Gösta Arturson

The tragedy of San Juanico--the most severe LPG disaster in history

During the early morning of Monday, 19 November 1984, one of the largest disasters in industrial history occurred in the Mexico City Area, causing the greatest rescue effort to assist population in an emergency ever undertaken. The tragic catastrophe started in a large LPG (Liquid Petroleum Gas) storage and distribution centre in San Juan Ixhuatepec, 20 km north of Mexico City. The facilities, owned by the Pemex State Oil Company, consisted of six spherical storage tanks (four with a volume of 1600 m3 and two with a volume of 2400 m3) and 48 horizontal cylindrical bullet tanks of different sizes. At the time of the disaster the storage tanks contained 11,000 m3 of a mixture of propane and butane. The inhabitants of San Juan Ixhuatepec numbered about 40,000, and a further 60,000 lived in the hills surrounding the village. The majority were poor country people living in one-story houses constructed of concrete pillars filled in with bricks and with roofs of iron sheets. The disaster started due to LPG leakage, probably a pipe leakage or rupture due to excess pressure. A vapour cloud built up and was slowly moved by the north-east wind towards the ground-placed flare pit located in the western part of the plant. The vapour cloud was ignited around 5:40 a.m. and was followed by an extensive fire at the plant area. The first explosion was registered on the seismograph at the University of Mexico at 05 h 44 min 52 s and was followed by a dozen explosions within the next hour, some of them of BLEVE type (Boiling Liquid Expanding Vapour Explosion) due to rupture of one or more storage tanks. Two of the explosions had an intensity of 0.5 on the Richter scale. Unburned and burning gas entered the houses south of the plant area and set fire to everything. Blast waves from the explosions not only destroyed a number of houses but also shifted several cylindrical tanks from their supports and added more gas to the fire. The smaller spheres and some of the cylinders exploded and fragments and even whole cylinders weighing around 30 tons, were scattered over distances ranging from a few to up to 1200 m.

Effect of cimetidine, hydrocortisone, superoxide dismutase and catalase on the development of oedema after thermal injury

A new hypothesis for the pathophysiological mechanism underlying the development of oedema after a thermal injury has been tested in an experimental burn model. Support was given to the suggestion that oxygen-derived free radicals produced by invading leucocytes which upon activation release the superoxide radical (O2-), may be partly responsible for the increase in microvascular permeability seen after thermal injury. By removal of oxygen-derived free radicals with radical scavengers (superoxide dismutase and catalases) it was possible to reduce significantly the post-burn oedema formation. For comparison, one series of rats was pretreated with hydrocortisone and another with the histamine H2-blocker cimetidine. Hydrocortisone reduced the very early post-burn oedema formation which might partly be due to its membrane-stabilizing influence and partly to a direct effect on the microvasculature, causing a reduction of the vasodilatation observed post-burn. The inhibition of post-burn oedema formation by cimetidine, earlier demonstrated in animal burn models, was confirmed in the present study. The mean arterial blood pressure (MAP) in the cimetidine-treated rats decreased, however, after treatment. It is therefore difficult to determine to what extent the concentration of oedema is attributable to histamine H2-receptor blockade and to what extent to the reduced blood pressure. The influence of MAP on post-burn odema formation was further illustrated in two series of rats anaesthetized with Inactin an Hypnorm/Valium respectively. The results underline the importance of using the same anaesthetic throughout the experimental series.

Oedema measurements in a standard burn model

A highly standardized, reproducible burn model on rat hind paw as well as a method to measure oedema volume non-invasively is described. Along with a review of the literature on earlier methods to measure post-burn oedema we present a statistical evaluation of the present model with notes on its applicability in various experimental settings.

The effect of prompt local cooling on oedema formation in scalded rat paws

A standardized, reproducible burn model on rat paw was used and the effect of prompt local cooling on the oedema formation was measured using a newly developed non-invasive method. A transient reduction in oedema formation was observed lasting for a longer period of time with decreasing temperature down to 0 degrees C and increasing cooling time up to 120 min. The decrease in oedema formation was followed by an increase towards or above the amount of oedema in untreated scald injury. This post-cooling increase in oedema formation was related to the temperature and the exposure time of the cooling fluid. The immediate effects of cooling are most likely due to local restriction of the blood flow as a result of cold-induced vasoconstriction. The increase of the oedema formation after the cooling period may be due to reactive hyperaemia.

Locomotion of neutrophil granulocytes from patients with thermal injury. Identification of serum-derived inhibitors

Seven variables related to the migration of the PMN have been evaluated in a consecutive study of 33 thermally injured patients. Random migration and chemotactic response of the isolated PMN showed both depressed and enhanced cellular function as compared to a reference group. No apparent relation to burn size was seen. A chemokinetic ratio was constructed to investigate the responsiveness of the patient PMN to chemokinetically active serum factors. Significant reductions in the chemokinetic ratio were observed during the first 8 days after injury both in major (≥40 per cent) and in minor (<40 per cent) burns with the heaviest reductions seen in the major burn group. An inverse and significant (P<0−02) relationship was found between skin burn area and the chemokinetic ratio. Serum obtained during the first 1–2 weeks after injury contained increased amounts of heat-labile chemokinetic activity with significantly higher amounts in the major burns. Heat treatment (56°C for 30 min) of the sera revealed a reduced amount of heat-stable chemokinetic activity most apparent in the sera from patients with major burns. The reduction during the first 1–2 weeks was in most cases shown to be due to a deficiency of stimulatory activity whereas the reduction during the subsequent weeks predominantly was due to the presence of cell-directed inhibitors. Two kinds of cell-directed inhibitors of PMN migration have been identified. Both were heat stable and revealed no chemotactic activities. One interfered with the chemotactic response of the PMN and had an apparent molecular weight of 20–30 000. The other inhibited both the chemotactic response and random migration of normal PMN. This migration inhibitor was eluated from a Sephacryl S-200 column mainly at a molecular weight of 150–300 000 dalton. Four of 8 patients who died developed migration inhibitory activity in their sera. One patient with migration inhibitory activity has survived possibly due to plasmapheresis. This study shows the variety of dysfunction in mechanisms involved in PMN migration. Some appear to be primarily of cellular origin but most seem to be found in the environment i.e. in plasma. The study of these variables may provide a basis for a more successful treatment of thermally injured patients including measures such as plasmapheresis, plasma or granulocyte transfusions.

Heart lymph: Electrolyte composition and changes induced by cardiac glycosides

Abstract The electrolyte content of heart lymph was compared with that of plasma in heart-lung preparations of dogs. The lymph was collected from a cannula in a lymph vessel, mainly draining the left ventricle. The potassium, sodium and calcium contents of lymph and plasma were determined by flame photometry. Changes of the potassium balance were provoked by rapid-acting cardiac glycosides. The time relations and magnitudes of changes in lymph and plasma were studied. The average potassium content in lymph was 5.80 m-equiv./1 and in plasma 3.90 m-equiv./1. In contrast, no significant difference was shown between plasma and lymph sodium content. Cardiac glycosides provoked a potassium loss from the myocardium which appeared more rapidly in the lymph than in the plasma. The potassium concentration change was of the same order in both the fluids, indicating that most of the potassium loss induced by the glycoside emanated from the heart in the heart-lung preparation. It is concluded that myocardial potassium changes are adequately and sensitively reflected in cardiac lymph.

Early post-burn oedema in leucocyte-free rats

A highly standardized, reproducible burn model on rat hind paws with objective measurement of oedema volume was used to study the post-burn oedema formation in leucocyte-free rats as compared to a matched group of normal rats. No difference in oedema volume could be detected during the first 4 h post-burn. Thus the mechanical effect of sticking leucocytes in the injured area or leucocyte derived substances do not seem to play any significant role in the early local oedema formation which we postulate is entirely mediated by local events.