ACUTE RENAL FAILURE

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ACUTE  RENAL  FAILURE
Results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions. The substances normally   eliminated   in   the   urine accumulate in the body fluids as a result of impaired renal excretion, leading to a disruption in endocrine and metabolic functions as well as fluid, electrolyte, and acid-base disturbances.  It is a systemic disease and is a final   common pathway of many different kidney   and urinary tract diseases. 


CATEGORIES OF ACUTE RENAL FAILURE 
➡️ PRERENAL
Occurs in 60 to 70% of cases,  is the result of impaired blood flow  that leads to hypoperfusion of the  kidney and a decrease in the GFR. Common   clinical   conditions  are:
1. volume-depletion states (hemorrhage  or  Gl  losses)
2. impaired  cardiac  performance (Mi, HF:or cardiogenic  shock)
3. vasodilation (sepsis or  anaphylaxis)

➡️ INTRARENAL 
Is the result of actual parenchymal damage  to glomeruli or kidney tubules. Nephrotoxic agents such  as aminoglycosides and radiocontrast agents  account for 30% of cases of acute tubular necrosis      (ATN),  and  ischemia  due  to  decreased  renal  perfusion accounts for more than 50& of cases. 

➡️POSTRENAL 
 Is usually the result of an obstruction somewhere distal to the kidneys. Pressure rises in the kidney tubules and eventually, the GFR decreases. 

CAUSES OF ACUTE RENAL FAILURE 
A. PRERENAL      
A  decrease  in  renal  function  secondary  to  decreased  renal  perfusion  but  without  renal parenchymal  damage  is  called  prerenal  failure. Causes  of prerenal  failure  include  fluid  volume  depletion,  shock  and impaired cardiac efficiency. 

1. Volume depletion resulting from:           a. Hemorrhage           
 b. renal losses (diuretics)               
 c. Gastrointestinal losses (vomiting, diarrhea. Ngaso gastric suctioning)      

2. impaired cardiac efficiency resulting from:            
a. Ml           
 b. Heart failure                
 c. Dysrhythmias         
 d. Cardiogenic shock     

 3. Vasodilation resulting from shock:         
  a. sepsis          
  b. anaphylaxis             
  c. antihypertensive medications or other  medications that cause vasodilation. 

B. INTRARENAL 
The  most  common  cause  of  intrinsic  or  intrarenal  failure,  or renal  failure  that  develops  secondary  to  renal  parenchymal damage,  is  acute  tubular  necrosis  (ATN). 
1. Prolonged renal ischemia resulting from:      
a. pigment nephropathy (associated with the breakdown of  blood cells containing pigments that in turn occlude           kidney structures). 
 b. Myoglobinuria (trauma, crush injury. Burns)        
c. Hemoglobinuria (transfusion reaction, hemolytic anernia)  

2. Nephrotoxic agents such as:      
a. Aminoglycosides antibiotics (gentamicin, tobramycin)      
 b. Radiopaque contrast media        
 c. Heavy metals (lead. Mercury)      
 d. Solvents and chemicals (carbon tetrachloride, arsenic)     
 e. NSAIDs, ACE inhibitors .

3. infectious processes such as:    
 a. acute pyelonephritis     
 b. acute GN

C. POST RENAL 
A  reduction  in  urine  output  because  of mechanical  obstruction  to  urine  flow  is  called  postrenal  failure. 
1. Urinary tract obstruction, including:  
a. calculi (stones)  
b. tumors 
c. BPH 
d. Strictures  
e. Blood clots

PATHOPHYSIOLOGY 
Acute  renal  failure  (ARF)  is  a  sudden  loss  of  renal  function as  a  result  of  reduced  blood  flow  or  glomerular  injury,  which may  or  may  not  be  accompanied  by  oliguria.  The  kidneys  lose their  ability  to  maintain  biochemical  homeostasis,  causing retention  of  metabolic  wastes  and  dramatic  alterations  in  fluid,  electrolyte,  and  acid-base  balance. 

PHASES OF ACUTE RENAL FAILURE 
1. INITIATION – begins with the  initial insult and  ends when oliguria develops 

2. OLIGURIA: The oliguria period is accompanied by an  increase  in  the  serum  concentration  of  substances usually excreted by the kidneys  (uric acid, urea, creatinine, organic acids). In  this phase uremic symptoms first appear  and  life-threatening  conditions  such  as     hyperkalemia develop. 
3. DIURESIS: The diuresis period is marked by a gradual   increase in urine output, which signals that     glomerular filtration has started to recover. 
4. RECOVERY: The recovery period signals the improvement of renal function and may take 3-12 months.  Lab values return to normal level. Although  a permanent 1-3 reduction in the GFR is  common. 

CLINICAL MANIFESTATION 
Almost every system of the body is affected when there is failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic, with persistent 
➡️ nausea
➡️ vomiting
➡️ diarrhea. 
The skin and mucous membranes are dry from dehydration, and the breath may have the odor of urine (uremic fetor). Central nervous system signs and symptoms include
➡️ drowsiness
➡️ headache
➡️ muscle twitching
➡️ seizures. 

ASSESSMENT 
➡️ PHYSICAL  ASSESSMENT :  Pallor,  edema  (peripheral,  periorbital,  sacral),  jugular  vein  distention,  crackles  (rales),  and  elevated  blood  pressure  (BP)  in  a  patient  who  has  fluid  overload. 
1. EXCESS  FLUID  VOLUME :  Oliguria,  pitting  edema,  hypertension,  pulmonary  edema. 
2. METABOLIC  ACIDOSIS :  Kussmaul  respirations  (hyperventilation),  lethargy,  headache. Electrolyte  disturbance:  Muscle  weakness  and  dysrhythmias. 
3. INFECTION :  Urinary  tract  infection,  septicemia,  pulmonary infections,  peritonitis. 
4. UREMIA  (retention  of  metabolic  wastes):  Altered  mental state,  anorexia,  nausea,  diarrhea,  pale  and  sallow  skin,  purpura, decreased  resistance  to  infection,  anemia,  fatigue.  Note: Uremia  adversely  affects  all  body  systems.
5. GI  SYSTEM :  Nausea,  vomiting,  diarrhea,  constipation,  gastrointestinal  (GI)  bleeding,  anorexia,  abdominal  distention.
6. HISTORY  OF :  Exposure  to  nephrotoxic  substances,  recent blood transfusion,  prolonged hypotensive episodes or decreased renal  perfusion,  sepsis,  administration  of  radiolucent  contrast media,  or  prostatic  hypertrophy.

DIAGNOSTIC  TESTS
➡️ CREATININE  CLEARANCE :  Measures  the  kidney’s  ability  to  clear the  blood  of  creatinine  and  approximates  the  glomerular  filtration  rate.  It  will  decrease  as  renal  function  decreases.  Creatinine  clearance  is  normally  decreased  in  older  persons.
➡️ BLOOD UREA NITROGEN (BUN) AND SERUM CREATININE : Assess progression and management of ARF. Although both  BUN and creatinine will increase as renal function decreases, creatinine is a better indicator of renal function because it is not affected by diet, hydration, or tissue catabolism.
➡️ URINALYSIS : Can provide information about the cause and location of renal disease as reflected by abnormal urinary sedi-ment (renal tubular cells and cell casts).
➡️ URINARY OSMOLALITY AND URINARY SODIUM LEVELS : To rule out renal perfusion problems (prerenal). In ATN, the kidney loses its ability to adjust urine concentration and conserve sodium, producing urine Na+ level greater than 40 mEq/L (in prerenal azotemia the urine Na+ is less than 20 mEq/L).

RENAL IMAGING 
➡️ RENAL ULTRASOUND : Provides information about renal anatomy and pelvic structures, evaluates renal masses, and detects obstruction and hydronephrosis. Because no intravenous (IV) contrast agent is used, this procedure limits risk of further compromise to renal function.
➡️ RENAL SCAN : Provides information about perfusion and function of the kidneys.
➡️ COMPUTED TOMOGRAPHY (CT) SCAN : Identifies dilation of renal calices in obstructive processes.
➡️ RETROGRADE UROGRAPHY: Assesses for postrenal causes (i.e., obstruction).

MEDICAL MANAGEMENT 
The kidney has a remarkable ability to recover from insult. Therefore, the objectives of treatment of Acute renal failure are to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can take place. Any possible cause of damage is identified, treated, and eliminated. Overall, medical management includes:
➡️ maintaining fluid balance
➡️ avoiding fluid excesses
➡️ performing dialysis.

PHARMACOLOGIC THERAPY 
a. Hyperkalemia is the most life threatening of the FE changes that occur in RF. The elevated RF may be reduced by administering cation’ exchange     resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema. It works by      exchanging sodium ions for potassium ions in the intestinal tract 

b. Sorbitol may be administered in combination with Kayexalate to induce diarrhea type effect (induce   water loss in the GIT)


c. If hemodynamically unstable,
IV dextrose 50%, insulin  and calcium replacement may be administered to shift potassium back into the cells. 

d. Diuretics  are often administered to control fluid  volume, but they have not been shown to hasten  the recovery for
From ARF. 


NUTRITIONAL THERAPY 
ARF 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 can be expected to lose 0.2 to 0.5 kg (0.5 to 1 lb) daily. If the patient gains or does not lose weight or develops hypertension, f luid retention should be suspected.
➡️ Dietary proteins are limited to about 1 g/kg during the oliguric phase to minimize protein breakdown and to prevent accumulation of toxic end products. 
➡️ Caloric requirements are met with high-carbohydrate meals because carbohydrates have a proteinsparing effect. 
➡️Foods and fluids containing potassium or phosphorus (bananas, citrus fruits and juices, coffee) are restricted.
➡️ Potassium intake is usually restricted to 40 to 60 mEq/day, and sodium is usually restricted to 2 g/day. 

NURSING MANAGEMENT 
1. Monitor fluid and electrolyte balance.  2. Reducing metabolic,rate’ 
3. Promotion pulmonary function.
4. Prevention infection 
5. Providing skin care.
6. Provision support

NURSING DIAGNOSIS 
1. Risk for Infection related to the presence of uremia
2. Excess Fluid Volume related to compromised regulatory mechanisms occurring with renal dysfunction: Oliguric phase
3. Deficient Fluid Volume related to active loss occurring with excessive urinary output: Diuretic phase
4. Imbalanced Nutrition Less Than Body Requirements related to nausea, vomiting, anorexia, and dietary restrictions
































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