So, just keep in mind, if you're looking at the blueprint for those taking the ABIM critical care exam, renal, metabolic, and endocrine questions comprise about 15 percent of the blueprint. So, this afternoon's session really highlights. And then, following that will be Dr. Zakaria's presentation on all the cardiac stuff, which is about 20 percent of the blueprint. So, this afternoon's sessions are critical. So, we're going to talk very, very quickly about endocrine emergencies. We're going to talk about thyroid disorders, hyperglycemic syndromes. We're going to talk about adrenal insufficiency, and then some pituitary problems like diabetes insipidus and pheochromocytoma. So, thyrotoxicosis just suggests, you know, an excess of thyroid hormones, elevated T4, T3, Graves' disease. Just keep in mind, it's the most common cause of thyrotoxicosis. You've seen patients with proptosis where their eyeballs are sticking out at you, and they have a very prominent goiter or thyroid gland enhancement. Thyroid storm is what we all need to be concerned about if we're taking care of these patients. It's a relatively rare but very serious cause of severe thyrotoxicosis. Typically, it's a patient that has been either partially or untreated with a thyroid disorder or maybe stopping their antithyroid medication, and then they get an acute stress like sepsis, infection, pregnant woman going to labor or delivery or having major surgical procedure. Manifestations are fever, high fever, hypertension, tachycardia, high output, congestive heart failure, alteration of mental status, as well as gastrointestinal symptoms like nausea, vomiting, and diarrhea. You need at least two tests to support a diagnosis of thyroid storm, and usually we look at an elevated T4, an elevated free thyroxin index, and a decrease in TSH. You need at least two of these four tests, usually, to make that diagnosis in the presence of your clinical manifestations. Treatment, there are generally four steps. The first step is to block further syntheses of thyroid hormones, and we usually do that with two drugs. PTU or propyl thiouracil is favored over methimazole. They can both be used. You can see the dosages there. The second step is to blunt the end organ effects. So you have to control the heart rate, the high blood pressure. So beta blockers are commonly used for that reason. Atenolol and metoprolol are favored because they're more cardio selective than propranolol. However, propranolol has an additional advantage in that it can also decrease the conversion peripherally of T4 to T3. And of course, if somebody needs an IV infusion for control of heart rate or blood pressure, esmolol can be very commonly used for that reason. The third step is to block thyroid hormone release and conversion of T4 to T3. In compounds like SSKI, potassium iodide, or Lugol solutions are used. IV radiocontrast dyes have also been used. Corticosteroids have always a place because there can be adrenal insufficiency in the mix. So if you haven't figured that out yet and you're treating somebody with thyroid storm, you typically have to also treat them with stress dose hydrocortisone. And lithium has also been used as a treatment for thyroid storm. Active care, of course, has to come in, treating the precipitating factors, treating any arrhythmias, bringing down the temperature in the febrile patients, correcting electrolyte abnormalities, and providing oxygen and mechanical ventilation if required. And these are patients that have to be in the ICU for very close monitoring and management. Shifting over to myxedema coma, so now we're looking at the other side here where you can have a patient with extremely low levels of thyroid hormone production. This can be triggered by infection, surgery trauma, use of sedatives. These patients can be very sensitive to getting opiates like morphine and other narcotics. And opiates generally you should not be giving these patients because they can get severe manifestations from that, including low temperature, bradycardia, congestive heart failure, weakness, mechanical ventilation. Many, many cancer patients may exhibit a lot of problems with their thyroid gland and it's very common for many of these patients, particularly those that are receiving certain therapy agents that they get in need of thyroid replacement. So think about those settings where they may develop this problem as well. Hypoglycemia is a very common abnormality in patients with hypothyroidism. Again in terms of laboratory criteria, unlike thyrotoxicosis or thyroid storm, you look at the opposite. So free thyroxin index is low, free T4 is low, and THH is usually very, very high. Treatment, again, besides ICU monitoring, respiratory support, hypoglycemia has to be corrected with glucose. It's had to be brought up to normothermia with passive rewarming. And then you have to usually use thyroid agents such as T4 and T3, and I mentioned hydrocortisone or stress dose steroids is often used in combination with thyroid hormone replacement because of the higher incidence of adrenal insufficiency in these patients that might be occult when you first encounter the patients. So just a quick question for you. Which of the following thyroid function test patterns is seen in patients with euthyroid sick syndrome? Since we don't have the ability to answer the questions, I'll just go very quickly to the answer. TSH actually is the least affected test in patients with sick euthyroid syndrome or euthyroid sick syndrome. In these patients, you actually see decreases in free T3. You actually see decreases in free T4. You also have decreases in reverse T3. So in sick euthyroid syndrome, the TSH, although it tends to usually be somewhat similar to patients with hypothyroidism, you can see increases as well as decreases in TSH levels, so it's hard to make that diagnosis alone relying on one level of TSH. This is commonly seen, and in fact, it's not usually recommended that we do thyroid function tests in critically ill patients because sometimes when you get these tests in a sick patient, you're going to get sometimes confused as to what to do. So in general, if you were to pull thyroid function tests in a critically ill patient, the consensus generally is not to treat the numbers unless you really have clinical manifestations suggesting that this is not sick euthyroid, that this is a patient that's truly hypothyroid and you do need to replace with thyroid hormone. I think the main thing here is to ensure that you are excluding hypothyroidism. In hypothyroidism, particularly severe, usually TSH levels are very, very high. In sick euthyroid, it may go up a little bit, but not as extreme as patients with clinical hypothyroidism. We shift over to hyperglycemic syndromes, DKA, and hyper or smaller hyperglycemic non-ketotic states. There's oftentimes an overlap, so sometimes you don't see the pure DKA or the pure HONC or HHNK syndrome, there can be overlap situations. So second question for you, which of the following is most likely correct in treating a patient with DKA? Is it A, acetone contributes to the anion gap? No, it's usually beta-hydroxybutyric acid and acetic acid. Half normal saline is the fluid of choice? No, it should be what? Isotonic saline, 0.9% sodium chloride. Beta blockers, are they useful for DKA? No. Stop the insulin infusion once the blood sugar level drops to 300? No. What's the number, usually? About 250, until it goes down to below 250. So correct answer here is the anion gap. It's not the glucose level to measure success. It's not the ketone level that measures success of DKA treatment. It's the anion gap. Is the anion gap closing? I remember this question because this came out in the last research that I took a few years ago. So DKA is typically seen in patients with type 1 diabetes. They present with a high anion gap. There's usually no insulin or there's insulin resistance. Infection or noncompliance with insulin therapy oftentimes is a trigger here. Patients tend to be volume depleted. They're altered in terms of their mentation, cusmal breathing. Their serum glucose levels are usually less than 800. And oftentimes it's somewhere between 350 to 500. And they do have ketones. As you can see, beta-hydroxybutyric acid and acetoacetic acid is really what you're measuring when you do your ketone levels. Euglycemic DKA, we're seeing this more and more in the last few years, particularly with the advent and use of HGL2 inhibitors. But you can also see euglycemic DKA in patients who have alcohol abuse disorders, patients with surgery for pancreatitis or infection. Here, unlike classic DKA, the glucose levels are not 350 to 500. They're usually more in the 150 to 250 kind of range. They can present with severe metabolic acidosis with pHs of less than 7.3. And the bicarbonate is usually less than 18. Isotonic saline or 0.9% saline is the solution of first choice. Insulin, of course, has to be given to these patients, usually 0.1 units per kilogram followed by a continuous infusion until the glucose levels fall below 250. There are other choices there, including Lispro with initial bolus. You can see the hourly dose. When the blood sugar then falls below 250, you can start decreasing your insulin infusion and then start the dextrose with the idea of keeping the blood sugar ranges somewhere between 150 to 200 until the gap has normalized. What about potassium replacement? It's not generally recommended unless the potassium levels are really below 3.3. And then in that situation, then you can add 20 to 30 milliequivalents of KCL to each IV fluid with the idea that you're keeping the range somewhere between 4 and 5. Sodium bicarbonate, again, is not routinely recommended unless the pH is below 6.9. What about hyper or smaller hyperglycemic non-ketotic states? Again, unlike in DKA, which is more common in those with type 1, this is usually typically seen in those with type 2 diabetes, older patients versus younger patients generally with DKA. Here you have partial insulin deficiency. The glucose levels are extremely high. They're usually over 1,000. And they don't get ketones usually are not present. The plasma osmolarity is usually as high as 380 millimoles per kilogram. This can be serious because it can cause a coma in up to a quarter to 50% of patients and actually has a higher mortality rate when compared to patients with DKA. So this is something that certainly you have to be jumping on patients. If they have this syndrome, unlike in DKA where the endpoint is, well, it's similar to DKA in that you're also looking for resolution of hyperglycemia, but more so than correction of the ketoacidosis. Here, these patients need very aggressive volume repletion with isotonic saline as compared to those with DKA. They don't require as much insulin. And you still have to supplement potassium and phosphorus in those that are deficient. Opposite of hyperglycemia is hypoglycemia. Generally, this is a blood sugar of less than 70 milligrams per deciliter. Drugs, alcohol, sepsis, hepatic failure are common causes. And then patients who get rapidly discontinued from TPN, this can sometimes occur where TPN is stopped for whatever reason. And then no glucose is given back. And then the next morning, the blood sugar is like 40. So this is something that we all want to recognize that if the TPN is being discontinued, particularly in a patient for whatever reason, that you have to have a dextrose infusion going to prevent severe hypoglycemia. Manifestations, we all know. Weakness, confusion, slurred speech, tachycardia, diaphoresis. We all know how to manage these patients with 50% dextrose. Glucagon can be substituted. IM, octreotide hydrocortisone usually will also increase your blood glucose levels. Which of the following laboratory abnormalities is found in adrenal insufficiency? So we're switching gears to adrenal insufficiency now. Is it hypernatremia, hypokalcemia, hyperkalemia, hyperglycemia, or hypokalemia? Everybody got this, or at least many of you got it. So typically in adrenal insufficiency, sodium is low, K is high, potassium, calcium is low as well, and the patients are usually hypoglycemic. So hyperkalemia is the correct answer in this particular question. Causes of adrenal insufficiency, you have primary. We don't usually tend to see this unless you see patients with metastatic cancer. But more commonly when we see adrenal insufficiency, it's usually in the setting of very severe critical illness, septic shock patients certainly would fit that category. Signs and symptoms for primary, more classic Addisonian picture would be, again, the hyperpigmentation that you see here in the picture. Very bronze-like look into the palms and feet. Patients can be febrile and hypotensive. So this is a syndrome that can mimic sepsis, but without an infection. So if somebody has ongoing fevers, they're hypotensive, but they're not septic, then they usually have adrenal insufficiency, and you have to recognize that. Treatment, again, is volume, expansion with isotonic saline or dextrose, normal saline. Hydrocortisone is usually prescribed. Stress dose is 100 milligrams Q8. Flutocortisone is another mineral or corticoid that sometimes can be given to these patients and, of course, treating glucose and monitoring electrolytes is also very important. Relative adrenal insufficiency, the main point I want to stress here is in patients with septic shock who are requiring vasopressors to maintain blood pressure, they need stress dose hydrocortisone, 50 milligrams hydrocortisone Q6, and plus minus flutocortisone can be given as well for those patients that remain with refractory hypotension. Finally, pituitary emergencies, central DI, nephrogenic DI. We talked about hypernatremia being the most common denominator. I think Dr. Conner already went over. Anybody who is hypernatremic, we check the urine osm. If the urine osm is less than 300, usually they're lacking in ADH, and we need to replete them. If it's over 800, they're usually water deprived or have an ADH receptor defect. So the way to do that is you give DD-AVP, and then you recheck the urine osmolality, and if it corrects more than 50%, then usually that means that the patient had complete central DI. If it's not fully corrected, they may have partial central DI, and if there's no change at all in the urine osmolarity, then they have nephrogenic diabetes insipidus. Treatment, again, fluid replacement and, of course, ADH replacement using DD-AVP or vasopressin can be given as well. Pheogorosarcoma follows the rule of tens, 10% malignant, familial, bilateral, multiple, and extramedullary. This was one of my earlier test questions. Patient with headache, high blood pressure, tremors, anxiety attacks can be manifestations. Again, this is a catechol-secreting tumor, so checking the plasma and urine for metanephrines as well as catecholamines will usually give you this diagnosis. Treatment, again, you have to control blood pressure, and the best agent in an exam situation for a patient with pheochromocytoma with hypertensive crisis is pentolamine. Preoperative preparation a few days before surgery to correct blood pressure and prepare the patient to avoid a hypertensive crisis, phenoxybenzamine is preferred, and then we talked about alpha short-acting blockers like doxasociin, which was in the test question. And then in patients that have already control of blood pressure, you can then use calcium channel blocker or nicardipine infusion to maintain blood pressure control on those patients. Surgery is the treatment of choice. I mentioned in the test question avoiding morphine because that can cause histamine release, catechol release, and that can exacerbate hypertensive crisis. So take home, TSH, single best test of thyroid function. If it's low and the T4 is high, it's hyperthyroid. If the THH is high and the T4 is low, it's hypothyroidism. Patients with DKA have to be managed with fluids, insulin infusion, and potassium replacement. In patients with adrenal insufficiency, refractory septic shock, IV hydrocortisone. For diabetes, insipidus, and hypernatremia, fluids and vasopressin are the mainstays. And for hypertensive crises in pheochromocytoma, pentolamine is the best agent of choice. Thank you. That was great. Thank you.

thyroid storm

DKA

adrenal insufficiency

diabetes insipidus

pheochromocytoma