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CHAPTER11 Endocrinology
Hypoglycaemia and diabetic renaldisease
Hypoglycaemia Suspect if known diabetes on oral/ insulin therapy.
Short history. Warning signs/ symptoms are usually present— sweating,
hunger, tremor. If untreated, may progress to odd/ violent behaviour, ts,
and ultimately coma. On examination, the patient may be sweaty, and have
tachycardia ± i BP. 0 Younger children may present atypically with behavioural changes or headache.
Emergency management Check capillary blood glucose on a blood testing
strip. Suspect hypoglycaemia if <2.5mmol/ L. If conrmed:
• If conscious give simple carbohydrate, e.g. 3 glucose tablets, 100mL of
milk or a sugar- containing soft drink, e.g. Lucozade®, 5 sweets (e.g. Jelly
Babies®), or GlucoGel
• If unable to take oral carbohydrate, give IM glucagon 1mg (children
<25kg— 0.5mg). Takes ≤5min to act but may have poor eect if the patient
is starved or drunk. Alternatively (if available) give IV glucose (adult:50–
250mL of 10% solution in 50mL aliquots; child:2– 5mL/ kg of 10% solution)
• Once the patient has regained consciousness supplement with simple
carbohydrate as for the conscious patient and, as symptoms improve,
give complex carbohydrate, e.g. biscuits
• Repeat glucose testing in <15min then monitor hourly blood sugars
over the next 4h and 4- hourly for the following 24h
• Maintain a high glucose intake for several hours if the patient has a
severe episode of hypoglycaemia due to an oral medication
• Review reasons for the hypoglycaemia
Advice forpatients
• Check blood sugar before driving and every 2h during a long journey
• Carry glucose everywhere and sandwiches on long journeys
• If warning signs of hypoglycaemia occur, stop hazardous activities and
take action
• Wait until fully recovered (usually 745min) before resuming activities
In case ofsevere hypoglycaemia Supply a responsible member of the family
with glucose gel (e.g. GlucoGel®) and glucagon injection— teach him/ her to
use it. Response is short- lived— give oral glucose (e.g. Lucozade®, glucose
tablets, milk) as soon as the patient is conscious.
Recurrent hypoglycaemia If hypoglycaemia occurs in a regular pattern, check
pattern of meals and activity and alter insulin to match needs. If erratic,
consider erratic lifestyle, alcohol, problems with absorption, errors in administration, and/ or gastroparesis. If no obvious cause, consider change in
underlying insulin sensitivity (e.g. age, CKD).
Hypoglycaemia unawareness To restore warning signs adjust insulin/ food intake to stop glucose levels dropping to <4mmol/ L. Consider undetected
night- time hypoglycaemia if HbA1c is lower than expected from blood
sugar diary.
0 Driving is not permitted if hypoglycaemic awareness has been lost or
>1 episode of severe hypoglycaemia while awake in the past 12mo (no
episodes permitted for Group2 licence).
®
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HYPOGLYCAEMIA AND DIABETIC RENALDISEASE
Renaldisease
Urinary tract infections More common in patients with poorly controlled
DM. May exacerbate renal failure and l renal scarring. Consider papillary
necrosis if recurrent (more common in DM).
Diabetic nephropathy Most common cause of end- stage renal failure
in adults starting dialysis in the UK. 25% of people with DM have renal
damage— more common if of Asian or African ethnic origin. Characterized
by proteinuria, i BP, and progressive d in renal function. Classication of
CKD (E p. 411).
Testing fornephropathy Before overt nephropathy occurs, there is a phase
(microalbuminuria) in which the urine contains traces of protein not detected by standard protein dipstick. Presence of i urine albumin levels and/
or iserum creatinine is associated with i CVD risk and i risk of CKD. Check
estimated glomerular ltration rate (eGFR) and urinary albumin:creatinine
ratio (ACR) at least annually if type 1 DM for >5y or type 2 DM of any
duration. Check more frequently as needed if known CKD— E p. 414.
Management ofnephropathy Discuss causes of CKD, risks (progression of
renal disease, i BP, CVD, i mortality), and management:
• Optimize blood glucose control; stop/ avoid nephrotoxic drugs (e.g.
NSAIDs). Consider d dose of other drugs as excretion/ metabolism
may be impaired. 0 Stop metformin if eGFR <30 mL/ min/ 1.73m
• Treat i BP— target <130/ 80mmHg; oer ACE inhibitor/ ARB if CKD
+ DM + ACR ≥3mg/ mmol; oer atorvastatin 20mg nocte for primary
prevention to all patients with DM + CKD (d CVD events and death
by 20%). i dose if <40% d in non- HDL cholesterol and eGFR ≥30mL/
min/ 1.73m2. If eGFR <30mL/ min/ 1.73m2, seek specialist advice
• Oer folic acid/ vitamin B12 supplements if d on laboratory testing/
poor diet
Refer forrenal USS If:
• eGFR of <30 mL/ min/ 1.73m2 (G4/ 5) or accelerated progression of
CKD:sustained d in eGFR of ≥25% and a change in GFR category in
<12mo, or sustained d in eGFR of ≥15mL/ min/ 1.73m2 per year
• Symptoms of urinary tract obstruction
• Family history of polycystic kidney disease and aged >20y
Refer torenal physician If:
• eGFR <30mL/ min/ 1.73m2 or ACR ≥70mg/ mmol or ACR ≥30mg/
mmol + haematuria (unless urgent referral for suspected cancer is
indicated— E p. 420)
• Sustained d in eGFR of ≥25% + change in GFR category or sustained d
in eGFR of ≥15 mL/ min/ 1.73m2 in <12mo
• Poorly controlled BP despite ≥4 antihypertensive drugs
• Known/ suspected rare/ genetic causes of CKD or renal artery stenosis
2
Further information
NICE (2014, updated 2015)Chronic kidney disease in adults. M www.
nice.org.uk/ guidance/ cg182
NICE (2015, updated 2016)Type 1 diabetes in adults:diagnosis and management. M www.nice.org.uk/ guidance/ ng17
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CHAPTER11 Endocrinology
Diabetic complications:cardiovascular
andskin
Cardiovascular complications Diabetic patients are at i risk of MI
(2– 5×), stroke (2– 3×), and peripheral vascular disease. Protective eect of
female sex is lost. Atherosclerotic disease accounts for most of the excess
mortality due to DM. Check arterial risk factors annually:
• Age
• Family history of arterial disease
• Abdominal adiposity
• BP
• Smoking— give smoking cessation advice at every opportunity. Help
patients who want to give up with advice, medication, and support
Blood glucose E p. 317. Target HbA1c:
• <48mmol/ mol if type 1 DM or type 2 DM controlled with diet and
lifestyle alone ± a single drug not associated with hypoglycaemia, e.g.
metformin, a DPP4i, or pioglitazone
• <53mmol/ mol if type 2 DM treated with a single drug associated with
hypoglycaemia or any combination of antidiabetic drugs
Statin E p. 223. Consider statin therapy for:
Primary prevention If:
• >85y (if appropriate)
• 10y CVD risk ≥10%— use a risk calculator that includes type 2 DM in its
risk calculation, e.g. QRisk3
• Type 1 DM + >40y or DM for >10y or established nephropathy or
other CVD risk factors
• eGFR <60 mL/ min/ 1.73 m and/ or albuminuria
Start treatment after optimizing lifestyle intervention, and treatment of
other modiable risk factors/ secondary causes of dyslipidaemia. Start
with high- intensity statin (e.g. atorvastatin 20– 40mg od). i dose as needed
aiming for a 40% d non- HDL cholesterol from baseline.
Secondary prevention If history of CVD— start treatment immediately irrespective of initial cholesterol levels. Use a high intensity statin (e.g.
atorvastatin 80mg od).
BP E p. 218. Any d in average BP d risk of cardiovascular complications.
Measure BP annually if not hypertensive and no renal disease. If BP is higher
than target, consider 24h BP monitoring.
• Type 1 DMN Target BP is ≤135/ 85mmHg unless microalbuminuria/
proteinuria or ≥2 features of the metabolic syndrome (E p. 313) when
treated if BP >130/ 80mmHg
• Type 2 DMN Target BP is <140/ 80mmHg or <130/ 80mmHg if kidney,
eye or cerebrovascular disease
Choice ofantihypertensive
• In all cases, discuss lifestyle modications (E p. 219)
• If i BP, start with an ACE inhibitor. If side eects with ACE inhibitor,
ARB is an alternative. For people of African- Caribbean descent, oer
ACE inhibitor + Ca2+ channel blocker or diuretic. If possibility of
N
• Lipid prole (LDL, HDL
cholesterol, and triglycerides)
• Albumin excretion rate
• Blood glucose control
(a) (b)
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DIABETIC COMPLICATIONS:CARDIOVASCULAR ANDSKIN
becoming pregnant, start with a Ca2+ channel blocker. Monitor BP every
1– 2mo until stable within target. Titrate dose to maximum tolerated
• If BP remains above target add a Ca2+ channel blocker (e.g. amlodipine
5mg od) and/ or a diuretic (e.g. indapamide MR 1.5mg od)
• Fourth line agents include α- blockers, β- blockers, or further diuretic
therapy, e.g. spironolactone 25mg od. Consider referral
Monitoring Monitor BP every 4– 6mo once stable on treatment. Check for
drug side eects (including erectile dysfunction and postural drop).
Antiplatelet therapy Give aspirin or clopidogrel 75mg od to all those
with a prior history of CVD. Do not use for 1° prevention.
Skin changes associated withDM Include:
• Predisposition to infection, e.g. candidiasis, staphylococcal infection
• Pruritus
• Xanthomas
• Diabetic bullae
• Neuropathic and/ or ischaemic ulcers— E p. 330
• Psoriasis— people with psoriasis have a 21% i risk of type 2 DM
• Necrobiosis lipoidica (Figure11.3a)— 50% associated with DM. Small,
dusky red, well- circumscribed nodule(s), usually on the shin. Enlarge
slowly becoming brownish yellow, irregular, and attened/ depressed.
Long- standing lesions may ulcerate. No eective treatment
• Diabetic dermopathy (Figure11.3b)— pigmented scars over shins
• Diabetic cheiroarthropathy— waxy skin- thickening over the dorsum of
the hand with restricted mobility
• Granuloma annulare — asymptomatic dermal nodules— association
with DM is controversial
• Vitiligo (type 1 DM)
• Fat atrophy/ hypertrophy at insulin injection sites
• Acanthosis nigricans
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Figure11.3 Diabetic skin changes:(a) necrobiosis lipoidica and (b)diabetic dermopathy
Figure 11.3 (a) reproduced with permission from New Zealand Dermatological Society
Incorporated, courtesy of Prof Raimo Suhonen. Published online at: www.dermnetnz.org
Further information
NICE (2014, updated 2016)Cardiovascular risk assessment and the modication of blood lipids for the primary and secondary prevention of cardiovascular disease. M www.nice.org.uk/ guidance/ cg181
NICE (2011, updated 2016)Hypertension in adults:diagnosis and management. M www.nice.org.uk/ guidance/ cg127
NICE (2015, updated 2016)Type 1 diabetes in adults:diagnosis and management. M www.nice.org.uk/ guidance/ ng17
NICE (2015, updated 2017)Type 2 diabetes in adults:management. M
www.nice.org.uk/ guidance/ ng28
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CHAPTER11 Endocrinology
Diabetic complications:eye andnerve
Eye disease 71 in 3 people with diabetes have eye problems at the time
of diagnosis.
Blurred vision May occur if control is poor— caused by osmotic changes in
the lens, corrects with normalization of blood sugar. Wait before changing
glasses.
Cataract Juvenile ‘snowake’ cataracts are more common and can develop rapidly (over days). Senile cataracts occur 710y earlier in DM. Surgical
complications from cataract removal are more common due to corneal
epitheliopathy related to DM.
Retinopathy Most common cause of blindness in people of working age in
industrialized countries (risk is i ×20 compared to non- diabetics). 20– 40%
patients with type 2 DM have retinopathy at diagnosis. 20y after diagnosis,
95% with type 1 DM, and 60% with type 2 DM have retinopathy— sightthreatening in 5– 10%.
Pathogenesis of retinopathy Small retinal blood vessels become blocked,
swollen (aneurysms), or leaky causing exudate formation, oedema, or
new vessels. Often asymptomatic until late stages. Laser treatment (photocoagulation) halts progression but does not restore vision. Good diabetic
control slows development of retinopathy. Monitor and treat risk factors—
BP, lipids (hard exudates), smoking.
Classication of retinopathy Various classications predict prognosis. All
are based on whether new vessels are present/ absent and if the macula
is aected:
• Non- proliferative or background retinopathy No new vessels; further
graded by severity (number of microaneurysms)
• Proliferative retinopathy New vessels present; further classied by
location of new vessels (how close to the optic disc) and severity
• Maculopathy Involvement of the macula
0 Retinal screening Digital retinal photography is available throughout the
UK. Ensure patients are referred early for retinal screening (<3mo after
diagnosis) and are screened ≥1×/ y to detect retinopathy before visual
loss occurs. Screening in pregnancy— E p. 806.
Glaucoma and rubeosis iridis DM is not a risk factor for primary glaucoma
but glaucoma is more likely to be found in patients with DM due to regular
eye checks. Rubeosis iridis is the growth of new vessels on the iris in eyes
with advanced retinal ischaemia. This predisposes to a severe form of secondary angle- closure glaucoma.
Retinal detachment More common in patients with proliferative diabetic
retinopathy. Caused by contraction of the vitreous gel in association with
haemorrhage from new vessels and subsequent brosis.
Other eye conditions more common inDM Optic neuropathy (type 2 DM;
due to vascular occlusion); retinal vein occlusion; ocular nerve palsies.
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DIABETIC COMPLICATIONS:EYE ANDNERVE
Refer toophthalmology if E=Emergency; U=Urgent; R=Routine
• Sudden loss of vision— E
• Rubeosis iridis— E
• Pre- retinal or vitreous
haemorrhage— E
• Retinal detachment— E
• New vessel formation— U
• Maculopathy— R
• Pre- proliferative retinopathy— R
• Cataract aecting visual acuity— R
• Unexplained drop in visual acuity— R
Neuropathy Enquire annually about painful and other symptomatic
neuropathy, erectile dysfunction in men, and manifestations of autonomic
neuropathy especially if renal complications or erratic blood glucose control. Optimize blood glucose control.
Symmetrical sensory progressive polyneuropathy Aects 40– 50% of patients
with DM eventually. Starts distally feet > hands. Glove- and- stocking distribution. May be asymptomatic or cause numbness, tingling, or neuropathic
pain. Pain can be depressing and disabling. Be supportive. If simple analgesia
with paracetamol or NSAID is ineective, try neuropathic painkillers (E
p. 188). When pain is controlled, review regularly and consider reducing
dose/ stopping.
Mononeuropathies/ mononeuritis multiplex Especially cranial nerves III and VI
resulting in ocular palsies— E p. 512
Amyotrophy Painful wasting of quadriceps muscles— reversible with improved blood sugar control.
Autonomicneuropathy
• Postural d BP Fall of >20mmHg systolic (or >10mmHg diastolic) BP
on standing. Common especially in the elderly. Review medication and
stop (if possible) drugs that may be contributing. i dietary salt intake
may help. Other treatments include udrocortisone 100– 400 mcg od
(unlicensed— uncomfortable oedema is a common side eect), and
midodrine (2.5– 10mg tds)
• Gastric paresis Treat with an antiemetic which promotes gastric transit,
e.g. domperidone 30mg tds. Use of erythromycin for treatment of
gastroparesis is controversial
• Diabetic diarrhoea Common. Exclude other causes of change in bowel
habit— E p. 378. Otherwise treat with loperamide 2mg prn
• Gustatory sweating Can be treated with antimuscarinics (e.g.
propantheline) but side eects are common. Hyperhidrosis— E p. 575
• Urinary retention E p. 428
• Erectile dysfunction E p. 754
N
Depression Prevalence of depression is i in patients with DM. Screen
for depression as part of the annual diabetic check (E p. 173)
Further information
NICE (2013) Gastroparesis in adults:oral erythromycin. M www.nice.org.
uk/ advice/ esuom13/ chapter/ Key- points- from- the- evidence
NICE (2015, updated 2016)Type 1 diabetes in adults:diagnosis and management. M www.nice.org.uk/ guidance/ ng17
NICE (2015, updated 2017)Type 2 diabetes in adults:management.
Mwww.nice.org.uk/ guidance/ ng28
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CHAPTER11 Endocrinology
The diabeticfoot
Foot problems are common in diabetes. Diabetic foot ulcers precede >80%
of amputations and DM is the most common cause of non- traumatic limb
amputation. 5- year mortality is 770% after an amputation. Foot problems
result from:
• Peripheral neuropathy l d foot sensation (Table 11.3) and
• Peripheral vascular disease l pain and predisposition to ulceration
(Table 11.3)
0 Patients with diabetes may have coexisting peripheral neuropathy and
peripheral vascular disease.
Information about footcare
• Self- care and self- monitoring:
• Daily examination of the feet for problems— colour change; swelling;
breaks in the skin; numbness
• Footwear— importance of well- tting shoes and hosiery
• Hygiene (daily washing and careful drying) and nail care
• Dangers associated with procedures, e.g. corn/ verruca removal
• Wound care
• Methods to help self- monitoring, e.g. mirrors if d mobility
• When to seek advice from a health professional— if any colour change,
swelling, breaks in the skin or numbness, or if self- monitoring is not
possible (e.g. due to mobility problems)
• For patients at moderate/ high risk or with ulcers, additionally advise no
barefoot walking and that, due to d sensation, extra care and attention
is needed, particularly with footwear
• If skin lesions, advise patients to seek help if any change in the lesion, if
i swelling, pain, odour, colour change or systemic symptoms
Riskfactors
• Age >70y
• Plantar callus
• Neuropathy
• Long DM duration
The diabetic foot check Part of the annual diabetic review.
History
• Foot problems since last review
• Visual or mobility problems aecting self- care of feet
• Self- care behaviours and knowledge of foot care
• History of numbness, tingling, or burning— may be worse at night
Table11.3 Clinical features ofneuropathic and vascular foot ulcers
Neuropathic Vascular
Warm foot
Bounding pulses, normal ABPI
Located at pressure points
Painless
Clearly dened or ‘punched out’
Surrounded by callus
• Peripheral vascular disease
• Previous ulceration or
amputation
• Social deprivation/ isolation
Cool foot
Absent pulses, d ABPI (0 may be normal
or i due to calcication of vessels)
Located at extremities (e.g. between toes)
Painful
Less clearly delineated
• Foot deformity
• Poor footwear
• Poor vision
• Smoking
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THE DIABETICFOOT
Table11.4 Classication offoot risk
Foot risk Features
Low risk No risk factors except callus alone
Moderate risk Deformity or neuropathy or non- critical limb ischaemia
High risk • Previous ulceration or amputation or
• On renal replacement therapy or
• Neuropathy and non- critical limb ischaemia together or
• Neuropathy in combination with callus and/ or deformity or
• Non- critical limb ischaemia in combination with callus and/ or
deformity
Active diabetic
foot problem
• Skin:ulceration or spreading infection or
• Vascular:critical limb ischaemia or gangrene or
• Joint:suspicion of an acute Charcot arthropathy, or an
unexplained hot, red, swollen foot ± pain
Examination
• Foot shape, deformity, joint rigidity, and shoes
• Skin condition— fragility, cracking, oedema, callus, ulceration, sweating,
presence of hair
• Foot and ankle pulses ± ABPI
• Sensitivity to 10g monolament
Management
General points Optimize diabetic control and risk factors for vascular disease (including smoking cessation); review drug therapy— stop β- blockers
if peripheral vascular disease; educate about foot care.
Specic management Classication— Table 11.4.
• Low risk Annual foot assessments. Education about foot care and risk
of progression to moderate/ high risk
• Moderate/ high risk Refer to the foot protection service to be seen in
<4wk if high risk and <8wk if moderate risk. Reassess feet every 3– 6mo
if moderate risk; every 1– 2mo if high risk or more frequently if concern
• Active diabetic foot problem If limb/ life- threatening condition
(Box11.1), admit as a same- day emergency; otherwise, refer for
assessment in <1 working day to the multidisciplinary foot care service
• Box 11.1 Limb- or life- threatening foot changes
requiring immediate hospitaladmission
• Ulceration + fever/ sepsis
• Ulceration + limb ischaemia
• Clinical concern about deep soft tissue infection/ osteomyelitis
• Gangrene
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Charcot osteoarthropathy (Charcot’s joint) Neuropathic foot
damaged because of trauma 2° to loss of pain sensation. Manage as for
‘Active diabetic foot problem’.
Further information
NICE (2015, updated 2016)Diabetic foot problems:prevention and management. M www.nice.org.uk/ guidance/ ng19
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CHAPTER11 Endocrinology
Lumps inthe thyroid gland andgoitres
Faced with a lump in the pre- tracheal region of the neck, ask:
• Is it in the thyroid (moves up and down on swallowing)?
• Is it a solitary lump or more generalized (a goitre)?
• Is the patient thyrotoxic, euthyroid, or hypothyroid?
• Is the trachea being compressed (patient is breathless or stridor)?
• Urgent management ofthyroidlumps
Refer to be seen immediately bya thyroid surgeon If symptoms of tracheal
compression including stridor due to thyroid swelling.
Refer urgently toa thyroid surgeonN (to be seen in <2wk) If any age and
unexplained thyroid lump.
Solitary thyroid nodule Investigate all solitary nodules. Check TFTs
and refer urgently to exclude thyroid cancer. Dierential diagnosis:
• Benign (790%):cyst, adenoma, discrete nodule in a nodular goitre
• Malignant (710%):primary— thyroid adenocarcinoma, lymphoma,
medullary carcinoma; secondary— direct spread from local tumour,
metastatic spread from breast, colon/ rectum, kidney, lung, lymphoma
Carcinoma ofthe thyroid Primary tumours:
• Papillary adenocarcinoma (60%) Typical age:10– 40y. ♀ > ♂. Low-
grade malignancy. Rarely fatal. Spreads to local LNs and/ or lung.
Sensitive to TSH. Treated with thyroidectomy then lifelong thyroxine
• Follicular carcinoma (25%) Typical age range:40– 60y. ♀ > ♂. May
arise in a pre- existing multinodular goitre. Spreads via bloodstream.
Bony secondaries are common. Treatment is with surgery and thyroxine
suppression therapy and/ or radioactive iodine
• Lymphoma (5%) Occurs at any age. Involvement of the thyroid may be
1° or 2°. Associated with Hashimoto’s thyroiditis. Staged/ treated as for
lymphoma elsewhere (E p. 656). Prognosis is good
• Anaplastic carcinoma (rare) Typical age:50– 60y. ♀ > ♂. Aggressive
tumour. Grows rapidly and inltrates tissues of the neck. Tracheal
compression is common. Metastasizes locally to LNs and via lymphatics.
Poor response to treatment
• Medullary carcinoma (rare) Occurs at any age. ♀=♂. Familial
incidence; associated with adenomas elsewhere. Often secretes
calcitonin (used as tumour marker). Spreads to local LNs. Treated by
excision then chemotherapy ± radiotherapy
Thyroid adenoma Benign tumours of the thyroid. 4 types classied ac-
cording to histological appearance— papillary, follicular, embryonal, Hürthle
cell. Afew produce thyroxine l thyrotoxicosis. Haemorrhage is rare and
results in rapid i in size. Refer for conrmation of diagnosis ± surgery.
Goitre There are 4 main types of goitre— Table 11.5.
Thyroid cyst Usually degenerative part of a nodular goitre though true
cysts do occur. Rapid enlargement/ pain may be caused by haemorrhage
into a cyst. Refer for conrmation of diagnosis.
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LUMPS INTHE THYROID GLAND ANDGOITRES
Table11.5 Types ofgoitre— presentation and management
Type Features Management
Congenital Enlarged thyroid gland
Physiological Occurs at puberty, during
Nodular Benign enlargement of the
present at birth ± hypo- or
hyperthyroidism
pregnancy, and in conditions
of iodine deciency
thyroid gland with areas of
hyperplasia and involution
Hypothyroid babies are treated
with thyroxine; if there is tracheal
compression or hyperthyroidism,
treatment is surgical
Usually requires no treatment. If
iodine decient, treat with iodine
supplements
No treatment is necessary unless:
• Thyrotoxic
• Compression of the neck
structures l dyspnoea or
dysphagia
• Worried by cosmetic appearance
• Focal i in size or recurrent
laryngeal nerve palsy
(hoarseness)— suggests malignant
change— refer for urgent review
(in <2wk)
If treatment is needed, refer
to surgery or endocrinology
depending on symptoms
Toxic Grave’s disease:smooth
Inammatory Hashimoto’s thyroiditis:
thyroid enlargement +
thyrotoxicosis
♀>♂. Antibodies to thyroid
tissue are produced. Initially
goitre and thyrotoxicosis.
Later myxoedema
De Quervain’s thyroiditis:
inammation due to viral
infection— usually Coxsackie
virus. Acutely swollen, tender
thyroid gland and transient
thyrotoxicosis often preceded
by sore throat/ malaise.
Settles spontaneously
Riedel’s thyroiditis:rare.
Thyroid becomes
inltrated by scar tissue l
hypothyroidism ± recurrent
laryngeal nerve palsy ± stridor
See management of
hyperthyroidism— E p. 334
In all cases refer to endocrinology
for conrmation of diagnosis and
management guidance
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Further information
NICE (2015, updated 2017)Suspected cancer:recognition and referral. M
www.nice.org.uk/ guidance/ ng12
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