Advanced gestational age and fetal lactate levels in flight.
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Biomedical subjects
Publications and source records attributed to C E Fife.
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During this study to determine the effects of smoking on diabetic patients undergoing hyperbaric oxygen therapy (HBO2T) for nonhealing wounds, one physician visited five hyperbaric facilities and reviewed records on 1,006 patients who had received HBO2T for diabetic wounds. Smoking history was documented on 469 patients, while 180 patients had complete information on number of HBO2Ts, outcome, age, duration of diabetes, transcutaneous oxygen baseline in air at ambient conditions, Wagner score of the worst wound, smoking history, and intensity of treatment. These factors were statistically significant predictors of treatment outcome using multiple regression modeling. No difference was found between smokers with less than 10 pack-years of cumulative history and nonsmokers. After that point there was a significant increase in the number of HBO2Ts needed to produce at least some healing in smokers vs. patients who had never smoked. The average patient with a greater than 10 pack-year smoking history who benefited from treatment was estimated to need between 8 and 14 more HBO2Ts. This translates into an added treatment cost of $4,000 to $7,000 for the average patient who has smoked, and an estimated $22-37 million annually for the United States.
We studied the effect of 9 h of simulated airplane cabin conditions at cruising altitude (8,000 feet; inspired oxygen equivalent to 15% O2 at sea level) on fetal plasma lactate in near-term pregnant rabbits. Controls (n = 19) spent 9 h at sea level (21% O2). Study group I (n = 21) experienced airplane cabin conditions. Study group II (n = 17) was studied at 8,000 feet with the inspired O2 concentration normalized to sea level. Study group III (n = 19) remained at sea level breathing 15% O2. Before ending each exposure, fetal blood sampling for lactate was performed under ultrasound guidance. Maternal lactates were obtained before and after sampling fetuses. Wilcoxon signed rank test, analysis of variance, and Bonferroni's method were used as appropriate. P < 0.05 denoted statistical significance. Study group I (altitude/hypoxia) had higher fetal lactates than controls (sea level/normoxia) and study group II (altitude/normoxia). Fetal lactates in study group I (altitude/hypoxia) were higher than in study group III (sea level/hypoxia). Maternal lactates were lower after fetal sampling. Fetal lactic acidemia was observed after 9 h of airplane cabin conditions. This was attributed to the combined effect of the lowered oxygen concentration and the decrease in atmospheric pressure.
The role of brain computerized tomography (CT) imaging in predicting clinical outcome was investigated in patients receiving hyperbaric oxygen therapy for serious carbon monoxide (CO) poisoning. From a series of 48 consecutive patients suffering loss of consciousness from CO exposures, the records of 40 selected patients were evaluated to determine how their CT findings correlated with clinical outcome. A neuroradiologist blinded to patient outcome confirmed the radiographic findings. CT abnormalities consisted of globus pallidus hypodensities (nine patients), subcortical white matter hypodensities (four), cerebral cortical lesions (one), cerebral edema (one), hippocampal lesions (one), and complete loss of gray-white differentiation (one). Of the patients with globus pallidus lesions, 44% manifested incomplete recovery, whereas white matter lesions reflected a 74% incidence of morbidity. Age, duration of CO exposure, and interval between CO exposure and treatment did not significantly relate to clinical outcome. The blood carboxyhemoglobin levels correlated with clinical prognosis (P < 0.05) and, importantly, CT results significantly predicted clinical outcome (P < 0.05). A normal scan correlated highly with a complete recovery, whereas an abnormal scan predicted incomplete recovery or death, despite prior HBO therapy. The current study establishes prognostic validity for brain CT imaging for evaluating clinical outcome after HBO therapy for CO poisoning.
The effects of ascent rate and post-dive exercise on the incidence of decompression sickness (DCS) were investigated in six groups of 20 rats exposed for 2 h at a pressure equivalent to 240 feet of sea water (fsw; 735 kPa). Ascent rates were 30, 45, and 60 fsw/min (92, 138, 184 kPa/min), and the rats either rested after the exposure or exercised by walking for 30 min on a treadmill at 1.6 m/min. Post-dive signs included respiratory distress, difficulty walking, paralysis, and death. DCS was scored as non-fatal at 30-min post-dive or fatal at any time. Analysis by ordinal logistic regression indicated more DCS with post-dive exercise (P = 0.0112) and at 45 (P = 0.0011) and 60 fsw/min (P = 0.0001) compared to 30 fsw/min. Survival analysis suggested earlier death at 60 fsw/min compared to 30 fsw/min (P = 0.0006). Similar effects have been reported for the less severe DCS that occurs in humans.
A patient with a cervical spinal cord injury receiving intrathecal baclofen for spasticity control underwent a 7 week course of hyperbaric oxygen therapy to induce healing of an ischial decubitus ulcer. After completion of this treatment and during a routine baclofen infusion pump refill, the actual pump reservoir volume exceeded computer measurements obtained with telemetry. Examination of the physiology of hyperbaric oxygen therapy in relation to infusion pump function revealed that the intraspinal pressures attained during hyperbaric oxygen therapy produced retrograde leakage of cerebrospinal fluid into the infusion pump reservoir.
Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.
A small body of literature has been published reporting the application of topical oxygen for chronic non-healing wounds . Frequently, and erroneously, this form of oxygen administration has been referred to as "topical hyperbaric oxygen therapy" or even more erroneously "hyperbaric oxygen therapy." The advocates of topical oxygen claim several advantages over systemic hyperbaric oxygen including decreased cost, increased safety, decreased complications and putative physiologic effects including decreased free radical formation and more efficient delivery of oxygen to the wound surface. With topical oxygen an airtight chamber or polyethylene bag is sealed around a limb or the trunk by either a constriction/tourniquet device or by tape and high flow (usually 10 liters per minute) oxygen is introduced into the bag and over the wound. Pressures just over 1.0 atmospheres absolute (atm abs) (typically 1.004 to 1.013 atm abs) are recommended because higher pressures could decrease arterial/capillary inflow. The premise for topical oxygen, the diffusion of oxygen into the wound adequate to enhance healing, is attractive (though not proven) and its delivery is certainly less complex and expensive than hyperbaric oxygen. When discussing the physiology of topical oxygen, its proponents frequently reference studies of systemic hyperbaric oxygen suggesting that mechanisms are equally applicable to both topical and systemic high pressure oxygen delivery. In fact, however, the two are very different. To date, mechanisms of action whereby topical oxygen might be effective have not been defined or substantiated. Conversely, cellular toxicities due to extended courses of topical oxygen have been reported, although, again these data are not conclusive, and no mechanism for toxicity has been examined scientifically. Generally, collagen production and fibroblast proliferation are considered evidence of improved healing, and these are both enhanced by hyperbaric oxygen therapy. Paradoxically, claims of decreased collagen production and fibroblast inhibition in wounds subjected to topical oxygen have been reported in studies of topical oxygen as a benefit of topical oxygen therapy. The literature on topical oxygen is mostly small case series or small controlled but not randomized trials. Moreover, the studies generally are not aimed at specific ulcer types, but rather at "chronic wounds." This non-specific approach is recognized as a major design flaw in any study of therapies designed to improve impaired wound healing. The only randomized trial for topical oxygen in diabetic foot ulcers actually showed a tendency toward impaired wound healing in the topical oxygen group. Contentions that topical oxygen is superior to hyperbaric oxygen are not proven. There are potentially plausible mechanisms that support both possibly beneficial and detrimental effects of topical oxygen therapy, and thus well designed and executed basic science research and clinical trials are clearly needed. There is some ongoing research in regard to the role of topical oxygen at established wound laboratories. Neither CMS nor other third party payors recognize or reimburse for topical oxygen. Therefore, the policy of the Undersea and Hyperbaric Medical Society in regard to topical oxygen is stated as follows: 1. Topical oxygen should not be termed hyperbaric oxygen since doing so either intentionally or unintentionally suggests that topical oxygen treatment is equivalent or even identical to hyperbaric oxygen. Published documents reporting experience with topical oxygen should clearly state that topical oxygen not hyperbaric oxygen is being employed. 2. Mechanisms of action or clinical study results for hyperbaric oxygen cannot and should not be co-opted to support topical oxygen since hyperbaric oxygen therapy and topical oxygen have different routes and probably efficiencies of entry into the wound and their physiology and biochemistry are necessarily different. 3. The application of topical oxygen cannot be recommended outside of a clinical trial at this time based on the volume and quality of scientific supporting evidence available, nor does the Society recommend third party payor reimbursement. 4. Before topical oxygen can be recommended as therapy for non-healing wounds, its application should be subjected to the same intense scientific scrutiny to which systemic hyperbaric oxygen has been held.