Intracranial hypertension

Refractory Intracranial Hypertension in Posterior Reversible Encephalopathy Syndrome

Authors: Facchini A, Magnoni S, Civelli V, Triulzi F, Nosotti M, Stocchetti N.

INTRODUCTION: Posterior reversible encephalopathy syndrome (PRES) is a largely reversible disease with long-term favorable outcome. A minority of patients, however, may develop progressive cerebral edema and ischemia resulting in severe disability or death. We report a case of severe intracranial hypertension associated with PRES that was successfully treated according to intracranial pressure (ICP)- and cerebral perfusion pressure (CPP)-driven therapy.
METHODS: Case report.
RESULTS: A 42-year-old woman underwent bilateral lung transplantation for severe bronchiectasis. Her immunosuppressive regimen consisted of azathioprine, prednisone, and tacrolimus. She acutely developed an aggressive form of PRES that rapidly resulted in severe refractory intracranial hypertension despite discontinuation of potentially causative medications and adequate supportive therapy. Accordingly, second-tier therapies, including barbiturate infusion, were instituted and immunosuppression was switched to anti-thymocyte globulin followed by mycophenolate mofetil. Within 10 h of barbiturate administration, ICP dropped to 20 mmHg. Thiopental was administered for two days and then rapidly tapered because of severe urosepsis. Six months after discharge from the intensive care unit the patient returned to near-normal life, her only complaint being short-term amnesia.
CONCLUSIONS: The decision to undertake ICP monitoring in medical conditions in which no clear recommendations exist greatly relies on physicians' judgment. This case suggests that ICP monitoring may be considered in the setting of acute PRES among selected patients, when severe intracranial hypertension is suspected, provided that a multidisciplinary team of neurocritical care specialists is readily available.

Assessment and management of cerebral edema and intracranial hypertension in acute liver failure

Authors: Mohsenin V.

Acute liver failure is uncommon but not a rare complication of liver injury. It can happen after ingestion of acetaminophen and exposure to toxins and hepatitis viruses. The defining clinical symptoms are coagulopathy and encephalopathy occurring within days or weeks of the primary insult in patients without preexisting liver injury. Acute liver failure is often complicated by multiorgan failure and sepsis. The most life-threatening complications are sepsis, multiorgan failure, and brain edema. The clinical signs of increased intracranial pressure (ICP) are nonspecific except for neurologic deficits in impending brain stem herniation. Computed tomography of the brain is not sensitive enough in gauging intracranial hypertension or ruling out brain edema. Intracranial pressure monitoring, transcranial Doppler, and jugular venous oximetry provide valuable information for monitoring ICP and guiding therapeutic measures in patients with encephalopathy grade III or IV. Osmotic therapy using hypertonic saline and mannitol, therapeutic hypothermia, and propofol sedation are shown to improve ICPs and stabilize the patient for liver transplantation. In this article, diagnosis and management of hepatic encephalopathy and cerebral edema in patients with acute liver failure are reviewed.

Euronews: Deep inside the brain (noninvasive intracranial pressure measurement)


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Spontaneous cerebrospinal fluid otorrhea and rhinorrhea in idiopathic intracranial hypertension patients

Authors: Rosenfeld E, Dotan G, Kimchi TJ, Kesler A.

BACKGROUND: Spontaneous cerebrospinal fluid (CSF) leakage may occur in patients with normal or increased intracranial pressure (ICP). We describe herein spontaneous CSF leakage as a result of chronic increased ICP in 4 patients with idiopathic intracranial hypertension (IIH). Although rhinorrhea previously has been described in IIH patients, to our knowledge this is the first report of otorrhea in these patients.
METHODS: Four patients with spontaneous CSF leakage were examined between 2001 and 2011; 3 presented with rhinorrhea and 1 with otorrhea. Clinical settings and manifestations were analyzed.
RESULTS: All patients were found to have IIH. Three had been diagnosed with IIH several years earlier and had been noncompliant with their medical treatment, whereas in 1 patient, CSF rhinorrhea was the presenting symptom of IIH.
CONCLUSION:  CSF leak is a rare complication in IIH patients. We have shown that rhinorrhea can be the presenting sign in these patients and that rhinorrhea and otorrhea can be a late sign of the disease.

Intracranial hemorrhage due to intracranial hypertension caused by the superior vena cava syndrome

Authors: Bartek J Jr, Abedi-Valugerdi G, Liska J, Nyström H, Andresen M, Mathiesen T.

We report a patient with intracranial hemorrhage secondary to venous hypertension as a result of a giant aortic pseudoaneurysm that compressed the superior vena cava and caused obstruction of the venous return from the brain. To our knowledge, this is the first patient reported to have an intracranial hemorrhage secondary to a superior vena cava syndrome. The condition appears to be caused by a reversible transient rise in intracranial pressure, as a result of compression of the venous return from the brain. Treatment consisted of surgery for the aortic pseudoaneurysm, which led to normalization of the intracranial pressure and resorption of the intracranial hemorrhage.

Predictive value of initial intracranial pressure for refractory intracranial hypertension in persons with traumatic brain injury: A prospective observational study

Authors:  Yuan Q, Liu H, Wu X, Sun Y, Zhou L, Hu J.

Abstract Objective: To prospectively investigate the predictive value of initial intracranial pressure (ICP) for refractory intracranial hypertension and outcomes in persons with diffuse traumatic brain injury (TBI). Methods: A prospective observational study was conducted in 107 adult persons with diffuse TBI (Marshall CT Class II-IV). Initial ICP was defined as the first ICP recorded in the operating room. Refractory intracranial hypertension was defined as ICP increases to more than 30 mmHg and/or reduces in cerebral perfusion pressure to less than 60 mmHg for a period longer than 15 minutes and failure to respond to the maximum medical treatment. Baseline demographics and injury-specific data were recorded. Multiple logistic regression models were used to determine independent risk factors for refractory intracranial hypertension and unfavourable outcomes. A receiver-operating characteristic (ROC) curve was then drawn. Results: The initial ICP allowed for a better refractory intracranial hypertension prediction (ROC area = 0.868; 95% CI = 0.799-0.937) than the Marshall Classification (ROC area = 0.670; 95% CI = 0.569-0.772) or Rotterdam Classification scores (ROC area = 0.679; 95% CI = 0.577-0.780). An initial ICP value higher than 20 mmHg had 83% sensitivity and 83% specificity, whereas an initial ICP value higher than 25 mmHg had 64% sensitivity and 92% specificity for refractory intracranial hypertension. A multivariable logistic regression model showed that any 5 mmHg pressure increase in a patient with initial ICP led to 2.884-times higher odds of refractory intracranial hypertension (95% CI = 1.893-4.395; p < 0.001). Head Abbreviated Injury Scale score, initial Glasgow Coma Scale (GCS) and initial GCS motor scores were not predictive of refractory intracranial hypertension (p > 0.05). Conclusion: For persons with diffuse TBI, the initial ICP provides great prognostic discrimination and is an independent predictor of refractory intracranial hypertension.


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