Rosen & Barkin's 5-Minute Emergency Medicine Consult (757 page)

Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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ICD9
  • 052.9 Varicella without mention of complication
  • 053.9 Herpes zoster without mention of complication
  • 053.21 Herpes zoster keratoconjunctivitis
ICD10
  • B01.9 Varicella without complication
  • B02.9 Zoster without complications
  • B02.31 Zoster conjunctivitis
VARICES
Galeta C. Clayton
BASICS
DESCRIPTION
  • Increased portal venous pressure results in portal–systemic shunts.
  • Shunts at gastroesophageal junction result in fragile submucosal esophageal varices.
ETIOLOGY
  • 10–30% of all cases of upper GI bleeding
  • 90% of upper GI bleeding in patients with cirrhosis
  • Variceal hemorrhage occurs in 30% of patients with cirrhosis:
    • 50% will stop bleeding spontaneously
    • 30% mortality per episode
    • 70% have recurrent bleeding
  • In adults:
    • Cirrhosis due to alcoholism or chronic hepatitis
    • Storage disease: Wilson or hemochromatosis
    • Middle East: Schistosomiasis
  • In children:
    • Intrahepatic obstruction from biliary cirrhosis
    • Biliary atresia
    • Cystic fibrosis
    • β-antitrypsin deficiency
    • Hepatitis
DIAGNOSIS
SIGNS AND SYMPTOMS
  • General:
    • Weakness and fatigue
    • Tachycardia
    • Tachypnea
    • Hypotension
    • Cool, clammy skin; prolonged capillary refill
  • Abdominal:
    • Significant active upper GI bleeding:
      • Hematemesis
      • Hematochezia
      • Melena
      • 20–40% of total blood volume loss possible
    • Abdominal pain
  • Stigmata of severe hepatic dysfunction:
    • Jaundice
    • Spider angiomata
    • Palmar erythema
    • Pedal edema
    • Hepatosplenomegaly
    • Ascites
  • History of portal hypertension:
    • Most commonly alcoholic cirrhosis
    • Others, including:
      • Primary biliary cirrhosis
      • Schistosomiasis
      • Budd–Chiari syndrome
      • Severe CHF
      • Sarcoidosis
  • Cardiovascular:
    • Chest pain/shortness of breath
  • CNS:
    • Syncope
    • Confusion and agitation initially
    • Lethargy and obtundation later
Pediatric Considerations
  • Massive hematemesis: Typical initial presentation:
    • Hypotension may be a late finding.
History
  • Gastroesophageal varices are present in 50% of patients with cirrhosis and correlate with severity of disease.
  • The most important predictor of hemorrhage is size of the varices. Other factors include number of varices, severity of hepatic disease and endoscopic findings.
  • Patients with PBC develop varices and variceal hemorrhage early in their course of disease, even prior to development of cirrhosis.
Physical-Exam
  • Vitals signs may be normal or may show tachycardia (early) and hypotension (late).
  • Altered mental status with encephalopathy or poor perfusion
  • Active hematemesis
  • Stigmata of alcoholic liver disease:
    • Ascites
    • General edema
    • Jaundice
ESSENTIAL WORKUP
  • Gastric tube placement:
    • Determines whether patient is actively bleeding
    • Decompresses stomach that may aid in hemostasis. Possible role in reducing aspiration risk
    • Facilitates endoscopic exam
    • Will not increase or cause esophageal variceal bleeding
  • Emergent endoscopy
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Type and cross-match 6–8 U:
    • Significant transfusion requirements
  • ABG for:
    • Acidosis
    • Hypoxemia
  • CBC:
    • Hematocrit is an unreliable indicator of early rapid blood loss.
    • Perform serial CBCs to follow blood loss.
  • Electrolytes, BUN, creatinine, glucose:
    • Evaluate renal function.
    • BUN:creatinine ratio >30 suggest significant blood in GI tract.
  • PT/PTT/INR and platelets:
    • Coagulopathy
    • Prolonged bleeding times
    • Thrombocytopenia
Imaging
  • Chest radiograph (portable) for aspiration/perforation
  • ECG for myocardial ischemia
DIFFERENTIAL DIAGNOSIS
  • Bleeding/perforated peptic ulcer
  • Erosive gastritis
  • Mallory–Weiss syndrome
  • Boerhaave syndrome
  • Aortoenteric fistula
  • Gastric varices
  • Gastric vascular ectasia
TREATMENT
PRE HOSPITAL
  • Airway stabilization
  • Treat hypotension 0.9% normal saline infusion bolus through 2 large-bore 16G or large IV lines.
  • Cardiac and pulse oximetry monitoring
INITIAL STABILIZATION/THERAPY
  • ABCs with early aggressive airway control/intubation:
    • Early intubation = easier intubation
    • For AMS or massive hemoptysis
    • Facilitates emergency endoscopy
  • Establish central IV access with invasive intravascular monitoring for hypotension not responsive to initial fluid bolus.
  • Replace lost blood as soon as possible:
    • Initiate with O-negative blood until type-specific blood available.
    • 10 mL/kg bolus in children
    • Fresh-frozen plasma and platelets may be required.
  • Place gastric tube nasally (awake) or orally (intubated)
  • Controversy:
    • Overly aggressive volume expansion may lead to rebound portal HTN, rebleeding, and pulmonary edema.
    • Transfusion goal is Hb = 8.
    • rFVIIa may decrease hemostasis failure rates in Child–Pugh class B/C patients
Pediatric Considerations
  • Initiate intraosseous access if peripheral access unsuccessful in unstable patient.
  • Most bleeding in children stops spontaneously.
  • Vital sign changes may be a late finding in children:
    • Subtle changes in mental status, capillary refill, mild tachycardia, or orthostatic changes may indicate significant blood loss.
    • Overaggressive correction in infants can quickly lead to significant electrolyte abnormalities.
ED TREATMENT/PROCEDURES
  • Emergent endoscopy required for active bleeding:
    • Use pharmacologic and tamponade devices as temporizing measures.
  • Endoscopy
    • Emergent with active bleeding in nasogastric tube
    • Procedure of choice in acute esophageal bleeding
    • Esophageal band ligation equivalent to sclerotherapy with fewer complications:
      • May be difficult to visualize in cases of massive bleeding
    • Sclerotherapy with massive bleeding
    • Gastric varices are not amenable to endoscopic repair due to high rebleeding rate:
      • Treat pharmacologically.
    • Administer antibiotics at time of procedure to decrease risk for spontaneous bacterial peritonitis:
      • Fluoroquinolone or ceftriaxone
  • Pharmacological Therapy
    • Somatostatin is 1st-line therapy where available (not widely available in US) due to greater efficacy and fewer side effects when compared to octreotide
    • Octreotide is 1st-line therapy where somatostatin not available:
      • Complications include hyperglycemia and abdominal cramping.
    • Vasopressin replaced by octreotide/somatostatin secondary to high incidence of vascular ischemia
  • Balloon Tamponade
    • Initiate in massive uncontrollable bleed.
    • Sengstaken–Blakemore and Minnesota tubes
    • Applies direct pressure but risks esophageal perforation and ulceration
    • Temporary benefit only with massive uncontrolled bleeding in the hands of experienced clinician
  • Refractory Bleeding Therapy
    • Interventional radiology:
      • Transjugular intrahepatic portosystemic shunt procedure. Recommended for refractory gastric varices or for patients who are poor surgical candidates
    • Surgical options:
      • Portacaval shunt
      • Variceal transection
      • Stomach devascularization
      • Liver transplantation
MEDICATION
  • Ceftriaxone: 2 g (peds: 50–75 mg/kg/24 h) IV q24h in Child–Pugh class B/C or in quinolone-resistant areas
  • Cefotaxime: 2 g (peds: 50–180 mg/kg/24 h) IV q8h
  • Erythromycin 250 mg IV:
    • Shown to aid in gastric clearing for better visualization during endoscopy
  • Norfloxacin 400 mg PO q12 or Ciprofloxacin 500 mg IV q12 if cannot tolerate PO (contraindicated in peds)
  • Octreotide: 50 μg bolus, then 50 μg/h infusion for 5 days
  • Somatostatin: 250 μg IV bolus followed by 250 μg/h IV infusion for 5 days
First Line

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