Rosen & Barkin's 5-Minute Emergency Medicine Consult (204 page)

• Aqueous AVP: 5–10 U SC in the unconscious patient from head trauma or postoperative
  
• Amiloride: 2.5–10 mg PO BID
  
• Chlorpropamide (Diabinese): 200–500 mg PO daily
  
• Clofibrate (Atromid-S): 500 mg PO q6h
  
• Desmopressin: 10–20 μg/d intranasally; 1–3 μg/d SC or IV; 0.1–1.2 μg/d PO
  
• Hydrochlorothiazide (HCTZ): 50 mg PO daily (peds: 2–4 mg/kg QD–BID)
  
• Lypressin nasal spray: 1–2 nasal spray TID–QID as needed
  

FOLLOW-UP

• AMS
  
• Seizure
  
• Severe dehydration
  
• Electrolyte abnormalities
  
• Associated trauma
  
• Patients requiring DDAVP testing or a trial of water restriction
  

• Known diagnosis of DI
  
• Stable electrolytes
  
• Adequately hydrated
  

Referral to specialist depends on underlying etiology of DI.

• Check urine osmolality and consider DI in polyuria.
  
• Central DI will typically respond to desmopressin.
  
• Nephrogenic DI will not respond to ADH:
  
  • Treat the underlying electrolyte abnormality, discontinue concerning drugs, and consult nephrology for further management.
    

• Di lorgi N, Napoli F, Allegri AE, et al. Diabetes insipidus – diagnosis and management.
  Horm Res Paediatr.
  2012;77:69–84.
  
• Fenske W, Allolio B. Current state and future perspectives in the diagnosis of diabetes insipidus: A clinical review.
  J Clin Endocrinol Metab
  . 2012;97(10):3426–3437.
  
• Gardner DG, Shoback
  D, eds. Endocrine emergencies. In:
  Greenspan’s Basic & Clinical
  Endocrinology
  . 9th ed. McGraw-Hill Professional; 2011.
  
• Kliegman RM. ed. Diabetes insipidus. In:
  Nelson Textbook of Pediatrics
  . 19th ed. Philadelphia,
  PA: Elsevier Saunders; 2011.
  
• Makaryus AN, McFarlane SI. Diabetes insipidus: Diagnosis and treatment of a complex disease.
  Cleve Clin J Med.
  2006;73:65–71.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Head Trauma
  
• Hypernatremia
  

CODES

• 253.5 Diabetes insipidus
  
• 588.1 Nephrogenic diabetes insipidus
  

BASICS

• Decrease in effective circulating insulin
  
• Increase in counter regulatory hormones including glucagon, catecholamines, cortisol, and growth hormone
  
• Hyperglycemia owing to:
  
  • Decreased peripheral glucose utilization
    
  • Increased hepatic gluconeogenesis
    
• Hyperosmolality and osmotic diuresis due to hyperglycemia
  
• Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonemia and metabolic acidosis, which is augmented with lactic acidosis from poor tissue perfusion
  
• Potassium deficit:
  
  • Intracellular shifts into extracellular space owing to hydrogen ion exchange
    
  • Loss from osmotic diuresis
    

Mechanism:

• Immune-mediated pancreatic islet β-cell destruction
  
• The overall incidence has been increased worldwide by 2–5% over the past 20 yr.
  
• Precipitating events leading to diabetic ketoacidosis (DKA):
  
  • Infection, often minor acute illness such as virus, group A streptococcal pharyngitis, or UTI
    
  • Stress
    
  • Endocrine: Pregnancy, puberty, hyperthyroidism
    
  • Psychiatric disorders, including eating disorders
    
  • Medication noncompliance, inappropriate interruption of insulin pump therapy, or treatment error
    
• Risk factors for cerebral edema:
  
  • Attenuated rise in measured serum sodium during DKA therapy (unrelated to the volume or sodium content of IV fluid or rate of change in serum glucose)
    
  • Bicarbonate treatment for acidosis correction
    
  • Hypocapnia
    
  • Increased serum urea nitrogen
    
  • No association with degree of hyperglycemia
    
  • Demographic factors that have been associated with an increased risk of cerebral edema include younger age, longer duration of symptoms, and new onset diabetes mellitus. These factors are also associated with increased risk of severe DKA.
    

DIAGNOSIS

• Polydipsia
  
• Polyuria (may have good urine output despite dehydration)
  
• Nocturia
  
• Polyphagia
  
• Malaise, weight loss
  
• DKA:
  
  • Initial presentation in 20–40% of patients
    
  • Often associated with tachypnea (Kussmaul respiration), tachycardia, orthostatic BP changes
    
  • Nausea
    
  • Vomiting
    
  • Abdominal pain, often resolving with reduction in ketosis/acidosis
    
  • Hyperpnea
    
  • Fruity breath secondary to ketones
    
• Rapid onset of DKA can occur within 7–8 hr with the use of insulin pump therapy if there is an infusion set or insulin delivery malfunction. This is due secondary to lack of long acting insulin to provide a safety net (more commonly seen in female >10 yr of age).
  
• Findings with more advanced disease
  
  • Dehydration, drowsiness, altered mental status, and ultimately, late stage coma and shock
    
• Cerebral edema:
  
  • The incidence ranges from 0.87–1.1%.
    
  • Cerebral edema accounts for 57–87% of all DKA deaths.
    
  • It typically occurs 4–12 hr after treatment is initiated, but can be presenting (subclinical) before treatment has started.
    
  • Headache
    
  • Change in neurologic status, such as drowsiness, irritability, or specific neurologic deficit, such as pupillary responses or cranial nerve palsies
    
  • Inappropriate slowing in pulse rate
    
  • Increase in BP
    
• Hyperglycemic hyperosmolar nonketotic coma:
  
  • Glucose level of 800–1,200 mg/dL
    
  • Rare in children; more common in adults
    

For DKA:

• The International Society for Pediatric and Adolescent Diabetes (ISPAD) defines DKA as blood bicarbonate level <15 mmol/L or venous pH <7.3 and hyperglycemia (>200 mg/dL) with related ketonemia or ketonuria.
  
• DKA classification:
  
  • Mild DKA: Venous pH <7.2–7.3 or HCO
    ₃
    <10–15 mmol/L
    
  • Moderate DKA: Venous pH <7.1–7.2 or HCO
    ₃
    <5–10 mmol/L
    
  • Severe DKA: Venous pH <7.1 or HCO
    ₃
    <5 mmol/L
    
• Hourly vital signs and neurologic checks
  
• Frequent blood chemistries
  
• ECG monitoring (in severe DKA) to assess T-waves for evidence of hyperkalemia or hypokalemia
  
• Accurate fluid input and output. Consider urinary catheterization in patients with impaired level of consciousness.
  

For DKA:

• Glucose, serum: Hyperglycemia
  
• Urinalysis:
  
  • Glycosuria
    
  • Ketonuria
    
  • Exclude UTI
    
• Blood chemistries every 2–4 hr until acidosis has resolved (more frequent as clinically indicated in the more severe cases)
  
• Electrolytes and venous pH
  
• Anion gap metabolic acidosis:
  
  • Potassium—high or normal (artifactual owing to extracellular shift)
    
  • Serum potassium rises 0.5 mEqL for each 0.1 decrease in pH
    
  • Sodium—low or normal (may be artifactual owing to hyperglycemia)
    
  • Corrected Na (mEq/L) = [measured serum Na (mEqL) + plasma glucose (mg/dL) – 100] × 0.016
    
  • Bicarbonate—low
    
  • Calculation: Na – (Cl + HCO
    ₃
    )
    
• Serum ketones—elevated. β-hydroxybutyrate (BHOB) is a quantitative test that is available to replace the classic nitroprusside test for serum ketones
  
• Serum osmolality
  
• CBC:
  
  • WBC often elevated owing to stress or infection
    
• Calcium
  
• Phosphate
  
• Cultures as indicated: Group A streptococcal pharyngeal swab, urine, etc.
  
• Pregnancy test if indicated
  
• ECG if potassium markedly abnormal