Rosen & Barkin's 5-Minute Emergency Medicine Consult (383 page)

• Failure of parathyroid gland:
  
  • Autoimmune destruction
    
  • Surgical interruption of blood supply or gland removal
    
  • Radiation damage
    
  • Hypomagnesemia (PTH cofactor)
    
• End-organ unresponsiveness to PTH
  

DIAGNOSIS

Neonates/infants:

• Transient hypoparathyroidism in 1st yr of life
  
• Below normal intelligence proportional to duration of hypocalcemia
  
• Dental hypoplasia
  

• Most common presentation is in the postoperative period after parathyroidectomy or thyroidectomy
  
• Prolonged severe hypomagnesemia, in the alcoholic or high-dose diuretic patient, is the next most common presentation and can be slow in onset; usually less symptomatic
  

• Related to severity, rapidity of onset, and duration of hypocalcemia
  
• General:
  
  • Weakness
    
  • Malaise
    
• Neuromuscular:
  
  • Paresthesias (especially circumoral and extremities)
    
  • Carpal pedal spasm
    
  • Latent spasm elicited by:
    
    • Chvostek sign (twitching of circumoral muscles after tapping facial nerve in front of the tragus)
      
    • Trousseau sign (spasm after inflating BP cuff 20 mm above patient’s systolic BP for 3 min)
      
  • Laryngospasm/bronchospasm
    
  • Blepharospasm
    
  • Muscle cramps
    
  • Tetany
    
  • Seizures (presenting symptom of 1/3 with hypoparathyroidism)
    
  • Increased intracranial pressure (ICP) with papilledema
    
  • Parkinson syndrome and other extrapyramidal disorders
    
  • Myelopathy
    
• Cardiovascular:
  
  • Prolonged QT interval (owing to ST-segment prolongation)
    
  • Heart block
    
  • CHF
    
  • Ventricular fibrillation (VFib)
    
  • Vasoconstriction
    
• Psychiatric:
  
  • Impaired memory
    
  • Confusion
    
  • Hallucinations
    
  • Dementia
    
• Dermatologic:
  
  • Brittle hair and nails
    
  • Psoriasis
    
• Hyperpigmentation:
  
  • Lenticular cataracts
    

• If
  no hypocalcemic symptoms
  with hypocalcemia, check albumin level:
  
  • If still low after correcting for hypoalbuminemia, check ionized Ca
    ²⁺
    
• If
  hypocalcemic symptoms
  with normal total Ca
  ²⁺
  , check pH for alkalosis:
  
  • If not alkalotic, check ionized Ca
    ²⁺
    (active form)
    
  • Metabolic or respiratory alkalosis increases the binding to albumin reducing the ionized Ca
    ²⁺
    
• If
  hypocalcemic symptoms
  with low ionized Ca
  ²⁺
  , check a PTH level:
  
  • Low in primary hypoparathyroidism and in vitamin D deficiency
    
  • Elevated in pseudohypoparathyroidism and hypocalcemia from renal failure
    

• Calcium: Correct for albumin using formula:
  
  • Corrected Ca
    ²⁺
    (mg/dL) = measured Ca
    ²⁺
    (mg/dL) + 0.8[4.0 – albumin (g/dL)]
    
• Ionized Ca
  ²⁺
  if symptomatic with low total calcium
  
• Electrolytes, BUN, creatinine, glucose
  
• Magnesium
  
• Arterial blood gas (ABG) if symptomatic with normal total Ca
  ²⁺
  
  • Elevation of 0.1 pH unit decreases the ionized Ca
    ²⁺
    by 3–8%.
    
• Phosphorus:
  
  • Elevated except when hypocalcemia caused by vitamin D deficiency
    
  • Metastatic calcification can cause hypocalcemia by tissue deposition when the calcium/phosphorus product is >60.
    

ECG:

• Prolonged QT interval:
  
  • Owing to ST-segment prolongation from hypocalcemia
    

• Must differentiate from a variety of causes of hypocalcemia
  
• Lab artifact:
  
  • Low total calcium that is normal when corrected for albumin level with no symptoms of hypocalcemia
    
• Alkalosis:
  
  • Symptomatic hypocalcemia with a normal total calcium
    
• Hypomagnesemia (needed for PTH secretion)
  
• PTH resistance (congenital)
  
• Vitamin D deficiency (low Ca
  ²⁺
  + low PO
  ₄
  ):
  
  • Anticonvulsant use (decreased vitamin D absorption)
    
  • Liver disease
    
  • Resistance to vitamin D
    
  • Malabsorption or dietary deficiency
    
• Gram-negative sepsis
  
• Renal failure or nephrotic syndrome
  
• Chelation:
  
  • Pancreatitis (fatty acids chelate calcium)
    
  • Ammonium bifluoride (tire cleaner spray)
    
  • Hydrofluoric acid
    
  • Citrated blood
    
  • Acute hyperphosphatemia:
    
    • Fleet enemas
      
    • Rhabdomyolysis
      
    • Acute renal failure
      

TREATMENT

• Administer calcium in refractory VFib or status epilepticus in addition to usual medications if known hypoparathyroidism or suspected hypocalcemia
  
• Stridor may herald laryngospasm
  

• Airway, breathing, and circulation management (ABCs):
  
  • Manage airway if laryngospasm
    
• Administer IV calcium bolus (chloride or gluconate) if unstable cardiac rhythm or tetany:
  
  • Slow infusion much safer unless patient markedly symptomatic
    
• Prepare for ventricular dysrhythmias including VFib.
  
• Seizure precautions
  

• Calcium replacement:
  
  • Calcium chloride 10% (27.2 mg elemental Ca
    ²⁺
    /mL):
    
    • For life-threatening conditions: 10 mL (1 g) IV over 5 min OR
      
  • Calcium gluconate 10% (9 mg elemental Ca
    ²⁺
    /mL):
    
    • For life-threatening conditions: 20–30 mL (2–3 g) over 3–5 min
      
  • For non–life-threatening conditions, administer calcium via slow infusion of 500–1,000 mg elemental Ca
    ²⁺
    over 6–24 hr (peds: 100 mg elemental Ca
    ²⁺
    /kg/24 hr)
    
  • Continuous cardiac monitoring
    
  • Stop infusion if bradycardia develops
    
  • Perform frequent checks of serum Ca
    ²⁺
    levels
    
  • Calcium administration may precipitate digitalis toxicity
    
  • Supplement to lowest possible Ca
    ²⁺
    level keeping the patient asymptomatic, then switch to oral replacement:
    
    • Soft tissue calcification may occur with calcium/phosphorus product of 60 (Ca × PO
      ₄
      )
      
• Replace magnesium if low
  
• Bind phosphorus:
  
  • Aluminum hydroxide–containing antacids (Maalox, Mylanta, or Gelusil) if creatinine <2
    
  • Calcium acetate (Phoslo) or calcium carbonate when concurrent renal failure if creatinine >2
    
  • Sevelamer HCl or carbonate (Renagel, Renvela)
    
• Vitamin D supplementation
  
• Avoid carbonated beverages (high in phosphorus)
  
• Assess for associated endocrinopathies
  

• Calcium gluconate: 10% (9 mg elemental Ca
  ²⁺
  /mL): 20–30 mL over 3–5 min if life-threatening condition; otherwise, slow infusion (peds: 20 mg/kg of calcium gluconate 10% or 2 mg/kg elemental Ca):
  
  • Follow with slow infusion: Calcium gluconate 10 g in liter of 5% dextrose infusedat 1–3 mg/kg/h in adults
    
  • Calcium gluconate has lower risk of venous irritation or extravasational injury compared to calcium chloride
    
• Magnesium sulfate: 2 g IV (peds: 25–50 mg/kg up to 2 g) over 2 hr—if severe, 6 g over 6 hr
  
• Calcium chloride 10% (27.2 mg elemental Ca
  ²⁺
  /mL): 10 mL (1 g) IV over 5 min if life-threatening condition; otherwise, slow infusion
  

• Calcium acetate: 667 mg (169 mg elemental Ca): 1 or 2 tabs TID with meals
  
• Calcium carbonate: 1,250 mg (500 mg elemental Ca): 1 or 2 tabs QID (2–4 g/d) (peds: 45–65 mg elemental Ca mg/kg/d div. QID)
  
• Sevelamer (Renagel, Renvela) 800 mg: 1 or 2 tabs TID with meals
  
• Magnesium oxide 400 mg: 1 tab daily or BID
  
• Vitamin D: 400 IU PO daily for supplement (if not responsive to standard supplement, then consider calcitriol (1,25(OH)
  ₂
  -D) 0.25 μg daily; titrate to 0.5–2 μg/d):
  
  • Preferred over other long-acting vitamin D analogues due to patient availability and lower cost, quicker onset and offset of action
    
• Thiazide diuretics: HCTZ 25 100 mg daily
  

FOLLOW-UP

• Symptomatic hypocalcemia
  
• Abnormal ECG
  
• Inability to take vitamin D or calcium orally
  
• Corrected calcium <5 mg/dL
  

• Asymptomatic hypocalcemia
  
• Not meeting any admission criteria
  

• Any patient requiring therapy or needing follow-up lab studies
  
• Repeat of calcium, phosphorus, magnesium levels in 1–2 days