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Morning Report 7/15/13

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Lindsey Riggin

on 15 July 2013

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Transcript of Morning Report 7/15/13

Notes
HERPES SIMPLEX VIRUS (HSV) ENCEPHALITIS
Objectives
Review the history and epidemiology of HSE
Learn about the pathogenesis of HSE
Describe the clinical presentation of HSE
Consider the differential diagnosis of HSE
Understand how to diagnose HSE
Know the appropriate treatment for HSE
Some History
Zarafonetis and coworkers (1944) –
HSV first isolated in adult brain
-Intranuclear inclusion bodies
-Temporal lobe localization
-Perivascular cuffs of lymphocytes
-Numerous small hemorrhages

Nahmias and Dowdle (mid-1960s) –
viral typing: HSV-1 & HSV-2
“Above the belt” and “below the belt”
A Devastating Disease
HSV infection of the brain is the most common cause of sporadic fatal encephalitis in the USA.

In patients who do not receive treatment:
Mortality rate > 70%

Only ~15-38% of survivors return to normal function after treatment.
Incidence

As of 2005, incidence was estimated between 1 in 250,000 and 1 in 500,000.

HSV encephalitis accounts for 10-20% of 20,000 annual viral encephalitis cases

75% of cases occur in adults, 1/2 of which are in patients older than 50 years

Both sexes equally affected
Acute neurologic/psychiatric symptoms (<1 week duration):
AMS and altered level of consciousness
Personality changes
Hallucinations
Cranial nerve deficits
Hemiparesis
Dysphasia/Aphasia
Ataxia
Focal seizures
Headache
Anosmia

PATIENTS NEARLY ALWAYS HAVE FEVER IN ADDITION TO ONE OF THE ABOVE SYMPTOMS!


CLINICAL PRESENTATION
CSF cell counts not specific for HSV.
Pleocytosis & proteinosis (average protein 100mg/dL)
Absence of bacterial & fungal pathogens in the CSF
Lymphocytic predominance

***PCR DETECTION of HSV DNA
-

diagnostic method of choice (94% sensitivity & 98% specificity)
CSF is indicated - assuming no signs of increased ICP
ABCs - Remember: Less than 8 [GCS] ... INTUBATE
DO NOT WAIT to start treatment...MUST BE STARTED BEFORE onset of HEMORRHAGIC NECROSIS and DETERIORATION OF CONSCIOUSNESS.
TREATMENT OF CHOICE:
ACYCLOVIR: 10 mg/kg/dose q8 hours for 14 days
(Per IDSA Guidelines 2008)

TREATMENT
Viral Intranuclear Inclusion Cells in temporal lobe of a patient with HSE
Herpes Simplex Figure 48.
HSV Viral Particles in an Intranuclear inclusion cell
This is seen in 50% of patients with HSE
Most often visible in the first week of infection
More Pathogenesis
Replicating HSV causes degeneration of cellular nuclei, loss of intact plasma membranes, and formation of multinucleated giant cells.
Results in acute inflammation (influx of mononuclear cells), congestion, and/or hemorrhage.
Most notably in the temporal lobes.
Adjacent limbic & frontal areas may also be involved.
After about 2 weeks, changes proceed to frank necrosis and liquefaction of involved brain tissue.
PATHOGENESIS
Due to HSV type 1 (HSV-1) in nearly all cases

Occurs through one of three routes:
-Immediate invasion in the CNS via trigeminal nerve following episode of primary HSV-1
-CNS invasion after episode of recurrent HSV-1, representing viral reactivation
-CNS infection without primary or recurrent infection, representing reactivation of latent HSV.
MRI -
Reveals temporal lobe abnormalities in >90% of PCR-proven cases.
Characteristic MRI changes occur early in the course of HSV encephalitis and include high signal intensity lesions on T2-weighted and FLAIR images involving the medial and inferior temporal lobes with extension into the insula.
EEG -
Non-specific, focal findings in >80% - slowing in temporal and frontal regions
Imaging
REFERENCES
"Love is for now, herpes is forever."
-Anonymous
Immunocompromised Patients with HSE
Study by Tan et al, 2012 published in American Academy of Neurology - retrospective review of patients at JHU from 1997-2010
Immunocompromised states - chronic HIV infection, transplant recipients, patients on immunosuppressive therapies, patients with active malignancy, diabetics, and patients with renal insufficiency
May predispose to HSE with atypical features
Fewer patients presented with prodromal symptoms and focal neurologic deficits
Immunocompromised individuals have worse outcomes and mortality
Mortality rate almost 6 times as high
Decreased performance by 23 points on the Karnofsky Performance Status Scale (p=0.018)
Two out of 14 immunocompromised patients had recurrent HSE.
1. Baringer (2008) Herpes simplex infections of the nervous system In Neurologic Clinics, 26: 657-674.

2. Riancho, Delgado-Alvarado, Sedano, Polo, and Berciano. (2013) Herpes simplex encephalitis: clinical presentation, neurological sequelae and new prognostic factors. Ten years of experience. In Neurological Sciences (Epub ahead of print)

3. Tan, McArthur, Venkatesan, and Nath. (2012) Atypical manifestations and poor outcome of herpes simplex encephalitis in the immunocompromised. In American Academy of Neurology, 79: 2125-2132.
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