Endocrine emergency cases
•Download as PPTX, PDF•
12 likes•2,262 views
A talk on endocrine emergencies from resident Abdalla Alzaabi
Recommended
More Related Content
What's hot
What's hot (20)
Similar to Endocrine emergency cases
Similar to Endocrine emergency cases (20)
More from RVHEM
Recently uploaded
Recently uploaded (20)
Endocrine emergency cases
- 1. Endocrine Emergency cases ABDALLA ALZAABI EM (FRCP) R1
- 2. Learning objectives To understand how the common Endocrine Emergencies present and how to initially treat them in the emergency department
- 3. Case 1 50 M CC: confused and ataxic with slurred speech. PMH: none Med: none Exam: Appear drunk. mildly tremulous, sweating. mildly tachycardic and hypertensive. Alcohol breath test Negative His fingerpick blood glucose reading was 1.6 mmol/L.
- 4. Is the presentation in keeping with hypoglycemia? YES He has a combination of autonomic symptoms (e.g. sweating, tachycardia, tremor) and neuroglycopenic symptoms (e.g. confusion, ataxia, dysarthria).
- 5. What is Whipple’s triad? Whipple’s triad confirms the diagnosis of clinically significant hypoglycemia. It consists of: The presence of symptoms consistent with hypoglycemia Low serum glucose level Resolution of the symptoms and signs of hypoglycemia with the administration of glucose
- 6. What are the causes of hypoglycemia?
- 7. What is the emergency treatment of hypoglycemia? In the awake, cooperative patient: Oral Glucose In the uncooperative or unconscious patient: No IV access give glucagon 1mg IM/SC IV access give 50 mL 50% glucose
- 8. Following the initial management of his hypoglycemia, the patient became more lucid. Meanwhile, his wife arrive and tell you that she found her diabetic medication bottle empty
- 9. What is the antidote for overdose? Octreotide 50–100 mcg IV or SC
- 10. Learning points Case 1: Always check blood glucose level in patient with Altered Mental Status The antidote for sulfonylurea overdose is Octreotide
- 11. Spot Diagnosis? Acanthosis nigricans
- 12. Case 2 20 M HPI: abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the previous day. He was diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago. Exam: BP 106/67 mmHg, HR123, RR32 , temperature 37.1°C (98.8°F). drowsy. deep and rapid respiration with acetone odor and mild generalised abdominal tenderness without guarding and rebound tenderness. Labs: BG (450 mg/dL), arterial pH 7.24, pCO2 25 mmHg, bicarbonate 12 mmol/l, WBC count 18.5 × 10^9/L , sodium 128 mmol/L , potassium 5.2 mmol/L , chloride 97 mmol/L , serum urea 11.4 mmol/L (32 mg/dL), creatinine 150.3 micromol/L (1.7 mg/dL), serum ketones strongly positive.
- 13. What is the diagnosis? Diabetes Ketoacidosis D= Blood Glucose Level >250mg/dl (450) K= moderate degree of ketonemia and ketonuria (serum ketones strongly positive) A= Arterial PH <7.3, HCO3 level <15mEq/l. (arterial pH 7.24, bicarbonate 12 mmol/l)
- 14. What is the trigger for DKA in this case? Incompliance with medication I= Infection I= Infarction/Ischemia I= Intrauterine pregnancy I= Interactions/Illegal (drugs) I= Idiopathic (newly diagnosed DM)
- 15. What is the pathophysiology of DKA? Relative lack of insulin + stressors causes hyperglycemia Hyperglycemia-induced osmotic diuresis causes polyuria, dehydration, hypovolemia, electrolyte loss (K, Mg, Phos) Switch over to fat breakdown for energy source causes ketonemia (acidosis) Metabolic acidosis causes compensatory hyperventilation (Kussmaul respirations= deep rapid respiration)
- 16. What is the management of DKA? Fluid Replacement NS bolus followed by 1/2NS when hemodynamically stable, then D5 1/2NS when glucose <300 Insulin Replacement insulin infusion at rate 0.1unit/kg/hr (5-10U/hr) aim for decrease glucose by 50mg/hr. Given until ketones cleared and anion gab normalized Potassium Replacement Serum K level; >5mmol/l no K, <5-3.3 add 20-30 mmol KCL in each litter of NS, <3.3 add 40mmol KCL in each L of NS and no insulin until K >3.3 Treat precipitant
- 17. Learning Points Case 2 Volume resuscitation is most important step in managing DKA Check potassium before giving Insulin !
- 19. Case 3 6 B CC: 5 days of vomiting. He was initially seen by his family doctor and treated for gastroenteritis. However, his vomiting has persisted and he is lethargic and no longer able to walk. He has no history of fevers, abdominal pain or diarrhoea. PMH: none Med: none Exam: T36.4C, P 120/min, BP 95/60mmHg, R24/min and SpO2 99%RA. He is drowsy and generally weak with no focal neurological deficits, and is able to protect his own airway. He has dry mucus membranes and his eyes appear sunken though his capillary refill time is <2 seconds.
- 20. What is your immediate management priority? Check the blood glucose
- 21. His fingerprick blood glucose is 1.9 mmol/L. He is immediately treated with 2mL/kg of 25% glucose IV. Blood tests were taken on arrival. Of note are the following: Sodium 117 mmol/L (135-145 mmol/L) Potassium 6.1 mmol/L (3-5 mmol/L) Urea 17.1 mmol/L (3-7 mmol/L) Creatine 111 umol/L (50-90 umol/L)
- 22. based on the laboratory data and the clinical information, what diagnosis must be suspected? Acute adrenal insufficiency • anorexia, vomiting, weakness, hypoglycemia, hypotension • dehydration, hyponatremia, hyperkalemia, pre-renal impairement
- 23. What are the possible underlying causes of this condition?
- 24. Describe the acute management of this condition? 1. ABCs 2. Treat shock if present 3. Correct hypoglycemia if present 4. Correct hyperkalemia if present 5. Give steroids 6. Give minerocorticoid if deficient 7. Treat precipitating causes 8. Refer to Endo for admission
- 25. Learning points case 3 Always check blood glucose level in patient with Altered Mental Status All that vomits is NOT gastroenteritis!
- 26. Skin hyperpigmentation in primary adrenal insufficiency
- 27. Case 4 24 F CC: fever, generalized abdominal and flank pain associated with severe nausea and vomiting, and dysuria for one day. She also had severe palpitations, poor concentration,anxiety, retro- bulbar pain, redness of eyes, painful eye movement and swelling around her eyelids. PMHx: Graves hyperthyroidism Dx 9month ago Med: methimazole: but non-compliant for past 2M Sx: tremendous stress due to post graduate examination. examination: restless, dehydrated, Temp 39.7 (F103.5), P132/min(IR), BP 120/76mmHg. generalized abdominal tenderness, Her thyroid was bilaterally enlarged with bruit. Eye examination revealed bilateral exophthalmoses. ECG: Atrial Fibrillation
- 28. Is the presentation keeping with thyroid storm? YES What are the precipitants in this case? UTI STRESS NON-Compliant Do you know of Any Diagnostic tool to help you in diagnosing Thyroid Storm? scoring system developed Burch and Wartofsky can help distinguish between thyrotoxicosis, impending thyroid storm, and frank thyroid storm A score of 45 or higher suggests thyroid storm, a score of 25-44 suggests impending storm, and a score below 25 is unlikely to represent thyroid storm
- 29. Fever, generalized abdominal and flank pain associated with severe nausea and vomiting, and dysuria for one day. She also had severe palpitations, poor concentration,anxiety, retro- bulbar pain, redness of eyes, painful eye movement and swelling around her eyelids. PMHx: Graves hyperthyroidism Dx 9month ago Med: methimazole: but non-compliant for past 2M Sx: tremendous stress due to post graduate examination. examination: restless, dehydrated, Temp 39.7 (103.5), P132/min, BP 120/76mmHg. generalized abdominal tenderness, Her thyroid was bilaterally enlarged with bruit. Eye examination revealed bilateral exophthalmoses. ECG: Atrial fibrillation
- 30. What is the treatment for thyroid storm?
- 31. Learning points case 4 Treat peripheral Prevent synthesis Prevent release
- 34. Sources Rosen’ Emergency medicine 8th edition Tintinalli Emergeny Medicine Life in the fast lane http://bestpractice.bmj.com/ High Yield emergency medicine
Editor's Notes
- He has a combination of autonomic symptoms (e.g. sweating, tachycardia, tremor) and neuroglycopenic symptoms (e.g. confusion, ataxia, dysarthria). Hypoglycemia accounts for over 5% of emergency presentations of ‘altered mental state’. Handy tips: Hypoglycemia can cause focal neurological signs — don’t miss hypoglycemia masquerading as stroke! The ‘drunk’ patient may be hypoglycemic — even when they are actually intoxicated with alcohol…
- Post-prandial hypoglycemia can also occur due to a rapid surge of insulin (‘late dumping’) following rapid entry of food into the small intestine. This may occur after gastric surgery, for instance. Distinguishing excess endogenous insulin from excess exogenous insulin Pancreas cleaves proinsulin to insulin plus immunoreactive C-peptide. Excess endogenous insulin has measurable C-peptide (not so with excess exogenous insulin) Finally, remember to consider pseudohypoglycemia — leukocytosis, thrombocytosis, or erythrocytosis can cause excess consumption of glucose in the collection vial while the sample awaits testing.
- In the awake, cooperative patient appropriate initial management may be as simple as: oral intake of simple carbohydrates (e.g. a sugary drink, jam, sugar lumps, barley sugars, etc.) followed by a sandwich or biscuits. In the uncooperative or unconscious patient, parenteral therapy is needed: 50 mL 50% glucose ’25g’= 1amp=100calories (or 5 mL/kg of 10% glucose in small children) by direct slow injection • Adults D50= 1AMP, Peds D25= 2-4ml/kg, Neonates D10= 5-10ml/kg Flush with 50ml saline as it is hypertonic and can cause phlebitis. Or glucagon 1mg IM/SC (converts liver glycogen to glucose)- this may be administered by family members or by paramedics at the scene when IV access is difficult. It is inappropriate in settings where liver glycogen stores are depleted (e.g. liver failure, elderly or chronic alcoholism). Remember: Vomiting may occur after glucagon administration, so the patient must be carefully monitored to prevent aspiration. Ongoing therapy: Begin a maintenance infusion of 5% dextrose or 10% dextrose IV at a rate of 100 mL/h if persistent hypoglycemia is anticipated (e.g. hepatic failure, seizure or coma). Repeat a fingerprick BGL in 1 hour and reassess the patient. Hypoglycemia because of an excess dose of oral hypoglycemic may require repeated doses of 50% dextrose because of the slow metabolism and excretion of these drugs. Octreotide 50–100 micrograms IV or SC can also be used to prevent further hypoglycemic episodes in these patients and may avoid the need for further boluses of
- Octreotide 50–100 micrograms IV or SC can also be used to prevent further hypoglycemic episodes in these patients and may avoid the need for further boluses Note: Octreotide – inhibits insulin secretion and helps prevent rebound hypoglycemia in the setting of glucose infusion treatment of refractory sulfonylurea-induced hypoglycemia
- Although the patient looks dry and will need fluid replacement, his ABCs are stable at present. The main concern is his altered mental state — we need to check his blood glucose ASAP.
- The manifestations of adrenal insufficiency are: glucocorticoid deficiency — anorexia, vomiting, weakness, hypoglycemia, hypotension (especially postural), shock mineralocorticoid deficiency — dehydration, hyponatremia, hyperkalemia, acidosis, pre-renal impairment The presence of features of both glucocorticoid and mineralocorticoid deficiency in this patient make it likely that this patient has primary adrenal insufficiency (see Q3). Hypotension is not always seen in adrenal insufficiency, but postural changes may go undetected unless they are specifically assessed. However, hypotension or shock out of proportion to the severity of the current illness is the key feature of adrenal crisis. Other points: Adrenal insufficiency is part of the differential diagnosis for normal anion-gap metabolic acidosis (NAGMA). The skin may be hyperpigmented in non-sun exposed regions. This suggests a primary cause of adrenal insufficiency, as it results from elevated ACTH levels. Features of androgen deficiency may also be seen, especially in women. All that vomits is NOT gastroenteritis!
- Adrenal insufficiency is most commonly seen in patients on steroids who have an inter-current illness or physiological stress, or have their steroids withdrawn. However, this child had no previous medical problems and was not taking steroids. Adrenal insufficiency can be primary or secondary, each with acute or chronic causes. In primary adrenal insufficiency there is failure of adrenal gland to produce cortisol and aldosterone. Secondary adrenal insufficiency is characterised by failure of the pituitary to produce ACTH, resulting in cortisol deficiency only — aldosterone is still produced because it is regulated by the still intact renin-angiotensin-aldosterone system. Primary adrenal insufficiency: acute — Adrenal hemorrhage — meningococcemia (Waterhouse-Friderichsen syndrome) and other sepsis, anticoagulation, anticardiolipin antibody syndrome, trauma chronic — Autoimmune adrenalitis (Addison’s disease) — isolated or polyglandular deficiency, HIV infection (direct involvement) TB and disseminated infections as seen in AIDS Metastatic cancer (breast, lung) Infiltrative diseases (e.g. sarcoid, hemochromatosis, amyloid) Congenital (e.g. adrenal hypoplasia, adrenoleukodystrophy, ACTH resistance) Bilateral adrenalectomy Drugs (e.g. etomidate, ketoconazole, rifampicin) Secondary adrenal insufficiency: acute — Pituitary apoplexy (hemorrhage into a pituitary tumor) Postpartum pituitary necrosis (Sheehan’s syndrome) Traumatic brain injury Relative adrenal insufficiency — e.g. sepsis, hepatic failure, severe acute pancreatitis, trauma chronic — Chronic steroid use with functional deficiency Pituitary tumor (primary or metastatic) Pituitary surgery or irradiation Infiltrative (e.g. sarcoid, eosinophilic granuloma, TB) Traumatic brain injury Postpartum pituitary necrosis (Sheehan’s syndrome) Empty sella syndrome Acute presentations may have an underlying chronic cause with an acute precipitating event. About 90% of the adrenals must be destroyed before function is affected. An inherited disorder such as polyglandular deficiency syndromes, adrenoleukodystrophy, adrenal hypoplasia, or ACTH unresponsiveness should be suspected in childhood presentations of adrenal insufficiency.
- Management of acute adrenal insufficiency: Attend to ABCs Treat shock if present — e.g. 20 mL/kg boluses of normal saline until capillary refill time <2 seconds. Detect and correct hypoglycemia — e.g. 5mL/kg 10% dextrose in infants, 2mL/kg 25% glucose in older children Treat hyperkalemia Administer steroids — hydrocortisone IV can be given IM initially if there is a delay in obtaining IV access typical doses according to age: <1y: 25 mg q6h, 1-3y: 25-50mg q6h, 4-14y: 50-75mg q6h, 15+y: 100mg q6h. IV fluid administration — add fluid deficit to maintenance requirements and replace over 24 hours [fluid deficit (mL) = %dehydration x wt(kg) x 10] use 0.9% NaCL with 5% glucose [use 0.45% NaCl if Na>130 mmol/L; use 10% dextrose if needed for ongoing hypoglycemia] seek and treat precipitating causes (e.g. sepsis) refer to the endocrinology team for admission. HDU/ ICU admission is often appropriate for regular monitoring of fluid status and electrolytes. Hydrocortisone is changed to an oral dose and the dose is gradually reduced once the patient is stable (typical maintenance dose is 10-15 mg/m2/d). In patients with mineralocorticoid deficiency, fludrocortisone (e.g. 0.1mg) is usually started as soon as the patient can tolerate oral fluids. Fludrocortisone is not required acutely because hydrocortisone has both glucocorticoid and mineralocorticoid activity.
- Always start with ABC intubation if resp compromise, severe AMS 3B- block of 1.production/release of thyroid hormones, 2.the sympathetic outflow, 3.peripheral conversion of T4 to T3 Aspirin is avoided in thyrotoxic patients as it decreases protein binding of T 4 and T 3, thereby elevating free T 4 and free T 3 concentrations. Dextrose-containing solutions are helpful as glycogen stores are often depleted. propranolol has been the beta-blocker of choice as it has the added benefit of blocking conversion of T 4 to T 3 ; its nonselective effects also improve tremor, hyperpyrexia, and restlessness Atrial fibrillation is often refractory to rate control until antithyroid therapy is administered. Thyroid-directed therapy has three goals: to reduce thyroid hormone production, to prevent thyroid hormone release, and to block peripheral conversion of T 4 to T. pseudoephedrine, ketamine, and albuterol should be used cautiously as they increase sympathetic tone and can exacerbate the adrenergic effects of thyrotoxicosis Either propylthiouracil (PTU) or methimazole can be used. PTU has the additional effect of impairing conversion of T 4 to T 3; methimazole has a longer duration of action. Inorganic iodine (SSKI) blocks the release of stored thyroid hormone. However, an iodine load can increase the synthesis of thyroid hormone, so these agents should not be administered until 1 hour after the initiation of PTU or methimazole therapy Corticosteroids are capable of both inhibiting peripheral conversion of T 4 to T 3 and blocking the release of hormone from the thyroid gland as well as treating relative adrenal insufficiency When steroids are used in conjunction with PTU and iodide, the concentration of T 3 can return to normal within 48 ho