IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR

NCM 103 (MEDICAL—SURGICAL NURSING) RLE

CASE STUDY:
UNDERSTANDING
THYROID STORM

SUBMITTED BY:
SANDOT, ALFRIEN B.

SUBMITTED TO:
MR. ZENAS B. PALOMA, RN, MN, MAN, EMT
MS. MARIZ ROCHELLE C. SEDON, RN, MN, MAN

SY: 2019-2020
 Acknowledgment

We, the third year level of Bukidnon State University College of Nursing would
like to extend our gratitude to the following persons who have contributed and
supported us in the Fulfillment of this Case Presentation.

To Our Almighty God, for giving us the knowledge, wisdom, strength, skills, and
the people who made time for our Case Presentation.

We would also like to thank our patient, Mrs. XY for the warm approach she gave
us throughout our assessments and for trusting us with all the information about
her case.

To Sir Zenas B. Paloma, RN, MN, MAN, EMT our Clinical Instructor for the
patience and time he has extended in checking the manuscript, and for sharing
his suggestions, constructive criticism, and for guiding us during our duty in the
Hospital that made every experience remembered, which means so much for the
all of us in his group.

To the Clinical Instructors for the Third Year Level, for guiding us and providing
us with information about Medical Surgical Nursing.

The hospital staff of Bukidnon Provincial Medical Center for helping us during
the times when we were on duty.

And last but not the least, to our ever supportive families who gave us the
encouragement and support to fulfill and achieve our requirements.
 TABLE OF CONTENTS

Acknowledgement
Table of Contents
I. Objectives ....... .................1
II. Introduction....... .................2
III. Data Base....... .................5
 Past Medical History
IV. Anatomy and Physiology....... .................7
V. Assessment....... .................12
 Review of System
VI. Concept Map....... .................21
VII. Medical Management....... .................25
 Ideal
 Actual
 Laboratory and Diagnostic
 Drug Study
VIII. Nursing Management....... .................49
 Theoretical Framework
 Nursing Care Plan
 Ideal
 Actual
IX. Discharged Plan....... .................57
 Methods
X. Prognosis ....... .................58
XI. Doctors Order....... .................61
XII. Journal/Related Readings....... .................64
XIII. Bibliography....... .................74
XIV. Documentation....... .................75

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I. OBJECTIVES

A. General Objective:

At the end of 4 hours case presentation, the learners will be able to gain
knowledge comprehensively about Thyroid Storm and will be able to pick up
some concepts that they believed will be useful in their future studies with the
same case. The learners will also be able to adapt some useful skills such as how
to thoroughly conduct a general assessment of a patient having the same case as
our patient and in utilizing an excellent communication skills which will be useful
for them in developing a positive and competitive attitude which we believed are
vital for creating and maintaining a healthy working relationship in their future
endeavour between their colleague, the hospital staffs, with the patient and their
significant others.

B. Specific Objectives:

At the end of 4 hours case presentation, the learners will be able to:

Knowledge:
1. Have an overview about what to expect in patient having a Thyroid Storm.
2. Learn and discuss in return about the important concepts needed in
conducting a thorough general assessment with a patient having a Thyroid
Storm.
3. Identify several factors that can trigger the disease including the risk factors
and its prevalence worldwide.
4. Learn the different nursing and medical management performed to the
patient with a Thyroid Storm throughout her stay in the hospital as well as
the actual and ideal management of the said disease of which will be
discussed by the presenters later in their case presentation.

Skills:
1. Elucidate the Anatomy and Physiology of Thyroid gland knowledgeably
and how it connects to the said disease.
2. Systematically illustrate the disease process of the Thyroid storm and
identify the organs involved with their corresponding signs and
symptoms.
3. Differentiate Thyroid Storm from other Thyroid gland disorders.
4. Formulate and plan their own nursing care plan based on the data
presented by the presenters.

Attitude:
1. Develop a positive approach towards the presented disease.
2. Establish and maintain rapport towards their colleague and the hospital
staffs, as well as their future patient and their significant others.

1
I. INTRODUCTION
"To keep the body in a good health is a duty, otherwise we shall not be able to keep
our
mind strong and clear"
-BUDDHA

In the field of Nursing, one can encounter a wide variety of disease conditions; and it
is necessary that nurses be equipped with proper knowledge and skills in dealing
with different health states. Thyroid Storm is just one of the conditions which
student nurses will encounter during their exposure in the medical field. We have
chosen this case in order for us to be able to have insight about the said condition.

The thyroid gland is an endocrine gland in your neck; it lies in the front and just
below your Adam’s apple. It is made up of two lobes—the right lobe and the left
lobe, each about the size of a plum cut in half—and these two lobes are joined by a
small bridge of thyroid tissue called the isthmus; the two lobes lie on either side of
your wind-pipe. It makes two hormones that are secreted into the blood stream. One
is called thyroxine, often called T4, which contains four atoms of iodine, and
triiodothyronine which contains three atoms of iodine and is often called T3. In the
cells and tissues of the body the T4 is converted to T3. It is the T3, derived from T4 or
secreted as T3 from the thyroid gland, which is biologically active and influences the
activity of all the cells and tissues of your body; these hormones are necessary for all
the cells in your body to work normally.

The thyroid gland is regulated by the Pituitary gland that lies underneath your brain
in your skull. It senses the levels of thyroid hormones in your blood stream, just as
the thermostat in your living room senses the temperature (British Thyroid
Foundation, 2019). Normally, if the hormone level drops below normal, the pituitary
gland releases a hormone called Thyroid Stimulating Hormone (TSH) to activate the
thyroid gland’s release of more T4 and T3. Similarly, if the hormone level rises above
normal, the pituitary stops secretion of TSH which in turn prevents the thyroid
gland from releasing T4 and T3.

T4, or rather the T3 derived from it, and the T3 secreted directly by the thyroid gland
influences the metabolism of your body cells. In other words, it regulates the speed
with which your body cells work. If too much of the thyroid hormones are secreted,
the body cells work faster than normal, and you have hyperthyroidism. On the other
hand if too little of the thyroid hormone are produced (known as hypothyroidism),
the cells and organs of your body slows down. Thyroid disorders are very common
and tend to mainly occur among women; although anybody—men, teenagers,
children and babies, too—can be affected. About one in 20 people has some kind of
thyroid disorder, which may be temporary or permanent (British Thyroid
Foundation, 2019).

According to the National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), a part of the National Institute of Health (NIH), hyperthyroidism affects
about 1.2 percent of the United States’ population; that is more than 1 person out of
100. Women are also 2 to 10 times more likely to develop hyperthyroidism than men.

2
Graves’ disease is the most common cause of hyperthyroidism. With this disease,
your immune system attacks the thyroid and causes it to make too much thyroid
hormone. The disease affects about 1 in 200 people (NIDDK, 2017). Graves’ disease
affects females more than males by a ratio of 5-10 to 1. The disorder usually develops
during middle age with a peak of incidence of 40-60, but can also affect children,
adolescents, and the elderly. It occurs almost any part of the world and is estimated
to affect 2-3% of the general population (NORD, 2016).

One of the complications of hyperthyroidism is thyroid storm. Thyroid storm is a

life-threatening health condition that is associated with untreated or undertreated
hyperthyroidism. Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-
threatening, hypermetabolic state induced by excessive release of thyroid hormones
(THs) in individuals with thyrotoxicosis (Ross, D., 2019). Thyroid storm may be the
initial presentation of thyrotoxicosis in undiagnosed children, particularly in
neonates. The clinical presentation includes fever, tachycardia, hypertension, and
neurological and GI abnormalities. Hypertension may be followed by congestive
heart failure that is associated with hypotension and shock. Because thyroid storm is
almost invariably fatal if left untreated, rapid diagnosis and aggressive treatment are
critical. Fortunately, this condition is extremely rare in children (Misra, M., 20198).
During thyroid storm, an individual’s heart rate, blood pressure, and body
temperature can soar to dangerously high levels. Without prompt, aggressive
treatment, thyroid storm is often fatal. Thyroid storm is rare. It develops in people
who have hyperthyroidism but aren’t receiving appropriate treatment. This
condition is marked by the extreme overproduction of the two hormones produced
by the thyroid gland. Not all people with hyperthyroidism will develop thyroid
storm (Moore, K., 2017).

In national surveys from the United States and Japan, the incidence of thyroid storm
was 0.57 to 0.76 and 0.20 per 100,000 persons per year, respectively, and 4.8 to 5.6 per
100,000 hospitalized patients per year. In the United States survey, 16 percent of
inpatients with thyrotoxicosis were diagnosed with storm. It may be precipitated by
an acute event such as thyroid or nonthyroidal surgery, trauma, infection, an acute
iodine load, or parturition. In addition to specific therapy directed against the
thyroid, supportive therapy in an intensive care unit (ICU) and recognition and
treatment of any precipitating factors is essential since the mortality rate of thyroid
storm is substantial (10 to 30 percent) (Ross, D., 2019).

3
Overview of our patient

Patient XY is a very accommodating married woman with two kids living in Sumilao
Bukidnon Province who willingly provided us with all the information we needed
for our case study. Year 2016, after she gave birth to her youngest child, her sister
noticed that her eyes had begun to bulge which led them to suspect that she might
have goiter, but never went to a physician/checkup to get an opinion. October last
year, the patient manifested the swelling of the neck, and with her sister finding a
job and being able to finance laboratory, she took a test at German Doctors in
Valencia City, but was unable to get the results. She has been experiencing weight
loss, palpitations, and heat intolerance which are typical symptoms of
hyperthyroidism since then.

With all the information provided by the patient, the group aims to present the
actual management done to improve the condition of our patient including the
Nursing Care Plan specifically formulated for our patient. We also aimed to enhance
our knowledge, skills and attitude to further improve ourselves in our nursing
practice.

4
 II. DATA BASE

DEMOGRAPHIC DATA

Pt. XY is a 30 years old female who presents a case of Thyroid Storm. She was born
on November 20, 1989. She was married but is now separated from her husband,
and lives with her mother and 2 children and resides in Sumilao, Malaybalay,
Bukidnon. She only managed to finish Elementary school and is a stay at home
mom. They are being supported and provided finances by her sister.

CHIEF COMPLAINTS

Difficulty breathing, palpitations and very high fever

HISTORY OF PRESENT ILLNESS

It was 3 years ago, on the fifth of September 2016 after she gave birth to her youngest
child, that they began suspecting that she had goiter when her sister had noticed that
her eyes were bulging. They even thought, back then that it was only because of her
hours of labor but had noticed no changes happening even a month after the day she
gave birth.

When the patient was asked about what she did after they had started suspecting it,
she told us that she did nothing and just relied mostly on medicinal plants and herbs
found around their home, like lagundi, tuba-tuba, and many others, every time she
feels sick. She also added, “Nanglarot baya ako buhok ay, ug usahay kay
makabantay ko na gapaminhod permi ako bagtak na murag naay kuryente.” When
asked about how she was for the past 3 years, she narrated: “Sige lang ko nerbyuson
ay, bisag wala ko gi-buhat. Unya kapoy ug luya permi akong lawas. Nakabantay
pud ko nga mura kog gakurog permi bitaw, unya pas-pas ang pitik sa akong
dughan permi. Igangon kayo sad ko ug nasingtanon mao galisod ko permi ug tulog
sa gabie. Dili man unta ko ingon-ani sauna.”

Due to lack of finances, it was only late last year, on October 12, 2018 did she had
her first check-up at German Doctors in Valencia City. She stated that a blood
sample was taken from her to be examined to confirm whether she really had goiter
or not but could not recall what test exactly was performed. She was then instructed
to return a month or two to get her results and only then will she receive
medications but was unable to return due to financial restraints resulting in her not
being able to confirm if she really had goiter or what exactly type of thyroid disorder
she was suffering to, and not being able to be treated and get proper intervention for
them.

And on November 3, 2019 at 9 am the patient stated: “Nag-pahilot ko kay sakit na

kaayo akong ulo ug kalawasan, ug galisod na gyud ko ug ginhawa tungod sa akong
ubo.” She also added “Pas-pas na kaayo ang pitik sa akong dughan.” When asked of
how she felt after that, she replied “Wala gyud na-wala ug ni samot pa nuon ako gi-
bati ug luya na kaayo ko.” She went home after that and told her mother that she
wants to be admitted. Later that day, at around 10am they then went to Bukidnon
Provincial Medical Hospital via a motorcycle with her mother; they arrived at the

5
hospital 2 hours later and was then received by the nurse on duty at the Emergency
Department at exactly 1:08pm with an initial vital signs of BP: 120/80mmHg, Temp:
38.3, PR: 130bpm, RR: 48cpm. She was assessed by the doctor on duty with the
following findings: mild agitation, high fever, and a history of possible
hyperthyroidism. She was started with an IV of D5LR 1L at 30gtts/min and O 2
inhalation at 3LPM. TSH, FT4 and FT3 to check for the Thyroid hormones (which
was later cancelled), CBC, Blood chem, SGPT/SGOT, BUN, UA, and 12 lead ECG
was ordered, and she be admitted to the ICU.

At about three weeks ago, prior to her admission, the patient verbalized: “Gaka-
hanap akong panan-aw, dili pareha sauna. Sige na pud ko gahilanat pero dili ra
kaayo ko grabe ka-init ato ug nawala ra pud siya.” She was already experiencing
palpitations, diaphoresis, intolerance to heat, tremors, significant weight loss (from
58 to 46, on admission then, 36.8 on assessment), fatigue and weakness, and
difficulty in sleeping for the past few years.

It was on October 24, 2019, 9 days before her date of admission that her copious
cough had started with yellowish sputum. She also had developed a fever but have
said the temperature was not that high (patient recalled her temperature was only
37.7). She was often irritated because she could not sleep due to a shortness of breath
that she thought was only because of her cough. The patient also only took
paracetamol along with some herbal medicine (lagundi) for her fever and cough; she
would only take paracetamol when she was experiencing fever and would stop if the
fever was no longer present.

HISTORY OF PAST ILLNESSES

The patient stated that she had not experienced chicken pox or measles ever since
she was born. She also said that she often experiences allergic reactions, like rashes,
when she eats shellfish.

The patient’s menstrual cycle began at the age of 10, and that it lasts only for about 3
days each; and can use up to 4 pads a day. She also added that she had always had
an irregular period since she started but only 4 years ago did her menstruation cease;
but she has now idea why that is so, and since she lacked the financial resources to
have herself checked by any doctor, she has still no explanation as to why.

FAMILY HISTORY

The patient mentioned that her biological father has Type 1 Diabetes Mellitus (DM)
and her mother is hypertensive. She also mentioned that there was no history of
hyperthyroidism in the family that she knows of and that nobody in the family other
than her has any history of any allergies and other chronic diseases.

6
IV. ANATOMY AND PHYSIOLOGY

The Thyroid Gland

The butterfly shape

Thyroid gland is located
just inferior to the larynx
(voice box). It is
composed of right and
left lateral lobes, one on
either side of the trachea,
that are connected by an
isthmus ,anterior to the
trachea. A small,
pyramidal-shaped lobe
sometimes extends
upward from the
isthmus. The normal
mass of the thyroid is
about 30 g. It is highly
vascularized and
receives 80-120 mL of
blood per minute.

Microscopic spherical
sacs called thyroid
follicles make up most of
the thyroid gland. The
wall of each follicle
consist primarily of cells
called follicular cells,
most of which extend to
the lumen (internal
space) of the follicle. A
basement membrane surrounds each follicle. When the follicular cells are inactive,
their shape is low cuboidal to squamous, but under the influence of TSH they
become active in secretion and range from cuboidal to low columnar in shape. The
follicular cells produce two hormones: thyroxin, which is also called
tetraidothyronine or T4 because it contains four atoms of iodine, and
triiodothyronine or T3, which contains three atoms of iodine. T3 and T4 are also
known as thyroid hormones. A few cells called parafollicular cells or C cells lie
between follicles. They helps regulate calcium homeostasis.

Thyrotoxicosis is a common endocrine condition that may be secondary to a number

of underlying processes.It is the clinical syndrome that results when tissues are
exposed to high levels of circulating thyroid hormone. In most instances,
thyrotoxicosis is due to hyperactivity of the thyroid gland, or hyperthyroidism

7
[Weetman, 2009]. Graves' disease, an autoimmune thyroid disease associated with
thyroid-stimulating hormone

(TSH)-receptor stimulating antibodies, is the most common form of thyrotoxicosis

leading to thyroid storm, whilst other causes of thyrotoxicosis such as toxic
multinodular goitre and toxic adenoma are less-frequent causes.Thyroid storm is
most commonly associated with underlying Graves' disease, although has been
reported with autonomous thyroid nodular disease. Traditionally, the condition was
experienced frequently following thyroidectomy for thyrotoxic state (due to
manipulation of the hyperactive thyroid gland during surgery), but modern
treatments aimed at reducing preoperative thyroid output and hormone stores have
dramatically reduced this complication.

Regardless of the underlying aetiology of thyrotoxicosis, the rare transition to a state

of thyroid storm usually requires a second superimposed insult. Most commonly
this is infection, although trauma, surgery, myocardial infarction (MI), diabetic
ketoacidosis (DKA), pregnancy and parturition have been reported as causes. The
administration of large quantities of exogenous iodine (such as with iodinated
contrast agents or amiodarone) can provide the substrate for significant thyroid
hormone production and secretion if there are areas of autonomous thyroid tissue
within the gland (i.e. Jod-Basedow phenomenon).

8
SYNTHESIS AND SECRETION OF T3 AND T4

IODIDE TRAPPING The thyroid follicular cells trap iodide ions by ACTIVELY
TRANSPORTING them from the blood into the cytosol. As a result, the thyroid
gland normally contains most of the iodide in the body.

SYNTHESIS OF THYROGLOBULIN. While the follicular cells are trapping, they

are also synthesizing the thyroglobulin (TGB), a large glycoprotein that is produced
in the rough endoplasmic reticulum, modified in the Golgi complex and packaged
into secretory vesicles. The vesicles then undergo exocytosis, which release TGB into
lumen of follicle.

OXIDATION OF IODIDE. Some of the amino acid in TGB are tyrosine that will
become iodinated. However negatively charged iodide ions cannot bind tyrosine
until they undergo oxidation (removal of electrons) to iodine. As the iodide ions are
being oxidized, they pass through the membrane into the lumen of the follicle.

IODINATION OF TYROSINE. As iodine molecules form, they react with tyrosine

that are part of thyroglobulin molecules. Binding of one iodine atom yields
monoiodotyrosine (T1), and a second iodination produce diiodotyrosine (T2). The
TGB with attached iodine atoms, a sticky material that accumulates and is stored in
the lumen of the thyroid follicle, is termed colloid.

COUPLING OF T1 AND T2. During the last step in the synthesis of thyroid
hormone, two molecules join to form T4 or one T1 and one T2, join to form T3.

PINOCYTOSIS AND DIGESTION OF COLLOID. Droplets of colloid reenter

follicular cells by pinocytosis and merge with lysosomes. Digestive enzymes in the
lysosomes break down TGB, cleaving off molecules of T3 and T4.

SECRETION OF THYROID HORMONES. Because T3 and T4 are lipid soluble,

they diffuse through the plasma membrane into interstitial fluid and then into the
blood. T4 normally is secreted in greater quantity than T3, but T3 is several times
more potent. Moreover after T4 enters a body cell, most of it is converted to T3 by
removal of one iodine.

TRANSPORT IN THE BLOOD. More than 99% of both the T3 and the T4 combine
with transport proteins in the blood, mainly thyroxin-binding globulin (TGB).

9
Functions of Thyroid Hormones

The thyroid hormones, T3 and T4, are

often referred to as metabolic hormones
because their levels influence the body’s
basal metabolic rate, the amount of
energy used by the body at rest. When
T3 and T4 bind to intracellular receptors
located on the mitochondria, they cause
an increase in nutrient breakdown and
the use of oxygen to produce ATP. In
addition, T3 and T4 initiate the
transcription of genes involved in
glucose oxidation. Although these
mechanisms prompt cells to produce
more ATP, the process is inefficient, and
an abnormally increased level of heat is
released as a byproduct of these
reactions. This so-called calorigenic
effect (calor- = “heat”) raises body
temperature.

Adequate levels of thyroid hormones are

also required for protein synthesis and
for fetal and childhood tissue
development and growth. They are
especially critical for normal
development of the nervous system both
in utero and in early childhood, and they
continue to support neurological
function in adults. As noted earlier, these
thyroid hormones have a complex
interrelationship with reproductive
hormones, and deficiencies can influence
libido, fertility, and other aspects of
reproductive function. Finally, thyroid
hormones increase the body’s sensitivity
to catecholamine’s (epinephrine and
norepinephrine) from the adrenal
medulla by up regulation of receptors in
the blood vessels. When levels of T3 and T4 hormones are excessive, this effect
accelerates the heart rate, strengthens the heartbeat, and increases blood pressure.
Because thyroid hormones regulate metabolism, heat production, protein synthesis,
and many other body functions, thyroid disorders can have severe and widespread
consequences.

10
In areas of the world with access to iodized salt, dietary deficiency is rare. Instead,
inflammation of the thyroid gland is the more common cause of low blood levels of
thyroid hormones called hypothyroidism, the condition is characterized by a low
metabolic rate, weight gain, cold extremities, constipation, reduced libido, menstrual
irregularities, and reduced mental activity. In contrast, hyperthyroidism an
abnormally elevated blood level of thyroid hormones is often caused by a pituitary
or thyroid tumor. In Graves’’ disease, the hyperthyroid state results from an
autoimmune reaction in which antibodies overstimulate the follicle cells of the
thyroid gland. Hyperthyroidism can lead to an increased metabolic rate, excessive
body heat and sweating, diarrhea, weight loss, tremors, and increased heart rate.
The person’s eyes may bulge (called exophthalmos) as antibodies produce
inflammation in the soft tissues of the orbits. The person may also develop a goiter.

CONTROL OF THROID HORMONE SECRETION

Thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid-

stimulating hormone (TSH) from the anterior pituitary stimulate synthesis and
release of thyroid hormones as:

Low blood levels of T3 and T4 or low metabolic rate stimulate the hypothalamus to
secret TRH.

TRH enters the hypophyseal portal veins and flows t9 the anterior pituitary, where it
stimulates thyrotrophs to secrete TSH.

TSH stimulates virtually all aspects of thyroid follicular cell activity, including
iodide trapping, hormone synthesis and secretion and in growth of follicular cells.

The thyroid follicular cells release T3 and T4 into the blood until the metabolic rate
returns to normal.

An elevated level of T3 inhibit release of TRH and TSH (negative feedback inhibition
)

Conditions that increase ATP demand – a cold environment, hypoglycemia, high

altitude and pregnancy – also increase the secretion of the thyroid hormones.

11
 Normal Laboratory Values
(www.endocrineweb.com)
Serum thyroxine T4 4.6-12 ug/dl
Free Thyroxine 0.7-1.9 ng/dl
Free Thyroxine index 4-11
Serum Triiodothyronine 80-180 ng/dl
Free Triiodothyronine l 230-619 pg/d
Free T3 Index 80-180
Serum thyrotropin 0.5-6 uU/ml
Thyroxine-binding globulin 12-20 ug/dl T4 +1.8 ugm
Thyroid hormone binding ratio 0.9-1.1
TRH stimulation test Peak 9-30 uIU/ml at 20-30 min

CALCITONIN

The hormone produce by the parafollicular cells of the thyroid gland is calcitonin
(CT). CT can decrease the level of calcium in the blood by inhibiting the action of
osteoclast, the cells feedback system.

When its blood is high, calcitonin lowers the amount of blood calcium and
phosphate by inhibiting bone resorption (breakdown of bone extracellular matrix)
by osteoclast and by accelerating uptake of calcium and phosphate into bone
extracellular matrix. Miacalcin, a calcitonin extract derived from salmon that is ten
times more potent than human calcitonin, is prescribed to treat osteoporosis.

12
 VIII. MEDICAL MANAGEMENT

Ideal Actual
 Radioactive Iodine therapy The patient had only medications to take
Overactive thyroid cells consume radioactive iodine such as antithyroid medications such as:
by the mouth. Some cells are damaged by iodine,  PTU (Propylthiouracil) 4 tablets
causing the thyroid to shrink and the levels of every 4hrs orally
thyroid hormones to fall. This usually results in  Methimazole 5mg 3 times a day
permanent thyroid destruction, which will cure orally.
hyperthyroidism. For the rest of their lives, most
patients receiving this treatment have to take Beta blocker such as:
thyroid hormone drugs to maintain normal levels of  Propanolol 4mg 1 tablet every 8hrs
hormones. orally
Some patients at high risk for complications of
hyperthyroidism may need pretreatment with Steroid such as:
antithyroid medications. Methimazole is given 4 to  Hydrocortisone 100mg 1 tablet
6 weeks prior to administration of radioactive every 8hrs IVTT
iodine. The antithyroid medications are stopped 3
days before and restarted 3 days after administering and Antibiotics such as:
radioactive iodine and then tapered over 4 to 6  Cefixime 1g every 8hrs IVTT
weeks.  Levofloxacin 750mg 1 tablet onc3
 Antithyroid medications daily orally.
Methimazole (Tapazole) or propylthioracil (PTU): The patient hasn’t undergone radioactive
these drugs block the hormone-making capacity of iodine therapy and surgery. The patient
the thyroid. They offer quick thyroid control. started PTU on November 2 along with
 Surgery Propanolol, Dexamethasone,
During surgery (thyroidectomy), the doctor can Paracetamol, Cefixime and N-
remove the thyroid gland. Typically this will induce acetylcysteine. IVF of D5LR
hypothyroidism. Thyroid supplements must be 30gtts/mins administered upon the
taken by patients with thyroidectomy to maintain admission.
hormone levels stable.

Source: Hinkle, J. L. & Cheever, K. H. (2014). Brunner

& Suddarth's textbook of medical-surgical nursing
(Edition 13.). Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.

LABORATORY/ DIAGNOSTIC RESULTS

Name: Patient XY

LABORATORY/ DIAGNOSTIC RESULTS

Name: Patient XY

13
Date: November 03, 2019

CHEST PA

FINDINGS:

Perihilar, peribronchial opacities are appreciated.

Tracheal air column is at the midline.

The heart is not enlarged.

Both hemidiaphragms and costophrenic sulci are intact.

The rest of the included osseous structures are unremarkable.

IMPRESSION:

 PNEUMONITIS.

Date: November 06, 2019

Exam: THYROID

14
 ULTRASOUND OPINION REPORT

HISTORY: Thyroid storm

Right and left thyroid lobes measure about 6.1 cm x 2.9 cm x 2.7 cm

(L x AP x W) and 5.6 cm x 2.3 cm x 2.8 cm, respectively, with uniformly hypoechoic

parenchyma. Increased vascular flow is noted on color Doppler. No focal lesions
seen.

Thyroid isthmus is 0.8 cm think.

No enlarged cervical lymph nodes seen.

IMPRESSION:

DIFFUSE THYROID ENLARGEMENT WITH HYPERVASCULAR PATTERN

CORRELATION WITH CLINICAL AND LABORATORYPARAMETERS
SUGGESTED.

Date: 11/03/2019
HEMATOLOGY

15
 DATE Normal
Parameters Result Significance
ORDERED Values
NOVEMBE COMPLETE
R BLOOD
03, 2019 COUNT
The patient was ordered to check
her WBC to look for possible
WBC 18.3 5-10
bacterial or viral infection.
Increased WBC signifies infection.
RBC 4.55 3.69-5.13 Normal
Hemoglobin was taken to measure
its levels in the blood. Low
Hemoglobi
11.4 11.7-14.5 hemoglobin levels indicates tissue
n
hypoxia due to the hypermetabolic
state of the body.
Hematocrit 35.5 34.1-44.3 Normal
MCV is to determine the condition
of blood components. Decreased
MCV 78.0 81.5-96.7
MCV indicates problem in RBC due
to cell dehydration.
MCH is to check the mass of her
hemoglobin. Decreased of
MCH 25.1 26.5-33.5 hemoglobin due an overactive
thyroid results in decreased in
MCH.
MCHC 32.1 31.9-39.5 Normal
Platelet
203 144-372 Normal
Count
Differential
Count:
Neutrophil 76 43.4-76.2 Normal
Lymphocyt
20 17.4-46.2 Normal
e
Monocyte 4 4.50-10.50 It decreases due to an infection.
Eosinophil
Basophil
Date: 11/06/2019 06:34 AM
Ward: IMCU

16
 HEMATOLOGY
DATE Normal
Parameters Result Significance
ORDERED Values
NOVEMBE COMPLETE
R BLOOD
06, 2019 COUNT
This was checked to monitor
WBC 13.3 5-10 the effectivity of the medical
management.
RBC 4.47 3.69-5.13 Normal
To determine the efficacy of
hemoglobin after medical
Hemoglobin 11.4 11.7-14.5 management. The result
indicates slight tissue
hypoxia.
Hematocrit 34.1 34.1-44.3 Normal
To monitor if the medical
MCV 76.0 81.5-96.7 intervention is effective to
restore balance of MCV
To monitor if the medical
MCH 25.4 26.5-33.5 intervention is effective to
restore balance of MCH.
To monitor the
concentration of
hemoglobin. Decreased
MCHC 31.4 31.9-39.5
levels of MCHC signifies
lack of hemoglobin and
hypoxia is still present.
Platelet Count 204 144-372 Normal
Differential
Count:
Neutrophil 64 43.4-76.2 Normal
Lymphocyte 36 17.4-46.2 Normal

17
 Date: 11/06/2019 03:39 PM
Ward: ICU

HEMATOLOGY
Norma
DATE
Parameters Result l Significance
ORDERED
Values
NOVEMBE COMPLET
R E BLOOD
06, 2019 COUNT
This was checked to determine if
WBC 12.1 5-10
medical management was effective
3.69-
RBC 4.47 Normal
5.13
To determine the efficacy of
Hemoglobi 11.7- hemoglobin after medical management.
11.2
n 14.5 The result indicates slight tissue
dehydration.
34.1-
Hematocrit 35.8 Normal
44.3
81.5- To continue monitor the restoration of
MCV 80.1
96.7 balance in MCV.
26.5- To continue monitor the restoration of
MCH 25.1
33.5 balance in MCH.
To continue monitor the concentration
31.9- of hemoglobin. Decreased levels of
MCHC 31.3
39.5 MCHC signifies lack of hemoglobin and
hypoxia is still present.
Platelet 144-
207 Normal
Count 372
Differential
Count:
43.4-
Neutrophil 65 Normal
76.2
Lymphocyt 17.4-
35 Normal
e 46.2

18
DATE: November 4, 2019

URINALYSIS
PHYSICAL RESULT NORMAL SIGNIFICANCE

Color Dark yellow Varying Highly concentrated due to

degrees dehydration of the cells.

Transparency Slightly Clear The result indicates infection

cloudy
pH 5.0 Usually Acidic Acidic

Specific 1.031 1.000 -1.030 Mild dehydration

Gravity

CHEMICAL RESULT NORMAL MICROSCOPIC RESULT

CELLS
Protein Negative Negative

Sugar Negative Negative Pus Cells /hpf

Ketones Negative Red Blood Cells 0-5/hpf

Blood Negative Epithelial Cells 10-15

Bilirubin Negative Bacteria Moderate

Urobilinogen 0.1- Mucous Threads

1.0mg/dL

Leukocytes Negative Amorphous Few

Urates

Nitrite Negative Amorphous

Phosphate

Others:

19
 MICROSCOPIC

/ NEGATIVE FOR ANY INTESTINAL PARASITIC OVA

Bacteria
DATE: November 4, 2019 MODERATE/LPF

FECALYSIS

PHYSICAL RESULT NORMAL SIGNIFICANCE

Color Brown Yellow-Brown Normal

Character Loose Soft – Formed Due to the body’s rapid

acceleration of metabolism
MISCELLANEOUS

Occult Blood Test Negative

20
 DATE: November 5, 2019

FECALYSIS

PHYSICAL RESULT NORMAL SIGNIFICANCE

Color Brown Yellow-Brown Normal

Character Formed Soft- Formed Normal

MISCELLANEOUS

Occult Blood Test Negative

MICROSCOPIC

/ NEGATIVE FOR ANY INTESTINAL PARASITIC OVA

Pus cells 0-1/HPF

Red blood cells 0-1/HPF

Bacteria Plenty/LPF

21
 Date: 11/04/2019
Room/Ward: ICCU

CLINICAL CHEMISTRY
TEST RESULT UNIT SIGNIFICANCE
REFERENCE
VALUES
Blood Urea 7.2 mg/dL 8.0-26.0 BUN was ordered to check the
Nitrogen L efficacy of the liver by measuring
the amount of nitrogen in the
blood. Decreased levels of BUN
indicates liver malfunctioning
due to extreme secretion of
thyroid gland.
Creatinine 0.4 mg/dL 0.5-1.2 This is to determine if the kidney
L is working properly. Low levels
of creatinine indicates kidney
malfunction.
SGOT (AST) 40 U/L 0-31 Increased levels of SGOT is due
H to hyperthyroidism that results
in fast conversions of T4-T3 that
causes liver to overworked and
damaged.
SODIUM 145.3 mmol/L 135.0-155.0 Normal
POTASSIUM 3.22 mmol/L 3.60-5.50 Decreased in potassium level is
L due to the hypermetabolic
activity of the body that causes
diarrhea and loss of potassium.
CHLORIDE 101.6 mmol/L 96.0-106.0 Normal
ENZYMES
SGPT (ALT) 41 U/L 0-32 Increased levels of SGPT
H indicates problem in the liver due
to the abnormal function of the
thyroid gland.

22
 Date: 11/07/2019
Room/Ward: Med

CLINICAL CHEMISTRY

REFERENCE VALUES
TEST RESULT CONVENTIONAL S.I UNITS
UNIT
ELECTROLYTES:
SODIUM 144.7 135-155 mEq/L 135-155
mmol/L
POTASSIUM 3.22 3.6-5.5 mEq/L 3.6-5.5
mEq/L
CHLORIDE 99.3 96-106 mEq/L 96-106
mEq/L

23
Date: 11/03/2019
Room/Ward: Med

COAGULATION TEST

PTPA RESULT Reference range

Patient 13.0 11.4-14.2 sec

Control 13.5

% Activity 100.0 100 %

INR 0.95 0.9-1.2

APTT RESULT Reference range

Patient *** 25-35 sec

Control ***

R *** 100 %

24
25
55
 IX. DISCHARGE PLAN

 Encouraged patient to follow and take the prescribed medications at the

right dose and timing to promote healing and to prevent further
complications.
 Instruct patient to take oral medicationCefixime 1 gram every 8 hours to
treat her infection.
 Advise patient to take drug exactly as prescribed and to continue to
take full amount prescribed even when feels better.
 Instruct to report any signs of allergic reactions and anaphylaxis
immediately.
 Instruct patient to take oral medication Propanolol 40 mg 1 tab every 8
hours.
 Instruct patient to comply with drug regimen: abrupt discontinuation
of antihypertensive drug may cause rebound hypertension.
 Encourage patient to increase fluid intake.
 Instruct patient to take oral medication Methimazole 5 mg 2 tab three times
a day.
Medication:  Instruct patient to take drug with meals to decrease GI symptoms
 Advise patient about the effects of iodine and its presence in iodized
salt, shellfish and OTC cough medicines
 Emphasize the importance of drug compliance, abruptly stopping the
antithyroid drug could bring on a thyroid crisis.
 Teach patient the signs and symptoms of hypothyroidism: lethargy,
puffy eyelids and face, thick tongue, low speech with hoarseness, lack
of perspiration and slow pulse. Hypothyroidism may result to
treatment of hyperthyroidism.
 Instruct patient to take oral medication Potassium chloride 600 mg 1 tablet
three times a day.
 Make sure the powder is completely dissolve before giving
 Instruct patient to take drug with full glass of water of fruit juice to
lessen GI distress.
 Teach patient about Deep Breathing Exercises to reduce apprehension and
promotes proper oxygenation.
 Teach patient about proper coughing such as performing DBE then suddenly
Exercise: coughing upon exhaling to excrete secretions retained in lungs and to avoid
wrong coughing.
 Instruct patient in extraocular muscle exercises to improve circulation
and maintains mobility of the eyelids.

56
  Instruct patient to elevate the head of the bed to promote lung expansion.
 Encourage chair rest or bedrest to prevent increase metabolic and circulatory
demands, which may potentiate cardiac failure.
 Instruct significant others to provide comfort measures such as touch
therapy or massage, or cool showers to promote relaxation to the patient.
Treatment:  Encourage the use of dark glasses when awake and taping the eyelids shut
during sleep as needed.
 Encourage patient to do diversional activities that are calming such as
reading, listening to music, and watching television to reduce anxiety.

 Instruct patient to comeback one week after the discharge for follow up
checkup.
Outpatient  Encouraged patient to visit their Barangay Health Center and have check-up
(checkup) and information drive
 Encourage patient to have yearly physical exam
 Instruct patient to consult gynecologist for menstrual cycle disturbance.
 Encourage patient to eat and increase the number of meals and snacks.
Suggest high-calorie foods that are easily digested such as avocados, sweet
potatoes, milk, beans and etc.
 Instruct patient to avoid fluids that cause diarrhea and foods that increase
peristalsis such as fiber-rich fruits like oranges, apples, bananas and
strawberries.
 Instruct patient to take the following diet:
 Low iodine diet - non-iodized salt, oats, honey, fresh fruits, eggwhites, etc.
Diet:
 Vitamins and minerals:
 Iron (dried beans, red meat, whole grains)
 Selenium (poultry, rice)
 Zinc (beef, mushrooms)
 Calcium and vitamin D (Spinach, okra, fatty fish)
 Healthy fats (olive oil, coconut oil)
 Spices (turmeric, black pepper)

57
 XI. PROGNOSIS
VERY
CRITERIA EXCELLENT GOOD FAIR POOR JUSTIFICATION
POOR
Physiologic The patient overall
Response of
condition is improving.
the body to
√ She’s now free from any
the
disease pain and can rest
process comfortably.

Relief of The patient is slightly

symptoms tachycardic. She’s easily
associated agitated and worried.
√
with the Her fever was relieved
disease and had a normalized
condition breathing pattern.

Ability of
the patient
The patient can now
to perform
perform activities of
activities of
√ daily living
daily living
independently
during
throughout the day.
hospital
stay

The patient complies

well with the
Patients medication therapy
compliance given to her by
to √ healthcare provider.
medication Symptoms that are
and therapy manifested are easily
relieved and it improves
the patient’s condition

Ability of √ Patient can take

the patient medication by herself.
and family Patient and significant
to follow others complies with the
through
medication and
with the
therapeutic regimen.
medication
and

58
therapeutic
regimen
The patient and
significant others give
Patient and attention to all
Family’s
instructions of a
response to
√ healthcare provider.
health Both perform all
teachings necessary advises to
improve the patient’s
condition.
The Patient is well
Patients oriented with her
perception condition. There’s
of their √
willingness in her to
condition follow instructions
given.
Patient experienced
problem in sleeping
during hospitalization
Adequacy
due to the cold and
of rest and √
sleep warm environment that
usually results in
excessive sweating and
uncomfortable feeling
Patient The patient interacts
social well with her family
interaction and healthcare provider.
and √
She’s able to verbalize
communicat her feelings and
ion opinions.

FORMULA:
(Total number of client’s response) / 45 (overall total of criteria) x 100 =
total

Frequency X Total
Excellent 5 5 25
Good 1 4 4
Fair 3 3 9
Poor 0 2 0
Very Poor 0 1 0

59
 Total Percentage (35/45) x 100 = 84.44 %

INTERPRETATION CRITERIA:

Excellent 81 – 100 %
Good 61 – 80 %
Fair 41 – 60 %
Poor 21 – 40 %
Very Poor 1 – 20 %
Source: https://journal.chestnet.org/article/S00123692(16)35422-8/pdf
INTERPRETATION: EXCELLENT
 Patient has a promising potential to meet expected outcomes of therapy due to her
motivation to return to her activity of daily living, and overall good physical
conditioning despite of her current illness.
 The symptoms manifested were properly treated with therapeutic medications and
is now showing improvement.
 The patient’s appetite is back to normal. She has no problem with regards to her diet
and her elimination pattern is already back to its usual pattern prior to her illness.
She was able to drink 8-10 glasses a day as well and reports no problem with urine
secretion.
 Patient is now able to moved independently throughout the day.
 Patient gets adequate rest but not continuously because of minimal interruptions
due to the environment in the ward.

60
XII. DOCTOR’S ORDER
 Please admit to ICU
 Secure consent to care of life
 No added salt in diet
 with IVF of D5LR 3L at 30 gtts/min
 Diagnostic exams:
11/ 03/ 19  TSH, T4, T3
1:08 PM  Chest xray, Serum sodium, Serum potassium
Burch Wartofsky  Creatinine, SGPT, SGOT, BUN
Diagnostic criteria  For xray PA
38.3 10  12 lead ECG
Mild agitation 10  Urinalysis
GI- Hepa 10  Treatment: give patient with PTU 5g12 tabs and then 4
HF 130 20 tabs every 6 hours
A1 0  Start propanollol 40 gram Thrice a day
Precipitant  Dexamethasone 5g every 8 hrs
history _10_  Paracetamol 500 gram every 4 hrs with temp of 38
60  Start cefixime 1 gram IV every 8 hours After Negative Skin
Test
 N acetylcysteine 600 grams with 150 cc water once daily
 02 at 1-3 lpm via nasal cannula
 Intake and output every shift
 Refer accordingly
11/ 03/ 19 Receiving notes
4:22 PM  S 1: 1 week prior to admission, onset of on and off fever ----
120/80 with cough productive of yellowish sputum
130  2: 3 years prior to admission, noted anterior neck mass,
48 associated with exophthalmos, palpitations and weight
38.3 loss. No consult & meds
98%  (+) vomiting, post-tussive (-)LBM
 O: Awake, irritable, febrile in respiration distress
AS, PPC
ECE, Crackels
AP, Tachycardic with RR, No murmur
Flabby, Soft, Non tender
(-) Bipedal edema
 A: Thyroid storm
Hyperthyroidism
 P Diagnostics: Repeat 12 Lead ECG at 10 PM today follow-
up labs (Protime, Ultrasound thyroid, ABG)
Therapeutics:
 Paracetamol 500 mg 1 tab every 4 hrsprn for
temperature higher than 37
 PTU 4 tabs per orem every 4 hrs
 Shift dexamethasone to hydrocortisone 100 mg every 8
hrs

61
  Propranolol 40 mg 1 tab every 8 hrs with bp precaution
 Cefixime 1 g IV stat, then every 8 hrs ANST
 Levofloxacin 750 mg 1 tab stat, then once daily
 N-acetylcysteine 600 mg 1 tab + 75cc H20 once daily
 Omeprazole 40 mg per orem once daily 30 minutes
prebreakfast
 O2 support at 2lpm via nasal cannula
 Head of bed 45
 For ICU admission
 VS every 1 hr taken 1 full minutes
 Intake & output every 8 hrs
 Refer accordingly
11/ 04/ 19  Continue medication
9:47 AM  IVF of D5 NM 2 Liters at 25 drops/minute
100/60  For transfer to IMCU
HR: 132
5:4
5 PM
RR: 62
T: 37.0
11/ 05/ 19 IVFF: D5NM 1 Liter at 25
9:00 AM drops/minutes
120/70 Diagnostics: TSH
HR: 105 FT4
RR: 26 UTZ- Thyroid
T: 36.1  Therapeutics:
O2: 99 %  KCL 600 mg 1 tab thrice a day
Positive Febrile  Increase Propanolol 40 mg 1 tablet every 6 hours
Episode  Continue medications
Decrease SOB  Hydrocortison 50 mg Intravenously every 8 hours
Negative times 3 more doses then discontinue
vomiting  Vital signs every hour
Awake, NIRD  Intake and Output every 8 hours
ECE, Crackles
 Refer accordingly
Unchanged
AP, Tachycardic
With RN
11/ 06/ 198:36  Diagnosis for 2Decho
AM  Still for Ultrasound of the neck
120/ 70  Repeat Complete Blood Count, PC
Day 3 ICU  Repeat Na, Potassium
admission  IVF D5 NSS at Keep Vein Open rate then shift to heplock
HR: 73  For compliance of medications
Positive tremors  Transfer to ward
Intake: 3,800  Please institutetime out
Output: 4,500
Awake,

62
 comfortable
Negative Bowel
Movement
Negative Fever
11/ 07/ 199:20 PTU 3 tabs thrice a day
AM Continue medications

11/ 08/ 19 Repeat CBC today

9:30 AM Continue meds

63
XIII. JOURNAL READINGS
Thyroid Storm

Clinical Recognition

Thyroid (or thyrotoxic) storm is an acute, life-threatening syndrome due to an exacerbation

of thyrotoxicosis. It is now an infrequent condition because of earlier diagnosis and
treatment of thyrotoxicosis and better pre- and postoperative medical management. The
incidence of thyroid storm currently may be as low as 0.2 cases/100,000 population.
Thyroid storm may be precipitated by a number of factors including intercurrent illness,
especially infections. Pneumonia, upper respiratory tract infection, enteric infections, or any
other infection can precipitate thyroid storm. Thyroid storm in the past most frequently
occurred after surgery, but this is now unusual. Occasionally it occurs as a manifestation of
untreated or partially treated thyrotoxicosis without another apparent precipitating factor.
In the Japanese experience approximately 20% of patients developed thyroid storm before
they received anti-thyroid drug treatment. Finally, if patients are not compliant with anti-
thyroid medications thyroid storm may occur and this is a relatively common cause.
Thyroid storm is typically associated with Graves' disease, but it may occur in patients with
toxic nodular goiter or any other cause of thyrotoxicosis.
Classic features of thyroid storm include fever, marked tachycardia, heart failure, tremor,
nausea and vomiting, diarrhea, dehydration, restlessness, extreme agitation, delirium or
coma. Fever is typical and may be higher than 105.8 F (41 C). Patients may present with a
true psychosis or a marked deterioration of previously abnormal behavior. Rarely thyroid
storm takes a strikingly different form, called apathetic storm, with extreme weakness,
emotional apathy, confusion, and absent or low fever.

Signs and symptoms of decompensation in organ systems may be present. Delirium

is one example. Congestive heart failure may also occur, with peripheral edema,
congestive hepatomegaly, and respiratory distress. Marked sinus tachycardia or
tachyarrhythmia, such as atrial fibrillation, are common. Liver damage and jaundice
may result from congestive heart failure or the direct action of thyroid hormone on
the liver. Fever and vomiting may produce dehydration and prerenal azotemia.
Abdominal pain may be a prominent feature. The clinical picture may be masked
by a secondary infection such as pneumonia, a viral infection, or infection of the
upper respiratory tract.

Death from thyroid storm is not as common as in the past if it is promptly recognized and
aggressively treated in an intensive care unit, but is still approximately 10-25%. In recent
nationwide studies from Japan the mortality rate was >10%. Death may be from cardiac
failure, shock, hyperthermia, multiple organ failure, or other complications. Additionally,
even when patients survive, some have irreversible damage including brain damage,
disuse atrophy, cerebrovascular disease, renal insufficiency, and psychosis.

64
Pathophysiology

Thyroid storm classically began a few hours after thyroidectomy performed on a patient
prepared for surgery by potassium iodide alone. Many such patients were not euthyroid
and would not be considered appropriately prepared for surgery by current standards.
Exacerbation of thyrotoxicosis is still seen in patients sent to surgery before adequate
preparation, but it is unusual in the anti-thyroid drug-controlled patient. Thyroid storm
occasionally occurs in patients operated on for some other illness while severely thyrotoxic.
Severe exacerbation of thyrotoxicosis is rarely seen following 131-I therapy for
hyperthyroidism; but some of these exacerbations may be defined as thyroid storm.
Thyroid storm appears most commonly following infection, which seems to induce an
escape from control of thyrotoxicosis. Pneumonia, upper respiratory tract infections, enteric
infections, or any other infection can cause this condition. Interestingly, serum free T4
concentrations were higher in patients with thyroid storm than in those with
uncomplicated thyrotoxicosis, while serum total T4 levels did not differ in the two groups,
suggesting that events like infections may decrease serum binding of T4 and cause a greater
increase in free T4 responsible for storm occurrence. Another common cause of thyroid
storm is a hyperthyroid patient suddenly stopping their anti-thyroid drugs.

DX and diff

Diagnosis of thyroid storm is made on clinical grounds and involves the usual diagnostic
measures for thyrotoxicosis. A history of hyperthyroidism or physical findings of an
enlarged thyroid or hyperthyroid eye findings is helpful in suggesting the diagnosis. The
central features are thyrotoxicosis, abnormal CNS function, fever, tachycardia (usually
above 130bpm), GI tract symptoms, and evidence of impending or present CHF. There are
no distinctive laboratory abnormalities. Free T4 and, if possible, free T3 should be
measured. Note that T3 levels may be markedly reduced in relation to the severity of the
illness, as part of the associated “non-thyroidal illness syndrome”. As expected, TSH levels
are suppressed. Electrolytes, blood urea nitrogen (BUN), blood sugar, liver function tests,
and plasma cortisol should be monitored. While the diagnosis of thyroid storm remains
largely a matter of clinical judgment, there are two scales for assessing the severity of
hyperthyroidism and determining the likelihood of thyroid storm. Recognize that these
scoring systems are just guidelines and clinical judgement is still crucial. Data comparing
these two diagnostic systems suggest an overall agreement, but a tendency toward
underdiagnosis using the Japanese criteria. Unfortunately, there are no unique laboratory
abnormalities that facilitate the diagnosis of thyroid storm.

Therapy

Thyroid storm is a medical emergency that has to be recognized and treated

immediately. Admission to an intensive care unit is usually required. Besides
treatment for thyroid storm it is essential to treat precipitating factors such as
infections. As would be expected given the rare occurrence of thyroid storm there
are very few randomized controlled treatment trials and therefore much of what is
recommended is based on expert opinion.

It should be noted that if any possibility is present that orally given drugs will not be
appropriately absorbed (e.g. due to stomach distention, vomiting, diarrhea or severe heart
failure), the intravenous route should be used. If the thyrotoxic patient is untreated, an
antithyroid drug should be given. PTU, 500–1000mg load, then 250mg every 4 hours,
should be used if possible, rather than methimazole, since PTU also prevents peripheral

65
conversion of T4 to T3, thus it may more rapidly reduce circulating T3 levels. Methimazole
(60–80mg/day) can be given orally, or if necessary, the pure compound can be made up in
a 10 mg/ml solution for parenteral administration. Methimazole is also absorbed when
given rectally in a suppository. After initial stabilization, one should taper the dose and
treat with Methimazole if PTU was started at the beginning as the safety profile of
Methimazole is superior. If the thyroid storm is due to thyroiditis neither PTU not
Methimazole will be effective and should not be used.
An hour after thiocarbamide has been given, iodide should be administered. A dosage of
250 mg every 6 hours is more than sufficient. The iodine is given after PTU or Methimazole
because the iodine could stimulate thyroid hormone synthesis. Unless congestive heart
failure contraindicates it, propranolol or other beta-blocking agents should be given at
once, orally or parenterally, depending on the patient's clinical status. Beta-blocking agents
control tachycardia, restlessness, and other symptoms. Additionally, propranolol inhibits
type 1 deiodinase decreasing the conversion of T4 to T3. Probably lower doses should be
administered initially, since administration of beta-blockers to patients with severe
thyrotoxicosis has been associated with vascular collapse. Esmolol, a short-acting beta
blocker, at a loading dose of 250 mcg/kg to 500 mcg/kg followed by 50 mcg/kg to 100
mcg/kg/minute can be used in an ICU setting. For patients with reactive airway disease, a
cardioselective beta blocker like atenolol or metoprolol can be employed.
Permanent correction of the thyrotoxicosis by either 131-I or thyroidectomy should be
deferred until euthyroidism is restored. Other supporting measures should fully be
exploited, including sedation, oxygen, treatment for tachycardia or congestive heart failure,
rehydration, multivitamins, occasionally supportive transfusions, and cooling the patient to
lower body temperature down. Antibiotics may be given on the presumption of infection
while results of cultures are awaited.
The adrenal gland may be limited in its ability to increase steroid production during
thyrotoxicosis. Therefore, hydrocortisone (100-300 mg/day) or dexamethasone (2mg every
6 hours) or its equivalent should be given. The dose can rapidly be reduced when the acute
process subsides. Pharmacological doses of glucocorticoids (2 mg dexamethasone every 6
h) acutely depress serum T3 levels by reducing T4 to T3 conversion. This effect of
glucocorticoids is beneficial in thyroid storm and supports their routine use in this clinical
setting.

Usually rehydration, repletion of electrolytes, treatment of concomitant disease,

such as infection, and specific agents (antithyroid drugs, iodine, propranolol, and
corticosteroids) produce a marked improvement within 24 hours. A variety of
additional approaches have been reported and may be used if the response to
standard treatments is not sufficient. For example, oral gallbladder contrast agents
such as ipodate and iopanoic acid in doses of 1-2 g, which inhibit peripheral T4 to
T3 conversion, may have value. Plasmapheresis can remove circulating thyroid
hormone and rapidly decrease thyroid hormone levels. Orally administered bile
acid sequestrants (20-30g/day Colestipol-HCl or Cholestyramine) can trap thyroid
hormone in the intestine and prevent recirculation. In most cases these therapies are
not required but in the occasion patient that does not respond rapidly to initial
therapy these modalities can be effective. Finally, in rare situations where medical
therapy is ineffective or the patient develops side effects and contraindications to
the available therapies thyroid surgery may be necessary.

Follow up

66
Antithyroid treatment should be continued until euthyroidism is achieved, when a
decision regarding definitive treatment of the hyperthyroidism with antithyroid
drugs, surgery, or 131-I therapy can be made. Rarely urgent thyroidectomy is
performed with antithyroid drugs, iodide, and beta blocker preparation.

Prevention of thyroid storm is key and involves recognizing and actively avoiding
common precipitants, educating patients about avoiding abrupt discontinuation of
anti-thyroid drugs, and ensuring that patients are euthyroid prior to elective
surgery and labor and delivery.

REFLECTION

Thyroid (or thyrotoxic) storm is an acute, life-threatening syndrome due to an

exacerbation of thyrotoxicosis and it is precipitated of the factors of such diseased
or having infection and complicated the thyroid to having pneumonia, upper
respiratory tract infection, enteric infections, or any other infection can precipitate
thyroid storm or it can occur after surgery, unthreated hyperthyriodism or abrupt
withdrawal of medications. If the patient is not aware about her hyperthyroidism ,
she suffered thyroid storm soon or if left untreated classic features of thyroid storm
include fever, marked tachycardia, heart failure, tremor, nausea and vomiting,
diarrhea, dehydration, restlessness, extreme agitation, delirium or coma are the
common signs and symptoms of hyperthyroidism.Signs and symptoms
decompensated in different organs and associated of congestive heart failure ,
peripheral edema, congestive hepatomegaly .Disorder in thyroid also have the
impact of the energy level and mood , anxiety due to having the diseased that
causing irritability and agitation because over secretions of thyroid hormones.

In the philippines there is increasing number of admissions for thyroid storm and
with decreasing the mortallity rate as the result of the studies in the philippines ,
the mortality rate of thyroid storm was lessen because the city health organization
instructed the barangay health worker to visit the community for the listing of
different diseases and to implemented or to aiding the patient fot having such
diseased.

A Case of Thyroid Strom Precipitated by Pneumonia

Christina PermataShalim, DewiCaturWulandari

Abstract: Thyroid storm is a rare but life-threatening condition that requires rapid
diagnosis and appropriate treatment. The symptoms that involve multiple organ
systems cause the diagnosis to be difficult because it can mimic other diseases.
Thyroid storm is usually precipitated by an acute illness, most commonly infection.
The symptoms of the infection itself are often make the diagnosis challenging
because they may mask the symptoms of thyroid storm. We present a case of
thyroid storm induced by pneumonia in a woman without history of
hyperthyroidism or other disease. Early recognition of thyroid storm and its
precipitating factor is important in preventing possible morbidity and mortality for
this patient.

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Thyroid storm is a complication caused by excessive amounts of thyroid hormone
which is rare but life threatening so it needs to be diagnosed quickly. The mortality
rate in this condition is not a common as in the past by still estimated to be 8-25%.

The symptoms that involve multiple organ systems cause the diagnosis to be
difficult because it can mimic other diseases. Thyroid storm is usually precipitated
by an acute illness, such as stroke, infection, trauma, surgery, or radioiodine
treatment of a patients with partially treated or untreated hyperthyroidism.
Infection is the most common precipitating factor for thyroid storm and the
symptoms of the infection itself are often make the diagnosis challenging because
they may mask the symptoms of thyroid storm.

Here, we present a case of thyroid storm likely precipitated by pneumonia.

Case report: A 41-year-old female patient presented in the emergency department

with 1-week history of nausea and vomiting. She also had cough with sputum,
shortness of breath, palpitation, subjective fever, and excessive sweating. There was
unintentional weight loss of 17kg over the last 2 months, anxiety, and heat
intolerance. She denied any stomach or chest pain. Her past medical history was
unremarkable, with no known personal or family history of thyroid diseases.

On presentation, she was agitated and diaphoretic. Her Glasgow Coma Scale was
15. She was tachycardic to 140bpm, subfebrile to 37.4°C, and tachypnea with
respiratory rate 40 times/minute. Her blood pressure was stable at 130/90 mmHg.
The physical examination showed mild exophthalmos, slightly enlarged thyroid,
and a fine tremor on both hands. Chest examination revealed mild rhonchi and
wheezing bilaterally throughout all lung fields.

Initial laboratory studies revealed hypokalemia (serum potassium: 2.8 mmol/L)

and increased AST (122 U/L) and ALT (100 U/L) level. Complete blood count was
within normal limit with white blood cells (WBC) count 6.08 x 10 3/uL, hematocrit
36.9%, and platelet count 248 x 103/uL. Chest X-ray showed bronchopneumonia.
Her electrocardiogram at that time showed sinus tachycardia with heart rate
125bpm.

Thyroid function test cannot be done at that time and was planned to be done the
next day, so for early diagnosis approach we tried to diagnosed hyperthyroidism
based on clinical symptoms and signs using Wayne’s Index. In this patient, the
Wayne’s Index score was at least 22 which was considered toxic.

Burch-Wartofsky score was used to assess the thyroid storm probability in this
patient. Patient’s Burch-Wartofsky score was calculated to be 60, which was highly
suggestive of thyroid storm.

The patient was admitted to the intensive care unit (ICU) and immediately treated
for thyroid storm with propylthiouracil (PTU) 200mg every 6 hours, propranolol
20mg every 8 hours, and hydrocortisone 100mg every day. Lugol’s solution was
planned to be given but it was not available in our hospital at that time. Empiric

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antibiotic certriaxoneintravenously also given for the pneumonia that has been
diagnosed based on the clinical symptoms that patient had, physical examination,
and her chest X-ray. Nebulization with salbutamol/ipratropium bromide was also
given. For the hypokalemia, patient was given potassium chloride 50mEq
intravenous solution diluted in 0.9% sodium chloride with infusion rate 12gtts/min.
other symptomatic therapy also given, including paracetamol, ranitidine,
ondansetron, and ambroxol.

Patient’s thyroid function tests on the next day were: thyroid stimulating hormone
(TSHs) <0.01µU/mL (normal range 0.27 to 4.27µU/mL) and free thyroxine (FT4)
37.00ng/dL (normal range 0.93-1.70 ng/dL). After potassium chloride infusion, the
serum kalium level was improved:4.2mmol/L.

During admission, patient’s blood pressure tends to be high with systolic blood
pressure range from 150-160 mmHg. Antihypertensive drug was initiated with
captopril 25mg every 12hours. On day 3 of admission, patient’s symptoms begin to
improve and her heart rate became normal 80bpm. Propranolol dose was lowered
to 20mg every 12 hours. On day 4 of admission, patient had stable condition and
discharge from the ICU to be admitted in general ward. Thyroid ultrasound was
done and revealed bilateral thyroiditis, left multiple thyroid nodule, and
nonspecific multiple bilateral cervical lymphadenopathy. Treatment was continued
until day 7 of admission. The only symptom that patient felt was mild shortness of
breath. Patient discharge with oral medications: PTU 200mg 3 times a day,
propranolol 10mg twice a day, captopril 25mg twice a day, and antibiotics
including cefixime and azithromycin for 5 days. For her next visit, we also planned
to evaluate her transaminase level because hepatotoxicity is one of the major
adverse effect of antithyroid therapy such as PTU or methimazole, so her liver
function should be monitored regularly during her therapy and that would be one
of the considerations for dose adjustment.

Discussion: Thyroid storm is a life-threatening manifestation of hyperthyroidism. In

this case report, a woman without history of hyperthyroidism or other disease came
to the emergency department with gastrointestinal symptoms of nausea and
vomiting.

Classic clinical symptoms of thyroid storm include fever, marked tachycardia,

heart failure, tremor, nausea, vomiting, diarrhea, dehydration, anxiety, delirium,
even coma. In this patient the main complaint was nausea and vomiting, which
turned out to be accompanied by fever and sever tachycardia. The patient also
seemed agitated, even though patient was still fully conscious.

Signs and symptoms that show decompensation in organ systems may also present,
such as delirium, peripheral edema, hepatomegaly, and respiratory failure. Sinus
tachycardia and tachyarrhythmia such as atrial fibrillation are also common. In this
patient we found sinus tachycardia and elevated transaminase, but other physical
findings as a result of other organ systems decompensation was not be found.
Clinical picture of the patient can also be masked by the presence of an infection

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that precedes the thyroid storm, such as pneumonia, viral infection, or upper
respiratory tract infection.

Hypokalemia in a patient with hyperthyroidism is usually associated with the

condition of hypokalemic periodic paralysis which is a rare complication of
hyperthyroidism characterized by acute paralytic attacks and hypokalemia. In this
patient, hypokalemia was present but there was no paralysis. This might be due to
the need for lower potassium levels to cause paralysis. In a case report that
reviewed 9 cases of hypokalemic periodic paralysis, potassium levels of 1.1-
2.3mmol/L were found in all of these cases, whereas our patient’s potassium levels
was 2.8 mmol/L

To diagnose thyroid storm, fist we have to confirm the hyperthyroidism status in

the patient. Because laboratory confirmation often delayed, Wayne’s index still
helpful to diagnose hyperthyroidism based in the clinical signs and symptoms. This
diagnostic index scores the presence or absence of various signs and symptoms of
hyperthyroidism for establishing a diagnosis. Then, thyroid function tests should be
ordered to confirm the diagnosis.

The diagnosis of thyroid storm is based on the clinical symptoms experienced by

the patient. The Burch-Wartofsky score can help to diagnose this condition. This
scoring system assigns points in the categories of thermoregulatory dysfunction,
central nervous system effects, gastrointestinal-hepatic dysfunction, cardiovascular
dysfunction and precipitant history. These points are totaled and a score of 45 or
more indicates a highly suggestive thyroid storm. In this patient, the total score
when the patient comes to the ER was 60.

Thyroid storm is usually precipitated by an acute illness, such as stroke, infection,

trauma, surgery, or radioiodine treatment. In this case, pneumonia that patient had
may be the precipitator of her thyroid storm.

After the diagnosis of thyroid storm is being made, appropriate therapy has to
immediately be given. Admission to an ICU is usually required. Specific therapies
for thyroid storm including antithyroid drugs (PTU or methimazole). Iodide
compound, propranolol, and corticosteroid such as dexamethasone or
hydrocortisone.

Antithyroid drugs directly inhibit thyroid peroxidase through the coupling of

iodotyrosine in thyroglobulin molecules. The major advantage of PTU compare to
methamazole is that PTU inhibits deiodination of T4 and therefore acutely decrease
T3 levels more than methamazole. This PTU’s action makes it the antithyroid drug
of choice on thyroid storm case.

Iodide compound, such as Logul’s solution or saturated solution of potassium

iodide (SSKI) in large doses can block the thyroid hormone synthesis and release by
inhibiting iodide oxidation and organification (the Wolff-Chaikoff effect). This
iodide solution should be administered at least one hour after the administration of
antithyroid drugs because iodine could stimulate thyroid hormone synthesis. The

70
delay allows the antithyroid drugs to prevent excess iodine from being used to
synthesize new hormone.

Propranolol is given to reduce tachycardia and other adrenergic manifestations.

Other beta blockers can be used for these effects, but high doses of propranolol
decreased conversion of T4 to T3 and the doses can be easily adjusted, therefore it
becomes beta blocker of choice on thyroid storm.

Corticosteroid such as dexamethasone or hydrocortisone should also be started

because there might be an adrenal insufficiency caused by the hyper metabolic state
in thyroid storm. Large doses of corticosteroids have also been shown to inhibit
peripheral conversion to T4 to T3.

Supportive therapy should be initiated based on the patient’s condition and

symptoms. In this case, an infection that likely precipitated thyroid storm is treated
with antibiotics. Treatment of hypokalemia in a patient with hyperthyroidism
includes correction of hypokalemia intravenously or orally and treatment of the
underlying hyperthyroid state. As for patient’s symptoms such as nausea and fever,
symptomatic drugs should be administered.

Once the patient is stable, the etiology of hyperthyroid underlying thyroid storm
should be investigated. Thyroid ultrasound can be useful for evaluation of gland’s
volume, echogenicity, vascularity, and presence of nodular disease.\

Conclusion: early recognition of thyroid storm and its precipitating factor is

important in preventing possible morbidity and mortality. Appropriate therapy has
too immediately be given, including specific therapy for the thyroid storm and
supportive therapy based on the patient’s condition and symptoms.

REFLECTION

Thyroid strom is a complication of the hypersecretions from your thyroid gland that
could potentially end a person’s life if left untreated when manifested. It is
triggered by one of the following: trauma, infection, surgery, radioiodine therapy,
stroke, or untreated hyperthyroidism. In this article, it was triggered by pneumonia,
an infection in the lungs (most cases of thyroid storm is usually triggered by
respiratory infections). Ultrasound could be used to identify if the patient has
adenoma on the thyroid gland, but checking of T4 serum could also be done, but in
emergency cases, you have to use what is readily available for diagnostics. The
article mentioned the medications given to the 41-year-old patient that helped
decrease the secretion of the T4 and T3, where it was altered to check if the patient
could tolerate and if the medicaitons has actually been working.

A person with this condition should be directed to the emergency room to be

admitted in the ICU, where they will then be monitored closely to prevent further
complications. It is not a condition that should be taken lightly, but with its
manifestations, it could be difficult to identify if the condition was thyroid storm or
not—since it could be mistaken for other conditions easily if the physician wasn’t

71
well aware or is not versed in the condition that is thyroid storm. The priority
should be the decreasing of secretion of your T4 and antibiotics to kill the bacterias
causing the infection to lessen the risk of complicating the condition.

Physicians and people in the medical field should be able to identify the
precipitating factors of thyroid storm to recognize the disease earlier rather than
later; being knowledgable about these conditions could save a person’s life and
prevent complications in cases where it’s too late—the condition affects other
systems and I have found that there are cases that neurologically, the person could
be impaired. It should be recognized that althought hypersecretion of T4 and T3 is
common, thyroid storm could practically be the one that could end the person’s life
all because of an infection in the lungs.

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 XIV. BIBLIOGRAPHY

Biggers, A. (2017). Thyroid storm. Retrieved from

https://www.healthline.come/health/thyroid-storm#causes

Binod, P., Kamal, B. (2019, June 3). Thyroid Storm. Retrieved from

https://www.ncbi.nlm.nih.gov/books/NBK448095/

British Thyroid Foundation. (2019, March 18). Your thyroid Gland. Retrieved from
https://www.btf-thyroid.org/what-is-thyroid-disorder

Moore, K. (2017, December 12). Thyroid Storm. Retrieved from

https://www.healthline.com/health/thyroid-storm

Misra, M., Talbot, F.B., et al. (2018, February 18). Thyroid Storm. Retrieved from
https://emedicine.medscape.com/article/925147-overview

Graves' Disease & Thyroid Foundation. (2019). About Graves’ Disease. Retrieved from
https://www.gdatf.org/about/about-graves-disease/

PermataShalim, C., Wulandari, D. (2019). International Journal of Science and Research. A

case of thyroid storm precipitated by pneumonia. Vol. 8, Issue 5. ISSN: 2319-7064.
DOI: 10.21275/ART20197563

Porth, C. M. (1998). Pathophysiology: Concepts of Altered Health States (7th ed.). Disorders
of endocrine control of growth and metabolism. Pg 970-976. Lippincott Williams &
Wilkins: Philadelphia

Ross, D. (2019, January 14). Thyroid storm. Retrieved from

https://www.uptodate.com/contents/thyroid-storm?fbclid=IwAR092-
BJUpUZotSH7wkRxklPUkMFQ30P6poc1A5nciSDD5RQ5iJ6OJTKbPQ#H1

Raboca, J.C., Jimeno, C., Kho, S., et al. (2012, March 22). The Philippine Thyroid Diseases
Study (PhilTiDeS 1): Prevalence of Thyroid Disorders Among Adults in the Philippines.
Retrieved from https://asean-
endocrinejournal.org/index.php/JAFES/article/view/9/400?
fbclid=IwAR1DQfVhxOjcnOB0hcr_fvJ0iPxnnH1tcHSl6K9jQcz2F0IaVAaePt1WQuo

National Organization for Rare Disease. (2016). Graves’ Disease. Retrieved from
https://rarediseases.org/rare-diseases/graves-disease/

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