Kesadaran dan Mati Batang Otak

Dr Khairul Ihsan Nasution SpBS

KESADARAN

Individu yang sadar adalah seseorang yang terbangun serta waspada terhadap diri dan lingkungannya. dua bagian utama sistem saraf1. formatio retikularis dibatang otak dan 2.cortex cerebri harus berfungsi aktif.

LOCATION OF BRAIN STEM

BRAIN STEM

Formatio reticularis berperan dalam keadaan bangun.Cortex cerebri dibutuhkan untuk keadaan waspada, yaitu keadaan yang memungkinkan individu beraksi terhadap stimulus dan berinteraksi dengan lingkungan.

Gerakan membuka mata merupakan fungsi batang otak ; berbicara adalah fungsi cortex cerebri. Secara selektif, obat-obatan yang menyebabkan ketidaksadaran seperti anestesia menekan mekanisme kesiagaan reticular ( reticular alerting mechanism ), sedangkan obat-obatan yang menyebabkan keadaan sadar memiliki efek stimulasi pada mekanisme ini.

Seorang dokter harus mampu mengenali berbagai tanda dan gejala yang ditimbulkan oleh berbagai tingkat kesadaran: Letargi Stupor Koma (tidak sadar).

Pada orang yang latergi, bicara lambat, serta gerakan voluntar berkurang dan lambat. Gerakan mata lambat.

Pasien stupor hanya bicara jika diberikan stimulus nyeri. Gerakan voluntar hampir hilang, mata tertutup dan sangat sedikit gerakan mata spontan. Pasien dengan stupor dalam tidak akan berbicara ; terdapat gerakan sekelompok otot pada bagian-bagiantubuh yang berbeda sebagai respons terhadap nyeri hebat. Gerakan spontan mata sangat kurang.

Pasien yang tidak sadar tidak akan berbicara dan hanya akan menimbulkan refleks bila diberikan stimulus nyeri, atau tidak bereaksi sama sekali ; mata tertutup dan tidak bergerak.

Secara klinis, tidak jarang didapatkan seorang pasien dengan, misalnya perdarahan intrakranial, mengalami penurunan kesadaran secara progresif menjadi letargi, stupor, koma, kemudian mengalami keadaan sebaliknya jika terjadi pemulihan.

Untuk menimbulkan perubahan atas kesadaran, sistem talamokortikal dan formatio reticularis harus berperan langsung secara bilateral atau secara tidak langsung melalui distorsi atau tekanan.

STATUS VEGETATIF PASIEN

Seseorang dapat memiliki formatio reticularis yang utuh, tetapi kortek serebrinya tidak berfungsi. Pasien tersebut terbangun (mata terbuka dan bergerak) dan memiliki siklus tidur bangun, namun pasien tidak mempunyai kewaspadaan sehingga tidak berekasi terhadap stimulus seperti perintah verbal atau nyeri.

Keadaan ini disebut status vegetatif persisten, biasanya terjadi setelah cedera kepala berat atau akibat anoksia serebri. Sayangnya, pengamat yang tidak berpengalaman menganggap pasien tersebut sadar .

Mungkin saja didapatkan keadaan bangunan tanpa kewaspadaan ; namun, tidak mungkin memiliki kewaspadaan tanpa keadaan bangun. Cortex cerebri membutuhkan input dari formatio reticularis untuk dapat berfungsi.

PERSISTENT PERMANENT VEGETATIVE STATE

Time Duration: 1 month; if persistent more than 1 year, almost always permanentFunction lost:No cognition: consistent responses to linguistic, symbolic, or mimetic instruction are absentNo semantically meaningful sounds or goal-directed movementsNo sustained head-ocular pursuit activity

PERSISTENT PERMANENT VEGETATIVE STATEFunction usually or often preserved:Brainstem and autonomically controlled visceral functions: homeothermia; osmolar homeostasis; breathing; circulation; gastrointestinal functionsPupillary and oculovestibular reflexes usually remain and are accentuatedBrief, inconsistent shifting of head or eyes toward new sounds or sights may occurSmiles, tears, or rage reactions may occur either spontaneously or to nonverbal soundsReflex postural responses to noxious stimuli remain

FORMULATIONS OF BRAIN DEATH

Whole-brain: complete and irreversible cessation of all brain function, including that of the brain stem

Brain-stem formulation: complete and irreversible cessation of brain-stem function alone

HARVARD CRITERIA (1968)Unreceptivity and unresponsivityNo movements or breathingNo reflexesFlat electroencephalogram (EEG)

All of the above four tests are to be repeated at, at least, 24 hrs with no change.Exclusion of hypothermia (below 90 F or 32.2 C) or Central nervous system depressants

American Academy of Neurology Guidelines (1995)

Demonstration of comaEvidence for the cause of comaAbsence of confounding factors, including hypothermia, drugs, electrolyte, and endocrine disturbancesAbsent brainstem reflexesAbsent motor responsesApneaA repeat evaluation in 6 hrs is advised, but the time period is considered arbitraryConfirmatory laboratory tests are only required when specific components of the clinical testing cannot reliably be evaluated.

CONFIRMATORY TESTS OF BRAIN DEATH IN ADULTS

Electroencephalography (EEG)Cerebral AngiogramTranscranial Doppler SonographyMagnetic Resonance Imaging (MRI)Single Photon Emission Computed Tomography (SPECT)Evoked PotentialsBrainstem Auditory Evoked Potentials (BAEP)Somatosensory Evoked Potentials (SSEP)Spiral Computed Tomography Scan (Spiral CT Scan)

Test 1 - PainCerebral motor response to painSupraorbital ridge, the nail beds, trapeziusMotor responses may occur spontaneously during apnea testing (spinal reflexes)Spinal reflex responses occur more often in youngIf pt had NMB, then test w/ train-of-fourSpinal arcs are intact!

Test 2 - PupilsRound, oval, or irregularly shaped Midsize (4-6 mm), but may be totally dilatedAbsent pupillary light reflexAlthough drugs can influence pupillary size, the light reflex remains intact only in the absence of brain deathIV atropine does not markedly affect responseParalytics do not affect pupillary sizeTopical administration of drugs and eye trauma may influence pupillary size and reactivityPre-existing ocular anatomic abnormalities may also confound pupillary assessment in brain death

Test 2 - PupilsRound, oval, or irregularly shaped Midsize (4-6 mm), but may be totally dilatedAbsent pupillary light reflexAlthough drugs can influence pupillary size, the light reflex remains intact only in the absence of brain deathIV atropine does not markedly affect responseParalytics do not affect pupillary sizeTopical administration of drugs and eye trauma may influence pupillary size and reactivityPre-existing ocular anatomic abnormalities may also confound pupillary assessment in brain death

Test 3Eye movementOculocephalic reflex = dolls eyesOculovestibular reflex = cold caloric test

Oculocephalic reflexRapidly turn the head 90 on both sidesNormal response = deviation of the eyes to the opposite side of head turningBrain death = oculocephalic reflexes are absent (no Dolls eyes) = no eye movement in response to head movementNot Barbie, but old fashioned type dolls

Cold caloricsElevate the HOB 30Irrigate one tympanic membrane with iced waterObserve pt for 1 minute after each ear irrigation, with a 5 minute wait between testing of each earFacial trauma involving the auditory canal and petrous bone can also inhibit these reflexes

Cold calorics interpretationNot comatoseNystagmus; both eyes slow toward cold, fast to midline Coma with intact brainstemBoth eyes tonically deviate toward cold water No eye movement Brainstem injury / deathMovement only of eye on side of stimulus Internuclear ophthalmoplegia Suggests brainstem structural lesion

Test 4Facial sensory & motor responsesCorneal reflexes are absent in brain deathCorneal reflexes - tested by using a cotton-tipped swabGrimacing in response to pain can be tested by applying deep pressure to the nail beds, supraorbital ridge, TMJ, or swab in noseSevere facial trauma can inhibit interpretation of facial brain stem reflexes

Test 5Pharyngeal and tracheal reflexesBoth gag and cough reflexes are absent in patients with brain deathGag reflex can be evaluated by stimulating the posterior pharynx with a tongue blade, but the results can be difficult to evaluate in orally intubated patientsCough reflex can be tested by using ETT suctioning, past end of ETT

Test 6ApneaPaCO2 levels greater than 60 mmHg, 20 mmHg over baselineTechnique:Pre-oxygenate with 100% oxygen several minAllow baseline PaCO2 to be ~40 mmHgPlace pt on CPAP or bag-ETTObserve for respirations for ~6-10 minutesGet ABG to determine PaCO2

Confirmatory testing4 vessel angiographyEEG30 minutesCerebral blood flow = perfusion scan

NEUROLOGIC STATES RESEMBLING BRAIN DEATH

HypothermiaAcute PoisoningAcute Metabolic EncephalopathiesAkinetic MutismPersistent Vegetative StateLocked-in-Syndrome

BRAIN DEATH DETERMINATION IN CHILDREN

No reports of children recovering neurological function who have met adult brain death criteria on clinical examinationGuidelines for children emphasize history and clinical examination in determining etiology of coma to eliminate reversible conditionsAge-related observation periods and need for specific tests recommended in guidelines for children under 1 year of age7 days to 2 months: Two examinations and EEGs 48 hrs apart2 months to 1 year: Two examinations and EEGs 24 hrs apart, or one examination and an initial EEG showing ECS combined with a radionuclide angiogram showing no CBF or bothMore than 1 year: Two examinations 12-24 hrs apart, EEG and isotope angiography are optional

HYPOTHERMIA: CLINICAL FEATURESBody Core Temperature

35 32 degrees CCentral Nervous System: apathy; dysarthria, impaired judgmentCardiovascular: tachycardia, then progressive bradycardia; cardiac cycle prolongation; vasoconstrictionRespiratory: tachypnia, to progressive bradypnea; bronchorrhea; bronchospasm

HYPOTHERMIA: CLINICAL FEATURES32 28 degrees CCentral Nervous System: decreased level of consciousness; hallucinations; papillary dilationCardiovascular: Progressive decrease in pulse and cardiac output; increased cardiac arrhythmias; Respiratory: Hypoventilation; 50% decrease in carbon dioxide production per 8 degree C drop in temperature; absence of protective airway reflexes; 50% decrease in oxygen consumptionNeuromuscular: hyporeflexia; diminishing shivering, rigidity

HYPOTHERMIA: CLINICAL FEATURES

Under 28 degrees CCentral Nervous System: coma; absent oculocephalic, corneal and bulbar reflexesCardiovascular: hypotension, bradycardia, dysrhythmias, decreased ventricular arrhythmia, asystoleRespiratory: pulmonic congestion and edema; apneaNeuromuscular: amobile; areflexia

RESEARCH DIRECTIONS FOR BRAIN DEATHImprovements in use of MRI and MRI angiographyUse of multimodality evoked potentials (MEPs), which test cerebral cortex as well as the brain stem, and include:brain-stem auditory evoked potentials (BAEP)flash-visual evoked potentials (flash VEPs), andmedian somatosensory evoked potentials (median SEPs)Refinements of imaging technologies (PET, MRI, SPECT) to achieve greater sensitivity and specificityImprovements in MEG (magnetoencephalography) to detect cellular activity in the brain stem

FUTURE DEVELOPMENTS AND BRAIN DEATHUse of electrodes on motor cortex to translate motor control commands, opens possibilities of translating and transferring ideas to a computer during process of dying

Use of electrodes may also provide means for determining that any organized activity doesnt exist, which in the absence of mechanical disruption, would demonstrate the brain is dead.

Understanding the process of neuronal death (apoptosis) may provide opportunities for intervention

SEKIAN & TERIMA KASIH

**********Fixed/dilated 3rd nerve compression (herniation, midbrain lesion)Pinpoint = pontine lesion*Fixed/dilated 3rd nerve compression (herniation, midbrain lesion)Pinpoint = pontine lesion*****Ice water to the right ear inhibits the right vestibular system and allows the normal left vestibular system to drive the eyes to the right (NORMAL RESPONSE)

*Corneal reflex tests integrity of CN 5 (sensory) and CN 7 (motor); watch medial lower eyelid/lashes for movement

Nasal stimulation should elicit a grimace and tests CN 7********