Cerebral blood flow and intracranial pressure

The Monro–Kellie hypothesis states that ‘if the skull is intact, then the sum of the volumes of the brain, cerebrospinal fluid (CSF) and intracranial blood volume is constant’. An increase in volume in one of the three components within the skull must be compensated for by a decrease in the volume of the other remaining components, otherwise the intracranial pressure (ICP) will increase. Brain tissue is not easily displaced; therefore changes in venous blood or CSF volumes initially act as the major buffers against a rise in ICP. In the normal adult, the ICP is 5–13 mm Hg, with minor cyclical variations owing to the effects of the arterial pressure waveform and respiration. Cerebral blood flow (CBF) is determined by a number of factors. It is closely linked to the metabolic activity of the brain to ensure adequate delivery of oxygen and substrates. The relationship between partial pressure of carbon dioxide in arterial blood (PaCO₂) and CBF is almost linear. CBF increases by 25% for each kPa increase in PaCO₂. Hypoxia (PaO₂ < 6.7 kPa) is also a potent stimulus for increasing CBF. The brain is intolerant of hypo- or hyperperfusion and therefore requires a constant flow of blood over a range of pressures, which is achieved by autoregulation. Below the lower limit of autoregulation, CBF mirrors mean arterial pressure (MAP), and eventually a reduced flow causes cerebral ischaemia. Monitoring of the central nervous system, including measurements of neuronal function, ICP, CBF and cerebral oxygenation, can guide pharmacological and surgical treatment according to the individual status of the patient.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the intracranial pressure–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure, which in turn determines global cerebral blood flow. Although the physiological process of autoregulation ensures that cerebral blood flow is tightly maintained over a range of cerebral perfusion pressures, large increases in the ICP can result in severely impaired autoregulation, meaning that cerebral blood flow may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and cerebral blood flow. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and cerebral blood flow.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the intracranial pressure–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure, which in turn determines global cerebral blood flow. Although the physiological process of autoregulation ensures that cerebral blood flow is tightly maintained over a range of cerebral perfusion pressures, large increases in the ICP can result in severely impaired autoregulation, meaning that cerebral blood flow may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and cerebral blood flow. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and cerebral blood flow.     

Brain blood volume and blood flow in patients with plateau waves

Plateau waves, characterized by acute transient rises of the intracranial pressure (ICP), are accompanied by a marked decrease of the cerebral perfusion pressure. Patients with plateau waves, however, often show no clinical symptoms of ischemia of the brain stem, such as vasopressor response or impairment of consciousness during the waves. The authors studied brain blood volume and blood flow with dynamic computerized tomography using rapid-sequence scanning in patients with plateau waves identified during continuous ICP recording. Following an intravenous bolus injection of contrast medium, density-versus-time curves were obtained for the regions of interest; that is, the frontal lobe, the temporal lobe, the caudate nucleus, the putamen, and the pons. The dynamic studies were undertaken when the ICP was high during a plateau-wave phase and when it was low during an interval phase between two plateau waves. The results indicate that, in the cerebral hemisphere (frontal lobe, temporal lobe, caudate nucleus, and putamen), plateau waves were accompanied by an increase in blood volume and, at the same time, a decrease in blood flow. In the pons, however, both the blood volume and blood flow showed little change during plateau waves as compared with the intervals between two plateau waves. These observations may explain why there is no rise in the systemic blood pressure and why patients are often alert during plateau waves.     

Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow.

Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of induced alterations in blood pressure on ICP and brain stiffness as indicated by the pressure-volume index (PVI) was studied during 58 tests of autoregulation of cerebral blood flow in 47 comatose head-injured patients. In patients with intact autoregulation mechanisms, lowering the blood pressure caused a steep increase in ICP (from 20 +/- 3 to 30 +/- 2 mm Hg, mean +/- standard error of the mean), while raising blood pressure did not change the ICP. When autoregulation was defective, ICP varied directly with blood pressure. Accordingly, with intact autoregulation, a weak positive correlation between PVI and cerebral perfusion pressure was found; however, with defective autoregulation, the PVI was inversely related to cerebral perfusion pressure. The various blood pressure manipulations did not significantly alter the cerebral metabolic rate of oxygen, irrespective of the status of autoregulation. It is concluded that the changes in ICP can be explained by changes in cerebral blood volume due to cerebral vasoconstriction or dilatation, while the changes in PVI can be largely attributed to alterations in transmural pressure, which may or may not be attenuated by cerebral arteriolar vasoconstriction, depending on the autoregulatory status. The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high. On the other hand, induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should only be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the ICP–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure (CPP), which in turn determines global cerebral blood flow (CBF). Although the physiological process of autoregulation ensures that CBF is tightly maintained over a range of CPPs, large increases in the ICP can result in severely impaired autoregulation, meaning that CBF may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and CBF. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and CBF.     

The effects of rapid infusions of saline and mannitol on cerebral blood volume and intracranial pressure in dogs

The role of osmotic brain dehydration in the early reduction of intracranial pressure (ICP) following mannitol administration has recently been questioned and a decrease in cerebral blood volume (CBV) proposed as the mechanism of action. To evaluate this hypothesis, relative CBV changes before and after mannitol infusion were determined by collimated gamma counting across the biparietal diameter of the exposed skull in six dogs. Red blood cells were labelled with chromium-51. Cerebral blood volume (CBV), total blood volume (TBV), ICP, mean arterial pressure (MAP), central venous pressure (CVP), haematocrit and osmolality were serially measured after infusions of 10 ml X kg-1 of normal saline (control study) and of 20 per cent mannitol (mannitol study). The solutions were administered over a two-minute period; a 30-minute equilibration period intervened between the saline and mannitol infusions. We demonstrated that the mannitol infusion was associated with significant increases in relative CBV (25 per cent), ICP (7 mmHg), CVP (11 cm H2O), and TBV (50 per cent). MAP declined significantly (14 per cent) after mannitol infusion. The administration of saline, although associated with an increase in TBV (18 per cent), was not associated with any significant change in CBV, ICP, MAP or CVP. The increase in relative CBV persisted for 15 minutes after mannitol infusion, while the ICP returned to control within five minutes and continued to decrease. This study supports the fact that after rapid mannitol infusion, ICP begins to decrease only once the dehydrating effect has counteracted the increase in brain bulk caused by the increase in cerebral blood volume.     

Role of the medulla oblongata in plateau-wave development in dogs

Plateau waves reflect both dilatation of the cerebral vessels and an increase in the cerebral blood volume under increased intracranial pressure (ICP). They are often associated with changes in arterial blood pressure (BP) and respiration, suggesting a role of the brain stem in their development. In experiments conducted on dogs in which intracranial hypertension was induced by occluding the neck veins, the authors stimulated the brain-stem reticular formation in the medulla oblongata and caudal pons to identify the brain sites that produce plateau-like responses. A rise in ICP was observed following stimulation of most areas of the brain stem and was associated with changes in arterial BP, cerebral perfusion pressure (CPP), cerebral blood flow (CBF), respiration, and pulse rate. The stimuli delivered to the medial reticular formation of the caudal medulla caused an arterial depressor response, a decrease in CPP and CBF, suppressed ventilation, and bradycardia; these responses were similar in many respects to plateau waves observed in clinical practice and almost corresponded to the depressor region of the vasomotor center. It is hypothesized that the medullary depressor area may play a role in eliciting cerebral vasomotor reaction concerned with the development of plateau waves in a state of increased ICP.     

Milieu intérieur et hypertension intracrânienne

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements accross the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An IV perfusion of 0.25 g-kg¹ is administered over 20 minutes when ICP increases. Hypertonie saline solutes act in the same way, however they are not more efficient than mannitol.CO₂ is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia.Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedema. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.     

Pediatric neck injuries. A clinical study

In a previous paper, the authors showed that mannitol causes cerebral vasoconstriction in response to blood viscosity decreases in cats. The present paper describes the changes in intracranial pressure (ICP) and cerebral blood flow (CBF) after mannitol administration in a group of severely head-injured patients with intact or defective autoregulation. The xenon-133 inhalation method was used to measure CBF. Autoregulation was tested by slowly increasing or decreasing the blood pressure by 30% and measuring CBF again. Mannitol was administered intravenously in a dose of 0.66 gm/kg; 25 minutes later, CBF and ICP were measured once again. In the group with intact autoregulation, mannitol had decreased ICP by 27.2%, but CBF remained unchanged. In the group with defective autoregulation, ICP had decreased by only 4.7%, but CBF increased 17.9%. One of the possible explanations for these findings is based on strong indications that autoregulation is mediated through alterations in the level of adenosine in response to oxygen availability changes in cerebral tissue. The decrease in blood viscosity after mannitol administration leads to an improved oxygen transport to the brain. When autoregulation is intact, more oxygen leads to decreased adenosine levels, resulting in vasoconstriction. The decrease in resistance to flow from the decreased blood viscosity is balanced by increased resistance from vasoconstriction, so that CBF remains the same. This might be called blood viscosity autoregulation of CBF, analogous to pressure autoregulation. Vasoconstriction also reduces cerebral blood volume, which enhances the effect of mannitol on ICP through dehydration of the brain. When autoregulation is not intact there is no vasoconstriction in response to increased oxygen availability; thus, CBF increases with decreased viscosity. With the lack of vasoconstriction, the effect on ICP through dehydration is not enhanced, so that the resulting decrease in ICP is much smaller. Such a mechanism explains why osmotic agents do not change CBF but decrease ICP in normal animals or patients with intact vasoconstriction, but do (temporarily) increase CBF in the absence of major ICP changes after stroke.     

Intrakranielle Druck-Volumen-Beziehung

Posttraumatic increase of intracranial pressure (ICP) is a strong prognostic factor for the outcome of patients after traumatic brain injury. After exhausting all compensatory mechanisms ICP increases exponentially, where ICP_norm=(CSF production*CSF flow resistance)+venous pressure_{(sinus sagittalis)}=10–15 mmHg. The ICP curve is influenced by the compliance (ΔV/ΔP) and elasticity (ΔP/ΔV) of the brain. Marmarou could demonstrate that the non-linear cranio-spinal pressure-volume relationship describes a logarithmic, mono-exponential, strongly linear relationship between pressure and volume and named this the pressure volume index (PVI=log ICP/ΔV). The pressure volume index describes the volume necessary to increase ICP by a factor of 10. Additionally to PVI the measurement of volume-pressure response (VPR) was introduced. The continuous intracranial compliance could be determined on the principle of pulsatile volume increases as an equivalent of very small intra-cranial volume increases. However, to ascertain functional status of the injured brain a combination of measurements of different parameters, such as tissue oxygen partial pressure (p_tiO₂), cerebral blood flow (CBF), microdialysis and electrocorticography (ECoG) is recommended.     

Prevention and treatment of intracranial hypertension

Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberoptic devices. Displaying the time course of pressure (high-resolution ICP tonoscopy) allows assessment of the validity of the signal and identification of specific pathological findings, such as A-, B- and C-waves. When ICP is pathologically elevated--at or above 20-25 mmHg--it needs to be lowered. A range of treatment modalities is available and should be applied with consideration of the underlying cause. When intracranial hypertension is caused by hematoma, contusion, tumor, hygroma, hydrocephalus or pneumatocephalus, surgical treatment is indicated. In the absence of a surgically treatable condition, ICP may be controlled by correcting the patient's position, temperature, ventilation or hemodynamics. If intracranial hypertension persists, drainage of CSF via external drainage is most effective. Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). When autoregulation of cerebral blood flow is compromised, hyperoncotic treatment aimed at reducing vasogenic edema and intracranial blood volume may be applied. When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.     

Changes in intracranial pressure and epidural pulse waveform following cold injury

Summary Using anaesthetized spontaneously breathing cats, intracranial pressure (ICP) was monitored for twenty hours following the insult of cold injury; simultaneous recordings were also made of cerebral blood flow (CBF), epidural pulse waveform (EDP-WF), and systemic arterial pressure (SAP). Results could be divided into two groups depending on whether or not ICP exceeded 30 mmHg. In group one, in which marked increase in ICP including occasional episodes of pressure waves were observed, an initial increase in CBF and the changes in EDP-WF from polyphasic to monotonous at about 20 mmHg were characteristic. On the other hand, in group two, ICP never exceeded 30 mmHg, CBF slightly and continuously decreased and EDP-WF was polyphasic throughout the course. There were no significant differences in trends in SAP, in the extent of spread of oedema and in water content of the white matter between both groups. Therefore, the amount of cerebral blood volume (CBV) due to cerebral vasodilatation was considered to account for the further increase in ICP. Moreover, changes in EDP-WF were regarded as a useful indicator in predicting the trends in ICP since these changes could be observed in a relatively lower pressure range prior to a marked increase in ICP.     

The relation of cerebral ischemia, hypoxia, and hypercarbia to the Cushing response.

A marked increase in intracranial pressure (ICP) produces a concomitant increase in systemic blood pressure (the Cushing response). In this study a comparison is made between this response of systemic blood pressure to increased ICP and the blood pressure responses produced by ischemia, hypoxia, and hypercarbia of the primate brain. A carotid-to-carotid cross-perfusion system was used to produce a purely cerebral hypoxia and hypercarbia. Each stimulus, except hypercarbia, produced a hypertensive response that was qualitatively and quantitatively similar. These responses were characterized by a short latent period, a rapid development, and an increase in mean arterial pressure of 60% or more. The similarity of the responses suggests that these stimuli act through a final common pathway independent of the purely mechanical effects of increased ICP upon the brain.     

Effect of cerebral perfusion pressure on contusion volume following impact injury

OBJECT: Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume. METHODS: The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin-stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12+/-1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9+/-1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16+/-2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18+/-1 mm Hg). CONCLUSION: Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.     

Effects of dihydroergotamine on cerebral circulation during experimental intracranial hypertension

Different cerebral vasoconstrictors have recently been suggested for the treatment of raised intracranial pressure (ICP) in patients with severe traumatic brain lesions. Such treatment may be associated with severe side effects. A porcine model simulating an intracranial mass lesion was utilized to examine the haemodynamic cerebral effects of dihydroergotamine (DHE), a recently introduced pharmacological treatment for raised intracranial pressure. Intracranial hypertension was induced by inflation of two tonometric gastric balloons placed extradurally covering the parieto-occipital region bilaterally. The animals were randomized into one group with six animals receiving 1.0 mg of DHE i.v. followed by a continuous infusion of 0.2 mg/h (high dose) and another group of six animals receiving 0.15 mg i.v. followed by 0.03 mg/h (low dose). Measurements of cerebral blood flow (CBF) and arterio-venous difference in oxygen content (Cavo₂) were performed 5, 20, and 60 min after the DHE infusion. Intracranial pressure (ICP), mean arterial blood pressure (MAP) and cerebral electrical activity (EEG) were recorded continuously.
In both groups infusion of DHE caused a lasting decrease in ICP probably achieved mainly by a decrease in cerebral blood volume due to constriction of both arterial and venous capacitance vessels. In the group treated with high-dose DHE, but not in that given low-dose DHE, a progressive increase in Cavo₂, a fall in jugular venous pH and an increase in EEG delta activity were observed indicating cerebral hypoxia. The study supports the view that DHE may be a valuable tool in the pharmacological treatment of increased ICP in traumatic brain lesions but underscores the importance of a proper dosage.     

Intracranial hypertension and brain oedema in albino rabbits. Part 3: Effect of acute simultaneous diuretic and barbiturate therapy

Summary Increased intracranial pressure due to brain oedema was produced in albino rabbits by combining a cryogenic lesion in the left hemisphere with the intraperitoneal administration of 6-aminonicotinamide (cytotoxic agent). The following parameters were assessed: intracranial pressure (ICP), systolic arterial pressure (SAP), central venous pressure (CVP), EEG, brain water and electrolyte content, gross pathology, and blood brain barrier integrity. Acute therapy to reduce ICP was performed by administering a bolus of mannitol (1 gm/kg) and 30 minutes later, also in bolus, frusemide (5 mg/kg). Immediately following the administration of mannitol an infusion of pentobarbitone was commenced; this was continued for one hour so that a total of 10 mg/kg was administered.There was a 50% reduction of ICP at one hour from initiation of treatment. The brains of the animals were extracted immediately upon cessation of therapy (pentobarbitone) and they revealed a significant reduction of water content for the right, uninjured, hemisphere only, when compared to controls; a slight but not significant reduction of the brain sodium and potassium was noted in both hemispheres. There was no change noted in the gross pathology and extent of blood brain barrier breakdown. In all animals epinephrine infusion had to be administered for between 20 and 30 minutes to maintain a SAP over 80 torr. There seems to be no advantage in the simultaneous administration of barbiturates and diuretics for the control of ICP due to brain oedema.     

Resuscitation from hemorrhagic shock. Alterations of the intracranial pressure after normal saline, 3% saline and dextran-40.

Resuscitation from hemorrhagic shock by infusion of isotonic (normal) saline (NS) is accompanied by a transient elevation in intracranial pressure (ICP), although cerebral edema, as measured by brain weights at 24 hours, is prevented by adequate volume resuscitation. The transient increase in ICP is not observed during hypertonic saline (HS) resuscitation. The effect of colloid resuscitation on ICP is unknown. Beagles were anesthetized, intubated, and ventilated, maintaining pCO2 between 30-45 torr. Femoral artery, pulmonary artery, and urethral catheters were positioned. ICP was measured with a subarachnoid bolt. Forty per cent of the dog's blood volume was shed and the shock state maintained for 1 hour. Resuscitation was done with shed blood and a volume of either NS (n = 5), 3% HS (n = 5), or 10% dextran-40 (D-40, n = 5) equal to the amount of shed blood. Intravascular volume was then maintained with NS. ICP fell from baseline values (4.7 +/- 3.13 mmHg) during the shock state and increased greatly during initial fluid resuscitation in NS and D-40 groups, to 16.0 +/- 5.83 mmHg and 16.2 +/- 2.68 mmHg, respectively. ICP returned to baseline values of 3.0 +/- 1.73 mmHg in the HS group with initial resuscitation and remained at baseline values throughout resuscitation. NS and D-40 ICP were greater than HS ICP at 1 hour (p less than .001) and 2 hours (p less than .05) after resuscitation. These results demonstrate that NS or colloid resuscitation from hemorrhagic shock elevates ICP and that HS prevents elevated ICP.     

Effects of positive end-expiratory pressure on intracranial pressure and compliance in brain-injured patients.

Hypoxic pulmonary disorders and head injuries associated with increased intracranial pressure (ICP) frequently co-exist. Positive end-expiratory pressure (PEEP) improves hypoxemia but has been reported to impede cerebral venous return, potentially causing a further increase in ICP. This study examined the effects of PEEP on ICP at different levels of brain compliance. continuous ICP recordings were obtained after insertion of Scott cannulas to the lateral ventricles of seven comatose patients. Brain compliance was assessed by calculation of the pressure volume index. Patients were maintained in a 30 degrees head-up position. Maintenance of PEEP to levels of 40 cm H2O pressure for as long as 18 hours did not increase ICP in patients with either normal or low intracranial compliance, and did not increase ICP in the absence of pulmonary disease. Central venous pressure and pulmonary artery wedge pressure increased proportionately as PEEP was increased. No consistent changes were found in blood pressure recordings, nor were there any reductions in cardiac output found during the studies. Abrupt discontinuation of PEEP did not result in increased ICP except for a transient rise on two occasions when respiratory secretions became copious and the patients were inadequately ventilated. Improved oxygenation in two patients as a result of PEEP was concomitant with improved intracranial compliance and neurological status. In patients with brain injuries, PEEP improves arterial oxygenation without increasing ICP as previously supposed. Consequently, PEEP is a valuable form of therapy for the comatose patient with pulmonary disorders such as pneumonia or pulmonary edema.     

Treatment of intracranial hypertension and aspects on lumbar dural puncture in severe bacterial meningitis

BACKGROUND: Brain stem herniation due to raised intracranial pressure (ICP) is a common cause of mortality in severe bacterial meningitis, but continuous measurements of ICP and the effects of ICP-reducing therapy in these patients have, to our knowledge, not been described. METHODS: During a four-year period, an ICP-monitoring device was implanted in patients admitted to our hospital with severe bacterial meningitis and suspected intracranial hypertension. ICP above 20 mmHg was treated using the Lund Concept, which includes antihypertensive therapy (beta1-antagonist,alpha2-agonist), normalization of the plasma colloid osmotic pressure and the blood volume, and antistress therapy. RESULTS: ICP above 20 mmHg was found in all 12 patients studied. It was effectively reduced in all but two patients, who died. Both patients had a low cerebral perfusion pressure (<10 mmHg), dilated pupils at start of therapy and were beyond recovery. Radiological signs of brain swelling were present in only five patients. Seven patients recovered fully, while mild audiological impairment was observed in two and minor neurological sequelae in one patient. Eight patients showed signs suggesting imminent brain stem herniation before start of ICP-reducing treatment, seven of whom had been subjected to diagnostic lumbar dural puncture shortly before development of the brain stem symptoms. These symptoms gradually regressed after initiation of therapy, and in one patient reversal of brain stem herniation was documented by MRI. CONCLUSIONS: Severe bacterial meningitis can be associated with increased ICP, which can be reduced using the Lund Concept. The high survival rate, the low frequency of sequelae and the reversal of signs of imminent brain stem herniation in these high-risk patients indicated beneficial effects of the intervention. The study confirms earlier observations that lumbar dural puncture is potentially hazardous in patients with intracranial hypertension, because it may trigger brain stem herniation. A normal CT brain scan does not rule out intracranial hypertension.