Important abdominal presentations Flashcards
Hepatomegaly: examination findings and causes
Pallor/anaemia: haemolysis, chronic liver disease, malignancy, marrow failure, infective endocarditis.
Jaundice: haemolysis, chronic liver disease, hepatitis.
Lymphadenopathy: lymphoma, metastatic disease, leukaemia, myeloproliferative disorders, connective tissue disorders, TB, viral hepatitis, infectious mononucleosis.
Cachexia: malignancy, TB.
Petechial rash: thrombocytopaenia in cirrhosis, leukaemia.
Herpes zoster, oral candidiasis: immunocompromised state in leukaemia, lymphoma, TB.
Stigmata of chronic liver disease: spider naevi, palmar erythema, leukonychia, digital clubbing, gynaecomastia.
Peripheral oedema: cirrhosis, right heart failure, hypoalbuminaemia.
Raised JVP: right heart failure.
Hepatomegaly: further examination of the abdomen
Look for visible masses, prominent veins, caput medusa.
Palpate in each quadrant for tenderness and masses.
Palpate specifically for the kidneys, gallbladder, and presence of ascites.
Auscultate for murmurs over the liver.
Hepatomegaly: causes
Infective: EBV, CMV, hepatitis, liver abscess, malaria, leptospirosis, amoebiasis, hydatid cyst, actinomycosis.
Neoplastic: hepatocellualr carcinoma, metastasis, myeloma, leukaemia, lymphoma, haemangioma.
Metabolic: haemochromatosis, amyloidosis, glycogen storage diseases (e.g. Hunter’s syndrome, Gaucher’s disease, Niemann-Pick disease), fat.
Congenital: Riedel’s lobe, polycystic disease.
Other: alcohol, right heart failure, Budd-Chiari syndrome, sarcoidosis.
Causes of mild hepatomegaly
Infection: hepatitis, HIV, EBV, hydatid disease.
Other: biliary obstruction, and the causes of moderate-massive hepatomegaly.
Causes of moderate hepatomegaly
Haematological: lymphoma, myeloproliferative disorders.
Infiltration: amyloidosis.
Haemochromatosis, and the causes of massive hepatomegaly.
Causes of massive hepatomegaly
Malignancy: HCC, metastasis.
Haematological: myeloproliferative disorders.
Vascular: right sided heart failure, tricuspid regurgitation.
Alcoholic liver disease and fatty infiltration.
Causes of hepatomegaly with irregular surface
Malignancy e.g. HCC, metastasis. Cirrhosis. Hydatid cysts. Amyloid. Sarcoid granulomas.
Causes of hepatomegaly with pulsatility
Vascular: tricuspid regurgitation, vascular malformation e.g. AVM.
Malignancy: HCC.
Causes of hepatomegaly with tenderness
Infection: hepatitis, malaria, EBV, hepatic abscess.
Malignancy: HCC, metastasis (stretching of liver capsule).
Vascular: right-sided heart failure, Budd-Chiari syndrome.
Biliary obstruction.
Ascending cholangitis.
Chronic liver disease: examination findings, general inspection
Pallor (anaemia).
Tattoos, needle track marks (may suggest viral hepatitis).
Digital clubbing.
Terry’s nails (proximal 2/3 of nail plate white with distal 1/3 red.
Muehrcke’s lines.
Palmar erythema.
Spider naevi (number and size correlate with severity).
Gynaecomastia.
Generalised muscle wasting.
Loss of body hair.
Testicular atrophy.
Evidence of alcohol misuse: Dupuytren’s contracture, parotid enlargement, cerebellar signs (past-pointing, ataxic gait).
Signs of decompensated liver disease: jaundice, purpura, asterixis.
Chronic liver disease: examination findings, abdominal inspection
Distension (ascites; a paraumbilical hernia may be visible).
Caput medusa.
Look also for scars, drain sites.
Chronic liver disease: palpation, percussion and auscultation
Palpate for hepatomegaly, splenomegaly.
Percuss for liver span, spleen, shifting dullness, fluid thrill.
Auscultate for either hepatic arterial bruit or venous hum (in portal hypertension; Cruveilheir-Baumgarten murmur).
Chronic liver disease: aetiology
Toxins: alcohol and other drugs, e.g. amiodarone, methotrexate.
Viral: hepatitis B and C, CMV, EBV.
Metabolic: non-alcoholic steatohepatitis (NASH), haemochromatosis, Wilson’s disease, alpha-1-antitrypsin deficiency.
Autoimune: autoimmune hepatitis, primary biliary cirrhosis, primary sclerosis cholangitis.
Chronic liver disease: clinical spectrum of alcoholic liver disease
Alcohol withdrawal syndrome including delirium tremens.
Wernicke’s encephalopathy: confusion, ataxia, and ophthalmoplegia.
Alcoholic fatty liver: fatty liver on ultrasound, abnormal liver enzymes on biochemistry with good synthetic function.
Alcoholic hepatitis: jaundice, raised liver enzymes, coagulopathy, encephalopathy.
Cirrhosis with portal hypertension.
Hepatic encephalopathy: overview
Neuropsychiatric disorder in patients with liver dysfunction (personality changes, intellectual impairment, reduced consciousness).
Diversion of portal blood into the systemic circulation via collaterals leads to a lack of hepatic detoxification.
Exposure of the brain to excessive concentrations of ammonia can cause neurotoxicity.
Severity can be graded by the West Haven classification.
Ammonia levels don’t always correlate with severity.
Other toxins implicated include mercaptans, short-chain fatty acids, and phenol.
Hepatic encephalopathy: epidemiology and prognosis
In decompensated cirrhosis, the risk of developing HE is 20% per year.
At any time, 30-45% of people with cirrhosis exhibit evidence of HE.
Development of HE is associated with a poor prognosis and strongly predicts short-term mortality in acute liver failure.
Hepatic encephalopathy: common precipitants
Increased nitrogen load: constipation, GI bleeding, blood transfusion, azotaemia, infection, hypokalaemia.
Decreased toxin clearance: dehydration (fluid restriction, diuretics, abdominal paracentesis, diarrhoea, vomiting), hypotension (bleeding, systemic vasodilatation), anaemia, portosystemic shunts.
Altered neurotransmission: benzodiazepines, psychoactive drugs.
Hepatocellular damage: continued alcohol use, hepatocellular carcinoma.
Jaundice: examination, inspection
Inspect the sclera and conjunctiva.
Using the left thumb, pull on the patient’s lower eyelid and ask them to look towards the ceiling.
Inspect the soft palate with a pen torch in cases of doubt (bilirubin is avidly taken up by tissues rich in elastin).
Check for signs of chronic liver disease.
Look for body piercings and tattoos (hepatitis risk).
Jaundice: examination, palpation
Palpate the abdomen for tenderness, masses, and organomegaly (including the gallbladder).
Jaundice: examination, percussion
Percuss for the liver, spleen, and presence of ascites.
Jaundice: examination, completion
Perform a digital rectal examination to look for pale stools (post-hepatic) or melaena (GI bleed complication).
Examine the external genitalia for hair growth and testicular size (atrophic in chronic liver disease).
Examine the hernial orifices.
Carry out a urinary dipstick test for bilirubin (post-hepatic).
Jaundice: prehepatic causes (unconjugated hyperbilirubinaemia)
Overproduction: haemolysis; ineffective erythropoiesis.
Impaired hepatic uptake: drugs (contrast agents, rifampicin), congestive cardiac failure.
Impaired conjugation: Gilbert’s syndrome, Crigler-Najjar syndrome.
Jaundice: hepatic causes (conjugated hyperbilirubinaemia)
Infection: viral hepatitis, leptospirosis, liver abscess, septicaemia.
Alcohol and toxins: carbon tetrachloride, fungi (Amanita phalloides).
Drug-induced hepatitis: paracetamol, anti-TB drugs (isoniazid, rifampicin, pyrazinamide), statins, sodium valproate, halothane.
Metabolic: haemochromatosis, alpha-1-antitrypsin deficiency, Wilson’s disease, Rotor syndrome.
Vascular: Budd-Chiari, right-sided heart failure.
Jaundice: posthepatic causes (conjugated hyperbilirubinaemia)
Luminal: gallstones.
Mural: cholangiocarcinoma, sclerosing cholangitis, primary biliary cirrhosis, choledochal cyst.
Extra-mural: pancreatic cancer, lymph nodes at porta hepatis.
Drugs: antibiotics (flucloxacillin, fusidic acid, coamoxiclav, nitrofurantoin).
Gallstones: background and epidemiology
Stones form due to the supersaturation of bile constituents, usually cholesterol.
Affects 10% of the population (and 2% of children).
Incidence increases with age (40% of women >80 years).
Male:female ratio roughly 1:2.
Typical patient: ‘5 Fs’ (female, forty, fair, fat, fertile).
Gallstones: examination, inspection
There may be no signs of gallstones.
Look for risk factors and complications.
Jaundice?
Scars of open or laparoscopic cholecystectomy.
If the patient has recently had surgery, a T-tube and drain may be visible.
A flexible tube arising from the right upper quadrant.
Gallstones: examination, palpation
Examine for a palpable gallbladder.
Gallstones: Murphy’s test
Using 2 fingers, palpate just below the costal margin in the right upper quadrant and maintain the position whilst the patient takes a deep breath.
Note any tenderness.
Repeat the procedure in the left upper quadrant.
If the patient experiences tenderness only when the right side is palpated, the test is positive.
Indicates acute cholecystitis, ascending cholangitis, empyema.
Gallstones: predisposing conditions
Haemolysis: sickle cell, hereditary spherocytosis, thalassaemia, pernicious anaemia, prosthetic heart valves.
Metabolic: diabetes, obesity, pancreatic disease, cystic fibrosis, hypercholesterolaemia, hyperparathyroidism, hypothyroidism, pregnancy.
Cholestasis: hepatitis, Caroli’s disease, parasitic infection, prolonged fasting (e.g. TPN), methadone use.
Malabsorption: (x10 risk of stone formation) IBD (especially Crohn’s), small bowel resection, bypass surgery.
Other: muscular dystrophy.
Ascites: definition and aetiology
Ascites is more than 25mL of fluid within the peritoneal cavity.
Common causes: cirrhosis with portal hypertension, peritoneal carcinomatosis.
Less common causes: hepatocellular carcinoma, Budd-Chiari syndrome, congestive cardiac failure, pancreatitis, and TB.
Ascites: complicating advanced cirrhosis
Ascites often marks the first sign of hepatic decompensation.
Occurs in >50% over 10 years of follow-up, worsens the course of disease, and reduces survival substantially.
If ascites becomes refractory to diuretics, 50% die within 1 year.
Spontaneous bacterial peritonitis is a frequent and serious complication of cirrhotic ascites and is defined as an ascitic neutrophil count >250 cell/mm^3.
Ascites: examination, inspection
If there is gross ascites, the abdomen may be distended.
Look for bulging of the flanks in a supine patient (fluid accumulates in the paracolic gutters).
Look for signs of chronic liver disease.
- Hands: clubbing, leukonychia, bruising, palmar erythema, Dupuytren’s contracture, hepatic flap, scratch marks.
- Face: anaemia, jaundice, xanthelasma, parotid enlargement, glossitis.
- Neck: Troisier’s sign/Virchow’s node (intra-abdominal malignancy).
- Trunk: spider naevi, gynaecomastia.
- Abdomen: distended superficial veins, caput medusa.
Ascites: examination, palpation
Palpate in each quadrant for tenderness and masses.
Palpation for organomegaly may be difficult in gross ascites.
Ascites: examination, percussion
Percuss borders of the liver, spleen, bladder, and any masses.
Shifting dullness.
Fluid thrill test.
Ascites: examination, completion
Examine the hernial orificies, lymph nodes and cardiovascular system (peripheral oedema and pleural effusion).
Primary biliary cirrhosis: overview
Autoimmune liver disease characterised by progressive destruction of intrahepatic bile ducts with cholestasis, portal inflammation and fibrosis.
May lead to cirrhosis, its complications, and eventually to liver transplantation or death.
Predominantly affects females in their 50s-70s.
Primary biliary cirrhosis: history
Majority are asymptomatic.
Fatigue (multifactorial: autonomic dysfunction, sleep disturbance, and excessive daytime somnolence, depression).
Pruritus (typically precedes onset of jaundice by months to years, develops independently of degree of cholestasis and stage of disease).
Vague right upper quadrant pain.
Night blindness, bony pain, easy bruising, fat-soluble vitamin malabsorption (A, D, E, and K).
Primary biliary cirrhosis: examination, inspection
Scratch marks. Pigmentation. Digital clubbing. Arthropathy (involving small joints). Xanthelasma. Xanthoma. Evidence of decompensated liver disease: jaundice, abdominal distension, dilated abdominal veins, hepatomegaly, splenomegaly, ascites, encephalopathy, asterixis.
Primary biliary cirrhosis: associated autoimmune conditions
Look for evidence of rheumatoid arthritis, thyroid dysfunction, Sjögren’s syndrome, scleroderma, SLE, coeliac disease.
Haemochromatosis: background
Autosomal recessive condition causing an abnormal accumulation of iron in the parenchymal organs, leading to organ toxicity.
Gene (HFE) for most genetic haemochromatosis (GH), lies on short arm of chromosome 6. The 2 major mutations are C282Y and H63D. Defective hepcidin (iron-regulatory hormone) gene expression or function may under most forms of non-HFE associated GH.
Carrier state ~1:10. Frequency of homozygosity ~1:200/400 but penetrance is low (higher with cofactors such as excess alcohol).
Male preponderance; menstruation has protective effect in females.
Haemochromatosis: symptoms
Often vague and non-specific: weakness, fatigue, lethargy, apathy, weight loss.
Organ specific: arthralgia, abdominal pain (hepatomegaly), amenorrhoea, loss of libido, impotence (pituitary dysfunction, hepatic cirrhosis), shortness of breath (CCF).
Impaired memory, mood swings, and irritability.
Haemochromatosis: examination findings
Hepatomegaly.
Cutaneous stigmata of liver disease (palmar erythema, jaundice, spider naevi).
Signs of portal hypertension (splenomegaly, ascites).
Arthritis and joint swelling: especially 2nd, 3rd metacarpophalangeal joints, wrists, hips, and knees.
Shortness of breath, oedema, raised JVP (dilated cardiomyopathy).
Arrhythmias (conduction abnormalities).
Altered pigmentation: bronzing or ‘slate-grey’ due to iron and melanin deposition.
Scars in cubital fossa (previous venesection).
Hair loss.
Hypogonadism (testicular atrophy, loss of axillary and pubic hair).
Increased blood and urine glucose levels (diabetes mellitus secondary to iron toxicity of pancreatic beta cells).
Signs of hypothyroidism.
Wilson’s disease: definition and epidemiology
Wilson’s disease or hepatolenticular degeneration is a rare autosomal recessive inherited disorder of copper metabolism characterised by excessive deposition of copper in the liver, brain, and other tissues.
Affects about 1/30,000 people, often manifesting as liver disease in children and adolescents, and as a neuropsychiatric illness in young adults.
Wilson’s disease: pathogenesis
The transport of copper by the P-type ATPase is defective due to one of several mutations (>300 identified) occurring within the ATP7B gene.
This gene has been mapped to chromosome 13q14.3.
Intestinal copper absorption and transport into the liver are intact, whilst incorporation into caeruloplasmin and excretion into bile are impaired.
Wilson’s disease: clinical features, neurological
Dysarthria. Dystonia. Tremor. Incoordination. Parkinsonian symptoms (rigidity, bradykinesia). Poor handwriting. Abnormal eye movements. Polyneuropathy.
Wilson’s disease: clinical features, hepatic
Acute hepatitis, chronic active hepatitis.
Cirrhosis.
Fulminant hepatic failure.
Wilson’s disease: clinical features, psychiatric
Irritability or anger, emotional lability. Hyperkinetic behaviour. Mania, depression. Psychosis. Impaired concentration. Personality changes.
Wilson’s disease: clinical features, ophthalmic
Kayser Fleischer rings.
Deposition of copper in Descemet’s membrane at the limbus of the cornea.
Greenish gold-brown, may be readily visible with the naked eye or can be identified on slit-lamp examination.
Seen in nearly all with neurological signs of Wilson’s disease.
Sunflower cataracts (visible only with slit-lamp).
Peutz-Jegher’s syndrome: background and epidemiology
Peutz-Jegher’s syndrome is due to germline mutations of the STK11 gene and is characterised by intestinal hamartomatous polyps and mucocutaneous melanocytic macules.
Autosomal dominant, with variable penetrance.
Incidence is estimated at between 1/50,000-200,000 live births.
The disease carries an increased risk of GI and other cancers, including pancreas, breast, cervix, ovary, uterus, lung, and testis.
Patients have a 93% cumulative risk of cancer by the age of 64.
~1/2 die from cancer by the age of 57.
Rapid increase in cancer risk >50 years.
Peutz-Jegher’s syndrome: examination, inspection
Pigmented macules of 1-5mm in diameter.
Most commonly around the mouth, crossing the vermilion border of the lip.
Dark brown to black (like freckles).
May also be present on hands and feet, and around the umbilicus, genitalia, and anus.
Similar lesions often occur on the buccal mucosa.
A prolapsed rectal polyp may be seen.
Peutz-Jegher’s syndrome: examination, other systems
Abdomen: inspect for scars (e.g. resulting from surgery for intussusceptions or malignancy).
A rectal mass due to a polyp may be palpable.
Testicular masses also occur: examine the testicles and check the chest for gynaecomastia (as a result of a Sertoli cell tumour).
In females, the breasts should be assessed for masses.
Appendicitis: epidemiology
The diagnosis is clinical, therefore investigations are only needed to exclude other pathology.
Lifetime risk 7%.
Overall mortality 0.2-0.8%, but higher in >70yrs due to diagnostic delay.
After the first 36hrs, perforation risk is 16-36%, with 5% risk for every subsequent 12hrs.
Appendicitis: examination, inspection
Fever.
Pain on movement.
Flexion of the right hip and a reluctance to extend it.
Flushed appearance.
Dry tongue.
Fetor oris.
Ask the patient to point to the site of pain with one finger- classically McBurney’s point (2/3 of the way along a line between the umbilicus and the right ASIS).
Appendicitis: examination, palpation
Tenderness and guarding at the right iliac fossa.
Maximal tenderness may be over McBurney’s point.
Percussion tenderness in the RIF.
Rovsing’s test: press the left iliac fossa and ask the patient if and where they feel pain, if felt at the right iliac fossa, test is positive.
Appendicitis: other tests
PR or PV examinations: tenderness on the right may indicate appendicitis, but examination may be normal.
Psoas sign: extension of the hip stretches the poses and is painful if irritated by a nearby inflamed appendix (especially retrocaecal).
Obturator sign: suprapubic pain on flexion and internal rotation of the right hip; due to obturator internus irritation by inflamed appendix.
Ulcerative colitis: definition and epidemiology
UC is an idiopathic inflammatory bowel disease characterised by colonic mucosal inflammation and a chronic relapsing course.
UC extends uninterrupted from the anal verge to involve part or all of the colon.
Apart from backwash ileitis, the small bowel is not involved.
Bimodal distribution with peaks at 15-30 years and 60s.
3x more common in non-smokers (some relapse on quitting).
Ulcerative colitis: associated conditions
Primary sclerosing cholangitis.
Cholangiocarcinoma.
Amyloidosis.
Uric acid renal stones.
Ulcerative colitis: history
Depends on extent and activity of the disease. Bloody diarrhoea. Mucous discharge. Faecal urgency. Tenesmus. Colicky abdominal pain. Fever. Malaise. Anorexia. Weight loss.
Ulcerative colitis: general inspection
Physical examination is often unremarkable, unless the patient is presenting acutely.
Aphthous ulcers.
Glossitis.
Pallor (anaemia is common).
Peripheral oedema.
Digital clubbing.
Ocular inflammation (uveitis, episcleritis, scleritis).
Cushingoid features (if steroid use).
Enteropathic arthropathy (large joint arthritis, seronegative spondyloarthropathy: sacroiliitis, ankylosing spondylitis).
Erythema nodosum (15%).
Pyoderma gangrenosum (1-2%).
Ulcerative colitis: inspection, abdomen
May be surgical scars (e.g. from hemicolectomy).
Stomas or healed stoma sites.
Abdominal drains or healed drain sites.
Ulcerative colitis: palpation
May find distended, tense abdomen.
Ulcerative colitis: percussion
Hyper-resonance (if abdomen distended).
Ulcerative colitis: auscultation
Tinkling bowel sounds (in obstruction).
Crohn’s disease: definition and epidemiology
Idiopathic inflammatory bowel disease characterised by transmural, granulomatous inflammation anywhere from mouth to anus (most common at ileocaecum).
It has a chronic, relapsing/remitting course.
Age of onset is bimodal with peaks at 15-30 and 60-80 years.
Smoking increases risk x3-4.
Crohn’s disease: intestinal complications
Malnutrition.
Fistulae.
Colorectal adenocarcinoma (Crohn’s colitis).
Short bowel syndrome (following surgical resection).
Crohn’s disease: extra-intestinal complications
Hepatic: fatty change, chronic active hepatitis, cirrhosis, amyloidosis.
Biliary tract: gallstones, sclerosing cholangitis, cholangiocarcinoma.
Renal: uric acid stones, oxalate stones.
Musculoskeletal: enteropathic arthropathy, osteoporosis.
Ocular: uveitis, episcleritis, scleritis.
Dermatological: erythema nodosum, pyoderma gangrenosum.
Haematological: anaemia (Fe, B12 and folate deficiency), thrombosis.
Crohn’s disease: history
Abdominal pain. Diarrhoea. Weight loss. Fever. Malaise. Anorexia.
Crohn’s disease: general inspection
Aphthous ulcers. Glossitis. Pallor (anaemia is common). Peripheral oedema. Digital clubbing. Ocular inflammation (uveitis, episcleritis, scleritis). Cushingoid features (if steroid use). Enteropathic arthropathy (large joint arthritis, seronegative spondyloarthropathy: sacroiliitis, ankylosing spondylitis). Erythema nodosum (15%). Pyoderma gangrenosum (1-2%).
Crohn’s disease: inspection, abdomen and perineum
Multiple surgical scars. Stomas or healed stoma sites. Enterocutaneous fistulae. Perianal skin tags, fissures, ulceration, sinuses. Abdominal drains or healed drain sites.
Crohn’s disease: palpation
May find distended, tense abdomen, mass (especially in right iliac fossa), hepatomegaly.
Crohn’s disease: percussion
Hyper-resonance (if abdomen distended).
Crohn’s disease: auscultation
Increased bowel sounds (in acute exacerbations).
Perianal disease: haemorrhoids
Hypertrophied endoanal cushions (causing symptoms).
Acute prolapse and inflammation with associated perianal lump, soreness and irritation.
May bleed.
Chronic = bleeding and pruritus ani.
Sites: primary (3, 7, 11 o’clock in the supine position- the locations of the main anal blood vessel pedicles.
Lord’s classification: 1st degree = bleeding, no prolapse; 2nd degree = prolapse, spontaneous reduction; 3rd degree = prolapse, digital reduction.
Perianal disease: fissure in ano
A superficial linear tear in the anoderm distal to the dentate line commonly caused by passage of hard stool.
Almost always in the midline: 90% posterior, 10% anterior.
Identified on inspection, often too painful to perform PR.
Causes acute, severe, localised ‘knife-like’ pain during defaecation with associated deep throbbing pain for minutes or hours after (pelvic floor spasm).
Blood is often seen on the paper when wiping.
Perianal disease: perianal abscess
Abscess within the soft tissues surrounding the anal canal.
Gradual onset, constant localised perianal pain.
Associated swelling with tenderness and possible discharge.
Perianal disease: fistula in ano
Abnormal communication between the anorectal lining and the perineal or vaginal epithelium.
Nearly always caused by a previous anorectal abscess.
Other less common causes include trauma, Crohn’s disease, carcinoma, radiation therapy, and TB.
Perianal or perineal pain.
Swelling and erythema of perianal skin.
Fever.
Tachycardia.
Discharge.
Goodsall’s rule: if the external opening is posterior to a line drawn transversely through the anus (in the supine position), the opening will be in the midline and thus have a curved tract; if the opening is anterior to this line it will have a radial tract.
Perianal disease: rectal prolapse
Protrusion of either the rectal mucosa or the entire wall of the rectum (complete prolapse).
Mainly occurs in the elderly and young children.
Obvious, large perineal lump, dark red/blue with surface mucosa and, occasionally, some surface ulceration.
Pain, constipation, faecal incontinence, mucous discharge, or rectal bleeding may occur.
Nephrotic syndrome: clinical diagnosis
Proteinuria >3g/24hrs.
Oedema.
Hypoalbuminaemia.
Hyperlipidaemia.
Nephrotic syndrome: common causes in adults
Minimal change disease (MCD).
Membranous nephropathy.
Focal segmental glomerulosclerosis.
Diabetic glomerulosclerosis.
Nephrotic syndrome: other causes
Renal amyloidosis. Lupus nephritis. Mesangiocapillary glomerulonephritis. Collapsing glomerulopathy (HIV-associated nephropathy). Light chain deposition disease.
Nephrotic syndrome: other causes of bilateral swollen legs
Right ventricular failure.
Lymphoedema.
Hypoalbuminaemia.
Hepatic failure.
Nephrotic syndrome: complications
Increased risk of thromboembolism (loss of anticoagulant factors in the urine).
Those with albumin <20g/L are often anticoagulated with warfarin.
Renal vein thrombosis: suspect if the patient develops loin pain, haematuria, and an acute deterioration in their renal function.
Pulmonary emboli.
Infection (loss of immunoglobulin and complement).
Hypercholesterolaemia.
Nephrotic syndrome: examination findings
Extensive oedema.
Periorbital swelling: typically worse in the morning.
Bilateral pitting oedema of the lower limbs: usually symmetrical, may extend up to the abdomen.
Also look for evidence of: pulmonary oedema, pleural effusion, ascites.
Chronic kidney disease: common causes in the UK
Diabetes mellitus. Glomerulonephritis, e.g. IgA nephropathy. Reflux nephropathy. Obstructive uropathy. Renovascular disease. Hypertension. Polycystic kidney disease.
Chronic kidney disease: other causes
Myeloma. Renal amyloidosis. SLE. Vasculitis. Tubulointerstitial nephritis. Scleroderma. Other inherited renal disease, e.g. Alpert's disease, oxalises, cystinosis.
Chronic kidney disease: history
Many patients with CKD are asymptomatic.
Symptoms usually develop at an advanced stage.
Fatigue, weakness (secondary to anaemia).
Breathlessness (due to fluid overload, acidosis).
Anorexia, vomiting, metallic taste in mouth (due to uraemia).
Pruritus.
Restless legs.
Bone pain.
Leg swelling.
Chronic kidney disease: examination findings
Pallor (due to chronic anaemia).
A lemon tinge to the skin (due to uraemia).
Scratch marks from pruritus.
Hypertension.
A pericardial rub (uncommon, due to uraemia).
Pleural effusions.
Palpable kidneys (causes include polycystic kidney disease, hydronephrosis).
Bilateral lower limb oedema (fluid overload or heavy proteinuria).
Distended bladder?
Chronic kidney disease: evidence that the patient is being prepared for dialysis
An arteriovenous fistula either at the wrist or in the antecubital fossa (usually non-dominant arm) for haemodialysis.
A peritoneal dialysis catheter situated in the abdomen.
Transplanted kidney: overview
A renal transplant is the most favourable and desired form of renal replacement therapy for patients with end-stage renal disease.
Simultaneous pancreas-kidney transplants are performed in patients with type 1 diabetes and stage 5 CKD.
Following a renal transplant, patients are required to take life-long immunosuppression to prevent graft rejection.
Transplanted kidneys may be from a deceased or living donor.
A transplanted kidney will lie in either the left or right iliac fossa.
Transplanted kidney: examination, inspection
Look around the bedside for clue that the patient has diabetes.
There may be lipoatrophy or lipohypertrophy at insulin injection sites.
Look for other complications of severe diabetes including signs of visual impairment due to diabetic retinopathy and peripheral vascular disease.
Transplanted kidney: examination, abdomen
A firm mass palpable deep to a diagonal scar.
It is possible that a patient may have had more than 1 transplant and could have a transplanted kidney in each iliac fossa.
An extended Lanz incision in either iliac fossa is called a Rutherford-Morrison incision.
The renal artery is usually anastomosed to the internal or external iliac artery and the renal vein to the external iliac vein.
The ureter is attached separately to the patient’s bladder.
Look for scars of previous nephrectomy (midline, chevron, or loin).
Transplanted kidney: evidence of end-stage renal disease
An arteriovenous fistula either at the wrist or in the antecubital fossa.
Small scars near the umbilicus consistent with previous peritoneal dialysis catheter placement.
Small scars beneath the clavicle on either side of the chest which might suggest previous tunnelled dialysis catheter placement.
A scar at the base of the neck consistent with parathyroidectomy (for advanced renal bone disease).
Adult polycystic kidney disease: overview
Adult polycystic kidney disease (APKD) is the commonest inherited form of renal disease with a prevalence of ~1/1000.
APKD is autosomal dominant.
25-40% of patients will have no family history.
Adult polycystic kidney disease: history
Flank or loin pain from enlarged or infected cysts.
Nocturia and polyuria (loss of urinary concentrating ability).
Hypertension.
Low grade proteinuria, persistent microscopic haematuria ± frank haematuria.
Uraemia symptoms if the patient presents late.
Adult polycystic kidney disease: examination findings
Bilaterally enlarged kidneys with irregular surfaces.
Ballotable flank masses which move caudally with inspiration and the examining hand can ‘get above’.
There may also be an enlarged liver with an irregular, lobulated edge.
Look for evidence of end-stage renal disease.
Adult polycystic kidney disease: evidence of advanced or end-stage renal disease
A scar in the iliac fossa and a mass consistent with a renal transplant.
An arteriovenous fistula either at the wrist or in the antecubital fossa for haemodialysis.
A peritoneal dialysis catheter situated in the abdomen or a scar consistent with previous catheter placement.
A scar at the base of the neck consistent with parathyroidectomy (for advanced renal bone disease).
Small scars beneath the clavicle on either side of the chest which might suggest previous tunnelled dialysis catheter placement.
Adult polycystic kidney disease: APKD associations
Cysts of other organs notably the liver, spleen, and pancreas.
Cardiac abnormalities: mitral valve prolapse, aortic regurgitation.
Intracranial aneurysms which on rupture present as subarachnoid haemorrhage- patients are screened for these if there is a strong positive family history of intracranial bleeding.
Colonic diverticula, abdominal and inguinal hernias.
Causes of bilateral renal enlargement
Adult polycystic kidney disease. Bilateral hydronephrosis. Amyloidosis (hepatosplenomegaly). Tuberous sclerosis (adenoma sebaceous or shagreen patches?). Von Hippel-Lindau disease.
