1.6 Brainstem Death Flashcards
What are the physiological changes seen after brainstem death?
The reasons for the altered pathophysiology of the heart-beating brainstem
dead person can be due to
- Primary pathology suffered by the patient
- Complications of ITU treatment
(mainly the resuscitation of the injured brain) - Specific physiological changes and a
systemic inflammatory response caused by the brainstem death
- Cardiovascular changes
- other changes
cardiovascular changes
Initial changes:
The first change to occur is the increase in intracranial pressure (ICP).
Mean arterial pressure increases to maintain cerebral perfusion in parallel with the increasing ICP.
Later brain herniation causes ischaemic changes in brainstem
and a hyper-adrenergic state.
This in turn increases both pulmonary and systemic vascular resistance.
Episodes of ‘sympathetic storm’ of variable duration occur
with tachycardia, vasoconstriction, and hypertension,
which can lead to myocardial ischaemia.
Hypertension and bradycardia (Cushing’s reflex)
occur in some patients secondary to reflex baroreceptor activation
and activation of the parasympathetic nervous system
Subsequent changes:
Cerebral herniation leads to loss of spinal cord sympathetic activity,
reducing vasomotor tone,
preload, and
cardiac output.
This is more consistent and called
‘syndrome with marked vasodilation and relative hypovolaemia’.
Myocardial perfusion can be affected due to low aortic diastolic pressure
Other changes
- Ischaemia to pituitary causes diabetes insipidus,
fluid and electrolyte loss,
leading to further cardiovascular instability - Reduced metabolic rate,
loss of hypothalamic control and
vasodilatation results in heat loss and hypothermia
- Reduced metabolic rate,
- Coagulation abnormalities can occur
due to original pathology and
release of coagulation activators
from the necrotic brain tissue and
hypothermia
- Coagulation abnormalities can occur
- Posterior pituitary function is lost,
but anterior pituitary function is preserved.
There is reduction in T3 levels with normal TSH levels
- Posterior pituitary function is lost,
What are the contraindications of organ donation?
In order to ensure that donations are as safe as possible, the donor’s
medical and behavioural history is reviewed to reduce the risk of transmitting
disease to a patient.
There are many absolute contraindications for various tissue donations,
but there are only two absolute contraindications for organ
donation along with organ specific contraindications.
Absolute contraindications for organ donation
- Known or suspected new variant CJD
and other neurodegenerative diseases
- Known or suspected new variant CJD
- Known HIV disease, not HIV infection alone
Relative contraindications for organ donation
organ and tissue specific contraindications
Relative contraindications for organ donation
- Disseminated malignancy
- Treated malignancy within 3 years (except non-melanoma skin cancer)
- Age >70 years
- Known active TB
- Untreated bacterial sepsis
Lungs
- Donor age >65
- Previous intra-thoracic malignancy
- Significant, chronic destructive or suppurative lung disease
- Chest X-ray evidence of major pulmonary consolidation
Liver
- Acute hepatitis (AST >1000 IU/L)
- Cirrhosis
- Portal vein thrombosis
Kidney
- Chronic kidney disease (CKD stage 3B and below; eGFR <45)
- Long-term dialysis
- Renal malignancy
- Previous kidney transplant (> 6 months previously)
Pancreas
Pancreas
- Insulin-dependent diabetes
(excluding ICU-associated insulin requirement)
- Insulin-dependent diabetes
- History of pancreatic malignancy
Heart
Heart
- Age >65
- Documented coronary artery disease
- Median sternotomy for cardiac surgery
- LVEF ≤ 30% on more than one occasion
- Massive inotropic or vasopressor support
You have confirmed brainstem death. How would you proceed
with organ donation?
1.Referral:
Early referral and communication with Donor Team
(Specialist Nurse for Organ Donation – SN-OD)
should be done once decision is made
to test for brainstem death.
Each acute trust in the UK has a nominated
SN-oD. If out of hours, the on-call SN-oD can be contacted.
- Patient/relatives:
once notified, the SN-oD will collect all the information
about the patient and his or her relatives. The specialist nurse will do a
detailed assessment of the patient for suitability of organ donation. Decision
is made on this assessment and after considering factors such as coroner
and relatives’ views.
- Transplant centre: A check on organ donation is then made by contacting
the NHS Blood and Transplant Duty office. - ITU: once decision is made, optimal organ support is continued in the ITU
and specific therapies are initiated to enhance the likelihood of successful
transplantation.
What do you do to preserve organ function while waiting for organ
retrieval
General care
Care should always take place in critical care environment.
once the brain death had been confirmed,
the care is mainly organ centred rather than
patient centred, as patient is legally dead.
Hence, in the brain-dead donor,
it is appropriate to insert new lines for invasive monitoring
if indicated for organ optimisation.
Continue all the basic critical care management
including enteral feeding,
essential drugs and
antimicrobial therapy,
correction of electrolytes,
glucose control with insulin,
prevention of hypothermia,
and blood product transfusion
to correct significant anaemia
and coagulopathy.
Organ specific management
Organ specific management
- Cardiovascular system:
Restoration of circulating volume without overload is essential.
Short-acting drugs are used during the periods of
Cushing’s reflux and sympathetic storm
such as esmolol, GTN, and sodium nitroprusside infusions.
Vasopressin is preferred to noradrenaline as this treats diabetes insipidus
and minimises catecholamine requirements.
T3 replacement can improve cardiac function.
Haemodynamic targets include
HR of 60–120/min,
MAP of > 70 but < 95 mmHg,
CVP of 10–15 mmHg,
cardiac index of > 2.1 L/min/m2,
and mixed venous saturation > 60%.
Respiratory system:
Methyl prednisolone 15 mg/kg given intravenously
at the earliest opportunity as this is proven to
reduce extra pulmonary lung water.
Use lung protective ventilation with low tidal volumes of 6–8 mL/kg,
inspiratory pressures limited to < 30 cmsH2o,
use of PEEP and recruitment manoeuvres on regular intervals..
Fio2 is adjusted to maintain Spo2 of > 90% or a Pao2 > 8.0 kPa.
Endocrine management:
T3 supplementation is part of many protocols
but it is beneficial only in patients with
poor cardiac performance after
fluid loading and vasopressin.
Desmopressin is also used if diabetes insipidus persisted.
Insulin may be useful as anti-inflammatory
and reduces cytokines in addition to glycaemic control.
