Decompression sickness cases treated with recompression therapy between 1963 and 1998 in Turkey: Review of 179 cases

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1 Decompression sickness cases treated with recompression therapy between 1963 and 1998 in Turkey: Review of 179 cases Akin Savas Toklu 1, Maide Cimsit 1, Senol Yildiz 2, Gunalp Uzun 2, Sefika Korpinar 1, Hakan Sezer 3, Samil Aktas 1 1 Department of Underwater and Hyperbaric Medicine, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey 2 Department of Underwater and Hyperbaric Medicine, Gulhane Military Medical Academy, Haydarpasa Teaching Hospital, Istanbul, Turkey 2 Turkish Naval Forces, Underwater and Salvage Command, Beykoz, Istanbul, Turkey CORRESPONDING AUTHOR: Akin Savas Toklu, M.D. akin@toklu.net ABSTRACT The purpose of this study was to review the cases diagnosed as decompression sickness (DCS) with recompression therapy treament between 1963 and 1998 in Turkey. The records of 179 cases were analyzed for age, gender, type of DCS, presenting signs and symptoms, time to onset of symptoms, time to recompression therapy, recompression table used, total number of treatments and outcomes. The diving depth on the day of injury ranged between 60 and 215 fsw (18 and 65 msw). The symptoms developed during ascent or within 10 minutes after surfacing in 47% of divers and within the first hour in 87% of the divers. The most frequent symptom was sensory loss in the extremities. The dive before the symptoms was a repetitive dive in 50% of the cases and the diagnosis was Type II DCS in 79% of these divers. Most of the divers (84%) received recompression therapy after a delay of more than 12 hours. Healing rate was 68% with the air recompression tables and 86% with the oxygen tables. Repetitive dives were associated with a higher incidence of Type II DCS than single dives (79% and 66%, respectively). The results using recompression tables with oxygen were more successful than the treatment with air tables. INTRODUCTION Decompression sickness (DCS) occurs when there is a rapid decrease in environmental pressure, such as during ascent from a dive, exit from a caisson (compressed tunnel) or fast ascent to altitude. The bubbles formed by the previously dissolved inert gases in blood vessels or tissues play a critical role in the pathophysiology of the disease [1]. DCS can cause a wide variety of symptoms such as pain, skin problems like itching and rashes, neurological symptoms as numbness and tingling, muscular weakness or paralysis, loss of bowel or bladder function, loss of coordination and even collapse or unconsciousness [2]. DCS cases should receive prompt recompression therapy in a hyperbaric chamber after diagnosis is established. The time interval between the onset of DCS and recompression therapy will affect the result of the recompression therapy and the course of the disease [3]. Commercial diving in Turkey began with sponge diving in the 1930s [4,5]. The sponge divers used to learn diving by apprenticeship. They utilized in-water recompression on air in the event of DCS until the Turkish Naval Forces established a recompression unit in the 1960s. At that time, the only land-based recompression chamber that was used for the treatment of DCS was in the Turkish Naval Forces Underwater & Salvage Command. The facility was located in Istanbul, and all DCS cases who required recompression treatment were referred to this facility until the new hyperbaric unit was established in 1984 in Bodrum, where the majority of sponge divers used to live. In 1989, another hyperbaric chamber was established in the Istanbul Faculty of Medicine, Department of Underwater and Hyperbaric Medicine for the treatment of DCS and other indications that require hyperbaric treatment. This study includes DCS cases treated in Copyright 2014 Undersea & Hyperbaric Medical Society, Inc. 217

2 these three recompression chambers between 1963 and The number of hyperbaric centers in Turkey has increased due to private companies opening centers since 1998 [6]. We retrospectively evaluated 179 DCS cases treated at the three hyperbaric facilities listed below between 1963 and 1998 to see the distribution and onset time of the symptoms, the delay in recompression therapy, and types and outcomes of the recompression treatments. Since this study spans a considerable period before the introduction of recent descriptive terminology on decompression disorders, classical terminology for the categorization of decompression sickness will be used throughout. METHODS The source of the data used in this study were records of the patients treated at three hyperbaric facilities in: 1. Turkish Naval Forces Underwater & Salvage Command in Istanbul; 2. Fishery Institute in Bodrum; and 3. Istanbul Faculty of Medicine, Department of Underwater and Hyperbaric Medicine in Istanbul. All facilities had a multiplace double-lock recompression chamber. Usually quick transfer was not possible from the diving site to the recompression chamber because of limited transportation facilities. We evaluated the medical records of 232 DCS cases. Of these, 53 (22%) cases were excluded due to incomplete data. The records of 179 cases who were treated between 1963 and 1998 in the three centers were analyzed for age, gender, type of DCS, presenting signs and symptoms, time to onset of symptoms after surfacing, time to recompression therapy, recompression table used, total number of recompression treatments, and outcomes. Although all the charts included the symptoms, onset time of the symptoms, type of recompression tables, delay in the treatments, some did not contain the details of the neurological examinations. Long-term follow up was not available in any patient. The denominator was 179 while calculating percentages for presence or absence of a condition. The continuous data were presented as mean, median, minimum, maximum and standard deviation (SD). RESULTS The data from 179 DCS cases were analyzed. All of the divers were male, the mean age was 29.6 years (16-57 years). There were 168 (94%) commercial divers and 11 (6%) recreational divers. The diving Table 1. Symptoms observed in divers n percentage sensory loss in the extremities weakness in the extremities pain in the extremities urinary incontinence chest pain paraplegia nausea and vomiting back pain dispnea rectal incontinence dizziness stomach ache skin rash numbness in trunk hemiplegia fainting headache speech disorders subcutaneus emphysema visual disturbance imbalance hearing loss tinnitus blackout convulsion depth on the day of injury ranged between 60 fsw (18 msw) to 215 fsw (65 msw). Fifty divers (28%) had Type I DCS, and 129 (72%) divers had Type II DCS. Type II DCS occurred in 70 of 89 divers (79%) who performed repetitive dives on the day of injury compared with 59 of 80 divers (66%) who had made only a single dive. The mean duration between surfacing and the onset of symptoms was 41 minutes with a range of minutes. The symptoms developed during ascent or within 10 minutes after surfacing in 47% of divers and within the first hour in 87% of the divers. The symptoms observed in the divers are listed in Table 1. After recompression treatment, 41 (23%) divers made a complete recovery. Significant improvements were achieved in 104 cases (%58). There were minimal residual symptoms such as slight weakness, numbness 218 A.S. Toklu, M. Cimsit, S. Yildiz, G. Uzun, et al.

3 and pain in these cases when recompression treatments were stopped. Fourteen (8%) divers had residual symptoms that affected their quality of life, and two divers died. Information about final outcomes could not be reached in 18 cases since they had been referred to hospitals for additional care. The mean delay from initial symptoms to recompression therapy was 47 hours (median: 24 hours), with a range of hours (Figure 1). The healing rate reduced with increased delay to recompression therapy. The complete or partial healing rate was 96% in divers treated in the first 10 hours after the onset of the disease. 74% of cases were treated within 24 hours of the onset of DCS. Of these, 83% had a complete or partial recovery. In divers who were treated more than 24 hours after the onset of DCS the full or partial recovery rate was 80%. In six divers the delay to treatment was greater than seven days. Four of these (57%) experienced significant improvement, with only mild residual symptoms. Divers received a variety of recompression treatments, including U.S. Navy Treatment Table (USNTT) 1A, 2A, 3, 4, 5, 6 and 6A and standard hyperbaric oxygen treatment table (Table 2). The oxygen treatment tables as USNTT 5, 6 and 6A were used after 1980 in 125 cases. Fifty-nine (33%) divers received more than one treatment. While the complete or partial healing rate was 68% after treatment using air tables, it was 86% after the oxygen tables. The information about the use of adjunctive medical treatments such as steroids or intravenous fluids was not sufficient in the charts for evaluation. Nearly one third (n=57, 32%) of the divers had tried in-water recompression on air after injury. Complete and partial healing was observed in 40 of 57 (70%) divers, while this rate was higher (81%) in divers who did not attempt in-water recompression. A few divers were urged to run after injury by other divers. Methods like massaging with olive oil, burying the divers in sand and keeping divers awake were other empirical procedures for managing the symptoms of DCS among sponge divers. Two divers (1.1%) died. Both were commercial divers with type II DCS. There was gross omitted decompression stops in their dive profiles. One diver went to 120 fsw (36 msw) depth four times, with about 40 minutes of bottom time for each dive and surface intervals of less than an hour. The other diver made number of divers _ Figure < 6 hr 7-12 hr hr hr 2-7 d > 7 d The time interval between initiation of symptoms and recompression therapy. Table 1. Recompression tables used in the treament of decompression sickness n % complete or partial recovery USNTT 1A USNTT 2A USNTT USNTT USNTT USNTT USNTT 6A Clinical HBO 2 therapy his last dive as a second dive to a depth of 215 fsw (65 msw) with a bottom time around 20 minutes. The deaths occurred during recompression treatment with USNTT 4. DISCUSSION In this retrospective study, we evaluated 179 divers who received recompression treatment between 1963 and 1998 in Turkey. The vast majority of the divers were commercial divers (94%). Two factors may have affected this distribution. First, the number of recreational divers was not significant until the mid-1970s. Second, sponge divers made up the majority of the diving population in Turkey during the study period, and the DCS rate was very high in these divers due to unsafe diving practices (4). The main purpose for diving A.S. Toklu, M. Cimsit, S. Yildiz, G. Uzun, et al. 219

4 between these two diving groups was different. While the commercial divers were compelled to dive for a living, recreational divers did because they had enough money to do so. This may in part explain why the dive profiles of two groups differed and why commercial divers violated the safe diving limits more frequently. In this study we have classified cases as Type I, Type II and arterial gas embolism. Arterial gas embolism refers to neurologic symptoms which manifest shortly after diving and results from introduction of air into the circulation by pulmonary barotrauma. Divers with musculoskeletal, skin or lymphatic symptoms were classified as Type I DCS and divers with neurologic, cardiorespiratory, audiovestibular symptoms or shock were classified as Type II DCS. Recently, a modification of this terminology, which combines arterial gas embolism and DCS as decompression illness, has been proposed [7]. This new terminology has removed the need to distinguish between cases with arterial gas embolism and Type II DCS. In this study most of the divers had Type II DCS (72%). The most frequent symptom (49.2%) was sensory loss in the extremities. In fact, pain in the extremities has been reported to be the most frequent symptom in DCS [8,9]. In our case series, pain was recorded in 40.8% of the cases. Most probably the majority of divers with complaints of pain alone (Type I DCS) did not seek recompression therapy. Subcutaneous emphysema was reported in four cases. It is possible that some of the cases who received recompression therapy had pulmonary barotrauma. Unless an accompanying pneumothorax presents, pulmonary barotrauma is not a contraindication for recompression therapy. In our study, we found that a significant number of divers (32%) tried in-water recompression on air after injury. All of these divers had serious decompression sickness, except one case, who had Type I DCS. Inwater recompression is the practice of diving back to the previous depth in order to eliminate the gas bubbles that are causing symptoms. It is used if DCS occurs in remote locations, where a recompression chamber is not available for treatment. Since divers symptoms can worsen underwater, they can become unconscious and drown. Because of this, in-water recompression should be attempted only if adequate equipment and educated personal are available. We found that complete or partial healing was lower in divers who attempted in-water recompression compared to divers who did not attempt in-water recompression (70% vs. 81%, respectively). In contrast to general recommendations, our cases used air rather than oxygen for inwater recompression. This may explain the unfavorable outcome of divers who attempted in-water recompression. Repetitive diving is a common practice in commercial divers in Turkey [5]. Turkish sponge divers frequently omit surface intervals between repetitive dives, which increases the risk of DCS. The rate of Type II DCS was higher in the divers who performed repetitive dives on the day of incident. Although we do not know the number of single and repetitive dives that were conducted during the period of this study, we believe that repetitive dives increase the risk of DCS. This study also demonstrated the change from air tables to oxygen tables in recompression treatments. The role of oxygen in the treatment of DCS either at atmospheric or hyperbaric conditions is well established. In our cases the results with recompression tables with oxygen were more successful than the treatment with air tables. Eighteen cases were referred to hospitals probably because they required intensive care or rehabilitation. The hyperbaric units were not hospital-based except the one in the Istanbul Faculty of Medicine. Ideally, it is better to treat severe DCS cases in a recompression chamber located at a hospital, or a hyperbaric unit with continuous hospital support. Most of the cases presented with delay for recompression therapy since the importance of quick transport was not fully understood. For the majority of the cases the time intervals between the onset of symptoms and recompression therapy was more than 10 hours. Those cases were delayed because of geographical factors. The location of dive sites and difficulties encountered during transport indicated the necessity of recompression chambers in remote areas. Currently hyperbaric units are available in those areas. LIMITATIONS There are limitations to our study. Due to the retrospective design of our study, we were unable to obtain all the necessary information from the medical records of all divers, and 22% of cases were excluded due to incomplete data. Secondly, outcome data were not available in 18 divers who were transferred to hospitals. In addition, long-term outcomes of the divers were not available. 220 A.S. Toklu, M. Cimsit, S. Yildiz, G. Uzun, et al.

5 CONCLUSION Divers who attempt in-water recompression on air may have unfavorable outcomes. DCS cases that occur after repetitive dives are more severe. Oxygen recompression tables are more successful than air tables. Delays in the recompression treatment clearly affect prognosis, but recompression treatment should be applied to DCS cases even after long delays. Acknowledgment This paper was supported by the Research Fund of The University of Istanbul, Project Number: Conflict of interest The authors have declared that no conflict of interest exists with this submission. n _ REFERENCES 1. Francis TJR, Mitchell SJ. Pathophysiology of decompression sickness. In: Brubakk AO, Neuman TS, eds. Bennett and Elliott s Physiology and Medicine of Diving, 5th edition. W. B. Saunders Co Ltd; 2003, p Eliott D, Kindwall E. Decompression Sickness. In: Kindwall E, Whelan TW, eds. Hyperbaric Medicine Practice 1st edition. Best Publishing Co. ; 2002, p Ball R. Effect of severity, time to recompression with oxygen, and re-treatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea Hyperb Med. 1993;20: Toklu AS, Cimsit M. Dysbaric osteonecrosis in Turkish sponge divers. Undersea Hyperb Med. 2001;28: Toklu AS, Cimsit M. Sponge divers of the Aegean and medical consequences of risky compressed-air dive profiles. Aviat Space Environ Med. 2009;80: Aktaş S, Toklu AS, Yildiz S, Uzun G. Development of underwater and hyperbaric medicine as a medical specialty in Turkey. Undersea Hyperb Med. 2013;40: Francis TJR, Mitchell SJ. Manifestations of decompression disorders. In: Brubakk AO, Neuman TS, eds. Bennett and Elliott s Physiology and Medicine of Diving, 5th edition. W. B. Saunders Co Ltd; 2003, p Lam TH, Yau KP. Manifestations and treatment of 793 cases of decompression sickness in a compressed air tunneling project in Hong Kong. Undersea Biomed Res. 1998;15: How JH, West D and Edmonds C. Decompression sickness in diving. Singapore Medical Journal. 1976;17:92-7. A.S. Toklu, M. Cimsit, S. Yildiz, G. Uzun, et al. 221