Lobar intracerebral hemorrhage
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Lobar intracerebral hemorrhage is a subtype of intracerebral hemorrhage defined by their location in the peripheral cerebral hemispheres. Compared to deep intracerebral hemorrhages (involving the deep grey nuclei or brainstem), lobar hemorrhages are less likely to be related to hypertension and more likely to be due to cerebral amyloid angiopathy or trauma. This article concerns spontaneous (non-traumatic) lobar intracerebral hemorrhages.
Primary lobar hemorrhage accounts for approximately 3.9% of acute strokes and 35% of intracerebral hemorrhages 1.
Cerebral amyloid angiopathy is a major risk factor for lobar hemorrhage, with estimates that over 20% of lobar hemorrhages were due to cerebral amyloid angiopathy (majority of which are seen in elderly patients). Hypertension, diabetes, smoking, short stature, dyslipidemia, and anticoagulant use are also significantly associated with primary intracerebral hemorrhage.
Younger patients may also develop lobar hemorrhages, but in such cases there is usually an underlying lesion (e.g. cerebral arteriovenous malformation) 2,8.
Clinical presentation will vary depending on the site and size of the hemorrhage.
headache and vomiting are the most common symptoms at initial presentation
focal neurological deficits
seizure can also occur during the onset of the lobar hemorrhage (focal or generalized with a brief duration)
delirium is increasingly being recognized as a common finding and can be the initial presenting illness
loss of consciousness or a decrease in GCS
Often the cause of a lobar hemorrhage is never established and the causes, when found, are varied including 9,10:
secondary to drug use (e.g. cocaine, amphetamines)
bleeding disorders or coagulopathies
anticoagulation - therapeutic or supratherapeutic levels
One of the strongest predictors of an underlying vascular lesion is the patient's age 11. The younger a patient, the more likely there is an identifiable cause: CT angiography found causes for hemorrhage in 47% of patients aged 18-45 years, 15% aged 46-70 years, and 4% aged 71-94 11.
Overall features of the hemorrhage that suggest an underlying secondary cause are 12:
internal density heterogeneity
highly irregular margin
internal hematocrit level
extensive surrounding vasogenic edema
extensive subarachnoid hemorrhage
CT is usually the modality first obtained when evaluating a suspected lobar hemorrhage. Noncontrast enhanced CT typically demonstrates a hyperdense collection of blood, located superficially within the lobes of the brain (i.e. not in the basal ganglia).
The hemorrhages can vary in size from only a centimeter or so (often asymptomatic) to larger hematomas where there may be extension into subdural, subarachnoid and even the intraventricular space (intraventricular extension being more common in basal ganglia hemorrhages). The ABC/2 formula gives reliable estimation of the intracerebral hematoma volume.
There are many predictors of hematoma expansion potentially evident on CT, which are discussed in depth in the main intracerebral hemorrhage article.
CTA is increasingly being used in the initial workup, not only to assess for an underlying abnormality such as arteriovenous malformations, vasospasm, and aneurysmal disease, but also to evaluate for the presence of ongoing bleed.
The CTA spot sign, characterized by a defined "spot" or foci, is a radiographic sign indicative of ongoing bleeding. The presence of the spot sign correlates with growth of the hemorrhage in the first few hours following the scan and is associated with a poorer prognosis 2,3.
Recent studies have demonstrated the presence of the spot sign on dynamic-enhancement CT (DECT or CT perfusion) to be an even stronger predictor of hematoma expansion 4,5, i.e. the most robust factor in predicting outcome 8.
MRI is usually obtained when concern exists that the bleed is from an underlying vascular malformation or neoplasm. Findings depend on the size and age of the bleed (see aging blood on MRI).
In cases of primary lobar hemorrhage, multiple small areas of susceptibility-induced signal drop-out may be evident on gradient echo (GRE) or susceptibility weighted (SWI) sequences, in-keeping with previous cerebral microhemorrhages, suggestive of cerebral amyloid angiopathy.
The presence of single lobar hemorrhage is still part of the Boston criteria for CAA.
Treatment and prognosis
Treatment depends on the age of the patient and the size or location of the hematoma. Medical management is the mainstay, typically treating the suspected underlying precipitant.
Management of raised intracranial pressure is similar to that of other conditions. Recommendations of supportive measures and lowering of systolic blood pressure have evidence in preventing further bleeding.
In cases of anticoagulation, cessation and reversal where applicable of the the anticoagulant is warranted, e.g. warfarin discontinuation and rapid reversal. With hematoma growth in an acute hemorrhage, there is moderate evidence of early hemostatic therapy to prevent early and subsequent growth. In situations where the hemorrhage is thought to be derived from inherited or acquired hemophilias i.e. hemophilia A, some studies recommend treatment with recombinant activated factor VIII.
Neurosurgical intervention currently has mixed evidence in patients with lobar intracerebral hemorrhage. One randomized trial (STITCH II) suggests early surgical therapy does not increase the rate of death or disability at six months 13. Nevertheless, there may be a slight but clinically relevant survival advantage for patients with spontaneous lobar intracerebral hemorrhage without intraventricular hemorrhage. More recent evidence, such as the ENRICH trial, offer more promising outcomes, demonstrating better functional outcomes for early and minimally invasive removal of intracerebral hemorrhages, specifically lobar hemorrhages 14.
The term lobar hemorrhage is often used to denote a primary hemorrhage. As such the differential includes:
an underlying vascular malformation (e.g. cerebral arteriovenous malformation)
hemorrhagic transformation of the venous infarct