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== | ==Clinical Features== | ||
| − | *Dehydration | + | *[[Dehydration]] |
| − | **Hypotension | + | **[[Hypotension]] |
| − | *Seizure (15% of | + | *[[Seizure]] (15% of patients) |
| − | * | + | *[[Altered mental status]] |
| − | *Lethargy/coma | + | *Lethargy/[[coma]] |
| − | ==Diagnosis== | + | ==Differential Diagnosis== |
| + | {{Hyperglycemia DDX}} | ||
| + | |||
| + | ==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 | *Glucose >600 | ||
| − | *Osm > | + | *Osm >320 |
*Bicarb >15 | *Bicarb >15 | ||
*pH >7.3 | *pH >7.3 | ||
*Serum ketones negative or mildly positive | *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 | |
| − | |||
| − | |||
| − | |||
| − | #Fluid replacement | ||
| − | # | ||
| − | # | ||
| − | # | ||
| − | #Hypokalemia | ||
| − | # | ||
| − | # | ||
| − | #Hyperglycemia | ||
| − | # | ||
| − | #Hypomagnesemia | ||
| − | # | ||
| − | #Hypophosphatemia | ||
| − | # | ||
| − | |||
[[File:HHS.jpg]] | [[File:HHS.jpg]] | ||
==Disposition== | ==Disposition== | ||
| − | *Most | + | *Most patients require ICU admission |
==See Also== | ==See Also== | ||
| − | *[[ | + | *[[Diabetes mellitus (main)]] |
| − | *[[ | + | *[[Diabetic ketoacidosis]] |
*[[Hypoglycemia]] | *[[Hypoglycemia]] | ||
| − | == | + | ==References== |
| − | + | <references/> | |
| − | + | [[Category:Endocrinology]] | |
| − | [[Category: | ||
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