The adrenal cortex

The cortex is divided structurally and functionally into three zones. Each zone is responsible for the secretion of a different class of steroid hormones, collectively called corticosteroids. The adrenal cortex, and therefore the corticosteroids, are under the influence of ACTH released by the anterior pituitary gland (Patton & Thibodeau 2010).

The following are examples of hormones synthesised and released by the adrenal cortex:

Given their role in glucose metabolism, glucocorticoids are often referred to as hyperglycaemic hormones

The adrenal medulla

The medulla, or inner portion of the adrenal glands, produces two similar hormones referred to as catecholamines: adrenaline (also referred to as epinephrine) and noradrenaline (also referred to as norepinephrine). When the medulla is stimulated by neurons of the sympathetic nervous system, the two hormones are released into the bloodstream. The physiological responses to the medullary hormones mimic those of the sympathetic nervous system, which are:

Adrenaline prepares the body for fight or flight, and its secretion is increased when the person feels threatened or experiences strong emotions such as fear, anger or excitement, thereby helping the body to cope with a stressful situation (Marieb & Hoehn 2010).

Gigantism

Disturbances to GH release are chronic progressive disorders marked by hormonal dysfunction and skeletal overgrowth, which most commonly can appear in two forms: gigantism and acromegaly. Hypersecretion of GH in childhood results in gigantism, and begins before epiphyseal closure (Marieb & Hoehn 2010). Children with gigantism may grow up to 15 cm a year, reach a height of 2.4 m, exhibit slow sexual development and may have slow mental development. Radiation therapy, surgical removal of the tumour and drug therapy may be used to decrease secretion of the growth hormone and slow down the excessive growth pattern (Monahan et al 2007; Craft et al 2011). With this treatment, prognosis for the individual with gigantism is generally good (Brown & Edwards 2012).

Acromegaly

Acromegaly is the manifestation of GH hypersecretion and occurs in adulthood after epiphyseal closure. It is characterised by atrophy of skeletal muscle and formation of new bone and cartilage. The long bones are unable to grow in length, but the smaller bones of the hands, feet and face grow, giving the individual a characteristic appearance, with an enlarged lower jaw, bulging forehead and thickened ears and nose (Fig 34.4). The extremities become elongated and enlarged, resulting in large hands and feet (Patton & Thibodeau 2010). Thickening of the tongue may cause the voice to sound deep and hollow, associated with slurred speech. Acromegaly is a chronic disfiguring disease that often shortens life expectancy, as it may lead to respiratory, cerebrovascular and congestive heart diseases (Monahan et al 2007). Surgical intervention to remove the pituitary tumour may lead to hypopituitarism or recur (Australian Pituitary Foundation 2011).

Figure 34.4 Acromegaly

(Dr P. Marazzi/Science Photo Library)

Prolactinoma

The most common tumour resulting from hypersecretion is prolactinoma (Australian Pituitary Foundation 2008). Hypersecretion of prolactin often results in gynaecomastia and galactorrhoea (breast swelling and milk production) in both males and non-breastfeeding females, and may be accompanied by menstrual or libido alterations. Evidence suggests that despite around 10% of the population possessing microprolactinomas, only 0.1% will be clinically affected each year in Australia (Australian Pituitary Foundation 2008).

SIADH

The syndrome of inappropriate antidiuretic hormone (SIADH) includes excessive ADH secretion from the posterior pituitary, but it may also be non-endocrine in origin. Individuals with pulmonary problems such as carcinoma, severe pneumonia and other lung dysfunctions often also suffer from SIADH (Craft et al 2011). As a result, a consideration of pulmonary health is important in the nursing diagnosis and management of SIADH.

Individuals with this disorder display enhanced renal water retention which leads to imbalances in sodium balance and blood osmolarity. Hyponatraemia is induced due to the relative increases in water, and is common in hospitalised patients. For example, one-quarter of the residents aged over 65 in an Australian geriatric facility had hyponatraemia, with half of these caused by SIADH (Anpalahan 2001).

Hyponatraemia suppresses the release of renin from the kidneys, which in turn regulates aldosterone release. The result is a loss of sodium in the urine. Diagnoses of SIADH include low serum osmolarity and sodium and urine hyperosmolarity; the symptoms are determined by the extent of severity of the continued ADH release.

Restricting and monitoring fluid intake, as well as the possible administration of diuretics, may reduce the underlying cause (Brown & Edwards 2008). Careful fluid restrictions for clients with SIADH of 0.5–1 L daily are suggested to allow sodium levels to increase slowly. Likewise, monitoring urine output and quality, weight and blood chemistries are indicated for individuals at risk (Monahan et al 2007).

Hypofunction of the anterior pituitary gland can also result from a tumour in the gland, secondary to trauma of the hypothalamus or infection (Monahan et al 2007). Hypopituitarism results in an absence or deficiency of GH and gonadotrophins and is marked by growth retardation, which in children causes dwarfism and delay of puberty. It can present in three forms, which share the characteristics of delayed or retarded growth, and decreased mentation and sexual development: Fröhlich’s syndrome, commonly caused by an anterior pituitary tumour; dwarfism, which results from hyposecretion of growth hormone and is characterised by proportionately small individuals; and Simmonds’ disease, atrophy of the anterior lobe of the pituitary gland, which is a rare disorder with widespread effects (Farrell & Dempsey 2011).

Treatment of hypopituitarism commonly involves hormone replacement of the target gland hormone (Australian Pituitary Foundation 2011; Endocrinology Expert Group 2009). Constant monitoring and adjusting of hormone levels is required to attain optimal results.

Diabetes insipidus

Diabetes insipidus is a rare condition characterised by a deficiency of ADH and may be of neurogenic (posterior lobe damage, resulting from head trauma, tumour or surgical or irradiative interventions) or nephrogenic in origin (kidneys failing to respond to adequate levels of ADH) (Craft et al 2011). Without ADH, the individual exhibits polyuria, passing vast quantities of dilute, colourless urine (volumes vary, but may be as high as 20 L daily), the osmolarity and specific gravity of which is very low. To compensate for the dehydration from the excessive fluid loss, the individual experiences polydipsia (excessive thirst, especially for cold drinks) and drinks large amounts of fluid (Farrell & Dempsey 2011).

Diagnostic procedures centre on fluid management. A fluid deprivation test in which the patient is unable to concentrate urine or continually passes large volumes is indicative of diabetes insipidus. This test is based on the principle that withholding fluid for several hours stimulates secretion of ADH. Other procedures include measurement of plasma ADH and osmolarity, or IV infusion of hypertonic saline (Craft et al 2011; Farrell & Dempsey 2011). Treatment for individuals with diabetes insipidus involves medication as opposed to limiting fluid intake, because the high volume of fluid loss through urine is independent of fluid intake. The replacement of ADH with synthetic analogues such as vasopressin or desmopressin has a good prognosis (Endocrinology Expert Group 2009; Monahan et al 2007). During the acute stage of this condition, clients need supportive care in relation to their polyuria and increased need for fluids.

Diagnostic tests

Pituitary function may be assessed by estimating the level of trophic hormones and by measuring the response to stimulation or suppression tests (Brown & Edwards 2008). The most common tests for evaluating anterior pituitary function are the serum growth hormone test and the insulin intolerance test. The insulin intolerance test, also called the growth hormone stimulation test, provides information about the secretion of growth hormone and ACTH. Investigations may also include x-ray, magnetic resonance imaging (MRI) or computerised tomography (CT) scan of the skull (Farrell & Dempsey 2011). Testing posterior pituitary function includes the water-deprivation test, which is performed when the client’s symptoms indicate diabetes insipidus.

Hyperthyroidism

Hyperthyroidism is one of the more common endocrine disorders and about 2% of Australian women will experience some hyperthyroidism (Queensland Health 2008a). Hyperthyroidism may be caused by many factors, such as thyroiditis or hypersecretion of TSH. An increase in the secretion of the thyroid hormones T₃ and T₄ affects the basal metabolic rate, as well as the functions of other body systems. The manifestations of hyperfunctioning are generally related to increased metabolic processes, and exhibit characteristic signs and symptoms which reflect heightened metabolism or adrenergic stimulation, and are sometimes collectively referred to as thyrotoxicosis. The presenting condition is often nervousness. The condition can also be caused by genetic or immunological factors (Michels & Eisenbarth 2007), thyroid gland nodules or chronic inflammation of the thyroid gland (Craft et al 2011). Table 34.2 lists the most common signs and symptoms of hyperthyroidism and hypothyroidism.

Table 34.2 Some common signs and symptoms of hyperthyroidism (including Graves’ disease) and hypothyroidism

Craft et al 2011; Monahan et al 2007

Graves’ disease

An autoimmune disorder, Graves’ disease is the most common hyperthyroid disease (Craft et al 2011; Farrell & Dempsey 2011; Thyroid Australia 2007). Elevated levels of circulating TSH receptor antibodies stimulate the thyroid gland, leading to the production and release of high concentrations of thyroid hormones and potential glandular hypertrophy. Graves’ disease more commonly affects young women, and is eight times more prevalent in females (Farrell & Dempsey 2011) (see Clinical Scenario Box 34.2). It may appear after a stressful episode, illness or shock. Symptoms include all the characteristics of hyperthyroidism: tachycardia, nervousness, hyperactivity and excitability. The individual will have a voracious appetite but loses weight and can be quite underweight. Diarrhoea is common, as peristaltic rate increases. Excessive sweating and extreme thirst are also common, because of the increased metabolic rate. One outstanding characteristic of Graves’ disease is that of exophthalmos, or protrusion of the eyeballs, which is due to oedema in the tissues behind the eye, and does not resolve even when the hyperthyroidism is corrected (Craft et al 2011) (Fig 34.5). A serious complication of Graves’ disease is thyroid crisis (or storm), which is discussed in Clinical Interest Box 34.1.

Figure 34.5 Exophthalmos and/or goitre

(Patton & Thibodeau 2012:574. Images: A Swartz MH: Textbook of physical diagnosis, 4th edn, Philadelphia, 2002, Saunders. B Stein HA, Slatt BJ, Stein RM: The ophthalmic assistant: fundamentals and clinical practice, 7th edn, Philadelphia, 2000, Mosby. C Swartz MH: Textbook of physical diagnosis history and examination, 5th edn, Philadelphia, 2006, Saunders)

Goitre

An enlarged thyroid gland (goitre) may be the result of thyroiditis, neoplasia, hyper- or hypoactivity. Goitre can cause local problems by exerting pressure on the trachea, which may produce dysphagia or respiratory distress (Monahan et al 2007). Simple goitre (non-toxic goitre) is due to an iodine deficiency that causes a compensatory enlargement of the thyroid gland in an attempt to maintain thyroid hormone production. Introduction of iodised salt has reduced the incidence in Australia and New Zealand, and in most other western countries (Farrell & Dempsey 2011), although localised iodine deficiency still persist in Australia (Australian Thyroid Foundation 2009; Endocrinology Expert Group 2009). Exophthalmic goitre occurs in hyperthyroidism (Fig 34.5).

Hypothyroidism

Hypothyroidism is the most common disorder of the thyroid and occurs more commonly in women (6–10%) (Endocrinology Expert Group 2009; Queensland Health 2008b). Hypothyroidism is characterised by a decreased secretion of thyroid hormones and may be congenital or it may develop later in life. Cretinism is the congenital form of hypothyroidism and typically results from absence or underdevelopment of the thyroid gland or from severe maternal iodine deficiency during pregnancy. The manifestations of cretinism are related to a marked depression of metabolic processes and progressive mental impairment. Typically the infant is overweight, lethargic, has dry thick skin, coarse features, a broad flat nose and protruding tongue and abdomen (Marieb & Hoehn 2010). If the disease goes unchecked, sexual organs fail to develop and muscle growth is retarded. Treatment is started as soon as diagnosis is made and involves lifelong thyroid hormone replacement therapy (HRT). Hypothyroidism can also result from surgical intervention used to correct hyperthyroidism.

The most common natural cause of hypothyroidism is an autoimmune disorder, Hashimoto’s disease. Symptoms of hypothyroidism are the opposite of those of hyperthyroidism (see Table 34.2). The individual is fatigued, drowsy and sensitive to cold temperatures, gains excessive weight, has thin nails and brittle hair, decreased pulse and respiratory rates and irregular menstruation (Monahan et al 2007) (Fig 34.6). Advanced hypothyroidism may produce personality and cognitive changes characteristic of other mental dysfunctions such as dementia or depression. Depression has been linked to, both causatively and symptomatically, and misdiagnosed as hypothyroidism (Chueire et al 2007; Krausz et al 2007). Diagnosis of hypothyroidism may be difficult due to the nonspecific nature of the symptoms, which are often diverse and atypical (Endocrinology Expert Group 2009). Despite this, hypothyroidism responds well to HRT and symptoms may disappear after a few months of treatment.

Figure 34.6 Myxoedema (A) and hypothyroidism (B)

(A Talley NJ & O’Connor S (2009) Clinical Examination, 6th edn. Churchill Livingstone, Elsevier Australia, Fig 10.8; B Dr P. Marazzi/Science Photo Library

Myxoedema is the characteristic sign of severe or prolonged hypothyroidism. The name refers to oedema in the dermis of the skin, especially around the eyes, hands and feet (Brown & Edwards 2012) (Fig 34.6). Myxoedema and myxoedema coma however—the decompensated state of severe hypothyroidism in which a patient may lose consciousness—if left untreated may lead to death. Maintenance of vital functions and monitoring for increasing severity of signs and symptoms is a major nursing intervention (Monahan et al 2007).

Diagnostic tests

A combination of tests is generally performed to evaluate thyroid function, including direct tests of thyroid function, tests that measure concentration and binding of the thyroid hormones and tests involving the use of scanning or imaging techniques (LeMone et al 2011). Blood tests are performed to measure serum hormone levels. The best screening test of thyroid function is the measurement of serum TSH concentrations, due to its sensitivity. This may be augmented by assessing serum free or bound T₃ and T₄. Radioactive iodine tests, such as the radioactive iodine uptake test, evaluate thyroid function by measuring the amount of orally ingested iodine that accumulates in the thyroid gland over a time regimen (Brown & Edwards 2012). Thyroid scanning is visualisation of the thyroid gland after administration of a radioisotope. Thyroid ultrasonography helps evaluate thyroid structure and differentiation between a cyst and a tumour on the thyroid gland. If an individual is to have thyroid tests, the nurse must ascertain medications taken by the person (especially if they contain iodine) (Farrell & Dempsey 2011).

Most people with classic hyperthyroidism rarely need hospitalisation. Critically ill individuals, those with extreme manifestations of thyrotoxicosis plus a significant concurrent illness, require inpatient acute care on a medical unit. Management of hyperthyroidism involves assisting the individual and their family to manage the symptoms associated with hyperthyroidism until it is controlled with medication (hormone replacement therapy is the preferred option) or surgery if indicated. Surgical intervention may involve a subtotal thyroidectomy, which removes part of the thyroid gland, leaving enough gland to produce adequate thyroid hormone, or a total thyroidectomy may be performed if the gland is cancerous (Monahan et al 2007). A person who has had a total thyroidectomy requires long-term hormone replacement (Australian and New Zealand Endocrine Surgeons 2011b).

The nurse should assess the nutritional and emotional status of a client with hyper- and hypothyroidism, and manage appropriately. The nurse should also reassure the client that the emotional reactions, especially with hypothyroidism, are normal for that condition (Farrell & Dempsey 2011).

Hyperparathyroidism

Hyperparathyroidism results in an overproduction of PTH. This condition can be caused by hereditary factors, tumours or enlargement of the glands. It is more common in women, and in patients above 60 years of age (Suliburk & Perrier 2007). Secondary hyperthyroidism can be caused by renal disease or other calcium perturbations such as osteomalacia or rickets. Excessive PTH production leads to hypercalcaemia (excessive calcium in the blood) as the hormone stimulates resorption of calcium from bone, the kidney and gut (Marieb & Hoehn 2010). As the calcium is pulled from the bones, individuals with this condition display manifestations that are widespread and include symptoms such as backache, bone curvature and pathological fractures from bone weakness (Farrell & Dempsey 2011). Renal stones may develop because of the excess calcium output in the urine, especially in conjunction with metabolic acidosis and alkaline urine. The digestive system increases absorption of calcium, causing abdominal pain, vomiting and constipation. Hypercalcaemia leads to hyperactivity of muscles, causing impaired neuromuscular coordination and cardiac arrhythmias.

Hypoparathyroidism

Hypoparathyroidism is relatively uncommon and is indicated by deficiency in PTH secretion. Causes may include familial hypoparathyroidism, autoimmune disorders or, most commonly, surgical removal of parathyroid glands in an effort to treat other thyroid disorders (Monahan et al 2007). Low or lack of circulating PTH causes hypocalcaemia and hyperphosphataemia (high phosphate levels in the blood), resulting in neuromuscular symptoms ranging from paraesthesia to tetany. Manifestations include muscle spasm, anxiety, hyperreflexia and laryngeal spasm (Marieb & Hoehn 2010).

Tetany results from hyperexcitability of nerves and skeletal muscles because of low calcium blood levels. It begins with tingling in the fingertips, toes and around the mouth (Brown & Edwards 2012). The tingling increases and produces muscle tension and spasms, with consequent adduction of the thumbs, wrists, elbows and toes (carpopedal spasm). The tetany associated with hypoparathyroidism mainly affects the face and hands, causing uncontrolled contraction of these muscles.

Diagnostic tests

The general diagnosis of both hyper- and hypoparathyroidism is often difficult due to the vague symptoms of pain or fatigue. Tests used to assess parathyroid function therefore include estimation of serum calcium and serum phosphorus levels (LeMone et al 2011). Elevated serum calcium alone is not definitive as blood calcium may be influenced by diet and medications also. A 24-hour urine collection may be performed to measure the total urine calcium, as hyperparathyroidism causes increased excretion of calcium in the urine, and hypoparathyroidism causes decreased excretion of calcium. Scans or x-rays to ascertain bone changes and antibody parathyroid tests may also be implemented. Testing for hypocalcaemia and hypoparathyroidism involves checking for a positive Chvostek’s sign (facial muscle spasm occurring when the facial nerve is tapped) and a positive Trousseau’s sign (hand muscle spasm when pressure is applied to the nerves and vessels of the upper arm) (Farrell & Dempsey 2011; Monahan et al 2007).

Treatment of hyperparathyroidism is directed at the cause and often results in good prognosis for the client. Surgical removal of tumours or removal of the parathyroid glands may be necessary, leaving half of one parathyroid gland, which is all that is required to maintain normal PTH levels. Other treatments include hydration or diuretic therapy to force increased excretion of calcium by the kidneys, and decreasing calcium intake in the diet (Farrell & Dempsey 2011).

An important aspect of the nursing care is the client education and management of dietary calcium and phosphate intake. Treatment of hypoparathyroidism with calcium supplements and vitamin D, which controls absorption of calcium in the gastrointestinal tract, gives a good prognosis (McCance & Huether 2010). Parathyroid autotransplantation, where the patient’s parathyroid glands are replaced during a thyroidectomy, is being implemented more often in Australia and New Zealand (Ebrahimi et al 2009). Following thyroidectomy, hypocalcaemia and tetany may occur. In this instance the client is infused calcium intravenously. Parenteral PTH may also be administered.

Disorders of the adrenal cortex—hyperadrenalism

Hyperadrenalism is usually confined to the cortex of the gland. It may be caused by neoplasia or hyperplasia, or it may be iatrogenic, that is, a condition caused by medical treatment or procedures. Other factors resulting in hyperfunctioning of the cortex include tumours or hyperplasia of the pituitary gland, whereby the negative feedback control of the adrenal cortex by ACTH is disturbed. Manifestations of hyperfunctioning are generally related to an excess of glucocorticoids, mineralocorticoids and sex hormones. Three major disorders can result.

Cushing’s syndrome

Cushing’s syndrome is a collection of endocrine disorders due to excess corticosteroids (Brown & Edwards 2012). This condition may result from excessive use of corticosteroids, hypersecretion of pituitary ACTH (Cushing’s disease) or a tumour of the adrenal glands or pituitary. Manifestations of this condition are related to hyperglycaemia, abnormal distribution of lipids and protein wasting. Classic symptoms include obesity of the trunk with a pad of fat across the shoulders (buffalo hump), a moon face, striae on the breasts, abdomen and legs, muscle weakness, osteoporosis and skin fragility (Craft et al 2011; Farrell & Dempsey 2011; Monahan et al 2007) (Fig 34.7). Persistent hyperglycaemia may develop into diabetes mellitus. Elevated cortisol levels exacerbate catecholamine effects and, as a result, hypertension is a common feature. This may lead further to atherosclerosis, ischaemic heart disease and nephrosclerosis.

Figure 34.7 Cushing’s syndrome

(A Seidel HM, Ball JW, Dains JE et al (2006) Mosby’s Guide to Physical Examination, 6th edn. Mosby, St Louis, Fig 50-11; B Lewis SL, Ruff Dirksen S, Heitkemper MM et al (2011) Medical-Surgical Nursing, 8th edn. Mosby, St Louis, Fig 50-12)

Women are more likely to develop Cushing’s syndrome, and excess androgen production causes virilisation in females of all ages (Farrell & Dempsey 2011). Male traits such as hirsutism and voice deepening and breast atrophy may occur. A complication of Cushing’s syndrome is the individual’s decreased immune response and increased susceptibility to infection (see Clinical Interest Box 34.2).

Primary aldosteronism

Primary aldosteronism, also known as Conn’s syndrome, is usually caused by an adrenal tumour and is the result of hypersecretion of the mineralocorticoid aldosterone (Craft et al 2011). Conn’s syndrome leads to impaired reabsorption of sodium and water in the renal tubules, resulting in hypertension, hypokalaemia, muscle weakness, polyuria, polydipsia, metabolic acidosis and neuromuscular dysfunction (Brown & Edwards 2012). Given the high incidence of hypertension in Australia and New Zealand (see Ch 23), alterations of aldosterone function should be of consideration and interest in the nursing assessment.

Androgenital syndrome

Hypersecretion of androgens may result in androgenital syndrome, especially in prepubertal children. Excessive secretion of androgens may cause contradictions in secondary sexual characteristics. For example, female children are seen with excessive hair growth on the legs, chest and abdomen, an enlarged clitoris, a deepened voice and amenorrhoea (features exhibited also by individuals suffering Cushing’s syndrome). Male children may experience precocious puberty (premature sexual development) and gynaecomastia (breast development) (Congenital Adrenal Hyperplasia Support Group Australia nd).

Addison’s disease

Hypofunctioning of the adrenal cortex may be caused by primary insufficiency, resulting in a condition known as Addison’s disease, or adrenocortical insufficiency. This is a rare condition thought to be due to an autoimmune reaction (Michels & Eisenbarth 2007), infection, acquired immunodeficiency syndrome (AIDS), cancer or adrenal gland atrophy. Up to 90% of the cortex can be destroyed before the symptoms become evident; as a result, the disease is often advanced before it is diagnosed (Australian Addison’s Disease Association 2006; Brown & Edwards 2012). The manifestations are related to a deficiency of all corticosteroids. The lack of mineralocorticoids depletes sodium, which leads to diarrhoea, dehydration, weakness, weight loss and hypotension. The lack of glucocorticoids affects blood sugar levels, leading to hypoglycaemia (Marieb & Hoehn 2010). An increased ACTH level, due to disturbed negative feedback control, may lead to brown pigmentation or bronzing of the skin and mucous membranes, affecting the palms, elbows, scars, skin folds and areolae (Australian Addison’s Disease Association 2006). Addison’s disease may also have profound effects on an individual’s mental state, with individuals exhibiting depression, confusion or apathy (Brown & Edwards 2012; Monahan et al 2007).

Congenital adrenal hyperplasia (CAH) is often classified together with Addison’s as general adrenal insufficiency. Similar to Addison’s disease, cortisol and aldosterone are either partially or not produced. The condition may be classified as ‘classic’ (congenital, a genetic defect in steroid synthesis) or ‘late-onset’ (early adult onset). Growth and adrenal problems may develop, as for other adrenal insufficiencies (Endocrinology Expert Group 2009). In New Zealand CAH is part of routine screening for newborns and about one in 10 000 children are born with CAH (Congenital Adrenal Hyperplasia Support Group New Zealand nd). Treatment centres on replacement of the corticoids with analogues such as dexamethasone and fludrocortisone.

Phaeochromocytoma

Phaeochromocytoma is a generally benign tumour of the medulla or of the sympathetic chain, which causes over-secretion of adrenaline and noradrenaline. Incidence peaks in middle age and is also high in familial members, and may occur as part of multiple endocrine neoplasia (MEN) (Farrell & Dempsey 2011). The resultant increase in sympathetic activity manifests as episodes of hypertension, tachycardia, chest pain, pallor, sweating, headaches, anxiety, tremor, nausea and vomiting and frequency of urination. These symptoms can cause life-threatening scenarios for the individual, so early diagnosis and treatment is imperative (Monahan et al 2007).

Diagnostic tests

Typically, blood and urine tests are performed that enable measurement of the levels of adrenal cortical hormones. Blood tests determine the level of serum aldosterone, serum cortisol or serum catecholamines (LeMone et al 2011). These levels aid in the diagnosis of adrenal function; for example, serum cortisol levels are increased in Cushing’s syndrome, while decreased serum cortisol levels are seen in Addison’s disease. A 24-hour urine collection may be performed to estimate the total daily free cortisol, aldosterone or catecholamine levels. A CT scan or suprarenal venography may also be used to aid in the diagnosis of tumours.

Surgical removal of the tumour or the dysfunctional adrenal gland (adrenalectomy) may correct Cushing’s syndrome for the individual (LeMone et al 2011). Lifetime hormone therapy to replace the cortical hormones is then required. Clinical Interest Box 34.2 provides an insight into cortisone therapy. Nurses should decrease risk of injury and infection, encourage rest and activity, promote skin care and stimulate mental activity for patients or clients with Cushing’s syndrome. Treatment and nursing care for Addison’s disease and CAH includes corticosteroid therapy, and the assessment and management of fluid levels, signs of shock and careful monitoring of symptoms (Craft et al 2011; LeMone et al 2011).

Measurements of blood and urine for catecholamines are the most direct and conclusive tests for disorders of the adrenal medulla like phaeochromocytoma. Likewise, the presence of hypertension, headache, hypermetabolism and hyperglycaemia indicates phaeochromocytoma. Imaging studies may also be carried out to identify the location of the suspected tumour, which is preferably removed surgically. Treatment and nursing management procedures include those for high blood pressure, high blood glucose and tachycardia, and HRT is often indicated following surgery (Brown & Edwards 2012; Monahan et al 2007).

Hypergonadism and hypogonadism

Gonadal disorders may reflect interruptions in the normal control by the pituitary, a tumour or congenital syndromes such as Turner’s or Klinefelter’s (Endocrinology Expert Group 2009; Craft et al 2011). Hypergonadism, as opposed to hypersecretion of gonadotrophins by the pituitary gland or androgenital syndrome, results from increased gonadal hormone production before puberty and leads to precocious sexual development and enhanced sexual characteristics in both sexes. Causes of hypergonadism are primarily unknown but some cases have been caused by ovarian tumours and testicular tumours (Funnel et al 2008). Treatment for both sexes involves removal or radiation of the tumours, and hormone therapy to suppress or counteract the effects of the sex hormone.

Hypogonadism results from decreased sex hormone production by the age of normal puberty. Due to the control of gonad function by the pituitary and adrenals, hypogonadism prior to puberty reflects abnormalities of these endocrine glands. Treatment with testosterone or oestrogen is usually effective (Endocrinology Expert Group 2009).

Endocrine deficiencies of the gonads in the adult female, for example, are implicated in two common disorders: osteoporosis and polycystic ovary syndrome (PCOS). This reflects the strong interrelationship between endocrine organs and hormones in the human body. Osteoporosis and PCOS are discussed further in Clinical Interest Boxes 34.3 and 34.4 respectively.

Diagnostic tests

Diagnoses of disorders of the gonads is based on a positive clinical history and, as for other disorders, are confirmed by blood tests showing elevated sex hormone levels.

Diabetes mellitus

Diabetes mellitus (DM) is a group of metabolic disorders characterised primarily by abnormal glucose metabolism, with the key feature of elevated blood glucose (hyperglycaemia). Diabetes mellitus affects a great number of the Australian and New Zealand population, with more than 7% of the Australian population over 25 having diabetes (Australian Institute of Health and Welfare 2008, 2009). In New Zealand, over 120 000 people suffer from diabetes (New Zealand Ministry of Health 2007), although current estimates suggest as many as 270 000 (Diabetes New Zealand 2011). Type 2 diabetes mellitus is more common than type 1, with over 95% of the population having type 2. Incidences and death rates in both Australia and New Zealand are higher for males than females, and both Indigenous Australians and Māori populations are almost twice as likely to be diagnosed (Australian Institute of Health and Welfare 2008, 2009; New Zealand Ministry of Health 2007). Such is the increasing prevalence in diabetes worldwide that diabetes nursing is becoming more specialised, with distinct nursing career and competency frameworks being developed (Davis et al 2008).

Diabetes mellitus is a disorder of glucose regulation characterised by abnormal metabolism of carbohydrate, protein and fat (Farrell & Dempsey 2011). A feature of the disorder is some degree of hyperglycaemia. Diabetes mellitus results from hyposecretion or hypoactivity of insulin, intolerance to insulin (hyperinsulinaemia) or from the production of substances antagonistic to insulin, which cause it to be ineffective. It may be caused by genetic or hereditary factors, pancreatic disorders or by disorders of other endocrine glands such as the pituitary or adrenal glands (recall that these endocrine glands secrete hormones that affect glucose metabolism). It is also thought to be autoimmune in origin: the destruction of β cells by the body may be a response to molecular mimicry by a pathogen, or due to possible diabetes susceptibility genes (Craft et al 2011; Farrell & Dempsey 2011; Marieb & Hoehn 2010).

A deficiency of insulin causes changes in the metabolism of glucose, which results in numerous physiological effects (Fig 34.3). In the liver glycolytic enzymes are inhibited, gluconeogenic enzymes are activated and amino acids are used to form glucose. Consequently, additional glucose is liberated into the bloodstream. Without insulin, glucose is unable to cross the cell membranes into muscle and fat cells, and hyperglycaemia ensues (Marieb & Hoehn 2010). The blood glucose level eventually exceeds the renal threshold, and the excess glucose is excreted in the urine (glycosuria). The most significant effect of elevated blood glucose level is dehydration of the tissue cells because the increased osmotic pressure in the extracellular fluids causes osmotic transfer of water out of the cells. In addition, the loss of glucose via the urine causes diuresis (polyuria), because of the osmotic effect of glucose in the renal tubules. The result is extreme thirst, or polydipsia (Monahan et al 2007).

Gestational diabetes is one form of the disorder and appears only during pregnancy (about 5% of pregnancies) (AIHW 2010; Diabetes Australia 2011b), and is characterised by impaired glucose tolerance. A woman who has had gestational diabetes runs a greater risk (50–60%) of developing diabetes mellitus later on in life (AIHW 2010; Craft et al 2011). Diabetes mellitus itself is classified into two types: type 1, or insulin-dependent diabetes mellitus (IDDM); and type 2, or non-insulin-dependent diabetes mellitus (NIDDM). A third minor type, pancreatic or type 3c diabetes (Hardt et al 2008), relates to exocrine insufficiency and may contribute to diabetes mellitus. It is believed therefore to be generally un- or misdiagnosed. The diagnosis of diabetes mellitus is confirmed, among other tests, by the presence of an elevated blood glucose level. The manifestations of diabetes mellitus vary according to the type.

Type 1 diabetes mellitus

Type 1 diabetes mellitus is characterised by the genetic or autoimmune destruction or deficiency of the pancreatic β cells that produce insulin and usually progresses so quickly it is often diagnosed in childhood, hence its previous name of juvenile-onset diabetes (Farrell & Dempsey 2011) (see Clinical Scenario Box 34.3). It can occur, however, at any age from infancy up to about age 40. There is a sudden onset of signs and symptoms related to hyperglycaemia, which includes weight loss, polyuria and polydipsia (related to osmotic diuresis), fatigue and the presence of glucose and ketones in the urine (glycosuria and ketonuria) (Craft et al 2011). Hyperglycaemia and dehydration accelerate the development of metabolic acidosis and, if untreated, can lead to coma and death.

Type 2 diabetes mellitus

Type 2 diabetes mellitus is a hyperglycaemia despite the availability of insulin (insulin resistance at the cell) and is more likely to occur after age 40. The signs and symptoms develop slowly and the individual is generally obese: obesity and metabolic syndrome are significant risk factors and often precursors for type 2 diabetes mellitus (Craft et al 2011). Type 2 diabetes mellitus may often go undetected, as the signs and symptoms of fatigue, polyuria and polydipsia can be quite insignificant. Diagnosis occurs when the individual presents with another disease, which is a common complication of diabetes mellitus (McDowell et al 2007). The individual with diabetes mellitus is prone to a range of complications, especially if the blood glucose level is uncontrolled. Complications include:

It is these complications that the nurse may need to assess and monitor. The maintenance of blood glucose levels are achieved by a balance between blood-borne stimuli, nervous input (e.g. the sympathetic nervous system) and hormonal influences. As such, there are a number of influences on blood glucose levels that the nurse should take into consideration.

Complications of diabetes mellitus

Complications may develop rapidly or progress insidiously over years before they become evident. The two main complications that occur because of uncontrolled blood glucose levels are hypoglycaemia and hyperglycaemia.

Long-term complications

Diagnostic tests

Laboratory evaluation of the pancreatic islets is mainly concerned with levels of glucose in the blood and urine. Urine is typically examined for the presence of glucose and ketones (see Ch 29). As a result of increased lipolysis, excess ketone bodies accumulate and are excreted in the urine. Urine may also be tested for the presence of protein (microalbuminuria), which may detect the early onset nephropathy. Blood tests measure the body’s use of glucose and include:

(Brown & Edwards 2012; LeMone et al 2011; McDowell et al 2007).

Cultural considerations: diabetes in the Māori population

In New Zealand, groups at risk of developing type 2 diabetes include not only those who are overweight, have familial history of the disease or who have a reduced physical activity, but also those of Asian, Māori or Polynesian descent (Diabetes New Zealand 2008a). The incidence of diabetes mellitus, particularly type 2, is both higher in Māori than Pākehā (European or white New Zealanders), and is expected to rise more quickly in the future. Currently about 1 in 32 New Zealand Pākehā adults has known diabetes, whereas 1 in 12 Māori and 1 in 12 Pacific Island adults have known diabetes (Diabetes New Zealand 2008a). In 2020 it is expected that 1 in 22 Pākehā and 1 in 6 Māori and Pacific Island adults will have known diabetes.

A contributing factor is the body size and weight status of Māori in New Zealand. A recent New Zealand Health Survey found that body size indicators (body mass index—BMI) for Māori male and female children and adults were consistently higher than those for non-Māori. The only exception was for males over 15 years where non-Māori males had a higher BMI than Māori. However, significantly more Māori men over 15 years were obese compared to non-Māori (New Zealand Ministry of Health 2010).

Associated with this increased prevalence and incidence is an increased risk of developing secondary complications, particularly renal and lower limb complications. According to the New Zealand Ministry of Health, renal failure is nine times more prevalent in Māori with concurrent diabetes compared to non-Māori. Likewise lower limb amputations are four times more likely in Māori (New Zealand Ministry of Health 2010). A descriptive analysis of Māori health status data is available in the form of Māori Health Chart books (Tatau Kahukura 2010 and Tatau Kura Tangata 2011) (New Zealand Ministry of Health 2011).

As a population group, Māori have on average the poorest health status of any ethnic group in New Zealand. The New Zealand Government and the Ministry of Health have made it a key priority to reduce the health inequalities that affect Māori and to close the gap in disease prevention and education between Māori and non-Māori. As a result, the Ministry of Health has developed Māori health strategies (He Korowai Oranga) and Health action plans (Whakatātaka Tuarua) which aim to set directions for Māori health development and to implement programs, policies and interventions (New Zealand Ministry of Health 2011). Table 34.3 is a summary of major endocrine imbalances.

Table 34.3 Summary of major endocrine imbalances

A major change in lifestyle

As a result of an endocrine imbalance, the individual may have to depend on lifelong medication, dietary and fluid intake modifications, reductions in activity or exposure to stressors, and potentially irreversible physical and physiological changes. In addition, individuals may experience sexual dysfunction, an often neglected complication of endocrine disorders (Bhasin et al 2007). For example, individuals with diabetes mellitus may have to depend on lifelong medication and dietary alterations, and a lifelong commitment to monitoring blood glucose. All clients with chronic conditions should also be encouraged to wear a medical alert bracelet.

The prospect of facing major surgery

Removal of the thyroid gland may be indicated in the presence of hyperthyroidism, goitre or carcinoma of a gland. Likewise, adrenalectomy may be the preferred intervention with adrenal gland tumour or hypersecretion of corticosteroids or catecholamines. A similar approach may be taken, in addition to medication, for pituitary tumours. Clients facing major surgery should be educated and counselled on the preparation for surgery, the procedure and care required postoperatively.

Possible postoperative changes

Surgical intervention may result in the balance of hormones shifting in the opposite direction. For example, thyroidectomy for hyperthyroidism or hyperparathyroidism may result in hypofunction of the gland after removal of much of the tissue. Individuals should be educated in the likelihood of having hypofunction of the gland and the reliance on medication to address these changes.

Alterations in nutritional status

Weight gain often occurs in hypothyroidism, whereas weight loss is common in people with type 1 diabetes mellitus. Nutritional status may also be affected if the individual is experiencing anorexia, nausea or vomiting. Hyperthyroidism is associated with increased cellular metabolism and individuals often experience rapid weight loss: management of calorific intake is therefore a concern. In addition, iodine intake may need to be restricted or increased in patients with goitre or thyrotoxicosis.

Nursing care plans should also consider the reduction or management of dietary intake of calcium for clients with parathyroid imbalances. Diabetes mellitus obviously requires the management of glucose intake by health professionals and educators, and most especially by the patient.

Alterations in fluid and electrolyte balance

Excessive loss of fluid (polyuria) may occur in diabetes mellitus or posterior pituitary gland disorders such as diabetes insipidus. Loss of fluid may also occur if the individual has diarrhoea, as may be present in disorders such as hyperthyroidism and Addison’s disease. To address polyuria, the increased thirst (polydipsia) and fluid intake of clients with diabetes mellitus and diabetes insipidus should be considered.

Conversely, retention of fluid may occur in disorders such as Cushing’s syndrome, the oedema associated with hypothyroidism (and myxoedema) and SIADH. Careful fluid restrictions for clients with SIADH are suggested to allow sodium levels to increase slowly. Where the effects of aldosterone are compromised or enhanced (e.g. primary aldosteronism), electrolyte intake (especially of sodium) as well as fluids should be considered.

Management of discomfort

Many endocrine disorders result in problems related to body temperature regulation. A person with hypothyroidism is very sensitive to cold, whereas an individual with hyperthyroidism is commonly intolerant to heat. Other factors that may cause discomfort include pruritus associated with hyperthyroidism or diabetes mellitus, and joint pain associated with acromegaly. Anxiety and nervousness associated with certain disorders such as hyperthyroidism, or hypertension and headache with phaeochromocytoma, may also cause discomfort as the individual is restless and finds it difficult to relax. Apathy and difficulty in concentration may occur in hypothyroidism.

Calcium imbalances potentially affect nervous and muscular function, and individuals with hyper- and hypoparathyroidism may experience anxiety, uncomfortable nervous tingling and muscle spasms, or backache associated with calcium resorption from bones.

Reduced independence

Extreme fatigue often accompanies endocrine disorders, and the individual may require assistance to carry out activities of daily living. Certain disorders (e.g. Cushing’s syndrome or hyperparathyroidism) may be accompanied by alterations in mental status, learning and memory (McCance & Huether 2010). Altered states of awareness or consciousness (hypothyroidism, decreases in fluid electrolyte levels) will also reduce the individual’s level of independence.

Hypertension and arteriosclerosis associated with disturbances to glucose and lipid metabolism (e.g. diabetes mellitus, Cushing’s syndrome) may also restrict clients to less exertive activities and a greater reliance on assistance.

Altered body image

Clients may experience both physical and mental alterations to body image and subsequent changes in behaviour to address these concerns. Healthcare professionals should be prepared to explain the manifestations to the client, and to consult and counsel the client in the event of changes in self-esteem or behaviour associated with physical changes.

Obvious changes in physical appearance occur with Cushing’s syndrome (e.g. buffalo hump, moon face), and exophthalmos and possible goitre associated with hyperthyroidism. Clients may also exhibit changes in height and appearance with gigantism and acromegaly. Hirsutism associated with adrenal, pituitary or gonadal dysfunction may severely affect the self-esteem of clients (especially females), and children suffering from androgenital syndrome are especially likely to suffer from psychological effects of an altered body image. Individuals with Addison’s disease may experience increased skin pigmentation (bronzing).

The plan of care that the nurse designs for a client should specifically address the need for comfort, psychological support, and maintenance of nutritional and fluid status. Clients should also be given information regarding professional support and self-help groups and should be encouraged to contact these organisations for further support and information. A list of organisations and websites is provided in online resources.

Diet, nutrition and energy requirements

Diet is an important aspect in control of both type 1 and type 2 diabetes mellitus. A dietitian works with the client to develop a well-balanced, healthy food intake. It is essential that the client gains understanding of the principles and can then modify and adapt the diet to meet demands experienced during illness, injury, emotional stress or major changes in lifestyle. The aims of the diet for a person with diabetes are to:

Normal or average blood glucose is around 5 mmol/L (4–6 mmol/L fasting), with a range of 3.5–8 mmol/L. Fasting plasma glucose in a non-diabetic individual is usually less than 6.1 mmol/L, and a repeated fasting level of at least 7.0 mmol/L is indicative of hyperglycaemia (LeMone et al 2011). The Heart and Diabetes Institute of Australia (Heart and Diabetes Institute of Australia 2011) recommend goals for dietary and nutrition management.

Alcohol should be limited, as not only is it high in sugar and may cause adverse reactions to some medications used in the treatment of diabetes mellitus, it may also mask hypoglycaemia (Endocrinology Expert Group 2009). The dietitian will supply the individual with instructions for planning nutritious and varied meals within the prescribed limitations. The importance of regular meals and snacks is emphasised, particularly an evening snack to prevent nocturnal hypoglycaemia. The diet is continually evaluated and adjusted as required. When the individual is in hospital it is important that the nurse observes the amount of each meal eaten because if nutrients are not all consumed the person may experience hypoglycaemia (Brown & Edwards 2012; Craft et al 2011; Farrell & Dempsey 2011).

Exercise

The amount of exercise required by the client should be estimated and planned to balance with the dietary intake and insulin (Farrell & Dempsey 2011). A well-planned program of regular exercise that is adjusted as necessary is beneficial in weight control, in its physiological and psychological effects and in terms of blood glucose control. Regular gentle exercise stimulates the uptake of glucose by muscle cells, lowering blood glucose levels and increasing the absorption of injected insulin. For these reasons, exercise can increase the likelihood of hypoglycaemia. To prevent hypoglycaemia after exercise, the individual needs to either increase the nutritional intake or decrease the insulin dosage. Education is essential for the client to gain understanding to correctly balance the level of exercise with dietary intake and insulin dosage under varying conditions. Exercise also has the benefits of decreasing cholesterol and triglycerides, and reducing the risk of cardiovascular disease (LeMone et al 2011). Strenuous exercise, however, can trigger the release of hyperglycaemic hormones, such as adrenaline and glucagon, so should be avoided (Brown & Edwards 2008).

Insulin

As insulin is essential for the normal metabolism of glucose, it is a major factor involved in the regulation of blood glucose levels. Many types of insulin are available and these may be rapid onset-fast acting, short-, intermediate- or long-acting, or mixed (Diabetes Australia 2011d). The different types of insulin vary in the time of onset and the duration of action, and are selected according to the time of day, activity and nutritional intake. As soon as possible after diagnosis, the client is given instruction on insulin administration and care for the equipment required. Insulin may be administered via syringe and needle (now less commonly used), specialised pens or by pump (CSII—continuous subcutaneous insulin infusion) (Diabetes Australia—Vic 2010; LeMone et al 2011; McDowell et al 2007). Clients are also instructed on rotating injection sites around the abdomen and thighs to prevent tissue atrophy or hypertrophy at regularly used injection sites. The abdomen provides the fastest and most consistent rate of absorption and is an accessible site for the person to use (Figs 34.8 and 34.9).

Figure 34.8 Insulin injection sites

(Lewis SL, Ruff Dirksen S, Heitkemper MM et al (2011) Medical-Surgical Nursing, 8th edn. Mosby, St Louis, Fig 49-5)

Figure 34.9 Insulin pen

(Getty Images/© Saturn Stills/Science Photo Library)

Short-acting insulin may also be delivered continuously at a basal rate subcutaneously by a CSII pump, with dosages entirely self-determined and monitored by the individual. Clients choosing this insulin regimen need to be motivated, and educated by a nurse or diabetes educator (Australian Diabetes Educator Association 2011b). Insulin pumps and associated equipment are subsidised in Australia by the NDSS (National Diabetes Services Scheme) (Endocrinology Expert Group 2009; Diabetes Australia–NDSS 2011).

Oral hypoglycaemic agents

Oral hypoglycaemic agents may be prescribed in the management of type 2 diabetes mellitus unresponsive to diet alone. The medications used in the treatment of diabetes mellitus act in a variety of ways, by stimulating the pancreas to release insulin (secretogogues), reducing insulin resistance (sensitisers), the promotion of glucose use or delaying glucose absorption across the gut (Endocrinology Expert Group 2009).

Hygiene and preventing infection

People with diabetes mellitus are susceptible to infection as a result of impaired body defence mechanisms and elevated glucose providing an environment for bacterial growth (Craft et al 2011). The person with diabetes is particularly at risk of developing urinary tract infections, fungal infections such as Candida and infected skin lesions (Brown & Edwards 2012). To minimise the risk of infection the person should understand the importance of good control of blood glucose levels, of maintaining a high standard of personal hygiene and of avoiding unnecessary exposure to infection (LeMone et al 2011). The skin should be kept clean and free from excessive irritation, friction or pressure. All injuries to, or infections of, the skin, however minor, should be cleaned with a mild antiseptic solution and covered with a dressing (McDowell et al 2007).

Skin lesions of the feet commonly occur in people with poorly controlled diabetes mellitus (Heart and Diabetes Institute of Australia 2011). Such lesions result from, or are exacerbated by, impaired circulation and peripheral neuropathy (Craft et al 2011). If a minor injury or lesion is undetected or untreated, ulceration and infection may develop (Fig 34.10). Between 50% and 75% of lower extremity amputations are performed on people with diabetes (Farrell & Dempsey 2011). The nurse should also consider the lesion or aberration to be of different origin: melanomas of the feet have been misdiagnosed as diabetic foot ulcers (Rogers et al 2007; Yesil et al 2007). Care of the feet and prevention of foot lesions is therefore of prime importance and national guidelines on the prevention, identification and management of foot complications in diabetes are available (Heart and Diabetes Institute of Australia 2011).

Figure 34.10 Diabetic foot ulcer

(B: Courtesy of Isabelle Ellis)

Guidelines for foot care in individuals with diabetes

(Craft et al 2011; Diabetes Australia 2011e; Farrell & Dempsey 2011; LeMone et al 2011; McDowell et al 2007).

Monitoring blood glucose levels

Blood glucose monitoring is an accurate method of assessing the effectiveness of diet, exercise levels and medication therapy and to gain information regarding a client’s current blood glucose level. Blood glucose monitoring is usually performed by obtaining a drop of capillary blood, which is applied to a reagent strip and read by one of the many types of glucometers available on the market. Most meters available currently show acceptable reading precision, and errors are clinically insignificant (Cohen at al 2006). A digital display of the glucose level is provided, or the colour of the strip may be compared with a standard, either visually or with a reflectance meter. A variety of blood glucose monitoring machines are available, including ones with automatic finger-pricking, which run either on batteries or from mains power (Fig 34.11).

Figure 34.11 Blood glucose meter and monitoring

(A, B, C: © Miriam Doerr/Shutterstock; D: © Lisa S./Shutterstock)

The aim of self blood glucose monitoring is to assist clients with diabetes to assume more independence in managing their condition. Each person using blood glucose monitoring receives individual instruction in the technique, from a diabetes health educator, for example (Australian Diabetes Educators Association nd, 1). People with diabetes are advised on the appropriate times at which to perform the test and are shown how to make suitable adjustments to their insulin dose if the blood glucose levels are above or below those recommended. If the nurse is required to perform blood glucose monitoring they should also receive instruction in the technique and should become familiar with the manufacturer’s instructions accompanying each monitoring device (see Procedural Guideline 34.1).

Although not as accurate or desirable, blood glucose and ketone analysis may be augmented by urinalysis, performed by either a nurse or the client at home. Glycosuria is also indicative of other disorders such as Cushing’s syndrome. As a result, information on the effects of treatments or severity of other endocrine disorders may be provided by the specific gravity, presence of ketones or pH recorded on urinalysis strips. For further information on urinalysis, see Chapter 29.

Education

The person with diabetes mellitus has to learn to accept the condition and the resulting lifestyle changes that need to occur. They need to gain confidence in managing the condition, which requires learning a considerable amount of medical information and technical skills. A well-planned education program helps alleviate anxiety, creates autonomy in management and results in well-managed clients. Involving family members and close friends in the education program also assists the individual. The aims of an education program are that the individual will:

A person with diabetes mellitus should always carry a form of diabetic alert identification with them, such as a card, bracelet or medallion. This ensures that appropriate care will be administered if a medical emergency occurs. Clients suffering from diabetes mellitus or at risk may be referred by their health professional to the Australian Government National Diabetes Services Scheme for access to subsidised products to assist in home blood testing (Australian Diabetes Educators Association nd, 2; Diabetes Australia–NDSS 2011). In New Zealand blood glucose meters are often provided free of charge to clients with a community services card (Diabetes New Zealand 2008b).