This article refers to fluid overload that occurs when the circulating volume is excessive, ie more than the heart can effectively cope with. This results in heart failure, which usually manifests as pulmonary oedema and peripheral oedema.
- Iatrogenic - excessive intravenous fluids, blood transfusions:
- The risk of fluid overload is higher in elderly patients and if there is cardiac or renal impairment, sepsis, major injury or major surgery.
- There may be insufficient training of junior doctors regarding intravenous fluid therapy. Postoperative patients may receive inappropriately large amounts of intravenous fluid and/or sodium.
- Heart failure.
- Acute kidney injury - depending on severity and whether oliguric or not.
- Increased antidiuretic hormone (ADH) secretion - eg, following head injury or major surgery.
- Responses to physiological stress:
- Excretion of excess sodium and water is more difficult for injured or surgical patients (owing to various physiological responses to injury and surgery which affect renal function and fluid balance regulation).
- It is now recognised that there are complex interactions between heart and kidneys which affect body fluid and sodium regulation. This is known as cardiorenal syndrome. Two main types have been identified - cardiorenal, and renocardiac - based on which organ is the main originator of disease. Each type may be acute or chronic. There can be a fifth subtype, integrating all cardiorenal involvement caused by systemic diseases[2, 3].
The recommended intake of sodium and water for normal adults is:
- Sodium 70 mmol/24 hours.
- Water 1.5 to 2.5 litres (25 to 35 mL/kg/24 hours).
In normal subjects the extracellular fluid sodium concentration and osmolality are maintained by the kidneys:
- Osmoreceptors and changes in vasopressin secretion affect urinary concentration and water excretion.
- If there is sodium depletion, the renin-angiotensin-aldosterone system is activated with consequent reduction in urinary sodium.
- However, the body's response to sodium excess is sluggish and even normal subjects are slow to excrete an excess sodium load.
For hospitalised patients requiring fluid therapy, be aware that:
- There are pros and cons of crystalloid and colloid solutions. The National Institute for Health and Care Excellence (NICE) recommends crystalloids that contain sodium in the range 130-154 mmol/L, with a bolus of 500 ml over less than 15 minutes for patients needing rapid fluid resuscitation.
- So-called 'normal saline' (0.9% sodium chloride) actually contains supranormal amounts of sodium chloride (154 mmol/L sodium and chloride compared with the physiological 140 mmol/L for sodium and 95 mmol/L for chloride).
- Several studies have demonstrated that even healthy subjects find it difficult to excrete solutions with a high chloride content (in comparison with solutions such as Hartmann's). Excretion of excess sodium and water is more difficult for injured or surgical patients.
- Acutely, fluid overload usually presents as acute pulmonary oedema with symptoms of acute dyspnoea. See the separate Acute Pulmonary Oedema article.
- Chronic fluid overload (in the context of intravascular fluid overload) usually presents with features of chronic heart failure; the main symptoms are fatigue, dyspnoea and pitting oedema. For details see the separate Heart Failure Diagnosis and Investigation article.
Other causes of dyspnoea (see the separate Breathlessness article):
- Bronchospasm - eg, asthma or chronic obstructive pulmonary disease (COPD).
- Pulmonary embolism (classically with no added lung sounds).
- Acute anaphylaxis may cause wheezing (may have swollen lips or tongue).
- Fibrosing alveolitis also causes fine inspiratory crackles (long-standing symptoms usually).
- Poor inspiratory effort may cause basal lung crackles - resolve after a few deep breaths.
Other causes of raised jugular venous pressure (JVP):
- Pulmonary embolism.
- Constrictive pericarditis or cardiac tamponade cause raised JVP - which unlike normal JVP will INCREASE on inspiration.
- Superior vena cava obstruction (distention of neck and upper limb veins, classically non-pulsatile).
Other causes of peripheral oedema:
- Pre-eclampsia (always check urine protein if >20 weeks pregnant and unwell/oedema).
- Hypoproteinaemia - nephrotic syndrome, malnutrition, malabsorption or liver failure.
- Lymphoedema (classically non-pitting oedema).
- Venous obstruction (may be unilateral) due to:
Note: if the patient is distressed with acute pulmonary oedema, start treatment before investigations.
Initial investigations which will help make a diagnosis in most cases:
- ECG - cardiac arrhythmias, infarction or hypertrophy.
- CXR - may identify pulmonary oedema; looks for other chest pathology - eg, pneumonia.
- Serum urea, creatinine and electrolytes - for renal function; to check if there is electrolyte imbalance contributing to problems.
- FBC - for anaemia and features of infection.
- LFTs - albumin and protein levels.
- Bedside echocardiography for a sick patient may help identify the cause of cardiac dysfunction - eg, ventricular failure, cardiac tamponade or large pulmonary embolus.
Other possible investigations:
- Arterial blood gases - for ill patients or if the cause of dyspnoea is unclear.
- B-type natriuretic peptide (BNP) and echocardiography help diagnose heart failure.
- Fluid balance charts and serial weights for monitoring response to treatment.
- Further investigations if necessary according to suspected cause.
- Optimise treatment of heart failure and acute kidney injury.
- Be aware that caution is needed with intravenous fluid replacement, including blood transfusion. NICE has published guidance on intravenous fluid therapy in adults in hospital with algorithms covering assessment, fluid resuscitation, routine maintenance and replacement and resuscitation.
- For surgical patients, guidelines on appropriate postoperative fluid replacement are now available.
- For patients with severe sepsis or septic shock, Surviving Sepsis Campaign guidelines include details of appropriate fluid therapy.
- Bedside assessment of postoperative patients with oliguria:
- In the absence of complications, oliguria occurring soon after operation is usually a normal physiological response to surgery.
- However, at the bedside a falling urine output may be interpreted as indicating hypovolaemia and patients may be given too much sodium-containing fluid.
- The key question is whether or not the oliguric patient has significant intravascular hypovolaemia which needs treatment - this can often be assessed clinically using signs such as capillary refill, jugular (central) venous pressure, and the trend in pulse and blood pressure. Interpret the urine output according to these clinical signs and the normal effects of surgery on urine output.
Further reading and references
Hahn RG, Geback T; Fluid volume kinetics of dilutional hyponatremia a shock syndrome revisited. Clinics (Sao Paulo). 2014 Feb
Sweeney RM, McKendry RA, Bedi A; Perioperative intravenous fluid therapy for adults. Ulster Med J. 2013 Sep82(3):171-8.
Siegemund M, Hollinger A, Gebhard EC, et al; The value of volume substitution in patients with septic and haemorrhagic shock with respect to the microcirculation. Swiss Med Wkly. 2019 Feb 4149:w20007. doi: 10.4414/smw.2019.20007. eCollection 2019 Jan 28.
Montomoli J, Donati A, Ince C; Acute Kidney Injury and Fluid Resuscitation in Septic Patients: Are We Protecting the Kidney? Nephron. 2019 Aug 8:1-4. doi: 10.1159/000501748.
Powell-Tuck J et al; British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical Patients, 2011.
Ronco C, Di Lullo L; Cardiorenal syndrome. Heart Fail Clin. 2014 Apr10(2):251-80. doi: 10.1016/j.hfc.2013.12.003. Epub 2014 Feb 4.
Bouchard J, Mehta RL; Fluid accumulation and acute kidney injury: consequence or cause. Curr Opin Crit Care. 2009 Dec15(6):509-13.
Intravenous fluid therapy in adults in hospital; NICE Clinical Guideline (Dec 2013, updated May 2017)
Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb39(2):165-228. doi: 10.1007/s00134-012-2769-8. Epub 2013 Jan 30.