KAMEDO--a Swedish Disaster Medicine Study organization.

Kamedo is a Swedish Disaster Medicine study organization that sends observers to disaster areas anywhere in the world to study recent events, collect useful information, and identify problems relative to the practice of Disaster Medicine. The results of these investigations are published in the KAMEDO Reports, and the English versions will be published in Prehospital and Disaster Medicine. Three of the recent reports follow: 1) KAMEDO Report 69: Ebolus Virus Epidemic in Zaire, 1995; 2) KAMEDO Report 70: The German Rescue and Emergency Organizations: a) Industrial Chemical Fire, Memmingen, Germany 23 January 1997; b) Fire at the Düsseldorf Airport, 01 April 1996; and c) Bus Accident on the Autobahn in Rosenheim, Germany; and 3) Terrorist Attack with Sarin, 20 March 1995. In addition, a catalog listing all of the KAMEDO Reports available in English is provided.

A placebo-controlled experimental study of steroid inhalation therapy in ammonia-induced lung injury.

BACKGROUND: The use of corticosteroids in toxic lung injury caused by exposure to an irritating gas such as ammonia has not been adequately studied. OBJECTIVE: To evaluate the effects of budesonide inhalation in a rabbit model of toxic lung injury induced by ammonia. DESIGN: Randomized, blind placebo-controlled laboratory investigation employing 16 New Zealand White rabbits. Lung injury was induced by inhalation of a defined amount of aerosolized ammonia. Thirty minutes later, the rabbits were randomized to receive either inhalation therapy with 0.5 mg budesonide or placebo. After another 2 hours, a second treatment inhalation, identical to the first one, was administered. RESULTS: Airway pressures, hemodynamics, and gas exchange were measured at baseline, 5, and 15 minutes after ammonia administration and every 30 minutes during a 6-hour period after the first blind inhalation of corticosteroids or placebo. The ammonia inhalation resulted in an acute severe lung injury, detected after 15 minutes as a decrease in Pao2 from 23.3 (+/- 3.6) to 11.0 (+/- 3.6) kPa (p < 0.005) and an increase in peak airway pressure from 13 (+/- 2) to 17 (+/- 2) cm H2O (p < 0.005). During the 6-hour observation period, the blood gas parameters improved gradually in all rabbits. In comparison with placebo, budesonide did not result in improved gas exchange or reduced airway pressure levels during the observation period. CONCLUSION: In this animal model corticosteroid inhalation therapy had no effect on ammonia-induced lung injury.

[When a disaster is a fact. Kamedo analyses how the help was functioning]. / När katastrofen är ett faktum. Kamedo analyserar hur hjälpen fungerade.

Kamedo (Organizing Committee for Disaster Medicine Studies) has for over 30 years compiled information on disasters in Sweden and abroad, analysed the data and published the results. The Kamedo reports supply knowledge and experience in the field of disaster medicine and form a basis for disaster medicine planning, education and research. Over 60 reports have been published so far, since 1980 including summaries in English. These summaries can be obtained from Kamedo, Swedish National Board of Health and Welfare (Socialstyrelsen), S-106 30 Stockholm, Sweden (fax +46 8 783 3287).

Renal impairment after acute diclofenac, naproxen, and sulindac overdoses.

Acute renal dysfunction has been described as a feature of acute overdoses of the nonsteroidal anti-inflammatory drugs benoxaprofen, fenoprofen, ibuprofen, mefenamic acid, piroxicam, suprofen, and zomepirac. The cases reported here include renal impairment after acute overdoses of another three nonsteroidal anti-inflammatory drugs: diclofenac (one case), naproxen (two cases), and sulindac (five cases). The eight patients presented with lumbar pain and oliguria and had protein and erythrocytes in the urine. Serum creatinine was increased to a maximum of 190-932 mumol/L. Renal impairment was generally transient but in one case was treated by hemodialysis and one by continuous arterio-venous hemofiltration dialysis. In all cases of significant acute overdose of nonsteroidal anti-inflammatory drugs, the risk of acute renal dysfunction must be considered.

Treatment of severe ethylene glycol intoxication with continuous arteriovenous hemofiltration dialysis.

Ethylene glycol is the major component of many antifreeze solutions and its metabolites may cause severe intoxication. Treatment involves correction of metabolic acidosis, ethanol administration and enhancement of elimination. The most commonly used elimination technique is hemodialysis but peritoneal dialysis has also been described. We report a case of severe ethylene glycol poisoning with multiple organ dysfunction. Treatment with continuous arteriovenous hemofiltration dialysis was associated with a favorable outcome and might be an alternative to hemodialysis in similar cases of circulatory instability or in situations where hemodialysis is unavailable.

Hospital treatment of victims exposed to combustion products.

Combustion toxicology is complex so, although victims exposed to combustion products are mainly treated symptomatically, it is important to identify those situations when specific therapeutic measures might be of importance. Victims presenting respiratory symptoms including severe cough, bronchoconstriction, hypoxia and respiratory distress should be given oxygen and ventilatory assistance or support. Furthermore, bronchoconstriction should be treated with bronchodilators (beta-2-adrenoreceptor agonists, theophylline). Corticosteroids should be considered both for inhalation and systemically due to the risk of developing toxic pulmonary oedema that may appear after a symptom-free interval that might last up to 48-72 h. Victims with impaired consciousness should be regarded as being exposed to carbon monoxide and cyanides. Apart from oxygen and optimal symptomatic treatment hyperbaric oxygen therapy should be considered in carbon monoxide poisoning. Certain cyanide antidotes, namely those with low intrinsic toxicity (as sodium thiosulphate, hydroxocobalamin) should be given liberally in these situations. Other specific therapeutic measures that might be considered when appropriate are administration of organophosphate antidotes (atropine, oximes), heavy metal chelators (e.g. dimercaptopropane sulfonate, dimercaptosuccinic acid) and methemoglobinemia antidotes (methylthionine, toluidine blue). Inhalation of hot fumes may cause upper respiratory tract oedema (e.g. laryngeal oedema) necessitating orotracheal intubation and ventilatory support.

Fatal systemic poisoning after skin exposure to monochloroacetic acid.

Little information is available on the toxicity of monochloroacetic acid. We report the case of a 38 year-old man who was splashed with an 80% monochloroacetic acid solution on 25-30% of his body surface. In addition to epidermal and superficial dermal burns, features of systemic poisoning occurred within a few hours including disorientation, agitation, cardiac failure and coma. He later developed severe metabolic acidosis, rhabdomyolysis, renal insufficiency and cerebral edema, and died due to uncal herniation on d 8. The 4 h post exposure plasma monochloroacetic acid concentration was 33 mg/L confirming skin absorption. In addition to its corrosive action, monochloroacetic acid probably blocks the tricarboxylic acid cycle (Kreb's cycle) and may also react with sulfhydryl groups in enzymes, causing severe tissue damage in energy-rich organs.