Rosen & Barkin's 5-Minute Emergency Medicine Consult (366 page)

ABCs:

• Secure airway in comatose patients.
  
• Cardiac monitor and 18G IV
  
• Naloxone, thiamine, and blood glucose for coma of unknown cause
  
• Restore hemodynamic stability with IV fluids.
  
• 0.9% NS 1–2 L over the 1st hr
  
• Larger volumes of fluid may be needed to normalize the vital signs and establish urine output.
  

• General strategy:
  
  • Frequent reassessment of volume and mental status
    
  • Electrolyte assessment difficult:
    
    • Serum levels of Na
      ⁺
      , K
      ⁺
      , PO
      ₄
      ⁻
      do not accurately reflect the total body solute deficits or the intracellular environment.
      
    • Repeat electrolyte and glucose levels hourly.
      
  • Search for a precipitating illness.
    
• Fluids:
  
  • Begin resuscitation with 0.9% NS 1–2 L over 1–2 hr to restore intravascular volume and achieve hemodynamic stability.
    
  • Use 0.45% saline after initial resuscitation
    
  • Calculate total body water (TBW) deficit using corrected serum sodium:
    
    • TBW deficit = 0.6 × weight (kg) × (1 – 140/corrected Na
      ⁺
      )
      
  • Average fluid deficit is 9 L.
    
  • Replace 50% of the fluid deficit over the next 12 hr.
    
  • Change fluid to D5 1/2 NS when serum glucose is <250 mg/dL.
    
• Potassium:
  
  • Anticipate hypokalemia:
    
    • Total body deficit of ∼5–10 mEq/kg body weight (replace over 3 days)
      
  • Begin potassium repletion after urine output is established. Do not start in anuric patients or if initial K
    ⁺
    level is >5 mEq/L.
    
    • If the initial K
      ⁺
      is normal (4–5 mEq/L), give 20–30 mEq KCl in the 1st L of fluids, then give 20 mEq/hr.
      
    • If the initial K
      ⁺
      is low (3–4 mEq/L), give 40 mEq in 1st L
      
    • If serum K
      ⁺
      is <3 mEq/L hold insulin and give 10–20 mEq/h until K
      ⁺
      >3.3, then add 40 mEq to each lister
      
    • Follow repeat serum K
      ⁺
      levels q1–2h and adjust treatment accordingly.
      
• Insulin:
  
  • No role in the early resuscitation
    
  • Earlier use of insulin may cause rapid correction of hyperglycemia with collapse of the intravascular space, hypotension, and shock or hypokalemia and dysrhythmias.
    
  • Some patients will not require insulin.
    
  • Use insulin as sole therapy in patients with fluid overload (i.e., acute renal failure [ARF]).
    
  • Begin only after achieving hemodynamic stability and evaluating for hypokalemia:
    
    • Do not use unless serum K
      ⁺
      >3.3 mEq/L
      
  • SC or IM insulin not recommended due to erratic absorption
    
  • Titrate drip to optimally decrease serum glucose by 50–90 mg/dL/hr. More rapid correction places the patient at risk for developing cerebral edema.
    
  • Decrease drip rate by 1/2 when serum glucose <250 mg/dL.
    
  • Adjust insulin drip to maintain serum glucose between 150–200 mg/dL, and continue until serum bicarbonate is >18 mg/dL and pH > 7.3
    
• Phosphate:
  
  • Routine replacement not recommended
    
  • If serum levels <1 mg/dL, give 20–30 mmol potassium phosphate over 24 hr
    
  • Monitor serum calcium levels closely
    
• Magnesium:
  
  • 0.35 mEq/kg magnesium in fluids for 1st 3–4 hr (2.5–3 g MgSO
    ₄
    in 70 kg patient)
    
  • Caution in ARF
    
• Anticoagulation:
  
  • Arterial thrombosis may complicate hyperosmolar state:
    
    • Consider SC heparin as prophylaxis.
      
  • Remain vigilant to detect thrombotic complications (e.g., MI, pulmonary embolus, mesenteric ischemia).
    

• Insulin: Begin with 0.05–0.1 U/kg/h; modify after assessing clinical response.
  
• MgSO
  ₄
  (magnesium sulfate): 50% (5 g/10 mL; dilute to at least 20% before IV use)
  
• Naloxone: 2 mg (peds: 0.1 mg/kg) IV push (IVP)
  
• Potassium phosphate IV: Phosphorous serum level <0.5 mg/dL: 0.5 mmol/kg IV infused over 4–6 hr; phosphorous serum level 0.5–1 mg/dL: 0.25 mmol/kg IV infused over 4–6 hr
  
• Potassium phosphate PO: Phosphorus 250 mg per tablet and potassium 1.1 mEq per tablet
  
• Thiamine: 100 mg (peds: 10–25 mg) IVP
  

FOLLOW-UP

• All but the mildest cases should be admitted to ICU:
  
  • Frequent serial labs for the 1st 24 hr
    
  • Rapid shifts in fluids and electrolytes and the potential for deterioration in mental status and arrhythmias mandate close monitoring.
    
• Mild cases may be managed in an observation unit over 12–24 hr.
  

• Patients meeting the diagnostic criteria for hyperosmolar syndrome should not be discharged.
  
• Mild hyperglycemia patients with mild volume deficits and normal serum osmolarity can be discharged after hydration and correction of hyperglycemia.
  

Patient should follow-up with endocrinology and with their primary physician within 1 wk postdischarge for long-term blood glucose monitoring and insulin therapy.

• Failure to look for precipitating event or cause
  
• Too rapid correction of glucose—may lead to hypotension
  
• Continuing isotonic fluids after volume resuscitation—may lead to hypernatremia
  
• Continuing hypotonic fluids without frequent electrolytes—may lead to cellular edema, cerebral edema
  
• Failure to prevent hypokalemia: Respiratory depression, dysrhythmias
  
• Avoid phenytoin in the event of seizure activity:
  
  • Inhibits the endogenous release of insulin
    

• Gaglia JL, Wyckoff J, Abrahamson MJ. Acute hyperglycemic crisis in the elderly.
  Med Clin North Am
  . 2004;88:1063–1084.
  
• Kitabchi AE, Nyenwe EA. Hyperglycemic crisis in diabetes mellitus: Diabetic ketoacidosis and hyperglycemic hyperosmolar state.
  Endocrinol Metab Clin North Am
  . 2006;35(4):725–751.
  
• Nyenwe EA, Kitabchi AE. Evidence-based management of hyperglycemic emergencies in diabetes mellitus.
  Diabetes Res Clin Pract
  . 2011; 94:340–351.
  

See Also (Topic, Algorithm, Electronic Media Element)

Diabetic Ketoacidosis

CODES

• 250.20 Diabetes with hyperosmolarity, type II or unspecified type, not stated as uncontrolled
  
• 250.21 Diabetes with hyperosmolarity, type I [juvenile type], not stated as uncontrolled
  
• 276.0 Hyperosmolality and/or hypernatremia
  

BASICS

• Parathyroid hormone (PTH) excess with symptoms owing to PTH actions:
  
  • Decreases urinary Ca
    ²⁺
    loss
    
  • Increases urinary PO
    ₄
    ²⁻
    loss
    
  • Stimulates vitamin D conversion from 25(OH)-D to 1,25(OH)-D in kidney
    
  • Liberates Ca
    ²⁺
    and PO
    ₄
    ²⁻
    from bone
    
  • Hypercalcemia is the primary metabolic finding
    
• Hypercalciuria from hypercalcemia (despite decreased urinary loss) produces increased magnesium loss in urine
  
• Magnesium (negative feedback to prevent hypercalcemia causes hypomagnesaemia):
  
  • Cofactor in the production of PTH
    
  • Essential for action of PTH in target tissues
    
• Genetics:
  
  • Associated with multiple endocrine neoplasia type 1:
    
    • Hyperparathyroidism
      
    • Pancreatic islet disease
      
    • Pituitary disease
      
  • Associated with multiple endocrine neoplasia type 2:
    
    • Hyperparathyroidism (type 2A, rare in 2B)
      
    • Medullary carcinoma of the thyroid (type 2A and 2B, less virulent in type 2A)
      
    • Pheochromocytoma (type 2A and 2B)
      
    • Mucosal neuroma (type 2B)
      

• Excess secretion of PTH owing to:
  
  • Primary hyperparathyroidism (adenoma 85%, hyperplasia 14%, carcinoma <1%)
    
  • Secondary hyperparathyroidism (response to vitamin D deficiency or chronic renal failure with hyperphosphatemia):
    
    • Calcium is low or normal, but PTH levels are elevated
      

DIAGNOSIS