SPONTANEOUS INTRACRANIAL HEMORRHAGE
A spontaneous intracerebral hematoma (SICH) is a clot that arises without immediately preceding trauma. It may be primarv 1 not due to other specific disease except indirectly as in the case of hypertension). or secondary (caused by a variety of congenital and acquired conditions). The evolution of the concepts of SICH can be gleaned from a number of sources.54.63.142.14,.1 Y.'.211'.2 I'
Interest in so-called apoplexy goes back to the dawn of written history. Apoplexy is a Greek word meaning "struck with violence as if by a thunderstorm" from which derives stroke. meaning a sudden loss of the senses with paralysis and the secondary fear it engenders.':" Indeed. there are said to be 30 reference, to sanguinous apoplexy in the Hippocratic writings.!" Gregor '\ymman ( 1594-1638) published De Apoplexia Tractus (16581. the first monograph on apoplexy. Johann Wepfer (1620-16951 published De Apoplexia (1658). a discussion on postmortem examination, that includes the first recognition of cerebral hernorrhages. Giovanni Morgagni (l682-1771) published De Sedibus 11-611 in which is found the first comprehensive clinical-pathologic correlations of SICH. Matthew Baillie (1761-1823) in his .\forbid Anatomv suggested that diseased vessels cause hemorrhages. John Abercrombie categorized apoplexy into infarction. intracerebral hemorrhage. and subarachnoid hemorrhage. Durer 118741 believed that the lenticulostriate artery was responsible for cerebral hemorrhage. Charcot and Bouchard (1868) described miliary aneurysmin hypertension. although the significance of these structure, wa-. argued for many years.54.20R Many cases of SICH in various anatomic locations were described in the late nineteenth and early twentieth centuries including hemorrhages in the cerebellum and pons.114.142.215 Westphal (1925) suggested that hypertension caused SICH. Sir Charles Symonds (1931) emphasized that intracerebral hemorrhage should be distinguished from subarachnoid hemorrhage. Russell and Cole and Yates discussed the relationships of microaneurysms to hypertension and hemorrhage. including their common distribution. 1 14 Fisher expanded this discussion and also discovered that disruption of nearby vessels contributed to the enlargement of the hemorrhage. 1 14
Macewen (l888) reported the first successful surgery for SICH (1883). By 1891 Chamboniere had reported 31 cases of SICH. Likewise. Lucas also had reported several cases. Cushing in 1903 successfully evacuated an SICH. In 1906 Ballance described the first successful evacuation of a cerebellar hemorrhage. Bagley in 1932 differentiated infiltrating deep hemorrhages from cont1uent
superficial hemorrhages and suggested that the latter could be removed. Penfield in 1933 stated that solid clots could not be successfully aspirated. 142 A number of papers were published on surgical evacuation as well as aspiration. However. the reports of \lcKissock and colleagues around 1960 suggested that surgical evacuation produced worse outcomes than nonoperative treatment. I". I '0.19- '\eurosurgeons seemed to accept that little could be done to alter the natural history of SICH and consequently lost interest in this problem.
However. interest slowly increased. possibly because of the high incidence in such places as Japan. and new experimental and clinical studies were begun a little over a decade ago. 15'l.IX6 Much has been learned about the origin of SICH and its manifestations through human autopsies. The pathophysiology of SICH is being better understood through the use of animal studies. It has been often difficult to clinically differentiate infarctions from clots: however, clots can now be accurately diagnosed by computed tomography (CT) or magnetic resonance imaging (MRI). which also has permitted clinical/anatomic correlation of their clinicalmanitestations. Many changes in the population as well as changes in health care. ranging from improved treatment of hypertension to the increased use of cocaine and an aging population with a higher incidence of amyloid angiopathy. have changed the total incidence of SICH and relative incidence from different etiologies. The epidemiology of SICH cannot be fully understood. however. until all patients in large populations suffering strokes are studied by neuroimaging and/or autopsy. Since a large percent of victims of SICH die immediately or soon after their hemorrhage. prevention i, the ultimate solution of the problem. Given the current situation. the question is how to optimize care. There is increased interest in treatment. both by controlling intracranial pressure and by evacuating the hematomas either with open surgery or by aspiration.
With growing interest. the literature dealing with SICH is increasing and now includes three monographs that were published in 1992.y7x.117 several overview chapters2.12.1.'.26.3., .. 'Y.47.74.114.142.157.177.1 XX.239.245 and review articles in
journals.'I1.'15.,r,.176.2" and literallv hundreds of more limited
. .
chapters and clinical and basic research articles published in the
last few ~ ears. A comprehensive and critical review of the literature would require a monograph of several volumes. Epidemiology
The epidemiology of SICH is problematic. although there have been many epidemiologic studies of stroke in general and SICH in panicular.">< .".:" Stroke is the third leading cause of death in the Lnited States. accounting for 2 to 4 percent of all deaths. SICH is the cause of 8 to 13 percent of strokes and 15 to 20 percent of death, due to strokes. There are about 37,000 incidences of SICH annually in the L'nited States.!" Hypertension is a contributing factor to at least 50 percent of SICH, with amyloid angiopathy beginning to assume more significance as the population ages. Risk factor, include age. race. hypertension, prior cerebral infarction. coronary artery disease. diabetes mellitus. and a variety of diseases .discussed laterl.:IY62 The incidence of strokes. including SICH, declined in the 1970s. at least partly due to the more frequent detection and effective treatment of hypertension62.242
Attempts to be more precise in detection are problematic for many reasons.I': In order to properly understand the incidence of SICH. we would need national figures to eliminate population
and all cases would have to be diagnosed and all contributing factors would have to be identified. Current information does not meet these standards, however. Some hemorrhages are minimally symptomatic and not reported; small ones may be diagnosed as infarcts if neuroimaging is not done . .16X'i.II.1.2.11I Large hematomas may be diagnosed but their cause not identified (e.g .. hemorrhages into the basal ganglia from aneurysms). Patients may die suddenly from SICH but since they are not autopsied their deaths are attributed to other causes (it is thought that intracranial bleeding causes 10 to 15 percent of sudden deathsr.':" On the other hand, patients may die of conditions such as cardiac disease but be presumed to have suffered SICH. Regional statistics. where populations are atypical with regard to race, age, and socioeconomic factors, may not be representative of national statistics. Additionally. medical knowledge and practices are changing. For example, drug therapy for hypertension may be less aggressive, more hemorrhages may be detected because more stroke patients have CT scans, and less patients may be dying of other diseases and thus develop strokes.i" Therefore, older statistics may not reflect current trends. Thus, when considering epidemiology, it is important to be aware of these problems and the limits of our current knowledge.
Some striking statistics have come from a recent study in Cincinnati where SICH was at least 1'/2 to 2 times as frequent as subarachnoid hemorrhage and equally as lethal.!"
Etiologies
A unified theory for the etiology of SICH has been proposed based on acute increase in blood tlow in areas of normal or ischemic arterioles or capillaries (or other vessels), or damage to penetrating blood vessels by chronic arterial hypertension.:" This can be applied to most specific etiologies. Larger vessels may also be subject to weakening, or insignificant acute injuries may not seal in the face of impaired hemostatic mechanisms.
Table 254-1 outlines the etiologies of SICH. There are, however. some obvious overlaps: the bleeding diathesis in disseminated intravascular coagulation (DIC) contributes to delayed posttraumatic SICH. anticoagulants contribute to hemorrhages after cardiac surgery that are related to emboli. and trauma and infection lead to aneurysms. Etiologies listed after cerebral amyloid angiopathy in Table 254-1 are less common. Part of the . 'unknown" group may include many patients in whom bleeding was caused by acute rises of blood pressure due to a variety of causes.
As mentioned. chronic hypertension (i.e .. known hypertension or left ventricular hypertrophy) is the most common cause of SICH, 11.1,2.111 and the incidence is related to the degree and duration of elevation of the blood pressure. III'! Racial (e.g .. Japanese, African Americans) predisposition to hypertension and socioeconomic problems that have limited detection and treatment may explain the high incidence of SICH in certain racial groups.i' ~ The incidence of fatal intracranial hemorrhage is actually many times greater in Japan than in the United States, which probably explains the high level of interest, aggressive approach, and number of studies coming from that country. Although some series implicate hypertension in as many as 90 percent of patients with SICH. this may not be completely accurate and may be changing dramatically.111 To put these issues in perspective, an approximation of frequency is indicated in Table 254-1. The future trends in the incidence of these problems are also projected based on assumptions that are fairly apparent (i.e .. increased use of street drugs,
TABLE 254-1 Etiologies of Spontaneous Intracerebral Hematoma
|
Hypertensive Chronic (Acute) Not hypertensive
Congenital vascular anomalies Aneurysms
Arteriovenous malformations Coagulopathy
Tumors
Vasculopathy. vasculitis Cerebral amyloid angiopathy Moyamoya
Vasculitis
Drug related SympathomimeticAnticoagulants Fibrinolytics
Postoperative Intracranial Carotid Cardiac
Stroke
Arterial infarction Venous occlusion
Delayed post-traumatic Parenchymal Aneurysmal Postoperative
Mycotic aneurysm Neonatal intraventricular" Other
Unknown/none
Secondary brain stem"' |
|
"'Not considered.
SOl/rce: From Kaufman HH. Spontaneous intracercbrul hematomas, In Grossman RG redi: Principles (~(,Vel/rmlfrJ . .;er.r. Ne«: York: Raven Press. 1991. P 66. with pcrmiscion. |
aging of the population so that amyloid angiopathy will be more common. less use and better control of anticoagulants, and treatment of DIC to avoid delayed traumatic SICH).
SICH has traditionally been considered in a bipartite fashion.
Because hematomas due to hypertension occur in typical locations (Table 254_2).99.111.11.1 this group will be considered first by site. The remaining hematomas often originate in the subcortical white matter: each etiology will be considered separately. Although it is true that subcortical clots may have a variety of specific etiologies. a large proportion (45 percent) may still be related to hypertension. On the other hand, clots in locations typical for hypertensive hemorrhage may often be due to other causes. For example. clots in the cerebellum and pons may result from such problems as cryptic vascular malformations. Of course. hypertensive patients may have clots caused by other etiologies such as aneurysms. Hypertensive Hemorrhage
Pathophysiology
The vasculopathy of chronic hypertension 1 1.1.12' affects the perforating arteries. 100 to 400 f.lm diameter. which arise directly from much larger trunks to enter the brain at right angles and which are end arteries. These vessels are subjected directly to changes til
|
TABLE 254·2 Relation of Hypertension to Location |
|
Hypertension 75 to 50'7c + |
|
:'\0 Hypertension 25 to 50,?( |
|
Basal ganglia Subcortical \\ hire matter Thalamus
Cerebellum
Pons |
|
Source: From Kaufman HH. Spont.mcou-. intracerebral hem.uorna-. In Gro-vmun RG red): Principles o(XclIroslIrgcry. :"L'\\ York: RJ\t'1l Pr. c "". 1991. I' 67. with pc-m!-. SIOIl. |
blood pressure. unlike cortical vessels which are protected by a series of bifurcations and have collaterals for run off."' These small arteries accumulate lipid and proteinaceous material in their walls ( lipohyalinosis j that in turn can cause a scarring (hyalinosis r or. alternatively. focal necrosis and even Charcot-Bouchard or miliary "aneurysms." Target arteries include the lenticulostriate arteries. the thalamoperforating arteries. and the paramedian branches of the basilar artery as well as the superior and anterior inferior cerebellar arteries. in whose distributions SICH may develop. This process is more common in the proximal part of the artery (explaining why putamina! hemorrhages are more common than those in the caudate r." In addition. autoregulation of blood flow is altered in chronic hypertension. and the vessels are less able to compensate for increased blood pressure. predisposing to bleeding as well as impaired compensation after."'1292.\'
Many other factors can contribute to bleeding. Damage to the parenchyma may compromise support to the vessels: the significance of this is not clear. however. Acute increases in blood pressure and flow may also be important. particularly where autoregulation may be compromised (as in trauma). or where pressure may be above the limits of autoregulation. as in toxemia. SICH generally occurs during the morning or early afternoon when a patient is active. Therefore. it has been postulated that the trigger for bleeding may be a diurnal rise or an acute increase in blood pressure from whatever cause."·1.lr.21 h.2.\' Last. compromise of hemostatic mechanisms may playa role. as in delayed traumatic SICH. a bleeding diathesis. or anticoagulant usage.
It had been thought that the bleeding event is relatively acute."" However, angiograms have shO\\I1 bleeding for several hours and. sometimes. even days from onset."le- In one systematic study. it was shown that six of eight patients with serial CT scans had an increase of the volume of their clot of over -1-0 percent. 1- In another series. late deterioration was seen in a small proportion.- It seems that most bleeding takes place within 6 h. and clots larger than 5 ern iii diameter are most likely to cvpand.?" which fits with the theory of expansion due to tearing. which would be more likely to occur in a larger clot. Many authors believe that this secondary bleeding is a very important mechanism in clot development.:ih.:iS 11.\.1 :is. I :i9 Small satellite hemorrhages. the marginal
hemorrhages of Stemmer. may be due to similar disruption of more distant small vessels. The pathologic evidence of such bleeding is the fibrin-platelet masses found within and at the margin of the clots. Blood pressure (systemic and local). size and rigidity of the vessel involved. state of autoregulation. state of the hemostatic system. and physical condition of the surrounding parenchyma probably all playa role in determining the size of the hematoma. A small number of patients will develop new clots. usually in a different location. e I e
The ultimate clinical manifestations of the clot relate to the speed and volume of the hemorrhage as well as its location. The
patterns of spread for each location have been described. as have the clinical manifestations related to location and extension.e9.IOI.II.\ A small hemorrhage may dissect along tissue planes (e.g .. a lobar hemorrhage). splitting the tissue apart rather than destroying it. with limited compromise and/or with restitution of function when the blood is absorbed."? A very large hemorrhage may explode into the brain substance. destroying large amounts of tissue. raising intracranial pressure to the level of the blood pressure before the bleeding is tamponaded, and causing herniation of that part of the brain from its normal position under the falx. through the tentorial incisura. or through the foramen magnum. depending on the location of the bleeding. Even if there is not acute herniation. the brain is plastic and can further deform or "creep" due to pressure from the original mass. Local pressure and edema. disconnection. and more distant changes in metabolism and blood flov, are also important29.e4:i
Blood may rupture into a ventricle (especially with caudate. thalamic. cerebellar. and pontine hemorrhages) and even cause hydrocephalus. On the other hand. the rupture may actually decompress the clot. Blood may also find its way into the subarachnoid space causing irritation and hydrocephalus as well. Distortion of the upper brain stcm may also lead to hydrocephalus.
Death is due to distortion or compression of the brain stem. development of secondary brain stem hemorrhages. or direct extension of the clot into the brain stem."" With posterior fossa hemorrhage. there may be direct compression of the brain stem. Basal ganglia clots of more than 85 ml or more than 6 percent of the volume of the brain. or cerebellar clots more than 3 cm in diameter have a poor prognosis if left untreated.
If the patient lives. the clot will eventually be broken down and reabsorbed. A six-phase process based on evolution of the clot has been described. It includes invasion by macrophages. development of surrounding edema. and development of microvessels at the margin of the clot. followed by quieting of these processes and development of gliosis (Table 25-1--3 ).12- In the case of a larger clot. this will take many months. A small number of patients will develop new clots. usu'ally in a different locauon.i:"
Models have been used to study various aspects of SICH.122 In vivo models mimic the natural dynamic milieu of human hematomas. But. animals are expeusivc, their hemostatic systems may be verv different from those of humans. and their brains arc too small to accept clots large enough to use to evaluate new surgical de\ ices. However, animal studies have revealed many details about pathologic and physiologic changes after SICH. They have demonstrated that blood is irritating to the parenchyma. causing a procressive hemorrhasic necrosis with edema at the margin of the ~Iot. This process ~is fixed by 6 h.222 Animal studies have also demonstrated changes in local and distant blood flow and metabolism.lee And. in animal studies. early evacuation of the clot has been shown to improve outcome.v ' In vitro models using human blood have been helpful in studying lytic drugs and aspiration devrces. but they lack the dynamic setting of an animal model.
Supratentorial Hematomas
Statistics
Supratentorial hematomas constitute about 80 percent of SICHs. 2262c.29.3.1.r'- 11.\ 1.\2.16e I 77. 197,2.\:i Perhaps half of these
hematomas are related to hypertension. Their highest incidence is in the fifth and sixth decades of life; males may predominate. Table 25-1---1- lists their distribution sites. They may be divided into
