**10. Intracerebral haemorrhage (ICH)**

#### **10.1. Introduction**

Placement of nasogastric tubes, indwelling bladder catheters, or intra-arterial pressure catheters should be delayed if the patient can be safely managed without them. A follow-up CT or MRI scan should be obtained at 24 hours after IV rt-PA before commencing anticoagulants

INR indicates international normalized ratio; IV, intravenous; NIHSS, National Institutes of Health Stroke Scale; and

**Table 2.** Additional inclusion and exclusion characteristics of patients with acute ischemic stroke who could be treated

This modality of treatment for acute ischaemic stroke is fast emerging. Mechanical clot retrieval with MERCI device (Mechanical Embolus Removal in Cerebral Ischaemia) has been employed. Other interventions have included mechanical clot aspiration with the Penumbra system. The Penumbra System (PS) is a new embolectomy device specifically designed to remove the thrombus in acute ischemic stroke secondary to large vessel thromboembolism. The device removes the thrombus through two mechanisms: aspiration and extraction [16]. Earlier trials, Trevo versus Merci Retrievers for Thrombectomy Revascularization of Large Vessel Occlusions in Acute Ischaemic Stroke (TREVO 2) and SWIFT, showed significantly higher recanalization rates associated with stent retriever

Patients who have sustained a stroke are prone to developing complications. About 30–60% of patients after acute ischaemic stroke develop these complications. The most frequent complications include respiratory and urinary tract infections, deep vein thrombosis (DVT) and pulmonary embolism (PE) [53]. Pulmonary embolism occurs in about 10% of patients post stroke. Deep vein thrombosis and pulmonary embolism tend to occur in the first three months post

devices compared to the first generation Merci Retriever [51, 52].

or antiplatelets (**Tables 1** and **2**).

**Inclusion criteria**

Aged >80 years

**Relative exclusion criteria**

Severe stroke (NIHSS>25)

 Taking an oral anticoagulant regardless of INR History of both diabetes and prior ischemic stroke

236 Essentials of Accident and Emergency Medicine

rt-PA, recombinant tissue plasminogen activator.

with IV rt-PA within 3 to 4.5 hours from symptom onset.

 Diagnosis of ischemic stroke causing measurable neurological deficit Onset of symptoms within 3 to 4.5 hours before beginning treatment

**7. Endovascular treatments**

**8. Complications**

This refers to bleeding into the brain parenchyma. Intracerebral haemorrhage is a devastating disease with increased morbidity and mortality constituting 15% of all stroke types [56, 57]. Factors associated with increased mortality include large clots, low Glasgow Coma Scale score, intraventricular haemorrhage and haematoma expansion. The causes of haematoma growth include a past history of stroke, liver disease, hyperglycaemia and hypertension [58]. The common sites for ICH include the basal ganglia, thalamus, brain stem and the cerebellum.

#### **10.2. Causes**

Causes of ICH have been classified into primary and secondary. Hypertension remains the most common modifiable risk factor for the development of ICH [59, 60] while cerebral amyloid angiopathy is the second most frequent risk factor in ICH leading to lobar haemorrhages . Other risk factors include increasing age, anticoagulation therapy, AV malformations, and aneurysms [61].

#### **10.3. Clinical features**

The symptoms are usually sudden in onset; most times occurring during exercise or emotional stress although it can also occur during routine activity [61, 62]. It is difficult, on the basis of clinical presentation, to distinguish ICH from ischaemic stroke as they may look similar.

Presentation of ICH differs depending on the size and location of the ICH. Symptoms that may suggest ICH include severe headache, vomiting, seizures, reduced level of consciousness. Headache is more frequent in patients with large haematomas and has been attributed to raised intracranial pressure and traction on the meningeal pain fibres. Small, deep haematomas rarely present with headache. [61]. About 15–23% of patients tend to have haematoma expansion and neurological deterioration in the first few hours of the event [63, 64].

#### **10.4. Assessment**

According to the guideline on the emergency diagnosis and assessment of an ICH patient, the following should be done:

had reported rapid reversal of transtentorial herniation and decreased intracranial pressure with the use of 23.4% of hypertonic saline [70]. Another study had observed the superiority of hypertonic saline over mannitol in the treatment of increased intracranial pressure [71]. The routine use of mannitol in small ICH and asymptomatic peri-haematoma oedema should be

Emergency Management of Acute Ischaemic Stroke http://dx.doi.org/10.5772/intechopen.75305 239

These are common in ICH occurring in up to 16% of the cases in the first week with most occurring at onset [72]. Lobar haematomas carry an increased risk of seizures than deep ICH [73]. A recent AHA/ASA guideline for management of spontaneous ICH recommend the use of antiepileptic drugs only in patients with clinical seizures and those with depressed mental status found to have electrographic seizures on EEG [74]. Drugs that have been used include intravenous Lorazepam (0.05–0.1 mg/kg), fosphenytoin (or Phenytoin 15-20 mg/kg),

Hyperglycaemia at presentation portends a worse outcome. This is independent of diabetes mellitus [75]. Treatment involves the use of Insulin. Hypoglycaemia should be avoided.

Symptomatic deep vein thrombosis occurs in 1–5% of patients with ICH with pulmonary embolism occurring in about 0.5–2% of such cases. It is therefore crucial to prevent both DVT and PE [76]. Prophylaxis for DVT includes the use of intermittent pneumatic compression devices (IPC) or compression stockings if IPC devices are not available. Subcutaneous lowdose unfractionated heparin can be used when the intracranial bleeding has been controlled

Lowering of blood pressure in the setting of ICH has been frequently practiced to reduce haematoma growth. However, the association between elevated BP and hematoma expansion remains controversial. An increasing blood pressure has been associated with haematoma expansion. The AHA/ASA guidelines recommend mean arterial Pressure of 130 mmHg. Titratable antihypertensive drugs such as Intravenous Labetalol (10–20 mg IV bolus, can be repeated up to max of 60 mg) and Nicardipine (5 mg/h up to 15 mg/h) are often used in acute ICH. Nitroprusside should be avoided because of its tendency to

This is a frequent occurrence in patients with ICH especially in those with intraventricular extension. Patients with persistent fever after ICH tend to have a worse prognosis [77].

discouraged.

*10.6.2. Seizures*

and valproic acid (15-45 mg/kg).

*10.6.3. Hyperglycaemia*

*10.6.4. Deep vein thrombosis*

*10.6.5. Blood pressure*

increase ICP.

*10.6.6. Fever*

within 48 hours of the admission [74].

A baseline severity score should be performed as part of the initial evaluation of patients with ICH (Class 1; level of evidence B); rapid neuroimaging with CT or MRI is recommended to distinguish ischaemic stroke from ICH (Class 1, level of evidence A); Computed Tomography Angiography (CTA) and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion (Class 11b, level of evidence B) and CTA, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MR angiography and magnetic resonance venography, and catheter angiography can be useful to evaluate for underlying structural lesions including vascular malformations and tumours when there is clinical or radiological suspicion (Class 11a, level of evidence B).

#### *10.4.1. Diagnosis*

Rapid diagnosis is essential in the management of the condition. Deterioration in the first few hours after onset has been reported due to haematoma expansion [64].

Initial assessment will include stabilization of patient by maintaining the airway. General physical examination and quick neurological examination should be performed on all patients. Vital signs should be measured. Baseline severity scale score like ICH score, Glasgow coma scale (GCS), NIHSS should be employed. The ICH score is a simple clinical grading scale, reliable and validated for rapid evaluation of ICH severity [63].

#### **10.5. Investigations**

Brain non- contrast CT Scan (NCCT) - this is the goal standard in diagnosing ICH. It is convenient and highly sensitive in the detection of ICH [65]. Other useful information that can be extracted from NCCT includes the location of ICH, intraventricular bleed, hydrocephalus, early signs of herniation, lesional oedema, and midline shift. ICH volume, a strong predictor of outcome can also be estimated. Brain MRI can help in identifying the exact neuroanatomic site as well as the aetiology [66]. Other investigations are same as for ischaemic stroke.

#### **10.6. Management**

Airway management is similar to that of acute ischaemic stroke.

#### *10.6.1. Peri-haematomal oedema*

This occurs in the first few days after intracerebral haemorrhage. It is significantly associated with hematoma expansion, increased intracranial pressure, mass effect, midline shift and brain herniation leading to poor functional outcome of ICH [67–69]. Agents that can reduce peri-haematomal oedema process provide protective effects for ICH. These include the use of osmotic diuretics such as Mannitol. Hypertonic saline can also be used. An earlier retrospective study had reported rapid reversal of transtentorial herniation and decreased intracranial pressure with the use of 23.4% of hypertonic saline [70]. Another study had observed the superiority of hypertonic saline over mannitol in the treatment of increased intracranial pressure [71]. The routine use of mannitol in small ICH and asymptomatic peri-haematoma oedema should be discouraged.

#### *10.6.2. Seizures*

**10.4. Assessment**

*10.4.1. Diagnosis*

**10.5. Investigations**

**10.6. Management**

*10.6.1. Peri-haematomal oedema*

following should be done:

238 Essentials of Accident and Emergency Medicine

suspicion (Class 11a, level of evidence B).

According to the guideline on the emergency diagnosis and assessment of an ICH patient, the

A baseline severity score should be performed as part of the initial evaluation of patients with ICH (Class 1; level of evidence B); rapid neuroimaging with CT or MRI is recommended to distinguish ischaemic stroke from ICH (Class 1, level of evidence A); Computed Tomography Angiography (CTA) and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion (Class 11b, level of evidence B) and CTA, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MR angiography and magnetic resonance venography, and catheter angiography can be useful to evaluate for underlying structural lesions including vascular malformations and tumours when there is clinical or radiological

Rapid diagnosis is essential in the management of the condition. Deterioration in the first few

Initial assessment will include stabilization of patient by maintaining the airway. General physical examination and quick neurological examination should be performed on all patients. Vital signs should be measured. Baseline severity scale score like ICH score, Glasgow coma scale (GCS), NIHSS should be employed. The ICH score is a simple clinical grading scale, reli-

Brain non- contrast CT Scan (NCCT) - this is the goal standard in diagnosing ICH. It is convenient and highly sensitive in the detection of ICH [65]. Other useful information that can be extracted from NCCT includes the location of ICH, intraventricular bleed, hydrocephalus, early signs of herniation, lesional oedema, and midline shift. ICH volume, a strong predictor of outcome can also be estimated. Brain MRI can help in identifying the exact neuroanatomic site as well as the aetiology [66]. Other investigations are same as for ischaemic stroke.

This occurs in the first few days after intracerebral haemorrhage. It is significantly associated with hematoma expansion, increased intracranial pressure, mass effect, midline shift and brain herniation leading to poor functional outcome of ICH [67–69]. Agents that can reduce peri-haematomal oedema process provide protective effects for ICH. These include the use of osmotic diuretics such as Mannitol. Hypertonic saline can also be used. An earlier retrospective study

hours after onset has been reported due to haematoma expansion [64].

able and validated for rapid evaluation of ICH severity [63].

Airway management is similar to that of acute ischaemic stroke.

These are common in ICH occurring in up to 16% of the cases in the first week with most occurring at onset [72]. Lobar haematomas carry an increased risk of seizures than deep ICH [73]. A recent AHA/ASA guideline for management of spontaneous ICH recommend the use of antiepileptic drugs only in patients with clinical seizures and those with depressed mental status found to have electrographic seizures on EEG [74]. Drugs that have been used include intravenous Lorazepam (0.05–0.1 mg/kg), fosphenytoin (or Phenytoin 15-20 mg/kg), and valproic acid (15-45 mg/kg).

#### *10.6.3. Hyperglycaemia*

Hyperglycaemia at presentation portends a worse outcome. This is independent of diabetes mellitus [75]. Treatment involves the use of Insulin. Hypoglycaemia should be avoided.

#### *10.6.4. Deep vein thrombosis*

Symptomatic deep vein thrombosis occurs in 1–5% of patients with ICH with pulmonary embolism occurring in about 0.5–2% of such cases. It is therefore crucial to prevent both DVT and PE [76]. Prophylaxis for DVT includes the use of intermittent pneumatic compression devices (IPC) or compression stockings if IPC devices are not available. Subcutaneous lowdose unfractionated heparin can be used when the intracranial bleeding has been controlled within 48 hours of the admission [74].

#### *10.6.5. Blood pressure*

Lowering of blood pressure in the setting of ICH has been frequently practiced to reduce haematoma growth. However, the association between elevated BP and hematoma expansion remains controversial. An increasing blood pressure has been associated with haematoma expansion. The AHA/ASA guidelines recommend mean arterial Pressure of 130 mmHg. Titratable antihypertensive drugs such as Intravenous Labetalol (10–20 mg IV bolus, can be repeated up to max of 60 mg) and Nicardipine (5 mg/h up to 15 mg/h) are often used in acute ICH. Nitroprusside should be avoided because of its tendency to increase ICP.

#### *10.6.6. Fever*

This is a frequent occurrence in patients with ICH especially in those with intraventricular extension. Patients with persistent fever after ICH tend to have a worse prognosis [77].

#### *10.6.7. Haemostatic therapy*

The outcome of ICH is made worse by coagulopathy as this causes expansion of haematoma. Coagulopathy should therefore be reversed. Intravenous Vitamin K 10 mg and fresh frozen plasma 20 ml/kg can be given to patients with Warfarin related ICH. Alternatives to fresh frozen plasma include prothrombin complex concentrate and activated factor VII (Novoseven) [78]. Although recombinant factor VIIa was shown to be efficacious in reducing haematoma growth in phase II trial, it failed to demonstrate consistency in efficacy in subsequent trials. It is often used in patients with ICH associated haemophilia.

Stroke rehabilitation usually commences during the acute hospitalization when the patient has been stabilized medically and neurologically. The major concern in the acute phase are prevention of a recurrent stroke, prevention of complications, mobilizing the patient, promoting resumption of activities of daily living as well as providing emotional support to the patient and family. Thereafter the focus shifts to evaluation and recovery of any residual

Emergency Management of Acute Ischaemic Stroke http://dx.doi.org/10.5772/intechopen.75305 241

A patient with stroke is at risk of developing joint and muscle contractures. The reasons for this are multifactorial and include hemiparesis, impaired sensation, reduced level of consciousness, older age, incontinence and pressures sores. Early rehabilitation can reduce the

Recent advances in neuroimaging, organized stroke care, dedicated Neuro-ICUs, medical and surgical management have changed the management of ICH. Early airway protection, blood pressure control, rapid reversal of coagulopathy and surgical intervention may increase the

[1] Hill MD, Liebeskind DS, Roberts S. Case fatality rates after hospital admission for stroke.

[2] Jones MR, Horner RD, Edwards LJ, Hoff J, Armstrong SB, Smith-Hammond CA, et al.

[4] Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: A review of population-based studies of incidence, prevalence, and case fatality in the late 20th cen-

[5] Welch KMA. Statins for the prevention cerebrovascular disease: The rationale for robust

[6] Bath PM, Lees KR.ABC of arterial and venous disease: Acute stroke. BMJ. 2000;**320**:920-923

[3] Gillum RF. Stroke mortality in blacks: Disturbing trends. Stroke. 1999;**30**:1711-1715

Racial variation in initial stroke severity. Stroke. 2000;**31**:563-567

intervention. European Heart Journal Supplements. 2004;**s6**:c34-c42

physical and cognitive deficits [90].

chance of survival for patients with severe ICH.

Address all correspondence to: nneninge@yahoo.com

University of Calabar Teaching Hospital, Calabar, Nigeria

contractures.

**10.8. Conclusion**

**Author details**

**References**

Ekanem Philip-Ephraim

BMJ. 2003;**326**:1085-1086

tury. Lancet Neurology. 2003;**2**:43-53

#### *10.6.8. Intraventricular haemorrhage and hydrocephalus*

About 45% of patients with intracerebral haemorrhage (ICH) develop intraventricular haemorrhage (IVH). ICH often predicts a poor outcome. There are two types of IVH; the primary –confined to the ventricles and secondary due to extension of an ICH. Secondary IVH is the commonest and is related to haemorrhages from hypertension involving the basal ganglia and the thalamus [79]. Treatment involves the use of intraventricular administration of rt-PA or urokinase. This was found to reduce mortality and morbidity by increasing blood clearance and clot lysis [80]. Unfortunately, the procedure was not without the risk of intracranial bleeding [81]. Other treatment options included an endoscopic surgical evacuation and ventriculostomy, ventriculoperitoneal shunting or lumbar drainage for hydrocephalus [82–84].

#### *10.6.9. Surgical intervention*

Controversies exist over the role of surgical haematoma evacuation. The International Surgical Trial in Intracerebral haemorrhage (ISTICH) and subsequent STICH 11 demonstrated no improvement for early haematoma evacuation in patients with supratentorial ICH [85, 86]. However in subgroup analysis, patients with superficial haematomas were more prone to a favourable outcome when managed surgically compared to deep ICH. In contrast to supratentorial haematomas, cerebellar ICH is a neurosurgical emergency requiring urgent evacuation as rapid deterioration can occur in the first 24 hours of onset. Indications for surgical intervention include haemorrhages greater than 3 cm and those with brainstem compression or hydrocephalus [87].

#### **10.7. Stroke recovery and rehabilitation**

Advancement in the treatment of acute stroke and the establishment of dedicated stroke units has led to an increase in the survival of stroke patients. Many of the survivors experience persistent difficulty in their activities of daily living. Moderate functional impairment has been observed in 40% of stroke patients with about 15–30% having severe disability [88]. Early initiation of effective rehabilitation post stroke has been found to enhance recovery process and minimize functional disability. Stroke rehabilitation is therefore crucial for recovery post stroke.

The services of rehabilitation involve a multidisciplinary approach comprising healthcare providers with training in neurology, rehabilitation nursing, physical therapy, occupational therapy and speech and language therapy. Other health professionals who play key roles in rehabilitation include social workers, psychologists, psychiatrists and counselors [89].

Stroke rehabilitation usually commences during the acute hospitalization when the patient has been stabilized medically and neurologically. The major concern in the acute phase are prevention of a recurrent stroke, prevention of complications, mobilizing the patient, promoting resumption of activities of daily living as well as providing emotional support to the patient and family. Thereafter the focus shifts to evaluation and recovery of any residual physical and cognitive deficits [90].

A patient with stroke is at risk of developing joint and muscle contractures. The reasons for this are multifactorial and include hemiparesis, impaired sensation, reduced level of consciousness, older age, incontinence and pressures sores. Early rehabilitation can reduce the contractures.

#### **10.8. Conclusion**

*10.6.7. Haemostatic therapy*

240 Essentials of Accident and Emergency Medicine

*10.6.9. Surgical intervention*

**10.7. Stroke recovery and rehabilitation**

is often used in patients with ICH associated haemophilia.

*10.6.8. Intraventricular haemorrhage and hydrocephalus*

The outcome of ICH is made worse by coagulopathy as this causes expansion of haematoma. Coagulopathy should therefore be reversed. Intravenous Vitamin K 10 mg and fresh frozen plasma 20 ml/kg can be given to patients with Warfarin related ICH. Alternatives to fresh frozen plasma include prothrombin complex concentrate and activated factor VII (Novoseven) [78]. Although recombinant factor VIIa was shown to be efficacious in reducing haematoma growth in phase II trial, it failed to demonstrate consistency in efficacy in subsequent trials. It

About 45% of patients with intracerebral haemorrhage (ICH) develop intraventricular haemorrhage (IVH). ICH often predicts a poor outcome. There are two types of IVH; the primary –confined to the ventricles and secondary due to extension of an ICH. Secondary IVH is the commonest and is related to haemorrhages from hypertension involving the basal ganglia and the thalamus [79]. Treatment involves the use of intraventricular administration of rt-PA or urokinase. This was found to reduce mortality and morbidity by increasing blood clearance and clot lysis [80]. Unfortunately, the procedure was not without the risk of intracranial bleeding [81]. Other treatment options included an endoscopic surgical evacuation and ventriculostomy, ventriculoperitoneal shunting or lumbar drainage for hydrocephalus [82–84].

Controversies exist over the role of surgical haematoma evacuation. The International Surgical Trial in Intracerebral haemorrhage (ISTICH) and subsequent STICH 11 demonstrated no improvement for early haematoma evacuation in patients with supratentorial ICH [85, 86]. However in subgroup analysis, patients with superficial haematomas were more prone to a favourable outcome when managed surgically compared to deep ICH. In contrast to supratentorial haematomas, cerebellar ICH is a neurosurgical emergency requiring urgent evacuation as rapid deterioration can occur in the first 24 hours of onset. Indications for surgical intervention include haemorrhages greater than 3 cm and those with brainstem compression or hydrocephalus [87].

Advancement in the treatment of acute stroke and the establishment of dedicated stroke units has led to an increase in the survival of stroke patients. Many of the survivors experience persistent difficulty in their activities of daily living. Moderate functional impairment has been observed in 40% of stroke patients with about 15–30% having severe disability [88]. Early initiation of effective rehabilitation post stroke has been found to enhance recovery process and minimize functional disability. Stroke rehabilitation is therefore crucial for recovery post stroke.

The services of rehabilitation involve a multidisciplinary approach comprising healthcare providers with training in neurology, rehabilitation nursing, physical therapy, occupational therapy and speech and language therapy. Other health professionals who play key roles in

rehabilitation include social workers, psychologists, psychiatrists and counselors [89].

Recent advances in neuroimaging, organized stroke care, dedicated Neuro-ICUs, medical and surgical management have changed the management of ICH. Early airway protection, blood pressure control, rapid reversal of coagulopathy and surgical intervention may increase the chance of survival for patients with severe ICH.
