Inroduction Abdominal compartment syndrome (ACS) is an unpredictable complication of posterior spinal fusion surgery. The condition is defined by elevated intra-abdominal compartment pressure (IAP) O 20 mm Hg, resulting in physiologic compromise and end organ dysfunction . Abdominal compartment syndrome can result from trauma, extreme fluid shifts, vascular compression, and mesenteric ischemia [2-4]. This case report describes delayed postoperative ACS in a patient with neuromuscular scoliosis resulting from cerebral palsy. This case outlines the clinical picture, risk for development, and indications for emergent surgical decompression of the abdomen in delayed onset of ACS. Case Presentation A 12-year-old African American boy with quadriplegic pattern cerebral palsy and multiple comorbidities presented with worsening scoliosis, difficulty with sitting, respiratory insufficiency, and discomfort with movement. He underwent a posterior spinal fusion from T1-pelvis with unit rod instrumentation and sublaminar wire fixation (Fig. 1). The abdomen was appropriately decompressed during positioning for the case and there were no intraoperative complications. Intraoperative parameters of surgery are shown in Table 1. Postoperatively, the patient was transferred to the pediatric intensive care unit on the ventilator in stable condition, placed supine with the head elevated approximately 20 to 30, and frequently turned as appropriate.
On postoperative day 1 (POD1) the patient had intermittent episodes of hypotension with mean arterial pressure ! 60 mmHg, necessitating fluid resuscitation. On POD2, the patient was positive 8.2 L overall. By the end of POD2, the intermittent hypotension episodes resolved and the patient was successfully weaned off of vasopressors. On the morning of POD3, the patient suddenly became tachycardic and hypotensive unresponsive to fluid resuscitation. Peak inspiratory pressures (PIP) rapidly increased to O 20 cm H2O. On examination, the abdomen was noted to be rigid. Empiric antibiotics were initiated, and an echocardiogram ruled out pericardial effusion. An Author disclosures: AB (none); KV (none); JPS (none); FM (none); KD (consultancy for DePuy Spine). *Corresponding author. Department of Orthopaedic Surgery, Jefferson Medical College, 1015 Walnut Street, Curtis Building, Sure 810, Philadelphia, PA 19107, USA. Tel.: (215) 955-1500; Fax: (215) 503-0530. E-mail address: firstname.lastname@example.org (A. Boniello). 2212-134X/$ - see front matter 2013 Scoliosis Research Society. http://dx.doi.org/10.1016/j.jspd.2013.07.011 Spine Deformity 1 (2013) 464e467 www.spine-deformity.org Author's personal copy urgent explorative laparotomy was performed at the bedside, because the patient was deemed unstable to transfer.
Inspection revealed an edematous colon and pancreas. The small bowel initially appeared pale but not frankly ischemic. Decompression resulted in immediate Fig. 1. (A) Preoperative AP view. (B) Preoperative lateral view. (C) Postoperative AP view. (D) Postoperative lateral view. A. Boniello et al. / Spine Deformity 1 (2013) 464e467 465 Author's personal copy improvement in the patient’s blood pressure as well as PIP. Within minutes, perfusion of the small bowel improved significantly. Ascitic fluid of 500 mL was removed and the abdomen was packed with a vacuum-assisted closure wound system applied. Repeat explorative laparotomies on POD4 and 6 failed to reveal intra-abdominal pathology. The abdomen was closed on POD6 and the patient was transferred from the intensive care unit. The remaining hospital course was uncomplicated, with discharge to home on POD17.
Postoperative parameters are shown in Table 2. Discussion Abdominal compartment syndrome can result in the compromise of multiple organ systems, leading to a mortality of 40% to 90% . Clinically, ACS can cause increased PIP, hypoxia, oliguria, and decreased cerebral perfusion pressure [5,6]. Physical examination has proven to be inaccurate at detecting IAP O 18 mmHg (sensitivities of 40% to 60%) . An IAP should be obtained with at least 2 of the following risk factors: surgery, trauma, high-volume fluid resuscitation, ileus, organ failure, prone positioning, or hypotension [1,8,9]. Other risk factors include acute pancreatitis, hemoperitoneum, sepsis, venous thrombosis, and burns. A described case of ACS developed during surgical neuromuscular scoliosis correction was related to impaired venous drainage . Another report described 2 cases of ACS that developed in patients with ankylosing spondylitis who underwent correction of hyperkyphosis deformity: 1 that occurred on POD13 and 1 that occurred intraoperatively. Development of ACS in the patient on POD13 likely resulted from alteration of the abdominal anatomy leading to small bowel obstruction, whereas massive fluid resuscitation was likely the causative factor in the intra-operative case. In the setting of scoliosis correction, superior mesenteric artery syndrome (SMAS) has also been described . Superior mesenteric artery syndrome is a phenomenon in which the angle between the SMA and the aorta is reduced, causing transient bowel edema and obstruction. Surgery can also lead to massive fluid shifts and significant third spacing, which may have precipitated the SMAS.
These factors may exacerbate transient bowel ischemia from SMAS and may go unrecognized in an intubated and sedated patient. To the authors’ knowledge, this is the first report of delayed ACS after scoliosis surgery in a patient with no prior abdominal surgeries or severe kyphotic deformity. Three mechanisms may have contributed to this pathology: fluid resuscitation postoperatively, third spacing after surgery, and SMAS causing bowel edema. This case illustrates the necessity for a high level of suspicion for increased IAP after major spinal surgery, because early intervention for ACS is lifesaving. ACS is a severe condition that can occur with correction of scoliosis requiring immediate surgical decompression of the abdomen. This case outlines complete recovery of delayed onset of ACS after neuromuscular spinal fusion. Increased awareness of ACS is imperative for timely recognition, rapid treatment, and ultimate survival. References  Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations.
Intensive Care Med 2007;33:951e62.  Sugrue PA, O’Shaughnessy BA, Nasr F, et al. Abdominal complications following kyphosis correction in ankylosing spondylitis. J Neurosurg Spine 2009;10:154e9.  Evarts CM, Winter RB, Hall JE. Vascular compression of the duodenum associated with the treatment of scoliosis: review of the literature and report of eighteen cases. J Bone Joint Surg Am 1971;53:431e44. Table 1 Intraoperative parameters of surgery: posterior spinal fusion, T1-pelvis. Anesthesia time 10 hours, 19 minutes Operative time 7 hours, 3 minutes Intravenous fluids 2,800 mL Packed red blood cells 570 mL Fresh-frozen plasma 1,350 mL Platelets 300 mL Cryoprecipitate 150 mL Estimated blood loss 3,000 mL Urine output 1,000 mL Table 2 Postoperative parameters. Postoperative day 0 123 45 6 Total in, mL* 9,411.96 3,520 2,883.5 6,769.38 3,743.9 2,867.96 3,093.12 Total out, mL* 5,271 4,753 4,098 4,006 5,522.5 3,062 2,869 Net, mL* 4,140.96 1,233 1,214.5 2,763.38 1,778.6 194.04 224.12 Mean arterial pressure, mm Hg 69 58 80 99 65 65 65 Serum sodium, mEq/L 136 135 133 135 130 135 136 Peak inspiratory pressure, (cm H2 O) 15 15 16 21 15 20 20 * Fluid values measured over 24-hour period beginning at 07:00. 466 A. Boniello et al. / Spine Deformity 1 (2013) 464e467 Author's personal copy  Carr JA.
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