Recognizing and Preventing Intracerebral Hematoma Expansion.

Oneearly anddramatic clinical accountofhematomaexpansion concerns amanwhodevelopedahematoma that evolved under observation in 1937.1 He was sent to the hospital because of “malignant hypertension.” While his medical history was being taken, the patient complained of weakness, dizziness, and numbness of his hands. He then reported an inability to hear, difficulty in swallowing, and dyspnea. The patient was placed on the examining table, and it was determined that his systolic blood pressure and diastolic blood pressurewere 245 and 170mmHg, respectively. Under the eyes of several examiners, complete bilateral palsy of the sixth nerves developed; both pupils dilated, and the corneal reflexesdisappeared.Thepatientwas still able to talk, butwith a bulbar speech, andhe appeared almost completely deaf.His left leg becameparetic, and rapid clonicmovementswere observed. The Babinski sign was present bilaterally. Within an hour, thepatient becamecomatose andquadriplegic and soon died.His brainstemhadbeen gradually destroyed by ahypertensive pontine hematoma while physicians watched helplessly.Kornyey1 commented that this rapidlyprogressivechain of eventswasmost unpleasant towitness and produced a depressing effect on the nurses and physicians. During the mid-1970s, several colleagues and I analyzed the course of illness of 54 well-documented patients with intracerebral hemorrhage (ICH)whowere in theHarvard Stroke Registry, andwe showed that 37 of the 57 patients had gradually developed symptoms during a period ofminutes or a few hours.2,3Asmooth,gradualworseningof functionwithina few minutes, followedbyheadache andvomiting,was the rule for patients with large hematomas. Some patients whose conditions had stabilized during the first 24 to 48 hours later developed progressively decreased alertness and increasing focal signswithin48 to72hours attributable to thedevelopment of edema around the hematomas. Fisher4 explained thegradual courseofhematomaexpansion in 1971 byusing observations of a necropsy specimen cut in serial sections of a pontine hematoma, the same condition thathadkilled thepatientsdescribed inKornyey’s case report.1 At the center of the lesion was a large mass of blood. Around theperipheryweremany fibrin globes, representing little caps of fibrinousmaterial that plugged small vessels that had broken and leaked during the patient’s lifetime. As the hemorrhage developed, pressure within the central core increased and compressed small vessels at the periphery of the hematoma.Theseperipheralarteriolesandcapillaries, in turn,broke, andblood escaped, enlarging the lesion. Thehematomagrew like a snowball rolling downhill, accumulatingmore snow on its outer circumferenceas it rolled.Tissuepressure around the lesionalso increased.Anequilibrium isultimately reachedbetween the pressure within the hematoma and the surrounding tissue pressure, and bleeding stops. If the hematoma reaches the ventricular or brain surface, it may communicate with the cerebrospinal fluid, discharge part of its contents at the same time, and, in doing so, decompress the pressure within the lesion. When brain imaging became available, sequential computed tomography (CT) studies of patients with acute ICH showed that hematomas relatively often expanded dramatically during a period of a few hours.5-8 Repeated CT often revealed the dramatic enlargement of the hematoma and ventricular drainage that developed within hours after the first CT scan. Invariably, clinical worsening was also present and was an indication for repeated scanning for some patients. In one study,8 41 of 204 patients with ICH had hematoma expansion detected on repeated CT scans. Expansion in this study8 was most often detected during the first 6 hours, but 5 of 33 patients (15%) had hematomas that expanded during an interval of 6 to 12 hours from symptom onset of ICH to initial CT scan, and 2 of 34 patients (6%) had hematomas that became enlarged during an interval of 12 to 24 hours from symptom onset of ICH to initial CT scan. Patients with ICH who have a bleeding diathesis (especially related to anticoagulation) are especially prone to hematomas that expand gradually and become enlarged often within a few days.9 A quarter of a century ago, it had been clearly shown that intracerebral hematomas enlarged gradually, and thedynamics of that enlargement were known. In patients with ICH, bleeding into the brain tissues from small, deep, penetrating vessels usually occurs under arteriolar or capillary pressure. Anumber of factors are important to considerwhen caring for a patient with hematoma expansion: (1) the arterial pressure, whichacts to increasebleeding; (2) thebloodcoagulability; (3) the vascular pathology (eg, cerebral amyloid angiopathy that renders vessels more fragile and breakable); and (4) the locationandpathof thebleeding.Hematomastendtoexpandalong whitematter tracts. The firmness and turgor of thewhitematter are important. Previously normal tissue tends to resist expansion, whereas soft gliotic white matter facilitates expansion. Bleeding into the cerebrospinal fluid on the pial surface or into the ventricles allows for the release of pressure and reduces further bleeding into the brain parenchyma, but introduces other problems. Clinicians have soughtways of predictingwhich hematomaswill expand.Computedtomographyangiographyhasbeen used to indicate active leakage of blood. The “spot sign,” a hyperdense, usually round, small region within the hemorrhage, can predict the enlargement of a hematoma and correlateswithmorbidityandmortality.10,11Other investigatorshave analyzedthedifference inHounsfieldunitsbetweenearly films after contrast injectionand films taken5minutes later.12A significant increase in Hounsfield units in a region of the hemaRelated article page 961 Opinion Editorial