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Fluid Overload
This article refers to fluid overload that occurs when the circulating volume is excessive, i.e. more than the heart can effectively cope with. This results in cardiac impairment.
Cardiac impairment (or cardiac failure) usually manifests as pulmonary and/or peripheral oedema. Cardiac failure activates the renin-angiotensin-aldosterone system, which further contributes to fluid retention.
- Iatrogenic: excessive intravenous fluids, blood transfusions. A fit person with normal kidneys can usually cope with excessive fluid administration up to a point. However, compensation for fluid overload is difficult or impossible for the elderly/frail patients and those with cardiac or renal impairment.
- Cardiac failure (aka cardiac impairment)
- LVF (left ventricular failure) causes pulmonary oedema ± pleural effusions
- RVF (right heart failure) causes peripheral oedema ± hepatomegaly and/or ascites
- Since one ventricle impinges upon the other, there is usually CCF (congestive cardiac failure or biventricular failure)
- Renal failure - depending on severity and whether oliguric or not
- Increased antidiuretic hormone (ADH) secretion due to head injury, or a stress response, e.g. following major surgery. This leads to hypotonic fluid retention.
- Interruption of usual treatment for cardiac or renal failure (e.g. omission of diuretics)
- Note that when the gut is oedematous, as occurs in right heart failure, oral diuretics may be poorly absorbed; this can contribute to the decompensation which occurs in exacerbations of cardiac failure
Clinical features depend upon the location and severity of the fluid overload. Acute severe pulmonary oedema causes severe respiratory distress and is an emergency. Peripheral oedema is better tolerated but may compromise skin and gut if the oedema is severe. There may be other symptoms related to cardiac or renal failure, such as general debility.
Left heart failure (pulmonary oedema)
Symptoms:
- If severe fluid overload: patient distressed, breathless and ill
- Dyspnoea: typically exertional, when supine (orthopnoea) or at night (paroxysmal nocturnal dyspnoea)
- Cough, haemoptysis or pink frothy sputum
Signs:
- Tachypnoea and/or tachycardia; respiratory distress if severe
- Breath sounds:
- In acute severe pulmonary oedema, wheezes and coarse crackles can mimic bronchospasm
- Classically, fine bilateral basal end-expiratory lung crackles. However, other sounds are possible, e.g. coarse crackles throughout the lungs
- Pleural effusions may be present
- Third heart sound ('gallop') possible
Right heart failure (peripheral fluid overload)
Symptoms and signs are:
- Raised JVP (jugular venous pressure)
- Pitting oedema of feet, legs, thighs or abdomen - depending on severity.
- Sacral oedema in bed-bound patients
- Swelling may redistribute according to posture (e.g. leg oedema improving in the morning)
- Ascites
- Hepatomegaly may occur with right heart failure
Children
Note that for young children with heart failure:
- Failure to thrive may be the main symptom
- Hepatomegaly is a more usual sign than oedema; fine lung crackles may be difficult to hear
Remember that other problems may co-exist and may contribute, e.g. pneumonia may precipitate cardiac failure in an elderly person with poor cardiac reserve.
Problems which can mimic fluid overload are:
Other causes of dyspnoea
- Pneumonia
- Bronchospasm, e.g. asthma or COPD
- Pulmonary embolism (classically with no added lung sounds)
- Acute anaphylaxis may cause wheezing (swelling of lips and tongue likely in this case)
- Fibrosing alveolitis also causes fine inspiratory crackles (though a longer history of dyspnoea is likely in this case)
Note that poor inspiratory effort may cause basal lung crackles, which will resolve after a few deep breaths.
Other causes of raised JVP
- Pulmonary embolism
- Constrictive pericarditis or cardiac tamponade cause raised JVP - which unlike normal JVP will INCREASE on inspiration
- SVC obstruction (superior vena caval obstruction) causes distention of neck and upper limb veins which is classically non-pulsatile
Other causes of peripheral oedema
- Pre-eclampsia N.B. always suspect pre-eclampsia and check urine protein if >20 weeks pregnant and unwell/oedema
- Loss of oncotic pressure due to hypoproteinaemia:
- Nephrotic syndrome
- Malnutrition or malabsorption
- Liver disease
- Lymphoedema (classically this is non-pitting)
- Venous obstruction (may be unilateral)
- Deep venous thrombosis (DVT)
- Severe varicose veins
- Pelvic mass
- IVC obstruction (inferior vena cava obstruction - unlikely to redistribute with posture)
- Pregnancy
- Pelvic or abdominal mass
- Hypothyroidism
Other causes of ascites
There are various other causes of ascites, e.g. cirrhosis, portal hypertension and malignancy. See article on ascites.
Note: if patient distressed, start treatment before investigations.
Initial investigations which will help make a diagnosis in most cases:
- ECG - cardiac arrythmias, infarction or hypertrophy
- Chest X-Ray - may identify pulmonary oedema, looks for other chest pathology, e.g. pneumonia
- Serum urea, creatinine and electrolytes - for renal function; to check if electrolyte imbalance contributing to problems
- Full blood count - for anaemia and features of infection
- Liver function tests - albumin and protein levels
- Bedside echocardiography for a sick patient may help identify the cause of cardiac dysfunction, e.g. ventricular failure, cardiac tamponade or large pulmonary embolus
Other possible investigations:
- Arterial blood gases - for ill patients or if cause of dyspnoea unclear
- BNP and echocardiography for possible heart failure
- Fluid balance charts and serial weights for monitoring response to treatment
- Further investigations if necessary according to suspected cause
This is described in the separate article on Acute Pulmonary Oedema.
Internet and further reading Acknowledgements EMIS is grateful to Dr N Hartree for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2008.
DocID: 2155
Document Version: 20
DocRef: bgp11
Last Updated: 15 Apr 2008
Review Date: 15 Apr 2010
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