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Biomedical subjects

R E Moon

Publications and source records attributed to R E Moon.

At least 19 recordsLinked to original sources
PubMed1992

Urinary vasopressin and aldosterone and plasma volume during a saturation dive to 450 m.

Urinary vasopressin (VP), aldosterone (ALDO), osmotic substances, sodium excretion, and plasma volume were assessed in 4 healthy male divers during 2 predive control days, 2 compression days, 6 days at 46 atm abs, and 26 days of decompression with stops at 37 and 27 atm abs. At pressure the ambient gas was trimix (0.5 atm abs O2:5% N2:remainder He). All urine was collected throughout the dive. Samples were divided into daytime (0700-1900) and nighttime (1900-0700). Indocyanine green dye dilution was used to determine plasma volume at predive 1, 46, and 24 atm abs. In agreement with previous dives at 31 atm abs, there was a decrease in VP excretion during compression lasting until return to 1 atm abs (P less than 0.05). Also similar to the shallower dives at 31 atm abs, the normal diurnal pattern of VP excretion, daytime higher than nighttime (P less than 0.05), disappeared at pressure. Urine osmolality showed alterations compatible with responses to VP. In contrast to previous studies at 31 atm abs, but in agreement with a previous study at 49.5 atm abs, there was no sustained increase in urinary ALDO excretion and only a transient natriuresis during the compression phase, followed by a reduced sodium excretion. In confirmation of earlier conclusions from indirect evidence, direct measurements of plasma volume indicated a reduction of about 20% (P less than 0.05) at 46 atm abs which remained reduced after decompression to 24 atm abs.

Adult↗
PubMed1992

Platelet count in deep saturation diving.

Platelet counts were measured in 10 divers during the course of 4 experimental deep dives (450 and 600 m) and different anticoagulants were tested. The use of sodium citrate as an anticoagulant was associated with artifactual thrombocytopenia, whereas ethylenediaminetetraacetic acid proved to be satisfactory. During one of the dives (450 m) the use of fluorocarbon to remove excess dissolved inert gas before decompression of the samples was systematically tested. Mean platelet count decreased from 272,600 +/- 29,400 mm-3 (mean +/- SD) on Day 7 (450 m) to 177,700 +/- 26,400 mm-3 on Day 12 (360 m). Platelet count had recovered to 209,900 +/- 20,700 mm-3 at the time of surfacing. Mean hematocrit (expressed in percent) increased from 44.7 +/- 2.2 predive to 59.4 +/- 2.0 on Day 7 (450 m) to 40.9 +/- 2.8 at the time of surfacing. These changes were statistically significant (P less than 0.05). Platelet counts on samples that had been degassed with fluorocarbon were not different from samples that had been decompressed without degassing.

Citrates↗
PubMed1992

Renal responses during a dry saturation dive to 450 msw.

Four subjects were compressed to a simulated depth of 450 msw (46 bar) for 37 days in the main research chamber of the German underwater simulator diving facility at the GKSS Research Center, Geesthacht. The ambient gas was trimix. Urine was collected at 0700, 1300, and 1900 h each day for analysis of Na+, K+, volume, osmolality, and creatinine. Urine, antidiuretic hormone (ADH), and aldosterone were analyzed separately. Daily fluid, Na+, and K+ intake were analyzed throughout the dive. The aim of the investigation was to confirm the existence of a diuresis and natriuresis which had been observed in earlier saturation dives to 31 atm abs using He-O2. A significant diuresis was observed during compression despite a decrease in fluid intake. After compression the diuresis decreased somewhat but remained significantly above precompression control levels during the entire hyperbaric exposure. No significant change in fluid intake was observed. Daily Na+ and K+ excretion increased significantly during compression, which was accompanied by a significant increase in nocturnal excretion of Na+ and K+. Daily intake of Na+ and K+ decreased throughout the dive. Daily urine ADH decreased immediately upon compression and was associated with a parallel decrease in urine osmolality. In contrast, urinary aldosterone excretion exhibited no change during the dive despite the increase in Na+ and K+ excretion and decrease in Na+ intake.

Aldosterone↗
PubMed1992

Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts.

We reviewed over 220 cases of acute carbon monoxide (CO) poisoning and now report on 17 patients whose poisoning occurred from the indoor use of propane-fueled forklifts. All patients in this series presented with neurologic symptoms or persistent headache and were given hyperbaric oxygen to resolve their symptomatology. We investigated the concentration of CO in the exhaust emissions of 12 propane-fueled forklifts used in various workplaces in our location. The average CO concentration in the exhaust during engine idling was 36,000 parts per million (3.6%). This value decreased slightly to 30,000 ppm (3.0%) at working engine speed. Measurements of exhaust flow indicate CO production rates of approximately 60 liters per minute at working engine speed. These quantities of CO constitute a significant occupational exposure risk to workers using propane-fueled forklifts in unventilated indoor environments.

Acute Disease↗
PubMed1991

Extubation after transsternal thymectomy for myasthenia gravis: a prospective analysis.

Recommendations concerning postoperative extubation after thymectomy for myasthenia gravis are presently based upon retrospective chart reviews. We present the results of a prospective investigation of time to extubation after thymectomy for 14 patients over a 12-month period based upon a protocol that included preoperative immunologic therapy, combined epidural and general anesthesia, postoperative epidural narcotic analgesia, and a standardized approach to discontinuation of ventilatory support. After a neurologist took measures to optimize preoperative neuromuscular function, all 14 patients received agents to produce lumbar epidural anesthesia and light general anesthesia. Muscle relaxants were avoided in all but one patient. Postoperative analgesia was initially maintained with epidural hydromorphone, then therapy was switched to patient-controlled intravenous morphine sulfate. Criteria for weaning from mechanical ventilation, first measured at the end of anesthesia, were partial pressure of oxygen (arterial) greater than or equal to 90 mm Hg (fraction of inspired oxygen = 0.40), partial pressure of carbon dioxide (arterial) less than or equal to 50 mm Hg, pH greater than or equal to 7.30, and respiratory rate less than or equal to 30 breaths/min. If these criteria were not met, ventilatory support was continued postoperatively with intermittent mandatory ventilation, and the patient was weaned gradually from this support. Criteria for extubation included meeting the criteria for weaning, vital capacity greater than or equal to 10 mL/kg, and inspiratory pressure better than -30 cm H2O. Criteria for reintubation included tachypnea (respiratory rate greater than 40 breaths/min), respiratory acidosis not due to narcotics, or vital capacity less than or equal to 8 mL/kg. The mean time to extubation was 9 hours (range, 0.75 to 25 hours). Mean preoperative vital capacity was 2.59 +/- 0.64 L (range, 1.90 to 4.20), which decreased approximately 50% to 1.19 +/- 0.39 L (range, 0.70 to 2.0) at the time of extubation. No patient required reintubation. Half of the patients required postoperative anticholinesterase therapy based upon serial neurologic examinations; there were no instances of cholinergic crisis. Thirteen patients returned to the ward on the first postoperative day, and one on the second day. Thirteen patients preferred epidural analgesia to patient-controlled analgesia. The time to extubation and average length of stay in an intensive care setting were markedly reduced compared to those reported in previous retrospective studies. We conclude that a multidisciplinary approach that optimizes neuromuscular function and decreases poststernotomy pulmonary insult will shorten the time to extubation and decrease the length of stay in the intensive care or recovery room after thymectomy.

Adolescent↗
PubMed1991

Venous gas emboli and complement activation after deep repetitive air diving.

Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.

Adult↗
PubMed1990

Barotrauma and air embolism in hyperbaric oxygen therapy.

A 69-year-old woman underwent hyperbaric oxygen therapy because of a nonhealing ulcer of her foot. During decompression, she developed a left-sided hemiplegia and confusion. Recompression resulted in transient neurologic improvement, but she eventually became comatose. Ventricular dysrhythmias developed and she died without regaining consciousness 17 h after onset of symptoms. An autopsy revealed diffuse interstitial pulmonary fibrosis with severe paracicatricial emphysema, chronic interstitial inflammation, and chronic bronchitis with abundant intrabronchial mucus. There was extensive multifocal ischemic injury of the cerebral cortex. The hippocampi, basal ganglia, and cerebellum were spared. Scattered acute myofiber necrosis was present in the heart. Clinical presentation and autopsy findings strongly support the diagnosis of air embolism and illustrate a potential risk of hyperbaric oxygen therapy in patients with preexisting pulmonary disease.

Aged↗
PubMed1990

Cerebral oxygen availability by NIR spectroscopy during transient hypoxia in humans.

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.

Adult↗
PubMed1990

Initial table treatment of decompression sickness and arterial gas embolism.

This descriptive, nonrandomized, multicenter-based study compares the treatment outcomes of two major categories of recompression treatment tables for recreational sport SCUBA divers suffering from decompression sickness and/or arterial gas embolism. Stratified and logistic regression analyses were used to compare the enhanced tables, which use pressures of 165 fsw (feet of salt water) or 60 fsw with extended recompression time, to the regular tables, which use pressures of 60 fsw or less without extended recompression time. A total of 113 cases were treated with enhanced tables, 54 being successes. A total of 214 cases were treated with regular tables, 135 being successes. The final logistic statistical model after adjusting for confounding factors found a significant improvement in successful treatment outcomes for divers treated with tables that use pressures of 60 fsw or less without extended recompression time (OR = 0.47, 95% CI = 0.28-0.78).

Adult↗
PubMed1990

Hyperbaric medicine: an integral part of trauma care.

In conclusion, HBO constitutes an important therapeutic tool in managing a variety of syndromes associated with trauma and is thought to possess potential benefits for the management of others. Because its therapeutic efficacy and limitations are as yet incompletely understood and appreciated, continuing research is warranted. This article provides a discussion of these conditions and applications as well as descriptions of the basic physics of gas behavior, the principle of the physiologic basis of HM, the general manner of clinical application of pressure and oxygen, and the special set of problems encountered when providing sophisticated medical care in the hyperbaric environment. Ultimately, this article encourages the highly motivated trauma anesthesiologist to enhance his or her contribution to and active participation in the field of HM.

Anesthesia↗
PubMed1989

Patent foramen ovale and decompression sickness in divers.

30 patients with a history of decompression sickness were examined for the presence of patent foramen ovale by bubble contrast, two-dimensional echocardiography and colour flow doppler imaging. With bubble contrast, 11 (37%) of the patients had right-to-left shunting through a patent foramen ovale during spontaneous breathing. 61% of a subset of 18 patients with serious signs and symptoms had shunting. This number was significantly higher than the 5% prevalence seen with the same diagnostic technique in 176 healthy volunteers. The presence of patent foramen ovale seems to be a risk factor for the development of decompression sickness in divers.

Acute Disease↗
PubMed1989

Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review.

Carbon monoxide (CO) is the leading cause of death due to poisoning. Although uncommon, CO poisoning does occur during pregnancy and can result in fetal mortality and neurological malformations in fetuses who survive to term. Uncertainty arises regarding the use of hyperbaric oxygen (HBO) as a treatment for the pregnant patient because of possible adverse effects on the fetus that could be induced by oxygen at high partial pressures. While the dangers of hyperoxia to the fetus have been demonstrated in animal models, careful review of animal studies and human clinical experience indicates that the short duration of hyperoxic exposure attained during HBO therapy for CO poisoning can be tolerated by the fetus in all stages of pregnancy and reduces the risk of death or deformity to the mother and fetus. A case is presented of acute CO poisoning during pregnancy that was successfully treated with HBO. Recommendations are suggested for the use of HBO during pregnancy.

Adolescent↗
PubMed1989

Effect of epidural lidocaine on spinal cord blood flow.

The effect of epidural lidocaine on spinal cord blood flow (SCBF) was measured in mongrel dogs. Spinal evoked potentials were used to measure spinal cord conduction and enabled us to time the measurement of SCBF associated with maximum reduction in latency and amplitude of spinal evoked potentials produced by instillation of 5 ml of 2% lidocaine in the epidural space. We used the radioactive microsphere technique to quantitate SCBF in the cervical, upper thoracic, lower thoracic, and lumbar regions of the spinal cord. A narcotic/relaxant technique was used to eliminate SCBF changes associated with other anesthetic agents. Other parameters known to affect SCBF were kept constant and within normal physiologic values. As compared with saline solution controls, there were significant decreases in SCBF in all the four areas of spinal cord in animals given epidural lidocaine, most marked in the lumbar area.

Anesthesia, Epidural↗
PubMed1988

Neuroimaging of scuba diving injuries to the CNS.

Diving accidents related to barotrauma constitute a unique subset of ischemic insults to the CNS. Victims may demonstrate components of arterial gas embolism, which has a propensity for cerebral involvement, and/or decompression sickness, with primarily spinal cord involvement. Fourteen patients with diving-related barotrauma were studied with MR imaging of the brain and spinal cord and with CT of the brain. In four patients with presumed cerebral gas embolism, cranial MR was abnormal in three patients while CT was abnormal in only one. Twelve patients had decompression sickness and spinal cord symptoms. MR documented spinal cord abnormalities in three patients. However, scans obtained early in our study were frequently limited by technical constraints. MR of the brain is more sensitive than conventional CT scanning techniques in detecting and characterizing foci of cerebral ischemia caused by embolic barotrauma to the CNS. Although spinal MR may be less successful in the localization of spinal cord lesions related to decompression sickness, these lesions were previously undetectable by other neuroimaging methods.

Adolescent↗
PubMed1986

Pulmonary gas exchange in humans exercising at sea level and simulated altitude.

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Adult↗