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Infective endocarditis remains an interesting and challenging disease in which the presenting features have been modified by medical progress. We report a case of a 63-year-old woman who presented with pyrexia, weight loss, night sweats and fatigue over a period of 7 weeks, at the end of which she developed severe right hypochondrial pain, mimicking acute abdomen. She was provisionally diagnosed with and treated for acute cholecystitis to no avail. An abdominal computed tomography scan was performed and revealed the presence of right kidney infarction, the source of which was later proven to originate from aortic valve endocarditis. The patient made a remarkable recovery following 6 weeks of treatment with intravenous antibiotics. This case demonstrates that endocarditis can present as an acute abdomen which is caused mainly by embolism in various organs (the kidney in our patient).
We report a case of endocarditis presenting as acute abdomen due to right renal infarction in a 63-year-old woman. Transoesophageal echo, blood cultures and computed tomography (CT) scan of the abdomen confirmed the diagnosis. Prompt treatment with antibiotics was initiated and the patient made a remarkable recovery. This is a very interesting presentation of a patient with endocarditis. The patient was initially thought to have a surgical cause for abdominal pain. It was subsequently found that the patient had a renal infarct that was presumed to be secondary to an embolus from a vegetation on the aortic valve.
A 63-year-old woman with type 2 diabetes presented to her general practitioner with a 7 week history of chills, fever and fatigue. She has also experienced intermittent earache during this time, prompting her GP to diagnose otitis media and prescribe oral antibiotics.
Her symptoms persisted and she developed nausea and loss of appetite, accompanied by bilious vomiting, night sweats, weight loss and right sided hypochondrial pain. Two weeks before admission an outpatient ultrasound scan was arranged which was suggestive of recent cholecystitis and splenomegaly. The patient continued to feel unwell and her family brought her to the accident and emergency department at Chorley Hospital.
On examination she had a low grade temperature (37.8°C) and was haemodynamically stable. There was no clubbing or splinter haemorrhages, jugular venous pressure (JVP) was not elevated, heart sounds were normal, her chest was clear, and an abdominal examination revealed severe abdominal tenderness at the right hypochondrium. The rectal examination was unremarkable. A urine dipstick was positive for nitrites and leucocytes. There was no evidence of haematuria on urine microscopy.
Initial blood tests showed normal white blood cell count (WBC) at 5.5 (range 4–11) ×109/l, haemoglobin 15.2 (11.5–16.5) g/dl, and platelets 180 (range 140–440) ×109/l, but raised erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) at 105 (range 1–18) mm/h and 133 (0–5) mg/l, respectively. Raised α-glutamyl transferase (GGT) was noted at 95 (range 1–65) u/l. Urea and electrolytes (U&E) were normal. Chest radiography was unremarkable and the electrocardiogram (ECG) revealed normal sinus rhythm.
As the patient presented with an acute abdomen she was referred to the surgeons who made the diagnosis of acute cholecystitis and she was accordingly started on cefuroxime 750 mg three times a day. An abdominal CT confirmed the presence of an enlarged spleen and revealed a wedge shaped low density area of infarction in the right kidney. The gallbladder and biliary tree appeared normal (fig 1).
The CT finding of right kidney infarction prompted the search for the potential source of the emboli. Therefore a transthoracic echocardiogram was arranged which showed moderate aortic regurgitation and good left ventricular function, but did not identify any vegetation. A previous echocardiogram, 4 years earlier, did not show any valvular abnormalities. At this stage blood culture grew Streptococcus oralis and a transoesophageal echocardiogram confirmed the presence of vegetations on both the non-coronary and left coronary aortic cusps.
On further questioning the patient denied any previous surgical procedures and she had no other gastrointestinal symptoms. Moreover, she did not have any history of congenital or acquired valvular heart disease.
The diagnosis was established as infective endocarditis. The patient was deemed suitable for medical treatment and improved following treatment with intravenous antibiotics (benzyl penicillin, 7.2 g daily in six divided doses, plus gentamicin, 1 mg/kg bodyweight every 8 h, modified according to renal function) for 6 weeks. She was then discharged home for outpatient follow-up.
Valvular heart disease, congenital heart disease, and prosthetic heart valves are well known predisposing factors to the development of infective endocarditis. In our patient both history and previous echocardiographic findings confirmed the absence of any predisposing factors.1 A population based case–control study from Philadelphia failed to identify pulmonary, cardiac, gastrointestinal, genitourinary procedures or surgery as risk factors for the development of community acquired endocarditis.2
An acute abdomen or abdominal pain in endocarditis patients has been attributed to rupture of mycotic aneurysm, and embolism into the liver, spleen, kidney or intestine.3 Mycotic aneurysms of the visceral arteries are life threatening with the potential for rupture and organ ischaemia.4 Mycotic aneurysms can result from direct bacterial invasion, embolic occlusion, and immune complex deposition within the blood vessels.5
The incidence of renal infarction associated with endocarditis is unknown. Renal infarction as a complication of endocarditis is frequently found at postmortem examination.6 In one series of 225 consecutive patients who were treated for native valve endocarditis, autopsy in 28 patients showed renal infarction in 17 (60.7%) of them.6
The diagnosis of renal infarction is often difficult to establish. Occasionally, a clinical event of flank pain or macrohaematuria may give a hint about infarction; however, haematuria can also be present in glomerulonephritis and drug induced interstitial nephritis.7 Our patient had a right hypochondrial pain but no haematuria.
Mesenteric ischaemia, an important differential diagnosis, is most frequently caused by dislodged thrombus from the left atrium, left ventricle, or cardiac valve. These patients have been classically described as having a rapid onset of severe periumbilical abdominal pain, which is out of proportion to the findings on physical examination.8
Renal infarction complicating endocarditis, although rare, is an important differential diagnosis of acute abdomen. A diagnosis should be suspected once flank pain and haematuria is presented in a patient with endocarditis. This case, in which the patient was treated with three different courses of antibiotics, illustrates early recognition and treatment of a rare illness. We therefore emphasise the importance of rapid diagnosis and institution of treatment, which can lead to excellent recovery.
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.