Risk factors for perioperative hyperglycemia in primary hip and knee replacements

Background and purpose — Perioperative hyperglycemia has been associated with adverse outcomes in several fields of surgery. In this observational study, we identified factors associated with an increased risk of hyperglycemia following hip and knee replacement.

Patients and methods — We prospectively monitored changes in glucose following primary hip and knee replacements in 191 patients with osteoarthritis. Possible associations of patient characteristics and operation-related factors with hyperglycemia (defined as glucose > 7.8 mmol/L in 2 consecutive measurements) and severe hyperglycemia (glucose > 10 mmol/L) were analyzed using binary logistic regression with adjustment for age, sex, operated joint, and anesthesiological risk score.

Results — 76 patients (40%) developed hyperglycemia, and 48 of them (25% of the whole cohort) had severe hyperglycemia. Glycemic responses were similar following hip replacement and knee replacement. Previously diagnosed diabetes was associated with an increased risk of hyperglycemia and severe hyperglycemia, compared to patients with normal glucose metabolism, whereas newly diagnosed diabetes and milder glucose metabolism disorders had no effect. In patients without previously diagnosed diabetes, increased values of preoperative glycosylated hemoglobin (HbA1c) and fasting glucose on the day of operation were associated with hyperglycemia. Higher anesthesiological risk score—but none of the operation-related factors analyzed—was associated with an increased risk of hyperglycemia.

Interpretation — Perioperative hyperglycemia is common in primary hip and knee replacements. Previously diagnosed diabetes is the strongest risk factor for hyperglycemia. In patients with no history of diabetes, preoperative HbA1c and fasting glucose on the day of operation can be used to stratify the risk of hyperglycemia.     

Suppressed neutrophil function as a risk factor for severe infection after cytotoxic chemotherapy in patients with acute nonlymphocytic leukemia

 Severe infections are a major problem in patients suffering from acute nonlymphocytic leukemia (ANLL) undergoing myeloablative chemotherapy. Possible factors leading to infectious complications in these patients are suppressed immune defense mechanisms existing prior to therapy, including those involving the neutrophil granulocyte department. In this study we investigated whether neutrophil function as measured by oxidative burst and phagocytosis before the start of treatment correlates with the severity of infection after therapy. Forty-four patients were included, 27 men and 17 women. Their median age was 46 years (range 20–70 years). According to the development of infectious complications the patients were assigned retrospectively to group 1 (no or only mild infections, n=29) or to group 2 (severe infection or death due to infection, n=15). The phagocytic activity was significantly reduced in group 2 as compared with group 1 [113.7±13.7 (SEM) vs 170.0±19.2, mean channel fluorescence;p=0.04]. In contrast, the oxidative burst as measured by FMLP stimulation was pronounced but not significantly enhanced in group 2 (24.8±6.1 vs 14.5±3.4, mean channel fluorescence). In conclusion, patients with severe infections after chemotherapy might already have preactivated neutrophils with suppressed function prior to treatment. Thus, evaluating function parameters could help to estimate the individual risk of infection for a patient with ANLL. Received: July 3, 1998 / Accepted: September 9, 1998     

Removal of endothelial function in coronary resistance vessels by saponin

Summary Studies of the role of the endothelium in coronary resistance vessels are limited to investigations of endothelium-derived relaxing factor mediated effects using various blocking agents. Endothelium removal as an alternative approach, is restricted to larger epicardial vessels.This study demonstrates the effect of endothelial damage by saponin on coronary resistance vessels remaining intact within the heart. In an isolated perfused guinea pig heart a saponin-containing solution (50 g/ml) was infused over 2 min to damage specifically the endothelium. Increases of coronary flow in response to carbachol, histamine, and serotonin were completely blocked and reversed to decreases. Angiotensin-I-induced vasoconstriction was attenuated, whereas angiotensin-II-induced vasoconstriction remained unchanged. Vasodilatory response to sodium-nitroprusside was not attenuated by saponin-treatment. In contrast inhibition of endothelium derived relaxing factor by gossypol inhibited carbachol-induced vasodilation but did not result in vasoconstriction. Electron microscopic examination ensured that while the endothelium was destroyed by saponin-treatment the vascular smooth muscle was left intact. Our data indicate a regulating influence of the vascular endothelium on coronary resistance vessels which can be totally eliminated by saponin-treatment.     

Terlipressin plus hydroxyethyl starch infusion: an effective treatment for hepatorenal syndrome

Ornipressin is a vasopressin analogue that can cause potent splanchnic vasoconstriction. It has been shown that, in combination with albumin infusion, ornipressin is able to reverse hepatorenal syndrome. However, its clinical use is limited by possible severe ischaemic complications. In our case, a 47-year-old man received a right hemihepatectomy for cholangiocellular carcinoma. On post-operative day three, he developed hepatorenal syndrome with ascites, peripheral oedema and oliguria (250-500 ml/day). Serum creatinine was increased to 3.5 mg/dl. The patient was treated with terlipressin, another vasopressin analogue with fewer side effects than ornipressin, (1 mg every 4 h intravenously) and hydroxyethyl starch (500 ml/day). Urine output increased to 3000 ml/day, serum creatinine decreased to normal range within 4 days and ascites and oedema disappeared. We hereby report the first case of successful treatment of hepatorenal syndrome with terlipressin and hydroxyethyl starch, which appears to be a safe and effective treatment.     

Predictors of New Airway Obstruction – An 11 Year’s Population-Based Follow-Up Study

In the present study we aimed to investigate the incidence and predictors of spirometry based airway obstruction in a representative population-based sample. Altogether 3,863 subjects, 1,651 males and 2,212 females aged ≥30 years had normal spirometry in year 2000. Fifty-three percent of them were never and 23% current smokers. A re-spirometry was performed 11 years later. Several characteristics, such as level of education, use of alcohol, physical activity, diet using Alternate healthy eating (AHEI) index, body mass index, circumwaist, sensitive C reactive protein (CRP) and cotinine of the laboratory values and co-morbidities including asthma, allergic rhinitis, sleep apnoea and chronic bronchitis, as potential risk factors for airway obstruction were evaluated. Using forced expiratory volume in one second/ forced vital capacity below the lower limit of normal, we observed 124 new cases of airway obstruction showing a cumulative 11-year incidence of 3.2% and corresponding to an incidence rate of 5.6/1,000 per year (PY). The incidence rate was higher in men than in women (6.3/1,000 PY vs. 5.0/1,000 PY, respectively). The strongest risk factors were current smoking (Odds ratio [OR] 2.5) and previously diagnosed asthma (OR 2.1). Sensitive CRP associated with the increased risk and high AHEI index with the decreased risk of airway obstruction. Using the similar study approach our findings on the incidence of airway obstruction are in line with the previously published figures in Europe. We were able to confirm the recent findings on the protective effect of healthy diet.     

How to use ECG for decision support in the catheterization laboratory. Cases with inferior ST elevation myocardial infarction

Treatment of acute myocardial infarction has changed considerably during the last few years with the introduction of primary coronary angioplasty. In the acute phase risk stratification is largely based on simple clinical parameters, laboratory markers of myocardial injury and 12-lead electrocardiography. The electrocardiogram is of crucial importance especially during the first few hours after initiation of chest pain when important therapeutic decisions are made. Biochemical markers of myocardial injury are usually not elevated at that time point. Cases with inferior ST-elevation myocardial infarction from our hospital are presented to show how anatomical interpretation of ECG recorded during chest pain helps to risk stratify patients.     

Role of kinin B2 receptor signaling in the recruitment of circulating progenitor cells with neovascularization potential

Reduced migratory function of circulating angiogenic progenitor cells (CPCs) has been associated with impaired neovascularization in patients with cardiovascular disease (CVD). Previous findings underline the role of the kallikrein-kinin system in angiogenesis. We now demonstrate the involvement of the kinin B2 receptor (B(2)R) in the recruitment of CPCs to sites of ischemia and in their proangiogenic action. In healthy subjects, B(2)R was abundantly present on CD133(+) and CD34(+) CPCs as well as cultured endothelial progenitor cells (EPCs) derived from blood mononuclear cells (MNCs), whereas kinin B1 receptor expression was barely detectable. In transwell migration assays, bradykinin (BK) exerts a potent chemoattractant activity on CD133(+) and CD34(+) CPCs and EPCs via a B(2)R/phosphoinositide 3-kinase/eNOS-mediated mechanism. Migration toward BK was able to attract an MNC subpopulation enriched in CPCs with in vitro proangiogenic activity, as assessed by Matrigel assay. CPCs from cardiovascular disease patients showed low B(2)R levels and decreased migratory capacity toward BK. When injected systemically into wild-type mice with unilateral limb ischemia, bone marrow MNCs from syngenic B(2)R-deficient mice resulted in reduced homing of sca-1(+) and cKit(+)flk1(+) progenitors to ischemic muscles, impaired reparative neovascularization, and delayed perfusion recovery as compared with wild-type MNCs. Similarly, blockade of the B(2)R by systemic administration of icatibant prevented the beneficial effect of bone marrow MNC transplantation. BK-induced migration represents a novel mechanism mediating homing of circulating angiogenic progenitors. Reduction of BK sensitivity in progenitor cells from cardiovascular disease patients might contribute to impaired neovascularization after ischemic complications.