Decompressive craniectomy has many known complications. The overall complication rates range up to 53.9% (14).

We suggest that complications be classified as those that occur in the first 4 weeks (early) and those that manifest later (late or delayed). Early complications, which occur in the first 4 weeks, are likely to happen while the patients is still at the hospital. Specific complications tend to occur during particular time periods and awareness of that information helps anticipate and treat them efficiently. Kurland et al. classified them as (i) hemorrhagic, (ii) infectious/inflammatory, and (iii) disturbances of the CSF compartment (15). They tabulated the overall average frequency of each of the complications from a total of 142 eligible reports of thousands of patients who underwent decompressive procedures. They found that one in ten patients who underwent DC develop a complication that required additional medical and/or neurosurgical intervention.

Ban et al. reported, from their analysis of 89 patients, that specific complications occurred in a sequential fashion (14). Complications like cerebral contusion expansion (2.2 ± 1.2 days), newly appearing subdural or epidural hematoma contralateral to the craniectomy defect (1.5 ± 0.9 days), epilepsy (2.7 ± 1.5 days), CSF leakage through the scalp incision (7.0 ± 4.2 days), and external cerebral herniation (5.5 ± 3.3 days) occurred early. Subdural effusion (10.8 ± 5.2 days) and postoperative infection (9.8 ± 3.1 days) developed between 1 and 4 weeks postoperatively. Syndrome of the trephined and post-traumatic hydrocephalus developed after 1 month postoperatively (at 79.5 ± 23.6 and 49.2 ± 14.1 days, respectively).

Patient-specific risk factors for developing complications include poor neurological status and age. A low preoperative GCS (below eight) has been shown to increase the possibility of all types of complications (16). Age over 65 years is another risk factor (14). Though these risk factors are not modifiable, the surgical team should identify these risk groups to diligently look for emerging complications.

An overview of the complications is provided in Table 1, 2 summarizes probable causes, consequences, and management options.

Expansion of conservatively managed contusions and other bleeds are major issues that occur early after the DC (Figure 1). Most expansions occur acutely after surgery and cause clinical deterioration, prolonged hospital stay, and can even prove fatal. One theory is that the hemostatic (or tamponade) effect is lost when removing the bone, and that, along with reduction in ICP facilitates the expansion mostly on the ipsilateral side. (17–19). This hypothesis is supported by the report from Flint et al. where the propensity was higher on the side of the decompression. In their series of 40 patients, new or expanded hemorrhagic contusions were observed in 23 (58%) of 40 patients and 80% of that occurred ipsilaterally (20). Other kinds of hematomas like extradural hematomas and acute subdural hematomas can either appear de novo or increase in size. Expansion or evolution of new, remotely located extradural hematomas, typically occur at a fracture site (21). Expansion of hematoma contralateral or remote from the side of the craniectomy has not been commonly reported in stroke patients.

A contralateral hematoma developed an average of 2.1 days after the primary decompression surgery (16) and an ipsilateral one happened after a mean of 1.5 days (14). In the multivariate analysis of the complications in 89 consecutive patients who underwent DC, only contusion expansion led to poor outcome (14). Hemorrhagic progression of infarcts occur at a frequency of about 23.7% (123/519) of malignant stroke patients who underwent DC (15).

We suggest mandatory CT scan(s) in the first 48 h after DC to help detect this complication quickly and limit the damage.

External cerebral herniation appears during the first week after surgery (Figure 2). Yang defined it as more than 1.5 cm of herniated brain tissue through the center of the craniectomy defect (16). The incidence is up to 25%. It is thought to be caused by the edema induced by cerebral re-perfusion and increased hydrostatic gradient from the capillaries, after decompression (17). Brain edema causes bulging of the brain and kinking of the draining veins at the edges of the craniectomy which in turn causes venous congestion, infarcts, further herniation, and brain parenchymal lacerations (22). Adequately large craniotomies and augmentative duraplasty avoid herniation (14). The Brain Trauma Foundation recommends that a large frontotemporoparietal DC (not less than 12 × 15 or 15 cm diameter) is needed over a small frontotemporoparietal DC for reduced mortality and improved neurologic outcomes in patients with severe TBI (23). Placing two small gelfoam pledgets on either side of drains at the craniectomy may prevent venous occlusion.

Paradoxical herniation is an unusual complication that tends to occur when there is negative, sub-atmospheric intracranial pressure under the caved-in scalp flap causing the brain to herniate when procedures like lumbar puncture CSF removal (24), ventriculoperitoneal shunt, subdural fluid drainage (25), or even making the patient assume a vertical position for postoperative mobilization is done (26). Intravenous hydration and Trendelenburg position has been used to successfully reverse the herniation.

Wound complications following DC or cranioplasty after DC have been classified as dehiscence, ulceration, or necrosis (27). The large size of the scalp flap and the increased probability of injury to the superficial temporal artery during emergency surgery predispose the wound edges to ischemia at the posterior parietal and temporal areas. The pressure of the brain bulge aggravates the ischemia. The underlying, exposed, injured, or ischemic brain is especially vulnerable to infective complications once the wound breaks down.

Meticulously preserving the superficial temporal artery and limiting the posterior extent of the flap to no more than 5 cm behind the ear could reduce chance of ischemic flap breakdown. A retrospective comparison of patients operated using an n-shaped incision with those who were operated using the conventional question mark flap showed that the former technique could accomplish greater bony decompression, allows more brain protrusion and is faster to perform (28). We have noticed that making a retroauricular incision could also reduce flap necrosis.

The overall prevalence of CSF leak/fistulae due to DC has been shown to be up to 6.3% (15). In patients undergoing DC for cerebral venous sinus thrombosis (CVST), it was seen in 2.9% (29). It appears intuitive that a meticulous augmentative duraplasty and watertight scalp closure would prevent the exodus of CSF from the wound and reduce infection risk. However, a recent randomized controlled trial where watertight duraplasty was compared with rapid-closure DC without watertight duraplasty, there was no statistically significant difference in complications like CSF leak between the two groups of 29 patients each (30). Rapid closure DC without water tight duraplasty was on an average 31 min faster and hence cheaper. Though the authors claim that both procedures are equivalent, the trial was never powered or designed to prove non-inferiority of the test procedure and hence the results should be taken with caution (31).

Superficial wound infections including wound breakdown, necrosis, surgical site infection, sub-galeal collections, and wound breakdown occurred in about 10% of patients and incidence of deeper infections like an epidural abscess, and subdural empyema was just under 4% (15). Figure 3 shows a brain abscess which developed 2 months after DC for CVST (Figure 3C).

The incidence of meningitis and ventriculitis is 4% probably due to the higher chances of CSF leaks. Early detection by looking for signs of meningeal irritation and guarded lumbar puncture CSF analysis is warranted.

Apart from the scalp wound complications, wound breakdown, and infection can occur when the bone flap is preserved in an abdominal pouch (Figure 4).

Postoperative epilepsy has been documented in a varying proportion of patients who have undergone DC (14, 32–36). Suggested mechanisms include graded increases in hyperexcitability and a reduced epileptogenic threshold (14, 37). Creutzfeldt et al. retrospectively assessed 55 patients who underwent DC for malignant middle cerebral artery infarction. Of these, 49% of the patients developed seizures within the first week and 45% developed epilepsy within 1 year of surgery (32). Similarly, Santamarina et al. observed occurrence of seizures in 47.5% of all patients and in 53.7% of survivors undergoing DC for malignant MCA infarction. Logistic regression revealed that only prolonged delay from the onset of stroke to decompression (>42 h) independently predicted the development of epilepsy (34). In another study, Brondani et al. reported the prevalence of seizures in 61% (21 out of 36) of the patients with malignant MCA infarction undergoing DC. Furthermore, 59% (19 out of 34) patients developed epilepsy (33). Although a non-significant difference existed between TBI patients with or without seizures (incidence of 10.8%), the hospital stay prolonged significantly in the former group (35). Identifying the key risk factors predisposing to seizures and their effect on clinical outcomes needs more prospective studies.

In the case of TBI, Ban et al. reported that only about 3% developed seizures despite the use of anticonvulsants. Seizures disappeared in all the patients after increasing the dosage or after adding other antiepileptic drugs and that is a reasonable approach to follow in the first 2 weeks post injury (14). An early cranioplasty might serve to mitigate their occurrence, however, studies addressing this issue are currently lacking. Phenytoin and levetiracetam can be considered as antiepileptic drugs.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.