ComaComa

Dr Ashraf AbdouDr Ashraf AbdouProfessor Neuropsychiatry dept.Professor Neuropsychiatry dept.

Alexandria UnivAlexandria Univ

22

OBJECTIVESOBJECTIVES

Anatomical & physiological basis of Anatomical & physiological basis of consciousnessconsciousness

What is coma?What is coma?

Glasgow coma scaleGlasgow coma scale

Causes of comaCauses of coma

Evaluation of comatosed patientEvaluation of comatosed patient

Management of comatosed patientManagement of comatosed patient

33

Consciousness Is Dependent on:

1) An Intact Ascending Reticular Activating System (central tegmental fasiculus) AROUSAL

2) Intact Cerebral Cortex AWARNESS

4

The Comatose Patient

Neurophysiology

Consciousness requires:

An intact pontine reticular activating system

An intact cerebral hemisphere, or at least part of a hemisphere

5

Conciousness

Arousal is regulated solely by physiological functioning and consists of more primitive responsiveness to the world, as demonstrated by predictable reflex (involuntary) responses to stimuli

Awareness allows one to receive and process all the information communicated by the five senses, and thus relate to oneself and to the outside world.

77

Consciousness requiresConsciousness requires::An intact pontine reticular activating An intact pontine reticular activating systemsystem

An intact cerebral hemisphere, or at An intact cerebral hemisphere, or at least part of a hemisphereleast part of a hemisphere

Coma requires dysfunction of either Coma requires dysfunction of either ::Pontine reticular activating system, orPontine reticular activating system, or

Bihemispheric cerebral dysfunctionBihemispheric cerebral dysfunction

8

Coma; koma=deep sleep

Coma is defined as a state of unarousable unresponsiveness in which there is no evidence of self or environmental awareness. Defining characteristic is absence of

sleep/wake cycles on EEG. No evidence of spontaneous movement (e.g.,

scratching), discrete localizing responses or language comprehension or expression.

Only reflex activity remains; this points toward a failure of both the reticular activating system and cortex.

99

States of Altered ConsciousnessStates of Altered Consciousness

State Description of Patient

Lethargy     fatigued with minimal difficulty maintaining alertness

Vegetative State recover the arousal component of consciousness but not awareness.

Stupor unresponsiveness with arousal only              vigorous/painful stimulus, return to unresponsiveness with removal of stimulus

10

Terminology

Delirium :a state of disturbed consciousness with motor restlessness and disorientation

Confusion: inability to maintain a coherent sequence of thoughts,usually by inattention and disorientation

Lethargy: decreases responsiveness but arousable

Obtundation: awake but not alert, psychomotor retardation is present

Drowsiness or lethargy: disorder to light stimuli

Stupor: be aroused by noxious stimuli only ; little motor or verbal activity once aroused

11

Coma Fact Number One

Coma implies dysfunction of: ARAS or Both hemi-cortices

Anatomically, this means central brainstem structures (bilaterally)

from caudal medulla to rostral midbrain both hemispheres

1212

Glasgow Coma Scale 3-15

Eye OpeningNever 1To pain 2To verbal 3Spontaneous 4

Best Verbal ResponseNone 1Sounds 2Inapp words 3disoriented 4oriented 5

Best Motor ResponseNone 1Extensor 2Flexor Posture 3Withdrawal 4Localization5obeys 6

COMA <8

1313

Common Etiologies of Coma

Approximate mortalityDrug Overdose 5-10%

Metabolic 50%

Head Trauma 50%

Anoxia 90%

Stroke 80%

Status Epilepticus 3-30%

1414

ClassificationsClassifications

Supratentorial lesions cause coma by either widespread bilateral disease, increased intracranial pressure, or herniation.

Infratentorial lesions involve the RAS, usually with associated brainstem signs

Metabolic coma causes diffuse hemispheric involvement and depression of RAS, usually without focal findingsPsychogenic

Plum and Posner, 1982

1515

1616

Supratentorial Mass Lesions

Hematoma

Neoplasm

Abscess

Contusion

Vascular Accidents

Diffuse Axonal Damage

1717

Supratentorial Mass LesionsSupratentorial Mass LesionsAcute epidural hematoma and Acute epidural hematoma and midline shiftmidline shift

1818

Supratentorial Mass LesionsSupratentorial Mass Lesions Cerebral AbscessCerebral Abscess

1919

Supratentorial Mass LesionsSupratentorial Mass Lesions

Differential CharacteristicsDifferential Characteristics

•Initiating signs usually of focal cerebral dysfunction

•Signs of dysfunction progress rostral to caudal

•Neurologic signs at any given time point to one anatomic area - diencephalon, midbrain, brainstem

•Motor signs are often asymmetrical Plum and Posner, Plum and Posner,

19821982

2020

Infratentorial LesionsInfratentorial Lesions

Cause coma by affecting Cause coma by affecting reticular activating system in reticular activating system in ponspons

Brainstem nuclei and tracts Brainstem nuclei and tracts usually involved with resultant usually involved with resultant focal brainstem findingsfocal brainstem findings

2121

Infratentorial LesionsInfratentorial LesionsCauses of ComaCauses of Coma

NeoplasmNeoplasm

Vascular accidentsVascular accidents

TraumaTrauma

Cerebellar hemorrhageCerebellar hemorrhage

Demyelinating diseaseDemyelinating disease

Central pontine myelinolysis (rapid Central pontine myelinolysis (rapid correction of hyponatremia)correction of hyponatremia)

2222

Infratentorial Mass LesionsInfratentorial Mass Lesions

Differential CharacteristicsDifferential Characteristics

History of preceding brainstem dysfunction or sudden onset of coma

Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality

Cranial nerve palsies usually present

“Bizarre” respiratory patterns common, usually present at onset of coma

Plum and Posner, 1982Plum and Posner, 1982

2323

Metabolic ComaMetabolic Coma

EtiologiesEtiologies

Respiratory– HypoxiaHypoxia– HypercarbiaHypercarbia

Electrolyte– HypoglycemiaHypoglycemia– HyponatremiaHyponatremia– HypercalcemiaHypercalcemia

Hepatic encephalopathy

Severe renal failure

Infectious–Meningitis–Encephalitis

Toxins, drugs

2424

Etiologies-toxic metabolic

Drug overdoseNarcotics, Tricyclics, Stimulants

MetabolicSepsisHepatic encephalopathyUremic encephalopathyHypoglycemiaHypothyroidismETOH withdrawal/intoxication

2525

Metabolic ComaMetabolic ComaDifferentiating FeaturesDifferentiating Features

Confusion and stupor commonly precede Confusion and stupor commonly precede motor signsmotor signs

Motor signs are usually symmetricalMotor signs are usually symmetrical

Pupillary reactions are usually preservedPupillary reactions are usually preserved

Asterixis, myoclonus, tremor, and Asterixis, myoclonus, tremor, and seizures are commonseizures are common

Acid-base imbalance with hyper- or Acid-base imbalance with hyper- or hypoventilation is frequenthypoventilation is frequent

2626

Infectious Etiology

History

Fever

Nuchal rigidity

Kernigs, Brudzinski

Rash

2727

Signs of increased ICP/Herniation

Pupils– Unilateral dilated pupil – Bilateral small poorly reactive pupils

Eye movements– Third nerve palsy– Sixth nerve palsy– Can be assessed by cold caloric

Fundoscopy– Signs of papilledema?

Respiratory pattern?

2828

Can be detected by a deterioration in mental status, pupils, or motor exam

– Withdrawal to pain transitioning to flexor withdrawal

– Flexor withdrawal to extensor posturing Decortication-Flexor withdrawal-lesion above red nucleus

Decerebration-Extensor posturing-lesion below red nucleus

2929

Approach to the Comatose PatientApproach to the Comatose Patient

PrioritiesPrioritiesNO MANAGEMENT NO MANAGEMENT OF COMA AT OF COMA AT HOMEHOMEABC’s are 1ABC’s are 1STST PRIORITYPRIORITYMust ensure oxygen and Must ensure oxygen and substrate reach CNS substrate reach CNS and vital organs and vital organs

Must address Must address immediately life immediately life threatening conditions threatening conditions before addressing CNSbefore addressing CNS

3030

Approach to the Comatose PatientApproach to the Comatose Patient

Initial TreatmentInitial TreatmentAirwayAirway

BreathingBreathing

CirculationCirculation

ABC - identify and address life ABC - identify and address life threatening inadequaciesthreatening inadequacies

Treat rapidly progressive metabolic Treat rapidly progressive metabolic disorders -- hypoglycemiadisorders -- hypoglycemiaEvaluate for intracranial hypertension and Evaluate for intracranial hypertension and imminent herniation and treatimminent herniation and treat

ABC

3131

Management of the Comatose Patient Management of the Comatose Patient

AirwayAirway

Evaluate -- is airway patent. Can patient move air without obstruction. Is there trauma or foreign body obstructing airway

Try chin lift to help open airway -- protect cervical spine

Place airway if indicated - nasal or oral airway

Intubation

3232

Management of the Comatose PatientManagement of the Comatose Patient

CirculationCirculation

Is patient in shock?Is patient in shock? Check pulses, heart rate, blood pressure, Check pulses, heart rate, blood pressure, perfusionperfusion

Remember hypotension is Remember hypotension is latelate sign of shock sign of shock

Start treatment for shockStart treatment for shockDo not restrict fluids in comatose patient with Do not restrict fluids in comatose patient with inadequate intravascular volume. inadequate intravascular volume.

Cardiac output and cerebral perfusion are Cardiac output and cerebral perfusion are much more important than fluid restrictionmuch more important than fluid restriction

3333

Management of the Comatose PatientManagement of the Comatose Patient

CirculationCirculation

Use isotonic solutions and blood, as indicated.

Do not use hypotonic solutions to treat shock, particularly patients with coma or possible cerebral edema

Identify life threatening hemorrhage and control it.

3434

Practical approach

NECK RIGIDITY

INFECTION or SAHFOCAL NEUROLOGICAL

SIGNS

METABOLICINTRACRANIAL

LESION

NO

YES

YES

NO

35

Quick approach to etiology

Comatose patient

YES No

YES NO

Focal SignsInfectionsSAH

Neck Rigidity

Intracranial lesion Metabolic or toxic

3636

Suspected bacterial meningitis or SAH

For SAH, STAT CT of brain– 90% yield for SAH

– Notify neurosurgery stat if suspected

If bacterial meningitis suspected,

do not delay for CT- – Start empiric therapy

Ceftriaxone 2 grams q12 hours IV

Vancomycin 750-1000 mg q 12 hours IV

Ampicillin 2 grams q 4 hours IV age > 65 or if   immunocompromised

– LP: L3-L4 interspaceObtain opening pressure

Cell count tubes 1 and 4

Tubes 2 and 3, Gram stain, Cocci, AFB, india ink,

Protein and glucose

3737

Management and Evaluation of the Comatose Management and Evaluation of the Comatose PatientPatient

PracticalitiesPracticalities

During ABC’s and secondary survey::– Have someone start IV and obtain labsHave someone start IV and obtain labs

ABG’sABG’s

Chem 7, LFT’s, ammonia, coagulation studiesChem 7, LFT’s, ammonia, coagulation studies

Toxin screensToxin screens

DextrostickDextrostick

– As soon as IV in and labs drawn, giveAs soon as IV in and labs drawn, giveGlucose (D25, 2 - 4 cc per kilogram)Glucose (D25, 2 - 4 cc per kilogram)

Consider thiaminConsider thiamin

3838

     

Increased ICPIncreased ICP

Hyperventilation: Reduces ICP immediately, peak effect 1-2 hours– NO BENEFIT TO drop PCo2 < 25, Ideal = 30

Mannitol: Onset in 30 minutes lasts 4-6 hours

Mannitol and lasix are synergistic.– 1 - 2 grams/kg bolus– 0.5 - 1 gram/kg q 6 hours– Monitor sodium, osmolality, BUN– Hyperosmolality with 3% NaCl

3939

Initial ManagementInitial ManagementHyperventilation: Reduces ICP immediately, peak   effect 1-2 hours– NO BENEFIT TO drop PCo2

< 25, Ideal = 30

Mannitol: Onset in 30 minutes lasts 4-6 hoursMannitol and lasix are synergistic.– 1 - 2 grams/kg bolus– 0.5 - 1 gram/kg q 6 hours– Monitor sodium, osmolality,

BUN

Hyperosmolality with 3% NaCl

Stat – fingerstick for dextrose– CBC, electrolytes, BUN/Cr,

Calcium, ABG, LFT’s, ammonia, UA, serum and urine tox screen, blood cultures if febrile

Dextrose (1 amp = 25 grams dextrose)– Always follow with Thiamine

100 mg IM

4040

Initial ManagementInitial Managementcontcont..

If Narcotic OD suspected, give– Naloxone 1 - 2 amps– repeat in 15 minutes

If benzodiazepine overdose suspected, – Flumazenil .2 mg – repeat q 1 minute up to 1.0

mg, may produce seizures.

If ETOH withdrawal (72-96 hrs post ETOH)– (confusion, hallucinations,

tremor, tachycardia, HTN) – Thiamine 100 mg/IM– Librium 25-100 mg q6hrs

For ETOH seizures – (12-24 hours post

withdrawal)Give thiamine 100mgStat fingerstick for dextroseLorazepam 2 mg IV q 6-8 hours

4141

Immediate TestsImmediate Tests

GlucoseGlucoseElectrolytesElectrolytes

CBC, BUN, CrCBC, BUN, CrOsmolalityOsmolality

ABGABGLP (if no mass lesion)LP (if no mass lesion)

Deferred TestsDeferred Tests

Tox ScreenTox ScreenLFT’sLFT’s

AmmoniaAmmoniaCoagsCoags

TSH, cortisolTSH, cortisolAED levelsAED levels

BCx/UcxBCx/Ucx

EEG/SSEPEEG/SSEP

Laboratory Work-upLaboratory Work-up

4242

Examination of the Comatose Examination of the Comatose PatientPatient

HistoryHistoryOnsetOnset

Recent complaintsRecent complaints

Recent InjuryRecent Injury

Prior IllnessPrior Illness

MedicationsMedications

General ExamGeneral ExamV.SV.S..

TraumaTrauma??

IllnessIllness??

DugsDugs??

Nuchal RigidityNuchal Rigidity

Neurologic ExamNeurologic ExamVerbal responsesVerbal responses

oriented speechoriented speech

confused conversationconfused conversation

inappropriate speechinappropriate speech

incomprehensible speechincomprehensible speech

no speechno speech

Eye openingEye opening spontaneousspontaneous

verbal responseverbal response

noxious responsenoxious response

nonenone

4343

Pupillary reactionsPupillary reactions presentpresent

absentabsent

Spont eye movtsSpont eye movts orientingorienting

rovingroving

miscmisc

nonenone

Oculocephalic responsesOculocephalic responses

normalnormal

fullfull

minimalminimal

nonenone

Oculovestibular responsesOculovestibular responses

normalnormal

tonic conjtonic conj

dysconjdysconj

nonenone

Corneal responsesCorneal responses presentpresent

absentabsent

Repiratory patternRepiratory pattern regularregular

periodicperiodic

ataxicataxic

Motor responsesMotor responses obeysobeys

localizeslocalizes

w/dw/d

abnormal flexionabnormal flexion

abnormal extensionabnormal extension

nonenone

DTR’sDTR’sNormal, incr, decrNormal, incr, decr

ToneToneNorm, para, flex, ext, flaccidNorm, para, flex, ext, flaccid

4444

Pupillary Responses in Various Lesions

4545

Oculocephalic and Vestibular Responses

4646

Abnormal Breathing Patterns

Cheyne-Stokes crescendo/decrescendo pattern mixed with apnea bilateral hemisphere dysfunction

Central neurogenic hyperventilation rapid deep breathing lesion between midbrain and pons

Apneustic breathing prolonged inspiration followed by apnea pontine dysfunction

Ataxic breathing irregular pattern medullary dysfunction-close to death

Coma with hyperventilation metabolic derangement

Coma with hypoventilation drug overdose COPD

4747

Guidelines to Determining Brain Death

Prerequisites -proximate cause is known and demonstrably irreversible -metabolic derangements corrected to extent possible -no drug intoxication -core temperature greater than 32C

Three Cardinal Findings in Brain Death 1) Coma- no cerebral response to noxious stimuli in all                   extremities 2) Absence of Brainstem Reflexes- no pupillary response, no oculocephalic response, no oculovestibular response, no corneal reflex, jaw reflex, grimace, gag, or cough 3) Apnea- core temp 36.5, SBP >90, no DI, no tidal volume with PCO2>60mm Hg

4848

Guidelines to Determining Brain Death

1) Above criteria must be present for >6 hours

• Purely spinal reflexes may be intact

3) Systemic circulation may be intact

4) EEG of some value though not required for confirmation

5) Should be confirmed by two physicians

4949

DECEREBRATE

DECORTICATE

Cheyne Stokes Cheyne Stokes

HV neurógena HV neurógena centralcentral

Respiraciones Respiraciones apneústicasapneústicas

NormalNormal

GCS Motor 6 5 4 3 2 1 GCS Motor 6 5 4 3 2 1