Decompression sickness (DS), also known as "the bends", can occur in scuba divers and others exposed to significant changes in atmospheric pressure. It is caused by nitrogen bubbles forming in the body if the pressure drops too quickly. DS is classified as type I or type II depending on whether skin/joints or other organs are affected. Common symptoms include joint pain, rashes, dizziness and paralysis. Treatment involves oxygen therapy followed by recompression in a hyperbaric chamber to dissolve the bubbles. Risk factors include ascent rate, depth, repetitive dives and individual traits like age and body type. Prevention focuses on following safe ascent procedures and dive tables to avoid dangerous pressure changes.

1. Decompression sickness Caribbean Emergency Care Conference 2011 J. van Leeuwen MD Surgeon

2. Introduction Classification DS is classified by symptoms The earliest descriptions of DS used the terms: "bends" for joint or skeletal pain "chokes" for breathing problems "staggers" for neurological problems

3. DS in a nutshell

4. Introduction Type I ('simple’) for symptoms involving only the skin, musculoskeletal system, or lymphatic syste Type II ('serious’) for symptoms where other organs (such as the central nervous system) are involved

5. Introduction Type II DCS is considered more serious and usually has worse outcomes

6. Signs and symptoms

7. Bubbles can form anywhere in the body Most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of DS cases, with the shoulder being the most common site

8. Musculoskeletal (mostly joints) Localized deep pain, ranging from mild to excruciating Red rash in skin Sometimes a dull ache, but rarely a sharp pain. Active and passive motion of the joint aggravates the pain

9. Itching, usually around the ears, face, neck, arms, and upper torso Sensation of tiny insects crawling over the skin Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema) CutaneousType I DS

10. Neurologic (brain)Type II DS Altered sensation, tingling or numbness paresthesia, increased sensitivity hyperesthesia Confusion or memory loss (amnesia) Visual abnormalities Unexplained mood or behaviour changes Seizures, unconsciousness

11. Neurologic (spinal cord) Ascending weakness or paralysis in the legs Girdling abdominal or chest pain Urinary incontinence and fecal incontinence

12. Constitutional (whole body) Headache Unexplained fatigue Generalised malaise, poorly localised aches

13. Audiovestibulair (inner ear) Loss of balance Dizziness, vertigo, nausea, vomiting Hearing loss

14. Pulmonary Dry persistent cough Burning chest pain under the sternum, aggravated by breathing Shortness of breath

15. Frequency symptoms Joint pain 89% Arm symptoms 70% Leg symptoms 30% Dizziness 5.3% Paralysis 2.3% Shortness of breath 1.6% Extreme fatigue 1.3% Collapse/unconsciousness 0.5%

16. Onset of DS within 1 hour 42% within 3 hours 60% within 8 hours 83% within 24 hours 98% within 48 hours 100% Although onset of DS can occur rapidly after a dive, in extreme cases even before a dive has been completed, in more than half of all cases symptoms do not begin to present until over an hour following the dive

17. What causes DS A reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude

18. Predisposing factors Although the occurrence of DS is not easily predictable, many predisposing factors are known environmental individual

19. Environmental (to increase risk) The magnitude of the pressure reduction ratio and duration Repetitive exposures – repetitive dives within a short period of time (a few hours) Repetitive ascents to altitudes above 5,500 metres The US Navy Dive Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DS, while recreational dive tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute

20. Individual Age Previous injury – there is some indication that recent joint or limb injuries to developing decompression-related bubbles Ambient temperature –exposure to very cold ambient temperatures may increase the risk of altitude DS High body fat content is at greater risk of DS. This is due to nitrogen's five times greater solubility in fat than in water

21. Alcohol consumption and dehydration Maintaining proper hydration is recommended. Patent foramen ovale Venous blood with microbubbles of inert gasbypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to arteries to the brain, spinal cord and heart In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, results in stroke, and in the spinal cordresults in paralysis

22. Mechanism Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DS

23. On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage

24. Diagnosis DS should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours The diagnosis is confirmed if the symptoms are relieved by recompression

25. Prevention To prevent ascend 10 metres (33 ft) per minute, and carry out a decompression schedule as necessary This schedule requires the diver to ascend to a particular depth, and remain at that depth until sufficient gas has been eliminated from the body to allow further ascent Dives that contain no decompression stops are called "no-stop dives", but divers usually schedule a short "safety stop" at 3 metres (10 ft), 4.6 metres (15 ft), or 6 metres (20 ft), depending on the training agency

26. Treatment 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development

27. Treatment Oxygen first aid has been used as an emergency treatment If given within the first four hours of surfacing, it increases the success of recompression therapy as well as a decrease the number of recompression treatments required

28. Treatment Give fluids, as this reduces dehydration In the past, both the Trendelenburg position and the left lateral decubitus position have been beneficial where air emboli are suspected

29. Prognosis Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long term effects Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed still had residual signs and symptoms from Type II DS and 7% from Type I DS

30. Epidemiology The incidence of decompression sickness is rare, estimated at 2.8 cases per 10,000 dives, with the risk 2.6 times greater for males than females DS affects approximately 1,000 U.S. scuba divers per year From 1998 to 2002, they recorded 50,150 dives, from which 28 recompressions were required — 0.05%

31. Treatment principles HBOT lies in its ability to drastically increase partial pressure of oxygen in the tissues of the body. The oxygen partial pressures achievable using HBOT are much higher than those achievable while breathing pure oxygen at normobaric conditions Under normal atmospheric pressure, oxygen transport is limited by the oxygen binding capacity of hemoglobin in red blood cells and very little oxygen is transported by blood plasma. Because the hemoglobin of the red blood cells is almost saturated with oxygen under atmospheric pressure, this transport cannot be used any further. Oxygen transport by plasma, however is significantly increased using HBOT

32. Indications Air or gas embolism Carbon monoxide poisoning Clostridal myositis and myonecrosis (gas gangrene) Crush injury, compartment syndrome, and other acute traumatic ischemias Decompression sickness

33. Hyperbaric Oxygen Therapy Involves intermittently breathing pure oxygen at greater than ambient pressure Think of oxygen as a drug and the hyperbaric chamber as a dosing device Elevating tissue oxygen tension is the primary effect

34. Hyperbaric Oxygen Therapy Primary therapy for: Decompression sickness Air embolism Carbon monoxide poisoning Adjunct therapy for: Surgical intervention Antibiotics

35. Accepted Indications Air or gas embolism Carbon monoxide poisoning Clostridialmyositis and myonecrosis Crush injury, compartment syndrome, acute traumatic ischemias Decompression sickness Enhance healing of wounds Necrotizing fasciitis Chronic osteomyelitis Radiation necrosis, brown recluse spider bites Thermal burns

36. Basic Mechanisms Boyle’s Law – pressure and volume inversely proportional under constant temperature By increasing ambient pressure to 2 atm, decreases the volume by ½ Henry’s Law – at a given temperature, the amount of gas dissolved in solute is directly proportional to the partial pressure of the gas. By increasing ambient pressure, more oxygen can be dissolved in the plasma

37. Mechanism of action Angiogenesis in ischemic tissues Bacteriostatic/bactericidal actions Carboxyhemoglobin dissociation hastened Clostridium perfringens alpha toxin synthesis inhibited Vasoconstriction Temporary inhibition of neutrophil Beta 2 integrin adhesion

38. Monoplace (1 person) or multiplace (2-14 patients) chamber Pressures applied inside the chamber are usually 2-3 xatm pressure, plus may have an additional hydrostatic pressure equivalent of 1-2 atm. Treatments last from 2-8 hours

39. Complications Middle ear barotrauma Middle ear barotrauma is the most common adverse effect of HBO treatment Hemorrhage or serous effusion develops Prevention: teaching patient auto-insufflation technique or use of decongestants If auto-insufflation fails, tympanostomy tubes are placed.

40. Complications Pulmonary barotrauma Rare Suspect if pulmonary or hemodynamic changes occur during or shortly after decompression Place chest tube if pneumothorax develops

41. Complications Oxygen Toxicity Can impair elasticity, vital capacity, and gas exchange. CNS toxicity Seizure Risk is higher in hypercapnic, acidotic, or septic patients Eyes Progressive myopia has been reported in patients undergoing repetitive daily therapy

42. CO Poisoning Leading cause of injury and death by poisoning in the world Affinity of CO for hemoglobin (forming carboxyhemoglobin) is 200 times that of oxygen

43. ClostridialMyonecrosis(gas gangrene) Mortality rates of 11-52% Diffused oxygen which raises capillary p02 levels at the wound site, stimulates capillary budding and granulation of new, healthy tissue

44. Necrotizing Fasciitis andFournier’s gangrene Addition of HBO to surgical and antibiotic treatment reduced mortality versus surgery and antibiotics alone May suppress growth of anaerobic organisms May increase leukocyte function and suppress bacterial growth

45. Crush injury Reduces infection and wound dehiscence and improves healing Improves oxygenation to hypoperfused tissue Causes arterial hyperoxia causing vasoconstriction and decreased edema formation. Also, intermittent pressure stimulates circulation and reduces edema Early use of HBO may reduce compartment pressures enough to avoid fasciotomy

46. Prevention Don’t push your limits and do all required decompression stops Keep physically fit and within a healthy weight range Don't exercise within 12 hours of diving Don't ascend to altitude or fly immediately after diving Make sure you're adequately hydrated before every dive Don't drink alcohol before or after diving and never dive when hungover Get checked out by a doctor to find out if you have a PFO

47. MASHA DANKI!