Brain death

brain death

1. Moderator: Prof. Dr R. N. Khadgaray Presenter: Dr Kundan Kishor Ghimire UCMS-TH BRAIN DEATH

2. Objectives Will be able to know when to, how to, and why to declare a patient as brain dead.

3. Historical Perspective Historically death defined as “permanent cessation of circulatory and respiratory function.” However, in 1968 a committee at Harvard Medical School decided to redefine death by using “irreversible coma” as a new criterion.

4. advancements in CPR techniques and widespread mechanical ventilators use, number of patients could be kept temporarily ‘alive. Consequently, Harvard criteria was developed and formed the basis for all brain death guidelines.

5. BRAIN DEATH Uniform Determination of Death Act(UDDA) 1981 An individual who has sustained either Irreversible cessation of circulatory and respiratory functions, or Irreversible cessation of all functions of the entire brain, including the brain stem

6. American Academy of Neurology(1995) Published practice parameter to describe medical standards for the determination of brain death essential findings necessary to confirm irreversible cessation of all functions of the entire brain, including brain stem.

7. Pathophysiology of brain death

8. cerebral hypoxia, traumatic head injury, subarachnoid or intracerebral hemorrhage and bacterial meningitis. primary brainstem pathology or conditions causing cerebral edema. E.g DKA, HE, Water intoxication, eclampsia, Aspirin overdose, Malignant hypertension. irreversible rise in ICP increased ICP compresses the entire brain including the brainstem total brain infract

9. Rise in ICP ➡️ massive release of catecholamine stores ➡️ increased systemic arterial blood pressure, sometimes associated with reflex bradycardia, bradyarrhythmia, or both. Decreased cardiac output, pulmonary edema, and cardiac ischemia may be encountered.

10. Once total brain infarction has occurred ➡️ catecholamines depletion ➡️ loss of sympathetic output ➡️ peripheral vasodilation and systemic hypotension. Other common problems after brain death include diabetes insipidus, hypothermia, metabolic acidosis and cardiac arrest .

11. Physiological change after brain death Neurological Changes:- temperature regulation center in hypothalamus is impaired. patient becomes poikilothermic and hypothermic. Cardiovascular Changes:- Raised ICP may cause rise in catecholamines, leading to 'sympathetic storm', responsible for the increased blood pressure, cardiac dysrhythmias, ECG abnormalities, myocardial damage and renal impairment.

12. Pulmonary Changes:- During the sympathetic storm, rapid rise in left atrial pressure exceeds pulmonary artery pressure may result in capillary disruption, protein-rich pulmonary edema and interstitial hemorrhage. Endocrine Changes:- Neurogenic diabetes insipidus. Electrolyte disturbances: hypernatremia, hypokalemia, hypocalcaemia, hypophosphatemia and hypomagnesemia occur rapidly without treatment.

13. Interrupt hypothalamic-pituitary axis leading to serum hormone depletion. Hypothyroidism & adrenal insufficiency Fall in insulin levels Leads to systemic hyperglycemia with severe osmotic diuresis and profound hypovolemia.

14. Hematological:- Release of fibrinolytic agents and plasminogen activators into the circulation can cause coagulation defects, DIC.

15. Incidence of pathophysiological changes following brain death: - Hypotension 81% - Diabetes Insipidus 65% - DIC 28% - Cardiac arrhythmias 25% - Pulmonary edema 18% - Metabolic acidosis 11%

16. DIAGNOSTIC CRITERIA Two examinations, separated by at least 6 hours Done by 2 or 3 physicians independent of the transplant team At least one physician should be a specialist in neurology/neurosurgery/ neuroanesthesia

17. Prerequisites Inclusion criteria Exclusion criteria Demonstration of clinical signs of brain death Ancillary tests for brain death

18. PREREQUISITES: Inclusion criteria patient must be totally unresponsive and ventilator dependent. Irreversible cause of brain death of known etiology: evidence of brain injury-clinical, radiological.

19. PREREQUISITES:     Exclusion criteria No drug intoxication or poisoning Recent administration or continued presence of neuromuscular blockers. Guillain-Barré or the locked-in syndrome

20. PREREQUISITES: Exclusion criteria   Metabolic or endocrine factors: Hypothermia(<32ºC) Hypoglycemia/ Hyperglycemia/ ketoacidosis Hepatic failure/ Reye’s syndrome Uremia Hyponatremia Hypercalcemia Panhypopituitarism Myxedema Adrenal cortical failure

21. Demonstration of clinical signs of brain death Coma or unresponsiveness GCS of 3 No cerebral motor response in all extremities or facial muscles to painful nail-bed pressure or supraorbital ridge pressure.

22. 2. Absence of brainstem reflexes   Pupils    No response to bright light     Size: midposition (4 mm) to dilated (9 mm)   Facial sensation and facial motor response No corneal reflex to touch with a cotton swab   No jaw reflex    No grimacing to deep pressure on nail bed, supraorbital ridge, or temporomandibular joint     

23. C . Pharyngeal(gag) and tracheal(cough) reflexes    No response after stimulation of the posterior pharynx with tongue blade No cough response to tracheal suctioning D. Ocular movement    No oculocephalic reflex (testing only when no fracture or instability of the cervical spine is apparent) No occulo -vestibular reflex

24. Oculocephalic reflex

25. Oculo-Vestibular Reflex “ Caloric Testing”

26. 3. Apnea test: considered as most important test. main components Prevent hypoxemia Ensure an adequate PaCO 2 Observe that spontaneous respiratory effort is absent

27. Prerequisites Normothermia (Core temperature>35ºC or 97ºF). Normotension (SBP >=100 mm Hg or MAP>60 mm of Hg)  Euvolemia.    Eucapnia(PaCO2 35-45 mm Hg) no prior evidence of CO2 retention

28. Procedure Adjust vasopressors to a systolic blood pressure 100 mm Hg Pre-oxygenate with 100% oxygen for at least 10 minutes to PaO2 of 200 mm Hg. Reduce ventilation frequency to 10 breath to eucapnia Reduce PEEP to 5 cm H2O. If oxygen saturation remains 95%, obtain baseline ABG

29. Disconnect the patient from the ventilator. Deliver 100% O 2 4-6 L/m via a insufflation catheter inserted at the level of carina. 6 L/m by T piece attached to the ETT tube Look closely for the respiratory effort for 8-10 mins. If no respiratory drive observed after 8 min draw blood for blood gas analysis and reconnect ventilator

30. Apnea test- Positive respiratory movements- absent and arterial PaCO 2  is ≥ 60 mm Hg or  20 mm Hg increase in PaCO 2  over a baseline Apnea test- Indeterminate Respiratory movement-absent PaCO2<60 mm Hg. Apnea test- Negative respiratory movements-present.

31. Criteria to abort test Presence of respiratory movements systolic blood pressure becomes < 90 mm Hg. significant oxygen desaturation. New cardiac arrhythmias.

32. Factors that can interfere the clinical diagnosis of brain death Severe facial or cervical spine trauma Preexisting pupillary abnormalities Toxic levels of any sedative drugs, aminoglycosides, TCA, anticholinergics, antiepileptic drugs, chemotherapeutic agents, or neuromuscular blocking agents Sleep apnea or severe pulmonary disease resulting in chronic retention of CO 2

33. Ancillary Testing Recommended when cause of coma is not known Apnea testing inconclusive or aborted confounding clinical conditions limit the clinical examination . Skull or cervical injuries Cardiovascular instability To reassure family member and medical staff

34. Choice of test Ideal ancillary test should meet all of the following criteria: no false positives results sufficient on its own to establish is or is not present. not susceptible to ”confounders” such as drug effect or metabolic disturbances. standardized in technology, technique and classification of results available, safe and readily applied in all medical centers with ICUs,

35. Ancillary test for brain death Electroencephalography Cerebral Angiography Nuclear brain scanning Transcranial doppler ultrasonography CT Scan MRI/ MRI-angiography SSEP

36. Spinal reflex Movements originating from the spinal cord or peripheral nerve. Common(33-75%), triggered by tactile stimuli or spontaneously. Examples include: Undulating toe flexion response- planter tactile stimulation Triple flexion response with flexion at the hip, knee and ankle. Pronator extensor reflex- head turning. Facial myokymia, repetitive twitching of facial muscles. Lazarus sign truncal movements including asymmetrical opisthotonic posturing of the trunk and preservation of superficial and deep abdominal reflexes.

37. Brain death in child Most commonly occurs as a result of trauma and anoxic encephalopathy. Anatomic neurodevelopment continues by 2 years of age or beyond the first dacade of life. Presence of open fontanelles and open sutures makes the skull an expandable chamber. ICP may not exceed MAP and cerebral blood flow continues.

38. History : determination of the proximate cause of coma to ensure absence of remediable or reversible conditions. 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.

39. 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. Examination results should remain consistent with brain death throughout the observation and testing period.

40. Exclusion of preterm infants younger than 37 weeks of gestational age. Observational period: 24 hours: neonates (37 weeks of gestation to term infants 30 days of age) 12 hours: Infants and children (>30 days to 18 years)

41. Management of organ Donors Consent from family for organ donation can be obtained after the diagnosis of brain death is established. primary goal: preserve organ viability. best achieved by ensuring oxygenation and ventilation, maintaining homodynamic stability, and correcting electrolyte problems and acid-base abnormalities.

42. “Rules of 100’s” - Maintain SBP > 100 mmHg - HR < 100 BPM - UOP > 100 ml/hr - PaO2 > 100 mmHg

43. Methylprednisolone 15mg/kg bolus Triiodothyronine (T3) 4mcg bolus, 3mcg/hr. Arginine vasopressin 1 unit bolus, 0.5-4 units/hr Insulin infusion 1 unit/ hr minimum

44. Donor organ preservation ( cold ischemic time): Heart & Lungs 3-4 hrs Pancreas 6 hrs Liver 8 hrs Kidneys 36 hrs

45. Conditions Distinct From Brain Death Deep coma Persistent Vegetative State Minimally Responsive State Locked in syndrome

46. Deep coma Non-responsive to external stimuli Dysfunctional cerebrum Brain stem intact  spontaneous breathing and heartbeat

47. Vegetative state Appears to be wakeful with cycles of eyes closure and opening. Normal Sleep-Wake Cycles No Response to Environmental Stimuli Can ventilate themselves Lack of higher brain function to control emotions, consciousness and cognition. Hypoxic brain injury.

48. Minimally Responsive State Unlike vegetative state, patients with MCS have partial preservation of conscious awareness. Diffuse or Multi-Focal Brain Injury

49. Locked in syndrome Lesion to the brainstem, most frequently an ischemic pontine lesion. complete disruption of the motor pathways face, trunk and limb movements, including breathing, swallowing and phonation. Consciousness and cortical functions are preserved .

50. Brain death verification chart FOR THE DIAGNOSIS AND CONFIRMATION OF DEATH Academy of Medical Royal Colleges 2008

51. References Miller’s Anesthesia, 8 th Edition ICU book. American Academy of Neurology guidelines for brain death determination. Textbook of Neuroanaesthesia and Critical Care.

52. Thank you