Emergency Medicine

Problem 3
Suddenly Unconscious,
What Could It Be?
Group 16
October 11th, 2016
 Group 16
• Tutor : dr. Twidi
• Leader : Yofishia Vandianto 405120175
• Secretary : Andi Eka Putra 405130132
• Scribe : Silvia Dwi Mustika 405120001
• Members :
 Julia Jennifer M. 405120053
 Albert 405130074
 Gishelly Marcella 405130083
 Suni Christina 405130111
 Florencia Santoso 405130133
 Mutiara Lirendra 405130147
 Jesica 405130151
 Skolastika Indah A. 405130224
Suddenly Unconscious, What Could It Be?
Female, 52 years old, was brought to the emergency
department by her husband when she was found to have a
decreased level of consciousness in their bedroom. When
she was found, she was lying face down, her body was cold,
but there is no apparent trauma to her head. The patient
was known to have diabetes and hypertension since 5 years
ago, and was treated regularly with glimepiride (1x2 mg),
metformin (2x500 mg), and amlodipine (1x10 mg). In the
past two days, the patient had a decreased appetite
because she said she was feeling nauseous. She also has
fever since last week, but haven’t taken any medicine to
treat it.
On her initial physical examination in the emergency
department, her findings are: GCS of E2M3V2, blood
pressure of 180 over 100 mmHg, heart rate of 112 beats per
minute, respiratory rate of 22 breaths per minute,
temperature of 36oC.
Suddenly Unconscious, What Could It Be?
Her neurology examination findings are: her pupil is
round, isocoric, with its diameter of 3mm/3mm, her
nuchal rigidity was absent, there aren’t any paresis on
her cranial nerves. There aren’t any weaknesses on her
motoric examination. Her physiologic reflexes are found
to be decreased on both sides of her extremities.
Her initial laboratory examination results are:
Hemoglobin of 10 g/dL, leukocytes of 17,500/ μL,
ureum of 40 mg/dL, and blood creatinine level of 1.2
mg/dL/ Other laboratory results such as blood glucose
test have not come out yet.
Discuss this case, assess the patient’s condition, and
plan a proper treatment for this patient while
considering all possibilities!
Unfamiliar Terms
• None
Perumusan Masalah
Perempuan 52 thn :
• Kesadaran menurun
• Badan dingin
• Riwayat DM + hipertensi, 5 thn • Suhu = 36 oC
lalu
• Obat : glimepiride +
metformin, amlodipine ,
regular
• Demam 1 minggu lalu
Perumusan Masalah
Pemeriksaan Fisik :
• GCS = 7
• TD = 180/110 mmHg
• HR = 112 bpm
• RR = 22 bpm
• Refleks Fisiologis menurun
Pemeriksaan Lab :
• Hb = 10 mg/dL
• WBC count 17,500 cells/μL 
leukositosis
• Ureum = 40 mg/dL
• Kreatinin = 1,2 mg/dL
Perumusan Masalah Curah Pendapat
Pertanyaan : 1. Penurunan Kesadaran
• Intra-kranial
1. Apa saja yang dapat (riwayat hipertensi dan DM 
menyebabkan stroke) , perdarahan
penurunan kesadaran? intrakranial.
• Ekstra-kranial
2. Pemeriksaan apakah o Riwayat minum obat
yang dapat dilakukan? glimepiride + metformin
3. Tatalaksana awal apakah dan nafsu makan menurun
 kadar glukosa darah
yang dapat diberikan? rendah  hipoglikemia 
penurunan kesadaran
o Jika minum obat tidak
teratur, risiko KAD dan HHS
 hiperglikemia 
penurunan kesadaran
Curah Pendapat
1. Penurunan Kesadaran
• Ekstra-kranial
o Gangguan ginjal (karena
riwayat DM dan hipertensi)
 ureum meningkat 
mual; penurunan kesadaran
 ensefalopati uremikum
o Gangguan elektrolit
o Gangguan asam-basa
o Infeksi : malaria serebral,
tifoid, sepsis
o Ensefalopati hipertensi
o Ensefalopati hepatikum
Curah Pendapat
2. Pemeriksaan ?
• Cek gula darah  hipo- dan
hiperglikemia
• Analisa gas darah  gangguan
asam basa
• Cek eletrolit  gangguan
elektrolit
• Cek hapusan darah  malaria
serebral
• EKG  pemeriksaan jantung
• CT scan  stroke, perdarahan
intrakranial
• Tes Widal  tifoid
• Kultur darah  sepsis
Curah Pendapat
3. Tatalaksana awal
Periksa ABC, pasang IV line, dan O2 jika dibutuhkan, kemudian
mencari etiologi :
• Hipoglikemia  glukosa / dekstrosa 5% IV
• Hiperglikemia  insulin
• Gangguan elektrolit  koreksi elektrolit
• Gangguan asam basa  koreksi cairan
• Tifoid  resusitasi cairan + antibiotik
• Sepsis  resusitasi cairan + antibiotik
• Malaria serebral  anti-malaria
• Ensefalopati uremikum  hemodialisis
• Ensefalopati hipertensi  anti-hipertensi
 Mind Map
Penurunan
Kesadaran

Ekstra-kranial Intra-kranial

• Stroke Iskemik
• Hipoglikemia • Stroke hemoragik
• Hiperglikemia • Perdarahan intrakranial
• Gangguan elektrolit
• Gangguan asam basa
• Ensefalopati uremikum Tatalaksana Tujuan
• Ensefalopati hipertensi
• Ensefalopati hepatikum • Memantau ABC
• Infeksi • Memulihkan
• Memasang IV
(malaria serebralis, kesadaran
line
tifoid dan sepsis • Mengurangi
• Memberikan O2
kerusakan saraf
• Segera mencari
Etiologi
 Learning Objective
1. MM Penurunan Kesadaran karena Intrakranial
2. MM Penurunan Kesadaran karena Ekstrakranial
• Patofisiologi
• Tanda dan Gejala
• Pemeriksaan Fisik
• Pemeriksaan Penunjang
• Tatalaksana
• Komplikasi
• Prognosis
 LO.1. Consciousness Disorders
Caused by Intracranial Components
Stroke (Ischemic and Hemorrhagic)
Intracranial Hemorrhage
Consciousness
Classification of Consciousness
Disorders
 Diagnosis
• History & Physical Examination
(including Vital signs)
• Neurologic examination  GCS
score, Pupillary reflex, eye
movements
• Head-to-toe examination
• Cardiopulmonary examination
• Lesions on skin
• Funduscopic examination
• Doll’s eyes, Vestibuloocular
reflex, Caloric testing
Rosen’s Emergency medicine : Concepts and Clinical Practice. 8 th ed.Philadelphia, Elsevier;2014.
Rosen’s Emergency medicine : Concepts and Clinical Practice. 8 th ed.Philadelphia, Elsevier;2014.
Rosen’s Emergency medicine : Concepts and Clinical Practice. 8 th ed. Philadelphia, Elsevier;2014.
STROKE
INTRACRANIAL
HEMORRHAGIC
Reference : http://emedicine.medscape.com/article/344342
 LO.2. Consciousness Disorders
Caused by Extracranial Components
• Hypoglycemia
• Hyperglycemia
• Electrolyte Disturbances
• Acid Base Disorders
• Uremic Encephalopathy
• Hypertensive Encephalopathy
• Hepatic Encephalopathy
• Cerebral Malaria
• Septic Encephalopathy
• DSS
HYPOGLYCEMIA
 HYPOGLYCEMIA
• Hypoglycemic  plasma glucose < 70 mg/dL
• Whipple’s triad
o Hypoglycemic symptoms (dizziness, headache,weakness, anxious, difficulty
with concentration, blurred vision)
o Low plasma glucose
o Symptoms reduced after treatment
 HYPERGLYCEMIA

- DIABETIC KETOACIDOSIS
-HYPERGLYCEMIA
HYPEROSMOLAR STATES
ELECTROLYTE
DISTURBANCES
Electrolyte Disturbances
ACID BASE DISORDERS
Acid – Base Disorders
Acid – Base Disorders
 UREMIC
ENCEPHALOPATHY
 UREMIC ENCEPHALOPATHY
• Is a constellation of nonspecific central neurologic
symptoms associated with renal failure
• Occurs due to buiid up of toxins which are normally
cleared by kidneys
• Develops in patiens with RF, usually when creatinine
clearance levels fall & remain below 15mL/min
• Four highly increased compound :
- creatinine
- guanidine
- guanidinosuccinic acid
- methylguanidine
• As uremia progresses  accumulation of GSA 
inhibition GABA receptors  myoclonus & seizures
 UREMIC ENCEPHALOPATHY
• History : • Physical examination :
- early symptoms : - confusion
anorexia, nausea, - nystagmus
diminished ability to - papilledema
cncentrate, slowed - hyperreflexia, clonus,
cognitive function asterixis
- agitation
- severe symptoms :
- dysarthria
vomit, decreased
- asterixis
cognitive function,
- seizure
confusion,
- myoclonic jerks, twitches
disorientation
 UREMIC ENCEPHALOPATHY
• Lab studies :
- electrolytes, BUN, creatinine, glucose
- CBC
- imaging (CT, MRI)
- EEG
- cognitive function test
• Treatment
- correcting metabolic disturbance
- seizure  anticonvulsants
- diet
 HEPATIC
ENCEPHALOPATHY
 Hepatic Encephalopathy
• Metabolic induced, potentially reversible,
functional disturbance of the brain.
• Etiologi : complication of acute or chronic liver
disease (commonly associated with cirrhosis)
• Two major mechanisms :
– Severe intrinsic hepatic dysfunction
– Portosystemic shunts
• Characterized : personality changes, impaired
intellect, disturbed sleep pattern and depressed
level of consciousness
Type Nomenclature Subcategories
A Associated with acute liver failure
B Associated with portal-systemic bypass and no intrinsic
hepatocellular disease
C Associated with cirrhosis and portal hypertension of portal- Episodic, persistent
systemic shunts and minimal
Pathophysilogy
 HYPERTENSIVE
ENCEPHALOPATHY
 Hipertensive emergency
• Severe elevation in blood pressure associated
with the presence of acute end-organ damage
Endocrine disorders Essential hypertension
Severe Hypertension
Pregnancy Renal disorders
Critical level
Drugs Or
Rapid rate of rise and increased
vascular resistance

Endothelial damage Spontaneous natriuresis

↑ Endothelial permeability Intravascular volume depletion

Platelet and fibrin ↓ vasodilators, NO, ↑ vasoconstrictors (renin-

deposition prostacycline angiotensin, catetholamines)

Fibrinoid necrosis and Further increase in blood

intimal proliferation pressure
Severe blood pressure
elevation

Tissue ischemia

End-organ dysfunction
CEREBRAL MALARIA
Cerebral malaria
Treatment
SEPTIC ENCEPHALOPATHY
DENGUE SHOCK SYNDROME
 DENGUE SHOCK SYNDROME
• dangerous complication of dengue infection and is associated with
high mortality.
• Increased vascular permeability, together with myocardial
dysfunction and dehydration, contribute to the development of
shock, with resultant multiorgan failure.
• Epid :
– The mortality rate
is around 1–2%
– The case fatality
of severe dengue
in Asian countries
is around 0.5–3.5%
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097561/ http://www.cdc.gov/dengue/clinicalLab/clinical.html
Risk Factors :
• more likely to
occur in infants
and the elderly
• patients with
chronic illness such
as diabetes
mellitus or asthm
• Malnutrition
• genetic
susceptibility
Pathophysiology

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097561/
 Diagnosis
• Serology
• RT-PCR
• Dengue-specific
IgG and IgM
ELISA

http://cid.oxfordjournals.org/content/32/2/204.full
 Management
• aggressive fluid resuscitation
 effective treatment
– normal saline, Ringer lactate,
5% glucose diluted 1:2 or 1:1
in normal saline, plasma,
plasma substitutes, or 5%
albumin.
– In the case of shock, fluids
should be administered as a
rapid (over less than 20 min)
intravenous bolus of 10–20
ml/kg body weight.
• a rapid bolus and repeated if
necessary to a total dose or
20–30 ml/kg of colloid.
• fresh whole-blood
transfusion may be required http://www.jped.com.br/conteudo/07-83-
(10 ml/kg). S22/ing_print.htm
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097561/
 Conclusion and Suggestion
• Female patient, 52 years old, was suddenly
unconscious. May caused by intracranial or
extracranial components, because of
inadequate data, should wait for the blood
glucose level and search for any electrolyte
imbalance.
• While waiting the data, we need to stabilize
patient by observing her ABC, give O2, and IV
line.