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Approach to diagnosis of coma
Citation preview
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
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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
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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
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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
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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
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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