Skin necrosis following sclerotherapy. Part 2: Risk minimisation and management strategies.

Tissue necrosis is a serious but rare complication of sclerotherapy. Early detection and targeted management are essential to prevent progression and minimise serious complications. In the first instalment of this paper, we reviewed the pathogenic mechanisms of post-sclerotherapy necrosis. Here, we describe risk minimisation and management strategies.Risk factors must be addressed to reduce the chance of necrosis following sclerotherapy. These may be treatment-related including poor choice of sclerosant type, concentration, volume or format, poor injection technique, suboptimal ultrasound visualisation and treatment of vessels in high-risk anatomical areas. Risk factors specific to individual patients should be identified and optimised pre-operatively.Tissue necrosis is more likely to occur with extravasation of irritant sclerosants such as absolute alcohol, sodium iodide, bleomycin and hypertonic saline, whereas extravasation of foam detergent sclerosants rarely results in tissue loss. Proposed treatments for extravasation of irritant sclerosants include infiltration of an isotonic fluid and hyaluronidase. Management of inadvertent intra-arterial injections may require admission for neurovascular observation and monitoring for ischaemia, intravenous systemic steroids, anticoagulation, thrombolysis and prostanoids infusion when required. Treatment of veno-arteriolar reflex vasospasm (VAR-VAS) necrosis follows the same protocol involving systemic steroids but rarely requires hospital admission and may not require anticoagulation.In general, treatment of post-sclerotherapy necrosis is challenging and most proposed treatment measures are not evidence-based and only supported by anecdotal personal experience of clinicians. Despite all measures, once the necrosis has set in, it is very difficult to reverse the process and all measures described here may only be useful in prevention of progression and extension of the ulceration.Mid to long-term measures include addressing exacerbating factors, management of medical and psychosocial comorbidities, treatment of secondary infections and referrals to relevant specialists. All ulcers should be managed with compression and prescribed dressing regimes in line with the healing stage of the ulcer.

Skin necrosis following sclerotherapy. Part 1: Differential diagnosis based on classification of pathogenic mechanisms.

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.

Recurrent Chronic Intervillositis: The Diagnostic Challenge - A Case Report and Review of the Literature.

BACKGROUND: Chronic intervillositis (CI) is a rare placental condition involving diffuse infiltration of intervillous spaces by CD68- or CD45-positive maternal mononuclear inflammatory cells. Because no validated clinical or biochemical markers are specific to CI, the diagnosis is purely histopathological and is made postpartum. CASE: This report describes a case of recurrent CI associated with adverse complications in two successive pregnancies. Both pregnancies were complicated by intrauterine growth restriction. Coexistent massive perivillous fibrin deposition was present in the first placenta. This case highlights the importance of CI in explaining and predicting adverse perinatal outcomes. CONCLUSION: CI is associated with adverse pregnancy outcomes and a high risk of recurrence, and it can coexist with massive perivillous fibrin deposition. Pathologists must ensure that the significance of these diagnoses is adequately conveyed to clinicians, to optimize management of subsequent pregnancies.

Intra-arterial injection of sclerosants: Report of three cases treated with systemic steroids.

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.

In search of risk factors for chronic pain in adolescents: a case-control study of childhood and parental associations.

OBJECTIVES: This 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. METHODS: Our 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. RESULTS: Migraine, 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. DISCUSSION: It 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.