Critical Care Nursing Theory: Endocrine Disorders (DKA/HHNS) 2024 PDF

Critical Care Nursing Theory Chapter 11 Endocrine Disorders DKA/HHNS Dr. Rana Al Awamleh 2024 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 1  Di...

Critical Care Nursing Theory Chapter 11 Endocrine Disorders DKA/HHNS Dr. Rana Al Awamleh 2024 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 1  Diabetes Mellitus/ Definition Diabetes mellitus refers to a group of diseases that affect how the body uses blood sugar (glucose). Glucose is an important source of energy for the cells that make up the muscles and tissues. It's also the brain's main source of fuel. DM is a metabolic disorder characterized by hyperglycemia due to an absolute or relative lack of insulin or to a cellular resistance to insulin Major classifications 1. Type 1 Diabetes 2. Type 2 Diabetes 2 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 1 ❑ Definition Metabolic condition in which the beta cells of pancreas no longer produce insulin; characterized by hyperglycemia, breakdown of body fats and protein and development of ketosis Accounts for 5 – 10 % of cases of diabetes; most often occurs in childhood or adolescence Formerly called Juvenile-onset diabetes or insulin-dependent diabetes (IDDM) 3 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 1 ❑ Pathophysiology Autoimmune reaction in which the beta cells that produce insulin are destroyed Alpha cells produce excess glucagon's causing hyperglycemia ❑ Risk Factors Genetic predisposition for increased susceptibility; Environmental triggers stimulate an autoimmune response Viral infections (mumps, rubella) Chemical toxins 4 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 1 ❑ Manifestations: 1. Process of beta cell destruction occurs slowly; hyperglycemia occurs when 80 – 90% is destroyed; often trigger stressor event (e. g. illness). 2. Hyperglycemia leads to: Polyuria (hyperglycemia acts as osmotic diuretic) Glycosuria (renal threshold for glucose: 180 mg/dL) Polydipsia (thirst from dehydration from polyuria) Polyphagia (hunger and eats more since cell cannot utilize glucose) Weight loss (body breaking down fat and protein to restore energy source Malaise and fatigue (from decrease in energy) 5 Blurred vision (swelling of lenses from osmotic effects)  Diabetes Mellitus/ Type 1 ❑ Diagnosis – Patient is symptomatic plus: Casual plasma glucose (non-fasting) is 200 mg/dl OR Fasting plasma glucose of 126 mg/dl or higher OR Two hour plasma glucose level of 200 mg/dl or greater during an oral glucose tolerance test 6 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 2 ❑ Definition: condition of fasting hyperglycemia occurring despite availability of body’s own insulin. Was known as non- insulin dependent diabetes or adult onset diabetes. ❑ Pathophysiology: Sufficient insulin production to prevent DKA; but insufficient to lower blood glucose through uptake of glucose by muscle and fat cells Cellular resistance to insulin increased by obesity, inactivity, illness, age, some medications 7 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 2 ❑ Risk Factors: 1. History of diabetes in parents or siblings 2. Obesity (especially of upper body) 3. Physical inactivity 4. Race/ethnicity: African American, Hispanic, or American Indian origin 5. Gender/Women: history of gestational diabetes, polycystic ovary syndrome, delivered baby with birth weight > 9 pounds 6. Clients with hypertension; HDL cholesterol < 35 mg/dL, and/or triglyceride level > 250 mg/dl. 8 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diabetes Mellitus/ Type 2 ❑ Manifestations: Client usually unaware of diabetes a. Discovers diabetes when seeking health care for another concern b. Most cases aren’t diagnosed for 5-6 years after the development of the disease c. Usually does not experience weight loss Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 9  Diabetic Ketoacidosis (DKA) ❑ Definition: A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis- producing derangements in intermediary metabolism, including production of serum acetone. DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. Diabetic ketoacidosis (DKA) is a serious complication of diabetes that can be life-threatening. Sometimes DKA is the first sign of diabetes in people who haven’t yet been diagnosed. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 10  Diabetic Ketoacidosis (DKA) ❑ Clinical features: The three main clinical features of DKA are: Hyperglycemia Dehydration and electrolyte loss Acidosis It Can occur in both Type I Diabetes and Type II Diabetes Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 11  Pathophysiology of DKA Three major physiological disturbances exist in DKA: (1) hyperosmolality due to hyperglycemia, (2) metabolic acidosis due to accumulation of ketoacids (3) volume depletion due to osmotic diuresis. Each of these three disturbances may be more or less severe in any patient. Interactions among these disturbances may occur, aggravating (or possibly partially compensating for) one another. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 12  Pathophysiology of DKA Without insulin, the amount of glucose entering the cells is reduced and the liver increases glucose production. Both factors lead to hyperglycemia. In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes (eg, sodium and potassium). This osmotic diuresis, which is characterized by excessive urination (polyuria), leads to dehydration and marked electrolyte loss. Patients with severe DKA may lose up to 6.5 liters of water and up to 400 to 500 mEq each of sodium, potassium, and chloride over a 24-hour period. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 13  Pathophysiology of DKA Another effect of insulin deficiency or deficit is the breakdown of fat (lipolysis) into free fatty acids and glycerol. The free fatty acids are converted into ketone bodies by the liver. In DKA there is excessive production of ketone bodies because of the lack of insulin that would normally prevent this from occurring. Ketone bodies are acids; their accumulation in the circulation leads to metabolic acidosis. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 14  Causes of DKA DKA can occur in patients with DM because of: 1. Decreased or missed dose of insulin. 2. Illness or infection, Pancreatitis. 3. Undiagnosed and untreated diabetes: (DKA may be the initial manifestation of diabetes). 4. Heart attack or stroke. 5. Certain medicines, such as some diuretics and corticosteroids (used to treat inflammation in the body). 6. Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. 15 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  DM/Insulin/DKA 1. Decreased or missed dose of insulin: ▪ An insulin deficit may result from an insufficient dosage of insulin prescribed or from insufficient insulin being administered by the patient. Errors in insulin dosage may be made by patients who are ill and who assume that if they are eating less or if they are vomiting, they must decrease their insulin doses. (Because illness, especially infections, may cause increased blood glucose levels, patients do not need to decrease their insulin doses to compensate for decreased food intake when ill and may even need to increase the insulin dose.) 16 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  DM/Insulin/DKA 1. Decreased or missed dose of insulin: ▪ Other potential causes of decreased insulin dose include patient error in drawing up or injecting insulin (especially in patients with visual impairments), intentional skipping of insulin doses (especially in adolescents with diabetes who are having difficulty coping with diabetes or other aspects of their lives), or equipment problems (eg, occlusion of insulin pump tubing). 17 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  DM/Insulin/DKA 2. Illness or infection Illness and infections are associated with insulin resistance. In response to physical (and emotional) stressors, there is an increase in the level of “stress” hormones—glucagon, epinephrine, norepinephrine, cortisol, and growth hormone. These hormones promote glucose production by the liver and interfere with glucose utilization by muscle and fat tissue, counteracting the effect of insulin. If insulin levels are not increased during times of illness and infection, hyperglycemia may progress to DKA 18 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Signs and Symptoms of DKA Diabetic ketoacidosis symptoms often come on quickly, sometimes within 24 hours. For some, these symptoms may be the first sign of having diabetes. Symptoms might include: Being very thirsty Urinating often Feeling a need to throw up and throwing up (Vomiting) Having stomach pain Being weak or tired Being short of breath Having fruity-scented breath Being confused 19 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Signs and Symptoms of DKA More-certain signs of diabetic ketoacidosis which can show up in home blood and urine test kits —include: High blood sugar level High ketone levels in urine 20 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diagnosis A physical exam and blood tests can help diagnose diabetic ketoacidosis. Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: 1. Blood sugar level: If there isn't enough insulin in the body to allow sugar to enter cells, the blood sugar level will rise. This is known as hyperglycemia. As the body breaks down fat and protein for energy, the blood sugar level will keep rising. 2. Ketone level: When the body breaks down fat and protein for energy, acids known as ketones enter the bloodstream. 21 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diagnosis 3. Blood acidity: A too-high blood ketone level will cause the blood to become acidic. This can change how organs throughout the body work. Other tests 1. Blood electrolyte tests 2. Urine analysis 3. Chest X-ray 4. ECG 22 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) HHNS is a serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium (sense of awareness). At the same time, ketosis is minimal or absent. An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics, A few reports of cases in type I diabetics. 23 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  PATHOPHYSIOLOGY of HHNS It is not known specifically why some people with diabetes develop HHS rather than DKA, although it is speculated that these patients may have just enough insulin to prevent ketosis. Pathophysiologically, the mechanisms of disease are the same as for DKA. A reduction in circulating insulin coupled with the effects of counterregulatory hormones such as cortisol and epinephrine leads to the development of hyperglycemia and the extreme hyperosmolar state. 24 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  PATHOPHYSIOLOGY of HHNS Usually, the patient has coexisting impaired renal excretion of glucose and antecedent renal insufficiency or prerenal azotemia. Because basal insulin levels are unaffected, excessive ketone production does not occur. The acidosis that these patients develop is attributed to lactic acidosis from poor tissue perfusion instead of ketoacidosis. Marked dehydration develops if the patient is unable to maintain an adequate fluid intake. As dehydration worsens, the patient develops increasing serum glucose and serum osmolality. 25 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  PATHOPHYSIOLOGY of HHNS The life-threatening cycle of hyperglycemia, hyperosmolality, osmotic diuresis, and profound dehydration triggers the sympathetic nervous system “fightor- flight” response. The counter-regulatory hormones epinephrine and cortisol stimulate gluconeogenesis and increase hepatic glucose production. Dehydration worsens and leads to CNS dysfunction. Confusion and lethargy ensue quickly. Hemoconcentration of the blood increases the risk of clot formation, thromboemboli, and infarcts in major organs. 26 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  PATHOPHYSIOLOGY of HHNS HHS may occur secondary to extreme stress associated with severe medical illness such as stroke, myocardial infarction, pancreatitis, trauma, sepsis, burns, or pneumonia. Often, HHS results from excessive carbohydrate intake or exposure such as through dietary supplements, total enteral support with tube feedings, or peritoneal dialysis. Elderly people are at particularly high risk, especially those who have impaired cognition and who are in long-term chronic care facilities. Drugs such as corticosteroids, thiazide diuretics, sedatives, and sympathomimetics affect carbohydrate metabolism adversely and may lead to glucose impairment. 27 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Pathophysiology of DKA/HHNS Insulin Deficiency Increased Lipolysis Hyperglycemia Increased ketogenesis Osmotic Diuresis Ketoacidosis Hyperosmolality Pure Diabetic Ketoacidosis Pure Hyperosmolar State 28 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Causes of HHNS HHNS develops when glucose levels surge (typically above 600 mg/dl), leading to severe dehydration. This dehydration occurs because elevated levels of glucose cause blood to become thicker and result in the body needing to produce more urine in order to lower them. The result is frequent urination, which can result in serious or even life-threatening dehydration. If these fluids are not adequately replenished, the condition may eventually result in a seizure, coma, or even death. Dr. Rana Al Awamleh/ Assistant Professor, 29 Critical Care Nursing  Causes of HHNS HHNS is typically brought on by: An infection, such as pneumonia or a urinary tract infection Poor management of blood sugar and/or not taking diabetes medications as prescribed Taking certain medications, such as glucocorticoids (which alter glucose levels) and diuretics (which increase urine output) Trauma and other medical emergencies like cardiovascular disease Having chronic conditions in addition to diabetes, such as congestive heart failure or kidney disease 30 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Signs and Symptoms of HHNS The symptoms of HHNS may appear slowly, taking days or even weeks to fully develop. Common symptoms include: Blood glucose levels over 600 milligrams per deciliter (mg/dl) Frequent urination Extreme thirst Dry mouth Confusion or sleepiness Unexpected weight loss Skin that is warm and dry without sweating Fever Weakness or paralysis on one side of the body Loss of vision 31Hallucinations Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Diagnosis HHNS is diagnosed based on symptoms and by measuring blood glucose levels, which can be performed with a finger stick. A blood glucose level of 600 mg/dL and low ketone levels are the main factors for diagnosis of HHNS. Serum osmolality, a test that measures the body's water/electrolyte balance, also is used to diagnose HHNS. Serum osmolality specifically measures the chemicals dissolved in the liquid part of blood (serum), such as sodium, chloride, bicarbonate, proteins, and glucose. The test is done by taking a sample of blood from a vein 32 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing Assessment and Diagnostic Findings for DKA, HHNS ❑ Physical Examination: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness 33 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing Assessment and Diagnostic Findings for DKA, HHNS ❑ Diagnostic tests: 1. Blood glucose levels may vary from 300 to 800 mg/dL: The severity of DKA is not necessarily related to the blood glucose level. Some patients may have severe acidosis with modestly elevated blood glucose levels, whereas others may have no evidence of DKA despite blood glucose levels of 400 to 500 mg/dL 34 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Assessment and Diagnostic Findings for DKA, HHNS ❑ Diagnostic tests: 2. Evidence of ketoacidosis is reflected in low serum bicarbonate (0 to 15 mEq/L) and low pH (6.8 to 7.3) values. A low PCO2 level (10 to 30 mm Hg) reflects respiratory compensation (Kussmaul respirations) for the metabolic acidosis. Accumulation of ketone bodies (which precipitates the acidosis) is reflected in blood and urine ketone measurements. 35 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Assessment and Diagnostic Findings for DKA, HHNS ❑ Diagnostic tests: 3. Sodium and potassium levels may be low, normal, or high, depending on the amount of water loss (dehydration). Despite the plasma concentration, there has been a marked total body depletion of these (and other) electrolytes. Ultimately, these electrolytes will need to be replaced. 36 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing  Assessment and Diagnostic Findings for DKA, HHNS ❑ Diagnostic tests: 4. Elevated levels of creatinine, blood urea nitrogen (BUN), hemoglobin, and hematocrit may also be seen with dehydration. After rehydration, continued elevation in the serum creatinine and BUN levels will be present in the patient with underlying renal insufficiency. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 37  Comparison of DKA and HHNS DKA HHNS Patients most Can occur in type 1 or type 2 Can occur in type 1 or type 2 commonly diabetes; more common in type 1 patients; more common in affected type 2 diabetes, especially elderly patients with type 2 diabetes Precipitating event Omission of insulin; physiologic Physiologic stress (infection, stress (infection, surgery, surgery, CVA, MI) CVA, MI) Onset Rapid (250 mg/dL Usually >600 mg/dL (>13.9 mmol/L) (>33.3 mmol/L) Arterial pH level