Lewis AKI Student 2025 PDF

NUR-213 2025 Julie Harris Lewis pp 1232-1238  LEARNING OBJECTIVES  Identify and discuss the pathophysiology, clinical manifestations, and medical/nursing management of clients experiencing AKI and prevention ARF  Examine risk factors for AKI across the lifespan and...

NUR-213 2025 Julie Harris Lewis pp 1232-1238  LEARNING OBJECTIVES  Identify and discuss the pathophysiology, clinical manifestations, and medical/nursing management of clients experiencing AKI and prevention ARF  Examine risk factors for AKI across the lifespan and nursing care to reduce these risks.  Distinguish between the three classifications of AKI.  Apply the nursing process as a framework to provide age appropriate, culturally sensitive care of the client with AKI.  Develop teaching strategies appropriate to the client experiencing AKI.  Definition Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal function with a loss of the kidneys' ability to excrete wastes, fluid and electrolyte balance and acid-base balance: Rise in Creatinine of >0.3 mg/dL or more within 48 hours….. or A 1.5 increase from a baseline drawn in the last 7 days…..or Urine volume less than 0.5 mL/kg/hr for 6 hours (call at 2 hours-ICU) The condition often is transient and completely reversible- if it is caught (by an observant critically thinking nurse) and the cause is treated! Incidence  20% of hospitalized clients (used to be 7% of hospitalized clients) develop AKI  60% of ICU patients (used to be 30% of ICU) patients develop AKI  Nsg Safety Priority: ASSESS in all clients  for low UOP  decreased SBP  decreased pulse pressure  thirst, etc. and intervene with oral fluids or an order for IVFs to PREVENT kidney damage!  ACUTE KIDNEY INJURY(AKI) Etiology 1. Kidneys not perfused (Pre-renal) problems before blood gets to kidneys) 2. Damage to kidney itself (Intra-Renal) 3. Obstructed urine flow out of kidney (Post-Renal) problems blocking urine from leaving kidneys TYPES OF AKI 1. Prerenal(kidney not perfused)(most common)- Decreased blood flow to the kidney.(MAP less than 65mmHg) & can lead to intrarenal if not corrected A. No damage to kidney itself (yet) B. Oliguria from decreased blood volume going through kidney caused by: 1. Severe dehydration (burns, GI lossess, hemorrhage, excessive diuresis) 2. Decreased Cardiac Output (CHF, cardiogenic shock, MI, dysrhythmias) 3. Decreased renal blood flow (renal artery thrombosis, embolism, Hepatorenal syndrome) 4. Decreased peripheral vascular resistance (anaphylaxis, neurologic injury, septic shock)-drop blood pressure and kidney perfusion Types of AKI 2. Intrarenal (Damage to the kidney itself) caused by inflammatory or immunologic processes or pre/post renal AKI. 1. nephrotoxic meds (aminoglycosides, CT contrast, lupus, vasculitis, blood transfusion reaction, myoglobin released from necrotic muscle cells) -Acute tubular necrosis (ATN)-most common cause of intrarenal AKI 3. Postrenal- Obstruction of urine flow out because of blockage in ureters, bladder or urethra. 1. BPH, tumors, stones, cancer 2. The back up causes hydronephrosis that increases hydrostatic pressure and tubular blockage  PUTTING IT TOGETHER  Indicate the type of AKI based on the underlying problem: Pre, Intra or Post  Glomerulonephritis  Systemic Lupus  Heart failure  Pelvic malignancy  BPH  Dehydration  Septic shock  CT scan with contrast  Motor vehicle accident with blood loss  Renal artery stenosis  ASSESSMENT (AKI) HISTORY  Recent surgery or trauma, hypotension/shock, NPO for surgery, bowel preps or excessive exercise  Ask about exposure to nephrotoxins.  Medication history especially treatment with antibiotics, ACE inhibitors(any HTN meds), and NSAIDS.  Diagnostic tests with use of a contrast.  Diseases that impair renal function (DM, SLE, HTN, GN, PVD, allergic reactions)  Recent acute illnesses (virus, influenza, cold, sore throats, gastroenteritis)  Ask about urine color, frequency and volume  Client & family hx of renal dx, trauma, cancer or obstruction KDIGO Classification System RIFLE Classification for AKI Phases of AKI  Oliguric Phase (kidneys not working)  Urine output of less than 400 ml/day  Diuretic Phase (kidneys starting to work but can’t concentrate urine)  Urine output of 1-3 Liters/day (that’s a lot)  Recovery Phase  Urine output normalizes and BUN and Creatinine return to normal levels If it starts as intrarenal, then it will progress: Diuretic phase (bc of damage to kidney & can’t concentrate) then Oliguric (if AKI not corrected) , repeat Diuretic phase and then Recovery Phase Phases of AKI (pre and post renal) Oliguric Phase: Manifestations (indications triggering event wasn’t caught and corrected so they are now in AKI) 1. Urinary Changes-oliguria< 400 mL/24hrs 2. Fluid Volume-fluid overload occurs (kidneys aren’t getting rid fluid or electrolytes) 3. Metabolic Acidosis 4. Sodium Balance 5. Potassium Excess 6. Hematologic Problems 7. Waste product Accumulation-elevated BUN/Crea 8. Neurologic problems Diuretic Phase  Daily Urine Output (UOP)- 1-3 liters a day, but up to 5 liters a day  Nephrons not fully functioning  Osmotic diuresis due to high urea concentration and tubules can’t concentrate urine  Kidneys can excrete waste but not concentrate it  Hypovolemia and hypotension are a concern  Monitor for hyponatremia, hypokalemia and dehydration  Lasts 1-3 weeks-at end Bun/Creatinine, acid base and electrolytes start to stabilize Recovery Phase  Identified by:  GFR increasing  BUN and Serum Creatinine decreasing  May take up to 12 months for full recovery  Full recovery doesn’t always occur depends on:  Overall health, severity of kidney injury, and complications Some do not recover and go into early CKD stages or End Stage Renal Disease (ESRD) Diagnosis  History-  Recent surgery or trauma, hypotension/shock, NPO for surgery, bowel preps or excessive exercise  Ask about exposure to nephrotoxins.  Medication history especially treatment with antibiotics, ACE inhibitors(any HTN meds), and NSAIDS.  Diseases that impair renal function (DM, SLE, HTN, GN, PVD, allergic reactions) or renal flow (BPH, bladder cancer, stones)  Laboratory  Rising BUN and creatinine, and abnormal electrolytes.(same as CKD)  AKI does not usually have the same anemia that is associated with CKD  Urine= it can be concentrated with specific gravity greater than 1.030(prerenal- dehydration) …or it can be not concentrated-pale, specific gravity of 1.000(intrarenal- myoglobin, sediment or hemoglobin may be present bc of the damage to the kidney itself)  Diagnostic  Ultrasound - identifies obstructions, kidney size and patency of ureters  Renal scan-identifies renal blood flow, tubular function  CT scan-lesions, masses, obstructions, vascular issues (usually without contrast)  Renal biopsy to determine intrarenal causes  MRI/MRA- usually not done in clients with renal failure  Responding-Fluid/Electrolytes  FLUID VOLUME DEFICIT (will cause or worsen prerenal AKI, or at risk for volume deficit if they are in the intrarenal-diuretic phase)  Treat cause-replace fluid & blood loss (adequate intravascular volume)  Strict I and Os  Assess for s/s of hypovolemia-dry mucous membranes, tachycardia, decreased UOP, hypotensive  Prerenal-Keep MAP 80 mmHg in ICU (use MAP b/c SBP isn’t always an indicator d/t RAAS system) and Heart rate WNL (adequate kidney perfusion)  May Tx with fluid challenges of 500-1000 ml of NS (prior to onset of AKI and oliguria) Responding-Fluid/Electrolytes  FLUID VOLUME EXCESS (oliguric phase)(late prerenal/late intrarenal/late postrenal)  Strict I & Os  Diuretics to increase UOP may be used  Fluid restrictions are implemented (UOP from last 24 hrs plus 600 ml; ex UOP yesterday 350 mL so 350 mL plus 600 = 950 mL allowed for today)  Possible electrolyte restrictions-Na and Potassium  Increase in Daily weights (1kg=1Liter fluid); assess for edema, neck vein distention, S3 heart sounds, HTN, & lung sounds(crackles or decreased) = all signs of hypervolemia  Leads to pulmonary edema, CHF, pericardial and pleural effusions  Nurses must continually assess creatinine & hourly UOP  Responding – Meds & Diet  Medications  Pharmacy – Stop nephrotoxic medications(table 49.3, p 1183) or adjust dose based on kidney function  Diuretics to remove excess fluids/electrolytes; doesn’t heal kidney though, do not give in anuria or ESRD  Caution regarding use of NSAIDS  ACEI-decrease perfusion pressure but cause hyperkalemia (use diuretics & diet to control); (they also decrease proteinuria and progression of kidney disease (CKD) Assess kidney function before CT Scan:  Pt medical hx (DM, HTN, lupus) and BMP  Limit contrast  Hydrate before and after contrast dye administered  1mL/kg/hr for 12 hours or 3mL/kg/hr for 1 hour before procedure  Goal is UOP of 150 ml/hr first 6 hours after contrast given  Responding – Diet  Nutrition Therapy  High rate of catabolism=breakdown of muscle for protein, which leads to an increase in azotemia & more elevated BUN so need good nutrition/calories:  30-35 kcal/kg/day and 0.8-1.0 protein/kg of desired body weight  Sodium intake– adjusted per lab values and restricted PRN for edema, HTN, HF  Fat intake is increased-used as nonprotein calories  Potassium intake adjusted per lab value-hyperkalemia tx Table 51.5, p. 1237  Monitor intake for calories  May need oral supplements, enteral nutrition (Tube feeds) or Parenteral (TPN or PPN – IV)  There are special solutions for kidney patients-low in sodium, potassium and phosphorus – Nepro, Suplena Renalcal Responding- Infection  Infection is leading cause of death in AKI  Use meticulous aseptic technique  Assess for any s/s of infection-swelling, redness, acute pain, fever, malaise, leukocytosis  Some don’t have fevers  Caution with antibiotics - may need lower dose or they will build up because kidneys not excreting them like expected  Kidney Replacement Therapy  INDICATIONS FOR DIALYSIS in AKI:  Symptomatic Uremia – BUN > 120 mg/dL  pericarditis, pericardial effusion or cardiac tamponade  Persistent Hyperkalemia or sudden rapid rise in Potassium (K > 6.5)  Severe Metabolic Acidosis (pH < 7.1 or HCO3 < 15 mEq/L )  Fluid Overload which compromises tissue perfusion  AKI d/t drug toxins may require KRT/RRT to remove toxins  Significant Mental status changes  DIALYSIS THERAPIES: If necessary  Hemodialysis – (intermittent); more emergent (4 hours 3x a week  Continuous Renal Replacement therapy (CRRT)(p1254) – over 24 hrs done slowly for the hemodynamically unstable client in AKI; Ex CVVH; Can’t be used for life threatening uremia Why?? Trialysis Catheter (Temporary) MANAGEMENT OF AKI AKI  PREVENTION  Prevent dehydration; drink 2-3 Liters of water/day  Monitor I&O on all patients, note urine color  Call for UOP less than 0.5/mg/kg/hr for more than 2 hours (ICU/patients with foleys); or patient without foley on med/surg- check every 6 hours not at the end of 12 hours.  Monitor Lab Values- CREATININE, BUN, potassium, sodium. What was their baseline eGFR?  Be aware of what is nephrotoxic….which medications  Stage of AKI  54 yo male 84 kg admitted 2 days ago for MVA (motor vehicle accident)/abd trauma, allergic to PCN, NS at 100 ml/hr, with admitting BUN of 15 mg/dL and Creatinine of 1.0 mg/dL, IV Vancomycin 1 g every 12 hrs via SW # 20 RFA, Ketorolac 50 mg every 6 hrs for pain prn, and hydromorphone 1 mg IV every 4 hours  AM labs today BUN 29 mg/dL and creatinine of 2.1 mg/dL, UOP of 75 ml for 3 hrs and 350 ml for night shift, pain level 8/10, WBCs 13,000, Hgb 9.0/hct 27, NS at 50ml/hr, urine specific gravity of 1.030  What stage of AKI KDIGO is he in? Describe.  Which type of AKI is this pre, intra or post? Why?  List nursing interventions in order of priority?  When would RRT/dialysis be considered? Web Resources  http://kidney.niddk.nih.gov/kudiseases/pubs/kustats/  http://www.kidneyfund.org  http://nkdep.nih.gov/  http://www.cdc.gov/ckd https://app.nearpod.com/?pin=WJZ8I