Thyroid storm

by
Prof s c
kohli
Thyroid storm
 Thyrotoxic crisis, or thyroid
storm
• Thyrotoxic crisis, or thyroid storm or
accelerated hyperthyroidism, is rare and
presents as a life-threatening
exacerbation of hyperthyroidism,
accompanied by fever, delirium, seizures,
coma, vomiting, diarrhea, and jaundice.
The mortality rate due to cardiac failure,
arrhythmia, or hyperthermia is as high as
30%, even with treatment.
 mechanism
• Cytokine release
• and acute immunologic disturbance
caused by precipitating factors
 Precipitating factors
• Thyrotoxic crisis is usually precipitated by
• acute illness (e.g., stroke, infection, trauma,
• diabetic ketoacidosis),
• surgery (especially on the thyroid),
• pregnancy parturition
• or radioiodine treatment of a patient with
partially treated or untreated
hyperthyroidism.
 Clinical features
• Fever is inveriable and severe
• Profuse sweating
• Tachycardia of sinus or ectopic origin
• Arrhythmias may be accompanied by
pulmonary oedema/ C C F
• Tremulousness & restlessness
• Delirium or frank psychosis may supervene
 Clinical features (contd)
• Nausia,vomiting,& abdominal pain
occur early in the course
• As disorder progresses
apathy,stupor,& coma may
supervene
• Hypotension may develop
• If unrecognised
condition is fatal
 apathetic storm.
• Sometimes thyroid crisis takes a
strikingly different form, which has been
called apathetic storm.
• This condition is characterized by
extreme weakness, emotional apathy
and sometimes confusion.
• The wild delirium and agitation of the
classic victim of thyroid storm are
missing, and fever, if present, does not
rise so high.
 diagnosis
Clinical picture with
history of preexisting thyrotoxicosis
With goitre/exophthalmos or both
is sufficient to establish the
diagnosis
 Mortality/Morbidity

Thyroid storm is an acute, life-threatening

emergency.
The adult mortality rate is extremely high
(90%) if early diagnosis is not made and the
patient is left untreated.
With better control of thyrotoxicosis and early
management of thyroid storm, adult mortality
rates have declined to less than 20%
 Management
• Management requires
1) intensive monitoring and supportive care,
2)identification and treatment of the
precipitating cause,
3)and measures that reduce thyroid hormone
synthesis & release
4)antagonising adrinergically mediated
aspects ofperipheral thyroid action
 management
Large doses of propylthiouracil (600 mg
loading dose and 200–300 mg every 6
h) given orally or by nasogastric tube or
per rectum;
the drug's inhibitory action on T4 T3
conversion makes it the antithyroid drug
of choice
& is preferable to methimazole
 reduce release of thyroid
hormone

One hour after the first dose of

propylthiouracil, stable iodide is given
to block thyroid hormone synthesis
(the delay allows the antithyroid drug to
prevent the excess iodine from being
incorporated into new hormone).
 reduce release of thyroid
hormone
A saturated solution of potassium iodide
(5 drops SSKI every 6 h),
or ipodate or iopanoic acid
(0.5 mg every 12 h), may be given orally.
Sodium iodide, 0.25 g intravenously every 6 h
is an alternative but is not generally
available.
 management
Propranolol given to reduce tachycardia and other
adrenergic manifestations (40–60 mg orally every
4 h;
or 2 mg intravenously every 4 h).
high doses of propranolol decrease T4 -T3
conversion, and the doses can be easily adjusted.
Lobetelol being shorter acting-safer
• Caution to avoid acute negative inotropic effects,
 management
Additional therapeutic measures include
glucocorticoids (e.g., dexamethasone, 2 mg every 6
h),
Inhibit both the release of hormone from gland
& peripheral generation of T3 from T4 synergizing with
Iodide & Propylthiouracil respectively
Combined use restoreT3 conc to normal in 48 hr
 Management Supportive
measures
Correction of dehydration & hypernatraemia
I V glucose administration
Treatment of hyperpyerexia
Acetominophen/wet pack
Avoid aspirin—it competes with T3,T4 in
binding with TBG & Transthyretin
Atrial fibrillation with high vent. Rate—agent
for blockade of AV Node conduction
Myxedema coma
 Myxedema coma
• Rare life threatening condition with
long standing untreated
hypothyroidism
• It is misnomer because pt is not
comatosed
• A precipitating event leads to
functional disorders of C V S & C N S
• Fatal if not recognised.
 Diagnostic Features
• Altered mental status – from disorientation to
lethargy to psychosis & coma
• Defective thermoregulation –hypothermia or
absence of fever despite infectious disease
• Precipitating event
• Cold exposure,infection
drugs(diuretics,sedatives,tranquilizers,)
• Trauma, stroke,heart failure, G I bleeding
 Precipitating factors
• Factors Known to Precipitate Myxedema
Coma Burns
• Carbon dioxide retention
• Gastrointestinal hemorrhage
• Hypoglycemia
• Hypothermia
• Infection Pneumonia Influenza Urinary
tract infection/urosepsis Sepsis
 Precipitating factors
• Medications
• Amiodarone (Cordarone)
• Anesthesia
• Barbiturates Beta blockers Diuretics
• Lithium Narcotics Phenothiazines
• Phenytoin (Dilantin) Rifampin
(Rifadin, Rimactane) Tranquilizers
• Stroke Surgery Trauma
 Physical findings in
myxedema coma
the classic myxedematous face,
• which is characterized by generalized puffiness,
macroglossia, ptosis, periorbital edema, and
coarse, sparse hair
Nonpitting edema of the lower extremities is
sometimes present.
A thyroid examination are usually normal, but a
goiter may be present in some patients.
 Clinical features
• Altered Mentation
All patients with myxedema coma display
deterioration of their mental status.
• This decline may be subtle, manifesting as
apathy, neglect or a decrease in intellectual
function;
• more obvious changes include confusion,
psychosis and, rarely, coma.
 Clinical features
• Hypoventilation
Hypoventilation in myxedema coma results
from the body's decreased ventilatory
response to hypoxia and hypercapnia.
• Respiratory dysfunction may lead to sleep
apnea,
• and respiratory difficulties may be
exacerbated by myxedematous infiltration of
the tongue and pharynx.
 Clinical findings
seen mostly in elderly women in winter
cool pale skin,
Cardiovascular
Elevated diastolic blood pressure—early
Hypotension—late Bradycardia
Gastrointestinal Decreased motility
Abdominal distension Paralytic ileus
Myxedema megacolon--late
 Lab findings
Typically, patients with myxedema coma
have primary hypothyroidism
manifested by
low serum levels of thyroxine (T4)
and triiodothyronine (T3)
 Summary of lab findings
Anemia
Elevated CPK
Elevated creatinine
Elevated transaminases
Hypercapnia
Hyperlipidemia
Hypoglycemia
Hyponatremia
Hypoxia ,Leukopenia ,Respiratory acidosis
 ECG changes
• ECG changes include
• bradycardia,
• decreased voltages,
• non-specific ST and T changes,
• varying types of block
• and a prolonged QT interval.
 treatment
• Rapid institution
• Levothyroxin 300 to 500 ug iv followed
by 50 to 100 ug iv daily till oral
medication is possible.
• Hypothermia
• Blankets ---rewarming dangerous—
peripheral vasodilatation may provoke
vascular cllapse
 treatment
• Hypoventilation—mechanical ventilation
• Treat anaemia---- blood transfusion
• Treat hyponatremia
• Hypoglycemia ----glucose administration
• Hypocortisolemia---glucocorticoids
• Hydrocortisone 200 -400 mg in 3 or divided
doses
 treatment
• Specific treatment for precipitating event
• Infection-- broad spectrum antibiotics
• Pneumonia / urosepsis in 35 %
• Fever, tachycardia,leucocytosis absent.
• Diuuretics/digoxin to be used with
caution
Save life Be Quick in
treatment