Rheumatology

د. حسين محمد جمعه

اختصاصي الامراض الباطنة
البورد العربي
كلية طب الموصل
2011

Steroids: a guide to their uses, side effects, and how to start and stop them

© 2011 BMJ Publishing Group Ltd

Steroid drugs are prescribed for 1% of the population at any one time. This prevalence increases with age.
The anti-inflammatory and immunosuppressive actions of steroids have changed how we manage common conditions such as asthma and rheumatoid arthritis.
Steroids have important side effects and risks which all health professionals should be aware .

Case study: vital lessons from a Fatal Accident Inquiry

The following case study shows why it is important to exercise care when starting patients on steroids.
In November 2001, a 5 year old girl was admitted to hospital with abdominal pain and lethargy. She had
ahistory of severe asthma and was being treated with high doses of fluticasone by inhaler. Her condition deteriorated rapidly. She was treated for suspected meningitis, but suffered repeated convulsions and died. A post-mortem failed to identify a cause of death.


A month later, her brother began to complain of similar symptoms, including abdominal pain and sickness. He also had a history of asthma and was being treated with a fluticasone inhaler. He was admitted to hospital, where a CT brain showed cerebral oedema. He was admitted to the intensive care unit, where he was sedated and ventilated. He made a full recovery and was discharged home. It was noted that his plasma cortisol was low. A short synacthen test showed adrenal suppression. On the basis of this, a diagnosis of severe adrenal suppression secondary to high dose steroid inhaler was made.

The above findings led to a Fatal Accident Inquiry in Scotland into the girl’s death. The inquiry criticised many aspects of her treatment and detailed how her death could have been prevented by improvements in her care. It was felt that there had been a failure to prescribe safely and a failure to anticipate the adverse effects of steroids. It was also felt that she should have been issued with a steroid card to help alert medical professionals to the risks of her treatment. Her case was later publicised by the National Patient Safety Agency.

Introduction

Glucocorticoids and mineralocorticoid hormones are collectively referred to as corticosteroids. The adrenal glands secrete the following hormones:
• Glucocorticoids (cortisol and corticosterone)
• Mineralocorticoids
• Sex steroid hormones.

The main naturally occurring (endogenous) glucocorticoids are cortisol and corticosterone. The main endogenous mineralocorticoid hormone is aldosterone.
Glucocorticoids affect carbohydrate and protein metabolism. Mineralocorticoids affect water and electrolyte balance.
Endogenous hormones usually have both mineralocorticoid and glucocorticoid actions.
Synthetic steroids have been developed in which these two actions have been separated, and this affects the choice of steroid in a given clinical situation.

The control of glucocorticoid release

Glucocorticoids are released from the adrenal glands in response to adrenocorticotrophic hormone (ACTH). ACTH is released from the anterior pituitary. Corticotrophin releasing factor, a hormone released from the hypothalamus, stimulates ACTH secretion. ACTH secretion is also stimulated by catecholamines and vasopressin.

Glucocorticoids in the bloodstream and, to a lesser extent, ACTH, have a negative feedback effect on the release of corticotrophin releasing factor from the hypothalamus (see figure 1). This decreases the release of ACTH and the production of endogenous steroids from the adrenal glands. This is why the use of steroids over as little as three weeks can cause adrenal suppression.

Normally, the adrenals secrete approximately 10 mg (± 3 mg) cortisol per day. This is equivalent to 20 mg to 30 mg of oral hydrocortisone per day.
Physiological factors and emotional or physical stress can act as a stimulus to the release of corticotrophin releasing factor from the hypothalamus. These factors include:
• Excessive heat or cold
• Toxins
• Injury and infection.


Learning bite: steroids and stress
Cortisol secretion can be increased tenfold in times of stress. In patients being treated with exogenous steroids for more than three weeks, the adrenal gland can become suppressed (this effect is related to dose and varies from patient to patient). As a result, the adrenal gland may not be able to adequately increase its steroid output during times of stress. This is why, during periods of stress, it is important to increase the dose of steroid that the patient is on.

Pharmacokinetics of steroids

Glucocorticoids are small lipophilic molecules that circulate in the blood, they are bound to albumin and corticosteroid binding globulin, and they are metabolised in the liver.
Glucocorticoids enter cells by diffusion and bind to their specific receptors in the cell nucleus. The resulting steroid receptor complex then binds to DNA and either induces or represses transcription of a particular gene.

Time is needed to affect gene transcription, so the effects of steroids are not immediate.
The half life of exogenous or endogenous hydrocortisone is 90 minutes once it reaches the plasma, and its main biological effects occur after two to eight hours.
The full effects may take days to occur.

Synthetic steroids

The main synthetic steroids in clinical use are prednisolone, hydrocortisone, and dexamethasone. Steroids are most commonly used in respiratory disease, followed by musculoskeletal and skin diseases.

Dose and potency of different steroids

Steroids are used in either replacement or therapeutic doses. The aim of replacement therapy is to restore steroid levels to physiological levels (as used in a patient with adrenal or pituitary insufficiency). When used therapeutically, steroids are used in greater than physiological doses to achieve certain (usually anti-inflammatory) effects.

The potency or efficacy of different steroid medications varies. The following comparison from the British National Formulary gives information about the anti-inflammatory glucocorticoid action of the drugs only.
A dose of 5 mg of prednisolone is equivalent to:
20 mg of hydrocortisone
4 mg of methylprednisolone
0.75 mg of betamethasone
0.75 mg of dexamethasone


This comparison does not take into account the potency of mineralocorticoid action or the duration of action (which will affect how often the drug has to be given). For example, it shows that in terms of glucocorticoid anti-inflammatory effects, prednisolone is four times as potent as hydrocortisone.
However, prednisolone is only 0.8 times as potent in terms of its mineralocorticoid action.

These varying potencies are the reason why different steroids are used in different clinical situations:
Dexamethasone has minimal mineralocorticoid action, but is 30 times as potent as hydrocortisone in terms of its anti-inflammatory glucocorticoid action. This is why dexamethasone is used to treat the inflammation associated with brain tumours.
Fludrocortisone is 150 times as potent as hydrocortisone in terms of its mineralocorticoid action, but is only 15 times as potent in terms of its glucocorticoid action. This is why it is used clinically for its mineralocorticoid effects in the treatment of adrenocortical insufficiency.

Actions of glucocorticoids

Glucocorticoids regulate protein and carbohydrate metabolism. They help mobilise sugars, fats, and amino acids during times of stress.
Glucocorticoids also suppress the natural inflammatory response and have immunosuppressive actions. They suppress all types of inflammation, including inflammation caused by infection, hypersensitivity, autoimmune disease, and chemical or physical injury. The anti-inflammatory and immunosuppressive effects of glucocorticoids are mediated in a number of ways. These include:

• Decreased histamine release from basophils

• Decreased production of the inflammatory mediators - cytokines, prostanoids, and leukotrienes
• Decreased clonal proliferation of T cells and decreased action of T helper cells
• Decreased vasodilation and capillary permeability.
The anti-inflammatory and immunosuppressive effects of glucocorticoids are mediated in a number of ways. These include:

These effects impair a patient’s response to infection and can delay the healing process.
Endogenous glucocorticoids also have some mineralocorticoid action, causing retention of sodium and loss of potassium. This can lead to hypertension, hypernatraemia, and hypokalaemia when in excess.

Clinical indications

The different actions of steroids mean that they are used for different clinical indications. These include:
Replacement therapy - in adrenal failure (Addison’s disease) and pituitary failure (hypopituitarism):
It is important to remember that patients with Addison’s disease will also need mineralocorticoid replacement in addition to glucocorticoid replacement. In pituitary failure, the renin-angiotensin-mineralocorticoid axis works independently of ACTH, so endogenous production of mineralocorticoids occurs


Anti-inflammatory or immunosuppressive treatment:
Asthma
Inflammatory bowel disease
Hypersensitivity or allergic reactions
Autoimmune diseases - rheumatoid arthritis and other connective tissue diseases, vasculitis
To prevent graft versus host disease in organ or bone marrow transplant
Topical inflammatory conditions of the skin, eyes, ears, and nose

Treatment of neoplastic disease:

Cytotoxic drugs in the treatment of malignancy
To decrease cerebral oedema in patients with brain tumours
Antiemetic therapy - the mechanism of action of the antiemetic effect is unknown6
As an investigative tool - to test hypothalamic-pituitary-adrenocortical function in the dexamethasone suppression test

Methods of delivery

All steroids can be given systemically (by the intravenous or intramuscular route), and most can be given orally. You can also give steroids:
Topically - as a cream, ointment, suppository, or as nasal or eye drops
By local injection - intra-articular or intralesional
By inhalation as an aerosol.
Although the likelihood of systemic side effects is reduced by topical treatment, these can still occur when patients use topical treatment in high doses. Please refer to the case study at the start of this module.


Side effects of steroids
Patients on high dose or prolonged treatment are at increased risk of unwanted effects. In patients who are on replacement doses of steroids, you need to look out for these unwanted effects as they can still occur, though the risk is greatly reduced.
In steroid replacement therapy, the aim is to restore physiological levels, so side effects should be minimal (the replacement dose is the lowest dose clinically needed and is usually 20 mg to 30 mg of hydrocortisone per day). When used therapeutically in greater than physiological doses, side effects are more likely to occur.

These side effects include the following:

Suppression of the natural response to injury or infection
The anti-inflammatory and immunosuppressive actions of steroids suppress the inflammatory response to injury and infection. This means that there is decreased or delayed wound healing. Patients are also more susceptible to infection and the clinical course can be atypical or fulminant. Although there is a concern that giving steroids to patients with infections may exacerbate the infection, steroids can be used in the treatment of infection where there is a large inflammatory response, for example, in certain patients with pneumocystis pneumonia.

One of the most common infections associated with steroid use is oral candidiasis. This is linked with inhaled steroid use. You should advise patients to rinse their mouth after using a steroid inhaler. This will reduce the absorption of steroid in the mouth.

Varicella zoster (chickenpox) and measles infection

There have been several case reports of patients on steroids suffering severe, life threatening infections with the varicella zoster virus. Complications of infection with the varicella zoster virus in a patient who is on steroid treatment may include:
Severe pneumonia
Hepatitis
Disseminated intravascular coagulation
Severe rash (may or may not be present).
Measles infection in patients on steroids can also be severe and cause complications such as interstitial pneumonitis and encephalopathy.

Learning bite: advice to patients on steroids with regards to chickenpox

You should advise patients who are on systemic steroids or who have used them in the previous three months to avoid exposure to chickenpox; if they have any suspected contact, they should inform their doctor. If patients have been exposed to chickenpox and are not known to be immune, it is recommended to give varicella zoster virus immunoglobulin. You should give this intramuscularly for passive immunisation.8
If a non-immune patient on steroids is exposed to measles, it is recommended to give normal immunoglobulin. You should give this intramuscularly for passive immunisation.8


Adrenal suppression
Exogenous glucocorticoids act to suppress the release of glucocorticoids from the adrenal glands. Steroid courses continued for more than about three weeks can lead to adrenal suppression. Patients with adrenal suppression can either be asymptomatic or they may have non-specific symptoms such as weakness, lethargy, postural dizziness, abdominal pain, and nausea. These patients may also have hyponatraemia, hypoglycaemic attacks, and fits.

Adrenal suppression can last for as long as a year after a patient has stopped taking steroids (or even longer in rare cases).
The following situations may result in an acute deficiency of steroids or an Addisonian crisis.Physiological or emotional stress in patients on steroids with adrenal suppression. Such patients do not increase their glucocorticoid secretion in response to stress .Abruptly stopping a steroid course without tapering the dose may not leave sufficient time for the adrenals to recover and hence may lead to a deficiency of endogenous steroid hormones .You can test the ability of the adrenals to respond to stimulation using the short synacthen test.

Addisonian crisis

Acute glucocorticoid deficiency may result from stopping steroids suddenly or from a failure to increase the dose of steroids during times of emotional or physiological stress.
During times of stress, the body increases cortisol production. If steroids are taken for a long time, the body reduces or stops its production of cortisol, so you need to give additional steroids to help mount the body’s natural stress response.

The case at the start of the module is an example of an Addisonian crisis brought on by high doses of inhaled steroids. It is important that, in patients who you suspect have Addison’s disease, you establish whether the patient has taken steroids in the past year and, if so, by what route and at what dose. The source of steroid use may not always be well defined; there are reports of steroids being present in herbal remedies and in skin lightening creams.

An Addisonian crisis is a medical emergency. It is characterised by nausea, vomiting, abdominal pain, postural hypotension, hyponatraemia, and hyperkalaemia.
You should treat it acutely with intravenous normal saline and systemic steroids (initially intravenous hydrocortisone 100 mg four times a day for at least 24 hours, and until symptoms settle).

Learning bite: short synacthen test

You should ideally perform a short synacthen test in the morning.
Cortisol secretion varies during the day and usually peaks in the early hours of the morning (between 4 am and 8 am), before falling to its lowest level in the evening (between 8 pm and 12 am). Performing the test in the morning makes it easier to interpret.

To perform a short synacthen test:

Take blood for baseline cortisol levels Give 250 mcg tetracosactrin (synthetic ACTH) intramuscularly or intravenously and note the time.
Perform further blood tests for cortisol levels 30 minutes and 60 minutes later (blood samples can be aspirated from a cannula, provided the initial 5 ml of blood is discarded and the cannula is flushed afterwards).


In a normal response, the cortisol level should rise above 550 nmol/l after giving synthetic ACTH.
A cortisol response that is subnormal suggests that there is adrenal or pituitary insufficiency.
If you suspect that a patient has pituitary insufficiency, you should take an ACTH level or perform a long synacthen test.

If you need to give steroids urgently to a patient with suspected Addisonian crisis and you also want to confirm the diagnosis of Addison’s disease, giving hydrocortisone makes it impossible to interpret a subsequent short synacthen test. You can give systemic dexamethasone instead as it has good glucocorticoid action and will not affect the results of the short synacthen test.

Metabolic side effects

Fat redistribution
Steroids cause breakdown of fat stores peripherally, with central redistribution. This results in the typical moon face, buffalo hump, and abdominal striae seen in Cushing’s syndrome. This is one of the most common side effects and has been recorded in 10.5% of patients treated with steroids (compared with 2.6% on placebo, P=0.001).

Osteoporosis

Steroids decrease bone formation by a direct effect on the activity and differentiation of osteoblasts and osteoclasts. This can lead to osteoporosis and an increased risk of fracture. The risk of hip fracture is approximately doubled with steroid use.
Fracture risk is proportional to the steroid dose. For example, the risk of vertebral fracture is increased by about 50% with low dose steroids (less than 2.5 mg prednisolone daily), while higher doses (greater than 7.5 mg prednisolone daily) increase the risk fivefold. Bone mineral density loss is greatest in the first few months of steroid use.

Management of osteoporosis in patients on steroids

You should consider patients aged over 65 years or those with previous fragility fractures to be at high risk of osteoporosis, and you should start them on bone protective treatment. In patients who you intend to treat with steroids for more than three months, you should consider measuring their bone mineral density in order to determine whether bone protective treatment is necessary. This is done using dual energy x ray absorptiometry (DEXA) scanning.

When deciding whether to start bone protective treatment in patients not at high risk of osteoporosis, you should take into account the age and bone mineral density of the patient, since these affect the probability of fracture.
The bisphosphonate drugs are the mainstay of bone protective treatment (alendronate, etidronate, and risedronate are all licensed for glucocorticoid induced osteoporosis).
Parathyroid hormone (PTH) can also be used.


Vitamin D and calcium supplements are given as adjuncts to treatment. To be effective in fracture prevention, you need to give vitamin D in high doses (800 IU daily).
You should always consider other general measures to reduce bone loss such as keeping steroid doses to a minimum, considering routes of administration with minimal systemic absorption, and using steroid sparing agents.

You should also advise all patients about general measures to avoid osteoporosis. These include:
Maintaining good nutrition with an adequate dietary calcium intake.
Regular weight bearing exercises to help maintain bone mineral density.
Avoiding smoking and excess alcohol.

Muscle weakness and wasting

Steroids increase protein breakdown and decrease protein synthesis.
This can cause muscle weakness and wasting, particularly proximal myopathy

Diabetes

Steroids cause decreased uptake and utilisation of glucose and increased gluconeogenesis.
This can lead to hyperglycaemia and an increased risk of developing impaired glucose tolerance or type 2 diabetes mellitus.
In a meta-analysis, diabetes occurred four times more frequently in patients on steroids than in patients on placebo.

Psychiatric effects

Steroids can have a variety of psychiatric effects, which occur more commonly at high doses. They are often associated with euphoria, but can also cause:
Depression
Suicidal ideation
Nightmares
Emotional lability
Irritability
Psychotic symptoms - known as steroid psychosis.


You should use steroids with care in patients with risk factors such as a known psychiatric illness or a family history of psychiatric disorders. If patients suffer psychiatric side effects, you should wean the steroids and stop them completely if possible.

In patients being treated with steroids for a condition with known psychiatric complications, such as cerebral lupus, it can be difficult to determine whether steroids are the cause of the psychiatric symptoms, or whether they may help by suppressing cerebral inflammation. In such patients, you should seek specialist advice from the psychiatric team and the relevant specialist team, for example the rheumatology team in a patient with cerebral lupus.

Peptic ulcers

Steroid therapy is only weakly linked with peptic ulceration and you should not consider this to be an important risk.
Hypertension
Hypertension is more frequent, due to the mineralocorticoid effect of steroids. It is seen in significantly more patients on steroids than on placebo (0.9% verses 0.2% in one meta-analysis).

Avascular necrosis of the femoral head

Avascular necrosis (also called osteonecrosis) most commonly affects the femoral head. It may also affect the head of the humerus, the femoral condyles, the tibial plateau, and the talus.
The mechanism behind avascular necrosis is thought to include vasoconstriction, decreased capillary permeability, and possibly fat embolism and hypercoagulability.

The incidence varies from 0.3% to 25% in different studies and is affected by the dose used and the condition studied (conditions such as renal transplant and systemic lupus erythematosus themselves predispose a patient to develop avascular necrosis).
There is an increased incidence of avascular necrosis with high doses and long courses of steroids, but the condition can also occur after short courses of high dose steroids.

Growth

Steroids are a potent growth suppressor in children. Steroid excess in children is usually caused by steroid treatment. You can greatly reduce growth suppression by giving steroids on alternate days.
Cataracts and glaucoma
Steroid treatment is associated with cataract formation and glaucoma.
Other
Other side effects include raised intracranial pressure and fever.


Cautions when using steroids
Infections
Because of the impaired immune response associated with steroid use, patients with an infection should not have live vaccines.
As viral herpes simplex can be a cause of an acute red eye, you should not prescribe topical steroids in a patient with an acute red eye as this may exacerbate the infection and lead to corneal ulceration.

Dermatology

You should not prescribe topical steroids for patients with a skin disease where you suspect an infective cause, for example in a patient with possible cellulitis.
Giving topical steroids to patients with psoriasis can cause paradoxical worsening of the condition. They should only be used under specialist supervision.

Head injury

A randomised controlled trial of steroid use in head injury showed that giving intravenous methylprednisolone after injury resulted in a slightly increased risk of death. The reason for this increased risk is not known, but you should not use steroids in patients who have a head injury.

Special situations

Pregnancy
Steroids can cross the placenta, but this varies according to the type of steroid. For example, dexamethasone crosses the placenta easily, while 90% of prednisolone is inactivated as it crosses the placenta.
Steroids can be used to help prevent neonatal respiratory distress.
They act by increasing surfactant production and assisting in the maturation of fetal lungs.

A possible side effect of steroid use is the risk of intrauterine growth restriction. Neonatal adrenal suppression from maternal steroid use is usually short lived and is not clinically important.
There is no evidence that steroid use during pregnancy predisposes to congenital abnormalities (including facial clefts).


Women of childbearing age are most likely to be on long term steroids for rheumatoid arthritis, systemic lupus erythematosus, or inflammatory bowel disease.
Rheumatoid arthritis usually remits during pregnancy, but if treatment is needed, prednisolone or hydrocortisone can be used.
In patients with systemic lupus erythematosus, the aim is to establish remission before pregnancy, then continue on the maintenance dose. If there is a flare up of disease, the dose is increased.

If a patient has a flare up of inflammatory bowel disease during pregnancy, prednisolone is used.
If a patient has an acute asthma attack while pregnant there is a risk of maternal and fetal hypoxaemia. Steroids should be used (prednisolone 40 mg to 50 mg for at least five days) as the beneficial anti-inflammatory effects for the mother and fetus far outweigh the possible risks.

Breast feeding

Steroids are excreted in small amounts in breast milk, but maternal doses of up to 60 mg to 80 mg prednisolone per day are unlikely to cause any effects in the infant.

Surgery

You should identify patients on steroids at the preoperative stage. It is important that you identify their steroid dose, length of treatment, and indication for treatment at an early stage and ensure that the anaesthetist is aware of these details. Patients need increased doses of steroids perioperatively due to the increased physiological stress of surgery. The amount of increase necessary depends on the likely physiological stress of the operation and will vary in different centres. For example3

Minor surgery*

Give the usual steroid dose on the morning of surgery or hydrocortisone 25 mg to 50 mg intravenously at induction
Restart the usual steroid therapy postoperatively.

Moderate or major surgery

Give the usual steroid dose on the morning of surgery and hydrocortisone 25 mg to 50 mg intravenously at induction
Follow this with hydrocortisone 25 mg to 50 mg three times a day intravenously for:
24 hours in moderate surgery
48 to 72 hours in major surgery
Restart the usual steroid therapy postoperatively.
*Minor surgery includes procedures involving the superficial structures of the body and does not involve general anaesthesia. Examples are dental procedures, excisions, and aspirations. These procedures have little anticipated physiological stress.


Learning bite
If a patient has an acute illness following surgery, such as postoperative pneumonia, you should increase hydrocortisone either to 50 mg to 100 mg intravenously three times a day or to 20 mg orally four times a day.
Learning bite
You should be aware that, in patients on long term steroids, you may need to increase the steroid dose for any physiological stress. This includes emotional stress as well as trauma or acute illness.

Interactions

Steroids are metabolised in the liver, so are affected by drugs which induce or inhibit liver enzyme systems. For example, drugs such as rifampicin and the antiepileptics carbamazepine and phenytoin induce liver enzymes and increase the metabolism of steroids.

The steroids may therefore have a decreased effect and higher doses may be needed.

Erythromycin inhibits the metabolism of steroids and may therefore result in a greater steroid effect, so you may need to decrease the dose of steroid.

How to start patients on steroids

Discussing the proposed therapy with the patient
When starting a patient on steroids, you must provide information on the intended benefits, the dose, and the length of the course. You must also explain when and how they should stop taking the steroids. This is not always done well; a recent study showed that one in seven patients on steroids were unable to recall the indication for treatment, and only half could recall their doctor’s advice on the likely side effects.

You should discuss the possible adverse effects of treatment with patients and explain the likely side effects. In particular, you should mention the following risks:
Immune suppression and infection
Adrenal suppression and the risks of sudden withdrawal of therapy
Psychiatric disturbance.
If you are giving the steroid in tablet form, you may need to provide the patient with a set number of tablets of smaller doses to make up their daily dose. The patient can then use these smaller doses when decreasing the dose of steroid.


Patient education
When starting a patient on steroids, you must advise them to:
Monitor themselves for side effects
Attend their doctor's surgery for regular reviews of their medication
Change the steroid dose when advised
Not start or stop other drugs without discussing it with their doctor
Never stop their steroids suddenly
Let health professionals know that they are taking steroids:
Patients can wear a medical alert bracelet for this purpose in the event that they are too unwell to give this information.

Steroid cards

You should give the patient written information in the form of a steroid card. Steroid cards were first designed in 1961 and are a patient held record of steroid use. They contain all the relevant information on dosing in one place. The patient or prescribing doctor should update the card whenever there is a change. They also contain warnings about the adverse effects of steroids. Note that the steroid card specifically warns about the danger of steroid use and varicella zoster infection.

Every patient on steroids should be given a steroid card as well as information about the indication, dose, and the duration of treatment being prescribed.
A recent study showed that the majority of patients (67%) did carry their steroid card with them.
The written warnings on the steroid card regarding stopping steroids suddenly and informing health professionals of steroid use up to a year after treatment are very important.

This is a good time to elicit a prior history of varicella zoster (chickenpox) infection. You can advise patients with no previous exposure that they need to avoid contact if possible and to inform their doctor of any suspected exposure

Selecting an appropriate product and dose

Strategies to reduce side effects include using routes of administration other than systemic where possible (for example, topical). You can also keep the total dose of steroids to a minimum by using short courses, weaning the courses as quickly as possible, and using steroid sparing agents.


When to take steroids
Patients should usually take steroids in the morning to reduce adrenal suppression. They may also cause sleep disturbance if taken in the evening

Monitoring therapy

You should monitor patients regularly for any adverse effects or side effects to steroid therapy. You should also monitor the illness for which the steroid was prescribed to see whether the steroid dose needs to be adjusted. This is often done using any available markers of disease activity, for example erythrocyte sedimentation rate (ESR) in rheumatoid arthritis.

Stopping therapy

You should decrease steroid treatment gradually, if treatment has continued for more than three weeks, in order to allow for the adrenals to restart synthesising steroid hormones. This helps to avoid acute adrenal insufficiency. In patients who have been on steroids for more than three weeks, you may need to perform a short synacthen test to assess adrenal function before stopping steroid treatment.

Table: Examples of steroid regimens in different conditions

Condition
Starting therapy
Stopping therapy
Acute asthma
Give 40 mg to 50 mg prednisolone orally daily for at least five days or until recovery. This is in addition to inhaled steroids.27
Stop oral therapy after five days or after recovery and continue inhaled treatment.27
If symptoms persist on stopping, you may wean the steroids by decreasing the dose by 5 mg every week.
Chronic asthma
Give regular inhaled steroids, such as beclometasone dipropionate or budesonide 100 µg to 200 µg, twice daily.27
Review the treatment every three months and, if good control is achieved, consider reducing the dose by up to 50%.8
Aim to maintain therapy at the lowest dose that controls symptoms.
Temporal arteritis
Start prednisolone immediately at 40 mg to 60 mg orally daily.8
Decrease the steroid dose slowly under specialist supervision, while monitoring the ESR.
Space occupying lesions affecting the brain or spinal cord
Give dexamethasone 4 mg intravenously four times a day, and continue at this dose until there is a clinical improvement.
Decrease the dose slowly over five to seven days, while monitoring for any clinical changes.8
• The following table gives some examples of the different steroid doses used in different conditions and regimens for how they are stopped (although local protocols may vary).


Steroid sparing agents
Steroid sparing agents are drugs which affect the underlying inflammatory disease process and thus allow you to decrease the steroid dose. Examples include
methotrexate, azathioprine, and sulfasalazine.

• Information on discharge from hospital

• You should ensure that you provide information to the patient's GP in a timely fashion, including the indication for steroid treatment, the dose, course length, and future plans for dose adjustment, as this will avoid medication errors. You should also make it clear to the GP who they should contact if they have any questions.

It is also important that the patient understands the treatment, duration, and plan for future monitoring. It is best to give this information to patients while they are in hospital in order that they have time to ask any questions before being discharged.
You can also use clinical audit to establish whether best practice is being followed in your place of work.