Management of Rotator Cuff Injuries in the Elite Athlete.

PURPOSE OF REVIEW: Rotator cuff injuries are a common cause of pain and dysfunction for the elite athlete and can result in time loss from participation. This review highlights the current management of these injuries. RECENT FINDINGS: Conservative management of rotator cuff injuries continues to be the "gold standard" in the elite athlete. This includes a comprehensive rehabilitation program, anti-inflammatories, and corticosteroid injections. Newer treatment techniques such as intramuscular dry needling and the use of biologics such as platelet-rich plasma and stem cells demonstrate early promising results; however, these modalities require further investigation to determine their effectiveness. Rotator cuff injuries can range from contusions and tendinopathy to full-thickness tears. A comprehensive evaluation is needed to determine the extent of injury and appropriate plan of care. Management strategies can range from rehabilitation to operative intervention and are guided by the size of the tear, time of season, sport, performance limitations, and presence of concomitant pathology.

Surgical anatomy of the radial nerve in the deltopectoral approach for revision shoulder arthroplasty and periprosthetic fracture fixation: a cadaveric study.

BACKGROUND: Radial nerve injury is a rare but clinically significant complication of revision shoulder arthroplasty and fixation of native and periprosthetic proximal humeral fractures. Understanding of the anatomic relationship between the radial nerve as it enters the humeral spiral groove and anterior shoulder landmarks in a deltopectoral approach is necessary to avoid iatrogenic radial nerve injury. METHODS: Eight forequarter cadaveric specimens were dissected through a deltopectoral approach. Distances between the radial nerve entry into the proximal spiral groove and the coracoid process, distal lesser tuberosity/inferior subscapularis insertion, superior latissimus insertion, and inferior latissimus insertion were measured. Means, standard deviations, and ranges were determined for each distance. RESULTS: The radial nerve entry into the proximal spiral groove averaged 133.1 mm (range, 110.3-153.0 mm) from the coracoid process, 101.9 mm (range, 76.5-124.3 mm) from the distal lesser tuberosity/inferior subscapularis insertion, 81.0 mm (range, 63.4-101.5 mm) from the superior latissimus insertion, and 39.6 mm (range, 25.5-55.4 mm) from the inferior latissimus insertion. The proximal spiral groove was distal to the inferior latissimus insertion in all specimens. CONCLUSION: The risk of iatrogenic injury to the radial nerve at the spiral groove may be minimized through proper identification and protection or avoidance of circumferential fixation. However, if encircling fixation with cerclage cables is necessary, instrumentation proximal to the inferior edge of the latissimus dorsi insertion may reduce the risk of radial nerve injury.

Management of the Biconcave (B2) Glenoid in Shoulder Arthroplasty: Technical Considerations.

Reconstruction of the biconcave (B2) glenoid presents a challenging clinical problem that has been associated with poor clinical outcomes and implant survivorship. The high failure rate from glenoid component loosening and subsequent premature implant failure can be substantially decreased with accurate glenoid component positioning and appropriate correction of the pathologic glenoid retroversion. Careful preoperative planning is essential for accurate preparation and execution of the optimal surgical plan. There are many surgical strategies to address the B2 glenoid, but no consensus on the optimal method exists, as the technique should be uniquely customized to the individual's pathology and surgeon preference. Cases with mild deformity may be corrected with eccentric reaming and total shoulder arthroplasty, while the more severe deformities may require posterior glenoid bone grafting, and/or augmented implants to restore native version. Finally, the reverse shoulder arthroplasty is a reliable option to restore stability and address bone deficiency for the severe B2 glenoid in an older, lower demand patient.

Roles of the subfornical organ and area postrema in arterial pressure increases induced by 48-h water deprivation in normal rats.

In rats, water deprivation (WD) increases arterial blood pressure (BP) in part due to actions of elevated osmolality in the brain to increase vasopressin levels and sympathetic activity. However, the osmoreceptors that mediate this response have not been identified. To test the hypothesis that osmoregulatory circumventricular organs are involved, BP and heart rate (HR) were continuously recorded telemetrically during 48 h of WD in normal rats with lesions (x) or sham lesions (sham) of the subfornical organ (SFO) or area postrema (AP). Although WD increased BP in SFOx and SFOsham rats, no significant difference in the hypertensive response was observed between groups. HR decreased transiently but similarly in SFOx and SFOsham rats during the first 24 h of WD. When water was reintroduced, BP and HR decreased rapidly and similarly in both groups. BP (during lights off) and HR were both lower in APx rats before WD compared to APsham. WD increased BP less in APx rats, and the transient bradycardia was eliminated. Upon reintroduction of drinking water, smaller falls in both BP and HR were observed in APx rats compared to APsham rats. WD increased plasma osmolality and vasopressin levels similarly in APx and APsham rats, and acute blockade of systemic V1 vasopressin receptors elicited similar depressor responses, suggesting that the attenuated BP response is not due to smaller increases in vasopressin or osmolality. In conclusion, the AP, but not the SFO, is required for the maximal hypertensive effect induced by WD in rats.

Is premorbid glenoid anatomy altered in patients with glenohumeral osteoarthritis?

BACKGROUND: Restoration of native, premorbid glenoid anatomy may be a goal in component placement during total shoulder arthroplasty. However, if patients with unilateral glenohumeral osteoarthritis are predisposed to the development of arthritis owing to abnormal native glenoid anatomy, this recommendation may be inappropriate. QUESTIONS/PURPOSES: The purpose of this study was to determine if patients with glenohumeral osteoarthritis have abnormal premorbid glenoid version or inclination, thereby predisposing them to subsequent glenoid disorders. We specifically tested whether: (1) premorbid glenoid version or inclination in the pathologic shoulder of patients with unilateral osteoarthritis, as determined by the glenoid vault model, is different from glenoid version or inclination in the contralateral nonpathologic shoulder of these patients; (2) there are differences between glenoid version or inclination in normal cadaver shoulders and the nonpathologic side of patients with unilateral osteoarthritis; and (3) there are differences between glenoid version or inclination in normal cadaver shoulders and the premorbid glenoid version and inclination in the pathologic shoulder of patients with unilateral osteoarthritis, as determined by the glenoid vault model. METHODS: Bilateral CT scans were obtained in 27 patients with unilateral glenohumeral osteoarthritis. Thirty normal cadaver control shoulders also underwent CT scans. Premorbid glenoid version and inclination in the pathologic shoulder, as measured by the glenoid vault model, were compared with the contralateral nonpathologic shoulder and the normal cadaver control shoulders. Glenoid version and inclination of the normal shoulders were compared with the nonpathologic side from patients with unilateral osteoarthritis. Measurements were made by two different methods using three-dimensional surgical simulation software: (1) a direct measurement technique and (2) measurements derived from placement of a glenoid vault model. Mean differences in these parameters were compared between shoulder groups using paired and unpaired Student's t-tests. RESULTS: Premorbid glenoid version and inclination in the pathologic shoulder as measured by the vault model averaged -7° (SD, 5) and 10° (SD, 6), respectively, compared with -7° (SD, 5) and 12° (SD, 6) as directly measured on the nonpathologic side, and -7° (SD, 4) and 12° (SD, 5) as directly measured in the normal cadaver control shoulders. There were no differences in glenoid version or inclination between the normal shoulders and the nonpathologic side of patients with unilateral osteoarthritis or between these shoulders and the premorbid version and inclination of the arthritic shoulder as measured by the vault model. CONCLUSIONS: Patients with glenohumeral osteoarthritis do not appear to have abnormal premorbid glenoid retroversion or inclination. The glenoid vault model can be used to determine premorbid glenoid version and inclination. CLINICAL RELEVANCE: The glenoid vault model may be a clinically useful tool to estimate patient-specific premorbid glenoid anatomy, which may help in preoperative or intraoperative surgical planning for total shoulder arthroplasty.

Comparison of patient-specific instruments with standard surgical instruments in determining glenoid component position: a randomized prospective clinical trial.

BACKGROUND: Glenoid component malposition for anatomic shoulder replacement may result in complications. The purpose of this study was to define the efficacy of a new surgical method to place the glenoid component. METHODS: Thirty-one patients were randomized for glenoid component placement with use of either novel three-dimensional computed tomographic scan planning software combined with patient-specific instrumentation (the glenoid positioning system group), or conventional computed tomographic scan, preoperative planning, and surgical technique, utilizing instruments provided by the implant manufacturer (the standard surgical group). The desired position of the component was determined preoperatively. Postoperatively, a computed tomographic scan was used to define and compare the actual implant location with the preoperative plan. RESULTS: In the standard surgical group, the average preoperative glenoid retroversion was -11.3° (range, -39° to 17°). In the glenoid positioning system group, the average glenoid retroversion was -14.8° (range, -27° to 7°). When the standard surgical group was compared with the glenoid positioning system group, patient-specific instrumentation technology significantly decreased (p < 0.05) the average deviation of implant position for inclination and medial-lateral offset. Overall, the average deviation in version was 6.9° in the standard surgical group and 4.3° in the glenoid positioning system group. The average deviation in inclination was 11.6° in the standard surgical group and 2.9° in the glenoid positioning system group. The greatest benefit of patient-specific instrumentation was observed in patients with retroversion in excess of 16°; the average deviation was 10° in the standard surgical group and 1.2° in the glenoid positioning system group (p < 0.001). Preoperative planning and patient-specific instrumentation use resulted in a significant improvement in the selection and use of the optimal type of implant and a significant reduction in the frequency of malpositioned glenoid implants. CONCLUSIONS: Novel three-dimensional preoperative planning, coupled with patient and implant-specific instrumentation, allows the surgeon to better define the preoperative pathology, select the optimal implant design and location, and then accurately execute the plan at the time of surgery.

The role of the subfornical organ in angiotensin II-salt hypertension in the rat.

Hypertension caused by chronic infusion of angiotensin II (Ang II) in experimental animals is dependent, in part, on increased activity of the sympathetic nervous system. This chronic sympathoexcitatory response is amplified by a high-salt diet, suggesting an interaction of circulating Ang II and dietary salt on sympathetic regulatory pathways in the brain. The present study tested the hypothesis that the subfornical organ (SFO), a forebrain circumventricular organ known to be activated by circulating Ang II, is crucial to the pathogenesis of hypertension induced by chronic Ang II administration in rats on a high-salt diet (Ang II-salt model). Rats were randomly selected to undergo either subfornical organ lesion (SFOx) or sham surgery (Sham) and then placed on a high-salt (2% NaCl) diet. One week later, rats were instrumented for radiotelemetric measurement of mean arterial pressure (MAP) and heart rate (HR) and placed in metabolic cages to measure sodium and water balance. Baseline MAP was slightly (but not statistically) lower in SFOx compared with Sham rats during the 5 day control period. During the subsequent 10 days of Ang II administration, MAP was statistically lower in SFOx rats. However, when MAP responses to Ang II were analysed by comparing the change from the 5 day baseline period, only on the fifth day of Ang II was MAP significantly different between groups. There were no differences between groups for water or sodium balance throughout the protocol. We conclude that, although the SFO is required for the complete expression of Ang II-salt hypertension in the rat, other brain sites are also involved.

Renal denervation attenuates long-term hypertensive effects of Angiotensin ii in the rat.

1. It is well accepted that some of the long-term effects of angiotensin (Ang) II are mediated via the central nervous system. Some of these actions that are mediated by the circumventricular organs and the baroreceptor reflex are thought to then alter sympathetic nervous system activity. In particular, there is some debate as to the role of renal nerves in the chronic effects of AngII. The aim of the present study was to assess the contribution of the renal nerves in a long-term model of progressive AngII-induced hypertension. 2. Male Sprague-Dawley rats were subjected to either bilateral renal denervation (RDX; n = 7) or sham surgery (SHAM; n = 8). Rats were instrumented with radiotelemetric transducers and venous catheters for the measurement of blood pressure and AngII infusion, respectively. A 4.0% NaCl diet and distilled water were provided ad libitum. The first 3 days served as the control period (7 mL/day, 0.9% NaCl, i.v.). This was followed by an infusion of AngII for 16 days (10 ng/kg per min, i.v.) and a 3 day recovery period identical to control. 3. Baseline arterial pressure between RDX and SHAM rats did not differ. Following AngII treatment, the arterial pressure of SHAM rats increased more rapidly than that of RDX rats. By Day 10 of treatment, the mean arterial pressure was significantly different between groups, having increased to 166 +/- 4 mmHg in SHAM rats and 135 +/- 11 mmHg in RDX rats. This trend continued for the remainder of AngII treatment. 4. The present results indicate that the renal nerves are necessary for the full expression of AngII-induced hypertension.

Effect of subfornical organ lesion on the development of mineralocorticoid-salt hypertension.

Accumulating evidence suggests that structures within the lamina terminalis; the organum vasculosm of the lamina terminalis (OVLT), the median preoptic nucleus (MnPO) and/or the subfornical organ (SFO); are required for the development of DOCA-salt hypertension. Lesion of the anteroventral tissue lining the third ventricle (AV3V), which destroys cell bodies in the OVLT and MnPO, as well as efferent projections from the SFO to the OVLT and MnPO, abolishes DOCA-salt hypertension in the rat. However, the individual contribution of these structures to DOCA-salt hypertension is unknown. The present study was designed to determine whether an intact SFO is required for hypertension development in the DOCA-salt model. In uninephrectomized SFO lesioned (SFOx; n=6) and SHAM (n=8) Sprague-Dawley rats, 24-h mean arterial pressure (MAP) and heart rate (HR) were continuously recorded telemetrically 4 days before and 36 days after DOCA implantation (100 mg/rat; s.c.); 24-h sodium and water balances were measured throughout the protocol. No differences in control MAP, HR, sodium and water balances were observed between groups. Following DOCA implantation, the magnitude of the elevation of MAP was similar between groups (approximately 40 mm Hg) so that by Day 40, MAP was 148+/-5 mm Hg in SFOx and 145+/-4 mm Hg in SHAM rats. The magnitude of decrease in HR from control values was similar in both groups. Differences in sodium and water balances were not observed between groups. We conclude that the SFO alone does not play a significant role in the development of mineralocorticoid-salt hypertension.

Chronic effects of angiotensin II and at1 receptor antagonists in subfornical organ-lesioned rats.

1. Angiotensin (Ang) II is known to exert some of its effects centrally via circumventricular organs. These unique central nervous system areas lack the normal blood-brain barrier and, therefore, allow peptide hormones access to the brain. Of these, the subfornical organ (SFO) has been shown to be involved in many of the acute dipsogenic and pressor effects of AngII, but much less is known about the role of the SFO in the chronic effects of AngII. We hypothesized that the SFO is a central site involved in the chronic hypotensive effects of endogenous AT(1) receptor blockade, as well as the chronic hypertensive effects of exogenously administered AngII. 2. In order to test these hypotheses, SFO-lesioned (SFOx) or sham Sprague-Dawley rats were instrumented with venous catheters and radiotelemetric pressure transducers for intravenous administration of losartan or AngII and continuous measurement of blood pressure and heart rate. Rats were given 3 days of saline control infusion (7 mL/day of 0.9% NaCl) and were then infused with either losartan (10 mg/kg per day) or AngII (10 ng/kg per min) for 10 days. 3. By day 4 of losartan treatment, arterial pressure had decreased 24 +/- 2 and 18 +/- 2 mmHg in sham (n = 9) and SFOx (n = 10) rats, respectively. Furthermore, by day 5 of AngII infusion, arterial pressure had increased 12 +/- 3 mmHg in sham rats (n = 9), but only by 4 +/- 1 mmHg in SFOx rats (n = 9). In each treatment group, these attenuated pressure responses in SFOx rats continued through day 10 of treatment. 4. These results support the hypotheses that the SFO plays a role in both the hypotensive effects of chronic AT(1) receptor blockade and the chronic hypertensive phase of exogenously administered AngII.

Sodium balance, arterial pressure, and the role of the subfornical organ during chronic changes in dietary salt.

The subfornical organ (SFO), one of the brain circumventricular organs, is known to mediate some of the central effects of angiotensin II related to sodium and water homeostasis. Because angiotensin II levels are altered with changes in chronic dietary salt intake, we reasoned that the actions of angiotensin II at the SFO might be involved in the regulation of arterial pressure during long-term alterations in dietary salt. The present study was designed to test the hypothesis that long-term control of arterial pressure during chronic changes in dietary salt intake requires an intact SFO. Male Sprague-Dawley rats were randomly selected for electrolytic lesion (SFOx, n = 8) or sham (n = 9) operation of the SFO. After a 1-wk recovery period, rats were instrumented with radio-telemetric blood pressure transducers for continuous 24-h measurement of mean arterial pressure (MAP) and heart rate (HR) and then were placed individually in metabolic cages. After another 1 wk of recovery, the rats were subjected to a 49-day protocol as follows: 1) a 7-day control period (1.0% NaCl diet), 2) 14 days of high-salt (4.0% NaCl) diet, 3) 7 days of normal-salt (1.0% NaCl) diet, 4) 14 days of low-salt (0.1% NaCl) diet, and 5) 7 days of recovery (1.0% NaCl diet). There were no significant differences in MAP or HR between SFOx and sham-operated rats throughout the protocol. These results do not support the hypothesis that the SFO is necessary for regulation of arterial pressure during chronic changes in dietary salt. However, SFOx rats demonstrated significantly less cumulative sodium balance than sham-operated rats on days 2-6 of the high-salt diet period. These data suggest that the SFO is important in the regulation of sodium homeostasis during chronic changes in salt intake.

Contribution of the subfornical organ to angiotensin II-induced hypertension.

Previous studies clearly demonstrated acute actions of angiotensin II (ANG II) at one of the central circumventricular organs, the subfornical organ (SFO), but studies demonstrating a role for the SFO in the chronic actions of ANG II remain uncertain. The purpose of this study was to examine the role of the SFO in the chronic hypertensive phase of ANG II-induced hypertension. We hypothesized that the SFO is necessary for the full hypertensive response observed during the chronic phase of ANG II-induced hypertension. To test this hypothesis, male Sprague-Dawley rats were subjected to sham operation (sham rats) or electrolytic lesion of the SFO (SFOx rats). After 1 wk, the rats were instrumented with venous catheters and radiotelemetric transducers for intravenous administration of ANG II and measurement of blood pressure and heart rate, respectively. Rats were then allowed 1 wk for recovery. After 3 days of saline control infusion (7 ml of 0.9% NaCl/day), sham and SFOx rats were infused with ANG II at 10 ng.kg(-1).min(-1) i.v. for 10 consecutive days and then allowed to recover for 3 days. A 0.4% NaCl diet and distilled water were provided ad libitum. At day 5 of ANG II infusion, mean arterial pressure increased 11.7 +/- 3.0 mmHg in sham rats (n = 9) but increased only 3.7 +/- 1.4 mmHg in SFOx rats (n = 9). This trend continued through day 10 of ANG II treatment. These results support the hypothesis that the SFO is necessary for the full hypertensive response to chronic ANG II administration.

Subfornical organ lesion attenuates chronic hypotensive effects of losartan in salt-replete rats.

UNLABELLED: HYPOTHESIS/INTRODUCTION: Circumventricular organs are central nervous system brain sites thought to participate in neuroendocrine regulation of neural output. We have previously demonstrated a profound chronic hypotensive response to the angiotensin II (Ang II) AT(1) antagonist, losartan (10 mg/kg/day), in normal rats. In addition, we have demonstrated that the area postrema, one of the circumventricular organs, partially mediates this response. The subfornical organ (SFO) is another circumventricular organ which has been shown to mediate actions of Ang II. The present study was designed to test the hypothesis that the SFO mediates the chronic hypotensive effects of losartan in normal rats. MATERIALS AND METHODS: Rats were randomly chosen for lesion of the SFO or sham operation and instrumented with intravenous catheters and radiotelemetric blood pressure transducers. After a control period, rats were infused with losartan (10 mg/kg/day) for nine days. Mean arterial pressure and heart rate responses were measured continuously throughout the protocol and examined as 12-hour day/night averages. RESULTS: By day 7 of losartan treatment, night-time mean arterial pressure had dropped to 75+2 mmHg in sham rats (n=8) but only to 83+2 mmHg in SFO-lesioned rats (n=10). This trend continued throughout the treatment protocol. CONCLUSIONS: These results suggest that the SFO partially mediates the chronic hypotensive effects of chronic losartan treatment in normal rats.

The role of Ang (1-7) in mediating the chronic hypotensive effects of losartan in normal rats.

HYPOTHESIS: The following studies were designed to test the hypothesis that Ang (1-7) contributes to the chronic hypotensive effects of the angiotensin II AT(1)-receptor antagonist, losartan, in normal rats. INTRODUCTION: We have previously shown a chronic, hypotensive response to the AT(1)-receptor antagonist, losartan, in normotensive rats. The mechanism of this response is not completely understood. Previous studies by others have demonstrated a role for Ang (1-7) in the beneficial antihypertensive effects of angiotensin-converting enzyme (ACE) inhibition. This is thought to be due to vasodilatory effects of increased levels of Ang (1-7) during ACE inhibition. Since it has now been shown that Ang (1-7) levels are also increased during AT(1) antagonism, we designed experiments to test the hypothesis above. MATERIALS AND METHODS: Sprague-Dawley rats were instrumented with venous catheters and radiotelemetric pressure transducers and commenced on a normal (0.4%) NaCl diet. Arterial pressure responses were measured in rats treated with losartan (10 mg/kg/day) (LOS rats, n=8) and compared with those treated with losartan and the Ang (1-7) antagonist, A779 (24 g/kg/hour) (A779/LOS rats, n=11) for 10 days. RESULTS: By day 7 of treatment, mean arterial pressure had dropped by 27+1 mmHg in LOS rats, in contrast with a decrease of only 21+2 mmHg in A779/LOS rats. This attenuated response in rats treated with A779 became more prominent and continued through day 10 of losartan treatment. CONCLUSION: These results support the hypothesis that the chronic hypotensive effects of losartan in normal rats are mediated in part through the actions of Ang (1-7).

Role of the subfornical organ in the chronic hypotensive response to losartan in normal rats.

Angiotensin II is known to act at a unique set of brain regions known as the circumventricular organs. These structures lack the normal blood-brain barrier and are therefore thought to participate in the central nervous system processing of neuroendocrine signals. We have reported that chronic treatment with the angiotensin type 1 (AT1) receptor antagonist, losartan, decreases arterial pressure in normotensive rats. Furthermore, this hypotension is attenuated in area postrema-lesioned rats, suggesting a role of endogenous angiotensin II at this circumventricular organ. Another circumventricular organ, the subfornical organ (SFO), has also been shown to mediate actions of angiotensin II. The present study tested the hypothesis that the SFO is a central site of action of endogenous angiotensin II at AT1 receptors. Adult male Sprague-Dawley rats were anesthetized and placed in a stereotaxic apparatus, and the SFO was sham or electrolytically lesioned. One week later, rats were instrumented with venous catheters and radiotelemetry pressure transducers for continuous infusion and monitoring of mean arterial pressure, respectively. After 3 days of control, losartan was administered intravenously (10 mg x kg(-1) x d(-1)) for 10 days in both SFO-lesioned and sham rats. By day 4 of losartan administration, mean arterial pressure had decreased to 75+/-2 mm Hg in sham rats (n=9) but had only fallen to 83+/-2 mm Hg in lesioned rats (n=10). This attenuated hypotensive response in SFO-lesioned rats continued through day 10 of losartan treatment. These results support the hypothesis that the SFO mediates part of the hypotensive effects of chronic AT1 receptor blockade in the normotensive rat.