Surgery for Ischemic Infarcts

Introduction

The first surgical procedures on patients with massive infarctions were performed to alleviate severe brain swelling often erroneously attributed to a tumor. With the common use of computed tomography (CT) and magnetic resonance imaging (MRI), the pathophysiologic cause of severe brain swelling is now rarely in question. Although anatomic imaging studies may not show signs of massive hemispheric or cerebellar infarction for the first few hours, the abrupt onset of any neurologic deficit is highly suggestive of a stroke or transient ischemic attack . The brain edema (usually a combination of cytotoxic and vasogenic edema) associated with an infarct increases usually 3–5 days after the insult, often resulting in massive swelling of the affected region and a dramatic change in tissue density. Depending on the location and size of the infarcted area, such massive swelling may cause life-threatening brain shift causing herniation and brainstem compression. Knowing the extent of the insult is of great importance—researchers who obtained quantitative tomographic measurements of cerebral blood flow within 1–2 h of the onset of symptoms that were related to a massive middle cerebral artery (MCA) stroke (malignant MCA stroke) observed an absence of perfusion throughout the entire territory of the MCA .

Despite enormous progress in the field of reperfusion therapy for ischemic strokes (medical and interventional therapies alike), the reestablishment of perfusion is unwarranted and potentially harmful for this kind of MCA infarction. Clinical studies indicate that reperfusion of a region that has already become irreversibly ischemic can accelerate vasogenic edema and convert ischemic infarcts to hemorrhagic ones . Medical therapies without the goal of reperfusion for massive infarction of the cerebral hemispheres or the cerebellum are directed toward preventing additional ischemic injuries and controlling brain edema. Depending on the cause of vascular occlusion, anticoagulation is often indicated to prevent additional embolic events or thrombus propagation. A moderately elevated perfusion pressure must be maintained while avoiding both hypotension and excessive hypertension. Ideally, at least in the initial days, this should take place in a neurointensive care unit. Traditionally, osmotic diuretics administration and intubation combined with hyperventilation have been used when the mass effect is accompanied by a decreased mental status. However, controlled hyperventilation and/or administration of mannitol or hypertonic saline is of little value if a decision against decompressive surgery has already been made, as these measures show only a transient effect in most cases and is possibly associated with a detrimental rebound phenomenon after discontinuation and thus result in increased intracranial pressure (ICP) . In case of concomitant hydrocephalus, placement of external ventricular drains with ICP monitors should be considered; however, shunt placement without performing a craniectomy is most likely not a successful strategy .

Despite such therapeutic efforts, 20–30% of massive infarctions resulted in irreversible secondary brainstem injuries caused by herniation and mass effect . In some cases, and to prevent these secondary brainstem injuries, decompressive surgery is suitable. In decompressive craniectomy, part of the skull is removed to create more space for the swelling brain, thus immediately reducing increased ICP and alleviating the mass effect. Usually this intervention includes opening and expanding the underlining dura. Rarely additional space is created by resection of infarcted brain tissue (e.g., temporal lobectomy). The bone flap is banked in a freezer or implanted in the patient’s abdominal wall, and patients wear helmets to protect the brain until the autologous bone or allograft prosthesis can be reimplanted in the second-stage procedure called cranioplasty. The optimal time to perform cranioplasty after decompressive craniectomy for strokes remains unknown, but the complication rate (e.g., hydrocephalus, infection) was slightly higher in case of early cranioplasty (within 10 weeks of craniectomy) and in patients with a ventriculoperitoneal shunt . On the other hand, if bone flap replacement is delayed further, communicating hydrocephalus may develop requiring shunt placement .

Decompressive craniectomy is typically done for two types of strokes: malignant MCA strokes and cerebellar strokes.