 |
|
 |
Google embedded. Try Me!
|
Login
Scuba Diving Article of the Month
Diving Accidents Requiring Recompression - Part1/4 |
|
I] Terminology
By including the evolution and manifestation terms in the phrase 'decompression illness', a highly flexible diagnostic label can be applied to any case. This label imparts a great deal of information and because it does not require the observer to guess at either a mechanism of the disease or location of the lesion, it should be possible for the diagnosis to be applied consistently. The term acute is used to distinguish these conditions from possible chronic consequences of diving such as dysbaric osteonecrosis (DON) - Dysbaric means “bad pressure” osteo means 'bone' and necrosis means 'cell death'. Therefore dysbaric osteonecrosis is simply bone cell death as a result of pressure changes. Examples of how the terminology is used include: acute, relapsing neurological, decompression illness or acute, progressive, limb pain and cutaneous decompression illness. In rare, highly complex cases, rather than enumerate a long list of manifestations, it may be appropriate to use the term 'multisystem'.
Symptoms and Signs: As a quick reminder we call symptoms what the patient is telling you and signs what you can see from outside. Since decompression illness can interfere with the function of a wide range of body tissues, the number of potential signs and symptoms is truly enormous. In the past, these have been lumped together into syndromes according to the anatomical site and presumed mechanism of disease. One of these syndromes has been further classified into types according to a dichotomy of perceived severity: Mild (Type I) and Serious (Type 2) decompression sickness. These terms are still used, but it is increasingly recognized that they are of very limited value.
Asymptomatic: without symptom
Stimulus modality (sensory modality): is one aspect of a stimulus. There are many modalities: temperature, taste, pressure....
Fistula: abnormal connection between the air-filled middle ear and the fluid filled inner ear.
Haemoptysis: expectoration of blood or blood-stained sputum.
Mediastinal shift: a shifting or moving of the tissues and organs that comprise the mediastinum to one side of the chest cavity. Often helpful in recognizing presence of pulmonary or pleural abnormality.
Hyper resonance: Exaggeration of normal resonance on percussion of the chest.
Lymph node: small clusters of cells - ball shaped, surrounded by a capsule. Ducts go in and out of them. The cells in lymph nodes are lymphocytes, which produce antibodies (protein particles that bind foreign substances including infectious particles) and macrophages which digest the debris. They act as the "cleaner" cells of the body.
The lymph nodes are a major site where foreign substances and infectious agents interact with the cells of the immune system.
Alternobaric caloric vertigo: is due to unequal pressures in the outer ears, the middle ears and can also be due to unequal stimulation of the ear drums by water of unequal temperature hitting the ears.
Additional Information
While the descriptive diagnostic terminology imparts a considerable amount of information, it is inadequate, of itself, to summarize a case of decompression illness. As was mentioned above, this a poorly understood syndrome and if a better understanding is to evolve, it is important that additional information is collected:
a) The Time of Onset: Decompression illness usually presents within a short period of time following a dive. Symptoms may become apparent before surfacing in saturation and occasionally in bounce dives, particularly where decompression has been omitted. However, most symptoms occur after surfacing and the majority of serious neurological or pulmonary symptoms are usually manifest within about 30 minutes. The onset of limb pain also occurs in this time period but this may be delayed for many hours after a dive. It should be remembered that decompression illness may be provoked or made worse many hours after a dive if the diver takes a flight. If a diver has been asymptomatic for 48 or more hours after a dive, and has not flown, then symptoms which develop subsequently are probably not dive-related. The time of onset should be recorded as the time in minutes or hours from surfacing from the last dive to the onset of each manifestation of decompression illness. If a flight was taken after the last dive, this should be recorded as well.
b) Gas Burden: When considering possible mechanisms for decompression illness, it is desirable to have an idea of the amount of gas that is likely to be present in the various tissues. At present there is no convenient means of summarizing this. Consequently it is important that the dive profile is recorded as accurately as possible. Where a dive computer or depth-time recorder was worn, the information should be retrieved from this source.
c) Evidence of Barotrauma: This is particularly important in the case of pulmonary and audio-vestibular decompression illness as discussed above. However, any evidence of barotrauma, such as in the middle ear should be recorded.
d) Response to Recompression: Quite often, the only means of confirming a diagnosis of decompression illness is if there is some measure of improvement following recompression. Consequently, it is important to record the response to recompression.
e) There are an increasing number of investigations which are performed on cases of decompression illness, such as tests for a PFO (see 2.5 below), electrophysiological tests and perfusion scans of the brain. The results of all investigations form an important part of any case notes.
II] Acute Decompression Illness
1. Background.
Acute decompression illness (DCI) is a syndrome of numerous possible manifestations which may develop following decompression. It is thought to be initiated by the presence of bubbles of gas in body tissues - including the blood stream. Although the means whereby these bubbles cause tissue dysfunction have yet to be fully elucidated, the manifestations have been recognized for many years and are described below.
 DCS localization
2. Disease Mechanisms.
There are a number of sources of these gas bubbles.
2.1 Dissolved Gas. The concentration of inert gas in arterial blood is approximately the same as in the gas mixture which is being breathed. For example, at sea level, both air and arterial blood contain approximately 0.8 atmospheres of nitrogen. During most dives or hyperbaric exposures, the partial pressure of inert gas which is breathed increases with depth and the concentration of that gas in arterial blood increases accordingly. Under these circumstances, the partial pressure of inert gas in tissues will gradually increase until it equals the ambient partial pressure. The dynamics of tissue gas exchange are beyond the scope of this text, but can be summarized by the statement that it is, at present, incompletely understood.
2.2 During decompression, inert gas moves in the opposite direction, from the tissues into the blood, where it is carried to the lungs and exhaled. If this process occurs in a controlled manner, so that the inert gas tension does not reach a sufficient level of super saturation for bubbles to form, the decompression will progress uneventfully. However, if the rate of decompression is such that the capacity of the tissues, cardiovascular system and lungs to remove inert gas is exceeded, bubbles of that gas may start to form. These bubbles may form in tissues or blood.
2.3 The human body is capable of tolerating a certain bubble burden. Bubbles in venous blood, for example, are efficiently removed from the circulation by the lungs and numerous studies have demonstrated the presence of such bubbles in asymptomatic divers. Furthermore, bubbles may form in some tissues (such as adipose tissue) without causing overt disease. However, other tissues, particularly nervous tissue, are much more sensitive and the presence of even a small number of gas bubbles may result in abnormal tissue function. How these bubbles provoke decompression illness has yet to be completely clarified. Hypotheses for the means whereby they exert their deleterious effects on tissue function include: the physical disruption of tissue architecture; interruption of tissue microcirculation and derangement of tissue biochemical activity at the tissue-bubble interface.
2.4 Arterial Gas Bubbles. As it was mentioned above, the lungs are excellent filters of gas bubbles. However, this capacity is finite and if the bubble burden is such that this is exceeded, they may transit the lungs and reach the arterial side of the circulation.
2.5 The transit of venous bubbles to arterial blood may occur before the pulmonary filter is overwhelmed. In approximately 25-30% of the normal, adult population, the septum which separates the upper chambers of the heart contains a potential or actual defect which is known as a Patent Foramen Ovale or PFO. This is a relic of the foetal circulation and normally results in no ill-effects. However, it does offer a possible route for bubbles to bypass the pulmonary filter and consequently, along with other right-to-left shunts, has the potential to promote the arterializations of otherwise relatively harmless venous bubbles.
 Red Arrow Shows the blood flow through the Patent Foramen Oval
2.6 How bubbles in arterial blood interfere with tissue function is another subject which is incompletely understood. One obvious mechanism is that they physically obstruct small blood vessels and thereby cause tissue ischaemia. The behavior of bubbles in the cerebral circulation has been studied extensively and, although the obstruction of blood vessels occurs as soon as bubbles arrive in the brain, this effect appears to be short-lived. Cerebral blood vessels respond to the presence of bubbles by dilating and thus allowing the bubbles to move on. It is now thought that much of the illness which results from bubble embolism of the brain is due to the consequences of traumatic injury to the delicate endothelial lining of cerebral blood vessels, which, in places may be stripped away from the vessel wall. This results not only in a breakdown of the blood-brain-barrier and the consequential leaking of potentially harmful blood constituents into the brain, but also, by exposing blood components such as white blood cells and platelets to the damaged blood vessel wall, a tissue reaction to injury is promoted. Ironically, it is the physical and biochemical consequences of this reaction which may actually result in a further deterioration of cerebral blood flow and function.
2.7 Although it is recognized that tissue bubbles may arise from two fundamentally different processes, it is often difficult, in individual cases, to be certain of the origins of the disease-provoking gas. Indeed, with respect to some organ systems, such as the ear and lungs, it may occasionally be difficult to distinguish between a condition caused by dissolved gas corning out of solution and the results of barotraumas. Consequently, it is now recognized that, for practical purposes, the distinction between the condition that used to be known as decompression sickness and arterial gas embolism was artificial. As a result, the term decompression illness, which encompasses the two, is increasingly being used to reflect this.
End of Part1 You can read directly the next part by following this Scuba Diving Accident Part2 then Scuba Diving Accident Part3 and finally Scuba Diving Accident Part4. WorlddivingReview |
