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Presentation on theme: "A CUTE R ENAL F AILURE /A CUTE K IDNEY I NJURY Dr. Sudarshan Singh."— Presentation transcript:


2 I NTRODUCTION Acute renal failure (ARF), or acute kidney injury (AKI), [as it is now referred to in the literature], is defined as An abrupt or rapid decline in renal filtration function Condition is usually marked by a rise in serum creatinine concentration or by azotemia (a rise in blood urea nitrogen [BUN] concentration)

3 C AUSES Acute kidney failure appears most frequently as a complication of serious illness, like Heart and/or liver failure, serious infection, dehydration, severe burns, and excessive bleeding (hemorrhage) May also be caused by an obstruction to the urinary tract or as a direct result of kidney disease, injury, or an adverse reaction to medicine These conditions divide AKF into 3 main categories: Prerenal Postrenal, and Intrinsic (inside) conditions

4 C AUSES Prerenal AKF Does not damage the kidney, but can cause diminished kidney function and significantly decreased renal (kidney) blood flow Most common type of acute renal failure, and is often the result of: Dehydration Extracellular fluid (ECF) volume depletion (or other acute fluid loss from the gastrointestinal tract, kidneys, or skin) Drugs (NSAIDS, cyclosporine, radiopaque contrast materials, or any substance toxic to the kidneys) Hemorrhage Septicemia, or sepsis Congestive heart failure (CHF) Liver failure Burns Decreased intravascular volume (referred to as third spacing, also found in the presence of pancreatitis, post surgical patients, and patients with a nephrotic syndrome)

5 C AUSES Postrenal AKF Result of an obstruction of some kind somewhere in the urinary tract, often in the bladder or ureters (the tubes leading from the kidney to the bladder) The kidneys compensate to such a degree that one kidney can be completely obstructed and the other will maintain nearly normal kidney function for the body The conditions that often cause postrenal AKF are: Inflammation of the prostate gland in men (prostatitis) Enlargement of the prostate gland (benign prostatic hyperplasia - BPH) Bladder or pelvic tumors Kidney stones (calculi)

6 C AUSES Intrinsic AKF Involves a type of kidney disease or direct injury to the kidneys. Accounts for 20-30% of AKF reported among hospitalized patients Intrinsic AKF can result from: Lack of blood supply to the kidneys (ischemia) Use of radiocontrast agents in patients with kidney problems Drug abuse or overdose Long-term use of nephrotoxic medications, like certain pain medicines Acute inflammation of the glomeruli, or filters, of the kidney (glomerulonephritis) Kidney infections (pyelitis or pyelonephritis) Infiltration by lymphoma, leukemia, or sarcoid carcinomas

7 T HE F OUR P HASES OF A CUTE R ENAL F AILURE Onset Phase – this period represents the time from the onset of injury through the cell death period. This phase can last from hours to days and is characterized by: 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.

8 T HE F OUR P HASES OF A CUTE R ENAL F AILURE Oliguric/Anuric Phase – this phase usually lasts between 8-14 days and is characterized by further damage to the renal tubular wall and membranes. Other characteristics in the oliguric- anuric phase include: Great reduction in the glomerular filtration rate (GFR) Increased BUN/Creatinine Electrolyte abnormalities (hyperkalemia, hyperphosphatemia and hypocalcemia) Metabolic acidosis

9 T HE F OUR P HASES OF A CUTE R ENAL F AILURE Diuretic Phase – this phase occurs when the source of obstruction has been removed but the residual scarring and edema of the renal tubules remains. This phase usually lasts and additional 7-14 days and is characterized by: 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.

10 T HE F OUR P HASES OF A CUTE R ENAL F AILURE Recovery Period Phase – The recovery phase can last from several months to over a year. During this phase, edema decreases, the renal tubules begin to function adequately and 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.

11 S YMPTOMS AND S IGNS The signs and symptom that may be experienced with ARF depend on Phase, degree of azotemia (abnormal levels of urea and creatinine) and degree of metabolic acidosis The following signs and symptoms are consistent with ARF: Decreased urine output (urine may be pink or reddish in color) Edema (face, arms, legs, feet eyes) Flank pain/Pelvic pain Poor appetite (nausea, vomiting) Bitter or metallic taste in mouth

12 S YMPTOMS AND S IGNS Symptoms and signs (Contd) Dry itchy skin Easy bruising Fatigue Seizures/LOC Shortness of breath Arrhythmias Sudden weight gain


14 D IAGNOSING ARF More about BUN and Creatinine Although elevated levels BUN/Creatinine are considered to be the “hallmarks” of acute renal failure, the rate of rise is actually dependant on the degree of renal ischemia and injury and in regards to BUN; the rate of protein uptake. BUN may also be elevated in other conditions not directly related to acute renal failure such as; GI or mucosal bleeding, steroid treatment therapy or protein loading.

15 D IAGNOSING ARF Imaging Studies/Procedures/Tests Creatinine Clearance Test Ultrasound Doppler studies

16 M EDICAL M ANAGEMENT OF A CUTE R ENAL F AILURE Medical management of acute renal failure must focus on first identifying and treating the cause Maintaining volume homeostasis and correcting biochemical abnormalities remain the primary goals of treatment. Gathering a detailed patient history (pre-hospital and current) Maintaining adequate intravascular volume Maintaining mean arterial pressure Discontinuing all nephrotoxic medications (NSAIDS, Gentamycin) Eliminating exposure to any other nephrotoxins

17 M EDICAL M ANAGEMENT OF A CUTE R ENAL F AILURE Correcting acidosis (sodium bicarbonate for severe acidosis) Correcting hemolytic abnormalities (blood transfusion may be required) Correcting all electrolyte abnormalities (Hyperkalemia is very common) Strict monitoring on intake and output/daily weight (Hydration for prerenal failure) Serial monitoring of labs (BUN/Creatinine/Osmolality [urine/blood], etc) Diet and fluid restrictions/replacement (in a state of oliguria or polyuria)

18 M EDICAL M ANAGEMENT OF A CUTE R ENAL F AILURE Dialysis: (a short term intervention when fluids and electrolytes cannot be managed by other means). This may involve the use of any of the following three methods: Peritoneal Dialysis – peritoneal dialysis is not commonly used as a treatment with acute renal failure. Although efficient, it is slow process that involves the transfer of fluid and solutes between the peritoneal cavity and the peritoneal capillaries. The clearance that occurs with peritoneal dialysis is thought to be less effective than other types of dialysis.

19 M EDICAL M ANAGEMENT OF A CUTE R ENAL F AILURE Hemodialysis – hemodialysis remains the primary method of renal replacement therapy in patients with acute renal failure Provides ultrafiltration for rapid water removal and diffusion for solute removal Indicated for uremia, electrolyte imbalances, fluid overload and severe metabolic acidosis Recommended when there is a need for quick removal of water and toxins One concern with using hemodialysis for critically ill patients with acute renal failure is that the process requires moving large amounts of fluid out of the intravascular system which can lead to acute and severe hypotension (secondary to hypovolemia).

20 M EDICAL M ANAGEMENT OF A CUTE R ENAL F AILURE Continuous Renal Replacement Therapy (CRRT) – CRRT therapy works similarly to hemodialysis except it is a continuous ongoing process that is less likely to cause acute hypotension. Other benefits to using CRRT as a method of dialysis include: Hemodynamic stability Correction of metabolic acidosis Quicker kidney recovery time Correction of malnutrition Solute removal

21 P HARMACEUTICAL I NTERVENTIONS Furosemide (Lasix) – a loop diuretic that can be used to increase urinary flow with the intent of flushing out cellular debris that may be causing an obstruction. Mannitol – an osmotic diuretic that can be used to dilate renal arteries by increasing the synthesis of prostaglandins (resulting in restored renal flow).

22 P HARMACEUTICAL I NTERVENTIONS Dopamine – at low doses (1-5 mcg/kg/min), dopamine dilates renal arterioles and increases renal blood flow and glomerular filtration. Because dopamine (even at low doses) can cause tachycardia, myocardial ischemia and arrhythmias it use should be considered carefully. N-acetylcysteine – this medication can help reverse acute renal failure when the cause is thought to be from a nephrotoxic source.

23 N URSING C ARE AND M ANAGEMENT Because acute renal failure often progresses through four phases, it is important for the nurse to detect which phase of failure the patient is experiencing in order to develop an appropriate plan of care A detailed history should be obtained to help direct nursing care; this history should include the following information: History of chronic illness (hypertension, diabetes) Recent infections (especially those that may have been streptococcal in nature) Recent episodes of hypotension (from surgery or bleeding) Exposure to nephrotoxins or chemical agents Recent blood transfusions

24 N URSING C ARE AND M ANAGEMENT Contd… Recent urinary tract disorders Toxemia from pregnancy or abortion Recent severe muscle damage Recent burn trauma

25 N URSING C ARE AND M ANAGEMENT Nursing assessment and subsequent interventions should focus around the following physical findings (based on the phase of renal failure): Onset Phase: Mild reduction in normal daily urine output Mild lethargy Mild malaise

26 N URSING C ARE AND M ANAGEMENT Oliguric/Anuric Phase: 24 hour urine total 400 ml or less Listlessness/fatigue Confusion or altered LOC (from electrolyte imbalances) ECG changes (elevated T waves, depressed ST segment, prolonged PR interval, loss of P wave, wide QRS complex, arrhythmias) S3 or S4 gallop Pericardial friction rub Pulsus paradoxus Fever Chest pain Crackles upon lung auscultation (due to fluid overload) Shortness of breath (due to fluid overload)

27 N URSING C ARE AND M ANAGEMENT Oliguric/Anuric Phase: Jugular vein distention (due to fluid overload) Periorbital, peripheral or sacral edema (due to fluid overload) Ascites (due to fluid overload) Capillary fragility as evidenced by easy bruising Metabolic acidosis Anorexia, nausea, vomiting, diarrhea, constipation Uremic frost (pale, yellow, dry or itchy skin) Diuretic Phase: Urine output of 3 to 5 liters in a 24 hour period Lethargy or muscle weakness (due to hypokalemia) Decreased blood pressure (due to fluid depletion) Dry mucous membranes (due to fluid depletion) Poor skin turgor and delayed capillary refill (due to fluid depletion)

28 N URSING C ARE AND M ANAGEMENT Recovery Phase: Urine output of 1500 to 1800 ml in a 24 hour period Stabilization of serum potassium, bicarbonate, BUN and creatinine Stabilization of cardiac rhythm and rate Reduction in lethargy and shortness of breath Reduction in adventitious breath sounds

29 N URSING R ESPONSIBILITIES FOR CRRT Patient family teaching regarding the procedure and equipment Monitoring of hemodynamic stability Frequent observation of the patients response to fluid removal Continuous assessment of vital signs/CVP/PAWP/PAP/Cardiac Output Monitoring changes in mental status Assessing breath sounds Assessing skin turgor/edema Monitoring for signs of bleeding/infection

30 N URSING R ESPONSIBILITIES FOR CRRT Monitor specifically for hypotension in response to hypovolemia (aggressive fluid replacement with a crystalloid and/or alteration of the ultrafiltration rate may be necessary). Monitoring for fluid volume overload (requiring a decrease or temporary discontinuation of replacement fluid). Monitor that all equipment connections are secure (due to the risk for vast hemorrhage if a break in the system occurs).

31 N URSING R ESPONSIBILITIES FOR CRRT Close monitoring of electrolyte and acid-base imbalances (prompt replacement is required). Adjusting care based on the mobility restrictions that occur with CRRT equipment. Close monitoring of extremity distal to catheter placement (pulses/perfusion). Assessment of catheter insertion site/dressing changes as per policy.

32 A PPROPRIATE N URSING D IAGNOSIS FOR C ONSIDERATION Alteration in urinary elimination (the goal is that the patient is euvolemic and has no symptoms suggestive of fluid deficit or overload). Fluid volume deficit (the goal is that the patient is euvolemic; with urine output that is approximately 30 ml/hr and has no symptoms suggestive of fluid deficit i.e. dry mouth, hypotension, poor skin turgor, delayed capillary refill). Fluid volume overload (the goal is that the patient is euvolemic and has no symptoms suggestive of fluid overload such i.e. edema, wt. gain, JVD). Altered nutrition (less than bodily requirement) - (the goal is that the patient will have balanced nutrition and fluid balance with weight within normal limits).

33 A PPROPRIATE N URSING D IAGNOSIS FOR C ONSIDERATION Potential for impaired skin integrity (the goal is that the patient remains free from pressure ulcers and dry itchy skin). Knowledge deficit (the goal is that the patient/family has a better understanding of the disease process and understand the need for follow up care). Decreased cardiac output (the goal for the patient is to have improved clinical findings based on adequate cardiac output i.e. normal vital signs, adequate capillary refill, absence of hypotension) Fear (anxiety) (the goal for the patient will have a low level of anxiety and be able to effectively express concerns and questions regarding care. The patient will also be able to verbalize symptoms of anxiety and mechanisms for dealing with these symptoms).

34 A PPROPRIATE N URSING D IAGNOSIS FOR C ONSIDERATION Potential for impaired skin integrity (the goal is that Activity intolerance - (the goal for the patient is to participate in activities of daily living without become exhausted). Ineffective individual/family coping the goal of the patient/family is to be able to participate in care without becoming overwhelmed. The goal is also to be able to verbalize where counseling/support can be found i.e. American Association of Kidney Patients or the National Kidney Foundation for example). Body image disturbance (the goal of the patient who may require a shunt for hemodialysis is to state or demonstrate acceptance of this change).

35 A PPROPRIATE N URSING D IAGNOSIS FOR C ONSIDERATION Altered thought processes (the goal of the patient is to demonstrate improved cognitive function and be able to participate in activities of daily living). Potential for injury (the goal for the patient is to remain injury free and be able to verbalize and explain methods to prevent injuries and/or falls). Risk of infection (the goal for the patient is to remain free from symptoms of infection (WBC’s within normal limits) and to be able to state what symptoms of infection are).


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