As this herbicide poisoning is frequent with poor outcomes so its management needs to be discussed and awareness should be raised among farmers about its use and pre-hospital treatments.
Paraquat poisoning causes severe oxidative stress and multi-organ failure. Ingestion has a high fatality rate. It is rapidly absorbed and concentrated in lungs, liver, and kidneys, causing cellular damage through redox cycling. Clinical features include oropharyngeal burns, respiratory distress, and acute kidney injury. Diagnosis is confirmed by positive urine dithionite test showing blue color change. Prognosis is poor for those with serum paraquat levels above the Sipp score threshold or rapidly increasing creatinine. Early extracorporeal removal within 4 hours may help severe cases, but long-term outcomes are generally poor with progressive lung fibrosis. Management focuses on supportive care, though antioxidants have been tried with
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
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
Rodenticides are chemicals used to kill rodent pests that can destroy large amounts of grains. They are commonly used but also pose risks to humans and pets through secondary poisoning. Common rodenticides include inorganic preparations like phosphorus and organic preparations like fluoroacetate compounds. Symptoms depend on the specific rodenticide ingested or inhaled and can include abdominal pain, vomiting, seizures, and bleeding. Treatment involves decontamination, supportive care, and antidotes like vitamin K for anticoagulants.
This document discusses drug-induced liver injury (DILI) caused by anti-tuberculosis (ATT) drugs. It notes that ATT drugs, particularly isoniazid, rifampin, and pyrazinamide, are common causes of DILI. Isoniazid metabolism varies depending on acetylator status, and its toxicity may be due to reactive metabolites. Rifampin induces liver enzymes and its toxicity is often seen in combination with other ATT drugs. Pyrazinamide toxicity depends on dose and can cause fatty liver. Presentations of ATT-induced DILI range from asymptomatic elevations in enzymes to acute liver failure. Careful screening and monitoring of patients on ATT is needed to prevent DILI
Aluminum phosphide poisoning is a common lethal poisoning that has caused many deaths in India in recent decades. Aluminum phosphide is marketed as pesticide pellets or tablets used to preserve food grains. When it reacts with water, it produces phosphine gas which is toxic as it inhibits cellular respiration. Symptoms include vomiting, hypotension, and organ damage. Diagnosis involves detecting phosphine in breath or vomit. Treatment focuses on managing shock through fluids and vasopressors, as there is no antidote. Prevention requires better regulation of aluminum phosphide distribution to limit accidental or intentional ingestion.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
This document discusses several types of rodenticides and poisons. It describes how rodenticides like warfarin work by disrupting the normal blood clotting process and can cause internal bleeding. Symptoms include nose bleeds, bleeding gums, and bruising. Overdoses of vitamin D3 can cause calcium deposition in organs and lead to conditions like heart problems. Phosphide poisons react with stomach acid to form phosphine gas, which is toxic and can cause respiratory failure. While there are some treatment approaches described, there are no known antidotes for many of these poisons.
Paraquat poisoning causes severe oxidative stress and multi-organ failure. Ingestion has a high fatality rate. It is rapidly absorbed and concentrated in lungs, liver, and kidneys, causing cellular damage through redox cycling. Clinical features include oropharyngeal burns, respiratory distress, and acute kidney injury. Diagnosis is confirmed by positive urine dithionite test showing blue color change. Prognosis is poor for those with serum paraquat levels above the Sipp score threshold or rapidly increasing creatinine. Early extracorporeal removal within 4 hours may help severe cases, but long-term outcomes are generally poor with progressive lung fibrosis. Management focuses on supportive care, though antioxidants have been tried with
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
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
Rodenticides are chemicals used to kill rodent pests that can destroy large amounts of grains. They are commonly used but also pose risks to humans and pets through secondary poisoning. Common rodenticides include inorganic preparations like phosphorus and organic preparations like fluoroacetate compounds. Symptoms depend on the specific rodenticide ingested or inhaled and can include abdominal pain, vomiting, seizures, and bleeding. Treatment involves decontamination, supportive care, and antidotes like vitamin K for anticoagulants.
This document discusses drug-induced liver injury (DILI) caused by anti-tuberculosis (ATT) drugs. It notes that ATT drugs, particularly isoniazid, rifampin, and pyrazinamide, are common causes of DILI. Isoniazid metabolism varies depending on acetylator status, and its toxicity may be due to reactive metabolites. Rifampin induces liver enzymes and its toxicity is often seen in combination with other ATT drugs. Pyrazinamide toxicity depends on dose and can cause fatty liver. Presentations of ATT-induced DILI range from asymptomatic elevations in enzymes to acute liver failure. Careful screening and monitoring of patients on ATT is needed to prevent DILI
Aluminum phosphide poisoning is a common lethal poisoning that has caused many deaths in India in recent decades. Aluminum phosphide is marketed as pesticide pellets or tablets used to preserve food grains. When it reacts with water, it produces phosphine gas which is toxic as it inhibits cellular respiration. Symptoms include vomiting, hypotension, and organ damage. Diagnosis involves detecting phosphine in breath or vomit. Treatment focuses on managing shock through fluids and vasopressors, as there is no antidote. Prevention requires better regulation of aluminum phosphide distribution to limit accidental or intentional ingestion.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
This document discusses several types of rodenticides and poisons. It describes how rodenticides like warfarin work by disrupting the normal blood clotting process and can cause internal bleeding. Symptoms include nose bleeds, bleeding gums, and bruising. Overdoses of vitamin D3 can cause calcium deposition in organs and lead to conditions like heart problems. Phosphide poisons react with stomach acid to form phosphine gas, which is toxic and can cause respiratory failure. While there are some treatment approaches described, there are no known antidotes for many of these poisons.
A 30-year-old unconscious housewife was brought to the hospital with a history of domestic violence. On examination, she had constricted pupils, low blood pressure, high blood sugar, metabolic acidosis on ABG, bradycardia on ECG, and elevated serum amylase. The diagnosis was organophosphorus poisoning based on the clinical features and laboratory findings.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
Super-vasmol hair dye poisoning is a major cause of suicidal poisoning in India, as its main toxic ingredient, paraphenylene diamine (PPD), is cheap and readily available. PPD poisoning can cause multi-organ dysfunction and failure through two phases - an initial acute presentation with angioedema and airway obstruction within 4-6 hours, followed by a subacute phase involving rhabdomyolysis, acute renal failure, hepatitis, and metabolic acidosis. Aggressive management is focused on airway protection, steroids to reduce angioedema, fluid resuscitation to prevent renal failure, and dialysis as needed.
This document discusses organophosphate poisoning. It begins by introducing organophosphates as a group of chemicals used in domestic and industrial settings that act as acetylcholinesterase inhibitors. It then describes the chemical structure and mechanisms of organophosphates, their routes of entry into the body, and how they cause toxicity by inhibiting acetylcholinesterase. The document goes on to describe the clinical features, phases, and syndromes of organophosphate poisoning as well as their treatment, which involves stabilization, decontamination, administration of the antidotes atropine and pralidoxime, and supportive care.
This document discusses Paraquat poisoning. It begins by introducing Paraquat as a widely used herbicide that is highly toxic to humans. It then summarizes the pathophysiology of Paraquat poisoning as involving oxidative stress and free radical generation that causes damage to multiple organs, particularly the lungs and kidneys. The clinical presentation, diagnosis, and severity classification of Paraquat poisoning are outlined. Management is described as primarily supportive care, with early extracorporeal removal via hemodialysis or hemoperfusion considered for severe cases. However, the prognosis remains poor even with aggressive treatment.
1) ATT induced hepatitis refers to drug-induced liver injury caused by anti-tuberculosis treatment medications like isoniazid, rifampin, and pyrazinamide.
2) These drugs can cause a spectrum of liver damage from asymptomatic transaminase elevations to acute liver failure via both idiosyncratic and dose-dependent mechanisms including intracellular calcium disruption and apoptosis.
3) Risk factors for tuberculosis drug-induced liver injury include older age, female sex, extra-pulmonary or meningeal tuberculosis, malnutrition, alcohol use, viral hepatitis coinfection, and certain genetic factors. Careful monitoring of liver enzymes is recommended during treatment.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
This document provides information on corrosive poisoning, including types, mechanisms of injury, clinical features, investigations, management, and treatment. It discusses three main types of corrosives - acids, alkalis, and oxidants. Alkalis are noted as the most dangerous due to their ability to rapidly cause liquifactive necrosis and injury. Clinical features involve the gastrointestinal tract, respiratory system, eyes and skin. Investigations include endoscopy, imaging, and labs. Management focuses on airway protection, dilution, antibiotics, and monitoring. Long term complications like stricture formation may require repeated dilations.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by irregular electrical activity in the atria. It increases in prevalence with age and can cause complications like heart failure, stroke, and systemic embolism.
2) Management of atrial fibrillation involves rate or rhythm control as well as long-term anticoagulation to prevent thromboembolism depending on stroke risk factors. The CHA2DS2-VASc score is used to assess this risk.
3) While antiarrhythmic drugs and cardioversion can restore normal sinus rhythm, rate control is preferred for many patients. Newer anticoagulants like dabigatran and rivar
Rat killer paste poisoining by Dr kandy Ajay Kandpal
This document discusses rat killer paste poisoning. It begins by providing statistics on its common occurrence and details on the historical use of yellow phosphorus as a rodenticide. It describes how yellow phosphorus causes direct tissue damage and toxicity to multiple organs. Clinical manifestations depend on the route of exposure and include gastrointestinal, neurological and cardiac effects. Treatment involves gastric lavage, charcoal, N-acetylcysteine, and supportive care. Liver transplant may be required for severe cases based on King's College criteria. Close monitoring of liver enzymes and prothrombin time is important to identify complications.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
1) Paracetamol is metabolized in the liver and can cause toxicity in high doses by depleting glutathione levels, allowing the reactive metabolite NAPQI to damage cells.
2) For paracetamol overdose, N-acetylcysteine should be administered within 8-10 hours as an antidote to replenish glutathione levels. The treatment involves intravenous administration over 21 hours.
3) Management also involves monitoring liver function tests and providing supportive care. Liver transplantation may be considered for severe liver failure due to paracetamol poisoning.
A 14-year-old boy presented to the emergency department with symptoms of an autonomic storm after being bitten by a scorpion. He was diagnosed with scorpion sting in autonomic storm. He was given prazosin, hydrocortisone, and other supportive treatments. His condition stabilized and he was discharged after 6 days. Scorpion stings can cause local effects and a systemic autonomic storm response due to neurotoxins that affect sodium channels and induce catecholamine release. Prazosin is an effective treatment as it blocks alpha receptors and counters the effects of venom.
1. Acute aluminum phosphide poisoning is an extremely lethal poisoning caused by ingestion of the toxic fumigant aluminum phosphide.
2. It liberates phosphine gas which inhibits the mitochondrial respiratory chain, causing multi-organ damage and failure.
3. The key treatments are decontamination through gastric lavage and activated charcoal, intensive care monitoring, management of shock and acidosis, and supportive care; however mortality remains very high between 37-100%.
This document provides an overview of the management of hypertensive crisis. It begins with definitions of hypertensive urgency and emergency. It then covers etiology, pathophysiology, clinical evaluation, workup, and management. The goals of management are to lower blood pressure gradually in hypertensive urgencies, and more rapidly in emergencies to prevent end organ damage, while avoiding too rapid a drop in pressure. Drugs discussed for acute treatment include sodium nitroprusside, nicardipine, clevidipine, labetalol, and esmolol. Special scenarios like myocardial ischemia and aortic dissection are also addressed.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
The document discusses oleandrin, the main toxic compound found in the plant Nerium oleander. It provides background on oleandrin's toxicity, structure, mechanism of action, and medical importance. While oleandrin is highly toxic and can be fatal, it is also under investigation for potential uses in cancer treatment and neuroprotection. However, its narrow therapeutic range and potential for drug interactions pose issues. The document also covers oleandrin's traditional uses in folk medicine, industrial applications, and current research developments regarding its medical potential.
This document discusses cannabis poisoning and provides key information about cannabis. It describes how cannabis is prepared in forms like bhang, ganja, and charas. Signs of acute cannabis poisoning include euphoria, confusion, and psychosis. Chronic use can cause apathy, dependence, and conditions like "hashish insanity." The minimum lethal doses are 2 grams per kg for charas and 8 grams per kg for ganja. Diagnosis involves clinical symptoms and urine tests. Treatment focuses on decontamination, controlling psychosis, and gradual withdrawal. Postmortem findings may show asphyxia but no distinctive signs. Medicolegal aspects note its use in robbery and potential for addiction.
1) Paraquat is a toxic herbicide that can cause severe poisoning if ingested. Its mechanism of toxicity involves generating reactive oxygen species that can damage lungs and other organs.
2) Management of paraquat poisoning involves decontamination procedures like activated charcoal and hemoperfusion within 4 hours of ingestion. Immunosuppressive therapies like cyclophosphamide, corticosteroids, and pulse dosing protocols may help reduce mortality from lung injury.
3) The prognosis is generally poor, especially with ingestion of concentrated solutions or levels over 1mg/mL detected on urine testing, as severe lung fibrosis often develops. Early and aggressive treatment offers the best chance of survival.
Paraquat poisoning by Dr.Jeevan Tc.pptxJeevan425844
- Paraquat is a highly toxic herbicide that is rapidly absorbed through the gastrointestinal tract and lungs. It causes oxidative stress by generating reactive oxygen species.
- Mild toxicity results from ingestion of less than 20 mg/kg, while more than 40 mg/kg is often fatal. Toxicity involves multiple organ systems and can cause acute respiratory distress syndrome.
- Management involves decontamination, supportive care, and antioxidants as adjunctive treatments. Decontamination includes removal of contaminated clothing and administration of activated charcoal or adsorbents. Supportive care focuses on hydration, ventilation, and treating complications like renal failure. High-dose antioxidants may help reduce oxidative damage from paraquat.
A 30-year-old unconscious housewife was brought to the hospital with a history of domestic violence. On examination, she had constricted pupils, low blood pressure, high blood sugar, metabolic acidosis on ABG, bradycardia on ECG, and elevated serum amylase. The diagnosis was organophosphorus poisoning based on the clinical features and laboratory findings.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
Super-vasmol hair dye poisoning is a major cause of suicidal poisoning in India, as its main toxic ingredient, paraphenylene diamine (PPD), is cheap and readily available. PPD poisoning can cause multi-organ dysfunction and failure through two phases - an initial acute presentation with angioedema and airway obstruction within 4-6 hours, followed by a subacute phase involving rhabdomyolysis, acute renal failure, hepatitis, and metabolic acidosis. Aggressive management is focused on airway protection, steroids to reduce angioedema, fluid resuscitation to prevent renal failure, and dialysis as needed.
This document discusses organophosphate poisoning. It begins by introducing organophosphates as a group of chemicals used in domestic and industrial settings that act as acetylcholinesterase inhibitors. It then describes the chemical structure and mechanisms of organophosphates, their routes of entry into the body, and how they cause toxicity by inhibiting acetylcholinesterase. The document goes on to describe the clinical features, phases, and syndromes of organophosphate poisoning as well as their treatment, which involves stabilization, decontamination, administration of the antidotes atropine and pralidoxime, and supportive care.
This document discusses Paraquat poisoning. It begins by introducing Paraquat as a widely used herbicide that is highly toxic to humans. It then summarizes the pathophysiology of Paraquat poisoning as involving oxidative stress and free radical generation that causes damage to multiple organs, particularly the lungs and kidneys. The clinical presentation, diagnosis, and severity classification of Paraquat poisoning are outlined. Management is described as primarily supportive care, with early extracorporeal removal via hemodialysis or hemoperfusion considered for severe cases. However, the prognosis remains poor even with aggressive treatment.
1) ATT induced hepatitis refers to drug-induced liver injury caused by anti-tuberculosis treatment medications like isoniazid, rifampin, and pyrazinamide.
2) These drugs can cause a spectrum of liver damage from asymptomatic transaminase elevations to acute liver failure via both idiosyncratic and dose-dependent mechanisms including intracellular calcium disruption and apoptosis.
3) Risk factors for tuberculosis drug-induced liver injury include older age, female sex, extra-pulmonary or meningeal tuberculosis, malnutrition, alcohol use, viral hepatitis coinfection, and certain genetic factors. Careful monitoring of liver enzymes is recommended during treatment.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
This document provides information on corrosive poisoning, including types, mechanisms of injury, clinical features, investigations, management, and treatment. It discusses three main types of corrosives - acids, alkalis, and oxidants. Alkalis are noted as the most dangerous due to their ability to rapidly cause liquifactive necrosis and injury. Clinical features involve the gastrointestinal tract, respiratory system, eyes and skin. Investigations include endoscopy, imaging, and labs. Management focuses on airway protection, dilution, antibiotics, and monitoring. Long term complications like stricture formation may require repeated dilations.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by irregular electrical activity in the atria. It increases in prevalence with age and can cause complications like heart failure, stroke, and systemic embolism.
2) Management of atrial fibrillation involves rate or rhythm control as well as long-term anticoagulation to prevent thromboembolism depending on stroke risk factors. The CHA2DS2-VASc score is used to assess this risk.
3) While antiarrhythmic drugs and cardioversion can restore normal sinus rhythm, rate control is preferred for many patients. Newer anticoagulants like dabigatran and rivar
Rat killer paste poisoining by Dr kandy Ajay Kandpal
This document discusses rat killer paste poisoning. It begins by providing statistics on its common occurrence and details on the historical use of yellow phosphorus as a rodenticide. It describes how yellow phosphorus causes direct tissue damage and toxicity to multiple organs. Clinical manifestations depend on the route of exposure and include gastrointestinal, neurological and cardiac effects. Treatment involves gastric lavage, charcoal, N-acetylcysteine, and supportive care. Liver transplant may be required for severe cases based on King's College criteria. Close monitoring of liver enzymes and prothrombin time is important to identify complications.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
1) Paracetamol is metabolized in the liver and can cause toxicity in high doses by depleting glutathione levels, allowing the reactive metabolite NAPQI to damage cells.
2) For paracetamol overdose, N-acetylcysteine should be administered within 8-10 hours as an antidote to replenish glutathione levels. The treatment involves intravenous administration over 21 hours.
3) Management also involves monitoring liver function tests and providing supportive care. Liver transplantation may be considered for severe liver failure due to paracetamol poisoning.
A 14-year-old boy presented to the emergency department with symptoms of an autonomic storm after being bitten by a scorpion. He was diagnosed with scorpion sting in autonomic storm. He was given prazosin, hydrocortisone, and other supportive treatments. His condition stabilized and he was discharged after 6 days. Scorpion stings can cause local effects and a systemic autonomic storm response due to neurotoxins that affect sodium channels and induce catecholamine release. Prazosin is an effective treatment as it blocks alpha receptors and counters the effects of venom.
1. Acute aluminum phosphide poisoning is an extremely lethal poisoning caused by ingestion of the toxic fumigant aluminum phosphide.
2. It liberates phosphine gas which inhibits the mitochondrial respiratory chain, causing multi-organ damage and failure.
3. The key treatments are decontamination through gastric lavage and activated charcoal, intensive care monitoring, management of shock and acidosis, and supportive care; however mortality remains very high between 37-100%.
This document provides an overview of the management of hypertensive crisis. It begins with definitions of hypertensive urgency and emergency. It then covers etiology, pathophysiology, clinical evaluation, workup, and management. The goals of management are to lower blood pressure gradually in hypertensive urgencies, and more rapidly in emergencies to prevent end organ damage, while avoiding too rapid a drop in pressure. Drugs discussed for acute treatment include sodium nitroprusside, nicardipine, clevidipine, labetalol, and esmolol. Special scenarios like myocardial ischemia and aortic dissection are also addressed.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
The document discusses oleandrin, the main toxic compound found in the plant Nerium oleander. It provides background on oleandrin's toxicity, structure, mechanism of action, and medical importance. While oleandrin is highly toxic and can be fatal, it is also under investigation for potential uses in cancer treatment and neuroprotection. However, its narrow therapeutic range and potential for drug interactions pose issues. The document also covers oleandrin's traditional uses in folk medicine, industrial applications, and current research developments regarding its medical potential.
This document discusses cannabis poisoning and provides key information about cannabis. It describes how cannabis is prepared in forms like bhang, ganja, and charas. Signs of acute cannabis poisoning include euphoria, confusion, and psychosis. Chronic use can cause apathy, dependence, and conditions like "hashish insanity." The minimum lethal doses are 2 grams per kg for charas and 8 grams per kg for ganja. Diagnosis involves clinical symptoms and urine tests. Treatment focuses on decontamination, controlling psychosis, and gradual withdrawal. Postmortem findings may show asphyxia but no distinctive signs. Medicolegal aspects note its use in robbery and potential for addiction.
1) Paraquat is a toxic herbicide that can cause severe poisoning if ingested. Its mechanism of toxicity involves generating reactive oxygen species that can damage lungs and other organs.
2) Management of paraquat poisoning involves decontamination procedures like activated charcoal and hemoperfusion within 4 hours of ingestion. Immunosuppressive therapies like cyclophosphamide, corticosteroids, and pulse dosing protocols may help reduce mortality from lung injury.
3) The prognosis is generally poor, especially with ingestion of concentrated solutions or levels over 1mg/mL detected on urine testing, as severe lung fibrosis often develops. Early and aggressive treatment offers the best chance of survival.
Paraquat poisoning by Dr.Jeevan Tc.pptxJeevan425844
- Paraquat is a highly toxic herbicide that is rapidly absorbed through the gastrointestinal tract and lungs. It causes oxidative stress by generating reactive oxygen species.
- Mild toxicity results from ingestion of less than 20 mg/kg, while more than 40 mg/kg is often fatal. Toxicity involves multiple organ systems and can cause acute respiratory distress syndrome.
- Management involves decontamination, supportive care, and antioxidants as adjunctive treatments. Decontamination includes removal of contaminated clothing and administration of activated charcoal or adsorbents. Supportive care focuses on hydration, ventilation, and treating complications like renal failure. High-dose antioxidants may help reduce oxidative damage from paraquat.
- Paraquat is a herbicide that causes toxicity through generation of reactive oxygen species, leading to lung and other organ damage.
- It is absorbed through the gastrointestinal tract and lungs, and accumulates primarily in the lungs. Clinical features range from mild gastrointestinal symptoms to multi-organ failure and death.
- Treatment involves gut decontamination, supportive care, antioxidants, and in some cases extracorporeal removal techniques. C-reactive protein levels may help predict prognosis.
Paraquat poisoning results from ingestion of the herbicide paraquat. It causes multi-organ damage through generation of reactive oxygen species. Clinical features include mouth ulcers, renal failure, liver damage, and pulmonary fibrosis. Diagnosis is confirmed by urine or blood tests detecting paraquat. Management focuses on decontamination, supportive care, and immunosuppression to reduce lung fibrosis. Prognosis is poor, even with treatment, due to progressive pulmonary damage.
Gut decontamination or methods of poison removal in clinical toxicology Soujanya Pharm.D
Gastrointestinal decontamination refers to removing toxins from the gastrointestinal tract. Methods include inducing vomiting, gastric lavage, cathartics, activated charcoal, and whole bowel irrigation. Inducing vomiting with ipecac or apomorphine is only recommended for alert patients within 4-6 hours of ingestion. Gastric lavage may be considered for life-threatening ingestions within 1-2 hours but has risks. Cathartics like sorbitol and magnesium can help purge the bowels. Activated charcoal binds toxins and is most effective within 1 hour. Whole bowel irrigation with solutions like PEG-ELS may help for late presentations over 4 hours after ingestion. These methods aim to reduce toxin
This document provides an overview of common drug and plant poisonings. It discusses acetaminophen, iron, and anticonvulsant poisonings in detail, outlining their pathophysiology, clinical features, investigations, and management including use of antidotes like N-acetylcysteine and desferoxamine. It also briefly mentions other common drug poisonings and plant toxins like oleander, datura, and jatropha. The goal is to educate about identifying and treating accidental or intentional overdoses of commonly ingested substances.
Therapeutic drug monitoring of cardiovascular agentsranjith lucky
This document discusses therapeutic drug monitoring of cardiovascular agents. It provides details about amiodarone and digoxin, including their clinical uses, mechanisms of action, dosing, toxicity, and monitoring. For amiodarone, it describes factors affecting drug concentrations, toxic effects, and patient tips. For digoxin it outlines dosing in various populations, factors influencing concentrations, side effects, and monitoring therapy.
The seminar discussed toxicity from 2,4-D and paraquat herbicides. 2,4-D is a systemic herbicide that can cause central nervous system and respiratory depression. It primarily targets the eyes, thyroid, kidneys, and reproductive organs. Paraquat poisoning primarily affects the lungs and kidneys due to accumulation and generation of toxic oxygen species. Ingestion of moderate amounts can cause gastrointestinal ulceration, renal failure, hepatotoxicity, and metabolic acidosis. Larger ingestions result in multi-organ failure and death within hours to days. Both herbicides are metabolized and excreted quickly in humans.
This document discusses the management of diarrhea through rehydration and drug therapy. It defines diarrhea and describes oral rehydration solutions for acute diarrhea treatment. Loperamide is recommended for acute diarrhea while opioids like codeine, diphenoxylate, and tincture of opium can be used for chronic diarrhea. Antimicrobial agents may be given if an infectious cause is known. Other drugs discussed for chronic diarrhea include clonidine, octreotide, cholestyramine, bulk forming agents, and certain plant alkaloids, calcium channel blockers, and chloride channel blockers.
This document discusses the use of antibiotics in patients with renal or hepatic failure. It begins by noting the risk of nephrotoxicity and hepatotoxicity from antibiotics. It then provides guidelines for dosing adjustments for various antibiotics based on renal function tests. These include reducing doses for aminoglycosides, tetracyclines, carbapenems, cephalosporins, and fluoroquinolones in renal failure. For hepatic failure, it recommends regimens for tuberculosis treatment that contain fewer hepatotoxic drugs. The document emphasizes individualizing treatment based on the severity of organ dysfunction.
Proton pump inhibitors (PPIs) like omeprazole irreversibly inhibit the gastric H+/K+-ATPase enzyme to reduce acid secretion. They are effective for treating acid-related disorders like GERD and peptic ulcers. PPIs have high bioavailability but require acidic conditions for activation. Common side effects include diarrhea and headache, while long term use may increase risks of infections, fractures, and nutrient deficiencies. Drug interactions are rare due to short half-lives, but some PPIs inhibit CYP2C19 and decrease clopidogrel effectiveness.
This document provides information about peritoneal dialysis (PD), including:
- An overview of PD, how it works, and the components of PD fluid.
- Details on different PD modalities, principles of exchanges, and factors in patient selection.
- Complications of PD like peritonitis and their treatment, as well as non-infectious complications.
- The PD program at Mansoura International Hospital, including patient education, catheter insertion, and home visits.
Racecadotril is a treatment for acute diarrhea that works by inhibiting the enzyme enkephalinase. This allows endogenous enkephalins to reduce intestinal secretion without affecting motility. A study found that in children with acute watery diarrhea, racecadotril combined with oral rehydration therapy decreased stool output and duration of diarrhea more than oral rehydration alone. Racecadotril is effective in both children and adults and shows promise for chronic diarrhea such as that associated with HIV. It provides benefits over loperamide such as more rapid relief of symptoms and less constipation as a side effect.
This document summarizes anthelmintic drugs used to treat helminthiasis. It discusses the major classes of anthelmintics including benzimidazoles (albendazole, mebendazole), piperazines (piperazine citrate), ivermectin, and praziquantel. For each drug, it outlines the mechanism of action, clinical uses, pharmacokinetics, contraindications, and adverse effects. The document provides an overview of the most common helminth infections (roundworms, hookworms, tapeworms, flukes) and highlights the anthelmintics recommended for treating different parasitic infections.
INTRODUCTION OF FUROSEMIDE
CLINICAL DATA
CHEMISTRY OF DRUG (INCLUDING DRUG PROPERTIES)
DRUG DATABASES (AVAILABILITY,STORAGE,DOSAGE,ROUTE PREFERENCE)
PHARMACOKINETICS (SITE OF ACTION,TIME/ACTION PROFILE)
MECHANISM OF ACTION
ACTIONS
DESIRED EFFECT
INDICATIONS
THERAPEUTIC USES
CONTRAINDICATIONS
PRECAUTIONS
ADVERSE EFFECTS/SIDE EFFECTS
WARNINGS INCLUDING DOSE ADJUSTMENT IN SPECIAL POPULATION
DRUG INTERACTIONS
TOXICOLOGY & IT’S MANAGEMENT
NURSING CONSIDERATIONS
;RESPONSIBILITIES;ASSESSMENT;POTENTIAL DIAGNOSIS; IMPLEMENTATIONS;EVALUATIONS DURING FUROSIDE ADMINISTRATION
PATIENT/FAMILY TEACHING
SPECIAL CALCULATIONS
CONCLUSION OF FUROSEMIDE
REFERENCES OF FUROSEMIDE
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
2. BACKGROUND
• Paraquat (1,1’- dimethyl-4,4’- bipyridinium) is a quaternary dipyridyl non-
specific contact herbicide
• Rapidly absorbed by the aerial plant and immediately inactivated on
contact to the clay in the soil, leaving minimal residue
• The solution is usually blue-green in color. It is present in varying
concentrations ranging from 10%-40% and requires to be diluted prior
to use.
• Paraquat, when ingested, is highly toxic. all formulations contain an
emetic to decrease absorption in case of accidental or suicidal ingestion
5. HISTORY
• First synthesized in 1882 as a redox indicator, and its herbicidal property was
recognized in the 1950s and found its way into agricultural use by 1962
• It was initially used to kill marijuana weeds in the United States and Mexico.
• Paraquat is a widely used for weed and grass control but is also a lethal poison.
In some low- and middle-income countries paraquat is commonly available and
inexpensive, making poisoning prevention difficult.
• Most of the people poisoned by paraquat have taken it as a means of self-
poisoning. its unregulated use in developing countries like India has made it a
commonly used pesticide.
6. WHY IT’S STILL IN USE ?
• Paraquat dichloride is being used for 25 crops in India, whereas it is approved
for use in only 9 crops by the Central Insecticide Board and Registration
Committee(CIBRC). This is in violation of the Indian Insecticides Act
• Syngenta, the Swiss-headquartered, Chinese-owned agrochemical giant that
inherited ICI’s pesticides business, continues to export thousands of tonnes of
Gramoxone each year from its factory - although the UK, Switzerland and China
have all banned its use on their own soil.
• Banned in 32 countries including Switzerland, where herbicide producing
company Sygenta is based.
• So far in India, only Kerala has banned the paraquat herbicide.
7. TOXICOKINETICS
• Gastrointestinal tract absorbs less than 10% of an ingested dose over 6 hours.
Presence of ulcerated mucosa or an empty stomach increases the fraction of
paraquat absorbed. peak plasma concentrations occurs within 4 hours.
• Poorly absorbed through intact human skin; however, damage to the skin by
paraquat itself or other means will permit greater systemic absorption
• It’s not actively metabolized in the body, and more than 90% is excreted
unchanged by the kidneys
• After absorption, paraquat is distributed to highly perfused organs such as the
lungs, kidneys, liver, and muscles, and remains partly in the intravascular space.
9. MECHANISMS OF TOXICITY
• The mechanism of toxicity in humans has not been clarified, but paraquat has
been shown in animals to induce complete oxidation of both NADPH and
NADH and increase peroxidation of vital lipid membranes
• Additionally, paraquat is a potent generator of acute reactive oxygen species
11. RANGE OF TOXICITY
1) MILD TOXICITY: Ingestion of less than 20 mg paraquat ion per kg body weight
(less than 7.5 mL of 20% [w/v] paraquat concentrate): No symptoms or mild GI
effects; recovery likely.
2) MODERATE to SEVERE TOXICITY: 20 to 40 mg paraquat ion per kg body weight
(7.5 to 15 mL of 20% [w/v] paraquat concentrate): Pulmonary fibroplasia develops.
Death occurs in most cases, but may be delayed 2 to 3 weeks.
3) FATAL: Greater than 40 mg paraquat ion per kg body weight (10 to 15 mL of
20% [w/v] paraquat concentrate): Multiple organ failure occurs; toxicity progresses
rapidly. Mortality is essentially 100% in 1 to 7 days
12. RANGE OF TOXICITY
• Based on the LD50 in humans (35 mg/kg), the estimated human lethal dose is
10 to 15 mL of a 20% solution.
• Mortality rates are as high as 65% in patients who ingest concentrated
formulation compared to 4% in those ingest diluted solution (25% w/v)
• Reformulation of products : Some variability may exist based on the formulation;
newer formulations may have an alginate that can increase emesis and act as a
purgative
13. CLINICAL FEATURES
• Ingestion/systemic toxicity : Nausea and vomiting, with or without diarrhoea, are
common together with a burning sensation, soreness and pain in the mouth, throat,
chest and abdomen (usually epigastric).
• Ulceration in the mouth (which may be severe), sloughing of the oropharyngeal
mucosae, an inability to swallow, dysphagia and aphonia ensue.
• Within hours generalised weakness, myalgia, giddiness, headache, anorexia and
fever develop.
• Oliguria or non-oliguric renal failure may supervene due to acute tubular necrosis.
• Most patients develop a cough which may be productive and blood stained.
Dyspnoea is a prominent feature in substantial amount of paraquat due to acute
respiratory distress syndrome (ARDS). In less severe cases, the onset of dyspnoea is
due to pulmonary fibrosis
14. CLINICAL FEATURES
• Inhalation : Epistaxis and sore throat.
• Dermal exposures : Especially in concentrated formulations, has a strong irritant
action on various types of epithelia. It will cause erythema, blistering, irritation
and ulceration of the skin and eczematous dermatitis.
• Eye exposure : Severe inflammation of the cornea and conjunctiva and may lead
to ulceration of the conjunctiva and cornea
• Intravenous or intramuscular injection : may lead to systemic toxicity.
15. LABORATORY MONITORING
A) Full laboratory analysis, including liver and renal function tests, basic metabolic
panel, complete blood count, chest x-ray and urinalysis, should be performed on
anyone ingesting paraquat. Arterial blood gas analysis should be performed on
those with a late presentation or those with hypoxia.
B) Urine dithionite test(UDT) : Bedside testing can be performed using a 1%
aqueous sodium dithionite in 0.1 normal sodium hydroxide to form a stable blue
radical in the urine. If paraquat is present, the urine will appear blue compared
with the control urine.
C) Serum paraquat concentrations can be useful for prognosis
17. LABORATORY TESTING
• If paraquat concentration is more than 1 mg/ml,
the urine will appear blue and this finding alone
indicates a very poor prognosis
• Urine testing that detects paraquat concentrations
of 1 mg/mL or above, gas chromatography (1
microgram/mL) and radioimmunoassay (< 0.1
microgram/mL)
19. DECONTAMINATION
• Remove contaminated clothing and wash skin with soap and water. Irrigate
exposed eyes.
• Gastric lavage not to be done due to corrosive injury.
• Consider gastric aspiration or lavage in adults who have ingested a potentially
lethal dose within 1 hour of ingestion.
• Gastric lavage followed by administration of 1 g/kg of activated charcoal in 250
mL of magnesium citrate or saline in patients presenting within 24 hrs.
• Activated charcoal's absorbing capacity for paraquat is increases when it is
suspended in magnesium citrate and is maximal at pH 7.8 (Intestine pH~7.0).
Also as cathartic it’s frequently administered to increase gastrointestinal transit
and decrease absorption of ingested toxins.
Gaudreault et al. Efficacy of activated charcoal and magnesium citrate in the treatment of oral paraquat intoxication. Ann Emerg
Med. 1985
20. DECONTAMINATION
• One of the following adsorbent should be given patients with an ingestion within the last
24 hours
I. Activated charcoal - dose : adult - 50 to 100 g; child: 1 g/kg
II. Bentonite clay (7% solution) - dose : adult -100 to 150 g; child less than 12 years of
age: : 2 g/kg
III.Fuller's earth (30% solution) – dose : adult -100 to 150 g; child less than 12 years of
age: 2 g/kg
IBM Micromedex
22. HEMOPERFUSION
• The first and the earliest modality of treatment of removal of paraquat. Ideally, it
should be started within 4 hours of exposure or ingestion. As early
hemoperfusion may reduce mortality.
• Two 8 hours courses of activated charcoal hemoperfusion within 24 hrs of
paraquat ingestion
• If the patient develops AKI, then standard indications for hemodialysis are
applicable but it is always useful to start hemofiltration at the earliest to avoid
subsequent development of acute kidney injury due to paraquat.
23. IMMUNOSUPPRESSIVE THERAPY
• Cyclophosphamide, methylprednisolone and dexamethasone should be
administered to treat the acute inflammatory process associated with paraquat
poisoning that can lead to lung injury and death
• To a patient at risk of moderate or severe pulmonary toxicity and those with
symptoms consistent with moderate to severe toxicity
• Several small studies suggest that it can reduce the mortality rate of severe
paraquat poisoning
24. PULSE THERAPY
• After hemoperfusion, IV cyclophosphamide 15 mg/kg/day in 200 mL D5NS infused over
2 hrs for 2 consecutive days and 1 g methylprednisolone in 200 mL D5NS infused over 2
hrs daily for 3 consecutive days.
• After the initial pulse therapy, administer dexamethasone 5 mg IV every 6 hrs until PaO2
is 80 mmHg (11.5 kPa) or greater.
• If PaO2 is less than 60 mmHg (8.64 kPa), repeat IV methylprednisolone 1 g in 200 mL
D5NS infused over 2 hours daily for 3 consecutive days.
• If WBC is greater than 3000/m3 and it has been 2 weeks since the initial pulse of
cyclophosphamide, repeat IV infusion of cyclophosphamide 15 mg/kg in 200 mL D5NS
infused over 2 hrs as a single dose.
• Then continue IV dexamethasone 5 mg every 6 hrs until PaO2 is 80 mmHg or greater.
Then reduce dexamethasone dose gradually.
IBM Micromedex
25. ALTERNATIVE THERAPIES
• High-dose therapy includes the same initial treatment (activated charcoal and
hemoperfusion) as pulse therapy along with high-dose cyclophosphamide (5
mg/kg/d) and dexamethasone 24 mg/d for 14 days.
• Another method includes early decontamination and 15 mg/kg of
cyclophosphamide in D5NS in 200 mL infused over 2 hrs for 2 days and
methylprednisolone 1 g in 200 mL D5NS IV infused over 4 hrs and repeated for
3 consecutive days. Mesna (15 mg/kg) was also administered over 4 days to
avoid side effects to cyclophosphamide.
IBM Micromedex
26.
27. OTHER THERAPIES
Antioxidants
• High-dose long-term antioxidants could potentially be a critical component
improving the survival rate in severe paraquat poisoning
(1) N-Acetylcysteine is renally protective with a low adverse reaction profile
• An infusion of N-acetylcysteine at 150 mg/kg for 1 hour, 50 mg/kg over the next
4 hours, then 100 mg/kg daily for 4 days
(2) Vitamin C 100 mg 4-hourly for 14 days
(3) Vitamin E 50 mg daily for 7 days
Lalloo et. al., 2008
28. SUPPORTIVE CARE
• ANTIDOTE - NO antidote available
• NAUSEA AND VOMITING - Antiemetics should be provided liberally. Stress ulcer
prophylaxis should be provided
• HYPOTENSION - Treat hypotension with isotonic fluid resuscitation, followed by addition of
vasopressors
• ACUTE TUBULAR NECROSIS - Adequate fluid resuscitation is key to limiting secondary
renal injury. Hemodialysis for oliguric renal failure is occasionally necessary as a
temporizing measure until renal function improves
• OXYGEN THERAPY - Should be withheld until the PaO2 is below 50 mmHg, because
supplemental O2 may lead to increased production of oxygen free radicals and increased
pulmonary toxicity
• Patients with QT prolongation, monitor serum electrolytes including potassium, calcium
and magnesium; correct any abnormalities.
Paraquat is available in commercial 20% concentrate form, as 2.5% granules, and 0.2% aerosol.
Paraquat is available in commercial 20% concentrate form, as 2.5% granules, and 0.2% aerosol.
*Paraquat is stopped (distribution, sale and use) in the State of Kerala since 2011, as per the Kerala Government order dated 07.05.2011
SOD, superoxide dismutase; CAT, catalase; Gred, glutathione reductase; Gpx, glutathione peroxidase; FR, Fenton reaction; HWR, Haber-Weiss reaction.
1–8: potential sites of action by available treatment options. 1: activated charcoal and Fuller’s earth; 2: dialysis; 3, 4, 6 and 8: salicylates; 5 and 8: N-acetylcysteine; 7 (P-glycoprotein induction): dexamethasone; 4: immunosuppression
Diluted paraquat is unlikely to irritate skin unless clothing soaked with spray is worn for prolonged periods.
Efficacy of activated charcoal declines rapidly with time since ingestion but there may be some potential benefit from later use, especially following ingestion of highly toxic substances.