Excessive menstrual loss: menorrhagia

Menorrhagia can be due to uterine or systemic disorders.

Some differential diagnoses and typical outline evidence

Fibroids	Suggested by: (sometimes) urinary frequency, constipation, recurrent abortion, infertility.
	Confirmed by: pelvic examination, ultrasound or CT.
	Management: OHCS pp276–7.
Endometrial carcinoma	Suggested by: abnormal uterine bleeding, blood-stained vaginal discharge, postmenopausal bleeding.
	Confirmed by: pelvic ultrasound, tissue sampling of endometrium, hysteroscopy.
	Management: OHCS pp278–9.
Pelvic endometriosis	Suggested by: dysmenorrhoea, dyspareunia, infertility, pelvic mass.
	Confirmed by: laparoscopy.
	Management: OHCS p288.
Chronic pelvic inflammatory disease	Suggested by: lower abdominal pain, fever, vaginal discharge, dysuria, ↑ ESR and ↑ CRP, leucocytosis.
	Confirmed by: high vaginal swab, pelvic ultrasound, ± laparoscopy.
	Management: OHCS p286.
Intrauterine contraceptive device	Suggested by: history of its insertion ± painful periods.
	Confirmed by: symptoms subside after removal of IUCD.
Primary hypothyroidism	Suggested by: cold intolerance, tiredness, constipation, bradycardia.
	Confirmed by: ↑ TSH, ↓ FT4.
	Management: OHCM p306.
Bleeding diathesis	Suggested by: family history, tendency to bleed, easy bruising.
	Confirmed by: abnormal clotting screen.
	Management: OHCM pp644–9.

Sudden diarrhoea, fever and vomiting

Sudden diarrhoea with fever, ± malaise, colicky abdominal pain, vomiting.

Some differential diagnoses and typical outline evidence

Antibiotic induced bacterial opportunist: Clostridium difficile	Suggested by: diarrhoea with a history of recent antibiotic therapy, ↑ WBC.
	Confirmed by: Cl. difficile toxin in stool culture.
	Management: OHCM pp218, 219.
Viral gastroenteritis: Rotavirus	Suggested by: diarrhoea in children <5>
	Management: OHCM p540.
Norwalk virus	Suggested by: diarrhoea in older children and adults, symptoms resolve in 2 weeks.
Food poisoning/ toxins Staphylococcus aureus	Suggested by: eating ‘doubtful’ meat, incubation period <6>
	Confirmed by: isolation of Staph. aureus from examination of suspected food.
	Management: OHCM p556.
Bacillus cereus	Suggested by: eating ‘doubtful’ rice, incubation period <6>
	Confirmed by: stool microscopy and culture.
	Management: OHCM pp556, 221.
Vibrio para haemolyticus	Suggested by: ‘doubtful’ seafood, incubation period 16–72 hours.
	Confirmed by: stool microscopy and culture.
	Management: OHCM pp596, 621.
Clostridium perfringens	Suggested by: eating ‘doubtful’ meat, incubation period 8–16 hours, abdominal cramps, little vomiting.
	Confirmed by: organism isolation from faeces or suspected food.
Botulism	Suggested by: eating ‘doubtful’ canned food, incubation period 18–36 hours, but may vary from 4 hours to 8 days, abdominal cramps, dry mouth, diplopia, progressive paralysis.
	Confirmed by: C. botulinum toxin in serum or faeces; C. botulinum toxin isolation from suspected food.
	Management: OHCM pp591, 830.
Salmonella typhimurium	Suggested by: eating ‘doubtful’ meat, egg, poultry. Fever (with relative bradycardia), headache, dry cough.
	Confirmed by: stool microscopy and culture.
	Management: OHCM p596.

Acute lower central (hypogastric) abdominal pain

Some differential diagnoses and typical outline evidence

Infective or ulcerative colitis	Suggested by: abdominal pain, diarrhoea with blood and mucus.
	Confirmed by: stool microscopy and culture, colonoscopy.
	Management: OHCM pp218–19, 244–5.
Large bowel obstruction	Suggested by: severe distension, late vomiting, visible peristalsis, resonant percussion, increased bowel sounds. Supine AXR showing peripheral abdominal large bowel shadow (with haustra partly crossing the lumen). Fluid levels on erect film.
	Confirmed by: abdominal ultrasound and laparotomy findings.
	Management: OHCM p492.
Cystitis	Suggested by: frequency, urgency, dysuria, ± haematuria.
	Confirmed by: MSUfor microscopy and culture.
	Management: OHCS p262.
Pelvic inflammatory disease	Suggested by: vaginal discharge, dysuria, dyspareunia, pelvic tenderness on moving cervix, ↑ ESR and CRP. WBC: leucocytosis.
	Confirmed by: High vaginal swab, pelvic ultrasound, ± laparoscopy.
	Management: OHCS p286.
Pelvic endometriosis	Suggested by: dysmenorrhoea, ovulation pain, dyspareunia, infertility, pelvic mass.
	Confirmed by: laparoscopy.
	Management: OHCS p288.
Ectopic pregnancy	Suggested by: constant unilateral pain ± referred shoulder pain, amenorrhoea, vaginal bleeding (usually less than normal period), faintness with an acute rupture.
	Confirmed by: pregnancy test +ve, bimanual examination reveals slightly enlarged uterus, pelvic ultrasound shows empty uterus with thickened decidua.
	Management: OHCS p262–3.

Acute lateral abdominal pain

Some differential diagnoses and typical outline evidence

Pyelonephritis	Suggested by: pain in loin (upper lateral), rigors, fever, vomiting, frequency of micturition, renal angle tenderness
	Confirmed by: FBC: leucocytosis. MSU: pyuria, urine culture and sensitivities.
	Management: OHCM pp258, 262, 276.
Renal calculus	Suggested by: renal colic mainly in loin (upper lateral), haematuria.
	Confirmed by: urinalysis, renal ultrasound, IVU, CT/MRI.
	Management: OHCM p264.
Ureteric calculus	Suggested by: renal colic, moving from loin (upper lateral) down to RLQ, haematuria.
	Confirmed by: urinalysis, renal ultrasound, IVU, CT/MRI.
	Management: OHCM p264.
Appendicitis	Suggested by: pain initially central, then radiating to right lower quadrant, anorexia, low grade fever, constipation. RLQ tenderness and guarding.
	Confirmed by: Inflamed appendix at laparotomy
	Management: OHCM p476.
Salpingitis	Suggested by: fever, nausea, vomiting, muco-purulent cervical discharge, irregular menses. Bilateral lower abdominal tenderness and guarding.
	Confirmed by: FBC: leucocytosis. High vaginal swab, laparoscopy.

Acute central abdominal pain

Some differential diagnoses and typical outline evidence

Small bowel obstruction	Suggested by: vomiting, constipation with complete obstruction.
	Confirmed by: AXR shows small bowel loops and fluid levels.
	Management: OHCM p492.
Crohn's disease	Suggested by: chronic diarrhoea with abdominal pain, weight loss, palpable RLQ mass or fullness, mouth ulcers.
	Confirmed by: colonoscopy with biopsy, barium studies showing ‘skip lesions’, string sign in advanced cases.
	Management: OHCM p246.
Mesenteric artery occlusion	Suggested by: vomiting, bowel urgency, melaena, diarrhoea.
	Confirmed by: mesenteric angiography, exploratory laparotomy.
	Management: OHCM p488.
Abdominal aortic dissection	Suggested by: tearing pain ± shock ± hypotension and peripheral cyanosis.
	Confirmed by: ultrasound or CT abdomen.
	Management: OHCM p480.

Acute pain in the upper abdomen

Trying to localise pain in the upper abdomen to the right, left or middle may be difficult for the patient.

Some differential diagnoses and typical outline evidence

Oesophagitis	Suggested by: retrosternal pain, heartburn.
	Confirmed by: oesophagogastroscopy.
	Management: OHCM p216.
Acute coronary syndrome (unstable angina or infarction)	Suggested by: chest tightness or pain on exertion.
	Confirmed by: exercise ECG ± coronary angiography if troponin normal, or later if troponin ↑.
	Management: OHCM pp120–4, 782.
Hiatus hernia	Suggested by: heartburn, worsens with stooping or lying, relieved by antacids.
	Confirmed by: oesophagogastroscopy, barium meal.
	Management: OHCM p532.
Gastritis	Suggested by: epigastric pain, dull or burning discomfort, nocturnal pain
	Confirmed by: oesophagogastroscopy, barium meal and pH study.
	Management: OHCM p214.
Gallstone colic (with no acute inflammation or infection)	Suggested by: jaundice, biliary colic, pain in epigastrium or RUQ radiating to right lower scapula. No fever or ↑WBC.
	Confirmed by: ultrasound of gallbladder and biliary ducts.
	Management: OHCM pp484, 485.
Acute cholecystitis	Suggested by: fever, guarding and positive Murphy's sign (abrupt stopping of inspiration when the palpating hand meets the inflamed gall bladder descending with the liver from behind the sub-costal margin on the right side—but not on the left side). ↑WBC.
	Confirmed by: ultrasound gallbladder and biliary ducts.
	Management: OHCM p484.
Duodenal ulcer	Suggested by: epigastric pain, dull or burning discomfort, typically relieved by food, nocturnal pain.
	Confirmed by: oesophagogastroscopy, barium meal and pH study: (Helicobacter pylori often present in mucosa or serology).
	Management: OHCM p214.
Gastric ulcer	Suggested by: epigastric pain, dull or burning discomfort, typically exacerbated by food, nocturnal pain.
	Confirmed by: oesophagogastroscopy, barium meal and pH study.
	Management: OHCM p214.
Gastric carcinoma	Suggested by: marked anorexia, fullness, pain, Troisier's sign (a ‘Virchow's’ node i.e. large lymph node in the left supraclavicular fossa).
	Confirmed by: upper GI endoscopy with biopsy.
	Management: OHCM p508.
Pancreatitis	Suggested by: pain radiating straight through to the back, better on sitting up or leaning forward.
	Confirmed by: ↑serum amylase, CT pancreas.
	Management: OHCD p478.

Sore throat

With odynophagia—painful swallowing.

Some differential diagnoses and typical outline evidence

Viral pharyngitis	Suggested by: sore throat, pain on swallowing, fever, cervical lymphadenopathy and injected fauces. ↑ lymphocytes, leucocytes normal in WBC.
	Confirmed by: negative throat swab for bacterial culture, self-limiting: resolution within days.
Acute follicular tonsillitis (streptococcal)	Suggested by: severe sore throat, pain on swallowing, fever, enlarged tonsils with white patches (like strawberries and cream). Cervical lymphadenopathy especially in angle of jaw. Fever, ↑ leucocytes in WBC.
	Confirmed by: throat swab for culture and sensitivities of organisms.
	Management: OHCS p564.
Infectious mononucleosis (glandular fever) due to Epstein–Barr virus	Suggested by: very severe throat pain with enlarged tonsils covered with creamy membrane. Petechiae on palate. Profound malaise. Generalised lymphadenopathy, splenomegaly.
	Confirmed by: ↑ atypical lymphocytes in WBC. Paul–Bunnel test positive. Viral titres.
	Management: OHCM p570.
Candidiasis of buccal or oesophageal mucosa	Suggested by: painful dysphagia, white plaque, history of immunosuppression/diabetes/recent antibiotics.
	Confirmed by: oesophagoscopy showing erythema and plaques, brush cytology ± biopsy shows spores and hyphae.
	Management: OHCM p210.
Agranulocytosis	Suggested by: sore throat, background history of taking a drug or contact with noxious substance.
	Confirmed by: low or absent neutrophil count.
	Management: OHCM p662.
Meningococcal meningitits	Suggested by: headache, photophobia, vomiting, sore throat, red fauces without purulent patches, neck stiffness. High blood neutrophil count.
	Confirmed by: lumbar puncture showing pus or neutrophil count and organisms on microscopy or culture.
	Management: OHCM p370.

Obstructive jaundice

Some differential diagnoses and typical outline evidence

	Suggested by: jaundice with pale stools and dark urine. Bilirubin in urine (i.e. conjugated and thus soluble).
	Confirmed by: ↑serum conjugated bilirubin and thus urine bilirubin but no ↑urobilinogen in urine. Markedly (↑↑) alkaline phosphatase, but less abnormal (↑) liver function tests and ↑↑GT.
	Management: OHCM p484.

Some differential diagnoses and typical outline evidence

Common bile duct stones	Suggested by: pain in RUQ ± Murphy's sign.
	Confirmed by: ultrasound liver: dilatation of biliary ducts.
	Management: OHCM pp484, 485.
Cancer of head of pancreas	Suggested by: progressive painless jaundice, palpable gall-bladder (Courvoisier's law), weight loss.
	Confirmed by: ultrasound liver: dilatation of biliary ducts. CT pancreas, ERCP or MRCP: obstruction within head of pancreas.
	Management: OHCM p248.
Sclerosing cholangitis	Suggested by: progressive fatigue, pruritus.
	Confirmed by: ↑ALP. Ultrasound liver: no gallstones. ERCP: (beading of the intra-and extra-hepatic biliary ducts)
	Management: OHCM p238.
Primary biliary cirrhosis	Suggested by: scratch marks, non-tender hepatomegaly, ± splenomegaly, xanthelasmata and xanthomas, arthralgia.
	Confirmed by: +ve anti-mitochondrial antibody, ↑↑serum IgM: infiltrate around hepatic bile ducts and cirrhosis on liver biopsy.
	Management: OHCM p238.
Drug-induced	Suggested by: drug history of oral contraceptive pill, phenothiazines, anabolic steroids, erythromycin, etc.
	Confirmed by: symptoms receding when drug discontinued.
	Management: OHCM p223.
Pregnancy (last trimester)	Suggested by: jaundice during pregnancy.
	Confirmed by: resolution following delivery.
	Management: OHCS p26.
Alcoholic hepatitis or cirrhosis	Suggested by: history of excess alcohol intake, presence of spider naevi and other signs of chronic liver disease.
	Confirmed by: ultrasound or CT liver, liver biopsy, improvement if abstinence.
	Management: OHCM p254.
Dubin–Johnson syndrome (decreased excretion of conjugated bilirubin, see OHCM p722)	Suggested by: intermittent jaundice, and associated pain in the right hypochondrium. No hepatomegaly.
	Confirmed by: normal ALP, normal LFT. ↑urinary bilirubin. Pigment granules on liver biopsy.

Hepatocellular jaundice (due to hepatitis or very severe liver failure)

Some differential diagnoses and typical outline evidence

	Suggested by: onset of jaundice over days or weeks, stools and urine pale or dark but dark urine.
	Confirmed by: ↑serum (conjugated) bilirubin and thus ↑urine bilirubin. Normal urine urobilinogen. Liver function tests all increasingly abnormal esp. ↑(ALT.

Some differential diagnoses and typical outline evidence

Acute (viral) hepatitis A	Suggested by: tender hepatomegaly.
	Confirmed by: presence of hepatitis A IgM antibody suggests acute infection.
	Management: OHCM p576.
Acute hepatitis B	Suggested by: history of iv drug user, blood transfusion, needle punctures, tattoos, tender hepatomegaly.
	Confirmed by: presence of HBsAg in serum.
	Management: OHCM p576.
Acute hepatitis C	Suggested by: history of iv drug user, blood transfusion, tender hepatomegaly.
	Confirmed by: presence of anti-HCV antibody, HCV-PCR.
	Management: OHCM p576.
Alcoholic hepatitis	Suggested by: history of drinking, presence of spider naevi and other signs of chronic liver disease. AST:ALT ratio >2.
	Confirmed by: resolution with abstinence.
	Management: OHCM p223.
Drug-induced hepatitis e.g. paracetamol halothane	Suggested by: drug history, recent surgery.
	Confirmed by: drug levels improvement after stopping the offending drug.
	Management: OHCM p223.
Primary hepatoma	Suggested by: weight loss, abdominal pain, RUQ mass.
	Confirmed by: ultrasound/CT liver, liver biopsy, ↑alpha-fetoprotein.
	Management: OHCM pp242, 243.
Right heart failure	Suggested by: ↑JVP, hepatomegaly, ankle oedema.
	Confirmed by: CXR: large heart. Echocardiogram: dilated right ventricle.
	Management: OHCM pp136–9.
Glandular fever (infectious mononucleosis)	Suggested by: cervical lymphadenopathy, sharp edge, ± Splenomegaly, ± jaundice.
	Confirmed by: Paul-Bunnell, +ve heterophil antibody test.
	Management: OHCM p570.

Hepatic jaundice due to congenital enzyme defect

Some differential diagnoses and typical outline evidence

	Suggested by: jaundice. Normal looking stools and normal looking urine.
	Confirmed by: ↑serum bilirubin (unconjugated), but no (conjugated) bilirubin in urine. No urobilinogen in urine and normal haptoglobin. Normal liver function tests.

Some differential diagnoses and typical outline evidence

Gilbert's syndrome (Normal lifespan)	Suggested by: above evidence of impaired conjugation, asymptomatic.
	Confirmed by: demonstration of unconjugated hyperbilirubinaemia with normal LFT, no haemolysis. Rise in bilirubin when fasting and after nicotinic acid.
	Management: OHCM p724.
Crigler–Najjar syndrome (Type I: Severe, neonatal and often fatal Type II: Normal lifespan)	Suggested by: above evidence of impaired conjugation.
	Confirmed by: unconjugated hyperbilirubinaemia with otherwise normal LFT, no haemolysis. No rise in bilirubin when fasting or after nicotinic acid.
	Management: OHCM pp222, 720.

Pre-hepatic jaundice due to haemolysis

Suggested by: jaundice and anaemia (the combination often seen as ‘lemon’ or pale yellow). Normal dark stools and normal looking urine.
	Confirmed by: ↑(unconjugated and thus insoluble) serum bilirubin but normal (conjugated and thus soluble) bilirubin and in turn no bilirubin in urine. Evidence of haemolysis as: ↑urinary urobilinogen and ↓serum haptoglobin. ↑Reticulocyte count. Normal liver function tests, Hb↓.

Some differential diagnoses and typical outline evidence

Hereditary haemolytic anaemia	Suggested by: family history, anaemia, splenomegaly, leg ulcers.
	Confirmed by: above evidence of haemolysis, ↑osmotic fragility; enzyme deficiency e.g. G6PD, pyruvate kinase.
	Management: OHCM pp624, 636, 638.
Acquired haemolytic anaemia	Suggested by: sudden onset, in later life, and on medication.
	Confirmed by: above evidence of haemolysis, blood film, +ve Coombs’ test in autoimmune type.
	Management: OHCM pp624, 636, 638.
Septicaemic haemolysis due to pneumonia, UTI, etc	Suggested by: fever, ± shock symptoms and signs of infection.
	Confirmed by: evidence of haemolysis, blood culture positive.
	Management: OHCM pp624, 636, 638.
Malaria	Suggested by: recent travel to malaria zone, periodic paroxysms of rigors, fever, sweating, nausea.
	Confirmed by: Plasmodium in blood smear.
	Management: OHCM pp549, 560–3

Jaundice

This can be a symptom reported by the patient or a physical sign. It is confirmed by ↑bilirubin in the plasma. Yellow sclerae and skin usually becomes visible when serum bilirubin level is >35µmol/L, so urine tests may provide the first clue. First subdivide into the 5 leads below. Remember that haemolysis causes ↑urinary urobilinogen and ↓serum haptoglobin. Hepatic failure causes ↑serum unconjugated bilirubin but intrahepatic or extra hepatic biliary obstruction results in ↑serum conjugated bilirubin.

Some differential diagnoses and typical outline evidence

Carotinaemia	Suggested by: onset over months. Skin yellow with white sclerae, normal stools and normal urine. Diet rich in yellow vegetables/fruits).
	Confirmed by: no bilirubin, no urobilinogen in the urine and normal serum bilirubin. Normal liver function tests. Response to diet change.
‘Pre-hepatic’ jaundice due to haemolysis	Suggested by: jaundice and anaemia (the combination seen as ‘lemon’ or pale yellow). Normal dark stools and normal looking urine.
	Confirmed by: ↑ (unconjugated and thus insoluble) serum bilirubin but normal (conjugated and soluble) bilirubin and thus no ↑bilirubin in urine. ↑urobilinogen in urine and ↓serum haptoglobin. Normal liver function tests. ↑Reticulocyte count, Hb↓.
	Management: OHCM pp222–3.
‘Hepatic’ jaundice due to congenital enzyme defect	Suggested by: Normal looking stools and normal looking urine.
	Confirmed by: ↑serum bilirubin (unconjugated), but no (conjugated) bilirubin in urine. No urobilinogen in urine and normal haptoglobin. Normal liver function tests.
	Management: OHCM pp222–3.
‘Hepatocellular’ jaundice (‘hepatic’ with element of ‘obstructive’ jaundice)	Suggested by: onset of jaundice over days or weeks, stools pale or normal but dark urine.
	Confirmed by: ↑serum (conjugated) bilirubin and thus ↑urine bilirubin. Normal urine urobilinogen. Liver function tests all abnormal esp. ↑(ALT.
	Management: OHCM pp222–3.
‘Obstructive’ jaundice	Suggested by: onset of jaundice over days or weeks with pale stools and dark urine. Bilirubin ↑ (i.e. conjugated and thus soluble) in urine.
	Confirmed by: ↑serum conjugated bilirubin and thus ↑ urine bilirubin but no ↑urobilinogen in urine. Markedly (↑↑) alkaline phosphatase, but less abnormal liver function tests and ↑↑GT.
	Management: OHCM p484.

Vomiting alone (unrelated to food and without abdominal pain or headaches)

Some differential diagnoses and typical outline evidence

Gastroenteritis	Suggested by: diarrhoea, decreased bowel sounds.
	Confirmed by: stools for WBC and culture.
	Management: OHCM p556.
Sliding hiatus hernia	Suggested by: occasional chest pain precipitated by heavy meals, lying flat.
	Confirmed by: barium meal showing reflux.
	Management: OHCM p216.
Acute viral labyrinthitis	Suggested by: vertigo, nystagmus.
	Confirmed by: being self-limiting over days.
	Management: OHCM p346–7.
Ménière's disease	Suggested by: vertigo, tinnitus, deafness.
	Confirmed by: audiometry: sensory hearing loss.
	Management: OHCM p346, OHCS p554.
Pregnancy	Suggested by: being worse soon after waking, amenorrhoea.
	Confirmed by: pregnancy test +ve.
Anaphylaxis	Suggested by: bronchospasm, laryngeal oedema, flushing, urticaria, angioedema.
	Confirmed by: relief with antihistamines or steroids.
	Management: OHCM p780, OHCS p237.
Renal failure (CRF)	Suggested by: fatigue, pruritus, anorexia, nausea, ‘lemon-tinge’ skin.
	Confirmed by: ↑serum creatinine, ↓creatinine clearance. If chronic CRF: Hb low, and small kidneys on renal ultrasound.
	Management: OHCM pp272–4.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol low ↓ and impaired response to short ACTH stimulation test (short Synacthen test).
	Management: OHCM p312.
Drugs e.g. antibiotics, cytotoxics, any overdose, excessive alcohol ingestion etc.	Suggested by: history of drug ingestion.
	Confirmed by: response of symptoms to avoidance of drug.
Functional	Suggested by: vomiting during or soon after a meal ± other psychological disturbance and no symptoms and physical signs of organic disease.
	Confirmed by: response to psychotherapy.

Vomiting with headache alone (unrelated to food and no abdominal pain)

Some differential diagnoses and typical outline evidence

Migraine	Suggested by: throbbing headache with preceding visual auras or other transient sensory symptoms and ‘trigger’ factors e.g. pre-menstrual, stress, particular foods.
	Confirmed by: history, but if in doubt MRI scan to exclude anatomical abnormalities.
	Management: OHCM p342.
Raised intracranial pressure	Suggested by: being worse in morning, on coughing and leaning forward, papilloedema.
	Confirmed by: CT scan head showing flattening of sulci and darkening of brain tissue.
	Management: OHCM p816.
Meningitis (viral or bacterial)	Suggested by: photophobia, fever, neck stiffness.
	Confirmed by: CT scan: no signs of ↑intracranial. pressure and LP: ↑lymphocytes in viral, ↑neutrophils in bacterial with organisms on staining and culture.
	Management: OHCM pp370–1.
Haemorrhagic stroke	Suggested by: sudden onset of headache, hemiparesis, sparing of upper face, dysarthia ± dysphasia, extensor plantar response.
	Confirmed by: CT brain scan: high attenuation area representing haemorrhage.
	Management: OHCM pp354–8.
Severe hypertension	Suggested by: continuous throbbing headache (non-severe hypertension is usually asymptomatic) but headache ± visual disturbance in malignant hypertension.
	Confirmed by: serial BP measurement: usually >140mmHg diastolic and/or >240mmHg systolic.
	Management: OHCM pp140–2.
Epilepsy	Suggested by: aura, altered consciousness, abnormal movements.
	Confirmed by: EEG result: spikes and waves over focus.
	Management: OHCM p380.
Acute glaucoma	Suggested by: blurred vision, painful red eye, coloured haloes.
	Confirmed by: ↑intraocular pressure on measurement.
	Management: OHCM p430.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol ↓ and impaired response to short ACTH stimulation test (short Synacthen test).
	Management: OHCM p312.

Vomiting with abdominal pain alone (unrelated to food and no fever)—metabolic causes

This is associated with a wide variety of GI and systemic disorders. It is non-specific.

Some differential diagnoses and typical outline evidence

Drugs overdose e.g. digoxin	Suggested by: drug history.
	Confirmed by: serum drug levels.
	Management: OHCM p830.
Diabetic ketoacidosis	Suggested by: polyuria, dehydration, ±Kussmaul respiration.
	Confirmed by: ↑blood glucose, ↓pH,ketonuria or plasma bicarbonate <15mmol/l.
	Management: OHCM p818.
Hypercalcaemia	Suggested by: lethargy, confusion, constipation, muscle weakness, polydipsia and polyuria.
	Confirmed by: ↑serum Ca2+.
	Management: OHCM p696.
Acute intermittentporphyria	Suggested by: family history, constipation, peripheral neuropathy, hypertension, psychoses, urine darkens on standing.
	Confirmed by: Elevated urinary-aminolevulinic acid and porphobilinogen, plasma porphyrins.
	Management: OHCM p708.
Lead poisoning	Suggested by: anorexia, personality changes, headaches, metallic taste.
	Confirmed by: elevated whole blood lead concentration >2.4µmol/L.
	Management: OHCM pp210, 628.
Vitamin A intoxication	Suggested by: ↑intracranial pressure, headache, irritability.
	Confirmed by: symptoms and signs disappearing within 1–4 weeks after stopping vitamin A ingestion.
Phaeochromocytoma	Suggested by: headache, sweating, palpitations, pallor, nausea, hypertension (intermittent or persistent), tachycardia.
	Confirmed by: 24 hour urinary metanephrines ↑, serum catecholamines ↑↑(adrenaline, noradrenaline), CT abdomen, MRI scan.
	Management: OHCM pp314, 822.

Vomiting with abdominal pain alone (unrelated to food and no fever)—non-metabolic causes

This is associated with a wide variety of GI and systemic disorders it is non-specific.

Some differential diagnoses and typical outline evidence

Large bowel obstruction e.g. malignancy, strangulated hernia	Suggested by: faecal vomiting, abdominal distension.
	Confirmed by: AXR showing bowel dilation, barium enema, colonoscopy.
	Management: OHCM p492.
Hepatic carcinoma, primary or secondary	Suggested by: RUQ pain and mass, jaundice.
	Confirmed by: weight loss over weeks to months, ultrasound/CT of liver showing hepatic mass.
	Management: OHCM pp242–3.
Mesenteric artery occlusion	Suggested by: periumbilical pain, diarrhoea, melaena.
	Confirmed by: mesenteric angiography showing filling defect.
	Management: OHCM p488.
Intussusception	Suggested by: child, usually between 6–18 months of life, acute onset of colicky intermittent abdominal pain, red currant ‘jelly’ PR bleed, ± a sausage shape mass in upper abdomen.
	Confirmed by: barium enema, may reduce with appropriate hydrostatic pressure.
	Management: OHCM p494.
Ectopic pregnancy, miscarriage	Suggested by: cramping pain, spotting, PV bleeding.
	Confirmed by: positive pregnancy test, USS of pelvis.
	Management: OHCS p262–3.
Renal calculi	Suggested by: colicky loin pain, haematuria.
	Confirmed by: plain abd X-ray, ultrasound, IVU.
	Management: OHCM p264.
Acute inferior myocardial infarction	Suggested by: retrosternal chest pain, sweating, nausea.
	Confirmed by: ↑ST on ECG, ↑cardiac enzymes e.g. CK-MB or troponin.
	Management: OHCM pp120–4.
Congestive cardiac failure (and liver congestion)	Suggested by: dyspnoea, orthopnoea, PND, liver enlargement and tenderness, leg oedema.
	Confirmed by: CXR and echocardiogram.
	Management: OHCM pp136–9

Vomiting with abdominal pain and fever

The vomiting is usually unrelated to eating.

Some differential diagnoses and typical outline evidence

Gastroenteritis	Suggested by: diarrhoea, ↑bowel sounds.
	Confirmed by: stools for WBC and culture.
	Management: OHCM p556.
Food poisoning	Suggested by: associated with diarrhoea, eating companions affected.
	Confirmed by: stools for WBC and culture, cultures of vomitus, food and blood.
	Management: OHCM p556.
Urinary tract infection	Suggested by: dysuria, frequency, abnormal dipstix.
	Confirmed by: MSU microscopy and culture. (US scan for possible anatomical abnormality.)
	Management: OHCM p262.
Acute appendicitis, mesenteric adenitis	Suggested by: RLQ pain anorexia, low grade fever.
	Confirmed by: RLQ guarding or right sided rectal tenderness.
	Management: OHCM p476.
Hepatitis A or B	Suggested by: RUQ pain, jaundice.
	Confirmed by: ALT ↑↑ and bilirubin ↑, hepatitis serology.
	Management: OHCM p576.
Toxic shock syndrome	Suggested by: use of tampons, high fever, vomiting and profuse watery diarrhoea, confusion, skin rash, hypotension, myalgia.
	Confirmed by: cultures of blood, stool, vaginal swab for Staphylococcus and toxin. Thrombocytopenia on FBC. ↑CPK.
	Management: OHCM p590.
Pneumonia (lower lobe)	Suggested by: cough, dyspnoea, fever.
	Confirmed by: CXR shows consolidation. Sputum and blood cultures. Serology if atypical.
	Management: OHCM p172.
Pelvic inflammatory disease	Suggested by: lower abdominal pain, fever, vaginal discharge.
	Confirmed by: high vaginal swab, elevated ESR and CRP. FBC: leucocytosis, pelvic ultrasound, ±laparoscopy.
	Management: OHCS p286.
Haemolytic uraemic syndrome	Suggested by: haematuria, fever, confusion.
	Confirmed by: FBC: thrombocytopaenia, fragmented RBCs on blood film, renal failure on U&E.
	Management: OHCM p282.
Malaria	Suggested by: recent travel to malaria zone, periodic paroxysms of rigors, fever, sweating, nausea.
	Confirmed by: Plasmodium in blood smear.
	Management: OHCM pp560–2.

Vomiting shortly after food

Some differential diagnoses and typical outline evidence

Gastritis/peptic ulcer disease	Suggested by: epigastric pain, dull or burning discomfort, (gastric ulcer pain typically exacerbated by food and duodenal ulcer pain relieved by it), ‘waterbrash’.
	Confirmed by: oesophagogastroscopy, barium meal and pH study.
Gastroparesis due to diabetes mellitus	Suggested by: intermittent vomiting, abdominal fullness or bloating, distended upper abdomen, succussion splash, history of diabetes.
	Confirmed by: oesophagogastroscopy, double contrast barium meal showing normal mucosa but dilatation.
Gastric outlet obstruction e.g. carcinoma, lymphoma, chronic scarring, congenital pyloric stenosis in newborn	Suggested by: intermittent vomiting, abdominal fullness or bloating, distended upper abdomen, succussion splash.
	Confirmed by: oesophagogastroscopy, double contrast barium meal shows structural abnormality.
Small intestinal tumour e.g. lymphoma	Suggested by: abdominal pain, anorexia, weight loss.
	Confirmed by: small bowel barium meal and follow-through showing filling defect, CT abdomen showing abnormal tumour in wall, flexible enteroscopy with biopsy showing abnormal histology.
Acute cholecystitis due to cholelithiasis	Suggested by: symptoms after fatty food with colicky abdominal pain.
	Confirmed by: ↑serum amylase, ultrasound scan of biliary tree/gallbladder.
	Management: OHCM pp484–5.
Acute pancreatitis	Suggested by: severe epigastric/central abdominal pain, jaundice, tachycardia, Cullen's sign (periumbilical discolouration) or Grey Turner's sign (discolouration at the flank).
	Confirmed by: ↑↑serum amylase, ↓Ca2+.
	Management: OHCM p478.

Vomiting without weight loss

Some differential diagnoses and typical outline evidence

Pharyngeal pouch	Suggested by: no pain, regurgitation of undigested food.
	Confirmed by: barium swallow showing saccular opacification outside pharynx.
	Management: OHCS p572.
Achalasia	Suggested by: vomiting after large meals, undigested solid food and fluid, dysphagia to fluid, nocturnal regurgitation.
	Confirmed by: barium swallow demonstrating the absence of peristaltic contractions, oesophagogastroscopy showing dilatation.
	Management: OHCM p212, OHCS p572.
Oesophagitisand ulceration	Suggested by: retrosternal pain, heartburn, dyspepsia, ‘waterbrash’.
	Confirmed by: oesophagogastroscopy showing inflammation and/or ulceration.
	Management: OHCM p216.

Vomiting with weight loss

Some differential diagnoses and typical outline evidence

Oesophageal carcinoma	Suggested by: dysphagia to solid food first, then semisolid and finally fluid.
	Confirmed by: barium swallow showing filling defect, fibreoptic gastroscopy with mucosal biopsy of visible tumour.
	Management: OHCM pp508, 718.
Gastric carcinoma	Suggested by: satiety after small meal.
	Confirmed by: oesophagogastroscopy showing and allowing biopsy of visible tumour, barium meal showing filling defect.
	Management: OHCM p508.
Achalasia	Suggested by: vomiting after large meals, undigested solid food and fluid, dysphagia to fluid, nocturnal regurgitation.
	Confirmed by: barium swallow demonstrating the absence of peristaltic contractions, oesophagogastroscopy showing dilatation.
	Management: OHCM p212.
Oesophageal stricture	Suggested by: undigested solid food and fluid in vomitus.
	Confirmed by: barium swallow, oesophagogastroscopy showing food residue and fixed narrowing.
	Management: OHCM p212.
Small intestinal tumour e.g. lymphoma	Suggested by: abdominal pain, anorexia.
	Confirmed by: small bowel follow-through, CT abdomen, flexible enteroscopy with biopsy.

Vomiting

Vomiting is not only a feature of GI disorders, but is also associated with a wide variety of local and systemic disorders. Therefore, more leads are needed. Ask about the amount, frequency and nature of vomitus—red blood, ‘coffee-ground’, timing of vomit i.e. in relation to meals, AND ask about weight loss, fever, headache and abdominal pain.

Try subdividing into

• Vomiting with weight loss
• Vomiting without weight loss
• Vomiting (within hours) of food
• Vomiting unrelated to food but with abdominal pain AND fever
• Vomiting unrelated to food, with abdominal pain but NO fever (non-metabolic)
• Vomiting unrelated to food, with abdominal pain but NO fever (metabolic)
• Vomiting unrelated to food without abdominal pain but with headaches
• Vomiting unrelated to food and without abdominal pain or headaches

Severe weight loss over weeks or months

The degree and speed of weight loss is relevant; the more severe, the more likely is it to be due to a demonstrable cause.

Some differential diagnoses and typical outline evidence

Any advancedmalignancy	Suggested by: progressive onset over weeks or months of specific symptoms e.g. neurological deficit, haemoptysis, rectal bleeding, change of bowel habit, etc.
	Confirmed by: metastases on CXR, metastases on ultrasound scan of liver or leukaemic changes on FBC or tumour on bronchoscopy, or GI endoscopy, etc.
Depression	Suggested by: sleep disorders, poor concentration, social withdrawal, lack of interest in usual activities etc.
	Confirmed by: response to antidepressants. Psychotherapy.
	Management: OHCS pp336–41.
Thyrotoxicosis	Suggested by: heat intolerance, tremor, nervousness, palpitation, frequency of bowel movements, goitre, fine tremor, warm and moist palm.
	Confirmed by: TSH↓, ↑FT4, ↑FT3.
	Management: OHCM p304.
Uncontrolled diabetes mellitus	Suggested by: thirst, polydipsia, polyuria.
	Confirmed by: Fasting blood glucose ≥7.0 mmol/L (on two occasions) OR fasting, random or GTT glucose ≥ 11.1mmol/L once only in the presence of symptoms.
	Management: OHCM pp292–6.
Infection e.g. tuberculosis	Suggested by: night sweats, fever, malaise, cough.
	Confirmed by: CXR showing opacification of pneumonia and presence of AFB in sputum on microscopy and culture.
	Management: OHCM pp564–6.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol ↓ and impaired response to short ACTH stimulation test (short Synacthen test).
	Management: OHCM p312.

Bilateral ankle swelling

Think of ↑ pressure within the veins or lymphatic vessels or low albumin in the vascular space, bilateral damage to veins, lymphatics or capillaries due to local inflammation.

Some differential diagnoses and typical outline evidence

Right ventricular failure due to pulmonary hypertension or congestive cardiac failure	Suggested by: ↑JVP, liver enlargement and pulsation, RV heave. Onset over months usually.
	Confirmed by: dilated RV on echocardiogram.
	Management: OHCM pp136–9.
Poor venous return due to abdominal or pelvic masses, post-phlebitic or thrombotic venous damage	Suggested by: onset over months. Worse on prolonged standing or sitting, varicosities, venous eczema, pigmentation or ulceration. Non-pitting oedema if chronic.
	Confirmed by: clinically with Trendelenberg test showing filling along extent of communicating valve leaks or on venous Doppler ultrasound.
Low albumin states caused by liver failure, nephrotic syndrome, malnutrition, etc.	Suggested by: generalised oedema often including face after lying down. Onset usually over months.
	Confirmed by: low serum albumin.
	OHCD p694.
Bilateral cellulitis often associated with diabetes mellitus	Suggested by: warm, red and tender legs, thrombophlebitis and tracking, ulcers etc. Onset over days.
	Confirmed by: positive blood cultures (usually streptococcal or staphylococcal). (Blood sugar ↑ in diabetes.)
	Management: OHCM pp298, 456, 486, 548.
Inferior vena cava obstruction due to prolonged immobility, carcinoma, and oral combined contraceptive use)	Suggested by: bilateral leg swelling onset over hours, assoc. risk factors (obesity, smoker, FH). Symptoms of PE.
	Confirmed by: CT abdomen, low flow on Doppler ultrasound scan or filling defect on venogram.
	Management: OHCM p194.
Bilateral thromboses	Suggested by: onset over hours, risk factor of obesity, history of immobility, carcinoma, contraceptive. Assoc. PE. Leg(s) firm, warm, tender.
	Confirmed by: no flow on Doppler ultrasound scan or filling defect on venogram.
	Management: OHCM pp446, 456, 457.
Impaired lymphatic drainage	Suggested by: firm non-tender, non-pitting oedema of gradual onset over months to years.
	Confirmed by: obstruction to flow lymphangiogram.