Davao Doctor College

Gen. Malvar St.

Davao City

A Book Base Case Study

Of Hyperthyroidism
Operative Review of Thyroidectomy

In Partial Fulfillment
Of NCM 103

Presented to:
Rufino M. Dayrit Jr. RN, MN
Of Davao Doctors College
Presented by:
Ken Alfred Pedreso

July 2014

TABLE OF CONTENTS

I.

INTRODUCTION

II.

ANATOMY

III.

PATHOPHYSIOLOGY

IV.

MEDICAL MANAGEMENT

V.

DIAGNOSIS

VI.

PROCEDURE PROPER (with Instrumentation)

VII.

Roles of Circulating and Scrub nurse

VIII.

Nursing Management
a.

Nursing Care Plan

IX.

Pharmacology

X.

Bibliography

CHAPTER I
INTRODUCTION

Hyperthyroidism, or overactive thyroid, is due to the overproduction of the thyroid

hormones T3 and T4, which is most commonly caused by the development of Graves'
disease, an autoimmune disease in which antibodies are produced which stimulate the
thyroid to secrete excessive quantities of thyroid hormones. The disease can result in
the formation of a toxic goiter as a result of thyroid growth in response to a lack of
negative feedback mechanisms.

About 1 in 500 women have hyperthyroidism during pregnancy. In some, it is a

preexisting condition; in others, the condition will develop during the course of the
pregnancy. It can be difficult to diagnose because the pregnancy often "masks" it; that
is, some of the symptoms may be attributed to the pregnancy itself rather than to
hyperthyroidism. Hyperthyroidism may affect a woman's ability to become pregnant.
The most common cause of hyperthyroidism in pregnancy is Graves' disease.
Symptoms generally will be worse in the first half of the pregnancy, will lessen during
the second half, and most likely will recur after the baby is born. The mother should
continue with her normal anti-thyroid medication during her pregnancy as prescribed by
her doctor. Most pregnant women and their babies will not experience significant
problems if the hyperthyroidism is mild to moderate. If properly treated, the pregnancy
can be expected to progress normally. Women with severe or uncontrolled
hyperthyroidism have an increased risk of infection, iron deficiency (anemia), and high
blood pressure accompanied by too much protein in the urine (a potentially dangerous
condition called pre-eclampsia). If a woman has severe hyperthyroidism, her baby has a
chance of having hyperthyroidism as well. There is a risk to the outcome of the
pregnancy, having a small baby or a premature birth.

Fortunately, most women who have hyperthyroidism in pregnancy can be

successfully treated with medication. The anti-thyroid drug which is Propylthiouracil is
commonly prescribed and can be safely used during pregnancy. It may take up to a
month on medication for the symptoms to resolve. Radioactive iodine cannot be used
during pregnancy. Rarely, if the symptoms and thyroid hormone levels cannot be
controlled, surgery needs to be considered to remove the thyroid gland.
Hyperthyroidism does not affect labor and delivery. However, thyroid storm can
develop which can be life threatening. The symptoms are an exaggeration of the normal
hyperthyroid symptoms with a very fast heart rate, tremors, nervousness, altered
consciousness, nausea, vomiting, diarrhea, and an extremely high fever. This will
require intensive care treatment to try normalizing the very high thyroid hormone levels
and keeping the patient cool.
Graves disease which is the most common form of hyperthyroidism in the US is
approximately 60-80% of cases of thryotoxicosis due to this disease. The annual
incidence of the disease is 0.5 cases per 1000 persons during a 20 year period, with the
peak occurrence in people aged 20-40 years.
Hyperthyroidism occurs in 2/1000 pregnancies in the United Kingdom. Graves
hyperthyroidism is the commonest cause of hyperthyroidism in young women (about
85% of cases) in the United Kingdom. The prevalence of undiagnosed hyperthyroidism
in women is about 4.7/1000, and 0.2% of UK women have been previously diagnosed
and treated. In areas of mild iodine deficiency the prevalence is higher.
In addition to true hyperthyroidism, the more common clinical entity of transient
gestational hyperthyroidism may be seen particularly in the first trimester, with
prevalence in Europeans of 2-3% but a much higher prevalence in South Asian
populations. Hyperthyroidism does not often arise for the first time in early pregnancy,
but clinicians need to be aware of the symptoms and signs.

CHAPTER II
ANATOMY
The thyroid gland or simply, the thyroid is one of the largest endocrine glands. The
thyroid gland is found in the neck, below the thyroid cartilage.

The thyroid gland

controls how quickly the body uses energy, makes proteins, and controls how sensitive
the body is to other hormones. It participates in these processes by producing thyroid
hormones, the principal ones being triiodothyronine (T3) and thyroxine which can
sometimes be referred to as tetraiodothyronine (T4). These hormones regulate the
growth and rate of function of many other systems in the body. T3 and T4 are
synthesized from iodine and tyrosine. The thyroid also produces calcitonin, which plays
a role in calcium homeostasis. Hormonal output from the thyroid is regulated by thyroidstimulating hormone (TSH) produced by the anterior pituitary, which itself is regulated
by thyrotropin-releasing hormone (TRH) produced by the hypothalamus. The thyroid
gets its name from the Greek adjective for "shield-shaped" due to the shape of the
related thyroid cartilage.

A. Anatomy
The thyroid gland is a butterfly-shaped organ and is composed of two cone-like
lobes or wings, lobus dexter (right lobe) and lobus sinister (left lobe), connected via the
isthmus. The organ is situated on the anterior side of the neck, lying against and around
the larynx and trachea, reaching posteriorly the esophagus and carotid sheath. It starts
cranially at the oblique line on the thyroid cartilage (just below the laryngeal
prominence, or 'Adam's Apple'), and extends inferiorly to approximately the fifth or sixth
tracheal ring. It is difficult to demarcate the gland's upper and lower border with
vertebral levels because it moves position in relation to these during swallowing.

The thyroid gland is covered by a thin fibrous sheath, the capsula glandulae thyroidea,
composed of an internal and external layer. The external layer is anteriorly continuous
with the pretracheal fascia and posteriorolaterally continuous with the carotid sheath.
The gland is covered anteriorly with infrahyoid muscles and laterally with the
sternocleidomastoid muscle also known as sternomastoid muscle. On the posterior
side, the gland is fixed to the cricoid and tracheal cartilage and cricopharyngeus muscle
by a thickening of the fascia to form the posterior suspensory ligament of Berry.[2][3]
The thyroid gland's firm attachment to the underlying trachea is the reason behind its
movement with swallowing. In variable extent, Lalouette's Pyramid, a pyramidal
extension of the thyroid lobe, is present at the most anterior side of the lobe. In this
region, the recurrent laryngeal nerve and the inferior thyroid artery pass next to or in the
ligament and tubercle.
Between the two layers of the capsule and on the posterior side of the lobes, there are
on each side two parathyroid glands.
The thyroid isthmus is variable in presence and size, can change shape and size, and
can encompass a cranially extending pyramid lobe (lobus pyramidalis or processus
pyramidalis), remnant of the thyroglossal duct. The thyroid is one of the larger endocrine
glands, weighing 2-3 grams in neonates and 18-60 grams in adults.

In a healthy patient the gland is not visible yet can be palpated as a soft mass.
Examination of the thyroid gland is carried out by locating the thyroid cartilage and
passing the fingers up and down, examining for abnormal masses and overall thyroid
size. Then, place one hand on each of the trachea and gently displace the thyroid tissue
to the contralateral side of the neck for both sides while the other hand manually
palpates the displaced gland tissue; having the patient flex the neck slightly to the side
when being palpated may help in this examination. Next, the two lobes of the gland
should be compared for size and texture using visual inspection, as well as manual or
bimanual palpation. Finally, ask the patient to swallow to check for mobility of the gland;
many clinicians find that having the patient swallow water helps this part of the
examination. In a healthy state, the gland is mobile when swallowing occurs due its
fascial encasement. Thus when the patient swallows, the gland moves superiorly, as
does the whole larynx.
The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of
the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical
trunk, and sometimes by the thyroid ima artery, branching directly from the subclavian
artery. The venous blood is drained via superior thyroid veins, draining in the internal
jugular vein, and via inferior thyroid veins, draining via the plexus thyroideus impair in
the left brachiocephalic vein.
Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the
pre- and parathracheal lymph nodes. The gland is supplied by parasympathetic nerve
input from the superior laryngeal nerve and the recurrent laryngeal nerve.

Embryological and fetal development

Floor of pharynx of embryo between 18 and 21 days.

In the embryo, at 34 weeks of gestation, the thyroid gland appears as an epithelial

proliferation in the floor of the pharynx at the base of the tongue between the
tuberculum impar and the copula linguae at a point later indicated by the foramen
cecum. The thyroid then descends in front of the pharyngeal gut as a bilobed
diverticulum through the thyroglossal duct. Over the next few weeks, it migrates to the
base of the neck, passing anterior to the hyoid bone. During migration, the thyroid
remains connected to the tongue by a narrow canal, the thyroglossal duct.

Thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) start

being secreted from the fetal hypothalamus and pituitary at 18-20 weeks of gestation,
and fetal production of thyroxine (T4) reach a clinically significant level at 1820 weeks.
Fetal triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks of gestation,
and increases to 50 ng/dL at term. Fetal self-sufficiency of thyroid hormones protects
the fetus against e.g. brain development abnormalities caused by maternal
hypothyroidism. However, preterm births can suffer neurodevelopmental disorders due
to lack of maternal thyroid hormones due their own thyroid being insufficiently
developed to meet their postnatal needs.
The portion of the thyroid containing the parafollicular C cells, those responsible
for the production of calcitonin, are derived from the neural crest. This is first seen as
the ultimobranchial body, which joins the primordial thyroid gland during its descent to
its final location in the anterior neck.

CHAPTER III
PHYSIOLOGY

B. Physiology
The primary function of the thyroid is production of the hormones T 3, T4 and
calcitonin. Up to 80% of the T4 is converted to T3 by organs such as the liver, kidney
and spleen. T3 is several times more powerful than T 4, which is largely a prohormone,
perhaps four or even ten times more active.
The system of the thyroid hormones T3 and T4.

Synthesis of the thyroid hormones, as seen on an individual thyroid follicular

cell:
1.

Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the

secretory pathway to enter the colloid in the lumen of the thyroid follicle by exocytosis.
2.

Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I-) actively into the

cell, which previously has crossed the endothelium by largely unknown mechanisms.
3.

This iodide enters the follicular lumen from the cytoplasm by the transporter

pendrin, in a purportedly passive manner.

4.

In the colloid, iodide (I-) is oxidized to iodine (I0) by an enzyme called thyroid

peroxidase.
5.

Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its

protein chain (in total containing approximately 120 tyrosyl residues).

6.

In conjugation, adjacent tyrosyl residues are paired together.

7.

The entire complex re-enters the follicular cell by endocytosis.

8.

Proteolysis by various proteases liberates thyroxine and triiodothyronine

molecules, which enters the blood by largely unknown mechanisms.

T3 and T4 production and action

Thyroxine (T4) is synthesised by the follicular cells from free tyrosine and on the
tyrosine residues of the protein called thyroglobulin (Tg). Iodine is captured with the
"iodine trap" by the hydrogen peroxide generated by the enzyme thyroid peroxidase
(TPO) and linked to the 3' and 5' sites of the benzene ring of the tyrosine residues on
Tg, and on free tyrosine. Upon stimulation by the thyroid-stimulating hormone (TSH),
the follicular cells reabsorb Tg and cleave the iodinated tyrosines from Tg in lysosomes,
forming T4 and T3 (in T3, one iodine atom is absent compared to T4), and releasing
them into the blood. Deiodinase enzymes convert T4 to T3. Thyroid hormone secreted
from the gland is about 80-90% T4 and about 10-20% T3.

Cells of the developing brain are a major target for the thyroid hormones T3 and T4.
Thyroid hormones play a particularly crucial role in brain maturation during fetal
development. A transport protein that seems to be important for T4 transport across the
bloodbrain barrier (OATP1C1) has been identified. A second transport protein (MCT8)
is important for T3 transport across brain cell membranes.
Non-genomic actions of T4 are those that are not initiated by liganding of the hormone
to intranuclear thyroid receptor. These may begin at the plasma membrane or within
cytoplasm. Plasma membrane-initiated actions begin at a receptor on the integrin
alphaV beta3 that activates ERK1/2. This binding culminates in local membrane actions
on ion transport systems such as the Na(+)/H(+) exchanger or complex cellular events
including cell proliferation. These integrins are concentrated on cells of the vasculature
and on some types of tumor cells, which in part explains the proangiogenic effects of
iodothyronines and proliferative actions of thyroid hormone on some cancers including
gliomas. T4 also acts on the mitochondrial genome via imported isoforms of nuclear
thyroid receptors to affect several mitochondrial transcription factors. Regulation of actin
polymerization by T4 is critical to cell migration in neurons and glial cells and is
important to brain development.
T3 can activate phosphatidylinositol 3-kinase by a mechanism that may be cytoplasmic
in origin or may begin at integrin alpha V beta3.
In the blood, T4 and T3 are partially bound to thyroxine-binding globulin (TBG),
transthyretin, and albumin. Only a very small fraction of the circulating hormone is free
(unbound) - T4 0.03% and T3 0.3%. Only the free fraction has hormonal activity. As with
the steroid hormones and retinoic acid, thyroid hormones cross the cell membrane and
bind to intracellular receptors (1, 2, 1 and 2), which act alone, in pairs or together
with the retinoid X-receptor as transcription factors to modulate DNA transcription.

T3 and T4 regulation
The production of thyroxine and triiodothyronine is regulated by thyroidstimulating hormone (TSH), released by the anterior pituitary. The thyroid and
thyrotropes form a negative feedback loop: TSH production is suppressed when the T4
levels are high. The TSH production itself is modulated by thyrotropin-releasing
hormone (TRH), which is produced by the hypothalamus and secreted at an increased
rate in situations such as cold exposure (to stimulate thermogenesis). TSH production is
blunted by somatostatin (SRIH), rising levels of glucocorticoids and sex hormones
(estrogen and testosterone), and excessively high blood iodide concentration.
An additional hormone produced by the thyroid contributes to the regulation of blood
calcium levels. Parafollicular cells produce calcitonin in response to hypercalcemia.
Calcitonin stimulates movement of calcium into bone, in opposition to the effects of
parathyroid hormone (PTH). However, calcitonin seems far less essential than PTH, as
calcium

metabolism

remains

clinically

(thyroidectomy), but not the parathyroids.

normal

after

removal

of

the

thyroid

CHAPTER III
PATHOPHYSIOLOGY

Schematic Diagram
Predisposing Factors
(Non modifiable factors)

Age
Sex/Gender
Genes
Family History

Precipitating factors
(Modifiable factors)
Lifestyle
Diet-decreased Iodine intake
Graves disease

Diagnosis
Physical Examination
Blood test
radioactive iodine

HYPERTHYROIDISM

If treated

Antithroid drugs
Beta blockers
Radioactive iodine
Surgery

If not treated

Arrhythmia
Cardiac dilation/
congestive heart failure
Sudden cardiac arrest
Hypertension
Osteoporosis

Pregnancy complications
increased risk of fetal loss
pre-eclampsia
heart failure
premature labor
Having a low birth weight
baby

Good prognosis

Poor prognosis

Death

Narrative
Any process that causes an increase in the peripheral circulation of unbound
thyroid hormone can cause signs and symptoms of hyperthyroidism. Disturbances of
the normal homeostatic mechanism can occur at the level of the hypothalamus, the
pituitary gland and the thyroid gland

Defect of hypothalamus and pituitary gland can be hyper-secreting of hormone

which can induce excessive secretion of thyroid hormone causing hyperthyroidism. But
this is rare. Hyper-secretion may be due to certain tumor or any other defects. On
investigation, this defect can increase level of tri-iodothyronine (T3) and level of
thyroxine (T4) in plasma. Level of Thyroid Releasing Hormone (TRH) and/or level of
Thyroid Stimulating Hormone (TSH) also may be increased. Goiter that is enlargement
of thyroid gland may be present.

Defect also can be originated from the thyroid gland itself. Hyper-secreting of
thyroid hormone may be one of the causes with absent of goitre. Other than that, is
Gravess Disease which is the common cause of hyperthyroidism. Gravess Disease is
an autoimmune disease in which the body abnormally produces thyroid-stimulating
immunoglobulin (TSI), an antibody whose targeting the TSH receptor on the thyroid
cells. TSI will stimulates both secretion and growth of the thyroid in a manner similar to
TSH.

Unlike TSH, TSI is not subjected for negative feedback inhibition by thyroid hormone, so
thyroid secretion and growth continued unchecked. On investigation, level of T3 and T4
may be high while level of TSH remains normal or low. Goiter may be present. Last
causes of hyperthyroidism are Apathetic Hyperthyroidism which refers to thyrotoxicosis
occurring in elderly, in whom old age and various co-morbidities may blunt typical
features of thyroid hormone excess seen in younger patients. The diagnoses of
throtoxicosis in these individual are often made during laboratory work-up for
unexplained weight loss or worsening cardiovascular disease.

Clinical manifestations of hyperthyroidism are induces by abnormal increased in thyroid

hormone. Thyroid hormone can cause three major effects that is hyper metabolic state,
over stimulation of sympathetic nervous system and cardiac effect as compensatory
mechanism of certain condition caused by increased thyroid hormone.

Thyroid hormone can lead to hyper metabolic state by increasing general

metabolic rate. Normally, thyroid hormone participated in inducing synthesis and
degradation of carbohydrate, fat and protein. However, overall metabolic effects of
thyroid hormone at normal physiologic level are to favor the consumption rather than
storage of body fuel. So, when thyroid hormone becomes abnormally high, it will
increase the overall basal metabolic rate by increasing rate of degradation. Skin of
patient may be soft, warm and flushed. Heat intolerance and excessive sweating also
can be noted.

Thyroid hormones has sympathomimetic action which the actions are similar to
one produced by sympathetic nervous system. Normally, thyroid hormone stimulates
proliferation of specific cathecholamines target cell receptors which can induce
sympathomimetic effect. Increased in thyroid hormone can induce overstimulation of
sympathetic effects which can lead to condition known as Thyroid Storm which is an
abrupt onset of acute hyperthyroidism. Thyroid Storm is a medical emergency situation
which significant number of untreated patients led to cardiac arrhythmias.

Overstimulation of gut will induce hypermotility which led to diarrhea and

eventually malabsoption. Overstimulation of levator palpebrae superioris of the eye will
result in ocular manifestation of wide, gaze, starring and lid lag of the eyes.
Overstimulation of neuromuscular will lead to nervousness, irritability and tremor. Nearly
50% develop proximal muscle weakness called thyroid myopathy.

Increasing thyroid hormone also can lead to thyroid effects. Heart rate and contractility
of heart muscle will be increase due to increase in hearts responsiveness towards
circulating cathecolamines. In addition, in response to heat load generated by
cholinergic effect of thyroid hormone as discussed above, peripheral vasodilatation
occurs to carry extra heat to body surface for elimination to the environment. Palpitation
that is conscious of increasing heart beat and tachycardia that is abnormally rapid
heartbeat is commonly seen in patient with hyperthroidosis.
Individuals with hyperthyroidism usually tell their doctors about symptoms such as rapid
heart rate, intense fatigue, inability to tolerate a hot environment, and constant
nervousness, jitteriness, or irritability. In addition, doctors look for physical signs such as
weight loss, rapid heartbeat, slight tremors of the hands, or excessive sweating. The
presence of such symptoms and signs strongly suggests the need for diagnostic testing
for hyperthyroidism.
Hyperthyroidism is diagnosed from blood tests: An abnormally high levels of T3
and T4 indicates that hyperthyroidism is present. An unusually low level of circulating
thyroid stimulating hormone (TSH) is normally due to an abnormality within the thyroid
gland.

In some cases of hyperthyroidism, a special diagnostic scan of the thyroid

gland using radioactive iodine called radioactive iodine uptake (RAIU) testing may be
particularly useful. This test is often done on an outpatient basis in the nuclear medicine
department of a hospital. RAIU testing shows whether: The entire thyroid gland is
overactive, in which case, a large amount of radioactive iodine is "taken up" by the
thyroid. Only portions of the thyroid are overactive. Significant amounts of radioactive
iodine are "taken up" by portions of the thyroid, not the entire gland.

There is no known cure for Graves' disease. Three forms of therapy are available for the
treatment of hyperthyroidism.These therapies work by decreasing the amount of thyroid
hormone made by the thyroid gland; therefore, an excess amount of hormone does not
get into the bloodstream. The treatments available are: Beta blockers, anti-thyroid drugs
and radioactive iodine, also known as radioiodine or 131I
Untreated hyperthyroidism can lead to serious complications, mainly related to the
heart. When the patient has hyperthyroidism, her body is, in a way, running on overdrive
all the time, and that can greatly affect her heart. Some possible heart-related
complications of uncontrolled hyperthyroidism are arrhythmia (abnormal heart beat,
such as atrial fibrillation), cardiac dilation (increase in the size of the heart cavities,
which actually thins the heart muscle) and congestive heart failure, sudden cardiac
arrest and hypertension
If the patient doesn't treat hyperthyroidism, she may also run the risk of
developing osteoporosis. She can gradually lose bone mineral density because
uncontrolled hyperthyroidism can cause her body to pull calcium and phosphate out of
the bones and to excrete too much calcium and phosphorous (through the urine and
stool). She needs calcium and phosphorous to maintain healthy bones, so if his bones
aren't absorbing enough those minerals or losing them at an increased rate, they can
become less dense. This can also make her body temporarily hungrier for calcium after
thyroid surgery if her conditions worsen.

CHAPTER IV
MEDICAL MANEGEMENT

Antithyroid Pharmacotherapy
Antithyroid drugs (eg, methimazole and propylthiouracil) have been used for
hyperthyroidism since their introduction in the 1940s. These medications are employed
for long-term control of hyperthyroidism in children, adolescents, and pregnant women.
In adult men and nonpregnant women, they are used to control hyperthyroidism before
definitive therapy with radioactive iodine.
Antithyroid medications inhibit the formation and coupling of iodotyrosines in
thyroglobulin. Because these processes are necessary for thyroid hormone synthesis,
this inhibition induces a gradual reduction in thyroid hormone levels over 2-8 weeks or
longer. A second action of propylthiouracil (but not methimazole) is inhibition of
conversion of thyroxine (T4) to triiodothyronine (T3). T3 is more biologically active than
T4; thus, a quick reduction in T3 levels is associated with a clinically significant
improvement in thyrotoxic symptoms
Radioactive iodine therapy is the most common treatment for Graves disease in
adults in the United States. Although its effect is less rapid than that of antithyroid
medication or thyroidectomy, it is effective and safe and does not require
hospitalization.
Concerns about radiation exposure after therapy have led to the issuance of new
recommendations by the ATA. These recommendations are compliant with Nuclear
Regulatory Commission regulations and are a practical guide for patient activity after
radioactive iodine therapy, with the aim of ensuring maximum radiation safety for the
family and the public.

Radioactive iodine is administered orally as a single dose in capsule or liquid form. The
iodine is quickly absorbed and taken up by the thyroid. No other tissue or organ in the
body is capable of retaining the radioactive iodine; consequently, very few adverse
effects are associated with this therapy. The treatment results in a thyroid-specific
inflammatory response, causing fibrosis and destruction of the thyroid over weeks to
many months.
Generally, the dose of131 I administered is 75-200 Ci/g of estimated thyroid tissue
divided by the percent of123 I uptake in 24 hours. This dose is intended to render the
patient hypothyroid.
Administration of lithium in the weeks following radioactive iodine therapy may extend
the retention of radioactive iodine and increase its efficacy. This may be considered in
Graves disease patients with especially large Graves glands (> 60 g) or in patients with
extremely high thyroidal iodine uptake (> 95% in 4 hours), which is associated with high
iodine turnover in the gland. However, studies have yielded inconsistent results, and the
benefits of using lithium with radioactive iodine must be weighed against the toxicities
associated with lithium.
Thyroidectomy
Subtotal thyroidectomy is the oldest form of treatment for hyperthyroidism. Total
thyroidectomy and combinations of hemithyroidectomies and contralateral subtotal
thyroidectomies also have been used.

Because of the excellent efficacy of antithyroid medications and radioactive iodine

therapy in regulating thyroid function, thyroidectomy is generally reserved for special
circumstances, including the following:

Severe hyperthyroidism in children

Pregnant women who are noncompliant with or intolerant of antithyroid

pharmacotherapy

Patients with very large goiters or severe ophthalmopathy

Patients who refuse radioactive iodine therapy

Patients with refractory amiodarone-induced hyperthyroidism

Patients who require normalization of thyroid functions quickly, such as pregnant

women, women who desire pregnancy in the next 6 months, or patients with
unstable cardiac conditions

Preparation for thyroidectomy includes antithyroid medication, stable (cold) iodine

treatment, and beta-blocker therapy. Generally, antithyroid drug therapy should be
administered until thyroid functions normalize (4-8 weeks). Propranolol is titrated until
the resting pulse rate is lower than 80 beats/min. Finally, iodide is administered as SSKI
(1-2 drops twice daily for 10-14 days) before the procedure. Stable iodide therapy both
reduces thyroid hormone excretion and decreases thyroid blood flow, which may help
reduce intraoperative blood loss.
With current operative techniques, bilateral subtotal thyroidectomy should have a
mortality approaching zero in patients who are properly prepared. Historically, operative
stress was the most common cause of thyroid storm, a physiologic decompensation in
patients who are severely thyrotoxic, with a mortality of about 50%. Adverse effects of
thyroidectomy include recurrent laryngeal nerve damage and hypoparathyroidism from
damage to local structures during the procedure.

Long-Term Monitoring
Care after initiation of antithyroid medication
After 4-6 weeks, antithyroid medications usually must be reduced; otherwise, the patient
becomes hypothyroid. Hypothyroidism causes the usual symptoms of fatigue and
weight gain, and in patients with Graves disease, it has been anecdotally associated
with worsening of thyroid ophthalmopathy. Initially, the patient should have thyroid
function tests performed every 4-6 weeks until thyroid hormone levels are stabilized on
a low dosage of antithyroid medication.
Patients with non-Graves hyperthyroidism rarely experience remissions. In patients who
are placed on long-term antithyroid drug therapy with the goal of remission, follow-up
tests of thyroid function should be performed at least every 3 months for the first year.
In patients with Graves disease, antithyroid medication should be stopped or decreased
after 12-18 months to determine whether the patient has gone into remission. In these
patients, remission is defined as a normal TSH level after cessation of antithyroid drug
therapy.

Once a patient with Graves hyperthyroidism becomes euthyroid on oral antithyroid

medication, other definitive treatment, such as radioactive iodine therapy or surgery,
should be considered. Although a significant fraction of patients with Graves disease go
into remission, as many as 20% become hypothyroid over subsequent years as a
consequence of autoimmune destruction of the gland.

Care after radioactive iodine ablation

Ablation of the gland occurs over 2-5 months after radioactive iodine therapy. Most
patients become hypothyroid. Checking thyroid functions every 4-6 weeks until the
patient stabilizes is recommended.

Once the thyroid hormone levels start falling into the low-normal range, it is reasonable
to stop antithyroid medications and to consider starting low-dose thyroid hormone
replacement before the patient becomes hypothyroid; however, some physicians prefer
to document persistently elevated TSH values with the patient off antithyroid medication
before starting thyroid hormone replacement.
Starting with partial or low-dose thyroid hormone replacement is recommended (50-75
g/day, adjusted every 6-8 weeks to normalize the TSH level). Several weeks after131 I
therapy, patients can, in rare cases, become thyrotoxic as a result of vigorous thyroid
destruction and release of preformed hormone. This process often is accompanied by a
painful, radiation-induced thyroiditis that can be treated with nonsteroidal antiinflammatory drugs (NSAIDs) or glucocorticoids.
In addition, radioablation can cause the release of thyroid antigens and exacerbate the
autoimmune thyroid disease process. In such cases, Graves disease can worsen.

Care after thyroid surgery

Patients whose thyroid functions normalize after surgery require routine follow-up
because hypothyroidism (from the chronic thyroiditis), recurrent hyperthyroidism, or
thyroid eye disease may develop at some time in the future. Most patients remain
euthyroid after a lobectomy or lobectomy plus isthmusectomy to treat a toxic adenoma
or toxic multinodular goiter with a dominant nodule. To ensure normal thyroid function,
thyroid function tests should be obtained 3-4 weeks after a lobectomy.

After subtotal thyroidectomy for hyperthyroidism and cessation of antithyroid therapy,

most patients become hypothyroid, depending on how much functional tissue is left by
the surgeon. Partial replacement (T4 50-75 g/day) is recommended in these patients,
beginning shortly after the procedure. Thyroid function tests should be monitored 4-8
weeks postoperatively, and the T4 dosage should be adjusted to maintain a normal
TSH level.

CHAPTER V
DIAGNOSIS

Hyperthyroidism is diagnosed using:

Medical history and physical exam. During the exam your doctor may try to detect
a slight tremor in your fingers when they're extended, overactive reflexes, eye
changes and warm, moist skin. Your doctor will also examine your thyroid gland as
you swallow.

Blood tests. A diagnosis can be confirmed with blood tests that measure the levels
of thyroxine and TSH in your blood. High levels of thyroxine and low or nonexistent
amounts of TSH indicate an overactive thyroid. The amount of TSH is important
because it's the hormone that signals your thyroid gland to produce more thyroxine.
These tests are particularly necessary for older adults, who may not have classic
symptoms of hyperthyroidism.

If blood tests indicate hyperthyroidism, your doctor may recommend one of the following
tests to help determine why your thyroid is overactive:

Radioactive iodine uptake test. For this test, you take a small, oral dose of
radioactive iodine (radioiodine). Over time, the iodine collects in your thyroid gland
because your thyroid uses iodine to manufacture hormones. You'll be checked after
two, six or 24 hours and sometimes after all three time periods to determine
how much iodine your thyroid gland has absorbed.
A high uptake of radioiodine indicates your thyroid gland is producing too much
thyroxine. The most likely cause is either Graves' disease or hyperfunctioning
nodules. If you have hyperthyroidism and your radioiodine uptake is low, you may
have thyroiditis.
Be sure to tell your doctor if you have had a recent X-ray or a computerized
tomography scan in which you had contrast material was injected. The results of
your radioiodine test may be influenced by these procedures.
Knowing what's causing your hyperthyroidism can help your doctor plan the
appropriate treatment. A radioactive iodine uptake test isn't uncomfortable, but it
does expose you to a small amount of radiation.

Thyroid scan. During this test, you'll have a radioactive isotope injected into the
vein on the inside of your elbow or sometimes into a vein in your hand. You then lie
on a table with your head stretched backward while a special camera produces an
image of your thyroid on a computer screen.
The time needed for the procedure may vary, depending on how long it takes the
isotope to reach your thyroid gland. You may have some neck discomfort with this
test, and you'll be exposed to a small amount of radiation.
Sometimes you may have a thyroid scan as part of a radioactive iodine uptake test.
In that case, orally administered radioactive iodine is used to image your thyroid
gland.

CHAPTER VI
PROCEDURE PROPER
Conventional thyroidectomy in a conventional thyroidectomy, a 3- to 4-inch
incision will be made through the skin in the low collar area of your neck (the lower front
portion of your neck, above the collarbones and breast bone). Next, a vertical cut will be
made through the strap-like muscles located just below the skin, and these muscles will
be spread aside to reveal the thyroid gland and other deeper structures. Then, all or
part of your thyroid gland will be cut free from surrounding tissues and removed. During
the entire procedure, the surgeon will pay attention to the location of the parathyroid
glands (two pairs of small glands located near the thyroid). The surgeon will focus on
preserving them, if possible. After your thyroid gland is removed, one or two stitches will
be used to bring your neck muscles together again. Then the deeper layer of your
incision will be closed with stitches, and your skin will be closed with sterile paper tapes.
A small suction catheter (tube) will be inserted near the area of your incision to drain
any blood accumulated inside your neck. Following surgery, you will be taken to a
recovery room, where you will be monitored for several hours until you are stable
enough to return to your hospital room. After about 24 hours, the suction catheter will be
removed from your neck. Most patients go home one or two days after the surgery.
Endoscopic thyroidectomy a viewing instrument called an endoscope and small
surgical instruments will be inserted into your neck through three or four small incisions.
Each incision is about 3 millimeters to 5 millimeters long (less than inches). Then the
surgeon will use a tiny camera on the endoscope to guide the instruments and remove
your thyroid tissue. At the end of the procedure, your neck incisions will be closed with
tiny stitches or surgical tape.

CHAPTER VI
INSTRUMENTATION

Surgical Instruments List

for the Thyroidectomy procedure:
(Quantity recommended is in parentheses)

(1) nylon needle holder

(4) short needle holders
(6) large towel clips
(2) straight mayo scissors
(1) baby Metzenbaum scissors
(1) regular Metzenbaum scissors
(1) nurses scissors
(1) fine iris scissors
(4) #3 knife handles (1Calibrated)
(1) #7 knife handle
(6) #10 blades
(4) #15 blades
(1) short plain forceps
(1) short multitoothed forceps
(2) vascular forceps
(1) fine Cushing forceps
(2) regular Cushing forceps
(1) Freer elevator
(2) Kelly clamps
(2) Ochners
(36) Criles
(12) curved mosquito clamps
(6) straight mosquito clamps
(2) Babcock clamps

(2) Senn rakes

(2) pairs of double skin hooks
(1) pair of single skin hooks
(1) pair vein retraction
(1) adenoid suction
(1) pair Green retractors
(1) double-ended medium-small Richardson retractors
(1) McCabe nerve dissector
(5) bullets (peanuts)
(2) army-navy retractors
(1) fiberoptic headlight unit
(1) bipolar cautery unit
(1) K1 Gardlok dissector
(1) Penrose drain
(1) pack Steri Strips
(1) pack I-Meds

CHAPTER VII
ROLES OF CIRCULATING AND SCRUB NURSE

Roles of a Circulating Nurse

The Circulating nurse is responsible for managing the nursing care of the patient within
the OR and coordinating the needs of the surgical team with other care provider
necessary for completion of surgery,

Observes the surgery and surgical team from broad perspective and assists the team to
create and maintain a safe and comfortable environment for the patient
Asses the patients condition before, during and after the operation to ensure an optimal
outcome for the patient and;
Must be able to anticipate the scrub nurses needs and be able to open sterile packs,
operate machinery and keep accurate records

Duties of a circulating nurse

Before an operation

Checks all equipment for proper functioning such as cautery machine, suction
machine, OR light and OR table

Make sure theater is clean

Arrange furniture according to use

Place a clean sheet, arm board (arm strap) and a pillow on the OR table

Provide a clean kick bucket and pail

Collect necessary stock and equipment

Turn on aircon unit

Help scrub nurse with setting up the theater

Assist with counts and records

During the Induction of Anesthesia

Turn on OR light

Assist the anesthesiologist in positioning the patient

Assist the patient in assuming the position for anesthesia

Anticipate the anesthesiologists needs

After the patient is anesthetized

Reposition the patient per anesthesiologists instruction

Attached anesthesia screen and place the patients arm on the arm boards

Apply restraints on the patient

Expose the area for skin preparation

Catheterize the patient as indicated by the anesthesiologist

Perform skin preparation

During Operation

Remain in theater throughout operation

Focus the OR light every now and then

Connect diatherapy, suction, etc.

Position kick buckets on the operating side

Replenishes and records sponge/ sutures

Ensure the theater door remain closed and patient s dignity is upheld

Watch out for any break in aseptic technique

End of Operation

Assist with final sponge and instruments count

Signs the theater register

Ensures specimen are properly labeled and signed

After an Operation
Hands dressing to the scrub nurse
Helps remove and dispose of drapes
Helps to prepare the patient for the recovery room
Assist the scrub nurse, taking the instrumentations to the service (washroom)

Roles of a Scrub nurse

Works directly with surgeon within the sterile field, passing instruments, sponges
and other items needed during the procedure

Members of the surgical team who prepares and preserves a sterile field in which
the operation can take place

Responsible for the sponge counts, the blades and needles and instruments
check throughout the operation

Has a job requiring anticipation, quick reaction and conscientious observation as

well as knowledge of anatomy and of operative procedures

Duties of a Scrub Nurse

Before an operation

Ensures that the circulating nurse has checked the equipment

Ensures that the theater has been cleaned before the trolley is set

Prepares the instruments and equipment needed in the operation

Uses sterile technique for scrubbing, gowning and gloving

Receives sterile equipment via circulating nurse using sterile technique

Performs initial sponges, instruments and needle count, checks with circulating
nurse

When surgeon arrives after scrubbing

Perform assisted gowning and gloving to the surgeon and assistant surgeon as
soon as they enter the operation suite

Assemble the drapes according to use. Start with towel, towel clips, draw sheet
and then lap sheet. Then, assist in draping the patient aseptically according to
routine procedure

Place blade on the knife handle using needle holder, assemble suction tip and
suction tube

Bring mayo stand and back table near the draped patient after draping is
completed

Secure suction tube and cautery cord with towel clips or allis

Prepares sutures and needles according to use

During an operation

Maintain sterility throughout the procedure

Awareness of the patients safety

Adhere to the policy regarding sponge/ instruments count/ surgical needles

Arrange the instrument on the mayo table and on the back table

Before the Incision Begins

Provide 2 sponges on the operative site prior to incision

Passes the 1st knife for the skin to the surgeon with blade facing downward and
a hemostat to the assistant surgeon

Hand the retractor to the assistant surgeon

Watch the field/ procedure and anticipate the surgeons needs

Pass the instrument in a decisive and positive manner

Watch out for hand signals to ask for instruments and keep instrument as clean
as possible by wiping instrument with moist sponge

Always remove charred tissue from the cautery tip

Notify circulating nurse if you need additional instruments as clear as possible

Keep 2 sponges on the field

Save and care for tissue specimen according to the hospital policy

Remove excess instrument from the sterile field

Adhere and maintain sterile technique and watch for any breaks

End of Operation

Undertake count of sponges and instruments with circulating nurse

Informs the surgeon of count result

Clears away instrument and equipment

After operation: helps to apply dressing

Removes and siposes of drapes

De-gown

Prepares the patient for recovery room

Completes documentation

Hand patient over to recover room

CHAPTER X
BIBLIOGRAPHY

http://www.sparkpeople.com/resource/health_a-z_detail.asp?AZ=468&Page=4
http://en.wikipedia.org/wiki/Thyroidectomy
http://nursingcrib.com/nursing-notes-reviewer/role-of-scrub-nurse/
http://nursingcrib.com/nursing-notes-reviewer/duties-of-scrub-nurse-2/
http://nursingcrib.com/nursing-notes-reviewer/role-of-circulating-nurse/
http://nursingcrib.com/nursing-notes-reviewer/duties-of-scrub-nurse/
http://nurseslabs.com/5-thyroidectomy-nursing-care-plans/
http://www.webmd.com/a-to-z-guides/hyperthyroidism-surgery
http://emedicine.medscape.com/article/121865-treatment