“Toxic Pancreatitis with an Intra- Abdominal Abscess which was Caused byOrganophosphate Poisoning (OP)”
Toxic pancreatitis, Intra-abdominal abscess, Organophosphate poisoning
Organophosphate insecticides are the potent inhibitors o the ace-tylcholinesterase enzyme which lead to an increased acetylcholineactivity, which are responsible or symptoms such as abdominalpain, diarrhoea, vomiting and hypersalivation. We are reporting ona young male with acute organophosphate poisoning, who pre-sented with unusual complications like toxic pancreatitis with anintraabdominal abscess.
Venugopal l, Dharma rao V, SriniVaS rao m, malliKarjuna Y
Organophosphorous poisoning is a major clinical problem in thedeveloping countries like India. Neurologic, cardiac and respiratorycomplications are the main causes o the morbidity and the mor-tality in these patients. The involvement o other systems can alsooccur, but it is very uncommon.In the recent years, a number o case reports o acute pancreatitiswhich were associated with acute organophosphorous poisoninghad been described [1-6]. The cause and the eect relationshipo this disease entity have been demonstrated in animal studies.However, this association may still have not been widely recog-nized. Acute pancreatitis usually ollows a subclinical course and it there-ore remains unrecognized and leads to increased morbidity andmortality in the patients who are aected by it.
A 25 year male patient presented to the emergency departmentwith a history o the ingestion o a pesticide 5 hours ago. At thetime o presentation, the patient had abdominal pain, vomiting,nausea and copious oral secretions. The patient denied having anyhistory o alcohol consumption or alcohol abuse. His past historywas unremarkable.On physical examination, the patient was drowsy, heart rate was88/min, regular and blood pressure was 100/60 mmHg and his re-spiratory rate was 26/min. The patient was hypoxic, with an SPO
level o 80-85%. His chest examination showed bilateral, diuse,coarse crepitations. Bilateral pinpoint pupils and diuse ascicula-tions were ound on his nervous system examination. His othersystem examinations were unremarkable. Based on the clinicalpicture, a provisional diagnosis o organophosphorous poisoningwas made. The treatment was initiated with gastric lavage. A bolus dose o 8mg atropine and 1.5 gms PAM was given. The atropine inusionwas continued with 4 mg /hr and it was titrated to maintain thepulse rate between 100-140 beats per minute. Bolus doses o 1.5gms o PAM were also continued every 8th hourly or 3 days. At the time o his admission, his serum pseudocholinesterase was412U/L (5000-13000 U/L) and his total count showed mild leu-cocytosis . His routine blood examination, liver unction tests, re-nal unction tests, ECG and chest radiography were within normallimits. The subsequent laboratory changes are shown in [Table/ Fig-1]. The patient responded to the initial treatment. His oral secretionsand bronchial secretions decreased but the patient was still hypox-ic. The saturation was maintained with O
administration, but on3rd day, it deteriorated urther, with poor respiratory eorts and hedeveloped type I respiratory ailure and worsening o the abdominalpain, with a localized swelling. Thereore, the patient was put onventilatory support. Due to the persistent abdominal pain and theappearance o the localized swelling, an ultrasound (USG) o theabdomen was done, which revealed a biloculated collection o pusin the subcapsular region (the let lobe o the liver), an oedematouspancreas which involved the body and the tail and ascites. An ul-trasound guided drainage o the liver abscess was attempted, butno pus was aspirated. The ndings o the ultrasound were laterconrmed by CT o the abdomen [Table/Fig-2a & b]. The patientwas kept nil per orally. Amikacin, metronidazole, 3rd generationcephalosporins and octreotide were started. The abdominal pain and the localized swelling gradually increasedin intensity and size respectively, over the next 5 days.On day 8, an ultrasound guided drainage o the abscess was doneand the collected sample was sent or culture and antibiotic sen-sitivity tests, which showed the growth o Klebsiella species whichwere sensitive to Imipenem [Table/Fig-3]. Subsequently, the cetri-axone was substituted with imipenem. The patient started improving symptomatically over the next ewdays and a repeat USG which was done, showed disappearanceo the liver abcess and resolution o the pancreatic abscess. Thepatient was discharged ater one month o the hospital stay. At onemonth o ollow up, the patient was ound to be absolutely normaland he was able to take up his routine activities.
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