Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
Acute Phosphine Poisoning? a Case Report and Review. D. Schoonbroodt, P. Guffens, P. Jousten, J. Ingels & J. Grodos To cite this article: D. Schoonbroodt, P. Guffens, P. Jousten, J. Ingels & J. Grodos (1992) Acute Phosphine Poisoning? a Case Report and Review., Acta Clinica Belgica, 47:4, 280-284, DOI: 10.1080/17843286.1992.11718243 To link to this article: http://dx.doi.org/10.1080/17843286.1992.11718243
Published online: 16 May 2016.
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View related articles
Citing articles: 9 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [University of Saskatchewan Library]
Date: 24 August 2017, At: 23:28
280
ACUTE PHOSP HINE POISON ING ? A CASE REPOR T AND REVIEW.
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
D . Schoonbr oodt*, P. Guffens*, P. Jousten *, J. lngels*, J. Grodos
**
SUMMARY
CASE REPORT
A case compatible with an acute phosphine poisoning after inhalation is presented. The observation was notably characterized by necrosis of the nasal mucosa, the delayed onset of a pulmonary edema and myocardia l injury with multisyste mic involvement. A review of literature, not very prolific in this field, is included in the discuss ion.
A 53-year-o ld man was admitted to the hospital with suspicion of POL YTANOL poisoning . POL YT ANOL contains 28% of calcium phosphid e (Chemi sche Fabrik Wi.ilfel , D-3000 Hannove r Germany) . Four days before the hospitaliz ation'' . the patient worked, during rainy weather, with this toxic powder for about two hours. He used it in hi s garden as a poison against moles and put into the mole galleries without the powder . . After about 18 hours, he measures protective experienc ed fever (40° C), dry cough, generali zed weakness associated with myalg ia, headac he di zziness and nausea. He also was dim-sight ed'. He was treated at home with cefazolin e (3 x I g IM/24 h), but respiratory symptom atology got
Acta Clin Belg. 47, 4: 280-4. INTROD UCTION Phosphin e poi soning after inhalation remains a rarely described entity with an as pecific clinical presentation and severe consequen ce . Phosphide , associated either with aluminum , zinc or calcium is a rodenti cide product. B y the action of water, it produces phosphin e (PH), a pote nti ally very toxic gas. lt may lead to multi system toxic ity, especially for the lungs, the heart, the kidneys and the brain. Phosphin e is frequently used as a fumi gant in grain elevators, cargo ships and in the manufact ure of si Iicon chips forthe computer industry. PH3 , a colourless gas, has a characteri stic odour of decay ing fi sh, detectable at 2 ppm. However , the threshold limit value of safe exposure (TL V) is 0 ,3 ppm. Hence, the odour threshold does not provide sufficient warning of dangerou s concentra tions.
* Innere Medizin , St Nikolaus Hospita l Eupen, Hufengasse 4, 4700 EUPEN tel. : 087174.45 .44 ** Pathologische Anatom.ie, St Nikolaus Hospi tal Eupen. Acta Clinica Belgica 47.4 ( 1992)
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Hi s past medical hi story was unremark able and there was no coronary risk factor. On the day of admi ssion , the patient was very anxious dys pneic, cyanotic, had a dry cough and com~ plained of severe nasal obstructio n. The temperature was 40°C; heart rate was 120/mi n., respiratory rate 30/min. and blood pressure 120/75 mmHg. On examinat ion , the patient had a healthy cons- ' titution. Inspirator y crackles were heard over the left upper lobe and right base of.the lung. There was no other abnormality. A chest-X-r ay examination showed interstitial infiltrates involving the left upper lobe and the apex of the rig ht inferior lobe with consolida tion and air bronchogram. A specimen of arterial blood , drawn while the patient was breathing room air, revealed: pH 7,49; Pa 0 2 55 mmHg; Pa C02 33 mm Hg; HCO3 _ ~i 23 mmol/I; BE - 1,2 mmol/1 ; 0 2 sat 85%.
r
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ACUTE PHOSPHINE POISONING ? A CASE R E PORT AND REVIEW.
28 1
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The ECG showed sinu s tachycardia, le ft
f anterior fascicular block without repolarisation
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
, abnonnality. Relevant laboratory data indicated: hematocrit 43 %, white blood cell count I 6.8x 109/1 with 90 % neutrophil s, platelet count 22 lxl0 9/I , urea 5,71 mmol/I (N: 2,67-8,03), fcreatinine 97,2 µmol/1 (N: 70,7 - 132,6), ASAT 48 U/l (N: 2-24), ALAT72 U/I (N: 2-24), LDH 503 U/l (N: 120 - 240), CPK 532 U/I (N: IO- 70) fwith 19 U MB subunit (N: < IO), amyl ase . 126 U/l (N: < 120), lipase 475 U/1(N:11 j V5-V6, conduction troubles, cardiac arrhythmias, of pericardia( damage (3,4) .
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A blood transaminase elevation was found after both inhal ation and ingestion ( l -3). Renal 05 ~ J injuries were characterized in two series of 16 0 and 25 patients who ingested phosphide by a :JC:: Je: significant proteinuria in 2 patients and by an 10 1 acute renal failure in 2 other pati ents (3, 5). We g. al so noted an elevation of the CPK mu scular fraction . Wilson et al (1) reported the sameobser-
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I
283
vation in 2 cases after phosphine inhalation. Aspecific neurological abnormalities were also reported: fatigue, headache, drowsiness, dizziness, diffuse alterations on EEG , paresthesia (6), CNS depress ion leading to coma, seizure (4), psychotic behaviour. Since admi ssion, amy lase and lipase serum levels remained abnormal for 2 weeks with a peak on day 17 and evidence of oedematous pancreatitis wasodetected on day 15 . Only Stephenson et al (7) noted a ri se of amylase without macro sc opic and micro sc opic abnormalities on post-mortem examination of the pancreas. The pathological action of phosphine has not been c learly establi shed . The organs with the greatest oxygen requirement appear to be especially sensitive to damage. Phosphine is a noncompetitive inhibitor of mitochondrial cytochrome oxidase in experimental animals (8). It is likely that interference with cellular respiration may lead to multi system toxicity . Phosphine poi soning is usually characterized by a poor prognosis. Wil son et al reported that 2 chi ldren and 29 adu lts of 31 crew members aboard a grain frei ghter became acutely ill after inhaling the toxic fumi gant phosphine; one child died (I). After ingestion of phosphide more data are avai lable (2,3,5, I 0) . In a series of25 pati ents, who had consumed 3 or more tablets of alumi nium phos phide, 10 succumbed. Because of the important toxic effects of phosphine, prevention remains the best protection. Thi s product should not be used in the presence of moi sture and without a face-mask. It is necessary to monitorthe patient for respiratory di stress and a 3 day observation is essential in order to detect a delayed onset of pulmonary edema. If cough or difficulties in breathing develop, it is important to make an evaluation for respiratory tract, irritation bronchitis or pneumoniti s, to administer I 00 % humidified oxygen with assisted ventilation if required and to manage the pulmonary edema with positive and end expiratory pressure breathing. It is also required to Acta Clinica Belgica 47.4 ( 1992)
284
ACUTE PHOSPHJNE POISONING ? A CASE REPORT AND REVIEW.
Ir I
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
check fluid balance, the electrolytes, the cardiac, hepatic, neurological and renal functions. This present case, compatible with an acute phosphine poi soning after inhalation, illustrates the possible delay and severity of the multisystemic involvement, which requires strict survei ll ance and adequate therapy.
RESUM E Nous rapportons,nn cas compatible avec une intoxication par inhalation de phosphine. L'observation se caracterise notamment par une necrose de la muqueuse nasale, !'apparition retardee d' un oedeme pulmonaire et de lesions myocardiques avec attei nte multiorganique. Une revue de la Jitterature est reprise dan la discussion.
SAMENVATilNG
Er wordt een geval voorge teld dat kompatibel is meteen intoxikatie door inhalatie van fos fin e. Bij deze casu wordt onder meer een neusslijmhuidnekrose, een laattijdig opgetreden longoedeem, en een aan tasting van hartspier en van meerdere andere organen beschreven. Van deschaarse litteratuurbestanden over dit onderwerp wordt een overzicht gegeven.
ACKNOWLEDGMENTS We wou ld like to thank, Pr. Mahieu, Cliniques Universitaires St Luc Brussels (Belgium), for his scientific help and interest.
Acta Clinica Belgica 47.4 ( 1992)
REFERENCES 1. Wilson R, Lovejoy FH, Jadger RJ et al. Acute phosphine poisoning aboard a grain freighter. JAMA. 1980; 244: 148-50. 2. Chopra JS, Kalra OP, Malik R et al. Aluminum phosphide poisoning: a prospective study of 16 cases inone year. PostgradMed J. 1986;62: I 11 315. 3. Khosla SN, Nand N, Kumar P. Cardiovascular complications of aluminum phosphide poisoning. Angiology. 1988; 39: 355-9. 4. Mi ra UK, Tripathi AK, Pandey R et al. Acute phosphine poi soning following inges tion or aluminum phosphide. Human Toxicol. 1988; 7: 343-5. 5. Singh S, Dilwari JB , Vashist R et al. Acute aluminum phosphide poisoning in man. Br Med J. 1985; 290: 1110- 1I. 6. Heyndrickx A, Van Peteghem C, Van Den Heede M et al. A double fatality with chi ld ren due to fumigated wheal. Eu r J Toxicol Environ Hyg. 1976; 9: I 13-8. 7. Stenphenson JPB . Zinc phosphide poisoning. Arch Environ' Health. 1967; 15: 83-8. 8. Chefurka W, Kashi KP, Bond EJ. The effect of phosphine on electron transport in mitochondria . Pestic Biochem Physiol. 1976; 6: 65-84. 9. Misra, Bhargava SK, Nag D, Kioway MM, Lal MM . Occupational phosphine exposure in India Workers. Toxicology Letters. 1988; 42: 257-63 . 10. Sepaha GC, Bharani AK, Jain SM et al. Acute aluminum phosphide poisoning. J Ind Med Assoc. 1985; 83: 378-9. 11. Hackenbe rg U. Chronic ingestion by rats of standard diet treated with aluminum phosphide. Toxicol Appl Pharmacol. 1972; 23: 147- 15 l 2. Rodenberg HD, Chang CC, Watson WA. Zi nc phosphide ingestion: a case report and review. Vet Hum Toxicol. 1989; 3 1: 559-62.
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ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
Acute Phosphine Poisoning? a Case Report and Review. D. Schoonbroodt, P. Guffens, P. Jousten, J. Ingels & J. Grodos To cite this article: D. Schoonbroodt, P. Guffens, P. Jousten, J. Ingels & J. Grodos (1992) Acute Phosphine Poisoning? a Case Report and Review., Acta Clinica Belgica, 47:4, 280-284, DOI: 10.1080/17843286.1992.11718243 To link to this article: http://dx.doi.org/10.1080/17843286.1992.11718243
Published online: 16 May 2016.
Submit your article to this journal
View related articles
Citing articles: 9 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [University of Saskatchewan Library]
Date: 24 August 2017, At: 23:28
280
ACUTE PHOSP HINE POISON ING ? A CASE REPOR T AND REVIEW.
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
D . Schoonbr oodt*, P. Guffens*, P. Jousten *, J. lngels*, J. Grodos
**
SUMMARY
CASE REPORT
A case compatible with an acute phosphine poisoning after inhalation is presented. The observation was notably characterized by necrosis of the nasal mucosa, the delayed onset of a pulmonary edema and myocardia l injury with multisyste mic involvement. A review of literature, not very prolific in this field, is included in the discuss ion.
A 53-year-o ld man was admitted to the hospital with suspicion of POL YTANOL poisoning . POL YT ANOL contains 28% of calcium phosphid e (Chemi sche Fabrik Wi.ilfel , D-3000 Hannove r Germany) . Four days before the hospitaliz ation'' . the patient worked, during rainy weather, with this toxic powder for about two hours. He used it in hi s garden as a poison against moles and put into the mole galleries without the powder . . After about 18 hours, he measures protective experienc ed fever (40° C), dry cough, generali zed weakness associated with myalg ia, headac he di zziness and nausea. He also was dim-sight ed'. He was treated at home with cefazolin e (3 x I g IM/24 h), but respiratory symptom atology got
Acta Clin Belg. 47, 4: 280-4. INTROD UCTION Phosphin e poi soning after inhalation remains a rarely described entity with an as pecific clinical presentation and severe consequen ce . Phosphide , associated either with aluminum , zinc or calcium is a rodenti cide product. B y the action of water, it produces phosphin e (PH), a pote nti ally very toxic gas. lt may lead to multi system toxic ity, especially for the lungs, the heart, the kidneys and the brain. Phosphin e is frequently used as a fumi gant in grain elevators, cargo ships and in the manufact ure of si Iicon chips forthe computer industry. PH3 , a colourless gas, has a characteri stic odour of decay ing fi sh, detectable at 2 ppm. However , the threshold limit value of safe exposure (TL V) is 0 ,3 ppm. Hence, the odour threshold does not provide sufficient warning of dangerou s concentra tions.
* Innere Medizin , St Nikolaus Hospita l Eupen, Hufengasse 4, 4700 EUPEN tel. : 087174.45 .44 ** Pathologische Anatom.ie, St Nikolaus Hospi tal Eupen. Acta Clinica Belgica 47.4 ( 1992)
I
(t .p
s j
(
v
r1u
p
·
~
rpc j
f1
worse.
I
Hi s past medical hi story was unremark able and there was no coronary risk factor. On the day of admi ssion , the patient was very anxious dys pneic, cyanotic, had a dry cough and com~ plained of severe nasal obstructio n. The temperature was 40°C; heart rate was 120/mi n., respiratory rate 30/min. and blood pressure 120/75 mmHg. On examinat ion , the patient had a healthy cons- ' titution. Inspirator y crackles were heard over the left upper lobe and right base of.the lung. There was no other abnormality. A chest-X-r ay examination showed interstitial infiltrates involving the left upper lobe and the apex of the rig ht inferior lobe with consolida tion and air bronchogram. A specimen of arterial blood , drawn while the patient was breathing room air, revealed: pH 7,49; Pa 0 2 55 mmHg; Pa C02 33 mm Hg; HCO3 _ ~i 23 mmol/I; BE - 1,2 mmol/1 ; 0 2 sat 85%.
r
l
ACUTE PHOSPHINE POISONING ? A CASE R E PORT AND REVIEW.
28 1
r '
The ECG showed sinu s tachycardia, le ft
f anterior fascicular block without repolarisation
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
, abnonnality. Relevant laboratory data indicated: hematocrit 43 %, white blood cell count I 6.8x 109/1 with 90 % neutrophil s, platelet count 22 lxl0 9/I , urea 5,71 mmol/I (N: 2,67-8,03), fcreatinine 97,2 µmol/1 (N: 70,7 - 132,6), ASAT 48 U/l (N: 2-24), ALAT72 U/I (N: 2-24), LDH 503 U/l (N: 120 - 240), CPK 532 U/I (N: IO- 70) fwith 19 U MB subunit (N: < IO), amyl ase . 126 U/l (N: < 120), lipase 475 U/1(N:11 j V5-V6, conduction troubles, cardiac arrhythmias, of pericardia( damage (3,4) .
f 1e ·
I
J
I
i~ I
A blood transaminase elevation was found after both inhal ation and ingestion ( l -3). Renal 05 ~ J injuries were characterized in two series of 16 0 and 25 patients who ingested phosphide by a :JC:: Je: significant proteinuria in 2 patients and by an 10 1 acute renal failure in 2 other pati ents (3, 5). We g. al so noted an elevation of the CPK mu scular fraction . Wilson et al (1) reported the sameobser-
LI'
I
283
vation in 2 cases after phosphine inhalation. Aspecific neurological abnormalities were also reported: fatigue, headache, drowsiness, dizziness, diffuse alterations on EEG , paresthesia (6), CNS depress ion leading to coma, seizure (4), psychotic behaviour. Since admi ssion, amy lase and lipase serum levels remained abnormal for 2 weeks with a peak on day 17 and evidence of oedematous pancreatitis wasodetected on day 15 . Only Stephenson et al (7) noted a ri se of amylase without macro sc opic and micro sc opic abnormalities on post-mortem examination of the pancreas. The pathological action of phosphine has not been c learly establi shed . The organs with the greatest oxygen requirement appear to be especially sensitive to damage. Phosphine is a noncompetitive inhibitor of mitochondrial cytochrome oxidase in experimental animals (8). It is likely that interference with cellular respiration may lead to multi system toxicity . Phosphine poi soning is usually characterized by a poor prognosis. Wil son et al reported that 2 chi ldren and 29 adu lts of 31 crew members aboard a grain frei ghter became acutely ill after inhaling the toxic fumi gant phosphine; one child died (I). After ingestion of phosphide more data are avai lable (2,3,5, I 0) . In a series of25 pati ents, who had consumed 3 or more tablets of alumi nium phos phide, 10 succumbed. Because of the important toxic effects of phosphine, prevention remains the best protection. Thi s product should not be used in the presence of moi sture and without a face-mask. It is necessary to monitorthe patient for respiratory di stress and a 3 day observation is essential in order to detect a delayed onset of pulmonary edema. If cough or difficulties in breathing develop, it is important to make an evaluation for respiratory tract, irritation bronchitis or pneumoniti s, to administer I 00 % humidified oxygen with assisted ventilation if required and to manage the pulmonary edema with positive and end expiratory pressure breathing. It is also required to Acta Clinica Belgica 47.4 ( 1992)
284
ACUTE PHOSPHJNE POISONING ? A CASE REPORT AND REVIEW.
Ir I
Downloaded by [University of Saskatchewan Library] at 23:28 24 August 2017
check fluid balance, the electrolytes, the cardiac, hepatic, neurological and renal functions. This present case, compatible with an acute phosphine poi soning after inhalation, illustrates the possible delay and severity of the multisystemic involvement, which requires strict survei ll ance and adequate therapy.
RESUM E Nous rapportons,nn cas compatible avec une intoxication par inhalation de phosphine. L'observation se caracterise notamment par une necrose de la muqueuse nasale, !'apparition retardee d' un oedeme pulmonaire et de lesions myocardiques avec attei nte multiorganique. Une revue de la Jitterature est reprise dan la discussion.
SAMENVATilNG
Er wordt een geval voorge teld dat kompatibel is meteen intoxikatie door inhalatie van fos fin e. Bij deze casu wordt onder meer een neusslijmhuidnekrose, een laattijdig opgetreden longoedeem, en een aan tasting van hartspier en van meerdere andere organen beschreven. Van deschaarse litteratuurbestanden over dit onderwerp wordt een overzicht gegeven.
ACKNOWLEDGMENTS We wou ld like to thank, Pr. Mahieu, Cliniques Universitaires St Luc Brussels (Belgium), for his scientific help and interest.
Acta Clinica Belgica 47.4 ( 1992)
REFERENCES 1. Wilson R, Lovejoy FH, Jadger RJ et al. Acute phosphine poisoning aboard a grain freighter. JAMA. 1980; 244: 148-50. 2. Chopra JS, Kalra OP, Malik R et al. Aluminum phosphide poisoning: a prospective study of 16 cases inone year. PostgradMed J. 1986;62: I 11 315. 3. Khosla SN, Nand N, Kumar P. Cardiovascular complications of aluminum phosphide poisoning. Angiology. 1988; 39: 355-9. 4. Mi ra UK, Tripathi AK, Pandey R et al. Acute phosphine poi soning following inges tion or aluminum phosphide. Human Toxicol. 1988; 7: 343-5. 5. Singh S, Dilwari JB , Vashist R et al. Acute aluminum phosphide poisoning in man. Br Med J. 1985; 290: 1110- 1I. 6. Heyndrickx A, Van Peteghem C, Van Den Heede M et al. A double fatality with chi ld ren due to fumigated wheal. Eu r J Toxicol Environ Hyg. 1976; 9: I 13-8. 7. Stenphenson JPB . Zinc phosphide poisoning. Arch Environ' Health. 1967; 15: 83-8. 8. Chefurka W, Kashi KP, Bond EJ. The effect of phosphine on electron transport in mitochondria . Pestic Biochem Physiol. 1976; 6: 65-84. 9. Misra, Bhargava SK, Nag D, Kioway MM, Lal MM . Occupational phosphine exposure in India Workers. Toxicology Letters. 1988; 42: 257-63 . 10. Sepaha GC, Bharani AK, Jain SM et al. Acute aluminum phosphide poisoning. J Ind Med Assoc. 1985; 83: 378-9. 11. Hackenbe rg U. Chronic ingestion by rats of standard diet treated with aluminum phosphide. Toxicol Appl Pharmacol. 1972; 23: 147- 15 l 2. Rodenberg HD, Chang CC, Watson WA. Zi nc phosphide ingestion: a case report and review. Vet Hum Toxicol. 1989; 3 1: 559-62.
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