Urine toxicology screen was sure for benzodiazepine, presumably secondary to intravenous midazolam, which was given to manage the seizures. His arterial blood gas demonstrated pH 7.49, PaO2 68 mmHg, PCO2 59.1 mmHg, and hydrogen bicarbonate 30 mEq/L with carboxyhaemoglobin level of 1.4%. The patient was remained in trans like state due to low GCS, patient was intubated to protect his airways. He was proceeded on levetiracetam, but sodium valproate and midazolam imbuement was added to manage the seizures. The patient stayed oblivious with inadequately controlled recurrent seizures. Throughout his hospital stay, he developed ventilator integrated pneumonia, sepsis with shock, and acute renal dysfunction. Expansive range anti-toxins, intravenous fluids, nor-adrenaline, and dopamine were included alongside other unfaltering measures. Tragically, the patient lapsed following 10 days of hospitalization.
3) Paraquat Poisoning: Paraquat or N, N′-dimethyl-4, 4′-bipyridinium dichloride is a green colored aromatic lethal compound that is broadly utilized as a herbicide basically for weeds and grass control. It is dangerous to humans, even a teaspoon of paraquat can be deadly. The most likely route of exposure would be through ingestion. Paraquat poisoning is likewise conceivable after skin exposure if skin exposure goes on for long time or skin that is not intact. The fundamental acute systemic impacts are pulmonary edema, convulsions, cardiac, renal and hepatic failure. It mainly meddles with the intracellular electron transfer framework and thus repressing the reduction of NADP to NADPH amid photosynthesis which result in accumulation of superoxide radical which causes decimation of lipid cell membranes.
Here is the case study of deadly paraquat poisoning from Eastern Indian state, Odisha 2017.
A 17 years of age female patient from a agriculturist family foundation was conveyed to the Emergency department of AMRI hospital, Bhubaneshwar with history of alleged utilization of approximately 5 ml of paraquat taken 11 hours prior to presentation. She had a dispute with her mother in regards to her marriage and she has taken paraquat which was kept in their home for cultivation reason. They brought the void container of paraquat by the trade name of Gramoxone II with them. She doesn’t have any past therapeutic or psychiatric ailment. She has devoured approximately 4 ml of herbicide as a self-destructive endeavor which is trailed by repeated vomiting. Primarily she was taken to Peripheral Health Centre after thirty minutes of consumption where gastric lavage done and she was alluded to higher Centre for further assessment and administration . Vitals at the time of presentation in ED are GCS-15/15, blood pressure at right arm 100/60mmHg, pulse rate- 108/min, respiratory rate-20/min, temperature at axillary-98.4 F, oxygen saturation-97% at room air, random blood glucose-103mg/dl, bilateral pupils were of typical size and receptive to light. On Primary overview, aviation route was patent, lungs were clear to auscultation, no respiratory pain, had normal heart sounds, capillary refill time was < 2 seconds and all peripheral pulses were available. Optional study demonstrated her oral mucosa red and congested and rest of the examination from head to toe were unremarkable. All primary investigations (CBC, RFT, LFT, PT/INR/APTT, ECG, X-RAY CHEST, URINE TOX SCREEN), UPT (Negative) were done from crisis. Patient then moved to ICU for consistent observing. On the First day in ICU, patient stayed asymptomatic. Introductory complete blood count, LFT, RFT were within normal limits. ECG uncovered sinus Tachycardia with no ST-T changes. Initial chest X-Ray was within normal limits. Patient was kept nil orally and on upkeep IV liquids, antiemetics, antacid and triamcinolone acetonide mouth paste to lessen the agony and swelling inside the mouth. On the second day she has developed oliguria and raise in urea and creatinine levels for which Nephrology meeting was done and advised to raise the IV liquids and made arrangement for hemodialysis if renal function further deteriorates. On fourth day patient had developed oliguria and further weakening of her renal function, hemodialysis was performed and continued on a regular basis .Patient had developed fever for which wide range antibiotic started. Urine routine examination demonstrated 20-25pus cells/HPF, RBC-10-15/HPF and granular cast suggestive of urinary tract infection and acute tubular necrosis. On fifth day, patient had 2 sessions of hamatemesis for which pantoprazole infusion and UGI Endoscopy done suggestive of extensive oropharyngeal and esophageal ulcerations with overflowing. On the next day, patient turned to be extremely hypoxic, spo2-85% while on 100% FIO2 on Non Invasive Ventilation was utilized. Heart rate was 124/min, Respiratory rate36/min and blood pressure was 120/66mmHg. Subsequently, patient became drowsy, Spo2 was 80% on 100% FIO2 on NIV.In perspective of ingenuity hypoxia patient was intubated and continued mechanical ventilation and hemodialysis was performed daily except her condition didn’t enhanced and she lapsed on 11th day.
4) Abrus Precatorius: Abrus precatorius or Rosary pea, a plant that grows wild in many parts of india. All parts of the plant are lethal particularly the seeds which contains high amount of abrin, a toxalbumin which hinders protein synthesis and causes cell demise. The lethal dosage of abrin in human beings is 0.1-1 µg/kg. The seeds are squashed which discharges toxin from within the protective external hard coat of seeds which raise the severity of toxicity and diminishing the onset of indications. Clinical features incorporates nausea, severe vomiting, diarrhea, abdominal pain, renal failure, encephalopathy.
A.Precatorius is an unprecedented cause of poisoning reported mainly from southern parts of India. Here is the case study of 2 year old boy passing rosary pea seeds which was dismissed by the guardians. There was no history of fever, vomiting or pain abdomen or rashes before the convulsions. On admission the pulse rate was 120/min, blood pressure was 100/70 mmHg and respiratory rate was 30/min. He was in altered sensorium, with discouraged reflexes and flexor plantars. Both pupils were of typical size, regular and receptive to light. Within few minutes of admission, the child had unspecialized tonic clonic seizures. The convulsions were dealt initially with intravenous dextrose and calcium gluconate and required midazolam and loading doses of both phenytoin and phenobarbitone to get controlled. As the respiration was sporadic and there was decay in Glasgow Coma Scale (GCS), the baby was intubated and put on ventilator support and antioedema measures were begin. The kid was set on wide range of antimicrobials and steady therapy.In the following 24 hours, he developed upper gastrointestinal bleeding without any skin or mucosal bleeds. The complete haemogram demonstrated microcytic hypochromic anaemia with haemoglobin of 7.2 gm/dl and mild thrombocytosis. The child was given cold saline stomach wash and intravenous ranitidine. Hypocalcaemia and hypokalaemia were corrected with intravenous calcium gluconate and KCl respectively. Cardiac monitoring did not uncover evidence of significant rhythm disturbances. ABG uncovered slight respiratory alkalosis. Chest X-ray was ordinary. CT scan brain uncovered bilateral diffuse cerebral oedema. The child was transfused with entire blood as the child was anaemic and had dynamic gastrointestinal