Hyperosmolar hyperglycemic state: Difference between revisions
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==Background==
==Background==
*Prototypical patient is elderly with uncontrolled type II [[DM]] without adequate access to H2O
*Occurs due to 3 factors:
**Insulin resistance or deficiency
**Increased hepatic gluconeogenesis and glycogenolysis
**Osmotic diuresis and dehydration followed by impaired renal excretion of glucose
***May result in TBW losses of 8-12L
*Ketosis usually absent (may be mild)
*Cerebral edema is uncommon complication (case reports)
*Estimated mortality 10-20%, usually due to underlying precipitant<ref>Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care.  2014; 37(11):3124-31.</ref>
**In contrast to [[DKA]], in which mortality is 1-5%
**Incidence of HHS < 1% of hospital admissions of patients with diabetes
===Precipitants===
===Precipitants===
# Renal failure
*[[Pneumonia (Main)]]
# Pneumonia, Sepsis
*[[Urinary tract infection]]
# GI bleed
*Medication non-adherence
# MI
*[[Cocaine intoxication]]
# CVA, bleed/ischemic
*Meds: [[Beta-blockers]], diuretics
# PE
*[[GI bleed]]
# Pancreatitis  
*[[Pancreatitis]]
# Burns
*[[Heat Emergencies|Heat related emergencies]]
# Heat Stroke
*[[Acute coronary syndrome]]
# Dialysis
*[[Stroke]]
# Recent Surgery
# Drugs, Meds: CCBs, Beta-blockers, carbamezapines, cimetidine, cocaine/alcohol, steroids, etc..


==Diagnosis==
==Clinical Features==
===History===
*[[Dehydration]]
# Fever
**[[Hypotension]]
# Thirst
*[[Seizure]] (15% of patients)
# Polyuria or Oliguria or Polydipsia
*[[Altered mental status]]
# Confusion
*Lethargy/[[coma]]
# Seizures (focal)
# Hallucinations


===Physical Exam===
==Differential Diagnosis==
# decrease consciousness
{{Hyperglycemia DDX}}
# tachy, hypotension
# fever
# focal seizures
# hemiparesis
# myoclonus
# quadriplegia
# nystagmus


==Work Up==
==Evaluation==
# CBC
===Work Up===
# UA
*Chemistry
# CXR
*Serum osm
# EKG
*[[Lactate]]
# cultures
*Serum ketones
# Head CT, LP if suspecting intracranial process
*CBC
*Also consider:
**Blood cultures
**[[Urinalysis]]/Urine culture
**[[LFTs]]
**Lipase
**[[Troponin]]
**[[CXR]]
**[[ECG]]
**[[Head CT]]


* 50-65% have no history of diabetes
===Diagnosis===
* Chem-10: Glucose> 600mg/dl (often > 1000), BUN/Cr ratio  >30
*Glucose >600
* Acetone:  no ketosis (lactic acidosis +/- present)
*Osm >320
* Serum, Urine osmolarity: serum osmolarity > 320-350 mOsm/L
*Bicarb >15
* Creatinine Kinase: often elevated due to rhabdo
*pH >7.3
*Serum ketones negative or mildly positive
*Neurologic abnormalities frequently present (coma in 25-50% of cases)


==Treatment==
==Management==
# Fluids- mean deficit is 9L. Start IV NS until BP and UOP OK.  Then, change to 1/2 NS & replace 50% deficit over 12h, & 50% over next 12-24h
#[[Fluid replacement]]
## ADA guidelines: 1/2 NS at 4-14 ml/kg/hr if corrected sodium normal or elevated
#*Average fluid deficit is 8-12L
## ADA guidelines: NS at 4-14 ml/kg/hr if low corrected sodium
#**50% should be replaced over the initial 12hr
# Add dextrose once glucose fall <=300 mg/dl
#**May have to replace slower if patient has cardiac/renal impairment
# Replace potassium (5-10 meq per h) when level available and OK UOP
#**Aggressiveness of fluid replacement must be weighed against the risk of cerebral edema, which increases with younger age<ref>Stoner GD. Hyperosmolar Hyperglycemic State. Am Fam Physician. 2005 May 1;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html</ref>
## if serum K <3.3 mEq/L add 40 mEq/L/hr
#[[Hypokalemia]]
## if serum K <5 mEq/L add 20 mEq to each liter of fluids
#*Must treat aggressively
## chemistry q1hr for first 4-6hrs of treatment
#*Once adequate urinary output has been established K+ replacement should begin
# Insulin: may be unnecessary in ED. Consider starting once hemodynamically stable and UOP is adequate
#[[Hyperglycemia]]
## consider 0.1 Unit/kg/hr IV and modify rate to lower glucose 50-75 dL/hour
#*Do not start insulin until K > 3.3 and adequate urinary output has been established
## once glucose is <=300 mg/dL, add D5 and decrease insulin to <= 0.5 Units/kg/hr
#[[Hypomagnesemia]]
# Empiric phosphate repletion, SC Heparin, Broad Spectrum PPx ABx may be needed
#*Repletion will help correct [[hypokalemia]]
# Avoid phenytoin for seizures since this agent inhibits the release of exogenous insulin and is associated with HHS 
#[[Hypophosphatemia]]
# Admit ICU, consider central line if underlying cardiac, or renal disease
#*Routine correction unnecessary unless phos <1.0
[[File:HHS.jpg]]
 
==Disposition==
*Most patients require ICU admission
   
   
==See Also==
==See Also==
Endo: DKA
*[[Diabetes mellitus (main)]]
 
*[[Diabetic ketoacidosis]]
Endo: Diabetes (Meds)
*[[Hypoglycemia]]
 
[[Hypoglycemia]]
 
==Source==
Sotelo 11/3/2009


[[Category:Endo]]
==References==
<references/>
[[Category:Endocrinology]]

Latest revision as of 16:06, 28 September 2019

Background

  • Prototypical patient is elderly with uncontrolled type II DM without adequate access to H2O
  • Occurs due to 3 factors:
    • Insulin resistance or deficiency
    • Increased hepatic gluconeogenesis and glycogenolysis
    • Osmotic diuresis and dehydration followed by impaired renal excretion of glucose
      • May result in TBW losses of 8-12L
  • Ketosis usually absent (may be mild)
  • Cerebral edema is uncommon complication (case reports)
  • Estimated mortality 10-20%, usually due to underlying precipitant[1]
    • In contrast to DKA, in which mortality is 1-5%
    • Incidence of HHS < 1% of hospital admissions of patients with diabetes

Precipitants

Clinical Features

Differential Diagnosis

Hyperglycemia

Evaluation

Work Up

Diagnosis

  • Glucose >600
  • Osm >320
  • Bicarb >15
  • pH >7.3
  • Serum ketones negative or mildly positive
  • Neurologic abnormalities frequently present (coma in 25-50% of cases)

Management

  1. Fluid replacement
    • Average fluid deficit is 8-12L
      • 50% should be replaced over the initial 12hr
      • May have to replace slower if patient has cardiac/renal impairment
      • Aggressiveness of fluid replacement must be weighed against the risk of cerebral edema, which increases with younger age[2]
  2. Hypokalemia
    • Must treat aggressively
    • Once adequate urinary output has been established K+ replacement should begin
  3. Hyperglycemia
    • Do not start insulin until K > 3.3 and adequate urinary output has been established
  4. Hypomagnesemia
  5. Hypophosphatemia
    • Routine correction unnecessary unless phos <1.0

HHS.jpg

Disposition

  • Most patients require ICU admission

See Also

References

  1. ↑ Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014; 37(11):3124-31.
  2. ↑ Stoner GD. Hyperosmolar Hyperglycemic State. Am Fam Physician. 2005 May 1;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html
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