Reduction Of Intracranial Pressure Research Articles

Effects of respiratory therapy on intracranial pressure

To determine whether respiratory therapy can be deleterious in patients with intracranial hypertension, we investigated the effects of passive and active respiratory therapy on intracranial pressure (ICP) and cerebral perfusion pressure in acute neurosurgical patients with normal (< 15 mm Hg) and increased (> 15 mm Hg) ICP. During passive respiratory therapy, moving the patients from a 30-degree head-up dorsal position to the lateral decubitus position increased ICP by 10 mm Hg ( P < .001) in normal ICP patients (n = 26) and by 6 mm Hg ( P < .001) in high ICP patients (n = 6). Cerebral perfusion pressure increased by 5 mm Hg ( P < .05) in both cases. Clapping did not further change ICP or cerebral perfusion pressure. During active respiratory therapy, ICP decreased by 2 to 3 mm Hg ( P < .05) in normal ICP patients (n = 11) and by 4 to 7 mm Hg ( P < .01) in high ICP patients (n = 7). Cerebral perfusion pressure decreased by 1 to 5 mm Hg and remained unchanged in normal and high ICP patients, respectively. The ICP reduction was attributed mainly to the decrease in PaCO 2 and the decrease in intrathoracic pressure during active hyperventilation. These results indicate that passive and active respiratory therapy can be performed safely in acute neurosurgical patients with normal or increased ICP, provided the therapy can be done in a position that does not deteriorate ICP.

Transcranial Doppler ultrasound in brain death: Experience in 140 patients

The interpretation of clinical tests for brain death is often complicated by the presence of facial trauma, or the use of barbiturate therapy for reduction of intracranial pressure. We propose a non-invasive technique--transcranial Doppler (TCD) sonography for the diagnosis of brain death. One hundred and forty comatose patients, 111 of whom were believed to be brain dead underwent TCD examinations. TCD assessments of the middle cerebral arteries (MCAs) and the basilar artery were performed before formal clinical testing for brain death. The TCD spectra recorded in the brain dead (BD) patients consisted of short, sharp systolic peaks followed by retrograde flow during diastole or just systolic peaks with absent flow in either direction. There were no survivors among patients who displayed these two TCD patterns. The 29 comatose control patients always showed flow throughout the cardiac cycle--no retrograde flow was ever recorded in these patients all of whom survived. Of particular interest were the basilar artery results. In nine BD patients no MCA signals could be obtained while good quality signals were recorded from the basilar artery. The TCD results agreed essentially with 100% accuracy with clinical testing and four vessel cerebral angiography. This paper illustrates the usefulness of TCD examination of the MCAs and especially the basilar artery in the diagnosis of brain death.

A novel treatment for ischemic intracranial hypertension in cats.

There is no accepted efficacious treatment for ischemic cerebral edema. We show in a cat model of focal cerebral ischemia that infarct volume can be reduced (p less than 0.05) by ventriculocisternal perfusion with an oxygenated fluorochemical emulsion (bis-perfluorobutylethylene). An accompanying effect of such ventriculocisternal perfusion is a reduction in intracranial pressure. At 18 hours following the start of the perfusion, there was a significant (p less than 0.05) difference in intracranial pressure between nonperfused controls (mean 11.4 [range 2.3-23.0] torr, n = 6) and cats perfused with an oxygenated nutrient solution not containing fluorochemical (mean 11.3 [range 3.0-29.0] torr, n = 8) or animals perfused with the oxygenated fluorochemical emulsion (mean 2.21 [range 0-3.5] torr, n = 7). Perfusion with this oxygenated fluorochemical emulsion warrants further study as a treatment for elevated intracranial pressure.

Dimethly sulphoxide lowers ICP after closed head trauma

Ten patients with closed head trauma and elevated intracranial pressure (ICP) ranging from 40-127 mm Hg were treated with intravenous dimethyl sulphoxide (DMSO) every 6 h for 1-10 days. Four patients received DMSO and intermittent oxygen. All patients showed a reduction of ICP after 24 h and 7 had normal ICP after 6 days of treatment. Two patients died of their injuries. Neurological assessment at the time of discharge showed 2 patients with severe neurological deficits and 6 patients with mild to no deficit. After a 3 month follow-up, 1 patient remained severely impaired and 7 patients showed mild to no deficit. It appears that intravenous DMSO can rapidly reduce elevated ICP in severe closed-head injury and that it improves neurological outcome.

Intracranial Pressure Responses During Hyperbaric Oxygen Therapy

The responses of intracranial pressure (ICP) to hyperbaric oxygen (HBO) therapy and arterial gas pressures were investigated. ICP was measured through a ventricular or spinal drainage catheter in patients with brain tumor or cerebrovascular disease. Changes in ICP, heart rate (HR), arterial blood pressure (ABP), and transcutaneous partial pressure of carbon dioxide (PtcCO2) or oxygen (PtcO2) were recorded continuously during air or 100% O2 breathing at 1 and 2.5 atmospheres absolute (ATA). HR and PtcCO2 decreased and mean ABP was unchanged during HBO inhalation. ICP was reduced at the beginning and tended to increase gradually during HBO inhalation. The change from air to O2 without altering respiratory frequency and volume caused a gradual increase of ICP and PtcCO2 with a transient ICP reduction in an artificially respirated patient. Intentionally reduced respiration to maintain PtcCO2 at the value at 2.5 ATA with air caused the ICP to return to near the value at 2.5 ATA with air even during HBO inhalation. These findings suggest that reduced ICP is initially due to direct cerebral vasoconstriction caused by hyperoxia and is maintained mainly by induced hypocapnia during HBO inhalation. Care is required when giving HBO therapy to patients with a high ICP and/or who are respirated artificially.

Dexamethasone Therapy for Bacterial Meningitis in Infants and Children

BACKGROUND Bacterial meningitis affects an estimated 15 000 infants and children in the United States each year. The case-fatality rates for these patients are from 5% to 10%; as many as 20% to 30% of survivors have long-term sequelae, the most common of which is hearing impairment.1 The reported incidence of hearing loss after meningitis has ranged from 5% to 20% of patients, depending on the selection of patients, techniques used to assess hearing, and etiology.2-5 In 1972 to 1977, Dodge and co-workers2 documented hearing loss in 31% of patients with Streptococcus pneumoniae meningitis, 10% with Neisseria meningitidis meningitis, and 6% with Haemophilus influenzae meningitis. Bilateral sensorineural hearing impairment occurred in 14%, 10%, and 3%, respectively. Newer antimicrobial agents with superior bactericidal activity in cerebrospinal fluid have not reduced morbidity and case-fatality rates compared with conventional therapy. The pathophysiologic events believed to contribute to adverse outcome from bacterial meningitis include alteration of cerebral capillary endothelial cells that comprise the blood-brain barrier, cytotoxic and vasogenic cerebral edema, and increased intracranial pressure.6 These events can lead to decreased cerebral perfusion pressure with a resultant diminution in cerebral blood flow causing regional hypoxia and focal ischemia of brain tissue. Because of its anti-inflammatory effects, corticosteroid therapy has been evaluated in experimental meningitis and in infants and children with meningitis. Dexamethasone produced significant reductions in intracranial pressure, brain edema, and lactate concentrations in cerebrospinal fluid in experimental H influenzae and S pneumoniae meningitis.7,8 In addition, the administration of dexamethasone was associated with decreased concentrations of prostaglandin E2 in cerebrospinal fluid and lowered mortality and clinically evident neurologic sequelae in rabbits with experimental pneumococcal meningitis.9

Regional cerebral blood flow in the pig after a localized cerebral contusion treated with barbiturates

Regional cerebral blood flow determined with microsphere technique in anaesthetized pigs was measured before and after a localized cerebral contusion as well as after treatment with pentobarbital. No overall reduction in intracranial pressure or perfusion pressure was observed. Flow reduction due to pentobarbital was different in different regions with a high percentage change in the highly perfused basal structures and cortical grey matter except in the centre of the contusion where the reduction was half compared to the rest of cortical grey matter. Changes in white matter were less than in cortical grey matter but more pronounced than in the very high flow areas (choroid plexus and pineal gland). The accumulated change was greatest in the damaged region. Contralateral to the contusion, where a significant increase in flow was noticed after the contusion, there was a very low accumulated change in flow. In white subcortical matter underlying the contusion a similar low flow change was observed but this was not accompanied by as large an accumulated change as in grey cortical matter. At each fraction of injected pentobarbital a short-lasting increase in intracranial pressure and a reduction in mean arterial blood pressure was observed. The amplitude and the height of the intracranial pressure change was reduced during the pentobarbital injections.

Ventricular Volume in Infantile Hydrocephalus and Its Relationship to Intracranial Pressure and Cerebrospinal Fluid Clearance before and after Treatment

The present study examines ventricular volume before and after shunting in 16 infants with hydrocephalus and mixed aetiology and relates this parameter to rates of cerebrospinal fluid clearance, intracranial pressure and outcome. Following treatment all patients showed reduction in intracranial pressure and amelioration of the clinical manifestations of hydrocephalus. Nevertheless, 4 patients showed persistence of marked ventriculomegaly, 4 had moderate ventricular enlargement, while 8 showed small or normal ventricles. Although the series was small there appeared to be a clear correlation between persistent ventriculomegaly, poor cerebrospinal fluid clearance and poor outcome despite reduction in intracranial pressure. The question is raised as to whether pressure-determined cerebrospinal fluid drainage provides optimum treatment of hydrocephalus in infants given the particular physical characteristics pertaining to the non-rigid cranium.

Role of Subtemporal Decompression in Severe Closed Head Injury

There is general agreement that aggressive management and monitoring of the patient with closed head injury with control of intracranial pressure (ICP) will improve patient survival and eventual outcome. Conversely, there is little agreement on the value of surgical craniectomy for increasing intracranial volume and subsequently decreasing ICP in these same patients. This study examines 115 patients with severe closed head injuries (Glasgow Coma Score 8 or less) seen at the North Carolina Baptist Hospital between July 1, 1983, and April 1, 1987. All 115 patients were started on a regimen of head elevation, fluid restriction, chemoparalysis, and hyperventilation at PCO2 25-30 torr. Fifty-seven patients failed to respond to that therapy and were given mannitol. Twenty-seven of these still failed to respond; 24 were placed in a pentobarbital coma therapy group and 3 underwent subtemporal decompression. Of the 24 patients in pentobarbital coma, 17 failed to respond, 7 of whom underwent subtemporal decompression and 10 of whom were not operated on. Of all 10 patients undergoing subtemporal decompression, 7 (70%) responded with an average reduction in ICP of 34% (+/- 19.5% SD). Of the 10, 4 died (40%), in contrast with a mortality of 82.4% among patients in pentobarbital coma without subtemporal decompression. These data strongly suggest that subtemporal decompression can be beneficial in patients with medically intractable elevations of ICP.

Continuous EEG and ICP monitoring as a guide to the administration of althesin sedation in severe head injury.

The effects of 142 intravenous boluses of althesin (0.05 ml/kg) on cerebral perfusion pressure (CPP) were studied in twelve head injured comatose patients. The data were divided into those where the mean pre-bolus intracranial pressure (ICP) was above or below 20 mmHg and then subdivided into those where the minimum pre-bolus voltage of the cerebral function monitor (CFM) was above or below 5 microV (representing marked reduction in cortical electrical activity). The pre-bolus ICP influenced the extent of the fall in ICP and thus the direction of the resulting change in CPP. A mean reduction in CPP was observed in both groups in which ICP was below 20 mmHg irrespective of the CFM voltage. In the subgroups with high ICP, CPP increased when CFM was not depressed and fell when CFM was below 5 microV. The effects of individual boluses varied within and between the subgroups and, occasionally, severe and unpredictable hypotension occurred. If althesin administration had been restricted to the high CFM and high ICP group, 90% of the episodes of reduced CPP would have been avoided. In fact, when cortical electrical activity is already severely depressed, further administration of hypnotic anaesthetic agents produces only small reductions in ICP and usually a fall in CPP. These findings suggest that the minimum voltage of the CFM trace is a clinically useful guide to the administration of intravenous anaesthetic agents and offers a relevant prediction of their effects on CPP.

The effect of nimodipine on intracranial pressure. Volume-pressure studies in a primate model.

Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p less than 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.

Effect of intravenous mannitol on cat pial arteries and veins during normal and elevated intracranial pressure.

In two series of cats, totaling 12 animals, the effect of 1 g of intravenous mannitol per kg over 15 minutes on pial vessels (cranial window technique, multichannel videoangiometry) and intracranial pressure (ICP) was investigated under circumstances of normal ICP and ICP elevated to 20 mm Hg by the cisternal infusion of mock cerebrospinal fluid. Under conditions of normal ICP, mannitol induced an 18% reduction of ICP at the end of the infusion and a further decrease to 38% below the initial level 10 minutes later. Pial veins and arteries remained more or less unreactive over 35 minutes, with changes never exceeding 2 to 3%. Administration of mannitol during elevated ICP (20 mm Hg) reduced ICP by 15% during the administration period; during the subsequent 15 minutes, ICP returned to pretreatment levels. Pial arteries remained unreactive during mannitol infusion; however, they started to dilate during the subsequent 15 minutes to +8%. Venous calibers showed no noticeable changes. It is concluded that mannitol in clinically relevant doses does not exert a significant constrictive effect on cerebral arteries and veins and that mannitol acts on ICP probably via an osmotic effect rather than by a direct effect on cerebral blood volume.

Effect of intravenous mannitol on cat pial arteries and veins during normal and elevated intracranial pressure

In two series of cats, totaling 12 animals, the effect of 1 g of intravenous mannitol per kg over 15 minutes on pial vessels (cranial window technique, multichannel videoangiometry) and intracranial pressure (ICP) was investigated under circumstances of normal ICP and ICP elevated to 20 mm Hg by the cisternal infusion of mock cerebrospinal fluid. Under conditions of normal ICP, mannitol induced an 18% reduction of ICP at the end of the infusion and a further decrease to 38% below the initial level 10 minutes later. Pial veins and arteries remained more or less unreactive over 35 minutes, with changes never exceeding 2 to 3%. Administration of mannitol during elevated ICP (20 mm Hg) reduced ICP by 15% during the administration period; during the subsequent 15 minutes, ICP returned to pretreatment levels. Pial arteries remained unreactive during mannitol infusion; however, they started to dilate during the subsequent 15 minutes to +8%. Venous calibers showed no noticeable changes. It is concluded that mannitol in clinically relevant doses does not exert a significant constrictive effect on cerebral arteries and veins and that mannitol acts on ICP probably via an osmotic effect rather than by a direct effect on cerebral blood volume. (Neurosurgery 21:142-146, 1987)

Clinical pharmacokinetic considerations in the treatment of increased intracranial pressure.

Life-threatening increased intracranial pressure can be reversed by a variety of drugs. These compounds all have some disadvantages, producing rebound effects, severe coma or cardiovascular depression and electrolyte imbalance. However, reduction of intracranial pressure is a prerequisite for recovery and the benefits of treatment outweigh the risks. Dexamethasone is rapidly eliminated, the short half-life (about 3 hours) indicating that dosage intervals should be kept small. As yet, however, its therapeutic efficacy has not been clearly demonstrated. Therefore, an association between pharmacokinetics and pharmacodynamics cannot be established. Osmotic diuretics are the most widely used agents for reduction of intracranial pressure. Pharmacokinetics show a very close relationship to changes in serum osmolality, but there are large variations in the clearance. For the use of osmotics, the blood-brain barrier must be intact. Osmotic diuretics may lead to intracerebral oedema or to acute renal failure as serum osmolality increases. Considering the pharmacokinetics of each drug, and the dynamics of intracerebral pressure and osmolality, an intermittent, individually titrated dosage should be administered, with simultaneous monitoring of intracranial pressure. Frusemide (furosemide) can be used as an adjunct, to enhance the effect of osmotic diuretics. Its pharmacokinetics are limited by renal function, depending on age as well as on the extent of renal impairment. Altered renal elimination of concomitantly administered drugs, and electrolyte imbalances should be anticipated when diuretics are used. Barbiturates are certain to decrease intracranial pressure in humans by an as yet unknown mechanism. Their administration is recommended for patients that do not respond to conventional therapy. As barbiturates can result in deep coma, knowledge of their pharmacokinetics is of great importance for recovery. Following single doses, pentobarbitone has a relatively long elimination half-life (about 22 hours). However, after repeated administration for several days, its elimination may be enhanced due to autoinduction. Thiopentone kinetics are characterised by distribution and redistribution into deep peripheral compartments. Administration of high and frequent doses leads to considerably delayed recovery. This is not true for methohexitone, which shows comparable pharmacokinetics after single and multiple dose administration. Elimination depends on liver blood flow. Thus, recovery from methohexitone-coma is rapid. Rapid elimination is also an important characteristic of etomidate and alphaxalone/alphadolone, two non-barbiturate hypnotics.(ABSTRACT TRUNCATED AT 400 WORDS)

A practical approach to head injuries, including intracranial pressure monitoring and protection of damaged tissue

The immediate care of head injuries includes provision of a secure airway and prevention of inhalation of gastric contents. Hypovolaemia must be urgently treated and care taken to diagnose other injuries, especially those of the cervical spine and chest. After resuscitation, a neurological assessment should be made and the appropriate radiological investigations performed. Intracranial haematoma must be diagnosed promptly and treated without delay. If anaesthesia is required for radiology or surgery, it must include tracheal intubation and hyperventilation, attenuating the effects of intubation by the use of thiopentone plus a β-receptor blocking agent or lignocaine. Isoflurane should be used to maintain anaesthesia, although in patients with gun-shot injuries and children, a total intravenous technique may be preferable. The principles of intensive care for head injuries are prevention of hypoxia and hypercapnoea, maintenance of systemic blood pressure and reduction of elevated intracranial pressure (ICP), continued vigilance for expanding haematoma and prevention and treatment of fits. It is also important to treat pyrexia, infection and fluid and electrolyte disturbances. Hyperglycaemia should be avoided. To achieve these aims, blood pressure should be continuously monitored and many patients require monitoring of ICP. Any unexpected deterioration is an indication for ultrasound or CAT scan. Controlled ventilation and specific treatment for raised ICP may also be required. The outcome after head injury depends inter alia on the severity of the injury, the presence of other injuries and the age of the patient. It is not surprising that it has proven difficult to demonstrate the efficacy of the various modalities of treatment or identify those patients who might benefit from more aggressive therapeutic regimens.

Effect on intracranial pressure of furosemide combined with varying doses and administration rates of mannitol.

The first part of this study investigated the combined use of furosemide and mannitol in the treatment of elevated intracranial pressure (ICP). Two groups of dogs were studied to determine if renal excretion of mannitol was altered in the presence of furosemide. No significant difference in excretion was noted between the two groups. Fifteen animals were used in other studies to identify the most advantageous sequence of administration of furosemide and mannitol. Infusion of mannitol followed by furosemide 15 minutes later resulted in the most profound and sustained ICP reduction. The effect on ICP reduction of varying the mannitol dose was observed in studies using single doses of 0.5 gm/kg, 0.75 gm/kg, and 1 gm/kg. The larger mannitol dose, resulting in a greater blood-brain osmotic gradient, proved to be the most efficacious in ICP reduction. A further 15 animals were used in investigations to determine whether changing the rate of delivery of the most effective mannitol dose (1 gm/kg) influenced resultant ICP reduction. The results indicated that rapid administration (2 ml/kg/min) produced higher peak serum concentrations of mannitol and more profound lowering of ICP than the same dose delivered at slower rates.

Effect of the barbiturate methohexital on cerebral vessels and intracranial pressure.

Reactions of pial arteries and veins as well as intracranial pressure (ICP) and mean arterial pressure during intravenous administration of methohexital were observed in two groups of cats totaling 24 animals in order to investigate hypothesized direct barbiturate effects on cerebral vascular volume. Group 1 had bolus injection of 1 mg/kg followed by infusion of 0.1 mg/kg/min over 60 minutes. This induced a 6 to 7% arterial dilatation at 50 to 60 minutes (not significant); a 20% reduction of pial vein calibers was observed (P less than 0.01). In Group 2, the same treatment protocol administered under conditions of ICP elevation to 20 mm Hg by the cisternal infusion of mock cerebrospinal fluid resulted again in consistent, although less extensive, venous caliber reduction (5 to 7%, P less than 0.01). In Group 2 controls, pial arteries dilated by 15 to 20%; this reaction was suppressed in the methohexital-treated animals. After stopping methohexital, however, arteries in the methohexital group dilated to almost the same extent as in controls. Mean arterial pressure remained stable in both groups. ICP was not reduced by methohexital. EEG-activity was slightly increased during treatment. We conclude that methohexital has a direct effect on vessel caliber and thus cerebral blood volume via absolute diminution of venous vessels and suppression of ICP-induced autoregulative arterial dilatation. This direct vascular effect, however, seems to be counterbalanced by unknown intracranial mass effects that prevent a reduction in ICP.

Responses of isolated canine and simian basilar arteries to thiopentone by a newly designed pharmacological method for measuring vascular responsiveness.

The stainless steel cannula inserting method was modified for application to observe vascular responses to thiopentone in the isolated basilar arteries of the dog and monkey. In the dog, thiopentone (0.01-3 mg) induced a monophasic vasoconstriction in a dose-dependent manner. On the other hand, in the monkey, thiopentone (0.01-3 mg) showed a biphasic vascular response, i.e., an initial vasoconstriction followed by a vasodilatation in a dose-dependent manner. Thiopentone usually produced much more potent vasoconstriction in the dog than that in the monkey, while potassium chloride made little difference of vasoconstriction between the dog and monkey basilar arteries. These findings suggest that thiopentone exerts a direct constrictive effect on cerebral vessels, the actions of which decrease the total cerebral blood volume and the brain bulk, allowing a reduction in intracranial pressure.

The effect of ketamine on intracranial pressure during haemorrhagic shock under the conditions of both spontaneous breathing and controlled ventilation

Seventeen piglets of both sexes, seven with O2/air-buprenorphine anaesthesia and controlled ventilation, and ten unanaesthetized animals with normal, spontaneous respiration, were used for the study. The intracranial pressure of both groups of animals was raised by insufflation of an epidural balloon and the arterial blood pressure was reduced to approximately 70% of the original value by controlled haemorrhage. 0.5 mg/kg body weight of ketamine was given intravenously, followed by a further dose of 2.0 mg/kg body weight of ketamine five minutes later. Both ketamine doses led to a significant rise in the intracranial pressure of those animals breathing spontaneously (31.8 mm Hg to 39.1 mm Hg). In contrast, the ventilated animals showed a significant reduction in intracranial pressure. No changes in arterial PCO2 were observed in this group, while those piglets breathing spontaneously had dangerous PCO2 rises. At both ketamine doses a significant correlation could be found between the PCO2 and the intracranial pressure.

In vivo effects of alpha-adrenoceptor agonists and antagonists on pial veins of cats.

Cerebral blood volume and intracranial pressure may be modified by influences on cerebral veins. The known adrenergic innervation of cerebral veins and their sensitivity to norepinephrine raised the question, whether pial veins can be selectively influenced through adrenoceptors in vivo. Therefore, alpha 1 and alpha 2 adrenoceptor agonists and antagonists were locally injected into the perivascular space of pial veins using the microapplication technique. The alpha 1 and alpha 2 adrenoceptor antagonists, prazosin and yohimbine, had only minor effects on pial veins. Both antagonists blocked constrictions induced by norepinephrine (10(-5)M) in a concentration dependent manner (10(-7)-10(-4)M). The alpha 1 adrenoceptor agonist phenylephrine caused significant (10(-7)-10(-3)M) constriction of pial veins, with a maximum of 11.6% of initial diameter at 10(-3)M. Oxymetazoline, an alpha 2 receptor agonist, induced a significant constriction only at 10(-3)M (5.1%). Since both alpha 1 and alpha 2 adrenoceptor agonists are less potent constrictors of pial veins than norepinephrine in vivo, a preferential use of alpha 1 or alpha 2 adrenoceptor agonists cannot be recommended from these experiments, if a therapeutic reduction of intracranial pressure or blood volume is desired.