AN UNUSUAL CASE

OF POISONING
PATIENT DETAILS:
◦ AGE -54 YRS
◦ GENDER-MALE
◦ OCCUPATION-FARMER
CHIEF COMPLAINTS:

◦ Alleged consumption of a herbicide (glyphosate)30 ml on the 6/08/2023 at 8 :00 am.

HOPI-
◦ Apparently asymptomatic till 6/8/23 when he allegedly consumed 30 ml of glyphosate
accidentally under the influence of alcohol.
◦ Patient then developed complaints of giddiness,vomitings-10 episodes –non blood stained/non
bilious,associated with hiccups,loose stools –multiple episodes.
◦ Was taken to Outside hospital (6/8/23)–Gastric lavage was done
◦ Went back home but I//v/o persistent symptoms was taken to Narayana medical college on
9/8/23 where patient received 3 cycles of HD I/v/o serum creatinine of 6.7.UGI scopy done
which revealed hiatus hernia II and corrosive oesophageal injury and patient was treated with
inj piptaz and clindamycin.
◦ Patient got discharged AMA and came to SRMC on 13/8/23
◦ PAST MEDICAL HISTORY-No known comorbidities
◦ PAST SURGICAL HISTORY-nil significant
◦ PERSONAL HISTORY-H/o alcohol consumption present since 10 years-18Units
per day,H/o smoking present-15 pack years.
◦ MARITAL HISTORY-unmarried
◦ FAMILY HISTORY-nil significant
GPE:
◦ @ER-Patient is conscious,coherent,Oriented to T/P/P
VITALS-Temp-afebrile
PR-114 bpm
BP-120/80 mm hg
Spo2-96 % on 6 l oxy (HM)
CBG-298 mg/dl
b/l pitting pedal edema +
No signs of pallor/icterus/cyanosis/clubbing/lymphadenopathy
Right HD line in place (9/8/23),Foleys in situ
SYSTEMIC EXAMINATION
◦ CVS-S1,S2 + ,no murmurs
◦ RS-BAE+,b/l diffuse crepts +(L>R),b/l wheeze +
◦ CNS-GCS-15/15,NFND
◦ P/A-soft,non tender.
 COURSE IN THE HOSPITAL:
◦ LABS -
CBC-hb-9.8,TC5850,MCV100,Plt-1.46
RFT-creat-6.4,Na 134,K -4.6,cl-101,bicarbonate 17,sr calcium 8.9,sr Uric acid 4.3,phosphate 5.8,CPK 76.
LFT-Normal
Urine r/e-glu +1,albumin +4,pus cells 17.4,nitrite +
Urine c/s-no growth
VM-non reactive
CXR-b/l infiltrates,bilateral CP angle blunting,predominant infiltrates in right lung fields.
ECG-NSR,T inversions in v1-v5.
USG-GB wall edema,mild ascites,b/l raised cortical echoes,b/l mild pleural effusion.
◦ In CCU- patient was started on NIV I/v/o (ABG showing Ph-7.3,Pco2 31,lac
2.6,bicarb 17.5-metabolic acidosis and Pao2/fio2 of 115) .
◦ I/v/o high creatinine and low urine output nephrology opinion was taken.I/O was
monitored and patient underwent 3 more cycles of HD and regular RFT and
electrolytes monitoring was done and patient didn’t require any further maintenance
dialysis.
◦ 2D ECHO was done which revealed RWMA,moderate LV systolic dysfunction,with
grade II diastolic dysfunction,EF 35 %,IVC non collapsing? Stress cardiomyopathy
◦ Cardio 3-trop I 0.03,BNP 5000.
◦ Patient was started on DAPT and statin ,T.metoprolol,T.hydralazine+ISDN,T.lasix.
◦ Patient was treated empirically with antibiotic(piperacillin and tazobactum )I/v/o b/l
infiltrates on CXR and CAUTI .
◦ Blood c/s sent from catheter line revealed growth of acinetobacter and piptaz was
continued for 14 days according to culture sensitivity.
◦ Patient was gradually weaned off NIV support to minimal oxygen requirement via
NP ,ARDS settled and Repeat CXR showed resolution ,urine output improved and
patient was shifted back to ward and creatinine at discharge was 0.8.
◦ Psychiatry opinion was taken for deaddiction .
◦ Repeat 2D ECHO was done at discharge and revealed improved systolic and diastolic
function and EF of 45 % and ?IVC thrombus .CT venogram was done I/v/o ?IVC
thrombus and showed no evidence of the same.
◦ ISSUES-AKI /ARDS/STRESS CARDIOMYOPATHY/CLABSI/CAUTI
DISCUSSION
◦ GLYPHOSATE-herbicide-isopropylamine salt of glyphosate -41%,surfactant
polyoxyethylene amine with water 15%
◦ MOA- uncoupling of oxidative phosphorylation and
POEA mediated cardiotoxicity.
oAlthough its structure is similar to OP it does not show any anticholinesterase
activity and OP like syndromes.
 Clinical manifestations
oTransient GI disturbance.
◦ Oral ulceration
◦ Esophagitis
◦ Lactic acidosis
◦ GI hemorrhage
◦ Hypotension
◦ Respiratory failure
◦ Arrythmias
◦ Cardiac arrest
◦ Death
◦ Case fatality rate—3-30 %
◦ Management-NO ANTIDOTE
◦ Aggressive Supportive treatment is the mainstay
◦ Gastric lavage within one hour if there is no evidence of burns
◦ Early UGI scopy in patients with GI involvement
◦ Decontamination for skin and eye exposure
◦ Early Renal replacement therapy
◦ IV fat emulsion has been useful in some cases with refractory hypotension as it lowers
serum concentration of free POEA by reducing its cardiotoxicity
◦THANK YOU