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VASCULAR LESIONS OF HEAD & NECK, BED SORES

VASCULAR LESIONS OF HEAD & NECK, BED SORES. Presenter – Dr. Neil D’Souza. HAEMANGIOMA. Most common vascular tumour in children (in 10% of term deliveries) Benign vascular endothelial tumour Common in girls (3 : 1). Onset is few weeks after birth

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VASCULAR LESIONS OF HEAD & NECK, BED SORES

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  1. VASCULAR LESIONS OF HEAD & NECK, BED SORES Presenter – Dr. Neil D’Souza

  2. HAEMANGIOMA

  3. Most common vascular tumour in children (in 10% of term deliveries) • Benign vascular endothelial tumour • Common in girls (3 : 1)

  4. Onset is few weeks after birth • Biphasic growth showing initial rapid growth with gradual involution over 5-7 years • Shows cellular endothelial hyperplasia with increased mast cells

  5. Commonly seen in skin and subcutaneous tissue • Common in head and neck region (60%) • Can occur anywhere in the body like in liver, brain, lungs, other organs

  6. It grows rapidly in first year and 70% involutes in 7 years • Early proliferative lesion is bright red, irregular; deep lesion is bluish coloured • Involution causes colour fading, softness, shrinkage leaving crepe paper like area

  7. Head and neck haemangioma is associated with ocular and intracranial anomalies • Ulceration, bleeding, airway block and visual disturbances are common complications. • Platelet trapping and severe thrombocytopenia • Rare, but important life-threatening complication • Presents as ecchymosis, petechiae, intracranial haemorrhage, massive GI bleed

  8. Raised angiogenic (fibroblastic) growth factor which is secreted in patient’s urine is useful lab investigation

  9. Classification • Capillary • Salmon patch (stork bite) • Strawberry haemangioma • Port-wine stain (naevus flammeus) • Cavernous

  10. CAPILLARY HAEMANGIOMA

  11. Salmon patch (stork bite)

  12. Presents at birth • Commonly occurs in the nape of the neck (50%), face, scalp and limbs • Usually involves a wide area of skin

  13. Caused by an area of persistent fetal dermal circulation • With age, it undergoes spontaneous regression and disappears completely (usually in one year) • Hence masterly inactivity is the treatment

  14. Strawberry haemangioma

  15. May start at birth • If the child is normal at birth; between one to three weeks it may appear as a red mark which rapidly increases in size within 3 months to form strawberry/raspberry haemangioma

  16. Contains immature vasoformative tissues • There will eventually be intravascular thrombosis, fibrosis and mast cell infiltration • It is a true capillary haemangioma

  17. It is 20 times more common than port wine stain. • It is common in white girls • Male to female ratio is 1 : 3 • It is common in head and neck region.

  18. It is clinically compressible, warm with bluish surface. • Bleeding, ulceration can occur after minor trauma and also • It involves skin, subcutaneous tissues and often muscles

  19. After one year of age, it slowly begins to fade, and disappears completelyin 7-8 years (70% in 7 years) • It is the most common haemangioma

  20. Port-wine stain (Naevus flammeus)

  21. It presents at birth and persists throughout life without change • Spontaneous regression will not occur • Due to defect in maturation of sympathetic innervation of skin causing localised vasodilatation of intradermal capillaries

  22. Presents as • Smooth, flat, reddish blue/intensely purple area • Eventually the surface becomes nodular and keratotic • Common in head, neck and face; • Often within the maxillary and mandibular dermatomes of 5th cranial nerve

  23. It is actually a capillary malformation even though considered under haemangioma • It is often associated with • Sturge-Weber syndrome, • Klippel-Trenaunay-Weber syndrome and • Proteus syndrome

  24. Treatment • Wait and watch policy commonly - allowed for spontaneous regression • Pulsed dye laser (diode laser) • Surgical excision and reconstruction • Sclerotherapy/ cryotherapy/ CO2 snow therapy cause unpleasant scarring

  25. Indications for surgery or intervention • Uncontrolled growth • Functional impairment like vision or hearing • Accidental haemorrhage

  26. Feeding vessels may need to be ligated after wide exposure before achieving complete extirpation • Preoperative embolisationfacilitates surgical excision and reduces the operative blood loss

  27. 10-year-male with left cheek hemangioma treated with percutaneous glue embolization followed by surgical resection

  28. Once embolisation is done, surgery should be done as early as possible otherwise recurrence occurs with enlarged collaterals • Materials used are—foam, plastic spheres, stainless/platinum steel coils, ethanol, polyvinyl alcohol foam of 1000 μmeters size, and rapidly polymerizing acrylic • Done with interventional radiology underC-Arm guidance

  29. Rapidly growing haemangioma may need systemic/oral and intralesional steroid therapy • Antiangiogenicinterferon 2a may be useful • Life-threatening platelet trapping may be controlled by cyclophosphamide chemotherapy • Haemangioma with drug resistane can be treated with radiotherapy

  30. CAVERNOUS HAEMANGIOMA

  31. Presents at birth • Gradually increases in size • Consists of a multiple venous channels • Often mixed with lymphatic component also

  32. Sites: • Head & neck • Limbs, • Tongue, • Liver and other internal organs

  33. Large or multiple cavernous haemangiomas can cause congestive heart failure (hyperdynamic) due to shunting of large quantity of blood • Cavernous haemangioma with dyschondroplasia is called as Maffucci syndrome

  34. Clinical Features • Non-pulsatile swelling • Smooth • Soft • Well localised • Warm • Fluctuant • Compressible • Bluish surface • Non-transilluminant

  35. Usually nontender unless it gets infected or undergoes thrombosis or causes haemorrhage

  36. Differential Diagnosis • Lymphangioma: it is brilliantly transilluminant unless it is infected or fibrosed • Lipoma • Cold abscess • Lymph cyst

  37. Complications • Haemorrhage • DIC • Thrombosis • Infection and septicaemia • Ulceration • Erosion into the adjacent bone • High output cardiac failure

  38. Investigations • Ultrasound with doppler • Angiogram to find out feeding vessel • Platelet count • MRI/MR angiogram to see feeding vessels and deeper extension

  39. Treatment • Sclerosant therapy: • Initial first line of therapy • Causes aseptic thrombosis and fibrosis • Sodium tetradecyl sulphate/ hypertonic saline are used • Often multiple injections are needed to achieve complete required effect • Later excision of the lesion is done

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