Escolar Documentos
Profissional Documentos
Cultura Documentos
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.
VII.
VIII.
Nursing Management
a.
IX.
Pharmacology
X.
Bibliography
CHAPTER I
INTRODUCTION
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.
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.
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.
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
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
7.
8.
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
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 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.
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.
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.
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.
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 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.
CHAPTER V
DIAGNOSIS
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
CHAPTER VII
ROLES OF CIRCULATING AND SCRUB 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
Before an operation
Checks all equipment for proper functioning such as cautery machine, suction
machine, OR light and OR table
Place a clean sheet, arm board (arm strap) and a pillow on the OR table
Turn on OR light
Attached anesthesia screen and place the patients arm on the arm boards
During Operation
Ensure the theater door remain closed and patient s dignity is upheld
End of Operation
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)
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
Before an operation
Ensures that the theater has been cleaned before the trolley is set
Performs initial sponges, instruments and needle count, checks with circulating
nurse
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
During an operation
Arrange the instrument on the mayo table and on the back table
Passes the 1st knife for the skin to the surgeon with blade facing downward and
a hemostat to the assistant surgeon
Watch out for hand signals to ask for instruments and keep instrument as clean
as possible by wiping instrument with moist sponge
Save and care for tissue specimen according to the hospital policy
Adhere and maintain sterile technique and watch for any breaks
End of Operation
De-gown
Completes documentation
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