Top Banner
DR. SHAHZAD HUSSAIN BDS, FCPS(Resident) Nishtar institute of Dentistry, Multan SNDENTALCARE.CO
30

Av malformation

Jan 22, 2018

Download

Health & Medicine

Welcome message from author
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
Page 1: Av malformation

DR. SHAHZAD HUSSAIN

BDS, FCPS(Resident)

Nishtar institute of Dentistry, Multan

SNDENTALCARE.CO

Page 2: Av malformation

Case PresentationPatient Name: Asia

Age/Gender: 30 year/Female

Page 3: Av malformation

Presenting Complaint

History Of Presenting Complaint

Past Medical & Dental History

Family History & Personal History

General Physical Examination

Page 4: Av malformation

Inspection Duration: since 3 year of age

Rate of progression: Slowly progressing lesion

Size: 3-5 cm

Site: lesion extended from 2 cm behind the angle of the mouth below the ear lobe. 2 cm posterior to the labiomental angle. Superiorly lesion extend to the pre auricular region and inferiorly it involves the lower border of the mandible.

Page 5: Av malformation

Extra Oral Examination The Swelling is

Diffuse, irregular

Surface, bluish

In color, normal

TMJ joint movements

& Normal mouth

Opening and lateral

Protrusive movemnt

Page 6: Av malformation

Palpation Firm, tender & warm swelling.

Page 7: Av malformation

Intra Oral Examination The lesion extended

from floor of the mouth to the retromolar pad area sparing the lingual side. It also involves the right lower buccalvestibule, soft & hard palate & fauces.

Page 8: Av malformation

Intra Oral Examintion

Page 9: Av malformation

Diffrential Diagnosis

Vascular Tumors:1:Benign:I. Infantile HemangiomaII. Congenital Hemangioma: a. Rapid involuting Congenital Hemangioma, (RICH)b. Non involuting Congenital Hemangioma(NICH)c. Partially involuting Congenital Hemangioma(PICH)

2:Locally Aggressive Vascular Tumors3:Malignant Vascular Tumors

Page 10: Av malformation

Basic Cell biology On basis of cell kinetics, there are two major types

of vascular anomalies:

Hemangiomas: lesions demonstrating endothelialhyperplasia.

Vascular Malformations : lesions with normalendothelial turnover.

Page 11: Av malformation
Page 12: Av malformation

Diffrential Diagnosis

Vascular Malformation:1. Capillary Malformation

a. Port Wine stains(Strug weber Syndrome)

1. Venous Malformation

2. Lymphatic Malformation

3. Arterio-Venous malformation

4. Arterior-Venous Fistula

5. HEREDITARY HEMORRHAGIC TELANGIECTASIA(Rendu Osler Weber disease)

Page 13: Av malformation

Diagnostic Tests

1. History & clinical examination2. Complete Blood Count3. CT Angiography4. Ultrasonography5. CT scan6. MRI7. Plain X-ray OPG (Shows soap bubble & honey comb

appearance) Other Investigations that are required:1. GLUT +ve for Hemangioma2. GLUT –ve for Vascular malformation

Page 14: Av malformation

CT Scan(Axial View)

Page 15: Av malformation

CT Scan(Coronal View)

Page 16: Av malformation

CT Scan(Saggital View)

Page 17: Av malformation

CT Scan(Report)

Page 18: Av malformation

Diagnosis Vascular malformation (AV)

Hemangioma can’t be ruled out.

Page 19: Av malformation

Treatment Options1. Non Surgical (Conservative)

2. Surgical (Non (Conservative)

Page 20: Av malformation

Non SurgicalI. Medications

A. Intra Lesional Cortecosteroids

B. Interferon Therapy

C. Cytostatic Therapy

D. Propanol Therapy

2: Sclerotherapy

3: Laser Therapy

Page 21: Av malformation

Surgical Resection Of the Lesion

Embulization

Compartmentalization

Page 22: Av malformation

Intralesional CortecosteroidsMechanism: Lead to increase in the level of cytochrome b

and induces apoptosis in hemangioma.

Benefits:

1. First line therapy

2. Conservative

3. Inexpensive

Disadvantages:

1. Sleep disorder

2. Irritability

3. GERD

4. Osteoprosis

Page 23: Av malformation

InterFeron Therapy Mechanism: Interferon alpha 2a and Alpha 2b based

on down regulation of fibroblasts growth factors.

Disadvantages: Due to neurotoxic side effects it is no longer recommended.

Page 24: Av malformation

CytotoxiC therapy Dosage: I/V weekly dosage of 1 mg/m3 over a period of

one to 8 months responds well in all patients

Disadvantages:

1. Loss of hear

2. Abdominal discomfort

Page 25: Av malformation

Proponol Therapy Mechanism: Exact mechanism not clearly understood.

The pro- angiogenic pathway could be suppressed by proponol therapy. Propnol therapy effect can be explained by premature apoptosis of Endothelial cells. It causes vasoconstriction of micro vessels.

It is the first line therapy for RICH. Within 24 hours after the first application , size reduction of upto 90 percent can be achieved within one two weeks.

Usual dose of 1-3 mg /kg daily

Page 26: Av malformation

Laser Therapy Controversial

It is believed that laser/phototherapy will not cure the pathology as it has a penetration depth of 0.75 mm to a maximum of 2mm.

Only indicated for the superfacial parts of infantile hemangioma.

Page 27: Av malformation

Sclerotherapy It is the most wide spread method.

In 1903, wyeth used boiling water as the sclerosing agent.

There are many sclerosing agents which are divided into following catogaries

1. Osmotic substances: Hypertonic saline, salicylate

2. Chemical Substances: Ethanol & iodine

3. Anticancer Substances: Bleomyocin

4. Detergents: Sodium tetradecylsulphate

Page 28: Av malformation

Resection with immediate replantation.

Goal of the surgery is to remove the lesionControl of hemorhageReconstruct the defectIncision: Extraoral incision is preferable when the lesion

extends proximally to the angle and ramus. Tran oral approach doesn’t allow good visibility & hemorrhage control

Procedure: An osteotomy can be made, distal to the lesion & involved segment can be rotated laterally to visulaize the lingual surface of the mandible. The resected mandible is replaced with the autologus bone grapt which is stabilized with bone plates.

IMF is done to maintain proper jaw position.

Page 29: Av malformation

Compartmentalization Jackson & colleagues treated 18 patients by this

technique in 1993.

They placed non resorbable sutures deep subcutaneous within the lesion

After placing the sutures, sclerosing agents were injected in the compartment followed by surgical resection with minimal risk of bleeding

The amount of infiltration is 3 cc to 35 cc depending upon the size of the lesion

Tracheotomy may be required To prevent airway compromise.

Page 30: Av malformation