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 respectivelyCombined 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 findingsseen 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