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).