Complications of treatment
Numerous complications can occur as a result of fluid therapy. Perhaps the most obvious is the administration of too much fluid. When this occurs, the heart can fail to pump the expanded circulatory volume effectively.
Over-distension of the left ventricle can cause heart failure and, consequently, pulmonary oedema. Patients suffering from this complication will display symptoms of a cough (producing a pink, frothy sputum) and respiratory distress — often worse when lying down. Renal failure and pre-existing ventricular impairment can exacerbate this condition.
Abdominal compartment syndrome and acute respiratory distress syndrome are both known consequences of excessive fluid resuscitation and fluid overload. Particular care has to be taken when treating any patient with co-existing cardiac or respiratory failure, or who is at risk of haemodynamic instability. By the time peripheral oedema or lung oedema are apparent, these patients have already been harmed by excessive volume or wrong choice of intravenous fluid.
Biochemical abnormalities occur frequently in patients receiving IV fluid therapy and reflect the response to the fluid administered. Infusions of NaCl 0.9 per cent can result in over provision of sodium and chloride — the latter being a strong anion that can result in hyperchloraemic acidosis.
In patients with underlying tendency to acidosis (eg, those with CO2 retention secondary to respiratory failure, or increased lactate levels following surgery), compensation mechanisms can easily be overwhelmed, resulting in severe metabolic acidosis.
Risks are also associated with over-rapid correction of disturbed sodium levels. When using fluids to alleviate hypernatraemia, particularly of chronic duration (more than two days), the aim should be to reduce plasma sodium levels by no more than 0.5mmol/L per hour. This prevents the development of cerebral oedema.
Too rapid correction causes brain cells to shrink in response to the rapid rise of extracellular osmolality, resulting in a syndrome called central pontine myelinolysis. To avoid this, the absolute change in sodium levels should not exceed 20mmol/L during the first 48 hours of treatment.
Hypertonic saline solutions must not be administered in fluid-overloaded patients because they can precipitate heart failure. Hyponatraemia due to excess fluid should be treated by fluid restriction or diuretics.
Administering IV fluids in large volumes will inevitably lead to haemodilution. Following successful resuscitation, the resulting fall in haemoglobin levels usually corrects itself within a few days as the extra fluid is cleared by the kidneys. However, a blood transfusion may be required depending on the patient’s condition and local transfusion criteria.
Dilutional coagulopathy is another effect of high volume administration. In addition, some colloid infusions impair components of the clotting cascade. This is probably of less clinical consequence with colloids of smaller molecular size, but starches of higher molecular weight have been associated with increased bleeding. For example, dextran solutions are known antithrombotic agents and are mainly used nowadays for this indication.
It has recently been suggested that starch solutions could potentially cause renal impairment. A possible explanation is hyperoncotic acute renal failure. If these products are given with insufficient water, the oncotic pressure of plasma is raised to the point where it effectively opposes the filtration pressure in the kidneys, thereby impairing normal glomerular filtration.
Current evidence for this suggests that certain types of HES are associated with increased morbidity. Although this may not be transferable to all starch infusions, serious consideration should be given before treating patients with large amounts of any HES.
A further risk associated with colloids, particularly high molecular weight starches and dextrans, is the occurrence of hypersensitivities and anaphylactic reactions.
Lobo DN, Dube MG, Neal KR, Simpson J, Rowlands BJ, Allison SP. Problems with solutions: drowning in the brine of an inadequateknowledge base. Clinical Nutrition 2001;20:125–30.
Rivers E, Nguyen B, Hanstad S, Ressler J, Muzzin A, KnoblichB, et al. Early goal-directed therapy in the treatment of severe sepsisand septic shock. New England Journal of Medicine 2001;345:1368–77.
Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, JaeschkeR, et al. Surviving sepsis campaign: International guidelines formanagement of severe sepsis and septic shock: 2008. Critical CareMedicine 2008;36:296–327.
Perel P, Roberts I. Colloids versus crystalloids for fluidresuscitation in critically ill patients. Cochrane Database ofSystematic Reviews 2007, Issue 3.
The SAFE study investigators. A comparison of albumin andsaline for fluid resuscitation in the intensive care unit. New EnglandJournal of Medicine 2004;350:2247–56.
Bunn F, Trivedi D, Ashraf S. Colloid solutions for fluidresuscitation. Cochrane Database of Systematic Reviews 2007, Issue 4.
Grocott MPW, Mythen MG, Gan TJ. Perioperative fluid managementand clinical outcomes in adults. Anesthesia and analgesia2005;100:1093–106.
Cotton BA, Guy JS, Morris JA, Abumrad NN. The cellular,metabolic and systemic consequences of aggressive fluid resuscitationstrategies. Shock 2006;26:115–21.
Morgan TJ. Clinical review: The meaning of acid-baseabnormalities in the intensive care unit – effect of fluidadministration. Critical Care 2005;9:204–11.
Katharina Floss is directorate pharmacist for critical care, theatres and anaesthetics at Oxford Radcliffe Hospitals NHS Trust.
Mark Borthwick is consultant pharmacist for critical care at Oxford Radcliffe Hospitals NHS Trust.
Christine Clark is a freelance journalist and former member of a nutrition group at Hope Hospital, Manchester