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1178 PART 10: The Surgical Patient
inadequate. Intravascular volume depletion can lead to a decrease in the GASTROINTESTINAL
renal blood flow, which leads to decreasing glomerular filtration rate,
renal cortical ischemia, and acute tubular necrosis. Aggressive volume Abdominal complications following electrical trauma are relatively
replacement is therapeutic by restoring the circulating plasma volume. infrequent. Most often, gastric atony and adynamic ileus are seen. These
The goal for urinary output is 0.5 to 1 mL/kg/h. complications usually resolve with nasogastric suction, intravenous
The precipitation of intravascular hemochromogens in the renal fluid administration, nutrition, and time. More serious complications
tubules is another cause of renal dysfunction. Hemochromogens can be such as gastrointestinal bleeding, acalculous cholecystitis, rupture
visualized in the urine in approximately 25% of patients with electrical of colon, gallbladder, and other organs have been reported. It is dif-
injuries. Myoglobin, secondary to rhabdomyolysis, and free hemoglo- ficult to know whether all of these processes are due to electricity or
13
bin, from lysed red blood cells, are the responsible pigments. The detri- the stresses of severe shock and systemic illness. If a contact point on
mental effect of pigments deposited in the tubules is thought to increase the abdomen has caused a full-thickness burn, the wound should be
with hypovolemia, which further underscores the need for adequate surgically excised. If this wound includes the posterior fascia of the
fluid resuscitation. The best prophylactic and therapeutic regimen to abdominal wall, then formal exploratory celiotomy should follow.
prevent renal toxicity secondary to hemochromogen deposition is to However, intra-abdominal pathology may be present even without
maintain adequate intravascular volume and high urine output. This abdominal wall injuries. Systemic signs of sepsis or changes on serial
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is accomplished with lactated Ringer solution and mannitol, infused physical examination of the abdomen should alert the clinician to
hourly in 12.5-g increments. The resulting solute diuresis must be moni- intra-abdominal pathology. White blood cell counts, liver function
tored carefully to prevent intravascular volume depletion and electrolyte tests, amylase and lipase levels, as well as examination of the abdomen
abnormalities. In the presence of urine pigments, the goal is to create a by ultrasound, computed tomography (CT), MRI, and peritoneal lavage
flow of urine of at least 1 to 2 mL/kg/h. It should be noted that the use may be required in making the correct diagnosis and directing therapy.
of mannitol has been controversial, in part, because studies have shown Virtually any abdominal catastrophe can be caused by electrical
conflicting results in preventing acute renal failure. 7,15-17 current, and thus the physician must be alert and respond appropriately
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Myoglobin is much more soluble and less likely to be retained by the to subtle clinical changes in abdominal signs and symptoms. If intra-
kidney when the urine is alkaline. Some contend that the provision of abdominal injury is not suspected, then enteral feedings should be
adequate resuscitation and a solute diuresis will automatically create instituted within 6 hours of admission if possible.
a urine pH that is clinically therapeutic. However, others recommend
maintaining a urinary pH of greater than 6.5 by adding sodium bicarbon- NEUROLOGIC
ate to the intravenous fluids. This treatment is continued until urinary
myoglobin has cleared, which may take from 48 to 60 hours. There is It is possible for any aspect of the human nervous system to be affected
evidence that bicarbonate also participates in the solute diuresis; hence its by high-voltage trauma. Neurologic deficits may appear in either the
value may be twofold. If the urine does not clear of hemochromogens central or peripheral nervous system. Evidence of injury may be imme-
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within 24 hours and the serum levels of CPK isoenzymes continue to diate or delayed. Finally, the duration of neurologic deficit ranges from
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rise, then a source of undetected muscle ischemia or myonecrosis should transient to permanent.
be actively sought. Careful, repeated physical examination, specifically Neurologic changes are often poorly described and documented
looking for areas of swelling and tenderness, should be performed. when they do occur, and hence evaluation of retrospective data is
Technetium 99 m nuclear scanning may be helpful in localizing areas of difficult. Immediate neurologic deficits occur in more than 40% of all
ischemic muscle, although its lack of specificity may lead to false-positive patients. The most common symptom is loss of consciousness. This
results. Xenon 131 scanning and arteriography have both been shown occurs in up to 65% of patients and usually resolves without permanent
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to be generally unhelpful in localizing areas of muscle ischemia or myo- sequelae. However, long-term complaints include headache, dizziness,
necrosis. Magnetic resonance imaging (MRI) provides a reliable method vertigo, and seizure activity, as well as psychosocial behavioral disorders
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of evaluating edematous muscle. When occult muscle ischemia is dis- such as impotence and personality changes.
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covered, surgical decompression or debridement may or may not lead to Spinal cord injuries can have acute or delayed presentations. Acute
functional recovery of that muscle group but may alleviate the systemic neurologic deficiencies can demonstrate frighteningly complete motor
problems related to toxic effects of injured or dying muscle. and sensory loss. Yet acute deficits have a tendency to resolve over hours
or days. Delayed spinal cord symptomatology is much more ominous
and less likely to resolve. The pathophysiology of these delayed findings
PULMONARY is not well understood. 2
Peripheral nerve injuries account for 5% to 23% of all posttrau-
There are relatively few pulmonary complications that are character- matic neurologic sequelae. The most common injury is to the median
istic of electrical injury. Acute ventilatory failure secondary to electri- nerve, followed by the ulnar, radial, and peroneal nerves. In the acutely
cal injury is usually related to CNS injury, or chest wall impairment damaged edematous arm and hand, immediate operative decompres-
from direct or indirect injury. Depressed respiratory drive due to CNS sion of the carpal tunnel, cubital tunnel, and Guyon canal is urgent if
damage may lead to respiratory failure, necessitating mechanical ven- peripheral neuropathy develops. Following appropriate release, signs of
tilation. The chest wall and the muscles of respiration may be directly acute peripheral nerve compression should dissipate if thermal injury to
injured, leading to suffocation secondary to tetanic contractions of the the nerve has not occurred.
respiratory muscles, which may occur when the thorax is an involved
pathway for the electric current. In addition, chest wall dynamics may EXTREMITY AND WOUND
be impaired by direct thermal or blunt injury.
Other pulmonary sequelae such as pneumonia or effusion are treated The care of the extremity as well as the wound caused by electrical
as in any other injury. There are isolated reports of current-induced trauma will be discussed concurrently. The rationale behind this
bronchopleural fistula, but in most cases the need for ventilatory approach is that the attempted salvage of the extremity, particularly the
support is not due to current injury to the pulmonary parenchyma. arm and hand, best demonstrates the principles of maximal tissue pres-
When the transient path of the current passes through the pharynx, ervation with optimal residual function.
significant upper airway swelling may develop. All patients at risk After life-threatening emergencies are addressed, attention should
should undergo serial examination of the upper airway by fiberoptic be turned to assessing the soft tissue injury. The injury should always
endoscopy and should be prophylactically intubated if hypopharyngeal be suspected of being more extensive than it initially appears, as visible
edema is found. cutaneous injury is only a portion of the total tissue destruction.
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