Rosen & Barkin's 5-Minute Emergency Medicine Consult (778 page)

Not applicable

• Fluid resuscitation with 0.9% NS IV; caution if concern about increased intracranial pressure.
  
• Determine bedside fingerstick glucose.
  

• Continue fluid resuscitation and correction of electrolyte imbalance if present.
  
• Decompress stomach with nasogastric or orogastric tube if abdomen distended or vomiting persistent.
  
• Continue evaluation for underlying cause.
  
• Consider antiemetic medications.
  
• Surgical consultation if acute abdomen; antibiotics if peritonitis or other systemic infection present
  

Antiemetics may be helpful once the underlying cause of vomiting has been determined.

Ondansetron: 4–8 mg (peds: 0.1 mg/kg per dose) IV or PO q6h

• Metoclopramide: 10 mg (peds: 0.1 mg/kg per dose) PO q6h
  
• Prochlorperazine: 2.5–5 mg (peds: 0.1 mg/kg per dose) IV, IM, or PR q6h
  
• Promethazine: 12.5–25 mg (peds: 0.25 mg/kg per dose) PO, PR, or IM q6h
  

FOLLOW-UP

• Unstable vital signs, including persistent tachycardia or other evidence of hypovolemia
  
• Serious etiologic condition or inability to exclude serious etiologic conditions
  
• Intractable vomiting or inability to take oral fluids
  
• Inadequate social situation or follow-up
  

• Stable; able to tolerate oral fluids
  
• Benign etiology considered most likely and serious or potentially important etiologies excluded
  
• Parental understanding of instructions to advance clear liquids slowly and return for continued vomiting, abdominal distention, decreased urination, fever, lethargy, or unusual behavior
  

• Chronic or recurrent episodes of vomiting or abdominal pain:
  
  • Pediatric gastroenterology
    

PCP in 1–2 days

• Determine presence or absence of bile or blood in emesis.
  
• Bilious vomiting in the neonate is an important anatomic abnormality such as malrotation until proven otherwise.
  
• Consider causes of vomiting other than just GI (see Differential Diagnosis).
  

• Chandran L, Chitkara M. Vomiting in children: Reassurance, red flag, or referral?
  Pediatr Rev.
  2008;29(6):183–192.
  
• Claudius I, Kou M, Place R, et al. An evidence based review of neonatal emergencies.
  Pediatric Emergency Med Practice.
  2010;7(6):1–22.
  
• Hostetler MA. Gastrointestinal disorders. In: Marx JA, Hockerberger RS, Walls RM, et al., eds.
  Emergency Medicine: Concepts and Clinical Practice.
  7th ed. St. Louis: Mosby; 2010:2168–2187.
  
• Pepper VK, Stanfill AB, Pearl RH. Diagnosis and management of pediatric appendicitis, intussusception and Meckel diverticulum.
  Surg Clin North Am.
  2012;92(3):505–526.
  

CODES

• 530.81 Esophageal reflux
  
• 787.03 Vomiting alone
  
• 787.04 Bilious emesis
  

BASICS

• Coagulopathy caused by deficiency or dysfunction of von Willebrand factor (vWF)
  
• vWF functions:
  
  • Mediates platelet–endothelial cell adhesion
    
  • Carrier protein for factor VIII
    
• Prevalence as high as 1–2% in the general population
  
• Genetics:
  
  • Most cases inherited—multiple genetic defects identified
    
  • Type 1—quantitative defect of vWF:
    
    • 70% of cases
      
    • Autosomal dominant
      
    • vWF deficiency results from decreased synthesis and increased clearance of protein.
      
    • Manifestation ranges from asymptomatic to moderate bleeding.
      
  • Type 2—qualitative defect of vWF:
    
    • 10–15% of cases
      
    • Divided into types 2A, 2B, 2M, 2N—all are autosomal dominant except 2N which is autosomal recessive.
      
    • Decrease in intermediate and high molecular-weight multimer
      
    • 2N—decreased binding to factor VIII
      
    • Leads to decreased levels of VIII and thus more serious coagulopathy
      
  • Type 3—absent or severe deficiency in amount of vWF:
    
    • Rare disease—1 per million cases
      
    • Autosomal recessive
      
    • Severe coagulopathy
      
  • vWD genetically associated with sickle cell disease, hemophilia A, factor XII deficiency, hereditary hemorrhagic telangiectasia, and thrombocytopenia
    

• In addition to genetic causes, acquired forms exist.
  
• Multiple mechanisms:
  
  • vWF antibody production
    
  • Decreased synthesis
    
  • Proteolysis
    
  • Increased clearance from binding to tumor cells
    
• Seen in association with the following:
  
  • Malignancy:
    
    • Wilms tumor
      
    • Multiple myeloma
      
    • Chronic lymphocytic leukemia
      
    • Non-Hodgkin lymphoma
      
    • Chronic myelogenous leukemia
      
    • Waldenstrom macroglobulinemia
      
    • Monoclonal gammopathy of uncertain significance
      
  • Immunologic:
    
    • Systematic lupus erythematosus
      
    • Rheumatoid arthritis
      
  • Medication induced:
    
    • Valproic acid
      
    • Ciprofloxacin
      
    • Hetastarch
      
    • Griseofulvin
      
  • Miscellaneous:
    
    • Hypothyroidism
      
    • Uremia
      
    • Hemoglobinopathies
      
    • Cirrhosis
      
    • Congenital heart disease
      
    • Disseminated intravascular coagulation
      

DIAGNOSIS

• Symptoms vary depending on type of disease.
  
• Many type 1 and some type 2 are asymptomatic, severe type 2 and type 3 are symptomatic:
  
  • Easy bruising
    
  • Menorrhagia
    
  • Recurrent epistaxis
    
  • Gum bleeding
    
  • GI bleeding
    
  • Soft-tissue bleeds and hemarthroses
    
  • Prolonged or excessive procedural bleeding
    
  • Postoperative hemorrhage
    

• Most often diagnosed in pediatric and adolescent populations
  
• Family history
  
• Minor/moderate recurrent mucosal bleeding most common historical clue
  
• Heavy menses
  

• Most will have normal exam
  
• Multiple large bruises
  
• Deep-tissue hematomas, hemarthroses
  

• Pregnancy causes increased vWF levels in patients with types 1 and 2 disease
  
• Pregnancy, labor, and delivery are usually uncomplicated
  
• vWF levels fall quickly after delivery:
  
  • Patients may suffer postpartum bleeding 10–28 days after delivery
    

Always consider nonaccidental trauma in an infant or child presenting with bruising or bleeding of unknown cause

• Screen and refer for testing if historical concerns or consistent physical findings
  
• For type 1 diagnosis, patient must have significant mucocutaneous bleeding, lab confirmation, and family history of type 1 disease
  

• CBC: Normal platelet count and morphology
  
• PT: Normal
  
• PTT:
  
  • Mildly prolonged in 50%
    
  • Due to low factor VIII levels or coexistent factor deficiency
    
• Measurement of vWF level and activity:
  
  • vWF ristocetin cofactor activity (vWF:RCo):
    
    • Uses platelet agglutination to determine vWF function
      
  • vWF antigen—tests for vWF level in serum using rabbit antibodies
    
• Bleeding time:
  
  • May be normal in type 1 (50%); prolonged in types 2 and 3
    
  • Not specific and hard to reproduce; has fallen out of favor for diagnosis
    

• Hemophilia A, B
  
• Platelet defects
  
• Use of antiplatelet drugs—NSAIDs
  
• Platelet-type pseudo vWD
  
• Bernard–Soulier syndrome
  

TREATMENT