Surgical Approaches to Intracerebral Hemorrhage
Pearls
Rapid correction of coagulopathies can reduce hematoma expansion with the use of appropriate reversal agents and in a timely fashion, which can reduce morbidity associated with volume expansion.
The combination of both stereotactically placed catheters and open surgical evacuation can be done in a safe manner and lead to reduced morbidity in intracerebral hemorrhage (ICH) patients.
Emergent hematoma evacuation remains a lifesaving intervention in younger patients with large ICH volume who are deteriorating clinically, and in patients with cerebellar ICH. These patients have generally been excluded from clinical trials.
Volume reduction or enhanced clearance rate of hematoma may be the operative goals of interventions for ICH in most patients with stable ICH and slow neurologic decline, as opposed to immediate and complete hematoma evacuation.
Intraventricular thrombolytics can be used safely and lead to increased clearing of intraventricular hemorrhage (IVH) and reduced rates of hydrocephalus without an increased risk of rehemorrhage. The effectiveness of this intervention is currently being tested in a phase III trial.
Spontaneous intracerebral hemorrhage (ICH), although accounting for only 10 to 30% of all stroke admissions to hospitals,1 – 3 represents the most devastating and costly1 – 3 type of stroke and harbors the poorest outcomes, with only approximately 20% of patients regaining any functional dependence at 6 months.1 , 3 The great majority of hemorrhagic strokes consist of intracerebral hemorrhage with or without intraventricular hemorrhage (IVH) and have been associated with 30-day mortality rates ranging from 30 to 50%2 – 9 and case disability rates above 80%.10 – 13 As such, the societal and financial burden continues to pose a serious health care economic load. Unlike ischemic strokes for which noteworthy therapeutic progress has been made through acute thrombolysis and several effective medical and surgical approaches for secondary stroke prevention, the management of spontaneous ICH has remained controversial. As technology and surgical techniques have continued to evolve and improve, the question regarding surgical treatment for ICH continues to be reassessed. McKissock and colleagues14 conducted the first prospective, randomized trial of surgical treatment of ICH in 1961 and raised the possibility that carefully selected patients may benefit from surgical therapy of ICH with and without accompanying IVH. This chapter discusses ICH and IVH, and the surgical management, outcomes, and future considerations and studies regarding this devastating type of stroke.
♦ Epidemiology
Intracerebral hemorrhage can be classified as primary or secondary. Primary ICH, accounting for over 70% of ICH cases, is typically the result of cerebral amyloid angiopathy (CAA) or chronic hypertension (hypertensive arteriopathy), most commonly in the elderly population.1 , 4 , 15 – 18 There is a slight male dominance of the disease, and incidence rates are approximately twice as high in African-American, Hispanic, and Asian populations.1 , 18 – 23 Primary ICH is often found in the deeper, subcortical areas of the brain. Secondary ICH often results from the use of anticoagulants or antithrombolytic agents, the presence of vascular anomalies, the use of illicit drugs, or from coagulation disorders, and is more often found in younger patients. Secondary ICHs are more commonly lobar in location24 ( Fig. 27.1 ).
The strongest risk factors for primary ICH are hypertension and advancing age. In addition, a wide variety of studies have demonstrated strong independent relationships of the Glasgow Coma Scale (GCS) score on presentation (inverse relationship), age, and ICH volume on outcome after ICH.25 – 32 The independent and negative impact of associated IVH and its relationship to increased mortality have also been reported.8 , 13 , 16 , 25 – 30 , 33 – 38 Clot location, smoking and drinking histories, cardiac disease, and diabetes are also related risk factors for ICH.6 , 27 30
Despite the suggested benefit of surgery in trauma-related ICH and the removal of subdural hematoma, the role of surgical intervention in nontraumatic, spontaneous ICH remains inconsistent in clinical practice. In spite of this discordant approach to patients with ICH, approximately 6000 to 7000 patients undergo operative removal of ICH annually.39 , 40 Recent study suggested potential eligibility for ICH evacuation in up to 15% of prospectively screened ICH cases, with up to 30% of cases benefiting from drainage of associated IVH.41 The goal of surgery in ICH and IVH is to decrease the size of the clot, reduce any mass effect, limit increases in intracranial pressure (ICP), and minimize the neurotoxic effects of blood-degradation products.
♦ Pathogenesis
Primary ICH is the result of chronic damage to the small blood vessels in the brain. The cerebral arterioles play an integral role in reducing blood pressure and pulse pressure in the microvasculature of the brain, but are susceptible to the effects of chronic hypertension. Chronic hypertension stimulates gradual, adaptive changes in an attempt to preserve the blood–brain barrier. Elevated blood pressure can lead to smooth muscle hyperplasia, vascular remodeling, and eventually cellular death. When this occurs, the affected arterioles become largely fibrotic, lacking viable smooth muscle cells, which is characterized by fibrinoid necrosis and lipohyalinosis, leading to the formation of Charcot-Bouchardaneurysms, which make vessels more susceptible to rupture.42 The small lenticulostriate vessels that originate as right-angle branches from the middle cerebral artery stem (a large diameter vessel with a vigorous, high pressure blood flow) are particularly susceptible to damage from hypertension.43 These vessels penetrate into the basal ganglia, and thus when a rupture occurs, it more frequently involves the deeper regions of the brain including the basal ganglia, thalamus, subcortical white matter, and pons.
Hypertension is of particular importance not only because it can cause ICH, but also because it is a potentially modifiable risk factor, and is hence amenable to primary prevention strategies. Hypertension increases the risk of stroke by two to more than four times, independent of other risk factors. Elevation of either systolic or diastolic pressure is associated with greater risk.44 Brott et al17 suggested that population strategies to control hypertension could decrease the incidence of ICH by 39%.
Cerebral amyloid angiopathy is a very common finding in the brains of Alzheimer’s disease (AD) patients and is recognized as a histopathologic attribute of the disease. CAA is the progressive process by which an amyloid protein deposits in the cerebral blood vessels, preferentially in the cortical and leptomeningeal arteries and arterioles, and results in degenerative vascular changes. The importance of CAA as a risk factor for ICH has become increasingly more significant in recent years as it was revealed that the same amyloid β (Aβ) peptide that was associated with AD was also responsible for a significant proportion of ICH (7–10%) occurring in nonhypertensive patients.45 These degenerative changes have been associated with decreased vascular integrity and fragility, which increase the susceptibility to rupture.46
Until recently, the diagnosis of probable CAA was based on neuropathologic findings in a biopsy specimen or in tissue obtained during hematoma evacuation. Staining techniques with Congo red allows ready identification of amyloid in tissue samples. In the absence of neuropathologic confirmation, the diagnosis of probable CAA has been based on the finding of frequent hemorrhages, and sometimes microhemorrhages, in patients over 60 years of age, or in instances where there is a solitary hemorrhage with no other obvious cause. From a current radiologic standpoint, the most sensitive techniques for detecting microhemorrhages associated with CAA are by T2-weighted gradient echo (GRE) and susceptibility-weighted magnetic resonance imaging (MRI), as these can detect a loss of signal from the presence of hemosiderin in the foci of the microbleeds.
The ApoE gene on chromosome 21 has been associated with many cases of CAA and is polymorphic in humans, encoding one of three alleles designated ε2, ε3, or ε4.47 – 50 Recent evidence suggests that although the ε3 allele is the normal genotype, the ε4 allele predisposes deposition of Aβ in the walls of the small blood vessels while the ε2 is associated with CAA-related hemorrhage.51 It has also been shown that carriers of the ε2 or ε4 allele have an increased risk of recurrent ICH.52 , 53 In addition, there may be an interaction between genetic and environmental factors that increases the risk of ICH in the presence of a genetic predisposition. It has been suggested that CAA patients exposed to clinical risk factors such as hypertension, antiplatelet/anticoagulant medication, and minor head trauma appear to be at most risk of lobar hemorrhage if those same patients were ApoE ε2 carriers than those who did not carry that allele.50
♦ Acute Resuscitation and Medical Management
The clinical presentation of ICH patients is highly variable but most often includes depressed mental status, focal neurologic deficits, and cardiovascular instability. After the primary survey of the patient, including the securing of an airway, assessment of breathing, and maintenance of adequate cerebral and systemic circulation and blood pressure, the patient can then be evaluated from a neurologic point of view.
Intracranial imaging with a noncontrast computed tomography (CT) scan of the head is the most common modality for evaluation of acute mental status and neurologic changes, and it is highly sensitive and specific for the diagnosis of ICH. Once the diagnosis of ICH has been made, then the management team can focus on the parameters that are important for minimizing hematoma expansion and secondary sequelae. At this point, it is important to consider potential etiologies of ICH. Once stabilization of the patient has occurred, other imaging modalities, such as computed tomography angiography (CTA) or MRI of the brain, can be used to delineate potential etiologic factors responsible for the ICH, such as aneurysm, arteriovenous malformation (AVM), tumor, and so on.
Intracranial Pressure Management
For patients who present with impaired level of consciousness (typically a GCS score <9) or for those whose neurologic exam is unreliable, intracranial pressure (ICP) monitoring should be considered. ICP can be monitored using a fiberoptic intraparenchymal monitor (“bolt”) or an external ventricular drain (EVD). The bolt is more accurate and can be combined with an intraventricular monitor. The intraventricular component allows therapeutic drainage of cerebrospinal fluid (CSF) and accurate monitoring of ICP, especially in cases of ventricular obstruction. Optimizing the patient’s position by elevation of the head while keeping the head midline and keeping the temperature <37°C, thus preventing hyperthermia and euvolemia, and draining CSF through the ventricular drain can be used to control ICP. Altering the carbon dioxide levels in the blood through mild hyperventilation can also alter the volume load and demand of the brain but should not be maintained for long periods of time. The effects of chronic hyperventilation can be compensated by metabolic acidosis over time, limiting its chronic effect on ICP, and increasing vulnerability to rebound hyperperfusion. Pharmacologic management of ICP may involve hyperosmotic solutions, for example, 3% sodium or mannitol. Diuretics can also lead to increased sodium levels and decreases in systemic volume. Finally, sedatives, paralytics, and barbiturates can be used to reduce the systemic and cerebral metabolic demands and thus reduce brain blood volume and facilitate ICP control
Blood Pressure Control
Patients with ICH often present with elevated systolic blood pressure (SBP) of >160 mm Hg. It has been shown that hematoma enlargement has been associated with elevated blood pressure and neurologic deterioration.15 , 16 Further, elevated pressure has been associated with the expansion of the original hematoma, intraventricular extension, and worse overall outcome.54 – 57 However, in the face of elevated ICP, the acute management of SBP can be a challenge; one must not decrease cerebral perfusion pressure (CPP) at the expense of BP management. The American Heart Association guidelines currently recommend blood pressure control if the SBP is >180 mm Hg or mean arterial pressure is >130 mm Hg. Several reports have suggested that reduced SBP within 6 hour was associated with improved mortality; however, these studies did not control for pretreatment GCS, ICH volume, and the presence of IVH—factors shown to be associated with increased morbidity and mortality. Acute and rapid reduction of SBP has also been shown to increase mortality primarily due to ischemic complications, both systemic and neurologic. Recent trials examining the effect of blood pressure control in patients with ICH have been completed. The Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT) demonstrated no significant difference in neurologic deterioration at 72 hours between ICH groups who presented within 6 hour of onset and whose blood pressure was reduced to <180 mm Hg or <140 mm Hg; however, there was a trend toward reduction of ICH volume growth in patients whose blood pressure was more aggressively reduced.58 Another trial, the Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial, did not preliminarily show a significant difference between three groups with targeted SBP targets.59 , 60 Worster et al61 recently reviewed the literature regarding whether early intensive lowering of blood pressure reduced hematoma volume and improved clinical outcomes, and found that although there are trends toward reduction in hematoma volume, there is no improvement in clinical outcomes. Therefore, it is currently reasonable to treat elevated blood pressures using the American Heart Association (AHA) guidelines. Ongoing clinical trials such as ATACH and INTERACT2 will continue to increase our understanding of the principles of blood pressure management in acute ICH.
Reversal of Coagulopathy
Hemostasis and correction of an underlying coagulopathy are important determinants of hematoma expansion. Patients who present with ICH often have been on some form of anticoagulant or antiplatelet therapy, thus presenting with an altered ability to maintain adequate hemostasis in the face of hemorrhage. It is estimated that approximately 15% of ICH cases are associated with warfarin use, which has been shown to increase the risk of ICH five to 10 times and doubles the risk of mortality and increases the risk of progressive bleeding and clinical deterioration. Furthermore, it has been shown that patients on warfarin therapy are associated with larger initial hematoma volumes and continue to expand for longer durations.62 Some studies have also shown that antiplatelet agents increase the risk of ICH63 , 64; for example, aspirin therapy has been shown to increase the risk of ICH by approximately 40% and in combination with clopidogrel up to approximately 60%, but some studies have refuted this claim.6 , 65 , 66 The cardiovascular benefits of these medications often outweigh their hemorrhage risks in most patients. However, when patients present with ICH and have been on anticoagulants, it is paramount to begin the correction of their coagulation parameters immediately so as to reduce the chance for hematoma expansion. In patients with mechanical heart valves or persistent atrial fibrillation requiring anticoagulant therapy, the patients’ international normalized ratio (INR) can be lowered to 1.5 to 2 without a significant increase in stroke risk over a short period of time (<2 weeks).67 , 68
There have not been any prospective randomized studies addressing the efficacy of anticoagulant reversal protocols. The available reversal agents for reversal of anticoagulation are vitamin K1, fresh frozen plasma (FFP), prothrombin complex conjugates (PCCs), and recombinant activated factor VII (rFVIIa). Vitamin K1 administration, either intravenous or oral, has been shown to be effective but not in the early hours, making this agent ineffective for the hyperacute period.69 Although the most common method of anticoagulant reversal has been the intravenous administration of FFP, the optimal dosing parameters have not been well established. Administration of FFP is normally delayed due to the requirement of compatibility testing and thawing of the blood products, which can significantly affect reversal; every 30-minute period that passes before administration has been shown to lead to a 20% reduction in the successful reversal of INR at 24 hours.70 With ICH growth most commonly documented in the first hours after symptom onset, reversal of coagulopathy with FFP is often too slow for timely benefit. Furthermore, administration of FFP can be complicated with circulatory overload, allergic reactions, transfusion-related acute lung injury, citrate toxicity, and transmission of viral infections.71 Although not available in the United States, but shown to be effective in several small European studies, PCC provides clotting factors that are deficient in anticoagulated patients and can reverse the INR in <30 minutes; however, improved clinical outcomes have also not been convincingly demonstrated.71
A promising agent in reduction of hematoma expansion has been rFVIIa, approved in the U.S. for bleeding complications of hemophilia. Several reports have documented rapid effective reversal of warfarin coagulopathy, allowing safe neurosurgical intervention in patients deteriorating from intracranial hemorrhage,70 – 77 The impact of rFVIIa on ICH growth in coagulopathic patients has not been carefully evaluated, although it is increasingly used (compassionate off-label indication) in deteriorating ICH patients and in cases requiring invasive interventions. Risks of thromboembolism with this agent have been reported,78 but mostly in non-ICH patients, and there is particular concern about prothrombotic complications in patients with critical coronary disease, mechanical heart valves, cerebrovascular stenoses, or hypercoagulable states, so the potential benefits of rapid arrest of ICH growth must be carefully weighed against these risks on a case-by-case basis.79
There has been interest in the potential benefit of rFVIIa in preventing early ICH volume expansion in noncoagulopathic patients. Although administration of rFVIIa has been shown to significantly reduce the incidence of ICH volume expansion within 3 hours of symptom onset, the clinical benefit of reduced mortality and morbidity did not reach statistical significance in the phase III Factor Seven for Acute Hemorrhagic Stroke (FAST) study.80 – 82 A very useful estimate of doserelated complications was provided in these studies. However, variant dosing of rFVIIa and lack of ICH risk stratification could have potentially masked benefits in some subgroups.83 Further, this FAST approach did not control for additional measures of reducing mortality and morbidity such as blood pressure reduction and replacement of vitamin K–dependent factors, or adjuvant interventions for ICH or IVH volume reduction that could enhance clinical benefit. It is thought that the combination of strategies could potentially lead to decreased hematoma expansion and improved clinical outcomes.
Despite the optimal correction of the INR, the patient may remain coagulopathic due to insufficient levels of factor IX, not assessed or corrected by examining the INR or by inadequate platelet function, most often in patients on chronic aspirin or clopidogrel oral therapy. Reversal of platelet dysfunction is often initiated with one to two packs of single donor platelets. The evidence for adding desmopressin (deamino-8-D-arginine vasopressin [DDAVP]) is lacking for efficacy. However, no published guidelines or general consensus exists regarding the reversal of antiplatelet agents in the face of ICH.63 , 65 , 84 , 85 However, decreased platelet activity in patients with ICH has recently been associated with IVH extension and worse clinical outcomes.86
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