Neurocritical Care

, Volume 15, Issue 3, pp 516–518

Decompressive Laparotomy for Refractory Intracranial Hypertension After Traumatic Brain Injury


  • Jon D. Dorfman
    • Department of SurgeryBoston University School of Medicine and Boston Medical Center
    • Department of NeurologyBoston University School of Medicine and Boston Medical Center
    • Department of NeurosurgeryBoston University School of Medicine and Boston Medical Center
  • Deborah M. Green
    • Department of NeurologyBoston University School of Medicine and Boston Medical Center
    • Department of NeurosurgeryBoston University School of Medicine and Boston Medical Center
  • Christina DeFusco
    • Department of NeurologyBoston University School of Medicine and Boston Medical Center
  • Suresh Agarwal
    • Department of SurgeryBoston University School of Medicine and Boston Medical Center
Practical Pearl

DOI: 10.1007/s12028-011-9549-0

Cite this article as:
Dorfman, J.D., Burns, J.D., Green, D.M. et al. Neurocrit Care (2011) 15: 516. doi:10.1007/s12028-011-9549-0



Intracranial hypertension is a crucial modifiable risk factor for poor outcome after traumatic brain injury (TBI). Limited evidence suggests that decompressive laparotomy may be an effective treatment for refractory ICH in patients who have elevated intra-abdominal pressure.


Case report.


We present a multi-trauma patient who sustained severe TBI in a motor vehicle collision. Intracranial pressure (ICP) was initially medically managed but became refractory to standard therapies. Emergent decompressive laparotomy performed in the surgical intensive care unit for abdominal compartment syndrome concomitantly improved the patient’s ICP.


Elevated intra-abdominal pressure can exacerbate intracranial hypertension in patients with TBI. Recognition of this condition and treatment with decompressive laparotomy may be useful in patients with intracranial hypertension refractory to optimal medical therapy.


Traumatic brain injuryIntracranial hypertensionIntra-abdominal hypertension


Intracranial hypertension is a crucial modifiable risk factor for poor outcome after severe traumatic brain injury (TBI) [1]. In most cases, it can be sufficiently managed with relatively conservative methods such as head elevation, sedation, and osmotherapy. In some cases however, the intracranial pressure (ICP) remains elevated despite the optimal use of these treatments. Commonly employed treatments for such refractory cases are directed at the brain and include craniectomy, barbiturate coma, and therapeutic hypothermia. Each of these treatments carries with it important risks and, if the process provoking intracranial hypertension is not reversed, can be ineffective.

Basic science and limited clinical evidence suggest a close relationship between intracranial, intra-thoracic, and intra-abdominal pressures [2, 3]. The proposed mechanism is decreased jugular venous outflow from increased central venous pressure. Cerebral venous congestion ensues. Treatment designed for improvement of intracranial pressure, particularly cerebral perfusion pressure augmentation and osmotherapy with hypertonic saline, may inadvertently elevate ICP. For example, resuscitation for hypovolemia intended to increase MAP, can lead to third spaced fluid, increased intra-abdominal hypertension (IAH) or even abdominal compartment syndrome (ACS). The IAH may subsequently lead to increased ICP. We present a case of a patient with multiple injuries including severe TBI who developed refractory intracranial hypertension after massive resuscitation with blood products whose ICP rapidly improved after laparotomy for ACS.

Case Summary

A 17 year old girl sustained severe TBI in a high speed motor vehicle collision. She was taken by ambulance to a local hospital, intubated and transferred to our Level 1 trauma center. Emergency medical services noted pre-hospital hypotension (systolic blood pressure < 90 mmHg). On arrival to the Emergency Department, her Glasgow Coma Score was 3 with 2 mm sluggishly reactive pupils. Her initial CT scan revealed diffuse cerebral edema, obliteration of the perimesencephalic cisterns and a right subdural hematoma with an 8 mm midline shift (Fig. 1).
Fig. 1

Admission CT showed obliteration of the perimesencephalic cisterns (a), diffuse cerebral edema, right subdural hematoma with 8 mm midline shift (b)

In addition to the TBI, she had extensive facial, thoracoabdominal and extremity injuries, including right lateral pterygoid plate fracture, left temporal bone fracture, bilateral pulmonary contusions, left hemo-pneumothorax, a mediastinal hematoma, comminuted fractures of the superior and inferior right pubic rami with diastases of the pubic symphysis, a left sacral fracture, comminuted and distracted fractures of the tibia and fibula with extensive soft tissue injury bilaterally. Her admission APACHE II Score was 26. Her mangled right lower extremity was not salvageable and required a completion amputation at the bedside in the intensive care unit on hospital day 1.

Because of massive blood loss from her multiple injuries, she required large volume resuscitation in the first 24 h of hospitalization. Over that time period, she was transfused 13 units of packed red blood cells, 6 units of fresh frozen plasma, a 10 pack of platelets, 10 units of cryoprecipitate in addition to more than 14 l of crystalloid.

An ICP monitor was placed within 4 h of admission to the ICU and showed an opening ICP of 27 mmHg. Over the first 18 h of admission, her intracranial pressure was kept <20 mmHg with standard medical therapy including maintenance of cerebral perfusion pressure >60 mmHg, systolic blood pressure >90 mmHg, PaCO2 35–40 mmHg, normothermia, head of bed elevation to greater than 30°, neutral head and neck positioning, adequate sedation and analgesia, and three doses of mannitol (25 gm each).

Over the following 6 h, her abdomen became increasingly distended and firm, the urine output dropped, her tidal volumes on airway pressure release ventilation (APRV) diminished from over 500 ml to less than 400 ml, and the bladder pressure was 32 mmHg. During this time period, her intracranial pressures increased and became refractory to mannitol and deep sedation (Fig. 2). This culminated in an ICP plateau wave of 35–40 mmHg, severe hypertension and bradycardia. Abdominal compartment syndrome with secondary intracranial hypertension was diagnosed. On hospital day 2, emergent decompressive laparotomy was performed at the bedside resulting in an immediate decline of her ICP to 5–10 mmHg and resolution of the ACS.
Fig. 2

Timeline of intracranial pressure (a) and pulmonary and renal dysfunction (b). Arrowhead denotes approximate time of decompressive laparotomy

She required one additional dose of mannitol 36 h later for elevated ICP. The remainder of her hospital stay was uneventful. Her right below-knee amputation was revised to an above-the-knee amputation (hospital day 3) and percutaneous tracheostomy was performed on hospital day 12. Her abdomen was closed with a biologic mesh and open gastrostomy feeding tube placed on hospital day 22. She was discharged to a rehabilitation center by hospital day 30.

Two months after her release from the hospital, she was steadily recovering from her TBI. Her Glasgow Outcome Score was 3. She is able to stand and communicate basic information, but requires frequent assistance with activities of daily living and constant supervision.


Dysfunction and failure of the renal, respiratory, cardiovascular, gastrointestinal, and hepatic systems is a well-described consequence of sustained intra-abdominal hypertension (>20 mmHg). This syndrome is known as the abdominal compartment syndrome [4]. A lesser-known potential complication of ACS is elevated ICP. This direct relationship between intra-abdominal pressure and ICP was first reported in a porcine experimental model by Josephs and colleagues in 1994 [5]. The pathophysiology of this phenomenon was investigated in a rigorous porcine model by Bloomfield and co-workers [2]. They measured intra-abdominal pressure, ICP, central venous pressure, and pleural pressure (PP) after inflating an intra-abdominal balloon. IAH positively correlated with CVP and ICP. The explanation for this observation has not been completely elucidated, but the authors hypothesized the following causal chain: ↑IAP → ↑PP → ↑CVP → ↓cerebral venous outflow → ↑ICP. Importantly, volume expansion with normal saline worsened intracranial hypertension, while surgical abdominal decompression lead to prompt normalization of ICP. Since then, ICP has been shown to positively correlate with IAP in an intensive care unit patient population with both traumatic and nontraumatic brain injury [6, 7].

The first report describing successful treatment of intracranial hypertension with abdominal decompression in a patient with simultaneous ACS was published in 1995 [8]. Subsequently, the group from the R. Adams Cowley Shock Trauma Center in Baltimore described a series of 17 patients with severe TBI and elevated IAP in whom decompressive laparotomy was successful in lowering ICP that was refractory to aggressive medical management, including barbiturate coma in 13. Interestingly, none of these patients had sufficient extracerebral organ dysfunction to meet criteria for abdominal compartment syndrome despite a mean pre-decompression IAP of 27.5 mmHg [9]. Eleven of the 17 patients survived to hospital discharge and 6 died.

Our case highlights the therapeutic potential of abdominal decompression in select patients with elevated IAP and intracranial hypertension refractory to traditional medical therapy. The easily overlooked effect of IAP on ICP should be considered in TBI patients with refractory intracranial hypertension, especially those who have received high-volume fluid resuscitation [3].

Conflict of interest

The authors report no conflicts of interest.

Copyright information

© Springer Science+Business Media, LLC 2011