Kidney Injury PDF

Week 9 Acute Kidney Injury Kidney Function Responsible for maintaining fluid and electrolyte homeostasis Ridding the body of water soluble wastes Regulating the amount and composition of the urine Performs 2 important endocrine functions ○ production of erythropoietin (hormone)...

Week 9 Acute Kidney Injury Kidney Function Responsible for maintaining fluid and electrolyte homeostasis Ridding the body of water soluble wastes Regulating the amount and composition of the urine Performs 2 important endocrine functions ○ production of erythropoietin (hormone) regulator of red blood cell quantity reduction of this you will have reduction of red blood cell less oxygen being delivered to kidney ○ activation of vitamin D cofactor(necessary) for intestinal calcium absorption; to be absorbed by intestines Filters more than 7 Liters per hour glomerulus is the kidney filter excrete hydrogen ions (excess); if not able to excrete patient will suffer Metabolic Acidosis Electrolytes (normal levels) Potassium 3.5-5.0 mEq/L ○ intracellular ○ To low or high heart becomes irritable Sodium 135-145 mEq/L ○ low causes mental confusion ○ high water retention ○ Low sodium causes muscle cramps and weakness ○ low sodium mental confusion ○ maintaining osmotic pressure in extracellular fluid Calcium 8.5-10.5 mg/dL  ○ in renal failure when calcium levels are low this will stimulate the parathyroid hormone ○ this will cause removal of calcium and phosphate from the bones ○ excessive parathyroid hormone stimulation will lead to Osteodystrophy weakened bones a greater risk of fractures in chronic kidney disease when calcium levels are low the body compensates by activating the parathyroid hormone this results in secondary parathyroidism ○ produces excessive amounts of this hormone ○ this is the most sensitive and earliest indicator that you are having abnormal metabolism in the bone Phosphorus 3.9-4.5 mg/dL ○ Kidney’s are the primary organ that excretes phosphorus ○ we get phosphorus in food that we consume ○ kidney failure we are not able to excrete ○ In kidney damage phosphorus is high and calcium is low ○ kidney’s are also involved in acid base balance ○ kidney’s excrete excess hydrogen ions ○ in Renal failure there is an excess of hydrogen ions ○ retaining will cause Metabolic acidosis Hormonal Regulation Erythropoietin (epogen) ○ in kidney failure this is reduced  ○ If this is reduced it causes reduction in red blood cells and decreases oxygen to the kidney’s ○ available through a therapeutic injection increase red blood cell and increase in the amount of oxygen delivered to the kidney’s Vitamin D ○ formed in the skin due to UV rays in sunlight ○ this is needed for calcium to be reabsorbed into the intestines positive Chevsek’s sign positive Trous ○ chronic renal failure the production of vitamin D is impaired and then there will be poor calcium absorption patients will experience hypocalcemia Addressing Clinical Problems When patients are anemic due to kidney problem ○ reduction in red blood cells leads to anemia erythropoietin (Epogen) replacement is given ○ reduced blood flow activation of the renin-angiotensin aldosterone system ○ hypertension damages the capillaries in the glomerulus waste products are filtered from the blood into the kidney tubules the blood is filtered by the glomerulus and this is what’s called GFR (Glomerular Filtration Rate) ○ 90-120 is adequate level ○ GFR above 60 mL per minute is more adequate level  ○ less than 15 mL you are experiencing END STAGE RENAL DISEASE ○ GFR is the best test to know just how well the kidneys are functioning and filtering leads to end stage kidney disease large amounts of protein in urine is a sign that glomerulus is not working properly Acute or Chronic Renal Injury (Azotemia) condition characterized by abnormal of nitrogen waste products in the blood ○ urea BUN liver produced and Kidney filters ○ creatinine muscle metabolism is waste product of muscle elevated BUN and creatinine ○ kidneys are not excreting waste properly Uremia abnormally high levels of waste products in the blood ○ dangerous condition that occurs when kidney no longer can filter properly ○ occurs when a person is in the final stage of chronic kidney disease Three types of Azotemia Prerenal Azotemia ○ Reduced blood flow to the kidneys without structural damage ○ Retain the ability to concentrate urine and reabsorb BUN ○ elevated BUN and Creatinine ○ This is reversible this occurs due to heart failure  dehydration ○ if untreated it can progress to intrinsic kidney damage Intrinsic (renal) Azotemia ○ direct damage to the kidneys themselves glomeruli tubules interstitial tissue ○ impairs the ability to filter blood, reabsorb solutions, and concentrate urine ○ causes acute tubular necrosis glomerulonephritis Postrenal Azotemia ○ obstruction of outflow kidney stones enlarged prostate tumors ○ kidneys may still concentrate urine but over time tubular function is lost ○ BUN 6-20 mg/dL normal ○ Creatinine 0.6-1.2 mg/dL normal Prerenal Injury (Azotemia) We are looking to restore the blood flow for the kidneys to function adequately ○ Hemorrhage ○ dehydration ○ burns ○ heart failure ○ myocardial infarction  ○ people that are hypotensive tend to have Azotemia tachycardia decrease in urinary output kidney tries to save itself by angiotensin the blood pressure helps to drive Specific Causes Medication that interfere with perfusion/blood flow to the kidney will precipitate pre renal failure ○ NSAIDS cause vasoconstriction of afferent arterioles Motrin/ibuprofen less blood will be delivered to the kidney’s afferent arterioles bring blood to the kidney ○ ACE inhibitors reduce glomerular perfusion pressure (decrease GFR) Zestril/lisinopril Capoten/captopril cause vasodilation of efferent arterioles exit with blood; so they will be less blood output ○ Angiotensin II Receptor Blockers reduce glomerular perfusion pressure (decrease GFR) Cozaar/losartan Diovan/valsartan Atacand/candesartan Intrarenal (intrinsic) Acute Kidney Injury Most common cause ○ acute tubular necrosis Nephrotoxic agents  ○ Radiographic contrast media causes tubular cell toxicity and ischemia ○ BUN and creatinine need to be tested before these tests are performed Rhabdomyolysis ○ breakdown of muscle tissue that release protein in the blood and damages renal tubules ○ trauma ex: MVC like a crushing injury ○ myoglobin protein that stores and transports oxygen in muscles sensitive indicator of muscle damage certain antibiotics ○ aminoglycosides this is given for serious infections but nephrotoxic to the kidney and ototoxic ( inner ear) gentamicin tobramycin streptomycin the effective dose is close to the toxic dose this is given by weight based monitor BUN and creatinine levels Acute Tubular Necrosis (Initial Phase) During this phase the kidney tubules start to suffer damage due to insufficient oxygenation or exposure to toxic substances ○ example ischemia contrast dye symptoms  ○ decreased urinary output with mild increased BUN and creatinine levels Reversibility ○ if recognized early less damage is done Acute Tubular Necrosis (Maintenance Phase) Duration 1-2 weeks; depends on severity period of maximum kidney dysfunction GFR rate drops oliguria low urine output ○ 400 ml/hr osmotic diuresis fluid and electrolyte depletion hypokalemia hyponatremia hypocalcemia gradual normalization of the BUN and creatinine levels Postrenal Acute Kidney Injury Benign prostatic hyperplasia kinked or obstructed catheters intra-abdominal tumors strictures calculi drugs  ○ form precipitates clogged ureters ○ acyclovir-antiviral used to treat herpes virus ○ indinavir- HIV protease inhibitor used to treat HIV/AIDS Clinical Manifestations Elevated blood pressure S3 heart sound indicates decreased left ventricular function of heart failure pulmonary crackles ○ volume excess ○ SOB ○ pulmonary edema jugular venous distention ○ due to volume excess anemia due to suppression of erythropoietin secretion Diagnostic Tests Urinalysis ○ proteinuria ○ RBCs and WBCs ○ tubular epithelial cells elevated serum creatinine ○ normal 0.6-1.2 mg/dL elevated Blood Urea Nitrogen (BUN) ○ normal 6-20 mg/dL serum electrolytes ○ potassium elevated ○ sodium decreased  arterial blood gasses ○ metabolic acidosis complete blood count Renal Ultrasonography End stage renal disease ○ will be shrinked (NEED TO LISTEN) used to identify obstructive cause of renal failure to differentiate between AKI from end stage renal disease (ESRD) Medications Loop diuretics ○ potassium excretion Bumex/bumetanide Edecrin/ethacrynic acid Lasix/furosemide Dermadex/torsemide Osmotic diuretics ○ will pull extracellular water into the vascular system Osmitrol/mannitol Ureaphil/urea ○ acute kidney injury need to maintain urinary output and further renal damage ○ can help flush out myoglobin protein that clogs kidney in Rhabdomyolysis Electrolyte Modifiers Used in Hyperkalemia ○ calcium chloride help to normalize calcium level and cause phosphorus levels to decrease ○ calcium gluconate  restores balance of cell membrane and reduces the heart muscle excitability ○ sodium bicarbonate ○ sodium polystyrene sulfonate used to remove excess potassium by changing sodium (NEED TO HEAR) Three types of Dialysis Hemodialysis ○ arteriovenous fistula connect artery to vein radial or brachial artery non dominant arm increase venous flow; takes about a month to increase and walls to thicken GOLD STANDARD ○ arteriovenous graft synthetic tube to surgically connect artery to vein ready for use in two weeks suitable for patients that have weak or small veins ○ central venous catheter this is done when someone is in an emergency state of kidney failure placed in a larger blood vein internal jugular, femoral vein, and (NEED TO LISTEN) ○ end stage and chronic ○ 3-4 times per week Peritoneal dialysis ○ peritoneal catheter ○ inserted in peritoneal cavity, lining of inside of stomach secured with sutures ○ has a dressing over it ○ done at home daily ○ aseptic technique when this is done gloves mask ○ two types of peritoneal dialysis continuous ambulatory dialysis Dialysate is left in abdomen for 4-5 hours Then it is drained out patient needs to do this exchange 3-5 exchanges per day total time is called one exchange (NEED TO HEAR) less restriction in their lifestyle automated peritoneal dialysis uses a machine cycles through multiple exchanges through the night you need to be connected 10-12 hours during nighttime you don’t need to be connected throughout the day aseptic technique needs to be used by patient or family member when they are helping with this dialysis the amount of fluid that goes in to stay in peritoneal space has a high concentration of glucose this helps the waste products and more fluid to be removed which increases the osmotic pressure  Continuous Renal Replacement therapy ○ acute kidney injury ○ 24 hours process Fistula you can auscultate and hear (NEED TO HEAR) you DO NOT want to do blood pressure on the arm that has fistula removes excess toxins dialysis is a life saving intervention ○ first used in 1924 ○ signed by law in 1972 lowers elevated drug levels Implementation of Care Monitor hourly intake and output daily weights assessing vital signs every 4 hours assessing breath sounds monitoring serum electrolytes ○ hyperkalemia ○ hyponatremia ○ hyperphosphatemia if elevated we need to be aware of hypocalcemia fluid restriction is pivotal