CMA Driving Guidelines

In addition to the discussion below about jolt accentuation and other tests for meningeal irritation, check out the CMA's driving guidelines.

We discussed patients who have had a TIA- as you can read on this website there is no clear time period during which patients cannot drive- they need to be seen by a physician and if no neurological deficits persist can go back to driving.

Patients with a stroke should not drive for at least one month- however how long exactly depends on the physician's assessment of their deficits and risk of recurrence.

This website is a great resource as it is nearly impossible to remember all the times for every condition you will encounter. http://www.cma.ca/determining-fitness-to-drive

How are your meninges?

Today in morning report we discussed a case of a patient with fever, headache, and focal neurological signs. Those in the room were appropriately concerned about a CNS cause.
Could this patient have meningitis or something else (such as blood in subarachnoid hemorrhage) irritating his meninges?

Symptoms suggestive of meningeal irritation are: headache, neck stiffness, photophobia, cranial nerve palsies. These, in addition to fever/chills and other infectious symptoms can suggest a diagnosis of meningitis.

In meningitis, clinical history does a poor job of leading us to the diagnosis. Neck stiffness on history has a sensitivity of only 28%.

For physical exam, Kernig's and Brudzinski's signs have poor sensitivity and specificity (based on little data) for meningitis.

Jolt accentuation of headache is quite sensitive (97%) based on one study of 54 patients with fever and headache, making it a good ruling-out test if it is negative. To perform the test, ask the patient to shake their head from side-to-side at about 2-3Hz and ask them if their headache is better, the same or worse. If it is not worse, this significantly decreases the likelihood of meningitis.

It generates a positive likelihood ratio of 2.4 and negative likelihood ratio of 0.05 for CSF pleiocytosis (increased cell count). In order to use a likelihood ratio, you multiply the pre-test probability by the LR to get the post-test probability. See the image below for a visual of this calculation:

You can read more about this in the JAMA Rational Clinical Exam Article "Does This Patient Have Acute Meningitis" follow link here http://jama.jamanetwork.com/article.aspx?articleid=774331#JRC80004T4

Renal Disease in Multiple Myeloma

Today we talked about a woman with acute kidney injury in the setting of multiple myeloma. Renal impairment is seen in 20-40% of newly diagnosed patients with myeloma.

There are many ways that MM can damage a kidney:

1) Pre-renal:
- Hypercalcemia via renal vasoconstriction and volume depletion

2) Renal Glomerular:
- Amyloid deposits in glomerulus
- Light Chain Deposition Disease (LCDD)
- rarely Type 1 cryoglobulinemia

3) Renal Tubulo-Interstitial
- Tubular Cast (aggregates of light chains and Tamm-Horsfall protein) formation- "Myeloma Kidney"
- Light chain toxicity to renal tubules
- Acquired Fanconi syndrome (also a form of light chain toxicity to the proximal tubule)- usually asymptomatic but detected because of hypouricemia
- Interstitial plasma cell infiltration
- Chronic urate nephropathy

One key question is whether or not a multiple myeloma patient with renal failure requires a kidney biopsy. If light chains are high in the urine, myeloma kidney is the likely cause. In a setting where 24-hour urine collection shows nephrotic syndrome but little to no light chains, a biopsy is useful to make the definitive diagnosis of amyloid or light-chain related glomerular disease.

Tubular cast on path:

Pemphi-What?

Today in morning report we heard about a patient with probable bullous pemphigoid. The pemphigoid/pemphigus question is a favourite on exams, and it can be a little confusing remembering the differences.

Here is a system to remember the characteristics of these two autoimmune skin conditions:

Pemphigus = Serious (thank you Grace for this trick!)

Pemphigus vulgaris is more serious because:
- loss of cohesion between cells leads to acantholysis, with flaccid, easily shearable bullae (and + Nikolsky sign)-> this leads to more denuded skin and thus more infections
- involves mucous membranes

Bullous pemphigoid= tense bullae (don't always break)- see pic below

- antibodies are to basement membrane, cells can still stick together
- usually seen in the elderly

- mucosal involvement less common

Definitive diagnosis of the two conditions relies on direct immunoflorescence microscopy of a biopsy sample to see where antibodies are located (epidermal basement membrane versus cell surface).


See you tomorrow!

Lady Windermere Syndrome: Mycobacterium avium complex-related lung disease affecting the right middle lobe and lingula in older, non-smoking women. This presents as bronchiectatic and nodular disease. The paper that originally described it: http://chestjournal.chestpubs.org/content/101/6/1605.short

Welcome

Hello and welcome. I just started as the new chief resident, and am looking forward to posting some good stuff for you! Stay tuned.

Pleuritic Chest Pain - Friday April 27, 2012

Thank you to Dr. Ho-Ping Kong for hosting today’s morning report, and thank you to team 7 for bringing the case.

Today we discussed a case with a man (in his 40’s) who presented with pleuritic chest pain.  We discussed the differential diagnosis of pleuritic chest pain that gets worse when lying down and improves with sitting up:  pulmonary embolism, pneumonia, pericarditis.  Also, given the nature of his pain, pancreatitis and GERD can sometimes have these symptoms, too.  This patient also had a history of upper respiratory tract infection few weeks prior.  ECG showed changes compatible with pericarditis (with negative troponin).  These changes may include diffuse ST elevation that is concave up (except for V1 and aVR) and PR segment depression.

We attributed his pericarditis to a viral illness.  One of the common viral causes is coxsackie virus (although we really cannot prove this).  We also discussed other causes of pericarditis include:  infection (viral, bacterial, TB, rarely fungal), transmural MI, after CABG, connective tissue disease (e.g. lupus), uremia, drugs, chest wall radiation, chest wall trauma, and neoplastic disease.

As always, we also learned some medical trivia along the way.  Banting and Best treated their first patient with insulin at Toronto General Hospital, it was a patient from the United States.  When someone has pneumonia and GI symptoms (e.g. diarrhea), it is important to consider Legionella as a causative organism.

You can find out more about ECG changes of pericarditis at ECG Made Simple (linked here).  It is a very good resource for learning many things about ECG.  You can also read more about pericarditis in this article (linked here).

Thank you everyone for a great month!  I have thoroughly enjoyed working with all of you.  Chris Smith will be back Monday.

Terence Tang

Anaphylaxis - Tuesday April 24, 2012

Thank you to Dr. A. Page for hosting morning report and to team 5 for bringing a case from overnight.

We discussed the diagnosis and management of someone presenting with anaphylaxis.  The diagnosis is made by meeting one of the following minutes to hours after exposure to a likely allergen:

- skin/mucosal manifestation + 1 of shock (decreased BP), or respiratory compromise.

- Two or more of:  skin/mucosal manifestation, respiratory symptoms, hypotension, or GI symptoms.

- Hypotension after exposure of an exposure to a known allergen for that patient.

We discussed the management of anaphylaxis which include

- Securing airway

- Obtaining IV access

- Epinephrine injection (0.3 mg IM)

- IV fluid

- Benadryl (diphenhydramine) 50 mg (H1 blocker)

- Ranitidine 50 mg (H2 blocker)

- Methyprednisolone 125 mg IV

- Bronchodilators may be used

We also discussed that there can be a biphasic reaction hours after the initial episode.

We also discussed that for patients on beta-blocker, epinephrine may be ineffective, and that glucagon is needed.

You can read more about anaphylaxis here.

Grand Morning Report - Friday April 20, 2012

Thank you to Dr. Y. Patel for hosting Grand Morning Report.  Last night, we had 10 cases, but they had a few themes in common.

The first theme is GI bleeding.  We discussed that stools can be black for a number of reasons (including iron supplementation).  It is important to decide whether the patient is having melena (by a digital rectal exam) and also to elucidate the temporal relation of dark stool to other events (such as beginning of iron supplementation).  We also discussed that fecal occult blood test is meant for a screening test for colon cancer and that its utility in a bleeding patient is not tested.  We also discussed the importance of establishing good IV access.

We also discussed when to transfuse.  There is a recently published clinical practice guideline in the Annals of Internal Medicine (March 26, 2012) (linked here) on transfusion threshold for hemoglobin.  For patients who are not bleeding and stable (without ACS), transfusion threshold of 70-80 is commonly used.  However, for bleeding patient, it depends on patient stability, symptoms, whether bleeding is on-going, etc …

We then moved on to the second theme of stroke.  We discussed that there are investigations that are sometimes helpful in patients presenting with a stroke, but not necessarily in ALL patients.  We must understand the purpose of each test before ordering.  For example, an MRI brain is sometimes ordered to confirm the diagnosis of strokes (for example, in the posterior circulation).  However, if the diagnosis is already very clear (e.g. on CT imaging), this may not be necessary.  Also, echocardiogram is used to look for source for cardio-embolic stroke.  If a patient is known to have atrial fibrillation and is already anti-coagulated, and that anticoagulation is planned to continue when safe to do so, there may not be a need for an echocardiogram as it does not change management.  We also discussed that carotid endarterectomy for symptomatic carotid artery stenosis has evidence-based support.  However, the benefit for asymptomatic disease is marginal.  See this review in the Mayo Clinic Proceedings (linked here).

The latest AHA stroke guidelines can be found here.  The “2010 update on the guideline for the prevention of stroke in patients with stroke or TIA” and the “2007 Guidelines for the early management of acute ischemic stroke” may be the most relevant to those on call.

Shortness of breath on exertion and pulmonary embolism - Thursday April 19, 2012

Thank you to team 5 for bringing an interesting case.

Today, we discussed a case of a man with significant previous coronary artery disease treated with coronary artery bypass graft surgery and multiple stenting.  He has known LVEF of 20-39%.  He presented to the Emergency Department with shortness of breath on exertion.

We discussed the pertinent history features when someone presents with previous coronary artery disease.  They include previous infarctions, interventions (surgery, interventional, or medical), presence of heart failure, and functional status (CCS class).  We also discussed the reason for dual anti-platelet therapy post-stenting and the minimum duration required for this therapy.  We discussed some of the typical medical management for patients with coronary artery disease (anti-platelet, beta-blocker, ACE-inhibitor, statin).  We compared this with the medications that our patient was on.  We then generated a list of differential diagnoses for our patient, which included heart failure (exacerbation), pulmonary embolism, pneumonia, new ischemia, bleeding, and less likely obstructive lung disease, or malignancy.  We also discussed the etiologies of heart failure and its triggers.

We looked at his CXR, which showed poor inspiration (we discussed how to determine this by counting ribs), with a right-sided consolidation.  The CT thorax showed pulmonary embolism (likely not acute) and right-sided consolidation.  Five months ago, this patient had a “high probability” V/Q scan followed by a negative CT PE study at a different hospital.  The team started this patient on anticoagulation.

We then discussed the etiology of his PE.  We discussed the usual risk factors for PE such as trauma, surgery, malignancy, immobility (including travel), and thrombophilia.  We did not have enough time to discuss this thoroughly, but we did note that this patient developed new-onset microcytic anemia and that a work-up is necessary.

We did not have time to discuss diagnosis of PE with the different modalities.  There was a systematic review on the different modalities used to diagnose PE in the BMJ in 2005 [331(7511):259], linked here.  Our patient had a “high probability” V/Q scan 5 months ago at a different hospital.  The PIOPED study (JAMA 1990, linked here) studied the diagnostic accuracy of V/Q scan.  In that study, 88% of patients with “high probability” V/Q scan had PE on angiogram (gold standard for that study).

Shortness of breath in a young person - Wednesday April 18, 2012

Thank you to Dr. P. Bunce for hosting today’s morning report and to team 7 for bringing a case.

We discussed a case of a previously healthy young person who presented with shortness of breath.  We discussed a list of differential diagnoses of this problem in a young person that is different than the one we usually use for an elderly person presenting with the same complaint.  The reason we did this is given that she is previously healthy, diagnoses such as heart failure is less likely in the absence of hypertension, diabetes or coronary artery disease.  For our patient, the differential diagnoses constructed were: asthma, pneumonia, pulmonary embolism, malignancy, pregnancy, pulmonary hypertension.  We also discussed that TB is a consideration depending on risk factors and exposure history.

We then looked at her CXR and CT of thorax and it showed an anterior mediastinal mass, and pulmonary embolism.  We discussed the differential diagnoses of T’s.  Teratoma, thymoma, thyroid, and terrible lymphoma.  Occasionally, TB can also be a cause.  Tissue was obtained.

This patient also had pericardial effusion.  We discussed that pulsus paradoxus is an important physical exam maneuver in someone with pericardial effusion for the concern of tamponade.  We discussed how to do this maneuver properly.  In normal individuals, systolic blood pressure drops slightly during inspiration.  In someone with pulsus paradoxus, this drop is exaggerated.  To measure, inflate BP cuff above systolic pressure, then slowly lower to the reading where you only hear sounds NOT with every beat (but only on expiration).  This is value 1.  Then lower it very slowly, and mark value 2 when you can hear sounds with every beat.  If the difference between the 2 values is more than 10, then that is abnormal.  Dr. P. Bunce has mentioned a figure from UpToDate and it is linked here (via U of T Library).

Hemochromatosis and Febrile Neutropenia - Tuesday April 17, 2012

Thank you Dr. A. Page for hosting morning report and to team 8 for bringing a fascinating case.

Today, we discussed a patient with hemochromatosis and many of its complications including liver cirrhosis, heart failure, diabetes, hypothyroidism, and hypogodnadism.  This patient was also started on oral iron chelation therapy (deferiprone) and presented with febrile neutropenia with a 1-day history of fever, malaise, dry cough, enlarged cervical lymph nodes, dysphagia, and rash on trunk.

We first discussed hemochromatosis as an autosomal recessive genetic disease (most common mutation is C282Y on the HFE gene) that results in iron overload.  Patients have high iron saturation (>45%) and high ferritin.  Genetic testing is done for diagnosis in the presence of iron overload.  Iron deposits can cause dysfunction in many organs including liver, heart, pancreas (diabetes), skin, gonads, and joints.  Main treatment is phlebotomy and/or iron chelation (which our patient is on).

We discussed the etiology of the patient’s neutropenia is likely secondary to deferiprone (known to cause agranulocytosis).  We also discussed other causes of neutropenia including bone marrow suppression from infection or drugs (e.g. levamisole, chemotherapy, …), nutritional deficiency, and infiltration of bone marrow.  He would be treated like any other patients with febrile neutropenia requiring empiric broad-spectrum antibiotics coverage until organism/source identified and/or recovery of neutrophil counts.

We also discussed the presentation of dry cough, enlarged lymph nodes, dysphagia, and malaise.  While a non-infectious cause (e.g. lymphoma) is possible, the onset is quite rapid.  We focused our discussion on infectious causes that included:  bacterial (group A strep, Arcanobacerium haemolyticum), viruses (HIV, hepatitis, EBV, CMV, Measle, Parvo virus), fungal disease (mucormycosis, less likely Candida), and TB.  We also discussed some syndromes involving infection of the head and neck area including Ludwig’s Angina, Lemierre’s syndrome (septic thrombophlebitis, most common Fusobacterium), and Vincent angina.

You can read more about hemochromatosis here.  There is one study, quoting the rate of agranulocytosis and neutropenia at 0.2 and 2.8 per 100-patient-year while on deferiprone (Cohen AR et al. Blood 2003.  102(5):1583-7; link here).