in Minor Procedures
Complications of central venous access catheters are common.
Steps to decrease complications include the following:
- Ensure that central venous access is indicated.
- Experienced (credentialed) personnel should insert the catheter,
or should supervise the insertion.
- Use proper positioning and sterile technique. Controversy
exists as to whether or not placing the patient in the Trendelenburg
position facilitates access.
- Central venous catheters should be exchanged only for specific
indications (not as a matter of routine) and should be removed as
soon as possible.
Common complications of central venous access include:
Occurrence rates from both subclavian and internal jugular vein approaches
are 1 to 6%. Pneumothorax rates appear to be higher among
the inexperienced but occur with experienced operators as well.
If the patient is stable, and the pneumothorax is small (<15%), close
expectant observation may be adequate. If the patient is symptomatic,
a thoracostomy tube should be placed. Occasionally, pneumothorax
will occur as late as 48 to 72 hours after central venous access
attempts. This usually creates sufficient compromise that a tube
thoracostomy is required. Prevention requires proper positioning
of the patient and correct technique. A postprocedure
chest x-ray is mandatory to confirm the presence or absence of a
pneumothorax, regardless of whether a pneumothorax is suspected.
Arrhythmias result from myocardial irritability secondary to
guidewire placement, and usually resolve when the catheter or guidewire
is withdrawn from the right heart. Prevention requires
electrocardiogram (EKG) monitoring whenever possible during catheter
The inadvertent puncture or laceration of an adjacent artery
with bleeding can occur, but the majority will resolve with direct
pressure on or near the arterial injury site. Rarely will angiography,
stent placement, or surgery be required to repair the puncture site,
but close observation and a chest x-ray are indicated. Prevention
requires careful attention to insertion technique.
A guidewire or catheter that migrates into the vascular space
completely can be readily retrieved with interventional angiography
techniques. A prompt chest x-ray and close monitoring of the patient
until retrieval is indicated.
Although estimated to occur in only 0.2 to 1% of patients,
an air embolism can be dramatic and fatal. Treatment may prove futile
if the air bolus is larger than 50 mL. Auscultation over the precordium
may reveal a “crunching” noise, but a portable
chest x-ray is required for diagnosis. If an embolus is suspected,
the patient should immediately be placed into a left lateral decubitus
Trendelenburg position, so the entrapped air can be stabilized within
the right ventricle. Aspiration via a central venous line accessing
the heart may decrease the volume of gas in the right side of the
heart, and minimize the amount traversing into the pulmonary circulation.
Subsequent recovery of intracardiac and intrapulmonary air may require
open surgical or angiographic techniques. Prevention requires careful
attention to technique.
Flow-directed, pulmonary artery (“Swan-Ganz”)
catheters can cause pulmonary artery rupture due to excessive advancement
of the catheter into the pulmonary circulation. There usually is
a sentinel bleed noted when a pulmonary artery catheter balloon
is inflated, and then the patient begins to have uncontrolled hemoptysis.
Reinflation of the catheter balloon is the initial step in management,
followed by immediate airway intubation with mechanical ventilation,
an urgent portable chest x-ray, and notification of the OR that
an emergent thoracotomy may be required. If there is no further
bleeding after the balloon is reinflated, the x-ray shows no significant
consolidation of lung fields from ongoing bleeding and the patient
is easily ventilated, then a conservative nonoperative approach
may be considered. This approach might include observation alone
if the patient has no signs of bleeding or hemodynamic compromise;
however, more typically a pulmonary angiogram with angioembolization
or vascular stenting is required. Hemodynamically unstable patients
rarely survive because of the time needed to perform the thoracotomy
and identify the branch of the pulmonary artery that has ruptured.
The Centers for Disease Control and Prevention (CDC) reports
mortality rates of 12 to 25% when a central venous line
infection becomes systemic, and this carries a cost of approximately $25,000
per episode.47–50 The CDC does not recommend
routine central line changes, but when the clinical suspicion is
high, the site of venous access must be changed. Additionally, nearly
15% of hospitalized patients will acquire central venous
line sepsis. In many instances, once an infection is recognized
as central line sepsis, removing the line is adequate. Staphylococcus
aureus infections, however, present a unique problem because
of the potential for metastatic seeding of bacterial emboli. The
required treatment is 4 to 6 weeks of tailored antibiotic therapy.
Arterial lines are placed to facilitate arterial blood gas sampling
and hemodynamic monitoring. They are often left in place to make
routine blood sampling easier, but this practice leads to higher
Arterial access requires a sterile Seldinger technique, and a
variety of arteries are used, such as the radial, femoral, brachial,
axillary, dorsal pedis, or superficial temporal arteries. Although
complications occur less than 1% of the time, they can
be catastrophic. Complications include thrombosis, bleeding, hematoma,
arterial spasm (nonthrombotic pulselessness), and infection. Thrombosis
or embolization of an extremity arterial catheter can result in
the loss of a digit, hand, or foot, and the risk is nearly the same
for both femoral and radial cannulation. Thrombosis with distal
tissue ischemia is treated with anticoagulation, but occasionally
surgical intervention is required to re-establish adequate inflow.
Pseudoaneurysms and arteriovenous fistulae can also occur.
The principal risk of GI endoscopy is perforation. Perforations
occur in 1:10,000 patients with endoscopy alone, but have a higher
incidence rate when biopsies are performed (up to 10%).
This increased risk is due to complications of intubating a GI diverticulum
(either esophageal or colonic), or from the presence of weakened
or inflamed tissue in the intestinal wall (e.g., diverticulitis,
glucocorticoid use, or inflammatory bowel disease).
Patients will usually complain of diffuse abdominal pain shortly
after the procedure, and then will quickly progress with worsening
abdominal discomfort on examination. In obtunded or elderly patients,
a change in clinical status may take several hours, and occasionally
as long as 24 to 48 hours, to become manifest. Radiologic studies
to look for free intraperitoneal air, retroperitoneal air, or a
pneumothorax are diagnostic. A delay in diagnosis results in ongoing
contamination and sepsis.
Open or laparoscopic exploration locates the perforation, and
allows repair and local decontamination of the surrounding tissues.
The patient who may be a candidate for nonoperative management is
one in which perforation arises during an elective, bowel-prepped,
endoscopy, and yet the patient does not have significant pain or
clinical signs of infection. The patient may be closely observed
in a monitored setting, on strict dietary restriction and broad-spectrum
The complications of bronchoscopy include bronchial plugging,
hypoxemia, pneumothorax, lobar collapse, and bleeding. When diagnosed
in a timely fashion, they are rarely life threatening. Bleeding usually
resolves and rarely requires surgery, but may require repeat endoscopy
for thermocoagulation or fibrin glue application. The presence of
a pneumothorax necessitates placement of a thoracostomy tube when
significant deoxygenation occurs or the pulmonary mechanics are
compromised. Lobar collapse or mucous plugging responds to aggressive
pulmonary toilet, but occasionally requires repeat bronchoscopy.
Tracheostomy facilitates weaning from a ventilator, decreases
length of ICU or hospital stay, and improves pulmonary toilet. Tracheostomies
are now performed open, percutaneously, with or without bronchoscopy,
and with or without Doppler guidance, and yet complications still
Recent studies do not support obtaining a routine posttracheostomy
chest x-ray after either percutaneous or open tracheostomy.51,52 However,
significant lobar collapse can occur from copious tracheal secretions
or mechanical obstruction.
The most dramatic complication of tracheostomy is tracheo-innominate
artery fistula (TIAF) (Fig. 12-8).53,54 This
occurs rarely (~0.3%), but carries a 50 to 80% mortality
rate. TIAFs can occur as early as 2 days or as late as 2 months
after tracheostomy. The prototypical patient is a thin woman with
a long, gracile neck. The patient may have a sentinel bleed, which
occurs in 50% of TIAF cases, followed by a most spectacular
bleed. Should a TIAF be suspected, the patient should be transported immediately
to the OR for fiberoptic evaluation. If needed, remove the tracheostomy,
and place a finger through the tracheostomy site to apply direct pressure
anteriorly for compression of the innominate artery.
This illustration depicts improper positioning (attitude)
of the percutaneous needle. It is possible to access the innominate
artery via the trachea, thus placing the patient at risk for early tracheo-innominate
A misplaced percutaneous endogastrostomy (PEG) may create intra-abdominal
sepsis with peritonitis and/or an abdominal wall abscess
with necrotizing fasciitis. As in other minor procedures, the initial
placement technique must be fastidious to avoid complications. Transillumination
of the abdomen may decrease the risk for error. Inadvertent colotomies,
intraperitoneal leakage of tube feeds with peritonitis, and abdominal
wall abscesses require surgery to correct the complications and
to replace the PEG with an alternate feeding tube, usually a jejunostomy.
A dislodged or prematurely removed PEG tube must be replaced
within 8 hours of dislodgment, because the gastrostomy site closes
rapidly. A contrast x-ray should be performed to confirm the tube’s
intragastric position before feeding.
Tube thoracostomy (chest tube insertion) is performed for pneumothorax,
hemothorax, pleural effusions, or empyema. A chest tube can be easily placed
with a combination of local analgesia and light conscious sedation.
Common complications include inadequate analgesia or sedation, incomplete
penetration of the pleura with formation of a subcutaneous track
for the tube, lacerations to the lung or diaphragm, intraperitoneal placement
of the tube through the diaphragm, and bleeding related to these
various lacerations or injury to pleural adhesions. Additional problems include
slippage of the tube out of position or mechanical problems related
to the drainage system. All of these complications can be avoided with
proper initial insertion techniques, plus a daily review of the
drainage system and follow-up radiographs. Tube removal can create
a residual pneumothorax if the patient does not maintain positive
intrapleural pressure by Valsalva’s maneuver during tube
removal and dressing application.
Diagnostic peritoneal lavage is performed in the emergent trauma setting
for the hemodynamically unstable patient with neurologic impairment
and an uncertain etiology for blood loss, when an abdominal trauma
ultrasound is not available or is unreliable. Nasogastric and bladder
catheter decompression is mandatory before diagnostic peritoneal
lavage to avoid injury during the procedure (Fig.
12-9). The small or large bowel, or the major vessels of the
retroperitoneum also can be punctured inadvertently, and these injuries
require surgical exploration and repair.
The illustration depicts improper positioning of the
diagnostic peritoneal lavage catheter, with overdistention of the
urinary bladder (A) and the stomach (B).
This error in technique clearly demonstrates the importance of decompressing
hollow viscus before embarking on a diagnostic peritoneal lavage.
Intramural dissection of a cannulated artery can lead to complications
such as ischemic stroke from a carotid artery dissection or occlusion,
mesenteric ischemia from dissection of the superior mesenteric artery,
or a more innocuous finding of “blue toe syndrome” from
a dissected artery in a peripheral limb. Invasive or noninvasive imaging
studies confirm the suspected problem. The severity of the ischemia
and the extent of the dissection determine if anticoagulation therapy
or urgent surgical exploration is indicated.
Bleeding from the vascular access site usually is obvious, but
may not be visible when the blood loss is tracking into the retroperitoneal
tissue planes after femoral artery cannulation. These patients can
present with hemorrhagic shock; an abdominopelvic CT scan delineates
the extent of bleeding into the retroperitoneum. The initial management
is direct compression at the access site and clinical observation
with resuscitation as indicated. Urgent surgical exploration may
be required to control the bleeding site.
Renal complications of angiography occur in 1 to 2% of
patients. Contrast nephropathy is a temporary and preventable complication
of radiologic studies such as CT, angiography, and/or venography.
Some studies suggest a benefit of N-acetylcysteine
for this condition. For the patient with impaired renal function
or dehydration before contrast studies, twice-daily dosing 24 hours before
and on the day of the radiographic study is suggested. Nonionic
contrast also may be of benefit in higher-risk patients. IV hydration
before and after the procedure is the most efficient method for preventing
Lymph node biopsies have direct and indirect complications that
include bleeding, infection, lymph leakage, and seromas. Measures
to prevent direct complications include proper surgical hemostasis,
proper skin preparation, and a single
preoperative dose of antibiotic to cover skin flora 30 to 60 minutes
before incision. Bleeding at a biopsy site usually can be controlled
with direct pressure. Infection at a biopsy site will appear 5 to 10
days postoperatively, and may require opening of the wound to drain
the infection. Seromas or lymphatic leaks resolve with aspiration
of seromas and the application of pressure dressings, but may require
Neurologic complications that occur after surgery include motor
or sensory deficits and mental status changes. Peripheral motor
and sensory deficits are often due to neurapraxia secondary to improper positioning
and/or padding during operations. Treatment is largely
clinical observation, and the majority will resolve spontaneously
within 1 to 3 months.
Direct injury to nerves during a surgical intervention is a well-known
complication of several specific operations, including superficial parotidectomy
(facial nerve), carotid endarterectomy (hypoglossal nerve), prostatectomy
(nervi erigentes), and inguinal herniorrhaphy (ilioinguinal nerve).
The nerve injury may simply be a stretch injury, or an unintentionally
severed nerve. In addition to loss of function, severed nerves can result
in a painful neuroma that may require subsequent surgery.
Mental status changes in the postoperative patient can have numerous
causes (Table 12-13). Mental status changes
must be carefully documented and continually assessed. CT scanning should
be used early to detect intracranial causes.
Table 12-13 Common
Causes of Mental Status Changes |Favorite Table|Download (.pdf)
Table 12-13 Common
Causes of Mental Status Changes
|Sodium||Ethanol||Closed head injury||Thyrotoxicosis||Aspirin|
|Magnesium||Methanol||Pain||Adrenal insufficiency||Beta blockers|
|Calcium||Venoms and poisons||Shock||Hypoxemia||Narcotics|
|Sepsis||Carbon monoxide||Dementia||Severe anemia||MAOIs|
|Cerebral abscess||ICU psychosis||Poor glycemic control||Amphetamines|
|Fever/hyperpyrexia||Hyperthermia||Corticosteroids, anabolic steroids|
Atherosclerotic disease increases the risk for intraoperative
and postoperative stroke (cerebrovascular accident). Postoperatively,
hypotension and hypoxemia are the most likely causes of a cerebrovascular
accident. Management is largely supportive once the diagnosis is
made, and includes adequate intravascular volume replacement plus
optimal oxygen delivery. Neurologic consultation should be obtained
so that decisions regarding thrombolysis or anticoagulation can
be made in a timely fashion.
Corneal abrasions are unusual, but are due to inadequate protection
of the eyes during anesthesia. Overlooked contact lenses in a trauma
patient may cause conjunctivitis.
Persistent epistaxis can occur after nasogastric tube placement
or removal, and nasal packing is the best treatment option if prolonged
persistent direct pressure on the external nares fails. Anterior and
posterior nasal gauze packing with balloon tamponade, angioembolization,
and fibrin glue placement may be required in refractory cases. The
use of antibiotics for posterior packing is controversial, but the
incidence of toxic shock syndrome is documented at approximately 17:100,000
External otitis and otitis media occasionally occur postoperatively.
Patients complain of ear pain or decreased hearing, and treatment
includes topical antibiotics and nasal decongestion for symptomatic
Ototoxicity due to aminoglycoside administration occurs in up
to 10% of patients, and is often irreversible. Recent data
show that iron chelating agents and alpha-tocopherol may be protective
against ototoxicity. Vancomycin-related ototoxicity occurs about
3% of the time when used alone, and as often as 6% when
used with other ototoxic agents, but is self limiting.55,56
of the Neck
Complications of carotid endarterectomy include central or regional
neurologic deficits or bleeding with an expanding neck hematoma.
An acute change in mental status or the presence of localized neurologic
deficit may require an immediate return to the OR to correct an
iatrogenic occlusion. An expanding hematoma may warrant emergent airway
intubation and subsequent transfer to the OR for control of hemorrhage.
Intraoperative anticoagulation with heparin during carotid surgery makes
bleeding a postoperative risk. Other complications can arise, such
as arteriovenous fistulae, pseudoaneurysms, and infection, all of
which are treated surgically.
Intraoperative hypotension during manipulation of the carotid
bifurcation can occur, and is related to increased tone from baroreceptors
that reflexly cause bradycardia. Should hypotension occur when manipulating
the carotid bifurcation, an injection of 1% lidocaine solution
around this structure should attenuate this reflexive response.
The most common late complication following carotid endarterectomy
is myocardial infarction. The possibility of a postoperative myocardial
infarction should be considered as a cause of labile blood pressure
and arrhythmias in high-risk patients.
Surgery of the thyroid and parathyroid glands can result in hypocalcemia
in the immediate postoperative period. Manifestations include EKG
changes (shortened P-R interval), muscle spasm (tetany, Chvostek’s
sign, and Trousseau’s sign), paresthesias, and laryngospasm.
Treatment includes calcium gluconate infusion, and if tetany ensues, chemical
paralysis with intubation. Maintenance treatment is thyroid hormone
replacement (after thyroidectomy) in addition to calcium carbonate and
Recurrent laryngeal nerve (RLN) injury occurs in less than 5% of
patients. Of those with injury, approximately 10% are permanent.
As the thyroid gland is dissected from lateral to medial, the dissection
near the inferior thyroid artery is a common area for RLN injury.
At the conclusion of the operation, direct laryngoscopy confirms
normal vocal cord apposition. The cord on the affected side will
be in the paramedian position. If bilateral RLN has occurred, the
chance of a successful extubation is poor. The cords are found to
be in the midline, and an early sign of respiratory distress is stridor
with labored breathing. If paralysis of the cords is not permanent,
function may return 1 to 2 months after injury. Permanent RLN injury
can be treated by various techniques to stent the cords in a position
Superior laryngeal nerve injury is less debilitating, as the
common symptom is loss of projection of the voice. The glottic aperture
is asymmetrical on direct laryngoscopy and management is limited
to clinical observation.
Surgical complications that put the respiratory system in jeopardy
are not always confined to technical errors. Malnutrition, inadequate pain
control, inadequate mechanical ventilation, inadequate pulmonary
toilet, and aspiration can cause serious pulmonary problems.
Pneumothorax can occur from central line insertion during anesthesia
or from a diaphragmatic injury during an abdominal procedure. Hypotension,
hypoxemia, and tracheal deviation away from the affected side may
be present. A tension pneumothorax can cause complete cardiovascular collapse.
Treatment is by needle thoracostomy, followed by tube thoracostomy.
A large-bore needle is placed either in the midclavicular line in
the second rib interspace, or where the chest tube will be inserted,
the fifth intercostal space in the anterior axillary line.
Hemothorax due to trauma or intrathoracic disease should be evacuated
completely. A delay in evacuation of the hemothorax leaves the patient
at risk for empyema and entrapped lung. If evacuation is incomplete
with tube thoracostomy, video-assisted thoracoscopy or open evacuation
and pleurodesis may be required.
Pulmonary atelectasis results in a loss of functional residual
capacity (FRC) of the lung, and can predispose to pneumonia. Poor
pain control in the postoperative period contributes to poor inspiratory
effort and collapse of the lower lobes in particular. An increase
in FRC by 700 mL or more can be accomplished by sitting patients
up to greater than 45°. For mechanically ventilated patients, simply
placing the head of the bed at 30 to 45° in elevation improves pulmonary
outcomes. The prevention of atelectasis is facilitated by delivering
adequate tidal volumes (8 to 10 mL/kg), preventing the
abdominal domain from impinging on the thoracic cavity, and by sitting
the patient up as much as possible. This includes having the ventilated
patient out of bed and sitting in a chair if possible.
Aspiration complications include pneumonitis and pneumonia. The
treatment of pneumonitis is similar to that for acute lung injury
(ALI) (see below in this section), and includes oxygenation with
general supportive care. Antibiotics are usually contraindicated
unless known organisms are detected with bacteriologic analysis.
Hospitalized patients who develop aspiration pneumonia carry a mortality
rate as high as 70 to 80%. Early, aggressive, and repeated
bronchoscopy for suctioning of aspirated material from the tracheobronchial
tree will help to minimize the inflammatory reaction of pneumonitis
and facilitate improved pulmonary toilet.
Patients with inadequate pulmonary toilet are at increased risk
for bronchial plugging and lobar collapse. Patients with copious
and tenacious secretions develop these plugs most often, but foreign
bodies in the bronchus can be the cause of lobar collapse as well.
The diagnosis of bronchial plugging is based on chest x-ray and
clinical suspicion when there is acute pulmonary decompensation
with increased work of breathing and hypoxemia. Fiberoptic bronchoscopy
can be useful to clear mucous plugs and secretions.
Pneumonia is the second most common nosocomial infection and
is the most common infection in ventilated patients. Ventilator-associated
pneumonia (VAP) occurs in 15 to 40% of ventilated ICU patients,
and accrues at a daily probability rate of 5% per day,
up to 70% at 30 days. The 30-day mortality rate of nosocomial
pneumonia can be as high as 40%, and depends on the microorganisms involved
and the timeliness of initiating appropriate treatment.
Once the diagnosis of pneumonia is suspected (an abnormal chest
x-ray, fever, productive cough with purulent sputum, and no other obvious
fever sources), it is invariably necessary to initially begin treatment
with broad-spectrum antibiotics until proper identification, colony
count [⩾100,000 colony-forming units (CFU)], and sensitivity
of the microorganisms are determined.57 The spectrum of
antibiotic coverage should be narrowed as soon as the culture sensitivities
are determined. Double-coverage antibiotic strategy for the two
pathogens, Pseudomonas and Acinetobacter spp., may
be appropriate if the local prevalence of these particularly virulent
organisms is high. One of the most helpful tools in treating pneumonia
and other infections is the tracking of a medical center’s antibiogram
every 6 to 12 months.58
Epidural analgesia decreases the risk of perioperative pneumonia.
This method of pain control improves pulmonary toilet and the early
return of bowel function; both have a significant impact on the
potential for aspiration and for acquiring pneumonia. The routine
use of epidural analgesia has a lower incidence of pneumonia than
ALI is a diagnosis applied to patients with similar findings
to those with acute respiratory distress syndrome (ARDS). These
should be considered a spectrum of the same disease process, with
the difference being in the degree of oxygenation deficits of patients. The
pathology, pathophysiology, and the mechanism of lung injury for
ALI are the same as for ARDS, except that the arterial oxygen to
inspired oxygen (partial pressure of arterial oxygen:fraction of
inspired oxygen) ratio is >200 for ALI and <200 for ARDS. Both
types of patients will require some form of positive pressure ventilatory
assistance to improve the oxygenation deficits, while simultaneously
treating the primary etiology of the initiating disease.
The definition of ARDS includes five criteria (Table
12-14). The recent multicenter ARDS Research Network (ARDSnet)
research trial demonstrated improved clinical outcomes for ARDS
patients ventilated at tidal volumes of only 5 to 7 mL/kg.60 It
is important to note that these ventilator setting recommendations
are for patients with ARDS, and not for patients requiring ventilatory
support for a variety of other reasons. The beneficial effects of positive
end-expiratory pressure (PEEP) for ARDS were confirmed in this study
as well. The maintenance of PEEP during ventilatory support is determined
based on blood gas analysis, pulmonary mechanics, and requirements
for supplemental oxygen. As gas exchange improves with resolving
ARDS, the initial step in decreasing ventilatory support should
be to decrease the levels of supplemental oxygen first, and then
to slowly bring the PEEP levels back down to minimal levels.61 This
is done to minimize the potential for recurrent alveolar collapse
and a worsening gas exchange.
12-14 Inclusion Criteria for the Acute Respiratory Distress Syndrome |Favorite Table|Download (.pdf)
12-14 Inclusion Criteria for the Acute Respiratory Distress Syndrome
|Pao2:FiO2 <200 (regardless
of positive end-expiratory pressure)|
|Pulmonary artery occlusion pressure <18 mmHg|
|No clinical evidence of right heart failure|
Not all patients can be weaned easily from mechanical ventilation. When
the respiratory muscle energy demands are not balanced, or there
is an ongoing active disease state external to the lungs, patients may
require prolonged ventilatory support. Protocol-driven ventilator weaning
strategies are successful and have become part of the standard of
care. The use of a weaning protocol for patients on mechanical ventilation
greater than 48 hours reduces the incidence of VAP and the overall
length of time on mechanical ventilation, when compared with nonprotocol
managed ventilator weaning. Unfortunately, there is still no reliable
way of predicting which patient will be successfully extubated after
a weaning program, and the decision for extubation is based on a
combination of clinical parameters and measured pulmonary mechanics.62 The
Tobin Index (frequency:tidal volume ratio), also known as the rapid
shallow breathing index, is perhaps the best negative predictive
instrument.63 If the result equals less than 105,
then there is nearly a 70% chance the patient will pass
extubation. If the score is greater than 105, the patient has an
approximately 80% chance of failing extubation. Other parameters
such as the negative inspiratory force, minute ventilation, and
respiratory rate are used, but individually have no better predictive
value than the rapid shallow breathing index.64
Malnutrition and poor nutritional support may adversely affect
the respiratory system. The respiratory quotient (RQ), or respiratory exchange
ratio, is the ratio of the rate of carbon dioxide (CO2)
produced to the rate of oxygen uptake (RQ = Vco2/V̇o2).
Lipids, carbohydrates, and protein have differing effects on CO2 production.
Patients consuming a diet consisting mostly of carbohydrates would
have an RQ of 1 or greater. The RQ for a diet mostly of lipids would be
closer to 0.7, and that for a diet of mostly protein would be closer
to 0.8. Ideally, an RQ of 0.75 to 0.85 suggests adequate balance
and composition of nutrient intake. An excess of carbohydrate may
negatively affect ventilator weaning because of the abnormal RQ
due to higher CO2 production and altered pulmonary gas
Although not without risk, tracheostomy will decrease the pulmonary
dead space and provides for improved pulmonary toilet. When performed before
the tenth day of ventilatory support, tracheostomy may decrease
the incidence of VAP, the overall length of ventilator time, and
the number of ICU patient days.
The occurrence of pulmonary embolism (PE) is probably underdiagnosed.
Its etiology stems from DVT. The diagnosis of PE is made when a
high degree of clinical suspicion for PE leads to imaging techniques
such as ventilation:perfusion nuclear scans or CT pulmonary angiogram.
Clinical findings include elevated central venous pressure, hypoxemia,
shortness of breath, hypocarbia secondary to tachypnea, and right
heart strain noted on EKG. Ventilation:perfusion nuclear scans are
often indeterminate in patients who have an abnormal chest x-ray.
The pulmonary angiogram remains the gold standard for diagnosing
PE, but spiral CT angiogram has become an alternative method because
of its relative ease of use and reasonable rates of diagnostic accuracy.
For cases without clinical contraindications to therapeutic anticoagulation,
patients should be empirically started on heparin infusion until
the imaging studies are completed if the suspicion of a PE is strong.
Sequential compression devices on the lower extremities and low-dose
subcutaneous heparin administration are routinely used to prevent
DVT, and, by inference, the risk of PE. Neurosurgical and orthopedic
patients have higher rates of PE, as do obese patients and those
at prolonged bed rest.
When anticoagulation is contraindicated, or when a known clot
exists in the inferior vena cava (IVC), therapy for PE includes
insertion of an IVC filter. The Greenfield filter has been most
widely studied, and it has a failure rate of less than 4%.
Newer devices include those with nitinol wire that expands with
body temperature and retrievable filters. Patients with spinal cord
injury and multiple long-bone or pelvic fractures frequently receive
IVC filters, and there appears to be a low long-term complication
rate with their use.
Arrhythmias are often seen preoperatively in elderly patients,
but may occur postoperatively in any age group. Atrial fibrillation
is the most common arrhythmia65 and occurs between
postoperative days 3 to 5 in high-risk patients. This is typically when
patients begin to mobilize their interstitial fluid into the vascular
fluid space. Contemporary evidence suggests that rate control is
more important than rhythm control for atrial fibrillation.66,67 The
first-line treatment includes beta blockade and/or calcium
channel blockade. Beta blockade must be used judiciously, because
hypotension, as well as withdrawal from beta blockade with rebound
hypertension, is possible. Calcium channel blockers are an option
if beta blockers are not tolerated by the patient, but caution must
be exercised in those with a history of congestive heart failure.
Although digoxin is still a faithful standby medication, it has
limitations due to the need for optimal dosing levels. Cardioversion
may be required if patients become hemodynamically unstable and
the rhythm cannot be controlled.
Ventricular arrhythmias and other tachyarrhythmias may occur
in surgical patients as well. Similar to atrial rhythm problems,
these are best controlled with beta blockade, but the use of other antiarrhythmics
or cardioversion may be required if patients become hemodynamically
unstable. Formal cardiac electrophysiology studies may be needed
to clarify the etiology of the arrhythmias so that medical or surgical
treatment can be tailored.
Cardiac ischemia is a cause of postoperative mortality. Acute
myocardial infarction (AMI) can present insidiously or it can be
more dramatic with the classic presentation of shortness of breath, severe
angina, and sudden cardiogenic shock. The work-up to rule out an
AMI includes an EKG and cardiac enzyme measurements. The patient
should be transferred to a monitored (telemetry) floor as soon as
a bed is available. Morphine, supplemental Oxygen, Nitroglycerine,
and Aspirin (MONA) are the initial therapeutic
maneuvers for those who are being investigated for AMI.
Hypertension in the immediate postoperative period may be merely
a failure of adequate pain control, but other causes include hypoxia, volume
overload, and rebound hypertension from failure to resume beta blockade
and/or clonidine. Perioperative hypertension carries significant
morbidity and aggressive control is warranted. Twenty to 50% of
patients with chronic atherosclerotic disease present with hypertension,
and causes of perioperative hypertension include cerebrovascular
disease, renal artery stenosis, aorto-occlusive disease, and rarely,
pheochromocytoma. Routine perioperative cardiac protection with
beta blockade is the standard of care for patients with a history of
Surgery of the esophagus is potentially complicated because of
its anatomic location and blood supply. The two primary types of esophageal
resection performed are the transhiatal resection and the transthoracic
(Ivor-Lewis) resection.68 The transhiatal resection
has the advantage that a formal thoracotomy incision is avoided.
The dissection of the esophagus is blind, however, and an anastomotic
leak occurs more than with other resections. However, when a leak
does occur, simple opening of the cervical incision and draining the
leak is all that is usually required.
The transthoracic Ivor-Lewis resection includes an esophageal
anastomosis performed in the chest near the level of the azygos
vein. These resections tend not to leak as often, but when they
do, they can be difficult to control. The reported mortality is
about 50% with an anastomotic leak, and the overall mortality
is about 5%, which is similar to transhiatal resection.
Nutritional support strategies must be considered for esophageal
resection patients to maximize the potential for survival.
Nissen fundoplication is an operation that is fraught with possibilities for
error. Bleeding is always a potential hazard, so dissection of the short
gastric vessels must be done with care. Laparoscopic port site bleeding,
injury to the aorta, and liver lacerations can also contribute to
significant blood loss. The fundoplication may be too tightly wrapped
or become unwrapped postoperatively. Postoperative edema and patient
noncompliance will produce symptoms of odynophagia and dysphagia.
Postoperative ileus is related to dysfunction of the neural reflex
axis of the intestine. Excessive narcotic use may delay return of
bowel function. Epidural anesthesia results in better pain control,
and there is an earlier return of bowel function, and a shorter
length of hospital stay. The limited use of nasogastric tubes and
the initiation of early postoperative feeding are associated with
an earlier return of bowel function.
Numerous studies have shown a decreased length of stay and improved
pain control when bowel surgery is performed laparoscopically. In
one study, however, patients with open colon resection were fed
at the same time as the laparoscopically treated patients and had
no difference in hospital length of stay.69
Pharmacologic agents commonly used to stimulate bowel function include
metoclopramide and erythromycin. Metoclopramide’s action is
limited to the stomach, and it may help primarily with gastroparesis.
Erythromycin is a motilin agonist that works throughout the stomach
and bowel. Several studies demonstrate significant benefit from
the administration of erythromycin in those suffering from an ileus.70
Small bowel obstruction occurs in less than 1% of early
postoperative patients. When it does occur, adhesions are usually
the cause. Internal and external hernias, technical errors, and
infections or abscesses are also causative. No one can accurately
predict which patients will form obstructive postoperative adhesions,
because all patients who undergo surgery form adhesions to some
extent, and there is little that can limit this natural healing process.
Hyaluronidase is a mucolytic enzyme that degrades connective tissue,
and the use of a methylcellulose form of hyaluronidase, Seprafilm,
has been shown to result in a 50% decrease in adhesion
formation in some patients.71,72 This should translate
into a lower occurrence of postoperative bowel obstruction, but
this has yet to be proven.
Fistulae are the abnormal communication of one structure to an
adjacent structure or compartment, and are associated with extensive
morbidity and mortality. Common causes for fistula formation are
summarized in the pneumonic FRIENDS (Foreign body, Radiation, Ischemia/Inflammation/Infection, Epithelialization
of a tract, Neoplasia, Distal
obstruction, and Steroid use). The cause of the
fistula must be recognized early, and treatment may include nonoperative
management with observation and nutritional support, or a delayed
operative management strategy that also includes nutritional support
and wound care.
GI bleeding can occur perioperatively (Table
12-15). Technical errors such as a poorly tied suture, a nonhemostatic
staple line, or a missed injury can all lead to postoperative intestinal
bleeding.73,74 The source of bleeding is in the
upper GI tract about 85% of the time, and is usually detected
and treated endoscopically. Surgical control of intestinal bleeding
is required in up to 40% of patients.75
12-15 Common Causes of Upper and Lower Gastrointestinal
Hemorrhage |Favorite Table|Download (.pdf)
12-15 Common Causes of Upper and Lower Gastrointestinal
|Upper GI Bleed||Lower GI Bleed|
|Gastric varices||Radiation proctitis|
|Aortoduodenal fistula||Neoplastic diseases|
|Peptic ulcer disease||Vasculitis|
|Neoplastic disease||Aortoenteric fistula|
|Inflammatory bowel disease|
When patients in the ICU have a major bleed from stress gastritis,
the mortality risk is as high as 50%. It is important to
keep the gastric pH greater than 4 to decrease the overall risk
for stress gastritis, particularly in patients mechanically ventilated
for 48 hours or greater and patients who are coagulopathic.76 Proton
pump inhibitors, H2 receptor antagonists, and intragastric
antacid installation are all effective measures.
Complications involving the hepatobiliary tree are usually due
to technical errors. Laparoscopic cholecystectomy has become the
standard of care for cholecystectomy, but common bile duct injury remains
a nemesis of this approach. Intraoperative cholangiography has not
been shown to decrease the incidence of common bile duct injuries, because
the injury to the bile duct usually occurs before the cholangiogram.77,78 Early
recognition of an injury is important, because delayed bile duct
leaks often require a more complex repair.
Ischemic injury due to devascularization of the common bile duct
has a delayed presentation days to weeks after an operation. Endoscopic
retrograde cholangiopancreatography (ERCP) demonstrates a stenotic,
smooth common bile duct. Liver function studies are elevated. The
recommended treatment is a Roux-en-Y hepaticojejunostomy.
A bile leak due to an unrecognized injury to the ducts may present after
cholecystectomy as a biloma. These patients may present with abdominal
pain and hyperbilirubinemia. The diagnosis of a biliary leak can
be confirmed by CT scan, ERCP, or radionuclide scan. Once a leak
is confirmed, a retrograde biliary stent and external drainage is the
treatment of choice.
Hyperbilirubinemia in the surgical patient can be a complex problem. Cholestasis
makes up the majority of causes for hyperbilirubinemia, but other
mechanisms of hyperbilirubinemia include reabsorption of blood (e.g.,
hematoma from trauma), decreased bile excretion (e.g., sepsis),
increased unconjugated bilirubin due to hemolysis, hyperthyroidism,
and impaired excretion due to congenital abnormalities or acquired
disease. Errors in surgery that cause hyperbilirubinemia largely
involve missed or iatrogenic injuries.
The presence of cirrhosis predisposes to postoperative complications. Abdominal
or hepatobiliary surgery is problematic in the cirrhotic patient.
Ascites leak in the postoperative period can be an issue when any
abdominal operation has been performed. Maintaining proper intravascular
oncotic pressure in the immediate postoperative period can be difficult,
and resuscitation should be maintained with crystalloid solutions.
Prevention of renal failure and the management of the hepatorenal
syndrome can be difficult, as the demands of fluid resuscitation
and altered glomerular filtration become competitive. Spironolactone
with other diuretic agents may be helpful in the postoperative care.
These patients often have a labile course and bleeding complications
due to coagulopathy are common. The operative mortality in cirrhotic
patients is 10% for Child class A, 30% for Child
class B, and 82% for Child class C patients.79
Pyogenic liver abscess occurs in less than 0.5% of adult
admissions, due to retained necrotic liver tissue, occult intestinal
perforations, benign or malignant hepatobiliary obstruction, and
hepatic arterial occlusion. The treatment is long-term antibiotics
with percutaneous drainage of large abscesses.
Pancreatitis can occur following injection of contrast during
cholangiography and ERCP. These episodes range from a mild elevation
in amylase and lipase with abdominal pain, to a fulminant course
of pancreatitis with necrosis requiring surgical débridement.
Traumatic injuries to the pancreas during surgical procedures on
the kidneys, GI tract, or spleen comprise the most common causes.
Treatment involves serial CT scans and percutaneous drainage to
manage infected fluid and abscess collections. A pancreatic fistula
may respond to antisecretory therapy with a somatostatin analogue,
Octreotide. Management of these fistulae initially includes ERCP
with or without pancreatic stenting, percutaneous drainage of any
fistula fluid collections, total parenteral nutrition (TPN) with
bowel rest, and repeated CT scans. The majority of pancreatic fistulae
will eventually heal spontaneously.
Renal failure can be classified as prerenal failure, intrinsic
renal failure, and postrenal failure. Postrenal failure, or obstructive
renal failure, should always be considered when low urine output
(oliguria) or anuria occurs. The most common cause is a misplaced
or clogged urinary catheter. Other, less common causes to consider
are unintentional ligation or transection of ureters during a difficult
surgical dissection (e.g., colon resection for diverticular disease),
or a large retroperitoneal hematoma (e.g., ruptured aortic aneurysm).
Oliguria is evaluated by flushing the Foley catheter using sterile
technique. When this fails to produce the desired response, it is
reasonable to administer an IV fluid challenge with a crystalloid fluid
bolus of 500 to 1000 mL. However, the immediate postoperative patient
must be examined and have recent vital signs recorded with total intake
and output tabulated, as well as urinary electrolytes measured (Table 12-16). A hemoglobin and hematocrit
level should be checked immediately. Patients in compensated shock
from acute blood loss may manifest anemia and end-organ malperfusion
12-16 Urinary Electrolytes Associated with Acute Renal Failure
and Their Possible Etiologies |Favorite Table|Download (.pdf)
12-16 Urinary Electrolytes Associated with Acute Renal Failure
and Their Possible Etiologies
|Intrinsic failure||>1||<350||>40||Sepsis, shock|
Acute tubular necrosis (ATN) carries a mortality risk of 25 to
50% due to the many complications that can cause, or result
from, this insult. When ATN is due to poor inflow (prerenal failure),
the remedy begins with IV administration of crystalloid or colloid
fluids as needed. If cardiac insufficiency is the problem, the optimization
of vascular volume is achieved first, followed by inotropic agents,
as needed. Intrinsic renal failure and subsequent ATN are often
the result of direct renal toxins. Aminoglycosides, vancomycin,
and furosemide, among other commonly used agents, contribute directly
to nephrotoxicity. Contrast-induced nephropathy usually leads to a subtle
or transient rise in creatinine. In patients who are volume depleted
or have poor cardiac function, contrast nephropathy may permanently
impair renal function.80–83
The treatment of renal failure due to myoglobinuria in severe
trauma patients has shifted away from the use of sodium bicarbonate
for alkalinizing the urine, to merely maintaining brisk urine output
of 100 mL/h with crystalloid fluid infusion. Mannitol and
furosemide are not recommended as long as the IV fluid achieves
the goal rate of urinary output.
A compartment syndrome can develop in any compartment of the body.
Compartment syndrome of the extremities generally occurs after a
closed fracture. The injury alone may predispose the patient to compartment
syndrome, but aggressive fluid resuscitation can exacerbate the
problem. Pain with passive motion is the hallmark of compartment
syndrome, and the anterior compartment of the leg is usually the
first compartment to be involved. Confirmation of the diagnosis
is obtained by direct pressure measurement of the individual compartments.
If the pressures are greater than 20 to 25 mmHg in any of the compartments,
then a four-compartment fasciotomy is considered. Compartment syndrome
can be due to ischemia-reperfusion injury, after an ischemic time
of 4 to 6 hours. Renal failure (due to myoglobinuria), foot drop,
tissue loss, and a permanent loss of function are possible results
of untreated compartment syndrome.
Decubitus ulcers are preventable complications of prolonged bedrest
due to traumatic paralysis, dementia, chemical paralysis, or coma.
Ischemic changes in the microcirculation of the skin can be significant
after 2 hours of sustained pressure. Routine skin care and turning
of the patient helps ensure a reduction in skin ulceration. This
can be labor intensive and special mattresses and beds are available
to help with this ubiquitous problem. The treatment of a decubitus
ulcer in the noncoagulopathic patient is surgical débridement.
Once the wound bed has a viable granulation base without an excess
of fibrinous debris, a vacuum-assisted closure dressing can be applied.
Wet to moist dressings with frequent dressing changes is the alternative,
and is labor intensive. Expensive topical enzyme preparations are
also available. If the wounds fail to respond to these measures,
soft tissue coverage by flap is considered.
Contractures are the result of muscle disuse. Whether from trauma, amputation,
or from vascular insufficiency, contractures can be prevented by
physical therapy and splinting. If not attended to early, contractures
will prolong rehabilitation and may lead to further wounds and wound
healing issues. Depending on the functional status of the patient,
contracture releases may be required for long-term care.
The transfusion guideline of maintaining the hematocrit level
in all patients at greater than 30% is no longer valid.
Only those patients with symptomatic anemia, or those who have significant
cardiac disease, or the critically ill patient who requires increased
oxygen-carrying capacity to adequately perfuse end organs, requires
higher levels of hemoglobin. Other than these select patients, the
decision to transfuse should generally not occur until the hemoglobin
level reaches 7 mg/dL or the hematocrit reaches 21%.
Transfusion reactions are common complications of blood transfusion.
These can be attenuated with a leukocyte filter, but not completely
prevented. The manifestations of a transfusion reaction include
simple fever, pruritus, chills, muscle rigidity, and renal failure due
to myoglobinuria secondary to hemolysis. Discontinuing the transfusion
and returning the blood products to the blood bank is an important
first step, but administration of antihistamine and possibly steroids
may be required to control the reaction symptoms. Severe transfusion
reactions are rare but can be fatal.
Infectious complications in blood transfusion range from cytomegalovirus
transmission, which is benign in the nontransplant patient, to HIV infection,
to passage of the hepatitis viruses, which can lead to subsequent
hepatocellular carcinoma. Although the efficiency of infectious
agent screening in blood products has improved, universal precautions
should be rigidly maintained for all patients (Table
Table 12-17 Rate of Viral Transmission
in Blood Product Transfusionsa |Favorite Table|Download (.pdf)
Table 12-17 Rate of Viral Transmission
in Blood Product Transfusionsa
Patients on warfarin (Coumadin) who require surgery can have
anticoagulation reversal by administration of fresh-frozen plasma.
Each unit of fresh-frozen plasma contains 200 to 250 mL of plasma and
includes one unit of coagulation factor per milliliter of plasma.
Thrombocytopenia may require platelet transfusion for a platelet count
less than 20,000/mL when invasive procedures are performed, or
when platelet counts are low and ongoing bleeding from raw surface
areas persists. One unit of platelets will increase the platelet count
by 5000 to 7500 per mL in adults. It is important to delineate the
cause of the low platelet count. Usually there is a self-limiting
or reversible condition such as sepsis. Rarely, it is due to heparin-induced
thrombocytopenia I and II. Complications of heparin-induced thrombocytopenia
II can be serious because of the diffuse thrombogenic nature of
the disorder. Simple precautions to limit this hypercoagulable state
include saline solution flushes instead of heparin solutions, and
to limit the use of heparin-coated catheters. The treatment is anticoagulation
with synthetic agents such as argatroban.
For patients with uncontrollable bleeding due to disseminated
intravascular coagulopathy, an expensive but useful drug is factor
VIIa.84–86 Largely used in hepatic trauma
and obstetric emergencies, this agent may mean the difference between
life or death in some circumstances. The combination of ongoing,
nonsurgical bleeding and renal failure can sometimes be successfully
treated with desmopressin.
In addition to classic hemophilia, other inherited coagulation
factor deficiencies can be difficult to manage in surgery. When
required, transfusion of appropriate replacement products is coordinated with
the regional blood bank center before surgery. Other blood dyscrasias
seen by surgeons include hypercoagulopathic patients. Those who
carry congenital anomalies such as the most common, Factor V Leiden
deficiency, as well as protein C and S deficiencies, are likely
to form thromboses if inadequately anticoagulated.
Abdominal compartment syndrome (ACS) and intra-abdominal hypertension
represent the same problem. Multisystem trauma, thermal burns, retroperitoneal
injuries, and surgery related to the retroperitoneum are the major
initial causative factors that may lead to ACS. Ruptured AAA, major
pancreatic injury and resection, or multiple intestinal injuries
are also examples of clinical situations in which a large volume
of IV fluid resuscitation puts these patients at risk for intra-abdominal
hypertension. Manifestations of ACS typically include progressive
abdominal distention followed by increased peak airway ventilator
pressures, oliguria followed by anuria, and an insidious development
of intracranial hypertension.87 These findings
are related to elevation of the diaphragm and inadequate venous
return from the vena cava or renal veins secondary to the transmitted
pressure on the venous system.
Measurement of abdominal pressures is easily accomplished by
transducing bladder pressures from the urinary catheter after instilling
100 mL of sterile saline into the urinary bladder.88 A
pressure greater than 20 mmHg constitutes intra-abdominal hypertension,
but the diagnosis of ACS requires intra-abdominal pressure greater
than 25 to 30 mmHg, with at least one of the following: compromised respiratory
mechanics and ventilation, oliguria or anuria, or increasing intracranial
The treatment of ACS is to open any recent abdominal incision
to release the abdominal fascia, or to open the fascia directly
if no abdominal incision is present. Immediate improvement in mechanical
ventilation pressures, intracranial pressures, and renal output
is usually noted. When expectant management for ACS is considered
in the OR, the abdominal fascia should be left open and covered
under sterile conditions with plans made for a second-look operation
and delayed fascial closure. Patients with intra-abdominal hypertension
should be monitored closely with repeated examinations and measurements
of bladder pressure, so that any further deterioration is detected and
operative management can be initiated. Left untreated, ACS may lead
to multiple system end-organ dysfunction or failure, and has a high
Abdominal wall closure should be attempted every 48 to 72 hours until
the fascia can be reapproximated. If the abdomen cannot be closed
within 5 to 7 days following release of the abdominal fascia, a large
incisional hernia is the net result.
There exist no prospective, randomized, double-blind, controlled
studies that demonstrate that antibiotics used beyond 24 hours in
the perioperative period prevent infections. There is a general
trend toward providing a single preoperative dose, as antibiotic
prophylaxis may not impart any benefit at all beyond the initial
dosing. Irrigation of the operative field and the surgical wound
with saline solution has shown benefit in controlling wound inoculum.92 Irrigation
with an antibiotic-based solution has not demonstrated significant
benefit in controlling postoperative infection.
Antibacterial-impregnated polyvinyl placed over the operative
wound area for the duration of the surgical procedure has not been
shown to decrease the rate of wound infection.93–97 Although
skin preparation with 70% isopropyl alcohol has the best
bactericidal effect, it is flammable, and could be hazardous when
electrocautery is used. The contemporary formulas of chlorhexidine
gluconate with isopropyl alcohol or povidone-iodine and iodophor
with alcohol are more advantageous.98–100
There is a difference between wound colonization and infection.
Overtreating colonization is just as injurious as undertreating
infection (Table 12-18). The strict definition
of wound (soft tissue) infection is more than 105 CFU per
gram of tissue. This warrants expeditious and proper antibiotic/antifungal
treatment.58,101 Often, however, clinical signs
raise enough suspicion that the patient is treated before a confirmatory culture
is undertaken. The clinical signs of wound infection include rubor, tumor, calor,
and dolor (redness, swelling, heat, and pain),
and once the diagnosis of wound infection has been established, the
most definitive treatment remains open drainage of the wound to
facilitate wound dressing care. The use of antibiotics for wound
infection treatment should be limited.102–105
12-18 Common Causes of Leukocytosis |Favorite Table|Download (.pdf)
12-18 Common Causes of Leukocytosis
|Systemic inflammatory response syndrome|
|Increases in interleukin-1 and tumor necrosis factor|
One type of wound dressing/drainage system that is gaining
popularity is the vacuum-assisted closure dressing. The principle of
the system is to decrease local wound edema and to promote healing
through the application of a sterile dressing that is then covered
and placed under controlled suction for a period of 2 to 4 days
at a time. Although costly, the benefits are frequently dramatic
and may offset the costs of nursing care, frequent dressing changes,
and operative wound débridement.
The four indications for applying a surgical drain are:
- To collapse surgical dead space in areas of redundant
tissue (e.g., neck and axilla)
- To provide focused drainage of an abscess or grossly infected
- To provide early warning notice of a surgical leak (either
bowel contents, secretions, urine, air, or blood)—the so-called sentinel
- To control an established fistula leak
Open drains are often used for large contaminated wounds such
as perirectal or perianal fistulas and subcutaneous abscess cavities.
They prevent premature closure of an abscess cavity in a contaminated wound,
but do not address the fact that bacteria are free to travel in either
direction along the drain tract. More commonly, surgical sites are
drained by closed suction drainage systems, but data do not support
closed suction drainage to “protect an anastomosis,” or
to “control a leak” when placed at the time of
surgery. Closed suction devices can exert a negative pressure of
70 to 170 mmHg at the level of the drain, therefore the presence
of this excess suction may call into question whether an anastomosis
breaks down on its own, or if the drain creates a suction injury
that promotes leakage (Fig. 12-10).106
This illustration demonstrates typical intraoperative
placement of closed suction devices in pancreatic or small bowel
surgery, where there may be an anastomosis. At negative pressures
of 70 to 170 mmHg, these devices may actually encourage anastomotic
leaks and not prevent them, or become clogged by them.
On the other hand, CT- or ultrasound-guided placement of percutaneous
drains is now the standard of care for abscesses, loculated infections,
and other isolated fluid collections such as pancreatic leaks. The
risk of surgery is far greater than the placement of an image-guided
drain, and the risk can often be reduced in these instances by a brief
course of antibiotics.
The use of antibiotics when drains are placed should be examined
from a cost-benefit perspective. Antibiotics are rarely necessary
when a wound is drained widely. Twenty-four to 48 hours of antibiotic
use after drain placement is prophylactic, and after this period
only specific treatment of positive cultures should be performed,
to avoid increased drug resistance and superinfection.
Several complications of urinary (Foley) catheters can occur
that lead to an increased length of hospital stay and morbidity.
It is recommended that the catheter be inserted its full length
up to the hub, and that urine flow is established before the balloon
is inflated, because misplacement of the catheter in the urethra
with premature inflation of the balloon can lead to tears and disruption
of the urethra.
Enlarged prostatic tissue can make catheter insertion difficult,
and a catheter coudé may be required. If this attempt is
also unsuccessful, then a urologic consultation for endoscopic placement
of the catheter may be required to prevent harm to the urethra.
For patients with urethral strictures, filiform-tipped catheters
and followers may be used, but these can potentially cause bladder
injury. If endoscopic attempts fail, the patient may require a percutaneously
placed suprapubic catheter to obtain decompression of the bladder.
Follow-up investigations of these patients are recommended so definitive
care of the urethral abnormalities can be pursued.
The most frequent nosocomial infection is urinary tract infection (UTI).
These infections are classified into complicated and uncomplicated
forms. The uncomplicated type is a UTI that can be treated with trimethoprim-sulfamethoxazole
for 3 days. The complicated UTI usually involves the hospitalized
patient with an indwelling catheter whose UTI is diagnosed as part
of a fever work-up. The interpretation of urine culture results
of less than 100,000 CFU/mL is controversial. Before treating
such a patient, one should change the catheter and then repeat the
culture to see if the catheter was simply colonized with organisms.
On the other hand, an argument can be made that, until the foreign
body (catheter) is removed, the bladder will continue to be the
nidus of infection, and antibiotics should be started. Cultures
with more than 100,000 CFU/mL should be treated with the
appropriate antibiotics and the catheter removed as soon as possible.
Undertreatment or misdiagnosis of a UTI can lead to urosepsis and
Recommendations are mixed on the proper way to treat Candida
albicans fungal bladder infections. Continuous bladder
washings with fungicidal solution for 72 hours have been recommended,
but this is not always effective. Replacement of the urinary catheter
and a course of fluconazole are appropriate treatments, but some
infectious disease specialists claim that C. albicans in
the urine may serve as an indication of fungal infection elsewhere
in the body. If this is the case, then screening cultures for other
sources of fungal infection should be performed whenever a fungal UTI
One of the most debilitating infections is an empyema, or infection
of the pleural space. Frequently, an overwhelming pneumonia is the source
of an empyema, but a retained hemothorax, systemic sepsis, esophageal
perforation from any cause, and infections with a predilection for
the lung (e.g., tuberculosis) are potential etiologies as well. The
diagnosis is confirmed by chest x-ray or CT scan, followed by aspiration
of pleural fluid for bacteriologic analysis. Gram’s stain, lactate
dehydrogenase, protein, pH, and cell count are obtained, and broad-spectrum
antibiotics are initiated while the laboratory studies are performed.
Once the specific organisms are confirmed, anti-infective agents
are tailored appropriately. Placement of a thoracostomy tube is
needed to evacuate and drain the infected pleural fluid, but depending
on the specific nidus of infection, video-assisted thoracoscopy
may also be helpful for irrigation and drainage of the infection.
Postsurgical intra-abdominal abscesses can present with vague
complaints of intermittent abdominal pain, fever, leukocytosis,
and a change in bowel habits. Depending on the type and timing of
the original procedure, the clinical assessment of these complaints
is sometimes difficult, and a CT scan is usually required. When
a fluid collection within the peritoneal cavity is found on CT scan,
antibiotics and percutaneous drainage of the collection is the treatment
of choice. There should still be a determination as to what the
cause of the infection was, so tailored antibiotic therapy can be initiated.
Initial antibiotic treatment is usually with broad-spectrum antibiotics
such as piperacillin-tazobactam or imipenem. Should the patient exhibit
signs of peritonitis and/or have free air on x-ray or CT
scan, then re-exploration should be considered.
For patients who present primarily (i.e., not postoperatively)
with the clinical and radiologic findings of an abscess but are
clinically stable, the etiology of the abscess must be determined.
A plan for drainage of the abscess and decisions about further diagnostic
studies with consideration of the timing of any definitive surgery
all need to be balanced. This can be a complex set of decisions, depending
on the etiology (e.g., appendicitis or diverticulitis); but if the
patient exhibits signs of peritonitis, urgent surgical exploration
should be performed.
Postoperative infections that progress to the fulminant soft
tissue infection known as necrotizing fasciitis are
uncommon. Group A streptococcal (M types 1, 3, 12, and 28) soft tissue infections, as
well as infections with Clostridium perfringens and C.
septicum carry a mortality of 30 to 70%. Septic
shock can be present and patients can become hypotensive less than
6 hours following inoculation. Manifestations of a group A Streptococcus
pyogenes infection in its most severe form include hypotension,
renal insufficiency, coagulopathy, hepatic insufficiency, ARDS,
tissue necrosis, and erythematous rash.
These findings constitute a surgical emergency and the mainstay
of treatment remains wide débridement of the necrotic tissue
to the level of bleeding, viable tissue. A gray serous fluid at
the level of the necrotic tissue is usually noted, and as the infection
spreads, thrombosed blood vessels are noted along the tissue planes
involved with the infection. Typically, the patient requires serial
trips to the OR for wide débridement until the infection is
under control. Antibiotics are an important adjunct to surgical
débridement and broad-spectrum coverage should be used
because these infections may be polymicrobial (i.e., so-called mixed-synergistic
infections). S. pyogenes is eradicated
with penicillin, and it should still be used as the initial drug
Response Syndrome, Sepsis, and Multiple-Organ Dysfunction Syndrome
The systemic inflammatory response syndrome (SIRS) and the multiple
organ dysfunction syndrome (MODS) carry significant mortality risks
(Table 12-19). Specific criteria have been
established for the diagnosis of SIRS (Table 12-20),
but two criteria are not required for the diagnosis of SIRS: lowered
blood pressure and blood cultures positive for infection. SIRS is
the result of proinflammatory cytokines related to tissue malperfusion
or injury. The dominant cytokines implicated in this process include
interleukin-1, interleukin-6, and tissue necrosis factor. Other mediators
include nitric oxide, inducible macrophage-type nitric oxide synthase,
and prostaglandin I2.
Table 12-19 Mortality Associated with Patients
Exhibiting Two or More Criteria for Systemic Inflammatory Response
Syndrome (SIRS) |Favorite Table|Download (.pdf)
Table 12-19 Mortality Associated with Patients
Exhibiting Two or More Criteria for Systemic Inflammatory Response
|2 SIRS criteria||5|
|3 SIRS criteria||10|
|4 SIRS criteria||15–20|
Table 12-20 Inclusion
Criteria for the Systemic Inflammatory Response Syndrome |Favorite Table|Download (.pdf)
Table 12-20 Inclusion
Criteria for the Systemic Inflammatory Response Syndrome
|Temperature >38°C or <36°C (>100.4°F or <96.8°F)|
|Heart rate >90 beats/min|
|Respiratory rate >20 breaths/min or Paco2 <32
|White blood cell count <4000 or >12,000 cells/mm3 or
>10% immature forms|
Sepsis is categorized as sepsis, severe sepsis, and septic shock.
An oversimplification of sepsis would be to define it as SIRS plus infection.
Severe sepsis is defined as sepsis plus signs of cellular hypoperfusion
or end-organ dysfunction. Septic shock would then be sepsis associated
with hypotension after adequate fluid resuscitation.
MODS is the culmination of septic shock and multiple end-organ failure.107 Usually
there is an inciting event (e.g., perforated sigmoid diverticulitis),
and as the patient undergoes resuscitation, he or she develops cardiac hypokinesis
and oliguric or anuric renal failure, followed by the development
of ARDS and eventually septic shock with death.
Management of SIRS/MODS includes aggressive global resuscitation
and support of end-organ perfusion, correction of the inciting etiology,
control of infectious complications, and management of iatrogenic
complications.108–110 Drotrecogin α,
or recombinant activated protein C, appears to specifically counteract
the cytokine cascade of SIRS/MODS, but its use is still
limited.111,112 Other adjuncts for supportive therapy
include tight glucose control, low tidal volumes in ARDS, vasopressin
in septic shock, and steroid replacement therapy.
and Metabolic Support Complications
A basic principle is to use enteral feeding whenever possible,
but complications can intervene such as aspiration, ileus, and to
a lesser extent, sinusitis. There is no difference in aspiration
rates when a small-caliber feeding tube is placed transpylorically
into the duodenum or if it remains in the stomach. Patients who
are fed via nasogastric tubes are at risk for aspiration pneumonia,
because these relatively large-bore tubes stent open the esophagus,
creating the possibility of gastric reflux. The use of enteric and
gastric feeding tubes obviates complications of TPN, such as pneumothorax,
line sepsis, upper extremity DVT, and the related expense. There
is growing evidence to support the initiation of enteral feeding
in the early postoperative period, before the return of bowel function, where
it is usually well tolerated.
In patients who have had any type of nasal intubation that are
having high, unexplained fevers, sinusitis must be entertained as
a diagnosis. CT scan of the sinuses is warranted, followed by aspiration
of sinus contents so the organism(s) are appropriately treated.
Patients who have not been enterally fed for prolonged periods secondary
to multiple operations, those who have had enteral feeds interrupted
for any other reason, or those with poor enteral access are at risk
for the refeeding syndrome, which is characterized by severe hypophosphatemia
and respiratory failure. Slow progression of the enteral feeding
administration rate can avoid this complication.
Common TPN problems are mostly related to electrolyte abnormalities
that may develop. These electrolyte errors include deficits or excesses
in sodium, potassium, calcium, magnesium, and phosphate. Acid-base
abnormalities can also occur with the improper administration of
acetate or bicarbonate solutions.
The most common cause for hypernatremia in hospitalized patients
is underresuscitation, and conversely, hyponatremia is most often caused
by fluid overload. Treatment for hyponatremia is fluid restriction
in mild or moderate cases and the administration of hypertonic saline
for severe cases. An overly rapid correction of the sodium abnormality
may result in central pontine myelinolysis, which results in a severe
neurologic deficit. Treatment for hyponatremic patients includes
fluid restriction to correct the free water deficit by 50% in
the first 24 hours. An overcorrection of hyponatremia can result
in severe cerebral edema, a neurologic deficit, or seizures.
In 2001, Van den Berghe and colleagues demonstrated that tight
glycemic control by insulin infusion is associated with a 50% reduction
in mortality in the critical care setting.113 This
prospective, randomized, controlled trial of 1500 patients had two
study arms: the intensive-control arm, where the serum glucose was
maintained between 80 and 110 mg/dL with insulin infusion;
and the control arm, where patients received an insulin infusion
only if blood glucose was greater than 215 mg/dL, but serum
glucose was then maintained at 180 to 200 mg/dL.
The tight glycemic control group had an average serum glucose
level of 103 mg/dL, and the average glucose level in the
control group was 153 mg/dL. Hypoglycemic episodes (glucose
<40 mg/dL) occurred in 39 patients in the tightly controlled
group, while the control group had episodes in 6 patients. The overall
mortality was reduced from 8% to 4.6%, but the
mortality of those patients whose ICU stay lasted longer than 5
days was reduced from 20% to 10%. Secondary findings included
an improvement in overall morbidity, a decreased percentage of ventilator
days, less renal impairment, and a lower incidence of bloodstream
infections. These finding have been corroborated by subsequent similar
studies, and the principal benefit appears to be a greatly reduced
incidence of nosocomial infections and sepsis. It is not known whether
the benefits are due to strict euglycemia, to the anabolic properties
of insulin, or both, but the maintenance of strict euglycemia appears
to be a powerful therapeutic strategy.113–115
“Stress dose steroids” have been advocated
for the perioperative treatment of patients on corticosteroid therapy,
but recent studies strongly discourage the use of supraphysiologic
doses of steroids when patients are on low or maintenance doses
(e.g., 5 to 15 mg) of prednisone daily. Parenteral glucocorticoid
treatment need only replicate physiologic replacement steroids in
the perioperative period. When patients are on steroid replacement
doses equal to or greater than 20 mg per day of prednisone, it may
be appropriate to administer additional glucocorticoid doses for
no more than two perioperative days.116–118
Adrenal insufficiency may be present in patients with a baseline
serum cortisol less than 20 μg/dL. A rapid
provocative test with synthetic adrenocorticotropic hormone may
confirm the diagnosis. After a baseline serum cortisol level is
drawn, 250 μg of cosyntropin is administered. At
exactly 30 and 60 minutes following the dose of cosyntropin, serum
cortisol levels are obtained. There should be an incremental increase
in the cortisol level of between 7 and 10 μg/dL
for each half hour. If the patient is below these levels, a diagnosis
of adrenal insufficiency is made, and glucocorticoid and mineralocorticoid
administration is then warranted. Mixed results are common, but
the complication of performing major surgery on an adrenally insufficient
patient is sudden or profound hypotension.108
Thyroid hormone abnormalities usually consist of previously undiagnosed
thyroid abnormalities. Hypothyroidism and the so-called sick-euthyroid
syndrome are more commonly recognized in the critical care setting.
When surgical patients are not progressing satisfactorily in the
perioperative period, screening for thyroid abnormalities should
be performed. If the results show mild to moderate hypothyroidism, then
thyroid replacement should begin immediately and thyroid function
studies monitored closely. All patients should be reassessed after
the acute illness has subsided regarding the need for chronic thyroid
Hypothermia is defined as a core temperature less than 35°C (95°F), and
is divided into subsets of mild [35 to 32°C, (95 to 89.6°F)], moderate [32
to 28°C (89.6 to 82.4°F)], and severe [<28°C,
(<82.4°F)] hypothermia. Shivering, the body’s
attempt to reverse the effects of hypothermia, occurs between 37
and 31°C (98.6 and 87.8°F), but ceases at temperatures below 31°C
(87.8°F). Patients who are moderately hypothermic are at higher
risk for complications than are those who are more profoundly hypothermic.
Hypothermia creates a coagulopathy that is related to platelet
and clotting cascade enzyme dysfunction. This triad of metabolic
acidosis, coagulopathy, and hypothermia is commonly found in long operative
cases, and in patients with blood dyscrasias. The enzymes that contribute
to the clotting cascade and platelet activity are most efficient
at normal body temperatures; therefore all measures must be used
to reduce heat loss intraoperatively.119
The most common cardiac abnormality is the development of arrhythmias
when body temperature drops below 35°C (95°F). Bradycardia occurs with
temperatures below 30°C (86°F). It is well known that hypothermia
may induce CO2 retention resulting in respiratory acidosis.
Renal dysfunction of hypothermia manifests itself as a paradoxic
polyuria, and is related to an increased glomerular filtration rate,
as peripheral vascular constriction creates central shunting of
blood. This is potentially perplexing in patients that are undergoing
resuscitation for hemodynamic instability, because the brisk urine
output provides a false sense of an adequate intravascular fluid
Neurologic dysfunction is inconsistent in hypothermia, but a
deterioration in reasoning and decision-making skills progresses
as body temperature falls, and profound coma (and a flat electroencephalogram)
occurs as the temperature drops below 30°C (86°F). The diagnosis
of hypothermia is important, so accurate measurement techniques are
required to get a true core temperature.
Methods used to warm patients include warm air circulation over
the patient, and heated IV fluids, and more aggressive measures
such as bilateral chest tubes with warm solution lavage, intraperitoneal
rewarming lavage, and extracorporeal membrane oxygenation. A rate
of temperature rise of 2 to 4°C/h (3.6 to 7.2°F/h)
is considered adequate, but the most common complication for nonbypass rewarming
is arrhythmia with ventricular arrest.
Hyperthermia is a core temperature greater than 38.6°C (101.5°F),
and has a host of etiologies (Table 12-21).120 Hyperthermia
can be environmentally induced (e.g., summer heat with inability
to dissipate heat or control exposure), iatrogenically induced (e.g., heat
lamps and medications), endocrine in origin (e.g., thyrotoxicosis),
or neurologically induced (i.e., hypothalamic).
Table 12-21 Common
Causes of Elevated Temperature in Surgical Patients |Favorite Table|Download (.pdf)
Table 12-21 Common
Causes of Elevated Temperature in Surgical Patients
|Neuroleptic malignant syndrome||Drug reaction|
|Carcinoid syndrome||Factitious syndrome|
Malignant hyperthermia occurs after exposure to agents such as succinylcholine
and some halothane-based inhalational anesthetics. The presentation
is dramatic, with rapid onset of increased temperature, rigors,
and myoglobinuria related to myonecrosis. Medications must be discontinued
immediately and dantrolene administered (2.5 mg/kg every
5 minutes) until symptoms subside. Aggressive cooling methods are
also implemented, such as an alcohol bath, or packing in ice. In
cases of severe malignant hyperthermia, the mortality rate is nearly
Thyrotoxicosis can occur after surgery, due to undiagnosed Graves’ disease.
Hyperthermia [>40°C, (104°F)], anxiety, copious
diaphoresis, congestive heart failure (present in about one fourth
of episodes), tachycardia (most commonly atrial fibrillation), and
hypokalemia (up to 50% of patients) are hallmarks of the
disease. The treatment of thyrotoxicosis includes glucocorticoids,
propylthiouracil, beta blockade, and iodide (Lugol’s solution)
delivered in an emergent fashion. As the name suggests, these patients
are usually toxic and require supportive measures as well. Acetaminophen,
cooling modalities noted in the paragraph above, and vasoactive
agents often are indicated.