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