Successful interventional management of abdominal compartment syndrome caused by blunt liver injury with hemorrhagic diathesis

Abdominal compartment syndrome (ACS) is a life-threatening disorder, resulting when the consequent abdominal swelling or peritoneal fluid raises intraabdominal pressures (IAP) to supraphysiologic levels. ACS is defined as IAP above 20 mmHg together with a new organ failure. The recommended treatment is initially medical while surgical decompression is indicated only when medical therapy fails[1‐3]. However, it is hardly possible to achieve operation without any complications on ACS, and more difficult in the aged patients or hemorrhagic diathesis. We report that a case of primary ACS, caused by blunt liver injury under the oral anticoagulation therapy, was successfully treated with interventional techniques. Additionally, we reviewed the previous reports of ACS treated with transcatheter arterial embolization (TAE). It may be considered as an alternative to surgical intervention for an ACS.

A 71-year-old man was admitted to emergency unit for abdominal trauma due to traffic accident. His consciousness was unclear and shock index was 1.8 (blood pressure, 70/39 mm Hg; pulse 125 beats/min). The electrocardiogram showed atrial fibrillation. His chest radiography showed markedly elevated diaphragms. The abdomen was distended, there were decreased sounds, and it was diffusely tender. Laboratory findings were as follows: hemoglobin 6.7 g/dL; international normalized ratio (INR) 3.2; because he was on the oral anticoagulation therapy for aterial fibrillation with warfarin and asprin. Arterial blood gas analysis revealed acute respiratory failure with a pH value of 7.344, PaO2 of 61.5 torr, PaCO2 of 49.0 torr under 5 L/min of oxygen supplementation by face mask. His urinary bladder pressure equal to intraabdominal pressures (IAP) was 26 cmH2O. He became hemodynamically unstable with hypotension. Transfusion of fresh frozen plasma and packed red blood cells was followed by a fluid overload and vitamin K. And he was placed on ventilator. Ultrasonography detected a hemoperitoneum and liver laceration. Enhanced computed tomography (CT) showed that contrast material extravasation was in the hepatic hilum on arterial phase (Figure 1a), and an uncovered laceration extended over segments 1, 4 and 8 of the liver with massive hemoperitoneum (Figure 1b,c). There were associated several rib fractures in the right upper quadrant and mild right hemothorax. Finally, we diagnosed as primary ACS. However, surgeons hesitated to perform laparotomy because of his hemorrhagic diathesis, therefore TAE was initially selected. The celiac artery was quickly cannulated with a 5-Fr shephered hook catheter (Clinical Supply Co. Ltd., Gifu, Japan). Digtal subtraction angiography (DSA) of the celiac artery demonstrated the perforated left hepatic arterial branch with exravasation (Figure 2a). The right hepatic artery was replaced on the superior mesenteric artery without extravasation. 2.0-Fr coaxial microcatheter (Progreat, Terumo Corp., Tokyo) was advanced nearby the bleeding point of the left hepatic arterial branch using a 0.014-in. microguidwire (Transend EX, Boston Scientific Corp., Watertown, MA, USA) (Figure 2b). Embolizaion was performed using mixtures of 0.1 mL of N-Butyl Cyanoacylate (NBCA) and 0.5 mL of Lipiodol. After TAE, DSA did not demonstrate extravasation (Figure 2c,d) and the patient became hemodynamically stable. Under ultrasonographic guidance, we inserted a 10.2-Fr pigtail drainage catheter (Cook Inc., Bloomington, IN, USA) into the right paracolic gutter using Seldinger’s technique. At the same time, IAP measured with the pigtail catheter was 30 cmH2O. About 3.2 L of intra-abdominal blood was evacuated through the pigtail catheter for the next two hours. IAP dropped to 12 cmH2O. He was discharged from the hospital without any major complications on 32 days after TAE.

ACS is a life-threatening condition resulting when the consequent abdominal swelling or peritoneal fluid raises intraabdominal pressures (IAP) to supraphysiologic levels, in massive abdominal hemorrhage, ascites, pancreatitis, ileus, as above[1‐3]. At the World Congress of ACS in 2004, the World Society of Abdominal Compartment Syndrome, ACS is defined as an IAP above 20 mmHg with evidence of organ dysfunction/failure[4, 5]. In our case, respiratory failure had been revealed. Increased IAP causes venous stasis and arterial malperfusion of all intra-and extra-abdominal organs, resulting in ischemia, hypoxia and necrosis. In parallel, respiratory, cardiocirculatory, renal, intestinal and cerebral decompensation can be seen.

Recently, ACS is divided to three types[4, 5]. Primary (postinjury) ACS, applied to our case, is a condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or interventional radiological intervention. Total body shock and subsequent reperfusion with intestinal edema and a tightly packed and closed abdomen increase abdominal pressure.

Secondary ACS refers to conditions that do not originate from the abdomino-pelvic region. The typical injury patterns are penetrating heart, major vessel, or extremity vascular trauma associated with profound shock and subsequent massive resuscitation resulting in whole-body ischemia or reperfusion injury. Recurrent ACS represents a redevelopment of ACS symptoms following resolution of an earlier episode of either prmary or secondary ACS.

Radiologically, Pickhardt et al.[1] described increased ratio of anteroposterior-to-transverse abdominal diameter over 0.8 on CT. However, Zissin[6], reported that valuable peritoneal diseases may increase this ratio without ACS, and Laffargue et al.[7] revealed that the ratio of anteroposterior-to-transverse abdominal diameter was under 0.8 in primary ACS. In our case, the ratio of anteroposterior-to-transverse diameter on CT was equal to 1:0.76 (Figure 1c).

We suppose that ACS is not always completed on that time when the CT is performed to the patient with active intraabdominal hemorrhage. Therefore, we should make a diagnosis of ACS as soon as possible; the most useful and simple examination is measurement of IAP, substituted by urinary bladder pressure.

ACS is generally required surgical decompression, whereas unaccustomed surgeons hesitate to perform laparotomy, because of perioperative high mortality rate, long staying at the intensive care unit, reoperation, and late complications including incisional hernia, gastrointestinal and pancreatic fistulas, abscess, polyneuropathy, psychic disorders, as above[1]. Additionally, our patient was on hemorrhagic diathesis with the oral anticoagulation therapy for atrial fibrillation, and attended with suspicious disseminated intravascular coagulation due to massive hemorrhage. But it wcxxas expected that the major vascular leakage was only in the hepatic arterial branch without any bowel perforation on the contrast-enhanced CT, so we performed interventional procedure. NBCA was the most appropriate embolic agent of TAE for our case with hemorrhagic diathesis, because it does not depend on the coagulation process for its therapeutic effect[8]. There are some reports of ACS treated with TAE[9]. However, combination treatment of TAE with NBCA and percutaneous catheter drainage (PCD) for ACS has not been reported (Table 1). We suggest that initial hemostasis by transcatheter arterial embolization is a safe, effective treatment method for abdominal compartment syndrome with active arterial bleeding in a patient undergoing anticoagulation.

The decompression is simultaneously essential to hemostasis for the treatment of primary ACS. There are some randomized controlled trials for ACS (Table 2)[31]. However, there have been no randomized controlled trials about which is better, PCD or decompressive laparotomy. PCD is easy and minimal invasive procedure compared with surgical decompression, and allows us to measure IAP. But it is not appropriate to perform catheter drainage for the patients with widespread peritonitis or bowel injury. When a heavy clot burden cannot be drained satisfactorily via catheter, we should transfer to decompressive laparotomy.

In summary, we described the case of primary ACS caused by blunt liver injury. Interventional procedures may improve primary ACS if the patient has hemorrhagic diathesis or coagulopathy discouraging surgeon from laparotomy, limited vascular injury, and no obvious peritonitis.

Written informed consent was obtained from the patient for publication of this Case report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.