Successful bilevel positive airway pressure therapy in a patient with amyotrophic lateral sclerosis after emergency laparotomy: A case report.

Patients with amyotrophic lateral sclerosis (ALS) present an increased risk of postoperative respiratory failure after general anesthesia. We report the case of a 71-year-old man with ALS who underwent emergency laparotomy for small bowel strangulation. After surgery, he remained intubated and was transferred to the high care unit under mechanical ventilation, due to unstable hemodynamics requiring inotropic support. On postoperative day (POD) 3, he was extubated under stable hemodynamics and respiratory status. Immediately after extubation, bilevel positive airway pressure (bilevel PAP) was prophylactically applied to prevent postoperative respiratory failure, which may have been caused by respiratory muscle fatigue, attributed to general anesthesia and surgical stress. On POD 7, bilevel PAP was smoothly weaned off because no signs and symptoms of respiratory failure were observed. On POD 10, he achieved 30 m-walk without rest. No postoperative complications were observed up to one month after surgery. Postoperative respiratory failure may lead to death in patients with neuromuscular disorder. Non-invasive ventilation (NIV) reduces respiratory muscle fatigue, resulting in easy sputum expectoration, promoting CO2 washout, and better oxygenation. Consequently, the prophylactic use of NIV to avoid postoperative respiratory insufficiency should be considered in patients with ALS after emergency operation under general anesthesia.

Interleukin-1 upregulates anaphylatoxin receptors on mononuclear cells.

BACKGROUND: The anaphylatoxins, C3a and C5a, that are generated during trauma, major surgery, or infection are potent proinflammatory mediators that increase interleukin (IL-1) cytokine synthesis. We investigated the effects of IL-1 on anaphylatoxin receptor expression in monocytes. METHODS: A human monocytic cell line, MONO-MAC-6, was used. C3a and C5a binding sites were assayed by competitive binding. Levels of messenger RNA for the C3a and C5a receptors were analyzed by reverse transcriptase-polymerase chain reaction. Changes of free cytosolic Ca(2+) concentration ([Ca(2+)]i) in response to C3a and C5a were measured. RESULTS: Basal MONO-MAC-6 cell sites for C3a and C5a binding were 10900 C3aR/cell (K(d)=2.0 nmol/L), 8700 C5aR/cell (K(d)=0.9 nmol/L). IL-1alpha increased sites for both C3a (61% increase; P <.01) and C5a (71% increase; P <.001). Levels of C3aR and C5aR messenger RNA also increased in IL-1alpha-stimulated cells. Receptors were coupled to functional responses, which were demonstrated by C3a- or C5a-induced [Ca(2+)]i increases. IL-1 receptor antagonist blocked the effects of IL-1alpha upregulation of anaphylatoxin receptors. CONCLUSION: These results suggest that there is an additional link between IL-1 and anaphylatoxins to amplify proinflammatory effects through monocytes and macrophages. Although C3a and C5a can increase the monocyte production of IL-1, IL-1 increases monocyte expression of receptors for these anaphylatoxins, which further amplifies inflammation.