Complications
This is relatively common with volume repletion, as many litres of volume may be required for adequate resuscitation. The ability to protect against oedema in the interstitium is limited in the setting of dilutional hypoalbuminaemia. The appearance of oedema does not necessarily indicate that volume repletion is adequate; haemodynamic parameters still need to be used as the guide for replacement.[5][9]
Pulmonary oedema caused by over-aggressive volume repletion is a concern in certain situations. The risk is greatest in patients with pre-existing heart disease, and in individuals with kidney failure in whom excess fluid cannot be excreted by the poorly functioning kidneys.[5]
The development of shock depends greatly on the cause of volume depletion. Massive haemorrhage for any reason can quickly lead to shock.
However, self-limiting gastroenteritis rarely results in shock in an otherwise healthy adult.
Progression to shock can be prevented if volume depletion is recognised in a timely fashion and appropriate resuscitation initiated promptly. Failure to do so in critical situations can be fatal.
Hypo- or hyperkalaemia may be a result of the underlying disorder (e.g., hypokalaemia in severe diarrhoea, hyperkalaemia in renal failure) or inappropriate inclusion of potassium in resuscitation fluids.[47]
Hypernatraemia can be observed at presentation, when water loss exceeds solute loss, or following the inappropriate use of hypertonic fluids during treatment.
Hyponatraemia can occur with excess resuscitation with electrolyte-free water or a replacement fluid that is hypotonic to the fluid that was lost. Risk is highest when water excretion by the kidney is limited by impaired kidney function or excessive vasopressin release.
Hyperchloraemic metabolic acidosis can result from rapid fluid resuscitation with isotonic saline, particularly in diabetic ketoacidosis in which ketoacids that are bicarbonate equivalents are lost in the urine.
In patients with liver disease or lactic acidosis, the lactate in lactated Ringer's solution is not converted to pyruvate and its accumulation can contribute to lactic acidosis.
Metabolic alkalosis can develop if sodium bicarbonate is used as the resuscitation fluid.
Volume depletion leads to poor renal perfusion, which is initially associated with an increased urea:creatinine ratio and low fractional excretion of sodium (FENa), a condition termed prerenal azotaemia. This disorder is reversible with correction of volume deficits.
If renal hypoperfusion is sufficiently severe and/or protracted, acute tubular necrosis (ATN) can occur. Once ATN develops, the renal damage cannot be reversed simply by restoration of normal perfusion. A longer period of time is required for recovery. ATN is characterised by the presence of granular and tubular casts in the urine and an elevated FENa. Biopsy findings are variable and inconsistent; it is usually a clinical diagnosis.
This broad term refers to renal damage manifested by an increase in creatinine, decreased urine output, or kidney failure in response to an acute event.
Specific criteria, described by the acronym RIFLE (Risk, Injury, Failure, Loss, and End stage renal disease), apply. This terminology for kidney injury was developed to provide standardised definitions for classification and research purposes and to permit diagnosis at an earlier stage. The latter could potentially provide an opportunity to intervene sooner, at a time when treatment might be more effective.[36]
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