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Surgical Treatment of Hemorrhagic Stroke 

Surgical Treatment of Hemorrhagic Stroke
Surgical Treatment of Hemorrhagic Stroke
Acute Stroke Management in the First 24 Hours: A Practical Guide for Clinicians

Vladimir Ljubimov

, Travis Dailey

, and Siviero Agazzi


1 Introduction

Although hemorrhagic strokes account for only 10–15% of all the strokes, they are the most fatal with a 30-day mortality of up to 40%.1 Only one-third of survivors will recover to functional independence. Hemorrhagic stroke can often be managed with medical therapy alone. Great controversy currently exists on the role of surgery in its overall management strategy. Past trials dealing with the surgical evacuation of the blood clot have failed to show much benefit, yet more recent trials, including minimally invasive surgical approaches and new emerging technologies, hold promise for treatment. Here, we discuss the decision-making process for surgical treatment of intracerebral and intraventricular hemorrhages (IVHs), epidural and subdural hematomas (SDHs), and subarachnoid hemorrhage (SAH) (Figure 14.1).

Figure 14.1 Surgical management of hemorrhagic stroke.

Figure 14.1 Surgical management of hemorrhagic stroke.

abbreviations: CT, computed tomography; EVD, external ventricular drain; IA, intra-arterial; ICH, Intracerebral hemorrhage, ICP, intracranial pressure; IVH, Intraventricular hemorrhage; LOC, level of consciousness; MRI, magnetic resonance imaging; SAH, subarachnoid hemorrhage.

Question 14.1: What is considered the “normal” intracranial pressure (ICP)?

Answer: The normal range of ICP depends on patient’s age. In adults, ICP below 10–15 mm Hg is considered normal.

2 Basic principles of intracranial pathophysiology

Published commentary on the effects of elevated ICP goes back to at least the description provided in 1783 by Monroe.2 Kellie further expanded on it in 1824.3 Over time, their collective work became known as the Monroe–Kellie doctrine. It describes the intracranial compartment as the set of three physiologic components: the brain, the cerebrospinal fluid (CSF), and the blood.

Because the skull is a closed and rigid structure, additional intracranial elements will cause displacement of the existing physiologic components and/or an increase in the ICP. Displacement can produce radiographic findings such as compression of the basilar cisterns, compression of the ventricles, midline shift, effacement of the sulci, and displacement of the brain parenchyma.

Elevation of the ICP, in additional to radiographic characteristics, may produce a combination of clinical findings including headaches, confusion, nausea, emesis, decrease in mental status, pupillary abnormalities, coma, loss of brainstem reflexes, and, finally, brain death. In the Emergency Department (ED), the diagnosis of an intracranial hemorrhage relies on radiographic findings (non-contrast computed tomography [CT] scan and magnetic resonance imaging [MRI]). The evidence of rising ICP is heavily factored in the decision-making process for medical versus surgical treatment (Figure 14.1).

As demonstrated in Figure 14.2, the rise in intracranial volume will initially cause only a very minor rise in ICP. This compensation mechanism is mostly mediated by a shift of CSF away from the brain into the lumbar spinal cistern. A critical aspect of this pressure volume curve is the “genu” of the curve or “critical volume.” Once the critical volume has been reached, further fluid shifts are not possible, and the brain is now devoid of any compensating mechanism. From this point forward, even a small increase in the intracranial volume will cause a dramatic increase in the ICP.

Figure 14.2 The Monroe Kelley doctrine and the intracranial pressure–volume curve.

Figure 14.2 The Monroe Kelley doctrine and the intracranial pressure–volume curve.

3 Initial clinical evaluation in the Emergency Department

The initial clinical assessment of a patient with hemorrhagic stroke should be aimed at determining the presence of increased ICP and immediately taking action to treat and prevent further elevation.

3.1 Awake patient

A patient arriving to the ED with an intracranial hemorrhage who is fully conscious has a normal cerebral perfusion pressure. However, he or she could still be in danger of deteriorating if the intracranial volume is approaching the knee of the pressure/volume curve and should therefore be closely monitored with frequent assessment of their neurological status. Increasing headaches, nausea and vomiting, and progressive somnolence should be considered alarming signs of impending neurological deterioration.

3.2 Somnolent or comatose patient

A patient with an intracranial hemorrhage arriving at the ED with an altered mental status should be considered as having an elevated ICP. The longer the period of elevated ICP is, the higher the risk of permanent damage to the brain is. Therefore, in these patients, steps should be taken quickly to measure and treat the ICP, and neurosurgical consultation should be immediately obtained. Administration of osmotic agents (mannitol and hypertonic saline), insertion of an external ventricular drain (EVD), or emergent evacuation of the hematoma should be considered depending on the overall condition and prognosis of the patient (Case 14.1). The American Heart Association (AHA) guidelines on the surgical management of increased ICP are summarized in Box 14.1.

Adapted from the 2015 AHA guidelines for the management of spontaneous ICH.20

3.3 Posterior fossa hemorrhage

The posterior fossa is a small space and contains some of the most critical cerebral structures such as the brainstem. Elevated pressure, compression of the brainstem, and herniation can occur there much more rapidly as compared to other locations that may require a larger volume of displacement.

Clinical evidence of neurological deterioration and radiographic effacement of the posterior fossa cisterns and fourth ventricle are considered to be an indication for evacuation of a posterior fossa hematoma (Box 14.2). Herniation of the cerebellar tonsils can result in brainstem compression and irreversible coma. In the setting of a posterior fossa hematoma, insertion of an external ventricular drain should be considered with great care as it could precipitate brainstem compression by upward transtentorial herniation.

Adapted from the 2015 AHA guidelines for the management of spontaneous ICH.20

Question 14.2: What are the indications for surgical treatment of intracerebral hemorrhage (ICH)?

Answer: Severity of neurological deficits, the size and location of the hematoma, and the presence of midline shift.

4 Surgical management of intracerebral hemorrhage

The current AHA guidelines on the surgical treatment of ICH are summarized in Box 14.2. The landmark trials on surgical evacuation of ICH are reviewed in the following discussion.

4.1 The STICH trial series

Among the first trials to evaluate surgical intervention for hemorrhagic stroke was the Surgical Treatment for IntraCerebral Hemorrhage (STICH) trial in 2005.4 The trial evaluated early surgical intervention versus non-operative management in patients with spontaneous supratentorial intracerebral hematomas. The study randomized 1033 patients to early surgery (within 96 hours) or conservative measures. The study showed no difference in mortality or functional outcome between the two groups. However, during subgroup analysis, it was found that lobar ICHs within 1 cm from the surface had an 8% absolute increase in good outcomes following surgery. Patients with deeper ICH randomized to early surgery tended to do poorly compared to the conservatively managed group. The trial ultimately concluded that there was no surgical benefit overall, and in patients with low Glasgow Coma Scale (GCS) scores, surgery was likely harmful.

The original STICH trial was criticized on a few points. First, 26% of patients in the medical management arm crossed over to the surgical arm. Generally, these patients were in grave condition. They had lower GCS scores and worse prognosis, and if they were not to have surgery, their presence in the medical group would have increased the group’s morbidity and mortality. Second, there were concerns as to the lack of standardization of surgical timing and the operation performed. The so-called early group had surgery on average within 30 hours postbleed, which could have contributed to poor outcomes.

In 2013 the STICH II trial was published.5 Like its predecessor, it examined early surgery versus initial conservative management of intracerebral hematomas. This trial aimed to address the weaknesses of the original STICH study. This study randomized 607 patients with spontaneous ICH, and early craniotomy was performed within 12 hours in the surgical arm. Inclusion criteria were depth of the hematoma <1 cm from the cortical surface; ICH volume of 10–100 ml, no IVH, and GCS >6. The overall outcome did not show any benefit with surgery. Within the subgroup analysis, the strongest benefit came in patients with poor predicted prognosis. This trial also faced criticism due to its high crossover rate of 21% and variability in the medical management of the nonsurgical arm.

4.2 Minimally invasive surgery

New technologies are evolving for ways of minimally invasive clot removal. Traditionally, large craniotomies were done for clot evacuation, and it was postulated that the poor outcome demonstrated by the early studies could be explained by surgical damage to surrounding brain tissue, in particular during access to deep-seated hematomas.

With advances in technology, including the widespread availability of intra-operative navigation, an attempt was made at evacuation of the blood clot with minimal damage to surrounding brain. Stereotactic needle aspiration and other less invasive methods are becoming more widespread (Case 14.1).

Stereotactic needle aspiration works by using imaging as a virtual intraoperative GPS, allowing the surgeon to know the precise location of the needle by looking at a rendered image on the screen, showing the tip of the navigation probe relative to the head. This allows precise insertion of a needle into the clot, with a desired trajectory bypassing critical structures and fiber tracts of the brain.

One of the first trials to assess minimally invasive surgery was the safety and efficacy of Minimally Invasive Surgery plus Tissue Plasminogen Activator (alteplase) in Intracerebral Hemorrhage Evacuation (MISTIE) pilot trial in 2005. The trial evaluated minimally invasive surgery for ICH evacuation plus alteplase administration and concluded in 2016.6 The trial evaluated 30-day mortality, 7-day procedure related mortality, 72-hour symptomatic bleeding, and 30-day CNS infections. There were no differences observed in primary outcomes assessed. It was found that hematoma evacuation was associated with lower perihematomal edema, considered by some to inflict cytotoxicity of surrounding tissue. Currently, the MISTIE III trial is ongoing with expected completion in 2019, with plans to enroll 500 patients in multiple countries.

Another surgical technique is image-guided endoscopic surgery. The Intraoperative Stereotactic Computer Tomography-Guided Endoscopic Surgery (ICES) trial enrolled 20 patients to test the safety for suction and transendoscopic irrigation of hematomas without alteplase. Based on its results, it was concluded that image-guided endoscopic surgery was safe and effective.7 The ongoing Evaluation of Minimally Invasive Subcortical Parafascicular Access for Clot Evacuation (MISPACE) trial focuses on assessing surgical performance while secondarily assessing complications and outcomes at 30- and 90-day intervals.8

Brain Path® is a new minimally invasive technology that aims to reduce subcortical injury by attempting to part cortical fibers without tearing them.9 Prior to surgery, advanced MRI diffusion tensor imaging allows for the identification of the major white matter fiber tracts. Then surgical trajectory is planned from the brain surface to the hematoma by using access routes parallel to those tracts, thereby displacing rather than transecting them. This new technology was tested at Cleveland Clinic in a single center trial on 18 patients. In this small trial, there were no hemorrhagic recurrences during the hospital stay, and median GCS improved from 10 before surgery to 14 afterwards.10

5 Intraventricular hemorrhage

IVH occurs in nearly half of patients with ICH.11 The main danger in these situations is the formation of obstructive hydrocephalus. As blood fills the ventricles, it will clot and may interrupt CSF flow. This, in turn, may lead to dangerous increases in ICP. Patients with IVH who have a GCS score less than 8 or are at high risk for transtentorial herniation should undergo placement of an EVD. Unfortunately, even with a drainage system in place, depending on the clot burden, obstruction of the EVD may occur.

The CLEAR III trial evaluated how intraventricular clot lysis affects outcomes. The investigators used alteplase to help lyse the clot, with the rationale that this will resolve the IVH faster, reduce ICP, and decrease CSF diversion.12 The trial showed that the use of low-dose alteplase had an acceptable safety profile and reduced time of clot elimination from the ventricular system. In a subgroup analysis, it was found that the best results were in patients with larger clots and with more than 20 mL of clot degradation. As far as the outcomes, clot lysis via EVD did not increase good functional recovery. There was no significant difference in Rankin score outcomes in the two groups. However, the use of alteplase resulted in a 10% reduction in mortality without an increase in poor functional outcome.

6 Epidural hematoma

Epidural hematomas are most frequently seen after trauma. Although uncommon, they are especially dangerous due to the arterial source of hemorrhage in 85% of the cases. One of the more common vascular structures damaged is the middle meningeal artery. Other rare nontraumatic causes exist such as iatrogenic postoperative complications, infection, coagulopathies, vascular malformations, tumors, and lupus among others.

Due to the arterial nature of the bleed, these hematomas can expand at a very rapid rate, which does not give the brain time to adapt to pressure changes and can lead to acute deterioration and death within hours of the original insult. Epidural hematomas are, therefore, surgical emergencies. The ICP increase can be very rapid, and surgical evacuation is the preferred treatment.

Epidural hematomas of smaller volume may electively be monitored. These patients will need vigilant neurological examinations and serial non-contrast CT images of the head, usually with the first 6 hours after the initial scan. If depression or lethargy is noted during an examination, a repeat CT scan is warranted immediately. If the hematoma expands on imaging, the patient should be taken to the operating room for evacuation without delay, to prevent further neurological decline or death.

All patients presenting with epidural hematomas should have anticoagulation stopped, coagulation factors assessed, and anticoagulants reversed. Generally, the risk of reversal of anticoagulation in patients in the context of epidural hematomas is less than the benefit incurred from stopping the hematoma spread.

7 Subdural hematoma

Similar to epidural hematomas, SDHs are often the result of trauma to the head, whether it is blunt force injury or rapid deceleration. SDHs are most often venous bleeds caused by rupture of bridging veins. The vulnerable populations for these are on opposite ends of the age spectrum: the infants and the elderly. SDHs can also form from low ICP, such as after a CSF leak or overdrainage in shunt patients.

SDH can range from acute to chronic. Acute SDHs can present very similarly to acute epidural hematomas. About half of acute SDH patients are comatose after their original injury. Chronic SDHs take a more insidious course. Because of the generally slower nature of the bleed, they may have a longer delay after the original trauma (up to weeks) before becoming symptomatic. These patients can present with headaches, confusion, light-headedness, apathy, or seizures. Chronic SDH found in neurologically intact patients might be observed with serial imaging and clinical exam.

In general, acute SDH with symptoms of elevated ICP should be managed similar to epidural hematomas. Symptoms may be associated with increased ICP and should be treated appropriately with head-of-bed elevation, hyperventilation, mannitol or hypertonic saline, and reversal of any anticoagulation, and the patient should be taken to the operating room for evacuation.

8 Subarachnoid hemorrhage

SAH is bleeding within the subarachnoid space between the arachnoid and the pia. These areas are normally filled with CSF. The most frequent cause of SAH is trauma. In the non-trauma population, the majority of SAH are from intracranial aneurysmal rupture.

8.1 Presentation

The most common presentation of SAH is the classic “thunderclap” headache, which patients frequently describe as the worst headache of their lives, which occurs acutely with an almost ictal onset. This can be associated with loss of consciousness, seizures, nausea, and meningeal signs.

8.2 Surgical and endovascular treatment

The current treatment for ruptured aneurysms is endovascular coiling or surgical clipping. The approach depends on aneurysm location, patient’s age, and comorbidities (Case 14.2). According to the Cochraine Database Review, in aneurysms suitable for both endovascular and surgical treatment, coiling is associated with a better clinical outcome.13 For aneurysms with challenging surgical approach, especially in the posterior circulation, endovascular coiling is preferred.

In more easily surgically accessed aneurysms, such as the middle cerebral artery trifurcation/bifurcation or ones that have a wide neck, craniotomy and surgical clipping may be preferred. Clipping is the more definitive treatment but carries higher risk due to being a more invasive procedure, whereas coiling has better outcomes but has higher chances of aneurysm recurrence.14,15

Question 14.3: What is the most common time of onset of vasospasm in SAH?

Answer: It typically occurs on day 6–10. However, in some cases, the onset can be as early as day 2–3 and as late as 3–4 weeks after the occurrence of SAH.

8.3 Treatment of complications

Complications of SAH include rebleeding, delayed cerebral ischemia from vasospasm, hydrocephalus, and increased ICP increase among others.16Patients with SAH should be admitted to an intensive care unit for close neurological and hemodynamic monitoring with appropriate neurocritical care management. In patients with decreased level of consciousness, it is advised to place an EVD that can treat hydrocephalus, a common complication of SAH, as well as to monitor ICP.

Vasospasm occurs in SAH, which can cause devastating cerebral ischemia. Nimodipine is believed to be protective against delayed cerebral ischemia from vasospasm, however, the exact mechanism is still debated. It does improve outcomes in SAH, and thus every SAH patient should be placed on nimodipine.17 In cases of severe vasospasm, patients can be taken to the angiography suite for intraarterial vasodilator infusions or balloon angioplasty.18,19

9 Clinical cases

Case 14.1 Intracerebral hemorrhage

Case presentation

A 65-year-old male with a history of hypertension was brought to the ED after he was found at home unresponsive. Upon arrival, the patient was obtunded and had a complete right-sided hemiplegia. His GCS was 7. Non-contrast CT of the head revealed a left hemispheric hematoma measuring about 7 × 4 cm with mass effect and a 6 mm of shift on the midline structures (Figures 14.3A and 14.3B). A small amount of IVH was also present.

Practical points

  • Although a hypertension-induced ICH was suspected, CT angiography was performed to rule out other causes of hemorrhage such as a middle cerebral artery aneurysm or an arteriovenous malformation/fistula. The study was unremarkable.

  • Intravenous mannitol was administered first, and the patient then underwent immediate surgical evacuation of the clot due given severe neurological deficit, evidence of midline shift, and high risk for herniation (Figure 14.3C).

  • Access to the hematoma was gained using a minimally invasive technique with tubular retractors. The patient’s mentation improved after the evacuation of the hematoma, and after a short stay in the neurosurgical intensive care unit, he was transferred out to the floor and then to inpatient rehabilitation. The patient never recovered a functional right hemibody but was able to be discharged home with his family and home health support.

Figure 14.3 Intracerebral hemorrhage.
(A) Non-contrast computed tomography, axial and (B) coronal views showing an intracerebral hematoma associated with significant midline shift. The hematoma is measuring 7 × 4 cm (approximately 40 ml of blood).
(C) Repeat non-contrast computed tomography after minimally invasive endoscopic evacuation of the hematoma. A small amount of residual blood is present.

Figure 14.3 Intracerebral hemorrhage.

(A) Non-contrast computed tomography, axial and (B) coronal views showing an intracerebral hematoma associated with significant midline shift. The hematoma is measuring 7 × 4 cm (approximately 40 ml of blood).

(C) Repeat non-contrast computed tomography after minimally invasive endoscopic evacuation of the hematoma. A small amount of residual blood is present.

Case 14.2 Subarachnoid hemorrhage

Case presentation

A 42-year-old female with no prior medical history was admitted to the ED after sudden onset of “thunderclap” headache, followed by loss of consciousness. Her GCS was 6. Non-contrast CT head showed a diffuse SAH (Figure 14.4A).

Figure 14.4 Subarachnoid hemorrhage.
(A) Non-contrast computed tomography showing a diffuse subarachnoid hemorrhage. Hydrocephalus is present in this case.
(B) Digital subtraction angiography, right internal carotid artery injection showing a 7 mm posterior communicating artery region aneurysm (arrow). The aneurysm has irregular shape and is the suspected source of the hemorrhage.
(C) The aneurysm was treated successfully with endovascular coiling (arrow).

Figure 14.4 Subarachnoid hemorrhage.

(A) Non-contrast computed tomography showing a diffuse subarachnoid hemorrhage. Hydrocephalus is present in this case.

(B) Digital subtraction angiography, right internal carotid artery injection showing a 7 mm posterior communicating artery region aneurysm (arrow). The aneurysm has irregular shape and is the suspected source of the hemorrhage.

(C) The aneurysm was treated successfully with endovascular coiling (arrow).

Practical points

  • This presentation fits a classic description of SAH. The first step is treatment of increased ICP and hydrocephalus with an external ventricular drain.

  • Once the patient is stabilized, an emergent CT or MR angiography is needed to rule out an intracranial aneurysm. In this case, a 7 mm right internal carotid artery saccular aneurysm was identified. The aneurysm was treated with endovascular coiling (Figures 14.4B and 14.4C). The patient had a prolonged hospitalization course complicated by severe delayed vasospasm requiring intra-arterial verapamil infusion and intracranial balloon angioplasty.


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