Dear Colleague,
Following the RITAs please bear the following in mind:
1. Carefully anonymise all patient details from anything you include in your
portfolio/log book.
2. Including individual clinic letters of all the patients you have seen in
your portfolio is not appropriate. It does not demonstrate learning. Only
inlcude a clinic letter if it demonstrates a learning outcome as specified
in the curriculum and specifically referr to it.
3. I have included examples, advice and a structure for reflective writing
with this e-mail.
4. Please provide evidence of learning the core Diabetes & Endocrine Topics
as outlined in an attachment to this e-mail.
5. Carefully follow Mini-CEX and MSF instructions and further guidance is
provided in an attachment to this e-mail.
6. Minimum requirements for the RITAs in May 2007 are:
* Thorough portfolio documentation
* Include Case based Discussions
* Include reflective accounts
* 4 Mini-CEXs since last RITA
* MSF from current unit
7. When completing competency sections in log book use Consultant level as
terminal outcome, i.e. if you put down 3 this implies you have achieved
autonomous competence in this area to Consultant level. Putting 3s down in
year 1 does not go down too well at the RITA.
8. Bear in my mind that the following audits stand out on your CV and the
RITA panel will be encouraged to see such audits:
* Process based audits
* Audits based on NICE or other important national/international
guidelines
* Audits that lead to service change/development
9. For next years RITA make sure that the requirements in your RITA report
from 2006 are fully achieved.
This e-mail will be posted on the ENDODIABOLOGY website as well.
Kindest of regards,
Shaz.
---------------------------------
CORE DIABETES AND ENDOCRINE TOPICS
It is essential to provide evidence of competence in your portfolio/log book of the following core topics:
Core Endocrine Topics
Mx of pt with functioning pituitary tumour
Hyponatraemia case
Case of delayed puberty
“Funny” thyroid function tests
Thyroid Eye disease case
Case of Thyroid cancer
Mx of thyroid disease in pregnancy
Patient with gonadal failure
Patient with suspected osteoporoses/osteomalacia
Ix and Mx of MEN
Core Diabetes Topics
Newly Dx pt with Type 1 Diabetes
Pt with poor glycaemic control
Pregnancy in diabetes
Microvascular diabetic complications
Macrovascular complications in Diabetes
Newly Dx pt with Type 2 diabetes
Surgical Mx in Diabetic pts
Insulin initiation
Hypoglycaemic problems
Monogenic diabetes
Metabolic emergencies
Alternative insulin therapies
New drugs for diabetes
Obesity in diabetes
Cultural/ethnic issues relating to diabetes
Evidence of learning the Core Topics
Min-CEX
Case based Discussions
- You may utilise the Foundation Programme Structure until specialty specific structures are published
Reflective (case) writing
Published case reports
- Peer reviewed journals
- Posters-published as abstracts
Presentations
- Include programme/certificate of attendance
DO NOT FORGET SUPERVISORS SIGNATURE
The majority of the topics should have been covered in your portfolio come your PYA and a minimum of 6 new topics should have been covered for each RITA
Shaz Wahid June 2006
----------------------------------
Documenting Mini-CEX and MSF assessments
PLEASE FOLLOW THE EXACT INSTRUCTIONS PROVIDED FOR MINI-CEX AND MSF ASSESSMENTS ON THE JCHMT WEBSITE
Until carbonated coloured pads are distributed to trainees please follow these instructions:
For each Mini-CEX once completed
1 copy to be retained by SpR
1 copy to be retained by Supervisor
1 copy to be made available for RITA panel
This will be retained by TPD
Mini-CEX summaries to be available for RITA panel and will be retained by TPD
MSF summaries only are to be included in SpRs portfolio
1 copy should be made available for RITA panel and will be retained by TPD
Shaz Wahid
June 2006
------------------------------------
REFLECTIVE WRITING
Helen Richardson, December 2003
Adapted from Effective learning number 11: Writing reflectively. Bob Price. Nursing Standard. 2003. Vol.17, Iss. 43;pg. 32A
Reflection is an important skill for those in clinical practice. It encourages clinicians to learn from events, and so can lead to continual improvement, as well as personal development for those who use it.
The process of reflective writing allows themes to develop, as the writer thinks in a focussed and analytical way about an event. Lessons which have been learned can be identified and recorded, as can learning needs which require action in the future.
There are four ‘stages’ in reflective writing, as described below.
Descriptions and perceptions
Clinical practice is made up of episodes that we remember and recall, based on both facts and perceptions. It is important that you are clear in your own mind, when you are writing a purely factual description, in contrast to when you are recording a perception.
This is because:
It is important to be able to describe events objectively.
It is also important to understand how your perception of events determines your interpretation of them. By understanding how you, personally, perceive events can be a great trigger for learning.
You may wish to persuade others of the reasonableness of your perceptions. You can only do this after you have learnt to recognise the difference between descriptions and perceptions.
Both descriptions and perceptual statements are acceptable in reflective writing, provided you use them with clear intent. If you wish to record a perception, use words that link behaviour to meanings, motives, feelings or beliefs. For example, 'The respiratory rate was dropping, which suggested a deterioration in the patient's condition. I informed the consultant.' If you wish to claim a description, record only that which could be seen. The respiratory rate was dropping and I informed the consultant.'
Explaining feelings
In reflective writing it is perfectly reasonable to record feelings.
Your reflections should:
Help the reader link feelings to specific events or behaviours.
Appreciate what you learnt about the feeling.
Avoid appeals to 'common sense'.
Acknowledge and respect the feelings of others.
Note that the word 'I' can be central to reflective writing, (unlike other types of academic writing.)
Sharing reasoning
Your writing will need to include an account of reasoning. You may wish to make bullet points of the factors that you took into account when making a decision. However, bullet points do not make arguments by themselves. You can show your reasoning by:
Acknowledging alternative choices or perspectives.
Describing the weight you gave to certain influences or information.
Acknowledging that reasoning could be different in other circumstances.
Drawing conclusions
Reflective writing is different from essay writing - it is not assumed that at the end of the work you will have solved all the problems or reached a neat conclusion. In practice we work constantly with unfinished business. One of the merits of reflective writing is that we can cope better with the uncertainties of practice because we set down the reflections on paper. So what sort of conclusions should you be able to reach as part of your reflective writing? The following are some suggestions:
What you think you understand about an episode.
What you believe about an episode.
What you feel about an episode.
What competing perspectives or accounts exist.
What has yet to be found out.
What learning needs you have identified.
How you might handle similar situations differently in the future.
You can express this sort of information by using terms that emphasise incremental analysis. That is, you have not completely closed the door on your ideas about such matters.
Conclusion
While there are different reflective frameworks, the thing that makes reflective writing stand out is the way it helps you to demonstrate your thoughts, perceptions and feelings to the reader. It should also help you to
identify things you have learned from an experience
identify remaining learning needs
formulate alternative strategies
While reflective writing may not involve pages of text, it does involve considerable thought. The more you plan what you want to say, and how you want to say it, the stronger your reflective writing will be.
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REFLECTIVE PRACTICE: LEARNING FROM EXPERIENCE
NAME: DATE:
An “experience” might be a particularly interesting/difficult example of your clinical practice or professional development. For example, attending a diabetic renal clinic, attendance at a Diabetes Clinical Network meeting, attending a local patient group meeting, teaching medical students or responding to a complaint.
WHAT WAS THE AIM OF THE EVENT?
WHAT WENT WELL AND WHAT WERE THE CONTRIBUTING FACTORS?
WHAT WENT LESS WELL AND WHAT WERE THE CONTRIBUTING FACTORS?
WHAT DID YOU LEARN FROM THIS EXPERIENCE: YOUR “KEY LEARNING POINTS”?
WHAT WILL YOU DO DIFFERENTLY IN PRACTICE AS A RESULT?
WHAT ADDITIONAL SKILLS OR KNOWLEDGE DO YOU NEED TO STRENGTHEN YOUR PRACTICE IN THIS AREA?
------------------------------------
Experience in diabetes care of renal inpatient and combined pancreatic renal transplant recipients in Freeman hospital
(1st Oct 2004- 30th Sept 2005)
The Specialist Registrars did 1 in 3 rota covering inpatients in Freeman. We
typically get 6- 12 new referrals weekly out of which at least 2-3 are from the renal and transplant ward. Other referrals are from of cardiothoracic wards and liver unit.
The problems encountered included
1. Patients in chronic renal failure with poor glycaemic control
2. Recurrent hypoglycaemic episodes in renal failure patients
3. Post renal transplant patients with difficult to control diabetes
4. Combined pancreatic renal transplant- Assessment before transplant and post transplant assessment.
The chronic renal failure patient are certainly one of the most challenging group in terms of glycaemic control. The reasons are many: Almost all of them have longstanding diabetes with poor quality of life secondary to visual impairment, cardiac disease, autonomic and peripheral neuropathy, and cerebrovascular disease in addition to the debility due to uraemia. In addition they are on multiple drugs with issues of side effects and compliance. They are prone for wide fluctuations in glycaemic control and most have poor hypo awareness thus putting them at a high risk with insulin treatment.
Treatment of hyperglyacemia induced by high dose steroids in post transplant patients is another difficult scenario. Use of high dose methyl prednisolone causes sudden worsening of glycaemic control and there is yet a clear plan on how much to put the insulin up although at least 20–30 % increase is used in practice. These patients sometimes unfortunately end up on a GI (Glucose insulin) regime, which still doesn’t control the sugars, as the patient’s postprandial hyperglycaemia is not well covered.
The hyperglyacemic effect of many anti-rejection drugs are well known. It is difficult to predict the increase in insulin requirement needed in these patients who will then have to be managed by close monitoring of sugars and adjustments of insulin.
The appropriate subcutaneous insulin regimes in the acute setting is also an interesting problem to solve. These patients are best managed at least temporarily by a basal bolus regime with short acting analogues with meals. The regime may be modified to give multiple short acting and twice a day, long acting in those requiring high doses especially those insulin resistant due to steroids.
Those being initiated on insulin treatment are another difficult group. There are several social issues because of frailty of patients, visual problems and tendency of hypos. The input of specialist nurses are invaluable. It is important to teach the hypo management thoroughly and go into detail of support at home once they go home.
Combined pancreatic renal transplant
2005 has seen the CPK transplant programme take off in a big way. We have been involved in the care of 7 CPK transplant patients during this period. I have personally been fully involved in the care of 3 patients while an inpatient (under supervision of Prof. ******* and Dr. *****). All three were assessed by me on arrival. The assessments included looking for any new macrovascular or microvascular complications i.e. new proliferative retinopathy, active foot ulcers which are contraindications for transplantation. Also autonomic neuropathy (gastroparesis) could have impact in the postoperative period. Their insulin regime is reviewed and GI commenced ~8 hours before transplant.
Postoperative period while in ITU is covered with a strict insulin infusion, which is in line with the Van de Berghe regime (NEJM 2001). We reviewed these patients regularly in ITU to monitor BM and decide whether transplant has been successful. Out of three patients I saw, 1 patient had a failed pancreatic graft needing further surgery and later went back on to insulin regime. Although postoperative period was stormy, the other 2 did remarkably well and had good graft function.
XYZ
DOB
IDDM- 32 years
End stage renal failure secondary to diabetic nephropathy
CAPD- October 2003
? retinopathy, ? peripheral neuropathy
severe hypo with unawareness
Cadaveric renal transplant- left kidney- 22nd May
Methyl prednisolone- day 1
Steroids, MMF- commenced
On GI infusion since 21st.
21/5- BM- 14, 18.7, 20.5,19.7
22/5- 18, 12.2, 11.3, 9.1, 6.3
23/5- 6.7
24/5- change to s/c insulin- humalog 12 tds, glargine 22
25/5- change to s/c insulin- humalog 16 tds, glargine 32
Points to note:
Immediate management of hyperglycaemia in renal transplant patients
Immunosuppressive/steroids use and effect on blood glucose control
ZYX
DOB
Combined pancreatic-renal transplant March 2005
Type 1 diabetes, End stage renal failure- on CAPD
Severe hypo with unawareness
Pre-proliferative retinopathy prior to transplant
Peripheral neuropathy, Diabetic foot ulcers
Reviewed 6 weeks later-
Insulin free,BM- 6-7 fasting
Eye- worsening of DR- new vessels, Feet- no ulcers
Inpatient:-
Assessment of inpatient
Protocol for pre and post transplant management of glucose control
---------------------------------
SAMPLE REFLECTIVE WRITING – RENAL CLINICS
I attended 2 general renal clinics and 2 diabetes renal clinics (Drs.****** & Dr. ********) at Freeman Hospital.
The objectives of attending these clinics were identified as:
Diagnosis of diabetic nephropathy
Management of diabetic nephropathy
Some experience of how the predialysis patients are managed.
Management of hypertension in renal disease
Some experience in investigation and management of non-diabetic renal disease.
Some important points I learned from these clinics were:
Hypertension treatment is the single most important factor that has an impact on renal function. Every attempt should be made to get this sorted.
Multiple agents of different action at a small dose are more useful than maximum dose of a single agent. Impact on BP lowering doesn’t increase proportionately with increase in dose of drugs like ACE inhibitor. Postural hypotension is an important side effect to look for.
Frequent follow-up is essential to achieve target levels.
Management of anaemia is important as this has been proven to delay worsening of renal function- Parenteral iron (if Ferritin is <200), and if not responding Erythropoetin therapy.
Address CVD risk factors aggressively as MI/strokes are the most important reasons for morbidity/mortality
Glycaemic control is most often poor but improving glycaemic control may not be easy as most patients will already be on large doses of insulin and have problems with hypos.
Renal function is monitored by creatinine in clinic and a GFR is calculated by MDRD calculator. This helps in monitoring these patients renal function.
This led to reading of renal NSF and NICE guideline which makes clear recommendations on management o f CKD.
I saw patients with nondiabetic renal disease –Glomerulonephritis, cystic renal disease, renal artery stenosis, polycyctic renal disease. In a clinic setting, once the cause of this has been investigated, the monitoring would be based on serum creatinine and protein-creatinine ratio. A decision when and how to investigate further especially with renal biopsy would depend on the rate of progression of disease.
NICE GUIDELINES & Renal NSF
Current recommendations into early management of diabetic nephropathy is based on NICE guidelines published in 2002. Diabetes patients are screened for Urine ACR or urine albumin concentration.
1.If microalbuminuria is present, then investigate for nondiabetic cause for renal disease in the absence of retinopathy.
Targets and interventions recommended in diabetic renal disease are as follows: HbA1c= 6.5-7.5%, BP=135/75, commence ACE inhibitor, address other cardiovascular risk factors.
2. Creatinine > 150 refer to specialist service or nephrology.
Part 1 Renal NSF looked at care of patients with established renal failure and at preparation for renal replacement therapy.
Part 2 Renal NSF published in February 2005
1. Focuses on chronic kidney disease. The emphasis is on identification and management in primary care to minimise its consequences.
2. Optimal management of acute renal failure & minimise risk of developing CKD
3. Looks also at care of people with ERF (Established renal failure) at their end of their lives.
Requirement : That patient becomes informed partners in their care.
CKD
Long term progressive
At its mildest , undetectable
Main risk- Cardiovascular disease
Minorotiy-Develop ERF.
Stages
Stage 1: Normal or raised GFR but other evidence of kidney damage
Stage 2: slight reduction in GFR (90 – 60 ml/m/1.73m2)
Stage 3: moderate reduction in GFR (59 – 30 ml/m/1.73m2)
Stage 4: severe reduction in GFR (29 – 15 ml/m/1.73m2)
Stage 5: ERF (<15 ml/m/1.73m2)
GFR 60 – 90 on its own doesn’t indicate CKD
Older adults will have slight decrease in GFR normally
Only a minority progress
Address CVD risk
Timely referral
3 things to look out for as kidney function deteriorates:
Anemia
Ca/ph imbalance
Poor growth/development
ARF
Important cause s- Infections, med, post op, hypotension
50 %- 90 day mortality
development of ERF- 7- 40 % in intensive care setting; 0-17 % outside
Quality requirement laid down by Renal NSF (markers of good practice)
1. Reduce number of patients developing CKD-
a. Target high risk groups- diabetes, hypertension, heart failure, urinary tract obstruction, family h/o
b. 24 hr urine collection unnecessary, spot urine, morning sample reliable
2. Reduce progression of CKD-
a. have a care plan
b. Risk factor management
c. Anemia treatment
d. Referral to specialist care when appropriate
3. Minimise impact of ARF
a. Timely identification and referral
b. Specialist management
4. End of life care
a. Appropriate care plan and multispecialist team involvement
b. Involvement of patient and family
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SAMPLE REFLECTIVE WRITING – Paediatric Endocrine Clinics, RVI
I identified the primary objectives of attending paediatric endocrine clinics as
1. Understanding about short stature and investigating the causes
2. Investigating and managing delayed puberty
3. Learn about the use of growth hormone in paediatric age group and
4. Management of childhood obesity.
I attended 4 clinics at the paediatric outpatient department at RVI and joined Dr. ******** and his team. There were several interesting problems that I saw during those clinics, to name a few, cases of congenital hypothyroidism, obesity with insulin resistance, primary adrenal failure, isolated growth hormone deficiency, congenital adrenal hyperplasia, Prader-Willi syndrome, constitutional growth delay, delayed puberty. There was a discussion of problems while the patients were being seen along with a demonstration of clinical signs when appropriate. There was also a detailed case discussion at the end of clinics lasting upto 2 hours.
Cases discussed :
1. A 5 year old boy with isolated growth hormone deficiency: This boy presented with height less than - 3 SD and truncal obesity. The age of presentation can vary from first few months of life to early teenage years and depends on severity of GH deficiency and the mutation. As either isolated GH deficiency and multiple hormone deficiency can present with short stature it is important to investigate all pituitary hormones. The diagnosis was suggested by low GH and IGF-1 and confirmed with 2 provocative tests (in this case, glucagon and arginine stimulation tests). He was commenced on GH and has shown good response. I thought it was important to understand how these patients are monitored in clinic. They are usually seen at 3- 4 months interval to assess compliance to treatment, any problems with injection technique, and any possible side effects. Questions should always be asked to rule out development of any other pituitary hormone deficiencies. Height and weight are the most important parameters used to assess response. The psychosocial aspect should not be forgotten and adequate support for the family in important. The role of specialist nurse is vital in this regard. Another important aspect is management of transition from childhood to adulthood. Traditionally, GH was given till linear growth is complete. NICE published guidance on use of GH in children in 2002 and in adults in 2003. Indications and how and when to use it were stated in these documents. The recommendation is that GH should be stopped at completion of linear growth (<2 cm/year) and then GH status reassessed. GH at adult doses should be restarted only if it meets the criteria for severe GH deficiency and then continued till adult bone mass has been achieved. The decision to further continue should be made by an Endocrinologist with special expertise and based on the following criteria: severe GH deficiency, QoL impaired and optimally replaced by other pituitary hormones if required.
2. A 7 year old boy with primary adrenal failure: Presented with tiredness,
failure to thrive, gastrointestinal symptoms and recurrent infections. He was hyperpigmented, hypotensive. He failed a short synacthen test and had a raised ACTH. The etiology was unclear there was no evidence of TB, no evidence of disorders of steroidogenesis, adrenal leucodystrophy or autoimmune polyglandular syndrome. There was also no evidence of other autoimmune disorders like Graves or type 1 diabetes. He has been on steroids for a while but came back to clinic being unwell for a few weeks, and with difficulty to eat. Issues were compliance to steroids (which his mother confirmed as good), oesophageal candidiasis (probably steroid related), needs to rule out TB, consider polyglandular autoimmune syndromes. The type and dose of glucocorticoids were also discussed. Hydrocortisone 2.5 mg tds was used in this boy. This is suggested by most authorities as likely to mimic the normal diurnal rhythm. However, long acting glucocorticoids administered as a single dose is another option. Main concerns are long-term risk of BMD but evidence is lacking on the superiority of one regimen over the other in the long-term.
3. 18 year old girl with obesity: Obesity is a major health concern at present in children and is a marker of insulin resistance which in later life lead on to Diabetes, PCOS and cardiovascular disease. However, rarely, genetic mutations can lead to severe obesity in children. This girl is the only member of the family who is obese and was found to have partial MC4 defect. She has problems with irregular periods, had some weight loss on sibutramine and is currently on Metformin. As the mutation involved is known MC4 receptor agonist could be a potential treatment option.
4. A 9 year old girl with idiopathic gonadotrophin dependent precocious puberty- Had breast development before the age of 8. The gonadotrophin dependent precocious puberty is a diagnosis of exclusion but account for 90% cases in girls. Think of secondary causes namely congenital anomalies, brain neoplasms, cysts, post infection, post trauma and post-cranial radiotherapy. Long acting gonadotrophin releasing hormone analogues are used nowadays. Initially it is given with cyproterone to prevent the stimulatory effect. However the effect of this on final height is dependent on the age of onset of treatment. Treatment is stopped usually when the child reaches an age where puberty is acceptable. No evidence that longer treatment improves final height. Then there is a growth spurt and most girls menstruate within a year of stopping treatment. Normal fertility documented but PCOS more common.
5. A 13 year old boy, refugee from Afghanistan, first seen by Community Paediatric team because of learning difficulties
Referred to Endocrine service in Dec 2003 with gynaecomastia, microphallus, glandular hypospadias and cryptorchidism.
Presenting history (from his father): 4th of 8 children, normal term delivery (? low birth weight,? neonatal problems)
Early months of life were normal, developed meningitis at the age of 1 year which left him with hemiparesis and speech problems, delayed developmental milestones. started walking only at 4-5 years of age, age 5- had surgery for left undescended testis, came to UK 2 years ago as a refugee.
At present, can say only 10-15 words, understands language, nonverbal communication. can walk but has difficulty running, no difficulty in eating, fully continent, noticed enlargement of breasts over the last few years, has small penis
Family history: Born out of a consanginous marriage (parents are first cousins); 7 siblings- 4 sisters (aged 18,14,8,5) ,3 brothers aged 16,3,1
Clinical examination:
Height between 75th to 91st centile, head circumference-3rd centile
Weight- 50th centile
Normotensive
Left ptosis, Other cranial nerves – normal, vision- normal,
Residual hemiparesis
Painless bilateral gynaecomastia, no discharge
Small penis, stretched length (2.5- 3cm).
Left testicle high in scrotal sac (6ml), right in inguinal region
Hypospadiasis with urethera opening at the base of the glans.
Other systems- CVS: no cardiac murmurs, Abdomen: No other palpable masses
Investigations:
Karytoype XY
LH=24.4, FSH=14.2, Testosterone=2.4
17 hydroxyprogesterone-17 (raised)
Homocysteine- normal range, baseline pituitary function tests- normal
MRI pituitary- NAD, ECHO= NAD
Ultrasound pelvis= no abnormality detected
Summary/key points
Gynaecomastia in a young man with cryptorchidism, small phallus and mild hypospadias. Biochemical evidence of primary gonadal failure with low testosterone.
? Testosterone Biosynthetic defect
Urine steroid profile:
1. Raised pregnanetriol- major metabolite of 17 hydroxyprogesterone
2. Mutation of 17 ,20 lyase activity than 17 hydroxylase activity of CYP 17.
3. 17- 20 lyase activity not completely abolished as androgen metabolites are still present.
4. Corticosterone/cortisol metabolites – ratio rises after synacthen suggesting that block exaggerated by synacthen.
Urinary steroid profile of siblings:
A
F
20 year old
Normal profile
T
M
17 year old
Normal
FA
F
15 year old
Incomplete 17-hydroxylase deficiency
Ta
M
13 year old
Incomplete 17-hydroxylase deficiency
Ma
F
10 year old
Normal
R
F
8 year old
Normal
Mu
M
6 year old
Corticosterone meatbolites raised ?cause
Mo
M
2 year old
Normal
FA (14)
No periods as yet
Stage 4 breast development
No androgenic
No axillary hair
No pubic hair
Short synacthen test- flat response
Molecular analysis – abnormal 17 alpha hydroxylase gene
Management
1.Mastectomy
2.Orchidopexy
3.Androgen replacement
Questions
Why Normotensive?
Why gynaecomastia?
How best to manage affected sister?
This case was presented and discussed at length with Dr. ********. I hope to present this again at the joint endocrine meeting at RVI/FRH in near future.
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SAMPLE REFLECTIVE WRITING – SPECIALITY FOOT CLINICS
My aim of attending the speciality foot clinic at diabetes centre, NGH, Newcastle (supervised by Dr. *******) was to gain specific experience in the following:
1. The functioning of multidisciplinary team in diabetic foot care
2. Assessment of complicated diabetes related foot problems
3. Learn about aspects of foot ulcer management and the appropriateness of antibiotic use in foot ulcer
4. Diagnosis and treatment of osteomyelitis and charcots arthropathy
5. Learn about the referral criteria to vascular surgeons and orthopaedics
6. Gain some insight into use of casts and newer modalities of treatment of ulcers
Personal experience obtained
The clinics I attended had a mixture of type 1 and type 2 patients with varying foot problems ranging from nonhealing ischaemic and neuropathic ulcers, osteomyelitis, to Charcots arthropathy. I felt that one of the major advantages of a specialty foot clinic was the presence of personnel with differing experiences namely, podatrists, doctors, specialist nurses who could deal with not only the foot itself but other factors like glucose control, concomitant medical problems, diabetes education and even social issues. This helped identify factors which might be either causing or aggravating foot problems. Typically a patient is referred to the clinic either from the community or from the hospital services. On arrival to the clinic relevant history is obtained followed by a proper assessment of vascular supply, nerve supply, shape of foot and condition of the skin. Any infection or inflammation is ruled out by clinical examination and foot wear is assessed to look for risk factors for ulceration. The doctor and specialist nurse then review medications, look for other complications of diabetes, assess glycaemic control and advice on management of diabetes as well as foot problems. Investigations and treatment would depend on the foot problem in question.
Examples of problems dealt with in the clinic:
Case 1
A 62 year old gentleman with type 2 diabetes, peripheral vascular disease, neuropathy , previous amputations of toes in both foot, CCF, AF on warfarin. Presented with a deep ulcer in the right metatarsal head in December 2002. Repeated course of antibiotics were used to treat enterococcus and anaerobes. Finally he developed multiple antibiotic resistance. Currently ulcer is not showing signs of infection and he is off antibiotics. Regular dressings and repeated swabs are being performed. Another issue is his lack of care of his foot – doesn’t rest the foot enough, uses improper foot wear and returns to the clinic with soiled dressings. Total contact cast was not possible because of leg oedema due to his CCF. A modified plaster cast slipper caused more ulcers around the edge possibly because of over use. Ulcer itself has overgrowing granulation tissue and slough but debridment is a problem because of anticoagulation. So far a below or above knee amputation has been prevented but an argument is that amputation might be more beneficial for him in the long run than a non healing ulcer which restricts mobility and affects quality of life.
Case 2
A 76 year old lady with insulin treated type 2 diabetes, recurrent DVT, diabetic retinopathy, registered partially sighted and left Charcots arthropathy. She developed an abscess in the Charcots foot needing incision and drainage. The ensuing wound was deep and probing to the bone. It was clear that pressure relief was paramount for any chance ulcer healing. She was intolerant to most antibiotics which made treatment of infection difficult. Anticoagulation and interaction of antibiotics with warfarin was another issue. The patient finally agreed to a total contact cast to sidestep the pressure area. This kept her mobile and started to make a difference to the ulcer healing. It should be noted that the care of the good leg is important in somebody like her who is on a plaster cast (which rubs against the other foot) and has neuropathy and poor vision. The ulcer itself started healing well although use of platelet derived growth factor may need to be considered once free of infection, as the ulcer is deep.
Case 3
A 32 year old rather unfortunate lady with poorly controlled long standing type 1 diabetes, peripheral neuropathy, autonomic neuropathy, Charcots arthropathy, laser treated proliferative retinopathy. Developed MRSA osteomyelitis of right foot leading on to septicaemia and ITU care last year. She was left with a large necrotic heel ulcer which needed muscle flap and skin graft. When seen in foot clinic she had an intact skin flap in the right foot overlying the previous ulcer with some superficial ulcers in the edges of graft, evidence of burn out charcots in the same foot with midfoot deformity. The heel itself was deformed making it difficult to find a suitable foot wear. Her glycaemic control remains poor with poor hypo awareness and she has visual impairment. The challenges in her are finding an appropriate foot wear in the short term so that the small ulcers don’t worsen and new ones don’t develop. In the longer term foot reconstruction surgery might need to be considered.
Case 4
A 30 year old lady whom I first met at Freeman hospital at the transplant ward when she came in for combined kidney pancreas transplant. She had long standing type 1 diabetes, recurrent debilitating hypoglycaemia, proliferative retinopathy and end stage renal failure. She had recurrent foot ulceration secondary to neuropathy and ischemia and deformed foot secondary to loss of arch. The transplant was delayed because of active foot ulcers which finally healed with regular input from foot clinic. She had a stormy post operative course after her transplant but pulled through with meaningful graft function (free of insulin and good renal function). Later, when she reviewed in the foot clinic she was free of foot ulcer although her neuropathy and PVD still puts her under risk of pressure ulcers.
Documents read as part of the learning process:
1. Hospital guidelines on diabetes care
2. NICE guidelines
3. NSF standards of care: intervention details and standard of care
4. Royal college of GPs foot problems in people with type2 diabetes guidelines (2000)
Conclusions:
Attending the speciality foot clinics helped me understand the importance of a multidisciplinary team approach in managing the foot problems. I learned to give correct advice to the patients with high risk feet, make a proper assessment of the foot investigate and treat pathologies accordingly. Identifying emergency foot problems and making appropriate referral to vascular surgeons is another aspect that I have gained experience in by attending these clinics. I hope to gain more expertise in writing up business plans and setting up of these types of speciality clinics.
