Rheumatology & Haematology — MCQs
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A 45-year-old woman presents with bilateral leg swelling 2 weeks after a long-haul flight. Doppler ultrasound confirms bilateral above-knee deep vein thrombosis. She has had two previous unprovoked DVTs. Thrombophilia screening reveals: antithrombin activity 45% (normal 80-120%), protein C 98%, protein S 105%, Factor V Leiden negative, prothrombin gene mutation negative, lupus anticoagulant negative. What is the most appropriate long-term management?
A 58-year-old woman is diagnosed with unprovoked pulmonary embolism. She has completed 6 months of anticoagulation with apixaban and has recovered well. She has no active cancer, normal renal function (eGFR >60), and no major bleeding risk factors. What is the most appropriate recommendation regarding duration of anticoagulation?
A 68-year-old man with atrial fibrillation on warfarin (target INR 2-3) presents to the emergency department following a fall with significant head trauma. CT head shows acute subdural haematoma requiring urgent surgical evacuation. His INR is 3.2. What is the most appropriate immediate management of his anticoagulation?
A 32-year-old woman who is 28 weeks pregnant presents with left leg swelling and pain. Ultrasound Doppler confirms left femoral deep vein thrombosis. She has no significant past medical history and no family history of thrombosis. What is the most appropriate anticoagulation management?
A 62-year-old man presents with fatigue. Blood tests show: Hb 92 g/L, MCV 88 fL, WCC 3.8 × 10⁹/L, platelets 145 × 10⁹/L, reticulocyte count 0.5% (normal 0.5-2.5%), ferritin 380 µg/L, ESR 78 mm/hr, CRP 45 mg/L. Renal and liver function are normal. Blood film shows normochromic normocytic red cells with rouleaux formation. What is the most appropriate next investigation?
A 45-year-old woman with rheumatoid arthritis on long-term methotrexate presents with fatigue. Blood tests show: Hb 102 g/L, MCV 104 fL, WCC 5.8 × 10⁹/L, platelets 165 × 10⁹/L. She is taking folic acid 5mg once weekly. What is the most appropriate management to address her anaemia?
A 35-year-old woman presents with a 3-month history of fatigue and shortness of breath on exertion. She follows a strict vegan diet. Blood tests show: Hb 88 g/L, MCV 118 fL, WCC 4.2 × 10⁹/L, neutrophils 2.8 × 10⁹/L, platelets 112 × 10⁹/L. Blood film shows hypersegmented neutrophils. Which single test would most reliably confirm the specific deficiency causing her anaemia?
A 28-year-old woman of Mediterranean origin presents with fatigue. Blood tests show: Hb 108 g/L, MCV 68 fL, ferritin 95 µg/L, serum iron 18 µmol/L (normal 10-30), transferrin saturation 28%, red cell count 5.8 × 10¹²/L. Blood film shows target cells and basophilic stippling. What is the most likely diagnosis?
A 68-year-old man presents with fatigue and pallor. Blood tests reveal: Hb 82 g/L, MCV 68 fL, MCH 22 pg, ferritin 8 µg/L, transferrin saturation 12%. He denies any obvious blood loss. Upper GI endoscopy and colonoscopy are both normal. What is the most appropriate next investigation?
A 55-year-old woman with type 2 diabetes and hypertension presents with sudden onset severe pain and swelling of her left knee. She has been feeling unwell with fever. Examination reveals a hot, swollen, tender knee with restricted movement. Knee aspiration yields turbid fluid. Microscopy shows weakly positive birefringent rhomboid-shaped crystals. Gram stain is negative. White cell count in synovial fluid is 28 × 10⁹/L with 85% neutrophils. What is the most appropriate immediate management?
Rheumatology & Haematology UK Medical PG Practice Questions and MCQs
Question 101: A 45-year-old woman presents with bilateral leg swelling 2 weeks after a long-haul flight. Doppler ultrasound confirms bilateral above-knee deep vein thrombosis. She has had two previous unprovoked DVTs. Thrombophilia screening reveals: antithrombin activity 45% (normal 80-120%), protein C 98%, protein S 105%, Factor V Leiden negative, prothrombin gene mutation negative, lupus anticoagulant negative. What is the most appropriate long-term management?
- A. Lifelong anticoagulation with warfarin (target INR 2-3) (Correct Answer)
- B. Six months anticoagulation followed by reassessment
- C. Lifelong anticoagulation with a direct oral anticoagulant
- D. Lifelong anticoagulation with warfarin (target INR 3-4)
- E. Low molecular weight heparin for 6 months then stop
Explanation: ***Lifelong anticoagulation with warfarin (target INR 2-3)***- The patient has **Antithrombin deficiency** (activity 45%) and a history of **recurrent unprovoked VTE**, which represents a high risk for future thrombotic events, necessitating **lifelong anticoagulation**.- **Warfarin** is often preferred over DOACs in antithrombin deficiency due to more extensive evidence and direct inhibition of vitamin K-dependent clotting factors, which is considered more robust in severe thrombophilias.*Six months anticoagulation followed by reassessment*- A 6-month course is insufficient for a patient with **multiple unprovoked DVT episodes** and a confirmed **inherited high-risk thrombophilia** like antithrombin deficiency.- Stopping anticoagulation after such a short period would lead to a very high **recurrence risk**, far exceeding the acceptable threshold for this clinical scenario.*Lifelong anticoagulation with a direct oral anticoagulant*- While **DOACs** are first-line for most VTE cases, current guidelines and clinical practice often still favor **warfarin** for **antithrombin deficiency** due to a lack of extensive data on DOACs in this specific high-risk population.- The mechanisms by which DOACs act (e.g., direct Factor Xa or thrombin inhibition) might be less optimally effective in all cases of antithrombin deficiency compared to the broad action of warfarin.*Lifelong anticoagulation with warfarin (target INR 3-4)*- An **INR target of 3-4** is considered high intensity and is typically reserved for very specific indications, such as **mechanical heart valves** or recurrent events despite a standard INR.- Maintaining a higher INR significantly increases the risk of **major bleeding complications** without providing additional proven benefit for venous thromboembolism in most cases.*Low molecular weight heparin for 6 months then stop*- **LMWH** is used for acute treatment and specific situations like VTE in pregnancy or cancer, but it is not practical or generally recommended for **long-term indefinite oral anticoagulation**.- Stopping therapy after 6 months, even with LMWH, would leave the patient unprotected against the **high risk of recurrence** due to her underlying antithrombin deficiency and prior events.
Question 102: A 58-year-old woman is diagnosed with unprovoked pulmonary embolism. She has completed 6 months of anticoagulation with apixaban and has recovered well. She has no active cancer, normal renal function (eGFR >60), and no major bleeding risk factors. What is the most appropriate recommendation regarding duration of anticoagulation?
- A. Stop anticoagulation after 6 months as treatment is complete
- B. Continue full-dose apixaban indefinitely
- C. Switch to aspirin 75mg daily indefinitely
- D. Continue reduced-dose apixaban (2.5mg twice daily) indefinitely if annual bleeding risk <2% (Correct Answer)
- E. Stop anticoagulation but restart if further thrombosis occurs
Explanation: ***Continue reduced-dose apixaban (2.5mg twice daily) indefinitely if annual bleeding risk <2%***- Patients with an **unprovoked pulmonary embolism** have a high annual risk of recurrence (approx. 10%), making **extended anticoagulation** the preferred strategy if bleeding risk is low.- Trials like **AMPLIFY-EXT** demonstrated that a **reduced-dose** (2.5 mg BID) is as effective as full-dose in preventing recurrence but carries a significantly lower risk of **major bleeding**.*Stop anticoagulation after 6 months as treatment is complete*- Stopping anticoagulation after 6 months for unprovoked VTE leads to unacceptably high **recurrence rates** compared to extended therapy.- Current guidelines recommend considering **indefinite treatment** for unprovoked events unless there is a high **bleeding risk**.*Continue full-dose apixaban indefinitely*- While effective, **full-dose apixaban** (5 mg BID) increases the risk of bleeding over the long term without providing superior protection against recurrence compared to the **reduced dose**.- The **2.5 mg BID** dose is specifically indicated for long-term prophylaxis after the initial 6-month treatment phase.*Switch to aspirin 75mg daily indefinitely*- **Aspirin** is significantly less effective than anticoagulants for the secondary prevention of **venous thromboembolism (VTE)**.- It should only be considered as a last resort for patients who refuse or cannot tolerate any form of **oral anticoagulation**.*Stop anticoagulation but restart if further thrombosis occurs*- This approach is reactive rather than preventative and exposes the patient to the potentially fatal risk of a **recurrent pulmonary embolism**.- **Unprovoked VTE** carries a long-term risk that necessitates a proactive, **preventative strategy** using low-dose anticoagulation.
Question 103: A 68-year-old man with atrial fibrillation on warfarin (target INR 2-3) presents to the emergency department following a fall with significant head trauma. CT head shows acute subdural haematoma requiring urgent surgical evacuation. His INR is 3.2. What is the most appropriate immediate management of his anticoagulation?
- A. Administer vitamin K 5mg intravenously slowly
- B. Administer prothrombin complex concentrate plus vitamin K 5mg intravenously (Correct Answer)
- C. Stop warfarin and recheck INR in 6 hours
- D. Administer fresh frozen plasma 4 units
- E. Administer protamine sulfate intravenously
Explanation: ***Administer prothrombin complex concentrate plus vitamin K 5mg intravenously*** - This patient has a **life-threatening intracranial hemorrhage** (acute subdural haematoma) requiring immediate and complete reversal of warfarin's anticoagulant effect for urgent surgery. - **Prothrombin complex concentrate (PCC)** provides rapid reversal by supplying activated clotting factors (II, VII, IX, X), while **intravenous vitamin K** ensures sustained new factor synthesis, preventing rebound anticoagulation. *Administer vitamin K 5mg intravenously slowly* - **Vitamin K** alone has a delayed onset of action, typically taking **4-6 hours** to significantly lower the INR. - This delay is unacceptable in a situation of acute, **life-threatening bleeding** requiring immediate surgical intervention, as the hematoma could expand significantly. *Stop warfarin and recheck INR in 6 hours* - Simply stopping **warfarin** is insufficient for **major or life-threatening bleeding** because of warfarin's long half-life and the slow clearance of depleted clotting factors. - Rechecking INR in 6 hours would delay critical treatment, putting the patient at high risk of **neurological deterioration** due to ongoing bleeding. *Administer fresh frozen plasma 4 units* - **Fresh frozen plasma (FFP)** contains all clotting factors but requires **large volumes** for effective reversal, posing a risk of fluid overload. - FFP also requires **blood group compatibility** and takes longer to thaw and administer compared to PCC, making it less ideal for immediate, critical reversal. *Administer protamine sulfate intravenously* - **Protamine sulfate** is the specific antidote for **heparin** (unfractionated and low molecular weight heparin) by neutralizing its anticoagulant effects. - It has **no effect on warfarin's anticoagulant action**, which works by inhibiting vitamin K-dependent clotting factor synthesis.
Question 104: A 32-year-old woman who is 28 weeks pregnant presents with left leg swelling and pain. Ultrasound Doppler confirms left femoral deep vein thrombosis. She has no significant past medical history and no family history of thrombosis. What is the most appropriate anticoagulation management?
- A. Low molecular weight heparin throughout pregnancy and 6 weeks postpartum (Correct Answer)
- B. Warfarin for remainder of pregnancy then 6 weeks postpartum
- C. Rivaroxaban throughout pregnancy and 6 weeks postpartum
- D. Low molecular weight heparin until delivery, then switch to warfarin for 6 weeks
- E. Low molecular weight heparin until delivery only, no postpartum anticoagulation needed
Explanation: ***Low molecular weight heparin throughout pregnancy and 6 weeks postpartum*** - **Low molecular weight heparin (LMWH)** is the preferred anticoagulant in pregnancy as it **does not cross the placenta** and carries no risk of fetal hemorrhage or teratogenicity. - Management of **Venous Thromboembolism (VTE)** in pregnancy requires treatment for the remainder of the pregnancy and at least **6 weeks postpartum**, ensuring a minimum total duration of 3 months. *Warfarin for remainder of pregnancy then 6 weeks postpartum* - **Warfarin** is generally **contraindicated** in pregnancy because it crosses the placenta and is **teratogenic**, especially during the first trimester (warfarin embryopathy). - It also increases the risk of **fetal intracranial hemorrhage**, particularly if used near the time of delivery. *Rivaroxaban throughout pregnancy and 6 weeks postpartum* - **Direct Oral Anticoagulants (DOACs)** like rivaroxaban are **contraindicated** in pregnancy due to a lack of safety data and potential for reproductive toxicity. - Animal studies have shown that DOACs cross the placenta and may lead to **fetal harm** and increased pregnancy loss. *Low molecular weight heparin until delivery, then switch to warfarin for 6 weeks* - While switching to **warfarin postpartum** is a valid clinical option because it is compatible with breastfeeding, continuing **LMWH** throughout is also an acceptable and often simpler management strategy. - This option is less ideal than the correct answer as it implies a mandatory switch, whereas LMWH alone is often preferred to avoid the complexities of **INR monitoring** in a new mother. *Low molecular weight heparin until delivery only, no postpartum anticoagulation needed* - The **postpartum period** (especially the first 6 weeks) is the time of highest weight-for-weight risk for VTE due to physiological changes and potential delivery trauma. - Stopping anticoagulation at delivery would be dangerous and is **incorrect management**, as guideline-directed therapy must continue for at least **6 weeks postpartum**.
Question 105: A 62-year-old man presents with fatigue. Blood tests show: Hb 92 g/L, MCV 88 fL, WCC 3.8 × 10⁹/L, platelets 145 × 10⁹/L, reticulocyte count 0.5% (normal 0.5-2.5%), ferritin 380 µg/L, ESR 78 mm/hr, CRP 45 mg/L. Renal and liver function are normal. Blood film shows normochromic normocytic red cells with rouleaux formation. What is the most appropriate next investigation?
- A. Bone marrow biopsy
- B. Serum protein electrophoresis and immunofixation (Correct Answer)
- C. Direct antiglobulin test (Coombs test)
- D. Flow cytometry for paroxysmal nocturnal haemoglobinuria
- E. JAK2 mutation analysis
Explanation: ***Serum protein electrophoresis and immunofixation***- The combination of **normocytic anaemia**, a significantly elevated **ESR (78 mm/hr)**, and **rouleaux formation** on the blood film is highly suggestive of a **paraproteinaemia**, such as **multiple myeloma**.- This investigation is the essential first-line screening test to identify a **monoclonal (M) protein spike**, which is characteristic of plasma cell dyscrasias.*Bone marrow biopsy*- While a **bone marrow biopsy** is crucial for confirming the diagnosis of **multiple myeloma** by quantifying plasma cell infiltration, it is typically performed *after* a paraprotein has been identified.- It is a more invasive procedure and follows initial non-invasive screening steps like **serum protein electrophoresis**.*Direct antiglobulin test (Coombs test)**- This test is used to diagnose **autoimmune haemolytic anaemia**, which would typically present with a **high reticulocyte count** due to increased red blood cell destruction and compensatory marrow activity.- The patient's **low reticulocyte count (0.5%)** indicates **underproduction** of red blood cells, not increased destruction, making hemolytic anemia unlikely.*Flow cytometry for paroxysmal nocturnal haemoglobinuria*- **Paroxysmal nocturnal haemoglobinuria (PNH)** is characterized by **intravascular haemolysis** (e.g., elevated LDH, low haptoglobin, dark urine) and often presents with **pancytopenia**.- It does not cause the striking **rouleaux formation** or the extremely high **ESR** and **CRP** seen in this patient.*JAK2 mutation analysis*- This analysis is primarily used to diagnose **myeloproliferative neoplasms** (e.g., polycythemia vera, essential thrombocythemia).- These conditions typically manifest with **elevated blood counts** (e.g., erythrocytosis, thrombocytosis) or specific cytopenias with marrow fibrosis, not the **anaemia** and rouleaux seen here.
Question 106: A 45-year-old woman with rheumatoid arthritis on long-term methotrexate presents with fatigue. Blood tests show: Hb 102 g/L, MCV 104 fL, WCC 5.8 × 10⁹/L, platelets 165 × 10⁹/L. She is taking folic acid 5mg once weekly. What is the most appropriate management to address her anaemia?
- A. Stop methotrexate and switch to alternative DMARD
- B. Increase folic acid to 5mg daily (Correct Answer)
- C. Check vitamin B12 level and commence supplementation
- D. Prescribe folinic acid rescue therapy
- E. Add oral iron supplementation
Explanation: ***Increase folic acid to 5mg daily*** - **Methotrexate** is a **folate antagonist** that inhibits **dihydrofolate reductase**, commonly leading to **macrocytic anaemia** as evidenced by the high **MCV (104 fL)**. - Increasing the frequency of **folic acid** supplementation (e.g., daily, avoiding the day of methotrexate administration) is the standard management to mitigate haematological side effects and improve tolerability, particularly when weekly dosing is insufficient. *Stop methotrexate and switch to alternative DMARD* - Stopping methotrexate is a premature step since the anaemia is **mild (Hb 102 g/L)** and can often be corrected with appropriate supportive care. - **Methotrexate** is a cornerstone treatment for **rheumatoid arthritis**, and switching should only be considered if dose adjustments or optimized supplementation fail to control toxicity or if there are more severe side effects. *Check vitamin B12 level and commence supplementation* - While **Vitamin B12 deficiency** can cause macrocytosis, the patient's current medication, **methotrexate**, is a direct cause of folate antagonism, making it the most probable cause of the macrocytic anaemia. - Although assessing B12 is part of a complete workup for macrocytic anaemia, given the clear precipitating factor, it is not the **most appropriate immediate** intervention compared to adjusting folate supplementation. *Prescribe folinic acid rescue therapy* - **Folinic acid (leucovorin)** is typically reserved for managing acute, severe **methotrexate toxicity** (e.g., myelosuppression, mucositis) or for high-dose methotrexate regimens. - It is not the standard approach for managing mild, chronic **macrocytosis** due to regular methotrexate use, where increased daily folic acid is preferred. *Add oral iron supplementation* - **Iron deficiency** typically results in **microcytic anaemia** (low MCV), whereas this patient clearly presents with **macrocytic anaemia** (MCV 104 fL). - Supplementing iron in a patient with a **macrocytic** profile would be inappropriate and would not address the underlying folate pathway interference caused by methotrexate.
Question 107: A 35-year-old woman presents with a 3-month history of fatigue and shortness of breath on exertion. She follows a strict vegan diet. Blood tests show: Hb 88 g/L, MCV 118 fL, WCC 4.2 × 10⁹/L, neutrophils 2.8 × 10⁹/L, platelets 112 × 10⁹/L. Blood film shows hypersegmented neutrophils. Which single test would most reliably confirm the specific deficiency causing her anaemia?
- A. Serum vitamin B12 level
- B. Serum folate level
- C. Serum methylmalonic acid level (Correct Answer)
- D. Bone marrow biopsy showing megaloblastic changes
- E. Anti-intrinsic factor antibodies
Explanation: ***Serum methylmalonic acid level*** - **Methylmalonic acid (MMA)** is a highly specific marker for **vitamin B12 deficiency** as B12 is a cofactor for its metabolism, leading to MMA accumulation when deficient. - Elevated MMA levels are seen in B12 deficiency but remain normal in **folate deficiency**, making it the most reliable test to differentiate the two causes of **megaloblastic anaemia**. *Serum vitamin B12 level* - Serum B12 levels can sometimes fall into a **"grey zone"** or be falsely normal despite **tissue-level deficiency**, especially in early stages. - This test might not always reflect the true functional B12 status, and other factors can influence its concentration. *Serum folate level* - While folate deficiency also causes **macrocytic anaemia** with **hypersegmented neutrophils**, it is less likely in a vegan, as many plant foods are rich in folate. - Testing folate directly does not confirm **vitamin B12 deficiency** and could lead to misdiagnosis if only folate is supplemented, masking a critical B12 deficiency. *Bone marrow biopsy showing megaloblastic changes* - A bone marrow biopsy would confirm **megaloblastic anaemia** by showing characteristic morphological changes, but it cannot differentiate between **B12** and **folate deficiency**. - It is an **invasive procedure** and less specific for identifying the *exact* deficiency compared to biochemical blood tests. *Anti-intrinsic factor antibodies* - These antibodies are specific for **Pernicious Anaemia**, an autoimmune condition causing **B12 malabsorption**, not direct dietary deficiency. - Given the patient's **strict vegan diet**, a **dietary deficiency** is the most probable cause, making tests for malabsorption secondary to confirming the deficiency itself.
Question 108: A 28-year-old woman of Mediterranean origin presents with fatigue. Blood tests show: Hb 108 g/L, MCV 68 fL, ferritin 95 µg/L, serum iron 18 µmol/L (normal 10-30), transferrin saturation 28%, red cell count 5.8 × 10¹²/L. Blood film shows target cells and basophilic stippling. What is the most likely diagnosis?
- A. Beta-thalassaemia trait (Correct Answer)
- B. Iron deficiency anaemia
- C. Anaemia of chronic disease
- D. Sideroblastic anaemia
- E. Alpha-thalassaemia trait
Explanation: ***Beta-thalassaemia trait*** - The patient's **Mediterranean origin**, combined with **microcytic anaemia** (low MCV 68 fL) and **normal iron studies** (ferritin 95 µg/L, serum iron, transferrin saturation), strongly points to thalassaemia. - The **elevated red cell count** (5.8 × 10¹²/L) despite anaemia and the presence of **target cells** and **basophilic stippling** on blood film are classic features of beta-thalassaemia trait. *Iron deficiency anaemia* - This is unlikely because **ferritin** and **iron studies** (serum iron, transferrin saturation) are within normal limits, directly contradicting iron deficiency. - In iron deficiency, the **red cell count** is typically decreased or normal, not elevated, and the MCV would usually be low but not always as low as 68 fL with these iron levels. *Anaemia of chronic disease* - While anaemia of chronic disease can be microcytic, the MCV is rarely as low as 68 fL, and although **ferritin** is usually normal or elevated, **serum iron** and **transferrin saturation** would typically be low. - The **red cell count** is usually normal or low, not elevated, differentiating it from thalassaemia. *Sideroblastic anaemia* - Sideroblastic anaemia often presents with **increased serum iron** and **ferritin** due to iron overload, which are not seen here. - The blood film might show **dimorphic red cell population**, and a definitive diagnosis requires a bone marrow biopsy for **ring sideroblasts**. *Alpha-thalassaemia trait* - While alpha-thalassaemia trait can also cause microcytic anaemia with a high red cell count and target cells, the patient's **Mediterranean origin** makes beta-thalassaemia more probable. - Differentiation typically relies on **haemoglobin electrophoresis**, which would show **increased HbA2** in beta-thalassaemia trait, while alpha-thalassaemia trait usually has normal HbA2.
Question 109: A 68-year-old man presents with fatigue and pallor. Blood tests reveal: Hb 82 g/L, MCV 68 fL, MCH 22 pg, ferritin 8 µg/L, transferrin saturation 12%. He denies any obvious blood loss. Upper GI endoscopy and colonoscopy are both normal. What is the most appropriate next investigation?
- A. Capsule endoscopy of small bowel
- B. Bone marrow biopsy
- C. Haemoglobin electrophoresis
- D. Coeliac serology including tissue transglutaminase antibodies (Correct Answer)
- E. CT chest, abdomen and pelvis
Explanation: ***Coeliac serology including tissue transglutaminase antibodies*** - This patient has **iron deficiency anaemia** (low ferritin, low MCV) with no source found on standard GI endoscopy; **Coeliac disease** is a common cause of iron malabsorption due to **duodenal villous atrophy**. - International guidelines recommend screening for Coeliac disease in all cases of unexplained iron deficiency, even in the absence of GI symptoms. *Capsule endoscopy of small bowel* - This is typically reserved for cases where both endoscopy and **Coeliac serology** are negative, to look for **angiodysplasia** or small bowel tumors. - It is a more invasive and expensive investigation that should follow simpler screening tests. *Bone marrow biopsy* - This is unnecessary when the iron studies (low **ferritin** and **transferrin saturation**) clearly establish a diagnosis of iron deficiency. - Biopsy is generally used for evaluating **myelodysplastic syndromes** or unexplained pancytopenia, not simple microcytic anaemia. *Haemoglobin electrophoresis* - This test screens for **haemoglobinopathies** like **Thalassaemia**, which also present with low MCV. - However, the low **ferritin** level specifically confirms iron depletion, whereas ferritin is typically normal or high in thalassaemia. *CT chest, abdomen and pelvis* - While used to search for **occult malignancy**, it is not the standard next step for iron deficiency after negative direct visualization of the GI tract. - It lacks the sensitivity to detect the functional malabsorption typical of **Coeliac disease**.
Question 110: A 55-year-old woman with type 2 diabetes and hypertension presents with sudden onset severe pain and swelling of her left knee. She has been feeling unwell with fever. Examination reveals a hot, swollen, tender knee with restricted movement. Knee aspiration yields turbid fluid. Microscopy shows weakly positive birefringent rhomboid-shaped crystals. Gram stain is negative. White cell count in synovial fluid is 28 × 10⁹/L with 85% neutrophils. What is the most appropriate immediate management?
- A. Start oral colchicine and arrange outpatient rheumatology review
- B. Administer intra-articular corticosteroid injection
- C. Start empirical intravenous antibiotics and await culture results (Correct Answer)
- D. Start oral NSAIDs and arrange urgent MRI knee
- E. Prescribe oral prednisolone and discharge with GP follow-up
Explanation: ***Start empirical intravenous antibiotics and await culture results*** - The patient presents with **fever**, a high synovial **WCC (28 x 10⁹/L)** with **85% neutrophils**, and turbid fluid, making **septic arthritis** the most critical diagnosis to rule out or treat immediately. - **Crystal arthropathy** (pseudogout) and infection frequently **coexist**; a negative Gram stain does not exclude sepsis, and delaying **empirical intravenous antibiotics** can lead to rapid **joint destruction**, osteomyelitis, or systemic sepsis. *Start oral colchicine and arrange outpatient rheumatology review* - While colchicine treats **calcium pyrophosphate deposition (CPPD)**, it is insufficient for a patient presenting with **systemic symptoms** like fever and severe joint pain, indicative of potential sepsis. - Outpatient review is inappropriate as the risk of **septic arthritis** requires immediate hospital admission for urgent diagnosis and IV therapy. *Administer intra-articular corticosteroid injection* - Injecting corticosteroids into a potentially **infected joint** is strictly **contraindicated** as it can worsen the infection by suppressing local immunity. - This intervention should only be considered after **septic arthritis** has been definitively ruled out by negative cultures. *Start oral NSAIDs and arrange urgent MRI knee* - **NSAIDs** may mask the pain and inflammation of infection but will not treat the underlying **bacterial source**, which is the primary concern given the fever and turbid fluid. - An **MRI** is not the primary diagnostic tool for septic arthritis; **synovial fluid culture** is the gold standard, and clinical urgency mandates treatment before imaging. *Prescribe oral prednisolone and discharge with GP follow-up* - **Systemic steroids** can facilitate the spread of **bacterial infection** and are not the first-line treatment for acute monoarthritis of unknown etiology with signs of sepsis. - Discharge is unsafe for a patient with **fever** and restricted movement, as they require immediate hospital admission, monitoring for clinical deterioration, and further management of the joint.
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