Metabolic and endocrine problems

CHAPTER 8 METABOLIC AND ENDOCRINE PROBLEMS

INTRODUCTION

Metabolic and endocrine disturbances are common in the ICU. They may be the patient’s primary presenting condition, or a consequence of the response to the primary disease process, the physiological stress response, fluid management and/or the effects of prescribed or illicit drugs.

Some typical electrolyte disturbances seen on the intensive care unit are discussed below. Long lists of possible causes have been deliberately omitted. In general, aim for slow correction of most abnormalities over a 24- to 48-h period to avoid major fluid shifts.

SODIUM

(Normal range serum sodium 135–145 mmol/L.)

Sodium is primarily an extracellular ion. Plasma or serum sodium concentrations are a result of the balance between the sodium and water content of the extracellular compartments. Most acute disturbances of sodium concentration represent changes in water balance rather than total body sodium.

Hyponatraemia

The causes of hyponatraemia are shown in Table 8.1.

TABLE 8.1 Causes of hyponatraemia

Excess water intake	Hypotonic fluids TURP syndrome Water intoxication
Reduced free water clearance	Stress response with raised ADH Syndrome of inappropriate ADH secretion Renal impairment Cardiac failure
Loss of body sodium	GI tract losses Renal losses including diuretic therapy Adrenal insufficiency Hyperpyrexia and sweating (inadequate salt replacement)

Hyponatraemia is most commonly due to an excess of extracellular fluid (rather than sodium loss). This is often the result of excessive use of hypotonic intravenous fluids. Hyponatraemia may also result from the chronic use of some diuretic drugs; this is more commonly seen in the elderly. More rarely, hyponatraemia is associated with other forms of organ dysfunction, including renal dysfunction and hepatic cirrhosis (where it is seen in association with secondary hyperaldosteronism). Treatment is not usually necessary unless the serum sodium falls below 130 mmol/L. Serum sodium below 120 mmol/L may be associated with altered conscious level and fits. Symptoms are related as much to the speed of change in concentration as to the actual measured level.

Consider the underlying cause.

Change maintenance fluids to 0.9% saline.

Restrict total fluid intake. Allow the kidneys to clear excess fluid.

If oliguric, consider the need for renal replacement therapy to remove excess fluid.

Rapid correction of severe hyponatraemia can cause central pontine demyelination (brainstem damage) and death. It is recommended that sodium should not rise more than 2 mmol / L per hour and by not more than 12 mmol / L in 24 h, to achieve an initial plasma sodium level of 120–130 mmol / L. The use of hypertonic saline solutions is controversial. Seek advice.

Excessive antidiuretic hormone (ADH) secretion

This is a cause of dilutional hyponatraemia due to reduced free water clearance. It is most commonly seen as part of the syndrome of inappropriate ADH secretion (SIADH), which may accompany the neuroendocrine stress response to trauma, surgery and critical illness. Rarely, ectopic ADH secretion by tumours may produce a similar picture. Oliguria is accompanied by increased urine osmolality (>500 mosmol/L) and reduced plasma osmolality (<280 mosmol/L).

Restrict fluids.

Consider a trial of diuretic therapy.

Hyponatraemia due to sodium loss

Significant sodium depletion is associated with a reduction in extracellular fluid volume. This stimulates the release of aldosterone and causes the kidneys to retain salt and water and lose potassium. Urinary osmolality is raised and urinary sodium is low, less than 10 mmol/L (unless there is an intrinsic renal problem or use of diuretics).

Replace sodium and ECF with isotonic (0.9%) saline.

Pseudohyponatraemia

Electrolytes are present and measured only in the aqueous phase of plasma, but the concentration is expressed according to the total plasma volume. If there is a raised lipid or protein content in the plasma this can produce a spurious result.

Hypernatraemia

High serum sodium usually represents free water depletion. This is associated with a raised serum urea (without a significant corresponding rise in serum creatinine) and an increased serum osmolality (&290 mosmol/L). In critically ill patients, this situation can arise despite the apparent appearance of widespread oedema and ‘fluid overload’ as a result of fluid shifting between ‘compartments’.

Assess patient’s clinical volume status (tissue turgor, sunken eyes, CVP, etc.).

Review fluid balance regimen.

Give additional free water as 5% dextrose (e.g. 1 L over 6–12 h) or water via NG tube. Consider diluting enteral feeds with sterile water.

If additional fluid is contraindicated or undesirable, consider renal replacement therapy. This should be discussed with the nephrologists, on a case-by-case basis.

Hypernatraemia due to genuine sodium overload is uncommon. It is usually due to excess sodium chloride ingestion or administration, and is therefore accompanied by a high serum chloride and a hyperchloraemic acidosis. Management is essentially the same. Increase free water intake to allow the kidneys to excrete the additional solute load.

Rapid correction of hypernatraemia, particularly if serum sodium is >160 mmol / L, can result in cerebral oedema as water enters the brain. As with hyponatraemia, correct slowly over 24–48 h.

POTASSIUM

(Normal range serum potassium 3.5–5 mmol/L.)

Potassium is primarily an intracellular ion. Small changes in serum concentration have significant effects on nerve conduction and muscle contraction.

Hypokalaemia

Causes of hypokalaemia are shown in Box 8.1.

Box 8.1 Causes of hyperkalaemia

Diarrhoea and vomiting

Nasogastric aspirates

Urinary losses (diuretics)

Dextrose and insulin

Hypomagnesaemia

Hypokalaemia is relatively common in the ICU. ECG changes include ST depression, flattening of the T wave and prominent U wave. If severe (<2 mmol/L), cardiac arrhythmias, including supraventricular and ventricular extrasystoles, tachycardias, atrial fibrillation, and ventricular fibrillation, may occur (Fig. 8.1).

Fig. 8.1 ECG changes associated with hypokalaemia.

Ensure adequate potassium concentration in maintenance fluids. The maximum safe concentration of potassium in peripheral fluid infusions is usually taken to be 60 mmol/L. In the intensive care unit where continuous monitoring is in place, a stronger potassium solution may be infused through a central line using a volumetric infusion pump or syringe driver

If additional potassium is required:

Do not give a rapid bolus injections of potassium, as there is a risk of sudden death.

Give 20 mmol of K⁺ in 20–40 mL of saline over 1 h via a central venous catheter using an infusion pump. Repeat as necessary.

Monitor the ECG during infusion.

Inadvertent and inappropriate injection of strong potassium solutions has been associated with death. These solutions should be treated as a controlled drug, and use should be governed by local protocols. Ideally, strong potassium infusions should be prepared by a pharmacy aseptic service. If you are required to prepare potassium infusions, ensure that fluids are thoroughly mixed before administration. Strong potassium chloride solution has a higher specific gravity than standard i.v. solutions and can ‘layer’ at the bottom of a bag / syringe. Administration should be via a central venous cannula to avoid the risk of extravasation injury. During infusion continuous ECG monitoring and regular blood sampling are mandatory.

In many patients, hypokalaemia is a reflection of a more widespread derangement of ionic homeostasis. It may be associated with an attempt to conserve magnesium in severe hypomagnesaemia. In this situation, correction of serum potassium is difficult and often transient until the hypomagnesaemia has also been corrected.

Hyperkalaemia

Causes of hyperkalaemia are shown in Box 8.2.

ECG changes include peaked T waves, broad QRS complexes and conduction defects (Fig. 8.2). Asystole may occur. Urgent treatment is usually required, although patients with long-term end-stage renal failure may be more tolerant of hyperkalaemia than the general intensive care patient population.

Fig. 8.2 ECG changes in hyperkalaemia.

Treatment to reduce risk of immediate arrhythmia

10 mL of 10% calcium chloride as a slow i.v. bolus will help to stabilize cardiac muscle.

In the presence of metabolic acidosis, give 50 mL 8.4% bicarbonate.

CALCIUM

(Normal range standard serum calcium 2.12–2.62 mmol/L.)

(Normal range ionized serum calcium 0.84–1 mmol/L.)

Most laboratories measure total calcium, which includes bound and unbound fractions. The unbound fraction (ionized Ca²⁺), which is the physiologically active component, varies with the albumin concentration. Therefore, look at the corrected figure, which takes account of protein binding. Alternatively, many blood gas analysers now measure ionized Ca²⁺ directly.

Hypercalcaemia

This occurs less commonly, and is generally due to an underlying disease process. Typical causes are listed in Box 8.4.

Box 8.4 Causes of hypercalcaemia

Hyperparathyroidism

Excessive intake vitamin D or calcium

Drug-induced (thiazide diuretics)

Symptoms include GI disturbance, confusion and polyuria. Treatment is by rehydration and the use of calcium-binding agents.

Give 0.9% saline to rehydrate the patient. Check plasma osmolality is within the normal range (280–290 mosmol/L).

A forced diuresis may be used to aid excretion. Furosemide (frusemide) is administered and the urine output replaced with alternating 0.9% saline and 5% dextrose.

Calcitonin reduces the rate of calcium and phosphate release from the bones. It is useful in patients with hypercalcaemia associated with malignancy, and generally reduces the calcium level within 2 h.

Bisphosphonates (e.g. disodium etidronate) also reduce release of calcium from bones but generally take a few days to achieve maximum effect.

Corticosteroids may be helpful in hypercalcaemia associated with sarcoidosis and malignancy.

PHOSPHATE

(Normal range serum phosphate 0.7–1.25 mmol/L.)

Hypophosphataemia

This is common in the ICU. It is usually multifactorial, resulting from reduced intake (particularly in patients receiving TPN), redistribution and increased losses (especially patients on renal replacement therapy). Hypophosphataemia causes muscle weakness, which may lead to heart failure or difficulty in weaning from artificial ventilation. It also contributes to failure of many metabolic processes and, if severe, results in depressed conscious level and seizures. It has also been associated with insulin resistance.

It is debatable at what level replacement is required. In most cases, as the patient’s overall condition improves, phosphate balance returns. Patients whose levels are below 0.8 mmol/L, particularly if symptomatic, may benefit from additional phosphate either in feeds or intravenously.

Use sodium phosphate or potassium phosphate depending upon requirements.

Give 30–60 mmol phosphate diluted in 100–500 mL 5% dextrose over 24 h.

Hyperphosphataemia

Hyperphosphataemia is caused by excessive intake or decreased excretion (e.g. renal failure). Maintain adequate hydration with 5% dextrose. If severe, consider the need for renal replacement therapy. Phosphate is effectively removed by continuous RRT techniques, with haemodialysis and haemodiafiltration performing better than simple filtration techniques.

MAGNESIUM

(Normal range serum magnesium 0.7–1 mmol/L.)

Hypomagnesaemia

Magnesium is the second most common intracellular cation and as such, serum levels are a poor guide to the need for replacement. Serum magnesium is frequently depleted in critical illness. Common causes of hypomagnesaemia are shown in Box 8.5.

Tags: Churchills Pocketbook of Intensive Care

Jun 4, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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