CASE WRITE UP Department of Surgery Cyberjaya University College of Medical Sciences
MULTINODULAR GOITRE Name: Harmeet Kaur a/p Daleep Singh Matric No.: 0908-1235 Year/Group: Year 3/Group 5 Supervisor: Mr Ahmed Awil Adam Core Component
Given Marks
History Physical Examination Investigation Provisional Diagnosis/Differential Diagnosis Discussion: Identify problems, management and progress of patient References
1. HISTORY
1.1 Demographic Data
1
Patient Name: Maslina Bt Ahmad Age: 66 years old Sex: Female Origin: Batu Pahat, Johor Date of admission: 25th December 2011 Date of Clerking: 30th December 2011 Place of clerking: Putrajaya Hospital
1.2 History of Presenting Illness
Chief complain: Madam Maslina presented to the Emergency Department following an episode of shortness of breath which lasted about half an hour on 25th December 2011 Madam Maslina’s history dates back to year 2000 where she first noticed a neck swelling on both sides of her neck. It was relatively small sized, with the right side being bigger than the left side. It was not painful and felt like multiple, small, seed like swellings (in her words) on her neck. It was soft and mobile too. There was no discharge or ulcers at the site of swelling and neither was it itchy or associated with any eczema. She noticed the swelling a few months after she had delivered her 4th child. At that time, she also had lethargy and had lost weight, about 5kg in the span of 3 months. She also had headache on and off. Her food intake was the same though, with no increase or decrease in appetite. She did not eat much seafood either. She had no heat or cold intolerance, difficulty in breathing or dysphagia at that time either. She did not notice any overt sweating or tremors as well. There was also no change in voice, diarrhea, palpitations or swelling anywhere else on her body. Her systemic review was unremarkable at that time.
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Due to her neck swelling, she went to Batu Pahat hospital at that time (year 2000) to see the doctor and was told that she most probably had a problem with her thyroid gland but nothing was done and no medications were given either. The swelling gradually increased in size over the years but she did not think that it was serious as she didn’t notice it becoming bigger until year 2009 where she was scheduled to do a surgery (thyroidectomy) in Batu Pahat hospital but the surgery was postponed as her thyroid hormone levels were high. Hence she was discharged with medications to stabilize her thyroid hormone level and was asked to come back again after a year and a half. She defaulted her follow up though. Now, in December 2012, she presented to the ED of Batu Pahat hospital with SOB which occurred at rest and lasted till she got to the ED, which was about half an hour. It had a sudden onset and was associated with syncopy which occurred while she was on the way to the hospital. The syncopy lasted about a few minutes though and she gained consciousness in the ED. She even had fever 1-2 days prior to admission which was intermittent in nature. She did not take any medications to relieve her fever though. She had no prior episodes of dyspnea, orthopnea or paroxysmal nocturnal dyspnea before this. She did not have any leg swelling or chest pain and did not have dysphagia prior to admission either. Her neck swelling was now much bigger in size, about 15cm in length. She had lost more weight over the years, gradually though but did not remember the amount. Systemic review was unremarkable. In Batu Pahat hospital, they took a long time to intubate her as it was difficult to do so and referred her to Putrajaya Hospital on that day itself.
1.3 Past Medical History
She was diagnosed to have hypertension in 2009 during her routine checkup. She does not have any other chronic illnesses though. She had not gone for any surgery before this either. 1.4 Family History
3
Her parents have passed away. Her father had asthma while he was alive while her mother had hyperthyroidism, hypertension and diabetes mellitus. She has 4 siblings whose ages range from 40-50 something years old. Her brother has hypertension and diabetes mellitus while her sister has rheumatoid arthritis and diabetes mellitus. Her other younger sister has hyperthyroidism too. She is married with 5 children whose ages range from 5-20 years old. They are all healthy. Hence, the ones with similar problems as her are her younger sister and mother.
1.5 Drug History
She used to take medications but only from year 2009. She takes a medication to reduce her thyroid hormone levels and is on anti-hypertensives. She does not remember the name of her drugs though. She is not compliant to her anti-hypertensives though as she takes them when she has headaches only. She is not allergic to any drugs and has not taken any traditional medicine previously.
1.6 Social History
She does not smoke nor consumes alcohol. She lives with her children and is generally well looked after. She is married with 5 children and her husband is still working as a contractor. She is a caterer and has a food business of her own.
2. PHYSICAL EXAMINATION
4
2.1 General Inspection
Post-op
On general inspection, she was conscious and was sitting up comfortably on her bed and was using a nasal prong. She was not in respiratory distress and was alert. She was orientated to time and space. She also had a branula inserted on the dorsal part of her hand and she was on CBD. Her palms were slightly moist. There was no clubbing or any other nail changes. There was slight tremor though. She was not pale or jaundiced and there was no central or peripheral cyanosis. She was slightly dehydrated though. Her face is not edematous.
2.2 Vital signs
Upon admission:
BP: 158/94 mm/Hg Heart rate: 103/min RR: 35/min
Post – op
5
BP: 130/85 Heart rate: 84/min RR: 16/min
2.3 Neck examination
Pre-op
Upon inspection of her neck, there is a swelling on both sides of the neck, with the right side being bigger than the left. It extends just above the suprasternal notch and lies deep to the sternoclaidomastoid muscles. The skin over the swelling is not red; there are no scars or eczema. There are slightly dilated veins visible on either side of the swelling. There are no sinuses or discharge from the swelling. There are no visible pulsations either. The swelling moved upward with swallowing. Upon palpation, the swelling was of normal temperature and was not hot. The right lobe measured 20x25 cm while the left lobe was 15x10cm. The swelling was not tender, firm and mobile. It’s surface was nodular and the tracheal rings were not palpable at the suprasternal notch. There were no thrills noted on the superior poles of the thyroid gland. Carotid pulse could be palpated, and it was strong and present. Upon percussion over the manubrium of sternum, dullness was noted. Upon auscultation of the superior poles of the gland, no bruits were noted. There were no lymph node enlargements.
Post-op
6
Post operatively, she has a fresh scar on her neck with visible stitches and no dressing. It is a horizontal scar measuring about 10cm. There is a catheter inserted at the operative area to drain blood from it. Her voice is now hoarse and she can barely whisper out words.
2.4 Systemic review:
Eyes: slight lid retraction and infrequent blinking pre operatively, no exopthalmos and she can converge her eyes, no ptosis Cardiovascular system: unremarkable Respiratory system: unremarkable Neurological system: unremarkable GI system: unremarkable Pulses: all present and strong Legs: No pretebial myxedema, no pitting edema
3. DIAGNOSES
3.1 Provisional Diagnosis
Multinodular goiter causing airway obstruction
3.2 Differential Diagnosis 7
1. Thyroid carcinoma 2. Graves’ disease 3. Lymphadenopathy
4. INVESTIGATIONS
4.1 Pre-Op (25th December 2011)
1. Full Blood Count
Component
Values
Normal Range
Total White Blood Cells
13.8
(4-11) x 109 cells
Red Blood cells
4.1
(3.8-5.5) x 1012 /L
Heamoglobin
12.2
(12-18) g/dL
Heamatocrit
35.5
(34-50) %
MCV
85.2
(83-100) fL
MCH
29.3
(27-32) pg
MCHC
34.4
(32-37) g/dL
RDW
14.7
(10-15) %
Platelet count
146
(150-400) x 109/L
Neutrophils
12.7
(2.5-7.5) x 109/L
Lymphocytes
0.5
(1.0-3.5) x 109/L
Monocytes
0.6
(0.2-0.8) x 109/L 8
Eosinophils
0
(0.04-0.4) x 109/L
Basophils
0
(0.1.0.1) x 109/L
2. Renal Profile
Component
Values
Normal Range
BUN
7.5
(2.5-6.4) mmol/L
Na
141.6
(132-144) mmol/L
K
4.40
(3.5-4.5) mmol/L
Cl
111.4
(95-105 ) mmol/L
Creatinine
80
(53-115) μmol/L
3. Coagulation Profile
Component
Value
Normal Range
PT
12.7
12.4-14.7
INR
1.146
<2.01
aPTT
23.7
31.7-41.1
4. Thyroid Function Test 9
Component
Value
Normal Range
T3
4.99
(3.1-7.7) pmol/L
T4
12.16
(9-23) pmol/L
TSH
0.129
(0.4-3.0) mU/L
5. Minerals
Component
Value
Normal Range
Phosphate
1.33
(0.8-1.5) mmol/l
Magnesium
1.06
(0.75-1.0) mmol/l
Calcium
2.09
(2.12-2.62) mmol/l
6. Ct scan – retrosternal expansion to level T1-T2
4.2 Post op (28th December 2011)
1. Full Blood Count 10
Component
Values
Normal Range
Total White Blood Cells
15.7
(4-11) x 109 cells
Red Blood cells
3.34
(3.8-5.5) x 1012 /L
Heamoglobin
9.74
(12-18) g/dL
Heamatocrit
26.7
(34-50) %
MCV
79.9
(83-100) fL
MCH
29.2
(27-32) pg
MCHC
36.6
(32-37) g/dL
Platelet count
122
(150-400) x 109/L
Neutrophils
13.9
(2.5-7.5) x 109/L
Lymphocytes
0.665
(1.0-3.5) x 109/L
2. Renal Profile
Component
Values
Normal Range
BUN
6.7
(2.5-6.4) mmol/L
Na
141.2
(132-144) mmol/L
K
3.47
(3.5-4.5) mmol/L
Cl
105.8
(95-105 ) mmol/L
Creatinine
95
(53-115) μmol/L
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3. Coagulation Profile
Component
Value
Normal Range
PT
13.9
12.4-14.7
INR
1.255
<2.01
aPTT
25.7
31.7-41.1
4. Minerals
Component
Value
Normal Range
Phosphate
1.00
(0.8-1.5) mmol/l
Magnesium
0.80
(0.75-1.0) mmol/l
Calcium
2.06
(2.12-2.62) mmol/l
5. Fasting Blood Sugar
Value 10.35 mmol/L
Normal Range < 7mmol/L
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6. Lipid profile Component
Value
Normal Range
HDL
1.3
(1.0-2.2) mmol/l
LDL
2.6
(2.0-3.4) mmol/l
Total cholesterol
4.7
(3.0-6.5) mmol/l
TG
1.7
(0.6-1.7) mmol/l
7. Biopsy done of goiter done: results unknown
5. DISCUSSION
This patient has a neck swelling. There are many causes to neck swelling such as: •
Bacterial 13
•
•
•
•
Bacterial pharyngitis
Peritonsillar abscess
Strep throat
Tonsillitis
Tuberculosis
Cancer
Hodgkin's disease
Leukemia
Non-Hodgkin's lymphoma
Thyroid
Thyroid carcinoma
Goitre
Graves' disease
Thyroglossal duct cysts
Thyroiditis
Viral
AIDS
Herpes infections
Infectious mononucleosis
Rubella (German measles)
Viral pharyngitis
Other
Allergic reactions
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In this patient, the cause of neck swelling is likely to be due to her thyroid gland as her history and the physical examination supports it. Her chief complain of shortness of breath together with a visible neck swelling is indicative of tracheal compression which is most probably due to enlargement of the thyroid gland. Her swelling was gradually increasing in size for the past 11 years and was not painful. No pain indicates that it most probably can’t be thyroiditis as that would cause pain. The swelling is also of a long standing one which also rules out thyroiditis as thyroiditis usually causes an acute swelling. She also described her swelling to be ‘many small seed like swellings’ which is indicative of a multinodular goiter. It was also soft and mobile which meant that it is most probably not malignant as there is no fixation of the swelling to the skin. She had developed it after giving birth to her 4th child which is a risk factor for hyperthyroidism too. She also felt lethargic and had lost 5kg in the span of 6 months. The lethargy could be due to increase metabolic rate of the body causing increased energy expenditure and increased metabolism also causes the weight loss. The weight loss also brings in the possibility of malignancy but she did not lose too much weight as significant weight loss in her case would be 6.6kg (10% of body weight). However, it cannot be ruled out yet. She also had headache on and off but this could be due to her hypertension which she developed in year 2009. A patient with hyperthyroidism could also have increased blood pressure as the thyroid hormone can cause activation of the sympathetic nervous system. She had no polyphagia though, which is normally a symptom seen with hyperthyroidism. She does not eat any seafood which means that her iodine level could be low and this can cause goiter too. She had no heat intolerance either which indicates that her BMR is not too high. She also did not have dysphagia which is normally the supporting symptom for retrosternal expansion, however the SOB is quite indicative of that already. Her SOB had also caused syncopy. SOB has many causes related to the heart and lungs but I think that it is highly unlikely as she has no history of orthopnea, dyspnea or PND before and neither does she have any chest pain or pedal edema. She also does not have any cough which again rules out other causes of SOB. Hence, given her symptoms which are more that of hyperthyroidism, I suspect that this is a case of hyperthyroidism with retrosternal expansion. She has a family history of hyperthyroidism as her mother and sister has it too. She also takes anti-hypertensive drugs and anti thyroid drugs which 15
were both given to her in year 2009 but she was not compliant to either of them. Hence, her neck swelling increased in size and has cause tracheal compression now. Upon admission her BP was high, she was tachycardic and tachypnic. The tachycardia and hypertension was probably due to her hyperthyroidism while the tachypnea was caused by the tracheal compression by the thyroid gland. Upon examining her neck, I noted that she had a large swelling which was bigger on the right side rather than the left and had a nodular surface. It was rather firm but was mobile. Her veins were also distended at the sides of the swelling. This could be due to pressure of the internal jugular veins in the thoracic inlet by the enlarged thyroid gland. The swelling moved with deglutition which is indicative that it was the thyroid gland as the thyroid gland is enclosed in the pretracheal fascia which is fixed to the thyroid cartilage so when the superior constrictor of larynx pulls the thyroid cartilage up during deglutition, the gland also moved up and down. Other swelling that moves with deglutition are thyroglossal cyst, pretracheal lymph nodes, subhyoid bursa, and extrinsic ca of larynx. The swelling was not tender and the tracheal rings were not palpable. This is indicative of a retrosternal expansion. To confirm it, I could have compressed her lateral lobes which would have caused stridor, indicating narrowing of trachea due to the presence of a scabbard trachea due to compression by an enlarged thyroid gland but I didn’t do so as she was already in respiratory distress. On percussion over the manubrium sternum, dullness was heard which once again indicates retrosternal expansion due to an enlarged thyroid gland. She had the hyperthyroidism eye signs of lid retraction and infrequent blinking but she did not have exopthalmos which indicates that she most probably does not have Graves’ disease. Her other systems were unremarkable which ruled out other reason of SOB such as pleural effusion and there was no lymph nodes enlargement when I palpated her cervical lymph nodes which indicates that the cause of her swelling is not due to lymphadenopathy either. She also did not have pretibial myxedema which once again indicates that she can’t be having Graves’ disease. Thus my provisional diagnosis is multinodular goiter as she had some symptoms of hyperthyroidism such as a neck swelling which was gradually increasing in size for the past 11 years, lethargy, weight loss, and headache and some signs too such as tremors, moist hands, lid retraction and infrequent blinking. The surface of the neck swelling was also nodular, mobile and painless which again supports the diagnosis. She also had SOB and her tracheal rings could not be 16
palpated and her manubrium sternum was dull to percussion which indicates a retrosternal expansion of the goiter. All the other differentials were already ruled out above. This is confirmed by the investigations especially the thyroid function test which showed that her TSH levels were low while her T4 and T3 levels were normal which is due to her antithyroid drugs that she has been on since year 2009. Her total white blood cell count was also high, probably due to reactive leucocytosis, and her calcium levels are slightly low which once again the surgeon must take note as if care is not taken during the surgery and her parathyroid glands are removed, her calcium level would go lower still which can cause future complications such as osteoporosis. Her CT scan also confirms the diagnosis as it shows retrosternal expansion to level T1-T2. Now we shall talk about the thyroid gland, the hormone it releases and hyperthyroidism. The thyroid gland consists of two lateral lobes connected by an isthmus. It is closely attached to the thyroid cartilage and to the upper end of the trachea, and thus moves on swallowing (like how hers did). Embryologically it originates from the base of the tongue and descends to the middle of the neck. Remnants of thyroid tissue can sometimes be found at the base of the tongue (lingual thyroid) and along the line of descent.
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Thyrotrophin-releasing hormone (TRH), a peptide produced in the hypothalamus, stimulates TSH from the pituitary. TSH stimulates growth and activity of the thyroid follicular cells via the G-protein coupled TSH membrane receptor. Circulating T4 is peripherally deiodinated to T3 which binds to the thyroid hormone nuclear receptor (TR) on target organ cells to cause modified gene transcription.
Physiological effects of thyroid hormones are: •
Cardiovascular system - increased heart rate and cardiac output.
•
Skeletal - increased bone turnover and resorption.
•
Respiratory - maintains normal hypoxic and hypercapnic drive in respiratory centre.
•
Gastrointestinal - increases gut motility.
•
Blood - increases red blood cell 2,3-BPG facilitating oxygen release to tissues.
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•
Neuromuscular - increases speed of muscle contraction and relaxation and muscle protein turnover.
•
Metabolism of carbohydrates - increases hepatic gluconeogenesis/glycolysis and intestinal glucose absorption.
•
Metabolism of lipids - increased lipolysis and cholesterol synthesis and degradation.
•
Sympathetic nervous tissue - increases catecholamine sensitivity and β-adrenergic receptor numbers in heart, skeletal muscle, adipose cells and lymphocytes. Decreases cardiac αadrenergic receptors. Hyperthyroidism (thyroid overactivity, thyrotoxicosis) is common, affecting perhaps 2-5%
of all females at some time and with a sex ratio of 5 : 1, most often between the ages of 20 and 40 years. Nearly all cases (> 99%) are caused by intrinsic thyroid disease; a pituitary cause is extremely rare. The causes of hyperthyroidism are :
Common •
Graves' disease (autoimmune)
•
Toxic multinodular goitre
•
Solitary toxic nodule/adenoma
Uncommon •
Acute thyroiditis
•
viral (e.g. de Quervain's)
•
autoimmune
•
post-irradiation
•
postpartum
•
Gestational thyrotoxicosis (HCG stimulated)
•
Neonatal thyrotoxicosis (maternal thyroid antibodies) 19
•
Exogenous iodine
•
Drugs - amiodarone
•
Thyrotoxicosis factitia (secret T4 consumption)
Rare •
TSH-secreting pituitary tumours
•
Metastatic differentiated thyroid carcinoma
•
HCG-producing tumours
•
Hyperfunctioning ovarian teratoma (struma ovarii)
The most common causes of hyperthyroidism are Graves’ disease and multinodular goiter (just as my patient has). The differences between the 2 are as below:
Characteristic
Graves disease
Multinodular goiter
Autoimmune antibodies
present
Absent
Opthalmopathy
Present with exopthalmos
Absent
Pretibial myxedema
present
Absent
Perspiration
More
Less
Age of patient
Usually younger since it is an 40 years or older autoimmune disease
Clubbing
Can occur if they have Thyroid Absent acropachy
Thyroid enlargement
Tracheal compression
Normally diffuse simple goiter, Nodular goitre, can be very not nodular
huge
Uncommon
Very common
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My patient has a multinodular goiter. Goitre is more common in women than in men and may be either physiological or pathological. Most commonly goiters are noticed as a cosmetic defect by the patient or by friends or relatives. The majorities are painless, but pain or discomfort can occur in acute varieties. Large goitres can produce dysphagia and difficulty in breathing, implying oesophageal or tracheal compression. My patient had a painless goiter which had caused tracheal compression. The nature can often be judged clinically. Goitres are usually separable into diffuse and nodular types, the causes of which differ. The causes of goiter are
Diffuse •
Simple
•
Physiological (puberty, pregnancy)
•
Autoimmune
•
Graves' disease
•
Hashimoto's disease
•
Thyroiditis
•
Acute (de Quervain's thyroiditis)
•
Iodine deficiency (endemic goitre)
•
Dyshormonogenesis
•
Goitrogens (e.g. sulfonylureas)
Nodular •
Multinodular goitre
•
Solitary nodular
•
Fibrotic (Reidel's thyroiditis)
•
Cysts
•
Tumours
•
Adenomas 21
•
Carcinoma
•
Lymphomas
Miscellaneous •
Sarcoidosis
•
Tuberculosis
Most common is the multinodular goitre, especially in older patients, such as my patient who is 66 years old. The patient is usually euthyroid but may be hyperthyroid or borderline with suppressed TSH levels but normal T4 and T3. This is also like my patient who had low levels of TSH but normal levels of T4 and T3 upon admission. Multinodular goitre is the most common cause of tracheal and/or oesophageal compression and can cause laryngeal nerve palsy. This also occurred to my patient as she had SOB. It may also extend retrosternally, just like my patient as her tracheal rings could not be palpated and there was dullness to percussion of the manubrium sternum. The classical 'multinodular goitre' is usually readily apparent clinically, but it should be noted that modern, high-resolution ultrasound frequently reports multiple small nodules in glands which are clinically diffusely enlarged and associated with autoimmune thyroid disease. These nodules are also found in up to 40% of the normal population. Malignancy should be considered in any solitary nodule - however, the majorities of such nodules are cystic or benign and, indeed, may simply be the largest nodule of a multinodular goitre. The diagnostic challenge is to identify the small minority of malignant nodules, which require surgery, from the majority of benign nodules, which do not. A history of rapid enlargement, associated lymph nodes or occasionally pain in such a situation suggests the possibility of thyroid carcinoma, but investigations are paramount. Risk factors for malignancy include previous irradiation, long-standing iodine deficiency and occasional familial cases. My patient did not have any lymph node enlargement and it was not a solitary nodule. Thus, it could not have been a malignancy.
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The clinical symptoms of hyperthyroidism in general are tiredness, emotional lability, heat intolerance, weight loss, excessive appetite and palpitations. The signs are tachycardia, hot, moist palms, exophthalmos, lid lag/retraction, agitation and thyroid goitre and bruit. Its comparison with hypothyroidism is illustrated as below:
My patient only had goiter, weight loss, tremors and moist palms as she was taking antithyroid drugs which controlled the other symptoms of hyperthyroidism. 23
Investigations that should be done if one suspects hyperthyroidism are: •
Thyroid function tests - TSH plus free T4 or T3
•
Thyroid antibodies - to exclude autoimmune aetiology.
•
Ultrasound. Ultrasound with high resolution is a sensitive method for delineating nodules and can demonstrate whether they are cystic or solid. In addition, a multinodular goitre may be demonstrated when only a single nodule is palpable. Unfortunately, even cystic lesions can be malignant and thyroid tumours may arise within a multinodular goitre; therefore fine-needle aspiration is often required and performed under ultrasound control at the same time as the scan.
•
Chest and thoracic inlet X-rays to detect tracheal compression and large retrosternal extensions in patients with very large goitre or clinical symptoms.
•
Fine-needle aspiration (FNA). In patients with a solitary nodule or a dominant nodule in a multinodular goitre, there is a 5% chance of malignancy; in view of this, FNA should be performed. This can be done in the outpatient clinic. Cytology in expert hands can usually differentiate
the
suspicious
or
definitely
malignant
nodule.
FNA reduces the necessity for surgery, but there is a 5% false-negative rate which must be borne in mind (and the patient appropriately counselled). Continued observation is required when an isolated thyroid nodule is assumed to be benign without excision. In my patient, they only did the thyroid function test. Thyroid antibodies were not done as it seemed highly unlikely given her age and the nature of her goiter. They did not have to do an ultrasound as a multinodular goiter was already palpable. They should have done a chest x-ray to confirm the tracheal compression though and they should have also done a FNA to rule out malignancy. The rest of their investigations were justified though, such as FBC was done to see whether there was any infection and whether her Hb and platelet levels are normal, given that she is scheduled for surgery and this should be reviewed before sending her in to avoid bleeding problems. Renal profile was also important as she has hypertension and is not compliant to her drugs, thus her kidneys should be assessed to avoid complications such as acute renal failure in future, post operatively. Coagulation profile must also be assessed as she is scheduled for surgery and the surgeon must confirm that she does not have any coagulopathy to avoid from complications such as bleeding. 24
Diagnosis of hyperthyroidism is usually straightforward. The patient is euthyroid, the nodules are palpable and often visible (smooth, usually firm and not hard) and the goitre is painless and moves freely on swallowing. Hardness and irregularity, due to calcification, may simulate carcinoma. A painful nodule or the sudden appearance or rapid enlargement of a nodule raises suspicion of carcinoma; however, such cases are usually due to haemorrhage into a simple nodule. Differential diagnosis from autoimmune thyroiditis may be difficult and the two conditions frequently coexist. My patient was euthyroid, her nodules were palpable and firm, painless, nodular and moved with swallowing. It was very indicative of multinodular goiter undeed. The general work up to reach a diagnosis is as below:
25
26
Long-term follow-up studies of hyperthyroidism show a slight increase in overall mortality, which affects all age groups, is not fully explained and tends to occur in the first year after diagnosis. Thereafter, the only long-term risk of adequately treated hyperthyroidism appears to be an increased risk of osteoporosis. Patients with persistently suppressed TSH levels have an increased likelihood of developing atrial fibrillation which may predispose to thromboembolic disease. Thus, hyperthyroidism should be corrected. Three possibilities are available: antithyroid drugs, radioiodine and surgery. Thyroidectomy should be performed only in patients who have 27
previously been rendered euthyroid. Conventional practice is to stop the antithyroid drug 10-14 days before operation and to give potassium iodide (60 mg three times daily), which reduces the vascularity of the gland. When thyroid function is abnormal the patient should be rendered euthyroid. Indications for surgical intervention are: •
The possibility of malignancy. A history of rapid growth, pain, cervical lymphadenopathy, change in voice or previous irradiation to the neck are worrying features. A positive or suspicious FNA makes surgery mandatory and surgery may be necessary if doubt persists even in the presence of a negative FNA (especially if the patient is concerned by the false negative rate).
•
Pressure symptoms on the trachea or, more rarely, oesophagus. The possibility of retrosternal extension should be excluded.
•
Cosmetic reasons. A large goitre is often a considerable anxiety to the patient even though functionally and anatomically benign.
The operation should be performed only by experienced surgeons to reduce the chance of complications: •
Early postoperative bleeding causing tracheal compression and asphyxia is a rare emergency requiring immediate removal of all clips/sutures to allow escape of the blood/haematoma.
•
Laryngeal nerve palsy occurs in 1%. Vocal cord movement should be checked preoperatively.
•
Transient hypocalcaemia occurs in up to 10% but with permanent hypoparathyroidism in fewer than 1%.
•
Recurrent hyperthyroidism occurs in 1-3% within 1 year, then 1% per year.
•
Hypothyroidism occurs in about 10% of patients within 1 year, and this percentage increases with time. It is likeliest if TPO antibodies are positive. Automated computer thyroid registers with annual TSH screening are used in some regions, and have demonstrated that a high proportion of patients become hypothyroid in the long term.
28
My patient underwent a total thyroidectomy in the hospital and this decision was made by the surgeon as there was presence of tracheal compression in her which had caused SOB. Hence, it was a good call by the surgeon as he had to relieve the SOB and this was already an emergency case. Post operatively, she did develop some of the complications as mentioned above as her left laryngeal nerve was preserved but her right laryngeal nerve was not. Thus, she has change in her voice where now it is coarse and can barely be heard. Her parathyroid gland was preserved but she does have slightly low calcium level post operatively as transient hypocalcaemia occurs in up to 10% of patients, as mentioned above. Before the operation, foot pump and stockings were applied for her and post operatively, she had somehow gotten a large ulcer on her leg which occurred when they removed the stockings post surgery. This is an unforeseen complication in her case.
29
