Abdominal compartment syndrome: A lethal disease

CASE REPORT A 63­year­old Caucasian male with a history of ventral hernia secondary to multiple motor vehicular accidents and prior abdominal surgeries was admitted for an elective ventral hernia repair. A primary closure of ventral hernia with a skin mesh was performed. Post­ operatively he remained intubated and was transferred to surgical intensive care unit. At baseline, his laboratory data included serum creatinine ­ 0.9 mg/dl, hemoglobin ­ 10 gm/dl, white cell count ­ 9x103/mm3 and lactic acid ­ 1 mmol/l. Peri­operatively, he was 10 liters net positive with a urine output (VOP) of 1200 cc in 24 hours. His serum creatinine was 1.3 mg/dl with one liter urine output on post­operative day (POD)­1. A two millimeter (mm) gap was noted in between the surgical staples. Intra­abdominal pressure (IAP) measured by transvesical route was noted to be elevated at 14 cm of H2O. He was started on the intensive regimen for management of intra­abdominal hypertension (IAH) including nasogastric decompression, elevation of head of the bed > 30°, discontinuation of intravenous fluids and a trial of neuromuscular blockage. On POD­2, he was noted to have increasing abdominal distension, with worsening hemodynamic parameters (table 1). The gap in the surgical wound increased to five mm (figure 1) and the IAP was noted to be 24 cm of H2O. His condition significantly deteriorated during next few hours with development of oliguric acute kidney injury (AKI) (UOP 200 cc/24hours), acute respiratory distress syndrome, high anion gap metabolic acidosis and refractory hypotension requiring escalating doses of multiple vasopressors (norepinephrine 3 μgm/kg/min, epinephrine 1 mcg/kg/min, vasopressin 0.04 units/minute), to maintain mean arterial pressure of about 60 mmHg. His laboratory data revealed serum creatinine ­ 5 mg/dL, hemoglobin ­ 7.8 gm/dL, white cell count ­ 20x103/mm3 and an elevated lactic acid ­ 18 mmol/liter. He was diagnosed with the refractory abdominal compartment syndrome (ACS). Given his clinical deterioration and hemodynamic instability, the treatment goals were addressed with the family. The patient was made comfortable care per his former wishes, at family’s request.

A 63yearold Caucasian male with a history of ventral hernia secondary to multiple motor vehicular accidents and prior abdominal surgeries was admitted for an elective ventral hernia repair. A primary closure of ventral hernia with a skin mesh was performed. Post operatively he remained intubated and was transferred to surgical intensive care unit. At baseline, his laboratory data included serum creatinine 0.9 mg/dl, hemoglobin 10 gm/dl, white cell count 9x10 3 /mm 3 and lactic acid 1 mmol/l. Perioperatively, he was 10 liters net positive with a urine output (VOP) of 1200 cc in 24 hours.
His serum creatinine was 1.3 mg/dl with one liter urine output on postoperative day (POD)1. A two millimeter (mm) gap was noted in between the surgical staples. Intraabdominal pressure (IAP) measured by transvesical route was noted to be elevated at 14 cm of H 2 O. He was started on the intensive regimen for management of intraabdominal hypertension (IAH) including nasogastric decompression, elevation of head of the bed > 30°, discontinuation of intravenous fluids and a trial of neuromuscular blockage.
On POD2, he was noted to have increasing abdominal distension, with worsening hemodynamic parameters (table 1). The gap in the surgical wound increased to five mm (figure 1) and the IAP was noted to be 24 cm of H 2 O. His condition significantly deteriorated during next few hours with development of oliguric acute kidney injury (AKI) (UOP 200 cc/24hours), acute respiratory distress syndrome, high anion gap metabolic acidosis and refractory hypotension requiring escalating doses of multiple vasopressors (norepinephrine 3 µgm/kg/min, epinephrine 1 mcg/kg/min, vasopressin 0.04 units/minute), to maintain mean arterial pressure of about 60 mmHg. His laboratory data revealed serum creatinine 5 mg/dL, hemoglobin 7.8 gm/dL, white cell count 20x10 3 /mm 3 and an elevated lactic acid 18 mmol/liter. He was diagnosed with the refractory abdominal compartment syndrome (ACS). Given his clinical deterioration and hemodynamic instability, the treatment goals were addressed with the family. The patient was made comfortable care per his former wishes, at family's request.

DISCUSSION
Abnormally elevated IAP has been increasingly recognized in the critically ill as a causes of significant morbidity and mortality [1]. Depending on the severity of increased IAP and organ function, the World Society  Causes can be divided based on the mechanism of IAP elevation: i) condition associated with increase in intraabdominal volume: gastric distention, ileus, volvulus, intraabdominal or retroperitoneal masses, ascites; ii) conditions leading to reduced abdominal wall compliance: abdominal surgery, especially with tight abdominal closures, rectus sheath hematomas, surgical correction of large abdominal hernias; iii) combination of decreased abdominal wall compliance and increased intraabdominal volume: obesity, sepsis, severe sepsis, and septic shock, severe acute pancreatitis, massive fluid resuscitation, major burns [1].
Increased IAP within the closed abdominal cavity can not only lead to decreased perfusion and ischemia of intraabdominal organs but can also cause organ dysfunction beyond the abdominal cavity due to the close anatomic relationships with contiguous cavities. [2]. Major clinical manifestations of the commonly involved organ systems are described in table 2. The key to recognizing ACS in a critically ill patient is the demonstration of elevated IAP. Clinical examination is an inaccurate indicator of IAP estimation with a sensitivity and positive predictive value of around 40 60% [3,4]. Moreover the radiologic investigations with plain radiography of the abdomen, abdominal ultrasound or CT scan are also insensitive [2]. Although Table 2: Clinical spectrum of IAH/ACS.

Organ system commonly involved
Major clinical manifestations medical treatment is not effective or in the presence of refractory ACS. Although invasive, decompressive laparotomy is effective in decreasing IAP and improving organ function [4,5].

CONCLUSION
IAH and ACS are an important cause of AKI in critically ill patients. It is crucial for the clinicians to be aware of the existence of IAH, its pathologic implications, and available methods for IAP measurement. If medical management fails and the patient progresses to ACS, an immediate surgical decompression is warranted.