Showing posts with label HSE. Show all posts
Showing posts with label HSE. Show all posts

Herpes Simplex Encephalitis Complications and Prognosis

HSE  Complications
Seizures are common and some authors recommend prophylactic anti-seizure therapy in patients with severe HSE. Brain edema that occurs sometimes can be resolved with steroid therapy, although the use of steroids in the HSE is still a controversy. Adjunct therapy for brain edema include hyperventilation and barbiturates. Other complications that looks similar to all patients and patients with severe pain severe consciousness disturbance (eg, aspiration pneumonia, venous thrombosis profundus, and decubitus.)  
HSE  Prognosis

Radiological HSE Examination

HSE Radiological examination
MRI is an examination of selected, able to show pathologic changes are usually bilateral, in the medial temporal lobe and the inferior frontal lobe. The existence of lesions in the temporal lobe is significant HSE in the allegation.
Head CT scans can show changes in the temporal and frontal lobes, but less sensitive than MRI. In a third patient HSE found a normal head CT scan.
Other Examination

Herpes Simplex Encephalitis: Lab Examination

Laboratory Examination for Herpes Simplex Encephalitis
CSS Analysis: Typically shows mononuclear pleocytosis with a mild increase in protein levels while the glucose levels normal or decreased slightly. In the early phases of disease, sometimes cell count may be normal, although on serial examination always found an increasing number of cells and proteins. If there is bleeding in the brain parenchyma, the number of erythrocytes is always increasing and the increase was settled on the all tube inspection. HSV CSF culture is rarely found in patients with HSE.

Herpes Simplex Encephalitis Clinical manifestations

Clinical manifestations HSE
HSE is acute or subacute with focal and general signs of cerebral dysfunction. Are sporadic and not associated with the pattern of a particular season. Although fever, headache, behavioral changes, confusion, focal neurological abnormalities and abnormalities in CSF supports the HSE, there are no clinical signs patognomonis to distinguish HSE from other neurological diseases (eg non-HSV encephalitis, brain abscess or brain tumor). Confirmation of the diagnosis depends on identification of HSV from CSF examination by PCR or in brain tissue with brain biopsy.

Herpes Simplex Encephalitis Patofisiology

HSE pathogenesis has not been understood. Part of the brain affected by ptekie very diffuse and scattered necrosis of the medial lobe asymmetry in the inferior temporal and frontal lobes. The exact mechanism is not clear cell damage and affects either directly or indirectly virus immune mediated process.
Brain infection is often a primary infection because of direct transmission of virus through neuronal path from the peripheral to the brain via nerve trigeminus or olfactorius. Factors that accelerate the HSE is not known. Although HSE is often found in patients with decreased immune system, most people have never experienced immune system suppression.

Herpes Simplex Encephalitis

In the last 2 decades there is rapid development of antiviral drugs, but the Herpes Simplex Encephalitis (HSE) remains a severe disease with high morbidity and mortality.In children and adults, HSE found in temporal and frontal lobe and is caused by herpes simplex virus type 1 (HSV-1). In neonates, brain damage caused greater and is caused by HSV-2 are usually obtained at delivery. HSE must be distinguished from herpes simplex meningitis, caused by HSV-2 and is often associated with genital herpes infections that occur simultaneously.