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Fluid resuscitation in critical care

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VOL: 98, ISSUE: 37, PAGE NO: 39

Daniel O’Neill, BSc, GIBiol, PGDip, RN, is staff nurse, A&E, Frimley Park Hospital, Surrey

Donna Perrin, RGN, is practice development sister, A&E, Frimley Park Hospital, Surrey

Fluid resuscitation is one of the most important aspects of the acute medical management of critically ill patients. 

Fluid volume deficits may be the result of excessive fluid loss, insufficient fluid intake or a combination of the two. Common situations leading to such deficits include blood loss, vomiting, diarrhoea and dehydration. A range of fluids are used in fluid resuscitation, the most common types being colloids and crystalloids. Colloids are mainly used as plasma volume expanders in the treatment of circulatory shock. They have large molecules that do not readily cross capillary walls and are retained in the blood vessels. They therefore restore vascular volume - stabilising circulatory haemodynamics - and maintain tissue perfusion when severe haemorrhage occurs. Common examples include the plasma substitutes Gelofusine and Haemaccel.

Crystalloids are balanced salt solutions that freely cross capillary walls (O’Neill, 2001). They are made up of water and electrolytes and stay in the intravascular compartment for a shorter time than colloids. Common examples include normal saline and sodium lactate preparations such as Hartmann’s and Ringer-Lactate solutions. Crystalloids are useful for maintaining fluid balance - for example, during the time after an operation when a patient is not able to drink - or can be used with colloids to replace intravascular volume after sudden blood loss. There is still some debate, however, about the best type of fluid for use in fluid resuscitation (Schierhout and Roberts, 1998).


Shock is a response to illness or injury characterised by a systemic imbalance between oxygen supply and demand (LeMone and Burke, 1996). Intravenous fluids are used to replace lost circulating volume and to try to reverse shock. There are five types of shock:

- Hypovolaemic shock is a reduction of intravascular volume by 15% or more, and is commonly caused by haemorrhage, burns, severe dehydration, and persistent and severe vomiting and diarrhoea;

- Cardiogenic shock occurs when the heart is unable to sustain cardiac output, for example owing to myocardial infarction, cardiomyopathy or cardiac arrest;

- Neurogenic shock is the result of an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle caused by a range of conditions including head injury, spinal trauma and prolonged heat exposure;

- Septic shock is caused by toxins produced by an infectious agent such as Pseudomonas aeruginosa, Escherichia coli or Klebsiella pneumoniae;

- Anaphylactic shock is a hypersensitivity reaction, which can be caused by a range of substances used to diagnose and treat disease, as well as foods.

The pathophysiology of shock

Fluids in the body are found within cells (intracellular fluid), between cells (intercellular fluid), and in blood vessels (vascular fluid). Intracellular and intercellular fluids form the extravascular compartment, and vascular fluid forms the intravascular compartment. Loss of circulating fluid causes decreased venous return (preload), with subsequent decreased stretch of the muscle in the right and left ventricles of the heart. This reduces cardiac output, resulting in hypotension and hypoperfusion.

The body’s response to loss of tissue fluid or blood (hypovolaemia) is directed at maintaining circulating volume. Fluid shifts from the tissues to the blood vessels and the heart rate rises (tachycardia) as a result of increased sympathetic outflow and reduced vagus nerve inhibition. The splenic bed and limb peripheries constrict (which causes the cold, pale extremities of shock), and urine output is reduced to retain fluid. At cellular level, hypoxic cells initially compensate by shifting to anaerobic metabolism. This results in the formation of lactic acid and the subsequent development of metabolic acidosis. If untreated, the cells swell and burst, resulting in marked tissue oedema and loss of function.

There are four stages of shock:

- Initial stage: the symptoms are almost imperceptible - pulse rate and blood pressure may decrease slightly and the skin may be pale, cool and moist;

- Compensatory stage: the compensatory mechanisms maintain blood pressure and tissue perfusion;

- Progressive stage: the compensatory mechanisms are unable to maintain mean arterial pressure;

- Irreversible stage: tissue anoxia is so generalised and cell death is so extensive that the damage cannot be reversed, resulting in death.

Treatment of shock aims to deal with the underlying cause, increase arterial oxygenation and improve tissue perfusion (Walsh and Kent, 2001). Volume expanders increase oncotic pressure (the component of total osmotic pressure which is due to colloids) in the intravascular space. Fluid moves from the interstitial space into the intravascular space, increasing circulating blood volume. This leads to an increase in central venous pressure and cardiac output, stroke volume, blood pressure and urinary output.

Intravenous fluids

Crystalloids - Sodium chloride 0.9% (normal saline). This provides short-term fluid replacement (30-60 minutes of blood volume replacement), because it is rapidly absorbed into the interstitial spaces. To achieve full fluid replacement, the volume that is infused must be three times the volume of blood lost.

Normal saline is useful for both short-term fluid replacement and when the fluid lost has been mostly sodium chloride (Kumar and Clark, 2002);

- Hartmann’s solution and Ringer-Lactate solution. These are buffered solutions similar to saline, but they also contain lactate, potassium, calcium and bicarbonate.

Colloids - Haemaccel and Gelofusine. These consist of modified fluid gelatin, which promotes osmotic diuresis, and have a half-life of several hours. These colloids provide excellent long-term volume replacement and are generally iso-oncotic (have equal osmotic pressure due to colloids) with blood, which they replace on a volume-for-volume basis.

The crystalloid versus colloid debate

Research has shown that colloids, although considerably more expensive than crystalloids, are no more effective (on a volume-for-volume basis) in restoring blood volume. A study of 37 randomised controlled trials of fluid resuscitation using either colloid or crystalloid preparations in critically ill patients (Schierhout and Roberts, 1998) found that colloids could cause pulmonary oedema, anaphylactic shock and lead to a small increase in risk of death. The authors of this systematic review concluded that the continued use of colloids was not supported for volume replacement. A similar review conducted in the USA (Bisonni, 1991), which looked at 26 randomised controlled trials of colloids versus crystalloids in fluid resuscitation of hypovolaemic patients, produced similar results, and the author concluded that colloids were not favoured in fluid resuscitation.

Delayed fluid management

The timing of fluid replacement has been the subject of some debate. A prospective trial comparing immediate with delayed fluid resuscitation (Bickell, 1994) included 598 adults with penetrating torso injuries who presented with a prehospital systolic blood pressure greater than 90mmHg. Patients assigned to the immediate resuscitation group received standard fluid resuscitation both before they reached the hospital and in A&E the delayed resuscitation group received intravenous cannulation but no fluid until they had reached the operating room. Among the 289 patients who received delayed fluid resuscitation, 203 (70%) survived to discharge from hospital, compared with 193 of the 309 (62%) who received immediate fluid resuscitation.

This study was one of many suggesting that it may be beneficial to delay fluid resuscitation in some situations, to ensure that the patient receives vital hospital treatment sooner (Deakin and Hicks, 1994). The timing and volume of fluid replacement are still subject to some debate, and there have been calls for further research into this area (Kwan et al, 2002).

Nursing observations and monitoring

Nurses overseeing an infusion of fluids and monitoring of hypovolaemia should be aware of the potential complications and their related symptoms. Complications of infusing large volumes of fluids can include hypothermia, acid/base disturbance, hyperkalaemia, hypocalcaemia, clotting problems and allergic reactions. Haemodynamic monitoring should be performed and, as is the case with the administration of any product, the patient should be closely observed in the first few minutes for any allergic reaction. If a reaction occurs, the fluids must be stopped immediately and the reaction noted. Patients receiving fluid infusions need to have regular checks of their blood pressure, temperature, pulse, respiration and mental state.


Although volume replacement for trauma patients is supported by the advanced trauma life support (ATLS) protocols, it may be of little benefit to the patient, particularly before admission to hospital, and may even increase the risk of death (Deakin and Hicks, 1994). Nurses who administer intravenous therapies must have a thorough knowledge of the relevant principles and applications. They must not be given without a full knowledge of the immediate and delayed effects, toxicity and implications for nursing care (Nursing and Midwifery Council, 2002). The NMC also emphasises that the administration of medicines is an important aspect of nursing practice. Nurses should not see it simply as a mechanical task to be performed to the written prescription of a doctor. It requires thought and the exercise of professional judgement.

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