Plenary Presentation

Group 5
Faculty of Medicine
Tarumanagara University
GROUP 5
Tutor: dr. Johan, Sp.FK & dr.
Haming, Sp.KFR
Leader: Andreas Satria (405130031)
Secretary: Carissa C C (405140168)
Writer: Ivana (405140259)
Members:
Laura Febriana (405130188)
Aditya Suksmawan (405140043)
Venia Endah Tamara (405140072)
Anggi Arini (405140096)
Clara Teny (405140108)
Jovian Lutfi Daniko (405140116)
Irnanto Fardik Kinanda
(405140129)
Dzuhri Al Okta (405140107)
Stefanie (405140259)
2
 A DIRE SITUATION(S)
• A 66-year-old male was brought to the ED by paramedics after he was found unconscious on the
bathroom floor by his wife. She told the paramedics that he was going to shower, and not long
after he went inside the bathroom there was a loud smashing noise. He has been complaining of
productive cough, fever, severe dizziness, vomiting and headaches for several days. He has a long
history of uncontrolled DM and HTN and had a stroke 5 years ago. On initial examination, the
patient appears obtunded and can only be aroused briefly with sternal rub. Temperature is 39∘C,
HR 68 bpm, BP 170/90 mmHg, RR 22 breaths per minute. There is a ø 10cm hematoma on the
back of his head. While he was being transported to the ED, the patient’s face starts to twitch
from his left side and spreads to his left extremities and finally develops into a generalized tonic-
clonic convulsion for more than 30 minutes.
• At the same time, a 2-year-old girl was brought to ED by her parents after seizing. She had been
coughing and feeling feverish for the past 5 days. The fever keeps worsening and she finally seized
30 mins ago. The seizure happened multiple times and lasted for <5 mins each time with a period
of unconsciousness in between seizures. She never got any vaccination since birth. Her mother
has a history of epilepsy and her father is on TB treatment. On initial examination, her temp is
39∘C, HR 100 bpm, RR 24 breaths per minute. On lung auscultation, there are crackles heard on
her right lung’s superior lobe
• Discuss the case, assess the patient’s condition, plan the necessary examination to diagnose and
plan proper treatment while considering all posibilities !
3
Step 1: Unfamiliar
terms
STEP 2
1. Apa hubungan DM, HTN, stroke dengan keluhan pasien?
1. Crackles: ronkhi
2. Mengapa kedutan wajah  ekstremitas  tonik
2. Obtunded: penurunan kesadaran krn klonik?
trauma atau kondisi medis
3. Apa hubungan kejang dengan hematoma di kepala?
4. Hub riwayat demam, batuk, vertigo dgn pasien tiba-tiba
terjatuh di kamar mandi?
5. Interpretasi PF?
6. Hubungan anak kejang dengan tidak pernah divaksinasi
sebelumnya?
7. Mengapa demam memburuk menyebabkan kejang?
8. Hubungan riwayat ibu epilepsi & ayah penderita TB
dengan keluhan anak?
9. Mengapa ronkhi (+) pada lobus superior paru kanan?

4
Step 3: brainstorming
1. Kemungkinan ada perdarahan 6. Kemungkinan tertular TB dari ayahnya
intrakranial, ensefalopati, SAH,  meningitis TB
meningoensefalitis
2. Pasien mengalami status epileptikus 7. Kejang demam
3. Adanya traumatic brain injury  post 8. Anak batuk mungkin tertular ayahnya,
traumatic seizure dan anak belum divakinasi sebelumnya.
4. Tidak ada, pasien jatuh kemungkinan Anak kejang kemungkinan karena ibu
krn Transient Ischemic Attack (TIA), ada riwayat epilepsi (genetik), tertular
vertigo, kurang elektrolit, DM TB
5. Temp 39∘C  infeksi, 9. Anak tertular TB paru
HR 68 bpm  Takikardi
BP 170/90 mmHg  HTN  TIA,
stroke
RR 22 bpm  takipneu

5
DIAGNOSIS BASED ON LEVEL OF CONSCIOUSNESS Conscious normal
Confused Disoriented, impaired This could be caused by sleep
deprivation, malnutrition, allergies,
thinking and responses environmental pollution, drugs
(prescription and nonprescription),
and infection.

Delirious Restlessness, in which a person may be restless

or agitated and exhibit a marked
hallucinations, sometimes deficit in attention
delusions
Somnolent Sleepy A somnolent person shows
excessive drowsiness and responds
to stimuli only with incoherent
mumbles or disorganized
movements
Obtunded Decreased alertness, Decreased interest in their
surroundings, slowed responses,
slowed psychomotor and sleepiness
responses
Stuporous Sleep-like state, little/no People with an even lower level of
consciousness, stupor, only
spontaneous activity respond by grimacing or drawing
away from painful stimuli
Comatose Cannot be aroused, no Do not even make this response to
stimuli, have no corneal or gag
response to stimuli reflex, and they may have no
pupillary response to light
Etiology
SEIZURE
SEIZURE
• Seizure : an episode of abn neurologic function
caused by inappropriate electrical discharge of
brain neurons.
• Neuronal electrical dischargehomeostasis of
glutaminergic(excitatory) & γ-aminobutyric
acid(inhibitory) activity.
• Epilepsy : clinical condition in which a person has
risk to recurrent seizures. It impliesmore
excitatory w/ a lower seizure threshold.
• Primary, or idiopathic : no evident cause can be
identified.
• Secondary, or symptomatic : identifiable
neurologic condition, such as a mass lesion,
previous head injury,/ stroke.

Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016

GENERALIZED SEIZURES
• Generalized seizures activation of the entire cerebral cortex, perhaps caused by
an electrical discharge originating deep in the brain & spreading outward.
• Clinical manif: loss of consciousness,/ variety of motor manifestations

• Generalized tonic-clonic seizures (grand mal)

• Typical attack(60-90s)pt suddenly rigid(tonic phase), trunk & extremitiespt
falls to the groundtonic phase subsides↑ coarse trembling that evolves into
a symmetric, rhythmic (clonic) jerking of trunk & extremities.
• Pt are often apneic during this period & cyanotic; urinate & may vomit.
• Attack ends, the pt : flaccid & unconscious, often w/ deep, rapid breathing.
• Consciousness returns gradually, postictal confusion, myalgias, & fatigue may
persist for several hours/more.

Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016

GENERALIZED SEIZURES
• Absence seizures (petit mal)
• Very brief, only few scnds.
• Pt suddenly develop altered consciousness but no change in postural tone.
• They appear confused, detached,/ withdrawn, & current activity ceases.
• They may stare/ have twitching of the eyelids; not respond to voice/ other
stimulation & may exhibit involuntary movements/ lose continence.
• The attack ceases abruptly, the pt resume previous activity without
postictal symptoms.
• The attacks can occur 100/more times daily.

Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016

PARTIAL (FOCAL) SEIZURES
• Partial seizures electrical discharges beginning in a localized region of the
cerebral cortex.
• Focal seizures: likely to be secondary a localized lesion of brain.

• Simple partial seizures localized; consciousness & mentation aren’t affected.

• It is possible to deduce the location of the initial cortical discharge from the
clinical features

• Complex partial seizuresconsciousness/mentation is affected.

• Caused by a focal discharge in the temporal lobe
• Symptoms may include automatisms, visceral symptoms, hallucinations, memory
disturbances, distorted perception, & affective disorders.

Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016

CLINICAL FEATURES
• History
• Important avenues of inquiry:
• The presence of a preceding aura
• Abrupt/ gradual onset
• Progression of motor activity
• Loss of bowel/ bladder control
• Presence of oral injury
• Whether the activity was localized/ generalized & symmetric/ unilateral.
• Ask: duration of the episode & determine the presence of postictal confusion/ lethargy.
• Common precipitating factors:
• Missed doses of antiepileptic drug
• Recent alterations in medication
• Dosage change/conversion fr brand name;
• Sleep ↓
• Strenuous activity ↑
• Infection
• Electrolyte disturbances
• Alcohol/substance use/ withdrawal.

Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016

• PHYSICAL EXAMINATION
• Immediately obtain a complete set of
vital signs & a point-of-care glucose
determination.
• In the post-seizure settingchecking for
injuries, especially to the head/ spine
• Lacerations of the tongue & mouth,
dental fracture, & pulmonary aspiration
: sequelae.
• Perform a directed, complete neurologic
examination
• Follow the pt’s level of consciousness &
mentation closely to avoid missing
nonconvulsant SE.
• A transient focal deficit (usually
unilateral) following a simple/ complex
focal seizure is referred to as Todd’s
paralysis & should resolve within 48h.
Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016
DIAGNOSIS
Clinical features that help to
distinguish seizures from other,
nonseizure attacks include:
• Abrupt onset & termination.
Some focal seizures: preceded by
auras 20-30s, but most attacks
begin abruptly. Most seizures
last 1 or 2 mnt.
• Lack of recall, (except for simple
partial seizures) pt usually can’t
recall the details of an attack.
• Purposeless movements/
behavior during the attack.
• Most seizures, (except for simple
absence/ simple partial seizures) are
followed by postictal confusion &
lethargy

• LABORATORY TESTING
• In a pt w/ a welldocumented seizure disorder
who has had a single unprovoked seizure
glucose level & pertinent anticonvulsant
medication levels.
• In case of adult w/ first seizure/unclear seizure
history, more extensive studies are needed &
depend on the clinical context. Obtain serum
glucose, basic metabolic panel, lactate, calcium,
magnesium, a pregnancy test, & toxicology
studies. Consider assays for anticonvulsant drug
levels.
• The therapeutic level of a drug is the level that
provides adequate seizure control without
unacceptable side effects.
Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016
IMAGING
• Concern for an acute intracranial
process is an important indication
for obtaining CT imaging, even if
there is a coexistent metabolic
process.
LUMBAR PUNCTURE
• In setting of acute seizure is
indicated if the pt is febrile/
immunocompromised/ if SAH is
suspected & noncontrast head CT
is N.
ELECTROENCEPHALOGRAPHY
• Emergent EEG can be considered
in the evaluation of a pt w/
persistent, unexplained altered
mental status, subtle SE,
paroxysmal attack,/ ongoing SE.
TREATMENT
• PATIENTS WITH ACTIVE SEIZURES
• Supportive & protective measures.
• If possible, turn the pt to the side to reduce
the risk of aspiration.
• Suction & airway adjuncts should be readily
available.
• It is not necessary/recommended to give IV
anticonvulsant medications during the course
of an uncomplicated seizure.
• Most seizures will self-resolve within 5 mnt.
Tintinalli_s Emergency Medicine - A Comprehensive Study Guide 8th 2016
• PATIENTS WITH A HISTORY OF SEIZURES
• Proper management of a pt w/ a well-
documented seizure disorder who presents
after 1/ more seizures depends on the
particular circumstances of the case.
• Identify & correct potential precipitants that
may lower the seizure threshold.
• PATIENTS WITH A FIRST UNPROVOKED
SEIZURE
• Guidelines don’t recommend hospital
admission/ initiation of anticonvulsant
therapy in the pt with a first unprovoked
seizure, as long as the patient has returned to
neurologic baseline.
STATUS EPILEPTICUS
Definition & Etiology
• Definition: continuous or intermittent seizures for more than 5
minutes without recovery of consciousness
• Most common causes of status epilepticus include:
• Subtherapeutic antiepileptic levels
• Preexisting neurologic conditions  prior CNS infection, trauma, hemorrhage,
or stroke
• Anoxia or hypoxia
• Metabolic abnormalities
• Alcohol or drug withdrawal

Tintinalli, Judith E., Gabor D. Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division,
Type of Status Epilepticus
• Nonconvulsive Status Epilepticus
• In nonconvulsive status epilepticus, the patient is comatose or has fluctuating
abnormal mental status or confusion, but no overt seizure activity or only subtle
activity
• The diagnosis is typically made by EEG
• Findings suggestive are include:
• Prolonged post-ictal period after a generalized seizure
• Subtle motor signs such as twitching, blinking, and eye deviation
• Fluctuating alterations in mental status
• Unexplained stupor or confusion in the elderly
• Epilepsia Parsialis Continua
• Is focal tonic-clonic seizure activity with normal alertness and responsiveness
• The distal leg and arm are most commonly affected

Tintinalli, Judith E., Gabor D. Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division,
Sign and Symptoms (GCSE) and Diagnosis
• S/S:
• Having overt convulsions
• May have mild clonic movements of only the fingers or fine, rapid movements
of the eyes
• There may be paroxysmal episodes of tachycardia, hypertension, and
pupillary dilation

• Diagnosis:
• EEG

a
https://3c1703fe8d.site.internapcdn.net/newman/gfx/news/hires/2016/newguideline.jpg
Prognosis
• Prognosis is related most strongly to the underlying process causing
SE
• The more advanced the stage of SE, the less favorable the response to
treatment
• Death most often is related to an underlying cause of brain injury
• In nonconvulsive status epilepticus, occasional patients have
reportedly had profound memory and behavioral changes after
episodes of complex partial SE

https://emedicine.medscape.com/article/1164462-overview#a6
STROKE & TIA
Stroke
https://www.nhlbi.nih.gov/health/health-topics/topics/stroke/types
MENINGITIS
Bacterial meningitis

Clinical features
• The most common causes  • Brudzinski sign & kernig sign (+)
Streptococcus pneumoniae (61%), • Neurologic examination should
Neisseria meningitidis (16%), group seek evidence of focal neurologic
dysfunction, such as  disordered
B streptococcus (14%), eye movements, homonymous
Haemophilus influenzae (7%), and visual field deficits, facial
Listeria monocytogenes (2%). asymmetry, and hemiparesis.
• The classic signs and symptoms are Diagnosis
 fever, neck stiffness, headache, • Lumbar puncture
and altered mental status. • CT Scan

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011.
Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011.
Viral meningitis
• cause viral meningitis  non-polio enteroviruses (echovirus,
coxsackievirus, and enterovirus), mumps, cytomegalovirus (CMV),
herpes simplex virus (HSV), lymphocytic choriomeningitis,
adenovirus, and human immunodeficiency virus.
• Dx: Lumbar puncture
• suspected HSV-2 meningitis, patients who present with neurologic
deficits, such as urinary retention or weakness, treated with acyclovir,
10 milligrams/kg IV every 8 hours

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011.
TUBERCULOSIS MENINGITIS
Clinical Presentation
• Headache, fever, and stiff neck, although meningeal signs may be
absent in the early stages
• Cranial nerve (CN) palsies, hemiparesis, paraparesis, and seizures
• Glasgow Coma Scale scores of 10 or less in resource-limited settings
• Multiple CN palsies, most commonly involving CN III, VI, and VII

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121465/
Diagnosis
• CSF in TBM
• CSF should be sent for routine analyses (cell counts and differential, protein
level, glucose level) and microbiologic tests for bacteria, fungi, and MTB
• Pleocytosis with lymphocytic predominance, high protein levels, and low
glucose levels are the hallmark findings in the CSF of patients with TBM
• CSF samples should be examined by Ziehl-Neelsen (ZN) staining for acid-fast
bacilli
• Contrast-enhanced brain CT or MRI can help support a diagnosis of
TBM because of the high frequency of abnormalities on initial
presentation

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121465/
Diagnosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121465/
Treatment

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121465/
ENCEPHALITIS
Viral encephalitis

Clinical features
• Viral encephalitis is a viral • cognitive deficits (e.g., aphasia,
infection of brain parenchyma amnestic syndrome, or acute
that produces an inflammatory confusional state), seizures, and
response. movement disorders.
• Cause viral encephalitis  HSV- • Features of meningeal
1, herpes zoster virus (HZV), involvement, such as headache
Epstein-Barr virus, CMV, and and photophobia, are usually,
rabies. but not invariably, present. The
same is true for fever.

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011.
 DD
• When fever and meningeal symptoms
predominate  bacterial meningitis.
• With severe headache  consider
subarachnoid hemorrhage.
• Tuberculosis
• fungal and neoplastic meningitis, and
• Subacute subarachnoid hemorrhage.
• When parenchymal features are
prominent  brain abscess, bacterial
endocarditis, postinfectious
encephalomyelitis, and toxic or
metabolic encephalopathies should be
considered.
Th/
• HSV encephalitis  acyclovir, 10
milligrams/kg every 8 hours.
• CMV encephalitis  ganciclovir, 5
milligrams/kg IV every 12 hours.

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011.
FEBRILE SEIZURE
Febrile seizure

• seizure accompanied by fever (temperature100.4°F or 38°C by any

method), without central nervous system infection, that occurs in
infants and children 6 through 60 months of age
• A child who has a seizure without a fever, then a febrile seizure is not
included in a febrile seizure
• If the child <6 months or >5 years experience seizures preceded by
fever  central nervous system infection or epilepsy

http://pediatrics.aappublications.org
 Classification febrile seizure

Simple febrile seizures Complex febrile seizure

• last for less than 15 minutes • focal

• generalized (without a focal
component)
• did not recur within 24
hours
• 80% of all febrile seizures
• prolonged (15 minutes)
• and/or recurrent within 24
hours.

http://pediatrics.aappublications.org
4
0
4
1
 How to give diazepam rectally

• Draw up the dose from an ampoule of

diazepam into a tuberculin (1-ml) syringe.
Base the dose on the weight of the child,
when possible. Then remove the needle
• Insert the syringe 4–5 cm into the
rectum, and inject the diazepam solution
• Hold the buttocks together for a few
minutes

Use phenobarbital (200 mg/ml solution) at a dose of 20 mg/kg to control

convulsions
in infants < 2 weeks of age:
Weight 2 kg – initial dose, 0.2 ml; repeat 0.1 ml after 30 min If convulsions
Weight 3 kg – initial dose, 0.3 ml; repeat 0.15 ml after 30 min continue
 Administration of drugs (indication)
• more prolonged (>15 min) anticonvulsant
• Focal seizure • valproic acid : 15-40 mg / kg / day in
2-3 doses
• The presence of a real neurological • phenobarbital 3-4 mg / kg per day in
disorder before or after a seizure 1-2 doses
(hemiparesis, paresis Todd, Treatment is given for 1 year free of
cerebral palsy, retardasi mental, seizures, then stopped gradually for
hidrosefalus) 1-2 months
• Seizures repeated twice or more in
24 hours
• Febrile seizures occur in infants
less than 12 months
• febrile seizure > 4 x/year

Konsensus Penatalaksanaan Kejang Demam. UKK neurologi.IDAI.2006

JUVENILE EPILEPSY
Juvenile myoclonic epilepsy (Janz syndrome)
• usually starts between the ages of 12 and 16. (girls > boy)
• People who have JME have 3 types of seizures:
Myoclonic seizures cause sudden jerks of the muscles, either in the arms, legs,
face or whole body. These seizures usually happen soon after waking up and
sometimes when getting dressed or having breakfast. They may also happen in
the evening or when the person is tired.
• Two thirds of people with JME also have tonic-clonic seizures. They usually
happen in the morning, within an hour or two of waking up. These are more likely
to occur if the person with JME has been to bed late the night before, or has
woken up earlier than usual.
• About one third to one half of children and young people with JME also have
absence seizures. These can happen at any time of the day, but are most likely in
the morning.
• The EEG shows a 4–6/sec
irregular spike and wave
pattern, which is enhanced by
photic stimulation
• The neurologic examination is
normal
• Treatment :
• sodium valproate
• lamotrigine
• clonazepam
West Syndrome
• Infantile spasms are brief episodes of tonic
flexor or extensor movements, or both, of the
body and limbs.
• These spasms are seen in infants and young
children up to 4 years of age
• One of the most common types of infantile
spasm is characterized by
forward flexion of the head and body, with
the arms flung forward or outward
• The EEG in infantile spasms
shows a characteristic pattern called
hypsarrhythmia, consisting of high-amplitude
multifocal spikes and slow wave
• During the spasm, the EEG shows an abrupt
generalized decrement in the amplitude of
the ongoing activity
• Infantile spasms are often treated with
adrenocorticotropic hormone or
corticosteroids. Clonazepam has
been used occasionally, and in some
refractory conditions, a ketogenic diet may be
helpful in controlling the seizures
•dietary approach to epilepsy
treatment
•high-fat,low carbohydrate
diet that helps to control
seizures
•fatsprimary fuel
•ketogenic diet( "long-
chain triglyceride diet”)
provides 3 to 4 grams of
fat for every 1 gram of
carbohydrate and protein.
•The kinds of foods :
butter, heavy whipping
cream, mayonnaise, and
oils (e.g., canola or olive).
TETANUS
Etiology & Epidemiology
• Clostridium tetani, a motile, gram-positive, spore forming obligate anaerob
 tetanospasmin/tetanus toxin (neurotoxin) that can cause spastic
paralytic illness
• Occurs in infants whose mother are not immunized
• Unimmunized women die each year of maternal tetanus, which result from
postpartum, postabortal or postsurgical wound infection with C. tetani
• Disease are associated with traumatic injury, often a penetrating wound
inflicted by a dirty object such as nail, fragment of glasses, or unsterile
injection. It may also occur in association with abscesses, ear and body
piercing, chronic skin ulceration, burns, fractures, gangrene

Nelson Textbook of Pediatric 19th Edition

Clinical manifestation
• Generalized tetanus  trismus, sardonic smile of tetanus (risus
sardonicus), opisthotonos
• Early symptoms  headache, restlessness, irritability, followed by
stiffness, difficulty chewing, dysphagia and neck muscle spasm
• Others:
• Seizure  sudden, severe tonic contraction of the muscle, with flexion and
adduction of the arms and hyperextension of the legs
• Dysuria & urinary retention
• Forced defecation
• Fever (40 degree C)
• Tachycardia, dysrhythmias, diaphoresis, cutaneous vasoconstriction

Nelson Textbook of Pediatric 19th Edition

Clinical manifestation
• Neonatal tetanus: within 3-12 days of birth as progressive difficulty in
feeding, associated hunger and crying
• Characteristics: paralysis or diminished movement, stiffness and rigidity to the
touch, spasm and with or without opisthotonos
• Umbilical stump may hold remnants of dirt, clotted blood or serum
• Cephalic tetanus (rare)  involving the bulbar musculature that
occurs with wounds or foreign bodies in the head, nostrils or face
• Characteristics: retracted eyelids, deviated gaze, trismus, risus sardonicus, and
spastic paralysis of tongue and pharyngeal musculature

Nelson Textbook of Pediatric 19th Edition

Management

• TIG 500 U IM to neutralize

systemic tetanus toxins
• Penicillin G 100,000
U/kg/day divided every 4-6
hr IV for 10-14 days
• Generalized tetanus 
muscle relaxant (diazepam
0.1-0.2 mg/kg every 3-6 hr
IV

http://accesssurgery.mhmedical.com/data/books/matt7/matt7_c047f001.png
Complication &
Prevention
Prognosis
• Complication: • Active immunization in early infancy with
• Aspiration of secretions and pneumonia combined diphteria toxoid-tetanus
• Laceration of mouth and tongue toxoid-acellular pertussis (DTaP) vaccine
• Long bone or spinal fractures at 2, 4, and 6 mo of age, with a booster at
• Pneumothorax & mediastinal emphysema
4-6 yr old of age and at 10 yr intervals
during ET intubation and mechanical thereafter throughout adult life
ventilation • Immunizationation of women with
• Prognosis: tetanus toxoid prevents neonatal tetanus
• Mortality is highest in the very young and
the very old
• Favorable prognosis  long incubation
period, absence of fever and localized
disease
• Unfavorable prognosis  onset of trismus
<7 days after injury and with onset of
generalized tetanic spasm <3 days after
onset of trismus

Nelson Textbook of Pediatric 19th Edition

EPIDURAL HEMATOMA
Epidural Hematoma *neurologic emergency
•epidural hematoma (EDH): accumulation of blood in potential space surrounding brain, between dura mater
and inner surface of skull
•physical findings & clinical presentation:
• history of head trauma (+)
• sx: altered LOC, nuchal rigidity, headache, drowsiness, confusion, aphasia, photophobia, paralysis
• signs: transient loss of consciousness, followed by lucid interval (pt is free of any neurologic S/S,
followed by clinical deterioration incl. vomiting, lethargy, confusion, seizures)
• other signs: paralysis of limbs, unequal pupils, coma.
• ↑ICP: Cushing reflex of hypoTN, bradycardia, respiratory distress
• external signs of skull fracture (75%-95%)— lacerations, ecchymoses, CSF rhinorrhea/otorrhea

5
3
• etiology:
• traumatic: A. meningea media
injury (>>), a. meningea anterior,
a dural arteriovenous fistula at
the vertex, or from venous
bleeding
• nontraumatic: infection/eroding
abscess, coagulopathy,
hemorrhagic tumors, vascular
malformations, postsurgical
procedures
5
4
• workup:
• imaging
• serial head CT: “lens shaped” /
“lentiform” hyperdensity
• head CT is not conclusive in cases due to
severe anemia, early scanning (before blood
has time to accumulate) and severe hypoTN
• Brain MRI: more sensitive
• LUMBAR PUNCTURE IS
CONTRAINDICATED IN EDH DUE TO RISK
OF BRAINSTEM HERNIATION 5
5
nonpharmacologic therapy
• immediate surgical
decompression, ideally within 1-2
hr after traumatic event
• craniotomy & hematoma
evacuation — treatment of choice
when indicated, identify & ligate the
bleeding vessels
• burr hole evacuation: drilling a
hole in skull to evacuate
hematoma
acute general tx:
cardiopulmonary resuscitation & assessment for
disability
medical resuscitation maneuvers: head
elevation, hyperventilation, monitor vital sign,
avoid hypoTN & hypothermia, sedation
medication: osmotic diuresis w/ IV mannitol,
cerebrosedating medication, PPI to decrease risk
of UGIB
eval for surgery: best available evidence points
toward advantages of decompression
proceduses
5
6
• nonoperative tx indicated if
pt has no sx, no focal
neurologic deficit, no coma
(GCS>8), EDH vol <30 mL by
CT scan with clot thickness
<15mm & midline shift <5
mm
• nonoperative tx: close
monitoring, hourly neurologic
checks, serial head CT scans
chronic tx
risk of permanent brain dmg whether
the disorder is treated/not. most
recovery occurs in the 1st 6mo, with
some improvement over 2yr
children recover more quickly
57
SUBARACHNOID HEMORRHAGE
SUBARACHNOID HEMORRHAGE
• hemorrhage into subarachnoid space
surrounding the brain.
• e/: nontraumatic / traumatic
• predominant sex: women >55yr — 25%
greater risk of developing SAH
• RF: genetic, lifestyle (smoking, HTN, oral
contraception, pregnancy, amphetamine /
cocaine use)
physical findings & clinical
presentation:
sudden, severe headache “worst
headache of my life” (thunderclap
headache) + N/V, neck pain, seizure,
complete loss of consciousness
30-60% history of headache preceding
the hemorrhage
acutely ↑ICP— loss of consciousness
posterior communication aneurysm
may present as oculomotor palsy
58
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9

treatment
•nonpharmacologic therapy
ABCs — neurologic exam
CSF drainage for pt who develop
hydrocephalus & ↑ICP; pt w Hunt and
Hess grade 3 or higher
•acute general th
stabilize pt & prevent re-hemorrhage
& hydrocephalus
BP control: nicardipine iv until SBP
<140 mmHg. after securing the
aneurysm, liberalization of BP
parameters.
pain ctrl: codeine, low dose morphine
vasospasm develop b/w day 4 and 14.
treatment strategies:
• hypertension, hypervolemia and
hemodilution (3H) to maintain
cerebral perfusion
• nimodipine adm between days 4 &
21 after hemorrhage
chronic therapy
management of reversible RF
(smoking, HTN, drug use)
physical therapy & rehabilitation
disposition
death rate 30-40%. 10-15% die before
they reach the hospital.
survive — cognitive impairment &
disability
60
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1
REFERENCES
1. Adams & Victor's Principles of Neurology, 10 ed
2. Netter, Frank H., et al. Netter's Neurology. 2nd ed. Philadelphia, PA: Elsevier
Saunders, 2012
3. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine : A Comprehensive
Study Guide. 6th ed. USA: McGrawHill; 2004.
4. Greenberg DA, Aminoff MJ, Simon RP.. Clinical Neurology. 8th ed. USA: McGraw-
Hill; 2012.
5. Kasper DL, Hauser SL, Jameson JL, Fauci AS, Longo DL, Loscalzo S, editors.
Harrison’s Principles of Internal Medicine. 19th ed. McGrawHill; 2015.
6. Clinical emergency medicine, Lange. p. 347-52
7. Rosen’s emergency medicine, 8th ed