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An audit looking at how many patients are with thyroid dysfunction

4156 words (17 pages) Essay in Psychology

5/12/16 Psychology Reference this

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What is the function of thyroid gland and thyroid hormones

The thyroid gland is located in the anterior part of the neck, attached to the thyroid cartilage. It consists of two lobes, approximately 5 cm each, that lie either side of the trachea joined in the middle by an isthmus. The thyroid gland is responsible for the production of three thyroid hormones: Calcitonin (involved with calcium homeostasis), Thyroxine (T4) and Triiodothyronine (T3). Everyday, approximately 100 ¿½g of T3 and T4 are secreted 90% of which are in the form T4. Most of T4 is later converted to T3 in the liver and Kidneys. T3 is 10 times more active than T4. [1] The thyroid hormones are responsible for the control of basal metabolic rate.

Expand?

How is Thyroid hormone regulated

The functional unit of the thyroid is the follicle. A spherical arrangement of secretory epithelial cells around a protein rich colloid. It is at this cell-colloid boundary that thyroid hormones are formed by iodination of thyroglobulin formed from tyrosine.[1] The follicular cells are involved in active absorption of iodine from the plasma which is required for thyroglobulin synthesis. The formed thyroid hormone is stored in the colloid until its secretion is triggered by thyroid stimulating hormone from the anterior pituitary which triggers the degradation of thyroglobulin in the follicular cells to release thyroid hormone.

Thyroid hormone secretion is under the control of the hypothalamic-pituitary axis. The hypothalamus releases Thyrotrophin Releasing Hormone (TRH) which stimulates the anterior pituitary to secrete Thyroid Stimulating Hormone (TSH). The TSH reaches the thyroid where it binds to the TSH receptors on the surface of the follicular cell, stimulating it to produce and release thyroid hormones. The homeostasis of thyroid hormone concentration is maintained by a negative feedback loop whereby increased concentration of thyroid hormone inhibits Thyroid Stimulating Hormone release from the anterior pituitary by decreasing the affinity for TRH. This leads to a decrease in TSH causing reduced amount of thyroid hormone to be released by the thyroid gland. This feedback loop enables us to monitor patients on thyroid hormone replacement therapy (such as Levothyroxine) by measuring TSH levels. If for instance the prescribed dose is insufficient, it would lead to inadequate inhibition of the pituitary gland and a raised serum TSH level. The reverse would occur with levothyroxine excess.

() This cannot be done in patients with secondary hypothyroidism. So what do we do then?

Common pathologies

Thyroid disease is the second most common endocrine disorder after diabetes.

¿½ Hypothyroidism

Hypothyroidism is defined as an underactive thyroid gland leading to decreased levels of T3 and T4. The annual incidence of hypothyroidism in the UK is 4 per 1000 in women and 0.6 per 1000 in men.[3] Symptomatic hypothyroidism is known as myxodema. Hypothyroidism is categorised into primary and secondary. Primary hypothyroidism results from disease processes affecting the thyroid gland itself, slowly decreasing thyroid function and thyroid hormone production. Onset of symptoms is therefore gradual, developing over months or even years. Secondary hypothyroidism is relatively uncommon. Secondary hypothyroidism develops when the pituitary is unable to produce enough TSH to induce enough T3 and T4 production from the thyroid gland. The causes of secondary hypothyroidism can include a pituitary tumour.

Patients with hypothyroidism could present with a number of signs and symptoms including:

¿½ Tiredness

¿½ Somnolence

¿½ Slow cognition

¿½ Cold Intolerance

¿½ Depression

¿½ Bradycardia

¿½ Weight gain

¿½ Calf stiffness

¿½ Menstrual disturbance

¿½ Carpal tunnel syndrome

¿½ Hearing impairment

¿½ Dry, thin and pale skin

¿½ Puffiness below the eyes

¿½ Bradycardia

The most common cause of primary hypothyroidism in the UK is autoimmune thyroiditis. In Hashimoto¿½s thyroiditis autoantibodies are produced against thyroglobulin. This leads to inflammation of the thyroid gland as it is infiltrated by lymphocytes causing goitre formation. Hashimoto¿½s thyroiditis is remarkable in this respect that it initially causes hyperthyroidism as inflammation of the thyroid gland releases stored thyroxine. Once this released thyroid hormone is metabolised the patient progresses to normal and then a hypothyroid state. [1]

Other notable causes of hypothyroidism include:[4]

¿½ Iatrogenic: Radioiodine ablation or thyroidectomy as a treatment for hyperthyroidism

¿½ Thyroiditis: Subacute (de Quervain¿½s) thyroiditis

¿½ Drugs: Lithium, Amiodarone, thalidomide, rifampicin and sutinib as well as drugs used in the treatment of hyperthyroidism

¿½ Iodine deficiency: common in some developing countries but very rare in the western world

At the opposite end of the spectrum lies Hyperthyroidism where there is increased Free T4 and a reduced level of TSH and has the opposite effect on the body than the one noticed in hypothyroidism e.g. tachycardia, heat intolerance etc. Hyperthyroidism is not covered further as this audit focuses on hypothyroidism.

Diagnosis and treatment

Symptoms of hypothyroidism are quite non-specific and can commonly occur with other medical conditions not related to the thyroid. Diagnosis of hypothyroidism therefore should not be made on clinical symptoms alone and it is essential to test thyroid function biochemically. This is done by measuring Thyroid Stimulating Hormone and Free Thyroxine (T4) in blood. The normal reference range for TSH is 0.4 ¿½ 4.0 mU/Litre.[4] A TSH level within the normal reference range has over a 99% predicted value to rule out primary hypothyroidism or hyperthyroidism.[5]

In hypothyroidism the patient would have a high Thyroid Stimulating Hormone level, with or without a low Thyroxine level. Depending on thyroid function tests hypothyroidism is further divided into:

a) Overt hypothyroidism: patients with a high Thyroid Stimulating hormone level and a Low serum free Thyroxine (T4)

b) Subclinical hypothyroidism: Patients with a high Thyroid Stimulating Hormone but a normal Thyroxine (T4) level

Treatment depends on whether the patient has overt or subclinical hypothyroidism. Patients with overt hypothyroidism should be treated with Levothyroxine to render them ¿½euthyroid¿½.[5] According to NHS statistics 12 million Levothyroxine prescriptions were issued during 2006.[6] The goal of the treatment is to reduce the TSH back to within the reference range. The dose of Levothyroxine is usually titrated up from 25-50 ¿½g daily however a recent trial has shown that this is unnecessary for most patients.[7] The study recommended that patients with no cardiac symptoms should be started on the full dose of 1.6 ¿½g/kg.

The following figure illustrates the algorithm for treatment of -pregnant adults with primary hypothyroidism:[4]

Algorithm for management of non-pregnant adults with primary hypothyroidism [4]

It is very important to monitor levothyroxine therapy as over or under prescription can be dangerous. Thyroid Stimulating Hormone (TSH) is the key method of monitoring levothyroxine therapy in patients with primary hypothyroidism. Unlike the thyroid function tests used to diagnose thyroid disease, free T3 and T4 levels are not very useful in monitoring treatment as their levels are influenced by the prescribed dosage of thyroid replacement hormone and are not accurate indicators of the individual¿½s requirement. TSH without T3 and T4 is also a cheaper test to carry out in General Practice. Current guidelines state that patients should have their Thyroid Stimulating Hormone level tested eight to twelve weeks after starting levothyroxine.[4] The dose can later be fine tuned accordingly to get the TSH level in the lower half of the reference range.[5] Besides monitoring TSH levels, an assessment of the patient¿½s symptoms should also be made as some younger patients may need higher doses to relieve their symptoms in which case it is acceptable to have the TSH between 0.1-0.4 mU/Litre. The Quality and Outomes Framework (QOF) guidance suggests that all Patients on long term thyroid hormone replacement therapy should have their TSH levels tested yearly to make sure their replacement dose remains optimal.[8]

Audit

1. Reason for audit move it to the top to include the rest of the study

Despite the yearly TSH tests, studies have shown that a considerable number of hypothyroid patients managed in primary care have TSH levels outside of the reference range. Okosieme et al reported that in 2009 data collected from 11 GP practices showed that 37.2% of the 1037 patients on the hypothyroidism register were inadequately managed.[9]

When we take into account the high prevalence of hypothyroidism (9.3% in women and 1.3% in men)[3] the results of the Okosieme et al study suggests that the total number of patients with suboptimal thyroid hormone replacement is significantly large.

Imperfect thyroid hormone replacement could have damaging repercussions for health. It may adversely affect blood pressure, body weight and lipid profile.

Since the basal metabolic rate of the body is controlled by thyroid hormones it is perhaps not surprising that a decrease in thyroid hormone levels leads to a decrease in metabolic rate and thus can cause weight gain. Even in euthyroid subjects there is a negative correlation between free T4 and Body Mass Index (BMI).[10] This suggests that even a small under-prescription of thyroid hormones could, over a period of time, lead to obesity.

Reduced Thyroxine levels also cause a dyslipidemia characterised by increased Low Density Lipoproteins (LDL) and a decrease in High Density Lipoproteins (HDL) with normal or slightly raised cholesterol levels.[11] Such a lipid profile is associated with a higher risk of atherosclerosis.

The thyroid hormones also seem to have a role in blood pressure homeostasis as hypothyroid patients recorded a higher systolic and diastolic blood pressure after stopping thyroid replacement therapy.[12] Thus inadequate replacement may cause hypertension which, together with the dyslipidemia described above adds to the risk of atherosclerosis and its subsequent cardiovascular complications.

Conversely, excessive thyroid hormone replacement has its own perils, having enhanced risk of atrial fibrillation, osteoporosis and fractures linked to it.

Excessive thyroid hormone increases the risk of developing atrial fibrillation especially in older patients. Studies have shown that a low TSH level in patients over 60 years old have a threefold higher risk of developing atrial fibrillation.[13] Patients over treated with levothyroxine also show increased loss of bone mineral putting them at increased risk of osteoporosis.[14] Subsequent studies have shown that patients with a suppressed TSH i.e. = 0.03 mU/Litre also had an increased risk of fractures however this was not observed in patients with low but unsuppressed TSH (0.04 ¿½ 0.4 mU/Litre).[15]

This highlights the need for maintaining optimal thyroid hormone replacement in primary hypothyroid patients in the General Practice setting to reduce the above mentioned risk factors. The 11 GP practices used by Okosieme et al showed that there is significant room for improvement as one third of the patient population on levothyroxine had TSH levels outside the reference range.[0.11]

Thus this is a worthwhile area for audit to establish current standards of care in our practice, Dr Dean & Partners, Heald Green Health Centre. Since this audit has not been carried out before in the practice it would give an idea of how well the practice manages patients on thyroid hormone replacement therapy. The suggestions for improvement would be beneficial to the patients of the practice and might also help with obtaining QOF points.

This audit would also be beneficial to me personally introducing me to the concept of audit cycles and giving me the opportunity to conduct my very first audit. It would also help me get a better understanding of management of hypothyroid patients which is the second most common endocrine disease in the UK after diabetes mellitus.

2. Criteria to be measured

Serum Thyroid Stimulating Hormone is used as the gold standard for biochemically diagnosing hypothyroidism and monitoring thyroid hormone replacement therapy.[4] The reference range indicating adequate replacement is usually around 0.4 ¿½ 4.0 mU/Litre.[4, 9] However this figure slightly varies according to local guidelines. For this I have chosen to use TSH between 0.1 ¿½ 4.0 mU/Litre as a reference range for adequate thyroid hormone replacement as this is the reference range used by the local Primary Care Trust (Stepping Hill Hospital) and the practice.

Patients with primary hypothyroidism on thyroid hormone replacement therapy should have a TSH level between 0.1 ¿½ 4.0 mU/Litre.

3. Setting standards

For setting the standard I have found that there are no specific guidelines stating what proportion of patients should be achieving the above mentioned criteria. There are no NICE guidelines for the treatment of hypothyroidism. The QOF guidance states that patients should have their TSH levels tested yearly but it does not state the standard of care required.

Having discussed this with GP at the practice I have decided that a theoretically ideal standard i.e. 100% of patients meeting the above criteria would be very impractical in theory from a resources perspective. Given the fact that suboptimal thyroid hormone replacement could be harmful, it is nonetheless important to achieve a high standard of care. Therefore I have decided on an optimum standard:

90% of patients with primary hypothyroidism on thyroid hormone replacement therapy should have a TSH level between 0.1 ¿½ 4.0 mU/Litre.

4. Preparation & planning

Before starting the audit I had a discussion with the GP tutor about worthwhile areas for audit. As I had never conducted an audit before he explained the audit cycle. As thyroid dysfunction was an area of interest for me I suggested undertaking this audit. The GP tutor agreed that this would be a useful area for audit and advised to me to review the literature to find out if it would be an appropriate audit from a clinical point of view and was an area where practice could be improved. After preliminary reading clinical reviews I formulated a step by step template of the things I felt should be covered and got the GP tutor¿½s approval to go ahead.

The data was collected with the help of the GP tutor. As the practice keeps electronic records of all patients, EMIS Population manger search function. Using the search function we identified all patients who had been prescribed thyroid hormone replacement medication for the past 12 months. We then identified patients who in the past 12 months had had their TSH levels tested. We then selected patients who had a TSH =0.1 mU/Litre and TSH =4. Subtracting the number of patients which meet the TSH search parameters from the total number of patients on thyroid hormone replacement would give us the number of patients who were outside the reference range of TSH.

5. Initial data collection

Criterion Number of Patients taking thyroid hormone replacement medication (n) Number of Patients with TSH levels within reference range Standard (%)

Patients with primary hypothyroidism on thyroid replacement therapy should have a TSH level between 0.1 ¿½ 4.0 mU/Litre. 206 167/206 (81%) 90%

Discussion

Results: what they are. How close to the standard. Are they good enough? (no, didn¿½t meet the standards). Why didn¿½t they meet the standard?

Merge results discussion with limitations discussion

The data collected shows that the current practice is 9% below the standard set. The standard required i.e. 90% of patients with primary hypothyroidism on thyroid hormone replacement therapy should have a TSH level between 0.1 ¿½ 4.0 mU/Litre. However this was the case with only 167 patients (81%). This means that 39 patients (19%) did not meet the standard set.

There could be several reasons why the results did not meet the standards set. One factor influencing TSH levels is the use of medicines which interact with thyroid function. Due to the limitations of the software used in data collection (as discussed below) we were unable to exclude patients who were on medication known to interact with thyroid function such as Amiodarone, Lithium, etc. Amiodarone, a fairly commonly prescribed drug to prevent arrhythmias, can cause deranged thyroid function as it contains iodine (37mg of iodine in 100mg of Amiodarone). This can cause a severe iodine overload and can lead to hypothyroidism as well as thyrotoxicosis.[0.16] Inclusion of such patients would bring the percentage down unfairly because management of such patients is a lot more complex and the TSH levels are not always a good indication of the adequacy of their thyroid hormone dosage. Patients with hypothyroidism due to Amiodarone are monitored by their Free T4 levels instead of TSH. [0.16]

Another factor which could have contributed to the high number of patients with TSH levels outside those defined in the criteria is the possibility that patients with abnormal TSH levels often don¿½t get their levothyroxine dose optimised. A study published in 1995 reported that at one GP practice in Suffolk 71% of patients with abnormal TSH levels did not have their medication dosage change as a result.[17]

If patients do not have their thyroid hormone replacement optimised as a result of abnormal TSH not only does it defeat the purpose of carrying out yearly TSH tests, it also means that these patients would continue to have an abnormal TSH when tested again. Currently we do not have the data to find out how many of the patients in our practice with abnormal TSH had not had their dose changed after a previous abnormal TSH in an attempt to bring it within the reference range specified in the criteria.

Ranging from poor patient compliance to the way the data has been collected

Lack of dose adjustment after abnormal TSH

The way results were collected. Limitations of software used. Limitations of the results collected ie things missed: how many patients actually had test done in the last 12 months (QOF points). How many were over and how many were under prescribed.

This audit has limitations. The data was collected from electronic records using the EMIS Population Manager. The limited search algorithms of the software meant that we couldn¿½t distinguish patients with a TSH below the reference range from those above it. All we were able to obtain was a single figure of how many people were within the reference range.

Due to the limitations of the EMIS Population Manager software we were also unable to test how many patients with hypothyroidism had actually had their TSH levels tested in the past 12 months as stated in the QOF guidance ¿½ 2004.[8] Thyroid Function Tests are done for a large number of patients whose symptoms are actually caused by a non-thyroid illness. Due to this reason we could not search for people who had their thyroid function tested in the past 12 months as that data would have included a lot of non-hypothyroid patients. Instead we had to search for patients who had been prescribed levothyroxine therapy in the past 12 months. And then further narrow the search parameters TSH levels in the past 12 months to obtain the data. This meant that the people who have not had their thyroid functions tested in the past 12 months were excluded from our data. The positive aspect of only testing people within the last 12 months is that the data reflects current level of care.

The data collection software shows patients as being within the normal TSH range if they have had at least one TSH test within the normal range during the last 12 months. If the patient has been started on levothyroxine therapy recently their TSH levels wouldn¿½t have had enough time to return to normal. However this is likely to be statistically insignificant.

The way to get round these limitations of the EMIS Population Manager would have been to study the clinical notes of all patients who were prescribed levothyroxine in the past year. By looking at the notes we would be able to exclude patients who are unsuitable for the purpose of this audit i.e. those patients in whom the TSH level is not a valid indicator of thyroid hormone requirement e.g. those on Amiodarone or lithium or patients with secondary hypothyroidism. Looking at the notes would also allow us to check the number of patients who had not had their TSH levels tested in the past year. Reading through the notes would also allow us to obtain more information such as age gender etc which might be helpful in indentifying some of the factors responsible for suboptimal thyroid hormone replacement. However reading the notes of over 206 patients would have taken a considerable amount of time. Since this was my first audit I decided to avoid gathering qualitative data and decided that the using electronic records would be sufficient for the purposes of this audit.

Changes to practice to hit the target. Tietable to implement that change and when to re-audit? Practicality, why change? Positives and negatives of changing.

There are a few approaches which could potentially be taken to improve the standard of care.

In order to improve the standard of care to meet the goal of 90% all patients on the hypothyroidism register should have yearly or six monthly blood tests to measure their TSH levels. all patients with abnormal TSH levels should be invited for an appointment with the GP and should be considered for a change in their current dosage. This would be a good opportunity to assess why their TSH levels are abnormal and check that the patient is adhering to the prescribed treatment regimen. If the dose remains unchanged the reason should be recorded in the notes so that the information is available for the second cycle of the audit.

Doing this will allow us to make sure that patients are kept at the optimum dose of levothyroxine to reduce the risks associated with under or over prescription. Seeing patients like this would however increase the workload placed on the surgery and its resources. However by talking the patients as and when they have their TSH levels tested the strain on the resources would be spread out over a year. Since the current audit identified 39 patients with abnormal TSH levels, this would mean an extra 3-4 patient appointments per month over the period of a 12 months. This should be discussed at the doctors¿½ meeting. Twelve months after the implementation of the change of practice a second data collection should be done to complete the audit cycle and evaluate the impact, if any, the change in practice has had on the management of hypothyroid patients.

Write to the patients to invite them to come in for a dose adjustment?

Consider collecting better data by reading the notes. That would take too long.

Consider specialist referral if symptoms persist.

What have I learned: 1 about the condition, 2 about auditing.

Conducting this audit has given me the chance to take an in-depth look at all aspects of hypothyroidism which has been an area of interest for me for some time. In the course of researching for the audit I have been able to review various guidelines, clinical reviews and other journal articles. Not only has that improved my understanding of the management of thyroid disease in primary care immensely. It has given me a sense of how a condition is followed through in general practice from first presentation to treatment to long term management.

I have also realised that management of chronic conditions such as hypothyroidism is an ongoing process as the patients¿½ condition and requirements change continuously for instance if their body mass index changes significantly their thyroid hormone requirements would also change and the dose would have to be altered. Also if a patient is planning on or has become pregnant they would need to be referred to specialist endocrinologists. I have been able to review the evidence which forms the basis of current practice. Researching this topic by reading clinical reviews has made me realise the advantages of using original literature and how much beneficial it can be in achieving a comprehensive understanding of a topic.

Being involved in a general practice standard-based audit has enabled me to learn about the role and significance of audits in healthcare. I have become familiar with the audit cycle and its different steps. Having conducted an audit myself, I can see the important role audits have in measuring and improving practice. It is a systematic way of monitoring standards of care and is very useful in facilitating change of practice through an evidence based approach. It has also allowed me to learn how to quickly and efficiently find relevant papers using such resources as ISI Web of science and medline.

Conclusion and summary

Timetable change re-audit

6. Description of change

7. Data collection (2)

8. conclusions

be almost impossible to achieve due to variables like poor patient compliance or use of interactive medications e.g. Amiodarone and Lithium. It would also be vastly impractical from a reasources point of view to aim for a 100% standard.

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