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Biomedical subjects

E F Wijdicks

Publications and source records attributed to E F Wijdicks.

At least 127 records · Page 7Linked to original sources
PubMed1995

Neurotoxicity in liver transplant recipients with cyclosporine immunosuppression.

We studied the clinical features, blood levels of cyclosporine, and neuroimaging findings in 46 patients with cyclosporine neurotoxicity after liver transplantation. The clinical presentation of cyclosporine neurotoxicity was characterized by tremulousness and restlessness in all patients and was associated with acute confusional state and psychosis in 20 patients, seizures in eight, speech apraxia or action myoclonus speech in three, and cortical blindness in two. In 35 patients, cyclosporine neurotoxicity occurred during IV treatment. Neuroimaging studies showed only minor white matter abnormalities in two patients despite dramatic clinical presentations, including speech difficulties, seizures, and cortical blindness. In only 19 of 31 patients (61%) did trough levels of cyclosporine suggest neurotoxicity. Neurologic findings were reversible in all patients after cyclosporine was withheld and then given in lower dosage. In three patients, substituting FK 506 did not result in neurotoxicity.

Adolescent↗
PubMed1995

Multifocal inflammatory leukoencephalopathy associated with levamisole therapy.

Cerebral demyelinating disease developed in a patient during adjuvant therapy with levamisole for malignant melanoma. This patient had no evidence of previous neurologic disease. Levamisole was administered for 5 weeks (total dose, 1,500 mg). Over a period of 3 weeks, the patient became progressively confused and ataxic. MRI with gadolinium enhancement demonstrated prominent multifocal enhancing white matter lesions. CSF examination revealed an inflammatory profile. After discontinuation of treatment with levamisole and a short course of corticosteroid therapy, the patient's condition dramatically improved. MRI also indicated improvement. Observations in our patient suggest that the leukoencephalopathy that developed in previously reported patients who received 5-fluorouracil and levamisole may have been caused at least partly by levamisole.

Antineoplastic Agents↗
PubMed1995

Sudden death from aneurysmal subarachnoid hemorrhage.

Some patients with aneurysmal subarachnoid hemorrhage (SAH) never reach the hospital alive ("sudden death") and, although their numbers are significant, they are not included in most studies of SAH. To clarify the clinical profile of sudden death from aneurysmal SAH, we reviewed the epidemiology and clinicopathologic features of patients with aneurysmal SAH who never reached medical attention. Using the medical record linkage system employed for epidemiologic studies for the population of Rochester, Minnesota, we identified all patients who were diagnosed with aneurysmal SAH between 1960 and 1989. There were 80 women and 33 men with a mean age of 55 years. Of these 113 patients, 13 (12%) died without reaching medical attention. The proportion of those with sudden death remained stable during the study period. In comparing patients with sudden death with those who reached medical attention, the only significant variable was the frequency of posterior circulation aneurysms that was found in 38%, compared with 14% in those who received medical attention (p = 0.042). At autopsy, intraventricular hemorrhage was present in 12 patients (92%) with sudden death, and intracerebral hemorrhage was present in two (15%). Twelve patients (92%) had acute pulmonary edema. In our community, the frequency of sudden death from aneurysmal SAH has not changed during the last three decades in spite of the advances in medical care. The typical clinical profile of sudden death in SAH includes intraventricular hemorrhage, pulmonary edema, and a ruptured posterior circulation aneurysm. Intracerebral hemorrhage is uncommonly associated with sudden death from aneurysmal SAH.

Adult↗
PubMed1995

The poor prognosis of ruptured intracranial aneurysms of the posterior circulation.

The first 48 hours after aneurysmal subarachnoid hemorrhage are critical in determining final outcome. However, most patients who die during this initial period are not included in hospital-based studies. We investigated the occurrence of subarachnoid hemorrhage in a population-based study to evaluate possible predictors of poor outcome. All patients diagnosed with aneurysmal subarachnoid hemorrhage between 1955 and 1984 were selected for analysis of mortality in the first 30 days using the medical record-linkage system employed for epidemiological studies in Rochester, Minnesota. One hundred and thirty-six patients were identified. The mean age of these 99 women and 37 men was 55 years. Rates for survival to 48 hours were 32% for the 19 patients with posterior circulation aneurysms, 77% for the 87 patients with anterior circulation aneurysms, and 70% for the 30 patients with a presumed aneurysm (p < 0.0001). Rates for survival to 30 days were 11%, 57%, and 53%, respectively, in these three patient groups (p < 0.0001). Clinical grade on admission to the hospital, the main variable predictive of death within 48 hours, was significantly worse in patients with posterior circulation aneurysms than in others (p < 0.0001). The prognosis of ruptured posterior circulation aneurysms is poor. The high early mortality explains why posterior circulation aneurysms are uncommon in most clinical series of patients with subarachnoid hemorrhage. The management of incidentally discovered intact posterior circulation aneurysms may be influenced by these findings.

Adolescent↗
PubMed1995

Clinical and radiologic features of cerebral edema in fulminant hepatic failure.

OBJECTIVE: To describe a series of consecutive patients with fulminant hepatic failure (FHF) and to present a new classification system for brain edema, an important cause of mortality in such patients. DESIGN: We reviewed 22 computed tomographic (CT) scans of the brain in 12 patients with FHF and classified the severity of cerebral edema by using predefined criteria. RESULTS: No cerebral edema was detected on CT scans in four patients with stage 1 or 2 hepatic encephalopathy at the time of admission, but it was noted in seven of eight patients with stage 3 or 4 hepatic encephalopathy. The severity of brain edema on CT scans was significantly correlated (P < 0.001) with the stage of hepatic encephalopathy. Three of the four patients who had stage 1 or 2 hepatic encephalopathy at the time of initial assessment ultimately had a good outcome. Of seven patients with stage 3 encephalopathy, two had rapid deterioration to brain death, three died of nonneurologic causes, and two had a good outcome after liver transplantation. One patient with stage 4 hepatic encephalopathy died, and autopsy showed cerebral edema. CONCLUSION: Stage 3 or 4 hepatic encephalopathy is associated with cerebral edema that can be detected on CT scans. The clinical and radiologic signs of cerebral edema in patients who have progression to stage 3 hepatic encephalopathy can be reversed with conventional treatment of increased intracranial pressure. Whether early recognition and treatment of cerebral edema result in increased survival of patients with FHF remains to be determined.

Adolescent↗
PubMed1995

Intracerebral hemorrhage in liver transplant recipients.

OBJECTIVE: To analyze possible causative mechanisms for intracranial hemorrhage after orthotopic liver transplantation. DESIGN: We conducted a retrospective survey of medical records and a case-control comparison in patients who had undergone liver transplantation during the period 1986 through 1992. MATERIAL AND METHODS: In a group of 8 patients with intracranial hemorrhage after orthotopic liver transplantation and a control series of 207 patients who had undergone liver transplantation but did not have intracranial hemorrhage, we summarized pertinent clinical and laboratory data and statistically analyzed potential risk factors for hemorrhage. RESULTS: In the eight study patients, intracerebral hematomas were located in the parietal or frontal lobe in six, the cerebellum in one, and the putamen in one. Autopsy demonstrated a Candida-associated mycotic aneurysm in one of the eight patients, and one had disseminated aspergillosis. No statistically significant differences in thrombocytopenia, hypertension, extracranial bleeding sites, or cyclosporine-related neurotoxicity were found when these patients were compared with the control series. Bacteremia or fungemia was found in five of the eight patients with intracerebral hemorrhages (62%) but in only 11% of the control group (P = 0.03; Fisher's exact test). CONCLUSION: Overwhelming infections, thrombocytopenia, or both may have a role in intracerebral hemorrhage after liver transplantation.

Adolescent↗
PubMed1994

Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage.

Retrospective surveys of patients with subarachnoid haemorrhage suggest that minor episodes with sudden headache (warning leaks) may precede rupture of an aneurysm, and that early recognition and surgery might lead to improved outcome. We studied 148 patients with sudden and severe headache (possible sentinel headache) seen by 252 general practitioners in a 5-year period in the Netherlands. Subarachnoid haemorrhage was the cause in 37 patients (25%) (proven aneurysm in 21, negative angiogram in 6, no angiogram done in 6, sudden headache followed by death in 4). 103 patients had headache as the only symptom, 12 of whom proved to have subarachnoid haemorrhage (6 with a ruptured aneurysm). Previous bouts of sudden headache had occurred in only 2. Other serious neurological conditions were diagnosed in 18. In the remaining 93, no underlying cause of headache was found; follow-up over 1 year showed no subsequent subarachnoid haemorrhage or sudden death. In this cohort, acute, severe headache in general practice indicated a serious neurological disorder in 37% (95% CI 29-45%), and subarachnoid haemorrhage in 25% (18-32%). 12% (5-18%) of those with headache as the only symptom. The notion of warning leaks as a less serious variant of subarachnoid haemorrhage is not supported by this study. Early recognition of subarachnoid haemorrhage is important but will probably have only limited impact on the outcome in the general population.

Acute Disease↗
PubMed1994

Prognostic value of myoclonus status in comatose survivors of cardiac arrest.

Generalized myoclonus status is common in comatose patients after cardiac resuscitation, but its prognostic value is uncertain. We studied the clinical, radiologic, and pathologic findings in 107 consecutive patients who remained comatose after cardiac resuscitation. Myoclonus status was present in 40 patients (37%). Features more prevalent in patients with myoclonus status were burst suppression on electroencephalograms, cerebral edema or cerebral infarcts on computed tomography scans, and acute ischemic neuronal change in all cortical laminae. All patients with myoclonus status died. Of 67 patients without myoclonus, 20 awakened. We conclude that myoclonus status in postanoxic coma should be considered an agonal phenomenon that indicates devastating neocortical damage. Its presence in comatose patients after cardiac arrest must strongly influence the decision to withdraw life support.

Adult↗
PubMed1994

FK506-induced neurotoxicity in liver transplantation.

We report FK506-induced neurotoxicity in 14 of 44 consecutive patients following orthoptic liver transplantation. In 10 of these 14 patients, postural hand tremors were found in the first weeks following surgery, transient apraxia of speech in 3, and generalized tonic-clonic seizures were noted in 2 patients. Other manifestations included nightmares, agitation, and acute delirium. Reduction of the FK506 dose resulted in resolution of symptoms, but in 1 patient mild speech difficulties and in 3 patients a fine tremor remained. Blood and plasma levels of FK506 were similar in patients with and without neurotoxicity. FK506 neurotoxicity in patients with liver transplantation commonly results in transient neurological manifestations. The incidence of neurotoxicity in FK506 is dramatically reduced in maintenance doses of 0.075 mg/kg twice a day.

Adult↗
PubMed1994

Absence of postoperative hyponatremia syndrome in young, healthy females.

Young and previously healthy females have been reported to develop severe postoperative hyponatremia with a fatal outcome. The clinical presentation is dramatic, with seizures, respiratory arrest, and permanent, often catastrophic, brain damage. The true incidence is unknown. We report a survey of 290,815 surgical procedures on females at the Mayo Clinic from 1976 to 1992. Postoperatively 1,498 females had cardiopulmonary arrest, 255 had a metabolic encephalopathy, 32 had new-onset seizures, and 6 had central pontine myelinolysis. We failed to identify any association of respiratory arrest with postoperative hyponatremia. Our findings indicate that the postoperative hyponatremia syndrome in young, healthy females with respiratory arrest is extremely uncommon.

Adolescent↗
PubMed1994

Acute acid-base disorders associated with status epilepticus.

OBJECTIVE: To analyze the acid-base abnormalities in patients with status epilepticus. DESIGN: We retrospectively reviewed the acid-base disturbances in 38 consecutive patients who had been admitted to the emergency department at a Mayo-affiliated hospital because of status epilepticus between 1982 and 1993. MATERIAL AND METHODS: On the basis of results of arterial blood gas analyses, the acid-base disorders were categorized. In addition, chest roentgenograms and electrocardiograms were reviewed for pulmonary infiltrates and cardiac arrhythmias. RESULTS: Arterial blood gas analysis performed immediately after admission revealed an acid-base abnormality in 32 of 38 patients (84%). Respiratory acidosis was most common (N = 16; 42%) and occurred either alone or in combination with metabolic acidosis. Pulmonary infiltrates were not more common in patients with respiratory acidosis than in other patients. Although cardiac arrhythmias were more common in patients with respiratory or metabolic acidosis (42%) than in those with respiratory alkalosis or normal blood gas values (36%), this difference was not statistically significant. CONCLUSION: We conclude that respiratory acidosis with or without metabolic acidosis is common in patients who have status epilepticus. Respiratory acidosis was not predictive of the final outcome. In our study patients, all acid-base abnormalities resolved spontaneously.

Acid-Base Imbalance↗
PubMed1994

The clinical spectrum of critical illness polyneuropathy.

OBJECTIVE: To describe the entity of critical illness polyneuropathy and review our experience with six cases. DESIGN: We present case reports of six patients with polyneuropathy associated with critical illness, who received medical care at the Mayo Clinic between 1992 and 1994, and discuss similar cases from the literature. RESULTS: Critical illness may damage peripheral nerves. In previous studies, sepsis and multiorgan failure have been found to trigger a peripheral neuropathy. Of our six patients with critical illness polyneuropathy, all had a preceding severe bacterial infection or septic shock. In one patient who had long-term administration of vecuronium bromide and had received massive intravenous doses of corticosteroids, sural nerve and quadriceps muscle biopsy specimens were available; they revealed axonal neuropathy and notable myopathic changes, respectively. The outcome was good in patients who survived the critical illness. CONCLUSION: Polyneuropathy in critically ill patients may be a cause of severe generalized limb weakness and occurs in the setting of a sepsis syndrome. The long-term outcome is good in patients who recover from the underlying critical illness. Compression neuropathies may be a cause of permanent sequelae.

Acute Disease↗
PubMed1994

Gastrointestinal bleeding in stroke.

BACKGROUND AND PURPOSE: Patients with ischemic or hemorrhagic stroke are at risk for systemic complications. The reasons why gastrointestinal bleeding occurs after stroke are unknown and have intuitively been attributed to stress ulcers. No study to date has addressed causes of gastrointestinal hemorrhage in stroke. METHODS: Between 1976 and 1994, 17 patients identified from the Mayo Clinic medical record system as having gastrointestinal hemorrhage and ischemic stroke (n = 14) or intracerebral hemorrhage (n = 3) were reviewed for presentation, associated causes, and outcome. Results of the endoscopic procedures were compiled, and available gastric biopsies were reviewed. RESULTS: In 17 patients with gastrointestinal bleeding after stroke, sudden hematemesis, a decrease in hemoglobin level, or orthostatic hypotension was found as a presenting feature. One patient presented with massive hematemesis, exsanguination, and cardiac arrest. Endoscopic findings were available in 14 patients and included gastroesophageal erosions, hemorrhagic gastritis, and gastric ulcer. In one patient, an adenocarcinoma of the gastric cardia was found. Putative pathogenetic agents were found in 16 of 17 patients and included a long history of nonsteroidal anti-inflammatory drugs (n = 6), acetylsalicylic acid (n = 3), grossly prolonged anticoagulation (n = 4), Helicobacter pylori (n = 2), and corticosteroids (n = 1). CONCLUSIONS: Gastrointestinal bleeding after stroke is rarely severe and may not contribute significantly to mortality. Medication-induced gastrointestinal hemorrhage may be underappreciated in this setting.

Anticoagulants↗