Difference between revisions of "Hyperosmolar hyperglycemic state"
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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=== | ||
− | + | *[[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]] | |
− | |||
− | |||
− | == | + | ==Clinical Features== |
− | + | *[[Dehydration]] | |
− | + | **[[Hypotension]] | |
− | + | *[[Seizure]] (15% of patients) | |
− | + | *[[Altered mental status]] | |
− | + | *Lethargy/[[coma]] | |
− | |||
− | |||
− | === | + | ==Differential Diagnosis== |
− | + | {{Hyperglycemia DDX}} | |
− | |||
− | |||
− | |||
− | |||
− | |||
− | |||
− | |||
− | ==Work Up== | + | ==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=== | |
− | * | + | *Glucose >600 |
− | * | + | *Osm >320 |
− | * Serum | + | *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]] | ||
+ | |||
+ | ==Disposition== | ||
+ | *Most patients require ICU admission | ||
==See Also== | ==See Also== | ||
− | + | *[[Diabetes mellitus (main)]] | |
− | + | *[[Diabetic ketoacidosis]] | |
− | + | *[[Hypoglycemia]] | |
− | |||
− | [[Hypoglycemia]] | ||
− | |||
− | |||
− | |||
− | [[Category: | + | ==References== |
+ | <references/> | ||
+ | [[Category:Endocrinology]] |
Latest revision as of 16:06, 28 September 2019
Contents
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
- Pneumonia (Main)
- Urinary tract infection
- Medication non-adherence
- Cocaine intoxication
- Meds: Beta-blockers, diuretics
- GI bleed
- Pancreatitis
- Heat related emergencies
- Acute coronary syndrome
- Stroke
Clinical Features
- Dehydration
- Seizure (15% of patients)
- Altered mental status
- Lethargy/coma
Differential Diagnosis
Hyperglycemia
- Physiologic stress response (rarely causes glucose >200 mg/dL)
- Diabetes mellitus (main)
- Hemochromatosis
- Iron toxicity
- Sepsis
Evaluation
Work Up
- Chemistry
- Serum osm
- Lactate
- Serum ketones
- CBC
- Also consider:
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[2]
- Average fluid deficit is 8-12L
- 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
Disposition
- Most patients require ICU admission
See Also
References
- ↑ Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014; 37(11):3124-31.
- ↑ Stoner GD. Hyperosmolar Hyperglycemic State. Am Fam Physician. 2005 May 1;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html