HHS Flashcards
Hyperglycemic hyperosmolar syndrome (HHS) dx:
BG>:
mOsm>:
ketones:
severe hyperglycemia (>600 mg/dl)
350 hyperosmolality
no or minimal urine ketones
Reduction of glomerular filtration rate (GFR) is essential. i.e.
The most important goals of therapy are:
how do fluids alone reduce BG levels via dilution and by
Prognosis for feline HHS patients is:
Dogs:
Renal failure and congestive heart failure are common
replace fluid deficits and SLOWLY decrease glucose concentration, thereby avoiding rapid intracranial shifts in osmolality and preventing cerebral edema
via dilution and increasing GFR
poor (12% long-term survival) -2 concurrent disease better px (62% discharged from hospital)
HHS accounted for ___% cats __% dog DM emergencies
6.4% cats 5% dogs
Hormonal Alterations MoA:
- relative or absolute lack of:
- increases in circulating levels of counterregulatory:
- counterregulatory elevated b/c:
- hepatic glycogenolysis and gluconeogenesis stimulated = diabetogenic hormones increase:
Pathogenesis of HHS is similar to DKA, except HHS is believed that small amounts of insulin and hepatic glucagon resistance inhibit:
insulin
glucagon, epinephrine, cortisol, and growth hormone concurrent disease
-protein catabolism, which in turn impairs insulin activity in muscle and provides amino acids for hepatic gluconeogenesis
lipolysis, thereby preventing ketosis and instead promoting HHSp
Hyperglycemia promotes_____ diuresis
and _____ diuresis increases magnitude of:
vicious circle of progressive diuresis, dehydration, and hyperosmolality
Neurologic signs develop secondary:
osmotic
hyperglycemia
cerebral dehydration
progressive dehydration, hypovolemia, and ultimately a reduction in____
severe hyperglycemia can ONLY occur in the presence of __
because:
GFR
reduced GFR
because no maximum rate of glucose loss via the kidney
ALL glucose that enters kidney in excess of the renal threshold will be excreted in the urine
______correlation exists between GFR and serum glucose in diabetic humans
inverse
Concurrent disease
initiating the hormonal changes associated with HHS:
predispose diseases include:
panc and HHS:
renal failure congestive heart failure (CHF) infection neoplasia endocrinopathies
panc and hepatic disease uncommon in cats with HHS
pancreatitis more common in dogs, 1/3 canine HHS
Dx vet.:
Dx human:
humans with HHS may have small quantities of:
Dogs with HHS have been classified as being ketotic or nonketotic at the time of the hyperosmolar event
Glucose concentrations can reach:
index of suspicion bc VBG will not read
600 mg/dl, absence of urine ketones,>350 mOsm/
600 mg/dl, arterial pH >7.3 ,>HCO3 15 mmol/L, >320 mOsm/kg, AG <12 mmol/
quantities of urine and serum ketones, measured by the nitroprusside method. Dogs with HHS have been classified as being ketotic or nonketotic at the time of the hyperosmolar event.
1600 mg/d
effective osmolality:
Na units
Gluc units
2(Na) + (Gluc/18)
mg/dl
mEq/L
VBG to assess degree of acidemia
Is it possible to differentiate HHS from DKA in cats based on the degree of metabolic acidosis?
Dogs, low pH and HHS has been associated with:
No
poorer outcome
HHS, metabolic acidosis is caused by
uremic acids and lactic acid
NOT ketones
Sodium is measured in _____
glucose is measured in _____
This effect is nonlinear, however; mild hyperglycemia leads to smaller changes in plasma sodium concentration than more severe hyperglycemia
mEq/L
mg/dl
Treatment 1. 2. 3. 4.
- replacing the fluid deficit, slowly
- reducing serum glucose and Na levels slow
- electrolyte abnormalities,
- treating concurrent disease
not to lower the serum:
glucose or sodium too rapidly
In humans, fluid losses HHS are ___X DKA patients
vascular volume is anticipated to decrease when water moves to the interstitium and intracellular space as intravascular glucose and osmolality decline =
first goal of therapy is to replace vascular volume in those patients with signs of hypovolemia or hypovolemic
shock:
On its own, fluid therapy will start to reduce blood glucose levels via:
2X
insufficient fluid resuscitation can contribute to cardiovascular collapse and death
initial 20 ml/kg (cat) to 30 ml/kg (dog) bolus
dilution
increasing GFR
subsequent urinary glucose excretion
How does isotonic saline (0.9% saline) preventing a rapid shift in osmolality?/why can you bolus?:
it both addresses the fluid deficits
and replaces glucose w. Na+ in extracellular space
preventing osmolality shifts
dehydration deficits should be replaced more slowly with Na closer to current .:. seperate IV
Correct hypernatremia with free water formula:
no more than:
but first must corr. Na:
may be necessary to switch back to isotonic saline if the sodium is dropping to quickly or if there are problems maintaining vascular volume which should be anticipated why?:
In humans the fluid deficit is assumed:
24 hrs
Free water deficit: 0.6 x Kg x (currNa - norm Na/normNa)
1 mEq/L/hr
severe hypernatremia may be masked by a hyperglycemia-induced pseudohyponatremia
hyperglycemia is corrected and water moves out of the vascular space (osmoltic pull intracell. now)
12% to 15% of body weight
insulin therapy is not as critical for reversal of HHS because much of the syndrome can be improved just by:
ketotic HHS patient, insulin may be needed somewhat sooner to:
insulin therapy should be instituted only after several hours of fluid therapy and only if:
improving GFR
reverse ketogenesis
potassium, magnesium, and phosphorus corrected
HHS when is time for insulin?:
glucose concentrations are no longer adequately declining <50 mg/dl/hr
goal is to decrease the glucose levels by no more than:
50 to 75 mg/dl/hr
or else decrease dose by 25% to 50%
Insulin protocol is slower/lower than DKA:
__U/kg into 250 NaCl
Dilute 1 U/kg of regular insulin in 250 ml 0.9% NaCl. Start this solution at 10 ml/hr (then same chart)
Monitoring 8):
- Serial neurologic
- BG <50-75mg/dl/hr
- Na <1mEq/L/hr
- hydration - expect osmotic shift and hypovolemia
- PCV/TP, kg, UOP, USG
- ELECTROLYTES
- EKG signs-of-life monitor
- ketones
Px: humans, the mortality rate children dogs cats
15% to 17%
72%
dogs better prognosis (62% discharged from hospital)
cats poor (12% long-term survival)
