Online Clinical Case Study (December 2015)

Clinical Cardiology Series

The content of the December Cardiology Series is provided by:
Dr. CHUI Shing Fung MBChB (CUHK), MRCP (UK), FHKCP, FHKAM (Med), Specialist in Cardiology
Dr. WONG Chi Yuen MBBS (HK), MRCP (UK), FHKCP, FHKAM (Med), Specialist in Cardiology

Sudden deterioration after myocardial infarction

A 65-year-old gentleman with history of hypertension and diabetes mellitus was admitted for retrosternal chest pain for 3 days. Blood pressure on admission was 165/85mmHg with heart rate 88bpm. Cardiac enzyme (high sensitive Troponin) was elevated to >50000ng/L (reference range <34.2ng/L). The ECG on admission is shown in Figure 1. He was treated as acute myocardial infarction with delayed presentation. His condition suddenly deteriorated on the next day of admission with blood pressure dropped to 92/48mmHg and heart rate raised to 118bpm, oxygen saturation was 88% on 100% oxygen mask. Chest auscultation revealed bilateral basal crepitation. There was also a systolic murmur at apex radiating to axilla.

Figure 1

1. What would be the most appropriate initial treatment for this patient?
a. Mechanical ventilation
b. Hemodynamic support
c. Diuretics
d. Emergent echocardiogram
e. All of the above
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After treatment, the patient was stabilized and an echocardiogram (transesophageal) was performed. The 2D image of mitral valve is shown in Figure 2. The color flow Doppler across mitral valve is shown in Figure 3, demonstrating severe mitral regurgitation.

Figure 2 Figure 3

What would be the most likely diagnosis?
a. Infective endocarditis
b. Chronic rheumatic heart disease
c. Rupture papillary muscle
d. Rupture chordae tendineae
e. Atrial myxoma

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3. What should be the definitive management for this patient?
a. Antibiotics treatment and percutaneous coronary intervention
b. Percutaneous coronary intervention only
c. Open heart surgery
d. None of the above
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1. E, 2. C, 3. C

This gentleman was admitted for recent inferior myocardial infarction (MI) complicated by cardiogenic shock secondary to rupture papillary muscle. The most common etiology of cardiogenic shock in such clinical setting is patient with left ventricular failure, but it can also be caused by mechanical complications, such as acute mitral regurgitation (MR), ventricular septal rupture or free wall rupture.

Delayed hospitalization (≥24 hours), undue in-hospital physical activity, and post-infarction angina increased the risk of mechanical complications in predisposed patients.

The causes of acute MR after acute MI include ischemic papillary muscle displacement (previously known as papillary muscle dysfunction) with left ventricular dilatation, and papillary muscle or chordal rupture.

Papillary muscle rupture is a life-threatening complication that accounts for approximately 5% of deaths in acute MI patients. It usually occurs two to seven days after the infarct. The rupture may be partial (occurring at one of the muscle heads) or complete.

Because of differences in blood supply, rupture of the posteromedial papillary muscle occurs more frequently than rupture of the anterolateral papillary muscle. The posteromedial papillary muscle is supplied with blood from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the left anterior descending and left circumflex arteries.

The clinical manifestations of papillary muscle rupture include acute onset hypotension and pulmonary edema with a new mid- or pansystolic murmur that may have widespread radiation.

The diagnosis of papillary muscle disease after MI is typically confirmed by echocardiography. Two-dimensional transthoracic echocardiography usually demonstrates a flail segment of the mitral valve, and a severed papillary muscle can frequently be seen moving freely within the left ventricular cavity. Color flow Doppler can demonstrate the presence of severe mitral regurgitation. In some cases, however, transthoracic echocardiography is not informative and transesophageal echocardiography (with addition 3D images, see Figure a) is required to establish the diagnosis. Left ventricular function is usually hyperdynamic as a result of ventricular contraction against the low impedance left atrium.

Figure a. 3D TEE of mitral valve viewed from left atrial side. The partially ruptured posteromedial papillary muscle (red arrow) is seen popping into left atrium during systole

Prompt diagnosis and initiation of medical therapy and emergent surgery are all necessary for a favorable outcome. Medical therapy includes aggressive afterload reduction with nitrates, sodium nitroprusside, diuretics, and intraaortic balloon pump counterpulsation. Afterload reduction decreases the regurgitant fraction, thereby increasing forward flow. Emergent surgical intervention remains the treatment of choice for papillary muscle rupture.

Mortality of patients with papillary muscle rupture are higher than those with other causes of ischemic mitral regurgitation, with an operative mortality rate of about 50% ; however, the outcome is worse with medical therapy with a mortality of 75% at 24 hours and 95% within two weeks after complete papillary muscle rupture. Risk factors for worse outcomes after surgery include older age, female gender, and poor left ventricular systolic function.

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Dermatology Series 皮膚科病例研究

Dermatology Series for December 2015 is provided by:
Dr. KWAN Chi Keung, Dr. TANG Yuk Ming, William, Dr. CHAN Hau Ngai, Kingsley, and Dr. LEUNG Wai Yiu
Specialists in Dermatology & Venereology

Itchy red spots on limbs

A 60-year-old man living in overcrowded temporary house complained sudden onset itchy papules over his forearms and legs in recent few months. Clinical examination reviewed multiple erythematous papules over his limbs.


1. What are your differential diagnoses?
The differential diagnoses include scabies, urticaria, papular eczema, drug eruptions and insect/arthropod bites.

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2. What is your diagnosis?
The diagnosis is insect / arthropod bites.

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3. What is the cause?
The cause is probably due to bedbugs. It is a parasitic arthropods from the family Cimicidae. They are less than 1 cm in length and reddish brown in colour. They can be found in furniture, floorboards, peeling paint or commonly in areas of clutter. They come out at night with peak feeding times just before dawn. They are attracted by sweating, body heat, carbon dioxide or ordour of human body.

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4. What investigation would you like to order?
The classical presentation makes the diagnosis and no investigation is needed. The typical bedbugs presentation is erythematous papules sometimes with urticarial components in a linear group of 3 - called "breakfast, lunch and dinner" (see the clinical photo).

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5. What is your treatment?
  Treatment of bedbug bites is not usually required. Topical steroid cream or oral antihistamines can be used for symptoms relief. Topical antibiotic or antiseptic lotion is used for secondary bacterial infections. The home environment should be maintained clean and advice from insect control and elimination experts may be needed to reduce and finally eliminate the bedbugs in living environment.
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