Fluid Volume Excess• Pathophysiology – may be related to fluid overload or diminished function of the homeostatic mechinisms responsible for regulating fluid balance• Contributing factors – CHF, renal failure, cirrhosis
Nursing Diagnosis and Goal• Fluid volume excess r/t CHF, excess sodium intake, renal failure AEB:Weight gain of 6 lb. in 24 hours; lungs with crackles in bases bilaterally; 2+ edema in ankles bilaterallyGoal: Client will have normal fluid volume within 48 hours AEB:Decreased weight of 1 lb. per day, lung sounds clear in all fields, ankles without edema
Fluid Volume Excess 3• Nursing management- Preventing FVE- Detecting and Controlling FVE- Teaching patients about edema
Electrolyte ImbalancesSodium!Normal range – 135 to 145 mEq/L- Primary regulator of ECF volume (a loss or gain of sodium is usually accompanied by a loss or gain of water)
Hyponatremia• Sodium level less than 135 mEq/L• May be caused by vomiting, diarrhea, sweating, diuretics, etc.
Hyponatremia 3• Medical management- Sodium Replacement- Water Restriction
Hyponatremia 4• Nursing Management- Detecting and controlling hyponatremia- Returning sodium level to normal
Critical Thinking Exercise: Nursing Management of the Client with Hyponatremia• Situation: An 87 year old man was admitted to the acute care facility for gastroenteritis, 2 day duration. He is vomiting, has severe, watery diarrhea and is c/o abd cramping. His serum electrolytes are consistent with hyponatremia r/t excessive sodium loss.
Critical Thinking Exercise: Nursing Management of the Client with Hyponatremia 2• 1. What is the relationship between vomiting, diarrhea, and hyponatremia?• 2. What s/s should the client be monitored for that indicate the presence of sodium deficit?• 3. In addition to examining the client’s serum electrolyte findings, how will the nurse know when the client’s sodium level has returned to normal?
Hypernatremia• Sodium level is greater than 145 mEq/L- Can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium
Hypernatremia 2• Pathophysiology- Fluid deprivation in patients who cannot perceive, respond to, or communicate their thirst- Most often affects very old, very young, and cognitively impaired patients
Critical Thinking Exercise: Nursing Management of the Client with Hypernatremia• Situation: A 47 year old woman was taken to the ER after she developed a rapid heart rate and agitation. Physical assessment revealed dry oral mucous membranes, poor skin turgor, and fever of 101.3 orally. The client’s daughter stated her mother had been very hungry recently and drinking more fluids than usual. Suspecting DM, the practitioner obtained serum electrolytes and glucose levels, which revealed serum sodium of 163 mEq/L and serum glucose of 360 mg/dL.
Critical Thinking Exercise: Nursing Management of the Client with Hypernatremia 2• 1. Interpret the client’s lab data.• 2. Why are clients with DM prone to the development of hypernatremia?• 3. What precautions should the nurse take when caring for the client with hypernatremia?• 4. List 4 food items this client should avoid and why.• 5. Identify 3 meds that could have an increased effect on the client’s sodium level.
All About Potassium• Major Intracellular electrolyte• 98% of the body’s potassium is inside the cells• Influences both skeletal and cardiac muscle activity• Normal serum potassium concentration – 3.5 to 5.5 mEq/L.
Hypokalemia 3• Nursing interventions:• Encourage high K foods• Monitor EKG results• Dilute KCl! – can cause cardiac arrest if given IVP
Hypokalemia 4• Administering IV Potassium- Should be administered only after adequate urine flow has been established- Decrease in urine volume to less than 20 mL/h for 2 hours is an indication to stop the potassium infusion- IV K+ should not be given faster than 20 mEq/h
Critical Thinking Exercise: Nursing Management of the Client with Hypokalemia• Situation: A 69 year old man has a history of CHF controlled by Digoxin and Lasix. Two weeks ago he developed diarrhea, which has persisted in spite of his taking OTC antidiarrheal meds. His partner transported him to the ER when she found him lethargic and confused. Initial assessment of the client reveals heart rate at 86 bpm, respiratory rate 10, and blood pressure 102/56 mmHg.
Critical Thinking Exercise: Nursing Management of the Client with Hypokalemia 2• 1. An electrolyte panel shows the client’s serum potassium is 2.9 mEq/L. Does the nurse have cause to be concerned about the client’s serum potassium? Why or why not?• 2. What data supports the presence of hypokalemia in this client?• 3. What, if anything, should the nurse do?• 4. What foods should the client be advised to eat that are high in potassium?
Hyperkalemia• Serum Potassium greater than 5.5 mEq/L- More dangerous than hypokalemia because cardiac arrest is frequently associated with high serum K+ levels
Hyperkalemia 2• Causes: - Decreased renal potassium excretion as seen with renal failure and oliguria - High potassium intake - Renal insufficiency - Shift of potassium out of the cell as seen in acidosis
Hyperkalemia 3• Clinical manifestations:- Skeletal muscle weakness/paralysis- EKG changes – such as peaked T waves, widened QRS complexes- Heart block
Hyperkalemia 4• Medical/Nursing Management:- Monitor EKG changes – telemetry- Administer Calcium solutions to neutralize the potassium- Monitor muscle tone- Give Kayexelate- Give Insulin and D50W
Calcium• More than 99% of the body’s calcium is located in the skeletal system• Normal serum calcium level is 8.5 to 10mg/dL• Needed for transmission of nerve impulses• Intracellular calcium is needed for contraction of muscles
Calcium 2• Extracellular needed for blood clotting• Needed for tooth and bone formation• Needed for maintaining a normal heart rhythm
Hypocalcemia• Serum Calcium level less than 8.5 mEq/L
Hypocalcemia 3• Clinical Manifestations- Tetany and cramps in muscles of extremitiesDefinition – A nervous affection characterized by intermitten tonic spasms that are usually paroxysmal and involve the extremities
Hypercalcemia• Serum Calcium level greater than 10.5 mEq/L
Hypercalcemia 2• Causes:- Hyperparathyroidism- Prolonged immobilization- Thiazide diuretics- Large doses of Vitamin A and D
Hypercalcemia 3• Clinical manifestations:- Muscle weakness, nausea and vomiting- Lethargy and confusion- Constipation- Cardiac Arrest (in hypercalcemic crisis, level 17mg/dL or higher)
Hypercalcemia 4• Medical/Nursing Management- Eliminate Calcium from diet- Monitor neurological status- Increase fluids (IV or PO)- Calcitonin
Calcitonin• - used to lower serum calcium level - useful for pts with heart disease or renal failure - reduces bone resorption - increases deposit of calcium and phosphorus in the bones - increases urinary excretion of calcium and phosphorus
• Parathyroid pulls, calcitonin keeps Parathyroid hormone pulls calcium out of the bone. Calcitonin keeps it there.
Magnesium- Normal serum magnesium level is 1.5 to 2.5 mg/ dL- Helps maintain normal muscle and nerve activity- Exerts effects on the cardiovascular system, acting peripherally to produce vasodilation- Thought to have a direct effect on peripheral arteries and arterioles
Hypomagnesemia• Serum Magnesium level less than 1.5 mEq/L
Hypomagnesemia• Causes- Chronic Alcoholism- Diarrhea, or any disruption in small bowel function
Hypomagnesemia 4• Clinical manifestations- Neuromuscular irritability- Positive Chvostek’s and Trousseau’s sign- EKG changes with prolonged QRS, depressed ST segment, and cardiac dysrhythmias- May occur with hypocalcemia and hypokalemia
STARVED• Starved – possible cause of hypomagnesemia• Seizures• Tetany• Anorexia and arrhythmias• Rapid heart rate• Vomiting• Emotional lability• Deep tendon reflexes increased
Hypomagnesemia 5• Medical/Nursing management- IV/PO Magnesium replacement, including Magnesium Sulfate- Give Calcium Gluconate if accompanied by hypocalcemia- Monitor for dysphagia, give soft foods- Measure vital signs closely
Hypomagnesemia 6• Foods high in Magnesium: - Green leafy vegetables
Hypermagesemia• Serum Magnesium level greater than 2.5 mEq/L
Hypermagnesemia 2• Causes- Renal failure- Untreated diabetic ketoacidosis- Excessive use of antacids and laxatives
Hypermagnesemia 3• Clinical manifestations- Flushed face and skin warmth- Mild hypotension
Hypomagnesemia 4- Heart block and cardiac arrest- Muscle weakness and even paralysis
RENAL• Reflexes decreased (plus weakness and paralysis)• ECG changes (bradycardia and hypotension)• Nausea and vomiting• Appearance flushed• Lethargy (plus drowsiness and coma)
Hypermagnesemia 5• Medical/Nursing management- Monitor Mg levels- Monitor respiratory rate- Monitor cardiac rhythm- Increase fluids- IV calcium for emergencies
Phosphorus- Normal serum phosphorus level is 2.5 to 4.5 mg/dL- Essential to the function of muscle and red blood cells, maintanence of acid-base balance, and nervous system- Phosphate levels vary inversely to calcium levels- High Calcium = Low Phosphate
Hypophosphatemia• Serum Phosphorus level less than 2.5 mEq/L
Hypophosphatemia 2• Causes- Most likely to occue with overzealous intake or administration of simple carbohydates- Severe protein-calorie malnutrition (anorexia or alcoholism)
Nursing Management in Cancer Care Larry Santiago, MSN, RN
7 Warning Signs of Cancer• Change in bowel or bladder habits A sore that does not heal Unusual bleeding or discharge Thickening or lump in breast or elsewhere Indigestion or difficulty in swallowing Obvious change in a mole or wart Nagging cough or hoarseness
Benign Tumors• Benign – Not recurrent or progressive. Opposite of malignant
Pathophysiology of the Malignant Process• Characteristics of Malignant Cells- All cancer cells share some common cellular characteristics- Cell membrane of malignant cells contain proteins called tumor-specific antigens, such as carcinoembryonic antigen and PSA
Pathophysiology 2• Invasion – growth of the primary tumor into the surrounding host tissues• Metastasis – dissemination or spread of malignant cells from the primary tumor to distant sites
Detection and Prevention of Cancer• Primary Prevention- Use teaching and counseling skills to encourage patients to partipate in cancer prevention and promote a healthy lifestyle
Detection and Prevention of Cancer 2• Secondary Prevention• Examples – breast and testicular self- examination, Pap smear
Detection and Prevention of Cancer 3• Tumor Staging and Grading – Staging determines size of tumor and existence of metastasis – Grading classifies tumor cells by type of tissue
Cancer Management- Cure, Control, or Palliation• Surgery• Radiation• Chemotherapy
Chemotherapy problems• Myelosuppression• Pulmonary or cardiac toxicity• Nausea and vomiting• Extravasation• Hypersensitivity reactions• Neuropathy• Pain at the injection site• Flulike syndrome• Hyperglycemia
Cancer Management- Cure, Control, or Palliation• Bone marrow transplantation
Nursing Process: The Patient with Cancer• Risk for Infection• Impaired Skin Integrity• Impaired Oral Mucous Membrane: Stomatitis• Imbalanced Nutrition: Less Than Body Requirements• Fatigue• Chronic Pain
Leukemia• A neoplastic proliferation of one particular cell type (granulocytes, monocytes, lymphocytes, or megakaryocytes)• Common feature is an unregulated proliferation of WBCs in the bone marrow
Acute leukemia• Progresses rapidly; characterized by ineffective, immature cells in the bone marrow pushing out the normal cells.• Acute myeloid leukemia (AML)--adults• Acute lymphocytic leukemia (ALL)--children• Signs and symptoms: Pallor, headache, fatigue, malaise, loss of appetite, weight loss, tachycardia, shortness of breath, petechiae, ecchymosis, splenomegaly, and bone tenderness.
Acute myelogenous leukemia (AML)• Normally, myelogenous line of cells mature into neutro-phils, monocytes, eosinophils, RBCs, and platelets. AML develops when cells commit to one type, typically neutrophils.• Diagnosis: Bone marrow biopsy• Prognosis: Favorably affected by age under 60 years, spontaneous rather than secondary leukemia, WBC less than 10,000/mm3 and remission after one round of chemotherapy.
AML treatment options• Induction chemotherapy – Goal is remission – Cytosine arabinoside and an anthracycle• Postinduction therapy (consolidation) – Goal is to prevent relapse after remission, but effective in only 25% to 35% of patients. – High-dose cytarabine has improved duration of first remission in young patients with AML. – Options: Standard chemotherapy, autologous stem cells, or human-leukocyte-antigen (HLA) matched sibling or donor (allogenic).
Acute lymphocytic leukemia (ALL)• Rapidly developing immature lymphocytes crowd our normal cells• Poor prognostic factors: High WBCs (> 25,000/mm3 at presentation), age over 50 years, and slow first remission (longer than 4 weeks).Treatment - Induction chemotherapy, administered in two phases, followed by maintenance therapy for up to 36 months.• Goal is complete remission.
Chronic leukemia• Progresses slowly and rarely affects people under age 20.• Chronic myeloid leukemia (CML) strikes ages 40 to 50, more in males.• Chronic lymphocytic leukemia (CLL) strikes after age 40 and is most common in older men.
Chronic myeloid leukemia (CML)• Too many neutrophils and the presence of the Philadelphia chromosome.• Chronic phase follows an indolent course, mild symptoms, <10% blasts in the marrow.• Accelerated phase characterized by spleen enlargement and progressive intermittent fevers, night sweats, and unexplained weight loss. 10% to 30% blasts and promyelocytes. It last 6 to 12 months.• Blast phase characterized by transformation to a very aggressive acute leukemia. 30% blasts and premyelocytes; patients die in this phase.
CML treatment options• Kinase inhibitor imatinib (Gleevec) is treatment of choice• Interferon alpha reduces growth and division 55% to 60%.• Hydroxyurea may prolong the chronic phase.• Stem cell transplant--greatest risk of dying in the first 100 days.
Chronic lymphocytic leukemia (CLL)Average survival is 2.5 years for advanced disease and 14 years for those with early- stage disease.• Indolent disease characterized by lymphocytosis, lymphadenopathy and hepatosplenomegaly. Risk of death from infection as the disease advances.
CLL treatment options• Standard chemotherapy, which can produce a remission not a cure and has harsh adverse reactions. Usually delayed till signs and symptoms appear. Chemotherapy, radiation, and Rituximab to enhance the response.
Lymphoma• Neoplastic disease in which lymphocytes undergo malignant changes and produce tumors• Classified as Hodgkin’s disease (accounts for 12% of lymphomas) and non-Hodgkin’s lymphoma (NHL)• Hodgkin’s disease accounted for 5 % of all cancer diagnoses in 2005; 3% NHL
Stages of lymphoma• Stage I – involves a single lymph node or localized involvement• Stage II – involves two or more lymph node regions on the same side of the diaphragm• Stage III – involves several lymph node regions on both sides of the diaphragm• Stage IV – involves extralymphatic tissue, such as the bone marrow
Hodgkin’s treatment options• Radiation is treatment of choice for stage IA or IIA nonbulky (<9 cm) Hodgkin’s. Over 95% achieve complete remission and 90% survive beyond 20 years.• Chemotherapy is appropriate for stage IIIB or IV, bulky disease. Standard ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) regimen is used.
Non-Hodgkin’s lymphoma (NHL)• Incidence has increased about 7% annually over 20 years, primarily older adults. Cause is unknown but increased risk: long-term immunosuppressant therapy, bone marrow transplant, inherited immune defects, rheumatoid arthritis, and prior Hodg-kin’s disease and treatment. Spread through the bloodstream.
NHL Treatment Options• Radiation, chemotherapy, or both• Stem cell transplant for recurrent disease
Multiple Myeloma• A malignant disease of the most mature form of B lymphocyte