Obstructive sleep apnoea and perioperative complications in bariatric patients.

BACKGROUND: The objective of this study was to determine the relationship between perioperative complications and the severity of obstructive sleep apnoea (OSA) in patients undergoing bariatric surgery who had undergone preoperative polysomnography (PSG). METHODS: The records of 797 patients, age >18 yr, who underwent bariatric operations (442 open and 355 laparoscopic procedures) at Mayo Clinic and were assessed before operation by PSG, were reviewed retrospectively. OSA was quantified using the apnoea-hypopnoea index (AHI) as none (≤ 4), mild (5-15), moderate (16-30), and severe (≥ 31). Pulmonary, surgical, and 'other' complications within the first 30 postoperative days were analysed according to OSA severity. Logistic regression was used to assess the multivariable association of OSA, age, sex, BMI, and surgical approach with postoperative complications. RESULTS: Most patients with OSA (93%) received perioperative positive airway pressure therapy, and all patients were closely monitored after operation with pulse oximetry on either regular nursing floors or in intensive or intermediate care units. At least one postoperative complication occurred in 259 patients (33%). In a multivariable model, the overall complication rate was increased with open procedures compared with laparoscopic. In addition, increased BMI and age were associated with increased likelihood of pulmonary and other complications. Complication rates were not associated with OSA severity. CONCLUSIONS: In obese patients evaluated before operation by PSG before bariatric surgery and managed accordingly, the severity of OSA, as assessed by the AHI, was not associated with the rate of perioperative complications. These results cannot determine whether unrecognized and untreated OSA increases risk.

Clinical characteristics of fatal pulmonary embolism in a referral hospital.

OBJECTIVE: To determine the clinical characteristics of hospitalized patients who died of pulmonary embolism, confirmed by evaluative autopsy. DESIGN: We retrospectively analyzed a series of autopsy cases of pulmonary embolism at a tertiary-care center for the period Jan. 1, 1985, through Dec. 31, 1989. MATERIAL AND METHODS: The medical and autopsy records of all hospitalized patients with autopsy-proven fatal pulmonary embolism were reviewed. Cases of tumor emboli, fat emboli, and contributory-only thromboembolic disease were excluded from the study. Specific symptoms and signs, diagnostic studies, and prophylactic measures were noted. RESULTS: Among 2,427 autopsies performed during the 5-year study period, death in 92 (3.8%) was clinically and pathologically judged to be caused by pulmonary embolism. No risk factors were noted in only 11 patients (12%). Prophylaxis against thromboembolism was used in 46%. Classic symptoms were often absent: dyspnea was present in only 59%, chest pain in only 17%, and hemoptysis in 3%. Pulmonary embolism was considered in 49% of the 92 patients and was correctly assigned as the cause of death on the death certificate or in the medical records in 32%. Testing for venous thromboembolic disease was performed in 22%. Comorbidity was present in most patients: 54% had guarded or poor prognoses independent of pulmonary embolism. CONCLUSION: The usual signs and symptoms associated with pulmonary embolism did not adequately identify most of our patients who died of pulmonary embolism. The reasons included the absence of these signs and symptoms, inability to communicate (for example, sedated or comatose patient), sudden death from acute massive pulmonary embolism, and presence of comorbid factors.

Cavitary pulmonary infarct in immunocompromised hosts.

Pulmonary disease in immunocompromised patients is common, but cavitary lung disease is less common and is usually associated with a fungal or mycobacterial infection. Pulmonary embolism is a noninfectious cause of a cavitary pulmonary process. Pulmonary embolism causes infarction in fewer than 15% of cases, and only about 5% of infarctions cavitate. Herein we describe two cases of cavitary infarcts in immunocompromised patients and review the clinical aspects of pulmonary infarcts and cavitation. Cavitary pulmonary infarction has been reported only rarely in immunocompromised patients. It is a dangerous but treatable pulmonary disease that must be considered in the differential diagnosis of immuno-compromised patients with lung disease.

Candida albicans stimulates arachidonic acid liberation from alveolar macrophages through alpha-mannan and beta-glucan cell wall components.

Candida albicans is an increasingly important fungal pathogen. Alveolar macrophages respond to fungal components such as zymosan by releasing arachidonic acid (AA) and AA metabolites. However, few studies hypothesized that macrophages respond to C. albicans by releasing AA and generating AA metabolites as a consequence of interaction of mannose and beta-glucan receptors with fungal cell wall components. [14C]AA-labeled rabbit alveolar macrophages released AA following stimulation with either live or heat-killed C. albicans. High-pressure liquid chromatography analysis revealed that 55% of the AA released was metabolized via cyclooxygenase and lipoxygenase pathways. The metabolites consisted of prostaglandin E2, prostaglandin F2 alpha, 6-ketoprostaglandin F1 alpha, thromboxane B2, and leukotrienes B4 and D4. We further examined the roles of alpha-mannan and beta-glucan components of C. albicans in mediating these alterations of eicosanoid metabolism. Prior work in our laboratory has shown that soluble alpha-mannan and beta-glucan inhibit macrophage mannose and beta-glucan receptors, respectively. Incubation of alveolar macrophages with soluble alpha-mannan derived from C. albicans (1 mg/ml) resulted in 49.8% +/- 2.6% inhibition of macrophage AA release during stimulation with intact C. albicans (P = 0.0001 versus control). Macrophage AA release in response to C. albicans was also inhibited to a significant but lesser degree by soluble beta-glucan (36.2% +/- 1.3%; P = 0.008 versus control). These results indicate that C. albicans stimulates macrophage AA metabolism and that these effects are partly mediated by alpha-mannan and beta-glucan constituents of the fungus.

Thymoma.

Thymomas and thymic carcinomas are thymic epithelial tumors that constitute approximately 15% of all mediastinal masses. From 28 to 66% of thymomas cause chest symptoms as the initial manifestation; the rest are discovered on routine chest roentgenograms or during investigations prompted by the presence of a paraneoplastic syndrome. Forty percent of patients with thymoma have one or more paraneoplastic syndromes, including myasthenia gravis, pure red cell aplasia, and hypogammaglobulinemia. Extrathymic malignant lesions develop in up to 20% of patients. Traditional histologic classifications have not accurately predicted tumor behavior; a recently developed classification based on cellular differentiation toward thymic medullary or cortical epithelium may correlate better with prognosis. Nevertheless, the prognosis is best predicted by stage of the tumor determined intraoperatively and is poorer in patients with incomplete resection than in those with complete resection of the thymoma. In addition to surgical intervention, irradiation and chemotherapy have important roles in the management of thymomas, particularly in advanced stages. In this article, the clinical manifestations, diagnosis, pathologic features, staging, and treatment of thymomas are reviewed, and the prognosis of affected patients is discussed.

Pneumocystis carinii induces the release of arachidonic acid and its metabolites from alveolar macrophages.

Pneumocystis carinii is an opportunistic organism that causes severe lung injury in immunocompromised hosts. Macrophage responses to P. carinii are poorly defined. Arachidonic acid (AA) and its metabolites are potent mediators of inflammation and have been implicated in host response to microorganisms. We therefore examined the production of eicosanoids from rat and rabbit alveolar macrophages stimulated with purified P. carinii. [14C]AA-labeled rabbit macrophages released 8.50 +/- 1.33% of the incorporated [14C]AA after 90 min in response to P. carinii (P = 0.0001 compared with unstimulated controls). In contrast, a similar number of rat alveolar macrophages exhibited a smaller but significant response to P. carinii, releasing 3.84 +/- 1.54% of their [14C]AA after 90 min (P = 0.001 compared with control). We further determined that P. carinii stimulated substantial production of prostaglandin E2 and concurrently a small amount of leukotriene B4 release from alveolar macrophages. To further investigate whether serum opsonization of P. carinii enhances these alterations in AA metabolism, we assessed the effect of P. carinii immune serum on P. carinii-induced AA release. P. carinii opsonized with this antiserum caused significantly greater AA release from rat alveolar macrophages than either unopsonized P. carinii or organisms opsonized with nonimmune serum. Previous studies suggest that P. carinii interacts with macrophage beta-glucan and mannose receptors. However, incubation of macrophages with P. carinii in the presence of either soluble beta-glucan or alpha-mannan failed to alter the release of AA from macrophages in response to P. carinii. Macrophage release of eicosanoids represents a potentially important host inflammatory response to P. carinii infection.

Analysis of microvascular water and solute exchanges in the renal medulla.

A theoretical model has been developed to simulate solute and water transport in the medullary microcirculation of the normal hydropenic rat. The model is formulated in terms of a countercurrent vascular unit consisting of one descending (DVR) and several ascending vasa recta (AVR) extending from the corticomedullary junction to the tip of the papilla. Steady-state mass balances relate gradients in NaCl, urea, and plasma protein concentrations and variations in the flow rates of plasma and red blood cells to permeability properties of the vasa recta and erythrocytes. In contrast to previous models, transmural volume fluxes are assumed to be present in both DVR and AVR. Available micropuncture measurements suggesting net volume removal from DVR within the inner medulla are found to be consistent with NaCl reflection coefficients in DVR between 0.10 and 0.80. The hydraulic permeability in the DVR is estimated to be greater than 0.18 X 10(-6) cm X s-1 X mmHg-1. Based on currently available data, reliable bounds cannot yet be placed on the hydraulic permeability of the AVR. The vascular unit is predicted to accomplish substantial net removal of NaCl and water from the inner medullary interstitium but relatively little removal of urea. Red cells leaving the inner medulla in the AVR are found to be slightly dehydrated. It is calculated that at a given blood flow rate, the lower the initial medullary hematocrit, the more effective the vascular unit is at removing water. Several unresolved issues are discussed, including the role of the capillary plexus that joins DVR with AVR. To the extent that the volume uptake observed in the exposed papilla in structures beyond the DVR occurs in the capillary plexus and not in the AVR, estimated values of AVR hydraulic permeability are reduced, as is predicted overall volume uptake by the vascular unit in the inner medulla.