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A 35-year-old male scuba diver returns from a diving trip complaining of joint pain, rash, and vertigo. Which of the following best describes this diving-related condition?
1. Type I decompression sickness (DCS I)
2. Type II decompression sickness (DCS II)
3. Nitrogen narcosis
4. Inner ear barotrauma
5. Arterial gas embolism
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1 or 2.
Plz explain this one
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Type I decompression sickness
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Type I DCS is characterized by one or a combination of the following: (1) mild pains that begin to resolve within 10 minutes of onset (niggles); (2) pruritus, or "skin bends," that causes itching or burning sensations of the skin; and (3) skin rash, which generally is a mottling or marbling of the skin or a papular or plaquelike violaceous rash. On rare occasions, skin has an orange-peel appearance.
Lymphatic involvement is uncommon and is usually signaled by painless pitting edema. The mildest cases involve only the skin or the lymphatics. Some authorities consider anorexia and excessive fatigue after a dive as manifestations of type I DCS.
Pain (the bends) occurs in the majority (70-85%) of patients with type I DCS. Pain is the most common symptom of this mild type of DCS and is often described as a dull, deep, throbbing, toothache-type pain, usually in a joint or tendon area but also in tissue. The shoulder is the most commonly affected joint. The pain is initially mild and slowly becomes more intense. Because of this, many divers attribute early DCS symptoms to overexertion or a pulled muscle.
Muscle splinting causes decreased function. Upper limbs are affected about 3 times as often as lower limbs. The pain caused by type I DCS may mask neurologic signs that are hallmarks of the more serious type II DCS. Dysbaric osteonecrosis is a phenomenon that occurs in divers with high numbers of dives. This is a persistent problem, suggesting that we do not yet understand the mechanisms involved in the disorder.
Type II decompression sickness
Type II DCS is characterized by (1) pulmonary symptoms, (2) hypovolemic shock, or (3) nervous system involvement. Pain is reported in only about 30% of cases. Because of the anatomic complexity of the central and peripheral nervous systems, signs and symptoms are variable and diverse. Symptom onset is usually immediate but may be delayed as long as 36 hours.
Nervous system
The spinal cord is the most common site affected by type II DCS; symptoms mimic spinal cord trauma. Low back pain may start within a few minutes to hours after the dive and may progress to paresis, paralysis, paresthesia, loss of sphincter control, and girdle pain of the lower trunk.
DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms confuses the diagnosis, differentiating DCS from traumatic nerve injuries.
When DCS affects the brain, many symptoms can result. Negative scotomata devoid of any lights or shapes is the earliest symptom. Negative scotomata become positive after a few minutes.
Other common symptoms include headaches or visual disturbances, dizziness, tunnel vision, and changes in mental status.
Labyrinthine DCS (the staggers) causes a combination of nausea, vomiting, vertigo, and nystagmus in addition to tinnitus and partial deafness. This alternobaric vertigo can be difficult to differentiate from dysbaric eustachian tube dysfunction. A history of eustachian tube problems depicted by past otitis media, past eustachian tube dysfunction, and problems equalizing pressure in the ears during the dive is associated with an increased prevalence of alternobaric vertigo.
Lungs
Pulmonary DCS (the chokes) is characterized by (1) burning substernal discomfort on inspiration, (2) nonproductive coughing that can become paroxysmal, and (3) severe respiratory distress.
This occurs in about 2% of all DCS cases and can cause death. Symptoms can start up to 12 hours after a dive and persist for 12-48 hours.
Circulatory system
Hypovolemic shock is commonly associated with other symptoms. For reasons not yet fully understood, fluid shifts from the intravascular spaces to the extravascular spaces. The signs of tachycardia and postural hypotension are treated via oral rehydration if the patient is conscious or intravenously if the patient is unconscious. The treatment of DCS is less effective if dehydration is not corrected.
Thrombi may form because of the activation of the early phases of blood coagulation and the release of vasoactive substances from cells lining the blood vessels. The blood-bubble interface may act as a foreign surface, causing this effect. Bubble formation in DCS has been believed not only to cause mechanical stretch or damage and blockage of blood flow by embolization, but also to act as a foreign body and to activate the complement and coagulation pathways, creating a thrombus. Recent studies appear to leave this concept unresolved. Some of the studies' authors indicate that they have supported this hypothesis, while others could not find a correlation with degree of injury.
A patent foramen ovale also comes into play in DCS. This allows bubbles to pass from right to left circulation, bypassing the screening effects of the pulmonary circulation. This has been found to correlate with a higher prevalence of high spinal cord and head/neck DCS injury, which was more profound when a procedural violation led to DCS. Patients with only a large patent foramen ovale had an increased risk of DCS when decompression rules were not violated. Although the overall prevalence of patent foramen ovale in the general population is significant (about 30%), the prevalence of serious type II DCS is very low; therefore, routine screening of divers for patent foramen ovale is not recommended. However, in the face of a serious DCS episode, it could be considered in evaluation of the patient for future diving.
Sorry , I wrote Type 1 but it is Type 2 .
