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Roberto Heros

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Jose I. Suarez

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Meg Verrees, Jose Americo Fernandes Filho, Jose I. Suarez and Robert A. Ratcheson

✓ Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. The parenchyma of the posterior fossa is infrequently involved. The authors report on two cases of isolated edema of the cerebellar hemispheres, which occurred in the setting of hypertensive crisis and led to complete obstruction of or significant impingement on the fourth ventricle and potentially lethal hydrocephalus. To the best of the authors' knowledge, these are the first reported cases of hypertensive encephalopathy centered in the posterior fossa.

Two patients presented with profound decreases in neurological status subsequent to development of malignant hypertension. Imaging studies revealed diffusely edematous cerebellar hemispheres with effacement of the fourth ventricle, causing dilation of the lateral and third ventricles. Following emergency placement of external ventricular drains, control of systemic blood pressure was accomplished, and neurological functioning returned to baseline.

Although neurological deterioration resolved swiftly following placement of ventricular catheters and administration of diuretic agents, systemic blood pressure did not fluctuate with the release of cerebrospinal fluid and resolution of increased intracranial pressure. Decrease in systemic blood pressure lagged well behind improvement in neurological status; the patients remained morbidly hypertensive until systemic blood pressure was controlled with multiple parenteral medications.

The authors hypothesize that the development of hypertension beyond the limits of cerebral autoregulation led to breakdown of the blood—brain barrier in the cerebellum and development of posterior fossa edema secondary to the focal transudation of protein and fluid. Correction of the elevated blood pressure led to amelioration of cerebellar edema. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered.

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Jose I. Suarez, Larry Shannon, Osama O. Zaidat, Muhammad F. Suri, Grwant Singh, Gwendolyn Lynch and Warren R. Selman

Object. Human albumin is used to induce hypervolemia (central venous pressure [CVP] > 8 mm Hg) after subarachnoid hemorrhage (SAH). Unfortunately, human albumin may increase the mortality rate in critically ill patients; because of this, its use became restricted in the authors' hospital in May 1999. The goal of this study was to determine the effect of human albumin on outcome and cost in patients with SAH before and after this restriction was put into place.

Methods. All patients with aneurysmal SAH who were admitted to the authors' institution between May 1998 and May 2000 were studied. Basic demographic information, dosage of human albumin given, length of stay, and the incidence of in-hospital deaths and complications were collected. The authors obtained Glasgow Outcome Scale (GOS) scores at 3 months after SAH (good outcome, GOS ≥ 4). Data were analyzed using t-test and chi-square analysis. Logistic regression was used to identify independent associations between use of human albumin and outcome.

The authors studied 140 patients: 63 who were admitted between May 1998 and May 1999 (Group 1) and 77 treated between June 1999 and May 2000 (Group 2). Two subgroups of patients were further analyzed. Group 1 patients who received human albumin (albumin subgroup, 37 patients) and Group 2 patients who would have received albumin under the old protocol (that is, those who failed to achieve CVP > 8 mm Hg after normal saline administration; nonalbumin subgroup, 47 patients). Patients in the nonalbumin subgroup were more likely to be male (38% compared with 16%), to experience hypertension (55% compared with 30%), to suffer from hypomagnesemia (49% compared with 5.4%), and to have hydrocephalus (47% compared with 27%). There was a trend for these patients to have more vasospasm (28% compared with 19%, p = 0.2). Patients in the albumin subgroup were more likely to have a good outcome at 3 months.

Conclusions. Administration of human albumin after SAH may improve clinical outcome and reduce hospital cost.

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Eric M. Bershad, Saeid Farhadi, M. Fareed K. Suri, Eliahu S. Feen, Olga H. Hernandez, Warren R. Selman and Jose I. Suarez


Acute subdural hematoma (SDH) is one of the most lethal forms of intracranial injury; several risk factors predictive of a worse outcome have been identified. Emerging research suggests that patients with coagulopathy and intracerebral hemorrhage have a worse outcome than patients without coagulopathy but with intracerebral hemorrhage. The authors sought to determine if such a relationship exists for patients with acute SDH.


The authors conducted a retrospective analysis of consecutive patients admitted to a neurosciences intensive care unit with acute SDH over a 4-year period (January 1997–December 2001). Demographic data, laboratory values, admission source, prior functional status, medical comorbidities, treatments received, and discharge disposition were recorded, as were scores on the Acute Physiology, Age, and Chronic Health Evaluation III (APACHE III). Coagulopathy was defined as an internal normalized ratio > 1.2 or a prothrombin time ≥12.7 seconds. Univariate and multivariate analyses were performed on 244 patients to determine factors associated with worse short-term outcomes.


The authors identified 248 patients with acute SDH admitted to the neurointensive care unit during the study period, of which 244 had complete data. Most were male (61%), and the mean age of the study population was 71.3 ± 15 years (range 20–95 years). Fifty-three patients (22%) had coagulopathy. The median APACHE III score was 43 (range 11–119). Twenty-nine patients (12%) died in the hospital. Independent predictors of inhospital death included APACHE III score (odds ratio [OR] 4.4, 95% confidence interval [CI] 1.4–13.4, p = 0.011) and coagulopathy (OR 2.7, 95% CI 1.1–7.1, p = 0.037). Surgical evacuation of acute SDH was associated with reduced inhospital deaths (OR 0.2, 95% CI 0.1–0.6, p = 0.003).


Coagulopathy is independently associated with inhospital death in patients with acute SDH. Time to treatment to correct coagulopathy using fresh frozen plasma and/or vitamin K was prolonged.

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Simone A. Dijkland, Blessing N. R. Jaja, Mathieu van der Jagt, Bob Roozenbeek, Mervyn D. I. Vergouwen, Jose I. Suarez, James C. Torner, Michael M. Todd, Walter M. van den Bergh, Gustavo Saposnik, Daniel W. Zumofen, Michael D. Cusimano, Stephan A. Mayer, Benjamin W. Y. Lo, Ewout W. Steyerberg, Diederik W. J. Dippel, Tom A. Schweizer, R. Loch Macdonald and Hester F. Lingsma


Differences in clinical outcomes between centers and countries may reflect variation in patient characteristics, diagnostic and therapeutic policies, or quality of care. The purpose of this study was to investigate the presence and magnitude of between-center and between-country differences in outcome after aneurysmal subarachnoid hemorrhage (aSAH).


The authors analyzed data from 5972 aSAH patients enrolled in randomized clinical trials of 3 different treatments from the Subarachnoid Hemorrhage International Trialists (SAHIT) repository, including data from 179 centers and 20 countries. They used random effects logistic regression adjusted for patient characteristics and timing of aneurysm treatment to estimate between-center and between-country differences in unfavorable outcome, defined as a Glasgow Outcome Scale score of 1–3 (severe disability, vegetative state, or death) or modified Rankin Scale score of 4–6 (moderately severe disability, severe disability, or death) at 3 months. Between-center and between-country differences were quantified with the median odds ratio (MOR), which can be interpreted as the ratio of odds of unfavorable outcome between a typical high-risk and a typical low-risk center or country.


The proportion of patients with unfavorable outcome was 27% (n = 1599). The authors found substantial between-center differences (MOR 1.26, 95% CI 1.16–1.52), which could not be explained by patient characteristics and timing of aneurysm treatment (adjusted MOR 1.21, 95% CI 1.11–1.44). They observed no between-country differences (adjusted MOR 1.13, 95% CI 1.00–1.40).


Clinical outcomes after aSAH differ between centers. These differences could not be explained by patient characteristics or timing of aneurysm treatment. Further research is needed to confirm the presence of differences in outcome after aSAH between hospitals in more recent data and to investigate potential causes.