I. What every physician needs to know.
Mallory-Weiss syndrome was initially described in 1929 by Mallory and Weiss as “hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting.” The tears can extend along the distal esophagus and proximal stomach and cause bleeding from submucosal arteries. Mallory-Weiss syndrome makes up about 5% of patients presenting with upper gastrointestinal bleeding.
Most patients with Mallory-Weiss syndrome have gastroesophageal tear due to increased abdominal pressure from forceful vomiting, straining with stool, or forceful cough or hiccups. Tears have also been associated with blunt abdominal trauma, iatrogenic from EGD, TEE, and esophageal intubation.
Patients with hiatal hernia, alcoholism and increased age have a higher incidence of Mallory-Weiss syndrome.
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Also known as: gastroesophageal tear.
II. Diagnostic Confirmation: Are you sure your patient has Mallory-Weiss Syndrome?
75% of patients diagnosed with Mallory-Weiss syndrome have the triad of alcoholism, hematemesis and vomiting.
40-80% of patients have a history of heavy alcohol use.
A. History Part I: Pattern Recognition:
Symptoms:
Forceful retching
Hematemesis
Abdominal pain
Back pain
The typical patient with Mallory-Weiss syndrome presents with forceful retching followed by hematemesis. The initial vomitus does not necessarily contain blood. In addition, the patient can also present with upper abdominal pain or back pain. If the patient has had significant hematemesis, patient may also have symptoms of hemodynamic instability.
B. History Part 2: Prevalence:
Mallory-Weiss patients tend to be men in their 40’s – 50’s with history of alcoholism and drinking binge immediately prior to episode. Although most tears occur in patients under 40, elderly patients may be predisposed to tears during endoscopy due to atrophic gastric mucosa.
Alcoholism plays a substantial role in Mallory-Weiss tears. 40-80% of patients with MWT have a history of heavy alcohol use with vomiting.
Other predisposing factors include hiatal hernia.
C. History Part 3: Competing diagnoses that can mimic Mallory-Weiss Syndrome.
Mallory-Weiss tears usually appear as focal lesions within normal mucosa. Bleeding usually self-limited in small amounts.
Ulcerative reflux esophagitis – No history of emesis. More diffuse involvement of esophagus.
Infectious esophagitis – diffuse esophagitis.
Pill induced esophageal ulcers – suspect with history of tetracycline or alendronate ingestion. Usually proximal in the esophagus.
Esophageal varices – suspect with history of cirrhosis, more profound bleeding, not necessarily associated with forceful vomiting.
D. Physical Examination Findings.
Assess for hemodynamic stability with vital signs, orthostatics.
Oral mucosa exam to look for source of bleeding (teeth, tongue, oral pharynx).
Abdominal exam for signs of acute abdomen suggesting possible perforation.
Signs of decompensated liver disease might suggest portal hypertension and esophageal varices.
E. What diagnostic tests should be performed?
EGD
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
CBC – look for baseline and current H/H as well as platelet levels.
PT/PTT/INR – looking for coagulopathy.
Type and crossmatch – for potential transfusion.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
KUB – if patient with significant abdominal pain associated with forceful emesis, might be useful to look for free air and evaluate for perforation.
EGD – diagnostic test of choice with benefit of treatment as well. The tear appears usually as single longitudinal tear in mucosa occasional clot present. Must be able to distinguish from other esophageal lesions. Can also treat with epinephrine injection and electrocoagulation with EGD.
F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.
LFT’s
III. Default Management.
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Stabilize patient.
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Assess need for transfusion.
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EGD.
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PPI, octreotide.
A. Immediate management.
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Stabilize patient first with fluid resuscitation if patient presents with hemodynamic compromise.
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Assess need for transfusion with CBC.
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EGD for diagnosis and treatment.
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PPI and possibly Octreotide infusion if history suggestive of PUD or esophageal varices.
B. Physical Examination Tips to Guide Management.
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Need to assess vital signs closely in first 24 hours.
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Abdominal exam for signs of perforation/peritonitis.
C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.
Follow H/H every 6 hours until level stable then evey 12 hours until no further bleeding. If patient presents with coagulopathy or thrombocytopenia, suggest following PT/INR and platelets daily until stable and no further bleeding.
D. Long-term management.
N/A
E. Common Pitfalls and Side-Effects of Management.
IV. Management with Co-Morbidities.
A. Renal Insufficiency.
No change in standard management.
B. Liver Insufficiency.
Patients with portal hypertension and esophageal varices might have more severe bleeding from Mallory-Weiss tears.
C. Systolic and Diastolic Heart Failure.
Be aware of respiratory status with volume resusciation in patients with heart failure.
D. Coronary Artery Disease or Peripheral Vascular Disease.
No change in standard management.
E. Diabetes or other Endocrine issues.
No change in standard management.
F. Malignancy.
No change in standard management.
G. Immunosuppression (HIV, chronic steroids, etc).
No change in standard management.
H. Primary Lung Disease (COPD, Asthma, ILD).
No change in standard management.
I. Gastrointestinal or Nutrition Issues.
Keep patient NPO in anticipation for EGD.
J. Hematologic or Coagulation Issues.
Decreased hemoglobin and platelet leveal at presentation increases risk of re-bleeding.
Patients with coagulopathy may experience more significant bleeding.
K. Dementia or Psychiatric Illness/Treatment.
No change in standard management.
V. Transitions of Care.
A. Sign-out considerations While Hospitalized.
Increased rate of rebleeding with shock on presentation or evidence of active bleeding on EGD.
Follow H/H every 6 hours during first 24 hours and consider transfusion and notification of GI for EGD emergently if H/H trends down.
Check out EGD findings as are important to predict possibility of rebleeding (i.e., active bleeding, visible vessels, pigmented protuberance, fresh adherent clot).
Monitor for signs of re-bleeding within first 24 hours of presentation.
B. Anticipated Length of Stay.
24 hours:
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No signs of active bleeding on EGD.
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No risk factors for re-bleeding (coagulopathy, portal hypertension).
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Hemodynamally stable.
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No hematochezia.
48 hours:
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No signs of active bleeding on EGD.
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Nonbleeding endoscopic stigmata (visible vessels, pigmented protuberance, fresh adherent clot).
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Risk factors of rebleeding (coagulopathy, portal hypertension).
72 hours:
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Active bleeding at endoscopy.
C. When is the Patient Ready for Discharge.
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Hemodynamic stability.
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H/H stable and not downtrending.
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No hematochezia.
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No further hematemesis.
D. Arranging for Clinic Follow-up.
1. When should clinic follow up be arranged and with whom.
General Medicine within 2 weeks to follow H/H.
2. What tests should be conducted prior to discharge to enable best clinic first visit.
None
3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.
H/H
E. Placement Considerations.
None
F. Prognosis and Patient Counseling.
10% of patients experience re-bleeding from Mallory-Weiss Syndrome. Have an increased awareness of re-bleeding if your patient has cirrhosis, experienced shock, had active bleeding on EGD, or had decreased hemoglobin and platelet level at presentation. Re-bleeding also occurs more frequently in patients requiring large number of tranfusions, pressors, or prolonged hospital stay.
VI. Patient Safety and Quality Measures.
A. Core Indicator Standards and Documentation.
None
B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.
No DVT pharmaco prophylaxis as increased risk of further bleeding.
May use SCD’s, Foot pumps if no contraindication.
Recommend PPI.
VII. What's the evidence?
Am J Emerg Med.. vol. 27. 2009. pp. 1010
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