Guest guest Posted March 27, 2004 Report Share Posted March 27, 2004 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 28, 2004 Report Share Posted March 28, 2004 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 28, 2004 Report Share Posted March 28, 2004 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 > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 28, 2004 Report Share Posted March 28, 2004 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 > > Quote Link to comment Share on other sites More sharing options...
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