Thromboangitis Obliterans( Buerger Disease) Informations

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TROMBO-ANGİTİS OBLİTERANS

(BUERGER Disease)

 

Leo Buerger (1879-1943)

In 1908, Mount Sinai Hospital, Dr. Leo Buerger’s disease, while studies on Buerger’s disease has managed to define the clinical entity, and histological features.

The disease is mainly young and male smokers, the lower extremity arteries is defined as a failure. Often associated tromboflebitle.
Histological appearance of a clearly tanımlanamasa; karekteritiktir segmental involvement. Occlusive lesions, recanalization mediada inward capillary growth and absence of elastic tissue is divided into aterosklerozisten.
Buerger’s disease, acute venous thrombophlebitis was noted that most attacks.

BIOGRAPHY


Leo Buerger was born in Vienna, his family emigrated to America.
Built in 1901 and based surgical training Colombiya graduated from the University. Lennox Hill hastenesinde Stajerliğini completed surgical section. Breslow surgery clinic in Germany in 1905 after working for a while and returned to NewYorka served as a professor of urology at Mount Sinai hastenesinde.
Buerger of the interest, as well as radiology and radium therapy on hematological tumors gelişimiylede concerned. Tilder F. Brown worked on the development in conjunction with cystoscopy and partly recognized as Brown-Buerger cystoscope later became known as Buerger cystoscope. Listen to the music, Dr. Leo is a good piano sniffer. Task used to do it again when they had married in 1929 in Los Angeles, chair of urology. California is seen as people who were offended and very negative in 1934 and again in New York Mt.Sinai Dr.Buerger in appointed.

.

ETYOLOJİ

Buerger’s disease (thromboangiitis obliterans) 75 years, although a pathology known for a long time, despite improvements in surgical or medical treatments, 2-in 4% of patients with chronic limb amputations, which are inevitable in a progressive inflammatory disease of non-atheromatous arterial (1.2) . Creates a group of small arteries in Buerger’s disease of unknown cause. Age, sex, race, hereditary factors (HLA antigen), and non-autoimmune mechanism is known as secondary etiologic factors. Smoking, the most important etiological factor is considered to be secondary. Recurrence of the disease, and the progress of agrevasyonu very tight link between smoking and there.

Amount of medium-sized vessels in the lower and upper extremity. The disease with an average around 28 years, male smokers are 95% (3). Due to the characteristics of the disease due to involvement of the distal vessel, a large group of patients, surgical revascularization is not a chance, conservative treatment techniques. The risk of peripheral gangrene in diabetic patients 70 years of age on the other hand, non-diabetic patients seen by more than 70 times. Microangiopathic dominated in this patient group, the microcirculation of functional disorders develop due to the non-glukolitik metabolism. The third clinical scenario is not applicable in the distal peripheral bypass surgery is the patient group as a result of atherosclerosis. These three clinical cases, limb amputation appears to be the last treatment option, but to be accepted by both patients and surgeons faced with extremely difficult as a result of which We remain a morbidity.

Modification of risk factors for peripheral vascular disease (smoking cessation, such as the regulation of hyperlipidemia and diabetes) can help slow the progression of the disease. Medical treatment antiagreganlar (4) (acetyl salicylic acid, klopidegrol), anticoagulants (warfarin), drugs that increase red blood cell fleksibilitesini (4), hyperlipidemia regulation (exercise, statins, fibrates), regulation of diabetes (or insulin with oral anticoagulants), α-receptor blockers, prostaglandin anaologları (5) (iloprost), Osijek hyperbaric therapy (6) options used to date. Not be performed when curative treatment is surgical sympathectomy, sympathetic blockade, debridement of infected tissue was used until the present day as the surgical approaches used with palliative intent (7). 12-in 15% of patients with ischemic foot ulcers of all kinds of medical treatment, limb amputation within 3-5 years required (8).

CLINICAL RESULTS

The disease most often begins with 20-35 years of age. Thromboangiitis obliterans, thrombophlebitis in 40% of patients seen roaming. Most of the patients seen in the lower extremity findings. The disease begins with a small artery. (Posterior tibial, anterior tibial, radial, ulnar, plantar, or palmar digital arteries). Medium and large arteries (popliteal, femoral, or brachial arteries) also affected by late season. Mayor arteries (aorta and iliac) disease involvement have been reported very rarely. Segmental lesions and episodic dağılımlıdır cruise tracks. In the acute stage, all the layers of the vessel wall is an acute inflammatory changes (panarteritis). Central thrombi and their purulent center and periphery of the foci of giant cells found. During the recovery period, (intermediate term), this characteristic is lost views. Is organized and recanalized thrombus. Recently, the lumen, which is the end product of the specified histological changes in tissue with konjektif is occluded by connective tissue.

Symptoms of the disease, pathological changes in the arterial occlusion Be cause, ie, inflammatory lesions and the destruction of the tissue after ischemia depends. Early symptoms appear as the bottom of the feet or fingers, pain and more pain is at rest. He’s mostly small-diameter arteries of the disease, intermittent claudication ASO’da (arteriosklerosis obliterans) is seen less often than seen. During periods of mild or the beginning of the disease, trophic changes, color changes, and may be changes in the form of coldness. Later periods, or standing on your toes gagren occurs. Inflammatory changes, causing ischemic pain at rest and thrombophlebitis can cause neuritis.

METHODS OF DIAGNOSIS

Ultrasound:
Doppler ultrasound method is determined with the flow and segmental pressure values ​​decreased.

Angiography:
Artery occlusion proximal to the smooth-looking, and usually the normal diameter. Anjiografideki most characteristic finding of occlusion of the vessel in view of increasingly finds ways to thinning and tree roots. Obstructions can also be seen around the short kolleteral network.

The diagnosis is taken into consideration the following criteria:
Coldness of the extremity ends of the asymmetric
Peripheral artery pulzasyonlarının (tibial and dorsalis pedis arteries) or the absence of relief
Tapering gradually, showing a sudden occlusion of blood vessels, and the corkscrew shaped structure showing kolleteral anjiogram
The absence of atheroma plaques
These findings are evaluated together with symptoms of the disease is decisive for diagnosis.

CLINICAL COURSE AND PROGNOSIS

At the end of a long-term observations, in terms of the natural course of disease is divided into 3 groups.

Group I: In this group, the initial period of transient ischemic attack, followed by a period without incident. Patients in this group, comprises 50% of all cases.

Group II: After the initial period, show a moderate periods of recurrence of symptoms occurs. Generates 42% of the patients in this group.

Group III: This group of patients, again during the acute attack, amputation, and often have serious clinical symptoms occur. This group covers 8% of cases.

TREATMENT

Constitute the mainstay of treatment, smoking cessation and supportive medical treatment. Foot hygiene is important to protect. Show multifocal lesions of the disease, the benefits of transactions prevents rekonsrüktif. Applicable to the method of surgical treatment of lumbar sympathectomy. In this method, the lumbar sympathetic ganglia outside the retroperitoneal ganglia removed first. The goal is to increase the blood supply by removing the vasomotor activity. Ticlopidine antiplatelet agent used in medical treatment, increases in erythrocytes fleksibiliteyi Pentoxifylline (Trental) and defibrinated Batroxobin’in agent shown to be effective as chronic arterial lesions. If no cases of wound healing and spread finger or foot amputation may be required.

THE END @ COPYRIGHT dR IWAN SUWANDY 2011

2 thoughts on “Thromboangitis Obliterans( Buerger Disease) Informations

  1. Michael Napier December 8, 2011 / 6:07 am

    I have lived with Buerger’s Disease for over 14 years now. I quit smoking for the first 3 years but after I started working again…I started up again. Human nature will see what he can get away with and what he can’t. But I have a very interesting theory as to Buerger’s Disease..and here it is.

    Why is it that in the Middle East and Asia Burger’s Disease is in epidemic preportions. About 1 in ten cigarette smokers get it there. In the USA it’s more like 1 in 10,000. Why is that??? Well…I will tell you why. Plain and simple. It is the chemicals the manufacturers add to it to make it more addictive, etc. You see..here in the USA we have the FDA which regulates the amount of chemicals added. In Asia and such…there is no FDA calling the shots telling them what they can or can’t add to them. So they just load them up as much as they can for the sake of selling cigs. One time I tried a Viet-Namese smoke called “Queen”. After two puffs on that thing, I could barely walk.

    Also look at it this way…American Indians have been using tobacco for centuries..perhaps even 1000’s of years. None of them ever got “Buerger’s Disease” or even Cancer. So…when the white man industrial machine got ahold of this product and mass produced it, then all sorts of bad things began to happen to smokers who were hypersensative to their chemicals they added. Dr. Buerger discovered this disease which he named after himself in 1903. That is about when RJ Reynolds started mass producing this stuff…think about it. And speaking from experience..When I was diagnosed in 1998, Marlboro reds were my brand. I still can’t handle them. I switched to Camel filter and got away with it for 8 years until they changed to slow burning papers in December of 2010. That chemical made it impossible for me to smoke ever again.

    • iwansuwandy December 8, 2011 / 8:41 am

      thanks vor visit my web blog and read about buerger disease, I had seen the case only one time during
      my intership in medical faculty,that was why I never soking.
      I hope what you told us about your experience against smoking, in Indonesia many smoker but they starting to used the very mild
      cigarette but the cases not many found,may be another factors related,as you told the Indian never seen with Buerger Disease.
      To stop your smoking habit very hard because your brain had change and if you stop something will happen, but you can starting to work anytime,never give time for smoking. I am collecting cigarette label and old pipe which antisipation for smoking habit, I will put them in my museum and
      one day after work hard the goverment will starting to stop the cigar ,In Indonesia in general place forbidden to smoke.
      My suggestions starting to used your time more for other social games than smoking and keep the smoking apparat as the museum collections to next generations.

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