Common intracranial complications following
head injury are
meningitis, usually associated with a
basilar skull fracture or open-
depressed skull fracture; delayed
hematoma;
hydrocephalus; and
vascular injuries. Prophylactic
antibiotics are not recommended for the management of
basilar skull fractures. The best means of preventing
infection from open-
depressed skull fractures is operative
debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed
hematomas. CT and MRI scans obtained several weeks or months after severe
head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical
hydrocephalus. Those that do, often benefit from a shunt.
Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with
cerebral contusions or other intracranial lesions, this may present an unacceptable risk for
intracranial hemorrhage. Pulmonary
infections frequently occur following
head injury, and can be associated with admission to the ICU and intubation. A large percentage of these
infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate
antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial
superinfection. The routine use of
antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric
therapy for
aspiration pneumonia should include
clindamycin.
Sinusitis is a frequent cause of
fever and
leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes.
Pulmonary edema is often caused by excessive fluid administration during
resuscitation of these patients, and can be avoided by monitoring central venous pressures.
Pulmonary edema may also be caused by ARDS, excessive
catecholamine release, or primary
cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose
heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive
gastritis is found in the majority of severely head-injured patients and may be due to
ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)