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chest pain

Hello!
My name is Celine and my question is: How great is the risk if I don't get treatment for my SMA syndrome after 2 years? I had a CT scan on april 08  that showed a possible SMA syndrome but by not having insurance I just deal with the pain right now hoping to have coverage soon.
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Below is info found on this condition....not being doctors and being a support forum I must advise u to see a dr even at a clinic and get on treatments ...u should be on a special diet...and not knowing about this condition myself....can only suggest u try the expert forum.....but do not self medicate when u have a serious condition.
I pray u r able to get some help.

Godspeed
"selma"


Superior mesenteric artery syndrome
From Wikipedia

SMA syndrome was first described in 1842 by Carl Freiherr von Rokitansky.

Superior mesenteric artery (SMA) syndrome is a very rare, life-threatening gastrointestinal disorder characterized by a compression of the third portion of the duodenum by the abdominal aorta (AA) and the overlying superior mesenteric artery. The syndrome is typically caused by an angle of 6°-25° between the AA and the SMA, in comparison to the normal range of 38°-56°, due to a lack of retroperitoneal fat. In addition, the aortomesenteric distance is 2-8 milimeters, as opposed to the typical 10-20. [1]
SMA syndrome was first described in 1842 by Carl Freiherr von Rokitansky in patients at autopsy. Only 0.013 - 0.3% of upper-gastrointestinal-tract barium studies support a diagnosis,[1] making it one of the rarest gastrointestinal disorders known to medical science. With only about 400 cases reported in English-language medical literature since the 1800s, recognition of SMA syndrome as a distinct clinical entity is controversial,[2] with some in the medical community doubting its existence entirely.[1] It is estimated that 1 of every 3 patients die of the condition [3]
Wilkie published the first comprehensive series of 75 patients in 1927, after which the eponym "Wilkie's syndrome" emerged.[4] It is also known as cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion.[5] It is distinct from Nutcracker syndrome, which is the entrapment of the left renal vein between the AA and the SM









TREATMENTS


In mild or acute cases, conservative treatment should be attempted first, involving the reversal or removal of the precipitating factor with proper nutrition and replacement of fluid and electrolytes, either by surgically-inserted jejunal feeding tube, nasogastric intubation, or peripherally inserted central catheter (PICC line) administering total parenteral nutrition (TPN). Symptoms typically improve after restoration of weight,[15] except when reversed peristalsis persists[16] or if regained fat refuses to accumulate within the mesenteric angle.
If conservative treatment fails, or if the case is severe or chronic, surgical intervention is required. The most common operation for SMA syndrome, duodenojejunostomy, was first proposed in 1907 by Bloodgood.[6] This invasive, open surgery involves the creation of an alternate route between the duodenum and the jejunum,[17] bypassing the compression caused by the AA and the SMA.[1] Less common surgical treatments for SMA syndrome include laparoscopic, Roux-en-Y, or robotically-assisted duodenojejunostomy; gastrojejunostomy; anterior transposition of the third portion of the duodenum; intestinal derotation; and division of the ligament of Treitz. Lysis of the duodenal suspensory muscle has the advantage that it does not involve the creation of an intestinal anastomosis.[8] The world's first robotically-assisted intestinal bypass for SMA syndrome was performed on July 30, 2008 at the London Health Sciences Centre in Ontario, Canada. In contrast to traditional open duodenojejunostomy which involves a 15-centimeter scar on the upper belly, inelastic internal staples, a one-week hospital stay and significant postoperative pain, the Da Vinci robot's range of motion allows for the use of stitches in place of staples, minimizes scarring to only five one-centimeter incisions and reduces both hospital recovery time and narcotic use by more than 50%.[18]
The possible persistance of symptoms even after surgical bypass can be traced to the remaining prominance of reversed peristalsis in contrast to direct peristalsis, even after the precipitating factor (the duodenal compression) has been bypassed or relieved. Reversed peristalsis has been shown to respond to an open surgery invented in China called duodenal circular drainage.[19]
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