Coma
a state of unrousable
unresponsiveness
Anatomical Basis of Consciousness
Consciousness is a complex phenomenon.
intact reticular activating system in the
brainstem.
cerebral cortex that provides the content of
consciousness.
neurotransmitters.
Diffuse hemisphere damage –
trauma, hypoxia, hypoglycaemia, infection, drugs
Bilateral thalamic damage
Brainstem compression, brainstem ischaemia or haemorrhage
Management
Airway
Breathing
Circulation
Diagnosis of Coma
Focal neurological signs – brain insults -
stroke, encephalitis
No focal neurological signs – systemic
causes – drugs, sepsis
Examination
History
Look for systemic signs of cause of coma
Look for focal neurological signs for cause of
coma
Assess level of coma
Features on Examination Possible Diagnoses
Fever Malaria, meningitis, encephalitis
Jaundice Malaria, Hepatic encephalopathy
Dehydration Diabetic coma
Ketotic breathing DKA
Acidotic breathing DKA, methanol
Petechial haemorrhage Meningococcal sepsis, S. suis
Hypersalivation Organophosphate poisoning
Orbital/Mastoid process bruising Basal skull fracture
Neck stiffness Meningitis, SAH, herniation
Papilloedema Raised intracranial pressure
Constricted pupils Opiate, pontine haemorrhage
Muscle fasciculation Organophosphate poisoning
Neurological examination
Assess level of coma (G.C.S.)
Pupils
Eye movements
Asymmetry of limb response
Glasgow Coma Scale
15 point scale
Best score for eye opening, verbal
response and motor response
Useful for monitoring comatose patients
Eye opening
1 Eyes closed
2 Eyes open to a painful stimulus
3 Eyes open to voice
4 Eyes open spontaneously
Motor Response
1 No motor response
2 Extensor response
3 Flexor response
4 Withdrawal from painful stimulus
5 Localises to pain
6 Responds to command
Verbal Response
1 No verbal response
2 Groans
3 Words only
4 Confused speech
5 Orientated
AVPU scale
Alert
Voice responsive
Pain responsive
Unrousable
Pupils
Reflex and spontaneous eye movements
Spontaneous bobbing
Oculocephalic
Oculovestibular
Focal neurological signs – think
catastrophic brain lesion (stroke)
No focal neurological signs – think
systemic illness (drugs, sepsis)
Head injury
Mechanisms of brain injury
Immediate management
Long term complications
Mechanisms of injury
Diffuse injury – from minor injuries to
diffuse axonal injury with axonal
retraction balls
Mass lesions – haematomas,
intracerebral contusions
Immediate Management
Goal:
Prevention of secondary brain injury
Avoiding hypoxia, treating sepsis,
controlling cerebral perfusion pressure
Immediate Management
Resuscitation ABC
Airway, Oxygen 100%
Intubate and hyperventilate if necessary
Immobilise neck
Immediate Management
Assess level of consciousness (GCS)
Scalp/face lacerations/bruises
Blood/CSF from ear/nose
Palpate neck and immobilise
Neuro exam: pupils,eye movts, power, reflexes
Immediate Management
I.V. blood count electrolytes
alcohol, toxicology
gases, clotting, group
Mannitol if pupils unequal
Diazepam for seizures
Antibiotics ATT for fracture CSF leak
?glucose ?thiamine
Immediate Management
Brief history from witnesses/relatives
X-ray skull, neck, chest, pelvis, femur
ECG
Immediate Management
CT if
GCS 14/15 in 2h LOC &
<=13/15 after high velocity injury
Focal deficit > 65 yrs
Seizure coagulopathy
Fracture
Vomitingx1
Immediate Management
VENTILATE if
GCS 8 or less or >8 but going down
Respiratory irregularity
Fits
Bleeding into mouth
Facial/jaw injury
PaO2 < 9kpa on air
PaO2 <13kpa on oxygen
Brain perfusion
Blood flow to the whole brain is proportional to the
cerebral perfusion pressure:
CPP = MAP - ICP
A healthy brain can regulate its own CPP despite
changes in MAP and ICP, though an injured brain
loses this ability
Intracranial pressure
Pressure α Blood + CSF +Tissue
Blood Position
Mannitol
Thiopentone
CSF Drain CSF
Mannitol
Tissue Surgery, hyperventilation
Box Craniectomy or burr hole
Long Term Complications
Seizures
Cognitive problems – post traumatic
amnesia (predictor of outcome)
Post concussion syndrome
Aetiology of non-traumatic coma in
Ethiopia
Infective (cerebral malaria, meningitis)
Metabolic causes (hepatic encephalopathy,
hypoglycaemia)
Catastrophic intracerebral events
Poisoning
Coma prognosis
In the Ethiopian study, 60% of patients died
Worse outcomes for HIV+ and infective
causes
In UK best predictor is whether comatose at
day 3
Differential diagnosis of coma
Vegetative state
Locked in syndrome
Catatonia
Psychogenic coma
Brain tumours - presentation
Headache
Seizures
Worsening focal neurological signs (hemiparesis,
dysphasia)
Confusion
Tumour types
Primary - glioma, schwannoma
Secondary - metastasis from almost any
tumour type
Non-brain cranial tumour - meningioma
HIV related - lymphoma
Glioma
Commonest tumour in adults
Low grade glioma usually progress to high grade
glioma
High grade glioma has a poor prognosis (1 to 3
years)
Complete resection is impossible, although
debulking may improve survival
Primary central nervous system lymphoma
HIV related lymphoma, though incidence is rising in
the immune competent
Perhaps related to EBV
Tumour cells present in CSF
Chemotherapy (methotrexate is mainstay of treatment
Mean survival 40 months
Meningioma
Slow growing tumour, arising from meninges
Histologically benign, although may have a
malignant course
Women more than men 3:1, associated with NF
2
If complete surgical removal is feasible, recovery
is usually complete
Acoustic neuroma
Arise most commonly on the 8th nerve
Slow growing, histologically benign
tumours
Present with unilateral deafness,
unsteadiness, though rarely vertigo
Metastatic tumours
Can arise from most tumour types
Differentiation from tuberculomas may
be difficult
Hunt for a primary cancer may not be
worthwhile (unless it is symptomatic)
Paraneoplatic neurological syndromes
Limbic encephalitis
Brainstem encephalitis
Paraneoplastic cerebellar degeneration
Opsoclonus myoclonus
Myelitis
Dorsal root gangionopathy
Neuropathies
Myopathies
Lambert Eaton syndrome
Management options
Surgery – diagnosis, debulking or
complete resection
Radiotherapy – high dose to area of
tumour
Chemotherapy – blood brain barrier
Symptom Management
Seizures may respond to carbamazepine
Headache and focal neurological signs may
in part be due to oedema, and may respond
to steroids
Nausea – consider centrally acting
antiemetics cyclizine, prochlorperazine
Case 1
A 23 year old woman comes to hospital and seems to
be unconscious. Her husband says she was well the
day previously, though overnight was agitated. She
was delirious at times.
She opens her eyes to your voice, though doesn’t look
at you directly. She cannot follow commands, though
draws her hand away as you insert a drip. She is
saying nothing.
Can you make a sensible differential diagnosis?
What questions would you ask her husband
What is her GCS?
She is pyrexial and has a stiff neck. She is
hypotensive (80/60mmHg) and tachycardic.
Both her pupils are equal and react to light.
What is your diagnosis now?
What is the nest thing you want to do?
Would you do any investigations?
Case 2
A 50 year old lady is brought to hospital by her family.
She has been behaving oddly for about a month,
often shouting at her husband and sons for trivial
reasons. She can no longer seem to hold the track of
a conversation, and she mumbles as she speaks.
She has bruises on her right arm and leg, from where
she has bumped herself and fallen. Her husband is
worried as she has fallen, and now cannot get up.
What is you differential diagnosis
What would you look for on a systemic examination?
She has a right hemianopia. You catch
a glimpse of her fundi, which look
normal. She has weak right arm,
especially the hand, and a weak right
leg. Her reflexes are all brisk and her
right plantar response is extensor.
She looks to have lost a lot of weight.
What is your differential diagnosis?
Would you do any other tests?
