Neuro Flashcards
What endocrine changes occur after brainstem death?
Decrease in
- ADH - which results in diabetes insipidus
- Cortisol - impairs the stress response
- Tri-iodothyronine - may contribute to cardiovascular collapse through depletion of high-energy phosphates
What are the features of diabetes insipidus?
Diuresis Hypovolvaemia Hyperosmolality Hypernatraemia Hypomagnesaemia/hypocalcaemia
What cardiovascular changes occur with brainstem death?
- Initial increase in BP in an attempt to maintain CPP. Cerebral herniation with pontine ischaemia occurs as ICP continues to rise which results in a catecholamine storm
- This adrenergic state causes marked sympathetic stimulation with intense vasoconstriction, raised SVR and tachycardia.
- The resultant increase in afterload to both ventricles causes acute myocardial ischaemia. - Cushings reflex may occur secondary to reflex baroreceptor activity and/or central midbrain activation of the parasympathetic nervous system.
- Eventual foramen magnum herniation results in loss of sympathetic tone leading to peripheral vasodilatation, hypotension and haemodynamic instability necessitating vasopressor treatment.
What respiratory changes occur in brainstem death?
- Raised pulmonary hydrostatic pressure aggravated by capillary endothelial damage results in pulmonary oedema
- Apnoea and cardiac arrest if ventilation is not supported
What endocrine changes occur in brainstem death?
- Pituitary ischaemia leads to cranial DI - resulting in fluid loss and electrolyte abnormalities.
- Hypothalamic dysfunction leads to hypothermia and functional hypothyroidism
What coagulation changes occur in brainstem death?
The catecholamine surge causes platelet dysfunction.
Damaged brain tissue impacts plasminogen activator and thromboplastin release.
How is the cardiovascular system managed in the heart beating donor?
The NHS blood and transplant group have the following cardiovascular goals to optimise the brain-dead donor.
- hr 60-120
- SBP > 10mmHg
- MAP 60-80mmHg
- PCWP 10-15mmHg
- CI > 2.1l/min/m2
- SvO2 > 60%
- CVP 6-10mmHg
- SVRI 1800-2400 dynes.sec./cm5/m2
Restoring the circulating volume should be the first priority, using CO monitoring to guide therapy.
Avoid fluid overload
Vasopressin is recommended if there is hypotension secondary to vasodilatation
If an inotrope is required then dopamine is the preferred inotrope in the NHSBT DBD care bundle.
What are the goals of ventilatory management in the brainstem dead donor?
- Lung recruitment maneouvres
- Lung protective ventilation
- Regular chest physiotherapy
- Head up tilt 30-45 degrees
- Aim pH 7.35-7.45, PaO2 > 10, PaCO2 4.5-6, SpO2 >84% for the lowest FiO2 - ideally < 0.4.
What are the principles of metabolic management in the heart beating donor?
- 15ml/kg methylpred attenuates the increase in extravascular lung water and improves oxygenation - its use is associated with increased organ retrieval and should be given asap.
- Active warming may be required to maintain temp 36-37.5
What are the principles of managing endocrine changes in the heart beating donor?
- Insulin infusion to maintain BM 4-10
- Early vasopressin may prevent the need for additional treatment for DI
- Routine T3 is no longer used as it increases risk of arrythmias.
- Hypernatraemia in the donor is associated with poor liver graft function - use water enterally or 5% dextrose to keep Na < 155.
What is cranial DI?
results from primary deficiency of anti-diuretic hormone due to pituitary ischaemia/dysfunction
How is DI treated?
Treat early based on dramatic/unexpected rise in urine output
Desmopressin (0.5-4mcg IV) is the drug of choice if DI is not effectively treated by the vasopressin used for cardiovascular management
