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 Table of Contents  
Year : 2016  |  Volume : 9  |  Issue : 3  |  Page : 339-341

Organophosphorus poisoning: A rare case of upper extremity deep vein thrombosis

1 Department of General Medicine, Sher-I-Kashmir Institute of Medical Sciences Medical College and Hospital, Srinagar, Jammu and Kashmir, India
2 Department of Radio Diagnosis, Sher-I-Kashmir Institute of Medical Sciences Medical College and Hospital, Srinagar, Jammu and Kashmir, India

Date of Web Publication21-Dec-2016

Correspondence Address:
Dr. Muzafar Naik
Department of General Medicine, Sher-I-Kashmir Institute of Medical Sciences Medical College and Hospital, Srinagar, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5006.196339

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A 32-year-old female was admitted with Organophosphorus (OP) poisoning and was managed with gastric lavage, intravenous pralidoxime, and atropine. On the 3rd day, she developed swelling and pain in the right upper extremity. Color Doppler confirmed upper extremity deep venous thrombosis (DVT). In addition to the neurologic manifestations patients of OP poisoning patients should also be monitored carefully for the development of DVT as these agents can lead to persistent inflammatory response which increases the risk of DVT. Upper limb DVT is rare and generally secondary to cancer, strenuous exercise, and insertion of central venous catheters. We hereby report a rare case of the upper limb DVT following OP poisoning.

Keywords: Deep vein thrombosis, organophosphorus, upper extremity thrombosis

How to cite this article:
Naik M, Bhat T, Mir MF, Jalaali U, Bhat A, Gowhar W, Naqash M. Organophosphorus poisoning: A rare case of upper extremity deep vein thrombosis. Indian J Health Sci Biomed Res 2016;9:339-41

How to cite this URL:
Naik M, Bhat T, Mir MF, Jalaali U, Bhat A, Gowhar W, Naqash M. Organophosphorus poisoning: A rare case of upper extremity deep vein thrombosis. Indian J Health Sci Biomed Res [serial online] 2016 [cited 2020 Sep 20];9:339-41. Available from: http://www.ijournalhs.org/text.asp?2016/9/3/339/196339

  Introduction Top

Organophosphorus (OP) poisoning is common wherever agriculture is a common profession.[1] It has been a major public health problem in developing countries.[2] Poisoning occurs mostly by voluntary ingestion, inhalation, or by absorption through the skin. OP toxicity primarily targets the nervous system.[3] OPs bind covalently and irreversibly at the active site of acetylcholinesterase (AChE).[3] This leads to decreased AChE levels and accumulation of acetylcholine at the peripheral nerve postsynaptic cleft, which in turn induces sympathetic and parasympathetic reactions through the activation of muscarinic and nicotinic receptors.[4] OP poisoning primarily targets nervous system; however, studies on the effect of OP poisoning on nontarget tissues have revealed that OP poisoning can lead to increased lipid peroxidation, induce oxidative stress, and reduce glutathione levels.[5] Under high-oxidative stress, tissues may sustain damage and persistently exhibit an inflammatory response, leading to cellular necrosis.[6] The Virchow's triad describes the three major risk factors that contribute to thrombosis, which are hypercoagulability, hemodynamic changes (stasis or turbulence), and endothelial injury or dysfunction.[7]

Chronic inflammatory response secondary to OP poisoning can lead to endothelial dysfunction or injury. This in turn can lead to coagulation abnormalities and increased risk of deep venous thrombosis (DVT) or PTE.[8] An unusual case of upper limb deep vein thrombosis following OP poisoning is reported here. The report, to the best of our knowledge, is the first of its kind in the literature.

  Case Report Top

A 35-year-old female was admitted to the Accident and Emergency department of our hospital with history of OP poisoning (Malathion). There was history of lacrimation, salivation, sweating, abdominal pain, and few episodes of vomiting. On examination, she was alert, oriented but uncooperative with Glasgow Coma Score of 13 (E4V4M5). Her pulse was 64 beats/min, blood pressure 130/90 mmHg, and respiratory rate of 16 breaths/min. She was maintaining oxygen saturation of 97% at room air. The pupils were constricted poorly reacting to light. There was sweating and lacrimation. Chest and cardiovascular examination was normal. On abdominal examination, there was mild epigastric tenderness and rest was normal. Nervous system examination revealed Grade IV power all over, reflexes Grade III, and fasciculation's.

Investigations revealed the following: Hemoglobin - 7.5 g/dL, mean corpuscular volume - 65 fL, total leukocyte count - 8.23 × 109/L, differential leukocyte count - neutrophils 66%, lymphocytes 13%, and mixed 13%, the platelet count - 164 × 109/L, urea - 39 mg/dL; creatinine - 0.55 mg/dL; bilirubin - 0.86 mg/dl; aspartate transaminase - 43 U/L; alanine transaminase - 27 U/L; alkaline phosphatase - 78 U/L; total protein - 7.09 g/dL; albumin - 3.91 g/dL; blood sugar (random) - 76 mg/dL; creatinine phosphokinase - 169 U/dL; uric acid - 2.7 mg/dL; serum calcium - 9.12 mg/dL; serum phosphorus - 3.3 mg/dL. Her arterial blood gas revealed pH: 7.44, PCO2- 37 mmHg, PO2- 88 mmHg, SO2- 96 %, Na + - 144, K + - 3.2, HCO3 - 25.1, Cl - 116 mEq/L (100–112). Electrocardiography and X-ray chest were normal. Her choline esterase levels were not done due to unavailability of the facility at our center.

She was managed by gastric lavage, intravenous atropine, and pralidoxime. On day 2nd, she developed swelling of the right forearm and arm. There was no history of strenuous activity involving force or abduction of the right upper arm. Doppler ultrasonography of the right upper limb revealed thrombosis of radial vein, ulnar vein, and distal part of brachial vein. The patient was managed with low-molecular weight heparin and warfarin overlap and was discharged on warfarin 5 mg OD after attaining a therapeutic INR.

  Discussion Top

OP poisoning can be accidental, suicidal, and rarely homicidal. The clinical features of OP poisoning are related to muscarinic effects, nicotinic effects, and central receptor stimulation.[9] The clinical features of OP poisoning can be subclassified into three stages: (i) Acute cholinergic crisis, which manifests within 24–72 h due to accumulation of acetylcholine at muscarinic and nicotinic sites and accumulation within the central nervous system resulting in seizures and altered sensorium; (ii) intermediate syndrome, which manifests after 24–96 h as a precipitous weakness of ocular, neck, limb, and respiratory muscles; and (iii) a delayed, often permanent peripheral neuropathy can result from the toxicity of certain OP compounds.[10]

OP compounds are lipophilic and may accumulate in various parts of tissues and organs after intoxication. OPs are subsequently released from these tissues into the bloodstream, and intoxication relapse may be prolonged, leading to various clinical manifestations.[10] OP intoxication may be associated with increased reactive oxygen species (ROS) production and lipid peroxidation.[11] ROS production can lead to an intense inflammatory response.[12] Inflammation leads to a procoagulant state as it increases procoagulant pathway and inhibits anticoagulant pathways.[13]

OP poisoning presenting as pulmonary thromboembolism has been described in a case report.[14] Recently, a nationwide cohort study in Taiwan indicated that the risk of developing deep vein thrombosis is markedly higher in patients with OP intoxication compared with that of the general population.[15] In this nationwide study, follow-up person-years showed that patients with OP intoxication have a 1.55-fold increased risk of DVT compared with the general population. The risks of DVT were significant and reached 2.12-fold of the hazard ratio of OP poisoning patients with any comorbidity compared with those without OP poisoning and comorbidities.[15] This study emphasizes the relation of OP poisoning with a chronic inflammatory state predisposing to the development of DVT and PTE and measures to minimize morbidity and mortality from these OP chemicals.

The incidence of the upper limb involvement is only 10% in cases of deep vein thrombosis. The increased use of central venous catheters and of cardiac pacemakers and defibrillators has led to increased incidence of the upper limb DVT. Among the other causes of the upper limb DVT is cancer and repeated microtrauma to the subclavian vein due to the strenuous activity. (Paget-Schroetter syndrome). OP poisoning leading to upper limb DVT has not been described till date as far as the English literature is concerned. In our patient, there was neither antecedent history of strenuous exercise involving the right upper limb nor there was the insertion of the central venous catheter.

  Conclusion Top

Keeping in view the chronic inflammatory state in patients of OP poisoning, these patients should be observed for DVT and upper limb DVT should be kept in mind. Further studies are advised to study the role of prophylactic heparin in patients of OP poisoning.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Goldman L, Tran N. Toxics and Poverty: The Impact of Toxic Substances on the Poor in Developing Countries. Washington, DC: The World Bank; 2002.  Back to cited text no. 1
Ecobichon DJ. Pesticide use in developing countries. Toxicology 2001;160:27-33.  Back to cited text no. 2
Banks CN, Lein PJ. A review of experimental evidence linking neurotoxic organophosphorus compounds and inflammation. Neurotoxicology 2012;33:575-84.  Back to cited text no. 3
Lionetto MG, Caricato R, Calisi A, Giordano ME, Schettino T. Acetylcholinesterase as a biomarker in environmental and occupational medicine: New insights and future perspectives. Biomed Res Int 2013;2013:321213.  Back to cited text no. 4
Mishra V, Srivastava N. Organophosphate pesticides-induced changes in the redox status of rat tissues and protective effects of antioxidant vitamins. Environ Toxicol 2015;30:472-82.  Back to cited text no. 5
Abdollahi M, Karami-Mohajeri S. A comprehensive review on experimental and clinical findings in intermediate syndrome caused by organophosphate poisoning. Toxicol Appl Pharmacol 2012;258:309-14.  Back to cited text no. 6
Bagot CN, Arya R. Virchow and his triad: A question of attribution. Br J Haematol 2008;143:180-90.  Back to cited text no. 7
Zöller B, Li X, Sundquist J, Sundquist K. Risk of pulmonary embolism in patients with autoimmune disorders: A nationwide follow-up study from Sweden. Lancet 2012;379:244-9.  Back to cited text no. 8
Richardson RJ. Assessment of the neurotoxic potential of chlorpyrifos relative to other organophosphorus compounds: A critical review of the literature. J Toxicol Environ Health 1995;44:135-65.  Back to cited text no. 9
Bardin PG, van Eeden SF, Moolman JA, Foden AP, Joubert JR. Organophosphate and carbamate poisoning. Arch Intern Med 1994;154:1433-41.  Back to cited text no. 10
Zunec S, Kopjar N, Zeljezic D, Kuca K, Musilek K, Lucic Vrdoljak A. In vivo evaluation of cholinesterase activity, oxidative stress markers, cyto- and genotoxicity of K048 oxime – A promising antidote against organophosphate poisoning. Basic Clin Pharmacol Toxicol 2014;114:344-51.  Back to cited text no. 11
Kmiecik B, Skotny A, Batycka M, Wawrzaszek R, Rybak Z. Influence of oxidative stress on tissue regeneration. Polim Med 2013;43:191-7.  Back to cited text no. 12
Samad F, Ruf W. Inflammation, obesity, and thrombosis. Blood 2013;122:3415-22.  Back to cited text no. 13
Umesh Babu R, Krishna Kumar BR, Kumar H, Gayathri BN. Organophosphorus poisoning presenting as pulmonary thromboembolism. Medicoleg Update 2012; 12: 40-41.  Back to cited text no. 14
Lim YP, Lin CL, Hung DZ, Ma WC, Lin YN, Kao CH. Increased risk of deep vein thrombosis and pulmonary thromboembolism in patients with organophosphate intoxication: A nationwide prospective cohort study. Medicine (Baltimore) 2015;94:e341.  Back to cited text no. 15

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