coma

Coma-GCS-Causes-Managment by dr mohamed i abunada

1. ComaComa
Dr Mohamed I. AbunadaDr Mohamed I. Abunada
Pediatric NeurologyPediatric Neurology
Dr Alrantisi specialized ped Dr Alrantisi specialized ped
HospitalHospital

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

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

4. Definitions of levels of arousal Definitions of levels of arousal
(Consciousness(Consciousness((
StuporStupor - - Deep sleep, patient can be Deep sleep, patient can be
aroused only by aroused only by vigorous and repetitivevigorous and repetitive
stimulation. Returns to deep sleep when stimulation. Returns to deep sleep when
not continually stimulatednot continually stimulated..
Coma (Unconscious)Coma (Unconscious) - - Sleep likeSleep like
appearance and behaviorally appearance and behaviorally unresponsiveunresponsive
to all external stimuli (to all external stimuli (UnarousableUnarousable
unresponsivenessunresponsiveness, , eyes closedeyes closed))

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

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

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

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

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

10. MODIFIEDMODIFIED GLASGOW COMA GLASGOW COMA
SCORE For InfantsSCORE For Infants

Eye opening Eye opening Motor Motor
spontaneous 4spontaneous 4 normal normal 66
To speech 3To speech 3 withdraws to touch withdraws to touch 55
To pain 2To pain 2withdraws to painwithdraws to pain 44
NoneNone 1 1 abnormal flexion abnormal flexion 33

VerbalVerbal abnormal extensionabnormal extension 22
Coos Coos 55 nonenone 11
Irritable cries 4Irritable cries 4
Cries to pain Cries to pain 33
Moans to painMoans to pain22
NoneNone 11

11. GCSGCS

Individual Individual elements as well as elements as well as the sumthe sum of of
the score are important. the score are important.

The score is expressed in the form "The score is expressed in the form "GCS 9GCS 9
= = EE2 2 VV4 4 MM3 3 at 07:35at 07:35
Generally, coma is classified as:Generally, coma is classified as:

SevereSevere, with GCS ≤ 8 , with GCS ≤ 8

ModerateModerate, GCS 9 - 12 , GCS 9 - 12

MinorMinor, GCS ≥ 13. , GCS ≥ 13.

12. Causes of COMA

13. Causes of Impaired ConsciousnessCauses of Impaired Consciousness
Possible CausesPossible Causes

AAlcohollcohol

EEpilepsypilepsy

IInsulin, nsulin, IIntoxicationntoxication

OOverdoseverdose

UUremia (and other metabolic causes)remia (and other metabolic causes)

TTraumarauma

IInfectionnfection

PPsychiatricsychiatric

SStroke, troke, SSyncopeyncope
AEIOU TIPS

14. EpilepticEpileptic

Absence status Absence status

Complex partial seizureComplex partial seizure

Post epileptic depressionPost epileptic depression

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

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

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

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

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

20. Causes of Impaired Consciousness Causes of Impaired Consciousness
contcont..
STRUCTURALSTRUCTURAL

TRAUMATRAUMA

NEOPLASMSNEOPLASMS

VASCULAR DISEASE VASCULAR DISEASE

FOCAL INFARCTIONFOCAL INFARCTION

HYDROCEPHALUS HYDROCEPHALUS
Stroke

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

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

23. AcuteAcute disseminated encephalomyelitis disseminated encephalomyelitis
(ADEM(ADEM((

Immune-mediated Immune-mediated disease of disease of
brainbrain. . It usually occurs It usually occurs
following a following a viral infectionviral infection or or
vaccination,vaccination, but it may also but it may also
appear spontaneously. appear spontaneously.

Abrupt onset and a Abrupt onset and a
monophasic course. monophasic course.

Symptoms usually begins 1-3 Symptoms usually begins 1-3
weeks after infection or weeks after infection or
vaccination. vaccination.

Major symptoms are Major symptoms are fevefever, r,
headache, drowsiness, headache, drowsiness,
seizuresseizures and coma. and coma.
Review: Pediatrics Aug 2002 Review: Pediatrics Aug 2002
110(2)110(2)

24. BRAIN ABSCESSBRAIN ABSCESS

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

26. 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.
Parenchymal haemorrhage

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

28. Multifocal hematoma , lt fronal & temporal
Hge extending to fourth ventricle

29. EPIDURAL HEMATOMAEPIDURAL HEMATOMA

30. Rt frontoparietal epidural hematoma +cephalohematoma

31. SUBDURAL HEMATOMASUBDURAL HEMATOMA
Subdural
bleeding
due to
tearing of
veins

32. Hgh in lateral ventricles
+ dilated ventricles

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

34. 
Inborn errors with a Inborn errors with a delayed onset of delayed onset of
encephalopathy include disorders of pyruvate encephalopathy include disorders of pyruvate
metabolism and respiratory chain disorders metabolism and respiratory chain disorders
,glycogen storage diseases , and primary carnitine ,glycogen storage diseases , and primary carnitine
deficiency. 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. HyponatremiaHyponatremia
Hyponatremia may result from water retention, Hyponatremia may result from water retention,
sodium loss, or both. sodium loss, or both.
The syndrome of inappropriate antidiuretic hormone The syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is an important cause of water secretion (SIADH) is an important cause of water
retention.retention.
Sodium loss results from renal disease, vomiting, Sodium loss results from renal disease, vomiting,
and diarrhea. and diarrhea.
Permanent brain damage from hyponatremia is Permanent brain damage from hyponatremia is
uncommon but may occur in otherwise healthy uncommon but may occur in otherwise healthy
children if the serum sodium concentration remains children if the serum sodium concentration remains
less than 115 mEq/L for several hours.less than 115 mEq/L for several hours.

36. Renal comaRenal coma
May occur in acute or chronic May occur in acute or chronic renal failurerenal failure
Raised blood ureaRaised blood urea alone cannot be alone cannot be
responsible for the loss of consciousness responsible for the loss of consciousness
but the but the
Metabolic acidosisMetabolic acidosis, , electrolyte disturbanceselectrolyte disturbances
and and Water intoxicationWater intoxication due to fluid due to fluid
retention may be responsibleretention may be responsible
Toxic CausesToxic Causes
Immunosuppressive drugsImmunosuppressive drugs
Substance abuseSubstance abuse
ToxinsToxins

37. COMA
History and Physical
Examination

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

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

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

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

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

44. Level of lesionLevel of lesion
Level of lesion Motor response Pupillary
response
Respiratory
Pattern
Cortex Flexion withdrawalSmall 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

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

46. Oculocephalic Reflex DOLLs EyeOculocephalic Reflex DOLLs Eye

Tests-sensory from the eighth nerveTests-sensory from the eighth nerve
Motor Part of the 3Motor Part of the 3
rdrd
, 4, 4
thth
6 6
thth
nerves nerves

Can only be done in patient with stable Can only be done in patient with stable
spine spine
Turn the head quickly to the side and the Turn the head quickly to the side and the
eyes should move to the opposite directions eyes should move to the opposite directions
of the movement of the movement

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

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

49. 
FlexionFlexion of the of the upperupper
limb with extension of limb with extension of
the lower limbthe lower limb
((decorticate responsedecorticate response) )
and and

extension of the upper extension of the upper
and lower limband lower limb
(decerebrate (decerebrate
response) response) indicate a indicate a
more severe more severe
disturbance and disturbance and
prognosis. prognosis.

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

51. Progression of LesionsProgression of Lesions

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

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

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

55. COMA
Treatment

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

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

58. 3%3% Na ClNa Cl

Give as 5ml/kg bolus over an hour Give as 5ml/kg bolus over an hour

Can be given in peripheral IV Can be given in peripheral IV

Sodium movement across the blood Sodium movement across the blood
brain barrier is low. brain barrier is low.

Therefore works similar to Mannitol Therefore works similar to Mannitol

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

60. THANK YOUTHANK YOU

THANK YOUTHANK YOU

THANK YOUTHANK YOU

THANK YOUTHANK YOU