Diabetes
Pancreatic Hormones and Metabolism
Pancreas Location and Function
Located near the duodenum and aorta.
Contains cells that secrete digestive juice via the pancreatic duct.
Contains Islets of Langerhans, which are endocrine cells responsible for secreting hormones directly into the bloodstream.
Pancreatic Endocrine Hormones (Islets of Langerhans)
Alpha cells: Secrete glucagon.
Beta cells: Secrete insulin.
Delta cells: Secrete somatostatin.
Comparison of Insulin and Glucagon
Insulin
Secreted by beta cells.
Released when blood glucose is high.
Promotes uptake and use of glucose by insulin-sensitive cells.
Tells the liver to convert glucose into glycogen (glycogenesis).
Uptake of amino acids and synthesis of proteins in cells.
Inhibits breakdown of stored glucose, protein, and fat.
Glucagon
Secreted by alpha cells.
Released when blood glucose is low.
Causes the liver to convert stored glycogen into glucose (glycogenolysis), which is released into the bloodstream.
Inhibits glycogen formation.
Definitions of Related Terms
Lysis: Breakdown.
Glycogenolysis: The breakdown of glycogen into glucose.
Genesis: Regeneration or formation of new.
Gluconeogenesis: The formation of glucose from non-carbohydrate substances (e.g., amino acids, fat, protein) through breakdown.
Glycogenesis: The formation of glycogen from glucose.
Blood Glucose Regulation
When blood sugar is high:
Pancreas promotes insulin release.
Insulin stimulates glucose uptake by tissue cells from the blood, thereby lowering blood sugar.
Insulin stimulates glycogen formation in the liver.
When blood sugar is low:
Pancreas promotes glucagon release.
Glucagon stimulates glycogen breakdown to glucose in the liver, thereby raising blood sugar.
Diabetes Mellitus
Definition of Diabetes
A group of diseases characterized by hyperglycemia (high blood glucose) due to defects in insulin secretion, insulin action, or both.
Physiology/Pathophysiology
Hyperglycemia can result from:
Impaired insulin secretion from the pancreas.
Increased basal hepatic glucose production by the liver.
Decreased insulin-stimulated glucose uptake by muscle tissue.
Gastrointestinal absorption of glucose.
Prevalence of Diabetes
Affects approximately 34.1 ext{ million} people in the U.S., with one-third undiagnosed.
Approximately 88 ext{ million} people aged 18 and older are prediabetic.
Prevalence is increasing and disproportionately affects ethnic and racial minority populations (African Americans, Hispanic Americans, Native Americans, Asian Americans, Pacific Islanders).
Classifications of Diabetes
Type 1 Diabetes
Characteristics: Characterized by the autoimmune destruction of pancreatic beta cells.
Former Names: Juvenile diabetes, insulin-dependent diabetes.
Onset: Can occur at any age but usually young ( < 30 ext{ years} ).
Typical Presentation: Usually thin at diagnosis with recent weight loss.
Etiology: Includes genetic, immunologic, and environmental factors.
Antibodies: Often have islet cell antibodies and antibodies to insulin, even before insulin treatment.
Insulin Production: Little or no endogenous insulin.
Treatment: Requires exogenous insulin to sustain life.
Ketosis: Prone to ketosis when insulin is absent.
Acute Complication: Diabetic ketoacidosis (DKA).
Pathophysiology Cycle (Insulin Deficiency):
Beta cell destruction leads to insulin deficiency.
Insulin deficiency causes decreased tissue glucose utilization, increased lipolysis (free fatty acids), and increased protein catabolism (amino acids).
These processes lead to glucogenesis (liver) and ketoacidosis.
Hyperglycemia results in glycosuria and ketonuria (kidney).
Glycosuria leads to polyuria and subsequently volume depletion, causing polydipsia.
Severe hyperglycemia and ketoacidosis can lead to diabetic coma.
Risk Factors:
Family history.
Environmental factors.
Presence of damaging immune system cells.
Geography.
Race or ethnicity.
Type 2 Diabetes
Characteristics: Characterized by a decrease in endogenous insulin secretion or increased insulin resistance.
Former Names: Adult-onset diabetes, non-insulin-dependent diabetes.
Onset: Can occur at any age, but usually ext{aged }
eq 30 ext{ years} and older.Typical Presentation: Usually obesity is present at diagnosis.
Antibodies: No islet cell antibodies.
Management: Most obese patients can control blood glucose through weight loss. Oral antidiabetic agents may improve blood glucose levels if diet and exercise are unsuccessful.
Insulin Needs: May need insulin on a short- or long-term basis to prevent hyperglycemia.
Ketosis: Uncommon, except in times of stress or infection.
Acute Complication: Hyperglycemic hyperosmolar syndrome (HHS).
Pathophysiology (B-cell dysfunction and insulin resistance):
Factors affecting insulin secretion and action include body weight, physical activity, smoking, heavy alcohol consumption, genetic predisposition, gene-environment interaction, and epigenetics.
These lead to B-cell dysfunction and insulin resistance.
Insulin resistance causes increased insulin-mediated glucose production by the liver and decreased insulin-mediated glucose uptake by adipose tissue and skeletal muscle, leading to hyperglycemia.
Risk Factors:
Increased weight.
Inactivity.
Family history of DM.
Race or ethnicity.
Older age.
History of gestational diabetes.
Polycystic ovary syndrome.
High blood pressure.
Abnormal cholesterol and triglyceride levels.
Prevention (Type 1 vs. Type 2)
Type 1: No known prevention.
Type 2:
Primary Prevention: Weight reduction, healthy diet, physical activities.
Secondary Treatment: Check HbA1c, adjust diet.
Tertiary Treatment: Exercise, healthy diet, blood sugar monitoring.
Gestational Diabetes
Onset: During pregnancy, usually in the second or third trimester.
Cause: Hormones secreted by the placenta inhibit insulin action.
Risks: Above-normal risk for perinatal complications, especially macrosomia (abnormally large babies).
Treatment: Diet and, if needed, insulin to strictly maintain normal blood glucose.
Prevalence: Occurs in about 18 % of pregnancies.
Prognosis: Glucose intolerance is transitory but may recur in subsequent pregnancies. 35-60 % will develop diabetes (usually Type 2) within 10-20 ext{ years} , especially if they have obesity.
Screening: Glucose challenge test performed on all pregnant women between 24 ext{ and } 28 ext{ weeks} of gestation. Should be screened for diabetes every 3 ext{ years} postpartum.
Risk Factors:
Age.
Family or personal history.
Increased weight.
History of previous large babies ( > 9 ext{ lbs} ).
Race or ethnicity.
Latent Autoimmune Diabetes of Adults (LADA)
Description: A subtype of diabetes where the progression of autoimmune beta cell destruction is slower than in Types 1 and 2.
Risk: High risk of becoming insulin dependent.
Diagnosis Criterial: Most patients have at least two of the following:
Age of onset less than 50 ext{ years} .
Body mass index (BMI) less than 25 ext{ kg/m}^2 .
History of autoimmune disease.
Acute symptoms prior to diagnosis.
Positive family history of autoimmune disease.
Diabetes Associated with Other Conditions
Accompanied by conditions known or suspected to cause the disease, such as pancreatic diseases, hormonal abnormalities, or medications (e.g., corticosteroids, estrogen-containing preparations).
Treatment may involve oral antidiabetic agents or insulin, depending on the pancreas's ability to produce insulin.
Prediabetes
Description: Previously classified as abnormality of glucose tolerance.
History: Previous history of hyperglycemia (e.g., during pregnancy or illness).
Current State: Current normal glucose metabolism.
Screening: Impaired glucose tolerance or impaired fasting glucose screening recommended after age 40 ext{ years} if there is a family history of diabetes or if symptomatic.
Management: Encourage ideal body weight, as a loss of 10-15 ext{ lbs} may improve glycemic control.
Diagnostic Criteria for Diabetes
A1C Test (Glycated Hemoglobin)
Diabetes: 6.5 % or above.
Prediabetes: 5.7 ext{-}6.4 %.
Normal: Below 5.7 %.
Fasting Blood Sugar Test
Diabetes: 126 ext{ mg/dL} or above.
Prediabetes: 100 ext{-}125 ext{ mg/dL} .
Normal: 99 ext{ mg/dL} or below.
Glucose Tolerance Test (2-hour Plasma Glucose)
Diabetes: 200 ext{ mg/dL} or above.
Prediabetes: 140 ext{-}199 ext{ mg/dL} .
Normal: 140 ext{ mg/dL} or below.
Medical and Nursing Management of Diabetes
Goals of Management
Normalize insulin activity and blood glucose levels.
Five main components: Nutritional therapy, Exercise, Monitoring, Pharmacologic therapy, and patient EDUCATION.
Need for Referrals
Ophthalmologist, Podiatrist, Dietitian, Diabetes educator, and others as indicated.
Nursing Assessment
Hyper/Hypoglycemia: Assess for signs of hyperglycemia and hypoglycemia. Assess blood glucose levels before meals and at bedtime.
HbA1c: Monitor the patient’s glycated hemoglobin (HbA1c).
Weight: Daily weight.
Feet: Assess feet for temperature, pulses, color, and sensation.
GI: Assess bowel sounds and note any reports of abdominal pain, bloating, nausea, or vomiting.
Renal: Monitor urine albumin and serum creatinine for renal failure.
Activity: Assess pattern of physical activity and exercise tolerance. Determine blood glucose levels before exercising.
Patient Knowledge: Assess the patient’s ability in self-monitoring of blood glucose and understanding of the prescribed diet.
Signs & Symptoms of Diabetes
Increased thirst (Polydipsia).
Frequent urination (Polyuria).
Extreme hunger (Polyphagia).
Unintended weight loss.
Fatigue and weakness.
Slow healing wounds.
Frequent infections.
Sexual dysfunction.
Blurred vision.
Numbness and tingling in hands and feet.
Monitor Labs/Diagnostics
Serum: Blood glucose, electrolytes, BUN/creatinine, HbA1c, fasting lipid profile.
Urine: Test for microalbuminuria, urinalysis, glycosuria.
Diagnostics: Electrocardiogram (ECG).
Nursing Interventions
Nutrition.
Exercise.
Blood sugar monitoring.
Pharmacology.
Patient education.
Nutrition Management
Goals
Achieve normal glucose levels, normal lipid panel, normal blood pressure (BP).
Prevent chronic complications.
Individualize nutrition needs.
Maintain quality of life.
Weight Loss: Essential if the patient is obese (especially for Type 2).
Meal Planning Considerations
Client preference, lifestyle, usual eating times, ethnic and cultural background.
Review diet history.
Consistency in amount of calories and carbohydrates.
Consistency in time intervals between meals.
Caloric Requirements/Distribution
Calorie control based on energy needs, activity, and weight maintenance.
Percentages of calories:
50 ext{% to }60 % from carbohydrates.
20 ext{% to }30 % from fat.
10 ext{% to }20 % from protein.
Increase fiber (soluble vs. insoluble).
Food Classification Systems
Exchange List: Categorizes foods into groups (starch, fruit, vegetable, meat, fat) with similar caloric and macronutrient content to aid meal planning (e.g., 2 ext{ slices bread} = 2 ext{ starch} ).
Nutrition Labels: Emphasizes reading labels carefully, especially for total fat, carbohydrates, dietary fiber, and sugars.
MyPlate Food Guide: Visual guide for balanced eating.
Glycemic Index (GI):
High GI Foods (cause quick increase in glucose levels): White bread, white rice, white potatoes, muffins, sugar, banana, pineapple.
Low GI Foods (slowly digested carbohydrates): Whole wheat bread, sweet potatoes, quinoa, oats, vegetables, apples, oranges.
Other Dietary Concerns
Alcohol: Use caution.
Sweeteners: Nutritive and nonnutritive sweeteners are alternatives to sugar.
Misleading Food Labels: Be aware of terms like "sugarless," "sugar-free," "dietetic," and "health foods" which may still contain significant calories or impact blood glucose.
Exercise for Diabetes Management
General Guidelines
Exercise three times each week, with no more than 2 consecutive days without exercise.
Perform resistance training twice a week if you have Type 2 diabetes.
Exercise at the same time of day (preferably when blood glucose levels are at their peak) and for the same duration each session.
Use proper footwear and, if appropriate, other protective equipment.
Avoid trauma to the lower extremities, especially with peripheral neuropathy.
Inspect feet daily after exercise.
Avoid exercise in extreme heat or cold.
Avoid exercise during periods of poor metabolic control.
Stretch for 10 ext{ to } 15 ext{ minutes} before exercising.
Exercise Precautions
Do not exercise if ketones are in urine and blood glucose is > 250 ext{ mg/dL} .
When on insulin, eat 15 ext{ g} carbohydrates before exercise.
For strenuous or prolonged exercise, eat a snack afterward.
For extended exercise, monitor blood glucose before, during, and after.
Monitoring Blood Glucose
Self-Monitoring of Blood Glucose (SMBG)
Typically via fingerstick.
Client needs physical capability to perform testing.
Ensure accuracy of the machine.
Frequency and timing of testing depend on individual needs and regimen.
Continuous Glucose Monitoring System (CGMS)
Used with or without an insulin pump.
Sensor/transmitter inserted subcutaneously.
Replaced every 7 ext{-}14 ext{ days} .
6 ext{ month} implantable monitors are now available.
Testing for Glycated Hemoglobin (HbA1c)
Indicates average glucose control for the past 3 ext{ months} .
Measures the amount of glucose attached to hemoglobin.
Diabetics typically aim for an HbA1c < 7 %.
Testing for Ketones
Ketones are by-products of fat breakdown.
Used for Type 1 diabetics.
Test for ketones when glycosuria is present, blood glucose is > 240 ext{ mg/dL} for two or more times in a row, during illness, or when pregnant.
Pharmacology: Insulin Therapy
Purpose: Required for Type 1 diabetes and often used for Type 2 and gestational diabetes.
Types: Vary by onset, peak, and duration.
Prescription: Insulin regimens are usually prescribed by an endocrinologist.
Dosing: Based on glucose levels (sliding scale), standing dose with meals, or long-acting at night.
Insulin Types and Characteristics (Subcutaneous)
Rapid-Acting Insulin (Lispro, Aspart, Glulisine)
Onset: 5 ext{-}30 ext{ min} .
Peak: 30 ext{-}90 ext{ min} .
Duration: 3 ext{-}5 ext{ hr} .
Indications: Rapid reduction of glucose, treat postprandial hyperglycemia, prevent nocturnal hypoglycemia.
Short-Acting Insulin (Regular)
Onset: 30 ext{-}60 ext{ min} .
Peak: 2 ext{-}3 ext{ hr} .
Duration: 4 ext{-}6 ext{ hr} .
Indications: Rapid reduction of glucose, treat postprandial hyperglycemia, prevent nocturnal hypoglycemia.
Intermediate-Acting Insulin (NPH)
Onset: 1 ext{-}1.5 ext{ hr} .
Peak: 4 ext{-}12 ext{ hr} .
Duration: Up to 24 ext{ hr} .
Indications: Food should be taken around the time of onset and peak.
Long-Acting Insulin (Glargine, Detemir)
Onset: 3 ext{-}6 ext{ hr} (Glargine); Unknown (Detemir).
Peak: Continuous (no peak) for both.
Duration: 24 ext{ hr} .
Indications: Used for basal dose.
Rapid-Acting Inhaled Powder (Afrezza)
Onset: < 15 ext{ min} .
Peak: ~50 ext{ min} .
Duration: 2 ext{-}3 ext{ hr} .
Indications: Administer at the beginning of a meal (Cost: $441 - $530 for 90 ext{ cartridges} of 4 ext{ units each} ).
Insulin Regimens
Often combinations of short-acting and longer-acting insulin.
Aims to mimic the normal pattern of insulin secretion based on food intake and activity patterns.
Conventional vs. Intensive Approach
Conventional Regimen:
Simplifies insulin regimen.
Aims to avoid hypo and hyperglycemia.
Requires consistent meal patterns and activity levels daily.
Intensive Regimen:
More complex.
Aims for maximal blood glucose control.
Allows for varied insulin doses based on flexible eating and activity patterns.
Complications of Insulin Therapy
Local Allergic Reaction: Redness, swelling, tenderness at injection site.
Systemic Allergic Reaction: Rare, but can involve generalized urticaria or anaphylaxis.
Lipodystrophy: Abnormal distribution of fat tissue at injection sites.
Lipohypertrophy: Increased fat tissue accumulation.
Lipoatrophy: Diminished fat tissue.
Insulin Resistance: Requires increasing doses of insulin to achieve desired glycemic control.
Morning Hyperglycemia
Dawn Phenomenon: Blood glucose levels start to rise around 3 ext{ AM} due to normal nocturnal increases in cortisol and growth hormone levels.
Management: Give evening insulin at bedtime instead of dinnertime.
Somogyi Effect: Early morning hypoglycemia leads to a rebound hyperglycemia ( 3 ext{ AM} low, followed by high morning glucose) due to counter-regulatory hormone release.
Management: Decrease evening insulin dose.
Insulin Waning: Progressive rise in glucose from bedtime until morning.
Management: Increase pre-dinner or bedtime insulin dose.
Diagnosis: Test blood sugar at bedtime, 3 ext{ AM} , and upon rising.
Methods of Insulin Delivery
Subcutaneous injections (traditional).
Jet injectors.
Insulin Pens (pre-filled devices).
Insulin Pumps (continuous subcutaneous infusion).
Implantation of insulin-producing pancreatic islet cells (experimental).
Pharmacology: Oral Antidiabetic Agents (for Type 2 Diabetes)
Overview of Actions: Act on different pathways including hepatic glucose output, glucose absorption, peripheral glucose uptake, glucagon secretion, and insulin secretion.
Specific Drug Classes
Second Generation Sulfonylureas (e.g., Glipizide, Glyburide, Glimepiride)
Actions: Stimulate beta cells to secrete more insulin.
Side Effects: GI symptoms, hypoglycemia, weight gain.
Nursing Implications: Contraindicated for sulfa allergy. Beta-blockers can mask S/S of hypoglycemia.
Biguanides (e.g., Metformin)
Actions: Increases sensitivity to insulin, inhibits glucose production by the liver.
Side Effects: Lactic acidosis, GI disturbances, hypoglycemia (rare alone).
Nursing Implications: Contraindicated for renal/liver impairment. Monitor kidney function and lactic acid levels. Hold 48 ext{ hours} before and after contrast procedures.
Alpha-Glucosidase Inhibitors (e.g., Acarbose, Miglitol)
Actions: Delay absorption of complex carbohydrates in the intestine (does not alter insulin secretion).
Side Effects: GI disturbances, hypoglycemia.
Nursing Implications: Only works when taken with the first bite of food.
Non-Sulfonylurea Insulin Secretagogues (e.g., Repaglinide, Nateglinide)
Actions: Stimulates the pancreas to secrete more insulin.
Side Effects: Hypoglycemia.
Nursing Implications: Take with food (rapid acting, short half-life). Monitor renal/liver function.
Thiazolidinediones (TZDs) (e.g., Pioglitazone, Rosiglitazone)
Actions: Makes tissue more sensitive to insulin.
Side Effects: Hypoglycemia, weight gain, anemia, liver issues.
Nursing Implications: Monitor liver function.
DPP-4 Inhibitors (e.g., Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Alogliptin)
Actions: Increases hormonal release that increases insulin release and decreases glucagon levels.
Side Effects: Hypoglycemia, GI issues, upper respiratory infection, stuffy nose.
Nursing Implications: Monitor kidney function.
GLP-1 Agonists (e.g., Liraglutide, Dulaglutide, Semaglutide)
Actions: Enhances insulin secretion.
Side Effects: GI disturbances, pancreatitis, weight loss.
Nursing Implications: Once-weekly SQ injection for some.
SGL-2 Inhibitors (e.g., Dapagliflozin, Anagliflozin, Empagliflozin)
Actions: Prevents kidneys from reabsorbing glucose, leading to glucose excretion in urine.
Side Effects: UTI, hypoglycemia, may increase LDL and HDL.
Nursing Implications: Daily before first meal in the morning.
Pramlintide (Amylin Agonist)
Actions: For Type 1 or Type 2 diabetics using insulin. Slows gastric emptying, suppresses post-meal glucagon secretion, increases satiety.
Side Effects: Hypoglycemia, gastroparesis, nausea and vomiting, headache.
Nursing Implications: Given SQ, 2 ext{ inches} from mealtime insulin injection site.
General Nursing Interventions
Patient Education: Crucial for self-management.
Blood sugar management and monitoring.
Medication administration and storage.
Identification of signs and symptoms of hyper- and hypoglycemia.
Weight management.
Managing Glucose Control in the Hospital Setting
Importance: Hyperglycemia can prolong lengths of stay and increase infection rates and mortality.
Occurrence: Often occurs in patients with known diabetes, newly diagnosed diabetes, or stress hyperglycemia.
General Principles:
Blood glucose targets are 140 ext{ to } 180 ext{ mg/dL} .
Insulin (subcutaneous or IV) is preferred over oral antidiabetic agents.
Hospital insulin protocols or order sets should minimize complexity.
Appropriate timing of blood glucose checks, meal consumption, and insulin dose are crucial for glucose control and to avoid hypoglycemia.
Example: Regular Insulin Sliding Scale (Low Dose)
< 70 ext{ mg/dL} : Initiate Hypoglycemia Protocol.
70 ext{-}130 ext{ mg/dL} : 0 ext{ units} .
131 ext{-}180 ext{ mg/dL} : 2 ext{ units} .
181 ext{-}240 ext{ mg/dL} : 4 ext{ units} .
241 ext{-}300 ext{ mg/dL} : 6 ext{ units} .
301 ext{-}350 ext{ mg/dL} : 8 ext{ units} .
351 ext{-}400 ext{ mg/dL} : 10 ext{ units} .
> 400 ext{ mg/dL} : 12 ext{ units} and call MD.
Complications of Diabetes Mellitus (Chronic)
Macrovascular Complications
Atherosclerotic changes in medium to large blood vessels.
Coronary artery vessels: Myocardial infarction (MI), silent MI.
Cerebral vessels: Transient ischemic attack (TIA), cerebrovascular accident (CVA), impaired recovery.
Peripheral arterial disease (PAD): Diminished pulses, intermittent claudication, gangrene, amputation.
Microvascular Complications
Retinopathy (Diabetic Eye Disease):
Painless, visual changes.
Requires ophthalmology to view vessels of the retina.
Prevention: Treat hypertension, stop smoking, tight glucose control.
Treatment: Photocoagulation (laser).
Nephropathy (Diabetic Kidney Disease):
High glucose causes stress on the kidney filtration system.
Manifestations: Elevated BUN/Creatinine ( ext{BUN/Cr} ext{ } ext{ extuparrow} ), decreased urine output.
Can change insulin needs.
Treatment: Kidney-protective measures, hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), or transplant.
Neuropathies
Peripheral Neuropathy: Affects extremities.
Symptoms: Tingling, prickling, burning sensations.
Decreased sensation to temperature and touch.
Decrease in proprioception (sense of body position).
Sudomotor Neuropathy: Affects sweat glands.
Change in anhidrosis pattern (lack of sweating).
Dryness in feet.
Autonomic Neuropathy: Affects involuntary body functions.
Cardiac: Tachycardia, orthostatic hypotension, lack of pain with MI.
Gastrointestinal: Constipation, nocturnal diarrhea, delayed gastric emptying (gastroparesis).
Renal: Urinary retention, decreased sensation of bladder fullness, urinary tract infections (UTIs).
Adrenal: Inability to feel symptoms of hypoglycemia.
Sexual Dysfunction: Erectile dysfunction in men.
Foot & Leg Problems
Diabetes accounts for 50 ext{% to }75 % of lower extremity amputations.
Causes:
Neuropathy: Changes in sensation (loss of protective sensation).
Peripheral Vascular Disease (PVD): Poor circulation to lower extremities.
Immunocompromised State: Hyperglycemia leads to decreased immune response to infections.
High-Risk Factors for Foot Problems:
Duration of diabetes greater than 5 ext{ years} .
Age greater than 40 ext{ years} .
Current smoker and history of smoking.
Decreased peripheral pulses.
Decreased sensation.
Anatomic deformities or pressure areas (e.g., bunions, calluses, hammer toes).
History of previous foot ulcerations or amputation.
Foot Care Guidelines:
Keep glucose level within a normal range.
Inspect feet daily.
Wash feet daily.
Keep skin soft and smooth.
Smooth corns and calluses gently.
Trim toenails weekly or as needed.
Wear shoes and socks at all times.
Protect feet from hot and cold.
Keep blood flowing to your feet.
Check with primary provider regularly.
Acute Complications of Diabetes Mellitus
Hypoglycemia
Definition: Blood glucose < 70 ext{ mg/dL} . Severe hypoglycemia is < 40 ext{ mg/dL} .
Causes: Excess insulin, too much medication, low food intake, physical activity, stress.
Symptoms:
Adrenergic (Autonomic): Sweating, palpitations, tachycardia, nervousness, hunger, tremors.
Neuroglycopenic (CNS): Headache, confusion, memory trouble, drowsiness, slurred speech, issues with coordination.
Severe: Seizures, disorientation, loss of consciousness.
Nursing Interventions:
Assess blood sugar and level of consciousness.
If possible and conscious, give 15 ext{ g} of carbohydrates (e.g., 4 ext{ oz} apple juice; do NOT add sugar).
For severe cases, IV glucagon or IV D50W.
Follow hospital-specific hypoglycemia protocol.
Diabetic Ketoacidosis (DKA)
Primary Cause: Severely low insulin levels, most common in Type 1 diabetes.
Precipitating Factors: Missed or incorrect insulin doses, human error, pump failure, physical or emotional stressors (e.g., illness, infection), new onset Type 1 diabetes.
Main Clinical Issues:
Hyperglycemia: Usually 250 ext{-}800 ext{ mg/dL} .
Dehydration and Electrolyte Loss: Can lose up to 6.5 ext{ L} water and up to 500 ext{ mEq} of Na, K, Cl over 24 ext{ hours} . Elevated BUN/creatinine.
Acidosis: Arterial pH 6.8 ext{-}7.3 , decreased bicarbonate ( ext{HCO}3 from 0 ext{-}15 ext{ mEq/L} ), decreased partial pressure of carbon dioxide ( ext{PaCO}2 from 10 ext{-}30 ext{ mmHg} ), positive ketones.
Assessment Findings:
Polyuria, polydipsia, anorexia.
Fatigue, headache, weakness, blurred vision.
Acetone breath (fruity).
Nausea/Vomiting, abdominal pain.
Alert, oriented, or confused.
Rapid respirations (Kussmaul's respirations).
Tachycardia (thready pulse), hypotension (orthostatic).
Treatment:
Hyperglycemia: IV insulin drip, hourly glucose checks, transition to SQ insulin when stable.
Fluid Loss (Hypotension, Tachycardia): Rehydrate (fluid concentrations depend on patient history, Na, glucose), monitor fluid status for signs of overload.
Acidosis/Ketosis (GI upset, N/V, acetone breath, Kussmaul respiration): Monitor electrolytes, electrolyte replacement, watch ECG, sodium bicarbonate infusion if severe acidosis.
Preventing DKA: "Sick Day Rules":
Take insulin or oral antidiabetic agents as usual.
Test blood glucose and urine ketones every 3 ext{ to } 4 ext{ hours} .
Report elevated glucose levels (as specified) or urine ketones to primary provider.
Take supplemental doses of regular insulin every 3 ext{ to } 4 ext{ hours} if needed (if on insulin).
Substitute soft foods (e.g., 1/3 ext{ cup} regular gelatin, 1 ext{ cup} cream soup, 1/2 ext{ cup} custard, 3 ext{ squares} graham crackers) six to eight times a day if unable to follow usual meal plan.
Take liquids (e.g., 1/2 ext{ cup} regular cola or orange juice, 1/2 ext{ cup} broth, 1 ext{ cup} sports drink) every 1/2 ext{ to } 1 ext{ hour} to prevent dehydration and provide calories, if vomiting, diarrhea, or fever persists.
Report nausea, vomiting, and diarrhea to primary provider, as extreme fluid loss may be dangerous.
Be aware that inability to retain oral fluids may require hospitalization to avoid DKA and possibly coma.
Hyperglycemic Hyperosmolar Syndrome (HHS)
Prevalence: Usually occurs in Type 2 diabetics, especially older patients.
Onset: Can occur over days to weeks (slower than DKA).
Signs & Symptoms:
Polyuria, severe dehydration leading to hypotension/tachycardia, kidney injuries, poor skin turgor.
Electrolyte imbalances.
More prominent neurological symptoms: altered level of consciousness, seizures, hemiparesis.
Treatment:
Vigorous fluid replacement.
Electrolyte correction/replacement.
Insulin therapy.
Treat underlying, precipitating illness.
Comparison of Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Syndrome (HHS)
Characteristics
DKA
HHS
Patients most commonly affected
Can occur in Type 1 or Type 2; more common in Type 1
Can occur in Type 1 or Type 2; more common in Type 2, especially older patients
Precipitating event
Omission of insulin; physiologic stress
Physiologic stress (infection, surgery, stroke, MI)
Onset
Rapid ( < 24 ext{ hours} ) | Slower (over several days) | | Blood glucose levels | Usually > 250 ext{ mg/dL} ( > 13.9 ext{ mmol/L} )
Usually > 600 ext{ mg/dL} ( > 33.3 ext{ mmol/L} )
Arterial pH level
< 7.3 | Normal | | Serum and urine ketones | Present | Absent | | Serum osmolality | 300 ext{-}350 ext{ mOsm/L} | > 350 ext{ mOsm/L}
Plasma bicarbonate level
< 15 ext{ mEq/L}
Normal
BUN and creatinine levels
Elevated
Elevated
Mortality rate
1 ext{%-}5 %
10 ext{%-}20 %
Specialized Care During Surgery/Hospitalizations
During hospitalization or surgery, closely monitor for HYPERGLYCEMIA and HYPOGLYCEMIA.
Be aware of Medication changes.
Diet changes: NPO (nothing by mouth), clear liquid diets (often high in sugar), enteral tube feedings (can have many simple carbs), parenteral nutrition (often includes insulin in the mix, requires SQ insulin to correct highs).