Factors predicting mortality in emergency abdominal surgery in the elderly

ABSTRACT: OBJECTIVE: This study aimed to investigate clinical features of abdominal emergency surgery in elderly patients, and to determine factors predicting mortality in these patients. METHODS: The study population included 94 patients aged 80 years or older who underwent emergency surgery for acute abdominal diseases between 2000 and 2010. Thirty-six patients (38.3%) were male and fifty-eight patients (61.7%) were female (mean age, 85.6 years). Main outcome measures included background of the patient's physical condition (concomitant medical disease, and performance status), cause of disease, morbidity and mortality, and disease scoring system (APACHE II, and POSSUM). Prognostic factors affecting mortality of the patient were also evaluated by univariate analysis using Fisher's exact test and Mann- Whitney U-test, and by multivariate analysis using multiple logistic regression analysis. RESULTS: Of the 94 patients, 71 (75.5%) had a co-existing medical disease; most patients had hypertension (46.8%). The most frequent surgical indications were acute cholecystitis in 23 patients (24.5%), followed by intestinal obstruction in 18 patients (19.1%). Forty-one patients (43.6%) had complications during hospital stay; the most frequent were surgical site infection (SSI) in 21 patients (22.3%) and pneumonia in 12 patients (12.8%). Fifteen patients died (overall mortality, 16%) within 1 month after operation. The most common causes of death were sepsis related to pan-peritonitis in 5 patients (5.3%), and pneumonia in 4 patients (4.3%). Multiple logistic regression analysis showed that time from onset of symptoms to hospital admission and the POSSUM scoring system could be prognostic factors for mortality. CONCLUSIONS: Mortality in elderly patients who underwent emergency surgery for acute abdominal disease can be predicted using the disease scoring system (POSSUM) and on the basis of delay in hospital admission. Keywords.     

Intrathoracic omental herniation through the esophageal hiatus: Report of a case

(Received for publication on Dec. 8, 1997; accepted on July 7, 1998)     

New Generation Extracorporeal Membrane Oxygenation With MedTech Mag‐Lev,a Single‐Use,Magnetically Levitated,Centrifugal Blood Pump: Preclinical Evaluation in Calves

We have evaluated the feasibility of a newly developed single‐use, magnetically levitated centrifugal blood pump, MedTech Mag‐Lev, in a 3‐week extracorporeal membrane oxygenation (ECMO) study in calves against a Medtronic Bio‐Pump BPX‐80. A heparin‐ and silicone‐coated polypropylene membrane oxygenator MERA NHP Excelung NSH‐R was employed as an oxygenator. Six healthy male Holstein calves with body weights of about 100 kg were divided into two groups, four in the MedTech group and two in the Bio‐Pump group. Under general anesthesia, the blood pump and oxygenator were inserted extracorporeally between the main pulmonary artery and the descending aorta via a fifth left thoracotomy. Postoperatively, both the pump and oxygen flow rates were controlled at 3 L/min. Heparin was continuously infused to maintain the activated clotting time at 200–240 s. All the MedTech ECMO calves completed the study duration. However, the Bio‐Pump ECMO calves were terminated on postoperative days 7 and 10 because of severe hemolysis and thrombus formation. At the start of the MedTech ECMO, the pressure drop across the oxygenator was about 25 mm Hg with the pump operated at 2800 rpm and delivering 3 L/min flow. The PO₂ of the oxygenator outlet was higher than 400 mm Hg with the PCO₂ below 45 mm Hg. Hemolysis and thrombus were not seen in the MedTech ECMO circuits (plasma‐free hemoglobin [PFH] < 5 mg/dL), while severe hemolysis (PFH > 20 mg/dL) and large thrombus were observed in the Bio‐Pump ECMO circuits. Plasma leakage from the oxygenator did not occur in any ECMO circuits. Three‐week cardiopulmonary support was performed successfully with the MedTech ECMO without circuit exchanges. The MedTech Mag‐Lev could help extend the durability of ECMO circuits by the improved biocompatible performances.     

Receptor activator of NF-κB ligand-dependent expression of caveolin-1 in osteoclast precursors, and high dependency of osteoclastogenesis on exogenous lipoprotein

Although extensive studies have done much to clarify the molecular mechanisms of osteoclastogenesis during the last ten years, there may still be unknown molecules associated with osteoclast differentiation. Thus, we used fluorescent differential display to screen for genes whose expression is induced by receptor activator of NF-κB ligand (RANKL), a crucial molecule for osteoclast formation. We identified caveolin-1 (Cav-1) as a RANKL-induced gene. Cav-1 is a major structural protein of caveolae and lipid rafts, cholesterol-enriched microdomains in the plasma membrane (PM). The RANKL-induced Cav-1 was immediately conveyed to lipid rafts. Conversely, expression of flotillin-1 (Flot-1), another scaffolding protein of lipid rafts, was reduced during osteoclastogenesis, indicating conversion of Flot-1-predominant rafts into Cav-1-enriched rafts. However, in vitro osteoclastogenesis of precursor cells from Cav-1-null mice was comparable to that of wild-type mice, while Cav-2 expression in the knockout osteoclasts was maintained. Conversely, Cav-2 gene silencing in Cav-1-null osteoclast precursors using siRNA for Cav-2 increased osteoclast formation, suggesting that the Cav-1/Cav-2 complex may act as a negative regulator for osteoclastogenesis. On the other hand, destruction of lipid rafts by removal of cholesterol from the PM by methyl-ß-cyclodextrin (MCD) treatment caused disordered signal transductions for osteoclastogenesis, such as hyperactivation of Erk1/2 and insensitivity of Akt to RANKL stimulus. The abnormal signaling was reproduced by deleting exogenous lipoproteins from the culture medium, which also resulted in reduced osteoclast formation. In addition, the deletion caused delayed expression of nuclear factor of activated T cells c1 (NFATc1), and depressed its activation in the cytosol and inhibited its translocation into nuclei. Simultaneously, the deletion reduced the level of FcRγ, a trigger protein for initiating the calcium signaling needed to activate NFATc1, and decreased Cav-1 in lipid rafts. These findings indicate that the molecular mechanisms of osteoclastogenesis are highly dependent on extracellular lipoprotein and the integrity of lipid rafts, and suggest possible involvement of cholesterol.     

Intraductal oncocytic papillary neoplasm of the extrahepatic bile duct: report of a case

We report a rare case of an intraductal oncocytic papillary neoplasm (IOPN) of the extrahepatic bile duct. A 66-year-old man was admitted to our hospital for investigation of right-sided back pain. Ultrasonography, computed tomography and magnetic resonance imaging showed a papillary lesion, 3?cm in diameter, in the middle bile duct, invaginating into the cystic duct. We made a provisional diagnosis of middle bile duct cancer and performed substomach-preserving pancreatoduodenectomy. Macroscopically, the middle bile duct contained a two-humped papillary tumor, one tip of which invaginated into the cystic duct. Microscopically, the tumor consisted of cuboidal cells with abundant eosinophilic cytoplasm resembling that of oncocytes and a fine fibrovascular core. The tumor cells were stained strongly with antimitochondria antibody. Based on these findings, the tumor was diagnosed histologically as IOPN of the extrahepatic bile duct. The patient died of prostate cancer 51?months after surgery, but without evidence of recurrence of the IOPN.     

Expression of type IV collagen in the developing human kidney

The distribution of α1–6 chains of type IV collagen (α1–6(IV)) in human fetal kidneys was examined by indirect immunofluorescence. By 11 weeks of gestation, α1, 2, 3, 4, and 6(IV) were already present, but α5(IV) appeared relatively late, at 21 weeks. α1(IV) and α2(IV) were present in all basement membranes, α3(IV) and α4(IV) were restricted to the glomerular basement membrane and parts of the tubular basement membrane. α5(IV) was distributed in the glomerular basement membrane, Bowman’s capsule, and parts of the tubular basement membrane. α6(IV) was present in the Bowman’s capsule, parts of the tubular basement membrane, and occurred in parts of the glomerular basement membrane at the early capillary loop stage, but disappeared during the later capillary loop stage. Received October 23, 1997; received in revised form and accepted February 6, 1998     

Suppression of energy requirement by lidocaine in the ischemic mouse brain

Effects of lidocaine on parameters of membrane functional integrity were investigated in the mouse brain. Changes in the direct-current potential shift in the cerebral cortex provoked by decapitation ischemia were compared in animals given lidocaine (0.05, 0.25, or 1.0 micromol, intracerebroventricular) or saline 15 minutes before ischemia. The brain content of adenosine 5'-triphosphate (ATP) was measured in animals subjected to 0, 0.5, 1, and 2 minutes of decapitation ischemia, and the effect of preischemic administration of lidocaine (0.25 micromol, intracerebroventricular) was evaluated. Na+, K+-ATPase, and Ca2+-ATPase activity was evaluated in brains pretreated with lidocaine (0.25 micromol, intracerebroventricular) or saline 15 minutes before decapitation. Changes in the intracellular Ca concentration ([Ca2+]i) were evaluated in hippocampal slices and the effects of lidocaine (50, 100, or 400 microM) were assessed in the hippocampal CA1 field and dentate gyrus at pH 7.4 and pH 6.8 every 60s for a duration of 50 min. The preischemic administration of lidocaine (1.0 and 0.25 micromol) delayed the onset of anoxic depolarization to 49 seconds and 44 seconds, respectively, as compared with that in the saline group at 27 seconds. Lidocaine maintained ATP levels higher than those in corresponding saline groups, values being 165% after 1 minute of ischemia and 212% after 2 minutes, respectively. Lidocaine did not affect Na+, K+-ATPase, and Ca2+-ATPase activity. Lidocaine did not affect changes in the [Ca2+]i in either area at either pH. The findings may suggest that lidocaine maintains the energy level by delaying depolarization in neurons, which may contribute to removal of cytosolic Ca2+ in ischemic states.     

Endovascular treatment of vertebral artery aneurysm manifesting as progressive hemifacial spasm

A 62-year-old woman presented with right hemifacial spasm persisting for 6 months. Brain magnetic resonance imaging and digital subtraction angiography showed a wide-neck aneurysm of the intracranial portion of the right vertebral artery. The patient underwent endovascular trapping of the aneurysm by coil embolization of the parent vessel on both sides of the aneurysm. The patient experienced gradual disappearance of the hemifacial spasm within 3 months. No relapses occurred during a follow-up period of 3 years. Magnetic resonance imaging revealed shrinkage of the vertebral artery aneurysm which had compressed the facial nerve. Endovascular trapping of a vertebral artery aneurysm can be used to treat hemifacial spasm caused by an aneurysm instead of surgical microvascular decompression.