One of the most formidable complications of traumatic brain injury (TBI) is increased intracranial pressure (ICP). An increased ICP is a neurologic emergency that if left untreated may cause cerebral ischemia, brain herniation, and possibly death. [1] The primary treatment for patients with TBI is to lower ICP readings below 20 mmHg and to maintain cerebral perfusion pressure (CPP) between 60 mmHg and 90 mmHg in order to provide sufficient cerebral perfusion. [1] Proper head elevation is an effective strategy promoting optimal venous flow for TBI, but more aggressive therapies are needed when elevated ICP accompanies severe TBI. Some of the therapies to lower ICP after TBI include hyperventilation (HV), intravenous mannitol and cerebrospinal fluid drainage from a ventriculostomy (EDV). Decompressive craniectomy and barbiturate-induced coma are at the desperate end of the continuum necessary to save a patient suffering from both TBI and increased ICP. [2] [3]

When all typical and heroic therapeutic treatments have been exhausted for sustained high ICP, an innovative approach termed a decompressive laparotomy can be implemented. This treatment which had been exclusively reserved for abdominal compartment syndrome involves cutting the anterior fascia of the abdomen allowing the abdominal viscera to expand thereby relieving intra-abdominal pressure. The elevation of intra-abdominal pressure displaces the diaphragm cephalad, increasing intrathoracic pressure and central venous pressure. The pressure is then transmitted through the venous system, causing increases in ICP and decreases in CPP. [4] [5] [6] We are presenting a case study of a 16-year-old male with a severe TBI and incessant elevated ICP who demonstrated a reduction in his ICP following a decompressive craniectomy without the presence of an abdominal compartment syndrome (ACS).

A 16-year-old male presented to our level I trauma center in Atlanta, Georgia after sustaining a single gunshot wound (GSW) to the left occipital region of head. He was confused and combative, requiring intubation in the trauma bay for a glasgow coma score of eight. Significant findings included comminuted fractures of the left thumb and an entry wound to the left temporal bone of the skull. The computed tomography (CT) scan of the head revealed retained bullet fragments and multiple facial fractures, it also revealed a comminuted fractures of the left posterior parietal, occipital and temporal bones. Intracranial damage included a left-sided subdural hematoma; intraparenchymal hemorrhage and diffuse cerebral edema with sulcal effacement of 6 mm with a left to right midline shift. (Figure 1)

The patient was taken to the operating room for debridement of the brain parenchyma and a right decompressive craniotomy by the neurosurgery service. Postoperatively, the ICP remained elevated (41–54) and would not respond to propofol sedation, 3% saline infusion and cerebrospinal fluid drainage. The following morning a repeated CT scan of the head was performed which revealed blossoming of the left intraparenchymal hematoma. The patient was transported to the operating room for a left hemicraniectomy and duraplasty. Despite this intervention, the ICP remained in the thirties and a metabolic coma with phenobarbital was induced.

On postoperative day-5, a decompressive laparotomy was performed as an intervention for his refractory intracranial hypertension. The abdominal fascia was left open allowing room for bowel evisceration. ICPs measured immediately following the decompressive laparotomy were lowered ranging between 11–12 mmHg. On postoperative day-14, the patient was taken to the operating room for an abdominal washout and fascial closure because of ICP measurements that were less than 20 for 9 days since the decompression. By postoperative day-18, the induced pentobarbital coma had been reversed and the external ventricular drain (EVD) had been removed. The patient survived and was discharged to a rehabilitation facility with a glasgow coma score of seven. One year following his gun shot wound to the head, the patient is at home with his parents. He is communicative and writing music. He has gained the ability to ambulate with the assistance of a cane and hopes to walk independently before reaching college.

Approximately, 1.7 million people sustain a TBI annually. [7] In the context of a TBI, the brain has a limited capacity to autoregulate the CPP because of increased intracranial pressure as established by the Monro–Kellie doctrine. The Monro–Kellie doctrine describes the brain as a fixed bone that has decreased compliance when compared to other body compartments. An increase in intracranial volume causes a significant increase in the ICP negatively impacting the CPP of the brain. [8] Systemic vasoactive responses from shock remote to the abdomen can cause "capillary leak" that leading to fluid accumulation inside the abdomen or thorax deleteriously increasing ICP. Intracranial pressure studies have demonstrated that there is a direct correlation between intracranial, intrathoracic and intra-abdominal compartments. [9] [10] Multiple-compartment syndrome or polycompartment syndrome, stresses the importance of increased pressure in closed anatomic spaces threatening the viability of surrounding tissue. [11] Joseph et al. demonstrated a decompressive laparotomy was successful in decreasing ICP, thus supporting the correlation of pressures in the polycompartment syndrome theory. In this study, decompressive laparotomies were utilized for 17 patients and all 17 patients experienced a decrease in the ICP of 10 mmHg or greater. [6] A case report by Dorfman et al. documented the treatment of a 17-year-old female following a motor vehicle collision with TBI that was effectively treated with a decompressive laparotomy in a last ditch effort to control intractable ICPs as a consequence of a massive resuscitation leading to an ACS. [12]

When bladder pressures are performed and measured above the normal range (greater than 20 mmHg), a decompressive laparotomy in selective patients can be performed to release an abdominal compartment syndrome. As mentioned by Scalea et al. the performance of decompressive laparotomies for refractory ICP can be associated with an unacceptably high rate of morbidity and mortality, and should be utilized with well-defined criteria. [10] In our study, and with subsequent success with an adult patient, we have expanded our decompressive laparotomies to not only include when medical management, which includes an induced pentobarbital coma, fails to reduce elevations of ICP above 20 mmHg, but also to include when the bladder pressures are normal. Our earlier intervention without bladder pressure elevation may suggest intervening before a measured increase in ACS that would negatively impact perfusion of the injured brain.

Our case outlines the utility of a decompressive laparotomy for an isolated head injury when the abdomen is affected by a massive trauma resuscitation and a polycompartment syndrome can be presumed while the bladder pressures may not yet reflect the volume expansion leading to an abdominal compartment syndrome. The immediate and significant drop of the ICP, which was sustained below 20 mmHg following the decompressive laparotomy highlights regarding the body as being multi-compartmented when treating intractable ICPs. Studies have demonstrated that the pediatric population performs more favorably to decompressive craniectomies than their adult counterparts. [13] [14]

This case study of a 16-year-old male patient and that of a 17-year-old patient by Dorfman et al. perhaps further demonstrates that the pediatric population with TBI with refractory intracranial hypetension can be treated more aggressively with less mortality and a lesser vegetative state when maximal medical therapy fails. The number of published cases and sample sizes are limited in the treatment of incessant intracranial pressures with abdominal compartment syndrome. Our success with this patient and another young adult demonstrates that a decompressive laparotomy can be safely applied as an alternative to improve cerebral perfusion in the absence of abdominal compartment syndrome when medical therapy fails.

1. Nakagawa K, Smith WS. Evaluation and management of increased intracranial pressure. Continuum (Minneap Minn) 2011 Oct;17(5):1077–93.   [Pubmed]    
2. Fortune JB, Feustel PJ, Graca L, Hasselbarth J, Kuehler DH. Effect of hyperventilation, mannitol, and ventriculostomy drainage on cerebral blood flow after head injury. J Trauma 1995 Dec;39(6):1091–7.   [CrossRef]   [Pubmed]    
3. Eisenberg HM, Frankowski RF, Contant CF, Marshall LF, Walker MD. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg 1988;69(1):15–23.   [CrossRef]   [Pubmed]    
4. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ. A Proposed Relationship between Increased Intra-abdominal, Intrathoracic, and Intracranial Pressure. Crit Care Med 1997 Mar;25(3):496–503.   [CrossRef]   [Pubmed]    
5. Josephs LG, Este-McDonald JR, Birkett DH, Hirsch EF. Diagnostic laparoscopy increases intracranial pressure. J Trauma 1994;36(6):815–8.   [CrossRef]   [Pubmed]    
6. Joseph DK, Dutton RP, Aarabi B, Scalea TM. Decompressive Laparotomy to Treat Intractable Intracranial Hypertension after Traumatic Brain Injury. J Trauma 2004 Oct;57(4):687–93.   [CrossRef]   [Pubmed]    
7. Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010.    
8. Kim DJ, Czosnyka Z, Kasprowicz M, et al. Continuous monitoring of the Monro-Kellie doctrine: is it possible? J Neurotrauma 2012 May 1;29(7):1354–63.   [CrossRef]   [Pubmed]    
9. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ. Effects of increased intra-abdominal pressure upon intracranial perfusion before and after volume expansion. J Trauma 1996;40(6):936–41.   [CrossRef]   [Pubmed]    
10. Scalea TM, Bochicchio GV, Habashi N, McCunn M, Shih D, McQuillan K, Aarabi B. Increased Intra-Abdominal, Intrathoracic, and Intracranial Pressure After Severe Brain Injury: Multiple Compartment Syndrome. J Trauma 2007 Mar;62(3):647–56.   [CrossRef]   [Pubmed]    
11. Malbrain ML, Wilmer A. The polycompartment syndrome: towards an understanding of the interactions between different compartments. Intensive Care Med 2007 Nov;33(11):1869–72.   [CrossRef]   [Pubmed]    
12. Dorfman JD, Burns JD, Green DM, DeFusco C, Agarwal S. Decompressive Laparotomy for Refractory Intracranial Hypertension After Traumatic Brain Injury. Neurocrit Care 2011 Dec;15(3):516–8.   [CrossRef]   [Pubmed]    
13. Rutigliano D, Egnor MR, Priebe CJ, et al. Decompressive craniectomy in pediatric patients with traumatic brain injury with intractable elevated intracranial pressure. J Pediatr Surg 2006 Jan;41(1):83–7.   [CrossRef]   [Pubmed]    
14. Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006 Jan 25;(1).   [CrossRef]   [Pubmed]