AKI (MedSurg) Ch.54
Describe postrenal AKI.
Postrenal AKI usually results from obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hypertrophy, malignancies, and pregnancy. Pressure rises in the kidney tubules, and eventually the GFR decreases.
What happens to urine sodium in pre-renal, intra-renal, and post-renal AKI?
Pre-renal: Decreases to <20 Intra-renal: Increases to >40 Post-renal: Varies, often increases to </= 20
Describe urine specific gravity in the 3 types of AKI.
Pre-renal: Increases Intra-renal: Low normal Post-renal: Varies
Describe urinary sediment in the 3 types of AKI.
Pre-renal: normal, few hyaline casts Intra-renal: Abnormal, casts, debris Post-renal: Usually normal
Prerenal AKI accounts for 60-70% of AKI, describe it.
Prerenal AKI, which occurs in 60% to 70% of cases, is the result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and renal artery stenosis, ultimately leading to a decrease in the GFR
General medical management for the 3 types of AKI.
Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Intrarenal azotemia is treated with supportive therapy, with removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors. Diuretics, albumin, dialysis
Intra renal failure causes
Prolonged renal ischemia resulting from: Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) Myoglobinuria (trauma, crush injuries, burns) Hemoglobinuria (transfusion reaction, hemolytic anemia) • Nephrotoxic agents such as: Aminoglycoside antibiotics (gentamicin, tobramycin) Radiopaque contrast agents Heavy metals (lead, mercury) Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic) Nonsteroidal anti-inflammatory drugs Angiotensin-converting enzyme inhibitors • Infectious processes such as: Acute pyelonephritis Acute glomerulonephritis
RIFLE classification system GFR criteria.
R (Risk) Increased serum creatinine 1.5 × baseline 0.5 mL/kg/h for 6 h OR GFR decreased ≥25% I (Injury) Increased serum creatinine 2 × baseline 0.5 mL/kg/h for 12 h OR GFR decreased ≥50% F (Failure) Increased serum creatinine 3 × baseline <0.3 mL/kg/h for 24 h OR OR GFR decreased ≥75% Anuria for 12h OR Serum creatinine ≥354 mmol/L with an acute rise of at least 44 mmol/L L (Loss) Persistent acute renal failure = complete loss of kidney function >4 wk E (ESKD) ESKD >3 mo
What is a major cause of hospital acquired AKI?
Radiocontrast-induced nephropathy (CIN) At risk patients have creatine greater than 2 mg/dL Prevention: N-acetylcysteine and sodium bicarbonate, prehydration with saline
Postrenal failure causes
Urinary tract obstruction, including: Calculi (stones) Tumors Benign prostatic hyperplasia Strictures Blood clots
Name 5 underlying causes for AKI that may treated before kidney function is impaired.
1. Hypovolemia 2. Hypotension 3. Reduced cardiac output, HF 4. Obstruction of the kidney or lower urinary tract by blood clot, tumor, kidney stone 5. Bilateral obstruction of renal arteries or veins
What are the 4 phases of AKI?
1. Initiation 2. Oliguria 3. Diuresis 4. Recovery
In AKI, urine volume may be normal or change may occur. What are possible changes?
1. Oliguria 2. Nonoliguria (>800 mL/day) 3. Anuria
How do the urine characteristics change in AKI?
1. Output varies from scanty to normal 2. Hematuria may be present 3. Low specific gravity due to inability to concentrate urine (normal:1.010-1.025) Patients with prerenal azotemia have a decreased amount of sodium in the urine (less than 20 mEq/L) and normal urinary sediment. Patients with intrarenal azotemia usually have urinary sodium levels greater than 40 mEq/L with urinary casts and other cellular debris.
What are the 3 major cateories of AKI?
1. prerenal (hypo perfusion of kidney) 2. intrarenal (actual damage to kidney tissue) 3. postrenal (obstruction to urine flow)
What is a widely accepted criterion for AKI?
50% or greater increase in serum creatinine
Assessment and prevention of environmental/medication causes of AKI
A careful history is obtained to identify exposure to nephrotoxic agents or environmental toxins. The kidneys are susceptible to the adverse effects of medications because they are repeatedly exposed to substances in the blood. Patients taking nephrotoxic medications (e.g., aminoglycosides, gentamicin [Garamycin], tobramycin, colistimethate [Coly-Mycin], polymyxin B, amphotericin B, vancomycin, amikacin [Amikin], cyclosporine [Neoral]) should be monitored closely for changes in renal function.
Why should an AKI patient be weighed daily?
AKI causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glucose use and protein synthesis, and increased tissue catabolism. The patient is weighed daily and loses 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (i.e., caloric intake falls below caloric requirements). If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected.
What are general clinical manifestations of AKI?
Almost every system of the body is affected with failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic. The skin and mucous membranes are dry from dehydration. Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures.
What activity level is recommended for AKI?
Bedrest to reduce the metabolic rate and catabolism. Catheters should be avoided for risk of UTI.
What kinds of conditions can lead to ATN?
CKD, diabetes, HF, hypertension, cirrhosis.
What is the classification system for AKI?
Classification criteria for AKI include assessment of three grades of severity and two outcome-level classifications. This five-point system is known as the RIFLE classification system. RIFLE stands for risk, injury, failure, loss and end-stage kidney disease.
Describe intra renal or intrinsic AKI.
Intrarenal AKI is the result of actual parenchymal damage to the glomeruli or kidney tubules. Acute tubular necrosis (ATN), or AKI in which there is damage to the kidney tubules, is the most common type of intrinsic AKI. Characteristics of ATN are intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate and decreased urine flow through the tubule), vasoconstriction, and changes in glomerular permeability. These processes result in a decrease of GFR, progressive azotemia, and fluid and electrolyte imbalances.
What is the most life threatening fluid and electrolyte imbalance that renal patients are at risk for?
Hyperkalemia (look for peaked T waves and K over 5)
If a patient is hemodynamically unstable how would potassium be shifted back into the cells? What might be prescribed?
Indications: low BP, change in mental status, dysrythmia IV dextrose 50%, insulin, calcium
What are nutritional considerations for AKI?
Individualized protein replacement High carb Restrict potassium, phosporus
What is sodium polystyrene sulfonate?
Kayexalate Reduces potassium Enema should be retained for 30 minutes, followed by a cleansing enema May be administered with Sorbitol to induce diarrhea and water loss.
3. Diuresis Phase
The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. Laboratory values stabilize and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal. Because uremic symptoms may still be present, the need for expert medical and nursing management continues. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase.
1. Initiation phase
The initiation period begins with the initial insult and ends when oliguria develops
2. Oliguria phase
The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, and the intracellular cations [potassium and magnesium]). The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL. In this phase, uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. Some patients have decreased renal function with increasing nitrogen retention but actually excrete normal amounts of urine (1 to 2 L/day). This is the nonoliguric form of renal failure and occurs predominantly after exposure of the patient to nephrotoxic agents, burns, traumatic injury, and the use of halogenated anesthetic agents.
After the diuretic phase of AKI, how are patient nutritional considerations changed?
The oliguric phase of AKI may last 10 to 14 days and is followed by the diuretic phase, at which time urine output begins to increase, signaling the patient is in the recovery phase (Ali & Gray-Vickrey, 2011). Results of blood chemistry tests are used to determine the amounts of sodium, potassium, and water needed for replacement, along with assessment for over- or underhydration. Following the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually.
4. Recovery phase
The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patient's normal level. Although a permanent 1% to 3% reduction in the GFR may occur, it is not clinically significant
Prerenal Failure causes
Volume depletion resulting from: Hemorrhage Renal losses (diuretic agents, osmotic diuresis) Gastrointestinal losses (vomiting, diarrhea, nasogastric suction) • Impaired cardiac efficiency resulting from: Myocardial infarction Heart failure Dysrhythmias Cardiogenic shock • Vasodilation resulting from: Sepsis Anaphylaxis Antihypertensive medications or other medications that cause vasodilation
