Complications and therapy after subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) is a subset of stroke with a poor prognosis, up to 40% of patients die. Besides the impact of the initial haemorrhage, several neurological and systemic complications contribute to a poor clinical outcome. The first part of this thesis describes several complications after SAH. It is well known that SAH patients often have hyperglycaemia, and in chapter 2 we showed that patients with hyperglycaemia have a higher risk of poor outcome than patients with lower glucose levels. In chapter 3, we assessed whether intracisternal or intraventricular blood and the severity of hydrocephalus on the initial CT scan were predictors for fever after SAH. Only intraventricular blood was a risk factor for the occurrence of fever. As hydrocephalus might lead to decreased cerebral perfusion, we studied in chapter 4 whether severity of hydrocephalus on the initial CT scan is related to a higher chance of delayed cerebral ischaemia (DCI). However, increasing enlargement of ventricles did not result in a higher chance of DCI. We showed in Chapter 5 that brain natriuretic peptide was elevated after SAH, and that it was related with severe hyponatraemia after SAH but that it could not distinguish hypovolemic from non-hypovolemic hyponatreamia. The second part addresses several grading scales for SAH. In chapter 6 and 7 we showed that the Prognosis of Aneurysmal Subarachnoid Haemorrhage scale (PAASH) has a good prognostic value and interobserver agreement when compared to two commonly used other scales. In chapter 8 we discussed the reliability of the mRankin scale, a commonly used outcome scale, when performed with a telephone interview compared with a face to face interview. We concluded that a telephone assessment with a structured interview can be safely used in clinical research. In the third part we describe several aspects of therapy after SAH. In chapter 9 we described a systematic review on the effects of antiplatelet therapy after SAH. Antiplatelet therapy does not have a beneficial effect on outcome. Likewise, we described in chapter 10 the effects of calcium antagonists, including magnesium. Only nimodipine decreased the occurrence of DCI and poor outcome after SAH, and should be routinely administered in SAH patients. In chapter 11 we showed that DCI is more common after clipping of the patients’ aneurysm than after coiling of the aneurysm. In chapter 12, later timing of aneurysm treatment was related to occurrence of DCI and poor outcome. In chapter 13 we studied the level of serum magnesium and its influence on the effect on DCI and poor outcome, in SAH patients treated with 64 mmol magnesium sulphate per day. A good effect on clinical outcome was seen with a broad range of magnesium levels. Apart from the assumed beneficial effect of magnesium on poor outcome, we showed in chapter 14 that magnesium therapy after SAH diminished headache and use of pain killers. Finally, chapter 15 describes the results of the MASH-II study: a large phase 3 randomised placebo controlled trial on magnesium therapy in SAH patients.