Electroencephalography and magnetic resonance imaging in neurological decompression sickness.

The purpose of this study was to evaluate the use of electroencephalography (EEG) and magnetic resonance imaging (MRI) in the clinical evaluation of acute decompression sickness (DCS) in the central nervous system (CNS). Twenty-one patients treated because of acute DCS in the CNS during 1999-2001 were included, 15 patients with clinical cerebral DCS and five with clinical spinal cord DCS. Seven patients had abnormalities in their EEG, five with cerebral DCS and two with spinal cord DCS. MRI showed high intensity lesions in the spinal cord in four patients with clinical spinal cord DCS and in one with clinical cerebral DCS. Cerebral lesions were not identified by MRI in any patient. In conclusion, EEG showed unspecific abnormalities in only one third of the cases. Conventional MRI with a 1.5 T scanner may be of help in the diagnosis of DCS in the spinal cord, but not in the brain. EEG and MRI have low sensitivity in the diagnosis of acute DCS in the CNS. Recompression treatment of DCS should still be guided by clinical neurological examination and assessment of symptoms.

Venous gas embolism in chamber attendants after hyperbaric exposure.

An initial occupational survey (OS) was initiated to investigate the prevalence of venous gas embolism (VGE) in chamber attendants assisting hyperbaric oxygen (HBO2) treatments. Nine female subjects were exposed for three consecutive days to the routine hospital procedure of compressed air exposure to 240 kPa for approximately 115 min with 12 min of terminal oxygen (O2) breathing. VGE was monitored with ultrasound Doppler in 15 min intervals for 2h after the first and third exposure. A follow-up experimental study was completed to investigate whether changed breathing gases and decompression would affect the high incidence of VGE observed in the OS. Ten female subjects were randomly exposed to the routine or revised profile (12 and 24 min of terminal O2 breathing respectively), and a Nitrox profile (breathing gas 40.5% O2 in Nitrogen during 90 min of the isobaric phase). VGE was monitored with transthoracic ultrasound scanner and Doppler. In the OS precordial VGE grade III (Doppler) was observed in five subjects, but median resting precordial VGE was Grade 0 both days and VGE score at all sites were equal Days 1 and 3. In the experimental study, median resting precordial VGE was Grade 0 (Doppler) and Grade 1 (Scanner). VGE Grade III (Doppler) was observed in all series, but VGE scores were not significantly different between the series. We conclude that chamber attendants assisting HBO2 treatment at 240 kPa for approximately 115 min are exposed to a significant decompression stress using the profiles tested in the present study.

Dehydration and body fluid-regulating hormones during sweating in warm (38 degrees C) fresh- and seawater immersion.

Body weight (BW) reductions of more than 4 kg have been observed during diving with the open hot water suit, a technique in which heated seawater (SW) continuously floods the skin surface. To test the hypothesis that osmotic effects may be involved in these fluid-loss processes, head-out immersion experiments in 38 degrees C freshwater (FW) and SW for 4 h were performed. Average BW reduction was 2.5 and 1.9 kg in SW and FW head-out immersion, respectively (P < 0.01). Atrial natriuretic peptide increased during the first 30 min of SW immersion (5.6-13.4 pmol/l, P < 0.01) followed by a reduction to 7.6 pmol/l (P < 0.01). This paralleled an initial decrease in aldosterone (from 427 to 306 pmol/l, P < 0.05) followed by an increase to 843 pmol/l (P < 0.01). The effects of temperature on fluid loss were studied in thermoneutral (34.5 degrees C) and 38 degrees C SW for 2 h. In thermoneutral SW, calculated sweat production was negligible (0.05 kg) compared with 1.2 kg in warm SW. We recommend that, if a dive is planned to last for more than 4 h, a mandatory break for fluid intake should be incorporated in the diving regulations.

[Hyperbaric oxygen treatment for radiation reactions]. / Hyperbar oksygenbehandling ved strålereaksjoner.

BACKGROUND: A national hyperbaric centre was established in 1994 at Haukeland Hospital with responsibility for all hyperbaric oxygen (HBO) treatment in Norway. In hypoxic tissues with symptomatic radiation reactions, hyperbaric oxygen induces the formation of collagen and angiogenesis resulting in permanently improved local microcirculation. MATERIAL AND METHODS: 234 patients received elective HBO treatment at Haukeland Hospital in 1997 with a total of 4,048 treatments. All 47 patients treated for radiation reactions in the pelvic area in 1997 received a questionnaire 3-15 months after HBO therapy; 81% responded. RESULTS: Rectal bleeding and haematuria were reported as much improved in 61% and 55% respectively, while bladder incontinence was much improved in 46%. INTERPRETATION: This treatment modality may be an alternative in symptomatic radiation reactions of the urinary bladder and the bowel when conventional treatment has given unsatisfactory results.

Effects of a standard hyperbaric oxygen treatment protocol on pulmonary function.

The prescription of hyperbaric oxygen (HBO) therapy for disorders not related to diving is increasing. Pulmonary oxygen toxicity is well known, but the effect of the cumulative oxygen exposure corresponding to a standard HBO treatment protocol has not been quantified before. Twenty patients (10 male) had 21 HBO treatments at a partial pressure of oxygen of 240 kPa for 90 min daily. None had any previous lung disease and all had normal chest radiography and lung function at the start of the study. Dynamic lung volumes, forced expiratory flows and the transfer factor of the lung for carbon monoxide (TL,CO) were measured before the HBO treatment, on days 7, 14 and 21 during treatment and then 3-4 weeks after treatment. Four patients (one male) reported nonproductive coughing during the last week of treatment. There was a progressive reduction in forced expiratory volume in one second (FEV1) (p<0.001), mean forced mid-expiratory flow rate (FEF25-75%) (p<0.001) and forced expiratory flows at 50 and 75% of forced vital capacity (FVC) expired during HBO treatment. The reduction in FEV1 on day 21 was 4.4+/-1.7% and in FEF25-75% 10.3+/-6.1%. Four weeks after treatment there was a partial normalization. There were no changes in FVC or peak expiratory flow (PEF). TL,CO was slightly reduced on day 21 of treatment only (p<0.01) and fully normalized 1 month later. A reduction in small airways conductance is consistent with other studies where total oxygen exposures have been below the limit causing toxic pulmonary effects traditionally measured as a reduction in vital capacity. This effect is not considered to be of any clinical significance for patients treated with hyperbaric oxygen unless repeated treatment series are to be given.

[Hyperbaric oxygen therapy. Now an established treatment in Norway]. / Hyperbar oksygenbehandling. Nå et etablert tilbud i Norge.

Hyperbaric oxygen therapy can be a life-saving form of treatment for certain acute medical conditions, e.g. cerebral gas embolism, clostridial infections, and smoke/carbon monoxide inhalation. It has long been used for treating decompression illness in divers. As from 1994 our hospital has been delegated the national responsibility for hyperbaric medicine in Norway. This paper describes the physiological basis, indications, and contraindications for hyperbaric oxygen treatment, and summarises hyperbaric oxygen treatment in Bergen over the last two years.

[Insulin pumps and drop in pressure]. / Insulinpumper og trykkfall.

Do insulin pumps deliver more insulin at lower environmental pressures and, if so, is this due to pump dysfunction or to formation of bubbles in the insulin solutions? H-TRON V-100 (Hoechst Infusor V-100), MRS-1 (Disetronic), Nordic Infusor MK II (Novo Nordisk) and Minimed 504-S (Minimed Technology) insulin pumps were studied at 0.9 ATA and 0.8 ATA with constant infusion 2.0 I.U./hour. H-TRON V-100 was also studied at 0.7 ATA at the same infusion rate and with the motor in stop position. The results indicated that all pumps delivered slightly more insulin than the set rate during decompression (max. single value 2.68 I.U. extra delivered at 0.7 ATA, max. average value 1.32 I.U. extra delivered at 0.8 ATA). An equivalent amount of insulin (1.72 I.U.) was delivered at 0.7 ATA without running the motor. This implies that the extra insulin supplied was caused by physically dissolved nitrogen and oxygen in the insulin solution, and was not due to dysfunction of the pumps.

[Intensive care of patients with burns]. / Intensivbehandling av brannskader.

We discuss the fluid requirements of burn patients and present the most common formulas for fluid resuscitation. The most commonly used formula is the Parkland formula containing 4 ml/kg/% Ringer acetate, which we still recommend for general use. Hypertonic Ringer acetate containing 240 mmol Na/l may reduce fluid requirement and edema generation. Regardless of formula applied, the fluid therapy is adjusted to individual requirements. We discuss nutritional demands and monitoring of nutritional status, and propose individual treatment based on weight development and nitrogen balance studies. We also consider upper and lower airway injuries, with emphasis on early diagnosis and treatment. We stress the need for prophylactic intubation before the upper airways become obstructed. Prophylactic use of steroids and antibiotics is not indicated after inhalation of smoke causing pulmonary injury. Prolonged nasal intubation gives less severe sequelae than tracheostomy.

Respiratory depression by analgesics at 41 bar.

The effects of morphine and fentanyl on respiration and tissue CO2 measured transcutaneously were studied at surface and at 41 bar ambient pressure in conscious, trained rats. Morphine and fentanyl were given in equianalgesic doses i.v., 7 and 0.025 mg/kg, respectively. Fentanyl caused a rapid but brief respiratory depression which was the same at 1 and 41 bar, and essentially the same results were found in the morphine groups, although there was a longer latency and duration of action. No statistical differences in the degree of respiratory depression were found at 41 bar compared to 1 bar for either analgesic.

EEG power spectra in rats during compression and during pentobarbital infusion at pressure.

The EEG of rats was studied with power spectrum analysis under compression to 71 ATA with He-O2 and during constant rate infusion of pentobarbital at 71 ATA and at surface. During compression the 1-4 Hz delta activity was increased, and 8-11 Hz alpha, 12-14 Hz spindle, and 16-10 Hz low beta activities were reduced compared to control animal recordings. During the course of pentobarbital infusion at 71 ATA, this picture changed: the delta activity was reduced while alpha and spindle activities (barbiturate spindles) increased, considerably more than in the rats studied at surface pressure. The findings may only in part be explained by pressure reversal of anesthesia.

Pharmacokinetics and tissue concentrations of ceftazidime in burn patients.

The pharmacokinetics and tissue concentrations of ceftazidime have been investigated in 8 patients with severe burns (20-80% of body surface area) undergoing skin transplantation 2 to 21 days after injury. Two prophylactic doses of ceftazidime were administered as 1 g i.v. bolus injections with an 8 h interval. Blood, urine, burn blister fluid and tissue were frequently sampled and drug concentrations were analyzed by HPLC. The kinetics of ceftazidime was the same after each dose. In these patients the pharmacokinetics of ceftazidime was greatly altered from that in other patients and there was much interindividual variation. The mean ceftazidime elimination half-life, apparent volume of distribution and total clearance were: 2.7 h, 30.91 (0.38 1.kg-1) and 139 ml.min-1, respectively. A linear correlation was found between creatinine clearance and the renal clearance of the ceftazidime, the mean values being 108 and 95 ml.min-1, respectively. No correlation was found between creatinine clearance and the total clearance of ceftazidime. The mean percentage urine recovery was 69% of the dose. Tissue and burn blister fluid concentrations were above the MIC, and ranged from 40.0 to 3.1 mg.kg-1. A substantial increase in the apparent volume of distribution and non-renal clearance of ceftazidime was observed, probably due to increased capillary permeability and drug loss through the wound surface replacement of prior to surgery and subsequently to lost and blood fluid.

Transcutaneous measurement of PCO2 at high ambient pressure (41 bar).

The accuracy of transcutaneous CO2 monitoring with the Kontron CO2 sensor was studied during compression to 41 bar and subsequent decompression. The PCO2 was stable and accurate during the test of the sensor in the pressure chamber, although an increase of 0.1-0.2 kPa during compression was found. The function of the transcutaneous sensor was tested in rats at 1 bar for the correlation between transcutaneous PCO2 (PtcCO2) and arterial PCO2 (PaCO2). The correlation coefficient between PtcCO2 and PaCO2 in the rat was found to be 0.93. The time difference between the 90% transcutaneous and 90% arterial response time was 4.6 +/- 0.6 min (mean +/- SEM). Finally, the use of the sensor in rats ventilated at constant minute volume during compression to 41 bar was examined. An increase in PtcCO2 of 0.2-0.4 kPa was found. The present results of transcutaneous PCO2 measurements indicate that this method may be useful in hyperbaric research and treatment.

Transcapillary colloid osmotic pressures in injured and non-injured skin of seriously burned patients.

Thermal skin injury is accompanied by rapid and excessive oedema formation implicating a dramatic increase in the transcapillary fluid transport. In order to clarify the pressure changes occurring across the microvasculature after a thermal skin injury we have measured colloid osmotic pressures (COP) in interstitial fluid (COPi) of injured and non-injured skin as well as in plasma (COPp) from patients suffering major cutaneous burns. Interstitial fluid was collected with a wick-technique and analysed for COP. Measurements were performed as early as 6 h and continued until 56 h after injury. A severe hypoproteinaemia occurred in all patients with a marked reduction in COPp down to about 10 mmHg. Up to 12h post-burn we found a higher COPi in injured skin than in plasma. The first measurement of COPp averaged 9.8 mmHg as compared to an average COPi of 11.1 and 9.3 mmHg in injured and non-injured skin respectively. Measurements performed later than 12h showed a return of the transcapillary COP gradient towards the normal direction (COPp greater than COPi). The gradient was considerably less than in a normal situation. Based on the present observations of transcapillary COP it is suggested that colloids should be withheld until the transcapillary COP gradient returns to the normal direction.

Anesthetic effect and distribution of infused pentobarbital in the rat at 71 ATA.

The anesthetic dose requirement and distribution of 14C-labeled pentobarbital were studied in rats at 1 ATA air and at 71 ATA He-O2. Pentobarbital was infused intravenously at a rate of 5 mg X kg-1 X min-1. The depth of anesthesia was assessed by EEG using the burst suppression of 1-s duration (silent second) as the biological end point. The mean anesthetic dose was 45.6 and 68.0 mg X kg-1 at 1 and 71 ATA, respectively, representing a 49% increase at pressure (P less than 0.001). The corresponding concentrations in the brain were 81.6 and 92.3 micrograms X g-1 (not significant). The hepatic and renal pentobarbital concentrations increased by 44 and 41%, respectively, at pressure (P less than 0.001). Interindividual variations in required doses and infusion lengths made comparison between tissue pentobarbital values difficult to interpret. A second series of experiments was therefore undertaken using a subanesthetic dose of pentobarbital infused at the same constant rate for 7 min. No significant changes were found in the organ distribution of the drug at pressure. The results show that high pressure antagonizes the narcotic effect of pentobarbital and that the distribution of pentobarbital is not significantly altered in the rat at 71 ATA.

The effect of high pressure on the kinetics of monoamine transmitters in the rat brain.

The effects of 71 ATA pressure on the turnover of serotonin (5-HT), noradrenaline (NA), and dopamine (DA) were studied. High pressure increased the concentration of the 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA) by 40%. A concomitant increase in 5-HT synthesis (measured by the accumulation of 5-hydroxytryptophan after inhibition of the decarboxylase) of 25% was found. The changes in NA and DA metabolites and synthesis were smaller and not statistically significant. The increase in 5-HT synthesis was not a result of changes in the neuronal uptake of transmitter. The observed change might be the result of a compensatory increase in the activity of the serotoninergic neurons at high pressure. Among the three monoamine transmitter systems, that mediated by 5-HT may be most important in the pathogenesis of the high pressure neurologic syndrome.

Effect of 71 ATA He-O2 on organ blood flow in the rat.

Cardiac output and organ blood flow to major organs were investigated in awake rats at 1 atmosphere absolute (ATA) air and at 71 ATA He-O2. Radioactively labeled microspheres [15 +/- 1 (SD) micron] were injected into the left ventricle during constant-rate arterial blood sampling at 1 ATA air and subsequently at 71 ATA He-O2. Intra-arterial blood pressure was continuously recorded. The partial pressure of O2 was kept between 0.4 and 0.6 ATA. The results indicate that the mean blood pressure, heart rate, cardiac output, and organ blood flow are essentially unaltered in the rat at 71 ATA except for increased blood flow to the liver (122%, P less than 0.05), whereas the blood flow to the adrenals, the diaphragm, and the leg muscle fell (P less than 0.05).

Tissue distribution of penicillin during constant rate infusion in rats at 71 ATA.

Benzyl[14C]penicillin was infused at a constant rate of 100 mg X kg-1 X h-1 for 90 min in rats at 1 ATA air for the control group (n = 10) and at 71 ATA He-O2 for the pressure group (n = 11). The radioactivity was measured in the arterial blood, brain, liver, kidney, muscle, and fat. The mean brain penicillin concentration after 90 min infusion was approximately 20% increased at 71 ATA (P less than 0.05), but the brain: blood concentration ratio was not significantly affected. The mean blood, liver, and muscle penicillin content was slightly higher and the mean kidney content was slightly lower at pressure, but no statistically significant changes were observed.