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Hyperosmolar Syndrome, Emergency Medicine


Basics


Description


  • Results from a relative insulin deficiency in the undiagnosed or untreated diabetic
  • Sustained hyperglycemia creates an osmotic diuresis and dehydration:
    • Extracellular space maintained by the osmotic gradient at the expense of the intracellular space
    • Eventually profound intracellular dehydration occurs.
  • Total body deficits of H2O, Na+, Cl-, K-, PO4-, Ca2+, and Mg2+
  • In contrast to diabetic ketoacidosis (DKA), severe ketoacidosis does not occur:
    • Circulating insulin levels are higher.
    • The elevation of insulin counter-regulatory hormones is less marked.
    • The hyperosmolar state itself inhibits lipolysis (the release of free fatty acids) and subsequent generation of keto acids

  • Most commonly seen in elderly type II diabetics who experience a stressful illness that precipitates worsening hyperglycemia and reduced renal function
  • In the elderly, 30-40% of cases are associated with the initial presentation of diabetes.

Hyperosmolar hyperglycemic states (HHS) rare in pediatric patients  

Etiology


  • Hyperosmolar state precipitated by factors that:
    • Impair peripheral insulin action
    • Increase endogenous or exogenous glucose
    • Decrease patients ability to replace fluid loss
  • Infection is the most common precipitating factor in 32-60% of cases.
  • Other precipitating causes include:
    • Inadequate diabetes therapy
    • Medication omission
    • Diet indiscretion
    • Infections
    • Pneumonia
    • UTI
    • Sepsis
    • Medications/drugs
    • Diuretics
    • β-blockers
    • Calcium channel blockers
    • Phenytoin
    • Cimetidine
    • Amphetamines
    • Ethanol
    • Myocardial infarction
    • Stroke
    • Renal failure
    • Heat stroke
    • Pancreatitis
    • Intestinal obstruction
    • Endocrine disorders
    • Burns
    • Heat stroke

Diagnosis


Signs and Symptoms


History
  • Progression of signs and symptoms typically occur over days to weeks.
  • Polyuria/polydipsia/weight loss
  • Dizziness/weakness/fatigue
  • Blurred vision
  • Leg cramps

Physical Exam
  • Dehydration
  • Tachycardia
  • Sunken eyes
  • Hypotension
  • Orthostasis
  • Dry mucous membranes
  • Decreased skin turgor
  • Collapsed neck veins
  • Coma/lethargy/drowsiness
  • Urinary output maintained until late
  • Seizures/focal neurologic deficits
  • Concurrent precipitating medical illness

Essential Workup


Diagnostic criteria:  
  • Serum glucose ≥600 mg/dL (usually >1,000 mg/dL)
  • Minimal ketosis
  • pH ≥ 7.30, HCO3 ≥15 mEq/L
  • Effective serum osmolality >320 mOsm/kg:
    • = 2 — Na+ + glucose/18
    • BUN not included because it is freely permeable between fluid compartments

Diagnosis Tests & Interpretation


Lab
  • Broad testing indicated to evaluate hyperosmolar syndrome and for precipitating causes
  • Electrolytes:
    • K+ may be elevated even in the presence of total body deficit owing to shift from intracellular space to extracellular space.
    • Mild anion gap metabolic acidosis owing to lactic acid, β-hydroxybutyric acid, or renal insufficiency
    • Increased sodium-correct for hyperglycemia: Corrected [Na+] = [Na+] + 1.6 — [(glucose in mg/dL) - 100]/100
  • BUN, creatinine:
    • Azotemia with elevated BUN/creatinine ratio owing to prerenal and intrarenal causes
  • Venous blood gas (VBG) or arterial blood gas (ABG) to rapidly determine pH:
    • ABG necessary to evaluate mixed acid-base disorders
  • Serum ketones, β-hydroxybutyrate, and lactate level if pH < 7.3 or significantly elevated anion gap to evaluate mixed acid-base disorder
  • Serum osmolarity
  • CBC:
    • Leukocytosis due to infection, stress, or hemoconcentration
    • Increased hemoglobin and hematocrit due to hemoconcentration
  • Lipase and amylase:
    • Pancreatitis common
    • Elevated amylase and lipase with no evidence of pancreatitis common
    • May be due to increased salivary secretion, hemoconcentration, or decreased renal clearance
  • Urinalysis:
    • Check for ketones/glucose.
    • Assess for UTI.
  • Magnesium, calcium, phosphate
  • Blood cultures in sepsis
  • Creatine kinase for rhabdomyolysis:
    • Incidence as high as 17%
  • Urine pregnancy test in females of childbearing years
  • Cardiac enzymes and troponin for myocardial infarction

Imaging
  • CXR to evaluate for possible underlying pneumonia
  • Head CT: When indicated for AMS or with focal neurologic deficit

Diagnostic Procedures/Surgery
ECG:  
  • Evaluate for electrolyte abnormalities causing conduction impairment
  • Evaluate for signs of ischemia as triggering event

Differential Diagnosis


Differentiate from DKA:  
  • If acidosis or significant anion gap present, must determine cause (i.e., ketosis, DKA, lactic acidosis, [hypoperfusion, sepsis, or postictal], or other causes of metabolic acidosis)
  • Mixed disorder of HHS and DKA present in up to 33% of patients

Treatment


Pre-Hospital


IV fluid resuscitation and initial stabilization  

Initial Stabilization/Therapy


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.

Ed Treatment/Procedures


  • General strategy:
    • Frequent reassessment of volume and mental status
    • Electrolyte assessment difficult:
      • Serum levels of Na+, K+, PO4- 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 MgSO4 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).

Medication


  • Insulin: Begin with 0.05-0.1 U/kg/h; modify after assessing clinical response.
  • MgSO4 (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


Disposition


Admission Criteria
  • 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.

Discharge Criteria
  • 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.

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

Pearls and Pitfalls


  • 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

Additional Reading


  • 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


ICD9


  • 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

ICD10


  • E11.01 Type 2 diabetes mellitus with hyperosmolarity with coma
  • E87.1 Hypo-osmolality and hyponatremia

SNOMED


  • 20313009 hyperosmolality (disorder)
  • 190331003 diabetes mellitus, adult onset, with hyperosmolar coma (disorder)
  • 190330002 diabetes mellitus, juvenile type, with hyperosmolar coma (disorder)
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