J. Douglas Miller

Traumatic Acute Subdural Hematoma — Major Mortality Reduction in Comatose Patients Treated within Four Hours

To discover which factors contributed to recovery after surgical intracranial decompression, we reviewed the records of 82 consecutive comatose patients with traumatic acute subdural hematoma (ASDH) who were treated in a single center under a uniform protocol. The delay from injury to operation was the factor of greatest therapeutic importance. Patients who underwent surgery within the first four hours had a 30 per cent mortality rate, as compared with 90 percent in those who had surgery after four hours (P less than 0.0001). Other important prognostic variables included results of the initial neurologic examination, sex, multimodality-evoked potentials, and postoperative intracranial pressure (ICP). If all patients with traumatic ASDH were taken directly to hospitals equipped to diagnose and remove the hematoma within four hours of injury, mortality rates could be reduced considerably.

Complete cerebral ischemia

SummaryNeuronal, astrocytic, and oligodendrocytic elements in several brain loci of the cat were examined at the light and electron microscopic level immediately after periods of complete cerebral ischemia (CCI) uncomplicated by post-ischemic recirculation. Such CCI episodes ranged from 1.5–25 min duration and were methodically produced in a cat model employing rigorous physiological controls. Subsequent to these CCI insults, morphological alterations occurred in a homogeneous manner within each cell type of all loci examined; however, variation in the temporal onset and magnitude of alterations among the various cell types was observed. With brief ischemic insults all cell nuclei demonstrated pronounced nuclear alterations, while their cytoplasmic organelles displayed minimal change. Chromatin clumping and nucleolar condensation were observed in both neurons and glia subsequent to 1.5–5 min of CCI, respectively. With increasing durations of CCI such changes were more dramatic and conspicuous alterations of the cytoplasmic organelles were observed. On the basis of extensive morphological analyses the present study illustrates that nuclear alterations are the first to occur subsequent to CCI. The homogeneity of neuronal involvement seen subsequent to CCI uncomplicated by post-ischemic recirculation is inconsistent with the “selective vulnerability” purported to occur by others. The significance of this inconsistency remains to be assessed; yet, the suggestion is advanced that post-ischemic recirculation may be a factor in the genesis of such vulnerability.

Delayed intracranial hematoma in patients with severe head injury.

Serial computed tomography was peformed on 119 consecutive patients suffering from severe head injury. The development of delayed intracranial hematomas, both intra- and extraaxial, was evaluated by comparing the initial scan with subsequent studies. Ten delayed intracerebral hematomas and nine delayed extracerebral collections were encountered. The occurrence of delayed intracerebral hemorrhage is more frequenct than previously reported and is associated with a poor outcome.

Volume-Pressure Response in Various Experimental and Clinical Conditions

The intracranial volume-pressure response (VPR) is the immediate change in ventricular fluid pressure (VFP) following an addition of 1 ml in 1 second to the ventricular CSF volume via the catheter used for VFP monitoring (1). This simple test yields information dP concerning intracranial elastance (inverse compliance dP/dV (2)) and relates both to resting VFP and presence of intracranial masses and brain shift (3,4). Further evaluation of the VPR has been undertaken under controlled conditions in baboons subjected to brain compression and in patients during continous monitoring of VFP.

CT Scan, ICP and Early Neurological Evaluation in the Prognosis of Severe Head Injury

The prognostic value of careful neurological evaluation using standard terminology performed serially over 72 hours in patients with head injuries of designated severity has been shown by Jennett and his colleagues. The growing use of muscle relaxants with artificial ventilation and the increasing interest in the use of induced barbiturate coma reduces the opportunity for serial neurological evaluations over an extended period. Furthermore, there is a need to identify at the earliest possible stage those patients in whom a particularly poor outcome is to be expected, because it is in this group that newer and perhaps riskier therapies are justified. Inclusion of patients in whom a better outcome is to be expected may yield a falsely optimistic view of a test therapy. One solution is to wait for a certain period of time to ascertain that the head injury is serious. This has the disadvantage that it may delay application of therapy to a point where no treatment can be effective because neurological deterioration has become irreversible.

Detection of occult abdominal trauma in patients with severe head injuries.

Among 109 consecutive victims of severe head injury, intra-abdominal injury could not be excluded in 87. These patients were considered to be at risk from occult intra-abdominal haemorrhage. 60 patients underwent diagnostic peritoneal lavage. 10 of these had a positive lavage, correctly indicating intra-abdominal haemorrhage. In each case a lesion requiring surgical repair was identified. 49 patients had a negative lavage, and only 1 of these patients subsequently showed signs of a missed intra-abdominal lesion. 13 patients had low systolic blood-pressure (< 90 mm Hg) on admission, and 4 of these had positive lavage. Of 47 patients with systolic blood-pressure of 90 mm Hg or greater on admission, 6 had positive lavage. 15 patients were deeply comatose with no eye-opening or verbal response and an extensor or no motor response to painful stimuli. 6 of these had positive peritoneal lavage. We conclude that diagnostic peritoneal lavage should form an integral part of the evaluation of comatose patients with head injury, particularly those whose level of consciousness is most depressed, whether or not clinical signs of shock, abdominal injury, or occult haemorrhage are present.

The Effect of Mannitol, Steroids and Hypocapnia on the Intracranial Volume/Pressure Response an Experimental and Clinical Study

The volume/pressure response (VPR) is defined as the change in ventricular fluid pressure (VFP) caused by a small induced change in the volume of fluid in the lateral ventricle. It has been shown, both in patients with raised ICP (1, 2) and in baboons undergoing experimental brain compression (3), that a direct relationship can be demonstrated between VFP and VPR. Therefore, during the reduction of intracranial hypertension, if the configuration of the volume/pressure curve remains unchanged, the fall in VFP should be paralleled by an equivalent fall in VPR.

Increased Intracranial Pressure: Theoretical Considerations

Publisher Summary This chapter describes the theoretical considerations of increased intracranial pressure (ICP). Increasing attention is being paid to the measurement and treatment of increased ICP in the management of acutely ill patients in the neurologic and neurosurgical intensive care unit. The ultimate source of ICP is the arterial blood pressure, and the systolic arterial pressure represents the asymptote of elevated ICP. It is found that when ICP rises, the pressure in the thin walled cerebral veins must rise equally. Otherwise, the veins would collapse with consequent cessation of cerebral blood flow. Elevated ICP may take the form of a steady increase in pressure or frequently be episodic in the form of pressure waves. It is the existence of these pressure waves that makes it necessary to measure ICP continuously over a period of time.

Management of Brain Edema in Head Injury

Strictly speaking, brain edema represents an increase in the bulk of the brain that has been produced by an increase in its tissue water content. In the context of the management of severely head-injured patients in the intensive care unit, however, the term brain edema is commonly used in a wider context, to include all conditions of increased brain volume or brain swelling frequently, but not always, associated with raised intracranial pressure (ICP). There are many potential causes of raised ICP after head injury. These include formation of true brain edema, development of an intracranial mass lesion (such as a subdural hematoma, which may also be associated with edema formation), acute swelling of the brain due to an increase in cerebral blood volume, and accumulation of cerebrospinal fluid in the form of acute hydrocephalus. For optimal management of the severely head-injured patient and effective treatment of raised ICP and its adverse sequelae, it is important to be aware of the several possible causes of intracranial hypertension and different mechanisms by which water content may increase and ICP rise. Wherever possible, therapy should be chosen that is appropriate to the underlying pathophysiological mechanism. In the comatose head-injury patient, the therapeutic “window” is narrow and time does not permit a random sequence of empirically applied therapies for reduction of ICP and resolution of brain edema.