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Toxic Pancre

Toxic Pancre

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Published by: Rhusiana Dhewie ItuSaia on Sep 26, 2013
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Journal o Clinical and Diagnostic Research. 2013 February, Vol-7(2): 366-368
366
 
366
DOI: 10.7860/JCDR/2013/4608.2771
Cas Rprt
“Toxic Pancreatitis with an Intra- Abdominal Abscess which was Caused byOrganophosphate Poisoning (OP)”
Ky Wds:
 
 Toxic pancreatitis, Intra-abdominal abscess, Organophosphate poisoning
 ABSTRACT
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 
InTRoduCTIon
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 eect 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 aected by it.
CASe RePoRT
 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
2
level o 80-85%. His chest examination showed bilateral, diuse,coarse crepitations. Bilateral pinpoint pupils and diuse 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 inusionwas 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
2
administration, but on3rd day, it deteriorated urther, with poor respiratory eorts and hedeveloped type I respiratory ailure and worsening o the abdominalpain, with a localized swelling. Thereore, 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 let 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 laterconrmed 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 cetri-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 ater 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.
    i  n   t  e  r  n  a   l   m  e   d     c     n  e    S  e  c   t     o  n
 
www.jcdr.net  Venugopal L et al., Toxic Pancreatitis with Intra-Abdominal Abscess Caused by Organophosphate Poisoning
Journal o Clinical and Diagnostic Research. 2013 February, Vol-7(2): 366-368
367
 
367
[Tab/Fig-2a & b]:
 
CT scan showing left subcapsular abscess extendinginto the lesser sac (A & B)
[1]. It is mainly caused by acetylcholine release rom the pancreaticnerves and the prolonged hyper stimulation o the acinar cells [2].Some patients may also develop serious complications like ab-scess ormations [2,3,6].In 1979, Dressel had described the rst case report o acute pan-creatitis with organophosphrous poisoning [7]. The patient was ahealthy young woman who was brought in a comatosed state. Atadmission, the serum amylase was ound to be 20 times elevated,which had returned to normal by the 4th day. In our patient, acutepancreatitis was suspected on the third day o his admission, withhis serum amylase being 20 times elevated and his ascitic fuidamylase also being very high ( 46,780 U), which returned to nor-mal in the second week o his admission [8]. In 1981, Moore andJames had described another case o acute pancreatitis whichhad presented to the hospital in a comatosed state, with signs o organophosphorous poisoning [9]. It was later conrmed by thelow pseudocholinesterase levels.In 1981, Dagli had reported a case o diazinon poisioning whohad developed acute pancreatits. Following this, Dagli and Sheikhstudied 75 cases who had been admitted to a general hospitalwith a denitive history o malathion ingestion [10,11]. Hyperamy-lasaemia was ound in 47 cases (63%) and in 10 cases (21%), thelevels were more than twice the upper limit o the normal levels. The higher level was more than our times the upper limit o thenormal level. In 42 cases (89%), the levels had returned to normalwithin 48 hours o the admission o the patients.Isoenzyme studies or pancreatitic biopsies were not done in thesecases and thereore, it was not clear whether the hyperamylasae-mia which was observed was due to pancreatitis. However, ex-periments which were done on dogs showed quite convincinglythat pancreatitis could be produced by the intra venous inusion o secretin and diazinon. Signicant increases o serum amylase andlipase were ound at 1, 2 and 3 hours.In our patient, acute pancreatitis was diagnosed, based on thelaboratory and the ultrasound abdomen ndings on the 3rd day o his admission to the hospital. The other possible aetiological ac-tors or acute pancreatitis like alcohol, biliary disease and medica-tions were excluded. A repeat ultrasound o the abdomen and CT o the abdomen showed regression o the oedema in the pancreasand the size o the abscess cavity, with the subsequent ollow upshowing disappearance o the abscess cavity.Liver involvement in the organophosphorus poisoning is very rare. A post-mortem study o the deaths which had been caused byorganophosphorus poisoning had shown the involvement o theliver in only 14 % o the cases [5]. It had mainly revealed micro-scopic ndings as atty changes in 4(36.36%) patients; congestionin 5(45.45%) patients; alcoholic hepatitis in 1 patient and sinusoidaldilatation in 1(9.09%) patient. In our patient, the liver abscess haddeveloped secondary to the acute pancreatitis.Hence, in the patients with organophosphorous poisoning, whocomplain o persistent abdominal pain, not only acute pancrea-titis, but also complications like liver abscesses should also besearched or, so that an early diagnosis can be made, to preventurther complications.
ConCluSIon
 The diagnosis o acute pancreatitis may be masked by the sys-temic eects o the OP poisoning like abdominal pain, nausea andvomiting, which are also the common eatures o acute pancreati-
dISCuSSIon
 Acute pancreatitis (toxic pancreatitis) is a rare complication o or-ganophosphorus poisoning. It generally shows a subclinical course
[Tab/Fig-1]:
 
Laboratory values at admission and follow up
[Tab/Fig-3]:
 
Culture and sensitivity
ivstts1st wk2dwk3d wk 4tw
PH7.417.447.38PaO2728276PaCO2394037HCO324.223.122.4Hb%10.6108.811.2 Total count24,20015,0001600015,000Dierential countN/L/M/B73/06/01/85/15/495/15/464/22/5RBS (mg/dl)120140124118Blood urea (mg/dl)24 262030Serum creatinine(mg/dl)0.80.81.00.9 ALT (U)35 291824 AST (U)68 254132 ALP (U)216 177283155 Albumin (mg/dl)0.61.82.02.3LDH (U/L)-254--Serum amylase (IU/L)2879 153147- Ascitic fuidamylase (IU/L)46 780---Serum lipase (U/L)114---Serum calcium (mg/dl)678.28.0Serum pseudocholinesterase(5000-13000 U/L)412497502850
Ct dsstvtyBd u Sbcbscss fde T Sct
FirstNegativeEnterococcusspp sensitiveto Imipenem, AmoxyclavKlebsiellasppsensitive toImipenemStaph. aureussensitive toNetilmycin, Tazobactum.Follow upculture-Klebsiellasensitiveto Imipenem,Gentamycinand NetilmycinSecondNegativeNegative-Negative ThirdNegativeNegative-Negative

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