In this case, he is describing the cardinal symptoms of polymyalgia rheumatica. Older patient, over 50 years of age, presenting with pain and stiffness in both girdles, associated with an elevation of acute phase reactants. He presents all the indispensable criteria: age equal to or greater than 50 years, bilateral omalgia and increased acute phase reactants. Of the optional criteria, he presents stiffness, pain or limitation in the hip. Initial treatment is corticosteroids at medium doses.

A 70-year-old woman who has been complaining for 1 month of pain and stiffness in the shoulder girdle and pelvic girdle, which predominates when she gets up and improves with mobilization, without fever, headache or general condition. Physical examination showed stiffness and pain on mobilization of the shoulders and hips. Laboratory tests show elevated ESR and C-reactive protein. What is the most likely diagnosis and what treatment would you prescribe?

Rheumatoid arthritis, would initiate treatment with methotrexate.

Fibromyalgia, would initiate treatment with duloxetine.

Polymyalgia rheumatica, would initiate treatment with corticosteroids.

Ankylosing spondylitis, I would initiate treatment with non-steroidal anti-inflammatory drugs.

[Polymyalgia rheumatica in daily routine practice].

Polymyalgia rheumatica (PMR) is a very painful inflammatory disease which regularly affects the shoulder region but in 70% of cases the pelvic girdle region is also affected. The disease occurs in people over the age of 50 years and reaches a peak at 72 years old. Women are affected twice as often as men. The prevalence is estimated to be 0.3-0.7% in the Caucasian population over 50 years old. Misdiagnosis of PMR is common. The differential diagnosis primarily includes impingement syndrome, osteoarthritis of the shoulders, calcifying tendinitis of the rotator cuff, bursitis, omarthritis or inflammatory rheumatic diseases, such as rheumatoid arthritis. Taking a structured medical history and performing a thorough clinical examination are crucial. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are usually highly elevated and should be investigated particularly in patients who present with new onset bilateral shoulder pain and pronounced general impairment of movement. Imaging shows characteristic inflammatory changes around the shoulders and hip joints. The new European League Against Rheumatism and American College of Rheumatology (EULAR/ACR) classification criteria of PMR including ultrasound imaging are superior to previous classification and diagnostic criteria in terms of positive and negative predictive values. Glucocorticoids are still the mainstay of treatment. Recommended daily prednisolone starting doses are between 15 mg and 25 mg with a weekly dose reduction until 10 mg/day and then further dose reductions of 1 mg per month. Methotrexate can aid reducing prednisolone doses in patients who fail to reach doses below the Cushing threshold quickly enough, which can have major side effects.

Polymyalgia Rheumatica (PMR) with Normal Values of Both Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP) Concentration at the Time of Diagnosis in a Centenarian Man: A Case Report.

The possibility that polymyalgia rheumatica (PMR) can be diagnosed when both ESR and CRP are normal at the time of diagnosis and before therapy with glucocorticoids, has been often discussed in the literature. We present a case report of a 100-year-old Caucasian man referred to our outpatient clinic, complaining of chronic pain in the shoulder and hip girdle associated with normal values of both ESR (21 mm/1st hour) and CRP (4 mg/dL). In the previous four months, several anti-inflammatory drugs and painkillers associated with physiotherapy treatments gave no significant improvement in pain and self-care. After an ultrasound (US) and an 18-fluorodeoxyglucose positron emission tomography associated with total body computed tomography (18-FDG PET/CT) examination, PMR was diagnosed and he started therapy with 17.5 mg prednisone, obtaining a fast improvement in pain and self-care. After 10 months of tapering, he stopped prednisone without relapse. During a 3-year follow-up, no alternative diagnosis was done. When a patient complains of chronic bilateral shoulder and hip girdle pain associated with normal inflammatory indices, it is reasonable to think in the first instance that this person is not suffering from PMR. Moreover, the possibility that PMR may onset in a centenarian person, is exceptional. In our patient, when we piece the puzzle together, the diagnosis of PMR was the most possible one.

[Diagnostics and treatment of polymyalgia rheumatica].

Polymyalgia rheumatica (PMR) is the most common autoimmune inflammatory disease in older persons with an average age of onset of 73 years. Typical symptoms include acute or subacute bilateral shoulder pain with severe stiffness and often neck and bilateral hip pain. Giant cell arteritis (GCA) occurs in approximately 20 % of cases and up to two thirds of patients with GCA have symptoms of PMR. There are many disease which mimic PMR, elderly onset rheumatoid arthritis is frequently misdiagnosed as PMR. Although there are no specific laboratory tests, C‑reactive protein and erythrocyte sedimentation rates are elevated in over 90 % of patients. The diagnosis may be aided by imaging, especially ultrasonography and magnetic resonance imaging (MRI). Treatment currently consists of glucocorticoids at an initial dose of 12.5-25 mg prednisone equivalent daily. Treatment duration is typically 2‑3 years but may be longer. Under certain conditions low-dose methotrexate can be used as adjuvant therapy.

Polymyalgia rheumatica.

Polymyalgia rheumatica is a syndrome that occurs in the elderly and is characterized by pain and stiffness involving the neck, the shoulder girdle, and the hip girdle. The aching should be present for greater than one month. Polymyalgia rheumatica may be more common than reported. The etiology remains unknown. There is generally little found pathologically in this disease. The physical examination is often not impressive. Synovitis may be a main contributing factor to many of the symptoms seen in patients with polymyalgia rheumatica. Symptoms often do not correlate with physical findings. Polymyalgia rheumatica must be differentiated from many conditions since the diagnosis remains entirely clinical. Osteoarthritis, flu syndromes, inflammatory myopathies, fibromyalgia, and depression all have features that may mimic polymyalgia rheumatica. Malignancies and infections may also be difficult to separate from polymyalgia rheumatica. Polymyalgia rheumatica may also be extremely difficult to differentiate from seronegative rheumatoid arthritis in patients older than 50 years. Although some patients with polymyalgia rheumatica have underlying giant cell arteritis, the majority apparently do not. The distinction between polymyalgia rheumatica and giant cell arteritis cannot be made on the basis of laboratory studies and relies solely on clinical symptoms and physical findings. Although nonsteroidal antiinflammatory medications may control symptoms in patients with mild disease, most patients with polymyalgia rheumatica require low-dose corticosteroids. The tapering schedule for the corticosteroids is contingent upon the response of symptoms and laboratory parameters. Polymyalgia rheumatica usually follows a benign course with almost complete response to an adequate treatment program. Recently, there have been several studies suggesting that the course of polymyalgia rheumatica may not be as short and simple as once proposed. Nevertheless, many patients may be completely weaned from corticosteroids. Other agents have been used in this disease, but for the most part their use remains somewhat controversial. Patients must be monitored carefully. Most patients do well, and treatment is effective.

Advances and challenges in the diagnosis and treatment of polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is a common inflammatory condition that often affects people over the age of 50 years. Characteristic symptoms are shoulder and hip girdle pain and prolonged morning stiffness. Markers of inflammation are often elevated. Clinicians are often faced with the challenge of distinguishing PMR from other conditions, particularly rheumatoid arthritis and spondyloarthropathy that can mimic symptoms of PMR in older people. Additionally, there is an association between PMR and giant cell arteritis, a common large-vessel vasculitis which also affects people over the age of 50 years. Imaging of the large vessels in asymptomatic patients with PMR often reveals findings of subclinical vasculitis. Presently, there are no tests that are specific for the diagnosis of PMR and clinicians rely on a combination of history, physical examination, laboratory tests and imaging studies to make a diagnosis. A recent undertaking by the European League Against Rheumatism/American College of Rheumatology has led to the publication of provisional classification criteria of PMR. Ultrasonography, which is being increasingly used by rheumatologists, can greatly aid in the diagnosis of PMR and often shows changes of synovitis and tenosynovitis. Treatment consists of low doses of glucocorticoids which are associated with morbidity. Evaluation of newer biologic therapies targeting inflammatory cytokines is underway. Despite treatment, relapses are common.

[Rheumatic polymyalgia].

Polymyalgia rheumatica (PMR) is a common clinical syndrome that is characterized by pain and stiffness in neck, shoulder girdle and pelvic girdle. The aetiology is unknown. However, recent studies have documented an association with HLA antigens and infectious agents. It occurs mostly after the age of 50 years and is often accompanied by systemic features such as fever, asthenia, hyporexia and weight loss. An erythrocyte sedimentation rate (ESR) of at least 40 mm/hour has been considered diagnostic criterion. Nevertheless, a normal ESR accounted for up to 20% of cases of PMR. A dramatic and prompt response to corticosteroid treatment is characteristic. Giant cell arteritis/temporal arteritis (GCA) has been found in 0-80% of cases of PMR. Temporal biopsy could initially be deferred in patients with PMR younger than 70 years with no cranial symptoms, in which the risk of GCA is very low.

Polymyalgia rheumatica--diagnosis and classification.

Polymyalgia rheumatica is the most common inflammatory rheumatic disease of the elderly, and shares many pathogenetic and epidemiological features with giant cell arteritis. The typical symptoms are bilateral aching of the shoulder girdle, associated with morning stiffness. The neck and hip girdle may also be involved. The diagnosis of polymyalgia rheumatica is made primarily on clinical grounds. There is no single diagnostic test, but sets of diagnostic or classification criteria have been suggested by several groups of investigators, based on the typical clinical presentation and laboratory evidence of acute-phase reaction. Other conditions that may mimic polymyalgia rheumatic, such as elderly-onset rheumatoid arthritis, must be excluded by appropriate testing and close monitoring of the disease course. Glucocorticoids at low doses (15-20 mg prednisone per day initially) are the mainstay of treatment.

[A case of polymyalgia rheumatica with excessive increase of rheumatoid factor].

A 76 year-old woman suffered from muscle pain and stiffness of acute onset in her shoulder girdle and pelvic girdle, which were followed by mild left temporal headache and transient arthralgia. Neither joint swelling nor sicca symptom was observed. Laboratory data showed high ESR (128 mm/hr), positive CRP (12.9 mg/dl), increased fibrinogen (485 mg/dl) and high titer of rheumatoid factor (RF) (RAHA x 640). Other autoantibodies examined were negative. Muscle enzymes and electromyogram were within normal limits. Joint X ray didn't reveal the finding suggestive of RA. After the treatment with prednisolone (PSL) 15 mg/day, clinical symptoms and laboratory data improved dramatically. Though she had excessive increase of RF (RAHA x 10240) during therapy, no recurrence of articular symptoms were recognized. She continues to be well with PSL 5 mg/day after 1 year 5 months from onset. As for polymyalgia rheumatica (PMR) followed by RA, the appearance or exacerbation of arthritis corresponding to the elevation of RF occurred in all previously reported 17 cases. Recurrence of arthralgia corresponding to the elevation of RF was not recognized in this case. In addition, Hunder et al reported that PMR with little or no observable joint swelling after several weeks of symptoms is unlikely to develope RA. Therefore, it is speculated that this case in unlikely to develope RA and assessment of arthritis corresponding to the elevation of RF is important to differentiate PMR and elderly-onset RA. This case of PMR is the 5th case with excessive increase of RF in Japan.

Polymyalgia Rheumatica After ChAdOx1 nCov-19 Vaccine: A Case Report.

Polymyalgia rheumatica (PMR) is an inflammatory rheumatic disease characterized by severe pain and morning stiffness, mainly affecting the shoulder girdle. A 75-year-old woman, previously healthy, received the first dose of ChAdOx1 vaccine and two weeks later started with pain in the shoulder and pelvic girdles and knees of inflammatory characteristics, accompanied by morning stiffness (about one hour), anorexia, asthenia, and activities of daily living (ADL) dependence. She started analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) with no improvement. The symptoms aggravated three days after the second vaccine dose, and she was referred to our center. At observation, she presented shoulder, hip, and knee active range of motion limitation. Blood analysis revealed an Erythrocyte Sedimentation Rate (ESR) of 120mm/h (reference value < 20mm/h) and C-Reactive Protein (CRP) of 80mg/L (reference value < 5mg/L). Ultrasound showed effusion on both shoulders, hips, and knees. The paraneoplastic syndrome was ruled out. She started oral corticosteroids and a rehabilitation program, and a month later, she presented controlled pain, normal analysis, and ADL independence. This case shows symptomatic and analytic features of PRM after the first vaccine dose and aggravation soon after the second. As such, we consider establishing a potential relationship between the inoculation and the development of PRM. A few cases were published reporting a PRM-like syndrome following a COVID-19 vaccine; however, the underlying mechanism and prognosis are still unknown.

Polymyalgia rheumatica: clinical update.

Polymyalgia rheumatica is a relatively common inflammatory rheumatic disease. There are no validated international guidelines available for the diagnosis and treatment of PMR; however, diagnostic and classification criteria are currently being developed. The aim of this article is to summarise the main management options suggested by American College of Rheumatology and discusses the role of the general practitioner in the diagnosis and early management of PMR. Diagnosis is made on the basis of a combination of clinical and laboratory findings. Patients typically present with shoulder and hip girdle pain with pronounced stiffness. Inflammatory markers are usually elevated and an ultrasound and MRI of the shoulder and hip can be done to localise inflamed tissues. Response to steroids should not be used as a defining feature of PMR but treatment with low dose prednisone should be considered. PMR has an excellent prognosis if diagnosis is prompt and therapy adequate.

Patient-reported outcomes in polymyalgia rheumatica.

To prospectively evaluate the disease course and the performance of clinical, patient-reported outcome (PRO) and musculoskeletal ultrasound measures in patients with polymyalgia rheumatica (PMR). The study population included 85 patients with new-onset PMR who were initially treated with prednisone equivalent dose of 15 mg daily tapered gradually, and followed for 26 weeks. Data collection included physical examination findings, laboratory measures of acute-phase reactants, and PRO measures. Ultrasound evaluation was performed at baseline and Week 26 to assess for features previously reported to be associated with PMR. Response to corticosteroid treatment was defined as 70% improvement in PMR on visual analog scale (VAS). At baseline, 77% had hip pain in addition to shoulder pain and 100% had abnormal C-reactive protein or erythrocyte sedimentation rate. On ultrasound, 84% had shoulder findings and 32% had both shoulder and hip findings. Response to corticosteroid treatment occurred in 73% of patients by Week 4 and was highly correlated with percentage improvement in other VAS measures. Presence of ultrasound findings at baseline predicted response to corticosteroids at 4 weeks. Factor analysis revealed 6 domains that sufficiently represented all the outcome measures: PMR-related pain and physical function, an elevated inflammatory marker, hip pain, global pain, mental function, and morning stiffness. PRO measures and inflammatory markers performed well in assessing disease activity in patients with PMR. A minimum set of outcome measures consisting of PRO measures of pain and function and an inflammatory marker should be used in practice and in clinical trials in PMR.

[Polymyalgia rheumatica].

Polymyalgia rheumatica is characterized by bilateral pain in the shoulder and pelvic girdles, malaise, morning stiffness and weight loss. The erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP) level are elevated. Imaging using ultrasound, magnetic resonance imaging (MRI) or positron emission tomography (PET) displays inflammatory changes in the painful anatomical areas. Nearly all patients are older than 50 years and the average age is 70-75 years. Polymyalgia rheumatica occurs 2-3 times more often in women than in men and some patients exhibit temporal arteritis or giant cell arteritis. Symptoms rapidly decrease with glucocorticoid treatment and the dose can normally be reduced during the course of the disease. Methotrexate may be given only if high glucocorticoid doses do not sufficiently control symptoms. On average treatment can be stopped after 2 years.

Polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is an inflammatory condition of unknown etiology characterized by aching and stiffness in the shoulder and in the pelvic girdles and neck. In the past, PMR was considered a manifestation of giant cell arteritis (GCA) or a variant of elderly-onset rheumatoid arthritis (EORA). The current diagnostic criteria for PMR were empirically formulated by clinical experts who had studied the disease extensively. Arthroscopic, radioisotopic and magnetic resonance imaging studies all have indicated the presence of a synovitis in proximal joints and periarticular structures. The synovitis is probably responsible for the musculoskeletal symptoms in PMR. The prominence assigned to the proximal symptoms has probably overshadowed the less well recognized and more variable distal musculoskeletal manifestations which are present in about half of the cases. A normal erythrocyte sedimentation rate does not exclude a diagnosis of PMR. C-reactive protein and interleukin-6 seem to be more sensitive indicators of disease activity both at diagnosis and during relapse/recurrence. Corticosteroids are the drugs of choice for treating PMR. A course of treatment of 1-2 years is often required. However, some patients have a chronic, relapsing course and require low doses of corticosteroids for several years. Large, multicenter, double-blind, placebo-controlled studies are required to define the role of methotrexate and anti-TNF-alpha agents as corticosteroid-sparing drugs in PMR.

[Dutch College of General Practitioner's practice guideline on polymyalgia rheumatica and temporal arteritis].

The practice guideline for general practitioners (GPs) on polymyalgia rheumatica and temporal arteritis was published in February 2010 by the Dutch College of General Practitioners. This guideline provides GPs with recommendations for the diagnosis and treatment of polymyalgia rheumatica. After other disorders have been excluded, the diagnosis of 'polymyalgia rheumatica' is made in patients over the age of 50 who have bilateral pain in the neck and shoulder girdle and/or hip girdle that has lasted for longer than 4 weeks, morning stiffness that lasts longer than 60 minutes and an ESR > 40 mm in the first hour. After the diagnosis is made treatment with prednisone or prednisolone 15 mg per day is started. This dosage is diminished very gradually according to a uniform treatment schedule during a period of 3 months, thereafter depending on the clinical course. The practice guideline pays attention to the diagnosis and management of temporal arteritis only when it occurs concurrently with polymyalgia rheumatica.

[Polymyalgia rheumatica update, 2015].

Polymyalgia rheumatica is an inflammatory musculoskeletal disorder of people aged 50 years or over, characterised by pain, aching and morning stiffness in the shoulder girdle and often hip girdle and neck. Marked systemic inflammation and rapid response to corticosteroid therapy are characteristic features. Giant cell arteritis is a well-known association of polymyalgia rheumatica. Recent clinical evidence and scientific results in the field have provided new challenges for rheumatologists. Besides the aspecific - although characteristic - proximal syndrome, less well recognizable and more variable distal musculoskeletal manifestations were observed. Magnetic resonance and ultrasound studies showed mild, remitting and non-erosive synovitis, with dominating inflammation of the extraarticular synovial structures. As no pathognostic sign is known, the diagnosis of polymyalgia rheumatica is based on its differential diagnosis, differentiation from the polymyalgia mimics; particularly from elderly onset inflammatory arthritides, such as elderly onset rheumatoid arthritis and late onset seronegative spondylarthritis. In 2012 the international polymyalgia rheumatica work group under the guidance of the American College of Rheumatology and European League Against Rheumatism elaborated new classification criteria, the scoring algorythm of which is based on clinical symptoms, with ultrasonography increasing the specificity. Corticosteroids remain the cornerstone of the therapy of polymyalgia rheumatica. No effective steroid-sparing drug has been found to date. Corticosteroids are generally needed for 1-1.5 years, though some patients have a chronic-relapsing course and require corticosteroids for several years. Well known corticosteroid-related side effects (diabetes, hypertension, hyperlipidaemia and osteoporosis) cause significant morbidity and economic burden on the society. Novel therapeautic approaches are on trial. Early recognition of the disease, early start of corticosteroids and a well-defined course, prevention and management of side effects are everyday tasks for rheumatologists and family doctors. Knowledge of polymyalgia rheumatica is essential for all medical specialties.

[Coexistence of polymyalgia rheumatica with ankylosing spondylitis: A case report].

Ankylosing spondylitis is a chronic inflammatory disease that affects the spine and peripheral joints. Polymyalgia rheumatica is an inflammatory disease characterized by aching and prolonged morning stiffness mainly in the shoulder and pelvic girdles. Many other diseases may mimic polymyalgia rheumatica, and thus differential diagnosis is predominantly required. A wide variety of diseases, including spondyloarthropathies, may present polymyalgia-like symptoms, and two diseases rarely coexist. We present a case of a 54-year-old man who had been followed-up for ankylosing spondylitis and presented with pain in the shoulder and pelvic girdles, restricted movement, and morning stiffness for 2 months. Physical examination revealed that the pain was located mostly in the shoulder and pelvic girdles. In addition, increased erythrocyte sedimentation rate revealed the coexistence of the two diseases. Corticosteroid treatment dramatically improved the patient's symptoms and supported the diagnosis. This case demonstrated that ankylosing spondylitis may present polymyalgia-like symptoms, and the two diseases may rarely coexist in the elderly. The coexistence of these two diseases has been rarely reported in literature. Accurate diagnosis of the two diseases is essential for improving the patient's symptoms and quality of life.

Diagnosis and management of polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is a common inflammatory condition of unknown aetiology with a prevalence of 1 in 133 in the over 50s, and a female to male ratio of 2:1. Symptoms develop over a matter of weeks; typically bilateral shoulder or pelvic girdle pain and stiffness, that is worse in the mornings. Associated symptoms include low-grade fever, malaise, fatigue, low mood, poor appetite, and weight loss. There is no specific diagnostic test for PMR but the usual pattern is a commensurate rise in CRP and ESR. A small proportion of PMR patients will have normal inflammatory markers. PMR is associated with giant cell arteritis (GCA). Half of patients with GCA will have some PMR symptoms and up to one fifth of patients with PMR will have evidence of GCA. Other conditions that can mimic PMR include: rheumatic disease in the elderly e.g. rheumatoid arthritis; inflammatory muscle diseases; thyroid disease; malignancy; infection; bilateral shoulder capsulitis; osteoarthritis, Parkinsonism and depressive illness. At diagnosis and each follow-up visit it is imperative to consider the potential for associated GCA. The patient should be asked about headaches, jaw claudication and visual disturbance. If there is any suspicion of GCA, urgent discussion with the rheumatologist should take place that day.

Polymyalgia rheumatica and temporal arthritis.

Polymyalgia rheumatica and temporal arteritis are closely related inflammatory conditions that affect different cellular targets in genetically predisposed persons. Compared with temporal arteritis, polymyalgla rheumatica is much more common, affecting one in 200 persons older than 50 years. Temporal arteritis, however, is more dangerous and can lead to sudden blindness. The diagnosis of polymyalgia rheumatica is based on the presence of a clinical syndrome consisting of fever, nonspecific somatic complaints, pain and stiffness in the shoulder and pelvic girdles, and an elevated erythrocyte sedimentation rate. Temporal arteritis typically presents with many of the same findings as polymyalgia rheumatica, but patients also have headaches and tenderness to palpation over the involved artery. Arterial biopsy usually confirms the diagnosis of temporal arteritis. Early diagnosis and treatment of polymyalgia rheumatica or temporal arteritis can dramatically improve patients' lives and return them to previous functional status. Corticosteroid therapy provides rapid and dramatic improvement of the clinical features of both conditions. Therapy is generally continued for six to 24 months. Throughout treatment, clinical condition is assessed periodically. Patients are instructed to see their physician immediately if symptoms recur or they develop new headache, jaw claudication or visual problems.

[Inflammatory Muscle Pain: Polymyalgia Rheumatica with or without Large Vessel Vasculitis].

Polymyalgia rheumatica (PMR) is characterized by rapidly evolving shoulder and pelvic girdle pain with fatigue, weight loss, night sweats and elevated CRP and ESR. Giant cell arteritis (GCA) can occur in PMR and vice versa. Headache and scalp tenderness are typical for GCA. GCA may be complicated by visual loss or by strokes.Imaging, particularly ultrasound, is helpful for distinguishing PMR from similar conditions such as shoulder osteoarthritis, rheumatoid arthritis and chondrocalcinosis. Subdeltoid bursitis, biceps tenosynovitis and hip joint effusions are common in PMR. The diagnosis of GCA needs to be either confirmed by imaging or by histology. Ultrasound is the imaging method of choice provided that expertise and adequate equipment are available. Inflamed arteries exhibit a concentric wall thickening. Patients with extracranial GCA are younger, more often female. Vasculitis commonly involves the aorta, subclavian arteries, axillary arteries and other arteries. The diagnosis of extracranial GCA may be confirmed by ultrasound, CT, MRI or PET.Prednisolone with a starting dose of 15-25 mg/d for PMR and of 40-60 mg/d for GCA results in rapid improvement of symptoms. Fast-track clinics provide clinical and ultrasound examinations by experts within 24 hours. Their introduction led to a decrease of visual loss in GCA. The prednisolone dose can be discontinued within 1 year in about 50 % of GCA patients. Additional treatment with tocilizumab allows to reduce flares and decrease glucocorticoid doses. Tocilizumab is particularly useful in patients with relapses and with increased risk of glucocorticoid side effects.

[Polymyalgia rheumatica].

Polymyalgia rheumatica is a disorder that affects people over 50 years of age. The etiology of the disease has not been hitherto clarified exactly. Its incidence among people over 50 is in the range of 0.1-0.5%. The incidence rate peaks in the age group of 60-70 years. It is also found in younger people, but far less frequently. The diagnosis is based primarily on locomotor complains--namely on pronounced pain, morning stiffness of the shoulder girdle, pelvic girdle and neck. Complaints relating to the arms and legs (such as muscular weakness, oedema, tendonitis etc.) are also observed, however, in one third of the cases. The diagnostic criteria are defined empirically. Polymyalgia rheumatica was formerly considered to be a form of elderly onset rheumatoid arthritis. The progressive erosion process is absent in the case of polymyalgia rheumatica unlike in the case of rheumatoid arthritis. Numerous factors are known, which point to a link between polymyalgia rheumatica and giant cell vasculitis, arthritis, but the precise nature of this relationship remains unknown. Both conditions affect the same age group in the general population and they are even found--not infrequently--in the same patient. Polymyalgia rheumatica can be found in 40% of the patients suffering from arthritis while the histological examination detected mild vasculitis in approximately 10% of the patients suffering for "isolated" polymyalgia rheumatica. The response to be given to the acute phase is similar in both disorders. Scandinavian authors consider polymyalgia rheumatica as the appearance of generalised arthritis. Arthroscopic, nuclear magnetic resonance imaging as well as isotopic studies show unequivocally, that in the background of the osteo-muscular symptoms, complaints, inflammation is to be found partly of the joints but primarily that of the periarticular synovial structures. The above mentioned--dominant--proximal symptoms can often mask the distal locomotor disorders (pitting oedema of the hands and feet, tendonitis, tendosynovitis, carpal tunnel syndrome). The disorder may be accompanied by atypical generalised symptoms (loss of appetite, weight loss, fever, fatigue). An excellent indicators of the acute phase reactions are erythrocyte sedimentation rate, C-reactive protein and interleukin-6. These are suitable for monitoring the effectiveness of the therapy, for indicating a relapse/recurrence. It should be noted, that polymyalgia rheumatica may also be present if the erythrocyte sedimentation rate and C-reactive protein values are low. This disorder is also characterised by fast and effective response to corticosteroid, which should be administered for 1-2 years. In some individual cases a different dosage regime may be necessary: steroid administered in low dosage over a longer period of time. Administration of methotrexate and anti-tumor necrotic factor-alpha may also be considered as alternative or adjuvant therapy for lowering the quantity of corticosteroid. Further multicenter, double blind studies should, however, be performed on large number of patients in this regard.

Diagnosis and management of polymyalgia rheumatica/giant cell arteritis.

There are no standardised diagnostic criteria for polymyalgia rheumatica. The combination of persistent pain (at least 1 month) with marked morning stiffness in at least 2 of the neck, shoulder or pelvic girdle is characteristic of polymyalgia rheumatica. The other criteria are age >50 years, erythrocyte sedimentation rate (ESR) >40 mm/hour, rapid response to corticosteroids and an absence of other diseases capable of causing the musculoskeletal symptoms. A normal ESR does not exclude a diagnosis of polymyalgia rheumatica. Diagnostic temporal artery biopsy is recommended in all patients suspected of having giant cell arteritis. The segment of temporal artery with abnormality on physical examination should be biopsied. The drugs of choice in the treatment of polymyalgia rheumatica/giant cell arteritis are corticosteroids. An initial prednisone dosage of 40 to 60 mg/day is adequate in almost all cases of giant cell arteritis. Higher dosages and/or intravenous pulse methylprednisolone can be tried on patients with partial response or with recent visual loss. Polymyalgia rheumatica in the absence of giant cell arteritis requires an initial dose of prednisone 10 to 20 mg/day. In some cases of mild polymyalgia rheumatica, a short course of nonsteroidal anti-inflammatory drugs may be tried. Long term corticosteroid therapy in polymyalgia rheumatica and giant cell arteritis is complicated by serious adverse effects in between 48 and 65% of patients. Vertebral fractures and infections are among the most dangerous and frequent complications. Although there are limited data on the use of cytotoxic or immunosuppressive drugs, such as methotrexate, azathioprine and cyclosporin, in these indications, they might be effective either in sparing corticosteroids or in treating patients who do not respond to treatment with corticosteroids.

Polymyalgia rheumatica

PMR was first established as a distinct disease in 1966 by a case report on 11 patients at Mount Sinai Hospital in New York, NY. It takes its name from the Greek word Πολυμυαλγία polymyalgia, which means "pain in many muscles". Signs and symptoms A wide range of symptoms can indicate if a person has polymyalgia rheumatica. The classic symptoms include: Pain and stiffness (moderate to severe) in the neck, shoulders, upper arms, thighs, and hips, which inhibits activity, especially in the morning/after sleeping. Pain can also occur in the groin area and in the buttocks. The pain can be limited to one of these areas as well. It is a disease of the "girdles" meaning shoulder girdle or pelvic girdle. Fatigue and lack of appetite (possibly leading to weight loss) Anemia An overall feeling of illness or flu-like symptoms. Low-grade (mild) fever or abnormal temperature is sometimes present. In most people, it is characterized by constant fatigue, weakness and sometimes exhaustion.

Polymyalgia rheumatica and giant cell arteritis in older patients: diagnosis and pharmacological management.

Giant cell arteritis (GCA) is an inflammatory vasculopathy that involves large- and medium-sized arteries and can cause vision loss, stroke and aneurysms. GCA occurs in people aged >50 years and is more common in women. A higher incidence of the disease is observed in populations from Northern European countries. Polymyalgia rheumatica (PMR) is a periarticular inflammatory process manifesting as pain and stiffness in the neck, shoulders and pelvic girdle. PMR shares the same pattern of age and sex distribution as GCA. The pathophysiology of PMR and GCA is not completely understood, but the two conditions may be related and often occur concurrently. A delay in the diagnosis should be avoided because of the risk of vascular ischaemic complications due to GCA. The diagnosis should be considered in patients aged >50 years presenting with symptoms such as new headache, visual disturbances, jaw claudication or symptoms of PMR. GCA can also present as a systemic inflammatory syndrome with fever of unknown origin. Marked elevation of acute-phase reactants, recognizable in higher erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, is often seen in both PMR and GCA. However, some patients can present with a normal ESR. Confirmation of the diagnosis of GCA by temporal artery biopsy is important because clinical findings and laboratory tests are not specific, and because a diagnosis of GCA commits patients to long-term treatment with corticosteroids. The role of imaging techniques for the diagnosis of GCA remains unclear, but these modalities can be helpful in assessing the extent of vascular involvement, especially when extra-cranial disease is present. In PMR, subdeltoid and subacromial bursitis can be identified by imaging techniques, especially ultrasound or MRI. The clinical manifestations of GCA and PMR respond dramatically within 12-48 hours of starting corticosteroid treatment. The initial corticosteroid dosage commonly used in GCA is oral prednisone 40-60 mg/day, and for patients with PMR a dosage of 15-20 mg/day is often sufficient. A prolonged course of treatment is necessary, and corticosteroids are gradually tapered, guided by regular clinical evaluation and ESR (and/or CRP) measurement. Methotrexate is the best studied corticosteroid-sparing agent in GCA, and may be useful for patients with frequent disease relapses and/or corticosteroid-related toxicity. Retrospective studies favour aspirin (acetylsalicylic acid) as an effective adjuvant treatment for reducing the ischaemic complications of GCA. The long-term course of corticosteroid therapy frequently exposes elderly patients with PMR/GCA to various adverse effects, which can be attenuated with appropriate prophylactic measures. Co-morbid diseases and polypharmacy can pose particular challenges in the geriatric population. In general, the life expectancy of patients with GCA does not appear to be shortened, whereas the morbidity associated with the disease and its treatment is well recognized.

Polymyalgia rheumatica with normal erythrocyte sedimentation rate: clinical aspects.

Polymyalgia rheumatica is a relatively common syndrome of the elderly characterized by severe pain and stiffness in the neck shoulder and pelvic girdles, along with increased acute phase reactants. The current diagnostic criteria include as a requirement an erythrocyte sedimentation rate (ESR) higher than 30 or 40 mm/1 hr. Nevertheless, in several reports, a sizable proportion of patients with PMR, from 7% up to 22%, had an ESR that was either normal or slightly increased at the time of diagnosis, supporting the notion that an increased ESR should not be an absolute requirement for its diagnosis. This subset is characterized by a younger age, a less marked predominance of females, a longer diagnostic delay and a lower frequency of constitutional symptoms such as fever or weight loss. When determined, a majority of these patients had increased levels of C reactive protein. The recognition of this subset of patients with PMR and a low ESR can be very useful to the clinician, avoiding unnecessary suffering of the patients and the risks of ineffective therapy with nonsteroidal antiinflammatory drugs. To avoid the over-diagnosis of PMR in patients with a low ESR, we propose a set of criteria that can be easily applied in daily practice to patients with a clinical picture consistent with PMR but with a normal or slightly increased ESR.

Developing classification criteria for polymyalgia rheumatica: comparison of views from an expert panel and wider survey.

This report summarizes the findings from a consensus process to identify potential classification criteria for polymyalgia rheumatica (PMR). A 3-stage hybrid consensus approach was used to develop potential PMR classification criteria. The first stage consisted of a facilitated meeting of 27 international experts who anonymously rated the importance of 68 potential criteria. The second stage involved a meeting of the experts, who were provided with the results of the first round of ratings and were then asked to re-rate the criteria. In the third stage, the wider acceptance of the 43 criteria that received > 50% support at round 2 was evaluated using an extended mailed survey of 111 rheumatologists and 53 nonrheumatologists in the United States, Canada, and Northern and Western Europe. A total of 68 and 50 criteria were identified and rated in round 1 and round 2, respectively. In round 2, 43 of the 50 items achieved at least 50% support, including 10 core criteria achieving 100% support. In round 3, over 70% of survey respondents agreed on the importance of 7 core criteria. These were age >or=50 years, duration >or=2 weeks, bilateral shoulder and/or pelvic girdle aching, duration of morning stiffness > 45 min, elevated erythrocyte sedimentation rate, elevated C-reactive protein, and rapid steroid response (> 75% global response within 1 wk to prednisolone/prednisone 15 20 mg daily). Among physical signs, more than 70% of survey respondents agreed on the importance of assessing pain and limitation of shoulder (84%) and/or hip (76%) on motion, but agreement was low for peripheral signs like carpal tunnel, tenosynovitis, and peripheral arthritis. There are differences in opinion as to what PMR is and how it should be treated. These findings make it important to develop classification criteria for PMR. The next step is to perform an international prospective study to evaluate the utility of candidate classification criteria for PMR in patients presenting with the polymyalgic syndrome.

Polymyalgia rheumatica: clinical picture and principles of treatment.

Polymyalgia rheumatica (PMR) is a common disease of the elderly. It is characterized by pain and stiffness in the neck, shoulders and the pelvic girdle. In most cases erythrocyte sedimentation rate and C-reactive protein levels are highly elevated. Polymyalgia rheumatica is frequently associated with giant cell arteritis. Steroids are the standard treatment for PMR but their dosage requires adjustment depending on clinical picture, co-morbid conditions and adverse effects. The most prominent features of the disease as well as the main principles of treatment are presented.

Clinical characteristics and prognostic factors for relapse in patients with polymyalgia rheumatica (PMR).

Polymyalgia rheumatica (PMR) is a common inflammatory disease of the elderly in western countries, but the prevalence is apparently different between races and countries. Until now, an epidemiologic study of PMR is limited in Korea. We retrospectively evaluated the clinical data of 78 patients with PMR who were treated in 5 tertiary hospitals, and analyzed initial laboratory data, symptoms, therapeutic responses, and prognostic factors for relapse 1 year after treatments. Sixty percent of patients had pain in both shoulder and hip girdles with 10.6 weeks of duration, 75.9 ± 32.7 mm/h of erythrocyte sedimentation rate (ESR), and 6.2 ± 6.4 mg/dl of C-reactive protein. The rate of relapse and remission at 1 year was 38.4 and 2.5 %, respectively. The rate of overall relapse was 46.1 %, and the relapse occurred mostly in a year, especially between 6 and 12 months after diagnosis. There were more female in relapse group (88.9 %, p = 0.037), and cumulative steroid dose of 1 year was significantly higher in relapse group (5.5 ± 2.7 vs. 4.4 ± 2.5 g, p = 0.018). Independent risk factors for relapse were initial CRP ≥ 2.5 mg/dl (OR 6.296, p = 0.047) and the use of hydroxychloroquine (OR 6.798, p = 0.035). Initial dosage or tapering speed of steroid did not influence on prognosis. In Korean patients with PMR, baseline clinical characteristics and relapse rate were similar to previous studies, but our patients accompanied no giant cell arteritis and showed lower remission rate as well as delayed therapeutic response and later occurrence of relapse. More aggressive management would be needed according to the clinical status of patients.

Diagnosing joint pain in the older people.

There are many potential causes of joint pain in older patients. The most likely aetiology is OA. However, the differential diagnosis includes conditions which should not be missed such as septic arthritis and inflammatory disease. The pattern of joint involvement points to the diagnosis. Bilateral symmetrical small joint pain, swelling and stiffness should arouse the suspicion of RA. The wrist and knee are commonly affected by pseudogout and the first metatarsophalangeal joint or knee joint involvement may represent gout. Stiffness in the shoulder and hip girdles, worse in the morning, suggests polymyalgia rheumatica. In straightforward cases of OA no specific investigations are required. If doubt exists, however, tests may be necessary including FBC, ESR and CRP, uric acid for suspected gout and X-rays of the affected joints especially following trauma, or pseudogout. Patients with OA should be offered education and advice as well as strengthening exercises and aerobic fitness training (if physically possible). If the patient is overweight, weight loss is critical, especially in OA of the knee. Paracetamol and topical NSAIDs are the first-line drug treatments. Elderly onset RA differs from younger onset RA in the following ways: a more balanced gender distribution; a higher frequency of acute onset; an association with systemic features; more frequent involvement of the shoulder girdle and higher disease activity. DMARD therapy should be used according to disease severity, as in younger onset RA. The current approach is for early, intensive intervention with combination therapy. Corticosteroids may be very effective in the elderly, however, prolonged use and/or high dosage may lead to marked toxicity especially osteoporosis and diabetes.

Update on treatment of polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is the second most common inflammatory rheumatic disease in the elderly after rheumatoid arthritis. It is clinically characterised by pain and stiffness in the neck, proximal shoulder and hip girdle. Glucocorticoids (GCs) are the cornerstone of PMR treatment, but they are associated with potentially severe side effects. Among GC-sparing agents, methotrexate revealed a modest benefit in clinical trials, and recently, there have been promising reports from tocilizumab. In this review, we summarize the available evidence on the treatment of PMR and the possible role in the future of other agents under investigation.

Polymyalgia rheumatica.

Polymyalgia rheumatica is a chronic, inflammatory disorder of unknown cause that affects people over age 50 years. Classic symptoms include pain and long-term morning stiffness of the neck, shoulders, hips, upper arms, and thighs. Although markers of inflammation are often raised, no specific laboratory test exists for the disorder and the diagnosis is based on clinical assessment. Provisional classification criteria were published in April, 2012, by a collaborative initiative of the European League Against Rheumatism and the American College of Rheumatology. Several other disorders can mimic polymyalgia rheumatica. In particular, clinical manifestations can be difficult to differentiate from other forms of inflammatory arthritis such as spondyloarthritis and rheumatoid arthritis. Imaging studies such as ultrasonography and MRI typically show a predominantly periarticular inflammatory process. A subset of patients has an associated inflammatory vasculopathy affecting large arteries (giant cell arteritis). The standard treatment is low-dose glucocorticoids, which provide symptomatic relief for most patients. However, disease relapses are common, and treatment with glucocorticoids is associated with substantial morbidity. Improved understanding of disease pathogenesis might allow for more targeted immunotherapy.

Diagnosis, differential diagnosis and treatment of polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is a common disorder in the elderly population. The diagnosis is based upon recognition of a clinical syndrome, consisting of pain and stiffness in the shoulder and pelvic girdle, muscle tenderness of the upper and lower limbs and nonspecific somatic complaints. In addition, in most cases the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) concentration are highly elevated. Although PMR and giant cell arteritis (GCA) are commonly regarded as two clinical variations of the same disease, their clinical picture is quite different. Whilst in PMR the musculoskeletal symptoms predominate, the major features of GCA are arterial inflammation and its consequences, which suggests clinical and pathological discrepancies between the two syndromes and important differences with respect to morbidity and mortality. The prognosis of correctly diagnosed PMR is excellent. It is well known that corticosteroid therapy in PMR usually leads to rapid and dramatic improvement of patients' complaints and returns them to previous functional status. However, prolonged corticosteroid treatment, sometimes for several years, may be necessary to maintain clinical improvement. Despite all the knowledge about the beneficial effects of corticosteroid treatment, data concerning the optimal dosage regimen are lacking. Long-term corticosteroid use can be associated with various adverse events, of which induction of osteoporosis, diabetes mellitus and infection among the worst. A Corticosteroid Side Effect Questionnaire has been shown to dose-dependently detect adverse effects perceived by patients. The European League Against Rheumatism (EULAR) response criteria for PMR comprise a core set of markers for monitoring therapeutic responses in PMR, namely ESR or CRP, the visual analogue scale of patient's pain and physician's global assessment, as well as morning stiffness and the ability to elevate the upper limbs. The PMR-disease activity score has been developed on the basis of EULAR response criteria as a means of expressing disease activity as an absolute number. A score <7 indicates low disease activity, scores 7-17 suggest medium activity, and a score >17 is indicative of high disease activity. The PMR-disease activity score has been proven to be highly correlated with patient's global assessment, patient satisfaction and ESR. It provides an easily applicable and valid tool for disease activity monitoring in patients with PMR. Improved knowledge of disease activity processes, exact monitoring of disease activity and treatment responses, and increased risk-estimation of treatment schedules should ultimately improve the care of patients with PMR.


It is the classic exploration: he had a fever and pain, he had pericarditis with effusion, and now this is causing tamponade. Hence the hypotension (his heart cannot fill well with blood and pump), jugular engorgement and dependence on respiration to achieve preload and cardiac output (i.e. paradoxical pulse).

A 45-year-old man with a history of febrile illness and chest pain comes to the hospital with dyspnea and tachypnea. On physical examination his blood pressure is low, jugular venous pressure is elevated with a prominent descending sinus x and he has a paradoxical pulse. What diagnosis would you suspect?

Pericardial effusion with cardiac tamponade.

[Purulent pericardial effusion with tamponade: a rare initial manifestation of o pneumococcal infection].

A 70-year-old man, admitted for a haemorrhoid operation, suddenly went into circulatory shock (heart rate 150/min, blood pressure 100/70 mm Hg), necessitating transfer to an intensive care unit. His neck veins were prominent and he had a paradoxical pulse. Heart sounds were distant and there was an arrhythmia (atrial fibrillation in the ECG). No murmurs were heard. Breath sounds were decreased, especially in the lung bases. Differential blood count showed 30% stab cells with 12,200 white cells per microliter. Erythrocyte sedimentation rate was 118 mm in the first hour, C-reactive protein was raised to 11.8 mg/dl. There was a partially compensated respiratory acidosis (pH 7.12; pO 93.4 mm Hg; pCO 16.3 mm Hg; base deficit -22.6 mmol/l). In the chest radiogram the cardiac silhouette was greatly enlarged bilaterally. The echocardiogram demonstrated a large pericardial perfusion with a "swinging heart". At pericardial needle puncture 700 ml of amber-coloured fluid, containing pneumococci, were aspirated with immediate circulatory improvement. Penicillin, 10 mill.U twice daily for 13 days, was administered intravenously, followed by amoxycillin, 1 g three times daily by mouth, for a further 15 days. In addition he was given anti-inflammatory treatment with diclofenac and methylprednisolone. Despite this pericardial effusion recurred after 14 days and 600 ml of sterile fluid were removed. Subsequently the inflammatory signs disappeared. Three months later no effusion was present and there were no signs of constrictive pericarditis.

A young man with intractable ascites and effort dyspnoea without echocardiographic signs of pericardial thickening: the importance of clinical investigation, CT scan and MRI in the diagnosis of constrictive pericarditis.

A 35-year-old male patient suffering from dyspnoea on effort for 8 months, with abdominal and jugular venous distension, was previously studied in another hospital and discharged with a diagnosis of restrictive cardiomyopathy. Physical examination revealed a blood pressure of 110/60 mm Hg and absence of pericardial knock and also of paradoxical pulse. Chest X-ray showed no cardio-pulmonary alterations. Transthoracic echocardiography showed mild LV dysfunction (LVEF 46%) and lack of pericardial effusion and thickening. Doppler interrogation of transmitral flow showed a restrictive pattern. Computed tomography showed diffusely thickened pericardium, with the absence of calcification and of pericardial effusion. Cardiac magnetic resonance confirmed pericardial thickening and showed lack of myocardial alterations. Mild LV dysfunction was noted with dyskinesia of interventricular septum. The patient underwent cardiac catheterization, demonstrating an equalisation of RV and LV diastolic pressures with "square root" sign. The patient underwent pericardiectomy with consequent resolution of his symptoms and improvement of LV function.

Diagnostic Challenges in Chronic Constrictive Pericarditis.

Chronic constrictive pericarditis (CCP) is a disease that has multiple possible causes and is associated with variable clinical findings, depending on its severity. It develops insidiously, and in many cases, particularly in developed countries, no antecedent diagnosis can be found. These cases are termed idiopathic. Tuberculosis is the leading cause of constrictive pericarditis in developing nations but represents only a small minority in developed countries. Here the authors describe two different case reports where tuberculosis was the probable cause of CCP. A 21-year-old man born in Cape Verde living in Europe for 4 years and a 24-year-old man born in Guiné Bissau were both admitted due to intense precordial pain and syncope after exertion. Interestingly both had fatigability, dyspnea, chest discomfort and palpitations on exertion, as well as progressive involuntary weight loss and decubitus cough. On physical examination they had tachycardia, jaundice, cachexia, elevated jugular venous pressure, hepatomegaly and ascites. Both electrocardiograms showed prominent P waves and chest X-ray showed bilateral pulmonary interstitial infiltrates and enlargement of the right cavities. Analytically, elevated bilirubin, leukopenia and thrombocytopenia was also found in both. Echocardiography revealed findings, in both cases, compatible with CCP including less common signs as annulus reversus and annulus paradoxus. Thoraco-abdomino-pelvic CT from both patients revealed chronic liver disease with congestion, pleural effusion, pericardial calcifications, ascites and massive mediastinal and abdominal adenopathies. Blood cultures and IGRA test were negative. However, given the presumptive diagnosis of tuberculosis (TB), anti-TB therapy was started. Despite the diagnosis of "end-stage" CCP with very high operative risk multidisciplinary team decided after informed consent, to perform total anterior pericardiectomy, that occurred without complications. Pericardial and mediastinal biopsies, pericardial/pleural fluid cultures/ immune-phenotyping were inconclusive. Anti- tuberculosis therapy was maintained. After surgery, the patients had a remarkable clinical improvement (NYHA I) that persisted in 6- month follow-up. These two case reports illustrate that despite the markedly elevated operative risk of pericardiectomy in "end-stage" forms of disease after patients informed consent must be a considered option. The other point to consider is that, despite rare, tuberculosis still is a possible diagnosis to consider in CCP in Portugal.

[A case of subacute effusive-constrictive pericarditis].

A 30-year-old female with effusive-constrictive pericarditis was admitted to our hospital because of dyspnea, ascites and edema. On examination, her blood pressure was 118/94 mmHg and her pulse rate was 90 bpm. Physical examination revealed pulsus paradoxus, markedly raised venous pressure and pericardial knock sound. Chest X-ray showed marked cardiomegaly and bilateral pleural effusion. After cardiac catheterization there was elevation of mean right atrial pressure, right ventricular end-diastolic pressure, pulmonary-capillary-wedge pressure, and their pressures during diastole were approximately 30 mmHg. After successful pericardiocentesis, their diastolic pressures still remained at 15 mmHg. Additionally, pressure wave of the right ventricle showed distinct diastolic dip and plateau pattern, and that of the right atrium showed deep x and y descents. The pressure pattern suggested that not only pericardial effusion but also decreased compliance of the pericardium was the main factor contributing to the cardiac diastolic dysfunction. Histological examination of the pericardium showed diffuse lymphocyte infiltration and fibrosis. These findings strongly suggested that there might have been viral infection.

Pericarditis

Physical examinations The classic sign of pericarditis is a friction rub heard with a stethoscope on the cardiovascular examination, usually on the lower left sternal border. Other physical signs include a person in distress, positional chest pain, diaphoresis (excessive sweating); possibility of heart failure in form of pericardial tamponade causing pulsus paradoxus, and the Beck's triad of low blood pressure (due to decreased cardiac output), distant (muffled) heart sounds, and distension of the jugular vein (JVD).

[Recurrent autoreactive pericardial effusion. Impact of an aetiological classification of pericarditis].

A 36 year-old man suffered from fever, fatigue, pleurodynia and precordial discomfort. His family physician suspected febrile tracheobronchitis and treated it with ampicillin for 5 days. Because symptoms persisted an ECG was done which suggested acute myocardial infarction. The patient underwent an emergency coronary angiography which excluded coronary artery disease and aortic dissection. Pericarditis was suspected and the patient put on aspirin, 500 mg/d. Because of persisting cardiac symptoms an echocardiography was performed which revealed systolic separation between epi- and pericardium, characteristic of a small pericardial effusion after acute pericarditis. The symptoms improved after one week of treatment with diclofenac and the ECG had become normal. Two months later the patient was seen at our cardiac outpatient clinic. He had night sweats, sporadic precordial pain and severe dyspnoe. Further investigations revealed tachycardia (120/min), hypotension (95/70 mm Hg), pulsus paradoxus and jugular vein sustension. Echocardiography revealed a large pericardial effusion ("swinging heart"), which explained the low voltage and the electrical alternans in the ECG. Pericardiocentesis was carried out the same day to relieve the tamponade. It was followed by pericardioscopy and epi- as well as pericardial biopsy. 485 ml of a serous effusion were drained. Cytology and histology demonstrated a lymphocytic fibrinous pericarditis. Polymerase chain reaction (PCR) on viral and bacterial RNA and DNA of potentially cardiotropic agents remained negative. The pigtail catheter was left in place and 80 mg of gentamycin were given intrapericardially on day 1 and 2, followed by 500 mg of crystalloid triamcinolone acetate after the PCR was found to be negative. Oral treatment with 0.5 mg colchicine three times a day (off-label use) was started and maintained for 6 months. After 9 months no effusion was detected and the patient was free of symptoms. After exclusion of bacterial and viral pericardial infection, a high single dose of intrapericardial triamcinolone combined with long-term oral colchicine has proven to be a highly efficacious treatment of autoreactive pericarditis which will avoid relapses in most cases.

Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?

[Constrictive pericarditis: the story of a constrained heart].

Symptoms of constrictive pericarditis may be nonspecific, misleading and may delay or lead to an incorrect diagnosis. We present the case of a 28-year-old male who was admitted to the hospital with progressive dyspnea, thoracic pain and a history of 25 kg of weight gain during the last 2 years. He was evaluated at another facility and his clinical presentation led to an erroneous diagnosis of primary hepatic disease (cirrhosis and portal hypertension). Physical examination showed that he was dyspneic, emaciated, had marked distention of his frontal cranial veins, diminished heart sounds, massive ascites and leg edema. Laboratory tests reported abnormal liver function tests and abdominal paracentesis chylous ascites. Electrocardiogram showed sinus rhythm with generalized low voltage and nonspecific repolarization changes. Heart size was normal on chest radiography. Doppler echocardiography reported bilateral atrial dilatation, a thickened pericardium and a short deceleration time of transmitral flow. A thickened and calcified pericardium was seen on CT scan. Pericardiectomy was performed. Spontaneous polyuria was observed during and after surgery with subsequent improvement of ascites and edema. The pericardium was found to be grossly thickened and inflamed. Clinician must be aware of the slow and progressive course of right ventricular failure, as well as to recognize constrictive pericarditis as a cause of chronic ascites.The hemodynamic aspects of the disease are of paramount importance for early diagnosis and opportune treatment.

InternalMed_Harrison

Viral or idiopathic acute pericarditis occurs at all ages but is more common in young adults and is often associated with pleural effusions and pneumonitis. The almost simultaneous development of fever and precordial pain, often 10–12 days after a presumed viral illness, constitutes an important feature in the differentiation of acute pericarditis from AMI, in which chest pain precedes fever. The constitutional symptoms are usually mild to moderate, and a pericardial friction rub is often audible. The disease ordinarily runs its course in a few days to 4 weeks. The ST-segment alterations in the ECG usually disappear after 1 or more weeks, but the abnormal T waves may persist for several years and be a source of confusion in persons without a clear history of pericarditis. Pleuritis and pneumonitis frequently accompany viral or idiopathic acute pericarditis. Accumulation of some pericardial fluid is common, and both tamponade and constrictive pericarditis are possible, but infrequent,

Myocardial infarction diagnosis

Physical examination The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular. If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung. Electrocardiogram

Purulent Pericarditis Due to an Infected Pacemaker Lead.

Intravenous drug users have a substantially increased risk of infective endocarditis, especially in the setting of implanted cardiac devices. Purulent pericarditis is a rare occurrence that can occur iatrogenically or through direct or hematogenous spread. A 75 year old man with a past medical history significant for hepatitis C, IV drug abuse, and sick sinus syndrome status post pacemaker was brought in by EMS with a chief complaint of diaphoresis and chest pain. Initial EKG revealed atrial fibrillation with ST elevations in multiple leads. The patient was taken urgently to the cardiac catheterization lab due to concern for STEMI. Left heart catheterization revealed nonobstructive CAD; bedside echo was significant for a pericardial effusion and a pacemaker lead vegetation. CT of the chest revealed extension of the ventricular pacemaker lead through the anterior right ventricular wall and pericardium and into the pleural cavity. Cardiothoracic surgery performed a pacemaker removal as well as pericardial window due to early tamponade; approximately 900 mL of purulent fluid was drained from the pericardial space. The patient was septic with initial blood cultures growing MSSA. He was also found to have multiple other foci of infection including a left-sided pleural effusion and a perihepatic fluid collection, both of which were drained and also grew out MSSA. The patient initially improved on antibiotics after his pacemaker removal and drainage of the infected fluid collections. However, several days after the pacemaker removal he gradually became more bradycardic; due to his multiple comorbidities and active infection, he was not a candidate for a replacement implanted pacemaker. He became profoundly bradycardic and hypotensive overnight and died despite the use of multiple pressors to maintain his blood pressure as well as transcutaneous pacing to maintain his heart rate. Purulent pericarditis has become a relatively uncommon occurrence since the development of effective antibiotics. This case illustrates a rare example of purulent pericarditis and cardiac tamponade secondary to the extension of an infected pacemaker wire through the pericardium and into the thoracic cavity. The presence of multiple other infected fluid collections in this case also illustrates the need to thoroughly assess for secondary foci of infection in cases of bacterial endocarditis.

Kussmaul's sign

Causes The differential diagnoses of Kussmaul's sign includes constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure. With cardiac tamponade, jugular veins are distended and typically show a prominent x descent and an absent y descent as opposed to patients with constrictive pericarditis (prominent x and y descent), see Beck's triad. Other possible causes of Kussmaul's sign include: Right ventricular infarction - low ventricular compliance Right heart failure Cardiac tumours Tricuspid stenosis Restrictive cardiomyopathy Pulmonary embolism Constrictive pericarditis History Kussmaul's sign is named after the German doctor who first described it, Adolph Kussmaul (1822-1902). He is also credited with describing Kussmaul breathing. See also Pulsus paradoxus References Symptoms and signs: Vascular

InternalMed_Harrison

Additional clues to the etiology and importance of a heart murmur can be gleaned from the history and other physical examination findings. Symptoms suggestive of cardiovascular, neurologic, or pulmonary disease help focus the differential diagnosis, as do findings relevant to the jugular venous pressure and waveforms, the arterial pulses, other heart sounds, the lungs, the abdomen, the skin, and the extremities. In many instances, laboratory studies, an ECG, and/or a chest x-ray may have been obtained earlier and may contain valuable information. A patient with suspected infective endocarditis, for example, may have a murmur in the setting of fever, chills, anorexia, fatigue, dyspnea, splenomegaly, petechiae, and positive blood cultures. A new systolic murmur in a patient with a marked fall in blood pressure after a recent MI suggests myocardial rupture. By contrast, an isolated grade 1 or 2 mid-systolic murmur at the left sternal border in a healthy, active, and asymptomatic young

Heart

Pericardial disease The sac which surrounds the heart, called the pericardium, can become inflamed in a condition known as pericarditis. This condition typically causes chest pain that may spread to the back, and is often caused by a viral infection (glandular fever, cytomegalovirus, or coxsackievirus). Fluid can build up within the pericardial sac, referred to as a pericardial effusion. Pericardial effusions often occur secondary to pericarditis, kidney failure, or tumours, and frequently do not cause any symptoms. However, large effusions or effusions which accumulate rapidly can compress the heart in a condition known as cardiac tamponade, causing breathlessness and potentially fatal low blood pressure. Fluid can be removed from the pericardial space for diagnosis or to relieve tamponade using a syringe in a procedure called pericardiocentesis. Congenital heart disease

Jugular venous pressure

Prominent 'x' descent Cardiac tamponade Slow 'y' descent Tricuspid stenosis Cardiac tamponade Prominent & deep 'y' descent Constrictive pericarditis Parodoxical JVP (Kussmaul's sign: JVP rises with inspiration, drops with expiration) Pericardial effusion Constrictive pericarditis Pericardial tamponade

A case of dilated cardiomyopathy.

Dilated cardiomyopathy is a significant health problem in Africa. Diagnosis and treatment can be challenging as it frequently affects young patients and those without risk factors for cardiac disease. A previously well HIV negative 17 year old boy presented to Mseleni hospital in December 2011 with a short history of worsening shortness of breath on exertion. The history had been preceded by a brief upper respiratory tract infection with general malaise and headache, from which he had recovered fully. On examination, he was clammy, peripherally shut down and clearly in respiratory distress. He had a raised jugular venous pressure (JVP) and palpable displaced apex beat. He had a loud P2, third heart sound and pansystolic murmur over the apex. He had scattered inspiratory crepitations bibasally. Routine blood tests on admission, including malaria and viral serology, were unremarkable. A chest x-ray showed a grossly dilated cardiac shadow and enlarged pulmonary trunk. A cardiac ultrasound ruled out pericardial effusion but did show a dilated and hypokinetic left ventricle. He was diagnosed with dilated cardiomyopathy secondary to a viral infection and managed accordingly. Dilated cardiomyopathy, although rare worldwide, is a significant problem throughout Africa. It has been shown to account for up to 48% of admissions with heart failure. Its aetiology is multifactorial and includes exposure to toxins and infectious agents. Presenting symptoms can be vague but improved prognosis and outcomes require prompt diagnosis and appropriate management.

Pericarditis

Complications Pericarditis can progress to pericardial effusion and eventually cardiac tamponade. This can be seen in people who are experiencing the classic signs of pericarditis but then show signs of relief, and progress to show signs of cardiac tamponade which include decreased alertness and lethargy, pulsus paradoxus (decrease of at least 10 mmHg of the systolic blood pressure upon inspiration), low blood pressure (due to decreased cardiac index), (jugular vein distention from right sided heart failure and fluid overload), distant heart sounds on auscultation, and equilibration of all the diastolic blood pressures on cardiac catheterization due to the constriction of the pericardium by the fluid.

A 63-year-old woman with a pericardial effusion, bilateral pleural effusions, and ascites: is the whole greater than the sum of its parts?

A 63-year-old female presented with dyspnea, leg edema, and abdominal distention. Exam revealed blood pressure of 104/58, pulse 108/min, jugular venous pressure of 8 cm, no pulsus paradoxus, a pericardial rub, muffled heart sounds, decreased basilar breath sounds, ascites, and ankle edema. Electrocardiogram showed low voltage. Imaging revealed thickened pericardium and a pericardial effusion. Hemodynamic tracings postpericardiocentesis revealed elevated right-sided pressures. The patient was diagnosed with effusive constrictive pericarditis. The case and review of this condition are described. Patients with a pericardial effusion and symptoms unresponsive to pericardiocentesis or with pericardial thickening should undergo evaluation for effusive-constrictive pericarditis.

Acute pericarditis

Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease. Prognosis One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Beck's triad). This condition can be fatal if not immediately treated.

Pericardial effusion

Signs and symptoms Pericardial effusion presentation varies from person to person depending on the size, acuity and underlying cause of the effusion. Some people may be asymptomatic and the effusion may be an incidental finding on an examination. Others with larger effusions may present with chest pressure or pain, dyspnea, shortness of breath, and malaise (a general feeling of discomfort or illness). Yet others with cardiac tamponade, a life-threatening complication, may present with dyspnea, low blood pressure, weakness, restlessness, hyperventilation (rapid breathing), discomfort with laying flat, dizziness, syncope or even loss of consciousness. This causes a type of shock, called obstructive shock, which can lead to organ damage.

Cardiac tamponade

Diagnosis may be suspected based on low blood pressure, jugular venous distension, or quiet heart sounds (together known as Beck's triad). A pericardial rub may be present in cases due to inflammation. The diagnosis may be further supported by specific electrocardiogram (ECG) changes, chest X-ray, or an ultrasound of the heart. If fluid increases slowly the pericardial sac can expand to contain more than 2 liters; however, if the increase is rapid, as little as 200 mL can result in tamponade.

InternalMed_Harrison

or absence of a third heart sound (S3). Accurate characterization of cardiac murmurs provides important insight into the natural history of many valvular and congenital heart lesions. Finally, the important role played by the physical examination in enhancing the clinician-patient relationship cannot be overestimated. THE GENERAL PHYSICAL EXAMINATION Any examination begins with an assessment of the general appear-ance of the patient, with notation of age, posture, demeanor, and 267 SEC Tion 2 DiAgnoSiS oF CARDiovASCulAR DiSoRDERS overall health status. Is the patient in pain or resting quietly, dyspneic or diaphoretic? Does the patient choose to avoid certain body positions to reduce or eliminate pain, as might be the case with suspected acute pericarditis? Are there clues indicating that dyspnea may have a pulmonary cause, such as a barrel chest deformity with an increased anterior-posterior diameter, tachypnea, and pursed-lip breathing? Skin pallor, cyanosis, and jaundice can be

Case Report: ST-Segment Elevation in a Man With Acute Pericarditis.

<bBackground:</b Acute pericarditis is a rapid inflammatory condition of the pericardium with both infectious and non-infectious etiology. Most acute pericarditis is self-limited, with a small portion evolving rapidly. The definitive diagnosis of acute pericarditis often requires detailed physical examination, ECG, echocardiography, blood analysis and chest X-ray. It's usually challenging to distinguish acute pericarditis from ST-elevated myocardial infarction (STEMI) due to the similar ECG characteristics (ST segment change). Here we present a case of purulent pericarditis probably caused by esophageal perforation. <bCase:</b A 52 year-old male presented with chest pain and dyspnea for 16 h. ST-segment elevation and positive cardiac markers lead to the initial diagnosis of ST-elevated myocardial infarction. Coronary angiography demonstrated normal coronary artery, while transthoracic echocardiography (TTE) showed massive pericardial effusion. Then, pericardiocentesis was performed with 250 ml of yellowish-green pus-like fluid extracted. A detailed history examination revealed a week history of possible esophageal perforation caused by a fishbone. And a further computed tomography (CT) demonstrated the presence of pneumomediastinum, and effusions in mediastinum, which lead to the diagnosis of purulent pericarditis. However, the patient's family refused further treatment and the patient died soon after discharge. <bConclusion:</b The differential diagnosis of chest pain should include acute pericarditis, which can be equally critical and fatal. And it's important to note the peculiar characteristics of acute pericarditis, which include concave and diffused ST-segment elevation, PR segment depression, and the ratio of ST-segment elevation to T wave >0.24 in lead V6. Moreover, comprehensive medical history and physical examination are crucial to the differential diagnosis of chest pain patients.

Cardiac Tamponade -- History and Physical

Patients with cardiac tamponade present similar to patients with other forms of cardiogenic or obstructive shock. They may endorse vague symptoms of chest pain, palpitations, shortness of breath, or in more severe cases, dizziness, syncope, and altered mental status.  They may also present in a pulseless electrical activity cardiac arrest. The classic physical findings in cardiac tamponade included in Beck’s triad are hypotension, jugular venous distension, and muffled heart sounds. Pulsus paradoxus, which is a decrease in systolic blood pressure by more than 10 mm Hg with inspiration is an important physical exam finding that suggests a pericardial effusion is causing cardiac tamponade. Pulsus paradoxus may be absent in patients with ASD, elevated diastolic pressures, pulmonary hypertension and aortic regurgitation. The Kussmaul sign - a paradoxical elevated in JVP and pressure during inspiration is sometimes seen in cardiac tamponade.

Constrictive-Effusive Pericarditis -- History and Physical

In effusive-constrictive pericarditis, patients commonly present with chronic symptoms that mimic volume overload. These include jugular venous distension, ascites, hepatomegaly, peripheral edema, and pleural effusions. Tachycardia occurs reflexively due to decreased cardiac output. Other signs and symptoms of decreased cardiac output include increased fatigue, hypotension, altered mental status, dyspnea, and tachypnea. Signs of active pericarditis may also ensue, including fever, pleuritic substernal chest pain, and a pericardial friction rub. Jugular venous distention also occurs due to decreased right heart filling and subsequent backup into the venous system.

Cardiac Syncope -- History and Physical

A careful physical exam will assess heart rate and rhythm. Any abnormalities will increase suspicion of cardiac arrhythmia. In addition, an elevated respiratory rate or hypoxia will increase suspicion of a pulmonary embolism. Jugular venous distention and hypotension are suggestive signs of an obstructive mechanical cardiac etiology. Pathological cardiac murmurs, specifically new ones, will clue one into a valvular etiology, hypertrophic cardiomyopathy, or an obstructive intracardiac lesion. Muffled sounds can be heard with pericardial tamponade. Pedal edema or other evidence of deep venous thrombosis increases a patient's risk of pulmonary embolism. [10]

[Lassa fever associated with effusive constrictive pericarditis and bilateral atrioventricular annular constriction: a case report].

A case of Lassa fever associated with effusive constrictive pericarditis and bilateral atrioventricular annular constriction was reported. A 49-year-old man, who had been diagnosed by indirect fluorescent antibody test as the first case of Lassa fever in Japan, was referred to the Hiroo Hospital because of syncope, progressive hepatomegaly, ascites and pericardial effusion in spite of pericardiocentesis and corticosteroid therapy. On admission, his blood pressure was 92/60 mmHg and he had a paradoxical pulse. Two-dimensional echocardiography revealed a localized pericardial effusion adjacent to the right ventricular wall and behind the left ventricular posterior wall. Bilateral atrioventricular annular constriction was also present. On pulsed Doppler echocardiography, the peak inflow velocities of the right and left ventricles increased during atrial systole. Right heart catheterization revealed a mean diastolic pressure gradient of 8 mmHg across the tricuspid valve. After pericardiectomy, a diastolic dip and plateau pattern became evident in the right ventricular pressure tracing, suggesting the presence of residual constriction. However, the atrioventricular annular constriction was no longer evident on two-dimensional echocardiography. This is considered the first reported case of subacute effusive constrictive pericarditis caused by Lassa fever.

Acquired Immune Deficiency Syndrome -- History and Physical -- Cardiac System [8]

HIV infection and ART likely contribute to increased cardiovascular disease in patients. Common presenting symptoms may include chest pain, shortness of breath, or fatigue. The examination should proceed as one would when assessing for acute coronary syndrome or valvular disease, palpating for chest wall pain, observing for jugular venous distension and peripheral edema, and auscultating for abnormal heart sounds, murmurs, or evidence of pulmonary edema. Cardiovascular AIDS-related illnesses could include purulent pericarditis or cardiac tamponade caused by Mycobacterium tuberculosis . If these conditions are suspected, observing for Beck’s triad of low blood pressure, jugular venous distension, and muffled heart sounds may confirm a compressive pericardial effusion.

Dilated cardiomyopathy

Signs and symptoms Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include: Shortness of breath Syncope (fainting) Angina, but only in the presence of ischemic heart disease A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

Acute Influenza Infection Presenting with Cardiac Tamponade: A Case Report and Review of Literature.

Cardiac complications associated with influenza infection can occur either via a direct effect of the virus on the heart or through exacerbation of preexisting cardiovascular disease. We present a case of a 57-year-old man with acute influenza infection complicated by pericardial effusion and cardiac tamponade. A 57-year-old white man presented to the Emergency Department with sudden onset of severe, nonexertional, retrosternal, pressure-like chest pain for a few hours and with fever and muscle aches for 2 days. The patient was initially admitted because of suspected acute coronary syndrome. The next morning, he complained of acute-onset shortness of breath and had hypotension and tachycardia. On examination, his peripheral extremities were cold and heart sounds were distant. Pulsus paradoxus was 20 mmHg. The electrocardiogram showed low-voltage QRS complex with electrical alternans. An urgently performed bedside echocardiogram showed moderate pericardial effusion with a small right ventricular cavity with diastolic collapse. Emergent pericardiocentesis was performed, with removal of 250 mL of fluid from the pericardial space. The patient's hemodynamic status immediately improved. Analyses of pericardial fluid demonstrated no bacteria, acid-fast bacilli, or malignant cells. The result of a rapid influenza diagnostic test with polymerase chain reaction was positive for influenza A virus, with other viral panels yielding normal results. The patient was treated with oseltamivir for 5 days. Pericardial involvement is a rare and perhaps underreported complication of influenza infection. Early recognition of cardiac symptoms and appropriate diagnostic workup in a patient presenting with influenza-like symptoms is important to avoid life-threatening complications.

InternalMed_Harrison

Subacute Effusive-Constrictive Pericarditis This form of pericardial disease is characterized by the combination of a tense effusion in the pericardial space and constriction of the heart by thickened pericardium. It shares a number of features with both chronic pericardial effusion producing cardiac compression and with pericardial constriction. It may be caused by tuberculosis (see below), multiple attacks of acute idiopathic pericarditis, radiation, traumatic pericarditis, renal failure, scleroderma, and neoplasms. The heart is generally enlarged, and a paradoxical pulse and a prominent x descent (without a prominent y descent) are present in the atrial and jugular venous pressure pulses. After pericardiocentesis, the physiologic findings may change from those of cardiac tamponade to those of pericardial constriction. Furthermore, the intrapericardial pressure and the central venous pressure may decline, but not to normal. The diagnosis can be established by pericardiocentesis

Jugular venous pressure

An exaggerated "y" wave or diastolic collapse of the neck veins from constrictive pericarditis is referred to as Friedreich's sign. Raised JVP, normal waveform Bradycardia Fluid overload Heart failure Raised JVP, absent pulsation Superior vena cava syndrome Large 'a' wave (increased atrial contraction pressure) Tricuspid stenosis Right heart failure Pulmonary hypertension Cannon 'a' wave (atria contracting against closed tricuspid valve) Atrial flutter Premature atrial rhythm (or tachycardia) Third degree heart block Ventricular ectopics Ventricular tachycardia Absent 'a' wave (no unifocal atrial depolarisation) Atrial fibrillation Large 'v' wave (c–v wave) Tricuspid regurgitation Absent 'x' descent Tricuspid regurgitation (sometimes 'x' wave is replaced by a positive wave) Prominent 'x' descent Cardiac tamponade Slow 'y' descent Tricuspid stenosis Cardiac tamponade Prominent & deep 'y' descent Constrictive pericarditis