ALSPA, HAGL,GLAD & BANKART

The 3 glenohumeral ligaments (GHLs) represent condensations of the shoulder capsule.The posterior capsule always inserts into the posterior labrum. The anterior capsule has a more variable medial insertion  on the labrum (47%) or glenoid neck (49%).The most important structure stabilizing the shoulder—one that limits gross anterior-inferior subluxations and dislocation—is the IGHL. This ligament forms a sling with discrete anterior and posterior bands. It is lax when the humerus is in the neutral position, and it allows normal shoulder movement. The ligamentous complex becomes taut in abduction and external rotation and, thus, stabilizes the joint at the end range of shoulder movement in the abduction external rotation (ABER) direction.

During a dislocation, forces exceed the threshold that the ligamentous complex can bear, leading to tears or stretching. This may lead to laxity and instability. Failure of the IGHL can occur at the insertion site (40%), in the ligamentous substance (35%), and at the humeral insertion site (25%).Bankart lesions represent failure of the IGHL at the glenoid insertion. IGHL capsule laxity represents intrasubstance ligamentous failure, whereas humeral avulsions of the GHL (HAGL) represent failure of the IGHL at its humeral insertion

A Bankart lesion is the most common lesion in anterior instability. The tear is usually large enough to involve not only the labrum, where the anterior band of the IGHL inserts, but also the middle labrum and, sometimes, the superoanterior labrum 

in a Bankart lesion, the scapular periosteum ruptures as the labroligamentous ligaments are avulsed from the glenoid. In Bankart variants, the scapular periosteum remains intact relative to the labroligamentous complex. If the labroligamentous complex is displaced medially and shifted inferiorly, rolling up on itself, the lesion is called an ALPSA lesion. An ALPSA lesion is associated with more severe injury.In the ALPSA, the labral fragment remains attached to the periosteum of the scapular margin and can be tethered in this abnormal position, increasing the likelihood further medial displacement and of re-dislocation.

A GLAD lesion is a tear of the anteroinferior labrum (nondisplaced) with avulsion of the adjacent glenoid cartilage. A glenoid chondral defect is therefore visualized. The labrum is not detached, and there is no capsular stripping. This lesion is clinically stable. The mechanism is glenohumeral impaction in the ABER position. Clinically, these patients complain of pain rather than instability. The lesion can be treated with arthroscopic debridement without need for a stabilization procedure

enoxaparin & fondparinux

     A critical pentasaccharide sequence inheparin molecules is required for their binding to ATIII and for promoting the change in conformation of ATIII. In unfractionated heparin, which has a molecular size distribution of 5,000 to 30,000 d, with the majority of chains containing ≥ 18 saccharide units and LMWHs (CLEXANE), produced by chemical or enzymatic depolymerization of unfractionated heparin to yield molecular species that range from 1,000 to 10,000 d,only approximately 30% of the molecules present in heparin preparations contain the ATIII-binding sequence. The remainder is composed of polyanionic chains that may bind nonspecifically, through electrostatic interactions, to a large number of other plasma proteins. This phenomenon possibly accounts for some of the  undesirable side effects of LMWH like HIT.  well-defined pentasaccharides constitutes more potent, more selective, and consequently safer drugs.  fondaparinux (ARIXTRA) is a synthetic pentasaccharide that selectively inhibits factor Xa.

          Enoxaparin( clexane) is a low molecular weight heparin marketed as Lovenox or Clexane.it binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and IIa. The anticoagulant effect of enoxaparin can be directly correlated to its ability to inhibit factor Xa. Factor Xa catalyzes the conversion of prothrombin to thrombin, so enoxaparin’s inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation.Enoxaparin does not affect the international normalized ratio (INR), prothrombin time (PT) or activated partial thromboplastin time (aPTT). anti factorXa is used to monitor its acitivity.