroban should be started until results from
the SRA are available. In one of the largest reviews to date, a
positive ELISA was not confirmed by the SRA 86% of the time.
It is prudent to withhold all heparinoids while the diagnosis of
HIT is being ruled out, unless the patient’s probability of HIT
before testing is exceedingly low.
Critical Illness Anemia and Transfusion
Anemia in the ICU is common and is the result of decreased
erythrocyte production, daily phlebotomy, hemodilution, and
bleeding events. Evidence shows that greater than 25% of patients
568 SECTION III  Trauma and Critical Care
in a surgical ICU on any given day receive a transfusion, most
often of packed red blood cells, and that 85% of patients who are
in the ICU for more than 1 week receive a transfusion. Most
critically ill patients with anemia do not have active blood loss,
and the issue is more often one of inadequate erythrocyte produc-
tion in the face of phlebotomy and dilution. Inflammatory condi-
tions upregulate hepcidin, which results in iron sequestration in
the liver and macrophages, diminishing erythropoiesis by the
bone marrow. Anemia in the ICU is assumed to result in decreased
oxygen carrying capacity and is theorized to contribute to poorer
outcomes, but evidence to support this contention is lacking;
however, there is a wealth of data showing that liberal transfusions
contribute to many complications and poor outcomes. In light of
these data, restrictive transfusion practices are the norm in most
ICUs at the present time, although some clinicians still adhere to
liberal transfusion strategies based on tradition. The exception to
restrictive transfusion is an actively bleeding patient in whom
transfusions need to replace not only what is lost but also what
will be shortly lost.
Blood therapy remains a challenging and sometimes contro-
versial topic in the ICU, despite a markedly decreased risk of
blood-borne infectious complications compared with the past.
Long gone are the days when blood was considered a “tonic” to
perk up patients, and most clinicians now recognize that the
oxygen carrying capacity of banked blood is limited because of
depletion of 2,3-diphosphoglycerate and adenosine triphosphate,
two factors critical to oxygen delivery at the cellular level. Addi-
tionally, many of the adverse effects of blood are being recognized
(e.g., transfusion-related acute lung injury and immunosuppres-
sion). Transfusion-related acute lung injury appears to be medi-
ated by soluble factors derived from the donor that cause
pronounced immune activation in the recipient that may lead to
ARDS and MSOF. In 1999, the TRICC trial, a landmark ran-
domized trial that examined transfusion requirements in critical
care, showed decreased mortality when a restrictive transfusion
practice was compared with a liberal transfusion practice. This
study established hemoglobin less than 7 mg/dL as a “transfusion
trigger” for most patients, and the mortality benefit was still
observed in patients with preexisting cardiac disease.33 Additional
research confirmed that hemoglobin levels of 7 mg/dL are well
tolerated by ICU patients, and the only patients who benefit from
more liberal transfusion are patients who are actively bleeding or
manifesting acute coronary ischemia.
Massive Transfusion Strategies
and Anticoagulation Reversal
Massive transfusion, defined as administration of 10 U of packed
red blood cells given over a 24-hour period, is occasionally
required for patients with severe trauma, gastrointestinal hemor-
rhage, or ruptured abdominal aneurysms. In these patients, large-
volume resuscitation with crystalloid fluids must be avoided
because this leads to worsening coagulopathy and death. Exsan-
guination is still the leading cause of death of trauma patients and
is often the result of the deadly triad of coagulopathy, acidosis,
and hypothermia; these conditions should be avoided and cor-
rected at all costs. Once surgical control of bleeding is obtained,
massive transfusion protocols can be lifesaving and aim to resus-
citate patients with a balance of packed red blood cells, fresh-
frozen plasma (FFP), and platelets, while minimizing the
administration of crystalloid. This resuscitation strategy has been
termed hemostatic resuscitation. Although the exact ratio of these
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products is still being defined and verified, it appears that patients
approaching a 1 : 1 : 1 ratio have favorable outcomes. A retrospec-
tive review of more than 400 patients with trauma-induced coagu-
lopathy confirmed that patients given a 1 : 1 ratio of FFP to red
blood cells had markedly lower mortality (28% versus 51%) than
patients given a 1 : 4 ratio. Concerns have arisen about the
increased administration of FFP because of its pooled nature and
potential to promote inflammatory responses such as transfusion-
related acute lung injury and ARDS, and these concerns have
been corroborated by a study that found elevated risk of ARDS
and MSOF with increasing amounts of FFP but decreased risk
when cryoprecipitate was used. Cryoprecipitate is a blood product
that contains high amounts of fibrinogen, von Willebrand factor,
and factor VIII. Many centers have added this product to their
massive transfusion protocols to decrease the use of plasma and
to avoid depletion of the factors in cryoprecipitate that are almost
absent in FFP.
Factor VIIa, prothrombin complex concentrates (PCC), and
tranexamic acid are massive transfusion protocol adjuncts that
decrease the use of blood products and help to control hemor-
rhage. Activated recombinant factor VII promotes clotting by
initiating a thrombin burst on the surface of activated platelets;
it showed great promise as the “universal hemostat,” but some of
this enthusiasm has waned because of the drug’s high cost and
limited evidence that it reduces mortality in patients with severe
traumatic injury. PCC is derived from human blood and contains
varying amounts of the vitamin K–dependent factors II, VII, IX,
and X and protein C and S. PCC is growing in popularity as a
reversal agent for patients taking anticoagulants, especially the
so-called novel anticoagulants. PCC was intended to counteract
the coagulopathy induced by warfarin, which is mediated through
inhibition of the terminal carboxylation of the vitamin K–
dependent clotting factors. Three PCCs are composed of factors
II, VII, and X, and four factor agents have those plus added factor
VII. The emergence of innovative anticoagulants such as dabiga-
tran and rivaroxaban, direct thrombin and factor Xa inhibitors,
respectively, has expanded the role of PCC. Previously, warfarin
was reversed through the administration of vitamin K or FFP if
urgent reversal was indicated. PCCs are stored in powder form
and can be quickly reconstituted for reversal of warfarin without
the concerns for volume overload associated with large quantities
of FFP administration. Tranexamic acid inhibits fibrinolysis by
blocking a binding site on plasminogen and has been shown to
reduce the risk of hemorrhage and death significantly in a study
of more than 20,000 bleeding trauma patients. This trial, the
CRASH-2 trial, demonstrated its mortality benefit without a
significant increase in vascular occlusive events; however, the role
of tranexamic acid outside of trauma is still being investigated.34
ENDOCRINE SYSTEM
Glucose Control
Hyperglycemia is common in the ICU and can be the result of
many different conditions, but the two main causes are increased
glucose production and peripheral insulin resistance. These condi-
tions can occur in the same patient and even at the same time;
thus, hyperglycemia is thought to be a marker of systemic inflam-
mation. Multivariate analysis has shown that hyperglycemia is an
independent risk factor for adverse outcomes after trauma, sepsis,
and TBI because it contributes to infections, neuropathy, immu-
nosuppression, and organ dysfunction. Many aspects of granulo-
cyte function are adversely affected by glycosylation, including

chemotaxis, phagocytosis, and the efficacy of the respiratory burst,
so bacterial infections are more prevalent in hyperglycemic indi-
viduals. Previously, most of the evidence concerning the effect of
hyperglycemia on outcomes was derived from patients undergo-
ing open heart surgery and patients with myocardial infarction,
but more recent data from diverse patient populations of critically
ill patients have clarified some of the controversy.
The term tight glucose control was derived from the experience
of patients undergoing open heart surgery and the finding that
hyperglycemia led to increased rates of sternal dehiscence or medi-
astinitis after coronary bypass operations. Several years later, van
den Berghe’s group published a landmark article showing that
patients with mechanical ventilation who had their glucose con-
trolled in a very narrow range of 80 to 110 mg/dL had lower
incidences of bloodstream infection, sepsis, need for renal replace-
ment, ICU neuropathy, and mortality.35 This single trial ushered
in the era of tight glucose control for all ICU patients, and most
quality organizations embraced this as “standard of care” drown-
ing out the voices of some providers who questioned the repro-
ducibility of the results. Later, the Normoglycaemia in Intensive
Care Evaluation Survival Using Glucose Algorithm Regulation
(NICE-SUGAR) study revealed that tight glucose control led to
more episodes of hypoglycemia, which significantly increased
mortality.36 Subsequent trials confirmed this finding, and hypo-
glycemia was recognized as an independent predictor of mortality.
At the present time, glucose values of most ICU patients are
maintained in the range of 150 to 180 mg/dL, which was the
range of the patients undergoing open heart surgery who had the
better outcomes decades before. The experience with tight glucose
control in the ICU is an excellent cautionary tale of what can
happen when major shifts in care are driven by a single random-
ized controlled trial, no matter how well designed it is.
Adrenal Insufficiency
The hypothalamic-pituitary-adrenal axis is central to the “fight-
or-flight” state and has served humans well in this capacity, but
in times of severe critical illness it can soon become exhausted.
Endogenous vasopressin and corticosteroids are often depleted in
shock states with profound adverse effects on hemodynamics. The
finding that supplementation of glucocorticoids and mineralocor-
ticoids to patients in septic shock decreased short-term mortality
began an era of widespread use of corticosteroids for shock, and
similar to the experience following the article by van den Berghe
and colleagues, steroid therapy became standard therapy based
on this single publication despite concerns about immunosup-
pression, wound healing, and glucose control. In this study,
patients were given a synthetic adrenocorticotropic hormone to
identify the patients who had relative adrenal insufficiency requir-
ing steroid supplementation; although steroids reduced pressor
requirements and 28-day mortality, mortality at 1 year was unaf-
fected.37 In 2008, the Corticosteroid Therapy of Septic Shock
(CORTICUS) randomized trial confirmed what many clinicians
had anecdotally observed—that steroids might reduce vasopressor
requirements, but mortality was not reduced.38 Adrenocortico-
tropic hormone stimulation testing has fallen out of favor since
CORTICUS confirmed that the results of this test are unimport-
ant to guide therapy, and steroid supplementation is reserved for
patients with shock refractory to fluids and vasopressors. ICU
patients who are on long-term steroids for medical comorbidities
should be given bioequivalent doses of intravenous hydrocorti-
sone and converted to their long-term dose when they resume oral
intake.
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CHAPTER 21  Surgical Critical Care 569
INFECTION IN THE INTENSIVE CARE UNIT
Fever and Approach to Infections
Critical illness increases the incidence of infections for a multitude
of reasons, but surgical patients have an even greater risk because
of factors unique to this patient population. Hemorrhagic shock,
trauma, wounds and incisions, drains, catheters, tubes, devitalized
tissue, hematomas, immunosuppressants, and malnutrition are
just some of the many reasons why surgical ICU patients have the
greatest risk of infection among all critical care settings. To com-
plicate matters further, surgical ICU patients often have manifes-
tations of SIRS, which limits the predictive value of the classic
signs of infection, such as fever and leukocytosis. In light of these
manifestations of SIRS, fever in surgical ICUs is typically defined
as 101.5° F and much higher in patient with burns or a heavy
burden of necrotic tissue.
The evaluation of fever should begin with consideration of all
potential sources of infection in the patient followed by a focused
physical examination that explores every one of those possibilities.
All dressings, wounds, and devices should be evaluated. The saying
“look for the hand of man” can help pinpoint the likely source of
infection, and operative reports and the medical record should
not be overlooked, keeping in mind that less than 20% of fever
in the first 2 days after elective surgery is due to an infection.39
Analogous to the secondary survey of trauma, the ICU patient
should be examined from head to toe looking for the infectious
source. Alterations in mental status, craniectomy, or monitoring
devices render meningitis a possibility, whereas nasogastric or
feeding tubes make sinusitis more likely. Intubation, aspiration,
pulmonary contusion, and altered mental status all increase the
risk of pneumonia, and chest tubes, surgery, and trauma make
empyema a distinct possibility. All indwelling tubes and devices
should be considered a breach in the normal host defense mecha-
nisms and are potential points of ingress for bacteria and infec-
tion. As is the case in blunt trauma, the evaluation of the abdomen
is most challenging because the potential sources here are almost
too numerous to list; in addition to infections resulting from
recent operations or injury, the patient may be at risk for common
intra-abdominal processes such as appendicitis. Anastomotic
breakdown, intra-abdominal abscess, infectious colitis, and acal-
culous cholecystitis are some of the more common causes of
intra-abdominal infection, and patients should be approached the
same methodical way as ICU patients with fever—a thorough
consideration of potential sources, followed by a focused examina-
tion. If the source of the fever or infection is not found or if the
provider is unsure, the decision to seek imaging studies or labora-
tory evaluation needs to be made.
For most patients, including patients on the ward, fever and
leukocytosis are usually indicative of infection, but as noted previ-
ously, this is not the case in the ICU. Other signs of infection
should be sought, including changes in vital signs such as
tachycardia, oliguria, hyperglycemia, and new-onset hypoxemia.
Feeding intolerance is often an early, subtle sign of an impending
infection, and ileus usually accompanies any intra-abdominal
process. Worsening liver dysfunction, increasing creatinine, new-
onset lactic acidosis, and a left shift on the differential are worri-
some findings and may be associated with infection. Any
degradation in a previously stable organ system may be a mani-
festation of sepsis, as illustrated by worsening oxygenation despite
stable ventilator settings in the case of VAP or peritonitis. In
contrast to medical intensivists, surgical intensivists have the
ability to obtain “source control.” Complete compliance with all
570 SECTION III  Trauma and Critical Care
elements of the sepsis bundle do the patient little good unless
perforated diverticulitis, fecal peritonitis, or necrotizing soft tissue
infection is not addressed first. Keeping this in mind should alter
how surgeons view antibiotics—that is to say, drainage of abscesses,
resection of necrotic or infected tissue, or removal of infected
devices should be undertaken without delay if possible, and anti-
biotics are adjuncts to this, the primary therapy. Occasionally,
antibiotics are not needed once source control has been obtained,
as is borne out by the treatment of a simple abscess, which is
primarily incision and drainage. In regard to antibiotic therapy in
ICU patients, less is often more, and the focus should be on
detecting and treating the source, with antibiotics used in a ratio-
nal fashion rather than indiscriminately starting or adding them
haphazardly.
Central venous catheters are common in the ICU and are
useful for medication or fluid administration, vasopressor agents,
TPN, and hemodynamic monitoring. CLABSI is a serious, iatro-
genic complication of ICU care that carries distinct morbidity and
mortality risks as well as increased length of stay and hospital
charges. Advances (e.g., antibiotic-impregnated catheters, antisep-
tic dressings and hubs) have had some positive effect on CLABSI
rates, but the most important way to reduce the risk of CLABSI
is remove the catheter. It is a good practice on ICU rounds to
evaluate the need for each tube, catheter, or device every day so
that the devices may be removed as soon as possible. Obviously
infected lines, indicated by draining purulence or erythema,
should be removed immediately, whereas catheters suspected of
being infected may be wire changed and the tip sent for culture.
Catheters must be removed if the tip culture returns with more
than 15 colonies of bacteria. If there are positive blood cultures
and a central line was present for more than 2 days including the
day before or the day the cultures were drawn, the CDC criteria
for a CLABSI have been met. Common pathogens are Staphylo-
coccus species; gram-negative and fungal pathogens may infect
lines placed in the femoral position. Central lines should be
inserted following a standard protocol or bundle that includes
hand washing, chlorhexidine skin preparation, maximal barrier
precautions, and a bedside nurse monitor looking for breaks in
sterility. Similar to many aspects of ICU patient care at the present
time, central line insertion, maintenance, and access are governed
by standardized protocols and bundles of care to reduce rates of
CLABSI.
Pneumonia, discussed extensively in the Respiratory System,
is the most common cause of death in patients with infections
acquired in the ICU, and most of these cases are associated with
mechanical ventilation. Ideally, VAP is diagnosed using quantita-
tive cultures because this allows for the most effective de-escalation
of antibiotics. Empirical antibiotics against the most likely organ-
ism should be started and then tailored as culture results become
available. Methicillin-resistant Staphylococcus aureus and the non–
lactose fermenting gram-negative rods termed SPACE organisms
(Serratia, Pseudomonas, Acinetobacter, Citrobacter, and Enterobac-
ter) should receive 14 days of therapy, whereas all other pathogens
can be treated for 1 week. Lung penetration of many antibiotics
is poor, and the pharmacokinetics of dosing antibiotics in criti-
cally ill patients can be challenging so input from a clinical phar-
macist should be sought out if available.
Catheter-associated urinary tract infection (CAUTI) in the
ICU is a common problem and typically due to the frequent
use of bladder catheters. Similar to central venous catheters, the
risk of developing an infection coincides with the duration the
catheter is indwelling. Coverage of the catheter with a biofilm
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facilitates bacterial colonization and migration, and this process
affects almost every indwelling foreign body over time. Workup
for CAUTI involves sending a urinalysis and urine culture;
however, the urinalysis can be unreliable because pyuria and leu-
kocyte esterase are often absent in ICU patients with documented
infections, whereas nitrates indicate only Escherichia coli or Entero-
bacter infection. In contrast to outpatient populations, ICU
CAUTI is often due to multidrug-resistant gram-negative rods or
fungal organisms, so duration of antibiotic treatment is typically
7 days because of the “complicated” nature of CAUTI in this
setting. The presence of Candida organisms in the urine of ICU
patients is termed candiduria and generally reflects colonization
rather than true infection. Candiduria is more common in patients
with poor glucose control and in patients who recently received
broad-spectrum antibiotics. Antifungal agents are indicated when
Candida organisms are recovered on culture from two different
sites; however, it is prudent to initiate coverage in patients who
have had recent genitourinary procedures, renal transplantation,
or marked neutropenia. Most Candida species are susceptible to
azole agents, such as fluconazole, but Candida glabrata and other
strains of yeast exhibit resistance to this agent and may require
treatment with an echinocandin such as caspofungin. For highly
resistant organisms, amphotericin may be required and should be
given as a bladder irrigant to avoid systemic toxicity. Similar to
CLABSI and VAP, it is difficult to get a CAUTI if the Foley
catheter is removed as soon as possible, so most institutions have
embraced this philosophy, including in ICU patients.
Clostridium difficile infection is not as common as VAP or
CAUTI, but it can follow a virulent course progressing rapidly to
florid septic shock, renal failure, acidosis, and death. C. difficile
infection is associated with dysbiosis or imbalances in colonic flora
caused by exposure to antibiotics, with agents having a broad
spectrum against anaerobes causing the greatest degree of dysbio-
sis. Treatment of C. difficile with metronidazole further disrupts
the normal colonic flora, which sets the stage for recurrent epi-
sodes and carrier states. Although C. difficile is the most common
cause of nosocomial diarrhea, it sometimes manifests as ileus and
constipation, so providers should not equate this disease only with
diarrhea. Most cases of diarrhea in the ICU are not due to C.
difficile but rather medications such as sorbitol-containing elixirs,
enteral tube feeds, and malabsorption. The diagnosis of C. difficile
is accomplished through polymerase chain reaction, which is more
sensitive than prior toxin assays, and standing orders for nurses
to send stool specimens as they see fit have been shown to reduce
time to diagnosis. The new NAP-1 strain of C. difficile often
progresses to megacolon, shock, and need for emergent colectomy.
Patients should initially be treated with metronidazole, but it is
acceptable to add oral vancomycin in areas where NAP-1 pre-
dominates. Fidaxomicin, which has activity against C. difficile but
causes less disturbance to normal colonic flora, has been shown
to be an effective therapy and is associated with lower recurrence
rates. C. difficile colitis that progresses to septic shock or renal
failure is best treated by emergent colectomy because it is unlikely
that antibiotics would be a successful therapy at that point. Initial
reports of less invasive approaches for toxic colitis, such as loop
ileostomy and colonic lavage with osmotic laxatives and antibiot-
ics, have shown promising results, as has fecal transplant, but
further investigation is necessary.
Sepsis Strategies
Approximately 40% of all ICU patients have sepsis on admission
or manifest it at some point during their ICU stay, and the

resource utilization and costs of treatment for it are staggering.
The term sepsis is derived from the Greek word meaning “to rot
or decay,” and sepsis lies on a continuum of illness progressing
from SIRS to severe sepsis and septic shock. These conditions were
defined more than 2 decades ago, and this common language has
helped guide therapy and the ability of clinicians to offer a prog-
nosis for critically ill patients.40 SIRS is defined by the presence
of two or more of the following criteria: temperature less than
36° C or greater than 38° C, heart rate greater than 90 beats/min,
white blood cell count less than 4000/mm3 or greater than
12,000/mm3 or band neutrophils greater than 10%, and respira-
tory rate greater than 20 or arterial carbon dioxide pressure less
than 32 mm Hg. As previously noted, many surgical patients
meet SIRS criteria on ICU admission, which can make the diag-
nosis of sepsis a challenge. Sepsis is defined by the presence of
SIRS with an infection, whereas severe sepsis is sepsis with signs
of end organ failure (e.g., oliguria, altered mental status, acidosis).
Finally, septic shock is at the end of the spectrum and is present
when patients with sepsis develop hypotension despite adequate
fluid resuscitation and require vasopressor support.
The Surviving Sepsis Campaign (www.survivingsepsis.org), ini-
tially launched in 2002 and revised several times since, is a notable
example of a strategy designed by clinicians and investigators to
improve outcomes. The original concept was driven by a strategy
that stressed early targeted physiologic goals of resuscitation that
changed the management of critically ill medical patients far more
than surgical patients. The campaign consists of two sets of bundled
elements to be fulfilled in the first 3 and 6 hours from the time the
patient is diagnosed with sepsis—the so-called time zero. The
3-hour bundle calls for measurement of lactic acid level, blood
cultures to be drawn before initiating antibiotics, administration
of broad-spectrum antibiotics, and boluses of 30 mL/kg of crystal-
loid fluid for hypotension or lactic acid greater than 4 mmol/liter.
The later bundle suggests the use of vasopressors to maintain MAP
greater than 65 mm Hg, measurement of CVP and ScvO2, and
rechecking lactic acid level levels. The targeted physiologic goals
are a CVP 8 mm Hg or greater, ScvO2 greater than 70%, and cor-
rection of lactic acidosis. The initial bundle elements of corticoste-
roids, tight glucose control, and activated protein C were modified
as new evidence emerged about their use as noted in previous sec-
tions. Although activated protein C was initially promising, this
drug was withdrawn from the market in 2011 after failing to
improve outcomes, although many surgical patients could not
receive this drug because of concerns over postoperative hemor-
rhage. The treatment of sepsis and septic shock continues to focus
on meeting the bundled care goals in a timely fashion because high
bundle compliance rates have been shown to reduce mortality.
Although the bundled care elements of the Surviving Sepsis Cam-
paign have benefited patients with sepsis syndromes, the impor-
tance of surgical source control cannot be overstated. Also, evidence
regarding the long-term sequelae of surviving sepsis is often unfa-
vorable because these patients have been shown to have significant
and lasting functional and cognitive impairments that adversely
affect quality of life.41 There is a great need for high-quality, risk-
stratified data on long-term outcomes of sepsis and critical illness,
as emerging data show that many of these patients have significant
issues regarding adverse quality of life.
Antibiotic Stewardship
It has been repeatedly shown that infected patients who receive
the right empirical antibiotic at the right time have better out-
comes because delays in effective antibiotic therapy lead to higher
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CHAPTER 21  Surgical Critical Care 571
BOX 21-2  Benefits of Antibiotic
Stewardship in the Intensive Care Unit
• Decreased development of resistant organisms
• Reduced nephrotoxicity and acute kidney injury
• Decreased Clostridium difficile risk
• Decreased opportunistic fungal infections
• Reduced costs and resource consumption
mortality. It has also been noted that unnecessary or extended
antibiotic use exposes the patient and other patients to immediate
and long-term hazards. These two conflicting truths highlight the
predicament that clinicians face when dealing with a patient with
a potential infection, and although most opt to start empirical
antibiotic therapy, this decision is often questioned when faced
with a patient in fulminant septic shock caused by unnecessary
antibiotic-induced C. difficile colitis. Unnecessary overuse of anti-
biotics led the World Health Organization to publish a statement
sounding the alarm as resistant pathogens are emerging at far
faster rates than novel antimicrobials are being developed, which
threatens to become a danger to the health of people worldwide.
In addition to concerns over the development of resistance and
C. difficile colitis, inappropriate antibiotic therapy exposes patients
to nephrotoxicity, allergic reactions, opportunistic fungal infec-
tions, and volume overload, there are global issues of costs, waste,
and drug shortages (Box 21-2). The concept of antibiotic steward-
ship is important in health care but more so in the ICUs because
the highest rates of antibiotic use occur here. The components of
this stewardship include a critical appraisal of the need for anti-
biotics on daily rounds, a review of culture results to eliminate
unnecessary agents, de-escalation from broad-spectrum to narrow-
spectrum agents whenever possible, and establishing a stop date
for the antimicrobial therapy. Multidisciplinary stewardship pro-
grams have been shown to reduce inappropriate antibiotic use,
decrease the development of resistance, and lessen hospital costs
without worsening patient outcomes.
PROPHYLAXIS IN THE INTENSIVE CARE UNIT
Stress Ulcer Prophylaxis
Critically ill patients have factors (e.g., decreased mucosal bicar-
bonate and mucus production and splanchnic ischemia) that
result in weakening of the gastric mucosal defenses setting the
stage for gastritis and bleeding. Although these events are rare,
occurring in less than 2% of ICU patients, bleeding may be heavy
resulting in the need for transfusions and emergency surgery. Most
critically ill patients have a reduction in their gastric acid secre-
tion, and bleeding episodes are due entirely to loss of mucosal
defenses. Stress ulcer bleeding is an ominous development because
these patients have been shown to have markedly higher mortality
rates. The classic finding on upper endoscopy is multiple areas of
ulceration or petechial erosions, particularly in the gastric fundus;
this entity cannot be treated endoscopically because diffuse bleed-
ing arises from superficial mucosal capillaries. The primary pre-
vention of stress ulcer bleeding centers around decreasing acid
production despite the fact that the pathophysiology suggests the
mucosal changes drive this process. In many ICU patients, pro-
phylaxis is likely overused, and some data suggest that this pre-
disposes the patient to pneumonia and C. difficile infections as
well as increasing health care costs. Retrospective reviews have
identified patients at high risk for stress ulcer bleeding, and
572 SECTION III  Trauma and Critical Care
patients with the following conditions should receive prophylaxis:
respiratory failure and mechanical ventilation, hemodynamic
instability requiring vasopressors, liver failure, coagulopathy, TBI,
spinal cord injury, organ transplantation, and burns.
Various medications have been tried over the years to prevent
stress ulcer bleeding, including anticholinergics and antacids,
which had unwanted side effects and limited efficacy. The intro-
duction of cimetidine, the first histamine 2 (H2) receptor antago-
nist, ushered in a new era in medicine that saw a dramatic
reduction not only in stress ulcer bleeding but also in peptic ulcer
disease. The addition of sucralfate, an aluminum sulfate com-
pound that functioned as a direct mucosal protection, offered
additional therapeutic options, but this agent was cumbersome to
use because medications and enteral feeding had to be held around
its dosing several times a day. At the present time, sucralfate and
cimetidine have been replaced entirely by more modern H2 recep-
tor antagonists and PPIs. The literature comparing the efficacy
and costs of these two agents is conflicting, and although PPIs are
far more potent than H2 receptor antagonists, this potency has
not been proven to offer superior efficacy against stress ulceration.
A meta-analysis suggested that PPIs may be marginally more effec-
tive than H2 receptor antagonists at reducing stress ulcer bleeding,
but these benefits are likely offset by their significantly higher cost.
At the present time, PPIs and H2 receptor antagonists both appear
to be effective agents against stress ulceration, and the choice boils
down to costs and drug availability until more randomized data
become available.
Venous Thromboembolism Prophylaxis
As mentioned in the Hematologic System, critically ill patients
are at high risk for VTE because almost all of them have the
factors comprising Virchow triad. Patients who have experienced
total joint replacement surgery, multisystem trauma, severe ortho-
pedic injuries, or recent spinal cord injury are at the highest risk
for VTE, although any patients with prolonged immobility should
be considered at risk. In contrast to stress ulcer bleeding events,
VTEs are a frequent occurrence in the ICU, and surveillance
studies of trauma patients found DVT rates of 50%.42 The most
significant consequence of VTE is pulmonary embolism (dis-
cussed in detail in the Respiratory System), which can be fatal.
All ICU patients should receive mechanical VTE prophylaxis in
the form of compression stockings and sequential pneumatic
devices, which are thought to activate tissue plasminogen and
promote local fibrinolysis. Patients with lower extremity fractures
or ischemic peripheral vascular disease may not be candidates for
these devices. For most ICU patients, mechanical VTE prophy-
laxis is inadequate, and pharmacologic prophylaxis is indicated.
Pharmacologic prophylaxis has been shown to reduce VTE and
pulmonary embolism compared with mechanical devices or no
prophylaxis at all. In the past, the most commonly used pharma-
cologic agent was unfractionated heparin given subcutaneously,
but there has been a move away from heparin as newer agents
have become available. Enoxaparin, a low-molecular-weight
heparin, was found to reduce the risk of DVT by 30% compared
with unfractionated heparin in a group of high-risk trauma
patients, without a difference in adverse events. This trial and
subsequent ones have established enoxaparin as preferred VTE
prophylaxis for high-risk patients. In contrast to enoxaparin, only
a small amount of unfractionated heparin is metabolized by the
kidneys, and it is often used in patients with AKI.
With the increasing obesity epidemic, it is likely that many
patients are receiving inadequate prophylactic doses of VTE
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prophylaxis. Enoxaparin was approved with fixed dosing, but the
advent of an assay for activated factor X along with treatment
failures in obese patients led to the interest in weight-based dosing.
Enoxaparin dosed 0.5 mg/kg twice daily based on actual body
weight, targeted for anti–factor Xa levels of 0.2 to 0.5 IU/mL has
been shown to be an appropriate and safe strategy for obese ICU
patients. Most of the data on dosing obese patients have come
from the bariatric literature, and few data on critically ill obese
patients are available. ICU patients who are at high risk for VTE
but cannot be anticoagulated for an extended period, such as
patients with hemorrhagic stroke, should receive an inferior vena
cava filter. These filters do not prevent DVTs; they prevent large
pulmonary embolisms, although small pulmonary embolisms
may make it through to the lungs. Inferior vena cava filters are
typically placed in the operating room, but bedside placement
using intravascular ultrasound or fluoroscopic guidance is gaining
interest. Bedside placement has realized savings in cost, operative
time, and need for transport, while increasing timeliness of place-
ment without problems of malpositioning.
SPECIAL ISSUES
Long-Term Intensive Care Unit Outcomes
Since the days of Semmelweiss and Codman, surgeons have been
at the forefront of advancing quality in health care, a concept that
has only more recently taken hold in the rest of health care as
governmental and other organizations have embraced the “quality
movement.” Modern ICU care has made significant progress as
technology and medications have improved, but some of the most
dramatic advancements in the quality of care have been driven by
the embrace of evidence-based practice. These changes coupled
with an aging population who are living longer with more comor-
bidities has called into question some of the purpose of critical
care as the focus turns from quantity of life to quality of life. Until
more recently, most research in the ICU was based on short-term
outcomes, such as 30-day mortality or survival to discharge, but
as the amount of organ failure that can be supported has grown
along with increasingly complex care, patients, families, and pro-
viders are questioning the outcomes of ICU survival. Research
into the long-term physical, cognitive, and emotional outcomes
of ICU discharge is in its infancy, and much remains to be
learned, but this begs the difficult question: What will be the
application of these outcomes data once known?
Some of the initial studies of long-term ICU care are becoming
available, and some of the revelations are disconcerting. “Surviving
intensive care: a report from the 2002 Brussels Roundtable” was
a landmark article in Intensive Care Medicine that suggested that
short-term outcomes such as in-hospital mortality were poor mea-
sures of “patient-centered outcomes.” The authors also introduced
the concept that the health and well-being of families of ICU
patients should also be included in research looking at outcomes
of critical care. Most importantly, the concept of health-related
quality of life (HRQOL) arose from this gathering in Brussels as
an outcomes measure to affirm focus on the patient beyond what
transpires in the ICU.43 Surgeons need to know about the long-
term outcomes of critical illness so that they can better counsel
patients and families during the perioperative period because care
is “beginning and ending outside the ICU box.”43
Most long-term ICU outcomes research has involved hetero-
geneous patient populations with far more medical ICU patients
than surgical patients, and although this limits the applicability
of these data to surgical patients, it does not completely invalidate

the data. In a 2011 prospective longitudinal study, Khouli and
associates44 showed that one third of patients admitted to the ICU
died within 6 months and that the oldest survivors had the poorest
results on HRQOL questionnaires. In that study, chronic obstruc-
tive pulmonary disease present before ICU admission was the
most significant predictor of mortality at 6 months. Mortality at
1 year after ICU discharge for septic patients was shown to be
surprisingly high, as was the presence of lasting cognitive impair-
ment. Compared with age-matched healthy control subjects, ICU
patients who survive to 6 months after discharge demonstrated
worse physical function, general health, and social functioning,
and their HRQOL outcomes remained poor compared with base-
line.45 The need for RRT after ICU discharge has been associated
with dismal results with almost uniform mortality at 3 months in
nonsurgical patients older than 75 years. Patients with ARDS
during their ICU stay have been shown to have lasting difficulties
with muscle weakness, depression, and significant physical limita-
tions but surprisingly few pulmonary limitations. Although long-
term data after traumatic injury are limited, it appears that many
of these patients return to their previous level of health and
employment as long as they do not have significant TBI. Based
on what little data we have about post-ICU outcomes, it appears
that outcomes after ICU discharge for patients with traumatic
injury and patients with ARDS are not as dismal as outcomes for
patients with sepsis and oncologic patients.
End-of-Life Care
One of the most difficult discussions that a physician can have
with a patient centers around goals of care, particularly as the
patient becomes elderly or develops a serious illness. Because this
discussion is so difficult, many patients arrive in the ICU with
their wishes regarding end-of-life care ill-defined. Similarly, less
than 50% of Americans have a “living will” establishing what level
of support they want if they are critically ill or if treatment is
medically futile or what their long-term goals after discharge from
the ICU would be. Patients with intra-abdominal catastrophes,
shock, altered mental status, major trauma, or burns are not in
any condition to have such a discussion. It is imperative that the
ICU team remain in close contact with family members and
health care representatives of critically ill patients at all times.
Soon after a critically ill patient is admitted to the ICU and after
the intensivist has had time to review the medical record, labora-
tory results, and other diagnostic studies, a meeting should be
held with the patient’s representatives to establish goals of care.
At that time, the provider needs to offer a frank assessment of the
patient’s status and a reasonable prognosis based on a synthesis of
all available data. It is equally important that the provider under-
stand what the patient’s wishes for outcomes after ICU discharge
are, what restrictions or limitations the patient would be willing
to accept, and how much the patient would be willing to endure
to achieve those goals (Table 21-4). If the patient is unable to
communicate the answers to these questions, the patient’s repre­
sentatives must provide answers. The amalgamation of all this
information is how the goals of therapy are established, and a
determination of an advance directive (i.e., code status) com-
monly is made at this time. Periodic meetings are needed as more
information becomes available and the clinical picture becomes
clearer. Open and nonadversarial communication becomes even
more important when a patient in the ICU experiences a decline
or has a complication of care, or there is an increased chance of
death. These discussions are best held in a quiet, private location,
rather than as an impromptu meeting in a hallway or the patient’s
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CHAPTER 21  Surgical Critical Care 573
TABLE 21-4  Adverse Long-Term
Outcomes for Intensive Care Unit Survivors
PHYSICAL COGNITIVE EMOTIONAL
LIMITATIONS LIMITATIONS ISSUES
Inability to do ADL Inability to do ADL Decreased social
functioning
Loss of independence Inability to concentrate Depression
Poor exercise tolerance Memory deficits Sleep disturbances
Neuromyopathies Poor problem solving PTSD
Unsteadiness Disorganization Anxiety
ADL, activities of daily living; PTSD, post-traumatic stress disorder.
room. Ideally, these meetings should be attended by representa-
tives from the ICU care team, family members, and the primary
surgeon if applicable. Small-scale meetings such as this typically
occur on a daily basis, and larger extended meetings are typically
held in response to significant developments, such as the need for
mechanical ventilation or RRT in response to major complica-
tions or if there has been a significant event such that previously
established goals are no longer possible. In the case of the latter,
this may open the door to a discussion of futility, not in terms of
medical futility, but rather futility that is patient defined.
Over the last 2 decades, there has been a major shift in how
end-of-life care is approached in the ICU. Previously, such
approaches used a paternalistic system where the physician was in
a dominant role establishing the plan; at the present time, patient
autonomy is foremost, and the physician serves more as an advisor
and facilitator of the patient’s wishes. Some authors call this “self-
determination,” which began in the early 1990s as more patients
were noted to seek “do not resuscitate,” “do not intubate,” and “do
not hospitalize” orders. Health care proxies were also more often
officially named as surrogate decision makers in cases where patients
lost mental capacity to make decisions. These trends have helped
guide the ICU team and have reduced the number of futile situa-
tions in the ICU. Another change is a better understanding of the
relationship between advances in ICU care, quality of life, and a
patient’s identity. With the vast technologic advances in critical
care, including salvage ventilation modes for ARDS, ECMO,
parenteral nutrition, and support devices such as left ventricular
assist devices, there is increasing ability to support patients and
stave off death for extended periods. End-of-life care has become
complicated because these therapies can make it difficult for family
members of patients to recognize just how ill or tenuous the patient
is. When communicating with families, it is important that the
ICU team convey the degree of illness and support the patient
requires to shift the discussion from meanings of biologic or physi-
ologic life to a different set of meanings. Walker and Lovat46 defined
a second level of life as a “sense of personhood and the essence or
meaningfulness of human life.” In essence, they were describing
the paramount importance of quality of life from the point of view
of the patient and the individuals who are meaningful to the
patient’s personhood. Thus, the discussion regarding end-of-life
care has morphed from “can we?” to “should we?”
When care has become medically futile or obtaining the
patient’s long-term goals is impossible, care shifts to alternative
strategies such as hospice care or withdrawal of support. Hospice
care aims to provide physical and emotional support to patients
and family members and may be rendered at home or in a facility.
A wide range of services are possible, including analgesia and
anxiolysis, oxygen, various medical devices, chaplain services, and
574 SECTION III  Trauma and Critical Care

counselors. For the sickest patients or patients on the highest levels
of organ support, it is impossible to leave the ICU because any
interruption of support would result in the patient’s death.
Hospice services can be arranged in an inpatient fashion, or the
patient can be made “comfort measures only” or “no escalation of
care” such that all potentially painful or invasive measures are
withheld. A “comfort measures only” patient per The Joint Com-
mission definition should receive only therapies that provide
maximum comfort during the natural process of dying, and all
other therapies should be avoided or discontinued. Mechanical
ventilation is often discontinued, and the patient’s air hunger is
treated with morphine, which is an example of the principle of
double effect. All attempts should be made to allow the patient’s
family to be at the bedside if the patient desires, and the patient
should be offered privacy as well as medical social work and chap-
lain support services so that the patient may die with dignity and
comfort in the presence of his or her extended family.
Iwashyna TJ, Ely EW, Smith DM, et al: Long-term cognitive
impairment and functional disability among survivors of severe
sepsis. JAMA 304:1787–1794, 2010.
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Kress JP, Pohlman AS, O’Connor MF, et al: Daily interruption of
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