Retrospective Study

Outcome following decompressive craniectomy in severe head injury: Rashid Hospital experience
Abrar Bukhari Syed, Imad Hashim Ahmad, Masood Hussain, Firas Al-Bya, Ammar Solaiman
Abstract Objectives: The aim of this study was to assess outcome of decompressive craniectomy in severe head injury. Methods: During period of June 2004 - June 2008 consecutive patients with severe head injury having subdural haematoma, midline shift and brain oedema underwent decompressive craniectomy along with intracranial pressure (ICP) monitoring with removal of clot to control (ICP) or to reverse the dangerous brain shifts. Total 80 cases were included in the study. Diffuse injury was demonstrated in 12 cases in which decompressive craniectomy had been performed. Decompressive craniectomy was performed urgently in 65 patients and in 15 patients the procedure was performed after ICP had become unresponsive to conventional medical management. Survivors were followed-up for at least 3 months post-treatment to determine the Glasgow outcome scale (GOS) score. Decompressive craniectomy lowered ICP to less than 20 mmHg in 85% of cases. Twelve of 80 patients died and 18 remained in vegetative state. Thirty patients were severely disabled and 20 patients had good recovery. Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift (as seen on CT scan) and patient age, possibly because of the small number of patients in each of the subsets. Complications included septicaemia (3 cases), extradural haematoma on the other side of craniectomy (1 case) and hydrocephalus (9 cases). Conclusions: Decompressive craniectomy was associated with a better than expected functional outcome in patients with medically uncontrollable ICP and brain herniation, compared with outcome in other control cohorts reported on in the literature. (p29-35) Key words: Severe head injury, traumatic brain injury, decompressive craniectomy, duralplasty, intracranial pressure and cerebral perfusion pressure

Introduction
In patients with traumatic brain injury (TBI) intracranial hypertension secondary to cerebral oedema is a major problem. The last treatment in these cases is decompressive craniectomy. Neurosurgical therapy aims to minimize the secondary brain damage after a severe head injury. This includes the evacuation of an intracranial space occupying bleeding, in ventricular haemorrhage by putting external ventricular drainage (EVD) and conservative therapy in the form of hyperventilation, mannitol and barbiturates coma in order to influence raised ICP. When conservative treatment fails to act then decompressive craniectomy might be successful in lowering ICP. Intracranial hypertension that does not respond to maximum medical management occurs in 10 - 15% of patients with severe head injury and contributes to increased morbidity and mortality rates.6 Miller, et al reported a 100% mortality rate when ICP above 25 was uncontrollable by medical means, particularly among patients with ICP above 40 mmHg.18 Marshall, et al recorded a 42% mortality rate.17 Seoul and Ducaer published a report in 1982 which shows 84% death rate when ICP is greater than 25 mmHg.21 Marou, et al also reported significant relationship between high ICP and outcome.15 Clifton, et al shows a significant relationship between an ICP greater than 25 mmHg and poor outcome.4 Marshall, et al reported patients with unilateral hemispheric or global brain swelling following TBI shows persistent raised ICP, despite maximum medical management i.e., barbiturate coma hyperventilation, mannitol, and there is

Department of Neurosurgery Rashid Hospital Dubai United Arab Emirates Correspondence: Dr. Abrar Bukhari Syed Department of Neurosurgery Rashid Hospital PO Box 4545 Dubai United Arab Emirates Tel: (971) 5 0469 2262 Email: drabrarns@yahoo.com

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high risk of morbidity and mortality as well.17 Eisenberg, et al reported a high rate of mortality even after a trial of high dose of barbiturate along with other conventional medical therapies.6 Cairns, et al result shows that decompressive craniectomy seems a reasonable alternative for treating intracranial hypertension and also for improving outcome following severe TBI, complicated by diffuse brain swelling.3 Literature on decompressive craniectomy indicates that during past four decades, the incidence of major disability or vegetative state has remained relatively constant, although there has been a gradual decrease in the mortality rate and an increase in the proportion of patients with good outcome.5,9,12,19,20,23 Improvement in outcome after decompressive craniectomy is due to early CT scan, better pre-hospital care, earlier and more aggressive surgical and intensive care of patient with TBI and application of guidelines for the management of severe head injury.2,8,15,17 Jaeger, et al also reported that decompressive craniectomy has significantly improved oxygen delivery to brain cells when incidence of cerebral ischaemia is at its peak.10 In this retrospective study we evaluated decompressive craniectomy for the treatment of 80 patients with severe head injury and brain swelling, and we report on the outcome following this surgical procedure.

Table 1 - Timing of decompressive craniectomy. Within 3 - 4 hours Within 2 - 3 days Unilateral decompressive craniectomy more than 12 cm Bilateral decompression craniectomy Artificial dura used (neural patch) Duragen used 65 15

73 7 65 15

Medical management prior to decompressive craniectomy Maximum medical management prior to decompressive craniectomy was provided according to the guidelines for the Management of Severe Head Injury.2 Immediately patient was intubated and ventilated and hyperventilation started keeping PC02 32 - 35 mmHg. Oxygenation (fraction of inspired O2 40 - 100%), head elevation (30 - 45) and fluid resuscitation started. A central venous catheter was inserted in each patient for central and pulmonary wedge pressure monitoring and fluid management. Every patient was subjected with arterial cannulae for blood gases assessment. Sedation with either sedatives shortacting benzodiazepines such as midazolam (1 - 2 mg/hour) or propofol (5 - 100 mg/kg/min) or fentanyl (25 - 100 mg/ kg/hour) were used. Muscle relaxant like nimbex (cisatracurium 0.05 - 0.1 mg/kg) was also used for brief periods. Osmotherapy (0.25 gm/kg mannitol/6 hourly) or hypertonic saline (3%, 250 - 500 cc bolus) up to a serum osmolality of 320 mOsm/kg H20 were the next steps. Blood pressure was supported if necessary with dopamine and noredrenaline (Tables 2 and 3). Barbiturate coma (pentobarbital 10 mg/kg/hour for 4 hours then 2 - 3 mg/kg/hour for 3 - 4 days) was used in 15 patients. Hypothermia was not used therapeutically. Imaging studies After resuscitation each patient underwent CT scan brain, cervical, chest and abdomen. Computed tomography brain findings of each patient was classified according to National Institute of Health Coma Traumatic Data Bank (Table 4).16 Technique and timing of decompressive craniectomy Sixty-five patients were directly taken to theatre within 3 - 4 hours after injury and 15 patients were initially treated medically (hyperventilation, mannitol, hypertonic saline and barbiturate coma) and only ICP insertion was done.

Clinical materials and methods

Patient population From June 2004 - June 2008 patients with severe closed head injury, Glasgow coma score ([GCS] 4 - 9) arrived at Rashid Hospital emergency after a mean time of 59 minutes, were included in the study. Sixty-five cases were immediately taken to theatre for urgent decompressive craniectomy while 15 patients were initially treated medically and only ICP monitoring was done. Within 1 - 2 days when ICP was uncontrolled with all possible medical measures, including hyperventilation and barbiturate coma these 15 patients were also subjected to decompressive craniectomy (Table 1). Pre-hospital management Pre-hospital management was completed according to the standard of American Guidelines of Basic Life Support (BLS). On admission to the emergency department of Rashid Hospital, the resuscitation was carried out according to American Guidelines for Advanced Trauma Life Support (ATLS).2,22

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Table 2 - Summary of characteristics in 80 patients with severe closed head injury who underwent decompressive craniectomy are as follows: Variables Total No. of patients Male Female Road traffic accident Fall from height Assault Mean age (years) Admission GCS 4-6 GCS 7-9 Abnormal pupils response to light ENT bleeding Hemiparesis Epilepsy CSF leakage Table 3 - Other associated injuries. Type of injury Spinal injury Chest injury Abdominal injury Long bone fracture Facial injury Subdural haematoma, midline shift and oedema Diffuse axonal multiple contusion, traumatic Subarachnoid haemorrhage Barbiturate coma was used 12 15 15 18.9 No. of patients 10 13 8 15 12 % No. of patients 80 78 2 48 30 2 35 19 61 56 64 72 8 7 23.7 76.3 70 80% 90 10 8.7 97.5 2.5 60 37.5 2.5 %

These 15 patients were also subjected to decompressive craniectomy within 1 - 2 days due to pupillary changes, worsening CT scan brain findings or persistent high ICP (ICP > 25). Standard unilateral frontoparietal temporal free bone flap with 15 cm in anterior posterior diameter with extension to temporal bone was removed in 73 patients. Four patients were initially subjected to unilateral frontoparietal temporal decompressive craniectomy but later on due to uncontrolled ICP, worsening of CT findings, pupillary changes or due to developing ischemia within 2 - 4 days, a contralateral decompression craniectomy was also performed (Fig. 1).

Figure 1 - Follow-up CT scan brain after bilateral decompressive craniectomy showing hydrocephalus.

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Bifrontal decompressive craniotomy was done in 3 cases. Intracranial pressure monitor (Codman type) was inserted in all cases. All cases were subjected to duraplasty either using artificial dura (neuropatch in 65 cases) or duragen (15 cases) (Fig. 2).

Table 4 - National Institute of Health Coma Traumatic Data Bank.16 CT class diffuse injury I II Definition No visible pathological component High or mixed density contusions < 25 ml, visible basal cisterns, and brain shift < 5 mm High or mixed density contusions < 25 ml, compressed or obliterated basal cisterns, and brain shift < 5 mm High or mixed density contusions < 25 ml, compressed or obliterated basal cisterns, and brain shift > 5 mm Any mass > 25 ml evacuated Any mass > 25 ml that was not evacuated Figure 2 - Operative picture showing large duraplasty with dural patch.

III

IV

Evacuated mass Non-evacuated mass

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Bone flap was stored in tissue bank at -4C for 1 - 6 months before re-implantation. Patients were followed-up from 3 - 24 months post-treatment and there Glascow outcome scale (GOS) was determined (Fig. 3).

later (50 days after decompression), due to septicaemia. The cumulative probability of survival in first 30 days after decompression was 87.5%. We analysed 6 established potential predictors of death during the first 30 days after decompressive craniectomy including patient age, admission GCS, abnormal pupillary response, midline shift, brain contusions and associated other injuries.9,13,21,22 Glasgow outcome scale Sixty-eight patients who survived after decompressive craniectomy were followed-up for at least 3 months posttreatment. Twenty patients (25%) have good recovery, 30 (37.5%) were severely disabled and 18 (22.5%) were in vegetative state, which are slightly better rates as compared to the results of Bizhan, et al.1 Several known predictors of good outcome were evaluated. Patient with admission GCS 6 - 9 were 10 times more likely to have good outcome as compared with patients having admission GCS 4 - 5. Abnormal pupil response to light, timing of decompressive cranioectomy, midline shift on CT scan and patients age were not statistically significantly associated with outcome in this study.9,11,13

Figure 3 - Patient who underwent bilateral decompressive craniectomy.

Statistical Analysis
The data was analyzed using excel software.

Results
Intracranial pressure and cerebral perfusion pressure (CPP) Fifteen patients, who were initially treated medically along with ICP insertion, were also subjected to decompressive craniectomy within 1 - 2 days due to uncontrolled ICP (ICP ranges between 20 - 30 mmHg), pupillary changes or worsening radiological findings. The ICP in these cases decreased from a mean of 24 mmHg to mean of 14 mmHg after decompression craniectomy. During decompressive craniectomy all 80 patients had Codman intraparenchymal ICP monitor. Postoperatively, ICP remained under 20 mmHg in 65 cases; in remaining 15 cases despite decompression craniectomy the ICP remained above 20 mmHg which responded very well to barbiturate coma. Intracranial pressure monitoring was kept for 7 - 10 days. The mean CPP in all patients with post-traumatic decompression craniectomy was 74.8 (range 60 - 100 mmHg). Mortality rate The overall mortality rate was 15% (total of 12 patients died) which is less as reported by Bizhan, et al in their study.1 Ten patients died during first 30 days and 2 patients died

Complications
Associated with decompressive craniectomy Subdural hygroma developed in 10 cases which resolved spontaneously in weeks or months. Two cases developed wound infection due to metheline resistant staphylococcus aureus (MRSA) but they responded well to medical management. One patient developed extradural haematoma on contralateral side which was causing mass effect (Fig. 4), so it was removed. In 3 cases radiological evidence showed increased brain swelling after decompressive craniectomy, which was treated medically. Eight patients (10%) developed parenchymal lucency (infarction) possibly

Figure 4 - Follow-up CT scan brain after decompressive craniectomy showing extradural haematoma on the opposite side.

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due to ischemia visualized on the postoperative CT scan brain (Fig. 5). Two patients developed global infarction (both died). Three patients developed unilateral hemispheric infarctions (remained vegetative) and occipital infarction in 3 cases (all with GOS ).

following severe head injury is challenged by the paucity of any strong scientific evidence.2 A negative attitude towards decompressive craniectomy arose from results of earlier studies of prophylactic decompressive craniectomy, which indicated high morbidity and mortality.5 In the present study, cumulative death rate in the first 30 days after decompressive craniectomy was 12.5% (10 patients out of 80) and 20 (25%) of 80 patients had a good outcome. The proportion of patients with a bad outcome (vegetative state) was 22.5% (18 out of 80 patients). Different studies data have also indicated that when better defined criteria are used, in conjunction with comprehensive management plan, decompressive craniectomy may improve outcome without increasing the proportion of patients in vegetative state (Table 5).6,9
Table 5 - Outcome following decompressive craniectomy for severe head injury.1 Author/year Gower, et al 1988 Gaab, et al 1990 Polin, et al 1997 Guerra, et al 1999 De Luca, et al 2000 Taylor, et al 2001 Whitfield, et al 2001 Schneider, et al 2002 Albanese, et al 2003 Bizher, et al 2006 Present study Total (%) Percentage No. of patients studied 10 37 35 55 22 13 26 62 13 50 80 403 (100%) GOS score (4 - 5) 4 29 13 33 9 7 18 18 5 20 20 176 (2 - 3) 2 3 14 11 9 3 2 30 5 16 48 143 (1) 4 5 8 11 4 3 6 14 3 14 12 84

Figure 5 - Follow-up CT scan after decompressive craniectomy showing multiple infarctions.

After replacement of bone flap in cases of decompressive craniectomy Six patients developed hydrocephalus after cranioplasty and ventriculoperitoneal shunt was done. Extradural haematoma developed in 5 cases in which 3 cases needed evacuation and 2 cases were treated conservatively due to their small size. Five cases developed wound infection. In these cases main causative factor was MRSA. Two cases treated medically but 3 cases developed osteomyelitis requiring removal of bone flap (later cranioplasty was done with titanium mesh after 3 months). Infection Intraoperative prophylactic antibiotic reduced wound infection up to 3%.3 In our study, 3 patients developed septicaemia (3.7%) in 2 patients (2.5%) developed wound infection which was due to MRSA. Duraplasty with a dural substitute has reportedly been associated with an increased chance of infection.14 We noted no such increase in infection. Cranioplasty with frozen bone implant also has an associated risk of infection.14 Five of our cases (6.2%) developed osteomyelitis due to MRSA and 2 of them were treated medically, 3 patients were subjected with removal of bone flap.

(43.6%) (35.4%) (20.8%)

Discussion
Although capable of controlling high ICP, the effectiveness of decompressive craniectomy in improving outcome In our study as in others, the admission GCS score, patients age and time of treatment was predictive of outcome.20,21

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Patient with good GCS (7 - 9), young age, and taken to operating theatre immediately have shown good outcome. The above results are good when compared with Miller, et al, Marshall, et al, Saul, et al and Clifton, et al who reported 42% mortality when an ICP is greater than 20 mmHg was not controlled in spite of maximum medical management.4,17,18,21 This comparison also favours the importance of decompressive craniectomy in maintaining controlled ICP (ICP below 20) and good outcome (43.6%) and decreased mortality rate (20.8%). Evidence for decompressive craniectomy One of the consequences of TBI is an acute increase in the total brain matter. Ischemia and energy failure at the level of mitochondria are some of the causes of cytotoxic brain oedema and ICP resistant to maximal medical management.3 Good pre-hospital care, intensive care and surgical guidelines for management of severe head injury has greatly reduced hypotension and hypoxia.2 Research on severe head injury has revealed no easy pharmaceutical therapy for severe head injury and brain oedema.3 Even after more than a dozen clinical trials there are no new clinically effective drugs to reduce cytotoxic or vasogenic brain oedema in acute phase, decreased ICP or improve outcome following severe head injury.6 Decompressive craniectomy reduces ICP independent of biochemical manipulation and maybe a valid management option in diffuse swelling when maximum medical management fails.9 Biological rationale in models of decompressive craniotomy in animals Cold-induced ICP in different experimental animals has been relieved by decompressive craniectomy, and in one study, resection of oedematous cortex improved glucose and oxygen metabolism as indicated by arteriovenous measures of 02 and glucose differences.5

Figure 6 - Operative picture showing craniotomy bone size is about 15 cm in AP diameter with temporal extension (Abrars flap).

One patient developed extradural haematoma on the contralateral side which was evacuated. Five cases (6.2%) developed extradural haematoma after cranioplasty in which 2 were treated conservatively, 3 needed evacuation. Postoperative infarction and oedema Bizhan, et al reported enhancement of brain oedema and at times fresh haemorrhage ipsilateral to the site of decompression craniectomy in 8 cases.1 In our study, 3 (3.7%) cases have radiological evidence of increased swelling which were treated with barbiturate coma and 8 patients developed infarction (10%). Among these 8 patients, 3 patients developed occipital infarction who recovered well, 2 patients developed global infarction (these patients died), 3 patients developed hemispheric infarction which resulted in vegetative state. Delayed hydrocephalus In our study 3 patients (3.7%) developed delayed hydrocephalus after decompressive craniectomy and 6 patients (7.5%) developed hydrocephalus after cranioplasty whom were subjected to VP shunt.

Conclusion
Studies of patient with traumatic brain injury indicate increased morbidity and mortality rates where ICP is not medically manageable. When the primary effects of severe head injury are not easily manageable by pharmaceutical agents, increased ICP can be relieved by decompressive craniectomy, and in turn reduce some of the events leading to secondary cerebral insult. Data from the last 7 series of decompressive craniectomy for persistent high ICP have indicated an improved outcome as compared to outcome following conservative treatment. In the present study, decompressive craniectomy in severe TBI has shown good results in controlling high ICP and

Surgery
Operatively, usual trauma frontoparietal flap was made but extended behind ear to allow more room for decompression along with temporal craniectomy. This is similar to hemicraniectomy and is called Abrars flap (Fig. 6). Subdural hygroma and extradural haematoma Subdural hygroma found as early as 15 days decompression may resolve several months thereafter.7 Ten patients (12.5%) in our study developed subdural hygroma and none of the patients needed surgical evacuation or insertion of shunt device.

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improving brain tissue oxygenation resulting in good outcome and decreased mortality rate. Furthermore, patients with severe head injury with admission GCS greater than 6 are especially good candidates for decompressive craniectomy. Decompressive craniectomy was associated with a better than expected functional outcome in patients with medically uncontrollable ICP and brain herniation, compared with outcome in other control cohorts reported in the literature.

References
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23: 417-422 10. Jaeger M, Soehle M: Effects of decompressive craniectomy on brain tissue oxygen in patients with intracranial hypertension. J Neurol Neurosurg Psych 2003, 74: 513-515 11. Jiang JY, Gao GY, Li WP, et al: Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma 2002, 19: 869-874 12. Kjellberg RN, Prieto A: Bifrontal decompressive craniotomy for massive cerebral edema. J Neurosurg 1971, 34: 488-493 13. Lannoo E, Van Rietvelde F, Colardyn F, et al: Early predictors of mortality and morbidity after severe closed head injury. J Neurotrauma 2000, 17: 403-414 14. Malliti M, Page P, Gury C, et al: Comparison of deep wound infection rates using a synthetic dural substitute (neural-patch) or pericranium graft for dural closure: A clinical review of 1 year. Neurosurg 2004, 54: 599-604 15. Marmarou A, Anderson RL, Ward JD, et al: Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 1991, 75: 59-66 16. Marshall LF, Marshall SB, Klauber MR, et al: A new classification of head injury based on computerized tomography. J Neurosurg 1991, 75: 14-20 17. Marshall LF, Smith RW, Shapiro HM: The outcome with aggressive treatment in severe head injury. Part 1: The significance of intracranial pressure monitoring. J Neurosurg 1979, 50: 20-25 18. Miller JD, Becker DP, Ward JD, et al: Significance of intracranial hypertension in severe head injury. J Neurosurg 1977, 47: 503-516 19. Polin RS, Shaffrey ME, et al: Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurg 1997, 41(1): 84-94 20. Ransohoff J, Benjamin MV, Gage EL Jr, et al: Hemicraniectomy in the management of acute subdural hematoma. J Neurosurg 1971, 34: 70-76 21. Saul TG, Ducker TB: Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982, 56: 498-503 22. Shakiba H, Dinesh S, Anne MK: Advanced trauma life support training for hospital staff. The Cochrane Database of Systemic Reviews: CD 004173, 2003 23. Venes JL, Collines WF: Bifrontal decompressive craniectomy in the management of head trauma. J Neurosurg 1975, 42: 429-433

GENTLE REMINDER
Glasgow outcome scale Classification Dead Vegetative Disabled Good recovery Sleep/ awake but not sentient Conscious but severely disabled May have minor sequelae Description

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