Nonimmune hydrops fetalis caused by G6PD deficiency hemolytic crisis and congenital dyserythropoietic anemia.

We present a case of a female neonate who had a nonimmune hydrops fetalis and severe hemolytic anemia due to a rare combination of glucose-6-phosphate dehydrogenase (G6PD) deficiency and congenital dyserythropoietic anemia. We conclude that in severe cases with persistent anemia one should search after delivery for a second reason other than G6PD deficiency alone.

Hyperbaric oxygen therapy in the pediatric patient: the experience of the Israel Naval Medical Institute.

UNLABELLED: The pediatric patient is to be found in hyperbaric facilities throughout the world, receiving hyperbaric oxygen (HBO) therapy for both life-threatening and chronic diseases. OBJECTIVE: To review the experience accumulated at the Israel Naval Medical Institute in the treatment of pediatric patients. DESIGN: A retrospective analysis and review of all records of patients younger than age 18 years. RESULTS: Between 1980 and 1997, 139 pediatric patients age 2 months to 18 years (mean, 7.7 years) received HBO treatment at the Israel Naval Medical Institute. Of the children, 111 (79%) suffered from acute carbon monoxide (CO) poisoning; 13 (9.2%) were treated after crush injury, traumatic ischemia, or compartment syndrome; 4 (2.8%) had clostridial myonecrosis; 1 (0.7%) had necrotizing fasciitis; 5 (3.6%) had refractory osteomyelitis; 2 (1.4%) had suffered massive air embolism; 2 (1.4%) had purpura fulminans; and 1 (0.7%) suffered from decompression sickness. Outcome, judged by neurologic sequelae, mortality, and extent of soft tissue loss and limb amputation, was favorable in 129 patients (93%). Two patients (1.4%) died, 1 as a result of CO poisoning and the other, gas gangrene; 2 of the patients in the CO group (1.4%) remained with neurologic sequelae, and 6 patients in the acute traumatic ischemia group (4.3%) underwent limb amputation. CONCLUSIONS: We had a favorable experience with 129 of a total 139 pediatric patients treated at our facility for the indications listed. A basic knowledge of HBO therapy is needed to refer the pediatric patient for treatment when indicated. The needs of the pediatric patient, especially the critically ill, require specific skills and equipment inside the hyperbaric chamber. Close collaboration between the pediatrician and the hyperbaric medicine physician is essential to ensure adequate care for infants and children.

Treatment of necrobiosis lipoidica diabeticorum by hyperbaric oxygen.

Necrobiosis lipoidica diabeticorum is a chronic cutaneous complication of diabetes mellitus with microangiopathy as an important pathophysiologic factor. Because of the known success of hyperbaric oxygen in the treatment of chronic non-healing wounds, we used this mode of therapy to treat a diabetic patient with ulcerated necrobiosis lipoidica of 7 years' duration, refractory to medical and surgical treatment. The patient received daily sessions of hyperbaric oxygen therapy. There was considerable improvement during the course of the treatment, with complete closure of all the ulcerations after 98 sessions. The success of this treatment emphasizes the role of hypoxia in the pathogenesis of the lesion. This simple and safe treatment method may be a good solution for patients with chronic nonhealing necrobiosis lipoidica which fails to respond to other therapeutic approaches.

Recovery of the hypoxic ventilatory drive of rats from the toxic effect of hyperbaric oxygen.

Hyperbaric oxygen (HBO) exposure reduces the hypoxic ventilatory drive (HVD), probably by damaging the carotid bodies. The recovery of the HVD from HBO exposure was studied. The HVD was calculated from whole body plethysmographic recordings of the ventilatory response to greater than 85% and 2% O2 in N2 mixtures. Five groups of rats were exposed to HBO for 9 h at pressures of 1.9, 2.0, 2.1, 2.2, and 2.4 ATA, respectively. Each rat underwent three control measurements on different days prior to HBO exposures and then at various intervals following the exposure. Postexposure HVD was reduced to 28% of control values in the high PO2s. Ninety percent recovery of pre-exposure HVD was evident by 12-48 h although in some animals exposed to relatively low PO2s (1.9 and 2.0 ATA) HVD stabilized at a level lower than 100%. The recovery of the HVD in percent during the first 4 d following exposure can be expressed as an exponential function of the time from the termination of HBO: HVD = 28 + 72(1 - exp-0.053t) (t in hours). This information may be of importance in cases of repeated exposures to HBO where one tries to avoid cumulative damage to the carotid bodies, and in the care of the poorly oxygenated patient after HBO treatment.