Myxedema Coma Case Study

DIFFERENTIAL DIAGNOSES

When it comes to our differentials, we want to first think of the most common and easiest fixes prior to moving onto the lesser seen unicorns. With that being said, never forget the unicorns exist.

PATHOPHYSIOLOGY

FOUNDATION

The pituitary gland is responsible for secretion of TSH (thyroid stimulating hormone); TSH tells the thyroid gland to, you guessed it, stimulate hormone - T3 and T4. Low T3 and low T4 indicate hypothyroidism. Yet, it is impossible to definitively state the origin of the hypothyroidism until you check TSH. If TSH is elevated (with low T3/T4), we have a thyroid gland problem (ex: surgical removal of thyroid). If TSH is low (with low T3/T4), we likely have a pituitary gland problem. 

When thinking of etiology, generally any stressor on the body can be a precipitating factor: sepsis, trauma, GIB, etc. 

What does this mean for patient presentation? Recall, hyperthroid is amped up (systemically: energy, heartrate, temp, etc.); hypothyroid is slowed down. 

Patients with hypothyroidism may present as: 

• obese: anywhere from "difficult to maintain healthy BMI" to morbid obesity
• bradycardic: anywhere from "they may just be athletic" 50s bpm or severely symptomatic 20s
• hypothermic: anywhere from "cold intolerance" to severe hypothermia 
• lethargic: anywhere from "always tired" to comatose 
• bradypneic
• anemic

MYXEDEMA COMA

All of the above bullets contain spectrums; the worst - and most lethal - side of these are what we are discussing in this post, Myxedema Coma. 

While a misnomer, because a diagnosis of "myxedema coma" does not necessitate a coma, it personally helps recalling how severe the altered mentation can be with these patients. Not only is the AMS severe, so is the level of mortality, with cited mortality "ranges from 30 to 60 percent" (Wall, 2000). What is a further slight misnomer is the "myxedema" aspect; simply put, often times these patients do not present with this widespread, facial predominating, edema as the name would suggest. 

TREATMENT 

Hypothyroid

The root of the problem for myxedema coma is ultimately low T3/T4. The only way to replace this in a hypothyroid individual at this severity is IV levothyroxine. It is important to note, though, that the trigger for this patient's episode of myxedema coma should still be sought after. 

Hyponatremia

The decrease in blood pressure results in hypoperfusion systemically which triggers a release of ADH to prompt water retention. While this results in an increase in systemic volume it also results in dilutional hyponatremia. And recall, hyponatremia plays a part in the altered mentation. Now, how does resolving this electrolyte imbalance work? The simple answer would be, "just get rid of the free water" however, this patient's cardiac output (look at that low HR and low BP) cannot handle that type of volume depletion. So, sodium replacement will come with gradual repletion (not aggressive). 

Acidosis

This is two-fold. The patient has been breathing slow for some time, resulting in carbon dioxide retention, hypercapnia, thus resulting in acidosis. Usually this can be compensated metabolically via the kidneys. However, due to the hypoperfusion secondary to the hypotension, the kidneys aren't even online enough (literally due to the reduction in GFR seen with myxedema) to properly maintain electrolyte levels, they're unable to adequately compensate this newfound acidosis. To treat this, IVF and tweaking ventilator settings (to target the respiratory source) will help. Pending severity of the acidosis, bicarb can be considered. 

Hypoglycemia

Hypoglycemia that persists is best treated with a dextrose containing maintenance fluid. D5-something where the "something" (NS, 1/2NS, LR etc.) will be dictated by the severity of the hyponatremia and acidosis. The efficacy of the D5 IVF will be assessed by frequent BBG checks and PRN D50 or D10.

Hypotension

These patients tend to have pressor-refractory hypotension, meaning no matter what pressors you throw their way, those numbers won't budge. That is, until you start successfully treating the initial trigger - think of that levothyroxine we discussed above. With that being said, it's important to remember our differential diagnoses could be our potential triggers; if our patient experienced sepsis as a precursor to the myxedema coma, we may have an aspect of our hypotension that may be reactive to pressors. 

Hypothermia 

Central warming (think warmed IVF or heated high flow) is the key for myxedema hypothermia. You want to avoid peripheral or external warming due to circulatory collapse secondary to vasodilation on an already compromised patient. Farkas (2020) delves into this further. 

Bradycardia

Atropine can be administered as warranted to prevent further cardiovascular collapse; however, just know it's a temporary that should only be needed until the levothyroxine can kick in. Further, pressors that target both pressure and HR should be considered as a two-fer deal.

Steroid

Lastly (for this blog's list), is steroids. Often times, adrenal crises can precipitate with myxedema coma. And other times, the two may be mistaken for one another. With that knowledge, it is both prudent and precautionary to administer stress dose steroids to these patients as well. These steroids will also inadvertently assist with bradycardia, hypertension, and hypoglycemia. 

PREHOSPITAL OR PROLONGED TRANSIT TIME

In the event of a prolonged prehospital transport time, it's likely that IV levothyroxine not available so we need to treat the symptoms until we arrive at a facility and get that definitive treatment on board. Now that airway and breathing have been stabilized, we take a step back and look at our patient. We readily identify four treatable ailments: hypothermia, hypotension, bradycardia, and hypoglycemia. But these tend to be PERSISTENT, so we prioritize continuous drips if available over single/push dose.

Hypothermia

• Remove wet clothing
• Warm patient cab
• Warmed fluids
• Environmental blanket
• Keep covered (especially head) 

Hypotension

As stated above, getting that blood pressure under control will likely pose a challenge. Further, this patient is likely on the fluid-overloaded side (recall the above increase in ADH) and thus will not benefit from the usual NS bolus. So, we think about our pressors, specifically ones that target HR and BP together, like norepi or epi. 

Bradycardia 

The norepi and epi that we started above may not cut it. Atropine should definitely be given; depending on the transit time, protocols, and availability, an atropine gtt can be considered. Lastly, don't forget pacing. The myxedema coma patient is an unstable patient that is prone to circulatory collapse given their symptoms are often non-reactive to treatment so ensure we are controlling cardiac output when where we can.

Hypoglycemia

Obviously follow protocol with the initial D50. Yet, frequently reassess BBG as the patient may not show any change in mentation as blood sugar fluctuates. Further, be quick to start a D10 gtt and glucagon as you'll likely be busy titrating pressors and assessing need for atropine or electricity.

RECAP

While the patient described at the beginning of this blog posed an interesting presentation, their lack of responsiveness to treatment in the ED was downright frustrating. Results from vent changes, medication administrations, aggressive rewarming, and more were SLOW. Also, given there was so much that we were simultaneously treating and correcting, by the time the metabolic panel came back from lab, we knew the labs were outdated. This was a patient presentation that I was immensely grateful for iSTAT chemistry panels and their minutes-to-results time. 

With all that being said, the sheer complexity and interconnectedness of each and every lab anomaly was intriguing. For example, the hypotension resulted in increased ADH which resulted in dilutional hypo-everything which resulted in altered mentation so we need to focus on diuresis without tanking cardiac output and sodium any further but we also can't forget about the temperature which if we just throw a warming blanket on and vasodilate, we'll exacerbate the hypotension which we're already on three pressors...and when's the last time we've even checked BBG and UOP?! This presentation demanded further research on my part to ensure I fully understood and ins-and-outs of myxedema coma and ultimately led to reigniting my appreciation of the interconnectedness of various body systems. There are so many more aspects I could have delved further on in this blog yet wanted to stay at a relatively surface level of critical care. 

QUESTIONS & COMMENTS

Have you had a patient with similar presentation or diagnosis? What did you do? What would you have done differently and why?