Discharge on the day of surgery following unicompartmental knee arthroplasty within the United Kingdom NHS.

AIMS: Unicompartmental knee arthroplasty (UKA) has been successfully performed in the United States healthcare system on outpatients. Despite differences in healthcare structure and financial environment, we hypothesised that it would be feasible to replicate this success and perform UKA with safe day of surgery discharge within the NHS, in the United Kingdom. This has not been reported in any other United Kingdom centres. PATIENTS AND METHODS: We report our experience of implementing a pathway to allow safe day of surgery discharge following UKA. Data were prospectively collected on 72 patients who underwent UKA as a day case between December 2011 and September 2015. RESULTS: A total of 61 patients (85%) were discharged on the same day. The most common reason for failure was logistical; five patients had their operation too late in the day. Three patients failed to mobilise safely, two had inadequate control of pain and one had a leaking wound. The mean length of stay for those who were not discharged on the same day was 1.2 nights (1 to 3). During the same time, 58 patients underwent planned inpatient UKA, as they were deemed inappropriate for discharge on the day of surgery. However, three of these were safely discharged on the same day. Follow-up data, 24 hours post-operatively, were available for 70 patients; 51 (73%) reported no or mild pain, 14 (20%) had moderate pain and five (7%) had severe pain. There were no re-admissions. All patients had a high level of satisfaction. CONCLUSION: We found that patients can be safely and effectively discharged on the day of surgery after UKA, with high levels of satisfaction. This clearly offers improved management of resources and financial savings to healthcare trusts. Cite this article: Bone Joint J 2017;99-B:788-92.

Infection in knee replacements after previous injection of intra-articular steroid.

We reviewed 231 patients who had undergone total knee replacement with an AGC (Biomet) implant over a period of 2.5 years. After applying exclusion criteria and with some loss to follow-up, there were 144 patients available for study. These were divided into two groups; those who had received intra-articular steroid in the 11 months before surgery and those who had not. There were three deep infections, all of which occurred in patients who had received a steroid injection. The incidence of superficial infection was not significantly different in the two groups. Five patients had undergone investigation for suspected deep infection because of persistent swelling or pain and all of these had received an intra-articular injection pre-operatively. We conclude that the decision to administer intra-articular steroids to a patient who may be a candidate for total knee replacement should not be taken lightly because of a risk of post-operative deep infection.

In-vivo sagittal plane knee kinematics: ACL intact, deficient and reconstructed knees.

Sagittal plane video fluoroscopy was used to analyse the bilateral knee kinematics of patients with unilateral ACL deficiency (ACLD) before, and 4 months after, hamstrings graft ACL reconstruction. Kinematics were studied during weight resisted knee extension, passive knee extension, and a step up. Thigh EMG records were also obtained from five subjects. In addition, six uninjured control subjects were analysed to establish normal kinematics. Kinematics were analysed by calculating the angle between the long axis of the tibia and the patella tendon through the range of knee flexion. Shear forces were calculated using a model of knee extension and force plate data. A maximum anterior TT of 7.3 (S.D. 2.1) mm was recorded in ACL intact (ACLI) knees during the weightbearing activity. Hamstrings activity was able to control ATT in the ACLD tibia to within the normal range of translation of the ACLI knee. Despite clinical improvements, ATT increased postoperatively in the reconstructed knees to 11.6 (S.D. 3.8) mm (P<0.048). The findings suggest that the ACL has only a minor role in the control of ATT during activity, and that the extent of ATT is more closely related to the level of quadriceps-generated shear force. A reduction in hamstrings force is proposed as the most likely cause for increased ATT post reconstruction. These findings have implications for the development of ACL rehabilitation regimes, and also may modify graft choice and the surgical aims of the procedure.

Acute precipitants of congestive heart failure exacerbations.

BACKGROUND: Few studies have prospectively and systematically explored the factors that acutely precipitate exacerbation of congestive heart failure (CHF) in patients with left ventricular dysfunction. Knowledge of such factors is important in designing measures to prevent deterioration of clinical status. The objective of this study was to prospectively describe the precipitants associated with exacerbation of CHF status in patients enrolled in the Randomized Evaluation of Strategies for Left Ventricular Dysfunction Pilot Study. METHODS: We conducted a 2-stage, multicenter, randomized trial in 768 patients with CHF who had an ejection fraction of less than 40%. Patients were randomly assigned to receive enalapril maleate, candesartan cilexetil, or both for 17 weeks, followed by randomization to receive metoprolol succinate or placebo for 26 weeks. Investigators systematically documented information on clinical presentation, management, and factors associated with the exacerbation for any episode of acute CHF during follow-up. RESULTS: A total of 323 episodes of worsening of CHF occurred in 180 patients during 43 weeks of follow-up; 143 patients required hospitalization, and 5 died. Factors implicated in worsening of CHF status included noncompliance with salt restriction (22%); other noncardiac causes (20%), notably pulmonary infectious processes; study medications (15%); use of antiarrhythmic agents in the past 48 hours (15%); arrhythmias (13%); calcium channel blockers (13%); and inappropriate reductions in CHF therapy (10%). CONCLUSIONS: A variety of factors, many of which are avoidable, are associated with exacerbation of CHF. Attention to these factors and patient education are important in the prevention of CHF deterioration.

Vascular and cardiac effects of amlodipine in acute heart failure in dogs.

BACKGROUND: Amlodipine improves exercise capacity in patients with chronic congestive heart failure (HF), but the mechanisms of this effect are unknown. OBJECTIVE: To test the hypothesis, in a canine model of acute, ischemic HF, that amlodipine increases vascular capacitance and reduces cardiac filling pressures. METHODS: Amlodipine was given to 13 anesthetized, splenectomized dogs (six controls and seven with HF). Aortic, left ventricular end-diastolic (LVEDP) and portal venous (Pportal) pressures, cardiac output, portal flow (ultrasonic probe) and intestinal blood volume (IBV, 99mTc blood-pool scintigraphy) were measured. Intestinal vascular conductance (= 1/resistance) and vascular capacitance (CAP) were measured before and 15 mins after repetitive 150 micrograms/kg dosages of amlodipine (maximum cumulative dosage, 1000 micrograms/kg). Pportal-IBV curves were obtained by impeding portal flow (pneumatic cuff), and change in CAP was defined by the change in IBV at Pportal = 7.5 mmHg. HF was induced by microsphere embolization of the left coronary artery. RESULTS: CAP increased in the control group (+ 28%, P < 0.01) but decreased (-9%, P < 0.05) in the HF group. Left ventricular stroke work increased in the control group (P < 0.05), while it decreased (P < 0.05) in the HF group, suggesting a negative inotropic effect. In the control group, LVEDP increased after amlodipine was given (P < 0.05) but did not change significantly in the HF group. CONCLUSIONS: In the acute experimental HF model, amlodipine failed to increase intestinal vascular CAP or decrease filling pressures, and may have had a negative inotropic effect. The experiment failed to demonstrate a beneficial hemodynamic effect of amlodipine in acute HF, and the mechanism of benefit of this agent in chronic HF remains unclear.

Wave-intensity analysis: a new approach to left ventricular filling dynamics.

In order to explore a new approach to the analysis of diastolic dysfunction, we adapted wave-intensity analysis (WIA), a time-domain analysis that provides information regarding both upstream and downstream events, to left ventricular (LV) filling. WIA considers the pressure and flow waves as summations of successive wavelets, characterised by the direction they travel and by the sign of the pressure gradient associated with them. Wave intensity is the product, dPdU, calculated from the incremental differences in LV pressure (dP) and mitral velocity (dU) and, during the diastolic filling interval, yields up to five dPdU peaks. Peak 1 is caused by backward-travelling expansion waves that accelerate the blood while LV pressure falls, and may be related to "diastolic suction". Peak 2 is caused by forward-travelling compression waves which occur if acceleration continues after LV pressure begins to increase. Peak 3 is caused by backward compression waves and is associated with rising LV pressure and deceleration. Peak 4 is caused by forward compression waves and is associated with the increasing LV pressure and acceleration caused by atrial contraction. Peak 5 is caused by backward compression waves and is associated with increasing pressure and deceleration. These preliminary observations suggest that WIA can be useful in describing the mechanics of LV filling and, after much further work has been accomplished, it might prove useful in the detection and characterization of diastolic dysfunction.