Surgical Management of Spontaneous Intracerebral Hemorrhage
Spontaneous intracerebral hemorrhage (sICH) constitutes 10–15% of first-ever strokes with an annual incidence of 20–30 cases per 100,000. It generally affects younger patients than ischemic stroke and has a peak incidence between 55 and 75 years. It is slightly more common in men and up to twice as common in blacks. Typical locations include deep structures (basal ganglia, thalamus, internal capsule) in 50%, hemispheres (lobar) in 35%, cerebellum in 10%, and brainstem in 5% of cases.
60–70% of cases are hypertensive in origin and are thought to follow rupture of small Charcot-Bouchard microaneurysms that develop in small cerebral arteries (e.g., lenticulostriates, thalamoperforators) as a result of long-standing hypertension. Other etiologies include cerebral amyloid angiopathy (15%), which typically causes lobar hemorrhages in nonhypertensive elderly patients, coagulation disorders (e.g., anticoagulants, liver disease), underlying vascular lesions (e.g., aneurysm, arteriovenous malformation) or hemorrhagic tumors (e.g., metastatic melanoma, glioblastoma), cerebral venous thrombosis, and illicit drugs (e.g., cocaine, amphetamines).
The nature and severity of symptoms depends on the location and size of the hematoma. Clinically, intracerebral hemorrhage (ICH) is often difficult to differentiate from ischemic stroke; thus, many patients are initially misdiagnosed and managed as such given the much higher incidence of the latter.
Computed tomography (CT) scan of the head should be urgently obtained in patients with acute neurologic symptoms and will promptly give the diagnosis of ICH. Intraventricular hemorrhage (IVH) may be present in 40–45% of cases.
Conventional or CT angiography should be performed when an underlying vascular lesion is suspected, such as in young patients (less than 45 years of age) and those with no preexisting hypertension, lobar ICH, isolated IVH, or unusual ICH location (e.g., sylvian fissure distribution).
Magnetic resonance imaging (MRI) without and with contrast should be performed to rule out a cavernous malformation or tumor in atypical cases. MR venography may be indicated if cerebral venous thrombosis is suspected.
In neurologically deteriorating patients who require emergent surgery, additional imaging should be withheld to avoid unnecessary delays. If presence of an underlying aneurysm or arteriovenous malformation is a concern, consideration may be given to intraoperative angiography.
30–40% of nonoperated hematomas may grow significantly by expansion or rehemorrhage in the first 24 hours, leading to clinical deterioration. Hydrocephalus may also develop in patients with IVH. Therefore, close monitoring and a repeat head CT in the first 24 hours are critical.
Medical treatment: All patients should be initially admitted to a neurosurgical intensive care unit (ICU) for aggressive medical treatment and monitoring. Standard ABC (airway, breathing, circulation) management, including intubation and mechanical ventilation when necessary, should be given priority.
Coagulopathies should be rapidly recognized and reversed. Patients on oral anticoagulants should receive intravenous (IV) vitamin K and fresh frozen plasma (FFP) aiming to drop their international normalized ratio (INR) below 1.5. If available, prothrombin complex concentrates (e.g., OctaplexTM, Octapharma AG, Lachen, Switzerland) are preferable to FFP given their faster therapeutic effect and smaller infusion volume. Patients on antiplatelet agents, particularly clopidogrel (PlavixTM, Bristol-Myers Squibb/Sanofi, Bridgewater, NJ), should receive platelet transfusions.
Blood pressure (BP) should be controlled to minimize the risk of hematoma growth. Intravenous antihypertensive agents (e.g., nicardipine, labetalol) may be used. A good rule of thumb is to lower systolic BP (SBP) by no more than 15–20% of its baseline value. In hypertensive patients, typical target values for SBP are 140–180 mm Hg. If BP is easy to control, noninvasive BP monitoring (brachial cuff) is sufficient. Otherwise, an arterial line should be placed to optimize BP control.
In patients with an intracranial pressure (ICP) monitor, ICP should be maintained below 20 mm Hg and cerebral perfusion pressure (CPP) above 60 mm Hg. Factors that may aggravate secondary neuronal injury (e.g., hyperglycemia, fever) should be treated aggressively.
Although activated recombinant factor VII (NovosevenTM, Novo Nordisk A/S, Kobenhavn, Denmark) may reduce early hematoma growth, it does not seem to improve outcome. Therefore, it should not be used routinely in ICH patients.
Withdrawal of care: This should be avoided in the early period (24–48 hours) given the current inability to precisely prognosticate. Exceptions include specific patient advance directives, clear family wishes, or elderly patients with very large ICH and poor neurologic exam.
An EVD should be placed in patients with obstructive hydrocephalus secondary to IVH. In patients with massive IVH and no underlying unsecured vascular lesion, intraventricular recombinant tissue plasminogen activator (rtPA) may be given to prevent EVD obstruction by clots and improve clearance of IVH.
Emergent craniotomy and hematoma evacuation should be considered on a case-by-case basis in patients with mass effect-related neurologic deterioration. Healthy young and middle-aged patients with a surgically accessible hematoma are the usual candidates (Fig. 87.1).
Surgical evacuation of supratentorial hematomas is not warranted on a routine basis. The STICH trial (International Surgical Trial in Intracerebral Hemorrhage) showed that routine early surgery (within 96 hours) in patients with supratentorial ICH did not improve patient outcome in terms of survival or functional outcome.
Surgical evacuation should be performed for cerebellar hematomas > 3 cm in size and those causing brainstem compression, obstructive hydrocephalus, or neurologic deterioration. EVD should not be performed before posterior fossa decompression given the risk of upward herniation.
Fig. 87.1 A 61-year-old female patient on warfarin for aortic valve replacement had sudden-onset severe headache with vomiting and decreased level of consciousness (Glasgow Coma Scale score = 10). International normalized ratio at presentation was 3, which was quickly reversed with vitamin K and fresh frozen plasma. (A) Urgent head computed tomography (CT) reveals a large right frontal intracerebral hemorrhage with significant midline shift. (B) Postoperative head CT following emergent craniectomy and hematoma evacuation shows resolution of mass effect with minimal disruption of adjacent brain tissue. Postoperatively, the patient regained a normal level of consciousness and had no significant neurologic deficits. (C) Follow-up head CT at 6 weeks.
The patient should be positioned and his or her head rotated so that the trajectory to the hematoma is as vertical as possible. The skin incision and craniotomy should be centered over this trajectory. The head is fixed in a Mayfield headholder and is elevated 30–45 degrees to improve jugular venous return. If available, intraoperative ultrasound may be helpful in localizing deep seated hematomas.
The approach should be planned in a way to minimize passage through healthy tissue while avoiding eloquent brain. When carefully reviewed, preoperative films will usually give a hint about the optimal surgical trajectory.
The importance of meticulous hemostasis cannot be overemphasized, given the significant risk of rebleeding. Before closing the dura, it may be worthwhile asking the anesthesiologist to raise the SBP to 140–160 mm Hg and watch for active bleeding in the hematoma cavity.
For lobar ICH, a horseshoe skin flap is typically used. The craniotomy should be large enough (at least 6–7 cm) to allow relaxation of swollen brain (Fig. 87.2 A). Dural incision is cruciate (X- or H-shaped) or curvilinear. For very extensive hematomas, a large trauma flap may be performed, particularly if concomitant decompressive hemicraniectomy is being considered.
Fig. 87.2 Illustration of the surgical technique used in the same patient. (A inset) Pterional craniotomy centered over the hematoma. 1. Craniotomy outline; 2. skin incision; 3. hematoma outline. (A) Small right frontal cortical-pial incision. (B) Coagulation of pia and cortex using bipolar cautery. (B inset) Incision of pia and cortex using microscissors. (C inset) Dissection of subcortical white matter using a Penfield #1 dissector. (C) Entry into hematoma cavity and evacuation of hematoma using fine suction with irrigation and pituitary forceps. Suctioning stops when white matter is encountered.
For basal ganglia ICH, a classical pterional skin incision and craniotomy with a curvilinear dural incision are typically used. These are followed by dissection of the sylvian fissure and exposure of the insular cortex using the operative microscope (transsylvian–transinsular approach).
For cerebellar hematomas, a midline or paramedian linear skin incision is often performed. Alternatively, a hockey-stick incision extending from the midline to the ipsilateral pinna may be used. A large suboccipital craniectomy is usually performed with exposure of the transverse and sigmoid sinuses and opening of the foramen magnum, followed by a cruciate dural incision.
Once the cortex overlying the hematoma is exposed, a small 1–2 cm pial-cortical incision is made using bipolar cautery and microscissors under microscope or loupe magnification (Fig. 87.2 B). The subcortical white matter is then progressively dissected using a Penfield #1 dissector until the hematoma cavity is entered (Fig. 87.2 C). Gentle retraction of the white matter is maintained by an assistant holding the dissector or by a self-retaining retractor (e.g., Greenberg retractor), and the hematoma is evacuated using a fine suction with intermittent irrigation by the assistant. Solid portions of the hematoma may be removed using a pituitary rongeur or tumor forceps (Fig. 87.2 C). Suctioning is continued until white matter is encountered in all planes. Injury to this potentially salvageable tissue should be avoided at all costs. Frequent changes in the orientation and position of the retractor will help expose more clot and achieve better hematoma evacuation. Meticulous hemostasis is obtained using bipolar cautery and application of local hemostatic agents (e.g., polyanhydroglucuronic acid oxidized cellulose polymer, SurgicelTM, Johnson & Johnson Inc., New Brunswick, NJ; microfibrillar collagen, AviteneTM, Davol Inc., Warwick, RI; or bovine-derived gelatin matrix component, FlosealTM, Baxter, Deerfield, IL). It may help to ask the anesthesiologist to raise the SBP moderately and watch for active bleeding in the hematoma cavity prior to dural closure.
In supratentorial craniotomies, decisions should be made whether to replace the bone flap and whether to insert an ICP monitor. The degree of intraoperative and anticipated postoperative cerebral edema should be taken into account when making such decisions.
Whenever an underlying vascular lesion is suspected, conventional or CT angiography should be performed preoperatively. If the patient’s condition is rapidly deteriorating and there is no time for additional imaging, consideration should be given to intraoperative angiography.
The patient should be mobilized as soon as he or she is medically stable. Physical, occupational, and speech therapy should be started in the hospital and transfer to a rehabilitation facility should be arranged.
Hematoma volume and GCS score are the two most important predictors of 30-day mortality. The latter varies from as low as 19% for patients with small (< 30 mL) ICH and GCS score ≥ 9 to as high as 91% for those with large (> 60 mL) ICH and GCS score ≤ 8.
Other negative prognostic factors include IVH (two- to fourfold increase in mortality), infratentorial location (hematomas > 5 mL in the brainstem or > 30 mL in the cerebellum are usually lethal), and older than 80 years of age.
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2 Broderick J, Connolly S, Feldmann E, et al. American Heart Association, American Stroke Association Stroke Council, High Blood Pressure Research Council, Quality of Care and Outcomes in Research Interdisciplinary Working Group. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke. 2007;38(6):2001-2023.
3 Morgenstern LB, Hemphill JCIII, Anderson C, et al. American Heart Association Stroke Council and Council on Cardiovascular Nursing. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010;41(9):2108-2129.
4 Mendelow AD, Gregson BA, Fernandes HM, et al. STICH investigators. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005;365(9457):387-397.