Page 1851 - Hall et al (2015) Principles of Critical Care-McGraw-Hill
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1320     PART 11: Special Problems in Critical Care


                 diving is expensive but effective and relatively safe to depths of 400 fsw.   preexisting medical conditions  or  injuries that compromise  regional
                 Most dives deeper than 400 fsw require saturation of the diver with inert   blood flow. Other serious forms of DCS involving the audiovestibular
                 gas at the approximate working depth of the dive. Saturation divers can   system (staggers) and pulmonary system (chokes), although relatively
                 live and work for weeks at pressure, for instance in a bell and chamber   rare, also occur. The most common clinical manifestations of DCS
                 system, and then undergo a single slow decompression to the surface.  are presented in  Table 132-2. The variable manifestations can make
                   The principle pathophysiologic problems of compressed gas diving   the clinical diagnosis difficult to establish, and there are no diagnostic
                 occur during ascent due to the uncontrolled emergence of inert gas from   laboratory studies.
                 tissues. During an ascent from diving or to altitude the extra inert gas in   Although bubbles do lead to bends, some bubbles are clinically silent.
                 the body at the higher pressure is eliminated as the pressure decreases by   As a result there is uncertainty about precisely how bubbles trigger the
                 the process of decompression.  The rates of uptake or elimination of inert   diverse features of DCS. The factors that govern bubble formation in
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                 gases from the body after a pressure change are determined primarily by   model tissues have been used to develop safe decompression tables
                 the solubility of the gas in blood and tissue, the blood flow, and the vol-    usually by assuming that DCS will not occur unless the inert gas tension
                 ume of tissue. In most tissues, inert gas exchange follows an exponential   exceeds the critical supersaturation threshold. The use of such a thresh-
                 function with respect to time. Tissues that behave this way are perfusion   old is empirical, and in the subcritical range of supersaturation, DCS
                 limited, and the characteristics of their inert gas exchange are defined   occurs as a stochastic event.  Therefore, even appropriate use of well-
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                 by a half-time. Because the body tissues receive different amounts of   tested decompression tables or a decompression computer is associated
                 blood flow and nitrogen is more soluble in fat, half-times for various   with a finite risk of DCS for dives deeper than about 25 fsw.
                 tissues vary considerably. The principle of multiple tissues was used to   In open water recreational diving, the incidence of DCS is probably
                 calculate the first safe decompression tables, with the assumption that   about one in 3000 dives, but increases with depth and duration, multiple
                 gas bubbles and DCS would occur only if the tissues were supersaturated   same day dives, cold water and strenuous work. In military and commer-
                 to allow a nitrogen partial pressure of about twice the absolute pressure.   cial divers and in military aviation, the risk is slightly higher, with a pre-
                 Modern decompression tables are still based on such parallel expo-  dominance of mild to moderate type I symptoms. Tunnel workers have
                 nential models, but with lower degrees of supersaturation. The most   a reported incidence of DCS of 0.7% to 1.5%, primarily consisting of
                 important variable affecting inert gas uptake and elimination is blood   type I symptoms of the knee and lower leg.  In recreational divers, some
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                 flow or tissue perfusion, but diffusion may limit tissue gas exchange   surveys have suggested frequent type II symptoms, but underreporting
                 under  some  conditions.   Diffusion  may  become important  when  two   of type I DCS and overdiagnosis of type II DCS are common.  Delays
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                 adjacent tissues have very different rates of perfusion. In such condi-  in the diagnosis and treatment of DCS may also allow more severe
                 tions, the more highly perfused tissue eliminates inert gas more quickly,   manifestations to evolve. Recreational divers are also more likely to omit
                 allowing inert gas to diffuse into it from the slower tissue. Thus, a faster   decompression than are professional divers, thus increasing the risk.
                 tissue may remain supersaturated for longer than expected. Diffusion is   One of the most serious forms of DCS is spinal paralysis.  Spinal cord
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                 also important during decompression once gas bubbles have formed in   DCS is not fully understood, but the injury may be related to intravas-
                 a tissue. Bubbles contain large amounts of N 2 gas that can be removed   cular bubbles  forming  in the  low-pressure,  epidural  venous  plexus of
                 by perfusion only after the N 2 diffuses back into the tissue. The rate at   the spinal cord.  Because of its low blood flow, the plexus is susceptible
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                 which N 2 diffuses away from a gas bubble is determined by the bubble   to bubble formation. Bubble-induced thrombi can obstruct venous out-
                 surface area, the intrabubble pressure, and the difference in partial pres-  flow, leading to spinal cord ischemia. Despite evidence for bubble for-
                 sure between bubble and tissue.                       mation in the spinal venous plexus, intravascular formation of bubbles is
                   Bubbles tend to form in specific nucleation sites in the body during   otherwise uncommon. Most intravascular bubbles probably originate at
                 decompression. Microscopic gas nuclei can be stabilized at hydropho-  the tissue-blood interface and stream into the circulation to be absorbed
                 bic sites in the body, but grow into bubbles during decompression.   by the lungs. Bubbles arising in the body of the spinal cord (autochtho-
                 The number of nucleation sites and their location and propensity to   nous) have also been implicated in the etiology of spinal DCS. 11
                 form macroscopic bubbles differ according to physiologic conditions.   Once bubbles enter the circulation, surface activity at the blood-
                 For example, exercise may increase the number of bubbles formed by   to-bubble interface produces complement activation, activation of
                 tribonucleation, a mechanism by which large negative pressures can   coagulation and fibrinolysis, platelet and neutrophil aggregation and
                 generate bubbles by traction between surfaces lubricated by a liquid,
                 such as joints.
                     ■  DECOMPRESSION ILLNESS                            TABLE 132-2    Clinical Manifestations of DCS
                                                                        Type I (mild DCS)
                 Decompression illness encompasses both decompression sickness (DCS)   Limbs
                 and arterial gas embolism (AGE) and these conditions, particularly after   Pain (bends), niggles, mild lymphatic obstruction, numbness, and paresthesias
                 an uncontrolled ascent by an inexperienced diver, may coexist.  As a   usually involving the large joints, eg, shoulders, elbows, and knees
                 rule, AGE has more serious implications, and it is a medical emergency.   Skin
                 Arterial gas blocking cerebral or coronary vessels and causing ischemia   Itching, rash, pallor, urticaria, edema (severe lymphatic obstruction, mottling,
                 must be eliminated promptly for the best outcome.           and edema is considered serious [cutis marmorata])
                   DCS is attributable to the growth of bubbles in body tissues that pro-
                 duce one or more clinical manifestations. The most common presenta-  Type II (serious DCS)
                 tion is pain-only or type I DCS, also known as bends. In type I DCS, the     CNS
                 primary sites of bubble growth are the joint spaces, tendon sheaths, and   Brain
                 periarticular tissues, including peripheral nerves. Type II or serious   Headache, seizures, loss of consciousness, visual disturbances, hemiparesis,
                 DCS is less common and usually involves the central nervous system,   aphasia, tremor, ataxia (staggers)
                 including the brain and spinal cord. Altitude DCS is similar, although   Spinal cord
                 symptoms appear most often during the exposure. Altitude DCS tends   Low back or pelvic girdle pain, paraparesis, urinary retention, incontinence
                 to be pain-only because the subject has often breathed an O 2-enriched   Audiovestibular DCS
                 gas  or  has  undergone  O 2  prebreathing.  Although  uncommon,  cases   Tinnitus, vertigo, nystagmus, decreased hearing, nausea, and vomiting
                 involving the CNS do occur.                              Cardiopulmonary DCS (chokes)
                   Most serious cases of DCS are due to omitted decompression and/  Dyspnea, cough, wheezing, hemodynamic collapse
                 or other risk factors such as exercise, cold, coexisting dehydration, or   CNS, central nervous system; DCS, decompression sickness.








            section11.indd   1320                                                                                      1/19/2015   10:56:10 AM
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