Rosen & Barkin's 5-Minute Emergency Medicine Consult (373 page)

TREATMENT

• Patients with abnormal vital signs require IV access and pulse oximetry.
  
• Supplemental oxygen if hypoxic
  

• Patients with abnormal vital signs require IV access and pulse oximetry.
  
• Initiate therapy for pathologic or physiologic cause of hyperventilation.
  

• Initiate treatment of hyperventilation syndrome if initial workup does not support a pathologic or physiologic cause, and history and physical exam findings suggest the diagnosis of hyperventilation syndrome.
  
• Reassurance, calming, and explanation of the voluntary component of the patient’s symptoms often have immediate dramatic results.
  
• Do not use paper bag rebreathing to increase the PCO
  ₂
  . This has not been supported in the literature:
  
  • It may be dangerous in patients with hypoxia or a pathologic or physiologic cause for hyperventilation.
    
• Clarification of the psychological stressors helps the patient avoid further attacks.
  
• Assess for need of psychiatric evaluation (i.e., suicidal ideation).
  
• Anxiolytics:
  
  • Benzodiazepine if symptoms persist to break the cycle of anxiety and hyperventilation
    
  • Short course of anxiolytics may benefit patients with definable temporary stressors.
    

• Alprazolam 0.25–0.5 mg PO
  
• Lorazepam: 1–2 mg PO or IV
  
• Diazepam: 2–5 mg PO or IV
  
• Outpatient treatment:
  
  • Buspirone: 5 mg PO TID
    
  • Diazepam: 2–5 mg PO BID–QID
    

FOLLOW-UP

Hyperventilation syndrome does not require admission.

• Exclusion or successful treatment of primary pathologic or physiologic causes of hyperventilation
  
• No acute psychiatric issues
  
• Adequate follow-up with a primary care physician
  

• Follow-up with primary care physician
  
• Assess the need for psychiatric follow-up.
  

• Exclude pathologic or physiologic causes of hyperventilation.
  
• Hyperventilation syndrome will not result in hypoxia.
  

• Gardner WN. The pathophysiology of hyperventi-lation disorders.
  Chest
  . 1996;109:516–534.
  
• Nardi AE, Freire RC, Zin, WA. Panic disorder and control of breathing.
  Respir Physiol Neurobiol
  . 2009;167(1):133–143.
  
• Niggerman B. How to diagnose psychogenic and functional breathing disorders in children and adolescents.
  Pediatr Allergy Immunol.
  2010;21:895–899.
  
• Rizzolo CL, Taylor JE, Cerciello RL. Anxiety and anxiety-related disorders in the adolescent population: An overview of diagnosis and treatment.
  Adolesc Med State Art Rev.
  2009:20(1):188–202.
  
• Saisch SG, Wessely S, Gardner WN. Patients with acute hyperventilation presenting to an inner–city emergency department.
  Chest
  . 1996;110(4):952–957.
  

CODES

306.1 Respiratory malfunction arising from mental factors

BASICS

• Hyperviscosity syndrome (HVS) is the clinical consequence of increased blood viscosity.
  
• The classic clinical symptoms are the triad of mucosal bleeding, visual disturbances, and neurologic signs.
  
• Viscosity is the resistance a material has to change in form.
  
• The higher the blood viscosity, the more the internal resistance to blood flows.
  
• Increased cardiac output is required to provide adequate perfusion of hyperviscous blood.
  
• Oxygen delivery is impaired as transit through the microcirculatory system slows. This impaired microcirculatory oxygenation gives rise to the clinical symptoms of this syndrome.
  

• Hyperviscosity occurs when there is elevation of either the cellular or acellular components of circulating blood.
  
• Acellular (protein) hyperviscosity:
  
  • The most common cause (85–90%) of hyperviscosity is increased concentration of γ globulins:
    
    • Monoclonal gammopathies: From malignant diseases like Waldenstrom macroglobulinemia and multiple myeloma
      
    • Polyclonal gammopathies: Usually rheumatic diseases (very rare)
      
• Cellular (blood cell) hyperviscosity:
  
  • Much less common (10–15%)
    
  • Increased numbers of RBC, as in polycythemia vera
    
  • Increased concentration (>100,000) of WBC, as in acute and chronic leukemia
    
  • Thrombocytosis
    

DIAGNOSIS

• Classic triad:
  
  • Mucosal bleeding
    
  • Visual disturbances
    
  • Neurologic
    
• Hematologic:
  
  • Bleeding is the most common manifestation. Mechanism thought to be platelet dysfunction.
    
  • Epistaxis
    
  • Gingival, rectal, uterine bleeding
    
  • Prolonged postprocedural bleeding
    
  • Blood dyscrasias
    
  • Pruritus owing to red cell breakdown products
    
  • Splenic enlargement
    
• Ocular:
  
  • Change in visual acuity:
    
    • Blurring
      
    • Diplopia
      
    • Visual loss
      
  • Characteristic “link-sausage effect” on funduscopy
    
  • Alternating bulges and constrictions within the retinal veins
    
  • Retinal hemorrhage, detachment
    
  • Exudate, microaneurysm formation
    
  • Papilledema
    
• Renal:
  
  • Nephritic or nephrotic syndrome
    
  • Hematuria
    
  • Sterile pyuria
    
• Neurologic:
  
  • Headache
    
  • Ataxia
    
  • Mental status changes/coma
    
  • Dizziness/vertigo
    
  • Nystagmus
    
  • Tinnitus, hearing loss
    
  • Paresthesia, peripheral neuropathy
    
  • Seizure
    
  • Intracranial hemorrhage
    
• Cardiovascular:
  
  • Angina or myocardial infarction
    
  • Dysrhythmias
    
  • CHF
    
• Dermatologic:
  
  • Raynaud phenomenon
    
  • Livedo reticularis
    
  • Palpable purpura
    
  • Eruptive spider nevus–like lesions
    
  • Digital infarcts
    
  • Peripheral gangrene
    

HVS should be considered in the following patient:

• Any patient presenting with the classic symptom triad of bleeding, visual disturbance, and neurologic dysfunction.
  
• Any patient with an established immunoglobulin-producing hematologic disease that presents with signs or symptoms of microvascular end-organ damage or cardiac decompensation.
  
• Any patient with an established hypercellular hematologic disease who presents with signs or symptoms of microvascular end-organ damage or cardiac decompensation.
  

There are no specific physical exam findings unique to HVS. However, patient will exhibit findings based on the affected end organs. Mucosal bleeding, petechial rash or bruising, focal neurologic findings, signs of decompensated heart failure, and funduscopic abnormalities have all been reported.

• Evaluate end-organ ischemia and bleeding.
  
• Measure serum or whole blood viscosity.
  
• Suspect diagnosis if the lab evaluation is hampered by serum stasis and increased viscosity causing analyzer blockage
  

• CBC with WBC differential:
  
  • Anemia or erythrocytosis can be seen in HVS.
    
  • Anemia usually normocytic and normochromic
    
  • Rouleaux of erythrocytes on the peripheral smear is an important diagnostic clue
    
  • WBC for leukemia
    
• Electrolyte, BUN, creatinine, and glucose levels:
  
  • Renal dysfunction is commonly noted in HVS.
    
  • Hypercalcemia and pseudohyponatremia in multiple myeloma
    
• Urinalysis:
  
  • Proteinuria
    
  • Hematuria
    
  • Sterile pyuria
    
• Coagulation profile
  
• Serum and urine protein electrophoresis
  
• Measurement of serum viscosity (not routinely available in ED setting):
  
  • Ostwald viscosimeter
    
  • Normal range for the serum viscosity relative to water is 1.4–1.8.
    
  • Minimal viscosity at which symptoms develop is 4 centipoise (cp).
    
• Elevated leukocyte alkaline phosphatase, lactate dehydrogenase, and serum vitamin B
  ₁₂
  levels