Pneumatosis intestinalis and hepatic portal venous gas caused by mesenteric ischemia in an aged person

Received: January 7, 2000 / Accepted: June 23, 2000     

Pneumatosis intestinalis and hepatic portal venous gas

We report two cases of pneumatosis intestinalis and hepatic portal venous gas. The first case was in a 67-year-old woman who complained of strong right lower abdominal pain and high fever on the twelfth day after pancreatoduodenectomy (PD) with portal vein (PV) resection. Abdominal X-ray and computed tomography showed hepatic portal venous gas and pneumatosis intestinalis. The emergency laparotomy performed disclosed extensive necrosis of the bowel from the jejunum to the ascending colon. All necrotic parts of the bowel were resected and a jejunostomy was performed. The residual intact small intestine was 30 cm in length. Her postoperative course was stable. This is a rare complication after PD and cannot be cured by any other treatment but surgery. The second case was in a 45-year-old woman with the chief complaint of abdominal pain and constipation. She had a past history of chronic toluene inhalation. Abdominal X-ray and computed tomography also showed hepatic portal venous gas and pneumatosis intestinalis, as well as free air, but no physical examination or laboratory test results supported a diagnosis of bowel necrosis. Hyperbaric oxygen (HBO) therapy effectively controlled the symptoms and signs.     

Pneumatosis Cystoides Intestinalis Following Steriod Pulse Therapy in a Patient with Polyarteritis Nodosa

We present a case of a 67‐year‐old female with polyarteritis nodosa, complicated by pneumatosis cystoides intestinalis. The definite diagnosis of polyarteritis nodosa was obtained by histological findings on a biopsy specimen from her sural nerve. Following steroid pulse therapy, she developed gastrointestinal symptoms such as nausea, abdominal fullness and watery diarrhea. Abdominal X‐ray and computed tomography showed an abundance of gas contrast within the large intestinal wall. Colonoscopy revealed submucosal tumor‐like multiple elevated lesions from the sigmoid to transverse colon. These findings indicated pneumatosis cystoides intestinalis and the patient was accordingly treated with a high concentration of oxygen via a nasal catheter. One week later, her symptoms and the gas in the bowel wall completely disappeared. Pneumatosis cystoides intestinalis may be one of the complications of steroid pulse therapy.     

Pneumatosis Intestinalis Developed in a Patient with Giant Cell Arteritis While in a Clinically Sustained Remission Phase

We herein report a patient with giant cell arteritis (GCA) who developed pneumatosis intestinalis (PI) while she was in a clinically sustained remission phase. A 79-year-old woman with GCA involving the thoracic aorta and its first branches to the posterior tibial arteries had been treated with high-dose prednisolone. Nine weeks after initiating treatment and while in clinically sustained remission with a normal CRP level, PI and pneumoperitoneum were incidentally found during scheduled positron emission tomography-computed tomography, which also revealed slight residual inflammation of GCA. This is a very rare case of PI complicated by GCA, and we discuss the possible relationships.     

Pneumatosis Intestinalis in Lung Cancer Induced Twice by Different Drugs: Bevacizumab and Pemetrexed

A 72-year-old man diagnosed with stage 4 lung adenocarcinoma developed asymptomatic pneumatosis intestinalis while undergoing treatment with first-line chemotherapy, which included carboplatin, paclitaxel, and bevacizumab (BEV). He was treated conservatively. The pneumatosis recurred while the patient was undergoing treatment with the third-line chemotherapy, which included pemetrexed (PEM). His condition resolved after 4 weeks of supportive therapy. To our knowledge, this is the first case in which pneumatosis intestinalis was induced twice by two drugs in a patient with lung cancer. BEV and PEM are often administered to patients with lung cancer; thus, it should be noted that pneumatosis intestinalis may occur as an adverse event in patients treated with these drugs.     

Pneumatosis Cystoides Intestinalis in a Patient with Polymyositis

A 29-year-old Japanese woman with polymyositis (PM) developed pneumatosis cystoides intestinalis (PCI). The patient experienced a gradual onset of mild epigastric abdominal pain and abdominal distension. Radiographs revealed pneumatosis intestinalis involving the small bowel, and colonoscopy revealed submucosal cysts. Treatment with antibiotics and high-flow oxygen resulted in remission. This is an extremely rare case of PCI in a patient with PM. Received: 27 December 1999 / Accepted: 29 May 2000     

Severe Acute Asthma with Bowel Infarction and Pneumatosis Intestinalis in a Young Adult

A young patient presented with a small bowel infarction with pneumatosis intestinalis in the early course of life-threatening severe acute asthma. Low cardiac output with severe congestive right heart failure combined with the use of high doses of epinephrine to reverse the near-fatal bronchospasm probably contributed to this previously unreported complication. The presence of gas collections in the submucosal space was possibly the consequence of diffuse small bowel mucosal disruption. Early recognition of this unusual complication is of major importance to ensure appropriate therapeutic management.     

CASE REPORT: Lactulose-Induced Pneumatosis Intestinalis and Pneumoperitoneum

A case of PI in a 57-year-old patient with colonic inertia treated with lactulose for PSE secondary to cirrhosis is described. The colonic inertia led to longer transit time. Retained lactulose and a build-up of carbon dioxide and hydrogen gas occurred in the setting of altered bacterial flora deficient in hydrogen metabolism. The increased gas pressure caused extravasation of air into the intestine, causing PI with pneumoperitoneum. They both resolved with discontinuation of lactulose.     

Pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis

We report a 58-year-old woman with pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis. She was receiving treatment for liver cirrhosis and hepatic failure when sudden severe right upper abdominal pain and fever developed. Abdominal radiograph disclosed pneumatosis intestinalis, involving the ascending colon, and small collections of free air along the right hemidiaphragm. The pneumatosis intestinalis appeared in both cystic and linear form. Autopsy revealed necrosis and multiple gas-filled mural cysts in the ascending colon. To our knowledge, this is the first case to be reported of pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis.     

Recurrent hepatic portal venous gas in a patient with hemodialysis- dependent chronic renal failure

We report a case of recurrent hepatic portal venous gas (HPVG). A 51-year-old woman who had been undergoing hemodialysis for 19 years was admitted with abdominal pain. Computed tomography (CT) scans revealed the presence of HPVG, and bowel necrosis was confirmed at operation. After 1 year, the abdominal pain recurred. CT scans on the second admission also revealed HPVG; however, an exploratory laparotomy was negative. Recurring presentation of HPVG in the same patient has not been described previously.     

PaO2-guided Low-dose Oxygen Therapy for Pneumatosis Cystoides Intestinalis to Prevent Acute Exacerbation of Interstitial Pneumonia

We herein report the first case of low-dose oxygen therapy for pneumatosis cystoides intestinalis (PCI) using PaO₂ as a therapeutic index to prevent acute exacerbation of interstitial pneumonia. An 86-year-old man was admitted to our hospital with abdominal distension. PCI was diagnosed by abdominal computed tomography. Low-dose oxygen therapy was started to avoid acute exacerbation of interstitial pneumonia. The oxygen dose was adjusted so that the PaO₂ value was approximately 100 mmHg. After seven days of treatment, the colon gas had disappeared, and no acute exacerbation of interstitial pneumonia was observed. A PaO₂ value around 100 mmHg is effective for PCI without inducing acute exacerbation of interstitial pneumonia.     

Pneumatosis cystoides intestinalis in intestinal pseudoobstruction

Summary A 66-year-old man with chronic idiopathic intestinal pseudoobstruction was admitted for pneumatosis cystoides intestinalis, complicated by pneumoperitoneum. The latter conditions resolved after treatment with metronidazole. There was no favorable effect of the prokinetic agents cisapride and erythromycin. To the authors' knowledge, this is the first reported case of successful treatment of pneumatosis cystoides intestinalis with metronidazole in primary chronic intestinal pseudoobstruction.     

Pathological study of idiopathic portal hypertension with an emphasis on cause of death based on records of Annuals of Pathological Autopsy Cases in Japan

BACKGROUND AND AIM: Idiopathic portal hypertension (IPH) is thought to be benign if bleeding gastroesophageal varices can be controlled or prevented. A recent autopsy of a woman with IPH who died of hemorrhagic intestinal infarction related to mesenteric thrombosis prompted the authors to examine the terminal antemortem features and causes of death of IPH. METHODS: Autopsy cases registered as IPH from 1986 to 1997 were surveyed in the records of the Annuals of Pathological Autopsy Cases in Japan, with permission from the Japanese Society of Pathology. The records of 65 of these cases were collected and examined pathologically. RESULTS: It was found that the most frequent cause of death in these cases was (i) bacterial infection (20 cases). The next three causes of death were directly or indirectly related to hepatic disease or its altered portal hemodynamics as follows: (ii) progressive hepatic failure (16 cases); (iii) massive hemorrhage from ruptured gastroesophageal varices (11 cases); and (iv) hemorrhagic intestinal infarction due to mesenteric venous thrombosis (5 cases). Although portal venous thrombosis was closely associated with (iv), (ii) and (iii) seemed not to be associated with portal venous thrombosis. In addition, intracranial hemorrhage and other heterogeneous factors were identified as the cause of death in five cases and eight cases, respectively. CONCLUSION: These results suggest that progressive hepatic failure and intestinal hemorrhagic infarction should be considered in addition to rupture of gastroesophageal varices when monitoring patients with IPH. Clinicians should be also aware of severe bacterial infection and intracranial hemorrhage as a fatal complication of IPH.     

Human hepatic infarction: histopathological and postmortem angiological studies

ABSTRACT— Twenty hepatic infarction cases selected from 5420 consecutive autopsy cases were investigated to clarify the pathogenetic aspects of this disease. Additional postmortem angiological studies of 24 normal human livers obtained at autopsy were also further performed to analyse the effects of blocking vascular structures on lesion development. Seventeen of the 20 cases (85%) were clinically associated with systemic circulatory insufficiency, especially hepato- and/or renal failure. Histopathologically, there was a significantly closer relationship between the location of infarcted regions and portal vein thrombosis than with either hepatic vein thrombosis or hepatic arterial damage. The borders between infarcted regions and surviving hepatic parenchyma were located around central veins, corresponding with the microcirculatory periphery of the portal venous system. Postmortem angiographic studies revealed that hepatic lobuli mainly consist of portal vein branches. Moreover, postmortem embolization studies of six normal livers using glass beads and bariumgelatin injection showed that physical occlusion of portal vein branches produced defects in broad areas of the hepatic parenchyma. Therefore, it is suggested that the development of hepatic infarction principally depends on disturbances of the portal venous system. In addition, systemic circulatory insufficiency, which reduces the intrahepatic blood flow, probably contributes greatly to the development of hepatic infarction.