Maintenance of a potential brain dead donor

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Maintenance of a potential brain dead donor

• Dr. Prashant Kumar

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Declaration of brain death

• Date
• Time
• Detailed documentation of Clinical Exam
  including specifics of Apnea Testing
• Physician signature

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Perioperative Management

• Aim
• Optimizing organ function for subsequent
  transplantation (not cerebral perfusion)
• Providing hemodynamic stabilization
• Support of body homeostasis
• Maintenance of adequate cellular oxygenation and
  donor organ health
• Saving the patient till organ retrieval

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Effective Donor Management

• Revision of existing orders or placement of new
  medical orders is intended to
• D/C medications no longer needed or appropriate
  (e.g., anticonvulsants, mannitol, sedatives,
  antipyretics)
• Continue needed medications, or therapy (e.g.,
  vasoactive drug infusions, IV fluids and vent
  settings)
• Create call orders that inform bedside
  personnel of the goals for physiologic parameters
  and alert OPC of changes in donor status.

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Incidence of pathophysiological complications
following Brain Death

• - Hypotension 81
• - Diabetes Insipidus 65
• - Coagulopathy/ DIC 28
• - Cardiac arrhythmias 25
• - Pulmonary edema 18
• - Metabolic acidosis 11

Physiologic changes During Brain Stem Death
Lessons for Management of the Organ Donor. The
Journal of Heart Lung Transplantation Sept
2004 (suppl)
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Maintenance Therapy Endpoints in the Brain-Dead
Organ Donor
Variable Therapeutic endpoint
Systolic blood pressure 100120 mm Hg or mean arterial pressure 60 mm Hg
Central venous pressure 810 mm Hg
Urine output 100300 mL/h
Core temperature gt35C
Partial arterial oxygen pressure 80100 mm Hg
Systemic arterial oxygen saturation 95
pH 7.377.45
Hemoglobin 1012 g/d
Hematocrit 3035
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What to expect after brain death
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Pathophysiology

• Loss of brain stem function results in systemic
  physiologic instability
• Loss of vasomotor control leads to a hyperdynamic
  state
• Cardiac arrhythmias
• Loss of respiratory function
• Loss of temperature regulation ? Hypothermia
• Hormonal imbalance ? DI, hypothyroidism

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Brain edema spreads
10

• Liquefied respirator brain

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Cardiovascular Management

• Aim
• CVP 6-10mmHg
• HRlt120bpm
• MAP 60-80mmHg

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Autonomic/Sympathetic Storm
?? ICP
Worsening Brainstem ischemia

• Tachycardia
• Elevated C.O.
• Vasoconstriction
• Systemic Hypertension
• Arrhythmia

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Cardiovascular System

• Rules of 100s
• - Maintain SBP gt 100mmHG
• - Hb gt 100 g.L-1
• - UOP gt 100ml/hr
• - PaO2 gt 100mmHg

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Clinical Concern Possible etiology Management Strategies
Hypotension (MAP lt60mmHg) 1. Hypovolaemia- blood loss, polyuria (diabetes insipidus DI), diuretics, hyperglycaemia or through therapeutic dehydration to ?ICP 2. Vasoplegia- absent central vasomotor control, after re warming 1. Replace volume- Aim CVP 6-10mmHg 2. Blood transfusion Aim for Hb gt70g/L if stable Aim for Hb gt90g/L if unstable 3. Vasopressors- Noradrenaline is the most commonly administered vasopressor. If Noradrenaline (NA) is gt0.2mcg/kg/min then vasopressin (1-2.4Units/h) may allow reduction of NA requirements.
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Clinical Concern Possible etiology Management Strategies
Hypertension MAPgt110mmHg Normally associated with herniation and is self-terminating Short acting beta blocker (esmolol 0.1-3mcg/kg/min) Vasodilator (sodium nitroprusside 1-5mcg/kg/min)
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Clinical Concern Possible etiology Management Strategies
Arrhythmias Supraventricular and Ventricular Tachycardia Bradycardia Normalise physiology- Maintain normal serum electrolytes (optimize K, Mg Ca2), optimise fluid status, normalise temperature. Standard arrhythmia management should be initiated (amioderone, cardioversion) Consider Adrenaline, Isoprenaline or pacing. Usually resistant to atropine or glycopyrrolate.
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Respiratory Management optimise tissue oxygen,
prevent lung injury and infection

• Aim
• pH 7.35-7.45
• pCO2 35-45mmHg
• pO2gt80mmHg
• Sats gt95

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Neurogenic Pulmonary Edema
01
Sympathetic Storm-increased capillary hydrostatic
pressure
02
Increased pulmonary capillary permeability
03
Inflammatory mechanisms
04
Other mechanisms - cell apoptosis
Šedý J, Kuneš J, Zicha J. Pathogenetic Mechanisms
of Neurogenic Pulmonary Edema. J Neurotrauma
2015 321135
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Impaired Gas Exchange

• Monitor ABGs q2h or as requested by organ
  procurement organization (OPO)
• HOB up 30o
• Prefer colloids to reduce use of crystalloid for
  resuscitation
• Increase ET cuff pressure immediately after BD
  declaration
• Aggressive pulmonary toilet (Keep suctioning
  turning q2h)
• CXR (Radiologist to provide measurements
  interpretation)
• OPO may request bronchoscopy
• CT of chest requested in some cases

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Correct Impaired Gas Exchange and Maximize
Oxygenation!

• Most organ donors are referred with
• Chest trauma
• Aspiration
• Long Hospitalization with bed rest resulting in
  atelectasis or ventilator associated pneumonia
• Impending Neurogenic Pulmonary Edema
• Brain Death contributes to and complicates all of
  these conditions

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Impaired Gas Exchange Goals

• Goals are to maintain health of lungs for
  transplant while optimizing oxygen delivery to
  other transplantable organs
• Avoid over-hydration
• Ventilatory strategies aimed to protect the lung
• Avoid oxygen toxicity by limiting Fi02 to achieve
  a Pa02 100mmHg PIP lt 30mmHg. For lung donors
  prefer PEEP to deal with hypoxia in non lung
  donors prefer increasing FiO2

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Clinical Concern Possible etiology Management Strategies
Hypoxaemia De-recruitment of lungs due to no cough or respiratory drive Orthostatic pneumonia and sputum retention Neurogenic pulmonary oedema Aspiration Acute lung injury Trauma Optimise mechanical ventilation Lung recruitment Optimisation of fluid management General Management
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Endocrine and Metabolic

• Aim for normal range
• Temperature 36-37.50C
• Electrolytes (Ca, Mg, KPO4, K, Na)
• Blood sugar 5-10mmol/L
• Urine Output 0.5-1ml/kg/h

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Failure of the Hypothalamus
Loss of ability to shiver
Hyperthermia
Pituitary Failure
Vasomotor failure and arrhythmias
Hypothermia
Nair-Collins M, Northrup J, Olcese J.
Hypothalamic-Pituitary Function in Brain Death A
Review. J Intensive Care Med. 2016
Jan31(1)41-50.
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Normal Pituitary Gland

• Controlled by the hypothalamus
• Releases ADH to conserve water
• Stimulates the release of thyroid hormone

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Pituitary Failure in brain death

• Anterior pituitary is supplied by inferior
  hypophyseal artery a branch of extradural
  internal carotid artery which is relatively
  preserved in brain death

• Hypothalamus and posterior pituitary failure
  leads to development of diabetes insipidus in
  upto 80 patients

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• May be responsible for impairment in myocardial
  cell metabolism and contractility which leads to
  myocardial dysfunction
• Severe dysfunction may lead to extreme
  hypotension and loss of organs for transplant
• ACTH levels have been variable in brain dead
  patients amongst different studies. Supplemented
  steroids have been shown to improve lung function
  in the recipients.
• Administration of Thyroid hormones T3 T4 have
  been debated in the past. Many studies have shown
  improved metabolic parameters and organ function
  on hormone supplementation.

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Clinical Concern Possible etiology Management Strategies
Hypothermia May cause an increased risk of arrhythmias, coagulopathy etc. Hypothalamic / pituitary malfunction Ensure temperature is maintained gt36C Early use of warming blankets, fluid warmers for large fluid volumes and humidification devices.  
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Central Diabetes Insipidus
Goal is UOP 1-3 ml/kg/hr Rule of thumb 500 ml
UOP per hour x 2 hours is DI
Treatment is aimed at correcting hypovolemia
hypernatremia and hypokalemia
Polyuria, Hypovolemia, Hypotension, and
Hypernatremia
NORD (National Organization for Rare Disorders).
2015. Archived from the original on 21 February
2017. Retrieved 28 May 2017.
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Vasopressin/ Desmospressin
4 Fluid Replacement Low sodium concentration
fluid such as 5D For fluid resuscitation consider
0.45 saline or Hartmans solution
UO gt3mls/kg for 2 consecutive hours
Send paired urine and plasma electrolytes and
osmolality
3
2
1
Vasopressin 2.4units/h (maximum ) or
Desmospressin (DDAVP) 2-4 micrograms every 2-6hrs
Nakagawa K, Tang JF. Physiologic response of
human brain death and the use of vasopressin for
successful organ transplantation. J Clin Anesth.
2011 Mar 23(2)145-8
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Clinical Concern Possible etiology Management Strategies
Hypernatremia (Nagt155mol/L) Adverse effect on the outcome of Liver recipients Hypokalemia Calcium, Magnesium, and Phosphorus As a consequence of DI or intracranial hypertension management.   Loss Remove all sources of sodium in IV solutions Review if DI contributory and follow DI management Replace
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Clinical Concern Possible etiology Management Strategies
Hyperglycaemia May be pre-existing IDDM/ NIDDM Insulin resistance due to brain death As a consequence of high volumes of 5 dextrose solution Insulin as per the unit policy should be administered to achieve plasma glucose levels 6 -10mmol/L
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Clinical Concern Possible etiology Management Strategies
Coagulopathy/ Disseminated Intravascular Coagulation (DIC) Passage of necrotic brain tissue into the circulation Hypothermia Release of catecholamines Hemodilution as a result of fluid resuscitation May require early organ recovery Replacement of clotting factors, platelets and PRBC is considered only if the bleeding is likely to effect organ recovery Target platelet count 50,000/cmm Target Hb- 10gm/dl
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Clinical Concern Possible etiology Management Strategies
Anemia Loss Critical illness Iatrogenic Target Hb- 7g/L in physiologically stable ? 10 g/L in unstable patients with significant inotropic support Transfuse 2 units PRBCs immediately Reassess after completion of 2nd unit and repeat infusion of 2 units if Hct remains below 30 Assess for source of blood loss and treat accordingly
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Clinical Concern Possible etiology Management Strategies
Infection Preexisting Acquired in the healthcare setting Prophylactic use of antibiotics do not have value Infection should be treated accordingly as in other ICU patients If culture reports are available- treat accordingly
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Hormonal therapy
Steroids administration shown to improve lung
function
Lack of agreement regarding benefits
Consider in cardiac dysfunction
Consider in Haemodynamically unstable patients
Donor hyperglycemia is a risk factor for poor
graft survival
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Normal Thyroid Gland

• Produces hormones that increase the metabolic
  rate and sensitivity of the cardiovascular system
• Levothyroxine (T4)
• Triiodothyronine (T3)

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Thyroid Failure

• Leads to
• Cardiac instability
• Labile blood pressure
• Potential coagulation problems

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Bolus Drug Dose
Bolus Methylprednisolone 15 mg/kg every 24 hrs
Bolus Triiodothyronine (T3) 20mcg
Bolus Regular Insulin 20 Units
Bolus D50W 50 ml
Infusion Triiodothyronine (T3) 4mcg/hr
Infusion Insulin Titrated dose to keep blood glucose upto 180 mg/dl
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Clinical Concern Possible etiology Management Strategies
Coagulopathy Tissue thromboplastin and plasminogen released from injured brain Hypothermia catecholamines Replacement of clotting factors, platelets and PRBC is only considered if the bleeding is likely to effect organ recovery Target platelet count 50,000/cmm Target Hb- 10gm/dl
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Organ Donor Management(in a nutshell)

• Hypertension ? Hypotension
• Excessive Urinary Output
• Impaired Gas Exchange
• Electrolyte Imbalances
• Hypothermia

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MONITORING, INVESTIGATION AND GENERAL CARE QUICK GUIDE MONITORING, INVESTIGATION AND GENERAL CARE QUICK GUIDE MONITORING, INVESTIGATION AND GENERAL CARE QUICK GUIDE

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Organ Preservation Time
Pancreas 12-18 hours
Heart 4-6 hours
Kidneys 72 hours
Lungs 4-6 hours
Small Intestines 4-6 hours
In Hours
Liver 12 hours
Edgardo E. et al. Organ Preservation Current
Concepts and New Strategies for the Next Decade.
Transfus Med Hemother. 2011 Apr 38(2) 125142.
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