Hyperosmolar hyperglycemic state: Difference between revisions
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Revision as of 11:20, 20 July 2015
Background
- Prototypical pt is elderly pt w/ 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)
Precipitants
- PNA
- UTI
- Medication non-compliance
- Cocaine use
- Meds: Beta-blockers, diuretics
- GI hemorrhage
- Pancreatitis
- Heat-related illness
- ACS
- CVA
Clinical Features
- Dehydration
- Hypotension
- Seizure (15% of pts)
- Altered mental status
- Lethargy/coma
Diagnosis
- Glucose >600
- Osm >315
- Bicarb >15
- pH >7.3
- Serum ketones negative or mildly positive
Work Up
- Chem
- Serum Osm
- Lactate
- Serum ketones
- CBC
- Also consider:
- Blood cx
- UA/UCx
- LFTs
- Lipase
- Troponin
- CXR
- ECG
- Head CT
Treatment
- Fluid replacement
- Average fluid deficit is 8-12L
- 50% should be replaced over the initial 12hr
- May have to replace slower if pt has cardiac/renal impairment
- 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 pts require ICU admission
See Also
Source
Tintinalli's