Vomiting complete topic medicine final year

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“Vomiting” for final-year medicine can be covered as:
  1. Physiology and vomiting reflex
  2. Causes and clinical classification
  3. History and examination
  4. Red flags and assessment of severity
  5. Investigations
  6. Initial stabilization and fluids/electrolytes
  7. Antiemetic pharmacology
  8. Cause-specific management
  9. Complications and prevention
  10. Important exam cases, differentials, and viva points
At a high level, vomiting is a symptom rather than a diagnosis. Final-year answers should begin with resuscitation and danger signs, then use the clinical pattern to identify gastrointestinal obstruction/inflammation, CNS disease, metabolic or endocrine causes, drugs/toxins, infection, pregnancy, or functional causes. Management combines rehydration, correction of electrolyte abnormalities, appropriate antiemetics, and definitive treatment of the cause.
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Choose the section or format to cover in detail first.

“Vomiting” for final-year medicine can be covered as:
  1. Physiology and vomiting reflex
  2. Causes and clinical classification
  3. History and examination
  4. Red flags and assessment of severity
  5. Investigations
  6. Initial stabilization and fluids/electrolytes
  7. Antiemetic pharmacology
  8. Cause-specific management
  9. Complications and prevention
  10. Important exam cases, differentials, and viva points
At a high level, vomiting is a symptom rather than a diagnosis. Final-year answers should begin with resuscitation and danger signs, then use the clinical pattern to identify gastrointestinal obstruction/inflammation, CNS disease, metabolic or endocrine causes, drugs/toxins, infection, pregnancy, or functional causes. Management combines rehydration, correction of electrolyte abnormalities, appropriate antiemetics, and definitive treatment of the cause.
Which format would help most?Choose what you want next:
  1. Complete exam note: structured final-year notes on vomiting
  2. Approach and management: emergency assessment, fluids, investigations, treatment algorithm
  3. Antiemetic drugs: classes, mechanisms, indications, adverse effects, contraindications
  4. Causes and diagnosis: differential diagnosis with clinical clues
  5. Exam cases and viva: short cases, long-answer framework, common questions

Give me complete final-year notes on vomiting

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vomiting AND management

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Merck Manual nausea vomiting adults evaluation treatment red flags antiemetics

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https://www.merckmanuals.com/professional/gastrointestinal-d…

A complete final-year note on vomiting is a large topic. The exam-oriented map is:
  1. Definitions and differentiation from regurgitation/rumination
  2. Physiology of the emetic reflex
  3. Causes and differential diagnosis
  4. Clinical assessment, red flags, history, and examination
  5. Investigations
  6. Emergency stabilization, fluids, and electrolyte correction
  7. Antiemetic drugs and their adverse effects
  8. Cause-specific management
  9. Complications
  10. Chronic vomiting syndromes, pregnancy, and exam cases
High-yield principle: first identify instability, dehydration, GI obstruction or peritonitis, intracranial pathology, poisoning, and pregnancy. Prolonged gastric fluid loss commonly produces hypochloremic, hypokalemic metabolic alkalosis, requiring saline-based volume replacement and potassium only after urine output is established. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 198-200.
Asking for Preferences

Which section should I write as a detailed final-year note first?

“Vomiting” for final-year medicine can be covered as:
  1. Physiology and vomiting reflex
  2. Causes and clinical classification
  3. History and examination
  4. Red flags and assessment of severity
  5. Investigations
  6. Initial stabilization and fluids/electrolytes
  7. Antiemetic pharmacology
  8. Cause-specific management
  9. Complications and prevention
  10. Important exam cases, differentials, and viva points
At a high level, vomiting is a symptom rather than a diagnosis. Final-year answers should begin with resuscitation and danger signs, then use the clinical pattern to identify gastrointestinal obstruction/inflammation, CNS disease, metabolic or endocrine causes, drugs/toxins, infection, pregnancy, or functional causes. Management combines rehydration, correction of electrolyte abnormalities, appropriate antiemetics, and definitive treatment of the cause.
Which format would help most?Choose what you want next:
  1. Complete exam note: structured final-year notes on vomiting
  2. Approach and management: emergency assessment, fluids, investigations, treatment algorithm
  3. Antiemetic drugs: classes, mechanisms, indications, adverse effects, contraindications
  4. Causes and diagnosis: differential diagnosis with clinical clues
  5. Exam cases and viva: short cases, long-answer framework, common questionsA complete final-year note on vomiting is a large topic. The exam-oriented map is:
  6. Definitions and differentiation from regurgitation/rumination
  7. Physiology of the emetic reflex
  8. Causes and differential diagnosis
  9. Clinical assessment, red flags, history, and examination
  10. Investigations
  11. Emergency stabilization, fluids, and electrolyte correction
  12. Antiemetic drugs and their adverse effects
  13. Cause-specific management
  14. Complications
  15. Chronic vomiting syndromes, pregnancy, and exam cases
High-yield principle: first identify instability, dehydration, GI obstruction or peritonitis, intracranial pathology, poisoning, and pregnancy. Prolonged gastric fluid loss commonly produces hypochloremic, hypokalemic metabolic alkalosis, requiring saline-based volume replacement and potassium only after urine output is established. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 198-200.# Vomiting (Emesis): Final-Year Medicine Notes

1. Definitions

  • Nausea: unpleasant subjective sensation of an urge to vomit, often associated with salivation, sweating, pallor, anorexia, and anxiety.
  • Retching: repeated spasmodic respiratory and abdominal contractions against a closed glottis, without expulsion of gastric contents.
  • Vomiting / emesis: forceful expulsion of gastric or intestinal contents through the mouth.
  • Regurgitation: effortless return of gastric or esophageal contents to the mouth, without nausea, retching, or forceful abdominal contraction.
    • Esophageal regurgitation: recently eaten, undigested food, as in achalasia.
    • Gastric regurgitation: sour material, often with heartburn, as in GERD.
  • Rumination syndrome: repetitive, effortless regurgitation of recently ingested food, usually soon after meals, which may be rechewed, reswallowed, or spat out.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 191-192.

2. Physiology of vomiting

Vomiting is coordinated by a brainstem network, principally involving the nucleus tractus solitarius and medullary vomiting centers.

Main afferent inputs

SourceImportant causes
GI tract via vagal and sympathetic afferentsgastroenteritis, obstruction, gastritis, pancreatitis
Chemoreceptor trigger zone (CTZ), area postremadrugs, toxins, uremia, DKA, chemotherapy
Vestibular apparatusmotion sickness, labyrinthitis, Ménière disease
Higher cortical centersanxiety, fear, unpleasant sights/smells, raised intracranial pressure
Other organsmyocardial infarction, renal colic, testicular torsion

Important receptors

  • 5-HT3 (serotonin): vagal afferents and CTZ
  • D2 (dopamine): CTZ
  • H1 histamine and M1 muscarinic: vestibular pathway
  • NK1 (substance P): central vomiting pathways
  • Cannabinoid receptors: modulate emetic pathways

Sequence

  1. Nausea, salivation, pallor, tachycardia
  2. Retching with closure of glottis
  3. Relaxation of lower esophageal sphincter
  4. Diaphragm and abdominal-wall contraction
  5. Expulsion of gastric contents while airway is protected by glottic closure

3. Causes of vomiting

A useful exam classification is by system.

A. Gastrointestinal causes

Acute causes

  • Acute gastroenteritis and food poisoning
  • Gastritis, peptic ulcer disease
  • Acute appendicitis
  • Acute cholecystitis or biliary colic
  • Acute pancreatitis
  • Hepatitis
  • Intestinal obstruction
  • Perforated viscus with peritonitis
  • Mesenteric ischemia
  • Diverticulitis
  • Incarcerated hernia
  • Gastric volvulus

Mechanical obstruction

SiteTypical pattern
Gastric outlet obstructionLarge-volume, non-bilious vomiting; retained food; early satiety; succussion splash
Proximal small-bowel obstructionEarly, profuse, often bilious vomiting; little distension
Distal small-bowel obstructionColicky pain, central distension, vomiting occurs later
Large-bowel obstructionMarked distension and constipation; vomiting late, sometimes feculent
Bilious vomiting suggests obstruction distal to the ampulla of Vater, unless there is another explanation.

Chronic GI causes

  • Peptic-ulcer-related gastric outlet obstruction
  • Gastric cancer
  • Gastroparesis, especially diabetic
  • Chronic intestinal pseudo-obstruction
  • Crohn disease with stricture
  • Coeliac disease
  • Achalasia or other esophageal motor disorders
  • Functional dyspepsia
  • Rumination syndrome

B. CNS and vestibular causes

  • Raised intracranial pressure due to tumor, hemorrhage, hydrocephalus, abscess
  • Meningitis, encephalitis
  • Migraine
  • Posterior circulation stroke
  • Vertigo, vestibular neuritis, labyrinthitis, Ménière disease
  • Head injury
  • Motion sickness
Early-morning vomiting with headache, papilledema, altered behavior, or focal neurologic signs suggests raised intracranial pressure.

C. Metabolic and endocrine causes

  • Diabetic ketoacidosis
  • Uremia
  • Adrenal insufficiency / Addisonian crisis
  • Hypercalcemia
  • Hyponatremia
  • Thyrotoxicosis
  • Acute intermittent porphyria
  • Severe metabolic acidosis
  • Pregnancy, especially hyperemesis gravidarum

D. Drugs, toxins, and substances

  • Opioids
  • NSAIDs
  • Digoxin toxicity
  • Theophylline toxicity
  • Antibiotics, especially macrolides
  • Metformin
  • Levodopa and dopamine agonists
  • Chemotherapy
  • Radiotherapy
  • Alcohol intoxication or withdrawal
  • Organophosphate poisoning
  • Salicylate toxicity
  • Iron poisoning
  • Cannabis: cannabinoid hyperemesis syndrome
  • Ingestion of toxins or corrosives

E. Infection and systemic disease

  • Sepsis
  • Malaria
  • COVID-19 or influenza-like viral illness
  • Pyelonephritis
  • Myocardial infarction, especially inferior-wall MI
  • Renal colic
  • Acute glaucoma
  • Testicular torsion
  • Severe pain of any cause

F. Psychiatric and functional causes

  • Anxiety disorders
  • Eating disorders, especially bulimia nervosa
  • Functional vomiting
  • Cyclic vomiting syndrome
  • Psychogenic vomiting
  • Rumination syndrome

4. Clinical assessment

A. Immediate priorities

Use an ABCDE approach in severe vomiting.

Assess urgently for:

  • Shock or severe dehydration
  • Reduced consciousness and aspiration risk
  • Acute abdomen or peritonitis
  • GI obstruction
  • GI bleeding
  • Raised intracranial pressure
  • DKA, uremia, adrenal crisis, or sepsis
  • Toxic ingestion
  • Pregnancy-related hyperemesis

Red flags

  • Hematemesis or coffee-ground vomitus
  • Bilious vomiting
  • Feculent vomiting
  • Severe abdominal pain, guarding, rigidity, or rebound tenderness
  • Marked abdominal distension with obstipation
  • Hypotension, oliguria, syncope, confusion
  • Fever with neck stiffness, rash, or photophobia
  • Severe headache, focal neurologic deficit, altered consciousness, papilledema
  • Persistent vomiting with weight loss or anemia
  • New vomiting in older age
  • Vomiting after head injury
  • Poisoning, overdose, or suspected toxic ingestion
The clinician should always consider pregnancy in a patient of childbearing potential. Merck Manual guidance also emphasizes acute abdominal and intracranial warning features.

B. History

Characterize the vomiting

Ask about:
  • Onset: acute or chronic
  • Frequency and volume
  • Relation to meals
  • Projectile or non-projectile
  • Contents:
    • Undigested food: achalasia, gastroparesis, gastric outlet obstruction
    • Bilious: distal duodenal or small-bowel obstruction
    • Feculent: distal intestinal obstruction
    • Blood or coffee-ground material: upper GI bleeding
  • Associated retching
  • Relief after vomiting
  • Relation to posture, motion, stress, migraine, or menstruation

Associated symptoms

SymptomsLikely diagnostic direction
Diarrhea, cramps, fevergastroenteritis
Colicky pain, distension, constipationintestinal obstruction
Severe epigastric pain radiating to backpancreatitis
Right-upper-quadrant painbiliary disease/hepatitis
Periumbilical pain moving to right iliac fossaappendicitis
Headache, visual symptoms, focal deficitCNS lesion / raised ICP
Vertigo, tinnitus, hearing lossvestibular disease
Polyuria, polydipsia, weight lossdiabetes / DKA
Amenorrhea, breast tendernesspregnancy
Flank pain, hematuriaureteric colic
Chest pain, sweating, dyspneaacute coronary syndrome
Hot bathing with chronic cannabis usecannabinoid hyperemesis syndrome

Relevant background

  • Medication review, including prescribed, OTC, herbal, recreational drugs
  • Alcohol and cannabis use
  • Diabetes, kidney disease, migraine, malignancy
  • Previous abdominal surgery or hernia
  • Previous similar attacks
  • Weight loss, dysphagia, early satiety
  • Travel, food exposure, sick contacts
  • Menstrual and obstetric history
  • Psychological stress, eating disorder behavior, self-induced vomiting

C. Examination

General examination

  • Hydration: dry tongue, poor skin turgor, thirst
  • Pulse, BP including postural BP, temperature, respiratory rate
  • Mental status
  • Weight and nutritional state
  • Pallor, jaundice, lymphadenopathy
  • Signs of endocrine disease
  • Peripheral edema or features of chronic organ failure

Abdominal examination

  • Distension
  • Scars and hernias
  • Bowel sounds:
    • High-pitched/tinkling: mechanical obstruction
    • Silent abdomen: ileus or peritonitis
  • Tenderness and localization
  • Guarding, rigidity, rebound tenderness
  • Palpable mass or organomegaly
  • Succussion splash: retained gastric contents, possible gastric outlet obstruction
  • Rectal examination when obstruction, bleeding, impaction, or pelvic pathology is suspected

Neurologic examination

  • Consciousness and cognition
  • Meningism
  • Fundus for papilledema
  • Cranial nerves, nystagmus
  • Cerebellar signs
  • Focal deficits

5. Investigations

Tests should be directed by the clinical diagnosis.

Basic investigations in significant, persistent, or unexplained vomiting

  • CBC
  • Serum electrolytes: sodium, potassium, chloride, bicarbonate
  • Urea, creatinine
  • Blood glucose
  • Liver-function tests
  • Serum amylase/lipase if pancreatitis possible
  • Urinalysis, ketones
  • Urine or serum beta-hCG in all patients who may be pregnant
  • ECG, particularly if electrolyte disturbance, cardiac symptoms, or QT-prolonging antiemetics are being considered
  • Venous or arterial blood gas in severe illness, DKA, sepsis, poisoning, or major acid-base disturbance
Recommended baseline evaluation for acute vomiting includes blood count, kidney function, thyroid and liver tests, electrolytes, glucose, amylase/lipase, and targeted toxicology when indicated. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 198.

Imaging and special tests

Clinical concernInvestigation
Suspected obstruction/perforationCT abdomen/pelvis with contrast when appropriate; abdominal radiograph may be used initially in selected settings
Biliary diseaseUltrasound abdomen
Pancreatitis complicationsContrast CT if indicated
Upper GI lesion, obstruction, cancerUpper GI endoscopy
GastroparesisGastric emptying study after exclusion of obstruction
CNS disease / raised ICPCT head urgently if unstable or suspected hemorrhage; MRI brain when appropriate
Meningitis/encephalitisBlood cultures, neuroimaging if needed before lumbar puncture, then CSF testing
Cardiac ischemiaECG, serial troponins
Toxic ingestionTargeted toxicology and poison-center advice
For chronic vomiting, endoscopy, contrast studies, CT/MR enterography, brain imaging, and motility studies are selected according to the suspected disorder. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 198.

6. Complications

A. Fluid and electrolyte complications

  • Dehydration
  • Hypovolemia and shock
  • Acute kidney injury
  • Hypochloremic, hypokalemic metabolic alkalosis
  • Hyponatremia
  • Hypomagnesemia
  • Cardiac arrhythmias
  • Muscle weakness, cramps, tetany
Gastric loss removes hydrogen and chloride ions. Volume depletion activates RAAS, increasing renal potassium and hydrogen loss, which sustains metabolic alkalosis.

B. Mechanical and respiratory complications

  • Aspiration pneumonitis or aspiration pneumonia
  • Mallory-Weiss tear causing hematemesis
  • Boerhaave syndrome: spontaneous esophageal rupture after forceful vomiting
  • Pneumomediastinum
  • Dental enamel erosion
  • Parotid enlargement in recurrent self-induced vomiting

C. Nutritional complications

  • Weight loss and protein-calorie malnutrition
  • Thiamine deficiency, especially in prolonged vomiting and hyperemesis gravidarum
  • Wernicke encephalopathy if carbohydrate is given before thiamine in a severely malnourished person
  • Vitamin and trace-element deficiencies
Protracted vomiting can rapidly cause hypotension, oliguria, arrhythmia, and hypochloremic alkalosis. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 199.

7. Management

A. General principles

  1. Stabilize the patient
  2. Assess aspiration risk
  3. Correct fluid and electrolyte deficits
  4. Identify surgical, neurologic, metabolic, infectious, toxic, and pregnancy-related causes
  5. Give an antiemetic appropriate to the cause
  6. Treat the underlying disease
  7. Monitor response and reassess frequently

B. Immediate supportive management

If unstable or severely dehydrated

  • Keep nil by mouth initially if active vomiting, obstruction, or surgery is possible.
  • Position laterally if drowsy or vomiting to reduce aspiration.
  • Give oxygen if hypoxemic.
  • Obtain IV access.
  • Give isotonic IV crystalloid, commonly 0.9% saline when chloride depletion/metabolic alkalosis is likely.
  • Monitor BP, pulse, urine output, mental state, and serial electrolytes.
  • Insert urinary catheter in shock, severe dehydration, or need for accurate output monitoring.
  • Consider NG tube decompression for bowel obstruction, gastric outlet obstruction, severe distension, or persistent large-volume vomiting.
  • Correct potassium after ensuring adequate renal function and urine output.
  • Give thiamine before glucose-containing fluids in malnutrition, alcoholism, or prolonged vomiting.
For repeated severe vomiting, IV saline plus potassium replacement after adequate urine output is the standard correction for chloride-depletion alkalosis. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 199-200.

If mild and no danger signs

  • Oral rehydration solution in small frequent sips
  • Advance diet gradually as tolerated
  • Avoid alcohol, excessive fat, and trigger foods
  • Treat the identified cause

8. Antiemetic drugs

Antiemetics should not delay evaluation of obstruction, peritonitis, intracranial pathology, poisoning, or other dangerous conditions.

A. 5-HT3 antagonists

Drugs

  • Ondansetron
  • Granisetron
  • Palonosetron

Uses

  • Acute undifferentiated vomiting
  • Gastroenteritis
  • Postoperative nausea/vomiting
  • Chemotherapy- or radiotherapy-induced nausea/vomiting

Adverse effects

  • Headache
  • Constipation
  • QT prolongation
  • Rare serotonin syndrome, particularly with serotonergic drugs
Ondansetron is commonly a preferred first-line antiemetic when an obstructive GI cause is not suspected because of its relatively favorable adverse-effect profile.

B. Dopamine D2 antagonists / prokinetics

Metoclopramide

Mechanism
  • D2 antagonist in CTZ
  • 5-HT4 agonist promoting gastric emptying
  • Weak 5-HT3 antagonism at higher doses
Uses
  • Gastroparesis
  • Migraine-associated nausea
  • General nausea/vomiting when obstruction is excluded
Adverse effects
  • Acute dystonia
  • Akathisia
  • Parkinsonism
  • Tardive dyskinesia with prolonged use
  • Hyperprolactinemia
  • Diarrhea
Avoid/caution
  • Mechanical bowel obstruction
  • GI perforation or bleeding
  • Parkinson disease
  • Previous dystonic reaction

Prochlorperazine

  • D2 antagonist
  • Useful for severe nausea, vestibular symptoms, migraine-related vomiting
Adverse effects: sedation, hypotension, dystonia, akathisia, QT prolongation.

Domperidone

  • Peripheral D2 antagonist and prokinetic
  • Fewer central extrapyramidal effects than metoclopramide
  • Risk of QT prolongation and arrhythmias
  • Availability varies by country.

C. H1 antihistamines

Drugs

  • Cyclizine
  • Dimenhydrinate
  • Meclizine
  • Promethazine
  • Diphenhydramine

Best uses

  • Motion sickness
  • Vestibular disease
  • Vertigo

Adverse effects

  • Sedation
  • Dry mouth
  • Blurred vision
  • Urinary retention
  • Confusion, especially in older adults

D. Antimuscarinic

Scopolamine / hyoscine

  • Particularly effective for motion sickness and vestibular nausea.
  • Adverse effects: dry mouth, blurred vision, urinary retention, confusion.

E. NK1 antagonists

Drugs

  • Aprepitant
  • Fosaprepitant

Uses

  • Highly emetogenic chemotherapy, usually in combination with a 5-HT3 antagonist and dexamethasone.

Important point

  • Significant drug interactions through CYP pathways.

F. Corticosteroids

Dexamethasone

  • Used mainly in chemotherapy-induced and postoperative vomiting.
  • Also useful in raised intracranial pressure due to tumor-related cerebral edema when indicated.
Adverse effects: hyperglycemia, dyspepsia, insomnia, mood change, infection risk.

G. Other agents

  • Olanzapine: effective in chemotherapy-induced nausea and refractory nausea, but may cause sedation and metabolic adverse effects.
  • Haloperidol: can be used in selected refractory cases, including palliative care; monitor QT interval and extrapyramidal effects.
  • Lorazepam: useful for anticipatory chemotherapy-related nausea and anxiety-associated symptoms, but is not a routine first-line antiemetic.
Antiemetic dosing should follow local hospital policy and individual factors such as QT interval, age, pregnancy, kidney/liver function, and concurrent medications.

9. Cause-specific management

A. Acute gastroenteritis

  • Oral rehydration if possible
  • IV fluids for severe dehydration
  • Ondansetron may facilitate oral intake in selected patients
  • Stool studies only when severe, bloody, prolonged, outbreak-related, immunocompromised, or recent antibiotic-associated illness
  • Antibiotics only for selected proven/suspected bacterial causes

B. Intestinal obstruction

  • NPO
  • IV fluids and electrolyte correction
  • NG decompression when indicated
  • Early surgical review
  • CT abdomen/pelvis to define site and cause
  • Antibiotics if strangulation, perforation, or sepsis suspected

C. Acute pancreatitis

  • IV fluids, analgesia, antiemetics
  • Early enteral nutrition as tolerated
  • Evaluate cause: gallstones, alcohol, hypertriglyceridemia, drugs, hypercalcemia
  • Urgent ERCP if cholangitis or persistent biliary obstruction

D. Biliary colic/cholecystitis

  • Analgesia, antiemetic, IV fluids
  • Ultrasound
  • Antibiotics and early cholecystectomy for acute cholecystitis where appropriate

E. DKA

  • IV fluids
  • IV insulin
  • Potassium-guided replacement
  • Identify and treat precipitant
  • Antiemetic as supportive care only

F. Raised intracranial pressure or CNS emergency

  • Urgent neuroimaging and specialist input
  • Airway protection if reduced consciousness
  • Treat the underlying cause
  • Avoid assuming “gastritis” in a patient with severe headache, neurologic deficit, or altered sensorium

G. Migraine

  • Antiemetic plus migraine-directed therapy such as NSAID, triptan when appropriate, or other acute migraine therapy
  • Metoclopramide or prochlorperazine is commonly useful

H. Motion sickness/vestibular vomiting

  • H1 antihistamine or scopolamine
  • Treat underlying vestibular disorder
  • Short-term vestibular suppressants only when appropriate

I. Gastroparesis

  • Small, low-fat, low-fiber meals
  • Optimize glycemic control in diabetes
  • Metoclopramide for short-term use where appropriate
  • Exclude mechanical obstruction
  • Specialist review for refractory disease

J. Hyperemesis gravidarum

  • Assess dehydration, ketonuria, weight loss, electrolyte disturbance, and alternate diagnoses.
  • IV fluids and electrolyte correction
  • Thiamine before dextrose if prolonged vomiting/malnutrition
  • Pregnancy-compatible antiemetic regimen according to local obstetric guidance
  • Consider admission if unable to tolerate oral intake, has dehydration, electrolyte imbalance, or significant weight loss

K. Cannabinoid hyperemesis syndrome

Clinical clues:
  • Long-term frequent cannabis exposure
  • Recurrent stereotyped vomiting episodes
  • Temporary relief with hot showers/baths
  • Normality between episodes
Management:
  • Cannabis cessation is definitive treatment
  • IV fluids and electrolyte correction
  • Antiemetics may be variably effective
  • Consider topical capsaicin or dopamine antagonist therapy under local protocol

L. Cyclic vomiting syndrome

  • Stereotyped recurrent discrete attacks separated by symptom-free intervals
  • Exclude metabolic, neurologic, obstructive, and toxic causes
  • Acute therapy: hydration, antiemetics, migraine-directed treatment where indicated
  • Prophylaxis and specialist management for recurrent disease

10. Important differential points for exams

FindingImportant diagnoses
Projectile non-bilious vomitinggastric outlet obstruction; in infants, pyloric stenosis
Bilious vomitingsmall-bowel obstruction until proven otherwise
Feculent vomitingdistal intestinal obstruction
Vomiting plus severe epigastric pain to backacute pancreatitis
Vomiting plus colicky abdominal pain and distensionintestinal obstruction
Vomiting plus diarrhea and fevergastroenteritis
Vomiting plus vertigo and nystagmusvestibular disorder or posterior circulation stroke
Morning headache and vomitingraised intracranial pressure
Vomiting, polyuria, polydipsia, abdominal painDKA
Vomiting, weight loss, early satietymalignancy or gastric outlet obstruction
Recurrent vomiting relieved by hot showerscannabinoid hyperemesis syndrome
Recurrent vomiting with normality between attackscyclic vomiting syndrome
Recurrent vomiting with erosive teeth, parotid enlargement, low K+bulimia nervosa
Vomiting with chest pain after forceful retchingBoerhaave syndrome

11. Long-answer structure for “Approach to a patient with vomiting”

In an exam, write in this sequence:
  1. Define vomiting and differentiate it from regurgitation.
  2. Assess severity using ABCDE.
  3. Identify red flags: obstruction, acute abdomen, CNS disorder, GI bleed, sepsis, poisoning, pregnancy.
  4. Take focused history: onset, content, pain, bowel symptoms, neurologic symptoms, drugs/toxins, pregnancy.
  5. Examine hydration, abdomen, neurologic system, and signs of systemic disease.
  6. Order directed investigations: CBC, electrolytes, renal function, glucose, pregnancy test, liver tests, lipase, ECG, imaging as indicated.
  7. Give supportive care: NPO if indicated, IV fluids, potassium replacement, thiamine in prolonged vomiting, aspiration precautions.
  8. Provide appropriate antiemetic.
  9. Treat the underlying cause and involve surgery, gastroenterology, obstetrics, toxicology, or neurology where appropriate.
  10. Monitor urine output, vitals, electrolytes, acid-base status, and nutritional state.

12. Viva questions and short answers

What is the common acid-base disturbance in prolonged vomiting?
Hypochloremic, hypokalemic metabolic alkalosis.
Why does hypokalemia occur?
There is direct potassium loss in vomitus plus renal potassium wasting due to volume depletion, RAAS activation, and alkalosis.
When is vomiting bilious?
Usually when obstruction is distal to the ampulla of Vater or with significant duodenal reflux.
What does feculent vomiting suggest?
Distal intestinal obstruction, often late small-bowel or large-bowel obstruction.
Which antiemetic is useful in gastroparesis?
Metoclopramide, because it has antiemetic and prokinetic actions, provided mechanical obstruction has been excluded.
Which drugs are useful in motion sickness?
H1 antihistamines such as meclizine/dimenhydrinate and antimuscarinic scopolamine.
What is the key management step in cannabinoid hyperemesis syndrome?
Complete cessation of cannabis.
Why give thiamine before glucose in prolonged vomiting?
To prevent precipitating Wernicke encephalopathy in thiamine-depleted patients.
When should an NG tube be considered?
In intestinal obstruction, gastric outlet obstruction, severe distension, persistent large-volume vomiting, or aspiration risk.
What is Boerhaave syndrome?
Transmural esophageal rupture following forceful vomiting, often presenting with severe chest pain, toxicity, and sometimes subcutaneous emphysema. It is a surgical emergency.
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