Organophosphate Poisoning PDF

Organophosphate Poisoning Complicated by RhabdomyolysisInduced Acute Kidney Injury A Case Report and Review of Literature: JB Gunasena, ST De Silva

ABSTRACT
Background: Rhabdomyolysis induced acute kidney injury (AKI) following organophosphate poisoning is a rare
complication. The mechanism responsible is uncertain.
Case report: A 42 years old male was admitted to a tertiary care hospital in Sri Lanka after deliberate self-ingestion of
Calcron® (Profenophos, an organophosphorus pesticide). He developed rhabdomyolysis induced AKI requiring
regular haemodialysis. During the hospital stay he also developed bronchopneumonia with acute respiratory distress
syndrome, requiring intubation and ventilation. The patient improved with intravenous antibiotics and repeated
renal replacement with haemodialysis. At discharge he had made a full recovery.
Conclusion: Organophosphate poisoning can rarely lead to rhabdomyolysis induced AKI. It is an adverse predictor
of outcome. Clinicians should be vigilant about this complication since, with early diagnosis and aggressive
treatment, a favourable outcome is possible.
Keywords: Organophosphate intoxication; Rhabdomyolysis; Acute kidney injury; Hemodialysis
INTRODUCTION
Farmers in agriculture-based economies of countries such as Sri
Lanka frequently use pesticides in their farming activities.
Organophosphates (OP) contribute to about 10% of the
pesticide imports to Sri Lanka. Chlorpyriphos is the most
frequently imported [1].
OP is a common cause of poisoning in the country, leading to
significant morbidity and mortality [2]. Over the counter
availability of OP has made it a common modality of poisoning
among agricultural communities [3,4]. Poisoning can either be
by deliberate self-ingestion or by occupational exposure.
Organophosphate poisoning leads to mainly three types of
clinical complications:
•Acute cholinergic syndrome
•Intermediate syndrome
•OP induced delayed polyneuropathy
Apart from these common complications rare manifestations
such as acute respiratory distress syndrome (ARDS), acute
kidney injury (AKI) and sub arachnoid haemorrhage have been
reported in literature [5-9].
We report a case of OP poisoning complicated by
rhabdomyolysis-induced AKI.
CASE REPORT
A 42 years old male was admitted to the emergency treatment
unit 90 minutes after deliberate self-ingestion of Calcron ®
(Profenophos, an organophosphorus pesticide). He had a history
of hypertension but was not on any regular medication. On
admission the patient was hemodynamically stable but had
clinical evidence of OP toxicity; pupils were meiotic, blood
pressure was 125/74 mmHg, pulse rate was 76 beats per minute
and there were increased oral secretions with bilateral lung
crepitations on auscultation. GCS on admission was 14/15.
Blood investigations were as follows: white blood cells 13,000/
μl, haemoglobin 10.8 g/dl, platelets 260,500/μl, creatinine
92.5 μmol/l, sodium 133 mmol/L, potassium 4.4 mmol/l,
Journal of Clinical Toxicology Case Report
Correspondence to: J B Gunasena, Colombo North Teaching Hospital, University Medical Unit, Ragama, Sri Lanka, E-mail:
janithag@outlook.com
Received: July 27, 2020; Accepted: August 12, 2020; Published: August 19, 2020
Citation: Gunasena JB, De Silva ST (2020) Organophosphate Poisoning Complicated by Rhabdomyolysis-Induced Acute Kidney Injury: A Case
Report and Review of Literature. J ClinToxicol. 10:450. DOI: 10.35248/2161-0495.20.10.450
Copyright: © 2020 Gunasena JB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
J Clin Toxicol, Vol.10 Iss.5 No:1000450 1
Journalof Clinical Toxicology
ISSN: 2161-0495
arterial pH 7.29, pCO2
43.6 mm Hg, pO2
72.6 mmHg,
HCO3
-21.1 mmol/l, lactate 1.1 mmol/l.
Treatment was commenced according to local guidelines and
treatment protocols. Intravenous atropine was administered,
and gastric lavage was performed. After the initial loading dose,
an infusion of atropine was given, followed by regular dosing of
pralidoxime.
On the third day after admission the patient developed
myoglobinuria with myalgia, oliguria and deterioration of renal
functions. Serum creatinine phosphokinase level rose to 23256
IU/l and rhabdomyolysis induced oliguric AKI was diagnosed.
Repeated laboratory investigations at this time showed white
blood cell count of 11,000/μl, haemoglobin 10.9g/dl, platelets
259,000/μl, serum creatinine 753 μmol/l, sodium 143
mmol/l, potassium 4.6 mmol/l, total calcium 2.2 mmol/l and
phosphate 1.4 mmol/l. Hemodialysis was commenced
immediately and repeated at regular intervals. Over the next few
days the patient developed bronchopneumonia with acute
respiratory distress syndrome (ARDS) and type 1 respiratory
failure. He required intubation, ventilation and broad-spectrum
intravenous antibiotics with ICU care. The patient improved
gradually with continued intravenous antibiotics and repeated
renal replacement therapy with hemodialysis. On the 41st day of
hospitalisation he was discharged after making a complete
recovery.
DISCUSSION
This is a rare case of OP poisoning complicated by
rhabdomyolysis-induced oliguric AKI. Organophosphates are
used as pesticides in agricultural activities, termite treatment and
anti-lice and tick products worldwide. The British Medical
Journal Best Practice-Organophosphate Poisoning defines OP
poisoning as “poisoning occurring after dermal, respiratory or
oral exposure to either organophosphate pesticide or nerve
agents causing inhibition of acetylcholine esterase at nerve
synapses” [10]. OP acts by inhibiting acetylcholinesterase enzyme
at neuromuscular junctions of the sympathetic, parasympathetic
and central nervous systems, leading to an excess of
acetylcholine. This results in parasympathetic effects such as
bronchospasms, bronchorrhoea, rhinorrhoea, bradycardia,
hypotension and pinpoint pupils. Cholinergic effects on the
central nervous system causes seizures, confusion and respiratory
failure. Fasciculations and weakness are due to neuromuscular
junction stimulation by excess acetylcholine. Treatment options
available for OP poisoning include the use of atropine,
pralidoxime and gastric decontamination as appropriate [10].
Literature on OP induced renal complications and OP induced
rhabdomyolysis is limited, with only a few cases of
rhabdomyolysis following OP poisoning being reported.
Rhabdomyolysis occurs as a result of skeletal muscle injury with
release of intracellular contents and there is a subsequent rise in
serum LDH, myoglobin and CPK. Common drugs abused in
society and known to cause rhabdomyolysis include cocaine,
amphetamines, LSD, heroine, alcohol and phencyclidine
[10,11]. The first reported case of OP poisoning induced
rhabdomyolysis was in a patient who developed post-synaptic
neuromuscular dysfunction with OP-induced intermediate
syndrome [12]. In this case, limited rhabdomyolysis was
confirmed by tibialis anterior muscle biopsy.
Two case reports of OP poisoning complicated by
rhabdomyolysis-induced AKI were reported by Gokel in 2002
[5]. Both patients developed myoglobinuria with elevated CPK,
deteriorating renal function and oliguria. They were managed
with renal replacement by peritoneal dialysis. Unfortunately,
both cases had unfavourable outcomes, with the patients
succumbing to cardiac arrest and myocardial infarction
respectively. Bardin et al. in a retrospective analysis reported that
13% of treated severe OP poisoning cases developed oliguric
AKI. The probable aetiology was thought to be hypovolemia or
rhabdomyolysis secondary to prolonged seizure activity [6].
However, our patient did not develop seizures during the course
of his illness and remained
haemodynamically stable. OP-induced rhabdomyolysis has also
been attributed to excessive muscular activity evoked by the
nicotinic effects of accumulated acetylcholine in a case report
published by Sheng et al. [13].
Few cases of OP poisoning complicated by renal impairment
have been reported in world literature so far. Abend et al.
reported a case of AKI following OP poisoning without any
evidence of rhabdomyolysis or haemodynamic instability; in
fact, the authors were unable to determine a cause for the renal
impairment [7]. Wedin et al. described crystalluria as a possible
cause of OP poisoning associated kidney injury [8]. Betrosian et
al. described a case of AKI secondary to OP poisoning and
speculated that acute tubular necrosis due to toxic effect of OP
was the likely aetiology [9].
Studies carried out in Sri Lanka in 1988 [2] and 2017 [14] have
not identified any cases of OP poisoning complicated by AKI. In
a recent study carried out in India, none of the patients who
presented with OP poisoning developed AKI as a complication
[15]. To the best of our knowledge, ours is the first ever case of
rhabdomyolysis induced AKI in a patient with OP poisoning
reported from Sri Lanka.
Information on the pathogenetic mechanism of AKI due to OP
poisoning is inconclusive since there is a lack of experimental
data in the literature and data derived from OP production
facilities. However, possible mechanisms are the level of plasma
choline esterase in distal convoluted tubules of the kidney, high
intralobular OP concentration, rhabdomyolysis and
hypovolemia from dehydration [16,17].
The majority of reported cases of OP poisoning induced AKI
had unfavourable outcomes despite the patients receiving
dialysis. This was attributed to several toxicokinetic effects of OP
such as rapid distribution to all tissues and high volume of
distribution [18]. The same toxicokineticsfavour the use of
continuous veno-venous hemofiltration (CVVH) over
haemodialysis in OP induced AKI [16].
CONCLUSION
Rhabdomyolysis induced AKI is a rare complication following
OP poisoning and is an adverse predictor of patient outcome.
Our patient developed rhabdomyolysis-induced AKI and
Gunasena JB, et al.
J Clin Toxicol, Vol.10 Iss.5 No:1000450 2
improved following repeated haemodialysis, compared to the few
previously reported cases managed with peritoneal dialysis.
Although both these complications are rare, surveillance of
patients following OP poisoning for AKI and rhabdomyolysis is
warranted. Haemodialysis appears to be beneficial in OP
poisoning induced AKI with rhabdomyolysis but, considering
the toxicokinetic effects of OP, CVVH may be a better
management option.
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