DIAGNOSIS AND IMPLICATIONS OF BRAIN DEATH

MANAGEMENT OF PATIENT FOLLOWING CARDIAC RESUSCITATION

Dr. Manish chopra

University College of Medical Sciences & GTB Hospital, Delhi

Part 9: Post–Cardiac Arrest Care

2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Mary Ann Peberdy, Clifton W. Callaway, Robert W. Neumar; Romergryko G. Geocadin; Janice L. Zimmerman; Michael Donnino; Andrea Gabrielli; Scott M. Silvers; Arno L. Zaritsky; Raina Merchant; Terry L. Vanden Hoek; Steven L. Kronick

Applying Classification of Recommendations and Level of Evidence

Class I Class IIa Class IIb Class III

Benefit >>> Risk

Procedure/Treatment SHOULD be performed/ administered

Benefit >> RiskAdditional studies with focused objectives neededIT IS REASONABLE to perform procedure/ administer treatment

Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpfulIT IS NOT UNREASONABLE to perform procedure/ administer treatment

Risk ≥ BenefitNo additional studies needed Procedure/Treatment should NOT be performed/ administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL

Level A Multiple (3-5) population risk strata evaluatedMultiple RCT or metaanalysis

o Recommendation that procedure or treatment is useful/effective o Sufficient evidence from multiple randomized trials or meta-analyses

o Recommendation in favor of treatment or procedure being useful/effective o Some conflicting evidence from multiple randomized trials or meta-analyses

o Recommendation's usefulness/efficacy less well established o Greater conflicting evidence from multiple randomized trials or meta-analyses

o Recommendation that procedure or treatment not useful/effective and may be harmful o Sufficient evidence from multiple randomized trials or meta-analyses

Applying Classification of Recommendations and Level of Evidence

Class I Class Iia Class IIb Class III

Level B Limited (2-3) population risk strata evaluatedSingle RCT or nonrandomized studies

o Recommendation that procedure or treatment is useful/effectiveo Limited evidence from single randomized trial or non-randomized studies

o Recommendation in favor of treatment or procedure being useful/effectiveo Some conflicting evidence from single randomized trial or non-randomized studies

o Recommendation's usefulness/efficacy less well established o Greater conflicting evidence from single randomized trial or non-randomized studies

o Recommendation that procedure or treatment not useful/effective and may be harmfulo Limited evidence from single randomized trial or non-randomized studies

Level C Very limited (1-2) population risk strata evaluatedOnly consensus opinion of experts case studies

o Recommendation that procedure or treatment is useful/effectiveo Only expert opinion, case studies, or standard-of-care

o Recommendation in favor of treatment or procedure being useful/effectiveo Only diverging expert opinion, case studies, or standard-of-care

o Recommendation's usefulness/efficacy less well established o Only diverging expert opinion, case studies, or standard-of-care

o Recommendation that procedure or treatment not useful/effective and may be harmful o Only expert opinion, case studies, or standard-of-care

Introduction

Increasing recognition of return of spontaneous circulation (ROSC) - good quality of life post cardiac arrest

Randomized controlled clinical trialsPost–cardiac arrest syndrome*#

Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury

*HACA. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic

hypothermia to improve the neurologic outcome after cardiac

arrest. N Engl J Med. 2002;346:549 –556.

#Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G,

Smith K. Treatment of comatose survivors of out-of-hospital cardiac

arrest with induced hypothermia. N Engl J Med. 2002;346:557–563.

(contd.)

Post–cardiac arrest care is a critical component of advanced life support

Most deaths occur during the first 24 hours after cardiac arrest

Multiple organ systems are affected after cardiac arrest

(contd.)

Significant cardiovascular dysfunction - requiring support of blood flow and ventilation- intravascular volume expansion, vasoactive and inotropic drugs, and invasive devices.

Therapeutic hypothermia, treatment of the underlying cause of cardiac arrest- improves survival and neurological outcomes

Protocolized hemodynamic optimization Multidisciplinary early goal-directed therapy protocols -

bundle of care Proactive titration of post–cardiac arrest hemodynamics

Difficult to distinguish between any specific component of care that is most important.

What should be our approach

Comprehensive

Structured

Multidisciplinary system of care

Interventions

Therapeutic hypothermia

Optimization of hemodynamics and gas exchange

Immediate coronary reperfusion- percutaneous coronary intervention (PCI)

Glycaemic control

Neurological diagnosis, management, and prognostication.

What I Will Talk About ??

Hemodynamic

Neurological

Metabolic

Initial objectives of post–cardiac arrest care

1. Optimize cardiopulmonary function and vital organ perfusion

2. Out-of-hospital cardiac arrest - appropriate hospital - comprehensive post–cardiac arrest treatment system of care

3. In-hospital post–cardiac arrest - appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care

4. Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest

Subsequent objectives of post–cardiac arrest care

1. Control body temperature to optimize survival and neurological recovery

2. Identify and treat acute coronary syndromes (ACS)

3. Optimize mechanical ventilation to minimize lung injury

4. Reduce the risk of multiorgan injury and support organ function if required

5. Objectively assess prognosis for recovery

6. Assist survivors with rehabilitation services when required

Overview of Post–Cardiac Arrest Care

Avoid using ties that pass circumferentially around the patient's neck

Elevate the head of the bed 30° Avoid 100% oxygen - titrate inspired oxygen SpO2 of >94%,

oxygen toxicity Avoid Hyperventilation or "overbagging" the patient

Ventilation_ 10 to 12 breaths per minute

Titrated to achieve a PETCO2 of 35 to 40 mm Hg or a PaCO2 of 40 to 45 mm

(Contd.)

Assess vital signs and monitor for recurrent cardiac arrhythmias

Intravenous / intraosseous access

Systolic blood pressure < 90 mm Hg- fluid boluses can be considered

Titrated vasoactive drug infusions - minimum SBP (90 mm Hg) or a MAP (65 mm Hg)

Therapeutic hypothermia

Coronary reperfusion (PCI)

Remember

Most common cause of cardiac arrest- cardiovascular disease and coronary ischemia - 12-lead ECG to detect ST elevation or new left bundle-branch block

High suspicion of acute myocardial infarction (AMI) - treatment of AMI and coronary reperfusion should be activated

Absence of ST elevation - medical or interventional treatments may be considered for treatment of ACS

Identify and treat - cardiac, electrolyte, toxicological, pulmonary, and neurological precipitants of arrest

Review the H's and T's mnemonic to recall factors

Targeted Temperature Management

Induced Hypothermia For protection of the brain and other organs - helpful therapeutic

approach in comatose patients

Specific indications

Timing and duration of therapy

Methods for induction, maintenance, and subsequent reversal of hypothermia

(contd.)

Studies of animal models of cardiac arrest showed that short-duration hypothermia (1 hour) achieved < 10 - 20 minutes after ROSC had a beneficial effect

Optimal duration of induced hypothermia is at least 12 hours and may be >24 hours

Hypothermia was maintained for 12 or 24 hours in the studies of out-of-hospital patients presenting in VF

Hypothermia for up to 72 hours was used safely in newborns

Methods for inducing hypothermia

Multiple, no single method has proved to be optimal. Feedback-controlled endovascular catheters and surface

cooling devices are availableCooling blankets, application of ice bags - require more labor

and closer monitoring. Iced isotonic fluid can be infused to initiate core cooling but

must be combined with a follow-up method for maintenance

of hypothermia#

# Bernard S , Buist M, Monteiro O, et al. Induced hypothermia using large volume, ice cold intravenous fluid in comatose survivors of out of hospital cardiac arrest: a preliminary report.

Resuscitation 2003;56:9-13

(contd.)

Patient's core temperature - Esophageal thermometer, bladder catheter, pulmonary artery catheter, Axillary and oral temperatures are inadequate for measurement of core temperature

Tympanic temperature - rarely available, unreliable

Bladder temperatures - anuric patients

Rectal temperatures - differ from brain or core temperature

Potential complications Coagulopathy Arrhythmias Hyperglycemia Pneumonia Sepsis Infections Decrease immune function Impairs coagulation Ongoing bleeding

(contd.)

RecommendationComatose adult patients with ROSC after out-of-hospital VF

cardiac arrest should be cooled to 32°C to 34°C for 12 to 24 hours. (Class I, LOE B)

Induced hypothermia also may be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of pulseless electric activity or asystole. (Class IIb, LOE B)

Active rewarming should be avoided in comatose patients who spontaneously develop a mild degree of hypothermia (>32°C) after resuscitation from cardiac arrest during the first 48 hours after ROSC.(Class III, LOE C)

Hyperthermia

After resuscitation, temperature elevation above normal can impair brain recovery

Etiology of fever after cardiac arrest - inflammatory cytokines.There are no randomized controlled trials evaluating the effect of

treating pyrexia with either frequent use of antipyretics or "controlled normothermia" using cooling techniques compared to no temperature intervention in post–cardiac arrest patients.

Patients can develop hyperthermia after rewarming

posthypothermia treatment. This late hyperthermia should also be identified and treated. Providers should closely monitor patient core temperature after ROSC and actively intervene to avoid hyperthermia (Class I, LOE C).

Organ-Specific Evaluation and Support

Pulmonary SystemPulmonary dysfunction after cardiac arrest is common. Etiologies - hydrostatic pulmonary edema from left ventricular

dysfunction

Noncardiogenic edema from inflammatory, infective, or physical injuries

Pulmonary atelectasis

Aspiration

Mismatch of ventilation and perfusion

ARDS/ ALI

Role of Positive end-expiratory pressure (PEEP), a lung-protective

strategy for mechanical ventilation, and titrated FiO2

(contd.)

Diagnostic tests in intubated patients - chest radiograph, ABG. Verify correct position of the ET tube, distribution of pulmonary infiltrates, edema

Identify complications - rib fracture, pneumothorax, and pleural effusions, pneumonia

Adjust mechanical ventilatory support - oxyhemoglobin saturation, ABG, MV and patient-ventilator synchrony

Reduce the work of breathing Titrate oxygen administration - maintain the SpO2 94%.

(contd.)

Significant metabolic acidosis after cardiac arrest- temptation to institute hyperventilation to normalize blood pH

1-mm Hg decrease in PaCO2 - decrease in cerebral blood flow of approximately 2.5% to 4%

Cerebral blood flow remains CO2-reactive after cardiac arrest - diminished for 1 to 3 hours after reperfusion

Initial hyperemic blood flow response that lasts 10 to 30 minutes, followed by a more prolonged period of low blood flow. During this latter period of late hypoperfusion, a mismatch between blood flow and oxygen requirement may occur. Hyperventilation at this stage may lower PaCO2, cause cerebral vasoconstriction, and exacerbate cerebral ischemic injury.

(contd.)

In one study, controlled ventilation with specific goals to keep PaCO2 37.6 to 45.1 mm Hg (5 to 6 kPa) and SaO2 95% to 98% as part of a bundle with multiple other goals (including hypothermia and blood pressure goals) increased survival from 26% to 56%.

Hyperventilation also may compromise systemic blood flow because of occult or auto-PEEP and is deleterious in all low-flow states, including cardiopulmonary resuscitation (CPR) and hypovolemia.

(contd.)

Recommendation - TV of 6 to 8 mL/kg and inspiratory plateau pressure 30 cm H2O to reduce ventilator-associated lung injury.

Furthermore, a recent historical comparison of ventilation practice after cardiac arrest reported no differences in pneumonia, oxygenation, lung compliance, and ventilator days when a low VT strategy versus a more liberal "old practice" VT was applied

Maintain PaCO2 (40 to 45 mm Hg) or PETCO2 (35 to 40 mm Hg)

while avoiding hemodynamic compromise (Class IIb, LOE C)

Treatment of Pulmonary Embolism After CPR

Use of fibrinolytics to treat pulmonary embolism after CPR has been reported

Surgical embolectomy

Mechanical thrombectomy

In post–cardiac arrest patients with arrest due to presumed or known pulmonary embolism, fibrinolytics may be considered (Class IIb, LOE C).

Sedation After Cardiac Arrest

Post–cardiac arrest - cognitive dysfunction, agitation, frank

delirium with purposeless movement, risk of self-injury

Opioids, anxiolytics, sedative-hypnotic agents, adrenergic agonists, butyrophenones

Neuromuscular blocking agents can be used for short intervals with adequate sedation

Daily interruptions and titrated to the desired effect.

Cardiovascular System

ACS is a common cause of cardiac arrest- 12-lead ECG and cardiac markers - aggressive treatment of STEMI - regardless of coma or induced hypothermia - emergent coronary angiography.

PCI alone or as part of a bundle of care - improved myocardial function and neurological outcomes.

Therapeutic hypothermia safely combined with primary PCI after cardiac arrest caused by AMI.

Antiarrhythmic drugs- lidocaine or amiodarone

There is no evidence to support or refute continued or prophylactic

administration of these medications.

Vasoactive Drugs for Use in Post–Cardiac Arrest Patients

(contd.)

(contd.)

Hemodynamic instability is common after cardiac arrest.Persistently low cardiac index during the first 24 hours -

multiorgan failureMetabolic acidosis - VasodilationIschemia/reperfusion of cardiac arrest and electric

defibrillation - myocardial stunning and dysfunctionEchocardiographic evaluation within the first 24 hours

Mean arterial pressure 65 mm Hg and an ScvO2 70% are generally considered reasonable goals.

Glucose Control

The post–cardiac arrest patient is likely to develop metabolic abnormalities such as hyperglycemia

Increased mortality or worse neurological outcomes Optimum blood glucose concentration and interventional strategy to

manage blood glucose in the post–cardiac arrest period is unknown Hypoglycemia may be associated with worse outcomes in critically ill

patients Strategies to target moderate glycemic control (144 to 180 mg/dL) may be

considered in adult patients with ROSC after cardiac arrest (Class IIb, LOE B)

Attempts to control glucose concentration within a lower range (80 to 110 mg/dL should not be implemented after cardiac arrest due to the increased risk of hypoglycemia (Class III, LOE B)

Steroids

Corticosteroids have an essential role in the physiological

response to severe stress, including maintenance of vascular tone and capillary permeability

In the post–cardiac arrest phase - adrenal insufficiency

At present there are no human randomized trials investigating corticosteroid use after ROSC

Hemofiltration

Hemofiltration has been proposed as a method to modify the humoral response to the ischemic-reperfusion injury that occurs after cardiac arrest

Future investigations are required to determine whether hemofiltration will improve outcome in post–cardiac arrest patients.

Central Nervous System

Brain injury

Common cause of morbidity and mortality in post–cardiac arrest patients.

Cause of death in 68% patients (out-of-hospital), 23% a (in-hospital) cardiac arrest.

Clinical manifestations - coma, seizures, myoclonus, neurocognitive dysfunction (ranging from memory deficits to persistent vegetative state), and brain death.

Seizure ManagementWhether there is any disease-specific management of seizures after cardiac arrest remains unknown Untreated seizures - detrimental to the brain EEG - as soon as possible and should be monitored frequently or continuously in

comatose patients after ROSC. (Class I, LOE C) Neuroprotective agents with anticonvulsant properties- thiopental, diazepam or

magnesium - not improved neurological outcome in survivors. The same anticonvulsant regimens for the treatment of seizures used for status

epilepticus caused by other etiologies may be considered after cardiac arrest. (Class IIb, LOE C)

Neuroprotective Drugs

Number of clinical trials performed to date is limited and has failed to demonstrate improved neurological outcome with potential neuroprotective drugs given after cardiac

arrest.

Prognostication of Neurological Outcome in Comatose Cardiac

Arrest Survivors

Early prognostication of neurological outcome - essential component of post–cardiac arrest care

Accurate and reliable tools to prognosticate poor outcome

Poor outcome is defined as death, persistent unresponsiveness, or

the inability to undertake independent activities after 6 months

No pre-arrest or intra-arrest parameters alone or in combination

accurately predict outcome in individual patients who achieve

ROSC

(contd.)

No post-arrest physical examination finding or diagnostic study has as yet predicted poor outcome of comatose cardiac arrest survivors during the first 24 hours after ROSC.

After 24 hours - SSEPs - absence of confounders (such as hypotension, seizures, sedatives, or neuromuscular blockers) - most reliable early predictors of poor outcome

However, the decision to limit care should never be made on the basis of a single prognostic parameter, and expert consultation may be needed.

Neurological Assessment

Most widely studied parameter to predict outcome in comatose post–cardiac arrest patients – check confounding factors (hypotension, seizures, sedatives, or neuromuscular blockers)

No clinical neurological signs reliably predict poor outcome < 24

hours after cardiac arrest. Absence of both pupillary light and corneal reflexes at 72 hours after cardiac arrest predicted poor outcome with high reliability

The absence of vestibulo-ocular reflexes at 24 hours or Glasgow Coma Scale (GCS) score < 5 at 72 hours are less reliable for predicting poor outcome

(contd.)

EEGNo electrophysiological study reliably predicts outcome in comatose

patients during the first 24 hours after ROSC. EEG pattern showing generalized suppression to <20 µV, burst-suppression

pattern associated with generalized epileptic activity, or diffuse periodic complexes on a flat background is associated with a poor outcome – check confounders

In the absence of confounding factors such as sedatives, hypotension,

hypothermia, neuromuscular blockade, seizures, or hypoxemia, it may be helpful to use an unprocessed EEG interpretation observed 24 hours after ROSC to assist with the prediction of a poor outcome in comatose survivors of cardiac arrest not treated with hypothermia (Class IIb, LOE B).

Evoked PotentialsAbnormalities in evoked potentials are associated with poor outcomes.

Neuroimaging

MRICTSingle-photon emission computed tomographyCerebral angiographyTranscranial Doppler

Blood and Cerebrospinal Fluid Biomarkers

NSE - most promising and extensively studied biomarker is serum for predicting poor outcome when measured between 24 and 72 hours after cardiac arrest

Routine use of any serum or CSF biomarker as a sole predictor of poor outcome in comatose patients after cardiac arrest is not recommended (Class III, LOE B).

Ethics

Advance directive – communicates thoughts, wishes, preferences for healthcare decisions in periods of inadequacy.

Living will – written direction to healthcare providers about the care that the individual approves should he or she becomes terminally ill and unable to make decisions.

Durable power of attorney for health care – legal document, appoints an authorized person to make healthcare decisions.

DNAR order – Licensed physician as per local regulation

Must be signed, valid date, preceded by discussion with familyAND (allow natural death) – allow natural consequences of a

disease or injury, emphasize ongoing end of life care.

A decision to limit care or withdraw life support is justifiable

If the patient is determined to be brain dead

If the physician and patient/surrogate agree that treatment goals cannot be met, or if the burden to the patient of continued treatment believed to exceed any benefits.

Organ Donation After Cardiac Arrest

Despite maximal support and adequate observation, some patients will be brain-dead after cardiac arrest.

No difference in functional outcomes of organs transplanted from patients who are brain-dead as a consequence of cardiac arrest when compared with donors who are brain-dead due to other causes.

Adult patients who progress to brain death after resuscitation from cardiac arrest should be considered for organ donation (Class I, LOE B).

Brain Death

Refinements in critical care medicine- appropriate diagnosis of brain death.

No global consensus on brain death diagnosis.

Legal requirement for organ donation.

History

First description of cessation of brain function – 1959

Criteria for brain death – first published in 1968

Brainstem definition for brain death - 1976- Conference of Medical Royal Colleges and their Faculties in the United Kingdom.

The document in 1995 - Criteria for the Diagnosis of Brain Stem Death encouraged the use of more correct term Brainstem Death.

The concept of Brain Death

Brain death – death of the organism and not merely death or necrosis of brain in a living body.

Physiologic significance of brain death and cardiac death are essentially equal- both represent irreversible loss of communication between the control centers and the peripheral cells.

Current concept - CNS, including the brain stem, is the control center, cessation of CNS functions represents cessation of harmony of life, without CNS control living organism is nothing more than an aggregation of living cells.

Diagnostic criteria for the clinical diagnosis of brain death

A Prerequisites

Brain death is the absence of clinical brain function when the proximate cause is known and demonstrably irreversible.

1. Clinical or neuroimaging evidence of an acute CNS catastrophe that is compatible with the clinical diagnosis of brain death.

2. Exclusion of complicating medical conditions that may confound clinical assessment

3. No drug intoxication or poisoning

4. Core temperature ≥ 32oC.

(contd.)

B Cardinal findings

1 Coma or unresponsiveness- no cerebral motor response to pain in all extremities.

2 Absence of brainstem reflexes Pupils

no response to bright light

size: midposition to dilated

(contd.)

Absent pupillary light reflex

Although drugs can influence pupillary size, the light reflex remains intact only in the absence of brain death

IV atropine does not markedly affect response

Paralytics do not affect pupillary size

Topical administration of drugs and eye trauma may influence pupillary size and reactivity

Pre-existing ocular anatomic abnormalities may also confound pupillary assessment in brain death

(contd.)

(contd.)

Ocular movement

no oculocephalic reflex

no deviation of eyes to irrigation (50ml, 1min, 5min)

Elevate the head by 30°Irrigate one tympanic membrane with iced water

Observe patient for 1 minute after each ear irrigation, with a 5 minute wait between testing of each ear

Facial trauma involving the auditory canal and petrous bone can also inhibit these reflexes

Cold caloric test interpretation

Not comatose Nystagmus; both eyes slow toward cold,

Coma with intact brainstem Both eyes tonically deviate toward cold water

No eye movement

Brainstem injury / death

Movement only of eye on side of stimulus Internuclear ophthalmoplegia Suggests brainstem structural lesion

(contd.)

Facial sensation and facial motor response

no corneal reflex

no jaw reflex

no grimacing to deep pressure Pharyngeal and tracheal reflexes

no response-posterior pharynx

no cough response- bronchial suctioning

(contd.)

3 Apnea testPrerequisites

Core temperature ≥ 36.5 OC

Systolic blood pressure ≥ 90 mmHg

Euvolemia: option- positive fluid balance in the previous 6 hours

Normal PaCO2: Option - PaCO2 ≥ 40 mmHg

Normal PaO2: Option - preoxygenation to obtain arterial PaO2 ≥ 200 mmHg

(contd)

Connect a pulse oximeter – disconnect ventilator

Deliver 100 percent oxygen, 6L/min, into the trachea

Look closely for the respiratory movements

Measure arterial PaCO2, PaO2 and pH after approximately 8 min and reconnect the ventilator

Interpretation of Apnea test

Respiratory movements - absent

arterial PCO2 ≥ 60 mmHg (option: 20 mmHg increase over baseline) – apnea test positiveRespiratory movements observed - apnea test negative - test

should be repeatedConnect the ventilator if - SBP ≤ 90 mmHg

Pulse oximeter indicates significant desaturation

Cardiac arrhythmias

(contd.)

Immediately draw an arterial sample- ABG

PaCO2 ≥ 60 mmHg or PaCo2 increase ≥ 20 mmHg - Apnea test positive

If PaCO2 ≤ 60 mmHg or PaCo2 increase < 20 mmHg- result is indeterminate - additional confirmatory test can be considered.

Brain death guidelines in children

A History

Determination of the proximate cause of coma to ensure absence of remediable or reversible conditions

B Physical examination

Coma and apnea

Absence of brainstem functions Midposition of fully dilated pupils Absence of spontaneous eye movements Absence of movements of bulbar musculature and corneal, gag,

cough, sucking and rooting reflexes Absence of respiratory movements with apnea testing Patient must not be hypothermic or hypotensive for age Flaccid tone and absence of spontaneous or induced movements

The examination results should remain consistent with brain death throughout the observation and testing period.

(contd.)

C Observation period according to age

7 days - 2 months: 2 examinations and EEGs separated by 48 hours

2 months - 1 yr: 2 examinations and EEG seperated by at least 24 hours

> 1 year : observation period of atleast 12 hours/ more prolonged period of atleast 24 hours if it is difficult to assess the extent and reversibility of brain damage.

(contd.)

D Laboratory testing

EEG – should be performed throughout a 30- min period using standardized techniques.

Angiography – cerebral radionuclide angiogram – lack of visualization of cerebral circulation

Techniques being investigated

Xenon CT, DSA, Real time cranial USG,

Doppler, Evoked potential

Confirmatory Testing for Determination of Brain Death

Cerebral angiography

Electroencephalograpgy

Transcranial Doppler USG

Cerebral Scintigraphy 99mTc- hexametazime

The diagnosis of brain death. N Engl J Med 344:1215,2001

Role of Anaesthesiologist in brain death/ Anaesthesiologists in Organ

Donation

With the development of organ transplantation, the concept of brain death has been developed.

Permits multiple vital organ procurement for transplantation.

Dead – donor rule : requires that patients must be declared dead before the removal of any life sustaining organs- ethical and legal implications

Required request/ presumed consent- to improve the rate of organ donation.

“Non-heart beating organ donor” protocols: life sustaining therapy is withheld on an imminently dying patient with the removal of transplantable organs after the patients cardiac arrest.

Anaesthesiologists- ample knowledge about brain death and organ donation.

Involved not only in brain death diagnosis but also in anaesthetic management of brain dead patients for organ procurement.

Special care is required for anaesthetic management as the spinal cord is intact and somatic and visceral reflexes are present.

Vasodilators- suppress hypertension and tachycardia by noxious stimuli.

Muscle relaxants – suppress the motor activity mediated by spinal reflexes.

Sedation and analgesia – an opinion – theoretically unnecessary.

References

1. Circulation . The journal of American heart association 2010

2. Miller’s anaesthesia 7th edition

3. Morgan’s clinical anaesthesiology 4th edition

4. Cardio pulmonary resuscitation 2010. improve the quality of care. Indian journal of anaesthesia. 2010;54; (2) :91- 94

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