11/1 VA Report: SVT and Valsalva – A REVERT Review

At today’s report Dr. Dixit took us through the complicated world of SVT’s and how to better incorporate our understanding of the electrophysiology into the assessment of each patient.

The VA team discussed initial maneuvers to break an SVT including carotid massage and Valsalva which lead us to the REVERT trial summarized below (3).

Major Points:

Valsalva maneuver is a safe first line treatment in ED’s for SVT with roughly the same efficacy between Valsalva and carotid massage (2). Cardioversion is rarely successful in clinical practice (5-20%) (1-2) and patients who remain in an SVT are usually treated with adenosine which is associated with substantial side effects. The REVERT researchers proposed to compare a modified Valsalva (15 second Valsalva + passive leg raise) to a standard Valsalva with a primary outcome of return to sinus rhythm at 1 minute.

Design:

  • Randomized controlled, multicenter parallel group trial
  • N = 433
    • Modified Valsalva (n=216)
    • Standard Valsalva (n=217)
  • Analysis: Intention-to-treat
  • Primary Outcome: Return to sinus rhythm at 1 minute
  • Secondary Outcomes: Use of adenosine, use of any emergency treatment for SVT (including adenosine), the need and reason for admission to the hospital, length of time participants spent in the ED, adverse events.

Population:

  • Inclusion Criteria: >18 yo, presented to ED with SVT (regular, narrow complex tachycardia with QRS duration <0.12s on ECG)
  • Exclusion Criteria: unstable SBP <90mmHg, suspected aflutter requiring adenosine trial, contraindication to Valsalva maneuver (AS, recent MI, glaucoma retinopathy), inability to lay flat or raise legs.

Intervention:

  • Standard Valsalva: pressure of 40 mmHg sustained for 15 seconds by forced expiration measured by manometer while SITTING at 45 degrees + standardized verbal instructions
  • Modified Valsalva: pressure of 40 mmHg sustained for 15 seconds by forced expiration measured by manometer while SITTING at 45 degrees + standardized verbal instructions + THEN laying flat and had their legs lifted by staff member to 45 degrees for 15 seconds

Outcomes:

Screen Shot Valsalva

  • Primary Outcome: 43% of participants in modified Valsalva maneuver group vs. 17% in standard Valsalva group achieved sinus rhythm at 1 minute. The absolute difference was 26.2% therefore 3 patients needed the modified Valsalva maneuver to avoid one case of further treatment.

Bottom Line:

This simple cost-free postural change to a standard Valsalva returns more people to sinus rhythm within 1 minute AND results in a substantial reduction in the number of patients needing other emergency treatments including adenosine.

** To do a Valsalva of about 40 mmHg you can use a 10mL syringe blown to just move the plunger **

References:

  1. Smith G et al. Use of valsalva manoeuvre in the prehospital setting: a review of the literature. Emerg Med J 2009; 26:8-10.
  2. Lim SH et al. Comparison of treatment of supraventricular tachycardia by valsalva manoeuvre and carotid sinus massage. Ann Emerg Med 1998; 31: 30-25.
  3. Appelboam A et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet 2015; 386: 1747-53.

 

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10/30 VA Report: Takotsubo’s vs. ACS

Today we discussed a 78 yo with a history of CAD s/p stenting x4 who presented with dyspnea/SOB in the setting of a recent hospitalization for reported Takotsubo’s Cardiomyopathy at OSH.

From a distance his Takotsubo presentation seemed plausible — he developed sudden onset CP/dyspnea in the setting of his wife’s death on the day of OSH admission. On the deep data dive things got complicated — his LHC at the OSH demonstrated a mid-LAD “thrombus and significant restenosis” and his ventriculogram demonstrated “apical ballooning consistent with stress cardiomyopathy.” They popped in a BMS. Now he’s back in the hospital with worsening SOB/dyspnea and an LVEF still 30% 2 months out from his initial presentation. So what actually qualifies as Takotsubo CM and how can we differentiate it from ACS?

Mayo Clinic diagnostic criteria for Takotsubo Cardiomyopathy:

LV wall motion beyond a single epicardial coronary artery perfusion territory, the absence of obstructive coronary artery disease or angiographic evidence of plaque rupture, the presence of new EKG abnormalities or elevation in troponins in the absence of pheo or myocarditis. (1)

First our team reviewed the data collected and published from the International Takotsubo Registry. The collected data demonstrated that most patients were >50 and about 90% female (1). Even though we THINK about emotional triggers — like in our patient — they actually only make up the trigger for about 1/3 of all Takotsubo patients with physical triggers the most common (36%) and 28.5% without a trigger that is identified! Most patients present with dyspnea (46.9%) and chest pain (75.9%) (1).

Troponin levels were elevated in MOST patients with Takotsubo’s and the mean was about the same as as those with ACS when they were admitted. However, during the course of the admission, Takotsubo’s patient trops only increased 1.8x whereas ACS patients trops increased by a factor of 6! Additionally while ST segment elevation rates were similar in Takotsubo and ACS EKGs, ST segment depression occurred in only 8.3% of Takotsubo patients as compared to 31% of ACS patients (1).

Most patients in the registry had apical ballooning, but as you can see below there are a few varieties of Takotsubo CM and they can look VERY different.

Screen Shot TTE

On reviewing the data for out patient, with a LHC demonstrating thrombus s/p stenting, a troponin peaking at 120, and a persistently reduced EF at 30% — he was recategorized as ICM. So why did it seem like this was a triggered event? Are MI’s triggered by the death of a spouse?

Two recent meta-analyses estimate an increase in the first 6 months after the death of a spouse — some up to a 41% increase (2). With regard to cardiac events, a recent cohort study in JAMA studied approximately 30,000 individuals aged 60-89 who experienced partner death with matched controls who did not experience a death.

Screen Shot Bereaved

Within 30 days of the partner’s death 0.16% of the bereaved group experienced MI or CVA as compared to 0.08% in the control group [IRR 2.20 95% CI 1.52-3.15] (3). This increased risk seemed to attenuate after 30 days (3). Of note, these MI’s did not have to be verified by LHC and so likely a subset of these patients have been lumped in to MI but were really Takotsubo’s CM — this in no way should take away from the fact that acute grief is associated with a short-term increased risk of CV events and may explain why our patient had what seemed to be a “triggered” MI.

References:

  1. Templin C et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med 2015;373:929-38. PMID 26332547
  2. Moon JR et al. Widowhood and mortality: a meta-analysis. PLos One. 2011;6(8):e23465. doi: 10.1371
  3. Carey IM et al. Increased Risk of Acute Cardiovascular Events After Partner Bereavement: A Matched Cohort Study. JAMA Intern Med. 2014;174(4):598-605. PMID: 24566983

 

 

10/23 VA Report: Pleural Effusions with Lymphocytosis

Today’s report focused in on a patient with a history of adenocarcinoma of the lung s/p Chemo/XRT/surgical resection and who lived in South East Asia for 10 years who presented with hemoptysis, chronic cough and a new pleural effusion.

We re-reviewed Light’s Criteria — acknowledging that we sacrifice specificity for sensitivity by pooling the three criteria — with a reported ~97% sensitivity and ~80% specificity.

Our patient had an effusion demonstrating >95% lymphs on diff — creating a nice tidy differential to work with — TB, malignancy, sarcoidosis, chronic rheumatoid pleurisy, yellow nail syndrome or chylothorax. We followed his work up narrowing the differential down to TB vs. malignancy.

In doing so we discussed the use of ADA and the proper time to send it — distinguishing between malignant and TB pleurisy with an exudative effusion that is lymphocytic AND has initial cytology and smear and culture negative for TB. We discussed that in patients with a lymphocytic:neutrophil radio >0.75 and ADA >40 empiric treatment for TB is reasonable — with pleural biopsy as a confirmatory test if either of those two criteria are not met. We discussed the diagnostic accuracy of the ADA in reviewing this paper. 

In the end our patient had an ADA <1.6 and is awaiting biopsy for continued malignancy work up.

References:

  1. Liang QL, Shi HZ, Wang K, Qin SM, Qin XJ. Diagnositc Accuracy of adenosine deaminase in tuberculous pleurisy: a meta-analysis. Respir Med. 2008 May; 102(5): 744-54. PMID: 18222681

 

 

10/9 VA Report: Chronic Kidney Disease Overview

In a delayed posting — I’d like to thank Lindsey Haddock for her excellent lecture on CKD Complete with picture-worthy whiteboard drawings!

Lindsey started off her overview highlighting the various stages of CKD and the importance of referring to nephrology when patients are stageIIIb (GFR 30-44) so that they can begin the vascular workup/preparations for dialysis.

IMG_0083 (1)

Next Lindsey tackled WHY patient’s get CKD with Hypertension and Diabetes taking the largest piece of the etiology pie at 30% and 45% respectively.

Importantly we reviewed the work up necessary and appropriate treatments/screening needed for the various sequelae of CKD including anemia, mineral bone disease and metabolic acidoses.

IMG_0084

Thanks again for a great lecture Lindsey — always proving that a picture is DEFINITELY worth a thousand words.

 

9/13 VA Report: Chronic Urticaria

The VA team conquered an interesting case of a 22 yo F who presented to the outpatient setting with chronic urticaria and “recurrent anaphylaxis.” She was a distance runner participating in multiple marathons. After a 13 mile run she developed SOB, hives, diarrhea and was rushed to the hospital for treatment.

We reviewed anaphylaxis how to clinically diagnose anaphylaxis:

2+ organ systems involved post exposure – skin/mucosa, respiratory, hypotension, GI

OR

Hypotension (as defined as SBP<90 or >30% decrease in SBP) following exposure to a KNOWN allergen

We also discussed the initial treatment algorithm including IM epi, benadryl, ranitidine, steroids — stressing the importance that only IM epinephrine has mortality benefit.

Our patient has resolution of the anaphylactic episode which was the second she’d had that year, but had persistent recurrence hives over the last year.

We discussed the difference in differential between urticaria + angioedema and angioedema ALONE — if angioedema WITHOUT urticaria and reviewed the work up for chronic urticaria (lasting >6 weeks) including: CBC, ESR/CRP, TSH and ANA (2). We also discussed that lesions lasting for >48 hours require biopsy. We reviewed an approach to chronic urticaria as outlined in the imaging below.

IMG_0034

After extensive testing, including inducing her hives with an exercise tolerance test, our patient was found to have exercise induced anaphylaxis NOT associated with food.  We discussed overall treatment of urticaria with ceterizine, avoidance of NSAIDs/ASA, H2 blocker, and avoidance of her triggers. Because exercise induced anaphylaxis can be triggered by various amounts of exertion, she was counseled to always have her IM Epi on hand and to only exercise with a friend (3).

References:

  1. Hosey RG, Carek PJ, Goo A. Exercise Induced Anaphylaxis and Urticaria. AAFP 2001;64 (8):1367-1372.
  2. Berstein, JA et al. The diagnosisand management of acute and chronic urticaria: 2014 update. AAAAI 2014;133(5):1270-1277.
  3. Barg W et al. Exercise Induced Anaphylaxis: An Update on Diagnosis and Treatment. Curr Allergy Asthma Rep (2011) 11:45-51.

8/29 PPMC Report: Microscopic Hematuria

Today at PPMC we covered one of the basics — microscopic hematuria. We see it ALL the time, we make sure we’ve made the PCP aware in the discharge paperwork — but what does the PCP actually need to DO in follow up? And when should we be forcing more aggressive workup and biopsy?

These were just a few of the great questions asked and answered today. First the PPMC team developed a basic algorithm, and then we moved forward to apply this algorithm to several cases.

Microscopic hematuria

We discussed that microscopic hematuria is NEVER normal and our risk stratification really depends on a triage between glomerular sources of bleeding vs. not and then the patients individual risk factors for malignancy. If glomerular in nature, we discussed factors that require an expedited workup with nephrology for biopsy — increasing protein in urine and worsening renal function.

Our first case was a 38 yo with a PMH of recurrent UTI’s and family history of an unknown “renal disease” who was found to have persistent microscopic hematuria. First, using the above algorithm, the team wanted to confirm that she didn’t have a benign reason for microscopic hematuria including her menses or another UTI. Once that testing came back negative we wanted to “start at the top” to determine if the bleeding was glomerular in nature. Her urine demonstrated dysmorphic reds and red cell casts but importantly NO protein and a normal creatinine. Based on this information we reviewed the data behind conservative medical management without biopsy  — with the presumptive diagnosis as either thin basement membrane or IgA nephropathy.

Our second case was a 65 yo M recently started on Xarelto for a RLE DVT who was found to have microscopic hematuria after starting anticoagulation. Again, benign causes for bleeding were ruled out and an assessment of his risk factors for malignancy  was performed: Age, Smoking status, history of gross hematuria, occupational exposure, h/o cycophosphamide exposure, use of some weight loss/diet preparations with aristolochic acid. This patient was found to have a transitional cell cancer of the bladder.

References:

  1. Cohen, RA and Brown RS. Microscopic Hematuria. N Engl J Med 2003;348:2330-8.

8/24 PPMC Report: Vertigo

Today’s case was a 47 yo F with congenital lymphangiectasia presenting with vertigo.

Obviously — the first thing we discussed was a quick review of congenital lymphangiectasia. It’s an exceedingly rare disease in which there are dilatation of intestinal lacteals resulting in lymph leakage into the small bowel. This disease is responsible for a protein-losing enteropathy leading to lymphopenia (CD4 count 36), hypoalbuminemia, and hypogammaglobulinemia.

Next we did a review of central vs. peripheral vertigo and how to differentiate between the two based on history and exam. While it’s not COMPLETELY black and white, the table below gives general guidelines to differentiate between the two.vertigo

 

Based on our patient’s presentation with vertical and horizontal nystagmus and positive skew deviation she was referred for MRI with c/f a central lesion.

Her MRI demonstrated multiple rim-enhancing brain lesions and we discussed the broad differential for an immunocompromised patient — including bacteria (abscess v. TB v. syphilis/gummas), fungal (crypto v. aspergillosis, v. histo v. coccidio v. actino v. mucor), Parasitic (toxo), Inflammatory (sarcoid v. whipple’s v. MS v. lupus v. PML v. Behcet’s) and Neoplastic (metastases vs. primary CNS lymphoma vs. GBM vs astrocytoma).

She had a biopsy that demonstrated primary CNS lymphoma.