Eso Varices/Mallory Weiss Flashcards
Portal Hypertension
general and common causes
An increase in the pressure within theportalvein
Common causes:
Cirrhosis due to chronic viral hepatitis C
Alcohol-induced liver disease
Portal Hypertension
Clin man
Manifestations:
Esophageal varices
Caput medusae
Hypersplenism = over active spleen
Anemia
Neutropenia
Thrombocytopenia
Marked ascites
Hemorrhoids
Portal HTN
Portal HTN
Varix
Most common sites
Abnormally dilated vessel with a tortuous course
Usually occurs in the venous system, but may also occur in arterial or lymphatic vessels
Most common sites for varix formation:
Distal esophagus
Proximal stomach
Umbilicus
Rectum
Retroperitoneum
Esophageal varices
general
Dilated submucosal veins in the distal esophagus connecting to the portal and systemic circulation
Most dangerous varices due to the risk of rupture → massive upper gastrointestinal bleeding
PAINLESS bleeding
Esophageal varices
Risk factors for bleeding
Risk factors for bleeding:
Size of the varices
Presence of red whale markings (longitudinal dilated venules on the varix surface)
Severity of liver disease
Active alcohol abuse
Variceal Bleeding
S/Sx of shock
Painless, upper GI bleeding
Acute, subacute, or chronic
Site of bleeding:
Distal esophagus – most often
Gastric fundus – less often
Acute massive bleed → shock
Systolic BP < 100 mm Hg
Pulse rate > 100 bpm, weak
Pale
Diaphoretic
Restless
Thirsty
Esophageal varices bleeding
Diagnostics
Endoscopy
Test of choice for esophageal and gastric varices
Evaluation for coagulopathy
High association of varices and hepatic disease
PT/INR and PTT
Additional tests
CBC – anemia and thrombocytopenia
Liver tests – AST, ALT, Alkaline phosphatase, bilirubin
esophageal varicose bleed
non pharm Tx
40% of variceal bleeds stop spontaneously
Bleeding varices - EMERGENCY
Airway management - Intubation
2 large-bore IVs
Fluid resuscitation
Blood transfusion
Type and cross-match 6 units of packed red blood cells
Correction of coagulopathy
1-2 units of fresh frozen plasma
Platelet transfusion (>50,000 mcL)
esophageal varicose bleed
Pharm Tx and intervention
Antibiotics
3rd generation cephalosporins (Rocephin) IV to prevent bacteremia and sepsis
IV octreotide
Synthetic analog of somatostatin that reduces portal pressure
Endoscopic banding or sclerotherapy
Performed when the patient is hemodynamically stable
Esophageal varicosity
prognosis
Chronic maintenance
Mortality depends primarily on the severity of the associated liver disease
20% mortality at 6 weeks
Recurrence rate of variceal bleeding is 50-75% within 1-2 years
β-blockers to ↓ recurrent bleeding- for chronic maintenance not acute Tx
Mallory-Weiss Syndrome
general
Syndrome characterized by esophageal bleeding caused by a longitudinal laceration(s) at or near the gastroesophageal junction as a result of vomiting or retching
Repeated episodes (typical presentation)
Single episode
3x more common in men
Accounts for 5-10% of upper gastrointestinal bleeding
Superficial bleeds
Mallory Weiss Syndrom
Patho
Pathogenesis:
Rapid ↑ in intraabdominal pressure and intragastric pressure
This pressure overcomes the lower esophageal sphincter pressure so the gastric contents are released into theesophagus
Normal autonomic reflexes cause theupper esophageal sphincter (UES) to relax → vomiting
Mallory Weiss
RF
Alcohol use disorder
Seen in 40-80% of patients; may coexist with esophageal varices
Events that create a sudden rise in thepressure gradient across thegastroesophageal junction:
Forceful or recurrent retching
Vomiting
Violent coughingspasms
Blunt abdominal trauma
Mallory Weiss
Clin man
Acute onset hematemesis
Presenting symptom in all patients
Variable amount
Streaks of blood → copious amount of fresh red blood
Severe bleeding
Shock (20% of patients)
Postural hypotension (45% of patients)
Normally preceded by one or more episodes of non-bloody emesis, retching, or coughing
Epigastric or back pain
Melena
Seen later in a patient Dx with a tear
May be light-headedness, dizziness, syncopal
Secondary to dehydration from underlying vomiting
typically bright red
mallory weiss
Dx
Clinical suspicion with a history of hematemesis occurring after episode(s) of non-bloody vomiting
Esophagogastroduodenoscopy (EGD) Diagnostic study of choice for esophageal tears
Allows for visual inspection of the esophagus, stomach, and duodenum
Minimal bleeding and the patient is stable, EGD may be deferred, but the patient should be referred to GI
Severe bleeding with hemodynamic instability – stability must be obtained prior to performing the endoscopy
After 96 hours, most tears are well-healed and difficult to visualize
only do EGD on STABLE pt
mallory weiss tear
Predictive Factors for Recurrent Bleeding
Initial presentation of shock
History of liver cirrhosis
Decreased hemoglobin requiring a blood transfusion
Low platelet count
Active bleeding noted at the time of endoscopy
mallory weiss
mallory weiss
non pharm Tx
Most episodes of bleeding stop spontaneously
Severe bleeding (10% of patients)
Close monitoring of vital signs
Place 2 large-bore IVs
Fluid resuscitation
Transfusion of PRBCs, if needed
mallory weiss
pharm Tx
Pharmacotherapy
IV proton pump inhibitor (PPI) - used for acidsuppression
mallory weiss
Labs
Labs
CBC and coagulation assessment (PT/INR, PTT)
Initially NPO; bleeding resolved → clear liquids
mallory weiss
Endoscopic hemostasis
Used for patients who are hemodynamically unstable
Dilute epinephrine injections made 3-5 mm apart circumferentially around the site of bleeding
Electrocautery
Esophageal clips
Band ligation
mallory weiss
Tx for difficult to treat tears
Arteriography with embolization
Surgical repair – rarely needed
Esophageal Perforation
general
Spontaneous transmural perforation of the esophagus exposing the mediastinum to GI contents
Iatrogenic perforation (85-90%)
Endoscopic procedures or other instrumentation
Penetrating injuries (gunshot wound > blunt injuries
Foreign body ingestion
Spontaneous perforation/rupture (Boerhaave syndrome)
Most lethal perforation of the GI tract
Mortality 30% → subsequent infection
esophageal perf
Best outcomes result from
early diagnosis and definite surgical management within 12 hours of rupture
esophageal perf
patho
Depends on the underlying cause
Boerhaave syndrome:
Sudden increase in intraluminal pressure in theesophagus, coupled with negative intrathoracic pressure, can lead to rupture
Most common site of rupture is the lower posterolateral third of the esophagus
esophageal perf
-Vomiting
-Severe retrosternal chest pain or epigastric pain
-Subcutaneous emphysema (SCE)
Occurs when gas or air (generally from the chest cavity) travels under the skin
Usually occurs on the chest, neck, and face
esophageal perf
other Sx aside from Macklers
Hematemesis: if present, diagnosis is often mistaken for Mallory-Weiss tear
Chest pain
Dysphagia
Fever
Shock
esophageal perf
Imaging
Chest x-ray
Suggests the diagnosis
Pneumomediastinum
Subcutaneous emphysema
Contrast esophagography (Gastrograffin)
Confirms the diagnosis
Contrast leakage from theesophagusto themediastinum
Length 0f the perforation and its location
CT scan of the chest
Performed when:
Chestx-rayor esophagography is inconclusive
Patient is unstable
esophageal perf
ABCDE survey
Airway: Ensure the patency of theairway
Breathing: Ensure properventilationis occurring
Circulation: Measure blood pressure and pulse, and administerIV fluids
Disability: Perform basic neurologic examination
Exposure: Search for injuries
esophageal perf
Tx
pharm and nonpahrm
ABCDE survey
Close monitoring of vital signs
Intravenous volume resuscitation
NPO
IV proton pump inhibitor (PPI)
Administration of broad-spectrum antibiotics
Prompt endoscopic stenting and/or surgical intervention
