British Journal of Radiology (2003) 76, 835-837
© 2003 British Institute of Radiology
doi: 10.1259/bjr/13712140
Hepatic portal venous gas: transient radiographic finding associated with colchicine toxicity
M Saksena, MD
M G Harisinghani, MD
J Wittenberg, MD
and
P R Mueller, MD
Department of Abdominal Imaging and Intervention, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White 270, Boston, MA 02135, USA
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Abstract
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Hepatic portal venous gas has traditionally been associated with a grave prognosis and high mortality. However, with the advent of ultrasound and CT, numerous less serious causes have been associated with this dramatic radiological finding. We present a previously unreported association with colchicine toxicity. The patient ingested a large dose of colchicine and was subsequently found to have portal venous gas on CT. The source of gas was felt to be intestinal gas penetrating through the demonstrated bowel injury. No surgical intervention was deemed necessary and the finding resolved spontaneously.
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Introduction
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Hepatic portal venous gas (HPVG) is an impressive radiological finding that has historically carried grave implications, often mandating emergency surgery. It is an established complication of bowel necrosis and has been associated with a high mortality rate [1]. However, owing to the increased resolution afforded by CT and ultrasound, HPVG has been recognized with more benign causes and spontaneous resolution [2–5]. We report a case of HPVG caused by the inadvertent ingestion of large amounts of colchicine. To our knowledge such an association has not been reported in world literature. This case report also illustrates the usefulness of CT in the detection, diagnosis and follow up of patients who are diagnosed with HPVG and are clinically stable.
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Case report
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A 57-year-old gentleman was transferred from an outside institution with a 2-day history of nausea, vomiting, diarrhoea and diffuse abdominal pain more pronounced towards the left of the midline. These symptoms were accompanied with fever of 101.8 degrees Fahrenheit. He also recounted a single syncopal episode during which he became weak and diaphoretic with subsequent collapse to the floor. A prior ECG and cardiac enzyme profile evaluated at the outside hospital were reported to be within normal limits. The patient had been fairly well till about 2 days ago when he developed an acute flare up of gout. He ingested colchicine tablets for the same and took a dose of 18 mg over the course of a single day (maximal permissible dose 4–8 mg per attack). On physical examination he appeared well developed and nourished and in no acute distress. The blood pressure, temperature and pulse rate was within normal limits. His abdomen was soft, non-tender and non-distended with good bowel sounds. The rest of the physical examination was unremarkable. Laboratory assessment revealed an increased white blood cell count 12 400 cells mm-3 (4500–11 000 cells mm-3), an elevated serum creatinine 2.3 mg dl-1 (0.6–1.5 mg dl-1) and blood urea nitrogen 40 mg dl-1 (8–25 mg dl-1), increased SGOT 80 units l-1 (10–40 units l-1) SGPT 83 units l-1 (111 units l-1) and lipase 10.8 units dl-1 (1.6–6.3 units dl-1). Bilirubin levels were mildly elevated with the total bilirubin of 1.1 mg dl-1 (0–1.0 mg dl-1) and direct bilirubin of 0.8 mg dl (0–0.4 mg dl-1). An arterial blood gas analysis showed mild hypoxia (PO2 82 on room air). Blood cultures did not show any growth. In view of the abdominal pain and elevated white blood cell count an abdominal CT scan was performed at the outside institution. Intravenous contrast medium was not given due to an elevated serum creatinine level. It revealed the presence of portal venous air predominantly in the left lobe of the liver (Figure 1a
). There was a 10 cm long segment of small bowel thickening extending from the ligament of Treitz distally (Figure 1b). There was no evidence of pneumatosis, diverticulosis or diverticulitis. A non-intravenous contrast CT scan repeated in our hospital on the same day confirmed the findings. As he was clinically stable, the patient was admitted and placed under observation. A nasogastric tube was placed for decompression. The elevated creatinine was deemed to be due to profound dehydration and normal saline was administered. Serial abdominal exams remained normal at all times with no evidence of peritoneal signs. The patient's pain resolved and he was able to ambulate the next day. An abdominal radiograph taken the next day did not show the presence of HPVG. CT scan of the abdomen and pelvis was repeated 4 days after the diagnosis was first made. It showed complete spontaneous resolution of the HPVG and the small bowel thickening seen on the initial CT scans. The patient progressively improved and was discharged after 9 days of admission. An ECG performed prior to discharge was normal.
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Figure 1. (a) Non contrast enhanced axial CT scan of the abdomen showing hepatic portal venous gas (arrow). (b) An axial CT scan a few sections lower shows multiple small bowel loops with wall thickening (arrows).
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Discussion
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Wolfe and Evans first described HPVG in infants with bowel distension, E. coli septicaemia and either ante mortem or post mortem evidence of HPVG [6]. Susman and Suturia reported the first case in an adult [7]. Subsequently, numerous clinical conditions have been associated with HPVG [8]. They can be serious pathological conditions such as necrotizing enterocolitis [6], sepsis secondary to appendicitis, diverticulitis, mesenteric infarction, intra-abdominal abscess, intestinal obstruction and peptic ulcer disease [1]. In these situations HPVG indicates a poor prognosis and often mandates emergency surgical intervention. On the other hand, HPVG is also seen in various non ischaemic conditions namely inflammatory bowel disease (IBD) [9], blunt abdominal trauma [3, 10], large gastric cancer [10], graft-versus-host reactions [10], paracolic abscess [10] and liver transplant [11]. Rare associations with seizures [2], cystic fibrosis [12] and child abuse [13] have also been reported. HPVG can be iatrogenic, occurring secondary to procedures such as barium enema especially in the presence of IBD, or if performed soon after rectal or colonic biopsy [8, 14–16], colonoscopy [17], endoscopic biliary sphincterotomy [4], hydrogen peroxide lavage [18], gastroscopic biopsy [10] and umbilical vein catheterization [8]. In these cases, HPVG has a favourable prognosis and often resolves spontaneously. In a recent series it was concluded that HPVG caused by non-ischaemic conditions was not associated with a bad clinical prognosis [10].
The primary factors favouring the development of HPVG are intestinal wall alterations, bowel distension and intra-abdominal sepsis [19]. Intestinal wall alterations and distension of bowel along with hypomotility in a diseased bowel may cause excessive gas to be absorbed into the mucosa and then into the portal system. The explanation of entry of the gas is uncertain and there exist two aetiological theories. One states, that gas under tension in a distended bowel, is forced through a wall altered by impaired circulation into the portal vein via the mesenteric veins. The other postulates that the gas is formed by submucosal or intravenous gas forming organisms (E. coli, Clostridia) [7, 8, 20]. These are essentially speculative and do not explain the occurrence of HPVG in multiple benign conditions like trauma and liver transplant.
The most likely explanation for the presence of portal vein gas in our patient is colchicine toxicity. The dose consumed was greatly in excess of the prescribed maximum dose of 4–8 mg per attack (1–1.2 mg at onset of symptoms followed by 0.5–1.2 mg every 12 h until pain is relieved or nausea, vomiting or diarrhoea occur) [21]. No other causative factors could be found. Acute colchicine toxicity is known to cause extensive mucosal damage in the gastrointestinal tract [22]. Abdominal pain, nausea and vomiting are the most common and earliest signs of colchicine toxicity [23]. This is consistent with our patient's clinical presentation. We hypothesized that severe bowel wall injury caused by high doses of colchicine may have facilitated the escape of enteric gas into the portal system. Colchicine induced mucosal damage is a likely concomitant of the thickening seen on the initial CT scan. The spontaneous resolution of both the HPVG and the small bowel thickening imply reversible damage, not requiring surgery. The main differential diagnosis on imaging is gas in the biliary tree [20, 24, 25]. Noting the distribution of the gas can often make this differentiation. Gas, in the biliary system is often central in the common hepatic duct owing to the centripetal flow of bile [7, 8]. The portal vein radicles are often seen at the periphery [1, 7]. This is attributed to the centrifugal flow of blood in the portal vein, which carries gas into the liver periphery outlining the distal fine portal venous radicles and branches [24]. The latter are much more numerous and thinner than distal branches of bile ducts. However, there are exceptions as not only does the position of gas in the portal vein vary with time, the biliary tree gas can also have both central and peripheral distribution [25]. Air in a parenchymal cavity such as an abscess usually shows coalescent collection of echoes on ultrasound and is not confused with HPVG. The distinction is fairly obvious on CT [25].
The pathological consequence of HPVG is not clear. For a long time it was thought to be an incidental radiological finding not causing any direct harm to the patient, with the high associated mortality being attributed to the underlying disease. Later, it was described that microbubbles of gas in the portal vein could cause protein denaturation in the portal sinusoids with subsequent slowing of the portal blood flow. Eventually the sinusoid could get blocked partially or completely, abolishing portal blood flow. This would decrease the venous return of the bowel, increasing transperitoneal exudation with resultant systemic absorption of bacteria and toxins leading to septicaemia [8]. However, with the increasing incidence of survival with HPVG, its actual contribution to patient mortality remains uncertain.
In conclusion, HPVG is not a disease but a manifestation of numerous causes. It may have a grave prognosis in certain clinical settings but is also associated with many less serious entities. Its association with colchicine toxicity, as seen in our patient, is previously undescribed. Although the exact pathologic mechanism behind this occurrence is not known, a plausible explanation is the escape of enteric gas into the portal system due to colchicine induced intestinal mucosal damage.
Received for publication June 28, 2002.
Revision received January 6, 2003.
Accepted for publication January 13, 2003.
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Abstract
Introduction
