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===
*[[Pneumonia (Main)]]
*[[Urinary tract infection]]
*Medication non-adherence
*[[Cocaine intoxication]]
*Meds: [[Beta-blockers]], diuretics
*[[GI bleed]]
*[[Pancreatitis]]
*[[Heat Emergencies|Heat related emergencies]]
*[[Acute coronary syndrome]]
*[[Stroke]]


Precipitants:
==Clinical Features==
*[[Dehydration]]
**[[Hypotension]]
*[[Seizure]] (15% of patients)
*[[Altered mental status]]
*Lethargy/[[coma]]


* Renal failure
==Differential Diagnosis==
* Pneumonia, Sepsis
{{Hyperglycemia DDX}}
* GI bleed
* MI
* CVA, bleed/ischemic
* PE
* Pancreatitis
* Burns
* Heat Stroke
* Dialysis
* Recent Surgery
* Drugs, Meds: CCBs, Beta-blockers, carbamezapines, cimetidine, cocaine/alcohol, steroids, etc..
== ==


==Evaluation==
===Work Up===
*Chemistry
*Serum osm
*[[Lactate]]
*Serum ketones
*CBC
*Also consider:
**Blood cultures
**[[Urinalysis]]/Urine culture
**[[LFTs]]
**Lipase
**[[Troponin]]
**[[CXR]]
**[[ECG]]
**[[Head CT]]


==Diagnosis==
===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==
#[[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<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>
#[[Hypokalemia]]
#*Must treat aggressively
#*Once adequate urinary output has been established K+ replacement should begin
#[[Hyperglycemia]]
#*Do not start insulin until K > 3.3 and adequate urinary output has been established
#[[Hypomagnesemia]]
#*Repletion will help correct [[hypokalemia]]
#[[Hypophosphatemia]]
#*Routine correction unnecessary unless phos <1.0
[[File:HHS.jpg]]


History:
==Disposition==
 
*Most patients require ICU admission
* Fever
* Thirst
* Polyuria or Oliguria or Polydipsia
* Confusion
* Seizures (focal)
* Hallucinations
== ==
 
 
Physical Exam:
 
* decrease consciousness
* tachy, hypotension
* fever
* focal seizures
* hemiparesis
* myoclonus
* quadriplegia
* nystagmus
 
==Work Up==
 
 
* CBC
* UA
* CXR
* EKG
* cultures
* Head CT, LP if suspecting intracranial process
== ==
 
 
* 50-65% have no history of diabetes
* Chem-10: Glucose> 600mg/dl (often > 1000), BUN/Cr ratio  >30
* Acetone:  no ketosis (lactic acidosis +/- present)
* Serum, Urine osmolarity: serum osmolarity > 320-350 mOsm/L
* Creatinine Kinase: often elevated due to rhabdo
== ==
 
 
==Treatment==
 
 
* 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
* ADA guidelines: 1/2 NS at 4-14 ml/kg/hr if corrected sodium normal or elevated
* ADA guidelines: NS at 4-14 ml/kg/hr if low corrected sodium
 
* Add dextrose once glucose fall <=300 mg/dl
* Replace potassium (5-10 meq per h) when level available and OK UOP
* if serum K <3.3 mEq/L add 40 mEq/L/hr
* if serum K <5 mEq/L add 20 mEq to each liter of fluids
* chemistry q1hr for first 4-6hrs of treatment
 
* Insulin: may be unnecessary in ED.  Consider starting once hemodynamically stable and UOP is adequate
* consider 0.1 Unit/kg/hr IV and modify rate to lower glucose 50-75 dL/hour
* once glucose is <=300 mg/dL, add D5 and decrease insulin to <= 0.5 Units/kg/hr
 
* Empiric phosphate repletion, SC Heparin, Broad Spectrum PPx ABx may be needed
* Avoid phenytoin for seizures since this agent inhibits the release of exogenous insulin and is associated with HHS 
* Admit ICU, consider central line if underlying cardiac, or renal disease
   
   
==See Also==
==See Also==
*[[Diabetes mellitus (main)]]
*[[Diabetic ketoacidosis]]
*[[Hypoglycemia]]


 
==References==
Endo: DKA
<references/>
 
[[Category:Endocrinology]]
Endo: Diabetes (Meds)
 
Endo: Hypoglycemia
 
 
==Source==
 
 
Sotelo 11/3/2009
 
 
 
 
[[Category:Endo]]

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