Fluid Overload

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

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.[1]
  • Heart failure
  • Renal failure - 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).[1]
    • It is now recognised that there are complex interactions between heart, lung and kidneys which affect body fluid and sodium regulation. When one of these organs is stressed it may affect the functioning of the others and impact on fluid balance.[2][3][4]

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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.
  • 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 separate article Acute Pulmonary Oedema.
  • 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 separate article Heart Failure Diagnosis and Investigation.

Other causes of dyspnoea (see separate article on Breathlessness):

Other causes of raised jugular venous pressure (JVP):

Other causes of peripheral oedema:

Other causes of ascites, eg cirrhosis, portal hypertension and malignancy.

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.
  • Chest X-Ray - may identify pulmonary oedema, looks for other chest pathology, eg 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, eg ventricular failure, cardiac tamponade or large pulmonary embolus.

Other possible investigations:

  • Arterial blood gases - for ill patients or if cause of dyspnoea 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.

See separate Acute Pulmonary Oedema article (for acute symptoms) and Heart Failure Management article (for chronic symptoms).

  • Optimise treatment of heart failure and renal failure.
  • Be aware that caution is needed with intravenous fluid replacement, including blood transfusion.
  • For surgical patients, guidelines on appropriate postoperative fluid replacement are now available.[1]
  • For patients with severe sepsis or septic shock, Surviving Sepsis Campaign guidelines include details of appropriate fluid therapy.[5]
  • Bedside assessment of postoperative patients with oliguria:[1]
    • 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 & references

  1. Powell-Tuck J et al; British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical Patients. BAPEN Medical 2008
  2. Liang KV, Williams AW, Greene EL, et al; Acute decompensated heart failure and the cardiorenal syndrome. Crit Care Med. 2008 Jan;36(1 Suppl):S75-88.
  3. Ricci Z, Ronco C; Pulmonary/renal interaction. Curr Opin Crit Care. 2010 Feb;16(1):13-8.
  4. Bouchard J, Mehta RL; Fluid accumulation and acute kidney injury: consequence or cause. Curr Opin Crit Care. 2009 Dec;15(6):509-13.
  5. Dellinger RP, Levy MM, Carlet JM, et al; Surviving Sepsis Campaign: international guidelines for management of severe Intensive Care Med. 2008 Jan;34(1):17-60. Epub 2007 Dec 4.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Naomi Hartree
Current Version:
Last Checked:
20/04/2011
Document ID:
2155 (v22)
© EMIS