NUR 265 EXAM #1: CONTENT REVIEW

NUR 265 EXAM #1: CONTENT REVIEW Unit 1: Care of Patients with Complex Renal & Gastrointestinal Problems Renal A & P • What do the kidneys do? o Kidneys receive 20-25% of cardiac output under resting conditions – more than 1L blood/min o Kidneys are controller of fluid & electrolyte homeostasis in the body o Kidneys secrete erythropoietin that inc. RBC synthesis in bone marrow o Kidneys convert Vitamin D into its active form o Loop of Henle concentrates urine and allows water reabsorption into bloodstream Question: The nurse is explaining to a group of nursing students that when there is a decrease in the secretion of renin, and aldosterone it can cause ▪ (Select all that apply.) • A. an excretion of sodium. • B. dilution of urine. • C. increased intestinal absorption of calcium. • D. increased bone density. • E. a decreased thirst. Physical Examination • Skin color (ashen, yellow); crystals on skin (uremic frost) • Tissue turgor: to detect dehydration or edema • Periorbital edema: suggests fluid retention. Inspect the mouth for moisture and odor • Observe respiratory rate, pattern, and effort • Auscultate the lungs for crackles or rhonchi • Inspect the abdomen for scars and contours, and palpate for tenderness and bladder distention • Edema • Inspect the genitalia Nephrotic Syndrome • Patho: o A condition of increased glomerular permeability that allows large molecules to pass through the membrane into the urine and then be excreted. o This process causes severe proteinuria, high serum lipid levels, fats in the urine, edema and hypertension. o Identified by kidney biopsy • Risk Factors: allergic reactions, reactions to medications, renal vein disease, sickle cell disease, HF • Clinical Manifestations o Massive proteinuria (Increased protein) 3.5g/day in a 24-hour urine sample o Hypoalbuminemia (Decreased albumin (serum)) 3g/dL o Hypertension o Edema (esp. facial and periorbital) o Hyperlipidemia (due to low albumin) o Fat bodies in urine o Delayed clotting or increased bleeding with higher-than-normal values of serum activated partial thromboplastin time (aPTT), coagulation or internation normalized ration for prothrombin (INR, PT) o Reduced kidney function with elevated BUN and serum creatinine and decreased GFR • Nursing Interventions: management varies, depending on which process is causing the disorder! o Maintain fluid (NS) & electrolyte balance o Monitor labs daily o Monitor and record I&O daily o Assess daily weight o Restrict sodium & potassium intake (diet changes) o Monitor skin due to edema o Protein intake restriction with decreased GFR; normal GFR dietary intake of protein is needed! o Medications: ▪ Administer steroids if needed for inflammation ▪ ACE inhibitors: Can decrease protein loss in the urine ▪ Cholesterol-lowering drugs can improve blood lipid levels • NOTE! NS may progress to end stage kidney disease (ESKD) but can be prevented with treatment!! Kidney Injury • Acute (AKI) vs Chronic (CRF) o Acute develops in a few hours to days with abrupt disruption in kidney function o Chronic is progressive deterioration over years with slow loss of kidney function o AKI affects MANY body systems. Chronic kidney disease affects EVRY body system. AKI • What is it? o Rapid reduction in kidney function resulting in a failure to maintain fluid & electrolyte balance, and acid-base balance. o Develops abruptly within hours to days o If AKI occurs in patients with decreased kidney function already  ESKD o Increase in serum creatinine by 0.3mg/dL or more within 48 hours; OR increase in serum creatinine to 1.5 times or more from baseline ▪ Occurred in previous 7 days; or a urine volume less than 0.5 mL/kg/hr for 6 hours o GFR is not accurate acute or critical illness although best overall indicator of kidney function! o HYPOPERFUSION (reduction in blood flow) ▪ Kidney compensates by constricting blood vessels and by activating renin-angiotension- aldosterone which RELEASES ADH ▪ ADH- increase blood volume increasing perfusion BUT will decrease UOP causing: • OLIGURIA = 400ml/24hour period o Less than 0.5mL/kg/hr for 2 or more hours o Min. UOP Q24 hours=720mL or 30mL/hr ▪ Symptoms of reduced blood volume  MAP 65, tachycardia, thread peripheral pulses, decreasing cognition o Timely interventions to remove the cause of AKI may prevent progression to ESKD and the need for lifelong renal replacement therapy or a renal transplant • S/S: same as fluid overload  Hypertension, dec. O2, high HR • AKI Causes o Reduced perfusion to the kidneys, damage to kidney tissue and obstruction of urine outflow o Pre-renal: decreased perfusion to glomeruli ▪ Reduced perfusion with a sustained mean arterial pressure (MAP) of less than 65mm Hg ▪ Conditions that contribute: Blood or fluid loss, BP drugs, heart attack/HF, infection, liver failure, use of aspirin/ibuprofen/NSAIDS, dehydration, burns, atherosclerosis o Intra-renal: nephrotoxic agents, kidney infections, occlusion of intrarenal arteries, hypertension, diabetes mellitus, or direct trauma to the kidney ▪ Reflects injury to the glomeruli, nephrons or tubules ▪ Conditions that contribute: glomerulonephritis, bleeding in the kidney, sepsis, lupus, TTP, drugs, multiple myeloma, scleroderma, vasculitis o Post-renal: caused by backward pressure on the kidney from an obstruction somewhere lower in the urinary system (Effects normal urine flow) ▪ Conditions that contribute: Kidney stones, cancers (bladder, cervical, colon, prostate), enlarged prostate, nerve damage, blood clots in the urinary tract Table 68-4 Conditions Contribute to AKI • Prerenal (Perfusion Reduction) o Blood or fluid loss (surgery, trauma, sepsis, shock, hypovolemic shock) o BP drugs resulting in hypotension o MI or heart failure o Infection o Liver failure o Use of aspirin, ibuprofen, Naproxen, NSAIDS o Severe allergic reaction o Severe burns o Severe dehydration o Renal artery stenosis o Bleeding or clotting in kidney blood vessels o Atherosclerosis or cholesterol deposits that block blood flow • Intrarenal (Kidney Damage) o Glomerulonephritis or inflammation o Bleeding in kidney o Thrombi or emboli o Hemolytic uremic syndrome (premature destruction of RBC’s) o Sepsis & local infection o Lupus o Chemo agents, abx, iodinated or hyperosmolar contrast, zoledronic acid o Multiple myeloma o Scleroderma o Thrombotic thrombocytopenic purpura o Ingested toxins (etoh, heavy metals, cocaine) o Vasculitis o Ischemia in kidney tissue • Postrenal (Urine Flow Obstruction) o Bladder, cervical, colon, prostate cancer o Enlarged prostate o Kidney stones o Nerve damage involving nerves that control bladder o Blood clots in urinary tract • Phases of AKI o Onset stage: from time of initial event to renal manifestations, symptoms can occur immediately up to a week after event ▪ increased BUN & serum creatinine with normal to decreased urine output. o Oliguric stage: can last 1 to 8 weeks (the longer this phase last the worse the prognosis. ▪ urine output decreases to 400 mls or less per day o Diuretic stage: gradual or abrupt return of glomerular filtration. ▪ Urine output may be 1-2L per day. Serum BUN & creatinine levels decrease. • Need a place of care that focuses on fluid and electrolyte REPLACEMENT and monitoring. • Onset of polyuria can signal the start of recovery from AKI. o Recovery stage: as renal tissue recovers, serum electrolytes, BUN & creatinine return to normal. ▪ Can last 3-12 months • Nursing Care of Patients with AKI o Avoid hypotension and maintain normal fluid balance to prevent and manage AKI o Thorough assessment and close monitoring of laboratory values is essential for signs of impending kidney dysfunction. (Na, K, USG, albumin creatine ratio, osmolarity, BUN and electrolytes) ▪ Evaluate fluid status ▪ Accurately measure I&O ▪ Measure body weight ▪ Note characteristics of urine (report of new sediment, hematuria (smoky or red color)), foul odor ▪ Report urine output 0.5 mL/kg/hr for more than 2 hours  ACT EARLY! ▪ Monitor kidney lab values • Increase in creatinine, esp. over hours or a few days (report to PCP) • BUN • Potassium, sodium, urine specific gravity, albumin-creatinine ratio and electrolytes • Reduced GFR makes pt more vulnerable for AKI ▪ Keep MAP at 80 mm/hg ▪ NO nephrotic agents ▪ Check kidney function before contrast dye • When nephrotoxic agents are used including contrast dye to protect kidney by administering a PRETREATMENT ORAL OR IV BOLUS OF FLUID VOLUME. ▪ DEHYDRATION REDUCES PERFUSION AND CAN LEAD TO AKI EVEN IN ADULTS WHO HAVE NO KNOWN KIDNEY PROBLEMS. ▪ Question medication for potentially nephrotoxic drugs • Table 68-5 Examples of Potentially Nephrotoxic Substances o Drugs Abx/antimicrobials ▪ Amphotericin B, Colistimethate, Methicillin, Polymyxin B, Rifampin, Sulfonamides, Tetracycline hydrochloride, Vancomycin. o Aminoglycoside Abx ▪ Gentamicin, Kanamycin, Neomycin, Netilmicin sulfate, Tobramycin. o Chemotherapy Agents ▪ Cisplatin, Cyclophosphamide, Methotrexate o NSAIDs ▪ Celecoxib, Flurbiprofen, Ibuprofen, Indomethacin, Ketorolac, Meclofenamate, Meloixcam, Naubmetone, Naproxen, Oxaprozin, Rofecoxib, Tolmetin o Other ▪ Acetaminophen, Captopril, Cyclosporine, Fluorinate anesthetics, Metformin, Phenazopyridine hydrochloride, Quinine ▪ Anticipate AKI following shock, hypotension, burns or heart failure exacerbation. • Dec. BP, dec. volume  dec. kidney function ⟶ CRITICAL RESCUE! o Preventing volume depletion and providing intervention early when occurrence are NURSING PRIORITIES. • Interprofessional Care: o History: ▪ Ask about recent sx or trauma, transfusions, allergic reactions, or other factors that might reduce kidney perfusion. ▪ Coexisting conditons of advanced age, diabetes, long term HTN, sepsis systemic inflammation, low cholesterol levels, coagulopathy or tx for bleeding or clotting disorders can increase risk. ▪ Anticipate AKI following shock, hypotension, burns or heart failure exacerbation ▪ Problems where blood volume depletes: cardiac bypass sx, extensive bowel preparations, being NPO before sx, or dehydration from exercise. o Physical Assessment/Signs & Symptoms: ▪ Assess urine output every hour after sx until stable during fluid resuscitation for shock or hypotension and when pt is high risk for AKI following hospital admission. ▪ Even brief period of oliguria, defined as less than 0.5 mL/kg/hour or output for 2 or more hours can signal AKI. ▪ Evaluate VS to recognize early hypoxemia and hypoperfusion. ▪ S/S of reduced blood volume such as MAP 65 mm Hg, tachy, thready pulses, or decrease cognition can indicate risk of AKI. • MAP 60-70 MM ▪ SpO2 88 may indicate potential hypoxemic or ischemic damage to kidneys. o Interventions: Responding ▪ Avoid Hypotension and maintain normal fluid balance ▪ Reduce exposure to nephrotoxic agents and drugs that alter perfusion. ▪ Observation about new onset or increased peripheral edema, increased daily weight, and reduced urine output can identify patients with + fluid balance from AKI who may require tx with FLUID RESPTRICTION OR DIURETIC THERAPY. ▪ Recognize elevated serum creatinine levels. ▪ During AKI with high volume output, hypovolemia, and electrolyte loss are main problems. • DIURETIC PHASE. • Drug therapy o Diuretics: used to increase urine output – doesn’t help to preserve kidney function just helps get the fluid off ▪ Furosemide o Fluid challenges: used to promote kidney perfusion ▪ Pts without fluid overload  500-1000 mL of NS infused over 1 hour ▪ Closely assess the response to fluid and slow the infusion is indications of fluid overload (particularly respiratory distress) • Nutrition Therapy o Work with dietitian for specific amounts of protein, sodium and fluids ▪ More protein is required in the diet if the patient is on dialysis ▪ For the patient who does not 0.6 g/kg of body weight or 40 g/day of protein is prescribed. ▪ For patient who require dialysis, the protein level needed ranges from 1 to 1.5 g/kg. o If high blood potassium levels are present, dietary potassium is restricted and pt is given fluid and Furosemide ▪ Dietary Na ranges from 60 to 90 meq/kg ▪ If high K dietary K is restricted to 60 to 70 meq/kg ⟶ CRITICAL RESCUE! o In an acute care setting, preventing volume depletion and providing intervention early when volume depletion occurs are nursing PRIORITIES. Reduced perfusion from volume depletion is a common cause of AKI. Assess continually to recognize the s/s of volume depletion (low urine output, decreased systolic BP, decreased pulse pressure, orthostatic hypotension, thirst, rising blood osmolarity). Respond by intervening early with oral fluids or in the patient who is unable to take or tolerate oral fluid, requesting an increase in IV fluid rate from the PCP to prevent permanent kidney damage • Renal Function Replacement o Hemodialysis o CRRT (Continuous Renal Replacement Therapy) o Kidney replacement therapy is used for patients with loss of kidney function and inadequate waste elimination. o A long term dialysis catheter may be placed in the radiology department using a tunneling technique under moderate sedation. o • Hemodialysis (nurse driven) o Continues to be the Gold Standard for treatment of AKI. o Large amounts of fluid can be removed & electrolytes replaced over 2-3 hours 3X’s a week o Creates shifts of fluid and electrolytes that may not be tolerated well in acutely or critically ill patients. Hypotension can occur(expected) and worsen renal function. • CRRT(Continuous Renal Replacement Therapy) o Concept is to dialyze patients in a more physiologic way, slowly over 24 hours – just like the kidney. o Removes about 1L/hour of fluid. o Suitable for hemodynamically unstable patients (ICU/critical pts) ▪ Occurs in the ICU because of the need for frequent monitoring and specialized skill set of the nurse to maintain safety during extracorporeal circulation (blood flow outside the body) and the need to ongoing monitoring and replacement of fluid and electrolytes ⟶ Chart 68-7: Caring for the Pt with an Arteriovenous Fistula or Arteriovenous Graft o DO NOT take BP readings using the extremity in which the vascular access is placed o DO NOT perform venipunctures or start an IV line in the extremity in which the vascular access is placed o Palpate for thrills and auscultate for bruits over the vascular access site every 4 hours while the patient is awake o Access that patient’s distal pulses and circulation in the arm with the access o Elevate the affected extremity after surgery o Encourage routine range of motion exercises o Check for bleeding at needle insertion sites o Access for indications of infection at needle sites o Instruct the patient not to carry heavy objects or anything that compress the extremity in which the vascular access is placed o Instruct the patient not to sleep with his or her body weight on top of the extremity in which the vascular access is places ⟶ ACTION ALERT! o Because repeated compression can result in the loss of the vascular access, avoid taking the BP or performing venipunctures in the arm with the vascular access. Do not use an AV fistula or graft for general delivery of IV fluids or drugs