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HYPOKALAEMIA IN ORGANOPHOSPHOROUS COMPOUND POISONING.

BACKGROUND

Organophosphorous compounds (OP) are one of the most commonly used insecticides in India and Asia. [1] They are the most commonly used agents for poisoning in India due to their easy availability. In some instances, severe poisoning may occur as an occupational hazard. [2] It is not a common health issue in developed nations, because access to poisons are restricted. Insecticides being used as suicidal agents, especially OP compounds, is an important public health problem worldwide and its incidence keep raising. [2]

Mechanism of action of OP compound is by inhibiting acetylcholinesterase (AchE) at muscarinic and nicotinic receptors. The commonly measured cholinesterases are butyrylcholinesterase (BuChE) and red cell cholinesterase. BuChE is produced in the liver. It is secreted into blood to metabolise xenobiotics. The latter is found in RBCs (PchE). Inhibition of these enzymes serves as the marker of poisoning. [3,4] Enzyme inhibition in RBCs will predict AchE inhibition at synaptic levels in acute poisoning. Hence, determination of PchE level is used for screening as well as for the diagnosis of OP poisoning so that proper and immediate intervention is possible. [5]

Although, we have understood the mechanism of OP toxicity as a result of cholinesterase inhibition, various health effects following exposure to OP are yet to be completely understood. It is apparent that although inhibition of cholinesterase plays a key role in OP toxicity, there are other factors which are important like individual susceptibility and direct effects of OP on tissues. [6] Electrolyte imbalances are one among the contributing factors for the severity of OP poisoning. In acute OP poisoning, the most common cause of mortality is respiratory failure as a result of respiratory muscle paralysis. [6] Hypokalaemia is also a frequent finding in OP poisoning either due to GI loss or through excessive secretions. Associated hypokalaemia increases muscle weakness. Hence, hypokalaemia can be considered as an important factor in the poisoning. [7]

MATERIALS AND METHODS

Following ethical clearance, a cross-sectional study was conducted in Department of Medicine, Victoria and Bowring and Lady Curzon Hospitals attached to Bangalore Medical College and Research Institute from February 2016 to June 2017. Patients with definitive history of OP poisoning were taken into the study. Patients with kidney disease, Heart disease and patients who are already on diuretics are excluded from the study. As soon as the patient is received, clinical features were observed and noted with severity assessment as per Proudfoot classification [8] (Table 4) along with measurement of serum potassium ion ([K+]) concentration and PChE level. The serum [K+] levels of less than 3.5 mmol/L were considered as hypokalaemia. [9] The PChE level was measured. The normal values of PChE range from 5320 to 11700. Data were analysed using descriptive statistics and unpaired student 't' test. Data were analysed using SPSS software (version 17).

RESULTS

Demographic Features

In this study, 50 OP poisoned patients (32 men, 18 women) were enrolled with median age of 30 +/- 0.56 years in men and 30 +/- 0.12 years in women. Chlorpyrifos was the commonest type (26%) of OP compound consumed followed by dichlorvos (24%), quinalphos (14%), methyl parathion (8%) and others (Table 2).

Baseline Clinical Features

Clinical manifestations of the patients are summarised in Table 3. The most common clinical manifestation was respiratory distress (50%) followed by neck muscle weakness/ fasciculations (44%), miosis (40%) and diaphoresis (30%). A total of 28 cases presented with one or more severe clinical features according to Proudfoot's classification (Table 4).

Serum Potassium Alterations in Severe Cases Among severe cases, 56% (20 out of 28) developed hypokalaemia. Among all patients, 44% (22 cases) had muscle weakness or fasciculation with mean serum [K+] of 3.39 [+ or -] 0.60 showing that as the serum [K+] level decreases below 3.5 mmol/L, these alarming signs can be recognised. The ventilatory support was required at the mean serum [K+] of 3.48 [+ or -] 0.61 mmol/L. No Fatality was noted. For these conditions, the correlation of the clinical effects and serum [K+] was significant (P < 0.05).

Plasma Cholinesterase Levels in Severe Cases

Among the cases with severe clinical features, the PChE level was remarkably reduced except in two cases. The relation between PChE and clinical manifestations was assessed independently at the time of presentation. As it is shown in Table 5, muscle weakness, fasciculation and respiratory distress were associated with marked suppression of PChE (>50%). For those patients with severe clinical effects, considerable reduction in serum [K+] was also evident (Table 5). Among those who required ventilatory support had the lowest PChE levels (1187 +/- 0.15 IU/L).

DISCUSSION

OP compounds bind to acetylcholinesterase (AChE), preventing hydrolysis of acetylcholine and resulting in its accumulation in muscarinic and nicotinic receptors. Accumulation at nicotinic receptors results in muscle fasciculation and flaccid paralysis. Decrease in serum [K+] may alter neuromuscular junction activity by hyperpolarising the muscle and impairing their ability to develop the depolarisation necessary for muscle contraction. Balali-Mood et al revealed that hypokalaemia may aggravate muscular weakness due to inhibition of AChE by OP compounds. [10] We also found that reduction in serum [K+] aggravate the OP toxicity induced muscle weakness and paralysis. The patients in the present study developed severe signs and symptoms of nicotinic effects of OP as the [K+] reduced. More than 98% of total body potassium is intracellular, chiefly in the muscle; buffering of extracellular potassium by this large intracellular pool plays a crucial role in the regulation of plasma K+ concentration. [11] Changes in the exchange and distribution of intra- and extra-cellular K+ can thus lead to hypo- and hyperkalaemia. The resting membrane potential and functional activity of electrically excitable cells undergo significant alteration even due to minute change in extracellular potassium concentration. [11] In acute cases of OP poisoning due to strong nicotinic actions, respiratory distress, muscle weakness and paralysis sets in. In such conditions, hypokalaemia acts as an add-on to the clinical severity of OP poisoning.

It is a well-known fact that Hypokalaemia and Hyperkalaemia can cause muscle weakness and periodic paralysis. [12,13] Hypokalaemia manifests with lassitude, muscular weakness, loss of deep tendon reflexes, paralysis and death (which is usually due to cardiac arrhythmias and respiratory distress). [11]

Cause of death in both acute OP poisoning and hypokalaemia is usually muscular weakness and respiratory distress. [13,14,9,15,16] Hypokalaemia and paralysis are potentially reversible medical emergencies [12,13]; however, when these features were coupled with reduction of PChE, higher chance of morbidity were observed. Hence, the level of PChE and serum [K+] can be proposed as OP poisoning predictive markers.

CONCLUSION

Serum [K+] and PchE level are greatly reduced in patients with OP poisoning with severe clinical features. Hence, these biochemical markers can be considered predictors of outcome in OP poisoning. Physicians should consider hypokalaemia associated with reduced PchE level as alarming signs of poor prognosis in OP poisoned patients and the need for ICU admission and ventilatory support.

REFERENCES

[1] Chitra GA, Muraleedharan VR, Swaminathan T, et al. Use of pesticides and its impact on health of farmers in South India. Int J Occup Environ Health 2006; 12(3):228-33.

[2] Gunnell D, Eddleston M, Phillips MR, et al. The global distribution of fatal pesticide self-poisoning: systematic review. BMC Public Health 2007; 7:357.

[3] Pillay VV. Comprehensive medical toxicology. 1st edn. Hyderabad, Inida: Paras Publications 2003.

[4] Naik B, Hirshhorn S, Dharnidharka VR. Prolonged neuromuscular block due to cholinesterase depletion by plasmapheresis. J Clin Anesth 2002; 14(5):381-4.

[5] Worek F, Koller M, Thiermann H, et al. Diagnostic aspects of organophosphate poisoning. Toxicology 2005; 214(3):182-9.

[6] Kamanyire R, Karalliedde L. Organophosphate toxicity and occupational exposure. Occup Med (Lond) 2004; 54(2):69-75.

[7] Prasad DRMM, Jirli PS, Mahesh M, et al. Relevance of plasma cholinesterase to clinical findings in acute organophosphorous poisoning. Asia Pac J Med Toxicol 2013; 2(1):23-7.

[8] Proudfoot AT. Acute poisoning: diagnosis and management. 2nd edn. Boca Raton, FL: CRC Press 1993.

[9] Van der Hoek W, Konradsen F. Analysis of 8000 hospital admission for acute poisoning in rural areas of Sri Lanka. Clin Toxicol (Phila) 2006; 44(3):225-31.

[10] Balali-Mood M, Ayati MH, Ali-Akbarian H. Effect of high doses of sodium bicarbonate in acute organophosphorous pesticide poisoning. Clin Toxicol (Phila) 2005; 43(6):571-4.

[11] Fauci AS, Braunwald E, Kasper DL, et al. Harrison's principles of internal medicine. 19th edn. New York: McGraw-Hill 2008.

[12] Lin SH, Lin YF, Halperin ML. Hypokalaemia and paralysis. QJM 2001; 94(3):133-9.

[13] Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation and therapy. Am J Emerg Med 1992; 10(2):143-8.

[14] Banday TH, Tathineni B, Desai MS, et al. Predictors of morbidity and mortality in organophosphorus poisoning: a case study in rural hospital in Karnataka, India. N AM J Med Sci June 2015; 7(6):259-65.

[15] Rodgers ML. OP poisoning. Am J Emerg Med 2006; 22:335-44.

[16] Nadia A, Jamal A, Ejaz K, et al. Acute organophosphate insecticide poisoning. J Surg Pak 2008; 13(2):71-4.

Diwakar Tumkur Narasimhamurthy (1), Shubha Vishnu Hegde (2)

(1) Associate Professor, Department of Medicine, Bangalore Medical College and Research Institute, Bangalore.

(2) Postgraduate Student, Department of Medicine, Bangalore Medical College and Research Institute, Bangalore.

'Financial or Other Competing Interest': None.

Submission 29-08-2017, Peer Review 07-10-2017, Acceptance 12-10-2017, Published 19-10-2017.

Corresponding Author:

Shubha Vishnu Hegde, PG girls Hostel, Victoria Hospital Campus, K R. Market, Bangalore.

E-mail: shubhahegde.bellimane@gmail.com

DOI: 10.14260/jemds/2017/1267
Table 1. Demographic Features

Gender   No. of Patients       Mean Age

Male         32(64%)       30 +/- 0.56 yrs.
Female       18(36%)       30 +/- 0.12 yrs.

Table 2. Type of Compounds Consumed

Compound Name      No.   Percentage %

Chlorpyrifos       13         26
Dichlorvos         12         24
Quinalphos          7         14
Methyl Parathion    4         8
Monocrotophos       3         6
Parathion           3         6
Phorate             3         6
Dimethoate          2         4
Diazinon            1         2
Pantothenate        1         2
Profenofos          1         2

Table 3. Clinical Manifestations
of OP Poisoning Patients (n= 50)

Clinical Manifestations   No.   %

Diaphoresis               15    30
Salivation                14    28
Bronchorrhoea             10    20
Vomiting                   6    12
Neck muscle weakness      22    44
Fasciculations            22    44
Respiratory distress      25    50
Miosis                    20    40
Seizures                   1    2

Table 4. Proudfoot Classification- Assessment of
Severity of Acute OP Poisoning [8]

                               Mild

                 Fatigue, Headache, Paraesthesia
Clinical         Nausea and Vomiting, Diaphoresis,
Manifestations      Salivation, Abdominal pain
                   Diarrhoea, Able to ambulate

Decline in                     <10%
Serum PchE

                           Moderate

                 Symptoms of Mild poisoning +
Clinical          Miosis, General weakness,
Manifestations   Dysarthria, Fasciculations,
                      Unable to ambulate

Decline in                  10-50%
Serum PchE

                              Severe

                 Generalised Fasciculation, Marked
Clinical            Miosis, Flaccid paralysis,
Manifestations         Respiratory distress,
                          Unconsciousness

Decline in                     >50%
Serum PchE

Table 5. Mean Potassium and Mean PChE Levels in association
with Severe Clinical Features of OP Poisoning

Clinical Features                  Mean K+             Mean PChE

Muscle weakness/      Yes        3.391+/-0.60       958.73+/-801.17
fasciculations        No         3.84+/- 0.43      3192.44+/-2927.01
                    P value         0.003                0.001
Respiratory           Yes        3.472+/-0.66       1006.17+/-836.04
Distress              No         3.82+/-0.35       3413.04+/-3007.49
                    P value         0.025                0.001
Miosis                Yes        3.635+/-0.54      1597.50+/-2039.598
                      No         3.653+/-0.56      2617.68+/-2721.184
                    P value         0.910                o.160

Ventilatory           Yes     3.48 [+ or -] 0.61   1187.24+/-1525.83
support               No         3.895+/-0.32      3743.15+/-3743.15
                    P value         0.008                0.001
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Title Annotation:Original Research Article
Author:Narasimhamurthy, Diwakar Tumkur; Hegde, Shubha Vishnu
Publication:Journal of Evolution of Medical and Dental Sciences
Date:Oct 19, 2017
Words:1893
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