Hyperglycemic Crisis Flashcards
What are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)?
DKA and HHS are serious and potentially life-threatening hyperglycemic crises in patients with diabetes
DKA is far more common in children, adolescents and young adults with type 1 diabetes mellitus
HHS is typically diagnosed in an older population with type 2 diabetes mellitus
What are the precipitating factors for DKA and HHS?
DKA - result of insulin deficiency and is usually precipitated by infection or other stress, insufficient insulin therapy, poor access to health care, or newly diagnosed diabetes
- infections and other serious illnesses increase secretion of counter-regulatory hormones (epinephrine, glucagon, growth hormone, and cortisol), which increase insulin requirements because of their anti-insulin effects
HHS - usually precipitated by infections (urinary tract infection or pneumonia) or cardiovascular events (myocardial infarction or stroke)
- increase in counter-regulatory hormones plays a role in causing hyperglycemia
- occasionally a patient is not aware of having type 2 diabetes (does not recognize symptoms such as polyuria and polydipsia) and the dx of diabetes is first established when pt presents with HHS
What is the pathophysiology of DKA and HHS?
Insulin is deficient in both DKA and HHS; both conditions have increased hepatic gluconeogenesis and glycogenolysis; both conditions have decreased glucose uptake by muscle and adipose tissue
degree of insulin deficiency is more severe in patients with DKA, permitting unrestrained lipolysis
in patients with HHS, there is sufficient insulin to exert antilipolytic effects
- higher concentrations of insulin are required to promote glucose uptake by insulin-sensitive tissues such as muscle and adipose tissue
different effect on lipolysis explains the difference in ketones between DKA and HHS
HHS is not associated with ketoacidosis
What are both DKA and HHS associated with?
Hyperglycemia, fluid losses, and increased serum osmolality
hyperglycemica, fluid loss and serum osmolality are much greater in patients with HHS
in both conditions, dehydration is associated with typical physical findings of dry mucous membranes, poor skin turgor (skin ‘tenting’), orthostatic hypotension, tachycardia
How would a patient present with DKA?
May have experienced polyuria, polydipsia, and weight loss for several days before rapid metabolic decompensation into DKA (sometimes within 24hrs)
often develop nausea, vomiting, and abdominal pain
Kussmaul breathing may be mistaken for respiratory distress due to asthma or other respiratory disorder
What is the criteria for diagnosing DKA?
Plasma glucose >250mg/dL
Serum bicarbonate <15mEq/L
Arterial pH < 7.3 (or venous pH <7.25)
Ketones positive at least +3 in undiluted serum
In addition, patietns with DKA usually have: arterial PaCO2 <20-30mmHg, increased anion gap, and increased serum osmolality
How would a patient with HHS present?
Usually older than 50 with type 2 diabetes
may have additional co-morbidities
HHS develops over a period of days to weeks, so the process is more gradual than DKA
may have existing type 2 diabetes or type 2 diabetes that has not been diagnosed with typical hyperglycemic symptoms such as polyuria and polydipsia that are not recognized
patients may not consume sufficient water because their thirst mechanism is impaired or because water is not easily accessible
usually do not have abdominal pain
typically present with changes in mental status, and often these have progressed to stupor or coma
no Kussmaul breathing but patient may have cough and respiratory distress if precipitating illness was pneumonia
What is the criteria for diagnosis of HHS?
Plasma glucose >600mg/dL
Arterioal pH >7.3 or venous pH >7.25
Serum bicarbonate >18mEq/L
Small ketonuria and negative or small ketonemia
Serum osmolality >320mOsm/kg plasma water
Altered consciousness
Compare the diagnostic criteria and characteristics of patients with DKA and HHS.
What would your initial laboratory assessment be?
Plasma glucose
Blood urea nitrogen (BUN)
serum creatinine
electrolytes (Na+, K+, Cl-; HCO3-) w/ calc of anion gap
Osmolality
Serum ketones*
Urine ketones*
*the total amt of ketone bodies present is greatly underestimated when using the sodium nitroprusside reagent (Acetest tablets or Ketostix), because the most abundant ketoacid (beta-hydroxybutyrate) is not measured; if avail, direct measurement of BHB is preferable
Arterial blood gas
How might you investigate for some precipitating factors?
CBC with differential
UTI: urinalysis and urine culture
Pneumonia: chest xray and sputum cultures
Septicemia: blood cultures
Myocardial Infarction: electrocardiogram
Hyperthyroidism: thyroid stimulating hormone (TSH)
What other acid-base disturbances might be on your diagnosis differential - alcoholic ketoacidosis (AKA)
Chronic alcoholism is sometimes associated with a form of ketoacidosis
in AKA, the history usually includes poor nutrition or short-term starvation with some degree of volume depletion
Ketonemia (primarily BHB) in AKA is greater than would be expected following an overnight fast, but usually less than with DKA
lesser degree of volume depletion, so BUN to creatinine ratio is not as high in AKA as it is in DKA
with better renal perfusion, patients with AKA are able to excrete more ketones in the urine - urine ketones are high, but serum ketones in AKA are usually lower than in DKA, so anion gap is usually smaller in AKA
glucose conc in AKA may vary, but it is usually not high enough to cause prolonged osmotic diuresis
Not assoc with severe depletion of sodium, water, and other electrolytes (differs from DKA)
What other acid-base disturbances might be on your diagnosis differential - lactic ketoacidosis
may present together with DKA, causing mixed acid-base disturbance resulting from an accumulation of lactate
the vast majority of cases of lactic acidosis are caused by cardiogenic or hypovolemic shock, severe heart failure, sepsis, or severe trauma
Type A lactic acidosis (most common): includes disorders associated with tissue hypoxemia (severe heart failure, cardiogenic shock, hypovolemic shock, sepsis, severe trauma, severe anemia, severe hypoxemia, carbon monoxide poisoning, or disorders causing increased oxygen requirements - seizures, vigorous exercise)
Type B lactic acidosis: includes a variety of other condiitons: disorders that may stimulate aerobic glycolysis (via excessive epinephrine stimulation of beta2 adrenergic receptors or metabolic activity of certain cancers), drugs that interfere with oxidative phosphorylation (toxic alcohols, cyanide, propofol, nucleoside reverse-transcriptase inhibitors, metformin, salicylates), or decreased lactate clearance (fulminant acute liver failure)
dx of lactic acidosis is confirmed by measurement of blood lactate concentration
What are some useful formulas?
Anion gap = [Na+] - [Cl-] - [HCO3-]
- as patients with DKA or HHS become gradually more dehydrated, this will be reflected as an increase in the plasma osmolality
Osmolality = 2(Na+K) + (BUN/2.8) + (glucose/18)
Sodium concentration correction in hyperglycemic states:
(glucose-100)/100 * 1.6 + plasma sodium concentration = actual sodium concentration
What are the main treatment options for DKA and HHS - rehydration?
As deydration worsens and BP decreases, kidney perfusion is decreased, which limits glomerular filtration
1 liter 0.9% NaCl within the first hour for adults with either DKA or HHS
If patients are in hypovolemic shock, more rapid administration of normal saline is indicated
approximately 5L of fluid should be admin during first 12hrs for adults
For children, fluid replacement adj based on severity
Cerebral edema may develop during treatment of DKA, especially in children
