Sweet Misery

Feb 28 2020

Today we presented our teaching activity to our fellow clerks on selectives. The topic I chose for my teaching session was Hyperglycemic Crises, reviewing the presentations, laboratory findings, and management of DKA and HSS. For the session, I wanted to use some of the strategies I had learned while doing the Student as Teachers program in second year medical school, as well as incorporate some new strategies I had learned from preceptors.

• Case-based: I have always enjoyed lectures and seminars with cases and thus wanted to make my teaching session case-based.  I find that case-based learning not only allows you to think critically through a case and build your knowledge, but also really engages the learners.
• Probing rationale: In a training session for an upcoming teaching activity I am involved in, we learned about probing the rationale of learners. When a learner gives an answer, it is useful to ask why they gave that answer., probing them further. This can help deepen their understanding and lead to further discussions.
• What if questions: In discussing my teaching project with Dr. C, he also suggested using "what if" questions to present variations on a case, encourage students to think differently, and enhance learning.

Overall, I think the teaching session today went well. The learners said that they enjoyed the interactive nature of the session, and the variations on the case helped solidify their learning. From the feedback of the learners and staff observing us, I also learned many strategies on how to improve my teaching for the future.

• I want to limit the amount of information I have on a slide. Learners can sometimes focus on reading the text on the slide, rather than listen to you talk. Instead, I will focus on just the key information on the slide, expanding more when I talk.
• In general, I will avoid covering too much material in a teaching session. I have the tendency to want to cover as many learning points, however this can lead to information overload for the learner.
• I also want to work on even further engaging learners during a talk. In small group sessions, if the learners are talking more than the teacher, that is often a good sign. I learned about other strategies that can be used to engage learners, such as online polling/answering tools.

I also saw the value that clinical experience adds to being an effective teacher. When building my teaching session, I referenced guidelines and resources such as UptoDate for information regarding presentation and management plans. However, in discussing with the staff, we learned how the guidelines sometimes differ from clinical practice. For example, although guidelines state to treat hypokalemia in DKA once the potassium level is less than 3.3 mmol/L, the staff explained that they would often start oral and IV potassium supplementation along with insulin once the potassium is below 4.0 mmol/L. Being able to have the perspective of experienced staff helped to enhance my understanding, and highlighted the differences between guidelines and practice.

I really enjoyed this teaching experience! It allowed me to try out some new teaching strategies, as well as learn ways to improve in the future. I want to be involved in teaching and medical education in my future career and look forward to improving my teaching skills as I move along in my training.

-MB-

Teaching Dermatology in Internal Medicine

February 28, 2020

After spending the past few weeks planning for my teaching exercise, the day had finally arrived where I would have the opportunity to lead a 30-minute session on dermatology in internal medicine to our fellow clerks. I decided on this topic because I felt that this is an area that we spend very little formalized curriculum time on (~ 1 week) and an area that people often feel uncomfortable with due to our limited experiences. The goal of my teaching exercise was to raise awareness about dermatological manifestations related to internal medicine conditions as there can be many cutaneous clues if one were to look for it on inspection. 

I approached this teaching session using a mixed approach involving didactic teaching and case-based learning with interactive components. 

I began the presentation with an overview of basic morphology to describe cutaneous lesions:

Then we went through a mini-quiz to describe various lesions. (However, I should have made sure to include dimensions for each lesion because it is challenging to tell on screen). 

Next, I went through 2 cases involving erythema nodosum. The first case was about sarcoidosis. This gave me an opportunity to have a discussion about sarcoidosis, Lofgren syndrome, and lupus pernio. The second case was about IBD. There are a lot of extra-intestinal manifestations of IBD but the two cutaneous ones that I covered were erythema nodosum and pyoderma gangrenosum. I brought up pyoderma gangrenosum because it can be easily mistaken to be infectious in etiology but it is actually inflammatory.  I then reviewed erythema nodosum, including its differential diagnoses, work-up, and management.

Reflecting on this experience, I realized that I tried to condense too much information into such a short-time period. If I were to do this again, I would have made just focused on erythema nodosum and the work-up for it, including the sensitivities and specificities for certain tests. I would have eliminated dermatological manifestations of internal malignancy all together. I would also summarized the information with a jeopardy format or have a pre- and post- mini-quiz to reflect on their learning. 

-JT-

Reference(s):
1. https://dermnetnz.org/
2. https://aad.org
3. Diagnosis and management of sarcoidosis. https://www.aafp.org/afp/2016/0515/p840.html
4. Erythema nodosum. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918049/
5. Erythema nodosum as a presentation of inflammatory bowel disease.        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1174850/

Short of breath

February 27, 2020

I spent this week following an elderly man who was recently discharged from the GIM ward for an upper gastrointestinal bleed due to an duodenal ulcer. He was referred to us for management of his shortness of breath.

Given that his shortness of breath only recently began within the past month, I attributed this to secondary to his anemia from his UGIB. However, we had to rule out other causes including CHF exacerbation and potentially COPD due to his smoking history. As such, we had ordered a chest x-ray and BNP which were negative. We also arranged for him to have a PFT. I also spent some time thinking about how I would best manage his symptomatic anemia. His most recent Hb was 86. Looking at the guidelines, a transfusion would be warranted to achieve a target Hb of >70, but a target Hb > 80 can be aimed for if he has coronary artery disease. At this time, it does not seem like he qualifies for a transfusion. There were also logistical things that would need to be arranged if he needed an outpatient transfusion. In order to get a transfusion, we would have to put in a referral to Women's College Hospital for this to be done as an outpatient. Fortunately, it seems this his SOB appears to be improving as his Hb is recovering.

This was a memorable case for me because I had the opportunity to follow him longitudinally over the past 2 weeks. I think longitudinal exposure to a patient's course of illness really allows the learning to settle in as you have can have the time to reflect on your medical decision making and see how it directly impacts your patient's outcomes.

This encounter also made me reflect on what it is like to care for patients with limited English proficiency. Although my patient did not speak English, I was fortunate to be able to communicate with him in my native language. Dr. Rawal recently had a talk during rounds about this topic as their is significant health disparities between patients who can speak English and those who cannot. Someone shared the experience of how a non-English speaking patient was diagnosed with COPD exacerbation and unfortunately the patient actually was having a NSTEMI but nobody had taken the time to communicate with this patient because of the "language barrier."

-JT-

Reference(s):

Barkun, A. N., Bardou, M., Kuipers, E. J., Sung, J., Hunt, R. H., Martel, M., & Sinclair, P. (2010). International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Annals of internal medicine, 152(2), 101-113.

Villanueva, C., Colomo, A., Bosch, A., Concepción, M., Hernandez-Gea, V., Aracil, C., ... & Guarner-Argente, C. (2013). Transfusion strategies for acute upper gastrointestinal bleeding. New England Journal of Medicine, 368(1), 11-21.

Harvey and murmurs

February 27, 2020

We had two Harvey teaching sessions this week, which I found to be incredibly valuable to my learning. Harvey functions as a high-fidelity simulator, which can be applied to teaching the cardiac physical exam. Learning in a small group with a facilitator to walk us through the different murmurs and then applying it to difference case scenarios really allowed me conceptualize murmurs.

I was really surprised by how much I retained from these Harvey sessions. During my cardiology clinic, I was able to appreciate a few murmurs including physiological S2 and severe regurgitation. I was also able to apply my knowledge in differentiating the different types of murmurs.

I would say that the 2 main ones that I focused on were:
1) aortic stenosis: systolic murmur, aortic area, crescendo-decrescendo, radiates to clavicles
2) mitral regurgitation: systolic murmur, holosystolic, radiates to axilla


I spent some time reading the literature around Harvey as a teaching tool. Interestingly, the article by Humphrey-Murto (2019) suggests that there are no differences between using Harvey and a standardized patient (SP) in teaching medical students physical examination skills but that the SP group had an improved ability at coming to a unifying diagnosis. Personally, I think that using both SP and Harvey would be of great value to medical students. I think it would be challenging to be able to get SPs for all the different types of murmurs that Harvey is able to reproduce. There are limitations to Harvey however that one must acknowledge and that it does not replace real life experiences.

-JT-

Reference(s):
Gauthier, N., Johnson, C., Stadnick, E., Keenan, M., Wood, T., Sostok, M., & Humphrey-Murto, S. (2019). Does Cardiac Physical Exam Teaching Using a Cardiac Simulator Improve Medical Students’ Diagnostic Skills?. Cureus, 11(5).

Feeling the Pressure

Feb 26 2020

In the GIM clinic today, I saw a patient who was been followed for findings of elevated RVSP on echocardiogram. He had symptoms of dyspnea with exertion, but was otherwise asymptomatic. We questioned the presence of pulmonary hypertension, however had no clear cause based on his current presentation and investigations. I always have difficulty remembering the classification for pulmonary hypertension, and so this was a great opportunity for me to review this topic.

Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure ≥ 25 mmHg. Clinically, PH is a pathophysiological disorder that may involve multiple clinical conditions. The WHO classification describes 5 groups of pulmonary hypertension:

• Group 1: Pulmonary artery hypertension (PAH). This develops due to an occlusive vasculopathy of the pulmonary arterioles, which may be idiopathic or associated with several disease states. Commonly associated conditions include: connective tissue diseases (scleroderma, lupus), congenital heart disease, portal hypertension, HIV or schistosomiasis infections, and drugs.
• Group 2: PH due to left heart disease. This develops due to chronically elevated left atrial pressure, which causes PH by a passive retrograde transmission of pressure. Causes include left ventricular systolic/diastolic dysfunction, and aortic or mitral valve disease.
• Group 3: PH due to lung diseases and/or hypoxia. This develops in patients with lung disease (COPD, interstitial lung disease), sleep disordered breathing, or other abnormalities of blood gases (hypoventilation, high altitude). Hypoxic pulmonary vasoconstriction (a normal physiologic response), loss of pulmonary capillary cross-sectional area, and pulmonary vascular remodeling can all be contributing factors.
• Group 4: Chronic thromboembolic PH. Approximately 3% of patients with acute pulmonary embolism go on to develop obstructive pulmonary arterial remodeling resulting in PH. These patients are often found to have an underlying thrombophilic disorder.
• Group 5: PH with unclear and/or multifactorial mechanisms. This is a diverse group of PH etiologies. Hematologic disorders (such as chronic hemolytic anemia), systemic disorders (such as sarcoidosis), metabolic disorders (such as glycogen storage diseases), and others may cause PH by unclear and/or multifactorial mechanisms.

For our patient, there was no obvious explanation for his elevated RVSP. He had no history of conditions associated with Group 1 PH, such as connective tissue disease, congenital heart disease or past infections, however could still have idiopathic PAH. His exam and echocardiogram showed no evidence of left ventricular or valvular disease, ruling out Group 2. There was no history of PE or thromboembolic disease, and no evidence of any systemic diseases, excluding Groups 4 and 5. We decided to send him for pulmonary function testing to assess for any underlying lung disease for Group 3 PH. His PFT will also determine his DLCO which will help in the diagnosis (DLCO is reduced in PH and an isolated reduction in DLCO is a typical finding in Group 1 PH). This case allowed me to gain a better understanding of pulmonary hypertension, the various classifications, and how to approach a patient with PH in the future.

-MB-

References:

1. Simonneau G, Gatzoulis MA, Adatia I, et al. Updated Clinical Classification of Pulmonary Hypertension. Journal of the American College of Cardiology 2013; 62(25): 35-41.

Pulsus Paradoxus

Feb 25 2020

Today in Cardiology clinic, I was preparing to see a patient who had a history of pericardial thickening, among other cardiac issues. Before going in for my assessment, my preceptor reminded me to screen for any symptoms of constrictive pericarditis and to examine for the presence of pulsus paradoxus. I took a moment to review the significance of pulsus paradoxus and how to perform this measurement.

Pulsus paradoxus refers to an exaggerated fall in a patient's blood pressure during inspiration by greater than 10 mmHg. It is caused by changes in the mechanical forces imposed on the chambers of the heart and pulmonary vasculature. The exact pathophysiology is quite complex and varies depending on the etiology, with several mechanisms involved. Pulsus paradoxus is often associated with pericardial disease, often cardiac tamponade and to a lesser extent constrictive pericarditis. However this finding can also been seen in non-pericardial diseases (such as right ventricular MI, restrictive cardiomyopathy), as well as non-cardiac diseases (severe COPD, asthma, tension pneumothorax).

Pulsus paradoxus is measured using a manual sphygmomanometer and stethoscope. Assessment is made by inflating the cuff until the Korotkoff sounds are absent. The cuff is than deflated very slowly. The first sounds auscultated will be heard only during expiration, and this pressure should be noted. As the cuff pressure is dropped further, the pressure when Korotkoff sounds are heard during both inspiration and expiration should be noted. The variation between these 2 systolic pressures is what quantifies pulsus paradoxus. Pulsus paradoxus can also be quantified by an invasive arterial measurement.

An important tip when assessing for pulsus paradoxus is to ensure the patient is breathing normally. Do not instruct them to change their breathing pattern as the depth of respiration influences the magnitude of pulsus paradoxus!

In the end, there was no finding of pulsus paradoxus in our patient and she had no clinical symptoms of pericardial disease. This was a great opportunity to review the significance of this physical exam finding and practice performing it in a real-life setting!

-MB-

References:

1. Van Dam MN, Fitzgerald BM. Pulsus Paradoxus. [Updated 2019 Jun 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.

Thrombocytopenia

February 21, 2020

In the GIM clinic today, I had a middle-aged patient referred for assessment of his incidental thrombocytopenia. 

My takeaway for an approach to thrombocytopenia is as follows:

• Etiology
• Decreased production of platelets
• Bone marrow suppression - e.g. methotrexate, alcohol, MDS, aplastic anemia
• Increased consumption/destruction of platelets
• Hematological - DIC, TTP, HUS
• These are particularly important to rule out
• Autoimmune - ITP (idiopathic thrombocytopenic purpura), Evan's syndrome
• Drug-induced - e.g. heparin (HIT), anti-convulsants
• Infectious - hepatitis C, HIV
• Sequestration in spleen
• Splenomegaly due to increased portal hypertension (e.g. cirrhosis)
• History
• Symptoms
• Bleeding
• Mucosal - epistaxis, gum bleeding, GU bleeding
• GI bleeding - hematemesis, BRBPR, and melena
• Bruising
• Rashes - particularly purpura and petechiae
• Risk factors
• Drug-related - e.g. heparin, anticonvulsants, antibiotics
• Malignancy, sepsis, cirrhosis
• Physical
• General
• Mucosal bleeding
• Bruising and rashes - petechiae, purpura
• Stigmata of liver disease
• Neuro: 
• Mental status 
• HEENT:
• lymphadenopathy
• Abdominal
• Assess for hepatosplenomegaly
• Investigations:
• CBC to monitor platelets but also assess for anemia
• Peripheral blood smear
• Consider 
• DAT to rule out hemolytic anemia
• hepatitis C and HIV serologies
• Management 
• Transfusion if platelets <10 or <50 for certain surgeries (in general)
• Immune suppression: IVIG +/- steroids, rituximab
• Consider splenectomy
• Treat underlying cause - e.g. discontinue heparin

My patient likely has a transient mild thrombocytopenia secondary to a viral infection or secondary to his use of anti-convulsants or PPI. I also recently found out about the importance of using a PPI for prophylaxis when using high-dose steroids. 

-JT-

Reference(s):

https://ashpublications.org/bloodadvances/article/3/23/3829/429213/American-Society-of-Hematology-2019-guidelines-for

Refractory hypertension

February 18, 2020

I had a patient today who was referred to the hypertension clinic for management of her refractory hypertension on 5 medications. This 50-something year old female patient was diagnosed with hypertension over 25 years ago after developing pre-eclampsia. She was on an ACE inhibitor, beta-blocker, calcium channel blocker, thiazide-like diuretic, and triamterene (potassium-sparing diuretic). Her past medical history also includes diet-controlled diabetes and dyslipidemia which were all at target. Interestingly, when I saw her, she was tapered down to 2 medications (ACE inhibitor and beta-blocker) as her blood pressure has been within target of 130/80 (given her diabetes). Upon further inquiry, she reports that the only change she's had since her referral is weight loss of about 10 kg. It is uncertain if she has had any work-up for secondary causes of her hypertension.

Looking into the literature, it seems that weight loss can have significant impact on blood pressure.

• "The Framingham Study found that hypertension is about twice as prevalent in the obese as the nonobese of both sexes." (Harsha, 2008)
• The Trial of Hypertension Prevention (TOHP), one of the largest of these studies, included a weight loss intervention arm.30 In this instance, a 2-kg loss in weight over a 6-month period resulted in a decline of 3.7 mm Hg in systolic and 2.7 mm Hg in diastolic blood pressure (Hypertension Prevention Trial Research Group, 1990)

This case highlights to me the importance of counselling patients on lifestyle modifications. For diet,  would recommend looking into the DASH (Dietary Approaches to Stop Hypertension).

-JT-

Reference(s):

Harsha, D. W., & Bray, G. A. (2008). Response to Weight Loss and Blood Pressure Control: The Pro Side. Hypertension, 51(6), 1420-1425.

Hypertension Prevention Trial Research Group. (1990). The Hypertension Prevention Trial: three-year effects of dietary changes on blood pressure. Archives of Internal Medicine, 150(1), 153-162.

https://www.heartandstroke.ca/get-healthy/healthy-eating/dash-diet

Can't Catch a Breath

Feb 21 2019

I spent the day in the Asthma and Airway Clinic today and had the opportunity to see several different bread-and-butter respirology cases, including COPD, asthma, and occupational-related lung diseases. During the morning, I saw a patient that had been referred for a possible diagnosis of COPD. He had experienced progressively worsening dyspnea over the last few years, and described feeling that he could not "catch enough air in a breath". The patient had a significant smoking history, as well as long-term exposure to occupational irritants in his work in construction. Although he had no history of asthma, he remembered being prescribed puffers in the past. His pulmonary function testing showed an obstructive pattern with no significant bronchodilator response. In discussing this case with my preceptor, we were quite certain this patient had COPD. However, my staff also raised the possibility of asthma-COPD overlap given some of his other characteristics.

Asthma-COPD overlap (ACO) is the presence of clinical features of both asthma and COPD, and is often not well recognized. There have been many different definitions of ACO over the years and thus the prevalence is difficult to determine exactly. The COPDGene study used the co-existence of diagnostic codes of asthma and COPD in the clinical history of the same patient and found a prevalence of 13% of this overlap. The study also found that asthma-COPD overlap was associated with an increased risk of exacerbations and hospitalizations (1). The Global Initiative for Chronic Obstructive Lung Disease (GOLD) developed a consensus document proposing that in order to diagnose ACO, 3 characteristics of asthma and 3 of COPD (taken from a list) should be fulfilled (2). In any case, numerous studies have demonstrated that ACO is a heterogenous disorder.

Management of ACO is challenging since these patients are often intentionally excluded from clinical trials. In addition, the heterogeneity of this syndrome makes it difficult to have a single approach to the management of all patients. General non-pharmacologic principles of management are not unlike those for COPD and asthma and include: smoking cessation, up-to-date vaccinations, proper inhaler technique, avoidance of allergens, and pulmonary rehabilitation. In terms of pharmacotherapy, all patients with ACO should have access to a rapid-acting inhaled bronchodilator (SABA, SAMA or combination) for as-needed symptom relief. Regular therapy with an inhaled corticosteroid is important in these patients. The addition of a long-acting beta-agonist (LABA) or long-acting muscarinic antagonist (LAMA) may be necessary to help adequately manage symptoms. Therapy can be escalated to help maintain control of symptoms. An important principle of ACO management is to avoid LABA monotherapy without inhaled corticosteroids.

Through this case, I was able to learn more about the complex entity of asthma-COPD overlap and will keep this diagnosis in  mind when I see patients that have features consistent with both of these conditions!

-MB-

References:

1. Hardin M, Silverman EK, Barr RG, et al. The clinical features of the overlap between COPD and asthma. Respir Res 2011; 12(1): 127-135.
2.  Vogelmeier CF, Criner GJ, Martinez FJ, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report: GOLD executive summary. Arch Bronconeumol 2017; 53: 128–149. 

AKI on CKD

February 21, 2020

In the GIM clinic today, I saw an elderly patient for follow-up of her acute kidney injury on chronic kidney disease due to initiation of Lasix for management of CHF.  She had a creatinine rise from 140s to 200s. Her creatinine clearance was less than 30. As she was euvolemic on exam, she was discontinued off her Lasix. Her ACE inhibitor and SGLT2 inhibitor were also temporarily discontinued.

After reading more about diabetes medications for renal insufficiency, I would have switched her from sitagliptin to linagliptin instead of fully discontinuing this as she would benefit from better blood glucose control given that her A1c was not at target.

As a big fan of mnemonics, one of the ones that I often go to when counselling patients about sick day medications is SADMANS:

S: sulfonylureas
A: ACE inhibitors
D: diuretics
M: metformin
A: ARBs
N: NSAIDs
S: SGLT2 inhibitors

-JT-

Reference(s):
https://www.diabetes.ca/DiabetesCanadaWebsite/media/Health-care-providers/2018%20Clinical%20Practice%20Guidelines/Appendix-8-sick-day-medication-list.pdf?ext=.pdf

https://guidelines.diabetes.ca/cpg/chapter13

https://care.diabetesjournals.org/content/31/Supplement_2/S194

Learning about POTS

Feb 19 2020

We saw a new referral in the Cardiology clinic for a woman who had been experiencing episodes of presyncope as well as intermittent palpitations for the past year. After reviewing and discussing her case, we considered the various possible causes for her symptoms. My staff mentioned the possibility of postural orthostatic tachycardia syndrome (POTS). I had never heard of this entity before and decided to do some further reading on the topic (1,2).

POTS is a condition characterized by insufficient blood return to the heart when moving from a lying to standing position. This orthostatic intolerance causes light-headedness and presyncope that can be eased by returning to the lying position. The hallmark of this disorder is an exaggerated heart rate increase in response to postural change - hence the name postural orthostatic tachycardia syndrome.

Epidemiology:

• It is the most prevalent form of orthostatic intolerance.
• It is commonly seen in younger patients between the ages of 15-50, and most commonly in women, with a female to male ratio of 4-5:1.

Etiology:

• The exact cause is unclear and many mechanisms have been proposed, including distal denervation, hypovolemia, changes in venous function, increased sympathetic activity, and more.

Symptoms:

• Patients report light-headedness, weakness, blurred vision, and fatigue upon standing. Other orthostatic symptoms experienced include palpitations, shakiness and anxiety.
• GI symptoms such as nausea, bloating, early satiety, constipation have also been observed.
• Syncope is less frequent but does occur in about 40% of patients.

Diagnosis:

• Diagnosis can be made by looking for an exaggerated increase in heart rate on tilt table testing or standing. Diagnostic criteria states a sustained heart rate increase of > 30 beats per minute or an increase to 120 bpm or greater within the first 10 minutes of tilt.
• There may be an increase in venous plasma norepinephrine levels at rest and with standing (>600 ng/mL), however the sensitivity and specificity of this is unknown.
• It is otherwise a diagnosis of exclusion.

Treatment:

• Goal of treatment is to improve circulatory problems that may be causing POTS, however no treatment has been systematically studied.
• In some patients, lifestyle changes such as increasing salt intake, drinking more fluids, exercising, and avoiding exacerbating factors, may improve symptoms.
• Some studies have shown benefit in using fludrocortisone (most effective when combined with increased salt and water intake). Midodrine has also been shown to be associated with improved symptoms and heart rate. 

Prognosis:

• Most patients have a good prognosis with improvement in their symptoms at the 1 year follow-up.

This patient did have several features in her history consistent with POTS. On physical exam, she had an increase in her heart rate of 20 beats upon standing, however it did not meet the cut off of a 30 bpm increase. Although we are not certain this patient has POTS and have ordered other investigations to rule out other diagnoses, it was an excellent opportunity to think critically through an interesting case and learn about a new syndrome!

-MB-

References:

1. Kaufmann H, Freeman R, Aminoff MJ (Ed.). Postural tachycardia syndrome. UpToDate. Accessed February 19, 2020 from: https://www-uptodate-com.myaccess.library.utoronto.ca/contents/postural-tachycardia-syndrome
2. Postural orthostatic tachycardia syndrome. Genetic and Rare Diseases Information Center. Accessed February 19, 2020 from: https://rarediseases.info.nih.gov/diseases/9597/postural-orthostatic-tachycardia-syndrome.

A bicuspid valve with double the issues

Feb 18 2020

This morning in clinic I saw a patient with a bicuspid aortic valve who was being followed for mixed aortic valvulopathy, with both moderate aortic stenosis and aortic regurgitation. Although I had seen patients in the past with either aortic stenosis or aortic insufficiency, I had not come across a case where the patient had both types of valvular disease. Before I went into the room, I thought about the questions I would ask to assess the patient's symptomology and what to look for on physical exam.

Patients with bicuspid aortic stenosis and bicuspid aortic regurgitation may remain asymptomatic for prolonged periods of time (1,2). In severe aortic stenosis, the classic symptoms are angina or chest discomfort, syncope, and dyspnea - the latter being associated with a worse prognosis. Severe aortic regurgitation can present with atypical chest pain, palpitations, and dyspnea.

In terms of the physical exam, a functionally normal bicuspid aortic valve produces a ejection click best heart at the left lower sternal border and may be accompanied by a short ejection murmur (1). When valve disease is present, the characteristics of the murmur depend on the severity of disease. With progressive aortic stenosis, the systolic ejection murmur becomes harsher and later peaking. In severe AS, the second heart sound becomes soft, pulsus parvus et tardus (weakened and delayed carotid upstroke) may be palpated, as well as a radial-brachial delay. The murmur of aortic regurgitation is a diastolic decrescendo murmur heard best at the left lower sternal border. When the AR murmur is loudest at the right sternal border, a dilated ascending aorta may be present, which warrants further investigation. With chronic severe AR, a variety of physical findings caused by the wide pulse pressure may be seen. A few examples are (3):

• Corrigan pulse: the rapidly rising and falling arterial pulse with a wide pulse pressure leads to a "water hammer" pulse; felt by palpating the radial or brachial arteries.
• De Musset's sign: a head bob with each heartbeat.
• Quincke's pulses: capillary pulsations in the fingertips or lips.
• Mueller's sign: systolic pulsations of the uvula.

In reading further about mixed aortic valve disease (MAVD), it appears that although current valvular heart disease guidelines provide well-validated parameters for following patients with isolated valvular heart disease, the data on the outcomes and appropriate follow-up of patients with combined stenotic and regurgitant valve lesions is more limited. A study by Egbe et al found there were high rates of adverse events associated with MAVD, comparable to those in severe isolated AS (4). Based on their findings, they recommended patients with severe MAVD be evaluated at least every 6 months. They also found that 50% of the patients became symptomatic and required an aortic valve replacement within 1 year. Thus, patients with MAVD should be considered seriously and monitored carefully.

This case allowed me to review the presentation and features of 2 common valve diseases, as well as learn more about bicuspid aortopathy. During the clinic, I had a stimulating discuss of the case with my preceptor and also had the opportunity to receive some valuable bedside teaching as we examined the patient. Intrigued by the case, I was able to do some further reading at home, helping to consolidate what I learned and also read about some new areas!

-MB-

References:

1. Braverman AC, Silversides C (Ed). Clinical manifestations and diagnosis of bicuspid aortic valve in adults. UpToDate. Accessed February 18, 2020 from: https://www-uptodate-com/clinical-manifestations-and-diagnosis-of-bicuspid-aortic-valve-in-adults
2. Unger P, Pibarot P, Tribouilloy C, et al. Multiple and Mixed Valvular Heart Disease. Circ Cardiovasc Imaging 2018; 11: 1-13.
3. Gaasch WH, Otto CM (Ed). Clinical manifestations and diagnosis of chronic aortic regurgitation in adults. UpToDate. Accessed February 18, 2020 from: https://www-uptodate-com/clinical-manifestations-and-diagnosis-of-chronic-aortic-regurgitation-in-adults
4. Egbe AC, Peterucha JT, Warnes CA. Mixed Aortic Valve Disease: Midterm Outcome and Predictors of Adverse Events. Eur Heart J 2016; 37(34): 2671-2678.

Secondary hypertension

February 11, 2020

During my GIM clinic, I saw a variety of patients in the longitudinal and rapid referral clinics.

After discussing with my team and reviewing the literature, I came away with the following general approach to secondary hypertension:

• Vascular
• Renal artery stenosis, fibromuscular dysplasia, coarctation of aorta
• Endocrine
• Cushing's
• Pheochromocytoma
• Hyperaldosteronism
• Hyper/hypothyroidism
• OSA
• Substance-induced
• Drugs: corticosteroids, OCPs, tacrolimus, cyclosporine, recreational (e.g. cocaine)
• Black licorice, caffeine, smoking, alcohol

In order to reduce unnecessary testing for secondary hypertension, it is important to do a thorough history and physical. For the history, a drug and substance use history can be quite significant. For the physical exam, I would like for features of the commonly associated endocrinopathies as well as auscultate for renal bruits.

-JT-

Reference(s):
https://guidelines.hypertension.ca/diagnosis-assessment/renovascular-hypertension/

https://guidelines.hypertension.ca/prevention-treatment/hypertension-endocrine-causes/

"Asthma"

February 14, 2020

During my respirology clinic, I had the opportunity to review many bread and butter cases of respirology including asthma and COPD. One of the patients that I saw today was an elderly patient who was referred to us for management of her "asthma" as she was experiencing shortness of breath. She reports a long-standing history of asthma since her childhood, which at some point had resolved and had in the past few years returned. She is a non-smoker. Her pulmonary function test did not show any evidence of obstruction or reversibility with bronchodilators. Instead, it showed evidence of restriction. On clinical exam and review of her chest x-ray, she has significant kyphosis which seems to be a large contributor to her restrictive lung disease. Looking at her CT spine, we were able to see some honeycombing in her lungs, which may suggest some type of interstitial lung disease. As such, decided to send her to get a high-resolution CT scan of her lungs for further work-up.

This encounter reminded me of the importance of getting the proper diagnosis even though a patient may have a clinical history that seems suggestive of asthma. We also recommended that she discontinue her puffers as she does not have any indication for its use and there can be side-effects despite it being considered relatively benign to the general public. She had been prescribed a long-acting cholinergic because at some point she was though to have COPD. A rare but serious side-effect is this is paradoxical bronchospasm. In someone with poor lung function, this can be fatal.

One of the interesting learning points is the option of using Symbicort as a single inhaler for both maintenance and rescue therapy given its fast onset of action (D'Urzo 2006). This may promote better adherence due to the simplicity of using a single inhaler rather than using an additional SABA (e.g. Ventolin) for rescue therapy.


-JT-

Reference(s):

D’Urzo, A. D. (2006). Inhaled Glucocorticosteroid and Long-Acting β 2-Adrenoceptor Agonist Single-Inhaler Combination for Both Maintenance and Rescue Therapy. Treatments in respiratory medicine, 5(6), 385-391.

Matters of the Heart

Feb 13 2020

Today in the Cardiology Clinic, I saw a patient who was being followed for his valvular disease and had undergone a transcatheter aortic valve replacement (TAVR) a few years ago. He had recently developed worsening symptoms of dyspnea and orthopnea which had actually led him to be hospitalized. His presentation was consistent with congestive heart failure and after responding to diuresis, he was sent home with a new prescription for furosemide. His echocardiogram done in hospital showed normal left ventricular systolic function, and no issues with his aortic valve prosthesis.

Today in clinic, his symptoms were much improved, although his exam still demonstrated signs of fluid overload. In reviewing his case, my preceptor helped guide me through the rationale for his new onset symptoms of heart failure. I realized that although the patient had undergone a valve replacement for his aortic stenosis, the reality is that his heart had been subjected to several decades of high afterload conditions as a result of his obstructive valve disease. In response to this increased afterload, his heart had undergone concentric remodelling and hypertrophy over the years. This was now causing diastolic dysfunction and leading to his symptoms of heart failure.

Knowing the physiologic changes causing his presentation, the key principles for acute management of his impaired diastolic function also become clear. Namely we had to 1) reduce his ventricular rate, using a beta-blocker, to help prolong diastolic filling time and 2) relieve his volume overload, using a diuretic, to help reduce preload. Longer term management options also included treatment of any underlying atrial fibrillation, controlling any hypertension, and use of ACEi/ARBs and aldosterone antagonists to regress left ventricular hypertrophy and optimize circulating volume.

By analyzing the physiology of his disease, I was able to understand what had led to his current presentation, as well as determine the most effective treatment options. I really appreciated that my preceptor encouraged me to explain my thinking process and work through this case. With his guidance, I was able to more fully grasp the case and gained a fulfilling learning experience.

-MB-

A Closer Look at Clubbing

Feb 12 2020

I saw a patient in clinic today referred from the emergency department for worsening dyspnea. This elderly gentleman had been experiencing shortness of breath on exertion for several months (and likely longer) which had become progressively worse. He did have a significant smoking history and potential history of workplace exposure to paints. In terms of associated symptoms, he denied any symptoms of cough or sputum production, had no symptoms of heart failure, and no infectious symptoms. He did note some unintentional weight loss in the past few months despite no changes in his diet or appetite. My initial physical exam for him was relatively unremarkable, although his respiratory exam showed slightly decreased air entry at the bases but no adventitious sounds. His investigations were notable for a venous blood gas showing a pattern consistent with chronic respiratory acidosis with a compensatory metabolic alkalosis. Given his presentation, smoking history and VBG, we were quite suspicious for COPD. After presenting the case to my preceptor and discussing our plan, she asked if I had examined him for clubbing, which I had forgotten to do.

When we returned to the room, we went over his respiratory exam and took some time to look at his nails. Indeed, the patient did have many features consistent with clubbing! Surprisingly, this was the first time I had seen features of clubbing in a patient. My preceptor carefully showed me the various ways to assess for clubbing. We examined the distal curvature of his nail, the nail-fold angle, the phalangeal depth ratio (comparing the distal phalangeal depth with the interphalangeal depth) and felt the pulp of his distal finger. I really appreciated the time my preceptor took to go over these details of the physical exam. As medical students we often just use the Schamroth sign to assess for digital clubbing, since it is a relatively quick way to qualitatively assess for clubbing. Although a study did show Schamroth sign was a reasonable way to assess for clubbing, having good concordance with other methods (Pallares-Sanmartin A et al., 2010), there are many other more quantitative measures to assess for clubbing. I also realized how going back to the basics of pre-clerkship and following the order of careful inspection, percussion, palpation and auscultation in the physical exam allows us to capture details which can be so telling!

After noting the findings of clubbing, we also reviewed which conditions are associated with this finding and built our differential. Although I remember being taught to look for clubbing in COPD patients, COPD itself is actually not a cause of clubbing. I use the mnemonic "CLUBBING", which I find helpful, to remember some of the diseases associated with clubbing:

• C: cyanotic heart disease, cystic fibrosis
• L: lung cancer, lung abscess
• U: ulcerative colitis
• B: bronchiectasis
• B: benign mesothelioma
• I: infective endocarditis, idiopathic pulmonary fibrosis
• N: neurogenic tumors
• G: gastrointestinal disease (biliary cirrhosis, celiac)

In this patient, it is possible he has underlying bronchiectasis or perhaps a malignancy contributing to his clubbing, in addition to a diagnosis of COPD. We have ordered PFTs and a CT chest to help elucidate the etiology of his dyspnea (and clubbing) and will see him again in clinic afterwards. This experience taught me the various ways to assess for clubbing and to not overlook the value of a head-to-toe inspection in patients!

-MB-

References:

1. Pallares-Sanmartin A, et al. Validity and Reliability of the Schamroth Sign for the Diagnosis of Clubbing. JAMA. 2010; 304(2):159–161. doi:10.1001/jama.2010.935.

Broadening the Differential

Feb 10 2020 (late entry)

I started the first day of my CEEP selective in the GIM Rapid Referral clinic today. After being away from medicine for the past month due to the all-consuming CaRMS process, I was both excited and nervous to restart clinical duties. Although the basics came back to me quickly, I definitely felt quite rusty.

The first case I saw was a young man who had been referred from the emergency department after an episode of hemoptysis. In reviewing the history with the patient, he had actually been experiencing a few month history of mild hemoptysis in the form of coughing up streaks of blood. However recently he had a more alarming event where he coughed up a more significant amount of blood.

I preceded to ask him questions to help build my differential and rule out the causes that commonly come to mind for hemoptysis, such as pulmonary embolism, bleeding from another source (such as the GI tract or from epistaxis), infectious causes, and malignancy. Although the patient did have some recent weight loss, which appeared to be related to improving his eating habits, there were no other associated symptoms. It did appear there was some temporal relation to his cigarette smoking and hemoptysis, although smoking alone would be unlikely to be the sole contributor to his more significant hemoptysis episode. The patient did also endorse significant marijuana use.

I presented the case to my preceptor and outlined my differential. Although I felt that certain causes of his hemoptysis such as pulmonary embolism, bleeding from another source, and tuberculosis were quite unlikely, I still did not have a clear explanation for the events other than irritation related to his cigarette smoking. My preceptor encouraged me to think more broadly about the differential and  to try and organize my list into categories.

After some teaching and discussion with my preceptor, we came up with a more comprehensive differential. We categorized this into the following:

• Thromboembolic causes, such as pulmonary embolism.
• Infectious causes, such as tuberculosis and fungal infectious. Namely due to his marijuana use, I learned he was at increased risk for aspergillosis.
• Inflammatory/Immune causes, such as sarcoidosis (given his ethnic background), Goodpasture's syndrome, granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis, systemic lupus erythematous.
• Malignant causes, such as bronchogenic cancer or carcinoid tumour.
• Genetic causes, namely hereditary hemorrhagic telangiectasia (HHT).
• And other causes, including GI bleeding, epistaxis, trauma.

After building this more thorough list, we were able to determine the best next steps for the patient, including ordering a CT chest to help investigate some of these potential causes. We also counselled the patient to maintain his smoking cessation and arranged a follow-up visit after his imaging.

As I reflected about the case, I realized I had thought of the common and/or life-threatening causes for the patient's presentation, but had forgotten to broaden my thinking to consider some of the other more rare but relevant causes. This case reminded me of the importance of constructing my differential in an organized and systematic manner in order to capture a broad yet reasonable differential. I also think that being used to the older patient population in Internal Medicine, I forgot to take into consideration the other patient characteristics in considering the differential. In this case, the patient's age, ethnic background, social history and family history also provided some clues to help build the differential. This was an extremely valuable learning case for me, not only in serving as a reminder to keep my differentials broad, but also as an opportunity to learn about new diseases. For example, I learned about the findings of aspergillosis on imaging, reviewed the physical exam findings for HHT, and discussed the classic features of GPA. I look forward to the rest of my weeks on this selective and to much more learning to come!

-MB-

Aortopathy

February 10, 2020


Having been away the past few weeks for CaRMS, I was excited to come back to medicine. I started my first day of my CEEP selective in the cardiology clinic. It was nice being able to review some common cardiology topics, such as post-MI management (i.e. dual-antiplatelet therapy, ACE inhibitor, beta-blocker, and high-dose statin) and its intricacies. Some of the more interesting cases that I saw that day were related to aortopathies. I had several patients with cardiovascular co-morbidities who presented with an incidental finding

After reviewing these cases with my team and additional readings, the following is my takeaways for thoracic aortic aneurysms.

Presentation: usually asymptomatic but can result in aortic rupture, dissection, and death.

Etiology:

• Degenerative
• Usually older patients with atherosclerotic risk factors (e.g. smoking, hypertension)
• Genetics: e.g. Marfan, Ehlers-Danlos, Loeys-Dietz syndrome, bicuspid aortic valve
• Consider if family history, physical exam findings in keeping with genetic syndrome, younger patients (no specific cut-off but ~<50 years old).
• Inflammatory: giant cell arteritis, Takayasu arteritis, Behcet's disease, ankylosing spondylitis

Management (in general):

• Consider genetics referral 
• Monitor every 6 months until stable then annually with imaging (echo, CT/MR angiography)
• Consider elective surgical management if symptomatic (e.g. malperfusion, compression), ascending aorta diameter >55 mm or annual expansion >5 mm (see guidelines for specifics)
• Evaluate for other aneurysms
• Preventative
• Blood pressure control 
• Beta-blocker preferred over ACEi/ARBs 
• Target 140/90 or if diabetic, 130/80 
• CV risk reduction - smoking cessation, lifestyle modification
• Avoid strenuous and isometric exercises
• Avoid fluoroquinolones - increase risk of aortic dissection/rupture
• Counsel patient on symptoms to watch out for, including sudden chest pain, and need for seeking immediate medical attention.

-JT-

Reference(s):
Boodhwani, M., Andelfinger, G., Leipsic, J., Lindsay, T., McMurtry, M. S., Therrien, J., & Siu, S. C. (2014). Canadian Cardiovascular Society position statement on the management of thoracic aortic disease. Canadian Journal of Cardiology, 30(6), 577-589.