384 Focus exam 1 Fluid and electrolyte imbalances (Na+, Calcium, K+, Magnesium) Sodium (Na) 135-145 *BRAIN/ Neurological* Imbalances typically associated with parallel changes in osmolality. Plays a major role in: Extracellular fluid (ECF) volume and concentration, generation and transmission of nerve impulses, muscle contractility & acid base balance HYPONATREMIA -Loss of sodium containing fluids or from water excess Causes: loss of sodium rich blood from draining wounds, diarrhea, vomiting, primary adrenal insufficiency, inappropriate use of sodium free or hypotonic IV fluids, giving fluids to patient w/ renal failure, SIADH Manifestations: Mild: headache, irritability, difficulty concentrating Severe: confusion, vomiting, seizures, coma Risk for: Electrolyte imbalance, injury, acute confusion Potential complication: Severe neurologic changes Nursing Implementation: Cause is water excess: Fluid restriction, loop diuretics à Severe symptom (seizures) give small amount of IV hypertonic saline solution (3% NaCl) Cause is abnormal fluid loss: fluid replacement with sodium containing solution, increase oral intake, withhold diuretics, drugs that block vasopressin (ADH) à Convaptan (Vaprisol): given for water excess & Tolvaptan (Samsca): given for hyponatremia from heart failure or SIADH -Sodium serum should not increase more than 6-12 mEq/L per hour in 24 hours à can cause osmotic demyelination syndrome w/ permanent damage to nerve cells in the brain -Accurate urine output is essential -Initiate seizure precautions HYPERNATREMIA -Inadequate water intake, excessive water loss or sodium gain -Causes hyperosmolality leading to cellular dehydration -Primary protection is thirst from hypothalamus Causes: Diabetes insipidus, IV administration of hypertonic saline or sodium bicarbonate, sodium containing drugs, excessive sodium intake Manifestations: Thirst, AMS (agitation, delirium, restlessness, confusion, lethargy), weakness, tetany, (High temp, BP, ADH & Aldosterone) Risk for: Electrolyte imbalance, fluid volume deficit & injury Potential complication: Seizures and coma Nursing Implementation: Treat underlying cause à Cause is water deficit- replace fluid orally or IV with isotonic or hypotonic fluids. Cause is excess sodium- dilute with sodium free IV fluids (such as 5% dextrose in water) and promote excretion with diuretics -Initiate seizure precautions & restrict sodium - Sodium serum shouldn’t decrease more than 8-15 mEq/L in an 8 hr period à can cause rapid shift of water into cells causing cerebral edema and neurological complications 1 Potassium (K) (3.5-5) *Cardiac) Major intracellular fluid (ICF) cation & regulated by kidneys. Necessary for transmission and conduction of nerve and muscle impulses, cellular growth, maintenance of cardiac rhythms, acid-base balance Sources: Fruits & veggies (bananas & oranges), salt substitutes, potassium medications & stored blood HYPOKALEMIA Causes: Increased loss of potassium via the kidneys or gastrointestinal tract (laxative misuse, vomiting, diarrhea, ileostomy drainage), increased shift of K+ from ECF to ICF, dietary K+ deficiency (rare) Manifestations: Cardiac (weak irregular pulse, arrythmias, ST depression, flattened T wave, prominent U wave), skeletal muscle weakness (legs), weakness of respiratory muscles, decreased GI motility, hyperglycemia, low tendon reflexes, fatigue & lethargy Risk For: electrolyte imbalance, activity intolerance, injury Potential complication: Dysrhythmias (heart block & lethal ventricular dysrhythmias) Nursing Implementation: KCl supplements orally or IV (always dilute IV KCl, NEVER give KCl via IV push or as a bolus, should not exceed 10 mEq/hr, use an infusion pump), consume potassium rich foods (fruits & veggies, bran, chocolate, peanut butter, milk, yogurt nuts and seeds) -Severe hypokalemia can cause paralysis HYPERKALEMIA Causes: impaired renal excretion, massive intake shift from ICF to ECF (includes acidosis, or massive cell destruction such as burns or severe infection) -Digoxin like drugs and b adrenergic blockers can impair entry of potassium into cells resulting in high ECF potassium concentrations -NSAIDS, potassium sparing diuretics, angiotensin II receptor blockers and ACE inhibitors can cause hyperkalemia by reducing kidneys ability to excrete calcium à Most common cause: Renal failure Manifestations: Cardiac dysrhythmias (bradycardia, peaked T wave, widened QRS, prolonged pr interval, elevated ST segment), cramping leg pain, weak or paralyzed skeletal muscles, abdominal cramping, Increased GI motility (diarrhea), paresthesia (pins & needles) Risk for: Electrolyte imbalance, activity intolerance, injury Potential complication: Dysrhythmias (heart block, ventricular fibrillation (Vfib), or cardiac standstill Nursing Implementation: Eliminate oral and parenteral K intake & Increase elimination of K (diuretics, dialysis, kayexalate). Force potassium from ECF to ICF by IV insulin and a b- adrenergic agonist or sodium bicarbonate. Stabilize cardiac membranes by administering IV calcium chloride or calcium gluconate. -Use continuous ECG monitoring (those with dangerous dysrhythmias à give IV calcium immediately & monitor BP, giving rapid calcium can result in hypotension) -Monitor for hypoglycemia when giving insulin and give glucose as needed 2 Calcium (Ca) 8.5-10.5 *Muscles* Functions: Formation of teeth and bones, blood clotting, transmission of nerve impulses, myocardial contractions, muscle contractions. Obtained from ingested foods & need vitamin D to absorb. Present in 3 forms: ionized calcium is biologically active. Changes in pH and serum albumin affect levels. Balance controlled by: parathyroid & calcitonin HYPOCALCEMIA Causes: Low levels caused by decreased production of PTH, multiple blood transfusions, alkalosis, increased calcium loss Manifestations: Positive Trousseau’s (carpal spasm from BP cuff being inflated) or Chvostek’s (facial muscle contraction when tapping Infront of ear) sign, laryngeal stridor, dysphagia, tingling or numbness around the mouth or in the extremities, cardiac dysrhythmia, tetany, hyperactive reflexes Risk for: Electrolyte imbalance, ineffective breathing pattern, acute pain, injury Potential complication: fracture, respiratory arrest Nursing Implementation: Treat cause à oral or IV calcium supplements, rebreathe into paper bag, treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis -Closely assess patient who had thyroid or neck surgery for manifestations of hypocalcemia due to proximity of surgery to the parathyroid glands HYPERCALCEMIA Causes: Hyperparathyroidism (two thirds of cases) & Cancer malignancy Manifestations: Fatigue, lethargy, weakness, confusion, hallucinations, seizures, coma, cardiac dysrhythmias, bone pain, fractures, nephrolithiasis, polyuria, dehydration, low muscle tone, low reflexes, stupor, N/V Risk for: Electrolyte imbalance, inactivity intolerance, injury Potential complication: Dysrhythmias à Heart block and ventricular tachycardia (Vtach) Nursing Implementation: Excretion of calcium w/ loop diuretic, hydration with isotonic saline infusion, low calcium diet, mobilization, bisphosphonates (gold standard treatment when caused by cancer), IM or SC calcitonin -Excess calcium acts like a sedative leading to reduced excitability of muscles and nerves -Must drink 3000-4000mL fluid daily to prevent kidney stone formation (cranberry and prune juice will also help prevent stone formation) -Receive calcitonin injection for immediate effect à can result in tachycardia 3 Magnesium (1.3-2.1) *Muscles/ neurological* Coenzyme in metabolism of carbohydrates. Required for DNA and protein synthesis, blood glucose control, BP regulation & necessary for ATP production. Acts directly on myoneural junction, important for normal cardiac function, 50-60% contained in bone, absorbed in GI tract & excreted by kidneys. HYPOMAGNESEMIA Causes: Prolonged fasting or starvation, chronic alcoholism, fluid loss from GI tract, prolonged parenteral nutrition without supplementation, diuretics, hyperglycemic osmotic diuresis, chronic alcohol use Manifestations: Hyperactive deep tendon reflexes, muscle cramps, tremors, seizures, dysrhythmias, tachycardia, corresponding hypocalcemia & hypokalemia, Positive Trousseau’s (carpal spasm from BP cuff being inflated) or Chvostek’s (facial muscle contraction when taping Infront of ear) sign, dysphagia, N/V Management: Treat underlying cause, oral supplements, increase dietary intake, parenteral IV or IM magnesium when severe -Diuretics, proton-pump inhibitors & certain antibiotics can lead to magnesium loss -If deficiency is severe or if hypocalcemia is present IV magnesium (mag sulfate) is given à use infusion pump and watch monitor since rapid administration can lead to hypotension and cardias or respiratory arrest HYPERMAGNESEMIA Causes: Increased intake or ingestion of products containing magnesium when renal insufficiency or failure is present & Excess IV magnesium administration Manifestations: Lethargy, N/V, impaired reflexes, muscle paralysis, bradycardia, low BP, respiratory and cardiac arrest Management: Prevention first à restrict magnesium intake in high risk patients. IV CaCl or calcium gluconate if symptomatic. Fluids and IV furosemide to promote urinary excretion & dialysis. -Can develop in a pregnant woman taking magnesium sulfate for treatment of eclampsia -Avoid magnesium containing foods (green veggies, nuts, bananas, oranges, peanut butter, chocolate) 4 What causes edema? Best objective way to assess fluid balance? • • • Edema occurs if venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic pressure rises. May also develop if an obstruction of lymphatic outflow causes a decrease in the removal of interstitial fluid o Plasma to interstitial fluid shift results in edema o Interstitial fluid drawn into plasma decreases edema Fluid spacing: distribution of body water o First spacing: normal distribution of fluid in ICF & ECF o Second spacing: abnormal accumulation of fluid (edema) o Third spacing: fluid collects in nonfunctional area of cells, (fluid is trapped where it is difficult or impossible for it to move back into cells or blood vessels) Assess fluid balance: o Daily weights o Intake (Proper fluid balance is intake of 2000-3000mL) o Output (urine specific gravity: Greater than 1.025 = concentrated & less than 1.010 = dilute) o Assess Skin turgor à à à à à à à à à o Labs § Fluid volume deficit = increased BUN, sodium, hematocrit, plasma & urine osmolality § Fluid volume excess= decreased BUN, sodium, hematocrit, plasma & urine osmolality When to use a hypertonic, hypotonic or isotonic solution Hypotonic • • More water than electrolytes Pure water lyses RBCs o Water moves from ECF to ICF by osmosis o Usually maintenance fluids o Monitor for changes in mentation à Treats hypernatremia & good maintenance fluid Isotonic • • • Expands only ECF No net loss or gain from ICF Ideal to replace ECF volume deficit àIdeal fluid replacement for patient with ECF volume deficits, surgery, burns, or GI fluid losses Hypertonic • • Initially expands and raises the osmolality of ECF Require frequent monitoring of: Blood pressure, lung sounds & serum sodium levels à Ideal for hyponatremia and trauma patients with head injury 5 ABG interpretation & assessment findings Practice: Respiratory alkalosis-Hyperventilation -Cause: hypoxemia from acute pulmonary disorders (pneumonia, pulmonary embolus) 6 Respiratory acidosis-Hypoventilation Metabolic acidosis- Acid other than carbonic acid accumulates in the body or when bicarbonate is lost in body fluids Metabolic alkalosis- Loss of acid or gain in HCO3 occurs 7 Anemia Decreased RBCs • Lack of B12, B9, FeSo4 Blood loss • Ulcer, trauma RBC destruction • Sickle cell, incompatible blood à Can lead to tissue hypoxia Mild = Hgb 10-12 g/dl (may not have symptoms) Moderate = Hgb 6-10 g/dl (increase in cardiopulmonary symptoms) Severe = Hgb <6 g/dl (many manifestations involving multiple systems) à Labs: HGB- (hemoglobin)Amount of oxygen carrying molecule in blood o Male: 14-18 o Female: 12-16 HCT- (hematocrit) Percent of RBC in blood o Male: 40-50% o Female: 36-44% MCV- (mean corpuscular volume): Measures the relative size of RBCS o 80-100fl CBC (complete blood count) to Diagnose à Check RBC & HGB to evaluate therapy response 8 Normocytic Anemia à 80-100fl Normal Usual causes: -Sudden blood loss -Prosthetic heart valves -Tumor -Long term disease -Decreased erythropoietin caused by renal failure -Blood loss can also be normocytic -Sickle cell disease Microcytic Anemia à < 80fl Decreased Usual causes: -Iron deficiency o Chronic blood loss -Lead poisoning -Thalassemia -Inflammation Macrocytic Anemia à > 100fl Increased Usual causes: -Chemotherapy -Folate deficiency -Cobalamin (Vit B12) deficiency -Alcoholism How to take orthostatic vital signs: 1. Have patient lie flat for 5 minutes. 2. Take heartrate and BP 3. Sit them up and wait 1-3 minutes 4. Take heartrate and BP 5. Stand them up and wait 1-3 minutes 6. Take heartrate and BP If systolic drops by 20/ diastolic drops by 10/ If HR increases by 20 / If patient dizzy when stands = Orthostatic vital signs TIBC – Total iron binding capacity • Measures proteins (i.e., transferrin) that bind or transport iron between bone marrow to tissues • Increased in iron deficiency, decreased in chronic dz (how much iron is in blood stream) Transferrin Saturation • Measures amount of iron ready to use for erythropoiesis • Ferritin is a carrier protein which transports iron in circulation • Decreased in iron deficiency, normal or decreased in chronic disease (total iron stores in body) 9 Ferritin • Correlates with normal body iron stores (1 mg/ml of ferritin = 8-10 mg of stored iron) • Ferritin is present I liver, spleen, bone marrow, brain, kidneys, etc. It is the storage form of iron. • Decreased in iron deficiency, normal in chronic disease (binds and transports iron in blood stream) Nursing Interventions: • Assess high risk patients • Assess for improving or worsening symptoms • Administer blood products – watch for reactions • Monitor lab values and vital signs • Oxygen therapy to stabilize patient • Keep environment safe - monitor for falls, burns, paresthesia • Patient education (increase folic acid and iron containing foods, stop drinking, medications) • Iron therapy • Medications such as erythropoietin (EPO) & vitamin supplements • Alternate periods of rest with activity (Especially after meals to decrease competition for supply to vital functions) • Aid with regular physical activities • Treat the cause Iron Deficiency Anemia à Most common nutritional disorder in the world (Inadequate diet intake, malabsorption, blood loss, or hemolysis) Drug Therapy: à Oral ferrous sulfate or ferrous gluconate (can stain teeth use straw & sit upright 30 min after taking) à IM or IV iron dextran, sodium ferrous gluconate, iron sucrose à Transfusion of RBCS Oral iron is a good option but consider these factors: • Enteric coated or sustained release tablets are counterproductive and expensive • Daily dose should be 150-200mg (can be taken in 3-4 doses) • Iron best absorbed in an acidic environment (take an hour before meals) • Take with vitamin C enhances absorption Blood Transfusions 1. 2. 3. 4. Consent signed Two licensed RNs must identify patient Vitals signs before for baseline ***Remain with the patient during the first 15 minutes or 50 ml of infusion, then retake vital signs 5. Give between 2-4 hours in most patients 6. Observe for reactions: hemolytic (due to ABO incompatibly), febrile, allergic, circulatory overload, etc. 10 How to know patient is having a reaction: • Free hemoglobin in urine or blood • Fever • SOB • Adventitious lung sounds • Any change in vital signs (i.e., hypertension, hypotension, tachycardia, tachypnea) • Nausea, weakness • Shivering or shaking What to do if patient is having a reaction: • Stop (if severe) or slow down (if mild) transfusion depending on agency protocol. • • • • • Infuse NS Notify provider Monitor Vital signs Administer medications and oxygen as prescribed. Notify the blood bank. DO NOT DISCARD BLOOD. Return blood to lab!! Polycythemia à Production and presence of increased numbers of RBCS: increase can be so great that blood circulation is impaired à bone marrow dysfunction v Causes hyper-viscosity & hypervolemia v Clotting is a complication à 2 types: Primary polycythemia (polycythemia vera) & Secondary polycythemia • Primary: referred to as Polycythemia Vera o a myeloproliferative chromosomal disorder o Increased RBCs, WBCs, and platelets o Median age 60 > males • Secondary: a physiological compensation to chronic hypoxemia o High altitudes, pulmonary disease & heart disease Medical Interventions: • Reduce blood volume o Phlebotomy (500 ml every 3 months) • Hydration to reduce viscosity • Medications o Myelosuppressive agents (Hydrea, Myleran) o Low dose ASA (prophylaxis of vascular events) o Interferon alpha o Allopurinol (reduce gouty attacks) • Nutritional evaluation 11 Symptoms: • Headache • • • • Shortness of breath Weakness Double vision Sweating, particularly at night Dizziness Weight loss Pain and swelling in the joint (especially in the big toe) • • • Diagnostic tests findings: • Elevated Hgb & RBC count Elevated WBC count Elevated Platelet count EPO levels elevated • • • Nursing Interventions: • • • • • Monitor lab values Control hypoxia to prevent secondary polycythemia vera Perform or assist with phlebotomy Monitor I & O – this ensures hydration Prevent thrombus formation o Ambulate patient o Give ASA Thrombocytopenia • • • • Reduction in platelets below 150,000/ microliter Under 80,000/microliter indicates high risk for hemorrhage Platelets live 10 days Interventions are working when Produced in bone marrow patient has no evidence of bleeding or bruising Major Types: 1. Hereditary • Hemophilia & Von Willebrand Disease (clotting factor abnormalities) 2. ITP (AKA: Immune thrombocytopenia) Prolonged bleeding usually • Lifespan of platelets decreased due to autoimmune processes does not occur until 50,000 3. TTP (AKA: Thrombotic thrombocytopenia) at 20,00 life threatening • Uncommon – caused by deficiency of plasma enzyme, meds, lupus bleeding usually occurs 4. DIC (AKA: Disseminated intravascular coagulation) • Clotting and bleeding occurs at same time due to causes such as arrest, septicemia, and hemorrhage 5. HIT (AKA: Heparin induced thrombocytopenia) Causes: • Decreased production (bone marrow suppression) • Trapped in the spleen (splenomegaly) • Medication o Aspirin, Quinine, Thiazides, Digoxin 12 Labs: Hereditary ITP DIC HIT Platelet Low Low Low Low Size platelets Normal Abnormal Normal Normal PT* Normal Normal ***High Normal Aptt* Normal Normal ***High Normal à Most lab values will be similar for different thrombocytopenia’s, except for DIC where there are low platelets and increased bleeding times. à PT – Prothrombin: Measure of Vitamin K dependent clotting ability. We are using mainly INR to replace the PT value now because it is more accurate. aPTT – Activated partial thromboplastin time: How long blood takes to clot with additives. Lab Values for DIC: • If PT and PTT are elevated – think DIC Assessment: • Petechia - tiny red dots under the skin that are a result of very small bleeds • Purpura - the purple color of the skin after blood has "leaked" under it. Diagnostic findings: • Platelets less than 150,000/ microliter • Normal PT, PTT • Bone marrow biopsy • à Prolonged bleeding usually does not occur until 50,000 at 20,00 life threatening bleeding usually occurs • àIf PT and PTT are elevated – think DIC Treatment: Medications: Depends on cause: -ITP: Corticosteroids and immunosuppressants • First step: Stop heparin and avoid future heparin (If HIT) -HIT: Anticoagulants with direct thrombin • Avoid other anticoagulant/antiplatelet medications inhibitors: • Platelet infusion for severely low counts - Argatroban, lepirudin, bivalirudin • Splenectomy -Recall that thrombin initiates hemostasis by activating other clotting factors • Immune suppression for autoimmune etiology -DIC: Anticoagulants (heparin) can be used to • Oprelvekin (Neumega) – a platelet growth factor decrease microclots from forming and using • Corticosteroids up clotting factors Collaborative Care: 13 • • • • • Early detection is essential Treatment of underlying cause Replacement of missing factors for severe hemorrhage o Cryoprecipitate, FFP, Platelets Prevent exsanguination Drug treatments are controversial and not highly effective (heparin, amicar, lovenox) Nursing Care: • Protect from injury • Transfusion of platelets • Avoid IM injections/procedures/central lines • Monitor labs, vital signs, assessments • Monitor response to and side effects from medications • Education: Soft toothbrush ok, avoid injury, pressure dressings, watch for signs bleeding (tarry stools, etc.) Immune Thrombocytopenia Causes: acquired immune disorder from impaired platelet production & T cell mediated destruction of platelets. Infection such as Helicobacter pylori or HIV contribute to this disorder. Treatment: High dose of IV immunoglobulin (IVIG) may be used for patient who is unresponsive to corticosteroids or splenectomy. Immunosuppressive therapy may be used in refractory cases & platelet transfusions may increase platelet counts in cases of life-threatening hemorrhage. DIC (Disseminated intravascular coagulation) à A serious disorder in which the proteins that control blood clotting become overactive. DIC begins with excessive clotting and followed by excessive bleeding. o Sudden DIC: follows surgery or childbirth, bleeding may be uncontrollable. Bleeding may occur at the site of an intravenous injection or in the brain, digestive tract, skin, muscles, or cavities of the body, sepsis. o Slow DIC: cancer, aneurysms (DVT, PE will develop) Causes: Inflammation in response to injury, infection, or an illness, severe tissue damage (burns or trauma), clotting factors by some cancers or pregnancy complications. Treatment: Treat underlying cause à IV fluids & blood transfusions & heparin Heparin- induced Thrombocytopenia (HIT) à A low platelet count caused by a reaction against heparin. • Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. o Develop 5-10 days after starting injection of heparin. Ptl drops by more than 50% o Tx: discontinue heparin. Monitor/prevent VBTE and PE o May use alternative antithrombotic (Argatroban) o HIT once= HIT forever! When receiving heparin 14 Test your Knowledge Questions: A nurse is caring for a client who has idiopathic thrombocytopenic purpura (ITP). The nurse should notify the provider and report possible small-vessel clotting when which of the following is assessed? A. Petechiae on the upper chest B. Hypotension C. Cyanotic nail beds D. Severe headache In a patient with prolonged vomiting, the nurse monitors for fluid volume deficit because vomiting results in a. Fluid movement from the cells into the interstitial space and the blood vessels b. Excretion of large amounts of interstitial fluid with depletion of extracellular fluids c. An overload of extracellular fluid with a significant increase in intracellular fluid volume d. Fluid movement from the vascular system into the cells, causing cellular swelling and rupture The nurse is administering 3.0 % saline solution IV to a patient with severe hyponatremia. It is most important for the nurse to observe for what? a. Decreased heart rate and blood pressure b. Prolonged QT interval and facial flushing c. Shortness of breath and increased respiratory rate d. Increased urine output and decreased urine specific gravity A patient is admitted with renal failure and an arterial blood pH level of 7.29. Which lab result would the nurse expect? a. Serum sodium 138 mEq/L b. Serum glucose 145 mg/dL c. Serum potassium 5.9 mEq/L d. Serum magnesium 0.4 mg/dL Pneumothorax à Open pneumothorax: air enters through an opening in the chest wall and parietal (outer) lining of the pleura. à Closed pneumothorax: occurs when the visceral (inner) lining of the pleura is disrupted, allowing air to enter the pleural space from the lung. There is no external wound. 15 Clinical manifestations: If a pneumothorax is small, mild tachycardia and dyspnea may be the only manifestations. If the pneumothorax occupies a large area, respiratory distress may be present, including shallow, rapid respirations; dyspnea; air hunger; and oxygen desaturation. On auscultation, there are no breath sounds over the affected area. A chest x-ray shows the presence of air or fluid in the pleural space and reduction in lung volume. Types: àA spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled sacs) located on the surface of the lung. • These blebs can occur in healthy, young individuals or as a result of lung disease such as COPD, asthma, cystic fibrosis, and pneumonia. • Smoking increases the risk for bleb formation. Other risk factors include being tall and thin, male gender, family history, and previous spontaneous pneumothorax. à Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures. • Example: transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, and transbronchial lung biopsy all have the potential to injure the lung. • Barotrauma from excessive ventilatory pressure during manual or mechanical ventilation can rupture alveoli or bronchioles. • Esophageal procedures may also be involved in the development of a pneumothorax. • Tearing during insertion of a gastric tube can allow air from the esophagus to enter the mediastinum and pleural space. Tension Pneumothorax: à Medical emergency, with both the respiratory and cardiovascular systems affected. • If the tension in the pleural space is not relieved, the patient is likely to die from inadequate cardiac output or severe hypoxemia. • Treat with needle decompression and chest tube insertion 16 Treatment: Depends on its severity and the nature of the underlying cause • • • • If the patient is stable, and has minimal air and/or fluid accumulated in the intrapleural space, no treatment may be necessary as the condition may resolve spontaneously. The most definitive and common form of treatment of pneumothorax and hemothorax is to insert a chest tube and connect it to water-seal drainage. Repeated spontaneous pneumothorax may need to be treated surgically by a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another. Tension pneumothorax is a medical emergency, requiring urgent needle decompression followed by chest tube insertion to water-seal drainage. Chest tube & pleural drainage: This unit has 3 chambers: (1) collection chamber; (2) water-seal chamber; and (3) suction control chamber. àSuction control chamber requires a connection to a wall suction source that is dialed up higher than the prescribed suction for the suction to work. In the water suction unit, the suction control chamber controls the wall suction pressure. àIf enough fluid or air accumulates in the pleural space, the negative pressure becomes positive and the lungs collapse. • As a result, chest tubes are inserted to drain the pleural space, reestablish negative pressure, and allow for proper lung expansion. • They may also be inserted in the mediastinal space to drain air and fluid postoperatively. • Chest tubes are approximately 20 inches (51 cm) long and vary in size from 12F to 40F. The size inserted is determined by the patient’s condition. Large (36F to 40F) tubes are used to drain blood, medium (24F to 36F) tubes are used to drain fluid, and small (12F to 24F) tubes are used to drain air. • Pigtail tubes are very small (10F to 14F) tubes with a curly end designed to keep them in place. They are a safe and effective alternative to larger bore chest tubes for treatment of pneumothorax. • Brisk bubbling of air often occurs in this chamber when a pneumothorax is initially evacuated. 17 • • • • • • Intermittent bubbling during exhalation, coughing, or sneezing (when the patient’s intrathoracic pressure is increased) may be observed as long as air is in the pleural space. Eventually, as the air leak resolves and the lung becomes more fully expanded, bubbling ceases. Normal fluctuation of the water within the water-seal chamber is called tidaling. This up-and-down movement of water in concert with respiration reflects intrapleural pressure changes during inspiration and expiration. Investigate any sudden cessation of tidaling, as this may signify an occluded chest tube. Gradual reduction and eventual cessation of tidaling is expected as the lung reexpands. Management: • Never elevate the drainage system to the level of the patient’s chest because this will cause fluid to drain back into the lungs. Secure the unit to the drainage stand. • Change the unit if the collection chamber is full. Do not try to empty it. • Mark the time of measurement and the fluid level on the drainage unit according to the unit standards. Report any change in the quantity or characteristics of drainage (e.g., clear yellow to bloody) to the physician and record the change. Notify physician if >100 mL/hr drainage. • Check the position of the chest drainage container. If the drainage system is overturned and the waterseal is disrupted, return it to an upright position and encourage the patient to take a few deep breaths, followed by forced exhalations and cough maneuvers. • Clamping of chest tubes during transport or when the tube is accidentally disconnected is no longer advocated. The danger of rapid accumulation of air in the pleural space, causing tension pneumothorax, is far greater than that of a small amount of atmospheric air that enters the pleural space. • If a chest tube becomes disconnected, the immediate priority is to reestablish the water-seal system. In some hospitals, when disconnection occurs, the chest tube is immersed in sterile water (about 2 cm) until the system can be reestablished. It is important to know the unit protocol, individual clinical situation (whether an air leak exists), and HCP preference before any chest tube clamping occurs. • Appearance of a new air leak warrants assessment of the drainage system to identify if the air leak is coming from the patient or the system. • Once again, the nurse is encouraged to become familiar with the policies and procedures of their workplace regarding specific clinical situations and circumstances when chest tubes may be clamped. à If unit overturned, have patient exhale and cough à Do NOT clamp à If break in system, place distal end in sterile water to maintain water seal 18 Test Your Knowledge When should a nurse check for leaks in the chest tube and pleural drainage system? a. When there is continuous bubbling in the water-seal chamber. b. There is constant bubbling of water in the suction control chamber. c. Fluid in the water-seal chamber fluctuates with the patient’s breathing. d. The water levels in the water-seal and suction control chambers are decreased. True or False: In tension pneumothorax, the trachea is deviated toward the unaffected side? Pneumonia à Acute infection of lung parenchyma Types: • Community-acquired (CAP) o Occurs in patients who have not been hospitalized or resided in a long-term care facility within 14 days of the onset of symptoms o Can be treated at home or hospitalized dependent on patient condition o Empiric antibiotic therapy started ASAP • Hospital-acquired (HAP) o HAP: Occurs 48 hours or longer after hospitalization and not present at time of admission o Associated with longer hospital stays, increased costs, sicker patients, and increased risk of morbidity and mortality • Ventilator-associated (VAP) o VAP: Occurs more than 48 hours after endotracheal intubation o Associated with longer hospital stays, increased costs, sicker patients, and increased risk of morbidity and mortality à Multidrug-resistant (MDR) organisms are major problem in treatment o Staphylococcus aureus o Gram-negative bacilli • Risk factors o Advanced age o Immunosuppression o History of antibiotic use o Prolonged mechanical ventilation 19 • • • • • • • • • Aspiration Pneumonia Results from abnormal entry of secretions into lower airway Major risk factors: o Decreased level of consciousness o Difficulty swallowing o Insertion of nasogastric tubes with or without tube feeding Empiric therapy based on severity of illness, where infection acquired, and probable causative organism Opportunistic Pneumonia Caused by microorganisms that do not normally cause disease Patients at risk o Severe protein-calorie malnutrition o Immunodeficiencies o Chemotherapy/radiation recipients o Long-term corticosteroid therapy • • • Necrotizing Pneumonia Rare complication of bacterial lung infection Often results from CAP Signs and symptoms o Immediate respiratory insufficiency and/or failure o Leukopenia o Bleeding into airways Pneumocystis jiroveci pneumonia (PJP) • Onset slow and subtle • Diffuse bilateral infiltrates to massive consolidation • Can be life threatening • Spread to other organs • Treat with trimethoprim/sulfamethoxazole IV or orally Cytomegalovirus (CMV) pneumonia Herpes virus Asymptomatic and mild to severe disease Life threatening in immunosuppressed person Treat with antiviral medications and high-dose immunoglobulin Manifestations: • Most common o Cough o Fever, chills o Dyspnea, tachypnea o Pleuritic chest pain o Green, yellow, or rust-colored sputum • Change in mentation for older or debilitated patients Physical examination findings: • Fine or coarse crackles • Bronchial breath sounds • Egophony • ↑ Fremitus • Dullness to percussion if pleural effusion present Interventions: • Pneumococcal vaccine o To prevent Streptococcus pneumoniae • Prompt treatment with antibiotics is essential o Response generally occurs within 48-72 hr o ↓ Temperature o Improved breathing o ↓ Chest discomfort • Repeat chest x-ray in 6-8 weeks à Supportive care • Oxygen for hypoxemia • Analgesics for chest pain • Antipyretics • Individualize rest and activity à No definitive treatment for majority of viral pneumonias 20 à Antivirals for influenza pneumonia Drug Therapy: • Start with empiric therapy o Based on likely infecting organism and risk factors for MDR organisms o Varies with local patterns of antibiotic resistance • Should see improvement in 3-5 days • Start with IV and then switch to oral therapy as soon as patient stable Nutritional Therapy: Be cautious giving oxygen to patient • Adequate hydration with COPD à over oxygenating o Prevent dehydration patient can lead to altered mental o Thin and loosen secretions status and further complications o Adjust for older adults, patients with heart failure, those with preexisting respiratory conditions • High calorie, small, frequent meals o Monitor for weight loss Complications: • Atelectasis • Pleurisy • Pleural effusion • Bacteremia • Pneumothorax • Meningitis • Acute respiratory failure • Sepsis/septic shock • Lung abscess How to know interventions are working: • Clear breath sounds • Normal breathing patterns • No signs of hypoxia • Normal chest x-ray • Normal WBC count • Absence of complications related to pneumonia Response Questions A 56-year-old normally healthy patient at the clinic is diagnosed with bacterial community-acquired pneumonia. Before treatment is prescribed, the nurse asks the patient about an allergy to a. amoxicillin b. erythromycin c. sulfonamides d. cephalosporins The nurse is caring for a patient with pneumonia. If a pleural effusion is developing, the nurse would expect which finding? a. Barrel-shaped chest b. Paradoxical respirations c. Hyperresonance on percussion d. Localized decreased breath sounds 21 What lung sounds could a nurse hear when assessing a patient with pneumonia? A. B. C. D. Rhonchi Rales Wheezes All of the above Neutropenia à Reduction in neutrophils (predisposing patient to infection) à ANC less than 1000 (normal range 2200 – 7700) à Severe neutropenia ANC less than 500 à Can be an expected effect of certain drugs, most common cause is chemotherapy and immunosuppressive therapy • Patient needs private room to be protected from staff and other patients (high priority) à positive pressure or high efficiency particular air (HEPA) • Nadir: lowest point of neutropenia in a patient treated with chemotherapy *Low grade fever great significance greater than 100.4F (38C) à blood culture drawn STAT and antibiotics started within 1 hour (usually IV route because of rapid lethal effects of infection) Diagnosis: primary diagnostic tests peripheral WBC count and bone marrow aspiration and biopsy Management: Identify and remove cause or site of infection (if possible), antimicrobial therapy, blood culture STAT before antibiotics, patient hygiene (strict hand washing) 1. Determine cause 2. Antibiotic therapy promptly 3. Identify offending organisms if infection developed 4. Give hematopoietic growth factors prophylactically after chemotherapy 5. Implement protective practices à Hand washing single most effective way to prevent à Avoid: Unwashed fruit and veggies, raw undercooked meats and eggs and soft cheese with molds 22 Nurse Civility à Foundation for patient safety, a healthy work environment, healthy staff • • Results in increased productivity Use clear communication verbally, on-verbally, and in writing & treat others with respect, dignity, and kindness Labs Sodium 136-145mEq/L Potassium 3.5-5.0mEq/L Calcium 9.0-10.5mg/dL Magnesium: 1.3-2.1mEq/L Phosphorus: 3.0-4.5mg/dL Glucose 74-106mg/dL HctFemale: 37%-47% (0.37-0.47) Male: 42%-52% (0.42-0.52) HgbFemale: 12-16g/dL Male: 14-18g/dL MCV80-100fL Platelets150,000-400,000x 103 /L WBC5,000-10,000/μl Banded neutrophils: 0%-8% Segmented neutrophils: 55%-70% SpO2 94%-99% SaO2: >95% PT: 11-12.5 seconds aPTT: 30-40 seconds (1.5-2.5 times the control value w/ heparin therapy) INR: 0.8-1.1 (Desired goal of 2 to 3 on warfarin therapy) 23 Medications Iron (Ferrous sulfate) Class: Antiemetics Action: Enters blood stream and is transported to organs where it becomes part of iron stores Indications: Treatment of iron deficiency anemia. Interventions: Do not take with acid suppressing agents (antacids, eggs, milk, coffee or tea) - take 2 hours apart. Orange juice and acid environment help with absorption. Peds patient should drink through a straw to decrease tooth staining. GI upset, constipation, green/black stools common. Give IM Z-track. Watch for CNS toxicity symptoms. Adverse Effects: Nausea, vomiting, dark stools, epigastric pain (constipation), staining of teeth Aspirin Class: Antipyretic, antiplatelet, analgesic NSAID Action: Produce analgesia and reduce inflammation and fever, decreases platelet aggregation Indications: Block prostaglandin activity which decreases inflammatory response. OD can lead to acidosis. Interventions: Administer with food, can cause antidiuretic effect Adverse Effects: Dyspepsia, epigastric distress, nausea, hypersensitivity reactions Erythropoietin Class: Antiemetics Action: Stimulates erythropoiesis (production of RBCs) Indications: Stimulates RBC production, common with renal failure, AIDS, post-surgical, chemo pts. Interventions: Caution if giving to patient with normal erythropoietin as could turn off the negative feedback loop. Watch for chest pain, thrombophlebitis, hypertension, facial flushing in athletes that are abusing this drug. Adverse Effects: Hypertension, cough, dizziness Neupogen Class: Colony stimulating factors Action: Binds to and stimulates immature neutrophils to divide and differentiate Indications: Decreases infection improves recovery of neutrophils in cancer treatment. Interventions: Prevent exposure to infection, provide mouth care and support. Adverse Effects: Bone pain, headache, fatigue, alopecia, rash, N/V, diarrhea, stomatitis, bone pain. Hydroxyurea Class: Antineoplastics Action: interferes with DNA synthesis and may alter characteristics of RBCs Indications: Reduction in frequency of painful crisis in sickle cell anemia Interventions: Anemia may occur, assess for signs of infection and bleeding Adverse Effects: leukopenia, chills, fever 24 Zithromax Class: Macrolide Action: Inhibits protein synthesis Indications: Used to fight infections Interventions: Take on empty stomach (best for most antibiotics - many cannot be taken with iron or calcium), complete full course of prescription even if feeling better, may suppress effectiveness of BCPs, liver enzymes (AST/ALT). Adverse Effects: GI, supra infections, c-diff. Can prolong QT interval and cause EKG changes which may result in chest pain and lethal arrhythmias. Ciprofloxacin & Levofloxacin Class: Fluoroquinolones Action: Inhibits bacterial DNA synthesis by inhibiting DN gyrase enzyme Indications: Used for more serious infections and patients who may be immunocompromised, such as HIV+. Interventions: Adding aminoglycosides, theophylline, steroids increase toxicity (note: theophylline does not go well with most drugs), Adverse Effects: Adding aminoglycosides, theophylline, steroids increase toxicity (note: theophylline does not go well with most drugs) Tazobactam & Ceftriazone Class: B-Lactams Action: Binds to bacterial cell wall membrane causing cell death à inhibits beta lactamase an enzyme that destroys penicillin’s Indications: Intraabdominal infections, Hospital acquired bacteria pneumonia (HAPB), complicated UTIs Interventions: Observe for anaphylaxis & monitor bowel function Adverse Effects: Diarrhea, Cdiff 25