Approach

The diagnosis of volume depletion relies on clinical suspicion, careful history, and physical examination, supported by appropriate laboratory investigation.

Children and older people are at most risk due to their more limited capability to compensate for volume loss and potentially diminished capacity to communicate symptoms. Other risk factors include diuretic therapy and reduced levels of consciousness with limited access to fluids.

History and physical examination

In cases of haemorrhage, there will often be clear physical evidence or historical context that indicates a likelihood of volume depletion. Fractures, lacerations, and crush injuries can rapidly lead to substantial volume depletion, with resultant hypotension and compensatory tachycardia. However, even in the absence of obvious injury, the potential for hidden intra-abdominal or intrathoracic haemorrhage should always be considered.

With volume depletion of a non-traumatic and less acute onset, diagnosis can be more difficult. Features of the history and physical examination that would support a diagnosis of volume depletion in these circumstances include:

Orthostatic hypotension, postural tachycardia, and postural dizziness

  • These are important features to elicit. Wherever possible, vital signs should be checked in both supine and standing positions, as postural change can often reveal a significant increase in pulse rate and decrease in blood pressure on standing.[2][5] When haemorrhage is suspected, postural dizziness has a sensitivity of 22% for moderate blood loss and 97% for severe blood loss. The specificity is 98%. This finding is less well established with volume depletion from other causes.[2] Postural dizziness can also be a sign of conditions other than volume depletion, such as autonomic insufficiency. In cases when the patient’s systolic BP is <90 mmHg, it is often not necessary and even dangerous to check for orthostatic vital signs.

  • Orthostatic hypotension is defined as a decrease of >20 mmHg in systolic blood pressure from supine to standing and/or a drop in diastolic pressure of >10 mmHg from supine to standing,[2] although this may also occur in cases of autonomic insufficiency or from treatment with certain antihypertensive medications.

  • An increase in pulse rate of >15 beats per minute indicates significant orthostatic changes. An increase in pulse rate of >30 beats per minute from supine to standing has a sensitivity of 22% for moderate blood loss and 97% for severe blood loss. The specificity is 98%. This finding is less well established with volume depletion from other causes.[2]

Thirst

  • Thirst is a non-specific symptom that may be seen with volume depletion when associated with true water deficit (i.e., dehydration with hypernatraemia), which may occur with or without accompanying hypovolaemia.

Fatigue

  • Although non-specific, patients with volume depletion frequently report fatigue, which is a manifestation of decreased tissue perfusion.

Muscle cramps

  • These can be a reflection of decreased tissue perfusion or electrolyte abnormalities.

Abdominal pain

  • Some people, especially older people, may have atherosclerotic changes of the mesenteric vasculature of sufficient severity that volume depletion can trigger ischaemic abdominal pain, sometimes termed abdominal angina. However, abdominal pain can also be a symptom of intra-abdominal bleeding, bowel obstruction, or pancreatitis, which can also be a cause of volume depletion.

Chest pain

  • Similarly, patients with coronary atherosclerosis can suffer cardiac ischaemia and angina due to hypotension associated with volume depletion.

Confusion

  • A non-specific sign, but may reflect poor cerebral blood flow or uraemia associated with impaired kidney function.

Decreased skin turgor

  • Suggests dehydration. This sign is less helpful in older adults, as they have decreased elasticity of their skin as part of ageing.

Dry mucous membranes

  • May be suggestive of volume depletion, particularly in the setting of prolonged poor oral intake, vomiting, or diarrhoea. Usually reflects associated dehydration. It is not a very useful sign in cases of acute, haemorrhage-related volume depletion.

Sources of volume loss

When a diagnosis of volume depletion is being considered, it is important to identify all the possible sources of volume loss, as these determine the most appropriate management.

Blood loss

  • Blood loss sufficient to manifest clinical changes is usually not subtle. Bleeding may be from haematemesis, melaena, haematochezia, or obvious traumatic injuries. Less apparent bleeding, such as intra-abdominal haemorrhage or crush injury causing haemorrhage into a large muscle, can also lead to hypovolaemia. The thigh, for example, can hold litres of blood despite only minimal apparent swelling. Massive blood loss can also occur with a vascular catastrophe such as a ruptured abdominal aortic aneurysm, where back pain may be the only initial symptom.

Gastrointestinal losses

  • Patients may describe frequent diarrhoea and/or vomiting, and be unable to maintain adequate oral intake to compensate for the losses. Hospitalised patients may become volume-depleted due to large volume losses from nasogastric suction or enteral drainage if they do not receive appropriate maintenance or replacement fluids.

Renal losses

  • Increased urine output may be difficult to document or confirm, as patients do not routinely record daily urine outputs. Volume depletion due to renal causes occurs if there is ongoing urinary solute and fluid loss without adequate replacement. A patient may present with a history of polyuria in the setting of uncontrolled diabetes or while receiving diuretic drugs.

Skin losses

  • Losses from sweating alone can cause hypovolaemia when there is limited access to solute and water replacement. This is generally seen in conditions of extreme heat and heavy physical exertion. Fluid loss from burns is more likely to lead to clinically significant hypovolaemia, as the fluid lost has a similar solute composition to plasma whereas sweat is hypotonic.

Respiratory losses

  • These are rarely sufficient to result in volume depletion, but it may occur in patients who lose a large amount of fluid through a draining pleural effusion or from increased bronchial secretions.

Third-space sequestration

  • Extracellular fluid becomes sequestered in a space other than the intravascular or interstitial space. Examples include severe pancreatitis (fluid in the retroperitoneal space), intestinal obstruction (fluid in the gastrointestinal [GI] tract), crush injury (fluid in damaged or devitalised muscle), and peritonitis (fluid in the peritoneal space).[9]

Diagnostic tests

Treatment of clinically confirmed cases of volume depletion must be instituted promptly. Nonetheless, laboratory investigations help to diagnose the severity and underlying causes of the volume depletion (particularly in less acute situations) and are important in guiding and monitoring treatment after the initial treatment phase.

Initial tests should include:

  • Basic metabolic profile (sodium, potassium, chloride, bicarbonate, blood urea nitrogen, creatinine, glucose, calcium): dehydration often presents with hypernatraemia. Hypokalaemia and decreased bicarbonate may be seen in diarrhoea. Elevated serum glucose may cause osmotic diuresis. Serum creatinine and urea may be elevated in the setting of acute kidney injury. A urea:creatinine ratio >20:1 infers poor renal blood flow and prerenal azotaemia, which often accompanies volume depletion. However, urea may also be elevated in GI bleeding or hypercatabolic states, or with glucocorticoid therapy.

  • For adults suspected of having sepsis, Surviving Sepsis Campaign guidelines suggest measuring blood lactate.[14] The presence of an elevated or normal lactate level significantly increases or decreases, respectively, the likelihood of a final diagnosis of sepsis in patients with suspected sepsis. However, lactate is neither sensitive nor specific enough to rule in or rule out the diagnosis on its own. Serum lactate level should be interpreted considering the clinical context and other causes of elevated lactate.[14]

  • FBC (to show haemoglobin and haematocrit): An elevated haematocrit may signify haemoconcentration due to plasma volume depletion. On the other hand, an acute decrease in haemoglobin and haematocrit may be indicative of massive blood loss.

  • Urinalysis: an elevated urinespecific gravity is consistent with dehydration.

In sepsis, serial measures of procalcitonin can be useful as a guide to the need to continue or stop empirical antibiotics, alongside clinical evaluation.[14][15][16] Urine sodium, urine chloride, urine creatinine, urine urea nitrogen, fractional excretion of sodium and/or urea, and urine osmolality may also be appropriate to assess renal response to volume depletion or the aetiology of accompanying acute renal failure. Urine sodium or urine chloride <20 mmol/L (mEq/L) suggests volume depletion. Fractional excretion of sodium (FENa) may also be calculated using the following formula: (urine sodium x plasma creatinine)/(plasma sodium x urine creatinine) x 100. FENa <1% suggests prerenal azotemia, which is a reflection of poor blood flow to the kidney that can be seen in volume depletion. FENa may not be accurate in the setting of diuretic use.[3] In this case, fractional excretion of urea (FE urea) may be calculated using the following formula: (urine urea x plasma creatinine)/(plasma urea x urine creatinine) x 100. FE urea <35% suggests prerenal azotemia. A urine osmolality >450 mOsm/kg is due to water conservation by the kidney, mediated by antidiuretic hormone. This occurs in response to hypertonicity from either dehydration or dehydration with volume depletion. This is not seen if urinary concentrating ability is impaired.

Arterial blood gases may be obtained to help assess the acid-base status of the patient. This is important as low bicarbonate levels may occur with prolonged diarrhoea or high levels of bicarbonate with prolonged vomiting. Hypotension and effective volume depletion from shock often cause lactic acidosis.

Nasogastric lavage, rectal exam, or faecal occult blood testing are done in the setting of non-critical GI bleeding. Upper GI endoscopy and/or colonoscopy can be used to identify, and potentially intervene on, sources of gastrointestinal bleeding.

Ultrasound and/or computed tomography scanning may be appropriate to identify the nature, position, and extent of third-space sequestration in cases of ascites, intestinal obstruction, or pleural effusion, and help to identify any underlying causes.

Stool culture may be appropriate in cases of severe diarrhoea.

A novel, portable, nuclear magnetic resonance (NMR) sensor may offer an alternative non-invasive way of evaluating the hydration status in dialysis patients. With this approach, fluid overload can be detected before it is apparent on clinical examination. While not yet available clinically, the NMR sensor holds great promise as a new tool to evaluate body water content.[17]

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