Case History:
An 87-year-old lady self-presented to the emergency department (ED) with a three-day history of bleeding PR associated with general malaise, subacute weight loss of 5 kg over three months and functional decline over a five-week period.
This octogenarian was frail (Clinical Frailty Scale score: 8) pre-admission with known severe aortic stenosis. Past medical history was otherwise significant for IHD with percutaneous coronary intervention five months previously, diverticular disease, anal squamous cell carcinoma (treated definitively with radiotherapy), dystonic tremor, hypertension and an 80 pack-year smoking history.
The patient denied any significant abdominal pain and had stable exertional dyspnoea without any recent deterioration in symptoms. Initial physical examination revealed a blood pressure of 116/50mmHg and heart rate of 82 beats per minute, an ejection systolic and early diastolic murmur consistent with mixed aortic valve disease and none of the stigmata of IE such as splinter haemhorrages, janeway lesions etc. There was no recorded pyrexia with a temperature of 36.7degrees C℃ and the patient denied any recent history of rigors. There was pallor and mild generalised abdominal tenderness on palpation. In the ED, she had blood cultures as part of her unwell adult (without obvious clinical cause) investigations, part of the protocol within our service. Intravenous (IV) co-amoxiclav 1.2g three times daily was commenced for suspected acute diverticulitis. This lady was anaemic on admission, with a haemoglobin of 7.7g/dL (reference range 12 - 15 g/dl), necessitating transfusion of one unit of red cell concentrate (RCC).
Both anaerobic and aerobic bottles of admission blood cultures flagged positive at 14 hours with Gram-positive cocci in pairs and chains, which later cultured on chocolate agar and identified as A. defectiva(Figure 1) Other laboratory values on admission included: white blood cell count (WBC) of 11.6 x 109/L (reference range 4 - 10 x 109/L), absolute neutrophil count of 9.24 x 109/L (reference range 2 - 7 x 109/L), mean corpuscular volume 85.0 fl (reference range 84 - 96 fl), platelet count of 320 x 109/L (reference range 150 - 400 x 109/L), serum C-reactive protein of 62 mg/L (reference range 0 – 5 mg/L), blood urea nitrogen of 8.6 mmol/L (reference range 2.9 – 8.2 mmol/L), serum creatinine of 108 µmol/L (reference range 49 – 90 µmol/L), serum albumin 31 g/L (reference range 39 – 51 g/L), and serum ferritin 1015 ng/mL (reference range 10 - 200 µmol/L). The haematological and biochemical parameters of the patient are tabulated in Table 1.
Thereafter, the patient had two episodes of bleeding PR with associated fall in haemoglobin and RCC transfusion. She underwent an oesophagogastroduodenoscopy on day five of admission, which did not reveal any active/recent bleeding or ulceration.
The patient stabilised over the next 48 hours with clinical improvement but then had further bleeding PR, although remaining haemodynamically stable. She was unfit for bowel preparation and/or colonoscopy. Computed tomography (CT) scans of the abdomen and pelvis were performed to investigate ongoing gastrointestinal(GI) blood loss against a background of subacute weight loss. This revealed appearances consistent with multiple splenic infarcts (Figure 2) and diverticular disease. Concurrently with the identification of splenic infarcts, the patient had further bleeding PR with requirement for 2 further units of RCC transfusion and developed clinical sepsis, evidenced by fluctuating consciousness, mild hypoactive delirium, tachycardia and low-grade pyrexia.
The combination of A. defectiva bacteraemia with ongoing pyrexia, known aortic murmur and apparent splenic infarcts on CT scan prompted the decision to treat as infective endocarditis (IE), as advised by Clinical Microbiology. Ceftriaxone 2 grams once daily was started empirically while sensitivity tests were pending. Transthoracic echocardiogram revealed a large mobile echo-density suggestive of a vegetation on a stenotic (maximum gradient 74mmHg) aortic valve with evidence of aortic regurgitation (Figure 3A). A diagnosis of A. defectiva IE was made. The Infectious Disease team was consulted and intravenous antimicrobial therapy was switched to amoxicillin 1 gram every four hours and gentamicin 50 milligrams three times daily, with monitoring of gentamicin serum levels as per protocol. A CT scan of the brain revealed no radiographic evidence of septic emboli in the brain parenchyma, a complication frequently associated with A. defectiva endocarditis [4].
The patient was deemed not to be a candidate for valve replacement given her frailty and significant pre-morbid co-morbidities. However, an initial clinical and biochemical response to antimicrobial therapy was noted.
.
Unfortunately, on day 15, the patient had further bleeding PR with a drop in Hb necessitating further RCC transfusion. Later that day, she was found pulseless and unresponsive and, being declared Not for Active Resuscitation, she died peacefully on the ward. She had a post-mortem which confirmed severe aortic stenosis with calcification and vegetation of the valve leaflets grossly and microscopically (Figure 3B-D) and severe widespread critical coronary atherosclerosis adjacent to coronary stents associated with 90% occlusion involving the three coronary vessels (Figure 4). There was no evidence of acute ischaemic changes within the heart. The entire aorta showed severe calcified atheroma. There was no bleeding focus found in the upper gastrointestinal(GI) tract, small bowel or large bowel which demonstrated mild diverticular disease. No evidence of recurrent tumour within the anal area which revealed evidence of internal haemorrhoids (Figure 5).
Unexpectedly, the spleen showed no evidence of infarction on detailed examination grossly and microscopically. Kidneys showed granular cortical surfaces with evidence of hypertensive changes represented by thickened blood vessels. Lethal cardiac arrhythmia secondary to severe triple coronary atheroma was the most likely cause of death.