Clostridium septicum sepsis and neutropenic enterocolitis in a patient treated with intensive chemotherapy for acute myeloid leukemia

Pouwels, M.J.M.; Donnelly, J. Peter; Raemaekers, John; Verweij, Paul E.; Pauw, B.E. de

doi:10.1007/s002770050273

Cited by 16 publications

(8 citation statements)

References 12 publications

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“…Secondly, prolonged exposure to antibiotics results in a marked shift in the gut microflora towards toxin producing bacteria 55 such as Staphylococcus aureus, Pseudomonas aeruginosa and Clostridium septicum. 56,57 In fact, Clostridium species are now more likely to predominate for reasons which are poorly understood so that bacteraemia due to C. tertium or C. septicum is almost pathognomonic for typhlitis. Antimicrobial pressure also predisposes to intestinal overgrowth by Clostridium difficile in transplant recipients.…”

Section: Neutropenic Typhlitis a Paradigm For Gut Mbimentioning

confidence: 99%

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Blijlevens¹,

Donnelly²,

Pauw³

2000

Bone Marrow Transplant

235

153

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Summary:Mucositis is an inevitable side-effect of the conditioning regimens used for haematopoietic stem cell transplantation. The condition is better referred to as mucosal barrier injury (MBI) since it is primarily the result of toxicity and is a complex and dynamic pathobiological process manifested not only in the mouth but also throughout the entire digestive tract. A model has been proposed for oral MBI and consists of four phases, namely inflammatory, epithelial, ulcerative and healing phases. A variety of factors are involved in causing and modulating MBI including the nature of the conditioning regimen, the elaboration of pro-inflammatory and other cytokines, translocation of the resident microflora and their products, for example, endotoxins across the mucosal barrier, exposure to antimicrobial agents and whether or not the haematopoietic stem cell graft is from a donor. Neutropenic typhlitis is the most severe gastrointestinal manifestation of MBI, but it also influences the occurrence of other major transplant-related complications including acute GVHD, veno-occlusive disease and systemic infections. The pathobiology, clinical counterparts and the means of measuring MBI are discussed together with potential approaches for prevention, amelioration and, perhaps, even cure. Bone Marrow Transplantation (2000) 25, 1269-1278. Keywords: mucositis; mucosal barrier injury; diagnosis; risk factors; treatment Mucositis is an inevitable side-effect of the intensive conditioning therapy used for haematopoietic stem cell transplantation 1 and usually refers to the mucosal ulceration of mouth and throat. However, it is generally accepted that oral mucositis is in reality the most obvious manifestation of damage or injury elsewhere particularly that of the gut. Hence, mucosal barrier injury (MBI) may be a more appropriate term for this biological process. There exists no clear definition of MBI which is defined by a constellation of signs and symptoms that vary in their clinical expression. Oral MBI is reported to affect 60% to 100% of transplant recipients 2,3 and is characterised by pain, oedema, erythema, lesions, pseudomembrane formation, excessive mucous production, reduced saliva and bleeding, all of which reduce the patient's ability to eat and drink. In contrast, there are no reliable data on the incidence of gut MBI although intestinal symptoms affect almost every transplant recipient to some extent and include nausea, vomiting, abdominal cramping and watery diarrhoea occasionally accompanied by macroscopic blood loss. The exact course and severity of bowel symptoms of MBI are also difficult to ascertain because many patients are in such pain due to oral MBI that they only gain relief from narcotic analgesia which induces constipation as a result of reduced gut motility. There are also a number of scoring systems for oral MBI 4 although none is universally accepted and all lack standardisation. As yet, there is no system for registering gut MBI although there are published definitions for grading toxicity o...

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Section: Neutropenic Typhlitis a Paradigm For Gut Mbimentioning

confidence: 99%

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Blijlevens¹,

Donnelly²,

Pauw³

2000

Bone Marrow Transplant

235

153

View full text Add to dashboard Cite

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“…1,4,7 In recent years survival has improved with aggressive medical management and broad spectrum antibiotics. [23][24][25] Recombinant hematopoeitic growth factors have been used to shorten the period of neutropenia which is essential in eradicating infection and restoring bowel mucosal integrity.…”

Section: Discussionmentioning

confidence: 99%

Typhlitis complicating autologous blood stem cell transplantation for breast cancer

Boggio

Pooley

Roth

et al. 2000

Bone Marrow Transplant

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Summary:Three cases of typhlitis occurring during autologous blood stem cell transplantation (ABSCT) for metastatic breast cancer are described. Typhlitis is a rare complication of neutropenia and has uncommonly been reported in the autologous transplant setting. Although it has been most commonly described in children with leukemia, typhlitis has increasingly been reported in adult leukemias and in association with neutropenia secondary to chemotherapy for a number of solid tumors. Only five previous cases of typhlitis in the setting of ABSCT have been described. Whereas diarrhea and fever are common toxicities associated with high-dose chemotherapy, it is likely that many cases of typhlitis go unrecognized. Bone Marrow Transplantation (2000) 25, 321-326. Keywords: typhlitis; neutropenic enterocolitis; breast cancer; stem cell transplantation Typhlitis was initially described in 1970 as a life-threatening condition occurring in children with leukemia.1 This condition is characterized by a necrotizing colitis usually localized to the cecum. Although most reports involve children with leukemia or aplastic anemia, 2-7 in recent years cases involving adults with hematologic malignancies have been described. [8][9][10][11][12][13] In addition, reports of typhlitis in patients with solid tumors treated with myelosuppressive doses of chemotherapy have appeared in the literature. [14][15][16] To date there have been five reported cases of typhlitis occurring in patients undergoing high-dose chemotherapy with autologous blood stem cell transplant (ABSCT), three from Hadassah University Hospital [17][18][19] and two from the Beth Israel-Deaconess Medical Center. 20 We describe our experiences with three additional cases of typhlitis complicating ABSCT for metastatic breast cancer. The frequency of typhlitis is likely to be underestimated given that Case 1A 33-year-old athletic white female with stage IV carcinoma of the breast was treated with three cycles of adriamycin and cyclophosphamide (AC) chemotherapy with good response. She was randomized to receive GM-CSF (Immunex, Seattle, WA, USA) 375 g/m 2 /day after cyclophosphamide for mobilization of peripheral blood progenitor cells (PBPC). Given the marginal numbers of total CD34 ϩ cells that were collected with two attempts at mobilization, a bone marrow harvest was performed to serve as a backup in the event of engraftment failure. She then received the STAMP V high-dose regimen (carboplatin, cyclophosphamide, thiotepa) with daily itraconazole and acyclovir for infection prophylaxis. After infusion of the PBPC, the patient received PIXY321 (Immunex) (a recombinant GM-CSF/IL3 fusion protein) 375 g/m 2 twice a day. On day ϩ2, she was noted to be neutropenic and febrile (38.3°C) with loose stools, and was placed on broad spectrum antibiotics. On day ϩ3, she developed abdominal pain with copious diarrhea (3 liters/day). Physical examination revealed diminished bowel sounds and a diffusely tender abdomen without rebound tenderness. A radiograph of the abdomen (Figure 1) on...

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“…A strong correlation between C. septicum bacteremia and digestive cancers is classical. Fulminant enterocolitis is a rare condition occurring in neutropenic patients [4], especially after chemotherapy inducing gastrointestinal toxicity [5].…”

Section: To the Editormentioning

confidence: 99%

A Fulminant Enterocolitis

et al. 2007

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A 54-year-old woman was referred to the intensive care unit (ICU) for shock and abdominal pain. There was a 4-month history of localized breast cancer treated by surgery and chemotherapy. Her performance status was not altered. The last course of chemotherapy (adriamycin and taxol) had been administered 10 days before. Abdominal pain, located initially in the right lower quadrant, and chills began 12 hr before ICU admission. Four hours after abdominal pain occurrence, the patient was oriented and had no circulatory or respiratory distress but presented with mild abdominal discomfort. There was neither diarrhea nor vomiting and nausea. Rectal temperature was 40 • C, and heart rate was 115 bpm. The abdomen was painful and slightly distended, without tenderness. Bowel sounds were rare and rectal examination was negative. White cell count was 200/µl. An abdominal x-ray and an ultrasound examination did not disclose any abnormalities. Blood cultures were drawn and intravenous ceftazidime (2 and 6 g/day) plus amikacine (25 mg/kg once a day) was started. Four hours before ICU admission, mild hypotension occurred, responding initially to administration of intravenous fluid. Two hours before ICU admission, confusion, recurrence of hypotension, and increased abdominal pain motivated ICU referral. The patient was obtunded but answered questions. Blood pressure was 81/36 mm Hg, and pulse rate was 126 bpm. Mottling was observed on the knees and the abdominal wall. Intravenous isotonic saline, norepinephrine, piperillin/tazobactam, 4 g/qid 6 hr, and ornidazole, 1 g/day, were administered. Abdominal computed tomography scan showed pneumoperitoneum and the presence of gas in the colonic wall and portal vein (Fig. 1). Emergent laparotomy were performed. The abdominal cavity contained serosanguinous liquid, and there was extensive digestive necrosis involving the last meter of the ileum, the right colon, and the terminal part of the left colon. Despite supportive care and large bowel resection, the patient died 36 hr after ICU admission.Histological examination showed necrosis of the wall of the ileum and right colon. Bacteriological examination showed Gram-positive rods. Culture yielded Clostridium septicum, producing lethal toxin for mouse. PCR amplification detected the gene encoding for the lethal toxin of C. septicum. C. septicum is known to be one of the agents Fig. 1 Abdominal computed tomography scan showing pneumoperitoneum and the presence of gas in the colonic wall and portal vein Springer

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Clostridium septicum sepsis and neutropenic enterocolitis in a patient treated with intensive chemotherapy for acute myeloid leukemia

Cited by 16 publications

References 12 publications

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Typhlitis complicating autologous blood stem cell transplantation for breast cancer

A Fulminant Enterocolitis

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