DKA & HHS Flashcards
what is DKA caused by?
caused by absence or a markedly inadequate amount of insulin that results in disorders in the metabolism of carbs, proteins, and fats
what are 3 main clinical features of DKA
- hyperglycemia
- dehydration & electrolyte loss
- acidosis
describe short patho of DKA
- no insulin so the amount of glucose that goes into cells is reduced
- because there’s a decrease in glucose, the liver will increase glucose production
- then in order to rid body of excess glucose, kidneys will excrete it (with water and electrolytes)
- osmotic diuresis (polyuria) leads to dehydration and electrolyte loss
- lipolysis converts into free fatty acids and glycerol
- free fatty acids are converted into ketone bodies by the liver
- insulin would normally prevent ketones from occurring but because people with DKA have no insulin
are ketones acids or bases?
ketones are acids! with accumulation of acids it leads to metabolic acidosis
what are 3 main causes of DKA
- decreased or missed dose of insulin
- Illness or infection
- undiagonosed/untreated DM
which hormones promote glucose production?
glucagon, epinephrine, norepinephrine, cortisol and growth hormone
how do the hormones interfere with glucose utilization?
normally hormones enhance break down of triglycerides into free fatty acids and gluconeogenesis (leading to increased glucose and ketones)
list mnfts of DKA
- hyperglycemia –> polyuria/polydipsia
- orthostatic hypotension from intravascular volume depletion
- ketosis and acidosis (GI symptoms will present)
- kussmaul respirations
what BG level range could you find with someone with DKA?
16.6-44.4mmol/L
what lab value shows evidence of ketoacidosis?
low serum bicarbonate (0-15mmol/L) and low pH (6.8-7.3)
would you have low or high PCO2 and why?
you would have low PCO2 (respiratory compensation) which are kussmaul respirations to compensate for metabolic acidosis (short, deeper breathing), blowing off more CO2
in addition to treating hyperglycemia, what is management aimed at?
correcting dehydration, electrolyte loss, and acidosis
why is rehydration important?
- maintains tissue perfusion
- fluid enhancement increases glucose secretion by kidneys
- monitor for FVE in elderly and those with renal/HF
what is the main electrolyte of concern with DKA?
potassium
what are factors of DKA that reduce serum K+ concentration?
- rehydration (leads to increased plasma volume with subsequent decreases in K and increased excretion)
- insulin admin which enhances movement of K from the ECF into cells
why must potassium be infused even if levels are normal?
because extracellular potassium drops during DKA
when would replacement of K be held?
only if hyperkalemia is present or if pt is not urinating
ketones accumulate in body as a result of what?
result of fat breakdown
how does insulin help with acidosis?
acidosis is reversed with insulin which inhibits fat breakdown, which stops acid buildup
when is the cue to stop IV insulin?
when the ketosis is resolved (you know this by having a normal anion gap)
at what BG level should IV dextrose be administered and why?
once its at 14mmol/L to avoid hypoglycemia
why is it crucial to flush the insulin solution through the entire IV infusion set and discard first 50ml?
because insulin molecules adhere to inner surface of IV infusion sets and can cause the initial fluid to cause a decreased concentration of insulin
what is monitored before potassium is administered?
urine output is monitored to prevent hyperkalemia
as DKA resolves and K+ replacement is decreased, what does the nurse ensure?
- that there are no signs of hyperkalemia in ECG
- lab values of K are normal or low
- patient is urinating
what is HHS?
a serious condition in which hyperosmolarity and hyperglycemia predominate with alterations of the sensorium (sense of awareness)
does ketosis occur in both DKA and HHS?
usually only in DKA
what occurs with HHS? (quick patho)
lack of effective insulin (insulin resistance) leads to patient persistent hyperglycemia that causes osmotic diuresis (resulting in losses of water and electrolytes)
what is the typical onset of people with HHS
50-70 years old with no known Hx of DM or with mild T2DM
what precipitating events can lead to HHS?
pneumonia, stroke, meds that exacerbate hyperglycemia or dialysis
what is the Hx of someone with HHS ?
days to weeks of polyuria with adequate fluid intake
what is the difference between DKA and HHS?
DKA= ketosis and acidosis HHS= NO ketosis and acidosis d/t difference in insulin levels
is there insulin present in DKA
insulin is NOT present. Because of this, it promotes breakdown of fats which lead to production of ketones
is there insulin present with HHS
insulin is present in small amounts and is too low to prevent hyperglycemia but high enough to prevent fat breakdown
Mnfts of HHS
- hypotension
- profound dehydration (dry mm, poor skin turgor)
- tachy
- variable neurologic signs
- bicarb level normal, BUN/creatinine elevated
is onset slower or faster in HHS?
onset is SLOWER
what are secondary signs of cerebral dysfunction for people with HHS
mental status changes, focal neurologic deficits, and hallucinations
what mnft accompanies dehydration with HHS
postural hypotension
what is the medical mgmt of HHS
- fluid replacement (0.9% or 0.45%)
- correction of electrolyte imbalances
- insulin admin (not as much needed as for DKA b/c not reversing acidosis)
- close monitoring of volume and electrolyte status
what is nursing mgmt of HHS
- close monitoring of vitals, fluid status and lab values
- strategies to prevent injury r/t changes in pt sensorium secondary to HHNS
- fluid status and urine output closely monitored
what are the hallmarks of HHS
- profound dehydration
- marked hyperglycemia-variable degrees of neurological impairment
- mild or no ketosis
what are mortality predictors of HHS
- age
- degree of dehydration
- hemodynamic instability (hypotension, absence of reflect tachy)
- degree of consciousness
- infection and Hx of cancer
describe the patho of HHS
- elevated levels of counterregulatory hormones initiate HHS by stimulating hepatic glucose production through glycogenolysis and gluconeogenesis
- this leads to hyperglycemia, intracellular water depletion and subsequent osmotic diuresis
- glycosuria causes greater loss of water leading to hyperosmolarity and dehydration
why are elderly with T2DM at increased risk for HHS
because they often take dehydrating meds (diuretics)
risk factors for HHS in children
- morbid obesity
- long term steroid use
- gastroenteritis
- black rate
- acanthosis nigricans
- fam HX of DM
what levels are almost always elevated in HHS
creatinine, BUN and hct
what is the four piece Tx approach to HHS
- vigorous IV rehydration
- electrolyte management
- IV insulin
- diagnosis and management of precipitating and coexisting problems
what is the first and most important step in treating HHS?
aggressively replacing fluids
why can total body potassium depletion be unrecognized in someone with HHS?
because initial K levels may be normal or high
what causes GI symptoms in DKA? (anorexia, N+V, pain)
ketosis and acidosis
what is the fruity breath of DKA r/t?
due to the elevated ketone bodies and acidosis
how do you prevent DKA
OT more often (q1-4hrs), diet teaching, rehydration
what’s important about rehydration in DKA
- maintain tissue perfusion
- increase low BP
- enhances kidney excretion (excrete glucose and K/Na)
what is the onset of DKA
rapid (<24hrs)
what is the onset of HHS?
slower (over several days)
what are the BG levels of someone with DKA
usually >13.9
what are the BG levels of someone with HHS
usually >33.3
are serum and urine ketones present or absent in both?
present in DKA and absent in HHS
are serum bicarb levels present in DKA and HHS
decreased in DKA and normal in HHS
are BUN and creatinine present in DKA and HHS
elevated in both
is the mortality rate higher in DKA and HHS
much higher in HHS (10-40% rate in HHS)
what is gluconeogenesis
makings glucose from proteins and fats
what is the precipitating event of HHS
physiologic stress (infection, surgery, CVA, MI)
what is the precipitating event of DKA?
omission of insulin; physiologic stress (infection, surgery, CVA, MI)
what is the onset of HHS?
50-70 years old
what is the arterial ph for DKA and HHS?
DKA is <7.3 and HHS is normal
what is the clinical presentation of HHS?
- hypotension
- dry mucous membranes, poor skin turgor)
- variable LOC, altered sensorium which can lead to seizures
what system is the most affected by blood sugar levels
the neuro system
how long do neurological systems take to resolve?
about 3-5 days
