Background Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies, but the results were not definitive. To study this issue, we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury. Methods The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were randomly assigned to be treated with hypothermia (body temperature, 33°C), which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling, or normothermia. All patients otherwise received standard treatment. The primary outcome measure was functional status six months after the injury. Results The mean age of the patients and the type and severity of injury in the two treatment groups were similar. The mean (±SD) time from injury to randomization was 4.3±1.1 hours in the hypothermia group and 4.1±1.2 hours in the normothermia group, a...

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Lack of effect of induction of hypothermia after acute brain injury.

✓ There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO3− buffer from CSF. The latter disadvantage might be overcome by the addition of the buffer tromethamine (THAM), which has shown some promise in experimental and clinical use. Accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (PaCO2 35 ± 2 mm Hg (mean ± standard deviation): control group), hyperventilation (PaCO2 25 ± 2 mm Hg: HV group), or hyperventilation plus THAM (PaCO2 25 ± 2 mm Hg: HV + THAM group). Stratification into subgroups of patients with motor score...

Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial

✓ This study describes the relationship between raised intracranial pressure (ICP), hypotension, and outcome from severe head injury. The study is based on information derived from the Traumatic Coma Data Bank where ICP records from a relatively large number of patients were available to help delineate the major factors influencing outcome. From the total data base of 1030 patients, 428 met minimum monitoring duration criteria for inclusion in the present analysis. Outcome was classified according to the Glasgow Outcome Scale score determined at 6 months postinjury. Arrays of comparably defined summary measures describing the patient's course were considered for ICP, blood pressure (BP), central perfusion pressure, and therapy intensity level. For instance, the array of ICP summary descriptors included the proportion of ICP readings greater than x, for x = 0 to 80 mm Hg by increments of 5 mm Hg. A total of 187 candidate summary descriptors were considered. A stepwise ordinal logistic regression was used t...

Impact of ICP instability and hypotension on outcome in patients with severe head trauma

Intracranial pressure (ICP) is derived from cerebral blood and cerebrospinal fluid (CSF) circulatory dynamics and can be affected in the course of many diseases of the central nervous system. Monitoring of ICP requires an invasive transducer, although some attempts have been made to measure it non-invasively. Because of its dynamic nature, instant CSF pressure measurement using the height of a fluid column via lumbar puncture may be misleading. An averaging over 30 minutes should be the minimum, with a period of overnight monitoring in conscious patients providing the optimal standard. Computer-aided recording with online waveform analysis of ICP is very helpful. Although there is no “Class I” evidence, ICP monitoring is useful, if not essential, in head injury, poor grade subarachnoid haemorrhage, stroke, intracerebral haematoma, meningitis, acute liver failure, hydrocephalus, benign intracranial hypertension, craniosynostosis etc. Information which can be derived from ICP and its waveforms includes cerebral perfusion pressure (CPP), regulation of cerebral blood flow and volume, CSF absorption capacity, brain compensatory reserve, and content of vasogenic events. Some of these parameters allow prediction of prognosis of survival following head injury and optimisation of “CPP-guided therapy”. In hydrocephalus CSF dynamic tests aid diagnosis and subsequent monitoring of shunt function.

https://jnnp.bmj.com/content/jnnp/75/6/813.full.pdf

Monitoring and interpretation of intracranial pressure

Objectives To define optimal cerebral perfusion pressure (CPPOPT) in individual head-injured patients using continuous monitoring of cerebrovascular pressure reactivity. To test the hypothesis that patients with poor outcome were managed at a cerebral perfusion pressure (CPP) differing more from the

Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury.

~," The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.

http://www.ventura.ind.br/media/artigos/05/14/contribution-of-csf-and-vascular-factors.pdf

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients.

The authors studied intracranial pressure (ICP) and intracranial compliance as defined by the pressure-volume index (PVI) in 34 severely head-injured patients with a Glasgow Coma Scale score of 8 or less. The objective of the research was to determine if there was a correlation between the pressure-volume status and subsequent increase in ICP. The PVI and ICP measurements were obtained serially, and the temporal course of the pressure-volume status and ICP was determined during the 5-day period following injury. Aggressiveness of ICP was quantified by a therapy intensity level scale. A clear relationship between the PVI measured soon after injury and subsequent development of ICP emerged. Following mechanical trauma the PVI is reduced, and the degree of reduction and extent of biomechanical recovery are closely related to outcome and development of raised ICP.

http://www.ventura.ind.br/media/artigos/05/14/pressure-volume-index-in-head-injury.pdf

Pressure-volume index in head injury

✓ The posttraumatic creatine kinase-BB isoenzyme (CKBB) activity and lactate concentration in ventricular cerebrospinal fluid (CSF) have been studied in 29 patients with severe head injuries. The CKBB activity reaches its maximum a few hours after trauma, and has a monoexponential drop with a half-time of approximately 10 hours. Ventricular CSF lactate concentration continues to rise in patients with a poor outcome, and decreases only slowly and inconsistently in most of the other patients. Thus, increase of lactate in the ventricular CSF is not, like CKBB, a direct one-stage consequence of the trauma but is due to continuous production from a derangement of metabolism caused by the trauma. Since even higher ventricular CSF lactate levels can be survived when not caused by head injury, and since no significant pH changes were related to the ventricular CSF lactic acidosis in these artificially ventilated patients, it is concluded that ventricular CSF lactic acidosis is indicative of a severe, although not...

CSF brain creatine kinase levels and lactic acidosis in severe head injury.

Our work and studies by other investigators have shown that the single most frequent cause of death in aggressively managed head injured patients is uncontrollable intracranial hypertension (Becker 1977, Marshall 1979). Studies in Richmond indicate thathigh ICP was initially present in two-thirds of those patients without intracranial spaceoccupying lesions who were comatose upon admission. Half of the patients who developed intracranial hypertension, or in whom elevated ICP persisted, died despite therapy. Raised ICP continues as the most frequent cause of death in head injury yet the sequence of events which leads to raised ICP is poorly understood. Our studies of ICP dynamics implicate at least three parameters which contribute to the level of pressure; the rate of fluid formation (If), the outflow resistance offered to the egress of fluid (Ro), and a component (Pv) identifying the vascular contribution to ICP. The objective of this study was to measure the changes in these parameters in head-injured patients and determine the relative contribution of CSF and vascular components to the ICP.

R. J. Moulton

Papers

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients.

Pressure-volume index in head injury

CSF brain creatine kinase levels and lactic acidosis in severe head injury.

Dynamics of Intracranial Pressure Rise in Severely Head Injured Patients