This document discusses various types of drug and chemical poisonings. It covers the classification, incidence, drugs commonly involved, clinical presentations, investigations, management principles, and specific treatments for paracetamol, salicylates, and NSAIDs. The key points are: accidental poisoning is most common in children under 5, deliberate self-poisoning is common in adults over 15, and management involves supportive care, preventing further absorption, enhancing elimination, and specific antidotes/treatments depending on the toxin. N-acetylcysteine is the antidote for paracetamol overdose, sodium bicarbonate and hemodialysis are used to treat salicylate poisoning, and activated charcoal and
This document discusses poisoning classifications and treatments. It provides statistics on poisoning incidence and the most common substances involved. Key points include:
- Accidental poisoning is most common in children under 5, while deliberate self-poisoning is common in adults over 15.
- Paracetamol and aspirin are among the most frequent causes of poisoning.
- Treatment focuses on preventing further drug absorption, increasing elimination, and using specific antidotes like n-acetylcysteine for paracetamol overdose.
- Poisoning management involves supportive care, monitoring, gastric decontamination methods, and increasing drug metabolism or excretion depending on the substance ingested.
This document discusses the assessment and management of drug overdoses. It covers evaluating the patient's history, performing examinations and investigations. Key poisoning agents discussed include paracetamol, aspirin, tricyclic antidepressants, benzodiazepines, opiates, and others. Management involves supportive care, decontamination, specific antidotes, and monitoring for complications depending on the toxin ingested.
1. Paracetamol (acetaminophen) toxicity results from formation of a reactive metabolite which causes liver and occasionally renal failure. Acetylcysteine treatment within 8 hours of overdose is highly effective at replenishing glutathione reserves and preventing toxicity.
2. Salicylate poisoning causes respiratory alkalosis, metabolic acidosis, and organ dysfunction. Treatment involves correcting dehydration and acidosis with sodium bicarbonate, and hemodialysis for severe or refractory cases.
3. Tricyclic antidepressant overdose can cause life-threatening arrhythmias, hypotension, and seizures due to sodium channel blockade and anticholinergic effects. Treatment involves
This document discusses poisoning classifications and treatments. It provides statistics on poisoning incidence and the most common substances involved. Key points include:
- Accidental poisoning is most common in children under 5, while deliberate self-poisoning is common in adults over 15.
- Paracetamol and aspirin are among the most frequent causes of poisoning.
- Treatment focuses on preventing further drug absorption, increasing elimination, and using specific antidotes like n-acetylcysteine for paracetamol overdose.
- Poisoning management involves supportive care, monitoring, gastric decontamination methods, and increasing drug metabolism or excretion depending on the substance ingested.
This document discusses drug poisoning and includes definitions, types of common drugs that cause poisoning like analgesics, barbiturates and benzodiazepines, narcotics. It covers topics like evaluation, management, and a case scenario of a child ingesting unknown tablets. Motive, symptoms, signs, and treatment approaches for an accidental poisoning are outlined. Drug abuse and addiction are also touched on.
1. Paracetamol toxicity results from formation of a reactive metabolite that binds to cellular proteins, causing cell death and hepatic or renal failure. Acetylcysteine replenishes glutathione stores and is highly effective if given within 8 hours of overdose.
2. Salicylate poisoning causes respiratory alkalosis, metabolic acidosis, and organ damage. Treatment involves correcting dehydration and acidosis with sodium bicarbonate. Hemodialysis is effective for removing salicylates from the body.
3. Tricyclic antidepressant overdose can cause arrhythmias, hypotension, and seizures due to sodium channel blockade. Treatment involves sodium bicarbonate to correct
A 17-year-old man was brought to the hospital drunk, depressed, and having taken pills and alcohol after failing exams. He was treated with IV fluids, monitored until sober, and discharged home with psychiatric support. Three days later he returned with jaundice, leading to the diagnosis of paracetamol poisoning.
This document discusses various cholinomimetic drugs that act directly or indirectly on acetylcholine receptors. Direct acting drugs such as carbachol, methacholine and pilocarpine mimic acetylcholine, while indirect acting drugs like neostigmine and pyridostigmine inhibit the acetylcholinesterase enzyme. The document also summarizes the pharmacological effects, therapeutic uses, and side effects of specific cholinomimetic drugs including atropine, homatropine, propantheline, neostigmine and pilocarpine.
This document discusses poisoning classifications and treatments. It provides statistics on poisoning incidence and the most common substances involved. Key points include:
- Accidental poisoning is most common in children under 5, while deliberate self-poisoning is common in adults over 15.
- Paracetamol and aspirin are among the most frequent causes of poisoning.
- Treatment focuses on preventing further drug absorption, increasing elimination, and using specific antidotes like n-acetylcysteine for paracetamol overdose.
- Poisoning management involves supportive care, monitoring, gastric decontamination methods, and increasing drug metabolism or excretion depending on the substance ingested.
This document discusses the assessment and management of drug overdoses. It covers evaluating the patient's history, performing examinations and investigations. Key poisoning agents discussed include paracetamol, aspirin, tricyclic antidepressants, benzodiazepines, opiates, and others. Management involves supportive care, decontamination, specific antidotes, and monitoring for complications depending on the toxin ingested.
1. Paracetamol (acetaminophen) toxicity results from formation of a reactive metabolite which causes liver and occasionally renal failure. Acetylcysteine treatment within 8 hours of overdose is highly effective at replenishing glutathione reserves and preventing toxicity.
2. Salicylate poisoning causes respiratory alkalosis, metabolic acidosis, and organ dysfunction. Treatment involves correcting dehydration and acidosis with sodium bicarbonate, and hemodialysis for severe or refractory cases.
3. Tricyclic antidepressant overdose can cause life-threatening arrhythmias, hypotension, and seizures due to sodium channel blockade and anticholinergic effects. Treatment involves
This document discusses poisoning classifications and treatments. It provides statistics on poisoning incidence and the most common substances involved. Key points include:
- Accidental poisoning is most common in children under 5, while deliberate self-poisoning is common in adults over 15.
- Paracetamol and aspirin are among the most frequent causes of poisoning.
- Treatment focuses on preventing further drug absorption, increasing elimination, and using specific antidotes like n-acetylcysteine for paracetamol overdose.
- Poisoning management involves supportive care, monitoring, gastric decontamination methods, and increasing drug metabolism or excretion depending on the substance ingested.
This document discusses drug poisoning and includes definitions, types of common drugs that cause poisoning like analgesics, barbiturates and benzodiazepines, narcotics. It covers topics like evaluation, management, and a case scenario of a child ingesting unknown tablets. Motive, symptoms, signs, and treatment approaches for an accidental poisoning are outlined. Drug abuse and addiction are also touched on.
1. Paracetamol toxicity results from formation of a reactive metabolite that binds to cellular proteins, causing cell death and hepatic or renal failure. Acetylcysteine replenishes glutathione stores and is highly effective if given within 8 hours of overdose.
2. Salicylate poisoning causes respiratory alkalosis, metabolic acidosis, and organ damage. Treatment involves correcting dehydration and acidosis with sodium bicarbonate. Hemodialysis is effective for removing salicylates from the body.
3. Tricyclic antidepressant overdose can cause arrhythmias, hypotension, and seizures due to sodium channel blockade. Treatment involves sodium bicarbonate to correct
A 17-year-old man was brought to the hospital drunk, depressed, and having taken pills and alcohol after failing exams. He was treated with IV fluids, monitored until sober, and discharged home with psychiatric support. Three days later he returned with jaundice, leading to the diagnosis of paracetamol poisoning.
This document discusses various cholinomimetic drugs that act directly or indirectly on acetylcholine receptors. Direct acting drugs such as carbachol, methacholine and pilocarpine mimic acetylcholine, while indirect acting drugs like neostigmine and pyridostigmine inhibit the acetylcholinesterase enzyme. The document also summarizes the pharmacological effects, therapeutic uses, and side effects of specific cholinomimetic drugs including atropine, homatropine, propantheline, neostigmine and pilocarpine.
General approach to treating poisoning cases with life threatening problemsSam George
The document provides guidelines for treating poisoning cases, including following advanced life support protocols, administering antidotes and fluids as needed, treating arrhythmias, seizures, hypoglycemia, and other symptoms, as well as avoiding potentially cardiotoxic drugs. It recommends aggressive cooling for hyperthermia and thiamine for those at risk of Wernicke's encephalopathy. The treatment aims to reverse toxins, support vital systems, correct electrolyte and acid-base imbalances, and use antidotes, pacing, or antibodies as indicated based on the poison involved.
This document provides guidance on the evaluation and management of poisoning and overdose. It discusses evaluating asymptomatic vs symptomatic patients, prioritizing treatment of life-threatening complications, and managing common complications including coma, hypothermia, hypotension, hypertension, arrhythmias, seizures, and hyperthermia. It also reviews decontamination methods, antidotes, and other treatments such as activated charcoal, whole bowel irrigation, and hemodialysis.
This document provides an overview of different classes of diuretic drugs used to treat conditions like hypertension and congestive heart failure. It discusses the pharmacology, mechanisms of action, uses, side effects and nursing considerations for each class including: loop diuretics like furosemide, thiazide diuretics like hydrochlorothiazide, potassium-sparing diuretics like spironolactone, osmotic diuretics like mannitol, and carbonic anhydrase inhibitors like acetazolamide. It also covers how to apply the nursing process when caring for patients taking diuretics by assessing, diagnosing, planning, implementing and evaluating care.
1) The document provides information on various medical conditions that may be covered in a local board exam, including abdominal aortic aneurysm, acne vulgaris, acromegaly, acute gastroenteritis, AIDS, Addison's disease, anemia, anaphylaxis, aphasia, arrhythmias, angina pectoris, appendicitis, arthritis, asthma, and autonomic dysreflexia.
2) For each condition, the summary includes information on the main problem, initial manifestations, relevant diagnostic data, priority nursing diagnoses, and key nursing interventions.
3) The document serves as a study guide for nurses preparing to take a local board exam, providing essential details on
This document provides an overview of salicylate (aspirin) overdose or toxicity. It discusses the therapeutic uses and inherent toxicity of salicylates. It covers the pathophysiology, diagnosis, clinical presentation, and treatment of both acute and chronic salicylate poisoning. Symptoms can involve multiple organ systems. Treatment focuses on decontamination, fluid resuscitation, urinary alkalinization, and hemodialysis in severe cases. Prognosis is generally good for acute overdoses but worse for chronic poisoning.
The document provides an overview of various drugs and medical topics. It discusses drugs used for deaddiction like opioids, cannabis, and alcohol. It also covers drugs used in CPR and emergencies like adrenaline and atropine. Additionally, it summarizes various vitamins and minerals, their functions, sources, and deficiency effects. The document also briefly outlines immunosuppressants, antidotes, antivenoms, and vaccines/sera.
SEMS 2014: Updates in paeds toxicology Rahul Goswami
1) A 6-year-old girl accidentally ingested her grandfather's heart medication, which were found to be missing from the bottle. 2) At the emergency department, her vitals showed bradycardia and hypotension. An ECG found sinus bradycardia and her potassium was low. 3) The symptoms and labs are consistent with calcium channel blocker poisoning from the grandfather's medication. She will require intensive care monitoring and treatment such as inotropes, calcium, high-dose insulin therapy, or intralipid infusion.
This document provides an overview of pediatric poisoning for emergency medical providers. It reviews the initial assessment and management of pediatric ingestions, focusing on activated charcoal, whole bowel irrigation, and enhancing excretion to prevent absorption. Common ingestions like acetaminophen, alcohols, and antihistamines are discussed. The document also addresses caustic ingestions and emphasizes supportive care and avoiding interventions that could worsen injury.
This document discusses drugs that modify blood coagulation. It begins by describing two case scenarios involving bleeding during tooth extraction. It then outlines the key learning objectives for medical students regarding drugs that achieve and prevent coagulation. The rest of the document provides details on the mechanisms, pharmacokinetics, uses, and adverse effects of various anticoagulant and coagulant drugs, including heparin, warfarin, vitamin K, fibrinolytics, antiplatelet drugs like aspirin, and dipyridamole.
1) Salicylate poisoning can occur from overdose of aspirin and other salicylate-containing medications and is a potentially serious toxicity.
2) Symptoms range from mild nausea and vomiting to seizures, coma and death depending on the dose ingested.
3) Treatment involves gastric decontamination, fluid resuscitation, urinary alkalinization to enhance elimination of salicylates, and hemodialysis for severe or refractory cases.
Management protocol for theophylline intoxicationKerolus Shehata
This document provides guidelines for managing intoxication from theophylline, a bronchodilator. Key points include:
1. Theophylline has a narrow therapeutic index and toxicity can occur even at low doses, presenting with nausea, vomiting, tachycardia, seizures and coma.
2. Initial treatment focuses on stabilizing vital signs and eliminating the drug through induction of vomiting, gastric lavage or activated charcoal. Hemodialysis may be needed for severe cases.
3. Patients with seizures, coma, cardiac issues or high initial blood levels require ICU admission for close monitoring and management of arrhythmias or acidosis. Serial blood levels guide further treatment.
1. The initial management of all poisoned patients should be similar and focus on stabilization, including maintaining the ABCDEs. Airway patency, breathing, circulation, disability, and exposure should be assessed and treated.
2. Definitive care involves identifying the toxic agent through history, physical exam including vital signs and toxic syndromes, and initial investigations like toxicology screening and basic labs.
3. Management then focuses on decreasing further absorption, administering antidotes if available, enhancing elimination, and treating complications through supportive care.
Drugs affecting the endocrine system presentationAamir Hussain
This document discusses anti-thyroid and parathyroid drugs. It provides information on drug classes that affect the thyroid and parathyroid glands, including thioamides, anion inhibitors, beta blockers, calcitonin, etidronate, and calcifediol. It also outlines nursing assessments, diagnoses, and care plans related to administering these medications and monitoring for effectiveness and adverse reactions.
This document discusses drug therapy considerations in the elderly population. Key points include:
- Physiological changes that occur with aging impact drug absorption, distribution, metabolism and excretion requiring dosage adjustments.
- Polypharmacy is common due to multiple diseases and increases risk of drug interactions.
- Adverse drug reactions are more frequent in the elderly. Drugs should be started at low doses and titrated carefully.
- Drug selection should consider potential side effects, dosage forms that are easy to take, and affordability. Close monitoring for side effects is important.
1. Diabetic ketoacidosis is caused by insulin deficiency and presents with hyperglycemia and metabolic acidosis. Symptoms include confusion, abdominal pain, and fruity breath odor. Treatment involves fluid resuscitation, insulin therapy, and bicarbonate for severe acidosis.
2. Hyperosmolar hyperglycemic state is characterized by extreme hyperglycemia without significant ketoacidosis. It presents with dehydration, confusion, and hypernatremia. Management consists of aggressive fluid replacement and insulin therapy to lower blood glucose levels.
3. Hypoglycemia can cause neurological symptoms like confusion and seizures. Treatment involves oral glucose for conscious patients or IV dextrose for
Allopurinol is a xanthine oxidase inhibitor used to treat gout and hyperuricemia. It works by decreasing uric acid production. Common brands include Zyloric, Allgoric, and Ciploric. Allopurinol is generally well tolerated but can cause rare severe hypersensitivity reactions. It interacts with several other drugs like azathioprine and increases risk of toxicity. Patients on allopurinol require monitoring of uric acid levels and kidney and liver function.
The main focus of this presentation is to discuss all the drugs used nowadays in clinical practice to treat/ manage bronchial asthma. Along with the mechanism of action, use and adverse effects of anti-asthma drugs, we have given a highlight of the pathophysiology of asthma and how the drugs individually act at individual set point(s) to bring the clinical outcome.
This document discusses various diagnostic procedures and dynamic tests used in chemical pathology, focusing on tests for disorders of growth hormone, cortisol, and aldosterone metabolism. It provides details on insulin hypoglycemic tests, glucose stimulation tests, clonidine stimulation tests, and exercise stimulation tests. These tests measure hormonal responses to stimuli like insulin-induced hypoglycemia, glucagon administration, clonidine administration, or exercise to evaluate the functioning of the hypothalamic-pituitary-end organ axes. The document outlines the procedures, normal responses, and interpretations for each type of dynamic test.
Aspirin is a medicine that relieves pain and reduces fever. It was first created in 1899 by a German chemist to treat his father's arthritis. Aspirin is quickly absorbed and provides rapid and long-lasting pain relief. It can be used to treat minor pains like headaches and toothaches, as well as more serious conditions like heart attacks. While it has many uses, aspirin also carries risks like Reye's syndrome in children and upset stomach or bleeding in some adults and animals. It works by reducing fever and pain but should only be used under a doctor or veterinarian's guidance.
This document summarizes the mechanisms of gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses how NSAIDs inhibit cyclooxygenase enzymes, which protect the gastrointestinal mucosa. This inhibition impairs the production of prostaglandins, compromising gastrointestinal integrity and increasing the risk of ulcers and complications. The document outlines risk factors for NSAID-induced toxicity and recommendations for prevention and management.
General approach to treating poisoning cases with life threatening problemsSam George
The document provides guidelines for treating poisoning cases, including following advanced life support protocols, administering antidotes and fluids as needed, treating arrhythmias, seizures, hypoglycemia, and other symptoms, as well as avoiding potentially cardiotoxic drugs. It recommends aggressive cooling for hyperthermia and thiamine for those at risk of Wernicke's encephalopathy. The treatment aims to reverse toxins, support vital systems, correct electrolyte and acid-base imbalances, and use antidotes, pacing, or antibodies as indicated based on the poison involved.
This document provides guidance on the evaluation and management of poisoning and overdose. It discusses evaluating asymptomatic vs symptomatic patients, prioritizing treatment of life-threatening complications, and managing common complications including coma, hypothermia, hypotension, hypertension, arrhythmias, seizures, and hyperthermia. It also reviews decontamination methods, antidotes, and other treatments such as activated charcoal, whole bowel irrigation, and hemodialysis.
This document provides an overview of different classes of diuretic drugs used to treat conditions like hypertension and congestive heart failure. It discusses the pharmacology, mechanisms of action, uses, side effects and nursing considerations for each class including: loop diuretics like furosemide, thiazide diuretics like hydrochlorothiazide, potassium-sparing diuretics like spironolactone, osmotic diuretics like mannitol, and carbonic anhydrase inhibitors like acetazolamide. It also covers how to apply the nursing process when caring for patients taking diuretics by assessing, diagnosing, planning, implementing and evaluating care.
1) The document provides information on various medical conditions that may be covered in a local board exam, including abdominal aortic aneurysm, acne vulgaris, acromegaly, acute gastroenteritis, AIDS, Addison's disease, anemia, anaphylaxis, aphasia, arrhythmias, angina pectoris, appendicitis, arthritis, asthma, and autonomic dysreflexia.
2) For each condition, the summary includes information on the main problem, initial manifestations, relevant diagnostic data, priority nursing diagnoses, and key nursing interventions.
3) The document serves as a study guide for nurses preparing to take a local board exam, providing essential details on
This document provides an overview of salicylate (aspirin) overdose or toxicity. It discusses the therapeutic uses and inherent toxicity of salicylates. It covers the pathophysiology, diagnosis, clinical presentation, and treatment of both acute and chronic salicylate poisoning. Symptoms can involve multiple organ systems. Treatment focuses on decontamination, fluid resuscitation, urinary alkalinization, and hemodialysis in severe cases. Prognosis is generally good for acute overdoses but worse for chronic poisoning.
The document provides an overview of various drugs and medical topics. It discusses drugs used for deaddiction like opioids, cannabis, and alcohol. It also covers drugs used in CPR and emergencies like adrenaline and atropine. Additionally, it summarizes various vitamins and minerals, their functions, sources, and deficiency effects. The document also briefly outlines immunosuppressants, antidotes, antivenoms, and vaccines/sera.
SEMS 2014: Updates in paeds toxicology Rahul Goswami
1) A 6-year-old girl accidentally ingested her grandfather's heart medication, which were found to be missing from the bottle. 2) At the emergency department, her vitals showed bradycardia and hypotension. An ECG found sinus bradycardia and her potassium was low. 3) The symptoms and labs are consistent with calcium channel blocker poisoning from the grandfather's medication. She will require intensive care monitoring and treatment such as inotropes, calcium, high-dose insulin therapy, or intralipid infusion.
This document provides an overview of pediatric poisoning for emergency medical providers. It reviews the initial assessment and management of pediatric ingestions, focusing on activated charcoal, whole bowel irrigation, and enhancing excretion to prevent absorption. Common ingestions like acetaminophen, alcohols, and antihistamines are discussed. The document also addresses caustic ingestions and emphasizes supportive care and avoiding interventions that could worsen injury.
This document discusses drugs that modify blood coagulation. It begins by describing two case scenarios involving bleeding during tooth extraction. It then outlines the key learning objectives for medical students regarding drugs that achieve and prevent coagulation. The rest of the document provides details on the mechanisms, pharmacokinetics, uses, and adverse effects of various anticoagulant and coagulant drugs, including heparin, warfarin, vitamin K, fibrinolytics, antiplatelet drugs like aspirin, and dipyridamole.
1) Salicylate poisoning can occur from overdose of aspirin and other salicylate-containing medications and is a potentially serious toxicity.
2) Symptoms range from mild nausea and vomiting to seizures, coma and death depending on the dose ingested.
3) Treatment involves gastric decontamination, fluid resuscitation, urinary alkalinization to enhance elimination of salicylates, and hemodialysis for severe or refractory cases.
Management protocol for theophylline intoxicationKerolus Shehata
This document provides guidelines for managing intoxication from theophylline, a bronchodilator. Key points include:
1. Theophylline has a narrow therapeutic index and toxicity can occur even at low doses, presenting with nausea, vomiting, tachycardia, seizures and coma.
2. Initial treatment focuses on stabilizing vital signs and eliminating the drug through induction of vomiting, gastric lavage or activated charcoal. Hemodialysis may be needed for severe cases.
3. Patients with seizures, coma, cardiac issues or high initial blood levels require ICU admission for close monitoring and management of arrhythmias or acidosis. Serial blood levels guide further treatment.
1. The initial management of all poisoned patients should be similar and focus on stabilization, including maintaining the ABCDEs. Airway patency, breathing, circulation, disability, and exposure should be assessed and treated.
2. Definitive care involves identifying the toxic agent through history, physical exam including vital signs and toxic syndromes, and initial investigations like toxicology screening and basic labs.
3. Management then focuses on decreasing further absorption, administering antidotes if available, enhancing elimination, and treating complications through supportive care.
Drugs affecting the endocrine system presentationAamir Hussain
This document discusses anti-thyroid and parathyroid drugs. It provides information on drug classes that affect the thyroid and parathyroid glands, including thioamides, anion inhibitors, beta blockers, calcitonin, etidronate, and calcifediol. It also outlines nursing assessments, diagnoses, and care plans related to administering these medications and monitoring for effectiveness and adverse reactions.
This document discusses drug therapy considerations in the elderly population. Key points include:
- Physiological changes that occur with aging impact drug absorption, distribution, metabolism and excretion requiring dosage adjustments.
- Polypharmacy is common due to multiple diseases and increases risk of drug interactions.
- Adverse drug reactions are more frequent in the elderly. Drugs should be started at low doses and titrated carefully.
- Drug selection should consider potential side effects, dosage forms that are easy to take, and affordability. Close monitoring for side effects is important.
1. Diabetic ketoacidosis is caused by insulin deficiency and presents with hyperglycemia and metabolic acidosis. Symptoms include confusion, abdominal pain, and fruity breath odor. Treatment involves fluid resuscitation, insulin therapy, and bicarbonate for severe acidosis.
2. Hyperosmolar hyperglycemic state is characterized by extreme hyperglycemia without significant ketoacidosis. It presents with dehydration, confusion, and hypernatremia. Management consists of aggressive fluid replacement and insulin therapy to lower blood glucose levels.
3. Hypoglycemia can cause neurological symptoms like confusion and seizures. Treatment involves oral glucose for conscious patients or IV dextrose for
Allopurinol is a xanthine oxidase inhibitor used to treat gout and hyperuricemia. It works by decreasing uric acid production. Common brands include Zyloric, Allgoric, and Ciploric. Allopurinol is generally well tolerated but can cause rare severe hypersensitivity reactions. It interacts with several other drugs like azathioprine and increases risk of toxicity. Patients on allopurinol require monitoring of uric acid levels and kidney and liver function.
The main focus of this presentation is to discuss all the drugs used nowadays in clinical practice to treat/ manage bronchial asthma. Along with the mechanism of action, use and adverse effects of anti-asthma drugs, we have given a highlight of the pathophysiology of asthma and how the drugs individually act at individual set point(s) to bring the clinical outcome.
This document discusses various diagnostic procedures and dynamic tests used in chemical pathology, focusing on tests for disorders of growth hormone, cortisol, and aldosterone metabolism. It provides details on insulin hypoglycemic tests, glucose stimulation tests, clonidine stimulation tests, and exercise stimulation tests. These tests measure hormonal responses to stimuli like insulin-induced hypoglycemia, glucagon administration, clonidine administration, or exercise to evaluate the functioning of the hypothalamic-pituitary-end organ axes. The document outlines the procedures, normal responses, and interpretations for each type of dynamic test.
Aspirin is a medicine that relieves pain and reduces fever. It was first created in 1899 by a German chemist to treat his father's arthritis. Aspirin is quickly absorbed and provides rapid and long-lasting pain relief. It can be used to treat minor pains like headaches and toothaches, as well as more serious conditions like heart attacks. While it has many uses, aspirin also carries risks like Reye's syndrome in children and upset stomach or bleeding in some adults and animals. It works by reducing fever and pain but should only be used under a doctor or veterinarian's guidance.
This document summarizes the mechanisms of gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses how NSAIDs inhibit cyclooxygenase enzymes, which protect the gastrointestinal mucosa. This inhibition impairs the production of prostaglandins, compromising gastrointestinal integrity and increasing the risk of ulcers and complications. The document outlines risk factors for NSAID-induced toxicity and recommendations for prevention and management.
Presentation by neha jain on aspirin induced alterations on liver and kidneyneha jain
The document presents a study that examined the effects of aspirin administration on the liver, kidney, and reproductive system of female albino rats. Various parameters were measured including organ weights, hematological factors, enzyme levels, histopathology, and estrus cycle. The results showed that aspirin induced toxicity in the liver and kidney and caused morphological changes in the ovaries, oviduct, and uterus along with effects on the estrus cycle.
presentation is based on mainly the chemistry of aspirin,A little bit introduction about nsaid is also here.The uses,doses and side effects are also in these presentation.
Aspirin is the common name for acetylsalicylic acid, which is used as a non-steroidal anti-inflammatory drug (NSAID) to relieve pain, reduce fever, and minimize swelling. It is also used as an anti-platelet drug to prevent blood clots and as a preventative measure for heart conditions. Aspirin is available over the counter and commonly used for headaches, colds, flu, and preventative heart care, though it can have gastrointestinal side effects.
The document provides an overview of antiplatelet agents, including their mechanisms of action, pharmacology, and places in therapy. It reviews how hemostasis involves platelet plug formation and coagulation, and how different medications can affect this process. The major classes of antiplatelet agents discussed are aspirin, P2Y12 receptor antagonists like clopidogrel and ticagrelor, glycoprotein IIb/IIIa inhibitors like abciximab, cyclic AMP inhibitors like dipyridamole, and thrombin receptor antagonists like vorapaxar. Each drug's mechanism of action, pharmacokinetics, indications, and safety considerations are outlined.
Acetylsalicylic acid, also known as aspirin, is a common analgesic, antipyretic, and anti-inflammatory drug. Aspirin was first isolated in 1897 by Felix Hoffmann working for Bayer. It is synthesized from salicylic acid and acetic anhydride. Aspirin works by inhibiting prostaglandin production. It has a long history of medicinal use and is effective for pain, fever reduction, and reducing heart attack risk. Common side effects include gastrointestinal irritation.
Aspirin toxicity remains an important clinical problem due to aspirin's widespread availability and use. Aspirin is rapidly absorbed in the stomach and metabolized in the liver. Toxicity can cause a wide range of symptoms affecting multiple organ systems. Diagnosis is based on history of ingestion and characteristic laboratory abnormalities. Management involves gastric decontamination, fluid replacement, urine alkalinization, and hemodialysis in severe cases.
Aspirin is the common name for acetylsalicylic acid, a medicine that relieves pain and reduces fever. It was first used in Europe in 1899 when a German chemist named Felix Hoffman developed it as a treatment for his father's arthritis. Aspirin works by blocking prostaglandins, which are chemicals that cause pain and fever in the body. It is produced through a process that involves weighing, mixing, and compressing its active ingredients along with fillers and lubricants into tablet form before packaging. While aspirin is still commonly used to treat minor pains, its popularity has declined somewhat with the release of alternatives like paracetamol and ibuprofen.
This document provides an overview of various drugs that affect the nervous system, organized by drug class. It discusses analgesics like opioids and NSAIDs; anesthetics like general gases and local anesthetics; anti-anxiety drugs like benzodiazepines and barbiturates; anti-seizure medications; CNS stimulants; antipsychotics; antidepressants; Parkinson's disease medications; and drugs that affect the autonomic nervous system, including cholinergic and anticholinergic drugs. Mechanisms of action, effects, and side effects are described for many of these drug classes and examples.
Aspirin is synthesized by reacting salicylic acid with acetic anhydride in the presence of sulfuric acid. It has the molecular formula C9H8O4 and is used to treat fever, pain, and inflammatory conditions like arthritis. Aspirin works by inhibiting prostaglandins and prevents blood clots, reducing the risk of heart attack and stroke. Regular aspirin use may also help prevent certain cancers. It decomposes in the presence of moisture but is stable when dry.
The document provides information on the approach to poisoning including triage, resuscitation, clinical assessment, investigations, management, and specific treatments. Some key points:
1) Poisoning is a major cause of death in young adults and hospital admissions, with most deaths occurring before medical help. Mortality is less than 1% for those admitted.
2) Intentional overdose of prescription drugs and accidental poisoning, especially in children and elders, are common causes.
3) Initial steps include identifying the poison, preventing reattempts, decontamination, resuscitation, monitoring, and giving antidotes.
4) Activated charcoal within 1 hour and other decontamination methods may help
This document summarizes information on various types of poisonings and drug overdoses. It discusses accidental, deliberate, and non-accidental poisonings. It then provides details on the incidence, common drugs involved, and general management approach for poisonings. The document also provides more in-depth information on the presentation, evaluation, and specific treatment approaches for paracetamol/acetaminophen, salicylate/aspirin, NSAID, and anticholinergic poisonings.
This document summarizes common types of drug poisonings, including accidental, deliberate self-poisoning, and homicide. It discusses incidence, common drugs involved like paracetamol and aspirin, clinical features, investigations, and general management principles like preventing absorption, enhancing elimination, and specific pharmacological interventions. For some specific drugs, it provides details on mechanisms of toxicity, clinical presentations, and treatment approaches.
This document provides an overview of poisoning, including its causes, approaches to triage and resuscitation of poisoned patients, clinical assessment of poisoning, investigations, management, and antidotes. Some key points include:
- Poisoning is a major cause of hospital admissions and deaths in young adults, with most fatalities occurring before medical help can be reached. Intentional overdose is most common.
- Initial focus is on stabilization of vital signs, identifying toxins, preventing reattempts, and decontamination if needed. Antidotes may be given.
- Assessment includes history, exam looking for toxic effects, and investigations like ECG, blood tests and toxicology screens.
- Management involves supportive
This document provides guidance on the general approach to triage, resuscitation, clinical assessment, investigations, and management of poisoning patients. It notes that poisoning is a major cause of death in young adults and hospital admissions. The most frequent causes are intentional overdose and accidental poisoning in children and elderly. It outlines steps for initial stabilization including vital signs, identifying toxins, decontamination, resuscitation, and use of antidotes when available. Long-term management focuses on supportive care, treatment of complications, and psychiatric evaluation for intentional overdoses.
This document summarizes organophosphorous (OP) poisoning. OP compounds are commonly used as agricultural insecticides and were historically developed as chemical warfare agents. They work by inhibiting the enzyme acetylcholinesterase, leading to excess acetylcholine in the body. Clinical effects range from acute cholinergic crisis to intermediate muscle weakness to delayed neuropathy. Diagnosis is based on history of exposure and clinical features. Treatment involves atropine to control muscarinic effects, pralidoxime to reactivate acetylcholinesterase, benzodiazepines for seizures, and supportive care. Prognosis depends on prompt diagnosis and treatment to prevent respiratory failure, intermediate syndrome, or delayed neuropathy.
Organophosphorus (OP) poisoning is a major cause of morbidity and mortality in Nepal. OP compounds inhibit acetylcholinesterase, leading to accumulation of acetylcholine and overstimulation of nicotinic and muscarinic receptors. Common presentations include excessive sweating, salivation, vomiting, diarrhea, bronchospasm, bradycardia, hypotension. Treatment involves atropine to block muscarinic effects, pralidoxime to reactivate acetylcholinesterase, benzodiazepines for seizures, and supportive care. Prognosis depends on severity of cholinergic crisis, and intermediate syndrome occurring 1-4 days later can cause respiratory failure if not properly managed.
General management of poisoning involves stabilization, evaluation, gastrointestinal decontamination if recent, urinary alkalinization for some toxins, haemodialysis/haemoperfusion, lipid emulsion therapy, supportive care, and antidotes if available. Stabilization focuses on airway, breathing, circulation. Evaluation includes examination. Gastrointestinal decontamination includes activated charcoal orally or via tube for some toxins within 1 hour, or whole bowel irrigation for sustained release drugs. Urinary alkalinization enhances excretion of weak acids/bases. Haemodialysis/haemoperfusion effectively removes some toxins. Lipid emulsion therapy counters cardiac effects of some lipophilic drugs. Supportive care monitors until effects
Poisoning can result from overdose of drugs, ingestion of toxic substances, or exposure to household/industrial chemicals. All poisoning patients should be admitted to the hospital. Treatment involves identifying the poison, administering antidotes if available, removing/preventing absorption of the poison, accelerated elimination, supportive care, and monitoring for complications. Activated charcoal and gastric lavage can help remove ingested poisons from the gastrointestinal tract before absorption.
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This document provides an overview of poisoning in children, including common toxins, clinical presentations, management principles, and case examples. The main points are:
1. Common toxins in children include acetaminophen, iron, organophosphates, and hydrocarbons. Clinical presentations depend on the toxin but may include gastrointestinal, neurological, or respiratory symptoms.
2. Management follows the ABCs - airway, breathing, circulation - along with decontamination using activated charcoal or whole bowel irrigation. Specific antidotes are given when available.
3. Case examples demonstrate iron poisoning presenting with GI bleeding, organophosphate poisoning with cholinergic symptoms, and acetaminophen overdose
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4. Poisoning classifiation:
• Accidental: most common in children < 5 years, less common in
adults as occupational exposure.
• Deliberate self poisoning: common in adults > 15 ys
( parasuicide).
• Non accidental: deliberate poisoning of a child by one of
parents( manchausen by proxy).
• Misadventure: By medical staff or nurse, usually error in dose or
admintration.
• Homicide: rare.
5. Incidence:
• Relatively a common problem in the our ER.
• Young persons specially females.
• In UK:
• 15-20% of all emergency medical admissions.
• ~6,300 suicides /year
– 20% of deaths in young people
– Important way of committing suicide.
• ~140,000 attempted suicides (parasuicides)
– Most common 15-19 year old females
– Most common method is poisoning
• 50% paracetamol
6. Incidence:
• 30% involve > 1 drug.
• Involve alcohol in addition of the ingested drug in 60% males &
40% females.
• 60% ingest drugs prescribed for themselves or a relative.
• The mortality from drug poisoning is < 1% & should be < 2% in
severely ill patient by effective ICU.
7.
8. • Drugs play an important role in suicidal &accidental poisoning
• Common drugs used in poisoning include:
• Analgesics (salicylates) > sedatives & hypnotics (barbiturates) >
psychotherapeutics (tranquilizers) > CNS stimulants
&depressants (amphetamines)
• Narcotics - Lomotilt, an antidiarrhetic with a similar lethal dose
as morphine; due to CNS depression.
– Propoxyphene , similar effect as methadone
– Overdose treated with Naloxone.
9. Major drugs involved in poisoning:
• Paracetamol.
• Aspirin.
• Benzodiazepines.
• SSRIs.
• TADs.
• Antionvulsants.
• Other analgesics inculding NSAIDs.
10. Poisoing by substanes other than drugs:
• Petrolium distilates.
• Nature toxines as mushrooms.
• Industrial chemicals.
• Toiletries.
• Household products.
• Agrochemicals.
• Others.
11. General Comments
• Try &get as much history as possible including witnesses
• People truly wanting to commit suicide often lie
• Remember the ABCs:
– Airway Clear mouth & throat, gag reflex
– Breathing O2 saturation, ABGs
– Circulation Venous access, IV fluids if shocked
• Assess GCS
• Examination
12. History
• When, what, how much ?
• Why?
• Circumstances
• PMHx, Drug history
• Psychiatric history
• Assess mental status & capacity
13. Care with names: Generic vs Chemical name!
• Dolostop: paracetamol+dextropropoxiphen.
• Valium: diazepan.
• Fluout: paraetamol + diphenhydramine.
16. Management
• Supportive
– Correct hypoxia, hypotension, dehydration, hypo- hyperthermia,
and acidosis
– Control seizures
– If comatose consider; DON’T( Dextrose,O2,Naloxone,Thaimine).
• Monitor
– PR, BP, ECG, Oxygenation, GCS
• General
↓ Absorption
↑ Elimination
– Specific antidotes
17. Principles of therapy:
1. Prevention of drug absorption
• Washing to remove cutaneous contamination by
acid or base or organophosphorous insecticides.
• Induction of vomiting to remove poison from
stomach by:
– a. Mechanical stimulation as inducing gag.
– b. Ipecac syrup.
– c. Apomorphine.
– d. Warm salt water or biarbonate gastric lavage .
18. Principles of therapy:
1. Prevention of drug absorption
• Binding of the poison by specific chelating agents e.g. EDTA inn heavy metal
poisoning as lead poisoning or deferxamine in Iron poisoning.
• Adsorption of the poison onto activated charcoal
– Should be given within 30 mm of ingestion
– Charcoal has no toxicity, may be given before inducing vomiting or gastric
lavage
– It is with a universal antidote (activated charcoal: magnesium oxide: tannic
acid 2:1:1)
– 50 g single or repeated dose (↑ elimination)
– Doesn’t bind heavy metals, ethanol, acids
20. ↓ Absorption
• Gastric lavage
– Only if within 1 hour & if life-threatening amount
– Never for corrosives as it may cause respiratory irritation&
more GIT damage specially esophage.
– If ↓ LOC intubate before gastric lavage.
21. ↑ Elimination
• Methods to inrease elimination:
• Multiple dose activated charcoal
– Can bind Quinine, phenobarbitone
• Charcoal haemoperfusion
– Can bind Barbiturates, theophylline
• Diuresis
• Urinary alkalinization: increase excretion of aspirin.
• Dialysis: can remove many substances from blood.
23. Principles of therapy:
2. Alteration of drug metabolism
• The enhancement of metabolism for drugs inactivated by
metabolism e.g. use of thiosulfate in cyanide poisoning
• The inhibition of metabolism of drugs which produce toxic
metabolites e.g. use of ethanol for methanol poisoning
24. Principles of therapy:
3. Enhancement of excretion
• Ion trapping & alteration of urinary pH
forced diuresis ,dialysis [hemodialysis),
peritoneal dialysis, gastric dialysis (add
acidic solution to stomach, pump out)]
• Hemoperfusion, pass blood over charcoal
• Laxatives (cathartics) e.g. sodium sulfate,
magnesium sulfate, citrate or phosphate
25. Principles of therapy:
4. Specific pharmacological intervention
• Direct chemical antagonism e.g acid-base
• Receptor competition e.g. nalorphine in morphine overdose
• Blockade of receptors that causes the toxic effects e.g. atropine in
organophosphate poisoning, Flumazenil in benzodiazepin
poisoning.
• Restoration of normal function using an agent exerting a direct
opposite effect e.g. barbiturate in CNS stimulant poisoning
26. Antidotes in most common use in clinical
toxicology:
• Paracetamol: n-acetyl cystein or methionine.
• Opoid: Naloxone.
• Benzodiazepines: Flumazenil.
• Iron: dexferoxamine.
27. Treatment of shock
• Shock is in all serious accidental poisoning
• Arterial blood pressure is low in shock
• The problem of shock is poor tissue
perfusion
• Present treatment: provide fluid, increase
arteriolar relaxation & C.O. using a
adrenergic blocker (isoproterenol) &
antiinflammatomy steroids.
28. Causes of hypotension in poisoning:
• Volume depletion from vomiting, diarrhea, GITB.
• Drug-induced dilation of the venous bed.
• Myocardial depresion as in TAD & BB poisoning.
• Severe brady or tahyrrhthmias.
• Drug-induced metabolic acidosis as in aspirin
poisoning.
29. Treatment of convulsion
• Many drugs stimulate CNS causing convulsion.
• Diazepam (Valium), a tranquilizer, is the drug of choice
31. Paracetamol Overdose
• Acetaminophen is a leading OTC analgesics
• Is one of the leading causes of drug overdose in the US & UK& a
leading cause of liver failure.
• It is metabolized in the liver & relatively safe in therapeutic doses.
• A small fraction is converted to a reactive toxic metabolite, N-
acetyl-p-benzoquinoneimine (NAPQI), by the cytochrome P-450
hepatic enzymes.
• With therapeutic doses, glutathione stores can detoxify NAPQI by
conjugation.
• Glutathione stores are depleted in overdoses, & NAPQI binds to
cellular proteins, producing hepatocellular necrosis.
• Toxicity occur after a minimum of 140 mg/kg, or about 10
g(20tabs) in an adult & much less in high risk
persons( alcoholics, ,on enzyme inducing drugs as antipileptics&
33. Paracetamol Overdose: features.
• Acetaminophen poisoning clinically produces only nausea,
vomiting, & anorexia 12 to 24 hours after ingestion.
• Hepatic coma & coagulopathy do not occur until 48 to 96 hours
after ingestion, after irreversible hepatic necrosis has occurred.
• Patient with significant paracetamol overdose should not be
discharged early from Hospital, even if appearing clinically well
in the first 48-96 hours.
34. Paracetamol Overdose: Treatment.
• N-acetylcysteine is the drug of choice.
• It effectively prevents hepatotoxicity if given within 8 hours.
• It is strongly effective if given within 16 hours & may be effective
up to & beyond 24 hours.
• N-acetylcysteine therapy should be instituted with a 4-hour
acetaminophen level of 150 mg/mL, an 8-hour level of 75 mg/mL,
or a 12-hour level of 37.5 mg/mL.
• Because this therapy may be effective 24 hours after ingestion,
the presence of any measurable acetaminophen or biochemical
evidence of hepatic injury at 24 hours is an indication to start N-
acetylcysteine therapy.
35. Paracetamol Overdose: Treatment.
• It causes hepatic damage in overdose& rarely renal failure.
• If presents within 1 hour of overdose, activated charcoal given in
addition to NAC.
• Antidote is IV N-acetylcysteine, provides complete protection if
given within 8-10 hours of overdose;efficacy declines thereafter.
• So, if a patient presents > 8 hours after ingestion, N-acetylcysteine
should not be delayed to await a paracetamol blood result, so it is
given & only stopped if the level subsequently shown to be below
the treatment line.
• Methionine 12 g orally 4-hourly, to a total of four doses, is a
suitable alternative when N-acetylcysteine is not available.
• If a patient presents > 15 hours after ingestion, liver function
tests, PT (or INR) & renal function tests should be performed&
the antidote started.
• In some cases ABGs will need to be taken.
• Liver transplantation should be considered in individuals who
develop acute liver failure.
36. Paracetamol Overdose: Treatment.
• Because the P-450 enzyme is present in the fetus by the 14th week
of pregnancy, acetaminophen is highly toxic to the fetus, & N-
acetylcysteine therapy should be given to the pregnant patient as
soon as possible.
37. Do not check a paracetamol
level
before 4 hours have elapsed;
it is uninterpretable.
If more than 8 hours since
ingestion, start
N-acetylcysteine
immediately & only stop
it if the concentration is
below the treatment line
38. The salicylates (aspirin).
• Is a leading cause of analgesic drug overdose.
• The association of Reye's syndrome with aspirin produced a
dramatic fall in use & accidental poisoning in the pediatric age
group.
• Salicylates inhibit the cyclooxygenase enzyme of the prostaglandin
synthetase complex, uncouple oxidative phosphorylation, &
produce respiratory alkalosis & a high anion gap metabolic
acidosis.
• Salicylates are metabolized by first-order kinetics & are
conjugated with glycine & glucuronic acid; as plasma
concentrations rise in overdose & glycine stores are depleted,
zero-order kinetics prevail & renal excretion of salicylate becomes
prominent.
39. The salicylates (aspirin).
• Salicylate ingestion at doses > 150, 250 & 500 mg aspirin/kg body
weight produces mild, moderate & severe poisoning respectively.
• Salicylate poisoning can also occur with ingestion of oil of
wintergreen or when salicylic ointment (e.g. wart remover) is
applied extensively to skin.
40. Salicylates (aspirin): Clinical presentation.
• Includes nausea, vomiting, tinnitus, hearing loss,sweating, facial
flushing, hyperpyrexia, & hyperventilation.
• With severe poisoning: progressive dehydration, hypernatremia,
pulmonary edema, purpura, GIB & death.
• Direct stimulation of respiratory centre produces
hyperventilation
• Peripheral vasodilatation with bounding pulses & profuse
sweating occurs in moderately severe poisoning.
• Petechiae &subconjunctival haemorrhages can occur due to
reduced platelet aggregation but this is self-limiting.
• Signs of serious poisoning include metabolic acidosis, renal failure
& CNS effects as agitation, confusion, coma& fits.
• Rarely, pulmonary& cerebral oedema occur.
• Death can occur as a result of CNS depression&CV collapse.
• The development of a metabolic acidosis is a bad prognostic sign,
because acidosis results in increased salicylate transfer across the
blood-brain barrier
• A plasma level of > 30 mg/dL indicates salicylate toxicity& 80-100
mg/dL indicates critical salicylate poisoning.
41. Salicylates (aspirin): treatment.
• It is important to measure a plasma level in all but the most
trivial overdose, best at 6 hours or later after ingestion because of
continued absorption of the drug.
• The salicylate concentration needs to be interpreted in
conjunction with the clinical features& acid-base status.
• The treatment of choice for salicylate poisoning is an alkaline
diuresis with sodium bicarbonate.
• Any significant metabolic acidosis should be treated with IV
sodium bicarbonate (8.4%)&the volume given titrated to give an
arterial Ph of 7.4-7.5.
• Patients are often very dehydrated& fluid loss from vomiting &
sweating &must be replaced, but over use of IVF may precipitate
pulmonary oedema.
• The use of multiple doses of activated charcoal in salicylate
poisoning is controversial, but this approach is currently
recommended unless salicylate level has peaked.
• Urinary alkalinisation is indicated for adult patients with
salicylate concentrations of 600-800 mg/l.
42. Salicylates (aspirin): treatment.
• Haemodialysis is very effective at removing salicylate &correcting
acid-base and fluid balance abnormalities & considered when:
• 1.Serum concentrations are > 800 mg/l in adults &> 700 mg/l in
the elderly.
• 2.Metabolic acidosis resistant to correction.
• 3.Severe CNS effects as coma or convulsions, pulmonary oedema
& acute renal failure
• Vitamin K supplementation should be given.
• Supportive care is paramount.
43. Other (NSAID) poisoning.
• Ibuprofen is the leading (NSAID).
• Usually causes little more than minor GI upset including mild
abdominal pain, vomiting & diarrhoea.
• 10-20% have convulsions; usually self-limiting & needs only
airway protection & oxygen, if persist IV diazepam.
• Serious features include coma, prolonged fits, apnoea ,
bradycardia but very rare.
• Deaths have been reported after massive overdose of ibuprofen,
but not with mefenamic acid.
• Rarely, renal failure ensues.
• Features of toxicity tend to occur early & unlikely to develop later
than 6 hours after the overdose.
• Liver/renal function may be affected, so electrolytes, liver
functions &CBP should be checked in all unless trivial overdoses.
• The 1/2t of most NSAIDs are < 12 hours, so elimination methods
are not needed.
• Activated charcoal should be given if > 100 mg/kg BW ibuprofen
or > 10 tablets of any other NSAID taken in the last hour.
• GI irritation is treated with oral H2-blockers (e.g. ranitidine).
44. Anticholinergic poisoning.
• The classic anticholinergic syndrome is produced by blockade of
acetylcholine with central & peripheral effects:
• Psychosis, delirium, seizures, flushing, dry mucous membranes &
skin, hyperpyrexia, dilated pupils & urinary retention.
• The antidote physostigmine should be reserved for severe cases of
pure anticholinergic poisoning.
• Physostigmine should not be used for agents with only some
anticholinergic properties, as tricyclic antidepressants.
• The initial dose of physostigmine is 0.5 - 2 mg IV slowly in adults
&0.02 mg/kg in children, maximum dose is not to exceed 4 mg in
30 minutes in adults.
• Cardiac monitoring is essential, because physostigmine has
caused asystole, bradycardia, & seizures.
45. Barbiturates poisoning.
• Still constitute a major source of overdose & mortality although
largely replaced as sleep medication by benzodiazepines.
• They are still present in headache prescriptions & sleep
medications & remain common drugs of abuse.
• Phenobarbital is one of the leading anticonvulsant medications.
• Thiopental is used as an IV anesthetic for in-hospital rapid-
sequence intubation or as a sedative before cardioversion &
surgery.
• Phenobarbital is excreted primarily unchanged by the kidney,
whereas most other barbiturates are metabolized by the liver.
46. Barbiturates poisoning: features.
• Overdose is associated with depression of CNS & CV system,
coma, hypotension, loss of reflexes, hypothermia, respiratory
arrest & death.
• 2 characteristic of a barbiturate overdose is:
• 1. The persistence of the pupillary light reflex even with stage IV
coma.
• 2. Bullous skin lesions often occur over pressure areas.
47. Barbiturates poisoning: treatment.
• Treatment of the critically ill patient involves mechanical
ventilation, resuscitation of CV status, gastric lavage & activated
charcoal (after securing the airway) & supportive care in an ICU.
• An alkaline diuresis with sodium bicarbonate is specifically
indicated for phenobarbital, which is a weak acid that is excreted
unchanged in the urine.
• Multiple-dose activated charcoal every 4 -6 hours is also
specifically indicated for phenobarbital, as it diffuses into the GIT
lumen.
• Charcoal hemoperfusion & hemodialysis have a role in
barbiturate overdose for critical patients who do not respond to
conservative therapy.
48. The benzodiazepines poisoning.
• Extremely popular & have replaced other sedative-hypnotics.
• All are effective anxiolytics & sedatives& are muscle relaxants,
anticonvulsants & amnestics.
• Diazepam, lorazepam, & midazolam, have major therapeutic
roles as IV drugs for in-hospital use as anticonvulsants,
preanesthetics & sedatives.
• Although common agents of overdose, cause only coma & ataxia;
mortality is rare & supportive care is all that usually necessary.
• The antidote flumazenil is reserved only for reversing pure in-
hospital benzodiazepine conscious analgesia&reversing coma in
zolpidem overdose.
• Its use in the general overdose patient or in a patient with head
injury or coma of unknown etiology is not recommended,
reported to cause seizures in patients who have co-ingested
benzodiazepines & cyclic antidepressants & has caused increased
intracranial pressure in patients with head injury.
51. The calcium channel blockers poisoning.
• Common antihypertensive agents
• the most common cause of cardiovascular drug death by
overdose.
• A special problem is presented by the sustained-release
preparations, which allow for continued absorption.
• Persistent hypotension, bradycardia with atrioventricular block
(especially with verapamil), coma, pulmonary edema, & cardiac
arrest constitute the clinical picture.
52. The calcium channel blockers poisoning.
• Treatment must be aggressive if these patients are to survive.
• Whole-bowel irrigation with polyethylene glycol is indicated if
sustained-release preparations have been ingested.
• An intravenous 10% calcium chloride 1-g bolus (over 5 minutes)
may be life-saving, and 1 gram IV every 15 minutes over the first
hour may be necessary in critically ill patients, followed by 10%
calcium chloride via continuous intravenous infusion (the dosage
and rate depending on the clinical condition) until blood pressure
stabilizes.
53. The calcium channel blockers poisoning.
• For patients who do not respond to high-dose calcium therapy,
dopamine, dobutamine, amrinone, epinephrine, and/or glucagon.
• Glucagon is indicated in patients with concomitant b-blocker
overdose.
• Pacing may be necessary, especially with verapamil overdose.
• Symptomatic patients and patients who have ingested sustained-
release preparations should be admitted to the critical care unit
for continuous ECG monitoring for at least 24 hours after
stabilization.
54. Digitalis poisoning.
• Still common.
• Patients who suffer yellow or blurred vision, nausea or vomiting,
& sinus bradycardia may improve simply by stopping the drug.
• Significant digitalis intoxication is heralded by hyperkalemia & a
variety of major cardiac arrhythmias.
• Digoxin-specific Fab antibodies (Digibind) offer a definitive
means of therapy &are indicated for:
• Life-threatening cardiac arrhythmia.
• Hyperkalemia.
• Aserum digoxin level of 10 ng/mL,
• A massive overdose of 10 mg or greater in adults or 4 mg in
children.
• Antidotal therapy should be instituted before conventional
therapy in life-threatening situations.
55. Antidiabetics:
• Sulphonylureas (e.g. chlorpropamide, glibenclamide, gliclazide,
glipizide, tolbutamide)
• Biguanides (metformin, phenformin)
• Insulins.
• Cause hypoglycaemia when taken in overdose.
• The onset & duration of hypoglycaemia vary, but can last for
several days with long-acting agents as chlorpropamide&
isophane / lente insulins.
• Hypoglycaemia may manifest as agitation, sweating, confusion,
tachycardia, hypothermia, drowsiness, coma or convulsions
• Permanent neurological damage can occur if the hypoglycaemia is
prolonged.
56. Antidiabetics:
• Metformin can cause a lactic acidosis in overdose, particularly in
elderly & those with renal or hepatic impairment, or when co-
ingested with ethanol.
• It is associated with a > 50% mortality.
• Metformin overdose may also cause nausea / vomiting, diarrhoea,
abdominal pain, drowsiness, coma, hypotension & CV collapse.
57. Antidiabetics: Management
• Activated charcoal should be given & gastric lavage considered in
all patients who present within 1 hour of ingestion of more than
the normal therapeutic dose of an oral hypoglycaemic agent.
• Formal measurement of venous blood glucose (not just visually
read strips or meter) , urea & electrolytes should be performed
&repeated regularly.
• For medico-legal purposes , a blood sample may be required for
subsequent measurement of insulin, pro-insulin and C-peptide.
• Hypoglycaemia should be corrected urgently with 50 ml 50%
dextrose, given i.v. if the patient is unconscious or with a sugary
drink if the patient is conscious, followed by an infusion of 10% or
20% dextrose titrated to the blood glucose to prevent further
hypoglycaemia&may be necessary for several days, depending on
the agent ingested or injected.
• Potassium replacement should be guided by frequent
measurement of urea &electrolytes.
58. Antidiabetics: Management
• Failure to regain consciousness within a few minutes of
normalisation of the blood glucose indicate either:
• 1. CNS depressant has also been ingested
• 2. Hypoglycaemia has been prolonged.
• 3. Another cause for the coma (e.g. cerebral haemorrhage) or
cerebral oedema.
• In cases of severe sulphonylurea overdose resistant to dextrose
infusions, use of IV octreotide as an antidote may be considered.
59. Carbon monoxide poisoning.
• Is the leading cause of death from poisoning in US.
• CO is a colorless, odorless, tasteless gas produced by incomplete
combustion of carbon materials.
• CO has a 200 times greater affinity for hemoglobin than oxygen
& thus produces cellular hypoxia & death.
• Fires, smoke, wood-burning stoves, gas space heaters& engine
exhaust are sources of unintentional poisoning.
60. Carbon monoxide poisoning.
• Because the heart & brain are the most sensitive to hypoxic insult,
clinical presentation usually involves CNS or cardiac symptoms—
headache, altered mental status, convulsions, chest pain, cardiac
arrhythmia, &/or AMI.
• Mild CO poisoning often is mistaken for influenza, as both occur
primarily in the winter months & cause headache/GI symptoms.
• Because most patients receive oxygen in an ambulance on the way
to the hospital, the carboxyhemoglobin level is usually an
unreliable indicator of the extent of poisoning.
• In general, the deeper the level of coma, the greater the chance of
neuropsychiatric sequelae.
61. Carbon monoxide poisoning.
• CO poisoning is treated with oxygen:
• Breathing room air, it takes a patient 6 hours to halve
carboxyhemoglobin level (T½); breathing 100% oxygen, 90
minutes; with hyperbaric oxygen at 2.5 atmospheres of pressure
absolute, < 1 hour.
• Hyperbaric oxygen therapy reduces the incidence of neurologic
sequelae & has become the standard of care for treating CO-
poisoned patients with coma & altered mental status
62. Carbon monoxide poisoning.
SPECIFIC INDICATIONS FOR HYPERBARIC OXYGEN THERAPY
All comatose patients
Patients with neurologic impairment by examination or psychometric testing
Patients with carboxyhemoglobin levels >40%
Cardiovascular involvement (chest pain, ECG changes, arrhythmias)
Pregnant patients with carbon monoxide levels >15%
Patients who do not respond to 100% oxygen
Patients with recurrent symptoms up to 3 weeks after exposure
63. Caustic alkali poisoning.
• Accidentally swallowing button batteries larger than 20 mm in
diameter & intentional ingestion of alkali substances are the
major causes of morbidity.
• Because solid crystals adhere to the tongue & cause burning, they
uncommonly produce esophageal burn.
• Drooling in children &inability to swallow are highly suggestive.
• Mouth burns are also suggestive, but the absence of mouth burns
does not exclude esophageal burn.
64. Caustic alkali poisoning.
• Milk is the only possible home antidote, but it must be given
immediately.
• To detect significant burns, some suggest UGI esophagoscopy
within 12 hours, whereas others prefer to wait 24-2 hours
following ingestion.
• A 3-week course of methylprednisolone, 2.5 mg/kg/day, to prevent
esophageal stricture has been the mainstay of therapy, but its
efficacy has been questioned.
• Esophageal dilation & gastric tube esophageal replacement are
indicated for treating esophageal stricture.
65. Cyanide poisoning.
• Most commonly is due to smoke inhalation.
• One public source is acetonitrile in acrylic nail remover.
• Hydrogen cyanide gas is a fumigant rodenticide.
• Prolonged administration of nitroprusside can result in elevated
cyanide levels.
66. Cyanide poisoning.
• Produces cellular hypoxia by binding with the ferric iron of
mitochondrial cytochrome oxidase & disrupting the electron
transport chain & the ability of cells to use oxygen.
• Rapidly develop coma, shock, seizures, lactic acidosis, respiratory
& cardiac arrest.
• Mild exposures following smoke inhalation may be difficult to
diagnose& Emergency administration of antidote may be life-
saving.
• Cyanide poisoning should be suspected in patients who have
inhaled smoke &who have evidence of lactic acidosis.
67. Cyanide poisoning.
• The cyanide antidote kit contains amyl nitrite, ampules of sodium
thiosulfate, & ampules of sodium nitrite.
• The body has a natural enzyme, rhodanese, that can complex
cyanide & sulfur to form thiocyanate, which is only mildly toxic.
• IV sodium thiosulfate provides the sulfur necessary to produce
thiocyanate & is relatively safe.
• Because sodium nitrite causes hypotension &
methemoglobinemia, its use is reserved for the most critical cases.
• The new antidote hydroxocobalamin (initial adult dosage 5 g IV),
not yet approved, is a safer alternative.
68. Iron poisoning.
• Has a direct corrosive action on the stomach & proximal small
bowel
• Once absorbed, produces shock, metabolic acidosis, liver
failure& death.
• Initially, GIsymptoms prevail with persistent vomiting,
abdominal pain& hemorrhage.
• A quiescent phase may be observed, followed by shock, coma,
metabolic acidosis& liver failure.
• Laboratory data may reveal leukocytosis, hyperglycemia&
radiopaque tablets on a flat plate of the abdomen.
69. Iron poisoning.
• A serum iron level should be determined (during peak levels) at 2
-4 hours after ingestion: > 300 mg/dL indicates mild
intoxication, ,> 500 mg/dL indicates serious intoxication, but a
serum iron level in excess of the total iron-binding capacity does
not serve as a useful predictor of iron poisoning.
70. Iron poisoning.
• Management of iron poisoning includes gastric lavage with
normal saline.
• Whole-bowel irrigation may be indicated after ingestion of
sustained-release capsules.
• The treatment of choice is the antidote deferoxamine, which
chelates free serum iron in the plasma to form ferrioxamine,
which is readily excreted & imparts a vin rosé color to the urine.
71. Iron poisoning.
• Deferoxamine is indicated for:
• All critical patients who present with coma, shock, or
hemorrhage,
• All patients with a serum iron level higher than 500 mg/dL,
• Patients who are symptomatic with a serum iron > 300 mg/dL.
• IV deferoxamine 15 mg/kg/hour is the preferred; up to 6 g may be
given in 24 hours.
72. Iron poisoning.
• Chelation therapy should continue until:
• The patient becomes stable for at least 24 hours.
• Vntil the vin rosé urine (when present) becomes clear.
• Until the serum iron level has fallen <300 mg/dL.
• Exchange transfusion may be indicated for the unusual patient
who is critically ill & does not respond to chelation therapy.
73. Methanol & ethylene glycol poisoning.
• True medical emergencies.
• Methanol is most commonly found as the active ingredient in
windshield washer fluid& ethylene glycol constitutes antifreeze.
• Moth are also found in many commercial & marine products.
• Methanol, or wood alcohol, is converted by alcohol
dehydrogenase to formaldehyde &then to formic acid.
74. Methanol & ethylene glycol poisoning.
• Signs & symptoms develop over a 24-hour period & may include
infarction of the putamen.
• Severe high anion gap metabolic acidosis occurs with an increase
in the osmolal gap.
• Treatment emphasizes IV ethanol, sodium bicarbonate &
hemodialysis.
75. Methanol & ethylene glycol poisoning.
• The diagnosis of ethylene glycol poisoning in adults, commonly
from antifreeze, is generally, but not always, evident from the
history.
• Metabolism of ethylene glycol by alcohol dehydrogenase causes
poisoning by producing severe metabolic acidosis due to aldehyde,
glycolate& lactate formation & deposition of oxalate crystals in
the lungs, heart& kidneys
• (4-methylpyrazole) inhibits alcohol dehydrogenase & may be an
alternative to intravenous alcohol for the treatment of ethylene
glycol poisoning.
• Hemodialysis is the treatment of choice for ethylene glycol
poisoning & should be instituted as early as possible once the
diagnosis is made.
76. Methanol & ethylene glycol poisoning.
POISONING WITH METHANOL OR ETHYLENE GLYCOL
Methanol
S&ss Altered mental status; coma; seizures; gastrointestinal disturbance with
abdominal pain; pancreatitis in some; visual disturbances: blurred
vision, diplopia, photophobia, sensation of "being in a snowstorm,"
blindness (end result).
Treat Aggressively prevent methanol conversion by infusing IV ethanol.
Correct metabolic acidosis with sodium bicarbonate;
Hemodialysis to remove methanol/metabolites—indicated for patients with
visual disturbance, serum methanol >50 mg/dL, or with intractable
metabolic acidosis.
77. Methanol & ethylene glycol poisoning.
Ethylene Glycol
Signs and symptoms Early
Altered mental status; seizures; hypocalcemic
tetany
12 hr after ingestion
Congestive heart failure
24–72 hr after ingestion
Profound renal failure
Treatment Treat ethylene glycol with:
aggressive gastric lavage;
ethanol infusion or 4-methylpyrazole,
sodium bicarbonate to correct metabolic acidosis,
Correct hypocalcemia with calcium chloride,
Hemodialysis
78. The organophosphates poisoning.
• Highly popular insecticides because they are effective,
disintegrate within days of application & do not persist in the
environment
• Even minute quantities can penetrate the skin & be lethal, as
evidenced by the use of organophosphate nerve gases sarin,
soman, tabun, & VX in chemical weapons.
79. The organophosphates poisoning.
• The organophosphates irreversibly inhibit acetylcholinesterase,
resulting in an overabundance of acetylcholine at synapses & the
myoneural junction.
• The acetylcholine initially excites & then paralyzes the CNS, the
parasympathetic nerve endings & the sweat glands (muscarinic
effects), somatic nerves & ganglionic synapses of autonomic
ganglia (nicotinic effects).
• Initial symptoms resemble a flulike syndrome with abdominal
pain, vomiting, headache, dizziness.
• The full-blown picture generally develops by 24 hours ,includes
coma, convulsions, confusion, or psychosis; fasciculation ,
weakness or paralysis; dyspnea, cyanosis,pulmonary edema;
sometimes pancreatitis.
• Torsades de pointes VF has also been described.
80. The organophosphates poisoning.
• Emergency management includes decontamination of the skin,&
removal of clothes; establishing an airway & ensuring proper
ventilatory support , cardiac monitoring; & administering the
specific antidote pralidoxime & the physiologic antidote atropine.
• A 25% reduction in red blood cell cholinesterase confirms
organophosphate poisoning.
• Atropine should be given as a physiologic antidote to reverse the
muscarinic effects & to dry the excessive pulmonary secretions
seen in patients with respiratory distress.
• Atropine use requires cardiac monitoring& proper oxygenation.
• Pralidoxime is the treatment of choice for organophosphate
poisoning & should be begun on clinical grounds before return of
any blood studies.
• To be effective, pralidoxime must be given in the first 48 hours
before irreversible binding of acetylcholinesterase occurs.
81. The organophosphates poisoning.
• The initial dose is 1 g IV given over 15 to 30 minutes;
the effect may be dramatic.
• Pralidoxime by continuous infusion of up to 500
mg/hour may be necessary in critically ill patients.
• Pralidoxime may obviate the need for high-dose
atropine therapy & reduce the incidence of late-onset
paralysis.
• Neither therapies exclude the use of the other.
82. The organophosphates poisoning.
• The carbamate insecticides include carbaril, methomyl,
& propoxur
• are reversible cholinesterase inhibitors.
• They produce clinical effects similar to those of the
organophosphates but without CNS signs;
• They are considerably more benign & shorter
duration.
• Atropine is the drug of choice for carbamate
poisoning.
• Pralidoxime is not indicated because the carbamate-
cholinesterase complex is quite reversible.
83. Theophylline poisoning.
• Mortality from both plain & sustained-release preparations occur
from acute overdose & long-term unintentional intoxication.
• Vomiting is often the first symptom, sinus tachycardia is the most
common sign in both acute - chronic toxicity.
• Seizures may be common when the serum concentration is higher
than 40 mg/mL in chronic toxicity or higher than 80 to 100
mg/mL in acute overdose.
• Cardiac arrhythmia, CVcollapse, respiratory arrest are seen
infrequently unless the concentration is higher than 50 mg/mL in
chronic toxicity or higher than 100 mg/mL in acute overdose.
• Profound hypokalemia, hyperglycemia, metabolic acidosis are
also seen.
• Serum theophylline is higher in acute overdose compared with
those in chronic toxicity.
84. Theophylline poisoning.
• Treatment includes
• withdrawing the drug, cardiac monitoring, supportive care.
• Gastric lavage &activated charcoal are indicated for acute
overdose.
• The serum half-life of theophylline can be reduced by serial
administration of activated charcoal, as it diffuses into the GIT
lumen; dosage is 1g/kg every 4 hours.
• Whole-bowel irrigation may be indicated for ingestion of
sustained-release capsules.
• Cardiac arrhythmias are often difficult to manage but may
respond to IV propranolol.
• Correction of hypokalemia, metabolic acidosis& fluid-electrolyte
balance is indicated.
• Although seizures may respond to IV diazepam, status epilepticus
& rhabdomyolysis may occur & signify a poor outcome.
85. Theophylline poisoning.
• Charcoal hemoperfusion is the treatment of choice for significant
theophylline toxicity.
• Hemodialysis is becoming an option equal to charcoal
hemoperfusion.
• Charcoal hemoperfusion is most beneficial for patients with a
serum theophylline > 80 to 100 mg/mL in acute overdose or > 40
mg/mL in chronic toxicity (especially in the elderly or patients
with hepatic disease or other conditions that delay theophylline
clearance) or patients in critical condition.
86. Tricyclic (or cyclic) poisoning.
• Still the leading cause of prescription drug death.
• CV toxicity (arrhythmia /hypotension), CNS effects
(especially coma /seizures), anticholinergic signs are
seen.
• The cardiotoxic effects are seen with ingestion of 1 g
(10 to 20 mg/kg) &account for the high mortality rate.
87. Tricyclic (or cyclic) poisoning.
• The hallmark on ECG is prolongation of the QRS complex.
• A QRS complex > 100 ms is a sign of severe toxicity & correlates
with a plasma level > 1000 ng/mL.
• Although sinus tachycardia & anticholinergic signs are evident
with mild toxicity, QRS complex prolongation is associated with
the development of ventricular arrhythmias, seizures, death.
• Ventricular tachycardia is the most common ventricular rhythm,
although ventricular bigeminy, slow ventricular rhythms,
torsades de pointes VF also have been described.
• VF/ sudden cardiac arrest are not uncommon.
88. Tricyclic (or cyclic) poisoning.
• The treatment of choice IV sodium bicarbonate.
• To maintain a blood pH of 7.5 reduce the incidence of cardiac
arrhythmia.
• IV bolus of sodium bicarbonate (1 to 2 mEq/kg) is the treatment
of choice for the sudden onset of ventricular tachycardia,
ventricular fibrillation& cardiac arrest.
• Sodium bicarbonate also may be useful for correcting
hypotension, although vasopressors may be necessary.
• Airway, proper oxygenation & ventilation, fluid replacement (but
avoid pulmonary edema), gastric lavage with serially
administered activated charcoal& supportive therapy are
indicated.
89. Tricyclic (or cyclic) poisoning.
• Phenytoin reverse QRS complex prolongation, but reserved for
managing seizures.
• Prophylactic IV phenytoin (15 mg/kg) before the onset of seizures
may be given in cases of amoxapine overdose, which has a high
incidence of status epilepticus.
• Diazepam is quite effective in controlling seizures, although
intensive therapy including thiopental & rapid-sequence
intubation may be necessary to manage status epilepticus.
• Physostigmine is no longer used in tricyclic overdose, because by
itself it can cause seizures, bradycardia, asystole.
• Death generally occurs within the first 24 hours after overdose.
• Because sudden death has occurred after apparent stabilization,
cardiac monitoring is indicated for at least 24 hours after
stabilization & normalization of the QRS complex.
90. Tricyclic (or cyclic) poisoning.
• Newer antidepressants that are not structurally related to the
cyclic agents include the serotonin reuptake inhibitors fluoxetine
(Prozac), sertraline (Zoloft), paroxetine (Paxil), and fluvoxamine
(Luvox),
• generally cause only sedation in overdose.
• Fatal serotonin syndrome from concomitant overdose of selective
serotonin reuptake inhibitors (SSRIs) and monoamine oxidase
inhibitors is now being reported.