Resume Sajian Kasus Berbasis Bukti

STATUS EPILEPTICUS (G41.0), BACTERIAL MENINGITIS (G00.9), PARTIAL TONIC

CLONIC EPILEPSY (G40.2), AND WELL NOURISHED

Status epilepticus has been conceptually defined as "a condition characterized by an epileptic
seizure that issues positively, or is repeated at a brief briefing interval to produce an unusing and
enduring epileptic condition" [1]. This conceptual definition is pragmatically defined by the
International League Against Epilepsy as 30 min of continuous seizure activity, or a series of
epileptic seizures during which the function is not regained between events in a longer than 30 min
period.

As for some groups of patients at risk of developing status epilepticus:

1. Epilepsy
About 10-20% of people with epilepsy will experience at least one episode of status epilepticus in
the course of their illness. In addition, SE can be the first manifestation of epilepsy in 12% of new
patients with epilepsy.
2. Critically ill patients. Patients who experience hypoxic-ischemic encephalopathy (EHI), head
trauma, CNS infection, cardiovascular disease, congenital heart disease (especially post-
operative), and hypertensive encephalopathy.
Pathophysiology
Seizures are triggered by excessive, spontaneous and synchronous stimulation of most neurons
resulting in activation of motor (seizure), sensory, autonomic or complex functions (cognitive,
emotional) locally or publicly.
The mechanism of seizure is several theories:
• Impaired ATP formation due to failure of Na-K pumps, for example in hypoxemia, ischemia,
and hypoglycemia. Whereas in self seizures can occur ATP reduction and hypoxemia occurs.
• Changes in nerve cell membrane permeability such as hypocalcemia and hypomagnesaemia.
• The relative changes in excitatory neurotransmitters compared to inhibitory neurotransmitters
can cause excessive depolarization. For example an imbalance between GABA or glutamate will
cause seizures.
 Figure 1. Algorithm for convulsive status epilepticus
The guideline, which is all available adult and pediatric evidence, provides a treatment
algorithm that comprises three phases of treatment. It also offers evidence-based answers to
effectiveness, safety and tolerability questions regarding the treatment of convulsive status
epilepticus.
 Stabilization phase (0-5 minutes of seizure activity), includes standard initial first aid for
seizures and initial assessments and monitoring.
 Initial therapy (5-20 minutes of seizure activity) when it is clear the seizure requires medical
intervention, a benzodiazepine (specifically IM midazolam, IV lorazepam, or IV diazepam) is
recommended as the initial therapy of choice, given its demonstrated efficacy, safety, and
tolerability.
 Second therapy phase (20-40 minutes of seizure activity) when the response (or lack of
response) to the initial therapy should be apparent. Reasonable options include fosphenytoin,
valproic acid and levetiracetam. There is no evidence for any of these options. Because of
adverse events, IV phenobarbital is a reasonable second-alternative therapy if none of the three
recommended therapies are available.
 Third therapy phase (40 + minutes of seizure activity). There is a clear evidence to guide
therapy in this phase. The guideline found strong evidence that the initial second therapy is
less effective than initial therapy, and the third therapy is substantially less effective than initial
therapy. Thus, if second fails to stop the seizures therapy, treatment considerations should
include repeating second-line therapy or anesthetic doses of either thiopental, midazolam,
pentobarbital, or propofol (all with continuous EEG monitoring).

Bacterial Meningitis
Bacterial meningitis is meningen inflammation, especially arachnoid and pyramidal, which
occurs due to bacterial invasion into the subarachnoid space. In meningitis, there is a recruitment
of leukocytes into the cerebrospinal fluid (CSS). Usually the inflammatory process is not limited
to meninges,but also affects the brain parenchyma (meningoencephalitis), ventricles
(ventriculitis), and can even spread to the spinal cord. Neuronal damage, especially in the
hippocampal structure, is thought to be a potential cause of persistent neuropsychological deficits
in patients recovering from bacterial meningitis.
Factors associated with an increased risk of bacterial meningitis include immunocompromised
status (human immunodeficiency virus infection, cancer, immunosuppressant drug therapy, and
splenectomy), cranial penetrating trauma, skull base fracture, ear infection, nasal sinus infection,
pulmonary infection, infection teeth, presence of foreign matter in the central nervous system (eg
ventriculoperitoneal shunt), and chronic diseases (congestive heart failure, diabetes, alcohol
abuse, and hepatic cirrhosis) .
Meningitis is divided into two groups based on changes in brain fluid, serous meningitis
and purulent meningitis. Serous meningitis is characterized by elevated cell and protein counts
with clear cerebrospinal fluid.
Based on the causative bacteria, meningitis can be caused by group B Streptococcus,
Eschericia coli, staphilococcus aureus, pseudomonas, Nisseria meningitidis, and Streptococcus
pneumoniae.
PATHOPHYSIOLOGY
Bacterial infections reach the central nervous system through direct invasion, hematogenous
spread, or embolization of infected thrombus. Infection can also occur through direct expansion
of infected structures via vv. diploica,erosional focus on osteomyelitis, or iatrogenic (post
ventriculo peritoneal shunt or other brain surgical procedures). Transmission of pathogenic
bacteria is generally through respiration droplets or direct contact with careers. The process of
entry of bacteria into the central nervous system is a complex mechanism. Initially, the bacteria
colonize the nasopharynx by binding to epithelial cells using villi adhesive and protein
membranes. The polysaccharide component of the bacterial capsule helps the bacteria to
overcome immunoglobulin. A defense mechanisms (IgA) in the host mucosa. Bacteria then pass
through epithelial cells into the intravascular space where bacteria are relatively protected from
complement humoral responses due to their polysaccharide capsules. Bacteria enter the
subarachnoid space and cerebrospinal fluid (CSS) through the choroid plexus or cerebral
capillaries. Bacterial displacement occurs through endothelial damage caused. All subarachnoid
space areas that include the brain, spinal cord, and optic nerve can be entered by bacteria and will
spread rapidly. The bacteria will multiply and the bacterial wall component or bacterial toxin will
induce an inflammatory process in the brain and parenchyma. As a result, barrier blood brain
barrier permeability increases and causes leakage of plasma proteins into CSS which will trigger
inflammation and produce purulent exudates in the subarachnoid space. Exudates will accumulate
quickly and will accumulate in the basal part of the brain and extend to the sheaths of the cranial
and spinal nerves. In addition, the exudate will infiltrate the arterial wall and cause thickening of
the intima and vasoconstriction, which can result in cerebral ischemia. Purulent exudate formed
can clog resorption of CSS by arachnoid villi or block the flow in the ventricular system which
causes obstructive hydrocephalus or communicants accompanied by cerebral edema. interstitial.
SIGNS AND CLINICAL SYMPTOMS
Acute bacterial meningitis has clinical trias, namely fever, severe headache, and stiff neck; not
infrequently accompanied by generalized seizures and impaired consciousness. Brudzinski and
Kernig signs can also be found and have the same clinical significance as stiff neck, but are
difficult to find consistently.8 Focal cerebral signs in the early stages of meningitis are most often
caused by pneumococci and H. influenza. Meningitis with etiology of H. influenza most
commonly causes seizures. Persistent focal cerebral lesions or difficult-to-control seizures usually
occur in the second week of meningial infection and are caused by infectious vasculitis, when
there is a superficial cerebral vein obstruction leading to infarction of brain tissue. Cranial nerve
abnormalities often occur in pneumococcal meningitis, due to invasion of purulent exudates that
damage the nerves through the subarachnoid space.
SUPPORTING INVESTIGATION
The diagnosis of bacterial meningitis is made through CSS analysis, blood culture, CSS staining,
and CSS cultures. In principle, lumbar puncture must be performed at any time for suspicion of
meningitis and / or encephalitis. On blood tests, bacterial meningitis is accompanied by an
increase in leukocytes and inflammatory markers. Brain imaging must be performed as soon as
possible to exclude mass lesions, hydrocephalus, or cerebral edema which are a contraindication
to the relative lumbar puncture.

Table 2: CSF forrmula characteristic

Management
Bacterial meningitis is a medical emergency. In general, the management of bacterial meningitis
can be seen in figure 1. The choice of the right antibiotic is a crucial step, because it must be
bactericidal in a suspected organism and can enter an effective amount of CSS. Antibiotics should
be started immediately while waiting for the results of the diagnostic tests and later can be
changed after laboratory findings. in patients with battery meningitis must be based on the local
epidemiology, the age of the patient, and the presence of underlying disease or concomitant risk
factors (table 3). Empirical antibiotics can be replaced with antibiotics that are more specific if
the results of the culture already exist. The duration of antibiotic therapy depends on the causative
bacteria, the severity of the disease, and the type of antibiotics used. Dexamethasone therapy
given before or together with the first dose of antibiotics can significantly reduce morbidity and
mortality, especially in pneumococcal meningitis. Dexamethasone can reduce the inflammatory
response in the subarachnoid space which can indirectly reduce the risk of cerebral edema,
increased intracranial pressure, impaired cerebral blood flow, vasculitis, and neuronal injury.
Dexamethasone is given for 4 days at a dose of 10 mg every 6 hours intravenously.

Figure 1. Management algorithm for infants and children with suspected bacterial meningitis.
Table 3. Antibiotics for bacterial meningitis after microorganism identification and in-vitro
susceptibility testing

General Seizures of Clonic Tonic

Grand MaL seizures are also known as generalized tonic-clonic seizures beginning with loss of
consciousness and excessive muscle contraction. This is the type of seizure most people imagine
when they think about seizures in general.
Grand Mal Seizure has two stages:
• Tonic phase. Loss of consciousness occurs, and the muscles contract then suddenly causing
people to fall. This phase usually lasts around 10 to 20 seconds. In this phase the patient often
experiences loss of consciousness, loss of balance and falls because the muscles tighten, scream
for no reason, bite the inner cheek and tongue
• Clonic phase. The muscles enter the rhythmic contraction stage, stretching and then relaxing
again, the patient can often wet the bed or remove uncontrolled large water. Seizures usually last
less than two minutes.
This type of attack is usually preceded by an aura. Aura is the feeling experienced before an attack
can be: abdominal pain, numbness, dizziness, buzzing ears. Superficial breathing and interrupted
at any time causes the lips and skin to look gray / blue. This is often followed by periods of
confusion, agitation and sleep. Headaches and pain are also common afterwards.
The diagnosis of epilepsy is established on the basis of recurrent epileptic seizures (minimum 2
times) without provocation, with or without the presence of epileptiform features in the EEG.
The complete order of examination to go to the diagnosis is as follows:
1. History
History must be done carefully, in detail and thoroughly. Explanation regarding everything
that happened before, during and after the attack (including symptoms and duration of attacks)
is very meaningful information and is the key to diagnosis.
History (auto and aloanamnesis), including:
a) Symptoms before, during and after seizure
• Circumstances when resurrected: sitting / standing / lying / sleeping / urinating.
• Onset symptoms (aura, movement / initial sensation / speech arrest).
• What appears during seizures (patterns / seizure forms): tonic / clonic movements,
vocalizations, automatism, incontinence, tongue biting, pale, sweating, and eye
deviation.
• Post-seizure conditions: confusion, awake, headache, sleep, restlessness, or Todd's
paresis.
 Is there more than one generation pattern, or is there a change in the pattern of
generation.
b) The presence/absence of other diseases currently suffered, as well as a history of
neurological diseases and a history of psychiatric illness or systemic diseases that may be
the cause.
c) Age of onset, duration, frequency of generation, and the longest interval between
generation.
d) History of neonatal seizures / febrile seizures.
2. General and neurological physical examination
Physical examination must ward off the causes of attacks by using age and disease history as
a handle. In pediatric patients, the examiner must pay attention to developmental delays,
organomegaly, and size differences between limbs can indicate the onset of unilateral brain
growth disorders.
3. Investigation
a) Laboratory examination
 Need to check the levels of glucose, calcium, magnesium, sodium, bilirubin, and urea in the
blood. Circumstances such as hyponatremia, hypoglycemia, hypomagnesia, uremia, and hepatic
encephalopathy can trigger seizures. Examination of serum electrolytes along with glucose,
calcium, magnesium, Blood Urea Nitrogen, creatinine and liver function tests may provide very
useful instructions.
b) Electro encephalography (EEG)
Electroencephalography is a device that can record electrical activity in the brain through
electrodes placed in the skin of the head. EEG abnormalities that are often found in people
with epilepsy are called epileptiform discharge or epileptiform activity. EEG examinations
must be carried out in all epileptic patients and are the most frequent investigations carried
out to establish a diagnosis of epilepsy. The presence of focal abnormalities in EEG indicates
the possibility of structural lesions in the brain, whereas the presence of a common
abnormality in EEG indicates the possibility of genetic or metabolic abnormalities. EEG
recordings are said to be abnormally determined on the basis of:
• Asymmetrical rhythm and wave voltage in the same area in both brain hemispheres.
• Irregular wave rhythms, slower waves than slower waves.
• There are waves that are usually not found in normal children, such as sharp waves,
spikes, spikes, compound nails, and slow waves that arise paroximal.
c) Radiological Examination
Ct scan (Computed Tomography Scan) head and MRI (Magnetic Resonance Imaging)
head is an examination known as neuroimaging which aims to see whether there is a
structural abnormality in the brain and complete EEG data.
This head CT scan is done if there is contradiction in the MRI, however this head MRI
examination is the preferred brain imaging procedure for epilepsy with high sensitivity and
more specific than CT scan. Therefore it can detect small lesions in the brain, hippocampal
sclerosis, cortical dysgenesis, tumors and cavernous hemangiomas, as well as refractory
epilepsy which is very possible surgical therapy. MRI is useful for comparing right and left
hippocampus.
ANTI EPILEPSY
I. Sodium Chanel Bloker

• CARBAMAZEPINE
 Carbamazepin is the main treatment as an epilepsy used for partial seizures and general
tonic-clonic seizures. CBZ is a tricyclic compound and was initially used primarily for the
treatment of trigeminal neuralgia, but then its ability as an anti-epileptic is very found. CBZ
working mechanism is to block sodium channels quickly, repeatedly, continuously to prevent
the potential of post tetanik.
Pharmacokinetics
Carbamazepin is a crystalline substance which is insoluble in water, which is used orally.
Because carbamazepin is a substance that is unstable, avoids heat or moisture, which reduces
bioavailability by 50%. It is extensively metabolized in the liver and induces its own
metabolism. The time of the serum half is reduced by 50olo during the first few weeks of
treatment. The elimination half-life ranges from 5-26 hours after repeated treatment of healthy
volunteers and patients with epilepsy. In children, half-life ranges from 3-32 hours. Available
formulations, including suspension, syrup, tablets (100 mg, 200 mg, 400 mg), chewable tablets
(100 mg, 200 mg), capsules (Tegretol XR; 100 mg, 200 mg, 400 mg), carbatrol (200 mg , 300
mg), and rectal suppositories.
Clinical Indications
Carbamazepin is one of the most widely used anti-epilepsy AEDs in the world. This is very
effective for partial onset seizures, including cryptogenic and partial seizure symptoms. It has also
shown kamanjuran both in general tonic-clonic seizure treatments.
Side effects and toxicity
CBZ can produce dose-related effects such as dizziness, diplopia, nausea, ataxia, and blurred
vision. Side effects that have been found are aplastic anemia, agranulocytosis, thrombocytopenia
and Stevens-Johnson syndrome. Asymptomatic elevations of liver enzymes generally occur during
therapy in 5-10% of patients. Rarely, severe hepatotoxic effects occur.
Drug interactions
Some drugs, such as macrolide antibiotics (erythromycin and clarithromycin), isoniazid,
chloramphenicol, calcium channel blockers, cimetidine, and propoxyphene, hepatic cytochrome
P-4503A4 (CYP3A4) enzyme inhibitors, which are responsible for metabolic breakdown of CBZ,
which causes an increase in levels. Phenobarbital, phenytoin, felbamate, and primidone also reduce
cbz levels via CYP3A4.

• PHENITOIN
Since its introduction in 1938, phenytoin has become the main drug in the treatment of partial
seizures and secondary generalized seizures in the United States. Phenytoin inhibits the movement
of ions through the sodium channel during the spread of the action potential, and therefore blocks
and prevents post tetanic potential, development of maximal seizure activity limits, and reduced
spastic spread. It also shows the effects that inhibit calcium channels and calcium ions of
quarantine in nerve terminals thus inhibiting the voltage dependent neurotransmission at the
synapse level. An antiepileptic effect is also seen in calmodulin and other secondary messenger
systems, an unclear mechanism.
Clinical indication
Phenitoin is one of the most commonly used anti epilepsy as the main treatment or adjuvant
treatment for partial seizures and generalized seizures, syndromes Lennox-Gastaut, status
epilepticus, and childhood epilepsy syndrome. This is not indicated for myoclonus

Table 2. selection of seizure medication

 Mengetahui,

dr. Dewi Sutriani., SpA(K)