Addressing DRESS

This is from the UCSD Medical Images site.

DRESS Syndrome - Drug Reaction with Eosinophilia and Systemic Symptoms. Also known as drug hypersensitivity reactions.

These commonly present 2 or more weeks after initiating a new medication, and is manifested by:

• Fever
• Rash: papular, macular, bullous
• Lymphadenopathy
• Arthralgias
• Hepatitis
• Eosinophilia (in many cases)

Medications commonly associated with DRESS syndrome include "aromatic" anticonvulsants (phenytoin, carbamazepine, and phenobarbitol) - but can occur with other anticonvulsants as well. Other classic drugs include NSAIDS, abacavir, and allopurinol. Treatment revolves around stopping the culpret agent, supportive care, and perhaps steroid therapy in severe cases.

In the case of abacavir, a drug used in HIV treatment, hypersensitivity reactions are known to occur in those who are HLA B5701-positive. Screening programs are now widely used to prevent this reaction. Here is the sentinel article from NEJM. You will be hearing a lot more about "personalized medicine" in the near future.

Pulmonary Hypertension

Pulmonary Hypertension is pretty common in hospitalized patients.

On Exam:

• JVP: may have a prominent "A" wave from right ventricular hypertrophy, "CV" waves from tricuspid regurgitation, and Kussmaul's sign along with Hepato-jugular reflux with right ventricular failure.
• General Inspection: You may see a pulsatile RUQ from hepatic congestion
• Precordial Exam: feel for a palpable P2 at the left second intercostal space. In addition, feel for a right ventricular heave. Heart sounds include a louder P2. S2 can be split pretty wide early on. You may also hear a right sided S3 in RV overload, or a right sided S4 with RV hypertrophy.
• Tricuspid Regurgitation: this is often a higher pitch, holosystolic murmur that is best heard at the left (sometimes right sternal border), and if heard on the left side may radiate to the right. 
• Special tests with Tricuspid Regurgitation: Increasing venous return will accentuate the murmur (eg. push on liver, passive leg raise), while decreasing venous return (eg. go from sit to stand) will decrease the murmur.  Watch for TR to be accentuated during inspiration....this is called Carvallo's sign.
• Other: look for cyanosis centrally and peripherally, and a pulsus paridoxus. Often you will be able to feel a pulsatile liver edge, and peripheral edema is common. 

A good approach to the etiology of Pulmonary Hypertension....think of pre-capillary, capillary, and post-capillary causes:

Precapillary:

• chronic thrombotic or embolic disease, pulmonary emboli, sickle cell disease

Capillary/Parenchymal

• Obstructive Lung Disease: COPD
• Interstitial Lung Disease
• Restrictive Lung Disease: chest wall or neuromuscular problems
• Obstructive Sleep Apnea
• Connective Tissue Disease: scleroderma (common), RA and SLE (rare)
• Vasculitis: eg Wegeners
• HIV 
• Medications/drugs like diet pills (fenfen), herbs (bush tea in some areas - Jamaica), cocaine, amphetamines

Post Capillary:

• Left Ventricular Issues: LVH, shunts, mitral or aortic valvular dysfunction
• Constrictive pericarditis
• Mediastinal fibrosis

Some Good Links:

Here a good review from NEJM on Pulmonary Hypertension, and an easy to read summary from JAMA.

Aortic Stenosis

An aerial view of the Hoover dam pictured left.

Aortic Stenosis. Know it. Love it. You will see it every day on the wards and in clinic.

Pathogenesis of Symptoms: large afterload leads to concentric left ventricular hypertrophy à high oxygen demand and ischemia (especially in subendocardium) à decreased compliance à fixed time of systole so when HR is high then diastole too short to fill ventricle àeventually leads to LV failure.

***if you do not remember how to perform one of the maneuvers below, please come find us ....we are happy to show you again***

Before you examine the precordium, have a look at:

• Carotid: parvus et tardus....a delayed and low volume carotid upstroke.
• JVP: look for prominent 'a' waves.

Precordium:

• Inspect: lateral displacement of the Point of Maximal Impulse (PMI)
• Palpate: the PMI may be displaced, greater in size, amplitude, and durations (longer than 2/3 of systole). You may feel a thrill.
• Auscultate: decreased or absent S2, may have an S3 or S4 present. Listen for a systolic ejection murmur at the right 2nd intercostal space. It should radiate past the clavicle towards both carotids. Time when the murmur peaks....later peaking correlates with increased severity of stenosis. The murmur intensity does not correlate with severity of stenosis.

Special Tests:

• Squatting: this increases pre-load, and will accentuate AS.
• Valsalva, or going from sit-to-stand will decrease pre-load and will minimize AS murmur.
• Apical Carotid Delay: palpate the precordial apex and the right carotid artery. Any delay in pulses is abnormal.
• Brachial Radial Delay: palpate the brachial artery and radial artery. Any delay between the two impulses is abnormal. Don't push too hard on the brachial artery as you will dampen the radial impulse!

Gallavardin phenomenon: this is when the AS murmur radiates to the apex with a more musical quality, imitating a murmur of Mitral Regurgitation.

Oy Vey....So what's the evidence for all this?

Here is a link to the classic JAMA paper, but it is summarized below....

-Rule Out AS (sensitive findings)

• Absence of systolic murmur
• Absence of murmur radiating to the right carotid

-Rule In AS (specific findings)

• Apical-carotid delay
• Slow rate of rise of the carotid artery
• Decreased intensity of S2
• Mid or late peaking murmur
• Brachio-radial delay

The same smart people from Toronto who wrote the above JAMA paper created another helpful bedside clinical prediction rule for diagnosing moderate to severe AS at this link.

Erythema Nodosum....and a word on Sarcoid

This is a good example of Erythema Nodosum [from Nature Clinical Practice Gastroenterology and Hepatology (2008) 5, 278-281] .

Remember that EN is an immunologic response, and presents as painful nodules, classically on the extensor surfaces, more on the shins but can also be seen on the arms. They are often dark purple or red in colour. This is a panniculitis - an inflammation of the subcutaneous fat. Imagine if somebody repeatedly hit your legs with a bat.....that is how EN looks and feels.

Causes:

• Infectious: TB, Streptococcal pharyngitis, fungal infections (histoplasmosis, blastomycosis, coccidiomycosis), Leprosy, Syphilis, and gastroenteritis from bacterial sources (eg Yersinia, Campylobacter) are the more common infectious causes.


• Autoimmune: Inflammatory Bowel Disease, Behcet's disease, and Lupus.


• Malignancy: lymphoma


• Sarcoid: See below


• Pregnancy and OCPs may be associated


• Medications: sulfa drugs have been implicated.

A word on sarcoid - we touched on the two acute manifestations of this condition:

1. Lofgren's Syndrome: this represents migratory arthralgias, erythema nodosum, and hilar adenopathy, often accompanied by fevers. Here is a cool article looking at prognostic variables in disease.


2. Uveoparotid Fever: This is exactly as advertised. Patients present with 1. uveitis, 2. parotitis, and 3. fever. This is also referred to as Heerford's syndrome, or Heerfort-Waldenstrom syndrome. Here is a great review of this syndrome.
   

Welcome

Welcome to "The Pulse," a blog dedicated to physical and clinical exam skills.

The aim of this blog is to complement what you have learned at the bedside. Here you will find links to relevant images, advice, and journal articles to round out your learning.

We encourage you to continue to enhance your clinical skills, and take what you have learned here and apply it at the bedside.

Feel free to drop by at any time for updates.

See you on the wards,

Your Clincal Exam Instructors