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Thyroid Storm

Last Updated: July 11, 2003 Rate this Article

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Synonyms and related keywords: thyrotoxic crisis, thyrotoxicosis

AUTHOR INFORMATION Section 1 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

Author: Abhay Singhal, MD, Attending Neonatologist, Department of

Pediatrics, Division of Neonatology, Children's Memorial Hospital,

Chicago

Coauthor(s): Deborah , MD, Chief, Associate Professor,

Department of Pediatrics, Division of Neonatology, Albert Einstein

College of Medicine and Montefiore Medical Center

Abhay Singhal, MD, is a member of the following medical societies:

Indiana State Medical Association

Editor(s): Phyllis Speiser, MD, Director, Division of Pediatric

Endocrinology, Children's Health Network of North Shore/LIJ Health

System, Clinical Professor, Department of Pediatrics, New York

University School of Medicine; Konop, PharmD, Clinical

Assistant Professor, Department of Pharmacy, Section of Clinical

Pharmacology, University of Minnesota; Lynne Lipton Levitsky, MD,

Chief, Pediatric Endocrine Unit, Massachusetts General Hospital;

Associate Professor, Department of Pediatrics, Harvard University

Medical School; Merrily Poth, MD, Professor, Department of

Pediatrics, Uniformed Services University of the Health Sciences; and

P Chrousos, MD, FAAP, FACP, MACE, Chief, Pediatric and

Reproductive Endocrinology Branch, Program Director, Pediatric

Endocrinology, NICHD/NIH; Clinical Professor, Department of

Pediatrics, town University Medical School

INTRODUCTION Section 2 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

Background: Thyroid storm is an acute, life-threatening, thyroid

hormone–induced hypermetabolic state in patients with thyrotoxicosis.

Thyroid storm may be the initial presentation of thyrotoxicosis in

undiagnosed children. Common clinical presentation includes fever,

tachycardia, neurologic abnormalities, and hypertension, followed by

hypotension and shock. Because thyroid storm is invariably fatal if

left untreated, rapid diagnosis and aggressive treatment are

critical. Fortunately, this condition is extremely rare in children.

Diagnosis is primarily clinical, and no specific laboratory tests are

available. Several precipitating factors can lead to progression of

thyrotoxicosis to thyroid storm. In the past, thyroid storm commonly

was observed during thyroid surgery, especially in older children and

adults, but improved preoperative management has decreased incidence

markedly. Today, thyroid storm occurs more commonly as a medical

rather than a surgical crisis.

Pathophysiology: Thyroid storm is a decompensated state of thyroid

hormone–induced, severe hypermetabolism involving multiple systems.

Thyroid storm is the most extreme state of thyrotoxicosis. The

clinical picture relates to severely exaggerated effects of thyroid

hormones (THs). Heat intolerance and diaphoresis are common in simple

thyrotoxicosis but manifest as hyperpyrexia in thyroid storm.

Cardiac findings of mild-to-moderate sinus tachycardia intensify to

accelerated tachycardia, hypertension, high-output heart failure, and

propensity to develop cardiac arrhythmia. Irritability and

restlessness in simple thyrotoxicosis progress to severe agitation,

delirium, seizures, and coma.

GI involvement is manifested by diarrhea, vomiting, jaundice, and

abdominal pain from mild elevation of transaminases and simple

enhancement of intestinal transport in simple thyrotoxicosis.

Extremely high metabolism also increases oxygen and energy

consumption.

The following factors are known to precipitate thyroid storm:

Infection

Surgery

Trauma

Radioactive iodine treatment

Pregnancy

Anticholinergic and adrenergic drugs

TH ingestion

Diabetic ketoacidosis (DKA)

Frequency:

In the US: The true frequency of thyrotoxicosis and thyroid storm in

children is unknown. Incidence of thyrotoxicosis increases with age.

Thyrotoxicosis may affect as many as 2% of older women. Children

constitute less than 5% of all thyrotoxicosis cases. Graves disease

is the most common cause of childhood thyrotoxicosis and, in a

possibly high estimate, reportedly affects 0.2-0.4% of the pediatric

and adolescent population. About 1-2% of neonates born to mothers

with Graves disease manifest thyrotoxicosis.

Mortality/Morbidity: Thyroid storm is an acute, life-threatening

emergency. Adult mortality 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

has declined to less than 20%.

Sex:

Thyrotoxicosis is 3-5 times more common in females than males,

especially in pubertal children.

Thyroid storm affects a small percentage of patients with

thyrotoxicosis. Incidence is presumed higher in females; however, no

specific data regarding sex-specific incidence are available.

Age:

Because thyrotoxicosis is more likely to occur in adolescents,

thyroid storm is more common in this age group, although thyroid

storm occurs in patients of all ages.

Infants younger than 1 year constitute only 1% of childhood

thyrotoxicosis. More than two thirds of cases occur in children aged

10-15 years. Overall, most thyrotoxicosis occurs during the third and

fourth decades of life.

Graves disease presents in 1-2% of neonates born to mothers who have

the condition.

CLINICAL Section 3 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

History: Patients may have known thyrotoxicosis. In the absence of

previously diagnosed thyrotoxicosis, history may reveal symptoms such

as irritability, emotional lability, voracious appetite with poor

weight gain, excessive sweating, and poor school performance caused

by short attention span.

General symptoms

Fever

Profuse sweating

Poor feeding and weight loss

Respiratory distress

Fatigue (more common in older adolescents)

GI symptoms

Vomiting

Diarrhea

Abdominal pain

Jaundice

Neurologic symptoms

Altered behavior

Seizures, coma

Anxiety (more common in older adolescents)

Physical:

Fever

Temperature consistently exceeds 38.5°C.

Patients may progress to hyperpyrexia.

Temperature frequently exceeds 41°C.

Excessive sweating

Cardiovascular signs

Hypertension with wide pulse pressure

Hypotension in later stages with shock

Tachycardia disproportionate to fever

Signs of congestive heart failure (CHF)

Cardiac arrhythmia (atrial fibrillation)

Neurologic signs

Agitation and confusion

Hyperreflexia and transient pyramidal signs

Tremors, seizures

Coma

Signs of thyrotoxicosis

Orbital signs

Goiter

Causes:

Thyroid storm is precipitated by the following factors in individuals

with thyrotoxicosis:

Sepsis

Surgery

Trauma

Drugs (eg, pseudoephedrine, other adrenergic and anticholinergic

drugs)

DKA

TH ingestion

Radioiodine therapy

Vigorous palpation of thyroid

Toxemia of pregnancy and labor in older adolescents

Most thyroid storm is associated with Graves disease in childhood.

Other reported causes of thyrotoxicosis associated with thyroid storm

include the following:

McCune-Albright syndrome with autonomous thyroid function

Hyperfunctioning thyroid nodule

Hyperfunctioning multinodular goiter

Thyroid-stimulating hormone (TSH)-secreting tumor

Graves disease also may occur in association with other autoimmune

conditions (and in children with Down or syndromes), including

the following:

Juvenile rheumatoid arthritis

disease

Myasthenia gravis

Chronic lymphocytic (Hashimoto) thyroiditis

Systemic lupus erythematosus

Chronic active hepatitis

Nephrotic syndrome

Although thyroid storm's exact pathogenesis is not fully understood,

the following theories have been proposed:

TH levels are not increased above levels observed in uncomplicated

thyrotoxicosis. Recent studies, however, have demonstrated relatively

high levels of free TH in patients with thyroid storm.

Adrenergic receptor activation is another hypothesis. In this theory,

sympathetic nerves innervate the thyroid gland, and catecholamines

can stimulate TH synthesis. This increased TH then increases the

density of beta-adrenergic receptors, thereby enhancing the effect of

catecholamines. Supporting this theory is the dramatic response of

thyroid storm to beta-blockers and the precipitation of thyroid storm

after accidental ingestion of adrenergic drugs such as

pseudoephedrine. This theory also explains normal or low plasma and

urinary excretion rates of catecholamines; it does not explain why

beta-blockers fail to decrease TH levels in thyrotoxicosis.

Another theory suggests a rapid rise of hormone levels as the

pathogenic source. A drop in binding proteins, which might occur

postoperatively, might cause a sudden rise in free hormone levels. A

rapid rise in hormone levels also may occur when the gland is

manipulated during surgery or by vigorous palpation during

examination.

Other proposed theories include tissue tolerance to THs, presence of

a unique catecholaminelike substance in thyrotoxicosis, and a direct

sympathomimetic effect of TH as a result of its structural similarity

to catecholamines.

DIFFERENTIALS Section 4 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

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Guest guest

thanks a lot, Tina! hugs, Sheila

tina83862 <tina83862@...> wrote:Thyroid Storm

Last Updated: July 11, 2003 Rate this Article

Email to a Colleague

Synonyms and related keywords: thyrotoxic crisis, thyrotoxicosis

AUTHOR INFORMATION Section 1 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

Author: Abhay Singhal, MD, Attending Neonatologist, Department of

Pediatrics, Division of Neonatology, Children's Memorial Hospital,

Chicago

Coauthor(s): Deborah , MD, Chief, Associate Professor,

Department of Pediatrics, Division of Neonatology, Albert Einstein

College of Medicine and Montefiore Medical Center

Abhay Singhal, MD, is a member of the following medical societies:

Indiana State Medical Association

Editor(s): Phyllis Speiser, MD, Director, Division of Pediatric

Endocrinology, Children's Health Network of North Shore/LIJ Health

System, Clinical Professor, Department of Pediatrics, New York

University School of Medicine; Konop, PharmD, Clinical

Assistant Professor, Department of Pharmacy, Section of Clinical

Pharmacology, University of Minnesota; Lynne Lipton Levitsky, MD,

Chief, Pediatric Endocrine Unit, Massachusetts General Hospital;

Associate Professor, Department of Pediatrics, Harvard University

Medical School; Merrily Poth, MD, Professor, Department of

Pediatrics, Uniformed Services University of the Health Sciences; and

P Chrousos, MD, FAAP, FACP, MACE, Chief, Pediatric and

Reproductive Endocrinology Branch, Program Director, Pediatric

Endocrinology, NICHD/NIH; Clinical Professor, Department of

Pediatrics, town University Medical School

INTRODUCTION Section 2 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

Background: Thyroid storm is an acute, life-threatening, thyroid

hormone–induced hypermetabolic state in patients with thyrotoxicosis.

Thyroid storm may be the initial presentation of thyrotoxicosis in

undiagnosed children. Common clinical presentation includes fever,

tachycardia, neurologic abnormalities, and hypertension, followed by

hypotension and shock. Because thyroid storm is invariably fatal if

left untreated, rapid diagnosis and aggressive treatment are

critical. Fortunately, this condition is extremely rare in children.

Diagnosis is primarily clinical, and no specific laboratory tests are

available. Several precipitating factors can lead to progression of

thyrotoxicosis to thyroid storm. In the past, thyroid storm commonly

was observed during thyroid surgery, especially in older children and

adults, but improved preoperative management has decreased incidence

markedly. Today, thyroid storm occurs more commonly as a medical

rather than a surgical crisis.

Pathophysiology: Thyroid storm is a decompensated state of thyroid

hormone–induced, severe hypermetabolism involving multiple systems.

Thyroid storm is the most extreme state of thyrotoxicosis. The

clinical picture relates to severely exaggerated effects of thyroid

hormones (THs). Heat intolerance and diaphoresis are common in simple

thyrotoxicosis but manifest as hyperpyrexia in thyroid storm.

Cardiac findings of mild-to-moderate sinus tachycardia intensify to

accelerated tachycardia, hypertension, high-output heart failure, and

propensity to develop cardiac arrhythmia. Irritability and

restlessness in simple thyrotoxicosis progress to severe agitation,

delirium, seizures, and coma.

GI involvement is manifested by diarrhea, vomiting, jaundice, and

abdominal pain from mild elevation of transaminases and simple

enhancement of intestinal transport in simple thyrotoxicosis.

Extremely high metabolism also increases oxygen and energy

consumption.

The following factors are known to precipitate thyroid storm:

Infection

Surgery

Trauma

Radioactive iodine treatment

Pregnancy

Anticholinergic and adrenergic drugs

TH ingestion

Diabetic ketoacidosis (DKA)

Frequency:

In the US: The true frequency of thyrotoxicosis and thyroid storm in

children is unknown. Incidence of thyrotoxicosis increases with age.

Thyrotoxicosis may affect as many as 2% of older women. Children

constitute less than 5% of all thyrotoxicosis cases. Graves disease

is the most common cause of childhood thyrotoxicosis and, in a

possibly high estimate, reportedly affects 0.2-0.4% of the pediatric

and adolescent population. About 1-2% of neonates born to mothers

with Graves disease manifest thyrotoxicosis.

Mortality/Morbidity: Thyroid storm is an acute, life-threatening

emergency. Adult mortality 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

has declined to less than 20%.

Sex:

Thyrotoxicosis is 3-5 times more common in females than males,

especially in pubertal children.

Thyroid storm affects a small percentage of patients with

thyrotoxicosis. Incidence is presumed higher in females; however, no

specific data regarding sex-specific incidence are available.

Age:

Because thyrotoxicosis is more likely to occur in adolescents,

thyroid storm is more common in this age group, although thyroid

storm occurs in patients of all ages.

Infants younger than 1 year constitute only 1% of childhood

thyrotoxicosis. More than two thirds of cases occur in children aged

10-15 years. Overall, most thyrotoxicosis occurs during the third and

fourth decades of life.

Graves disease presents in 1-2% of neonates born to mothers who have

the condition.

CLINICAL Section 3 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

History: Patients may have known thyrotoxicosis. In the absence of

previously diagnosed thyrotoxicosis, history may reveal symptoms such

as irritability, emotional lability, voracious appetite with poor

weight gain, excessive sweating, and poor school performance caused

by short attention span.

General symptoms

Fever

Profuse sweating

Poor feeding and weight loss

Respiratory distress

Fatigue (more common in older adolescents)

GI symptoms

Vomiting

Diarrhea

Abdominal pain

Jaundice

Neurologic symptoms

Altered behavior

Seizures, coma

Anxiety (more common in older adolescents)

Physical:

Fever

Temperature consistently exceeds 38.5°C.

Patients may progress to hyperpyrexia.

Temperature frequently exceeds 41°C.

Excessive sweating

Cardiovascular signs

Hypertension with wide pulse pressure

Hypotension in later stages with shock

Tachycardia disproportionate to fever

Signs of congestive heart failure (CHF)

Cardiac arrhythmia (atrial fibrillation)

Neurologic signs

Agitation and confusion

Hyperreflexia and transient pyramidal signs

Tremors, seizures

Coma

Signs of thyrotoxicosis

Orbital signs

Goiter

Causes:

Thyroid storm is precipitated by the following factors in individuals

with thyrotoxicosis:

Sepsis

Surgery

Trauma

Drugs (eg, pseudoephedrine, other adrenergic and anticholinergic

drugs)

DKA

TH ingestion

Radioiodine therapy

Vigorous palpation of thyroid

Toxemia of pregnancy and labor in older adolescents

Most thyroid storm is associated with Graves disease in childhood.

Other reported causes of thyrotoxicosis associated with thyroid storm

include the following:

McCune-Albright syndrome with autonomous thyroid function

Hyperfunctioning thyroid nodule

Hyperfunctioning multinodular goiter

Thyroid-stimulating hormone (TSH)-secreting tumor

Graves disease also may occur in association with other autoimmune

conditions (and in children with Down or syndromes), including

the following:

Juvenile rheumatoid arthritis

disease

Myasthenia gravis

Chronic lymphocytic (Hashimoto) thyroiditis

Systemic lupus erythematosus

Chronic active hepatitis

Nephrotic syndrome

Although thyroid storm's exact pathogenesis is not fully understood,

the following theories have been proposed:

TH levels are not increased above levels observed in uncomplicated

thyrotoxicosis. Recent studies, however, have demonstrated relatively

high levels of free TH in patients with thyroid storm.

Adrenergic receptor activation is another hypothesis. In this theory,

sympathetic nerves innervate the thyroid gland, and catecholamines

can stimulate TH synthesis. This increased TH then increases the

density of beta-adrenergic receptors, thereby enhancing the effect of

catecholamines. Supporting this theory is the dramatic response of

thyroid storm to beta-blockers and the precipitation of thyroid storm

after accidental ingestion of adrenergic drugs such as

pseudoephedrine. This theory also explains normal or low plasma and

urinary excretion rates of catecholamines; it does not explain why

beta-blockers fail to decrease TH levels in thyrotoxicosis.

Another theory suggests a rapid rise of hormone levels as the

pathogenic source. A drop in binding proteins, which might occur

postoperatively, might cause a sudden rise in free hormone levels. A

rapid rise in hormone levels also may occur when the gland is

manipulated during surgery or by vigorous palpation during

examination.

Other proposed theories include tissue tolerance to THs, presence of

a unique catecholaminelike substance in thyrotoxicosis, and a direct

sympathomimetic effect of TH as a result of its structural similarity

to catecholamines.

DIFFERENTIALS Section 4 of 10

Author Information Introduction Clinical Differentials Workup

Treatment Medication Follow-up Miscellaneous Bibliography

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Guest guest

glad to hear she is doing better---she needs to get off that and use

armour you know---even thyrodine would be better---she would need to

find the correct does though but it would be worth a try.

tina

Thyroid Storm

> Last Updated: July 11, 2003 Rate this Article

> Email to a Colleague

>

>

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Guest guest

yeah, she wants to try Armour. Her doc has not been unopposed to letting her try

it. He just wanted to wait. He said if she got to up 100 mcg of Synthroid

without success he would definitely try it. i don't understand his logic nor

does she. he's been on vacation while she's been going thru all this. she is

planning on asking the endo she sees to try Armour.

take it easy, sheila

tina83862 <tina83862@...> wrote:

glad to hear she is doing better---she needs to get off that and use

armour you know---even thyrodine would be better---she would need to

find the correct does though but it would be worth a try.

tina

Thyroid Storm

> Last Updated: July 11, 2003 Rate this Article

> Email to a Colleague

>

>

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