Musculoskeletal Injuries & Treatments PDF

TUTOR NOTES PICTURES/MY NOTES Contusion = soft tissue injury STRAINS - Trauma (excessive stretching) to a muscle body or a tendon, tendons are fibrous cords that attach muscles to bones Occurs with twisting motion or misuse Occur...

TUTOR NOTES PICTURES/MY NOTES Contusion = soft tissue injury STRAINS - Trauma (excessive stretching) to a muscle body or a tendon, tendons are fibrous cords that attach muscles to bones Occurs with twisting motion or misuse Occur in the large muscle groups Acute: d/t vigorous exercise Chronic: d/t repetitive muscle overuse SPRAINS - Damage to ligaments or their attachments to a bone ANKLE MOST FREQUENT AREA OF INJURY s/s of strain and sprains: - pain - edema - decreased function ALSO KNOWN AS RICE METHOD! Acute Care R: Rest If immediate injury occurs, care focuses on: I: Ice; *20-30 minutes at a time* 1. Stopping the activity and limiting movement – do a C: Compress(with elastic bandage) neurovascular assessment E: Elevate above heart 2. Applying ice packs to the injured area 3. Compressing the involved area 4. Elevating the extremity 5. Providing analgesia as needed - applying heat after the acute phase(24-48) helps with pain management and stiffness - movement of injured muscle improves circulation and resolution of contusion and swelling How do we educate our pts to prevent contusions, strains, and sprains? - prevention strategies, stretching, correct footwear or protective gear etc Diagnostics: - X-ray 1. What’s the difference between strain, and sprain?  2. When do you apply warm moist heat? 3. What are the steps in caring for acute sprains? REPETITIVE STRAIN INJURY (RSI) / OVERUSE SYNDROMES - Injuries resulting from prolonged forces or repetitive movements and awkward postures - Repeated movements strain the tendons, ligaments, and muscles causing tiny tears that become inflamed. - risk factors: - repetitive jobs like: dancers, butchers, athletes, keyboard operators Interventions for Overuse Syndrome: - Warm ups before exercise - Rest - NSAIDS ♐□❒ pain - Steroid injection for short term relief - Rehabilitation LATERAL/MEDIAL HUMERAL EPICONDYLITIS = TENNIS/GOLFER’S ELBOW CARPAL TUNNEL SYNDROME - Compression of the median nerve - Most common compression neuropathy in the upper extremity - Weakness, pain, numbness or impaired distribution of the median nerve - Common in musicians, carpenters, computer operators bc they require continuous wrist movement POSITIVE TINEL’S SIGN - Tinel’s Sign: can be elicited by tapping over the median nerve as it passes through the carpel tunnel in the wrist - (+) response: sensation of tingling in the distribution of the median nerve over the hand POSITIVE PHALEN’S SIGN - Phalen’s Sign: can be elicited by allowed the wrists to fall freely into maximum flexion and main the position for longer than 60 seconds (+) response 🡪 sensation of tingling in the distribution of the median nerve over the hand ROTATOR CUFF INJURIES **T’s for Tear in Tendons** - A tear in the tissues connecting muscle to bone (tendons) around the shoulder joint - Occurs with repetitive motion or traumatic injury of shoulder joint Other causes: 1. Falling onto an outstretched arm and hand 2. A blow to the upper arm 3. Heavy lifting 4. Repetitive work motions S/S - shoulder weakness, pain, and decreased ROM rotator cuff: four muscles in the shoulder that - Severe pain when arm abducted between 60 and 120 stabilize and protect humeral head degrees - tears usually are caused by repetitive - Positive drop arm test if patient’s arm falls suddenly stress, aging, or acute injury from 90 degrees then a rotator cuff injury suspected TEAR CONFIRMED BY MRI - For inflammation 🡪 conservative interventions 🡪 Sling, NSAIDS, steroid injection, analgesic injection - AFTER acute phase 🡪 exercise to strengthen and improve ROM - Surgery: Arthroscopy(restoration of joint), acromioplasty Surgery 🡪 post op care 🡪 EXERCISE BEGINS 1st POST-OP DAY/ Shoulder immobilizer to limit shoulder movement MENISCUS INJURIES - Meniscus = fibrous cartilage on top of tibia and femur; absorbs shock - there are different types of tears: - longitudinal: down the meniscus - rotational: twisting from opposite ends like wringing out a rag. the knee is twisting while the foot is planted Time to Recall!!! - s/s: 1. What can cause a rotator cuff injury? - popping, slipping, catching, buckling of knee 2. When do you begin exercises to with injury, swelling, pain strengthen and improve ROM? POSITIVE McMURRAY TEST = click heard with maneuver, pain 3. When does exercise begin after to the medial or lateral joint line surgery? https://youtu.be/lwDFPAyGGgI KNEE LIGAMENT TEAR (LATERAL, MEDIAL, ACL, PCL) - Ligaments between tibia and femur - Most common injured knee ligament is the ACL - Usually when the athlete pivots, lands from a jump, or slows down when running - Positive Lachman’s Test will suggest an ACL tear 🡪 flexing knee 15 to 30 degrees and pulling the tibia forward while the femur is stabilized treatment: - RICE method - pain management - immobilizer or hinged knee brace - Physical therapy(6-8 months depending on progress) FRACTURES Disruption or break in the continuity of the bone Classifications: - open vs closed - extent of break (complete or incomplete) - displaced or nondisplaced(out of their normal position Lachman’s Test or still aligned) - →→→→be familiar with different types of fractures!! S/S = swelling, bruising, pain, tenderness, deformity, loss of function, abnormal movement, crepitus, neurovascular changes Potential complications: KNOW THESE!!! - Shock (hemorrhage) - Fat embolism syndrome: systemic fat globules from fractures that are distributed into tissues, lungs and other organs after a traumatic skeletal injury - DVT🖳 order prophylactic anticoagulants - Compartment syndrome: a condition in which swelling causes increased pressure within the fascia (muscle compartment) o Compromises the function of blood vessels and nerves o Capillary perfusion reduced below level of tissue viability o caused by decreased compartment size after surgery OR increased contents within injury site due to edema and/or hemorrhage d/t “suffocation”  - WATCH FOR 6 P’s: o pain: does not match level of injury o pressure o paresthesia o pallor paralysis o pulselessness (peripheral pulse) - Treatment of Fat Embolism Syndrome: - Treatment: fluid resuscitation to prevent o Do not elevate extremity above heart level hypovolemic shock and blood o Do not use cold compresses transfusion o relieve pressure(surgical decompression - fasciotomy) o amputation - Nerve injury - Infection: o usually associated with open fractures and soft tissue injuries o Delayed treatment can lead to chronic osteomyelitis - Pressure ulcers TRACTION application of a pulling force to an injured or diseased body part or extremity Used to: early signs: - Prevent or reduce pain and muscle spasm - pain that isn't relieved, paraesthesia! - Immobilize a joint or part of the body - Reduce a fracture or dislocation late signs: - treat a pathologic joint condition - pulselessness, paralysis Skin Traction - for short term tx - Make sure the line of pull is parallel to the bed and not angled downward. **don’t use cold compress because it - Ensure the patient is positioned in the center of the constricts the blood flow that is already being bed, with the affected leg aligned with the trunk of the “suffocated” by the swelling inside the fascia patient’s body. Check overall alignment of the patient’s body. - Weights should hang freely, off the floor and bed. Infection: Knots should be secure. Ropes should move freely - treat with Antibiotics through the pulleys. The pulleys should not be constrained by knots LOOK AT THE PICTURES IN YOUR PPT!!! Nursing Considerations - Skin breakdown: monitor skin in contact - Assess for tingling, numbness  - Avoid wrapping area tightly or pressure on peroneal nerve or tibia may cause foot drop - Circulatory impairment 🡪 cool skin temp, decreased peripheral pulses, slow cap refill, blush skin - DVT 🡪 calf tenderness, swelling and positive Holman’s sign (calf pain with dorsiflexion of the foot) Skeletal Traction External Fixation with Traction = External fixator is a device composed of metal pins that are inserted into the bone and Time to Recall!!! attached to external rods to stabilize the fracture while it 1. What is the most common injured knee heals ligament? Regularly inspect exposed skin areas 2. What is fat embolism syndrome? Observe pin sites for signs of infection 3. What is compartment syndrome? 4. What is ordered to prevent DVT? Arm Casts Long arm cast: ELEVATE the immobilized arm Leg Casts Elevate on pillows and apply ice pack How do you properly place a crutch and use one????? KNOW IT - Distance between axilla and the arm pieces on the crutches should be 2-3 finger widths in the axilla space - Elbows should be slightly flexed, 20-30 degrees when client is walking - When ambulating with client stand on affected side - Never rest axillae on the axillary bars - Instruct the client to look up and outward when ambulating and to place the crutches 6-10 inches diagonally in front of the foot Internal fixation (IF) - surgical realignment of bony fragments using devices such as pins, plates, rods, and screws External fixation (EF) - metal pins and wires attached to external rods Nursing Management: Fractures Assessment:  - teach about immobilization and limitations that will occur after the surgery - pain regimen - be attentive to limitations with turning Q2 hrs - monitor for complications: External: Internal: - compartment syndrome - fat embolisms - DVT - hemorrhage Management: Nutrition - increase protein, vitamins, calcium, phosphorus, magnesium, and fluids so their body can heal! Time to Recall!!! 1. What are nursing considerations with traction? 2. True or False. We should always instruct the client to look down at their feet when walking with crutches so they know how to properly walk. 3. What is Volkmann’s contracture? 4. What is the most common cause of death with a pelvis fracture?  Diabetes Mellitus What is it? Chronic multisystem disease characterized by hyperglycemia related to: abnormal insulin production (type 1) , impaired insulin utilization (type 2), OR BOTH. Very prevalent disease in the US - 8th leading cause of death Leading cause of: end stage renal disease (people on dialysis), adult blindness, non traumatic lower limb amputations. Risk Factors Family history Gestational diabetes - could lead to diabetes, start living like you have diabetes. Minority groups (American Indians, AA, Hispanics, Asian Americans) Age > 35 Obesity (BMI of > 30) Given birth to an infant > 9lbs Inactivity Etiology and Pathophysiology Combination: genetic, autoimmune, environmental Regardless of its cause, DM is mainly a disorder of glucose metabolism related to absent or insufficient supply and/or ineffective use of available insulin. Normal insulin metabolism ○ Produced by B cells in islets of Langerhans ○ Released continuously into bloodstream in small increments with larger amounts released after food ○ Stabilizes glucose level in range of 70 to 120 mg/dL **Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. GLUCOSE SHOULD BE IN THE CELL NOT IN THE BLOOD. INSULIN IS THE KEY TO ALLOW GLUCOSE INTO THE CELL AND OUT OF THE BLOODSTREAM. Other hormones (counterregulatory hormones): glucagon, epinephrine, GH, cortisol ○ Work against the effects of insulin ○ These hormones increase glucose levels by (1) stimulating glucose production and release by the liver and (2) decreasing the movement of glucose into the cells. ○ Counterregulatory hormones and insulin work together to maintain glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting. ○ Glucagon = opposite of insulin - release from the liver Increase the amount of glucose in the bloodstream by: Glycogenolysis: breakdown of stored glucose Gluconeogenesis: the liver converts fats and proteins into glucose ○ Cortisol = rises with stress; rises in the morning; when cortisol is released, sugar goes up Ketones, the result of the breakdown of fats are excreted in the urine Protein metabolism causes an elevated Blood Urea Nitrogen (BUN) Prediabetic need to PREVENT diabetes, live life like a diabetic before complications occur. At risk for type 2 diabetes Defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. Diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 IFG is diagnosed when fasting glucose levels are 100 to 125. Usually no symptoms Patient Teaching ○ Have glucose A1C checked regularly. ○ Monitor for symptoms of diabetes such as fatigue, frequent infections, or slow-healing wounds. ○ Maintain a healthy weight, exercise regularly and make healthy food choices. Type 1: insulin dependent (abnormal insulin production) The result of the destruction of the beta cells in the pancreas, the only cells in the body that make insulin When beta cells are destroyed, insulin is no longer produced. Signs/Symptoms ○ POLYDIPSIA- excessive thirst ○ POLYURIA - frequent urination ○ POLYPHAGIA- excessive hunger ○ fatigue/weakness due to the body’s inability to get energy from glucose ○ GI : N/V - body’s attempt to get rid of excess glucose Treatment: must be on both a long acting and short acting insulin Type 2: insulin resistant (impaired insulin utilization) Combination of inadequate insulin secretion and insulin resistance. The pancreas usually makes some endogenous insulin, but the body may not produce enough of it or use it effectively. Signs/Symptoms ○ Slow onset of manifestations, the person may go for many years with undetected hyperglycemia and few, if any, symptoms. ○ May have polyuria and polydipsia ** To differentiate between type 1 and type 2, we can look at the beta cells and insulin. Gestational Develops during pregnancy Increase risk for c-section and perinatal complications Screen high risk patients at first visit; others at 24 - 28 weeks Usually glucose levels normal 6 weeks postpartum Diagnostics (Can be used for all types but mostly secondary onset) Fasting plasma glucose (FPG) ○ Impaired fasting glucose: >100 and < 126 ○ If glucose is greater than 126, DM is present ○ Goal = keep FPG of 99 or lower Hemoglobin A1C ○ Gives an average of glucose levels for the past 3 months  ○ Glucose “sticks” to red blood cells. RBCs last about 3 months ○ Goal: 6.5% - 7% ○ 6.5% or > = DIABETIC Estimated Average Glucose (eAG) ○ A calculated conversion of HbA1c ○ It’s reported in mg/dL, the same units as their home blood glucose tests ○ Makes results more meaningful to patients Urine glucose, ketone, and protein levels ○ The presence of glucose in the urine indicates hyperglycemia ○ Ketonuria occurs with the breakdown of fats ○ Albuminuria may indicate early onset of nephropathy Serum cholesterol ○ Diabetics are at risk for atherosclerosis ○ Treatment goal is LDL < 100 Insulin - KNOW! Mixing Insulin (NR -> RN) Wipe off tops of vials with alcohol wipe Draw air for NPH dose, inject air into NPH Draw air for regular insulin, inject air into regular insulin Draw back regular insulin Draw back NPH **draw clear then cloudy Storage of Insulin Do no heat/freeze In-use vials may be left at room temperature for up to 4 weeks Extra insulin should be refrigerated Avoid exposure to direct sunlight, extreme heat or cold Stored prefilled syringes upright for 1 week if two insulin types; 30 days for one Administration of Insulin Typically given by subcutaneous injection. Regular insulin can be given IV when immediate onset of action is desired Insulin is NOT taken orally because it is inactivated by gastric fluids. Absorption is the fastest from the abdomen,followed by the arm, thigh, and buttock. Teach patients to rotate the injection within and between sites to prevent excess bruising. Usually available as U100 insulin (1mL contains 100 U of insulin) Inject at 45 to 90 degree angle NO alcohol swab for self injection; wash with soap and water - can dry out skin Insulin Pump Delivers a continuous subcutaneous insulin infusion through a small device worn on the belt, in the pocket, or under clothing. Deliver short-acting insulin Preprogrammed to deliver varying hourly basal rates. Ideal candidate ○ A person who has failed to control diabetes on other regimens ○ Pregnant ○ Desires increased daily flexibility Very expensive ($7,000) Risk of infection at site progressing to sepsis Change the infusion site every 24-48 hours. Problems with Insulin Therapy Hypoglycemia ○ Treatment includes administering glucagon 0.5-2 mg IM. After 20 minutes of no progression, administer again ○ When aroused, give 15 g of carbs and wait 15 minutes Allergic reaction ○ Local inflammatory reactions to insulin may occur, such as itching, and burning around the injection site. ○ Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. Lipodystrophy ○ Changes in subcutaneous tissue ○ May occur if the same injection sites are used frequently.  Somogyi Effect ○ Hyperglycemia in the morning may be due to the Somogyi effect. ○ Pt takes insulin at night time, then in morning the sugar is very low ○ Rebound hyperglycemia occurs because a high dose of insulin causes a decline in glucose levels overnight, and counterregulatory hormones are released. Dawn Phenomenon ○ Also characterized by hyperglycemia that is present on awakening ○ Due to the release of counterregulatory hormones ○ Unrelated to amount of insulin given at night. ○ The treatment for the dawn phenomenon is an increase in insulin or an adjustment in administration time. Acute Complications Diabetic ketoacidosis (DKA): associated excessive levels of ketones in the body ○ Serious condition that proceeds rapidly and must be promptly treated, and is caused by a profound deficiency of insulin. ○ It is characterized by hyperglycemia, ketosis, acidosis, and dehydration. Hyperglycemia: cells don't have insulin to allow glucose in. This forces the body to use fat cells to break down glucose for energy. Ketoacidosis: the after-effect of fat cells being broken down for glucose stores Dehydration: cells are hungry. They have no food, so the body goes into severe dehydration. Overload of sugar in the ECF leads to vomiting in an attempt to excrete excess sugar. ○ Clinical manifestations Dehydration, lethargy SWEET FRUITY BREATH! KUSSMAUL RESPIRATIONS (rapid, deep breathing w/dyspnea) Labs - Blood Glucose > 250, pH < 7.3 ○ Interprofessional Care First goal = establish IV for fluid and electrolyte replacement Assess renal status, cardiopulmonary status, LOC Hyperosmolar Hyperglycemic Syndrome (HHS): due to insulin deficiency ○ Blood sugar like 600, will be in ICU, very life-threatening ○ Life-threatening syndrome that can occur in a patient with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia. ○ HHS is less common than DKA. It often occurs in patients over 60 years of age with type 2 diabetes. ○ HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usually a history of inadequate fluid entail, increasing mental depression or cognitive impairment. ○ Lab values in HHS include a blood glucose level > 600 mg/dL and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine. ○ Nursing Management HHS is a medical emergency and has a high mortality rate Immediate IV administration of insulin and either 0.9% or 0.45% NaCl Monitor administration of (1) IV fluids to correct dehydration (2) insulin therapy to reduce blood glucose and serum ketone levels, and (3) electrolytes given. Hypoglycemia: low blood glucose due to too much insulin ○ IV access available - obtain blood glucose level, administer glucagon 0.5 - 2 mg IM  ○ When aroused - give 45 g carbohydrates to replace glycogen stores Drug Therapy (Oral Agents) Only for type 2 diabetes (insulin resistance, decreased insulin production, increased hepatic glucose production) For oral medications we want glucose to be 70 - 99 mg/dL **a patient can be on both oral and insulin injection at the same time. Drug: MOA: Nursing Considerations: Biguanides: Metformin Decreases the overproduction of causes moderate weight loss; glucose by the liver; decreases can be used for people with type insulin resistance. 2 diabetes and prediabetes who are overweight or obese. a-Glucosidase Inhibitors: Works in the small intestine to Taken with the first bite of Glyset, Precose slow carb metabolism and each main meal, they are most delays glucose absorption effective in lowering postprandial blood glucose. Their effectiveness is measured by checking 2-hour postprandial glucose levels. Sulfonylureas: Glucotrol, Stimulates the pancreatic cells Most common side effect is Glynase to secrete more insulin and hypoglycemia peripheral cells’ sensitivity to insulin Meglitinides: Prandin Stimulates the of insulin from Hypoglycemia is a common the pancreatic islet cells; rapid side effect acting Long term Diabetes Complications Nephropathy ○ Damage to the kidneys ○ Early glomerular hypertrophy ○ Increased glomerular filtration ○ Microalbuminuria Cardiovascular ○ Coronary artery disease ○ Stroke ○ Hypertension American diabetes association recommends < 140/90 130/80 if high risk  Retinopathy ○ Can lead to blindness ○ Encourage eye exam once a year Neuropathy ○ Decreased feeling in feet or hands ○ Hot, burning sensation Gastroparesis - low GI motility ○ Constipation, vomiting, anorexia, heartburn Infections Sexual Dysfunction Nursing Assessment Health history: visual changes, numbness in hands or feet, pain when walking, appetite, N/V, frequent vomiting, infections Physical assessment: height/weight, VS, peripheral pulses, skin, feet, injection sites Patient Education ○ Medications ○ How to administer insulin ○ Finger sticks or CGM ○ Foot care ○ Diet Tests and/or Areas to check annually ○ Glycohemoglobin (2-4 times a year) ○ Kidney function ○ Cholesterol & triglycerides, foot exam, eye exam, BP **If a patient is sick, you SHOULD still take your oral antidiabetic because because of the stress from sickness, cortisol is released and increases the blood sugar. Disorders of the Parathyroid Glands Parathyroid gland: four small glands that are located on the posterior surface of the thyroid and releases parathyroid hormone; about the size of a grain of rice PRIMARY FUNCTION: regulate calcium levels; to a lesser degree regulates phosphate levels Calcium is stored in the bones; it is readily available to the rest of the body at the request of the parathyroid glands. Osteoclasts = deconstructs bone Osteoblasts = build bone Parathyroid Hormone ○ Regulates how much calcium is: Absorbed from diet Excreted by kidneys Stored in bones ○ Increases formation of active vitamin D  ○ Active vitamin D increases intestinal calcium and phosphorus absorption HYPERPARATHYROIDISM Most common disease of the parathyroid glands Characterized by excess PTH - so you get excess calcium in the blood Parathyroid glands continue to make large amounts of PTH even when the calcium level is normal. Most common cause: benign tumor called an adenoma on one of parathyroid glands that secretes too much PTH Symptoms: ○ Kidney stones - due to kidneys’ inability to keep up with the excretion of calcium ○ Abdominal pain ○ Bone and joint pain - too much calcium in the blood and not in the bone ○ Fragile bones (osteoporosis) ○ irritability/Depression/Anxiety ○ Heart palpitations/arrhythmias Diagnostic Studies: Serum PTH: Serum Calcium: Serum Urine Calcium: Bone Density Phosphate: ⬆ ⬆(8.5-10) ⬇(2.5-4.5) ⬆ ⬇ Management: It depends on the severity of disease Surgical: partial or complete removal of the parathyroid glands Nonsurgical: ○ Ongoing measures of lab values ○ Exercise ○ Increase fluids ○ Moderate calcium intake ○ Calcimimetic agents, bisphosphonates, and phosphate Severe: ○ IV sodium chloride ○ Loop Diuretics ○ IV bisphosphonates: rapidly lower serum calcium in patients with dangerous levels Nursing Management: Patient education If postoperative: ○ Pain control ○ Monitor for bleeding ○ Monitor for tetany (due to sudden decrease in calcium level) HYPOPARATHYROIDISM Very rare; characterized by inadequate circulating PTH Most common cause: iatrogenic (this may include accidental removal of parathyroid glands or damage to the vascular supply of the glands during neck surgery) Symptoms Due to hypocalcemia: ○ Tetany ○ Tingling of lips and stiffness of limbs ○ Painful spasms of muscles ○ Trousseau’s sign Inflate BP cuff above SBP for several minutes Positive response: muscle contractions in hand Indicates hypocalcemia ○ Chstvoek’s Sign Elicited by tapping the patient’s face slightly over the facial nerve anterior to the ear lobe Positive finding: facial muscle twitching Indicates hypocalcemia Diagnostic Studies: Serum PTH: Serum Calcium: Serum Phosphate: ⬇(10-65) ⬇ ⬆(2.5-4.5) Management: Calcium supplements Vitamin D Magnesium High calcium diet Teach patient that it is a lifelong disorder Treatment goals are to treat acute complications, such as tetany, maintain normal calcium levels, and prevent long-term complications Give IV calcium slowly. USE ECG monitoring when giving calcium (can cause arrhythmias/cardiac arrest) Need to be in ICU Anatomy and Physiology: Thyroid Gland: The thyroid gland is located in the front of the neck with the primary function being to produce thyroid hormone. the thyroid hormone controls:  ○ metabolic rate ○ Metabolism ○ growth/development Thyroid Hormones ○ Calcitonin: controls body use of calcium; lowers excess calcium in the blood (calciTONin TONES down calcium in the blood) ○ T3: composed of iodine, regulates metabolism - iodine comes from salt! You can get goiter from lack of iodine. ○ T4 : composed of iodine and regulates metabolism ○ With iodine deficiency, the thyroid is unable to secrete sufficient thyroid hormone. ○ TSH: released from the pituitary gland that stimulates the thyroid to release T3/T4 Disorders of the Thyroid Gland TSH and T4 levels are measured to determine whether a goiter is associated with normal thyroid function, hyperthyroidism, or hypothyroidism. HYPOTHYROIDISM Condition in which the thyroid gland produces inadequate amounts of thyroid hormone Primary hypothyroidism: thyroid gland malfunction; the thyroid gland fails to produce sufficient thyroid hormone to sustain normal metabolic function. ○ Causes: Insufficient iodine diet Hashimoto’s disease: autoimmune disease in which the body attacks its own thyroid gland Surgical removal of the thyroid Therapeutic radiation as a result of hyperthyroidism Atrophy of the thyroid gland Tumors of the thyroid gland Secondary hypothyroidism: cause is related to pituitary tumors and other pituitary disorders; results from alterations in the hypothalamic-pituitary axis. Clinical manifestations - Fatigue Weight gain Cold intolerance Constipation Dry skin Thinning hair Periorbital edema Myxedema Coma Severe hypothyroidism A loss of brain function as a result of severe, long standing low level of thyroid hormone Life-threatening! Causes: acute illness, surgery, chemo, or DC of medications Lab Tests TSH = high T4 Low Thyroid Scan Fine-needle biopsy Ultrasonography Management **restore a euthyroid state as safely and rapidly as possible with hormone therapy Administration of synthetic thyroid hormone ○ Levothyroxine (Synthroid) : drug of choice for hypothyroidism Taken in the morning on an empty stomach Follow-up: TSH and T4 levels will be drawn in 4-8 weeks to assess levels Nursing Management Guided by the severity of the disease Directed at symptom management Note signs and symptoms Monitor patient progress ○ Weight loss ○ Resolution of fatigue ○ Skin and hair returning to normal Nursing Diagnosis Activity intolerance RT fatigue & depressed cognitive process Altered body temperature Constipation RT depressed GI function Altered thought process RT depressed metabolism & altered CV & respiratory status. HYPERTHYROIDISM - Excessive production of thyroid hormone. Patient is in a continuous hypermetabolic state Etiology: Graves Disease: Most common cause of hyperthyroidism ○ Autoimmune disorder ○ TSH is activated ○ Thyroid produces too much thyroid hormone Thyroiditis Nodules on thyroid gland Over treatment of hypothyroidism Signs/Symptoms - CAN LEAD TO THYROID STORM Weight loss tachycardia/palpitations Warm, moist skin Heat intolerance Fine tremors of the hand and tongue Hyperactivity, weakness, insomnia, exophthalmos , goiter Diagnostic Tests TSH: extremely low T4: high Management Synthroid dose will be decreased dose if applicable Antithyroid drugs: Tapapzole, PTU (Propylthiouracil) ○ Inhibit production or conversion of active thyroid hormone (T4 to T3) Beta-Blockers Radioactive Iodine ○ Destroys all or part of the thyroid gland ○ Post treatment: hypothyroid ○ Potassium iodine (SSK) and Lugol’s solution  Give with a straw Metallic taste Surgical Therapy ○ Subtotal thyroidectomy ○ Indications: failure of antithyroid drugs, not good candidate for radioactive iodine, large goiter (tracheal compression), malignancy ○ Makes thyroid gland unable to produce excessive thyroid hormone ○ Complication: accidental removal of parathyroid gland (hypocalcemia) ○ Post-op Assess for hemorrhage and tracheal compression Vital signs Voice Symptoms of hypocalcemia Paresthesia Facial spasm Muscular twitching Spasm of larynx Check for positive Chvostek’s sign ○ Nursing Management VS:BP, Pulse, respirations Exopht  Hematologic System Structures & Functions of Hematologic System Bone marrow (yellow & red) - red marrow is found in flat bones and is responsible for making blood cells. Blood is a connective tissue that transports, regulates, and protects (maintains homeostasis of coagulation) ○ Plasma (55%) - composed mainly of water, but also contains proteins, electrolytes, gasses, nutrients, and waste. ○ Blood cells (45%) Erythrocytes (RBCs) - O2 transportation Leukocytes (WBCs) - protects from infection Thrombocytes (Platelets) - promotes blood coagulation Anemia is a deficiency in: Number of erythrocytes (RBCs) Quantity or quality of hemoglobin (Hgb) Volume of packed RBCs (hematocrit) Causes Decreased RBC production Blood loss Increases RBC destruction Hereditary (intrinsic) Because RBCs transport O2, RBC disorders can lead to tissue hypoxia. Manifestations of anemia result from the body's response to hypoxia Normal CBC Hemoglobin (Hgb) ○ Female: 12-16 g/dL ○ Male: 14-18 g/dL WBC - 5000 - 10,000/uL Platelets - 150,000 - 400,000 Mild (10-12g/dL) Moderate (6-10g/dL) Severe ( < 6g/dL) Asymptomatic Fatigue Pallor Palpitations - bounding Dizziness Response to heavy exercise pulse headache/vertigo/impaired Palpitations Dyspnea thought process Dyspnea exhausted/lethargic Mild fatigue Severe palpitations, tachy Orthopnea, dyspnea at rest Sensitive to cold, anorexia  Morphology Etiology Normocytic, Normochromic Acute blood loss, hemolysis, chronic kidney Normal size and color disease, sickle cell anemia, pregnancy, cancer MCV 80-100fL, MCH 27-34 pg Microcytic, hypochromic Iron deficiency anemia, Vit B6 deficiency, Small size, pale color Thalassemia, lead poisoning MCV < 80 fL MCH < 27 pg Macrocytic (megaloblastic), Normochromic Cobalamin (Vit B12 deficiency), folic acid Large size, normal color deficiency, liver disease, effects of ETOH abuse MCV > 100 fl MCH > 34 pg Diagnostic Studies for Anemia CBC (Hgb, Hct, WBC, platelets) Reticulocyte count Red blood cell indices - MCV, MCH Serum ferritin - measures iron stores. First to drop. Serum iron - measures circulating iron, carried by transferring. Drops after serum ferritin. TIBC (transferrin & iron binding capacity) B12 Folate Schilling Test - to evaluate vit absorption (rarely done) Etiology and Management of Anemia Decreased RBC production - iron deficiency thalassemia Decreased number of RBC precursors - aplastic anemia Nutritional anemias - iron deficiency, macrocytic or megaloblastic anemias (B12 or folate deficiency) Blood loss - acute or chronic Hereditary (intrinsic) - sickle cell anemia Assessment ○ H&H Clinical problems - depends on H&H Planning - goal = normal activities Nursing Implementation Varies ○ Numerous causes of anemia ○ Patient-specific needs  ○ Acute interventions may include blood transfusions, drug therapy (eg. iron supplements), and O2 therapy. Patients with fatigue ○ Alternate rest and activity ○ Prioritize activities Accommodate energy levels Maximize O2 supply for vital functions ○ Aid to minimize risk of injury from falls ○ Monitor cardiorespiratory response ○ Evaluate nutrition needs Acute interventions ○ Blood transfusions ○ Drug therapy (iron supplements) ○ O2 therapy National Patient Safety - Eliminate Transfusion Error GOAL: eliminate transfusion errors related to patient misidentification. “PATIENT SAFETY” Two-person patient identification process includes: ○ Person who will give the blood ○ Another person who is qualified to identify the patient Match blood to the provider’s order. Match patients to blood. Nutritional Anemia Iron Deficiency Anemia Causes ○ Chronic blood loss (GI or GU systems), or hemolysis ○ Menstruation ○ Inadequate dietary intake ○ Inadequate absorption of iron from GI tract (small intestine is where iron is best absorbed) - think about if they’ve had GI surgery ○ GI surgeries, involving bypass of duodenum ○ Malabsorption syndromes Signs/Symptoms - depends on age and severity Few symptoms until HCT < 30 ○ Pallor, glossitis (inflammation of tongue), cheilitis (inflammation of lips), headache, paresthesia History & Physical ○ Menstrual history ○ Onset & duration of symptoms ○ Change in stool patterns ○ Color of stool ○ Dietary intake ○ Medication history  ○ Observe skin - pallor, jaundice, pruritus ○ Examine tongue - atrophic glossitis, burning sensation ○ Look at the corners of the mouth - cheilosis ○ Examine nails - koilonychias (spooning) ○ Palpate abdomen tenderness ○ Splenomegaly ○ Obtain stool for occult blood Diagnostics ○ Labs Low Hgb Decreased serum iron - measures circulating iron, carried by transferring. Drops after serum ferritin. High TIBC - ability of cells to bind to iron Low serum ferritin - measures iron stores. First to drop. Low MCV Low MCH **normally is inversely related to serum iron, eg. when serum iron is low, TIBC is high ** ○ Stool occult blood test ○ Endoscopy and colonoscopy ○ Bone marrow biopsy Nursing Management ○ Goal - treat underlying problems causing loss, reduced intake, or poor absorption of iron ○ Replace iron Nutrition therapy Oral iron supplements Transfusion of packed RBCs Treatment: Self-Care Plan ○ Oral iron therapy ○ Teach about foods high in iron - eggs, lean beef, red kidney beans, oats, spinach ○ Take iron between meals or one hour before - iron is best absorbed in acidic environment ○ *Taking with vitamin C improves iron absorption ○ *May cause constipation - patient should start on stool softeners or laxatives ○ Correct cause of bleeding ○ What do you need to teach patients about their stool when taking iron?? - stools may be black in color Thalassemia A group of diseases involving inadequate production of normal Hgb Results in decreased RBC production Due to absent or reduced globulin protein - abnormal Hgb synthesis Hemolysis occurs Genetic link - autosomal recessive genetic basis Clinical Manifestations Thalassemia minor (Thalassemia trait) ○ Often asymptomatic** ○ Mild to moderate anemia (Hgb 6 - 12) ○ Mild splenomegaly, bronzed skin color, and bone marrow hyperplasia ○ Body adapts to the reduction of Hgb - thus no treatment is indicated Thalassemia major ○ Life-threatening disease** ○ Growth and development deficits ○ Jaundice is prominent ○ Splenomegaly, hepatomegaly, cardiomyopathy ○ Symptoms develop in childhood ○ *Bone marrow responds to the reduced O2-carrying capacity of the blood by increasing RBC production ○ Cardiac complications from iron overload, lung disease, HTN ○ Endocrine problems, thrombosis Interprofessional Care Thalassemia major ○ Blood transfusions or exchange transfusions with chelating agents that bind to iron to reduce iron overloading ○ Luspatercept-aamt (Reblozyl) Improves Hgb levels and reduces transfusion needs Blocks inhibitors of late-stage RBC production ○ Splenectomy ○ Hematopoietic stem cell transplantation (HSCT) Megaloblastic Anemias (Macrocytic) Characterized by abnormally large RBCs, which are easily destroyed Caused by impaired DNA synthesis - result sin defective RBC maturation B12 (Cobalamin) Deficiency Most common cause = pernicious anemia (prevents body from absorbing B12) Defect of the gastric mucosa resulting in decreased formation of intrinsic factor (IF) necessary for absorption of B12 Gastrectomy, gastric bypass Other causes preventing absorption - small bowel resection, involving ileum Ileitis (inflammation of ileum) Crohn's disease Signs/Symptoms *Smooth beefy red tongue, fatigue, lab values Also desire to eat ice or other non-food things (pica) Neurological symptoms ○ Peripheral neuropathy - paresthesia hands and feet, loss of balance (ataxia) ○ Altered mental status - impaired memory, confusion to dementia **may be confused with alzheimer’s disease - this is a nutritional problem Diagnostics Hgb may be low, MCV is high (macrocytic), everything else may be fine Transferrin and ferritin may be up Vitamin B12 is low Folate level is normal Abnormal schilling test - pernicious anemia cause Demonstrates inability to absorb vit B12, without IF Elevated serum MMA and homocysteine levels Interprofessional and Nursing Management Parenteral or intranasal administration of cobalamin is the treatment of choice ○ Patients will die in 1-3 years without treatment ○ Anemia can be reversed with ongoing treatment, but long-standing neuromuscular complications may not be reversible Folic Acid Deficiency Folic acid is needed for DNA synthesis ○ RBC formation and maturation Manifestations are similar to B12 deficiency, but if neurologic symptoms present, may be caused by thiamine deficiency Common causes include ○ Diet deficiency, malabsorption syndromes ○ Alcohol use and anorexia ○ Loss during hemodialysis Folate is a water-soluble vitamin It is not stored in the body. Deficiency can occur in just a few weeks. Diagnostics Hgb may be low MCV is high (macrocytic) Transferrin and ferritin may be elevated Vitamin B12 is normal Folate level is low Signs/Symptoms Symptoms of anemia as previously mentioned ○ Smoothie beefy red tongue, fatigue, lab values Neural tube defects in pregnant individuals ○ Deficiency can result in spina bifida  Folate supplements are given when pregnant Anemia of Chronic Disease - Anemia of Inflammation Underproduction of RBCs and mild shortening of RBC survival Can be caused by: ○ Cancer ○ Autoimmune and infectious disorders (HIV, hepatitis, malaria) ○ Chronic inflammation ○ Heart failure ○ Bleeding episodes Usually develops after 1-2 months of disease activity Can become severe if the underlying disorder is not treated Diagnostics High serum ferritin Increased iron stored Normal folate and cobalamin Treat underlying causes is best Blood transfusions for severe cases Limited use of erythropoietin therapy History Determine onset, duration of symptoms Obtain a complete medical and surgical history Physical Exam Guided by history Symptoms similar to that of iron deficiency anemia Findings depend more on the nature of underlying disease than on the anemia ALWAYS obtain stool for occult blood. Aplastic Anemia Pancytopenia (decrease in ALL blood cell types) ○ RBCS, WBCs, platelets Hypocellular bone marrow Ranges from moderate to very severe - potentially fatal *Activity of bone marrow is depressed or has ceased Affects all cells made by the bone marrow (pancytopenia) Cause - congenital or acquired; idiopathic or autoimmune Exposure to certain drugs (antineoplastics, sulfonamides, anticonvulsants such as dilantin) Infections (hepatitis B & C, cytomegalovirus) Radiation Clinical Manifestations Abrupt or insidious development Symptoms caused by suppression of any or all bone marrow elements General manifestations of anemia ○ Fatigue, dyspnea ○ CV and cerebral responses ○ Neutropenia, thrombocytopenia Diagnosis by laboratory studies Decreased Hgb, WBC, platelet values Decreased reticulocyte count Elevated serum iron and TIBC Hypocellular bone marrow with increases yellow marrow (fat content) Management Prognosis of severe untreated aplastic anemia is poor Immunosuppressive therapy and HSCT transplantation can be curative Anemia Caused by Blood Loss (Acute & Chronic) Anemia from blood loss may be caused by acute or chronic problems Acute blood loss occurs because of sudden bleeding ○ Trauma, complications or surgery, problems that disrupt vascular integrity ○ 2 clinical concerns: hypovolemic shock, compensatory increased plasma volume within diminished O2 carrying RBCs Clinical manifestations ○ Caused by the body’s attempt to maintain adequate blood volume and meet oxygen requirements ○ Clinical s/s Pain - internal bleeding, tissue distention, organ displacement, nerve compression Retroperitoneal bleeding - numbness, pain in lower extremities ○ SHOCK is a major complication Interprofessional and Nursing Management ○ Replace blood volume ○ Promote coagulation ○ Find the source of bleeding/stop blood loss ○ Correct RBC loss ○ Provide supplemental iron ○ May be challenging to prevent blood loss if caused by trauma ○ Postoperative patients - monitor blood loss, give blood products for anemia Chronic blood loss ○ Sources: bleeding ulcer, hemorrhoids, menstrual and postmenopausal blood loss ○ Management involves Identifying the source and stop bleeding Providing supplemental iron as needed Hemolytic Anemia Destruction or hemolysis of RBCs at a rate that exceeds production ○ Caused by problems intrinsic or extrinsic to the RBCs Intrinsic forms are usually hereditary and result from defects in RBCs themselves RBCs are normal in acquired forms, but damage is caused by external factors General manifestations of anemia Specific manifestations - jaundice, enlargement of spleen and liver Maintenance of renal function is a major focus of treatment Signs/symptoms ○ Cold reacting symptoms (Raynaud’s disease) Red cells clump in capillary beds Cyanosis, pain, paresthesia ○ Warm reacting symptoms Severe hemolysis-jaundice, splenomegaly CHF, palpitation Diagnosis ○ Coombs test - presence of antibody or complement Treatment - corticosteroids, transfusion, splenectomy Sickle Cell Disease (SCD) Group of inherited, autosomal recessive disorders (genetic) ○ An abnormal form of Hgb in RBC ○ Genetic disorder usually found routine neonatal screening ○ incurable , significantly affects quality of life An inherited disorder that affects the synthesis of Hgb HB S (sickle), replaces HB A (normal) Can carry oxygen, but when oxygen levels fall, the cells go into sickle shape which causes plugs in the circulation, leading to tissue ischemia also RBCs have a shortened life spain (7-20 days) Predominantly in african-american population Symptoms The results of blockage from the sickle cells ACUTE: ○ Pain in back, chest, extremities ○ Low grade fever, 1-2 days after onset of pain ○ Could have a stroke ○ Jaundiced CHRONIC: ○ Kidney ○ Vision ○ Musculoskeletal  ○ Spleen Complications Infection is a major cause of mortality ○ Spleen function becomes compromised from sickled RBCs ○ Pneumococcal pneumonia most common ○ Severe infections can cause gallstones ○ Can lead to shutdown of RBC production Acute chest syndrome ○ Pneumonia, tissue infarction, and fat embolism ○ Fever, chest pain, cough, lung infiltrates, and dyspnea ○ Pulmonary infarctions may cause: pulmonary hypertension, MI, cor pulmonale, HF, retinal detachment and blindness, renal failure, stroke Management Maintain adequate fluids Pain management Oxygen therapy Avoid high altitudes - why? - low oxygen! Treat infections promptly Screening for retinopathy Immunizations - pneumococcal, H. influenzae, Hepatitis Urgent visit to the hospital during crises Patient and caregiver support Polycythemia The production and presence of increased number of RBCs Primary polycythemia/polycythemia vera ○ A bone marrow disorder leading to an abnormal increase in blood cells: RBCs (mostly HCT) ○ Cause: genetic defect (primary) or oxygen deficit (secondary) ○ Result: HCT rises (>48% in women and > 52% in men); blood viscosity is high and patient is at risk for blood clots - DVT, strokes, MI ○ Increased blood viscosity and blood volume - now at risk for clotting!! ○ Splenomegaly and hepatomegaly Secondary polycythemia ○ Can be hypoxia-driven or hypoxia-independent ○ Hypoxia-driven hypoxia stimulates the kidneys to make EPO which stimulates RBC production ○ Hypoxia-independent - cancer or benign tumor tissue makes EPO Clinical Manifestations ○ Headache, dizziness, blurred vision, tinnitus, plethora, or ruddy complexion ○ Erythromelalgia (painful redness and burning of hands and feet) ○ Thrombo-embolism events, with stroke the most common event ○ Hemorrhagic events: bruising, GI bleed Treatment ○ Monitor Hgb, HCt levels ○ Periodic phlebotomy to maintain normal Hgb and HCT ○ Hydration to reduce blood viscosity ○ Chemotherapy to reduce number of RBCs or interferon to lower blood counts  Vascular Disorders Peripheral Artery Disease (PAD) Peripheral artery disease: Pathophysiology, Causes, Symptoms,… Involves thickening of the artery walls and progressive narrowing of arteries of upper and lower extremities. Lower limbs are most affected. ○ Symptomatic age 50-70; and earlier with diabetes ○ Increased prevalence in blacks Higher risk of mortality, CVD mortality, major coronary events, and stroke Pathophysiology and Etiology Atherosclerosis is the leading cause in majority of cases Gradual thickening and buildup of plaque from cholesterol Exact causes unknown; inflammation and endothelial injury play a major role Symptoms occur when vessels are 60-75% blocked Risk Factors SMOKING Diabetes HTN High cholesterol Age greater than 60 **having multiple risk factors increases risk for PAD Atherosclerosis often affects coronary, carotid, and lower extremity arteries Clinical Manifestation Intermittent claudication (ischemic muscle pain from lactic acid buildup) ○ Pain when walking - temporary ○ Resolves within 10 mins or less with REST. Paresthesia: numbness or tingling in the toes or feet from nerve tissues ischemia (loss of pressure and deep pain sensations from reduced blood flow). Pain at rest (aggravated by limb elevation, relieved by gravity) ○ Occurs more often at night Reduced blood flow to limb: ○ Thin, shiny, and taut skin ○ Loss of hair on lower legs ○ Diminished or absent pedal, popliteal, or femoral pulses ○ Pallor of foot with leg elevation - **remember pain is relieved by gravity ○ Reactive hyperemia (redness) of foot with dependent position Critical Limb Ischemia (CLI)  ○ Chronic ischemic rest pain lasting more than 2 weeks ○ Non Healing arterial leg ulcers or gangrene ○ At increased risk: diabetes, HF, history of stroke ○ Interprofessional care Revascularization via bypass surgery using autogenous vein Percutaneous transluminal angioplasty (PTA) IV prostanoids (iloprost) - not FDA approved for CLI Continue to decrease risk for CVD risk: statins, antiplatelet, ACE, and B-blocker ○ Conservative treatment Protect from trauma Decreases ischemic pain prevent/control infection Improve arterial perfusion - healing is unlikely without increasing blood flow Spinal cord stimulation - pain Angiogenesis - new blood vessel growth Complications of PAD Prolonged ischemia leads to: ○ Atrophy of skin and underlying muscles ○ Delayed wound healing and infection ○ Tissue necrosis ○ Arterial ulcers over bony prominences Most serious: ○ Non Healing arterial ulcers and gangrene - collateral circulation may prevent gangrene ○ May result in amputation if adequate blood flow is NOT restored and severe infection occurs (indicated with uncontrolled pain and spreading infection) Diagnostic Studies Doppler ultrasound - segmental BP Duplex Imaging - bidirectional, color doppler Ankle-brachial index (ABI) ○ Done using hand-held doppler ○ Calculated by dividing ankle systolic BP by the higher of the brachial SBPs ○ Falsely elevated results can be seen in older patients or those with diabetes Angiography and MRI Interprofessional Care & Risk Factor Modification Goal = reduce CVD risk factors ○ BP control (reduce sodium), smoking cessation, A1C < 7%, aggressive tx of hyperlipidemia Drug Therapy  ACE Inhibitors Decreases CV morbidity Ramipril (Altace) Decreases mortality Increases peripheral blood flow Increases walking distance Antiplatelet Aspirin - low dose Aspirin Clopidogrel (Plavix) For aspirin-tolerant pts Can be used in combination for high-risk patients Cilostazol (Pletal) Inhibits platelet aggregation **for tx of intermittent claudication Increase vasodilation Pentoxifylline (trental) Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity **for intermittent claudication Intermittent claudication - Walking is most effective exercise for individuals with claudication (30-45 mins 3/week) - Women have faster decline in mobility than men Nutrition Therapy ○ BMI < 25 ○ Waist circumference < 40 for men and < 35 for women ○ 3-5% weight loss yields reduces triglycerides, glucose, A1C, and decreased risk for type 2 diabetes ○ Recommend reduced calories and salt for obese or overweight persons Conservative Therapy ○ Protect from trauma ○ Decrease ischemic pain ○ prevent/control infection ○ Improve arterial perfusion - healing is unlikely without increasing blood flow ○ Spinal cord stimulation - pain ○ Angiogenesis - new blood vessel growth Interventional Radiology & Surgical Procedures ○ Percutaneous transluminal angioplasty (PTA) - catheter with balloon tip is inflated, dilating the vessel & stent is placed to hold artery open ○ Atherectomy - removal of obstructing plaque ○ Cryoplasty - combines PTA and cold therapy ○ Endarterectomy - open artery and remove plaque ○ Peripheral artery bypass surgery ○ Amputation - considered if necrosis, gangrene, or osteomyelitis develop ○ Nursing Assessment and Management  ○ Subjective data: health history, nutritional-metabolic, activity, exercise, functional health patterns ○ Objective: integumentary, CV, neuro, diagnostic ○ Overall goals Adequate tissue perfusion Relief of pain Increased exercise tolerance Intact, healthy skin on extremities Long-term antiplatelet/ASA therapy Graduated compression stockings Smoking cessation Acute Arterial Ischemic Disorders Etiology and Pathophysiology Sudden interruption in arterial blood supply to a tissue, organ, or extremity Can result in tissue death Causes: embolism, thrombosis, or trauma Thrombi from the left side of the heart may dislodge and travel anywhere in the systemic circulation Sudden local thrombosis may occur at the site of athersclerotic plaque Traumatic injury to an extremity may cause partial or complete blockage Clinical Manifestations 6P’s = pain, pallor, pulselessness, paresthesia, paralysis. Poikilothermia (inability to maintain temp in limb) ○ Should notify HCP if changes in 6Ps occur. Management ○ Early diagnosis and treatment ○ Anticoagulant - IV unfractionated heparin ○ Restore blood flow - remove thrombus ○ Percutaneous catheter ○ Thrombolytic dissolves clot over 24 to 48 hours ○ Requires close monitoring or catheter positions and bleeding at the insertion site ○ Surgical revascularization ○ Amputation Thromboangiitis Obliterans (Buerger’s Disease) Nonarthersclerotic, segmental, recurrent inflammatory disorder of the small and medium arteries and veins of the arms and legs ○ Discoloration of tips of fingers Most common in men younger than 45 years old with a history of tobacco and/or marijuana use without other CVD risk factors. Acute phase: inflammatory thrombus blocks vessel Chronic phase: thrombosis and fibrosis cause ischemia Symptoms:  ○ Intermittent claudication of feet, hands, or arms ○ Rest pain ○ Ischemic ulcerations ○ Changes in color and temp ○ Paresthesia ○ Superficial vein thrombosis ○ Cold sensitivity Raynaud’s Phenomenon May occur alone or with other diseases Hands cold, color change, throbbing pain Contributing factors: ○ Use of vibrating machinery ○ Work in cold environments ○ Exposure to heavy metals ○ High homocysteine levels Diagnosis: persistent symptoms for at least 2 years Nursing Care Patient education: prevent episodes ○ Avoid temperature extremes ○ No tobacco products ○ Avoid caffeine ○ No vasoconstrictor drugs ○ Stress management Drug Therapy ○ Sustained release calcium channel blockers to decrease vasospasm ○ Topical nitroglycerin 2% ointment Digital ulceration or critical ischemia ○ Prostacyclin infusion, antibiotics, analgesia ○ Surgical debridement ○ Botox and statins ○ Sympathectomy Nursing Management HR and BP control Anxiety Pain management Semi-fowler's position & quiet environment to decrease HR and SBP Observation of changes in the quality of peripheral pulses Discharge teaching If pain returns or symptoms progress, instruct the patient to seek immediate help Acute and Chronic Venous Disorders  Phlebitis: acute inflammation of the walls of small cannulated veins of the hand or arm (related to IV) ○ Manifestations: pain, tenderness, warmth, erythema, swelling, and palpable cord ○ Risk factors: irritation from the catheter, infusion of irritating drugs, and catheter location (area of flexion) ○ Treatment: remove catheter Edema - elevate Pain + inflammation - NSAIDs & warm/moist heat Venous Thrombosis ○ Formation of a thrombus (clot) with vein inflammation ○ Virchow’s triad - 3 key factors that cause venous thrombosis 1. Venous stasis - dysfunctional valves Dysfunctional valves, inactive extremity muscles At risk: ○ Obese, pregnant, long-distance travel ○ Chronic HF or Afib ○ Prolonged surgery or prolonged immobility 2. Endothelial damage: stimulates platelet activation and starts coagulation cascade, which predisposes the patient to thrombus development Direct damage - surgery, burns, IV catheter, trauma, prior VTE Indirect damage - chemo, diabetes, sepsis 3. Hypercoagulability of blood Very high risk for women who use tobacco, are childbearing age, take estrogen oral contraceptives, postmenopausal, over age 35, have family history of VTE Manifestations Lower extremity ○ Unilateral edema ○ Pain and tenderness with palpation ○ Dilated superficial veins ○ Full sensation in the thigh or calf ○ Red, warm, fever greater than 100.4 Inferior vena cava - legs edematous and cyanotic Superior vena cava - similar symptoms of arms, neck, back and face. Superficial vein thrombosis - deep veins of arms or legs, pelvis, vena cava, and pulmonary system Deep vein thrombosis (DVT) - most often occurs in iliac and/or femoral veins  Complications PE - pulmonary embolism - most serious complication Chronic thromboembolic pulmonary hypertension Post-thrombotic syndrome (PTS) - pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, and venous claudication Interprofessional Care Interventions based on: bleeding and thrombosis risk, PMH, current drugs, medical diagnoses, schedules procedures, and patient preferences. 3 VTE prevention measures: ○ Early and progressive mobilization ○ Graduated compression stockings (not recommended if VTE already exists) - if you already have clot, we do NOT want it to move! ○ Intermittent SCDs Drug therapy ○ Anticoagulants VTE prophylaxis: prevent clot formation Existing VTE: prevent new clot formation, spread of clot and embolization ○ Three classifications Vitamin K antagonists (VKA) - Warfarin/Coumadin Do not give with antiplatelets/NSAIDS Measure PT, INR Thrombin inhibitors (heparin) - monitor PTT Lovenox - LMWH Factor Xa Inhibitors: Apixaban (Eliquis) ○ Monitor INR (therapeutic 2-3), PTT Nursing Management Assessment ○ Subjective, objective data, important health information, functional health patterns, clinical problems, Planning goals ○ Nursing implementation: acute care - prevent thrombi and reduce inflammation ○ Monitor and reduce risk of bleeding ○ Teach importance of physical activity Discharge teaching ○ VTE risk factors: smoking, hormone therapy, travel, prolonged sitting, s/s of PE ○ Guidelines for follow-up - report or call ER Bleeding (urine, stool, vomit, nose, gums, skin) Severe headache, stomach pain, chest pain, palpitations, dyspnea, mental status changes  Inform all HCPs and dentists of anticoagulation Varicose Veins (varicosities) - Dilated greater than or equal to 3mm, tortuous (twist & turns)superficial veins Primary - weakness of vein walls Secondary - direct injury, previous VTE, or excessive dilation Congenital - chromosomal defects Reticular - flat, less tortuous, blue-green Telangiectasis - (spider veins) smaller than 1mm, blue-black, purple, or red Etiology and Pathophysiology - superficial veins in legs become dilated and tortuous from retrograde blood flow (flowing opposite direction of normal) and increased venous pressure Risk Factors: family history of venous problems, female, tobacco use, aging, obesity, multiparity, history of VTE, venous obstruction, phlebitis, leg injury, prolonged sitting or standing Diagnosis: examination & duplex ultrasound Interprofessional care Rest with limb elevation Graduated compression stockings Leg-strengthening exercises Weight loss Drug Therapy (venoactive drugs) Antioxidants Micronized Rutosides Proanthocyanidins Ruscus Interventions and Surgical Therapies Sclerotherapy - ablation of vein by direct injection of sclerosing agent Transcutaneous laser therapy or high intensity pulsed light therapy Endovenous ablation - radiofrequency or laser therapy Traditional = ligation of vein and branches (surgical procedure closing off blood vessel, closing off) Ambulatory phlebectomy Transilluminated powered phlebectomy Nursing Management Prevention ○ Avoid prolonged sitting or standing ○ Maintain ideal weight ○ Avoid injury ○ Avoid restrictive clothing ○ Walk every day Postoperative ○ Deep breathing ○ Neurovascular assessment ○ Elevate legs  ○ Graduated compression stockings Long term management ○ Improve circulation and appearance ○ Relieve discomfort ○ Avoid complications and ulcerations ○ Patient teaching Chronic Venous Insufficiency and Venous Leg Ulcers Abnormalities of the venous system include edema, skin changes, and venous leg ulcers Etiology and Pathophysiology ○ Primary varicose veins and Post thrombotic syndrome (PTS) ○ Ambulatory venous HTN Serous fluid and RBC leak results in edema and chronic inflammatory changes Hemosiderin - brown skin discoloration Skin is hard, thick, and contracted Clinical manifestations ○ Lower leg - brown, leather and edematous ○ Eczema with itching and scratching ○ Venous ulcers ○ Pain especially in dependent position ○ Risk of infection Interprofessional and nursing care ○ Compression for healing and prevention of recurrence ○ Activity guidelines and limb positioning ○ Wound care and dressings - moist environment ○ Nutrition - adequate protein, vitamins A and C, zinc ○ Monitor for infection ○ Drug therapy - pentoxifylline or micronized flavonoid fraction ○ Other: skin replacement (graft) ○ Daily moisturizing  Test = CBC - low hgb, low hct, MCV (high or low): high = macrocytic, low = microcytic Serum ferritin (low = iron def) TIBC (high = iron def.) Type Cause Symptoms Labs Nursing Management Treatment Nutritional anemia Chronic blood loss, menstruation, Few symptoms until HCT < 30 (Iron Deficiency) inadequate dietary intake, pallor , glossitis, cheilitis, inadequate absorption of iron headache, paresthesia from GI tract, GI surgeries Megaloblastic Anemias - Large SIZE **below Thalassemia Inadequate production of normal Thalassemia minor - often n/a Blood transfusions or exchange Hgb that results in decreased - asymptomatic transfusions RBC production - mild to moderate anemia Thalassemia major Luspatercept-aamt (Reblozyl) - Life threatening - Improves Hgb levels - Jaundice, enlarged SPlenectomy organs, growth and Hematopoietic stem cell development deficits transplantations (HSCT) B12 (Cobalamin) Deficiency Most common - pernicious Smooth beefy red tongue, Hgb - low If not treated, it can be fatal. Parenteral or intranasal anemia fatigue, desire to eat ice or other MCV - high (macrocytic) administration of cobalamin non-food things B12 - low Early detection and tx is Gastrectomy, gastric bypass, Transferrin and ferritin - higher important. small bowel resection (causes Neurological symptoms: Folate - low preventing absorption) peripheral neuropathy, altered Abnormal schilling test Assess for neurological problems mental status not corrected by replacement therapy. Ensure safety from falling. Folic Acid Deficiency Diet deficiency, malabsorption Smooth beefy red tongue, fatigue Hgb - low syndromes - Similar to other anemias MCV - high (macrocytic) Folic acid is needed for DNA Folate - low synthesis (RBC formation and Alcohol use and anorexia Neural tube defects in pregnant Transferrin and ferritin - higher maturation) Loss during hemodialysis individuals (can result in spina bifida) Anemia of Chronic Disease Cancer, autoimmune, chronic Similar to iron deficiency anemia Serum ferritin - high History - onset, duration of (Anemia of Inflammation) inflammation, heart failure, Iron stores - increased symptoms bleeding episodes Normal folate and cobalamin Physical Exam -symptoms similar to iron deficiency anemia -ALWAYS obtain stool for blood occult Aplastic anemia Congenital or acquired General anemia Hgb - low **prognosis of severe untreated manifestations: Fatigue, WBC - low aplastic anemia is poor *pancytopenia - decrease in ALL Infections, radiation, certain dyspnea, CV and cerebral Platelets - low blood cell types drugs responses, neutropenia, Serum iron and TIBC - high Immunosuppressive therapy and thrombocytopenia HSCT transplantation can be Bone marrow cannot make curative. enough new blood cells Acute Blood Loss Occurs from sudden bleeding *caused by body’s attempt to - Trauma, complications of maintain adequate blood volume surgery and meet oxygen requirements - Pain - internal bleeding - Retroperitoneal bleeding - SHOCK Chronic Blood Loss Bleeding ulcers, hemorrhoids, Identify source and stop menstrual and postmenopausal bleeding, provide supplemental  blood loss iron as needed Hemolytic Anemia Sickle Cell Inherited disorder, genetic, Acute: pain in back, chest, Oxygen therapy!! incurable extremities, low grade fever, Maintain fluids -inherited disorder that affects jaundice Pain management synthesis of hemoglobin. **low oxygen causes cells to Treat infections promptly sickle and RBCs have shortened Chronic: kidney, vision, life spain (7-20 days) musculoskeletal, spleen Infection is a major cause of mortality. Polycythemia Vera -bone marrow disorder leading to Headache, dizziness, blurred High HCT Patient at risk for blood clots, abnormal increase in RBCs vision, tinnitus, erythromelalgia, DVT, strokes MI *increased RBCs (increased HCT) thrombo-embolism events, -bone marrow disorder leading to hemorrhagic events Monitor Hgb and Hct abnormal increase in RBCs -increases blood viscosity and Periodic phlebotomy (increased HCT) blood volume (thicker blood) hydration  Alterations in Urinary Elimination Urinary System Upper (kidneys and ureters) ○ KIDNEYS = principal organ - maintaining homeostasis Functions: regulate volume and composition of ECF, excrete waste products, control BP, make erythropoietin (RBC production) , activate vitamin D, and regulate acid-base balance. Lower: ○ Bladder: serve as a reservoir for urine and to eliminate waste products from the body. Normal urine output = 1500 mL/day An adult will typically urinate 5-6 timers per day ○ Urethra Functions: allows passage of urine and semen Kidneys (Microstructure) - filter blood Nephron = functional unit of the kidney which contains: ○ Glomerulus: blood is filtered here! GFR - amount of blood filtered each minute by the glomeruli Normal rate = 125mL/min Want it to be > 60mL/min Low GFR is an indication that your kidney is failing. ○ Bowman’s capsule: unfiltered blood crosses the membrane and enters the Bowman's capsule ○ Tubular system: reabsorption of nutrients Blood flow to the kidneys = 1200 mL/min - accounts for 20-25% of CO Renal arteries -> arterioles -> capillaries -> glomerulus Aging & the Urinary System Decrease in size & weight with age Around age 70, glomeruli function is reduced Atherosclerosis - can cause reduced blood flow to GU system Altered urinary concentration & excretion - incontinence Not able to compensate as well Female - loss of elasticity & muscle support (encourage kegel exercise) Male - prostate enlarges ○ ¼ males will have BPH (enlarged prostate) Lab Changes ○ GFR ○ BUN/Creatinine ○ Creatinine clearance Assessment of the Urinary System 1. Health History: ask about presence or history of kidney disease or other urologic problems. Note specific urinary problems such as cancer, infection, BPH, and stones. a. Are there any other health problems that may affect kidney function? - HTN, diabetes, HIV, trauma, etc. HTN is #1 risk factor for kidney issues! 2. Current Symptoms/Vital Signs 3. Medications a. Many drugs are nephrotoxic and certain drugs may alter the quantity and character of urine output (diuretics). b. Anticoagulants may cause hematuria. c. Antibiotics: penicillins, gentamicin, steroids 4. Surgeries & radiation/chemo 5. Nutrition & fluid intake a. Dehydration may contribute to UTIs, stones, and kidney failure b. Large intake of dairy or high protein may lead to stone formation c. Asparagus can cause urine to smell musty d. Beets can cause red urine e. Caffeine can cause frequent urination 6. Elimination issues a. Daytime voiding frequency? b. Nocturia? c. Urgency, incontinence, retention? 7. Occupation Urinalysis - general exam of urine to establish baseline information or provide data to establish a tentative diagnosis and determine if further studies are needed. **clean catch (voided) ** catheter (from port) Test Normal Abnormal Possible Cause & Significance Bilirubin none present Liver problems. May appear before jaundice is visible. Casts None. occasional present Molds of the renal hyaline tubules that may contain protein, WBCs, RBCs, or bacteria. Noncellular casts (hyaline) occasionally found in normal urine. Color Amber yellow Dark, smoky color Hematuria Yellow-brown to olive Excess bilirubin. green  Orange-red to Phenazopyridine or orange-brown rifampin Cloudiness of fresh UTI urine Colorless urine Excess fluid intake, kidney disease, or diabetes insipidus. Culture for organisms No organisms in Bacteria counts > 10^5 UTI bladder Glucose none glycosuria Diabetes, low renal threshold for glucose. Pituitary problems. ketones none present Altered carbohydrate and fat metabolism in diabetes and starvation; dehydration, vomiting, severe diarrhea. odor aromatic Ammonia-like Urine allowed to stand. Unpleasant odor UTI Osmolality 50-1200 < 50 Tubular dysfunction > 1200 Kidney lost ability to concentrate or dilute urine pH 4.6-8.0 >8.0 UTI Protein Random protein Persistent proteinuria Acute and chronic kidney disease. HF RBCs 0-4 < 4.0 Respiratory or metabolic acidosis > 4.0 Stones, cystitis, cancer, UTI, trauma, etc. Specific Gravity 1.005-1.030` Low Dilute urine, excess diuresis, diabetes insipidus High Dehydration, glycosuria Fixed at 1.010 Renal inability to  concentrate urine; end stage renal disease. WBCs 0-5 >5 UTI, inflammation Diagnostics/Labs Diagnostic Test Description Therapeutic range/Test findings BUN/Creatinine Detect renal problems; regulated BUN: 10-20 by the rate at which urea is Cr: 0.5 - 1.2 excreted Creatinine Clearance Waste product of protein Male: 107-139 ** measure or creatinine in a breakdown (primarily body Female: 87-107 24-hour period muscle mass); approximates the GFR Culture/Sensitivity Tests to see if bacteria are Should be unremarkable ** tells us what antibiotic we present in urine. need to use Urine Cytology Takes biopsies of the bladder if Should be unremarkable ** looks for cancer cells there is a suspicion of bladder cancer KUB X Ray Look at kidneys, ureters, and the Should be unremarkable bladder. IVP (intravenous pyelogram) Evaluates size of the kidneys Should be unremarkable bladder and ureters after iodine injection. Can be nephrotoxic to pt; hydration is important **need dye! **should ask if they are allergic to dye Ultrasound/CT **ultrasound is safer than CT Should be unremarkable Urinary Tract Infection (UTI) Description Infections of the urinary tract. E.coli is the most common pathogen (75% of cases) Other: pseudomonas, streptococci, staphylococci, enterococci, fungal, klebsiella Classification - based on location. Upper ○ kidneys/ureters ○ Systemic symptoms ○ Pyelonephritis - inflammation of renal parenchyma and collecting system Inflammation of the renal parenchyma and collecting system. Most common cause is bacterial infection. (inflammation of kidneys) Clinical Manifestations - **systemic effects! fever/chills N/V Malaise Flank pain They may include - dysuria, urgency, frequency CVA tenderness usually present ] Treatment/Interprofessional Care Involves upper urinary system (can start from the bladder) Tests ○ Utilize many of same tests ar uncomplicated UTI ○ May also do CT, urogram, cystoscopy ○ Labs: CBC, CMP/BMP, urine cultures, blood cultures renal function studies ○ Urinalysis - results may show pyuria (WBCs), bacteriuria, and hematuria ○ Urine for culture and sensitivity ○ Ultrasound ○ CT - can assess for signs of infection in kidney and complications ○ CBC ○ Percussion for CVA tenderness (flank pain) Medication ○ Antibiotics (empiric until C&S returns) Ampicillin, fluoroquinolones (ciprofloxacin, levofloxacin), vancomycin (ototoxicity, red man's syndrome) May need to be given IV Longer course of antibiotics Goal = to convert to PO meds when/if possible Patient teaching ○ Finish all antibiotics ○ Do not hold in urine ○ May need to refer to kidney specialist ○ Drink more fluid Nursing diagnosis: altered urinary function, risk for decreased kidney perfusion Lower ○ bladder/urethra ○ Usually local symptoms ○ Cystitis - inflammation of the bladder (bladder infection) ○ Urethritis - inflammation of the urethra Causes: STI, ,bacteria, viruses, fungal  Treatment = depends on causative organism Difference between cystitis and urethritis is in urethritis you will see discharge. Often tied to chlamydia, so need to get the partner tested if they have urethritis. Urosepsis: UTI spread beyond GU system ○ life-threatening! ○ Can lead to shock and organ failure ○ Encourage fluid intake, avoidance of irritants, voiding hygiene, monitor VS! ○ Most common cause of bacterial sepsis in elderly ○ TIME (when it comes to sepsis, it’s about TIME) Temperature (higher or lower than normal) Infection (may have s/s) Mental Decline (confused, sleepy, difficult to arouse) Extremely ill (“i feel like I might die,” severe pain or discomfort) ○ Nursing Care Ensure adequate fluid intake Educate pt to avoid irritants Encourage pt to void Correct cleaning after voiding Monitor VS for s/s of sepsis Medication administration Uncomplicated: occurs in pts with no urinal structure/function deficit ○ Localized infection in lower urinary tract; typically bladder ○ Usually respond well to antibiotics. Complicated: occurs in pts with an underlying disease or with a structural or functional proble