Detection of impending abdominal compartment syndrome.

Abstract

Abdominal compartment syndrome (ACS) is the end result of sustained and uncorrected intra-abdominal hypertension (IAH). IAH is defined as a urinary bladder pressure greater than 18 mmHg (25 cm H2O) [1]. Various clinical conditions are associated with this syndrome, including massive intra-abdominal or retroperitoneal haemorrhage, severe gut oedema, intestinal obstruction, ascites under pressure, burn eschars, tight abdominal closures and repair of large hernias [2, 3]. Successful therapy often requires abdominal decompression followed by sequential or delayed closure of the abdomen after appropriate resuscitation [2, 4]. We report a case in which impending ACS was averted by a timely detection of changes in various parameters and modifying the surgical technique. A 70-year old man with a long-standing, massive left inguino-scrotal hernia was scheduled for a hernia repair with mesh. He had been treated for hypertension, and had had one episode of chest pain 20 years previously. Following induction and tracheal intubation, anaesthesia was maintained with halothane in oxygen. Nitrous oxide was avoided to prevent an increase in gas volume of trapped bowel within the hernia. Following induction, a urinary catheter was inserted and the intravesical pressure was measured by filling the bladder with 50 ml of sterile water and transducing an 18-gauge cannula inserted through the culture aspiration port. The baseline intravesical pressure was 4 mmHg. A routine mesh repair was performed after reducing the hernia with primary opposition and closure. At skin closure there was a fall in systolic blood pressure from 130 to 90 mmHg and rises in peak airway pressure to 35–40 cm H2O and intravesical pressure to 18–22 mmHg. The peripheral blood oxygen saturation fell to 90%. Other complications such as tension pneumothorax, cardiac temponade and severe bronchospasm were excluded and a fluid challenge given. There was no improvement in the patient's condition and the surgical repair was modified to a loose mesh hernioplasty. Lung ventilation was continued for 4 h postoperatively and the blood pressure, peak airway pressure, oxygen saturation and intravesical pressure returned to baseline values. The increase in intra-abdominal pressure in ACS decreases lung compliance and raises peak airway pressure during mechanical ventilation, resulting in hypoxaemia and hypercapnia. It also decreases venous return, reducing the cardiac output and perfusion of abdominal organs causing oliguria and splanchnic ischaemia. Decreased venous return may cause raised intracranial pressure, leading to brain death [1, 5]. During surgical procedures on patients at high risk for developing ACS, the use of urinary bladder pressure measurement as guide for closure of abdomen is recommended [6]. Various methods of abdominal closure to prevent ACS have been suggested, for example, temporary closure with towel clips, use of a silastic Bagota bag, application of partial-thickness skin graft to granulating bowel and expanding the lateral abdominal wall muscles, fasciae and skin with tissue expanders [2, 3]. This case highlights the role of anaesthetist in the timely detection of changes in pertinent parameters to avert an impending ACS.