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.

CaptureCapture

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 🙂

 

 

Necrotizing Fasciitis: Clinical Suspicion Is your Only Chance

Dr. Glenn Harris discussed a case of an elderly man with diabetes and end stage renal disease who presented with sepsis from a right groin skin infection draining pus.

We used this opportunity to review our Sepsis-3 guidelines and discuss some of the newer evidence around the way we treat our septic patients.

Sepsis-3 guidelines tell us that sepsis should be defined based on the following 3 criteria:

– known or suspected infection

– organ dysfunction

– life-threatening

There are various scores we can use to increase the accuracy of our clinical judgment in our determination of the life-threatening nature of a septic patient’s disease, or in other words, their risk of mortality. The SIRS criteria is the scoring system most of our residents were taught in medical school, but according to Sepsis-3, this score has fallen out of favor. It is thought to be too nonspecific. Regardless of the underlying pathology, too many patients present to the ED meeting SIRS criteria. Sepsis-3 encourages the use of the qSOFA score, with only three binary criteria of RR, SBP, and the presence of altered mental status. However, since the guidelines came out, multiple studies have cast doubt on the utility of the qSOFA score, criticizing it as too insensitive. A large study comparing it with SIRS and the NEWS (National Early Warning Signs) score concluded that it fared worse in predicting outcomes. The NEWS score actually fared the best and we may see this score pop up in future studies or guidelines.

Treatment of sepsis includes fluid administration (30cc/kg) within three hours, cultures before antibiotics, and antibiotics within 1 hour. Fluid choice has been a hotly debated topic in the past. The evidence seems to support the use of crystalloids, but our classic dilemma is whether to us NS or LR. Normal saline carries with it a risk of hyperchloremic nonanion gap metabolic acidosis as well as a chloride load which decreases renal blood flow. These concerns lead many clinicians to resuscitate their septic patients with Lactated Ringers, but some give up to 2L normal saline and then switch to LR.

Antibiotic choice in cellulitis is guided by which type of pathogen you are concerned for. Typically, your first branch point is whether you believe the cellulitis is purulent (fluctuant, aka has a potentially drainable pocket of pus) or nonpurulent.

Purulent cellulitis is most commonly caused by staph, with a                                          high prevalance of MRSA

Nonpurulent cellulitis is most commonly caused by strep

However, if you have any suspicion for a necrotizing infection, you should cover for a polymicrobial infection. The LRINEC scoring system has been used to help guide our clinical suspicion for necrotizing fasciitis, but lacks sensitivity and does not take into account the patient’s physical exam or vital signs. The score should not be used to rule out necrotizing fasciitis. Clinical findings that should push you to consult surgery as soon as possible out of concern for a necrotizing skin or soft tissue infection are rapid progression, septic shock, crepitus, and hemorrhaghic bullae. These patients also frequently have pain out of proportion to exam. Your index of clinical suspicion is your most useful tool and you should treat for necrotizing fasciitis regardless of a LRINEC score if you are concerned. 

Unstable Bradycardia with a side of Sgarbossa

Dr. Soumya Murag presented an exciting case of unstable bradycardia in a hyperkalemic patient who also met Sgarbossa’s criteria and turned out to have a concomitant inferior STEMI from 99% ostial stenosis of the RCA.

Here are some high-yield clinical pearls we discussed today:

  • First line treatment for unstable sinus bradycardia is atropine
    • Atropine will not work in Mobitz II 2nd degree heart block or complete heart block (atropine acts on increasing the frequency of firing at the SA node, but these P waves will not be conducted in these situations)
    • The vagus nerve is not always connected in transplanted hearts so atropine may be ineffective in heart transplant patients
  • U waves can be seen in sinus bradycardia without underlying electrolyte abnormalities
  • Acute myocardial ischemia should always be on your differential diagnosis in unstable bradycardia
  • A new LBBB in a patient with chest pain or any presentation concerning for acute coronary syndrome is not a STEMI equivalent, but should prompt you to apply the Sgarbossa Criteria
    • Sgarbossa criteria: 1mm or more ST elevation in any lead with an upward QRS complex (concordant ST elevations) gives 5 points, 1mm or more ST depression in leads V1-V3 gives 3 points, and ST elevations 5mm or more in any lead with a downward QRS complex (discordant ST elevations) gives 2 points
    • A score of 3 or more should prompt urgent cardiac cath
  • Hyperkalemia causes a specific pattern of EKG abnormalities as potassium levels increase, which goes as follows: peaked T waves –> wide, low amplitude P waves with prolonged PR interval –> widening of the QRS –> sine wave
  • Nitrates should be avoided in inferior STEMI patients because they are preload dependent and nitrates can precipitate hypotension
    • Morphine can act in a similar manner so should be used only with extreme caution in inferior STEMI patients

 

Bright Red Blood Per … ULCER!!

Dr. Sylvia Cardounell presented a case of H.pylori induced peptic ulcer disease with a few interesting twists.

One atypical feature of this patient’s case was that he presented with bright red bloody bowel movements initially despite having an upper GI bleed. Upper GI bleeds (upper meaning proximal to the ligament of Treitz or 4th portion of the duodenum) classically present with melena, but when brisk and accompanied by other systemic signs and symptoms such as presyncope, tachycardia, and hypotension, can manifest as hematochezia. The BUN:Cr ratio is sometimes used to aid in differentiating between upper and lower GI bleeding. Due to digestion of blood in the stomach, the BUN increases in upper GI bleed, however a significant portion of lower GI bleeds also have increased BUN due to hypovolemia-induced prerenal azotemia. Some authors suggest various ratios 36:1-100:1 as more specific for upper GI bleeds, but our take home message is that the higher the ratio, the more likely it is for your GI bleed to be upper.

The classic presentation of a patient with peptic ulcer disease is epigastric abdominal pain about 2 to 5 hours after a meal when acid is secreted in the absence of a food buffer. Pain may also manifest at night between 11pm and 2am when circadian stimulation of acid secretion is maximal. Other food-provoked symptoms may occur as well including pain worse with eating (due to visceral sensitization and gastroduodenal dysmotility), belching postprandially, early satiety, fatty food intolerance, nausea, and occasional vomiting. Alarm features for dyspepsia that should provoke further testing and looking for alternate diagnoses are unintentional weight loss, dysphagia, odynophagia, unexplained iron deficiency anemia, persistent vomiting, palpable mass or lymphadenopathy, and a family history of upper GI cancer. Our patient’s initial vital signs showed mild tachycardia and hypotension when laying supine, indicating a blood loss of about 40% of total blood volume. Tachycardia typically starts at <15% blood loss, orthostatic hypotension requires a blood loss of at least 15%, and supine hypotension indicates a minimum blood loss of 40%.

The following are good rules of thumb for initially stabilizing your patient bleeding from their upper GI tract:

  • Prioritize access: they should have at least 2 large bore (18 gauge or larger). You can look at the color of your IV catheter to ascertain the gauge. Green is 18g, grey is 16g, and orange is 14g. 14g are not usually used for IV access due to their large size. Smaller IVs are pink, blue, and yellow.
  • Monitor for airway protection, place patient NPO, type and cross, consent for blood transfusion
  • Resuscitate: 
    • Crystalloids should be started for resuscitation if blood products cannot be obtained initially. Be judicious due to the risk of volume overload with subsequent transfusions.
    • Blood products:
      • A transfusion goal of Hgb 7 is appropriate for most patients, but those with unstable coronary artery disease should aim for a hemoglobin of 9. Clinical judgement is necessary in these cases and those who are elderly or with many comorbidities may need a higher transfusion goal.
        • In patients with cirrhosis, overtransfusion has been shown to lead to worse outcomes, likely due to worsening of underlying portal hypertension
      • Transfuse platelets if platelet <50 
        • Platelet transfusion can also be considered in patients on chronic antiplatelet therapy. However, evidence is lacking and given the risks of transfusion, platelet transfusion should not be routine in these patients
      • Goal INR <2. If your patient requires significant PRBC transfusion, you may dilute the concentration of clotting factors in the serum, creating an iatrogenic coagulopathy. Therefore, for every 4u PRBCs transfused, you should give 1u FFP.
  •  Acid suppression: Increasing the gastric pH allows blood to form clots and hopefully stop active hemorrhage. Traditionally, PPI infusion was used for UGIB cases, but more recent evidence has shown no difference in outcomes when comparing continuous PPI infusion and PPI bolusing BID. In fact, there was a trend toward lower rates of rebleeding in the bolusing group. Because of this evidence, the decreased cost, less resource utilization, and increased patient comfort, intermittent bolusing of PPIs is recommended. A loading dose of 80mg IV should still be given before starting 40mg IV BID dosing. Protonix and Nexium are the only PPIs available IV, but there is increasing evidence that oral PPIs may be sufficient.
  • In cirrhotics: octreotide and antibiotics should be added
  • Consider prokinetic agents such as erythromycin or Reglan 30-90 minutes before EGD if your patient has severe bleeding or has recently eaten as these may help your gastroenterologist visualized the stomach

Once you diagnose peptic ulcer disease, your differential remains broad. 

Peptic ulcer disease accounts for >50% of upper GI bleeds. It has myriad causes and risk factors. H.pylori, NSAID-induced, steroid-induced, and stress ulcers are our most commonly considered components on the differential, but ulcers have been associated with other more rare disorders such as gastrinoma, IgG4 related infilrative gastropathy, polycythemia vera, and sarcoidosis. There is also an association with acetaminophen of 2-3g/day or higher, bisphosphonates, Sirolimus, and an increasing body of evidence indicating that SSRIs increase risk of PUD as well. Smoking also increases the risk of peptic ulcer disease through many mechanisms.

Our patient received testing for H.Pylori via stool antigen test, which returned positive. Another atypical aspect of his case was that he received biopsy of his gastric mucosa during his EGD as well, but this came back negative. Typically, biopsy has a sensitivity of 90-95%, but active GI bleeding, antibiotics, PPIs, and bismuth-containing compounds decrease the sensitivity of biopsy, stool antigen test, and urea breath testing. If biopsy is negative for H.Pylori and you are worried about the sensitivity of biopsy in your clinical case, doing noninvasive H.Pylori testing 2 weeks after cessation of PPIs and 4 weeks after cessation of bismuth compounds is indicated. If EGD is indicated for another reason, biopsy is always first line for H.Pylori diagnosis. If no EGD is indicated, stool antigen or urea breath test should be used. 

Serology is not used to diagnose H.pylori because it remains positive after H.pylori treatment or after exposure that is not causing clinical disease.

H.Pylori Treatment:

Triple therapy should be used unless there is significant local resistance to clarithromycin (15% or more) or the patient has risk of macrolide resistance (has received macrolides for any reason). 

Triple therapy: Clarithromycin, amoxicillin, and PPIx14d

Quadruple therapy: Tetracycline, Flagyl, PPI, and Bismuth Subsalicylate x14d

One month after treatment of H.pylori, you should confirm eradication with urea breath test or stool antigen.