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DKA & HHS
Hyperglycemia Crisis Management
Dieni Azra
• DKA & HHS associated with high mortality rates if left not treated.
• significant likelihood of morbidity & mortality, including cerebral edema,
permanent neurological injury & death.
• mortality rate for DKA is < 1% & ~ 15% for HHS.
• DKA & HHS have similar pathophysiology with some few differences.
• occur because of lack of insulin effect
• Typically, pts with T1DM more likely to exhibit DKA because of absolute
insulin deficiency, & T2DM more likely to experience HHS
Pathophysiology basic cause: insufficient insulin effect
Precipitating cause
Diagnosis – History & Physical exam
DKA
• develops rapidly, over a
time span of <24 h
• nausea & vomiting:
common symptom
• Abdominal pain,
sometimes mimicking an
acute abdomen
• full alertness to profound
lethargy
• fruity breath odor,
• Kussmaul
HHS
• several days before
admission
• polyuria, polydipsia &
weight loss
• mental obtundatioh & coma
 more frequent
Laboratory
• Immediate: BG, ABG, & Ureum/BUN
• serum electrolytes,osmolality, creatinine & ketones
• urinalysis; ketonuria
• CBC with differential.
• Bacterial cultures of urine, blood, & other tissues 
appropriate antibiotics should be administered if
infection is suspected.
Diagnosis
Diagnosis
Treatment
• Cornerstones: fluids, insulin, correction of electrolyte
abnormalities & close monitoring
• therapeutic goals:
1) improving circulatory volume and tissue perfusion
2) decreasing serum glucose & plasma osmolality to normal
levels
3) clearing serum & urine of ketones at a steady rate
4) correcting electrolyte imbalances
5) identifying & treating precipitating events
Deficit
DKA
• Total water: 5-7 l
(100ml/kg)
• Sodium: 7-10 mmol/kg
HHS
• 7-9 l
(100-200ml/kg)
• Sodium: 5-13mmol/kg
Fluid rescucitation
• improving circulatory volume & tissue perfusion
• decreasing serum glucose & plasma osmolality to
normal levels
• correcting electrolyte imbalances
• Dilution: reduce BG & contra insulin hormone
concentration
• Fluids: NS
Sodium >/= 140 mEq/L: NaCl 0.45%
Date of Download: 7/25/2023 Copyright © 2023 American Diabetes Association. All rights reserved.
Protocol for management of DKA or HHS
Diabetes Care. 2009;32(7):1335-1343. doi:10.2337/dc09-9032
serum Na should be corrected for hyperglycemia (for each 100 mg/dl glucose 100 mg/dl, add 1.6 mEq to sodium value for corrected serum
value
Monitoring
• serum glucose: every 1-2 h during treatment
• Serum electrolytes: every 2-6 h, depending on the clinical
response of the patient
• the precipitating factor must be identified & treated.
Resolution
Date of Download: 7/25/2023 Copyright © 2023 American Diabetes Association. All rights reserved.
From: Management of Hyperglycemic Crises in Patients With Diabetes
Diabetes Care. 2001;24(1):131-153. doi:10.2337/diacare.24.1.131
Thank you

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hyperglycemic crisis, IGD Juli 2023.ppt

  • 1. DKA & HHS Hyperglycemia Crisis Management Dieni Azra
  • 2. • DKA & HHS associated with high mortality rates if left not treated. • significant likelihood of morbidity & mortality, including cerebral edema, permanent neurological injury & death. • mortality rate for DKA is < 1% & ~ 15% for HHS. • DKA & HHS have similar pathophysiology with some few differences. • occur because of lack of insulin effect • Typically, pts with T1DM more likely to exhibit DKA because of absolute insulin deficiency, & T2DM more likely to experience HHS
  • 3. Pathophysiology basic cause: insufficient insulin effect
  • 5. Diagnosis – History & Physical exam DKA • develops rapidly, over a time span of <24 h • nausea & vomiting: common symptom • Abdominal pain, sometimes mimicking an acute abdomen • full alertness to profound lethargy • fruity breath odor, • Kussmaul HHS • several days before admission • polyuria, polydipsia & weight loss • mental obtundatioh & coma  more frequent
  • 6. Laboratory • Immediate: BG, ABG, & Ureum/BUN • serum electrolytes,osmolality, creatinine & ketones • urinalysis; ketonuria • CBC with differential. • Bacterial cultures of urine, blood, & other tissues  appropriate antibiotics should be administered if infection is suspected.
  • 9.
  • 10. Treatment • Cornerstones: fluids, insulin, correction of electrolyte abnormalities & close monitoring • therapeutic goals: 1) improving circulatory volume and tissue perfusion 2) decreasing serum glucose & plasma osmolality to normal levels 3) clearing serum & urine of ketones at a steady rate 4) correcting electrolyte imbalances 5) identifying & treating precipitating events
  • 11. Deficit DKA • Total water: 5-7 l (100ml/kg) • Sodium: 7-10 mmol/kg HHS • 7-9 l (100-200ml/kg) • Sodium: 5-13mmol/kg
  • 12. Fluid rescucitation • improving circulatory volume & tissue perfusion • decreasing serum glucose & plasma osmolality to normal levels • correcting electrolyte imbalances • Dilution: reduce BG & contra insulin hormone concentration • Fluids: NS Sodium >/= 140 mEq/L: NaCl 0.45%
  • 13.
  • 14.
  • 15. Date of Download: 7/25/2023 Copyright © 2023 American Diabetes Association. All rights reserved. Protocol for management of DKA or HHS Diabetes Care. 2009;32(7):1335-1343. doi:10.2337/dc09-9032 serum Na should be corrected for hyperglycemia (for each 100 mg/dl glucose 100 mg/dl, add 1.6 mEq to sodium value for corrected serum value
  • 16.
  • 17.
  • 18. Monitoring • serum glucose: every 1-2 h during treatment • Serum electrolytes: every 2-6 h, depending on the clinical response of the patient • the precipitating factor must be identified & treated.
  • 20. Date of Download: 7/25/2023 Copyright © 2023 American Diabetes Association. All rights reserved. From: Management of Hyperglycemic Crises in Patients With Diabetes Diabetes Care. 2001;24(1):131-153. doi:10.2337/diacare.24.1.131