Uploaded byAbhinav Srivastava
Vomiting
This document discusses nausea and vomiting. It begins by classifying vomiting as primary or secondary and acute or chronic. It then describes the reflex mechanism of vomiting which occurs in three phases: nausea, retching, and vomiting. Various causes of vomiting are provided for both general and pediatric populations. Evaluation involves taking a history and performing a physical exam and tests. The major types of antiemetics are described along with their mechanisms and clinical uses. Specific conditions like cyclic vomiting syndrome and nausea/vomiting of pregnancy are also discussed. The document concludes by outlining approaches to managing nausea and vomiting.
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Vomiting
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- 2. OUTLINE • Classifications • Reflexmechanism of vomiting • Causes of Vomiting • History • Physical Examination • Special Considerations In Pediatric Group • Tests DDx In General Population • DDx In Pediatric Population • Cyclic vomiting syndrome • Evaluation of nausea and vomiting of pregnancy • The management of Nausea &Vomiting • Sequelae Of Vomiting
- 3. What is themajor physiological function of vomiting Remove non-toxic or harmless substances from the body after ingestion Valuable physiological response to ingestion of toxic substances e.g. alcohol
- 4. Classifications Primary : Usuallydue to a GI illness ( Obstruction Or Gastroenteritis ) Secondary : Due to either : 1- Sever visceral pain . 2- Sever Systemic illnesses ( MI , Sepsis , Shock ) 3- Specific conditions like : pregnancy “ Hormonal “ , Raised ICP “ CNS pathology “ , Toxins “ Homeostatic Reflex “ Motion Sickness “ Neuroendocrine “ Or Chemo “ CTZ “
- 5. Classifications Acute Vomiting :Occurs ( < or = 1 Week ) , Usually associated with : obstruction , ischemic , toxic , metabolic , infectious , neurological and post-operative reasons . Chronic : Occurring for more than 1 Month , Usually due to partial obstruction , motility disorder , neurological chronic condition , pregnancy or functional reasons .
- 6. Reflex mechanism ofvomiting Three phases: NAUSEA, RETCHING and VOMITING
- 7. Nausea • an unpleasantsensation that immediately precedes vomiting. Cold sweat, pallor, salivation. Noticeable disinterest in the surroundings Loss of gastric tone Reflux of intestinal contents into the stomach Accompanying symptoms
- 8. Retching • follows nausea Compriseslabored spasmodic respiratory movements against a closed glottis with contractions of the abdominal muscles, chest wall & diaphragm without any expulsion of gastric contents. can occur without vomiting but normally it generates the pressure gradient that leads to vomiting.
- 9. Vomiting caused by: • Thepowerful sustained contraction of the abdominal and chest wall musculature accompanied by • The descent of the diaphragm and the opening of the gastric cardia. It results in the • Rapid and forceful evacuation of stomach contents upto and out of the mouth Reflex activity that is not under voluntary control
- 11. Neuronal pathways, transmitters and receptorsinvolved in nausea and vomiting
- 12. Mechano and Chemoreceptors located in • stomach, jejunum and ileum involved with • detection of emetic stimuli in the gastrointestinal tract • Mechanoreceptors are tension receptors that initiate emesis in response to distension and contraction • Chemo receptors respond to a variety of toxins in the intestinal lumina
- 13. Afferent neuronal pathways fromthe abdomen are the same regardless of the stimulus
- 14. Receptors and neurotransmittersinvolved in mediating vomiting: Structures Receptors Agonists Antagonists Area postrema CTZ D2 Apomorphine L-DOPA Antidopaminergic drugs Vestibular nuclei N. tractus solitarius M, H1 Cholinomimetics Histamine Scopolamine Dramamine Vomiting center M Cholinomimetics (e.g., physostigmine) Scopolamine Vagal sensory nerve endings 5-HT3 Serotonin Ondansetron Granisetron Tropisetron
- 15. Vomiting Centre Final commonpathway for efferent responses that produce emesis • controls the act of vomiting not a discrete anatomical site, but represents inter-related neuronal networks. • inputs include: vagal sensory pathways from the gastro- intestinal tract and neuronal pathways from the labyrinths, higher centers of the cortex, intracranial pressure receptors and the chemoreceptor trigger zone. • When activated induces: vomiting via stimulation of the salivary and respiratory centers and the pharyngeal, gastrointestinal and abdominal muscles.
- 16. Chemoreceptor Trigger Centre (CTZ) •Area prostrema of the 4th ventricle of the brain • acts as the entry point for emetic stimuli • CTZ is outside the blood-brain barrier • Responds to stimuli from either the cerebral spinal fluid (CSF) or the blood.
- 19. Main neurotransmitters involvedin control of vomiting • Acetylcholine • Histamine • 5-HT • Dopamine • Enkephalins • Substance P
- 20. Class Drug Anti-cholinergic scopolamine(L-hyoscine) Anti-histamine cinnarizine cyclizine promethazine Dopamine antagonists metoclopramide domperidone droperidol (withdrawn 2001) haloperidol Cannabinoid nabilone Corticosteroid dexamethasone Histamine analogue betahistine 5HT3-receptor antagonist granisetron ondansetron tropisetron
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- 22. Drug/treatment - inducedCancer chemotherapy Opiates, Nicotine Antibiotics, Radiotherapy Labyrinth disorders Motion, Meniere's disease Endocrine causes Pregnancy Infectious causes Gastroenteritis Viral labyrinthitis Increased intracranial pressure Haemorrhage, Meningitis Post-operative Anaesthetics, Analgesics Procedural CNS causes Anticipatory Migraine, Bulimia nervosa
- 23. Drugs causing emesis. Drugsacting on CTZ • Apomorphine • Emetine (when given parenterally and only at large doses) • L-DOPA • Estrogens (morning sickness of pregnancy) • Chemotherapeutic agents • Eardiac glycosides • Opiates
- 24. Drugs acting locallyon the G-I tract Activate enterochromaffin cells secrete serotonin acts on the 5-HT3 receptors at the nerve endings of the vagal sensory fibers. • Afferent fibers transmit excitation to the N. tractus solitariusVC. • Traditionally called "local irritants” • Ipecac, zinc salts, copper sulfate,
- 25. Cancer chemotherapeutic agentsand radiation therapy Produce free Radicals Enterochromaffin cells Serotonin Stimulate CTZ receptors
- 26. History Duration : todefine the type of vomiting and to give you a close picture of what kind of sequelae might have this patient developed Time + Onset / Offset : to define the type or the etiology causing it : Acute Onset : Gastroenteritis , Pancreatitis , cholecystitis, Appendicitis , Anaphylaxis , Medication Effect Or Toxicity . Morning : Raised ICP , Primary Tension or Migraine Headaches , Pregnancy , Uremia , Alcoholism . 1 Hour After Eating : Gastric Outlet Obstruction Or gastroparesis. 12 Hours After Eating : Gastric Or Intestinal Obstruction .
- 27. Content Of TheVomit : • Bilious Gastric outlet obstruction is out of the question , cause the area between the stomach and duodenum is intact • If Undigested Food Achalasia Or Stricture • If Digested Food Might be due to toxins or anaphylaxis • If Hematemesis Suspect Upper GI Bleed • If Fecal Matter/Foul Smelling Distal Bowel Obstruction , Fistula , Bacteria Overgrowth due to long standing outlet obstruction .
- 28. Associated Symptoms : •Hyper-salivation, defecation, tachycardia, bradycardia, atrial fibrillation, and termination of ventricular tachyarrhythmia’s • Chronic headaches with nausea and vomiting intracranial lesion Past Medical & Surgical Hx : any GI disease or previous surgeries Social & Traveling Hx : alcohol or other substance abuse. Medications & Dietary Habits : Nutritional history is valuable in the consideration of failure to thrive in infancy thorough medication list, including over-the-counter drugs, should be included.
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- 30. Special Considerations InPediatric Group • Bulging Fontanel Meningitis • Projectile Vomiting Pyloric Stenosis • Unusual Odors Metabolic Or Toxicological Causes • Visible Bowel Loops Obstruction • Enlarged Parotid Gland + Loss Of Dental Enamel Bulimia
- 31. • Mild Reflux& Rumination & Regurgitation might be normal in first few months of life • First Week Vomiting Obstructive , Inborn Error Of Metabolism , Serious Infection • After 1 Week Pyloric Stenosis , Feeding Problems • First Month Infections , Metabolic Causes , Failure To Thrive , Subdural Hematoma in Abused Children • Adolescents + Teenagers Cyclic Vomiting , Food Poisoning , Pneumonia , DKA , Anorexia Nervosa , Bulimia , Drug Abuse
- 32. Tests - CBC :If Hb and HCT are High >>> Dehydration - Electrolytes : Hypochloremia , Hypokalemia . - BUN / Creatinine Ratio : If 20:1 >> Sever Dehydration . - Amylase & Lipase : Pancreatitis >>> Dehydration - Urine analysis : For UTI , Pregnancy Test , DKA , Hematuria , Stones , Sterile Pyuria in Appendicitis . - Culture , Sensitivity & Titers : To Rule In Or Out Infection - LFTs + Ammonia : Cholycystitis , Ascending Cholangitis , Liver Failure . -
- 33. • Chest &Abdominal X-Rays : Focus ,Perforation , Obstruction • CT & Angio : Ischemia & Infarction • ECG : MI • TFT : Thyroid Disease • Drug Levels
- 34. DDx In GeneralPopulation
- 35. DDx In PediatricPopulation
- 36. The management of Nausea&Vomiting
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- 38. Class Drug Anti-cholinergic scopolamine(L-hyoscine) Anti-histamine cinnarizine cyclizine promethazine Dopamine antagonists metoclopramide domperidone droperidol (withdrawn 2001) haloperidol Cannabinoid nabilone Corticosteroid dexamethasone Histamine analogue betahistine 5HT3-receptor antagonist granisetron ondansetron tropisetron
- 39. Receptors antagonists Which receptors H1 - Histamine receptors Muscarinic receptors 5 HT 3 receptors
- 41. Antiemetic Drugs H1- receptorantagonist • Cyclizine • Meclizine • Cinnarazine • Promethazin • Diphenhydramine • Dimenhydrinate • Hydroxyzine Muscarinic antagonist • Hyoscine (Scopolamine)
- 42. D2-receptor antagonist Phenothiazine • Chlorpromazine •prochlorperazine • Promethazine • Trifluoperazine • Thiethylperazine Butyrophenones: • Haloperidol • Droperidol Metoclopramide Domperidone
- 43. 5 HT3-receptor antagonist Ondansetron Granisetron Dolasetron Cannabinoids •Nabilone • Dronabinol Steroids • Dexamethasone • Methylprednisolone
- 44. Clinical Uses ofAnti emetics • Histamine H1 receptor antagonist Cyclizine Motion sickness Cinnarazine Motion sickness, vestibular disorders Promethazine Morning sickness of pregnancy
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- 46. Dopamine D2 receptorantagonist Phenothiazines vomiting caused by Prochlorperazine uremia, radiation,viral gastroenteritis, severe morning sickness of pregnancy. Metoclopramide uremia, radiation, GI disorders, cytotoxic drugs.
- 47. 5-HT3- receptor antagonist DrugsVomiting caused by Ondansetron Granisetron Dolasetron cytotoxic anticancer drugs, post operative vomiting, radiation induced vomiting Cannabinoids Vomiting caused by anticancer drugs
- 48. 5 HT3 Antagonists •Ondansetron, • Granisetron, • Dolasetron, • Tropisetron Primary site of action: CTZ Therapeutic Use: chemotherapy and radiation induced nausea & vomiting DOSE: Adult:4mg IV single dose paeds : up to 40kg 0.1mg/kg, >404mg IV Adverse effects: Rare headache , GI upsets
- 49. Phenothiazines • Antipsychotics • Commonlyused for: nausea and vomiting associated with vertigo, motion sickness, and migraine. • Act mainly as: antagonist at dopamine D-2 receptors in the CTZ • Also block: muscarinic and histamine receptors • Adverse effects: sedation hypotension extra pyramidal symptoms
- 50. Metoclopramide and Domperidone •D2 receptor antagonist in CTZ. • Peripheral prokinetic activity: • Domperidone does not cross BBB. • DOSE:10-20mg tid max 2.4mg/kg or 80max • Peads:250ug-500ug/kg tid max 2.4 mg/kg total daily dose Incontrast • Metoclopramide crosses BBB Movement disorder, fatigue, spasmodic torticollis, occulogyric crises, increased prolactin release galactorrhea , menstrual irregularities DOSE:10mg IM/IV Q6hr Increase the motility of esophagus, stomach, and intestine
- 51. Cannabinoids Dronabinol, Nabilone • Syntheticcannabinol derivative Mechanism of action: unknown Adverse effects: common: • Drowsiness , dizziness, dry mouth. • Mood changes • Postural hypotension • Hallucinations DOSE:4.2mg/m2 PO 1-3hr before chemotherapy for total of 4-6 doses/day
- 52. Corticosteroids High dose Glucocorticoids •Dexamethasone • Methylprednisolone Mechanism of action: unclear may involve inhibition of PGs DOSE : 8-12mg/PO/IV
- 53. Cyclic vomiting syndrome •CVS was first described in France in 1861 • In 1882, described three essential clinical features of the disorder Three or more recurrent discrete episodes of vomiting Varying intervals of completely normal health between episodes Episodes are stereotypical with regard to timing of onset, symptoms & duration Absence of an organic cause of vomiting
- 54. PATHOGENESIS • Unknown • CVSand migraines • Food allergy • Catamenial CVS • Chronic cannabis use
- 55. DIAGNOSIS Rome IV criteria •Stereotypical episodes of vomiting regarding onset (acute) and duration (less than one week) • Three or more discrete episodes in the prior year, and two episodes in the past six months, occurring at least one week apart • Absence of vomiting between episodes, but other milder symptoms can be present between cycles • The criteria should be fulfilled for the last three months with symptom onset at least six months before diagnosis.
- 56. Supportive criteria • Historyor family history of migraine headaches. • North American Society for Pediatric Gastroenterology Hepatology and Nutrition — Recommendations apply to children and adolescents (all must be met) At least five attacks in any interval, or a minimum of three attacks during a six- month period Episodic attacks of intense nausea and vomiting lasting 1 hour to 10 days and occurring at least one week apart Stereotypical pattern and symptoms in the individual patient Vomiting during attacks occurs at least four times per hour for at least one hour Return to baseline health between episodes Not attributed to another disorder
- 57. Treatment • antimigraine medications •coenzyme Q10 is 10 to 20 mg/kg per day, or 200 mg twice daily • L-carnitine is 50 or 100 mg/kg per day, or one gram twice daily • During vomiting episodes intravenous administration of a 10 percent dextrose solution can decrease the frequency and duration of vomiting episodes high dose ondansetron (0.3 to 0.4mg/kg/dose, max 20 mg/dose) sedation (eg, with diphenhydramine or lorazepam) quiet, dark room are often helpful.
- 58. Evaluation of nauseaand vomiting of pregnancy • Hyperemesis gravidarum severe end of the symptom spectrum (weight loss exceeding 5 percent of prepregnancy body weight) • no universally accepted criteria distinguish between mild and severe disease
- 59. Sequelae Of Vomiting -Aspiration: altered mental status low or depressed level of consciousness extremely repetitive cycles lead to aspiration of gastric contents aspiration pneumonia
- 60. Mallory Weiss Syndrome Dueto sever and repetitive retching and vomiting partial tear of the mucosa and sub-mucosa in the stomach & gastroesophageal junction Bleeding
- 61. Boerhaave's Syndrome : Dueto repetitive extreme prolonged bouts of retching and vomiting full tear of all the layers of the esophagus most commonly the posterolateral lower part of the esophagus
- 62. Hypovolemia due to alot of vomiting high water volume content and sodium and chloride will be lost contraction of the extracellular fluid space activation of the Renin – Angiotensin – Aldosterone system .
- 63. Electrolyte Imbalance : MainlyHypokalemia Volume depletion Hyperaldosteronism Increased re-absorption of Sodium Increased Excretion of large amounts of Potassium in the urine
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