ACUTE RENAL FAILURE

Cabalfin, Ma. Isabel Cisneros, Reuben Chu, Johntone Contega, Janine Dacles, Steven Paul

DISCUSS THE FF.:

Pathophysiology Categories/ Causes of ARF Stages of ARF Assessment and Diagnostic Findings Complications Medical Management Nursing Management

RENAL FAILURE

It is the inability of nephrons in kidneys to maintain fluid, electrolyte & acid-base balance, excrete nitrogen waste products & perform regulatory function such as maintaining calcification of bones & producing erythropoietin.

PATHOPHYSIOLOGY
Hemorrhage, Dehydration, Vascular Obstruction Glomerular Inflammation Drugs, myoglobinemia, hemaglobinemia

Decrease Renal Blood Flow

Nephrotoxicity

Ischemia Increase tubular permeability Tubular damage & obstruction

Decrease glomerular filtration & impaired tubular secretion

Oliguria

Azotemia

Electrolyte Imbalance

Acid-base Imbalance

CATEGORIES/ CAUSES OF ARF

Prerenal

Hypoperfusion, as from volume depletion disorders, extreme vasodilation, or impaired cardiac performance
Parenchymal damage to the glomeruli or kidney tubules, as from burns, crush injuries, infections, transfusion reaction or nephrotoxicity, which may lead to acute tubular necrosis (ATN) Urinary tract obstruction, as from calculi, tumor, strictures, prostatic hyperplasia, or blood clots

Intrarenal

Postrenal

STAGES OF ARF

Initiation phase

onset of injury through the cell death period further damage to the renal tubular wall and membranes source of obstruction has been removed but the residual scarring and edema of the renal tubules remains can last from several months to over a year

Oliguric phase

Diuretic phase

Recovery phase

INITIATION PHASE
Renal flow at 25% of normal Oxygenation to the tissue at 25% of normal Urine output at 30 ml (or less) per hour Urine sodium excretion greater than 40 mEq/L In this phase only 50% of the patients are noted to be oliguric. With prompt treatment, irreversible damage can be achieved during this pre renal failure onset phase.

OLIGURIC/ANURIC PHASE
Great reduction in the glomerular filtration rate (GFR) Increased BUN/Creatinine Electrolyte abnormalities (hyperkalemia, hyperphosphatemia and hypocalcemia) Metabolic acidosis

DIURETIC PHASE
Increase in glomerular filtration rate (GFR) Urine output as high as 2-4 L/day Urine that flows through renal tubules Renal cells that cannot concentrate urine Increased GFR in this phase contributes to the passive loss of electrolytes which requires the administration of IV crystalloids to maintain hydration.

RECOVERY PHASE
edema decreases renal tubules begin to function adequately fluid and electrolyte balance are restored (if damage was significant, BUN and Creatinine may never return to normal levels). At this point the GFR has usually returned to 70% to 80% of normal.

ASSESSMENT(CLINICAL MANIFESTATION)
Critical illness and lethargy with persistent nausea, vomiting & diarrhea Skin & mucous membranes are dry; breath has odor of urine(uremic fetor) CNS manifestations

Drowsiness, Headache, muscle twitching, seizures

Urine Output scanty to normal; urine may be bloody with low specific gravity

ASSESSMENT(CLINICAL MANIFESTATION)
Steady rise in BUN may occur depending on degree of catabolism; serum creatinine values increase with disease progression Hyperkalemia

may lead to dysrhythmias and cardiac arrest

Progressive acidosis
increase in serum phosphate concentration low serum calcium levels

Anemia

from blood loss due to uremic gastrointesitnal lesions, reduced RBC life-span & reduced erythropoietin production

DIAGNOSTIC FINDINGS
BUN, Creatinine, Electrolyte analyses Urine output measurements Renal ultrasonography, CT and MRI scans

COMPLICATIONS
Water overload Hyperphosphataemia Hyperkalaemia Chloride levels raised (plasma or serum) Hypernatraemia Amylase levels raised (plasma or serum) Hypocalcaemia Metabolic acidosis Reduced level of consciousness Nausea and vomiting Diabetes insipidus, nephrogenic Weight loss

COMPLICATIONS
Pyruvic acid levels raised (blood) Urea levels raised (plasma or serum) Pericarditis Immune deficiency Hypermagnesaemia Bicarbonate levels low (plasma) Oedema Weight gain Creatinine levels raised (plasma or serum) Acute confusional state Bleeding tendency Pulmonary edema

MEDICAL MANAGEMENT
Fluid balance Blood flow Dialysis Ion exchange resin Intravenous glucose & insulin & calcium glutamate Sodium Bicarbonate Parenteral erythropoietin Shock and infection Arterial blood gas

MEDICAL MANAGEMENT

Ventilatory measures if respiratory problems develops Phosphate-binding agents to control elevated serum phosphate concentration Dietary protein is limited to about 1g/kg during oliguric phase Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition Foods and fluids containing potassium and phosphorus are restricted Blood chemistries are evaluated to det. Amt. Of replacement Na, K and H2O during oliguric phase After the diuretic phase, high protein, high-calorie diet is given with gradual resumption of activities

NURSING MANAGEMENT
Monitoring Fluid and Electrolyte levels Reducing Metabolic Rate Promoting Pulmonary Function Avoiding Infection Providing Skin Care Providing Support During Dialysis