Patients admitted to acute care hospitals from high-acuity LTCFs (ie, VSNFs and LTACHs) were more likely to be colonized with KPC-producing Enterobacteriaceae than were patients admitted from the community. Identification of healthcare facilities with a high prevalence of colonized patients presents an opportunity for focused interventions that may aid regional control efforts.

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A 54-year-old male Caucasian was admitted to North Manchester General Hospital with a 5-day history of confusion and hallucinations. A history taken from his family revealed a prior 4-week history of decreased appetite and weight loss coupled with episodes of urinary incontinence. Three months before this the patient had been diagnosed with squamous cell carcinoma of the soft palate, confirmed to be locally invasive by computed tomography scan. He had been booked for radical resection of the tumour in the coming week. Past medical history included coeliac disease and hypertension. He was a current heavy smoker and a heavy consumer of alcohol until 1 month ago. He was not taking any regular medications. On examination the patient appeared agitated and confused. He was apyrexial, with a heart rate of 103 beats per minute, blood pressure 128/75 mmHg and low pulse oximetry at 93%. Systemic clinical examination was otherwise unremarkable. Initial blood investigations including full blood count, urea and electrolytes and liver function tests were normal except for raised inflammatory markers and markedly raised corrected calcium of 4.08 mmol/litre. His parathyroid hormone level was 6 ng/litre. Other investigations included a normal mid-stream urine sample, electrocardiogram and chest X-ray; computed tomography of the head and neck did not show any change from a previous scan showing soft palate lesion with local invasion. The differential diagnosis at this point was sepsis of unknown origin, hypercalcaemia secondary to bony metastasis or confusion secondary to hypercalcaemia or infection. He was treated with aggressive intravenous fluids (4 litres in the first 24 hours) and intravenous pamidronate for his hypercalcaemia, intravenous broad spectrum antibiotics for sepsis and lorazepam for his agitation. His confusion persisted despite corrected calcium coming down to 3.27 mmol/litre over the next few days. Subsequently computed tomography of the abdomen, pelvis and thorax was performed which showed diffuse liver metastatic deposits. There was no bony metastasis to account for the hypercalcaemia. A bone scan did not show evidence of any lytic or sclerotic metastases. His inflammatory markers remained high but blood and urine cultures revealed no growth. Tumour markers showed normal carcinoembryonic antigen and alpha-fetoprotein levels. CA19-9 was raised at 841 U/ml (normal range <35 U/ml). He was reviewed by oncology who deemed him unfit for any intervention but suggested liver biopsy to try and get any clues for the primary as oral squamous cell carcinoma was suggested to be unlikely to metastasize to the liver. He started becoming increasingly drowsy and his calcium started to rise again (corrected calcium 5.26 mmol/litre). A further dose of intravenous pamidronate (90 mg course) made little difference to his hypercalcaemia. He continued to deteriorate and eventually died 22 days after admission. His parathyroid hormone-related protein level was high at 13.8 pmol/litre (normal range <1.8 pmol/litre). The post-mortem examination revealed diffuse infiltration of the liver by a tumour which was squamous cell carcinoma on histology. There were no other sites found to have squamous cell carcinoma.