Abstract Low back pain (LBP) is a prevalent health issue in the Western world. It is the leading cause of disability in adults under the age of 45 and the second highest symptomatic complaint seen by primary care physicians in the United States. Consequently, patients with LBP make up the largest client population seen by outpatient physical therapists. While most low back pain cases result from mechanical etiologies, the clinician must be alert to the non-orthopedic causes of LBP that emanate from multifarious organ systems. The purpose of this project was to create a reference guide in the form of a mobile or web application for physical therapists, athletic trainers, and other clinicians who work with patient populations suffering with LBP. The guide presents details on non-orthopedic pathologies that result in pain to the low back. It includes evidence based findings on incidence, etiology, pathogenesis, clinical manifestations, and treatment for each disease. Content of the guide is based on an extensive literature review and is geared toward clinicians who work regularly with LBP patients but rarely see patients whose primary source of pain is not from the low back itself. This clinical application will help clinicians quickly consider other pathological possibilities as they navigate through the differential diagnostic process. Introduction Low back pain (LBP) is a prevalent issue in the Western world.1 LBP is the leading cause of disability in adults under the age of 45 and it is the second most common symptomatic reason for visits to primary care physicians in the United States, behind upper respiratory tract infections.2, 3 Consequently, patients with LBP make up the largest client population seen by outpatient physical therapists (PT).4 This pain has ramifications for those affected. Missed work, extended sick leave, physical disability, and depression are all difficult and costly concerns associated with LBP.5 Most causes of LBP are benign in nature and resolve with time and therapeutic intervention. Rarely, pain is caused by a more serious underlying condition such as malignancy, infection, or inflammatory disease.6 Of these conditions, malignancy is the most common underlying cause of back pain, with an incidence rate of less than 1% of all patients experiencing LBP.7 It is a vital responsibility of the PT to be aware of non-orthopedic pathology that can result in LBP so that when a client with LBP of suspected mechanical origin does not respond to conservative treatment or presents with other significant findings upon evaluation, the therapist can make the informed decision to make referral to a physician for further review and diagnosis. This study of non-orthopedic sources of low back pain is based on three categories of back pain described by Deyo.8 The three categories include “mechanical” spine disorder, non-mechanical spine disease, and visceral disease as possible causes of LBP (see Figure 1). Mechanical low back pain is described as having no underlying inflammatory or neoplastic cause. Pathologies of mechanical nature are associated with accidental, postural, or structural problems resulting in a disorder of the skeletal system and associated muscles, joints, or ligaments. Similarities exist in initial treatment for most back pain of mechanical cause compared to non-mechanical and visceral causes of LBP. PTs are primarily trained in rehabilitation of illness and injuries of this nature. Some examples of mechanical LBP include lumbar strain or sprain, spondylolysis, spondylothisthesis, herniated disk, and spinal stenosis. Non-mechanical sources of LBP are systemic in nature and include infection, neoplasm, and inflammatory disease.8 Nonspecific

nerve endings surrounding the visceral structures near the spine can also cause referred pain from the diseased organ to the lumbar spine.9 Visceral causes of back pain include diseases of internal organs, most notably the kidneys, gastrointestinal, and reproductive organs.8 Low Back Pain and Physical Therapist Practice Low back pain presents a particular challenge to the healthcare provider. Only 15% of acute low back pain cases ever receive a definitive pathoanatomical diagnosis, the remaining 85% being of unknown cause.10 The majority of LBP is benign in nature, however sometimes it is triggered by an underlying medical disorder.9 It is the job of the primary care physician to rule out low back pain that is caused by a serious pathology such as infection, malignancy, or inflammatory disease.11,12 Although rare, not all patients with non-orthopedic pathologies are identified during primary care evaluation, however, as evidenced by physical therapists’ encounter with such pathologies in clients referred to physical therapy.13 The differential diagnosis process during primary care evaluation of LBP must screen for and identify any serious disease as the source of pain. Early diagnosis of these conditions is the key to preventing further deterioration of the patient’s condition, and particularly to preventing the metastasis of malignancies.11 Once in physical therapy, it is possible that these conditions may continue to go undiagnosed because of their rarity in LBP populations and the therapist’s relative lack of training and clinical experience with these types of pathologies. Additionally, the complex nature of LBP and sheer volume of LBP patients may dull the therapist’s awareness of presenting signs and symptoms. The diseases investigated in this study demonstrate diversity in clinical presentation that can make diagnosis difficult without a high level of clinical suspicion. Although there may be reason for suspicion of a particular diagnosis, a high level of suspicion of any one of these potentially rare conditions is not necessary on part of the therapist for the patient to receive the appropriate medical attention. A number of red flags may arise that indicate more serious illness. Common red flags in patients with low back pain that necessitate referral to a physician include abdominal pain, colicky pain, costovertebral tenderness, excruciating pain, diaphoresis, hyper- or hypotension, pain at night, fever, and shock.9 Patients are also at greater risk of having back pain due to cancer if they have a history of cancer, are over 50 at age of onset, have unexplained weight loss, or fail to respond to conservative treatment.14 Physical therapists may potentially encounter clients with medical causes of back pain more frequently due to increasing use of direct patient access to physical therapy.15 Currently, patients are allowed to be evaluated by PTs in all 50 states and the District of Columbia without referral from a physician. In 48 states and the District of Columbia, patients are allowed to be evaluated and receive treatment for musculoskeletal conditions from a PT without physician referral.16 Recent research supports the safety, cost efficiency, and positive patient outcomes associated with patient self-referral to physical therapy compared to physician-referred care.17 Implications of direct patient access in physical therapy include even greater responsibility on behalf of the therapist to screen for medical conditions which fall beyond the scope of practice of a PT. Growing autonomy in the profession of physical therapy requires ease of access to evidencebased resources to aid in clinical decision making.

Mechanical

Pregnancy Pancreatic Cancer Ovarian Cancer Neoplasia

Multiple Myeloma

Prostate Cancer Testicular Cancer Spondylodiscitis Osteomyelitis Non-Mechanical Spine Disease

Infection

Bacterial endocarditis

Low Back Pain

Skeletal Tuberculosis Ankylosing spondylitis Reactive arthritis Crohn’s Disease

Inflammatory arthritis

Inflammatory Bowel Bowel Disease

Paget's disease

Psoriatic arthritis

Ulcerative Colitis

Systemic Lupus Erythematosus Prostatitis Pelvic organs

Endometriosis Pelvic Inflammatory Disease

Nephrolithiasis Urinary Tract Infection Visceral

Renal disease

Polycystic Kidney Disorder Pyelonephritis Perinephric abscess

Gastrointestinal disease Abdominal Aortic Aneurysm

Pancreatitis Irritable Bowel Syndrome

Figure 1: Concept map of pathologies that refer pain to the low back, categorized by type and organic location

Evidence-based practice, as defined by the American Physical Therapy Association, is “access to, and application and integration of evidence to guide clinical decision making to provide best practice for the patient/client.”18 Physical therapists are faced with the challenges of an aging population, a culture that places growing interest in health and fitness, and an extensive existing body of research which continues to grow in time. Information management inherently becomes more complex due to these factors, and PTs must determine the most efficient ways to locate and access information resources to guide clinical decision making.19 Thus, a reference guide in the form of a computer or mobile application may prove a valid tool for the clinical professional. The Role of Technology in Physical Therapy With an 84 million dollar global market for healthcare applications, the prevalence of Apple mobile device ownership by healthcare professionals in the US, and increased integration of technology into healthcare, an opportunity to explore the possibility of mobile application integration into physical therapy practice presents itself.20 Current advances in technology related to healthcare include thought-controlled robotic prosthetics, wearable health and fitness sensors, consumer health apps, and health professionals’ use of healthcare information technology (IT), particularly electronic medical records and health information exchanges.21,22 It is seen that utilization of healthcare IT can play a significant role in improving patient outcomes, reducing costs, and increasing patient management.23 Regarding mobile healthcare applications specifically, many apps are helpful in communicating information about a patient to a clinician or for conveying educational information to a patient. It is not entirely clear what role mobile technology plays in providing educational information for the clinician. Technology is of ever increasing relevance in the physical therapy field, particularly for young professionals who have been raised and educated in a computerized age. A 2012 study found that the primary sources of information PTs are using to make clinical decisions are journal articles, likely due to increasing accessibility of free articles through the Internet, followed in frequency of use by databases and Internet search engines.19 Creating a Clinical Reference Tool The present literature review examined 28 non-orthopedic pathologies that refer pain to the low back. These included diseases of the immune, renal/urologic, gastrointestinal, cardiovascular, musculoskeletal, hepatic/pancreatic/biliary, and female and male reproductive systems. With this information, an electronic reference tool was designed for the physical or sports therapy clinician who may encounter LBP patients who do not respond to treatment or have other signs, symptoms, or risk factors that may suggest a non-orthopedic origin of back pain. Because these types of pathologies are not common to outpatient physical therapy practice, a quick reference guide detailing these pathologies may prove a valuable clinical tool. With this guide, the clinician will be able to reference findings on incidence, etiology, pathogenesis, clinical manifestations, treatment, and therapy considerations for each disease processes without having to go to a computer and use valuable time in research. Information in this guide may assist the clinical professional objectify patient findings and, if an underlying pathology is suspected, make referral to a physician for further evaluation.

The final mobile product is a web application developed using the online database program Knack.24 After searching current available programs for building mobile applications, it was determined that more than a simple free app builder for mobile devices would be required. The database format allows the user to implement filters, use search functions, and organize results as desired, all contributing to make the application a practical tool. Knack allows individuals to create a web-based database and build an interface through which the user can access the information. All 28 pathologies and corresponding findings on incidence, etiological factors, pathogenesis, signs and symptoms, diagnosis, treatment, and implications for the therapist were included in the database. The interface was then designed to bring the user to a home page from which one can navigate to a search tab or list view of all pathologies. To reference a pathology, the “view details” link next to each pathology takes the user to a page with information and references for that pathology. Literature reviewed for each pathology was consolidated into a succinct overview designed for quick review by the clinician. The user who wants deeper reading can scroll down to the references, included in the application with each pathology. References are included at the conclusion of each pathology in this paper as they would be seen in the application. A medical disclaimer is also included in the site (see appendix A). Each of the 28 installments are presented below, organized alphabetically. The following information is included in the application and is available at: http://plnuhonors.knackhq.com/backology. Non-Orthopedic Pathologies that Refer Pain to the Low Back Abdominal Aortic Aneurysm Condition

Aneurysm is defined as a dilation of an arterial, venous, or heart wall to greater than 50% its normal size.1 Abdominal aortic aneurism (AAA) is the dilation of the aortic artery in the abdomen. Incidence/Etiological Factors

Each year, 200,000 people in the United States are diagnosed with AAA, of which 15,000 rupture. Incidence increases with age, beginning around 50 years. Prevalence of AAA among Americans ages 50 to 84 is estimated to be around 1.4%. Prevalence among men ages 65 to 75 with smoking history is estimated to be near 5%.2 Men are at greater risk than women, as are those who smoke, have hypertension, high cholesterol, are overweight, or have family history of AAA.1,3 Abdominal aortic aneurisms occur four times more often than thoracic aortic aneurisms, likely because the aorta in this location is not supported by skeletal muscle.1 Pathogenesis

Over time, plaque formation begins to erode the vessel wall and elastin in the aorta breaks down, exposing collagen fibers to the pulsating and erosive force of blood flow. Collagen fibers,

although they have twenty times the tensile strength of elastin, cannot stretch as far as elastin without being damaged. With each systole, the vessel becomes more vulnerable to dilation and possible rupture. Individual differences in collagen fiber architecture may vary the risk of rupture from person to person.1,2 Most ruptures occur between the renal arteries and iliac bifurcation, located between L2 and L4 vertebrae.2 Atherosclerosis or injury to the muscular layer (tunica media) of the arterial wall is responsible for most aneurisms. Additional causes may include trauma, Marfan’s syndrome, Ehlers-Danlos syndromes (EDS), hereditary abnormalities of connective tissues, inflammatory diseases, or infectious agents.1 Family history of aneurysm puts an individual at greater risk likely because of inherited defects in elastin and collagen composition that weaken the aortic wall. For example, Marfan’s disease is caused by a gene that codes for fibrillin, a glycoprotein that effects elastin, weakening the aortic media and causing dilation. Genetics may also influence enzymatic activity that leads to break down of vessel wall components.2 Signs and Symptoms

Most abdominal aortic aneurysms are asymptomatic, but abdominal pain or backache are common first manifestations of pathology.2 In some cases, back pain is the only presenting symptom prior to rupture. Twenty to thirty percent of people with AAA experience mild to severe pain in the mid-abdominal or lower back region that is intermittent or constant.1 Other early symptoms and signs include feelings of fullness and pulsation in the abdomen, palpable pulsating abdominal mass, nausea, and weak or absent peripheral pulses.2,4 As the aneurysm grows and impinges local structures, persistent, substernal back, neck, or jaw pain may develop.1 The patient may describe pain as throbbing or pulsating, and may have difficulty finding relief in any position.5 Early warning signs of rupture include presence of an abdominal heart beat while lying down, dull ache in mid-abdominal, left flank, or lower back. A full rupture will cause intense flank pain with pain referred to the back at the level of the rupture. Radiating pain may present in the lower abdomen, groin, or genitalia.1 The PT’s level of clinical suspicion should be increased for the individual with a history of smoking, increased weight, myocardial infarction, claudication, or hypertension. Differential diagnosis for the older male patient who presents with sudden onset back or flank pain accompanied by shock and/or syncope should include AAA.2 Diagnosis

Since most AAAs are asymptomatic, diagnosis is usually incidental, with findings being discovered on radiographic images taken for another purpose.1,2,4,6 A pulsating mass may be palpable upon routine physical examination. Overall sensitivity for this is low, but for patients with an abdominal girth of less than 100cm, sensitivity is very high.1,2 Clinical suspicion for AAA should be followed up with ultrasound to confirm diagnosis. Ultrasound has high sensitivity, 100% specificity, and a positive predictive value for AAA.2 Treatment

Treatment is based on the size, rate of growth, and clinical presentation of the bulge. For small aneurysms, watchful waiting is recommended. Preventive medicine may be prescribed to lower cholesterol and/or control blood pressure. If the aneurism reaches 5cm in diameter, surgery is recommended because the risk of rupture becomes greater than the risk of repair.2 Open surgery is often a life-saving procedure for those at risk for rupture, but it is not without risk. Surgery requires clamping of the aorta above and below the aneurysm which can cause ischemic damage to other tissues. If the aneurysm extends above the level of the renal artery, blood flow during surgery is impeded to the kidneys and renal ischemic damage is likely to increase mortality.4 The endovascular stent-graft is a less invasive procedure which implants a stent, typically through the femoral artery, to bypass the aneurysm. Benefits of the procedure are lower mortality rates, quicker procedure time, reduced risk of acute kidney injury, reduced risk of thoracic aortic rupture, and reduced short-term morbidity and duration of hospital stay.1,4,7 Overall mortality rate for elective surgery is about 3%.2 Mortality rate for undetected rupture is 90% and for emergency rupture repair is estimated around 36%.7,8 Implications for the Therapist

As the aneurysm grows larger, sensitivity of abdominal palpation increases for detecting AAA. Thus, it is important that the physical therapist include abdominal palpation and auscultation in the examination of a LBP patient, particularly if the patient is suspected to have abdominal pathology, is at risk for developing an AAA, displays nonmechanical pain patterns (does not find relief with change in posture, activity, etc.), or does not respond to treatment. Differences noted when comparing and contrasting a patient’s current episode of LBP compared to previous episodes may alert the PT to potential pathological sources of pain.5 References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 607-610. 2. Crawford CM, Hurtgen-Grace K, Talarico E, Marley J. Abdominal aortic aneurysm: An illustrated narrative review. Journal of Manipulative and Physiological Therapeutics. 2003; (26)3:184-195. 3. Kent K, Zwolak R, Greco G, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. Journal Of Vascular Surgery. September 2010;52(3):539-548. 4. Woodrow P. Abdominal aortic aneurysms: clinical features, treatment and care. Nursing Standard. August 17, 2011;25(50):50-58. 5. Mechelli F, Probaski Z, Boissonnault W. Differential diagnosis of a patient referred to physical therapy with low back pain: abdominal aortic aneurysm. Journal Of Orthopaedic & Sports Physical Therapy. September 2008;38(9):551-557. 6. Tsuchie H, Miyakoshi N, Shimada Y, et al. High prevalence of abdominal aortic aneurysm in patients with chronic low back pain. The Tohoku Journal Of Experimental Medicine [serial online]. 2013;230(2):83-86.

7. Schermerhorn M, Bensley R, Landon B, et al. Changes in abdominal aortic aneurysm rupture and short-term mortality, 1995-2008: a retrospective observational study. Annals Of Surgery. October 2012;256(4):651-658. 8. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. 6th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2010: 319.

Ankylosing Spondylitis Condition

Ankylosing spondylitis (AS) is an inflammatory disease marked by inflammation of the attachment sides of tendons, ligaments, and cartilage to the bone. Inflammation at ligamentous attachment sites to the vertebrae is most common in AS. Incidence/Etiological Factors

Over 21% of adults in the United States have self-reported physician diagnosed arthritis. Ankylosing spondylitis is the most common of a group of inflammatory diseases called spondyloarthritides, affecting primarily the spine and sacroiliac joints.1,2 Spondyloarthritides are reported to affect from 0.6 million to 2.4 million adults. Reported prevalence of AS is shown to vary by race, between 0.03 and 0.1% in Caucasian populations, and much lower prevalence in African American populations.1,2 More males are affected by the disease than females and typical age of diagnosis is between 30 and 50 years old.1 Back pain and stiffness beginning in adolescence and early adulthood is typical of early disease. Diagnosis typically is delayed many years as symptoms will initially be minimal.3 Ankylosing spondylitis, like other spondyloarthritides, is linked to the presence of human leucocyte antigen (HLA)-B27 gene, although the link is unclear. In Caucasian populations, 90% of those with AS have the gene, yet only 1 in 15 individuals with the gene develop AS, suggesting that environmental factors play a role in development of the disease.1,3 Pathogenesis

Spondyloarthritides commonly arise in individuals who are genetically predisposed and encounter an environmental trigger which starts the disease process.3 Pathogenesis is not well understood, but the primary pathology is inflammation at the attachment sides of tendons, ligaments, and cartilage to the bone. Inflammation of ligamentous attachments to the vertebrae is the mark of AS. This begins typically in the lumbar spine and moves down to the sacroiliac joint. Chronic inflammation leads to osseous growth at the lesion and subsequent stiffening and fusing of vertebrae in end-stage disease.4 Signs and Symptoms

A common symptom is stiffness in the morning, lasting at least 30 minutes after rising from bed. Patients typically experience pain in the low back and sacroiliac region that develops slowly over weeks and months that is relieved with exercise and worsens with rest.1,3 Low back pain

develops insidiously typically before age 45.3 Persistent fatigue that does not go away with rest, shortness of breath as disease progresses, and flaring of symptoms with periods of dormancy are seen in patients with AS.1 Patient may have history of acute anterior uveitis, requiring urgent ophthalmic care, impaired spinal and/or chest mobility, or family history of AS or other spondyloarthritides.3 Tenderness over sacroiliac joints, spine, heels, iliac crest, and anterior chest wall may be indicators of enthesitis, another clinical indicator of AS.3 Diagnosis

The Modified New York criteria are used for diagnosis.1,3 Clinical criteria for this system include: (1) LBP lasting more than three months that is relieved with exercise and not by rest (2) Limited lumbar range of motion in sagittal and frontal planes (3) Limited chest expansion compared to normal for age and sex of the patient. Imaging criteria must include radiographic imaging evidence of sacroiliitis bilaterally or unilaterally depending on the degree of fusion. A definite diagnosis of AAA is confirmed in the presence of positive radiographic imaging in addition to at least one clinical criterion.1,3,6 Diagnosis is probable if all three clinical criteria are present but there is no imaging evidence or if there is evidence of sacroiliitis but no clinical criteria.1 One difficulty with diagnosis of this disease is that radiographic imaging will not be positive for sacroiliitis until years after the disease process has begun and there may already be significant joint damage. MRI and other more advanced imaging techniques may be useful for diagnosis as they can detect inflammatory changes in the tissue years before bone damage occurs.1 Treatment

Daily exercise is helpful non-pharmacological intervention for many patients seeking to relieve pain. There is also evidence that when a patient with AS is educated about his or her disease, more positive outcomes are achieved.1 Pharmacologic interventions widely include the use of NSAIDs such as ibuprofen or naproxen. 75% of patients with AS show good response to NSAIDs 48 hours after treatment begins. In contrast, only 15% of those with mechanical low back pain experience the same relief, suggesting that this may be a helpful tool for discrimination between the two.5 NSAIDs in combination with analgesics tend to provide the best relief compared to either treatment alone.1 Disease-modifying anti-rheumatic drugs are commonly used to treat rheumatic conditions. AntiTNF drugs have demonstrated the best effectiveness in reducing activity of the disease.1,3 Implications for the Therapist

Stretching is shown to improve joint range of motion in patients with AS. Although all forms of stretching demonstrate positive outcomes, the global postural reeducation approach to stretching, which involves active overall stretching of muscle chains as opposed to isolated singular muscle stretches, is superior for decreasing morning stiffness and increasing spine mobility, thoracic

expansion, and overall quality of life.7 Recommended home-based exercise programs for patients with AS include muscle relaxation and flexibility exercises for the cervical, thoracic and lumbar spine, stretching, muscle strengthening, and postural and respiratory exercises. Exercise should be conducted at least five days per week for 30 minutes per day.8,9 References

1. Bond D. Ankylosing spondylitis: diagnosis and management. Nursing Standard. December 18, 2013;28(16-18):52-59. 2. Helmick, C.G, Felson, D.T, Lawrence, R.C, Gabriel, S., Hirsch, R., Kwoh, C.K., Liang, M.H., Kremers, H.M., Mayes, M.D., Merkel, P.A., Pillemer, S.R., Reveille, J.D., Stone, J.H. and National Arthritis Data Workgroup (2008), Estimates of the prevalence of arthritis and other rheumatic conditions in the United States: Part I. Arthritis & Rheumatism, 58: 15–25. doi: 10.1002/art.23177 3. Khan M. Update on spondyloarthropathies. Annals Of Internal Medicine. June 18, 2002;136(12):896-907. 4. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1282. 5. Kain T, Zochling J, Taylor A, et al. Evidence-based recommendations for the diagnosis of ankylosing spondylitis: Results from the Australian 3E initiative in rheumatology. Med J Aust. 2008;188(4):235-7. 6. National Institute for Health and Care Excellence. Adalimumab, etanercept and infliximab for ankylosing spondylitis. NICE Technology Appraisal Guidance 143. October 2010;47. 7. Silva E, Andrade S, Vilar M. Evaluation of the effects of Global Postural Reeducation in patients with ankylosing spondylitis. Rheumatology International. July 2012;32(7):21552163. 8. Yigit S, Sahin Z, Demir S, Aytac D. Home-based exercise therapy in ankylosing spondylitis: short-term prospective study in patients receiving tumor necrosis factor alpha inhibitors. Rheumatology International. January 2013;33(1):71-77. 9. Aytekin E, Caglar N, Ozgonenel L, Tutun S, Demiryontar D, Demir S. Home-based exercise therapy in patients with ankylosing spondylitis: effects on pain, mobility, disease activity, quality of life, and respiratory functions. Clinical Rheumatology. January 2012;31(1):91-97.

Autosomal Dominant Polycystic Kidney Disease Condition

Autosomal polycystic kidney disease (ADPKD) is characterized by the formation of fluid filled epithelial cysts in kidneys that progressively enlarge and lead to progressive renal failure.1,2 Incidence/Etiological Factors

In the United States in 2011, prevalence of ADPKD as the primary diagnosis in patients with end-stage renal disease (ESRD) was 4.7%, with a mean age of 59. From 2007-2011, ADKPD

was the primary diagnosis of 2.3% of new cases of ESRD, with a mean age of 54 being reported.3 This genetic disorder affects approximately 1 in 1000 people.2 Mutations on the PKD1 gene on chromosome 16 and on PKD2 gene on chromosome 4 have been identified as responsible for autosomal dominant polycystic kidney disease (ADPKD).1 Pathogenesis

Mutations of PKD1 and PKD2 genes alter the functions of their encoded proteins, resulting in the development of fluid-filled epithelial cysts that arise from a nephron, grow, detach from the nephron. Once detached, the cyst continues to proliferate. Multiple cysts may cause destruction of renal parenchyma, interstitial fibrosis, cellular infiltration, and loss of functional nephrons. ADPKD is a systemic disorder which may include defective cardiac valves, incracranial arterial aneurysms, colonic diverticulosis, and cyst formation of the liver, spleen, and pancreas.2,4 Signs and Symptoms

Abdominal and flank pain are common symptoms, though chronic low back pain is most commonly reported by patients, followed by hematuria and non-specific abdominal pain. In patients who report pain, it is common to have more than one source of pain (back, abdominal, radiating hip or leg, and/or chest pain, headache).5 Hematuria occurs in many patients as a result of cyst rupture, urinary tract infection, or nephrolithiasis.6 Other signs and symptoms include hypertension, renal insufficiency, and proteinuria.1 Mechanical low back pain may be caused by subtle postural changes assumed over time as kidney and liver cysts grow, resulting in exaggerated pelvic tilt, subsequent lumbar lordosis, and observed hypertrophy of the lumbodorsal muscle group.6 Diagnosis

Diagnosis is primarily based off of patient symptoms, known family history and incidental finding.5 Ultrasonography is used to screen for polycystic kidney disorder. Criteria for diagnosis of an individual under 30 years is at least two cysts in one kidney, for those ages 30-59 diagnosis requires two cysts in each kidney, and for individuals over 60 four cysts per kidney should be present. CT and MRI are other imaging methods available. Urinalysis may reveal hematuria and/or proteinuria. Kidneys may be enlarged and palpable upon examination.4 Treatment

Treatment for mild to moderate pain relief first includes non-pharmacologic therapies including psychobehavioral modification, ice massage, heating pad, whirlpool treatment, and the Alexander technique. If these do not reduce pain, non-narcotic analgesics such as Acetaminophen, Salsalate, NSAIDs, COX-2 inhibitors, Tramadol, and/or Clonidine may be used alone or in combination with the previously listed techniques. Physical interventions include transcutaneous electrical nerve stimulation (TENS), acupuncture, and autonomic plexus blockade.6

Major invasive procedures for pain treatment include neuromodulation of the spinal column and use of neuraxial opioids and local anesthetics. Surgical intervention may be necessary if conservative treatment measures do not adequately relieve pain symptoms. Laparoscopic cyst decortication is shown to be effective in permanently relieving pain in many PKD patients. Nephrectomy may be the only surgical option for relieving pain in patients reaching end-stage renal disease, and may be performed in preparation for kidney transplant. Renal denervation procedures have also been effective in improving pain.6 Treatment for cyst infection involves antibiotic therapy (ciprofloxacin or other agents effective in cyst penetration), and fluid intake of greater than 3 liters per day is encouraged for management nephrolithiasis. Hypertension is managed using ACE inhibitors.1 Implications for the Therapist

Therapists should be aware of the signs and symptoms of renal cystic disease and recognize signs that disease may be worsening. Any changes in signs and symptoms in the patient with ADPKD warrant physician referral. Patients with ADPKD are also at increased risk for hypertension, UTI, cerebral and aortic aneurysms, and mitral valve problems. The development of symptoms associated with these conditions will also warrant referral to a physician.4 References

1. Masengu A, Courtney A. Improving recognition of inherited renal disease. The Practitioner. February 2012;256(1748):17. 2. Chang M, Ong A. Autosomal dominant polycystic kidney disease: recent advances in pathogenesis and treatment. Nephron. Physiology. 2008;108(1):p1-p7. 3. U.S. Renal Data System, USRDS 2013 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 2013.* *The data reported here have been supplied by the United States Renal Data System (USRDS). The interpretation and reporting of these data are the responsibility of the author(s) and in no way should be seen as an official policy or interpretation of the U.S. government.

4. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 936. 5. Bajwa Z, Sial K, Malik A, Steinman T. Pain patterns in patients with polycystic kidney disease. Kidney International. October 2004;66(4):1561-1569. 6. Bajwa Z, Gupta S, Warfield C, Steinman T. Pain management in polycystic kidney disease. Kidney International. November 2001;60(5):1631-1644.

Chronic and Acute Pancreatitis Condition

Acute pancreatitis is pancreatic inflammation typically triggered by binge drinking or cholelithiasis. Chronic pancreatitis is the result of permanent changes to tissues of the pancreas secondary to chronic inflammation. Incidence/Etiological Factors

Incidence of chronic pancreatitis is around 3.34 cases per 100,000 people per year. Males have a slightly higher incidence rate than females, with a ratio of 1.5:1.1 Acute pancreatitis has higher incidence than chronic pancreatitis. Overall incidence of acute pancreatitis is estimated around 13 cases per 100,000 people per year.2 In their early 20s, women have higher incidence of acute pancreatitis than men, but between the ages of 44 and 84 the opposite is true, with men 30-63% higher observed incidence.2 Acute pancreatitis (AP) is typically triggered by binge drinking or cholelithiasis.3,4 Alcohol abuse is the most common etiology for acute pancreatitis in the United States, with about 5055% of all cases being alcohol related.1 Chronic pancreatitis (CP) develops as a result of permanent changes to the pancreas secondary to chronic inflammation.5 The pancreas, in this condition, begins digesting itself, causing severe tissue destruction.3 Chronic inflammation can be related to alcohol abuse, autoimmune disease, history of acute pancreatitis, genetic factors, or idiopathic.5 The typical alcohol abuse patient with CP is a 35 to 45 year old male who has consumed large amounts of alcohol for over six years. Patients with a family history of two or more people with the disease, including cystic fibrosis, are at greater risk for developing pancreatitis.5 Pathogenesis

The exact initiatory mechanism of pancreatitis is unknown.4 Some hypotheses for CP relate to a pathological cascade in the pancreas due to chronic alcohol consumption. One hypothesis is that alcohol consumption causes the release of pancreatic fluid that is high in protein and low in volume and bicarbonate. This leads to the precipitation of protein that creates plugs in pancreatic ducts. These plugs calcify and produce pancreatic stones, damaging tissue and increasing pressure within the ducts. Pancreatic stones are found in many types of CP, but their presence is not required for tissue damage to occur.5 Another alcohol-related hypothesis is that alcohol or one of its metabolites act as a toxin that causes acinar cells to be sensitive to pathologic stimuli. The presence of alcohol may stimulate the release of cholecystokinin (CCK) which triggers transcription of inflammatory enzymes within the pancreas.5 In the healthy pancreas, pancreatic stellate cells (PSC) maintain normal extracellular matrix (ECM). PSC cells have the ability to migrate and phagocytize, suggesting some sort of a role in immunity. In the pathogenic pancreas, PSC cells are activated by alcohol and its metabolites to secrete cytokines and secrete excess amount of ECM proteins. The presence of cytokines forms a cycle of PSC activation and continues ECM production, causing tissue fibrosis.6

Multiple bouts of acute pancreatitis can lead to development of chronic pancreatitis. With each episode, the healing of necrotic tissue results in formation of scar tissue or fibrosis. Similar to the process of liver cirrhosis, the cycle of tissue damage and scarring can lead to chronic inflammation and potentially cancer.5 Signs and Symptoms

Signs and symptoms of AP are typically sudden and severe enough that immediate medical attention is sought. Sudden onset of upper abdominal pain that radiates to the back is most common, and may be accompanied with jaundice or sympathetic responses that include sweating, flushing, nausea, vomiting, and anorexia.7 CP is characterized by insidious onset of upper abdominal pain, also radiating to the back. Associated symptoms and signs of progressive pancreatic destruction include weight loss, steatorrhea, azotorrhea, and loss of vitamins A, D, E, and K. Diabetes mellitus may also develop due to loss of islet cells.5,7 Back pain from pancreatitis is usually referred to the region from the 10th to 12th thoracic vertebrae, and from there may radiate to the sub or midscapular regions or left shoulder.4 Pain is worsened after meals and can be relieved by forward bending or the raising of knees to chest. The pain may be acute, with episodes of the patient feeling well, or it may be chronic with gradual increase in intensity.5 Physical examination is usually significant for abdominal tenderness.5 Diagnosis

Imaging used to aide in diagnosis of pancreatitis includes transabdominal ultrasonography or CT. Significant findings reveal structural changes such as dilation of pancreatic ducts, strictures, pancreatic stones, lobularity, or atrophy.5 Diagnosis of acute pancreatitis is based on the Atlanta criteria which include: (1) abdominal pain suggestive of AP, (2) serum amylase (and/or lipase) at levels three times greater than normal, and (3) appearances characteristic of AP on CT or ultrasound.7 During an acute episode of pancreatitis, lab tests may reveal elevated levels of lipase and amylase.3,5 Abnormal bilirubin may indicate significant compression of a bile duct by a pseudocyst or fibrosis.5 If AP is suspected, immediate referral must be made to the emergency department.7 Chronic pancreatitis can be diagnosed using a variety of laboratory tests that test enzyme activity from samples taken directly from the pancreas or from fecal matter. Imaging tests include abdominal ultrasound, abdominal CT scan, and endoscopic ultrasound.8 For those with suspected CP, referral should be made based on the current severity of symptoms. The patient or client with an acute form of the disease should be referred and treated much as those with AP. If the disease has a more chronic presentation, it is recommended that referral be made to a gastroenterology or hepatopancreaticobiliary outpatient clinic for further assessment and investigation.7 Treatment

The primary goals of treatment are to prevent further pancreatic injury, relieve pain, and replace lost endocrine/exocrine function.5 For acute pancreatitis, elimination of the initiating factor is critical for management.7 For example, alcohol intake must be limited or ceased in alcohol related disease.5 Inpatient supportive therapy includes support for other failing organ systems, oxygen replacement, replenishment of circulatory volume, and nutritional supplementation.7 Since pain is the most debilitating symptom of chronic pancreatitis, immediate treatment for this condition is focused on pain relief. Cessation of alcohol intake and smoking help slow the inflammatory processes and improve response to other treatment. Depression is common in individuals with chronic disorders and is indicative of poor outcomes. Support groups and counseling can help improve quality of life for those struggling with depression and its effects.7 Pain is treated first with non-narcotics and will advance to narcotics if needed. High-dose enzyme therapy, for those with small duct disease, and nerve blocks may also help aid in pain reduction. For large duct disease, stents and pancreatic duct sphincterotomy improve pain in over 50% of clients. Surgical drainage or removal of pseudocysts may be used to treat severe pain.5 Final treatment for refractory pain is pancreatectomy. Removal of the pancreas requires subsequent supplemental oral enzyme replacement before, during, and after meals.5 Implications for the Therapist

Beware of a client’s health history that includes patterns of high alcohol consumption, as alcohol abuse is a risk factor for development of pancreatitis. People with alcohol related chronic pancreatitis often exhibit peripheral neuropathy. Additional red flags suggestive that indicate physician referral include aggravating and relieving factors and failure to respond to conservative treatment.1 References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 915-916. 2. Klineberg E, Mazanec D, Orr D, Demicco R, Bell G, McLain R. Masquerade: medical causes of back pain. Cleveland Clinic Journal Of Medicine. December 2007;74(12):905913. 3. Decina P, Vallee D, Mierau D. Acute pancreatitis presenting as back pain: a case report. Journal Of The Canadian Chiropractic Association. June 1992;36(2):75. 4. Yadav D, Timmons L, Benson J, Dierkhising R, Chari S. Incidence, prevalence, and survival of chronic pancreatitis: a population-based study. The American Journal Of Gastroenterology. December 2011;106(12):2192-2199. 5. Spanier B, Bruno M, Dijkgraaf M. Incidence and mortality of acute and chronic pancreatitis in the Netherlands: a nationwide record-linked cohort study for the years 1995-2005. World Journal Of Gastroenterology: WJG. May 28, 2013;19(20):3018-3026. 6. Skipworth J, Shankar A, Pereira S. Managing acute and chronic pancreatitis. The Practitioner. October 2010;254(1733):23.

7. Apte M, Pirola R, Wilson J. New insights into alcoholic pancreatitis and pancreatic cancer. Journal Of Gastroenterology & Hepatology. October 4, 2009;24:S51-S56. 8. Banks P. Classification and diagnosis of chronic pancreatitis. Journal Of Gastroenterology. 2007;42:148-151. Crohn’s Disease Condition

Crohn’s disease is an autoimmune chronic inflammation of any region of the gastrointestinal tract, but most commonly involving the ileum and proximal portion of the colon. Crohn’s disease and ulcerative colitis are collectively known as inflammatory bowel diseases.1,2 Incidence/Etiological Factors

The highest incidence of Crohn’s disease is reported in northern Europe, the United Kingdom, and North America. Incidence in North America ranges between 3.1 and 14.6 cases per 100,000 persons per year. Prevalence ranges between 26 and 199 cases per 100,000 persons. Crohn’s disease affects more females than males and more white and African Americans than Native, Asian, and Hispanic Americans. Established risk factors include family history of inflammatory bowel diseases, cigarette smoking, and appendectomy.3 Pathogenesis

Random mutation of the NOD2 gene is believed to be the genetic root of Crohn’s disease. A pathologic interaction between the immune system and normal gut microbiota leads to the misdirected attack of the immune system on the colon. Three mechanisms are thought to drive this faulty interaction. First, the introduction of pathogenic bacteria may induce a chronic immune response. Second, a loss of protective bacteria can lead to increased mucosal permeability and an increased immune response. Finally, dysfunction of regulatory T cells or antigen presenting cells can lead to a loss of tolerance for resident gut microbiota.2 Signs and Symptoms

Symptoms include diarrhea, abdominal cramping and pain, fever, and sometimes rectal bleeding. Loss of appetite, weight loss, and fatigue may also occur. Blocking of the intestine due to inflammation and scar tissue can lead to abdominal cramps, vomiting, and bloating.1 Three fourths of patients with Crohn’s disease will complain of abdominal cramps in the lower right quadrant. 2 The disease is not limited to the gastrointestinal tract and the patient may experience symptoms that affect the joints, eyes, skin, and liver.1 Sacroiliitis is a common finding in patients with Crohn’s disease, and the majority of these patients complain of low back pain.4 Ankylosing spondylitis develops in approximately 60% of Crohn’s patients who are serum positive for the HLA-B27 gene.2

Diagnosis

The mean age of diagnosis is around late adolescence and early adulthood.3 The presence of antibodies for E. coli and S. cerevisiae are indicative of Crohn’s disease. Increased fecal lactoferrin and calprotectin levels are both markers for bowel inflammation and also indicative of Crohn’s. Colonoscopy, capsule endoscopy, CT, and MRI are diagnostic tests useful in aiding diagnosis.5 Treatment

Goals of treatment include symptom control, clinical remission of disease, and maintenance of remission. Corticosteroids may be prescribed first, with pharmacologic treatment progressing to immunomodulators or anti-tumor necrosis factor (TNF) agents as necessary. Antibiotics have an anti-inflammatory and anti-infectious affect in patients with mild disease. Surgery is indicated in severe disease in which there is obstruction of the intestine or an abdominal mass.5 Implications for the Therapist

When a client presents with back, sacroiliac, or hip pain of unknown origin, the therapist should ask questions about accompanying gastrointestinal symptoms, family history of inflammatory bowel disease, and if symptoms are relieved upon passing stool or gas.6 Findings suggestive of nonmechanical pathology warrant physician referral. References

1. Centers for Disease Control and Prevention. Inflammatory Bowel Disease. http://azhin.org/content.php?pid=326216&sid=2670252. Updated January 14, 2014. Accessed April 5, 2014. 2. Engel M, Neurath M. New pathophysiological insights and modern treatment of IBD. Journal Of Gastroenterology. June 2010;45(6):571-583. 3. Loftus, EV. Clinical Epidemiology of Inflammatory Bowel Disease: Incidence, Prevalence, and Environmental Influences. Gastroenterology. 2004;125:1504-1517. 4. Orchard T, Holt H, Wordsworth B, et al. The prevalence, clinical features and association of HLA-B27 in sacroiliitis associated with established Crohn’s disease. Alimentary Pharmacology & Therapeutics. January 15, 2009;29(2):193-197. 5. Wilkins T, Jarvis K, Patel J. Diagnosis and management of Crohn's disease. American Family Physician. December 15, 2011;84(12):1365-1375. 6. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 857.

Infective Endocarditis Condition

Infective endocarditis is a bacterial infection of the endocardium of the heart. Structures involved include heart valves, chordae tendineae, cardiac septum, or lining of the chambers.1

Incidence/Etiological Factors

Incidence in the United States has risen in the last 15 years, and is estimated to be about 12.7 per 100,000 people, representing an annual hospital admission rate increase of 2.4% from 19982009. Average age of diagnosis is 60 years old.2 History of underlying cardiac valvular disease, congenital heart disease, prosthetic cardiac valve, and intravenous drug abuse all increase risk of developing endocarditis.3 Pathogenesis

Endothelial injury results in the formation of a sterile-fibrin thrombus. The thrombus is vulnerable to bacterial colonization from normal transient bacteremia. Infection of the thrombus leads to the development of valvular vegetations, an accumulation of bacterium, white blood cells, fibrin, and platelets which collects on the endothelial surface of the heart. These infected valvular vegetations can cause local tissue damage, embolic events, and immune complexes.3 Any microorganism can cause bacterial endocarditis, but Streptococcus viridans and Staphylococcus aureus are the most common bacterial organisms causing endocarditis in patients with musculoskeletal symptoms.3,4 Signs and Symptoms

Symptoms often are nonspecific and may include fever, chills, night sweats, fatigue, anorexia, weight loss, and muscle and joint pain.1 Infective endocarditis can have a broad spectrum of clinical manifestations, affecting a variety of organs and systems. Immunological, cutaneous, splenic, pulmonary, neurological, hematologic, musculoskeletal, and renal manifestations have all been documented.5 Nearly 50% of patients with infective endocarditis have some sort of musculoskeletal manifestation. Of those with musculoskeletal manifestations, one fourth have low back pain. When low back pain is present, it is often one of the chief complaints, with spinal tenderness and decreased range of motion present. Additional musculoskeletal manifestations include arthralgias, arthritis, diffuse myalgias, leg myalgias, and disc space infection.4 Diagnosis

Infective endocarditis can be an elusive diagnosis due to its systemic manifestations and subtle or delayed cardiac involvement.4 Thus, a high index of suspicion for the disease is required for diagnosis, which is guided by the modified Duke criteria.3 Modified Duke Criteria for diagnosis of bacterial endocarditis is widely utilized and accepted.3 These criteria are divided into major and minor criteria. The four major criteria include: (1) positive blood culture of a typical microorganism consistent with infective endocarditis, (2) evidence of endocardial involvement, (3) positive echocardiogram for infective endocarditis, and (4) new valvular regurgitation. The minor criteria include: (1) presence of a predisposing condition for infective endocarditis, (2) fever, (3) vascular phenomena, (4) immunologic

phenomena, and (5) microbiological evidence of infection but not consistent with organisms indicated in the major criterion.6 Definitive diagnosis of infective endocarditis is reached in the presence of: (1) 2 major criteria (2) 1 major criteria and 3 minor criteria (3) 5 minor criteria. Diagnosis is classified as possible in the presence of: (1) 1 major and 1 minor criterion (2) 3 minor criteria. Diagnosis is rejected if firm diagnosis of other pathology is reached that explains symptoms indicative of infective endocarditis, symptoms resolve after four days or less of antibiotic therapy, there is no evidence of infective endocarditis upon surgery or autopsy, or if none of the criteria for diagnosis are reached.6 Treatment

Goals of treatment are to preserve cardiac function, clear infection, and prevent complications such as embolism and heart failure.1 Streptococcus infections respond well to antibiotic treatment in most cases. Staphylococcus infections are less susceptible to antibiotic treatment alone and usually will require surgical intervention.3 Implications for the Therapist

A feature of back pain due to infective endocarditis that distinguishes it from mechanical back pain is lack of previous known injury or history of back pain. These cases of back pain also resolve with antibiotic treatment, indicating that they are of infectious origin.4 References

1. HolComb S. Recognizing and managing endocarditis. Nursing. February 2004;34(2):32cc1-32cc2. 2. Bor D, Woolhandler S, Nardin R, Brusch J, Himmelstein D. Infective Endocarditis in the U.S., 1998–2009: A Nationwide Study. Plos ONE. March 2013;8(3):1-8. 3. Murtagh B, Frazier OH, Letsou GV. Diagnosis and management of bacterial endocarditis in 2003. Curr Opin Cardiol. Mar 2003;18(2):106-110. 4. Churchill M, Geraci J, Hunder G. Musculoskeletal manifestations of bacterial endocarditis. Annals Of Internal Medicine. December 1977;87(6):754-759. 5. Heffner JE. Extracardiac manifestations of bacterial endocarditis. West J Med. Aug 1979;131(2):85-91. 6. Li J, Sexton D, Corey G, et al. Proposed Modifications to the Duke Criteria for the Diagnosis of Infective Endocarditis. Clinical Infectious Diseases. April 2000;30(4):633.

Endometriosis Condition

Endometriosis is a condition defined by the presence of endometrial tissue outside of the uterus.1 Incidence/Etiological Factors

Affecting an estimated 5.5 million women in North America, incidence rates of endometriosis are highest among women ages 25-29 and lowest among women over 44 years old.3,2 Estimates of prevalence vary between 2-10% of women of reproductive age having endometriosis.3 Women of childbearing age are at more risk for the condition, and it is more common in those who have postponed pregnancy. Additional risk factors include early menarche, 27-day or shorter menstrual cycles, menstrual periods lasting longer than 7 days, and genetic predisposition.1 There is no variability in risk among women of different ethnic origins, backgrounds, and geographic locations.2 Pathogenesis

The condition becomes apparent in early teen years after menses have begun and may continue until menopause. Endometrial cells migrate to other parts of the body where they form pockets of tissue called implants. The implants then swell in response to cyclic estrogen and progesterone surge, causing cysts on underlying organs and, in time, development of fibrosis and adhesions.1,6 Pelvic organs are the most commonly affected sites, although organs beyond this region, such as the lungs, are sometimes affected.6 The mechanism by which endometrial tissue is relocated to other areas of the body is unknown. The most widely accepted explanation is that of retrograde menstrual flow, in which endometrial tissue travels up through the fallopian tubes during menstruation and into the peritoneal cavity.4 Signs and Symptoms

Endometrial implants can lead to false-positive findings upon initial examination by a physical therapist.1,7 It is important to recognize the following signs and symptoms that may be present in a female presenting with low back pain. Signs and symptoms are largely dependent on the location of the implants. Pain and infertility are the two most common symptoms.2 Intermittent, cyclical, or constant pelvic and/or low back pain by present itself unilaterally or bilaterally.1 If implants are located on the uterosacral ligaments, dysmenorrhea is a chief complaint. Dyspareunia, pain during defecation, low-grade fever, diarrhea, constipation, and rectal bleeding are also possible symptoms. Pain may be referred to the low back or sacral region, groin, posterior leg, upper abdomen, or lower abdominal and suprapubic regions.1 Diagnosis

The triad of dysmenorrhea, dyspareunia, and infertility are strongly suggestive of endometriosis. It is difficult to diagnose endometriosis based off of symptoms alone because its presentation is variable depending on location of the implants.6 To obtain a definitive diagnosis, direct visual examination by laparoscopy is required and considered to be the gold standard.1,4,6 An additional benefit of laparoscopy is that implants can be removed as they are discovered. Ultrasound and

MRI are also used to examine the pelvis. MRI is more sensitive for detecting implants. Research is currently being conducted in the development of a blood test to aid in detection.1 Treatment

As there is no cure for endometriosis, goals of treatment are preservation of tissues and pain relief. NSAIDs are safe to be taken for pain relief.1 Progestins and oral contraceptives are considered the first line in treatment against endometriosis. Hormonal drugs used to suppress ovarian function such as danazol and gestrinone are effective in reducing pain associated with endometriosis, but have undesirable side effects and should be considered a second-line option for treatment.5 Because these therapies work by suppressing ovarian function, they are recommended for women who do not wish to become pregnant in the near future. Surgical interventions may be sought for patients with mild to extensive adhesions. Laparoscopic cauterization or laser surgery is effective in most cases. For women over 35-40 years old who are done with childbearing and experiencing disabling pain, total hysterectomy, bilateral slpingooophorectomy, or implant removal are all considerable options.1 Nontraditional therapies sought include yoga, aromatherapy, reflexology, naturopathic medicine, or homeopathy.1 Implications for the Therapist

Cyclic back pain is often attributed to the hormonal changes of the menstrual cycle that result in ligamentous laxity and subsequent stress on the pelvic joints. Pelvic disease such as endometriosis may also result in the same type of pain, however. Consideration should be taken when considering dyspareunia, for example, a common symptom of endometriosis. Patients with back pain associated with joint dysfunction may experience painful intercourse in certain positions and not others. If dyspareunia is due to endometriosis, relief will not be achieved regardless of position. Location of the implants in different regions may also result in falsepositive findings in various muscle groups. Awareness of signs and symptoms of pelvic disease will enhance the therapist’s differential diagnosis process in female clients with LBP.3 References

1. Endometriosis. Rockville, Md: National Institutes of Health, National Institute of Child Health and Human Development, US Department of Health and Human Services; 2002. NIH Publication 02-2413. 2. Missmer S, Hankinson S, Spiegelman D, Barbieri R, Marshall L, Hunter D. Incidence of laparoscopically confirmed endometrosis by demographic, anthropometric, and lifestyle factors. American Journal Of Epidemiology. October 15, 2004;160(8):784-796. 3. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 995-997.

4. Kennedy S, Agneta B, Chapron C, D’Hooghe T, Dunselman G, Greb R, et al. ESHRE guideline for the diagnosis and treatment of endometriosis. Human Reproduction. 2005;20(10):2698-2704. 5. Mao A, Anastasi J. Diagnosis and management of endometriosis: the role of the advanced practice nurse in primary care. Journal Of The American Academy Of Nurse Practitioners. February 2010;22(2):109-116. 6. Troyer MR. Differential diagnosis of endometriosis in a young adult woman with nonspecific low back pain. Phys Ther. 2007;87:801–810. 7. Vercellini P, Somigliana E, Viganò P, Abbiati A, Barbara G, Crosignani PG. Endometriosis: Current therapies and new pharmacological developments. Drugs. 2009;69(6):649-75.

Irritable Bowel Syndrome Condition

Irritable bowel syndrome (IBS) is a heterogeneous set of conditions characterized by episodes of abdominal pain or discomfort accompanied by changes in frequency or consistency of stool without an organic etiology.1 Incidence/Etiological Factors

In the United States, incidence of clinical diagnosis of IBS is approximately two per 1000 persons per year. Incidence increases with age and prevalence is higher in women than men. True incidence is predicted to be much higher than reported, as many people do not seek medical care for their symptoms.2 Pathogenesis

Irritable bowel syndrome has no known medical etiology.1 A combination of altered gastrointestinal motility, visceral hyperalgesia, and psychopathology are believed to contribute to irritable bowel syndrome. Altered GI motility is hypothesized to be the result of hyperresponsiveness of the smooth muscle of both the small intestine and colon. Psychopathology and increased perception of visceral pain are common in patients with IBS.3 Psychiatric disorders such as depression and anxiety are often comorbid in patients lacking organic etiology. Associations have been demonstrated among psychiatric or medically unexplained conditions including low back pain, chronic fatigue syndrome, irritable bowel syndrome, major depression, chronic tension headache, temporary mandibular joint disorder, fibromyalgia, panic attacks, and posttraumatic stress disorder.4 Signs and Symptoms

Patients may present clinically with a wide range of symptoms. These may include abdominal distension, pain or discomfort, bloating, diarrhea, constipation, lower abdominal pain alleviated with bowel movement, mucus in stools, incomplete emptying of bowels, fatigue, irritable

bladder, flatulence, back pain, dyspareunia, nausea, headache, poor appetite, muscle pain, and heartburn. Anxiety, depression, and other psychiatric disorders may accompany this condition.5 Diagnosis

Since this syndrome does not have any structural or biochemical markers, diagnosis is confirmed based on reported symptoms and firm exclusion of organic diseases with similar symptomology.1 According to NICE guidelines6, diagnosis of IBS is considered when a patient has had abdominal pain, discomfort, or change in bowel habits lasting at least six months and at least two of the following symptoms: (1) Altered stool passage (2) Abdominal bloating (3) Worsening symptoms upon eating (4) Passage of mucus from the rectum Although these symptoms are required for diagnosis of IBS, a wide range of symptoms associated with the syndrome may be presented to the clinician. These may include abdominal distension, pain or discomfort, bloating, diarrhea, constipation, lower abdominal pain alleviated with bowel movement, mucus in stools, fatigue, irritable bladder, back pain, dyspareunia, nausea, headache, poor appetite, muscle pain, and heartburn. Mental symptoms that also may accompany this condition are anxiety and depression.5 Treatment

Treatment should be oriented at establishing a strong patient-provider relationship that includes reassurance and patient education. Dietary recommendations include fiber supplementation for patients with constipation and diarrhea and increased water for patients primarily dealing with constipation. Psychotherapy and antidepressants have also demonstrated effectiveness in improving GI symptoms.3 Implications for the Therapist

Patients with IBS may benefit from increased body awareness therapy, as it helps increase flexibility and reduce tension.7 Patients with IBS may use breath holding patterns or hyperventilation to manage their stress. The physical therapist should emphasize healthy breathing patterns to use during exercise and relaxation techniques.8 References

1. Yale S, Musana A, Kieke A, Hayes J, Glurich I, Po-Huang C. Applying Case Definition Criteria to Irritable Bowel Syndrome. Clinical Medicine & Research. May 2008;6(1):916. 2. Locke III G, Yawn B, Wollan P, Melton III L, Lydick E, Talley N. Incidence of a clinical diagnosis of the irritable bowel syndrome in a United States population. Alimentary Pharmacology & Therapeutics. May 2004;19(9):1025-1031. 3. Lehrer JK, Lichtenstein GR. Irritable Bowel Syndrome. Medscape. http://emedicine.medscape.com/article/180389-overview#a0104. Accessed April 5, 2014.

4. Schur E, Afari N, Buchwald D, et al. Feeling bad in more ways than one: Comorbidity patterns of medically unexplained and psychiatric conditions. Journal Of General Internal Medicine. June 2007;22(6):818-821. 5. Shan Y. Irritable bowel syndrome: treatment and management. Primary Health Care. October 2009;19(8):28-34. 6. National Institute for Health and Clinical Excellence. Irritable bowel syndrome in adults: Diagnosis and management of irritable bowel syndrome in primary care. NICE Clinical Guideline 61. February 2008. 7. Eriksson E, Nordwall V, Kurlberg G, Rydholm H, Eriksson A. Effects of body awareness therapy in patients with irritable bowel syndrome. Advances In Physiotherapy. September 2002;4(3):125-135. 8. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 861.

Multiple Myeloma Condition

Multiple myeloma (MM) is a malignant monoclonal tumor of bone marrow plasma cells that leads to lytic lesions of the bone.1 Incidence/Etiological Factors

Multiple myeloma is the second most prevalent hematopoietic malignancy. An estimated 24,000 new cases will be diagnosed in the United States in 2014.1 Risk of MM increases with age and is twice as high in Africans and African Americans than in other populations.2 Pathogenesis

The development of multiple myeloma is preceded by development of asymptomatic monoclonal gammopathy of undermined significance (MGUS).3 This premalignant plasma cell tumor, like MM, exhibits total dysregulation of the cyclin D/retinoblastoma pathway, an important pathway involved in regulation of the cell’s lifecycle.4,5 Presence of the tumor in the microenvironment of the bone marrow causes activation of osteoclasts and suppression of osteoblasts, leading to lytic bone disease.4 Lytic bone lesions of the spine may develop into fractures of the vertebrae that may be mistaken for mechanical back pain.6 Signs and Symptoms

Presenting features of MM include symptoms of bone disease, impaired kidney function, anemia, hypercalcemia, recurrent bacterial infection, and hyperviscosity.3 The most common signs and symptoms at diagnosis are weight loss, bone pain, and anemia-related fatigue.7 Most multiple myeloma patients will develop bone disease, greatly increasing risk for pain, fracture, spinal cord compression, and hypercalcemia.3 Diagnosis

Patients may be diagnosed following incidental findings of raised ESR, plasma viscosity, or serum protein during routine blood tests. Monoclonal (M) protein is produced by the myeloma cells and is used as a market to track disease progress and treatment efficacy. Levels of Mprotein less than 30g/l, bone marrow clonal plasma cells of less than 10%, and no related organ or tissue impairment are three diagnostic criteria for MGUS. M-protein levels greater or equal to 30g/l and/or bone marrow clonal plasma cells of greater or equal to 10% along with no evidence of organ or tissue damage are criteria for asymptomatic myeloma. Criteria for symptomatic myeloma diagnosis include the presence of M-protein in serum and/or urine sample, increased bone marrow plasma cells, and related organ or tissue impairment such as bone lesions. Some patients with symptomatic myeloma will not demonstrate increased M-protein or increased clonal plasma cells in the bone marrow, but will have myeloma-related organ or tissue damage.3 A full skeletal survey to screen for bone lesions is recommended upon diagnosis and follow up imaging using CT or MRI should be conducted for ambiguous plain radiographic findings or if bone disease is suspected.3 Treatment

Genetic heterogeneity makes this cancer a high risk drug resistant disease. Advances in treatment and technology have doubled the median survival time from three to six years, but multiple myeloma still remains an incurable disease.3,7 Patients with asymptomatic myeloma should be regularly monitored by a hematologist. Treatment for asymptomatic myeloma is not recommended, but chemotherapy may be commenced as levels of M-protein rise. Chemotherapy is indicated once organ or tissue related symptoms arise.3 Upon diagnosis of symptomatic myeloma, the patient should also be considered for hematopoietic stem cell transplant.7 Implications for the Therapist

It is vital for the therapist to be ever vigilant for clients who do not respond to conservative therapy.6 Patients with MM may be reluctant to exercise due to pain, fatigue, low motivation, and fear of infection. Individualized exercise programs may be helpful for addressing the both psychological and physical recovery needs of patients diagnosed with MM.8 Weight bearing considerations must be made for patients with lytic bone lesions. Recommendations for patients with bone metastases include: (1) >50% cortical metastatic involvement: no weight bearing, touch down okay (2) 25-50% cortical metastatic involvement: some weight bearing, avoid stretching and twisting (3) 0-25% cortical metastatic involvement: full weight bearing, avoid straining and lifting.9 References

1. Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA: A Cancer Journal For Clinicians. 2014;64(1):9-29.

2. Greenberg A, Vachon C, Rajkumar S. Disparities in the prevalence, pathogenesis and progression of monoclonal gammopathy of undetermined significance and multiple myeloma between blacks and whites. Leukemia (08876924). April 2012;26(4):609-614. 3. Bird J, Owen R, Behrens J, et al. Guidelines for the diagnosis and management of multiple myeloma 2011. British Journal Of Haematology. July 2011;154(1):32-75. 4. Kuehl W, Bergsagel P. Molecular pathogenesis of multiple myeloma and its premalignant precursor. Journal Of Clinical Investigation. October 2012;122(10):34563463. 5. Bartek J, Bartkova J, Lukas J. The retinoblastoma protein pathway in cell cycle control and cancer. Experimental Cell Research. November 25, 1997;237(1):1-6. 6. Gebhardt M. Pathological cause of low back pain in a patient seen through direct access in a physical therapy clinic: a case report. Orthopaedic Physical Therapy Practice. June 2013;25(2):73-76. 7. Lee K, De Bellis D. Therapeutic considerations in managing multiple myeloma. Formulary. July 2009;44(7):204-213. 8. Craike M, Hose K, Courneya K, Harrison S, Livingston P. Perceived benefits and barriers to exercise for recently treated patients with multiple myeloma: a qualitative study. BMC Cancer. August 2013;13(1):1-10. 9. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 709-713.

Nephrolithiasis Condition

Nephrolithiasis, also known as renal calculi or kidney stones, refers to the formation and passage of crystalline stones in and through the kidneys and urinary tract.1 Incidence/Etiological Factors

In the United States an estimated 10% of the populace will be diagnosed with a kidney stone in their lifetime. Prevalence is greater in men and risk increases with age, peaking in those 40-59 years old.2 Warmer temperature is also a contributing factor for disease, as increased temperature and sun exposure alter the composition of urine to be highly saturated in calcium oxalate and calcium phosphate.3 Pathogenesis

Renal calculi are categorized into two types: staghorn and non-staghorn. Staghorn stones fill in numerous major and minor calices while non-staghorn stones are identified by their location in the renal pelvis or in a major or minor calyx. Stones may also be located in the ureters and urinary bladder.4 The pathogenesis of stone formation is complex. Stones develop 80% of the time as the result of urine supersaturation of calcium oxalate (CaOx) and calcium phosphate (CaP). Supersaturation of uric acid or struvite cause stones 9% and 10% of the time respectively.3 Supersaturation may

be the result of low urine volume, hyperuricosuria, hypercalciuria, hyperoxaluria, low urine pH, dietary habits, altered gut microbiota, or genetic predisposition. Calculi formation is hypothesized to occur through one of three pathways, (1) overgrowth on Randall’s plaque, (2) growth on plugs in the ducts of Bellini, and (3) in free solution.1,4,5 Signs and Symptoms

If a stone becomes lodged at the junction between the kidney and ureter, severe colicky flank pain may result. Pain may be localized at the costovertebral angle and hematuria may be present. As the stones pass into the ureter, the patient may experience ureteral colic and hematuria. Further descension through the ureters toward the bladder will cause spasms and colicky pain radiating laterally to the umbilical region. Sharp pain radiating to the groin, testicles, or labia may occur as the stone passes near the bladder. Immediate relief follows the passing of the stone through the system.1 Diagnosis

Diagnosis is based upon history and physical examination, blood and urine tests, and a radiologic imaging study. Urinalysis may reveal hematuria, altered pH, and the presence of small crystals. Serum analysis revealing elevated WBC count is suggestive of a systemic urinary infection and reduced RBC count may be indicative of chronic disease or severe ongoing hematuria. The primary diagnostic tool for identifying calculi is the intravenous pyelogram (IVP). It provides accurate information on size and location of the stone and severity of the obstruction, helping guide subsequent treatment. CT scan allows the diagnostician to find changes secondary to a urinary obstruction such as renal enlargement, ureteral dilation, and periureteral edema. Renal scan, plain radiographs, and ultrasound are additional imaging modalities used in guiding the diagnosis and treatment process.1 Treatment

Stones of less than 5mm are very likely to be passed. Stones 5-7mm in size have a 50% chance of being passed, and stones greater than 7mm will almost always require special intervention.3 Two to three quarts of water intake per day will help progress the stone through the urinary system. The process of letting the stone pass can be done at home with the help of pain medicine as needed. If the stone is too large to be passed, extracorporeal shockwave lithotripsy (ESWL) is commonly used to transmit shock waves which break up the stone into smaller, passable fragments. In severe cases when ESWL is contradicted, percutaneous nephrolithotomy is used to remove the stone surgically.1 Implications for the Therapist

Renal colic is typically not confused with musculoskeletal pain of the back, but sometimes depending on the location of the obstruction, symptoms can be intermittent, manageable, and manifest as unilateral back pain. The therapist should be alert to reported symptoms of urinary dysfunction. A positive Murphy’s percussion test should warrant referral to a physician.6 References

1. Colella J, Kochis E, Galli B, Munver R. Urolithiasis/Nephrolithiasis: What's It All About?. Urologic Nursing. December 2005;25(6):427-475. 2. Stamatelou K, Francis M, Jones C, Nyberg L, Curhan G. Time trends in reported prevalence of kidney stones in the United States: 1976–19941. Kidney International. May 2003;63(5):1817-1823. 3. Eisner B, Sheth S, Humphreys M, et al. The effects of ambient temperature, humidity and season of year on urine composition in patients with nephrolithiasis. BJU International. December 15, 2012;110(11c):E1014-E1017. 4. Evan A. Physiopathology and etiology of stone formation in the kidney and the urinary tract. Pediatric Nephrology. May 2010;25(5):831-841. 5. Sakhaee K. Recent advances in the pathophysiology of nephrolithiasis. Kidney International. March 15, 2009;75(6):585-595. 6. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 939.

Osteomyelitis Condition

Osteomyelitis is characterized by inflammatory bone changes or necrosis due to a bacterial infection.1 Incidence/Etiological Factors

Incidence of osteomyelitis is around five cases per million per year, and highest incidence is found within the 60-69 year old age group.2 Adults who develop osteomyelitis often have an underlying medical condition such as diabetes mellitus, cancer, chronic renal disease, or history of intravenous drug use. However, children are naturally more susceptible to hematogenous osteomyelitis because their bones are highly vascular and more vulnerable to trauma.1 Pathogenesis

Chronic osteomyelitis is typically secondary to infection from surgery, an open fracture, bacteremia, or soft tissue infection.1,3 Staphylococcus aureus infection is the most common cause of both acute and chronic forms of hematogenous osteomyelitis.1 Infection is spread through the blood stream, predominantly through arteries. When a septic embolus reaches the bone it causes inflammation and infarct of the tissue. Extensive necrosis narrows the disc space, causing wedging, cavitation, and compression fractures which lead to spinal instability, deformity, and cord compression.4 Signs and Symptoms

Systemic indicators of infection include fever, irritability, and local erythema, swelling, and tenderness over the involved bone. Bone infection in adults most often involves vertebrae but can also occur in the long bones, clavicle, or pelvis. Back pain is usually the primary presenting

symptom.1 Roughly 70% of vertebral osteomyelitis has lumbar involvement.5 Other nonspecific symptoms include chronic pain, poor wound healing, malaise, and fever.1 Diagnosis

In children, diagnosis is made based on the localization and rapid onset of symptoms. In adults, diagnosis is difficult and requires a high index of clinical suspicion. The clinician should inquire about history of systemic symptoms or predisposing risk factors. Exam should focus on identifying the origin of infection, assessing peripheral and sensory function, and exploring ulcers for the presence of bone.1 Laboratory tests are not specific for osteomyelitis, but may reveal leukocytosis, raised erythrocyte sedimentation rate, and/or raised C-reactive protein. Consistently normal ESR and C-reactive protein rule out osteomyelitis. A positive culture from bone biopsy is preferred for definitive diagnosis. Imaging modalities are useful for measuring the extent of disease as well as ruling out other causes of symptoms.1 Treatment

Infection is treated with antibiotics and sometimes surgery to remove infected and necrotic tissue.1 Implications for the Therapist

Back pain caused by vertebral osteomyelitis will not respond to conservative treatment by a therapist. Beware if the patient develops fever, fatigue, and/or neurological deficits.6,7 Spinal infection is a rare, but potentially morbid cause of back pain in older adult populations and should be included in the differential diagnosis of back pain without previous known injury in patient populations over 60 years and older.8 References

1. Hatzenbuehler J, Pulling T. Diagnosis and management of osteomyelitis. American Family Physician. November 2011;84(9):1027-1033. 2. Krogsgaard M, Wagn P, Bengtsson J. Epidemiology of acute vertebral osteomyelitis in Denmark: 137 cases in Denmark 1978-1982, compared to cases reported to the National Patient Register 1991-1993. Acta Orthopaedica Scandinavica. October 1998;69(5):513517. 3. Quesnele J. Spinal infection: a case report. Journal Of The Canadian Chiropractic Association. September 2012;56(3):209-215. 4. Gouliouris T, Aliyu SH, Brown NM. Spondylodiscitis: update on diagnosis and management. J Antibmicrob Chemother.2010;65(Suppl3):iii11-iii24. 5. Mete B, Kurt C, Ozturk R, et al. Vertebral osteomyelitis: eight years' experience of 100 cases. Rheumatology International. November 2012;32(11):3591-3597. 6. Petrie C, Marzban F, Sokhansanj A, Tofan C, Garrett K. Salmonella spondylodiscitis in a 15 year old male presenting with back pain: a case report. Journal Of Chiropractic Education. March 2009;23(1):87.

7. Ursprung W, Kettner N, Boesch R. Vertebral osteomyelitis: a case report of a patient presenting with acute low back pain. Journal Of Manipulative & Physiological Therapeutics. November 2005;28(9):713-718. 8. Hutchinson C, Hanger C, Wilkinson T, Sainsbury R, Pithie A. Spontaneous spinal infections in older people. Internal Medicine Journal. December 2009;39(12):845-848.

Ovarian Cancer Condition

Ovarian cancer is cancer that forms in the tissues of the ovary. Most ovarian cancers are epithelial (arising out of the outer epithelium of the ovary) or germ cell (develops in an egg cell). Incidence/Etiological Factors

It is estimated that 225,500 new cases of ovarian cancer are diagnosed worldwide each year and at 140,200 deaths per year, this represents the second most deadly of gynecological cancers. Although there are more cases of ovarian cancer in developing countries than developed countries, incidence rates in developed countries are higher, at 9.4 per 100,000 in developed nations and 5.0 per 100,000 in developing nations.1 Epithelial and germ cell are the two predominant types of ovarian tumor. Epithelial tumors are most likely to occur in women who are middle aged and older. These types of tumors are rare in young adults, particularly in those who are prepubescent.4 Germ cell tumors are much more common in children, making up more than half of ovarian tumors in this population, with one third of these being malignant.2 Family history of two or more cases of breast or ovarian cancer may indicate increased risk possibly associated with genetic mutations of the tumor suppressor genes BRCA1 and BRCA2. Not all cases are associated with the mutated BRCA gene, and mutations can also be acquired in an individual over time.3 Any factor that causes an increase in ovarian activity is associated with higher risk for development of disease. For this reason, nullipary and infertility appear to increase risk as well as the use of hormone replacement therapy and fertility drugs. Conversely, pregnancy, childbirth, breast feeding, and use of oral contraceptives all correspond with a decreased risk for ovarian cancer.3 Pathogenesis

There are three main types of ovarian malignancies: germ cell, epithelial stromal, and sex chord stromal tumors. Surface epithelial stromal tumors arise from the surface epithelium of the ovary and account for 60% of all ovarian tumors and 90% of all malignant ovarian tumors.2 Sex chord stromal tumors are associated with hormonal expression and arise from the theca, granulosa, and other stromal cells, as well as their testicular counterparts the Sertoli and Leydig cells. They make up 8% of all ovarian tumors and 7% of ovarian malignancies. Germ cell tumors are

believed to rise out of the egg cells of the ovary, making up around 25% of all ovarian tumors but only 3-7% of malignancies. In adults this type of tumor is rare and usually benign, but in children this tumor type makes up greater than 50% of all ovarian tumors and about one third of these are malignant.2 Signs and Symptoms

Unusual abdominal or lower back pain is reported in over 50% of cases.4 The next most common symptom is unusual bloating, fullness and pressure in the abdomen or pelvis. Gastrointestinal distress including gas, constipation, diarrhea, food intolerance, gastroenteritis, nausea and/or vomiting is also common.4 Less common symptoms include frequent, urgent, or burning urination. Symptoms affecting reproductive health include abnormal vaginal bleeding, and infertility. Irritable bowel syndrome is also reported by a number of patients.4 The non-specificity of symptoms often leads to diagnosis only in the later stages of the disease when prognosis is poor. Awareness of these symptoms in the cancer’s earlier stages may lead to better outcome.3 Diagnosis

Tumor proliferation and subsequent tissue damage in the ovary leads increased CA125 in blood serum.3 The CA125 tumor marker the best single representative marker for diagnosing ovarian cancer. However, combined analysis of CA125 and HE4 improves diagnostic accuracy, particularly in individuals with early stages of the disease.5 Normal value for CA125 is 35IU/ml. If the patient has marker values greater than this, ultrasound is used to initially identify the presence of ovarian masses. If ultrasound findings are positive, then risk of malignancy (RMI) is calculated. Score of 250 or higher on the RMI algorithm warrants referral to a specialist for cancer care and treatment. A symptomatic patient with normal CA125 levels or unremarkable ultrasound findings should be monitored and other causes of symptoms investigated.3 Treatment

Surgery and chemotherapy are standard treatment for women with ovarian cancer. Early stage malignancy, defined as being localized only to the ovaries, is treated surgically with total hysterectomy or bilateral salpingo oophorectomy. These interventions typically are typically curative. Postoperative assessment is vital to ensure that cancer does not return or surface in the lymph nodes or elsewhere. Women who are young and wish to spare fertility may undergo a unilateral salpingo oophorectomy if malignancy is contained to one ovary.3 Advanced disease that has metastasized requires surgery to remove as much of the malignancy as possible. Chemotherapy follows to treat remaining disease and help promote quality of life with the disease. Chemotherapy treatment may also be employed to reduce tumor size prior to surgery.3 Implications for the Therapist

Therapists must be alert to the moderate to high rates of ovarian cancer recurrence and the signs and symptoms of ovarian cancer or its metastases. Gait interruption is a sign of paraneoplastic syndrome associated with gynecologic cancer. Other metastatic symptoms may present as thoracic or shoulder pain due to lymph node metastasis, symptoms of lung or liver disease, weight loss, and overall fatigue.5 References

1. Jemal A, Bray F, Center M, Ferlay J, Ward E, Forman D. Global cancer statistics. CA: A Cancer Journal For Clinicians. March 2011;61(2):69-90. 2. Chen VW, Ruiz B, Killeen JL, Coté TR, Wu XC, Correa CN, Howe HL. Pathology and classification of ovarian tumors. Cancer. 2003:97(10S);2631–2642. doi: 10.1002/cncr.11345 3. Rooth C. Ovarian cancer: risk factors, treatment and management. British Journal Of Nursing. September 27, 2013;22(17):S23-30. 4. Behtash N, Ghayouri Azar E, Fakhrejahani F. Symptoms of ovarian cancer in young patients 2 years before diagnosis, a case-control study. European Journal Of Cancer Care. September 2008;17(5):483-487. 5. Lenhard M, Stieber P, Hertlein AK, Furst S, Mayr D, Nagel D, Hofmann K, Krocker K, Burges A. The diagnostic accuracy of two human epidydmis protein 4 (HE4) testing systems in combination with CA125 in the differential diagnosis of ovarian masses. Clin Chem Lab Med. 2001;49(12);2081-2088. 6. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1007-1009.

Paget Disease of Bone Condition

Paget disease of bone (PDB) is an increased and unorganized turnover of bone that can affect one or more focal skeletal sites.1 Incidence/Etiological Factors

The highest prevalence of PDB is found in the United Kingdom, Australia, New Zealand, North America, and Western Europe, while the disease is quite rare in Scandinavian countries, India, Japan, China, the Middle East, and Africa.2 Worldwide prevalence has been decreasing and developed countries have seen a decrease in both prevalence and severity of disease.3-5 Age of onset is almost always after 40 years, with prevalence doubling each decade after 50 years of age. Family clustering points to genetic factors affecting PDB development, as 15-40% of PDB patients have family history of the disease.2 Pathogenesis

Dysregulation of osteoclastic activity in the bone leads to excessive and unorganized bone remodeling. The precise cause of dysregulation is unknown, but genetic factors are suspected. The predisposing gene SQSTM1 contains mutations that speed osteoclast activity in 5-20% of PDB patients.1 Environmental factors are also hypothesized to play a role in the pathogenesis of PDB, and this is supported by decreasing prevalence and severity of the disease in many countries.1-5 Pagetic lesions exhibit increased bone resorption, marrow fibrosis, increased vascularity, and increased bone formation. The high rate of turnover results in a mixture of woven and lamellar bone, the unorganized structure of which decreases the mechanical integrity of the bone. Decreased mechanical strength increases risk of fracture and bone deformity. Lesions commonly develop in the pelvis (70% of cases), femur (55%), lumbar spine (53%), skull (42%), and tibia (32%).1 Periosteal stretching, vertebral microfractures, vascular enlargement, facet arthritis, intervertebral disc disease, vertebral or sacral fracture, and spondylolysis/-listhesis associated with PDB result in back pain, the most common symptom in patients with lumbar spine involvement.6 In the worst cases (0.2%), malignant degeneration may occur with osteosarcoma being the most common malignancy. This is to be suspected in the case of long lasting disease with persistent or worsening bone pain or new segmental involvement.2 Signs and Symptoms

Most cases are asymptomatic. Deep, aching bone pain is the primary complaint in symptomatic cases. PDB bone pain is typically constant day and night and often worse at night. Pain may be accompanied by bone deformities including bending of long bones and skull enlargement. Due to the high vascularity of the lesions, temperature of the skin directly over the affected bone is often increased. Osteoarthritis secondary to PDB may develop when there is long bone involvement in the limbs. Skull involvement may lead to neurological symptoms including hearing loss and cranial nerve palsies. The high vascular demand of the bony lesions may “steal” blood supply from the local tissue. Resultant decreased blood supply to the brain can cause drowsiness and apathy. With spine involvement the vascular deficit can cause pain, dysthesias, and paralysis. Thoracic spine involvement is the most likely to result in radiculopathies.2 Diagnosis

Radiographic evidence of osteolysis is the cornerstone for diagnosis.2 Since most cases are asymptomatic, the majority of PDB cases are discovered incidentally by radiographic imaging ordered for another purpose.7 Biochemical markers are useful for assessing disease activity and monitoring treatment. PDB is marked by serum elevation of alkaline phosphatase. An elevation of more than 15% is considered clinically significant for a healthy person.2 Treatment

Nitrogen-containing bisphosphonates are the front line drug against PDB. These pharmacologic drugs inhibit bone resorption, improve bone density, and reduce fracture risk long after the completion of treatment. Pain may be controlled with NSAIDs or other anti-inflammatory drugs.

Surgery may be indicated when there is nerve involvement, severe deformity, or severe degenerative joint disease.2,8 Implications for the Therapist

Back pain is the most common complaint in individuals with spine involvement of PDB. Beware of deep, achy pain unrelated to activity and unrelieved by rest.6 Be alert to older clients who report headaches, hearing loss, tinnitus, diplopia, trouble swallowing, or incontinence, as these are indicative of cranial nerve palsy potentially associated with undiagnosed PDB. The reporting of any of these symptoms warrants communication with the physician. Exercise is encouraged to help maintain skeletal health. Strengthening, endurance, stretching, aerobic, endurance, coordination, and balance exercises are all valuable. Exercises should be low impact (no running or jumping), avoid flexion and rotation movements when spinal involvement is present.8 References

1. Ralston S, Layfield R. Pathogenesis of Paget Disease of Bone. Calcified Tissue International. August 2012;91(2):97-113. 2. Colina M, Corte R, Leonardis F, Trotta F. Paget’s disease of bone: a review. Rheumatology International. September 2008;28(11):1069-1075. 3. Bastin S, Bird H, Gamble G, Cundy T. Paget's disease of bone—becoming a rarity?. Rheumatology. October 2009;48(10):1232-1235. 4. Cundy H, Gamble G, Wattie D, Rutland M, Cundy T. Paget’s Disease of Bone in New Zealand: Continued Decline in Disease Severity. Calcified Tissue International. November 2004;75(5):358-364. 5. Corral-Gudino L, Borao-Cengotita-Bengoa M, Del Pino-Montes J, Ralston S. Epidemiology of Paget's disease of bone: A systematic review and meta-analysis of secular changes. Bone. August 2013;55(2):347-352. 6. Dell'atti C, Cassar-pullicino V, Lalam RK, Tins BJ, Tyrrell PN, M. The spine in paget's disease. Skeletal Radiol. 2007;36(7):609-26. 7. Cortis K, Micallef K, Mizzi A. Imaging Paget’s disease of bone—from head to toe. Clinical Radiology. July 2011;66(7):662-672. 8. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1176-1181.

Pancreatic Cancer Condition

Pancreatic cancer is cancer of the tissue of the pancreas. Most pancreatic cancers arise from exocrine cells of the pancreas. Incidence/Etiological Factors

Pancreatic cancer is the fourth leading cause of cancer mortality in the United States. Incidence and mortality rates of pancreatic cancer are strikingly similar, with the five year survival rate under 5%.1 The American Cancer Society projects that in 2014, 46,420 Americans will receive diagnosis and 39,590 people will die of pancreatic cancer.2 Since 1977, incidence rates have remained stable at around 11 per 100,000 people.1 This cancer is most common in the Western world and it is more common in black men and women than in whites.3 Risk factors include advancing age (>60 years), family history of pancreatic cancer, smoking, tobacco use, chemical exposure, obesity, diets high in fat and meat, and family history of chronic pancreatitis.2,4 Pathogenesis

Pancreatic cancer is categorized into two major types: exocrine and endocrine pancreatic cancers. Ninety-five percent of pancreatic neoplasms are adenocarcinomas that arise from exocrine cells. Endocrine pancreatic cancer makes up the remaining five percent of diagnoses, arising from the islet cells.5 Genetic factors contributing to pancreatic cancer are currently under investigation. K-ras mutations are found in more than 90% of people with pancreatic adenocarcinomas.3 These mutations are present in the early stages of carcinogenesis, so their presence may be helpful for detecting earlier stages of disease. The SMAD-4 oncogene is disrupted in 60% of pancreatic cancer cases. Absence of this gene is diagnostic in cases of difficult tissue biopsies. It may also prove helpful for suggesting the pancreas as the possible primary site for metastases of unknown origin. Germline mutations of the STK-11 gene also predispose carriers to a 36% lifetime risk of developing pancreatic cancer. Familial history of pancreatic cancer secondary to germline mutations makes up about 5% of pancreatic cancer cases.5 History of chronic pancreatitis is a risk factor for pancreatic cancer. Both of chronic pancreatitis and pancreatic cancer are characterized by heavy fibrosis of the pancreas. This fibrosis has been considered only the result of repeated damage and scarring, but researchers are also discovering a dynamic relationship between alcohol, pancreatic stellate cells (PSC), and fibrosis. In the healthy pancreas, PSC cells maintain normal extracellular matrix (ECM). PSC cells have also demonstrated ability to migrate and phagocytize, suggesting some sort of a role in immunity. In the pathogenic pancreas, PSC cells are activated by alcohol and its metabolites to secrete cytokines and secrete excess amount of ECM proteins. The presence of cytokines forms a cycle of PSC activation and continues ECM production, causing tissue fibrosis. A mutualistic relationship is formed in the presence of both PSC and pancreatic cancer cells. Pancreatic cancer cells increase PSC cell proliferation, ECM synthesis, and migration. In turn, PSC cells increase pancreatic cancer cell proliferation and migration and decrease pancreatic cancer cell apoptosis. PSC cells have been found to accompany pancreatic cancer cells to distant metastatic sites, thus demonstrating their ability to facilitate the establishment and growth of pancreatic cancer at various sites throughout the body. In light of this, future therapies may be targeted at interrupting the PSC cell and pancreatic cell interaction to help inhibit cancer progression.6 Signs and Symptoms

Presentation is non-specific and vague initially. Up to as long as 24 months prior to traditional symptoms of pancreatic cancer, dysgeusia, pruritis, pancreatitis, diabetes mellitus, skin changes, thrombophlebitis, and psychological disturbances may arise. Up to six months before traditional pancreatic symptoms occur, anorexia, early satiety, and sudden onset asthenia may present.7 Clients seek medical care for pain (80-85%), weight loss (60%), and jaundice (47%), although these symptoms already suggest that disease has progressed to advanced stages. Severe pain is a common symptom because of tumor invasion into the nerves. The physical therapist, if presented with this disease, will likely be presented with thoracolumbar back pain that is the result of radiating epigastric abdominal pain.3 Jaundice, itching, dark urine, and acholic stools occur when the tumor compresses the biliary tree. Pancreatitis may develop as an early sign of disease. Deep venous thrombosis may also occur. One third of people with malignancy also present with a palpable gall bladder. Cervical lymphadenopathy (Virchow’s node) may be the first sign of distant metastases.3 Diagnosis

Ultrasound is often used as an initial imaging test for patients who present with non-specific abdominal pain. If ultrasound yields suspicious findings, then a contrast enhanced CT is used for follow up.8 The most common imaging test to aid in diagnosis of pancreatic cancer is a spiral CT with intravenous contrast of the abdomen (90% sensitivity, 95% specificity).3 CT is preferred to MRI because of its greater availability. CT guided biopsy or endoscopic ultrasound are necessary in cases attempting to differentiate malignancy from chronic or autoimmune pancreatitis.8 Laboratory tests are of limited usefulness, but may reveal elevated bilirubin if biliary tree obstruction is present. Elevated serum tumor marker CA 19-9 is helpful for monitoring treatment, though it is a nonspecific sign for pancreatic cancer and not sufficient for diagnosis.3 Treatment

Appropriate treatment depends on the stage of the tumor. Tumors are divided into three categories: resectable, locally advanced, and metastatic.3 Surgical resection is the only curable therapy. Pancreaticoduodenectomy, also called Whipple procedure, is performed to resect tumors of the head, neck, and uncinate process of the pancreas. Body or tail lesions are removed using distal pancreatectomy.8 For a tumor that has a high chance of not being completely resectable, chemoradiation may be prescribed adjuvantly to reduce the tumor’s size until it is completely resectable. Chemoradiation therapy is employed for locally advanced disease and chemotherapy for metastasized disease. Most therapy is palliative.3 Patients with locally advanced or metastatic disease have median survival of 2-3 months without treatment.8 Opioids and celiac plexus block may help improve quality of life. Celiac plexus block is not shown to demonstrate significantly greater reductions in pain compared to opioids, but remains an important option for patients because it has fewer adverse side effects.9 Pancreatic enzyme replacement is also used to aid with malabsorption and steatorrhea.3

Implications for the Therapist

A physical therapist may encounter a client with pancreatic cancer who has vague low back pain as the first presenting symptom. Palpation of an enlarged supraclavicular lymph node is a sign of distant metastasis and must be reported to the physician.3 Patients undergoing treatment for gastrointestinal cancer may benefit physically and psychologically from an individualized walking program.10 References

1. Shaib Y, Davila J, El-Serag H. The epidemiology of pancreatic cancer in the United States: changes below the surface. Alimentary Pharmacology & Therapeutics. July 1, 2006;24(1):87-94. 2. American Cancer Society. Pancreatic Cancer. 2013. Available at: http://www.cancer.org/acs/groups/cid/documents/webcontent/003131-pdf.pdf 3. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 916-918. 4. Zhou J, Enewold L, Zhu K, et al. Incidence rates of exocrine and endocrine pancreatic cancers in the United States. Cancer Causes & Control: CCC. June 2010;21(6):853-861. 5. Matthaios D, Zarogoulidis P, Balgouranidou I, Chatzaki E, Kakolyris S. Molecular Pathogenesis of Pancreatic Cancer and Clinical Perspectives. Oncology. December 2011;81(3/4):259-272. 6. Apte M, Pirola R, Wilson J. New insights into alcoholic pancreatitis and pancreatic cancer. Journal Of Gastroenterology & Hepatology. October 4, 2009;24:S51-S56. 7. Halls B, Ward-Smiths P. Identifying Early Symptoms of Pancreatic Cancer. Clinical Journal Of Oncology Nursing. April 2007;11(2):245-248. 8. Kanji Z, Gallinger S. Diagnosis and management of pancreatic cancer. CMAJ: Canadian Medical Association Journal. October 2013;185(14):1219-1226. 9. Arcidiacono P. Celiac plexus block for pancreatic cancer pain in adults. Cochrane Database Of Systematic Reviews. August 29, 2013;(8). 10. Heislein DM, Bonanno AM. Effect of exercise on quality of life and functional performance for patients undergoing treatment for gastrointestinal cancer. Rehabilitation Oncology. 2009;27(1):3-8.

Pelvic Inflammatory Disease Condition

Pelvic inflammatory disease (PID) is characterized by bacterial infection and inflammation of the female upper genital tract. It is made of a variety of conditions that may include endometriosis, salpingitis, tubo-ovarian abscess, pelvic peritonitis, or any other condition that causes inflammation of the female reproductive organs.1 Incidence/Etiological Factors

PID is a common cause of infertility, chronic pain, and ectopic pregnancy.1,2 The most likely cause of pelvic inflammatory disease is bacterial infection, particularly untreated gonorrhea, chlamydia, and bacterial vaginosis.1-3 In 2012, nearly 1.5 million cases of chlamydia were reported in the United States, at a rate of 456.7 people per 100,000. Approximately 335,000 cases of gonorrhea infection were reported at a rate of 107.5 cases per 100,000 people, an increase of 4.1% from 2011. Both gonorrhea and chlamydia are most prevalent Americans ages 15-24 years old.4 Roughly 3% of women who test positive for Chlamydia trachomatis infection and go untreated develop PID within two weeks.2 The infection can be introduced to the body by the skin, vagina, or gastrointestinal tract and is often associated with STI/STDs, but it can develop after a birth or surgical procedure. Risk factors include history of previous pelvic infection, being under age 15 at first vaginal intercourse, having multiple male partners, having partners with symptoms or known history of chlamydia or gonorrhea, and non-use of barrier methods of contraception.1,3 Pathogenesis

Pelvic inflammatory disease is the result of bacterial migration from the vagina and cervix into the upper genital tract, causing infection and inflammation of the uterus, fallopian tubes, and ovaries.1-3,5 Chronic inflammation leads to scarring and adhesions in organs of the upper genital tract. Inflammation of the fallopian tubes is the primary cause for PID associated infertility, ectopic pregnancy, and chronic pelvic pain.6 Signs and Symptoms

This disease is often asymptomatic. When symptoms present, they often include lower abdominal pain, vaginal bleeding and discharge, adnexal tenderness, and cervical motion tenderness. Symptoms associated with infection such as fever, chills, nausea, and vomiting may also arise. Many women experience dyspareunia, painful menstruation, and back or pelvic pain. Moderate to severe back, abdominal, and/or pelvic pain is possible, with pain becoming chronic if scarring of the pelvic organs occurs.1,3 Diagnosis

Early diagnosis is the key to best patient outcome, as chlamydial and gonorrheal infections are curable with prompt treatment.7,8 Laparoscopy is considered the gold standard for diagnosis of PID, but the invasive procedure is not the best option for all patients.8 Laparoscopic findings consistent with PID include edema and erythema of fallopian tubes and the presence of purulent exudate and adhesions on the fallopian tubes.3 Other methods for evaluation include ultrasound, endometrial biopsy, and laboratory analysis of a vaginal swab or urine sample.8,3 Dilated fallopian tubes are the most significant finding on a transvaginal ultrasound. The presence of leukocytes in an endometrial biopsy sample is highly sensitive and specific, but this tool is of limited usefulness because of the minimum 2-day delay for results. Microscopic analysis of a vaginal wet smear revealing the presence of three or more leukocytes has high sensitivity (87-91%) and absence of white blood cells boasts high negative predictive value (94.5%).3

Diagnosis of subclinical, or mild, PID is difficult. Gold standard this diagnosis is considered to be endometrial biopsy revealing endometritis.8,3 Treatment

Goals of treatment are to relieve the acute symptoms and inflammation and prevent the development of long-term sequelae, particularly infertility.3 Pelvic inflammatory disease is curable with antibiotics, but treatment cannot reverse tissue damage.1 Cure rates after recommended antibiotic treatment range from 93-100%.3 Outpatient antibiotic therapy typically consists of a cephalosporin in combination with either doxycycline or azithromycin.6 Severe PID may require hospitalization to rule out tuboovarian abscess.1,6 The CDC recommends hospitalization for women with PID who (1) are severely ill, (2) are pregnant, (3) cannot take or do not respond to oral medication, (4) have a fallopian tube or ovarian abscess, or (5) need to be monitored for another possible condition requiring surgery, such as appendicitis.9 Implications for the Therapist

When presented with a female client with LBP, it is important to consider pelvic disease during differential diagnosis. Gynecologic symptoms and signs and symptoms of infection necessitate referral to a physician. References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1010. 2. Haggerty C, Gottlieb S, Taylor B, Low N, Fujie X, Ness R. Risk of Sequelae after Chlamydia trachomatis Genital Infection in Women. Journal Of Infectious Diseases. June 16, 2010;201:S134-S155. 3. Beigi RH, Wiesenfeld HC. Pelvic inflammatory disease: new diagnostic criteria and treatment. Obstetrics and Gynecology Clinics of North America. 2003;30:777-793. 4. Centers for Disease Control and Prevention. Reported STDs in the United States: 2012 National Data for Chlamydia, Gonorrhea, and Syphilis. http://www.cdc.gov/nchhstp/newsroom/docs/STD-Trends-508.pdf. Published January 2014. Accessed February 15, 2014. 5. Sweet R. Pelvic inflammatory disease: current concepts of diagnosis and management. Current Infectious Disease Reports. 2012;14:194-203. 6. Soper D. Pelvic inflammatory disease. Obstetrics & Gynecology. August 2010;116(2 Pt 1):419-428. 7. Centers for Disease Control and Prevention. Incidence, Prevalence, and Cost of Sexually Transmitted Infections in the United States. http://www.cdc.gov/std/stats/STI-EstimatesFact-Sheet-Feb-2013.pdf. Published February 2013. Accessed February 15, 2014. 8. Gaitán H, Angel E, Diaz R, Parada A, Sanchez L, Vargas C. Accuracy of five different diagnostic techniques in mild-to-moderate pelvic inflammatory disease. Infectious Diseases In Obstetrics And Gynecology. 2002;10(4):171-180. 9. Centers for Disease Control and Prevention. Pelvic Inflammatory Disease (PID) – CDC Fact Sheet. http://www.cdc.gov/std/pid/PID-factsheet-press-Sept-2011.pdf. Published September 27, 2011. Accessed February 16, 2014.

Perinephric Abscess Condition

Perinephric abscess, an uncommon complication of upper urinary tract infection, is defined as a collection of purulent material in the surrounding spaces of the kidneys.1 Incidence/Etiological Factors

Perinephric abscess is uncommon, making up 1-10 out of 10,000 hospital visits. Men and women are equally affected.1 Conditions that contribute to the development of perinephric abscess include diabetes mellitus, lithiasis, ureteral obstruction, immunosuppression, and chronic urinary retention.3 Pathogenesis

Infective staghorn renal calculi proliferate in the presence of bacteria and result in an insoluble mass of calcium, ammonium, magnesium, and phosphate. Together, infection and obstruction damage the kidney, meanwhile high pressure within the tissue drives purulent material into the perinephric space where there is little resistance to increased accumulation.1 E. coli, K. pneumoniae, S. aureus, and P. mirabilis cultures are most commonly responsible for infection and development perinephric abscesses.3 Signs and Symptoms

Symptoms are typically indicative of an upper urinary tract infection, although some patients may present with only one symptom. Eighty-five percent of patients with perinephric abscess experience fever and 65% have lumbar pain.2,3 Malaise, nausea and vomiting, abdominal pain, and weight loss are the next most common symptoms. Palpation of an abdominal or flank mass and painful percussion of the vertebral angle are signs found in 38 and 52% of patients respectively.3 Blood and/or urine samples may be positive for bacterial culture.1 Most patients will experience symptoms for 14 days or longer before hospital admission.3 When the accumulation of purulent material is large, there may be local rigidity and fullness. Scoliosis due to psoas irritation may be noticeable in thin patients.1 Diagnosis

Diagnosis of renal and perinephric abscesses can be difficult because symptoms are nonspecific and develop insidiously.1 Positive tests for urine and blood culture may help guide antimicrobial treatment, as they are usually parallel to the culture of the abscess. Abscesses are identified typically with ultrasound and followed up with CT imaging.3 Treatment

Percutaneous or urinary drainage with adjuvant antibiotic therapy is the first line of treatment performed on most abscesses.4 Surgical drainage and nephrectomy are considered in cases of more severe infection or in the presence of renal failure, typically secondary to nephrolithiasis. Rarely, in the case of an otherwise healthy individual with an abscess less than 3 cm, broadspectrum antibiotics may be curative.3 Depending on the severity of infection, average hospital stay is between 10-30 days.4 Implications for the Therapist

In new cases of back pain in patients with recent history of recurring (upper) urinary tract infection, take note of signs or symptoms listed above as they are almost all indicative of some type of infection. References

1. Gardiner R, Gwynne R, Roberts S. Perinephric abscess. BJU International. April 2011;107 Suppl 3:20-23. 2. Thomas J, Vrocher D, Khoury C. Images in emergency medicine. Man with back pain and rash. Perinephric abscess presenting as rash. Annals Of Emergency Medicine. November 2010;56(5):454. 3. Coelho R, Schneider-Monteiro E, Mesquita J, Mazzucchi E, Marmo Lucon A, Srougi M. Renal and perinephric abscesses: analysis of 65 consecutive cases. World Journal Of Surgery. February 2007;31(2):431-436. 4. Meng M, Mario L, McAninch J. Current treatment and outcomes of perinephric abscesses. The Journal Of Urology. October 2002;168(4 Pt 1):1337-1340.

Pregnancy Condition

Pregnancy is the period from conception to birth of a child. Pregnancy usually lasts 40 weeks and includes all stages of development from fertilization and implantation of the fertilized ovum in the uterus to birth. Incidence/Etiological Factors

About 45% of pregnant and 25% of postnatal women suffer from pregnancy-related pelvic girdle and/or back pain (PGP/PLBP). Strong evidence supports that strenuous work, previous low back pain associated with menstruation, and previous lumbopelvic pain during or after pregnancy are risk factors for having low back pain during pregnancy. Weak evidence exists that maternal height, maternal weight, fetal weight, use of oral contraceptives, smoking, epidural anesthesia, and a prolonged second stage of labor are risk factors for pregnancy-related lumbopelvic pain.1 A combination of biomechanical, hormonal, and vascular factors are believed to contribute to the occurrence of low back pain during pregnancy.2 Pathogenesis

Biomechanical causes for low back pain are typically related to weight gain associated with pregnancy. Originally it was hypothesized that the shift in the center of gravity anteriorly promoted posterior tilt of the upper body and head, resulting in hyperlordosis of the lumbar spine. Subsequent stress placed on the disks, facet joints, and ligaments of the lumbar spine lead to inflammation and synovial fluid production, increasing sensitivity to movement. Hyperlordosis of the lumbar spine before pregnancy is a predictor of back pain during pregnancy. Anterior weight gain and expansion of the uterus also results in significant weakening of abdominal muscles, placing extra strain on the lumbar musculature.2 Increased relaxin during pregnancy is the most strongly associated hormonal factor related to PLBP. Current theory suggests that relaxin stimulates collagenase expression, increasing joint laxity, and thus promoting low back pain through increased pelvic instability and joint range of motion.2 A third vascular component is suggested to increase susceptibility to PLBP. As the uterus expands, it places pressure on the vena cava between L1-L5. This increased pressure along with pregnancy related hypervolemia decreases cardiac output, decreases blood pressure, and increases heart rate. Increased blood flow to pelvic organs because of the baby, progesteroneinduced increased venous distensibility, and inadequate venous circulation distal to the point of constriction all contribute to exacerbation of low back pain symtpoms.2 Signs and Symptoms

Pregnancy classically presents itself with amenorrhea, nausea, vomiting, malaise, and breast tenderness. Physical signs include enlargement of the uterus, breast changes, and softening of the cervix, evident beginning at about six weeks.3 Onset of pain typically is around week 18, with the most severe back pain around weeks 24-36. Pain is typically localized in the lumbosacral and gluteal region, is described as anything between stabbing and a dull ache, and varies in intensity between mild and bearable in roughly 50% of cases, to quite intense in about 25% of cases.1 Most cases of PLBP are characterized as a dull pain experienced in forward flexion. Restricted spine motion is observable as well as increased pain upon palpation of the erector spinae.4 Diagnosis

Diagnosis of pregnancy is typically made following a missed menstrual cycle and confirmed through medical history and examination, laboratory evaluation, and ultrasonography. The most common hormone tested for is beta-human chorionic gonadotropin (hCG). Concentration of 25mIU/mL of greater is the traditional measurement required for a positive pregnancy test. By day 8 of pregnancy, hCG is present in 5% of women, and by day 11 it is present in 98% of women. False positive serum hCG tests occur 0.1-2% of the time. Progesterone and early pregnancy factor (EPF) are additional hormones that may be useful indicators of pregnancy in lab testing.3

Transvaginal ultrasonography is the most accurate way of detecting intrauterine pregnancy. However, it is typically only utilized for the high-risk obstetric patient or in cases when the woman presents with vaginal bleeding or abdominal pain early in gestation.3 Treatment

Patients are encouraged to utilize the best configuration of pillows to provide support for various areas of the body, particularly when lying down to sleep.4 Individually tailored stretching and strengthening exercises as well as water gymnastics may reduce back pain and sick leave in pregnant women.3 Pelvic belts, TENS and acupuncture are additional modalities that may aid in back pain relief. Use of NSAIDs and other pharmaceutical drugs is not recommended, and is prohibited during the third trimester of pregnancy.4 Implications for the Therapist

Pregnancy must be considered in the differential diagnosis of any woman of reproductive age. Lower extremity and core strengthening exercises may help reduce low back and pelvic girdle pain, although evidence is not conclusive enough to make exercises standard treatment.6 References

1. Wu W, Meijer O, Ostgaard H, et al. Pregnancy-related pelvic girdle pain (PPP), I: Terminology, clinical presentation, and prevalence. European Spine Journal. November 2004;13(7):575-589. 2. Sneag D, Bendo J. Pregnancy-related low back pain. Orthopedics. October 2007;30(10):839-847. 3. Shields A. Pregnancy Diagnosis. Medscape. http://emedicine.medscape.com/article/262591-overview#a1. Accessed March 29, 2014. 4. Vermani E, Mittal R, Weeks A. Pelvic girdle pain and low back pain in pregnancy: a review. Pain Practice. 2010 Jan-Feb 2010;10(1):60-71. 5. Stuge B, Hilde G, Vollestad N. Physical therapy for pregnancy-related low back and pelvic pain: a systematic review. Acta Obstetricia Et Gynecologica Scandinavica. November 2003;82(11):983. 6. Lillios S, Young J. The Effects of Core and Lower Extremity Strengthening on Pregnancy-Related Low Back and Pelvic Girdle Pain: A Systematic Review. Journal Of Women's Health Physical Therapy. September 2012;36(3):116-124.

Prostate Cancer Condition

Prostate cancer is a slow growing cancer that rises from tissue of the prostate. Incidence/Etiological Factors

Prostate cancer is the second most commonly diagnosed malignancy in men in developed countries, with 7.8% risk of developing the disease by age 75. Prostate cancer is the second leading cause of cancer related death in males.1 The greatest risk factor in developing prostate cancer is family history of the disease.2-4 Hereditary factors play a larger role in developing this cancer than any other cancer, with brothers and sons of men with history of the disease at greatest risk.3 The next greatest risk factors are age (>50 years), being of African descent, environmental exposure to cadmium, having a diet high in fat, and heavy alcohol consumption.4 Pathogenesis

Prostate cancer is a slow growing cancer that begins with early prostatic lesions that may or may not develop into cancer. Its development is believed to be affected by lifestyle factors.5 Tumors develop in the periphery of the prostate, slowly invading local structures including the seminal vesicles and urinary bladder.4 Ninety percent of metastases of prostatic carcinomas involve the spine, with metastasis into the lumbar spine by way of Batson’s venous plexus accounting for 15-30% metastases.6 Bony metastasis to the lumbar spine results in osteoblastic tumors that can cause spinal cord compression with subsequent pain and neurological complications.4,6 Signs and Symptoms

Presentation may be variable until the disease has reached advanced stages. Early presenting symptoms may include urinary obstruction, onset of pain, fatigue, and weight loss. Symptoms of urinary obstruction include urinary urgency, frequency, dysuria, hematuria, difficulty initiating or continuing a urine stream, decreased urine stream, or blood in ejaculate.4 Bone and other musculoskeletal pain in the low back can be a late manifestation of prostatic cancer which has metastasized to the bone.7 For patients over the age of 50, acute onset of low back pain with an unknown mechanism of injury should increase the clinician’s level of suspicion.6,7 Localized back pain (90-95%), weakness (75-80%), autonomic nervous dysfunction (57%), and sensory changes (50%) are signs and symptoms suggestive of spinal cord compression due to lumbar metastasis.6 Progressive radicular pain that is aggravated by movement and is not alleviated by reclining is suggestive of compression due to metastasis and not to be confused with pain due to an osteodegenerative process in the spine. Muscle weakness of the proximal muscles of the lower extremity may develop days or weeks after the onset of pain. Autonomic dysfunction may cause urinary retention or bowel or bladder incontinence. Neurologic symptoms are rarely the first manifestations of prostatic cancer.6 Diagnosis

Prostate-specific antigen (PSA) screening is followed up by tissue biopsy if PSA is elevated for unknown reasons. Digital rectal examination may reveal a hardened, fixed structure, or a heavily swollen gland. MRI can aid in evaluation of the prostate gland and local lymph nodes, though

lymph node involvement would have to be advanced to be detectable, and radiograph or bone scan can be used to identify any metabolically active lesions.4 Treatment

Treatment will vary depending on individual assessment of the patient’s disease based on life expectancy, comorbidities, biopsy grade, clinical stage, and PSA levels.4,8 Patients with low risk cancer may decide to forego immediate treatment and begin a period of surveillance which includes PSA testing every 3-6 months, DRE every 6-12 months, and biopsy every 12 months unless PSA and DRE results change. For those with a longer life expectancy and low risk cancer, active surveillance, radical prostatectomy, or radiation therapy are all viable treatment options.8 It is recommended that patients with intermediate and high risk stages of cancer undergo radical prostatectomy and radiation therapy. Administration of androgen deprivation therapy (ADT) before, during, and after radiation is shown to improve survival in patients.8 ADT is the preferred treatment for symptomatic metastatic disease because androgens promote prostatic tissue growth and malignancy. Luteinizing hormone receptor agonists, gonadotropin-releasing hormone receptor agonists and antagonists, and complete androgen blockade are all examples of ADTs.8 Moderate to high intensity exercise should be considered the frontline treatment, as it has been shown to combat the effects of ADT such as fatigue, muscle loss, slower gate, decreased strength and functional performance, and overall quality of life.9-11 Both acute and chronic exercise in patients with prostatic cancer have been shown to slow tumor growth by reducing the rate of active DNA synthesis and inducing apoptosis in tumor cells, respectively.5 A regimented walking routine for men currently receiving or who have received ADT in the past may help alleviate some of the cognitive and psychosocial issues (memory deficits, low self-esteem, depression) that result from the reduced levels of testosterone.12 Patients who participate in a supervised exercise program, such as one prescribed by a PT, show greater benefit than those who are simply advised to exercise.9 Implications for the Therapist

Physical therapists often see clients with pre-existing prostate conditions. Understanding and recognizing signs and symptoms associated with common prostate conditions can help the therapist have a baseline from which to determine when different or more serious pathology develops. A client may seek PT for pain located in the thoracic, lumbar, or sacral regions of the spine mistakenly thinking it is of mechanical origin. The presence of urinary symptoms, history of prostate cancer, being over 50 years in age, and an unknown cause of musculoskeletal pain should alert the therapist to make physician referral in cases of men with LBP.4 References

1. Jemal A, Bray F, Center M, Ferlay J, Ward E, Forman D. Global cancer statistics. CA: A Cancer Journal For Clinicians. March 2011;61(2):69-90. 2. Lichtenstein P, Holm N, Hemminki K, et al. Environmental and heritable factors in the causation of cancer--analyses of cohorts of twins from Sweden, Denmark, and Finland. The New England Journal Of Medicine. July 13, 2000;343(2):78-85.

3. Bratt O. What should a urologist know about hereditary predisposition to prostate cancer?. BJU International. April 2007;99(4):743-748. 4. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 970-978. 5. Rundqvist H, Augsten M, Östman A, et al. Effect of Acute Exercise on Prostate Cancer Cell Growth. Plos ONE. July 2013;8(7):1-9. 6. Benjamin R. Neurologic complications of prostate cancer. American Family Physician. May 2002;65(9):1834-1834-40, 1733-6, 2p passim. 7. Lishchyna N, Henderson S. Acute onset-low back pain and hip pain secondary to metastatic prostate cancer: a case report. Journal Of The Canadian Chiropractic Association. March 2004;48(1):5-12. 8. Ghavamian R. Prostate Cancer Treatment Protocols. Medscape. http://emedicine.medscape.com/article/2007095-overview. Updated January 3, 2014. Accessed March 27, 2014. 9. Murphy R, Wassersug R, Dechman G. The role of exercise in managing the adverse effects of androgen deprivation therapy in men with prostate cancer. Physical Therapy Reviews. August 2011;16(4):269-277. 10. Clay C, Perera S, Wagner J, Miller M, Nelson J, Greenspan S. Physical Function in Men With Prostate Cancer on Androgen Deprivation Therapy. Physical Therapy. October 2007;87(10):1325-1333. 11. Cramp F. Exercise for the management of cancer-related fatigue in adults. Cochrane Database Of Systematic Reviews. October 10, 2012;(11). 12. Lee C, Kilgour A, Lau Y. Efficacy of walking exercise in promoting cognitivepsychosocial functions in men with prostate cancer receiving androgen deprivation therapy. BMC Cancer. January 2012;12(1):324-330.

Prostatitis Condition

Prostatitis is an inflammation of the prostate gland of unknown etiology that results in urogenital pain, urinary symptoms, and decreased overall quality of life. Incidence/Etiological Factors

The National Institutes of Health classification system for prostatitis includes: (1) Acute bacterial prostatitis, (2) Chronic bacterial prostatitis, (3) Chronic prostatitis/Chronic pelvic pain syndrome (CP/CPPS), and (4) Asymptomatic inflammatory prostatitis.1 Most men diagnosed with prostatitis are diagnosed with CP/CPPS.2 An estimated 50% of men experience a form of prostatitis as some point in their lifetime. Men in their 40s and men prone to UTI are more likely to develop prostatitis. UTI is the most common cause of prostatitis, followed by bladder outlet obstruction.3 Etiology for CPPS is poorly understood, but patients with cardiovascular disease, neurologic disease, psychiatric conditions, non-specific urethritis, and hematopoietic, lymphatic, or infectious disease have higher lifetime prevalence of the disease.2,4

Recent urethral catheterization and having multiple sexual partners increases risk for developing prostatitis. Additional triggers for disease include stress, emotional factors, alcohol, spicy foods, or caffeine. Poorly managed diabetes mellitus may also increase risk because urine glucose provides a substrate for bacterial growth.3,4 Pathogenesis

Pathogenesis is poorly understood for CP/CPPS. Theories suggest an infectious or inflammatory process, autoimmunity, and pelvic floor muscle spasm with undiagnosed pelvic floor disorders that mimic prostatitis. When evidence of a bacterial pathogen in present, it is most commonly that of gram-negative enterobacteria.3 Signs and Symptoms

Symptoms and signs of bacterial prostatitis (types I and II) include urinary frequency, urgency, nocturia, dysuria, urethral discharge, UTI, high fever, chills, malaise, myalgia, and arthralgia. Pain may be located in lower abdominal, rectal, low back, sacral, and/or the pelvis regions.3 Characteristic symptoms of CP/CPPS (type III) include urinary frequency, urgency, and dysuria. Impairments to sexual function include erectile dysfunction, ejaculatory and post-ejaculatory pain, and decreased libido.5,6 Pain may be located in the low back, scrotal, and/or pelvis regions.3 Asymptomatic prostatitis (type IV) has no symptoms and is typically discovered as a result of investigations into infertility.3 Diagnosis

Urine culture should be obtained from a symptomatic patient rule out UTI. Presence of chronic pelvic pain and voiding in the absence of UTI is supportive of a chronic pelvic pain syndrome diagnosis.7 Digital rectal examination may reveal a swollen, tender, or warm prostate. CT and transrectal ultrasonography imaging should be ordered to follow up with anatomical details.3 NIH guidelines advise using NIH Chronic Prostatitis Symptom Index (NIH-CPSI) to assess symptoms and quality of life of men with CP/CPPS and guide treatment. Three subscores of the system address pain, urinary symptoms, and quality of life.8 Treatment

Treatment for bacterial prostatitis includes antibiotics and suprapubic drainage for men with voiding issues.3 CP/CPPS is difficult to treat, and antibiotics and anti-inflammatories often fail to relieve symptoms. Treatment is typically aimed at symptom control and relief because the cause of nonbacterial prostatitis is unknown. Longer courses of treatment lasting 4-6 months have better outcomes than shorter courses. Despite the unknown etiology of nonbacterial prostatitis,

approximately one half of men with CPPS respond to antibiotic therapy.3 Alpha-blockers, antiinflammatories, and antibiotics all demonstrate a clinically significant decrease in symptoms when compared with placebo, with α-blockers and anti-inflammatories having the greatest effect. For optimal management of symptoms, a combination of two or three of these treatment options is recommended over therapy with only one.9 Biofeedback, pelvic floor reeducation, and αblocker therapy all help the relax the smooth muscle of the prostate and base of the bladder and have demonstrated effectiveness. Additional treatment options include medicine to treat neuropathic pain, anticholinergic medicine, phytotherapies, physical therapy, and surgery to treat bladder neck obstruction.3 Research has provided mixed results as to the efficacy of various treatment options, suggesting large heterogeneity of CP/CPPS. Many individuals with a chronic pain syndrome have experienced several previously failed treatment attempts and are more likely to expect new treatments to fail. Interestingly, many studies still demonstrate a placebo effect. This evidence may suggest more research into the qualitative aspects of the disease that affect the patient’s response to treatment.10 Implications for the Therapist

Patients with CPPS may be referred to physical therapy for treatment, particularly in cases where there appears to be no evidence of infection and antibiotic therapy fails to provide relief. Physical therapy treatment may include pelvic floor tender point release, muscle relaxation training, aerobic exercise, and postural and flexibility exercises to help relieve pain and restore sexual function.5 References

1. Krieger JN, Nyberg L Jr, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA. 1999;282:236-7. 2. Pontari M, McNaughton-Collins M, Litwin M, et al. A case-control study of risk factors in men with chronic pelvic pain syndrome. BJU International. September 2005;96(4):559-565. 3. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 964-967. 4. Chung S, Lin H. Association between Chronic Prostatitis/Chronic Pelvic Pain Syndrome and Anxiety Disorder: A Population-Based Study. Plos ONE. May 2013;8(5):1-5 5. Van Alstyne L, Harrington K, Haskvitz E. Physical therapist management of chronic prostatitis/chronic pelvic pain syndrome. Physical Therapy. December 2010;90(12):1795-1806. 6. Chung S, Keller J, Lin H. A case-control study on the association between chronic prostatitis/chronic pelvic pain syndrome and erectile dysfunction. BJU International. September 2012;110(5):726-730. 7. Schaeffer A. Epidemiology and evaluation of chronic pelvic pain syndrome in men. International Journal Of Antimicrobial Agents. February 2, 2008;31:108-111. 8. Propert K, Litwin M, McNaughton-Collins M, et al. Responsiveness of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI). Quality Of Life Research. March 2006;15(2):299-305.

9. Thakkinstian A, Attia J, Anothaisintawee T, Nickel J. α-blockers, antibiotics and antiinflammatories have a role in the management of chronic prostatitis/chronic pelvic pain syndrome. BJU International. October 2012;110(7):1014-1022. 10. Cohen J, Fagin A, Eldabe S, et al. Therapeutic Intervention for Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS): A Systematic Review and MetaAnalysis. Plos ONE. August 2012;7(8):1-12.

Psoriatic Arthritis Condition

Psoriatic arthritis (PsA) belongs to a group of conditions called spondyoarthropathies. It is a chronic inflammatory disease with predominantly cutaneous and musculoskeletal manifestations.1 Incidence/Etiological Factors

Family history, stress, infection, trauma, myocardial infarction, and surgery may increase risk. Psoriatic arthritis develops in less than 10% of patients with psoriasis. Joint manifestations precede skin disease in roughly 15% of cases and in less than 2% of cases skin disease never develops.1 Pathogenesis

The precise etiology of psoriatic arthritis is unknown, but it is believed that interaction between genes, the environment, and immunologic factors play a role in its development. Studies have found a large percent of individuals who develop PsA have immediate family members who have psoriasis or PsA. Environmental factors include infection and trauma. Trauma to the skin is reported in many patients who develop psoriatic lesions in the same area, and joint trauma precedes 24% of PsA cases. Immunologic factors are a point of interest for developing treatments. Found on the skin and within joints of PsA patients is a lymphocytic filtrate containing an abundance of activated T cells and B lymphocytes. The activiated T cells release pro-inflammatory cytokines that cause adhesion molecules such as TNF to be expressed. The TNF molecule is responsible for joint damaging processes that include cartilage erosion, inhibition of bone formation and proteoglycan synthesis, and stimulation of bone resorption.2 Signs and Symptoms

Psoriasis precedes psoriatic arthritis in most cases, with scalp, plaque, nail, and inverse psoriasis the most common forms.1 Psoriatic arthritis is usually asymmetric, with distal joints predominantly affected. When uveitis is present, it is often chronic and bilateral.3 Lumbosacral back pain is a common complaint in patients hospitalized for PsA. Nearly half of PsA patients who complain of low back pain are found to have sacroiliitis upon radiographic imaging.1 Diagnosis

Laboratory reports yield no specific findings, but ESR, fibrinogen, C-reactive protein, and haptoglobin levels are commonly elevated in individuals with PsA.1 Radiographs may reveal erosive arthritis, frequently with distal interphalangeal joint involvement.3 The CAPSAR criteria are used for confirming diagnosis. To meet the CAPSAR criteria, the patient must have articular joint inflammation and at score at least three points from the following five categories: (1) Current psoriasis (2pts), history of psoriasis, or family history of psoriasis (1pt) (2) Psoriatic nail dystrophy (1pt) (3) Negative rests for presence of rheumatic factor (1pt) (4) Swelling of an entire digit (dactylitis) or history thereof confirmed by a rheumatologist (1pt) (5) Radiographic evidence of ossification near joint margins of the hand or foot (1pt).4 Treatment

Treatment is targeted toward both skin and joint manifestations. Topical therapies for psoriasis include corticosteroids, retinoids, and UV light therapy. NSAIDs are the first line therapy for treating joint swelling and tenderness. Generalized disease may respond to oral corticosteroids, and intra-articular corticosteroid injection may help control localized joint disease. Second line treatments include methotrexate, sulfasalazine, cyclosporine, TNF inhibitors.3 Implications for the Therapist

When a client is being treated for joint pain it is important that the therapist recognize the signs and symptoms of arthritis that may require further medical diagnosis. The presence of psoriatic skin lesions in conjunction with joint pain warrants referral to the physician. References

1. Pavlica L, Perić-Hajzler Z, Jovelić A, Šekler B, Damjanović M. Psoriatic arthritis: a retrospective study of 162 patients. Vojnosanitetski Pregled: Military Medical & Pharmaceutical Journal Of Serbia & Montenegro. September 2005;62(9):613-620. 2. Turkiewicz A, Moreland L. Psoriatic arthritis: current concepts on pathogenesis-oriented therapeutic options. Arthritis And Rheumatism. April 2007;56(4):1051-1066. 3. Kataria R, Brent L. Spondyloarthropathies. American Family Physician. June 15, 2004;69(12):2853-2853-60, 2757-9, 2934 passim. 4. Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. Aug 2006;54(8):2665-73.

Pyelonephritis Condition

Pyelonephritis is an infection of the kidney that results from the ascension of a lower urinary tract infection to the pelvis of the kidney.1

Incidence/Etiological Factors

Women are at six times greater risk of developing pyelonephritis than men.1 Incidence rates among females are approximately 12-13 cases per 10,000 persons per year. Incidence among males is approximately 2-3 cases per 10,000 persons.2 Other groups at risk include those with type 1 and type 2 diabetes, the immunocompromised, those with stress incontinence, who engage in anal sex, have structural abnormalities that may impede urinary flow, or who have recently been catheterized.1 Pathogenesis

Infection results from the ascension of a pathogen from the bladder through the ureters to the kidney. Typically kidney infection is preceded by a lower urinary tract infection.3 E. coli is responsible for 80% of cases of acute pyelonephritis in women and 70% of cases in men.2 Signs and Symptoms

Signs and symptoms indicative of pyelonephritis are consistent with those of a lower urinary tract infection. Most common signs and symptoms include flank pain, hematuria, polyuria, foulsmelling urine, dysuria, tachycardia, tachypnea, fever, malaise, chills, anorexia, and nausea and/or vomiting, and costovertebral angle tenderness.1,3,4 Kidney involvement may also irritate the diaphragm, leading to ipsilateral shoulder or lumbar back pain.3 Diagnosis

Pyuria, bacteriuria, and hematuria may be revealed by urinalysis, but urinalysis is not specific enough for diagnosis of pyelonephritis.1,3 Collectively, patient history, physical examination, and urinalysis can provide enough evidence to begin treatment.1 Treatment

In otherwise healthy individuals, treatment can be done by oral antibiotics on an outpatient basis. Hospital admission may be required if the patient has other complications requiring intravenous medication.1 Implications for the Therapist

The physical therapist who notices the onset of the above symptoms in a client may help in early detection of UTI. Insidious onset of back or shoulder pain, particularly following an infection, may be indicative of a recurring or worsening infection and warrants medical referral.3 References

1. Bethel J. Acute pyelonephritis: risk factors, diagnosis and treatment. Nursing Standard. October 3, 2012;27(5):51-56. 2. Czaja CA, Scholes D, Hooton TM, Stamm WE. Population-Basted Epidemiologic Analysis of Acute Pyelonephritis. Clin Infect Dis. 2007;45(3):273-280.

3. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 928-931. 4. Guay D. Contemporary Management of Uncomplicated Urinary Tract Infections. Drugs. May 2008;68(9):1169-1205.

Reactive Arthritis Condition

Reactive arthritis (ReA), formerly called Reiter’s syndrome, belongs to the group of conditions called spondyoarthropathies. It is an aseptic arthritis commonly triggered by a bacterial urogenital or gastrointestinal infection.1-3 Incidence/Etiological Factors

Incidence rates have been reported between 1-30 cases per 100,000 people per year. Prevalence is equal among men and women when the root cause is a gastrointestinal infection, but when the triggering infection is of Chlamydia trachomatis, men are more frequently affected. Twenty to forty year olds are most commonly affected as are white adults due to the higher genetic frequency of the HLA-B27 allele.4 The majority of patients who contract reactive arthritis are HLA-B27 positive.2 Pathogenesis

Onset is usually one to four weeks following a gastrointestinal infection by Chlamydia, Ureaplasma, Shigella, Salmonella, Yersinia, and Campylobacter bacterial species.2 The precise interactive mechanism between the pathogen and host is unknown. With ReA, synovial fluid is negative for bacterial culture, leading researchers to hypothesize that arthritis develops as a result of either an overstimulated autoimmune response or the body’s immune response to bacterial antigens deposited in the joint space. Presence of the HLA-B27 allele is not believed to factor in the onset of ReA, but it may perpetuate chronic disease.4 Signs and Symptoms

Onset is usually acute, with pain and swelling in joints of the lower extremities.2 The classic triad of comorbidities are arthritis, urethritis, and conjunctivitis.4 Weight loss, fever, enthesitis, dactylitis, and inflammatory back pain are also common. Additional extraarticular manifestations may include uveitis, acute diarrhea, cervicitis in women, oral ulcers, and hyperkaratonic lesions on the palms of hands or soles of feet.2 Diagnosis

Guidelines for diagnosing reactive arthritis were developed in 1999 at the 4th International Workshop on Reactive Arthritis in Berlin.5 Diagnosis is “definite” when both major criteria and one relevant minor criteria is met. If both major and no minor criteria are met or only one major and one or more minor criteria are met, diagnosis is “probable.” Additionally, identification of

the disease triggering infection is required for diagnosis. The major criteria for diagnosis include: (1) Arthritis that has two or more of the following qualities: asymmetric, mono or oligoarthritis, and involving the lower limbs. (2) Arthritis follows a symptomatic infection of enteritis, urethritis, or both. Minor criteria include: (1) Evidence of a triggering infection (2) Evidence of synovial infection.4,5 Treatment

Reactive arthritis is typically self-resolving in three to twelve months, but symptomatic treatment is warranted. NSAIDs, sulfasalazines, and corticosteroid injections may be used to manage symptoms.2 Antibiotic therapy for bacterial infections usually includes azirthromycin, tetracyclines, or a combination of the two.4 Although the underlying etiology for ReA is bacterial infection, the role and effectiveness of antibiotic treatment is debateable.2 Implications for the Therapist

It is important that anyone who develops a new onset joint problem during or following a gastrointestinal or urogenital infection be evaluated for a bacterial or infectious cause. The presence of joint involvement with accompanying diarrhea, bloating, abdominal pain, fever, or positive obturator or iliopsoas signs must be reported to the physician.6 References

1. Lu DW, Katz KA. Declining use of the eponym "Reiter's syndrome" in the medical literature, 1998-2003. J Am Acad Dermatol. Oct 2005;53(4):720-3. 2. Kataria R, Brent L. Spondyloarthropathies. American Family Physician. June 15, 2004;69(12):2853-2853-60, 2757-9, 2934 passim. 3. Barth W, Segal K. Reactive arthritis (Reiter's syndrome). American Family Physician. August 1999;60(2):499. 4. Selmi C, Gershwin EM. Diagnosis and classification of reactive arthritis. Autoimmunity Reviews. 2014;13(4/5):546-549. 5. Braun J, Kingsley G, van der Heijde D, Sieper J. On the difficulties of establishing a consensus on the definition of and diagnostic investigations for reactive arthritis. Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, July 3-6, 1999. The Journal Of Rheumatology. September 2000;27(9):2185-2192. 6. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1290.

Skeletal Tuberculosis Condition

Extrapulmonary tuberculosis (TB) is a bacterial infection of Mycobacterium tuberculosis that is spread to other organ systems during initial pulmonary infection via lymphatic and hematogenous routes.1-3 Skeletal tuberculosis most often involves the spine (Pott’s disease). Tuberculous arthritis of weight bearing joints and tuberculous osteomyelitis are also expressions of skeletal tuberculosis.2 Incidence/Etiological Factors

Skeletal tuberculosis is a relatively uncommon manifestation of TB. 10-15% of tuberculosis cases are extra pulmonary and of those, 10%-35% of extrapulmonary cases are skeletal.1,2 Fifteen million people in the United States are estimated to have TB, an increase due in part to the presence of AIDS. New York, California, and Hawaii have the highest incidence rates in the US.1 Tuberculosis is rare in developed countries, but is still common in tropical climates. Individuals are at increased risk following travel to a tropical climate or underdeveloped country. The elderly and immune-compromised patients, such as those with HIV/AIDS, are most susceptible to contracting tuberculosis.4 Rates of extrapulmonary tuberculosis have risen with the rise of HIV and AIDS cases in the United States. 50% of patients with concurrent AIDS and tuberculosis have extrapulmonary manifestation of the disease.2 Pathogenesis

The spread of mycobacterium from the original pulmonary site of infection to the skeleton is hematogenous.1,3 Once infection reaches the skeleton, a lesion develops and caseation of the tissue causes bony expansion, trabecular, and cortical destruction resulting in skeletal fragility. In cases of tuberculous arthritis, infection typically originates in the epiphyseal plate and breaks through the epiphysis to enter the joint. Rarely does infection directly enter the highly vascularized synovium of the joint.3 In the spine, infection begins in the anteroinferior aspect of the vertebral body, causing destruction of the disk and adjacent vertebrae. Destruction causes subsequent anterior wedging of the vertebrae, possibly developing a Gibbus deformity and resultant palpable spinous prominence at that segment.2 Progressive increase in pain is caused by nerve root irritation, pressure from abscess, and collapse of the vertebral body leading to cord compression and possible paraplegia.1 Signs and Symptoms

Early signs and symptoms include pain and stiffness, with pain localized or radicular from the lower thoracic and lumbar spine or other weight bearing joints.1,2 Symptoms are often consistent with chronic sciatica.1 Systemic signs such as fever, chills, weight loss, and fatigue may develop in late stages of the disease. In time, joint effusion may affect the muscles and nerves around the joint.1

Diagnosis

Skeletal tuberculosis is of insidious onset, developing 2-3 years after the initial infection.1,4 Early diagnosis is important for preservation of articular cartilage and joint space, but is often delayed by months or years in the absence of signs or symptoms suggesting extrapulmonary TB. Plain radiography, computed tomography, and magnetic resonance imaging all have some usefulness in detection of skeletal TB.1,3 Plain radiograph imaging has very low sensitivity for detecting tuberculous spondylitis.3 Radiographic images can present similar to osteoporotic compression fractures or metastatic disease, with findings including bone destruction, intervertebral disk destruction, and/or paravertebral abscess.4 Bone destruction is not detectable on a radiograph until at least 50% of the vertebra is destroyed. CT scan is adequate for sensing both bony and soft tissue changes associated with skeletal tuberculosis and it is more sensitive than MRI for depicting subtle calcification of soft tissue. MRI is the primary imaging modality used in Western countries for investigation of the spine. It is sensitive to early inflammatory bone marrow changes characteristic of tuberculous osteomyelitis and arthritis.3 In challenging cases, diagnosis can be confirmed by microbiologic assessment of culture collected from the spine by CT-guided fine-needle aspiration.1,3 Treatment

Pharmacologic treatment is the same as for pulmonary TB.1 Patients with skeletal manifestation of TB typically improve with the appropriate antimicrobial therapy, analgesia, and rehabilitation. Surgical intervention is rare and typically reserved for those with persistent instability, severe kyphosis, radiculopathy, or other neurological compromise.4 The standard course of antibiotic treatment runs for six to nine months. The first two months consist of the antibiotic cocktail isoniazid, rifampin, pyrazinamide, and ethambutol, with four to seven months of isoniazid and rifampin follow to conclude the nine month treatment. For patients with extrapulmonary skeletal manifestations, duration of antibiotic therapy may be extended to 12 months.2 Decompressive surgery is employed if Pott’s paraplegia is present. Rehab from decrompressive surgery follows standard orthopedic principles and is individualized to the patient. Extraarticular infections may require curettage and bone grafting. Surgical treatment for a joint infection includes arthrotomy or synovectomy, and treatment of articular erosions. More advanced infections may require resection of bones and joints, arthrodesis, and limb salvage or amputation.1 Implications for the Therapist

Skeletal tuberculosis may present itself similarly to arthritis, sciatica, or another musculoskeletal dysfunction of unknown origin. The LBP patient who has the above signs and symptoms and fails to respond to treatment presents as a red flag. If a patient demonstrates consistencies with this type of clinical presentation, fails to show improvement, and is at increased risk (age, immunodeficiency, travel abroad to underdeveloped nation when TB is endemic), a medical screening should be performed and the patient referred to a physician.1 If a diagnosis of

tuberculosis is suspected, it is required that healthcare providers and allied professionals report to the appropriate local and state health agencies.5 References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 1198. 2. Golden M, Vikram H. Extrapulmonary tuberculosis: an overview. American Family Physician. November 2005;72(9):1761-1761-8, 1651-4, 1917 passim. 3. De Vuyst D, Vanhoenacker F, Gielen J, Bernaerts A, De Schepper A. Imaging features of musculoskeletal tuberculosis. European Radiology. August 2003;13(8):1809-1819. 4. Choo CY, Pan WJ, Lee HC. Spinal Tuberculosis as a Cause of Low Back Pain – A Timely Reminder. Pain Medicine. 2012;13:613-614. 5. The Centers for Disease Control and Prevention. Tuberculosis Control Laws and Policies: A Handbook for Public Health and Legal Practitioners. http://www.cdc.gov/tb/programs/TBlawPolicyHandbook.pdf. Published October 1, 2009. Accessed April 10, 2014.

Spondylodiscitis Condition

Spondylodiscitis is a pyogenic infection of the spine. The term encompasses vertebral osteomyelitis, spondylitis, and discitis.1 Incidence/Etiological Factors

Incidence rates of spondylodiscitis range from 1 per 100,000 to 1 per 250,000 persons per year. Men are affected one and a half to three times more often than women, with children and 50-60 year olds being the most commonly affected. Risk factors include high blood pressure, diabetes, previous disc infection, extended steroid use, chronic kidney failure, liver failure, and serious trauma.2 Pathogenesis

Infection is spread through the blood stream, predominantly through arteries. When a septic embolus reaches the disc it causes infarct that is limited to the disc in children, but usually spreads to the neighboring vertebrae and discs in adults. Extensive necrosis narrows the disc space, causing wedging, cavitation, and compression fractures which lead to spinal instability, deformity, and cord compression.1 Nearly 50% of spondylodiscitis cases originate from the spread of distant infections. These infections may be of the genitourinary tract, skin and soft tissue, intravascular devices, gastrointestinal tract, respiratory tract, and oral cavity. Infective endocarditis has been reported in 12% of spondylodiscitis cases. Direct inoculation is the most common iatrogenic cause of

spondylodiscitis, making up 25-30% of cases. This may occur following spinal surgery, prosthetic implantation, lumbar puncture, or epidural procedures.1 Signs and Symptoms

Infective spondylodiscitis is characterized by back pain, fever, and neurological deficits depending on the location of the infection.3 The patient may experience lumbar pain and rigidity that is worse in flexion and does not respond to conservative treatment. Pain may increase when digital pressure is placed over the involved vertebrae. Radiating pain into the periumbilical, sciatic, or crural fascia regions has also been reported. Radicular pain is indicative of nerve root and/or cord compression due to purulent material entering the epidural space. Untreated infections may lead to increasing instability and progressive thoracic kyphosis with para- or tetraplegia. Many patients with spondylodiscitis also demonstrate anorexia, asthenia, and weight loss. 2 Diagnosis

Due to the non-specific nature of signs and symptoms, diagnosis can be delayed 2-6 months from the onset of symptoms. Diagnosis requires isolation of a bacterial culture found through biopsy or blood sample. MRI is the gold standard for identifying spinal infections, with 96% sensitivity and 94% specificity, and is used for spondylodiscitis identification and monitoring.2 Treatment

Treatment involves immobilization followed by four weeks in a reinforced canvas corset. Antibiotic treatment is prescribed in accordance with positive biopsy or blood culture. Surgery is indicated in patients who do not respond to conservative treatment with antibiotics, show deterioration of neurological symptoms, or instability and progressive kyphosis. Most patients recover with conservative treatment that involves spinal decompression, immobilization and antibiotic therapy.2 Implications for the Therapist

Back pain caused by spondylodiscitis will not respond to conservative treatment by a therapist. Beware if the patient develops fever, fatigue, and/or neurological deficits.4 Spinal infection is a rare, but potentially morbid cause of back pain in older adult populations and should be included in the differential diagnosis of back pain without previous known injury in patient populations over 60 years and older.5 References

1. Gouliouris T, Aliyu SH, Brown NM. Spondylodiscitis: update on diagnosis and management. J Antibmicrob Chemother.2010;65(Suppl3):iii11-iii24. 2. Bettini N, Girardo M, Dema E, Cervellati S. Evaluation of conservative treatment of non specific spondylodiscitis. European Spine Journal. June 2, 2009;18:143-150. 3. Flitsch J, Fritzsche E, Papavero L. Spondylodiscitis caused by occult endocarditis. Acta Neurochirurgica. December 2004;146(12):1377-1378.

4. Petrie C, Marzban F, Sokhansanj A, Tofan C, Garrett K. Salmonella spondylodiscitis in a 15 year old male presenting with back pain: a case report. Journal Of Chiropractic Education. March 2009;23(1):87. 5. Hutchinson C, Hanger C, Wilkinson T, Sainsbury R, Pithie A. Spontaneous spinal infections in older people. Internal Medicine Journal. December 2009;39(12):845-848.

Systemic Lupus Erythematosus Condition

SLE is an inflammatory autoimmune disease of largely unknown etiology.1,2 Incidence/Etiological Factors

Systemic Lupus Erythematosus (SLE) primarily affects women of childbearing years. Women are affected eight times more than men and women of African, Hispanic, Asian, and Native American descent are more often and more severely affected by SLE than Caucasian women.1,2 Yearly incidence of SLE in the US is estimated to be around 7 cases per 100,000 and prevalence of SLE in the US has been estimated between 81-103 cases per 100,000.3 Incidence is higher in first degree relatives than in the general population, indicating a hereditary component to the disease, although its development is believed to be the result of both genetic and environmental factors. Combined immunologic, environmental, hormonal, and genetic factors all play a role.1 Additional predisposing factors include physical or mental stress that affects immune cell function, streptococcal or viral infections, exposure to sunlight or UV light that can cause tissue damage and inflammation, pregnancy, and abnormal estrogen metabolism, as there is higher incidence of SLE exacerbation among women taking low-dose estrogen contraceptives. Drugs such as hydralazine, anticonvulsants, penicillins, sulfa drugs, and oral contraceptives have also been found to induce SLE.1,2 Pathogenesis

SLE is an inflammatory autoimmune disease, the exact cause of which is unknown.1,2 Dysregulation of B- and T- lymphocytes, autoantibody production, and formation of immune complex collectively result in pathologic immune response to a microbial pathogen or other tissue trauma.4,5 Local inflammation of the endothelial cells combined with the deposit of immune complex lead to inflammation of blood vessels and subsequent thrombosis. Thrombosis is the result of clot inducing properties of autoantibodies specific to SLE. These coagulopathic responses lead to a cascade of pathologic processes in the tissue that ultimately affect organ function. Clinical manifestations of SLE will be dependent on the organ or system that is pathologic.4 Precise cause of the dysfunctional immune response is unknown, but believed to be related to a genetic defect. Presence of the defective gene does not, however, mean that the disease will manifest.4,6 SLE is likely the result of a combination of genetic influence and environmental triggers.1,2,4

Signs and Symptoms

Clinical presentation of SLE is heterogeneous between affected clients due to the diversity of tissues the disease can potentially affect. Most patients with SLE experience cycles of exacerbation and remission of symptoms.1-3 Signs and symptoms are discussed below according to the tissue or organ system affected.1,2,4,5,7 Musculoskeletal System Arthralgias and arthritis are the most common manifestations of SLE affecting the musculoskeletal system. These may be of an acute or insidious onset. Early symptoms include fever, weight loss, malaise, and fatigue. Acute arthritis may affect any joint, but most commonly involved are the small joints of the hands, wrists, and/or knees. SLE associated arthritis is differentiated from rheumatoid arthritis in that it is typically not destructive to the bone or severe enough to cause gross deformity. Nonetheless, pain can be significant enough to cause functional impairment. Cutaneous and Membranous Lesions Skin rash is common in areas exposed to UV light. Classic manifestation of this is the butterfly rash over the nose and cheeks. Vasculitis, inflammation of cutaneous blood vessels, may cause infarctive lesions on fingers, splinter hemorrhages, necrotic leg ulcers, digital gangrene, or Raynaud’s syndrome. Additionally, patient may display discoid lesions, alopecia, and painless ulcers in the mouth, vagina, and nasal septum. Cardiopulmonary System Pleuritis, pericarditis, dyspnea, myocarditis, endocarditis, tachycardia, pneumonitis (acute or chronic) may all result from SLE affecting the cardiopulmonary system. Pulmonary hypertension and congestive heart failure are complications secondary to the listed conditions. These individuals are at high risk for thrombosis. Central Nervous System Also referred to as neuropsychiatric manifestations, these include headaches, irritability, and depression. The patient may experience emotional lability and instability, psychoses, seizures, cerebrovascular accidents, cranial neuropathy, or organic brain syndrome. Verbal memory, attention, language skills, and psychomotor speed may also be impaired. Renal System Destruction of glomerulus, hematuria, and proteinuria may lead to renal failure. Other systems Additional signs and symptoms may include: anemia, amenorrhea, enlargement of spleen and cervical, axillary, and inguinal nodes, nausea, diarrhea, and abdominal pain with gastrointestinal involvement. Diagnosis

Diagnosis of SLE is difficult because the symptoms are vague and may mimic other diseases.1 The American Rheumatism Association has developed the following criteria for diagnosis of SLE.7 Four or more of the following eleven criteria must be present for diagnosis:1,7 (1) Abnormal titer of ANAs (2) Butterfly (malar) rash (3) Discoid rash (4) Hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia (5) Neurologic disorder: seizures or psychosis (6) Nonerosive arthritis of 2+ peripheral joints characterized by tenderness, swelling, or effusion (7) Oral or nasopharyngeal ulcerations (8) Photosensitivity (9) Pleuritis or pericarditis (10) Positive lupus erythematosus cell preparation, anti-DNA, or anti-splice sosomal test or chronic false-positive serologic test for syphilis (11) Renal disorder: profuse proteinuria (>0.5 g/day) or excessive cellular casts in urine Treatment

Treatment is primarily pharmacologic with the goal being to reverse the autoimmune process and relieve symptoms.1 Pharmacological treatment is individualized to the patient based on symptoms, specific organ system involved, and severity of disease.5 NSAIDS are used to relieve mild symptoms and reduce inflammation and muscle or joint pain. Corticosteroid-sparing agents can help preserve bone health and prevent cardiovascular disease and anticoagulants are recommended for patients with antiphospholipid antibody syndrome. For dermatologic, arthritic, and renal symptoms, antimalarial agents are prescribed. Immunomodulating drugs that suppress the immune system can be taken during periods of active disease, particularly when there is severe kidney involvement. Finally, corticosteroids and cytotoxic drugs are given only in severe cases that have not responded to other types of pharmacologic therapy.1 Non-pharmacologic treatment consists primarily of sun protection.1,5 Implications for the Therapist

Recognition of signs and symptoms of SLE in a LBP patient should alert the physical therapist referral. Physical therapy and an individualized exercise prescription may help with disease management, as prolonged bed rest can worsen fatigue. Exercise should be designed to strengthen muscles and increase endurance while being careful to avoid undue stress on the joints.1 References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 284. 2. Richman S, Schub T. Systemic Lupus Erythematosus. June 29, 2012. 3. Furst D, Clarke A, Fernandes A, Bancroft T, Greth W, Iorga S. Incidence and prevalence of adult systemic lupus erythematosus in a large US managed-care population. Lupus. January 2013;22(1):99-105.

4. Childs S. The pathogenesis of systemic lupus erythematosus. Orthopaedic Nursing. March 2006;25(2):140-147. 5. Bernknop A, Rowley K, Bailey T. A review of systemic lupus erythematosus and current treatment options. (cover story). Formulary. May 2011;46(5):178-194. 6. Pan H, Leng R, Tao J, Li X, Ye D. Ets-1: a new player in the pathogenesis of systemic lupus erythematosus?. Lupus. March 2011;20(3):227-230. 7. Hochberg M. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis And Rheumatism. September 1997;40(9):1725.

Testicular Cancer Condition

Testicular cancers are a highly treatable form of cancer that is the most common type of cancer found in younger males.1 Incidence/Etiological Factors

Testicular cancer is uncommon, making up 1-2% of all malignancies in men, but it is the most common cancer in young men ages 15-35 years, with average age of diagnosis at about 33.1,2 The American Cancer Society estimates there will be 8,820 new cases of testicular cancer diagnosed in the United States in 2014 and 380 deaths from the disease.3 Cryptorchidism, or undescended testis, is the most established risk factor for developing testicular cancer, increasing risk of development by four to eight times. Additional risk factors include history of testicular cancer in the contralateral testis and family history.1 Testicular tumors are also four times more prevalent in Caucasian than African American populations.4 Pathogenesis

Ninety-five percent of testicular cancers are germ-cell tumors (GCTs). GCTs are classified into pure seminomas and non-seminomas. Pure seminomas make up 40% of GCTs, originating from the seminiferous tubules. Non-seminomas collectively make up 60% of GCTs and are further categorized into embryonal carcinomas, teratomas, choriocarcinomas, and yolk sac tumors.2 Non-seminomas are more common in younger males and yolk sac tumors are the most common type of testicular tumor in children.2,4 Seminomas metastasize through the lymphatic system while non-seminomas spread throughout the body via both blood and the lymphatic system. Back pain is most commonly caused by lymphatic metastasis to the para-aortic lymph nodes. Hematogenous spread most commonly results in metastases to the lungs, liver, and brain.5 Outcomes are better for men who detect the disease in earlier stages, however testicular cancer is highly curable and 90% of men who present with metastasized cancer have five year survival.2 Signs and Symptoms

The most common symptom is an enlargement of the testicle with diffuse testicular pain, swelling, or hardness. Men may also experience a dull ache in the abdomen or scrotum or have enlargement of the scrotum.6 Back pain, breathlessness, and hemoptysis are indicative of metastatic disease. Around 10% of men with testicular cancer will present with one of these symptoms.2 Diagnosis

Urologic history and physical examination may reveal a painless testicular mass. Serum tumor markers (AFP, hCG, and LDH) are elevated in 40-60% of cases, but definitive diagnosis is achieved by microscopic examination of the tissue. Ultrasound may be used to differentiate between cancer, epididymitis, orchitis, hydrocele, and hematocele, and CT and MRI are utilized to assess metastatic spread.6 Treatment

Testicular cancer has been considered to be the “model of curable cancers,” and survival rate for men with this cancer is extremely high. Greater than 99% of patients with early stage disease experience full recovery and greater than 50% of those with metastatic disease have good prognosis at time of diagnosis.7 The first step in treatment is a radical unilateral inguinal orchiectomy, sometimes followed up with subsequent lymph node dissection of the local lymph nodes to help cure lymphatic metastases and provide more accurate staging information.8 Following orchiectomy, cisplatinbased combination chemotherapy is standard treatment for testicular cancer, and therapy results in a complete recovery rate of 70-80%. For metastatic cancer, resection of any residual tumor with concurrent chemotherapy is recommended, and should be performed at a specialized center for treatment.7,9 Implications for the Therapist

The therapist may encounter a patient with undiagnosed testicular cancer who displays thoracic or lumbar back pain secondary to metastasis or low lumbar pain that radiates to the iliac crest and groin. Low lumbar and iliac crest pain may be the result of biomechanic dysfunction, but pain radiating into the groin is suggestive of cancer. Knowledge of superficial lymph nodes is helpful for observation and palpation of a mass. Positive iliopsoas sign or palpation of a nodule requires medical referral. Following orchiectomy and/or retroperitoneal lymph node dissection, the patient may experience lymphedema and altered mechanics of the trunk, pelvis, and hip regions.6 References

1. Manecksha R, Fitzpatrick J. Epidemiology of testicular cancer. BJU International. November 15, 2009;104(9B):1329-1333. 2. McCullagh J. Testicular cancer: Epidemiology, assessment and management. Nursing Standard. 2005;19(25):45-53.

3. American Cancer Society. Testicular Cancer. http://www.cancer.org/acs/groups/cid/documents/webcontent/003142-pdf.pdf. Updated February 11, 2014. Accessed March 27, 2014. 4. Alanee S, Shukla A. Paediatric testicular cancer: an updated review of incidence and conditional survival from the Surveillance, Epidemiology and End Results database. BJU International. November 2009;104(9):1280-1283. 5. Dearnaley DP, Huddart RA, Horwich A. Managing testicular cancer. Br Med J. 2001;322(7302):1583-8. 6. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 980-982. 7. Kopp H, Kuczyk M, Hartmann J, et al. Advances in the treatment of testicular cancer. Drugs. March 2006;66(5):641-659. 8. Jayachandran J, Freedland S, Moul J. Long-Term Effects of Testicular Cancer Treatment. Current Medical Literature: Urology. March 2008;14(1):1-8. 9. Nakamura T, Miki T. Recent strategy for the management of advanced testicular cancer. International Journal Of Urology. February 2010;17(2):148-157.

Ulcerative Colitis Condition

Ulcerative colitis is an autoimmune chronic inflammation of the colon, unlike Crohn’s disease which can affect any part of the gastrointestinal tract. Ulcerative colitis and Crohn’s disease are collectively known as the inflammatory bowel diseases. Incidence/Etiological Factors

Incidence and prevalence rates are highest in Northern European countries, the United Kingdom, and North America. Incidence is estimated to range between 2.2-14.3 cases per 100,000 person years and prevalence ranges from 37-246 cases per 100,000 persons. Prevalence is higher in males than females.1 Family history of UC is a risk factor for disease, while appendectomy and cigarette smoking exhibit a protective effect.2 Pathogenesis

Genetic factors may predispose individuals to an abnormal response to gut flora. Family history of UC is reported in 20% of cases.3 It is hypothesized that a pathologic interaction between the immune system and normal gut flora leads to a misdirected immune response on the colon. Three mechanisms are thought to drive this faulty interaction. First, the introduction of pathogenic bacteria may induce a chronic immune response. Second, a loss of protective bacteria can lead to increased mucosal permeability and an increased immune response. Finally, dysfunction of regulatory T cells or antigen presenting cells can lead to a loss of tolerance for resident gut microbiota.2 Signs and Symptoms

Symptoms of inflammatory bowel disease often cycle unpredictably between remission and relapse. The most common symptoms are abdominal pain and cramping, diarrhea, weight loss, and rectal bleeding. Severe inflammation may result in intestinal blockage that leads to abdominal cramps, vomiting, and bloating.4,5 Diagnosis

Inflammatory bowel diseases are most often diagnosed in late adolescence and early adulthood.2 Diagnosis is first suspected clinically and then confirmed by endoscopic biopsy. Lab tests may or may not reveal anemia, increased erythrocyte sedimentation rate, or increased C-reactive protein. These results may indicate ulcerative colitis, but these findings may be absent.6 Treatment

Goals of treatment are to induce remission and prevent relapse. Once the diagnosis is made, the patient with mild to moderate disease distal to the descending colon will be prescribed topical 5aminosalicylic acid (5-ASA). For disease proximal to the sigmoid colon, oral 5-ASA therapy is commenced. If either topical or oral treatment is not effective on its own, they will be prescribed together. The combination of oral and topical treatment is superior to either one alone. Should these treatments fail, a short course of oral corticosteroids may be effective. If the disease still fails to respond to the maximum course of outpatient management, hospital admission is required for intravenous admission of corticosteroids. If symptoms still do not improve, intravenous cyclosporine or infliximab are the next treatment options, followed by surgical proctolectomy in severe cases.6 Implications for the Therapist

When a client presents with back, sacroiliac, or hip pain of unknown origin, the therapist should ask questions about accompanying gastrointestinal symptoms, family history of inflammatory bowel disease, and if symptoms are relieved upon passing stool or gas.7 References

1. Loftus, EV. Clinical Epidemiology of Inflammatory Bowel Disease: Incidence, Prevalence, and Environmental Influences. Gastroenterology. 2004;125:1504-1517. 2. Engel M, Neurath M. New pathophysiological insights and modern treatment of IBD. J Gastroenterol. 2010;45:571-583. 3. Sands B. Inflammatory bowel disease: past present, and future. J Gastroenterol. 2007;42:16-25. 4. Farrell D, Savage E. Symptom burden in inflammatory bowel disease: Rethinking conceptual and theoretical underpinnings. International Journal Of Nursing Practice. October 2010;16(5):437-442. 5. Centers for Disease Control and Prevention. Inflammatory Bowel Disease. http://azhin.org/content.php?pid=326216&sid=2670252. Updated January 14, 2014. Accessed April 5, 2014. 6. Adams S, Bornemann P. Ulcerative colitis. American Family Physician. May 15, 2013;87(10):699-705.

7. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 857.

Urinary Tract Infection Condition

A urinary tract infection (UTI) is a bacterial infection of the urinary tract, typically by gramnegative fecal-associated bacteria. Incidence/Etiological Factors

Urinary tract infections can affect any person of any age, but occur most frequently in women and older adults.1 A woman’s lifetime risk of contracting a UTI is greater than 50%, and it is estimated that 25% of women diagnosed with UTI will experience reinfection.2 Escherichia coli infection is the number one cause of UTI.2,3 Most UTIs occur in adult women. Young, sexually active women, pregnant women, and women with poor perineal hygiene due to dementia or stroke are at increased risk. Prevalence of UTI is greater in the older population, particularly those living in an assisted living, skilled nursing, or extended care facility.4 UTIs account for 40% of nosocomial infections, and catheterization is the leading cause of UTI in hospital facilities.1 Pathogenesis

The bacteria most often responsible for urinary tract infections are fecal-associated gramnegative bacteria. E. coli account for 80% of urinary tract infections.1-3 Infection often begins when the vagina and urethra are colonized by fecal bacteria that ascend through the urethra into the bladder.2 Very rarely, infection may be bloodbourne of acquired via the lymphatic system.1 UTIs are categorized into two types. Bladder infection, or cystitis, is an infection of the lower urinary tract. Infection of the upper urinary tract or kidneys, is pyelonephritis.3 Signs and Symptoms

Common signs and symptoms of urinary tract infection include urinary frequency and/or urgency, dysuria, nocturia, suprapubic pain, hematuria, malaise, fever, vague or mild abdominal pain, and incontinence.2 Self-reported symptoms in women with suspected cystitis are wide and vary individually, but the most commonly reported symptoms include feelings of malaise, fever, and back pains. Heytens et al.5 found low back pain was reported by 48.6% of women suspected of having UTI. Additionally, urine may be cloudy, bloody, or foul-smelling, and a burning sensation during urination or intercourse may occur. Older adults may experience malaise, anorexia, or mental status changes (i.e. confusion).1 Signs and symptoms indicative of pyelonephritis are consistent with those for cystitis but also include flank pain, fever, chills, nausea and/or vomiting, and costovertebral angle tenderness.1,3

Kidney involvement may irritate the diaphragm, leading to ipsilateral shoulder or lumbar back pain.1 Diagnosis

Diagnosis can usually be reached and treatment commenced based on history and signs and symptoms alone. Urine dipstick analysis for leukocyte esterase and nitrites is commonly used to screen for UTI. Tests revealing the presence of leukocyte esterase and nitrites demonstrate high specificity but low sensitivity for UTI.2 A urine leukocyte count of greater than10 leukocytes per mL urine is considered high. Bacterial count over100,000 organisms per mL urine is also accepted criterion for diagnosis of UTI.1 Treatment

The most commonly prescribed antimicrobials for UTI include fluouroquinolones, cotrimoxazole, and nitrofurantoin.3 For women with recurring infections, prophylactic antibiotics may be prescribed for self-treatment following sexual intercourse or as symptoms are recognized.2 Increased fluid intake is recommended and probiotic supplements such as Lactobacillus acidophilus may be taken to replace naturally occurring bacteria in the intestines that may be interrupted by antibiotic treatment.1 Implications for the Therapist

The physical therapist who notices the onset of the above symptoms in a patient or client may help in early detection of UTI. Insidious onset of back or shoulder pain, particularly following an infection, may be indicative of a recurring or worsening infection and warrants medical referral.1 Underlying pelvic floor dysfunction may be an underlying cause in women with recurrent UTIs who do not respond appropriately to antibiotic treatment. Physical therapist intervention involving pelvic floor muscle training and biofeedback in such cases may prove beneficial.1,2 References

1. Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. Saunders Elsevier; 2009: 928-931. 2. Nosseir S, Lind L, Winkler H. Recurrent Uncomplicated Urinary Tract Infections in Women: A Review. Journal Of Women's Health. March 2012;21(3):347-354. 3. Guay D. Contemporary Management of Uncomplicated Urinary Tract Infections. Drugs. May 2008;68(9):1169-1205. 4. Dwyer L, Harris-Kojetin L, Thompson N, et al. Infections in Long-Term Care Populations in the United States. Journal Of The American Geriatrics Society. March 2013;61(3):341-349. 5. Heytens S, De Sutter, De Backer ,, Verschraegen G, Christiaens T. Cystitis: Symptomatology in Women with Suspected Uncomplicated Urinary Tract Infection. Journal Of Women's Health. July 2011;20(7):1117-1121.

Conclusion Low back pain is a prevalent complaint addressed by outpatient physical therapists. Although roughly 97% of LBP cases are mechanical in nature and respond to treatment or resolve over time, it is critical that physical therapists are competent in understanding non-orthopedic pathologies that can be a source of back pain. In the 3% of cases of LBP that are not of mechanical etiology, diagnosis is typically made in the primary care setting.25 Nonetheless, it is a rare, yet distinct possibility that back pain in a physical therapy setting can be caused by an undiagnosed non-mechanical or visceral disease.13 Timely recognition of signs and symptoms of these pathologies is crucial for preventing serious illness or even death. Therefore, the PT must also be attentive to non-orthopedic etiologies of pain in addition to the typical mechanical causes of musculoskeletal dysfunction in order to ensure the best patient care. Without exhaustive training in these diseases however, PTs must find the most efficient ways to locate and access information resources to guide clinical decision making. For this reason, the present study of non-orthopedic pathologies that refer pain to the low back is presented in the form of a mobile web application reference guide. The guide presents details on non-orthopedic pathologies that result in pain to the low back and includes evidence based findings on incidence, etiology, pathogenesis, clinical manifestations, and treatment for each disease. This application allows the user to implement filters and search functions to help make the application a practical tool. The information in this guide may assist the clinical professional to objectify patient findings and, if an underlying pathology is suspected, make referral to a physician for further evaluation. Areas for future research in the field include further investigation into the usefulness of mobile applications in physical therapy practice and research into how physical therapists currently gather resources to support clinical decision making. For the application presented in this project, the next step in development may include trial use for education purposes by undergraduate students pursuing careers in allied health fields.

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19. Fell DW, Burnham JF, Dockery JM. Determining where physical therapists get information to support clinical practice decisions. Health Information & Libraries Journal. 2012;30:3548. 20. Ardito S. Mobile Apps for the Health Professional. Searcher. July 2011;19(6):46-50. 21. Health Care Technology Today. PT In Motion. December 2013;5(11):24-28. 22. Wilkinson SG, Chevan J, Vreeman D. Establishing the Centrality of Health Informatics in Physical Therapist Education: If Not Now, When?. Journal of Physical Therapy Education. 2010;24(3):10-15. 23. Overview of AHRQ Projects Points to Importance of Health IT. Physical Therapy. March 2, 2014:14. 24. Knack. https://www.knackhq.com/. Accessed September 10, 2013. 25. Jarvik J, Deyo R. Diagnostic evaluation of low back pain with emphasis on imaging. Annals Of Internal Medicine. October 1, 2002;137(7):586-597.

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