(Stroke. 1995;26:1953-1955.)
© 1995 American Heart Association, Inc.
Articles |
Acute Fatal Deterioration in Putaminal Hemorrhage
From the Departments of Neurology, Neurology/Neurosurgery Intensive Care Unit, Saint Mary's Hospital, Mayo Medical Center, Rochester, Minn.
Correspondence to E.F.M. Wijdicks, MD, Department of Neurology, W8A, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
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Abstract |
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Background Clinical deterioration in patients with spontaneous intracerebral hemorrhage has rarely been studied. It has been previously thought that intracranial hematomas bleed in a monophasic fashion. Recent studies have demonstrated continuous active bleeding within hours after the event, resulting in enlargement of the hematoma. However, acute sudden and fatal deterioration suggesting a rebleed is rarely reported.
Summary of Reports An 84-year-old man was admitted with a moderate-size hemorrhage in the putamen and was treated for hypertension during the first day of admission. He acutely demonstrated extensor posturing and light-fixed pupils. Repeat CT scan showed massive enlargement of the intracranial hematoma and extension into the ventricles causing acute hydrocephalus. A 72-year-old man was admitted with a mid-size hemorrhage in the putamen. Acute deterioration with loss of all brain stem reflexes except for cornea reflexes was associated with a large increase in volume of the hematoma, 7 hours after the initial hemorrhage. An 85-year-old woman was admitted with a small hemorrhage in the putamen and recovered to be able to walk unassisted. She suddenly died from a recurrent massive putaminal hemorrhage 2 weeks after the ictus.
Conclusions Patients with spontaneous intracerebral hemorrhage in the putamen may die acutely from fatal catastrophic enlargement of the initial hematoma hours to days after the ictus. In some patients with spontaneous intracerebral hemorrhage and clinical deterioration, rebleeding may be a possible mechanism.
Key Words: rebleeding • intracerebral hemorrhage • death
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Introduction |
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Patients with deep-seated intracerebral hematomas may deteriorate in the first 24 hours after the ictus.1 2 3 4 5 Early clinical deterioration is often gradual and has been attributed to progressive brain displacement from edema4 or from growth of intracerebral hematoma, particularly within the first 6 hours after onset.1
Most earlier studies of clinical deterioration have been retrospective,1 2 3 4 and prospective studies of neurological deterioration in intracerebral hemorrhage are scarce.5 Acute secondary deterioration is very unusual in patients with basal ganglia hemorrhages.
During a 3-year epoch, we followed a series of 29 patients with intracerebral hematoma admitted within 8 hours of ictus. Within this cohort, we observed 3 elderly patients admitted to the neurological intensive care unit with acute fatal deterioration from massive enlargement, which in 1 patient occurred after a virtually asymptomatic interval of 2 weeks.
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Case Reports |
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Patient 1
An 84-year-old man with a history of hypertension was admitted to the emergency department after sudden onset of speech difficulties and right-sided weakness. Medications he was taking at admission were hydrochlorothiazide and regular daily aspirin. Neurological examination showed that he was able to follow commands. A marked expressive aphasia and right hemiparesis were noted. Eyes were conjugately deviated to the left. Pupils were equal and reactive to light.
Laboratory investigations including international normalized ratio (INR), activated partial thromboplastin time (APTT), and platelet counts were normal. A bleeding time, however, was not performed. Initial blood pressure of 230/120 mm Hg was initially controlled by esmolol infusion of 50 µg/kg per minute.
In the first hour of admission, blood pressure became more difficult to
manage, and systolic blood pressures ranged from 200 to 230 mm Hg,
with diastolic pressures ranging from 110 to 150 mm Hg.
Labetalol and later nitroprusside were added. The patient acutely
deteriorated approximately 12 hours after the ictus with a fixed and
dilated pupil and posturing on the left. He was intubated and needed
mechanical ventilation to counter several apneas. CT scan showed a
massive enlargement of the hematoma into the diencephalon and
ventricular system (Fig 1
). He fulfilled the clinical
criteria of brain death within 1 hour of this second event. Autopsy was
not permitted.
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Patient 2
A 72-year-old man with a history of coronary artery
disease, hypertension, atrial fibrillation, and chronic obstructive
pulmonary disease suddenly fell at home and was unable to move
the right side of his body. He did not use aspirin or nonsteroidal
anti-inflammatory agents, nor had he been recently anticoagulated.
Neurological examination in the emergency department revealed a maximal
Glasgow Coma Scale (GCS) score, paraphasic errors, and a flaccid right
hemiplegia. Blood pressure on admission averaged 170/75 mm Hg.
Laboratory investigations including INR, APTT, and platelet counts
were normal. In the first hours, he was somewhat restless but could
clearly communicate that he had a severe headache. His GCS score did
not lessen during 4 hours of close observation in the intensive care
unit. Seven hours after the ictus, he acutely developed spontaneous
bilateral posturing, agonal breathing, and anisocoria but retained
pupillary light reflexes. CT scan showed massive enlargement of the
initial hemorrhage in the putamen with midline shift and
significant intraventricular blood (Fig 2). One hour after acute deterioration, mid-position
pupils nonreactive to light and absent doll's eyes were noted, but the
corneal reflexes remained preserved. He died after withdrawal of
support. Autopsy was not permitted.
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Patient 3
An 85-year-old woman with a history of long-standing
hypertension and lacunar stroke presented to the neurological
intensive care unit with sudden onset of dysarthria and right
hemiparesis. She was occasionally confused, but the GCS score was
maximal during most of the day. Laboratory investigations were normal,
including INR, APTT, and platelet counts. A repeat CT scan 2 days
after admission showed an unchanged volume of the putaminal
hemorrhage. After a brief observation in the neurological
intensive care unit for blood pressure control, the patient was further
rehabilitated. She needed only minimal assistance for walking 1 week
after the initial event. Her short-term memory was poor, and formal
cognitive testing after transfer to the ward demonstrated deficits
evident in estimated level of global intellectual functioning, language
abilities (particularly in the receptive domain), and attention
concentration abilities. Two weeks after the ictus, she was suddenly
found unresponsive in the hospital with spontaneous posturing on the
right side and bilateral fixed pupils. She was intubated and
mechanically ventilated. CT scan showed a recurrent hemorrhage
in the putamen (Fig 3). She died hours after the event.
No autopsy was permitted.
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Discussion |
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The traditional teaching that spontaneous intracerebral hematomas are monophasic and do not continue to bleed has recently been challenged.1 2 Rupture of small penetrating arteries forms a pressure mass that may rapidly expand from breakage of surrounding arteries. Why some putaminal hemorrhages are cushioned earlier and therefore remain small and others rapidly expand to gigantic proportions is not known, although bleeding diathesis from liver disease, use of aspirin, and persistent hypertension has been implicated.6 7
Hematoma enlargement has only recently been studied with imaging studies. Broderick and colleagues1 5 are credited for their serial CT scan study, the first to demonstrate that bleeding may continue in the first 6 hours after ictus, often with a clinical accompaniment of progressive deterioration in level of consciousness. This observation of enlarging hematoma was recently confirmed in a large retrospective survey but, surprisingly, without any detailed clinical correlation6 and in one small series of patients with rapid expansion of hypertensive intracerebral hematoma but without any attempt to correct the invariably extremely high blood pressures.7
Our patients are unique in several respects, and our findings permit two key observations. First, massive enlargement of an intracerebral hematoma associated with acute deterioration to virtually minimal GCS scores and loss of many brain stem reflexes is a very unusual clinical course for a deep-seated hematoma. In the study by Broderick et al,1 expansion of the hematoma ranged from 48% to 338%, but in seven of these patients the volume remained less than 50 mL. In this study, follow-up cranial CT scans were prospectively scheduled and, in many patients, not dictated by a changing clinical status. Gradual clinical deterioration often lagged behind increased volume that was demonstrable on CT scan.
Hematoma enlargement was previously reported in 2 of 10 patients with massive expansion of hematoma, but 1 of these patients had a new hematoma in the frontal lobe.8 A recent review by Mayer et al4 emphasized early cerebral edema as the most common cause of deterioration in intracerebral hematoma. In this clinical study, deterioration was gradual in all patients and was arbitrarily defined as a change of two points on the GCS score.4
A second important observation in our cases is rebleeding into the putamen with catastrophic consequences after a relatively asymptomatic interval of 2 weeks. This phenomenon has not been previously reported to our knowledge. In the study of Bae et al,8 one patient developed a 400% increase in volume after 3 days, but the clinical course was not well detailed.8
Without pathological examination (rejection of autopsy is commonplace for elderly patients with stroke9 ), we can only speculate about a possible mechanism. Admittedly, in two of our patients continued bleeding may have caused deterioration, but both patients were lucid in the interim, only to deteriorate with sudden loss of pupil reflexes and agonal breathing. In our third patient, hemiparesis had resolved significantly, and rehabilitation had resulted in an independent outcome. Therefore, rebleeding seems a more likely mechanism than expansion from active bleeding.
The very advanced ages of our patients are of potential interest and may superficially indicate that amyloid angiopathy plays a role. However, although two reports have located severe amyloid deposition in perforating arteries,10 11 these vessels are usually less commonly affected than large vessels supplying the occipital and temporal lobes. An arteriovenous malformation cannot be excluded, but a rebleed very soon after the initial event or even within the first year is very uncommon.
The frequency of acute deterioration in spontaneous intracerebral hemorrhage in the putamen seems low in our initial survey, but prospective studies of secondary deterioration (preferably with autopsy) in patients with hemorrhage in the putamen are needed.
Received April 4, 1995; revision received June 15, 1995; accepted July 11, 1995.
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References |
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1. Broderick JP, Brott TG, Tomsick T, Barsan W, Spilker J. Ultra-early evaluation of intracerebral hemorrhage. J Neurosurg. 1990;72:195-199. [Medline] [Order article via Infotrieve]
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attributed to cerebrovascular disease. Stroke. 1993;24:71-75.
10. Bruni J, Bilbao JM, Pritzker KPH. Vascular amyloid in the aging central nervous system: clinicopathological study and literature review. Can J Neurol Sci. 1977;4:239-244. [Medline] [Order article via Infotrieve]
11. Lie SS, Stemmerman GN. Congophilic angiopathy and cerebral hemorrhage. Arch Pathol Lab Med. 1978;102:317-321.[Medline] [Order article via Infotrieve]
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