Monitoring Renal Function

MONITORING FLUID BALANCE

Monitoring fluid balance in critical illness is paramount. Constant monitoring and vigilance by the nurse coupled with an understanding of disease processes are vital because clinical conditions can deteriorate rapidly (Murphy and Byrne 2010). Fluid and electrolyte overload is sometimes difficult to avoid because in critical illness the basic senses such as hunger and thirst are abolished by disease processes or treatments. Therefore survival depends on the appropriate administration of volumes of fluids and appropriate quantities of electrolytes and nutrition to match often excessive losses.

Careful monitoring of the fluid balance chart must be maintained and this should include all input and output. Monitoring the patient for signs of fluid loss/gain should also be undertaken and Table 7.1 provides an overview of this. The importance of monitoring urine output, urine osmolality and specific gravity of urine has already been discussed.

Table 7.1 Systemic signs and symptoms of fluid loss and gain

Reprinted by permission of Baillière Tindall from Sheppard & Wright (2000).

Daily measurement of serum sodium, potassium, urea and creatinine is required to assess fluid and electrolyte balance. In addition, fluid balance charts from the preceding few days should be compared with serum and urine urea and electrolyte values. This will help evaluate the patient’s response to fluid administration and guide the fluid regimen over the next 12–24 hours. The nature and volume of any fluid replacement therapy will depend on fluid losses.

MANAGEMENT OF ACUTE RENAL FAILURE

Acute renal failure, or acute kidney injury (AKI) as it is being termed in the literature, is a syndrome characterised by a rapid (hours to days) decrease in the kidneys’ ability to eliminate waste products, which results in an accumulation of end-products of nitrogen metabolism (urea and creatinine). It has been reported to occur in up to 20% of the ICU population, with associated high mortality rates of 60–80%, particularly if multiorgan dysfunction syndrome (MODS) coexists.

The kidney is a very vascular organ and acquires about 25% of cardiac output (Murphy and Byrne 2010). Prerenal failure, i.e. when the kidney is affected by systemic factors that cause a reduction in the glomerular filtration rate (GFR), is by far the most common form in critical illness (Bellomo 2009). Inadequate renal perfusion resulting from reduced cardiac output, hypotension or raised intra-abdominal pressure leads to reduced GFR (Bellomo 2009). However, around 50–60% of patients who have ARF will revert to normal renal function after treatment (Murphy and Byrne 2010). ARF can be attributed to a multiplicity of different diseases and pathophysiological mechanisms and is classified according to precipitating factors:

Prerenal: caused by inadequate renal perfusion due to (Holcombe and Kern Feeley 2009; Murphy and Byrne 2010):
- Decreased intravascular volume:
  - Dehydration
  - Haemorrhage
  - Hypovolaemic shock
  - Third-space losses, e.g. burns
- Cardiovascular failure:
  - Heart failure
  - Myocardial infarction (MI)
  - Cardiogenic shock
  - Valvular heart disease
- Drugs:
  - Angiotensin-converting enzyme (ACE) inhibitors
  - Non-steroidal anti-inflammatory drugs (NSAIDs)
  - Ciclosporin
  - Radiocontrast dye
  - Ethylene glycol (anti-freeze)
  - anaesthetics
- Decreased effective renal perfusion:
  - Sepsis
  - Cirrhosis
  - Neurogenic shock
Intrinsic (parenchymal): occurs when there is structural damage to the renal parenchyma such as acute tubular necrosis (ATN). ATN occurs because of sustained renal hypoperfusion (Perkins and Kisiel 2005). Causes include (Bellomo 2009):
- Glomerulonephritis
- Vasculitis
- Interstitial nephritis
- Malignant hypertension
- Pyelonephritis
- Bilateral cortical necrosis
- Amyloidosis
- Malignancy
- Nephrotoxins
Postrenal: caused by obstruction of urine drainage due to (Holcombe and Kern Feeley 2009):
- Ureteral obstruction:
  - Intrinsic – stones, carcinoma of the ureter, blood clots, strictures
- Bladder obstruction:
  - Tumours
  - Blood clots
  - Neurogenic bladder – due to spinal cord injury, diabetes mellitus, ischaemia, drugs
- Urethral obstruction:
  - Prostate cancer or benign hypertrophy
  - Stones
  - Strictures
  - Blood clots
  - Blocked in-dwelling catheter.

Diagnosis

The clinical presentation of ARF despite adequate resuscitation:

Anuria or profound oliguria
Progressive rise in blood creatinine and urea levels
Developing metabolic acidosis
Rising serum potassium and phosphate levels
MODS is common.

Clinical Course

The clinical course of ARF can be classified into three distinct phases (Murphy and Byrne 2010):

1. Initial phase: this is the phase between the exposure to the insult and a reduction in renal function when renal damage can be reversed

2. Maintenance phase: this can last from days to weeks or sporadically up to 2 months; during this time renal damage cannot be reversed. Patients can be anuric, oliguric or non-oliguric during this time.

3. Recovery phase: this is marked by a return to normal ranges of urea and creatinine. Patients may experience a polyuric stage when fluid and electrolyte imbalances may occur.

Prevention of ARF

Due to the poor prognosis, prevention of ARF in critical illness is paramount. The fundamental prevention strategy in ARF is to treat the cause (Bellomo 2009). If prerenal factors are likely to contribute they must be identified quickly and resuscitation instigated without delay (Bellomo 2009). Murphy and Byrne (2010) suggest the following to attempt to prevent ARF:

Early identification of those patients at risk based on pre-existing disease, type of surgery planned and planned use of nephrotoxic substances
Maintenance of euvolaemia and stable haemodynamics
Invasive monitoring where indicated and accurate interpretation of results
Avoidance of hypoxia
Intravenous acetylcysteine for the prevention of radiocontrast nephropathy
Monitoring of levels of nephrotoxic drugs and avoidance of using two together.

Complications of ARF

Hyperkalaemia is a serious electrolyte imbalance seen in ARF (Holcombe and Kern Feeley 2009). Characteristic ECG changes include elevated and pointed T waves. Cardiac arrhythmias and cardiac arrest may ensue and active treatment is normally required, e.g. insulin (and dextrose), RRT and in extreme situations intravenous calcium chloride. Continuous cardiac monitoring is essential to ensure early detection of cardiac arrhythmias. Metabolic acidosis is also a serious complication of ARF and may be intensified in critical illness due to the patient’s high metabolic rate which releases intracellular acids (Holcombe and Kern Feeley 2009). In severe metabolic acidosis bradycardia and hypotension may manifest due to myocardial suppression. Sodium bicarbonate is reserved for severe metabolic acidosis only, due to complications of extracellular volume increases, metabolic alkalosis and hypokalaemia. Refractory acidosis is an indicator for the commencement of RRT.

Patients with ARF are immunosuppressed and are therefore at greater risk of developing infections such as pneumonia, UTI, wound infection and sepsis, which can be a major cause of mortality (Murphy and Byrne 2010).

Adequate nutritional support is required. Nutrition in critical illness is always preferred by the enteral route; however, patients in ARF may require parenteral nutrition (TPN) because they may have impaired gastrointestinal (GI) function and absorption capacity (Holcombe and Kern Feeley 2009). Patients who are critically ill need their caloric requirements met and adequate protein intake to prevent further catabolism. Protein restriction in ARF is controversial and should not compromise meeting anabolic needs (Holcombe and Kern Feeley 2009). Whichever method of nutrition is instigated regular monitoring of the patient must be undertaken, i.e. serum protein, electrolytes, haemoglobin and urea are essential. Potassium, sodium and fluid intake should be restricted if the patient is not on RRT. Close monitoring of blood glucose levels is essential, particularly if the patient is on dietary supplements.

The patient who is in the oliguric phase of ARF requires careful fluid balance assessment. To prevent volume overload, a general working rule is the previous day’s urine output plus 500 ml for insensible loss. Consideration must be given to such variables as pyrexia, diarrhoea and wound drainage.

Serial weights may be more reliable than fluid balance assessment but are not widely used due to technical difficulties; rapid daily gains and losses in weight are usually related to changes in fluid volume. It is also important to observe for signs of fluid overload, e.g. raised central venous pressure (CVP), generalised oedema, pulmonary oedema and dyspnoea.

Clinical features of uraemia include nausea, vomiting, hiccoughs, confusion, irritability, altered conscious level, infection and bleeding. It is important to observe for these complications and treat appropriately.

Criteria for the initiation of RRT:

Oliguria (urine output: <200 ml/12 h)
Anuria (urine output 0–50 ml/12 h)
Urea >35 mmol/l
Creatinine >400 µmol/l
K⁺ >6.5 mmol/l or rapidly rising
Pulmonary oedema unresponsive to diuretics
Uncompensated metabolic acidosis (pH <7.1)
Na⁺ <110 and >160 mmol/l
Temperature >40°C
Uraemic complications (encephalopathy, neuropathy, pericarditis)
Overdose with a dialysable toxin, e.g. lithium.

If two of the above criteria are met, RRT is strongly recommended (Bellomo 2009).

MONITORING DURING RENAL REPLACEMENT THERAPY

Renal replacement therapy in the ICU is usually continuous venovenous haemodiafiltration, which is an extracorporeal venous system whereby blood is driven through a semi-permeable membrane to remove water, electrolytes, and small- and medium-sized molecules from the blood via diffusion, osmosis and convection (Bellomo 2009) (Fig. 7.2). Venous access is via a double lumen venous catheter often in the internal jugular, subclavian or femoral veins. To maximise the removal of solutes dialysate fluid is added to the circuit, which flows in a countercurrent direction to the blood around the fibres of the filter. Modern methods of RRT minimise the risks associated with intermittent haemodialysis, e.g. haemodynamic instability and should be instigated early in ARF in the critically ill patient (Bellomo 2009).

Fig. 7.2 Continuous renal replacement therapy.