CASE 38
Incident
Clinical information prior to arrival:
• P 58.
• BP 190/105 mmHg.
• SaO2 100%.
Relevant information
▪ Aircraft: Rotary wing
▪ Local resources: General hospital, no neurosurgery or ICU on-site
▪ Retrieval options: Regional neurosurgical centre 45 minutes by air
▪ Other: Nil
Questions
38.1 Outline your plan for initial clinical management.
A quick bedside review of the patient soon after your arrival reveals the following:
• P 60.
• BP 85/55 mmHg.
• SaO2 93% on 50% inspired oxygen.
• Bilateral fixed and dilated pupils.
The neurosurgical team at the receiving hospital has now reviewed the CT scans and telephones as you arrive to say that ‘the intracranial haemorrhage is inoperable and unsurvivable’. They are concerned that the patient may have ‘already coned’.
38.2 Describe the procedures to diagnose brain death. Are you able to diagnose brain death in this case?
38.3 What are the options in this scenario?
38.4 What are the key points of discussion with the family?
Discussion
38.1 The initial clinical management plan should focus on good neurointensive care. The patient should be managed 30 degrees head-up, making sure the tracheal tube tie is not applied too tightly (impairing cerebral venous drainage). Although currently hypertensive, cerebral perfusion should be protected. A mean arterial blood pressure (MAP) of at least 80 mmHg should be targeted in the absence of invasive intracranial pressure monitoring. Vasoactive agents should be used if necessary. Hypoxia should also be aggressively defended and ventilation must be controlled to achieve normocapnoea (ETCO2 30–35 mmHg [4.0–4.5 kPa]). If there is evidence of localising neurological signs, early consideration should be given to hypertonic solutions such as mannitol or hypertonic saline. In addition, large intraparenchymal cerebral haemorrhages are highly eleptogenic and seizure prophylaxis is often advisable (intravenous phenytoin 1.5 mg/kg). Both hyperglycaemia and hypoglycaemia are potentially injurious to already damaged neuronal tissue. Therefore, aim for euglycaemia. Finally, hyperthermia should be actively managed with antipyretics and cooling. Induced hypothermia is not recommended in this scenario.
38.2 Although there is some regional variation (particularly between the United Kingdom and Australasia), the clinical diagnosis of brain death universally requires demonstration of irreversible cessation of brain function. The Australian and New Zealand Intensive Care Society statement on death and organ donation 20081 states that:
‘Determination of brain death requires that there is unresponsive coma, the absence of brainstem reflexes and the absence of respiratory centre function, in the clinical setting in which these findings are irreversible. In particular, there must be definite clinical or neuroimaging evidence of acute brain pathology (e.g. traumatic brain injury, intracranial haemorrhage, hypoxic encephalopathy) consistent with the irreversible loss of neurological function.’
It should be noted that, in Australia and New Zealand, whole brain death is required for the legal determination of brain death. This contrasts with the United Kingdom where brainstem death (even in the presence of cerebral blood flow) is the standard.
Brain death may either be determined by clinical testing (if the preconditions outlined below are met) or imaging that demonstrates the absence of intracranial blood flow (e.g. four-vessel angiography or radionuclide imaging).
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