Discussion:
Herpes simplex virus is a neuro-tropic virus that enters the body
through the mucosal surface. It travels along the axons through
retrograde transport and lies dormant in the sensory ganglia. The exact
mechanism of transport to CNS is not described but it is postulated that
it is a similar mechanism of retrograde transport along the sensory
nerves, given its predilection to mesiotemporal lobe and orbitofrontal
cortex(9). Once in the CNS, the manifestations of encephalitis prevail.
CNS complications include seizures (38.4%), status epilepticus (5.5%),
acute respiratory failure (20.1%), ischemic stroke (5.6%) and
intracranial hemorrhage (2.7%)(10). Thus, intracranial hemorrhage being
rare but fatal consequence in many instance(10). Untreated, the
mortality rate in herpes encephalitis due to its complication can reach
to 70% and most of the survivors can have serious neurological deficits
like neuropsychiatric or neurobehavior issues. HSE encephalitis needs a
prompt treatment with IV acyclovir for the reduction of mortality and
morbidity from HSV encephalitis and its complication.
The exact mechanism of hemorrhage has not been found but few theories
have been described to show the relationship of HSV encephalitis and
lobar hemorrhages. Vasculitis or transient hypertension caused by
increased ICP plays a major role in having lobar hemorrage. The
hypothesis include the rupture of the small vessels due to these above
causes(11). Magnetic resonance imaging (MRI ) of the brain is the
preferred imaging study; T2 images may be more helpful than T1
images(12).
Our patient’s presentation was consistent with HSV encephalitis but
later he developed brain hematoma. Otherwise, the clinical features of
brain hemorrhage were not distinctive and overlapped significantly with
those of HSV encephalitis. It is thus difficult to suspect this
complication on clinical grounds alone. The lack of clinical improvement
or the worsening of initial symptoms, particularly during first to
second week of admission, should lead to this suspicion and be followed
by a neuroimaging study. If the evidences discard the possibility of
structural complication, a lack of improvement with the treatment of
acyclovir may raise concern of acyclovir resistance or treatment adverse
effect. This scenario may warrant the start or switch the therapy to
foscarnet(13).
During management of this complication, supportive care and intensive
monitoring was sufficient, and surgical intervention was not required.
Mannitol was used for management of raised ICP but corticosteroids were
not used, the role of which remains still debatable in this area(14). A
multicenter randomized controlled trial was done to study the role of
corticosteroid in treatment of HSV encephalitis but was prematurely
terminated due to small no of study participants(15). Thus, higher level
of evidence to support the use of corticosteroid is lacking. Intensive
care physicians involvement in the care team seems imminent as up to
32% require ICU stay and 17% require mechanical ventilation(16).
Similarly, need for surgical intervention may be as high as 50%
following intracerebral hemorrhage as reported by Sainz et. al(17).The
neurological outcome in the non-operated group was similar, although in
this case it could be argued that they were less severely affected.
Thus, the role of neurosurgery in these patients is still unclear.