Borborygmus

Cardiology Pearls

2011-08-24T08:29:00.003-04:00

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

2011-08-19T14:33:00.002-04:00

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!!

2011-08-15T13:47:00.003-04:00

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"

2011-08-15T13:35:00.002-04:00

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!

2011-08-09T10:37:00.002-04:00

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

2011-08-05T09:29:00.004-04:00

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

2011-08-04T09:54:00.005-04:00

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

Elevated CK

2011-08-03T10:59:00.004-04:00

Rhabdomyolysis

August 2nd, 2011 - Morning Report

Definition: the rapid breakdown of striated muscle with subsequent release of cellular contents into the extracellular fluid and circulation.

Fun fact:
First description of Rhabdomyolysis is thought to be in the Book of Numbers (Bible or Torah) after the Israelites ate quail and were poisoned. Scholars believe this to be due to cicutoxin from the Hemlock plant that the quail were believed to feed on.

Elevated CK
- CK-MM muscle
- CK-MB heart
- CK-BB brain

DDx for elevated CK-MM (rhabdo)
1. Crush: compartment syndrome; lying on ground immobile
2. Drugs:(statins - risk significantly increases with co-use of fibrates, ecstasy, heroin, cocaine, neuroleptics - NMS), malignant hyperthermia
3. Ischemia: DVT with compartment syndrome, arterial embolus
4. Exertion: seizure, marathoners, muscle builders (think fit vs non-fit)
5. Inflammatory: polymyositis (personal or famil hx of autoimmune disease?), dermatomyositis (look for an underlying tumor)
6. Infection (especially viruses like EBV, coxsackie), Legionnaire's disease
7. Genetic: most common is McArdle's disease (congenital myophosphorylase deficiency), Tarui disease (phosphofructokinase disease), carnitine deficiency
8. Endocrine: hypo > hyperthyroid

*The schematic above showing the causes and complications of rhabdomyolysis was taken from the article: Cervellin G, Comelli I, Lippi G. Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med. 2010 Jun;48(6):749-56.

Clinical features:

- classic triad: muscle pain, brown pigmented urine (myoglobinuria), weakness seen in <10% of patients

- can be asymptomatic with only elevated CK

- myalgias, pain, pigmented urine, fever, malaise, tachycardia, nausea/vomiting

- AKI can be seen if CK>5000

- complications: renal failure, DIC, and death in ~5% of cases

- urine myoglobin is not useful in diagnosis

- CK is the biochemical gold standard

- other investigations: elevated AST>ALT, LDH, UA

Treatment:

- FLUIDS!

- little support for the use of mannitol, Lasix, or bicarb

- manage the electrolyte derangements (hyperkalemia, hypocalcemia)

- severe hyperkalemia may require dialysis - shifting with insulin may not work if extensive tissue damage led to rhabdo

Moderate-intensity exercise (HR 55-90% max) is enough to elevate CK levels to the mid-thousands, particularly if "eccentric muscle contractions" like weight lifting or running downhill. More info can be found in the article:

Latham J , Campbell D , Nichols W , Mott T . Clinical inquiries. How much can exercise raise creatine kinase level--and does it matter? J Fam Pract. 2008 Aug;57(8):545-7.

Geripsych Morning Report

2011-08-03T09:52:00.004-04:00

This morning we discussed some common geripsych issues...

Form 1
- any physician can fill out within 7 days of seeing a patient
- mandates mental health assessment, can hold patient up to 72 hrs to do this
- mental health assessment does not have to be done by a psychiatrist; can be done by any physician comfortable with this assessment
- if patient deemed unsafe, next steps either: 1) put on Form 3 if involuntary, or 2) patient can stay voluntarily
- rarely use Box B (except psychiatrists who know the patient well because addresses patient's history)
- must give pt the Form 42: notifies the patient of why they're being held and by what authority (otherwise illegal to detain them)

Agitation
- clarify what agitation means and whether it warrants treatment
- treatment responsive versus non-treatment responsive
- treatment non-responsive: example -> wandering doesn't warrant treatment - there's no specific treatment except zonking them out
- treatment responsive: yelling, behavior driven by psychosis, striking/violence
- non-pharmacologic therapy: some "agitated" patients just need something to do like fold towels or stuff envelopes
- pharmacotherapy:

1. Atypical antipsychotics: mainly oral
- Risperidone: highest EPS, least sedating, ex: 0.25 OD or BID
- Olanzapine: most anticholinergic therefore avoid in elderly, mid EPS, mid sedating
- Quetiapine: Lowest EPS, most sedating, causes orthostatic hypotension (huge variation in dose, 6.25-200mg! Start low go slow, first couple days will have sedation)

Here is the Results portion of the article: L.B. Ozbolt; M.A. Paniagua ; R.M. Kaiser Atypical Antipsychotics for the Treatment of Delirious Elders. Journal of the American Medical Directors Association (January 2008), 9 (1), pg. 18-28

"Results: Risperidone, the most thoroughly studied atypical antipsychotic, was found to be approximately 80% to 85% effective in treating the behavioral disturbances of delirium at a dosage of 0.5 to 4 mg daily. Studies of olanzapine indicated that it was approximately 70% to 76% effective in treating delirium at doses of 2.5 to 11.6 mg daily. Very few studies have been conducted using quetiapine; it also appears to be a safe and effective alternative to high-potency antipsychotics. In comparison to haloperidol, the frequency of adverse reactions and side effects was found to be much lower with the use of atypical antipsychotic medications. In the limited number of trials comparing atypical antipsychotics to haloperidol, haloperidol consistently produced a higher rate (an additional 10% to 13%) of extrapyramidal side effects."

2. Typical
- Haldol: can be given po/im so gives you options, most EPS, least anticholinergic (ex 0.5-1mg po q4h prn); NB Haldol iv better for EPS but less safe from cardiac perspective ie long Qt
- Loxapine: slightly sedating, available in liquid form

3. Other
- Trazadone: good for nighttime restlessness

Stimulants in Depression:
- use for depression in the medically ill elderly who are anergic (apathetic) as opposed to sad, ex: flat affect, fatigued, low energy, no interest in eating in patient with no history of depression
- one week to titrate up and if it's going to work you expect it to work quickly within first week
- options: Buproprion or SSRIs
- NB: can use mirtazapine to stimulate appetite but caution because can increase cholesterol

Leukemia Cutis

2010-03-02T10:52:00.005-05:00

Today at morning report we discussed rash and acute leukemia.

Rash (or other dermatologic complaints) are often difficult for internists to deal with, as we often lack a lot of experience with them. However, going back to basics, a few key points to make are:

(1) A description of the rash is important. This includes the features of the lesions (i.e. macules, papules, plaques, nodules, bullae, etc), a description of the distribution (localized vs. diffuse, major regions of the body affected, areas spared) and the progression of the lesions over time. It is also important to describe the associated symptoms - fever, pruritis, pain, parasthesia or anasthesia, etc.

(2) Rule out acutely dangerous things. A few key rashes internists should know about are:

Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis
Pemphigus
Infections of skin/soft tissue (in particular, necrotizing fasciitis)
Purpura fulminans (meningococcemia)
Staphylococcal toxic shock
Viral exanthems (Note that varicella, measles, etc can be severe and even fatal in adults, especially the elderly)

(3) If in doubt, stop all possible offending drugs and get an urgent dermatology opinion and biopsy.

We talked in more detail about leukemia cutis, a disease caused by infiltration of the skin with leukemic cells. The Canadian Medical Association Journal recently published a short case report with images (although in a child) on this syndrome. Leukemia cutis may portend a worse prognosis in adults with AML.

Management of Ascites

2010-02-05T09:10:00.004-05:00

Today at morning report, we discussed the management of ascites.

I wanted to share with you some guidelines and literature:

Chronic Outpatient Management of Ascites

Sodium restriction (88 mmol/day [2000 mg/day])

Diuretics (oral spironolactone with or without oral furosemide).

Fluid restriction only if serum sodium is less than 120 to 125 mmol/L.

Chronic Outpatient Management of REFRACTORY Ascites

Serial therapeutic paracenteses.

Postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L.

For large-volume paracenteses, an albumin infusion of 6 to 8 g/L of fluid removed can be considered.

Transjugular intrahepatic portasystemic stent-shunt (TIPS) may be considered in appropriately selected patients who meet criteria similar to those of published randomized trials.

Who Needs SBP Prophylaxis?

Anyone who has had SBP before.

Anyone with cirrhosis admitted with a variceal bleed. See the NEJM paper

Anyone with cirrhosis, ascites ascitic protein less than 1.5, creatinine greater than 106 mmol/L OR BUN greater than 8.9 mmol/L), serum Na less than 130, MELD greater than 9 points with bilirubin greater than 3 mg/dL.

One question that came up was whether prophylaxis should be daily or intermittently. Both regiments have been shown to be of benefit in clinical trials, but there is concern that intermittent dosing will lead to bacterial resistance and therefore the preferred regimen according to the AASLD is daily.

Renal Failure in Ascites

Erik mentioned using albumin in patients with SBP. The major evidence supporting this practice is from an article published in the NEJM in 1999 which randomized patients with SBP to either antibiotics alone or antibiotics with albumin. The investigators found a statistically significant reduction in renal dsyfunction and mortality with this regimen.

There was aslo a recent review article on renal failure and cirrhosis in the NEJM.

See the AASLD Guidelines for more information on the management of ascites.

Graves' Disease

2009-12-08T11:15:00.003-05:00

Here is a NEJM review on Graves.

We also discussed anti-NMDA receptor encephalitis - there is a case presentation here. A discussion of paraneoplastic syndromes involving the CNS is posted here.

Back in Business

2009-12-03T12:09:00.004-05:00

Articles from yesterday's morning report:

NEJM article on acute pericarditis here:

The classic Art of Pimping article here:

Today at morning report we discussed Wegener's Granulomatosis. An older NEJM review of small vessel vasculitis that I like is here

Hyponatremia - no it's Hyperhydroemia

2009-09-11T16:51:00.009-04:00

CLINICAL PEARLS WHEN TREATING HYPONATERMIA?

1. In patients on diuretics, the fractional excretion of urea can be used to help determine if patient is hypovolemic. FeUrea= (Uurea/Purea)/(UCr/Pcr)
FeUrea <35% suggests prerenal state.

2. Before accusing someone of having SIADH, you must check TSH and adrenal function (ACTH stim).

3. Acute recognition of a chronic problem (chronic hyponatremia) does not require acute treatment.

4. To prevent overly rapid correction of hyponatremia, consider the role for DDAVP (often given as 1-2mcg SC/IV). If you do correct too quickly (want to correct 0.5 mmol/h at the absolute most) also consider giving D5W in addition to DDAVP - see the article below.

5. If volume repletion is required, give fluid that is isotonic to the patient by using a combination of NS and D5W.

6. Attach the foley catheter to the IV (figuratively) - be sure to monitor urine osm and output - and consider calculating a tonicity balance

Extras:
When seeing hyponatremia in the ER:

First rule out acute hyponatremia that needs acute correction.

Recheck the lytes as they were often done a while ago and the patient has possibly received intravenous fluids that may have significantly altered the sodium concentration - especially if the stimulus (often ECF volume depletion) for ADH secretion has been removed. Following the urine output may help to identify this (although recording can be an issue outside of the ICU) as a brisk, dilute diuresis can be bad sign.

An article on DDAVP to prevent rapid correction is posted here.

Familial Mediterranean Fever

2009-09-11T16:51:00.001-04:00

Doctor, There's a Hole in my Heart!?

2009-09-02T09:36:00.002-04:00

An interesting article published by one of our staff and residents on morning report can be found here.

A prior blog on the causes of platypnea and orthodeoxia can be found here.

Review of PFO formation:

The endocardial cushions fuse, separating the heart into R and L sides.

Early in utero the septum primum grows and fuses with the endocardial cushion, closing the formaen primum, however perorations have developed in the septum primum to fuse, forming the foramen secundum (still allowing right to left shunting)

A second membrane, the septum secundum, grows on the right atrial side of the septum primum. The septum secundum overlaps the foramen secundum, forming an incomplete septal partition that becomes the foramen ovale. The remaining septum primum forms a flap-like valve over the foramen ovale.
After birth, normal circulation is established (left sided pressures>right sided) and the flap fuses in 75% of people by age 2. The remainder have a PFO.
The PFO is completed covered, but not sealed and shunting can occur if there is a reversal in intracardiac pressures (i.e. right to left shunt).
If an open communication exits (no flap) this is an ASD.

In studies, PFO prevalance is as high as 25%

A debate on PFO closure (with respect to cryptogenic stroke) can be found in these two Circulation articles: Close v. Don't Close (or at least do an RCT).

SIGNOVER SAFETY

2009-09-02T09:22:00.005-04:00

An effective handover is critical to safe and efficient patient care.

The mneumonic "SIGNOUT?" was developed as part of a signover curriculum discussed in this article.

S - Is the patient sick? Stable? Code Status?
I- ID
G - General Hospital Course
N - New events of the day
O - Overall clinical condition
U - Upcoming possibilities (those that can reasonably anticipated) with plan/rationale
T - Tasks to complete overnight (explicit instructions) and rationale
? - Any questions?
Slide 24

Quality of Care

2009-08-19T10:46:00.001-04:00

A previous blog on quality of care can be found here.

Platypnea

2009-08-19T10:02:00.008-04:00

PLATYPNEA and ORTHODEOXIA

After discussing an approach to dyspnea on exertion, the symptom of platypnea was discussed.

Platypnea is an increase in dyspnea in the upright position that improves on lying down.

Orthodeoxia is a decrease in oxygen saturation that occurs upon rising from supine.

These often occur together. They happen when there is right to left shunting that only occurs or is more pronounced, in the upright position. Shunts can be intracardiac (ASD, PFO) or intrapulmnary (AVM, hepatopulmonary syndrome).

This often occurs in HHT, when larger pulmonary AVMs are in bases of the bases of the lungs and therefore recevie a greater proportion of blood when the patient is upright. It can also occur for anatomic reasons in patients with intracardiac shunts.

Shunting can be seen with contrast ECHO where agitated saline bubbles are injected into peripheral veins. They appera in the right heart, and if a right to left shunt exists then they will appear in the left side of the heart. If they appear in 1-2 beats, the shunt is intracaridac, in 3-8 beats then it is likely intrapulmonmary.

Shunt fraction can be calculated by testing SaO2 and PaO2 before and after breating 100% oxygen fro 15 minutes. Normal is less than 5%.

International guidelines for the diagnosis and management of HHT (published by Toronto clinicians) can be found here.
A NEJM review of HHT can be found here.
A NEJM review of hepatopulmonary syndrome can be found here.

Parkinsonism

2009-08-14T15:47:00.005-04:00

Here is a link to the JAMA Rational clinical exam article for Parkinson's Disease
Here is a link to a CMAJ review article on Parkinson's disease

When examining someone with potential Parkinsonism (in real life, but also consider if relevant on an exam), be sure to consider the "Parkinson plus" syndromes.

JEOPARDY

2009-08-14T09:31:00.002-04:00

Here is a website with some interesting/rare medical conditions - not completely accurate descriptions and genetic causes for many are being discovered. Interesting nevertheless.

Here is the wikipedia page on Ken Jennings, the winningest player in Jeopardy history. He was defeated by Nancy Zerg in his 75th appearance.

"My, that is a cute joint"

2009-08-13T13:47:00.009-04:00

ACUTE MONOARTHRITIS

A great advanced discussion today that focused on monoarthritis.

The first step in assessing an "acute joint" is to determine if the process is articular, periarticular or referred.

If it is indeed an acute articular process the differential includes:

Infectious: SEPTIC UNTIL PROVEN OTHERWISE!!!
- a very good general rule, although as we learned today in classic presentations of other diseases, joint tap may be deferred
Crystal Arthropathy: Gout, Pseudogout (CPPD), Hydroxyapatite
Inflammatory
Seropositive arthritis (early RA or SLE)
Seronegative arthritis (psoriatic, Ankylosing spondilitis, IBD, reactive)
Degenerative: Osteoarthritis

Trauma: Hemarthrosis, joint trauma

Extra-articular: Bursitis, cellulits, ruptured Baker’s cyst, tendonitis, etc…

A JAMA rational clinical exam article on septic arthritis is linked here and a CMAJ article on approach to acute monoarthritis is here. Gout is unusual in premenopausal women. An article on acute calcific periarthritis is linked here.

IMAGING
Not always necessary - may be helpful for
1)Trauma
2)Evidence of crystal disease
3)Baseline study (i.e. to follow for development of pathology in future if septic joint, etc.)/to assess for obvious coexisting osteomyelitis.

Antihyperuricemic Treatment
Indications:
Recurrent kidney stones
Gout and renal failure
Tophi
Associate chronic joint changes
Frequent/severe attacks of gout

Options:
Uricosuric agents: - best in uric acid undexcretors (normal urine uric acid with high serum levels). Avoid if renal stones/uric acid nephropathy. Less effective in renal failure.

Xanthine oxidase inhibitor - decrease uric acid synthesis. Good for almost everyone, but need to consider drug interacations and adjusft for comorbidities (renal failure)

Use minimum dose to achieve effect (follow serum urate levels)
Azathioprine (Imuran) is mteabolized by xanthine oxidase (decrease Imuran dose by >50% and follow for toxicity)

Febuxostat - ?available here soon - xanthine oxidase inhibitor - but not a purine analog

Not clear what its role will be vs allopurinol, and ongoing safety monitoring will be important to follow (as with any new med)

CONSIDER prophylaxis with colchicine (0.6 mg up to BID if normal CrCl) when initiating/titrating antihyperuricemic drugs - stop once normouricemic for 6 months.

"When I grow up...."

2009-08-11T10:01:00.008-04:00

When discussing career planning a number of issues arise. It is important to start thinking about what you want your career to look like/what you enjoy doing. Try to figure out if you like inpatient vs outpatient, procedures vs not, clinical/admin/teaching/research etc.

The most important thing is to work hard and do good work - that is how you will build a good reputation.

Two relevant articles publised by MSH MDs - One on Mentorship and the other on how academic Practice plans are structured can be found using the links.

SEPTOID? What's that?

2009-08-11T09:22:00.006-04:00

SEPSIS

Definitions:
SIRS: Two or more of the following: T>38.5°C or <35.0°c;>90 beats/min; RR >20 breaths/min or PaCO₂ of <32>12,000 cells/mL, <4000>10 percent immature (band) forms.

Sepsis: SIRS secondary to an infection

MANAGEMENT:
Early goal directed therapy for sepsis is now the standard of care. A trial showing improved mortality using an early goal directed approach to sepsis can be found here, this trial is frequently referred to in the ICU as the Rivers' protocol.

Aimed at maintaining tissue perfusion:
1) Ensure adequate airway/breathing - intubate if necessary. Provide supplemental oxygen

2) Evaluate for signs of poor perfusion - frequent BP monitoring (consider art line - NEJM video on insertion here), LOC, Urine output, lactic acidosis, shock liver, etc.

3) Improve perfusion - FLUIDS!!!!!. Crystalloids (NS or Ringer's) are currently used as the first line resuscitation fluid. Patients often need >6L in the early stages of sepsis - be sure to monitor for signs of fluid overload, especially in those with renal or heart failure. Consider placing a central venous catheter - this provides secure venous access, can allow infusion of inotropes/pressors and can be used to monitor central venous oxygen saturatino and CVP.

4) Monitoring/"Advanced measures" - Involve the ICU/CCRT team. Activated Protein C (Xigris) and/or steroids should be considered in the right clinical context. Steroids are generally used now when shock persists despite adequate fluids and inotrope administration, or in patients on chronic steroids.

5) TREAT THE SOURCE - Identify and treat the cause of infection. In a large retrospective study, antimicrobial administration within the first hour of hypotension was associated with increased survival to hospital discharge in patients with septic shock. Culture potential sources and use appropriate broad spectrum antibiotics based on the suspected source and patient characteristics. Surgical evaluation and debridement should be rapdily arranged if necessary.

Hypercalcemia - "Milk does a body good?"

2009-08-06T17:13:00.011-04:00

Corrected Calcium:
The physiologically important calcium (Ca2+) is ionized calcium. This can be measured in the lab, however, total calcium is the value most commonly reported.

Calcium is bound to serum proteins, most importantly albumin. Therefore, in patients with low serum albumin concentration, the fraction of total serum Ca2+ that exists as ionized Ca2+ will be higher.
It is important to know the serum albumin when interpreting total serum calcium levels. A correction for total serum calcium can be made using the following formula (alternatively ionized Ca2+ could be measured):

Ca = SerumCa + 0.02 * (NormalAlbumin - PatientAlbumin) (SI UNITS)

Pseudohypercalcemia can occur when patients are hyperalbuminemic or have a multiple myeloma with a paraprotein that binds calcium (rare) - in these cases total CA2+ will be high, but ionized CA2+ will be normal.

TREATMENT
FLUIDS!!!!!!!!

Infusion rate depends on volume status, heart function, etc, but should target 100-1500 cc urine output/hr - do not need to hydrate beyond euvolemia

If severe/symptomatic consider: Bisphosphonates (IV) - will not take effect for 48-72 hrs, but will help maintain normal calcium when achieved.

Calcitonin by nasal spray or subQ is also very effective.
If hyperCa2+ is from sarcoid or lymphoma consider steroids (20-40 mg/day) - this works by decreasing calcitriol production from activated mononuclear cells in the lung and lymph nodes.

AVOID LASIX since most patients are profoundly volume depleted initially and once replete can cause hypokalemia, hypomagnesemia, and lead to recurrence of volume depletion. A recent Annals of Internal Medicine article reviews the use/concerns regarding Lasix in hypercalcemia.

Dialysis should be consider if the above fail/can't be done because of renal failure or heart failure.

Wegener's Granulomatosis

2009-08-06T17:13:00.010-04:00

Some important points regarding diagnostic approach:

When patients with chronic disease (such as Wegener's) present with an acute problem, one should consider if this is a process related or unrelated to their underlying disease. Attempts to evaluate the "activity" of the chronic disease should also be made.

When patients are admitted to hospital, careful thought should be given to what tests are ordered at time of admission. Although we should all try to attempt to minimize unnecessary investigations, if a patient is going to be in hospital for more than a few days it may be helpful to get "baseline" CXR, ECG and "routine bloodwork". This will may serve as a useful comparison should they develop further complications associated with their admission diagnosis or adverse events from hospitalization or treatment.

A 1997 NEJM review of small vessel vasculitis is available here.

A review of the evidence of PCP prophylaxis in non HIV infected patients is available here.

Quality of Care

2009-07-31T07:48:00.004-04:00

An interesting paper examining the discussion of medical errors in morbidity and mortality conferences was published in JAMA.

It found that in GIM M+M conferences case presentations were longer than those in surgery M+M. Less time was spent on audience discussion, fewer case presentations included adverse events or errors causing adverse events. At surgery M+M, errors were more likely (P=.17) to be attributed solely to an individual rather than a team or system.

"That's Tight" - How to assess for Aortic Stenosis

2009-07-28T20:32:00.008-04:00

We discussed EVAR (Endovascular Aneurysm Repair). A NEJM review can be found here. The precise role for EVAR (rather than open) repair is still debated. 2005 AHA guidleines suggest EVAR of infrarenal AAA could be considered in patients at high risk of complications following open repair and may be considered in those at low or average surgical risk. Longterm monitoring, including imaging, should be performed to ensure late complications do not develop. Several studies have been published since then and EVAR is being more widely used.

We also briefly discussed multiple myeloma. A review in BLOOD was published in 2008. Treatment in this field has evolved rapidly over recent years.

Finally, we discussed the physical exam diagnosis of aortic stenosis. The findings of a paper examining a clinical prediction rule for AS is summarized in the following figure from the article.

Abscence of a murmur over the right clavicle (see article Table 1 for how to auscultate for this) as performend by a staff internist or senior medical resident, effectively rules out moderate to severe AS (usually more important clinically than ruling in AS, as to rule it in a TTE will often be performed).

The JAMA rational clinical exam "Does this patient have an abnormal systolic murmur?" can be found here.

The Pneumonia formerly known as PCP

2009-07-27T13:15:00.015-04:00

Pneumocysitis jirovecii pneumonia was previosuly named Pneumocystis carinii pneumonia. Some of the debate regarding the name change can be found here and in the associated references. Previously classified as a protozoa, but molecular studies have shown it to likely be a FUNGUS.

Generally occurs in HIV+ patients with a CD4 count below 200 cells/mm3. Can also occur in other immunosuppressed hosts.

PRESENTATION
Subacute onset of (exertional) dyspnea, dry cough +/- "low-grade" fever.
Physical Exam shows tachypnea, tachycardia and normal lung auscultation in 50% (the remainder having crackles etc.).
CXR - classically bilateral, perihilar interstitial infiltrates, but can show almost anything (or nothing). However, pleural effusions and/or lymphadenopathy is very rare.

DIAGNOSIS
In addition to the clinical presentation, microscopic examination of (induced) sputum, BAL fluid or tissue can be performed. PJP cannot be readily cultured (be sure to specify you want sputum tested for PJP if it is in your Ddx), it can be seen with methenamine silver or immunofluorescence stains.

Laboratory data is generally not very informative. LDH is elevated in 90%, but this is very non-specific.

TREATMENT
TMP-SMX - high dose (see reference) x 21 days. Alternatives included inhaled pentamidine and atovaquone. Remember to start prophylaxis after finishing treatment!

Patients with PCP may worsen after two to three days of therapy, possibly from inflammation in response to dying organisms.

Corticosteroids are of benefit in patients who are hypoxic at presentation (PaO2 on room air less than 70mmhg or oxygen saturation <90%)

The benefit of steroids in PCP was shown in a study conducted in Toronto in 1987.

A NEJM review article can be found here

Thanks to prior CMRs for some of the above.

As discussed at noon rounds: Nystatin was isolated from Streptomyces noursei by Elizabeth Lee Hazen and Rachel Fuller Brown. The soil sample where they discovered nystatin was from the garden of Hazen's friends, Walter B. Nourses, therefore the strain was called noursei. It contained a substance that they first named fungicidin, a name that had already been used for another substance. They then renamed the substance nystatin in honor of the New York State Public Health Department, where they worked.

What's the diff?

2009-07-21T11:00:00.023-04:00

CLOSTRIDIUM DIFFICILE

Gram positive anaerobic bacillus - cytotoxin producing. Disease caused when toxin(s) bind to the surface of intestinal epithelial cells, where they are internalized and catalyze the glucosylation of cytoplasmic rho proteins, leading to cell death.

Typical occurs in elderly/instiutionalized especially after receiving antibioitics. Historically Clindamycin has been associated with high risk of C diff, in the Quebec outbreak in 2003, fluoroquinolone use was also associated with the development of infection. Direct person-to person spread occurs and previously healthy/younger/non institutionalized patients have also been infected.

PREVENTION

need responsible antibiotic use
infection-controlmeasures (contact precautions, hand hygiene, environmentaldecontamination)

DIAGNOSIS
Microbiology

C. diff toxin assay (EIA) detects toxins A and B and has ~70% sensitivity, with ~90-95% sensitivity on three tests. The specificity is> 95%.
The most sensitive assay is the test for cytopathic effect, which is not available here
You can also culture Clostridium difficile from the stool, but this is not routinely done, as there are nonpathogenic strains
A positive toxin assay in a patient with minimal or no symptomsshould not prompt treatment. (i.e. only send for toxin testing if there is sufficient pre-test probability)

Radiology

Consider AXR to assess for toxic megacolon -a maximum colonic diameter greater than 6 cm is consistent with megacolon, may also see bowel wall changes
CT scan helpful for further assessment and to R/O other causes of colonic distension etc.. May show thickening of the bowel wall, colitis, ileus

Sigmoid/Colonoscopy
Generally avoided with typical presentation and positive toxin EIA

Concern regarding endoscopy/insuflation of air causing perforation, especially if toxic megacolon present

May see pseudomembranes diagnostic of pseudomembranous colitis
Consider endoscopy if:

Atypical presentation (ileus etc.)
Other diagnoses suspected/need to be ruled out
Failure of C. difficile infection to respond to therapy

TREATMENT

See table from NEJM review here.

First Episode
***If possible stop offending antibiotics***

Mild/Moderate Disease
- Metronidazole OR Vancomycin (PO) duration 10-14d
Severe Disease
- Defined as:
  - Two of (Age above 60, Febrile, WBC above 15, Albumin below 25)
  - OR hypotension/shock or Cr greater than 1.5x normal, or toxic megacolon, peritoneal signs, perforated bowel
- Infectious Disease +/- General Surgery Consultation
- ICU Consult for patients with hemodynamic comprimise
- Vancomycin (PO) unless severe illeus/toxic megacolon, then Metronidazole (IV) duration 10-14d (Vanco has more rapidsymptom resolution and a lower risk of treatmentfailure).

Relapse

First relapse --> can repeat last treatment depending on severity
Second relapse --> vancomycin taper. ID consult.

NEJM Review article (2008) can be found here.
A paper discussing Vanco as first line treatment can be found here.
Thanks to Dr. T.C Lee for some of the above post.

Gallstone Ileus

2009-07-16T09:52:00.012-04:00

Occurs after gallstone lodges in bowel (generally terminal ileum - the narrowest intestinal area). The stone gets into the gut through a biliary enteric fistula.

Average age of affected patients is 70 years, more common in women.

In a large surgical series of patients undergoing cholecystectomy described here:

1.8% had a cholecystoenteric fistula
90% of patients with a cholecystoenteric fistula had Mirrizi syndrome (common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct)
5.7% of patients had Mirrizi syndrome

PRESENTATION
Classically a subacute obstruction in an elderly female that occurs episodically as the stone passes through and transiently obstructs the GI tract. (Transient) abdo pain, vomitting, abdo distension, increased bowel sounds

Bouveret's syndrome - gastric outlet obstruction secondary to an impacted gallstone in the duodenum or pylorus

Less than 15% of gallstones can be seen on plain film. Other AXR findings - parital or total SBO, pneumobilia. CT scan is likely better to visualize the stone/obstruction and MRCP may be best to define biliary anatomy

TREATMENT
Supportive until definitive treatment.

Surgical - enterolithotmy (with care to examine for >1 stone) +/- concurrent cholecystectomy or delayed laparoscopic cholecystectomy

Alternatives - extracorporeal lithotripsy, endoscopy (not first line)

"When you're sliding into first...."

2009-07-14T15:22:00.011-04:00

BLOODY DIARRHEA

A good discussion on the differential diagnosis of bloody and none bloody diarrhea of acute onset occurred today.

As always, a good history (as always) goes a long way in helping to focus the picture. In addition to a travel/sick contacts/dietary/medication history, sexual history is also important.

It is recommended that all patients with acute bloody diarrhea (including on history and FOB +) undergo stool culture.

DIFFERENTIAL DIAGNOSIS
Infection:
cytoxic - E. coli (EHEC) O157:H7 (often present with no fever), C. Difficile
invasive - E. coli (EIEC), Salmonella, Shigella, Yersinia, Campylobacter
Inflammatory: Inflammatory Bowel disease, radiation proctitis/colitis
Ischemic Colitis

Non diarrheal causes of Lower GI bleed should also be considered (diverticular disease, etc.)
Other considerations are rarer and depend on immunosuppression (CMV colitis) and exposure (GI anthrax, Intestinal TB, intestinal amebiasis, HSV procitis etc.)

A study of infectious etiologies (determined by stool culture) of acute bloody diarrhea in patients presenting to the ER in the US is posted here. If found enteropathogens in 12.5% of cases that were cultured despite the physician's presumptive diagnosis of a noninfectious cause.

A second study of the clinical and epi factors of diarrhea in the U.S. is posted here.

For an excellent blog on Infectious Disease issues see: http://www.idologist.com/Blog/

NASH

2009-07-10T10:00:00.001-04:00

Non Alcoholic SteatoHepatitis

CAUSES:
Metabolic Syndrome - obesity, diabetes, hyperlipidemia

Metabolic - hypothyroidism, TPN, rapid weight loss

GI surgery - gastroplasty, jejunal bypass, small bowel resection

Drugs - Tamoxifen, amiodarone, prednisone, estrogens

TREATMENT: Modify risk factors. Weight loss should be gradual as rapid weight loss can worsen the liver injury. Identify and treat underlying causes (hypothyroid, meds, etc.). Preliminary studies have shown that metformin or pioglitazone may one day have a role in treatment, but their exact longterm benefit is not clear.

Click here for a 2002 NEJM Review article.

Cholesterol Emboli

2009-07-10T09:56:00.009-04:00

Cholesterol Emboli Syndrome was discussed in the context of acute renal failure and raised lots of interesting issues.

ACUTE RENAL FAILURE:
A standard approach

Prerenal: Volume depletion, hemorrhage, decreased effective circulating volume (CHF, cirrhosis), renal artery stenosis

Renal: Glomerular - Glomerulonephritis (and its associated long list of causes), Acute interstitial nephritis, Acute tubular necrosis (either ischemic or nephrotoxic), Vascular

Postrenal: Obstruction of collecting system or extrarenal drainage

PERIPHERAL EOSINOPHILA
While discussing laboratory findings of AIN, the differential diagnosis of a peripheral eosinophilia was reviewed:
Allergic - rhinitis, asthma, meds.
Infectious - parasitic (helminths), fungal, other
Hematologic - Hypereosinophilia Syndrome, leukemia, lymphoma
Specific Organ Involvement - blood eosinophilia can occur when tissue eosinophilic infiltration is present in pulmonary, GI, derm, cardiac, rheumatologic or renal disease

CHOLESTEROL EMBOLI SYNDROME
Occurs in people with atherosclerotic disease
Spontaneous or as a result of intravascular procedure
Result of cholesterol crystal embolism causing occlusion of multiple small arteries leading to further inflammation and intimal proliferation

Pathology - "ghosts" of cholesterol crystals as they are dissolved during fixation

Symptoms:
Non specific H/A, myalgia, fever
Derm -livedo reticularis (lacy rash), ulceration, gangrene, "blue toe syndrome"
Acute Renal Failure -

GI - intestinal ischemia
Eyes - Hollenhorst plaques (cholesterol crystals in retinal arteries)

Labwork - nonspecific: elevated WBC/ESR, hypocomplementemia, Cr and urine eosinophils (if renal involvement), eosinophila

In the abscence of other symptoms consistent with cholesterol emboli, post angiogram renal failure will often be diagnosed as contrast nephropathy. Ways to try to distinguish the two:

Presence of other signs of cholesterol emboli (obviously)
Transient eosinophilia/hypocomplementemia
Persistent renal failure (much less common in contrast nephropathy)

Links to a prosepctive study on CES risk factors and incidence can be found here and the associated editorial here. They found elevated baseline CRP to be an independent risk factor for CES after cardiac cath. Thanks to the facilitator for these.

See a picture of Hollenhorst plaque (from UMich) below:

"Poncho Sign" and Heliotrope Rash

2009-07-08T09:27:00.003-04:00

DERMATOMYOSITIS

Dermatomyositis and polymyositis = inflammatory myopathies that are often discussed together because they often present as symmetric proximal muscle weakness.

Dermatomyositis, however, is associated with skin findings and is much more likely to be associated with an underlying malignancy.

SKIN FINDINGS - Heliotrope rash (see picture),Gottron's papules, periungual changes, "mechanic's hands", and the shawl sign - which some MDs felt appeared more like a poncho sign in certain patients.

Lung Involvement - ILD, respiratory muscle weakness

GI Involvement - Dysphagia, regurgitation, aspiration

Cardiac Involvement - Myocarditis, pericarditis, arrhythmias

SEROLOGY - ANA+ in 80%. Ongoing research into myositis specific antibodies (currently felt to be present in 30%) to help determine likely clinical progression and treatment response

MALIGNANCY - Incidence of cancer is 5-7x higher than general pop'n. Peak incidence of diagnosis is within 2 years before or after the DM diagnosis. Search guided by complete history and physical. Bloodwork, imaging and tumor markers (CA125, CA 19-9, PSA) and age appropriate cancer screening.

Ongoing cancer surveillance suggested for 3-4 years after diagnosis or recurrence, with the exception of ovarian CA which can occur >5 years after diagnosis (therefore screen for longer).

Publications on malignancy frequency in DM/PM can be found here (don't forget they have a higher baseline incidence of nasopharyngeal CA in China - it isn't the most common DM associated cancer here) and here.

THERAPY- Treat the cancer!! (If you can find it without going overboard looking!)

Involves steroids at relatively high doese for prolonged periods of time. Steroid sparing agents such as azathipone and methotrexate are also used. Guided by clinical exam/weakness rather than CK/other markers.

As steroid course will be prolonged, be sure to consider the associated side effects and posible infections including TB.

Patients with polymyositis/dermatomyositis who have interstitial pulmonary fibrosis may be at increased risk for PCP with glucocorticoids alone compared to other populations.

A review of treatment can be found here.

Atrial Fibrillation

2009-07-06T19:01:00.000-04:00

Acute management of atrial fibrillation:

First question - STABLE vs UNSTABLE?
(Instability rare if HR<150)>

Unstable if - hypotension, chest pain, altered mental status, other signs of shock

If Unstable - requires immediate synchronized cardioversion (with appropriate sedation, monitoring, etc).

If stable - consider rate control (oral or IV) with agents such as beta blockers, calcium channel blockers (Non-dihydropyridines) and amiodarone - depending on the clinical situation/contraindications.

The ACLS Tachycardia algorithim can be found here.

ANTICOUAGULATION in chronic/paroxysmal AFIB:
Initiated to prevent embolic stroke.
Risk similar in chronic vs paroxysmal AFib

CHADS2 score - used to risk stratify patients
C-Congestive Heart Failure (1point)
H-Hypertension (1point)
A-Age>75 (1point)
D-DM (1 point)
Stroke/TIA - (2 points)

CHADS2 score of 0 associated with 0.5%/year chance of stroke without coumadin
CHADS2 score >=3 associated with >5.3%/year chance of stroke without coumadin]
Patients with higher stroke risk will have greater benefit with anticoagualtion.

See the original article here.

Informed discussions should take place with patients to determine the risk/benefit of starting on anticoagulation with coumadin (target INR 2-3).

MDs are often concerned about starting anticoagulation in patients who fall. A decision analysis conducted in part by a Toronto based researcher suggested that patients with an average risk of stroke from AFib would have to fall 300 times in one year for the risk of anitcoagulation to outweigh its benefit - see article here.