This document discusses coma and disorders of consciousness. It defines coma as a state of unresponsiveness and unconsciousness, and notes that coma can be a medical emergency requiring intervention. The document outlines different levels of arousal from alert to coma and describes conditions like encephalopathy, locked-in syndrome, and persistent vegetative state. Causes of impaired consciousness discussed include alcohol, epilepsy, intoxication, trauma, infection, stroke, and hypoxia-ischemia. The Glasgow Coma Scale for assessing coma is also summarized.

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

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

3. Definitions of levels of arousalDefinitions of levels of arousal
(conciousness(conciousness((
AlertAlert (Conscious)(Conscious) -- Appearance ofAppearance of
wakefulness, awareness of the self andwakefulness, awareness of the self and
environmentenvironment
LethargyLethargy -- mildmild reduction in alertnessreduction in alertness
ObtundationObtundation -- moderatemoderate reduction inreduction in
alertness. Increasedalertness. Increased response timeresponse time to stimuli.to stimuli.
DeliriumDelirium -disturbed consciousness with motor-disturbed consciousness with motor
restlessness, disorientation and hallucinationrestlessness, disorientation and hallucination

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

5. EncephalopathyEncephalopathy
 EncephalopathyEncephalopathy describes a diffusedescribes a diffuse
disorder of the brain in which at leastdisorder of the brain in which at least
two of the following symptoms aretwo 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 encephalopathyis an encephalopathy
accompanied by cerebrospinal fluidaccompanied by cerebrospinal fluid
(CSF) pleocytosis.(CSF) pleocytosis.

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

7. Persistent Vegetative StatePersistent Vegetative State PVSPVS
 PVS is a form ofPVS is a form of eyes-open permanenteyes-open permanent
unconsciousnessunconsciousness after recovery from coma withafter recovery from coma with lossloss
of cognitive functionof cognitive function andand awareness of theawareness of the
environmentenvironment butbut preservation of sleep-wake cyclespreservation of sleep-wake cycles
andand 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 anoxiaThe usual causes, in order of frequency, are anoxia
and ischemia, metabolic or encephalitic coma, andand ischemia, metabolic or encephalitic coma, and
head trauma.head trauma.
 Anoxia-ischemia has the worst prognosis. ChildrenAnoxia-ischemia has the worst prognosis. Children
who remain in a PVS for 3 months do not regainwho remain in a PVS for 3 months do not regain
functional skills.functional skills.

8. Glasgow Coma ScaleGlasgow Coma Scale GCSGCS
 Developed to define outcome in adultDeveloped to define outcome in adult
patients with head injurypatients with head injury
 Coma: score of 8 or lessComa: score of 8 or less
 There is a modified scale used for infantsThere 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 5localizes pain 5
 To pain 2To 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 COMAGLASGOW COMA
SCORE For InfantsSCORE For Infants
 Eye openingEye opening MotorMotor
 spontaneous 4spontaneous 4 normalnormal 66
 To speech 3To speech 3 withdraws to touchwithdraws to touch 55
 To pain 2To pain 2withdraws to painwithdraws to pain 44
 NoneNone 11 abnormal flexionabnormal flexion 33
 VerbalVerbal abnormal extensionabnormal extension 22
 CoosCoos 55 nonenone 11
 Irritable cries 4Irritable cries 4
 Cries to painCries to pain 33
 Moans to painMoans to pain 22
 NoneNone 11

11. GCSGCS
 IndividualIndividual elements as well aselements as well as the sumthe sum ofof
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
== EE22 VV44 MM33 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 statusAbsence status
 Complex partial seizureComplex partial seizure
 Post epileptic depressionPost epileptic depression

15. Hypoxia-ischemiaHypoxia-ischemia
 ShockShock
 Cardiac or pulmonary failure (Cardiac or pulmonary failure (CardiacCardiac
arrest, arrhythmia, CHF)arrest, arrhythmia, CHF)
 Near drowningNear drowning
 Carbon monoxide poisoningCarbon monoxide poisoning
 StrangulationStrangulation

16. Hypoxia and IschemiaHypoxia and Ischemia
 Hypoxia and ischemia usually occur togetherHypoxia and ischemia usually occur together
 acute anoxiaacute anoxia results in immediate loss ofresults in immediate loss of
consciousness.consciousness.
 ProlongedProlonged hypoxia causes personality changehypoxia causes personality change
first, then loss of consciousness;first, then loss of consciousness;
 Prolonged hypoxiaProlonged hypoxia can result fromcan result from
severe anemiasevere 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, andchronic lung disease, and
neuromuscular disorders.neuromuscular disorders.

17. Diagnosis.Diagnosis.
Cerebral edema is prominent during the firstCerebral edema is prominent during the first
72 hours after severe hypoxia.72 hours after severe hypoxia.
CT during that time shows decreased densityCT during that time shows decreased density
with loss of the differentiation between graywith loss of the differentiation between gray
and white matter.and white matter.
Severe, generalized loss of density on the CTSevere, 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-suppressionAn EEG that shows a burst-suppression
pattern or absence of activity is associatedpattern 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 wavespattern of burst of slow and mixed waves
often of high amplitude alternating with aoften of high amplitude alternating with a
flat baseline.flat baseline.
 It is usually seen after severe brain injuryIt is usually seen after severe brain injury
such as post ischemia or post anoxiasuch as post ischemia or post anoxia

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

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

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

22. Viral encephalitisViral encephalitis
 EnterovirusesEnteroviruses andand herpes simplex virusherpes simplex virus (HSV)(HSV)
are now the most common viral causes ofare 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 thatIn addition to viruses that directlydirectly infect theinfect the
brain and meninges, encephalopathies maybrain and meninges, encephalopathies may
follow systemic viral infections. These probablyfollow 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 encephalomyelitisdisseminated encephalomyelitis
(ADEM(ADEM((
 Immune-mediatedImmune-mediated disease ofdisease of
brainbrain.. It usually occursIt usually occurs
following afollowing a viral infectionviral infection oror
vaccination,vaccination, but it may alsobut it may also
appear spontaneously.appear spontaneously.
 Abrupt onset and aAbrupt onset and a
monophasic course.monophasic course.
 Symptoms usually begins 1-3Symptoms usually begins 1-3
weeks after infection orweeks after infection or
vaccination.vaccination.
 Major symptoms areMajor symptoms are fevefever,r,
headache, drowsiness,headache, drowsiness,
seizuresseizures and coma.and coma.

24. BRAIN ABSCESSBRAIN ABSCESS

25. TraumaTrauma
 ConcussionConcussion
 Cerebral contusionCerebral contusion
 Epidural hematomaEpidural hematoma
 Subdural hematoma/effusionSubdural 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 statesThe inborn errors of metabolism that cause states
of decreased consciousness are usuallyof decreased consciousness are usually
associated withassociated with hyperammonemia, hypoglycemia, orhyperammonemia, hypoglycemia, or
organic aciduriaorganic aciduria..
Neonatal seizures are an early feature in most ofNeonatal seizures are an early feature in most of
these conditions, but some may not causethese conditions, but some may not cause
symptoms until infancy or childhood.symptoms until infancy or childhood.
 HypoglycemiaHypoglycemia
 AcidosisAcidosis
 HyperammonemiaHyperammonemia
 UremiaUremia

34.  Inborn errors with aInborn errors with a delayed onset ofdelayed onset of
encephalopathy include disorders of pyruvateencephalopathy include disorders of pyruvate
metabolism and respiratory chain disordersmetabolism 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 hormoneThe syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is an important cause of watersecretion (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 isPermanent brain damage from hyponatremia is
uncommon but may occur in otherwise healthyuncommon but may occur in otherwise healthy
children if the serum sodium concentration remainschildren 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 chronicMay occur in acute or chronic renal failurerenal failure
 Raised blood ureaRaised blood urea alone cannot bealone cannot be
responsible for the loss of consciousnessresponsible for the loss of consciousness
but thebut the
 Metabolic acidosisMetabolic acidosis,, electrolyte disturbanceselectrolyte disturbances
andand Water intoxicationWater intoxication due to fluiddue 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) thethe eventsevents leading to the behavioralleading 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 medicineoften at fault than substances of abuse, and a medicine
cabinet inspection should be ordered in every home the childcabinet inspection should be ordered in every home the child
has visited);has visited);
(3)(3) a personal ora personal or FH of migraine or epilepsyFH of migraine or epilepsy;;
(4)(4) recent or concurrent fever, infectiousrecent or concurrent fever, infectious
disease, or systemic illnessdisease, or systemic illness
(5)(5) a previous personal or family history ofa previous personal or family history of
encephalopathy.encephalopathy.

39. General Physical ExamGeneral Physical Exam
The important variables in locating the site of abnormalityThe important variables in locating the site of abnormality
areare 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 mildThe cause of lethargy and obtundation is usually mild
depression of hemispheric function.depression of hemispheric function.
 Stupor and coma are characteristic of much moreStupor and coma are characteristic of much more
extensive disturbance of hemispheric function orextensive 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 strokeVery high temperature and dry skin – consider heat stroke
 Hypothermia often seen inHypothermia often seen in drug intoxicationdrug intoxication
 BPBP

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

41. NEUROLOGIC EXAM
 Examination of the eyes, in addition to determining theExamination of the eyes, in addition to determining the
presence or absence of papilledema,presence or absence of papilledema, provides otherprovides other
etiological clues.etiological clues.
 Small or large pupilsSmall or large pupils that respond poorly to light, orthat respond poorly to light, or
impaired eye movementsimpaired eye movements suggest a drug or toxicsuggest a drug or toxic
exposure.exposure.
 Fixed deviation of the eyes in one lateral direction mayFixed deviation of the eyes in one lateral direction may
indicate thatindicate 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 shouldThe general and neurological examinations should
specifically include a search forspecifically include a search for evidence of traumaevidence of trauma,,
needle marks on the limbsneedle marks on the limbs,, meningismusmeningismus, and, and cardiaccardiac
disease.disease.

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

44. Level of lesionLevel 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

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

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 3rdrd
, 4, 4thth
66thth
nervesnerves
 Can only be done in patient with stableCan only be done in patient with stable
spinespine
 Turn the head quickly to the side and theTurn the head quickly to the side and the
eyes should move to the opposite directionseyes should move to the opposite directions
of the movementof the movement

47. Cold Caloric ResponseCold Caloric Response
 Oculovestiublar reflexOculovestiublar reflex
 Tests the same pathway as doll’s eyes but can be done inTests 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 earElevate the head 30 degrees place a catheter in the ear
and inject ice water.and inject ice water.
 In an awake patient: nystagmusIn an awake patient: nystagmus COWSCOWS::
CCold water - fast componentold water - fast component ooppositepposite
WWarm water –arm water – SSame sideame side
 When supratentorial disease developsWhen supratentorial disease develops
 Due to metabolic depression of cortical function - the fastDue to metabolic depression of cortical function - the fast
component disappears and the eyes move toward the coldcomponent disappears and the eyes move toward the cold
water stimuluswater stimulus

48. Respiratory PatternRespiratory Pattern
 Injury location and type of breathingInjury location and type of breathing
 Post hyperventilation apnea -bilateral hemisphericPost hyperventilation apnea -bilateral hemispheric
dysfunctiondysfunction or can result from bilateral damageor can result from bilateral damage
anywhere along the descending pathway betweenanywhere along the descending pathway between
the forebrain and upper ponsthe forebrain and upper pons
 Cheyne-stokes breathingCheyne-stokes breathing ((periods of hyperpneaperiods 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, deepa sustained, rapid, deep
hyperventilation ,hyperventilation ,loss of involuntary respiration-loss of involuntary respiration-
medulla (medulla (Lesions just ventral to the aqueduct orLesions just ventral to the aqueduct or
fourth ventricle)fourth ventricle)

49. FlexionFlexion of theof the upperupper
limb with extension oflimb with extension of
the lower limbthe lower limb
((decorticate responsedecorticate response))
andand
extension of the upperextension of the upper
and lower limband lower limb
(decerebrate(decerebrate
response)response) indicate aindicate a
more severemore severe
disturbance anddisturbance and
prognosis.prognosis.

50. Infratentorial lesionsInfratentorial lesions
 Brainstem symptoms are often seenBrainstem symptoms are often seen
initiallyinitially
 Sudden onset of comaSudden onset of coma
 Cranial nerve abnormalitiesCranial nerve abnormalities
 Alteration of the respiratory patternAlteration of the respiratory pattern

51. Progression of LesionsProgression of Lesions

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

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

54. Other test to considerOther test to consider
 EEGEEG
 MRIMRI
 EchocardiogramEchocardiogram
 Head CTHead CT with contrast enhancementwith contrast enhancement
promptly to exclude the possibility ofpromptly 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
 INTUBATIONINTUBATION
 Hyperventilate for a short period of timeHyperventilate for a short period of time
 Keep head elevatedKeep head elevated
 Midline position to enhance venous drainage into theMidline position to enhance venous drainage into the
chestchest
 Check electrolytesCheck electrolytes
 Correct hyponatremia - produces brain swellingCorrect hyponatremia - produces brain swelling
 Restore low BPRestore low BP

57. Medical Intervention of increased ICPMedical Intervention of increased ICP
 Decrease CSFDecrease CSF
 Shunt fluid with external ventricultomy tubeShunt fluid with external ventricultomy tube
 Diamox 25-100 mg/kg/day in 3 dosesDiamox 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/ kgMannitol –0.25 to 1.0 gm/ kg
 Infuse over 10 to 15 minutesInfuse over 10 to 15 minutes
 Place foleyPlace foley
 May need to provide NS bolus to maintain BPMay need to provide NS bolus to maintain BP

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

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

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