Association of metabolic syndrome and surgical factors with pulmonary adverse events, and longitudinal mortality in bariatric surgery.

BACKGROUND: Postoperative pulmonary complications (PPC) in bariatric surgery have not been well studied. Additionally, many bariatric patients suffer from the metabolic syndrome (MetS), contributing to surgical risk. We examined the incidence of PPC and MetS in a large national bariatric database. Furthermore, we analysed the relationships between morbidity, mortality, PPC, MetS, and several other comorbidities and also surgical factors. METHODS: The Bariatric Outcomes Longitudinal Database (BOLD™) is a registry that includes up to 365 day outcomes. We analysed data between January 2008 and October 2010. The PPC tracked included pneumonia, atelectasis, pleural effusion, pneumothorax, adult respiratory distress syndrome, and respiratory failure. A composite pulmonary adverse event (CPAE) included the occurrence of any of these. MetS was defined as the combination of hypertension, dyslipidaemia, and diabetes mellitus. The association of MetS and additional comorbibities, procedural data, and patient characteristics with CPAEs was examined with appropriate statistical tests. RESULTS: A total of 158 405 patients had a low incidence of PPC (0.91%) and a low mortality (0.6%) after bariatric surgery. MetS was prevalent in 12.7%, and was a significant risk factor for CPAE and mortality. Age, BMI, ASA physical status classification, surgical duration, procedure type, MetS (P<0.001), and additional comorbidities were significantly associated with CPAEs. CONCLUSIONS: The incidence of PPC was low after bariatric surgery. Increasing age, BMI, ASA status, MetS, obstructive sleep apnoea, asthma, congestive heart failure, surgical duration, and procedure type were independently significantly associated with PPC. Pulmonary complications and MetS were significantly associated with increased postoperative mortality.

Ophthalmic complications after spinal surgery.

STUDY DESIGN: A retrospective review of 3450 spinal surgeries was performed. OBJECTIVES: To review ophthalmic complications and their etiologies, as well as treatments and outcomes, in patients who have undergone spinal surgery. SUMMARY OF BACKGROUND DATA: Ophthalmic complications after major spinal reconstructive surgery are rare and have not been adequately addressed in the orthopedic literature. METHODS: In a series of 3450 spinal surgeries at three institutions, the authors identified seven patients (incidence = 0.20%) whose postoperative course was complicated by loss of visual acuity. These perioperative ophthalmic complications included posterior optic nerve ischemia, occipital lobe infarcts, and central retinal vein thrombosis. Operative time, estimated blood loss, and medical history of peripheral vascular, cardiovascular, or ophthalmic disease were obtained from the charts, as were follow-up data. RESULTS: Three patients recovered completely, and one had partial return of visual function. In the remaining three patients, significant visual loss persisted. CONCLUSIONS: The risk of ophthalmic complications with spinal surgery has not been fully appreciated. Because ophthalmic complications in spinal surgery may be reversed with prompt recognition and intervention, it is important for clinicians to be aware of their possible occurrence.

Surgical and anesthetic management of patients undergoing major hepatectomy using total vascular exclusion.

Total vascular exclusion (TVE) of the liver is accomplished by complete occlusion of inflow and outflow of the liver during hepatectomy. It affords the opportunity for bloodless, anatomically precise parenchymal transection but has not been widely used in this country. TVE should make it possible to treat large or unfavorably located lesions safely. To evaluate the benefit of this modality, we have examined the results of TVE in 49 major resections. Forty-nine patients with liver tumors (mean age, 50 +/- 17 years; range 3 to 75 years) were treated by the authors over 5 years with a mean age of 50 +/- 17 years (range 3-75). Thirty-five (71%) patients were females and 38 (78%) had malignant tumors (hepatocellular CA n = 15, liver metastases n = 20, other n = 3), whereas 11 (22%) had benign tumors (hemangiomas n = 7 other n = 4). Six (12%) had histological cirrhosis but normal liver function test results. Twenty two (45%) had previous surgery. Forty-seven (96%) underwent total or extended lobectomies. Two patients had segmental resection of benign tumors (one in segment 4 and one in segment 8). Mean surgical time was 4.7 hours (2.5-8.3 hours) and mean red blood cell requirement was 2.2 U (0 to 11). Twenty-two (45%) procedures were performed without transfusions. Hospital mortality rates were 0%. The mean postoperative hospital duration was 11 days (5 to 41 years). Complications occurred in 18 (36%), requiring reoperation in 1 case for wound debridement and in another for lysis of postoperative adhesions. Hepatic insufficiency occurred transiently in 2 patients with prolongation of protime and cholestasis and resolved within 4 days in 1 patient and 10 days in the other (with cirrhosis). The perception of hepatic resection as a prohibitive undertaking with high mortality rate may limit the use of resection in patients who might benefit from this modality. Our data document the effectiveness and safety of major hepatectomy even in cirrhotic patients using TVE. Expanded use of TVE and other advances in liver surgery should be considered to decrease the morbidity rate of resection and make the benefits of this therapy more widely available.

The effect of x-irradiation on cell loss in five solid murine tumours, as determined by the 125IUdR method.

The rate of cell loss in irradiated RIF-1, EMT6, KHJJ, B16 and KHT tumours was studied using the 125IUdR loss technique. Administration of 125IUdR preceded localized tumour irradiation by 2 days. Loss of tumour radioactivity was measured for 6-8 days after irradiation. The blood flow to some tumours was occluded during, and for 30 min following, injection of the label to measure the amount of radioactivity entering the tumour as a result of reutilization of label from the gut epithelia and influx of labelled host cells. Irradiation did not significantly alter the amount of radioactivity entering these clamped tumours during the 8-10 days after injection of 125IUdR. This permitted comparison of irradiated and control groups based on the loss of radioactivity from the non-occluded tumours. Irradiation of RIF-1, EMT6, KHJJ or B16 tumours with doses of 600, 1400, 2400 or 4400 rads produced no significant increase in the rate of loss of tumour radioactivity. This suggested that, in the population of labelled cells, cell lysis following irradiation proceeded slowly. In contrast, KHT tumours showed a significant increase in loss rate following each radiation dose, although the increase was dose-independent. In all tumour systems, the constant rate of cell loss after radiation appeared to coincide with published reports of tumour growth responses after irradiation. The present data suggest that the manner of expression of radiation-induced cell killing results from the cellular proliferative status, i.e. whether a cell is cycling or non-cycling.

125IUdR loss as a measure of tumour cell loss: influence of reutilization and influx of labelled host cells.

Two potential artifacts, the reutilization of label released from the gut and the influx into solid tumours of labelled host cells, have been measured by occluding the blood flow to tumours during, and for 30 min after, injection of 125IUdR. Previous work has shown that occluded EMT6 and KHJJ tumours exhibit a substantial increase in label, to 30-40% of the total activity in non-occluded tumours within 4 days post-125IUdR injection. In B16 and RIF-1 tumours the influx of label is minimal. Almost all of this entry of 125IUdR results from the influx of labelled host cells. Significant influx was also demonstrated in Lewis lung and KHT tumours. Minimal changes in the extent of influx of labelled host cells were found following irradiation of EMT6 and RIF-1 tumours with 600 or 1400 rad. These doses also resulted in little or no additional loss of 125IUdR despite the fact that 60 to 95% of the tumour cells were killed. Thus, the lysis of the killed cells must proceed very slowly. The conditions necessary for the use of 125IUdR loss to assess cell killing, as opposed to cell lysis, are reviewed.