An 80-year-old gentleman presented with sudden-onset right-sided upper abdominal pain for 1 day. He also had a swollen and tender right leg for the previous 3–4 days following a fall. Additionally, the patient had experienced weight loss and night sweats. Medical history included variceal haemorrhage, type 2 diabetes mellitus, transient ischaemic attack, left knee replacement and chronic liver disease. There was no history of recent alcohol abuse, blood transfusion, intravenous drug abuse or high-risk sexual encounters and no significant travel history.
On admission, he was pyrexial (37.5 ºC), blood pressure was 114/54 mm Hg, pulse 81 bpm regular, respiratory rate 15 with no icterus and no peripheral lymphadenopathy. Clinical examination revealed minimal right upper quadrant abdominal tenderness on deep palpation but no rebound tenderness. Splenomegaly was not clinically detectable. Normal bowel sounds were audible. The significant finding was a swollen, warm, erythematous right knee joint with tenderness on palpation. A patellar tap was positive indicating a right knee effusion. An x-ray of the right knee revealed no fracture and no chondrocalcinosis but mild osteoarthritic changes.
Laboratory investigations revealed a haemoglobin (Hb) of 11.6 g/dl and a white cell count of 9.5×109/l with raised neutrophils at 7.6×109/l. The platelet count was depressed at 62×109/l, C reactive protein (CRP) 40, alanine transaminase (ALT) 58 IU/l, alkaline phosphatase (ALP) 113 IU/l, total bilirubin 34, albumin 28, estimated glomerular filtration rate (eGFR) 42, creatinine 141, sodium 130 and potassium 4.6. α-fetoprotein (AFP) was raised at 242 but serum ferritin was in the normal range at 216 μg/l.
Aspiration of the right knee effusion revealed a turbid, cloudy yellow fluid with leucocytes ++ and a gram stain revealed gram negative rods identified as Klebsiella pneumoniae, which was sensitive to co-amoxiclav, ceftriaxone, tazocin and timentin. Culture report confirmed identification of K pneumoniae (pnenotype unavailable). Unfortunately, no blood cultures were taken, but the results of joint fluid culture were reviewed with a consultant microbiologist who suggested that since gram negative rods were seen on gram stain and a heavy growth of K pneumoniae was obtained on direct culture, there is ample evidence to indicate K pneumoniae as the causative organism for septic arthritis. However, it is important to stress that in cases of septic arthritis, the causative organism should ideally be isolated from both blood and joint fluid. The patient was commenced on a 5-day course of intravenous timentin 3.2 g three times daily. This was followed up by a course of oral co-amoxiclav following discharge. The patient responded to antibiotic therapy and the temperature, swelling, redness and tenderness improved.
Here, we present a case of septic arthritis due to K pneumoniae in a cirrhotic patient, which is an extremely unusual causative organism for joint infection.