Ascites and oedema

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Fluid accumulates when hydrostatic pressure rises, oncotic pressure falls, renal sodium retention develops or lymphatic drainage is obstructed. Portal hypertension drives splanchnic vasodilatation and neurohormonal sodium retention; peritoneal malignancy increases vascular permeability and blocks lymphatics. Heart failure raises venous pressure, nephrotic or hepatic disease lowers effective circulating volume, and immobility impairs dependent return. Several mechanisms commonly coexist.

Start with the problem the person wants solved: abdominal pressure, early satiety, breathlessness, immobility, painful tight legs, leaking skin or fear about appearance. Establish speed of change, previous drainage response and how much travel, blood testing or procedure burden is acceptable. A small fluid reduction may provide more value than normalising weight, while aggressive diuresis can cause dizziness, kidney injury and loss of remaining mobility.

Examine observations, perfusion, jugular venous pressure, heart and lungs, abdomen, hernias, liver and spleen, pitting distribution, sacrum, genital area and skin. Unilateral warmth or tenderness suggests DVT or cellulitis; bilateral oedema with raised venous pressure suggests systemic congestion. Tense ascites can impair ventilation, renal perfusion and oral intake. Marked oedema may coexist with intravascular depletion.

Diagnostic paracentesis is important in new ascites, decompensated cirrhosis, hospital admission or clinical deterioration when treatment remains appropriate. Send cell count and differential promptly, culture inoculated at the bedside into blood-culture bottles, albumin and total protein; add cytology when malignancy is suspected. A neutrophil count of at least 250 cells per microlitre supports spontaneous bacterial peritonitis and requires urgent treatment under the local cirrhosis pathway.

Ultrasound-guided therapeutic drainage can relieve malignant tension quickly. Agree a symptom target, observations, drainage rate and stopping criteria; reassess pain, blood pressure, breathlessness and leakage. Routine albumin replacement after malignant-ascites drainage is not supported in the same way as cirrhotic large-volume paracentesis. In cirrhosis, British guidance recommends albumin when more than 5 litres is removed, commonly 8 g per litre drained, with lower-volume use considered in selected high-risk patients.

Diuretic prescribing must follow mechanism. Cirrhotic first-presentation moderate ascites commonly begins with spironolactone; recurrent or severe ascites often uses spironolactone and furosemide in a 100:40 mg ratio, titrated under protocol. Frail palliative patients may need lower starts and slower changes. Monitor sodium, potassium, creatinine, blood pressure and weight, usually limiting loss to about 0.5 kg daily without peripheral oedema or 1 kg with oedema.

Key points

Ascites is free peritoneal fluid; peripheral oedema is interstitial fluid. Both are signs with malignant, portal-hypertensive, cardiac, renal, venous, lymphatic, drug and low-albumin causes.
First-line assessment establishes onset, breathlessness, pain, fever, urine output, weight trend, medicines, liver and cardiac signs, unilateral versus bilateral swelling and the desired outcome.
Urgently assess fever with abdominal pain, shock, new encephalopathy, oliguria, rapidly worsening dyspnoea, unilateral painful swelling or threatened skin.
Ultrasound confirms and maps ascites before drainage; new, unexplained or clinically changed fluid usually needs diagnostic paracentesis when the result will alter care.
The serum-ascites albumin gradient supports mechanism: 11 g/L or more favours portal hypertension, whereas a lower gradient favours peritoneal disease, but interpret in clinical context.
Therapeutic paracentesis is first-line for rapid relief of tense, symptomatic malignant ascites; repeated procedures or a tunnelled catheter may suit recurrent fluid.
In cirrhotic ascites, sodium moderation, spironolactone with or without furosemide and carefully monitored paracentesis follow a different pathway; give albumin after more than 5 litres according to the cirrhosis protocol.
Diuretics are less predictably effective in pure peritoneal carcinomatosis and more likely to help when portal hypertension, heart failure or renal sodium retention contributes.
Compression is not an automatic treatment for every swollen leg: first exclude acute DVT, severe arterial disease, decompensated heart failure, infection and fragile or leaking skin.
The gold-standard plan names the mechanism, target symptom, expected time to benefit, biochemical and weight limits, escalation route and explicit stop point.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Portal hypertension

Cirrhosis, portal or hepatic venous obstruction and extensive liver metastases increase splanchnic pressure and activate renal sodium and water retention.

Peritoneal malignancy

Carcinomatosis increases capillary leak, impairs normal peritoneal lymphatic drainage and may produce protein-rich ascites that recurs rapidly.

Systemic congestion

Heart failure, renal failure, medicines and excessive fluid administration raise venous or total-body sodium load, producing dependent and sometimes abdominal fluid.

Low oncotic or lymphatic states

Advanced hepatic disease, nephrotic protein loss, severe malnutrition and lymphatic obstruction promote oedema, often alongside another hydrostatic mechanism.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Hydrostatic filtration
Raised portal or venous pressure drives water out of capillaries faster than lymphatics can return it to the circulation.
2
Effective-volume signalling
Splanchnic vasodilatation and low effective arterial volume activate renin, aldosterone and sympathetic pathways, retaining sodium despite visible fluid excess.
3
Reduced oncotic retention
Low serum albumin reduces plasma colloid pressure and facilitates interstitial fluid movement, although hypoalbuminaemia alone rarely explains all ascites.
4
Peritoneal and lymphatic leak
Tumour, inflammation or infection increases permeability and blocks resorption, creating protein-rich fluid that can recur rapidly after drainage.
5
Pressure consequences
Rising abdominal pressure limits diaphragmatic movement, compresses stomach and veins, reduces mobility and may impair renal perfusion or cause hernia leakage.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Symptomatic ascites

Increasing girth, flank fullness, shifting dullness, early satiety, reflux, breathlessness and reduced bending or mobility suggest clinically important fluid.

Portal-hypertensive pattern

Chronic liver signs, splenomegaly, thrombocytopenia, varices and a high serum-ascites albumin gradient support portal pressure as the dominant mechanism.

Malignant pattern

Known pelvic or abdominal cancer, nodularity, weight loss, lower albumin gradient and positive cytology support peritoneal disease, although cytology can be negative.

Systemic oedema

Bilateral dependent pitting, sacral swelling, raised jugular pressure or pulmonary congestion indicates cardiac, renal, hepatic or medicine-associated fluid retention.

Lymphatic oedema

Persistent asymmetric swelling, skin thickening, reduced pitting and previous nodal surgery or radiotherapy favour lymphatic obstruction.

Spontaneous bacterial peritonitisRed flag

Abdominal pain, fever, hypotension, encephalopathy or renal decline in cirrhotic ascites requires urgent diagnostic tap and antibiotics.

Red flags requiring action

Fever, abdominal tenderness, new confusion, hypotension or rising creatinine with ascites suggests infected fluid even when pain is mild.
Severe breathlessness, hypoxia or inability to lie flat may reflect tense ascites, pleural fluid, pulmonary oedema or embolism and needs cause-focused assessment.
New oliguria, postural collapse, hyponatraemia or rapid creatinine rise may follow intravascular depletion despite visible oedema.
Unilateral painful leg swelling, chest pain or haemoptysis raises venous thromboembolism and should not be treated simply with elevation or compression.
Red, hot, tender or blistering oedematous skin suggests cellulitis, necrosis or severe pressure injury.
New ascites with weight loss, a pelvic mass or altered bowel habit requires diagnostic evaluation if disease-directed treatment remains an option.
Rapid diuretic escalation without renal, sodium, potassium, blood-pressure and weight review can precipitate encephalopathy, arrhythmia and kidney injury.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line bedside assessmentFirst stepFirst line
Why
Define observations, perfusion, weight trend, girth, jugular pressure, lungs, abdominal tension, pitting distribution, skin and unilateral features.
Interpretation and limitations
This separates urgent infection or organ compromise from stable symptom burden and guides whether drainage, diuresis, venous imaging or skin care comes first.
02
Abdominal ultrasound
Why
Confirm fluid, estimate distribution, identify loculation and mark a safe drainage site; add liver, portal, ovarian or mass assessment when relevant.
Interpretation and limitations
Ultrasound is first-line imaging and improves procedural safety but does not alone establish malignant versus portal-hypertensive mechanism.
03
Diagnostic paracentesis
Why
Send cell count and differential, bedside-inoculated culture, albumin and protein; add cytology, amylase or other tests for the clinical question.
Interpretation and limitations
Neutrophils at least 250 per microlitre support spontaneous bacterial peritonitis; positive cytology supports malignancy but a negative result does not exclude it.
04
Serum-ascites albumin gradient
Why
Subtract ascitic albumin from serum albumin sampled near the procedure to estimate whether portal pressure drives fluid.
Interpretation and limitations
A gradient at least 11 g/L favours portal hypertension; lower values favour peritoneal inflammation or malignancy but require clinical correlation.
05
Blood and urine profile
Why
Check full blood count, CRP, renal function, sodium, potassium, albumin, liver tests, clotting and urinalysis or protein quantification where relevant.
Interpretation and limitations
Results identify infection, synthetic failure, nephrotic loss and safe limits for drainage and diuretic adjustment; INR alone does not predict every procedural bleed.
06
Cause-directed gold-standard imaging
Why
Use contrast CT abdomen and pelvis, echocardiography or venous duplex when malignancy, cardiac failure or DVT needs anatomical definition.
Interpretation and limitations
The gold-standard test depends on the suspected mechanism; order it only when the result can change a goal-concordant treatment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Bowel distension

Constipation, ileus or obstruction causes tympanitic enlargement, colic and vomiting and can coexist with a smaller ascitic volume.

Bladder retention or mass

A central lower abdominal swelling, urinary symptoms or focal contour suggests retention, organ enlargement, cyst or tumour rather than free fluid.

Deep-vein thrombosis

New unilateral swelling, tenderness, warmth or asymmetry requires prompt venous assessment rather than routine oedema treatment.

Cellulitis and lymphoedema

Erythema, fever and tenderness suggest infection; non-pitting thickened skin and stemmer change support chronic lymphatic failure.

Venous or cardiac oedema

Dependent pitting, varicosities, raised jugular pressure, crackles or orthopnoea points to venous insufficiency or systemic cardiac congestion.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Immediate assessmentExclude infection and organ compromiseFirst stepAscites or oedema is new, rapidly worse, painful, febrile or associated with breathlessness, confusion or oliguria.

1EscalationAssess ABCDE, sepsis, respiratory effect, perfusion, urine output, unilateral leg signs and skin; clarify escalation wishes without delaying immediate comfort.
2Obtain urgent bloods and ultrasound and perform diagnostic paracentesis promptly in cirrhosis or suspected peritonitis when safe; investigate DVT or cardiac failure as indicated.
3Treat infection, thrombosis or decompensated organ failure within goals and use monitored therapeutic drainage when pressure is causing severe symptoms.

02Malignant ascitesDrain for a defined symptom targetTense or recurrent ascites from peritoneal or advanced malignant disease causes pressure, dyspnoea, early satiety or immobility.

1Confirm accessible fluid by ultrasound, discuss prognosis and choose a target such as easier breathing or eating; check procedure and bleeding risks under local protocol.
2Perform symptom-led paracentesis with observations, controlled flow and stop criteria; routine albumin is not automatically required for malignant drainage.
3Record duration of benefit and recurrence burden; consider repeat day-case drainage, tumour treatment or a tunnelled catheter with specialist and community support.

03Portal-hypertensive ascitesCombine sodium control, diuresis and safe drainageCirrhosis or portal hypertension is the dominant mechanism and active management remains beneficial.

1Moderate dietary sodium without worsening intake, stop contributing medicines where possible and select spironolactone alone or with furosemide according to first versus recurrent ascites.
2Titrate by weight, symptoms, blood pressure, sodium, potassium and renal function; pause or reduce for excessive loss, severe hyponatraemia, potassium change, encephalopathy or kidney injury.
3For tense or refractory fluid, arrange large-volume paracentesis and give albumin under the cirrhosis protocol when more than 5 litres is removed; seek hepatology advice about recurrence options.

04Peripheral oedemaProtect skin and match treatment to causeDependent swelling, discomfort, leakage or reduced mobility dominates rather than abdominal tension.

1Assess systemic congestion, medicines, renal and hepatic function, venous disease, DVT, arterial supply, infection, skin and the person's ability to tolerate compression.
2Treat the cause where beneficial and use elevation, ankle movement, pressure relief, emollient, absorbent non-adherent dressings and appropriate footwear; never puncture oedematous skin to release fluid.
3Use diuretics for systemic sodium retention and specialist compression for venous or lymphatic oedema only after contraindications are addressed; review comfort and skin frequently.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Aldosterone antagonism is first-line diuresis for cirrhotic sodium retention and may help malignant ascites with a portal-hypertensive component.

Spironolactone for portal-hypertensive ascites

A common cirrhosis regimen starts at 100 mg orally daily and titrates at intervals toward 400 mg if required; frail palliative patients often need a lower individual start under local hepatology guidance.

Monitor potassium, sodium, creatinine, blood pressure and weight; avoid or pause in severe hyperkalaemia, progressive kidney injury or symptomatic volume depletion and review interacting medicines.

Adds loop diuresis, balances potassium effects and can relieve concurrent pulmonary or peripheral congestion more rapidly.

Furosemide with spironolactone

For recurrent or severe cirrhotic ascites, a common paired start is furosemide 40 mg with spironolactone 100 mg orally daily, titrated in the same 40:100 ratio under protocol.

Over-diuresis causes hypovolaemia, hyponatraemia, hypokalaemia, kidney injury, gout and encephalopathy; ototoxicity is a concern with high or rapid intravenous dosing.

Reduces post-paracentesis circulatory dysfunction and renal complications in cirrhotic large-volume drainage.

Human albumin after cirrhotic paracentesis

When more than 5 litres is removed in cirrhosis, give 20% or 25% albumin equivalent to 8 g per litre removed according to the local large-volume paracentesis protocol.

This rule should not be transferred automatically to malignant ascites; verify product concentration and total grams and monitor for pulmonary oedema or fluid overload.

Treats a time-critical infection that may present with encephalopathy or renal decline rather than prominent abdominal signs.

Antibiotics for suspected ascitic infection

Give the local empiric spontaneous bacterial peritonitis or intra-abdominal sepsis regimen promptly after cultures when possible, adjusting for allergy, renal function, acquisition setting and resistance risk.

Do not wait for culture or cytology when sepsis is likely; review microbiology, renal dosing, Clostridioides difficile risk and secondary prophylaxis with hepatology or microbiology.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Infection and peritonitis

Ascitic infection may cause pain, fever, encephalopathy, renal deterioration or shock and can present subtly in advanced cirrhosis.

Respiratory and nutritional compromise

Tense fluid elevates the diaphragm, reduces tidal volume, causes reflux and early satiety and worsens frailty and breathlessness.

Renal and electrolyte injury

Disease, over-diuresis or rapid haemodynamic change can cause hyponatraemia, potassium disturbance, acute kidney injury and hepatorenal physiology.

Skin failure and infection

Oedematous skin becomes fragile, painful and leaky, with increased pressure damage, fungal disease, cellulitis and poor wound healing.

Procedure burden

Repeated drainage can cause bleeding, infection, leakage, hypotension, protein loss and recurrent travel that may outweigh short-lived symptom benefit.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record the specific target before drainage or diuresis: breathlessness, pressure, eating, walking, sleep or skin comfort.
During drainage monitor pain, pulse, blood pressure, respiratory symptoms, flow, volume, leakage and the agreed stopping threshold.
During diuresis monitor daily weight initially, postural symptoms, urine output, sodium, potassium and creatinine at a frequency matched to instability.
In cirrhosis keep weight loss within the protocol range, commonly no more than 0.5 kg daily without oedema or 1 kg with oedema.
Inspect oedematous skin for weeping, maceration, fungal change, cellulitis and pressure injury and reassess any compression plan.
After each malignant drainage document symptom gain, time to recurrence and procedure or travel burden to inform the next decision.
Review whether prognosis, performance or goals have changed enough that repeated blood tests, diuresis or drainage now causes more burden than benefit.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Visible fluid can hide depletion

A person with litres of ascites can still have low effective arterial volume and develop postural symptoms or kidney injury during diuresis.

Mechanism predicts diuretic benefit

Portal and cardiac sodium retention usually responds better than isolated peritoneal carcinomatosis, where drainage often gives faster relief.

Albumin rules are context specific

Evidence for albumin after large-volume cirrhotic paracentesis should not be assumed to apply to routine malignant-ascites drainage.

A negative cytology is not exclusion

Tumour type, sampling and peritoneal shedding affect sensitivity, so imaging and the wider clinical picture remain important.

Compression needs diagnosis

Elastic pressure can harm severe arterial disease and be intolerable in decompensated heart failure, cellulitis or fragile leaking skin.

Duration of relief matters

Recording days of symptom benefit after drainage is more useful for future planning than recording volume alone.

11Common pitfallsFrequent interpretation and management errors.

01
Calling every enlarged abdomen ascites without ultrasound or considering constipation, retention and mass.
02
Missing spontaneous bacterial peritonitis because fever or guarding is absent.
03
Treating visible oedema as proof of adequate intravascular volume.
04
Using the serum-ascites albumin gradient as a stand-alone cancer test.
05
Prescribing escalating diuretics for peritoneal malignant ascites without a response target.
06
Removing large-volume cirrhotic fluid without the appropriate albumin protocol.
07
Giving albumin routinely after every malignant-ascites drainage without an indication.
08
Applying compression before excluding DVT, severe arterial disease, infection and decompensated heart failure.
09
Focusing on litres drained while failing to record symptom benefit and recurrence interval.
10
Continuing burdensome drainage or blood monitoring after the agreed outcome is no longer achieved.