Barbiturate-augmented hypothermia for reduction of persistent intracranial hypertension

1974 ◽  
Vol 40 (1) ◽  
pp. 90-100 ◽  
Author(s):  
Harvey M. Shapiro ◽  
Stephen R. Wyte ◽  
John Loeser

✓ Thiopental and pentobarbital caused further reductions in intracranial pressure (ICP) in five patients with persistent intracranial hypertension who had been previously treated with diuretics, steroids, and hyperventilation therapy. The ICP reduction obtained with these patients at normothermia was rapid. Abrupt increases in ICP could be quickly checked by barbiturate treatment. Frequently, the ICP reduction was accompanied by an improvement in the cerebral perfusion pressure. Reduction of ICP by thiopental was brief while that due to pentobarbital was more prolonged. Sustained intracranial pressure reduction could be maintained for up to 5 days by combining pentobarbital (serum concentration 3 mg%) and hypothermia (30°C) without cardiovascular instability or other untoward side-effects. The cerebral metabolic depression due to this combined therapy may be additive and therefore offer a greater protection to the brain during periods of elevated ICP.

1993 ◽  
Vol 79 (5) ◽  
pp. 705-709 ◽  
Author(s):  
Johan van Loon ◽  
Bharati Shivalkar ◽  
Chris Plets ◽  
Jan Goffin ◽  
T. Budya Tjandra-Maga ◽  
...  

✓ To determine the catecholamine response to progressive intracranial hypertension, intracranial pressure (ICP) was raised gradually by continuous expansion of an epidural balloon in seven dogs. Hemodynamic parameters, ICP, and cerebral perfusion pressure (CPP) were monitored continuously and serum catecholamine levels began to rise when CPP was in the low-positive range (20 to 30 mm Hg), reaching a peak just after brain death (CPP ≤ 0 mm Hg). There was no correlation between ICP and the catecholamine peak. Compared to control values, the mean increase was 286-fold for epinephrine and 78-fold for norepinephrine. Temporally, the catecholamine peak corresponded well with the observed hemodynamic changes. These results suggest that ischemia in certain parts of the brain stem is responsible for the hemodynamic changes observed in intracranial hypertension (such as the Cushing response), and they show that catecholamines play an important role in these hemodynamic changes.


1981 ◽  
Vol 55 (5) ◽  
pp. 704-707 ◽  
Author(s):  
Jon S. Huseby ◽  
John M. Luce ◽  
Jeffrey M. Cary ◽  
Edward G. Pavlin ◽  
John Butler

✓ Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in its absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.


1990 ◽  
Vol 73 (5) ◽  
pp. 725-730 ◽  
Author(s):  
Julio Cruz ◽  
Michael E. Miner ◽  
Steven J. Allen ◽  
Wayne M. Alves ◽  
Thomas A. Gennarelli

✓ Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.


1975 ◽  
Vol 43 (3) ◽  
pp. 318-322 ◽  
Author(s):  
Lawrence F. Marshall ◽  
David I. Graham ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
Frank Welsh ◽  
...  

✓ The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.


1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.


1978 ◽  
Vol 48 (3) ◽  
pp. 329-331 ◽  
Author(s):  
James E. Cottrell ◽  
Katie Patel ◽  
Herman Turndorf ◽  
Joseph Ransohoff

✓ Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 ± 1.85 to 27.61 ± 3.33 torr (p > 0.0005) and cerebral perfusion pressure decreased from 89.32 ± 3.5 to 43.23 ± 4.60 torr (p < 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.


2021 ◽  
Vol 8 (29) ◽  
pp. 2639-2643
Author(s):  
Sruthy Unni ◽  
Ranju Sebastian ◽  
Elizabeth Joseph ◽  
Remani Kelan Kamalakshi ◽  
Jamsheena Muthira Parambath

BACKGROUND Anaesthesia for neurosurgery requires special considerations. The brain is enclosed in a rigid cranium, so the rise in intracranial pressure (ICP) which impairs cerebral perfusion pressure (CPP), results in irrepairable damage to various vital areas in the brain. Stable head position is required in long neurosurgical procedures. This is obtained with the use of clamps which fix the head rigidly. This is done usually under general anaesthesia because it produces intense painful stimuli leading to stimulation of sympathetic nervous system which in turn causes release of vasoconstrictive agents. This can impair perfusion in all organ systems. The increase in blood pressure due to sympathetic nervous system causes increase in blood flow. This causes increases in intracranial pressure which result in reduction in cerebral perfusion pressure once the auto regulatory limits are exceeded. We compared the effects of dexmedetomidine 1 µgm/kg and propofol 100 µgm/kg given as infusion over a period of 10 minutes before the induction of anaesthesia and continued till 5 minutes after pinning to attenuate the stress response while cranial pinning. In this study, we wanted to compare the effects of dexmedetomidine and propofol as infusion to attenuate the stress response while cranial pinning in patients undergoing neurosurgical procedures. METHODS This is a randomized interventional trial. Patients were divided into 2 groups of 20 each. Group 1 receiving dexmedetomidine and group 2 receiving propofol, both drugs given as infusion. Haemodynamic variables were monitored before and after cranial pinning. Data was analysed using IBM statistical package for social sciences (SPSS) statistics. The parameters recorded were analysed with the help of a statistician. RESULTS The two groups were comparable in demographic data. Incidence of tachycardia between group 1 and 2 showed that tachycardia to pinning was better controlled with propofol than dexmedetomidine (P < 0.05) which is statistically significant. There is no statistically significant difference in blood pressure values between group 1 and 2 after pinning. CONCLUSIONS From our study, we came to a conclusion that propofol was superior to dexmedetomidine in attenuating the heart rate response to cranial pinning. The effect of propofol and dexmedetomidine was comparable in attenuating the blood pressure response to cranial pinning. KEYWORDS Cranial Pinning, Dexmedetomidine, Propofol


2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall

Object. Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.Methods. The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-d-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.Conclusions. Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.


2001 ◽  
Vol 95 (4) ◽  
pp. 569-572 ◽  
Author(s):  
Bon H. Verweij ◽  
J. Paul Muizelaar ◽  
Federico C. Vinas

Object. The poor prognosis for traumatic acute subdural hematoma (ASDH) might be due to underlying primary brain damage, ischemia, or both. Ischemia in ASDH is likely caused by increased intracranial pressure (ICP) leading to decreased cerebral perfusion pressure (CPP), but the degree to which these phenomena occur is unknown. The authors report data obtained before and during removal of ASDH in five cases. Methods. Five patients who underwent emergency evacuation of ASDH were monitored. In all patients, without delaying treatment, a separate surgical team (including the senior author) placed an ICP monitor and a jugular bulb catheter, and in two patients a laser Doppler probe was placed. The ICP prior to removing the bone flap in the five patients was 85, 85, 50, 59, and greater than 40 mm Hg, resulting in CPPs of 25, 3, 25, 56, and less than 50 mm Hg, respectively. Removing the bone flap as well as opening the dura and removing the blood clot produced a significant decrease in ICP and an increase in CPP. Jugular venous oxygen saturation (SjvO2) increased in four patients and decreased in the other during removal of the hematoma. Laser Doppler flow also increased, to 217% and 211% compared with preevacuation flow. Conclusions. Intracranial pressure is higher than previously suspected and CPP is very low in patients with ASDH. Removal of the bone flap yielded a significant reduction in ICP, which was further decreased by opening the dura and evacuating the hematoma. The SjvO2 as well as laser Doppler flow increased in all patients but one immediately after removal of the hematoma.


1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.


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