Decompressive craniectomy (DC) and cranioplasty are common operations which appear deceptively straightforward. However, there are many potential pitfalls and complications of these operations most of which can be avoided with an experienced neurosurgeon involved, careful planning, anticipation of the risks, meticulous surgical technique and assiduous post-operative care. This chapter outlines the relevant applied anatomy, the general and specific complications of these operations and presents strategies for avoidance of these complications. The common complications of DC are postoperative haemorrhage, hydrocephalus, delayed subdural effusion and syndrome of the trephined. The common complications of cranioplasty are resorption of the bone flap, subflap hematoms and infection. We advocate early cranioplasty following DC once brain swelling has subsided and before the longer term complications of DC have developed. Paradoxical herniation following DC and massive brain swelling following cranioplasty are uncommon life-threatening complications which the neurosurgeon should be aware of.
Keywordsdecompressive craniectomy, cranioplasty, complications, neurosurgery
The common complications of decompressive craniectomy are acute postoperative hemorrhage (subgaleal, epidural, subdural), delayed subdural effusion, hydrocephalus, and syndrome of the trephined.
The common complications of cranioplasty are resorption of cranial bone flap, subflap hematomas, and infection.
The cranioplasty should be performed as early as possible after the brain swelling has subsided and before the late complications of decompressive craniectomy have developed. The management of decompressed patients with secondary hydrocephalus is challenging.
An uncommon but serious complication of decompressive craniectomy is paradoxical herniation with brainstem compression, which is a life-threatening emergency.
An uncommon but serious complication of cranioplasty is massive postoperative cerebral swelling with subsequent death.
Careful surgical planning, meticulous surgical technique, and assiduous postoperative care will help prevent much of the morbidity associated with decompressive craniectomy and cranioplasty.
The commonest error in surgical technique is to make the craniectomy too small, which results in inadequate relief of intracranial hypertension and results in brain herniation out of the defect and further secondary brain injury.
Decompressive craniectomy (DC) and subsequent cranioplasty are common operations in neurosurgical practice. The purpose of DC is to control elevated intracranial pressure (ICP). The indications for DC are blunt or penetrating severe traumatic brain injury (TBI), malignant middle cerebral artery occlusion syndrome, acute cerebellar infarction, acute cerebellar hemorrhage, acute intra- or postoperative cerebral swelling/hematoma, and refractory nontraumatic intracranial hypertension in children due to infection, infarction, or Reye’s syndrome.
The controversies surrounding the indications, timing, and selection of patients for DC are not discussed in this chapter. The surgical technique for unilateral hemicraniectomy and bilateral frontotemporo-parietal DC has been well described. The size of the craniectomy is an important consideration because an inadequately sized craniectomy will not adequately control the intracranial hypertension and will result in a brain herniation out of the defect with secondary injury to this brain, particularly at the edges of the defect where veins are occluded. The herniated brain may be hemorrhagic and infarcted when re-explored.
The fourth edition of the Brain Trauma Foundation guidelines recommends that a unilateral frontotemporo-parietal DC in the civilian context be not less than 12 × 5 cm or 15 cm in diameter. Bell et al., from their military experience with bomb blasts and penetrating TBI due to gunshot wounds, recommend that a hemicraniectomy for frontotemporo-parietal decompression have at a minimum dimensions of 14 cm anteroposterior by 12 cm superioinferior.
The systematic review by Kurland et al. subtyped DC-associated complications into three main types: (1) hemorrhagic, (2) infection/inflammatory, and (3) disturbances of the cerebrospinal compartment. According to their analysis, one in 10 patients undergoing a DC suffers a complication necessitating additional medical or surgical intervention. Individual studies have reported a high incidence of complications overall. In a series of 164 patients who had DC for TBI, 81 patients (55.5%) had at least one complication. The occurrence of at least one complication was significantly associated with an increased risk of prolonged hospital or rehabilitation stay after adjusting for the predicted risk of unfavorable outcome from the TBI. In a series of 108 patients with TBI, 50% developed complications related to the surgical decompression, and of these, 25.9% of patients developed more than one type of complication. Older patients and those with more severe head trauma had a higher occurrence of complications. In a series of 12 children who had DC after severe TBI, the most frequent complications were hygroma formation (83%), aseptic bone resorption of the reimplanted bone (50%), hydrocephalus (42%), secondary infection or dysfunction of ventriculoperitoneal shunt (25%) or cranioplasty (33%), and epilepsy. 75% of the patients required reoperation in addition to the cranioplasty, with up to 8 interventions.
The common complications after DC are acute postoperative hematoma, brain herniation through the bone defect, subdural effusion, expansion of hemorrhagic contusions, seizures, hydrocephalus, and syndrome of the trephined. New contralateral or remote subdural or epidural hematomas may also occur, usually during the first week after DC. Hemorrhagic transformation of ischemic infarction has been reported after DC. Infectious complications include meningitis, ventriculitis, and wound infection ( Figs 44.1–44.3 ).
The common complications of cranioplasty are new ipsilateral hematoma (usually epidural); infectious, inflammatory, and wound healing complications (superficial or deep, including abscess formation and osteomyelitis); meningitis and ventriculitis; cerebrospinal fluid (CSF) disturbance including subdural effusion/hygroma and CSF leak/fistula; bone flap aseptic necrosis and resorption and cosmetic defects; less commonly, seizures; and hydrocephalus. A rare, fatal allergy to titanium bone replacement has been reported. Zanaty et al. reported an overall complication rate of 31.3% and a mortality rate of 3.16% in a mixed series of 348 cranioplasties.
The scalp flaps for DC should be planned carefully. The scalp flaps are large, and the main blood supply for the hemicraniectomy flap is from the superficial temporal artery (STA). The STA and its accompanying draining veins should be preserved to avoid scalp flap ischemia and subsequent wound breakdown. The STA should be palpated and marked on the scalp so that the incision avoids it. The scalp flap can reach the midline, but the bone cuts must avoid the major venous sinuses (sagittal and transverse). Some neurosurgeons leave a central bone strut over the sagittal sinus to protect the sinus. It is helpful to mark out the position of the venous sinuses and the scalp incision before draping commences.
A flap design that lessens the risk of ischemia of large scalp flaps is the T-shaped incision that is favored by some military surgeons. A midline sagittal incision with a “T-bar” extension was described by Ludwig G. Kempe for hemispherectomy. The midline incision extends from the hairline to the inion. The T-bar incision starts 1 to 2 cm anterior to the tragus at the root of the zygoma and extends superiorly to meet the midline incision just behind the coronal suture. This incision largely preserves the STA and occipital artery angiosomes.
Falx. The anterior falx is frequently divided along with the sagittal sinus during the bifrontal craniectomy. A bilateral horizontal fish-mouth opening in the dura including falx and sagittal sinus division was described by Polin et al. This theoretically permits both cerebral hemispheres and the corpus callosum to expand forward without being tethered or injured by the falx. An alternative is to open the dura separately on each side without dividing the falx.
Frontal sinus. The lower bone cut for the bifrontal craniectomy may open the frontal sinus. The surgeon can avoid the sinus by steering the craniotome above it, but a small opening should be covered with pericranial flap. A larger opening requires “cranialization” of the sinus, including removal of the posterior wall of the sinus and the mucosa of the sinus. This will help prevent infection and late mucocele formation.
Air cells are present in the temporal and sphenoid bones. The hemicraniectomy may open these air cells. The surgeon should carefully examine the exposed bone edge for any air cells and occlude them with bone wax to prevent CSF leaks. Larger air cell openings will require a flap of pericranium to close them.
Cerebrospinal fluid pathways. CSF dynamics are disturbed after DC. CSF fistula between the subarachnoid space or ventricles could lead to subdural hygromas and pseudomeningoceles. Also, the entry of blood into the ventricular system could lead to communicating hydrocephalus. A further suggested mechanism is an increased venous outflow to the sagittal sinus after DC that results in an increase in extracellular fluid absorption, reduced brain parenchyma volume, and increased ventricular size. The development of an interhemispheric hygroma that occurs within the first 9 days after DC is a predictive radiologic sign for hydrocephalus developing within the first 6 months in patients with severe TBI.
Coagulopathy will increase the risk of hemorrhagic complications. Reversal of the coagulopathy should occur preoperatively or be continued intraoperatively in an emergency.
Hemorrhagic cerebral contusions frequently expand after DC. In a retrospective study of 40 consecutive patients, new or expanded hemorrhagic contusions ≥5 cc were observed in 48% of patients having a hemicraniectomy. Expanded hemorrhagic contusion volume >20 cc after hemicraniectomy was strongly associated with poor outcome and mortality. The expansion of contusions may also occur in the absence of a DC. Particular attention should be directed to optimizing coagulation parameters in these patients.
Inadequate wound debridement in compound injuries to the cranium will increase the risk of wound breakdown and infection.
Dura left open. The dura should ideally be closed watertight after DC by duroplasty using a dural patch of fascia, pericranium, or dural substitute. This prevents CSF fistula as well as subflap and subgaleal collections and reduces the risk of infection.
Open frontal sinus will increase the risk of CSF rhinorrhea, infection, and mucocele.
One-layer scalp closure will increase the risk of poor scalp healing and CSF fistula and wound infection. The scalp should be closed in two layers.
Tense scalp closure will increase the risk of wound edge necrosis, wound dehiscence, CSF fistula, and infection.
Seizures may indicate progressive intracranial pathology such as postoperative hemorrhage, infection, and swelling and should be investigated.
Fever may indicate intracranial infection. Cranial infections typically do not manifest in the first five postoperative days and may be accompanied by fever, reddening of the wound site, and elevated white cell counts and C-reactive protein (CRP) values.
Deteriorating cognitive function or conscious state requires urgent imaging and further investigation.
CSF fistula (wound/nose/ear)
Chronic headaches, seizures, and cognitive decline may be signs of a low-grade infection that will need to be investigated with infection markers and imaging. If a collection is developing around the bone flap or substitute, re-exploration and removal of the flap may be required if infection is the likely cause.
Sunken scalp flap. The development of new focal neurologic deficits and cognitive decline raises the possibility of the syndrome of the trephined or sinking skin flap syndrome. In this condition, the difference between atmospheric and intracranial pressure due to the absence of the cranium causes the scalp to be infolded, and mass effect to be exerted on the cerebral cortex, affecting cerebral perfusion and CSF flow dynamics. This syndrome occurs 5.1 ± 10.8 months after the DC for trauma. The presenting symptoms include unilateral motor deficits, cognitive deficits, language deficits, altered level of consciousness, headache, seizure, and cranial nerve deficits. Investigations include electroencephalography, computed tomography (CT) perfusion scan, and phase contrast magnetic resonance imaging. The neurologic deficits are usually recoverable in the ensuing days to months after the cranioplasty. In many cases improvement is seen within 24 hours of cranioplasty. Minimizing the time interval to cranioplasty will reduce the risk of this complication. The bone should be replaced when the brain swelling has subsided and the patient is fit enough for surgery. This is usually at 4 to 6 weeks after the DC.
CSF drainage by lumbar puncture, ventriculostomy, lumbar drain on continuous drainage, or ventriculoperitoneal shunt exacerbates the pressure gradient of atmospheric pressure exceeding ICP, which may precipitate downward shift of the brain, tonsillar herniation, and death. This is called paradoxical herniation (PH) because it occurs in the presence of a sunken bone flap. This is a life-threatening emergency. PH occurred in 13/429 (3.03%) consecutive DCs, and all 13 patients were treated and survived beyond 6 months. PH may also occur in the absence of CSF drainage. Upright posture, mannitol, and hyperventilation may also be risk factors. The patient is placed in the Trendelenburg position (15 degrees, head down) and hydrated intravenously, and CSF drainage is ceased.
Unprotected brain at the site of the craniectomy. The patient should be fitted with a custom-made plastic helmet ( Fig. 44.1 ) to protect the exposed brain, and this should be worn even before the patient is mobilized. Direct trauma to the craniectomy site may have serious consequences or result in death ( Fig. 44.4 ).