This document provides an overview of coma, including definitions, terminology, causes, assessment approach, management, and prognosis. It defines coma as a state of unarousable unresponsiveness and discusses related altered states of consciousness like stupor, delirium, and vegetative state. Common causes of coma are categorized as those with focal signs, without focal signs but without meningeal irritation, and without focal signs but with meningeal irritation. The rapid assessment approach is outlined, including stabilization, history, neurological exam, investigations like CT/MRI, and management of identified issues. Prognosis depends on etiology, depth and duration of impaired consciousness, with infectious causes generally having better outcomes than hypoxic-

1. PRESENTER: DR. MUFEEDA ALUNGAL
MOHAMED
MODERATOR: DR. RATHIKA. D. SHENOY

2.  Definition of coma
 Terminology – States of altered consciousness
 Causes of coma
 Approach to coma:
Rapid assessment and stabilisation
History
Examination and neurological assessment
Investigations
Management
 Prognosis

3. State of arousal (wakefulness) with awareness of self and
environment
Arousal mediated by - Brainstem
- Subcortical structure
- Cerebral cortex
 Awareness primarily mediated by cerebral cortex with
subcortical connections

4.  State of ‘unarousable unresponsiveness’
 Even strong exteroceptive stimuli fail to elicit
recognisable psychologic response; unresponsive to pain

5.  Stupor – Spontaneous unarousability interruptive only by
vigorous, direct external stimulation ; responsive only to
pain
 Delirium – An acute or subacute reduction in awareness,
attention, orientation and perception (clouding of
consciousness), associated with abnormal sleep/wake
patterns and often psychomotor disturbances
 Syncope – Brief loss of consciousness caused by global
failure of cerebrovascular perfusion

6.  Dementia – A sustained multidimensional or global
decline in cognitive function
 Vegetative state – A sustained, complete loss of cognition,
with sleep/wake cycles and other autonomic functions
being relatively intact; either follow acute, severe bilateral
cerebral damage or develop gradually as the end stage of
progressive dementia

7.  A state of preserved arousal and awareness
 Preservation of intellectual activity accompanied by
severe or total incapacity to express voluntary responses ,
vertical eye movement is present
 Due to damage to or dysfunction of descending motor
pathways in the brain or peripheral motor nerves
 Normal EEG activity
 Sparing midbrain – Caused by severe neuromuscular
disease

8. COMA
STRUCTURAL
LESIONS
(FOCAL)
Supratentorial
(Hemispheric)
Infratentorial
(Brainstem)
METABOLIC
DISORDERS
(DIFFUSE ,
SYMMETRIC)

9. Clinically categorized causes of coma :
1) Coma with focal signs
2) Coma without focal signs and without meningeal
irritation
3) Coma without focal signs and with meningeal irritation

10.  Coma with focal signs
• Intracranial hemorrhage
• Stroke: arterial ischemic or sinovenous thrombosis
• Tumors
• Focal infections-brain abscess
• Post seizure state: Todd’s paralysis
• Acute disseminated encephalomyelitis

11. Coma without focal signs and without meningeal irritation
• Hypoxia-Ischemia
• Metabolic disorders
• Systemic Infections
• Post infectious disorders
• Post immunization encephalopathy
• Drugs and toxins
• Cerebral malaria
• Hypertensive encephalopathy
• Post seizure states
• Non-convulsive status epilepticus

12. Coma without focal signs and with meningeal irritation
• Meningitis
• Encephalitis
• Subarachnoid hemorrhage

15.  Establish and maintain Airway
 Ventilation, Oxygenation as indicated
 Circulation : Establish IV access, send investigations,
check blood glucose levels
 Identify signs of cerebral herniation or raised ICP
 Temperature: treat fever & hypothermia

16.  History
 Physical examination
 Rapid neurological examination

20. 1) Level of consciousness
2) Pupillary abnormalities
3) Brainstem function
4) Motor response
5) Herniation Syndromes
6) Other neurological findings

24. Light reaction: Absent - deep sedative poisoning or acute
or chronic structural brainstem damage
Equality: 15% of normal patients have mild anisocoria,
but new or >2-mm dilation means parasympathetic (3rd
nerve) palsy
Extraocular movements: Absent - deep drug poisoning,
severe brainstem damage, polyneuropathy, or botulism
Dysconjugate deviation: Acute 3rd, 4th, or 6th nerve palsy
or internuclear ophthalmoplegia

25. Spontaneous eye movements: Nystagmus, bobbing, and
independently moving eyes - brainstem damage
Oculocephalic or oculovestibular responses: Absence of
responses means drug overdose or severe brainstem
disease
- dysconjugate responses with equal pupils-
internuclear ophthalmoplegia
- unequal pupils - 3rd nerve disease

27.  Observe the respiratory pattern, assessing corneal
reflexes, and testing oculocephalic (doll’s eye) or
oculovestibular (cold caloric) reflexes
Cheyne–Stokes respiration - bilateral hemispheric or
diencephalic dysfunction. It may also precede
transtentorial herniation. The hyperpneic periods have a
characteristic smooth, crescendo-decrescendo pattern
 Central neurogenic hyperventilation- midbrain
dysfunction (tachypneic and hyperpneic)

28.  Apneustic breathing- damage in the middle to lower
pontine region (prolonged pause at full inspiration)
Clusters of breaths separated by periods of apnea- low
pontine to upper medullary lesions
Ataxic or irregular breathing, slow regular breathing, or
agonal respiration- Medullary lesions

31.  Assessing muscle tone, observe spontaneous and stimulus-elicited
movements, and test deep tendon reflexes.
 Painful stimuli- to elicit motor responses in an unconscious child.
 Asymmetries suggest involvement of the corticospinal tracts in the
cerebral hemisphere or brainstem.
 Presence of spontaneous limb movements (eg, withdrawing from or
pushing away a painful stimulus) suggests a lighter depth of coma.
 Decerebrate posturing includes extension and internal rotation of the arms
and legs- brainstem involvement from a compressive or destructive process
 Decorticate posturing produces adduction and flexion at the elbows,
wrists, and fingers, with leg extension and rotation- implies a more rostral
and potentially less dire insult

33.  Brain tissue deforms intracranially and moves from higher to lower
pressure when there is asymmetric, unilateral or generalized
increased intracranial pressure.
 Signs of herniation tend to progress in a rostrocaudal manner.
 The importance lies in recognition and prompt treatment, before
the damage becomes irreversible

35.  Neuro-ophthalmologic examination.
Funduscopy - Papilledema , Haemorrhages
 Signs of meningeal irritation- Neck rigidity -- meningitis, tonsillar
herniation or cranio cervical trauma
- The Kernig’s and Brudzinski’s
signs are more reliable signs of meningeal irritation

36.  Basic laboratory investigations:
Immediate blood glucose by reagent strips
CBC + differential, Peripheral smear, RDT for malarial
parasite Electrolytes Coagulation profiles Liver Function
test Renal function test Calcium, Magnesium Lactate
Arterial blood gas Urine for reducing substance and ketone
 CT - intracranial hemorrhage, cranial trauma, stroke,
herniation and cerebral edema. A contrast study may reveal
features of infection in the form of meningeal enhancement,
brain abscess or neurocysticercosis

37.  Lumbar puncture: CSF should be tested for cell count, glucose,
protein, Gram stain, Ziehl-Neelsen stain, bacterial culture, viral
polymerase chain reaction for Herpes Simplex virus, Latex
agglutination test, and additional cultures guided by clinical
suspicion (fungal or tubercular)
 MRI: to evaluate parenchymal abnormalities. Imaging may reveal
subtle signs of edema, ischemia, or demyelination before these signs
are visible on CT scan
 If MRI results are normal, the most likely causes of coma are
intoxication, psychologic factors, or related to seizure

39.  Electroencephalogram — In coma of unknown etiology- only means
of recognizing non convulsive status epilepticus (NCSE), especially
in patients who are paralyzed.
 Periodic epileptiform discharges may occur in NCSE but also in
underlying brain injury without seizures
 Periodic lateralized epileptiform discharges- herpes encephalitis or
infarction.
 Multifocal or generalized periodic discharges can also be seen with
metabolic and infectious etiologies and are characteristic of subacute
sclerosing panencephalitis

40.  Stabilization of vitals: airway, breathing and circulation
 Identification and treatment of brain herniation and raised
intracranial pressure: hyperventilation, mannitol/3% saline etc.
 Identify and treat hypoglycemia with intravenous dextrose (2 ml/kg
10% D, Then glucose infusion rate of 6–8 mg/kg/min)
 Identification and treatment of seizures: Tonic clonic movements,
tonic deviation of eyes or nystagmus, history of a seizure preceding
the encephalopathy - anticonvulsant should be administered.
Lorazepam should be given (0.1 mg/kg), followed by phenytoin
loading (20 mg/kg)

41.  Maintenance of normothermia
 Acid base and electrolyte abnormalities should be corrected
 Treatment of infections: In case of suspected sepsis/ meningitis - broad spectrum
antibiotics (ceftriaxone, vancomycin) should be instituted immediately.
 If viral encephalitis is likely, then samples for PCR for herpes simplex virus
should be sent and acyclovir should be started
 Antimalarials(quinine/artesunate)- If there is a clinical suspicion of cerebral
malaria.
 Antidotes: Naloxone (0.1 mg/kg) should be used in case of suspected opiate
poisoning. Flumazenil is useful for benzodiazepine overdosage
 Steroids- Acute disseminated encephalomyelitis, meningococcemia with shock,
enteric encephalopathy, tubercular meningitis, and pyogenic meningitis.
 If metabolic causes have been identified, e.g. diabetic ketoacidosis, hepatic
encephalopathy, uremia or hyperammonemia, these should treated appropriately.

42.  The outcome of coma depends on the etiology, depth and duration of
impaired consciousness
 In a study by Wong CP et al , of the 283 episodes of pediatric coma
(defined as GCS <12 for at least 6 h), mortality at 1yr ranged from 3%
(intoxication) to 84% (accident), depending on etiology (3).
 Prolonged coma after a hypoxic-ischemic insult carries a poor prognosis(4).
 Most children surviving infectious encephalopathies have a comparatively
better outcomes, often surviving with mild or moderate difficulties only(5,6).
 Worse outcome in younger children with lower GCS score on presentation,
or had absent brainstem reflexes, worse motor responses, hypothermia, or
hypotension (7).

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