7 HMRS anak mengeluh lemas, mudah capek

saat aktifitas, pucat(+), pusing (-), periksa

ke dokter disarankan minum tonikum, ada
perubahan lebih baik, BAB,BAK normal,Nafsu
makan turun disarankan rawat inap RS
HMRS anak lemas, mudah capek ,mudah
mengantuk, pusing
(-),demam(-),Mual(-),muntah (-) BAK tak ada
keluhan,BAB tak ada keluhan, nafsu makan
turun

 Ketika datang ke IGD kejang 1x

selama + 30 menit, demam (-),
riwayat jatuh (-)

 RPD:
Pernah mondok di RS selama 1 hari
pada usia 2 tahun karena kejang
demam
1 bulan yang lalu didiagnosis

 HR : 143
RR: 24
T: 36,2
BB :26 kg
A: Status Epileptikus
P:Diazepam supp 10 mg 5 menit pertama
Diazepam ke 2 10mg
O2 2L/menit
IVFD 15 tpm
Sodium Valproat 15mg/kgBB
Sulfas Ferous 1x1tab

WBC: 14,00
RBC :3,70
HGB : 8,2
HCT : 26,7
PLT: 644

Definisi
on-going or recurrent clinical or sub-clinical
seizure activity for more than 30 minutes
Status Epilepticus is a life threatening condition
where prolonged seizures >30 minutes can cause
neuronal death and may result in serious
neurological sequelae
Consequently, it is generally recommended that
seizures lasting for more than 5 minutes should
be treated as for status epilepticus
Applicable in children >1 month of age

Causes of status
epilepticus in children
In approximately one-quarter of children
affected, status epilepticus is the sign of an
underlying acute brain disorder, such as
traumatic brain in jury or meningitis.
Approximately onethird of children affected will
have a history of previous epileptic seizures,
developmental delay, or other neurological
abnormality.
One-quarter of children affected will have a
prolonged febrile convulsion and no other
cause will be demonstrated

pathophysiologi
SE is thought to result from failure of mechanisms that normally
terminate an isolated seizure. This failure can arise from
abnormal persistence of excessive excitation or ineffective
recruitment of inhibition. Experimental studies suggest that there
is an induction of reverberating seizure activity between
hippocampus and parahippocampal structures and seizure
progresses through a sequence of distinct electrophysiological
changes. [32] The proposed mechanisms of SE are as follows:

Constant activation of hippocampus.

Loss of GABA-mediated inhibitory synaptic transmission in
hippocampus.
Glutaminergic excitatory synaptic transmission, important for
sustaining SE.

Summary Recommendations for SE Definition and

Classification
1. SE should be defined as 5 min or more of continuous
clinical and/or electrographic seizure activity or recurrent
seizure activity without recovery between seizures (strong
recommendations, moderate quality).
2. SE should be classified as either convulsive SE
(convulsions that are associated with rhythmic jerking of the
extremities) or non-convulsive SE (seizure activity seen on
EEG without the clinical findings associated with convulsive
SE) (strong recommendation, high quality).
3. Refractory SE should be defined as SE that does not
respond to the standard treatment regimens, such as an
initial benzodiazepine followed by another AED (strong
recommendations, moderate quality).
4. The etiology of SE should be diagnosed and treated as
soon as possible (strong recommendation, high quality).

Physiological and Systemic

Changes
In the early stage of SE, there is massive release of catecholamines which
result in tachycardia, arrhythmias, high systemic, pulmonary, and left atrial
pressure, and occasionally pulmonary edema.
Blood glucose is elevated.
Blood glucose is elevated.
Respiratory failure and lactic acidosis result in metabolic acidosis.
Hyperpyrexia with increased white cell counts in SE may be mistaken for
infection.
Low-grade cerebrospinal fluid (CSF) pleocytosis may follow SE.
BP declines 15 to 30 minutes after SE and may be markedly low after 2 hours
of continuous seizure activity.
Besides, there may be hypoglycemia.
Renal failure may occur because of rhabdomyolysis and myoglobinuria.
In the initial phase of SE, cerebral blood flow increases to meet the elevated
demands, thereby increasing the intracranial pressure.
Later, cerebral edema ensues; in focal seizures, focal brain edema may be
present

 the physiological changes in SE can be

divided into two phases.
In phase 1, compensatory mechanisms
prevent cerebral damage
In phase 2, these mechanisms fail and
there is an increasing risk of cerebral
damage as the status progresses. The
transition from phase 1 to phase 2 occurs
after about 30 to 60 minutes of continuous
seizures