PATIENT WITH

ENDOCRINE
DYSFUNCTION
•Thyroid emergencies:
•- Thyroid storm (crisis)
•- Myxoedema coma
• At the end of the learning session, the students should be able
to:
• 1. explain briefly the following thyroid emergencies:
• 1.1 Thyroid storm (crisis)
• 1.2 Myxoedema coma
• 2. correlate the clinical presentation of the above thyroid
emergencies with its pathophysiology
• 3. state the relevant laboratory data concerning the above
acute thyroid emergencies
• 4. describe the management related to the above acute
thyroid emergencies
• 5. use the nursing process as a framework to formulate
individualized care of patients with the above acute thyroid
emergencies
• 6. appreciate the importance of prompt management to the
patient’s clinical prognosis
How the Thyroid Gland
Works
•The thyroid is part of the endocrine
system, which is made up of glands that
produce, store, and release hormones into
the bloodstream so the hormones can
reach the body's cells. The thyroid gland
uses iodine from the foods you eat to
make two main hormones:
•Triiodothyronine (T3)
•Thyroxine (T4)
•two types of thyroid hormones:
thyroxine (T4), which contains
four iodine atoms and
triiodothyronine (T3), which
contains three iodine atoms.The
thyroid gland mainly produces T4.
•It is important that T3 and T4
levels are neither too high nor too
low. Two glands in the brain—the
hypothalamus and the pituitary
communicate to maintain T3 and
T4 balance.
•The hypothalamus produces TSH
Releasing Hormone (TRH) that signals
the pituitary to tell the thyroid gland
to produce more or less of T3 and T4
by either increasing or decreasing the
release of a hormone called thyroid
stimulating hormone (TSH).
•When T3 and T4 levels are low in the
blood, the pituitary gland releases
more TSH to tell the thyroid gland to
produce more thyroid hormones.
•If T3 and T4 levels are high, the
pituitary gland releases less TSH to
the thyroid gland to slow production
of these hormones.
thyrotoxicosis
thyrotoxicosis
A condition resulting from excessive
concentrations of thyroid hormones in the body,
as in hyperthyroidism.

thyrotoxicosis
the condition caused by excessive quantities of
thyroid hormones ; it may be due to
overproduction by the thyroid gland (as in Graves'
disease), overproduction originating outside the
thyroid, or loss of storage function and leakage
from the gland.
thyrotoxicosis
•Causes of thyrotoxicosis
•There are four main causes of
thyrotoxicosis,
•Graves' Disease (70%)
•Toxic multinodular goitre (15%)
•Toxic adenoma (5%)
•Thyroiditis (5%)
Graves' Disease (70%)
• Graves' disease is an autoimmune disease, like
Type 1 diabetes and rheumatoid arthritis, where
the body's immune system forms antibodies to
attack its own organs.

• In the case of Graves' disease, the immune

system attacks the thyroid, with production of
thyroid stimulating antibodies, which bind to the
TSH receptor (anti-TSH receptor antibodies). The
autoantibodies stimulate the thyroid cell to
make excess thyroid hormone, which results in a
state of thyrotoxicosis.
manifestation
• 1) Symptoms due to stimulation of metabolic processes and
the sympathetic nervous system

• Hypermetabolism symptoms such as palpitations, tremor,

irritability, weight loss, etc. although in the elderly the cardiac
and neurological symptoms tend to predominate. Eye changes
of lid lag and lid retraction, commonly found in all forms of
thyrotoxicosis, are caused by sympathetic nerve stimulation of
the upper eyelid muscles.
• 2) Symptoms due to the autoantibodies.
• Specific to Graves' disease is Graves'
Ophthalmopathy (Thyroid Eye Disease - TED),
which is distinct from the lid lag and lid
retraction common to all forms of thyrotoxicosis.
TED is thought to be caused by reaction to
antigens in the retroorbital tissues (behind the
eye) that cross react with the TSH receptor,
resulting in swelling of the orbital contents, lids
and periorbital tissues, with marked lid
retraction, vision effects and a characteristic
stare .
.2: Thyroid eye disease
showing characteristic
stare
hyperthyroidism
•Anxiety
•Irritability or moodiness
•Nervousness, hyperactivity
•Sweating or sensitivity to high
temperatures
•Hand trembling (shaking)
•Hair loss
•Missed or light menstrual periods
hypothyroidism
•Trouble sleeping
•Tiredness and fatigue
•Difficulty concentrating
•Dry skin and hair
•Depression
•Sensitivity to cold temperature
•Frequent, heavy periods
•Joint and muscle pain
THYROID EMERGENCIES
•Definition
•1. Thyroid storm (crisis)
•Thyroid storm is an acute,
life-threatening complication of
hyperthyroidism and represents
the extreme manifestation of the
disease.
•Thyroid storm is a serious
complication of
thyrotoxicosis usually of an
abrupt onset.
•Thyroid storm is a
decompensated state of thyroid
hormone–induced, severe
hypermetabolism involving
multiple systems and is the most
extreme state of thyrotoxicosis.
Etiology
• Thyroid storm is precipitated by the following factors in
individuals
with thyrotoxicosis:
• Sepsis
• Surgery
• Anesthesia induction[2]
• Radioactive iodine (RAI) therapy[3]
• Drugs (anticholinergic and adrenergic drugs, eg,
• pseudoephedrine; salicylates; nonsteroidal anti-inflammatory
• drugs [NSAIDs]; chemotherapy[4]
• Excessive thyroid hormone (TH) ingestion
• Withdrawal of or noncompliance with antithyroid medications
• Diabetic ketoacidosis
• Direct trauma to the thyroid gland
• Vigorous palpation of an enlarged thyroid
• Toxemia of pregnancy and labor in older adolescents; molar
• pregnancy
Clinical manifestation
Laboratory Findings
• Thyrotoxicosis
• o Thyroid function test: f T4 and fT3 are usually increased,
though this does not correlate with clinical severity. TSH is
undetectable.
• o Hyperglycemia in non-diabetics.
• o Leukocytosis with a left shift, even in the absence of
infection (leukopenia may be present in patients with Graves
disease).
• o Abnormal liver function tests and hyperbilirubinaemia.
• o Hypocalcaemia due to haemoconcentration and the effect of
thyroid hormones on bone resorption.
• o Hypokalemia and hypomagnesaemia (particularly in
apathetic thyrotoxicosis).
•Serum cortisol should be elevated. If low
values are found, adrenal insufficiency
should be considered and treated. Adrenal
reserve in thyrotoxic patients is often
exceeded in the absence of absolute
adrenal insufficiency.
Management Throid Storm
•Supportive therapy:
•Hyperthermia:
•IV fluids
• Antipyretics
• Cooling blanket
Thyroid-directed therapy:
• Inhibition of thyroid hormone synthesis:
• o Propylthiouracil: 800 mg PO/PR first dose, then 200-300 mg
PO/PR q 8 h, or
• o Methimazole: 80 mg PO/PR first dose, then 40-80 mg PO/PR
q 12 h
• Block release of thyroid hormones from the gland:
• o Telepaque (iopanoic acid): 1g PO once daily (if available), or
• o SSKI: 5 drops PO q 8 h, or
• o Lugol’s solution: 10 drops PO q 8 h, or
• o Lithium: 800-1200 mg PO once daily; achieve serum lithium
levels 0.5-1.5 mEq/L
β-Adrenergic blocking
drugs:
• o Propranolol: 1 mg IV/min to a total dose of 10
mg, then 40-80 mg PO q 6 h, or
• o Esmolol: 500 mg/kg/min IV, then 50-100
mg/kg/min, or
• o Metoprolol: 100-400 mg PO q 12 h, or
• o Atenolol: 50-100 mg PO daily
• o Other:
• - Vasopressors
• - Digoxin
2. Myxoedema coma
• Myxedema coma is a rare syndrome that
represents the extreme expression of severe
long-standing hypothyroidism.

• It carries a mortality ranging from 30% to 60%.

• The syndrome includes decompensated
hypothyroidism,central nervous system
impairment, and cardiovascular compromise.
•As with thyroid storm, myxedema coma is
usually caused by a precipitating event in
the untreated or partially treated
hypothyroid patient.
•The crisis occurs most commonly in elderly
women with long-standing undiagnosed or
undertreated hypothyroidism in whom an
additional significant stress is experienced.
Myxoedema coma

• Myxoedema coma can be defined when

decreased mental status, hypothermia
• and clinical features of hypothyroidism are
present. When these features are
• present, diagnosis is straightforward; however,
asymptomatic or atypical presentation (e.g.
decreased mobility) may occur.
Investigation Myxoedema
• Thyroid function tests: will reveal low T4 and T3;
TSH is raised in primary and low in secondary
and tertiary hypothyroidism.
• o Hypernatremia is common and usually
develops due to free water retention resulting
from excess vasopressin secretion or impaired
renal function. It may be severe and can
contribute to diminished mental function.
Although total body water is increased,
intravascular volume is usually decreased.
•Hypoglycemia may result from
hypothyroidism alone, or as a result of
concurrent adrenal insufficiency
(Schmidt’s syndrome). The mechanism is
probably reduced gluconeogenesis, but
infection and starvation may contribute.
•Azotemia and hypophosphatemia
are common; renal function may
be severely abnormal due to low
cardiac output and
vasoconstriction.
•Azotemia is an elevation of blood
urea nitrogen (BUN) and serum
creatinine levels. The reference
range for BUN is 8-20 mg/dL, and
the normal range for serum
creatinine is 0.7-1.4 mg/dL.
•Mild leukopenia and normocytic anemia
are frequently present, though macrocytic
and pernicious anemia due to
autoimmune dysfunction may occur.
•o Arterial blood gases often reveal
respiratory acidosis, hypoxia and
hypercapnia.
Clinical presentation
Investigation
• Thyroid function tests: will reveal low T4 and T3;
TSH is raised in primary and low in secondary
and tertiary hypothyroidism.

• o Hypernatremia is common and usually

develops due to free water retention resulting
from excess vasopressin secretion or impaired
renal function. It may be severe and can
contribute to diminished mental function.
Although total body water is increased,
intravascular volume is usually decreased.
•Hypoglycemia may result from
hypothyroidism alone, or as a result of
concurrent adrenal insufficiency
(Schmidt’s syndrome). The mechanism is
probably reduced gluconeogenesis, but
infection and starvation may contribute.
•Azotemia and hypophosphatemia are
common; renal function may be severely
abnormal due to low cardiac output and
vasoconstriction.
•o Mild leukopenia and normocytic anemia
are frequently present, though macrocytic
and pernicious anemia due to
autoimmune dysfunction may occur.
•Arterial blood gases often reveal
respiratory acidosis, hypoxia and
hypercapnia.
b. Myxoedema coma
• Supportive:ICU admission
• Assisted ventilation – respiratory support- intubation
• If HCT < 30% - transfuse blood to provide adequate perfusion and
oxygen carrying capacity
• Hemodynamic support
• Poikilothermic – cool blood
• Passive rewarming for hypothermia
• No aggressive warning – vasodilatation vascular collapse
• Intravenous glucose for hypoglycemia
• o Water restriction or hypertonic saline for severe hyponatremia
• Avoid fluid overload
• o Hydrocortisone IV ( 40- 100 mg 6 hly for 1 week than taper)
• o Treatment of precipitating factor(s)
•Avoidance of all CNS-acting medications -
sedation
•o Thyroid Hormone Replacement
•- L-T4: 200-300 μg loading dose IV, up to
500 μg IV in the first 24 h and/or
•- L-T3: 12.5 μg IV q 6 h
Nursing Care

• Problem 1: Decrease cardiac output secondary to increase

demand
• Clinical assessment findings
• Agitated and restless
• Profuse sweating
• Tachycardia
• Deterioration in mental status
• Poor capillary refill
• Decrease urine output
Intervention
• 1. Assess the parameters which indicate
decrease in cardiac output.
• 2. Administer fluid to increase circulating
volume.
• 3. Provide oxygen therapy through ventimask.
• 4. Prepare for intubation and ventilation if
unstable haemodynamic or dropped in GCS
below 8.
• 5. Control the heart rate – consider beta blocker,
if haemodynamically stable and no
contraindication.
•6. Watch up for the cardiac
arrhythmias, cardioversion may be
required.
•7. Look for the precipitating cause for
thyroid crisis leading to reduce
cardiac output such as infection.
Identify the causative organism.