Ligament of Treitz: Anatomy and Duodenal Landmark

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

The ligament of Treitz is the suspensory muscle of the duodenum (musculus suspensorius duodeni), a fibromuscular band that attaches the duodenojejunal flexure to the connective tissue around the celiac and cranial mesenteric arteries and to the right crus of the diaphragm. It is the classic boundary between foregut and midgut, and in clinical medicine it is the landmark that separates upper gastrointestinal bleeding from lower gastrointestinal bleeding.

This structure matters for three separate reasons that converge on one small piece of anatomy. First, it is a functional anchor, holding the sharp duodenojejunal angle in place so that luminal contents pass smoothly from the extraperitoneal duodenum into the mobile small intestine [1]. Second, it is a clinical dividing line that determines how a bleeding patient is triaged, scoped, and imaged. Third, it is a surgical and radiographic reference point that appears in operative planning for pancreatic and duodenal disease [2]. Students who learn it only as a name on a bleeding-classification list miss most of its value.

Václav Treitz (1819 to 1872) described the structure while working as a professor of pathological anatomy in Prague. He identified a small muscle connecting the duodenojejunal flexure to the celiac axis. The name "ligament of Treitz" persisted for decades even though the structure is muscular, and anatomists now prefer the term suspensory muscle of the duodenum [3].

Key Facts at a Glance

Anatomy and Structure of the Suspensory Muscle

Origin, insertion and tissue composition

The suspensory muscle is not a simple tendon. Cadaver studies show that it consists largely of smooth muscle fibers that arise from connective tissue around the stems of the celiac and superior mesenteric arteries and insert into the third and fourth parts of the duodenum in about 53 percent of specimens, with additional insertion into the duodenojejunal flexure in about 40 percent [4]. The muscle bundles continue the longitudinal and circular muscle coats of the duodenum itself, but they are not supplied by Auerbach's plexus, which separates them functionally from the rest of the gut wall [4].

Near the diaphragmatic end, striated muscle fibers appear. A study of 31 cadavers (21 adults and 10 fetuses) confirmed that the muscle is unstriped throughout most of its length, with striped fibers visible cranially near the insertion on the right side of the diaphragmatic esophageal opening [5]. This mixed composition is the single most commonly tested detail about the ligament: it contains skeletal muscle from the diaphragm and smooth muscle from the duodenum.

Between the muscle bundles lies loose connective and adipose tissue, and microganglia of up to about 90 cells can be found in these spaces [7]. The superior part of the muscle is enclosed in connective sheaths that are continuous with the adventitia of the aorta and celiac trunk [7]. This relationship explains why the structure is difficult to isolate cleanly at surgery.

Development

The suspensory ligament begins as a superior retention band in the fetus. As the gut rotates, this band is transformed into the suspensory ligament of the duodenum, and the muscle of Treitz develops within it. The inferior retention band atrophies, and a separate structure, the phrenicocolic ligament, forms during fetal life and develops its own smooth muscle cells [6]. This embryologic sequence links the ligament directly to intestinal rotation. Errors in that rotation process produce the malrotation syndromes discussed below. A 1966 study explicitly examined the relationship between the suspensory muscle and rotation of the intestinal loop, reinforcing that the two processes are developmentally coupled [8].

Innervation and proposed function

The suspensory muscle receives nonmyelinated nerve fibers from the celiac and superior mesenteric plexuses [4]. Because it lacks Auerbach's plexus input, several authors propose that it acts less like a segment of bowel and more like a sphincter, with innervation patterned opposite to that of the duodenum [7]. A related anatomical study described the Treitz ligament and duodenojejunal flexure as a valve that regulates emptying of duodenal contents, and reported that transecting the ligament altered evacuatory function in dogs [9].

In dogs, the electrical activity of the duodenojejunal flexure differs from that of the duodenum under normal conditions. After pyloroplasty, electrical activity at the flexure increases in amplitude and frequency. Adding transection of the Treitz ligament suppresses electrical activity in both the antrum and the flexure, which suggests a close functional interrelationship between the pylorus and the duodenojejunal junction [10]. That is a useful reminder that the ligament is not inert connective tissue.

Anatomical variants

The ligament is not uniform across individuals. Depending on how the duodenum fixes to the posterior abdominal wall, anatomists distinguish normoduodenum, dolichoduodenum (an elongated duodenum), and duodenoptosis (a downward-displaced duodenum). In normoduodenum and dolichoduodenum, the ligament contains a considerable amount of striated muscle tissue. In duodenoptosis, it consists of loose fibrous connective tissue with only single smooth muscle fibers [11]. This variation matters because a lax or fibrous ligament offers less suspension, which is exactly the situation described in a recent case of recurrent duodenal obstruction where the suspensory tissue corresponding to the ligament of Treitz was lax [12].

The Ligament as a Duodenal and Embryologic Landmark

The duodenum is unusual among gut segments because most of it is retroperitoneal and immobile. The peritoneal fossae around the duodenum form where fusion with the posterior parietal peritoneum is incomplete. In a dissection study of 24 cadavers, investigators found that the duodenal loop is usually completely fused with the posterior parietal peritoneum except at the duodenojejunal flexure. Ten distinct peritoneal fossae were catalogued, including right and left retroduodenal fossae, inferior duodenal fossae, and the paraduodenal and superior duodenal fossae. These recesses mostly result from incomplete adhesion of Treitz's fascia and provide an anatomical basis for paraduodenal hernias [13].

That single observation ties together three topics that students often learn separately. The ligament of Treitz is a landmark because it is the point where the fused, retroperitoneal duodenum gives way to the mobile, mesenteric jejunum. The fossae around it are the places where intestine can herniate. And the flexure itself is the pivot around which the whole proximal bowel can rotate abnormally.

Foregut and midgut boundary

The embryonic foregut gives rise to the esophagus, stomach, and proximal duodenum, supplied by the celiac artery. The midgut gives rise to the distal duodenum through the proximal transverse colon, supplied by the superior mesenteric artery. The duodenojejunal flexure, suspended by the ligament of Treitz, sits near the junction between these two vascular territories. Fewer than 10 publications have presented malignant sigmoid-duodenal fistulas, and in one of them the sigmoid colon cancer was found at laparotomy to be directly invading the duodenojejunal flexure arising from the ligament of Treitz on the left side of the superior mesenteric artery [14]. That case shows how the landmark's position relative to the superior mesenteric artery matters in real operative anatomy.

Clinical Significance

Bleeding localization

Upper gastrointestinal bleeding originates proximal to the ligament of Treitz. Lower gastrointestinal bleeding originates distal to it. This is the definition most often quoted in clinical practice, and it is the reason the structure appears in nearly every discussion of GI hemorrhage [2]. The practical consequence is that a patient with melena or hematemesis is assumed to have a lesion above the ligament until proven otherwise, while bright red rectal bleeding points below it. In one case report, a patient presented with melena and was ultimately found to have both a sigmoid colon tumor and extrinsic invasion into the horizontal duodenum, showing that the landmark guides initial reasoning even when the final diagnosis crosses the boundary [14].

Malrotation and abnormal fixation

The ligament plays a role in the embryologic rotation of the bowel [1]. When fixation is incomplete, the duodenojejunal junction becomes abnormally mobile. A published case described a 77-year-old man with recurrent aspiration pneumonia secondary to duodenal obstruction. Computed tomography showed dilation from the stomach to the proximal duodenum, with the third portion of the duodenum coursing caudally without passing between the abdominal aorta and the superior mesenteric artery. The superior mesenteric vein lay to the right of the artery at the L2 vertebral level but to the left of it at L4, suggesting mesenteric rotation. At surgery, no intestinal malrotation or internal hernia was found, but the duodenojejunal junction showed incomplete retroperitoneal fixation and the suspensory tissue corresponding to the ligament of Treitz was lax [12]. This is a clean example of a primarily ligamentous problem producing a functional obstruction.

Superior mesenteric artery syndrome

Vascular compression of the duodenum, also called superior mesenteric artery syndrome, occurs when the third part of the duodenum is compressed between the aorta and the superior mesenteric artery. The ligament of Treitz contributes to the effects of this compression [1]. A review of 10 cases plus 125 cases from the literature since 1962 found the lesion more common in women than in men. It may follow supine immobilization, use of a body cast, or rapid weight loss, and in about one third of patients no predisposing factor is identified. Diagnosis is best made by cinefluoroscopy. Most patients require surgery, and section of the suspensory muscle with relocation of the duodenojejunal junction relieves symptoms in many, while duodenojejunostomy is required in others [15]. Untreated vascular compression may run a chronic course or become acute with fatal results [15].

Surgical landmarking

Surgeons use the ligament and the foramen associated with it to enter the distal duodenum and proximal jejunum. A described "duodenal window first" approach to pancreatoduodenectomy accesses and mobilizes the second, third, and fourth parts of the duodenum and the first part of the jejunum through the duodenal window and Treitz's foramen, achieving an almost complete Kocher maneuver before opening the gastrocolic ligament. The technique was applied in 15 open and robotic pancreatoduodenectomies with no specific morbidity [2].

Postoperative and iatrogenic complications

Iatrogenic small bowel obstruction from rotation of the distal duodenum around the ligament of Treitz is rare. One report described proximal small bowel obstruction following an open right radical nephrectomy. Serial CT showed rightward displacement of the duodenojejunal flexure, and the diagnosis was iatrogenic rotational malposition of the proximal small bowel requiring surgical relief. The report emphasizes that the duodenojejunal flexure should remain in its anatomical left-sided position on postoperative imaging [16]. This is a concrete reason to know where the flexure normally sits.

Comparative Anatomy: Dogs, Cats and Horses

The suspensory apparatus differs across domestic species, and those differences change how disease presents.

In dogs and cats, the duodenojejunal flexure is less rigidly fixed than in humans. The mesenteric root allows more mobility, and the ligament does not form the same dense, well-defined band. Clinical consequences follow from this looseness. Abnormal mobility of the duodenojejunal junction can produce intermittent obstruction, and the proximal bowel can rotate around a lax attachment point. The functional coupling between the pylorus and the duodenojejunal junction described in dogs supports the idea that the region acts as a regulatory valve even where the gross ligament is subtle [10][9].

In horses, the duodenocolic fold is far more prominent than the suspensory muscle. The equine duodenum is closely associated with the base of the cecum and the right dorsal colon, and this fold is a consistent landmark during abdominal exploration. The relatively stronger duodenocolic attachment means the equine duodenojejunal region is defined more by its relationship to the large colon than by a discrete suspensory band. Students transitioning between species should not assume that the human pattern of a robust suspensory muscle transfers directly to the horse.

The practical takeaway is that the ligament of Treitz in small animals is best understood as a functional anchor and a radiographic landmark rather than a distinct palpable cord. In horses, the fold named for the duodenum and colon serves the comparable landmarking role.

How the Landmark Is Identified in Practice

Radiologists and surgeons rely on position rather than direct visualization. The ligament itself resists imaging: its fibromuscular structure makes visualization by CT or MRI challenging, and this is a genuine limitation rather than a technique gap [1].

Indirect identification uses several checkpoints:

1. The duodenojejunal flexure should sit to the left of the spine at approximately the L1 to L2 level in humans. Rightward displacement suggests rotational malposition [16].
2. The third part of the duodenum should pass between the abdominal aorta and the superior mesenteric artery [12].
3. The superior mesenteric vein should lie to the right of the superior mesenteric artery at the L2 vertebral level [12].
4. Cinefluoroscopy is the preferred diagnostic method for vascular compression of the duodenum [15].
5. On cross-sectional imaging after abdominal surgery, a change in the position of the flexure from left to right is a red flag [16].

Veterinary imaging applies the same logic with species-adjusted anatomy. The relative positions of the cranial mesenteric artery, the duodenum, and the flexure are the working references.

Common Misconceptions

Several errors appear repeatedly in student work and even in clinical writing.

The first is treating the ligament of Treitz as a true ligament. It is a muscle, and calling it a ligament obscures its contractile and sphincter-like behavior [1]. Anatomists prefer suspensory muscle of the duodenum for this reason [3].

The second is conflating the ligament with the duodenojejunal flexure. The flexure is a position. The ligament is a structure that suspends it. Literature frequently uses the ligament's name to designate the flexure, and this shorthand causes confusion about what the structure actually is [1].

The third is assuming the muscle attaches only to the diaphragm. Cadaver work shows the suspensory muscle arises from connective tissue around the celiac and superior mesenteric arteries and inserts into the duodenum, while a separate diaphragmatic slip (the Hilfsmuskel) attaches to the margin of the esophageal hiatus. The Hilfsmuskel and the suspensory muscle are separate entities [4]. Skeletal muscle does appear at the cranial end of the suspensory muscle near the diaphragm [5], but the structure should not be reduced to a diaphragmatic band.

The fourth is expecting the ligament to look the same in every patient. In duodenoptosis it is little more than loose fibrous tissue with scattered smooth muscle fibers [11].

The fifth is assuming the ligament is always visible on advanced imaging. It usually is not [1].

Quick Review

• The ligament of Treitz is the suspensory muscle of the duodenum, not a true ligament.
• It attaches the duodenojejunal flexure and distal duodenum to connective tissue around the celiac and cranial mesenteric arteries, with a diaphragmatic relationship at its cranial end.
• It contains smooth muscle throughout most of its length and skeletal muscle near the diaphragm.
• It is innervated by the celiac and superior mesenteric plexuses and lacks Auerbach's plexus supply.
• It separates upper from lower GI bleeding and foregut from midgut.
• It contributes to the effects of superior mesenteric artery syndrome and to disorders of intestinal rotation.
• In dogs and cats the flexure is less fixed. In horses the duodenocolic fold is more prominent.

This article is educational and is not a substitute for veterinary diagnosis or treatment.

Clinical Relevance, Limitations and Common Mistakes

The ligament of Treitz earns its place in the curriculum because it converts a small anatomical structure into a decision point. A clinician deciding whether to scope a vomiting dog from above or to image for lower tract disease uses the same foregut and midgut logic that the landmark encodes. A surgeon planning a pancreatoduodenectomy enters through the duodenal window and Treitz's foramen [2]. A radiologist reviewing a postoperative scan checks that the duodenojejunal flexure has not migrated rightward [16].

Limitations deserve honest treatment. Direct imaging of the ligament is difficult by CT or MRI [1]. Diagnosis of vascular compression relies on cinefluoroscopy rather than static cross-sectional images [15]. Variants in the amount of striated muscle and in the density of fibrous tissue mean that two patients with the same symptoms can have very different ligaments [11]. The relationship between the ligament and duodenal motor function is supported by experimental work in animals rather than by large human trials [10][9].

Common mistakes in clinical reasoning cluster around three habits. Mistaking the landmark for the structure leads to errors in operative reporting. Assuming that a normal upper endoscopy rules out pathology near the flexure overlooks lesions that sit at the boundary itself, as in malignant invasion of the duodenojejunal flexure [14]. And treating the ligament as anatomically constant ignores the lax variants that produce intermittent obstruction [12][17]. Chronic intermittent duodenal obstruction in children, for example, has been attributed to tight fixation of the ligament of Treitz, compression from mesenteric lymphomas, or abnormal attachment of the mesocolon [17]. Each of these requires different management.

Individual patients require evaluation by a veterinarian. Signs such as persistent vomiting, postprandial fullness, or unexplained weight loss near a suspected duodenal problem warrant imaging and clinical assessment rather than assumptions based on anatomy alone.

Frequently Asked Questions

What is the ligament of Treitz?

The ligament of Treitz is the suspensory muscle of the duodenum, a fibromuscular band that attaches the duodenojejunal flexure to connective tissue near the celiac and cranial mesenteric arteries and to the right crus of the diaphragm. It contains both smooth and skeletal muscle.

Why is the ligament of Treitz called a ligament if it is a muscle?

The name is historical. Václav Treitz described the structure in the nineteenth century, and the term ligament persisted long after anatomists recognized its muscular nature [3]. The preferred modern name is suspensory muscle of the duodenum.

What does the ligament of Treitz mark clinically?

It marks the boundary between upper and lower gastrointestinal bleeding and between the embryologic foregut and midgut [2]. Lesions above it are treated as upper GI sources, and lesions below it as lower GI sources.

Can the ligament of Treitz cause bowel obstruction?

Yes. Abnormal mobility or lax suspensory tissue at the duodenojejunal junction can permit recurrent duodenal obstruction [12]. Rotation of the distal duodenum around the ligament after abdominal surgery is a rarer cause of proximal small bowel obstruction [16].

Is the ligament of Treitz the same in dogs, cats and horses?

No. In dogs and cats the duodenojejunal flexure is less rigidly fixed than in humans. In horses the duodenocolic fold is the more prominent landmark.

What is superior mesenteric artery syndrome?

It is compression of the third part of the duodenum between the aorta and the superior mesenteric artery, and the ligament of Treitz contributes to its effects [1]. It may follow supine immobilization, body cast use, or rapid weight loss, and many patients need surgery [15].

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