Brain Death presentation

1. BRAIN DEATH
Presenter- Ranjith R Thampi
PG Resident, AIMS, Kochi
Dept of Anaesthesiology and Critical Care

2. 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 Barnard
1968- Irreversible coma and brain death by Harvard Medical College

3. INTRODUCTION
• CEREBRAL DEATH
Cessation of function of cerebral cortices. Brainstem function
controlling respiratory centers ANS & Endocrine & immune
systems are preserved with a flat cortical EEG
• BRAINSTEM DEATH
Does not require EEG for confirmation
Based 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

4. CAUSES
• Cerebrovascular Accident
- Stroke
-Ruptured Aneurysm
• Anoxia
Hanging, drowning, smoke inhalation, CO poisoning
• Trauma- RTA, Fall
Open- Gun shot wounds
Closed- Blunt Injury

5. Traumatic Brain Injury
Generalized 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

6. MECHANISM OF BRAIN DEATH
Brain odema
Cytotoxic
Vasogenic
Brain Death

7. • 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

8. 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 levelsBrain Death

9. • 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

10. 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

11. 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

12. 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.]

13. CHECKLIST
 loss of consciousness,
 loss of brainstem responses,
 apnea, and
 confirmatory tests, including lack of EEG activity

14. 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

15. • Brainstem Responses
Criteria of the American Academy of Neurology
include
• Light reflex
• Oculocephalic reflex
• Caloric test
• Corneal reflex
• Jaw reflex
• Pharyngeal reflex
• Cough reflex

16. 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 response
1. No corneal reflex to touch with a throat swab

17. • Pharyngeal and tracheal reflexes
1. No response – stimulation of posterior pharynx with tongue blade
2. 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

18. 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

19. Connect pulse oximeter and disconnect ventilator
Deliver 100% O2 at 6L/min into trachea
Look 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 ventilator
If 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

20. 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

21. • 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

22. 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.

23. CONFIRMATORY TESTS
• Instances where clinical criteria not met.
• Not always mandatory in adults but strongly
recommended in children.

24. • EEG
- Minimum of 8 scalp electrodes to be used
Loss 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.

25. 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.

26. 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.

27. 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.

28. SOMATOSENSORY
EVOKED POTENTIALS
After electrical stimulation of peripheral nerves waves are
generated from neural structures along the afferent
somatosensory pathway

29. SSEP
5 waves:
• Wave I : Brachial plexus
• Wave II : Upper cervical cord
• Wave III : Posterior column
• Wave IV : Thalamus
• Wave V : Sensory cortex

30. 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.

31. 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!

32. 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

33. 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.

34. 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.

35. • 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

36. 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.

37. 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.

38. 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

39. 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.

40. 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

41. 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

42. 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

43. 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

44. 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.

45. 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.

46. MANAGEMENT OF THE HEARTBEATING
BRAIN-DEAD ORGAN DONOR

47. GOALS OF ORGAN DONOR
MANAGEMENT
• Maintain body temperature
• Ensure adequate oxygenation
• Circulating volume
• Cardiovascular stability
• Adequate urine output

48. ‘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’

50. PRINCIPLES OF DONOR
MANAGEMENT
GENERAL CARE RESPIRATORY CVS
FLUIDS AND
NUTRITION
BLOOD &
COAGULATION
SYSTEMIC
EFFECTS
INVESTIGATIONS

51. 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.

52. 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.

53. 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

54. 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.

55. 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)

56. 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.

57. 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.

58. 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.

59. 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

60. 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

61. 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

62. 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

63. HORMONE-REPLACEMENT
THERAPY
BOLUS INFUSION
TRI IODOTHYRONINE 4 mcg/kg 3mcg/kg/hr
THYROXINE 20 mcg/kg 10mcg/kg/hr
METHYLPREDNISOL
ONE
15mg/kg Repeat in 24 hrs
VASOPRESSIN 1 u 0.5-4 u/hr
INSULIN 10 u (50%
dextrose)
Maintain btw 80-
150mg/dl

64. 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.

65. 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.

66. 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

67. 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

68. PRE PRESERVATION INJURY
• Pre – existing hepatic disease  steatosis
• Injury associated with brain death  hypotension/ hypoxia
warm ischaemia.
• During organ harvesting  intra-op hypotension.

69. 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.

70. • 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

71. ISCHEMIA
• Decreased mitochondrial
function
• Anaerobic conditions -
depletion of ATP
• Alterations in ion
permeability
• Accumulation of lactate
• Accumulation of hypoxanthine
• Cell swelling
• Cytosolic calcium accumulation

72. 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

73. REWARMING INJURY
• During anastomosis, organ rewarms but not perfused.
• Oxygen & ATP level further falls.
• Anaerobic glycolysis

74. REPERFUSION INJURY
• Leukocyte & platelet activation
• Kupffer cell activation
• Reactive oxygen species

75. 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.

76. 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.

77. • 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

78. BRETSCHNEIDER’S / HTK
SOLUTION
• Cardiac preservation.
• Histidine - retard acidosis
• Tryptophan - prevent membrane injury
• Ketoglutarate – substrate for energy metabolism.

79. COMPOSITION OF
PRESERVATIVE SOLUTIONS
EUROCOLLINS UW
POTASSIUM 115 125
SODIUM 10 125
MAGNESIUM 30 5
CHLORIDE 15 -
BICARBONATE 10 -
SULPHATE 30 5
PHOSPHATE 57.5 25
GLUCOSE 140

80. EUROCOLLINS UW
LACTOBIONATE 100
RAFFINOSE 30
ADENOSINE 5
GLUTATHIONE 3
ALLOPURINOL 1
HYDROXYETHYL
STARCH
50g/L
mOsm/L 320 320
pH 7 7.4

81. 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.

82. 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.

83. •Salient Features Of
THE TRANSPLANTATION OF
HUMAN ORGAN ACT 1994

84. 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.

85. 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.

86. 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.

87. 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.

88. 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

89. 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