Delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage
A 48-year-old woman is day 3 after a WFNS grade 2, Fisher grade 3 subarachnoid haemorrhage from an anterior communicating artery aneurysm. Her GCS was 14 (E4V4M6) with no focal deficit. Blood pressure is 158/92 mmHg, heart rate 88/min, sodium 132 mmol/L and haemoglobin 11.2 g/dL. She is receiving nimodipine 60 mg every 4 hours. She is listed for endovascular coiling. Overnight she becomes drowsy with a GCS of 12 and develops right arm weakness. Blood pressure is 172/96 mmHg. Transcranial Doppler shows a left middle cerebral artery mean velocity of 165 cm/s. CT perfusion shows a small area of delayed ischaemia in the left frontal lobe. The team asks whether to induce hypertension, give more fluid and how to anaesthetise her for coiling.
1. Explain the pathophysiology of vasospasm and delayed cerebral ischaemia, and critically appraise induced hypertension and hypervolaemia.
Read the worked answer
After subarachnoid haemorrhage, erythrocyte breakdown releases oxyhaemoglobin and other blood products into the subarachnoid space. These trigger an inflammatory cascade, endothelial dysfunction, smooth muscle contraction and microthrombosis, producing angiographic vasospasm and, more importantly, delayed cerebral ischaemia. The process typically begins on day 3 and peaks between days 5 and 14. Nimodipine improves outcome even though it does not reliably reverse large-vessel spasm, which suggests that microvascular and neuroprotective effects matter. The traditional triple-H therapy has been reappraised: induced hypertension can improve cerebral perfusion pressure and collateral flow in the ischaemic penumbra, and is widely used in delayed cerebral ischaemia, but hypervolaemia has not been shown to improve outcome and can cause pulmonary oedema, hyponatraemia and worsening cerebral oedema. Haemodilution reduces oxygen-carrying capacity and is potentially harmful. The modern approach is euvolaemia, avoidance of hypotension, and induced hypertension with a vasopressor such as noradrenaline if delayed ischaemia develops, titrated to neurological improvement and with cardiac and pulmonary monitoring. I would avoid prophylactic hypervolaemia and treat the patient's volume status carefully.
2. Outline your anaesthetic management for endovascular coiling in this patient.
Read the worked answer
The priorities are to maintain cerebral perfusion pressure, avoid hypotension and prevent a further decrease in cerebral blood flow. I would place an arterial line before induction and use a balanced total intravenous anaesthetic with propofol and remifentanil, or volatile anaesthesia, while maintaining normocapnia and normothermia. I would avoid hyperventilation because hypocapnia causes cerebral vasoconstriction and can worsen ischaemia in an already compromised brain. Induction should be slow and titrated, with vasopressor support ready; I would target a mean arterial pressure at or above her baseline, particularly given the new delayed ischaemia. During coiling the neuroradiologist will heparinise the patient, so I would monitor activated clotting time and have protamine available. I would watch for aneurysm rupture, which may present as sudden hypertension and bradycardia, and for contrast reactions or catheter-related complications. After the procedure, I would ensure a smooth emergence, avoid hypertension and hypoxaemia, and arrange close neurological monitoring. If delayed ischaemia progresses, induced hypertension may need to continue into the postoperative period.
3. She develops hyponatraemia of 126 mmol/L on day 4. How do you differentiate SIADH from cerebral salt wasting and manage it?
Read the worked answer
Both conditions cause hyponatraemia with a high urine sodium and concentrated urine, but the volume status differs. In SIADH the patient is euvolaemic or slightly hypervolaemic, with low serum osmolality, high urine osmolality and no evidence of dehydration; treatment is fluid restriction and treatment of the underlying cause. In cerebral salt wasting the patient is hypovolaemic because of renal sodium wasting, with low central venous pressure, weight loss, high urine sodium and sometimes postural hypotension; treatment is volume and sodium replacement with isotonic saline. In subarachnoid haemorrhage, cerebral salt wasting is more common than SIADH. I would assess volume status carefully using fluid balance, weight, CVP, urine output and clinical signs, and review the urine sodium and osmolality. I would avoid hypotonic fluids in both conditions and correct sodium slowly, aiming for a rise of no more than 8–10 mmol/L in 24 hours to avoid osmotic demyelination. If the patient is hypovolaemic, I would give 0.9% saline; if euvolaemic, I would restrict fluids. Fludrocortisone or hypertonic saline may be required in refractory cases, with close monitoring.