Content
Collaboration
About Us
Contact Us
SEARCH RESULTS FOR:
Hyperosmolar-Hyperglycemic-State
Hyperosmolar Hyperglycemic State
![Hyperosmolar Hyperglycemic State (HHS)
Note: HHS is only seen in Type II DM patients!
Note: In patients with either DKA or HHS, always look for an underlying cause (i.e. an infection)
Author: Yan Yu Reviewers:
Peter Vetere
Gill Goobie
Hanan Bassyouni* * MD at time of publication
Alters total body water & ion osmosis
Inadequate insulin production, insulin resistance, non- adherence to insulin Tx
Relative Insulin deficit
Stresses that ↑ Insulin demand: infections, pneumonia, MI, pancreatitis, etc)
Hyperglycemia
(Very high blood [glucose], higher than in DKA)
When blood [glucose] > 12mmol/L, glucose filtration > reabsorption, ↑ urine [glucose]
Glucosuria
Glucose in filtrate promotes osmotic diuresis: large- volume urine output
Polyuria
Dehydration
(↓ JVP, orthostasis: postural hypotension/ postural tachycardia, ↑ resting HR)
Some insulin still present, but not enoughsome glucose is utilized by muscle/fat cells, some remain in the blood
Cells not “starved”, but still need more energy
↑ release of Catabolic hormones: Glucagon, Epinephrine, Cortisol, GH
Body tries to ↑ blood [glucose], to hopefully ↑ cell glucose absorption
Hypothalamic cells sense low intra-cellular glucose, triggering feelings of hunger
Polyphagia
Note: the presence of some insulin directly inhibits lipolysis; thus, in HHS there is no ketone body production, and no subsequent metabolic acidosis and ketouria (unlike in DKA). If ketones are detected in an HHS patient it’s likely secondary to starvation or other mechanisms.
↓ ECF volume, ↑ ECF osmolarity (i.e. hypernatremia)
↑ Gluconeogenesis ↑ Glycogenolysis (in liver)
↓ Protein synthesis, ↑ proteolysis
(in muscle)
↑ Gluconeogenic substrates for liver If the patient doesn’t drink enough
water to replenish lost blood volume If pt is alert and
Electrolyte imbalance
water is accessible
Water osmotically leaves neurons, shrinking them
Neural damage: delirium, lethargy, seizure, stupor, coma
↓ renal perfusion, ↓ GFR
Renal Failure
(pre-renal cause; see relevant slides)
Polydipsia Note: in HHS, body K+ is lost via osmotic diuresis. But diffusion of K+ out of cells
may cause serum [K+] to be falsely normal/elevated. To prevent hypokalemia, give IV KCl along with IV insulin as soon as serum K+ <5.0mmol/L. But ensure patient has good renal function/urine output first, to avoid iatrogenic hyperkalemia!
Note: Electrolyte imbalances (i.e. hyperkalemia, hypernatremia) are worsened by the acute renal failure commonly coexisting with DKA/HHS
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published November 3, 2016 on www.thecalgaryguide.com](http://calgaryguide.ucalgary.ca/wp-content/uploads/2015/05/Hyperosmolar-Hyperglycemic-State-HHS.jpg "Hyperosmolar Hyperglycemic State (HHS)
Note: HHS is only seen in Type II DM patients!
Note: In patients with either DKA or HHS, always look for an underlying cause (i.e. an infection)
Author: Yan Yu Reviewers:
Peter Vetere
Gill Goobie
Hanan Bassyouni* * MD at time of publication
Alters total body water & ion osmosis
Inadequate insulin production, insulin resistance, non- adherence to insulin Tx
Relative Insulin deficit
Stresses that ↑ Insulin demand: infections, pneumonia, MI, pancreatitis, etc)
Hyperglycemia
(Very high blood [glucose], higher than in DKA)
When blood [glucose] > 12mmol/L, glucose filtration > reabsorption, ↑ urine [glucose]
Glucosuria
Glucose in filtrate promotes osmotic diuresis: large- volume urine output
Polyuria
Dehydration
(↓ JVP, orthostasis: postural hypotension/ postural tachycardia, ↑ resting HR)
Some insulin still present, but not enoughsome glucose is utilized by muscle/fat cells, some remain in the blood
Cells not “starved”, but still need more energy
↑ release of Catabolic hormones: Glucagon, Epinephrine, Cortisol, GH
Body tries to ↑ blood [glucose], to hopefully ↑ cell glucose absorption
Hypothalamic cells sense low intra-cellular glucose, triggering feelings of hunger
Polyphagia
Note: the presence of some insulin directly inhibits lipolysis; thus, in HHS there is no ketone body production, and no subsequent metabolic acidosis and ketouria (unlike in DKA). If ketones are detected in an HHS patient it’s likely secondary to starvation or other mechanisms.
↓ ECF volume, ↑ ECF osmolarity (i.e. hypernatremia)
↑ Gluconeogenesis ↑ Glycogenolysis (in liver)
↓ Protein synthesis, ↑ proteolysis
(in muscle)
↑ Gluconeogenic substrates for liver If the patient doesn’t drink enough
water to replenish lost blood volume If pt is alert and
Electrolyte imbalance
water is accessible
Water osmotically leaves neurons, shrinking them
Neural damage: delirium, lethargy, seizure, stupor, coma
↓ renal perfusion, ↓ GFR
Renal Failure
(pre-renal cause; see relevant slides)
Polydipsia Note: in HHS, body K+ is lost via osmotic diuresis. But diffusion of K+ out of cells
may cause serum [K+] to be falsely normal/elevated. To prevent hypokalemia, give IV KCl along with IV insulin as soon as serum K+ <5.0mmol/L. But ensure patient has good renal function/urine output first, to avoid iatrogenic hyperkalemia!
Note: Electrolyte imbalances (i.e. hyperkalemia, hypernatremia) are worsened by the acute renal failure commonly coexisting with DKA/HHS
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published November 3, 2016 on www.thecalgaryguide.com")
