Hemorrhagic shock secondary to GI bleed with recent PCI for NSTEMI on DAPT… Did I mention severe aortic stenosis as well? How about all of these in one patient at the same time? 11/29/2018

Narges presented a very complicated patient, who presents with 2 days of abdominal pain and melena. He had a PCI 4 days prior with a drug-eluting stent deployed at the LAD, and he was discharged on aspirin and ticagrelor (PLATO trial, superior to clopidogrel). On presentation he was in hemorrhagic shock, with notable hematochezia on exam, encephalopathy, and a 4/6 systolic murmur with carotid radiation which turned out to be an undiagnosed severe aortic stenosis.

To briefly summarize his main problem list:

  1. Hemorrhagic shock secondary to UGIB
  2. CAD with recent NSTEMI s/p DES to LAD x1 on DAPT
  3. Severe aortic stenosis, newly diagnosed

Question is, what to do if you see a patient like this? Let’s break it down.


 

Antiplatelet and PCI

  • Drug eluting stents (DES) are designed to have lower rates of late re-stenosis than bare metal stents (BMS), but they are at higher risk for in-stent thrombosis due to delayed endothelialization.
  • Some terminology:
    • Stent re-stenosis:
      • Gradual narrowing of the stent segment, usually occurs 3-12 months after stent placement.
      • Can present as recurrent angina vs full blown MI
    • Stent thrombosis
      • Abrupt thrombotic occlusion of a previously patent stent, usually catastrophic MI
  • Duration of DAPT? It depends! Per the 2016 ACC/AHA guidelineDAPT.png

In a nut shell:

Elective PCI in stable CAD:

  • BMS: At least 1 month of DAPT
  • DES: At least 6 months of DAPT

Exact duration is yet to be determined; there is some evidence of decreased stent restenosis (DAPT trial) with longer duration of DAPT but at the expense of all cause mortality and bleeding complications. There are also newer studies (i.e. ARCTIC Interruption) that found no benefits with longer duration of DAPT.

For PCI in setting of ACS, however, the guideline is different:

Anti-platelet duration in setting of ACS

  • Medical Therapy: At least 12 months of DAPT
  • PCI (BMS or DES, doens’t matter): At least 12 months of DAPT
  • CABG: Also at least 12 months of DAPT

In patients with high bleeding risk or personal history of bleeding and/or long term NSAID use, preemptive prophylaxis with a PPI can be considered. If bleeding risk is significant, you can potentially decrease DAPT duration to at least 6 months, on a case-to-case basis.

Now keep in mind our patient has a DES deployed 4 days ago and he’s now bleeding…


GI Bleed

Risk Factors

  • Alcohol
  • NSAID
  • Anticoagulation
  • Cirrhosis
  • Cancer

Presentation

  • UGIB: BUN/Cr ratio > 30 usually (not sensitive but specific), melena (gut transit of blood)
  • LGIB: bright red hematochezia, lower BUN/Cr ratio, but do not be fooled, can be seen in brisk UGIB (especially in this patient).

Management

  • Airway protection
  • Large bore IVs (18 G), Cordis, IO (they work wonders in a pinch!)
  • Fluid resuscitation
  • Anti-acid (i.e. Protonix)
  • Octreotide if suspecting variceal bleed, if catastrophic variceal bleed, consider deployment of a Blakemore/Minnesota tube
  • Antibiotics for primary SBP prophylaxis if cirrhotic
  • Blood product administration
  • GI consultation, urgency depending on clinical status, EGD

High risk features on Endoscopy

The patient underwent EGD and a duodenal ulcer that was actively bleeding was found. There are certain features of an ulcer that we can use to risk stratify and determine how likely intervention will be successful, and how likely the ulcer will rebleed. This is the Forrest Classification, first published in the Lancet in 1974. Our patient in this case is class 1B, and he ended by rebleeding twice requiring additional endoscopic intervention.

Picture1

Source: Alzoubaidi DLovat LBHaidry R. Management of non-variceal upper gastrointestinal bleeding: where are we in 2018? 

Failure of endoscopic therapy

  • Predictors: active bleeding at time of endoscopy, visible vessel, > 2cm, posterior duodenal ulcers, and gastric ulcers on the lesser curvature are associated with higher risk of treatment failure/rebleeding.
  • First line: 2nd endoscopic intervention
  • If recurrent bleeding persists, surgical options or IR embolization should be considered

The key question here is, when to resume DAPT? The decision will have to be individualized and most would recommend restarting ASAP as soon as patient is clinically stable… At the same time, pt has one other newly diagnosed problem that makes his management tricky…


aorticvalvearea-classification-aorticstenosis-meangradient-cardiology-original

Source: grepmed

Severe Aortic Stenosis

Criteria:

  1. Area < 1cm2
  2. Mean trans valvular gradient > 40 mmHg
  3. Peak velocity > 4m/s

Referral to Cardiology because it is actually more complicated than this, there is also pseudo severe where AVR is not recommended, Low flow AS, low gradient AS, or both LF LG AS.

  • Pseudo-severe: mild to moderate AS, low gradient, underlying myocardial dysfunction leading to poor valve opening. No benefit in AVR
  • LF LG AS:
    • AVA < 1cm2, but gradient < 35mmHg
    • Must distinguish from pseudo severe AS. Do dobutamine stress echo
      • If AVA remains the same, gradient inc, confirms true severe AS
      • If AVA improves while mean gradient remains the same, this is pseudo-severe AS, manage medically.

Epidemiology

  • < 70: Suspect bicuspid aortic valve
  • > 70: Progressive valvular fibrosis/calcification
  • Developing country: Rheumatic fever

Pathophysiology

  • Over time leads to LV hypertrophy (concentric), muscle hypertrophy. Leads to heart failure over time.

Presentation

  • Asx
  • Sx: SAD syncope, angina, dyspnea

Management

  • TAVR (transcatheter) vs SAVR (surgical), TAVR is non-inferior (PARTNER A, PARTNER B, SURTAVI trials) but has other complications to consider,
  • Can think about the transcatheter approach in high surgical risk patients.

In setting of hypotension

  • Patients with critical AS are highly preload dependent:
  • Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV). In patients with severe AS, CO is fixed due to physiologic limitations of a small outlet.
    • Increasing HR can help with CO but you run the risk of increasing myocardial O2 demands…
    • Also in terms of volume, pts with severe AS usually has a degree of diastolic dysfunction (decreased compliance due to a hypertrophied ventricle). As you can imagine, if you push too much fluids into a non-compliant system, back up can occur leading to pulmonary edema thus respiratory failure…
  • Choice Pressors: no absolute contraindication to any but phenylephrine has been suggested in some anesthesia text books as first line
    • Rationale: Pure alpha, increases DBP (diastolic blood pressure), which in turns inc coronary perfusion pressure (CPP = DP – PCWP (LVEDP))
    • Won’t induce tachycardia (if anything induces a mild reflexive bradycardia which decreases myocardial O2 demands).
    • Epi has been associated with higher incidences of arrhythmias

Stress-induced cardiomyopathy – 9/5/18

Thanks to Eric for presenting the case of an “late middle-age” woman with chest pressure, found to have ST depressions, troponin elevation, TTE with apical akinesis, and clean coronaries on cardiac cath concerning for Takotsubo cardiomyopathy.


Clinical Pearls

  • Think of heart failure as ischemic vs non-ischemic
  • Most common causes of heart disease are ischemia (CAD), HTN, idiopathic, valvular, infectious (viral), and drugs.
  • MINOCA or myocardial infarction with nonobstructive coronary arteries is MI in the absence of coronary artery disease with >50% vessel occlusion and includes the following etiologies
    • Stress induced cariodmyopathy (Takotsubo)
    • Coronary vasospasm
    • Microvascular dysfunction
  • Takotsubo cardiomyopathy most commonly presents in postmenopausal women and triggered by physical or emotional stress.  The pathogenesis is not well understood and the course is self-limited.  Treatment is largely supportive.  Prognosis to recovery of cardiac function is 1-4 weeks.

Heart failure

  • Ischemic
    • CAD
    • Bridge
  • Non-ischemic
    • HTN
    • Valvular disease
    • Idiopathic
    • Infectious (viral is most common)
    • Infiltrative (sarcoid, amyloid, hemochromatosis)
    • Stress induced cardiomyopathy (Takotsubo)
    • Arrhythmia
    • High output (secondary to anemia, Paget’s disease, pregnancy, AV fistula, beriberi, hyperthyroidism)
    • Post-partum
    • Hypothyroidism
    • OSA
    • Connective tissue disease

MI with non-obstructive coronary arteries (MINOCA)

  • Diagnosis: requires the following
    • Clinical documentation of MI
    • Exclusion of obstructive CAD
    • No overt cause for acute MI present
  • Etiologies: significant overlap with non-ischemic causes of heart failure
    • Non-cardiac
      • Reduced troponin clearance (i.e. renal impairment)
      • Increased right heart pressures (ex PE)
    • Cardiac causes
      • Stress induced cardiomyopathy
      • Inflammation (myocarditis)
      • Coronary artery spasm (vasospastic angina)
      • Microvascular dysfunction (microvascular angina, microvascular spasm, coronary slow flow phenomenon)
      • Thrombophilia
  • Work up
    • MINOCA is a working diagnosis
      • Exclude non-cardiac cause
      • Rule out ischemic etiology
      • TTE
      • Cardiac MRI is often indicated
      • Provocative spasm testing (with acetylcholine etc in the case of coronary vasospasm)

Takotsubo cardiomyopathy

  • First described in Japan in 1990
  • It is the underlying etiology in ~1-2% of patients presenting with ACS
  • More common in post-menopausal women (mean age 66.4)
  • Pathogenesis:
    • Not well understood
  • Clinical manifestations
    • Often triggered by emotional or physical stress but ~30% of the time, no trigger is identified
    • Symptoms
      • Most commonly present with acute substernal chest pain.  Less commonly present with SOB or syncope or heart failure symptoms
    • Exam
      • May have late peaking systolic murmur similar to HOCM
    • EKG changes:
      • ST elevation in anterior leads (43.7%)
      • ST depression (7.7%)
      • QT prolongation, T wave inversion, abnormal Q waves
    • Troponin elevation in most patients (mean initial troponin is ~7-8)
    • Diagnostic criteria
      • Transient LV systolic dysfunction (hypokinesis, akinesis, or dyskinesis), wall motion abnormalities that extend beyond a single epicardial coronary distribution
      • Absence of CAD based on cath
      • New EKG abnormalities
      • Absence of pheochromocytoma or myocarditis
    • Work up
      • Rule out ACS
      • Cardiac MRI to rule out other causes of MINOCA
    • Management
      • Supportive
    • Prognosis
      • Recovery in 1 to 4 weeks

Picture1

Picture above and cool video from NEJM here.

 

 

Thyroid storm! Or is it?… 8/28/18

Thanks Hong for presenting the case of a middle-aged woman with recent diagnosis of Grave’s disease off methimazole who presented with A fib with RVR and congestive heart failure, raising a debate on thyroid storm!


Clinical Pearls:

  • Thyroid storm is an extremely rare (1 in 500,000) but life-threatening diagnosis (up to 30% mortality) that should not be missed.
  • Degree of thyroid hormone elevation or TSH suppression is not a criteria for diagnosing thyroid storm! In fact, levels are typically similar to those of patients with uncomplicated thyrotoxicosis.
  • Common clinical feature is cardiovascular symptoms (heart failure, arrhythmia, tachycardia) but more specific finding is AMS.
  • Scoring criteria to screen for thyroid storm include Burch/Wartofsky and the Akamizu criteria, but they have not been validated.
  • Consult endocrine early if you suspect thyroid storm!

Thyroid storm: 

Risk factors:

  • Longstanding untreated hyperthyroidism
  • Precipitants:
    • Thyroid/non-thyroidal surgery
    • Trauma
    • Infection
    • Acute iodine load
    • Parturition
    • Irregular use or discontinuation of antithyroid treatment

Etiology: not clearly understood, but possibly related to the following

  • Rapid rate of increase in thyroid hormone levels?
  • Increased responsiveness to catecholamines?
  • Enhanced cellular responses to thyroid hormone?
  • The degree of thyroid hormone elevation or TSH suppression is not typically more profound than uncomplicated thyrotoxicosis

Clinical features:

  • CV (>60% of cases)
    • Tachycardia
    • CHF
    • Arrhythmias
  • Hyperpyrexia
  • AMS (considered by many to be essential to diagnosis)
    • Agitation, anxiety, delirium, psychosis, stupor, coma
  • Features associated with worse outcomes?
    • AMS
    • Older age >60
    • Mechanical ventilation
    • Not using antithyroid drugs or beta blockers

Diagnosis: 

  • Clinical! No universally accepted criteria or validated clinical tools.  Degree of hyperthyroidism is not a criterion for diagnosis.  Some to know of that might be helpful:
    • Burch and Wartofsky (sensitive, not specific)
      • > 45: highly suggestive of thyroid storm
      • 25 – 44: impending storm
      • <25: thyroid storm unlikely
    • Akamizu (Japanese) system developed in 2012 (less sensitive but more specific)

Treatment

  • ICU admission!
  • Regimen
    • Beta blockers ⇒ control symptoms from increased adrenergic tone
    • Thionamide ⇒ block new hormone synthesis. PTU is preferred because it blocks peripheral conversion of T4 to T3.
    • Iodine solution ⇒ block release of thyroid hormone (saturated solution of potassium iodide)
    • Iodinated radiocontrast agent (not available anymore in most places) ⇒  inhibit peripheral conversion of T4 to T3
    • Glucocorticoids ⇒ reduce T4 to T3 conversion, promote vasomotor stability, and treat any associated relative adrenal insufficiency
    • Bile acid sequestrants ⇒ decrease enterohepatic recycling of thyroid hormones (only in very severe cases)
  • Principles
    • Start with beta blockers + PTU, and stress dose steroids
    • 1 hour later: start SSKI q6h (after hormone synthesis has been halted with PTU, otherwise SSKI can make thyroid storm worse)

Digi-Tox? DigiFab! – 8/8/18

Thanks to Michelle for presenting the case of an elderly man with CKD5 presenting with GI symptoms and bradycardia, found to have regularized A fib consistent with dig toxicity!


Clinical Pearls

  • A “regularized” atrial fibrillation rhythm should trigger work up for digoxin toxicity.  This rhythm is generated because of complete heart block.  So the atria continue to fibrillate but no impulse is getting through to the ventricles.  As a result, a junctional (narrow complex) escape rhythm takes over.
  • Elevated digoxin levels can rule in the diagnosis of dig toxicity but normal levels do not rule it out.
  • Risk factors for dig toxicity include: renal dysfunction, hypokalemia, hypomagnesemia, and hypercalcemia.

Clinical manifestations of dig toxicity:

  • Acute: predominantly GI symptoms (nausea/vomiting, anorexia, non-specific abdominal pain)
  • Chronic: predominantly neurologic symptoms (delirium, confusion, weakness, lethargy, disorientation, vision changes)
  • Cardiac manifestations: can be acute or chronic and of greatest concern!

EKG findings:

  • Most common finding ⇒ PVCs!
  • Other arrhythmias: AVB, atrial tachyarrhythmia, ventricular bigeminy, junctional rhythm, bidirectional ventricular tachycardia (RARE and only a few drugs can cause this)
  • Scooped ST depressions (the famous Salvador Dali mustache)
  • Increased U waves
  • QT shortening

Risk factors for developing toxicity:

  • Renal dysfunction
  • Hypokalemia, hypomagnesemia, hypercalcemia

Treatment:

  • Ingestion 1-2 hours ago? ⇒ activated charcoal
  • Indications for using Digoxin-specific antibody fragments (AKA DigiFab)
    • Severe poisoning
      • life threatening/hemodynamically unstable arrhythmia
      • K > 5
      • Organ hypoperfusion (AMS, renal failure)
      • Other considerations before giving DigiFab:
        • Hyperkalemia ⇒ do NOT treat.  DigiFab will lower levels
        • Hypokalemia ⇒ Treat! DigiFab will make it worse
        • Hypomagnesemia ⇒ Treat!
    • Serum digoxin concentration is irrelevant!
  • You’ve ordered DigiFab but pharmacy is taking too long? ⇒ atropine!

Want more? 

Infective endocarditis – 8/6/18

Thanks to Janhavi for presenting the case of a middle-aged man with no significant PMH presenting with acute onset of malaise, myalgias, and a “stubbed toe,” septic with petechiae on palms and soles, found to have mitral valve endocarditis.


Clinical Pearls:

  • Endocarditis is more common in men (2:1)
  • ~50% of cases of endocarditis occur in people with no known underlying valve disease
  • 80% of cases are caused by staph and strep species
  • TEE is the gold standard for diagnosis and recommended when clinical suspicion for endocarditis is high.  TTE is more helpful to rule out disease when clinical suspicion is low.
  • Indications for early surgery based on this NEJM article include:
    • Heart failure
    • Uncontrolled infection
    • Prevention of embolic events

Duke’s criteria:

Major criteria:

  • Blood culture positive:
    • Typical organism in two separate blood cultures
    • Persistently positive blood cultures
    • Single positive culture for Coxiella
  • E/o endocardial involvement
    • Echo positive for vegetation
    • New valve regurgitation

Minor criteria:

  • Predisposition to IE (i.e. IVDU, prosthetic valve, congenital cyanotic heart disease)
  • Fever >38
  • Vascular phenomena ⇒ arterial emboli, pulmonary infarcts, mycotic aneurysms, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions
  • Immunologic phenomena ⇒ GN, Osler’s nodes, Roth’s spots, RF
  • Microbiologic evidence: positive blood culture not meeting major criteria

Probability of endocarditis:

Definite IE:

  • 2 major, 1 major + 3 minor, 5 minor

Possible IE:

  • 1 major + 1 minor, or 3 minor

Rejected IE:

  • Firmly established alternative diagnosis
  • Resolution of symptoms < 4 days with antibiotics
  • Does not meet definite/possible criteria

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

Complications:

  • Most common cause of death: heart failure
  • Heart block
  • Emboli
    • More likely with s. aureus or S. bovis, veg > 1 cm, or increased veg mobility on echo
    • Antiplatelet therapy initiation is not recommended because of increased risk of hemorrhagic conversion of septic emboli

Want more?

  • Check out this blog post and this great review article in the NEJM.

New A fib, severe MR, and papillary muscle rupture… 7/17/18

Thank you Naina for presenting the case of an elderly man with 20 packyear smoking history presenting with acute onset of dyspnea and scant hemoptysis, found to have new onset A fib and L heart failure secondary to severe mitral regurgitation resulting from papillary muscle rupture!


Clinical Pearls

  • In patients with severe mitral regurgitation (MR) and a normal L atrium size, think about acute causes of MR.  TEE is often indicated to better visualize the valve structure and determine need for operative intervention.
  • MR can be caused by papillary muscle rupture, especially 3-7 days post MI.  Other etiologies of rupture include endocarditis and myxomatous valve degeneration.
  • Patients with rupture present with acute onset hypotension, pulmonary edema, and a hyperactive precordium. A systolic murmur is not always present!
  • Treatment:
    • Aggressive afterload reduction AND
    • Surgery (high mortality rate 20-25%)

Atrial Fribrillation

Categories:

  • Paroxysmal (terminates within 7 days)
  • Persistent (>7 days)
  • Long-standing persistent (>1 year)

Differential for new onset A fib: (PIRATES!)

  • Pulmonary (OSA, PE, COPD, PNA)
  • Ischemia/infarction/CAD*
  • Rheumatic heart disease/mitral regurgitation
  • Alcohol/anemia (high output failure
  • Thyrotoxicosis/toxins (stimulants)
  • Electrolytes/endocarditis
  • Sepsis/sick sinus syndrome
  • Other: HTN*, congenital heart disease, previous cardiac surgery, viral infections

* Most common causes in the US.

Treatment:

  • Rate control (preferred method based on AFFIRM and RACE trials)
    • Beta blockers
    • Calcium channel blockers ⇒ contraindicated in decompensated heart failure
    • Digoxin ⇒ avoid use in renal failure, hypokalemia, hypomagnesemia, or hypercalcemia
    • Amiodarone
  • Rhythm control
    • Methods:
      • Chemical (~30% success rate)
        • Class III (amiodarone, sotalol, ibutilide)
      • Electrical (synchronized to QRS, ~80% success rate)
    • Preferred modality in
      • Hemodynamically unstable
      • Young patient (age <65) or good functional status
      • Early in natural history of disease
      • Failure of rate control agents
      • Heart failure

Capture

Complications post MI:

Picture1

Figure from article by Reed et al. Lancet. 2017.

Papillary muscle rupture:

  • Posteromedial muscle is 6-12x more likely because blood supply is through PDA only. Anterolateral muscle receives dual supply from LAD and LCx.
  • Clinical presentation
    • Acute onset hypotension, pulmonary edema
    • Hyperactive precordium
    • Mid, late, or holosystolic murmur with widespread radiation (though many have no murmur!)
    • Diagnosis requires TTE/TEE
    • Treatment:
      • Aggressive afterload reduction
      • Urgent/emergent surgical intervention (20-25% mortality)