CASE ICM II

Intracranial lesion à unconsciousness

Objectives:

1. Examination of unconscious person

Quick cause checklist: COMA:

• CO narcosis
• Overdose
• Metabolic
• Apoplexy

Inspection

 ABC: Airway, Breathing, Circulation.

 Breathing type is important clue:
• Cheyne-Stokes (diencephalic).
• Biot's [irregular, ataxic] (advanced brainstem).
• Kussmaul (DM).
 Circulation: shock, dehydration, cyanosis, BP, pulse rate.
• Cherry red (CO poisoning).
 Posture: trauma, hyperextension, decerebrate, decorticate.
 Involuntary movements:
• Recurrent convulsions (status epilepticus).
• Myoclonic jerks (hypoxia, metabolic encephalopathy).

Consciousness level

 Press knuckles over sternum to cause pain and assess consciousness.

 Note stage:
• Drowsiness: normal sleepiness, can we roused to wakefulness.
• Stupor: unconsciousness, can be aroused with effort, purposeful pain responses.
• Light coma: unconscious with reduced semi-purposeful response.
• Deep: no response, no reflex.
 To assign a value, See Glasgow Coma Scale Reference.

Head, neck

 If no evidence of neck trauma, assess neck stiffness, Kernig's sign (SAH, meningitis).

 Inspect, palpate for head injures, including Battle's sign.
 Facial asymmetry (affected side sucked in/ out with respiration).
 Jaundice (hepatic coma).
 Myxoedema manifestations.

Eyes

 Pupils:
• Constricted (narcotic OD).
 • 1 dilated (subdural, raised ICP, SAH).
• Dilated (atropines, cloning from raised ICP).
 Dolls eye test:
• Open lids, turn head from side to side.
• Normal: eyes fixate like a moved doll, don't follow head. Brainstem lesion: follow head.
 Eye deviations:
• 1 eye deviated (CN III, IV, VI palsy).
• Both eyes deviated (cerebral hemisphere [look towards lesion]).
• Up/down deviation (brainstem).
• Also skull fracture could restrict an eye muscle, so deviate.

Ears, nose

 Blood leaking from ears/ nose.

 CSF leaking from ears/ nose (skull fracture).
• CSF test of watery discharge: test for glucose.

Mouth

 Gum hyperplasia: epilepsy clue (taking phenytoin).

 Trauma (previous seizure).
 Smell breath (ketoacidosis, alcohol, hepatic coma, uremia).
 Gag reflex: absent (brainstem dz, deep coma).
 Mouth corrosion (could be poison).

Limbs

 Injection marks (addict, DM).

 Tone: pick up arm, let fall.
 Deep tendon reflexes (coma: may be absent on paralyzed side).
 Pain: press pen on distal toe/ finger and see if leg/ arm withdrawal (if grimace/twitch and not
withdrawal, could be sensation but paralyzed).
• Grimacing important: segmental reflexes alone can cause withdrawal.

Body

 Signs of trauma.
 Examine heart, lungs, abdomen.

Temperature

 Hypothermia (hypothyroidism), fever (meningitis).

Urine

 Incontinence.
 Test urine for glucose, ketones (diabetes), protein (uracemia), blood (trauma).
Glucose

 Prick finger, drop of blood on test strip.

• If can't give an IV of glucose (saves hypoglycemia, won't harm ketoacidosis).
 If Wernicke's possible, give thiamine.

Stomach contents

 Perform if suspect drug OD, or no other obvious cause.

 While protecting airway, examine stomach by nasogastric tube.

Examination unconsciousness
Signs of Trauma
Basilar skull fracture
 Raccoon eye
 Battle sign
 Hemotympanum
 Cerebrospinal fluid, rhinorrhea
Palpation of head shows depressed skull fracture, swelling of soft tissue

Temperatur
 Hiper menandakan heatstroke, status epilepticus
 Hipo menandakan ethanol intoxication, hypoglycemia, Wernicke
encephalopathy, hepatic encephalopathy

Meningeal irritation
 Meningitis
 SAH

Funduscopy
 Papilloedema pada peningkatan ICP
 Terson Syndrome : Intraocular, subhyaloid hemorrhage pada SAH

GCS
GCS dapat juga menilai 
Status kesadaran
Compos mentis : Kesadaran penuh
Apatis : Sikap acuh. GCS 12-13.
Delirium : Disorientasi (orang, tempat dan waktu), berteriak, berhalusinasi, 10-11.
Somnolence : Kesadaran menurun, sering tertidur, tapi bangun dengan mudah
apabila dirangsang, kemudian tertidur lagi. 7-9.
Stupor : Tertidur lelap, respon dengan nyeri saja. GCS 4-6.
Coma : Tidak bisa dibangunkan. <8 dengan brainstem function tidak intak, atau
dibawah 3.
Brainstem Function
Respiration
Pulse and blood pressure 
Bisa hipotensi kalau medullary depression karena keracunan barbiturate. Bisa
hipertensi kalau brainstem dysfunction.
Pupils Reaction
Yang dicek CN II dan CN III
Corneal Refleks
Untuk menilai CN V 1 sebagai sensorik dan VII sebagai motoric
Positif apabila setelah diberikan respon pada kornea menghasilkan kedipan

Pergerakan Bola Mata Abnormal

Occulocephalic (Doll’s Eye)
Menilai CN III, IV, VI dan VIII
Ga boleh dilakukan pada pasien dengan cedera cervical

Occulovestibular
Menilai CN III, IV, VI, VIII
Ga boleh dilakukan pada pasien dengan rupture timpani/ otorrhea
Cold Opposite, Warm Same
Gag Reflex
Untuk menilai CN IX sebagai sensorik dan X sebagai motorik
Normalnya muntah
Motoric
Cek
 Tones
 Deep tendon reflex
 Plantar reflex
 Kesimetrisan

Abnormal Motor Function

 Jerking of limbs and eye fluttering
 Myoclonus pada pasien anoxic
 Asterixis pada hepatic encephalopathy atau keadaan uremic

 Decorticate
  Decerebrate

Lokasi Lesi
Supratentorial lesion
 Pupil size and light reaction : Normal size and reactive or large and
unreactive if transtentorial herniation.
 Reflex eye movement : Normal (kalau ada gaze mendekati sisi lesi)
 Motor response : Asymmetric, kecuali kalau sudah transtentorial herniation
bisa symmetric.
Subtentorial lesion
 Pupil size and light reaction : Midsized and unreactive with midbrain lesion,
pinpoint and unreactive with pontine lesion.
 Reflex eye movement : Impaired adduction with midbrain lesion, impaired
adduction and abduction with pontine lesion.
 Motor response : Asymmetric if unilateral lesion and symmetric lesion if
bilateral lesion.

Diffuse encephalopathy
 Pupil size and light reaction : Normal size and reactive, pinpoint and
unreactive with opiates, large and unreactive with anticholinergic.
 Reflex eye movement : Normal, or impaired by sedative drugs or Wernicke
encephalopathy
 Motor response : Symmetric, tapi asymmetric apabila hypoglycemia, HHS,
hepatic encephalopathy.

Etiology of Coma
Supratentorial Lesion
 Subdural Hematoma
Collection of blood in the subdural space between dura mater and arachnoid
mater. Yang kena bridging vein. Biasanya terjadi pada orang tua karena otak
sudah atrofi. Biasanya ada headache, altered consciousness, hemiparesis
contralateral and ipsilateral pupillary dilation. Diagnosis dengan CT/ MRI.
Therapy surgery.
 Epidural Hematoma
Associated with lateral skull fracture and tearing of middle meningeal artery
and vein. Ada lucid interval. Diagnosis dengan CT/ MRI. Therapy surgery.
 Cerebral Contusion
Bruising of the brain caused by head trauma 🡪 Cerebral oedema may cause
the level of consciousness fluctuate, seizure and focal neurologic signs may
develop.
LP is dangerous, jadi pakai CT/ MRI aja. Terapi ga usah di surgery.
 Intracerebral Hemorrhage
Bisa disebabkan oleh trauma dan non trauma (HTN)
Occurs when the patient is awake. Localized headache nausea and vomiting,
altered consciousness, HTN, hemiparesis, nuchal rigidity, gaze deviation
toward the putaminal or lobar hemorrhage. Diagnosis dengan CT/MRI non
kontras. Terapi dengan target BP 140, cerebral oedem diterapi dengan
mannitol/ hypertonic saline/ glucocorticoid, bisa juga terapi dengan surgery.
 Brain Abscess
Biasa berasal dari infeksi paru dan parameningeal (otitis, sinusitis,
osteomyelitis). Disebabkan oleh kuman aerob, anaerob, microaerophilic,
streptococci, and gram – anaerob.
Lesinya expanding, jadi sampai menyebabkan coma itu cukup lama (dalam
hitungan hari). Waspada karena bisa aja ga demam dan leukosit <10.000.
 Diagnosis dengan CT dan MRI kontras. LP ga boleh karena bisa
memperburuk.
 Stroke
 Brain Tumor
Diagnosisnya dengan CT/ MRI. Diperlukan juga CXR dan CT karena meta otak
biasanya dari paru. Terapi untuk edema otak biasanya dengan corticosteroid,
sedangkan terapi spesifik dengan surgery, radiotherapy, chemotherapy.

Subtentorial Lesion
 Basilar Artery Thrombosis or Embolic occlusion
 Pontine Hemorrhage
 Cerebral Hemorrhage or Infarction
 Posterior Fossa Subdural and Epidural Hematoma

Diffuse Encephalopathy
 Meningitis : Harus CSF exam dan CT.
 Encephalitis
 SAH
 Hypoglycemia : Biasanya apabila gula <30 mg/dL
 Global Cerebral Ischemia
Biasanya setelah cardiac arrest. Manifestasinya pupillary dilation, tonic
clonic, fecal incontinence.
 Drugs Intoxication
 Hepatic Encephalopathy
 HHS
 Hyponatremia
 Hypothermia
 Hyperthermia
 Seizure

2. Pathophysiology of traumatic unconsciousness

 

The initial traumatic insult results in mechanical damage including:

1. Rupture of cellular and vascular membranes with release of intracellular contents,
ultrastructural damage of axons, and changes in cerebral blood flow. 
2. Increased intra-cranial pressure, decreased cerebral blood flow, tissue ischemia, cerebral
edema, and functional blood brain barrier dysfunction. 
3. Subsequent metabolic derangement includes widespread release of excitatory
neurotransmitters such as glutamate, severe dysregulation of calcium homeostasis, energy
failure due to ATP depletion, free radical generation, and cell death by necrotic and apoptotic
pathways. 
4. Initial damage, repair and recovery processes begin through the removal of cellular debris, glial
scar formation, and plastic (tissue) changes in neural networks.
Leads to:
1. Brain dysfunction involving either the hemispheres or the deep structures of the brain (including
the reticular activating system, which governs sleep and wake cycles
RAS
RAS tidak menerima sensory input penghidu, letaknya di 2/3 brainstem superior.
Dari brainstem ke thalamus melalui formasio reticularis. Kemudian dilanjutkan ke cerebral cortex.
Talamus sebagai relay station, mengarahkan stimuli ke lokasi tertentu, mengontrol motoric pada jalur
descending.

Unconscious
Patofisiologi
Disfungsi dari cerebral cortex dan gray matter akibat nekrosis, hypoxia, hypoglycemia dan penyebab
metabolic lain sehingga terjadi acute reticular shock. 
Atau kerusakan langsung di brainstem atas (pada bagian RAS).
Demyelinasi yang menyebabkan diskoneksi korteks dan subkorteks, pada kejadian CO poisoning
sehingga hipoperfusi serebral.
Intinya semuanya mengganggu arousal.

 
3. Diagnostic Analysis of Unconsciousness

Systematic team approach to the unconscious patient. ABCDE = airway, breathing, circulation,
disability, exposure; CT = computed tomography; CXR = chest X-ray
History
A collateral history from relatives or other witnesses, including paramedics, is vital. 4 The
patient's recent health, functional status and previous medical history may provide diagnostic
clues as well as guiding decisions regarding ongoing care, such as admission to a critical care
unit. Previous hospital records must be requested urgently and the next of kin contacted. Hospital
pharmacists can obtain a drug history from primary-care shared records. Bystanders may have
witnessed the patient collapse, while paramedics are skilled in surveying the scene for clues, such
as empty drug packets, alcohol or a suicide note.
Examination
After the initial ABC assessment, the level of consciousness should be formally measured and
documented using the Glasgow Coma Scale (GCS) (see Table
Table2).
2). Coma is defined as having a GCS <8 or scoring U on the AVPU (Alert, responsive to Voice,
responsive to Pain, Unresponsive) scale.7 A focused neurological examination should be
undertaken. Motor responses can be purposeful, such as the patient pulling on an airway adjunct,
or reflexive, including withdraw, flexion or extension responses.3 Motor response to graded
stimuli should be assessed in a stepwise approach:8

 verbal stimulus – eg ‘Can you hear me?’

 tactile stimulus – to hands or face
 noxious stimulus – intense but not causing injury, eg pressure on nailbed or supraorbital
ridge.

Eye movements cannot be fully assessed in an unconscious patient. If there is no concern

regarding a neck injury, the doll's eyes or oculocephalic reflex can be performed. A loss of
conjugate eye movement away from the direction the head is moved, with the eyes remaining in a
midorbit position, suggests brain stem dysfunction. Fundoscopy should be performed; important
findings include papilloedema in posterior reversible encephalopathy syndrome (PRES) or
subhyaloid haemorrhage in subarachnoid haemorrhage. Pupil examination can aid diagnosis:3–5

 small pupils (<2 mm) – opioid toxicity or a pontine lesion

  midsize pupils (4–6 mm) unresponsive to light – midbrain lesion
 maximally dilated pupils (>8 mm) – drug toxicity, eg anticholinergic overdose
 mixed and dilated pupil(s) – 3rd (oculomotor) nerve lesion from uncal herniation.

A full examination must be performed, although there are areas of specific relevance in the
unconscious patient. The breath may exhibit the musty smell of hepatic encephalopathy or the
garlic smell of organophosphate poisoning.9,10 When the breath suggests alcohol consumption, a
thorough search for other causes of unconsciousness should continue. In older people, especially
those taking anticoagulant medication, an intracranial bleed remains a strong possibility, even in
the absence of a history of falls or external injury. However, older people often have evidence of
minor injuries, such as bruises, which should alert the attending physician to more serious
intracranial pathology. The presence of generalised tremor or myoclonus points towards a
metabolic cause. Examination of the skin may reveal drug injection sites.
The pattern of breathing should be assessed as well as the respiratory rate.

 Kussmaul respiration – deep, laboured breathing, indicative of severe metabolic acidosis

and commonly associated with diabetic ketoacidosis.
 Shallow with an extremely depressed respiratory rate seen in opiate overdose.
 Ataxic breathing (Biot's respiration) – groups of quick, shallow inspirations followed by
regular or irregular periods of apnoea, suggesting a lesion in the lower pons.11
 Central neurogenic hyperventilation – breathing characterised by deep and rapid breaths
at a rate of at least 25 breaths per minute indicating a lesion in the pons or midbrain.12
 Cheyne–Stokes breathing is seen with many underlying pathologies and is not helpful in
making a firm diagnosis.

Investigations
Investigations aid diagnosis, assessment of severity and monitoring of ongoing care. Before
considering any further investigations, a bedside capillary blood glucose must be performed to
exclude hypoglycaemia (Box 1).
 Urgent imaging of the brain is important and a structural pathology should always be considered
if the cause of unconsciousness is not obvious from the initial rapid assessment. 3–6 Computed
tomography (CT) of the brain is the investigation of choice to exclude common pathologies such
as intracranial blood, stroke or space-occupying lesions. If the CT brain scan is normal and the
diagnosis remains unclear, further imaging with a magnetic resonance scan may be required. If
there is no contraindication, a lumbar puncture should be considered when the cause of
unconsciousness remains unclear or a central nervous system infection is suspected.
Electroencephalography (EEG) should be performed in suspected cases of non-convulsive status
epilepticus. In this condition there is prolonged seizure activity but in the absence of motor signs.
It is more common in older patients. Clinically, patients appear to stare into space with
nystagmus-like eye movements, lip smacking or myoclonic jerks.

4. Importance of “triad of signs”

Triad’s signs ini menandakan Increase Cranial Presure , kalau kita ICPnya naik maka
akan mengakibatkan komplikasi yang ada di bawah yang akan berujung pada kematian
jaringan otak.
  

Brain herniation complications

Brain herniation complications may include:

 extensive brainstem ischemia

 Duret hemorrhage. Duret hemorrhage is a small hemorrhage (or multiple
hemorrhages) seen in the medulla or pons of patients who are rapidly
herniating.
 contralateral midbrain compressed against the tentorium may cause
Kernohan phenomenon
 compression of the ipsilateral posterior cerebral artery will result in
ischemia of the visual cortex with resultant homonymous hemianopsia
 Brain death
 Permanent and significant neurologic problems
Prompt treatment of increased intracranial pressure and related
disorders may reduce the risk for brain herniation.

5. Pathophysiology of expanding Intracranial masses

Tumor progression continues as additional mutations occur within cells of the tumor population. Some
of these mutations confer a selective advantage to the cell, such as more rapid growth, and the
descendants of a cell bearing such a mutation will consequently become dominant within the tumor
population. The process is called clonal selection, since a new clone of tumor cells has evolved on the
basis of its increased growth rate or other properties (such as survival, invasion, or metastasis) that
confer a selective advantage. Clonal selection continues throughout tumor development, so tumors
continuously become more rapid-growing and increasingly malignant.
Like healthy cells, cancer cells can't live without oxygen and nutrients. So they send out signals called
angiogenic factors. These encourage new blood vessels to grow into the tumour. This is called
angiogenesis. Without a blood supply, a tumour can't grow much bigger than a pin head.

Once a cancer can stimulate blood vessel growth, it can grow bigger. It stimulates hundreds of new small
blood vessels (capillaries):
 to grow 
 to bring in nutrients and oxygen

6. Emergency management protocols

Emergency Management
Immediate
 1. Harus amankan ABC dahulu. 
 Tanda-tanda ventilasi yang adekuat adalah tidak adanya cyanosis, RR>8
kali per menit, adanya breath sound pada auskultasi. Apabila ventilasi
tidak adekuat maka diperlukan ventilasi mekanik.
 Sirkulasi dapat diasses melalui pulse dan BP, managementnya adalah
dengan IV fluid replacement, pressor dan obat anti arrhythmia.
2. Lakukan pemeriksaan gula, elektrolit, hepatic and renal function, CBC, PTT aPTT dan cek
obat-obatan. 
3. Pemberian IV 50 ml 50% dextrose, thiamine 100g dan naloxone 0,4-1,2 mg. Dextrose
untuk terapi hipoglikemia, thiamine untuk mencegah perburukan Wernicke
encephalopathy karena pemberian gula secara tunggal, naloxone sebagai antagonis
opioid. Flumazenil 1-10mg dapat diberikan sebagai antidote benzodiazepine. 
4. Lakukan pemeriksaan ABG dan pH untuk menentukan penyebab coma secara metabolic
Respiratory acidosis
 Sedative drug intoxication
 Pulmonary encephalopathy
Respiratory alkalosis
 Hepatic encephalopathy
 Salicylate
 Sepsis
Metabolic acidosis
 Diabetic Ketoacidosis
 Uremic Encephalopathy
 Lactic acidosis
 Methanol intoxication
 Sepsis terminal
Metabolic alkalosis
 Coma unusual
5. Treat seizure bila ada

Next
1. Apabila ada tanda-tanda meningeal lakukan LP
2. Lakukan pemeriksaan neurologis dan PF yang lenkap
3. Order CT apabila curiga structural lesion/ SAH
Later
1. EKG
2. Correct hypo/hyperthermia
3. Correct severe acid base imbalance and electrolyte abnormalities
4. CXR
5. Blood and urine toxicology
6. EEG
 Tambahan LO:

7. cushing Triad

Cushing’s triad refers to a set of signs that are indicative of increased intracranial
pressure (ICP), or increased pressure in the brain. Cushing’s triad consists of bradycardia
(also known as a low heart rate), irregular respirations, and a widened pulse pressure. A
widened pulse pressure occurs when there is a large difference between the systolic blood
pressure(the blood pressure when the heart is contracting) and the diastolic blood
pressure (the blood pressure when the heart is relaxing). Cushing’s triad is indicative of
a medical emergency and medical attention is required. 

What causes Cushing’s triad?

 Increased ICP results in a lack of oxygen in brain tissue and a restriction of cerebral
blood flow in the brain. 
 This is most commonly caused by a head injury, bleeding in the brain (i.e.
hematoma or hemorrhage), tumor, infection, stroke, excess cerebrospinal fluid, or
swelling of the brain. 
 Increased ICP activates the Cushing reflex, a nervous system response resulting in
Cushing’s triad. 
  As the ICP begins to increase, it eventually becomes greater than the mean arterial
pressure, which typically must be greater than the ICP in order for the brain tissue
to be adequately oxygenated. 
i. The difference in pressure causes a decrease in the cerebral perfusion pressure (CPP),
or the amount of blood and oxygen the brain is receiving, therefore leading to the brain
not receiving enough oxygen (also known as a brain ischemia). 
1. To compensate for the lack of oxygen, the sympathetic nervous
system is activated, causing an increase in systemic blood pressure
and an initial increase in heart rate. 
1. The increased blood pressure then signals the carotid and
aortic baroreceptors to activate the parasympathetic
nervous system, causing the heart rate to decrease. 
 As the pressure in the brain continues to rise, the brain stem may start to
dysfunction, resulting in irregular respirations followed by periods where
breathing ceases completely. This progression is indicative of a worsening
prognosis. 

What are the signs and symptoms of Cushing's triad?

 Widened pulse pressure

 Bradycardia 
 Irregular respirations (also known as Cheyne–Stokes respirations) 
o Cheyne-Stokes respirations consist of periods of slow, deep breaths followed by
periods of apnea, when breathing comes to a complete stop. 
 Hypertension, or increased blood pressure 
 Additional symptoms 
o Headaches
o Vomiting
o Blurred vision
o Weakness
o Changes in behavior or level of consciousness

What are the assessment findings of Cushing’s triad?

 Procedural diagnosis is necessary to definitively diagnose Cushing’s triad by measuring

ICP.
o Lumbar puncture (spinal tap) in which the cerebrospinal fluid is measured.
o Continuous monitoring by a catheter placed in the ventricle of the brain. 
 Clinical evaluation can be performed to help determine the underlying cause.
o Medical history review
o Physical examination 
 Imaging may be required to determine the underlying cause.
o CT scans 
o MRI

How do you treat Cushing’s triad?

Treatment is aimed at decreasing the ICP, as well as reversing the cause of the increased
intracranial pressure. Prescribed treatment is often individualized and will depend on the severity
of the symptoms. 

 Medications
o Mannitol (osmotic diuretic medication) is often provided intravenously and can be
highly effective in lowering ICP and increasing cerebral perfusion pressure
(CPP). 
o Other medications often used in combination with mannitol:
 Diuretics (e.g. furosemide)
 Steroids (e.g. methylprednisolone)
 Sedatives (e.g. propofol) 
 Hyperventilation, or breathing very fast, is recommended to help lower ICP. 
 Laying in the reverse Trendelenburg position (with the head elevated) 
 Drainage of the extra cerebrospinal fluid may be required to decrease the pressure. 
 Rarely, a craniotomy, or removal of a small portion of the skull, may be performed to
alleviate the rising pressure. 

If Cushing's triad is left untreated for too long, 

a. Herniation can occur, causing the brain tissue to shift to the opposite side of the brain or
down towards the brainstem (uncal herniation). 
b. Uncal herniation can lead to various symptoms, including loss of certain reflexes, loss
of consciousness, and potentially death. 
c. Infarction, or death of the brain tissue, can occur. 

8. Epdiural hematoma classic triad

  

9. DD of unconscious dan pemeriksaan penunjang unconscious

DD Coma
• Psychogenic unresponsiveness
• Persistent vegetative state
• Locked in syndrome
• Brain Death
10. Derajat Head Injury
 Minimal (Simple Head Injury)

 Nilai GCS 15, tidak mengalami penurunan kesadaran, tidak ada amnesia pasca
trauam (APT), tidak ada defisit neurology.

Cedera Otak/Trauma Kapitis Ringan (Mild Head Injury)

 Nilai GCS 13-15, CT Scan normal, pingsan <30 menit, tidak ada lesi operatif, rawat
rumah sakit <48 jam, amnesia pasca trauam (APT) < 1 jam.

Cedera Otak/Trauma Kapitis Sedang (Moderate Head Injury)

 Nilai GCS 9-12 dan dirawat >48 jam, GCS >12 akan tetapi ada lesi operatif
intrakranial atau abnormal CT Scan, pingsan >30 menit – 24 jam, APT 1-24 jam.

Cedera Otak/Trauma Kapitis Berat (Sever Head Injury)

 GCS <9 yang menetap dalam 48 jam sesudah trauma, pingsan >24 jam. APT > 7 hari.

 
          A 45-year-old male presented in the emergency unit. Around one hour prior to
admission, he fell when getting off a bus, and fall head-first into the street – hitting his
head on a post. Initially, He was unconscious initially but quickly improved. The
paramedics who arrived at the scene then stabilized his airway and applied a cervical
collar to his neck.

On arrival to the ER, the examining physician finds that his GCS was E3M6V3, no obvious
weakness could be determined, Pupils were 3mm, round equal and reactive to light.
There was an abrasion on the Right scalp but no other signs of trauma. His Cervical
Spine X-ray was normal, He was observed in the Emergency Department.

1. What are his problems?

2. Describe the pathophysiology of traumatic unconsciousness

When reassessed 1 hour later, his neurological status had changed. His level of
consciousness was now E2M4V3. His RR is 28, the Rt pupil is 4mm - nonreactive, Left
pupil 2mm and reactive and he has Left sided weakness.  His eye movements are
normal.
5. Please describe and interpret the CT scan

6. Describe your management for this patient in the Emergency department

7. Explain the reasons why you choose this management plan.