Clubbing

Today in morning report we discussed a patient, who among other problems, was clubbed.

Clubbing is the enlargement of the terminal segments of the fingers and/or toes that results from the proliferation of the connective tissue between the nail matrix and the distal phalanx. It develops in the context of a number of neoplastic, infectious, inflammatory and vascular conditions.

Features on physical exam that make clubbing more likely include changes in nail-fold angles, as well as changes in the shape, depth, and width of the terminal phalanges.

1) Phalangeal Depth - This ratio compares the depth of the distal phalanges to the inerphalangeal areas. Normally, this is less than 1. Once this ratio exceeds 1, clubbing is more likely.

2) Nail Fold angles - Two angles are commonly discussed: the profile angle and hyponychial angle.

a) The profile angle can be estimated by the angle the nail projects from the nail fold. normally this is about 160 degrees but exceeds 180 degrees when the finger is clubbed.

b)The hyponychial angle compares two lines, (1), from the DIP joint to the nail fold and (2), from the nail fold to the point where the nail meets the finger tips. This angle is should not exceed 190 degrees normally and if it does, clubbing is likely present.

3) Nail bed squishiness - Palpation of the nail bed in clubbed fingers tends to be spongier than a normal nail with the sensation that the nail is floating.

Check out the JAMA rational clinical exam series here for an evidence based review.

Grade 4 Left Ventricles

Today in morning report, we discussed a patient presenting with complications related to their grade-4 left ventricle. Much of our discussion focused on the management of these patients. Specifically, what about device therapy? Here is a summary:



Device Therapy
This really came to the forefront with the MADIT-2 trial where patients with a history of MI and severe LV dysfunction (grade 3 or worse) after optimal medical therapy had prophylactic ICDs placed. This showed improved survival. The SCD-HeFT trial looked at amiodarone vs. ICDs and again, device therapy appeared superior. Cost effective analysis has been favourable, but controversial. Check out this editorial for another look.


The MADIT-CRT trial looked at relatively asymptomatic patients (NYHA class 1 and 2) with depressed LV function (less than 30%) and prolonged QRS durations and found that CRT decreased rates of CHF exacerbations.

Recently, results of the RAFT trial were presented in NEJM and found that "among patients with NYHA class II or III heart failure, a wide QRS complex, and left ventricular systolic dysfunction, the addition of CRT to an ICD reduced rates of death and hospitalization for heart failure." More adverse events were noted, however.

All in all, this is a rapidly progressing area in medicine and it may not be too long until we find ourselves here!

Toxic Epidermal Necrolysis

Today in Morning Report, we discussed the case of toxic epidermal necrolysis likely secondary to allopurinol use.

Allopurinol and its metabolite, oxipurinol (alloxanthine), decrease the production of uric acid by inhibiting the action of xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Indications are most commonly for disorders of hyperuricemia (urate nephropathy, tumor lysis sydrome prophylaxis, and gout). When used for gout, most would agree that >3 flares/year (or tophaceous deposition) would merit its use. Incidentally discovered hyperuricemia is not an on-label indication.

With regards to the side-effect profile, the biggest concern, as seen in our patient, is toxic epidermal necrolysis. This is a very rare, but acute and potentially fatal skin reaction in which there is sheet-like skin and mucosal loss. It exists in a spectrum with Stevens-Johnson Sydrome and is mainly differentiated by the degree of epidermal involvement.

Treatment is mostly supportive but begins with the discontinuation of the offending drug. Wound care is very important to prevent excess fluid loss and secondary infections. In severe cases, consultation with a burn unit may be appropriate. Adjunct treatment with corticosteroids, cyclosporin, cyclophosphamide and IVIg have been trialed with variable success.

TEN is reviewed nicely at this link, check it out for a summary on the diagnosis and treatment.

Hyperkalemia

Last week, a patient with hyperkalemia was discussed in morning report.

Causes of hyperkalemia always come down to renal handling of potassium. Dietary (or iatrogenic!) intake of potassium may play a role, but most clinical scenarios revolve around limitations in excretion.

Management options include:
1) Stop the exogenous potassium - this seems simple but is embarassing when missed.

2) Stop offending drugs - this is not the right time for any potassium sparing diuretics or ACE inhibitors

3) Shift the Potassium - This does not equal excretion and is only a temporary fix. Classically, a high glucose load (1 amp of D50W) with an intravenous insulin chaser (1o units iv) is the mainstay cocktail. Other options include intravenous sodium bicarbonate and inhaled beta agonists (8 puffs with aerochamber). Interestingly, beta agonists may be more efficacious than previously believed (see the article below).

4) Dump the Potassium - at the end of the day, you need to rid the body of the excess. A number of options exist. High dose furosemide (assuming this is not oliguric renal failure) is an effective way to mobilize potassium. Potassium binders are often used (kayexalate) but are slow and have other side effects (colonic necrosis!). Finally, hyperkalemia refractory to medical management is an indication for hemodialysis.

Check out CMAJ for a very recent review.

Aches and Pains

Today we discussed an interesting case of a man with fevers and progressive muscle pain and weakness. Among the many things on the differential diagnosis was Giant Cell Arteritis.

GCA (formerly known as temporal arteritis) should be considered in patients with new headaches, abrupt onset of visual disturbances, symptoms of polymyalgia rheumatica, jaw claudication, unexplained fever or anemia, high erythrocyte sedimentation rate and/or high serum C-reactive protein.

A temporal artery biopsy is part of the workup but can be negative in some patients who have the disease (7-13% will have a negative unilateral biopsy but a postive bilateral biopsy).

The treatment for GCA are glucocorticoids. Prednisone at 1mg/kg is the commonest initial therapy with tapering initiated after 4 weeks (providing a normalized ESR).

Here is a link to a NEJM review on the topic and here is a look at the topic in the JAMA rationale clinical exam.