Case Of Abdominal Compartment Syndrome Research Articles

Translumbar Extraperitoneal Decompression for Abdominal Compartment Syndrome After Endovascular Treatment of a Ruptured AAA

Purpose: To report an unusual case of abdominal compartment syndrome (ACS) following endovascular repair of a ruptured abdominal aortic aneurysm (rAAA) that had been treated with a stent-graft 3 years prior. Case Report: A 68-year-old man with a 3-year-old Vanguard bifurcated aortic stent-graft experienced sudden back pain and collapse. Aneurysm rupture documented by computed tomography was due to dislocation of the left graft limb. A Talent aortomonoiliac graft was deployed, followed by a femorofemoral bypass. No endoleak was evident. A few hours later, the patient became oliguric and hemodynamically unstable. Increased intraabdominal pressure (IAP) was recorded. Abdominal decompression was performed, removing 1500 mL of blood from the retroperitoneum through an 18-cm lumbotomy; the peritoneum was opened, and another 500 mL of blood was aspirated. The IAP fell immediately, followed by diuresis a few hours later. The patient recovered and was discharged after 27 days. Conclusions: Some of the perioperative complications seen after conventional rAAA repair are also encountered after endovascular treatment. ACS requires urgent decompression, and less invasive approaches, such as translumbar extraperitoneal decompression, may be a good alternative to a midline laparotomy.

Translumbar Extraperitoneal Decompression for Abdominal Compartment Syndrome after Endovascular Treatment of a Ruptured AAA

To report an unusual case of abdominal compartment syndrome (ACS) following endovascular repair of a ruptured abdominal aortic aneurysm (rAAA) that had been treated with a stent-graft 3 years prior. A 68-year-old man with a 3-year-old Vanguard bifurcated aortic stent-graft experienced sudden back pain and collapse. Aneurysm rupture documented by computed tomography was due to dislocation of the left graft limb. A Talent aortomonoiliac graft was deployed, followed by a femorofemoral bypass. No endoleak was evident. A few hours later, the patient became oliguric and hemodynamically unstable. Increased intra-abdominal pressure (IAP) was recorded. Abdominal decompression was performed, removing 1500 mL of blood from the retroperitoneum through an 18-cm lumbotomy; the peritoneum was opened, and another 500 mL of blood was aspirated. The IAP fell immediately, followed by diuresis a few hours later. The patient recovered and was discharged after 27 days. Some of the perioperative complications seen after conventional rAAA repair are also encountered after endovascular treatment. ACS requires urgent decompression, and less invasive approaches, such as translumbar extraperitoneal decompression, may be a good alternative to a midline laparotomy.

Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation

BackgroundThe term secondary abdominal compartment syndrome (ACS) has been applied to describe trauma patients who develop ACS but do not have abdominal injuries. The purpose of this study was to describe major trauma victims who developed secondary ACS during standardized shock resuscitation. MethodsOur prospective database for standardized shock resuscitation was reviewed to obtain before and after abdominal decompression shock related data for secondary ACS patients. Focused chart review was done to confirm time-related outcomes. ResultsOver the 30 months period ending May 2001, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 ± 5 mm Hg, base deficit 8.6 ± 1.6 mEq/L), with severe injuries (injury severity score 28 ± 3) and required aggressive shock resuscitation (26 ± 2 units of blood, 38 ± 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and did not maintain decreased bladder pressure. Conclusions:Secondary ACS is an early but, if appropriately monitored, recognizable complication in patients with major nonabdominal trauma who require aggressive resuscitation.

Release of Abdominal Compartment Syndrome Improves Survival in Patients with Burn Injury

Abdominal compartment syndrome (ACS) has rarely been described as a complication of burn injury. This study describes cases of ACS in patients with burn injury and the physiologic results of abdominal release. Charts for all patients admitted to two major burn center intensive care units from January 1998 through August 2000 were reviewed for ACS. Physiologic parameters were compared before and after abdominal release. Ten of 1,014 patients developed ACS. Abdominal release improved peak inspiratory pressures and Acute Physiology and Chronic Health Evaluation II scores (p < 0.03). The amount of fluid required to maintain adequate urine output also decreased substantially. Forty percent of patients with ACS survived to discharge. Abdominal release for patients with ACS and severe burn injury results in physiologic improvement and a 40% survival rate. We recommend bladder pressure monitoring for all patients with severe burn injuries and abdominal decompression in any patient who develops pressures greater than 30 mm Hg if they have signs of physiologic compromise. Aggressive expectant management can effect a 40% survival rate in this group of severely injured patients.

Secondary abdominal compartment syndrome is a highly lethal event

Background: Recent reports have described resuscitation-induced, “secondary” abdominal compartment syndrome (ACS) in trauma patients without intra-abdominal injuries. We have diagnosed secondary ACS in a variety of nontrauma as well as trauma patients. The purpose of this review is to characterize patients who develop secondary ACS. Methods: Our prospective ACS database was reviewed for cases of secondary ACS. Physiologic parameters and outcomes were recorded. Data are expressed as mean ± SEM. Results: Fourteen patients (13 male, aged 45 ± 5 years) developed ACS 11.6 ± 2.2 hours following resuscitation from shock. Eleven (79%) had required vasopressors; the worst base deficit was 14.1 ± 1.9. Resuscitation included 16.7 ± 3.0 L crystalloid and 13.3 ± 2.9 red blood cell units. Decompressive laparotomy improved intra-abdominal, systolic, and peak airway pressures, as well as urine output; however, mortality was 38% among trauma and 100% among nontrauma patients. Conclusions: Secondary ACS may be encountered by general surgeons in a variety of clinical scenarios; resuscitation from severe shock appears to be the critical factor. Early identification and abdominal decompression are essential. Unfortunately, in our experience, this is a highly lethal event.

Abdominal compartment syndrome after mesenteric revascularization

Abdominal compartment syndrome (ACS) results from increased pressure within the abdominal cavity leading to multisystem organ dysfunction. The most common cause of ACS is increased intraperitoneal volume from any source, but extrinsic compression can also cause increased intra-abdominal pressure. Although ACS has been well described in patients with trauma, little has been reported on ACS in postoperative patients without traumatic injuries. We report on a patient who had acute ACS 2 days after surgical revascularization for chronic mesenteric ischemia. With appropriate treatment, the patient made a rapid and complete recovery. We present this case of acute ACS in the postoperative patient without trauma to increase awareness and help minimize death caused by this devastating syndrome. (J Vasc Surg 2001;34:559-61.)

Acute renal failure due to abdominal compartment syndrome: report on four cases and literature review.

We report on 4 cases of abdominal compartment syndrome complicated by acute renal failure that were promptly reversed by different abdominal decompression methods. Case 1: A 57-year-old obese woman in the post-operative period after giant incisional hernia correction with an intra-abdominal pressure of 24 mm Hg. She was sedated and curarized, and the intra-abdominal pressure fell to 15 mm Hg. Case 2: A 73-year-old woman with acute inflammatory abdomen was undergoing exploratory laparotomy when a hypertensive pneumoperitoneum was noticed. During the surgery, enhancement of urinary output was observed. Case 3: An 18-year-old man who underwent hepatectomy and developed coagulopathy and hepatic bleeding that required abdominal packing, developed oliguria with a transvesical intra-abdominal pressure of 22 mm Hg. During reoperation, the compresses were removed with a prompt improvement in urinary flow. Case 4: A 46-year-old man with hepatic cirrhosis was admitted after incisional hernia repair with intra-abdominal pressure of 16 mm Hg. After paracentesis, the intra-abdominal pressure fell to 11 mm Hg.

Abdominal compartment syndrome

Two cases of abdominal compartment syndrome are described and the pathophysiology associated with it is reviewed. The first patient was a 46-yr-old man who sustained extensive blunt abdominal injuries following a fall. The second was a 54-yr-old man involved in a motor vehicle accident with blunt abdominal trauma. In both cases, the patients developed an extremely tense abdomen, increasing peak inspiratory pressures, hypercarbia and oliguria. Both demonstrated improvement in cardiac performance and ventilatory variables following an emergency decompressive celiotomy. Abdominal compartment syndrome results in impairment of organ function secondary to increased intraabdominal pressure. These patients require emergency decompressive celiotomy to relieve the symptoms. However, the incidence of intractable asystole and hypotension during this procedure is high and vigilance must be maintained during the release of the increased intraabdominal pressure.