Sindrom Mallory-Weiss

01Pathophysiology

Mallory-Weiss syndrome results from sudden, forceful increases in intra-abdominal and intragastric pressure against a closed glottis or a contracted cardia. This is the same mechanical principle behind a Valsalva maneuver. When a patient retches or vomits violently, the intragastric pressure spikes, and the resulting transmural stress causes longitudinal tears in the mucosa and submucosa at the gastroesophageal junction, the anatomical point where the relatively rigid esophageal squamous epithelium meets the more pliable gastric columnar epithelium. This transitional zone is inherently vulnerable to shearing forces.

The tears characteristically involve the mucosa and submucosa only, meaning the muscularis propria and serosa remain intact. This is the single most important distinction from Boerhaave syndrome, where a full-thickness transmural rupture occurs. Because the tear does not penetrate the full wall, there is no mediastinal contamination, no pneumomediastinum, and no risk of mediastinitis. Instead, the clinical consequence is arterial or venous bleeding from submucosal vessels exposed by the laceration.

The majority of tears (approximately 80 to 90 percent) occur on the gastric side of the gastroesophageal junction, which is why this is sometimes described as a tear at the cardia. Tears may extend proximally into the distal esophagus, but isolated esophageal tears are less common. The reason this matters clinically is that the gastric cardia has a rich submucosal vascular plexus, and disruption of these vessels is what produces the brisk hematemesis.

Importantly, the classic vignette sequence is: the patient vomits first (nonbloody emesis), and then subsequent vomiting produces bright red blood or coffee-ground material. The initial vomiting episode creates the tear, and the hematemesis follows. This temporal relationship (retching first, bleeding second) is the hallmark that separates Mallory-Weiss tears from other causes of upper GI hemorrhage.

Chronic alcohol use is the most commonly tested predisposing factor because it promotes both frequent, forceful vomiting and coexisting conditions like portal hypertension and coagulopathy, which impair hemostasis and can make the bleeding more difficult to control. Hiatal hernias also predispose by creating an anatomical setup where the gastric mucosa is more susceptible to mechanical disruption during episodes of increased abdominal pressure.

02Classification and Clinical Manifestation

Mallory-Weiss tears are not formally staged in clinical practice, but they can be organized by the severity of bleeding and depth of the tear, which directly influences management decisions.

03Diagnostic Workup

Upper endoscopy is the cornerstone of the diagnostic approach. Unlike many other GI conditions where you start with a noninvasive test and escalate, in Mallory-Weiss syndrome the endoscopy serves a dual role: it confirms the diagnosis by directly visualizing the mucosal tear, and it allows therapeutic intervention at the same time if active bleeding is found. There is no separate "screening test" followed by a "confirmatory test." The endoscopy is both.

The reason endoscopy is performed urgently (rather than waiting) is that the differential diagnosis for hematemesis is broad. You cannot distinguish a Mallory-Weiss tear from a bleeding peptic ulcer, esophageal varices, or a Dieulafoy lesion based on clinical history alone. Endoscopy clarifies the source, grades the severity of the lesion using Forrest classification principles, and directs therapy.

On endoscopy, the tear appears as a linear, longitudinal mucosal laceration at the gastroesophageal junction. The tear typically runs parallel to the long axis of the stomach/esophagus, not circumferentially. Most tears are solitary, though multiple lacerations can occur. The endoscopist will assess for stigmata of recent hemorrhage: a clean-based tear with no visible vessel indicates low risk for re-bleeding, while a tear with active spurting, oozing, or a nonbleeding visible vessel may warrant intervention.

Laboratory studies are supportive rather than diagnostic. The CBC helps quantify blood loss, though it is important to remember that in the first several hours of acute hemorrhage, hemoglobin may not yet reflect the true degree of blood loss because hemodilution has not occurred. A falling hemoglobin on serial checks is more informative. Coagulation studies are particularly relevant in the alcoholic patient population, where coexisting liver disease may contribute to a prolonged INR and impair clot formation at the tear site.

An elevated $BUN:CreatinineBUN:Creatinine$ ratio above 20:1 is a classic laboratory finding in upper GI bleeding and can be a helpful clue in the vignette, suggesting the bleeding source is proximal to the ligament of Treitz.

04Management and Treatment

The first priority in any patient presenting with hematemesis is hemodynamic assessment and stabilization. Establish two large-bore IV lines, begin rapid infusion of isotonic crystalloids (normal saline or lactated Ringer's), and send blood for a type and crossmatch. If the patient is tachycardic or hypotensive, volume resuscitation takes precedence over diagnostic workup.

Antiemetic therapy is a frequently overlooked but important step. The ongoing cycle of vomiting is what created the tear in the first place, and continued retching will worsen the laceration and prevent healing. Ondansetron (4 mg IV every 6 to 8 hours as needed) is the standard choice.

Proton pump inhibitor (PPI) therapy reduces gastric acid exposure at the tear site, promoting mucosal healing and reducing the risk of re-bleeding. Pantoprazole 40 mg IV once daily is commonly used in the inpatient setting. For mild cases managed on an outpatient basis, oral omeprazole 20 to 40 mg daily or an equivalent PPI for 4 to 8 weeks is appropriate. Note that high-dose continuous PPI infusion (as used for peptic ulcer bleeding with high-risk stigmata) is generally not necessary for Mallory-Weiss tears unless the clinical scenario overlaps with ulcer disease.

The critical teaching point for management is that 80 to 90 percent of Mallory-Weiss tears stop bleeding spontaneously without any intervention beyond supportive care. This is a high-yield fact. The tears are superficial, and the normal hemostatic mechanisms are usually sufficient to achieve hemostasis as long as the inciting vomiting has ceased. This means most patients do well with fluids, antiemetics, PPIs, and observation.

For the 10 to 20 percent who continue to bleed, endoscopic hemostasis is the next best step. The preferred approach is combination therapy: injection of dilute epinephrine (which causes local vasoconstriction and tamponade) followed by a definitive modality such as hemoclip application or thermal coagulation. Monotherapy with epinephrine alone is discouraged because the vasoconstrictive effect is temporary and re-bleeding rates are higher.

If endoscopic therapy fails (after two attempts), the next step is angiographic embolization by interventional radiology, not surgery. Surgery (oversewing the laceration via an anterior gastrotomy) is reserved only for cases where both endoscopic and angiographic approaches have failed, which is extremely uncommon.

A contraindication to be aware of: in patients with suspected or confirmed Boerhaave syndrome (transmural perforation), endoscopy may worsen the perforation and should be approached with caution or deferred. If the clinical picture suggests perforation (subcutaneous emphysema, chest X-ray showing pneumomediastinum, severe chest/back pain out of proportion), the management shifts entirely to surgical consultation and broad-spectrum antibiotics rather than endoscopy.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students miss questions on Mallory-Weiss syndrome is by confusing it with Boerhaave syndrome. Both conditions involve forceful vomiting, but they differ in a fundamental way: Mallory-Weiss is a partial-thickness mucosal tear that causes bleeding, while Boerhaave is a full-thickness transmural rupture that causes mediastinal contamination. The vignette will distinguish them by the dominant symptom. If the stem emphasizes hematemesis after vomiting, think Mallory-Weiss. If the stem emphasizes severe chest or back pain, subcutaneous emphysema, or signs of sepsis after vomiting, think Boerhaave. Students who fixate on the "vomiting" trigger and ignore the presenting complaint will select the wrong answer.

A second common trap involves the temporal sequence of symptoms. In Mallory-Weiss, the patient vomits first (nonbloody), and then the bloody vomiting follows. If the vignette describes a patient whose very first episode of vomiting is bloody (without prior retching), the diagnosis is more likely a peptic ulcer or variceal bleed, not a Mallory-Weiss tear.

Another tested concept is the management sequence. Students frequently jump to endoscopic therapy or surgery when asked about the "next best step." For a hemodynamically stable patient with a clinical picture consistent with Mallory-Weiss, the answer is supportive care (IV fluids, antiemetics, PPI, monitoring), because the vast majority of these tears stop bleeding on their own. Endoscopy is appropriate for diagnosis and for patients with ongoing bleeding, but it is not the immediate next step in a stable patient who has already stopped vomiting blood.

Finally, be alert for vignettes that test the elevated BUN-to-creatinine ratio as a clue to an upper GI source of bleeding. A patient who presents with melena or hematemesis and has a $BUN:Creatinine>20:1BUN:Creatinine\; >\; 20:1$ is digesting and absorbing blood proximal to the ligament of Treitz. This lab finding does not confirm Mallory-Weiss by itself, but it points you toward the upper GI tract and away from lower GI bleeding sources, which is often the actual question being asked.

The core competency tested by Mallory-Weiss questions is pattern recognition: identifying the classic sequence of forceful vomiting followed by hematemesis, linking it to a partial-thickness mucosal tear, distinguishing it from transmural perforation, and knowing that most cases resolve with conservative management alone.