COMA

Dr Bako Istifanus Bintum

Senior registrar, Neurology unit, JUTH
Introduction
• Consciousness comprises state of wakefulness, awareness, or
alertness in which most humans function while not asleep or one of
the recognized stages of normal sleep from which the person can be
readily awaken.
• Unconsciousness/ loss of consciousness or lack of consciousness, is
an alteration of mental state that involves complete or near-complete
lack of responsiveness to people and other environmental stimuli.
Coma
• Coma is a state of unarousable unresponsiveness
• Coma is a deep sleep-like state from which the patient cannot be
aroused.
• It is a profound state of unconsciousness.
• A person in a coma cannot be awakened
• Fails to respond normally to pain, light or sound
• Does not have sleep-wake cycles, and
• Does not take voluntary actions.
• A person in a state of coma can be described as comatose.
Differential diagnosis
• Coma(Unconsciousness) should not be confused with-
• Syncope
• Brain death
• Locked-in syndrome
• Vegetative state

• All persons in coma are unconscious, but all who are unconscious are
not in coma
• Fainting due to a drop in blood pressure and a decrease of the oxygen
supply to the brain is an illustration of a temporary loss of
consciousness.
• Syncope is the medical term for fainting, a sudden,
usually temporary, loss of consciousness
• Generally caused by insufficient oxygen in the brain either by
• Cerebral hypoxia
• Hypotension
• Brain death is the irreversible state when there is no brain activity
(including involuntary activity necessary to sustain life) due to total
necrosis of the cerebral neurons following loss of brain oxygenation
• Reflexes in brain death-
• Pupillary response – none (fixed pupils)
• Oculocephalic reflex- none
• Corneal reflex- None
• Response to the caloric reflex test- none Spontaneous respirations
• Locked-in syndrome is a condition in which a
patient is aware and awake but cannot move or
communicate verbally due to complete paralysis of
nearly all voluntary muscles in the body except for the
eyes.
• It is the result of a brain stem lesion in which the ventral
(anterior) part of the pons is damaged
• Also known as cerebromedullospinal disconnection, de-
efferented state, pseudocoma, and ventral pontine
syndrome.
• A vegetative state is a condition of patients with severe brain
damage who were in a coma, but progressed to a state of partial
awareness.
• After four weeks in a Vegetative State (VS), the patient is classified as
in a Persistent Vegetative State.
• This diagnosis is classified as a Permanent Vegetative State (PVS)
after approximately 1 year of being in a Persistent Vegetative State.
• Patients in the deepest level of coma:
• -Do not respond with any body movement to pain,
• -Do not have any speech, and
• -Do not open their eyes

• Comas typically last for no more than a few weeks.

• However, if the coma continues, the patient is usually considered to be
in a persistent vegetative state with Very less chance of awakening
after remaining in that state for one year.
Causes of coma
• Vascular
• Infectious
• Neoplastic
• Degenerative
• Inflammatory-immunologic
• Congenital-developmental
• Autoimmune
• Toxic/ traumatic
• Endocrine/ metabolic
Pathophysiology
• The pathophysiology of unconsciousness results from neuronal
dysfunction due to a reduction in the supply of glucose or oxygen to
the brain.
• In cases involving structural lesions of the central nervous system,
coma can occur through either the direct destruction of brain arousal
centers or secondary damage caused by the shifting of intracranial
structures, vascular compression, or elevated intracranial pressure
• The anatomical seat of arousal is the ascending reticular activating
system(RAS) in the brainstem.
• Neurons of this system originate in the dorsal pons and midbrain,
form connections in the thalamus, and project to various regions
within the cortex.
• The cortex plays a pivotal role in processing, integrating, and
providing context to the information it receives, ultimately generating
awareness.
• The RAS receives impulses from the spinal cord and cortex,
facilitating awareness of the surrounding environment
• Damage to the below-mentioned 3 significant areas of the brain results
in unconsciousness
• 1. Bilateral Hemispheric Damage -Extensive damage to the cerebral
cortex, resulting from conditions such as hypoxic or ischemic injuries
or brain trauma, leads to neuronal death and denervation of cortical
regions.
• 2. Diencephalic (Thalamic) Injury - bilateral thalamic lesions can
manifest findings similar to those observed in cases of bilateral
cortical injury, because it harbors relay nuclei responsible for directing
afferent input to the cortex.
• 3. Upper Brainstem Injury -The dorsal pons and midbrain contain
the RAS. Lesions in this area can inhibit consciousness and result in a
comatose state.
Management of coma
• History
• Events from attendance/ visitors focusing on probable causes
• Trauma, Drug ingestion, Alcohol
• Rapidity with which neurologic symptoms developed
• Preceding medical/Neurologic symptoms (Fever, Headache, Vomiting,
Seizures, dizziness, Diplopia)
• Medical diseases: Hepatic/Renal/cardiac/Respiratory
• Past history: TIA,
• General physical examination:
• Vitals: Pulse, BP, Temperature, Respiratory rate and pattern of
breathing
• Oxygen saturation
• Skin rash
• Bleeding manifestation
• Odour
• Anemia/ Jaundice/ Cyanosis
• Pattern of Breathing:
• Cheyne-stokes breathing- Periods of apnea alternate with periods of
hyperapnea seen in Brain damage (bihemispheral damage) due to cerebral
hemorrhage or trauma
• Kussmaul’s respiration- Deep and rapid respiration due to stimulation of
respiratory center seen in Metabolic acidosis due to Ketoacidosis or Uremia
• Hyperventilation- Rapid and shallow breathing resulting in alkalosis and
tetany
• Ataxic breathing- Irregular in time and depth seen in Brain stem damage.
• Shallow,slow,regular- Metabolic/Drug related
• Neurologic assessment:
First observe the patient without intervention
Assess the level of arousal/Elicited movements
Glasgow coma scale
Response to noxious stimuli
Pupillary light reflex:
• -Normal reactive mid size pupil-Excludes mid brain lesion
• -One unreactive and dilated pupil-Compression of third cranial nerve
• -Bilateral dilated and unreactive pupil-Severe mid brain damage
• -Reactive but bilateral small pupil-Metabolic encephalopathy, Deep
hemispheric lesion
• -Bilateral pin point pupil-Pontine hemorrhage, Barbiturate/ Opioid
overdose
• Ocular movements
• -Note resting eye position
• -Look for rectus palsy
• -Roving eye movements-slow random deviation of eye position and
are common in metabolic/hepatic encephalopathy and sometimes
disappears in deep coma
• -Nystagmus
Oculocephalic reflex
• -Elicited by moving head from side to side-normally, the eye moves in
the opposite direction (doll’s eye)
• -Doll’s eye reflex is negative if the eye remain in the midline or move
in same direction with head and signifies brainstem dysfunction
Oculovestibular reflex
• -Caloric stimulation:-Irrigating external auditory canal with either cold
or warm water-Observe for the tonic deviation of the eyes(nystagmus)-
absence signifies brainstem death.
• Remember-cold opposite/warm same(COWS)
Corneal reflex
-slightly touching the cornea with tissue or cotton swab induces rapid
bilateral blink reflex (direct and consensual)
-it assesses the integrity of the trigeminal and facial cranial nerves in the
brainstem
• Other Neurologic examination • SYSTEMIC EXAMINATION:
in detail • Cardiac
• - Cranial nerve • Respiratory
• -Motor • Hepatic
• -Meningeal signs • Renal
• -Skull and Spine
• Investigation:
• 1. Blood• TC, DC, Hb • Glucose, Electrolytes, Calcium, Urea,
Creatinine, ABG, NH3 • Toxicological screening
• 2. CSF analysis
• 3. Neuroimaging -CT scan head, MRI head
• 4. EEG
• Contraindications of LP
• Signs and symptoms of raised ICP (Papilloedema, decreased LOC,
progressive deficit, headache) due to mass lesion,Do CT first and then
proceed to lumbar puncture (LP) if there is no neurologic findings
suggestive of localized mass lesion
• Obstructive hydrocephalus, or evidence of blood infection at LP site
• Coagulopathy (e.g. anticoagulant drugs) or thrombocytopenia
• Developmental abnormality (i.e. tethered spinal cord)
• Diagnostic Tests with CSF
• Opening pressure
• Protein and Glucose
• Cell counts
• Color
• VDRL • Viral PCR • IgG levels • Oligoclonal bands • Fungal antigens
• Microbiological stains (Gram, ZN, fungal)
• Bacterial culture and PCR-Correlate with typical CSF Findings in
CNS Infections
• Treatment: • Treat the metabolic cause:
• Immediate goal: • Glucose, Electrolytes, Acid Base
• To prevent further brain damage imbalance
• -ABC • Antidotes:
• -Oropharyngeal airway • -Naloxone (For morphine/
• -Tracheal intubation heroin)
• -Correction of Hypotension • Assess for head injury/ Cervical
• -Securing IV access/Drawing blood spine injury
samples
• -Hypo/Hyperthermia
• Control of Raised ICP • Control of seizures
• -Head end elevation:15-30 ̊ • Treatment of underlying cause
• -Hyperventilation to decrease
PaCo2
• -Osmotic agent: Mannitol,
Furosemide