Surgical management of posthemorrhagic hydrocephalus in 22 low-birth-weight infants.

In order to assess the complication rates of cerebrospinal fluid diversion techniques used at our institution, a retrospective study of the surgical management of posthemorrhagic hydrocephalus was conducted from a population of 547 premature infants admitted to the neonatal intensive care unit from 1987 to 1989. The incidences of periventricular-intraventricular hemorrhage in the 3 years studied were 44%, 37%, and 27%, respectively. Thirty-nine of the infants developed posthemorrhagic hydrocephalus as determined by serial cranial ultrasonography; 22 required cerebrospinal fluid diversion. During the study period, we began using subcutaneous ventricular reservoirs and a low-pressure Neonatal Shunt (customized device) in infants weighing less than 1500 g at the time of instrumentation. This change in management was associated with a significant reduction (P < 0.005) in the morbidity and mortality compared to the use of external ventricular drainage devices. On the basis of these findings, the use of external ventricular drainage devices was discontinued.

Postinjury scopolamine administration in experimental traumatic brain injury.

A single bolus dose of scopolamine (1.0 mg/kg) or saline (equal volume) was injected (i.p.) at 15, 30 or 60 min after fluid percussion traumatic brain injury in the rat. Scopolamine administered at 15 min postinjury significantly reduced beam walking deficits and body weight loss assessed for 5 days after injury. Scopolamine treatment at 30 or 60 min postinjury had no effect on behavioral outcome assessed for 5 days after injury. Plasma concentrations of scopolamine were measured with a radioreceptor assay. The plasma half-life for scopolamine was 21.6 min in injured rats and 17.3 min in normal rats (P less than 0.05). These results, along with evidence from previous studies, suggest that a brief period of excessive neuronal excitation can produce relatively long-lasting behavioral deficits. The temporal effectiveness of receptor antagonist intervention in this process appears to be brief.

Penetrating intracranial wood wounds: clinical limitations of computerized tomography.

The case history of a patient with a periorbital penetrating wooden foreign body is presented. The computerized tomography (CT) densities of several different sources of wood were compared using an experimental model. The clinical usefulness and practical limitations of CT in the evaluation of intracranial foreign bodies is discussed, and the management of this type of injury is reviewed.

Midline central nervous lipomas in children.

We review the clinical, radiologic, surgical, and pathologic features of 15 children with central nervous system lipomas. Three were situated in the corpus callosum and 12 at the conus medullaris. The intracranial and the intraspinal disorders share several features suggesting that they are related. Both are midline developmental abnormalities associated with dysraphism and both may have extrinsic as well as intrinsic components. Both can occur as occult asymptomatic lesions, particularly early in life, or can be part of extensive dysraphic malformations. Computed tomography is the best way to demonstrate the nature and extent of these lesions prior to treatment.

Evaluation of acute nonpenetrating cervical spinal cord injuries with CT metrizamide myelography.

Computerized tomography metrizamide myelography was performed in 46 patients with acute, nonpenetrating cervical spinal cord injuries. By visualizing the spinal canal, spinal cord, and any compressive lesion, the study proved valuable in the decision as to whether surgical decompression was indicated and what approach should be used. Eleven patients were found to have significant spinal cord compression, 10 of whom were treated surgically. The technique, results, and complications resulting from the study are discussed.

Papilledema after acute head injury.

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.

Gastric secretory and mucosal injury response to severe head trauma.

The problem of gastric secretory and mucosal injury response was evaluated in 19 patients who had suffered a severe head injury. Fifteen of 19 patients had some evidence of gastrointestinal hemorrhage. In 7 cases, this was marked. The mean volume of gastric secretions ranged from 36.4 ml/hour on Day 1 to 47.6 ml/hour on Day 6. The mean value of titratable acidity ranged from 3.4 meq/hour on Day 1 to 3.9 meq/hour on Day 6. Possible risk factors were analyzed as a means of predicting specific subgroups of severely injured patients who would be more prone to have gastrointestinal complications. During the first 6 days after injury, there was no significant association (correlation coefficient not significant at the 0.05 level of significance) of the presence of an intracranial mass lesion, elevated intracranial pressure, brain stem dysfunction or prior episodes of hypotension or hypoxia, sepsis, shock, or the requirement for pressor agents with elevated gastric acid output, mucosal erosion, or hemorrhage. Because no specific risk factor or factors could be identified, all severely brain-injured patients should be on some form of therapy for the prevention of gastrointestinal complications.

Sarcoid optic neuropathy.

Three patients presented with unilateral progressive optic neuropathy. None of these patients had signs of symptoms referable to the chiasm or eye, thus confining their decline in vision to the optic nerve. Clinical and neuroradiographic evidence suggested a meningioma involving the optic nerve at the orbital-canalicular junction in one patient and the intracranial optic nerve in another patient. Surgical exploration in both patients, however, revealed a noncaseating granuloma. Decline in vision from granulomatous invasion of the retrobulbar optic nerve is an uncommon manifestation of sarcoidosis. Review of our patients' findings suggests that a nonsurgical diagnosis of sarcoid optic neuropathy may have been tenable.

Operative treatment in head injury.

Improved outcome will result only from improvement in the total care of the head-injured patient. Each aspect of care is dependent on the other: rescue services; aggressive emergency evaluation and resuscitation; monitoring of the patient's physical, chemical, and neurological status; CT scanning; and intensive medical therapy and early rapid surgical decompression. The injured brain is particularly prone to further secondary insults. Intracranial mass lesions must be removed quickly and thoroughly; the brain should be handled in a careful and gentle fashion intraoperatively, and medical complications should be prevented. Dysfunctional cells in a marginal state can only be expected to return to normal with the proper management and environment.

Computed tomography in the evaluation of incidence and significance of post-traumatic hydrocephalus.

Two hundred consecutive patients with severe head injury underwent sequential computed tomography (CT) on admission, after 4, 14, and 90 days, and after one year. Ventricular enlargement was evaluated in the surviving patients, based upon serial CT examinations. Significant ventricular enlargement was further evaluated with radionuclide cisternography. A significant correlation was shown between clinical outcome and presence or absence of ventricular enlargement. Radionuclide cisternography provided an additional means of determining those patients whose recovery was impaired by persistent obstruction of cerebrospinal fluid circulation and who would therefore benefit from cerebrospinal fluid shunting.

Flaccidity after head injury: diagnosis, management, and outcome.

Upon admission, 17 of 223 (8%) consecutive patients with severe head injury exhibited a flaccid, wholly unresponsive motor examination. In this study alcoholic intoxication neither caused depressed motor responsiveness in head-injured patients with high serum ethanol levels nor accounted for the motor examination in those exhibiting the flaccid state. Flaccidity was attributed principally to impaired ventilation in 4 patients, a major intracranial mass in 12, and a spinal cord injury in 1. Compared to the larger group of head-injured patients, the flaccid patients had a significantly greater incidence of hypercapnia (P less than 0.001), acidosis (P less than 0.01), and both elevated and uncontrollable intracranial pressure (ICP) (P less than 0.001). These findings and the high mortality rate (76%) in this study suggest that the magnitude of respiratory complications and the severity of mechanical brain injury are greater in flaccid patients. The flaccid patients undergoing surgical decompression for major intracranial mass lesions (11 cases) have all died and, although still small in number, this group may represent an important subset with a poor prognosis. Nonetheless, a protocol that encourages rapid radiological and electrophysiological assessment and vigorous surgical and ICP management until the probable cause of flaccidity is identified and treated has benefit. The flaccid state was reversed and a good recovery was attained after the restoration of blood pressure and/or ventilation in 2 patients who appeared to have sustained a very grave head injury. In another patient, absent somatosensory evoked potentials greatly facilitated the diagnosis of a spinal subdural hematoma. This program of prompt diagnosis and intense therapy did not result in a protracted course or undue numbers of severely brain-damaged survivors.

Further experience in the management of severe head injury.

A prospective and consecutive series of 225 patients with severe head injuries who were managed in a uniform way was analyzed to relate outcome to several clinical variables. Good recovery or moderate disability were achieved by 56% of the patients, 10% remained severely disabled or vegetative, and 34% died. Factors important in predicting a poor outcome included the presence of intracranial hematoma, increasing age, abnormal motor responses, impaired or absent eye movements or pupil light reflexes, early hypotension, hypoxemia or hypercarbia, and elevation of intracranial pressure over 20 mm Hg despite artificial ventilation. Most of these predictive factors were assessed on admission, but a subset of 158 patients was identified in whom coma was present on admission and was known to have persisted at least until the following day. Although the mortality in this subset (40%) was higher than in the total series, it was lower than in several comparable reported series of patients with severe head injury. Predictive correlations were equally strong in the entire series and in the subset of 158 patients with coma. A plea is made for inclusion in the definition of "severe head injury" of all patients who do not obey commands or utter recognizable words on admission to the hospital after early resuscitation.

Delayed sequelae of head injury.

The evaluation of delayed sequelae of head injury is greatly facilitated by CT. This non-invasive technique provides us with the opportunity to evaluate the head trauma patients sequentially to detect the development and clinical significance of post-traumatic sequelae like delayed intracerebral hemorrhage, hydrocephalus, and post-traumatic atrophy.

Failure of high-dose steroid therapy to influence intracranial pressure in patients with severe head injury.

While corticosteroids in standard neurosurgical dosage do not appear to influence recovery from severe head injury or elevated intracranial pressure (ICP), some reports claim that a much higher dose is effective. A resultant hypothesis is that an abrupt increase in corticosteroid dosage in patients with severe head injury should cause a detectable reduction in ICP and in cerebral elastance within 48 hours. To test this hypothesis 20 consecutive patients with severe head injury, 12 of whom had had surgical decompression of mass lesions, were studied. All patients were artificially ventilated, and had continuous monitoring of ICP and intermittent testing of elastance by measurement of the volume-pressure response (VPR). For the first 12 hours after admission, patients received methylprednisolone, 40 mg every 6 hours. The dose was then increased abruptly by giving a single dose of 2 gm and 500 mg every 6 hours for the next 24 hours, then tapering rapidly. No significant change in ICP or VPR could be detected after 24 or 48 hours of high-dose steroid therapy. Of the 20 patients, 50% had good recovery or were moderately disabled, 15% were severely disabled or vegetative, and 35% had died. The course of ICP and the outcomes in these patients were not significantly different from those observed in a previous group of 262 patients managed in the same way for the high-dose regimen. There was, however, high incidence of gastric hemorrhage (50%) and of hyperglycemia with glucosuria (85%) in these 20 patients. These negative results in patients with head injury stand in marked contrast to our experience of the benefit of methylprednisolone in patients with brain tumors.

The genesis and significance of delayed traumatic intracerebral hematoma.

During a 34-month period, 12 cases of delayed traumatic intracerebral hematoma (DTICH) were diagnosed among 162 consecutive prospectively studied patients admitted to the Medical College of Virginia with severe closed head injuries. All patients were unresponsive to command and unable to utter formed words at the time of admission. The interval from injury to diagnosis of DTICH by computerized tomography (CT) was within 48 hours in 11 of the 12 cases. Six patients had no decompressive surgery before the development of the lesion. Four patients had undergone decompressive surgery and then developed DTICH on the contralateral side. Two patients developed lesions in the vicinity of the operative site that were thought not to be the result of operation. The development of DTICH was not heralded by neurological deterioration nor by elevation of intracranial pressure. Eleven of the 12 patients had suffered a secondary hypoxic insult soon after the head injury. We suggest that the CT appearance of DTICH is likely to represent hemorrhage into an existing traumatized area and is an epiphenomenon rather than a cause of severe primary and secondary brain damage.