Coma approach

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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Coma, Indian J Pediatr (2010) 77:1279–1287 DOI 10.1007/s12098-010-0191-1
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bacterial meningitis: further evidence for persisting effects. Arch Dis Child.
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6) Lahat E, Barr J, Barkai J, et al. Long term neurological outcome of herpes
encephalitis. Arch Dis Child. 1999;80:69–71
7) Johnston B, Seshia SS. Prediction of outcome in nontraumatic coma in childhood.
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