Hypertensive encephalopathy with a focal cortical edema in MRI

2001 ◽  
Vol 248 (10) ◽  
pp. 900-902 ◽  
Author(s):  
Christina Haubrich ◽  
Michael Mull ◽  
Jörg Hecklinger ◽  
Johannes Noth ◽  
Frank Block
Keyword(s):  
Hypertensive Encephalopathy ◽  
Cortical Edema

Hypertensive Encephalopathy in Children with Sickle Cell Disease.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3790-3790
Author(s):  
Caterina P. Minniti ◽  
Steven L. Weinstein ◽  
Zarir Khademian
Keyword(s):  
Magnetic Resonance ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Complete Resolution ◽  
Clinical Symptoms ◽  
Hypertensive Encephalopathy ◽  
Cell Disease ◽  
Acute Infarction ◽  
Cortical Edema

Abstract Cerebrovascular (CVA) accidents are a serious complication of Sickle Cell Disease (SCD). Acute cerebral infarction occurs in approximately 10% of children with SCD under the age of 16 years, with silent infarcts identified in an additional 22%. Children however can present with acute neurologic deterioration mimicking a CVA but demonstrate a picture consistent with hypertensive encephalopathy (HTNE). The incidence of HTNE in children with SCD is unknown with few annedoctal reports available in the literature. We retrospectively identified 83 children with SCD, who received their care at Children’s National Medical Center in Washington, DC, from 1992 to 2005, who presented with neurologic complaints that prompted Magnetic Resonance Imaging (MRI). There were 37 females and 46 males, age 13 months to 17 years, with mean age of 5 years and 8 months. Clinical and neuro-imaging data identified 8 children (7 females and 1 male) with clinical picture compatible with HTNE (BP > 2 std deviation for age), prior to neuroimaging. At the time of the hypertensive episode, the ages ranged from 6 to 16 years and 8 months, with an average of 14 years and 2 months. All patients had Hb SS. Neurologic complaints included seizure, sudden onset headache, confusion, loss of consciousness, and urinary retention. Elevated blood pressures were aggressively treated and all patient received an exchange transfusion. No specific etiology for the hypertension was determined. Initial MRI, obtained within 24–48 hours of presentation, did not show acute or prior infarction in this group. However, there was absence of diffusion restriction on T1 and T2 weighted images, and presence of cerebral cortical edema, which differentiate HTNE from acute infarction. The magnetic resonance angiogram (MRA) did not demonstrate evidence of arteriopathy. The hallmark of HTNE is a complete resolution of abnormalities of both the neurologic exam and the imaging studies at follow up. There was complete resolution of cerebral edema in all patients and mild interval prominence of the cerebral sulci, which can indicate cerebral volume loss, in three out of the 8 patients, in follow up studies obtained 10 days to 4 months later. No recurrences of the symptoms have been reported, with follow up ranging from 5 months to 8 years. None of the patients with HTNE has received chronic transfusions. We conclude that HTNE should be considered in the differential diagnosis of an acute neurologic event in a child with SCD. Accurate recording of vital signs and prompt correction of hypertension is indicated. MRI can accurately distinguish between HTNE and acute infarction, even when clinical symptoms are similar. This distinction helps physicians to establish proper treatment such as chronic transfusion following infarction.

A case of hypertensive encephalopathy with prominent brainstem presentation

2009 ◽  
Vol 30 (2) ◽  
pp. 133-135 ◽  
Author(s):  
E. Medici ◽  
S. Arabi ◽  
M. Sebastianelli ◽  
O. Pirani ◽  
E. Giaccaglini
Keyword(s):  
Hypertensive Encephalopathy

Posterior Reversible Encepalopathy Syndrome in A Child With Post Streptococcal Glomerulonephritis- A Rare Case Report

Med Phoenix ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 50-52
Author(s):  
Sunita Ghimire ◽  
Shree Krishna Shrestha ◽  
Ram Chandra Bastola ◽  
Anita Dahal ◽  
Pragya Shakya
Keyword(s):  
Posterior Reversible Encephalopathy Syndrome ◽  
Vasogenic Edema ◽  
Female Child ◽  
Hypertensive Encephalopathy ◽  
Posterior Reversible Encephalopathy ◽  
Radiological Features ◽  
Rare Case Report ◽  
Post Streptococcal Glomerulonephritis ◽  
Reversible Encephalopathy ◽  
Timely Treatment

Posterior reversible encephalopathy syndrome is a condition occurring  in majority of case of  hypertensive encephalopathy mainly due to vasogenic  edema in parieto occipital region in neuroimaging. It is reversible if timely treatment is done .Here we are reporting a 11 year old female child with acute post streptococal glomerulonephrtitis leading to typical clinical and radiological features of posterior reversible encephalopathy syndrome

HYPERTENSION IN EMBRYOMA (WILMS' TUMOR)

PEDIATRICS ◽  
1949 ◽  
Vol 3 (2) ◽  
pp. 201-207
Author(s):  
JAMES G. HUGHES ◽  
HERMAN ROSENBLUM ◽  
LACY G. HORN
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Clinical Features ◽  
Wilms Tumor ◽  
Hypertensive Encephalopathy ◽  
Renal Ischemia ◽  
Cerebral Anoxia ◽  
Cardiac Decompensation ◽  
First Case ◽  
The Right

A case of Wilms' tumor of the right kidney is presented, in which the dominant clinical features were extreme elevation of blood pressure and hypertensive encephalopathy, associated with cardiac decompensation and death. Generalized convulsions and right hemiplegia developed, believed to have been due to cerebral anoxia incident to angiospasm. No metastases were found, and no other cause for arterial hypertension was discovered. This patient is thought to be the first case reported where death from Wilms' tumor was due to the hypertensive factor. The literature with reference to the association of hypertension with Wilms' tumor is reviewed. The mechanisms by which Wilms' tumors may produce unilateral renal ischemia with arterial hypertension are discussed. The presence of clearcut hypertension in a child with a kidney area mass points toward the probability of a Wilms' tumor.

Hypertensive encephalopathy: Report of a case

1986 ◽  
Vol 86 (9) ◽  
pp. 85-89
Author(s):  
Gilbert J. Toffol ◽  
Robert A. Norman
Keyword(s):  
Hypertensive Encephalopathy

HYPERTENSIVE ENCEPHALOPATHY

1944 ◽  
Vol 37 (12) ◽  
pp. 698-700
Author(s):  
Arnold McNitt
Keyword(s):  
Hypertensive Encephalopathy
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