exam 8 L. 9: DKA Flashcards Preview

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Flashcards in exam 8 L. 9: DKA Deck (48):


-Stable, uncomplicated canine
-stable, uncomplicated feline
-stable, ketotic
-diabetic ketoacidotic


Stable uncomplicated canine

1) history: excessive drinking and urination, how is hungry but losing weight
2) physical exam:
-may be relatively normal
-**cataracts common**: lens freely permeable to glucose, metabolized to sorbitol via the enzyme aldose reductase, potent hydrophilic agents, lens fibers swell and rupture


Minimum database


-mild elevation liver enzymes


urine culture/susceptibility as part of minimum database!
-24% of diabetic dogs had bacterial UTIs with no evidence of pyuria
-glucose may be substrate for bacteria
-immune system compromise with diabetic state



1) dogs are insulin-dependent
-little to no functional beta cells
-absolute insulin deficiency
2) we must provide insulin



Canine and porcine insulin have identical amino acid sequences!

Also, it is uncommon for antibody to develop versus insulin and cause issues, although it did happen versus cattle insulin


Neutral protamine Hagedorn (NPH) insulin

1) crystalline suspension with protamine and zinc
2) intermediate acting
3) good 1st choice for dogs (not good choice for cats)


Lente insulin

1) more zinc added to delay absorption
2) mixture of short acting and long-acting insulin
3) Vetsulin
-porcine derived Lente insulin
-FDA approved for use in dogs and cats


Protamine zinc insulin (PZI)

1) more protamine than NPH results in longer duration
2) ProZinc
-recombinant human insulin
-FDA approved for use in cats

*Cats tend to need a longer acting insulin while dogs a shorter acting insulin*


Long-acting analogs: insulin glargine

1) in solution at acidic pH, precipitates at normal pH in SC tissue
-slow release of insulin from SC microprecipitates


Long-acting analogs: insulin detemir

1) similar to glargine
2) reversible binding between albumin and insulin
-gradual release of bound fraction from albumin


Goals of therapy: diabetic canine

1) eliminate clinical signs of diabetes mellitus
- PU/PD; polyphagia; weight loss
2) reduce risk of complications
-ketoacidosis, infection, neuropathy (cataracts don't seem to be avoidable, eventually they occur)


Initiate therapy-stable canine

1) initiate insulin (NPH or Lente)
-Ensure animals eat prior to insulin*
-0.25-0.5 U/kg subcutaneously every 12 hours*
2) treat any complicating conditions
3) recheck clinical signs, blood glucose curve and urine in about 1-2 weeks


Feline diabetic: differences from canine

1) majority have type II diabetes**
2) obesity is an important risk factor
-insulin resistance
3) occurs concurrently with other endocrinopathies
-Cushing's, acromegaly


Feline diabetic: differences from canine

1) stress hyperglycemia more problematic
-affects diagnosis and monitoring
2) different complications
-cataracts versus diabetic neuropathy
3) relative importance of dietary management
-higher in cats


Goals of therapy: diabetic feline

1) eliminate clinical signs of diabetes mellitus
-100 < BG >250 mg/dl*
2) reduce risk of complications
-ketoacidosis, infection, neuropathy
3) promote diabetic remission, if possible!


Initiate therapy-stable feline

1) initiate insulin therapy
-cornerstone of management of DM and cats-optimize chance of remission
-PZI, Lente, or glargine appropriate 1st choices
-1 U/cat SC BID
2) implement dietary management


Oral hypoglycemic drugs

1) Glipizide
-stimulates insulin secretion
2) treatment is successful in 1/3 of cats
3)**only use in situations in which owners are unwilling or unable to give insulin


Nutritional management

1) cats are true carnivores and best adapted to a diet composed mainly protein and fat
2) high protein, low carbohydrate diets are ideal
-improve clinical control, increased rate of remission
3) weight management
-reversal of obesity induced insulin resistance


Diabetic remission

1) maintains normal glycemia without insulin
2) usually occurs within the 1st 3 months of treatment
3) remission DOES NOT equal cure
-new sources of insulin resistance can precipitate relapse (i.e. illness)
-lifelong weight and dietary management recommended



1) ketone bodies derived from fatty acid oxidation
2) in states of cellular glucose deficiency, ketone bodies can be used as energy source
3) As ketone bodies increase in vascular space, exceed renal threshold = osmotic diuresis=>


Urine ketones

1) urine strips measure: acetoacetic acid, acetone
2) strips do NOT measure beta-hydroxybutyrate
3) ketosis indicates more prolonged cellular "starvation"


Stable ketotic diabetic

1) very similar to stable diabetic
2) urine ketones present
3) clinically: still leading, still drinking, maintain hydration, no vomiting
4) if suspect ketosis with negative urine ketones, check the blood
5) most can be treated as stable diabetic
-watch more closely


Diabetic ketoacidosis

1) ketosis plus metabolic acidosis = diabetic ketoacidosis
2) these animals are SICK
3) warrant immediate care = hospitalization, emergency therapy**
4) consider referral to 24 Hour Care Ctr.


Diabetic Ketoacidosis: why are they so sick?

1) dehydrated:
-osmotic diuresis: glucose, ketones
-vomiting and diarrhea: acidosis
-volume depleted, GFR falls
-worsens prerenal azotemia
2) acidotic
-hydrogen ions produced to buffer bicarbonate, overwhelms buffering system (renal)
3) life-threatening if not corrected**


Precipitating causes of DKA

1) concurrent disease:
-pancreatitis, UTI/pyelonephritis, HAC, pneumonia, neoplasia, renal/hepatic disease
2) diestrus
3) insulin withdrawal
4) fasting/dehydration

**diabetes alone may eventually lead to DKA**


signalment and history

1) middle to older aged dogs and cats, no sex predilection
2) historical signs
- PU/PD/PP; weight loss
3) acute signs
-anorexia, vomiting/diarrhea, dehydration, weakness/depression


Physical exam

1) dehydration (may also have hypovolemia-hypothermia, weak pulses etc.)
2) muscle wasting (especially uncontrolled diabetes)
3) variable BCS
4) poor hair coat
5) weakness/depression
6) cataracts (dogs)
7) peripheral neuropathy (cats)



1) hyperglycemia
2) glucosuria
3) ketonuria
4) acidosis
5) sick
6) may be initial diagnosis or may be diagnosed and previously stable diabetic


Treatment goals

1) restore intravascular volume
2) correct dehydration
3) correct electrolyte disturbances
4) correct acid-base imbalance
5) reduced blood glucose concentration
6) eliminate ketones
7) address underlying diseases



Fluid therapy in DKA

1) method of administration: IV catheter
2) rate of replacement
-maintenance + % dehydration + ongoing losses
-typically correct dehydration over 6-24 hours
-may give initial fraction of replacement volume as bolus, depending on patient status


Fluid therapy DKA

1) fluid choices
-buffered crystalloid solution (plasmalyte, LRS)
-after initial stabilization: may also need maintenance solutions depending on individual patient needs
2) fluid additives
-dextrose (0-5%, depending on blood glucose)
-electrolytes (DO NOT BOLUS!)


Potassium supplementation

1) initial serum potassium variable
-insulin promotes intracellular potassium shift
2) prepare for potassium to drop following insulin therapy**
3) high rates of potassium supplementation are common
-monitor frequently!
-Dose potassium on a body weight basis (not a per liter basis)


Phosphate supplementation

1) phosphorus follows potassium
-both are driven intracellularly with insulin administration
2) serum phosphorus <1.5 mg/dl clinically significant


Insulin therapy

1) regular insulin
-rapid onset, potent, short acting
2) IV protocol
-insulin added to 0.9% NaCl administered as CRI
-per 250 mL saline: 2.2 U/kg (dogs), 1.1 U/kg (cats)


Helpful hints

1) place a central line or sampling catheter
-frequent glucose and electrolyte monitoring
2) use burette for frequent changes in fluid composition
3) feeding assistance may be necessary
4)**DKA may be brought on by concurrent illness, therefore LOOK FOR ONE**


Once through DKA crisis

1) change to longer acting insulin (if newly diagnosed, start at the starting dose)
-patient is eating and drinking
-vomiting is resolved
-acidosis is resolved
-ketosis is resolved


To summarize

DKA is a serious complication of diabetes mellitus, usually brought on by one or more concurrent disease

prognosis can be good if:
1) precipitating condition can be treated
2) aggressive treatment is implemented (24-hour intensive care)


To summarize #2

1) remember your priorities when treating DKA!
-Begin addressing hypovolemia and dehydration 1st
-pay attention to electrolytes
-begin cautious insulin therapy after addressing the above issues


Diabetic monitoring: blood glucose curve

1) procedure: blood glucose recorded every 2 hours after insulin administration
-increased hourly if blood glucose is low in-ideally sample for 12 hours
2) mimic home environment as much as possible (minimize stress)
-feed/give insulin at home*


Blood glucose curve

1) pre-insulin blood glucose (if possible)
2) Nadir (lowest blood glucose level in that 12 hour period)
3) duration of insulin effect
4) highest BG
5) average BG

**MUST interpret curve in light of other clinical parameters before making decisions regarding insulin administration


Glucose curve: indications

1) 1-2 weeks after any change in insulin dose or formulation
2) any patient with poor control of clinical signs
3) routine monitoring in any patient every 3-6 months


Glucose curve: pitfalls

1) day-to-day variability
-insulin recommendations based on blood glucose curve alone differed in 50% of cases!!
2) effect of stress hyperglycemia
3) expense
4) potential to miss hypoglycemia
-note: you are still more likely to miss hypoglycemia with other modalities (fructosamine, glucose spot-checks)


Diabetic monitoring: fructosamine

1) fructosamine is the product of an irreversible reaction between glucose and the amino group of plasma proteins
- **Reflects average blood glucose for past approximately 2 weeks**
-use: eliminates confounding effect of stress hyperglycemia
2) limitations:
-can be normal in recent-onset DM
-reduced in hypoproteinemia and hyperthyroidism!


Poor owner compliance

**Most common cause of persistence of diabetic clinical signs**
1) may mimic insulin resistance
2) diagnose by history and observe the technique of the owner
-blood glucose curve after insulin administered by clinician


Insulin under-dose

1) anticipate increasing dose (0.25 U/kg BID)
2) MOST diabetics will have glycemic control with 1 U/kg insulin BID or lower
- doses higher than 1.5 U/kg BID ==> suspect insulin resistance or another problem


Insulin resistance

1) concurrent disease process impairs insulin activity
-**action of diabetogenic hormones**
2) common diseases: obesity, infection, acromegaly (cats), hyperadrenocortiscism (dogs), pancreatitis


Insulin induced hypoglycemia

1) Somogyi Effect
2) etiology: hypoglycemia (brought on by insulin overdose) ==> stimulation of diabetogenic hormones ==> increases BG levels ==> rebound hyperglycemia

3) can induce insulin resistance for up to 72 hours
4) clinical signs of hyperglycemia dominate
- glucouria is common

**The body is good at protecting the brain against hypoglycemia


Inadequate insulin duration

1) rapid metabolism of insulin
-duration <8-10 hours
- Nadir occurs less than 8 hours after injection with hyperglycemia (>300 mg/dl) recurring before next insulin dose