Medical management

Medical management

Patients should be placed on bed rest with hourly neuro - observations. They require strict input–output monitoring and intravenous fluid replacement with normal saline initially . Oral - nimodipine at a dose of 60 /uni00A0 mg every 4 hours is administered to reduce the incidence of vasospasm and dela yed ischaemic neurological deficit. Analgesics, laxatives, antiemetics, gastric protection and compression stockings are also likely to be necessary . After resuscitation, the priorities in SAH are to: 1 prevent rebleeding by identifying and controlling any underlying lesion; 2 recognise and manage: /uni25CF neurological complications, especially vasospasm, delayed ischaemic neurological deficit and hydro - cephalus; ance, severe hypertension, cardiac infarct and arrhyth mia, and neurogenic pulmonary oedema. These goals are best served by early transfer of the patient to a neurosurgical centre. In elderly patients with a poor WFNS grade, a decision to o ff er only supportive management may be appropriate. Neurological deterioration should prompt a repeat scan to exclude evidence of rebleeding and of hydrocephalus. T his is typically the communicating type, which is a common complication of haemorrhage. Where these complications are not demonstrated, deterioration may reflect delayed ischaemic neurological deficit (DNID), which commonly develops 3–10 days after aneurysmal haemorrhage and can progress rapidly to infarction. The process is attributed to cerebral vasospasm in response to, and correlating with, the blood load. This process can be visualised angiographically or by perfusion CT , and the velocity of blood flow in the cerebral vasculature measured using transcranial Doppler ultrasound can also provide an indirect assessment of the degree of stenosis. Outcomes are optimised by the prophylactic administration of nimodipine and maintenance of fluid volume, typically with 2.5–3 /uni00A0 L/day of normal saline. In established vasospasm, the goal is to maintain cerebral perfusion by administration of fluid and inotropes. Hyponatraemia is a frequent complication of SAH, attributed to cerebral salt wasting in the context of fluid depletion and to the syndrome of inappropria te antidiuretic hormone secretion otherwise. This is associated with a higher incidence of DNID; practical management, irrespective of the underlying pathology , is based on sodium replacement with hypertonic infusions if necessary . Fluid restriction is not appro priate in these patients since this risks further compromising perfusion. Summary box 48.7 Subarachnoid haemorrhage /uni25CF /uni25CF /uni25CF

Most result from rupture of an aneurysm in the circle of Willis Plain CT and lumbar puncture are /f_i rst-line investigations Even ‘good grade’ patients treated promptly have a signi /f_i cant morbidity owing to vasospasm, cardiac arrhythmias, neurogenic pulmonary oedema, etc.

Medical management

Patients should be placed on bed rest with hourly neuro - observations. They require strict input–output monitoring and intravenous fluid replacement with normal saline initially . Oral - nimodipine at a dose of 60 /uni00A0 mg every 4 hours is administered to reduce the incidence of vasospasm and dela yed ischaemic neurological deficit. Analgesics, laxatives, antiemetics, gastric protection and compression stockings are also likely to be necessary . After resuscitation, the priorities in SAH are to: 1 prevent rebleeding by identifying and controlling any underlying lesion; 2 recognise and manage: /uni25CF neurological complications, especially vasospasm, delayed ischaemic neurological deficit and hydro - cephalus; ance, severe hypertension, cardiac infarct and arrhyth mia, and neurogenic pulmonary oedema. These goals are best served by early transfer of the patient to a neurosurgical centre. In elderly patients with a poor WFNS grade, a decision to o ff er only supportive management may be appropriate. Neurological deterioration should prompt a repeat scan to exclude evidence of rebleeding and of hydrocephalus. T his is typically the communicating type, which is a common complication of haemorrhage. Where these complications are not demonstrated, deterioration may reflect delayed ischaemic neurological deficit (DNID), which commonly develops 3–10 days after aneurysmal haemorrhage and can progress rapidly to infarction. The process is attributed to cerebral vasospasm in response to, and correlating with, the blood load. This process can be visualised angiographically or by perfusion CT , and the velocity of blood flow in the cerebral vasculature measured using transcranial Doppler ultrasound can also provide an indirect assessment of the degree of stenosis. Outcomes are optimised by the prophylactic administration of nimodipine and maintenance of fluid volume, typically with 2.5–3 /uni00A0 L/day of normal saline. In established vasospasm, the goal is to maintain cerebral perfusion by administration of fluid and inotropes. Hyponatraemia is a frequent complication of SAH, attributed to cerebral salt wasting in the context of fluid depletion and to the syndrome of inappropria te antidiuretic hormone secretion otherwise. This is associated with a higher incidence of DNID; practical management, irrespective of the underlying pathology , is based on sodium replacement with hypertonic infusions if necessary . Fluid restriction is not appro priate in these patients since this risks further compromising perfusion. Summary box 48.7 Subarachnoid haemorrhage /uni25CF /uni25CF /uni25CF

Most result from rupture of an aneurysm in the circle of Willis Plain CT and lumbar puncture are /f_i rst-line investigations Even ‘good grade’ patients treated promptly have a signi /f_i cant morbidity owing to vasospasm, cardiac arrhythmias, neurogenic pulmonary oedema, etc.

Medical management

Patients should be placed on bed rest with hourly neuro - observations. They require strict input–output monitoring and intravenous fluid replacement with normal saline initially . Oral - nimodipine at a dose of 60 /uni00A0 mg every 4 hours is administered to reduce the incidence of vasospasm and dela yed ischaemic neurological deficit. Analgesics, laxatives, antiemetics, gastric protection and compression stockings are also likely to be necessary . After resuscitation, the priorities in SAH are to: 1 prevent rebleeding by identifying and controlling any underlying lesion; 2 recognise and manage: /uni25CF neurological complications, especially vasospasm, delayed ischaemic neurological deficit and hydro - cephalus; ance, severe hypertension, cardiac infarct and arrhyth mia, and neurogenic pulmonary oedema. These goals are best served by early transfer of the patient to a neurosurgical centre. In elderly patients with a poor WFNS grade, a decision to o ff er only supportive management may be appropriate. Neurological deterioration should prompt a repeat scan to exclude evidence of rebleeding and of hydrocephalus. T his is typically the communicating type, which is a common complication of haemorrhage. Where these complications are not demonstrated, deterioration may reflect delayed ischaemic neurological deficit (DNID), which commonly develops 3–10 days after aneurysmal haemorrhage and can progress rapidly to infarction. The process is attributed to cerebral vasospasm in response to, and correlating with, the blood load. This process can be visualised angiographically or by perfusion CT , and the velocity of blood flow in the cerebral vasculature measured using transcranial Doppler ultrasound can also provide an indirect assessment of the degree of stenosis. Outcomes are optimised by the prophylactic administration of nimodipine and maintenance of fluid volume, typically with 2.5–3 /uni00A0 L/day of normal saline. In established vasospasm, the goal is to maintain cerebral perfusion by administration of fluid and inotropes. Hyponatraemia is a frequent complication of SAH, attributed to cerebral salt wasting in the context of fluid depletion and to the syndrome of inappropria te antidiuretic hormone secretion otherwise. This is associated with a higher incidence of DNID; practical management, irrespective of the underlying pathology , is based on sodium replacement with hypertonic infusions if necessary . Fluid restriction is not appro priate in these patients since this risks further compromising perfusion. Summary box 48.7 Subarachnoid haemorrhage /uni25CF /uni25CF /uni25CF

Most result from rupture of an aneurysm in the circle of Willis Plain CT and lumbar puncture are /f_i rst-line investigations Even ‘good grade’ patients treated promptly have a signi /f_i cant morbidity owing to vasospasm, cardiac arrhythmias, neurogenic pulmonary oedema, etc.