A more recent study suggested that the formation of "fibrinous" adhesions is preceded by the aggregation of cavity macrophages, that can act like extravascular platelets in the abdominal cavity.If this is allowed to happen, tissue repair cells such as macrophages, fibroblasts, and blood vessel cells penetrate into the fibrinous adhesion and lay down collagen and other matrix substances to form a permanent fibrous adhesion. In 2002, Giuseppe Martucciellos research group showed a possible role could be played by microscopic foreign bodies (FB) inadvertently contaminating the operative field during surgery. These data suggested that two different stimuli are necessary for adhesion formation: a direct lesion of the mesothelial layers and a solid substrate foreign body (FB). While some adhesions do not cause problems, others may prevent muscle and other tissues and organs from moving freely, sometimes causing organs to become twisted or pulled from their normal positions. Regions affected
Adhesive capsulitis
In the case of adhesive capsulitis of the shoulder (also known as frozen shoulder), adhesions grow between the shoulder joint surfaces, restricting motion. Abdominal adhesions
Abdominal adhesions (or intra-abdominal adhesions) are most commonly caused by abdominal surgical procedures. The adhesions start to form within hours of surgery and may cause internal organs to attach to the surgical site or to other organs in the abdominal cavity. Adhesion-related twisting and pulling of internal organs may result in complications such as  abdominal pain or intestinal obstruction. Small bowel obstruction (SBO) is a significant consequence of post-surgical adhesions.
In 2018, the American College of Chest Physician stated that it is presents if there is an inadequate response to high-dose vasopressor therapy defined as ≥ 0.5 mg/kg/min norepinephrine-equivalent dose. Management
Reversing the underlying causes of vasodilatory shock, stabilizing hemodynamic, preventing renal, myocardial, and other organs from injuries due to hypoperfusion and hypoxia, and taking necessary measures to safeguard against complications including venous thromboembolism are served as the top priorities during the treatment.The initial treatment aiming at restoring effective blood pressure in patients that have refractory shock typically starts with introducing norepinephrine and dopamine. Vasopressin comes as the second-line agent.However, high-dose therapy is linked to excessive coronary, splanchnic vasoconstriction, and hypercoagulation. Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak myocardial function.In those whose vasodilatory shock is caused by hypocalcemic cardiomyopathy in the context of dilated cardiomyopathy with documented both reduced heart ejection fraction and contractile performance, the uses of calcium and active vitamin D or recombinant human parathyroid hormone treatment are viable since there were many successful cases reported while given the physiological role of calcium on muscle contraction.A successful treatment requires leveraging the respective unique contributions of a multi-disciplinary team not only critical care doctors and often, infectious disease specialists but also respiratory therapy, nursing, pharmacy and others in collaboration. Epidemiology
Observational studies suggest that, about 6% to 7% of critically ill people may end up developing refractory shock. Prognosis
Early recognition and rapid treatment initiation are crucial to saving life.