Pericardial Effusion and Stable Cardiac Tamponade

Stable cardiac tamponade you say?? That’s right! Today, our esteemed Dr. Whitney Chew presented a fascinating case of a middle-aged woman with a remote history of malignancy who presented with a month of progressive fatigue, shortness of breath, and pleuritic chest pain, found to have a large pericardial effusion with compression of the right atrium and ventricle on echocardiogram concerning for cardiac tamponade. Vital signs were stable (BP 131/71 without tachycardia) and the patient was reported to be in no acute distress on documented physical exams.

Clinical Pearl: Cardiac tamponade can be acute OR subacute. When acute, the fluid accumulates quickly and the pericardium has no time to stretch or allow the body to compensate for the decreased diastolic filling. Hemodynamic collapse occurs quickly in this case. In subacute cardiac tamponade, usually from renal failure or malignancy, the fluid accumulates slowly, allowing the pericardial compliance to increase gradually. In this case, as much as 2L of fluid can accumulate in the pericardium before hemodynamic collapse occurs.

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CXR of pericardial effusion: Above are images of pericardial effusion on chest X-ray. On the left, cardiomegaly with a slight water bottle appearance can be appreciated. In addition, a retrocardiac air-fluid level with the air lower than the fluid despite the upright position of the patient is indicative of a pericardial effusion. The fluid is contained within the pericardium and sitting atop some aerated lung, creating this reverse air-fluid level. On the right, the later film shows the “Oreo Cookie Sign” of a vertical opaque line between 2 radiolucent vertical lines indicative of pericardial fluid between the pericardial and epicardial fat. With large pericardial effusions, widening of the subcarinal angle may also be seen.

A Gift for All You Budding Nephrons

Before I begin, I would like to thank Dr. Frank Luo and Dr. Amit Gohil for coming to today’s report and sharing with us their wisdom from years of clinical experience. I also would like to thank Dr. Jacobson for his continuous attendance and invaluable guidance at our reports. As Osler said, “the work of an institution in which there is no teaching is rarely first class” and we owe a debt of gratitude to all of our teachers for their service to us.

To proceed…esteemed colleagues: every once a while you get a case that pushes every aspect of your medical knowledge, diagnostic skills, and clinical reasoning — this was that case. Megan and Trevor presented a case of acute encephalopathy and hypothermia in a patient who ultimately was found to have the following:

  1. Lactic Acidosis
  2. Ketoacidosis
  3. Renal Failure
  4. Respiratory Acidosis
  5. Elevated Osmolar Gap

…among many many other derangements.

We first went through a focused differential of acute encephalopathy and hypothermia

  1. Sepsis
  2. Cardiogenic Shock
  3. Ingestions
  4. Adrenal Crisis
  5. Myxedemic Crisis
  6. Severe Hypoglycemia
  7. Neurologic Crises – brain mass, stroke
  8. Severe Trauma

We then learned that the patient was on Metformin and an SGLT-2 inhibitor and postulated the following sequence of events:

  • Empagliflozin is an SGLT-2 inhibitor known to cause euglycemic DKA, which may have been the etiology of his ketoacidosis. (on an unrelated note — remember that SGLT-2 inhibitors are known to increase the risk of genitourinary infections, particularly fungal infections)
  • The time course of renal failure is difficult to be certain of – but perhaps it was volume depletion from his SGLT-2 inhibitor (via an osmotic diuresis) that led to a pre-renal AKI
  • Metformin is known to cause a Type B lactic acidosis, which may have occurred in the setting of his AKI from above
  • Additionally, his HCO3 may have been so low, that he developed shock as a result of severe acidemia and subsequent type A lactic acidosis as well
  • His acidemia was so profound, that he could not fully compensate, leading to a respiratory acidosis
  • The combination of lactic acidosis, ketoacidosis and renal failure all could have contributed to his osmolar gap

Which leads us to a discussion of the osmolal gap. Checking the serum osms is useful in cases of ingestions, particularly when we suspect it could be a glycol or methanol. We calculate the osmolality based on readily available formulas, then compare it to the measured osmolality. If the measured is greater than the calculated by more than 10, you expect there are added extra osmoles in the blood. UpToDate has a fantastic way of approaching this:

  • With AGMA
    • Major causes of of a large osmolal gap
      • ethylene glycol
      • propylene glycol
      • methanol 
    • Causes of a smaller osmolal gap
      • ketoacidosis
      • lactic acidosis
      • severe CKD without regular dialysis
      • paraldehyde ingestion or injection
  • Without AGMA
    • ethanol
    • isopropanol
    • diethyl ether
    • infusion of mannitol, sorbitol or glycine
    • pseudohyponatremia (severe hyperlipidemia or hyperproteinemia)

Courtesy of UpToDate

Mucormycosis

Today, Dr. Trevor Rafferty presented an extremely interesting case of acute sinusitis in an uncontrolled diabetic that was rapidly progressive and progressed to include right facial edema, erythema, and numbness.

Management of acute sinusitis:

Acute sinusitis can be managed with supportive care in most cases as it is of viral etiology 98% of the time. Less than 2% are bacterial, with an extremely small percentage being of fungal etiology. If symptoms persist and/or worsen over 7-10 days or if the patient endorses a “double worsening” (symptoms getting better and then getting worse again), bacterial sinusitis should be suspected and antibiotics given. In immunocompromised hosts, antibiotics should be considered on a case by case basis and fungal sinusitis should always be on the differential diagnosis. In addition, one should always evaluate for signs of complications of sinusitis, which are orbital cellulitis, preseptal cellulitis, meningitis, abscesses, osteomyelitis, and infections of other adjacent structures. Worrisome signs and symptoms include nuchal rigidity, sepsis, proptosis, painful extraocular movements, diplopia, focal neurological deficit, eschar, and altered mental status.

Diagnosis of fungal sinusitis:

Diagnosis of fungal sinusitis is ONLY possible with a very high index of suspicion. It should be suspected in any and all patients with acute sinusitis in the setting of uncontrolled diabetes, organ transplant, chronic steroids, AIDS, IVDU, or other immunosuppressing medications or conditions. If the patient is in diabetic ketoacidosis or if there is clinical or imaging evidence of erosive disease, invasive fungal sinusitis must be ruled out surgically. Mucor especially thrives in patients with DKA due to an enzyme called ketone reductase, which causes it to thrive in environments rich in ketones. Mucor is angioinvasive and therefore, spreads quickly and produces eschar, necrosis, and frequently focal neurological deficits.

Endoscopic biopsies by ENT are the initial test of choice to obtain the histopathology and culture necessary to diagnosed fungal sinusitis, but are not very sensitive and if negative, do not rule out mucor. In most cases, more invasive exploration in the OR is necessary to look for necrotic tissue and eschar. B-D Glucan is not helpful in diagnosis as mucor does not have the cell wall components that make the test positive.

Treatment of mucormycosis:

The mainstay of treatment is surgical debridement, which often results in significant disfigurement. Multiple debridements are often necessary for source control. Antifungal treatment is also necessary and consists of amphotericin B initially and as a clinical responsive is observed, usually over several weeks, may be transitioned to posaconazole or isavuconazole. Mortality of sinus mucor is around 50%, pulmonary mucor 76%, and 96% for disseminated mucor. Antifungal treatment can be necessary for months and is usually continued until the period of immunosuppression can be stopped (if possible). For patients that cannot stop their immunosuppressing medications or diseases, they may required lifelong antifungal treatment. In addition to surgical debridement and antifungal therapy, aggressive treatment of predisoposing factors is necessary, including hyperglycemia, acidosis, and if possible, immunocompromise.

The Sword of Damocles

If you missed the heart-melting and gut-wrenching portrayal by the talented Dr. Harris of Cicero’s famous story of Damocles and Dionysius II — you truly missed out.

Luckily for you, we have some myxedemic coma pearls we would like to drop as today we reviewed a case of a presumed immmune-checkpoint inhibitor mediated autotoimmune thyroiditis leading to a severely elevated TSH and undetectable T4 in a patient with acute encephalopathy.

Clinical Presentation of Myxedemic Crisis

  • severe hypothyroidism leading to altered level of consciousness, hypothermia and findings of organ slowing
  • can be due to chronic, severe hypothyroidism and/or be precipitated by an acute inciting factor such as , infection, MI, cold exposure and certain medications
  • suspect it in any patient with unexplained ALOC, but particularly in those with some other typical finding of myxedemic crisis such as hypothermia, hyponatremia or bradycardia.

Treatment

  • IV Levothyroxine 200-400mcg x1 as a loading dose followed by daily doses of 50-100mcg until the patient can tolerate oral medications
  • The use of T3 may be useful (center-dependent)
  • Hydrocortisone 100mg q8hrs until you exclude adrenal insufficiency
  • Supportive measures

Bonus!

If you liked the framework for acute encephalopathy but still wanted a mnemonic, never fear — we’ve always got your back!

AuNTie MIA!

Neurologic / Toxic / Metabolic / Infectious / Assorted.

I’ll see myself out 🙂