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.