A 56-year-old man with history of hypertension presented to our emergency department with complaints of severe headache and visual changes. At the first encounter his level of alertness was normal and his only neurological deficit was a right visual field deficit. His blood pressure was 194/112 mmHg. He was treated with intravenous labetalol. Shortly after his arrival he became sleepier, and repeat examination showed right-sided weakness and hypoesthesia. An emergency CT scan showed a large left lobar hematoma (estimated volume 65 cm3) with regional mass effect. (Figure 1.1A) Coagulation values were normal. The blood pressure remained elevated despite repeated doses of labetalol, but became finally better controlled after initiation of a nicardipine infusion.
When we see the patient in the emergency department immediately after the CT scan he is arousable to strong voice but does not remain awake unless he is stimulated. His pupils are symmetric and reactive to light. He does not blink to visual threat on the right and has a moderate right hemiparesis and sensory loss. He has a right Babinski sign, but plantar response remains flexor on the left.
What do you do now?
FIGURE 1.1 A) CT scan of the head before surgical evacuation showing a large left lobar hematoma with extensive regional mass effect. B) Complete evacuation of the hematoma with resolution of the mass effect is shown in a CT scan obtained 72 hours after surgery.
No doubt this is a disconcerting clinical situation. Most of us know that surgery for cerebral hematoma—dissecting through healthy neuronal tissue to reach the clot—is no sinecure. There is evidence that surgery does not improve outcome in deep seated ganglionic hemorrhages but faced with a patient worsening from a lobar hematoma a more nuanced understanding is necessary. Here is some useful information to help in making a decision.
Intracerebral hemorrhage (ICH) often has devastating consequences. Four in ten patients with ICH die, and many survivors can remain disabled. Furthermore, the medical treatment of ICH is limited to supportive care, control of severe hypertension, and correction of coagulation abnormalities when present. In patients with spontaneous ICH, hemostatic therapy reduces hematoma expansion, but has not been proven to result in better functional outcomes. Some hematoma enlargements do not translate in measurable clinical differences, or the treatment—mostly recombinant factor VIIa—may be helpful only in patients who continue to bleed. The challenge now for clinical researchers is to identify patients who would benefit most. Therefore, the combination of poor prognosis and lack of effective medical therapy makes the alternative of a surgical intervention appealing. Yet, multiple studies comparing medical and surgical management of spontaneous ICH have shown disappointing results.
The largest trial evaluating surgical evacuation for spontaneous ICH was the Surgical Trial in Intracerebral Hemorrhage (STICH). Over 500 patients—with similar numbers of hematomas in the putamen/thalamus and lobar locations—were randomized to surgical or medical treatment within 3 days of ICH onset (median time to surgery was 30 hours). Six months later, only one quarter of patients in both groups had achieved good recovery or had no more than moderate disability. Therefore, surgery did not improve the outcome of patients with spontaneous ICH at large, which confirmed the results of previous smaller trials. Subgroup analyses in the STICH population however, disclosed that patients who were not comatose and had superficial lobar hematomas (< 1 cm from the brain surface) did better when they underwent surgery. Patients with these characteristics are currently being enrolled in another trial (STICH II).
We need to keep in mind that trials evaluating surgery in ICH have typically not enrolled rapidly deteriorating patients (in fact, “rescue” surgery took place in more than one in four patients randomized to the medical group in the STICH trial). Although in three quarters of patients outcome is still poor, we have seen patients with signs of clinical and radiological brainstem compression or displacement who recovered well after emergency evacuation. If those patients have good potential for recovery, surgery should at least be considered.
We know a few other things about surgery for ICH. Deep-seated hematomas do not benefit from evacuation via a traditional open craniotomy but some case series and one randomized study indicated that stereotactic surgery with needle aspiration could be useful in deep seated hematoma. The safety and efficacy of stereotactic evacuation facilitated by instillation of a thrombolytic agent into the hematoma to liquefy it requires further evaluation of experience in this regard is limited. Ultra-early hematoma evacuation was a concept that made a lot of sense a priori, but a clinical trial testing this strategy had to be terminated because of increased numbers of deaths among patients operated within hours. This was explained by difficulty to maintain hemostasis and frequent postoperative rebleeding. On the other hand, hovering between “wait and see” or “do something” to then proceed with a surgical intervention only after the patient has become comatose from mass effect seems poor practice. Surgery was ineffective in comatose patients in STICH. Furthermore, in reality, waiting for the patient to decline before offering surgery often results in not offering surgery at all. Once the patient is “too poor for surgery” the opportunity is gone.
Surgery is standard practice in certain circumstances. We do know that sizable cerebellar hematomas must be evacuated to avoid obstructive hydrocephalus and brainstem compression, all of which can be fatal or result in irreversible complications. Delaying evacuation of the clot in these patients is ill-advised.
Another population in which surgery is indicated is when the ICH is secondary to a vascular anomaly (such as an arteriovenous malformation or an aneurysm) because of the high risk of recurrent bleeding, and when there is suspicion of an underlying tumor. Generally, suspicion of amyloid angiopathy does not contraindicate surgery (in the past the fragility of the arteries has worried neurosurgeons). Some patients with pathologically confirmed amyloid angiopathy can recover well after surgery, especially those younger than 75 years, without intraventricular hemorrhage, and without history of dementia.
Another neurosurgical issue is the placement of a ventriculostomy in a patient with cerebral hematoma and obstructive hydrocephalus. This intervention seldom results in clinical improvement because obstructive hydrocephalus is often the result of a large clot compressing the ventricles. CSF diversion alone in these cases is not sufficient.
So what did we decide to do with our patient? Neurosurgery was consulted in the emergency department. We discussed the situation with the family, since the patient was not able to sustain attention sufficiently to participate in the conversation we told them that we had a favorable experience with early intervention, but without scientific proof of benefit. We mentioned that later surgery would not be a good option. After the family provided informed consent, our neurosurgical team performed a craniotomy and clot evacuation. Surgery started 6 hours after patient presentation and approximately 8 hours after symptom onset and achieved successful hematoma evacuation. The following day the patient was awake and could be safely extubated. He was discharged from the hospital with a right visual deficit and minimal right arm weakness and numbness. He continued to improve and was back to work 6 months later, and this time he was taking his antihypertensive medications (unlike before the ICH, when he had been noncompliant).
When considering surgery for ICH, we need to take into account various factors related to the ICH itself, the patient’s chances of recovery, and the patient’s preferences, which often have to be discussed with the family or proxy (Table 1.1). When the decision is to go to surgery, first the patient needs to be fully stabilized (i.e., adequate ventilation and oxygenation, control of hypertension below a systolic blood pressure of 180–160 mmHg, and correction of anticoagulation as discussed in chapter 2). Realistic expectations are discussed with the family. In many cases, surgery may reduce mortality but without improving function. While some cases can get better when the clot is removed, as illustrated by our example, in most situations surgery is far from a standard approach for these patients. Careful patient selection is probably the key to optimizing functional results, but we still do not know which patients are the best candidates for surgical treatment. Yet, if surgery is being considered, one should not wait until the patient markedly worsens.
TABLE 1.1 Factors Favoring Surgery for ICH
Worsening clinical signs
Absence of severe comorbidities
Absent or corrected coagulopathy
Absent brainstem injury
Absent intraventricular hemorrhage
Good rehabilitation potential
KEY POINTS TO REMEMBER REGARDING SURGERY FOR CEREBRAL HEMORRHAGE
· Surgery cannot be recommended as a routine intervention for patients with spontaneous ICH.
· Selected patients with spontaneous ICH might benefit from surgery, especially noncomatose patients with good rehabilitation potential and superficial hematomas without associated intraventricular hemorrhage.
· When surgery is considered, it is most reasonable to perform it early, but in stable patients preferably not during the first 4 hours after ICH onset because of problems with hemostasis in this ultra-early period.
· Surgery is indicated in patients with large cerebellar hematomas, and underlying vascular anomalies or tumors.
Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, Karimi A, Shaw MD, Barer DH, STICH investigators. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral hematomas in the International Surgical Trial in Intracerebral Hemorrhage (STICH): a randomized trial. Lancet 2005; 365:387-397.
Petridis AK, Barth H, Buhl R, Hugo HH, Mehdorn HM. Outcome of cerebral amyloid angiopathic brain hemorrhage. Acta Neurochir (Wien) 2008; 150:889-895.
Prasad K, Mendelow AD, Gregson B. Surgery for primary supratentorial intracerebral hemorrhage. Cochrane Database Syst Rev 2008; 8(4):CD000200.
Rabinstein AA, Atkinson JL, Wijdicks EFM. Emergency craniotomy in patients worsening due to expanded cerebral hematoma: to what purpose? Neurology 2002; 58: 1367-1372.
Rabinstein AA, Wijdicks EFM. Surgery for intracerebral hematoma: the search for the elusive right candidate. Rev Neurol Dis 2006; 3:163-172.
Rabinstein AA, Wijdicks EFM. Determinants of outcome in anticoagulation-associated cerebral hematoma requiring emergency evacuation. Arch Neurol 2007; 64: 203-206.