The effects of Hurricane Sandy on trauma center admissions.

BACKGROUND: Hurricane Sandy was a particularly unusual storm with regard to both size and location of landfall. The storm landed in New Jersey, which is unusual for a tropical storm of such scale, and created hazardous conditions which caused injury to residents during the storm and in the months following. This study aims to describe differences in trauma center admissions and patterns of injury during this time period when compared to a period with no such storm. METHODS: Data were collected for this study from patients who were admitted to the trauma center at Morristown Medical Center during Hurricane Sandy or the ensuing cleanup efforts (patients admitted between 29 October 2012 and 27 December 2012) as well as a control group consisting of all patients admitted to the trauma center between 29 October 2013 and 27 December 2013. Patient information was collected to compare the admissions of the trauma center during the period of the storm and cleanup to the control period. RESULTS: A total of 419 cases were identified in the storm and cleanup period. 427 were identified for the control. Striking injuries were more common in the storm and cleanup group by 266.7% (p = 0.0107); cuts were more common by 650.8% (p = 0.0044). Medical records indicate that many of these injuries were caused by Hurricane Sandy. Self-inflicted injuries were more common by 301.3% (p = 0.0294). There were no significant differences in the total number of patients, mortality, or injury severity score between the two cohorts. CONCLUSION: The data we have collected show that the conditions caused by Hurricane Sandy and the following cleanup had a significant effect on injury patterns, with more patients having been injured by being struck by falling or thrown objects, cut while using tools, or causing self-inflicted injuries. These changes, particularly during the cleanup period, are indicative of environmental changes following the storm which increase these risks of injury.

HIF-1: a key mediator in hypoxia.

The transcription factor HIF-1 is one of the principal mediators of homeostasis in human tissues exposed to hypoxia. It is implicated in virtually every process of rapid gene expression in response to low oxygen levels. The most common causes of tissue hypoxia are inflammation and/or insufficient circulation or a combination of both. Inflamed tissues and the areas surrounding malignant tumors are characterized by hypoxia and low concentrations of glucose. Serious and generalized inflammation can lead to sepsis and circulatory collapse resulting in acute or chronic tissue hypoxia in various vital organs which induces a rapid homeostatic process in all nucleated cells of affected organs in the human body. Under hypoxic conditions the alpha and beta subunits of HIF-1 make an active heterodimer and drive the transcription of over 60 genes important for cell survival, adaptation, anaerobic metabolism, immune reaction, cytokine production, vascularization and general tissue homeostasis. In addition, HIF-1 plays a key role in the development of physiological systems in fetal and postnatal life. It is also a critical mediator of cancer, lung and cardiovascular diseases. The better understanding of the functions of HIF-1 and the pharmacological modulation of its activity could mean a successful therapeutic approach to these diseases.

Effects of intravenous famotidine on gastric acid secretion in patients undergoing cardiac surgery.

OBJECTIVE: To determine the effects of cardiopulmonary bypass and famotidine on gastric acid secretion in adults undergoing cardiac surgery. DESIGN: Prospective, randomized, double-blind, placebo-controlled study. SETTING: University teaching hospital. PARTICIPANTS: Eighteen patients undergoing elective cardiac surgery with cardiopulmonary bypass. MAIN OUTCOME MEASURES: Famotidine 20 mg or NaCl 0.9% placebo was administered intravenously following induction of anesthesia and placement of a nasogastric pH probe. A second dose was given 12 hours after surgery in the intensive care unit. Gastric pH was measured continuously and gastric volume was measured every 4 hours for up to 24 hours after cardiopulmonary bypass. RESULTS: Following famotidine administration, pH increased by 43% within 45 minutes and remained above 5.5 throughout the study period (p < 0.05 vs placebo and baseline). The gastric pH did not increase, but remained above 4.0 in most patients in the placebo group for up to 12 hours after cardiopulmonary bypass. Gastric volumes were on average 24% lower in the famotidine group (p > 0.05). CONCLUSIONS: Gastric acid secretion is decreased during and for 12 hours after cardiopulmonary bypass. Perioperative administration of famotidine suppresses gastric secretion in cardiac surgery patients.

Hemodynamic effects of intravenous famotidine in patients undergoing cardiac surgery.

STUDY OBJECTIVE: To determine the hemodynamic effects of famotidine in patients undergoing cardiac surgery. DESIGN: A prospective, randomized, double-blinded, placebo-controlled study. SETTING: A large university teaching hospital. PATIENTS: Twenty-one patients undergoing elective cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: The patients received a rapid intravenous bolus injection of famotidine 20 mg or saline placebo after anesthesia induction. A second dose was given 12 hours after surgery in the intensive care unit. MEASUREMENTS AND MAIN RESULTS: Serial hemodynamic measurements (heart rate, arterial blood pressure, cardiac index, pulmonary arterial pressure, central venous pressure, systemic vascular resistance) were obtained after each famotidine or placebo dose and analyzed by ANOVA: The values were not altered (p > 0.05) after intraoperative or postoperative famotidine or placebo administration. CONCLUSIONS: Rapid intravenous bolus administration of famotidine does not alter patient hemodynamics after anesthesia induction or in the intensive care unit after cardiac surgery.

Multiple platelet surface receptors mediate platelet adhesion to surfaces coated with plasma proteins.

The interactions between platelets and plasma proteins previously shown to adhere to biomaterials were evaluated, using monoclonal antibodies (mAbs) against specific platelet surface glycoprotein (GP) receptors. Purified 51Cr-labeled human platelets in plasma-free medium were incubated with each of the following antibodies: mAb 10E5 [anti-GP IIb/IIIa; fibrinogen, von Willebrand factor (vWF), and fibronectin receptor]; mAb 6D1 (anti-GP Ib-IX; vWF receptor); mAb IV.3 (anti-Fc gamma RII; IgG receptor); polyclonal antiserum A108 or mAb BIIG4 (anti-GP Ic-IIa; fibronectin receptor). Antibody-treated platelets were added to microtiter wells coated with fibronectin, fibrinogen, vWF, IgG, vitronectin, albumin, or platelet-poor plasma (PPP). 51Cr-labeled platelet adhesion to matrix proteins was expressed as a percentage of that measured on PPP-coated surface. Platelets adhered to fibrinogen, fibronectin, vWF, or IgG immobilized on polystyrene. Limited binding to either vitronectin or albumin was detected. Binding to fibrinogen and IgG was blocked by mAb 10E5. Binding to IgG was also blocked by mAb IV.3. Binding to fibronectin, reduced in the presence of mAb 10E5, mAb BIIG4, or the polyclonal antiserum A108 alone, was further reduced by combined 10E5 and BIIG4 or 10E5 and A108. Neither mAb 10E5 nor 6D1 alone blocked adhesion to vWF; however, the combination of 10E5 and 6D1 significantly reduced platelet adhesion to this matrix. Finally, platelet adhesion to the plasma-coated surface was reduced by mAbs 10E5 and BIIG4. These results indicate that multiple adhesion receptors can mediate platelet adhesion to matrix proteins immobilized on surfaces.

Pharmacokinetics of iodamide in normal subjects and in patients with renal impairment.

The pharmacokinetic characteristics of iodamide, a contrast agent for excretion urography, were studied in seven normal subjects and in 15 patients with various degrees of renal impairment. Two different formulations were administered, namely, a 65% solution (iodamide 300) by slow intravenous injection and a 24% solution by slow intravenous (drip) infusion. Both preparations of iodamide exhibited characteristics of an open two-compartment model. In both normal subjects and patients, the contrast agent was excreted almost exlusively in urine. In normal subjects, the pharmacokinetic parameters of both formulations were similar, with a distribution half-life (1/2alpha) of about 3 minutes and a disposition half-life (t1/2beta) of about 69 minutes. An average of 84 per cent of the dose was excreted in urine within 4 hours after administration of iodamide with net renal tubular secretion of about 38 per cent. The binding of iodamide to plasma proteins was negligible, and the extent of biotransformation of iodamide was minimal. In patients with renal impairment, the disposition half-life (t1/2beta) of iodamide ranged from 4.1 to 16.4 hours. Other changes in pharmacokinetic parameters were also seen in patients with renal impairment.

Metabolism of the (+)-, (+/-)-, and (-)-enantiomers of alpha-methylfluorene-2-acetic acid (cicloprofen) in rats.

1. After oral or intraperitoneal administration of (+/-)-[14C]cicloprofen to rats, the peak plasma concentrations of radioactivity and the areas under the plasma concentration/time curves did not increase proportionally with dose; total urinary and faecal excretions of radioactivity did increase with dose, suggesting saturation of plasma protein binding of drug and faster elimination of unbound drug at higher doses. 2. [14C]Cicloprofen and its metabolites were eliminated mainly via biliary excretion. Ratios of faecal to urinary excretion ranged from 2 to 3 and depended on dose administered. 3. Rats with cannulated bile ducts excreted the drug almost exclusively in bile, whereas intact rats excreted up to 32% of the dose in urine in 6 days, suggesting that [14C]cicloprofen or its metabolites or both undergo extensive enterohepatic recirculation in the rats. 4. The major metabolites of [14C]cicloprofen excreted in urine or bile were the 7-hydroxy, 9-hydroxy-, 7,9-dihydroxy-, and 9-hydroxy-9-methoxy-derivatives and their glucuronide or sulphate conjugates. 5. The (+)-enantiomer of [14C]cicloprofen was hydroxylated and excreted by rats at a faster rate than its (-)-antipode; no qualitative stereoselective metabolism of the individual enantiomers of [14C]cicloprofen was observed.

Human serum protein binding of cephalosporin antibiotics in vitro.

The published values for serum protein binding of antibiotics vary considerably depending upon the method and experimental conditions used. A rapid, simple, and standardized ultrafiltration procedure for determination of the serum protein binding of antibiotics has been developed and used to compare the binding characteristics of four marketed cephalosporins. The human serum protein binding of cephradine, cephalexin, cephalothin, and cefazolin at 37 degrees C. and physiological pH (7.4) was found to be 13.8, 12.4, 71.2, and 89.2 per cent, respectively. These values fall within the range of published values for these antibiotics.

Inversion of optical configuration of alpha-methylfluorene-2-acetic acid (cicloprofen) in rats and monkeys.

A simple and sensitive radiometric method to determine the individual enantiomers of cicloprofen has been developed. 14C-Cicloprofen was converted to its L-leucine diastereoisomers, which were separated by thin-layer chromatography and quantified by measuring the radioactivity in the area corresponding to each individual diastereoisomer. This technique has also been used to measure the enantiomers of unlabeled cicloprofen by condensing with 14C-labeled L-leucine. By using the radiometric method, a unique biotransformation process, the inversion of the (-)-enantiomer of alpha-methylfluorene-2-acetic acid to its (+)-enantiomer, has been demonstrated in the rat and monkey. The rate of (-)- to (+)-inversion was found to be faster in the rat than in the monkey. After single or repeated oral adminstration of the racemic modification or the (-)-enantiomer of cicloprofen to both species, the ratio of (+)- to (-)-enantiomers of cicloprofen in plasma, urine, or bile increased with time. At 5, 22, and 48 hr after oral administration of a single 50-mg/kg dose of the (-)-enantiomer, 14C-cicloprofen in rat plasma contained 20, 50, and 79%, respectively, of the (+)-enantiomer. After receiving the same dose of (-)-enantiomer, monkey plasma contained 16.5% and 32% of (+)-enantiomer at 8 and 24 hr, respectively. After oral administration of a single 50-mg/kg dose of the (+)-enantiomer of 14C-cicloprofen to rats and monkeys, the percentage of (-)-enantiomer in plasma varied from 2 to 15%. Since the administered (+)-enantiomer contained 4% of (-)-enantiomer and the (+)-enantiomer was excreted at a faster rate than its (-)-antipode by rats or monkeys, it is not known whether an occasional small percentage increase of (-)-enantiomer in plasma resulted from the (+)-to-(-) inversion, or from faster elimination of the (+)-enantiomer. Nevertheless, if (+)-to-(-) inversion does occur in these two species, the rate is much slower than for the (-)-to-(+) inversion.

A new contrast medium for cholangio-cholecystography: meglumine iodoxamete.

A preliminary study of 18 patients following a single bolus intravenous injection of 10 to 30 cc. of meglumine iodoxamate (Cholovue), a new contrast medium for cholangio-cholecystography, showed no significant adverse clinical or laboratory effects with 10 to 20 cc., and only transient, minor changes with 30 cc. Early and persistent visucalization of the subsegmented and major bile ducts and the gallbladder was obtained. Good to excellent opacification was obtained in all cases with doses ranging between 0.11 cc./kg. (19.7 mg. iodine) to 0.59 cc./kg. (108 mg. iodine). Meglumine iodoxamate appears to be highly effective agent for cholangio-cholecystography.