Ascites Lecture Notes
Ascites is the abnormal accumulation of fluid within the peritoneal cavity. It is a clinical manifestation of an underlying disorder, rather than a single disease. Assessment must establish why the fluid has accumulated, whether infection or organ dysfunction is present, and how the abdominal swelling is affecting breathing, nutrition, movement and comfort.
These notes cover ascites under Surgical Nursing II: conditions of the abdominal cavity. Most cirrhotic ascites is managed medically, but nurses also care for patients undergoing abdominal paracentesis, investigations, shunt procedures and surgery for the underlying cause.
- Anatomy and fluid balance
- Causes, risk factors and classification
- Pathophysiology
- Clinical features and assessment
- Investigations and ascitic fluid interpretation
- Medical and procedural management
- Paracentesis: nursing responsibilities
- Nursing care plans and rationales
- Complications and emergencies
- Prevention, discharge teaching and revision questions
Anatomy and Physiology Relevant to Ascites
- Peritoneum: the parietal layer lines the abdominal wall and the visceral layer covers abdominal organs. Between these layers is a potential space containing a small amount of lubricating fluid.
- Portal circulation: blood from much of the digestive tract passes through the portal vein to the liver. Obstruction to its passage increases portal pressure.
- Hepatic veins: drain blood from the liver towards the inferior vena cava. Venous outflow obstruction can cause hepatic congestion and ascites.
- Albumin: a major plasma protein produced by the liver. It contributes to colloid osmotic pressure, helping retain water within the circulation.
- Lymphatic drainage: returns interstitial and peritoneal fluid to the circulation. Increased production or impaired drainage can overwhelm this system.
- Kidneys: regulate sodium and water excretion. Hormonal responses to reduced effective circulation can make the kidneys retain fluid even when the abdomen and legs are visibly swollen.
Clinical implication: a patient may have excess total body fluid and still have poor effective circulating volume. Abdominal swelling alone does not justify aggressive diuresis or withholding all fluid.
Causes of Ascites
1. Liver and Portal Vascular Disorders
- Cirrhosis: chronic scarring increases resistance to portal blood flow. Relevant underlying disorders include chronic hepatitis B or C, alcohol-associated disease, metabolic dysfunction-associated steatotic liver disease and autoimmune or cholestatic liver disease.
- Budd–Chiari syndrome: obstruction of hepatic venous outflow produces congestion, abdominal pain, hepatomegaly and sometimes rapid ascites formation.
- Portal vein thrombosis: may contribute to portal hypertension, particularly with additional liver disease.
- Other portal hypertensive disorders: include advanced hepatic schistosomiasis; assessment must distinguish portal hypertension from other causes of abdominal swelling.
2. Cardiovascular Causes
Right-sided heart failure and constrictive pericarditis raise systemic venous pressure. The liver becomes congested and fluid enters the abdominal cavity. Associated findings can include raised jugular venous pressure, dependent oedema and breathlessness.
3. Malignancy
Ovarian, gastrointestinal, pancreatic and other cancers may produce ascites through peritoneal involvement, lymphatic obstruction or extensive liver disease. Weight loss, early satiety, a mass, progressive abdominal enlargement or bleeding may accompany it. Ascites alone does not establish a cancer diagnosis.
4. Infection and Inflammation
- Peritoneal tuberculosis: consider when ascites is accompanied by prolonged fever, night sweats, weight loss or relevant exposure. Obtain diagnostic evidence rather than assuming all chronic ascites is tuberculosis.
- Pancreatitis or pancreatic duct disruption: enzyme-rich fluid may leak into the abdomen.
- Other peritoneal inflammatory disease: can increase vascular permeability and fluid production.
5. Low Oncotic Pressure and Other Causes
- Nephrotic syndrome: substantial urinary protein loss reduces plasma albumin and promotes oedema.
- Severe protein deficiency or protein-losing enteropathy: can contribute to low oncotic pressure.
- Chylous ascites: results from disruption or obstruction of lymphatic flow; the fluid may appear milky.
- Urinary or biliary leakage: can follow trauma, obstruction or procedures and requires specific investigation.
- Mixed causes: a patient with cirrhosis may also have heart failure, cancer or infection.
Related study: Diploma in Nursing Direct curriculum.
Risk Factors and Predisposing Conditions
Risk follows the underlying cause: chronic liver disease; harmful alcohol use; untreated viral hepatitis; obesity and diabetes associated with fatty liver disease; established cardiac or kidney disease; abdominal malignancy; tuberculosis; pancreatic disease; previous abdominal operations; and lymphatic injury. Ask about medicines and herbal preparations because some can damage the liver or kidneys. Avoid attributing ascites to alcohol without a respectful history and appropriate investigation.
Classification
| Category | Meaning | Nursing relevance |
|---|---|---|
| Grade 1 | Small volume detected by ultrasound. | Clinical examination may appear normal; investigate the cause. |
| Grade 2 | Moderate symmetrical abdominal distension. | Assess diet, mobility, fluid balance and response to prescribed treatment. |
| Grade 3 | Large or tense ascites with marked distension. | Assess respiratory compromise and need for therapeutic drainage. |
| Recurrent | Fluid repeatedly returns after initial control. | Review treatment access, adherence, sodium intake and progression of disease. |
| Refractory | Cannot be adequately controlled with tolerated medical treatment, or effective doses cause unacceptable adverse effects. | Specialist review, repeated drainage and selected advanced therapies may be needed. |
| Uncomplicated / complicated | Ascites without, or with, infection, kidney dysfunction or other major complications. | A change in condition requires reassessment rather than routine continuation of care. |
Pathophysiology
- Resistance to blood flow rises: in cirrhosis, distorted hepatic architecture obstructs portal flow.
- Pressure and fluid filtration increase: fluid movement from the hepatic and splanchnic circulation rises and lymphatic drainage may become insufficient.
- Splanchnic vessels dilate: the circulation effectively underfills despite the presence of excess fluid elsewhere.
- Compensatory mechanisms activate: the sympathetic nervous system, renin–angiotensin–aldosterone system and antidiuretic hormone favour sodium and water retention.
- Retained fluid accumulates: peritoneal fluid increases, and dependent oedema may develop. Reduced albumin can further favour movement out of the circulation.
Use this to organise the mechanisms, but remember that malignant, pancreatic and tuberculous ascites have different initiating processes.
With malignancy, tumour deposits may obstruct lymphatics and increase permeability. With heart failure, elevated venous pressure promotes congestion. With pancreatic disease, leaking secretions irritate the peritoneum. Correct treatment therefore depends on identifying the mechanism.
Signs and Symptoms
- Increasing abdominal size: clothing becomes tight and the abdomen may feel heavy or stretched.
- Weight gain: reflects retained fluid; simultaneous loss of muscle and body fat can be concealed.
- Abdominal discomfort: pressure, fullness or a dragging sensation. New severe pain suggests a complication.
- Early satiety: abdominal pressure limits meal size and contributes to inadequate intake.
- Breathlessness: large-volume fluid elevates the diaphragm and limits comfortable lung expansion.
- Reduced movement and fatigue: a tense abdomen makes walking, bending and self-care difficult.
- Dependent oedema: legs, ankles or sacral tissues may be swollen.
- Umbilical changes: the umbilicus may evert or an umbilical hernia may become prominent.
- Underlying-disease features: jaundice, easy bruising, enlarged superficial veins, muscle wasting, cardiac signs, fever or a palpable mass.
History Taking
Establish onset and progression; previous episodes and drainage; abdominal pain; fever; vomiting; bowel changes; urinary output; shortness of breath; orthopnoea; appetite and weight changes. Ask about hepatitis, liver, cardiac, renal and pancreatic disease; tuberculosis exposure; malignancy; prior operations; pregnancy possibility where appropriate; alcohol intake; medicines; allergies; and access to previous treatment. Explore how swelling affects sleep, work, relationships and ability to obtain food or attend follow-up.
Physical Assessment
- General observation: assess distress, alertness, nutritional state, jaundice and peripheral oedema.
- Vital observations: record temperature, pulse, blood pressure, respiratory rate and oxygen saturation. Interpret trends against the patient's baseline.
- Inspect the abdomen: observe distension, flank fullness, scars, visible veins, skin integrity, umbilicus and hernias.
- Auscultate: bowel sounds are assessed before palpation in a conventional abdominal examination. Sounds alone cannot exclude serious disease.
- Percuss: fluid commonly produces flank dullness with more central tympany. Shifting dullness is assessed by changing the patient's position and repeating percussion.
- Fluid wave: transmission of an impulse across the abdomen may support large-volume ascites, but obesity and abdominal wall movement can mislead.
- Palpate gently: assess tenderness, guarding, masses and organ enlargement. Avoid repeatedly eliciting painful signs.
- Measure consistently: use the same scale and timing for weight; if girth is measured, use the same anatomical level, position and tape tension.
A distended abdomen is not automatically ascites. Ultrasound helps distinguish fluid from obesity, pregnancy, a large cyst, a tumour, bowel distension or urinary retention.
Urgent Red Flags
Escalate immediately for fever or hypothermia, new abdominal pain or tenderness, hypotension, rapidly worsening breathlessness, altered consciousness, gastrointestinal bleeding, falling urine output, persistent vomiting, a painful irreducible hernia, or leakage of fluid through damaged umbilical skin. Infection can be present without dramatic fever or pain.
Investigations
| Investigation | Purpose | Practical interpretation |
|---|---|---|
| Abdominal ultrasound, with Doppler when indicated | Confirms fluid; evaluates liver, spleen, masses and vascular flow; helps select a safe drainage site. | Imaging supports the diagnosis but does not by itself determine whether fluid is infected. |
| Diagnostic paracentesis | Obtains fluid for cell count, albumin, total protein and culture; additional tests depend on suspected cause. | New-onset ascites and clinical deterioration need prompt diagnostic evaluation. |
| Full blood count | Assesses anaemia, inflammatory changes and platelet count. | Consider bleeding, infection and chronic liver disease alongside the result. |
| Urea, creatinine and electrolytes | Assess kidney function, sodium and potassium before and during treatment. | A rising creatinine or significant electrolyte change requires review of the treatment plan. |
| Liver tests and serum albumin | Evaluate liver injury and synthetic function; serum albumin is paired with fluid albumin for SAAG. | Normal aminotransferases do not exclude advanced chronic liver disease. |
| Coagulation studies | Evaluate liver disease and relevant bleeding concerns. | An elevated INR in cirrhosis does not directly quantify paracentesis bleeding risk. |
| Urinalysis / urine protein assessment | Investigates renal causes and intercurrent urinary disease. | Heavy proteinuria supports evaluation for nephrotic syndrome. |
| CT, MRI, echocardiography or endoscopy | Investigates suspected malignancy, vascular disease, cardiac disease or associated gastrointestinal problems. | Select tests from the clinical question rather than ordering all tests routinely. |
Ascitic Fluid Analysis and SAAG
SAAG = serum albumin − ascitic fluid albumin. Use samples taken close together and the same units. A gradient ≥1.1 g/dL (11 g/L) supports portal hypertension; a lower gradient suggests causes such as peritoneal malignancy, tuberculosis or pancreatic disease. Combine SAAG with the total protein and clinical findings: a high gradient with protein ≥2.5 g/dL can suggest a cardiac contribution. These are diagnostic patterns, not stand-alone diagnoses.
Worked example: serum albumin 2.8 g/dL and ascitic albumin 1.2 g/dL give a SAAG of 1.6 g/dL. This supports a portal hypertensive mechanism, but further assessment is needed to identify its cause.
Fluid neutrophils ≥250 cells/mm³ warrant prompt assessment and treatment for spontaneous bacterial peritonitis when no surgically treatable source is identified. A negative culture does not exclude infection. Send cultures promptly, with bedside inoculation into blood culture bottles according to laboratory practice. Cytology, amylase, triglycerides, tuberculosis studies or other tests are requested selectively. AASLD: diagnostic paracentesis and infection assessment.
Appearance: straw-coloured, cloudy, bloody or milky fluid can provide a clue but is not definitive. Never label bloody fluid as cancer or cloudy fluid as infection solely by looking at it.
Aims and Principles of Management
- Identify and treat the underlying cause.
- Relieve pressure and improve breathing, eating and mobility.
- Reduce fluid accumulation without causing circulatory depletion.
- Prevent or promptly treat infection and kidney injury.
- Maintain nutrition, dignity and independence.
- Plan follow-up, specialist referral and supportive or palliative care when appropriate.
Initial Support and Referral
For severe breathlessness or deterioration, begin structured airway, breathing and circulation assessment; summon clinical assistance; position for comfort; monitor observations; and administer prescribed oxygen for hypoxaemia. Obtain vascular access and investigations when indicated. Fluids and diuretics must be selected by the clinical team according to circulation, kidney function and the cause of illness. Avoid treating all abdominal swelling with unprescribed diuretics or home drainage.
Diet, Fluid and Nutrition
For cirrhotic ascites, a commonly used sodium target is approximately 2 g sodium daily, equivalent to about 5 g salt. Teach practical choices: reduce added salt, salty seasonings, stock cubes, processed meats and heavily salted snacks. Preserve adequate food intake; an excessively restrictive diet can worsen malnutrition. Routine fluid restriction is usually unnecessary unless a clinician prescribes it for significant hyponatraemia or another indication. Provide small frequent meals and a late snack when suitable. Maintain adequate protein rather than automatically imposing a low-protein diet. AASLD: outpatient cirrhosis care.
Diuretic Therapy
Spironolactone blocks aldosterone-related sodium retention; furosemide promotes sodium and water excretion through a different nephron site. Depending on presentation, spironolactone may be used alone or with furosemide. A common adult combination is spironolactone 100 mg with furosemide 40 mg daily, adjusted by the prescriber. This is an educational example, not a universal starting prescription. AASLD: rationale for combined diuretics.
- Check the prescription, renal function, sodium, potassium and blood pressure before giving treatment.
- Measure weight and intake/output; do not judge response only from the size of the abdomen.
- Monitor dizziness, cramps, dehydration, confusion and reduced urine output.
- Spironolactone may cause hyperkalaemia and breast tenderness; furosemide may cause hypokalaemia and volume depletion.
- Escalate significant abnormalities before the next dose and follow the clinician's instructions.
- Review NSAIDs and other medicines that can worsen kidney perfusion; avoid recommending unprescribed potassium supplements or salt substitutes.
Therapeutic Paracentesis and Albumin
Therapeutic drainage relieves tense or symptomatic ascites. It does not remove the underlying cause, so fluid can recur. For cirrhotic ascites, removal of more than 5 litres generally requires prescribed intravenous albumin; a commonly recommended replacement is 6–8 g per litre of total fluid removed. Smaller drainage volumes may also require albumin when acute kidney injury or circulatory vulnerability is present. For example, 6 litres at 8 g/L corresponds to 48 g; the exact product, volume and rate follow the prescription. AASLD practice guidance.
Treatment of the Cause and Advanced Options
- Liver disease: address viral hepatitis, alcohol-associated disease and other treatable causes; assess for specialist liver care.
- Cardiac disease: manage the heart disorder and congestion through the appropriate cardiac plan.
- Tuberculosis: use an established diagnostic pathway and prescribed multidrug treatment; monitor toxicity and adherence.
- Malignancy: oncology and surgical teams determine systemic therapy, procedures and symptom control. Selected patients benefit from palliative drainage.
- Pancreatic or other leakage: may require endoscopic, radiological or operative management.
- TIPS: a transjugular intrahepatic portosystemic shunt can reduce portal pressure in selected patients. Selection must consider cardiac function, liver reserve and encephalopathy risk.
- Transplantation: may offer definitive treatment for eligible patients with advanced liver disease, subject to specialist assessment and service availability.
Refractory disease needs review rather than indefinite escalation of diuretics. Consider relief of symptoms, patient priorities and access to care alongside disease-directed treatment.
Paracentesis: Nursing Preparation and Care
Diagnostic paracentesis removes a sample for tests. Therapeutic paracentesis drains a larger quantity for relief. The procedure is performed by a suitably trained clinician using aseptic technique and a selected safe site, preferably with ultrasound guidance when available.
Equipment
Prepare the prescribed drainage or sampling kit; sterile gloves and drapes; approved skin antiseptic; local anaesthetic and appropriate syringes; dressing materials; correctly labelled specimen containers and blood culture bottles if requested; a closed collection system; monitoring equipment; protective underpad; sharps container; and intravenous equipment or albumin when ordered. Check that emergency assistance and equipment are accessible according to facility policy.
| No. | Nursing action | Rationale |
|---|---|---|
| 1 | Confirm identity, indication, consent, allergies and the clinician's plan. Explain the difference between taking a sample and draining for relief. | Promotes informed participation and prevents an incorrect procedure. |
| 2 | Review medicines, relevant results and previous procedural problems; communicate bleeding concerns, pregnancy possibility, abdominal surgery or infection at a proposed site. | Allows the operator to assess individual risks and select the approach. |
| 3 | Record baseline blood pressure, pulse, respiration, oxygen saturation, pain, weight and relevant abdominal measurements. | Provides a comparison for the effect of drainage and recognition of deterioration. |
| 4 | Ask the patient to empty the bladder where feasible. Assist with the prescribed position and maintain privacy. | Reduces bladder distension and improves comfort and safe access. |
| 5 | Prepare equipment, maintain the sterile field and assist without contaminating connections or insertion materials. | Reduces introduction of organisms into the peritoneal cavity. |
| 6 | Label samples at the bedside; record time and send the requested tests promptly. | Prevents identification errors and protects diagnostic usefulness. |
| 7 | Observe the patient and drainage system; document the quantity and appearance of fluid. Follow the operator's rate and monitoring instructions. | Supports accurate fluid balance and detection of complications. |
| 8 | Immediately report faintness, hypotension, severe new pain, bleeding, increasing breathlessness or altered consciousness. | These may indicate circulatory disturbance, bleeding or visceral injury. |
| 9 | Administer prescribed albumin after checking the concentration, calculated grams, infusion volume and compatibility; monitor for reactions and overload. | Supports circulation while avoiding medication and infusion errors. |
| 10 | Apply the prescribed dressing, inspect for bleeding or persistent leakage, reassess observations and organise follow-up tests. | Identifies local and delayed systemic complications. |
| 11 | Record total drainage, specimens, medicines, observations, response, adverse events and instructions. | Provides continuity for subsequent staff and outpatient care. |
Aftercare: assist gradual mobilisation when stable, assess comfort and breathing, observe urine output, and reinforce the ongoing diet and medication plan. Do not leave a drain in place beyond the documented clinical plan. Persistent leakage, fever or new pain needs review.
Nursing Assessment, Problems, Outcomes and Interventions
Individualise the care plan. Distinguish actual problems from risks and use the assessment to support each problem. The goals below are examples; agree achievable targets with the patient and clinical team.
| Nursing problem | Evidence / contributing factors | Expected outcome |
|---|---|---|
| Excess fluid volume | Abdominal swelling, oedema and rising weight with sodium and water retention. | Fluid burden improves without hypotension, kidney injury or harmful electrolyte changes. |
| Ineffective breathing pattern | Diaphragmatic restriction from tense fluid; tachypnoea or discomfort. | Patient breathes more comfortably with appropriate respiratory observations. |
| Inadequate nutritional intake | Early satiety, poor appetite, weakness or reduced access to food. | Patient takes an agreed amount of nourishing food and maintains function. |
| Impaired comfort / pain | Abdominal stretching, procedures or underlying disease. | Pain and discomfort decrease while new concerning pain is promptly investigated. |
| Risk of impaired skin integrity | Oedema, stretched skin, pressure and reduced mobility. | Skin remains intact without pressure injury or unnoticed leakage. |
| Risk of infection | Underlying disease and invasive access. | Infection is prevented where possible and recognised early when present. |
| Knowledge and self-management needs | Unfamiliar medicines, diet, warning signs or follow-up arrangements. | Patient explains the plan using teach-back and knows where to seek help. |
| No. | Intervention | Rationale |
|---|---|---|
| 1 | Trend weight, oedema, girth if used, observations and intake/output. Distinguish measured output from estimates. | Combined measures describe response more reliably than a single abdominal measurement. |
| 2 | Review laboratory trends with the team and report rising creatinine or significant sodium/potassium abnormalities. | Fluid removal can worsen effective circulation and produce dangerous biochemical changes. |
| 3 | Position in a supported semi-upright posture if this eases breathing; reassess respiratory effort and oxygen saturation. | Reduces the mechanical discomfort from an elevated diaphragm and identifies ongoing compromise. |
| 4 | Assist pacing of activity, rest periods and safe transfers; provide a nearby toilet or urinal during diuretic treatment. | Supports independence while reducing exertion and falls. |
| 5 | Offer smaller meals, maintain oral hygiene, ask about nausea and involve a dietitian when available. | Makes intake more manageable when abdominal pressure reduces appetite. |
| 6 | Assess food availability and affordability before giving a diet plan; use familiar local foods that fit the agreed restriction. | Practical teaching is more likely to be followed than an inaccessible menu. |
| 7 | Assess pain location, severity, timing and change; give prescribed analgesia and reassess. | Measures comfort and prevents new infection or surgical pathology being dismissed as routine stretching. |
| 8 | Inspect sacrum, heels, skin folds, legs and umbilical region; reposition and provide pressure relief according to risk. | Swollen or stretched tissues and reduced movement increase skin vulnerability. |
| 9 | Keep skin clean and dry; use suitable protection from friction; avoid tight clothing and adhesive injury. | Reduces maceration and damage to fragile skin. |
| 10 | Monitor alertness, orientation and sleep pattern; promptly report new confusion. | Confusion can signal infection, electrolyte disturbance, medication effects or hepatic encephalopathy. |
| 11 | Use hand hygiene and asepsis for invasive care; inspect insertion sites and minimise unnecessary devices. | Limits preventable infection. |
| 12 | Listen to concerns about body image, repeated admissions, finances and prognosis; involve chosen supporters with permission. | Addresses barriers and distress that influence participation in care. |
| 13 | Use teach-back for medicines, sodium guidance, weight monitoring and warning signs; give clear written follow-up details. | Confirms understanding and makes discharge instructions usable. |
Evaluation
Review whether breathlessness and fullness have improved; circulation and kidney function remain stable; nutrition and mobility are improving; skin is intact; new infection signs are absent; and the patient can explain the care plan. Persistent or worsening swelling requires review of cause, complications, treatment tolerance and practical adherence barriers.
Complications
- Spontaneous bacterial peritonitis: infection of ascitic fluid without an evident surgical source. It can progress to sepsis and kidney dysfunction. Obtain diagnostic fluid promptly and begin prescribed antibiotics without avoidable delay.
- Secondary peritonitis: infection from perforation, an abscess or another intra-abdominal source. Persistent pain, unusual fluid findings or failure to improve warrants imaging and surgical assessment.
- Acute kidney injury and hepatorenal syndrome: assess infection, volume depletion, nephrotoxic medicines, obstruction and intrinsic kidney disease; do not assume every creatinine rise is hepatorenal syndrome.
- Hyponatraemia and potassium disturbances: can cause weakness, confusion and arrhythmias; management must follow a monitored clinical plan.
- Hepatic hydrothorax: fluid may enter the pleural space and aggravate breathlessness.
- Hernias and umbilical rupture: rising pressure can weaken the abdominal wall. A painful irreducible hernia or sudden fluid leakage is an emergency.
- Malnutrition and muscle loss: fluid-related weight gain can mask declining nutritional reserve.
- Paracentesis complications: include leakage, bleeding, infection, visceral injury and circulatory dysfunction.
SBP care: antibiotic selection depends on community versus hospital acquisition, severity, previous antimicrobial exposure and local resistance. Albumin is prescribed for selected patients under the infection protocol. Monitor observations, urine output, cognition and treatment response; specialist teams decide prophylaxis after recovery. Never use prophylactic antibiotics for every patient with ascites.
Prevention and Discharge Education
- Control the cause: attend hepatitis, liver, kidney, cardiac or cancer follow-up and take the prescribed treatment.
- Avoid alcohol in alcohol-associated and advanced liver disease: assess support needs and arrange safe care if withdrawal risk exists.
- Use medicines safely: keep an updated list; avoid self-prescribed diuretics, NSAIDs and unverified herbal remedies.
- Follow the agreed sodium plan: identify salt sources without sacrificing adequate nourishment.
- Monitor at home: record weight if a scale is available and note swelling, breathing and urine changes. Use the team's threshold for seeking help.
- Recognise danger signs: fever, new pain, confusion, bleeding, fainting, severe breathlessness or markedly reduced urine output require urgent review.
- Protect the skin: report sores, hernia changes and leakage instead of applying home punctures or drains.
- Keep appointments: bring medication and monitoring records; organise transport and a contact point before discharge.
Revision Questions and Clinical Reasoning
- Define ascites and explain why it is a manifestation rather than a single diagnosis.
- Classify its major causes and compare cirrhotic, cardiac, malignant and tuberculous presentations.
- Explain how portal hypertension and renal sodium retention lead to ascites.
- Describe shifting dullness and explain the limitations of physical examination.
- Calculate SAAG from paired albumin results and interpret the result with fluid protein.
- Outline the nursing preparation, monitoring and aftercare for paracentesis.
- Develop a care plan for breathlessness, poor intake and excess fluid volume.
- Explain why fever, new pain or confusion in a patient with ascites must be escalated urgently.
Do not simply increase the diuretic. Assess immediate stability, report deterioration, review kidney function and electrolytes, and assist prompt evaluation for infection and other precipitants. The apparent excess fluid does not rule out effective circulatory depletion.
References and Further Reading
The explanations and nursing applications above are written for revision. Use current facility protocols for clinical decisions and prescribed treatments.