Handbook of Practical Medicine Stroke

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 746 746 Chapter 14 Specific treatment of aneurysmal subarachnoid haemorrhage 14.8 Management of acute hydrocephalus 14.8.1 Diagnosis About 20% of unselected patients admitted within 3 days of SAH develop acute hydrocephalus, defined as a bicaudate index above the 95th percentile for age (Fig. 14.16). 26,215,216 Predisposing factors are frank intra- ventricular haemorrhage (Fig. 14.17), 26,217,218 extensive haemorrhage in the perimesencephalic cisterns in the tentorial hiatus (Fig. 14.18) 217,219 and – in only a single study – increasing age. 218 Fenestration of the lamina terminalis as part of any surgical treatment may reduce the risk of hydrocephalus according to observational studies, 220,221 but the increasing application of Fig. 14.17 CT scan of a patient with hydrocephalus from intraventricular extension of the haemorrhage. The lateral (upper black arrow) and temporal horns (lower black arrow) are enlarged; there is blood in the lateral (upper white arrow) and third (lower white arrow) ventricles. endovascular techniques for aneurysm occlusion will make this procedure less feasible. The typical presentation of acute hydrocephalus is that of a patient who is alert immediately after the initial haemorrhage, but who in the next few hours becomes increasingly drowsy, to the point that he or she only moans and localizes to pain. Nonetheless only half of all patients with acute hydrocephalus present in this way. 26 In the others consciousness is impaired from the onset, or the course is unknown because the patient was alone at the time of haemorrhage. If the patient is admitted very early and secondary deterioration occurs because of hydrocephalus, serial investigation by CT may show that the level of consciousness correlates more or less Fig. 14.16 CT brain scan of a patient with hydrocephalus 27 inversely with the width of the lateral ventricles. But (same patient as in Fig. 14.12) showing the bicaudate index when different patients are compared within one series, (A/B), a simple and linear method for measuring the size of the the relationship between the level of consciousness and ventricular system. A is the width of the frontal horns between the degree of ventricular dilatation is rather erratic. 26,215 the parallel walls of the caudate nuclei, at the level of the Ocular signs do not always accompany the obtunda- foramina of Monro, B the diameter of the brain at the same level. The 95th percentile for the bicaudate index is 0.16 at tion as a result of acute hydrocephalus; they help to age 30 years or under, 0.18 at 50 years, 0.19 at 60 years, 0.21 corroborate but not to exclude the diagnosis. In a pro- at 80 years, and 0.25 at 100 years. spective study in which 30 of 34 patients with acute .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 747 14.8 Management of acute hydrocephalus 747 (a) (b) (c) Fig. 14.18 CT scans of a patient with hydrocephalus from subarachnoid blood (white arrowheads) and no blood in the diffuse subarachnoid blood without intraventricular extension fourth ventricle (black arrow). The lateral and third ventricles of the haemorrhage. The hydrocephalus was treated with are enlarged (white arrows). (c) Later CT scan showing lumbar punctures. (a, b) CT scan on admission showing diffuse disappearance of the hydrocephalus. hydrocephalus had an impaired level of consciousness, Table 14.9 Management of acute hydrocephalus nine of these 30 had small, non-reactive pupils, and four of these nine also showed persistent downward Consider diagnosis if level of consciousness gradually deviation of the eyes, with otherwise intact brainstem deteriorates, particularly on the first day after the bleed reflexes. 26 These eye signs reflect dilatation of the pro- Repeat the CT brain scan and compare the bicaudate index with that on any previous scan ximal part of the aqueduct, which causes dysfunction of Spontaneous improvement occurs within 24 h in 50% of the pretectal area. 222 All nine patients with non-reactive patients (except those with massive intraventricular pupils had a relative ventricular size of more than 1.20 haemorrhage); take action if patient further deteriorates and were in coma, i.e. they did not open their eyes, obey or fails to improve within 24 h commands or utter words. Lumbar punctures are reasonably safe if there is no brain shift, and effective in about 50% of the patients who have Repeat CT scanning is required to diagnose or exclude no intraventricular obstruction hydrocephalus in a patient with subarachnoid External drainage of the ventricles is very effective in haemorrhage who deteriorates within hours or days restoring the level of consciousness, but may increase the of the initial event, with or without eye signs of risk of rebleeding (consider emergency clipping or coiling at the same time), and does increase the risk of infection hydrocephalus (small, unreactive pupils and (this may to some degree be prevented by prophylactic downward deviation of gaze). Patients with antibiotics, subcutaneous tunnelling, or both) intraventricular blood or with extensive haemorrhage in the perimesencephalic cisterns are particularly likley to develop acute hydrocephalus. is decreased because spontaneous improvement within this period has been documented in approximately 14.8.2 Possible interventions half of the patients (7 of 13) with acute hydrocephalus Possible interventions are listed in Table 14.9. who were only drowsy, and in almost half (19 of 43) who had a Glasgow Coma Score of 12/14 or worse but no massive intraventricular haemorrhage. 215 It is not Wait-and-see always easy to make a definitive decision on the need for A policy of wait-and-see for 24 h is eminently justified surgical measures even after 1 day has elapsed because in patients with dilated ventricles who are alert because patients may temporarily improve to some extent but only about one-third of them will become symptomatic then reach a plateau or again deteriorate; such fluctua- in the next few days. 215 Postponing interventions for tions are encountered in about one-third of patients a day can also be rewarding if the level of consciousness with symptomatic hydrocephalus. 215 Any further .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 748 748 Chapter 14 Specific treatment of aneurysmal subarachnoid haemorrhage deterioration in the level of consciousness warrants External ventricular drainage active intervention. External drainage of the cerebral ventricles by a catheter inserted through a burr hole is, in many centres, the Lumbar puncture most common method of treating acute hydrocephalus; Lumbar puncture was suggested as a therapeutic measure the improvement is usually rapid and sometimes dra- a long time ago, 223 but formal studies are scarce. In a matic. 26,215 Internal drainage, to the right atrium or prospective but uncontrolled study, 17 patients were peritoneal cavity, is rarely considered in the first few days treated in this way because they had acute hydrocephalus because the blood in the cerebrospinal fluid will almost with neither a haematoma nor gross intraventricular inevitably block the shunt system. However, a major haemorrhage. 28 Between one and seven lumbar punc- concern is that the abrupt lowering of the intracranial tures per patient were performed in the first 10 days, the pressure could precipitate rebleeding due to decreased number depending on the rate of improvement; each transmural pressure, or removal of clot sealing the time a maximum of 20 mL of cerebrospinal fluid was ruptured aneurysm. Therefore, the pressure of the cere- removed, the aim being a closing pressure of 15 cmH O. brospinal fluid after external ventricular drainage should 2 Of the 17 patients, 12 showed initial improvement: of be kept between 15 and 25 mmHg, 225 although this these 12, six fully recovered, two showed incomplete does not abolish the risk of rebleeding. 215 Aneurysm improvement but fully recovered after insertion of an pulsatilty and size increase after ventricular drainage, internal shunt, and four patients died of other complica- which further supports the notion of an increased risk of tions several days after the lumbar punctures had been rebleeding. 226 Indeed, several studies have suggested a started. Of the five remaining patients in whom lumbar significantly increased risk of rebleeding in patients with puncture had no effect, two recovered after an internal external ventricular drainage, compared with patients shunt and three died of other complications. without it. 227 However, many variables that could Whether the risk of rebleeding is increased by lumbar affect the rebleeding rate, such as the timing of surgery, punctures or drainage is uncertain. In a study of the risk the timing and duration of drainage, the size of the of rebleeding after lumbar puncture, a series of patients aneurysm, as well as the severity of the initial haemor- with SAH and hydrocephalus treated with one or more rhage, do not seem to have been adequately explored in lumbar punctures within 4 days after the haemorrhage most of these studies. 227 In a recent study, the risk of and before aneurysm occlusion was compared with rebleeding after external ventricular drainage within 4 control patients with untreated hydrocephalus and days after the haemorrhage and before aneurysm occlu- with control patients without ventricular enlargement. sion was compared with control patients with untreated Patients and controls were matched for interval since hydrocephalus, and with control patients without SAH, use of tranexamic acid, clinical condition on ventricular enlargement. Patients and controls were admission, and age. In the group treated with one or matched for interval since SAH, duration of exposure, more lumbar punctures, rebleeding occurred in one of use of tranexamic acid, clinical condition on admission, 21 patients (5%), in three of 21 controls (14%) with and age. Rebleeding occurred in seven of 34 patients untreated hydrocephalus and in none of the 21 controls treated with external ventricular drainage (21%), in seven without hydrocephalus. Thus, this study did not confirm of 34 controls (21%) with untreated hydrocephalus, and an increased risk of rebleeding after lumbar puncture, in six of 34 controls (18%) without hydrocephalus. 224 but because of the small number of patients it could not Thus, this study did not confirm an increased risk, but rule this out. 224 Until randomized controlled trials are because of the small number of patients it could not rule available, and we think these are still needed and ethic- it out. 224 ally justifiable, the tentative conclusion is that lumbar Ventriculitis is a frequent complication of external puncture seems a safe and reasonably effective way of drainage, especially if it is continued for more than a few treating those forms of acute hydrocephalus that are not days. 215 But regular exchange of the intraventricular obviously caused by intraventricular obstruction. catheter, in a randomized controlled study, did not decrease the risk of infection. 228 Likewise, a review of In patients deteriorating from acute hydrocephalus studies, all retrospective, before that trial was published after subarachnoid haemorrhage it is worth trying found prophylactic catheter exchange did not modify lumbar punctures if spontaneous improvement does 229 the risk of developing later infection. Some advocate not occur within 24 h, and if the probable site of very rigid antiseptic techniques and prophylactic anti- obstruction is in the subarachnoid space, not in the 230 biotics, but without proper evidence. Implementation ventricular system. of a protocol for insertion and for handling the drain in .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 749 14.9 Management of systemic complications 749 the intensive care unit with strict surveillance of adher- thereby with the development of delayed cerebral ing to the protocol may be helpful; in one single-centre ischaemia. After the syndrome of inappropriate secre- study it reduced the rate of infections compared with tion of antidiuretic hormone (SIADH) had been initially the period before the protocol. 231 Long subcutaneous described in the 1950s, 243 hyponatraemia in SAH was tunnelling has also been recommended, but infection incorrectly attributed to this syndrome. In SIADH there has only been compared with risks reported in the liter- is a continuing secretion of ADH, inappropriate to ature, 232 or with the risk of percutaneous drainage via changes of plasma volume and osmolality. The extra- Rickham reservoirs in a hospital where neurosurgeons cellular volume increases and the expansion of the could choose between these two methods. 233 intravascular component of this volume causes a dilu- External lumbar drainage probably carries a lower tional hyponatraemia. Natriuresis takes place because the risk of infection than ventricular drainage, 234 although volume expansion increases the glomerular filtration not all studies agree; 235 obviously lumbar drainage cannot rate and inhibits the secretion of aldosterone. Balance be used in patients with large intracerebral haematomas studies have shown that the degree of natriuresis is rel- or extensive intraventricular haemorrhage. As with lumbar atively small and approximately equals intake. The high punctures and external ventricular drainage, external concentration of urinary sodium in SIADH can be simply lumbar drainage may increase the risk of rebleeding, 236 explained by the fact that the sodium intake must be but there are no data from randomized trials. excreted in a smaller volume of urine. To shorten the period for which ventricular catheter- By contrast, hyponatraemia after SAH results from ization is necessary, test occlusion is often applied. excessive natriuresis, or cerebral salt wasting. 244 Serial But gradual weaning by sequential increases in the pres- measurement of plasma volume shows that this is sure of the external ventricular drainage system over decreased in most patients who developed hypona- 4 days preceding drain closure conferred no advantage, traemia, and is preceded by a negative sodium balance in according to a randomized study of 81 patients. 237 all instances. 42 Plasma volume considerably decreases, even in some patients with normal sodium levels, usu- ally as a result of excessive natriuresis. Serum ADH levels are increased or normal on admission, but decrease by the time hyponatraemia occurs. 14.9 Management of systemic Predisposing factors for the development of hypona- complications traemia are hydrocephalus, particularly enlargement of the third ventricle, 245 and ruptured aneurysms of the anterior communicating artery. 246 Mechanical pressure Neurologists and neurosurgeons are regularly confronted on the hypothalamus can perhaps disturb sodium and by non-neurological complications in patients with water homeostasis. Four substances have been identified aneurysmal subarachnoid haemorrhage: fever, anaemia, that are related to natriuresis and may act as inter- hypertension and hypotension, hyperglycaemia, hyper- mediary factors: a digoxin-like substance, 247 atrial natraemia and hyponatraemia, hypomagnesaemia, natriuretic factor, 248–252 brain natriuretic peptide 252–255 cardiac failure and arrhythmias, and pulmonary oedema and dendroaspis natriuretic peptide. 256 and pneumonia. More than half the patients have one The frequency of hyponatraemia depends on the or more of these complications and they are an import- cut-off point; if defined as a sodium level of 134 mmol or ant contributor to poor outcome. 238–240 The importance less on at least two consecutive days, it occurs in about of medical complications is further underlined by the one-third of patients. 182 It develops most commonly finding that grading scales in which they are taken into between the second and tenth day. Severe hypona- account are more accurate predictors of outcome than traemia (120–124 mmol/L) occurs in 4%. 42 scales made up only of neurological characteristics. 241 Correction of hyponatraemia in SAH is in practice a problem of correcting volume depletion (Table 14.10). Acute symptomatic hyponatraemia is rare and requires 14.9.1 Hyponatraemia and other electrolyte urgent treatment with hypertonic saline (1.8% or even disturbances 3%). However, over-rapid infusion of sodium may pre- Both hyper- and, more often, hyponatraemia can occur cipitate myelinolysis in the pons and the white matter after SAH, 242 although not all studies agree. 240 Hyper- of the cerebral hemispheres. 257 If possible, correction natraemia has been independently associated with should not be faster than 8 mmol/L/day. 258,259 A mild poor outcome in some studies, 242 but not in others. 240 degree of hyponatraemia (125–134 mmol/L) is usually Hyponatraemia is associated with hypovolaemia and well tolerated, self-limiting and need not be treated .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 750 750 Chapter 14 Specific treatment of aneurysmal subarachnoid haemorrhage Table 14.10 Management of hyponatraemia. unsettled. The influence of serum potassium on delayed cerebral ischemia and outcome has been investigated Almost invariably caused by sodium depletion, not by in only a single retrospective study without consecutive sodium dilution data collection in operated patients between 1971 and Associated hypovolaemia increases the risk of delayed 1987; potassium levels were not related to delayed cere- cerebral ischaemia 263 bral ischemia or death. Give isotonic saline (with or without plasma expander) or a mixture of glucose and saline; no free water If necessary, add fludrocortisone acetate, 400 mg/day in two 14.9.2 Hyperglycaemia doses, orally or intravenously Keep central venous pressure between 8 and 12 mmHg, Hyperglycaemia defined as a plasma concentration of or pulmonary capillary wedge pressure between 14 and > 11.1 mmol/L is found in one-third of the patients 18 mmHg during their clinical course, and is associated with a poor clinical condition on admission. 240 From admission through day 10, glucose levels remain higher in patients with a poor outcome compared with those with a good in itself. Hyponatraemia in patients with evidence of clinical outcome. 264 Hyperglycaemia is independently a negative fluid balance or excessive natriuresis is associated with poor outcome. 264,265 Whether correction corrected with saline (0.9%; sodium concentration of hyperglycaemia results in improved outcome is an 150 mmol/L). unresolved issue. Hyponatraemia after subarachnoid haemorrhage 14.9.3 Disorders of cardiac rhythm and usually reflects cerebral salt wasting (sodium function depletion) and not secretion of antidiuretic hormone (sodium dilution). Because hyponatraemia may lead Aneurysmal rupture is commonly associated with car- to hypovolaemia, it should not be treated with fluid diac arrhythmias, ischaemia-like electrocardiographic restriction. (ECG) abnormalities, and sometimes with cardiac arrest. 13 It is therefore not surprising that patients Hypomagnesaemia is found in half the patients on are sometimes initially misdiagnosed as having acute admission, or during the clinical course. 154 On admis- myocardial infarction and admitted to coronary care sion it is related to poor clinical condition and large units. Cardiogenic shock may also occur, usually in amounts of extravasated blood, but not with the later combination with pulmonary oedema (section 14.9.4). occurrence of delayed cerebral ischaemia or poor out- The probable explanation is sustained sympathetic come, at least not independently. By contrast, hypo- stimulation, associated with massive excretion of cate- magnesaemia developing between day 2 and 12 after cholamines, 266,267 and also of cortisol and ADH. 267 This SAH is independently associated with the development may result in structural damage to the myocardium, of delayed cerebral ischaemia. 154 Why hypomagnesemia according to echocardiographic evidence, 268 raised tro- occurs after SAH is unclear; renal excretion of magne- ponin I levels, 269–272 and histological features at post- sium is an unlikely explanation because hypomagne- mortem – contraction bands, focal myocardial necrosis saemia occurs within hours of the haemorrhage. and subendocardial ischaemia. 273 Secretion of B-type Hypomagnesaemia has been linked to cardiac arrhyth- natriuretic peptide is probably a consequence of myo- mias, 260 and in cases of acute arrhythmia 4–8 mmol cardial damage. 274 Low magnesium levels may play an as an intravenous load in 5–10 min, followed by intermediary role. 275 25 mmol per day is recommended. 260 The aim is to keep The most common ECG abnormalities in SAH the magnesium concentration above 0.4 mmol/L. Infu- (Fig. 14.19) are ST depression and elevation, T-wave sion of 64 mmol per day results in concentrations changes, pathological Q waves and bundle branch between 1.0 and 2.0 mmol/L, 261 and is associated with a block. 276 Life-threatening arrhythmias such as ventricu- reduced risk of developing delayed cerebral ischaemia, 157 lar fibrillation and ‘torsade de pointe’ may occur, 277,278 but whether this regimen results in improved overall but in under 5% of patients. 12,13,279 A striking finding outcome is not yet clear (section 14.5.3). in a large series of patients investigated by serial ECGs Low serum potassium occurs in approximately half was that every patient had at least one abnormal ECG. 280 the patients with SAH, and is associated with an increased Virtually all ECG abnormalities changed to other abnor- risk of severe Q–Tc prolongation. 262 But whether malities, in no consistent order, and then disappeared, hypokalaemia is associated with overall outcome is in an observation period of 10 days. .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 751 14.9 Management of systemic complications 751 V 1 V 4 V 1 V 4 V 1 V 4 V 2 V 5 V 2 V 5 V 2 V 5 V 3 V 6 V 3 V 6 V 3 V 6 Day 0 Day 1 Day 9 (a) (b) (c) Fig. 14.19 ECG abnormalities in a 74-year-old woman with prolonged Q–Tc interval and signs of left ventricular subarachnoid haemorrhage. (a) Day 0: ischaemic ST segment, hypertrophy. (c) Day 9: sinus tachycardia, transient prominent U wave and prolonged Q–Tc interval. (b) Day 1: pathological Q wave and ischaemic ST segment. sinus bradycardia, ischaemic ST segment, ischaemic T wave, A prolonged Q–T interval often represents delayed 14.9.4 Pulmonary oedema ventricular repolarization and predisposes to ventricular arrhythmias, but in patients with SAH it is more import- Pulmonary oedema occurs to some degree in approxi- ant as an indicator of severe intracranial disease than of mately one-third of patients with SAH 36,288 but the ful- potentially serious cardiac complications. 280,281 Rhythm minant variety is much rarer (2% in the largest series to disturbances have some association with lesions of the date). 289 The onset is usually rapid, within hours of the insular cortex, 282 more often with right- than with SAH. What triggers pulmonary oedema is unclear. Raised left-sided haemorrhages, 3,283 an association that is not intracranial pressure can lead to a massive sympathetic limited to ruptured aneurysms. 284 discharge, mediated by the anterior hypothalamus – the same location that is held responsible for electrolyte dis- Abnormalities of heart rhythm after subarachnoid turbances (section 14.9.1). This would lead to increased haemorrhage mostly represent ‘smoke’ rather than permeability of endothelial cells in the pulmonary ‘fire’ and rarely need to be treated. capillary bed. Any cardiac failure may aggravate the pulmonary oedema. 36 Generally, severe ventricular arrhythmias are brief. Beta- The typical clinical picture consists of unexpected dys- blockade has been proposed as preventive treatment pnoea, cyanosis and the production of pink and frothy aimed at lowering the sympathetic tone. In patients with sputum. Many patients are pale, sweat excessively and are head injury a double-blind, randomized study found hypertensive. A chest X-ray usually demonstrates impres- that beta-blockers reduced catecholamine-induced car- sive pulmonary oedema (Fig. 14.7) which may disappear diac necrosis, but not in-hospital case fatality. 285 In in a matter of hours following positive end-expiratory patients with SAH, routine administration of beta-blockers pressure ventilation. A problem is that liberal adminis- is not warranted until there is evidence of improved tration of fluids is beneficial for brain perfusion but may overall outcome; the net benefits may be disappointing delay recovery of pulmonary oedema and hence impair because beta-blockers lower blood pressure. brain oxygenation, and that positive end-expiratory Left ventricular dysfunction also occurs, most often pressure ventilation increases intracranial pressure. in the initial days after the SAH. 286 In a review of four If there is associated left ventricular failure, clinically studies of consecutive series of patients examined by manifested by sudden hypotension following initially echocardiography, irrespective of clinical condition or elevated blood pressure, transient lactic acidosis and ECG findings, left ventricular dysfunction was found in mild elevation of the creatine kinase MB fraction, 37,290 12% of patients. 287 These patients had an increased risk inotropic agents are indicated (intravenous dobutamine, of delayed cerebral ischaemia and poor outcome. 5–15 µg/kg/min). 291 .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 752 752 Chapter 14 Specific treatment of aneurysmal subarachnoid haemorrhage patients within the first year. 64 A long-term study in 14.10 Late sequelae and complications Japan estimated the rebleeding rate after initially suc- cessful clipping was 2.2% after 10 years and 9% after 20 years, 85 while in a Dutch cohort the rate of new episodes In general, functional outcome improves significantly be- of SAH (from newly developed aneurysms, incidental tween 4 months and 18 months after SAH with improved aneurysms that were left untreated and from regrowth quality of life. 292 Nevertheless, specific late complica- aneurysms combined) was 3.2% after 10 years. 86 Despite tions require attention. Therefore, we favour a multidis- this relatively high risk of new episodes of SAH after ciplinary clinic for patients who have had an SAH where successful surgical treatment of the initial episode, a neurologists and rehabilitation physicians are at hand. modelling study estimated that repeated screening and treatment of newly detected aneurysms could not be recommended, because the prevented episodes of new 14.10.1 Vitreous haemorrhages episodes of SAH would be outweighed by the complica- Preretinal haemorrhages associated with SAH (section tions of the diagnostic and therapeutic procedures. For 3.7.1) may break into the vitreous cavity (Terson syn- patients with an increased risk of both aneurysm devel- drome). This has been documented in 13% of patients opment and aneurysm rupture, screening was beneficial in prospective studies; 293 the rates were three times as in this model, but at present we cannot identify who high in patients who had lost consciousness at some these patients are (section 15.2.5). stage. 294 These haemorrhages occur in one or both eyes, After endovascular occlusion of the aneurysm, there is usually at the time of the initial haemorrhage, but some- still little information about the rate of rebleeding in the times several days later, and then mostly in association long term (section 14.4.2). with rebleeding. It may, however, take days or weeks before the patient is sufficiently alert to complain about 14.10.3 Late hydrocephalus blurred vision. In most cases, the vitreous haemorrhage clears spontaneously in a matter of weeks to months. If Permanent shunting for hydrocephalus persisting for not, vitrectomy may be indicated to improve vision. 295 2–4 weeks after the initial haemorrhage is needed in Operation is unnecessary if preretinal haemorrhages approximately 20% of patients, according to two neuro- have not involved the vitreous body. 296 surgical series. 299,300 Aneurysm site (anterior commun- icating artery complex or posterior circulation) is an established risk factor for late hydrocephalus. 301,302 14.10.2 New episodes of subarachnoid Putative risk factors, identified only in single studies, are haemorrhage 303 301 age, intraventricular haemorrhage and the clear- When the ruptured aneurysm is left untreated, the rate ance rate of subarachnoid blood. 304 The risk of chronic of rebleeding after the first 6 months have passed is hydrocephalus is no lower after endovascular treatment 3.5% per year during the first decade, but of course than after surgical clipping. 305–307 If fenestration of the this situation is now increasingly unusual. 297 However, lamina terminalis is performed, as part of the microsurg- even in patients with successfully occluded ruptured ical procedure for aneurysm repair, late hydrocephalus is aneurysms new episodes of bleeding do occur – from de a rare event. 308 novo aneurysms, incidental aneurysms that were left untreated at the time of the initial haemorrhage, or from 14.10.4 Epilepsy regrowth of the aneurysm that caused the first bleed. From the patient’s perspective the source of a new New-onset epilepsy (two or more unprovoked seizures) episode is not very relevant, but from a management in the first year after discharge from hospital was perspective it is. In a study of 30 patients with late reported in 17 of 242 patients (7%) from Columbia Uni- rebleeding (after an average period of more than 7 years) versity, New York, while an additional 10 patients (4%) the ruptured aneurysm had developed at a new location had a single seizure. 309 In a British cohort late epilepsy in somewhat more than half the cases, it had regrown occurred in 4.9% in the first year after the haemorrhage at the previous aneurysm site in about a quarter, and in (23 of 872 patients). 310 Unfortunately neither cohort the rest the source of bleeding was an additional recorded a possible relationship with seizures at the aneurysm that had been overlooked at the time of the time of the haemorrhage or during hospital stay; this is first episode. 298 important because in a small cohort of 95 patients from In the surgical arm of the ISAT trial rebleeding from Detroit all eight with epileptic seizures after discharge the clipped aneurysm occurred in 1% of the operated fell into this category. 311 Putative risk factors (identified .. ..

9781405127660_4_014.qxd 10/13/07 2:15 PM Page 753 References 753 in single studies only) include focal lesions such as sub- Netherlands. J Neurol Neurosurg Psychiatry 2000; dural haematoma and cerebral infarction, 309,312 as well 68:337–41. as disability on discharge, 310 which of course is largely 5 Wiebers DO, Whisnant JP, Huston J, III, Meissner I, Brown a consequence of structural brain damage. De novo RD, Jr., Piepgras DG et al. Unruptured intracranial epileptic seizures are relatively rare after coiling. 64,313 aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003; 362:103–10. 14.10.5 Cognitive dysfunction and psychosocial 6 Stegmayr B, Eriksson M, Asplund K. Declining mortality impact from subarachnoid hemorrhage: changes in incidence and case fatality from 1985 through 2000. Stroke 2004; It is important to appreciate just who should be asked if 35:2059–63. a patient has ‘recovered’. The patients rate their own 7 Bardach NS, Zhao SJ, Gress DR, Lawton MT, Johnston SC. outcome worse than the treating physician, but better Association between subarachnoid hemorrhage outcomes than their spouses. 314 Even patients who seem to make and number of cases treated at California hospitals. Stroke a good functional recovery and who are independent 2002; 33:1851–6. in activities of daily living often can have psychoso- 8 Sasaki T, Sato M, Oinuma M, Sakuma J, Suzuki K, cial and cognitive deficits in the first year after the Matsumoto M et al. Management of poor-grade patients SAH. 3,315,316 Although improvement still occurs between with aneurysmal subarachnoid hemorrhage in the acute stage: importance of close monitoring for neurological 4 and 18 months after the SAH, many patients and their grade changes. Surg Neurol 2004; 62:531–5. partners still experience reduced quality of life 1–2 years 9 Inagawa T, Kamiya K, Ogasawara H, Yano T. Rebleeding of after the haemorrhage. 317 The psychosocial impact at ruptured intracranial aneurysms in the acute stage. Surg even longer follow-up is considerable. In a survey of 610 Neurol 1987; 28(2):93–9. patients who were interviewed about 9 years after their 10 Fujii Y, Takeuchi S, Sasaki O, Minakawa T, Koike T, SAH, a quarter of the employed patients had stopped Tanaka R. Ultra-early rebleeding in spontaneous working and another quarter worked shorter hours or subarachnoid hemorrhage. J Neurosurg 1996; 84:35–42. had a position with less responsibility. 318 On average, 11 Ohkuma H, Tsurutani H, Suzuki S. Incidence and patients returned to work about 9 months after discharge significance of early aneurysmal rebleeding before (range 0–96). A total of 60% of the patients reported neurosurgical or neurological management. 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Proposed use of 4 Roos YBWEM, de Haan RJ, Beenen LFM, Groen RJM, prophylactic decompressive craniectomy in poor-grade Albrecht KW, Vermeulen M. Complications and outcome aneurysmal subarachnoid hemorrhage patients presenting in patients with aneurysmal subarachnoid haemorrhage: with associated large sylvian hematomas. Neurosurgery a prospective hospital based cohort study in the 2002; 51:117–24. .. ..