Endocrine Emergency Part 1
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DKA, HHS, Hypoglycemia, Thyroid Storm, Myxedema Coma, Adrenal Insufficiency
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Endocrine Emergency Part 1
- 1. Presented by: Dr. Stacy Arvinna Department : Emergency, HDOK.
- 2. 1. Hypoglycaemia 2. Diabetic Ketoacidosis 3. Hyperosmolar Hyperglycaemic State Pituitary apoplexy 1. Addisonian Crisis 2. Phaeochromocytoma hypertensive crisis 1. Thyroid storm 2. Myxoedema coma Parathyroid gland Hypo / hypercalcaemia
- 3. OVERVIEW DIABETIC KETOACIDOSIS HHS HYPOGLYCEMIA THYROID STORM MYXEDEMA COMA ADRENAL INSUFFICIENCY
- 5. DIABETIC KETOACIDOSIS DKA is a triad of hyperglycaemia, ketosis and acidaemia DKA is a potentially life threatening medical emergency due to absolute or relative insulin deficiency coupled with counter-regulatory hormones excess. Diagnostic criteria (ADA) : - Blood glucose > 13.8 mmol/l - pH < 7.3 - Serum bicarbonate < 18mmol/l, - Anion gap > 10 - Ketonaemia
- 7. Clinical Features : - Polyuria - Polydipsia - Weight loss - Vomiting - Abdominal pain - Weakness - Tachypnea - Altered mental status Physical findings: - Dehydration - Hypotension - Tachycardia - Poor skin turgor - Precipitating causes present (infection, vascular events, drug abuse etc)
- 8. Laboratory Findings : - Hyperglycaemia (> 13.8 mmol/l) - Hyperosmolality [2x(Na+K) + Urea + Glucose] - Ketones - Widened anion gap metabolic acidosis (pH < 7.3) - Elevated urea and creatinine - Hyperkalaemia - Leucocytosis
- 10. Differential diagnosis. Hyperglycemic hyperosmolar state is not associated with ketosis. Starvation and alcoholic ketoacidosis are not characterized by hyperglycemia >200 mg/dl and bicarbonate level <18 meq/L. With hypotension and history of metformin use, lactic acidosis (lactic acid level >7 mmol/L) should be suspected. Ingestion of methanol, isopropyl alcohol, and paraldehyde can also alter anion gap and/or osmolality and need to be investigated.
- 13. Management A.Fluid therapy B.Insulin infusion C.Electrolyte management D.Treatment of underlying cause According to ENDOCRINE UNIT HOSPITAL UNIVERSITI SAINS MALAYSIA KOTA BHARU, KELANTAN
- 14. FLUID THERAPY Rate Action Fluid Step 1 1 pint over 30 min for 1 hour To review 1 litre Step 2 1 pint over 1 hour for 2 hour To review 1 litre Step 3 1 pint over 2 hour for 4 hour To review 1 litre Step 4 1 pint over 4 hour for 8 hour To review 1 litre Fluid replacement is priority one in the treatment of DKA. Replace fluid deficit in DKA (~6 L) within 24-36 hours with the goal of 50% volume replacement within first 12 hours.
- 15. INSULIN INFUSION Start IVI at 0.1 unit/kg/ hr based on estimated body weight (50 units human soluble insulin;Actrapid/ Humulin R + 0.9% NaCl= 50 ml) Irrespective of blood glucose level Bolus insulin is not recommended Monitor blood glucose level hourly Aim for blood glucose drop of 2-4mmol/L per hour Initially, aim for CBG~10mmol/L (range 8-12mmol/L) until DKA has improved oWithold insulin infusion if serum potassium <3.5mmol/L or ECG changes of hypokalaemia. o Transition to SC insulin by giving long-acting insulin 2 hours before the discontinuation of IV insulin.
- 16. ELECTROLYTE MANAGEMENT Potassium Begin preplacement at the second hour of fluid therapy Start with 0.5 gm KCL per hour over 2 hour (eg. Add 0.5gm KCL in 1 pint of normal saline and run over 1 hour for 2 hour). Once result is available, replace according to the result Aim-Serum Potassium 4.0-5.0mmol/L Sodium If serum sodium is normal, use 0.9% NaCl(normal saline) in fluid therapy If elevated (>160mmol/L) use 0.45% NaCl (half normal saline) in fluid therapy Bicarbonate Bicarbonate replacement is not routinely indicated in the management of DKA Consider giving bicarbonate replacement if pH <7.0 and/or serum bicarbonate <10mmol/L if pH is < 7.0 or bicarbonate level is < 5 meq/L, administer 100 mmol (2 ampules) of bicarbonate in 200 ml of water with 20 meq of potassium chloride over two hours.
- 17. Outline monitoring regimen Hourly capillary blood glucose Vital signs and input-output charting hourly Venous bicarbonate and potassium at 60minutes, 4 hours and 6-hourly thereafter 6-hourly plasma electrolytes and urine ketone Continuous pulse oximetry (if indicated) Continuous cardiac monitoring (if indicated) Look for precipitating cause and start broad spectrum antibiotic if infection suspected.
- 19. HYPEROSMOLAR HYPERGLYCAEMIC STATE Hyperosmolar hyperglycaemic state (HHS) is caused by deficiency of insulin usually in elderly patients; 2/3 have previously undiagnosed diabetes Mortality up to 50% Diagnostic criteria: •Hypovolaemia •Marked hyperglycaemia (BG>30mmol/L) •Osmolality >320 mosmol/kg
- 21. Precipitants : - Infection - Myocardial infarction / cerebrovascular accident - Inadequate insulin treatment / noncompliance - High sugar intake - Other endocrine disorders e.g. acromegaly - Drugs e.g. glucocorticoids, thiazides, loop diuretics, phenytoin
- 23. Laboratory Findings : - Hyperglycaemia - Hyperosmolarity [2x(Na+K) + Urea + Glucose] - Hypo or hypernatraemia - Hyperkalaemia
- 27. HYPOGLYCAEMIA IN CONTEXT OF DIABETES; excess insulin in absence of enough carbohydrate. Most common in insulin treated patient. Low blood glucose concentrations lead to adrenergic activation and neuroglycopenia . Symptomatic hypoglycemia is diagnosed clinically using Whipple’s triad: symptoms of hypoglycemia, plasma glucose concentration<50 mg/dl (2.8 mmol/l), and resolution of those symptoms after the plasma glucose concentration is raised. ALL UNCONSCIOUS PATIENTS SHOULD BE ASSUMED TO BE HYPOGLYCAEMIC UNTIL PROVEN OTHERWISE
- 28. Hypoglycaemia unawareness occurs in up to 1/3 patients with type 1 diabetes Conversely, some patients have hypoglycaemic symptoms when their glucose is above the target range (> 7.0 mmol/l) Patients post total pancreatectomy have more frequent and severe episodes because they have also lost their glucagon producing cells
- 29. PATHOPHYSIOLOGY Redundant counter-regulatory mechanisms are in place to prevent or correct hypoglycemia. As glucose levels decline, major defenses include: 1) a decrease in insulin secretion; 2) an increase in glucagon secretion; 3) an increase in epinephrine secretion. Increased cortisol and growth hormone secretion also occur. If these defenses fail, plasma glucose levels will continue to fall. In type 1 and longstanding type 2 diabetes these counter-regulatory responses to hypoglycemia are frequently impaired. This increases the risk of hypoglycemia and also contributes to hypoglycemia unawareness.
- 30. Causes : 1. Drugs - insulin/oral hypoglycaemics - alcohol - salicylates - quinine - beta-blockers, pentamidine, disopyramide - prescription errors e.g. chlorpropamide for chlorpromazine 2. Tumours - Insulinoma - Retroperitoneal sarcomas 3. Miscellaneous - Liver dysfunction - adrenal insufficiency / hypopituitarism - renal failure - myxoedema
- 31. Presentation : 1. Autonomic (Blood glucose 3.3 – 3.6 mmol/l) - diaphoresis - anxiety - palpitations / tachycardia - tremor - warm feeling 2. Neuroglycopenic (Blood glucose <2.6 mmol/l) - confusion - slurred speech - visual disturbances - being uncoordinated - tiredness - focal neurological defects - coma / seizures (usually with glucose <1.5 mmol/l)
- 32. Diagnosis : - Blood glucose - U and E, liver profile - Insulin and C-peptide levels - Sulphonylurea screen - IGF-2
- 35. Thyroid gland
- 36. Thyroid Storm A life threatening exacerbation of the hyperthyroid state with evidence of decompensation in one or more organ systems. The mortality is 20 - 30 %. It may be precipitated by stress including concurrent infections, surgery or pregnancy. It is a clinical diagnosis with features of severe thyrotoxicosis, hyperpyrexia and neuro-psychiatric manifestations such as delirium. Malaysian Endocrine and Metabolic Society (MEMS)
- 37. Precipitating factors General: Infection. Non-thyroidal trauma or surgery. Psychosis. Parturition DKA Myocardial infarction or other acute medical problems. Thyroid specific: Radioiodine. High doses of iodine-containing compounds (for example, radiographic contrast media). Discontinuation of antithyroid drug treatment. Thyroid injury (palpation, infarction of an adenoma). New institution of amiodarone therapy.
- 40. Scoring. <25 : unlikely thyroid storm 25-44 : supports the diagnosis >45 : highly suggestive of thyroid storm Adapted from: Burch HB, Wartofsky L. Life threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am 1993: 22:263
- 41. Laboratory investigation Free T4, free T3 elevated TSH suppressed Note that findings are not different than that of hyperthyroidism, but the difference is in the setting Biochemical features include hyperglycaemia, leucocytosis, mild hypercalcaemia, and abnormal liver function tests.
- 42. Uncomplicated Thyrotoxicosis Thyroid Storm Heat intolerence, diaphoresis Hyperpyrexia, temperature >38.5C, dehydration Sinus tachycardia, Heart rate 100-140 HR >140bpm, hypotension, atrial dysrhythmias, congestive heart failure Diarrhea, increase appetite with loss of weight Nausea, vomitting, severe diarrhea, abdominal pain, hepatocellular dysfunction-jaundice Anxiety, restlessness Confusion, agitation, delirium, frank psychosis, seizures, stupor or coma
- 43. Management of Thyroid Storm Asses ABCDE Rehydration Treat hyperpyrexia (use fans, tepid sponging and oral paracetamol) Do NOT use aspirin or NSAIDs
- 44. Treatment of Thyroid Storm Sympathetic outflow Production and release of thyroid hormone Peripheral conversion (T4 T3) Triangle of Treatment
- 45. Management of Thyroid Storm Beta sympathetic blocking agents o Oral propanolol 40 mg qid, or I/V 1-2 mg 4-6 hourly Iodide o Oral saturated solution of potassium iodide (SSKI) 5 drops 6-hourly o or I/V Sodium Iodide 500 mg 8 hourly o or oral Lugol's iodine 5-10 drops, 6-hourly Antithyroid Drugs o Carbimazole 15-20 mg 6-hourly o or propylthiouracil 150-200 mg 6-hourly Corticosteroids o I/V dexamethasone 2 mg 6-hourly o or I/V hydrocortisone 200 mg 6-hourly
- 46. Take home points 1.Patients susceptible to developing thyroid storm have increased sensitivity to catecholamines. Therefore, any stressor that leads to outpouring of catecholamines, can lead to thyroid storm. 2.Thyroid storm is a true medical emergency; these patients should be managed in the ICU and beta-blockers should be started early (esmolol is a great choice because of its short half-life (on the order of seconds). 3.Remember the “triangle of treatment”: decrease sympathetic outflow, decrease production of thyroid hormone, and decrease peripheral conversion of T4 to T3.
- 48. Myxedema Coma Severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. It is a medical emergency with a high mortality rate. Fortunately, it is now a rare presentation of hypothyroidism, likely due to earlier diagnosis as a result of the widespread availability of thyroid-stimulating hormone (TSH) assays. End stage of untreated or insufficiently treated hypothyroidism History: Previous thyroid surgery Radioiodine Default thyroid hormone therapy
- 49. Precipitating factors Hypothermia. Infections especially pneumonia. Myocardial infarction or congestive heart failure. Cerebrovascular accident. Respiratory depression due to drugs (for example, anaesthetics, sedatives, tranquillisers). Trauma or gastrointestinal blood loss
- 52. Physical Findings Comatose or semi comatose Dry coarse skin Hoarse voice Thin dry hair Delayed reflex relaxation time Hypothermia Pericardial, pleural effusions, ascites
- 53. Lab Tests Free T4 low and TSH high If the T4 is low and TSH low normal consider pituitary hypothyroidism Blood gasses Electrolytes and creatinine Distinguish from euthyroid sick syndrome Low T3, Normal or low TSH, normal free T4
- 54. Management 1. ABCDE assesment 2. Gradual rewarming with blankets. 3. Accurate core temperatures should be recorded with a low reading Rectal thermometer. 4. Thyroid hormone replacement with L-thyroxine 300-400 ug given orally via nasogastric tube or parenterally if available. Alternatively, doses of tri- iodothyronine 10 ug 8-hourly (IV or orally) may be used.
- 55. 5. I/V hydrocortisone should be given, 200 mg stat and 100 mg 6-hourly until patient regains consciousness. Controversial but necessary in hypopituitarism or multiple endocrine failure 6. Ensure adequate hydration and nutrition; Use 5-10% dextrose solution to maintain normal blood glucose levels. 7. Correct electrolyte imbalance (patients tend to be hyponatraemic). 8. Ensure adequate ventilation. Patients tend to hypoventilate, resulting in hypercapnoea. 9. Treat precipitating cause. 10. Infection may be masked by the hypothyroid state.
- 57. Adrenal Gland
- 60. ACUTE ADRENAL INSUFFICIENCY Clinical Features : - Hypotension (mineralocorticoid deficiency) - Postural hypotension - Nausea and vomiting, weight loss, fatigue - Hypoglycaemia - Hyperpigmentation
- 62. Clues to Underlying Chronic Adrenal Insufficiency Pigmentation in unexposed areas of the skin Creases of hands Buccal mucosa Scars Consider adrenal insufficiency if hypotension does not respond to pressors
- 63. Lab Tests Hyponatremia and hyperkalemia (Hyponatremia might be obscured by dehydration) Random cortisol is not helpful unless it is very low (<5 mg/L) during a period of great stress
- 64. Lab Diagnosis ACTH (cosyntropin) stimulation test Failure of cortisol to rise above 552 nmol/L 30 min after administration of 0.25 mg of synthetic ACTH IV Basal ACTH will be raised in primary adrenal insufficiency but not in secondary CT of abdomen will reveal enlargement of adrenals in patents with adrenal hemorrhage, active TB or metastatic malignancy
- 65. Management of Acute Adrenal Insufficiency ABCDE assesment Hydrocortisone 100 mg IV stat then 50 mg 4 hly for 24 h Taper slowly over the next 72 h When oral feeds is tolerated change to oral replacement therapy Overlap the first oral and last IV doses Replace salt and fluid losses with 5% dextrose in normal saline IV
- 66. Patients with primary adrenal insufficiency may require mineralocorticoid therapy (fludrocortisone) when shifted to oral therapy Treat precipitating diseases
- 67. SOURCES Practice Guidelines For Thyroid Disorders The Malaysian Consensus 2000 Postgraduate Medical Journal Clinical Practice Guidelines Management Of Type 2 Diabetes Mellitus(5th Edition) 2015 http://www.endotext.org http://www.ncbi.nlm.nih.gov www.medscape.org Greenspan Fs. The Thyroid Gland – Thyrotoxicosis Crisis. In Basic And Clinical Endocrinology. Greenspan Fs, Gardner Dg, Eds. New York: Lange Medical, 2001. Pp. 247-8 Hyperthyroidism: Management Guidelines Of The American Thyroid Association And American Association Of Clinical Endocrinology
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- Pathogenesis : - insulin deficiency - increased counter-regulatory hormones (glucagon, catecholamines, cortisol and GH) This leads to increased glucose production by the liver and decreased utilisation in peripheral tissues. Lipolysis results in ketone body production and acidosis.
- Most patients usually present to emergency and ICU within 24 h of development of polyuria, polydipsia, weakness, and weight loss. There may be complaints of anorexia, abdominal pain, fatigue and muscle cramps. Intravascular volume depletion due to osmotic effects leads to dry mucous membranes, sunken eyeballs, tachycardia, orthostatic hypotension, and even supine hypotension. Tachypnea occurs to compensate the biochemical effects of metabolic acidosis. Infection and sepsis can aggravate the clinical effects of volume depletion. Altered sensorium ranging from mild confusion to coma may prevail.
- The first goal of therapy is to correct tissue hypo-perfusion, improve glomerular filtration and reverse the insulin resistance and deficiency. Note: 1.Starting point depend on severity ofdehydration. If a patient is not severely dehydrated, may start with Step 2or Step 3. 2.After each step, review the patient for adequacy of fluid replacement and evidence of fluid overload . a)Symptom eg. Breathlessness b)Sign eg. BP,PR, JVP, Lung Examination(for basal crepitation) c)Monitoring-Input/output chart (Aim for urine output ~1ml/min) -CVP (When indicated; aim for CVP reading 8-10cm H2O) d)Laboratory values-Hb, Hct,Urea (if available) 3.At review •If patient still hemodynamicallyunstable ie. dehydrated and hypotensive with no urine output – repeat same step •If patient is improving, follow from step 1- step 4, and continue step 4 as maintenance •If patient developed fluid overload, withhold fluid therapy and manage the fluid overload accordingly. Once stable, restart fluid therapy at slower rate ie. Skip the next step and go directly the step after that (eg. Step 2–fluid overload-skip Step 3-go to Step 4) 4.Usual deficit in moderate DKA is 6L (range 4-8L)-aim 50% replacement in 6 hour, and total replacement within 24-48 hours. 5.In the acute stage, do not order fluid regimen for 24 hour. Always review after each steof fluid regime. 6.Caution in the elderly, those with heart failure or renal failure, slow replacementis imperative and frequent review is necessary to detect sign of fluid overload. 7.Use 0.45% NaCl (half normal saline) if serum Na>160mmol/L. 8.Once blood glucose level ~10mmol/L-change to 5% dextrose.
- I.Aim for blood glucose drop of 2-4mmol/L per hour oIf CBG is dropping at <2mmol/L per hour-increase insulin dose by 2u/hr. Continue increasing the dose by 2u/hr until blood glucose fall by 2-4mmol/hr, ORinsulin dose more than 6u/hr oIf CBG is reducing at the rate of 2-4mmol/L per hour- maintains the current dose oIf CBG is reducing at the rate >4 mmol/L per hour – reduce insulin infusion by 2u/hr (or if present insulin dose is ≤2u/hr, half the current dose) II.Initially, aim for CBG~10mmol/L (range 8-12mmol/L) until DKA has improved, inform doctor if CBG <8mmol/L OR > 12 mmol/L. Once DKA has resolved (fully conscious, acidosis normalized) aim for CBG of 4-6mmol/L. Inform the doctor if CBG <4mmol/L OR >8mmol/L. Consider changing to s/c insulin if patient is able to take regular meal. III.Caution: oInform endocrinologist on-call if insulin rate is >6u/hr. oWithold insulin infusion if serum potassium <2.5mmol/L with ECG changes of hypokalaemia. – Correct potassium under continuous cardiac monitoring. –restart insulin therapy once serum potassium ≥3.0mmol/L or normalization of ECG changes. Cerebral edema is reported in young adult patients. This condition is manifested by appearance of headache, lethargy, papillary changes, or seizures. Mortality is up to 70%. Mannitol infusion and mechanical ventilation should be used to treat this condition.
- Danger a.Rapid infusion of KCL may cause cardiac arrest b.KCL must neverbe administered by IV bolus or IM injection e)Caution a.Do not give potassium if urine output is poor ie. ≤30ml/hr (patient may need to be catheterized for accurate urine output charting) b.Withold potassium replacement if serum potassium is >5.5mmol/L c.Withold insulin if serum potassium < 2.5mmol/L f)Aim-Serum Potassium 4.0-5.0mmol/L Consider giving bicarbonate replacement if pH <7.0 and/or serum bicarbonate <10mmol/L •Give 50ml 8.4% NaHCO3 over 1 hour •Repeat ABG 1 hour after completion of infusion •Repeat NaHCO3 infusion if pH is still <7.0 Caution-HCO3 over correction may cause complication including: •Hypokalaemia •Cerebral oedema •Pulmonary oedema •Lactic acidosis Bicarbonate (mmol) = base deficit × weight (kg) × 0.3 Half of the amount is given as bolus dose and rest as slow infusion over 8 hours period. Phosphate a)Phosphate replacement is not routinely indicated in the management of DKA b)Consider giving phosphate replacement if serum phosphate <0.3mmol/L or in patient with severe hypoxia
- severe hyperglycemia, often >600 mg/dl, and hyperosmolality with preservation of near normal pH and bicarbonate, and minimal or absent serum and/or urine ketones. Diagnostic criteria of HHS (Level III) •Hypovolaemia •Marked hyperglycaemia (BG>30mmol/L) •Osmolality >320 mosmol/kg
- PATHOPHYSIOLOGY HHS and diabetic ketoacidosis (DKA) represent the two ends of the spectrum of markedly decompensated diabetes, differing mainly in severity of acidosis, ketosis and dehydration. HHS usually occurs with lesser degree of insulinopenia compared with DKA, but the pathophysiology is otherwise thought to be similar. In both entities, there is a decrease in net effective insulin action with concomitant elevation of counterregulatory hormones. In the setting of relative insulin deficiency, glucagon, catecholamines and cortisol stimulate hepatic glucose production though glycogenolysis and gluconeogenesis. High catecholamines and low insulin reduce peripheral glucose uptake. Unlike DKA, it is thought that there is adequate insulin available in HHS to restrain lipolysis and ketogenesis. However, there is significant hyperglycemia with resultant glycosuria leading to loss of water and electrolytes, dehydration, and ultimately decreased renal perfusion, decreased glucose clearance, and exacerbation of hyperglycemia.
- If the cause of the hypoglycemia is not evident, measure plasma glucose, insulin, c-peptide, proinsulin, and beta-hydroxybutyrate concentrations and screen for oral hypoglycemic agents (sulfonylurea and glinide drugs) during an episode of spontaneous hypoglycemia. Glucagon, 1 mg IV, should then be administered with careful follow up of the glucose response. The diagnosis of insulinoma is supported if insulin, c-peptide and proinsulin levels are elevated, beta-hydroxybutyrate is <2.7 mmol/l, and sulfonylurea/meglitinide levels are undetectable during the hypoglycemic episode. If testing cannot be performed during a spontaneous episode of hypoglycemia, a 72 h fast or a mixed meal test, done in a monitored setting, followed by administration of glucagon is the most useful diagnostic strategy. During a 72 hour fast, patients are allowed no food but can consume non-caloric caffeine-free beverages. Insulin, c-peptide and glucose samples are obtained at the beginning of the fast and every 4-6 hours. When the plasma glucose falls to <60 mg/dl, specimens should be taken every 1-2 hours under close supervision. Patients should continue activity when they are awake. The fast continues until the plasma glucose falls below 45 mg/dl (2.5 mmol/l) [plasma glucose <55 mg/dl (3.0 mmol/l) is recommended in the most recent Endocrine Society guidelines] and symptoms of neuroglucopenia develop, at which time insulin, glucose, c-peptide, oral insulin secretagogue, proinsulin and beta-hydroxybutyrate levels are obtained and the fast is terminated. Additional samples for insulin antibodies, anti-insulin receptor antibodies, IGF-1/IGF-2 and plasma cortisol, glucagon or growth hormone can also be obtained at this time if a non-islet cell tumor, autoimmune etiology, or hormone deficiency is suspected. Patients are fed at the conclusion of the fast. For patients with hypoglycemic symptoms several hours after meals, a mixed meal test may be performed. This test has not been well standardized. Patients eat a meal similar to one that provokes their symptoms. A plasma glucose level is drawn at the time of symptoms to verify hypoglycemia. Table 4. Distinguishing causes of symptomatic hypoglycemia [glucose < 55 mg/dl (3.0 mmol/l)] after a prolonged fast Insulin (µU/ml) C-peptide (nmol/L) Proinsulin (pmol/L) Oral hypoglycemic Interpretation »3 <0.2 <5 No Exogenous insulin ≥3 ≥0.2 ≥5 No Endogenous insulina ≥3 ≥0.2 ≥5 Yes Oral hypoglycemic a Insulinoma, noninsulinoma pancreatogenous hypoglycemia (NIPHS), post gastric bypass hypoglycemia. In a patient with documented hypoglycemia with laboratory findings consistent with endogenous hyperinsulinism localizing studies should be done to evaluate for insulinoma. These may include computed tomography or magnetic resonance imaging (MRI), transabdominal and endoscopic ultrasonography, and, if necessary, selective pancreatic arterial calcium injections with measurements of hepatic venous insulin levels.
- Life threatening thyrotoxicosis or thyroid storm is a rare, occasionally iatrogenic disorder characterized by multisystem involvement and a high mortality rate if not immediately recognized and treated aggressively. A high index of suspicion for thyroid storm should be maintained in patients with thyrotoxicosis associated with any evidence of systemic decompensation. Precise criteria for thyroid storm have been defined (Table ) and include tachycardia, arrhythmias, congestive heart failure, hypotension, hyperpyrexia, agitation, delirium, psychosis, stupor and coma, as well as nausea, vomiting, diarrhea, and hepatic failure.
- Pathophysiology: •There is no evidence that increased productionof T3 or T4 causes thyroid storm •Increased catecholamine receptors (increased sensitivity to catecholamines) plays a key role •Decreased binding to TBG (increased free T3 or T4) may play a role •Bottom line: patients who are susceptible to thyroid storm have increased sensitivity to catecholamines; therefore, in states of stress (= catecholamine excess), thyroid storm can rear its ugly head! by:Greenspan FS. The Thyroid Gland – Thyrotoxicosis Crisis. In Basic and Clinical Endocrinology. Greenspan FS, Gardner DG, eds. New York: Lange Medical, 2001. pp. 247-8
- Remember that elderly patients often present atypically (apathetic thyroid storm)
- To confirm the diagnosis, both serum levels of free T4 and supersensitive TSH should be assayed. Results of serum total T4 measurements can be affected by protein binding abnormalities and may be misleading. Supersensitive TSH assay is useful for screening but a suppressed TSH level by itself may not be due to thyrotoxicosis. A result of normal free T4 (fT4) level may miss a small number of cases of thyrotoxicosis due to T3 toxicosis. In patients suspected of T3 toxicosis, serum free T3 (fT3) measurement is indicated. Isotope uptake scan may be performed in cases suspected of thyroiditis and toxic adenoma.
- Airway assessment is always the first as it is imperative that the airway is not obstructed. For detailed advice on management of the airway see the WHO ETAT course (1). Check consciousness Assess ability to take a deep breath Assess ability to speak in a full sentence – can the patient speak a full sentences, juse phrases, single words, or not at all Assess if the airway is clear Breathing should be adequate; if breathing assistance is required use a bag valve mask device or give oxygen if available. Only when problems with airway and breathing are addressed should the clinician move onto circulation. Look, listen and feel for the movement of air Assess the adequacy of the breathing process – is their sufficient rate and volume of air being moved? Assess work of breathing (patient effort versus efficacy) Listen to the chest (through Auscultation) and identify any variances of normal breathing. Normal breathing should sound like soft air movements; absent breath sounds is very bad; wheezes suggests bronchospasm; crackles and rales indicates pulomonary oedema or infection. Expose chest (while maintaining patient’s dignity) and assess for accessesory muscle involvement, such as sternocloidomastoid arching, pectoral muscles,external and internal intercostal muscles, which are all signs of increased respiratory distress Circulation. The chart gives guidance on the use of fluids. It is important to recognise malnutrition at this stage, as rapid infusion of intravenous fluids to a malnourished child can be very dangerous. Depending upon measurement of capillary refill, heart rate and blood pressure, give fluids: rapidly IV, slowly IV, or orally. Examine for life- threatening haemorrhage Assess perfusion (level of consciousness, skin colour, pulse rate and blood preasure Assess the pule mannually – is it regular or irregular, what is the rate (15 seconds x 4), skin colour, temperature, central and peripheral cap refil. Disability. If the patient shows signs of disability (either coma or convulsion) airway and breathing management are top priority. It is then appropriate to insert an IV cannual and measure the blood sugar if possible. These patients are at risk of low blood sugar and often it is safer to give glucose as soon as possible. Measure level of consciousness (AVPU – Patient is Alert, responding to verbal stimuli, responds to pain, unconscious; GCS: Glascow Coma Score) Dehydration - is so common in tropical countries that checking for signs of dehydration should be routine. The signs of shock have already been looked for while assessing circulation but specific examination for loose skin, lethargy and sunken eyes should occur. Exposure. Finally it is important to look at the whole patient, to look for signs of a rash, trauma or swollen abdomen. Expose the patient (while maintaining their dignity) so that you can see any injuries, watch breathing, etc. Check temperature
- “Triangle of treatment” −Decrease the sympathetic outflow (beta-blockers – esmolol is a great choice) −Decrease production of thyroid hormone (PTU or methimazole); super-saturated iodine solution (SSKI) can also be used to block outflow of thyroid hormone from the thyroid gland. −Decrease peripheral conversion of T4 >T3 (PTU, beta-blockers, steroids)
- The above regime should be instituted simultaneously. Once the clinical situation stabilises (usually after 3 - 4 days), iodide and corticosteroids may be stopped and the dose of anti-thyroid drugs and beta-blockers may be reduced. The precipitating cause should be treated. Subsequently, appropriate treatment for thyrotoxicosis should be continued.
- Typical clinical picture: Elderly obese female Becoming increasingly withdrawn, lethargic, sleepy and confused Slips into a coma
- elderly patients with hypothyroidism may have atypical symptoms. They may just present with reduced mobility, and some patients with compensated hypothyroidism are asymptomatic The physical signs of hypothyroidism are usually obvious and most patients have respiratory depression secondary to a decreased hypoxic ventilatory drive and an impaired response to hypercapnia: the more severe the latter, the more likely coma is. Cardiac enlargement, bradycardia, decreased ventricular contractility, hypotension, and ECG changes (low voltage, non-specific ST wave changes and sometimes torsades de pointes with a long QT interval) are common. Many patients have anorexia, abdominal pain and distention, and constipation and these changes may rarely lead to paralytic ileus and megacolon.
- hyponatraemia, normal or increased urine sodium excretion, raised creatine phosphokinase and lactate dehydrogenase, hypoglycaemia, and normocytic or macrocytic anaemia. Thyroid stimulating hormone values may only be modestly raised (and will be normal or low in secondary hypothyroidism) but free thyroxine levels are usually very low.
- The adrenal glands are two, triangular-shaped organs that measure about 1.5 inches in height and 3 inches in length. They are located on top of each kidney. Their name directly relates to their location (ad—near or at; renes—kidneys). Each adrenal gland is comprised of two distinct structures—the outer part of the adrenal glands is called the adrenal cortex. The inner region is known as the adrenal medulla. The adrenal cortex—the outer part of the gland—produces hormones that are vital to life, such as cortisol (which helps regulate metabolism and helps your body respond to stress) and aldosterone (which helps control blood pressure). Adrenal Cortex Hormones The adrenal cortex produces two main groups of corticosteroid hormones—glucocorticoids and mineralcorticoids. The release of glucocorticoids is triggered by the hypothalamus and pituitary gland. Mineralcorticoids are mediated by signals triggered by the kidney. When the hypothalamus produces corticotrophin-releasing hormone (CRH), it stimulates the pituitary gland to release adrenal corticotrophic hormone (ACTH). These hormones, in turn, alert the adrenal glands to produce corticosteroid hormones. Glucocorticoids released by the adrenal cortex include: Hydrocortisone: Commonly known as cortisol, it regulates how the body converts fats, proteins, and carbohydrates to energy. It also helps regulate blood pressure and cardiovascular function. Corticosterone: This hormone works with hydrocortisone to regulate immune response and suppress inflammatory reactions. The principle mineralcorticoid is aldosterone, which maintains the right balance of salt and water while helping control blood pressure. There is a third class of hormone released by the adrenal cortex, known as sex steroids or sex hormones. The adrenal cortex releases small amounts of male and female sex hormones. However, their impact is usually overshadowed by the greater amounts of hormones (such as estrogen and testosterone) released by the ovaries or testes. The adrenal medulla—the inner part of the gland—produces nonessential (that is, you don’t need them to live) hormones, such as adrenaline (which helps your body react to stress). The hormones of the adrenal medulla are released after the sympathetic nervous system is stimulated, which occurs when you’re stressed. As such, the adrenal medulla helps you deal with physical and emotional stress, fight-or-flight response. Hormones secreted by the adrenal medulla are: Epinephrine: Most people know epinephrine by its other name—adrenaline. This hormone rapidly responds to stress by increasing your heart rate and rushing blood to the muscles and brain. It also spikes your blood sugar level by helping convert glycogen to glucose in the liver. (Glycogen is the liver’s storage form of glucose.) Norepinephrine: Also known as noradrenaline, this hormone works with epinephrine in responding to stress. However, it can cause vasoconstriction (the narrowing of blood vessels). This results in high blood pressure.
- Acute adrenocortical insufficiency may be due to primary failure of adrenal function (primary adrenal insufficiency, PAI) or secondary due to lack of adrenocorticotrophic hormone (ACTH) drive from the pituitary (secondary adrenal insufficiency, SAI).