Effect of ambient temperature on the risk of decompression sickness in surface decompression divers.

BACKGROUND: Several studies have noted an apparent increase in decompression sickness (DCS) risk with surface decompression diving in warm water or with hot water suits (Van Der Aue 1951, Shields 1986, Leffler 1997), but did not perform statistical tests to control for the pressure-time profile. METHODS: The 1986 data, including 73 DCS cases out of 14,891 dives, were analyzed by Mantel-Haenszel analysis to control for depth and bottom time. Dive profiles from the 1951 U.S. Navy report, including 147 DCS cases from 1507 dives, were analyzed with logistic regression analysis to control for depth, bottom time, and aspects of the decompression profile. RESULTS: In the 1986 data, hot water suits, as compared with passive thermal protection, were associated with an odds ratio (OR) of 1.81 (95% confidence interval, CI = 0.96 to 3.42) for DCS. In the 1951 data, each 10 degree C increase in water temperature yielded an OR for DCS of 1.96 (95% CI = 1.33 to 2.90). The interaction of temperature and bottom time suggested that the effect was more pronounced in shorter dives. Among DCS cases, the OR for type 2 symptoms with hot water suits was not significant in the 1986 data (p = 0.18). In the 1951 data, the probability of type 2 symptoms among DCS cases was better explained by the dive profile than by the temperature. Thermal effects on gas physics, metabolism, hemostasis, and nociception were reviewed. CONCLUSION: Surface decompression divers who are warm at depth face an increased risk of DCS. Vasodilatation in warm divers may result in more rapid on-gassing of tissues with short time constants. A full evaluation of DCS risk should consider physiological and physical effects of ambient temperature.

Median neuropathy at the wrist: diagnostic utility of clinical findings and an automated electrodiagnostic device.

Clinical findings have limited value in predicting electrophysiologically confirmed median neuropathy at the wrist (MNW). To determine the value of clinical findings and an automated electrophysiologic neurodiagnostic device (AEND) in diagnosing MNW, we studied two groups of 75 consecutive patients (an initial group and a validation group, 150 total) referred to an academic electrophysiology laboratory for upper extremity complaints. The definitive standard for MNW was the neurologist's diagnosis after formal clinical and electrodiagnostic evaluation. The neurologist was blinded to the results of the AEND (NC-Stat, NeuroMetrix, Inc). In the validation group, the AEND yielded a distal motor latency (DML) in 97% of hands with a conventional motor response, and the correlation of the AEND DML with the conventional DML was 0.94 (P < 0.001). Of 248 symptomatic hands, the neurologist diagnosed 117 (47%) with MNW. At 90% specificity, the AEND DML had a sensitivity of 86% for MNW. Age, body mass index, sensory symptoms in digits 1 to 3, and nocturnal awakening were independent clinical predictors of MNW. Each 1-msec increase in the adjusted AEND DML was independently associated with an OR of 298 (95% confidence interval, 40 to 2233) for MNW. Each 1-msec increase in the F-wave latency was independently associated with an OR of 2.6 (95% confidence interval, 1.3 to 4.9) for MNW. Compared with a model based solely on clinical variables, an algorithm including symptom variables plus the AEND DML had an odds ratio for correct diagnostic classification of 6.3 (95% confidence interval, 3.8 to 12.3). The sensitivity at 90% specificity improved from 40% for the clinical model to 86% for the model with DML. A practical method for integrating clinical and electrophysiologic findings to assess the risk of MNW was proposed. This method correctly stratified 79% of control and MNW patients into very low- and high-risk groups, respectively. We concluded that MNW diagnosis is significantly improved with an AEND.

Occupational asthma and contact dermatitis in a spray painter after introduction of an aziridine cross-linker.

A 23-year-old spray painter developed contact dermatitis and respiratory difficulty characterized by small airways obstruction shortly after the polyfunctional aziridine cross-linker CX-100 began to be used in his workplace as a paint activator. The symptoms resolved after he was removed from the workplace and was treated with inhaled and topical steroids. Painters may have an increased risk of asthma due to exposure to a variety of agents, such as isocyanates, alkyd resins, and chromates. This case illustrates the importance of using appropriate work practices and personal protective equipment to minimize exposure. Occupational asthma is diagnosed by a history of work-related symptoms and exposure to known causative agents. The diagnosis is confirmed by serial pulmonary function testing or inhalational challenge testing. The risk of asthma attributable to occupational exposures is probably underappreciated due to underreporting and to inappropriate use of narrow definitions of exposure in epidemiologic studies of attributable risk.

Glucosamine, chondroitin, and manganese ascorbate for degenerative joint disease of the knee or low back: a randomized, double-blind, placebo-controlled pilot study.

OBJECTIVE: A 16-week randomized, double-blind, placebo-controlled crossover trial of a combination of glucosamine HCl (1,500 mg/day), chondroitin sulfate (1,200 mg/day), and manganese ascorbate (228 mg/day) in degenerative joint disease (DJD) of the knee or low back was conducted. METHODS: Thirty-four males from the U.S. Navy diving and special warfare community with chronic pain and radiographic DJD of the knee or low back were randomized. A summary disease score incorporated results of pain and functional questionnaires, physical examination scores, and running times. Changes were presented as a percentage of the patient's average score. RESULTS: Knee osteoarthritis symptoms were relieved as demonstrated by the summary disease score (-16.3%; p = 0.05), patient assessment of treatment effect (p = 0.02), visual analog scale for pain recorded at clinic visits (-26.6%; p = 0.05) and in a diary (-28.6%; p = 0.02), and physical examination score (-43.3%; p = 0.01). Running times did not change. The study neither demonstrated, nor excluded, a benefit for spinal DJD. Side effect frequency was similar to that at baseline. There were no hematologic effects. CONCLUSIONS: The combination therapy relieves symptoms of knee osteoarthritis. A larger data set is needed to determine the value of this therapy for spinal DJD. Short-term combination therapy appears safe in this setting.

Recompression treatments during the recovery of TWA Flight 800.

After the crash of TWA flight 800, U.S. Navy (USN) and civilian divers recovered the aircraft and the victims' remains from 117 feet of sea water (fsw). Safety information was gathered from observations, interviews, and medical and diving records. Of 752 dives employing surface decompression using oxygen (SDO2), 10 divers required recompression treatments, mainly for type 2 decompression sickness (DCS). When using hot water heating, the DCS risk was high until the dive profiles were modified. Divers made nearly 4,000 no-decompression scuba dives. In eight scuba divers and one tender treated with recompression, the diagnoses included DCS (3), arterial gas embolism (AGE) (1), and vascular headache (2). All USN divers recovered fully. The experience is consistent with previous work suggesting an increase in DCS risk in warmer SDO2 divers. The USN SDO2 tables can be made safer by limiting bottom time and extending decompression. Even under stressful conditions, rapid ascents resulting in AGE are uncommon. Vascular headaches can mimic DCS by responding to oxygen.

NASPE Young Investigator Awardee-1993. Computer model of the atrioventricular node predicts reentrant arrhythmias.

INTRODUCTION: Following atrial premature beats, the AV node may exhibit sustained reentrant tachyarrhythmias, isolated echo beats, or discontinuities in the recovery curve (the plot of conduction time versus atrial cycle length). A computer model was used to examine the hypothesis that spatial variation of AV nodal passive electrical resistance may account for these phenomena. METHODS AND RESULTS: A computer model of a rectangular lattice of electrotonically linked elements whose ionic kinetics simulated nodal ionic flux was developed. The model showed that there exists a resistance value that minimizes the effective refractory period, because high resistance prevents depolarization of distal elements, while low resistance allows leakage of depolarizing current by electrotonic transmission, preventing activation of proximal elements. High resistances stabilized reentry by slowing conduction. Simulations incorporating equal resistance values between elements predicted increased AV nodal conduction times with increasing prematurity of atrial impulses. A model with a gradual change in resistance between fibers produced discontinuities and tachycardia, but not both simultaneously. Uniform anisotropy produced preferential transverse block, leading to echo beats and "fast-slow" tachycardia, but not recovery curve discontinuities. Nonuniform anisotropy could produce reentry, but tachycardia often occurred without discontinuities. Dividing the lattice into two electrotonically linked parallel pathways with different resistance values ("dual pathway model") predicted recovery curve discontinuities, echo beats, and tachycardia. At critical atrial cycle lengths, only the (high resistance) slow pathway conducted antegradely, while the fast pathway conducted retrogradely, to generate the typical "slow-fast" tachycardia. Responses of the dual pathway model to ablation were consistent with clinical data, including the previous observation of a decrease in fast pathway effective refractory period after slow pathway ablation. CONCLUSION: Differences in passive electrical resistance of electronically linked dual pathways within the AV node may account for functional longitudinal dissociation, reentrant arrhythmias, and responses to catheter ablation therapy.

Rate-related and autonomic effects on atrioventricular conduction assessed through beat-to-beat PR interval and cycle length variability.

INTRODUCTION: Atrioventricular (AV) conduction time varies on a beat-by-beat basis in response to the influences of cardiac efferent autonomic activity and rate-dependent electrical recovery processes. The goals of this study were to distinguish these effects on AV conduction time and to compare the variability in sinoatrial and AV nodal function. METHODS AND RESULTS: The PR interval on the surface ECG served as an index of AV conduction time in this study of 14 adult human subjects undergoing a random interval breathing protocol. P and R waves were located by a template-matching algorithm. Spectral analysis allowed frequency-domain comparisons between PR and RR interval variability. Spectra of PR and RR intervals had similar power distributions, although the power of the RR interval spectra was much greater. Autonomic blockade with atropine plus propranolol reduced the power of both spectra. Standing significantly decreased the spectral power from 0.15 to 0.5 Hz for PR and RR spectra, and introduced a peak near 0.1 Hz in the mean PR and RR spectra, although the latter finding was significant only for the RR interval spectra. Propranolol had no significant effects on the PR and RR interval spectra. Linear regression analysis allowed quantification of the autonomic and recovery effects on AV conduction and showed which effect predominated. Simple linear regression confirmed in adults a previous finding in children that conduction time may be either positively or negatively correlated with cycle length. By multiple regression and transfer function analysis, the inverse relation seen in some subjects was attributed to the effect of recovery from the preceding cycle. With the preceding recovery period accounted for, the conduction time and cycle length of the current beat were positively correlated, presumably due to the parallel autonomic effects on the sinoatrial and AV nodes. The magnitude of the recovery effect predicted by the regression analysis was similar to published values. CONCLUSION: A noninvasive evaluation of the surface ECG can be used to compare variability in AV conduction time and cycle length and characterize the effects of autonomic efferent activity and rate-related recovery on AV nodal function.

A comparative study of subcutaneously administered terbutaline and epinephrine in the treatment of acute bronchial asthma.

Terbutaline, a new bronchodilator drug reported to have selective affinity for beta 2-adrenergic receptors, was compared with epinephrine in the treatment of 49 adult subjects with acute bronchial asthma. Under double-blind conditions, 24 subjects received 1.0 mg of terbutaline sulfate, and 25 subjects received 0.5 mg of epinephrine hydrochloride subcutaneously. Spirometric measurements, heart rate, and blood pressure, as well as subjective responses, were recorded prior to, and then at 5, 15, 30, 60, and 120 minutes after administration of the drug. The results indicate that terbutaline is an effective bronchodilator drug in subjects with acute asthma; however, the heart rate rose significantly after administration of terbutaline, with a maximal increase of 25 percent above control. Review of the literature reveals that tachycardia is a consistent finding when subcutaneous doses of terbutaline in excess of 0.25 mg are administered. Stimulation of beta 1-adrenergic receptors in the heart appears to be the most important factor involved in this response. A lesser cardioaccelerator effect was observed after administering epinephrine in a dose producing an equivalent degree of bronchodilatation.