by Shanyar Qadirby Shanyar Qadir

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From the Greek koma, meaning "deep sleep" It is an alteration of consciousness in which a

person appears to be asleep, cannot be aroused even by painful stimuli, and shows no awareness of the environment

Acute life-threatening neurological emergency Requires prompt intervention for preservation

of life & brain function

Introduction

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Lethargy: difficulty maintaining an aroused state, can be aroused with little difficulty

Obtundation: decreased arousal but responsive to stimuli, cannot fully be aroused

Stupor: responsiveness to pain but not to other stimuli

Coma: unresponsive even to painful stimuli

Disorders of Consciousness

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Complete paralysis: locked-in state, GBS, botulism

Akinetic-mutism: frontal lobe lesions, tone & reflexes intact

Catatonia

Coma mimics

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Consciousness can be diminished or abolished by Dysfunction within the brainstem Impairment of both cerebral hemispheres Insults that globally depress neuronal activity

(e.g. metabolic disturbances) Unilateral cerebral lesions may cause coma if

they compress or injure contralateral or brainstem structures.

Etiology

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Infection Meningitis Encephalitis Brain abscess

Trauma Shaken baby syndrome Intracerebral hemorrhage Concussion

Toxins Narcotics Antihistamines Anticonvulsants

Hypoxia-ischemia Near-drowning Cardiac arrhythmia Carbon monoxide intoxication Strangulation

Etiologies-1

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Epilepsy Subclinical status epilepticus Postictal states

Stroke Arterial ischemic stroke Cerebral sinovenous thrombosis Hemorrhage

Metabolic derangements Hypoglycemia Hyponatremia or its correction Hypernatremia or its correction Hyperosmolality or its correction Hypercapnia

Etiologies-2

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Vital signs and general and trauma examination Neurologic examination and GCS Screening laboratories (CBC, glucose, electrolytes, BUN,

creatinine, blood cultures, LFTs, urinalysis, urine drug screen) Head CT scan: do emergently if focal neurologic signs,

papilledema, fever - consider rapid MRI instead if available. Lumbar puncture: do emergently after CT scan if fever, elevated

WBC, meningismus; otherwise do according to level of suspicion for diagnosis or if cause remains obscure

Other laboratory tests: for metabolic conditions, coagulation tests, carboxyhemoglobin, specific drug concentrations - do according to level of suspicion for diagnosis or if cause remains obscure

EEG: for possible nonconvulsive seizure, or if diagnosis remains obscure

Brain MRI with DWI, if cause remains obscure

Evaluation

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Size Possible interpretation

Normal eye with two pupils equal in size and reactive to light. This means that the patient is probably not in a coma and is probably lethargic, under influence of a drug, or sleeping.

Pinpoint pupils: opiate overdose, damage to pons. The pinpoint pupils are still reactive to light, bilaterally.

One pupil is dilated and unreactive, while the other is normal. Damage to the oculomotor nerve or possibility of vascular involvement.

Both pupils are dilated and unreactive to light. This could be due to overdose of certain medications, hypothermia or severe anoxia.

Pupillary reflex

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Pediatric GCSSign Pediatric GCS Scor

e

Eye opening

Spontaneous 4

To sound 3

To pain 2

None 1

Verbal response

Smile, orientation to sound, interacts, follows objects

5

Cries, irritable 4

Cries to pain 3

Moans to pain 2

None 1

Motor response

Spontaneous movements (obeys command)

6

Withdraws to touch (localizes pain) 5

Withdraws to pain 4

Abnormal flexion to pain (decorticate) 3

Abnormal extension to pain (decerebrate)

2

None 1

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ABCs: Intubate if GCS ≤8 or respiratory failure Stabilize cervical spine Supplement O2 IV access Blood pressure support as needed

Dextrose 0.25 g/kg (2.5 mL/kg of 10 % dextrose solution)

Treat definite seizures. Lorazepam (0.1 mg/kg, maximum single dose 5 mg). If seizures continue treat as for status epilepticus.

Management-1

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Infection: Ceftriaxone 100 mg/kg (maximum single dose

2 grams) and Vancomycin Acyclovir

Ingestion: Naloxone 0.1 mg/kg IV; maximum 2 mg IV (use

if opioid toxidrome: miosis, respiratory depression, hypotonia)

Increased ICP: Mannitol 0.5 - 1 gram/kg IV

Management-2

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Largely specific to the etiology Mortality rates according to a study in

England: near-drowning - 84% infection - 60% metabolic causes 27% intoxication - 3.4%

Prognosis

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Coma Sequelae

Coma is transient, patients either recover, die or go into a more permanent state of impaired consciousness

Persistent vegetative state (PVS): permanent if lasts > 12 mo after traumatic injury or > 3 mo after non-traumatic injury

Minimally conscious state: severe alteration in consciousness who do not meet criteria for PVS

Brain death: coma, apnea, and absent brainstem reflexes. No chance of recovery, synonymous with death in most countries

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No evidence of awareness of self or environment and no ability to interact with others.

No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli.

No evidence of language comprehension or expression. Intermittent wakefulness manifested by the presence of

sleep-wake cycles. Sufficiently preserved hypothalamic and brainstem

autonomic function to permit survival with medical and nursing care.

Bowel and bladder incontinence. Variably preserved cranial nerve reflexes and spinal reflexes.

Persistent Vegetative State (PVS)

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Thank You!

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1. Nelson Essentials of Pediatrics, 7e – 20152. The Harriet Lane Handbook, 20e - 20153. Plum & Posner's Diagnosis of Stupor & Coma,

4e – 20074. Evaluation of stupor & coma in children. In:

UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2013.

5. Coma on Wikipedia(http://en.wikipedia.org/wiki/Coma)

References