• Prevalence: Nausea affects up to 50% of adults in community surveys over a given year. It is one of the top 10 reasons for primary care visits.
• Emergency presentations: Nausea/vomiting account for ~5% of all emergency department visits.
• Hospitalised patients: Extremely common; post-operative nausea and vomiting (PONV) affects 25–30% of all surgical patients (up to 80% in high-risk groups) ^[2].
• Hong Kong context: Gastroenteritis (both viral and bacterial, particularly Norovirus and food-borne pathogens) is a leading cause in the community. Early pregnancy-related nausea ("morning sickness") is almost universal (70–80% of pregnancies).

Risk factors for PONV include ^[2]:

• Patient: Young female, non-smoker, early pregnancy, previous history of PONV / motion sickness, obesity
• Anaesthetics: GA > RA, opioids, inhalational agents (→ try to use IV propofol)
• Surgery: Eye, ENT, laparoscopy (abdominal / pelvic)
• Post-op: pain, movement, hypotension

The "vomiting centre" is not a discrete anatomical nucleus but rather a network of loosely organised neurons in the medulla oblongata (within the lateral reticular formation, near the nucleus tractus solitarius [NTS]). It coordinates the motor act of vomiting.

• Key receptors at the vomiting centre: muscarinic acetylcholine (mACh) receptors ^[2]
• It receives input from four main sources (detailed below).

The NTS is the crucial relay and integration centre. It receives input from all four sources above and projects to the vomiting centre. Key receptors here include mACh and H1 receptors ^[2].

Once the vomiting centre is activated, the coordinated motor output includes:

1. Pre-ejection phase: Retrograde giant contraction of small intestine → duodenal/gastric relaxation → nausea and retching.
2. Ejection phase:
   • Deep inspiration against closed glottis (↑intrathoracic pressure).
   • Forceful contraction of diaphragm and abdominal wall muscles (↑intra-abdominal pressure).
   • Relaxation of lower oesophageal sphincter (LOS) and oesophageal body.
   • Retrograde expulsion of gastric contents.
3. Protective reflexes: Elevation of soft palate (closes nasopharynx), laryngeal closure (protects airway), salivation (protects dental enamel from acid).

Efferent pathways involve:

• Vagus nerve (CN X): to GI tract smooth muscle
• Phrenic nerve: to diaphragm
• Spinal nerves: to abdominal wall muscles

Hong Kong–specific considerations:

• Norovirus gastroenteritis is extremely common in Hong Kong, especially in winter (October–March), often in institutional outbreaks.
• Food poisoning ^[1] from seafood (V. parahaemolyticus, V. cholerae), raw pork (Streptococcus suis), and undercooked poultry (Salmonella, Campylobacter) is prevalent.
• Hepatitis B is endemic (8% chronic carrier rate) — acute flares or hepatocellular carcinoma can present with nausea/vomiting.
• Gastric cancer remains an important diagnosis in the Hong Kong Chinese population (higher incidence than Western populations) ^[5].

Drugs are a major cause (multiple) ^[1]. Think of the mechanism for each:

Pregnancy (early) is listed as a key pitfall ^[1].

• Nausea and vomiting of pregnancy (NVP): Affects 70–80% of pregnant women, typically weeks 6–12 (peaks at 9 weeks), usually resolves by week 20.
• Mechanism: hCG surge stimulates CTZ (via thyrotropic cross-reactivity and direct effects); also oestrogen/progesterone → ↓LOS tone and ↓gastric motility.
• Hyperemesis gravidarum: Severe end of the spectrum — persistent vomiting leading to > 5% weight loss, dehydration, ketonuria, electrolyte disturbances. Incidence ~0.3–3%.

Is the patient trying to tell me something? Possibly: extreme stress and anxiety (e.g. panic attacks). Consider bulimia (self-induced vomiting) and functional (psychogenic). ^[1]

• Post-operative nausea and vomiting (PONV) ^[2]: Multifactorial — anaesthetic agents stimulate CTZ (inhalational agents), opioid analgesics, surgical manipulation activates visceral afferents, pain, hypotension.
• Post-embolisation syndrome ^[16]: After TOCE for HCC — nausea, vomiting, abdominal pain, loss of appetite, fever ^[16]. Mechanism: tumour necrosis releasing inflammatory mediators.

Bilious vomiting in a neonate is a surgical emergency until proven otherwise — it strongly suggests malrotation with midgut volvulus, which can lead to complete midgut infarction within hours.

Malignancy is listed separately as a "serious disorder not to be missed" ^[1]. Key points:

• Gastric cancer ^[5][22]: Nausea and vomiting from GOO (distal tumours) or poor distensibility (linitis plastica); also early satiety, weight loss, anaemia. Presenting features: weight loss (62%), abd pain (52%), nausea (34%) ^[22]
• Oesophageal cancer: Progressive dysphagia (solids → liquids) with regurgitation
• Pancreatic cancer: Epigastric pain radiating to back, jaundice, weight loss; GOO from head of pancreas tumour compressing duodenum
• Brain tumours: Vomiting ↑when exertion/cough and worse when supine ^[11] — from raised ICP

Intracranial disorders: malignancy, cerebellar haemorrhage, PICA infarction ^[1]

• NVP (weeks 6–12): most common; diagnosis of exclusion
• Hyperemesis gravidarum: > 5% weight loss, ketonuria, electrolyte disturbance
• Molar pregnancy: exaggerated NVP, uterus large for dates, very high β-hCG
• Ectopic pregnancy: pelvic pain + vaginal bleeding + positive β-hCG; vomiting from peritoneal irritation if ruptured

• PONV ^[2]: onset within 24 hours; risk factors as per previous section
• Prolonged paralytic ileus ^[6]: onset post-op day 4 or later; rule out surgical complications
• Adhesive SBO: especially if previous abdominal surgery; colicky pain, distension, absolute constipation
• Anastomotic leak: fever, tachycardia, peritoneal signs, rising inflammatory markers

The elderly deserve special attention because:

• Atypical presentations are the norm: MI may be painless ^[1][24]; meningitis may lack neck stiffness; UTI may present only with vomiting and confusion
• Polypharmacy: drugs (multiple) ^[1] is a leading cause
• Malignancy: gastric, pancreatic, and brain tumours are more common
• Metabolic: uraemia ^[1], hypercalcaemia ^[1] (from malignancy or hyperparathyroidism)

As discussed in the previous sections, the structured history should cover:

Diagnostic tips from lectures ^[1]: The common cause of acute nausea and vomiting in most age groups is gastroenteritis.

Key examination ^[1] highlights what the physical examination should focus on. Let's expand this with the pathophysiological rationale for each component:

These are rapid, cheap, and can immediately change your management.

These are the "standard panel" you should order for virtually any patient with significant or unexplained nausea and vomiting. The lecture slides explicitly state: Look for the cause and also consider biochemical abnormalities resulting from fluid and electrolyte loss ^[1].

Interpretation of electrolyte abnormalities from vomiting — a worked example:

Suppose your bloods come back showing Na⁺ 131, K⁺ 2.8, Cl⁻ 88, HCO₃⁻ 34, urea 12, creatinine 95. What does this tell you?

• Hypokalaemia (K⁺ 2.8): Loss of K⁺ from vomiting (small direct loss) + renal K⁺ wasting (secondary hyperaldosteronism from hypovolaemia + alkalosis driving K⁺ into cells → kidneys exchange Na⁺ for K⁺ to compensate)
• Hypochloraemia (Cl⁻ 88): Direct loss of HCl in gastric fluid
• Metabolic alkalosis (HCO₃⁻ 34): Loss of H⁺ in gastric acid → unopposed alkaline tide; maintained by chloride depletion (kidneys can't excrete HCO₃⁻ without Cl⁻)
• Mild hyponatraemia (Na⁺ 131): Na⁺ lost in vomitus + ADH-driven water retention from hypovolaemia → dilutional effect
• ↑Urea (12) with normal-ish creatinine (95): Pre-renal state — urea is preferentially reabsorbed in hypovolaemia (↑urea:creatinine ratio)

This electrolyte pattern — hypokalaemic, hypochloraemic metabolic alkalosis — is the hallmark of prolonged vomiting and should prompt you to think about the underlying cause (GOO, pyloric stenosis, bulimia) while initiating IV NS with KCl replacement.

These are ordered when first-line workup is inconclusive or when a specific diagnosis is suspected:

Diagnostic criteria ^[7]:

• Hyperglycaemia: plasma glucose > 14 mmol/L
• HAGMA: arterial pH < 7.3, plasma HCO₃⁻ < 15 mmol/L ± ↑anion gap
• Ketosis: moderate ketonuria or ketonaemia or ↑serum β-hydroxybutyrate (BHBA)

Why these three? DKA is defined by the triad of uncontrolled glucose (insulin deficiency), ketone production (unrestrained lipolysis → hepatic ketogenesis), and acidosis (ketoacids overwhelm buffering capacity).

Diagnostic criteria (Revised Atlanta classification, 2013) ^[34]: Fulfilment of 2 out of 3:

• Clinical: typical epigastric pain
• Lab: serum amylase or lipase > 3× ULN
• Imaging findings (USG/CT/MRI)

Important nuance: Imaging is typically only required if amylase/lipase is negative but clinical suspicion remains high ^[36]. You do NOT need a CT to diagnose pancreatitis if the clinical picture and enzyme levels are clear.

Enzyme details ^[34]:

• Serum amylase: rise within 6-12h of onset, normalize in 3-5 days
• Serum lipase: rise within 4-8h of onset, normalize in 8-14 days (longer t½)
• False positive amylase: PPU, ruptured AAA, DKA, macroamylasemia ^[34]
• Prolonged elevation indicates complications e.g. pancreatic pseudocyst ^[34]

Modified Alvarado score (MANTREL) ^[37]:

Interpretation ^[37]:

• 0-3 points → unlikely to have acute appendicitis → evaluate for other diagnoses
• 4-6 points → should consider imaging before surgery
• 7 points → surgical exploration if imaging unavailable, otherwise consider imaging

No formal "diagnostic criteria" but radiological criteria on AXR are well-established:

• Proximal dilatation ( > 3cm SB, > 5cm LB, > 9cm caecum) with distal collapse ^[36]
• *** > 5 air-fluid levels on erect AXR diagnostic of IO*** ^[36]
• Transition point identified on CT confirms mechanical obstruction and often reveals the cause

Chronic nausea and vomiting disorder (CNVD) — Rome IV criteria:

• Bothersome nausea occurring ≥ 1 day per week AND/OR ≥ 1 episode of vomiting per week
• Self-induced vomiting and eating disorders excluded
• No evidence of organic disease to account for symptoms (including OGD, metabolic screen)
• Criteria fulfilled for the last 3 months with symptom onset ≥ 6 months before diagnosis

Cyclic vomiting syndrome (CVS) — Rome IV criteria:

• Stereotypical episodes of vomiting regarding onset (acute) and duration ( < 1 week)
• ≥ 3 discrete episodes in the prior year AND ≥ 2 episodes in the past 6 months, occurring ≥ 1 week apart
• Absence of vomiting between episodes (but other milder symptoms can be present between episodes)
• Not attributable to another disorder

No universally accepted formal criteria, but commonly defined as:

• Persistent vomiting in pregnancy not due to other causes
• Acute starvation (ketonuria on urine dipstick)
• Weight loss ≥ 5% of pre-pregnancy weight
• Electrolyte derangement (typically hypokalaemic metabolic alkalosis)

• Positioning: Lateral (recovery) position if reduced consciousness — prevents aspiration of vomitus into the airway.
• NGT insertion: For ongoing vomiting, especially in bowel obstruction, gastroparesis, or reduced consciousness.
  • Placed on free drainage with 4-hourly aspiration ^[39] or continuous/intermittent suction ^[40].
  • Functions: decompression proximal to obstruction; reduce risk of aspiration during induction of anaesthesia and post-extubation ^[39].
  • Aspirate stomach if unconscious or vomiting ± ETT for airway protection if necessary ^[7].
• Intubation: If GCS ≤ 8, ongoing haematemesis with airway compromise, or before OGD in unstable patients with massive upper GI bleeding.

The fluid of choice is dictated by the metabolic consequence:

Potassium replacement is almost always needed in prolonged vomiting:

• Target K⁺ 3.5–5.0 mmol/L
• Give KCl 10–40 mmol/L in IV fluids (max rate 10–20 mmol/h peripherally, up to 40 mmol/h centrally with cardiac monitoring)
• Replace K first if K < 3.3 before giving insulin in DKA ^[7] — why? Because insulin drives K⁺ into cells, and giving insulin to a profoundly hypokalaemic patient can cause fatal arrhythmia.

Treatment targets the maintenance factors:

• Treat underlying cause: remove NG aspiration, treat vomiting, stop diuretics ^[44]
• Saline repletion to ↑volume, ↑Cl⁻ in saline-responsive cases (i.e. volume-depleted ones) ^[44]
• Potassium repletion to ↑K⁺ ^[44]
• Acetazolamide (carbonic anhydrase inhibitor) to ↓HCO₃⁻ reabsorption in PCT ^[44] — for refractory cases
• Dialysis in those with AKI or CKD (cannot excrete HCO₃⁻) ^[44]

Drug ingestion is a common cause of nausea and vomiting so check for prescribed drugs and illicit street drugs such as heroin and ecstasy ^[1].

• First step: Always review and withdraw or substitute the offending drug if possible.
• Opioid-induced: Switch to alternative opioid; add anti-emetic (ondansetron or metoclopramide). Tolerance usually develops within 3–5 days.
• Chemotherapy-induced (CINV): See dedicated section below (Section 5.3).
• Digoxin toxicity: Withhold digoxin; check level; digoxin-specific antibodies (DigiFab) if life-threatening arrhythmia.

Risk factors for PONV ^[2]:

• Patient: Young female, non-smoker, early pregnancy, previous Hx of PONV / motion sickness, obesity
• Anaesthetics: GA > RA, opioids, inhalational agents (→ try to use IV propofol)
• Surgery: Eye, ENT, laparoscopy (abdominal / pelvic)
• Post-op: pain, movement, hypotension

Prevention (high-risk patients):

• Use IV propofol instead of inhalational agents for induction/maintenance ^[2]
• Minimise opioid use (multimodal analgesia: paracetamol, NSAIDs, regional anaesthesia)
• Prophylactic anti-emetics: dexamethasone 4–8mg at induction + ondansetron 4mg at end of surgery (combination more effective than either alone)
• Adequate hydration

Treatment (if PONV occurs):

• Ondansetron 4mg IV (first-line)
• ± dexamethasone 4–8mg IV if not already given
• ± droperidol 0.625–1.25mg IV or prochlorperazine 12.5mg IM
• Ensure adequate pain control and hydration

This table ties together the pharmacology and the clinical scenario:

Chemotherapy-induced nausea and vomiting is classified by timing:

• Acute ( < 24h): Primarily 5-HT mediated (enterochromaffin cell damage → 5-HT release → vagal 5-HT3)
• Delayed (24h–5 days): Primarily substance P / NK1 mediated
• Anticipatory: Conditioned response (higher centres)

Standard prophylaxis for highly emetogenic chemotherapy (e.g. cisplatin):

For moderately emetogenic chemotherapy: 5-HT3 antagonist + dexamethasone ± NK1 antagonist.

For any patient with bowel obstruction or surgical abdomen with vomiting ^[39][40]:

1. NPO (nil per os) ^[39] — to limit further bowel distension
2. IV fluids: crystalloids (NS, Ringer's lactate, Hartmann's) ^[39] — replace losses including third-space sequestration
3. NGT decompression ^[39][40] — "suck" component; reduces aspiration risk
4. K⁺ replacement ^[39] — but given cautiously in patients with AKI from severe dehydration ^[39]
5. Pain relief: opioids are reasonable ^[39] — although caution as they ↓GI motility
6. Broad-spectrum antibiotics: mandatory for all patients undergoing surgery for intestinal obstruction ^[39]
7. Gastrografin meal and follow-through ^[39] — both diagnostic (level and completeness of obstruction) and therapeutic

N/V in DKA is treated by treating the DKA — the anti-emetic is insulin, not ondansetron:

• Aspirate stomach if unconscious or vomiting ± ETT for airway protection ^[7]
• Fluid + insulin + K ^[7] — as per the DKA protocol
• Anti-emetics (ondansetron, metoclopramide) may provide symptomatic relief but are adjunctive

GI upset: abdominal discomfort, anorexia, nausea/vomiting is common with anti-TB drugs ^[47]:

• Should exclude hepatitis (ensure ALT < 3× and total bilirubin > 2× ULN) ^[47]
• Symptomatic relief: administer with food ± antiemetic (but should avoid antacids → ↓H/R absorption) ^[47]
• Other measures: consider daily regimens (instead of intermittent) or fixed combination drugs ^[47]

Mechanism: Each episode of vomiting expels gastric fluid (containing water, Na⁺, K⁺, Cl⁻, H⁺). Concurrently, oral intake is reduced or impossible due to nausea. The result is progressive negative fluid balance.

Clinical features: Dry mucous membranes, ↓skin turgor, sunken eyes, tachycardia, postural hypotension, ↓urine output, ↑urine specific gravity.

Why it matters: Hypovolaemia → ↓cardiac output → ↓renal perfusion → pre-renal acute kidney injury (AKI). In bowel obstruction, the problem is compounded by fluid sequestration in bowel lumen ("third-space loss") ^[48] — fluid is trapped in the dilated bowel proximal to the obstruction and is functionally lost from the circulation even though it hasn't left the body.

Dehydration and electrolyte loss in intestinal obstruction arises from: decreased oral intake, loss due to vomiting, defective intestinal absorption, fluid sequestration in bowel lumen, transudation of fluid into extracellular space and peritoneal cavity ^[48].

This is the signature electrolyte disturbance of prolonged vomiting and is a favourite exam topic. Let's trace it step by step from first principles:

1. Loss of HCl in vomitus: Gastric parietal cells secrete H⁺ and Cl⁻ into the stomach lumen. Normally, when this acid reaches the duodenum, it stimulates pancreatic HCO₃⁻ secretion, neutralising the "alkaline tide" (the HCO₃⁻ that entered the blood when the parietal cell made HCl). When you vomit, H⁺ is lost before reaching the duodenum → the alkaline tide goes unopposed → metabolic alkalosis.

2. Hypochloraemia: Direct loss of Cl⁻ in gastric juice. This is critical because Cl⁻ depletion maintains the alkalosis — the kidney cannot excrete HCO₃⁻ efficiently without adequate Cl⁻ (the principal anion exchange partner in the collecting duct).

3. Hypokalaemia: Through three mechanisms:

   • Small direct K⁺ loss in vomitus (gastric K⁺ concentration is only ~5-10 mmol/L, so direct loss is modest)
   • Renal K⁺ wasting — hypovolaemia activates the RAAS → aldosterone drives Na⁺ reabsorption at the expense of K⁺ and H⁺ excretion in the collecting duct
   • Transcellular shift — alkalosis drives K⁺ into cells (H⁺ comes out of cells to buffer the alkalosis; K⁺ goes in to maintain electrical neutrality)

4. Paradoxical aciduria: Despite systemic alkalosis, the urine becomes acidic. Why? The kidneys are desperately reabsorbing Na⁺ (because the patient is hypovolaemic) and excreting H⁺ instead of K⁺ when K⁺ is severely depleted — perpetuating both the alkalosis and the hypokalaemia in a vicious cycle.

Clinical significance: Severe hypokalaemia (K⁺ < 2.5 mmol/L) → muscle weakness, paralytic ileus, cardiac arrhythmias (U waves on ECG, risk of torsades de pointes). Severe alkalosis (pH > 7.55) → ↓ionised calcium → tetany, seizures.

Investigation: RFT for hydration status, electrolyte disturbance; ABG for metabolic alkalosis ^[32].

Management: IV 0.9% NaCl + KCl (repletes volume, chloride, and potassium simultaneously).

In the specific context of gastric outlet obstruction: Risk of dehydration and electrolyte abnormalities including hyponatraemia, hypokalaemia and metabolic alkalosis ^[49]. Management includes Normal saline and KCl is administered when indicated for prolonged vomiting leading to hyponatraemia, hypokalaemic, hypochloremic metabolic alkalosis ^[50].

Mechanism: Dual hit — Na⁺ is lost in vomitus (gastric Na⁺ ~20–70 mmol/L), PLUS hypovolaemia triggers ADH release → water retention → dilutional hyponatraemia.

Severity: Usually mild (130–135 mmol/L) in uncomplicated vomiting, but can become moderate-severe in prolonged cases (GOO, hyperemesis gravidarum, bowel obstruction).

Mechanism: Hypovolaemia → ↓renal perfusion → ↓GFR → ↑urea and creatinine. Classic pattern: urea rises disproportionately to creatinine (urea:creatinine ratio > 100:1) because urea is preferentially reabsorbed in the hypovolaemic, slow-flowing proximal tubule.

Significance: Usually rapidly reversible with volume resuscitation, but if unrecognised and prolonged, can progress to acute tubular necrosis (intrinsic renal disease).

Mechanism: Prolonged vomiting → inability to eat → hepatic glycogen depletion (within 24–48h) → gluconeogenesis becomes the only glucose source → simultaneously, lipolysis generates ketone bodies for alternative fuel → starvation ketoacidosis (mild, usually pH > 7.30, low-normal glucose).

Significance: More common in children (lower glycogen reserves) and in hyperemesis gravidarum. Distinguish from DKA (where glucose is high, not low).

Emetogenic injury, eg. Mallory-Weiss tears ^[32][51].

What it is: A longitudinal mucosal tear at the gastroesophageal junction (GEJ), typically on the gastric side (lesser curvature of the cardia).

Mechanism: Forceful retching → sudden ↑↑intra-abdominal pressure against a closed upper oesophageal sphincter → mechanical shearing force at the GEJ (which is the point of maximum stress because it transitions from the negative-pressure thorax to the positive-pressure abdomen) → mucosal tear.

Clinical features: Haematemesis (bright red blood or coffee-ground) following an episode of forceful vomiting. Classically described in alcoholics after a binge/vomiting episode, but can occur with any violent vomiting.

Diagnosis: OGD — reveals a longitudinal mucosal laceration at the GEJ.

Prognosis: 80–90% stop bleeding spontaneously; endoscopic haemostasis (clips, thermal coagulation) for persistent bleeding. Rarely requires angiographic embolisation or surgery.

What it is: A transmural (full-thickness) rupture of the oesophagus, almost always on the left posterolateral distal oesophagus (the weakest point, where it lacks serosal covering).

Mechanism: Same as Mallory–Weiss but the force is greater and the tear extends through all layers (mucosa → submucosa → muscularis → adventitia) → gastric contents and air leak into the mediastinum → mediastinitis and chemical pneumonitis.

Clinical features: "Mackler's triad" — (1) forceful vomiting, (2) lower chest/epigastric pain, (3) subcutaneous emphysema. Also dyspnoea, fever, sepsis. Hamman's sign: mediastinal crunch (crackling sound synchronous with heartbeat on auscultation).

Diagnosis:

• CXR: pneumomediastinum, left-sided pleural effusion, subcutaneous emphysema
• Water-soluble contrast swallow (Gastrografin): demonstrates leak site
• CT thorax with oral contrast: most sensitive

Prognosis: Lethal if untreated (mortality > 90% if delayed > 24h). Requires urgent surgical repair ± drainage of mediastinum and pleura. Earlier presentation has better outcomes with endoscopic stenting or primary repair.

Mechanism: Forceful retching → sudden ↑venous pressure in the head and neck (Valsalva effect) → rupture of small conjunctival capillaries → blood spreads under the bulbar conjunctiva.

Clinical significance: Alarming in appearance but benign and self-limiting (resolves in 1–3 weeks). No treatment needed. Important to reassure the patient.

Mechanism: Same Valsalva mechanism as subconjunctival haemorrhage → venous congestion in the head → rupture of dermal capillaries, particularly in the periorbital region and face.

Clinical significance: Can be a clinical clue to forceful/prolonged vomiting. In children, consider non-accidental injury (NAI) as an alternative cause of facial petechiae.

Mechanism: Forceful retching can cause alveolar rupture (similar mechanism to Valsalva) → air tracks along perivascular sheaths into the mediastinum → pneumomediastinum.

Clinical significance: Usually self-limiting if the oesophagus is intact; but must exclude Boerhaave syndrome with a contrast study.

Mechanism: Vomitus enters the trachea and lower airways. Two distinct processes:

1. Aspiration pneumonitis (Mendelson syndrome): Chemical injury from gastric acid (pH < 2.5) → acute inflammatory response in bronchial and alveolar epithelium → diffuse alveolar damage → pulmonary oedema, hypoxia. Onset is rapid (within hours). Sterile initially.

2. Aspiration pneumonia: Bacterial infection from aspiration of oropharyngeal flora and gastric contents → typically anaerobic and gram-negative organisms → lobar or segmental pneumonia, often in dependent lung segments (right lower lobe if supine, posterior segments if recumbent).

Risk factors ^[52]: Depressed sensorium (eg. stroke, drug intoxication), increased gastro-oesophageal reflux, overfeeding ^[52]. Also: absent gag reflex, supine positioning, ↓consciousness (from any cause including intoxication, anaesthesia, seizures), NGT feeding errors.

Clinical features: Cough, fever, dyspnoea, crackles on auscultation, hypoxia. CXR may show consolidation in dependent segments ± air bronchograms.

Prevention:

• Lateral positioning of vomiting patients with ↓consciousness
• NGT decompression in bowel obstruction/gastroparesis before anaesthesia
• Elevate head of bed to 30–45° during enteral feeding ^[52]
• Pre-operative fasting ("nil by mouth" rules)

Aspiration pneumonia is listed as a complication of intestinal atresia, gastric outlet obstruction, and enteral nutrition across multiple sources ^[49][52][53].

Mechanism: Large food particles or copious vomitus can physically occlude the larynx or trachea → acute upper airway obstruction → asphyxiation.

Risk factors: Reduced consciousness, absent gag reflex, supine position, copious vomiting (e.g. bowel obstruction, massive upper GI bleed).

Management: Emergency suctioning, lateral positioning, basic airway manoeuvres, intubation if needed.

Mechanism: Thiamine (vitamin B1) is a water-soluble vitamin with limited body stores (depleted within 2–3 weeks of inadequate intake). Vomiting → ↓oral intake → rapid depletion. Thiamine is an essential cofactor for pyruvate dehydrogenase (links glycolysis to TCA cycle) and transketolase (pentose phosphate pathway).

Clinical triad: Confusion, ophthalmoplegia (CN III/VI palsies, nystagmus), ataxia. In reality, the complete triad is present in only ~30% of cases — have a low threshold for suspicion.

At-risk populations: Hyperemesis gravidarum, chronic alcoholism, prolonged vomiting of any cause, eating disorders, refeeding.

Prevention: IV thiamine 100mg BEFORE any dextrose-containing fluids.

Why this is dangerous: If you give glucose (IV dextrose) to a thiamine-depleted patient, you accelerate glucose metabolism without the cofactor needed to process pyruvate → lactate accumulates → further neuronal damage. This is why the teaching is: "Thiamine before dextrose, ALWAYS."

Mechanism: Gastric acid (pH ~1–2) repeatedly contacts dental enamel during vomiting → chemical dissolution of enamel. The pattern is characteristic: lingual and palatal surfaces of the upper incisors and molars are affected first (because vomitus flows over these surfaces as it exits the mouth).

Clinical significance: Pathognomonic finding in bulimia nervosa (chronic self-induced vomiting). Also occurs in chronic vomiting of any cause (GERD, gastroparesis, cyclic vomiting syndrome).

Dental consequences: Sensitivity to hot/cold/sweet; yellowing of teeth (dentin becomes visible); ↑caries risk; eventually tooth loss.

Mechanism: Chronic stimulation of the parotid glands by repeated vomiting → hypertrophy and hyperplasia of acinar cells → bilateral, painless parotid enlargement.

Clinical significance: Characteristic finding in bulimia nervosa. Takes weeks to months of repeated vomiting to develop.

Mechanism: Repeated exposure to gastric acid → chemical inflammation of pharyngeal and oesophageal mucosa → sore throat, hoarseness, odynophagia. Can progress to oesophagitis and stricture formation if chronic.

Mechanism: Repeated association of eating with subsequent nausea/vomiting → conditioned food aversion (classical conditioning). The patient subconsciously avoids eating to avoid the unpleasant consequence.

Clinical significance: Leads to further weight loss, malnutrition, and perpetuates the cycle. Particularly problematic in gastroparesis, cyclic vomiting syndrome, and functional nausea.

Mechanism: Chronic N/V → reduced quality of life, inability to work, social isolation, fear of vomiting in public (emetophobia), disrupted sleep → secondary anxiety and depression.

Chronic unexplained N/V can lead to repeated ED visits, hospitalisations, invasive investigations, and opioid prescription (for associated pain), with risk of iatrogenic harm.