Cardiology Pearls

Three main causes of Aortic Stenosis:
1. Congenital bicuspid aortic valve: age 50-60, men>women
2. (Acquired) Calcific aortic stenosis: age 70-80, men=women
3. (Acquired) Rheumatic aortic stenosis: middle-aged women>men, will also have mitral valve disease (note: rheumatic heart disease usually affects mitral, then tricuspid, then aortic in sequence)

Troponins
Troponins are a confirmatory test fo ACS in the setting of a history/clinical picture that suggests ACS. In other settings, it's a marker of myocyte necrosis but completely non-specific. It is only specific for ACS if ordered because the history suggested ACS.

Infective Endocarditis
Strep viridans does not generally cause large vegetations
- Staph and fungal infections cause large vegetations
- ECHO has low sensitivity

Acute versus Chronic Aortic Insufficiency (AI)

1. Chronic AI:
- LV has adapted by eccentric hypertrophy and dilatation to compensate for volume overload
- displaced apex beat
- long, loud, early diastolic decrescendo murmur, best heard at aortic area when the patient is seated and leans forward with breath held in expiration; often goes all the way to S1
- S1 is normal
- Wide pulse pressure, and related signs: waterhammer pulse, Corrigan's pulse, de Musset's sign, Quincke's sign (pulsations in the capillary nail bed), Duroziez's sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethescope)

2. Acute AI:
- equalization of aortic pressure with LV pressure because LV can't compensate acutely for all the extra volume = diastasis
- Premature S1 that is very soft (the massive reflux of blood from the aorta fills the left ventricle during diastole, increasing LVEDV and filling pressure, and closes the mitral valve prematurely), normal S2
- increased LA pressures leading to pulmonary edema (florid CHF)
- Very quiet and short early diastolic murmur
- Signs of vasoconstricted state, tachycardia, low sBP, dBP and MAP (and low stroke volume)
- pulse pressure not as wide
- Main causes: aortic dissection, aortic valve IE

Skin & Soft Tissue Infections

Layers of the Skin & Soft Tissue (out to in) with their corresponding infections:
- Epidermis -> erysipelas
- Dermis -> cellulitis
- Subcutaneous fat -> panniculitis
- Fascia -> fasciitis
- Muscle -> pyomyositis

CLINICAL PEARLS:
1. Differentiating erysipelas versus cellulitis
- Erysipelas has a raised, distinct border
- Cellulitis is less well demarcated

2. Gestalt...
- Red with no pus -> likely Group A Strep
- Red with lots of pus -> likely Staph

3. The number 1 bug for ALL layers is GROUP A STREP.
Number 2 is Staph.

4. Lympangitic streaking can be seen with cellulitis, but not with fasciitis because there is no lymphatic drainage of the fascia.

Recognize sepsis!!
Upon presentation, a patient's chance of dying is 5-10% with an MI, 15% with a stroke, and 50% with sepsis! Yet it remains under-recognized...

Treatment of cellulitis: (to cover both Strep and Staph)
#1 - Cefazolin / Cephalexin (first generation cephalosporins)
- Cloxacillin
- Vanco if suspecting MRSA
- If PCN allergy: Levofloxacin or moxifloxacin

Strep is highly resistant to Septra and Macrolides.
Doxycycline is good for Staph but not so great for GAS.

Click here for the IDSA practice guidelines for the Dx and Rx of SKIN AND SOFT TISSUE INFECTIONS.

Mumps at Ki Restaurant!!

For all you foodies out there (I am one), note that TPH has reported a mumps outbreak, with 9 cases among employees at a popular Toronto restaurant (a favourite amongst Cardiologists!)..

See link for TPH update:

http://www.toronto.ca/health/cdc/communicable_disease_surveillance/monitoring/pdf/mumps_2011.pdf

MUMPS CLINICAL FEATURES:

Signs and Symptoms:
- viral prodrome (myalgias, anorexia, malaise, headache, and fever)
- unilateral or bilateral parotitis
- respiratory symptoms

Complications:
- meningitis,
- encephalitis,
- orchitis,
- oophoritis,
- pancreatitis
- deafness

Transmission:
- direct contact with respiratory droplets or saliva
- incubation period 12 to 26 days

Diagnostic testing:
- virus isolation/detection from buccal or throat swab + urine collection
- serology (IgM and IgG for mumps)

A classic case of "brain rot"

We had a particularly entertaining Morning Report last Friday where we discussed the case of an elderly woman with subacute onset of memory disturbances, incontinence, ataxia and multiple focal neurologic deficits. Pending brain biopsy, her preliminary diagnosis is ...

HSV ENCEPHALITIS

Click the link below for a review of viral encephalitis:
http://journals1.scholarsportal.info.myaccess.library.utoronto.ca/tmp/10753946288144476016.pdf

("Brain rot" is not a term routinely used to describe HSV encephalitis, but rather was thrown out there by our MR facilitator and I found it somewhat amusing..)

Doctor my back hurts!

Today in Morning Report we reviewed a case of a 60F with acute onset of low back pain.

Remember the Red Flags of Back Pain:

1. Saddle anesthesia

2. Bowel/bladder changes

3. Constitutional symptoms (fever, chills, sweat, anorexia, weight loss)

4. Prior or current history of malignancy

5. Night pain

6. Hx of IVDU

7. Older age> 65 with new onset back pain

Why do we care about these red flags?

- Impending neurologic compromise

- Malignancy

- Abscess

The role of imaging in the management of low back pain: bottom line - in the absence of red flags, imaging for LBP doesn't significantly influence management and is associated with substantial cost.

http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/15031430 (use your UtorID for access)

A systematic review published in the Annals of Internal Medicine in 2004 concluded that in adults < 50 years old with no systemic symptoms (or red flags), symptomatic therapy without imaging is appropriate. In adults > 50 years, or those with systemic symptoms, routine bloodwork and plain radiographs are usually sufficient to rule out underlying systemic disease.

http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/12353946

Aphasia

Today in Morning Report we talked about a woman with acute onset of word-finding difficulties and recognition. Here is simple approach to aphasia:



*Remember: APHASIA = impairment in language. DYSARTHRIA = motor speech problem.



Broca's area and Wernicke's area are the main language areas located in the perisylvian language area, they are joined by the arcuate fasciculus.



*All aphasias have naming problems.

1) Can the patient repeat? (Assess repetition)
- Repeat after me: "no ifs, ands, or buts"

- if yes: perisylvian language area intact, therefore lesion in area around perisylvian language area = transcortical aphasia

• 2) Is the patient able to comprehend? (Assess comprehension, simple commands)


• easy questions: close your eyes, to more difficult: point to your nose with your right hand


• If yes: "Transcortical motor aphasia"


• If no: "Transcortical sensory aphasia"

- if no repetition: lesion within perisylvian language area

• 2) Is the patient able to comprehend?


• If yes: "Broca's aphasia"


• If no: "Wernicke's aphasia"

Summary:

Broca's Aphasia
- can understand, cannot repeat ("patient is frustrated")
- not fluent

Wernicke's Aphasia
- cannot comprehend, cannot repeat
- fluent (but non-sensical speech, not coherent) - word salad ("examiner is frustrated")

Transcortical Motor Aphasia
- like Broca's aphasia but CAN repeat
- usually lesion near Broca's area but not in the perisylvian area (in the frontal cortex)

Transcortical Sensory Aphasia
- like Wernicke's aphasia but CAN repeat

Global Aphasia
- cannot comprehend, cannot repeat, not fluent, cannot read, cannot write (usually mute)
- suggests large lesion affecting both Broca's and Wernicke's areas (ex. Large MCA stroke)

Anomic Aphasia
- difficulty naming but no other deficits
- does not localize

Conduction Aphasia
- cannot repeat, but everything else intact
- lesion in the Arcuate Fasciculus (the fibers that connect Broca's and Wernicke's); the two main areas are intact but the listening and the speaking parts of the brain can't connect

"Rapid Fire" MR

August 4, 2011 - Today we had "rapid fire" post-call morning report and reviewed several cases from last night. Here are some synopses:



Case 1. 57M mucosal bleeding. PMHx: APLA, ITP with splenectomy. Meds: Prednisone 15mg daily, no warfarin. O/E: petechiae, ecchymosis, cushingoid.



What do you think is causing his bleeding?



Investigations: Plt 285, INR 1.0, PTT 25.7, bleeding time >15s, U/A 2+ blood, creat 78



Does this change your differential diagnosis?



Remember the components of coagulation:
- factors, inhibitors (check via INR, PTT)
- Plt fxn (uremia, antiplt)
- fibrinogen
- vWF/factor 8 deficiency

Disorders of primary hemostasis:
- Acquired: antiplatelet agents (ASA, Plavix), thrombocytopenias (ITP, HIT, TTP), primary bone marrow diseases (myeloproliferative disorders, MDS, plasma cell dyscrasias), severe renal failure (so called "uremic platelets")
- Congenital: vWD, some platelet dysfunction disorders


Disorders of coagulation/fibrinolysis:
- Acquired: liver failure, Vit K deficiency, anticoagulant meds, factor inhibitors, scurvy
- Congenital: coagulation factor deficiencies (hemophilias), antiplasmin deficiency

Initial lab tests:
- CBC, liver enzymes, ABO blood group
- INR, aPTT, if abnormal: consider 1:1 mixing studies
- fibrinogen
- vWF antigen, ristocetin cofactor, factor VIII
- platelet aggregation test
- standardize bleeding time


***
Case 2. 58F 6-weeks post-THR (PMHx: JRA). Recent C. Diff treated with Flagyl, returning with worsening diarrhea, abdo pain.

C. diff recurrence - Definition: complete abatement of C. diff infection symptoms while on appropriate therapy, followed by subsequent reappearance of diarrhea and other symptoms after treatment has been stopped; must distinguish from persistent diarrhea without resolution during initial therapy.

Treatment of C. diff:
Initial episode: Flagyl 500 mg PO TID x 10 to 14 days
Alternative ($$$): Vanco 125 mg PO QID x 10 to 14 days

First relapse: repeat treatment as in initial episode (Flagyl)

Second relapse: tapering course of PO Vanco, +/- probiotics (Saccharomyces boulardii 500 mg orally twice daily).

***
Case 3. 78M from ICU post hypercapneic resp failure due to severe COPD

NB: The traditional teaching of supplemental oxygen decreasing the "drive to breathe" in CO2-retaining COPDers, is incorrect. The current thinking is that therapy with supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates the Haldane effect (decreased carriage of CO2 by oxyhemoglobin when compared with reduced hemoglobin), resulting in changes in physiologic deadspace and worsening hypercarbia.

Published in:
Hanson, C William III et al. Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease. Crit Care Med 1996; 24(1): 23-28.

***
Case 4. 50F 6-week abdo pain, diarrhea. CT abdo shows: Terminal ileitis.

What is your differential diagnosis?

DDx terminal ileitis:
- Crohns (#1, 2, 3!)
- infectious (especially Yersinia, TB)
- spondyloarthropathies
- vasculitides
- ischemia
- neoplasm
- medication-induced (especially NSAIDS)
- eosinophilic enteritis