Download Thyroid Crises: Myxedema Coma and Thyrotoxic Crisis and more Lecture notes Pathology in PDF only on Docsity!
Myxoedema coma (Myxoedema crisis) Myxedema coma (myxedema crisis) is a rare but life-threatening condition that represents severe hypothyroidism with physiological decompensation. At risk patients: Occurs in patients with long-standing undiagnosed or undertreated hypothyroidism Precipitating factor(s): “Pathological” stress: eg. Critical illness: eg. Infection, CVA, Heart failure Trauma Post-operative stress C/F Hypothyroidism: PMH of hypothyroidism: may be +, but background hypothyroidism may be undiagnosed, so Myxedema crisis can be the initial presentation of hypothyroidism Hypothermia Heart rate: Bradycardia Hypotension (poor cardiac contractility due to profound deficiency of thyroxine) Hypoactivity: Altered sensorium/Behavioural disturbance/Confusion/Convulsion/Coma/Delirium/Drowsiness
Hypoventilation: Drowsiness (CO2 retention due to central depression of ventilatory drive) Hyponatremia: asymptomatic or symptomatic (Lack of thyroxine promotes Natreuresis) Hypoglycemia: asymptomatic or symptomatic
Investigations: Diagnostic purpose: Thyroid function test: Hypothyroid pattern: Elevated TSH with low FT4 and FT3 indicates primary thyroid disorder Low TSH level with low FT4 and FT3 indicates pituitary or hypothalamic dysfunction. Assessment purpose: To look for any ppting factor+ biochemical disturbance associated with severe hypothyroidism CBC CRP Ur+ Cr Electrolytes: Na/K ABG ECG Infection/sepsis screen: CxR/Urine R.E/M.E/C.S+ Blood C/S+ Procalcitonin Treatment: Definitive: 1.Thyroxine replacement: Ideally initially IV Levothyroxine (T4) + T3, Once stable start PO Levothyroxine Because the rate of conversion of T4 to the active hormone T3 can be reduced in these patients, the addition of T3 along with T4 has been recommended. (IV thyroxine preparation is NOT available in India, so we rely on PO/Ryles tube administration) 2.Corticosteroid: IV Hydrocortisone should be administered until the possibility of adrenal insufficiency is excluded by ACTH stimulation test because otherwise there is a potential risk of precipitating acute adrenal insufficiency caused by the accelerated metabolism and increased demand of cortisol that follows T4 therapy. Primary hypothyroidism may have concomitant primary adrenal insufficiency while patients with secondary hypothyroidism may have associated hypopituitarism and secondary adrenal insufficiency. Supportive: ≥ 1 of the followings depending on clinical scenario Hypothermia: Passive rewarming using ordinary blankets and a warm room Active rewarming using external devices: Bair Hugger blanket is the temperature management system that uses forced-air warming (but carries a risk of vasodilatation and worsening hypotension and should be avoided) Hypotension: intravenous fluids with normal saline is advised. Refractory hypotension can be treated with vasopressors Hypoventilation: Intubate and ventilate Hyponatremia: saline and free water restriction Hypoglycemia: intravenous dextrose Treat any precipitating factor
Thyrotoxic crisis Thyroid storm (thyrotoxic crisis) is an acute, life-threatening, hypermetabolic state induced by excessive release of Thyroxine in individuals with thyrotoxicosis.
Pathogenesis: Severely exaggerated effects of Thyroxine due to increased release (with or without increased synthesis) Precipitating factors: Thyroid storm is precipitated by the following factors in individuals with thyrotoxicosis: Sepsis Surgery Anesthesia induction RAI therapy Noncompliance with antithyroid medications
Direct trauma to the thyroid gland Vigorous palpation of an enlarged thyroid Toxemia of pregnancy Molar pregnancy
C/F: are due to ≥ 1 of the followings: Hyperthyroidism: background of thyrotoxic manifestations Hyperpyrexia Hyperphagia: voracious appetite Hyperhydrosis: excessive sweating Hyperactivity: anxiety/agitation/behavioural disturbance/confusion/convulsion/ delirium/emotional lability Heart Hypertension with wide pulse pressure Hypotension in later stages with shock Tachycardia disproportionate to fever Arrhythmia Hyperperistalsis: Nausea, vomiting, diarrhoea, abdominal pain Hyperreflexia
Investigations: Thyroid function test: Low TSH level with high FT4 and FT3 indicates primary thyroid disorder Elevated TSH with high FT4 and FT3 indicates excess TSH secretion: pituitary or nonpituitary source
Management: 1.Antiadrenergic drugs: Propranolol: orally or via nasogastric tube :dose based on heart rate and blood pressure 2.Iodine compounds: Lugol iodine or KI: orally or via a nasogastric tube to block the release of Thyroxine- to be given at least 1 hour after starting antithyroid drug therapy 3.Antithyroid drugs: Carbimazole/Methimazole- to block further synthesis of thyroid hormones 4.Glucocorticoids to decrease peripheral conversion of T4 to T 5.Bile acid sequestrant: Cholestyramine prevents reabsorption of free Thyroxine in the gut Supportive measures: ≥ 1 of the followings depending on clinical scenario 1.Supplemental oxygen 2.Ventilatory support 3.IV fluid: Dextrose solutions are the preferred to cope with continuously high metabolic demand. 4.Correct electrolyte abnormalities. 5.Treat cardiac arrhythmia, if necessary. 6.Aggressively control hyperthermia by applying ice packs and cooling blankets and by Paracetamol
Investigation: Diagnostic purpose: 1.Random Serum cortisol: Very low level is indicative of adrenal insufficiency. 2.ACTH stimulation test: diagnostic test- treatment SHOULD be started on the basis of suspicion pending the result Assessment purpose: To look for any ppting factor+ biochemical disturbance associated with severe hypothyroidism CBC CRP Ur+ Cr Electrolytes: Na/K ABG ECG Infection/sepsis screen: CxR/Urine R.E/M.E/C.S+ Blood C/S+ Procalcitonin Treatment: Definitive: Glucocorticoids in supraphysiologic or stress doses. Dexamethasone does not interfere with serum cortisol assay and, thus, may be the initial drug of choice. However, because Dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement are essential. Hydrocortisone 100 mg IV every 6 hours is the preferred treatment to provide mineralocorticoid support. Delaying glucocorticoid replacement therapy while awaiting the results of the ACTH stimulation test is inappropriate and dangerous. Supportive: Aggressive fluid replacement with 5% or 10% intravenous dextrose and saline solutions Treatment of hyperkalemia Look for a precipitating cause and administration of empiric antibiotics is indicated. Vasopressors (Dopamine/Noradrenaline) may be necessary to combat hypotension.
Refer to notes for: DKA (“prepare” for LQ as well as Sh. Notes) HHS/HONC (“prepare” for LQ as well as Sh. Notes) Pituitary apoplexy Sheehan syndrome (Expecting a post “dada/sir, can you please write DKA and HHS as a short note type answer”!!)
Aortic dissection Aortic dissection is defined as separation of the layers within the aortic wall. Tears in the intimal layer result in the propagation of dissection as blood enters the intima-media space Symptoms: include the following: Chest pain Sudden onset of severe chest pain that often has a tearing or ripping quality (classic symptom) Anterior chest pain: Usually associated with anterior arch or aortic root dissection Neck or jaw pain: With aortic arch involvement and extension into the great vessels Tearing or ripping intrascapular pain: May indicate dissection involving the descending aorta No pain in about 10% of patients Syncope Cerebrovascular accident (CVA) symptoms Dyspnea Signs: include the following: Hypertension Hypotension Interarm blood pressure differential greater than 20 mm Hg Signs of aortic regurgitation Asymmetrical pulses
Diagnosis Blood: Falling Hb & Hct: Leaking or rupture of the dissection Elevation of the Urea & Creatinine: Renal artery involvement or prerenal azotemia Elevation of the myocardial enzymes: Myoglobin/ TropI &T level: Myocardial ischemia from coronary artery involvement Lactate dehydrogenase elevation: Hemolysis in the false lumen Imaging : CxR: Widening of the mediastinum is the classic finding Contrast CT Chest: definitive test in most patients with suspicion of aortic dissection Echo: Transoesophageal echocardiography (TEE) is more accurate than transthoracic echocardiography (TTE) MRI: Most sensitive method for diagnosing aortic dissection Management Surgical: Emergency surgical correction Medical: Decreasing the blood pressure and the shearing forces of myocardial contractility:Antihypertensive therapy with beta blockers, is the treatment of choice for all stable chronic aortic dissections Pain management: Narcotics and opiates are the preferred agents
Anaphylaxis An acute, potentially fatal reaction caused by the release of chemical mediators from mast cells and basophils. The classic form involves prior sensitization to an allergen with later reexposure, producing symptoms via an immunologic mechanism. C/F: commonly affects the cutaneous, respiratory, cardiovascular, and gastrointestinal systems. Symptoms: Dermatologic: Flushing, urticaria, pruritus, warmth and swelling Ocular: Conjunctival congestion/itching Respiratory: Nasal congestion, rhinorrhea, sneezing, throat tightness, wheezing, shortness of breath, cough Cardiovascular: Dizziness, syncope, chest pain, palpitation Gastrointestinal: Dysphagia, nausea, vomiting, diarrhoea Neurologic: Headache, dizziness, blurred vision Signs: Vital signs: Vary according to the severity of the anaphylactic episode Respiratory: Severe angioedema of the tongue and lips; tachypnea; stridor/wheezing Cardiovascular: Tachycardia, hypotension- shock can occur immediately Neurologic: Altered sensorium Dermatologic: Urticaria anywhere on the body; angioedema (soft-tissue swelling) Investigations: Usually not required and are rarely helpful. However, if the diagnosis is unclear, especially with a recurrent syndrome, or if other diseases need to be excluded, the following laboratory may be ordered in specific situations: Serum tryptase may help confirm the diagnosis of anaphylaxis Urinary 24-hour histamine may help in the diagnosis of recurrent anaphylaxis Skin testing/ Immunoglobulin E (IgE) tests, or both- to determine the stimulus causing the anaphylactic reaction. Management Nonpharmacotherapy: Supportive care includes the following: Airway management: ventilator support with bag/valve/mask, endotracheal intubation( if required) High-flow oxygen Cardiac monitoring and/or pulse oximetry Intravenous access Fluid resuscitation with isotonic crystalloid solution Supine position (or position of comfort if dyspneic or vomiting) with legs elevated
