EMERGENCY MEDICINE BLOCK

CASE 6

Ronald Chrisbianto Gani

405090223
Faculty of Medicine
Tarumanagara University

CRANIOCEREBRAL INJURY

MECHANISM

Adams and Victors Principle of Neurology 9th

GLASGOW COMA SCALE

Classification
Severe
7 or less

Moderate
8-12

Mild
12 or more

Adams and Victors Principle of Neurology 9th

PATHOPHYSIOLOGY
Increased Intracranial Pressure (ICP)
Caused by edema and traumatic mass
lesion
If Cerebral Perfusion Pressure (CPP)
compromised vasoparalysis no
autoregulation massive cerebral
vasodilation outpouring fluid into
etravascular space vasogenic edema
increase ICP brain death
Can cause herniation syndrome
brainstem compression

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Brain swelling and Cerebral Edema
Brain swelling : increased intracranial
blood volume, as compensatory
mechanism to increased metabolic
needs
Cerebral edema : increase in brain
volume caused by an absolute increase
in cerebral tissue water content
(vasogenic or cytotoxic)

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Altered level of conciousness
Interruption of the RAS or cortex
Other causes : hypotension, hypoxic,
hypoglycemia, post-traumatic seizure,
brain swelling

Cushings Phenomenon
Hypretension, bradycardia, respiratory
irregularity
As response to increased ICP

Rosens Emergency Medicine 7th E

PATHOPHYSIOLOGY
Cerebral Herniation
Increasing cranial volume and ICP
overwhelm the natural compensatory
capacities of CNS
Result of : brain swelling, edema,
traumatic mass lesion
Mortality rate 100% if without
immediate neurosurgical intervention

Rosens Emergency Medicine 7th E

DIAGNOSIS
History
Mechanism of injury
Past medical history and medications
Recent drugs or alcohol use
Complaints immediately after event

Physical Examination
Mental status, GCS, pupilarry size and
responsiveness, motor strength and
symetry

Rosens Emergency Medicine 7th E

DIAGNOSIS
Pupilarry exam
Pupilarry assymetry, loss of responsiveness,
dilated, suggest herniation syndrome

Motor Examination
Hemiparesis contralateral to a fixed and
dilated pupil herniation syndrome
Decorticate postu
ring injury above midbrain
Decerebrate posturing caudal injury (bad
prognosis)

Rosens Emergency Medicine 7th E

DIAGNOSIS
Brainstem function
Oculocephalic response (dolls eye maneuver)
Oculovestibular response (cold water calorics)
CN Exam : CN III, V, VII, IX, X

Deep Tendon Reflexes and Pathologic

Reflexes
Babinski sign
Rectal tone and anal reflexes

Other
Head and neck for external trauma
Carotid artery dissection

Rosens Emergency Medicine 7th E

MANAGEMENT OF
TRAUMATIC BRAIN INJURY (TBI)
Severe TBI (GCS 8 or less) or
presence of any intracranial
contusion, hematoma, laceration
Moderate TBI (GCS 9-13)
Mild TBI (GCS 14-15)

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI
Clinical prognostic indicators
Initial motor activity
Pupilarry responsiveness
Patients age and premorbid conditions
Occurence of secondary systemic insult

Overall mortality : 60%

Divided in : Out-of-Hospital and ED
management

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI
Out of hospital management
Airway and IV access
Assessment : GCS, pupil exam,
consciousness, motor strength and
symmetry
Cardiac monitor in transport
Search for external head trauma
Avoid excessive blood loss
Sedative for agitated patients
Intubation is still a controversy

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI
Emergency Department Management
Airway : intubation, Lidocaine,
Succinylcholine, or Ethomidate
Hypotension : search for other cause,
sign for profound blood loss, give fluid
(NS or RL) or blood tranfusion
Hyperventilation : to reduce PCO2 to 3035mmHg induce vasoconstriction
reduce risk of herniation

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI
Osmotic agents : Mannitol (0,25-1g/kg)
and hypertonic saline to reduce
increased ICP
Barbiturates : Pentobarbital. Reduce
cerebral metabolic demands.
Cranial decompression : Burr Holes
Seizure prophylaxis : Diazepam
(0,1mg/kg up to 5mg IV every 10 mins
up to total 20mg) for acute setting,
phenytoin or fosphenytoin for long term
Antibiotic prophylaxis

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI
Recombinant Factor VIIIa : hemostatic
agent
Ancilarry evaluation
Lab test : urine tox screen, blood alcohol
level, CBC, Electrolytes, Glucose,
coagulation study
Neuroimaging

Rosens Emergency Medicine 7th E

HEAD IMAGING MODALITIES

Rosens Emergency Medicine 7th E

MANAGEMENT OF SEVERE
TBI

Rosens Emergency Medicine 7th E

MANAGEMENT OF
MODERATE TBI
Clinical features
Change in consciousness, progressive
headache, post-traumatic seizure, vomiting,
post-traumatic amnesia
Talk and deteriorate / die : in elders and and
anticoagulant patient

Management :
Close clinical observation
Early CT-Scan
Aggresive neurosurgical intervention

Rosens Emergency Medicine 7th E

MANAGEMENT OF
MODERATE TBI
Complication
Overall mortality rate : 20%
Memory difficulties
Persistent headache
Long-term diasbility

Rosens Emergency Medicine 7th E

MANAGEMENT OF MINOR
TBI

Rosens Emergency Medicine 7th E

MANAGEMENT OF MINOR
TBI
Temporary and brief interruption of
neurologic function after head
trauma and loss of consciousness
Clinical Features
Headache, nausea and emesis, transient
disorientation, confusion, post-traumatic
amnesia
Balance deficit, impaired verbal
memory, delayed language
comprehension, slowed speech

Rosens Emergency Medicine 7th E

MANAGEMENT OF MINOR
TBI
Imaging : CT-Scan
Low Risk : usually not indicated
Moderate risk : selective or only observation
High risk : consider to indicate

MRI for detecting diffuse axonal injury,

ischemia after TBI, some hemmorhagic
lesions
Ancilarry studies
Urine tox screen, blood alcohol level, CNS
biomarkers (not clinically useful in emergency
state)

Rosens Emergency Medicine 7th E

MANAGEMENT OF MINOR
TBI
Disposition
Discharged after normal normal
examination and a reasonable period of
observation (4-6h)
If any doubt exist prolonged
observation (12-24h)
If patient return with delayed
complications CT-Scan
Neurosurgical intervention is rarely
needed

Rosens Emergency Medicine 7th E

SHOCK

SPECIFIC CAUSES
Hemmorhagic shock
Rapid reduction in blood volume
vasoconstriction + cardiac contraction
and HR (compensation)
Cells produce and release lactic acid
acidemia
After loss of 1/3 of total blood severe
hypotension
During resuscitation neutrophils
attack organs cell injury

Rosens Emergency Medicine 7th E

SPECIFIC CAUSES
Septic Shock
Mostly caused by gram-positive organism
Results : relative hypovolemia, cardiovascular
depression, systemic inflammation ARDS
Pulmonary symptoms more severe than others

Cardiogenic Shock
Myocardial pump failure
Occurs when >40% myocardium undergoes
necrosis caused by many other pathologic
factors (hypoxemia, toxins, ishcemia, immunemediated)

Rosens Emergency Medicine 7th E

CLINICAL FEATURES

Rosens Emergency Medicine 7th E

CLINICAL FEATURES AND

DIAGNOSIS

Rosens Emergency Medicine 7th E

SPECIFIC DIAGNOSIS

Rosens Emergency Medicine 7th E

SPECIFIC DIAGNOSIS

Rosens Emergency Medicine 7th E

MANAGEMENT
Monitoring perfusion status
Continuous ECG
Pulse oxymetry
Repeated BP measurement
Urine output (N : 1ml/kg/hr)
Serum lactate concentration
CVP

Rosens Emergency Medicine 7th E

RESUSCITATION
FLOW
DIAGRAM

Rosens Emergency Medicine 7th E

SPECIFIC MANAGEMENT

Rosens Emergency Medicine 7th E

SPECIFIC MANAGEMENT

Rosens Emergency Medicine 7th E

SPECIFIC MANAGEMENT

Rosens Emergency Medicine 7th E