656
Intracerebral
haemorrhage
LOUIS R. CAPLAN intracerebral haemorrhage (ICH) describes into brain parenchyma with formation of a focal bleeding haematoma. ICH accounts for about 10% of all strokes and is slightly more common among US blacks and individuals of Chinese and Japanese ancestry. The
term
Aetiology Most haematomas are attributed to chronic or acute arterial hypertension. Bleeding may be due to rupture of arteries damaged by chronic hypertension. Long-term increases in blood pressure may also lead to infiltration of the walls of penetrating arteries by lipid and hyaline material (lipohyalinosis) and microaneurysmal outpouchings (Charcot-Bouchard aneurysms).1 However, surgical and necropsy specimens of acute ICH usually show breakage of penetrating arteries that have no aneurysmal changes. Moreover, about 50% of patients with spontaneous ICH give no past history of hypertension and have no retinal, cardiac, or renal evidence of hypertensive changes. Most do have raised blood pressure on arrival at hospital with ICH. Circumstances associated with acute rises in blood pressure or cranial blood flow can provoke ICH in locations typically associated with hypertension;2examples include use of amphetamines and cocaine, exposure to extreme cold, trigeminal nerve stimulation, post carotid endarterectomy, post heart transplantation, and post correction of congenital heart lesions. Vasadar malformations, notably arteriovenous and cavernous angiomas, are a common cause of ICH, especially in young normotensive individuals. These lesions often abut on ependymal or pial surfaces or involve the choroid plexus. Cavernous angiomas tend to be multiple and can be familial. Seizures and headaches commonly antedate haemorrhage. Traumatic haematomas are usually multiple and abut on the basal brain surfaces, especially of the orbital frontal and medial and inferior temporal lobes. A haematoma may become visible with computed tomography (CT) only days after the injury ("spat apoplexy") because of delayed bleeding into an area of injured blood vessels. Bleeding diatheses are often associated with multiple foci of haemorrhage in the brain and systemic bleeding; warfarin treatment now accounts for most of these haematomas and is associated with slowly evolving lobar or cerebellar haematomas with high fatality rates.4 Thrombocytopenia, leukaemia, and haemophilia are usually apparent before ICH develops. Amyloid angiopathy accounts for up to a third of haematomas in elderly patients. Small arteries in the cerebral white matter and subarachnoid space, which are fragile because of congophilic amyloid material infiltrating their walls, break and cause lobar haematomas that are often multiple. Episodes of subarachnoid bleeding, and dementia of the Alzheimer type or multi-infarct dementia are common in patients with amyloid angiopathy. Occasionally haematomas develop in regions reperfused after brain infarction or after systemic administration of fibrinolytic agents. Dural sinus occlusion, and bleeding into primary and metastatic brain tumours account for a few haematomas. Aneurysmal rupture usually leads to subarachnoid haemorrhage but the blood can track into both the brain and the spinal fluid. These meningocerebral
haemorrhages are located near the base of the brain in sites typical of berry aneurysms.7
Pathogenesis and general signs and symptoms Breakage of capillaries, arterioles, and small arteries leads to extravasation of blood into brain parenchyma. The haematoma causes an increase in pressure locally, which then leads to disruption of surrounding capillaries. Consequently, the haematoma enlarges on its outer circumference like a rolling snowbal1.1 Increased systemic blood pressure and decreased blood coagulability foster enlargement whereas increased tissue pressure favours containment. Haematomas often dissect along fibre tract pathways. The expanding haematoma may decompress itself by dissecting into a ventricle or into the spinal fluid on the brain surface. Symptoms and signs often begin while patients are physically active and relate to the function of the parenchymal site of bleeding.8 Thus, in putaminal haemorrhage there might be weakness and/or numbness of the opposite limbs, whereas in cerebellar haemorrhage ataxia is often the earliest feature. The neurological symptoms and signs gradually increase over seconds or minutes, or rarely hours. Weakness in one limb might spread to the face and other limb on the same side of the body, and hemiplegia and hemisensory loss might develop, ataxia could worsen, making walking impossible. If the haematoma remains small, no other signs develop. If the ICH becomes large with increased intracranial pressure, there will be headache, vomiting, and decreased level of consciousness. Seizures are also common in patients with subcortical haematomas.
Neurological signs in relation to location of haematomas As shown in the table, the commonest sites of hypertensive ICH are lateral ganglionic (putamen and internal capsule), caudate nucleus; thalamus ; cerebral lobes; pons; and cerebellum. These areas are supplied by penetrating branches of the anterior, middle, and posterior cerebral arteries and the basilar artery. Motor signs, pupillary responses, and oculomotor functions vary according to the site of the haematoma.8 Lateral ganglianic ICH usually causes contralateral hemiparesis, hemisensory loss, and ipsilateral conjugate eye deviation. Pupillary responses are normal. Large lesions that cause pressure shifts and an ipsilateral dilated or non-reactive pupil or a bilateral conjugate gaze palsy have a poor prognosis. Haematomas in the middle portion of the putamen affecting the genu of the internal capsule cause persistent hemiparesis whereas more anteriorly placed haematomas cause less severe and less persistent motor signs. Posterior putaminal lesions may cause hemisensory loss and aphasia (left putamen) or visual neglect of left hemispace (right putamen). Caudate nucleus haemorrhages lead to changes in ADDRESS: Department of Neurology, Tufts University, 750 Washington Street, NEMCH 314, Boston, Massachusetts 02111, USA (Prof L. R. Caplan, MD).
657
LOCATION OF INTRACEREBRAL HAEMORRHAGE BY CAUSE
cognition and behaviour such as apathy and aboulia (lack of will power), restless agitation, and poor memory. Dissection of the haematoma posterolaterally to the internal capsule will lead to hemiparesis. Thalamic haemorrhages usually cause a contralateral hemisensory loss and ataxia with only minor motor weakness. The pupils are often small and react poorly to light. Oculomotor abnormalities include loss of vertical gaze, especially upwards, deviation of eyes down and in at rest, hyperadduction of one or both eyes with poor abduction (pseudo-VIth palsy), and conjugate eye deviation to the side opposite the haemorrhage or ipsilateral deviation. Behavioural abnormalities are common and include diminished alertness, somnolence, apathy, amnesia, and decreased ability to make new memories; aphasia and visual neglect are often found. Some thalamic haematomas are small and limited to the anterolateral, ventrolateral, posterior, and dorsal regions of the thalamus. Involvement of the medial thalamic structures is associated with behavioural abnormalities and pupillary and oculomotor signs whereas ventrolateral haemotomas cause mostly sensory and ataxic abnormalities. In lobar haematomas, signs depend on the lobe: occipital lesions cause hemianopia; frontal haematomas lead to behavioural and motor signs; parietal haematomas are accompanied by sensory, cognitive, and behavioural abnormalities and visual neglect; and temporal lobe ICH causes aphasia, agitation, and
hemianopia. Large pontine haematomas involve the paramedian tegmento-basal junction and often spread into the tegmentum and IVth ventricle and extend rostrally towards the midbrain. There will be quadriplegia, coma, small reactive pupils, and bilateral paralysis of horizontal conjugate gaze. Spontaneous downward eye movements (ocular bobbing) indicate preservation of rostral brainstem vertical gaze centres. These large central pontine haematomas are fatal or devastating. Smaller unilateral basal pontine haematomas cause a contralateral hemiparesis, often with some ataxia in the weak limbs. Lateral tegmental pontine haematomas cause contralateral hemisensory loss, ipsilateral conjugate gaze palsy, and sometimes an ipsilateral internuclear ophthalmoplegia. Ataxia is present and may be bilateral or either ipsilateral or contralateral to the haematoma. Cerebellar ICH usually involves the dentate nucleus region and less often the vermis. The cardinal findings are an inability to walk, leaning or veering to one side, dizziness, and vomiting. The ipsilateral pupil may be smaller and there may be an ipsilateral VIth nerve or conjugate gaze palsy. Intraventricular haemorrhage usually causes headache, vomiting, decreased level of consciousness, and bilateral extensor plantar responses. Sometimes there are asymmetrical motor, visual, or sensory abnormalities. The table shows the common sites of ICH according to aetiology.
Diagnosis ICH should be suspected when an individual with risk factors for bleeding—eg, hypertension, bleeding diathesis, anticoagulant treatment, or cocaine use-manifests focal neurological signs over a few minutes without preceding warning attacks. Signs of increased intracranial pressure such as headache, vomiting, and decreased level of consciousness favour the diagnosis. ICH should be confirmed by neuroimaging. CT not only defines the size, location, and site of the haematoma but also provides information about extension into the ventricular system, presence of surrounding oedema, and shifts in brain contents. Acute haematomas are very well defined on CT and have smooth borders. In patients who worsen abruptly, repeat CT may show enlargement of the ICH. Haematomas often dissect along white matter pathways. Findings with magnetic resonance imaging (MRI) depend on the timing of the investigation. Very recent haematomas may show only slight hypointensity (black) on Tl weighted images and hyperintensity (white) on T2 weighted images. By 72 hours, there will be hyperintensity on Tl and hypointensity on T2 weighted images. After 1 week, both Tl and T2 weighted images show focal hyperintensity (white) at the site of the haematoma. Years after the ICH, the cavity collapses to form a slit-like defect. MRI can help differentiate these old slit haemorrhages from old bland infarcts by showing haemosiderin within the walls of the haematoma. Old haematomas and haemorrhagic infarcts can be separated only by the site and shape of the lesions. MRI may also display heterogeneous images characteristic of angiomas or vascular malformations. Angiography is usually indicated in normotensive patients with white matter, subcortical, and superficial haematomas to reveal underlying vascular malformations and aneurysms. Angiography is especially important in patients with cocaine-related ICH since they often have vascular abnormalities. Coagulation studies should be carried out, especially if there is evidence of a present or past bleeding tendency.
Prognosis Outcome largely depends on four factors: (a) location of the haematoma; (b) size of the haematoma; (c) level of consciousness on admission; and (d) later progression of neurological signs and development of increased intracranial pressure.9 In general, pontine, thalamic, and lateral ganglionic haematomas have the highest fatality rates and most often leave severe neurological disabilities. Haematomas over 2 cm in diameter on a CT slice are more often associated with increased intracranial pressure, and haematomas over 4 cm in diameter are usually fatal unless decompressed. In all studies, patients’ level of consciousness on admission was the most important clinical determinant of survival. Stupor or coma indicates either direct involvement of the brainstem reticular activating system bilaterally in the brainstem tegmentum (usually paramedian pons or thalamus) or increased intracranial pressure with shifts in brain contents or frank herniation. Stupor or coma is a grim prognostic sign except in patients with thalamic haemorrhage. Clinical deterioration characterised by increase in focal neurological signs or decrease in level of alertness is likewise associated with a poor outcome. Serious deterioration warrants urgent treatment unless the neurological deficit is so severe that survival would only be compatible with a vegetative state. The outlook for improvement in neurological deficits is better for ICH
658
patients than for those with
infarcts of similar size.
Haematomas separate and disconnect normal brain tissues whereas infarcts cause tissue destruction. Recurrence
depends on aetiology. Haemorrhages due to amyloid angiopathy and arteriovenous malformations usually recur; by contrast, patients with hypertensive haemorrhages seldom rebleed if their blood pressure is well controlled.
Treatment Warfarin anticoagulation should be reversed quickly with vitamin K or fresh frozen plasma. Other bleeding diatheses should be treated specifically when possible. Blood pressure mm Hg should be lowered when it is very high (> 170 systolic) and I favour labetalol for this purpose, but hypoperfusion should be avoided. Frequent monitoring of the state of alertness and neurological signs provides a better index of brain perfusion than do measures of arterial pressure. Small haematomas heal well without additional medical measures except blood pressure control after hospital discharge. Very large haematomas cause devastating neurological deficits, usually before patients can be treated effectively. Patients with medium-sized haematomas (2-4 cm in largest diameter on a CT slice) are most likely to benefit from treatment. Open surgical drainage is possible in patients with medium-sized haematomas located in the cerebral lobes, cerebellum, and right putamen. Surgery should be considered if there are signs of increased intracranial pressure, and especially if the patient’s overall condition is worsening.7 Medical decompression by use of intubation with forced
hyperventilation, mannitol or glycerol, and corticosteroids is often useful in reducing increased intracranial pressure. Intracranial pressure can be monitored by a gauge or other measuring device. Sequential CT scans can show pressure shifts and the status of the haematoma and surrounding oedema. Haematomas are easier to drain acutely before they solidify. Stereotactic haematoma drainage guided by CT or MRI, sometimes with instillation of fibrinolytic agents to liquefy the haematoma, is being studied. Patients with angiomas or with vascular malformations that have bled causing an ICH are candidates for surgery, radiotherapy, or interventional neuroradiological treatment to obliterate the lesions. These treatments are generally best initiated after resolution of the haematoma, unless surgical drainage is required. REFERENCES 1. Fischer CM. 2.
Pathological observations in hypertensive cerebral hemorrhages. J Neuropathol Exp Neurol 1971; 30: 536-50. Caplan LR. Intracerebral hemorrhage revisited. Neurology 1988; 38:
624-27. 3. Levine SR, Welch KMA. Cocaine and stroke. Stroke 1988; 19: 779-83. 4. Kase CS, Robinson K, Stein R, et al. Anticoagulant-related intracerebral hemorrhage. Neurology 1985; 35: 943-48. 5. Gilbert J, Vinters H. Cerebral amyloid angiopathy: incidence and complications in the aging brain, I: cerebral hemorrhage. Stroke 1983; 14: 915-23. 6. Kase CS. Intracerebral hemorrhage: non-hypertensive causes. Stroke 1986; 17: 590-94. 7. Ojemann R, Heros R. Spontaneous brain hemorrhage. Stroke 1983; 14: 468-74. 8. Feldmann E. Intracerebral hemorrhage. Stroke 1991; 22: 684-91. 9. Tuhrim S, Dambrosia JM, Price TR, et al. Prediction of intracerebral hemorrhage survival. Ann Neurol 1988; 24: 258-63.
CLINICAL PRACTICE
Investigation of selected patients with hypertension by the rapid-sequence intravenous urogram
The rapid-sequence intravenous urogram (IVU) has tended to fall from favour for investigating hypertension because of its perceived imprecision for detecting renovascular disease. However, no study has examined the value of the IVU as a screening test in appropriately selected patients. We have analysed the diagnostic yield of the rapid-sequence IVU in hypertensive patients selected for features suggesting renal or renovascular disease in a retrospective review of case records from a hypertension clinic. The IVU was abnormal in 27% (95% Cl 21-32%) of 241 consecutive patients. The most common abnormalities were chronic pyelonephritis (6%); proven renovascular disease (5%); stone (4%); possible renovascular disease and simple cyst (each 3%); hydronephrosis (2%); and tumour and active tuberculosis (each 1%). The IVU led to intervention aiming to correct hypertension in 5% (95% Cl 2-8%) of patients, and revealed an abnormality needing intervention in its own right in 4% (95% Cl 2-6%). The IVU led to unnecessary
invasive investigation in 3% of cases. Individual abnormalities could not be predicted from the clinical or laboratory features. The initial investigation in hypertensive patients with suspected renal or renovascular disease should be a general purpose test able to detect a wide range of abnormalities. The rapid-sequence IVU is the only single test capable of satisfying this requirement. In patients with features suggesting renovascular disease, a normal rapid-sequence IVU excludes renovascular disease with 93% probability, but is an imperfect screening test since it fails to diagnose about 20% of cases. Renal arteriography should be done despite a normal IVU when it is essential to exclude renovascular disease.
ADDRESS.
University Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK (H. A. Cameron, MRCP, C. F. Close, MRCP, W. W Yeo, MRCP, P. R. Jackson, MRCP, L. E. Ramsay, FRCP) Correspondence to Professor L. E Ramsay
Intracerebral
haemorrhage
LOUIS R. CAPLAN intracerebral haemorrhage (ICH) describes into brain parenchyma with formation of a focal bleeding haematoma. ICH accounts for about 10% of all strokes and is slightly more common among US blacks and individuals of Chinese and Japanese ancestry. The
term
Aetiology Most haematomas are attributed to chronic or acute arterial hypertension. Bleeding may be due to rupture of arteries damaged by chronic hypertension. Long-term increases in blood pressure may also lead to infiltration of the walls of penetrating arteries by lipid and hyaline material (lipohyalinosis) and microaneurysmal outpouchings (Charcot-Bouchard aneurysms).1 However, surgical and necropsy specimens of acute ICH usually show breakage of penetrating arteries that have no aneurysmal changes. Moreover, about 50% of patients with spontaneous ICH give no past history of hypertension and have no retinal, cardiac, or renal evidence of hypertensive changes. Most do have raised blood pressure on arrival at hospital with ICH. Circumstances associated with acute rises in blood pressure or cranial blood flow can provoke ICH in locations typically associated with hypertension;2examples include use of amphetamines and cocaine, exposure to extreme cold, trigeminal nerve stimulation, post carotid endarterectomy, post heart transplantation, and post correction of congenital heart lesions. Vasadar malformations, notably arteriovenous and cavernous angiomas, are a common cause of ICH, especially in young normotensive individuals. These lesions often abut on ependymal or pial surfaces or involve the choroid plexus. Cavernous angiomas tend to be multiple and can be familial. Seizures and headaches commonly antedate haemorrhage. Traumatic haematomas are usually multiple and abut on the basal brain surfaces, especially of the orbital frontal and medial and inferior temporal lobes. A haematoma may become visible with computed tomography (CT) only days after the injury ("spat apoplexy") because of delayed bleeding into an area of injured blood vessels. Bleeding diatheses are often associated with multiple foci of haemorrhage in the brain and systemic bleeding; warfarin treatment now accounts for most of these haematomas and is associated with slowly evolving lobar or cerebellar haematomas with high fatality rates.4 Thrombocytopenia, leukaemia, and haemophilia are usually apparent before ICH develops. Amyloid angiopathy accounts for up to a third of haematomas in elderly patients. Small arteries in the cerebral white matter and subarachnoid space, which are fragile because of congophilic amyloid material infiltrating their walls, break and cause lobar haematomas that are often multiple. Episodes of subarachnoid bleeding, and dementia of the Alzheimer type or multi-infarct dementia are common in patients with amyloid angiopathy. Occasionally haematomas develop in regions reperfused after brain infarction or after systemic administration of fibrinolytic agents. Dural sinus occlusion, and bleeding into primary and metastatic brain tumours account for a few haematomas. Aneurysmal rupture usually leads to subarachnoid haemorrhage but the blood can track into both the brain and the spinal fluid. These meningocerebral
haemorrhages are located near the base of the brain in sites typical of berry aneurysms.7
Pathogenesis and general signs and symptoms Breakage of capillaries, arterioles, and small arteries leads to extravasation of blood into brain parenchyma. The haematoma causes an increase in pressure locally, which then leads to disruption of surrounding capillaries. Consequently, the haematoma enlarges on its outer circumference like a rolling snowbal1.1 Increased systemic blood pressure and decreased blood coagulability foster enlargement whereas increased tissue pressure favours containment. Haematomas often dissect along fibre tract pathways. The expanding haematoma may decompress itself by dissecting into a ventricle or into the spinal fluid on the brain surface. Symptoms and signs often begin while patients are physically active and relate to the function of the parenchymal site of bleeding.8 Thus, in putaminal haemorrhage there might be weakness and/or numbness of the opposite limbs, whereas in cerebellar haemorrhage ataxia is often the earliest feature. The neurological symptoms and signs gradually increase over seconds or minutes, or rarely hours. Weakness in one limb might spread to the face and other limb on the same side of the body, and hemiplegia and hemisensory loss might develop, ataxia could worsen, making walking impossible. If the haematoma remains small, no other signs develop. If the ICH becomes large with increased intracranial pressure, there will be headache, vomiting, and decreased level of consciousness. Seizures are also common in patients with subcortical haematomas.
Neurological signs in relation to location of haematomas As shown in the table, the commonest sites of hypertensive ICH are lateral ganglionic (putamen and internal capsule), caudate nucleus; thalamus ; cerebral lobes; pons; and cerebellum. These areas are supplied by penetrating branches of the anterior, middle, and posterior cerebral arteries and the basilar artery. Motor signs, pupillary responses, and oculomotor functions vary according to the site of the haematoma.8 Lateral ganglianic ICH usually causes contralateral hemiparesis, hemisensory loss, and ipsilateral conjugate eye deviation. Pupillary responses are normal. Large lesions that cause pressure shifts and an ipsilateral dilated or non-reactive pupil or a bilateral conjugate gaze palsy have a poor prognosis. Haematomas in the middle portion of the putamen affecting the genu of the internal capsule cause persistent hemiparesis whereas more anteriorly placed haematomas cause less severe and less persistent motor signs. Posterior putaminal lesions may cause hemisensory loss and aphasia (left putamen) or visual neglect of left hemispace (right putamen). Caudate nucleus haemorrhages lead to changes in ADDRESS: Department of Neurology, Tufts University, 750 Washington Street, NEMCH 314, Boston, Massachusetts 02111, USA (Prof L. R. Caplan, MD).
657
LOCATION OF INTRACEREBRAL HAEMORRHAGE BY CAUSE
cognition and behaviour such as apathy and aboulia (lack of will power), restless agitation, and poor memory. Dissection of the haematoma posterolaterally to the internal capsule will lead to hemiparesis. Thalamic haemorrhages usually cause a contralateral hemisensory loss and ataxia with only minor motor weakness. The pupils are often small and react poorly to light. Oculomotor abnormalities include loss of vertical gaze, especially upwards, deviation of eyes down and in at rest, hyperadduction of one or both eyes with poor abduction (pseudo-VIth palsy), and conjugate eye deviation to the side opposite the haemorrhage or ipsilateral deviation. Behavioural abnormalities are common and include diminished alertness, somnolence, apathy, amnesia, and decreased ability to make new memories; aphasia and visual neglect are often found. Some thalamic haematomas are small and limited to the anterolateral, ventrolateral, posterior, and dorsal regions of the thalamus. Involvement of the medial thalamic structures is associated with behavioural abnormalities and pupillary and oculomotor signs whereas ventrolateral haemotomas cause mostly sensory and ataxic abnormalities. In lobar haematomas, signs depend on the lobe: occipital lesions cause hemianopia; frontal haematomas lead to behavioural and motor signs; parietal haematomas are accompanied by sensory, cognitive, and behavioural abnormalities and visual neglect; and temporal lobe ICH causes aphasia, agitation, and
hemianopia. Large pontine haematomas involve the paramedian tegmento-basal junction and often spread into the tegmentum and IVth ventricle and extend rostrally towards the midbrain. There will be quadriplegia, coma, small reactive pupils, and bilateral paralysis of horizontal conjugate gaze. Spontaneous downward eye movements (ocular bobbing) indicate preservation of rostral brainstem vertical gaze centres. These large central pontine haematomas are fatal or devastating. Smaller unilateral basal pontine haematomas cause a contralateral hemiparesis, often with some ataxia in the weak limbs. Lateral tegmental pontine haematomas cause contralateral hemisensory loss, ipsilateral conjugate gaze palsy, and sometimes an ipsilateral internuclear ophthalmoplegia. Ataxia is present and may be bilateral or either ipsilateral or contralateral to the haematoma. Cerebellar ICH usually involves the dentate nucleus region and less often the vermis. The cardinal findings are an inability to walk, leaning or veering to one side, dizziness, and vomiting. The ipsilateral pupil may be smaller and there may be an ipsilateral VIth nerve or conjugate gaze palsy. Intraventricular haemorrhage usually causes headache, vomiting, decreased level of consciousness, and bilateral extensor plantar responses. Sometimes there are asymmetrical motor, visual, or sensory abnormalities. The table shows the common sites of ICH according to aetiology.
Diagnosis ICH should be suspected when an individual with risk factors for bleeding—eg, hypertension, bleeding diathesis, anticoagulant treatment, or cocaine use-manifests focal neurological signs over a few minutes without preceding warning attacks. Signs of increased intracranial pressure such as headache, vomiting, and decreased level of consciousness favour the diagnosis. ICH should be confirmed by neuroimaging. CT not only defines the size, location, and site of the haematoma but also provides information about extension into the ventricular system, presence of surrounding oedema, and shifts in brain contents. Acute haematomas are very well defined on CT and have smooth borders. In patients who worsen abruptly, repeat CT may show enlargement of the ICH. Haematomas often dissect along white matter pathways. Findings with magnetic resonance imaging (MRI) depend on the timing of the investigation. Very recent haematomas may show only slight hypointensity (black) on Tl weighted images and hyperintensity (white) on T2 weighted images. By 72 hours, there will be hyperintensity on Tl and hypointensity on T2 weighted images. After 1 week, both Tl and T2 weighted images show focal hyperintensity (white) at the site of the haematoma. Years after the ICH, the cavity collapses to form a slit-like defect. MRI can help differentiate these old slit haemorrhages from old bland infarcts by showing haemosiderin within the walls of the haematoma. Old haematomas and haemorrhagic infarcts can be separated only by the site and shape of the lesions. MRI may also display heterogeneous images characteristic of angiomas or vascular malformations. Angiography is usually indicated in normotensive patients with white matter, subcortical, and superficial haematomas to reveal underlying vascular malformations and aneurysms. Angiography is especially important in patients with cocaine-related ICH since they often have vascular abnormalities. Coagulation studies should be carried out, especially if there is evidence of a present or past bleeding tendency.
Prognosis Outcome largely depends on four factors: (a) location of the haematoma; (b) size of the haematoma; (c) level of consciousness on admission; and (d) later progression of neurological signs and development of increased intracranial pressure.9 In general, pontine, thalamic, and lateral ganglionic haematomas have the highest fatality rates and most often leave severe neurological disabilities. Haematomas over 2 cm in diameter on a CT slice are more often associated with increased intracranial pressure, and haematomas over 4 cm in diameter are usually fatal unless decompressed. In all studies, patients’ level of consciousness on admission was the most important clinical determinant of survival. Stupor or coma indicates either direct involvement of the brainstem reticular activating system bilaterally in the brainstem tegmentum (usually paramedian pons or thalamus) or increased intracranial pressure with shifts in brain contents or frank herniation. Stupor or coma is a grim prognostic sign except in patients with thalamic haemorrhage. Clinical deterioration characterised by increase in focal neurological signs or decrease in level of alertness is likewise associated with a poor outcome. Serious deterioration warrants urgent treatment unless the neurological deficit is so severe that survival would only be compatible with a vegetative state. The outlook for improvement in neurological deficits is better for ICH
658
patients than for those with
infarcts of similar size.
Haematomas separate and disconnect normal brain tissues whereas infarcts cause tissue destruction. Recurrence
depends on aetiology. Haemorrhages due to amyloid angiopathy and arteriovenous malformations usually recur; by contrast, patients with hypertensive haemorrhages seldom rebleed if their blood pressure is well controlled.
Treatment Warfarin anticoagulation should be reversed quickly with vitamin K or fresh frozen plasma. Other bleeding diatheses should be treated specifically when possible. Blood pressure mm Hg should be lowered when it is very high (> 170 systolic) and I favour labetalol for this purpose, but hypoperfusion should be avoided. Frequent monitoring of the state of alertness and neurological signs provides a better index of brain perfusion than do measures of arterial pressure. Small haematomas heal well without additional medical measures except blood pressure control after hospital discharge. Very large haematomas cause devastating neurological deficits, usually before patients can be treated effectively. Patients with medium-sized haematomas (2-4 cm in largest diameter on a CT slice) are most likely to benefit from treatment. Open surgical drainage is possible in patients with medium-sized haematomas located in the cerebral lobes, cerebellum, and right putamen. Surgery should be considered if there are signs of increased intracranial pressure, and especially if the patient’s overall condition is worsening.7 Medical decompression by use of intubation with forced
hyperventilation, mannitol or glycerol, and corticosteroids is often useful in reducing increased intracranial pressure. Intracranial pressure can be monitored by a gauge or other measuring device. Sequential CT scans can show pressure shifts and the status of the haematoma and surrounding oedema. Haematomas are easier to drain acutely before they solidify. Stereotactic haematoma drainage guided by CT or MRI, sometimes with instillation of fibrinolytic agents to liquefy the haematoma, is being studied. Patients with angiomas or with vascular malformations that have bled causing an ICH are candidates for surgery, radiotherapy, or interventional neuroradiological treatment to obliterate the lesions. These treatments are generally best initiated after resolution of the haematoma, unless surgical drainage is required. REFERENCES 1. Fischer CM. 2.
Pathological observations in hypertensive cerebral hemorrhages. J Neuropathol Exp Neurol 1971; 30: 536-50. Caplan LR. Intracerebral hemorrhage revisited. Neurology 1988; 38:
624-27. 3. Levine SR, Welch KMA. Cocaine and stroke. Stroke 1988; 19: 779-83. 4. Kase CS, Robinson K, Stein R, et al. Anticoagulant-related intracerebral hemorrhage. Neurology 1985; 35: 943-48. 5. Gilbert J, Vinters H. Cerebral amyloid angiopathy: incidence and complications in the aging brain, I: cerebral hemorrhage. Stroke 1983; 14: 915-23. 6. Kase CS. Intracerebral hemorrhage: non-hypertensive causes. Stroke 1986; 17: 590-94. 7. Ojemann R, Heros R. Spontaneous brain hemorrhage. Stroke 1983; 14: 468-74. 8. Feldmann E. Intracerebral hemorrhage. Stroke 1991; 22: 684-91. 9. Tuhrim S, Dambrosia JM, Price TR, et al. Prediction of intracerebral hemorrhage survival. Ann Neurol 1988; 24: 258-63.
CLINICAL PRACTICE
Investigation of selected patients with hypertension by the rapid-sequence intravenous urogram
The rapid-sequence intravenous urogram (IVU) has tended to fall from favour for investigating hypertension because of its perceived imprecision for detecting renovascular disease. However, no study has examined the value of the IVU as a screening test in appropriately selected patients. We have analysed the diagnostic yield of the rapid-sequence IVU in hypertensive patients selected for features suggesting renal or renovascular disease in a retrospective review of case records from a hypertension clinic. The IVU was abnormal in 27% (95% Cl 21-32%) of 241 consecutive patients. The most common abnormalities were chronic pyelonephritis (6%); proven renovascular disease (5%); stone (4%); possible renovascular disease and simple cyst (each 3%); hydronephrosis (2%); and tumour and active tuberculosis (each 1%). The IVU led to intervention aiming to correct hypertension in 5% (95% Cl 2-8%) of patients, and revealed an abnormality needing intervention in its own right in 4% (95% Cl 2-6%). The IVU led to unnecessary
invasive investigation in 3% of cases. Individual abnormalities could not be predicted from the clinical or laboratory features. The initial investigation in hypertensive patients with suspected renal or renovascular disease should be a general purpose test able to detect a wide range of abnormalities. The rapid-sequence IVU is the only single test capable of satisfying this requirement. In patients with features suggesting renovascular disease, a normal rapid-sequence IVU excludes renovascular disease with 93% probability, but is an imperfect screening test since it fails to diagnose about 20% of cases. Renal arteriography should be done despite a normal IVU when it is essential to exclude renovascular disease.
ADDRESS.
University Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK (H. A. Cameron, MRCP, C. F. Close, MRCP, W. W Yeo, MRCP, P. R. Jackson, MRCP, L. E. Ramsay, FRCP) Correspondence to Professor L. E Ramsay
