Complications
A common cause of death in patients with rabies.
The patient loses the ability to control body temperature, and the paralyzed body adopts the temperature of the local environment. Control of ambient temperature is required to control body temperature. This condition does not respond to antipyretics.
Progressive CSF lactic acidosis has been seen in the few patients where this has been measured, independent of noninvasive measures of cerebral perfusion.
Coma occurs in all patients in the late stages of infection. The diagnosis of brain death poses particular challenges in these patients. Rabies can mimic brain stem death by causing denervation in the presence of ongoing electrical activity. Clinical brain-death criteria do not apply; electrical activity and cerebral perfusion studies are more reliable to confirm brain death.[13][42]
These occur within the first 10 days of symptomatic infection. Arrhythmias include tachycardia or supraventricular tachycardia, which occur with hypertension, or bradycardia and asystole. Bradycardia or asystole lead to death in some patients. Arrhythmias usually respond to increased sedation but may require cardiac pacing. Bradycardia is often unresponsive to anticholinergics.
Can occur at any time from the onset of symptoms. Produced by dehydration, and may also be related to insufficiency of adrenal medulla from tetrahydrobiopterin (BH4) deficiency.
Secretions may be viscous and cause aspiration. Some patients may require intubation. Aspiration may require bronchoscopy for adequate clearance.
Typically occurs during the second week after symptoms begin and lasts 5-7 days. Nasojejunal feedings are recommended.
The onset is in the second week. Can be confused with salt-wasting syndrome. Monitoring of urine output and serum glucose and electrolytes is required. Diuretics should be avoided.
Onset in second week, concurrent with onset of immune response (possibly in bat rabies only). Appears to be related to the presence of high rabies antibody titers in the CSF (>10 U/mL). This antibody response can be halted by methylprednisolone pulse therapy.
Occurs at presentation, originating from dehydration or salt wasting rather than SIADH. Monitoring of serum sodium and urine output is required.
Occurs before the onset of paralysis. May cause reflex dysautonomia.
Heart failure can occur at any time during the symptomatic infection, and is possibly related to myocarditis or catecholamine stunning.
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