Colonic intussusception.
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Abdominal Pain↗
Biomedical subjects
Michael C Ott
Publications and source records attributed to Michael C Ott.
Inhalation of carbon monoxide prevents liver injury and inflammation following hind limb ischemia/reperfusion.
The induction of heme oxygenase (HO), the rate limiting enzyme in the conversion of heme into carbon monoxide (CO) and biliverdin, limits liver injury following remote trauma such as hind limb ischemia/reperfusion (I/R). Using intravital video microscopy, we tested the hypothesis that inhaled CO (250 ppm) would mimic HO-derived liver protection. Hind limb I/R significantly decreased sinusoidal diameter and volumetric flow, increased leukocyte accumulation within sinusoids, increased leukocyte rolling and adhesion within postsinusoidal venules, and significantly increased hepatocyte injury compared with naive animals. Inhalation of CO alone did not alter any microcirculatory or inflammatory parameters. Inhalation of CO following I/R restored volumetric flow, decreased stationary leukocytes within sinusoids, decreased leukocyte rolling and adhesion within postsinusoidal venules, and significantly reduced hepatocellular injury following hind limb I/R. HO inhibition did not alter microcirculatory parameters in naive mice, but did increase inflammation, as well as increase hepatocyte injury following hind limb I/R. Inhalation of CO during HO inhibition significantly reduced such microcirculatory deficits, hepatic inflammation, and injury in response to hind limb I/R. In conclusion, these results suggest that HO-derived hepatic protection is mediated by CO, and inhalation of low concentrations of CO may represent a novel therapeutic approach to prevent remote organ injury during systemic inflammatory response syndrome, or SIRS.
Administration, Inhalation↗
Management of blunt thoracic aortic injuries: endovascular stents versus open repair.
BACKGROUND: Endovascular stent graft (EV) technology has been successfully adapted to the repair of blunt traumatic aortic injuries. The purpose of this study was to compare the outcomes of patients treated with EV repair and open repair after blunt thoracic aortic trauma. METHODS: A review of a tertiary trauma center's prospective trauma registry identified all patients who suffered a blunt traumatic thoracic aortic injury over an 11-year period (1991-2002). Operative interventions and outcomes were then compared. RESULTS: Over an 11-year period, 18 patients underwent repair of a blunt thoracic aortic injury (EV, 6; open, 12). There were no significant differences in demographics, injury, or crash statistics between groups. The open group had a 17% early mortality rate (n = 2), a paraplegia rate of 16% (n = 2), and an 8.3% incidence of recurrent laryngeal nerve injury (n = 1). This is in contrast to a 0% rate of mortality, paraplegia, and recurrent laryngeal nerve injury in the EV group. A definite trend toward decreased morbidity, mortality, intensive care unit length of stay, and number of ventilator-dependent days was seen with EV repair. CONCLUSION: We observed a clear trend toward improved outcomes after EV repair of thoracic aortic injuries compared with standard open repair. EV repair is emerging as the preferred method of repairing blunt thoracic aortic injuries in trauma patients with multiple injuries.
Adult↗
Pulmonary toxicity in patients receiving low-dose amiodarone.
RATIONALE: Although there have been reports of pulmonary toxicity with low-dose amiodarone, it is generally believed that low-dose therapy is safe. METHODS: The clinical data for eight patients identified from a retrospective chart review are presented. RESULTS: All of the patients were receiving amiodarone, 200 mg/d, for an average of 2 years. The average age was 77 years (range, 65 to 89 years). Seven of the eight patients were male. Seven of the eight patients presented with dyspnea on exertion, and three of the eight patients presented with cough. All of the patients had a clinical diagnosis of amiodarone-induced pulmonary toxicity. Open-lung biopsies were obtained on two patients that were consistent with amiodarone-induced pulmonary toxicity. None of the patients were in congestive heart failure. Treatment involved cessation of amiodarone. In addition, three patients received corticosteroids. Five of the patients improved symptomatically with this conservative approach, and four patients improved radiographically. One patient died with progressive respiratory insufficiency (presumably from amiodarone pulmonary toxicity). One patient was unavailable for follow-up. CONCLUSION: Amiodarone-induced pulmonary toxicity can occur at a daily dose of 200 mg. Clinicians must remain alert to this possibility even with this low-dose therapy.
Aged↗
Pulmonary microcrystalline cellulose deposition from intravenous injection of oral medication in a patient receiving parenteral nutrition.
A 50-year-old man who had been dependent on home parenteral nutrition (HPN) for 24 years presented with shortness of breath. A computed tomography scan of the lungs revealed a diffuse micronodular parenchymal infiltrate. On bronchoscopy, a crystalloid material was identified. This organic material was determined to be consistent with codeine. The patient had been injecting codeine into his intravenous catheter.
Analgesics, Opioid↗