Malignant Brain Edema Research Articles

H1N1 Encephalitis with Malignant Edema and Review of Neurologic Complications from Influenza

BackgroundInfluenza virus infection of the respiratory tract is associated with a range of neurologic complications. The emergence of 2009 pandemic influenza A (H1N1) virus has been linked to neurological complications, including encephalopathy and encephalitis.MethodsCase report and literature review.ResultsWe reviewed case management of a 20-year old Hispanic male who developed febrile upper respiratory tract signs and symptoms followed by a confusional state. He had rapid neurologic decline and his clinical course was complicated by refractory seizures and malignant brain edema. He was managed with oseltamavir and peramavir, corticosteroids, intravenous gamma globulin treatment, anticonvulsants, intracranial pressure management with external ventricular drain placement, hyperosmolar therapy, sedation, and mechanical ventilation. Reverse transcriptase polymerase chain reaction analysis of nasal secretions confirmed 2009 H1N1 virus infection; cerebrospinal fluid (CSF) was negative for 2009 H1N1 viral RNA. Follow-up imaging demonstrated improvement in brain edema but restricted diffusion in the basal ganglia. We provide a review of the clinical spectrum of neurologic complications of seasonal influenza and 2009 H1N1, and current approaches towards managing these complications.Conclusions2009 H1N1-associated acute encephalitis and encephalopathy appear to be variable in severity, including a subset of patients with a malignant clinical course complicated by high morbidity and mortality. Since the H1N1 influenza virus has not been detected in the CSF or brain tissue in patients with this diagnosis, the emerging view is that the host immune response plays a key role in pathogenesis.

Identification and Clinical Impact of Impaired Cerebrovascular Autoregulation in Patients With Malignant Middle Cerebral Artery Infarction

To study cerebrovascular autoregulation and its impact on clinical course in patients with impending malignant middle cerebral artery infarction, we used invasive multimodal neuromonitoring, including measurement of cerebral perfusion pressure, tissue oxygen pressure, and microdialysis. Fifteen patients with a stroke that involved >50% of the middle cerebral artery territory were included. Probes were placed into the ipsilateral frontal lobe. Autoregulation was assessed by calculation of the cerebral perfusion pressure-oxygen reactivity index (COR) and the correlation coefficient (R) of cerebral perfusion pressure and tissue oxygen pressure at 24 and 72 hours after stroke. COR and R at 24 hours after stroke were higher in the 8 patients with a malignant course (ie, massive edema formation) compared with the 7 patients with a benign course (COR, 1.99+/-1.46 versus 0.68+/-0.29; R, 0.49+/-0.28 versus 0.06+/-0.31; P<0.05), indicating impaired autoregulation in the malignant course group. At 72 hours, further increases in COR and R were observed in the malignant course group in contrast to the benign course group with stable values over time (COR, 3.31+/-2.38 versus 0.75+/-0.31; R, 0.75+/-011 versus 0.36+/-0.27; P<0.05). With a COR of 0.99, a cutoff value for prediction of a malignant course was found. The lactate-pyruvate ratio was higher in patients with a malignant compared with a benign course at both time points. COR, R, and the lactate-pyruvate ratio showed significant correlations with outcome parameters as a midline shift on cranial computed tomography and score on the modified Rankin scale after 3 months. We found early impairment of cerebrovascular autoregulation in peri-infarct tissue of patients who developed malignant brain edema, whereas autoregulation was preserved in patients with a benign course. Impaired cerebral autoregulation seems to play a key role for development of a malignant course and might serve as a predictive marker. Impaired cerebral autoregulation also accentuates the need for consequent adjustment of cerebral perfusion pressure in patients with impaired autoregulation.

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Malignant brain edema after MCA infarction is determined by the severity of ischemia within the infarction

Malignant brain edema after MCA infarction is determined by the severity of ischemia within the infarction

Relevance of ICP and ptiO2 for indication and timing of decompressive craniectomy in patients with malignant brain edema

The exact effects of decompressive craniectomy on intracranial pressure (ICP) and cerebral tissue oxygenation (ptiO2) are still unclear. Therefore, we have monitored ICP and ptiO2 intra-operatively and correlated these values to different operative steps during craniectomy. ICP and ptiO2 values have been monitored both, simultaneously and continuously, in 15 patients with cerebral edema due to posttraumatic or postischemic brain swelling. Indications for craniectomy were an increase in ICP above 25 mmHg or a decrease in ptiO2 below 10 mmHg resistant to conservative treatment (e.g. mannitol, hyperventilation, adequate arterial blood oxygenation, etc.). In all cases, we performed a fronto-temporo-parietal craniectomy (15 x 12 cm) and dura enlargement with galea-periosteum. During craniectomy, monitoring of ICP and ptiO2 in the affected hemisphere was continued. Values were recorded and correlated with the different operative steps. We performed craniectomy according to our treatment protocol in 5 patients. Prior to surgery, mean ICP values were 25.6 mmHg (range: 23-29 mmHg), mean ptiO2 values were 5.9 mmHg (range: 2.4-9.5 mmHg), and mean CPP values were 66 mmHg (range: 60-70 mmHg). After removing the bone flap, ICP values dropped to physiological values (mean: 7.4 mmHg), whereas ptiO2 values increased only slightly (mean: 11 mmHg). Opening of the dura resulted in a further decrease of ICP (mean 4.8 mmHg) and an increase of ptiO2 to normal limits (mean: 18.8 mmHg). After skin closure, mean ICP was 6.8 mmHg and mean ptiO2 was 21.7 mmHg, respectively. We found a significant decrease of ICP after craniectomy (p<0.042) and after dura enlargement (p<0.039) as well as a statistically significant increase in ptiO2 after craniectomy (p<0.043) and after dura enlargement (p<0.041). As a large bone flap in decompressive craniectomy is essential for adequate ICP reduction, the results of the presented cases suggest that dura enlargement is the crucial step to restore adequate brain tissue oxygenation and that ptiO2 monitoring could be an important tool for timing craniectomy in the future.

Severe Ethylene Glycol Intoxication Mimicking Acute Basilar Artery Occlusion

We report a patient with severe ethylene glycol poisoning initially mimicking acute basilar artery occlusion and elucidate the importance of immediate diagnosis and treatment: a previously healthy 59-year-old truck driver presenting with hallmarks of basilar artery syndrome after having consumed an unknown substance. Immediate application of intravenous ethanol and hemodialysis could not prevent the development of a malignant brain edema within hours. This report describes a new clinical presentation of severe ethylene glycol intoxication mimicking acute basilar artery occlusion with the development of a fatal brain edema within hours, despite adequate treatment.

Cerebral Microdialysis in Stroke Patients: Potentials and Limitations of a Method with Longitudinal Information: Response

Cerebral Microdialysis in Stroke Patients: Potentials and Limitations of a Method with Longitudinal Information: Response

Identification of malignant brain edema after hemispheric stroke by PET-imaging and microdialysis.

Cerebral blood flow (CBF) and extent of irreversible tissue damage as well as the time course of extracellular concentration of amino acids, substrates of energy metabolism, and purine metabolites, intracranial pressure and tissue oxygen tension were assessed in 34 patients with large strokes covering more than 50% of the MCA territory. The results were compared to findings in the experimental model of transient (for 3 hours) MCA occlusion in cats. In the experimental model as well as in the clinical setting development of malignant brain infarcts (due to formation of space occupying brain edema) was predicted by the size of critically hypoperfused tissue and the volume of irreversibly damaged tissue. The course of malignant infarcts was characterized by progressive increase in concentrations of excitatory amino acids, lactate, pyruvate, glycerol, hypoxanthine and in intracranial pressure, while cerebral perfusion pressure and tissue oxygen tension decreased. These results clearly differentiate a malignant from a benign course of large hemispheric infarction. The methods can be used to identify patients at risk for formation of space occupying edema and to select patients who could benefit from invasive therapeutic strategies.

Extracellular markers of impending malignant brain edema in large hemispheric stroke

117 Background: The development of malignant brain edema is a life-threatening complication of large hemispheric stroke. Hemicraniectomy and hypothermia are two invasive therapeutic options aiming to reduce mortality and to improve outcome in space-occupying MCA-infarction. The earlier such interventions are initiated the better is the chance of favourable outcome. However, therapeutic decision making is quite arbitrary as clinical observation, imaging or ICP measurement do not yield reliable prognostic criteria. Objective: To assess potential predictors of evolution of malignant brain edema in large MCA-infarction by microdialysis. Subjects and Methods: Following an ongoing prospective clinical trial invasive monitoring was performed in eight patients with large MCA-infarction. 18–36 hours after stroke onset a microdialysis probe was inserted in the parenchyma of the ipsilateral frontal lobe together with an ICP measuring device. Extracellular concentrations of glutamate, lactate, pyruvate, glycerol and various aminoacids were measured continuously for five days. CCT scans were performed on admission, after 6–12 h and at day 5. Scans were scrutinized for presence of mass-effect and size of infarction. Neurological deficit was assessed using the National Institutes of Health Stroke Scale (NIHSS). Results: Median NIHSS at baseline was 18 pts. (range 15–29 pts.). All patients suffered from a large stroke covering more than two thirds of the MCA-territory. In 4/8 patients an infarction of the entire territory of the MCA developed, in 3 of them with fatal space-occupying brain edema. The dynamics of the different substances varied in accordance with the clinical course, size of infarction and local brain edema: in patients with a massive edema in CCT an increase in glutamate concentrations and lactate/pyruvate-ratio was found, whereas patients without mass-effect demonstrated generally low and stable concentrations of these substances. Conclusion: In patients with large hemispheric infarction, bedside monitoring with microdialysis is feasible and may be valuable to predict impending malignant brain edema.

Extracellular markers of impending malignant brain edema in large hemispheric stroke

117 Background: The development of malignant brain edema is a life-threatening complication of large hemispheric stroke. Hemicraniectomy and hypothermia are two invasive therapeutic options aiming to reduce mortality and to improve outcome in space-occupying MCA-infarction. The earlier such interventions are initiated the better is the chance of favourable outcome. However, therapeutic decision making is quite arbitrary as clinical observation, imaging or ICP measurement do not yield reliable prognostic criteria. Objective: To assess potential predictors of evolution of malignant brain edema in large MCA-infarction by microdialysis. Subjects and Methods: Following an ongoing prospective clinical trial invasive monitoring was performed in eight patients with large MCA-infarction. 18–36 hours after stroke onset a microdialysis probe was inserted in the parenchyma of the ipsilateral frontal lobe together with an ICP measuring device. Extracellular concentrations of glutamate, lactate, pyruvate, glycerol and various aminoacids were measured continuously for five days. CCT scans were performed on admission, after 6–12 h and at day 5. Scans were scrutinized for presence of mass-effect and size of infarction. Neurological deficit was assessed using the National Institutes of Health Stroke Scale (NIHSS). Results: Median NIHSS at baseline was 18 pts. (range 15–29 pts.). All patients suffered from a large stroke covering more than two thirds of the MCA-territory. In 4/8 patients an infarction of the entire territory of the MCA developed, in 3 of them with fatal space-occupying brain edema. The dynamics of the different substances varied in accordance with the clinical course, size of infarction and local brain edema: in patients with a massive edema in CCT an increase in glutamate concentrations and lactate/pyruvate-ratio was found, whereas patients without mass-effect demonstrated generally low and stable concentrations of these substances. Conclusion: In patients with large hemispheric infarction, bedside monitoring with microdialysis is feasible and may be valuable to predict impending malignant brain edema.

HEAD INJURY - FOOTBALL

480 HISTORY - A 16 year-old center, during the varsity football game, was struck in the back of the head while lying face down on the ground. He appeared to be momentarily unconscious, but is awake when the trainer evaluates him. Athlete complained of a headache the remainder of the game. He was also noted to have some post-traumatic amnesia. The parents became increasingly concerned when the athlete developed dizziness and unsteady gait. In the ER the athlete was noted to have an ataxic gait, left-sided headache and post-traumatic amnesia. The parents found the athlete to be more lethargic the next day and a half, following which examination by the neurologist was negative. Further the parents state that the athlete had sustained a mild head injury 3 days prior. The initial head injury occurred while blocking. At that time the athlete complained of headache, dizziness, and feeling“funny.” PHYSICAL EXAMINATION - Athlete appeared pleasant, cooperative and in good hygiene. Mini-Mental Status Exam was 30 out of 30. Vital signs, heart and lungs were within normal limits. Neck and back were supple, non-tender, and without deformity. Cranial nerves were intact. Negative Romberg's and heel to shin bilaterally. Gait without abnormality. Deep tendon reflexes were 2+ and equal bilaterally at the knees. 1+ and equal at the elbow and ankles. Babinski's were negative. Strength was 5 out of 5 and equal bilaterally upper and lower extremity. Muscle tone and range of motion normal through out. DIFFERENTIAL DIAGNOSIS: Recurrent Mild Brain Injury. Second Impact Syndrome. Epidural Hematoma. Subdural Hematoma. Post-concussion Syndrome. Malignant Brain Edema Syndrome. Rule out associated neck sprain. TESTS AND RESULTS: CT Scan of the Head without Contrast: No evidence of acute or old bleed. No evidence of edema. Neck X-rays: No evidence of fractures or dislocations. FINAL WORKING DIAGNOSIS: Recurrent Mild Brain Injury: Initial mild head injury followed by a moderate. MANAGEMENT: Athlete was held out of participation for 1 month. He was symptom free for at least 3 weeks. School performance returned to base line after the rest period.

Einsatz von Gamma-Hydroxybuttersäure in der Therapie des erhöhten Hirndrucks und des Vasospasmus

Gamma-hydroxybutyrate (GHB), a suspected neurotransmitter, has sedative properties, reducing brain metabolism and body temperature and thus inducing effects resembling hibernation. Introduced as a narcotic 25 years ago, it has been employed in recent years for basic sedation of intensive-care patients in need of long-term respiratory support. In this study we analysed the effects of continuous GHB application in 19 patients suffering from increased intracranial pressure (ICP) subarachnoid haemorrhage (SAH), or both. GHB, which is only available as a sodium salt, frequently causes hypernatremia and metabolic alcalosis when given continually in dosages higher than 12 mg/kg body weight per hour. GHB is, therefore, often limited to preserve the potential usefulness of controlled hyperventilation or osmotherapy, respectively, when ICP increases. In 7 out of 8 patients with total infarctions in the territory of the middle cerebral artery GHB could not prevent the development of a malignant brain edema. The survivors with territorial infarctions or SAH in whom ICP was monitored showed no critical decreases in cerebral perfusion pressure during GHB application. Early GHB administration seemed beneficial in the prevention of vasospasm subsequent to severe SAH. The intracranial blood flow velocities did not exceed 90 cm/s in all three cases treated with GHB within the first three days after SAH, whereas three out of four cases without GHB showed marked acceleration with values over 90 cm/s. In two patients, the administration of GHB after the development of severe vasospasm was followed by a continuous decrease of flow velocities in the cerebral arteries.

Characteristics and Prognosis of Extradural Hematomas in Children

This is a report on 31 children with operated extradural hematoma. The aim of the study was to elucidate the characteristics of extradural hematoma in childhood and the different clinical pattern and outcome compared to adults. For that reason the charts of the patients seen at the Department of Surgery of the Children's University Hospital Zurich between 1972 and 1990 have been revised. Follow-up criteria were recorded according to the Glasgow Outcome Scale. Most hematomas have been provoked by minor injuries and almost all children presented with at least one typical clinical sign. Associated intracranial injuries have been found in four patients, while two were polytraumatised. 30 of the 31 patients survived. One patient died of malignant brain edema. The mean range of follow-up was seven years. 28 patients had a "good recovery", "moderate disability" and "severe disability" was found in a patient one each. Our results demonstrate that the long-term outcome in children with extradural hematoma is far better than in adults regarding survival as well as quality of life. The causes may be minor traumas with fewer associated lesions and presentation with typical clinical findings and therefore early diagnosis and treatment.

Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema".

The commonest initial computerized tomography (CT) finding in head-injured children is bilateral diffuse cerebral swelling. Cerebral blood flow and CT density studies suggest that this swelling is due to cerebral hyperemia and increased blood volume, not to edema. The clinical history, course, and outcome of 63 children with this CT pattern are reviewed. Fourteen children had a Glasgow Coma Scale score of greater than 8; all made a complete recovery and follow-up CT scans were normal. Forty-nine children had Glasgow Coma Scale scores of 8 or less. Fifteen had a history of a lucid period following the initial unconsciousness. One of these children died of delayed brain swelling, the others recovered well with minimal neurological deficit. Thirty-four children were rendered immediately and continuously unconscious. There was a high incidence of second lesions on the CT scan, 50% of this group developed intracranial hypertension and five died. All of the others were in coma for periods ranging from weeks to months. Follow-up CT scans showed an extracerebral collection with a density of cerebrospinal fluid in 27% of the patients, and ventriculomegaly with large sulci in 35%, whereas this pattern was seen only once in those with a lucid period. The difference between those with and without a lucid period is related to the degree of primary diffuse impact injury to the white matter.