Fig. 10.2 Blood glucose monitoring chart (Walsall Hospitals NHS Trust).

Sources of blood glucose measurement inaccuracy (Ginsberg 2009):

• Strip factors: strips must be in date and not exposed to high temperatures or humidity in an open vial
  
• Patient factors: variations in haematocrit, high levels of triglycerides, high or low oxygen values, uric acid
  
• Medications: L-dopa, tolazamide, ascorbic acid, icodextrin (used in peritoneal dialysis solutions
  
• High levels of bilirubin (>0.43 mmol/l, e.g. in jaundice).

Systems should be in place to ensure that any point-of-care testing devices are subject to rigorous quality control processes and. if any results are incongruent with the patient’s physical condition, a laboratory sample should be taken (Higgins 2008).

Newer devices are currently being developed to enable non-invasive methods of monitoring blood glucose (Higgins 2008). Current research into non-invasive testing of blood glucose (using breath analysis) in type 2 diabetes mellitus is currently under way (American Diabetes Association 2010).

Hyperglycaemia and Diabetic Ketoacidosis

There are many causes of hyperglycaemia including diabetes mellitus, acute pancreatitis, parenteral nutrition and sepsis (Bersten and Soni 2009). Twenty-five per cent of patients who present with acute coronary syndrome have diabetes mellitus which is an independent risk factor with a risk similar to elevated troponin (Aroney 2011). Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency (Jerreat 2010). It is a serious life-threatening metabolic complication of diabetes mellitus consisting of three concurrent abnormalities: hyperglycaemia, hyperketonaemia and metabolic acidosis (Savage et al. 2004).

Acute illness, particularly infection, major surgery, myocardial infarction and critical illness, will stimulate the release of stress hormones, including glucagon, which will cause glucose imbalance (Higgins 2008). Criteria for diagnosis of DKA are (Jerreat 2010):

• Blood sugar >11 mmol/l
  
• Moderate ketonuria or blood ketone levels > 3 mmol/l
  
• Significant acidosis bicarbonate ≤15 mmol/l or an arterial pH <7.

Signs and symptoms of severe DKA include reduced consciousness, hyperventilation (Kussmaul’s respirations) and hypotension (Kapustin 2009b).

Monitoring priorities include the following:

• Airway patency (if the patient is semiconscious or in a coma)
  
• Arterial blood gas analysis: indicated if there is altered conscious level or if breathing is compromised (Savage et al. 2004)
  
• Pulse oximetry: breathing may be compromised
  
• Pulse, blood pressure and CVP measurements: hypovolaemia
  
• ECG monitoring: cardiac arrhythmias
  
• Blood ketone measurements: the use of blood ketone tests is preferred to urine ketone tests for diagnosis and monitoring of DKA (American Diabetes Association 2010)
  
• Blood glucose measurements: hourly (Savage et al. 2004) to monitor hyperglycaemia and the effect of prescribed insulin
  
• Strict fluid balance: fluid replacement should be closely monitored
  
• Cultures: blood, urine, throat swab to detect infection
  
• Serum potassium measurements: to detect hypokalaemia or hyperkalaemia (Jerreat 2010).

Hypoglycaemia

Hypoglycaemia is described as a blood glucose level that does not meet metabolic demands (typically <3.9 mmol/L) (Higgins 2008). Causes include hepatic dysfunction, malnutrition, inadequate oral intake and exercise following administration of insulin or oral anti-hypoglycaemic agents, and intentional or accidental overdose (Higgins 2008; Keays 2009). Blood glucose levels <1 mmol/l are a medical emergency (Keays 2009). Regular blood glucose measurements are required.

PRINCIPLES OF MONITORING ADRENAL GLAND FUNCTION

The adrenal glands comprise the medulla and cortex. The adrenal medulla secretes the hormones adrenaline and noradrenaline (catecholamines) in response to sympathetic stimulation. The adrenal cortex secretes three categories of hormones, all of which are steroids.

Phaeochromocytoma

Phaeochromocytoma (tumour of the adrenal medulla) can lead to the secretion of high levels of catecholamines, usually intermittently (Savage et al. 2004). Common symptoms include severe hypertension, headache, tachycardia, hyperglycaemia, bowel disturbances and blurred vision (Adam and Osborne 2005). Hypertension is paroxysmal initially, but later becomes sustained, severe hypertension (Myburgh 2009). Monitoring priorities include:

• Arterial pressure monitoring: hypertension
  
• ECG monitoring: cardiac arrhythmias
  
• Blood glucose measurements: to monitor hyperglycaemia and evaluate treatment.

Addisonian Crisis

Addisonian crisis results from acute adrenocortisol insufficiency. Acute adrenocortical insufficiency can be caused by a primary failure of the adrenal gland or secondary to the lack of adrenocorticotrophic hormone (ACTH) drive from the pituitary gland (Venkatesh and Cohen 2009). The clinical features, which result mainly from the deficiency of aldosterone, include thirst, polyuria, dehydration, cardiac arrhythmias, electrolyte imbalance and hypotension (Adam and Osborne 2005). Monitoring priorities include:

• Arterial blood gas analysis: metabolic and respiratory acidosis may occur
  
• ECG monitoring: cardiac arrhythmias
  
• Arterial pressure monitoring: hypotension
  
• CVP monitoring: hypotension
  
• Strict fluid balance: polyuria
  
• Blood glucose measurements: hypoglycaemia.

PRINCIPLES OF MONITORING THYROID GLAND FUNCTION

The thyroid gland secretes three hormones: thyroxine (T₄), triiodothyronine (T₃) and calcitonin. T₃ and T₄ are responsible for the metabolic rate of all bodily tissues. Calcitonin reduces serum calcium levels. Thyroid crisis and myxoedema coma result from over- and under-secretion of the thyroid gland, respectively. If untreated they have a high mortality rate (Handy 2009).

Thyroid Crisis

Hyperthyroidism (also known as thyrotoxicosis) results from over-secretion of T₃ and T₄, leading to hypermetabolism. Thyroid crisis (thyroid storm) is a rare but life-threatening syndrome that often occurs in untreated or undiagnosed hyperthyroidism (Karanikolas et al. 2009).

Thyroid crisis is characterised by fever, tremors, tachycardia, diarrhoea, nausea and vomiting, dehydration, apathy, generalised weakness, seizures, stroke, coma, abdominal pain, liver failure and circulatory instability (Karanikolas et al. 2009). If the patient has underlying cardiac disease or has a compromised cardiovascular system, the risk of serious complications increases. Thyroid crisis carries a relatively high mortality rate, so careful and accurate monitoring is therefore essential. Monitoring priorities include:

• Respiratory rate, pulse oximetry and arterial blood gas analysis: patient may develop pulmonary oedema
  
• ECG monitoring: cardiac arrhythmias
  
• Arterial blood pressure monitoring: hypotension may develop
  
• CVP monitoring: patient can develop heart failure; there may also be considerable fluid loss
  
• Strict fluid balance: considerable fluid loss (excessive sweating)
  
• Blood glucose measurements: hypoglycaemia
  
• Core temperature measurements: patient may develop extreme pyrexia (>40°C) (Adam and Osborne 2005)
  
• Neurological monitoring: extreme agitation and coma may develop.

Myxoedema Coma

Myxoedema coma results from decreased T₄ production and occurs most commonly in the elderly female population with long-standing or undiagnosed hypothyroidism (Handy 2009). Effects include unconsciousness, hypothermia (as low as 23°C), hypoventilation, hypotension and hypoglycaemia (Handy 2009). Monitoring priorities include:

• Airway: unconscious patient
  
• Respiratory rate, pulse oximetry and arterial blood gas analysis: hypoventilation
  
• ECG monitoring: bradycardia
  
• Arterial blood pressure monitoring: hypotension
  
• CVP monitoring: patient may develop heart failure; also there may be considerable fluid gain
  
• Strict fluid balance: there may be considerable fluid gain
  
• Blood glucose measurements: hypoglycaemia
  
• Core temperature measurements: hypothermia
  
• Neurological monitoring: coma.

PRINCIPLES OF MONITORING PARATHYROID GLAND FUNCTION

The parathyroid glands secrete parathyroid hormone, which raises serum calcium levels. Calcium is essential for a variety of bodily functions, including muscle contraction, blood clotting and maintenance of cell membrane integrity. Abnormalities in parathyroid function (hyperparathyroidism and hypoparathyroidism) can lead to calcium disorders which can be life threatening.

Hypercalcaemia

Symptomatic hypercalcaemia requires urgent treatment and if it is severe the patient should be admitted to the ICU (Adam and Osborne 2005). Severe hypercalcaemia (corrected serum calcium >3.0 mmol/l) requires urgent treatment and is usually caused by malignancy (Muzzy and Adams Snyder 2009). Monitoring priorities include:

• ECG monitoring: cardiac arrhythmias
  
• Arterial blood pressure monitoring: hypertension
  
• CVP monitoring: hypovolaemia
  
• Strict fluid balance: dehydration, polyuria and hypovolaemia.

Hypocalcaemia

Hypocalcaemia is present in approximately 70–90% of critically ill patients (Venkatesh 2009). Acute symptomatic hypocalcaemia is a medical emergency, requiring urgent treatment (Venkatesh 2009). Monitoring priorities include:

• Airway patency: stridor
  
• Respirations, pulse oximetry and arterial blood gas analysis: respiratory compromise
  
• ECG monitoring: cardiac arrhythmias
  
• Arterial blood pressure: hypotension
  
• CVP monitoring: hypotension
  
• Neurological monitoring: convulsions and altered conscious level.

Scenario

James, a 28-year-old man, was admitted to the high dependency unit (HDU) with a history of weight loss, general malaise, polyuria, polydipsia, lethargy and deep sighing Kussmaul’s respirations. He was known to have diabetes but had omitted his insulin injections over the preceding few days and was also complaining of diarrhoea and vomiting. A provisional diagnosis of diabetic ketoacidosis was made. What are the monitoring priorities?

BP 90/60, pulse 125/min, respiratory rate 35/min, temperature 38.5°C, SpO₂ 95%, blood glucose 40 mmol/l. The patient’s vital signs were consistent with acute circulatory failure secondary to dehydration caused by excessive fluid loss. The pyrexia may be associated with the diarrhoea and vomiting. Blood glucose measurements and urinalysis were undertaken. The presence of hyperglycaemia, glycosuria, ketonuria and ketonaemia helped to confirm the diagnosis of DKA.

Arterial blood gas results are as follows:

pH 7.1

PaCO₂ 2.9 kPa (15 mmHg)

PaO₂ 11.8 kPa (88.5 mmHg)

HCO₃⁻ 12 mmol/l

BE −13

SaO₂ 97%

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