Rheumatoid arthritis is a symmetrical, polyarthritis that is characterized by early morning joint pain and stiffness. A positive prognosis is associated with negative anti-CCP antibodies and negative rheumatoid factor. When anti-CCP antibodies are present, they are usually seen in conjunction with positive rheumatoid factor, which is a strong predictor of early transformation from transient to persistent synovitis. A gradual onset of symptoms is also linked to a poor prognosis for rheumatoid arthritis, rather than a sudden onset. Additionally, female gender is associated with a worse prognosis for rheumatoid arthritis, while male gender is not. Finally, HLA-B27 is not associated with rheumatoid arthritis, but rather with seronegative spondyloarthropathies like psoriatic and reactive arthritis.

Prognostic Features of Rheumatoid Arthritis

A number of factors have been identified as predictors of a poor prognosis in patients with rheumatoid arthritis. These include being rheumatoid factor positive, having anti-CCP antibodies, presenting with poor functional status, showing early erosions on X-rays, having extra-articular features such as nodules, possessing the HLA DR4 gene, and experiencing an insidious onset. While there is some discrepancy regarding the association between gender and prognosis, both the American College of Rheumatology and the recent NICE guidelines suggest that female gender is linked to a poorer prognosis. It is important for healthcare professionals to be aware of these prognostic features in order to provide appropriate management and support for patients with rheumatoid arthritis.

The reactivation of TB is a possible side effect of TNF-α inhibitors.

Managing Rheumatoid Arthritis with Disease-Modifying Therapies

The management of rheumatoid arthritis (RA) has significantly improved with the introduction of disease-modifying therapies (DMARDs) in the past decade. Patients with joint inflammation should start a combination of DMARDs as soon as possible, along with analgesia, physiotherapy, and surgery. In 2018, NICE updated their guidelines for RA management, recommending DMARD monotherapy with a short course of bridging prednisolone as the initial step. Monitoring response to treatment is crucial, and NICE suggests using a combination of CRP and disease activity to assess it. Flares of RA are often managed with corticosteroids, while methotrexate is the most widely used DMARD. Other DMARDs include sulfasalazine, leflunomide, and hydroxychloroquine. TNF-inhibitors are indicated for patients with an inadequate response to at least two DMARDs, including methotrexate. Etanercept, infliximab, and adalimumab are some of the TNF-inhibitors available, each with their own risks and administration methods. Rituximab and Abatacept are other DMARDs that can be used, but the latter is not currently recommended by NICE.

Understanding Osteoporotic Vertebral Fractures

Osteoporotic vertebral fractures are a common consequence of osteoporosis, a condition where bones gradually decrease in bone mineral density, leading to an increased risk of fragility fractures. These fractures often present with acute onset back pain, but patients can also be asymptomatic. Osteoporosis is more prevalent in females than males, with a male-to-female ratio of 1:6. Advancing age is a major risk factor for osteoporotic fractures, with women over 65 and men over 75 being at increased risk. Other risk factors include a previous history of fragility fractures, frequent or prolonged use of glucocorticoids, history of falls, family history of hip fracture, alternative causes of secondary osteoporosis, low BMI, tobacco smoking, and high alcohol intake.

Patients with osteoporotic vertebral fractures may present with acute back pain, breathing difficulties, gastrointestinal problems, loss of height, kyphosis, and localised tenderness on palpation of spinous processes at the fracture site. X-ray of the spine is the first investigation ordered, which may show wedging of the vertebra due to compression of the bone. Other investigations such as CT spine and MRI spine may be used to visualise the extent/features of the fracture more clearly and differentiate osteoporotic fractures from those caused by another pathology.

To assess the likelihood of future fractures, risk factors are taken into account, and a dual-energy X-ray absorptiometry (DEXA) scan should be considered. The FRAX tool or QFracture tool can be used to estimate the 10-year risk of a fracture. These tools require the clinician to input patient information into a form, which is then used by the programme to calculate the risk. Understanding osteoporotic vertebral fractures and their risk factors is crucial in preventing and managing this condition.

Prescribing folate alongside methotrexate is an effective way to decrease the risk of myelosuppression. This patient’s symptoms suggest that she may have rheumatoid arthritis, which is often treated with methotrexate as a first-line option. However, methotrexate can inhibit dihydrofolate reductase, an enzyme involved in folate metabolism, which can lead to bone marrow suppression. To prevent this, folate is prescribed alongside methotrexate to ensure that the patient’s red blood cells, white blood cells, and platelets are not reduced to dangerous levels.

B12 supplementation is not necessary in this case, as methotrexate is not known to cause deficiencies in B12. Calcium and vitamin D supplementation may be considered if blood tests or symptoms indicate a deficiency, but they are not necessary at this time. Similarly, bisphosphonates are not needed as the patient is not at significant risk of osteoporosis due to her short-term use of corticosteroids.

Methotrexate: An Antimetabolite with Potentially Life-Threatening Side Effects

Methotrexate is an antimetabolite drug that inhibits the enzyme dihydrofolate reductase, which is essential for the synthesis of purines and pyrimidines. It is commonly used to treat inflammatory arthritis, psoriasis, and some types of leukemia. However, it is considered an important drug due to its potential for life-threatening side effects. Careful prescribing and close monitoring are essential to ensure patient safety.

The adverse effects of methotrexate include mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis. The most common pulmonary manifestation is pneumonitis, which typically develops within a year of starting treatment and presents with non-productive cough, dyspnea, malaise, and fever. Women should avoid pregnancy for at least 6 months after treatment has stopped, and men using methotrexate need to use effective contraception for at least 6 months after treatment.

When prescribing methotrexate, it is important to follow guidelines and monitor patients regularly. Methotrexate is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. The starting dose is 7.5 mg weekly, and folic acid 5mg once weekly should be co-prescribed, taken more than 24 hours after the methotrexate dose. Only one strength of methotrexate tablet should be prescribed, usually 2.5 mg. It is also important to avoid prescribing trimethoprim or co-trimoxazole concurrently, as it increases the risk of marrow aplasia, and high-dose aspirin increases the risk of methotrexate toxicity.

In case of methotrexate toxicity, the treatment of choice is folinic acid. Methotrexate is a drug with a high potential for patient harm, and it is crucial to be familiar with guidelines relating to its use to ensure patient safety.

The most specific test for limited cutaneous systemic sclerosis among patients with systemic sclerosis is the anti-centromere antibodies.

Understanding Systemic Sclerosis

Systemic sclerosis is a condition that affects the skin and other connective tissues, but its cause is unknown. It is more common in females, with three patterns of the disease. Limited cutaneous systemic sclerosis is characterised by Raynaud’s as the first sign, affecting the face and distal limbs, and associated with anti-centromere antibodies. CREST syndrome is a subtype of limited systemic sclerosis that includes Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, and Telangiectasia. Diffuse cutaneous systemic sclerosis affects the trunk and proximal limbs, associated with scl-70 antibodies, and has a poor prognosis. Respiratory involvement is the most common cause of death, with interstitial lung disease and pulmonary arterial hypertension being the primary complications. Renal disease and hypertension are also possible complications, and patients with renal disease should be started on an ACE inhibitor. Scleroderma without internal organ involvement is characterised by tightening and fibrosis of the skin, manifesting as plaques or linear. Antibodies such as ANA, RF, anti-scl-70, and anti-centromere are associated with different types of systemic sclerosis.

During active SLE, complement levels tend to decrease due to the formation of complexes that consume complement. As a result, monitoring complement levels can be useful in tracking SLE flares. In contrast, CRP is not a reliable marker of disease activity as it may remain normal unless there is an infection or serositis. ESR is a better indicator for monitoring disease activity. Additionally, high levels of anti-dsDNA titres are typically observed during active SLE and can also be used for disease monitoring.

Systemic lupus erythematosus (SLE) can be investigated through various tests, including antibody tests. ANA testing is highly sensitive, making it useful for ruling out SLE, but it has low specificity. About 99% of SLE patients are ANA positive. Rheumatoid factor testing is positive in 20% of SLE patients. Anti-dsDNA testing is highly specific (>99%), but less sensitive (70%). Anti-Smith testing is also highly specific (>99%), but only 30% of SLE patients test positive. Other antibody tests include anti-U1 RNP, SS-A (anti-Ro), and SS-B (anti-La).

Monitoring of SLE can be done through various markers, including inflammatory markers such as ESR. During active disease, CRP levels may be normal, but a raised CRP may indicate an underlying infection. Complement levels (C3, C4) are low during active disease due to the formation of complexes that lead to the consumption of complement. Anti-dsDNA titres can also be used for disease monitoring, but it is important to note that they are not present in all SLE patients. Proper monitoring of SLE is crucial for effective management of the disease.

If a patient presents with renal impairment, respiratory symptoms, joint pain, and systemic features, ANCA associated vasculitis should be considered. Granulomatosis with polyangiitis (Wegener’s granulomatosis) is a type of ANCA associated vasculitis that often presents with these symptoms, as well as ENT symptoms. A chest X-ray may show nodular, fibrotic, or infiltrative opacities. The best diagnostic test for granulomatosis with polyangiitis is cANCA. ANA is typically associated with autoimmune conditions like SLE, systemic sclerosis, Sjogren’s syndrome, and autoimmune hepatitis. pANCA is more specific for eosinophilic granulomatosis with polyangiitis (Churg-Strauss), which presents with asthma and eosinophilia and is often associated with conditions like ulcerative colitis, primary sclerosing cholangitis, and anti-GBM disease. If a patient presents with haemoptysis, weight loss, and cavitary lesions on chest X-ray, sputum acid-fast stain would be the appropriate diagnostic test for tuberculosis. However, if the patient also has haematuria, arthralgia, sinusitis, and epistaxis, granulomatosis with polyangiitis is more likely.

ANCA Associated Vasculitis: Common Findings and Management

Anti-neutrophil cytoplasmic antibodies (ANCA) are associated with small-vessel vasculitides such as granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, and microscopic polyangiitis. ANCA associated vasculitis is more common in older individuals and presents with renal impairment, respiratory symptoms, systemic symptoms, and sometimes a vasculitic rash or ear, nose, and throat symptoms. First-line investigations include urinalysis, blood tests for renal function and inflammation, ANCA testing, and chest x-ray. There are two main types of ANCA – cytoplasmic (cANCA) and perinuclear (pANCA) – with varying levels found in different conditions. ANCA associated vasculitis should be managed by specialist teams and the mainstay of treatment is immunosuppressive therapy.

ANCA associated vasculitis is a group of small-vessel vasculitides that are associated with ANCA. These conditions are more common in older individuals and present with renal impairment, respiratory symptoms, systemic symptoms, and sometimes a vasculitic rash or ear, nose, and throat symptoms. To diagnose ANCA associated vasculitis, first-line investigations include urinalysis, blood tests for renal function and inflammation, ANCA testing, and chest x-ray. There are two main types of ANCA – cytoplasmic (cANCA) and perinuclear (pANCA) – with varying levels found in different conditions. ANCA associated vasculitis should be managed by specialist teams and the mainstay of treatment is immunosuppressive therapy.

Common Causes of Elbow Pain

Elbow pain can be caused by a variety of conditions, each with their own characteristic features. Lateral epicondylitis, also known as tennis elbow, is characterized by pain and tenderness localized to the lateral epicondyle. Pain is worsened by resisted wrist extension with the elbow extended or supination of the forearm with the elbow extended. Episodes typically last between 6 months and 2 years, with acute pain lasting for 6-12 weeks.

Medial epicondylitis, or golfer’s elbow, is characterized by pain and tenderness localized to the medial epicondyle. Pain is aggravated by wrist flexion and pronation, and symptoms may be accompanied by numbness or tingling in the 4th and 5th finger due to ulnar nerve involvement.

Radial tunnel syndrome is most commonly due to compression of the posterior interosseous branch of the radial nerve, and is thought to be a result of overuse. Symptoms are similar to lateral epicondylitis, but the pain tends to be around 4-5 cm distal to the lateral epicondyle. Symptoms may be worsened by extending the elbow and pronating the forearm.

Cubital tunnel syndrome is due to the compression of the ulnar nerve. Initially, patients may experience intermittent tingling in the 4th and 5th finger, which may be worse when the elbow is resting on a firm surface or flexed for extended periods. Later, numbness in the 4th and 5th finger with associated weakness may occur.

Olecranon bursitis is characterized by swelling over the posterior aspect of the elbow, with associated pain, warmth, and erythema. It typically affects middle-aged male patients. Understanding the characteristic features of these conditions can aid in their diagnosis and treatment.

Understanding Gout: Symptoms and Diagnosis

Gout is a type of arthritis that causes inflammation and pain in the joints. Patients experience episodes of intense pain that can last for several days, followed by periods of no symptoms. The acute episodes usually reach their peak within 12 hours and are characterized by significant pain, swelling, and redness. The most commonly affected joint is the first metatarsophalangeal joint, but other joints such as the ankle, wrist, and knee can also be affected. If left untreated, repeated acute episodes of gout can lead to chronic joint problems.

To diagnose gout, doctors may perform a synovial fluid analysis to look for needle-shaped, negatively birefringent monosodium urate crystals under polarized light. Uric acid levels may also be checked once the acute episode has subsided, as they can be high, normal, or low during the attack. Radiological features of gout include joint effusion, well-defined punched-out erosions with sclerotic margins in a juxta-articular distribution, and eccentric erosions. Unlike rheumatoid arthritis, there is no periarticular osteopenia, and soft tissue tophi may be visible.

Psoriatic arthropathy is a type of inflammatory arthritis that is associated with psoriasis. It is classified as one of the seronegative spondyloarthropathies and is known to have a poor correlation with cutaneous psoriasis. In fact, it often precedes the development of skin lesions. This condition affects both males and females equally, with around 10-20% of patients with skin lesions developing an arthropathy.

The presentation of psoriatic arthropathy can vary, with different patterns of joint involvement. The most common type is symmetric polyarthritis, which is very similar to rheumatoid arthritis and affects around 30-40% of cases. Asymmetrical oligoarthritis is another type, which typically affects the hands and feet and accounts for 20-30% of cases. Sacroiliitis, DIP joint disease, and arthritis mutilans (severe deformity of fingers/hand) are other patterns of joint involvement. Other signs of psoriatic arthropathy include psoriatic skin lesions, periarticular disease, enthesitis, tenosynovitis, dactylitis, and nail changes.

To diagnose psoriatic arthropathy, X-rays are often used. These can reveal erosive changes and new bone formation, as well as periostitis and a pencil-in-cup appearance. Management of this condition should be done by a rheumatologist, and treatment is similar to that of rheumatoid arthritis. However, there are some differences, such as the use of monoclonal antibodies like ustekinumab and secukinumab. Mild peripheral arthritis or mild axial disease may be treated with NSAIDs alone, rather than all patients being on disease-modifying therapy as with RA. Overall, psoriatic arthropathy has a better prognosis than RA.

AMA (Anti-mitochondrial antibodies)

Understanding Systemic Sclerosis

Systemic sclerosis is a condition that affects the skin and other connective tissues, but its cause is unknown. It is more common in females, with three patterns of the disease. Limited cutaneous systemic sclerosis is characterised by Raynaud’s as the first sign, affecting the face and distal limbs, and associated with anti-centromere antibodies. CREST syndrome is a subtype of limited systemic sclerosis that includes Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, and Telangiectasia. Diffuse cutaneous systemic sclerosis affects the trunk and proximal limbs, associated with scl-70 antibodies, and has a poor prognosis. Respiratory involvement is the most common cause of death, with interstitial lung disease and pulmonary arterial hypertension being the primary complications. Renal disease and hypertension are also possible complications, and patients with renal disease should be started on an ACE inhibitor. Scleroderma without internal organ involvement is characterised by tightening and fibrosis of the skin, manifesting as plaques or linear. Antibodies such as ANA, RF, anti-scl-70, and anti-centromere are associated with different types of systemic sclerosis.

The flexor retinaculum is the only structure that is divided in the surgical treatment of carpal tunnel syndrome. It is important to protect all other structures during the procedure as damaging them could result in further injury or disability. The purpose of dividing the flexor retinaculum is to decompress the median nerve.

Understanding Carpal Tunnel Syndrome

Carpal tunnel syndrome is a condition that occurs when the median nerve in the carpal tunnel is compressed. Patients with this condition typically experience pain or pins and needles in their thumb, index, and middle fingers. In some cases, the symptoms may even ascend proximally. Patients often shake their hand to obtain relief, especially at night.

During an examination, doctors may observe weakness of thumb abduction and wasting of the thenar eminence (not the hypothenar). Tapping on the affected area may cause paraesthesia, which is known as Tinel’s sign. Flexion of the wrist may also cause symptoms, which is known as Phalen’s sign.

Carpal tunnel syndrome can be caused by a variety of factors, including idiopathic reasons, pregnancy, oedema (such as heart failure), lunate fracture, and rheumatoid arthritis. Electrophysiology tests may show prolongation of the action potential in both motor and sensory nerves.

Treatment for carpal tunnel syndrome may include a 6-week trial of conservative treatments, such as corticosteroid injections and wrist splints at night. If symptoms persist or are severe, surgical decompression (flexor retinaculum division) may be necessary.

The triad of symptoms for this individual includes respiratory distress, neurological issues, and a petechial rash that typically appears after the first two symptoms. It is suspected that the individual may be experiencing fat embolism syndrome due to a recent injury and physical signs that align with this condition. Meningococcal sepsis is not typically associated with initial hypoxia, and pyrexia is not commonly linked to pulmonary emboli.

Understanding Fat Embolism: Diagnosis, Clinical Features, and Treatment

Fat embolism is a medical condition that occurs when fat globules enter the bloodstream and obstruct blood vessels. This condition is commonly seen in patients with long bone fractures, particularly in the femur and tibia. The diagnosis of fat embolism is based on clinical features, including respiratory symptoms such as tachypnea, dyspnea, and hypoxia, as well as dermatological symptoms such as a red or brown petechial rash. CNS symptoms such as confusion and agitation may also be present. Imaging may not always show vascular occlusion, but a ground glass appearance may be seen at the periphery.

Prompt fixation of long bone fractures is crucial in the treatment of fat embolism. However, there is some debate regarding the benefit versus risk of medullary reaming in femoral shaft or tibial fractures in terms of increasing the risk of fat embolism. DVT prophylaxis and general supportive care are also important in the management of this condition. While fat embolism can be a serious and potentially life-threatening condition, prompt diagnosis and treatment can improve outcomes for patients.

Reactive arthritis, also known as Reiter’s syndrome, can be effectively treated with NSAIDs if there are no contraindications. The patient’s presentation of asymmetrical oligoarthritis with accompanying dysuria and conjunctivitis, following a recent diarrhoea illness, is a classic indication of this condition. Reactive arthritis is typically caused by exposure to certain gastrointestinal and genitourinary infections, with Chlamydia trachomatis, Salmonella enterica, and Campylobacter jejuni being the most common culprits. In this case, NSAIDs should be the first-line treatment option. Intra-articular glucocorticoids may be considered for cases of reactive arthritis that are limited to a small number of joints and are unresponsive to NSAID treatment. Methotrexate may be used for chronic cases of reactive arthritis that do not respond to NSAIDs or glucocorticoids. Oral glucocorticoids may also be considered if NSAIDs fail to control symptoms.

Reactive arthritis is a type of seronegative spondyloarthropathy that is associated with HLA-B27. It was previously known as Reiter’s syndrome, which was characterized by a triad of urethritis, conjunctivitis, and arthritis following a dysenteric illness during World War II. However, further studies revealed that patients could also develop symptoms after a sexually transmitted infection, now referred to as sexually acquired reactive arthritis (SARA). Reactive arthritis is defined as arthritis that occurs after an infection where the organism cannot be found in the joint. The post-STI form is more common in men, while the post-dysenteric form has an equal incidence in both sexes. The most common organisms associated with reactive arthritis are listed in the table below.

Management of reactive arthritis is mainly symptomatic, with analgesia, NSAIDs, and intra-articular steroids being used. Sulfasalazine and methotrexate may be used for persistent disease. Symptoms usually last for less than 12 months. It is worth noting that the term Reiter’s syndrome is no longer used due to the fact that Reiter was a member of the Nazi party.

Understanding Drug-Induced Lupus

Drug-induced lupus is a condition that shares some similarities with systemic lupus erythematosus, but not all of its typical features are present. Unlike SLE, renal and nervous system involvement is rare in drug-induced lupus. The good news is that this condition usually resolves once the drug causing it is discontinued.

The most common symptoms of drug-induced lupus include joint pain, muscle pain, skin rashes (such as the malar rash), and pulmonary issues like pleurisy. In terms of laboratory findings, patients with drug-induced lupus typically test positive for ANA (antinuclear antibodies) but negative for dsDNA (double-stranded DNA) antibodies. Anti-histone antibodies are found in 80-90% of cases, while anti-Ro and anti-Smith antibodies are only present in around 5% of cases.

The most common drugs that can cause drug-induced lupus are procainamide and hydralazine. Other less common culprits include isoniazid, minocycline, and phenytoin.

In osteogenesis imperfecta, the levels of adjusted calcium, PTH, ALP, and PO4 are typically within the normal range. This rare genetic disorder is characterized by frequent bone fractures, blue-grey sclera, micrognathia, and kyphoscoliosis. Biochemical tests usually show normal levels of calcium, phosphate, and parathyroid hormone. If parathyroid hormone levels are elevated along with high calcium, it may indicate primary hyperparathyroidism caused by parathyroid adenoma, hyperplasia, or parathyroid cancer. On the other hand, elevated parathyroid hormone with low calcium may suggest secondary hyperparathyroidism due to kidney failure or vitamin D deficiency. Hypercalcemia without elevated parathyroid hormone may indicate primary malignancy or sarcoidosis. Hypocalcemia with low parathyroid hormone levels may suggest parathyroid dysfunction, which is commonly seen after thyroid or parathyroid surgery or as part of an autoimmune syndrome.

Osteogenesis imperfecta, also known as brittle bone disease, is a group of disorders that affect collagen metabolism, leading to bone fragility and fractures. The most common type of osteogenesis imperfecta is type 1, which is inherited in an autosomal dominant manner and is caused by a decrease in the synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides. This condition typically presents in childhood and is characterized by fractures that occur following minor trauma, as well as blue sclera, dental imperfections, and deafness due to otosclerosis.

When investigating osteogenesis imperfecta, it is important to note that adjusted calcium, phosphate, parathyroid hormone, and ALP results are usually normal. This condition can have a significant impact on a person’s quality of life, as it can lead to frequent fractures and other complications. However, with proper management and support, individuals with osteogenesis imperfecta can lead fulfilling lives.

The initial management for ankylosing spondylitis (AS) involves exercise regimes and NSAIDs. Intra articular steroids are not the primary treatment for AS, but may be considered by a rheumatologist if sacroiliitis is advanced or unresponsive to first-line therapies. DMARDs are not suitable for first-line treatment of AS and are typically used for other rheumatological conditions or when there is peripheral joint involvement in AS. The use of paracetamol and NSAIDs, or NSAIDs alone, is not effective in reducing back pain caused by AS.

Investigating and Managing Ankylosing Spondylitis

Ankylosing spondylitis is a type of spondyloarthropathy that is associated with HLA-B27. It is more commonly seen in males aged 20-30 years old. Inflammatory markers such as ESR and CRP are usually elevated, but normal levels do not necessarily rule out ankylosing spondylitis. HLA-B27 is not a reliable diagnostic tool as it can also be positive in normal individuals. The most effective way to diagnose ankylosing spondylitis is through a plain x-ray of the sacroiliac joints. However, if the x-ray is negative but suspicion for AS remains high, an MRI can be obtained to confirm the diagnosis.

Management of ankylosing spondylitis involves regular exercise, such as swimming, and the use of NSAIDs as the first-line treatment. Physiotherapy can also be helpful. Disease-modifying drugs used for rheumatoid arthritis, such as sulphasalazine, are only useful if there is peripheral joint involvement. Anti-TNF therapy, such as etanercept and adalimumab, should be given to patients with persistently high disease activity despite conventional treatments, according to the 2010 EULAR guidelines. Ongoing research is being conducted to determine whether anti-TNF therapies should be used earlier in the course of the disease. Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis, and ankylosis of the costovertebral joints.

The correct answer is engorged pale optic disc with blurred margins. This presentation is highly suggestive of polymyalgia rheumatica (PMR) in a female patient of this age, with preceding proximal muscle pain and stiffness that improves throughout the day. The current bilateral headaches and vision loss are likely due to giant cell arthritis (GCA), a complication strongly associated with PMR. GCA can cause anterior ischemic optic neuropathy, leading to optic disc pallor and swelling, as the immune system damages arteries supplying the optic nerve, leading to thrombus formation and occlusion. Cotton wool spots, hard exudates, and blot hemorrhages are incorrect, as they are seen in diabetic retinopathy, which is not present in this patient. Retinal whitening and a cherry red spot are also incorrect, as they describe central retinal artery occlusion (CRAO), which presents as sudden-onset painless visual loss, unlike the current presentation of GCA-induced vision loss.

Temporal arthritis, also known as giant cell arthritis, is a condition that affects medium and large-sized arteries and is of unknown cause. It typically occurs in individuals over the age of 50, with the highest incidence in those in their 70s. Early recognition and treatment are crucial to minimize the risk of complications, such as permanent loss of vision. Therefore, when temporal arthritis is suspected, urgent referral for assessment by a specialist and prompt treatment with high-dose prednisolone is necessary.

Temporal arthritis often overlaps with polymyalgia rheumatica, with around 50% of patients exhibiting features of both conditions. Symptoms of temporal arthritis include headache, jaw claudication, and tender, palpable temporal artery. Vision testing is a key investigation in all patients, as anterior ischemic optic neuropathy is the most common ocular complication. This results from occlusion of the posterior ciliary artery, leading to ischemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins. Other symptoms may include aching, morning stiffness in proximal limb muscles, lethargy, depression, low-grade fever, anorexia, and night sweats.

Investigations for temporal arthritis include raised inflammatory markers, such as an ESR greater than 50 mm/hr and elevated CRP. A temporal artery biopsy may also be performed, and skip lesions may be present. Treatment for temporal arthritis involves urgent high-dose glucocorticoids, which should be given as soon as the diagnosis is suspected and before the temporal artery biopsy. If there is no visual loss, high-dose prednisolone is used. If there is evolving visual loss, IV methylprednisolone is usually given prior to starting high-dose prednisolone. Urgent ophthalmology review is necessary, as visual damage is often irreversible. Other treatments may include bone protection with bisphosphonates and low-dose aspirin.

When a patient with a history of cancer complains of back pain, it is important to investigate further. Even if the pain seems to be caused by a simple musculoskeletal injury, there may be underlying issues related to the patient’s cancer history. In this case, the patient has three red flags that require urgent attention in a hospital setting: a history of cancer, thoracic back pain, and worsening pain when lying down (which could indicate pressure on a growth or tumor). The concern is that the back pain may be caused by spinal metastases, which can lead to cord compromise.

Performing a digital rectal exam (DRE) is not necessary in this case, as the patient does not exhibit symptoms of cauda equina syndrome or cord compromise. DRE is typically used to assess for reduced anal tone and saddle anesthesia, which are signs of cauda equina syndrome. This condition can cause sciatic-like lower back and leg pain.

While prescribing stronger pain medication may help alleviate the patient’s symptoms, the priority in managing this case is to rule out any serious underlying causes of the back pain. Physiotherapy may be helpful in managing musculoskeletal back pain, but it is important to first rule out the possibility of spinal metastases due to cancer recurrence.

An X-ray of the spine may not be sensitive enough to detect small lytic lesions or assess for canal compromise. It is typically only considered if there has been recent significant trauma or suspicion of osteoporotic vertebral collapse. In cases where metastases are suspected, an MRI or CT scan is preferred.

Lower back pain is a common issue that is often caused by muscular strain. However, it is important to be aware of potential underlying causes that may require specific treatment. Certain red flags should be considered, such as age under 20 or over 50, a history of cancer, night pain, trauma, or systemic illness. There are also specific causes of lower back pain that should be kept in mind. Facet joint pain may be acute or chronic, worse in the morning and on standing, and typically worsens with back extension. Spinal stenosis may cause leg pain, numbness, and weakness that is worse on walking and relieved by sitting or leaning forward. Ankylosing spondylitis is more common in young men and causes stiffness that is worse in the morning and improves with activity. Peripheral arterial disease may cause pain on walking and weak foot pulses. It is important to consider these potential causes and seek appropriate diagnosis and treatment.

The patient in question presents with a deep foot ulcer and signs of systemic inflammation, including fever and tachycardia, which suggest an infection. Given his history of diabetic neuropathy and a diabetic foot ulcer that has penetrated the bone, osteomyelitis is a likely diagnosis. It is important to note that patients with reduced sensation may not be aware of the ulcer’s presence, so the patient’s apparent lack of concern should not be taken as a sign that the condition is not serious.

To determine the surgical anatomy and the depth of the infection, MRI is the preferred imaging modality. A biopsy is not recommended as it may cause further damage to the area and will not provide information on the depth of the infection. While a CT scan may be used if MRI is not available, it is not as effective in this scenario.

Repeat clinical examination would not provide any additional information, so urgent imaging is necessary. Blood cultures should also be taken, and the patient should be started on empirical IV antibiotics while awaiting the results. Treatment will likely involve a prolonged course of antibiotics, and repeat scans will be compared to the initial MRI to monitor progress.

Understanding Osteomyelitis: Types, Causes, and Treatment

Osteomyelitis is a bone infection that can be classified into two types: haematogenous and non-haematogenous. Haematogenous osteomyelitis is caused by bacteria that enter the bloodstream and is usually monomicrobial. It is more common in children, with vertebral osteomyelitis being the most common form in adults. Risk factors include sickle cell anaemia, intravenous drug use, immunosuppression, and infective endocarditis. On the other hand, non-haematogenous osteomyelitis results from the spread of infection from adjacent soft tissues or direct injury to the bone. It is often polymicrobial and more common in adults, with risk factors such as diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.

Staphylococcus aureus is the most common cause of osteomyelitis, except in patients with sickle-cell anaemia where Salmonella species predominate. To diagnose osteomyelitis, MRI is the imaging modality of choice, with a sensitivity of 90-100%. Treatment for osteomyelitis involves a six-week course of flucloxacillin. Clindamycin is an alternative for patients who are allergic to penicillin.

In summary, osteomyelitis is a bone infection that can be caused by bacteria entering the bloodstream or spreading from adjacent soft tissues or direct injury to the bone. It is more common in children and adults with certain risk factors. Staphylococcus aureus is the most common cause, and MRI is the preferred imaging modality for diagnosis. Treatment involves a six-week course of flucloxacillin or clindamycin for penicillin-allergic patients.