340
Bums (1992) 18,(4), 340-341
Printed in Great Britain
Phosphorous pentachloride a slowly healing injury
chemical burn -
A. Eldadl, M. Chaouat”, A. Weinberg I, A. Neumanl, P. Ben Meirl, M. Roteml and M. R. Wexler’ IDepartment Israel
of Plastic Surgery and Bum Unit and 2The Skin Bank, Hadassah University
A 51-year-old chemical engineer sustained phosphorous penfachloride partial skin thickness burns over 20 per cent of his body surface area. Alfhough macroscopically and microscopically the wound seemed fo be superficial, fhe course of clinical healing of fhis injury was very slow and painful. Retrospectively this burn should have been freuted by early excision and grafting.
Introduction Phosphorous pentachloride (Pa,) is a yellowish-white fuming crystalline mass with a pungent odour, having a molecular weight of 208.22Da, a melting point of 148’C and a boiling point of 160°C. It is widely used as a catalyst, a chlorinating and a dehydrating agent. It is toxic if taken orally (LD,, for rats 66Omg/kg) or inhaled through the respiratory system (LD,, for rats 205 mg/m3 (Sax and Lewis, 1989). No data exists for the LD,, of PCl, when it is absorbed through the skin, although severe eye, skin and mucous membrane irritation is a well-described phenomena in animals. Its corrosive effect is via direct chemical action on tissue proteins that are converted to an acid proteinate which dissolves in the concentrated acid (Dreisbach and Robertson, 1987). With haemoglobin it forms dark acid haematin and is then precipitated. Intense stimulation by the acid causes reflex loss of vascular tone. Its toxicometric indices and some of its toxic effects, as well as its characteristics as a skin irritant, and its highest admissible concentrations have been studied by Roshin and Molodkina (1977). We present an example of an accidental chemical bum with PCl, and our recommendations for treatment.
Case report A 51-year-old chemical engineer was working in a chemistry laboratory when he sustained splashes of PCI, over his back, shoulders, face and eyes. He washed himself immediately with tapwater for IS min but the pain became worse under water. He was treated in a peripheral hospital for 24h and then transferred to our unit. His past medical history revealed Crohn’s disease known for 14 years and treated with 5-aminosalicylic acid. On admission he was 0 1992 Butterworth-Heinemann 0305-4179/92/04034002
Ltd
Hospital, Ein Kerem, Jerusalem,
in a general good condition, but suffered pain, mainly in the eyes and back. His eyes were irritable with superficial cornea1 erosions. Superficial hyperpigmented bums covered his shoulders, back and forehead. The rest of the physical examination did not reveal any additional pathological findings.
laboratory results Hb 12.5 g/dl, Hct 36 per cent, WBC 11.9/mm”, platelets 238000/mm3, prothrombin time (PT) (in s) 83 per cent, partial thromboplastin time (PTT) 37.6 s. Blood electrolytes, urea, sugar, creatinine, uric acid, bilirubin, cholesterol, alkaline phosphatase, LDH, liver enzymes, calcium and phosphate were all within the normal range. Total protein was low (49 g/l) and albumin was 29 g/l. Creatinine clearance for the first 24 h was 5 1 ml/min and 129 and 132 ml/min for the following days. In order to assess the depth of the bums punch biopsies were taken from the back (the most affected area) and the histological findings were of a superficial bum with viable adnexa in the depth of the dermis (Figure I). It was decided on a conservative approach and the patient was treated twice daily with I per cent silver sulphadiazine cream (SSD). A high caloric, high protein diet was given orally in an attempt to improve his hypoalbuminaemia which was interpreted as a result of his longstanding colon disease. An average energy input of 2447 Kcal/day was taken with an average protein intake of 117 g/day. A gradual rise in the albumin level was recorded up to 34 g/l 3 weeks after the bum. All other laboratory results were normal throughout the period of his stay in hospital except for an elevation of aspartic amino transferase 50 (normal range 7-40 units), alanine amino transferase 167 (normal range 0-40 units) and gamma glutamic transferase I12 (normal range O-40 units). The erosions of his cornea healed within 72 h, a similar timespan was expected from the superficial skin lesions, but the healing course for the back bums was very slow. Another set of punch biopsies was taken to rule out transformation of the lesions into full skin thickness bums but these biopsies demonstrated the same picture of superficial bums without any signs of healing. Not until the end of week 4 after injury were some small islands of epidermis observed in the wound bed. Although no signs of infection were apparent, healing was slow and painful. It was only by week 6 that the patient could be discharged for further
A. Eldad et al.: Phosphorous
pentachloride
341
chemical burn
No reports of PCI, bums were found in our search of the literature so we could only rely on our clinical judgement and the histological appearance of the bums when we decided to embark on a conservative form of treatment. Retrospectively this patient would have been better treated if he had been operated and his wounds excised and grafted early. In this patient we could not detect any signs of systemic absorption of the toxic material. Elevation of liver enzymes is a well-described phenomena of bums and not necessarily a sign of renal or hepatocellular damage. Low levels of albumin are well described in bums (which reflect a catabolic sequence of events) but with this patient they were low to start with and reached normal levels while healing was still incomplete, so we do not tend to blame hypoalbuminaemia or a toxically induced organ failure for the slow course of healing shown by this patient. It seems that PCl, has some special deleterious effect on the wound healing process, not unlike the effects of mustard gas where the lesions appear to be superficial blisters, but in some patients these blisters healed only after 70 days (Willems, 1989). We therefore suggest that the long period of healing shown by these chemical bums is not caused exclusively by the extent of immediate cell death, but may be due to some further damage incurred by the epidermal cells. Although epidermal adnexa appeared normal in biopsies, these cells were very slow to replicate and migrate across the wound. An aggressive policy of excision and grafting will probably shorten the morbidity in patients with injuries caused by phosphorous pentachloride.
Figure 1. Necrosis of epidermis and superficial dermis with intact
adnexa in the depth of the dermis 24 h after chemical bums. ( x 40, Haematoxylin & eosin.)
ambulatory treatment and only by week 8 were all his wounds healed. No signs of hypertrophic follow-up.
scarring were evident
in the
Discussion Chemical bums are notorious for their slow course of healing, When compared to similar size thermal injuries the stay in hospital for chemical bums was 30 per cent longer (Curreri et al., 1970). A recent report (Mozingo et al., 1988) reviewing clinical data from the same institute (Brooke Army Medical Center) showed that the stay in hospital for all chemical bums is longer when compared to similar size thermal injuries, but this result is mainly due to white phosphorous bums that were included in the chemical bum group. When the non-white phosphorous chemical bums were compared to thermal injuries, the stay in hospital for the latter was 25 per cent shorter.
References Curreri P. W., Asch M. J. and Pruitt B. A. (1970) The treatment of chemical bums: specialized diagnostic therapeutic and prognostic considerations. J. Tvatima 10, 634. Dreisbach R. H. and Robertson W. 0. (1987) In: Handbook of Poisoning, 12th edn. Norwalk, Connecticut: Appleton & Lange, p. 199. Mozingo D. W., Smith A. A., McManus W. F. et al. (1988) Chemical bums. 1. Trauma 28, 642. Roshin A. V. and Molodkina N. N. (1977) Chloro compounds of phosphorous as industrial hazards. 1. Hyg. Epidemiol. Microbial. lmwlol. 21, 387. Sax N. I. and Lewis R. J. (1989) In: Dungerotls Properfies of Industriu~ Materials, vol. 3, 7th edn. New York: Van Nostrand Reinhold, p. 2778. Willems J. L. (1989) Clinical management of mustard gas casualties. Ann. Med. Milit. Belg. 3, (suppl.), l-60. Paper accepted
9 December
1991.
Correspondence should be addressed to: Dr Arieh Eldad, Bums Unit, Hadassah University Hospital, Ein Kerem, Jerusalem, Israel, 91120.
Bums (1992) 18,(4), 340-341
Printed in Great Britain
Phosphorous pentachloride a slowly healing injury
chemical burn -
A. Eldadl, M. Chaouat”, A. Weinberg I, A. Neumanl, P. Ben Meirl, M. Roteml and M. R. Wexler’ IDepartment Israel
of Plastic Surgery and Bum Unit and 2The Skin Bank, Hadassah University
A 51-year-old chemical engineer sustained phosphorous penfachloride partial skin thickness burns over 20 per cent of his body surface area. Alfhough macroscopically and microscopically the wound seemed fo be superficial, fhe course of clinical healing of fhis injury was very slow and painful. Retrospectively this burn should have been freuted by early excision and grafting.
Introduction Phosphorous pentachloride (Pa,) is a yellowish-white fuming crystalline mass with a pungent odour, having a molecular weight of 208.22Da, a melting point of 148’C and a boiling point of 160°C. It is widely used as a catalyst, a chlorinating and a dehydrating agent. It is toxic if taken orally (LD,, for rats 66Omg/kg) or inhaled through the respiratory system (LD,, for rats 205 mg/m3 (Sax and Lewis, 1989). No data exists for the LD,, of PCl, when it is absorbed through the skin, although severe eye, skin and mucous membrane irritation is a well-described phenomena in animals. Its corrosive effect is via direct chemical action on tissue proteins that are converted to an acid proteinate which dissolves in the concentrated acid (Dreisbach and Robertson, 1987). With haemoglobin it forms dark acid haematin and is then precipitated. Intense stimulation by the acid causes reflex loss of vascular tone. Its toxicometric indices and some of its toxic effects, as well as its characteristics as a skin irritant, and its highest admissible concentrations have been studied by Roshin and Molodkina (1977). We present an example of an accidental chemical bum with PCl, and our recommendations for treatment.
Case report A 51-year-old chemical engineer was working in a chemistry laboratory when he sustained splashes of PCI, over his back, shoulders, face and eyes. He washed himself immediately with tapwater for IS min but the pain became worse under water. He was treated in a peripheral hospital for 24h and then transferred to our unit. His past medical history revealed Crohn’s disease known for 14 years and treated with 5-aminosalicylic acid. On admission he was 0 1992 Butterworth-Heinemann 0305-4179/92/04034002
Ltd
Hospital, Ein Kerem, Jerusalem,
in a general good condition, but suffered pain, mainly in the eyes and back. His eyes were irritable with superficial cornea1 erosions. Superficial hyperpigmented bums covered his shoulders, back and forehead. The rest of the physical examination did not reveal any additional pathological findings.
laboratory results Hb 12.5 g/dl, Hct 36 per cent, WBC 11.9/mm”, platelets 238000/mm3, prothrombin time (PT) (in s) 83 per cent, partial thromboplastin time (PTT) 37.6 s. Blood electrolytes, urea, sugar, creatinine, uric acid, bilirubin, cholesterol, alkaline phosphatase, LDH, liver enzymes, calcium and phosphate were all within the normal range. Total protein was low (49 g/l) and albumin was 29 g/l. Creatinine clearance for the first 24 h was 5 1 ml/min and 129 and 132 ml/min for the following days. In order to assess the depth of the bums punch biopsies were taken from the back (the most affected area) and the histological findings were of a superficial bum with viable adnexa in the depth of the dermis (Figure I). It was decided on a conservative approach and the patient was treated twice daily with I per cent silver sulphadiazine cream (SSD). A high caloric, high protein diet was given orally in an attempt to improve his hypoalbuminaemia which was interpreted as a result of his longstanding colon disease. An average energy input of 2447 Kcal/day was taken with an average protein intake of 117 g/day. A gradual rise in the albumin level was recorded up to 34 g/l 3 weeks after the bum. All other laboratory results were normal throughout the period of his stay in hospital except for an elevation of aspartic amino transferase 50 (normal range 7-40 units), alanine amino transferase 167 (normal range 0-40 units) and gamma glutamic transferase I12 (normal range O-40 units). The erosions of his cornea healed within 72 h, a similar timespan was expected from the superficial skin lesions, but the healing course for the back bums was very slow. Another set of punch biopsies was taken to rule out transformation of the lesions into full skin thickness bums but these biopsies demonstrated the same picture of superficial bums without any signs of healing. Not until the end of week 4 after injury were some small islands of epidermis observed in the wound bed. Although no signs of infection were apparent, healing was slow and painful. It was only by week 6 that the patient could be discharged for further
A. Eldad et al.: Phosphorous
pentachloride
341
chemical burn
No reports of PCI, bums were found in our search of the literature so we could only rely on our clinical judgement and the histological appearance of the bums when we decided to embark on a conservative form of treatment. Retrospectively this patient would have been better treated if he had been operated and his wounds excised and grafted early. In this patient we could not detect any signs of systemic absorption of the toxic material. Elevation of liver enzymes is a well-described phenomena of bums and not necessarily a sign of renal or hepatocellular damage. Low levels of albumin are well described in bums (which reflect a catabolic sequence of events) but with this patient they were low to start with and reached normal levels while healing was still incomplete, so we do not tend to blame hypoalbuminaemia or a toxically induced organ failure for the slow course of healing shown by this patient. It seems that PCl, has some special deleterious effect on the wound healing process, not unlike the effects of mustard gas where the lesions appear to be superficial blisters, but in some patients these blisters healed only after 70 days (Willems, 1989). We therefore suggest that the long period of healing shown by these chemical bums is not caused exclusively by the extent of immediate cell death, but may be due to some further damage incurred by the epidermal cells. Although epidermal adnexa appeared normal in biopsies, these cells were very slow to replicate and migrate across the wound. An aggressive policy of excision and grafting will probably shorten the morbidity in patients with injuries caused by phosphorous pentachloride.
Figure 1. Necrosis of epidermis and superficial dermis with intact
adnexa in the depth of the dermis 24 h after chemical bums. ( x 40, Haematoxylin & eosin.)
ambulatory treatment and only by week 8 were all his wounds healed. No signs of hypertrophic follow-up.
scarring were evident
in the
Discussion Chemical bums are notorious for their slow course of healing, When compared to similar size thermal injuries the stay in hospital for chemical bums was 30 per cent longer (Curreri et al., 1970). A recent report (Mozingo et al., 1988) reviewing clinical data from the same institute (Brooke Army Medical Center) showed that the stay in hospital for all chemical bums is longer when compared to similar size thermal injuries, but this result is mainly due to white phosphorous bums that were included in the chemical bum group. When the non-white phosphorous chemical bums were compared to thermal injuries, the stay in hospital for the latter was 25 per cent shorter.
References Curreri P. W., Asch M. J. and Pruitt B. A. (1970) The treatment of chemical bums: specialized diagnostic therapeutic and prognostic considerations. J. Tvatima 10, 634. Dreisbach R. H. and Robertson W. 0. (1987) In: Handbook of Poisoning, 12th edn. Norwalk, Connecticut: Appleton & Lange, p. 199. Mozingo D. W., Smith A. A., McManus W. F. et al. (1988) Chemical bums. 1. Trauma 28, 642. Roshin A. V. and Molodkina N. N. (1977) Chloro compounds of phosphorous as industrial hazards. 1. Hyg. Epidemiol. Microbial. lmwlol. 21, 387. Sax N. I. and Lewis R. J. (1989) In: Dungerotls Properfies of Industriu~ Materials, vol. 3, 7th edn. New York: Van Nostrand Reinhold, p. 2778. Willems J. L. (1989) Clinical management of mustard gas casualties. Ann. Med. Milit. Belg. 3, (suppl.), l-60. Paper accepted
9 December
1991.
Correspondence should be addressed to: Dr Arieh Eldad, Bums Unit, Hadassah University Hospital, Ein Kerem, Jerusalem, Israel, 91120.
