In treatment of subacromial impingement syndrome, subacromial injection of Ketorolac 30 mg was equivalent to corticosteroid injection in terms of effectiveness. In patients with diabetes or those who have concerns about the adverse effects of steroids, subacromial injection of Ketorolac can be considered a suitable alternative. Research Ethics. Financial support. Conflict of interest.
National Center for Biotechnology Information , U. Journal List Clin Shoulder Elb v. Clin Shoulder Elb. Published online Feb Author information Article notes Copyright and License information Disclaimer. Abstract Background As nonsteroidal anti-inflammatory drugs NSAIDs and steroids have similar effects, steroids can be avoided to reduce adverse effects.
Methods Sixty patients with rotator cuff syndrome for at least 3 months were enrolled and divided into steroid and NSAID groups. Results Both groups showed improvements in the clinical outcomes. Conclusions Subacromial injection of NSAIDs for rotator cuff tendinitis with shoulder pain had equivalent outcomes with those of steroid injection at the week follow-up. Keywords: Anti-inflammatory agents, non-steroidal; Impingement syndrome; Ketorolac; Rotator cuff injuries; Triamcinolone.
Table 1. Patient demographics by injection group. Open in a separate window. Treatment Method A subacromial injection as indicated on the chosen card was administered with an opaque syringe in an injection room. Assessment or Outcomes Clinical evaluation was performed before treatment and at 3, 6, and 12 weeks after treatment. Table 2. Clinical scores by injection method. Financial support None. Conflict of interest None. Anatomical and biomechanical mechanisms of subacromial impingement syndrome.
Clin Biomech Bristol, Avon ; 18 — Subacromial impingement syndrome. J Am Acad Orthop Surg. Shoulder impingement syndrome. Am J Med. Cakmak A. Conservative treatment of subacromial impingement syndrome. Acta Orthop Traumatol Turc. Subacromial infection following corticosteroid injection. J Shoulder Elbow Surg. Corticosteroid injection for shoulder pain: single-blind randomized pilot trial in primary care.
Shoulder disorders in general practice: incidence, patient characteristics, and management. Ann Rheum Dis. Effect of a single subacromial prednisolone injection in acute rotator cuff tears in a rat model. Knee Surg Sports Traumatol Arthrosc. Incidence of full-thickness rotator cuff tear after subacromial corticosteroid injection: a week prospective study. Mod Rheumatol. Blood glucose levels in diabetic patients following corticosteroid injections into the hand and wrist.
J Hand Surg Am. Effect of steroid injections on the rotator cuff: an experimental study in rats. Subacromial injection of autologous platelet-rich plasma versus corticosteroid for the treatment of symptomatic partial rotator cuff tears.
Eur J Orthop Surg Traumatol. All will be fixed within 48 hours. Transition pack 50 — Videohive Swift II — Videohive Photo Album Comic Book — Videohive Overflow Logo Reveal — Videohive Hand Drawn Letters and Numbers — Videohive Connect with D. I allow to create an account. When you login first time using a Social Login button, we collect your account public profile information shared by Social Login provider, based on your privacy settings.
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An official cutoff for the definition of aortic dilatation has not been determined because of the variability of this measure, but most experts agree that ascending aorta size should be correlated to size and gender. In addition, some authors suggest using the aortic size index [2] which takes into account the body surface area, thus minimizing classification of normal aorta as pathologically dilated and vice versa.
Unfortunately, the mortality rate of patients presenting with complications of TAA has remained relatively stable in the last two decades, in contrast to the improved survival observed in patients presenting with complications of coronary artery disease CAD. As Clouse et al. The incidence of TAA has been reported to be only 5. Women and men have similar incidences of thoracic aortic aneurysm but the age at diagnosis is a decade higher in women 70s than in men 60s.
The aorta is an elastic vessel composed of three main layers: the tunica intima, the tunica media and the tunica adventitia. The internal elastic lamina separates the intima from the media.
Elastic fiber in the medial layer of the aorta allows continuous forward flow during the whole cardiac cycle. During systole, expansion of the aorta allows kinetic energy from left ventricular contraction to be stored as potential energy in the aortic wall.
In diastole, recoil of the aorta transforms the stored potential energy back to kinetic energy, propelling the blood distally into the arterial bed. With aging, there is fragmentation of elastic fiber, smooth muscle dropout and replacement by amorphous material known as cystic medial degeneration , which leads to increased stiffness and weakening of the aortic wall which predisposes to dilatation of the ascending aorta.
In addition, according to Laplace's law, the dilation of the aorta increases wall tension, triggering vascular wall remodeling and even further aortic dilatation. Recent developments have helped better explain the cellular changes that lead to aneurysmal ascending aortas. The different conditions that cause TAAs either affect structural components of the aortic wall or alter the intracellular signaling cascade that maintains vascular wall integrity.
The main culprit in this disease seems to be the TGF-B1 signaling mechanism that is responsible for activating matrix degradation through increased production of plasminogen activators and release of matrix metalloproteinases [5]. In addition, the MYH11 gene affects the C-terminal coiled-coil region of the smooth muscle myosin heavy chain, a specific contractile protein of smooth muscle cells [7] and increases TAA formation.
Other mutations can affect both the structure and the metabolic homeostasis of the vascular wall. For instance, the mutation of fibrillin 1 in Marfan syndrome weakens the vascular wall given that it is a reinforcing structure [8] and it also alters the regulation of the bioavailability of TGFB1 [9].
Other mutations alter the regulatory mechanisms that inhibit the activity of the TGF-B pathway such as the mutation of GLUT10, a glucose transporter whose deficiency is associated with arterial tortuosity syndrome [11] or the mutation of the SMAD3 gene that encodes a protein necessary for the signaling downstream of the TGF-B pathway [12].
Many other structural anomalies and metabolic alterations have also been implicated in the pathogenesis of TAAs but will not be extensively reviewed in this article. The process of cystic medial degeneration can be either due to an innate defect or an acquired one. As can be seen in Table 1 , ascending TAA is frequently seen with connective tissue diseases such as Marfan syndrome, Ehlers—Danlos syndrome, or familial aneurysms syndrome [13].
Data suggests that this process can also occur in congenital disease such as tetralogy of Fallot [14] and bicuspid aortic valve BAV. Hypertension and smoking appear to accelerate the process by increasing elastolytic enzymes in the aortic medial layer [13].
Atherosclerosis has long been considered as a second cause of aortic aneurysm formation, with atheromatous plaques destroying small muscle cells and elastic fiber architectures, resulting in weakening of the aortic wall. However, this concept has recently been challenged; and it is now thought that atherosclerosis is not a primary cause, but a concomitant process in the diseased medial layer of the aortic wall [13].
Other less common etiologies can contribute to TAA formation. These include post-traumatic aortic transection, aortic cannulation post-CABG surgery, chronic aortic dissection, bacterial or syphilitic infection and vasculitic aortitis.
These uncommon etiologies are not discussed in this review. Different studies have shown that the ascending aorta diameter significantly correlates with age, waist circumference, smoking history and hypertension; the latter being the most prevalent risk factor for acute aortic dissection [15].
In a recent study, mean carotid intimal media thickness as well as epicardial adipose tissue were associated with ascending aorta dilatation [16]. In a study examining autopsy cases, six risk factors age, sex, body height, smoking history, hypertension and severe atherosclerosis have been associated with ascending aorta dilations with age being the most important predictor of dilatation [17].
Dilatation of the ascending aorta is a very indolent process as it takes many years to develop and it is asymptomatic initially. In patients who develop an ascending aortic aneurysm secondarily to a systemic disorder, signs of the primary disease are the ones who lead the clinician to look for the dilatation such as in Marfan syndrome.
Otherwise, this pathology remains quiet until its catastrophic complications occur or when it is incidentally seen on cardiovascular imaging related to other causes.
We can prevent these complications by screening asymptomatic patients. Feared events include aortic dissection or rupture, pericardial hemorrhage, cardiac tamponade and occlusion of aortic branches. In addition, some patients, in a lesser proportion, can also develop intramural hematomas or penetrating aortic ulcers. As shown in Table 2. They are greatly dependent on the predisposing condition and, as discussed later, on the management of this disease.
As can be seen in Table 3 , many imaging modalities can be used to image the ascending aorta. We will discuss the advantages and disadvantages of each of these modalities in this section. TAA produces a widening of the mediastinum characterized by a width on AP film of greater than 8 cm at the T4 or carinal level. In the lateral view, there is loss of the retrosternal space. However, this simple and non-invasive test is not neither sensitive nor specific.
Transthoracic echocardiography TTE provides a simple non-invasive technique to evaluate the aortic root, proximal ascending aorta, aortic valve and left ventricular morphology and function in the vast majority of patients.
For aorta assessment, images should be obtained in the parasternal long axis view and the aorta size measured at the onset of the QRS complex at 4 levels of the ascending aorta: annulus, sinuses of Valsalva, ST junction, and ascending tubular aorta maximal diameters. Aortic dimensions can be obtained using a leading-to-leading edge technique [18]. Measurements obtained from two-dimensional images are preferred as m-mode techniques may underestimate the size of the aorta due to translation of the heart during the cardiac cycle.
Even though TTE does not provide consistently an adequate imaging of mid and distal segments of the ascending aorta, nor does it well visualize the descending aorta, it is the recommended imaging technique for screening of patients with suspected aortic aneurysm root or proximal aorta and for follow-up.
A recent study [19] showed that TTE can substitute TEE in the follow-up of TAA dilatation with both modalities having relatively the same accuracy and a very little inter-observer variability. Although, transesophageal echocardiogram TEE provides better view of almost the entire thoracic aorta, it is a semi-invasive technique and it is not the preferred routine study for follow-up or screening.
Since the introduction of CT scanning in the 80s, it has become the preferred imaging technique to define aortic anatomy and its side branch vessels because of its easy accessibility and of its rapid results.
With 3D reconstruction, the accuracy is further enhanced for measurement of aneurysms and the diagnosis of dissection, penetrating ulcer or intramural hematoma. The main disadvantages of CT scanning are the radiation exposure and the risks related to contrast injection such as contrast induced nephropathy CIN , carcinogenicity and teratogenicity.
While CIN can be easily prevented with adequate hydration and reduction of contrast volume, carcinogenicity remains an important issue to consider especially in younger patients i. Marfan syndrome patients who require serial evaluations even in the context of newer generation low dose CT scanners.
For this reason, screening with CT scanning is not routinely recommended, but it is the imaging method of choice to diagnose complications of ascending TAA dilatation and for preoperative visualization of the entire aortic anatomy. MR angiography is an imaging modality that provides accurate measurement and definition of the entire aorta anatomy.
Combined with cardiac MRI, this technology can better assess ventricular function, aortic valve function and aortic root anatomy. While it has the advantages of not requiring any radiation exposure, it is a less accessible and a more time consuming imaging technique.
In addition, it is contraindicated in patients having metallic parts in them and in patients with advanced renal failure because of the possible risk of systemic nephrogenic fibrosis related to gadolinium injection. Normal aorta grows slowly with age. From the Framingham Heart Study echo sub-study , aorta diameter increases 0.
Similar rate of growth is also observed for the tubular portion of the ascending aorta [23]. By the age of 75, normal ascending aorta diameter is approximately 3. Nearly all studies found that hypertension increases ascending aorta dilatation in pre-existing TAAs and predisposes to the formation of TAA. Unlike inherited forms of ascending aortic aneurysms, hypertension related TAAs complicate at diameters over 6. Once the aorta becomes aneurysmal, its rate of growth is somehow accelerated and is strongly influenced by its size.
The database from the Yale Center shows that aneurysms of the thoracic aorta grow at approximately 0. The annual growth varies from 0. The rate of growth is also affected by the location of aneurysm. Aneurysms arising from ascending aorta grow slower 0. Nistri et al. While the valvular complications are directly related to the valve anatomy and its underlying embryological defects, the pathophysiology of the vascular complications is still under debate.
Aortic dilatation could be easily attributed to hemodynamic abnormalities across an abnormally shaped valve but many studies seem to show that valvular dysfunction is not significantly related to increased aortic size. For instance, Ferencik and Pape showed that in patients with BAV with normal valve function, progressive aortic dilatation was more severe than in patients with tricuspid aortic valve TAV [28]. In a case—control study done by Keane et al.
Most studies done so far seem to show an underlying congenital anomaly in the aortic media associated with BAV that predisposes these patients to develop aortic dilatation with an aggravation induced by the valve dysfunction. Very few studies succeeded in establishing a growth rate pattern for patients with BAV, and the evidence remains contradictory. A prospective TEE study has compared the growth rates of the dilated ascending aorta 4. Among the patients studied, 86 had bicuspid and 27 had tricuspid valve and there was no difference in the rate of growth between the two groups [30].
In addition, a recent study at the Montreal Heart Institute showed that ascending aortas in patients with BAV had a growth rate of 0. While it may seem that the natural history of TAA in patients with bicuspid aortic valve disease remains ill-defined, there seems to be a great tendency towards faster growth rate in this population.
Marfan syndrome, first described by Antoine Marfan in , is a connective tissue disorder with manifestations mainly involving the cardiovascular, respiratory, skeletal and ocular systems. While Marfan syndrome predisposes to many other conditions, its most serious complications are related to aortic valve regurgitation and ascending root dilatation. Aortic dissection constitutes the most common cause of death in these patients. Plus, women often complicate at smaller ascending aorta size compared to men [33].
Different studies have tried to establish the growth rate of the ascending aorta in these patients. As shown in Table 4 , the results varied widely, ranging from 0. It has also been noted in certain studies that there are two specific subsets of patients in terms of growth rate: fast growers and slow growers. In a study by Meijboom et al. In the study by Roman et al.
Genetic predisposition other than Marfan syndrome appears to be linked with the development of ascending TAA. Biddinger et al. In this study, patients with family history of TAA, aortic dissection or sudden death exhibited higher prevalence of TAA development and sudden death.
Recently, similar studies support the role of genetic factors in the familial aggregation of TAA [13] , [37] , [38]. Albornoz et al. It seems to be transmitted in an autosomal dominant pattern with variable degree of penetrance. They are older than Marfan group but younger than sporadic group. In some cases, familial TAA appears to be an aggressive aortic disease and family history of TAA, aortic dissection or sudden death needs to be considered as risk factor for rapid growth of TAA and its complications.
Loeys—Dietz syndrome is an autosomal dominant genetic disorder mainly associated with mutations of the genes responsible for the transforming growth factor B receptors 1 and 2. It is a rather rare disease characterized by the triad of hypertelorism, a bifid uvula, cleft palate or both, and generalized arterial tortuosity with widespread vascular aneurysm and dissection [11].
This disorder is nearly always associated with aortic root aneurysm and they tend to have complications very early on in life. In the study by Loeys et al. In addition, women with this disease have higher tendency to have aortic dissection during pregnancy. Ehlers—Danlos regroups a multitude of connective tissue disorders characterized by laxity of the Joints and skin disorders. This population has not been extensively studied but the associated TAA seems to be of little clinical importance as a recent retrospective study suggested that these aortas seem to normalize in size when children with EDS become adults [41].
However, type IV Ehlers—Danlos syndrome autosomal dominant disorder is characterized by characteristic skin manifestations associated with arterial, uterine and intestinal dissection and rupture [42]. Arterial complications are usually preceded by aneurysm formation but they can also occur spontaneously.
Arterial tortuosity syndrome is an autosomal recessive disorder characterized by tortuosity and aneurysm formation in the major arteries caused by a deficiency in glucose transporter GLUT 10 causing an upregulation of TGFBR1 signaling [11]. Aneurysms osteoarthritis syndrome is an autosomal dominant syndromic characterized by thoracic aortic aneurysms and dissections associated with the presence of arterial aneurysms, early-onset osteoarthritis and cutaneous manifestations.
As has been previously mentioned, complications of ascending aorta aneurysms can be disastrous even if diagnosed promptly and properly managed. It is therefore essential to diagnose a pathologically dilated ascending aorta in a timely fashion and to ensure a proper follow-up in order to start medical therapy and recommend prophylactic surgical repair. Several studies have demonstrated the reduction in mortality associated with prophylactic surgery Table 5.
Corrective surgery is recommended when the aorta reaches a size where the risk of complications equals or exceeds the risk related to the surgery.
There have been many studies that tried to establish a specific size at which surgery should be performed, but it has been shown that this criterion depends on the underlying pathology, the rate of growth, the family history and to some extent the individual morphology of each patient. A retrospective study that included a few patients with Marfan syndrome showed that the median size associated with an increased risk of aortic dissection, rupture or sudden death was 6.
In the same study, we see that the odds ratio of acute dissection for an aorta between 5. It is therefore safe to recommend prophylactic surgery when the aorta reaches a diameter of 5. These results led some experts to develop other measures that can possibly better predict the risk of complications. For example, a novel method that takes into account the body surface area called the aortic size index ASI , measured by MRI, by dividing the maximal aortic diameter with the body surface area [2].
This formula allowed to identify 3 different risk groups: those with an ASI higher than 4. This index allows a certain individualization of the size at which people should be recommended surgery. As of today, it is recommended to offer prophylactic ascending aorta repair to patients without predisposing conditions other than hypertension when the aorta reaches 5.
As has been already mentioned in this review, patients with Marfan syndrome tend to have acute aortic syndromes at a younger age and at smaller aortic diameters than other patients refer to Table 2.
The newest American guidelines recommend prophylactic surgery for patients with Marfan syndrome in 6 settings [46] :. When the aorta reaches a diameter of 4. When the patient is undergoing aortic valve replacement, if the aorta exceeds 4. Associated significant aortic valve regurgitation, if the aorta exceeds 4. Some references even suggest lowering the threshold for surgery to all patients with Marfan syndrome to 4.
Choice of surgical procedure is discussed in the following section. For patients born with a bicuspid aortic valve, data is still somewhat contradictory about the diameter at which complications occur. It is now widely accepted that this is a heterogeneous population. Therefore, there is variability with the determination of a specific diameter at which the risk of complications increases.
Most centers recommend elective replacement when the ascending aorta reaches 5. Choice of surgical procedure has not been extensively studied. In patients diagnosed with Loeys—Dietz syndrome, complications from TAA occur at a much younger age and at smaller ascending aortic diameters than most other patients, thus requiring even more aggressive prophylactic therapy. The authors of the main study on aneurysm syndromes in patients with Loeys—Dietz syndrome recommend prophylactic surgery at experienced centers when the aorta reaches 4.
Likewise, the latest guidelines from the ACCF recommend prophylactic surgery when the ascending aorta reaches 4. As can be noticed, all international guidelines recommend prophylactic surgery for TAA at sizes somewhat equivalent. Comparison of national guidelines for the management of TAA in patients without any genetic predisposition. Comparison of national guidelines for the management of TAA in patients with Marfan syndrome. Progressive aortic regurgitation, especially if the surgeon believes the aortic valve can be spared and an aortic valve-sparing procedure is planned.
Progressive dilation of more than 2 mm per year as confirmed by repeated measurements. Comparison of national guidelines for the management of TAA in patients with bicuspid aortic valve. If diagnosed early, mild to moderate dilated ascending aortas can certainly benefit directly from medications such as beta blockers and ACE inhibitors.
In addition, it is very important to prevent and treat risk factors such as hypertension and metabolic syndrome. In patients with Marfan syndrome, a landmark trial by Shores et al. The physiological effect of beta blockers on the natural history of the dilated ascending aorta is not clearly understood, and a combination of reduced wall stress and vascular remodeling has been proposed.
As mentioned earlier, patients with mildly dilated ascending aorta are those who benefit the most from beta blockade as shown in a study by Haouzi et al. In addition, many authors have shown interest in the effect of angiotensin converting enzyme inhibitors ACEIs on the rate of dilation of TAA.
In one study, the addition of perindopril to beta-blockers significantly reduced the aortic diameter as well as the aortic stiffness in a small sample of 10 patients with Marfan syndrome [51].
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