By V. Dan. Virginia Military Institute. 2018.
Arthritis—Nonerosive arthritis involving two or more peripheral joints with tender- ness cheap sildalis 120 mg with amex, swelling and effusion 6 buy sildalis 120 mg with mastercard. Hematologic disorder—Hemolytic anemia, leukopenia, thrombocytopenia, lymphopenia 10. Immunologic—(+)LE cell preparation or Anti-DNA antibody, or Anti-SM, false positive test for syphilis 11. ANA Clinical Fatigue, fever, weight loss, GI complaints Alopecia Vasculitis Arthritis Jaccoud’s Arthritis – Small joints of the hands, wrist, Nonerosive deforming arthritis and knees Ulnar deviations of the fingers and sublux- – Symmetric ations which are reversible early – Migratory, chronic, nonerosive May become fixed – Soft tissue swelling – Subcutaneous nodules – Synovial analysis—ANA (+) – Jaccoud’s arthritis Arthralgias Muscle pain and weakness 112 RHEUMATOLOGY Labs Depressed complement—C3 and C4 Ds-DNA Anti-SM Treatment NSAIDs, corticosteroids, antimalarials, methotrexate, cyclophosphamide, azathioprine, cyclosporine A PROGRESSIVE SYSTEMIC SCLEROSIS (SCLERODERMA) Progressive Chronic Multisystem Disease Classified by the degree of skin thickening Fibrosis-like changes in the skin and epithelial tissues of affected organs Subsets: – Diffuse Cutaneous Scleroderma Heart, lung, GI, kidney ANA(+) Anticentromere Antibody (–) Rapid onset after Raynaud’s phenomenon Variable course—poor prognosis – Limited cutaneous Scleroderma—CREST Syndrome Crest Syndrome Progression after Raynaud’s phenomenon Calcinosis Anticentromere Antibody (+) Raynaud’s phenomenon Good prognosis Esophageal dysmotility – Overlap syndromes Sclerodactyly Combinations of connective tissue disease Telangiectasia – Undefined CTD No clinical or laboratory findings – Localized scleroderma Morphea, linear scleroderma Clinical Skin thickening—face, trunk, neck Symmetric arthritis with involvement of the fingers, hands, arm, legs Initial symptoms—Raynaud’s phenomenon with fatigue, and musculoskeletal complaints Raynaud’s Phenomenon Vasospasm of the muscular digital Causes of Raynaud’s arteries can lead to ischemia, Collagen vascular disease—PSS, ulceration of the fingertips SLE, RA, Dematomyositis/ Triggered by cold and emotional stresses Polymyositis Reversal of episode occurs after Arterial occlusive disease stimulus has ended—and digits rewarmed Pulmonary HTN Present in 90% of patients with scleroderma Neurologic—SCI, CVA Treatment Blood dyscrasia – Education against triggers—cold, smoking Trauma – Rewarming Drugs—ergots, beta blockers, – Calcium channel blockers—nifedipine cisplatin – EMG and biofeedback—self-regulation (Braunwald, et al. ANA AND RF ANA RF MCTD + + RA + + SLE + – Scleroderma (PSS) + – Polymyositis + – Sjögren’s + + (+) HLA-B27 A S Reiter’s Psoriatic arthritis Enteropathy arthropathy Pauciarticular JRA RHEUMATOLOGY 115 VASCULITIS POLYARTERITIS NODOSA Systemic necrotizing vasculitis Male:female ratio is 2:1 Also seen in: Small, medium artery involvement R Glomerulonephritis—#1 cause of death SLE Lungs spared Sjögren’s Skin—palpable purpura Mononeuritis multiplex, arthritis GIANT CELL ARTERITIS: ALSO KNOWN AS TEMPORAL ARTERITIS (TA) More common in females > 50 years old Large arteries Tenderness of the scalp and in the muscle of mastication Headaches, abrupt visual loss in 15% of patients Diagnosis: Elevated ESR, temporal artery biopsy Treatment: High dose steroids imperative to prevent permanent visual loss Polymyalgia Rheumatica (PMR) In view of clinical similarities between PMR patients with and without signs of arteritis in a temporal artery biopsy, many authors believe that PMR is an expression of giant cell arteritis Fever, weight loss, malaise Proximal muscles—neck, pelvic Shoulder Morning stiffness—muscle tenderness Abrupt myalgias/arthralgia Diagnosis: ↑ ESR > 50 Treatment: steroids WEGENER’S GRANULOMATOSIS Small artery involvement Male, middle aged Necrotizing granulomatous vasculitis involving – Upper/lower respiratory tract – Focal segmental glomerulonephritis “Saddle-nose” deformity Pulmonary, tracheal, ocular, and cutaneous manifestation 116 RHEUMATOLOGY TAKAYASU Elastic large arteries—Aorta Asian females, 40 years old Erythema nodosum on the legs Pulselessness, arm claudication BEHÇET’S Small vessels Oral and genital skin ulcers 20% experience venous thrombosis GOODPASTURE’S Pulmonary and kidney involvement SJÖGREN’S SYNDROME Autoimmune-mediated disorder of the exocrine glands CLINICAL PRESENTATION: (sicca symptoms) Dry eyes Dry mouth Skin lesions Parotid involvement LABS: ANA (+), RF (+) Classification: Primary and secondary forms Primary—Dry eyes and mouth with ANA (+) , RF (+) Secondary—sicca symptoms – Sjögren’s syndrome plus evidence of SLE, RA, PSS, Polymyositis EXTRAGLANDULAR MANIFESTATIONS Arthralgias Raynaud’s phenomenon RHEUMATOLOGY 117 ARTHRITIS AND INFECTIOUS DISORDERS SEPTIC ARTHRITIS Clinical Picture: Septic Arthritis Rapid onset of moderate to severe joint pain, erythema, and decreased ROM Monoarticular, leukocytosis Knee is the most common joint Risk factors—age, prosthetic joints, comorbidities such as anemia, chronic diseases, hemophilia. Coli) Bone scans 118 RHEUMATOLOGY Treatment Antibiotic coverage Frequent needle aspirations with arthroscopic lavage TABLE 3–7. Joint Fluid Analysis Property Normal Noninflammatory Inflammatory Septic Viscosity High High Low Variable Color Colorless Straw Yellow Turbid-Yellow Clarity Transluscent Transluscent Transluscent Opaque WBC < 200 < 5000 1000–75000 > 100,000 PMN% < 25 < 25 > 50 > 85 Culture Negative Negative Negative Positive Mucin clot Good Good Fair Poor Glucose Equal to blood Equal to blood < 50 mg/dl > 50 mg/dl lower than lower than blood blood OTHER INFECTIOUS CAUSES OF ARTHRITIS Viral Infections—Rubella, infectious hepatitis Fungi—Seen in Immunocompromised adults Mycobacterium—tuberculosis of the spine (Pott’s disease) – Thoracic involvement – TB arthritis—Hips and knees Monoarticular Radiologic findings—Phemister’s triad Juxta-articular osteoporosis Marginal erosions Joint space narrowing Lyme Disease – Tick borne—Borrelia burgdorferi – Classic presentation Erythema migrans—bull’s eye rash Cardiac, neurologic, articular manifestations – Intermittent migratory episodes of polyarthritis – Commonly affects the knee – Synovial fluid—Inflammatory – Diagnosis—ELISA, Western blot analysis – Management—First-line antibiotics: Adults: Doxycycline Children: Amoxicillin – Pattern of Onset: Bite Rash Systemic dz. Neurologic involvement RHEUMATOLOGY 119 DEPOSITION AND STORAGE DISEASE HEMOCHROMATOSIS Organ damage and tissue dysfunction secondary to excessive iron stores and the deposi- tion of hemosiderin Organs → Hepatic cirrhosis, cardiomyopathy, DM, pituitary dysfunction Skin pigmentation Chronic progressive arthritis – Occurs commonly in second and third MCP, PIP joints. It may also affect the hip joints Males ~40–50 years old Treatment: Phlebotomy, NSAIDs ALKAPTONURIA (OCHRONOSIS) Autosomal recessive Deficiency in the enzyme homogentisic acid oxidase leads to its increase Alkalinization and oxidation causes darkening of tissue parts termed ochronosis – Blueish discoloration of the urine, cartilage, skin, sclera secondary to the accumulation of homogentisic acid Progressive degenerative arthropathy – Onset—in the fourth decade – Spinal column involvement – Arthritis of the large joints, chondrocalcinosis, effusions, osteochrondral bodies WILSON’S DISEASE Autosomal recessive Deposition of copper leads to destruction: – Liver leading to cirrhosis – Brain – Kidneys – Ocular—Kayser-Fleischer rings OA—wrists, MCP, knees, spine Osteoporosis Treatment: Copper chelation with penicillamine, dietary restriction GAUCHER’S DISEASE Autosomal recessive—Ashkenazi Jews Glucocerebroside accumulates in the reticuloendothelial cells of the spleen, liver, and bone marrow Monoarticular hip and knee degeneration 120 RHEUMATOLOGY OTHER SYSTEMIC DISEASES SARCOIDOSIS Systemic chronic granulomatous disease—can affect any organ system Pathogenesis: disseminated noncaseating granulomatous Eight times more common in blacks, females > males Clinical features: – Pulmonary – Hilar adenopathy – Fever, weight loss, fatigue – Arthritis: polyarthritis, 4-6 joints Knees, PIP, MCP, wrists – Skin—Lofgren’s Syndrome – Arthritis, Hilar adenopathy, Erythema nodosum AMYLOIDOSIS Homogeneous eosinophilic material seen with Congo red dye Deposition of amyloid in the kidneys, liver and spleen Clinical features: – Renal disease is primary clinical feature – Cardiomyopathy – Median neuropathy – Pseudoarthritis—periarticular joint inflammation – Effusions: Arthrocentesis—“Shoulder-pad” sign HEMOPHILIA ARTHROPATHY X-linked recessive disorder, predominately in males—associated with HIV 2° to transfu- sions of factor and blood Blood coagulation disorder caused by Factor VIII deficiency (classic hemophilia A) and Factor IX deficiency (Christmas disease, hemophilia B) Bleeding into bones and soft tissue causes hemarthrosis, necrosis and compartment syn- drome Elbow, knee, wrist are common Arthritis is caused by the remaining blood in the joint depositing hemosiderin into the synovial lining → proliferation of the synovium and pannus formation Radiologic: Joint space narrowing, subchondral sclerosis and cyst formation Treatment: Conservative care (immobilization, rest, ice), Factor VIII replacement, reha- bilitation, joint aspiration as a last resort SICKLE-CELL DISEASE Biconcave RBC changes to an elongated crescent sickle-shape causing obstruction of the microvasculature Musculoskeletal complications: – Painful crisis—Most common event Abdomen, chest, back Pain in the large joints from juxta-articular bone infarcts with synovial ischemia RHEUMATOLOGY 121 – Dactylitis—“Hand-Foot” Syndrome Painful non-pitting swelling of the hands and feet – Osteonecrosis Local hypoxia with occlusion to the venous system by the sickled cells 1/3 femoral heads and 1/4 humeral heads go on to osteonecrosis – Osteomyelitis—most commonly caused by Salmonella NEUROPATHIC ARTHROPATHY (CHARCOT’S JOINT) DEFINITION Chronic progressive degenerative arthropathy, secondary to a sensory neuropathy with loss of proprioception and pain sensation, leading to instability and joint destruction CAUSES → “STD” “SKA” → SHOULDER, KNEE, ANKLE Syringomyelia → Shoulder Tabes dorsalis # 2 → Syphilis → Knee Diabetic Neuropathy → # 1 cause → Ankle CLINICAL Early findings: Painless swelling, effusion and joint destruction Late findings: Crepitation, destruction of cartilage and bones, intra-articular loose bodies Subtle fractures RADIOLOGIC Joint destruction Hypertrophic osteophytes Loose bodies caused by micro fractures Disorganization of the joint—Subluxation and dislocation TREATMENT Immobilization Restriction of weight bearing Charcot Joint vs. Osteoarthritis May mimic OA early in the disease— Both have: Soft tissue swelling Osteophytes Joint effusion Charcot joints have: Bony fragments Subluxation Periarticular debris 122 RHEUMATOLOGY TABLE 3–8. Hip Pain in Children (Janig and Stanton-Hicks 1996; Kaggs and Tolo 1996; Koop Quanbeck 1996; Jensen et al. Growth arrest— Proximal and lateral epiphysis avascular stage migration of the femoral Grade I: < 33% 2. Subchondral fracture— head from the Grade II: 33–50% “Crescent sign” acetabulum Grade III: > 50% 3. Healed RHEUMATOLOGY 123 TABLE 3-8 (Continued) Congenital Slipped Capital Femoral Legg-Calve-Perthes Hip Dislocation Epiphysis (SCFE) Disease (LCPD) Treatment Goal—return the hip into Bed rest—weight relief 1. Prevent femoral head pathologic changes Surgery is the preferred collapse Closed Reduction— method of treatment— Containment techniques < 6 mo Knowles pinning Permit weight bearing Position devices Nonsurgical—traction, of the femoral head to Triple diapers body casts, hormonal assist healing and Frejka pillows therapy remodeling Splints: Craig, Von Greater than 6 years old Rosen-Pavlik harness: Abduction braces allows hip motion Petrie casts, Toronto within the safe zone brace, Salter stirrup while maintaining Surgical— abduction Epiphysiodesis Traction, casting, surgical Valgus Osteotomy Complication 1. OA Thomas Test: To detect flexion contractures of the hip and evaluate range of hip flexion 1. Have patient hold one leg on chest, lower other leg flat Indicators of fixed flexion contracture/deformity: 1. Emotional stress May be associated with Irritable Bowel Syndrome, RA, Lyme, hyperthyroidism ARA CLASSIFICATION: 1. Widespread pain—pain in the left and right side of the Classification body above and below the waist. Pain in 11–18 tender points (Figure 3-5) months Bilateral involvement Occipital, lower cervical, trapezius, supraspinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knee FMS SHOULD BE DIFFERENTIATED FROM MYOFASCIAL PAIN SYNDROME AND CHRONIC FATIGUE SYNDROME Myofascial Pain Syndrome Local pain and tender points that resolves with local treatment, but may recur Fatigue, morning stiffness uncommon Chronic Fatigue Syndrome Disabling fatigue at least six months Preceded by a viral syndrome TREATMENT OF FMS Patient education and reassurance Nortriptyline—sleep disturbance RHEUMATOLOGY 125 NSAIDs and corticosteroids Combination therapy is effective Biofeedback, tender point injection Acupuncture, aerobic exercise Greater Trochanter FIGURE 3–5. Fibromyalgia: Location of Specific Tender Points COMPLEX REGIONAL PAIN DISORDER (CRPD) OTHER NAMES Sudeck’s atrophy Algodystrophy Shoulder hand syndrome RSD: Reflex Sympathetic Dystrophy 126 RHEUMATOLOGY CHARACTERISTICS Limb pain, swelling, and autonomic dysfunction Most commonly caused by minor or major trauma CLINICAL FEATURE Pain, deep burning exacerbated by movement – Allodynia—pain induced by a nonnoxious stimulus – Hyperalgesia—lower pain threshold and enhanced pain perception Local edema and vasomotor changes – Extremity is warm, red, and dry initially – Later becomes cool, mottled, and cyanotic Muscle weakness Dystrophic changes – Thin, shiny skin, brittle nails CLINICAL STAGES 1. Acute—few weeks–6 months – Pain, hypersensitivity, swelling, and vasomotor changes – Increased blood flow creating temperature and skin-color changes – Hyperhidrosis 2. Dystrophic—3–6 months – Persistent pain, disability, and atrophic skin changes – Decreased blood flow, decreased temperature – Hyperhidrosis 3.
The discipline of psychology must play a central role in the study order sildalis 120mg overnight delivery, as- sessment 120mg sildalis with visa, and management of pain. It is not surprising that Ronald Melzack, one of the developers of the most influential theory in the field of pain, is a psychologist. Nor is it unexpected that at least 2 of the 10 most influential clinicians and researchers in the field of pain (as assessed by survey of a random sample of members of the International Association for the Study of Pain [IASP]) are psychologists (Asmundson, Hadjistavropoulos, & Anto- nishyn, 2001). These two individuals (Ronald Melzack and Dennis Turk) are contributors to this volume. In this book we have tried to capture major features of the psychology of pain and the most influential contributions of psychologists to pain re- search and management. We are primarily interested in the ultimate impact of advances in understanding and controlling pain. Hence, although much of the volume covers applied issues, basic processes are also given careful consideration. FROM DESCARTES TO THE NEUROMATRIX Historical trends demonstrate the importance of psychological mechanisms. Descartes’s (1644/1985) early mechanistic conceptions of pain resulted in the biomedical specificity theory that proposed that a specific pain system transmits messages from receptors to the brain. This theory is sometimes referred to as “the alarm bell” or “push button” theory (Melzack, 1973), INTRODUCTION 3 because of its apparent simplicity. Descartes’s early views were refined substantially over the years, and more complex mechanistic views gradu- ally emerged as investigators struggled to incorporate in their models of pain the complexities and puzzles of pain that dismayed patients and clini- cians struggling with pain control. Nevertheless, biomedical specificity theory continued to exert an enormous influence through the first half of the 20th century. There was little room for recognition of the importance of psychological processes such as emotion, attention, past experience, and cognitive processes in the study of pain. Patients suffering from pain without a pathophysiological basis or signs often were considered “crocks” (Melzack, 1993). Despite dominance of sensory specificity and biomedical models of pain, clinicians were increasingly finding emotional and motivational processes to be important in understanding pain. Merskey (1998) observed that psy- chological explanations about motives for complaints about pain and psy- chodynamic theories gradually became popular during the early and mid- dle parts of the 20th century (e. Early investigation of psychiatric patients with pain had led to the erroneous conclusion that physical and psychological factors in pain were mutually exclusive and that pain is either physical or psychologi- cal (IASP Ad Hoc Subcommittee for Psychology Curriculum, 1997). Persis- tent pain with no identifiable causes was frequently labeled as psychogenic, a regrettable construct because it perpetuates mind/body dualistic thinking (Liebeskind & Paul, 1977) and fails to recognize that biological mechanisms are integral to all psychological phenomena, including pain. Freud (1893–1895) viewed pain as a common conversion symptom and favored the position that pains encountered in hysteria were originally of somatic origin. In other words, he argued that the pain was not created by the neurosis, but rather the neurosis served to maintain it. Dynamic con- ceptions of pain emphasize the role of psychic energies derived from innate drives linked to aggression, dependency, and sexuality and postulate that the pain experience is associated with the gratification or frustration of these drives (Pilowsky, 1986). For example, pain can be construed as the product of aggression that is inflicted either on oneself or on others and can be related to the formation of a cruel superego with an associated chronic sense of guilt and low self-esteem (Pilowsky, 1986). Although psychodynamic approaches were frequently used to charac- terize patients whose pain unfortunately had been labeled as “psycho- genic,” they have not led to any major empirically supported advances in pain management, and this perspective has been losing favor over the years (e. Efforts to bolster the psychodynamic perspec- tive come from case studies, although some work has linked suppressed an- ger to the experience of persistent pain. Pilowsky and Spence (1975), for ex- 4 HADJISTAVROPOULOS AND CRAIG ample, found that a pain clinic group reported a higher incidence of anger inhibition than 40 hospital outpatients who reported pain as their most prominent symptom. Perhaps the most significant and systematic involvement of psycholo- gists in the field of pain began with the correspondence of Donald Hebb, a McGill University psychologist, and George A. The starting point of their discus- sion was Hebb’s treatment of pain in his classic text The Organization of Be- havior (1949).
Treatment for a patient’s suffering order sildalis 120mg amex, however discount sildalis 120mg fast delivery, involves more than control of pain. Emotional sup- General Treatment 43 port is essential, and uninterrupted sleep is beneficial. Other problems burn pa- tients often experience are anxiety, itching, and posttraumatic stress disorder. Back- ground pain is always present and its range of fluctuation is very small. The second type of pain is the excruciating, intolerable pain that occurs when something is done to the patient, such as procedural pain during dressing changes, line change, or physiotherapy. It is the worst pain a patient can encounter, and patients cannot make any comparison to other experiences in life. Pain control is one of the great challenges in the burn unit, and it is an unsolved problem. Anxiety, sleep disor- ders, and posttraumatic stress are problems often encountered along with pain. They need to be treated at the same time in order to obtain a perfect response. It must be remembered, however, that anxiety or other disorders are not treated with opioids, and pain should likewise not be treated with anxiolytics. The patient’s pre-existing psycho- logical make-up, ethnocultural background, the experience of the injury, and its meaning modulate the individual response to pain. Analgesics are most effective when given on a regular basis (not as needed or required). Intramuscular injections are not usually appropriate because the patient fears the injection and intramuscular flow may be altered. Pain management protocol should be initiated with the starting doses, which can be modified as the situation dictates. Pain Assessment The patient’s pain can be assessed using the 10-point scale or the Faces scale (Fig. In the 10-point scale, the sliding scale is moved until the patient feels FIGURE 2 Faces pain rating scale. Patients point at the face that best describes the pain they are suffering. A laughing face means no pain at all; a sad, crying face describes intensive, non-bearable pain. A scale of 1 hurts just a little bit, whereas 10 is the worst experience a person can ever imagine. For children less than 3 years old, the Faces pain-rating scale is best used. The child points to the face that best describes the pain he or she is experiencing. A smiling face with a pain score of 0 is happy because it does not hurt at all. For children who are preverbal or communicate nonverbally, the observer scale is used (see Table 6). Both background and procedural pain occur in the emergency, acute, and rehabilitation phase. Therefore different methodologies should be applied depend- ing on the patient’s phase of the disease in order to obtain good pain control. Unless patients have a pre-existing drug abuse problem, they will not become opioid dependent from its use during the acute phase of the burn.
Certainly cheap 120mg sildalis otc, it is preferable to MR imaging which cally treated unstable fracture buy sildalis 120mg, which extends to the may require a general anaesthetic. However, ultrasonography has recently cians have found it to be helpful in guiding the reduc- been shown to be capable of ruling out joint involve- tion of difficult paediatric forearm fractures. The diagnosis of fracture in a child’s elbow One emergency department has described the use is further complicated by the variable ages at which of US to demonstrate uncomplicated greenstick and the ossification centres are visible on plain films. There has been a case report of Inexperienced casualty officers may not be aware the detection of a radiographically occult fracture of of the order of epiphyseal ossification around the the radial neck with US. Ultrasonography can be used to study the diaphyseal fractures and fractures of the forearm. It was less dependable for compound injuries, non-dis- placed epiphyseal fractures (Salter-Harris type 1) and Table 2. Supracondylar fractures carry a high rate of complications including neurovascular Radial head 4 years (2–6 years) compromise. There may be few clues to the presence Medial epicondylea 7 years (4–6 years) of a supracondylar fracture on the plain film, partic- Trochlea 10 years (9–10 years) ularly when the fracture involves the cartilaginous Olecranon 10 years (6–10 years) growth plate. Superior displacement of the coronoid fat pad is the most sensitive indicator of a traumatic Lateral epicondyle 11 years (9–12 years) joint effusion. However, this may be missed if an ade- aLast to fuse Trauma and Sports-related Injuries 25 hypoechoic, unossified epiphysis around the elbow 2. MR findings may vary depending on the time elapsed since the injury, but usually show char- Foreign body demonstration is notoriously dif- acteristics of methaemoglobin with increased signal ficult with radiographs particularly with wooden on both T1- and T2-weighted sequences. Haema- splinters, which are non-radiopaque, and can cause tomas tend to resorb over a period of 6 to 8 weeks, significant morbidity if they remain undetected. It is possible to mainly in the rectus femoris but also in semimembra- localize foreign bodies as small as 1 to 2 mm using nosus and semitendinosus muscles. The use of haematoma are dependent on the time of imaging fol- US to detect and remove foreign bodies by emer- lowing injury. In the acute phase, haematoma may be gency physicians has been described and intra- echogenic and difficult to discriminate from normal operative US by surgeons has been recommended by muscle (Fig. US on the day of injury shows haematoma (H) in the deep infrapatellar bursa (PT). The acute hae- matoma (H) has the classical appearance of mixed hyper and hypoechogenicity. Thickening of the distal patellar tendon (PT) is now present (arrows); T tibia b 26 P. There is usually a lack of inflammatory change in the The same is true of myotendinous junction injury surrounding subcutaneous soft tissues. This in part results from Muscle and tendon injuries are uncommon in the muscle anisotropy making the assessment of muscle immature skeleton since the weakest link in the echotexture difficult. This means that US has a low muscle-tendon-bone chain is the growth plate. How- sensitivity for grade 1 tears and really only demon- ever, young athletes may incur sprains and tears, strates the size of the haematoma and the degree of particularly at myotendinous junctions, although structural disruption. Strains most often separating muscle oedema, haematoma and struc- affect muscles that cross two joints since these are tural disruption, and as a result tends to overesti- susceptible to greater degrees of stretch. These hamstring muscles, particularly the biceps femoris, methods must be used in combination to achieve an are the most commonly injured muscles in jump- accurate assessment of muscle injury. Each hamstring myotendi- nous junction extends almost the full length of the muscle so that when injury occurs it can be located 2. Tendon injury is unusual in this age group and will Young athletes involved in throwing, swimming not be discussed in depth.