Undifferentiated Oedema — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr James Whitfield is a 70-year-old retired builder presenting with three weeks of progressive bilateral leg oedema, abdominal distension and exertional dyspnoea, on a background of heart failure with reduced ejection fraction (EF 34 per cent), cirrhosis from non-alcoholic fatty liver disease, type 2 diabetes and hypertension. He is on the four pillars of the heart failure therapy (bisoprolol, ramipril, spironolactone, dapagliflozin) plus furosemide 80 mg daily, and amlodipine 10 mg daily for the hypertension. [1]

His main problems are:

1. A decompensated heart failure with the raised JVP to the jaw, the bilateral basal crackles and the gallop, supported by the NT-proBNP of 2100, which is above the PRIDE rule-in cutpoint for a patient over 50.
2. A cirrhotic ascites with the portal hypertension confirmed by the SAAG of 14 g per litre (the serum albumin 28 minus the ascitic albumin 14), and the spontaneous bacterial peritonitis excluded by the ascitic neutrophil count of 30.
3. A mild proteinuria (1+ on the urinalysis) with the rising creatinine (145 from the baseline 110), most consistent with the diabetic nephropathy and the early hepatorenal syndrome rather than a primary nephrotic syndrome.
4. A drug-induced component from the amlodipine 10 mg daily, which contributes to the peripheral oedema through the arteriolar vasodilatation. [1]

My immediate priorities are the ABCDE assessment, the cautious intravenous diuresis (the furosemide uptitrated to 120 mg, monitored for the renal function and the electrolytes), the reduction or the discontinuation of the amlodipine, the consideration of the large-volume paracentesis with the albumin replacement for the symptomatic ascites, and the continuation of the four pillars of the heart failure therapy. I will reassess at 24 to 48 hours — if the creatinine rises by more than 30 per cent or the sodium falls further, I will slow the diuresis and consider the hepatorenal syndrome." [1]

Examiner probing questions and model answers

Q1: "His SAAG is 14. How does that change your management?" [1]

"The SAAG of 14 g per litre is at or above the cutpoint of 11 g per litre, which confirms the portal hypertension as the mechanism of his ascites, as established by the Runyon study of 901 paired samples [4]. The confirmation shifts my management towards the management of the portal hypertension — the spironolactone (which he is already on for the heart failure), the consideration of the large-volume paracentesis with the albumin replacement for the symptomatic relief, the evaluation for the liver transplant, and (in the selected patients) the TIPS. The SAAG also raises the question of the cardiac contribution to the portal hypertension — the raised right heart pressures from his decompensated heart failure transmit to the hepatic sinusoids and contribute to the ascites, which is why the management of his cardiac failure and the management of his cirrhosis are the two sides of the same coin. The trap to avoid is the over-diuresis — the cirrhotic target weight loss is 0.5 kg per day without the peripheral oedema and 1 kg per day with it, and a faster diuresis precipitates the hepatorenal syndrome, which is already a concern given his rising creatinine."

Q2: "How much of his oedema is cardiac and how much is cirrhotic?" [1]

"I do not try to separate them at the first assessment — I treat both in parallel and I reassess. The cardiac component is the dominant cause given the JVP to the jaw, the bilateral basal crackles, the gallop, and the NT-proBNP of 2100, and it is addressed with the cautious diuresis and the four pillars of the heart failure therapy. The cirrhotic component is confirmed by the SAAG of 14 and the ascites, and it is addressed with the spironolactone, the sodium restriction, and the consideration of the paracentesis. The reassessment at 24 to 48 hours tells me which is responding — if the JVP falls and the crackles reduce with the diuresis, the cardiac component was dominant; if the ascites persists and the creatinine rises, the cirrhotic component and the hepatorenal syndrome are the concerns. The integrated management is safer than forcing a single diagnosis at the cost of missing the other." [1]

Q3: "His NT-proBNP is 2100. How do you interpret this in the context of his cirrhosis and his renal impairment?" [1]

"The NT-proBNP of 2100 is above the PRIDE age-stratified rule-in cutpoint of 900 pg per mL for a patient over 50, which supports the cardiac contribution to his oedema and his dyspnoea [5]. But I interpret it in the clinical context — he has cirrhosis, a rising creatinine, and an acute decompensation, all of which elevate the peptide, and the value does not by itself quantify the cardiac contribution. The false-positive causes of the elevated NT-proBNP include the renal failure (the reduced clearance), the cirrhosis (the reduced clearance and the cardiac stress), and the acute illness. The synthesis is that the peptide confirms the cardiac component but does not exclude the cirrhotic or the renal contribution, and I weigh the value with the JVP, the crackles, the gallop, and the echocardiogram. The trap is treating the number rather than the patient — the diuresis is titrated to the clinical response, not to a target NT-proBNP."

Q4: "He is on amlodipine 10 mg. Should you stop it?" [1]

"Yes, I would reduce and discontinue the amlodipine. The amlodipine is contributing to his peripheral oedema through the preferential arteriolar vasodilatation that raises the capillary hydrostatic pressure, and it is not an evidence-based therapy for the heart failure. The mechanism, reviewed by Sica, is the arteriolar-venous mismatch, not the volume overload [3]. The corollary is that the diuretics are ineffective and potentially harmful in the amlodipine-induced oedema — they reduce the plasma volume and may worsen the capillary pressure mismatch. I would switch his antihypertensive to the uptitration of the ramipril (or the consideration of the ARNI if the heart failure therapy is being optimised) and the addition of the thiazide-like diuretic if the blood pressure requires it. The teaching point is that the drug history is the single most cost-effective investigation in the oedematous patient, and the discontinuation of the offending drug is often the entire treatment."

Q5: "His creatinine has risen from 110 to 145. How does that change your management?" [1]

"The rising creatinine is the early warning. The differential is the pre-renal AKI from the over-diuresis or the volume depletion, the hepatorenal syndrome from the cirrhotic decompensation, and the intrinsic renal disease from the diabetic nephropathy or the ACE inhibitor. My first step is to assess the volume status — if he is over-diuresed (the dry mucous membranes, the postural drop, the low JVP), I slow the diuresis and give a fluid challenge. If he is volume-overloaded (the raised JVP, the crackles, the ascites), the rising creatinine is the hepatorenal syndrome or the cardiorenal syndrome, and I am more cautious with the diuresis but I do not stop it — the treatment of the decompensated heart failure requires the diuresis, and the cardiorenal syndrome improves as the congestion is relieved. The 50 per cent rise rule for the ACE inhibitor — I would hold the ramipril temporarily if the creatinine rises by more than 30 per cent from the baseline, and the potassium exceeds 5.5, and I would reconsider the SGLT2 inhibitor if the eGFR falls below the threshold. The teaching point is the monitoring — the daily weight, the daily renal function, and the readiness to adjust the diuretic and the ACE inhibitor in response to the creatinine trend." [1]

Q6: "What is the role of the SGLT2 inhibitor (dapagliflozin) in his management?" [1]

"The dapagliflozin is one of the four pillars of the guideline-directed therapy for the heart failure with reduced ejection fraction, as established by the 2021 ESC Heart Failure Guidelines [5]. It reduces the heart failure hospitalisations and the cardiovascular mortality, it causes a mild osmotic diuresis and a reduction in the preload, and it is renoprotective in the diabetic kidney disease. In Mr Whitfield, it is particularly valuable because it addresses both the heart failure and the diabetes, and the mild diuresis helps the oedema. I would continue it unless there is a contraindication (the eGFR below the threshold, the volume depletion from the over-diuresis, the diabetic ketoacidosis). The four pillars together — the bisoprolol, the ramipril, the spironolactone, and the dapagliflozin — reduce the oedema by improving the ventricular function and the sodium excretion over the weeks to the months, and the oedema resolves as the heart failure improves."

Short Case Discussion

The examination for oedema

Examiner instruction: "Examine this patient for oedema. Present your findings and offer a differential diagnosis." [1]

Candidate's model answer: [1]

*"My routine is to assess the distribution, the pitting, the JVP, the cardiovascular system, the abdomen, the skin, and the Stemmer sign. Before I touch the patient, I take five seconds at the end of the bed: is the swelling localised or generalised, is the patient orthopnoeic, is the colour normal? [1]

Distribution. I inspect the face (the periorbital oedema of the renal or the hypothyroid cause), the hands, the legs (the dependent oedema of the cardiac or the venous cause), the sacrum (the recumbent or the immobile patient), and the abdomen (the distension of the ascites). [1]

Pitting. I press my thumb firmly on the medial malleolus for 5 seconds and I grade the depth and the recovery time — grade 1 (2 mm, immediate), grade 2 (4 mm, 10 to 15 seconds), grade 3 (6 mm, more than 30 seconds), grade 4 (8 mm or more, minutes). I repeat at the sacrum if the patient is recumbent. The non-pitting oedema is the lymphoedema or the myxoedema. [1]

JVP. I assess the JVP at 45 degrees — the raised JVP indicates the right heart failure, the constrictive pericarditis, the restrictive cardiomyopathy, the cor pulmonale, or the fluid overload. The Kussmaul sign (the rise on inspiration) suggests the constriction. [1]

Cardiovascular. The apex (displaced in the dilated left ventricle), the murmurs (the aortic stenosis, the mitral regurgitation, the tricuspid regurgitation), the third heart sound (the systolic heart failure), the pericardial knock (the constriction), the loud P2 (the pulmonary hypertension). [1]

Abdomen. The hepatomegaly, the splenomegaly, the ascites (the positive fluid thrill and the shifting dullness), the caput medusae (the cirrhosis), the palpable bladder or the enlarged kidneys. [1]

Skin. The haemosiderin, the lipodermatosclerosis, the venous ulcer (the venous insufficiency), the woody non-pitting skin (the lymphoedema), the palmar erythema and the spider naevi (the cirrhosis), the butterfly rash (the lupus), the orange-peel pretibial plaques (the Graves dermopathy), the dry coarse skin (the hypothyroidism). [1]

Stemmer sign. I try to pinch a fold of skin at the base of the second toe — if I cannot, the Stemmer sign is positive and the diagnosis is the lymphoedema. [1]

The examination does not stop at the legs — the oedema is a systemic sign, and the integrated assessment of the cardiac, the hepatic, the renal, the endocrine, and the skin is what identifies the mechanism and frames the first-tier investigations."* [1]

Examiner: "What is the significance of the Stemmer sign?" [1]

"The Stemmer sign — the inability to pinch a fold of skin at the base of the second toe — is the bedside discriminator between the lymphoedema and the venous oedema. The skin is thickened and tethered in the lymphoedema (the protein-rich interstitium, the chronic fibrosis) and cannot be lifted; in the venous oedema the skin is of normal thickness and can be pinched. The Stemmer sign, combined with the non-pitting quality and the woody texture, makes the clinical diagnosis of the lymphoedema and redirects the management from the compression stockings alone to the complete decongestive therapy." [1]

Examiner: "What is the single most important lesson from this examination for a registrar managing undifferentiated oedema?" [1]

"The single most important lesson is that the oedema is a systemic sign, not a local one. The registrar who examines only the legs has examined only a fraction of the patient. The integrated assessment — the distribution, the pitting, the JVP, the cardiovascular, the abdominal, the skin, and the Stemmer sign — identifies the mechanism (the hydrostatic, the oncotic, the lymphatic, the myxoedematous) and frames the first-tier investigations (the urinalysis, the albumin, the NT-proBNP, the TFTs, the chest X-ray, the echocardiogram). The corollary is that the mechanism determines the treatment — the cardiac oedema responds to the diuresis and the heart failure therapy, the cirrhotic oedema responds to the spironolactone and the paracentesis, the nephrotic oedema requires the treatment of the glomerular disease, the drug-induced oedema requires the discontinuation of the offending drug, and the lymphoedema requires the complete decongestive therapy. The registrar who reaches for the furosemide before the mechanism is identified has confused a bridge with a destination." [1]