Approach to coma

Moderator: Dr. Yirgalem

MD, Internist, Neurologist
Prepared by: Helina Tesfamichael
 Outline
• Terminologies
• Introduction
• Etiologies
• History
• Physical examinations
• Investigations
• Management
• Prognosis
 Terminologies
• Coma: a deep sleeplike state with eyes closed, from which the
patient can’t be aroused.
• Stupor: a lower threshold for arousability; the pt can be transiently
awakened by vigorous stimuli, accompanied by motor behavior
that leads to avoidance or withdrawal from noxious stimuli.
• Drowsiness: light sleep; easy arousal that may persist for brief
periods.
 Cont’d
• Vegetative state: an awake-appearing but nonresponsive state, usually
encountered in a patient who has emerged from coma.
• Minimally conscious state(MCS): severely impaired consciousness;
minimal but definite behavioral evidence of self/ env’tal awareness is seen.
• Akinetic mutism: a partially or fully awake state in which the patient
remains virtually immobile and mute but can form impressions and think,
as demonstrated by later recounting of events.
 Cont’d

• Catatonia: a hypomobile and mute syndrome; pts make few

voluntary or responsive mov’ts
• Locked-in state: a type of pseudocoma
• an awake but paralyzed pt has no means of producing speech or
volitional limb mov’t but retains voluntary vertical eye mov’ts and lid
elevation, thus allowing the pt to communicate .
 Cont’d
• Brain death: state of irreversible cessation of all cerebral
and brainstem function with preservation of cardiac
activity and maintenance of respiratory and somatic
function by artificial means.
 Introduction
• Consciousness is a state of full awareness of the self and one’s
relationship to the env’t.
• Coma is a severe impairement of consciousness, when the
patient is in a state of unresponsiveness from which they cannot
be aroused.
• The most common neurologic emergency and requires an
organized approach
 Reticular formation
• It resembles a net(reticular) that is made up of nerve cells and
nerve fibers.
• The net extends up through the axis of the CNS from the spinal
cord to the cerebrum.
• It receives input from most of the sensory systems and has
efferent fibers that descend and influence nerve cells at all CNS
levels.
 Ascending Reticular Activating System(ARAS)
• Multiple ascending pathways carrying sensory information to
higher centers are channeled through the reticular formation,
which in turn, projects this information to different parts of the
cerebral cortex, causing a sleeping person to awaken.
• Different degrees of wakefulness seem to depend on the degree
of activity of the reticular formation.
• Acetylcholine plays a key role as an excitatory neurotransmitter
in this process.
 Pathophysiology
• Almost all instances of coma can be traced to either
– widespread abnormalities of the cerebral hemispheres or
– reduced activity of the thalamocortical alerting system, the reticular
activating system (RAS)
 Cont’d
• Coma Due to Cerebral Mass Lesions and Herniation Syndromes
• Coma Due to Metabolic, Drug, and Toxic Disorders
• Epileptic Coma
• Coma Due to Widespread Structural Damage to the Cerebral
Hemispheres
 Differential diagnosis of coma
• The causes of coma can be divided into 3 broad categories:
– those without focal neurologic signs (e.g., metabolic and toxic
encephalopathies)
– those with prominent focal signs (e.g., stroke, cerebral hemorrhage)
– meningitis syndromes (e.g., bacterial meningitis, subarachnoid
hemorrhage, encephalitis).
 Cont’d
• Causes of sudden coma: drug ingestion, cerebral hemorrhage,
trauma, cardiac arrest, epilepsy, and basilar artery occlusion.
• Coma that appears subacutely: preexisting medical or
neurologic problem or, less often, to secondary brain swelling
surrounding a mass such as tumor or cerebral infarction.
 HISTORY
• The cause of coma may be immediately evident as in cases of
trauma, cardiac arrest, or observed drug ingestion.
• In the remainder, certain points are useful:
– the circumstances and rapidity with which neurologic symptoms dev’ped
– antecedent symptoms
– the use of medications, drugs, or alcohol; and
– chronic liver, kidney, lung, heart, or other medical disease.
 Physical Examination
• Signs of head trauma
• Fever or hypothermia
• Tachypnea and aberrant respiratory patterns
• Marked hypertension or hypotension
• Fundoscopic examination
• Cutaneous petechiae
• Cyanosis and reddish or anemic skin coloration
 Neurologic examination
• Level of arousal
• Brainstem reflexes
• Pupillary signs
• Ocular movements
• Respiratory patterns
• Motor exam
 Glasgow Coma Scale( GCS)
Eye response Verbal response Motor respnose

6- obeys command

5- oriented 5- localizing pain

4- eyes open simultaneously 4- confused 4- withdrawal from pain

3- eye opening to verbal command 3- inappropriate words 3- flexion response to pain

2- eye opening to pain 2- incomrehensible sounds 2- extension response to pain

1- no eye opening 1- no verbal response 1-no motor response

9-12 – moderate brain injury

≤8- severe brain injury

 Cont’d
• LEVEL OF AROUSAL
– Compression of nailbeds, supraorbital ridge or the temporomandibular
joint
– Tickling the nostrils
– Pressure on bony prominences and pinprick stimulation

Posturing – severe damage to the corticospinal system

Abduction-avoidance mov’t of a limb- intact corticospinal system
 Cont’d
• Brainstem reflexes
– Pupillary size and reaction to light,
– Spontaneous and elicited eye movements,
– Corneal responses, and
– The respiratory pattern
 Cont’d
• Pupillary Signs
– Reactive and round pupils of midsize (2.5–5 mm)
– One enlarged (>6 mm) and poorly reactive pupil
– An oval and slightly eccentric pupil
– Bilaterally dilated and unreactive pupils
– Reactive and bilaterally small (1–2.5 mm) but not pinpoint pupils
– Unilateral miosis
 Cont’d
• Ocular Movements
– Spontaneous eye movements in coma often take the form of conjugate
horizontal roving
– Conjugate horizontal ocular deviation to one side:damage to the frontal
lobe on the same side or less commonly the pons on the opposite side
• “wrong-way eyes”
 Cont’d
– Eyes turn down and inward :thalamic and upper
midbrain lesions, typically thalamic hemorrhage.
– “Ocular bobbing”:bilateral pontine damage, usually from
thrombosis of the basilar artery.
– “Ocular dipping”: diffuse cortical anoxic damage
 Cont’d
• Oculocephalic reflexes
– “Doll’s eyes”
• presence: reduced cortical influence on the brainstem and intact brainstem
pathways
• absence: damage within the brainstem OR from overdoses of certain drugs
– Oculocephalic maneuvers should not be attempted in patients with
neck trauma
 Cont’d
• Corneal reflex: useful test of pontine function
– CNS-depressant drugs diminish or eliminate the corneal
responses soon after reflex eye movements are paralyzed but
before the pupils become unreactive to light.
– May be lost for a time on the side of an acute hemiplegia
 Cont’d
• Respiratory Patterns
– Shallow, slow, but regular breathing: metabolic or drug-induced
depression of the medullary respiratory centers.
– Cheyne-Stokes respiration: bihemispheral damage or
metabolic suppression and commonly accompanies light
coma.
 Cont’d
– Rapid, deep (Kussmaul) breathing: metabolic acidosis but may
also occur with pontomesencephalic lesions.
– Agonal gasps: lower brainstem (medullary) damage and are
recognized as the terminal respiratory pattern of severe brain
damage.
 Cont’d
• Motor responses
– Motor tone
– Motor reflexes
• Deep tendon reflexes and cutaneous reflexes
– Motor responses
• Posturing : decerebrate or decorticate rigidity
 Investigations
• Chemical-toxicologic analysis of blood and urine
• ABG analysis: in patients with lung disease and acid-base
disorders.
• Serum electrolytes, glucose, calcium, magnesium, osmolarity
• Renal fuction test; BUN
• Hepatic function test : NH3
 Cont’d
• Toxicologic analysis
• Cerebrospinal fluid (CSF) examination
• Cranial CT scan
• MRI
• CT angiography or MRI :if acute posterior circulation
stroke is considered.
• MR spectroscopy, neurosonography
 Cont’d
• EEG
– Predominant high-voltage slowing (δ or triphasic waves) in
the frontal regions
• metabolic coma, as from hepatic failure
– Widespread fast (β) activity
• overdose with sedative drugs (e.g., benzodiazepines)
 Cont’d
• A special pattern of “alpha coma”
– pontine or diffuse cortical damage and is associated with a poor
prognosis.
• A unique EEG pattern in adults of “extreme delta brush”
– Anti–N-methyl-D aspartate [NMDA] receptor form of
autoimmune encephalitis.
 Cont’d
• Normal α activity on the EEG, which is suppressed by
stimulating the patient
– locked-in syndrome
– hysteria, or
– catatonia
 Management
• Immediate goal: prevention of further nervous system damage.
• ABC of life
• Hypotension, hypoglycemia, hypercalcemia, hypoxia,
hypercapnia, and hyperthermia should be corrected rapidly.
• Hyponatremia should be corrected slowly to avoid injury from
osmotic demyelination .
 Cont’d
• An oropharyngeal airway is adequate to keep the pharynx open
in a drowsy patient who is breathing normally.
• Tracheal intubation: if there is apnea,UAO,emesis or
hypoventilation, or if the patient is at risk for aspiration.
• Mechanical ventilation: if there is hypoventilation or a need to
induce hypocapnia in order to lower ICP.
 Cont’d
• IV access is established and naloxone and dextrose: if opioid
overdose or hypoglycemia are possibilities.
• Thiamine with glucose: to avoid provoking Wernicke’s
encephalopathy in malnourished patients.
• IV tissue plasminogen activator or mechanical embolectomy:
– Suspected ischemic stroke including basilar thrombosis with brainstem
ischemia,
– after cerebral hemorrhage has been excluded .
 Cont’d
• Physostigmine
– patients with anticholinergic-type drug overdose
– used only with careful monitoring
• Fomepizole for ethylene glycol ingestion
• Administration of hypotonic IV solutions should be monitored
carefully in any serious acute brain illness because of the
potential for exacerbating brain swelling.
 Cont’d
• Acute bacterial meningitis is suspected:
– Antibiotics including at least vancomycin and a third-generation
cephalosporin are typically administered rapidly along with
dexamethasone
• Anticonvulsants like Lorazepam for pts with seizure
 Prognosis
• Early prognostication of patients with coma outside of brain
death is unwise.
• Medical judgments must be tempered by factors such as age,
underlying systemic disease, and general medical condition.
• Metabolic comas have a far better prognosis than traumatic.
• In patients with head injury, the GCS has predictive value
• For anoxic coma: the pupillary and motor responses after 1 day,
3 days, and 1 wk week have predictive value.
 Reference
• Harrison’s Internal Medicine, 21st edition
• Snell’s clinical neuroanatomy, 8th edition
• Plum and Posner’s diagnosis and treatment of stupor
and coma, 5th edition
Thank You