Acute Kidney Injury Reversible PDF

Preview

Summary

notes for acute kidney injury from lectures from class 9...

Description

ACUTE KIDNEY INJURY( REVERSIBLE) -

SUDDEN decrease of renal failure DUE TO: 1. Prerenal: issues with perfusion to the kidney. ( from the heart to the renal arteries) The blood that gets oxygenated goes to the nephrons; which is the functional unit of the kidneys that filters blood and reabsorbing nutrients and makes urine. - Decreases the function of the kidney: decreased blood to the kidney to filter and deprives kidneys of nutrients. ( can lead to intrarenal injury) - What can lead to this: Cardiac issues. MI: damaged heart muscles that cant pump the blood leading to decrease cardiac input. Bleeding: decrease bf going to the kidney not perfusing it. Dehydration: hypovolemia . Burns: which depletes the body of fluids. - The renal system senses decrease in perfusion and activates RAAS and RAAS conserves water and sodium in order to maintain BP. Low urine output and increase BUN and Creatinine. 2. Intrarenal: damage to the nephrons. - Decreased ability to filter the blood. Which leads to excessive waste, water and can't maintain electrolyte levels. Increase of urea, nitrogen, and creatinine and progressive increase of potassium - What can lead to this: Nephrotoxic drugs: NSAIDs, antibiotics “Aminoglycosides”, chemo drugs and contrast dye. Infection: glomerulonephritis . Injury-stenosis/thrombosis - Hemoglobin released from hemolyzed RBCs and myoglobin released from necrotic muscle cells.{TB} 3. Postrenal: blockage in the urinary tract “AFTER” the kidneys to the urethra. - Prevents urine from draining out of the system: Pressure and waste builds in the kidneys and decreases kidney function. - What can lead to this: Renal Calculi, enlarged prostate(BPH),cancer, neuro injury “stroke”. Bladder doesn't empty properly.

BASICS ABOUT THE KIDNEY/LABS - Adults should void 1-2 L/day, greater than 30 ml/hr

-

-

-

Urine consists of water and ions…. Urea: waste product from protein breakdown(BUN), Creatinine waste product from muscle breakdown. Creatinine normal level 0.6-1.20 mg/dl Creatinine is solely filtered out via glomerulus and is not reabsorbed or secreted in the nephron. If there is too much creatinine then there is a decrease of function in the kidneys because creatine is not being filtered out. Creatinine clearance: the amount of blood the kidneys make per minute that is FREE of creatinine. Female: 85-125ml/min Male 95-140 ml/min Glomerular filtration rate(GFR): 90 ml/min or higher. If gfr is decreased…. - urinary output is decreased: oliguria ( less than 400 ml/day) - water is increased in the body: hypertension, edema. - Waste is increased( Azotemia). BUN and Creatinine elevated. Metabolic acidosis. - Electrolyte imbalance: hyperkalemia. High phosphate and low calcium. Phosphate and calcium are related when one is up the other one is down. BUN: 6-20 mg/dl: breakdown of protein liver, secreted in the blood and filtered in the kidneys. Dehydration can cause BUN to increase.

STAGES 1. Initiation: starts from the cause of injury to the kidneys and ends when s/s appear. ( few hours to several days). Must find cause and prevents. - Decrease in circulating volume, resulting in decrease tissue oxygen. Compensatory mechanisms the release of angiotensin 2, aldosterone, norepinephrine, and antidiuretic hormone to preserve the blood flow to the essential organs. Vaosoconstriction occurs. {TB} 2. Oliguric: ( last a week to 2 weeks) MAY SKIP THIS PHASE AND GO TO THE DIURES STAGE…. Urine output less than 400 ml/day because glomerulus decreases the ability to filter blood. - Increase BUN and Creatinine: Neuro changes (confusion, sluggish), Build up goes to the skin and may cause itching. - NI- low protein diet, safety - Hyperkalemia: watch out for cardiac issues. Tall peak T waves, wide QRS, prolonged PR interval.

-

-

-

NI- Restrict potassium rich food, monitor ekg, labs, “kayeoxolate” lowers potassium. Increased fluid in the body: edema, pulmonary + cardiac issues. - NI- Limit fluid intake, strict I&O. daily weights. Monitor BP, lung sounds, O2 sat, swelling. Metabolic acidosis- Ph < 7.35: confusion, kussmaul breathing- decreased rapid breathing to blow off excess CO2. - NI- Safety, resp. Status. Mild hyponatremia( can run low because of the extra fluid build up diluting), increase phosphate and decreased calcium, high specific gravity >1.020( very dark urine)

TX- DIALYSIS 3. Diureses:( Last 1 week to 3 weeks) Nephrons are on their way to recovery. Filters blood but can't concentrate urine. - GFR starts improving( still abnormal).. Allows BUN and Creatinine to decrease ( still abnormal). Mental status improves - Voiding 3-6 liters per day due to osmotic diuresis. The patient was peeing so now everything is coming out. High amounts of urea is coming out. - Hypovolemic due to the excess output of urine… dehydration, hypotension, hypokalemia, < 1.020 specific gravity very diluted urine. - NI- I&Os, daily weights, s/s of dehydration, supplements and Iv fluids. 4. Recovery:(Can a year or more) Starts when GFR returns to normal. - 1-2 L/day urine ouput - Labs return to normal Some people never make it to this stage due to the amount of damage and end up having CKD or renal failure. THE BOOK -s/s: edema, pulmonary edema, sob, hf, jvd, htn, dysrhythmias, chest pain/pressure. Anorexia, constipation or diarrhea, nausea, confused, lethargic. Crackles. FLANK pain - Restrict potassium. Restrict sodium because of the edema,htn, and chf. -hyperkalemia- decreases the threshold necessary to generate an action potential.

- meds- furosemide(lasix), bumetanide(bumex), and osmotic diuretic(mannitol) - dextrose,insulin, and calcium can reduce potassium

CHRONIC KIDNEY DISEASE( IRREVERSIBLE) Significant decreased renal function that occurs over a period of time. Early stages will be asymptomatic. GFR decreases leads to: - Increase BUN and creatinine - Hypervolemia - Increase potassium - decreased urinary output - Increase phosphate...