Serotonergic thrombocytopathy and its effects on platelets during orthopaedic surgery.

The serotonergic effects on platelet dysfunction (thrombocytopathy) can cause deficient hemostasis during orthopaedic surgery. Peripheral serotonin located within the granules of platelets assists in initial platelet aggregation. Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs) are drugs used to treat a myriad psychological-related, mental-related, and psychosocial-related disorders. A correlation exists between low levels of peripheral serotonin and a bleeding diathesis during orthopaedic surgery. The relationship of excessive bleeding during orthopaedic surgery secondary to thrombocytopathy and low levels of serotonin caused by drugs that inhibit the reuptake of serotonin is presented.

Pathogenesis of tendon rupture secondary to fluoroquinolone therapy.

Tendon rupture related to trauma and corticosteroid injection, in and about tendon insertion sites, is well documented in the literature. Rupture of tendon after fluoroquinolone therapy has been identified in the recent past. Both short- and long-term courses of antibiotic treatment with fluoroquinolone may precipitate alteration in tendon matrix leading to tendinopathy with subsequent rupture. The pathogenesis of tendon rupture secondary to fluoroquinolone therapy is presented.

The pathogenesis and biomechanics of turf toe.

Sprain injury to the 1st metatarsophalangeal joint is referred to as turf toe. The incidence of this injury has increased over the years secondary to athletic fields being covered by artificial turf and also by increased flexibility of the toe box in athletic shoes. The pathogenesis of turf toe will be presented in this article.

The pathogenesis of systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease that causes inflammation in the tissues of the brain, endothelial cells, gastrointestinal/genitourinary (GI/GU), joints, kidneys, muscles, and skin. Lupus comprises a range of multisystem disorders involving the deposition of aberrant immune complexes into tissues. Inflammation occurs as a result of autoantibodies attacking organ systems. The pathogenesis of systemic lupus erythematosus is presented.

Dupuytren's disease.

Dupuytren's disease is a nonmalignant fibroproliferative disease that causes progressive and permanent contracture of the palmar fascia with subsequent flexion contracture of the digits. Although the exact etiopathology in the development of Dupuytren's disease is unknown, certain familial, racial, and physiologic factors have been determined. The latest prospective pathogenesis of Dupuytren's disease are presented.

Rhabdomyolysis.

Rhabdomyolysis is the dissolution of skeletal muscle. Breakdown of the myocyte causes the extravasation of intracellular constituents, leading to a clinical syndrome--the classic triad of brown urine, muscle pain, and weakness. The pathogenesis of rhabdomyolysis is presented.

Osteonecrosis: death of bone cells.

Osteonecrosis is a pathologic process resulting from direct and indirect injury to the bones' vascular supply. Varying microangiopathic entities cause the death of bone. Bone cell death subsequently causes loss of joint function, impaired mobility, and microfractures leading to collapse of the joints' articular surface. The pathogenesis of osteonecrosis is presented.

Stimulators of bone healing. Biologic and biomechanical.

Bone is a dynamic biologic tissue. Metabolically active, the stimuli for bone degeneration and regeneration is influenced and modulated by biomechanical and biologic (cellular, hormonal, and molecular) physiologic processes. This article discusses the biologic and biomechanical stimulators and inhibitors of bone healing.

Pathogenesis of anterior cruciate ligament injury.

Pathology, part of the basic science of medicine and nursing, is an understanding of how cellular mechanisms and organ systems function conjointly in the physical body. An awareness of the biomechanics and pathophysiology related to a particular mechanism of injury (MOI) provides a more appreciative sense of how tissues become damaged. Cognizance of the variables and risk factors involved in MOI specific to anatomic structures not only helps the Health Care Provider (HCP) decide which treatment options are necessary, but knowing risk factors helps in preventive tactics, counseling an athlete for optimal training, and rehabilitation of the injured athlete. This article discusses the pathophysiology related to anterior cruciate ligament (ACL) injury, one of the most common and costly ligamentous knee injuries. The differentiation between contact versus noncontact mechanisms and risk factors plaguing women athletes will be listed.

Cervical whiplash syndrome. Hyperextension-hyperflexion injury.

Cervical whiplash syndrome, or hyperextension-hyperflexion injury, is a common traumatic injury to the soft tissue structures around the cervical spine. The mechanisms of injury that cause cervical whiplash syndrome vary, yet they may be sufficient enough to cause cervical spine fracture, resulting in partial or complete neurologic deficit. The pathogenesis of cervical whiplash syndrome are presented.

Double crush syndrome.

Nerve entrapment conditions and peripheral neuropathies are sometimes related to injurious events, toxicosis, and repetitive microtrauma to soft tissue and nerve structures. An interesting theory concerning peripheral entrapment neuropathy has been discussed in the literature. This theory is called the double crush syndrome. This article briefly discusses the biologic/metabolic, structural, toxicogenic, and vasculopathic rationale for the pathogenesis of double crush syndrome.

Muscle wasting.

The loss of lean body mass (muscle wasting) is initiated by cascades or events that precipitate increased proteolysis. Muscle wasting is stimulated by internal and external factors. Humorally related feedback loops stimulated by disease states, e.g., cancer, inflammatory myopathies, leukemia, or sepsis, and initiated as a response to systemic inflammatory response syndrome can cause a downward progression of events, resulting in chronic illness or even death. This article discusses the pathogenesis of muscle wasting, which is often referred to as cachexia.

Diffuse idiopathic skeletal hyperostosis: Forestier's disease.

Diffuse idiopathic skeletal hyperostosis (DISH) or Forestier's disease is characterized by calcification and ossification of soft tissue entheses of ligaments and tendons. DISH is believed to be a variant of osteoarthritis (OA) without the degenerative intervertebral disc and joint degenerative qualities seen in classic OA. The likely pathoetiologic causes of DISH are presented.

Reactive arthritis. Immune-mediated synovitis or joint infection.

Reactive arthritis is one form of the seronegative Spondyloarthropathies. Susceptibility to reactive arthritis is closely linked to individuals who have the genetic predisposition to the HLA-B27 allele (gene form). Although there is a reactive-inflammatory joint reaction present, the synovium is not damaged by infectious agents (bacteria, fungi, or virus). This article discusses the pathogenesis of reactive arthritis.

Syndesmotic ankle sprain.

Ankle sprain injuries are the most common type of joint sprain. The prevalence of ankle joint sprains accounts for 21% of joint injuries in the body. Although somewhat rare, high-ankle or syndesmotic ankle sprains occur in up to 15% of ankle trauma. This article will present the pathomechanics of the high-ankle or syndesmotic sprain.

Musculoskeletal manifestations of Ehlers-Danlos syndrome.

Ehlers-Danlos syndrome is a disorder caused by mutations in connective tissue and muscle tissue genes. Alteration in genes disrupts the functional ability of muscles, ligaments, and joints. Adaptation in the formation of collagen also affects the support and elasticity that collagen provides to the musculoskeletal system. The pathogenesis of Ehlers-Danlos syndrome, as it relates to the musculoskeletal system, is presented.

Biofilm: the pathogenesis of slime glycocalyx.

Biofilm is a complex aggregation of microorganisms. Biofilm, also called glycocalyx, functions within an extracellular slimy exopolysaccharide material. The morphology and pathogenesis of biofilm as it relates to Staphylococcus epidermidis in orthopaedic implant patients are presented.

Care of the orthopaedic trauma patient.

The perianesthesia nursing care of the orthopaedic trauma patient focuses on injuries of the musculoskeletal system and the associated muscles, ligaments, tendons, and joints. Multitrauma patients often sustain more than one musculoskeletal injury at the time of the traumatic event. Early stabilization, astute nursing assessments, and interventions are imperative to the patient's functional outcome and rehabilitation. Knowing the mechanism of injury is essential to understanding and caring for musculoskeletal trauma injuries. Because patients with traumatic orthopaedic injuries are at a higher risk for wound infections, it is important for perianesthesia nurses to initiate careful infection control practices. Recognizing significant orthopaedic trauma complications that include compartment syndrome, fat embolism syndrome, and hypovolemic shock is vital for saving the life or limb of the patient.

Tension pneumothorax: a pulmonary complication secondary to regional anesthesia from brachial plexus interscalene nerve block.

Interscalene brachial plexus anesthesia is often used for surgeries involving the shoulder and upper arm. This method of regional anesthesia decreases pain, nausea, and vomiting associated with general anesthesia. One infrequent complication of interscalene brachial plexus block is tension pneumothorax. Recognition of early signs and symptoms of tension pneumothorax and expeditious treatment for rapid decompression before physiologic decompensation is mandatory. This article discusses the interscalene brachial plexus block procedure leading to the pathogenesis, clinical presentation, diagnosis, and treatment of tension pneumothorax.