Evacuation of Intracerebral Hemorrhages

13

Evacuation of Intracerebral Hemorrhages JAMES E. SIEGLER, PATRICIA ZADNIK, H. ISAAC CHEN, and SHIH-SHAN LANG

Introduction Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with a high rate of morbidity and mortality. Multiple studies have established the need for careful blood pressure control1 and dedicated neurocritical care; however, the role for surgical decompression and hematoma evacuation has been debated.2–6 This is partially due to the inherent heterogeneity of the patient population, as well as the expanding use of oral anticoagulants. Furthermore, ICH may be associated with devastating neurological sequelae, and patient goals of care and quality of life should be considered prior to intervention.7 In this chapter, we review the neurosurgical and neuromedical approaches for the various etiologies and locations of ICH, as well as literature guiding surgical decision making for patients with ICH.

Neuroanatomy and Procedure Key Concepts • ICH is found within the brain tissue (or ventricle for intraventricular hemorrhage [IVH]). • ICH, from hypertensive vasculopathy, is typically found in the basal ganglia (putamen/caudate), thalamus, pons, cerebellum, and subcortical white matter.

ANATOMY AND PATHOLOGY ICH is found within the brain tissue, whereas epidural, subdural, and subarachnoid hemorrhages are found outside of brain tissue. Clinical presentation is variable depending on the location of the hemorrhage. Hematoma in the basal ganglia or thalamus may present with contralateral sensorimotor deficit. Pontine hemorrhage typically presents with coma and pinpoint pupils due to damage within the reticular activating system. Cerebellar hemorrhage manifests as vertigo/ dizziness, ataxia, and nausea/vomiting and also may cause hydrocephalus due to compression of the fourth ventricle.8 Spontaneous ICH (sICH) is most commonly caused by hypertensive vasculopathy and cerebral amyloid angiopathy but may also be due to other etiologies (Table 13.1). Hypertensive vasculopathy is generally thought to be due to intimal hyperplasia and lipohyalinosis of penetrating arteries, which leads to focal necrosis and ultimately rupture of the vessel wall. This type of vasculopathy typically affects vessels supplying the thalamus, putamen, caudate, pons, midbrain, and cerebellum. Cerebral amyloid

angiopathy is characterized by amyloid beta peptide deposits within small to medium-sized blood vessels. These deposits preferentially affect cortical vessels and thus predispose to lobar hemorrhages.9,10 The size, location, and intraventricular extension dictate surgical approach, and intraparenchymal hemorrhage often necessitates craniotomy for access to the lesion of interest. In sICH with associated intracranial hypertension, decompressive hemicraniectomy is a life-saving approach to improve cerebral perfusion and subsequent ischemia.11 Enlargement of the hematoma is associated with neurological deterioration and worse outcomes. These observations indicate that significant improvements in patient outcome from ICH may be achieved by minimizing both secondary brain ischemia and hematoma enlargement. Computed tomography angiography has been shown to identify the “spot sign,” which is a focal area of enhancement within hematomas. Studies show that this sign is associated with expansion of the hematoma, which leads to worse clinical outcomes.12,13 Hematoma enlargement also commonly occurs in anticoagulant-related hemorrhages. Conventional anticoagulation (i.e., warfarin) increases the risk of any ICH up to 10 times.14 Some studies show that reversing the anticoagulation effect improves the outcome of warfarin-related ICH in terms of preventing neurological deterioration and hematoma expansion.15 However, other studies show the rate of hematoma expansion in ICH patients taking anticoagulation is similar to nonanticoagulated ICH patients.16 As a standard of care for all patients with ICH, it is important to immediately reverse the anticoagulation effects to prevent hematoma enlargement. Surgical intervention for spontaneous supratentorial ICH has been studied extensively in the literature, with a recent series of randomized controlled clinical trials comparing the efficacy of surgical intervention versus optimal medical management for patients with intracerebral hemorrhage.5,6 The Surgical Trial in Intracerebral Haemorrhage (STICH) compared outcomes of patients with spontaneous supratentorial ICH who received conservative medical management in a neurocritical care unit with patients undergoing early surgical intervention (mostly craniotomy and evacuation) and concluded that there was no overall benefit for patients receiving early surgery compared with initial conservative treatment.5 This study was the first to utilize rigorous, randomized controlled trial methods to evaluate ICH outcomes; however, there was a 26% crossover rate for patients originally randomized to the initial conservative management group. Despite the failure of randomization, the results suggested a potential 133

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Table 13.1 Anatomical Sites of ICH Etiology of ICH

Anatomical Predilection

Hypertension

Deep gray nuclei, brainstem, cerebellar, lobar

Trauma

Cortical/lobar

Coagulopathy

Lobar, cerebellar

Vascular Conversion of ischemic infarction

Deep gray nuclei, brainstem, cerebellar, lobar

Amyloid angiopathy

Lobar, deep gray nuclei

AVM/cavernoma/AVF/aneurysm

Cortical/lobar, deep gray nuclei, cerebellar, brainstem

Venous sinus thrombosis

Cortical/lobar, thalamic (straight sinus, vein of Galen)

Neoplastic Secondary: lung carcinoma, breast, renal cell, melanoma, choriocarcinoma, papillary thyroid carcinoma

Juxtacortical/lobar, cerebellar

Primary: glioblastoma multiforme, glioma

Lobar

Infectious Septic emboli

Juxtacortical/lobar

Herpes simplex virus encephalitis

Mesial temporal lobe(s)

Toxicity Cocaine

Deep gray nuclei, brainstem, lobar

Amphetamines

Deep gray nuclei, brainstem, lobar

ICH, intracranial hemorrhage; AVM, arteriovenous malformation; AVF, arteriovenous fistula.

benefit for those patients with hemorrhagic lesions within 1 centimeter from the cortical surface. The high crossover rate and potential improvement for patients with lobar ICH led to STICH II. STICH II compared extended Glasgow Outcome Scale scores for patients undergoing early surgical evacuation within 12 hours plus medical therapy versus medical therapy alone.6 The authors concluded that early surgery did not increase death or disability at 6 months and resulted in a small survival advantage for patients without IVH.6

NEUROSURGICAL INTERVENTIONS The primary surgical interventions for ICH are either cerebrospinal fluid (CSF) diversion with ventriculostomy, craniotomy with hematoma evacuation, or decompressive hemicraniectomy. Minimally invasive approaches to hematoma evacuation are alternative approaches to open surgical intervention and show promise as potential novel therapeutic options. Craniotomy utilizes one or more burr holes connected via a high-speed air drill to create a bone flap. A burr hole involves drilling a single hole into the skull using a

pneumatic or handheld device at a region near the known hematoma. The bone flap is removed, and the hematoma is removed without opening the dura. The dura is typically reapproximated unless there is elevated intracranial pressure (ICP). The bone flap is replaced and secured in place with titanium or plastic plates and screws. Decompressive craniectomy follows similar methods compared with the craniotomy described earlier, with creation of a bone flap by making several burr holes and connecting them with a pneumatic drill. The dura is subsequently incised in a cruciate or stellate fashion and left open or covered with a dural substitute such as Duragen (Integra LifeSciences, Plainsboro, NJ) to further reduce brain swelling and improve cerebral perfusion pressure (CPP). In contrast to craniotomy, the bone flap is then placed in the patient’s abdomen or a bone bank for storage.17 Studies suggest that a craniectomy at least 12 cm in diameter provides the greatest benefit for patients with elevated ICP.18 In some cases, such as bilateral frontal lobe injury, bilateral frontal subdural hematoma, or diffuse injury, a bifrontal craniectomy may be performed. In cases of ICH complicated by IVH, an external ventricular drain (EVD) is almost universally required for prevention or management of obstructive hydrocephalus. This device is coupled with an external pressure transducer for ICP monitoring. EVDs and other ICP monitors are also used to continuously illustrate ICP waveforms, which can be used to predict future alterations in ICP and even clinical deterioration in experienced hands.19 EVDs are often preferred for ICP monitoring because they permit removal of CSF for the identification of its chemical contents and for the treatment of elevated ICP.20 Unfortunately, this device is limited largely by its risk of infections such as meningitis and ventriculitis, seen in up to 10% of patients, and this risk is greater for patients with ICH than other neurological conditions.21 This device, as well as any other implantable ICP monitor, is also associated with a small risk of subdural and intraparenchymal hemorrhage during insertion.22 In ICH extending to the ventricular system, blood products can reduce CSF resorption, leading to obstructive hydrocephalus, and an EVD functions to divert CSF out of the brain. Further, hemorrhage size and initial Glasgow Coma Scale (GCS) correlate with 30-day mortality in patients with ICH23; thus efforts have been made to reduce hemorrhage size. Because an EVD offers direct access to the ventricular system, it can be used for the administration of therapeutic agents. In the CLEAR-IVH trial, authors studied the effect of intraventricular recombinant tissue plasminogen activator (rtPA) on clot lysis in patients with IVH.24 Intraventricular rtPA, administered 12 to 24 hours after hemorrhage, was found to accelerate the radiographic resolution of IVH; however, the effectiveness varied by hemorrhage location, with greatest effectiveness on midline ventricles and with higher doses of rtPA.25 Infusion of rtPA was least effective on hemorrhage clearance in the posterolateral ventricles.25 Minimally invasive methods of hematoma evacuation have been proposed as an alternative to open craniotomy. Stereotactic and endoscopic evacuation of hemorrhage, coupled with local administration of rtPA, have also been studied in the neurosurgical treatment of IVH.26 In the Minimally Invasive Surgery plus rtPA for Intracerebral

13 • Evacuation of Intracerebral Hemorrhages

Hemorrhage Evacuation (MISTIE) trial, patients received rtPA via EVD followed by endoscopic hematoma aspiration.24 The investigators reported a reduction in mean clot size of 46% in the treatment group compared with 4% in the medical management group.24 In MISTIE-II, investigators also found a reduction in perihemorrhage edema in patients undergoing surgical evacuation of IVH.26 Although these results are encouraging, these trials have been powered to assess treatment safety and efficacy, and no survival benefit has been demonstrated to date.

POSTERIOR FOSSA HEMORRHAGE As in the case of supratentorial hemorrhage, posterior fossa hemorrhage (PFH) is caused by hypertension in 60% to 90% of cases.27 PFH may also be related to traumatic injury or vascular malformations. Cerebellar hemorrhages are occasionally reported in patients after supratentorial surgery, spinal surgery, and in patients with spontaneous intracranial hypotension.1,2 The mechanism is thought to be removal of large amounts of CSF or continuing CSF leak from a dural breach. The hemorrhage is remote from the surgical site or anatomical defect and may result from transient occlusion or rupture of superior cerebellar bridging veins. Rarely, cerebellar ICH may be related to metastases. Among metastatic tumors that produce ICH, lung adenocarcinoma and melanoma are the most common, accounting for over one-quarter of all intracranial metastases regardless of hemorrhage.9 In contrast, metastatic lesions that carry a higher propensity of hemorrhage include choriocarcinoma, papillary thyroid carcinoma, and renal cell carcinoma; however, these lesions are less frequently encountered.10 Location of the hemorrhage (midline vs. hemispheric) is important in determining symptoms and clinical course. Location may be more important than absolute hematoma size for prognosis. Generally speaking, the more lateral the hemorrhage and the smaller the hematoma, the more likely the brainstem structures are spared and the better the prognosis. 27 Surgical management for PFH involves bilateral suboccipital craniectomy (SOC) for decompression of the brainstem, with or without EVD placement, to treat obstructive hydrocephalus from fourth ventricle compression. Current evidence guiding surgical decision making comprises case series and clinical practice guidelines, as PFH are generally excluded from randomized controlled trials due to the lack of clinical equipoise.4,5 Current literature supports aggressive surgical intervention for patients with grade III fourth ventricular compression with complete obliteration of the fourth ventricle or distortion of the brainstem,28 or intracerebellar hemorrhage diameter greater than 40 mm and GCS
13.4 In patients with flaccid tetraplegia and severe brainstem or ventricular compression, surgical intervention is unlikely to improve outcome.4,283,22,29 SOC is the approach of choice for PFH and proceeds via a midline incision at the posterior aspect of the neck. A bone flap typically extends from the foramen magnum upwards toward the torcula, and the posterior ring of C1 may be removed for greater exposure.30 The dura is incised for access to the hematoma, which is then evacuated with

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irrigation and suctioning. Unlike supratentorial hematomas, the bone flap is typically not replaced at the time of surgery or later.

Perioperative Considerations Key Concepts • Initial management of ICH includes airway protection, hemodynamic stabilization, and consideration of advanced neurological monitoring and/or neurosurgical intervention. • In cases of anticoagulant-associated ICH, the underlying coagulopathy should be rapidly reversed in order to facilitate surgical intervention, prevent hematoma expansion, and mitigate neurological deterioration.

Initial medical management of ICH relies on hemodynamic and ventilatory support to promote adequate organ perfusion and function.22 Admission to a neurocritical care unit equipped with all necessary resources and manned with appropriately trained personnel improves mortality in this patient population.31 Strict blood pressure goals must be set because elevation may cause ICH progression, herniation, or even death.1 However, caution should be exercised because rapid reduction of arterial blood pressure may lead to cerebral ischemia. Invasive monitoring using an arterial catheter allows for continuous assessment of blood pressure changes. Fever is commonly observed in ICH and may be central in origin or due to medical complications of ICH (e.g., pneumonia, urinary tract infection, deep vein thrombosis; see Table 13.2). Although there are no randomized trials to support targeted temperature management or therapeutic cooling, maintenance of normothermia should be achieved in these patients because fever is significantly associated with greater mortality.32

Clinical Pearl Early admission to a Neuro ICU prevents mortality in cases of ICH.

Many patients with ICH may require intubation due to altered mentation, irregular respiratory patterns (e.g., Kussmaul’s or Cheyne-Stoke respirations), and impaired clearance of secretions. In acute or chronic hypertension, evaluation for other signs of end organ damage, especially renal and cardiac injury, should be assessed using serological and electrocardiographic assessment. Hematologic parameters must also be checked to ensure normal platelet count and coagulation function, the alterations of which may increase the likelihood for rebleeding. Hyperglycemia is associated with deleterious outcomes in ICH.33 However, tight glucose control has not been proven effective in the neurocritical care of patients with ICH because it may precipitate systemic hypoglycemia. There are no guidelines for targeted glucose management in ICH, but in the authors’ experience, a liberal blood glucose goal (160–180 mg/dL) is a safe and effective approach

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Table 13.2 Associated Medical and Neurological Complications Complications of ICH Neurological Hemorrhagic expansion Cerebral edema with/without herniation Intracranial hypertension Obstructive hydrocephalus Hematoma after ICH clot evacuation Stroke Medical Nosocomial infections Ventilator-associated pneumonia Indwelling urethral catheter–associated urinary tract infection Central venous catheter–associated bacteremia Ventriculitis/meningitis due to intracranial pressure monitoring Cellulitis/wound infection due to EVD placement or craniotomy/ craniectomy Fever Infection Fever due to deep venous thrombosis Central nervous system fever Vasculitis End organ dysfunction Acute kidney injury Ventilator-dependent respiratory failure Congestive heart failure exacerbation Delirium Delirium due to metabolic abnormalities or infection ICU delirium Pharmacological delirium Intoxication or withdrawal of substances of abuse ICH, intracranial hemorrhage; EVD, external ventricular drain; ICU, intensive care unit.

to critically ill patients with ICH. The use of insulin infusions may be considered on a case-by-case basis but should not be routinely implemented.

HEMOSTASIS Correction of an underlying coagulopathy should be performed within the first several hours of ictus and is a standard of care.22 Platelet counts less than 10,000/mL may contribute to spontaneous ICH in otherwise healthy individuals and ought to be treated with transfusion to prevent major bleeding.34 The most common causes of platelet dysfunction are platelet inhibitors such as aspirin, and this

warrants correction with platelet transfusion in ICH. Other causes of platelet dysfunction, such as uremia, do not have guidelines in place for cases of ICH. Desmopressin is not strongly supported in these instances but may be considered.35 Defects in the coagulation cascade (genetic or acquired hemophilia) should be corrected with specific factor replacement or treatment of the underlying cause of acquired hemophilia (e.g., plasma exchange or intravenous steroids may be considered in the setting of autoantibodies toward procoagulant factors).36 Hepatic insufficiency may produce a mixed coagulopathy/thrombophilia. Although coagulation markers may be abnormal in patients with underlying liver failure and ICH, there are limited data to support the efficacy of treating these laboratory abnormalities. One in eight cases of ICH are attributed to oral anticoagulant use, and this may be rising with the use of newer oral anticoagulants, such as direct thrombin inhibitors.37 It is imperative to recognize coagulopathies and correct them as rapidly as possible. Vitamin K antagonists (VKAs), such as warfarin, have long been heralded as the number-one culprit for iatrogenic coagulopathic ICH. For patients on VKAs, the historical recommendation had been to correct the international normalized ratio (INR) to <1.3 within 2 hours using fresh frozen plasma (FFP) and IV vitamin K.38 FFP is advantageous in that it contains all the human procoagulant factors, specifically those whose production are directly inhibited by VKAs. However, there are many limitations of FFP treatment, including transfusion reactions and infections. Additionally, the volume of FFP required to reverse coagulopathy may result in transfusion-associated circulatory overload or transfusion-related lung injury. Furthermore, because plasma is stored in a frozen state, it needs to be thawed prior to infusion, increasing the time to medication delivery, and thus reversal. The current recommendation for reversal of lifethreatening VKA-related hemorrhages is 4-factor PCC (prothrombin complex concentrate), which contains the four procoagulant factors inhibited by VKAs (II, VII, IX, X) in combination with 5 to 10 mg of IV vitamin K.39 When reconstituted, the volume is quite small, which allows for rapid preparation and infusion. It also does not have effects on mean arterial pressure (MAP), as do large volumes of FFP. In comparison to FFP, which may take several hours to achieve INR normalization, 4 F-PCC has been shown to reverse VKAs in minutes.40 Recombinant FVIIa is another alternative for reversing coagulopathic ICH; however, it is associated with a higher risk of thrombotic complications and confers no significant survival benefit to placebo.41

Clinical Pearl Prothrombin complex concentrate is the preferred reversal agent for warfarin or rivaroxaban-induced ICH.

Data regarding factor Xa inhibitors (rivaroxaban, apixaban, and edoxaban) have demonstrated a superiority to VKA in (1) the prevention of ischemic stroke in nonvalvular

13 • Evacuation of Intracerebral Hemorrhages

atrial fibrillation, (2) risk of anticoagulant-associated ICH, and (3) all-cause mortality.42 The data regarding appropriate reversal agents in humans are scant; animal data demonstrate mixed results regarding the benefit of PCC over activated PCC, factor eight inhibitor bypassing agent.43 Currently, there are no data to support reversal efficacy in apixaban-related ICH. Reversal of unfractionated heparin is achieved with protamine sulfate at a dose of 1 mg protamine for every 100 U of IV heparin, with a maximum dose of 50 mg. Reversal of IV bolus or infusion is warranted; prophylactic doses do not require reversal. The goal of treatment is to normalize the partial thromboplastin time (PTT) per the institution’s laboratory standards and stop bleeding. PTTs should be serially assessed over the first 6 hours of reversal given the half-life of heparin. Low-molecular-weight heparins are thought to be less responsive to protamine sulfate during reversal attempts. Dabigatran is a direct thrombin inhibitor used in secondary stroke prevention in patients with nonvalvular atrial fibrillation.44 Previously, the only option to reverse dabigatran was hemodialysis in the event of an emergency. This requires insertion of a large-bore dialysis catheter, which may take time and carries a high risk of secondary hemorrhage in the patient who is already coagulopathic. Recently idarucizumab has been approved by the Food and Drug Administration as a monoclonal antibody reversal agent for dabigatran and has been shown to effectively reverse the anticoagulant effect of dabigatran.45,46

Clinical Pearl There is evidence for surgical intervention for a subset of patients with ICH; however, an open discussion regarding goals of care and patient quality of life is appropriate in all patients with ICH.

Clinical Pearl In ICH patients receiving conservative management prior to planned surgical intervention, close monitoring in a Neuro ICU is important to improve clinical outcome.

When medical management has failed to prevent significant neurological deterioration in ICH, surgical management may be necessary. Hemorrhage increases ICP, which decreases cerebral perfusion, thus resulting in delayed ischemic changes in the penumbra surrounding the initial hematoma if it is not evacuated. Once identified, surgical management reduces ICP through removal of the hematoma, bone, or both to reduce compression on the brain parenchyma in an effort to reduce cerebral edema. Access to the hematoma may be through a burr hole, craniotomy, or craniectomy. Hematoma removal involves drainage or irrigation, with or without placement of a drain. Reversal of oral anticoagulation is recommended to slow hematoma

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expansion and improve intraoperative hemostasis prior to surgical intervention.22

Postoperative ICU Management Key Concepts • In facilities with appropriately trained personnel and adequate resources, invasive ICP monitoring and treatment are recommended for a goal ICP <20 cm H2O. • ICP may be reduced via reduction in central nervous system metabolic demand (e.g., sedation), hyperventilation, osmotic therapy (e.g., mannitol or hypertonic saline), and neurosurgical decompression.

ICP MONITORING Although the neurocritical management of ICH is largely based on standard critical care practices as stated earlier, the neuromedical aspects focus on physiological principles behind ICP management. In adults, elevated ICP can be loosely defined as >15 to 20 cm H2O when the patient is lying in the lateral decubitus position.20 The current practice of invasive ICP monitoring as a means to determine management in ICH and other neurocritical care scenarios remains extensively debated. ICP is traditionally monitored using an EVD, as described earlier.47 The use of a Licox Brain Oxygen Monitoring System (Integra LifeSciences, Plainsboro, NJ) may provide added insight into hypoxic injury after ICH,48 but its ability to improve outcomes after ICH has not been fully explored in prospective trials. Currently, experts recommend invasive ICP monitoring at centers where this is performed on a routine basis and clinicians are experienced at the interpretation and management of alterations in ICP. In cases where subtle changes early in the course of a patient’s care may alter emergent treatment decisions, these changes may be detected early by using invasive monitoring devices.

Clinical Pearl In experienced hands, invasive ICP monitoring may improve outcome in ICH.

With few exceptions (e.g., infants whose cranial sutures have not yet closed), the calvarium can be considered a rigid container enclosing a fixed volume of contents. In comparison, fluid and other soft tissues within the cranial vault are somewhat more compliant and may be slightly compressible with rising pressure changes.20 However, the compressibility of neural parenchyma and surrounding fluid is trivial, rendering the pressure/volume adaptability of these tissues clinically negligible.20 These theoretically distensible and compressible intracranial contents include three main components: brain, arterial and venous blood, and CSF. The Monro-Kellie doctrine states that because the volume of the cranial vault remains constant, any

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change in ICP or volume of a single intracranial component will produce a change in volume of the remaining components.

Clinical Pearl The Monro-Kellie doctrine: If the volume of any one component within the skull increases, the volume of the remaining components must decrease.

CPP ¼ MAP  ICP When represented mathematically, ICP is equivalent to MAP minus the CPP.20 This simple formula is of paramount importance in neurocritical care because it demonstrates the dynamic nature of CPP as it is affected by changes in ICP and systemic arterial pressure. Any increase in ICP or reduction in systemic blood pressure will effectively reduce cerebral perfusion. Conversely, any reduction in ICP or rise in blood pressure will increase cerebral perfusion. The relationship between MAP and CPP is not linear. Autoregulatory mechanisms within the central nervous system permit a stable CPP while MAP fluctuates (Fig. 13.1), except in certain conditions of impaired autoregulation such as ICH. These mechanisms remain highly effective except in situations of extreme hypotension (MAP <50 mm Hg) or hypertension (MAP >150 mm Hg) and intracranial insult producing autonomic disruption.49

MANAGEMENT OF INTRACRANIAL HYPERTENSION In the event of elevated ICP, the CPP should be kept at a goal of 60 to 150 mm Hg in order to preserve susceptible neural parenchyma.22 The artificial augmentation of CPP may only affect cerebral blood flow when (1) cerebral autoregulation has failed (e.g., acute ischemic stroke or ICH) or (2) CPP is too low for cerebral autoregulatory mechanisms to compensate (e.g., distributive shock in the setting of sepsis). Goal ICP should be <20 cm H2O. The head of bed

Cerebral blood flow (ml/min/100g)

80

50

20 20

60

100

140

180

Mean arterial pressure (mmHG) Fig. 13.1 Logarithmic relationship between mean arterial pressure and cerebral blood flow with dynamic autoregulation. (Adapted from Peterson E, Chesnut RM. Static autoregulation is intact in majority of patients with severe traumatic brain injury. J Trauma. 2009;67:944–949.)

should be raised to >30 degrees, and the patient’s neck should be midline in order to optimize jugular venous drainage. Metabolic demands of the central nervous system should be reduced—for example, fevers controlled, seizures treated with antiepileptic agents, etc. In patients who have indwelling EVDs that permit drainage of CSF, CSF removal should be considered. For patients with elevated ICP, intubation and sedation should be considered first. Hypocarbia hyperventilation leads to cerebral vasoconstriction, which temporarily reduces cerebral blood flow and decreases ICP. This may be used as a bridge to more definitive therapy.50 Deep sedation with propofol or barbiturates while intubated confers a secondary benefit of also reducing cerebral activity, which can reduce ICP.22 The mainstay of treatments for intractable elevated ICP includes hyperosmolar therapy, namely mannitol or hypertonic saline (HTS) infusions. Mannitol is typically considered a first-line pharmacological agent for elevated ICP, except in the case of renal insufficiency, where it is relatively contraindicated. HTS may have neuroprotective effects; however, currently the literature suggests that these agents are equivalent in efficacy. Both mannitol and HTS increase the osmotic gradient across the blood–brain barrier and may effectively “draw out” osmoles from the brain parenchyma, thereby reducing ICP.51

Clinical Pearl Osmotic therapy should be implemented in cases of ICH where life-threatening edema or herniation is likely.

As a final resort, patients with refractory ICH should be considered for EVD drainage first and then decompressive hemicraniectomy as described previously in this chapter. Fig. 13.2 outlines a recommended ICP management algorithm.

RESUMPTION OF ANTICOAGULATION One major difficulty in the treatment of anticoagulantassociated ICH is the timing of anticoagulant resumption. Current guidelines recommend against anticoagulation resumption in lobar ICH but may be considered in cases of other ICH; however, the level of evidence is moderate and further investigations are needed.22 Data on resumption of antiplatelet therapies such as aspirin or clopidogrel are also lacking. Recommendations suggest there is utility in antiplatelet resumption after ICH as long as there are definite indications.22 At our center, we resume antithrombotic therapy primarily in patients with a higher risk of recurrent thrombosis than of ICH. Special circumstances need to be addressed for patients on clopidogrel or other antiplatelet agents used to manage cardiovascular health. In patients with a recent coronary artery stent, clopidogrel is essential for reducing the risk of in-stent restenosis. The decision to resume antithrombotic therapy should be made on a case-by-case basis with the risks and benefits discussed with the patient and/or decisionmaking care provider.

13 • Evacuation of Intracerebral Hemorrhages

139

ICH confirmed Suspicion of elevated ICP, or confirmation via invasive monitoring

Early intervention

Raise head of bed to 30 degrees & face head forward

Maintain normotension, normothermia, normoglycemia

Treat seizure, if present

Fail Consider noninvasive intervention Pharmacologic intervention Mannitol 1g/kg IV bolus every 6 hrs

SOsm <320 mg/dL, SOsm gap <20

3% HTS IV infusion

SOsm >320 mg/dL

23.4% or 5% HTS IV bolus every 6 hours

Na >160 mg/dL

Na <160 mg/dL (goal 145–160)

Fail If EVD in place, drain CSF as tolerated Surgical intervention

Fail Consider surgical intervention

Fig. 13.2 Management algorithm for elevated ICP.

A

B

Fig. 13.3 A 48-year-old female with history of hypertension developed acute-onset aphasia and right-sided hemiplegia. (A) HCT illustrated a left basal ganglia intraparenchymal hemorrhage. After developing signs of herniation, she underwent an emergent decompressive hemicraniectomy (B).

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Value

the literature discussing operative decision making and the type of operation to perform. Perioperative management of ICH requires a multidisciplinary team and dedicated neurocritical unit to optimize care.

<80 years

0 points

References

80 years

1 point

1. Anderson CS, Huang Y, Arima H, et al. Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the intensive blood pressure reduction in acute cerebral haemorrhage trial (interact). Stroke. 2010;41:307–312. 2. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58:S16–S24. discussion Si–iv. 3. Chen SH, Chen Y, Fang WK, Huang DW, Huang KC, Tseng SH. Comparison of craniotomy and decompressive craniectomy in severely head-injured patients with acute subdural hematoma. J Trauma. 2011;71:1632–1636. 4. Kobayashi S, Sato A, Kageyama Y, Nakamura H, Watanabe Y, Yamaura A. Treatment of hypertensive cerebellar hemorrhage: surgical or conservative management? Neurosurgery. 1994;34:246–250. discussion 250–241. 5. Mendelow AD, Gregson BA, Fernandes HM, et al. 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;365:387–397. 6. Mendelow AD, Gregson BA, Rowan EN, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet. 2013;382:397–408. 7. Honeybul S, Janzen C, Kruger K, Ho KM. Decompressive craniectomy for severe traumatic brain injury: is life worth living? J Neurosurg. 2013;119:1566–1575. 8. Hallevi H, Albright KC, Aronowski J, et al. Intraventricular hemorrhage: anatomic relationships and clinical implications. Neurology. 2008;70:848–852. 9. Barnholtz-Sloan JS, Sloan AE, Davis FG, Vigneau FD, Lai P, Sawaya RE. Incidence proportions of brain metastases in patients diagnosed (1973 to 2001) in the metropolitan detroit cancer surveillance system. J Clin Oncol. 2004;22:2865–2872. 10. Soffietti R, Ducati A, Ruda R. Brain metastases. Handb Clin Neurol. 2012;105:747–755. 11. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of traumatic parenchymal lesions. Neurosurgery. 2006;58:S25–S46. discussion Si–iv. 12. Demchuk AM, Dowlatshahi D, Rodriguez-Luna D, et al. Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the ct-angiography spot sign (predict): a prospective observational study. Lancet Neurol. 2012;11:307–314. 13. Wada R, Aviv RI, Fox AJ, et al. CT angiography “spot sign” predicts hematoma expansion in acute intracerebral hemorrhage. Stroke. 2007;38:1257–1262. 14. Hart RG, Boop BS, Anderson DC. Oral anticoagulants and intracranial hemorrhage. Facts and hypotheses. Stroke. 1995;26:1471–1477. 15. Le Roux P, Pollack Jr CV, Milan M, Schaefer A. Race against the clock: overcoming challenges in the management of anticoagulant-associated intracerebral hemorrhage. J Neurosurg. 2014;121(Suppl):1–20. 16. Horstmann S, Rizos T, Lauseker M, et al. Intracerebral hemorrhage during anticoagulation with vitamin k antagonists: a consecutive observational study. J Neurol. 2013;260:2046–2051. 17. Iwama T, Yamada J, Imai S, Shinoda J, Funakoshi T, Sakai N. The use of frozen autogenous bone flaps in delayed cranioplasty revisited. Neurosurgery. 2003;52:591–596. discussion 595–596. 18. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58:S7–S15. discussion Si–iv. 19. Chesnut R, Videtta W, Vespa P, Le Roux P. The Participants in the International Multidisciplinary Consensus Conference on Multimodality M. Intracranial pressure monitoring: fundamental considerations and rationale for monitoring. Neurocrit Care. 2014;21(2): 64–84. 20. Steiner LA, Andrews PJ. Monitoring the injured brain: ICP and Cbf. Br J Anaesth. 2006;97:26–38.

Table 13.3 List of Variables for Scoring ICH ICH Score Item Age

Location Supratentorial

0 points

Infratentorial

1 point

Level of Consciousness GCS 13–15

0 points

GCS 5–12

1 point

GCS 3–4

2 points

ICH volume <30 cc

0 points

30 cc

1 point

Intraventricular Extension No

0 points

Yes

1 point

ICH, intracranial hemorrhage; GCS, Glasgow Coma Scale.

PROGNOSTICATION Clinical classification of ICH based on severity and location is crucial in guiding surgical management, and rapidly acquired CT imaging is a necessary adjunct to the neurological examination when evaluating patients with suspected hemorrhage. Commonly, the validated ICH score is used to quantify the clinical severity of ICH, with higher scores associated with poorer outcomes (Table 13.3).46 The Graeb score may be used to prognosticate for patients with significant IVH.52 The Graeb score is calculated by adding together a score for each lateral ventricle separately (1 ¼ trace blood, 2 ¼ < 50% ventricle filled with blood, 3 ¼ >50% ventricle filled with blood, 4 ¼ ventricle completely casted and expanded). The third and fourth ventricles, separately, are added to this total (1 ¼ blood present, ventricle normal size; 2 ¼ ventricle filled with blood and expanded) for a maximum score of 12. The Graeb scale is the most commonly reported scale in adults and correlates significantly with short-term outcome (Glasgow Outcome Score at 1 month).12

Conclusions ICH in the adult population is a common and important cause of neurological morbidity and mortality. Trauma, use of anticoagulation, and hypertension are the most frequent causes of ICH. In the appropriate setting, occult causes such as cerebral venous sinus thrombosis ought to be investigated given the dramatically different management (e.g., anticoagulation). There are limited studies in

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