Progressing haemorrhagic stroke: categories, causes, mechanisms and managements

Abstract

Haemorrhagic stroke is a severe stroke subtype with high rates of morbidity and mortality. Although this condition has been recognised for a long time, the progressing haemorrhagic stroke has not received adequate attention, and it accounts for an even worse clinical outcome than the nonprogressing types of haemorrhagic stroke. In this review article, we categorised the progressing haemorrhagic stroke into acute progressing haemorrhagic stroke, subacute haemorrhagic stroke, and chronic progressing haemorrhagic stroke. Haematoma expansion, intraventricular haemorrhage, perihaematomal oedema, and inflammation, can all cause an acute progression of haemorrhagic stroke. Specific 'second peak' of perihaematomal oedema after intracerebral haemorrhage and 'tension haematoma' are the primary causes of subacute progression. For the chronic progressing haemorrhagic stroke, the occult vascular malformations, trauma, or radiologic brain surgeries can all cause a slowly expanding encapsulated haematoma. The mechanisms to each type of progressing haemorrhagic stroke is different, and the management of these three subtypes differs according to their causes and mechanisms. Conservative treatments are primarily considered in the acute progressing haemorrhagic stroke, whereas surgery is considered in the remaining two types.

Fig. 1

Mechanism of acute progressing haemorrhagic stroke

Fig. 2

Patient with ‘spot sign,’ demonstrating extravasation and haematoma expansion [166]. Reproduced from Wolters Kluwer Health with permission

Fig. 3

Haematoma heterogeneity and haematoma growth border. These two patients were admitted to our hospital with the impression of spontaneous ICH. Patient 1: a CT on admission shows haematoma heterogeneity with an initial haematoma volume of 15 mL. b Repeated CT after 32 h shows a haematoma volume of 30 mL. Patient 2: c CT on admission shows haematoma growth border (black arrow). d Repeated CT after 10 h shows haematoma expansion with increased midline shift

Fig. 4

A case of subacute progressing stroke. The patient was admitted to our hospital because of dysphagia, hemiparalysis, and conscious disturbance. a CT on hospital admission showed left parietal and frontal intracerebral haemorrhage. After the initial treatment, the patient regained consciousness. b 10 days after hospital admission, the patient became lethargic, and repeated CT showed an increased mass effect and midline shift, with enlargement of the perihaematomal oedema. Stronger osmotic therapy was applied immediately and the patient’s consciousness improved. c Repeated CT at 17 days post hospital admission showed that the initial haematoma shrank further, the density of the brain oedema decreased, and the mass effect alleviated modestly. d An enhanced CT at 17 days showed no ring-enhancement, eliminating the tension haematoma

Fig. 5

Management of subacute progressing stroke

Fig. 6

Mechanisms of CEICH