Rosen & Barkin's 5-Minute Emergency Medicine Consult (377 page)

• Symptomatic or severe ionized hypocalcemia (<3.2 mg/dL)
  
• Continuous IV calcium preparations necessary to maintain calcium levels
  

• Asymptomatic hypocalcemia
  
• Ionized calcium >3.2 mg/dL in healthy patients with no comorbid illness
  

Close follow-up with an endocrinologist may be necessary for impaired PTH or vitamin D action or synthesis.

• Hypocalcemia has many causes
  
• Treatment of hypocalcemia varies with its severity and underlying cause
  
• Patients who are severely symptomatic require rapid correction with IV calcium therapy
  
• To effectively treat hypocalcemia with concurrent magnesium deficiency, magnesium must first be normalized
  

• Al-Azem H, Khan AA. Hypoparathyroidism.
  Best Pract Res Clin Endocrinol Metab.
  2012;26(4):517–522.
  
• Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcemia.
  BMJ
  . 2008;336(7656):1298–1302.
  
• Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: An Endocrine Society clinical practice guideline.
  J Clin Endocrinol Metab
  . 2011;96(7):1911–1930.
  
• Liamis G, Milionis HJ, Elisaf M. A review of drug-induced hypocalcemia.
  J Bone Miner Metab
  . 2009;27(6):635–642.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Hypercalcemia
  
• Hyperparathyroidism
  
• Hypoparathyroidism
  

CODES

• 775.4 Hypocalcemia and hypomagnesemia of newborn
  
• 275.41 Hypocalcemia
  
• 275.5 Hungry bone syndrome
  

BASICS

• Deficiency in counterregulatory hormones (glucagon, epinephrine, cortisol, growth hormone) or excessive insulin response
  
• Serum glucose < 70 mg/dL
  

• Strict glycemic control with insulin
  
• Prior hypoglycemia episodes
  
• Hypoglycemia unawareness
  
• Decreased counterregulation
  
• <5 years of age or elderly
  
• Comorbid conditions:
  
  • Renal disease
    
  • Malnutrition
    
  • Coronary artery disease
    
  • Liver disease
    

• Congenital metabolic and endocrine disorders that decrease gluconeogenic ability (e.g., hereditary fructose intolerance)
  
• Congenital hyperinsulinism
  
• Neonatal diabetes mellitus (often a mutation effecting an ATP-dependent potassium channel)
  

• Increased insulin levels:
  
  • Overdose of oral hypoglycemic agent or insulin
    
  • Oral antihyperglycemics (i.e., α-glucosidase inhibitors, biguanides, and thiazolidinediones) do not cause hypoglycemia alone, but may enhance the risk when used with insulin or sulfonylureas.
    
  • Sepsis
    
  • Insulinoma
    
  • Autoimmune hypoglycemia
    
  • Alimentary hyperinsulinism
    
  • Renal failure (partially responsible for insulin metabolism)
    
  • Liver cirrhosis (responsible for significant insulin metabolism)
    
• Underproduction of glucose:
  
  • Alcohol (inhibitory effect on glycogen storage and gluconeogenesis)
    
  • Drugs
    
  • Salicylates
    
  • β-blockers (including eye drops)
    
  • SSRIs
    
  • Some antibiotics (e.g., sulfonylureas, pentamidine)
    
  • Adrenal insufficiency
    
  • Malnutrition
    
  • Dehydration
    
• Cerebral edema
  
• Extremes of age
  
• Congestive heart failure
  
• Counterregulatory hormone deficiency
  
• Hypothyroidism or hyperthyroidism
  

• 3rd-trimester pregnant patients risk relative substrate deficiency–induced hypoglycemia.
  
• The fetus is less likely to become hypoglycemic during mother’s hypoglycemic episode secondary to active glucose transport across placenta:
  
  • Oral hypoglycemic use in pregnancy may lead to profound and prolonged neonatal hypoglycemia.
    

Most common cause of hypoglycemia in the 1st 3 mo of life is persistent hyperinsulinemic hypoglycemia of infancy (PHHI) in mothers with diabetes.

DIAGNOSIS

• Adrenergic caused by excessive counter-regulatory hormones (i.e., epinephrine):
  
  • Diaphoresis
    
  • Anxiety
    
  • Tachycardia/palpitations
    
  • Hunger
    
  • Paresthesias
    
  • Chest pain
    
  • Ischemic ECG changes
    
• Neuroglycopenic:
  
  • CVA mimic
    
  • Any focal or general neurologic change
    
  • Dizziness
    
  • Confusion
    
  • Mood changes
    
  • Hyperactive or psychotic behavior
    
  • Slurred speech
    
  • Cranial nerve palsies
    
  • Seizures
    
  • Hemiplegia
    
  • Decerebrate posturing
    
• Neonatal presentation:
  
  • Asymptomatic
    
  • Limp
    
  • Bradycardia
    
  • Irritable
    
  • Tremulous
    
  • Seizures
    
  • Poor feeding
    

• Underlying diseases or conditions: Diabetes, renal failure, liver failure, alcohol use.
  
• Certain medications—long-acting insulin and oral hypoglycemic agents—are more concerning.
  
• Possible insulin or oral hypoglycemic overdose.
  

See Signs and Symptoms

• Diagnosis requires:
  
  • Demonstration of neuroglycopenic signs and symptoms as defined above
    
  • Lab evidence of hypoglycemia
    
  • Clearing of symptoms following glucose administration
    

• Blood glucose (initial and post-treatment)
  
• Electrolytes, BUN, creatinine
  
• Prothrombin time
  
• Urinalysis for possible infection
  
• Urine and other cultures as appropriate in evaluation for infection
  
• C-peptide if concern for exogenous insulin overdose
  

CXR for:

• Possible aspiration during hypoglycemic episode
  
• Pneumonia as source of sepsis
  

• ECG if MI/ischemia owing to hypoglycemia or as cause of hypoglycemia suspected.
  
• Hypoglycemia may affect cardiac electrical conduction.
  

The differential diagnosis is extensive; see Altered Mental Status for a complete list. Major concerns include:

• Neurologic:
  
  • Cerebral vascular accident/transient ischemic attack (CVA/TIA)
    
  • Seizure disorder
    
• Drug or alcohol intoxication
  
• Hypoxia
  
• Sepsis
  
• Metabolic derangements
  
• Endocrine derangements
  
• Environmental stressors
  
• Psychosis, depression, or anxiety
  

• Growth hormone deficiency
  
• Inborn errors of metabolism
  
• Ketotic hypoglycemia
  
• Reye syndrome
  
• Salicylate ingestion
  

TREATMENT