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Poisoning severity score, Glasgow
coma scale, corrected QT interval
in acute organophosphate poisoning
Okhan Akdur
1
, Polat Durukan
2
, Seda Ozkan
2
,
Levent Avsarogullari
2
, Alper Vardar
2
, Cemil Kavalci
3
and
Ibrahim Ikizceli
2
Abstract
The aim of this study was to investigate effectiveness of the poisoning severity score (PSS), Glasgow coma scale
(GCS), and corrected QT (QTc) interval in predicting outcomes in acute organophosphates (OP) poisoning.
Over a period of 2 years, 62 patients with OP poisoning were admitted to emergency department (ED) of
Erciyes University Medical School Hospital. The age, sex, cause of contact, compound involved, time elapsed
between exposure and admission to the ED, duration of hospital stay, and cardiac manifestations at the time of
presentation were recorded. GCS and poisoning severity score (PSS) was calculated for each patient. Electro-
cardiogram (ECG) analysis included the rate, rhythm, ST-T abnormalities, conduction defects, and measure-
ment of PR and QT intervals. Sixty-two patients with OP poisoning presented to our ED from January
2007 to December 2008 from which 54 patients were included in the study. The mean age was 34.1 +
14.8 years. Of the cases, 53.7% were female. Twenty-six patients had a prolonged QTc interval. Mean PSS
of men and women was 1.8 +1.0. No statistically significant correlation was found between the PSS and QTc
intervals of the cases. A significant correlation was determined between the GCS and PSS of grade 3 and grade
4 cases. GCS is a parameter that helps clinician to identify advanced grade OP poisoning patients in the initial
assessment in the ED. However, ECG findings, such as prolonged QTc interval, are not effective in determi-
nation of short-term prognosis and show no relationship with PSS.
Keywords
clinical toxicology, organophosphates, poisoning
Introduction
Organophosphates (OP) are used as insecticides in
agricultural and domestic settings throughout the
world.
1
Poisoning with OP compounds is responsible
for great morbidity and mortality in developing coun-
tries. According to the World Health Organization,
1 million serious accidental and 2 million suicidal
poisonings with insecticides occur worldwide every
year, and of these, approximately 200,000 die, mostly
in developing countries.
2
Mortality rates were
reported to be 9.1%for adults in a study performed
in Turkey.
3
OPs inhibit the enzymes acetylcholinesterase
(AChE) in cholinergic synapses and on red cells
and butyrylcholinesterase in plasma. As a result of
this enzyme inhibition, the substrate acetylcholine
accumulates. The continued stimulation of the acetyl-
choline receptor account for the clinical signs and
symptoms of OP poisoning.
1
Cardiac complications that often accompany poi-
soning with these compounds may be serious and are
1
Canakkale Onsekiz Mart University Faculty of Medicine,
Departments of Emergency Medicine, Canakkale, Turkey
2
Department of Emergency Medicine, Erciyes University Faculty
of Medicine, Kayseri, Turkey
3
Department of Emergency Medicine, Trakya University Faculty
of Medicine, Edirne, Turkey
Corresponding author:
Okhan Akdur, Departments of Emergency Medicine, Canakkale
Onsekiz Mart University Faculty of Medicine, Canakkale, Turkey.
Email: oakdur@hotmail.com
Human and Experimental Toxicology
29(5) 419–425
ªThe Author(s) 2010
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DOI: 10.1177/0960327110364640
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often fatal. Cardiac complications include tachycardia
or bradycardia, prolonged corrected QT (QTc) inter-
val, PR interval prolongation, and dysrhythmias.
4,5
Prolongation of the QTc interval is one of the the most
common electrocardiogram (ECG) abnormality.
4,6
There are a lot of investigations about the cardiac
toxicity of OP poisoning, but its pathogenesis and
underlying mechanism are not known.
7-9
Oxidative
stress in the heart cells may be the cause of myocar-
dial damage that may result in several conduction
problems.
10
A number of systems have been proposed for pre-
dicting outcome in OP poisoning, many are reliant on
laboratory tests.
11
Working from a simple grading
scale proposed by the European Association of Poison
Centres and Clinical Toxicologists, a poisoning sever-
ity score (PSS) has been developed jointly with the
International Programme on Chemical Safety and the
European Commission.
12
PSS has been shown to be
effective in determining the severity of cases of vari-
ety intoxication.
12-14
The aim of this study was to investigate effective-
ness of the PSS, Glasgow coma scale (GCS), and QTc
interval in predicting outcomes in OP poisoning. We
also was to describe the clinical characteristics of
adult OP poisoning cases admitted to our hospital.
Methods
Over a period of 2 years (January 2007 to December
2008), 62 patients with OP poisoning were admitted
to emergency department (ED) of Erciyes University
Medical School Hospital in Central Anatolia, in
Turkey.
Fifty-four cases of poisoning were included and
eight excluded due to insufficient data and a past his-
tory significant for cardiac disease.
Patients were admitted to the intensive care unit
directly from the ED. The diagnosis of OP poisoning
was based on the following criteria: a history of intake
or exposure to organophosphorus insecticide, clinical
manifestations of OP poisoning, including excessive
salivation, miosis, and fasciculations, and improve-
ment of the signs and symptoms of OP poisoning after
administration of atropine. Exclusion criteria included
carbamate poisoning or severe pre-existing chronic
health status and co-ingestion of other drugs.
The age, sex, cause of contact, compound
involved, time elapsed between exposure and admis-
sion to the ED, duration of hospital stay, need for
assisted ventilation, and cardiac manifestations at
the time of presentation were recorded. GCS and
PSS were calculated for each patient using the
criteria in Tables 1 and 2. Pulse rate, blood pressure,
andECGrecordingstakenonarrivalintheEDor
general medical ward were selected for analysis
before the start of atropine treatment.
ECG analysis included the rate, rhythm, ST-T
abnormalities, conduction defects, and measurement
of PR and QT intervals. QT intervals were measured
from the first deflection of the QRS complex to the
point of T-wave offset. The QT interval was corrected
according to the formula of Bazett.
15
QTc was consid-
ered prolonged when it was longer than 0.41 sec in
men and longer than 0.42 sec in women.
7
All patients received standard medical treatment
under the direction of the hospitals’ consultant physi-
cians. This followed a standard protocol, which was
dictated by the patients’ clinical condition and was
independent of the identity of the OP involved. The
protocol included rapid atropinization, with doubling
dose of atropine at 5–10 min intervals, starting at 1–3
mg, given until muscarinic signs were abolished. The
decision to intubate and mechanically ventilate was
made by the medical team. All symptomatic patients
received pralidoxime chloride 1 g intravenously
(IV) four times a day for 1–3 days.
Data were recorded using standardized data collec-
tion forms and were analyzed with SPSS software
(SPSS Inc., Chicago, Illinois, USA). The results were
Table 1. The Glasgow coma scale provides a score in the
range 3–15
Measure Response Score
Eye
opening
Opens:
Spontaneously 4
To verbal comand 3
To pain 2
No response 1
Verbal Oriented and converses 5
Disoriented and converses 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Motor Obeys verbal command 6
To painful stimulus:
Localize pain 5
Flexion-withdrawal 4
Abnormal flexion (decorticate
rigidity)
3
Extension (decerebrate rigidity) 2
No response 1
420 Human and Experimental Toxicology 29(5)
Table 2. Poisoning severity score (11)
Organ
None Minor Moderate Severe Fatal
01 2 3 4
No symp-
toms or
signs
Mild transient, and spontaneously
resolving symptoms
Pronounced or prolonged signs or
symptoms Severe or life-threatening Death
Cardiovascular
system
Isolated extrasystoles Bradycardia (HR 40-50 in adults) Bradycardia (HR < 40 for adults)
Tachycardia (HR 140-180 in adults) Tachycardia (HR > 180 for adults)
Chest pain Cardiac arrest
Conductance, disturbance
Hypertension
Hypotension
Respiratory
system
Irritation, coughing, breathlessness,
mild dyspnea, mild bronchospasm
Prolonged coughing, bronchospasm, dys-
pnea, stridor, hypoxemia requiring extra
oxygen
Manifest respiratory insufficiency airway
obstruction, pulmonary edema, ARDS,
pneumonitis
Chest X-ray: abnormal with minor
or no symptoms
Chest X-ray: abnormal with moderate
symptoms
Chest X-ray: abnormal with severe symptoms
Nervous
system
Vertigo, tinnitus, ataxia Unconsciousness with appropriate response
to pain
Deep coma unresponsive to pain
Mild extrapyramidal symptoms Confusion, agitation, hallucinations,delirium Extreme agitation
Paresthesia Infrequent, generalized, or local seizures Generalized seizures, status epilepticus
GI tract Vomiting, diarrhea, pain Pronounced or prolonged vomiting, diar-
rhea, pain ileus
Massive hemorrhage, perforation
Dysphagia Severe dysphagia
Metabolic
imbalance
Mild acid-base disturbances More pronounced acid-base disturbances Severe acid-base disturbances
Mild electrolyte and fluid
disturbances
More pronounced electrolyte and fluid
disturbances
Severe electrolyte and fluid disturbances
Mild hypoglycemia More pronounced hypoglycemia Severe hypoglycemia
Liver Minimal rise in serum enzymes Rise in serum enzymes no diagnostic bio-
chemical or clinical evidence of liver
dysfunction
Rise in serum enzymes biochemical or clinical
evidence of liver dysfunction
Kidney Minimal proteinuria/hematuria Massive proteinuria/hematuria Renal
dysfunction
Renal failure.
Muscular
system
Mild pain, tenderness Pain, rigidity, cramping, fasciculations Intense pain, extreme rigidity, extensive
cramping,fasciculations
Rhabdomyolysis Rhabdomyolysis with complications
Local effects on
skin
Irritation, 1st degree burns 2nd degree burns in 10%–50% of body sur-
face or 3rd degree burns in <2% of body
2nd degree burns in >50% of body surface or
3rd degree burns
Local effects on
eye
Irritation, redness, lacrimation, mild
palpebral edema
Intense irritation, corneal abrasion Minor
(punctate) corneal ulcers
Corneal ulcers (other than punctate),
perforation
ARDS, Acute Respiratory Distress Syndrome.
421
expressed as mean +SD. Chi-square test was used in
the statistical analysis of gender distribution. After
one Sample-Kolmogorov Simirnov test for normality,
statistical significance was calculated using a one-
way ANOVA test post hoc Scheffe for normally dis-
tributed data, and the Kruskal-Wallis test for data not
normally distributed. To determine differences
between groups was used Mann-Whitney Utest with
Bonferroni correction. Findings were considered sig-
nificant at p< .05.
Results
Fifty-four patients with OP poisoning presented to our
ED from January 2007 to December 2008. The ages
of the patients ranged from 17 to 80 years. The mean
age was 34.1 +14.8 years. There was no significant
difference in the mean age between males (34.0 +
14.8) and females (33.9 +14.9; p> .05). Of the
cases, 29 (53.7%) were female.
Fourty-seven (87%) patients had ingested the
OP compound. The average time lapse between
exposure to the time of administration at the ED
(pre-hospitalization period) was 4.4 +4.3 hours
(range2–24 hours), with a median of 3.00 hours.
Acute exposure were either suicidal (n¼40); acci-
dental (n¼12) or occupational (n¼2). The type of
OP compound that caused the intoxication could
be determined in 25 of the cases. The most common
OP compounds that cause poisoning seemed to be
Dichlorvos (n¼14), Diazinon (n¼3) and methyl-
parathion (n ¼3).
Cardiac manifestations and electrocardiographical
changes that were recorded before the administration
of atropine are shown in Tables 3 and 4. Twenty
six (53.7%) patients had a prolonged QTc interval.
The mean QTc interval was 0.403 +0.036 sec
(min: 0.33 max: 0.55). Prolonged of the QTc interval
was the most common ECG abnormality. Non-
specific ST segment elevation (<0.2 mV above the
isoelectric line) and low amplitude T wave changes
were seen in 13 cases.
All of the cases according PSS were assessed in
four grades. As 32 (59.3%) of the cases had a grade
of 1, 6 (11.1%) had grade of 2, and 13 (24.1%) had
grade of 3 (Table 5). Mean PSS score of men and
women was 1.8 +1.0. There was no significant cor-
relation between the PSS score and gender difference
(p> .05). No statistically significant correlation was
found between the PSS and QTc intervals of the cases.
Mean hospitalization period was 6.7 +3.7. There
was no statistically significant correlation between
this period and PSS (p> .05; Table 6).
There were seven (13%) cases that needed entuba-
tion and mechanically ventilation support. The PSS in
three (5.6 %) cases was 4 and in four (7.4 %) cases 3.
During the study, 3 (5.6 %) cases were fatal. The
PSS of these three cases was 4.
Discussion
OP poisoning is a major global health problem and
high mortality is seen in resource-poor settings. We
aimed to evaluate whether clinical parameters that
can be obtained rapidly in cases presenting to the
Emergency Service with OP poisoning could help
determination of the severity of OP poisoning. In
order to achieve this target, we analyzed the clinical
pictures as well as PSS, GCS, ECG findings.
According to the demographic data that we
reviewed, OP poisonings were found to take place
usually at 20–40 years age and due to suicidal inten-
tions. There was no significant difference between the
two genders. Our data were consistent with the results
achieved in the previous studies on OP poisoning.
16,17
Scoring systems are employed to evaluate the
severity of the cases and manage the patients on the
basis of clinical characteristics.
18
PSS and GCS are
the most commonly used ones in poisonings.
13,19,20
Table 3. Cardiac manifestations of acute organophosphate
poisoning
Cardiac manifestations n(%)
Sinus bradycardia
a
6 (11.1)
Sinus tachycardia
b
3 (5.6)
Hypertension
c
9 (16.7)
Hypotension
d
2 (3.7)
a
Heart rate < 60/min.
b
Heart rate > 100/min.
c
Systolic pressure > 160 mm Hg or diastolic pressure
>95 mm Hg.
d
Systolic pressure < 80 mm Hg.
Table 4. Electrocardographic (EGC) findings of acute
organophosphate poisoning
ECG abnormalities n(%)
Prolonged QTc interval 29 (53.7)
ST-T change 13 (24.1)
Extrasystole 1 (1.9)
Prolonged PR interval (>0.20 sec) 1 (1.9)
422 Human and Experimental Toxicology 29(5)
PSS measures the severity of the illness after the acute
poisoning.
12,19
It is used for describing the severity of
the poisoning,
20
allows comparison of the severity
and outcomes of the poisonings. PSS is not a prognos-
tic score. GCS is a neurological scale, which is
commonly employed in Emergency Services for the
assessment of the consciousness of patients.
20
We measured the PSSs of our cases with OP
poisoning on admission to Emergency Service and
evaluated those along with GCSs and other clinical
symptoms.
All the cases that demonstrated mortality were
grade 4 (PSS). GCSs of these cases were significantly
lower than those of others. This result suggests PSS
and GCS as effective tools for determination of the
severity of OP poisoning. Moreover, because GCS
has less complex parameters, it is more easily used
in clinical settings. Grmec et al.
21
reported that GCS
would be useful in determination of prognosis and
prevention of complications among OP poisoning
cases. Davies et al.
19
described a similar efficacy for
PSS and GCS in predicting mortality among patients
with OP poisoning. Our results show consistency with
those two studies.
No statistical correlation was found between
pre-hospitalization period and PSS. Actually, as this
duration increases, poisoning severity is expected to
rise. Because, the delay in treatment enables poison
to increase its initial peak serum level, which leads to
irreversible tissue damage. Sam et al. found a linear
correlation between those two parameters as well,
however, they concluded that this duration had no
influence over the clinical outcome.
20
Nevertheless,
early intervention is known to be one of the most
important factors that could affect survival.
22
Another
important result of our study was the significantly high
PSS scores in OP poisoning cases over 50 years of age.
Moreover, our mortal cases had a high mean age.
No relationship was found between PSS and the
decrease in plasma cholinesterase levels of cases.
Table 5. Effect of demography and manner of exposure on poisoning severity score
PSS (mean +SD) Grade 0 Grade 1 nGrade 2 nGrade 3 nGrade4 n
Gender
Male(n¼25) 1.8 +1.1 15 1 7 2
Female(n¼29) 1.7 +0.9 17 5 6 1
Age distribution
<20 years (n¼11) 2.2 +0.9 33 5
20–29 years (n¼13) 1.2 +0.4 11 2
30–39 years (n¼14) 1.4 +0.9 11 3
40–49 years (n¼8) 1.9 +1.0 41 3
>50 years(n¼8)
a
2.6 +1.4 323
Manner of exposure
Suicidal (n¼40) 1.8 +1.0 23 5 10 2
Accidental (n¼12) 1.8 +1.1 61 31
Occupational (n¼2) 1.0 2
PSS, poisoning severity score.
a
p< .05 significantly different PSS scores compared to other exposure groups.
Table 6. Effect of clinical characteristics on poisoning severity score
Mean +SD
Grade 0
mean +SD
Grade 1
mean +SD
Grade 2
mean +SD
Grade 3
mean +SD
Grade 4
mean +SD
Variables
Pre-hospitalization
period (hour)
4.4 +4.3 – 4.7 +5.2 2.2 +0.4 4.8 +2.8 3.3 +0.6
Cholinesterase 1782.5 +1965.7 – 2094.5 +1961.3 1757.2 +1365.8 1062.6 +2265.8 1625.3 +1531.1
Glasgow coma score 13.4 +3.1 – 14.8 +0.9 13.2 +2.9 11.9 +3
a
4.7 +0.6
a
QTc interval (s) 0.403 +0.036 – 0.397 +0.039 0.405 +0.018 0.410 +0.029 0.403 +0.040
Hospitalization
period (day)
6.7 +3.7 – 5.9 +3.9 5.5 +1.8 9.0 +3.0 6.7 +4.7
a
p< .05 significantly different.
Akdur O et al.423
Tsao et al. conducted a study on 107 cases and
determined a significant rise of survival rate in cases
demonstrating a slight decrease in cholinesterase
level.
23
Although there are studies and case reports
which show that cholinesterase level can show the
poisoning severity, recent studies and our results do
not support this view.
20
Nouira et al. found low cho-
linesterase levels in life-threatening OP poisoning
cases but reported no statistical difference associated
with this finding and noted that cholinesterase cannot
be used as a prognostic parameter.
16
ECG results associated with OP poisoning cases
can be mentioned among the remarkable results of our
study. The mechanism of cardiac symptoms occurring
in OP poisoning cases is not yet understood clearly.
However, more than one mechanism is thought to
be involved in the process. Parasympathetic and sym-
pathetic overactivity, hypoxemia, acidosis, electrolyte
disturbances, and direct effects of the compounds are
indicated as the underlying causes of myocardial
damage.
24
Ludomirsky et al. described three phases
of cardiac toxicity after OP poisoning: phase 1 is a
brief period of increased symphatetic tone; phase 2
is a prolonged period of parasympathetic activity; and
in phase 3, QT prolongation is followed by torsades
de pointes ventricular tachycardia and then ventricu-
lar fibrillation.
25
Therefore, continuous cardiac mon-
itorization is recommended for detection of dynamic
cardiac alterations. In the current study, most com-
mon ECG finding in OP poisoning cases was the pro-
longed QTc interval. This result is consistent with the
literature.
4
Another important result of our study was the
absence of a relationship between QTc interval and
PSS. However, there are studies that show different
results concerning the value of ECG for determining
poisoning severity and prognosis in cases with OP
poisoning.
4,6,7
Jang et al.
26
found significant eleva-
tions in mortality and respiratory rates among cases
showing prolonged QTc intervals. Nevertheless,
another study described prolonged QTc interval as a
poor indicator for prognosis.
25
In light of our results,
we believe that ECG findings of OP poisoning cases
cannot solely suffice to determine the severity of the
poisoning.
Conclusion
We have two striking results in this study; GCS is a
parameter that helps clinician to identify advanced
grade OP poisoning patients in the initial assessment
in the ED, the second important result is that ECG
findings, such as prolonged QTc interval, are not
effective in determination of short-term prognosis and
show no relationship with PSS.
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Akdur O et al.425
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