The goals of therapy are to reduce morbidity, to shorten the clinical course of the disease, to prevent complications, and to prevent recurrences. Pharmacotherapy for herpes simplex encephalitis (HSE) is available in the form of acyclovir. Patient outcome is improved when this agent is used for treatment.
The goals of using antivirals are to shorten the clinical course, prevent complications, prevent development of latency and subsequent recurrences, decrease transmission, and eliminate established latency.
Acyclovir is the drug of choice for HSE. It has demonstrated inhibitory activity against both herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) and is taken up selectively by infected cells. Mortality from HSE before use of acyclovir was 60-70%; since acyclovir, it is approximately 30%.
After ingestion, drug is rapidly biotransformed into the active compound penciclovir and phosphorylated by viral thymidine kinase. By competition with deoxyguanosine triphosphate, penciclovir triphosphate inhibits viral polymerase, subsequently inhibiting viral DNA synthesis/replication.
Adjust the dose in patients with renal insufficiency or hepatic disease.
Anticonvulsants are used to terminate clinical and electrical seizure activity as rapidly as possible and to prevent seizure recurrence.
Carbamazepine is effective in treatment of complex partial seizures; it appears to act by reducing polysynaptic responses and blocking posttetanic potentiation.
Phenytoin is a hydantoin. Its primary site of action appears to be the motor cortex, where it may inhibit spread of seizure activity; it may reduce maximal activity of the brain stem centers responsible for the tonic phase of grand mal seizures.
The dose should be individualized; if daily dosage cannot be divided equally, larger dose should be given before bedtime. A phosphorylated formulation, fosphenytoin, is available for parenteral use.
These agents are used for the management of increased intracranial pressure in complications resulting from herpes simplex encephalitis.
Furosemide is a loop diuretic that increases the excretion of water by interfering with the chloride-binding co-transport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It increases renal blood flow without increasing the filtration rate. The onset of action generally is within 1 hour. It increases potassium, sodium, calcium, and magnesium excretion.
Furosemide is used in the acute setting for reduction of increased ICP. The proposed mechanisms in lowering ICP include following: (1) suppression of cerebral sodium uptake, (2) carbonic anhydrase inhibition resulting in decreased CSF production, and (3) inhibition of cellular membrane cation-chloride pump, thereby affecting the transport of water into astroglial cells.
The dose must be individualized to the patient. Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 hours after the previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.
Mannitol reduces cerebral edema with the help of osmotic forces, and it decreases blood viscosity, resulting in reflex vasoconstriction and lowering of ICP.
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