Signs and symptoms
Significant pain, sometimes felt along the arm past the shoulder. Sensation that the shoulder is slipping out of the joint during abduction and external rotation. Shoulder and arm held in external rotation (anterior dislocation), or adduction and internal rotation (posterior dislocation). Resistance of all movement. Numbness of the arm. Visibly displaced shoulder. Some dislocations result in the shoulder appearing unusually square. No palpable bone on the side of the shoulder. Diagnosis
A diagnosis of shoulder dislocation is often suspected based on the persons history and physical examination. Radiographs are made to confirm the diagnosis. Most dislocations are apparent on radiographs showing incongruence of the glenohumeral joint. Posterior dislocations may be hard to detect on standard AP radiographs, but are more readily detected on other views. After reduction, radiographs are usually repeated to confirm successful reduction and to detect bone damage. After repeated shoulder dislocations, an MRI scan may be used to assess soft tissue damage. In regards to recurrent dislocations, the apprehension test (anterior instability) and sulcus sign (inferior instability) are useful methods for determining predisposition to future dislocation.There are three main types of dislocations: anterior, posterior, and inferior. Anterior (forward)
In over 95% of shoulder dislocations, the humerus is displaced anteriorly. In most of those, the head of the humerus comes to rest under the coracoid process, referred to as sub-coracoid dislocation. Sub-glenoid, subclavicular, and, very rarely, intrathoracic or retroperitoneal dislocations may also occur.Anterior dislocations are usually caused by a direct blow to, or fall on, an outstretched arm.
This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy including aortic insufficiency, nonischemic dilated cardiomyopathy, and noncompaction cardiomyopathy. Because the papillary muscles, chordae, and valve leaflets are usually normal in such conditions, it is also called functional mitral regurgitation.Acute MR is most often caused by endocarditis, mainly S. aureus. Rupture or dysfunction of the papillary muscle are also common causes in acute cases, dysfunction, which can include mitral valve prolapse. Pathophysiology
The pathophysiology of MR can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase. Acute phase
Acute MR (as may occur due to the sudden rupture of the chordae tendinae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume) but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction); this happens because of more complete emptying of the heart. However, as it progresses the LV volume increases and the contractile function deteriorates, thus leading to dysfunctional LV and a decrease in ejection fraction.