An 8-year-old boy presented with multiple episodes of erythematous painful necrotic eruptions since the age of 18 months. The lesions had initially developed on the patient's heels and toes (Fig. 1), and over time had also started to involve his ears, inner thighs and hips. During each episode, the lesions began as small purple macules, which increased in size during a few hours. The lesions were extremely painful and could persist for several months. They occurred more frequently and were more severe during the winter months. The child was otherwise healthy, and no relevant family history was reported.Extensive laboratory investigations (Table S1) for vasculitis and vasculopathy were performed. Vasculitis screens were negative. Fibrinogen, plasma viscosity, antithrombin, Protein S and Protein C levels were normal.Genetic testing found no evidence of prothrombin G20201A mutation. A heterozygous Factor V Leiden mutation was detected; however, as this confers only a slightly increased risk of thrombosis, it was felt that this mutation was insufficient to explain the full clinical presentation. 1 Cryoglobulinaemia, cryofibrinogenaemia and congenital thrombotic thrombocytopenic purpura were excluded. Screening tests for anticardiolipin and anti-b2-glycoprotein I antibodies were negative. Lupus anticoagulant (LA) was negative by three independent methods [dilute Russell viper venom time (dRVVT), kaolin clotting time and
We report a case of a 65-year-old man with multiple myeloma being treated with bortezomib who suffered necrotising fasciitis (NF) due to Salmonella enteritidis.The patient was admitted with a pathological fracture of the humerus in August 2006, which subsequently was found to be due to a plasmocytoma. Further investigation revealed an IgG kappa paraproteinaemia of 12.8 g/l with immune paresis, no Bence-Jones protein in the urine, but bone marrow trephine (BMT) showed 14% plasma cells. Skeletal survey showed no further bony abnormalities. Full blood count and renal function were normal. He was diagnosed with Salmon Durie stage 3 multiple myeloma. Only past medical history of note was hypertension. He received four cycles of vincristine, adriamycin and dexamethasone. However, his paraprotein started to increase on treatment; therefore, he received second-line treatment with cyclophosphamide, thalidomide and dexamethasone. His paraprotein decreased from 18 to 6 g/l. In December 2007, he underwent a melphelan conditioned autologous stem-cell transplant. He suffered a rapid relapse in August 2008 with hyperviscosity and a paraprotein of 59.8 g/l. BMT at this time showed complete infiltration of the bone marrow by plasma cells. He was commenced upon bortezomib (1.3 mg/m 2 ) and dexamethasone as per local protocol. Subsequently, dose reductions were necessary due to suspected bortezomib-induced hepatitis.After his eleventh dose of bortezomib, he presented as an emergency with fever, pain and slight swelling of his right thigh; 5 days previously, he had been commenced upon oral flucloxacillin by his primary care physician for a finger splinter. There were no gastrointestinal symptoms prior to admission. Blood results showed a haemoglobin 13.1 g/l, white cell count 2.6 9 10 9 per L, platelets 95 9 10 9 per L, neutrophils 1.94 9 10 9 per L, creatine kinase 836 U/L, urea 15.6 lmol/L, creatinine 86 lmol/L and C-reactive protein 154 mg/L. Cultures of blood and urine were ordered upon initial review, a diagnosis of right thigh cellulitis was made and he was commenced upon intravenous flucloxacillin. After 2 h, he deteriorated with shock secondary to sepsis. Piperacillin-tazobactam and gentamicin were administered. The surgical team made a clinical diagnosis of NF and he was admitted directly to the intensive care unit (ICU) for resuscitation pending urgent surgical debridement.During surgery, NF was confirmed, the necrotic areas were debrided and fascia excised. Intraoperative tissue and pus samples were taken from the right thigh. Antibiotic treatment was changed to piperacillin-tazobactam and clindamycin. S. enteritidis was isolated in pure culture from tissue and tissue fluid from the right thigh and in initial blood cultures. This was found to be sensitive to amoxicillin, ciprofloxacin, trimethoprim, meropenem, piperacillin-tazobactam and azithromycin. Identification was confirmed by Vitek (bioMerieux) and typed as S. enteritidis phage type 11 (stool specimens were unobtainable). A 16S ribosomal subunit polymerase chain re...
Vaccine-induced thrombosis with thrombocytopenia (VITT) is a recently-described condition associated with arterial and venous thrombosis following vaccination with the ChAdOx1 nCoV-19 (AstraZeneca) vaccine. This report describes two cases of stroke caused by arterial and venous thromboses presenting within 28 days of receiving the AstraZeneca vaccine. The patients were otherwise young and healthy with minimal risk factors for thrombosis yet developed a rapid, ultimately fatal neurological deterioration.The patients were significantly thrombocytopenic with disproportionately raised D-dimers, both of which are widely reported in this condition. Both cases had measurable immunoglobulin G platelet factor-4 antibodies detected via enzyme-linked immunosorbent assay, similar to those described in heparin-induced thrombocytopenia.These cases illustrate that physicians should be especially mindful of VITT in the context of evolving evidence on treatment and in view of the potentially rapid and catastrophic neurological deterioration, leading to fatality despite best supportive care.
Introduction Since the introduction of a venous thromboembolism (VTE) risk assessment tool in 2011 there has been an increase in the workload of the combined Obstetric-Haematology clinic. In view of this increase a retrospective review of the size and composition of clinics during the first 12 weeks of 2011 and 2012 was carried out. Method Clinic lists for the relevant weeks were obtained and the letters reviewed. New referrals were categorised as VTE risk assessment or other. The type of clinic and number of antenatal visits was obtained from the patient activity summary. Results The total number of new referrals to the clinic increased by 51.4% when the first 12 weeks of 2011 and 2012 were compared. The number of referrals for VTE risk increased by 40%. 51.4% (18/35) of the VTE risk assessment new referrals made in 2012 were women with a family history of VTE, compared with 16% (4/25) in 2011. In 2012 of the women referred for a family history of VTE 61.1% (11/18) were reviewed at one further follow up appointment in the combined clinic. Conclusions The introduction of the VTE risk assessment tool has contributed to the increase in new referrals. Many of the women reviewed do not require further Consultant input and may be suitable for review by a Specialist Midwife. The development of a Specialist Midwife role may increase Consultant clinic capacity and provide midwifery input for women who are reviewed frequently and may miss out on holistic care from their community Midwife.
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