Erna Wati

405140024
Kejang demam
Definition & classification
• occur between the age of 6 and 60 mo
• temperature of 38°C or higher
• not the result of central nervous system infection or any metabolic imbalance
• occur in the absence of a history of prior afebrile seizures

• Simple febrile seizure

• primary generalized; tonic-clonic
• attack associated with fever
• lasting for a maximum of 15 min
• not recurrent within a 24-hour period
• Complex febrile seizure
• Focal; more prolonged (>15 min)
• recurs within 24 hr
• Febrile status epilepticus  febrile seizure lasting > 30 minutes
• Risk factor for recurrency
Work up & evaluation
Febrile seizures often occur in the context
of otitis media, roseola and human
herpesvirus 6 (HHV6) infection, shigella,
or similar infections
• Lumbar puncture
• children <12 mo of age after their first febrile seizure; to rule out meningitis
• children >18 mo of age, a lumbar puncture is indicated in the presence of clinical
signs and symptoms of meningitis
• EEG
• delayed until or repeated after >2 wk have passed (because if < 2 wk  nonspecific
slowing)
• performed for at least 30 min in wakefulness and in sleep according to international
guidelines
• Blood studies
• Neuroimaging
• CT or MRI is not recommended in evaluating the child after a first simple febrile
seizure
Treatment
• antiepileptic therapy, continuous or intermittent, is not recommended for children with
one or more simple febrile seizure
• If the seizure lasts for >5 min  acute treatment with diazepam, lorazepam, or
midazolam
• recurrence of febrile seizure lasting >5 min  rectal diazepam
• Febrile status epilepticus  Intravenous benzodiazepines, phenobarbital, phenytoin, or
valproate
• < risk of febrile seizure
• intermittent oral diazepam can be given during febrile illnesses (0.33 mg/kg every 8 hr during
fever)
• Intermittent oral nitrazepam, clobazam, and clonazepam (0.1 mg/kg/day)
• intermittent diazepam prophylaxis (0.5 mg/kg administered as a rectal suppository every 8 hr)
• Phenobarbital (4-5 mg/kg/day in 1 or 2 divided doses)
• Valproate (20-30 mg/kg/day in 2 or 3 divided doses)
Kejang demam
• Bangkitan kejang yang terjadi pada kenaikan suhu tubuh (>38 derajat
celcius) karena suatu proses ekstrakranium
• Terjadi tanpa adanya infeksi intrakranial, gangguan metabolik
• Kejang dengan demam pada anak yang pernah mengalami kejang
tanpa demam sebelumnya tidak termasuk dalam kriteria ini
• Pada anak usia 6 bulan-5 tahun
Etiologi
• Infeksi saluran napas atas (paling sering)
• Gastroenteritis
• ISK
Patofisiologi
• Diduga merupakan respon otak imatur terhadap peningkatan suhu yang
cepat
• Hipertermia  mengurangi mekanisme yang menghambat potensial aksi
dan meningkatkan transmisi sinaps eksitatorik
• Mutasi genetik dari kanal ion natrium dan reseptor GABA  gangguan
genetik yang mendasari kejang demam
• Faktor yang mungkin berperan:
Demam itu sendiri
Efek produk toksik dari mikroorganisme terhadap otak
Respon alergik atau keadaan imun abnormal
Perubahan keseimbangan atau elektrolit
Ensefalitis viral
Gabungan faktor tsb
Faktor resiko
• Demam
• Usia
• Riwayat kejang dalam keluarga
• Faktor perinatal dan pascanatal
• Faktor vaksinasi/imunisasi
Klasifikasi
KEJANG DEMAM SEDERHANA
• Singkat, <15 mnt
• Berhenti sendiri
• Kejang tonik dan/atau klonik, tanpa fokal
• Tidak berulang dlm 24 jam

KEJANG DEMAM KOMPLEKS

• Lama, >15 mnt
• Kejang fokal atau kejang umum yg didahului parsial
• Berulang >1x dalam 24 jam
Tanda & gejala
• Singkat
• Kejang klinik atau tonik-klonik bilateral
• Sering berhenti sendiri  anak tidak memberi reaksi apapun sejenak
 bbrp detik atau menit: sadar kembali
• Peningkatan suhu tubuh mendadak hingga >38 derajat celcius
Diagnosis
• Umur 6bln-4th
• sebentar, <15 mnt
• Kejang umum
• Timbul dalam 16 jam pertama setelah demam
• Px neurologis sblm dan sesudah demam  normal
• Px EEG 1 mg stlh suhu normal  tdk ada kelainan
• Frek bangkitan kejang dalam 1 th <4x
Tatalaksana
PENANGANAN FASE AKUT
• Pertahankan jalan napas
• Lindungi dr trauma
• Posisikan stgh duduk
• Longgarkan pakaian
• Oksigen
• Suction jika diperlukan
• Demam  kompres dan antipiretik
• Monitor tanda vital
• Antikonvulsan rektal  diazepam
• Antikonvulsan IV kalo 2x diazepam rectal ttp kejang atau masih kejang >15 mnt 
diazepam IV, atau lorazepam IV
MENCARI DAN MENGOBATI PENYEBAB
• Px cairan serebrospinal
• Px lab

PENGOBATAN PROFILAKSIS
• Profilaksis intermiten pd waktu demam
• Profilaksis terus menerus dengan antikonvulsan setiap hari 
diazepam intrarektal
Prognosis
• Kemungkinan mengalami kecacatan atau kelainan neurologis
• Perkembangan mental dan neurologis normal pd pasien yg sblmnya
normal
• Kemungkinan berulang
• Kemungkinan epilepsi  faktor resiko:
Kelainan neurologis atau perkembangan yang jelas sebelum kejang demam
pertama
Kejang demam yang pertama adalah kejang demam kompleks
Riwayat epilepsi pada orangtua atau saudara kandung
 Bila setelah pemberian diazepam rektal
kejang belum berhenti,
dapat diulang lagi dengan cara dan dosis
yang sama dengan
interval waktu 5 menit.

setelah 2 kali pemberian diazepam rektal masih

tetap kejang,
dianjurkan ke rumah sakit. Di rumah sakit
dapat diberikan
diazepam intravena dengan dosis 0,3-0,5
mg/kg.

Bila kejang telah berhenti,

pemberian obat selanjutnya
tergantung
dari jenis kejang demam apakah
kejang demam sederhana
atau kompleks dan faktor risikonya.
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Status Epilepticus
• Recurrent generalized convulsions at a frequency that precludes regaining of consciousness in the interval between seizures
(convulsive status)  serious problem in epilepsy
• Some patients who die of epilepsy do so because of
• uncontrolled seizures of this type
• Complicated by the effects of the underlying illness
• An injury sustained as a result of a convulsion
• Sign and symptoms :
• Rising temperature
• Acidosis
• Hypotension
• Renal failure from myoglobinuria
• Prolonged convulsive status (longer than 30 minutes)  carries a risk of serious neurologic sequelae  epileptic encephalopathy
• Etiology :
• Viral or paraneoplastic encephalitis
• Old traumatic injury
• Epilepsy with severe mental retardation
• Stroke
• Brain tumor
 Treatment

Adams and Victor’s Principles of Neurology 10th ed

Treatment
• Fact : that no one of them is altogether satisfactory and none is clearly superior
• Steps :
1. When the patient is first seen  an initial assessment of cardiorespiratory function is made
and an oral airway established
2. A large-bore IV line is inserted  blood is drawn for glucose is given (with thiamine if
malnutrition and alcoholism are potential factors)
3. To rapidly suppress the seizures  diazepam IV at a rate of about 2 mg/min until the
seizures stop or a total of 20 mg has been given or lorazepam 0,1 mg/kg IV push at a rate not
to exceed 2 mg/min
4. Immediately thereafter  loading dose (20 mg/kg) of phenytoin is administered by vein at a
rate of less than 50 mg/min  must be given through a freely running line with normal
saline and should not be injected IM-ly
5. In an epileptic patient known to be taking seizure medications chronically but in whom the
serum level of drug is unknown  it’s probably best to administer the full recommended
dose of phenytoin : if it can be established that the serum phenytoin is above 10 mg/mL 
lower loading dose may be advisable  if this fails to suppress seizures and status has
persisted for 20 to 30 min, an endotracheal tube should be inserted and O2 administered
Treatment

Clinical Neurology Lange 9th ed

www.aesnet.org/about_aes/press_releases/guidelines2016
Meningitis
• Consider meningitis if 
• headache + classic triad (fever, altered mentation & neck stiffness)
• high index of suspicion 
• Immunosuppression ps (AIDS, HIV, cancer history, chemotherapy, chronic steroids)
• LP is indicated for suspected meningitis
• If the LP is delayed (e.g., CT, coagulopathy, thrombocytopenia, agitation)
and meningitis is strongly suspected, administer antibiotics without delay.
• Ps who are awake, are alert with no evidence of papilledema or focal
neurologic deficit, and have no history to suggest immunocompromised
state or new-onset seizure  the head CT can be delayed until after the LP
Meningitis
• Classical symptoms 
• fever, headache, photophobia, nuchal rigidity,
lethargy, malaise, altered sensorium, seizures,
vomiting, and chills
• Subtle presentations  common esp in
immunosuppressed & geriatric patients 
ONLY alternation in mental status
• If (-) of fever, stiff neck, and mental status
change  excludes meningitis
• in children  clinical fx that increasing the
likelihood of bacterial meningitis 
• bulging fontanel, neck stiffness, and seizures in
children outside the age typical for febrile
convulsions
Meningitis
• The physical findings in meningitis  depending
on the host, causative organism, and severity of
the illness.
• Kernig’s sign & Brudzinski’s sign  (+) in
approximately 50% of adults.
• the sensitivity of Kernig’s sign, Brudzinski’s sign, &
(+) nuchal rigidity  5%, 5%, & 30%  these
physical findings have limited diagnostic value
• Ps w/ coma (GCS <9)  should not LP (risk for
herniation)
• Systemic findings in meningitis  obvious source
of infection (sinusitis, OM, mastoiditis,
pneumonia, or UTI), endocarditis, arthritis
Meningitis
Meningitis
Meningitis
Meningitis
MENINGITIS
• BACTERIAL MENINGITIS  acute confusional states
• Predisposing conditions include
• systemic (especially respiratory) or
• parameningeal infection,
• head trauma,
• anatomic meningeal defects,
• prior neurosurgery,
• cancer,
• alcoholism, and
• other immunodeficiency states.
• Bacteria  to the CNS by colonizing the mucous membranes of the
nasopharynx
•  leading to local tissue invasion, bacteremia, and hematogenous seeding of the
subarachnoid space.
• Bacteria can also spread to the meninges directly,
• through anatomic defects in the skull or
• from parameningeal sites such as the paranasal sinuses or middle ear.
•  Polysaccharide bacterial capsules, lipopolysaccharides, and outer
membrane proteins may contribute to bacterial invasion and virulence.
• The low levels of antibody and complement present in the cerebrospinal fluid are
inadequate to contain the infection.
 •  inflammatory response
• associated with the release of inflammatory cytokines that promote blood–brain barrier
permeability, vasogenic cerebral edema, changes in cerebral blood flow, and perhaps
direct neuronal toxicity
• Bacterial meningitis is characterized by
• leptomeningeal and perivascular infiltration with polymorphonuclear
leukocytes and an inflammatory exudate.
• tend to be most prominent in Streptococcus pneumoniae and Haemophilus infection
and Neisseria meningitidis.
• Brain edema
• hydrocephalus
• cerebral infarction
•  may occur, although bacterial invasion of the brain parenchyma is rare
• Clinical Findings
• most patients have had symptoms
of meningitis for 1 to 7 days.
• These include:
• fever,
• confusion,
• vomiting,
• headache, and
• neck stiffness,
•  but the full syndrome is not usually
• Physical examination
• Fever
• Signs of systemic or parameningeal infection
• such as skin abscess or otitis.
• A petechial rash is seen in 50% to 60% of patients with N. meningitidis meningitis.
• Signs of meningeal irritation (meningismus) are seen in approximately 80% of cases
•  often absent in the very young and very old, or with profoundly impaired consciousness.
• These signs include
• neck stiffness on passive flexion,
• thigh flexion on flexion of the neck (Brudzinski sign), and
• resistance to passive extension of the knee with the hip flexed (Kernig sign)
• The level of consciousness, when altered, ranges from mild confusion to coma.
• Focal neurologic signs, seizures, and cranial nerve palsies may occur.
• Papilledema is rare
• Laboratory Findings
• polymorphonuclear leukocytosis from systemic infection or leukopenia
caused by immunosuppression.
• organism can be cultured from the blood
• Images of the chest, sinuses, or mastoid bones may indicate a primary site of
infection.
• A brain CT or MRI scan  contrast enhancement of the cerebral convexities,
the base of the brain, or the ventricular ependyma.
• The EEG is usually diffusely slow, and focal abnormalities suggest the
possibility of focal cerebritis, abscess formation, or scarring.
• prompt lumbar puncture and CSF examination.
• CSF pressure is elevated in approximately 90% of cases, and the appearance
of the fluid ranges from slightly turbid to grossly purulent.
• CSF white cell counts of 1,000 to 10,000/μL are usually seen, consisting chiefly
of polymorphonuclear leukocytes
• Protein concentrations of 100 to 500 mg/dL are most common.
• The CSF glucose level is lower than 40 mg/dL in approximately 80% of cases
and may be too low to measure.
• Gram-stained smears of CSF
• CSF culture, which is positive in approximately 80% of cases,
• PCR has also been used with CSF specimens to identify the etiologic.
• Differential Diagnosis
• Signs of meningeal irritation also be seen with nonbacterial meningitis and
subarachnoid hemorrhage.
• However, the combination of an acute to subacute course (days rather than
weeks), polymorphonuclear pleocytosis, and low CSF glucose point to a
bacterial cause.
• Early viral meningitis can produce polymorphonuclear pleocytosis and
symptoms identical to those of bacterial meningitis,
• but a repeat lumbar puncture after 6 to 12 hours should demonstrate a shift to
lymphocytic predominance in viral meningitis, and the CSF glucose level is normal.
• Subarachnoid hemorrhage is distinctive in that lumbar puncture yields bloody CSF, which
does not clear as increasing amounts of CSF are removed
• Prevention
• Vaccines are available for three bacteria that can cause meningitis:
• H. influenzae type b,
• N. meningitidis, and
• S. pneumoniae.
• Children ages 2 to 15 months should be routinely immunized against H.
influenzae and S. pneumoniae,
• Children and adolescents ages 1 to 18 years against N. meningitidis, and
adults 65 years of age and older against S. pneumoniae.
• prophylactic administration of rifampin 20 mg/kg/d orally given as a single daily dose for
4 days (H. influenzae) or as two divided doses for 2 days (N. meningitidis)
• Treatment
• Unless the physical examination shows focal neurologic abnormalities or
papilledema, suggesting a mass lesion, lumbar puncture should be performed
immediately;
• if the CSF is not clear and colorless  antibiotic treatment is started without delay.
• When focal signs or papilledema are present,
• blood and urine should be taken for culture, antibiotics begun, and a brain CT scan obtained.
• If the scan shows no focal lesion that would contraindicate lumbar puncture, the puncture is
then performed.
• The initial choice of antibiotics is empirical, based on the patient’s age and predisposing
factors
• Therapy is adjusted as indicated when the Gram stain or culture and sensitivity results
become available
• Lumbar puncture can be repeated to assess the response to therapy.
• CSF should be sterile after 24 hours, and a decrease in pleocytosis and in the proportion of
polymorphonuclear leukocytes should occur within 3 days.
• Dexamethasone, given immediately before the onset of antibiotic treatment and
continued for 4 days,
•  may improve outcome and decrease mortality in immunocompetent patients with
confirmed bacterial meningitis
• Prognosis
• Complications of bacterial meningitis
• headache, seizures, hydrocephalus, syndrome of inappropriate secretion of antidiuretic hormone
(SIADH), residual neurologic deficits (including cognitive disturbances and cranial—especially VIII—
nerve abnormalities), and death.
• a CT or MRI scan will confirm suspected hydrocephalus, and fluid and electrolyte status should be
carefully monitored to detect SIADH.
• N. meningitidis infections may be complicated by adrenal hemorrhage related to meningococcemia
(Waterhouse-Friderichsen syndrome),  hypotension and often death.
• Morbidity and mortality from bacterial meningitis are high.
• Fatalities occur in approximately 20% of affected adults, and more often with some pathogens (eg,
S. pneumoniae, gram-negative bacilli) than others (eg, H. influenzae, N. meningitidis).
• Factors that worsen prognosis include extremes of age, delay in diagnosis and treatment,
complicating illness, stupor or coma, seizures, and focal neurologic signs
VIRAL MENINGITIS & ENCEPHALITIS
• Viral infections of the meninges (meningitis) or brain parenchyma
(encephalitis)  acute confusional states.
• viruses (eg, herpesviruses) can cause either meningitis or encephalitis,
• but others preferentially affect the meninges (eg, enteroviruses) or brain
parenchyma (eg, arthropod-borne—or arbo—viruses).”
• Viral infections can affect the CNS in three ways
• hematogenous dissemination of a systemic viral infection (eg, arthropod-borne
viruses),
• neuronal spread of the virus by axonal transport (eg, herpes simplex, rabies),
• autoimmune postinfectious demyelination (eg, varicella, influenza).
• Pathologic changes in viral meningitis consist of an inflammatory
meningeal reaction mediated by lymphocytes.
 • Encephalitis is characterized by
• perivascular cuffing,
• lymphocytic infiltration, and
• microglial proliferation mainly involving subcortical gray matter regions.
• Intranuclear or intracytoplasmic inclusions are often seen
• Clinical manifestations of viral meningitis
• include fever, headache, neck stiffness, photophobia, pain with eye movement, and mild
impairment of consciousness.
• Patients usually do not appear as ill as those with bacterial meningitis.
• Systemic viral infection may cause
• skin rash, pharyngitis, lymphadenopathy, pleuritis, carditis, jaundice, organomegaly, diarrhea, or orchitis,
and these findings may suggest a particular etiologic agent.
• Because viral encephalitis involves the brain directly,
•  more marked alterations of consciousness, seizures, and focal neurologic signs can occur.
• When signs of meningeal irritation and brain dysfunction coexist, the condition is termed
meningoencephalitis
• LAB FINDING
• CSF analysis is the most important laboratory test.
• CSF pressure is normal or increased,
• a lymphocytic or monocytic pleocytosis is present, with cell counts usually less than
1,000/mL.
• Higher counts can be seen in lymphocytic choriomeningitis or herpes simplex encephalitis.
• A polymorphonuclear pleocytosis can occur early in viral meningitis,
• whereas red blood cells may be seen with herpes simplex encephalitis.
• Protein is normal or slightly increased (usually 80-200 mg/dL).
• Glucose is usually normal, but may be decreased in mumps, herpes zoster, or herpes simplex
encephalitis.
• An etiologic diagnosis often can be made from
• CSF by virus isolation, polymerase chain reaction, or detection of antiviral antibodies.
• Blood counts may show a normal white cell count, leukopenia, or mild leukocytosis.
• Atypical lymphocytes in blood smears and a positive heterophil (Monospot) test suggest
infectious mononucleosis.
Meningitis

• Meningitis is a clinical syndrome characterized by inflammation of the

meninges
• Etiology : Bacterial, Viral, Fungus, Secondary (Malignancy)

https://emedicine.medscape.com/article/232915
Signs and symptoms

The classic triad of bacterial meningitis consists of the following:

• Fever
• Headache
• Neck stiffness
Other symptoms can include nausea, vomiting, photalgia
(photophobia), sleepiness, confusion, irritability, delirium, and coma.

https://emedicine.medscape.com/article/232915
Diagnosis

The diagnostic challenges in patients with clinical findings of meningitis are as

follows:
• Early identification and treatment of patients with acute bacterial meningitis
• Assessing whether a treatable CNS infection is present in those with suspected
subacute or chronic meningitis
• Identifying the causative organism
Blood studies that may be useful include the following:
• Complete blood count (CBC)
• Serum electrolytes
• Serum glucose (which is compared with the CSF glucose)
• Blood urea nitrogen (BUN) or creatinine and liver profile

https://emedicine.medscape.com/article/232915
Management

Initial measures include the following:

• Shock or hypotension – Crystalloids
• Altered mental status – Seizure precautions and treatment (if necessary), along with
airway protection (if warranted)
• Stable with normal vital signs – Oxygen, IV access, and rapid transport to the emergency
department (ED)
Treatment of bacterial meningitis includes the following:
• Prompt initiation of empiric antibacterial therapy as appropriate for patient age and
condition
• After identification of the pathogen and determination of susceptibilities, targeted
antibiotic therapy as appropriate for patient age and condition
• Steroid (typically, dexamethasone) therapy
• In certain patients, consideration of intrathecal antibiotics

https://emedicine.medscape.com/article/232915
http://www.aafp.org/afp/2010/1215/afp20101215p1491-f1.gif
Seizures
• Seizures are disorders characterized by temporary neurologic signs or
symptoms resulting from abnormal, paroxysmal, and
hypersynchronous electrical neuronal activity in the cerebral cortex
Seizures require 3 conditions
• A population of pathoogically excitable neurons
• An increase in excitatory, mainly glutaminergic, activity through
recurrent connections in order to spread the discharge
• A reduction in the activity of the normally inhibitory GABAergic
projections
Etiology

Clinical Neurology Lange 9th ed

 Clinical Neurology Lange 9th ed

Adams and Victor’s Principles of Neurology 10th ed

IDIOPATHIC (CRYPTOGENIC) SEIZURES
• These account for two-thirds of new onset seizures in the general population

HEAD TRAUMA
• Is a common cause of epilepsy, particularly when it occurs perinatally or is
associated with a depressed skull fracture or intracerebral or subdural hematoma

STROKE
• Stroke affecting the cerebral cortex produces seizures in 5% to 15% of patients
and can occur after thrombotic or embolic infartion or intracerebral hemorrhage
• Vascular malformations may be associated with seizures, presumably as a result
of their irritative effects on adjacent brain tissue
MASS LESIONS
• Mass lesions, such as brain tumors or abscesses, can present with seizures
• Glioblastomas, astrocytomas, andmeningiomas are the most common tumors
associated with seizures

MENINGITIS OR ENCEPHALITIS
• Bacterial (Haemophilus influenzae or tuberculous), viral (HSV), fungal, or parasitic
(cysticercosis) infections can also cause seizures

DEVELOPMENTA ANOMALIES
• Cortical dysgenesis and neuronal migration disorders can predispose to epilepsy
Systemic disorders
• Hypoglycemia: especially with serum glucose levels of 20-30 mg/dL
• Hyponatremia: associated with seizures at serum sodium levels <120 mEq/L or at
higher levels after a rapid decline
• Hyperosmolar states: including both hyperosmolar nenketotic hyperglycemia and
hypernatremia
• Hypocalcemia: with serum calcium levels 4,3-9,2 mg/dl can produce seizures with
ot without tetany
• Uremia
• Hepatic encephalopathy
• Porphyria
• Drug overdose: the drugs most frequently associated with seizures are
antidepressants, antipsychotics, cocaine, insulin, isoniazid, lidocaine, and
methylxanthines
• Global cerebral ischemia from cardiac arrest, cardiac arrhytmias, or
hypotension  may produce, at onset, a few tonic or tonic-clonic
movements
• Hypertensive encephalopathy may be accompained by generalized
tonic-clonic or partial seizures
• Eclampsia
• Hyperthermia can resut from infection, exposure, hypothalamic
lesions, or drugs
Classification
• Generalized seizures
Tonic-clonic (grand mal)
Absence (petit mal)
Other types (tonic, clonic, myoclonic, atonic)
• Partial (focal) seizures
Simple partial
Complex partial
Partial seiures with secondary generalization
• Unclassifiable
Clinical Neurology Lange 9th ed
 Treatment of
Seizures

Tatalaksana farmakologi
• tujuan: menciptakan seizure free state
dengan efek samping minimal
• u/ pengobatan inisial: berikan 1 macam obat
sampai dosis terapeutik maksimal tercapai,
jika tetap tidak dapat menangani kejangnya,
ganti dengan obat lain

Adams and Victor’s Principle of Neurology 10th ed

Harrison Principle of Internal

Medicine
https://microbiologyinfo.com/wp-content/uploads/2015/12/Difference-Between-Meningitis-and-Encephalitis.jpg
 Encephalitis
• Inflammation in brain parenchyma resulting in neurologic dysfunction

• Most common in children <1 yo and young children

HSV Encephalitis
HSV - 1 HSV - 2
• HSV 1 infection (most common)  • Usually occurs in neonate (vertical infection
gingivostomatitis (herpetic lesion of oral
mucosa)  axonal transport to trigeminal from the mother during labor)
ganglion (latent infection)  invasion of • In adults caused by aseptic meningitis,
olfactory bulb trough nasal mucosa 
invasion to inferomedial or lateral portion of polyradiculitis, myelitis, and recent HSV-2
frontal & temporal lobes and the insula infection
• Resulting in olfactory/gustatory
hallucinations, anosmia, temporal lobe • Causing acute generalized encephalitis 
seizures, personality change, bizzare or much severe than HSV-1 type
psychotic behavior or delirium, aphasia,
hemiparesis, disturb memory function
• Swelling of temporal lobes  herniation 
coma in the 1st few days (poor prognostic
signs)
Encephalitis signs and symptoms

• fever,
• headache,
• nausea and vomiting,
• lethargy, and
• myalgias

https://emedicine.medscape.com/article/791896
Diagnosis
A lumbar puncture (LP) should be performed in all cases of suspected viral encephalitis.
Imaging modalities that may be helpful include the following:
• CT
• MRI
• EEG
Blood and urine tests that may be helpful include the following:
• Complete blood count (CBC)
• Serum electrolyte levels
• Serum glucose level
• Blood urea nitrogen (BUN) and creatinine levels
• Urine or serum toxicology screening

https://emedicine.medscape.com/article/791896
Imaging Findings
• CT : hypodensity of the affected temporal lobe
 Management

Management in the prehospital setting includes the following:

• Evaluation and treatment for shock or hypotension
• Airway protection (in patients with altered mental status)
• Seizure precautions
• Oxygen and IV access secured en route to the hospital (all patients)

*Acyclovir IV 30mg/kg/d and continued for 10-14 days in order to prevent relapse

https://emedicine.medscape.com/article/791896
INTRACRANIAL HEMORRHAGE

• Traumatic intracranial hemorrhage can be epidural, subdural, or intracerebral

• Epidural hematoma
• most often results from a lateral skull fracture that lacerates the middle
meningeal artery or vein.
• may or may not lose consciousness initially,
• event a lucid interval (several hours to 1 to 2 days )
• of headache,
• progressive obtundation,
• hemiparesis, and
• finally ipsilateral pupillary dilatation from uncal herniation.
• Death may follow if treatment is delayed.
• Subdural hematoma
• after head injury can be acute, subacute, or chronic.
• In each case, headache and altered consciousness are the principal
manifestations.
• Delay in diagnosis and treatment  fatal outcome.
• In contrast to epidural hematoma,
• the time between trauma and the onset of symptoms is typically longer,
• the hemorrhage tends to be located over the cerebral convexities, and
• associated skull fractures are uncommon.
• diagnosis  CT scan or MRI.
 • Epidural hematoma 
• appear as a biconvex, lens-shaped, extra-
axial mass that may cross the midline or the
tentorium
• but not the cranial sutures.
• Subdural hematoma 
• is typically crescent shaped and may cross
the cranial sutures
• but not the midline or tentorium.
• treated by surgical evacuation.
• depends on the clinical course and
location.
• Evacuation, decompression, or shunting
for hydrocephalus may be indicated.
 Epidural Haematoma
• Sign & symptoms
• Severe headache
• Nausea & vomiting
• Dizziness
• Seizure
• Sleepiness
• Level of consciousness may be decreased, with decreased or fluctuating GCS
• Contusion, laceration, or bony step-off may be observed in the area of injury

Hostetler MA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier. 2013
http://emedicine.medscape.com/article/824029-clinical#b4
 Epidural Haematoma
• On CT scan, an EDH appears hyperdense, biconvex, ovoid, and
lenticular
• The EDH does not usually extend beyond the dural attachments at
the suture lines
• The margins are sharply defined and the hematoma usually bulges
inward toward the brain
• EDHs of mixed density on CT may be actively bleeding

Hostetler MA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier. 2013
 Epidural Haematoma

Figure 41-9. Non–contrast-enhanced computed tomography scan of

acute epidural hematoma at the level of right midconvexity. There is an
associated mass effect and moderate midline shift.

Hostetler MA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier. 2013
 Epidural Haematoma
• Treatment
• Establish IV access, administer oxygen, monitor, and administer IV crystalloids as
necessary to maintain adequate blood pressure
• Intubate, which generally includes premedication with lidocaine, a cerebroprotective
sedating agent (eg, etomidate), and a neuromuscular blocking agent
• Elevate head of the bed 30° after the spine is cleared, or use reverse Trendelenburg
position to reduce ICP and increase venous drainage
• Administer mannitol 0.25-1 g/kg IV after consulting a neurosurgeon if MAP is greater
than 90 mm Hg with continued clinical signs of increased ICP
• Phenytoin  early posttraumatic seizures
• Epidurals greater than 30 cm^3 in volume should be evacuated surgically, regardless
of the patient’s GCS score
• It is strongly recommended that comatose patients with an acute EDH and anisocoria
on pupillary examination undergo surgical evacuation as soon as possible
Hostetler MA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier. 2013
http://emedicine.medscape.com/article/824029-treatment#d10
 Epidural Haematoma
• Complication
• Neurobehavioral changes
• Vegetative state
• Death

http://emedicine.medscape.com/article/824029-followup#e6
http://surgicalneurologyinternational.com/blog/wp-content/uploads/2011/09/BTF_EDH_FC.gif
 Subdural Haematoma
• Clinical presentation • Clinical presentation (Acute
(Chronic SH) SH)
• Decreased level of • Headache
consciousness • Nausea
• Headache • Confusion
• Difficulty with gait or • Personality change
balance
• Decreased level of
• Cognitive dysfunction or consciousness
memory loss
• Speech difficulties
• Personality change
• Other change in mental
• Motor deficit (eg,
hemiparesis) status
• Aphasia • Impaired vision or double
vision
• Weakness
http://emedicine.medscape.com/article/1137207-overview#a7
 Subdural Haematoma
• Physical Examination  • Physical Examination 
neurologic findings
(Chronic SH)
• Mental status changes
• Papilledema
• Hyperreflexia or reflex
asymmetry
• Hemianopsia
• Hemiparesis
• Third or sixth cranial
nerve dysfunction
neurologic findings (Acute
SH)
• Altered level of
consciousness
• A dilated or nonreactive pupil
ipsilateral to the hematoma
(or earlier, a pupil with a
more limited range of
reaction)
• Hemiparesis contralateral to
the hematoma
http://emedicine.medscape.com/article/1137207-clinical#b3
 Subdural Haematoma
• Initial blood tests include the following:
• Complete blood count
• Hemoglobin or hematocrit
• Coagulation profile
• Basic metabolic panel

http://emedicine.medscape.com/article/1137207-workup
 Subdural Haematoma
• On noncontrast CT scan, an acute subdural hematoma appears as a
hyperdense (white), crescent-shaped mass between the inner table of
the skull and the surface of the cerebral hemisphere
• Subdural hematomas are concave toward the brain and unlimited by
suture lines, as opposed to epidural hematomas, which are convex
toward the brain and restricted by suture lines
• Acute subdural hematomas are usually unilateral

http://emedicine.medscape.com/article/1137207-workup#c9
Subdural Haematoma

Acute right-sided subdural hematoma associated with significant

midline shift shown on CT scan

http://emedicine.medscape.com/article/1137207-workup#c9
 Subdural Haematoma
• Treatment
• As with any trauma patient, resuscitation begins with the ABCs (airway,
breathing, circulation)
• All patients with a Glasgow Coma Scale (GCS) score of less than 8 should be
intubated for airway protection
• Patients often require intensive care postoperatively for ventilator-dependent
respiration, strict blood pressure control, and management of intracranial
hypertension
• Surgery for emergent decompression has been advocated if the acute
subdural hematoma is associated with a midline shift greater than or equal to
5 mm

http://emedicine.medscape.com/article/1137207-treatment
http://emedicine.medscape.com/article/1137207-treatment#d10
https://www.researchgate.net/figure/256451993_fig3_Fig-3-Recommended-treatment-algorithm-for-patients-with-
traumatic-posterior-fossa
 Subdural Haematoma
• Complication:
• Brain herniation
• Persistent symptoms such as memory loss, dizziness, headache, anxiety and
difficulty concentrating
• Seizures
• Temporary or permanent weakness, numbness, difficulty speaking

https://medlineplus.gov/ency/article/000713.htm
Delirium
• Delirium, acute confusional state,
acute cognitive impairment, acute
encephalopathy, altered mental
status, and other synonyms  refer
to a transient disorder with
impairment of attention and
cognition.
• The patient has difficulty focusing,
shifting, or sustaining attention.
• Confusion may fluctuate
Coma
• PATHOPHYSIOLOGY
• can result from deficiency of substrates
needed for neuronal function (as with
hypoglycemia or hypoxia).
• systemic causes  the brain is globally
affected  lacking the signs of localize
dysfunction to a specific area of the
brainstem or cortex.
 MM infark serebral (STROKE)
• Stroke is generally defined as any disease process that interrupts blood flow to
the brain.
• Injury is related to the loss of oxygen and glucose substrates necessary for high-energy
phosphate production and the presence of mediators of secondary cellular injury.
• Subsequent factors, such as edema and mass effect, may exacerbate the initial insult.
• STROKETYPE
• Stroke results from two major mechanisms:
• ischemia and hemorrhage.
• Ischemic strokes account for 87% of all strokes and are categorized by cause:
•  thrombotic, embolic, or hypoperfusion related.
• Hemorrhagic strokes are subdivided into
• intracerebral (accounting for 10% of all strokes) and
• nontraumatic subarachnoid hemorrhage (accounting for 3% of all strokes)
• The final common pathway for all of these mechanisms is altered neuronal perfusion.
• Neurons are exquisitely sensitive to changes in cerebral blood flow and die within minutes of complete
cessation of perfusion—hence, the current treatment emphasis on rapid reperfusion strategies.
CLINICAL FEATURES
• The clinical presentation of stroke can range from
• the obvious (facial droop, arm drift, abnormal speech) to
• the subtle (generalized weakness, lightheadedness, vague sensory changes,
altered mental status).
• Sudden onset of symptoms suggests an embolic or hemorrhagic stroke,
• whereas a stuttering or waxing and waning deficit suggests a thrombotic or
hypoperfusion-related stroke
• Risk factors for vessel thrombus include:
• hypertension, diabetes mellitus, and coronary atherosclerotic disease.
• In contrast, atrial fibrillation, valvular replacement, or recent myocardial
infarction  suggests embolism.
PHYSICAL EXAMINATION
• Airway, breathing, and circulation are the top priorities.
• Next, the goals of examination are to confirm the diagnosis of stroke, exclude
stroke mimics, and identify comorbidities.
• Fever should prompt an investigation for potential infection.
• CNS infections (meningitis, encephalitis) may mimic a stroke, or
• an infection such as aspiration pneumonia or a urinary tract infection may be a
complication of the stroke.
• Look for meningismus, signs of emboli (Janeway lesions and Osler nodes), and bleeding
diatheses (ecchymoses or petechiae).
• A funduscopic examination may identify signs of
• papilledema (suggesting a mass lesion, cerebral vein thrombosis, or hypertensive crisis)
• or preretinal hemorrhage (consistent with subarachnoid hemorrhage).
ISCHEMIC STROKE SYNDROMES
• ANTERIOR CEREBRAL ARTERY INFARCTION
• Occlusion of the anterior cerebral artery is uncommon (0.5% to 3% of all
strokes),
• but when unilateral occlusion occurs, it can cause contralateral sensory and
motor symptoms in the lower extremity, with sparing of the hands and face.
• In addition, a left-sided lesion is typically associated with akinetic mutism and
transcortical motor aphasia (repetition ability retained),
• whereas right-sided infarction can result in confusion and motor hemineglect.
• Bilateral occlusion can cause a combination of the above symptoms, but was
particularly associated with mutism, incontinence, and poor outcome in one
small series.
• MIDDLE CEREBRAL ARTERY INFARCTION
• is the vessel most commonly involved in stroke, and clinical findings can be quite
variable, depending on exactly where the lesion is located and which brain
hemisphere is dominant.
• (In right-handed patients and in up to 80% of left-handed patients, the left
hemisphere is dominant.)
• A middle cerebral artery stroke typically presents with
• hemiparesis, facial plegia, and sensory loss contralateral to the affected cortex.
• These deficits variably affect the face and upper extremity more than the lower extremity.
• If the dominant hemisphere is involved,
• aphasia (receptive, expressive, or both) is often present.
• If the nondominant hemisphere is involved,
• inattention, neglect, extinction on double simultaneous stimulation,
• dysarthria without aphasia, and constructional apraxia (difficulty in drawing complex two-
dimensional or three-dimensional figures) may occur.
• A homonymous hemianopsia and gaze preference toward the side of the infarct may also be
seen, regardless of the side of the infarction.
• POSTERIOR CEREBRAL ARTERY INFARCTION (DISTAL POSTERIOR
CIRCULATION)
• The classic symptoms and signs of posterior circulation strokes include
• ataxia, nystagmus, altered mental status, and vertigo, but presentation can sometimes be
rather subtle.
• Crossed neurologic deficits (e.g., ipsilateral cranial nerve deficits with contralateral
motor weakness) may indicate a brainstem lesion.
• Symptoms of posterior cerebral artery involvement include
• unilateral limb weakness, dizziness, blurry vision, headache, and dysarthria.
• Common presenting signs include visual field loss, unilateral limb weakness, gait ataxia,
unilateral limb ataxia, cranial nerve VII signs, lethargy, and sensory deficits.
• Visual field loss, classically described as contralateral homonymous hemianopsia and
unilateral cortical blindness, is thought to be specific for distal posterior circulation stroke
because the visual centers of the brain are supplied by the posterior cerebral artery.
• Light-touch and pinprick sensation deficits, loss of ability to read (alexia) without agraphia,
inability to name colors, recent memory loss, unilateral third nerve palsy, and hemiballismus
have also been reported.
• Motor dysfunction, although common, is typically minimal, which can keep some patients
from realizing they have had a stroke.
• BASILAR ARTERY OCCLUSION (MIDDLE POSTERIOR CIRCULATION)
• Occlusion of the basilar artery most commonly presents with symptoms of unilateral
limb weakness, dizziness, dysarthria, diplopia, and headache.
• The most common presenting signs are unilateral limb weakness, cranial nerve VII
signs, dysarthria, Babinski sign, and oculomotor signs.
• Dysphagia, nausea or vomiting, dizziness, and Horner’s syndrome are positively
correlated with basilar artery occlusion.
• Basilar artery occlusion can also rarely cause locked-in syndrome, which occurs with
bilateral pyramidal tract lesions in the ventral pons and is characterized by complete
muscle paralysis except for upward gaze and blinking.
• Basilar artery occlusions have a high risk of death and poor outcomes
• VERTEBROBASILAR INFARCTION (PROXIMAL POSTERIOR CIRCULATION)
• Patients with vertebrobasilar infarction most commonly present with symptoms of:
• dizziness, nausea or vomiting, headache, dysphagia, unilateral limb weakness, and unilateral
cranial nerve V symptoms
• Common presenting signs include:
• unilateral limb ataxia, nystagmus, gait ataxia, cranial nerve V signs, limb sensory deficit, and
Horner’s syndrome.
• CEREBELLAR INFARCTION
• Patients with cerebellar infarction can present with very nonspecific symptoms and
frequently present with:
• dizziness (with or without vertigo), nausea and vomiting, gait instability, headache, limb ataxia,
dysarthria, nystagmus, and cranial nerve abnormalities.
• Mental status may vary from alert to comatose.
• Because CT is inadequately sensitive for posterior fossa lesions, obtain a diffusion-weighted
MRI (DWI-MRI) when this diagnosis is suspected.
• The clinical presentation and course of cerebellar infarction can be frustratingly difficult to
predict, but the clinician must remain vigilant to the possibility of rapid deterioration
secondary to increased brainstem pressure caused by cerebellar edema.
• Therefore, extremely close serial examinations (especially looking for gaze palsy and altered mental
status) and prompt neurologic and neurosurgical bedside consultations are needed.
• Obtain early neurosurgical consultation for patients with cerebellar infarction.
• Cerebellar edema can lead to rapid deterioration with herniation, and consultation is required to
determine the need for emergency posterior fossa decompression in these patients.
• Acute obstructing hydrocephalus requires treatment of elevated intracranial pressure and emergent
surgical decompression.
HEMORRHAGIC STROKE SYNDROMES
• INTRACEREBRAL HEMORRHAGE
• may be clinically indistinguishable from ischemic infarction, but the two conditions are
distinct clinical entities in terms of management, with higher levels of morbidity and
mortality for hemorrhage than for ischemic infarction
• Therefore, perform imaging to differentiate between the two.
• Headache, nausea, and vomiting often precede the neurologic deficit, and the patient’s
condition may quickly deteriorate
• CEREBELLAR HEMORRHAGE
• may be clinically indistinguishable from cerebellar infarction.
• SUBARACHNOID HEMORRHAGE
• typically characterized by a severe occipital or nuchal headache.
• Patient history includes the recent sudden onset of a maximal-intensity headache in many
cases.
• Careful history taking may reveal activities associated with a Valsalva maneuver, such as
defecation, sexual activity, weight lifting, or coughing, at stroke onset
 Diagnosis
• Brain Imaging Obtain emergency non–contrast-
enhanced CT for suspected acute stroke.
• Most acute ischemic strokes are not visualized by a
noncontrast brain CT in the early hours of a stroke.
• Therefore, the utility of the first brain CT is primarily
to exclude:
• intracranial bleeding,
• abscess, tumor, and other stroke mimics, as well • However, in the vast majority of EDs, a non–
as to detect current contraindications to contrast-enhanced CT is the most readily
thrombolytics available imaging study and is the only
• The CT scan should be reviewed by the most expert imaging study necessary prior to
interpreter available within 45 minutes of patient administration of rtPA
arrival, especially if thrombolytic therapy is being
considered.
• Despite these caveats, the current AHA/ASA acute
ischemic stroke guidelines recommend either non–
contrast-enhanced CT or MRI as the initial imaging in
the acute stroke patient.
GENERAL TREATMENT OF ACUTE ISCHEMIC
STROKE
• STANDARD TREATMENT
• DEHYDRATION
• Dehydration can contribute to poor stroke outcomes secondary to increased blood viscosity,
hypotension, renal impairment, and venous thromboembolism.
• Correct dehydration with IV isotonic crystalloid.
• For euvolemic patients, provide maintenance fluids.
• HYPOXIA
• The 2013 AHA/ASA consensus guidelines recommend oxygen administration to patients in stable condition only
as necessary to maintain oxygen saturation >94% and to maintain normoxia.
• Routine normobaric oxygen administration does not appear to improve short- or long-term outcomes in mild to
moderate stroke and oxygen administration has been associated with increased stroke mortality.
• Hyperbaric oxygenation is not currently recommended
• HYPERPYREXIA
• Fever is associated with increased morbidity and mortality in stroke, possibly due to increased metabolic
demand and free radical production
• Identify the source of fever and treat with acetaminophen. 7

• HYPERTENSION
• For patients who are not candidates for thrombolytics or reperfusion measures, the guidelines call for
permissive hypertension, with no active attempts made to lower blood pressure unless the systolic
blood pressure is >220 mm Hg or the diastolic blood pressure is >120 mm Hg or if the patient has
another medical condition that would benefit from lowering blood pressure.
• If the decision has been made to initiate blood pressure control, a suggested target is a 15% reduction in
systolic blood pressure for the first 24 hours
• Conversely, blood pressure control is essential prior to, during, and after
thrombolytic therapy.
• A systolic blood pressure >185 mm Hg or a diastolic blood pressure >110 mm Hg is a
contraindication to the use of rtPA
•  because elevated blood pressure is associated with hemorrhagic transformation of ischemic
stroke.
• Therefore, if a patient is a candidate for rtPA, actively attempt to lower blood pressure to meet
these entry parameters.
• If the target arterial blood pressures for rtPA administration cannot be reached with these
measures, then the patient is no longer a candidate for rtPA therapy.
• HYPERGLYCEMIA
• The current AHA/ASA guidelines recommend the maintenance of blood glucose from 140
milligrams/dL (7.77 mmol/L) to 180 milli- grams/dL (9.99 mmol/L). Avoid, and treat,
hypoglycemia (<60 milli- grams/dL [3.33 mmol/L]).
• Hyperglycemia is common in acute stroke, and glycemic control has been recommended
82

based on data that associate less favorable outcomes with hyperglycemia

• However, glycemic control must avoid hypoglycemia, which in itself can result in brain
dysfunction
• ASPIRIN
• The current AHA/ASA guidelines recommend the oral administration of
aspirin (initial dose is 325 milligrams) within 24 to 48 hours after stroke onset.
• However, no antiplatelet agent (including aspirin) should be given within 24
hours of rtPA therapy.
• Studies demonstrate significant reduction in mortality and morbidity rates (at
4 weeks and 6 months) when aspirin is administered to acute ischemic stroke
patients within 48 hours.
• The benefit seems due mainly to reduction of recurrent stroke.
• aspirin is cost-effective and adds no risk to the outcome of ischemic stroke
LI12 Subarachnoid Hemorrhage
• Subarachnoid hemorrhage  resulting from rupture of an
intracranial aneurysm “worst headache of my life”
• Early detection & appropriate management  lead to improved
clinical outcome
• 1st step in evaluation  Obtain a noncontrast head CT
• If head CT: (-) for blood but suspicion for SAH is strong  next step is
LP to detect blood or xanthochromia in the cerebrospinal fluid
Subarachnoid Hemorrhage
• SAH  extravasated blood in the
subarachnoid space.
• (+) of the blood  activates meningeal
nociceptors  diffuse occipital pain + signs
of meningismus.
• SAH >10% of all strokes the most common
cause of sudden death from a stroke.
• Cerebral aneurysms  focal arterial pouches
typically located in areas of bifurcation of the
circle of Willis
• larger aneurysms (>5–10 mm)  more likely to
rupture
Subarachnoid Hemorrhage
• CLINICAL FEATURES:
• Classically present to the ED w/  severe headache of acute onset
(“thunderclap” headache)  reaches max intensity within minutes
• Headaches associated w/ loss of consciousness, seizure, diplopia or other
neurologic signs, or nuchal rigidity  require clinical investigation
• Less frequent  may (+) w/ nausea & vomiting, altered mental status,
photophobia, or symptoms suggestive of ischemic stroke
• Ps develop symptoms while engaged in activities that cause increased BP
(exercise, sexual intercourse, or defecation).
• If uncomplicated true syncope without head trauma, headache, seizure,
neurologic deficits, nuchal rigidity, or other symptoms of SAH  does not
require evaluation for SAH .
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
• Dx:
• Patients with SAH who are
misdiagnosed at their initial ED visit
 have worse outcomes
• Misdiagnosis is associated w/ 
• normal mental status (+ ½ of ps w/
SAH)
• smaller size of hemorrhage
• Imaging
• Initial dx/ modality of choice 
noncontrast CT of the head
• sensitivity highest shortly after
symptoms begin & 98% within 6 to 12
h of the onset
• LP  For suspected SAH + (-) head CT
• CT/CT angiography (CTA) & MRI/MRA
 options
• Lumbar Puncture
• CSF analysis  when normal result on
head CT.
• advantage of LP  identify other
causes of headache (meningitis /
intracranial hypertension)
• disadvantages of LP  post-LP
headache & inability to perform in the
patient with coagulopathy or
thrombocytopenia.
• (+) Xanthochromia
• normal findings on head CT, the (-) of
xanthochromia, and zero or few
RBCs (<5 x 106 RBCs/L) in the CSF 
exclude SAH
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
• TREATMENT
• Medical management of the SAH ps in the ED  occur in a monitored critical care area and
should target the prevention of complications.
• Check the GCS & pupillary responses regularly  decrease of 1 GCS point can indicate the
onset of complications.
• The risk of rebleeding  >> in the first 24 hours  can be reduced by adequate BP control
• MAP of <140 mm Hg  reasonable target while avoiding hypotension
• The BP  fluctuate through the course of the disease  a titratable IV antihypertensive is preferred.
• Labetalol and nicardipine  most often used.
• Avoid nitroprusside and nitroglycerin  can increase cerebral blood volume and ICP
• Pain management
• Antiemetics
• Vasospasm  most common 2 days to 3 weeks after SAH
• Nimodipine  60 mg PO every 4 hours  initiated within 96 hours of symptom onset unless
contraindicated
 LI12 Subarachnoid Haemorrhage
• Sign & symptoms
• Sudden onset of severe headache (the classic feature)
• Accompanying nausea or vomiting
• Symptoms of meningeal irritation
• Photophobia and visual changes
• Focal neurologic deficits
• Sudden loss of consciousness at the ictus
• Seizures during the acute phase
 Subarachnoid Haemorrhage
• Diagnosis  laboratory studies
• Serum chemistry panel - To establish a baseline for detection of future
complications
• Complete blood count - For evaluation of possible infection or hematologic
abnormality
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For
evaluation of possible coagulopathy
• Blood typing/screening - To prepare for possible intraoperative transfusions
• Cardiac enzymes - For evaluation of possible myocardial ischemia
• Arterial blood gas (ABG) - Necessary in patients with pulmonary compromise

http://emedicine.medscape.com/article/1164341-workup#c1
 Subarachnoid Haemorrhage
• Diagnosis  CT-scan
• CT without contrast is the most sensitive imaging study in SAH
• When carried out within 6 hours of headache onset, CT has 100% sensitivity
and specificity

A 47-year-old woman presented

with headache and vomiting; her
CT scan in the emergency
department revealed subarachnoid
hemorrhage

http://emedicine.medscape.com/article/1164341-workup#c8
 Subarachnoid Haemorrhage
• Diagnosis
• Lumbar puncture
• Cerebral angiography
• CT angiography
• MRI

http://emedicine.medscape.com/article/1164341-workup#c9,c10,c11,c12
 Subarachnoid Haemorrhage
• Treatment
• Assess the level of consciousness and airway, breathing, and
circulation (ABCs)
• Post-traumatic vasospasm is common, occurring approximately
48 hours after injury and persisting for up to 2 weeks
• Calcium channel blockers (e.g., nimodipine and nicardipine)
have been used in the acute intensive care unit setting
• to prevent or reduce vasospasm after TSAH
• Monitoring should include the following:
• Cardiac monitoring
• Pulse oximetry
• Automated and/or arterial blood pressure monitoring (arterial BP
monitoring is indicated in high-grade SAH or when blood pressure is
labile)
• Urine output via placement of a Foley catheter
Hostetler MA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier. 2013
http://emedicine.medscape.com/article/1164341-workup#c9,c10,c11,c12
Diagnostic Algorithm for Subarachnoid Hemorrhage

https://www.ahcmedia.com/articles/125011-is-the-lp-necessary-in-sah-with-new-generation-scanners
 Subarachnoid Haemorrhage
• Complications
• Hydrocephalus
• Rebleeding
• Vasospasm
• Seizures
• Cardiac dysfunction

http://emedicine.medscape.com/article/1164341-clinical#b4
 Subarachnoid Haemorrhage
• Prognosis
• Approximately 25% of patients die within 24 hours, with or without medical
attention
• Hospitalized patients have an average mortality rate of 40% in the first month
• About half of affected individuals die in the first 6 months
• Rebleeding, a major complication, carries a mortality rate of 51-80%

http://emedicine.medscape.com/article/1164341-clinical#b4
 Intracerebral Hematoma
Intracerebral Hematoma(ICH)
• Define as an accumulation of blood within the brain matter

• Most common can be caused by trauma, aneurysm rupture, amyloid, and

hypertension

• Associated with blunt/non-penetrating/closed head injury

• The brain is usually contused (bruised), swollen, or lacerated, and there are
hemorrhages, both meningeal and intracerebral , as well as ischemic hypoxic
lesion
Etiology
Primary
absence of any underlying vascular
malformation or coagulopathy.
Ex: Hypertensive arteriosclerosis
and cerebral amyloid angiopathy
(CAA)

Secondary
due to underlying vascular
malformation, hemorrhagic
conversion of an ischemic
stroke, coagulopathy,
intracranial tumor, etc.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291314/ The Acute Management of Intracerebral Hemorrhage: A Clinical Review. Justine Elliott, FRCA, and Martin Smith, FRCA
 Sign & Symptomps
• The classic presentation: sudden onset of a focal neurological deficit (depending on the
area of the brain involved) that progresses over minutes to hours with accompanying :

• Headache, nausea, and vomiting

• decreased consciousness or comatose

• Dyspneu and irregular respiration

• Elevated blood and intracranial pressure

• Dilatation of pupil

• Bilateral Babinski signs

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291314/
Intracerebral Hemorrhage. Carlos S. Kase and Ashkan Shoamanesh Bradley's Neurology in Clinical Practice, 66, 968-982.e3
Cont.
• 1st few hours after injury : bleeding point in contused area may appear
small and innocuous
• First several days after injury : swelling from the contused area or to
develop hematoma
• Swelling  compress surrounding structure
 Herniation of the brain
• Lesion : coup-countercoup
Imaging findings
• 1st line : CT non contrast
• Appear as a small areas of high density with surrounding edema which
appears hypodense
• Can cause blood in ventricles
• May displace or compress surrounding structures due to mass effect from
the collection
• Can result herniation
 The ED algorithm for early diagnosis and emergent intervention.

Cyrus K Dastur, and Wengui Yu Stroke

Vasc Neurol 2017;svn-2016-000047
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
Prognosis : ICH SCORE

http://emedicine.medscape.com/article/2172479-overview#a1
 Cerebral Malaria
• Cerebral malaria is a common, life-threatening complication of P. falciparum infection.
• Parasitized RBCs express malarial cell surface glycoproteins called knobs that are sticky. They
adhere to capillary walls, causing sludging in the cerebral microvasculature, localized
ischemia, capillary leak, and petechial hemorrhages.
• Clinical manifestations include fever, altered mentation including obtundation, coma, and
occasionally seizures.
• A careful history and early diagnosis and therapy are essential to prevent severe morbidity
and death.

Rosen’s Emergency Medicine 7th Ed

Management
• Intravenous quinine, quinidine, or artemisinin (if it is available)
• Supportive care, including mechanical ventilation for comatose
patients and patients with noncardiogenic pulmonary edema
• Antiepileptics and correction of acidosis and hypoglycemia
• The mortality rate is high, especially in children, but if the patient
recovers, neurologic sequelae are rare. Corticosteroids, including
dexamethasone, provide no benefit and can worsen outcome in
cerebral malaria.

Rosen’s Emergency Medicine 7th Ed

Harrison’s Principles of Internal Medicine.19th ed.
Signs of Specific Disorders Causing Confusional States
Diagnosis
• Both historical & p.examination finding indicating delirium are necessary to
confirm the diagnosis
• Obtaining a history
• the acute onset of attention deficits & cognitive abnormalities fluctuating
in severity throughout the day & worsening at night virtually the
diagnostic of delirium
• Examine medication history
• Asses for an underlying process such as pneumonia /urinary tract
infection,urinalysis ,CBC & a chest radiograph ,hepatic & renal studies &
chest radiograph
• 1 key for detecting delirium is the mental status examination & other
cognitive screening instrument
Treatment
• Direct treatment at the underlying cause
• Sedation may be needed
• Haloperidol is a frequent intial choice at dose of 5-10 miligram PO
,IM/IV with reduced dosing of 1-2 mg in the elderly.Repeated at 20-30
min interval as needed
• Benzodiazepines such as lorazepam 0,5-2.0 mg PO,IM/IV may be used
in combination with haloperidol in doses of 1-2 mg with dose varying
widely depending on the age & size of the patient & the degree of
agitation.
http://www.mc.vanderbilt.edu/documen
ts/NeuroICU/files/ENLS_Coma.pdf
 Bila setelah pemberian diazepam rektal
kejang belum berhenti,
dapat diulang lagi dengan cara dan dosis
yang sama dengan
interval waktu 5 menit.

setelah 2 kali pemberian diazepam rektal masih

tetap kejang,
dianjurkan ke rumah sakit. Di rumah sakit
dapat diberikan
diazepam intravena dengan dosis 0,3-0,5
mg/kg.

Bila kejang telah berhenti,

pemberian obat selanjutnya
tergantung
dari jenis kejang demam apakah
kejang demam sederhana
atau kompleks dan faktor risikonya.
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
www.aesnet.org/about_aes/press_releases/guidelines2016
 ENSEFALOPATI HIPERTENSIF
• Sindrom yang berkembang cepat, terdiri dari :
• Hipertensi berat
• Sakit kepala
• Mual dan muntah
• Gangguan penglihatan
• Penurunan kesadaran (s/d koma)
• Kejang multipel dapat timbul, lebih terlihat pada 1 sisi tubuh

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles
of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
 ENSEFALOPATI HIPERTENSIF
• Sindrom neurologis → dominasi gejala dari daerah oksipital dan
parietal
• Perubahan patologi : mikroinfark multipel dan petechiae
• Saat manifestasi neurologis muncul, hipertensi biasanya sudah
mencapai tahap maligna (TDD > 125 mmHg, perdarahan retina,
eksudat retina, papiledema, penyakit ginjal dan jantung)
• ↑ tekanan darah mendadak → ensefalopati pada tekanan yang lebih
rendah (terkait perubahan permeabilitas)

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles
of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
 PENCITRAAN PADA ENSEFALOPATI
HIPERTENSIF
• Daerah luas substansia alba mengalami edema
• CT-scan : hipodensitas, terutama pada bagian posterior hemisfer
serebri
• Hasil akumulasi cairan

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles
of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
 PENCITRAAN PADA ENSEFALOPATI
HIPERTENSIF
• Daerah luas substansia alba mengalami edema
• CT-scan : hipodensitas, terutama pada bagian posterior hemisfer
serebri
• Hasil akumulasi cairan

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles
of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
 Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL,
Jameson JL, et al., editors. Harrison’s principle of internal
medicine. 18th ed. USA: The McGraw-Hill Medical; 2012.
 Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL,
Jameson JL, et al., editors. Harrison’s principle of internal
medicine. 18th ed. USA: The McGraw-Hill Medical; 2012.
Tanda & gejala
Terjadi mendadak dengan ketegangan otot yang
makin bertambah terutama pada rahang dan
leher, dlm waktu 48 jam penyakit ini menjdi
nyata dengan ketegangan dengan:
• Trismus  spasme otot2 mastikatoris
• Kaku kuduk smpai opistotonus  ketegangan
otot2 erektor trunki
• Ketegangan otot dinding perut
• Kejang tonik
• Risus sardonikus
• Kesukaran menelan, mudah terangsang, nyeri
kepala,
• Spasme khas  badan kaku dan epistotonus, extr. Inferior dalam
extensi, lengan kaku dan mengepal kuat,
• Asfiksia dan sianosis  serangan pda otot pernapasan dan laring

Menurut beratnya gejala  3 stadium:

1. Trismus 3 cm tanpa kejang tonik umum meskipun dirangsang
2. Trismus 3 cm atau lebih kecil dengan kejang tonik umum bila di
rangsang
3. Trismus 1 cm dengan kejang tonik umum spontan
Komplikasi
• Spasme otot faring  terkumpulnya otot air liur di dalam saliva
rongga mulut dan hal ini memungkinkan terjdinya aspirasi sehingga
dapat tjdi pneumonia aspirasi
• Asfiksia  serangan pd otot pernapasan
• Atelektasis  krna obsturksi o/ sekret
Pencegahan
• Mencegah terjadinya luka
• Perawatan luka yang adekuat
• Pemberian AST  dlm beberapa jam stelah luka yaitu u/ mmberikan
kekebalan pasif. AST 1.500 U IM dengan di dahului dengan uji kulit
dan mata
• Pemberian TT pada anak2 yg belum pernah setelah pemberian ATS
• Penisilin prokain selama 2-3 hri setelah mendapat luka berat dosis
50.000 U/kgBB/hari
• Imunisasi aktif  dimulai umur 3 bulan, booster 1 thun kemudian pd
usia 5 tahun
Tatalaksana
• AST 20.000 U/hari selama 2 hri berturut2 scra IM dengan di dahului o/ uji
kulit dan mata, bila +  pemberian AST hrus dilakukan dengan desenitisasi
• Antikonvulsan dan penenang  kejang hebat: fenobarbital dosis awal jika
umur < 1thun 50 mg dan u/ anak umur >1 thun 75 mg, dosis lanjutan 5
mg/kgbb/d dibagi 6 dosis. Diazepam dengan dosis 4 mg/kgbb/day dibagi 6
dosis IV. Largaktil dosis 4 mg/kgbb/d dibagi 6 dosis
• Penisilin prokain 50.000 U/kgbb/hari IM  sd 3 hari panas turun
• Diet cukup kalori dan protein. Jika trismus  makanan cair melalui
lambung
• Isolasi u/ mnghindari rangsangan
Tetanus neonatorum
• Disebabkan o/ clostridium tetani yang masuk melalui luka tali pusat
 karena tindakan yang tidak memenuhi syarat kebersihan (
memotong tali pusat dengan gunting yang tdk steril)
• Tanda & gejala:
Tiba-tiba demam
Tidak mau atau tidak dapat menetek lagi (trismus), sblmnya bayi menetek
biasa
Gejala khas mencucu sprti mulut ikan (karpermond), mudah kejang disertai
sianosis, suhu tinggi, kaku kuduk smpai epistotonus
Tatalaksana
• Cairan IV dengan larutan glukosa 5%: nacl fisiologis 4:1 selama 48-72
jam sesuai dengan kebutuhan, sedangkan selajutnya IVFD hanya u/
memasukkan obat.
• Bila sakit > 24jam atau sering kejang atau apnea diberikan lar.glukosa
10%: natrium bikarbonat 1,5% 4:1
• Diazepam dosis awal 2,5 mg iv perlahan2 selama 2-3 menit.
• ATS 10.000 U/d dan diberikan selama 2 hri berturut2
• Ampisilin 100 mg/kgbb/d dibagi 4 dosis scra iv selama 10 hari
• Tali pusat dibersihkan dengan alkohol 70% atau betadine
Pencegahan
• TT yang dberikan pada trimester ke3 kehamilan dikatakan sangat
bermakna mencegah tetanus neonatrum
Malaria serebral
Tanda & gejala
• Headache
• Seizures
• Coma
• Diffuse cerebral edema
• Very rarely by focal features, such as :
• Hemiplegia
• Aphasia
• Hemianopia
• Cerebellar ataxia
• Usually the neurologic symptoms appear in the second or third week of the infection, but they may be the
initial manifestation
• Children in hyperendemic regions are the ones most susceptible
• Among adults in nonendemic areas  only pregnant woman and nonimmune individuals who discontinue
prophylactic medication are liable to CNS involvement
• With plasmodium vivax infection  there may be drowsiness, confusion and seizures without invasion of
the brain by the parasite
Treatment
• Quinine and artesunate
• Newer drugs  mefloquine, artemether with lumefantrine and
atovaquone
• Large doses of dexamethasone given as soon as cerebral symptoms
appear may be lifesaving
• Blood or exchange transfusion may confer a modest benefit on
survival in severe cases