Tuesday, May 18, 2010


Today we discussed hyponatremia and its management:

Some take home points - rapid correction of hyponatremia is often not required unless it is clear that the patient is acutely symptomatic from their hyponatremia - if you do need to give hypertonic saline (often in marathon runners, ecstasy overdose, etc.) it is often given as 3%NS with a 100cc bolus, then reassessment for further doses. The patient should be in a monitored setting and have frequent repeat electrolytes sent.

Consulting nephrology is never a bad idea for these patients.

We also discussed "BEER POTOMANIA" (apparently potomania is: An intense and persistent desire to drink alcohol to excess).

Malnourished patients (low-protein, high water intake diets) often do noy have enough solute excretion to deal with their water intake . Beer and other primary carbohydrates meals have little solute, however their CHO content suppresses endogenous protein catabolism/urea production.

Normal subject - 600 mosm/day of solute intake (and output). If they are hyponatremic and make a maximally dilute urine of 60 mosm/L (assume the kidneys cannot make a more dilute urine), their solute load allows a maximum of 10L of urine/day i.e. - their free H2O intake would have to exceed 10L for them to get more hyponatremic.

In malnourished patients - their solute intake/output can be 240 mosm/day. Therefore with a maximally dilute urine of 60 mosm/L (the kidneys cant make it more dilute) then their maximum urine output will be 4L/day. If their intake of fluid is >4L (>11 beers)/ day they will worsen their hyponatremia.

Other tips:
When seeing hyponatremia in the ER:

First rule out acute hyponatremia that needs acute correction.

Recheck the lytes if they were done several hours previously- the patient has possibly received intravenous fluids in the ER that may have significantly altered the sodium concentration - especially if the stimulus (often ECF volume depletion) for ADH secretion has been removed. Following the urine output may help to identify this (although recording can be an issue outside of the ICU) as a brisk, dilute diuresis can be bad sign.

Further tips from a nephrologist who attends on GIM are posted here, as well as an article about the use of DDAVP to prevent overly rapid sodium correction.

Monday, May 17, 2010

End of Life Care

Many people have strong beliefs regarding feeding and end of life care. It is imperative to examine the goals of care with patients when making end of life care decisions and to remember that there will be a number of social, cultural and religious factors to be considered. Enlisting help from palliative care physicians, chaplaincy and other professionals with experience in helping make these decisions is often very important.

An article that examines some important points surrounding the use of feeding tubes in severe dementia is posted here. We often dont focus on promoting oral intake in hospital, but it is important to consider strategies to address this as well.

An article reviewing artificial nutrition and hydration at the end of life can be found here (Pub med abstract) or here (if logged through the university libraries)

Friday, May 14, 2010

Tuesday, May 11, 2010


Some interesting articles about morning report:

The Matrix article

The Pimping article

Points about COPD

Definition: (WHO)"Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases."


Diagnosis: symptoms compatible with COPD, airflow obstruction (FEV1/FVC ratio less than 0.70 with no alternative cause.

Severity based on FEV1

Mild: FEV1 over 80% of predicted, with or without symptoms

Moderate COPD -FEV1 50-80% predicted

Severe COPD- FEV1 30-50%

Etiologies of exacerbations:
Majority are infection-related (80%) - H. Flu; S. Pneumo; M. Catarrhalis; P. Aeruginosa (5-10%); Rhinoviruses (20-25%).

15-20% are from other causes (inhaled irritants, air pollution)

Treatment consists of

1) Bronchodilators

2) Systemic steroids

3) ABx

4) Ventilatory support if needed (including BiPAP)

Abx - NOT needed for all exacerbations. Some advocate using only if increased sputum purulence. Classically used in all exacerbations requiring assisted ventilation (possible mortality benefit) or when there are 2 or more of increased dyspnea, sputum production or sputum purulence. One of the earlier papers to address that is referenced here.

Steroids: Trials have demonstrated benefit of systemic steroids for vs. placebo. No mortality benefit, but shorter length of stay, PFT improvement, and symptomatic improvement.
Original trial used Solumedrol 125mg IV q8h; no advantage to this high dose over Prednisone 40-60mg PO x 5-7d. No need for taper of this duration.

A NEJM paper from 2002 reviewing AECOPD is here

Monday, May 10, 2010


A prior post on this topic with some good references is posted here


The classic definition of FUO from the early 1960s was: fever greater than 38 degrees Celsius on several occasions over a 3 week period of time with week worth of hospital investigations. With changes in our healthcare system, it is now generally accepted that the definition applies if only 2-3 weeks have past and there have been initial investigations performed (the list of which tests varies)

When thinking about FUO remember the 4 major categories
Inflammatory, Infectious, Malignancy and up to 50% do not end up with a diagnosis (and generally have a good prognosis)

A proposed algorithm based on existing evidence was created by a Toronto internist and published in Archives of Internal Medicine. Dont forget that investigations should be tailored/expanded based on a comprehensive history and physical.