Successful management of severe unilateral re-expansion pulmonary edema after mitral valve repair with mini-thoracotomy using extracorporeal membrane oxygenation.

A 60-year-old man received mitral valve repair via right mini-thoracotomy, which was followed by unilateral re-expansion pulmonary edema on the right side and severe hemoptysis just after the surgery. Despite differential lung ventilation with unilateral high positive end expiratory pressure was initiated for the affected right lung, respiratory function did not improved and hemodynamics was collapsed in the next day. Veno-venous extracorporeal membrane oxygenation was initiated by cannulation of the right jugular and the left femoral vein. After pulmonary function recovered gradually, veno-venous extracorporeal membrane oxygenation was terminated on the fifth postoperative day. He was discharged in ambulatory condition on postoperative day 52.

[Airway management in a patient with cavernous hemangioma of the hypopharynx and larynx].

A 48-year-old woman was diagnosed with cavernous hemangioma of hypopharynx and larynx, which extended to the trachea and mediastinum. She was scheduled for tracheostomy and open surgical excision of hypopharynx hemangioma under general anesthesia. On induction of anesthesia, we planned awake fiberoptic intubation according to the difficult airway algorithm of the American Society of Anesthesiologists. Under continuous infusion of remifentanil at 0.1-0.2 microg x kg(-1) x min(-1), the patient became sedated while spontaneously breathing, and her pain and laryngeal reflexes were reduced. Although tracheal intubation was successfully accomplished without injuring the hypopharynx hemangioma, tracheostomy was difficult because of bleeding from the surgical site. After 3 hr of surgery with 1880 g of blood loss, the surgeons quitted tracheostomy and the patient was transferred to the intensive care unit. Her airway was managed with endotracheal tube for 7 days, and open surgical excision of hypopharynx hemangioma was performed on day 7. The patient was successfully extubated on day 9 with the support of non-invansive positive pressure ventilation. Awake fiberoptic intubation under remifentanil infusion is safe and useful approach for patients with airway hemangioma.

Epidural analgesia prevents endotoxin-induced gut mucosal injury in rabbits.

In the present study, we evaluated the effect of epidural analgesia on the alterations of gut barrier function elicited by endotoxin in rabbits. After the placement of an epidural catheter, 28 male rabbits were randomized into either 0.5% lidocaine (group E) or saline (group C) group. The solutions (0.4 mL/kg) were epidurally injected, followed by continuous infusion (0.1 mL . kg(-1) . h(-1)) throughout the study period. Under a continuous infusion of lipopolysaccharide (15 microg . kg(-1) . h(-1)), mean arterial blood pressure, intramucosal pH, and plasma thrombomodulin concentrations were measured. At 4 h, mean arterial blood pressure was lower (P < 0.05), intramucosal pH was higher (P < 0.01), and the progression of hemodilution more profound (P < 0.05) in group E versus group C, whereas plasma thrombomodulin levels were increased to a similar extent between the groups. With less wet-to-dry weight ratio of ileum, histopathological injury scores of gut mucosa were significantly less in group E versus group C (P < 0.01). In a separate series of experiments (n = 10 each group), mucosal permeability in group E was significantly less compared with group C (P < 0.05). Collectively, these studies showed that despite a significant decrease of perfusion pressure and arterial oxygen content, epidural analgesia minimized endotoxin-induced functional and structural injury of gut mucosa possibly through endothelium-independent mechanisms.

Olprinone, a phosphodiesterase III inhibitor, reduces gut mucosal injury and portal endotoxin level during acute hypoxia in rabbits.

BACKGROUND: Preservation of gut integrity has become a therapeutic goal to obviate bacterial translocation in the critically ill. The authors examined whether olprinone, a phosphodiesterase III inhibitor, protected functional and structural integrity of gut mucosa against acute progressive hypoxia. METHODS: Thirty-two animals were randomly allocated to a control group (n = 12), a low-dose group (0.2 microg x kg-1 x min-1 olprinone; n = 10), or a high-dose group (0.6 microg x kg-1 x min-1 olprinone; n = 10) after preparatory surgery. Ascending aortic and portal blood flow, intramural pH of the ileum, and portal endotoxin levels were measured at normoxia and through three stages of progressive hypoxia (fraction of inspired oxygen = 0.17, 0.13, and 0.10). RESULTS: At normoxia, ascending aortic flow in the high-dose group was approximately 20% higher than in the control and low-dose groups. During progressive hypoxia, both ascending aortic and portal flow in the control group were depressed, whereas olprinone infusion attenuated such alterations and redistributed blood to the splanchnic area in a dose-dependent manner. On the contrary, the reduction of intramural pH of the ileum and the elevation of portal endotoxin levels observed in the control group were significantly minimized in both the low- and high-dose groups to a similar extent during acute hypoxia. Histopathologic alterations of gut mucosa observed in the control group were minimized by olprinone infusion dose-independently, accompanied by reduction of mortality rate of the animals. CONCLUSIONS: Olprinone slows progression of intestinal mucosal acidosis and gut barrier dysfunction, concurrently with preservation of microscopic structures, through both flow-dependent and -independent mechanisms under acute hypoxia. Such properties of olprinone may serve to protect the host under insult.