I am often asked whether physical activity has a positive or negative effect on the overall health of knee cartilage. The answer is unclear. Published data are conflicting.
What is known and generally agreed on:
1) Physical activity has been shown to facilitate cartilage development in children
2) Forced immobility (spinal cord injury) results in rapid cartilage loss
3) The medial knee compartment experiences significant mechanical loads during weight-bearing activity and is often the primary site of knee OA
A recent study attempted to answer whether 1) long-term (10yrs) participation in vigorous physical activity would benefit knee cartilage in healthy adults and 2) whether there were certain subgroups with asymptomatic preexisting structural knee changes which predict a harmful cartilage response to long-term physical activity.
Vigorous = activity generating sweating or SOB at least 20min 1/wk
Healthy older adults (mean age 57.8 yr) performing persistent vigorous physical activity had an increased risk (odds ratio 1.5) of worsening medial knee cartilage defects but not of a change in cartilage volume
In those w/ asymptomatic preexisting structural knee changes, there was worsening of cartilage defects (odds ratio 3.4) and a trend toward increased rate of loss of cartilage volume (again in the medial knee compartment)
Long-term effects of vigorous physical activity may depend on the preexisting health of the joint
Intussusception is the telescoping or prolapse of one portion of the bowel into an immediately adjacent segment.
Transplant patients are the norm now in the ED. Their drug lists are immense and are usually on some form of immunosuppression to prevent rejection of the transplanted organ. Two common medications are cyclosporine and tacrolimus. They share many adverse effects like hepatotoxicity, nephrotoxicity and hypertension. Here is the mechanism of action and some unique adverse effects to these powerful immunosuppressants (there are many more so be wary):
1) Cyclosporine - suppresses T-cell activation and growth. Unique toxicity - painful neuropathy of the fingertips and toes, cortical blindness
2) Tacrolimus - simiar to cyclosporine but actually hampers T-cell communication/signal transduction. Unique toxicity - can also cause cortical blindness but is also known to cause diabetes/hyperglycemiad
Two recently presented abstracts at the 2012 Society of Critical Care Medicine conference suggest that the combination of vancomycin and piperacillin-tazobactam may lead to acute kidney injury (AKI) in the critically ill. There may also be evidence to suggest that piperacillin-tazobactam alone increases the risk of AKI.
Both abstracts retrospectively compared patients who received either vancomycin alone or the combination of vancomycin and piperacillin-tazobactam. In both studies, the rates of AKI were significantly lower in patients treated with vancomycin alone as compared to patients receiving both vancomycin and piperacillin-tazobactam.
Bottom line: Although the current evidence does not support a change in our clinical practice, more prospective studies exploring this topic are necessary.
79 year old male with headaches, ataxia, falls, and difficulty urinating. What's the diagnosis?
For patients presenting to the ED with chest pain, we've been taught that “classic” or “typical” presentations for ACS (chest pressure with radiation to the left neck/jaw/shoulder/arm, dyspnea, diaphoresis, nausea, vomiting, lightheadedness) are most worrisome. Yet, many of the patients that present with typical symptoms end up having negative workups for ACS. What are the symptoms that truly predict ACS? Three major studies have demonstrated that the best predictors of ACS in patients presenting to the ED with chest pain are (not necessarily ranked in order):
1. chest pain that radiates to the arms, especially if the pain radiates bilaterally or to the right arm
2. chest pain associated with diaphoresis
3. chest pain associated with vomiting
4. chest pain associated with exertion
The description of the chest pain (e.g. "pressure" or "squeezing," etc.), the dyspnea, nausea, lightheadedness, and pain at rest were, surprisingly, not helpful at predicting ACS.
The simple takehome point is the following: always ask your patient with chest pain if the pain radiates, if there was associated diaphoresis, if there was associated vomiting, and if the pain is associated with exertion. If the answers to any of these 4 questions is "yes," think twice before labeling the patient with a non-ACS diagnosis.
Contrast Allergy:
Many patients will report that they have a allergy to iodinated contrast by saying that they are allergic to iodine
Iodine, itself, is not an allergen and is a required element for thyroid homrone production. Plus could you imagine the hordes of people that would be having allergic reactions everyday when they add salt to their french fries. Our EDs would be completely swamped.
A recent meta-analysis by Drs. Schabelman and Witting also showed the following:
As we enter Crab eating season in Maryland, lets stop giving shellfish a bad name. A patent with any allergy is at increased risk, but shellfish is no higher a risk than those allergic to Strawberries.
Definition: Fracture of the humerus just proximal to the epicondyles.
Use the Measured Sodium Concentration!
19 year-old male presents with L ankle pain and obvious deformity after jumping out of a window and landing on his inverted foot. What's the diagnosis?
New studies are utilizing mild therapeutic hypothermia as a treatment option in cardiogenic shock. These studies have reported improved circulatory support, an increase in systemic vascular resistance, and reduction in vasopressor use which ultimately may result in lower cardiac oxygen consumption. The preliminary results suggest that mild therapeutic hypothermia could be a therapeutic option in hemodynamically unstable patients independent of current recommendations which support its use in cardiac arrest survivors.
• Wedge compression fractures
http://jbjs.org/data/Journals/JBJS/855/JBJA0851224560G02.jpeg
It may not be necessary to give oral vitamin K to patients that are not bleeding that have INRs between 4.5 and 10.
Patients who were supratherapeutic on warfarin were randomized to vitamin K 1.25 mg (n=355) versus placebo (n=369).
In the 90 days after enrollment, 15.8% of patients allocated to vitamin K and 16.3% allocated to placebo had a bleeding event. Major bleeding events occurred in 9 patients in the vitamin K group and 4 in the placebo.
Thromboembolic events occurred in 1.1% of patients in the vitamin K group, compared to 0.8% of patients in the placebo group. An equal number of patients died in each group (n=7).
Consider rhabdomyolyisis secondary to heat exposure as summertime approaches; have a low threshold to screen patients if they are at risk (e.g., people exercising in high-ambient temperatures).
Symptoms include muscle tenderness, cramping, and swelling with associated weakness. Patients with altered mental status (e.g., heat stroke) should be examined for limb induration, skin discoloration (i.e., ischemia), or compartment syndrome.
Complications:
Treatment
Naltrexone and methylnaltrexone are both mu-receptor antagonists that look similar and have similar names. But, they have very different uses.
Severe UGIB
Ultrasound is useful during intubation; here is a video explaining how: http://ultrarounds.com/ultrarounds.com/Visual_Pearl_May_28,_2012.html
Today's Bonus Pearl:
EMRA has developed a great antibiotic guide for the iphone (http://itunes.apple.com/us/app/2011-emra-antibiotic-guide/id393020737?mt=8) or android (https://play.google.com/store/apps/developer?id=Emergency+Medicine+Residents'+Association). This app is a bit pricey ($15.99), but is easy to use and well organized. Enjoy!
[pearl provided by Dr. Semhar Tewelde]
Myocarditis is an under-diagnosed cardiac disease resulting from a broad range of infectious, immune, and toxic etiologies
