Ascariasis pneumonitis: a potentially fatal complication in smoke inhalation injury

Ascariasis pneumonitis: a potentially fatal complication in smoke inhalation injury

Burns Vol. 21, No. 2, pp. 149-151, 1995 Copyright 0 1995 Elsevier Science Ltd for ISBI Printed in Great Britain. Ail rights reserved 0305-4179/95 $10...

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Burns Vol. 21, No. 2, pp. 149-151, 1995 Copyright 0 1995 Elsevier Science Ltd for ISBI Printed in Great Britain. Ail rights reserved 0305-4179/95 $10.00 + 0.00

Ascariasis pneumonitis: complication in smoke

a potentially fatal inhalation injury*

J. P. Heggersxp2, M. J. Mwllerz, E. Elwood3 and D. N. Herndonlp2 ‘Departments of Surgery and Microbiology and Immunology, University of Texas Medical Branch, Galveston, 3hriners Bums Institute, Galveston, Texas and 3Department of Surgery, Grady Bum Center, Atlanta, Georgia, USA

Ascaris pneumonifis in areas of endemic infestation is considered a benign condition. Smoke inhalation with any burn injury can be pofenfially fafal. A heavy infestation of Ascaris could further exacerbate the smoke-induced lung injury. After ingested eggs hatchin the small intestine, the larvaepenefrafe the mucosa and invade the blood sfream and are then carried to the lungs. The hrvae break out info fhe aveolar spaces as fhey are too large to cross the capillary bed and are carried up the bronchial free and evenfually swallowed. This study describes three cases of Ascarisinfection in thermally injured children. While the burns were < 30 per cent total body surface area, two patients who were injured in the same fire had a further complication of smoke inhalation which necessitated sophisticated fherapy in order to promote survival. All patients were treated initially with Vermox. The one patient without smoke inhalafion did nof develop ascariasis pneumonifis even with positive stool samples and was discharged with no complications, whereas the two with smoke inhalation developed severe pneumonifis. One patient was placed on ECMO and did not receive a full course of the Vermox freafmenf. This patient died after several weeks of ECMO freafmenf. The fhird pafienf received a full course of Vermox, slowly recovered, and wenf home. Supportive therapy only is recommended during the lung migration phase of fhe Ascarislifecycle. We feel that continuation of chemofherapy (Vermox) would have been beneficial in fhefatal case based on the survival of the second patient. Ascaris-induced lung injury superimposed upon severe smoke-induced lung injury may have had an additive effect that precipitated severe, unrecoverable respiratory failure.

causedby nematode infections are based primarily upon the number of invading parasites.The number may be so small as to give no sign of the infection or so large as to overcome completely the resistanceof the host. Generally nematodes need only one host, the definitive host, in which they exist in both larval and adult form. The pathogenesis of the damage wrought by the nematodesis varied. Those directly invading the intestinal tract produce symptoms by mechanical irritation (Enferobius, Ascaris) and obstruction of a viscus (Ascaris), by excretion of toxic, lytic, and sensitizing products (Trichuris), by damageto vesselswith lossof blood (Anclyosfoma), and by invasion of the intestinal wall (Sfrongyloides, Trichinella,

Trichuris).

Introduction Nematodes, roundworms, are widely distributed in nature and exhibit remarkable diversity of habitat and form. Relatively few are parasitic and the great majority are free living, either in the soil or water. Parasitic nematodesvary considerably in size; some are hardly visible to the naked eye and others are several feet in length. Roundworms do not multiply in man, hence the lesions

*Presented

31October

in part at the ASTMH/ASP to 4 November 1993.

Joint Meeting, Atlanta, Georgia,

of the intestinal

nematodes,

Ascariasis Lifecycle Ascaris ltimbricoides

Burns,Vol. 21, No. 2,149-X1,1995

Some

entering not through the alimentary tract but through the skin (Ascuris, Strongyloides, Anclyosfoma), have a circuitous route of migration during which the larvae often affect tissuesnot ordinarily damagedby the adult. Nematode infections, particularly those causedby the intestinal nematodes,are transmitted directly from man to man or indirectly by insects which act as mechanical carriers of the ova. These infections although of universal distribution, are naturally more prevalent in the tropics where primitive living habits and poor sanitation serve to increasethe incidence of infectionl,‘.

is the largest roundworm which commonly occursin man asthe result of hand to mouth transfer of ova without an intermediate host. After ova are excreted in faecesthe second-stagelarvae develop outside the body. The motile, rhabditiform larvae emerge from the shellsof the ova in the duodenum, traverse the intestinal wall, invade both lymphatics and venules to reach the lungs by way of the thoracic duct or the portal vein and vena cava. In the lungs most of the larvae enter the alveoli from the pulmonary capillariesalthough some,not filtered out in the pulmonary circulation, may be carried to any part of the body. Two moults occur in the alveoli within approximately 10 days, then the larvae ascendthe bronchi and trachea and descend the oesophagus to reach the intestine. After the fourth moult in the small intestine, approximately 10 weeks after infection, the adult female Ascurismeasuresasmuch as 35 cm in length and begins to deposit ova’,‘.

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The lesions associatedwith ascariasisinfection are varied becauseof the systemic migrations of the larvae. As the first-stage larvae penetrate the intestinal wall, haemorrhagesmay occur in the mucosaand along the tract of the larva. If the infection is heavy, haemorrhagesoccur in the lungs as the larvae penetrate the alveoli. There is marked local eosinophile reaction to the larvae in the alveoli and often focal or confluent bronchopneumonia. Children frequently succumb to pneumonia at this stage, haemorrhages and abscessformation may occur in any organ becauseof ectopic localization of larvae which have not been trapped in the pulmonary circulation. During febrile states,the adults in attempting to escape, may migrate up the oesophagusand into the trachea, nose, and even the eustachiantube. There is danger in treatment that the sudden death of a great many adult worms may result in intestinal obstruction and that constitutional symptoms may occur from the liberation of toxin from the dead worms’,‘.

Results 1. Chest film of patient on ECMC) showing diffuse infiltratesthroughout both lungsconsistentwith ARIA.

Three thermally injured patients with bums < 30 per cent TBSA had a concomitant Ascaris infection. Two had a further complication of smokeinhalation. This necessitated sophisticated therapy in order to promote survival. All patients were treated initially with Vermox. The one patient without smoke inhalation did not develop pneumonitis and was discharged with no complications, whereas the two with smoke inhalation developed severe pneumonitis. One patient was placed on Extra Corporal Membrane Oxygenation (ECMO) and did not receive a full course of the Vermox treatment and subsequently died due to adult respiratory distresssyndrome (ARDS) (Figwe I). Histological lung sections revealed larval infestation (Figure 2). The third patient survived and was eventually discharged (Figure 3), although he did develop a pneumonitis. Multiple adult worms were found on the bed linens of both patients, apparently after regurgitation or migration of the worms. FiguresJa and b are representative of the adult worms found.

Figure

Conclusions

Figure

If large numbers of infective eggs are ingested, the larvae may causeintensive tissue reactions in the lung associated with dyspnoea often of the asthma type, fever, cough, rales. X-ray’s show an infiltrative shadow suggestive of pulmonary tuberculosis or viral pneumonia. Eosinophilia during this phase is prominent. The sputum characteristically contains many eosinophils and at times abundant Charcot-Leyden crystals. Although ascarid pneumonitis has its onset suddenly and causessevere symptoms, it is characteristic in clearing up spontaneously within 1-2 weeks’,‘. However this was not the casewhen two siblings were simultaneously injured in a house fire with complications of smoke inhalation. Chest X-rays revealed a lung infiltrate consistent with ARDS (Figure I) in the ECMOtreated patient, while the other patient only had a left lower lobe infiltrate (Figure 3). While supportive therapy is only recommendedduring lung migration, we felt that our patient was in double jeopardy with a combined ascariasis pneumonitis and smoke inhalation. Therefore we continued chemotherapy The patient placed on ECMO was not continued on

3. Chest film of patient not on ECMO showing dense consolidationin left lower lobeposteriorly. Sameinfiltrate may alsobe presentin the left upperlobe.

2. Histological preparation of Infected iung tissue showingcross-section of Ascaris larvae.(t-l &z E x: Tn.)

Figure

Heggers

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Figure 4. Photograph of male Ascaris which was recovered from the nasophaxyngeal head of the adult male Axuris.

chemotherapy. This patient died after several weeks of ECMO treatment. The third patient received a full course of Vermox, slowly recovered, and went home. Supportive therapy only is recommended during the lung migration phase of Ascaris lifecycle. We feel that continuation of chemotherapy (Vermox) would have been beneficial in the second, and fatal, case. Ascaris-induced lung injury superimposed upon severe smoke-induced lung injury may have had an additive effect that precipitated severe, unrecoverable respiratory failure.

Acknowledgements The authors wish to acknowledge MS CassieManess for her devoted and conscientiousefforts in the preparation of this manuscript. We would also like to acknowledge our Graphic Arts department: MS Sandra Baxter, our medical illustrator, who provided timely and preciseillustrations of our data, and Mr Lewis Milutin, Jr and MS Tina Garcia for their photographic expertise.

area: a, note coiled tail of the male with spicule; b,

This study was supported in part by the Shriners Hospital for Crippled Children, Shriners Bums Institute, Galveston. Texas.

References I Yamaguchi T, Kamo H, Masamitsu 0, Toshio S, Yukio Y. Color Atlas of Clinical Parasitiology. Pennsylvania: Lea & Febiger, 1981; pp 36, 76-80, 156. 2 Ash LR, Orihel TC. Intestinal helminths. In: Balows A, Hausler Jr WJ, Herrmann Isenberg HD, Shadomy HJ eds. Manual of Clinical Microbiology 5th edn. Washington, DC: American Society for Microbiology, 1991; pp 782-785.

Paper accepted 5 June 1994.

Correspondence should be addressed to: Dr John P. Heggers, Shriners Bums Institute, 815 Market Street, Galveston, TX 77550, USA.