Endocrine Emergencies Flashcards
What are the 2 factors that must happen in order for diabetic ketoacidosis to occur?
1) Insulin deficiency (relative or absolute)
2) Circulation of diabetogenic hormones, most notably glucagon, will:
- Accentuate insulin deficiency by promoting insulin resistance
- Stimulate lipolysis, leading to ketogenesis
- Stimulate hepatic gluconeogenesis, which worsens hyperglycemia
Other diabetogenic hormones include: cortisol, catecholamines and growth hormone
What is the pathogenesis of Diabetic Ketoacidosis?
- Insulin resistance + Insulin deficiency + increased circulating concentrations of diabetogenic hormones
- FFA mobilization from triglycerides stored in adipose tissue
- Increased lipolysis at the liver, thus promoting ketogenesis
- Ketones accumulate in the body, the buffering system becomes overwhelmed and metabolic acidosis occurs
- Ketones accumulate and the renal threshold for resorption is surpassed, leading to spillover into the urine –> osmotic diuresis
- Overall result in excess water loss, electrolyte loss (Na, K, Ca, Mg), dehydration, hypovolemia, poor perfusion, prerenal azotemia and hyperosmolality
What are the clinical signs associated with Diabetic Ketoacidosis?
- Dehydration
- Vomiting
- Anorexia
- lethargy
- tachypnea or slow deep breathing is severe metabolic acidosis
- tachycardia
- abdominal pain: often pancreatitis is happening concurrently
- PU/PD
- hypovolemic shock
+/- acetone breath
There is often a Triggering Event that causes the shift from uncomplicated DM to DKA, what are the most common causes (6)?
What are some less common causes?
Most commonly: Pancreatitis, UTI, Chronic renal disease, Hyperadrenocorticism, Diestrus, or administration of corticosteroids
Less commonly:
- Any significant bacterial infection: Pneumonia, Pyometra, Pyoderma, Prostatitis
- Hepatic failure
- Neoplasia
- Hyperthyroidism (cat)
- Hypothyroidism (dog)
What is the Hyperosmolar Hyperglycemic State?
The hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, without significant ketoacidosis.
It most often occurs in type 2 diabetes, often in the setting of physiologic stress
How do you know if a patient is in a Hyperosmolar Hyperglycemic State?
This syndrome is characterized by:
- Severe hyperglycemia (blood glucose concentration >600 mg/dL)
- Hyperosmolality (>350 mOsm/kg)
- Dehydration in the absence of significant ketosis
You can calculate the Osmolality:
2[Na] + BUN + Glucose
What is the pathogenesis of the Hyperosmolar Hyperglycemic State?
1) Triggering Event: chronic kidney disease, infections, cardiac failure, neoplasia, hyperthyroidism, pancreatitis, hyperadrenocorticism
2) Relative insulin deficiency leads to hyperglycemia
3) Excessive urination due to osmotic diuresis leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level
4) Ketosis is not usually seen as the presence of some functioning insulin inhibits the breakdown of FFAs
How can DKA be diagnosed?
The minimal database is required:
- PCV + TP
- Glucose
- Electrolytes
- Acid-base
- Urinalysis
- Urine culture: possible triggering event?
- cPL/fPL: possible triggering event?
- Abdominal ultrasound: possible triggering event
DM is diagnosed based on clinical signs, a persistent fasting hyperglycemia + glycosuria
The presence of Ketonuria establishes Diabetic Ketosis
The presence of Metabolic acidosis establishes the diagnosis of Diabetic Ketoacidosis
You test for ketonuria using a dipstick, however, the owner mentions the animal is on N-acetyl cysteine or Captopril, why is this important?
Both of these drugs can lead to a false positive ketonuria
N-acetyl cysteine (used for the treatment of acetaminophen toxicity, degenerative myelopathy, respiratory disease, chronic renal failure and feline immune deficiency virus (FIV))
Captopril (is an ACE inhibitor and works by relaxing blood vessels so that blood can flow more easily)
You test for ketonuria, and it comes up as positive, what should the owner be asked?
Is the animal on any drugs?
Specifically N-acetyl cysteine or Captopril, which can lead to a false positive ketonuria
You suspect an animal has DKA, you test the urine for ketones on a dipstick and it comes up as negative.
Could this be a false negative?
What could have caused this test result?
This could be a false negative
This can occur when:
- BACTERIAL METABOLISM: many animals have a concurrent UTI which can be the triggering event
- Urine sample is exposed to air for too long
- Excess Vitamin C is in the diet/ urine
- Early-onset of the disease: dipstick does not detect beta-hydroxybutyrate, which is the major ketone involved
What are the 5 goals of treatment for a dog or cat with DKA?
1) Provide adequate amounts of insulin to suppress lipolysis, ketogenesis and hepatic gluconeogenesis
2) Restore water and electrolyte losses
3) Correct acidosis
4) Identify the precipitating/ triggering event
5) Provide a CHO substrate (Dextrose) when necessary to allow for administration of insulin without causing hypoglycemia
What is the treatment protocol for patients with DKA?
1) Fluid therapy: 0.9% saline +/- KCl supplementation
2) Insulin therapy: low dose IM insulin therapy of Actrapid
3) Treat underlying disease/ triggering event
Concurrent pancreatitis = give nothing by mouth + aggressive fluid therapy
Concurrent infections = broad-spectrum, parenteral Ab’s
4) Once blood glucose concentrations reach 10-15 mmol/L (usually within 4-8 hours) we need to maintain that BG to avoid hypoglycemia and hyposomolality. Because we need to continue to suppress ketogenesis, thus administer 2.5-5% dextrose IV fluids + SC or IM insulin
Fluid Rate/ Therapy:
- Hypovolemia present = bolus
- Rate then calculated for maintenance + dehydration status + continued losses taking renal disease into account if present
What are the potential complications of correcting DKA?
- Hypoglycemia: supplement Dextrose as needed and monitor BG every 1-2 hours
- Too rapid drop in BG: only use low dose insulin therapy
- Hypokalemia: Supplement KCl according to serum [K+], or if this is not possible, take 0.9% saline and add 40mEq to make a 40mEq/L solution
- Anemia: correction of acidosis and insulin can lead to PO4 moving from the vessels to the cells and causing hypophosphatemia, this can lead to hemolytic anemia, rhabdomyolysis and impaired cerebral function. Correct with Phosphate supplementation
