📋 Key Information Summary
- Nausea and vomiting are symptoms, not diagnoses — always pursue the underlying cause using a systematic age- and mechanism-based approach.
- Red flags demanding urgent assessment include projectile vomiting in neonates, bilious (green) vomiting at any age, haematemesis, signs of raised intracranial pressure, and dehydration ≥5 % body-weight loss.
- Vomiting in adults — categorise by acute (<7 days) versus chronic (>4 weeks), then by suspected mechanism (gastrointestinal, neurological, metabolic/endocrine, drug-induced, pregnancy).
- Hypertrophic pyloric stenosis typically presents at 2–8 weeks of age with progressive non-bilious projectile vomiting; the diagnostic triad is visible peristalsis, palpable olive, and metabolic (hypochloraemic, hypokalaemic) alkalosis.
- Intestinal atresia presents within the first 24–48 hours of life with bilious vomiting and abdominal distension; abdominal X-ray shows a "double-bubble" sign for duodenal atresia — this is a surgical emergency.
- Acute gastroenteritis in Australia is most commonly viral (rotavirus, norovirus); management is primarily oral rehydration therapy (ORT), with ondansetron as an adjunct to facilitate oral intake in moderate-to-severe vomiting.
- Gastroparesis is defined as delayed gastric emptying without mechanical obstruction; the most common cause in Australia is diabetes mellitus; diagnosis requires gastric emptying scintigraphy (4-hour egg-beater study).
- Oral rehydration solution (WHO-ORS) is the first-line fluid for rehydration in acute gastroenteritis across all age groups; intravenous fluids (Normal Saline or Plasmalyte) are reserved for patients unable to tolerate oral intake or with severe dehydration.
- Ondansetron (Zofran®) is the most widely used anti-emetic in Australian general practice and emergency departments; it is available as an orally disintegrating tablet (ODT), making it ideal for vomiting patients.
- Diabetic gastroparesis requires optimisation of glycaemic control (HbA1c target <7 %), dietary modification (small, frequent, low-fat, low-fibre meals), and prokinetic therapy with metoclopramide or domperidone as first-line agents.
- Pregnancy-related nausea and vomiting affects up to 80 % of pregnancies; hyperemesis gravidarum (0.3–3 %) requires IV rehydration, thiamine supplementation, and exclusion of molar pregnancy or other pathology.
- Aboriginal and Torres Strait Islander peoples have higher rates of gastroenteritis-related hospitalisation, delayed presentation, and complications — culturally safe care, health-worker support, and community-based ORT education are essential.
Introduction & Australian Epidemiology
Nausea and vomiting are among the most common presenting complaints across all age groups in Australian general practice and emergency departments. While often self-limiting, these symptoms may signal serious underlying pathology — from life-threatening surgical emergencies in neonates to intracranial pathology or metabolic derangement in adults. A structured, mechanism-based approach is essential to avoid missed diagnoses and unnecessary investigations.
Nausea is the subjective, unpleasant sensation of an urge to vomit, mediated by the vomiting centre in the medulla oblongata. Vomiting (emesis) is the forceful retrograde expulsion of gastric contents through the mouth, coordinated by the vomiting centre receiving inputs from the chemoreceptor trigger zone (CTZ), vagal and sympathetic afferents, the vestibular system, and higher cortical centres.
Australian Burden of Disease
- Acute gastroenteritis accounts for an estimated 17.2 million cases annually in Australia, with ~50,000 hospitalisations and approximately 80 deaths per year (AIHW, 2023). Rotavirus vaccination has reduced rotavirus-coded hospitalisations by over 70 % since its introduction onto the National Immunisation Program (NIP) in 2007.
- Gastroparesis prevalence in the general population is estimated at 1.8–4 %, but rises to 40–50 % in patients with long-standing type 1 diabetes mellitus. Australian hospital admissions for gastroparesis have increased approximately 150 % over the past two decades, driven by rising diabetes prevalence.
- Pyloric stenosis occurs in 2–5 per 1,000 live births in Australia, with a male-to-female ratio of approximately 4:1. It is more common in first-born males and is associated with macrolide antibiotic exposure in the neonatal period.
- Nausea and vomiting of pregnancy (NVP) affects 50–80 % of pregnancies. Hyperemesis gravidarum (HG) complicates 0.3–3.0 % and is the most common reason for hospital admission in the first trimester.
Physiology of Emesis
The vomiting centre (nucleus tractus solitarius and adjacent reticular formation) integrates signals from four key pathways:
- Chemoreceptor trigger zone (CTZ) — located on the floor of the fourth ventricle, outside the blood-brain barrier; detects circulating emetogens (drugs, metabolites, toxins). Targets: dopamine D₂, serotonin 5-HT₃, NK₁ receptors.
- Vagal afferents — from the GI tract (pharynx, stomach, small bowel, hepatobiliary system); primarily serotonergic (5-HT₃) and mechanoreceptor/chemoreceptor mediated.
- Vestibular system — motion sickness; histaminergic (H₁) and muscarinic (M₁) pathways.
- Higher cortical centres — anticipatory, psychogenic, or conditioned vomiting.
Vomiting in Adults — Diagnostic Model
A systematic approach to vomiting in adults involves determining the acuity (acute vs chronic), identifying alarm features, and then considering the most likely mechanism based on clinical context.
Acute vs Chronic Classification
| Feature | Acute Vomiting (<7 days) | Chronic/Recurrent (>4 weeks) |
|---|---|---|
| Common causes | Gastroenteritis, food poisoning, drug side-effect, acute abdomen, migraine, DKA | Gastroparesis, GERD, functional dyspepsia, cyclical vomiting syndrome, chronic medication effect, pregnancy, intracranial pathology |
| Priority | Exclude surgical abdomen, obstruction, MI, raised ICP, metabolic emergency | Exclude malignancy, gastroparesis, Addison disease, medication-related, rumination syndrome |
| Initial workup | FBE, UEC, LFTs, lipase, glucose, β-hCG (women of childbearing age), ECG if cardiac risk | FBE, UEC, LFTs, lipase, glucose, HbA1c, TFTs, cortisol, CT abdomen/pelvis, upper endoscopy, gastric emptying study |
Red Flags — Urgent Referral Required
- Bilious (green) vomiting — suggests proximal bowel obstruction until proven otherwise
- Haematemesis or melaena — upper GI bleeding
- Signs of peritonism or acute abdomen
- Severe headache, altered consciousness, papilloedema — raised intracranial pressure
- Chest pain with vomiting — exclude acute coronary syndrome (inferior MI)
- Severe dehydration: oliguria, hypotension, tachycardia, confusion
- New-onset vomiting in a patient >55 years with weight loss — alarm for malignancy
Mechanism-Based Diagnostic Framework
| Mechanism | Examples | Key Distinguishing Features |
|---|---|---|
| Gastrointestinal obstruction | Small/large bowel obstruction, pyloric stenosis, gallstone ileus, hernia | Colicky pain, distension, constipation/absolute obstipation, high-pitched tinkling bowel sounds, air-fluid levels on AXR |
| Infectious / inflammatory | Gastroenteritis, cholecystitis, pancreatitis, appendicitis, hepatitis | Fever, diarrhoea, localised tenderness, raised inflammatory markers |
| Drug-induced | Opioids, chemotherapy, antibiotics, metformin, SSRIs, digoxin, alcohol | Temporal relationship to medication initiation/dose change |
| Neurological | Raised ICP (tumour, haemorrhage, meningitis), vestibular neuritis, migraine, basilar artery stroke | Headache, vertigo, neurological focal signs, papilloedema, nausea often disproportionate to vomiting |
| Metabolic / endocrine | DKA, uraemia, Addison disease, hypercalcaemia, pregnancy | Biochemical abnormality on UEC/glucose/electrolytes, other endocrine features |
| Functional / motility | Gastroparesis, cyclic vomiting syndrome, functional nausea/vomiting, rumination | Chronic, recurrent, exclusion of organic pathology, Rome IV criteria |
Investigations in Adults
Symptomatic Anti-emetic Therapy in Adults
Vomiting in Infancy
Vomiting is extremely common in infancy, with physiological gastro-oesophageal reflux (GOR) affecting up to 50 % of infants under 3 months. However, persistent or bilious vomiting in a neonate or young infant must be investigated urgently, as several surgical and metabolic emergencies present in this age group.
Approach to Vomiting in Infants
| Feature | Likely Benign (GOR) | Alarm Features |
|---|---|---|
| Vomitus colour | White/milky (non-bilious) | Green (bilious), bloody, or "coffee-ground" |
| Projectile? | No — effortless regurgitation | Yes — forceful, distance projectile |
| Growth | Thriving, appropriate weight gain | Poor weight gain, falling percentiles |
| Distress | Comfortable between feeds | Persistent irritability, lethargy, abdo distension |
| Timing of onset | After feeds, from early weeks | Onset <24 h (atresia) or 2–8 weeks (PJS) |
Hypertrophic Pyloric Stenosis (PJS)
Incidence: 2–5 per 1,000 live births in Australia. Male:female ratio 4:1. Peak presentation 2–8 weeks of age. Associated with first-born males, family history, and macrolide antibiotic exposure in the neonatal period (erythromycin, azithromycin). More common in Caucasian populations.
Hypertrophy and hyperplasia of the circular muscle layer of the pylorus, leading to progressive gastric outlet obstruction. The elongated, thickened pylorus forms a palpable "olive" in the right upper quadrant.
Clinical Features
- Progressive non-bilious projectile vomiting beginning at 2–6 weeks, worsening over days to weeks
- Vomiting typically occurs immediately or within 30 minutes of feeding
- Infant remains hungry after vomiting and wants to feed again
- Visible peristalsis — wave-like movement from left to right across the upper abdomen before vomiting
- Palpable olive — firm, mobile, non-tender mass in the right upper quadrant or epigastrium, best palpated post-vomiting when the stomach is empty (sensitivity ~60–80 % in experienced hands)
- Dehydration, weight loss, and hypochloraemic hypokalaemic metabolic alkalosis in advanced cases
Diagnosis
Management
Intestinal Atresia
Intestinal atresia refers to congenital absence of a segment of the intestinal lumen, presenting in the first 24–48 hours of life with bilious vomiting and abdominal distension. It occurs in approximately 1 in 1,500–5,000 live births.
Types
| Type | Location | Presentation | Imaging |
|---|---|---|---|
| Duodenal atresia | Second part of duodenum (most common) | Bilious vomiting within hours of birth; polyhydramnios antenatally; associated with Down syndrome (30 %), annular pancreas | "Double bubble" sign on AXR — dilated stomach and proximal duodenum with no gas distally |
| Jejunoileal atresia | Jejunum (45 %), ileum (45 %), multiple sites (10 %) | Bilious vomiting at 24–48 hours; progressive abdominal distension; failure to pass meconium | Multiple dilated loops on AXR; no "double bubble"; contrast enema shows microcolon (unused distal bowel) |
| Colonic atresia | Rare (5 % of intestinal atresias) | Presentation similar to jejunoileal; abdominal distension prominent | AXR: dilated loops; contrast enema: microcolon, no air in rectum |
Management of Intestinal Atresia
- Duodenal atresia: Duodenoduodenostomy (diamond-shaped anastomosis) — no bowel resection required
- Jejunoileal atresia: Resection of atretic segment with primary anastomosis (end-to-oblique or functional end-to-end). In cases of significant length discrepancy, a Bishop-Koop or Santulli enterostomy may be required.
- Colonic atresia: Resection with primary anastomosis, or staged approach (initial stoma formation) in unstable patients
- Post-operative: Prolonged ileus is expected; TPN may be required until enteral feeding is tolerated. Monitor for short bowel syndrome in cases of extensive resection.
Other Important Causes of Vomiting in Infancy
| Condition | Age of Onset | Key Features |
|---|---|---|
| Gastro-oesophageal reflux (GOR) | 2 weeks – 12 months | Effortless regurgitation, thriving infant, no alarm features. Self-resolving in 90 % by 12 months. |
| Intestinal malrotation ± volvulus | Any age (peak: neonatal – 1 year) | Bilious vomiting, acute abdomen, shock. URGENT upper GI contrast study. Ladd procedure. |
| Cow's milk protein allergy (CMPA) | 1–6 months | Vomiting ± bloody stools, eczema, failure to thrive. Trial of extensively hydrolysed formula or maternal elimination diet. |
| Inborn errors of metabolism | Neonatal period (often days 2–5) | Vomiting, lethargy, encephalopathy, metabolic acidosis. Screen with blood ammonia, lactate, amino acids, urine organic acids. Emergency metabolic referral. |
| Hirschsprung disease | Neonatal (failure to pass meconium in first 48 h) | Abdominal distension, bilious vomiting, delayed meconium passage. Rectal suction biopsy (absence of ganglion cells). Contrast enema: transition zone. |
| Raised intracranial pressure | Any age | Projectile vomiting, irritability, bulging fontanelle, sunset sign. CT/MRI brain. Urgent neurosurgical referral. |
Acute Gastroenteritis
Acute gastroenteritis (AGE) is defined as diarrhoea (≥3 loose stools in 24 hours) with or without vomiting, nausea, fever, or abdominal pain, lasting <14 days. It is one of the most common reasons for emergency department attendance and hospitalisation in Australia, particularly in children under 5 years and older adults.
Australian Aetiology
- Viral (most common, 60–80 %): Rotavirus (decreasing since NIP introduction), norovirus (most common in adults and outbreaks), adenovirus, astrovirus
- Bacterial (10–20 %): Campylobacter (most common bacterial cause in Australia), Salmonella spp., Shigella spp., Shiga toxin-producing E. coli (STEC), Clostridioides difficile
- Parasitic (5–10 %): Giardia lamblia, Cryptosporidium (associated with daycare, swimming pools, remote communities)
Assessment of Dehydration Severity
Management of Acute Gastroenteritis
1. Rehydration
- Mild dehydration: Continue usual feeds/ORS ad libitum; reassess in 24–48 hours
- Moderate dehydration: ORS 50–100 mL/kg over 3–4 hours, then maintenance fluids + replacement of ongoing losses
- Severe dehydration or inability to tolerate oral intake: IV 0.9 % Normal Saline 20 mL/kg bolus over 1–2 hours, repeat as needed. In children: Plasmalyte-148 or 0.9 % NaCl + 5 % dextrose for maintenance
2. Anti-emetics — Facilitating Oral Rehydration
3. Dietary Management
- Do NOT restrict diet — early refeeding (within 4 hours of commencing ORT) reduces illness duration and improves nutritional status
- Continue breastfeeding in infants (more frequent, shorter feeds)
- Avoid fruit juices, carbonated drinks, and high-sugar fluids (osmotic diarrhoea)
- Age-appropriate diet: complex carbohydrates (rice, bread, potatoes), lean meats, yoghurt, fruits, and vegetables
- Lactose-containing feeds may be continued — routine lactose-free formula is NOT recommended unless there is evidence of secondary lactase deficiency (protracted diarrhoea >7 days)
4. Specific Antimicrobial Therapy
| Pathogen | Indication for Treatment | First-Line Agent | Dose (Adult) |
|---|---|---|---|
| Campylobacter spp. | Severe/protracted illness, immunocompromised, pregnancy, bacteraemia | Azithromycin | 500 mg PO daily × 3 days (or 1 g day 1 then 500 mg days 2–5) |
| Salmonella spp. (non-typhoidal) | Bacteraemia, immunocompromised, age <3 months, prosthetic implants, severe illness | Ciprofloxacin or azithromycin | Ciprofloxacin 500 mg PO BD × 5–7 days; or azithromycin 500 mg PO daily × 3 days |
| Shigella spp. | All confirmed cases (reduces transmission and duration) | Azithromycin | 1 g PO stat (single dose) or 500 mg PO daily × 3 days |
| Giardia lamblia | Confirmed diagnosis | Tinidazole (preferred) or metronidazole | Tinidazole 2 g PO single dose; or metronidazole 400 mg PO TDS × 5–7 days |
| Cryptosporidium | Immunocompetent: self-limiting. Immunocompromised (HIV with CD4 <200): treat. | Nitazoxanide | 500 mg PO BD × 3 days (adults); not PBS-listed — Special Access Scheme |
| C. difficile | All confirmed cases with diarrhoea | Vancomycin (oral) | 125 mg PO QDS × 10 days (first episode); fidaxomicin 200 mg PO BD × 10 days as alternative |
5. When to Refer / Admit
- Severe dehydration not responding to oral rehydration
- Inability to tolerate any oral fluids for >6–8 hours
- Bloody diarrhoea or suspected STEC/haemolytic uraemic syndrome (HUS)
- Signs of peritonitis or toxic megacolon
- Immunocompromised patients (HIV, transplant recipients, chemotherapy)
- Infants <3 months with fever and vomiting
- Significant comorbidities (chronic kidney disease, heart failure) where fluid balance is critical
Rotavirus Vaccination — Australian NIP
Rotavirus vaccine is funded on the NIP for all Australian infants:
- Rotarix® (RV1): 2-dose schedule at 2 and 4 months of age (oral)
- RotaTeq® (RV5): 3-dose schedule at 2, 4, and 6 months of age (oral)
- First dose must be administered before 15 weeks of age; course must be completed before 8 months of age
- Vaccination has reduced rotavirus-coded hospitalisations by over 70 % in Australia
Gastroparesis
Gastroparesis is a chronic disorder of gastric motility characterised by delayed gastric emptying of solids in the absence of mechanical obstruction. It significantly impairs quality of life, nutrition, and glycaemic control, and presents a substantial burden on Australian healthcare services.
Aetiology
| Category | Examples | Frequency |
|---|---|---|
| Diabetic | Type 1 > Type 2 diabetes mellitus; chronic hyperglycaemia damages the interstitial cells of Cajal and vagal nerve function | ~30–40 % of cases |
| Post-surgical | Fundoplication, bariatric surgery (sleeve gastrectomy, Roux-en-Y), vagotomy, lung/heart transplantation | ~15–25 % |
| Idiopathic | No identifiable cause; may follow viral illness ("post-viral gastroparesis"); more common in young women | ~30–40 % |
| Medication-induced | Opioids, anticholinergics, GLP-1 receptor agonists (liraglutide, semaglutide), pramlintide, calcium channel blockers | Important to exclude |
| Other | Systemic sclerosis, Parkinson disease, amyloidosis, hypothyroidism, chronic mesenteric ischaemia | Rare |
Clinical Presentation
- Cardinal symptoms: Nausea (90 %), vomiting (85 %), early satiety (60 %), postprandial fullness (75 %), bloating (75 %), upper abdominal pain (45 %)
- Vomitus characteristically contains food ingested many hours previously (retained food)
- In diabetic gastroparesis: erratic glycaemic control, recurrent hypoglycaemia (from mismatched insulin absorption and food delivery), and weight loss
- Patients may restrict oral intake to minimise symptoms, leading to malnutrition
Diagnostic Criteria
Gastroparesis Severity (GCSI-based)
Management of Gastroparesis
1. Dietary and Lifestyle Modifications
- Small, frequent meals (5–6 per day) — smaller volumes are better tolerated
- Low-fat, low-fibre diet — fat delays gastric emptying; indigestible fibre (raw vegetables, legumes) may form bezoars
- Well-cooked, blended, or pureed foods for severe cases
- Sit upright during meals and for 1–2 hours postprandially
- Avoid carbonated beverages and alcohol
- Supplemental liquid nutritional supplements (e.g., Sustagen®, Ensure®) if solid intake is inadequate
- Dietitian referral is recommended for all patients with confirmed gastroparesis
2. Glycaemic Optimisation (Diabetic Gastroparesis)
3. Pharmacological Management
4. Refractory Gastroparesis — Specialist Interventions
Monitoring
- Regular review (every 4–8 weeks initially) to assess symptom control, weight, nutritional status, and medication tolerability
- Gastroparesis Cardinal Symptom Index (GCSI) — validated symptom score for serial monitoring
- HbA1c every 3 months in diabetic gastroparesis
- FBE, UEC, LFTs, iron studies, vitamin B12, folate, zinc — monitor for nutritional deficiencies
- Bone densitometry (DEXA) if chronic malnutrition or prolonged use of prokinetics associated with reduced oral intake
- Screen for depression and anxiety — prevalence up to 50 % in gastroparesis patients
Special Populations
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander peoples experience a significantly higher burden of gastrointestinal illness, including acute gastroenteritis, compared to the non-Indigenous Australian population. Culturally safe, community-informed approaches are essential to improving outcomes.
📚 References
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