Rosen & Barkin's 5-Minute Emergency Medicine Consult (42 page)

• D
  ₅₀
  W: 1 ampule of 50% dextrose (25 g) IVP
  
• Lorazepam (benzodiazepine): 2 mg IV and titrate to effect
  
• Narcan: 2 mg IVP
  
• Ondansetron: 4–8 mg IVP
  
• Prochlorperazine: 5–10 mg IVP slowly (not >5 mg/min)
  
• Promethazine: 12.5–25 mg IVP
  
• Thiamine: 100 mg IVP
  

FOLLOW-UP

• Persistent metabolic acidosis
  
• Persistent signs of hypovolemia
  
• Persistent nausea and vomiting
  
• Abdominal pain of uncertain etiology
  
• Comorbid illness requiring admission for treatment
  
• Need for monitored bed due to electrolyte abnormalities requiring continued treatment
  

• Many patients can be managed in observation unit over 12–24 hr.
  
• Tolerating oral fluids well
  
• Resolution of metabolic abnormalities
  
• No other associated illnesses requiring additional therapy
  
• Most will warrant at least observation
  

Counseling regarding alcohol cessation

• Aggressive volume repletion with dextrose containing fluid is key.
  
• Volume resuscitate with NS as necessary
  
• Thiamine repletion
  
• Monitor electrolytes before and after treatment.
  
• Unrecognized increased osmolal gap
  
• Inadequate monitoring of glucose levels
  
• Failure to recognize initial electrolyte abnormalities and electrolyte shifts caused by treatment.
  
• Must be placed on monitor:
  
  • Cases of sudden death in AKA:
    
    • Possible alcoholic cardiomyopathy
      
    • Dysrhythmias
      
    • Electrolyte derangements
      

• Cartwright MM, Hajja W, Al-Khatib S, et al. Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes.
  Crit Care Clin
  . 2012;28(4): 601–631.
  
• Diltoer M, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: Common signs of a single condition.
  Eur J Emerg Med
  . 2004;11(3):172–175.
  
• McGuire L, Cruickshank A, Munro P. Alcoholic ketoacidosis.
  Emerg Med J
  . 2006;23:417–420.
  
• Yanagawa Y, Kiyozumi T, Hatanaka K, et al. Reversible blindness associated with alcoholic ketoacidosis.
  Am J Opthalmology
  . 2004;137(4):775–777.
  
• Yanagawa Y, Sakamoto T, Okada Y. Six cases of sudden cardiac arrest in alcoholic ketoacidosis.
  Intern Med.
  2008;47(2):113–117.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Acidosis
  
• Diabetic Ketoacidosis
  

CODES

276.2 Acidosis

BASICS

• Respiratory alkalosis:
  
  • Elevated serum pH secondary to alveolar hyperventilation and decreased PaCO
    ₂
    
  • Hyperventilation occurs through stimulation of 2 receptor types:
    
    • Central receptors—located in the brainstem and respond to decreased CSF pH
      
    • Chest receptors—located in aortic arch and respond to hypoxemia
      
  • Increased alveolar ventilation secondary to:
    
    • Disorders causing acidosis
      
    • Hypoxemia
      or
      
    • Nonphysiologic stimulation of those receptors by CNS or chest disorders
      
  • Rarely life threatening with pH typically <7.50
    
• Metabolic alkalosis:
  
  • Primary increase in serum HCO
    ₃
    ⁻
    secondary to loss of H
    ⁺
    or gain of HCO
    ₃
    ⁻
    
  • Pathogenesis requires an initial process that generates the metabolic alkalosis with a secondary or overlapping process maintaining the alkalosis.
    
• Generation occurs through 1 of the following mechanisms:
  
  • Gain of alkali through ingestion or infusion
    
  • Loss of H
    ⁺
    through the GI tract or kidneys
    
  • Shift of hydrogen ions into the intracellular space
    
  • Contraction of extracellular fluid (ECF) volume with loss of HCO
    ₃
    ⁻
    -poor fluids
    
• Renal maintenance is required to sustain a metabolic alkalosis secondary to the kidney’s enormous ability to excrete HCO
  ₃
  ⁻
  . This occurs through the following:
  
  • Decreased GFR (renal failure, ECF depletion)
    
  • Elevated tubular reabsorption of HCO
    ₃
    ⁻
    secondary to hypochloremia, hyperaldosteronism, hypokalemia, ECF depletion
    
• Mortality 45% if pH >7.55 and 80% if pH >7.65
  

• Respiratory alkalosis:
  
  • CNS:
    
    • Hyperventilation syndrome
      
    • Pain
      
    • Anxiety/psychosis
      
    • Fever
      
    • Cerebrovascular accident (CVA)
      
    • CNS infection (meningitis, encephalitis)
      
    • CNS mass lesion (tumor, trauma)
      
  • Hypoxemia:
    
    • Altitude
      
    • Anemia
      
    • Shunt
      
  • Medications/drugs:
    
    • Progesterone
      
    • Methylxanthines
      
    • Salicylates
      
    • Catecholamines
      
    • Nicotine
      
  • Endocrine:
    
    • Hyperthyroidism
      
    • Pregnancy
      
  • Chest stimulation:
    
    • Pulmonary embolism
      
    • Pneumonia
      
    • Pneumothorax
      
  • Other:
    
    • Sepsis
      
    • Hepatic failure
      
    • Heat exhaustion
      
• Metabolic alkalosis:
  
  • GI loss of H
    ⁺
    :
    
    • Vomiting
      
    • Nasogastric (NG) suctioning
      
    • Bulimia
      
    • Antacid therapy
      
    • Chloride-losing diarrhea (villous adenoma)
      
  • Renal loss:
    
    • Diuretics (loop and thiazide)
      
    • Post (chronic) hypercapnia
      
    • Mineralocorticoid excess
      
    • Hyperaldosteronism
      
    • Drug/medication (carbenicillin)
      
    • Glucocorticoid excess (Cushing disease)
      
    • Gitelman syndrome
      
    • Hypercalcemia
      
    • Milk–alkali syndrome
      
    • Low chloride intake
      
    • Bartter syndrome
      
  • Intracellular H
    ⁺
    shift:
    
    • Hypokalemia
      
    • Refeeding
      
  • Contraction alkalosis:
    
    • Diuretics
      
    • Sweat loss in CF
      
    • Gastric losses
      
  • HCO
    ₃
    ⁻
    retention:
    
    • NaHCO
      ₃
      infusion
      
    • Blood transfusions
      

DIAGNOSIS

• Signs and symptoms secondary to:
  
  • Arteriolar vasoconstriction
    
  • Hypocalcemia secondary to decreased ionized calcium from increased calcium binding to albumin
    
  • Associated hypokalemia
    
  • Underlying cause
    
• Weakness
  
• Seizures
  
• Altered mental status
  
• Tetany
  
• Chvostek sign
  
• Trousseau sign
  
• Arrhythmias
  
• Myalgias
  
• Carpal–pedal spasm
  
• Perioral tingling/numbness
  
• Hypoxemia
  
• Dehydration
  

• Electrolytes:
  
  • Elevated HCO
    ₃
    ⁻
    with metabolic alkalosis
    
  • Evaluate for hypokalemia and hypocalcemia.
    
• BUN/creatinine:
  
  • Evaluate for renal failure or dehydration.
    
• Blood gas (arterial/venous):
  
  • pH
    
  • PCO
    ₂
    decreased in respiratory alkalosis
    
  • PO
    ₂
    for hypoxemia
    
  • Venous versus arterial blood gas
    
    • pH—good correlation within 0.03–0.04 units
      
    • pCO2—good correlation, although VBG may not correlate with severe shock
      
    • HCO3—good correlation
      
    • Base excess—good correlation
      
• Calculate compensation to identify mixed acid–base disorders:
  
  • Acute respiratory alkalosis:
    
    • HCO
      ₃
      ⁻
      decreases secondary to intracellular shift and buffering within 10–20 min.
      
    • Expected HCO
      ₃
      ⁻
      decreased by 2 mEq/dL for each 10 mm Hg decrease in PCO
      ₂
      .
      
  • Chronic respiratory alkalosis:
    
    • HCO
      ₃
      ⁻
      decreased secondary to renal secretion of HCO
      ₃
      ⁻
      
    • Requires 48–72 hr for maximal compensation
      
    • Expected HCO
      ₃
      ⁻
      decreased by 5 mEq/dL for each 10 mm Hg decrease in PCO
      ₂
      .
      
    • If HCO
      ₃
      ⁻
      greater than predicted, concomitant metabolic alkalosis
      
    • If HCO
      ₃
      ⁻
      less than predicted, concomitant metabolic acidosis
      
  • Metabolic alkalosis:
    
    • Expected PCO
      ₂
      = 0.9 [HCO
      ₃
      ⁻
      ] + 9
      
    • If PCO
      ₂
      greater than predicted, concomitant respiratory acidosis
      
    • If PCO
      ₂
      less than predicted, concomitant respiratory alkalosis
      
• Urine chloride:
  
  • More accurate marker than urine Na
    ⁺
    for patient’s volume status:
    
    • UCl
      ⁻
      <20 mEq/L in volume depletion
      
    • UCl
      ⁻
      >40 mEq/L in euvolemia or edematous states
      
• Useful in therapy for determining saline-responsive vs. saline-resistant causes of metabolic alkalosis