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BRAIN DEATH IN CHILDREN AND CARE OF THE POTENTIAL ORGAN DONOR

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Assistant Professor of Pediatrics. University of Minnesota ... of brain death by the Ad Hoc Committee of the Harvard Medical School in 1968 ... – PowerPoint PPT presentation

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Title: BRAIN DEATH IN CHILDREN AND CARE OF THE POTENTIAL ORGAN DONOR


1
BRAIN DEATH IN CHILDRENAND CARE OF THE POTENTIAL
ORGAN DONOR
  • Andrew W. Kiragu, MD, FAAP
  • Medical Director, PICU
  • Hennepin County Medical Center
  • Assistant Professor of Pediatrics
  • University of Minnesota

2
  • Think of your child then, not as dead, but as
    living not as a flower that has withered, but as
    one that is transplanted, and touched by a divine
    hand, is blooming in richer colors and sweeter
    shades .
  • Richard Hooker

3
OBJECTIVES OF THIS PRESENTATION
  • To discuss a representative patient case report
  • To briefly discuss brain death in pediatric
    patients.
  • To discuss the pathophysiologic changes that
    occur as a result of brain death.
  • To discuss the ICU management of these
    physiologic derangements.
  • To discuss some of the other challenges faced in
    the management of the potential organ donor.

4
CASE REPORT
5
CASE REPORT
  • EP is an 8 yo boy admitted to the PICU for
    management after he was struck by a van while
    riding his bicycle.
  • Sustained a severe brain injury with an initial
    GCS at the scene of 3.
  • Patient noted to have agonal respirations and
    intubated at the scene.
  • Brought to ED for initial evaluation and
    management. Local OPO contacted.

6
CASE REPORT
  • The patient sustained significant thoracic trauma
    with initial radiographs showing multiple rib
    fractures and bilateral pulmonary contusions as
    well as fractures of his pelvis and right tibia
  • On exam the patient is hypotensive and
    tachycardic with BP 80/30 and HR 140. His exam is
    significant for a laceration and swelling over
    the right temporal region of his skull with no
    noted step-off.
  • Pupils are fixed and dilated. ETT in place with
    notable bloody aspirate. Patient has no cough or
    gag reflexes with suctioning.

7
CASE REPORT
  • Chest exam shows significant bruising and coarse
    rhonchi bilaterally
  • Cardiac exam significant for tachycardia and a
    flow murmur
  • Abdominal exam shows significant ecchymosis over
    LUQ. Abdominal CT shows Grade 2 splenic
    laceration. RLE splint placed.
  • Neurologic exam remarkable for no response to
    noxious stimulus. Absent reflexes. Head CT shows
    diffuse cerebral edema and evidence for severe
    diffuse axonal injury.

8
CASE REPORT
  • The patient is sent up to the PICU for ongoing
    management
  • Ventriculostomy placed and initial ICP is 40. No
    significant response to hypertonic saline and
    hyperventilation
  • The patient receives significant fluid
    resuscitation but remains hypotensive and is
    therefore started on inotropic support
  • Also started on insulin drip for glycemic control
    and triiodothyronine drip given significant
    inotrope requirement

9
CASE REPORT
  • The patient is subsequently noted to put out
    significant amounts of dilute urine and lab
    evaluation consistent with DI. Vasopressin drip
    initiated.
  • The patients clinical status/exam concerning for
    brain death.
  • Brain death examination and cerebral blood flow
    study confirm the clinical suspicion.
  • These findings discussed with the family who
    request information about organ donation.

10
INTRODUCTION
OPTN Data 9/18/08
11
INTRODUCTION
OPTN Data 8/28/08
12
INTRODUCTION
  • Medicine and society continue to struggle with
    the definition of death.
  • The progression of life-sustaining ICU therapies
    challenge our concepts of death.
  • Questions about when a disease process is
    irreversible, when additional treatment is
    ineffective or when death has occurred preoccupy
    us and are independent of and galvanized by the
    practice of organ donation.

13
INTRODUCTION
  • Historically, death identified with cessation of
    pulse and respiratory effort since these findings
    herald the dissolution of the individual.
  • In 1950s and 1960s with advent of ICUs, a
    group of patients began to emerge who had
    persistent pulse and circulation in the absence
    of detectable neurologic function
  • The concept of death as the absence of clinical
    brain function began to develop

14
INTRODUCTION
  • Advances in transplantation technology
  • Brain dead patients a potential source of
    organs but during those earlier years fraught
    with legal and ethical difficulties
  • Need for a medical and legal definition of brain
    death
  • First certification of brain death by the Ad Hoc
    Committee of the Harvard Medical School in 1968
  • In the 1990s the Uniform Determination of Death
    Act legally recognized that death could be
    defined using neurological criteria

15
DETERMINATION OF BRAIN DEATH
  • Begins with formal neurological examination
  • AAN has set forth practice parameters for
    diagnosis of brain death
  • AAP guidelines developed to help in the diagnosis
    of brain death in pediatric patients. These
    guidelines for the most part similar to adult
    guidelines except for timelines
  • Radiographic support for intracranial catastrophe

16
DETERMINATION OF BRAIN DEATH
  • Based upon the absence of brainstem and
    hemispheric function
  • Patients in a persistent vegetative state are not
    brain dead
  • It is not necessary to diagnose brain death in
    order to discontinue extraordinary measures of
    support or to tell the parents the childs
    outlook is hopeless
  • Once brain death criteria are met, the patient is
    legally dead

17
DETERMINATION OF BRAIN DEATH
  • Exclusion and correction of conditions that
    confound diagnosis of brain death (electrolyte
    abnormalities, intoxication, hypothermia, drugs)
  • The child should not have received recent doses
    of sedative hypnotic or neuromuscular blocking
    agents
  • The child must not be significantly hypotensive
    for age
  • Neurologic exam then proceeds with aim of
    determining three principle findings in brain
    death coma, absence of brainstem reflexes and
    apnea (coma and apnea must coexist)

18
DETERMINATION OF BRAIN DEATH
  • Absence of brainstem function as defined by
  • Mid-position or fully dilated pupils that do not
    respond to light
  • Absence of spontaneous eye movements induced by
    occulocephalic or occulovestibular (cold
    calorics) testing
  • Absence of bulbar function including facial and
    oropharyngeal muscles (Corneal, cough, gag, and
    rooting reflexes are absent)
  • Respiratory movements are absent off ventilator
    support
  • Flaccid tone and absence of spontaneous or
    induced movements (excluding spinal cord events
    such as reflex withdrawal or spinal myoclonus)

19
DETERMINATION OF BRAIN DEATH
  • The recommended observation period depends on the
    age of the patient and the ancillary testing
    utilized
  • 7 days to 2 months Two examinations and EEGs
    separated by at least 48 hours
  • 2 months to one year of age Two examinations
    and EEGs separated by at least 24 hours. A
    repeat EEG is not necessary if a cerebral
    radionuclide scan or cerebral angiography
    demonstrates no flow or visualization of the
    cerebral arteries

20
DETERMINATION OF BRAIN DEATH
  • Older than one year of age When an irreversible
    cause exists, ancillary testing is not required
    and an observation period of 12 hours is
    recommended.
  • The observation period may be decreased if the
    EEG demonstrates electrocerebral silence or the
    cerebral radionuclide or cerebral angiography
    study demonstrates no flow or visualization of
    the cerebral vessels.

21
CONFIRMATORY TESTING
  • Not required in adults or children older than 1
    year. However, often helpful in providing an
    additional objective finding
  • In situations where neurological exam cannot be
    dependably done and in children younger than 1
    year, recommended
  • Classified in two groups assessment of
    electrical activity and assessment of blood flow

22
CONFIRMATORY TESTING
  • EEG
  • Radionuclide Scans
  • Intracranial pressure monitoring
  • Somatosensory evoked responses
  • Transcranial Doppler
  • Cerebral angiography

23
ELECTROENCEPHALOGRAPHY
  • The absence of electrical activity during at
    least 30 minutes of EEG recording supports
    diagnosis of brain death.
  • Validated for adults but not pediatric patients
  • Concerns also about preservation of EEG activity
    despite a clinical exam consistent with brain
    death and absence of cerebral blood flow

24
SOMATOSENSORY EVOKED POTENTIALS
  • SEP are a measure of electrical potentials
    produced in response to stimulation of the
    sensory system
  • Stimulus typically applied to a peripheral mixed
    sensory and motor nerve e.g. median nerve and
    potential measured at downstream site along
    neural pathway
  • Bilateral absence of response to nerve
    stimulation consistent with brain death
  • SEP found useful in confirming brain death in
    children and infants.

25
CEREBRAL ANGIOGRAPHY
  • Performed by injection of contrast into aortic
    arch and looking for blood flow to carotids and
    vertebral vessels
  • When ICP exceeds MAP angiography demonstrates
    absence of blood flow beyond carotid bifurcation
  • This study not routinely performed although in
    cases where brain dead patient is in a
    barbiturate coma it can be used without the
    necessary wait for the medication to leave the
    system

26
NUCLEAR STUDIES
  • Radionuclide studies performed by measuring a
    tracer intravenously and obtaining static images
    at between 30 and 60 minutes and 2 hours
  • Absence of uptake of isotope in brain parenchyma
    is supportive of a diagnosis of brain death
  • Caution needed in the child age lt2 months.

27
NUCLEAR STUDIES
28
TRANSCRANIAL DOPPLER
  • Blood flow through MCA can detected by applying a
    Doppler US probe over the temporal bone
    bilaterally.
  • Small systolic peaks in early systole without
    diastolic flow or reverberating flow indicate
    very high vascular resistance and are supportive
    of the diagnosis of brain death
  • However 10 of patients do not have adequate
    windows for insonation and so results need to be
    interpreted cautiously.

29
MANAGEMENT OF THE BRAIN-DEAD ORGAN DONOR
  • Trauma patients represent a large percentage of
    those declared brain dead in the PICU and
    therefore a large pool of potential organ donors
  • Significantly wide gap between organs available
    for transplantation and those awaiting
    transplantation
  • Improvement in consent rates for transplantation
    from current 40-60 will help bridge this gap

30
MANAGEMENT OF THE BRAIN-DEAD ORGAN DONOR
  • ICU management of the potential organ donor plays
    a key role in maintaining and increasing current
    number of donor organs
  • Early identification of potential donors e.g.
    patients with catastrophic TBI
  • Early notification of OPO
  • Preparation of the family

31
DONOR ACCEPTANCE CRITERIA
  • Exclusion criteria include infectious diseases
    such as HIV, viral hepatitis, encephalitis,
    active CMV infections, active HSV, active TB and
    untreated syphilis
  • Disseminated malignancies also preclude organ
    donation
  • Age gt 65years generally precludes donation,
    although approximately 10 of organ donors gt65

32
PATHOPHYSIOLOGY OF BRAIN DEATH
  • The potential organ donor at high risk for
    instability due to the loss of homeostatic
    mechanisms dependent on the CNS
  • Hemodynamic instability and cardiac arrest after
    brain death accounts for the loss of as many as
    25 of potential organ donors
  • Loss of hormonal and metabolic equipoise also a
    significant contributor to the physiologic
    derangements seen in brain dead patients

33
CARDIOVASCULAR CHANGES
  • Hypertension and bradycardia preceding brain
    death characterize the Cushings response.
  • Ischemia of the vagal nucleus in the medulla
    oblongata results in uncontrolled sympathetic
    stimulation-the catecholamine storm
  • This results in systemic hypertension,
    tachycardia and possibly tissue ischemia
    including pituitary ischemia.
  • Duration and severity of this storm varies but
    within hours results in depletion of
    catecholamines with subsequent generalized
    vasodilation and hemodynamic collapse

34
CARDIOVASCULAR CHANGES
  • Total infarction of the vasomotor centers in the
    brain lead to an abrupt loss in sympathetic tone
    and hypotension
  • Myocardial injury can result in right and/or left
    ventricular dysfunction
  • This contributes to hemodynamic instability and
    organ dysfunction

35
HORMONAL CHANGES
  • Infarction of the HPA during the course of brain
    death impairs the release of ADH
  • The consequent DI results in problems with
    hemodynamic stability and fluid and electrolyte
    balance
  • Absence of DI after brain death likely due to
    preserved pituitary circulation

36
HORMONAL CHANGES
  • Notable reduction in thyroid hormone levels after
    brain death
  • Study evidence that thyroid hormone
    supplementation may reverse metabolic
    abnormalities and stabilize hemodynamic
    parameters
  • Hormonal resuscitation now a management strategy
    for UNOS

37
HORMONAL CHANGES
  • Studies regarding ACTH and cortisol levels
    inconclusive.
  • Unclear whether steroids make any significant
    improvement in organ preservation
  • Hyperglycemia with catastrophic TBI common likely
    due to increased catecholamines and relative
    insulin resistance

38
ELECTROLYTE AND ACID-BASE DISTURBANCES
  • Hypernatremia
  • Hypokalemia
  • Hypophosphatemia
  • Hypomagnesemia
  • Hypocalcemia
  • Metabolic acidosis

39
HEMATOLOGIC ABNORMALITIES
  • Coagulation abnormalities may be present due to
    previous anticoagulant use, dilution, consumption
    of factors, DIC, etc.
  • Coagulation and platelet function may also be
    affected by hypothermia
  • Blood loss from trauma may lead to anemia,
    hemodynamic instability etc
  • Questions regarding transfusion

40
IMMUNE SYSTEM PATHOPHYSIOLOGY
  • Following brain death, increased secretion of
    proinflammatory cytokines, chemokines and
    adhesion molecules resulting in a systemic
    inflammatory response
  • Cytokine release may exacerbate tissue injury
    associated with the catecholamine surge
  • Inflammatory upregulation may also impact organ
    function post transplant and increase likelihood
    of rejection
  • Effect of steroids

41
ICU MANAGEMENT OVERVIEW
  • Key to management is anticipation of
    complications, frequent reassessment and
    titration of therapies
  • Maintenance of vital organ function and
    prevention and treatment of complications are
    goals of therapy
  • Routine care of the ICU patient applies to the
    potential organ donor as well

42
ICU MANAGEMENT OVERVIEW
  • Resuscitation
  • Oxygen delivery to the tissues
  • Hydration and perfusion
  • Restoration of normal ventilation
  • Thermal regulation
  • Regulation of neuroendocrine function

43
MONITORING
  • Arterial and central venous pressure monitoring
  • If necessary, pulmonary artery catheter placement
  • Core temperature monitoring and pulse oximetry
  • Routine laboratory testing e.g. blood gases,
    electrolytes and hematologic indices monitoring

44
HEMODYNAMIC AND CARDIOVASCULAR SUPPORT
  • Hemodynamic Goals
  • Blood Pressure is age related
  • Birth to 2 months Systolic gt 60 mm Hg and lt 90
    mm Hg
  • 2 months to 1 year Systolic gt 70 mm Hg and lt
    100 mm Hg
  • 1 year -10 years Systolic gt (2 x age 70) and
    lt 40 (2 x age 70)
  • gt 10 years Systolic gt 100 mm Hg and lt 140 mm Hg

45
HEMODYNAMIC AND CARDIOVASCULAR SUPPORT
  • CVP 5-10 mm Hg
  • SvO2 saturation (mixed venous saturation) gt 70
  • SaO2 saturation gt 93
  • Normal serum lactate and base deficit
  • Urine output gt 1 ml/kg/hr and lt 10 ml/kg/hr
  • Good capillary refill and pulse quality

46
HEMODYNAMIC AND CARDIOVASCULAR SUPPORT
  • Initial period of severe HTN may be managed with
    short-acting B-blocker such as esmolol
  • Hypotension, however, poses the greatest risk to
    organ viability
  • Management of this involves use of crystalloid,
    colloid, blood products as needed.
  • Also judicious use of vasopressor agents

47
HEMODYNAMIC AND CARDIOVASCULAR SUPPORT
  • Initial vasopressor choice unclear. Many centers
    start with dopamine. Epinephrine and
    norepinephrine are also choices
  • Second-line therapy includes vasopressin
  • A levothyroxine (4-10mcg/hour) and other hormonal
    replacement an integral part of UNOS management
    protocols
  • Regimen may use a T3 ( 0.05-0.2mcg/kg/hour drip)
    instead of levothyroxine

48
RESPIRATORY SUPPORT
  • Ventilatory support should aim to provide
    adequate ventilation and oxygenation
  • Goal FiO2 is 40, PEEP 5, PIPlt 30-35 mmHg, TV of
    8-10 ml/kg (or 6-8 ml/kg if ARDS)
  • Goals are normal pH and pCO2, PaO2gt100, PaO2FiO2
    ratiogt300
  • Minimize potential for VILI and hemodynamic
    instability
  • Aggressive pulmonary toilet including VEST
    therapy
  • Bronchoscopy with BAL pre-transplant and as
    needed for refractory atelectasis etc.

49
METABOLIC EQUIPOISE
  • Fluid management to maintain euvolemia
  • Significant challenge is management of fluid
    status in face of DI
  • Use of vasopressin or DDAVP
  • Treatment of electrolyte abnormalities
    particularly hypernatremia, hypophosphatemia and
    hypomagnesemia
  • Aggressive glycemic control

50
HEMATOLOGIC INTERVENTIONS
  • Correction of consumption coagulopathy which is
    secondary to release of tissue thromboplastin
    from the injured brain. Hypothermia can worsen
    this coagulopathy
  • Therapy includes FFP, Cryoprecipitate, platelets,
    Vitamin K
  • In some situations, transfusion with packed red
    blood cells may be required
  • Prevention or correction of hypothermia which may
    exacerbate the coagulopathy

51
HORMONAL THERAPY
  • As neurologic death occurs, alteration in the
    hypothalamic-pituitary-adrenal axis (HPA axis) is
    inevitable.
  • Thus, we should be using HRT early on in the
    course of donor management. No contraindications
    in using prior to neurologic death.
  • HRT decreases the need for inotropic support in
    children and associated with increased number of
    organs donated

52
HORMONAL THERAPY
From Rosendale Transplantation, Volume
75(4).February 27, 2003.482-487
53
HORMONAL THERAPY
  • Thyroid replacement, increases cardiac output,
    increases heart rate, increases ventilation rate
    and increases basal metabolic rate
  • Thyroid hormone administration typically with T3
    (triiodothyronine) which is the active form of
    thyroid hormone.
  • T3 is converted from T4 by deiodinase. T3 is 4 X
    more active than T4
  • Dose of T3 0.05-0.15 mcg/kg/hour titrate to
    effect

54
HORMONAL THERAPY
  • Steroid production will be inhibited or lost due
    to CNS insult and loss of the HPA axis.
  • Steroids upregulate adrenergic receptors thus
    enhancing response to inotropes. May also help
    pulmonary function.
  • Protocols may use hydrocortisone (Solucortef) 1.5
    mg/kg IV Q 6 hours (max dose of 100 mg) or single
    dose of methylprednisolone 15 mg/kg in adults
    and 1 mg/kg in children (max dose of 2 gm)

55
  • Vasopressin (0.5mU/kg/hour) for management of
    diabetes insipidus. Titrate up as needed to
    maintain UOP at less than 4 ml/kg/hr
  • Insulin 0.05-0.1U/kg/hour titrated to maintain
    glucose at 80-120
  • Hourly glucose checks so as to avoid hypoglycemia

56
OTHER ASPECTS OF MANAGEMENT
  • Temperature control
  • Antibiotic therapy
  • Nutrition
  • Support of the family

57
CONSENT AND COORDINATION WITH THE OPO
  • Optimum medical management key to successful
    donation
  • However, significant impediment to organ donation
    is refusal of families to consent
  • Donor consent rates approximately 50
  • A number of factors contribute to this and
    include both patient/family factors and health
    care professional/facility factors

58
CONSENT AND COORDINATION WITH THE OPO
  • Early involvement of OPO personnel
  • Designated requestor (usually OPO coordinator)
  • Preparation of family including previous
    discussion of brain death
  • Multidisciplinary support for entire family
  • Clarification of ongoing physiologic support
    despite brain death
  • Sensitivity to familys psychological, religious
    and cultural needs

59
CHALLENGES
  • Supply of cadaveric organ donors is limited
  • Societal concerns about the definition of brain
    death
  • Cultural and familial concerns
  • The challenges of medical management of the brain
    dead organ donor
  • Legal and logistical concerns

60
CHALLENGES
  • Medical and ethical questions remain despite
    current guidelines
  • Is the brain truly dead when clinical diagnosis
    of brain death made.
  • Some patients meeting brain death criteria still
    produce AVP
  • Others may still have electrical activity on EEG
  • No neurophysiologic testing exists that can
    accurately verify the permanent cessation of
    functioning of the entire brain

61
CHALLENGES
  • In addition clinician differences in application
    of testing for determination of brain death
  • State differences in criteria for brain death
    determination also confounds the issue.
  • Difficulty in grasping concept of brain death
    given personal, ethnic and religious beliefs

62
CHALLENGES
  • Education
  • Sensitivity to cultural and family concerns
  • Concerns about child abuse victims as donors
  • Additional research and improvements in the
    medical management of the brain dead donor

63
CONCLUSIONS
  • Medicine and society continue to struggle with
    the definition of death.
  • Determination of brain death a clinical diagnosis
    although age-related issues can make confirmation
    of brain death more difficult.
  • Most organ recipients rely on the gift of an
    organ from a brain dead donor.
  • There continues to be a significant gap between
    those patients needing transplants and the number
    of available organs.

64
CONCLUSIONS
  • Recognition and proper care of the brain dead
    potential organ donor key in increasing the
    number of organs available for transplantation.
  • Significant physiologic derangements occur as a
    result of brain death and the importance of
    skilled management of these derangements cannot
    be overstated.
  • Preparation of the potential donors family also
    key to this process
  • There continue to be significant challenges in
    increasing consent rates for organ donation,
    particularly in minority populations.

65
QUESTIONS?
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