Acute Kidney Injury

Question 1

What is AKI?

Answer 1

the sudden cessation of renal function that occurs when blood flow to the kidneys is significantly compromised.

Can be reversible

There is build of waste, fluid, and electrolyte imbalances due to kidneys not functioning properly

Complications like metabolic acidosis and fluid/electrolyte imbalances can occur

Question 2

What are the phases of AKI?

Answer 2

(OODR)

• Onset: Begins with the onset of the event, ends when oliguria develops, and lasts for hours to days.
• Oliguria: Begins with the kidney insult; urine output is 100 to 400 mL/24 hr with or without diuretics; and lasts for 1 to 3 weeks. In this phase, uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. Kidney labs goes up.
• Diuresis: Begins when the kidneys start to recover; diuresis of a large amount of fluid occurs; and can last for 2 to 6 weeks. Signals that glomerular filtration has started to recover. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase. Labs are stabilizing.
• Recovery: Continues until kidney function is fully restored and can take up to 12 months.

Question 3

What are the causes of AKI?

Answer 3

1. Prerenal (before the kidneys; issues with perfusion to the kidneys):
   
   • cardiac issue; damage to heart and muscle can’t perfuse fluids to the kidneys = decrease cardiac output (hypotension, sepsis, shock)
   • intravascular volume depletion (blood loss associated with trauma or surgery, dehydration, burns, decreased cardiac output as with cardiogenic shock)
   • decreased peripheral vascular resistance
   • decreased renovascular blood flow (renal artery stenosis)
   • prerenal infection or obstruction
2. Intrarenal (within the kidneys; damage to the nephrons):
   
   • Note: there is decreased ability to filter blood, remove waste and excessive water
     
     • tubular necrosis (type of AKI in which there is damage to the kidney tubules)
     • prolonged prerenal ischemia
     • nephrotoxicity (Nephrotoxicity drugs: NSAIDs, antibiotics “amino-glycosides”, chemo drugs, contrast dye)
     • infection
3. Postrenal (between the kidney and urethral meatus; blockage in urinary tract AFTER the kidney to the urethra that prevents urine draining out of system):
   
   • Note: the is increase pressure in kidney and wast and this decreases kidney function
     
     • bladder neck obstruction
     • bladder cancer
     • renal calculi
     • postrenal infection
     • enlarged prostate
     • Neuro injury like a stroke, bladder doesn’t empty properly (neurogenic bladder)

Question 4

What are the clinical manifestations of AKI?

Answer 4

• CNS: drowsiness, headache, muscle twitching, and seizures
• skin and mucous membranes are dry (from dehydration)
• Urinary: low urine output, hematuria may be present, low specific gravity (normal: 1.010 - 1.025)
• metabolic acidosis (patients cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by decreased serum carbon dioxide (CO2) and pH levels.)
• anemia (reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan, and blood loss from the GI tract)
• low calcium levels (may be low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for the elevated blood phosphate levels)

Question 5

What is the non oliguric form of kidney injury?

Answer 5

It occurs predominantly after exposure of the patient to nephrotoxic agents (any substance, medication, or action that destroys kidney tissue), burns, traumatic injury, and the use of halogenated anesthetic agents.

Some patients have decreased renal function with increasing nitrogen retention but actually excrete normal amounts of urine (1 to 2 L/day)

Question 6

What are the nursing interventions?

Answer 6

• monitor labs :
  
  • BUN (it is increased)
  • Creatinine (it is increased)
  • Potassium (With a decline in the GFR, oliguria, and anuria, patients are at high risk for hyperkalemia ; will lead to dysrhythmias, such as ventricular tachycardia and cardiac arrest) WHY??
  • ABGs (the arterial blood gases and serum bicarbonate levels (CO2) must be monitored because the patient may require sodium bicarbonate therapy or dialysis)
• monitor urine output
• treat fluid and electrolyte imbalances
  
  • Hyperkalemia is the most immediate life-threatening imbalance seen in AKI!!!
• watch out for ECG changes (tall, tented, or peaked T waves)
• changes in clinical status
• strict I&Os
• renal diet (restrict K+, sodium and phosphorus; no bananas, citrus fruits, juices, milk products, and coffee)
• if pt is bed rest, to prevent atelectasis and respiration infection, have pt turn, cough, and deep-breathe

Question 7

What are the meds given?

Answer 7

• High K+ levels: administer cation-exchange resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema.
  
  • Kayexalate works by exchanging sodium ions for potassium ions in the intestinal tract. Sorbitol may be given in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract). If a Kayexalate retention enema is given (the colon is the major site of potassium exchange), a rectal catheter with a balloon may be used to facilitate retention if necessary. It is given either orally or by enema, not IV. It also induces diarrhea to get ride of the excess potassium
• If the patient is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia): administer IV dextrose 50%, insulin, and calcium replacement may be given to shift potassium back into the cells.
• Control fluid volume: diuretics
• Elevated serum phosphate: may be controlled with phosphate-binding agents (e.g., calcium or lanthanum carbonate) that help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract.

Question 8

What are the treatments?

Answer 8

• IV fluids or transfusions of blood products
• If AKI is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed
• Dialysis may be initiated to prevent complications of AKI, such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and promotes wound healing.
• Hemodialysis (a procedure that circulates the patient’s blood through an artificial kidney [dialyzer] to remove waste products and excess fluid)
• peritoneal dialysis (PD; a procedure that uses the patient’s peritoneal membrane [the lining of the peritoneal cavity] as the semipermeable membrane to exchange fluid and solutes)

Question 9

What are other nursing concerns that you as a nurse should be aware of?

Answer 9

• nephrotoxic agents (with age, pre-existing kidney disease, the simultaneous administration of several nephrotoxic agents increase the risk of kidney damage)
• Any agent that reduces renal blood flow (e.g., long-term analgesic use) may cause renal insufficiency. Chronic use of analgesic agents, particularly nonsteroidal anti-inflammatory drugs (NSAIDs), may cause interstitial nephritis (inflammation within the renal tissue) and papillary necrosis. Patients with heart failure or cirrhosis with ascites are at particular risk for NSAID-induced kidney disease.
• exposure to contrast dye WHY??
• gerontologic considerations (Suppression of thirst, enforced bed rest, lack of access to drinking water, and confusion all contribute to the older patient’s failure to consume adequate fluids and may lead to dehydration, further compromising already decreased renal function)
• avoid fluid overload
• Many medications are eliminated through the kidneys; therefore, dosages must be reduced when a patient has AKI. Examples of commonly used agents that require adjustment are antibiotic medications (especially aminoglycosides), digoxin (Lanoxin), phenytoin (Dilantin), ACE inhibitors, and magnesium-containing agents.

Question 10

What is the major cause of hospital acquired AKI? What are the preventable measures?

Answer 10

Radiocontrast-induced nephropathy (CIN)

This is a potentially preventable condition. Baseline levels of creatinine greater than 2 mg/dL identify patients at high risk. Limiting the patient’s exposure to contrast agents and nephrotoxic medications will reduce the risk of CIN (Rank, 2013). Administration of N-acetylcysteine and sodium bicarbonate before and during procedures reduces risk, but prehydration with saline is considered the most effective method to prevent CIN