Acute Complications of Chapter 67
Jan 21, 2016
Acute Complications of Diabetes Mellitus
Acute Complicationsof
Chapter 67 OverviewIn the U.S., DM leading cause of new cases of:BlindnessEnd-stage renal disease requiring dialysis or transplantationFoot or leg amputationsGlycemic (blood glucose) control reduces complications of DMTreatment of hyperlipidemia and hypertension essential to prevent complications
PathophysiologyChronic hyperglycemia (main feature for all diabetics)Problems with insulin secretionProblems with insulin actionCombination of both
Disease is classified by underlying problem causing lack of insulin
PathophysiologyPancreasIslets of langerhansAlpha cells produce glucagonBeta cells produce insulinInsulinAllows glucose in the blood to move into cells to make energyIn the liver, promotes production and storage of glycogen and inhibits glycogen breakdownIncreases protein and lipid synthesis in the liverPromotes protein and glycogen synthesis in the musclePromotes triglyceride storage in fat cells
Insulin is a hormone secreted by the pancreas in response to increased glucose levels in the blood. Glucose HomeostasisGlucose is main fuel for the CNS
Brain cannot store glucose
Combined action of insulin and counterregulatory hormones maintain range of 68 to 105 mg/dL to support brain function
With Falling Glucose Levels.Insulin secretion stopsGlucagon released from pancreas and causes the liver to convert glycogen to glucose: glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (conversion of amino acids into glucose.)When liver glucose is unavailable, lipolysis (breakdown of fat) and proteolysis (breakdown of proteins) provide fuel
Other counterregulatory hormones that increase blood glucose levels:EpinephrineNorepinephrineGrowth hormoneCortisolBlood GlucoseAbsence of InsulinPrevents cells from using glucose for energy
Body breaks down fat and protein
HyperglycemiaGlucose builds up in the bloodFluid and electrolyte imbalance resultsSymptoms: polyuria, polydipsia, polyphagiaInsulin
PolyuriaFrequent and excessive urination
Excess glucose in the urine results in osmotic diuresis
NaCl and K are excreted in the urine
Water loss is severe > Dehydration results
Polydipsia and PolyphagiaPolydipsiaExcessive thirst resulting from dehydration caused by polyuria
PolyphagiaExcessive eating resulting from cells receiving no glucosePerson remains in starvation despite excessive eating until insulin is available
Insulin DeficiencyFat breaks down releasing free fatty acids
Conversion of fatty acids to ketone bodies provides backup energy source
Accumulation of ketones in the blood results in metabolic acidosis
Dehydration leads to hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, and hypoxiaInsulin DeficiencyExcess acids increase hydrogen ion and carbon dioxide levels in the bloodIncreases rate and depth of respiration Kussmaul respiration
Acetone is exhaled giving fruity odor to the breath
Insulin DeficiencyPotassium depletion from hyperglycemia
Hyperkalemia in acidosis from shift of K from inside cells to the blood
Can have hyperkalemia, hypokalemia, or normal K depending on hydration, severity of acidosis, and response to treatment
Type 1 DiabetesPrimary beta cell destruction leading to absolute insulin deficiencyAutoimmune processIdiopathic
Also called insulin-dependent (IDDM)Type 2 DiabetesRanges from insulin resistance with and insulin deficiency to secretory deficit with insulin resistance
Also called non-insulin dependent diabetes (NIDDM)Gestational DiabetesCarbohydrate intolerance with onset or first recognized during pregnancyRisks for mothersHigher risk for developing DM after pregnancyRisk for childNeonatal mortality, congenital malformation, and macrosomiaIncreased risk for obesity and glucose intolerance later in life
What is macrosomiaAcute Complications of DiabetesThree glucose-related emergenciesHypoglycemiaDiabetic ketoacidosis (DKA)Hyperglycemic-hyperosmolar- syndrome (HHS)
Require emergency treatment
Can be fatal if treatment is delayed or incorrect
HypoglycemiaBrain stores only a few minutes supply of glucose as glycogen
CNS function depends on it
Medical emergency!
HypoglycemiaCauses:Insulin excessInsufficient food intakeExcessive activityAlcoholPoor client education
HypoglycemiaThe first defense against falling blood glucose in non-diabetics: - Decreased insulin secretion (about 83) - Decreased glucose use - Increased glucose production
Blood glucose is raised by stimulating liver glycogen breakdown: ~ Glucagon (main counterregulatory hormone)activated about 67 mg/dL ~ Epinephrine (limits insulin secretion)
HypoglycemiaType 1 DiabetesBodys response to hypoglycemia is disruptedResponse to decreased blood glucose levelsResponse to glucagon and epinephrine
Hypoglycemic unawarenessNo warning symptoms - to take actionOccurs in 25% of diabetic clients, 50% of all clients with type 1 for 30 years or longer
HypoglycemiaNeuroglycopenic symptomsBrain glucose gradually declines to a low level
Neurologic symptomsAutonomic nervous system activity triggered by a rapid decline in blood sugar
Neuroglycopenic Signs and SymptomsWarmth Weakness/fatigueDifficulty thinkingConfusionBehavior changesEmotional labilitySeizuresLoss of consciousnessBrain damageDeath
GradualNeurogenic Signs and SymptomsAdrenergicShaky/tremulousHeart poundingNervous/anxious
CholinergicSweatyHungryTinglingRapidHypoglycemia occurs in Diabetics:
When there is an excess of insulinWhen the dose of insulin or oral agent is : ~ill timed ~excessive ~wrong type of agentWhen meals are missedWhen food is intake is not increased after exercise,When there is alcohol intake without food
Hypoglycemic ManagementMonitor blood glucose levels Before giving antidiabetic drugsBefore mealsBefore bedtimeWhen symptomatic
Hypoglycemia ManagementDiet therapy ~Follow carbohydrate replacement per facility standing orders or protocol: Example:
~If BG 30 ml/hr
Bicarbonate used for severe acidosis (pH less than 7.0)
Serum Sodium bicarbonate level less than 5 mEq/LAcidosis ManagementCorrected with fluid replacement and insulin therapy
Focus on determining cause of DKA after acid-base disturbances are correctedUsually infection
Sick Day RulesMonitor blood glucose at least every 4 hoursTest urine for ketones when blood glucose > 300Continue to take insulin or oral antidiabeticsDrink 8 to 12 ounces of sugar free liquids every hour that you are awakeContinue to eat mealsConsume tolerated meals including liquid carbs
Sick Day Rules (cont.)Call PCP for:Persistent N/VModerate or large ketonesElevated glucose after two supplemental doses of insulinHigh temp or increasing feverTreat symptoms as directedGet plenty of rest
Hyperglycemic-Hyperosmolar StateFormerly called HHNS, now HHSCan occur in DM I and DM II but more common in DM IIMorbidity rate is very high up to 15%Mortality usually due to shock, coma, ATN, and vascular thrombosisWhat is HHS?Hyperosmolar state caused by hyperglycemia and dehydration Gradual onset vrs. rapid onset in DKAAbsence of ketones and much higher blood glucose levels and blood osmolarityHHS is the end result of a sustained osmotic diuresis, as glucose impairs the concentrating ability of the kidney
See chart p:1455HHS EtiologyCause is usually: infection sepsis MI stroke and some drugs
HHSElderly are very prone because they tend to be dehydrated, have lower body water content, as well as thirst perception changes and poor urine-concentrating abilities
CNS changes from confusion to coma, and seizures are seen
TreatmentFluid therapyGoal is: rehydration in 36-72 hours
Electrolyte issues same as with DKA
Acidosis is not present
Treatment of HHSFluid therapy Objective of therapy is to increase blood volume1L/hr until BP and urine output are adequateThen decrease to 100-200 ml/hrASSESS for abrupt changes in mental status, coma, pupillary changes, or seizuresA slow but steady improvement in CNS function is best evidence that fluid management is satisfactory
HHS TreatmentInsulin therapyIV insulin drip- bolus +0.15 u/kg/hr a. Goal-reduction of blood glucose levels by 50- 70 mg/dL an hour is the goalK+ may drop quickly when insulin therapy started. Begin supplement when urine output adequate