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.
DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation. The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy.
• Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
Thyroid Storm and post-surgical hypoparathyroidismJin-Yi Hsu
Thyroid storm is a life-threatening condition, and early detection and early management are the most important. This is a case presentation about Grave's disease s/p subtotal thyroidectomy. However, the Grave's disease recurred and some precipitating factor induced the thyroid storm. Besides, post-surgical hypoparathyroid was found incidentally due to the seizure episode.
Myxoedema coma Pharmacotherapeutic viewPranatiChavan
Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.
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
Perioperative Management of Hypothyroid Patients Undergoing Nonthyroidal SurgeryTerry Shaneyfelt
In these annotated PowerPoint slides I describe the perioperative evaluation and management of patients with hypothyroidism needing nonthyroid surgery. Remember to download these slides to view the annotations for each slide.
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.
DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation. The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy.
• Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
Thyroid Storm and post-surgical hypoparathyroidismJin-Yi Hsu
Thyroid storm is a life-threatening condition, and early detection and early management are the most important. This is a case presentation about Grave's disease s/p subtotal thyroidectomy. However, the Grave's disease recurred and some precipitating factor induced the thyroid storm. Besides, post-surgical hypoparathyroid was found incidentally due to the seizure episode.
Myxoedema coma Pharmacotherapeutic viewPranatiChavan
Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.
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
Perioperative Management of Hypothyroid Patients Undergoing Nonthyroidal SurgeryTerry Shaneyfelt
In these annotated PowerPoint slides I describe the perioperative evaluation and management of patients with hypothyroidism needing nonthyroid surgery. Remember to download these slides to view the annotations for each slide.
The presentation deals with the basics of hemorrhage i.e. classification, etiology. It also covers the mechanism of hemostasis and the various methods to achieve hemostasis.
Hope you like it! Suggestions and feedback will always be well appreciated. :)
The prevalence of well-documented, permanent adrenal insufficiency is 5 in 10,000 in the general population. Hypothalamic-pituitary origin of disease is most frequent, with a prevalence of 3 in 10,000, whereas primary adrenal insufficiency has a prevalence of 2 in 10,000. Approximately one-half of the latter cases are acquired, mostly caused by autoimmune destruction of the adrenal glands; the other one-half are genetic, most commonly caused by distinct enzymatic blocks in adrenal steroidogenesis affecting glucocorticoid synthesis (i.e. congenital adrenal hyperplasia.)
Adrenal insufficiency arising from suppression of the HPA axis as a consequence of exogenous glucocorticoid treatment is much more common, occurring in 0.5–2% of the population in developed countries.
This presentation describes updated management of thyroid related emergencies. Anaesthetic considerations of myxoedema coma and thyrotoxic crisis is highlighted.
The thyroid gland is the body's largest single organ specialized for endocrine hormone production. Its function is to secrete an appropriate amount of the thyroid hormones, primarily (thyroxine, T4) , and a lesser quantity of triiodothyronine (T3) , which arises mainly from the subsequent extrathyroidal deiodination ofT4.
Thyroiditis is a general term that refers to “inflammation of the thyroid gland”. Thyroiditis includes a group of individual disorders causing thyroidal inflammation but presenting in different ways. For example, Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
3. MIXEDEMA COMA
Myxedema coma is the extreme expression of
severe hypothyroidism and fortunately is
rare, with an incidence rate of 0.22 per million
per year.
Myxedema coma occurs in younger patients as
well, with 36 documented cases of pregnant
women
Med Clin N Am 96 (2012) 385–403
4. MIXEDEMA COMA
A pituitary or hypothalamic basis for
hypothyroidism is encountered in about 5%
According to some studies, in up to 10% to
15% of patients
Med Clin N Am 96 (2012) 385–403
6. MIXEDEMA COMA
Clinical Signs and Symptoms
Hypothermia (often profound to 80F [26.7C]) and
unconsciousness constitute 2 ofthe cardinal features of
myxedema coma.
Underlying hypoglycemia may further compound the
decrement in body temperature.
Although coma is the predominant clinical presentation, a
history of disorientation,depression, paranoia, or hallucinations
Med Clin N Am 96 (2012) 385–403
7. MIXEDEMA COMA
The mechanism for hypoventilation in profound
myxedema is a combination of a depressed
hypoxic respiratory drive and a depressed
ventilatory response to hypercapnia
Typical electrocardiographic (ECG) findings
include bradycardia, varying degrees of
block, low voltage, flattened or inverted T
waves, and prolonged Q-T interval, which can
result in torsades de pointes ventricular
tachycardia.
Med Clin N Am 96 (2012) 385–403
8. MIXEDEMA COMA
Reduced stroke volume in severe cases may also
be due to the cardiac tamponade caused by the
accumulation of fluid rich in
mucopolysaccharides within the pericardial sac.
Hyponatremia is a common finding observed in
patients with myxedema coma. The mechanism
accounting for the hyponatremia is associated
with increased serum antidiuretic hormone and
impaired water diuresis caused by reduced
delivery of water to the distal nephron
Med Clin N Am 96 (2012) 385–403
9. MIXEDEMA COMA
The gastrointestinal tract in myxedema may be
marked by mucopolysaccharide infiltration and
edema of the muscularis, as well as neuropathic
changes leading to gastric atony, impaired
peristalsis, and even paralytic ileus.
Gastrointestinal bleeding secondary to an
associated coagulopathy
Med Clin N Am 96 (2012) 385–403
10. MIXEDEMA COMA
Severe hypothyroidism is associated with a
higher risk of bleeding caused by coagulopathy
related to an acquired von Willebrand syndrome
(type 1) and decreases in factors V, VII, VIII, IX,
and X
Med Clin N Am 96 (2012) 385–403
11. MIXEDEMA COMA
DIAGNOSIS
Physical findings could include
bradycardia, macroglossia, hoarseness, delayed
reflexes, dry skin, general
cachexia, hypoventilation, and
hypothermia, commonly without shivering.
Med Clin N Am 96 (2012) 385–403
12. MIXEDEMA COMA
DIAGNOSIS
Laboratory evaluation may indicate hypoxemia,
hypercapnia, anemia, hyponatremia,
hypercholesterolemia, and increased serum
lactate dehydrogenase and creatine kinase. On
lumbar puncture there is increased pressure and
the cerebrospinal fluid has high protein content
Med Clin N Am 96 (2012) 385–403
13. MIXEDEMA COMA
TREATMENT
VENTILATION AND AIR WAY
The patient’s comatose state is perpetuated by
hypoventilation, with CO2 retention and respiratory
acidosis
14. MIXEDEMA COMA
TREATMENT
HORMONAL THERAPY
The single intravenous bolus of T4 was
popularized by reports suggesting that
replacement of the entire estimated pool of
extrathyroidal T4 (usually 300–600 mg) was
desirable to restore nearnormal hormonal status
Med Clin N Am 96 (2012) 385–403
15. MIXEDEMA COMA
TREATMENT
HORMONAL THERAPY
Rodriguez and colleagues performed a prospective
trial in which patients were randomized to receive
either a 500-mg loading dose of T4 followed by a 100-
mg daily maintenance dose, or only the maintenance
dose.
The overall mortality rate was 36.4%, with a lower
mortality rate in the high-dose group (17%) than in
the low-dose group (60%)
Med Clin N Am 96 (2012) 385–403
16. MIXEDEMA COMA
HYPOTHERMIA
Treatment with T4 and/or T3 enables restoration of
body temperature to normal.
Simultaneously, blankets or increasing the room
temperature can be used as additional interventions
to keep the patient warm until the thyroid hormone
effect is achieved.
Too aggressive warming may cause peripheral
vasodilatation, which may then lead to hypotension or
shock.
17. MIXEDEMA COMA
HYPOTENSION
Hypotension should also be correctable by
treatment with T4 and/or T3.
However, a hypotensive patient may require
additional volume-repletion therapy.
Fluids may be administered cautiously as 5% to
10% glucose in 0.5 N sodium chloride if
hypoglycemia is present, or as isotonic normal
saline if hyponatremia is present
Med Clin N Am 96 (2012) 385–403
18. MIXEDEMA COMA
HYPOTENSION
Low serum sodium may cause a semicomatose
state or seizures even in euthyroid patients, and
the severe hyponatremia (105–120 mmol/L) in
profound myxedema is likely to contribute
substantially to the coma in these patients.
Med Clin N Am 96 (2012) 385–403
19. MIXEDEMA COMA
General supportive measures
In addition to the specific therapies
outlined, other treatments will be indicated as in
the management of any other elderly patient
with multisystem problems.
Management might include the treatment of
underlying problems such as
infection, congestive heart failure, diabetes, or
hypertension.
Med Clin N Am 96 (2012) 385–403
20. MIXEDEMA COMA
Prognosis
Even with this vigorous therapy, the prognosis for
myxedema coma remains grim, and patients with
severe hypothermia and hypotension seem to do
the worst. In the past the mortality rate was as
high as 60% to 70%, but this has now been
reduced to 20%–25% with the advances in
intensive care management.
Med Clin N Am 96 (2012) 385–403
21. THYROTOXIC STORM
Thyroid crisis or thyrotoxic storm is characterized
by severely exaggerated manifestations of
thyrotoxicosis. The underlying cause of
thyrotoxicosis is commonly Graves disease or
toxic multinodular goiter.
Rarely, thyrotoxic storm may occur with subacute
thyroiditis or factitious thyrotoxicosis caused by
intentional thyroxine overdose.
Med Clin N Am 96 (2012) 385–403
22. THYROTOXIC STORM
Epidemiology and Precipitating Events
An accurate estimation of the incidence of
thyroid storm is impossible to determine because
of the considerable variability in the criteria for
its diagnosis.
Med Clin N Am 96 (2012) 385–403
23. THYROTOXIC STORM
Clinical Signs and Symptoms
The clinical diagnosis is based on the
identification of signs and symptoms that suggest
decompensation of several organ systems.
Some of these cardinal manifestations include
fever out of proportion to an apparent infection
and dramatic diaphoresis
Med Clin N Am 96 (2012) 385–403
24. THYROTOXIC STORM
Cardiovascular Manifestations
Tachycardia, atrial fibrillation, or other
supraventricular tachyarrhythmias, and
rarely, ventricular tachyarrhythmias, which can
be observed even in patients without previous
heart disease.
Med Clin N Am 96 (2012) 385–403
25. THYROTOXIC STORM
Respiratory Manifestations
The main pulmonary symptom is dyspnea and
tachypnea related to an increased oxygen
demand. The excessive work of the respiratory
muscles may eventually lead to diaphragmatic
dysfunction.
Med Clin N Am 96 (2012) 385–403
26. THYROTOXIC STORM
Gastrointestinal Manifestations
The most common symptoms are diarrhea and
vomiting, which can aggravate volume
depletion, postural hypotension, and shock with
vascular collapse. The diffuse abdominal
pain, possibly caused by impaired
neurohormonal regulation of gastric
myoelectrical activity with delayed gastric
emptying, may even lead to a presentation such
as acute abdomen or intestinal obstruction.
Med Clin N Am 96 (2012) 385–403
27. THYROTOXIC STORM
Electrolyte Disturbances and Renal Manifestations
Increased serum calcium levels, caused by both
hemoconcentration and known effects of thyroid
hormone on bone resorption, may be seen.
The sodium, potassium, and chloride levels are
usually normal.
Med Clin N Am 96 (2012) 385–403
28. THYROTOXIC STORM
Hematological Manifestations
A moderate leukocytosis with a mild shift to the left is
a common finding, even in the absence of infection.
Hyperthyroidism may be associated with
hypercoagulability caused by increased
concentrations of fibrinogen, factors VIII and IX, tissue
plasminogen activator inhibitor 1, von Willebrand
factor, increase in red blood cell mass secondary to
erythropoietin upregulation, and a tendency to
augmented platelet plug formation.
Med Clin N Am 96 (2012) 385–403
29. THYROTOXIC STORM
Diagnosis
Diagnosis can be established predominantly on the
basis of clinical presentation, because the laboratory
findings may not be much different than those
observed in uncomplicated hyperthyroidism.
Indeed, serum total T3 levels may be even within
normal limits, as these patients may have some
underlying precipitating illness that reduces T4 to T3
conversion as is seen in the euthyroid sick syndrome
Med Clin N Am 96 (2012) 385–403
30.
31. THYROTOXIC STORM
Treatment
To avoid a disastrous outcome, a complex
approach to management is recommended.
First, specific antithyroid drugs must be used to
reduce the increased thyroid production and
release of T4 and T3. The second approach
comprises treatment intended to block the
effects of the remaining but excessive circulating
concentrations of free T4 and T3 in blood.
Med Clin N Am 96 (2012) 385–403
32. THYROTOXIC STORM
Treatment
Therapy directed to the thyroid gland
Inhibition of new synthesis of the thyroid
hormones is achieved by administration of
thionamide antithyroid drugs, such as
carbimazole, methimazole (Tapazole), and
propylthiouracil.
Given by nasogastric tube or per rectum as
enemas or suppositories
Med Clin N Am 96 (2012) 385–403
33. THYROTOXIC STORM
Prognosis
Even with early diagnosis, death can occur, and
reported mortality rates have ranged from 10%
to 75% in hospitalized patients
Med Clin N Am 96 (2012) 385–403
34. THYROTOXIC STORM
Total thyroidectomy is the procedure of
choice, in view of reports of recurrent severe
thyrotoxicosis and thyroid crisis after less than
total thyroidectomy.
Med Clin N Am 96 (2012) 385–403