Organophosphate Poisoning: Prediction of Severity and Outcome by Glasgow Coma Scale, Poisoning Severity Score, Acute Physiology and Chronic Health Evaluation II Score, and Simplified Acute Physiology Score II

Organophosphate Poisoning: Prediction of Severity and Outcome by Glasgow Coma Scale, Poisoning Severity Score, Acute Physiology and Chronic Health Evaluation II Score, and Simplified Acute Physiology Score II

PHARM/TOX CORNER ORGANOPHOSPHATE POISONING: PREDICTION OF SEVERITY AND OUTCOME BY GLASGOW COMA SCALE, POISONING SEVERITY SCORE, ACUTE PHYSIOLOGY AND ...

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PHARM/TOX CORNER

ORGANOPHOSPHATE POISONING: PREDICTION OF SEVERITY AND OUTCOME BY GLASGOW COMA SCALE, POISONING SEVERITY SCORE, ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION II SCORE, AND SIMPLIFIED ACUTE PHYSIOLOGY SCORE II Authors: Shobha Churi, MPharm, Krunal Bhakta, BPharm, and Ramesh Madhan, PhD, Mysore, India Section Editor: Allison A. Muller, PharmD, D.ABAT

Earn Up to 10 CE Hours. See page 503. rganophosphates (OPs) are a diverse group of chemicals (eg, insecticides [malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, ethion], nerve gases [soman, sarin, tabun], ophthalmic agents [echothiophate, isoflurophate], and antihelmintics [trichlorfon]) used in both domestic and industrial settings.1 Toxic exposures to OPs can occur through ingestion, dermal exposure, or inhalation. OP poisoning is one of the major health concerns in developing countries.1-3 This also has been a great concern to developed countries vulnerable to terrorist or military attacks with nerve agents.4 The principal pharmacologic action of OPs is the inhibition of acetylcholinesterase. Most deaths occur in the acute stage from cardiorespiratory failure.1-3 The high mortality rate of OP poisoning is often related to a

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Shobha Churi is Assistant Professor, Department of Pharmacy Practice, JSS College of Pharmacy, JSS University, Mysore, India. Krunal Bhakta is PharmD Student, Department of Pharmacy Practice, JSS College of Pharmacy, JSS University, Mysore, India. Ramesh Madhan is Professor, Department of Pharmacy Practice, JSS College of Pharmacy, JSS University, Mysore, India. For correspondence, write: Shobha Churi, MPharm, Department of Pharmacy Practice, JSS College of Pharmacy, JSS University, SS Nagar, Mysore570015, Karnataka, India; E-mail: [email protected]. J Emerg Nurs 2012;38:493-5. Available online 21 July 2012. 0099-1767/$36.00 Copyright © 2012 Emergency Nurses Association. Published by Elsevier Inc. All rights reserved. doi: 10.1016/j.jen.2012.05.021

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delay in diagnosis or to improper management. Traditional diagnosis relies heavily on history of possible exposure and physical signs and symptoms (eg, rhinorrhea, wheezing, dyspnea, pulmonary edema, lacrimation, salivation, sweating, vomiting, abdominal cramps, diarrhea, pupil constriction, bradycardia, tachycardia, hypotension, raised blood pressure, muscle twitching, fasciculations, weakness, headache, vertigo, confusion, restlessness, tremor, slurred speech, ataxia, drowsiness, convulsions, and coma with respiratory failure) consistent with exposure. However, the onset of symptoms may take some time to develop, and delayed treatment can cause irreversible or even fatal toxicity.2 In addition, subjective evaluation of clinical status by individual clinicians may differ in measurement of illness severity. Traditionally, OP concentrations and serum cholinesterase levels in plasma or urine are determined to correlate with the mortality rate. 5 The laboratory methods, however, are not always available in developing countries and some hospitals in developed countries. Hence, various descriptive and prognostic evaluation scales (scoring systems) have been developed and used in the emergency department to predict the severity and mortality rate of OP poisoning.6 Standard Treatment in OP Poisoning

On admission to the emergency department, all poisoned patients received standard medical treatment that included (1) treatment of respiratory manifestations by frequent suctioning, endotracheal intubation, and assisted ventilation; (2) gastric lavage; (3) atropinization with a dose of 2 to 4 mg every 15 minutes, until signs of atropinization were apparent (tachycardia, papillary dilation, dry skin); (4) slow

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TABLE 1

Prediction and categorization of patient's severity, predicted mortality rate, and clinical outcome (improved, discharged with severe morbidity, and dead) of acute OP poisoning using GCS, PSS, APACHE II, and SAPS II scoring systems Severity level/grade/score

GCS Mild (≥13) Moderate (9-12) Severe (≤8) PSS Grade 1 (low) Grade 2 (moderate) Grade 3 (high) Grade 4 (death) SAPS II 0-10 11-20 21-30 31-40 41-50 >50 APACHE II 0-4 5-9 10-14 15-19 ≥20

Improved (n = 119) [n (%)]

Discharged with severe morbidity (n = 10) [n (%)]

Dead (n = 7) [n (%)]

Total (n = 136) [n (%)]

76 (55.89) 43 (31.62) 0 (0)

3 (2.20) 3 (2.20) 4 (2.94)

0 (0) 1 (0.74) 6 (4.41)

79 (58.09) 47 (34.56) 10 (7.35)

83 34 2 0

(61.02) (25) (1.48) (0)

0 2 8 0

(0) (1.48) (5.88) (0)

0 0 0 7

(0) (0) (0) (5.14)

83 36 10 7

(61.02) (26.48) (7.36) (5.14)

8 61 37 11 1 1

(5.88) (44.85) (27.20) (8.08) (0.74) (0.74)

1 1 1 4 3 0

(0.74) (0.74) (0.74) (2.94) (2.21) (0)

0 0 0 1 4 2

(0) (0) (0) (0.74) (2.93) (1.47)

9 62 38 16 8 3

(6.62) (45.59) (27.94) (11.76) (5.88) (2.21)

0.67 3.20 10.04 23.14 35.26 84.93

± ± ± ± ± ±

0.16 2.07 1.65 4.03 6.84 8.83

56 41 16 6 0

(41.18) (30.15) (11.76) (4.41) (0)

1 2 3 3 1

(0.73) (1.47) (2.21) (2.21) (0.73)

0 0 0 2 5

(0) (0) (0) (1.47) (3.68)

57 43 19 11 6

(41.91) (31.62) (13.97) (8.09) (4.41)

4.24 7.76 13.8 27.47 46.55

± ± ± ± ±

0.87 1.5 2.71 4.6 17.36

intravenous administration of pralidoxime with a dose of 1 to 2 g; and (5) supportive treatment if necessary. How to Predict the Severity and Outcome of OP Poisoning

The study was conducted over a period of 1 year in an Indian tertiary-care teaching hospital. A total of 136 patients (116 men and 20 women, aged 18 to 60 years [mean ± SD, 31.2 ± 11.4 years]) were involved in the study. We collected information related to demography, poison (name and type of OP, route of exposure, and circumstance of poisoning), patient medical history, signs and symptoms, diagnosis, investigation report, supportive and decontamination methods, and antidote. All patients were followed up until discharge from the hospital or death. The Glasgow Coma Scale (GCS) score was calculated by assessing the motor response to pain, as well as verbal and eye responses.7 On the basis of signs and symptoms

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Predicted mortality rate (mean ± SD) (%)

in the various systems and metabolism (eg, acid-base disturbances),8 the poisoning severity score (PSS) (where grade 1 [or mild] indicates mild, transient, and spontaneously resolving symptoms or signs; grade 2 [or moderate], pronounced or prolonged signs or symptoms; grade 3 [or severe], severe or life-threatening symptoms or signs; and grade 4, death or fatal outcome) was calculated. The Acute Physiology and Chronic Health Evaluation (APACHE) II score and Simplified Acute Physiology Score (SAPS) II values were calculated in accordance with the original methodology by using the worst physiological values (temperature, blood pressure, heart rate, and respiratory rate; laboratory parameters such as serum sodium, potassium, creatinine, HCO3–, and pH; and hematologic parameters) on the first day of admission.9,10 Then, on the basis of calculated APACHE II and SAPS II scores and mortality rate, the severity and outcome were determined. A higher score indicates higher severity and mortality rate.

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TABLE 2

Comparison of calculated severity score and predicted mortality rate of different scoring systems with clinical outcome (improved, discharged with severe morbidity, and dead) Groups

GCS score

PSS

SAPS II

APACHE II

Score

Predicted mortality rate (%)

Score

Predicted mortality rate (%)

Improved Discharged with severe morbidity Dead

13.2 ± 1.8 10.1 ± 2.8

1.3 ± 0.5 2.5 ± 0.8

21.0 ± 10.5 29.7 ± 12.5

5.7 ± 10.1 15.8 ± 14.6

6.1 ± 4.5 12 ± 5.5

7.9 ± 5.6 17.9 ± 11.9

6.6 ± 1.3

4.0 ± 0

50.5 ± 13.6

43.8 ± 25.9

43.1 ± 17.6

Total P

12.9 ± 2.4 < .001*

1.5 ± 0.7 < .001*

23.3 ± 12.8 .002

9.5 ± 14.5 .002

23.2 ± 6.4 9.4 ± 6.0 < .001*

10.4 ± 10.8 < .001*

Values represent mean ± SD. * Significant difference among various outcome variables (Kruskal-Wallis test).

Significance of GCS, PSS, APACHE II Score, and SAPS II Systems

GCS values provided information about the consciousness of patients.7 PSS values indicated the severity of the illness.8 The values of the APACHE II score and SAPS II, which are relatively advanced scoring systems, provided the general condition of patients during the first 24 hours of OP poisoning.9,10 We found a significant association between the clinical outcome and values of the GCS, PSS, and APACHE II score and the predicted mortality rate (Tables 1 and 2). For example, a majority of patients whose severity was predicted to be mild to moderate recovered from the poisoning (improved category), whereas patients whose illness was predicted to be severe were either discharged with severe morbidity or had died. Not surprisingly, the predicted mortality rate was higher for those patients whose predicted illness was severe. The prediction of severity and clinical outcome using these scoring systems was simple and less time-consuming and provided beneficial information. The use of these scoring systems in the emergency department enables clinicians/ nurses to identify the patients at high risk of death soon after presentation, allowing more intensive monitoring and treatment. A simple system based on clinical features is likely to be most useful in low-income countries where the majority of OP poisoning occurs.

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REFERENCES 1. Konradsan F. Acute pesticide poisoning—a global public health problem. Dan Med Bull. 2007;54(1):58-9. 2. Paudyal BP. Organophosphorous poisoning. JNMA. 2008;47:251-8. 3. Akdur O, Durukan P, Ozkan S, Avsarogullar L, Vardar A, Kavalci C, Ikizceli I. Poisoning severity score, Glasgow coma scale, corrected QT interval in acute organophosphate poisoning. Hum Exp Toxicol. 2010;29(5):419-25. 4. Buckley NA, Roberts D, Eddleston M. Overcoming apathy in research on organophosphate poisoning. BMJ. 2004;329(7476):1231-3. 5. Surjit S. Organophosphorous poisoning: an evidence based approach. MJAFI. 2004;60(1):2-4. 6. Stefek G, Gasparovic V. Comparison of APACHE 2, MEES and Glasgow coma scale in patients with nontraumatic coma for prediction of mortality. Critical Care. 2001;5(1):19-23. 7. Teassdale G, Jennett B. Assessment of coma impaired consciousness. A practical scale. Lancet. 1974;2(7872):81-4. 8. Persson H.E, Sjoberg G.K, Haines J.A, Pronczuk J.G. Poisoning severity score: grading of acute poisoning. Clin Toxicol. 1998;36(3):205-13. 9. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. Apache II: a severity of disease classification system. Crit Care Med. 1985;13(10):818-29. 10. Le Gall JR, Lemeshow S, Saulnier F. A new Simplified Acute Physiologic Score (SAPS II) based on an European/North American multicenter study. JAMA. 1993;270(24):2957-63.

Submissions to this column are encouraged and may be sent to Allison A. Muller, PharmD, D.ABAT [email protected]

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