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Complex II; Final Review; Acute renal Injury
Nursing Care- Complex Health Problems II (11-63-375)
University of Windsor
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COMPLEX II: FINAL EXAM REVIEW: ACUTE RENAL FAILURE: Acute Renal Failure: Kidney disease may result in partial or complete impairment of kidney function. Results in inability to excrete waste products and water and disturbance in the function of all body systems. Acute Kidney Injury (AKI): - Term referring to mild to severe renal impairment - Abrupt decline in renal function → ↑ creatinine and/or ↓ urine output - Potentially reversible, but mortality rate is high - Commonly follows severe, prolonged hypotension, hypovolemia, or exposure to nephrotoxic agents Added: Need to know lab values for the BUN and Creatnine Need to know the electrolyte values as well Acute Kidney Injury (AKI): Acute renal failure = severe AKI – Requires aggressive management – Frequently requires RRT (renal replacement therapy) – Develops in > 60% of critical care patients, mortality rates 70-80% Added: Neurogenic shock and spinal cord injury or someone who is septic Someone might need dialysis because they have kidney failure Acute Kidney Injury: Develops over hours-days – ↑ Urea – ↑ Creatinine – ↑ K+ – +/- oliguria Added: Within hours the creatnine and BUN can rise Antibioics that affect the kidney We see the changes in their blood work Why would someone have increased potassium when they have kidney failure- the kidneys cannot get rid of the potassium They wont have just no urine, they might have just decreased urine output Added: GFR- glomerular filtration rate Increase in creatnine and or they have the urine output that is dropping- that puts them at risk Patients who are older or diabetic they have decreased kidney function They might have decreased BP as well Categories of Causes of AKI: Pre-renal (external to kidney) Intra-renal (direct damage to renal tissue) Post-renal (mechanical obstruction to urine outflow) Added: Pre-renal- something is happening before the kidneys Intra- something is within the kidneys Post- something after the kidneys Pre-renal Causes of AKI: Those leading to ↓ renal blood flow,& therefore to ↓ glomerular perfusion and filtration: - Hypovolemia - Decreased C - Vasodilation (decreased SVR) - Renal vascular obstruction Intra-Renal Causes of AKI: Those that result in direct damage to renal tissue → nephron dysfunction Renal ischemia → ATN Nephrotoxins (e. contrast dye, aminoglycosides) → ATN Blocked tubules Hgb from hemolyzed RBCs Myoglobin from necrotic muscle cells Renal diseases (e., glomerulonephritis) Acute Tubular Necrosis (ATN) – most common Added: - vasoconstriction going into the kidneys is considered PRE-RENAL ****** Aminoglycosides- another type of antibiotics Acute tubular necrosis- in our burn patients- destruction of the tissues- myoglobin release, blocks the tubules HgB from hemolyzed RBC- someone who gets the wrong blood type – when it INTIIALLY starts they complain FLANK pain (this is how we know the kidneys are affected) Someone going for a coronary angiogram and they need contrast dye we need to assess their BUN and creatnine and their GFR- we need to make sure they can filter out the dye If someone has borderline kidney dysfunction, and they NEED the contrast dye- we give them fluids before and after to help flush the dye an save the kdineys We might also give them medication We give them musomyst- it breaks up muscus- but it also helps them with their bladder Acute Tubular necrosis: (ATN): - Most common intra-renal cause of ARF - Involves necrosis of tubular cells d/t - Ischemia - → disrupted basement membrane and destruction of tubular epithelium - Nephrotoxins - → necrosis of tubular epithelium → sloughing → plug tubules 2. Maintenance (oliguric) phase: Duration: days to weeks Patients may be anuric, oliguric or non-oliguric (~ 30%) Added: Some patients might not have any changes in their urine output - But they are not clearing it out properly - Their specific gravity is not changing which is a MAIN sign - If we drink a lot it becomes diluted and if we don’t its very concentrated - We need to watch to make sure that the patients specific gravity is changing - Even if they have dialyss they still need to pee Maintenance phase continued: -Oliguria (<400 ml/24 hrs) Most common initial sign Usually 10-14 days, but can be longer 2° to reduced GFR → Fluid volume excess → manifestations? -Urine casts, RBCs, WBCs, protein, ↑ Na SG ~ 1, indicating inability to concentrate urine Added: Normal urinalysis we should NOT see protein - if we do this is teling us that the basement membrane of the nephrons is not working, now what happens is molecules that are generally kept in the blood are able to get into the urine - If we think about the diabetic patients we need to watch their urine for proteins If we have early interventions the kdineys will be okay Specific gravity is NOT changing Maintenance phase continued: Metabolic Acidosis Cannot excrete H; bicarb as buffer gets used Acidosis → Kussmaul’s resp Acidosis → hyperkalemia Added: Kussmauls resp- DKA- a complication- rapid breathing because we are trying to blow off CO2 in order to compensate the PH The body can only blow off so much CO2 When they are acidotic it PULLS potassium OUT of the cells and they become hyperkalemic Maintenance Phase Continued: Serum electrolytes Hyponatremia Tubules cannot conserve Na Lethargy, stupor if untreated Hyperkalemia Due to Impaired excretion, acidosis, tissue destruction, transfusions Life threatening Added: Need to know normal electrolyte ranges******** Hyponatremia- the sodium is LOW This is going to affect the central nervous system We need to look up the signs and symptoms of this *** Hyperkalemia- increased potassium Life threatnening This is life threatnening This can cause VENTRIULAR arrythmais (must review this) Maintenance Phase Continued: Calcium deficit Kidneys cannot activate Vit D → impaired GI absorption of Ca 2+ → hypocalemia → PTH secretion → bone demineralization and Ca 2+ and PO4 release Phosphate excess Due to release from bones and impaired excretion Added: Calcium and phosphate goes in the opposite direction CalciumErythropoetin- stimulates the bone marrow to make RBC this also activates vitamin D Meaning we cannot absorb it properly Leadings to hypocalcemia This causes PTH secretion- this is going to try and get the calcium up but this also leads to phosphate being released Hypocalcemia signs ***** When you take this BP and their hand goes crazy- trousseau Chostveks sign- when they have a facial twitch Diagnostic Studies: History UA (cells, casts, protein, hematuria, crystals, SG, osmolality) Labs – BUN (N = 3.6-7 mmol/L) – Creatinine (N = 44 – 133 umol/L) – CBC, electrolytes Creatinine Clearance (N = 85-135 mL/min) Renal Ultrasound (anatomy and function) CT (lesions, masses, obstructions; contrast) Renal scan – blood flow and collecting system Added: eatine clearance- this is looking at how much is being cleared per minute- need to memorize this value Renal ultrasounds are important to look for post-renal causes - We need to be careful if we have to use contrast though - - cyctocsopy- they put a scope through the urethra- they can take biopsies and retreieve stones - Transurethral resection of the prostate Collaborative Care: Prevent/Eliminate cause Manage S/S Prevent complications Prevent/eliminate cause – See health promotion, pg 1338 – Hydrate post angiogram – Fluids for hypovolemia, etc. – Manage heart failure – Monitor renal function with nephrotoxic drugs (e., NSAIDS) Close monitoring of fluid, electrolyte status – S/S electrolyte disturbances – I & O; Daily weights 1 kg weight gain = 1000 ml fluid retention Added: If they need mucomyst- acetylsystoline which is the generic name (look this name up) Acetylsystoline- also used for Tylenol overdose- because when people OD they are at risk of kidney problems We need to manage their heart failure we need to make sure their kdineys are being profesusd Daily weights- are the most important We always weigh them Even if we are watching in and outs there is room for msitakes We don’t weigh the patient at different times, we always need to be consistent ARF: collaborative Care continued: Fluid management – Fluid resuscitation For pre-renal AKI r/t hypovolemia; may be accompanied by diuretics to prevent fluid overload Generally not indicated if renal failure has set in Fluid restriction During oliguric stage Intake = previous 24 hr fluid loss + 600 ml (insensible losses) Fluid removal Diuretics (generally not if renal failure has set in) or Renal replacement therapy Added: Manage their fluids If someone is on a oliguric phase- we might need to give them fluid restriction Memorize that formula previous 24 hr fluid loss + 600 ml (insensible losses) - Previous fluid loss includes urine, and NG tube, if they have 800 from previous loss plus 600 ml that would mean they need 1400ml - Need to know this Insensible loses- sweat, breathing, gut Fluid removal- diuretics Furosemide we are NOT going to give this type of diruretic We are going to remove fluid by hemodialysis or peritoneal dialysis but if the kidneys aren’t working we don’t gve them Lasix because they cannot excrete the fluid Collaborative Care: continued: Treat hyperkalemia – Stabilize myocardium with calcium gluconate – Enhance K removal Kayexalate (oral, rectal, NG) Diuretics (if producing urine) Dialysis Added: Know the medications for the hyperkalemia removal Kayexalate- exchange of potassium and sodium through the gut- the patient NEEDS to have a properly working gut meaning asses for paralytic ileus Someone with extreme hyperkalemia- we can give them insulin- 50% glucose- and they all go back into the cell We give them regular insulin IV and 50% glcose and they all attach to the potassium and goes into the cells Added: Need adequate calories Catabolic state Prevent ketosis we don’t want them breaking down fat Sodium potassium and phosphate One of the break down of proteins is ammonia and nitrogen and hydrogen Watch protein intake Kidney diets are very difficult to maange Phosphate binders- bind up phosphate and gets rid of it Collaborative Care Continued: Renal replacement therapy – Indications Volume overload affecting cardiac or pulmonary function Hyperkalemia Metabolic acidosis BUN > 43 mmol/L Mental status changes Pericarditis, pericardial effusions, or cardiac tamponade Added: Mental status changes- from waste products in the blood going into the brain pericardial effusions-and pericardial tamponade- from the fluid moving to other places Collaborative Care: Continued Renal replacement therapy (cont’) – Movement of fluid and molecules across semi-permeable membrane from one compartment to another – Corrects fluid/electrolyte imbalances; removes wastes – PD vs HD vs CRRT Added: Peritoneal dialysis or hemodialysis Continuous renal replacement therapy some typeof membrane needs to be used to filter out waste products from the patient Collaborative Care Continued: Most common forms of RRT for AKI are – Hemodialysis (HD) Intermittent removal (4 hr/day – 3 or 4 times/wk) Preferred when rapid change over short period needed – Continuous renal replacement therapy (CRRT) Continuous over 24 hrs or longer Slower rate of change Preferred for hemodynamically unstable patients Added: 3-4 times a week hemodialysis CRRT- special type of machine, continuous over 24 hours- initially patients aren’t always stable so this is the type that we would use for the patient If someone is on hemodialysis and their BP is low, the blood is going to clot in the tubing they need to be hemodynamically stable Collaborative Care: Continued CRRT = Continuous renal replacement therapy – Continuous dialysis (and/or ultrafiltration) lasting 12 – 24 hrs or longer (days) – For hemodynamically unstable patients – Less aggressive than HD in terms of speed of removal of fluid/toxins Nursing Diagnosis: Excess fluid volume Risk for infection r/t lines, toxins, ↓ immunity Imbalanced nutrition r/t altered metabolism and dietary restrictions Disturbed thought processes r/t uremic toxins Fatigue r/t anemia, acidosis, uremic toxins Anxiety Potential complications: dyrhythmias; metabolic acidosis **know reasons for why a person might have these diagnosis*** Nursing Management: Prevention Control nephrotoxic drugs/industrial chemicals (insecticides, organic solvents, cleaning agents) Prevent prolonged hypotension, hypvolemia – Careful monitoring of fluid status; – Fluid replacement to prevent renal ischemia Monitor renal fxn with nephrotoxic drugs Identify and monitor high risk populations Ambulatory and Home Care Recovery is variable depending on – Age, general condition – Duration of oliguria – Severity of nephron damage Promote good nutrition, rest and activity Dietary restrictions in accordance with renal function Teach prevention & S/S recurrent disease 3-12 month convalescence May need long term dialysis
Complex II; Final Review; Acute renal Injury
Course: Nursing Care- Complex Health Problems II (11-63-375)
University: University of Windsor
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