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The venous bubble load in the body after diving may be used to infer risk of decompression sickness (DCS). Retrospective analysis of post-dive bubbling and DCS was made on seven studies. Each of these investigated interventions, using an 18 meters of sea water (msw) air dive profile from Royal Navy Table 11 (Mod Air Table), equivalent to the Norwegian Air tables. A recent neurological DCS case suggested this table was not safe as thought. Two-hundred and twenty (220) man-dives were completed on this profile. Bubble measurements were made following 219 man-dives, using Doppler or 2D ultrasound measurements made on the Kisman-Masurel and Eftedal-Brubakk scales, respectively. The overall median grade was KM/EB 0.5 and the overall median maximum grade was KM/EB 2. Two cases of transient shoulder discomfort ("niggles") were observed (0.9% (95% CL 0.1% - 3.3%)) and were treated with surface oxygen. One dive, for which no bubble measurements were made, resulted in a neurological DCS treated with hyperbaric oxygen. The DCS risk of this profile is below that predicted by models, and comparison of the cumulative incidence of DCS of these data to the large dataset compiled by DCIEM [1, 2] show that the incidence is lower than might be expected.

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Lidocaine is the most extensively studied substance for adjuvant therapy in neurological decompression illness (DCI), but results have been conflicting. In this retrospective cohort study, we compared 14 patients who received adjuvant intravenous lidocaine for neurological decompression sickness and cerebral arterial gas embolism between 2001 and 2011 against 21 patients who were treated between 1996 and 2001 and did not receive lidocaine. All patients were treated with hyperbaric oxygen (HBO2) therapy according to accepted guidelines. Groups were comparable for all investigated confounding factors, except that significantly more control patients had made an unsafe dive (62% vs. 14%, p = 0.007). Groups had comparable injury severity as measured by Dick and Massey score (lidocaine 2.7 +/- 1.7, control 2.0 +/- 1.6), an adapted version of the Dick and Massey score, and the Blatteau score. Number of HBO2 sessions given was comparable in both groups (lidocaine 2.7 +/- 2.3, control 2.0 +/- 1.0). There was neither a positive nor a negative effect of lidocaine on outcome (relative risk for objective neurological signs at follow-up in the lidocaine group was 1.8, 95% CI 0.2-16). This is the first retrospective cohort study of lidocaine in neurological DCI. Since our study is under-powered to draw definitive conclusions, a prospective multicenter study remains the only way to reliably determine the effect of lidocaine in neurological decompression illness.

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BACKGROUND: Symptoms of neurological decompression incidents (DCS/AGE) can be severe or mild. It is unknown if these differences of symptom presentation represent different clinical entities or if they represent just the spectrum of DCS/AGE. METHODS: 267 cases with DCS/AGE were compared retrospectively and classified into two subgroups, the Type A-DCS/AGE for cases with a severe and often stroke-like symptomatology and the Type B-DCS/AGE for those with milder and sometimes even doubtful neurological symptoms. The main outcome measures were the number of hyperbaric treatments (HTs) needed and the clinical outcome. RESULTS: 42 patients with DCS/AGE were classified as Type A- and 225 patients met the criteria for a Type B-DCS/AGE. Patients with Type A-lesions were more severely affected, needed more hyperbaric treatments and had a less favorable outcome than patients with the Type B-variant. CONCLUSIONS: The Type A- and the Type B-DCS/AGE are likely to be different entities with better clinical outcome in the Type B-variant and possibly significant differences in the underlying pathophysiologies of both variants. Future studies with a particular focus on the up to now inadequately investigated Type B-DCS/AGE are necessary to elucidate such differences in the pathophysiology.

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Neurological complications are common in recreational divers diagnosed with decompression illness (DCI). Prior reports suggest that hemoconcentration, with hematocrit values of 48 or greater, increase the risk for more severe and persistent neurological deficits in divers with DCI. Herein we describe our experience with neurological DCI and hematocrit values in a large series of consecutively treated divers. We performed a retrospective chart review of 200 consecutive recreational divers that received treatment for DCI. Standard statistical analyses were performed to determine if there were any significant relationships between diving-related or demographic parameters, neurological manifestations, and hematocrit. In 177 of the 200 divers (88.5%), at least one manifestation of neurological DCI (mild, moderate, or severe) was present. The median hematocrit value was 43, for both male and female divers, with a range of 30 to 61. Hematocrit values did not correlate with diver age or level of diving experience. In male divers, the hematocrit did not correlate with neurological symptoms, including the sub-group with values of 48 or greater. In contrast, female divers with hematocrit values of 48 or greater were significantly more likely to develop motor weakness (p=0.002, Fisher's exact test) and an increased number of severe sensory symptoms (p=0.001, Kendall's tau statistic). Neurological complications are common in recreational divers treated for DCI. Hematocrit values of 48 or higher were correlated with the presence of motor weakness and severity of sensory symptoms in female divers. The hematocrit did not correlate with neurological DCI in male divers.

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Decompression illness (DCI) is a potentially life-threatening disease, often requiring hyperbaric oxygen therapy (HBO2) for symptom resolution. Once treated, current guidelines recommend an observation period of at least six hours for patients with neurological symptoms in case of relapse. Surveys have shown a symptom relapse rate as high as 38.5%, with half of those occurring in the first twenty-four hours. We propose that a short-term observation unit (OU) would be an ideal setting for these patients to be monitored. To evaluate this, we did a retrospective study of patients presenting with DCI at a major hyperbaric facility. One hundred and two consecutive patients were evaluated with DCI diagnosis and receiving HBO2. Forty-two (41.2%) patients had neurological sequelae; ten required more than one treatment for refractory symptoms or relapse. Thirty-eight of the forty-two patients received up to three treatments, which can be done within the time requirements of short-term observation. We conclude that OUs would provide a safe and efficient disposition for patients after receiving HBO2.

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Diving is a high-risk sport. There are approximately between 1 to 3 million recreational scuba divers in the USA (with over a quarter-million learning scuba annually); there are about 1 million in Europe and over 50,000 in the United Kingdom. In this population 3-9 deaths/100,000 occur annually in the US alone, and those surviving diving injuries far exceeds this. Diving morbidity can be from near-drowning, from gas bubbles, from barotrauma or from environmental hazards. In reality, the most common cause of death in divers is drowning (60%), followed by pulmonary-related illnesses. The mean number of annual diving fatalities in the USA from 1970 to 1993 was 103.5 (sd 24.0) and the median was 106. This article will focus primarily upon pressure effects on the health of a diver. There are two principle ways pressure can affect us: by direct mechanical effects and by changing the partial pressures of inspired gases. Dysbarism is a general term used to describe pathology from altered environmental pressure, and has two main forms: barotrauma from the uncontrolled expansion of gas within gas-filled body compartments and decompression sickness from too rapid a return to atmospheric pressure after breathing air under increased pressures. Greater than 90% of the human body is either water or bone, which is incompressible; the areas directly affected by pressure changes thus are those that are filled with air or gas. These sites include the middle ear, the eustachian tube, the sinuses, the thorax, and the gastrointestinal tract. Air in these cavities is compressed when the ambient pressure rises because the pressure of inhaled air must equilibrate with the ambient pressure.

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High-pressure neurological syndrome (HPNS) is a condition encountered in diving beyond a depth of 100 m. Manifestations include headache, tremor, myoclonus, neuropsychiatric disturbances and EEG changes. Convulsions are seen only in experimental animals. Most of the changes are reversible on surfacing but some such as memory disturbances may linger on for long periods. Excessive atmospheric pressure is the most important factor in the pathogenesis of HPNS. Neurotransmitter changes occur of which serotonin appears to be a more likely mediator because of the resemblance of HPNS to serotonin syndrome. Anesthetics and anticonvulsants have been used in experimental animals but are unsuitable for use in human divers. Breathing gas mixtures such as heliox have enabled the extension of depth of diving without HPNS. Use of 5-HT1A receptor antagonists may provide an interesting approach to prevention of HPNS.

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