Remove Continuous Positive Airway Pressure and Bilevel Positive Airway Pressure
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ساعت ٧:٠٧ ‎ب.ظ روز ۱۳٩٠/٥/٤   کلمات کلیدی:

Calcium, magnesium and phosphate


Over 99% of body calcium is in bone, of which about 1% is freely exchangeable with

extracellular fluid (ECF). Ionised calcium is crucial to many excitatory processes,

including nerve and neuromuscular conduction/contraction and coagulation. Normal

daily intake is of the order of 10–20mmol and normal total serum calcium is in the range

2.25–2.7mmol l−1. Intestinal calcium absorption is enhanced by 1,25-dihydroxy-vitamin

D3 (1,25(OH)2D3). Around 40% is bound to albumin and total serum calcium decreases

0.02mmol l−1 for each 1g l−1 decrease in albumin. Ionised calcium is the physiologically

important form and the normal level is 1.15mmol l−1.



Hypocalcaemia occurs when calcium is lost from the ECF (most commonly through renal

mechanisms) in greater quantities than can be replaced by bone or the intestine. Common

causes of hypocalcaemia are:

• Renal failure.

• Hypoparathyroidism.

• Sepsis.

• Burns.

• Hypomagnesaemia.

• Pancreatitis.

• Malnutrition.

• Osteomalacia.

• Alkalosis (reduced ionised calcium).

• Citrate toxicity (massive transfusion).

As a result of reduced absorption of dietary divalent cations or poor dietary intake,

hypocalcaemia and hypomagnesaemia often coexist.

Clinical features

The symptoms of hypocalcaemia correlate with the magnitude and rapidity of the

decrease in serum calcium. The main features include neuromuscular irritability

evidenced by extremity and circumoral paraesthesiae, Chvostek and Trousseau signs,

muscle cramps, tetany, laryngospasm and seizures. A prolonged QT is seen on ECG and

may progress to VT/VF and hypotension.


Appropriate therapy depends on the severity of the hypocalcaemia and its cause. The

serum magnesium and phosphate should be checked and, if low, corrected. Chronic

asymptomatic mild hypocalcaemia can be treated with oral calcium supplements. If

metabolic acidosis accompanies hypocalcaemia, calcium must be corrected before the

acidosis is corrected. Calcium and hydrogen ions compete for protein-binding sites, so an

increase in pH will lead to a rapid decrease in ionised calcium. In the presence of acute

symptomatic hypocalcaemia, an intravenous bolus of calcium (100–200mg or 2.5–

5mmol) should be given over 5min. This can be followed by a maintenance infusion of

1–2mg kg−1 h−1. Calcium chloride 10% contains 27.2mg Ca ml−1 (0.68mmol ml−1) and

calcium gluconate 10% contains 9mg ml−1 (0.225mmol l−1). Calcium gluconate causes

less venous irritation than calcium chloride.

Calcium management following parathyroidectomy

In chronic renal failure the glomerular filtration rate (GFR) decreases and phosphate

(PO4) is not excreted. Phosphate levels in the blood rise and this decreases the level of the

active metabolite of 1,25(OH)2D3. As a result, patients have hypocalcaemia and defective

bone mineralisation. The low calcium stimulates the parathyroid gland to increase

production of parathyroid hormone, PTH (secondary hyperparathyroidism). If the

secondary hyperparathyroidism is prolonged, the secretion of PTH becomes

autonomous—tertiary hyperparathyroidism. This leads to high calcium levels. High

calcium and high PO4 levels cause precipitation of calcium in tissues and organs. After

total or partial parathyroidectomy the calcium level can fall rapidly, particularly in

patients who have evidence of ‘hungry bone syndrome’ (high alkaline phosphatase).

These patients may need large quantities of i.v. calcium replacement. Some patients have

hypercalcaemia with calcification of small and medium blood vessels, leading to skin

necrosis and ulcers particularly on their legs. This is called calciphylaxis and these

patients’ calcium levels should be kept at the lower limit of normal.

Calcium infusion after parathyroidectomy

Following parathyroid surgery, calcium infusions are best given through central

intusions, as peripheral i.v. may cause necrosis. Calcium levels should be checked 4-

hourly until stable, then 6-hourly. Check the patient’s alkaline phosphatase level

preoperatively: the higher the level, the more likely postoperative low serum calcium

levels and symptoms will occur. Prescribe oral calcium medications. If the corrected

calcium level is <2.4mmol l−1, commence a calcium infusion.

Dilute 20ml 10% calcium chloride in 100ml 0.9% sodium chloride (Table 2). Check

corrected calcium 4-hourly, and adjust rate (Table 3).

If the patient has tertiary hyperparathyroidism or calciphylaxis, choose the lower

infusion rate; if they have alkaline phosphatase >300units/l, choose the higher infusion


All patients require oral calcium, 1g, 8-hourly, and calcitriol, 0.5–1.0μg daily in two

divided doses, as soon as they are able to drink





Hypercalcaemia occurs generally when the influx of calcium from bone or the intestine

exceeds renal calcium excretory capacity. Common causes include:

• Hyperparathyroidism (accounts for >50% of cases).

• Neoplasms (primary with ectopic PTH secretion, secondary with bone metastases).

• Sarcoidosis (increased production of 1,25(OH)2D3 by granulomatous tissue).

• Drugs (thiazides and lithium).

• Immobilisation of any cause.

• Vitamin D intoxication.

• Thyrotoxicosis.

Clinical features

The symptoms associated with hypercalcaemia depend on the rate of rise as well as the

absolute level of calcium. Mild hypercalcaemia is usually asymptomatic. Severe

hypercalcaemia causes neurological, gastrointestinal and renal symptoms. Neurological

features range from mild weakness, depression, psychosis and drowsiness but may

progress to coma. Gastrointestinal effects include nausea, vomiting, abdominal pain,

constipation, peptic ulceration and pancreatitis. Nephrogenic diabetes insipidus (DI),

renal stones, nephrocalcinosis and ectopic calcification may occur.


The underlying cause of hypercalcaemia must be treated. The measures taken will depend

on the calcium level. Most cases of mild hypercalcaemia are caused by primary

hyperparathyroidism and many will require parathyroidectomy. Patients with

symptomatic moderate (serum calcium >3.0mmol l−1) or severe (>3.4mmol l−1)

hypercalcaemia require intravenous saline to restore intravascular volume and enhance

renal calcium excretion. Thiazide diuretics should be avoided but furosemide (frusemide)

will enhance calcium excretion. Patients with severe hypercalcaemia associated with

raised PTH should be referred for urgent parathyroidectomy. Bisphosphonates (e.g.

etidronate, sodium pamidronate) have become the main therapy for the management of

hypercalcaemia due to enhanced osteoclastic bone reabsorption. Steroids are effective in

hypercalcaemia associated with haematological malignancies and in diseases related to

1,25(OH)2D3 excess (e.g. sarcoidosis and vitamin D toxicity).


Magnesium is essential for normal cellular and enzyme function. The total body

magnesium store is about 1000mmol, of which 50–60% is in bone. The normal plasma

range is 0.7–1.0mmol l−1 but because it is primarily an intracellular ion the plasma level

does not reflect total body stores. The normal daily intake is 10–20mmol, which is

balanced by urine and faecal losses. The kidney is the primary organ involved in

magnesium regulation.


Hypomagnesaemia occurs in up to 65% of critically ill patients and is often associated

with hypokalaemia.


Usually follows loss of magnesium from the gastrointestinal tract or kidney.

• Gastrointestinal causes include prolonged nasogastric suction or vomiting, diarrhoea,

extensive bowel resection, severe malnutrition and acute pancreatitis.

• Renal losses occur with volume expanded states, hypercalcaemia, diuretic therapy,

alcohol, aminoglycosides and cisplatin exposure and the polyuric phase of acute

tubular necrosis.

• Other causes include phosphate depletion, hyperparathyroidism and diabetes mellitus.

Clinical features

Most of the symptoms of hypomagnesaemia are rather non-specific. The accompanying

ion abnormalities such as hypocalcaemia, hypokalaemia and metabolic alkalosis account

for many of the clinical features. Neurological signs include confusion, weakness, ataxia,

tremors, carpopedal spasm and seizures. A wide QRS, long PR, inverted T, and U wave

may be seen on ECG. Arrhythmias may occur, including severe ventricular arrhythmias

(torsades de pointes), and there is increased potential for cardiac glycoside toxicity.


The underlying cause must be addressed. Symptomatic moderate-to-severe

hypomagesaemia will require parenteral therapy. In the event of an acute arrhythmia or

seizure, 8–10mmol of magnesium sulphate can be given over 5min followed by 25mmol

over 12h. The rate should be titrated against serum levels. Potassium should be replaced

at the same time. Oral magnesium sulphate is a laxative and may cause diarrhoea.


Hypermagnesaemia is usually iatrogenic (e.g. excess i.v. administration). High

magnesium levels antagonise the entry of calcium and prevent excitation.

Clinical features

These include hypotension, bradycardia, drowsiness and hyporeflexia (knee jerk is a

useful clinical test and is lost above 4mmol l−1). Levels >6mmol l−1 cause coma and

respiratory depression.


Administration of magnesium should be stopped. Calcium chloride will antagonise the

effect of magnesium. Diuretics increase renal loss. In severe cases dialysis may be


Total body phosphate in adults is about 700g: approximately 85% is in bone and 15% is

in extracellular fluid and soft tissue. Phosphate is found in adenosine triphosphate (ATP),

2,3-diphosphoglycerate (2,3-DPG) in red blood cells, phospholipids and phosphoproteins.

Phosphate is essential in many cellular functions and also acts as a buffer. The normal

serum level is 0.85–1.4mmol l−1.



Hypophosphataemia results from internal redistribution, increased urinary excretion and

decreased intestinal absorption.

• Internal redistribution of phosphate may result from respiratory alkalosis, refeeding

after malnutrition, recovery from diabetic ketoacidosis and the effects of hormones

and other agents (insulin, glucagon, adrenaline (epinephrine), cortisol, glucose).

• Increased urinary excretion of phosphate occurs in hyperparathyroidism, vitamin D

deficiency, malabsorption, volume expansion, renal tubular acidosis and alcoholism.

• Decreased intestinal absorption of phosphate occurs in antacid abuse, vitamin D

deficiency and chronic diarrhoea.

Clinical features

The clinical features are usually seen when the phosphate level has fallen below 0.3mmol

l−1. They are often non-specific but may include weakness (which may contribute to

respiratory failure and problems with weaning from mechanical ventilation), cardiac

dysfunction, paraesthesia, coma and seizures.


The underlying cause should be corrected. Oral phosphate can be given in doses of 2–3g

daily. When needed, 10mmol potassium phosphate can be given i.v. over 60min and

repeated depending on measured levels (a sodium phosphate preparation is also

available). There is a risk of hypocalcaemia associated with i.v. replacement and serum

calcium must be maintained.



Renal failure is the most common cause.

• Reduced renal excretion: renal failure, hypoparathyroidism, acromegaly,

bisphosphonate therapy and magnesium deficiency.

• Increased exogenous load: i.v. infusion, excess oral therapy, phosphate-containing


• Increased endogenous load: tumour lysis syndrome, rhabdomyolysis, bowel infarction,

malignant hyperthermia, haemolysis and acidosis.

• Pseudohyperphosphataemia: multiple myeloma.

Clinical features

Hypocalcaemia and tetany may occur with rapid rise in level. A large rise in

calcium×phosphate product causes ectopic calcification in tissues, nephrocalcinosis and

renal stones.


Aluminium hydroxide is used as a binding agent. Magnesium and calcium salts are also

effective and aluminium accumulation is a risk. Dialysis may be required.

Further reading

Aguilera IM, Vaughan RS. Calcium and the anaesthetist. Anaesthesia 2000; 55:779–90.

Bushinsky DA, Monk RD. Calcium. Lancet 1998; 352:306–11.

Weisinger JR, Bellorin-Font E. Magnesium and phosphorus. Lancet 1998; 352:391–6.

Yudd M, Llach F. Current medical management of secondary hyperparathyroidism. Am J Med Sci

2000; 320:100–6.


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