Aluminum phosphide is a common pesticide used worldwide that releases phosphine gas which is toxic. It is frequently used as a suicide method in India and causes death in 60-90% of cases from cardiac issues within 1-48 hours. Symptoms include vomiting, chest pain, and coma. There is no antidote so management focuses on supportive care. A case study describes a 7-year-old girl who died of phosphine poisoning after being near a granary during rainy weather.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
COPPER POISONING
Appear within 15-30 min
Metallic taste
Increased salivation
Burning pain in stomach
Nausea, vomiting (vomited matter : blue / green colour)
Diarrhoea with much straining (motions are liquid and brown)
Oliguria, haematuria, albuminuria, acidosis, uraemia
In severe cases, haemolysis, jaundice, pancreatitis, convulsions, spasm of legs
Breathing difficulty, cold perception, severe head ache
Death due to HEPATIC or RENAL failure or both
Rodenticide Poisoning + Rat Killer paste poisoning managementVasif Mayan
Rodenticide paste poisoning
Case Study
Clinical features
Management
Investigations
Treatment guidelines
pathogenesis
N acetyl cysteine
Coumarins
other rodenticides
COPPER POISONING
Appear within 15-30 min
Metallic taste
Increased salivation
Burning pain in stomach
Nausea, vomiting (vomited matter : blue / green colour)
Diarrhoea with much straining (motions are liquid and brown)
Oliguria, haematuria, albuminuria, acidosis, uraemia
In severe cases, haemolysis, jaundice, pancreatitis, convulsions, spasm of legs
Breathing difficulty, cold perception, severe head ache
Death due to HEPATIC or RENAL failure or both
Rodenticide Poisoning + Rat Killer paste poisoning managementVasif Mayan
Rodenticide paste poisoning
Case Study
Clinical features
Management
Investigations
Treatment guidelines
pathogenesis
N acetyl cysteine
Coumarins
other rodenticides
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Health Impacts of Water Fluoridation. Presentation includes data on the contrubution of fluoride to pulmonary disease, metabolic disorders, neurological disorders and cancer.
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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2. Introduction
Aluminum phosphide (AlP) is a solid fumigant pesticide sold as tablets in use since the
1940s. It is considered to be an ideal pesticide because of its cheapness, efficiency and
easy availability in the market and is widely used as a grain preservative worldwide
Although the chemical does not accumulate in the food chain, aluminum phosphide
poisoning is one of the most common forms of poisoning in India. The incidence of
the poisoning has been increasing steadily, and most of the poisoning is from suicide
in the agricultural community. Occupational exposure or accidental exposure of
individuals in railroad boxcars, cargo ships or close proximity to grain storage facilities
has been reported. The mortality in cases of aluminum phosphide poisoning varies
between 60% and 90%, even in experienced and well-equipped hospitals.
3. None of the patients who had ingested more than three tablets survived. The average
time interval between ingestion of AlP and death is 3 h (1–48 h), 95% of the patients
die within 24 h and the most common cause of death in this group is cardiac
dysrhythmia. Death is reported to result from profound shock, myocarditis and
multiorgan failure. In some countries, the use of AlP is strictly controlled, and it
cannot be freely supplied. Aluminum phosphide is capable of releasing phosphine gas
if it comes in contact with moisture in the air. Phosphine gas is colorless, extremely
flammable and explosive; very toxic to insects; and useful as a fumigant for stored
products for controlling pests; it has a unique smell of garlic or decaying fish, with an
odor threshold of 0.14 ppm and a vapor density of 1.17. Phosphine poisoning
following inhalation has also been reported. The fatal dose of aluminum phosphide
was stated to be in the range of 150–500 mg/ 70 kg
4. Toxicokinetic:
Phosphine can easily be distributed into all tissues and excreted in the urine and
expelled through the lungs .The most important urine metabolites of phosphine are
phosphite and hypophosphite. Phosphine toxicity to humans occurs with a common
mechanism of respiratory inhibition .Phosphine is a noncompetitive inhibitor of
cytochrome oxidase in mitochondria, with electron transfer blockage, which inhibits
oxidative phosphorylation and, in turn, cellular respiration and production of peroxide
radicals. This inhibits oxidative respiration by 70% and ultimately results in a marked
decrease in the mitochondrial membrane potential .Phosphine can inhibit catalase and
deplete glutathione, which may result in cellular wall and canal dysfunction as well .It is
likely that interference with cellular respiration may lead to multisystem toxicity.
5.
6.
7. Clinical Finding :
Human phosphine poisoning occurs after inhalation of phosphine generated from
metal phosphides pellets used as fumigants, leading to systematic clinical symptoms
including the damage of the nervous system and respiratory system. Acute phosphine
poisoning has a quick onset; severe poisoning symptoms occur in a few minutes,
although some patients have a long latency to response of 48 h. It mainly causes
dizziness, headache, fatigue, nausea, vomiting, loss of appetite, cough, chest tightness,
dry throat, abdominal pain and diarrhea, and patients often recover in one week with
appropriate treatment. Severe poisoning can cause coma, convulsions, pulmonary
edema, shock, significant myocardial damage, and significant liver and kidney damage .
8. The symptoms of respiratory and nervous system damage occur quickly after
inhalation of phosphine, while the gastrointestinal symptoms occur early, in
particular in acute poisoning caused by ingestion of zinc phosphide or
aluminum phosphide. Acute phosphine poisoning can be diagnosed according
to the history of exposure, clinical examination, on-site investigation, with
other diseases excluded, and it is rather difficult for diagnosis of phosphine
poisoning in children .
Clinical Finding :
9. Management:
Management should be started as soon as history and clinical examination
support AlP poisoning, and should not be delayed for the confirmatory
diagnosis . Unfortunately, due to no known specific antidote, management
remains primarily supportive care. As each poison has a definite elimination
time, so also is the case with AlP. Early arrival, resuscitation, diagnosis, intensive
monitoring and supportive therapy may result in good outcome. Care of
patients with severe poisoning can be enhanced by consultation with a medical
toxicologist or a regional poison center.
10. Case Study :
Case 5 A 7-year-old girl presented with clinical symptoms of vomiting and
abdominal pain in the morning; her grandmother presented with mild vomiting
symptom. She was sent to the hospital and back home after treatment. She was
dead at midnight that night, and phosphine poisoning was suspected because
she lived near a granary. Furthermore, it had been rainy for a week. Forensic
autopsy indicated no trauma or fatal disease. The metabolites of phosphine
were found in the liver and bladder flush fluid by GC–MS.
11. References :
1- Journal of Analytical Toxicology, 2018;42:330–336 doi: 10.1093/jat/bky005
Advance Access Publication Date: 25 January 2018 Article.
2- Hashemi-Domeneh, B., Zamani, N., Hassanian-Moghaddam, H., Rahimi, M.,
Shadnia, S., Erfantalab, P., et al. (2016) A review of aluminium phosphide poisoning
and a flowchart to treat it. Arhiv za higijenu rada i toksikologiju, 67, 183–193
3- Kalawat, S., Thakur, V., Thakur, A., Punjabi, N.D. (2016) Cardiovascular profile of
aluminium phosphide poisoning and its clinical significance. International Journal of
4- Advances in Medicine, 3, 859–864. 12. Meena, M.C., Mittal, S., Rani, Y. (2015) Fatal
aluminium phosphide poisoning. Interdisciplinary Toxicology, 8, 65–67