BRAIN DEATHPresenter- Ranjith R Thampi

PG Resident, AIMS, KochiDept of Anaesthesiology and Critical Care

INTRODUCTION

• Definitions:DEATH- Irreversible loss of capacity for consciousness, combined with irreversible loss of capacity to breathe.

• BRAIN DEATH- Loss of Cerebral cortex and Brainstem function.

Etiology is known and demonstrably irreversible.Spinal cord reflexes may be preserved in some.Introduced by Harvard medical school in 1968

1967 – Discussion started after first heart implantation by Christian Barnard1968- Irreversible coma and brain death by Harvard Medical College

INTRODUCTION

• CEREBRAL DEATHCessation of function of cerebral cortices. Brainstem function controlling respiratory centers ANS & Endocrine & immune systems are preserved with a flat cortical EEG

• BRAINSTEM DEATHDoes not require EEG for confirmationBased on rationale that brainstem and not cortices control respiration, circulation homeostasis and reticular formation for consciousness.

Brain Death- Does not include lower portion of spinal cord caudal to C2

CAUSES

• Cerebrovascular Accident- Stroke-Ruptured Aneurysm

• AnoxiaHanging, drowning, smoke inhalation, CO poisoning

• Trauma- RTA, FallOpen- Gun shot woundsClosed- Blunt Injury

Traumatic Brain InjuryGeneralized Hypoxia

Vasogenic Cerebral Edema

Brain Liquefication-

Total Brain Infarction

Raised ICP-

Exceeds Arterial BP

Cytotoxic Cerebral Edema

Cerebral Circulation Ceases-

Aseptic Brain Necrosis

ICP > MAP

MECHANISM OF BRAIN DEATH

Brain odema

CytotoxicVasogenic Brain Death

• Vasogenic edema - induced by an increase in cerebrovascular permeability after leaking of serum proteins into the brain parenchyma.

• Cytotoxic brain edema - hypoxic and ischemic conditions. results from disturbance of cellular osmoregulation.

• Brain oedema – focal initially – then spreads – increase ICP – ICP > arterial BP – cerebral circulation ceases- aseptic necrosis of brain- liquidified mass – respirator brain.

Brain Death

CARDIOVASCULAR SYSTEM

• Vasomotor and cardioaccelerating neurons diffusely in the pontine and medullary reticular core.

• Activation of these cells induces sympathetic nervous outflow, thereby increasing HR & BP.

• Hypertension then suppresses these cells through the feedback mechanism and circulation returns to preactivation levels

Brain Death

• When ICP is elevated, arterial blood pressure suddenly decreases sign of tonsillar herniation through the foramen magnum on the cervical spinal cord, in which outflow to the spinal cord suddenly ceases.

• Vasomotor and cardioaccelerating neurons of the spinal cord obtain automaticity within several days of disconnection and arterial blood pressure returns to normal without supplementation with vasopressors

Brain Death

HYPOTHALAMIC PITUITARY ENDOCRINE FUNCTIONS

• Preserved to a certain degree for a certain period after the onset of brain death.

• Thyroid hormones & vasopressins levels are markedly reduced after brain death.

• Hormonal therapy for hemodynamic stabilization of brain-dead organ donors T3, vasopressin, methylprednisolone, and insulin.Brain Death

DIAGNOSTIC CRITERIA

• Two examinations are required, separated by atleast 6 hours.

• Diagnosis done by 2 or 3 physicians who are independent of transplant team

• Atleast one physician should be a specialist in neurology/neurosurgery/anesthesia

DIAGNOSTIC CRITERIA

A. PREREQUISITES-Clinical/neuroimaging evidence of acute CNS catastrophe-Exclusion of complicating causes[Acid Base Disorders, Electrolyte imbalances, Endocrine disturbances.]-No drug intoxication, poisoning-Core Temp >32 oC (90 oF)

Lazarus Sign- Spontaneous/ reflex movements due to intact spinal cord at time of skin incision or in synchrony with respiration produced by mechanical ventilation. [Arm Flexion, Shoulder adduction, hands crossed and opposed just below the chin.]

CHECKLIST

loss of consciousness, loss of brainstem responses, apnea, and confirmatory tests, including lack of EEG activity

B. Clinical Findings:

Loss of Consciousness and Unresponsiveness• Patient should be in coma; GCS of 3• Motor responses of limbs or facial muscles to painful

supraorbital pressure – absent

• Motor responses may occur spontaneously during apnea testing; of spinal origin – observed during hypoxic or hypotensive episodes

• Spontaneous movements of spinal origin observed

Brain Death- Does not include lower portion of spinal cord caudal to C2

• Brainstem ResponsesCriteria of the American Academy of Neurology include

• Light reflex• Oculocephalic reflex• Caloric test• Corneal reflex• Jaw reflex• Pharyngeal reflex• Cough reflex

Pupils• No response to bright light• Size midposition(4mm) to dilated(9mm)

Ocular Movement• No Oculocephalic reflex (Testing only when no fracture or

instability of the cervical spine is apparent)• Caloric Test: No deviation of eyes to irrigation of ear with

50ml cold water. (Allow 1 minute after injection and 5 minutes between testing on each side)

Facial sensation and facial motor response1. No corneal reflex to touch with a throat swab 2. No jaw reflex 3. No grimacing to deep pressure on nail bed,

supraorbital ridge, or TMJ

Brainstem Reflex Testing

• Pharyngeal and tracheal reflexes1. No response – stimulation of posterior pharynx with tongue

blade2. No cough response to bronchial suctioning

• Apnea Testing:-Mandatory and most important test-Performed as the last test after other tests fulfill the criteria of brain death

Brainstem Reflex Testing

PREREQUISITES-Core Temp > 36.5 oC or 97 oF-Systolic BP > 90 mm Hg-Euvolemia/positive fluid balance in last 6 hrs-Normal PaCO2 (PaCO2 ≥ 40 mm Hg)-Normal PaO2 (preoxygenation to obtain arterial PaO2 ≥ 200 mm Hg)

-Connect pulse oximeter and DC ventilator-Deliver 100% O2 at 6L/min into trachea

APNEA TESTING

Connect pulse oximeter and disconnect ventilatorDeliver 100% O2 at 6L/min into tracheaLook closely for respiratory movements (abdominal or chest

excursions that produce adequate tidal volumes)Send ABG, Measure arterial PaO2, PCO2, and pH after

approximately 8 minutes and reconnect the ventilatorIf respiratory movements are absent & arterial PCO2 ≥ 60 mm Hg

(or; 20 mm Hg increase in PCO2 over baseline normal PCO2), apnea test is positive; supports the diagnosis of brain death

If respiratory movements observed, the apnea test result is negative (does not support the diagnosis of brain death), the test should be repeated

APNEA TESTING

Connect the ventilator if the SBP ≤ 90 mm Hg or significant oxygen desaturation and cardiac arrhythmias occur during testing – immediately analyse the ABG

If PCO2 is ≥ 60 mm Hg or PCO2 increase is ≥ 20 mm Hg over baseline normal PCO2, the apnea test result is positive; supports diagnosis of brain death

If PCO2 is < 60 mm Hg or PCO2 increase is < 20 mm Hg over baseline normal PCO2 – result is indeterminate; an additional confirmatory test can be considered

APNEA TESTING

• Controversies marked hypotension severe cardiac arrhythmias, Inadequate preoxygenation and acid-base or electrolyte abnormalities, pneumothorax intracranial pressure can increase markedly time for observation of apnea

APNEA TESTING

BRAIN DEATH GUIDELINES IN CHILDREN

Differences from adult guidelines:-3 separate longer observation periods required-2 corroborating EEGs and 1 EEG with radionuclide angiography required.- Can be used as confirmatory test when clinical criteria are not met.

Mandatory for kids less than 1yr.

CONFIRMATORY TESTS

• Instances where clinical criteria not met.

• Not always mandatory in adults but strongly recommended in children.

ANCILLARY TESTING

• EEG - Minimum of 8 scalp electrodes to be usedLoss of bioelectrical brain activity as shown on the EEG (i.e., isoelectric EEG) is a reliable confirmatory test for brain death• False positive - drug intoxication – barbiturates.• False negatives – residual electrical activity that persist after

brain death.

EEG

ELECTROCEREBRAL INACTIVITY (ECI)/SILENCE (ECS)

Normal Electrocerebral Silence

No electroencephalographic activity above 2 µV/mm when recording from scalp electrode pairs placed 10 or more cm apart and with interelectrode impedances less than 10,000 ohms but more than 100 ohms.

2.EVOKED RESPONSES

• Brainstem auditory evoked potentials (BAEPs):

Signals generated in auditory nerves and brainstem after an acoustic stimulus

5 identifiable waves from specific brainstem structures along auditory pathway.

BRAINSTEM AUDITORY EVOKED POTENTIALS (BAEPS)

• Wave I : 8th nerve

• Wave II : cochlear nerve

• Wave III : lower pons

• Wave IV : upper pons

• Wave V : midbrain

The loss of waves III to V or II to V or no reproducible BAEP on both sides is usually regarded as brain death.False positives - Preexisting deafness or severe peripheral auditory system damage.

SOMATOSENSORY EVOKED POTENTIALS

After electrical stimulation of peripheral nerves waves are generated from neural structures along the afferent somatosensory pathway

SSEP5 waves:

• Wave I : Brachial plexus• Wave II : Upper cervical cord• Wave III : Posterior column• Wave IV : Thalamus• Wave V : Sensory cortex

ADVANTAGES

• Unlike EEG signals, the early components of BAEPs and SSEPs are minimally affected by sedative drugs and anesthetics.

• However, drugs and metabolic derangements affect middle and late BAEPs and SSEPs.

3.DEMONSTRATION OF BRAIN PERFUSION AND MEASUREMENT OF CEREBRAL BLOOD

FLOW-ANGIOGRAPHY

I. Contrast Catheter Angiography

• Four-vessel cerebral angiography is a traditional “gold standard”.• The contrast medium should be injected under high pressure in

the anterior and posterior circulation.

• Advantage: neither influenced by CNS depressant drugs nor by hypothermia!

CONFIRMATORY TESTING• No intracerebral filling should be

detected at the level of entry of the carotid or vertebral artery to the skull.

•  External carotid circulation - patent.

• Filling of superior longitudinal sinus may be delayed

Normal

No Intracranial Flow

DISADVANTAGES

• Transported to radiology suite

• Invasive –Experienced neuroradiologist

• Complications - vasospasm, subintimal injection, arterial dissection, and thromboembolism, leading to a false image of absent flow and cerebral ischemia.

• Intra-arterial (aortic arch) or intravenous (vena cava) digital subtraction angiography has been shown to be as effective as conventional four-vessel angiography, less invasive, and easier to perform.

II) RADIONUCLIDE ANGIOGRAPHY

• Less invasive

• cannot image the posterior fossa well

• Radioligands such as technetium 99m (99mTc) hexamethylpropyleneamine-oxime (HMPAO), which cross the blood-brain barrier and are picked up and held by viable cells for several hours, are recommended to confirm.

• The lack of uptake of isotope in brain parenchyma ( hollow skull phenomenon) is characteristic for brain death.

• 99mTc-HMPAO single-photon emission computed tomography (SPECT) provides much more precise regional information - effective in the diagnosis of brain death both in children and adults

• The lack of signal from the intracranial compartment and the normal uptake in other parts of the head produce the “empty light bulb” and “hot nose” signs

Technetium-99 Isotope Brain Scan

Radionuclide Angiography

III) COMPUTED TOMOGRAPHY• Noninvasive test• intravenous injection of contrast media-time density analysis

• Advantages –• 1) easily accessible• 2) fairly inexpensive• 3)only minutes• 4) can also be combined with CT perfusion imaging• 5) noninvasive • 6) the images are easy to interpret. Xenon-CT cerebral blood flow method – average global flow of less than

5 mL/dL/min confirms brain death.

4. MAGNETIC RESONANCE

MR- Angiography Magnetic resonance (MR) imaging (MRI) and MR angiography.

MRI allows an assessment of intracranial contents and in defining abnormalities in the posterior fossa.

TRANSCRANIAL DOPPLER ULTRASONOGRAPHY

• Safe, noninvasive, and inexpensive

• Cerebral circulatory arrest can be confirmed if the following extracranial and intracranial Doppler sonographic findings have been recorded and documented both intracranially and extracranially and bilaterally on two examinations at an interval of at least 30 minutes:

Transcranial Ultrasonography

1.“Systolic spikes” or “oscillating flow” in any cerebral artery can be recorded by bilateral transcranial insonation of the internal carotid artery and middle cerebral artery.

   2.The diagnosis established by the intracranial

examination must be confirmed by the extracranial bilateral recording of the common carotid artery, ICA, and vertebral arteries.

POSITRON EMISSION TOMOGRAPHY

• Intravenous injection of radiotracers labeled with positron-emitting nuclides (e.g., oxygen 15 [15O], carbon 11 [11C], nitrogen 13 [13N]).

• Radionuclides are incorporated into organic compounds that are chemically similar to those present in the body, and several physiologic parameters can be measured.

• Use of PET in brain dead or comatose pts –early stage of development

CONSIDERATIONS REGARDING CHILDREN

• The anatomic neurodevelopment continues by 2 years of age or beyond the first decade of life.

• The presence of open fontanelles and open sutures in young children makes the skull an expandable chamber. Intracranial pressure may not exceed mean arterial blood pressure, and cerebral blood flow continues.

• The child's brain is more resistant to insults leading to death

A.    History: Determination of the proximate cause of coma to ensure absence of remediable or reversible conditions

B.    Physical examination criteria:   1.    Coma and apnea 2.    Absence of brainstem function

• Midposition or fully dilated pupils  • Absence of spontaneous eye movements  • Absence of movement of bulbar musculature and corneal, gag, cough, sucking,

and rooting reflexes    • Absence of respiratory movements with standardized testing for apnea

3.    Patient must not be hypothermic or hypotensive for age.   

4.   Flaccid tone and absence of spontaneous or induced movements, excluding spinal cord events.    5.    The examination results should remain consistent

with brain death throughout the observation and testing

period

C.    Observation period according to age :  

1. Seven days to 2 months: two examinations and EEGs separated by at least 48 hours.

  2. Two months to 1 year: two examinations and EEGs

separated by at least 24 hours

3. Older than 1 year: An observation period of at least 12 hours or, if it is difficult to assess the extent and reversibility of the brain damage, a more prolonged period of at least 24 hours.

D.    Laboratory testing:  

1. EEG:     2. Angiography

3. Techniques being investigated:    Xenon CT, digital subtraction angiography, visualization of cerebral arterial pulsations by real-time cranial ultrasound, Doppler determination of cerebral blood flow velocity, and evoked potential.

MANAGEMENT OF THE HEARTBEATING BRAIN-DEAD ORGAN DONOR

GOALS OF ORGAN DONOR MANAGEMENT

• Maintain body temperature• Ensure adequate oxygenation• Circulating volume• Cardiovascular stability• Adequate urine output

‘RULE OF 100’!!

• Systolic arterial pressure 100 mm Hg

• Urine output 100 ml/h

• PaO2 -100 mm Hg

• Haemoglobin concentration 100 g/litre.

• Blood sugar 100% normal’

PRINCIPLES OF DONOR MANAGEMENT

GENERAL CARE RESPIRATORY CVS

FLUIDS AND NUTRITION

BLOOD & COAGULATION

SYSTEMIC EFFECTS

INVESTIGATIONS

GENERAL CARE• The first priority when managing a patient with vasoplegia

and hypotension is to maintain an adequate effective intravascular volume.

• Plasma cytokine concentrations are increased in donors who are inadequately resuscitated and ‘preload-responsive’ and organ yields are lower.

• There is no evidence that any specific fluid has particular advantage for resuscitation in donors.

GENERAL CARE• Balanced salt solutions –avoid hyperchloraemic acidosis.

• Blood and blood products -if indicated

• Artificial colloids :

Starch-based colloids-are a/w delayed graft function.

• The choice of i.v. fluid and rate of administration should account for previous therapy, polyuria from diabetes insipidus, and consideration of effects of excessive fluid on respiratory system.

GENERAL CARE• Avoid excessive fluid loading in donor management

increase the number of transplantable lungs.

• CVP measurement alone is a poor guide for directing resuscitation - alternative techniques can be used to assess effective fluid administration.

• Fluid management of DBD directed by pulse-pressure variation can increase the viability of lungs and other organs.

• ‘Restrictive’ fluid regimens do not affect other donor organs

GENERAL CARE• Catecholamines have anti-inflammatory and preservation

effects, used by transplant retrieval services, for cardiac donation.

• High doses of norepinephrine (>0.05 microgram/ kg/ min) in donors is a/w increased cardiac graft dysfunction, particularly right ventricular performance, and higher early and late mortality in recipients.

GENERAL CARE

• Minimum invasive CVS monitoring includes arterial &CVP.

• Cardiac output monitoring .

• Stop unnecessary drugs(sedatives)

• Reduce heat loss and actively warm if necessary to maintain core temperature >35OC.

• Identify and treat infections.

• Bronchoalveolar lavage (after lung recruitment)

CVS• Review fluid balance

• Correct hypovolaemia

• Use CO monitoring to titrate fluids and inotropic or pressor drugs to intended goals as guided by retrieval team.

CVS• If vasopressor drugs required, vasopressin 2.4

units /h may reduce catecholamine requirements.

• High doses of catecholamines (e.g.norepinephrine > 0.05 microgram/kg/min) should be avoided if possible.

FLUIDS AND NUTRITION

• Administer maintenance fluids (can use enteral route), but avoid positive balance and hypernatraemia.

• Monitor U/O and maintain at 0.5–2.5 ml/kg/h.

• If urine output is >4 ml/kg/h, consider diagnosis of DI and treat with vasopressin infusion or DDAVP.

FLUIDS AND NUTRITION

• Insulin infusion (1 unit/h minimum).

• Maintain feeding or glucose source.

• Blood glucose target concentrations 4–8 mmol/litre.

• Correct electrolyte abnormalities to normal values

RESPIRATORY

• Use ‘lung protective’ ventilation.

• Tidal volume 6–8 ml/kg with optimal PEEP to allow min FIO2 .

• Recruitment manoeuvres initially, and repeated after apnoea testing or tracheal suction.

• Maintain tracheal cuff pressure @ 25 cm H2O and head up to reduce risk of aspiration

• Avoid administration of excessive i.v. fluids.

• Consider diuretics if fluid overload

• Avoid high inspired oxygen concentration-limit bronchiolitis obliterans syndrome in lung

recipients. Hennessy SA, Hranjec T, Swenson BR, et al. Donor factors are associated with bronchiolitis obliterans syndrome after lung transplantation. Ann Thorac Surg 2010; 89: 1555–62

BLOOD AND COAGULATION• Correct coagulation if evidence

of active bleeding

• Consider need for coagulation support during retrieval.

• Consider need for transfusion.

• Maintain thromboprophylaxis as there is a high incidence of pulmonary emboli found at retrieval

SYSTEMIC EFFECTS

• Methylprednisolone 15 mg/kg bolus immediately after brain death confirmed.

USE:

• A/w improved oxygenation

• Reduce increase in extravascular lung water so increased lung yields.

• Inflammation in the liver, heart and kidney is also reduced. Kainz A, Wilflingseder J, Mitterbauer C, et al. Steroid pretreatment of organ donors to

prevent Postischemic renal allograft failure. Ann Intern Med 2010; 153: 222–30

HORMONE-REPLACEMENT THERAPY BOLUS INFUSION

TRI IODOTHYRONINE 4 mcg/kg

3mcg/kg/hr

THYROXINE 20 mcg/kg 10mcg/kg/hr

METHYLPREDNISOLONE

15mg/kg Repeat in 24 hrs

VASOPRESSIN 1 u 0.5-4 u/hr

INSULIN 10 u (50% dextrose)

Maintain btw 80- 150mg/dl

MANAGEMENT OF LIVER FUNCTION

• Liver suffers from acute haemodynamic changes at the time of brainstem death, but continues to be affected by the systemic response even after restoration of arterial pressure.

• Ischaemic preconditioning of liver in heartbeating donor reduce IR injury.

• Volatile anaesthetic drugs and remifentanil have potentially beneficial preconditioning effects in hepatic and cardiovascular surgery.

RENAL AND PANCREATIC FUNCTION

• Effective donor management with good renal graft function avoids liberal fluid therapy.

• 1-deamino-8-D-arginine-vasopressin (DDAVP)does not affect graft function if blood volume is well maintained.

• Dopamine has no renal protective effect on renal function can be deleterious in donors if fluid management is inadequate, but might have beneficial effects in renal transplantation.

RENAL AND PANCREATIC FUNCTION

• Increasing obesity in the population is a significant factor reducing numbers of suitable organs.

• Achievement of donor goals, low vasopressor use, and good glycaemic control are a/w increased no: of retrieved grafts

ORGAN PRESERVATION

• Graft dysfunction occurs in the early post-op after transplantation preservation injury.

• Mechanism of preservation injury• Pre preservation injury• Cold preservation injury• Rewarming injury• Reperfusion injury

PRE PRESERVATION INJURY

• Pre – existing hepatic disease steatosis

• Injury associated with brain death hypotension/ hypoxia warm ischaemia.

• During organ harvesting intra-op hypotension.

COLD PRESERVATION INJURY

• Final temperature on ice 10 c

• Lowering the temperature lowers metabolic activity by 50 % for every 100 c of temperature reduction.

• At 10c the metabolic activity reduces to 5% of normal.

• Effects of cold• Anaeobic glycolysis reduced ATP & increased lactic acid.• Increased xanthine oxidase oxygen free radicals.• Inhibit Na – K ATPase loss of gradient

cell swelling

ISCHEMIA

• Decreased mitochondrial function

• Anaerobic conditions - depletion of ATP

• Alterations in ion permeability

• Accumulation of lactate

• Accumulation of hypoxanthine• Cell swelling• Cytosolic calcium accumulation

REPERFUSION

• Generation of reactive oxygen species

• Increased oxidative stress• Lipid peroxidation of cellular

membranes• Free radical formation leads to

cellular destruction• Results in macrophage/Kupffer cell

activation • Increased serum tumor necrosis

factor (TNF)• Damage can lead to prolonged

hypoxia after reperfusion

REWARMING INJURY

• During anastomosis, organ rewarms but not perfused.

• Oxygen & ATP level further falls.

• Anaerobic glycolysis

REPERFUSION INJURY

• Leukocyte & platelet activation

• Kupffer cell activation

• Reactive oxygen species

PRESERVATIVE SOLUTIONS

• Eurocollins solution• First clinically adapted solution.• Isotonic • High potassium • Glucose as impermeant.• Phosphate buffer• Effective for preservation of less than 6 hours.• Low viscosity – washout for blood & reduce the volume of

UW solution.

UNIVERSITY OF WISCONSIN SOLUTION

• Folkert Belzer & James Southard

• Isotonic, high potassium phosphate buffered solution.

• Osmotic concentration maintained by the use of metabolically inert substances like lactobionate and raffinose rather than with glucose.

• Hydroxyethyl starch is used to prevent edema

• Glutathione & allopurinol are added to scavenge free radicals, along with steroids and insulin.

• Adenosine substrate for ATP resynthesis on reperfusion.

• Dexamethasone membane stabilizer.

University of wisconsin solution

BRETSCHNEIDER’S / HTK SOLUTION

• Cardiac preservation.

• Histidine - retard acidosis

• Tryptophan - prevent membrane injury

• Ketoglutarate – substrate for energy metabolism.

COMPOSITION OF PRESERVATIVE SOLUTIONS

EUROCOLLINS UWPOTASSIUM 115 125SODIUM 10 125MAGNESIUM 30 5CHLORIDE 15 -BICARBONATE 10 -SULPHATE 30 5PHOSPHATE 57.5 25GLUCOSE 140

EUROCOLLINS UW

LACTOBIONATE 100RAFFINOSE 30ADENOSINE 5 GLUTATHIONE 3ALLOPURINOL 1 HYDROXYETHYL STARCH

50g/LmOsm/L 320 320 pH 7 7.4

ANESTHESIOLOGISTS IN ORGAN DONATION

• The main purpose of diagnosis of brain death is that it permits multiple vital organ procurement for transplantation.

• The “dead-donor rule” requires that patients must be declared dead before the removal of any life-sustaining organs.

• “Non–heart beating organ donor” protocols, in which life-sustaining therapy is withheld on a imminently dying patient with the removal of the transplantable organs after the patient's cardiac arrest, have been introduced.

MANAGEMENT

• Muscle relaxants are necessary to suppress motor activity mediated by spinal reflexes.

• Vasodilators usually are employed to suppress hypertension and tachycardia by noxious stimuli.

•Salient Features Of THE TRANSPLANTATION OF HUMAN ORGAN ACT 1994

SALIENT FEATURES OF HOTA, 1994•

1. The Transplantation of Human Organs Act, 1994 is meant to “provide for the regulation of removal, storage, and transplantation of human organs for therapeutic purposes and for the prevention of commercial dealings in human organs.” The Central Act illegalises the buying and selling of human organs and makes cash-for-kidney transactions a criminal offence.

• 2. The law establishes an institutional structure to authorise and regulate human organ transplants and to register and regulate, through regular checks, hospitals that are permitted to perform transplants.

• 3. It recognises, for the first time in India, the concept of brain-stem death, paving the way for a cadaver-based kidney transplant programme.

• 4. The Act details actions that amount to direct participation in or abetment of the organ trade; these offences are punishable under Section 19 of the Act.

• 5. The Act defines two categories of donors:-• First, it permits a near relative, defined as a patient's spouse, parents, siblings, and children, to donate a kidney to the patient. 

SALIENT FEATURES OF HOTA, 1994

•• Secondly, in Section 9(3) of the Act, live donors who are not near relatives but are willing to donate kidneys to the recipients “by reason of affection or attachment towards the recipient or for any other special reasons,” are permitted to do so, provided that the transplantations have the approval of the Authorisation Committee, established under the Act.

• 6. The Act makes the offence of kidney trading non-cognisable. In other words, the police cannot look into complaints of kidney trading independently but must wait for a complaint to be made by the Appropriate Authority set up under the Act or by an officer authorised by it or by an individual who has given prior notice of not less than 60 days to the Appropriate Authority.

SALIENT FEATURES OF HOTA, 1994

•7. It is not clear whether Section 9(3) was deliberately meant - under pressure from special interests - to provide a loophole that could be exploited in practice, or whether the law-makers thought they were sympathetically making provision for donations from second-degree relatives and others who might act out of genuine love and affection or altruism. But whatever be the reasoning and motivation behind the provision of a loophole, the practical operation of Section 9(3), combining with the non-cognisability of the offences to be prosecuted, has rendered the 1994 Act virtually unenforceable.

• 8. The Act very sensibly provides for registration of hospitals claiming to have the necessary competence and facilities to perform particular organ transplantation. This is a regulatory measure intended to protect the interests of patients. It is with the Appropriate Authority, set up by the State government under the Act, that hospitals intending to do transplants must register. Approvals are granted only after the institutions fulfill certain technical, infrastructural and medical requirements.

THE TRANSPLANTATION OF HUMAN ORGANS (AMENDMENT) BILL, 2009

Highlights of the Bill(HOTA)

• The Bill amends the Transplantation of Human Organs Act, 1994, which regulates removal, storage and transplantation of human organs. 

• In addition to human organs, the Bill seeks to regulate transplantation of tissues of the human body. 

• The Act permits donations from living persons who are near relatives. The Bill expands the definition of “near relative” to include grandparents and grandchildren in addition to parents, children, brother, sister and spouse. 

THE TRANSPLANTATION OF HUMAN ORGANS (AMENDMENT) BILL, 2009

Highlights of the Bill

• The doctor in an ICU has to inform the patient or relatives of patient about the option of organ donation and ascertain whether they would consent to the donation.

• A pair of donor and recipient who are near relatives but whose organs do not medically match for transplantation are permitted by the Bill to swap organs with another pair of such persons.

• The Bill enhances the penalty for unauthorised removal of human organs and for receiving or making payment for human organs

THANK YOU

“Concern for man and his fate must always form the chief interest of all technical endeavors. Never forget

this in the midst of your diagrams and equations”

Albert Einstein