This document provides information about coma, including definitions, levels of arousal, causes, Glasgow Coma Scale assessment, and approach to history and physical examination. Coma is defined as a state of unresponsiveness and unconsciousness. The Glasgow Coma Scale is used to assess levels of arousal from alert to coma and classify coma severity. Potential causes of coma discussed include hypoxia-ischemia, infections, structural injuries or diseases of the brain, metabolic disorders, and toxic exposures. The history and physical exam aim to identify potential causes and clues about neurological function by evaluating vital signs, skin exam, neurological exam of eyes and motor responses.

1. Coma
Dr Tanvi Vyas

2. Definitions
 Coma is defined as a state of unresponsiveness
and unconsciousness
 Coma from the Greek word "koma,"
meaning deep sleep
 Coma can be a medical emergency
 That requires intervention without always knowing
the cause
 Knowledge of CNS anatomy can give clues to the
cause

3. Definitions of levels of arousal
((conciousness
Alert (Conscious) - Appearance of
wakefulness, awareness of the self and
environment
Lethargy - mild reduction in alertness
Obtundation - moderate reduction in
alertness. Increased response time to stimuli.
Delirium -disturbed consciousness with motor
restlessness, disorientation and hallucination

4. Definitions of levels of arousal
((Consciousness
Stupor - Deep sleep, patient can be
aroused only by vigorous and repetitive
stimulation. Returns to deep sleep when
not continually stimulated.
Coma (Unconscious) - Sleep like
appearance and behaviorally unresponsive
to all external stimuli (Unarousable
unresponsiveness, eyes closed)

5. Encephalopathy
 Encephalopathy describes a diffuse
disorder of the brain in which at least
two of the following symptoms are
present:
(1)altered states of consciousness,
(2)altered cognition or personality, and
(3)seizures.
 Encephalitis is an encephalopathy
accompanied by cerebrospinal fluid
(CSF) pleocytosis.

6. locked-in syndrome
 a brainstem disorder in which the
individual can process information
but cannot respond .

7. Persistent Vegetative State PVS
 PVS is a form of eyes-open permanent
unconsciousness after recovery from coma with loss
of cognitive function and awareness of the
environment but preservation of sleep-wake cycles
and vegetative function.
 Survival is indefinite with good nursing care.
 The usual causes, in order of frequency, are anoxia
and ischemia, metabolic or encephalitic coma, and
head trauma.
 Anoxia-ischemia has the worst prognosis. Children
who remain in a PVS for 3 months do not regain
functional skills.

8. Glasgow Coma Scale GCS
 Developed to define outcome in adult
patients with head injury
 Coma: score of 8 or less
 There is a modified scale used for infants
and children

9. Glasgow Score
 Eye opening Motor Response
 Spontaneous 4 obeys commands 6
 To command 3 localizes pain 5
 To pain 2 withdraws to pain 4
 None 1 abnormal flexion 3
 Verbal abnormal extension 2
 Oriented 5 none 1
 Confused 4
 Inappropriate words 3 TOTAL 3-15
 Incomprehensible sounds 2
 None 1

10. MODIFIED GLASGOW COMA
SCORE For Infants
 Eye opening Motor
6
 spontaneous 4 normal
 To speech 3 withdraws to touch 5
 To pain 2 withdraws to pain 4
3

 None 1 abnormal flexion
Verbal abnormal extension 2
1
 Coos 5 none
 Irritable cries 4
 Cries to pain 3
 Moans to pain 2
 None 1

11. GCS
 Individual elements as well as the sum of
the score are important.
 The score is expressed in the form "GCS 9
= E2 V4 M3 at 07:35
Generally, coma is classified as:
 Severe, with GCS ≤ 8
 Moderate, GCS 9 - 12
 Minor, GCS ≥ 13.

12. Causes of COMA

13. Causes of Impaired Consciousness
Possible Causes
 Alcohol
 Epilepsy
 nsulin, Intoxication
Insulin, Intoxication
 Overdose
 Uremia (and other metaboliccauses)
 Trauma
 Infection
 Psychiatric
 Stroke, Syncope
AEIOU TIPS

14. Epileptic
 Absence status
 Complex partial seizure
 Post epileptic depression

15. Hypoxia-ischemia
 Shock
 Cardiac or pulmonary failure (Cardiac
arrest, arrhythmia, CHF)
 Near drowning
 Carbon monoxide poisoning
 Strangulation

16. Hypoxia and Ischemia
 Hypoxia and ischemia usually occur together
 acute anoxia results in immediate loss of
consciousness.
 Prolonged hypoxia causes personality change
first, then loss of consciousness;
 Prolonged hypoxia can result from
severe anemia (oxygen-carrying capacity reduced by at least half),
congestive heart failure,
chronic lung disease, and
neuromuscular disorders.

17. Diagnosis.
Cerebral edema is prominent during the first
72 hours after severe hypoxia.
CT during that time shows decreased density
with loss of the differentiation between gray
and white matter.
Severe, generalized loss of density on the CT
scan correlates with a poor outcome.
An EEG that shows a burst-suppression
pattern or absence of activity is associated
with a poor neurological outcome or death.

18. BURST SUPRESSION
 pattern of burst of slow and mixed waves
often of high amplitude alternating with a
flat baseline.
 It is usually seen after severe brain injury
such as post ischemia or post anoxia

19.  Maintaining oxygenation, circulation, and blood glucose
concentration is essential.
 (hyperventilation) Regulate intracranial pressure to levels that
allow satisfactory cerebral perfusion
 Anticonvulsant drugs manage seizures
 Anoxia is invariably associated with lactic acidosis. Restoration of
acid-base balance is essential.
 barbiturate coma to slow cerebral metabolism is common
practice .
 Hypothermia prevents brain damage during the time of
hypoxia and ischemia but has questionable value after the
event.
 Corticosteroids do not improve neurological recovery in
patients with global ischemia after cardiac arrest.

20. Causes of Impaired Consciousness
.cont
STRUCTURAL
 TRAUMA
 NEOPLASMS
 VASCULAR DISEASE
 FOCAL INFARCTION
 HYDROCEPHALUS
Stroke

21. Infectious Causes of Coma
 Bacterial meningitis
 Brain abscess
 Epidural, subdural empyema
 Fungal meningitis
 Viral encephalitis
 Postinfectious encephalomyelitis ADEM

22. Viral encephalitis
 Enteroviruses and herpes simplex virus (HSV)
are now the most common viral causes of
encephalitis in children.
 Specific viral identification is possible,
however, in only 15% to 20% of cases.
 In addition to viruses that directly infect the
brain and meninges, encephalopathies may
follow systemic viral infections. These probably
result from demyelination caused by immune-
mediated responses of the brain to infection.

23. Acute disseminated encephalomyelitis
((ADEM
 Immune-mediated disease of
brain. It usually occurs
following a viral infection or
vaccination, but it may also
appear spontaneously.
 Abrupt onset and a
monophasic course.
 Symptoms usually begins 1-3
weeks after infection or
vaccination.
 Major symptoms are fever,
headache, drowsiness,
seizures and coma.

24. BRAIN ABSCESS

25. Trauma
 Concussion
 Cerebral contusion
 Epidural hematoma
 Subdural hematoma/effusion
 Intracerebral hematoma

26. Parenchymal haemorrhage
May cause a rapid decline in consciousness,
from
1. Rupture into the ventricles
2. or subsequent herniation and brainstem
compression.
 Cerebellar haemorrhage or infarct with
1. Subsequent oedema
2. Direct brainstem compression, early
decompression can be lifesaving.

27. Lt frontoprietal intracerebral he (hyperdense(
(Massive (midline shift

28. Multifocal hematoma , lt fronal & temporal

29. EPIDURAL HEMATOMA

30. Rt frontoparietal epidural hematoma +cephalohematoma

31. SUBDURAL HEMATOMA
Subdural
bleeding
due to
tearing of
veins

32. Hgh in lateral ventricles
+ dilated ventricles

33. Metabolic Disorders
The inborn errors of metabolism that cause states
of decreased consciousness are usually
associated with hyperammonemia, hypoglycemia, or
organic aciduria.
Neonatal seizures are an early feature in most of
these conditions, but some may not cause
symptoms until infancy or childhood.
 Hypoglycemia
 Acidosis
 Hyperammonemia
 Uremia

34.  Inborn errors with a delayed onset of
encephalopathy include disorders of pyruvate
metabolism and respiratory chain disorders
,glycogen storage diseases , and primary carnitine
deficiency.
DKA ( diabetic Ketoacidosis)
Hepatic coma
Hypernatremia The usual causes
Dehydration or overhydration with hypertonic saline
solutions.
Hypernatremia is a medical emergency and, if not
corrected promptly, may lead to permanent brain
damage and death.

35. Hyponatremia
Hyponatremia may result from water retention,
sodium loss, or both.
 The syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is an important cause of water
retention.
 Sodium loss results from renal disease, vomiting,
and diarrhea.
 Permanent brain damage from hyponatremia is
uncommon but may occur in otherwise healthy
children if the serum sodium concentration remains
less than 115 mEq/L for several hours.

36. Renal coma
 May occur in acute or chronic renal failure
 Raised blood urea alone cannot be
responsible for the loss of consciousness
but the
 Metabolic acidosis, electrolyte disturbances
and Water intoxication due to fluid
retention may be responsible
Toxic Causes
Immunosuppressive drugs
Substance abuse
Toxins

37. COMA
History and Physical
Examination

38. History and Physical Examination
 Obtain a careful history of the following:
(1)the events leading to the behavioral
change;
(2)drug or toxic exposure (prescription drugs are more
often at fault than substances of abuse, and a medicine
cabinet inspection should be ordered in every home the child
has visited);
(3)a personal or FH of migraine or epilepsy;
(4)recent or concurrent fever, infectious
disease, or systemic illness
(5)a previous personal or family history of
encephalopathy.

39. General Physical Exam
The important variables in locating the site of abnormality
are state of consciousness, pattern of breathing,
pupillary size and reactivity, eye movements, and
motor responses.
 The cause of lethargy and obtundation is usually mild
depression of hemispheric function.
 Stupor and coma are characteristic of much more
extensive disturbance of hemispheric function or
involvement of the diencephalon and upper brainstem.
Vital signs
 Fever (may mean infection)
 Very high temperature and dry skin – consider heat stroke
 Hypothermia often seen in drug intoxication
 BP

40. Skin examination
 Cyanosis
 Cherry red - carbon monoxide (almond
odor)
 Café au lait spots - neurofibromatosis
 Shagreen patches - tuberous sclerosis
 Hyperpigmentation - Addison disease
 Petechiae and purpura - meningococcemia
 Signs of trauma – suspicious bruises

41. NEUROLOGIC EXAM
 Examination of the eyes, in addition to determining the
presence or absence of papilledema, provides other
etiological clues.
 Small or large pupils that respond poorly to light, or
impaired eye movements suggest a drug or toxic
exposure.
 Fixed deviation of the eyes in one lateral direction may
indicate that
(1)The encephalopathy has focal features
(2)Seizures are a cause of the confusional state
(3)Seizures are part of the encephalopathy.
The general and neurological examinations should
specifically include a search for evidence of trauma,
needle marks on the limbs, meningismus, and cardiac
disease.

42. Cranial Nerve Exam
 I. olfactory-smell
 II. Optic-Visual acuity, visual fields, pupils reaction, color
 III. Oculomotor - eye movement
 IV. Trochlear eye movement
 V. Trigeminal Nerve - facial sensation, corneals,
 VI. Abducens-eye movement
 VII. Facial nerve - motor and sensory to face
 VIII. Acoustic nerve - hearing
 IX. Glossopharyngeal - gag reflex, elevate palate
 X. Vagus - swallowing movement of the cords
 XI. Accessory Nerve - sternocleidomastoid muscle , trapezius
function
 XII. Hypoglossal nerve - tongue movement, fasciculations

43. Level of lesion
Level of lesion Motor response Pupillary
response
Respiratory
Pattern
Cortex Flexion withdrawal Small reactive Normal or cheyne
stokes
Thalamus Abn. Flexion
( decortication)
Small reactive Normal or cheyne
stokes
Midbrain Abn. Extension
(decerebration)
Fixed midposition Hyperventilation
Pons No response pinpoint Normal or
apneustic
Medulla No response Small reactive irregular

44. Corneal reflex
 Test the fifth nerve sensory and seventh
nerve motor
 Cotton on cornea and look for a blink or
watch the lower eyelashes move toward
the midline
 Good test for mid and low pontine
dysfunction

45. Oculocephalic Reflex DOLLs Eye
 Tests-sensory from the eighth nerve
 Motor Part of the 3rd, 4th6thnerves
 Can only be done in patient with stable
spine
Turn the head quickly to the side and the
eyes should move to the opposite directions
of the movement

46. Cold Caloric Response
 Oculovestiublar reflex
 Tests the same pathway as doll’s eyes but can be done in
patient with unstable cervical cord.
 Elevate the head 30 degrees place a catheter in the ear
and inject ice water.
 In an awake patient: nystagmus COWS:
Cold water - fast component opposite
Warm water – Same side
 When supratentorial disease develops
 Due to metabolic depression of cortical function - the fast
component disappears and the eyes move toward the cold
water stimulus

47. Respiratory Pattern
 Injury location and type of breathing
 Post hyperventilation apnea -bilateral hemispheric
dysfunction or can result from bilateral damage
anywhere along the descending pathway between
the forebrain and upper pons
 Cheyne-stokes breathing (periods of hyperpnea
alternate with periods of apnea)
 Central Neurogenic Hyperventilation (formerly known as
Ondine’s curse) a sustained, rapid, deep
hyperventilation ,loss of involuntary respiration

48. Flexion of the upper
limb with extension of
the lower limb
(decorticate response)
and
extension of the upper
and lower limb
(decerebrate
response) indicate a
more severe
disturbance and
prognosis.

49. Infratentorial lesions
 Brainstem symptoms are often seen
initially
 Sudden onset of coma
 Cranial nerve abnormalities
 Alteration of the respiratory pattern

50. Progression of Lesions

51. Laboratory Work up


CBC with diff PT,PTT, INR
LFT’s
 Toxic screen
 Blood, urine culture
 Chest x-ray
 Urine ketones, glucose
 Electrolytes Ca, Mg, BUN, creatinine

52. Other Lab work
 Blood ammonia
 Lead levels
 Serum cortisol
 Skeletal survey
 Amino acid profile
 Blood pyruvate and lactate
 Organic acid analysis

53. Other test to consider
 EEG
 MRI
 Echocardiogram
 Head CT with contrast enhancement
promptly to exclude the possibility of
a mass lesion and herniation.

54. COMA
Treatment

55. TREATMENT OF ELEVATED ICP
 INTUBATION
 Hyperventilate for a short period of time
 Keep head elevated
 Midline position to enhance venous drainage into the
chest
 Check electrolytes
 Correct hyponatremia - produces brain swelling
 Restore low BP

56. Medical Intervention of increased ICP
 Decrease CSF
 Shunt fluid with external ventricultomy tube
 Diamox 25-100 mg/kg/day in 3 doses
 Reduce the size of other compartment
 Mannitol or 3% NaCl
 Mannitol –0.25 to 1.0 gm/ kg
 Infuse over 10 to 15 minutes
 Place foley
 May need to provide NS bolus to maintain BP

57. Na Cl 3%
 Give as 5ml/kg bolus over an hour
 Can be given in peripheral IV
 Sodium movement across the blood
brain barrier is low.
 Therefore works similar to Mannitol

58. Treatment of elevated ICP
 Progression of treatment
Mannitol, or 3% NaCl
Sedation and pain medication
Fever control
Intubation
ICP monitor and drainage of CSF
Pentobarbital coma
Surgery for decompression craniotomy

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