VA ICU report 7.21.17: Hypertriglyceridemia and pancreatitis

Case summary: Thanks to the ICU team for presenting a great case of a 61M HIV on ARVs (CD4 >400), abdominal gunshot wound c/b SBO, HCV without cirrhosis, HFpEF, PSA including EtOH abuse who presented with acute onset abdominal pain, nausea/vomiting, who was found to have severe acute pancreatitis and hypertriglyceridemia to the 1000s.

Top pearls:

1. Why are the labs taking forever to come back!? Recall that there are both endogenous (hemolysis, lipids, proteins, antibodies, bilirubin) and exogenous substances (drugs, poisons, herbals, IV fluids, IVIg, digibind, and collection tube/sample additives/clotting in the tube) that can interfere with lab tests.
2. Hypertriglyceridemia can be congenital (due to familiar hyperlipiemias) or acquired (usually due to obesity, EtOH, pregnancy or DMT2). Levels >1000 are associated with pancreatitis.
3. There is debate whether hypertriglyceridemia is a cause or a consequence of pancreatitis. Nevertheless, the key features of management are: hydration!, pheresis, IV insulin +/- heparin.

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Why are the labs taking forever to come back!? Aka Causes of lab interference

• Endogenous interference- originates from substances found naturally in the patient sample.
  • hemolysis (haemoglobin and other substances)
  • bilirubin
  • lipids
  • proteins
  • antibodies (autoantibodies, heterophile antibodies)
  • excessive analyte concentration (e.g. the lab doesn’t dilute the sample enough)
  • cross-reacting substances (e.g. bicarb can react with some of the lab machinery)
• Exogenous interference– results from substances not naturally found in the patient’s specimen
  • drugs (parent drug, metabolites, and additives)
  • poisons
  • herbal products
  • IV fluids
  • substances used as therapy (e.g. monoclonal antibodies, IVIg, digi-bind)
  • collection tube components, test sample additives, processes affecting the sample (e.g. transport, storage, centrifugation), clots (post-refrigeration in heparin plasma, slow-clotting serum)

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Hypertriglyeridemia: a brief review

• Defined as:
  • Normal – <150 mg/dL (1.7 mmol/L)
  • Borderline high – 150 to 199 mg/dL (1.7 to 2.2 mmol/L)
  • High – 200 to 499 mg/dL (2.3 to 5.6 mmol/L)
  • Very high – ≥500 mg/dL (≥5.6 mmol/L)
  • important to test fasting levels
• Causes:
  • congenital:

• • acquired: obesity, diabetes, alcohol, nephrotic syndrome, hypothyroidism, pregnancy, medications (estrogen, tamoxifen, beta blockers except carvedilol, immunosuppressive medications (steroids, cyclosporine), ARVs, retinoids
• Findings:
  • limited data linking hypertriglyceridemia to cardiovascular outcomes
  • patients with congenital etiologies can have xanthomas and xanthelasmas
  • greatest risk is of pancreatitis at levels >1000
  • some clinicians will treat outpatients with fasting levels >886 because this is associated with postprandial levels that can cause pancreatitis, but there are limited data to guide this decision
    • Non-pharmacological therapy includes lifestyle modification (weight loss, exercise, and restricting fat and simple sugars)
    • Fibrates are first-line therapy, niacin and omega 3 fatty acids are second line. These drugs can be used alone or in combination with statins.
• Hypertriglyceridemia and pancreatitis:
  • The incidence of AP in patients with TG > 1,000 is 5%, which increases to 10-20% with levels > 2,000
  • Elevated TG are associated with more severe end-organ complications of pancreatitis and increased mortality
  • Treatment:
    • Hydration!
    • Pheresis
    • IV insulin (increases the activity of lipoprotein lipase, which breaks down TG-rich chylomicrons)
    • +/- heparin (contraversial)

Chaudhary A, Iqbal U, Anwar H, Siddiqui HU, Alvi M. Acute Pancreatitis Secondary to Severe Hypertriglyceridemia: Management of Severe Hypertriglyceridemia in Emergency Setting. Gastroenterology Research. 2017;10(3):190-192.

Berglung L, et al. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012 Sep;97(9):2969-89.

Brunzell JD. Hypertriglyceridemia. N Engl J Med 2007;357:1009-1017

Moffitt Pearls 7/21/17 – renal report – salicylate toxicity

Thank you to Jocelyn for presenting a case of a middle aged male with a history of depression admitted for altered mental status in the setting of possible ingestion found to have a profound metabolic acidosis and salicylate toxicity.

Key Pearls:

1. From the Ditty: a brief differential diagnosis for microcytic anemia includes iron deficiency anemia, thalassemia, and sideroblastic anemia. You can use the Mentzer Index (MCV/RBC count) to help differentiate between the two most common causes, IDA and thalassemia. Because b-thal results in MANY small RBCs & IDA decreases the size and number of RBCs relatively equally.
   1. MCV/RBC count < 13 = beta thalassemia
   2. MCV/RBC count > 13 = IDA
2. We reviewed the approach to acid-base abnormalities – see below for the updated mnemonic for anion gap acidosis:
3. We also discussed the management of salicylate overdose. Key learning point – an indication for emergent HD in a patient with salicylate toxicity is any sign of AMS as this could represent cerebral edema.

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MUDPILES vs. GOLDMARK

In this 2008 article from the Lancet, the mnemonic MUDPILES for anion-gap metabolic acidosis got a makeover.  GOLDMARK is the new jam – it’s updated to cover topics more germane to the 21^st century.  See the differences below:

MUDPILES:

Methylene

Uremia

DKA

Paraldehyde

INH

Lactic acidosis

Ethylene glycol

Salicylate

 

GOLDMARK:

Glycols (ethylene and propylene)

Oxaloprolene (aka pyroglutamic acid) – seen in chronic APAP use

L-lactate

D-lactate

Methanol

Aspirin

Renal failure

Ketoacidosis

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Indications for Dialysis – another mnemonic!

A-           Acid base disturbance

E-            Electrolyte abnormalities (usually hyper K)

I-             Ingestion – depending on what, may be able to dialyze off

O-           Overload – severe volume overload

U-           Uremia

 

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Management of Salicylate Toxicity

• Fluids
• Bicarbonate – Alkalinizing the urine “traps” the ion in the tubule, enabling you to enhance excretion of salicylates
• Dialysis – HD is preferred – Remember that the rate of filtration is markedly increased in hemodialysis compared to CRRT
• Potassium repletion
• Maintenance of normoglycemia à Dr. Liu may get back to us re: mechanism for cerebral hypoglycemia with normal serum glucose in patients with salicylate toxicity

Here’s an article describing some of the risk factors associated with adverse outcomes in patients with salicylate toxicity: https://www.ncbi.nlm.nih.gov/pubmed/28064509.  The authors highlight the significant public health impact of salicylate toxicity with more than 20,000 US cases annually!  The study found that older age, tachypnea, and elevated serum lactates all predicted severe outcome. Interestingly, the serum salicylate concentration alone, did not!

Evernote: https://www.evernote.com/shard/s462/sh/2d3baded-e438-47b8-89db-b5cefd7f0671/47a327ebb1b968467c017cb8e04380e8

Ambulatory Report 7.19.17 – Secondary Hypertension and a Hemorrhagic Stroke in a young patient

Thanks John for presenting this great case!  We discussed the case of a 31 yo male with a pmhx of hypertension and hemorrhagic stroke who was presenting for primary care now undergoing a work-up for secondary hypertension.

High-yield pearls

• The most common causes of a hemorrhagic stroke in a young person are vascular malformations and hypertension
• Consider an age-based approach to secondary hypertension work-up
• LT pearl: If you are concerned about pheo, check orthostatics.  Untreated pheo patients will have positive orthostatics because they are chronically vasoconstricted and cannot adjust adequately to postural changes
• Recognize lots of medications and dietary sodium will affect your renin/aldosterone ratio.  If your patient is on an ACEi or ARB, you do not need to stop the medication in your first pass you evaluation but know that a normal result does not exclude primary hyperaldosteronism.

 

Hemorrhagic CVA in the young:

• Most frequent RISK FACTOR: tobacco use, HYPOcholesterolemia, HTN, alcohol use
• Most frequent ETIOLOGY: vascular malformation and HTN
• The final neurologic outcome was favorable in 60%
• Causes overall:
  • Aneurysm/vascular malformation
  • Trauma
  • Severe HTN
  • Tumor
  • Septic/mycotic aneurysm
  • Bleeding d/o
  • CNS infection (eg HSV encephalitis)
  • Vasculitis
  • Drugs (cocaine, meth)
  • Secondary transformation from central venous thrombosis

 

Secondary Hypertension

Who should I work-up a patient for secondary hypertension?

• 5-10% of all adults with HTN will have a secondary cause of HTN
• Consider evaluation in patients with:
  • Resistant HTN: Defined as inadequately controlled BP when on three anti-hypertensives one of which must be a diuretic
  • Early or late onset HTN
  • Severe or accelerated course of HTN
  • Antihypertensive drug intolerance
  • Suggestive features on history or physical

When thinking about secondary hypertension consider an age-based approach to focus your differential. (Thanks for sharing Abbi and Jackie!)

Secondary Hypertension Differential and Suggestive Clues on history, physical, and basic labs

• Renal Vascular Disease: Renal artery stenosis or fibromuscular dysplasia
  • Look for creatinine increases by >30% after starting ACEi or ARB, asymmetric size of kidneys, recurrent flash pulm edema, bruit on exam (not very sensitive)
• Primary renal disease
  • Will see abnormal creatinine and UA
• Endocrine causes
  • Pheochromocytoma
    • Triad; headache, palpitations, sweating,
    • LT pearl: check orthostatics!  Untreated pheo patients are chronically vasoconstricted so cannot adjust blood pressure with positional changes
  • Hyperaldosteronism
    • Unexplained hypokalemia, urine potassium wasting
    • One half of patients will have normal serum potassium
    • Typically mild HTN presenting in middle age
  • Cushing’s
    • Cushinoid features on physical exam
    • History of steroid use
  • Hypothyroid
  • Primary hyperparathyroidism
    • Hypercalcemia
• Coarctation of the Aorta
  • Diminished or delayed femoral pulses
  • Asymetric BPs: BP in right arm > left arm or HTN in arms and low BP in legs
• OSA
  • Obesity, daytime somnolence, snoring
• Drugs
  • Cocaine, amphetamines
• Medications
  • NSAIDs, OCPs, antidepressants, calcineurin inhibitors, decongestants, steroids,

 

Things that affect renin/aldo ratio: 

• Meds
  • Mineralocorticoid receptor antagonist
  • Diuretics
  • ACEi or ARB
    • You do not need to take your patient off their ACEi or ARB in your first pass work-up because many with primary hyperaldosteronism will have an abnormal result.  However, if the result is normal you cannot exclude primary hyperaldosteronism and may need to recheck it off the medication.
  • Beta blockers
  • Clonidine
  • NSAIDs
  • SSRIs
  • OCPs
• Hypokalemia/Hyperkalemia
• Na restricted diet/Na loaded diet
• Pregnancy
• Renovascular HTN
• Malignant HTN
• Liddle syndrome: Liddle syndrome is a genetic disorder characterized by early, and frequently severe HTN with low plasma renin activity, metabolic alkalosis, hypokalemia, and normal to low aldosterone.

At the VA, endocrine clinic helps with obtaining this test and providing your patient with the appropriate instructions to avoid spurious results.

 

References:

Intracranial hemorrhage in Young People: http://stroke.ahajournals.org/content/30/3/537

Age Based Approach to Secondary Hypertension from the AAFP: http://www.aafp.org/afp/2010/1215/p1471.html

 

Moffitt Pearls 7.19.17 – Morning Report – H&N infxn and more!

Image & Mini-case Potpourri!!!

Thank you Mike Thomashow for presenting a mini-case of an older patient with MM on chemotherapy with Ludwig’s Angina.

Thank you, HH for sharing the story of a young, otherwise healthy man admitted to the medical service who developed a sore throat and then several days later developed high fevers and rigors. Blood cultures returned positive fusiform bacteremia!

And finally, thank you to Brad Monash for telling us about space occupying lesions of infectious, malignant and inflammatory etiologies. Brad shared with us an image of a patient with Rosei Dorfman disease!

Key Pearls

• Ludwig angina: infection begins in the floor of the mouth, is aggressive with rapid spreading cellulitis involving the submandibular space
• Lemierre Syndrome is jugular vein suppurative thrombophlebitis: infection involvement of the carotid sheath vessels with bacteremia.
• Airway stridor is the end game of airway compromise and requires emergent evaluation by ENT. Patient with airway concern need admission to ICU.
• Space occupying lesions – 1) infections 2) malignant 3) inflammatory and NEW 4) infiltrative – including histiocytosis. Check out this great Clinical Care Conundrum – you may recognize several of the authors 🙂

 

 

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Ludwig angina

• Has been traditionally loosely applied to a heterogeneous array of infections involving the sublingual and submylohyoid (submaxillary) spaces.
• True definition: infection begins in the floor of the mouth. An aggressive, rapidly spreading “woody” or brawny cellulitis involving the submandibular space.
• Present without lymphatic involvement and generally without abscess formation.
• Both the submylohyoid and sublingual spaces are involved.
• The infection is often bilateral.

Microbiology of Ludwig Angina

• Most common organism isolated from deep neck space infections is Streptococcus viridans. Most abscesses originating from the teeth also harbor oral anaerobes, including Peptostreptococcus species, Fusobacterium nucleatum, pigmented Bacteroides (eg, Prevotella melaninogenica [formerly Bacteroides melaninogenicus] and Porphyromonas spp), and Actinomyces species.
• In immunocompromised patients, gram-negative aerobes may also be present.

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Lemierre Syndrome

• Jugular vein suppurative thrombophlebitis: infection involvement of the carotid sheath vessels with bacteremia.
• Often preceded by pharyngitis, usually in association with tonsil or peritonsillar involvement. Other antecedent conditions include primary dental infection or infectious mononucleosis.
• Infection progresses from the oropharynx to the parapharyngeal or lateral pharyngeal space. The anterior part of this space consists of the anterior neck muscles; the posterior section contains the carotid sheath that encloses the internal jugular vein, internal carotid artery, the vagal nerve, and lymph nodes

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Head and Neck Infection – Overview of Microbiology

• Epiglottitis à H. Flu
• Peritonsil abscess à Group A Strep
• Ludwigs angina (above)à tongue displacement (mixed peri-dontal including bacteroidies, Fusibacterium)
• Actinomyces
• Nocardia

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Acute bacterial sialadenitis

• Acute bacterial sialadenitis (suppurative sialadenitis) in the absence of sialolithiasis is a condition that typically affects older adults, malnourished, or postoperative patients. The parotid gland is most commonly involved. It is characterized by sudden onset of a very firm and tender swelling over the involved gland. Fever and chills are usually present, generally with fairly marked systemic toxicity. Purulent drainage can often be expressed from the effected duct orifice.
• Staphylococcus aureus is the most frequent microbiologic isolate, but Streptococcus pneumonia, Streptococcus viridans, Haemophilus influenzae, and Bacteroides species have also been isolated. Broad-spectrum therapy should be initiated. Prompt surgical drainage and decompression is required if an abscess develops.

Quick Guide based on patient characteristics:

• ICU patient who is critical ill –> think Gram negative bacteria
• Outpatient setting –> Staph aureus (Sjogrens is a risk factor)
• More often in the pediatric or global population –> Mumps

 

Evernote: https://www.evernote.com/shard/s462/sh/4fa562e7-815d-41c9-a7a0-0b6cc002850b/6e5606181240beedc3afa93611cc6d9a

ZSFG AM Report Pearls 7/18/2017: Syncope, Bradycardia, and Controversies in Risk Stratification!

 

Thank you to Mike Incze for presenting a case of symptomatic bradycardia with syncope from complete heart block that was initially thought to be due to hyperkalemia but has now persisted despite correction of electrolyte abnormalities.

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Top Pearls:

• SF Syncope Rule is a controversial tool used to risk stratify patients presenting to ED with unexplained syncope using Hx of CHF, Hct <30%, Abnml EKG, SOB, SBP <90
• Bradycardia DDx is broad but should include medications, electrolytes, ischemia, infiltrative and infectious etiologies.
• A complaint of bradycardia should be evaluated initially by determining if stable or unstable (CP, SOB, AMS, low BP, evidence of end organ damage)

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SF Syncope Rule:

• For patients with unexplained syncope
• Potentially can be used to risk stratify and identify patients who need admission
• NOTE: Controversial in the literature (with an impressive back and forth that is played out in Annals of Emergency Medicine)
  • Hx of CHF
  • Hct <30%
  • Abnormal EKG (Any non-sinus rhythm, ANY new change on EKG)
  • Shortness of Breath
  • Systolic BP <90mmHg at triage

If all absent, may be low risk for having a significant event in the next 30 days and may not need inpatient admission.

Note: Remember, at UCSF, ED providers decide about the need for admission and especially given the controversy about this “rule,” we would not recommend using this to frame your thoughts about the appropriateness of admissions.

Original Study:

• Excluded pts w/ trauma, EtOH, or drug-associated loss of consciousness
• Outcome measurement = serious outcome within 30 days of their ED visit (death, MI, arrhythmia, PE, stroke, subarachnoid hemorrhage, enami, procedural intervention, hospitalization, return ED visity)
• The rule was 98% sensitive (95% confidence interval [CI] 89% to 100%) and 56% specific (95% CI 52% to 60%) to predict these events. In this cohort, the San Francisco Syncope Rule classified 52% of the patients as high risk, potentially decreasing overall admissions by 7%. If the rule had been applied only to the 453 patients admitted, it might have decreased admissions by 24%.

External Validation Study:

• Sixteen of 61 (26%; 95% confidence interval [CI] 16% to 39%) patients with a serious outcome were not identified as high risk by the rule. Rule performance to predict serious outcomes was sensitivity 74% (95% CI 61% to 84%), specificity 57% (95% CI 53% to 61%); negative likelihood ratio 0.5 (95% CI 0.3 to 0.7) and positive likelihood ratio 1.7 (95% CI 1.4 to 2.0)

Response to External Validation Study:

• Authors argue that the institution doing validation had small number of ED visits for syncope and a high number of admissions  for syncope
• Also argue that they incorrectly applied the EKG part of the SF Syncope Rule in the validation study

 

Bradycardia:

Etiologies:

• Medications: BB, CCB, Amio, Lithium, Digoxin, Clonidine, acetylcholinesterase inhibitors
• Ischemia: Acute MI (15-25% of patients with acute MI)
• Increased Vagal Tone: athletes, sleep, IMI
• Metabolic: hypoxia, sepsis, myxedema, hypothermia, hypoglycemia, hyperkalemia
• OSA
• Increased intracranial cranial pressure (Cushing)
• Infectious: Chagas, Lyme disease, legionella, Q fever, babesia, malaria, RMSF, lepto, yellow fever, dengue, trichinosis
• Infiltrative/Myocarditis: sarcoid, amyloid, hemochromatosis
• Treatment: none if asymptomatic, atropine, B1 agonists, or temp pacing

Sick Sinus Syndrome:

• Features can include unprovoked sinus bradycardia, SA arrest, paroxysms of SB and atrial tachyarrhythmias, chronotropic incompetence w. ETT
• Treatment: meds alone usually fail (Adequate tachy -> unacceptable brady) usually need combination of meds (BB, CCB, dig) for tachy & PPM for brady.

 

Link to JAMA Rational Clinical Exam Podcast Series on ACS: Here

 

Sources:

• Quinn J, McDermott D, Stiell I, Kohn M, & Wells G. (2006). Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 47(5): 448-454.
• Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ. (2008). Failure to validate the San Francisco Syncope Rule in an independent emergency population. Ann Emerg Med. 53(2): 151-159.
• Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. (2009). Yield of diagnostic test in evaluating syncopal episodes in older patients. Arch Intern Med. 169(14): 1299-1305.

 

Also, a reminder about EKG Change in Hyperkalemia, check out prior Chief’s Blog Post:  https://ucsfmed.wordpress.com/2017/06/27/zsfg-am-report-pearls-6272017-non-stemi-st-segment-elevations-and-ekg-changes-in-hyperkalemia/

 

Evernote links

• SF Syncope Rule: https://www.evernote.com/shard/s509/sh/8343bc1e-99f2-4b8f-bff7-8c5aab93117f/c2b36c31e86d0f45afce14a8ead30162
• Syncope Work-Up: https://www.evernote.com/shard/s509/sh/83aa4cba-b22e-454d-8b0c-5218053e5d75/553fdf4812a5801a15a6e7c8777e748e
• Bradycardia and More: https://www.evernote.com/shard/s509/sh/8576116d-598c-4419-b151-d29adcaa9630/e566d44f2f605c07041fc256d573d71d
• EKG Changes in Hyperkalemia: https://www.evernote.com/shard/s509/sh/4d049bad-bb46-4a46-94b2-f4927c8a2d27/65eef1fe332b1cd1a94b83e6758b653b

 

VA Morning report 7.18.17: Acute liver injury and aortic dissection deep cuts

Case summary: Huge thanks to Jin Ge for presenting a fascinoma: 33M with PMH cocaine abuse, who was admitted to the liver transplant unit with acute liver injury and was found to have an aortic dissection extending from the aortic root to the iliac arteries leading to multi organ ischemic injury.

 

Top pearls:

1. Northern California had an outbreak of amanita mushroom poisoning this year, which starts with GI symptoms 9 hours after ingestion and can progress to fulminant hepatic failure. There is an ongoing RCT testing a new antidote called silibinin.
2. Many of us are familiar with the triumvirate of acute liver failure: toxin, viral hepatitis, ischemia; consider using an anatomic approach the includes more rare causes.
3. Aortic dissection is due to weakening of the vessel wall. This is most commonly caused by HTN but can result from any aortopathy, either acquired (infection, inflammation) or genetic (collagen/vascular disease, bicuspid valve, familial TAAD).

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Amanita “deathcap” mushroom poisoning

• Paul Blanc (international expert in toxicology/occupational health) and Jody Garber (international expert in the VA ED, beer, and Northern California in general) gave us some great deep cuts on amanita mushroom poisoning.
• Amanita phalloides is responsible for most mushroom-related deaths worldwide.
• The toxin is activated in the GI tract and is “heat stable,” meaning that cooking doesn’t dilute their potency.
• They taste good!
• They’re found under trees after heavy rainfall.
• Northern California experienced an outbreak this year because of our wet weather; the CDC released a report on 14 cases in 2016-2017 (as compared to the typical 1-2 cases/year).
  • all patients developed severe GI symptoms (abdominal pain, diarrhea) 9 hours after eating the mushrooms
  • Eleven patients recovered, although three required liver transplants
  • One of those patients, a child, developed cerebral edema despite liver transplant and suffered permanent neurologic sequelae
• Ask a mycologist (mushroom expert) to examine your mushrooms before eating!
• There’s an ongoing clinical trial testing an antidote that is licensed in Europe called silibinin (the cases described above received it empirically)

 

http://www.latimes.com/local/lanow/la-me-ln-mushroom-sickness-20170602-htmlstory.html

https://www.cdc.gov/mmwr/volumes/66/wr/mm6621a1.htm?s_cid=mm6621a1_w#T1_down

https://clinicaltrials.gov/ct2/show/NCT00915681

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Anatomic approach to acute liver injury

• Courtesy of Rabih Geha:

 

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Causes of aortopathy

• This patient had dissection of the almost the entire length of his aorta, and the presumed etiology is cocaine/HTN.
• It’s important to remember, particularly in a young patient, the spectrum of diseases that can cause aortopathy.
• Dissection develops due to a weak aortic wall leading to a tear of the intima.
  • Acquired
    • HTN- vessel wall degeneration over time; by far the most common cause
    • Infection- septic embolism, bacterial inoculation (e.g. syphilis!) or contiguous infection (e.g. extension of perivalvular abscess) of vessel wall
    • Inflammation- giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, ankylosing spondylitis, Wegener’s granulomatosis, reactive arthritis, and Behcet syndrome cause inflammation of vessel wall
  • Genetic–
    • Abnormal collagen/vasculature- Marfan syndrome, vascular Ehlers Danlos syndrome, Loeys-Dietz syndrome, and Turner syndrome
    • Familial thoracic aortic aneurysm and dissection (TAAD)-patients with a family history of aneurysmal disease who don’t have a connective tissue disorder
    • Bicuspid aortic valve- independent association with aortopathy; most commonly recognized congenital abnormality in adulthood, and 25 percent require intervention on aortic valve, aorta, or both
• Note that these risk factors also increase the risk of aortic aneurysm, which can lead to dissection as well as rupture.

Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA. Acute Aortic Dissection and Intramural HematomaA Systematic Review. JAMA. 2016;316(7):754-763.

Thrumurthy Sri G, Karthikesalingam Alan, Patterson Benjamin O, Holt Peter J E, ThompsonMatt M. The diagnosis and management of aortic dissection  BMJ  2012;  344 :d8290 

Moffitt Pearls 7.18.17 – Cardiology Report – WCT

 

Thank you to Armond for presenting a case of an elderly (but very fit and with great taste in burgers) male with chest pain, palpitations, and light-headedness with a wide complex tachycardia!

Key Pearls

1. From the ditty, aplastic anemia is a disorder of the pluripotent hematopoietic stem cells resulting in decreases in cell lines. If severe and in a young patient, the treatment of choice is an allogeneic stem cell transplant.
2. The differential for a long R-P tachycardia includes both sinus tachycardia and the very rare condition of sinus node re-entrant tachycardia! Arvind shared with us a very cool ECG from a patient with this condition!
3. DDx for a regular wide complex tachycardia is short!! See below…

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Long and Short RP Tachycardia – to distinguish between LONG R-P and SHORT R-P tachycardia, assess the RP duration compared to the PR duration.  If the RP is longer than the PR, we think of that as a long-RP tachycardia. Conversely, if the RP is shorter than the PR, then we classify that as a short-RP tachycardia.

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There’s a relatively short differential diagnosis for Wide Complex Tachycardia. The most important entity to rule out is ventricular tachycardia.

Step 1: Hemodynamic Instability? If present à manage as if Ventricular Tachycardia and perform synchronized cardioversion. If HD stable, you have time to think (and to breath!) – go to Step 2.

Step 2: Turn to your DDx for WCT

• VT
• SVT with aberrancy
• antidromic AVRT
• Pacemaker mediated tachycardia
• toxin-mediated widening of the QRS à TCA

*** Your job is RULE OUT ventricular tachycardia ***

Remember Brugada criteria – a set of rules that can be employed to identify VT. These are not rules you should necessarily memorize, but at least be somewhat familiar with. Some of the first steps, such as concordance, A-V dissociation, capture and fusion beats are reasonable to keep in your memory bank. Use an algorithm (like this one from UpToDate) to remind you of the finer details.

Short-cut: look at aVR first à if you have a regular, wide complex tachycardia that is POSITIVE in aVR, there’s a good chance this is VT. This is NOT 100% sensitive, but it’s relatively specific. Check out this paper from Heart Rhythm exploring the use of aVR alone compared to a Brugada algorithm. In this study of 483 patients with wide complex tachycardias, the aVR algorithm actually outperformed the Brugada criteria! This is probably directly related to its simplicity of use (and therefore being more difficult to mess up) compared to Brugada. This is just one of the reasons why aVR happens to be my favorite lead – check out this article titled “aVR – the forgotten lead” – about the often under-recognized value of aVR.

Evernote: https://www.evernote.com/shard/s462/sh/cd1740b7-4b6b-4073-93c3-cdc941f78160/bc8b91ef0bbc26a74d3c05daca48f173