ObjectivesThis study was designed to investigate whether an individual and parental history of functional pain syndromes (FPS) is found more often in adolescents suffering from chronic pain than in their pain-free peers.MethodsOur case–control study involved 101 adolescents aged 10–18 years. Cases were 45 patients of the Chronic Pain Clinic at Sydney Children’s Hospital with diverse chronic pain disorders. Controls consisted of 56 adolescent volunteers who did not have chronic pain. Adolescents and their parents filled out questionnaires assessing demographic data as well as known and potential risk factors for chronic pain. A history of FPS was assessed by questionnaire, including restless legs syndrome (RLS). Chi-squared tests and t-tests were used to investigate univariate associations between chronic pain in adolescents and lifetime prevalence of FPS. Logistic regression was used to test multivariate associations, while controlling for possible confounders.ResultsMigraine, non-migraine headaches, recurrent abdominal pain (RAP), and RLS were reported significantly more frequently in cases than controls (P-values of 0.01, <0.001, 0.01, and 0.03, respectively). Parental migraine, RAP, and RLS were also significantly associated with adolescent chronic pain in the multivariate analyses. Individual history of migraine, non-migraine headaches, and RAP, along with parental history of RAP and depression significantly accounted for 36%–49% of variance in chronic pain. Other associations with chronic pain were generally in accordance with previous reports.DiscussionIt may be helpful when assessing a child who has chronic pain or is at risk of chronic pain, to enquire about these associations. Based on the current findings, an individual history of migraine, non-migraine headaches, and RAP, as well as parental migraine, RAP, and RLS are symptoms that are of particular relevance to assess.

Intra-arterial injection of sclerosants is a significant but uncommon complication of sclerotherapy that may result in extensive tissue necrosis and in rare cases digit or limb amputation. We have managed three cases in the past 10 years. One patient was referred for immediate treatment following intra-arterial injection of liquid polidocanol. The other two had undergone foam sclerotherapy with polidocanol and sodium tetradecyl sulphate, respectively. All patients were treated with a combination of oral steroids (prednisone 0.5-1 mg/kg) and systemic anticoagulants (enoxaparin 1.5 mg/kg daily subcutaneous injection). One case progressed to skin ulceration where prednisone was started five days after the adverse event and prematurely stopped after four weeks. The other cases did not progress to necrosis or other long-term sequelae. In these patients, prednisone was commenced immediately and slowly reduced over the following 12 weeks. The inflammation that follows ischemia plays a significant role in tissue necrosis and the immediate management of this adverse event may benefit from anti-inflammatory measures and in particular systemic steroid therapy unless contraindicated.

Background: Tissue necrosis is a significant but uncommon complication of sclerotherapy. The pathogenic mechanisms of this often-debilitating complication have been poorly described in the literature. Purpose: To elucidate the pathological mechanisms, we propose a morphological approach to classify sclerotherapy-induced skin necrosis into two categories of round and stellate (star-like) necrosis. Research Design: Comprehensive literature review was conducted. Results: Round necrosis is typically caused by extravasation of sclerosants. It typically presents as an ulcer with smooth and non-geographic borders. Historically, extravasation has been cited as the main cause of sclerotherapy-related necrosis. While this may be the case with osmotic or irritant sclerosants, it is far less likely with the use of detergent agents particularly in the foam format.The more commonly encountered pattern of stellate necrosis is an ischaemic ulcer secondary to arterial/arteriolar occlusion. In contrast to round necrosis, stellate necrosis follows an intra-vascular injection of sclerosants such as an inadvertent intra-arterial injection. But more frequently, stellate necrosis may follow a perfectly executed intra-venous or intra-telangiectatic delivery of sclerosants. Several pathogenic pathways can be considered. The physiologic response of veno-arteriolar reflex vasospasm (VAR-VAS) is possibly the most frequent pathway. It follows a high-pressure injection of the sclerosant in a target vein resulting in a rapid rise of intravenous pressures which in-turn would trigger a sympathetic neuronal reflex vasospasm of the pre-capillary sphincters and a corresponding opening of the normally closed arterio-venous anastomoses (AVAs). This communication would allow entry of the sclerosing agent into the arteriolar side of the circulation resulting in arteriolar occlusion and infarction of the corresponding skin. Similarly, an intravenous administration of sclerosants in the vicinity of defective boundary valves or persistently open AVAs can result in the entry of detergent agents into the arteriolar side of the microvasculature causing an ischemic stellate ulcer. Conclusions: In this first instalment of these two-part series, we review the pathogenic mechanisms of post-sclerotherapy necrosis. In the second instalment, we describe risk minimisation and management strategies.