Hyperosmolar hyperglycemic state: Difference between revisions
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==Background== | ==Background== | ||
*Prototypical | *Prototypical patient is elderly with uncontrolled type II [[DM]] without adequate access to H2O | ||
*Occurs due to 3 factors: | *Occurs due to 3 factors: | ||
**Insulin resistance or deficiency | **Insulin resistance or deficiency | ||
Line 8: | Line 8: | ||
*Ketosis usually absent (may be mild) | *Ketosis usually absent (may be mild) | ||
*Cerebral edema is uncommon complication (case reports) | *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- | *Medication non-adherence | ||
*Cocaine | *[[Cocaine intoxication]] | ||
*Meds: Beta-blockers, diuretics | *Meds: [[Beta-blockers]], diuretics | ||
*GI | *[[GI bleed]] | ||
*Pancreatitis | *[[Pancreatitis]] | ||
*Heat | *[[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 | *[[Altered mental status]] | ||
*Lethargy/coma | *Lethargy/[[coma]] | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
{{Hyperglycemia DDX}} | |||
== | ==Evaluation== | ||
===Work Up=== | ===Work Up=== | ||
* | *Chemistry | ||
*Serum | *Serum osm | ||
*Lactate | *[[Lactate]] | ||
*Serum ketones | *Serum ketones | ||
*CBC | *CBC | ||
*Also consider: | *Also consider: | ||
**Blood | **Blood cultures | ||
** | **[[Urinalysis]]/Urine culture | ||
**LFTs | **[[LFTs]] | ||
**Lipase | **Lipase | ||
**Troponin | **[[Troponin]] | ||
**CXR | **[[CXR]] | ||
**ECG | **[[ECG]] | ||
**Head CT | **[[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 | |||
[[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== | ||
<references/> | |||
[[Category: | [[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
- 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