Francis Wattel

Handbook on hyperbaric medicine

Physiology and Physiopathology of Hyperbaric Oxygen.- Physiological Principles of Hyperbaric Oxygenation.- Toxic Effects of Oxygen.- Pulmonary Effects.- HBO Dose Titration.- Clinical Indications.- Decompression Illness - Final Report.- Acute Indications of HBO Therapy - Final Report.- Chronic Hyperbark Oxygen Therapy Indications - Final Report.- Recommendations of the Jury.- Decompression Illness.- Epidemiology of Decompression Accidents During Recreational Diving.- Pre-Hospital Treatment of Decompression Sickness in Recreational Divers.- Hospital Medical Treatment of Decompression Sickness in Sport Scuba Diving.- Hyperbaric Treatment of Decompression Accidents.- Medical Specificities of Diving for Children and Women.- The Treatment of Decompression Sickness in Commercial Diving.- Effect of Gas Bubbles on the Blood.- Gas Embolism.- The Divers Alert Network: Epidemiology of Diving Accidents.- Divers Alert Network and its Programs.- The Divers Alert Network in Europe: Risk Evaluation and Problem Management in a European Recreational Divers Population.- Divers Alert Network Japan Report.- Carbon Monoxide Poisoning: Mechanism, Clinical Presentation and Management.- Carbon Monoxide Poisoning in the United States.- Hyperbaric Oxygen Therapy for CO Intoxication During Pregnancy.- Heart Damage Caused by Carbon Monoxide Poisoning.- The CO-Poisoned Child.- Soft Tissue Infections Including Clostridial Myonecrosis: Diagnosis and Treatment.- Clostridial Myonecrosis.- Radionecrosis.- Brain Injuries and HBO.- HBO in Orthopedic Disorders.- Hyperbark Oxygen Therapy in Crush Injuries.- Applications of Hyperbaric Oxygen Therapy in Plastic Surgery.- Oxygen and Healing Wounds: Tissue-Bone Repair Enhancement.- HBO Therapy in Burns and Smoke Inhalation Injury.- Hyperbaric Oxygen Therapy and Diabetic Problems.- Diabetes Mellitus: Diagnosis, Epidemiology, Therapy and Long-Term Complications.- Hyperbaric Oxygen Therapy in Diabetic Foot Ulcer and Gangrene.- Vascular Diseases and HBO.- Hyperbaric Oxygen Therapy in Ophthalmology.- Pigmentous Retinopathy (PR) and Hyperbaric Oxygen Therapy (HBO).- Hearing Disorders.- Monitoring of Clinical Parameters in Hyperbaric Chamber.- Management of HBO Patients.- Transcutaneous Oxymetry.- Oxymetry.- Transcutaneous Oxymetryin Hyperbaric Medicine.- Effect of Hyperbaric Oxygen on Activity of Antibacterial Agents.- Safety and HBO Therapy.- Future Prospects in Research for Hyperbaric Oxygen.- Adapting the Hyperbaric Chamber to the Health Care Environment: History and Future Trends.- New Frontiers.- New Frontiers: Hyperbaric Oxygen Therapy (HBO) in Open Heart Surgerys Complications.- New Frontiers: Dermatology.- New Frontiers: HBO in Treatment of Fetal Growth Deficiencis.- New Frontiers: Obstetrical Indications for Hyperbaric Oxygen Therapy.- New Frontiers: Use of Combined Hyperbaric Oxygenation and In-Water Rehabilitation for Neurological Conditions due to Stroke and to Spinal Decompression Sickness.- New Frontiers: Treatment of Radiation-Induced Xerostomia with Hyperbaric Oxygen: Is There a Room for such a Complicated Treatment?.- New Frontiers: Tumor Oxygenation and Radiotherapy.- New Frontiers: Sickle Cell Anemia.- New Frontiers: Brain Abscess.- New Frontiers: Endothelin 1 and HBO.- Medical Oxygen: Characteristics, Use, Safety Guidelines.- Personal, Professional and Educational Requirements for the Staff of a Hyperbaric Medical Center.- Cost-Benefit and Cost-Efficiency Evaluation of Hyperbaric Oxygen Therapy.

Acute Carbon Monoxide Poisoning Risk of Late Sequelae and Treatment by Hyperbaric Oxygen

The indications for hyperbaric oxygen therapy (HBO) in the treatment of acute carbon monoxide (CO) poisoning are discussed far too little in the literature. Depending on the author reasons for referral to a hyperbaric center include the carboxyhemoglobin level, change in state of consciousness or neurological abnormalities. In our opinion, HBO should be used on much wider indications than is usual, not only because of the rapid relief from symptoms it provides but mainly because it may prevent severe delayed sequelae. During a period of 9 months 230 patients with CO poisoning were admitted to our intensive care unit; 203 were treated with HBO and 27 with normobaric oxygen. Our indications for HBO treatment were: coma, pathological neurological findings or loss of consciousness during CO exposure irrespective of normal clinical findings on admission. Four patients died and the others were discharged 12 hours to 25 days after the incident. Seven patients had minor neurological problems within two weeks of discharge and which disappeared within one month. Two patients were re-hospitalized for neuropsychiatric sequelae and recovered in 3 and 6 months respectively. Neither the clinical status upon admission nor COHb predicted the outcome of the poisoning. Referral to a HBO center should be considered when: --the patient is comatose --there are abnormal clinical findings --patients have been unconsciousness during exposure, irrespective of whether they are conscious on admission and have normal clinical status.

Dobutamine improves gastrointestinal mucosal blood flow in a porcine model of endotoxic shock.

OBJECTIVE To test the hypothesis that saline solution plus dobutamine increases gastrointestinal mucosal perfusion better than saline solution alone in a model of endotoxic shock. DESIGN Prospective, randomized, unblinded study. SETTING Animal research laboratory affiliated with a university teaching hospital. SUBJECTS Twelve female pigs, weighing 30 to 32 kg. INTERVENTIONS Animals were anesthetized, and their lungs were mechanically ventilated. Catheters were inserted into the right atrium, pulmonary artery, and carotid artery for blood sampling and blood pressure and cardiac output measurements. A tonometer and a laser Doppler probe were placed in the lumen of the stomach and the ileum for determination of mucosal acid-base status and measurement of mucosal blood flow. Group 1 animals (n = 6) received an infusion (T = 0 min) of 150 mcirog/kg Escherichia coli endotoxin and normal saline solution (0.3 mL/kg/min). Group 2 animals (n = 6) received an infusion of endotoxin and were resuscitated with the same method as used in group 1, but an infusion of dobutamine (5 microg/kg/min) was begun at T = 60 mins, and continued for the duration of the experiment. MEASUREMENTS AND MAIN RESULTS Both experimental regimens produced shock, with decreased mean arterial pressure and systemic vascular resistance, without change in cardiac output and oxygen delivery. Endotoxin plus saline infusion decreased gastrointestinal mucosal blood flow to <60% of baseline and decreased gastrointestinal pH. In contrast, gastrointestinal mucosal blood flow returned to baseline values, and intramucosal pH tended to normalize by the end of the saline solution plus dobutamine resuscitative protocol. CONCLUSION Compared with saline solution alone, saline solution plus dobutamine increased blood flow to the gastrointestinal mucosa, and may have partially improved oxygenation.

Small intestine intramucosal Pco2 and microvascular blood flow during hypoxic and ischemic hypoxia

OBJECTIVE To determine whether small intestine intramucosal PCO(2) and mucosal blood flow changes would be different between ischemic and hypoxic hypoxia. DESIGN Randomized animal experiment. SETTING Research laboratory. SUBJECTS Anesthetized, mechanically ventilated, and surgically instrumented pigs. INTERVENTIONS Systemic oxygen delivery was lowered in a stepwise manner to decrease it beyond critical oxygen delivery by lowering either FIO(2) or blood volume. MEASUREMENTS AND MAIN RESULTS In hypoxic hypoxia pigs (n = 6), arterial oxygen concentration and oxygen delivery decreases were achieved by progressively reducing arterial PO(2) while cardiac index remained unchanged. In ischemic hypoxia pigs (n = 5), oxygen delivery reduction was achieved by progressively reducing cardiac index while arterial PO(2) remained unchanged. In control pigs, oxygen delivery remained unchanged. The lowest oxygen delivery measured in both hypoxia and ischemia experiments was 3.60 +/- 0.26 vs. 2.93 +/- 0.77 mL x kg(-1) x min(-1), respectively (p =.23). At the lowest oxygen delivery level, differences between ischemic hypoxia and hypoxic hypoxia experiments were observed for arterial lactate concentration (468 +/- 308 vs. 1070 +/- 218 mmol/L, respectively; p =.03), mixed venous arterial PCO(2) difference (10 +/- 7 vs. 4 +/- 2 torr, respectively; p =.04), and small intestine mucosal blood flow (6.2 +/- 2.1 vs. 15.7 +/- 7.4 perfusion units, respectively; p =.02). Small intestine intramucosal-arterial difference was higher in ischemic hypoxia than in hypoxic hypoxia (52 +/- 15 vs. 31 +/- 12 torr, respectively; p =.03). CONCLUSION Small intestine intramucosal PCO(2) increases may indicate systemic oxygen uptake supply limitation in ischemic and hypoxic hypoxia related to conditions of mucosal flow stagnation and CO(2) generation.

Non-Healing Wounds

A large body of pathophysiological evidence supports the beneficial role of HBO in reversing a delayed healing process. Daily experience supports its use in the clinical management of patients with non-healing wounds. TCPO2 measurement is a valuable and helpful method for patient selection, follow-up and treatment monitoring.

Inhaled nitric oxide modulates leukocyte kinetics in the mesenteric venules of endotoxemic rats.

Objective: to determine whether inhaled nitric oxide (NO) would alter leukocyte kinetics in the septic microvasculature. Design: Randomized, controlled trial. Setting: Experimental laboratory. Subjects: Male Sprague Dawley rats. Interventions: Rats were treated with either saline or endotoxin (10 mg/kg, iv) and then allowed to breathe either air or air plus NO (10 ppm). Measurements and Main Results: After a 4‐hr period, rolling, firm adhesion, and emigration of leukocytes and endothelial dysfunction were monitored in mesenteric venules by using intravital videomicroscopy. Compared with controls, endotoxemic rats exhibited a profound influx in mesenteric venule rolling leukocytes (55 ± 17 vs. 70 ± 19 leukocytes/min; p < .05), associated with a reduction of leukocyte rolling velocity (83 ± 14 vs. 34 ± 3 μm/sec; p < .05). In endotoxemic rats, venular endothelium leukocyte firm adhesion (1.15 ± 0.32 vs. 4.08 ± 0.96 leukocytes/100 μm; p < .05) and emigration (0.84 ± 0.47 vs. 4.23 ± 1.2 leukocytes/100 μm; p < .05) increased compared with controls. Inhaled NO had no effect on leukocyte kinetics in control rats. Inhaled NO significantly attenuated endotoxin‐induced venular endothelium leukocyte adhesion (4.08 ± 0.96 vs. 1.86 ± 0.76 leukocytes/100 μm; p < .05) and emigration (4.23 ± 1.2 vs. 1.68 ± 0.72 leukocytes/100 μm; p < .05). Compared with control rats, macromolecular (FITC‐dextran) vascular leakage, expressed as the perivenular/intravenular fluorescence intensity ratio, increased in endotoxemic rats (0.56 ± 0.02 vs. 0.81 ± 0.05; p < .01). Endotoxin‐induced macromolecular vascular leakage increases were partially prevented by inhaled NO (0.66 ± 0.01 vs. 0.56 ± 0.02; p < .05). Conclusion: These observations suggest that inhaled NO reduces leukocyte adhesion and the degree of vascular permeability dysfunction in mesenteric venule of endotoxemic rats.

Pedicle Musculocutaneous Flap Transplantation: Prediction of Final Outcome by Transcutaneous Oxygen Measurements in Hyperbaric Oxygen

In pedicle musculocutaneous flaps, a local circulatory insufficiency with a total or subtotal ischemia may occur and jeopardize the result of the reconstructive surgery. Transcutaneous oxygen pressure (PtcO2) monitoring has been shown to reflect tissue perfusion and has been advocated to predict the final outcome of ischemic flaps. Unfortunately, under normal atmospheric conditions, this test is not sufficiently discriminative. We evaluate the effect of hyperbaric oxygen conditions on the efficiency of this test. Fifteen patients with pedicle musculocutaneous flap were evaluated by clinical examination and transcutaneous oxygen tension measurements. The final outcome was healing in 7 and failure in 8. In order to determine the predictive value of transcutaneous oxygen tension, measurements were done immediately after the surgical procedure. In ambient air, neither the absolute value of transcutaneous oxygen tension (2.6 ± 3.6 versus 11.7 ± 12.6 torr; N.S.) nor the difference or the ratio between the transcutaneous oxygen tension of the flap and the subclavicular reference shows any significant difference according to the outcome (failure or success). The same is true in normobaric oxygen. In hyperbaric oxygen, however, there is a significant difference in transcutaneous oxygen tension between the two groups (12 ± 12 versus 378 ± 385 torr; p < 0.01). A transcutaneous oxygen tension higher than 50 torr in hyperbaric oxygen (2.5 atm abs) is the best cutoff value to discriminate success from failure.

PHYSIOLOGIC EFFECTS OF HYPERBARIC OXYGEN ON MICROORGANISMS AND HOST DEFENCES AGAINST INFECTION

Physiologic effects of hyperbaric oxygen on microorganisms and host defence mechanisms against infection fall into three categories: a direct action on anaerobic bacteria an indirect action on the microbicidal capability of polymorphonucleocytes and macrophages by raising or restoring normal oxygen pressure within the infected areas. an enhancement of the antimicrobial activity of some antibiotics.

A History of Hyperbaric Medicine

On June 19th, 1997 a first careful attempt was done to compare the European Committee indications with those of the HBO Committee of the UHMS. Not only indications were discussed but also recommended protocols, pressures and threshold treatment levels. The conclusion was that similarities were far greater than differences, and that in the future the two tables should be harmonized. Conditions not on both lists were to be evaluated to resolve differences as soon as possible. It was also planned to include the levels of recommendation for the ECHM indications as in the HBO Therapy UHMS Committee Report. A joint meeting took place during the Annual Meeting of the UHMS in Sydney in 2004; but a lot more work is required, involving both the UHMS Committee and the ECHM.

Carbon dioxide rebreathing method of cardiac output measurement during acute respiratory failure in patients with chronic obstructive pulmonary disease.

Objective: To compare measurement of cardiac output by the CO2 rebreathing method vs. the thermodilution cardiac output technique in the setting of acute respiratory failure in patients with chronic obstructive pulmonary disease. Design: Prospective, comparative study of two methods in a consecutive sample. Setting: Intensive care unit. Patients: Twenty‐five patients with chronic obstructive pulmonary disease with acute respiratory failure were studied. The patients were being mechanically ventilated and monitored with systemic and pulmonary artery catheters. Measurements and Main Results: Cardiac output was determined, using both the thermodilution technique and an indirect CO2 Fick method. Veno‐arterial CO2 content difference was calculated from an estimated mixed venous Pco2 obtained by an equilibrium CO2 rebreathing method and measured Paco2. Pco2 was converted to content using the equation of the CO2 dissociation curve described by McHardy. A wide range of cardiac output was studied. There was a significant correlation between thermodilution and CO2 rebreathing methods (r2 = .92, p < .001). The mean difference between thermodilution and CO2 rebreathing methods was ‐0.06 L/min/m2, standard deviation for the bias was 0.028 L/min/m2, and 95% confidence interval for the bias was ‐0.120 to ‐0.001 L/min/m2. Conclusion: Our results suggest that the CO2 rebreathing method may be a reliable noninvasive technique to determine cardiac output in mechanically ventilated patients with chronic obstructive pulmonary disease. (Crit Care Med 1994; 22:81‐85)