Constrictive Pericarditis

Thanks to Phuong today for presenting the case of a young woman who presented with volume overload, found to have constrictive pericarditis!


Clinical Pearls

  • Constrictive pericarditis and restrictive cardiomyopathy can have similar clinical presentations.  Cardiac cath is generally needed to help distinguish between the two.
  • The most common cause of constrictive pericarditis is idiopathic!
  • Exam findings in constrictive pericarditis include volume overload, pulsus paradoxus, Kussmaul’s sign, pericardial knock, and occasionally (<20% of the time) pericardial friction rub.
  • ECG and CXR can be normal in constrictive pericarditis.
  • Treatment of early disease is supportive care.  Treatment of late stage constrictive pericarditis is pericardiectomy.

Etiologies of constrictive pericarditis:

  • Idiopathic (42-61%) ⇒ most common cause!
  • Post-cardiac surgery (11-37%)
  • Post-radiation therapy (2-31%) particularly after Hodgkin disease or breast cancer
  • Connective tissue disorder (3-7%)
  • Post-infectious – TB or purulent pericarditis (3-15%)
  • Miscellaneous causes (malignancy, trauma, drug-induced, asbestosis, sarcoidosis, uremic pericarditis) (1-10%)

Clinical Presentation

  • Symptoms related to fluid overload
  • Symptoms related to diminished cardiac output in response to exertion
  • Exam:
    • Elevated JVP
    • Pulsus paradoxus – drop in SBP >10 mmHg due to drop in stroke volume and cardiac output with inspiration (20%)
    • Kussmaul’s sign – lack of an inspiratory decline in JVP.  (Also present in people with severe tricuspid valve disease or R heart failure.
    • Pericardial knock – 47%
    • Pericardial friction rub – 16%
    • Stigmata of heart failure
  • ECG: can be normal
  • CXR: Majority of people do NOT have pericardial calcifications
    • Interestingly, calcifications are more common in people with idiopathic disease, a longer duration of symptoms, and those with TB!

Management of Constrictive Pericarditis

  • Early disease is usually managed with supportive care.  Diuretics can help mitigate symptoms of volume overload but must be used cautiously due to preload dependent physiology.
  • Late stage disease is treated with pericardiectomy.  Complication rates tend to be high and operative mortality can reach 12%!

Constrictive Pericarditis vs Restrictive Cardiomyopathy:

CP vs RCM

We also talked about a helpful way of breaking up new onset ascites to help generate a DDx:

Ascites fluid distribution

Culture Negative Endocarditis 5/7/2019

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!


Septic Arthritis

  • Epidemiology
    • 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.
  • Microbiology
    • 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
  • Presentation
    • 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
  • Diagnosis
    • 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
    • Imaging:
      • Always get a radiograph to evaluate for concurrent bone/joint involvement
      • CT/MRI can be useful if looking for an effusion
  • DDx
    • Infectious
      • Gonococcal arthritis
      • Lyme disease
      • TB arthritis
      • Viral (usually polyarticular), i.e. Zika, Dengue, chikungunya, parvo, rubella, adenovirus
    • Non-infectious
      • Crystal dz
      • Reactive arthritis
  • Management
    • Joint drainage, severe infectious may require repeated aspiration or even wash out.
    • Abx
      • 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
      • Duration:
        • 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
  • Epidemiology
    • 2-7% of IE cases
    • 3 most common causes:
      • Previous abx
      • Inadequate samples
      • Atypical organisms (fastidious bacteria i.e. zoonotic microbes, fungal)
  • Microbiology
    • Farm animal exposure: Brucella, Coxiella (Q-fever)
    • Homeless: Bartonella Quintana
    • Cat: Bartonella hensale
    • Ingestion of unpasteurized milk: Brucella, Coxiella
    • Immunocompromised: Fungi, Coxiella
    • HACEK: Most common agents of culture negative endocarditis
      • Haemophilis aphrophulus
      • Actinobacillus
      • Cardiobacterum hominis
      • Eikenella corrdens
      • Kingella
  • Diagnosis
    • PCR, histology, special cultures are helpful.
    • PCR
      • 16S Ribosomal DNA: Bacteria
      • 18S Ribosomal DNA: Fungi
  • Non-infectious DDx
    • APLS, associated with Q fever
    • Acute rheumatic fever
    • Atrial myxoma
    • Libman Sachs endocarditis (non-bacterial thrombotic endocarditis or NBTE)
      • Seen in:
        • SLE
        • Advanced cancer
        • Hypercoagulable state
    • Vasculitis
    • Mural thrombus

NBTE (Non-bacterial thrombotic endocarditis)

  • Epidemiology
    • Rare affected all age group with no sex preference, most commonly 40s – 80s
    • Most commonly associated with pts with concurrent SLE or advanced malignancy (lung cancer, pancreatic cancer, gastric cancer)
    • Other associated conditions: APLS, rheumatic heart disease, RA.
  • Pathophysiology
    • A form of non-infectious endocarditis characterized by deposition of thrombi on halve valves, most commonly mitral or aortic
  • Presentation
    • Usually asx but high risk of thromboembolic events
    • May present with acute stroke or coronary ischemia
  • Diagnosis
    • Exclusion: Demonstration of vegetations on echo in absence of systemic infection in patients with risk factors.
  • Management
    • Systemic anticoagulation
      • Clinical experience and retrospective studies had shown this is beneficial due to high rate of emboli in pts with NBTE
    • Treat underlying condition
    • Surgery
      • Surgical excision for NBTE vegetation, can be considered in only selective cases and generally avoided.

Caffeine Overdose! 5/1/2019

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!


Caffeine Intoxication

  • Epidemiology
    • Caffeine = world’s #1 psychoactive compound consumed
    • Pure caffeine can be easily obtained, caffeine pills introduced in 2004.
    • Death from caffeine overdose is rare, only 92 cases have been described in literature.
    • Caffeine pills heavily advertised as weight loss supplements
  • Risk factors
    • Psychiatric conditions
    • Athletes (weight loss/work out supplements, these things are NOT regulated!)
    • Infants/young kids (accidental ingestion)
  • Pathophysiology
    • Dose-dependent MOA
    • CNS and cardiac stimulation, usually occurs at plasma concentration of 15mg/L or higher
    • Usually not food/beverages related. Most cases are related to caffeine-containing medications.
    • Lethal cases reported over 10g ingestion, highest reported ingestion is 100g (1000 double shots of Expresso)
    • Absorbed in the GI tract within 30 minutes
    • Half life 5-6 hours, metabolized in the liver
  • Presentation
    • Agitation, diaphoresis, anxiety, restlessness, insomnia, GI disturbances, tremors, psychomotor agitation
    • Complications
      • Serious cases: arrhythmias (SVT, VT), even V-fib (most common cause of death in caffeine intoxication)
      • Hypotension
      • Hypokalemia
      • Seizures
      • Lactic acidosis
      • Rhabdomyolysis
      • Renal failure
  • Diagnosis
    • Life threatening caffeine overdose more commonly associated with blood concentration > 80mg/L
    • Clinical history, serum measurement, ingestion history
  • Management
    • Activated charcoal for ingestions:
      • Effective only within a short time of ingestion, typically within 1-2 hour and patients have to be mentating
      • Interacts with caffeine and prevents it from being absorbed.
    • Hydration
    • Electrolyte repletion
    • Anti-arrhythmic agents (amiodarone, even lidocaine) in setting of arrhythmias, ACLS if unstable arrhythmias
    • Dialysis: Dialyzable

Source: GrepmedToxidrome Flow

A summary of toxidromes:

Toxidrome.jpg

Infective endocarditis

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.


Clinical Pearls

  • 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 early surgery:
    • Heart failure
    • Uncontrolled infection
    • 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.

ECG Report

Some pearls from our ECG report today:

  • DDx for ST elevations on ECG:
    • Pericarditis (diffuse)
    • Ischemic heart disease (MI, Prinzmetal angina, ventricular aneurysm) –> tends to present in one vascular territory
    • LBBB
    • 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.

RCA infarct, bradycardia, & hyperkalemia!

Today, we discussed the case of an elderly woman with significant history of vasculopathy and ESRD who presented with weakness, found to be bradycardic to 30s, hypotensive, and hyperkalemic to 7.2.  Her hyperkalemia was treated with dialysis but she underwent cardiac cath due to up trending troponins, found to have a 100% occlusion of the RCA!


Clinical Pearls

  • First step in managing a patient with bradycardia is ABCs!
  • First medication for symptomatic bradycardia is atropine.  Remember that atropine works at the level of the AV node and higher so if the block is occurring somewhere below the AV node, then atropine will not be effective.
  • Other pharmaceutical agents are dopamine, epi, or isoproterenol
  • Anyone with bradycardia and unstable hemodynamics in spite of above treatments should receive transcutaneous pacing.  This buys you time until you can place a transvenous pacemaker (less painful, more effective)
  • ECG has a low sensitivity but high specificity for hyperkalemia-induced cardiomyocyte instability.
  • ECG changes associated with hyperkalemia in progressive severity:
    • Peaked T waves
    • P wave widening, PR prolongation, P wave disappearance
    • QRS widening, AV block, bradycardia
    • Sine wave
    • VF/asystole/PEA

Bradycardia approach

1. ABCs!

  • Pharmaceutical agents
  • Atropine (0.5 mg – 1 mg q3-5 mins for a total of 0.03 mg/kg)
  • If no improvement, consider dopamine or epi
  • If still symptomatic, then start transcutaneous pacing

2. Find underlying cause and treat it 

  • Meds: BB, CCB, amio, digoxin, clonidine, lithium, acetylcholinesterase inhibitors
  • Ischemia (up to 25% of patient with acute MI present with bradycardia)
  • ↑ vagal tone: if young, athlete
  • Metabolic: hypoxia, sepsis, ↓T4, hypothermia, hypoglycemia, hyperkalemia
  • OSA
  • Elevated ICP
  • Infections: legionella, lyme, Q fever, typhoid, malaria, RMSF, yellow fever, leptospirosis, dengue, Chagas disease
  • Infiltrative processes: sarcoid, amyloid, hemochromatosis

In our patient, the cause was severe hyperkalemia as well as an RCA infarct.  Given her clinical instability, and the potential for worsening hyperkalemia from cardiac catheterization alone, the team normalized her serum potassium before performing cardiac cath which led to the RCA MI diagnosis.

Hyperkalemia

  • ECG changes are not sensitive for hyperkalemia and can miss up to 39% of patients even with a K of 7-9.
  • Sweet spot for potassium appears to be a mean K of 3.5 to 4.5 mEq/L. There is not a well-defined treatment threshold.
  • Bottom line for management: if you have the kidneys available, use the kidneys to excrete as much potassium as possible.
  • Newer agents like sodium zirconium and patiromer. Mix with water. Well tolerated and highly effective.

Agents that reduce serum potassium via transient intracellular shift:

  • Insulin: give with D50 if normoglycemic to avoid hypoglycemia and be sure to check FSG hourly for 4 hours after to ensure no hypoglycemia develops
  • Albuterol (10-20 mg) nebs: this is significantly higher than the dose we give in COPD (2.5 mg) and is equal to ~8 treatments! So make sure to continue the nebs when the patient arrives on the floor from the ER if they are still hyperkalemic.
  • NaHCO3: best for management of chronic hyperkalemia in the outpatient setting.  In the acute management of hyperkalemia, alkalinization of serum with a large bicarb load can lead to a reduction in serum calcium levels.  Lower serum calcium can lead to more cardiac membrane instability and fatal arrhythmias!

Agents that eliminate potassium from the body:

  • Loop diuretics: first choice if a functioning kidney is available!
  • Cation exchange binders: preferred when kidneys are not available
    • Patiramer (available at VMC), much more tolerable than kayexalate and highly effective at lowering serum potassium.  Like kayexalate, it works over hours to days.
    • Sodium zirconium: similar to patiramer but not currently available
    • Kayexalate: not pleasant to take orally. Also carries with it the slight risk of colonic ischemia especially in post renal transplant patients and those with baseline colonic dysfunction (due to infection or inflammation).
  • Dialysis

Indication for using calcium gluconate: when EKG changes are noted.  Repeat doses (maximum 3) until EKG changes have resolved.

EKG Changes in Hyperkalemia:

  • K > 5.5 ⇒ repolarization abnormalities:
    • Peaked T waves are the earliest sign
  • K > 6.5 ⇒ progressive paralysis of the atria:
    • P wave widens and flattens
    • PR segment lengthens
    • P wave eventually disappears
  • K > 7.0 ⇒ conduction abnormalities and bradycardia:
    • QRS widens
    • High-grade AV block, slow junctional and ventricular escape rhythms
    • Any kind of conduction block (bundle branch blocks, fascicular blocks)
    • Sinus bradycardia or slow AF
    • Sine waves
  • K > 9.0 ⇒ cardiac arrest:
    • Asystole
    • Ventricular fibrillation
    • PEA with bizarre, wide complex rhythm

ECG Report #2!

Thanks everyone for yet another high yield report on ECGs with Dr. Zhao!  Here are the main pearls from today:

  • Remember that a negative p wave amplitude in lead I is seen in two diagnoses only: dextrocardia and limb lead reversal.  To distinguish between the two, look at the amplitude of the QRS complexes as you advance through the precordial leads.  In dextrocardia, you should see a loss of amplitude as you go from V1 to V6, because you are getting further away from the heart.  In limb lead reversal, this is not the case.
  • Remember that ST depressions in anterior leads V2 and V3 should raise your suspicion for a posterior MI and prompt further evaluation with a posterior ECG!
  • When dealing with an irregularly irregular wide complex tachycardia, think of these three differential diagnoses:
    • Atrial fibrillation with aberrancy (i.e. with a bundle branch block)
      • QRS waves should largely look similar in morphology
      • Rates should not exceed 170 bpm because all conduction is still going down the AV node
      • Treatment: shock if unstable, AV nodal blocking agents or amiodarone
    • Atrial fibrillation with an accessory pathway (WPW, also known as a preexcitation pathway)
      • QRS waves have varying shapes because they are conducted down the accessory pathway and the AV node
      • Because the accessory pathway has a much shorter refractory period than the AV node, heart rate can be very high and >200 bpm.
      • Treatment: shock if unstable.  Do NOT give AV nodal blocking agents (including amiodarone) because blocking the AV node can force all conduction down the much faster accessory pathway and lead to VF arrest.  The agent of choice is IV procainamide.
    • Polymorphic VT
      • QRS morphology varies (Torsades)
      • Rates should not exceed 170 bpm
      • Treatment: shock if unstable, otherwise amiodarone