Decompressive Hemicraniectomy for Malignant Hemispheric Infarction

Trial

Nation

Patientage (years)

Surgical timing

Patient no. (surgicalgroup, medical group)

Publication

DESTINY

Germany

18–60

<36 h

17, 15

Stroke, 2007

DECIMAL

France

18–55

<24 h

20, 18

Stroke, 2007

HAMLET

Netherlands

18–60

<4 days

32, 32

Lancet Neurol, 2009

DESTINY II

Germany

>60

<48 h

49, 63

N Engl J Med, 2014

DECIMAL trial DEcompressive Craniectomy In MALignant middle cerebral artery infarcts trial, DESTINY trial DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY trial, DESTINY II trial DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY II trial, HAMLET Hemicraniectomy After Middle cerebral artery infarction with Life-threatening Edema Trial

Three of the trials were conducted between 2001 and 2007; however, the DECIMAL (DEcompressive Craniectomy In MALignant middle cerebral artery infarction) trial and DESTINY (DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY) trial were both stopped due to a lack of cases and a significant difference in the mortality between the surgical and medical groups [2, 5, 15].

Notwithstanding, the HAMLET (Hemicraniectomy After Middle cerebral artery infarction with Life-threatening Edema Trial) study was completed, and the results were published in 2009 [2]. Over a 5-year period, 32 patients were randomly assigned to undergo surgical decompression, while another 32 patients received the medical treatment. As a result, for those patients with large hemispheric infarction who were treated within 48 h of stroke onset, a decompressive hemicraniectomy was found to reduce both the fatality rate and the poor outcomes (mRS 5).

Meanwhile, a pooled analysis of three European randomized controlled trials (DECIMAL, DESTINY, and HAMLET), which included patients aged <60 years who underwent decompressive surgery within 48 h after stroke onset, reported a high (43%) survival rate with functional independence (mRS ≤3) [4].

In a more recent prospective randomized clinical trial, Decompressive Surgery for Treatment of Malignant Infarction of Middle Cerebral Artery-II (DESTINY II trial) published in 2014, the efficacy of a decompressive hemicraniectomy within 48 h after stroke onset was investigated for elderly patients aged >60 years [3]. In this trial, while survival was increased, most survivors experienced severe disability (mRS 4) following surgery with only 6% having functional independence (mRS 3).

15.3 Surgical Timing and Indications

15.3.1 Timely Surgery

Although originally intended as a last resort to prevent a fatal cerebral herniation, recent European clinical trials have proposed the early use of a decompressive hemicraniectomy for better functional outcomes. In particular, patients who underwent decompressive surgery within 48 h after stroke onset were included in both a pooled analysis of three European randomized controlled trials and the DESTINY II trial [2–5, 9].

However, neurological deterioration due to brain swelling varies significantly from <24 h to >6 days, affecting the appropriate timing of early surgery. When Qureshi et al. [16] investigated the timing of neurological deterioration related to cerebral edema after massive MCA infarction, 36 and 32 % of the patients experienced neurological deterioration <24 h and 24–48 h after stroke onset, respectively, while the remaining third (33%) experienced clinical deterioration on day 3 (19%), day 4 (4%), day 5 (4%), and day 6 or after (6%). Thus, instead of a strict timing, the appropriate surgical timing should be before or immediately after the initiation of neurological deterioration related to brain edema, which could be on day 1, day 2, or even day 7 after stroke onset [17–21].

15.3.2 Early Predictors of Malignant Hemispheric Infarction

Various early predictors of malignant hemispheric infarction have already been reported based on clinical and radiological data [17, 22–30]. However, none of these predictors have a sufficient predictive value that allows them to be used to schedule an early decompressive craniectomy before any neurological deterioration. Thus, the decision for decompressive surgery is invariably made on the basis of radiological data and a concomitant clinical course.

While the volume of the infarcted brain tissue can often be used to predict the development of fatal cerebral edema and herniation after acute infarction, infarcts smaller than the cutoff value can also cause fatal cerebral edema due to a variety of other unpredictable factors, including expansion of the initial infarct territory, delayed spontaneous recanalization of the occluded vessel, hemorrhagic transformation of the infarcted brain tissue, and the hydration status of the patient. Thus, monitoring in an intensive care unit (ICU) or stroke unit setting is needed for all patients with acute large hemispheric infarction to expedite timely surgical decompression.

In previous studies, assessing the infarct volume using early CT scans after stroke onset does not provide a satisfactory predictive value: (1) hypodensity covering >50% of the MCA territory within 5 h after symptom onset was predictive of a malignant course with a sensitivity of 61% and specificity of 94% [30]; (2) hypodensity covering >50% of the MCA territory within 12 h was predictive with a sensitivity of 64% and specificity of 66% [31]; and (3) hypodensity covering >50 and 67% of the MCA territory within 18 h was predictive with a sensitivity of 58% and 45%, respectively, and specificity of 94% and 100%, respectively [23].

In contrast, assessing the initial infarct volume using diffusion-weighted imaging (DWI) would seem to be a more promising predictor. In the study by Oppenheim et al. [28], an initial infarct volume >145 cm³ within 14 h after an acute MCA occlusion was predictive of a malignant course with a sensitivity of 100% and specificity of 94%.

Another useful predictor of malignant hemispheric infarction is a midline brain shift. Gerriets et al. [32] reported that a midline shift of ≥2.5, 3.5, 4.0, and 5.0 mm in transcranial color-coded duplex sonography at 16, 24, 32, and 40 h, respectively, after stroke onset was predictive of a malignant course with a specificity of 100% and positive predictive value of 100%.

An ICU setting can also facilitate the use of predictors with a high cutoff value, providing a high specificity and high positive predictive value for deciding on early surgery before clinical deterioration and thereby avoiding over-inclusive indications of surgical decompression [17]. However, the cutoff values for the lesion volume and associated midline brain shift for predicting a malignant clinical course differ according to the timing of the brain imaging after stroke onset and the severity of brain atrophy [17, 32]. In a retrospective study of radiological predictors for 61 patients with large hemispheric infarction, Park et al. [17] proposed strict cutoff criteria with a high specificity according to the timing of the imaging. For patients without severe brain atrophy (bicaudate ratio <0.16), an initial infarct volume >160 ml in DWI within 14 h of stroke onset was predictive of a malignant course with a 97% specificity and 76% sensitivity, while an infarcted lesion volume >220 ml and midline shift >3.7 mm in follow-up CT scans 24 h after stroke onset were predictive with a 100% and 98% specificity, respectively.

The final infarct volume can also be assessed using the perfusion CT or perfusion MR images on admission [29, 33]. In the MR perfusion study by Thomalla et al. [29], a perfusion lesion volume >162 mL on a time-to-peak (TTP) map with a TTP delay threshold of >4 s was predictive of a malignant course with a sensitivity of 83% and specificity of 75%.

15.4 Surgical Technique

The surgical decompression of intracranial masses can be performed using external and/or internal decompression. In cases of malignant hemispheric infarction, external decompression can be used with or without internal decompression.

External decompression, including a hemicraniectomy and expansive duraplasty, enables external herniation of the swollen infarcted brain tissue. In the clinical trials DECIMAL, DESTINY, HAMLET, and DESTINY II, the standard surgical technique was external decompression without internal decompression [2, 3, 5, 15]. Internal decompression, including resection of the infarcted brain tissue and/or temporal lobe, is not commonly used for simple MCA infarction due to the difficulty in differentiating between salvageable ischemic and irreversibly infarcted brain tissue. However, when external decompression is unable to reduce the intracranial pressure and relieve brain stem compression (e.g., in the case of whole hemispheric infarction), additional internal decompression should be considered [34].

Figure 15.1 illustrates a decompressive hemicraniectomy using external decompression, where the frontal, temporal, and parietal bones overlying the infarcted hemisphere are removed, allowing for external herniation of the swollen infarcted brain. After administering general anesthesia, a skin incision is initiated just above the zygomatic arch 0.5 cm anterior to the tragus and then continued superiorly and posteriorly over the ear and around the parietal bone to the contralateral frontal midpupillary line. The hemicraniectomy requires the removal of a large fronto-temporo-parietal bone flap, where a minimum diameter of 12 cm is widely accepted [35, 36], although the author recommends a diameter >14 cm for an effective decompressive hemicraniectomy [37].

Fig. 15.1

Illustration of decompressive hemicraniectomy. The medial limit of the craniectomy is 2 cm from the midline (dotted curved line), while the posterior limit is 5–6 cm posterior to the external auditory canal

The craniectomy is limited by the following boundaries: (1) To avoid violation of the frontal sinus, the bone flap is made anteriorly, except in the case of a large frontal sinus. (2) To minimize venous bleeding on the dura, the medial limit is 2 cm from the midline. (3) The posterior limit of the bone flap is approximately 5–6 cm posterior to the external auditory canal, which covers the MCA territory posteriorly and allows for a neutral head position in bed without compressing the swollen brain. (4) Inferiorly, the temporal squama is removed to the level of the zygomatic arch [38].

Following a stellate-shaped dural incision, the infarcted brain tissue is not normally removed due to the presence of a salvageable penumbra area or viable tissue [2, 5, 15]. Expansive duraplasty is then performed using a large flap of pericranial tissue or an artificial dura substitute. The dimensions of the expansive duraplasty should be lengthened to accommodate subsequent aggravation of the brain swelling.

Meticulous hemostasis is critical for preventing a postoperative epidural/subgaleal hematoma, which includes the use of multiple dural tenting sutures, the bipolar coagulation of bleeding points on the dural surface, the application of commercial hemostatic materials, and the placement of one or two closed suction drains in the epidural/subgaleal space. The dural tenting sutures require small holes along the margin of the craniectomy. In addition, self-drilling anchor screws can be used around the sphenoid ridge for easy anchoring of the dural tenting sutures (Fig. 15.2) [39].

Fig. 15.2

Intraoperative photograph of decompressive hemicraniectomy showing self-drilling anchor screws (arrows) for anchoring the dural tenting sutures around the sphenoid ridge

Lastly, the temporalis muscle and skin flap are re-approximated and sutured layer by layer. However, the temporalis muscle and fascia can be resected to maximize the external herniation of the swollen brain [38]. Removing the temporalis muscle has a minimal impact on the maximal bite force and does not create problems with chewing, as the grinding phase of the closure stroke only needs one-third of the maximal bite force [40, 41]. On average, resection of the temporalis muscle and fascia creates a twofold volume expansion of the external herniation on postoperative day 3 when compared with the conventional technique (Fig. 15.3) [38]. The technical obstacles to achieving effective external decompression include an insufficient craniectomy size, postoperative epidural/subgaleal hematoma, thick and swollen temporalis muscle compressing the temporal lobe, tough and inelastic temporalis fascia, and tight scalp [36, 38, 42]. Thus, maximizing the external herniation of the infarcted brain requires the hemicraniectomy to be as large as possible, meticulous hemostasis, and resection of the temporalis muscle and fascia. The bone flap is stored in a tissue bank at –70°C, and cranioplasty using the autogenous bone flap is then performed 2–3 months after the craniectomy.

Fig. 15.3

Axial CT scans after decompressive hemicraniectomy and resection of the temporalis muscle on postoperative day 1 (a) and day 3 (b). Progressive and considerable external herniation of the infarcted brain is noted

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