case write up_harmeet_multinodular goitre
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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
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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 25 th 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
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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
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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
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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
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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
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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
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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
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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
4.2Post op (28th December 2011)
1. Full Blood Count
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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
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Value Normal Range
10.35 mmol/L < 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
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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 pressureas 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 asshe 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
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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
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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 anti-
thyroid 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 de-
iodinated 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 α-
adrenergic 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 isextremely 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)
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• 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
autoimmune disease
40 years or older
Clubbing Can occur if they have Thyroid
acropachy
Absent
Thyroid enlargement Normally diffuse simple goiter,
not nodular
Nodular goitre, can be very
huge
Tracheal compression 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
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• 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 anti-
thyroid drugs which controlled the other symptoms of hyperthyroidism.
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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.
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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:
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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
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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 rareemergency 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.
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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.
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