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ReviewComplications of intracerebral haemorrhage
Introduction
Spontaneous or primary intracerebral haemorrhage (ICH) is a major cause of morbidity and mortality worldwide. It is the second most common form of stroke, accounting for 10–30% of first-ever strokes.1, 2, 3 The 30 day mortality for ICH has been reported to be 30–55%,1, 2, 3, 4, 5, 6 with half the deaths occurring in the acute phase, especially in the first 48 h.1, 2, 5 The complications of ICH are among the major predictors of early mortality and poor outcome.
ICH complications include haematoma expansion (HE), perihaematomal oedema (PHE), intraventricular extension of haemorrhage (IVH) with hydrocephalus, seizures, venous thromboembolic events (VTE), hyperglycaemia, increased blood pressure (BP), fever, and infections. Complications such as HE,7, 8 IVH with obstructive hydrocephalus,9, 10, 11 and hyperglycaemia4, 12, 13 are major predictors of increased early mortality and adverse outcome during the hyperacute phase of ICH. Similarly, HE, hydrocephalus, and PHE have been associated with early neurological deterioration (END) and poor outcome.14 A prospective observational study reported END in about 33% of patients with ICH within 48 h of onset, with an associated 30 day mortality of 47% in those with END.14
The complications of ischaemic stroke (IS) and their management have been reviewed extensively,15, 16 with little discussion of the complications of ICH. Despite its seriousness, the treatment options for ICH are restricted and few evidence-based data exist to guide the management of ICH complications. By contrast with IS, for which therapeutic advances have been made to improve clinical outcome, the management of ICH is generally supportive, but with poor prognosis because no specific treatments have been shown to improve outcome after ICH. For example, the management of HE is of unproven value because all measures aimed at restricting HE have so far not improved outcome in controlled trials. Similarly, PHE management is mainly supportive and measures aimed at decreasing intracranial pressure (ICP) are also of unproven value. Also, insufficient evidence exists with regard to the efficacy of surgical treatment for ICH, and whether or not surgical approaches are beneficial remains controversial.
Additional therapeutic dilemmas can arise over the safest and most effective approach to VTE prevention in patients with ICH because prophylaxis with anticoagulants can increase the risk of HE or further bleeding. Perhaps a more difficult therapeutic dilemma is how to manage patients with clinical thromboembolic complications after ICH, balancing the risk of subsequent life-threatening thromboembolism if untreated against the risk of recurrence of ICH. A related issue is whether or when to resume anticoagulation after ICH in patients with cardiac disease associated with high embolism risk, such as those who need mechanical valve prostheses or those with atrial fibrillation.
In this review, we focus on the early complications of ICH, discussing emerging therapies and relevant preventative and management strategies based on available evidence and guidelines. We draw attention to the scarcity of evidence to guide the management of many important and common complications of ICH.
Section snippets
Clinical features
HE, defined as an increase in volume of 33–50% or an absolute change in haematoma volume of 12·5–20 mL (on repeat CT), is a common early and severe complication of ICH.8, 17, 18, 19, 20 Although HE is one of the main pathophysiological phases of ICH, it can also be a serious complication subsequent to the acute phase—up to 40% of the haematoma grows in the first few hours post ictus. Various terms such as haematoma extension, expansion, progression, growth, enlargement, and rebleeding have been
Clinical features
PHE, which is present in most patients with ICH, can be associated with increased mass effect and END14, 73 and is a predictor of poor functional outcome and mortality.1, 73, 74, 75 PHE develops early in the hyperacute phase (increasing in volume by 75% in the first 24 h),75 evolves over many days, and increases strongly during the first week 74 before it reaches its maximum during the second week after bleeding.1, 14, 76
Although the mechanisms of oedema formation after ICH are not fully
Clinical features of IVH
IVH is common after ICH, occurring in 30–50% of patients, and is a major additional predictor of poor prognosis (figure 2).9, 10, 11, 95, 96, 97 A relation exists between the location and volume of ICH and the presence of IVH.11, 95 A subanalysis of the activated rFVIIa phase 2 trial showed a relation between thalamic ICH and increased frequency of IVH.11 This was attributable to the anatomical closeness of the thalamus to the third ventricle and the predisposition for blood to spread medially.
Clinical features
Seizures are a frequent complication of ICH and can even be the presenting symptom.123 Seizures most commonly occur at the onset of ICH, but can be delayed. About 50–70% of seizures occur within the first 24 h, and 90% in the first 3 days,124, 125, 126, 127 with an overall 30 day risk of seizures of about 8%.123
Early seizures are defined as those occurring within 2 weeks of initial ictus, late seizures occurring thereafter.124, 125 Whereas early seizures are thought to be caused by structural
Clinical features
VTE are a common and potentially fatal complication in patients with ICH that can manifest as either deep-vein thrombosis (DVT) or pulmonary embolism (PE).138, 139 The reported rate of clinically symptomatic VTE is 3–7%.138, 140, 141 Overall, studies have estimated the short-term post-ICH risk of PE to be 1–2% and of DVT to be 1–4%.138 Subclinical DVT is more common than is clinically apparent DVT, with asymptomatic DVT rates occurring in up to 17% of patients with ICH.142 In a small
Clinical features
Fever occurs in up to 40% of patients after ICH,162, 163 and is independently associated with a poor outcome and increased mortality.163, 164, 165, 166, 167 The incidence of fever (temperature >38·3°C) is high in basal ganglionic and lobar ICH, especially in patients with IVH.45, 162, 163 The cause of high temperature after stroke is not always apparent, although increased body temperature might be a direct consequence of brain damage caused by stroke or accompanying infections.164, 168
Clinical features
A high proportion of patients (about 60%) might develop hyperglycaemia even in the absence of a previous history of diabetes after ICH.174 Increased blood glucose in the acute setting of ICH is probably a response to stress and severity of ICH13 and can persist for up to 72 h after ICH.174
Many studies have shown that increased serum glucose on admission is associated with larger haematoma size, HE, PHE, cell death, and increased risk of poor outcome,12, 32, 174, 175, 176 and that it is a potent
Clinical features
Increased BP (≥140/90 mm Hg) is common in the acute phase of ICH, occurring in more than 70% of patients on presentation.180, 181 Increased BP in the acute setting of ICH occurs even in the absence of a previous history of hypertension and is independently associated with poor outcome.180, 182
The mechanism for the acute increase of BP after ICH is unknown. However, it is proposed to be a multifactorial process that includes activation of the neuroendocrine systems (sympathetic nervous system,
Conclusions
Complications occurring during the acute phase of ICH add further detrimental effects to an already potentially fatal disorder and substantially affect the clinical outcome. In view of the small number of therapeutic options available for ICH, a need exists to provide the best evidence-based supportive care. Patients should be managed in a neuroscience ICU or a similar setting during the acute phase of ICH, with continuous monitoring of vital signs and frequent neurological assessment. Improved
Search strategy and selection criteria
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