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occur. The return of bowel activity is heralded by the presence of
bowel sounds, flatus, and bowel movements.
Patients with early postoperative small bowel obstruction do
not show manifestations of bowel activity or have temporary
return of bowel function. In adynamic ileus, the stomach, small
bowel, and colon are affected. In mechanical obstruction, the
obstruction may be partial or complete, may occur in the proxi-
mal part of the small bowel (high obstruction) or in the distal part
of the small bowel (low obstruction), and may be a closed-loop
or open-ended obstruction.33 There is stasis and progressive accu-
mulation of gastric and intestinal secretions and gas; the bowel
may lose its tone and dilate, resulting in abdominal distention,
pain, nausea and vomiting, and obstipation. The extent of the
clinical manifestations varies with the cause, degree, and level of
obstruction. Patients with high mechanical small bowel obstruc-
tion vomit early in the course and usually have no or minimal
distention. The vomitus is generally bilious. Patients with distal
obstruction vomit later in the course and have more pronounced
abdominal distention. The vomitus may initially be bilious and
then becomes more feculent. Differentiation between adynamic
ileus and mechanical obstruction can be difficult. With adynamic
ileus, patients have diffuse discomfort but no sharp colicky pain
and a distended abdomen. They often have a quiet abdomen, with
few bowel sounds detected on auscultation with a stethoscope.
With mechanical obstruction, high-pitched, tinkling sounds may
be detected. Fever, tachycardia, manifestations of hypovolemia,
and sepsis may also develop.
The diagnosis of bowel obstruction is usually based on clinical
findings and plain radiographs of the abdomen.33 However, in the
postoperative period, differentiation between adynamic ileus and
mechanical obstruction is imperative because the treatment is
completely different. A CT scan, abdominal radiographs, and
small bowel follow-through are variably used to establish the
diagnosis and assist in treatment decision making. In adynamic
ileus, abdominal radiographs reveal diffusely dilated bowel
throughout the intestinal tract, with air in the colon and rectum.
Air-fluid levels may be present, and the amount of dilated bowel
varies greatly. With mechanical bowel obstruction, there is small
bowel dilation with air-fluid levels and thickened valvulae con-
niventes in the bowel proximal to the point of obstruction and
little or no gas in the bowel distal to the obstruction. A CT scan
is more accurate for differentiating functional from mechanical
obstruction by identifying the so-called transition point or cutoff
at the obstruction site in cases of mechanical obstruction. It also
determines the level (high or low) and degree of obstruction
(partial versus high-grade or complete), differentiates between
uncomplicated and complicated (compromised bowel, perfora-
tion) obstruction, and identifies specific types of obstruction
(closed-loop obstruction, intussusception). In addition, CT may
identify other associated disease states (e.g., bowel ischemia,
phlegmon, abscess, pancreatitis). Small bowel follow-through is
indicated if the clinical picture of postoperative small bowel
obstruction is confusing, radiographs of the abdomen are not
diagnostic, or the response to expectant management is inade-
quate. A standard battery of laboratory tests is also obtained,
including complete blood cell count with differential; determina-
tion of amylase, lipase, electrolyte, magnesium, and calcium levels;
and urinalysis.
Treatment
Preventive measures must be started intraoperatively and contin-
ued in the immediate postoperative period. A concerted effort
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CHAPTER 12  Surgical Complications 307
must be made during any abdominal operation to minimize
injury to the bowel and other peritoneal surfaces, the recognized
source of adhesion formation. During the operation, the surgeon
must handle the tissues gently and limit peritoneal dissection to
only what is essential. The bowel must not be allowed to desiccate
by prolonged exposure to air without protection. Moist laparot-
omy pads must be used to cover the bowel and must be moistened
frequently if contact with the bowel is prolonged. Instrument
injury to the bowel must be avoided. Given the importance of
adhesion formation and the large magnitude of serious problems
related to adhesions, adjunctive measures, such as antiadhesion
barriers, may be considered. Numerous antiadhesion barriers are
available, including an oxidized cellulose product and a product
that is a combination of sodium hyaluronate and carboxymethyl
cellulose. These agents may inhibit adhesions wherever they are
placed. However, a decrease in the number of adhesions at the
site of application does not translate into a decrease in the rate of
small bowel obstruction.
In the postoperative period, electrolyte levels are monitored,
and any imbalance is corrected. Alternative analgesia to narcotics,
such as NSAIDs and placement of a thoracic epidural with local
anesthetic, may be used when possible. Intubation of the stomach
with an NG tube needs to be applied selectively. Routine intuba-
tion does not confer any appreciable effect and is associated with
discomfort; inhibits ambulation; and predisposes to aspiration,
sinusitis, otitis, esophageal injury, and electrolyte imbalance. The
use of prokinetic agents does not alter the outcome after colorectal
surgery, and other pharmacologic manipulations, such as para-
sympathetic agents, adrenergic blocking agents, and metoclo-
pramide, have no impact on resolving postoperative ileus.32 The
role of early postoperative feeding is unclear.
When early postoperative obstruction is suspected or diag-
nosed, a three-step approach is essential to guarantee a favorable
outcome—resuscitation, investigation, and surgical interven-
tion.33 Emergency repeat laparotomy is performed if there is a
closed-loop, high-grade, or complicated small bowel obstruction,
intussusception, or peritonitis. Adynamic ileus is treated by resolv-
ing some of the abnormalities listed in Box 12-10 and waiting
expectantly for resolution, with surgery not usually being required.
Partial mechanical small bowel obstruction is also initially
managed expectantly and for a longer period, 7 to 14 days, if the
patient is stable and clinical and radiologic improvement contin-
ues. During this time, nutritional support is initiated, and surgical
intervention is performed if there are signs of deterioration or no
improvement.
Acute Abdominal Compartment Syndrome
Cause
Abdominal compartment syndrome (ACS) comprises increasing
organ dysfunction or failure as a result of IAH. IAH is present
when there is consistent increased IAP greater than 12 mm Hg,
determined by a minimum of three measurements conducted 4
to 6 hours apart, measured at the end of expiration in a relaxed
patient. ACS may be primary or secondary and develops when
IAP is 20 mm Hg or greater, with or without abdominal perfu-
sion pressure less than 50 mm Hg (at least three measurements
performed 1 to 3 hours apart); it is associated with failure of one
or more organ systems that was not present previously.
Primary ACS develops as a result of pathologic IAH caused by
intra-abdominal pathology, and secondary ACS develops in the
absence of intra-abdominal primary pathology, injury, or inter-
vention. Primary ACS is most commonly encountered in victims
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308 SECTION II  Perioperative Management
of multiple trauma, especially after damage control surgery, and
develops as a result of ileus caused by bowel edema and contami-
nation, continued bleeding, coagulopathy, packing used to control
bleeding, capillary leak, and massive fluid resuscitation and trans-
fusion. Closure of a noncompliant abdominal wall under tension
in these situations is associated with IAH in 100% of cases. In
nontrauma patients, IAH and possibly primary ACS have been
reported to occur in patients with ascites, retroperitoneal hemor-
rhage, pancreatitis, or pneumoperitoneum and after reduction of
chronic hernias that have lost their domain, repair of ruptured
abdominal aortic aneurysm, complex abdominal procedures, and
liver transplantation. Secondary ACS is in part iatrogenic and
commonly encountered in patients with shock requiring aggres-
sive fluid resuscitation with crystalloids, thermally injured and
shock trauma victims, critically ill hypothermic and septic patients,
and patients who have sustained cardiac arrest. Shock and isch-
emia increase capillary permeability; combined with excessive
crystalloid resuscitation (leading to dilution of plasma) and gut
reperfusion, which further increase microvascular permeability,
exudation of fluid with resultant interstitial edema, bowel wall
edema, and ascites occurs.
In healthy individuals, IAP ranges from subatmospheric to
5 mm Hg and fluctuates with respiration, body mass index, and
activity. IAP ranges from 3 to 15 mm Hg after uncomplicated
abdominal surgery. IAP reflects intra-abdominal volume and
abdominal wall compliance. With increased volume, there is a
decrease in compliance, and any further change in volume results
in an increase in pressure, leading to IAH. In the early stages of
IAH, changes in organ function are not detectable and of
questionable clinical significance. With further increase in IAP,
deleterious effects are observed in the intra-abdominal and extra-
abdominal organs and abdominal wall.27 Upward displacement of
the diaphragm results in decreased thoracic volume and compli-
ance and increased intrapleural pressure. An increase in peak
airway pressure (PAP), ventilation-perfusion ( V/Q � � ) mismatch,
hypoxia, hypercapnia, and acidosis result. When IAP reaches
25 mm Hg, there is an increase in end-respiratory pressure to
achieve a fixed tidal volume. However, modest IAH can exacerbate
acute lung injury, inhalation injury, or respiratory distress syn-
drome. Compression of the inferior vena cava and portal vein
occurs and results in decreased venous return and a decrease in
preload and pooling of blood in the splanchnic and lower extrem-
ity vascular beds and increased peripheral vascular resistance.
Venous return decreases with IAP greater than 20 mm Hg. As a
result, CO, cardiac index, and right atrial and pulmonary artery
occlusion pressures decrease. Increased intrathoracic pressure also
decreases left ventricular compliance, reducing contractility and
further decreasing CO. Ventricular compliance is reduced when
IAP is greater than 30 mm Hg. CO decreases, despite normovole-
mia or apparent high filling pressures and a normal ejection, when
the IAP is 20 to 25 mm Hg. Systemic delivery of oxygen decreases
and whole body oxygen consumption is significantly reduced at
an IAP greater than 25 mm Hg.
Direct compression of the kidneys and obstruction of venous
outflow, with resultant increase in prerenal vascular resistance
and shunting of blood from the cortex to the medulla, results in
a decrease in the glomerular filtration rate, renal plasma flow,
glucose reabsorption, and urine output. In a postoperative patient
admitted to the ICU with an IAP greater than 18 mm Hg, renal
function is impaired by 30%, independent of prerenal circula-
tion. Renal output decreases in 65% of patients with an IAP
greater than 25 mm Hg and in 100% of patients with an IAP
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greater than 35 mm Hg. Compression of the mesenteric vascula-
ture leads to a decrease in splanchnic perfusion, mesenteric
venous hypertension, and decreased hepatic arterial flow. This
results in severe intramucosal acidosis, intestinal edema, and vis-
ceral swelling; increased intestinal permeability; and possible bac-
terial translocation. Gastric intramucosal acidosis develops with
IAP greater than 20 to 25 cm H2O or 15 mm Hg. Elevated
central venous pressure interferes with venous cerebral outflow,
with consequent cerebral pooling and increase in intracerebral
pressure. Also, with diminished CO and increasing intracerebral
pressure, cerebral perfusion pressure decreases. Interleukin 6
(IL-6) and IL-1β levels increase in response to increased IAP.
Blood flow to the abdominal wall decreases with a progressive
increase in IAP; this may result in an increased rate of abdominal
wound complications.
Diagnosis
The clinical manifestations of primary and secondary ACS are
similar. However, the effects of secondary ACS are more subtle,
so the diagnosis may be missed, and the clinical deterioration of
the patient is usually attributed to severity of the primary illness
or occurrence of irreversible shock. Secondary ACS often occurs
during aggressive fluid resuscitation in patients with burns, extra-
abdominal injury, or sepsis. Patients with ACS have difficulty
breathing or are difficult to ventilate and exhibit increasing PAP,
decreased volumes, hypoxia, worsening hypercapnia, and deterio-
rating compliance. Oliguria rarely occurs in the absence of respira-
tory dysfunction or failure. The CO is reduced, despite apparent
high filling pressures, and vasopressor therapy is required. The
abdomen becomes distended and tense, and neurologic deteriora-
tion may occur. The central venous pressure, PCWP, and PAP
become elevated, and acidosis develops. Anuria, exacerbation of
pulmonary failure, cardiac decompensation, and death ultimately
occur.
Use of the urinary bladder catheter has been the gold standard
and is the indirect method used to measure IAP.28 IAP is measured
in the following ways: (1) using a regular Foley catheter, discon-
nect from drainage tubing, directly inject 50 mL, clamp, insert
needle, and measure; (2) using a three-way Foley catheter, inject
saline into one port, and measure IAP through the other; or (3)
serially connect a regular Foley catheter to a three-way stopcock
and a transducer. Other measurement kits are commercially avail-
able. Once measured, the pressure is graded: GI (IAP <10 to
15 cm H2O), GII (IAP <16 to 25 cm H2O), GIII (IAP <26 to
35 cm H2O), and GIV (IAP >36 cm H2O).
Treatment
The prevention of primary ACS entails leaving the peritoneal
cavity open in patients at risk for IAH and after high-risk surgical
procedures. Patients at risk for secondary ACS receiving crystal-
loid resuscitation must be monitored closely, and IAP must be
measured when patients are given more than 6 liters of crystalloid
in a 6-hour period. In addition to blood pressure and urine
output, monitoring abdominal perfusion pressure (abdominal
perfusion pressure = mean arterial pressure − IAP) by continu-
ously measuring IAP throughout resuscitation is a helpful indica-
tor of the resuscitation end point. Routine measurement of IAP
also must be considered in critically ill patients because IAH is
the leading cause of chest wall impairment in ARDS. Monitoring
gastric pH can detect cases of secondary ACS early after admission
to the ICU. A high incidence of suspicion is paramount, especially
in cases of secondary ACS, in which the onset is insidious and
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manifestations are subtle. Patients exhibiting the prodromal phase
of ACS benefit from timely intervention to relieve IAH and
prevent progression to ACS (Box 12-11). Conservative fluid resus-
citation; administration of analgesia, sedatives, and pharmaco-
logic paralysis; patient positioning; drainage of intra-abdominal
fluid; escharotomy; renal placement therapy; and diuretics are
measures that may prevent progression to ACS.
Optimizing treatment and identifying patients with IAH-ACS
likely to benefit from decompression is a challenging task. The
decision to intervene surgically is not based on IAH alone but
rather on the presence of organ dysfunction in association with
IAH. Few patients with a pressure of 12 mm Hg have any organ
dysfunction, whereas IAP greater than 15 to 20 mm Hg is signifi-
cant in every patient. With grade III IAH, decompression may be
considered when the abdomen is tense and signs of extreme ven-
tilatory dysfunction and oliguria develop. In grade IV IAH, with
signs of ventilator and renal failure, decompression is indicated.
In patients with severe head injury and IAP greater than
20 mm Hg, even without overt ACS, or intractable intracranial
hypertension without obvious head injury, abdominal decompres-
sion must be considered. In contrast to primary ACS, in which
reopening of the preexisting laparotomy incision for decompres-
sion can be easily done, there is usually reluctance to perform a
formal laparotomy for decompression in cases of secondary ACS,
especially in the absence of primary intra-abdominal pathology.
If nonoperative measures (see earlier) prove ineffective, fascial
BOX 12-11 Prevention of Abdominal
Compartment Syndrome
Patients at risk for IAH and abdominal compartment syndrome are identified
(e.g., major trauma, complex abdominal procedure).
Organ function is monitored and assessed:
• Lungs: Hypercapnia, hypoxia, difficult ventilation, elevated pulmonary
artery pressure, decrease in PaO2/FIO2 ratio, decreased compliance,
intrapulmonary shunt, increased dead space
• Heart: Decreased CO and cardiac index and need for vasopressors
• Kidneys: Oliguria unresponsive to fluid therapy
• Central nervous system: Glasgow Coma Scale score <10 or neurologic
deterioration in the absence of neurotrauma
• Abdomen: Distention; CT scan to check for fluid collections, narrowing
of inferior vena cava, compression of kidneys, and rounding of abdomen
Intra-abdominal pressure is measured and monitored with a urinary bladder
or gastric catheter.
Other tests are done to check organ dysfunction:
• Gastric mucosal pH
• Near-infrared spectroscopy to measure muscle and gastric tissue
oxygenation
• Abdominal perfusion pressure = mean arterial pressure − intra-
abdominal pressure
• Renal filtration gradient = mean arterial pressure − 2 × intra-abdominal
pressure
• CT scan
Measures to lower IAH are implemented:
• Drainage of intra-abdominal fluid collections
• Muscle relaxation
Avoid primary closure of the incision—laparotomy or mesh, Bogota bag,
biologic mesh, or vacuum-assisted closure.
CO, cardiac output; CT, computed tomography; FIO2, fraction of
inspired oxygen; IAH, intra-abdominal hypertension; PaO2, partial
arterial oxygen pressure.
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CHAPTER 12  Surgical Complications 309
release without exposing the peritoneal cavity using minimally
invasive techniques has proven effective in lowering IAP in experi-
mental animals.34 Decompression (formal laparotomy) is an emer-
gency and is performed in the operating room. Decompression
leads to reduction of IAH, severe hypotension as a result of sudden
decrease in systemic vascular resistance, and abrupt increase in the
true tidal volume delivered to the patient, with washout of the
byproducts of anaerobic metabolism from below the diaphragm.
Respiratory alkalosis; decrease in effective preload; and a bolus of
acid, potassium, and other byproducts delivered to the heart,
where they cause arrhythmia or asystolic arrest, result. Decom-
pression is performed after adequate preload with volume has
been established. Most patients respond to decompression and
survive. When stable, the patient may be returned to the operating
room for definitive closure. If primary closure is impossible,
closure may be effected with skin flaps only, composite mesh,
bioprosthesis, bilateral medial advancement of rectus muscle and
its fascia with lateral skin relaxation incisions, or tissue expanders
and myocutaneous flaps.
Postoperative Gastrointestinal Bleeding
Causes
Postoperative GI bleeding is one of the most worrisome complica-
tions encountered by general surgeons. Possible causes in the
stomach include peptic ulcer disease, stress erosion, Mallory-Weiss
tear, and gastric varices; possible causes in the small intestine
include arteriovenous malformations and bleeding from an anas-
tomosis; and possible causes in the large intestine include anasto-
motic hemorrhage, diverticulosis, arteriovenous malformations,
and varices.
In critically ill patients, GI bleeding caused by stress ulceration
is a serious complication. The incidence of bleeding from stress
ulceration has decreased in the past 15 years, mainly because of
improved supportive care, superior acid suppression, and enhanced
resuscitative measures. Clinically significant bleeding that leads to
hemodynamic instability, the need for transfusion of blood prod-
ucts, and occasionally operative intervention occurs in less than
5% of cases and is associated with significant mortality. Risk
factors for stress ulceration are listed in Box 12-12.
Presentation and Diagnosis
When considering the source of the hemorrhage, a previous
history is important when assessing the patient. A history of
peptic ulcer disease and previous upper GI bleeding leads one to
consider a duodenal ulcer. Severe trauma, major abdominal
surgery, central nervous system injury, sepsis, or MI may be associ-
ated with stress ulceration. An antecedent history of violent emesis
leads to consideration of Mallory-Weiss tear, and a history of
portal hypertension or variceal bleeding is a clue regarding the
BOX 12-12 Risk Factors for Development
of Stress Erosions
Multiple trauma
Head trauma
Major burns
Clotting abnormalities
Severe sepsis
Systemic inflammatory response syndrome
Cardiac bypass
Intracranial operations