We discussed a case about an elderly woman with history of HTN, HLD, CVA, and rheumatic heart disease, who presented with palpitations and dyspnea on exertion, found to have severe mitral stenosis and atrial fibrillation. Unfortunately her hospital course was complicated by bilateral lower extremity arterial thromboemboli.
Rheumatic heart disease is the leading cause of mitral stenosis that affects females more than males (4:1).
Clinical manifestations Patients can be asymptomatic for years until they develop severe stenosis.
Dyspnea (due to pulmonary congestion)
Fatigue (due to low cardiac output)
LE edema (due to right heart failure)
MS and atrial fibrillation About 50% of patients with MS will have afib. Without anticoagulation, these patients have a risk of thromboembolism of 20-25%.
Valvular afib = afib in the setting of…
Moderate to severe MS OR
Presence of a mechanical heart valve
A: at risk of MS
B: progressive MS
C: asymptomatic severe MS
D: symptomatic severe MS
Severe MS measurements:
Mitral valve area ≤1.5 cm2
Mean mitral valve gradient > 10 mm Hg
Pulmonary artery systolic pressure > 30 mm Hg
Treatment If the patient is a candidate, percutaneous mitral balloon valvuloplasty (PMBV) is the treatment of choice.
We discussed a case of a middle aged man presenting with acute onset chest pain and bradycardia in the setting of recurrent syncope. Our patient had negative troponins but ST elevations that met criteria for STEMI. STEMI alert was called, however repeat EKG did not meet STEMI criteria. Patient was admitted for unstable angina and received a stress test during which he experienced chest pain with EKG evidence of STEMI. Coronary angiogram was negative for coronary artery disease however he responded to intracardiac nitroglycerin with significant increase in the caliber of left PDA. He was diagnosed with a type of MINOCA (MI in the absence of obstructive CAD), known as vasospastic angina.
It is important to think of “do not miss” chest pain differentials using the 4:2:1 method:
Today we presented a case of syncope 2/2 to age-related degeneration of the conducting system leading to complete heart block. We first went through a framework for Syncope (taken from Dr. Eric Strong’s awesome lecture series)
Definition: Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery.
We then emphasized the importance of choosing wisely in the workup of syncope. All patients with syncope should receive the following:
A spectacular history
A splendid physical examination
Orthostatic vital signs
Depending on the above, target your further testing accordingly
Remember, it’s the cardiogenic syncope that is highly concerning and so the San Francisco Syncope Rule can be useful in deciding who is safe to discharge…BUT, as a recent paper reported, the sensitivity of clinical judgement for adverse outcomes secondary to a syncope is higherthan decision making rules. Therefore, if something doesn’t feel right, trust your instincts!
Our patient was found to have complete heart block on an EKG and we reviewed the three major classifications for its etiology:
Today’s case was a 60-year-old man with acute onset atypical chest pain, tachycardia, mild leukocytosis, and concave ST elevations without anatomical distribution, who was found to have acute pericarditis.
We recently had a case of a middle age man with SLE on chronic prednisone, ESRD on PD, presenting with acute on chronic shoulder pain x 10 days. Presentation was initially concerning for septic arthritis, and joint washout revealed gross purulence from the shoulder joint. Cultures were sent but no additional fluid studies were obtained.
A subsequent TTE, and later a TEE, confirmed a mitral valve vegetation concerning for concurrent infective endocarditis. However, multiple sets of blood cultures, fungal cultures, synovial fluid culture from the initial I&D/wash out, and even 16S PCR of the synovial fluid were all negative. This is a rare case of culture negative endocarditis which is later thought to be more likely Libman Sacs!
Risk factors: Advanced age, pre-existing joint dz, recent surgery or injection, SSTI, IVD, indwelling catheter, immunosuppression.
Most cases arise from hematogenous seeding, hence bacteremia is common.
Direct inoculation: usually due to trauma, surgery/injections, or wounds.
Usually mono-microbial, and Staph aureus is the most common cause of septic arthritis in adults.
GNR can be seen in older adults or in immunocompromised patients
Monoarthritis is most common
Edematous, painful, warmth, limited ROM
Older patients may not be febrile
20% of cases can present as oligoarticular or polyarticular infection. Polyarticular septic arthritis is more likely to occur in pts with RA
Most common affected joint is the knee
Could be a manifestation of infective endocarditis, esp amongst IVDU
Synovial fluid analysis and culture, should be obtained prior to abx
Positive gram stain or culture is gold standard and diagnostic
PCR only required in rare cases since most non-gonococcal cultures obtained prior to antibiotics return positive. Negative cultures can result due to recent abx or atypical organism.
In pts with purulent synovial fluid (WBC 50k-150k) but culture negative, a presumptive dx can be made.
Likelihood of septic arthritis inc with inc leukocyte count
Blood cultures should be obtained
Should also evaluate for endocarditis given most common organism is staph aureus
Always get a radiograph to evaluate for concurrent bone/joint involvement
CT/MRI can be useful if looking for an effusion
Viral (usually polyarticular), i.e. Zika, Dengue, chikungunya, parvo, rubella, adenovirus
Joint drainage, severe infectious may require repeated aspiration or even wash out.
Most cases are staph, MRSA cases on the rise
Suspect pseudomonas if pt is immunocompromised or has h/o IVDU
Intra-articular abx: typically not used
Staph aureus with bacteremia: At least 4 weeks
Staph aureus without bacteremia: at least 14 days IV, followed by 1-2 weeks PO
Bone involvement: 4-6 weeks
Any organisms, any bone involvement: 4-6 weeks
Other organisms: Typically at least 4 weeks
Culture Negative Endocarditis
Definition: Endocarditis without an identified organism in at least 3 independent blood cultures with negative growth after 5 days
2-7% of IE cases
3 most common causes:
Atypical organisms (fastidious bacteria i.e. zoonotic microbes, fungal)
The world’s #1 addictive substance of choice… Caffeine! And yes you can OD on it!
A 37yo F with history of anxiety presented with nausea and palpitations after ingesting 160 pills of Diurex in an attempt to fix her constipation for the past 2 weeks. Prior to arrival to the hospital, the paramedics administered activated charcoal. She was tachycardic, mildly hypotensive, hypokalemic, and acidotic (AG 20). Methamphetamine was found in her system as well. Fortunately she improved with fluids and supportive measures, but lethal cases of caffeine overdose, while rare, have been described in the medical literature!
Of note: An expresso doubt shot contains roughly 60-100mg of caffeine.
This patient took 16000mg (16g) of caffeine, equivalent to 160-260 shots of double expresso!
Thanks to Dr. Olivia Lee for letting us know of the case of this middle-aged woman with h/o endometrial cancer s/p TAH/BSO who was BIBA on a 5150 for GD after being found living in her yard. Her medical clearance work up led to the diagnosis of endocarditis with a large abscess on the mitral valve leading to septic emboli to the brain, spleen, and kidneys as well as vitritis and endophthalmitis. She was also noted to have an indwelling mediport with a vegetation at its tip, showering emboli into her lungs. She successfully underwent urgent surgical replacement of her infected/destroyed valve.
Use Duke’s criteria to help with your pre-test probability of endocarditis. If patient meets criteria for definite endocarditis, consider going straight to a TEE.
TTE is not sensitive but highly specific for endocarditis. However, in a patient with concerning clinical features (see next bullet point), a TEE is necessary to evaluate valve condition and plan for surgical intervention. TTE is more useful if pre-test probability of endocarditis is low.
Indications for surgery
Valve dysfunction causing heart failure
Perivalvular extension with development of abscess, fistula, and/or heart block
Fungi or other highly resistant organisms that are difficult to treat with abx alone
Persistent bacteremia despite maximal treatment
Recurrent embolization with persistent vegetations
Large vegetations (>1 cm) with severe valvular regurg
S aureus prosthetic valve endocarditis
Indications for earlysurgery:
Prevention of embolic events
Most common cause of death in endocarditis is heart failure.
For a thorough review of endocarditis, please see our previous blog post here.
Ischemic heart disease (MI, Prinzmetal angina, ventricular aneurysm) –> tends to present in one vascular territory
Early report variant (AKA J point elevation)
A flutter at its fastest (2:1 block) would have a rate of 150 bpm (meaning atrial rate is 300 bpm). So if you have a regular, narrow complex tachycardia that is going faster than 150 bpm, then start thinking AVRT or AVNRT.
A rough estimate of maximum SA node rate possible in a patient is 220 – age.
If you see a slow a fib with QRS waves at regular intervals, think of dig toxicity! Because dig increases atrial and ventricular ectopy, the atria start to fibrillate. At the same time, the AV node is being blocked. So what you are actually seeing on ECG is fibrillating atrium with complete heart block causing a slow junctional escape rhythm. Keep in mind though that the most common abnormality on ECG for dig toxicity is PVCs.