Silent brain infarct in thrombotic thrombocytopenic purpura.
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Adult↗
Biomedical subjects
E F Wijdicks
Publications and source records attributed to E F Wijdicks.
Perimesencephalic subarachnoid hemorrhage. Additional perspectives from four cases.
BACKGROUND: Nonaneurysmal perimesencephalic hemorrhage, a distinct form of subarachnoid hemorrhage, is a recently described variant of intracranial hemorrhage. We describe two patients who presented with unusual features of this type of subarachnoid hemorrhage and also two patients who had a perimesencephalic pattern of hemorrhage due to a ruptured posterior circulation aneurysm. CASE DESCRIPTIONS: The first patient, a 41-year-old woman with perimesencephalic hemorrhage, underwent an exploratory craniotomy because angiography had suggested an anomaly of the basilar tip. No source of hemorrhage could be identified at the time of surgery. The second patient was a 3-year-old boy who presented with opisthotonos and who was found to have a perimesencephalic hemorrhage. Angiography revealed no source for the hemorrhage. The third patient, a 54-year-old man, had a perimesencephalic pattern of subarachnoid hemorrhage from a vertebrobasilar junction aneurysm associated with a fenestration that was missed on the initial angiographic study. The fourth patient, a 43-year-old man, suffered a perimesencephalic pattern of subarachnoid hemorrhage from a small posterior cerebral artery aneurysm, which had not been recognized on two angiograms. CONCLUSIONS: These patients elaborate on the clinical spectrum of subarachnoid hemorrhage with a perimesencephalic pattern. First, a negative exploratory craniotomy suggests that the source of nonaneurysmal perimesencephalic hemorrhage may not be arterial. Second, nonaneurysmal perimesencephalic hemorrhage may also occur in children. Finally, the index of suspicion for a posterior circulation aneurysm should remain high in patients who present with a perimesencephalic pattern of subarachnoid hemorrhage, and these aneurysms may rise from unusual locations.
Adult↗
Neurologic complications associated with internal jugular vein cannulation in critically ill patients: a prospective study.
To determine the frequency of neurologic complications after internal jugular cannulation, we performed a prospective study in 66 consecutive critically ill patients. Of these 66 patients, one had Horner's syndrome probably associated with a large carotid sheath hematoma (2%; 95% CI, 1 to 8%). No cerebrovascular complications occurred. The frequency of neurologic complications following internal jugular vein catheterization is low in critical illness.
Adolescent↗
Phenytoin toxicity associated with hypoalbuminemia in critically ill patients.
Four critically ill patients developed phenytoin toxicity. Hypoalbuminemia or concomitant displacing drugs resulted in an increased fraction of unbound drug. Clinical findings included gradual decrease in level of consciousness and cerebellar signs. Marked phenytoin toxicity can occur in critically ill patients with hypoalbuminemia and can often be detected only by direct measurement of free phenytoin levels.
Adult↗
Failure of high dose intravenous immunoglobulins to alter the clinical course of critical illness polyneuropathy.
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Adult↗
Subcortical hemorrhage in disseminated intravascular coagulation associated with sepsis.
Cranial CT features of two patients with intracerebral hemorrhages in the setting of sepsis and disseminated intravascular coagulation are reported. Multiple predominantly subcortical hemorrhages were seen. This pattern of cerebral hemorrhage should raise suspicion of disseminated intravascular coagulation as an underlying cause.
Aged↗
Intracerebral hemorrhage after fibrinolytic therapy for acute myocardial infarction.
BACKGROUND AND PURPOSE: Intracerebral hematoma may complicate treatment of acute myocardial infarction in patients treated with fibrinolytic agents. We studied the clinical presentation and computed tomographic characteristics. METHODS: We studied eight patients with lobar intracerebral hematomas after fibrinolytic treatment of acute coronary occlusion. All patients had electrocardiographic and laboratory evidence of acute myocardial infarction and were treated with tissue plasminogen activator or streptokinase followed by heparin infusion to prevent reocclusion. Computed tomography scans of 17 patients with cerebral hemorrhage from other causes were used for comparison. RESULTS: For most patients, outcome was fatal within hours of the ictus. Computed tomography scans showed superficially large lobar hematomas in six patients. One patient had a putaminal hemorrhage, and one had a vermis hemorrhage. Multiple sites of intracerebral hemorrhage were noted in three patients. Fluid levels inside the hematoma suggesting continuing hemorrhage into multiple compartments were common. Radiologically, fluid levels in hematomas, multiple hematomas, and blood in multiple compartments served to differentiate fibrinolysis-induced hemorrhage from hemorrhage of other causes. Severe amyloid angiopathy was found in one patient who was operated on. CONCLUSIONS: Hemorrhages in multiple compartments and the presence of fluid levels inside the hematoma suggest fibrinolysis-associated cerebral hematomas. Severe amyloid angiopathy may be a crucial factor in this clinical entity. Outcome is poor, and a high proportion of patients have rapid progression to brain death. Therefore, emergency neurosurgical evacuation will probably be unsuccessful.
Aged↗
Fulminant brain necrosis from atrial myxoma showers.
BACKGROUND: Atrial myxoma is uncommon and may be associated with brief isolated ischemic events. We describe a patient with atrial myxoma and an incompletely evaluated ischemic stroke followed 1 year later with almost complete brain necrosis. SUMMARY OF REPORT: A 63-year-old woman presented with a rapidly progressive illness resulting in coma within 24 hours from multiple myxomatous emboli. Cranial computed tomographic scan demonstrated multiple hypodensities in both cerebellar and cerebral hemispheres. Postmortem examination revealed virtually complete brain necrosis, multiple peripheral artery embolizations, embolization in the coronary arteries with acute myocardial infarction, and tumor emboli in the spleen and kidneys. CONCLUSIONS: Although uncommon, atrial myxoma may present as a fatal multiple organ embolization that includes both anterior and posterior circulation territories of the brain.
Adult↗
Subarachnoid hemorrhage without detectable aneurysm. A review of the causes.
BACKGROUND: In 15% to 20% of patients with a spontaneous subarachnoid hemorrhage, no aneurysm is found on the first angiogram. This review emphasizes that this group of patients is in fact heterogeneous and describes the clinical features, pattern of hemorrhage on early computed tomographic (CT) scan, prognosis, and proposed management in the several and distinct subsets of these patients. SUMMARY OF REVIEW: Patients in whom no aneurysm is revealed on the initial angiogram can be subdivided mainly according to the pattern of hemorrhage on an early CT scan. In two thirds of these patients the CT scan shows a perimesencephalic pattern of hemorrhage (ie, blood confined to the cisterns around the midbrain); these patients invariably have a good prognosis, which obviates the need for a second angiogram. Patients with diffuse or anteriorly located blood on CT scan are at risk of rebleeding. In most of these patients the source of hemorrhage is an occult aneurysm, but intracranial artery dissections, dural arteriovenous malformations, mycotic aneurysms, trauma, bleeding disorders, substance abuse, or a cervical origin of the hemorrhage should also be considered. Patients with no blood revealed on an early CT scan but with xanthochromic cerebrospinal fluid are extremely rare. These patients deserve a second reading of the scan for blood in the prepontine cistern, which can be the only site of hemorrhage in perimesencephalic hemorrhage. CONCLUSIONS: The prognosis and management of patients in whom no aneurysm is found on the initial angiogram depends on the pattern of hemorrhage on the initial CT scan. Patients should no longer be designated with the umbrella term "angiogram-negative subarachnoid hemorrhage."
Anemia, Sickle Cell↗
New-onset seizures in critically ill patients.
We studied causes of new-onset seizures in 55 patients admitted to medical and surgical intensive care units between 1981 and 1991. In one-third of the patients, sudden withdrawal of narcotic agents was associated with tonic-clonic seizures. In another third, acute metabolic changes, predominantly severe hyponatremia (sodium < or = 125 mEq/l), accounted for new-onset seizures. In eight patients, drug toxicity (antibiotics and antiarrhythmic agents) predisposed to seizures. Only five patients had previously unrecognized structural CNS abnormalities that were manifested by focal or generalized tonic-clonic seizures. In six patients, the cause remained unknown. Twenty-four patients had recurrent seizures despite treatment with standard antiepileptic drugs. Status epilepticus occurred in four patients. Outcome was poor in only 34% of the patients, particularly in those with metabolic causes. Sudden withdrawal of narcotic drugs may be a significant cause of new-onset seizures in patients with life-threatening disorders.
Adult↗
[Peri-mesencephalic hemorrhage: a benign subarachnoid hemorrhage].
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Adult↗
The role of hypotension in septic encephalopathy following surgical procedures.
To study the risk factors for septic encephalopathy, we reviewed a consecutive series of 84 patients with septic syndrome and multiple-organ failure. Septic encephalopathy developed in 14 of these patients. Univariate analysis revealed that severe hypotension was significantly associated with the development of septic encephalopathy. In stepwise multiple logistic regression analysis, no other variable made a significant contribution in the presence of severe cardiovascular failure. Septic encephalopathy may be related to ischemic damage rather than to metabolic causes.
Adult↗
Infarction after aneurysm rupture does not depend on distribution or clearance rate of blood.
BACKGROUND AND PURPOSE: We sought to determine the contribution of the amount, distribution, and clearance rate of extravasated blood in relation to occurrence of infarction and outcome in patients with aneurysmal subarachnoid hemorrhage. METHODS: We prospectively studied 59 consecutive patients with aneurysmal subarachnoid hemorrhage admitted within 72 hours by means of serial computed tomographic scanning, close clinical observation, and assessment of outcome after 3 months. RESULTS: Infarction occurred in 17 of the 59 patients. The arterial territories involved hardly reflected the distribution of subarachnoid blood in the basal cisterns on computed tomography, and even the side of the infarcts corresponded only weakly with the side on which most extravasated blood was seen. Infarction occurred twice as often in patients with large amounts of subarachnoid blood; this difference was not significant on its own but is in agreement with previous studies. A low clearance rate of cisternal blood was not related to the occurrence of infarction; a relation between clearance rate and poor outcome was largely explained by the amount of subarachnoid blood on the initial computed tomogram and by a low Glasgow Coma Scale score on admission. CONCLUSIONS: The fact that infarction is related to the total amount but not to the distribution or clearance rate of extravasated blood argues against a direct role of extravasated blood and in favor of systemic factors, dependent on the severity of the initial hemorrhage.
Cerebral Infarction↗
Acute hydrocephalus in nonaneurysmal perimesencephalic hemorrhage: evidence of CSF block at the tentorial hiatus.
The acute hydrocephalus in patients with nonaneurysmal perimesencephalic hemorrhage suggests an extraventricular obstruction of CSF flow. We studied the occurrence of acute hydrocephalus and the site of cisternal blood in 40 consecutive patients with perimesencephalic hemorrhage. In all 11 patients with hydrocephalus, all perimesencephalic cisterns were filled with blood; this occurred in only five of the 29 patients (17%) without hydrocephalus (p less than 0.0001). We conclude that in the absence of intraventricular blood, filling of all perimesencephalic cisterns with blood is a necessary factor for the development of acute hydrocephalus.
Acute Disease↗
Outcome in patients with subarachnoid haemorrhage and negative angiography according to pattern of haemorrhage on computed tomography.
15% of patients with spontaneous subarachnoid haemorrhage have normal cerebral angiograms; they fare better than patients with demonstrated aneurysms, though rebleeding and cerebral ischaemia can still occur. In patients with a normal angiogram and accumulation of blood in the cisterns around the midbrain--"perimesencephalic nonaneurysmal haemorrhage"--outcome is excellent. To test the hypothesis that rebleeding and disability in angiogram-negative subarachnoid haemorrhage might be limited to those with other patterns of haemorrhage on initial computed tomography (CT), complications and long-term outcome were studied in 113 patients with angiogram-negative subarachnoid haemorrhage, admitted between January, 1983, and July, 1990. All patients were investigated with third-generation CT scans within 72 h of the event, and with cerebral angiography. The mean follow-up period was 45 (range 6-96) months. None of 77 patients with a perimesencephalic pattern of haemorrhage on CT died or was left disabled as a result of the haemorrhage (0% [95% confidence interval 0-5%]). Among the other 36 patients, who had a blood distribution on CT indistinguishable from that in proven aneurysmal bleeds, 4 had rebleeds and 9 died or were left disabled as result of the haemorrhage (25% [14-43%]). Thus, two distinct subsets of patients with angiogram-negative subarachnoid haemorrhage should be recognised. Patients with a perimesencephalic pattern of haemorrhage have an excellent prognosis. Rebleeding, cerebral ischaemia, and residual disability occur exclusively in patients with aneurysmal patterns of haemorrhage on initial CT. Repeated angiography in search of an occult aneurysm is justified only in the patients with aneurysmal patterns.
Acute Disease↗
The clinical course of perimesencephalic nonaneurysmal subarachnoid hemorrhage.
We studied the early clinical course of 65 patients with perimesencephalic (nonaneurysmal) subarachnoid hemorrhage. None of the patients rebled; none had delayed cerebral ischemia; and only 3 patients (5%) developed clinical signs of acute hydrocephalus, 2 requiring ventricular shunting. Hyponatremia and electrocardiographic changes were found in the same proportions as in patients with aneurysmal rupture. All patients had a good outcome after 3 months. To control for the influence of the relatively small amount of cisternal blood in perimesencephalic hemorrhage on the absence of delayed cerebral ischemia, we compared these 65 patients with 49 patients who had aneurysmal subarachnoid hemorrhage. This control group with aneurysms was selected according to a similar amount of cisternal blood, a comparable level of consciousness on admission, and absence of other factors known to increase the risk for delayed cerebral ischemia. We found that 4 of the 49 patients with aneurysmal hemorrhage developed delayed cerebral ischemia (Fisher's exact test, p = 0.03); therefore the relatively small amount of blood does not account for the absence of delayed cerebral ischemia in perimesencephalic hemorrhage. Patients with a perimesencephalic pattern of hemorrhage and a normal angiogram should be considered to have a distinct subset of subarachnoid hemorrhage and should be excluded from future treatment trials of patients with subarachnoid hemorrhage.
Adult↗
Fatal disseminated hemorrhagic toxoplasmic encephalitis as the initial manifestation of AIDS.
A 28-year-old woman presented with progressive coma after being asymptomatic for 1 year after the demonstration of seropositivity for human immunodeficiency virus and high serum immunoglobulin G toxoplasma titers. Computed tomographic scanning showed multiple rounded cerebral hemorrhages and massive cerebral edema. Postmortem examination disclosed Toxoplasma gondii cysts scattered throughout the brain. An overwhelming fatal toxoplasmosis associated with multiple cerebral hemorrhages may be the first presentation of the acquired immunodeficiency syndrome. We raise the possibility that frequent neuroradiological monitoring may be indicated in asymptomatic human immunodeficiency virus-infected patients with high immunoglobulin G toxoplasma titers.
Acquired Immunodeficiency Syndrome↗
Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.
BACKGROUND AND PURPOSE: The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances. METHODS: We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. RESULTS: Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. CONCLUSIONS: A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.
Adult↗