Week two required Flashcards
Include AKI in a differential diagnosis based on various signs and symptoms
Recognize signs like anorexia, fatigue, nausea, vomiting, pruritus, seizures, and dyspnea. Also, evaluate lab results for ↑ Serum Creatinine and ↓ in urine output.
Recognize AKI quickly and efficiently based on lab work and urine output
AKI is typically recognized by an increase in serum creatinine and a decrease in urine output, with KDIGO stages providing a guideline for severity.
Stage the degree of AKI based on established baseline creatinine
Stage 1: ↑ x 1.5–1.9 or ↑ 0.3 mg/dl; Stage 2: ↑ x 2.0–2.9; Stage 3: ↑ x 3 or ↑ Cr > 4.0 mg/dl or need for dialysis.
Recite the etiology of AKI (prerenal, postrenal, intrinsic) from most common to least common
Prerenal: ↓ Renal perfusion; Postrenal: Obstruction; Intrinsic: AIN, GN, ATN.
Formulate a differential using initial lab work as well as physical exam and history to assist in patient care on rounds
Use lab work (BUN:Cr ratio, Urine osmolality, FeNa) and history (volume loss, medications, comorbid conditions) to guide diagnosis.
Provide a stepwise approach to workup and diagnosis to avoid unnecessary/costly workups
1) Review H&P and hospital records. 2) Analyze lab results and urine output. 3) Consider renal ultrasound and further tests if needed.
Recognize possible warning signs of ‘zebras’ when considering the etiology of AKI
Zebras include rare causes like glomerulonephritis, vasculitis, or drug-induced nephropathy, requiring a high index of suspicion.
Recommend treatment for AKI based on the etiology
Prerenal: Restore perfusion; Postrenal: Relieve obstruction; Intrinsic: Treat underlying cause, support renal function.
Recognize and recite the indications for emergent dialysis
Emergent dialysis is indicated for severe acidosis, hyperkalemia, toxin ingestion, volume overload, and uremia.
Recommend strategies to help prevent AKI
Prevent hypotension, avoid nephrotoxic drugs, ensure adequate hydration, and monitor renal function in at-risk patients.
Epidemiology of AKI
2-3 cases per 1000 persons; 7% of hospitalized patients; 2/3 of ICU patients; Typically because of sepsis; 2/3 of AKI cases resolve within 7 days; Mortality: 25-80%.
Definition of AKI
↓ Kidney function within 48 hours, ↑ Serum Creatinine, ↓ in urine output, and Need for Renal Replacement Therapy (RRT).
KDIGO Stages of AKI
Stage 1: ↑ x 1.5–1.9 OR ↑ 0.3 mg/dl, <0.5 ml/kg/h x 6–12hrs; Stage 2: ↑ x 2.0–2.9, <0.5 ml/kg/h x 12 hrs; Stage 3: ↑ x 3 OR ↑ Cr > 4.0 mg/dl, need for dialysis, or <35 GFR.
Symptoms of AKI
Nonspecific symptoms: Anorexia, Fatigue, Change in mentation, Nausea & vomiting, Pruritus, Seizures, Dyspnea.
Signs of AKI
Asterixis, Myoclonus, Pericardial rub, Edema, Lung Rales, ↓ Urine output (Oliguria: < 400 cc per day; Anuria: <100cc per day).
Prerenal AKI: Epidemiology
Accounts for 70% of community-acquired AKI and 40% of hospital-acquired AKI.
Prerenal AKI: Etiology
Systemic Volume Depletion, ↓ Mean Arterial Pressure, Isolated ↓ Renal Perfusion, Medications (e.g., ACE/ARB, NSAIDs).
Prerenal AKI: Treatment
Stop nephrotoxic medications, ensure adequate blood pressure (MAP > 65 mmHg), and maintain normal urine output with intravenous fluids.
Postrenal AKI: Epidemiology
Accounts for 17% of community-acquired AKI.
Postrenal AKI: Etiology
Extrarenal obstruction: BPH, Neurogenic bladder, Retroperitoneal fibrosis, Cancer. Intrarenal obstruction: Stones, Crystals, Clots, Tumors.
Postrenal AKI: Treatment
Relieve obstruction and hydrate if needed.
Intrinsic AKI: Classification
Glomerular (GN), Interstitial (AIN), Tubular (ATN), Vascular causes (e.g., renal vein thrombosis, malignant hypertension).
Acute Tubular Necrosis (ATN): Epidemiology
85% of intrinsic disease is ATN; 50% ischemic, 35% toxic.
ATN: Pathology
Tubular necrosis occurs due to decreased blood flow or direct toxic effect, leading to cast formation and tubule obstruction.