This document discusses the management of thyroid storm, a life-threatening condition characterized by a hypermetabolic state caused by underlying hyperthyroidism. Key points include:
- Thyroid storm is diagnosed clinically or using scoring tools like the Burch-Wartofsky Point Scale.
- Management aims to inhibit thyroid hormone synthesis/release and peripheral effects while reversing decompensation. This involves high-dose antithyroid drugs, beta blockers, corticosteroids, inorganic iodide, and treating any precipitating factors.
- Supportive treatments like IV fluids and nutrition are also important, along with considering urgent thyroidectomy or radioactive iodine in some cases. Patient education is crucial
Thyroid storm is a life-threatening syndrome that results from an acute exacerbation of thyrotoxicosis. Prevention, prompt recognition, and appropriate intervention as discussed herein are key to the prevention of death and morbidity in affected patients. I hope you find it educating as well as enlightening.
Thyroid storm is basically a life threatening acute exacerbation of the clinical features of thyrotoxicosis.
Thyroid storm also known as thyroid crisis is an acute, life threatening hypermetabolic state induced by excessive activity of thyroid hormones in individuals with thyrotoxicosis.
Exact pathogenesis not understood.
No clear cut clinical feature separation from thyrotoxicosis.
precipitants of thyroid storm include the following
Infection, especially pneumonia
Cerebrovascular accident
Acute coronary syndrome, Congestive heart failure
Pulmonary embolus
Diabetic ketoacidosis
Parturition / toxemia
Major trauma
Surgery
Iodine 131 Rx or iodine contrast agents
Rapid withdrawl of antithyroid medications
Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased.
Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines.
The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines.
However, 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 protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
General symptoms
Fever
Profuse sweating
Poor feeding and weight loss
Respiratory distress
Fatigue (more common in older adolescents)
GI symptoms
Nausea and vomiting
Diarrhea
Abdominal pain
Jaundice
Neurologic symptoms
Anxiety (more common in older adolescents)
Altered behavior
Seizures, coma
Thyroid storm is a life-threatening syndrome that results from an acute exacerbation of thyrotoxicosis. Prevention, prompt recognition, and appropriate intervention as discussed herein are key to the prevention of death and morbidity in affected patients. I hope you find it educating as well as enlightening.
Thyroid storm is basically a life threatening acute exacerbation of the clinical features of thyrotoxicosis.
Thyroid storm also known as thyroid crisis is an acute, life threatening hypermetabolic state induced by excessive activity of thyroid hormones in individuals with thyrotoxicosis.
Exact pathogenesis not understood.
No clear cut clinical feature separation from thyrotoxicosis.
precipitants of thyroid storm include the following
Infection, especially pneumonia
Cerebrovascular accident
Acute coronary syndrome, Congestive heart failure
Pulmonary embolus
Diabetic ketoacidosis
Parturition / toxemia
Major trauma
Surgery
Iodine 131 Rx or iodine contrast agents
Rapid withdrawl of antithyroid medications
Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased.
Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines.
The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines.
However, 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 protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
General symptoms
Fever
Profuse sweating
Poor feeding and weight loss
Respiratory distress
Fatigue (more common in older adolescents)
GI symptoms
Nausea and vomiting
Diarrhea
Abdominal pain
Jaundice
Neurologic symptoms
Anxiety (more common in older adolescents)
Altered behavior
Seizures, coma
This lecture includes classification of antithyroid drugs, mechanism of action, adverse effect, therapeutic uses and advantage and disadvantages of them
Thyrotoxicosis is any syndrome caused by excess thyroid hormone and
can be related to excess hormone production (hyperthyroidism).It is Also called as overactive thyroid.Symptoms include unexpected weight loss, rapid or irregular heartbeat, sweating and irritability, although the elderly often experience no symptoms.
Treatments include radioactive iodine, medication and sometimes surgery.
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
Dive into the world of AI! Experts Jon Hill and Tareq Monaur will guide you through AI's role in enhancing nonprofit websites and basic marketing strategies, making it easy to understand and apply.
Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
Biological screening of herbal drugs: Introduction and Need for
Phyto-Pharmacological Screening, New Strategies for evaluating
Natural Products, In vitro evaluation techniques for Antioxidants, Antimicrobial and Anticancer drugs. In vivo evaluation techniques
for Anti-inflammatory, Antiulcer, Anticancer, Wound healing, Antidiabetic, Hepatoprotective, Cardio protective, Diuretics and
Antifertility, Toxicity studies as per OECD guidelines
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
Honest Reviews of Tim Han LMA Course Program.pptxtimhan337
Personal development courses are widely available today, with each one promising life-changing outcomes. Tim Han’s Life Mastery Achievers (LMA) Course has drawn a lot of interest. In addition to offering my frank assessment of Success Insider’s LMA Course, this piece examines the course’s effects via a variety of Tim Han LMA course reviews and Success Insider comments.
Safalta Digital marketing institute in Noida, provide complete applications that encompass a huge range of virtual advertising and marketing additives, which includes search engine optimization, virtual communication advertising, pay-per-click on marketing, content material advertising, internet analytics, and greater. These university courses are designed for students who possess a comprehensive understanding of virtual marketing strategies and attributes.Safalta Digital Marketing Institute in Noida is a first choice for young individuals or students who are looking to start their careers in the field of digital advertising. The institute gives specialized courses designed and certification.
for beginners, providing thorough training in areas such as SEO, digital communication marketing, and PPC training in Noida. After finishing the program, students receive the certifications recognised by top different universitie, setting a strong foundation for a successful career in digital marketing.
2. DEFINITION
Mortality 11-25%
(especially if you miss it)
Characterized by a multisystem disorder by
triggering event in conjunction with underlying
hyperthyroid conditions.
3. WHO DOES IT HAPPEN TO ?
Underlying thyroid disorders
• Grave’s disease
• Multinodular Goitre
• Hashimoto
• Thyroid adenoma
• Administration of iodinated contrast/radioactive iodine
• Diabetic ketoacidosis
• Severe Infection/sepsis
• Cardiac event
• Thyroidal or non-thyroidal surgery
• Trauma
• Pregnancy/post natal
• Adrenal insufficiency
Untreated / Undiagnosed/ Non-
compliant/discontinuation ATH
5. DIAGNOSIS OF THYROID STORM
• MADE CLINICALLY IN A THYROTOXIC PATIENT WITH EVIDENCE OF
DECOMPENSTATION, ITS OFTEN OVERLAP WITH CLINICAL FEATURES OF OTHER
CRITICAL MEDICAL CONDITIONS
• AID DIAGNOSTIC METHODS
• BURCH–WARTOFSKY POINT SCALE (RECOMMENDED TOOL, MORE SENSITIVE)
• THE NEWER JAPAN THYROID ASSOCIATION
6. BURCH–WARTOFSKY POINT SCALE
Score
• more/equal 45
thyroid storm
• 25-44 : Impending
thyroid storm
• <25 : Thyroid
storm unlikely
Score of 25-44,
requires clinical
judgement to look
for decompensation
7. THE NEWER JAPAN THYROID ASSOCIATION
*Grade TS2 :
requires clinical
judgement to
look for
decompensatio
n
8. MANAGEMENT
AIM OF MANAGEMENT OF THYROID STORM ;
• INHIBITING SYNTHESIS AND RELEASE OF THYROID HORMONE
• INHIBITING PERIPHERAL ACTION OF THYROID HORMONE
• REVERSING SYSTEMIC DECOMPENSATION
• TREATING PRECIPITATING EVENT
• ADDRESSING DEFINITIVE THERAPHY
9. ANTI-THYROID DRUG: MMI/PTU
• HIGH DOSE OF PROPYLTHIOURACIL(PTU) RECOMMENDED, WITH LOADING DOSE 500-1000MG THEN
250MG 4H
• IN THE PRESENCE OF CONTRAINDICATIONS, HIGH DOSE OF METHIMAZOLE (MMI) 60-80MG/DAY,
SINGLE DOSE OR DIVIDED INTO TWO EQUAL DOSES.
• PTU IS PREFERRABLY USED FOR COMPARED TO MMI IN THYROID STORM, AS LATTER HAS THE ADDED
BENEFITS OF INHIBITING TYPE 1 DEIODINASE ACTIVITY IN THE THYROID GLAND AND OTHER
PERIPHERAL ORGANS( REDUCE THE CONVERSION OF T4 TO T3), T3 LEVELS DROP BY 45% WITHIN
ONE HOUR OF PTU ADMINISTRATION BUT ONLY ABOUT 10-15% AFTER STARTING MMI.
• NO OUTCOME DIFFERENCES BETWEEN MMI AND PTU
ADJUVANT TREATMENT FOR THYROID STORM
LITHIUM CAN BE USED ALTERNATIVE FOR PATIENT WHO CANNOT TOLERATE MMI/PTU.
• WORKS BY INHIBITING RELEASE OF THYROID HORMONE BY THYROID GLAND THROUGH UNKOWN
MECHANISM
• DOSE: 300MG TDS, MONITORED LITHIUM TOXICITY
10.
11. BETA ADRENERGIC RECEPTOR ANTAGONISTS.
• KEY TO CONTROL HEART RATE AND INHIBIT OTHER PERIPHERAL ACTIONS OF
THYROID HORMONES IN THYROID STORM.
• ABILITY INHIBITS TYPE 1 DEIODINASE SUCH AS PROPRANOLOL, 60-80MG/4H
• BETA BLOCKERS WITH SELECTIVE B-1 BLOCKADE SUCH AS BISOPROLOL,
LANDIOLOL AND ESMOLOL INFUSION HAVE MORE FAVORABLE CVS BENEFITS IN
THYROID STORM WITH CARDIAC COMPROMISE.
• IV ESMOLOL LOADING DOSE 250-500MCG , MAINTAINANCE 50-1OOMCG/KG/MIN
• CONTRAINDICATIONS TO BETA BLOCKERS SUCH AS PATIENT WITH BRONCHIAL
ASTHMA OR COPD, DILTIAZEM CAN BE USED IN INTENSIVE CARE SETTING TO
CONTROL HR.
• AF PATIENT, CARDIOVERSION CONSIDERED AFTER R/OUT CARDIAC THROMBOSIS
IF HEMODYNAMICS ARE IMPAIRED.
12. CORTICOSTEROIDS
• TO INHIBIT BOTH THYROID HORMONE SYNTHESIS AND PERIPHERAL CONVERSION
OF T4-T3
• GIVEN AS PROPHYLAXIS FOR RELATIVE ADRENAL INSUFFICIENCY CAUSED BY
HYPERMETABOLIC STATE IN THYROID STORM.
• IV IS PREFERRED WHEN RAPID REACTION IS PREFFERED , WITH THE
IMPROVEMENT IN CLINICAL CONDITION DOSES SHOULD BE REDUCED AND
TAPERED OFF TO PREVENT ADVERSE EFFECT.
• DEXAMETHASONE (MEDIAN DOSE 6MG/DAY)
• HYDROCORTISONE (300MG/DAY)
• PREDNISALONE (25MG/DAY)
13. INORGANIC IODIDE(LUGOL’S IODINE/SATURATED SOLUTIONS OF POTASSIUM
IODIDE,SSKI)
• USED TO DECREASE T4 LEVELS BY INHIBITION OF IODIDE OXIDATION AND
ORGANIFICATION AND INHIBITS RELEASE OF THYROID HORMONE.
• RECOMMENDED DOSE 5DROPS OF LUGOL’S IODIDE 6H(6.25MG IODINE/DROP) OR
10DROPS OF LUGOL’S IODINE 8H
• THIS SOLUTION SHOULD BE DILUTED IN WATER OR TAKEN WITH BREAD TO AVOID
MUCUSAL IRRITATION.
• THIS AGENTS CAN BE USED IN COMBINATION WITH ATT.
• THESE AGENTS SHOULD ONLY BE GIVEN AT LEAST AFTER ONE HOUR OF ATT
DRUGS ADMINISTRATION, TO PREVENT USE OF IODINE AS SUBTRATE FOR
THYROID HORMONE SYNTHESIS.
• AFTER CLINICAL IMPROVEMENT, THE LUGOL’S SHOULD BE TAPERED AND
STOPPED BEFORE THE ANTITHYROID.
• LUGOL’S IODINE SHOULD NOT GIVEN BEYOND 10DAYS OR ELSE THIS WOULD
LEAD TO ESCAPE FROM WOLFF-CHAIKOFF PHENOMENON.
• CONTRAINDICATED: KNOWN TO BE ALLERGIC TO INORGANIC IODIDE
14.
15. SUPPORTIVE TREATMENT
• INTRAVENOUS FLUIDS
• RESPIRATORY SUPPORT INCLUDES INVASSIVE/NON-INVASSIVE
• NUTRITIONAL SUPPORT
• ACUTE INFECTIONS- SHOULD BE TREATED WITH BROAD SPECTRUM ABX
DEFINITIVE THERAPHY
URGENT/ EARLY THYROIDECTOMY
• IS AN OPTION IN PATIENTS WHO HAVE CONTRAINDICATIONS TO ATT, LARGE GOITRE
• PATIENTS SHOULD RENDERED TO EUTHYROID STATE PRIOR TO SURGERY TO MINIMISE RISK OF
THYROID STORM
• RAI IODINE IS CONSIDERED AND LUGOL’S IODINE HAS BEEN ADMINISTERED DURING THYROID STORM ,
THE RAI SHOULD BE DEFERRED UNTIL ABOUT 3-4 MONTHS AFTER.
PRECIPATING FACTORS: NON-COMPLIANCE
• PATIENT SHOULD BE EDUCATED ON THIS ASPECT
Editor's Notes
thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) to be transported. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of thyroid storm may be triggered by conditions (as explained earlier, the causes) that lead to the following:
Individuals with thyroid storm tend to have increased levels of free thyroid hormone, although total thyroid hormone levels may not be much higher than in uncomplicated hyperthyroidism.[9] The rise in the availability of free thyroid hormone may be the result of manipulating the thyroid gland. In the setting of an individual receiving radioactive iodine therapy, free thyroid hormone levels may acutely increase due to the release of hormone from ablated thyroid tissue
increases in thyroid hormone availability, it is also suggested that thyroid storm is characterized by the body's heightened sensitivity to thyroid hormone, which may be related to sympathetic activation
Sympathetic nervous system activation during times of stress may also play a significant role in thyroid storm.[3] Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in thyroid storm.
As with hyperthyroidism, TSH is suppressed. Both free and serum (or total) T3 and T4 are elevated.[5] An elevation in thyroid hormone levels is suggestive of thyroid storm when accompanied by signs of severe hyperthyroidism but is not diagnostic as it may also correlate with uncomplicated hyperthyroidism.
The diagnosis of thyroid storm is based on the presence of signs and symptoms consistent with severe hyperthyroidism.[9] Multiple approaches have been proposed to calculate the probability of thyroid storm based on clinical criteria, however, none have been universally adopted by clinicians.
Burch-wartofsky assigning a numerical value based on the presence of specific signs and symptoms organized within the following categories: temperature, cardiovascular dysfunction (including heart rate and presence of atrial fibrillation or congestive heart failure), central nervous system (CNS) dysfunction, gastrointestinal or liver dysfunction and presence of a precipitating event
Japanese Thyroid Association (JTA) criteria, derived from a large cohort of patients with thyroid storm in Japan and published in 2012, provide a qualitative method to determine the probability of thyroid storm. The JTA criteria separate the diagnosis of thyroid storm into definite versus suspected based on the specific combination of signs and symptoms a patient exhibits and require elevated free triiodothyronine (T3) or free thyroxine (T4) for definite thyroid storm.[14]