Cranioplasty with autologous cryopreserved bone after decompressive craniectomy: complications and risk factors for developing surgical site infection.

BACKGROUND: Renewed interest has developed in decompressive craniectomy, and improved survival is shown when this treatment is used after malignant middle cerebral artery infarction. The aim of this study was to investigate the frequency and possible risk factors for developing surgical site infection (SSI) after delayed cranioplasty using autologous, cryopreserved bone. METHODS: This retrospective study included 74 consecutive patients treated with decompressive craniectomy during the time period May 1998 to October 2010 for various non-traumatic conditions causing increased intracranial pressure due to brain swelling. Complications were registered and patient data was analyzed in a search for predictive factors. RESULTS: Fifty out of the 74 patients (67.6 %) survived and underwent delayed cranioplasty. Of these, 47 were eligible for analysis. Six patients (12.8 %) developed SSI following the replacement of autologous cryopreserved bone, whereas bone resorption occurred in two patients (4.3 %). No factors predicted a statistically significant rate of SSI, however, prolonged procedural time and cardiovascular comorbidity tended to increase the risk of SSI. CONCLUSIONS: SSI and bone flap resorption are the most frequent complications associated with the reimplantation of autologous cryopreserved bone after decompressive craniectomy. Prolonged procedural time and cardiovascular comorbidity tend to increase the risk of SSI.

Comparison of faecal and intestinal concentrations of granulocyte marker protein and localization of gastrointestinal tumours in rats.

BACKGROUND: Increased faecal concentrations of the granulocyte marker protein (GMP) have been found in rats with azoxymethane (AOM) induced carcinoma of the colon, but the origin of this GMP is unknown. The aims were to investigate the concentrations of GMP in different parts of the gastrointestinal (GI) tract in rats with or without AOM-induced carcinoma and to correlate the GMP concentrations to localization of the carcinomas. METHODS: Nineteen rats were given intramuscular injections of AOM, 15 mg/kg, once weekly for 6 weeks and were killed after 22 weeks. Five rats that were not given AOM injections served as controls. RESULTS: All rats given AOM developed tumours; 18 developed a total of 33 adenocarcinomas in the GI tract and one developed an adenoma in the colon. Nine animals had carcinoma in the small bowel, seven of which also had carcinoma of the colon, and nine animals had carcinomas in the large bowel only. No other tumours were found. All except one of the animals that had carcinoma of the colon had elevated faecal GMP concentrations, and from week 11 there was a significant difference in the GMP values between the control group and the group that developed colon carcinoma. In all rats that developed carcinoma in the small bowel, the tumour was localized in the proximal part. In the rats that had been given AOM, the luminal GMP concentrations were significantly higher in the proximal part of the small bowel than in the distal part, but there were no significant differences in the GMP concentrations between animals with and without carcinoma in the small bowel. Sixteen rats developed a total of 24 carcinomas in the colon, and one rat developed an adenoma. Luminal GMP concentration in the distal part of the colon was elevated in all animals with carcinomas in the colon, and the GMP concentrations were significantly higher in the distal part than in the proximal part. Rats with one carcinoma in the colon had significantly lower GMP values in the distal part, compared to rats that had two carcinomas in the colon. CONCLUSIONS: The animal model described is suitable for further studies on many aspects of tumour development in the colon. Furthermore, it is likely that increased faecal GMP concentration in rats with colon carcinoma is a result of an inflammatory process in or around tumours.