Pancreatic injury after thoracoabdominal aortic occlusion in a porcine model

BACKGROUND: The aim of this study was to investigate pancreatic injury after 45 min of thoracoabdominal aortic occlusion in a porcine model. METHODS: Twenty-four pigs were used. Six pigs underwent sham operation and 18 intravascular balloon thoracoabdominal aortic occlusions for 45 min. The animals were randomly killed at 12, 48 and 120 h after reperfusion. After killing, all pancreata were examined macroscopically for any signs of acute pancreatitis, whereas gland specimens were harvested for histological study to evaluate pancreatic injury (haematoxylin and eosin staining) and acinar cell apoptosis (Terminal deoxynucleotidyl transferase mediated dUTP Nick-End Labelling staining). RESULTS: Pancreatic injury severity score was mildly increased in terms of oedematous features at 12 h after reperfusion, but normalized to sham levels by the second day and thereafter. Necrotic injury was not statistically significant at any time point. Acinar cell apoptotic index was mildly increased at 12 and 48 h, but showed a tendency to decrease towards sham levels by the fifth day. One animal developed acute pancreatitis. CONCLUSION: Acute pancreatitis is unlikely to occur after 45 min of thoracoabdominal aortic occlusion. However, an early, mild oedematous and apoptotic injury that occurs subclinically seems to be a constant event. This injury might have clinical significance when combined with pre-existent pancreatic pathologies.     

Nonsteroidal anti-inflammatory drugs and coma: a case report of fenoprofen overdose

We present the case of a 17-year-old girl who ingested 24 to 36 g fenoprofen as a suicidal gesture. She presented with coma, hypotension, metabolic acidosis, and respiratory depression within four hours of ingestion. The most common adverse effects of the nonsteroidal anti-inflammatory drugs occur in both therapeutic and toxic doses and include gastrointestinal upset, blood dyscrasias, and analgesic nephropathy. The propionic acid derivatives of nonsteroidal anti-inflammatory drugs, including fenoprofen and ibuprofen, are rarely associated with severe toxic effects. This is the first report of pure fenoprofen overdose presenting as coma and metabolic acidosis.     

Comparison of standard external CPR, open-chest CPR, and cardiopulmonary bypass in a canine myocardial infarct model

STUDY OBJECTIVES: After cardiac arrest, open-chest CPR (OCCPR) and cardiopulmonary bypass (CPB) have demonstrated higher resuscitation rates when compared individually with standard external CPR (SECPR). We compared all three techniques in a canine myocardial infarct ventricular fibrillation model. TYPE OF PARTICIPANTS: Twenty-six mongrel dogs were block-randomized to receive SECPR and advanced life support (nine), CPB (nine), or OCCPR (eight). DESIGN AND INTERVENTIONS: All dogs received left anterior descending coronary artery occlusion followed by four minutes of ventricular fibrillation without CPR and eight minutes of Thumper CPR. At 12 minutes, dogs received one of three resuscitation techniques. After resuscitation, all animals received four hours of intensive care. Animals that were resuscitated had histochemical determination of ischemic and necrotic myocardial areas. MEASUREMENTS: Intravascular pressures were measured and coronary perfusion pressure was calculated during baseline, cardiac arrest, resuscitation, and postresuscitation periods. Percent necrotic myocardium, percent ischemic myocardium, and necrotic-to-ischemic ratios were determined for resuscitated animals. Epinephrine dosage and number of countershocks were determined for each group. MAIN RESULTS: Nine of nine CPB and six of nine OCCPR, compared with two of eight SECPR animals, were resuscitated (P less than .01). Three of nine CPB and OCCPR and two of eight SECPR dogs survived to four hours (P = NS). Coronary perfusion pressure two minutes after institution of technique was significantly higher with CPB (75 +/- 37 mm Hg) and OCCPR (56 +/- 31 mm Hg) than in SECPR animals (16 +/- 16 mm Hg, P less than .04). Epinephrine required for resuscitation was significantly less with CPB (0.10 +/- 0.02 mg/kg) than for SECPR (0.28 +/- 0.11 mg/kg, P less than .002). The ratio of necrotic to ischemic myocardium at four hours was significantly lower with CPB (0.15 +/- 0.31) and OCCPR (0.39 +/- 0.25) than for SECPR (1.16 +/- 0.31, P less than .02). CONCLUSION: OCCPR and CPB produce higher coronary perfusion pressures and improved resuscitation rates from ventricular fibrillation when compared with SECPR in this canine myocardial infarct cardiac arrest model. CPB and OCCPR yielded similar resuscitation results, although less epinephrine was required with CPB.     

Human herpesvirus 8 (HHV-8) infection in healthy urban employees from Greece: seroprevalence and associated factors

A cross-sectional study was carried out in healthy company employees from Greece with the aim of assessing the prevalence of human herpesvirus 8 (HHV-8) and identifying risk factors for this herpesviral infection. Serum samples obtained from 955 subjects were tested for antibodies to HHV-8 by the K8.1 enzyme-linked immunosorbent assay (ELISA). Associations between HHV-8 serostatus and potential risk factors were examined using t-test, chi square test, and multivariate logistic regression analysis. HHV-8 prevalence was 7.6% (95% confidence interval (CI): 6.0%, 9.5%) and it increased with age from 6.5% among <30 years old to 13.8% among > or =50 years old subjects (P = 0.006). HHV-8 seropositivity was independently associated with endoscopic examination (odds ratio (OR): 2.01; 95% CI: 1.09, 3.70; P = 0.026), HBsAg positivity (OR: 5.16; 95% CI: 2.02, 13.20; P = 0.001) and age (OR > or =50 years old vs. <50 years old: 2.09; 95% CI: 1.23, 3.52; P = 0.006). No statistically significant associations between HHV-8 positive status and gender, occupational status, surgery, transfusion, tattoos/body piercing, multiple sex partners, weakness/fatigue, HCV status were observed. HHV-8 is prevalent in Greece. The strong association between HBV infection and HHV-8 positive status supports the hypothesis of an association between these two viral infections. The association between HHV-8 seropositivity and endoscopic examination requires further investigation.     

Role of oxygen in postischemic myocardial injury

Myocardial function is dependent on a constant supply of oxygen from the coronary circulation. A reduction of oxygen supply due to coronary obstruction results in myocardial ischemia, which leads to cardiac dysfunction. Reperfusion of the ischemic myocardium is required for tissue survival. Thrombolytic therapy, coronary artery bypass surgery and coronary angioplasty are some of the treatments available for the restoration of blood flow to the ischemic myocardium. However, the restoration of blood flow may also lead to reperfusion injury, resulting in myocyte death. Thus, any imbalance between oxygen supply and metabolic demand leads to functional, metabolic, morphologic, and electrophysiologic alterations, causing cell death. Myocardial ischemia reperfusion (IR) injury is a multifactorial process that is mediated by oxygen free radicals, neutrophil activation and infiltration, calcium overload, and apoptosis. Controlled reperfusion of the ischemic myocardium has been advocated to prevent the IR injury. Studies have shown that reperfusion injury and postischemic cardiac function are related to the quantity and delivery of oxygen during reperfusion. Substantial evidence suggests that controlled reoxygenation may ameliorate postischemic organ dysfunction. In this review, we discuss the role of oxygenation during reperfusion and subsequent biochemical and pathologic alterations in reperfused myocardium and recovery of heart function.     

Compared to angiotensin II, epinephrine is associated with high myocardial blood flow following return of spontaneous circulation after cardiac arrest

INTRODUCTION: Epinephrine (adrenaline) and vasopressin are used currently to improve myocardial blood flow (MBF) during cardiac arrest. Angiotensin II has also been shown to improve MBF during CPR. We explored the effects of angiotensin II or epinephrine alone, and the combination of angiotensin with epinephrine, on myocardial and cerebral blood flows in a swine model of cardiac arrest. METHODS: Swine were instrumented for regional blood flow measurements. Ventricular fibrillation was induced and CPR begun. Angiotensin II 50 mcg/kg (ANG), epinephrine 0.02 mg/kg (EPI) or the combination (ANG+EPI) was administered. Blood flow was measured during baseline normal sinus rhythm (NSR), before (CPR) and after drug administration (CPR+DRUG), and post reperfusion return of spontaneous circulation (ROSC). RESULTS: All groups had a significant increase in MBF during CPR following drug administration (P<0.05). [table: see text] There was a trend toward higher flows in the EPI groups. The group receiving both EPI and ANG did not have higher blood flows than the EPI or ANG alone groups. Both groups that received EPI had markedly elevated MBF following ROSC compared with angiotensin II (P<0.05). CONCLUSIONS: The combination of ANG and EPI did not improve MBF during cardiac arrest. Epinephrine may increase MBF compared with angiotensin II post-reperfusion.     

Activity of ampicillin-sulbactam and oxacillin in experimental endocarditis caused by beta-lactamase-hyperproducing Staphylococcus aureus.

Using a rat model of aortic valve infective endocarditis, we previously found that oxacillin was equally effective against an oxacillin-susceptible strain of Staphylococcus aureus and a beta-lactamase-hyperproducing borderline oxacillin-susceptible strain of S. aureus; also, ampicillin-sulbactam was less effective than oxacillin against both isolates and at low doses was less effective against the borderline-susceptible strain than against the fully oxacillin-susceptible strain (C. Thauvin-Eliopoulos, L. B. Rice, G. M. Eliopoulos, and R. C. Moellering, Jr., Antimicrob. Agents Chemother. 34:728-732, 1990). In the present study, we extended this work, using alternative treatment schedules and additional bacterial strains. Extending treatment with low doses of ampicillin-sulbactam (500 and 250 mg/kg of body weight per day, respectively) to 6.5 days resulted in equalization of effectiveness against the previously studied strains BOSSA-1 and OSSA-1 (3.75 +/- 1.61 log10 and 4.71 +/- 1.79 log10 CFU of residual viable bacteria per g, respectively). Against the borderline oxacillin-susceptible strain BOSSA-1, increasing the sulbactam dosage from 500 to 2,000 mg/kg/day while maintaining a fixed dose of ampicillin (1,000 mg/kg/day) by continuous infusion resulted in lower bacterial counts (4.93 +/- 1.84 log10 versus 3.65 +/- 1.26 log10 CFU of residual viable bacteria per g, respectively), but this difference was of only borderline significance; differences in efficacy between the low-dose and high-dose sulbactam regimens were exaggerated when intermittent intravenous administration was used (6.19 +/- 1.90 log10 versus 3.37 +/- 1.41 log10 CFU/g, respectively; P < 0.001). However, for any individual sulbactam dosage, the model of administration (continuous versus intermittent infusion) did not affect the activity of the regimen. When additional strains were used in the model, oxacillin and ampicillin-sulbactam (1,000 plus 2,000 mg/kg/day) were equally effective against both oxacillin-susceptible and borderline oxacillin-resistant strains of S. aureus. These results support the predictions that oxacillin would be clinically effective in the treatment of infections caused by borderline oxacillin-susceptible strains of S. aureus and that, except at very low doses, ampicillin-sulbactam would also be as effective against borderline-susceptible strains as against fully oxacillin-susceptible strains of S. aureus.     

Serum osmolal gap in clinical practice: usefulness and limitations

Background: Although serum osmolal gap can be a useful diagnostic tool, clinicians are not familiar with its use in clinical practice.

Objectives: The review presents in a series of questions-answers and under a clinical point of view the current data regarding the use of osmolal gap.

Discussion: The definition and the best formula used for the calculation of osmolal gap, the main causes of increased osmolal gap with or without increased anion gap metabolic acidosis, as well as the role of concurrent lactic acidosis or ketoacidosis are presented under a clinical point of view.

Conclusions: The calculation of osmolal gap is crucial in the differential diagnosis of many patients presenting in emergency departments with possible drug or substance overdose as well as in comatose hospitalized patients.