스쿠버 다이빙 합병증, 감압병(잠함병), 비행기 여행, Complications of SCUBA diving, decompression sickness, air travel

감압병(잠함병)은 원래 caisson의 압축된 환경에서 대기압으로 복귀한 후 터널 작업자들 사이에서 1843 년에 처음 발견되었을 때 "caisson disease"으로 기술되었습니다. 감압병(잠함병)을 앓고 있는 노동자들은 때때로 약간의 굽은 자세[19 세기 후반 브루클린 다리 건설 당시의 여성 사회인들에 의해 영향을 받는 자세, 또한 Grecian Bend로 알려져 있음]로 걷기 때문에 "the bends"라는 용어가 이 질병에 자주 적용됩니다.

네이버 지식백과 https://terms.naver.com/entry.nhn?docId=3353636&cid=40942&categoryId=32095

다이버가 하강하여 압력이 증가한 상태에서 공기를 흡입하면 Henry의 법칙에 따라 조직에 산소와 질소 양이 증가합니다. 다이버가 표면으로 돌아 오면 조직의 가스 장력의 합이 주변 압력을 초과하여 기포 형태로 조직에서 자유 가스가 방출될 수 있습니다. 기포 형성의 위치는 조직 특성에 다소 의존적입니다. 방출된 기포는 혈관을 차단하거나 조직을 파열 또는 압축하거나 응고 및 염증성 cascade를 활성화시켜 장기 기능을 변화시킬 수 있습니다. 이 기포의 부피와 위치에 따라 증상이 발생하는지 여부가 결정됩니다.

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위험 인자들로는 1) Right-to-left shunt 2) air travel 3) gender 4) additional factors들이 있고 드라마 하우스3 18편에서 나오는 장면은 스쿠버 타이빙 직후 비행기를 탄 환자에서 발생한 decompression sickness입니다.

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스쿠버 다이빙 직후 비행기로 여행하는 환자는 기내 감압병 (developing decompression sickness (DCS) in-flight) 발병 위험이 높아집니다. 따라서 많은 전문가들은 다이빙 후 비행 전 대기 시간을 제안하지만 연구는 제한적이며 최적의 대기 시간을 알 수는 없습니다. 우리는 승객이 하루에 한 번만 다이빙을 한다면 비행하기 전에 12 시간을 기다려야 한다고 동의합니다. 여러 번의 다이빙에 참여한 사람 또는 감압 정지가 필요한 사람은 비행하기 전에 최대 48 시간 동안 대기하는 것을 고려해야 합니다.

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참고문헌 UpToDate 219.08.13

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Symptoms — Approximately 75 percent of patients with decompression sickness develop symptoms within one hour and 90 percent within 12 hours of surfacing; only a small number become symptomatic more than 24 hours after diving. Scuba divers should wait 12 to 48 hours before flying on a commercial airliner, depending upon the length of their diving exposures, to avoid decompression sickness in a diver who has subclinical gas bubbles .

Prodromal manifestations of decompression sickness include malaise, fatigue, and a sense of foreboding. Other constitutional symptoms include anorexia and headache. Decompression sickness is classified into two types based on the clinical manifestations.

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Type I decompression sickness — Type I decompression sickness involves mild insults and typically affects the following organ systems:

●Musculoskeletal – Localized joint pain is the most common manifestation of decompression sickness. Joints appear particularly vulnerable to the development of gas bubbles because local regions of negative pressure are created during the movement of lubricated articular surfaces. Symptoms are believed to result from the presence of bubbles in the periarticular tissues, which impair blood flow and stretch noncompliant tissues. Pain generally develops within an hour of surfacing and gradually increases over the next one to two days. The elbow and shoulder are affected three times more commonly than the knee and hip. Motion of the joint usually does not worsen the pain, and localized tenderness or signs of inflammation are rarely seen.

●Cutaneous – Pruritus, usually over the upper torso, is relatively common and thought to result from the presence of small bubbles in the skin. It generally resolves within 30 minutes, even without treatment. Localized erythema, potentially evolving into mottled areas of cyanosis, can also be seen. It likely is due to vasospasm or obstruction of venous drainage by the bubbles and resolves without treatment.

●Lymphatic – Lymphatic obstruction by bubbles, although rare, can lead to pain, lymphadenopathy, and localized edema, usually with follicular depressions and a peau d'orange effect. These lesions are mainly seen on the chest and torso.

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Type II decompression sickness — Type II decompression sickness is more severe and can lead to permanent injury and death. The following systems are typically affected:

●Neurologic – Approximately 60 percent of divers with decompression sickness have signs and symptoms of nervous system involvement. The vast majority of these cases are characterized by damage to the spinal cord, usually in the upper lumbar or lower thoracic regions. Paresthesias and weakness may progress to paraplegia, and loss of sphincter control, particularly of the bladder, may occur. Cerebral manifestations can also occur and include memory loss, ataxia ("the staggers"), visual disturbances, and changes in personality, speech, and affect. Most of these manifestations are believed to result from the formation and coalescence of gas bubbles within low pressure venous plexi and consequent venous obstruction. However, microvascular arterial embolization or bubble formation within nervous tissue may also play a role.

●Pulmonary – In about 5 percent of cases of decompression sickness, the burden of venous air bubbles is sufficient to precipitate symptomatic venous gas embolism. Gas bubbles can occlude portions of the pulmonary circulation and produce chest pain, wheezing, dyspnea, and pharyngeal irritation ("the chokes"). Embarrassment of right ventricular outflow with acute right-sided cardiac failure ("air lock"), circulatory collapse, and death may ensue, or some gas bubbles may traverse the pulmonary capillary bed or a patent foramen ovale to produce arterial gas emboli.