Unconscious Patient

Dr. A.M Iyagba,

Department of Medicine,
Faculty of Clinical Sciences,
CHS, University of Port Harcourt.
Lecture outline

1. Components of consciousness
2. What is coma?
3. Causes of coma
4. Pathogenesis of coma
5. Approach to the unconscious patient
6. Prognosis
7. Differential diagnosis of coma
8. Herniation syndromes
9. Brain death
 Components of consciousness
• Consciousness has two components:
 Arousal (or wakefulness)
 Awareness (or responsiveness)
• These two components are used to identify the
major conditions of abnormal consciousness such
as:
 Coma
 Vegetative state
 Locked-in state
 What is coma?
• Coma is characterized by the absence of arousal
and awareness.
• It is a state of un-arousable unawareness.
• It is a sleep-like state in which the patient makes
no purposeful response to the environment and
from which he or she cannot be aroused.
• It results from a disturbance of either:
 Brainstem RAS above the mid-pons or
 Both cerebral hemispheres
Causes of coma

The causes of coma can be classified under

two broad groups:

Structural or Metabolic
Structural causes of coma
1. Tumors → primary brain tumors, metastasis.

2. Trauma → SDH, EDH, traumatic SAH.

3. Vascular → Ischaemic stroke, haemorrhagic stroke,

SAH.

4. Infections → Meningitis, encephalitis, brain abscess.

5. Demyelination → Multiple sclerosis, acute

disseminated encephalomyelitis (ADEM)
 Metabolic causes of coma
1. Endocrine
-Hypoglycaemia,
-DKA, HHS, Lactic acidosis 6. Gases
-Myxoedema coma
-CO poisoning
2. Alcohol overdose
-Organophosphate
3. Drug overdose
-Benzodiazepines
-Barbiturates 7. Toxins
- Tri-cyclic antidepressants
-Cyanide
-Opiates

4. Electrolyte derangement
8. Disordered temperature
-↓Na+
regulation-
5. Systemic diseases -Hypothermia,
-Uremic encephalopathy
-Hepatic encephalopathy
-Hyperthermia.
-Anoxic encephalopathy
Pathogenesis of coma
Coma arises by one or a combination of two main
mechanisms:

1. Structural transection/destruction of neuronal tracts

and or structures of the RAS, thalamo-cortical
projections or cerebral hemispheres.

2. Metabolic alteration of the function of cells of the RAS

and its projections.
-Hypoglycaemia, hypoxia, drug overdose, etc
Anatomic basis of coma
Approach to evaluating coma

This consists of:

1. Emergency assessment and stabilization.
2. Perform a focused physical and neurologic
examination.
3. Review history
4. Perform relevant diagnostic tests to
establishing an etiologic diagnosis.
5. Treat the cause if possible
Emergency management
ABCDE!
• A-Airway
• B-Breathing
• C-Circulation & collection of blood samples
(serum glucose, E/U/Cr, LFTs, prothrombin time,
partial thromboplastin time, FBC + ESR, blood
culture, drug screens, ABGs.)
• D-Drugs to stabilize patient emergently
• E-exposure/examination looking out for physical
clues that could point to cause of coma
D-Drugs for stabilization
1. IV mannitol to reduce cerebral oedema
2. 50ml of 50% DW → hypoglycaemia
3. Naloxone(0.4-1.2mg)→ opiate overdose
4. Thiamine (100 mg, IV) → alcoholics and
malnourished
5. Flumazenil(1-10mg) → benzodiazepine overdose
6. Abort seizures → diazepam, lorazepam
7. Antipyretics → fever, hyperthermia
E-Exposure/examination
• Signs of basilar skull fracture
 Racoon eyes→ periorbital ecchymoses
 Battle sign → swelling and discolouration of
mastoid bone behind the ear
 Haemotypanum → blood behind the tympanic
membrane
 CSF rhinorrhoea or otorrhoea
• Depressed skull fracture
• Soft tissue swelling
 History
• Temporal progression of coma is crucial
• Rapid onset → vascular origin e.g stroke or SAH
• Protracted course (days to weeks or more)-
tumors, abscess, chronic SDH.
• Coma preceded by a confusional state or agitated
delirium without lateralizing signs or symptoms is
probably due to metabolic derangement or
infection (meningitis or encephalitis).
• Patients circumstances at the time of onset.
• Fever → meningitis, encephalitis, septicaemia, brain
abscess.

• Headaches, neck stiffness, photophobia → meningitis.

• Head trauma → SDH, SAH, EDH

• Renal symptoms → uraemic encephalopathy

• Hepatic symptoms → hepatic encephalopathy

• Any evidence of empty pill bottles, prescription, or
suicide notes
• Last meal → hypoglycaemia
• Known hypertensive or DM
• IV drug use or drugs of abuse → drug overdose
• Any previous neurosurgery, for e.g, intracranial shunts
• Alchohol abuse
• Exposure to toxins, gas fumes or possible CO/cyanide
• Recent travel to north or meningitis belt→meningitis.
 Neurologic examination in coma

1. Glasgow coma score

2. Signs of meningeal irritation
3. Fundoscopy
4. Pupil examination
5. Occulocehalic responses
6. Occulocaloric responses
7. Limb posture/Motor response to pain
8. Respiratory pattern
9. Reflexes
Signs of meningeal irritation

• Nuchal rigidity

• Kernig’s sign

• Brudzinski’s sign

NB: These signs may be lost in deep coma so

their absence does not exclude these conditions.
 Fundoscopic findings in coma
• Papilloedema → sign of increased ICP.

• Hypertensive eye changes

• Diabetic eye changes

• Choroidal tubercles→ tuberculous meningitis

• Subhyaloid (superficial retinal) haemorrhage →

Subarchnoid haemorrhage
Pupils in coma

• Normal

• Pin point

• Thalamic pupils

• Fixed, midsized (mid-positioned)

• Fixed, dilated pupils

 Normal pupil

• 3-4mm in diameter

• Equal in size bilaterally

• Constrict briskly

• Symmetrical in response to light

• Normal pupils may be found in structural or metabolic

causes of coma
Thalamic pupils

• 2mm in size

• Reactive to light

• Seen in early stages of thalamic compression

from mass lesions

• Due to interruption of descending sympathetic

pathways
Pinpoint pupils
• Pinpoint pupils
• 1-1.5mm in size
• Usually indicates:
 opiate overdose
 focal structural lesion in pons
 organophosphate poisoning or
 miotic eye drops
• Naloxone can distinguish between pinpoint
pupil from pontine lesion or opiate overdose
Fixed, midsized pupil

• 5-6mm in diameter.

• Due to brainstem damage at midbrain level

which interrupts both sympathetic
pupilodialtor and parapsympathethic
pupilloconstrictor fibers.
Fixed, dilated pupils
• >7mm in size.
• Fixed (unreactive to light)
• Due to compression of III and associated
pupilodilator nerve fibres) anywhere along its
course, from midbrain to the orbit.
• May also be seen in anticholinergic or
sympathomimetic drug intoxication.
• Bilateral fixed dilated pupils is one of the signs
of brain death
Eye movements

• Assesses the integrity of brainstem from

cranial nerve III to VIII.

• Occulocephalic or dolls-head maneuver

• Occulovestibular reflex or cold water caloric

testing
Oculocephalic reflexes (doll’s eye movement)
• These are elicited by brisk turning of the head
• Response in metabolic coma or that caused by
bihemispheric structural lesions consists of
conjugate movements of the eyes in the opposite
direction.
• Elicitation of these reflexes in coma patients provide
two pieces of information:
1. Integrity of structures that control ocular
movements and the ocular motor nerves.
2. Loss of cortical inhibition that holds these reflexes
in check
Localization from eye movements
• Lateral downward deviation of one eye→ third
nerve palsy
• Medial deviation of one eye → VI palsy
• Destructive hemispheric lesion → both eyes look
to the side of the lesion.
• Irritative hemispheric lesion (e.g seizure focus)
→both eyes look to the side opposite the lesion.
• Conjugate downward deviation of both eyes
→midbrain lesion or bi-hemispheric lesion.
• Asymmetric eye movements → brainstem disease
 Oculovestibular reflexes/caloric test
• This assesses integrity of brainstem from III to VIII
• It is done with either cold or warm water
• Caveat!
1. Tympanic membrane must be intact
2. No neck fracture.
COWS pneumonic
Cold → Opposite side
Warm → Same side
 Limb posturing
• Assessed by applying strong pressure on the
supra-orbital ridge, sternum or nail beds.

• Limb posturing/motor response to pain is

observed.

• Response can indicate whether condition

causing the coma affects the brain symmetric-
ally (metabolic or diffuse encephalopathy) or
asymmetrically (unilateral focal cause).
Forms of abnormal posturing

• Decorticate posturing → associated with

lesions that involve the thalamus directly or
large masses that compress the thalamus from
above.
• Decerebrate posturing → occurs when brain
dysfunction has descended to the level of the
midbrain
• Bilateral symmetric posturing → may be seen
in both structural and metabolic disorders
• Asymmetric or unilateral posturing → suggests
structural disease in the contralateral cerebral
hemisphere or brainstem.

• Myoclonic jerks → point toward an anoxic cause

of coma & portend a bad prognosis.

• Subtle rhythmic movements → may suggest

ongoing seizures.
 Respiratory patterns in coma patients

1. Normal
2. Kussmaul’s
3. Cheyne-Stokes
4. Central neurogenic
hyperventilation or
pontine respiration
5.Apneusis
6.Ataxic
7.Gasping or agonal gasps
Investigating a coma patient
• Brain CT scan/Brain MRI • Complete blood count

• EEG • Blood culture

• Blood glucose
• CSF analysis
• E/U/Cr plus Ca, Mg
• Chest xray
• LFTs

• ECG • ABG

• Echocardiogram • Toxicologic analysis of blood

& urine
Some brain CT findings in coma

Subdural haemorrhage Extradural haemorrhage

Intracerbral haemorrhage Subarachnoid haemorrhage
Ischaemic strokes
 Treatment of coma
This depends on the underlying cause
• Acute bacterial meningitis→antibiotic
• Tuberculous meningitis →anti-Koch’s
• Septicaemia →antibiotics
• Subdural haemorrhage →burr hole drainage
• Extradural haemorrhage →surgical drainage
• Hypoglycaemia →50% DW, i.m glucagon
• Seizures-AEDs
 Prognosis
• This depends on the underlying cause.
• Reversible lesions such as metabolic, toxic and
surgically amenable lesions have a better
prognosis.
• Anoxic brain injury, diffuse cortical or
brainstem lesions carry a bad prognosis.
• Prognostication should be guarded initially in
all cases of coma.
Differential diagnosis of coma

• Locked-in state.

• Persistent vegetative state

• Psycogenic unresponsiveness or coma

Locked-in state
• This disorder is caused by bilateral injury to
the motor pathways in the ventral pons,
disrupting all voluntary movement except for
up-down ocular movements and eyelid
blinking.
• Function of the cortex and RAS are unaffected.
• The patient is fully awake and aware.
• It can mimic a vegetative state.
Persistent vegetative state-1
• This refers to patients who regain wakefulness
but not awareness that has lasted for at least 1
month following a coma.
• They have:
o Spontaneous eye-opening and sleep-wake cycles.
o Intact brainstem function
o Intact autonomic functions
• They neither comprehend nor produce language
• They make no purposeful movements.
Persistent vegetative state-2
• This condition may persist for years
• Recovery from non-traumatic causes is rare
after 3 months.
• Recovery from traumatic causes is rare after
12 months.
• A subset of these patients have minimal but
definite environmental awareness→this state
is referred to as a minimally conscious state.
Psychogenic unresponsiveness-1

• This is a diagnosis of exclusion and should only

be made on the basis of compelling evidence.
• It may be a manifestation of:
-Catatonic schizophrenia
-Somatoform disorders or
- Malingering.
• The aim of evaluating a patient with
psychogenic coma is to demonstrate clinical
and EEG evidence of wakefulness.
 Psychogenic unresponsiveness-2
• Physical examination reveals no abnormality.
• Neurologic examination reveals:
-Normal pupils that react briskly to light
-Normal eye movements
-Symmetrically decreased tone,
-Normal reflexes and normal (flexor) response to
plantar stimulation.
-Occulo-caloric testing shows brisk nystagmus usually
seen in conscious patients whereas no nystagmus
occurs in unconscious patients.
• EEG is usually that of an awake normal person.
Herniation syndromes
A-Transcalvarial

B-Subfalcine

C-Transtentorial (uncal)

D-Transtentorial (upward)

E-Tonsilar

F-Axial (Central or ‘coning’)