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��������	�	//����8W\�<k3$��`�ZD�$�2�2�2�2�2�2�2$�5�18<3�\`��3//W%3r&r&r&�/V�2r&��2r&r&r�.T���/�����[���#��.�2;30k3/�m8�$�m8�/m8�/,��r&�����33�%����k3������������������������������������������������������������������������m8����������		�:	Hypokalemia: Strong predictor of morbidity and mortality in acute organophosphorous compound poisoning.
 Introduction 
Morbidity and mortality due to poisoning is a worldwide problem. As per World Health Organization three million cases of pesticide poisoning occur every year and estimated two million people die; most of the deaths occur in Asia and at least 50% are due to organophosphorous poisoning.1 The total number of poisoning cases is constantly increasing in all developing and developed countries in all age groups irrespective of sex due to various reasons. Accidental poisoning has become more common in children due to increased use of chemicals both in households and in agriculture.2 
Pesticide poisoning in developing countries have high rates of morbidity and mortality as facilities are limited for early diagnosis and treatment. Most of the ill health associated with exposure to organophosphorous compound has been attributed to inhibition of enzymes, acetyl cholinesterase and plasma cholinesterase in nerve, neuromuscular and glandular tissues where these enzymes plays a key role in cell to cell communication.3 
Despite significant progress in understanding the potential mechanisms of toxicity far beyond the commonly accepted mechanism of cholinesterase inhibition in intentional exposure, the precise health effects following exposure are yet to be completely defined. The inhibition of cholinesterases by itself cannot account for the wide range of disorders that have been reported. It is becoming apparent that, although inhibition of cholinesterases plays a key role in the toxicology of organophosphates, individual susceptibility, the inhibition of other enzyme systems and the direct effects of organophosphates on tissues are also important.4 Electrolyte imbalance in such case adds on to the clinical burden contributing in the mortality and morbidity. As a consequence of intracellular shift, due to reentry of potassium ions fatal cardiac arrhythmias in organophosphorous poisoning may occur. This also results in tissue hyperkalemia and serum hypokalemia. Distribution of potassium is affected by chronic illness like cardiac failure, renal failure and other factors like hormones, acid-base balance, osmolality and cell turn over, disturbances in acid-base balance. Factors like decreased intake, increased net loss by gastrointestinal tract or excessive sweating leading to integumentary loss and shift into intra-cellular compartment can result in hypokalemia.5 Since potassium is the major intra-cellular cation, the ratio between intra-cellular to extra-cellular potassium concentrations which is 38:1 plays a crucial role in cell membrane resting potential (RMP) maintenance.5 Thus RMP and cellular excitability will be very much altered even in relatively small change in extra-cellular potassium concentration. The normal neuro-muscular function entirely depends upon the extra-cellular potassium concentration.
           Literature survey revealed little about hypokalemia in acute organophosphorous compound poisoning. Thus we aim to study the significance of hypokalemia in relation to clinical manifestations in cases of acute organophosphorous compound poisoning.








Materials and methods
After the approval from the Ethical Committee on Human Studies and informed consent, this double blind clinical cross-sectional study was conducted at KLE�s Dr.Prabhakar Kore Medical and Research Center, Jawaharlal Nehru medical College, Belgaum, Karnataka, India from November 2009 to April 2010. The gastric aspirate of patients with history of consumption of organophosphorous compound was tested in the Poison Detection Center, Department of Forensic Medicine and Toxicology, by thin layer chromatography and UV-Vis spectrophotometry, confirmed to be organophosphorous compound were involved in the study. Cases with severe vomiting and, those associated with chronic illness, renal and cardiac failure were excluded from study as these conditions may be associated with altered potassium levels. 
 Pre-interventional routine investigations and serum electrolyte assay were done using venous blood in 50 consecutive patients. The potassium level was estimated using C311 fully automated biochemistry analyser where 3-5ml of blood was subjected to centrifugation and the plasma was separated. 25micro liter of plasma was added with 25micro liter reagent and subjected for potassium estimation. Thus the values at the time of admission were considered. Low potassium levels were observed at the time of grave clinical features also. The potassium level of less than 3.5m mol/L was considered as hypokalemia.6 The coupled grave clinical features like fasciculation, muscle weakness, respiratory distress, convulsion and death, were noted.  Ventilators were used in cases where there was respiratory failure. The criteria for diagnosis of respiratory failure and ventilator support were based on the following: 7 
apnoea, 
obvious hypoventilation,
persistent cyanosis in spite of oxygen supplementation, 
persistent tachypnoea - respiratory rate more than 24/minute, 
persistent oxygen saturation level less than 90% with oxygen supplementation by non invasive means,
active involvement of accessory muscles of respiration,
The clinical status of the patients was assessed and tabulated. (Table- 3, 4, 5 and 6)

















Observations
There were 50 cases in the median age group of 27.14 year. Out of them 1case was occupational, 7cases were accidental and 42 were suicidal in incidence. A total of 13 cases presented with hypokalemia (Table-1) along with one or more grievous clinical features. (Table-2) However there were certain cases, which showed grievous clinical features without absolute hypokalemia ([K]+  < 3.5mmol/L).  The average potassium concentration among the cases with the grievous clinical features was in sub-normal zone. (Table- 3, 4, 5, and 6) Monocrotophos was the commonest type of organophosphorus compound detected.











Discussion
Organophosphorous compounds are used around the world as pesticides because of the relatively easy availability, affordability, and effectivity. However, suicidal and accidental ingestion of organophosphorous compounds have become rampant. It is readily absorbed by alimentary system following ingestion and by skin, following prolonged dermal contact. Toxicity is expressed when organophosphorous compound binds to acetylcholinesterase, preventing hydrolysis and resulting in an accumulation of acetylcholine in the synaptic cleft. Mahdi Balali-Mood et al. revealed that hypokalaemia is the cause for the muscular weakness due to inhibition of acetylcholineesterase by organophosphorus compound which was noted on admission in 5/60 patients with organophosphorous compound poisoning.8 In our study it is 17/50 patients revealed muscle weakness and fasciculations with an average serum potassium level of 3.32 +/- 0.11.
The present study reveals that as the potassium level decreased below 3.5 mmol/L, alarming signs were recognized. At the mean level of +/- SEM [K+] 3.32 +/- 0.11 mmol/L patients developed fasciculation and muscle twitching in association with steady decrease in oxygen saturation level and gradually progressed to respiratory distress to such a level that there were  requirement of ventilator support at the mean level of  +/- SEM [K+] 3.28 +/- 0.10 mmol/L. When the mean concentration reduced drastically to 2.90 +/- 0.06 mmol/L, the patients died. In all these cases the P-value is less than 0.0001. Mean while, some patients presented with convulsions with the mean level of +/- SEM [K+] 3.83 +/- 0.12 m mol/L. However the P-value in this case came to be insignificant. (Table-7) Potassium homeostasis appears to be altered in acute organophosphorous compound poisoning. Alteration in potassium concentration may alter neuro-muscular junction activity and contribute to overall morbidity and mortality. The patients in the present study developed grievous signs and symptoms sequentially as the serum potassium concentration reduced. As the potassium concentration decreased gradually patients start to show signs like muscle weakness, fasciculation, twitching, convulsion, respiratory distress and death, in succession. The decrease in serum potassium concentration was directly proportional to the onset of grievous signs and symptoms.
 Potassium ion is tightly balanced, in that urinary potassium excretion (1- 1.5mmol/Kg/day) is directly proportional to the total body potassium and is a good marker of total body potassium.6 The resting membrane potential and functional activity of electrically excitable cells undergo significant alteration even due to minute changes in extra-cellular potassium concentration. In acute cases of organophosphorous poisoning, due to strong nicotinic actions, respiratory distress, muscle weakness and paralysis sets in.  In such stressful conditions, hypokalemia, the alarming sign can be established, which can add on to the clinical burden and/or these signs and symptoms can be aggravated in presence of associated hypokalemia. Hypokalemia presents with lassitude, muscular weakness, loss of deep tendon reflexes, paralysis, and death will be sudden, which is usually due to respiratory distress, a complication of respiratory muscle weakness and paralysis. Cause of death in both acute organophosphorous poisoning and hypokalemia is due to muscular weakness and respiratory distress. It is not uncommon for patients to present to the emergency room with severe weakness and a markedly low plasma potassium concentration.9 
Hypokalemia and paralysis  are potentially reversible medical emergencies.10 Morbidity and mortality are related to complications secondary to hypokalemia such as  cardiac arrhythmia or respiratory failure.11 Although there are many potential causes of hypokalemia, there are far fewer entities in the differential diagnosis of hypokalemia and paralysis.10 Hypokalemia and paralysis can be divided into 2 types, hypokalemic periodic paralysis due to a short-term shift of potassium into cells12, 13, 14 and non- hypokalemic periodic paralysis resulting from a large deficit of potassium.15, 16 The differential diagnosis in a patient with hypokalemia and paralysis can be challenging, but it is important to make the diagnosis promptly because different therapies are required for each type. 
Organophosphate induces cardiac toxicity in a significant form by elongation of the repolarization period in the ventricles. This is clinical marked and measured in electrocardiogram as long- QT syndrome. The primary membrane currents responsible for this condition are two. Potassium modulation of the sodium current and reduction of the potassium currents mimic the experimentally observed change in slope of the depolarization in the presence of organophosphates as well as the prolongation and shape of repolarization. This is a precursor to the onset of Torsade de Pointes and ventricular fibrillation, the fatal complications due to alteration in potassium concentration. Animal experimental data show that organophosphorous intoxication results in lesions of the cardiac tissue, acidosis, and anoxia. These effects in terms of the membrane currents can be expressed and simulated by ion channel conductivity changes. Potassium conductivity changes, which can be caused by ligand blocking the channel, are a major contributor to increased cycle length and consequently long- QT syndrome.11
The hypokalemia in acute organophosphorous poisoning cases and the associated grievous features is alarming and a strong predictor of morbidity and mortality. During the whole course of treatment, the treating physician should watch the serum potassium concentration and maintain at normal level to prevent the unexpected morbidity and mortality.


Conclusion 
Hypokalemia is relatively common and an alarming sign in acute organophosphorous compound poisoning cases and carries higher risk of mortality. It is simple, economical to investigate and a powerful marker of morbidity and mortality in acute organophosphorous compound poisoning cases. 














References
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Mahadeshwaraprasad DR, Kamble DD, Aramani SC, Gouda HS, Honnungar RS, Jirli PS. Accidental mass poisoning in children � a case report. Journal of the Indian Society of Toxicology. 7;1 Jan-June 2011
Karalliedde L. Cholinesterase estimation revisited: the clinical relevance. European Journal of Anesthesiology 2002 May; 19(5): 313
Kamanyire R,  Karalliedde L. Depth Review- Organophosphate toxicity and occupational exposure. Occupational Medicine 2004; 54: 69�75
Gawarammana I B, Kularathna K S, Dawson A H. Potassium homeostasis in patients with acute organophosphorous poisoning. South Asian Clinical Toxicology Research Collaboration, Faculty of Medicine, University of Peradeniya. Sri Lanka.
Fauci, Braunwarld, Issclbacher, Wilson, Kasper, Hauser, Longo. Harrison�s Principles of Internal Medicine, 17th ed. Mc Graw hill health Division Company.
 Frank G. Toxicological Emergencies. 4th ed. London. Appleton and Lange Publications;  1998
Mahdi Balali-Mood et al. Use of high doses of sodium bicarbonate in acute organophosphorous pesticide poisoning is advancing. Clinical Toxicology 2007; 45(1): 9
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Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation and therapy. Am J Emerg Med. 1992; 10: 143-146. 
 Ober KP. Thyrotoxic periodic paralysis in the United States: report of 7 cases and review of the literature. Medicine. 1992; 71:109-120. 
McFadzean AJS, Yeung R. Periodic paralysis complicating thyrotoxicosis in Chinese. British Medical Journal. 1967; 25: 451- 455. 
 Ko GT, Chow CC, Yeung VT, Chan HH, Li JK, Cockram CS. Thyrotoxic periodic paralysis in a Chinese population. QJM. 1996; 89: 463- 468. 
Lin SH, Lin YF. Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis. Am J Kidney Dis. 2001; 37: 620- 623. 
Huang YY, Hsu RS, Tsai JS. Paralytic myopathy: a leading clinical presentation for primary aldosteronism in Taiwan. J Clin Endocrinol Metab. 1996; 81: 4038- 4041
Dowd JE, Lipsky PE. Sj�gren's syndrome presenting as hypokalemic periodic paralysis. Arthritis Rheum. 1993; 36:1735-1738


















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