A term neonate was born with a grossly swollen and discoloured left hand and forearm. He was transferred from the local hospital to the plastic surgical unit, where a diagnosis of compartment syndrome was made and he underwent emergency forearm fasciotomies at six hours of age. Following serial debridements of necrotic tissue, he underwent split-thickness skin grafting of the resultant defects of his forearm, hand and digits. At the clinic follow-up appointment two months after the procedure, he was found to have developed severe flexion contractures despite regular outpatient hand therapy and splintage. He has had further reconstruction with contracture release, use of artificial dermal matrix, and K-wire fixation of the thumb and wrist. Despite this, the long term outcome is likely to be an arm with poor function. The key learning point from this case is that despite prompt transfer, diagnosis and appropriate surgical management, the outcome for neonatal compartment syndrome may still be poor.
The clinical pathways for craniosynostosis and nonsynostotic skull deformity are entirely different. At the Dutch Craniofacial Center (DCFC), all patients were assessed in the same multidisciplinary craniofacial clinic, a common practice in countries with developed health care. However, the high volume of referrals of nonsynostotic cases frequently resulted in the capacity of these clinics being exceeded, with some patients being assessed in the general pediatric plastic surgery clinic instead. In these general clinics, not all the multidisciplinary team members are routinely present, so patients with craniosynostosis had to make a second journey for further assessment, causing inconvenience, expense, and potential delay in treatment. With triage at the community level unreliable and triage at clinic level inefficient, we decided to trial a triage system to increase efficiency and to ensure patients enter the correct clinical pathway earlier.The 2 craniofacial secretaries were issued with a flowchart to be completed for each new referral. The flowcharts were designed to triage the patients into true craniosynostosis with an appointment for the multidisciplinary clinic or nonsynostotic deformity with an appointment with the craniofacial nurse practitioner (CNP). During a 3-month period, 107 referrals were made. The triage category listed on the initial flowchart for each patient was compared, with the final diagnosis made in the multidisciplinary and CNP clinics.None of the patients triaged as nonsynostotic deformity on the flowcharts were found to be true craniosynostosis after clinical assessment by the CNP. Radiographic assessment or assessment by the craniofacial surgeons in the DCFC confirmed this.The flowchart questionnaire used at the DCFC is a highly sensitive and therefore safe method for detecting craniosynostosis. It has helped to improve efficiency by ensuring patients are seen in an appropriate setting.
These results suggest that enhanced cell proliferation and procollagen gene expression are both involved in LDS development. Furthermore, fibrotic changes may occur in the absence of, or subsequent to, any significant inflammatory response, indicating that additional profibrotic factors produced in the skin as a consequence of chronic venous insufficiency may play a role in LDS formation.
Lymphangioma circumscriptum (LC) is an uncommon skin condition characterized by large muscular-coated lymphatic cisterns that lie deep with in the subcutaneous tissue and communicate with dilated dermal lymphatics. Patients suffer from edema and lymphatic leakage. Surgical excision and reconstruction is the gold standard for therapy. However, this can be mutilating. The authors present a patient who suffered widespread disease of his scrotum who had excellent symptomatic relief by treatment with the CO(2) laser.
Patients with chronic venous disease may develop characteristic changes in the skin of the lower limb known as lipodermatosclerosis (LDS). The affected skin becomes indurated and pigmented and often ulcerates. The degree of induration associated with LDS correlates directly with ulcer formation and leads to a subsequent delayed rate of healing. However, there is limited information regarding the cellular and molecular events that lead from venous dysfunction to LDS development. This article reviews the current knowledge of the clinical progression of chronic venous disease, summarizing the histological findings from these authors' laboratory and other studies on LDS, and offers possible mechanisms to explain the fibrotic changes associated with this condition.
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