Correlation of cerebral perfusion pressure and Glasgow Coma Scale to outcome.

Cerebral Perfusion Pressures (CPP) and Glasgow Coma Scale (GCS) scores were monitored to guide the management of severely head-injured patients. These measures were correlated to outcome (Glasgow Outcome Scale-GOS) in 136 consecutive patients at least 1 year after injury. The GOS showed highly significant positive correlations to either CPP or GCS assessments (p less than 0.001). Two parameters that are correlated with subsequent death in most patients include 1) highest (h) GCS = 3 or 4 (Day 1: 31 of 32 patients died, and Day 2: 19 of 19 patients died), and 2) CPP less than or equal to 60 mm Hg more than 33% of the hourly measures during Day 2 (36% of all subsequent deaths; 11% overlap with the highest Glasgow Coma Scale). The Day 2 measures identifying two groups that have a greater than 75% incidence of "good outcome" or GOS = 4 or 5 include 1) hGCS greater than or equal to 6 (N = 45) and 2) the average (a) CPP greater than or equal to 90 mm Hg (N = 26). Of the 45 patients with a GOS = 4 or 5 who had both CPP and GCS recorded on the third day, 44 were identified by these "good outcome" parameters.

Accurate intracranial pressure monitoring: technical note.

Intracranial pressure (ICP) monitoring may be misleading or inaccurate in patients who have sustained cerebral death or who have had cerebrospinal fluid drainage (e.g., due to skull fracture or craniotomy). ICP recording in these patients requires particular attention to the monitoring technique to avoid misleading values that may result in inappropriate therapy. We review methods for obtaining accurate ICP readings from fluid-interface systems using either a ventricular catheter or a subarachnoid screw. We suggest attention to the following: (a) elevation of the pressure in the external tubing and connections to ensure that there are no microleaks , (b) injection of a small volume of saline intracranially, and (c) awareness of what constitutes a true ICP reading.

Effect of mannitol on increased intracranial pressure.

We studied 61 patients with a closed head injury and increased intracranial pressure (ICP). The ICP was monitored continuously, concomitant with the administration of 20% mannitol. If the ICP remained higher than 25 mm Hg for 10 minutes or more, the patient was included in the study. Analysis of monitoring records delineated four variables that were related to the response of ICP to mannitol: (a) the level of ICP 1 hour before mannitol was administered, (b) the level of ICP when mannitol was administered, (c) the amount of mannitol that was administered immediately before the resulting changes in ICP were measured, and (d) the cumulative amount of mannitol given over the 6 hours before the most recent mannitol dosage was administered. The level of the ICP measurements and the cumulative amount of preceding doses of mannitol influenced the response of ICP to mannitol more than did the size of the dose of mannitol. These findings imply that: (a) the initial administration of more mannitol than is absolutely needed may lead to larger doses being required to control ICP and (b) for that reason, mannitol given on a gram/kilogram, an hourly, or a serum osmolarity basis to control increased ICP has negative long term effects because more mannitol may be required to decrease ICP when an excessive amount of it has been given previously.

Treatment of cerebral infarction with dimethyl sulfoxide in the mongolian gerbil.

Dimethyl sulfoxide (DMSO) has been reported to have beneficial effects in the treatment of central nervous system trauma, possibly due to its reported anti-inflammatory, antiedemic, anticoagulate, diuretic, hypothermic, vasodilatory, and respiratory stimulatory effects as well as an ability to correct membrane instability and penetrate the blood-brain barrier. In this paper we discussed these properties, and how they may be of benefit in ischemic cerebral infarction and elevated intracranial pressure. We also described a study we performed to determine if treatment with DMSO would decrease the morbidity and mortality from experimental cerebral infarction.

Effect of DPPD (diphenyl-para-phenylenediamine) on stroke and cerebral edema in gerbils.

Diphenyl-para-phenylenediamine (DPPD) is an antioxidant that has been shown to decrease liver damage due to the peroxidative process of carbon tetrachloride in rats and to ameliorate cold-induced cerebral edema in cats. Because lipid peroxidation disrupts the integrity of the plasma membrane, a process believed to occur in cerebral infraction, which is a major cause of cerebral edema. DPPD was tested for its protective effect against cerebral infarction. When given intraperitoneally in gerbils with unilateral ligation of the common carotid artery, DPPD had no effect on resultant incidence, morbidity, or mortality of cerebral infarction. Despite these findings, the authors believe, on the basis of what is known about free radical pathology, that DPPD and other antioxidants deserve further laboratory trials as possible drugs in the treatment of brain trauma and cerebral edema.

Effect of aminophylline on cerebral infarction in the Mongolian gerbil.

The effects of aminophylline in Mongolian gerbils subjected to unilateral carotid ligation were studied. The drug was given in varying intraperitoneal doses at varying postoperative intervals and the animals observed for 5 days for clinical signs of stroke. Doses of 100 mg per kg caused early death and were discontinued. Doses of 50 mg per kg had no significant effect on morbidity, mortality, time until death, stroke incidence or lesion size, as compared to saline given as a control. Doses of 80 mg per kg caused a higher mortality, higher morbidity, and a shorter interval to death, but a smaller infarct. Thus, aminophylline did not have a protective effect against stroke in gerbils and was actually detrimental during the first 16 hours following the carotid ligation.

Effect of dose and dose schedule on the response of intracranial pressure to mannitol.

Analysis of monitoring records of 150 patients given over 1000 infusions of 20% mannitol delineared three variables affecting the response of intracranial pressure (ICP) to mannitol: the original ICP; the current dose; and the dose given over the preceding three hours. The level of ICP influenced the response to mannitol as much as the amount of mannitol; giving more mannitol than was required to bring ICP below 25 mm Hg led to the need for larger following doses. One hundred-milliliter-bolus doses were often as effective as larger doses. The results suggest that doses of mannitol given to control increased ICP should be kept as small as possible.

Experimental cerebral infarctioneffects of pentobarbital in Mongolian gerbils.

Unilateral ligation of thecarotid artery was done in 110 gerbils anesthetized with either and 78 anesthetized with pentobarbital sodium. Thirty of the ether-anesthetized animals received no tratment. Starting one hour after ligation, 38 animals from each anesthesia group were given 3 mg/50 gm of body wight of pentobarbital intraperitoneally every eight hours for 72 hours. The remaining animals received normal saline on the same treatment schedule. Morbidity and mortality were recorded for the next six days. Eighty-five animals (45.2%) developed cerebral infarction. Only ten of the 38 animals (2693%) anesthetized and treated with pentobarbital developed infarction. The percentage of infarction in the remaining groups ranged from 45% to 53%. There were no significant differences among the groups in the number of deaths or in the location or extent of the lesion.

Durometer for measurement of intracranial pressure.

The tensity of the skin over a supratentorial craniectomy was measured with a durometer placed on the skin flap. Tensity values were obtained on 124 occasions in 28 patients in whom lumbar or intracranial pressure was being recorded simultaneously. Corrections were made for differences in the level of the durometer and the level at which the device measuring lumbar or intracranial pressure was placed. The skin tensity and lumbar or intracranial pressure were then correlated and the correlation studied statistically. It was found that the durometer could be used to predict quantitatively the intracranial pressure with a very low standard error (estimation of +/- 28 mmH2O). An experimental model confirmed these findings. The system was less accurate at pressure below 68 mmH2O and above 680 mmH2O.

Cerebral infarction in the Mongolian gerbil exacerbated by phenoxybenzamine treatment.

In a double-blind study, the effects of a large dose (20 mg per kilogram) of phenoxybenzamine (PBZ) on cerebral infarction were evaluated in 120 Mongolian gerbils. The left common carotid artery was ligated in 100 animals; a sham operation was done in 20 animals. One hour later, 25 animals were given 2 mg per kilogram of PBZ, 25 animals were given 20 mg per kilogram of phenoxybenzamine, and 50 animals were given 0.5 cc of nomal saline, all doses being repeated at 24, 48, and 72 hours. Five sham-operated animals were given 2 mg per kilogram of phenoxybenzamine, five were given 20 mg per kilogram of phenoxybenzamine and ten were given 0.5 cc of normal saline on the same treatment schedule. Morbidity and mortality were recorded for one week and then all surviving animals wer killed. All brains were studied for signs of infarction. Of the saline-treated animals, 32% had cerebral infarction and 81% of these died. Of the animals treated with phenoxybenzamine, 36% of those receiving 2 mg per kilogram and 68% (p less than 0.05) of those receiving 20 mg per kilogram had cerebral infarction and all of those with infarction died during the observation period. The animals receiving phenoxybenzamine had a larger stroke index than those treated with saline. The authors concluded that phenoxybenzamine is harmful in postischemic treatment of strokes.

Continuous intracranial pressure monitoring: review of techniques and presentation of method.

Continuous monitoring of intracranial pressure has proved to be of value in guiding the treatment of patients with diffuse cerebral trauma or edema. The evolution of monitoring devices is reviewed from simple lumbar puncture through intraventricular, subdural, epidural and external monitoring with progressively more sophisticated equipment. The device reported in detail connects the subarachnoid space to an on-line data reducer that calculates the percentage time the intracranial pressure is in 16 pressure ranges of 5 mmHg each and portrays it on a histogram. The pressure at that moment, the total range of the intracranial pressure, the level of pressure the patient has had for the largest percented of time, and pressure waves, if present, can all be determined by this process.

Effects of hyperventilation, CO2, and CSF pressure on internal carotid blood flow in the baboon.

The combined effect upon cerebral blood flow (CBF) of an elevation of cerebrospinal fluid pressure (CSFP) and changes in respiratory CO2 was studied in nine baboons under chloralose anesthesia. The animals were mildly hyperventilated and provided with increasing amounts of CO2 in O2-air. Arterial CO2 tensions (PaCO2) increased from 17 to 58 mm Hg. Internal carotid blood flow (ICBF) was measured at normal CSFP and at hydrostatically maintained 50 mm Hg CSFP. It was found that: 1) end-tidal CO2 may be used as a substitute for arterial PaCO2 determinations; 2) this elevation of CSFP has little effect on ICBF during hypercapnia and normocapnia; however, 3) during hypocapnia the ICBF is reduced an additional 20% when CSFP is elevated; that is, ICBF is reduced 50% from normal when end-tidal CO2 is reduced to 2% at this elevated level of CSFP. Caution should be exercised during hyperventilation therapy particularly if the elevated CSFP or intracranial pressure (ICP) is not reduced to approach normal levels; in these conditions, the combination of decreasing PaCO2 and elevated ICP may reduce CBF below critical levels and thus lead to cerebral hypoxia.