Louis A. Johnson VA Medical Center

Introduction:Spontaneous recurrent hemarthrosis of the knee following a total knee arthroplasty is a rare complication with varying time of onset from 2 months to 18 years. It needs a prompt diagnosis and treatment to prevent complications of stiffness, chronic pain, and limited function. We present a case of spontaneous recurrent hemarthrosis presenting at 3 months following a total knee arthroplasty with a follow-up to 1 year.Case Report:A 66-year-old male presented at 3 months following a right total knee arthroplasty with a history of increased pain and swelling of the knee joint. Initially, he was treated with anti-inflammatories when the pain and swelling recurred, an aspiration demonstrated hemarthrosis of the knee. Further evaluation demonstrated no infection, a femoral angiography demonstrated prominence of medial superior and inferior geniculate arteries with a tumor blush appearance. Therapeutic embolization of both the arteries resulted in complete resolution of the symptoms in 1 month with return of full knee function. At the end of 1-year follow-up, the patient had return of full knee function with no pain and no recurrence.Conclusion:An algorithmic approach is helpful in identifying the etiology of spontaneous recurrent hemarthrosis of knee and a course of conservative treatment should always be the first line of treatment. Angiography and selective arterial embolization of the geniculate arteries can be an effective treatment in the management of recurrent spontaneous hemarthrosis.

A popular choice for lateral epicondylitis (LE), corticosteroid injections have been associated with prominent side effects, which has led to the conception of modalities like platelet-rich plasma (PRP). This randomised trial aimed to evaluate and compare the 6-week, 3-month and 1-year outcomes with PRP and corticosteroid injections in LE. We hypothesised that PRP would prove more effective in relieving pain and improving function. At the sports medicine unit of our tertiary care teaching centre, 80 patients with LE were randomised into either receiving PRP (group A) or corticosteroids (group B) injections. Pre-injection visual analogue scale (VAS), disabilities of the arm, shoulder and hand (DASH) score, Mayo elbow performance score (MEPS) and grip strength score (GSS) were recorded. Common extensor origins were identified and infiltrated with 3ml of either PRP or corticosteroid (triamcinolone in 2% xylocaine) using a peppering technique. Follow-up scores and extent of pain relief were recorded and compared. At 6weeks, there were greater improvements in group B versus A in mean VAS (13.8 vs. 44.5; p < 0.001), DASH (64.2 vs. 53.3; p < 0.001), MEPS (88.0 vs. 74.5; p = 0.004) and GSS (89.3 vs. 73.4; p = 0.039). These scores showed a reversed pattern at 3months when group A outcomes superseded group B (VAS p = 0.002; DASH p < 0.001; MEPS p = 0.002; GSS p = 0.045). At 1-year follow-up, group A continued to enjoy better pain relief and function (VAS p = 0.024; DASH p < 0.001; MEPS p = 0.009; GSS p = 0.028). Albeit corticosteroid injections show good short-term results at 6weeks, patients receiving PRP injections fare better at 3 and 12months.

Compelling clinical reports reveal that behavioral stress alone is sufficient to cause reversible myocardial dysfunction in selected individuals. We developed a rodent stress cardiomyopathy model by a combination of prenatal and postnatal behavioral stresses (Stress). We previously reported a decrease in percent fractional shortening by echo, both systolic and diastolic dysfunction by catheter-based hemodynamics, as well as attenuated hemodynamic and inotropic responses to the β-adrenergic agonist, isoproterenol (ISO) in Stress rats compared with matched controls (Kan H, Birkle D, Jain AC, Failinger C, Xie S, Finkel MS. J Appl Physiol 98: 77-82, 2005). We now report enhanced catecholamine responses to behavioral stress, as evidenced by increased circulating plasma levels of norepinephrine (P < 0.01) and epinephrine (P < 0.01) in Stress rats vs. controls. Cardiac myocytes isolated from Stress rats also reveal evidence of oxidative stress, as indicated by decreased ATP, increased GSSG, and decreased GSH-to-GSSG ratio in the presence of increased GSH peroxidase and catalase activities (P < 0.01, for each). We also report blunted inotropic and intracellular Ca(2+) concentration responses to extracellular Ca(2+) (P < 0.05), as well as altered inotropic responses to the intracellular calcium regulator, caffeine (20 mM; P < 0.01). Treatment of cardiac myocytes with N-acetylcysteine (NAC) (10(-3) M) normalized calcium handling in response to ISO and extracellular Ca(2+) concentration and inotropic response to caffeine (P < 0.01, for each). NAC also attenuated the blunted inotropic response to ISO and Ca(2+) (P < 0.01, for each). Surprisingly, NAC did not reverse the changes in GSH, GSSG, or GSH-to-GSSG ratio. These data support a GSH-independent salutary effect of NAC on intracellular calcium signaling in this rodent model of stress-induced cardiomyopathy.

We have previously reported echocardiographic evidence of myocardial dysfunction in male rats with prenatal stress (PS) and restraint stress (R) (PS+R). We now report significant differences in hemodynamic effects of PS+R between male vs female rats. PS + R blunted both systolic and diastolic function in male rats. In contrast, PS+R enhanced systolic function and had no effect on diastolic function in female rats. PS+R blunted both systolic and diastolic responses to isoproterenol (ISO) in male rats, but enhanced the systolic and diastolic responses to ISO in female rats. No differences in baseline hemodynamics or responses to ISO were noted between male and female rats after PS alone or R alone. This cardiomyopathy model may provide insights into sex differences in behavioral and cardiovascular responses to stress in animal models and humans.Mean± SE; #p&lt;0.05, ##p&lt;0.01, vs Control.

Obesity is a risk factor for deep vein thrombosis (DVT), and as obesity increases, DVT rates will also elevate. The purpose of this article is to assist nurses in correctly selecting evidence-based interventions found effective in preventing DVT formation. To promote full understanding of this disease process, pathophysiologic changes associated with obesity will be linked with current research-based therapies of anticoagulation, compression therapy, and mobilization. A call for future research is proffered in multiple areas, to include assessment, determination of interventional effectiveness, and establishment of outcome measurements for both surgical and medical obese populations.