Every month we summarize our simulation cases. No deep dive here, just the top 5 takeaways from each case.
Hyperosmolar Hyperglycemic State (HHS)
1. HHS is similar to Diabetic Ketoacidosis in many ways except for a few key points.
Higher mortality (up to 30% HHS vs 10% DKA)
Minimum to no formation of ketoacids.
Treatment priority is fluids
2. HHNS often has more insidious/develops over a longer period of time. The most common patient profile is [2-3]:
7th decade of life
Elderly/resident of NH, demented, Type II DM (new or old dx)
Decreased oral intake
Impaired renal function
3. Search for a precipitating cause – the I’s
Insulin lack (diabetes is a NEW diagnosis in 30-50% of cases)
Ischemia/Infarction (CVA, MI, mesenteric ischemia)
4. Successful treatment of both DKA and HHS includes correction of the dehydration and hyperglycemia, resolution and anticipation of the electrolyte abnormalities, identification of precipitating or comorbid illnesses .
0.9% NS at 1-1.5 bolus and continue at 1L/hr if continued shock
Choice and rate of fluids should be based on corrected serum sodium and fluid status
If serum sodium is high or normal (0.45% NaCl at 250-500 ml/hr)
If normal or low serum sodium (0.9% NaCl at 200-500 ml/hr)
Regular insulin IV
Insulin protocols very per institution
Using the American Diabetic Association Protocol :
0.14 units/kg/hour infusion
If serum glucose does not fall by at least 10% in the first hour, give 0.14 units/kg IV bolus, then resume previous infusion rate
Upon resolution of hyperosmolar hyperglycemic state, transition to multiple dose subcutaneous regimen with shorter-acting and intermediate or longer acting insulins
Potassium- Close monitoring and repletion of potassium unless serum potassium > 5 mEq/L (5 mmol/L)
Other FOAMed Reviews on HHS
Here is another great reivew on HHS by Life in the Fast Lane
Written by Jeffrey A. Holmes, MD
1. Chaithongdi N, Subauste JS, Koch CA, et al. Diagnosis and management of hyperglycemic emergencies. Hormones (Athens). 2011;10(4):250-260. (Review)
2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009 Jul;32(7):1335-43.
3. Scott A, Claydon A. Joint British Diabetes Societies Inpatient Care Group. The management of hyperosmolar hyperglycaemic state (HHS) in adults with diabetes. Joint British Diabetes Societies 2012 Aug.
4. American Diabetes Association (ADA) position statement on standards of medical care in diabetes can be found in Diabetes Care 2017 Jan; 40 Suppl 1: S1 PDF
1. Thyroid storm is decompensated (organ system dysfunction) hyperthyroidism or exaggerated effects of thyrotoxicosis. It is a clinical diagnosis with no immediate confirmatory test and is most commonly marked by:
Altered mental status (agitation, delirium, psychosis, stupor, or coma)
Tachycardia (>140 bpm) 
Hyperpyrexia (104-106F common)
Underlying hyperthyroidism, that is either known (Grave’s disease, toxic adenoma, Toxic multinodular goiter) or potentially undiagnosed
2. Like most endocrine emergencies, there is a precipitating cause (stress to the body) that tips the patient into decompensation. This event increases catecholamines that activates the increased number of hypersensitive beta adrenergic receptors.
Severe infection (may be most common cause)
Infarction (MI, PE)
3. It is a clinical diagnosis with no immediate confirmatory test and high mortality (20%).
Vigorous resuscitation with IVF as dehydration is common in thyroid storm (unless concern for high output failure)
Treat fever with acetaminophen (AVOID ASA as it can increase peripheral conversion of T4 to T3); employ aggressive cooling measures as needed (cool mist, fans, ice packs, cooling blanket)
Block Peripheral Adrenergic Effects of Thyroid Hormone
Propanolol (60-80 mg po or 0.5-1 mg IV q 15 min) preferred because it also block peripheral conversion of T4 to T3 
Esmolol 250-500 mcg/kg IV bolus, then 50-100 mcg/kg/minute by continuous infusion is alternative
Block further production/release of thyroid hormone
PTU (600 to 1000 mg by mouth, followed by 300 mg every 6 hours, to a maximum daily dose of 1200 mg) 
Iodide (given at least one hour after PTU to avoid being used as a substrate for new hormone synthesis)
Potassium iodide (SSKI) 5 gtts every 6 hours
Lugol’s solution 4 to 8 gtts every 4 to 6 hours
Prevent peripheral conversion of T4 to T3
Propanolol(60-80 mg po or 0.5-1 mg IV q 15 min); goal is HR 90-100 
Dexamethasone (1-2 mg IV q 6 hr)/hydrocortisone (100 mg IV q 8 hr)
4. Be wary of the patient with high output heart failure.
Avoid diuretics (these patients are typically volume depleted)
Consider esmolol over propanolol IV (rare reports of CV collapse after IV propanolol if there is severe heart failure or hypotension) [3 ]
Use bedside echo to guide fluids/therapy
5. Pan culture and consider broad spectrum antibiotics due to high incidence of concomitant infection and difficulty in differentiating the two syndromes.
1. Nayak B, Burman K: Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 35:663-686, 2006.
2. Cooper DS: Antithyroid drugs. N Engl J Med. 352:905-917, 2005.
3. Dalan R, Leow MC. Cardiovascular collapse associated with B-Blockade in thyroid storm. Exp Clin Endocrinol Diabetes. 2007; 115 (10) 696.
4. Swee du S, Chng CL, Lim A. Clinical characteristics and outcome of thyroid storm: a case series and review of neuropsychiatric derangements in thyrotoxicosis. Endocr Pract. 2015;21(2):182.
A Five Step Approach to Myxedema Coma (Decompensated Hypothyroidism)
1. Have a high index of suspicion – it is rare but deadly.
Myxedema coma requires neither myxedema nor coma
The clinical hallmarks are altered mental status and hypothermia
Consider the diagnosis in the patient with the ‘hypo’s’ (hypothermia, hypotension, bradycardia, hypoventilation, hyponatremia)
The "typical patient" is an elderly woman with chronic hypothyroidism that is untreated or unrecognized and presents in the winter 
2. Support the ABC’s and passively rewarm.
Due to a low metabolic rate, peripheral vasoconstriction is increased to conserve heat
Active external heating (i.e. BAIR hugger) can cause peripheral vasodilation and cardiovascular collapse
3. Like most endocrine emergencies, there is a precipitating cause that tips the patient into decompensation. Identify and treat the precipitating cause [2-3].
Long standing untreated hypothyroidism
Sedative medications (especially opioids)
4. Order a TSH, free T4 and cortisol.
5. Treat aggressively (40% mortality untreated) with thyroxine (T4) 300-500 mg IV and hydrocortisone 100 mg IV (give hydrocortisone first) .
The cardiotoxic effects of T3 are reduced by giving T4 instead, allowing the body to generate T3
T4 is mostly protein bound (buffering effect)
Peripheral conversion to T3 is reduced in illness
Concomitant hydrocortisoine is important because:
Hypopituitarism and hypoadrenalism can mimic myxedema
Patients with autoimmune-mediated primary hypothyroidism may have concomitant primary adrenal insufficiency
Treatment with thyroxine can deplete cortisol causing relative adrenal insufficiency
1. Vaidya B, Pearce SH. Management of hypothyroidism in adults. BMJ. 2008 Jul 28;337:a801
2. Wartofsky, L. Myxedema coma. In: The Thyroid, Braverman, LE, Utiger RD (Eds). Lippincott-Raven, Philadelphia,
1996, p. 871.
3. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 200635(4):663-686,vii.
4. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism. Thyroid. 2014 Dec;24(12):1670-751 full-text
Written by Jeffrey A. Holmes, MD