Definition-Acute Kidney Injury

INTRODUCTION
Kidney failure (also called renal failure) is the partial or complete impairment of kidney function. It results in an
inability to excrete metabolic waste products and water, it contributes to disturbances of all body systems.
TYPES
Kidney disease can be classified as:
• Acute kidney injury
• Chronic kidney disease
DEFINITION- ACUTE KIDNEY INJURY
AKI, previously known as acute kidney failure, is the term used encompass a wide range of the syndrome, ranging
from slight deterioration to severe impairment.
Acute Kidney Injury is characterized by rapid loss of kidney function. This loss can develop over hours or days
accompanied by a rise in serum creatinine, blood urea nitrogen, potassium and with or without reduction in urine
output. AKI is potentially reversible.
ETIOLOGY
The cause of renal failure are multiple and complex, are categorised as prerenal, intra renal (intrinsic) and post
renal causes
Prerenal: those factors external to the kidneys
1. HYPOVOLEMIA
• Dehydration
• Hemorrhage
• GI losses(vomiting, diarrhea)
• Excessive diuresis
• Hypoalbuminemia
• Burns
2. DECREASED CARDIAC OUTPUT
• Cardiac dysrhythmias
• Cardiogenic shock
• Heart failure
• Myocardial infraction
3. DECREASED PERIPHERAL VASCULAR RESISTANCE
• Anaphylaxis
• Neurologic shock
• Septic shock
4. DECREASED RENO VASCULAR BLOOD FLOW
• Bilateral renal vein thrombosis
• Embolism
• Renal artery thrombosis
Intrarenal: The conditions that cause direct damage to the kidney tissue, resulting in impaired nephron function.
1. NEPHROTOXIC INJURY
• Drugs: aminoglycoside (gentamycin, amikacin)
• Contrast media
• Hemolytic blood transfusion reaction
• Severe crush injury
• Chemical exposure: ethylene glycol, lead, arsenic
2. INTERSTITIAL ACUTE KIDNEY INJURY
• Allergies(antibiotics, NSAIDS, ACE inhibitors)
• Infection[acute pyeloacute kidney injury, CMV, candidiasis]
3. OTHER CAUSES
• Prolonged pre renal ischemia
• Acute glomeruloacute kidney injury
• Toxemia of pregnancy
• SLE
Post renal: It involves mechanical obstruction in the outflow of urine.
• BPH
• Bladder cancer
• Calculi formation
• Prostate cancer
• Spinal cord disease
• Strictures
• Trauma (back, pelvis, perineum)
PATHOPHYSIOLOGY
These factors reduce the systemic circulation
A reduction in renal blood flow
Decrease glomerular perfusion and filtration of kidneys.
GFR is reduced.
Prerenal oliguria, azotemia, increased sodium & water retention,

decreased urine output
Prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged. The kidneys loses its ability to
compensate and damage to kidney parenchyma occurs.
Intrarenal causes
Prolonged ischemia, nephron-toxins, hemoglobin from hemolysed RBC,

myoglobin from necrotic muscle cells
Damage to the renal parenchyma
Nephro-toxin obstruction of intrarenal structures by

crystalizing and causing damage to the epithelial cells of tubules.
Hemoglobin and myoglobin block the tubules and cause

vasoconstriction.
Post renal: It involves mechanical obstruction in the outflow of urine.
Urine flow is obstructed
Urine reflexes into the renal pelvis
Hydrostatic pressure increases
Tubular blockage
Disruption of kidney function
If obstruction is relived within 48 hours, complete recovery is likely. Prolonged obstruction, after 12 weeks, can
lead to tubular atrophy and irreversible kidney fibrosis.
CLINICAL FEATURES
•  Oliguric phase
•  Diuretic phase
•  Recovery phase
Oliguric phase
 Urinary changes-The most common initial manifestation of AKI is oliguria, a reduction in urine output less
than 400 mL/day.
Occurs within 1 to 7 days.
If ischemia, occurs within 24 hours
If nephrotoxic drugs, onset is delayed for as long as 1 week
Lasts on an average of 10 to 14 days.
 Fluid volume
Fluid retention due to decreased urine output.
Distended neck vein
Bounding pulse
Edema
Hypertension
Fluid overload eventually leads to heart failure, pulmonary edema, and pericardial and pleural effusion
 Metabolic acidosis- the kidneys cannot synthesis ammonia or excrete uric acid. The serum bicarbonate
level decreases because HCo3 is depleted in buffering hydrogen ions.
Kussmaul respiration
 Hyponatremia- Damaged tubules can consequently, the urinary excretion of sodium may increase, resulting
in normal or below-normal levels of serum sodium. Excessive intake of sodium should be avoided because it can
lead to volume expansion, hypertension, and HF. Uncontrolled hyponatremia or water excess can lead to cerebral
edema.
 Hyperkalemia
 Leukocytosis
 Elevated BUN and creatinine
DIURETIC PHASE
Daily urine output is usually 1-3L, but may reach 5 L or more. High urine output is due to osmotic diuresis from
the region of high concentration in the glomerular filtrate and the inability of tubules to concentrate the urine.
•  Hypovolemia, hypotension hyponatremia, hypokalemia and dehydration can occur.
•  Kidneys starts to excrete waste, but not concentrate urine.
•  The diuretic phase lasts for 1 to 3 weeks.
RECOVERY PHASE
The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and
then decreases. Although major improvements take place in the first 1 to 2 weeks of this phase, kidney function
may take upto 12 months to stabilize.
DIAGNOSTIC STUDIES
• History collection
• Physical examination
• Serum creatinine and BUN level
• Serum electrolytes
• Urinalysis- urine sediment containing abundant cells, casts or proteins suggest intrarenal disorders.
• Renal ultrasound- A kidney ultrasound is often the first test done, since it provides imaging without
exposure to potentially nephrotoxic contrast agents. It is useful for evaluating for possible kidney
disease and obstruction of the urinary collection system.
• Renal scan - A renal Scan can assess abnormalities in kidney blood flow, tubular function, and the
collecting system.
• CT scan - A computed tomography (CT) scan can identify lesions, masses, obstructions, and vascular
anomalies.
• Renal biopsy - A renal biopsy is considered the best method for confirming intrarenal causes of AKI.
MEDICAL MANAGEMENT
The goal of treatment in patients with AKI is to eliminate the cause, manage the signs and symptoms and prevent
complications while kidney recovers.
•  Treatment of the precipitating factor
•  Fluid restriction
Fluid intake= previous 24hrs output +600ml

NB: Output means all losses for the previous 24 hrs: urine diarrhoea, emesis, blood
600ml for insensible loss: respiration, diaphoresis
 Nutritional therapy
o Adequate protein intake (0.6-2 g/kg/day) depending on the catabolism.
o Potassium restriction - 40mEq/day
 DIURETIC THERAPY is often administered along with volume expanders to prevent fluid overload. The
therapy includes loop diuretics e.g furosemide [Lasix], bumetanide or osmotic diuretic like mannitol.
 HYPERKALEMIA is the most common complication in AKI.
Regular Insulin IV
• Potassium moves into cells when insulin is given.
• IV glucose is given concurrently to prevent hypoglycemia.
• When effects of insulin diminish, potassium shifts back out of cells.
Sodium Bicarbonate
• Therapy can correct acidosis and cause a shift of potassium into cells.
Calcium Gluconate IV
• Generally used in advanced cardiac toxicity (with evidence of hyperkalemic ECG changes).
• Calcium raises the threshold for excitation, resulting in dysrhythmias.
Hemodialysis
• Most effective therapy to remove potassium.
• Works within a short time.
Sodium Polystyrene Sulfonate
• Cation-exchange resin is administered by mouth or retention enema.
• When resin is in the bowel, potassium is exchanged for sodium.
• Therapy removes 1 mEq of potassium per gram of drug.
• It is mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of potassium-
rich stool from body
Dietary Restriction
Potassium intake is limited to 40 mEq/day.
Primarily used to prevent recurrent elevation; not used for acute elevation.
RENAL REPLACEMENT THERAPY
Renal replacement therapy (RRT) is a term used to refer to modalities of treatment that are used to replace the
waste filtering functions of a normal kidney.
The most common indication for RRT in AKI are
a) Volume overload resulting in compromised cardiac or pulmonary status
b) Elevated serum potassium level
c) Metabolic acidosis[serum HCo3 less than 15mEq/L]
d) BUN level greater than 120mg/Dl
e) Significant change in mental status
f) Pericarditis, pericardial effusion or cardiac tamponade.
.NURSING MANAGEMENT
Nursing assessment
• Monitor vital signs and fluid intake and output.
• Examine urine for color, specific gravity, glucose, protein, blood, and sediment.
• Assess the patient general appearance, including skin color, edema, neck vein distension and bruises.
• Assess the patient’s level of consciousness and mental status.
Nursing diagnoses
• Excess fluid volume related to kidney failure and fluid retention
• Fatigue related to anemia, metabolic acidosis and uremic toxins
• Anxiety related to disease processes, therapeutic interventions and uncertainty of prognosis
• Risk for infection
Planning
• The overall goals are that patient with AKI will
• Completely recover without any loss of kidney function.
• Maintain normal fluid and electrolyte balance.
• Have decreased anxiety.
• Adhere to and understand the need for careful follow up care.
Interventions
• Prevention and early recognition of the AKI are the most important components of care.
• Careful monitoring of I/O fluid and electrolyte.
• Assess and record extra-renal losses of fluid from vomiting, diarrhea hemorrhage etc.
• Prompt replacement of significant fluid loss.
• Diuretic therapy for patient with fluid overload, but aggressive diuretic therapy should be avoided
because it can cause reduction in renal blood flow.
• Take daily weight with same scale at the same time of each day to detect excessive weight gain or
loss[1kg=1000 mL of fluid]
• Meticulous aseptic technique is critical.
• Perform skin care and take measures to prevent ulcers
• Mouth care
Evaluation
The expected outcomes are that the patient with AKI will
• Regain and maintain normal fluid and electrolyte
• Adhere to the treatment regime
• Experience no complication
• Have a complete recovery..

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INTRODUCTION

These factors reduce the systemic circulation

A reduction in renal blood flow

Decrease glomerular perfusion and filtration of kidneys.

Prerenal oliguria, azotemia, increased sodium & water retention,

Prolonged ischemia, nephron-toxins, hemoglobin from hemolysed RBC,

Damage to the renal parenchyma

Nephro-toxin obstruction of intrarenal structures by

Hemoglobin and myoglobin block the tubules and cause

Urine flow is obstructed

Urine reflexes into the renal pelvis

Hydrostatic pressure increases

Disruption of kidney function

Fluid intake= previous 24hrs output +600ml

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