External ventricular drainage--a new aspect in the operative treatment of head injury (author's transl)

It is not only for CSF-removal in conservative treatment of oedema and control of the effectiveness of osmo-onco-therapy, contricosteroids, anticholinergics and aldosterone-antagonists, that external CSF drainage in severe cerebral trauma has proved of value. It has also made it possible to assess objectively the indications for bitemporal craniotomy in raised intracrainial pressure with an acute midbrain syndrome caused by tentorial herniation. Continuous monitoring of ICP permits an intervention at the right time and prevents one from operating too late, namely at a moment, when manifest neurological signs already indicate cerebral decompensaervative steps failing, a bitemporal craniectomy is indicated: in this way we lower intracranial pressure, liberate the rostral brain stem out of its strangulation and improve cerebral perfusion and metabolism.     

Impulsive and compulsive self-injurious behavior in bulimia nervosa: prevalence and psychological correlates

Acute ischemia in the complete territory of the carotid or the middle cerebral artery may lead to cerebral edema with raised intracranial pressure and progression to coma and death. Although clinical data suggest benefit for patients undergoing decompressive surgery for massive space occupying hemispheric stroke, little data about the effects of this procedure on morbidity and outcome is available. The experimental data support an early surgical approach. For early and probably most effective treatment of severe, space-occupying cerebral ischemia, the "malignant" character of the brain edema has to be recognized early after onset of vessel occlusion. Hereby magnetic resonance imaging (MRI) may allow to determine the clinical significance of brain edema early after onset, simultaneously allowing to monitor the evolution of ischemia. We performed serial SE-MRI in rats with acute hemispheric infarctions treated by decompressive craniectomy. Focal cerebral ischemia was induced in 36 rats using an endovascular occlusion technique. Decompressive craniectomy was performed 4 and 24 hours after vessel occlusion in groups of 12 animals each. Twelve animals were not treated by decompressive craniectomy (control group). Four, 24, 48, 72 and 168 hours after MCAO all animals were examined with conventional T1- and T2-weighted SE-MRI. Shift of the midline structures and compression of the ventricles were scored. Changes in weight and neurological performance were measured daily. The infarction volume was calculated by triphenyltetrazolium chloride staining 168 hours after MCAO. While mortality in the untreated group was 33.3%, none of the animals treated by a decompressive craniectomy died (mortality 0%). Neurological behaviour, weight loss and infarction volume were significantly better in the animals treated by early decompressive craniectomy (p < 0.05). Four hours after MCAO all untreated animals showed a massive shift of the midline structures and a massive compression of the ventricles; only 7 of 12 animals treated early by craniectomy showed mild mass effects. Correlation of the histological brain damage with T2-weighted MRI 4 hours after MCAO was poor (r = 0.41); later than 24 hours there was a good correlation (r > 0.7). Our results suggest that decompressive craniectomy in malignant cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. In the acute phase of hemispheric infarction conventional SE-MRI is not sensitive in estimation of infarction size. Later than 24 hours, conventinal SE-MRI proved to be useful in monitoring brain edema and infarction size in this rat model of malignant hemispheric stroke.     

Intravascular ultrasound in endovascular stent-grafts for peripheral aneurysm: a clinical study

The present series of experiments was performed to investigate the influence of acute intracranial hypertension on the upper limit (UL) of cerebral blood flow (CBF) autoregulation. Three groups of eight rats each--one with normal intracranial pressure (ICP) (2 mmHg), one with ICP = 30 mmHg, and one with ICP = 50 mmHg--were investigated. Intracranial hypertension was maintained by continuous infusion of lactated Ringer's solution into the cisterna magna, where the pressure was used as ICP. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure (MABP)-ICP, was increased stepwise by continuous intravenous infusion of norepinephrine. CBF was calculated by the intracarotid 133Xe method. In all three groups the corresponding CBF/CPP curve included a plateau where CBF was independent of changes in CPP, showing intact autoregulation. At normal ICP the UL was found at a CPP of 141 +/-2 mmHg, at ICP = 30 mmHg the UL was 103+/-5 mmHg, and at ICP = 50 mmHg the UL was found at 88+/-7 mmHg. This shift of the UL was more pronounced than the shift of the lower limit (LL) of the CBF autoregulation found previously. We conclude that intracranial hypertension is followed by both a shift toward lower CPP values and a narrowing of the autoregulated interval between the LL and the UL.     

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.     

Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain

OBJECTIVE: To determine the effect of continuous hypertonic (3%) saline/acetate infusion on intracranial pressure (ICP) and lateral displacement of the brain in patients with cerebral edema. DESIGN: Retrospective chart review. SETTINGS: Neurocritical care unit of a university hospital. PATIENTS: Twenty-seven consecutive patients with cerebral edema (30 episodes), including patients with head trauma (n = 8), postoperative edema (n = 5), nontraumatic intracranial hemorrhage (n = 8), and cerebral infarction (n = 6). INTERVENTION: Intravenous infusion of 3% saline/acetate to increase serum sodium concentrations to 145 to 155 mmol/L. MEASUREMENTS AND MAIN RESULTS: A reduction in mean ICP within the first 12 hrs correlating with an increase in the serum sodium concentration was observed in patients with head trauma (r2 = .91, p = .03), and postoperative edema (r2 = .82, p = .06), but not in patients with nontraumatic intracranial hemorrhage or cerebral infarction. In patients with head trauma, the beneficial effect of hypertonic saline on ICP was short-lasting, and after 72 hrs of infusion, four patients required intravenous pentobarbital due to poor ICP control. Among the 21 patients who had a repeat computed tomographic scan within 72 hrs of initiating hypertonic saline, lateral displacement of the brain was reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SEM]) and in patients with postoperative edema (3.1 +/- 1.6 to 1.1 +/- 0.7). This effect was not observed in patients with nontraumatic intracranial bleeding or cerebral infarction. The treatment was terminated in three patients due to the development of pulmonary edema, and was terminated in another three patients due to development of diabetes insipidus. CONCLUSIONS: Hypertonic saline administration as a 3% infusion appears to be a promising therapy for cerebral edema in patients with head trauma or postoperative edema. Further studies are required to determine the optimal duration of benefit and the specific patient population that is most likely to benefit from this treatment.     

Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats

This study on conscious rats with occluded left carotid artery investigates the influence of cerebral edema after acute carbon monoxide (CO) poisoning on cerebrospinal fluid pressure (CSFp) and evaluates the therapeutic effectiveness of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2). The CSFp was continuously recorded via a cannula placed in the left cerebral ventricle before, during, and for up to 6 h after exposure to 0.27% CO for 1 h. A non-sustained small increase in the CSFp and identical degrees of hypoxemia, hypocapnia, arterial hypotension, and acidosis were found during the exposure in all rats. After the CO exposure, all non-edema control rats without carotid artery ligation (n = 7) recovered completely with normal CSFp, behavior, and brain water content. All untreated (n = 7) and NBO2-treated rats (n = 7) developed a severely increased CSFp (> 50 mmHg) with neurologic motor dysfunction, and died of a severely increased CSFp (> 100 mmHg) with considerable cerebellar herniation. Except in one rat, the CSFp did not reach a dangerous level (> 25 mmHg) after the HBO2 session (300 kPa O2 for 1 h, beginning at 20 min post CO). All HBO-treated rats (n = 7) survived with less neurologic motor dysfunction and less left hemispheric edema than those in untreated and NBO2-treated rats. The results demonstrated that the increase in the CSFp was related to the left hemispheric edema, and that the cerebellar herniation was the predominant cause of death after the CO exposure. HBO2, but not NBO2, prevented the severe increase in the CSFp and thus saved the life after the CO exposure.     

Insulin improves cardiac contractile function and oxygen utilization efficiency during moderate ischemia without compromising myocardial energetics

Insulin improves myocardial contractile function during moderate ischemia, but the mechanism is unknown. To determine effects of insulin on myocardial oxygen utilization efficiency (O2UE) and energetics, regional left coronary perfusion pressure (CPP) was lowered sequentially from 100 to 60, 50, and 40 mmHg in 24 anesthetized, open-chest dogs. Regional power index (PI), myocardial oxygen consumption (MVO2), and O2UE index (PI/MVO2) were determined in untreated and insulin treated (4 U/min, i.v.) hearts. Biopsies were obtained from six untreated and six insulin-treated hearts at CPP=40 mmHg for determining high energy phosphates and the cytosolic phosphorylation potential. Measurements were compared with data from normal, untreated myocardium (n=11). MVO2 fell (P<0.05) in all hearts as CPP was lowered to 40 mmHg, and was unaffected by insulin treatment. PI decreased 32 and 75% in untreated hearts at CPP=50 and 40 mmHg, respectively (P<0.05). In insulin treated hearts, PI was not significantly depressed at CPP>40 mmHg, and fell only 26% at CPP=40 mmHg. O2UE increased (P<0.05) in all hearts at CPP=60 mmHg. In insulin treated hearts, O2UE was greater (P<0.05) at CPP=50 and 40 mmHg than at CPP=100 mmHg, and greater (P<0.05) than in untreated hearts at CPP=40 mmHg. Reducing CPP to 40 mmHg produced similar metabolic changes in all hearts. Compared to normal myocardium, ATP content of untreated and treated hearts was unchanged, creatine phosphate content decreased 21 and 14%, creatine content increased 24 and 30%, inorganic phosphate concentration increased 108 and 140%, and phosphorylation potential decreased 80 and 77%. We conclude that insulin markedly improves PI and O2UE without altering cytosolic energetics during moderate myocardial ischemia.     

Diaspirin cross-linked hemoglobin resuscitation improves cerebral perfusion after head injury and shock

BACKGROUND: Shock associated with traumatic brain injury (TBI) doubles the mortality of TBI alone by inducing a secondary ischemic injury. Rapid correction of cerebral perfusion pressure (CPP) is thought to be essential to improving outcome. Diaspirin cross-linked hemoglobin (DCLHb) has been shown to improve cerebral blood flow, increase mean arterial pressure (MAP), and reduce lesion size in models of occlusive cerebral ischemia but has not been evaluated in a model of TBI combined with hemorrhagic shock. METHODS: We studied the effects of DCLHb resuscitation in a porcine model of cryogenic TBI and hemorrhagic shock (MAP = 50 mmHg). After combined insults, animals were randomized to receive a bolus of 4 mliters/kg of either lactated Ringer's solution (n = 5) or DCLHb (n = 6). Lactated Ringer's solution was then infused in both groups to maintain MAP at baseline. Shed blood was returned 1 hour after the initiation of resuscitation (R1). Animals were studied for 24 hours. RESULTS: DCLHb infusion resulted in a significantly greater MAP at R1 and R24 (95 +/- 4 vs. 82 +/- 2 and 99 +/- 3 vs. 85 +/- 3 mm Hg, respectively) and a significantly greater CPP at R1 and R24 (83 +/- 10 vs. 68 +/- 5 and 89 +/- 6 vs. 71 +/- 11 mm Hg, respectively). Intracranial pressure was lower in the DCLHb group, but this difference was not significant. There was no significant difference between the groups in cerebral oxygen delivery. DCLHb animals required less fluid to maintain MAP (12,094 +/- 552 vs. 15,542 +/- 1094 mliters, p < 0.05). CONCLUSION: These data suggest that DCLHb is beneficial in the early resuscitation of head injury and shock and that further investigation is warranted. Key Words: Diaspirin cross-linked hemoglobin, Head injury, Shock, Cerebral perfusion pressure.     

An experimental study on the occurrence of brain edema after retrograde cerebral perfusion

To assess the safety of retrograde cerebral perfusion, the occurrence of brain edema after this procedure was investigated. Twenty-eight adult mongrel dogs were divided into three groups that underwent the following treatments: antegrade perfusion (group 1, n = 9); retrograde perfusion alone (group 2, n = 11); or tetrograde perfusion with drugs (manuitol, thiopental sodium, and methylprednisolone; group 3, n = 8). After 90 minutes of cerebral perfusion at 20 degrees C of the pharyngeal temperature, evans blue (EB) was administered to check for disruptions of the blood-brain-barrier (BBB) and brain tissue water content was measured. Intracranial pressure after cerebral perfusion was markedly higher in group 2 than in group 1 (26.4 +/- 9.4 vs. 11.2 +/- 3.6 mmHg), and brain tissue water content was also significantly higher in group 2 than in group 1 (80.7 +/- 2.0 vs. 77.8 +/- 0.9%). These data suggested that brain edema was more prominent after retrograde perfusion than after antegrade perfusion. The extent of EB to brain tissue was greater in group 2 than in group 1 (169.8 +/- 97.7 vs. 54.7 +/- 31.5 micrograms/dl). The BBB was highly disrupted in group 2 and vasogenic edema appeared after retrograde cerebral perfusion. Maximum intracranial pressure, brain tissue water content and EB concentration were significantly lower in group 3 than in group 2, and did not differ significantly between group 3 and 1. Administration of pharmacologic agents suppressed edema formation and extravasation of EB. We conclude that 90 minutes of retrograde cerebral perfusion at 20 degrees C of the pharyngeal temperature causes brain edema and disrupts the BBB in a manner different from that associated with antegrade perfusion. Mannitol, thiopental sodium, and methylprednisolone prevent these phenomena, indicating that pharmacologic intervention may improve the safety of retrograde cerebral perfusion.     

Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema

OBJECTIVE: The management of malignant posttraumatic cerebral edema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high despite refinements in medical and pharmacological means of controlling elevated intracranial pressure; therefore, a comparison of medical management versus decompressive craniectomy in the management of malignant posttraumatic cerebral edema was undertaken. METHODS: At the University of Virginia Health Sciences Center, 35 bifrontal decompressive craniectomies were performed on patients suffering from malignant posttraumatic cerebral edema. A control population was formed of patients whose data was accrued in the Traumatic Coma Data Bank. Patients who had undergone surgery were matched with one to four control patients based on sex, age, preoperative Glasgow Coma Scale scores, and maximum preoperative intracranial pressure (ICP). RESULTS: The overall rate of good recovery and moderate disability for the patients who underwent craniectomies was 37% (13 of 35 patients), whereas the mortality rate was 23% (8 of 35 patients). Pediatric patients had a higher rate of favorable outcome (44%, 8 of 18 patients) than did adult patients. Postoperative ICP was lower than preoperative ICP in patients who underwent decompression (P = 0.0003). Postoperative ICP was lower in patients who underwent surgery than late measurements of ICP in the matched control population. A statistically significant increased rate of favorable outcomes was seen in the patients who underwent surgery compared to the matched control patients (15.4%) (P = 0.014). All patients who exhibited sustained ICP values above 40 torr and those who underwent surgery more than 48 hours after the time of injury did poorly. Evaluation of the 20 patients who did not fit into either of those categories revealed a 60% rate of favorable outcome and a statistical advantage over control patients (P = 0.0001). CONCLUSION: Decompressive bifrontal craniectomy provides a statistical advantage over medical treatment of intractable posttraumatic cerebral hypertension and should be considered in the management of malignant posttraumatic cerebral swelling. If the operation can be accomplished before the ICP value exceeds 40 torr for a sustained period and within 48 hours of the time of injury, the potential to influence outcome is greatest.     

Effects of sufentanil on cerebral hemodynamics and intracranial pressure in patients with brain injury

BACKGROUND: The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). METHODS: Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. RESULTS: Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. CONCLUSIONS: The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.     

Glare test in clinical ophthalmology]

Hemoperfusion with local heparin before and protamine after the column was used in the treatment of patients with grave craniocerebral injury. Effect of such treatment on the cerebral perfusion pressure (CPP) is analyzed. The treatment did not increase the liquor pressure but decreased it by 20-25 mm H2O in both groups of patients. CPP in the survivors improved and normalized. In the other group (dead patients) CPP did not change, despite a decrease of the liquor pressure, and remained high. These values can be prognostically important.     

Effects of cisatracurium on cerebral and cardiovascular hemodynamics in patients with severe brain injury

BACKGROUND: For neuroanesthesia and neurocritical care the use of drugs that do not increase or preferentially decrease intracranial pressure (ICP) or change cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) are preferred. The current study investigates the effects of a single rapid bolus dose of cisatracurium on cerebral blood flow velocity, ICP, CPP, mean arterial pressure (MAP) and heart rate (HR) in 24 mechanically ventilated patients with intracranial hypertension after severe brain trauma (Glasgow coma scale <6) under continuous sedation with sufentanil and midazolam. METHODS: Patients were randomly assigned to receive either 2xED95 (n=12) or 4xED95 (n=12) of cisatracurium as a rapid i.v. bolus injection. Before and after bolus administration mean cerebral blood flow velocity (BFV, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system, ICP (mm Hg) was measured using an extradural probe, and MAP (mm Hg) and HR (b/min) were measured during a study period of 20 min. Cerebral perfusion pressure (CPP=MAP-ICP) was also calculated. RESULTS: Our data show that a single bolus dose of up to 4xED95 cisatracurium caused no significant (P<0.05) changes in BFV, ICP, CPP, MAP and HR. Possible histamine-related events were not observed during the study. CONCLUSIONS: The results from this study suggest that cisatracurium is a safe neuromuscular blocking agent for use in adult severe brain-injured patients with increased ICP under mild hyperventilation and continuous sedation.     

Renal artery reconstruction in transplant kidney. Case report

Diaspirin cross-linked haemoglobin (DCLHb) is a new oxygen carrying blood substitute with vasoactive properties. Vasoactive properties may be mediated via high affinity binding of nitric oxide by the haem moiety. Using a rodent model of head injury combined with ischaemia, we studied the effects of DCLHb on cerebral blood flow (CBF) and intracranial pressure (ICP). Twenty anaesthetized rats were allocated randomly to receive treatment with DCLHb 400 mg kg-1 i.v. or placebo (oncotically matched plasma protein substitute 4.5% i.v.). To produce diffusely increased ICP, after a severe weight drop injury, all animals underwent a 30-min period of bilateral carotid ligation combined with a period of induced hypotension. After reperfusion, DCLHb or placebo was infused and the animals instrumented for measurement of intraventricular ICP and CBF in the region of the sensorimotor cortex using the hydrogen clearance technique. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP) (CPP = MAP - ICP) and CBF were measured 4 h after injury in all animals. DCLHb significantly reduced ICP from mean 13 (SEM 2) to 3 (1) mm Hg (P < 0.001), increased CPP from 52 (8) to 95 (6) mm Hg (P < 0.001) and increased CBF from 21 (2) to 29 (2) ml 100 g-1 min-1 (P = 0.032). We conclude that DCLHb improved CPP without a reduction in CBF in a rodent model of post-traumatic brain swelling.     

Low clinical ischemic threshold for cerebral blood flow in severe acute brain trauma. Case report

A case of severe acute brain trauma is presented in which the patient made a satisfactory recovery after suffering a marked reduction in cerebral blood flow, to a level previously reported in association with impending brain death (10 ml/100 gm/min). This is believed to be the first report of a patient with severe acute brain injury in whom serial clinical and physiological assessments allowed documentation of the reversibility of such a critical level of cerebral hypoperfusion.     

Effects of various degrees of compression and active decompression on haemodynamics, end-tidal CO2, and ventilation during cardiopulmonary resuscitation of pigs

The effects of various degrees of compression and active decompression during cardiopulmonary resuscitation were tested in a randomized cross-over-design during ventricular fibrillation in eight pigs using an automatic hydraulic chest compression device. Compared with 4/0 (compression/decompression in cm), mean carotid arterial blood flow rose by 60% with 5/0, by 90% with 4/2 and 4/3, and 105% with 5/2. Two cm active decompression increased mean brain and myocardial blood flow by 53% and 37%, respectively, as compared with 4/0. Increasing standard compression from 4 to 5 cm caused no further increase in brain or heart tissue blood flow whether or not combined with active decompression. Tissue blood flow remained unchanged or decreased when active decompression (4/3) caused that 50% of the pigs were lifted from the table due to the force required. Myocardial blood flow was reduced with 5/0 vs. 4/0 despite no reduction in end decompression coronary perfusion pressure ((aortic-right atrial pressure) (CPP), (7 +/- 8 mmHg with 4/0, 14 +/- 11 mmHg with 5/0)(NS)). End decompression CPP increased by 186% with 4/2 vs. 4/0, by 200% with 4/3, and by 300% with 5/2. Endo-tracheal partial pressure of CO2 was significantly increased during the compression phase of active decompression CPR compared with standard CPR. Active decompression CPR generated an significantly increased ventilation compared with standard CPR. Conclusion: Carotid and tissue blood flow, ventilation, and CPP increase with 2 cm of active decompression. An attempt to further increase the level of active decompression or increasing the compression depth from 4 to 5 cm did not improve organ blood flow.     

Hypertensive encephalopathy in childhood. Diagnostic problems

Oppenheimer and Fischberg's vasoconstriction-hypothesis on the pathogenesis of hypertensive encephalopathy was subsequently supported by animal experiments. Later on the role of decompensation of the autoregulatory mechanism of the cerebral blood flow was revealed. The transient symptomatology comprises headache, seizures, focal cerebral symptoms (hemiplegia etc.), visual disturbances, mental disorders, papiledema etc. The age-dependency of the influence of edema is probably expressed by the predominance of seizures in childhood and the long duration of the symptoms in our third and fourth patient. The differentiation between hypertensive encephalopathy and a local complication of hypertension (hemorrhage) can be difficult, not at least because the first disturbance may be followed by the second (patient 3). Hypertension is not always present as initial symptom (patient 1 and 2). Hence a series of blood pressure readings is required in acute cerebral incidents in childhood. Steroid-treatment may lead, especially in patients suffering from a hypocomplementemic form of membranoproliferative glomerulonephritis, to a sudden rise of the blood pressure and subsequently to hypertensive encephalopathy (patients 2 and 3). Hypertensive encephalopathy is a neuropediatric emergency. The urgent treatment with dioxaside, fursemide and sodium nitroprusside is shortly reviewed.     

Cerebral edema in acute hepatic failure: clinicopathologic correlation

A child developed acute fulminant viral hepatitis and cerebral edema confirmed on postmortem examination. Clinical evidence of herniation, effacement of cortical sulci on computed tomography, and elevated cerebrospinal fluid pressure preceded complicating terminal events, demonstrated that cerebral edema was associated with acute hepatic failure, rather than complicating factors, and led to the patient's death. The mechanism is unknown.     

Use of adrenocorticotrophic hormone analog to minimize brain injury

STUDY OBJECTIVES: To investigate the effects of a vasoactive analog of adrenocorticotrophic hormone (GMM2) on time-dependent disturbances in regional cerebral blood flow, permeability-capillary surface area products, and intracranial pressure in a rat model of moderate concussion/brain injury. SETTING AND DESIGN: Regional permeability-capillary surface area products and cerebral blood flow were measured at two hours after trauma. Intracranial pressure was monitored for 120 hours after trauma. SUBJECTS: Male Wistar rats (330 to 430 g) (regional cerebral blood flow studies, n = 35; permeability-capillary surface area product studies, n = 36; intracranial pressure studies, n = 32). INTERVENTIONS: Post-traumatic subcutaneous administration of nanomolar concentrations of GMM2 (31 nmol per rat). MEASUREMENTS AND MAIN RESULTS: Untreated trauma acutely increased average brain permeability-capillary surface area products for sucrose and decreased average brain cerebral blood flow. Moreover, it produced marked and prolonged increases in intracranial pressure. Post-traumatic subcutaneous administration of nanomolar concentrations of GMM2 effectively reduced the early hypoperfusion, blood-brain barrier leakiness, and pathologic elevation of intracranial pressure. CONCLUSION: Post-traumatic administration of GMM2, in nanomolar amounts, can prevent or reverse significantly the serious cerebrovascular sequelae of moderate head injury in this animal model. In view of its potency, low toxicity, and other neuroprotective properties, in both rats and human beings, these data suggest that GMM2 may have considerable clinical benefits in the treatment of central nervous system trauma.     

Comparison of the effect of etomidate and desflurane on brain tissue gases and pH during prolonged middle cerebral artery occlusion

BACKGROUND: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. METHODS: After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. RESULTS: During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). CONCLUSION: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.