U Because skeletal dysplasias are primary disorders of bone, they have not been commonly understood as neurosurgical diseases. Nevertheless, neurosurgical complications are commonly encountered in many cases of dysplasia syndromes. The authors present two cases of skeletal dysplasia that caused overt instability of the cervical spine. One patient with a diagnosis of Gorham disease of the cervical spine was treated with prolonged fixation in a halo brace after an initial attempt at instrumentation with a posterior occiput‐C4 fusion. The other patient, who at birth was identified to have camptomelic dysplasia, has been treated conservatively from the outset. Although these two patients presented with different disorders—in one patient adequate mature bone never formed and in the other patient progressive bone loss became apparent after a seemingly normal initial development—these cases demonstrate unequivocally that surgical options for fusion are ultimately limited by the quality of the underlying bone. In patients in whom the bone itself is inadequate for use as a substrate for fusion, there are currently limited treatment options. Future improvements in our understanding of chondrogenesis and ossification may lead to the design of superior methods of encouraging fusion in these patients; however, at the present time, long-term maintenance in a halo brace may, in fact, be the only treatment.

/pdf/report-of-two-cases-and-review-of-the-literature-12jmr5r1y4.pdf

Report of two cases and review of the literature

Though rare in incidence, chylothorax can lead to significant morbidity and mortality. Its occurrence corresponds to increased mortality following esophagectomy. Leakage of chyle and lymph leads to significant loss of essential proteins, immunoglobulins, fat, vitamins, electrolytes and water. The presence of chylomicrons and a triglyceride level >110 mg/dl in the aspirated pleural fluid confirms the diagnosis of chylothorax. Identifying the aetiology using different diagnostic tests is important in planning treatment. While therapeutic thoracentesis provides relief from respiratory symptoms, the nutritional deficiency will continue to persist or deteriorate unless definitive therapeutic measures are instituted to stop leakage of chyle into the pleural space. Definitive therapy consists of obliteration and prevention of recurrence of chylothorax. Aggressive surgical therapy is recommended for post-traumatic or post-surgical chylothorax.

/pdf/aetiology-and-management-of-chylothorax-in-adults-394dkg1tqb.pdf

Aetiology and management of chylothorax in adults

Cutaneous vascular malformations are rare disorders representing errors in vascular development. These lesions occur much less commonly but are often confused with the common infantile hemangioma. It is important to properly diagnose vascular malformations because of their distinct differences in morbidity, prognosis and treatment. Vascular malformations may be associated with underlying disease or systemic anomalies. Several of these syndromes are well defined and can often be distinguished on the basis of the flow characteristics of the associated vascular malformation. Learning objective At the completion of this learning activity, participants should have a better understanding of the different types of cutaneous vascular malformations. Because of the importance of proper diagnosis of these lesions, participants should also be better able to direct correct management and treatment.

Vascular malformations: Part I

Venous Malformations: Classification, Development, Diagnosis, and Interventional Radiologic Management

The lymph vascular system parallels the blood vasculature and as one of its key functions returns liquid and solutes to the bloodstream, including macromolecules that have escaped from blood capillaries and entered the interstitium. In conjunction with interspersed lymph nodes and lymphoid organs, the lymphatic vasculature also acts as a conduit for trafficking immune cell populations. Echoing the explosion of knowledge about blood vessel angiogenesis (properly termed "hemangiogenesis"), the past two decades have also witnessed a series of significant, yet less-noticed discoveries bearing on "lymphangiogenesis," along with delineation of the spectrum of lymphedema-angiodysplasia syndromes. Failure of lymph transport promotes a brawny proteinaceous edema of the affected limb, organ, or serous space that is disfiguring, disabling, and on occasion even life-threatening. Key members of the vascular endothelial growth factor (VEGF) and angiopoietin families of vascular growth factors (and their corresponding tyrosine kinase endothelial receptors) have been identified which preferentially influence lymphatic growth and, when manipulated in genetically engineered murine models, produce aberrant "lymphatic phenotypes." Moreover, mutations in VEGF receptor and forkhead family developmental genes have now been linked and implicated in the pathogenesis of two familial lymphedema-angiodysplasia syndromes. Thus, recent advances in "molecular lymphology" are elucidating the poorly understood development, physiology, and pathophysiology of the neglected lymphatic vasculature. In combination with fresh insights and refined tools in "clinical lymphology," these advances should lead not only to earlier detection and more rational classification of lymphatic disease but also to better therapeutic approaches, including designer drugs for lymphangiostimulation and lymphangioinhibition and gene therapy to modulate lymphatic growth.

Lymphangiogenesis and lymphangiodysplasia: From molecular to clinical lymphology

1 There now exists the basis for a new syndrome which is supported by a remarkable similarity of clinical and roentgenographic findings in twenty-four cases, and by an equally convincing similarity of the histological picture in eight of these, which we have personally studied2 However it is acco

Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone); its relation to hemangiomatosis.

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Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone); its relation to hemangiomatosis.