Page 1853 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1322 PART 11: Special Problems in Critical Care

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potential for permanent injury, and AGE should never be regarded as RECOMPRESSION THERAPY
benign; however, the severity of injury in general appears to be related Gas bubbles in tissue or circulation slowly resolve spontaneously, but
to the volume of intravascular gas. In the heart, the myocardial response the rate at which they are removed can be greatly enhanced by oxygen
to AGE is similar to coronary insufficiency of any etiology. Ventricular breathing and recompression. Recompression and hyperbaric oxygen
arrhythmias and ST-segment elevation or depression are common and (HBO) administration are primary therapy for DCS and AGE. Bubble
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may lead to myocardial infarction. 25,26 Cerebral manifestations of AGE resolution is related to size and the partial pressure difference between
are similar to those of arterial thromboembolism and include focal the bubble and tissue. This partial pressure difference is due to the
neurologic deficits, loss of consciousness, seizures, and death. The inherent unsaturation of venous blood that results from the difference
distinction between AGE and VGE may become clinically indistinct in solubility of CO 2 and O 2 in body tissues. CO 2 is 20 times more soluble
because the possibility of arterial spillover is difficult to exclude, and than is O 2 in tissues. As O 2 is consumed, it is replaced by CO 2 from
either may manifest with cardiovascular collapse. substrate oxidation at a ratio of about 0.8 mol of CO 2 for each mole
Divers who experience AGE are most often inexperienced and fre- of 100 mm Hg leaves
quently arrive suddenly at the surface after diving. They may cry out, of O 2. Thus, O 2 entering tissue at an arterial P O 2
of 40 mm Hg. In contrast, CO 2 enters at
indicating a rapid ascent with a closed glottis, or they may surface the venous capillary at a P O 2
40 mm Hg and leaves at only 46 mm Hg. The remaining gas pressure in
unconscious. Somewhat surprisingly, AGE is only occasionally com- tissues is primarily N 2, which is inert and has the same partial pressure
plicated by pneumothorax or pneumomediastinum or accompanied at equilibrium, 573 mm Hg, on both sides of the circulation. Therefore,
by clinical signs of pulmonary barotrauma, such as mediastinal crunch the sum of partial pressures in the venous system is 54 mm Hg less than
(Hamman sign), subcutaneous air, or tension pneumothorax. The onset in the arterial system. This “oxygen window” provides a pressure gradi-
of AGE is quite sudden, virtually always within 15 minutes of surfacing, ent to eliminate N 2. As O 2 is removed by metabolism, a bubble collapses
and presents with symptoms of cerebral ischemia, which may be pro- as
gressive. Initial symptoms of AGE appearing more than 1 hour after an because the internal pressure of N 2 (P N 2 ) increases above tissue P N 2
the pressure in the bubble stays in equilibrium with ambient pressure. In
ascent should not be attributed to AGE but to serious DCS, drowning, or this way, N 2 is gradually absorbed. The oxygen window can be expanded
stroke. Common clinical findings of AGE include headache, confu- during and after decompression and during recompression by adminis-
sion, nausea, vomiting, blindness, hemiparesis, seizures, and uncon- , which decreases tissue PN 2 and increases the
sciousness. Chest pain, hemoptysis, and shortness of breath may also tration of high inspired P O 2
partial pressure gradient for N 2 between bubble and tissue. Immediate
occur. Laboratory abnormalities may include elevated serum creatine O 2 administration at the scene of a diving accident before recompression
kinase levels, signifying injury to skeletal and cardiac muscle. 27 therapy is clearly beneficial in the management of DCS and AGE.
Various recompression schedules are effective for AGE and DCS if treat-
ment is begun promptly, but the treatment of choice is recompression tables
THERAPY OF DECOMPRESSION ILLNESS that use HBO and minimal recompression. US Navy (USN) Treatment
■ ADJUNCTIVE THERAPY Table 6 (Fig. 132-2), which uses intermittent HBO at a maximum depth
of 2.8 ATA (60 fsw), is a standard for primary DCS and for recurrent
The optimal care of patients with decompression illness begins with a symptoms. Recurrent or persistent symptoms should be retreated with
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heightened suspicion of the problem in the appropriate setting. High flow daily recompression according to Table 6 or with USN Treatment Table
oxygen, if available, should be administered at the scene and a thorough, 5 once or twice a day. As a rule, a point of diminishing returns is reached
but rapid neurological examination performed as soon as feasible. The after a few (usually four to eight) sessions. Persistent bladder and bowel
management of AGE (as with VGE) begins with prompt identification dysfunction or neuromuscular weakness also may respond to saturation
of the problem and efforts to prevent further emboli. In VGE of any therapy (eg, USN Table 7), if the resources and expertise are available for
etiology, a “mill wheel” murmur produced by air in the right ventricle conducting prolonged treatments. Rarely, recompression using oxygen is
4
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may be audible with a stethoscope. The clinical practice of positioning not available, and air recompression tables must be used. These tables are
the patient in the left lateral decubitus and Trendelenburg position in longer and less effective than HBO tables and are more likely to produce
an effort to avoid PFO crossover and brain emboli had been proposed DCS in chamber attendants. Recompression of the seriously ill patient
to reduce cerebral bubble diameter by increasing hydrostatic pressure can present significant logistical challenges for the intensive care team,
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in the cranium ; however, later evidence suggested that positioning is particularly in monoplace chambers. 35
not efficacious because blood flow rather than buoyancy of the bubble HBO is used to treat AGE and serious neurological manifestations of
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determines the course of air emboli. Further, Trendelenburg position- VGE on the basis of the following rationale. First, an increase in ambi-
ing has been associated with increased cerebral edema. The use of 100% ent pressure compresses the gas and increases the ratio of surface area
O 2 helps correct hypoxemia and increases the diffusion gradient for to volume of the bubble, thus improving nitrogen diffusion out of the
nitrogen out of the bubbles, promoting shrinkage. Vasopressors and bubble. Second, greater oxygen tension in the blood increases the nitro-
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antiarrhythmic agents may be required for hypotension and ventricular gen gradient across the blood-bubble interface. Third, the amount of O 2
arrhythmias associated with AGE. Lidocaine at 2 to 4 mg/min intrave- physically dissolved in plasma during HBO (∼6 mL O 2/dL of plasma at
nously after a 1-mg/kg loading dose ameliorated cerebral injury after 2.8 ATA) may avert or reverse ischemia because plasma streaming can
experimental cerebral AGE. 31 occur around emboli that obstruct erythrocyte flow.
Adjunctive therapy for AGE and serious DCS, other than oxygen The optimal treatment of AGE using HBO is not known. Experience
consists of correction of hemoconcentration with intravenous fluids by the US Navy with air embolism after diving accidents led to the
and management of complications. 32,33 Parenteral corticosteroids such development of USN Table 6A, which uses initial recompression of the
as dexamethasone, 4 mg every 6 hours, have been recommended to patient breathing air to an equivalent pressure of 165 fsw (6 ATA) fol-
decrease cerebral or spinal cord edema after AGE and serious DCS, but lowed by decompression to 60 fsw (2.8 ATA) and O 2 breathing in cycles
the evidence for efficacy in either case is lacking. Stress ulceration may alternating with air. The intent of the initial, deep compression is reduc-
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occur after AGE, and prophylaxis should be used routinely. Because tion of emboli size to 55% of their original diameter (assuming spherical
of blood-bubble physical interactions discussed earlier, treatment of geometry). This approach may be appropriate for very recent AGE or
cerebral AGE with heparin was once recommended, but has not proven when the quantity of intravascular gas is very large. Deep compression
efficacious, and is associated with hemorrhage into areas of cerebral on air, however, may actually allow nitrogen into the emboli so that they
infarction induced by the air embolus. However, heparin prophylaxis of increase in size. This problem can be circumvented in part by having the
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deep venous thrombosis and pulmonary emboli should be given for spinal patient breathe a mixture of 50% O 2 and 50% N 2 during compression to
cord DCS because of the immobility of the patient. limit the driving force of N into the emboli. Recent experience using
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