Acute kidney injury

Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.

1. Acute kidney injury (AKI) By:Mr.Jagdish sambad M.Sc. Nursing IKDRC COLLEGE OF NURSING

2. Learning outcome To understand the different types and causes of acute kidney injury (AKI). To help and support the patient and family during an episode of AKI. To describe the signs and symptoms of AKI. To analyse the management of those with AKI. To evaluate the various treatment options for AKI.

3. INTRODUCTION The kidney has multiple functions and the management of the patient with AKI has been likened to ‘juggling’ as the nurse has to be aware of many different aspects of care at one time (Davies 2009). Approximately one in five people who are admitted to hospital as an emergency will suffer some degree of acute kidney injury(AKI )

4. Introduction Acute kidney injury is viewed as a spectrum of injury, which may result in organ failure and the need for renal replacement therapy (RRT ). Clinically AKI is characterized by a rapid reduction in kidney function resulting in a failure to maintain fluid , electrolyte and acid-base homoeostasis Depending on its severity and duration, AKI is often transient in nature and, with careful nursing care, the patient can regain normal renal function. However, without appropriate specialized treatment, the patient may be denied the opportunity to make a full recovery and a precipitation of further impairment may lead to chronic kidney disease (CKD) and established renal failure (ERF ).

5. Mortality There are a number of patient groups for which AKI has a particularly high mortality rate . For example, AKI occurs in up to 65% of patients with septic shock and is independently associated with an increased risk of death in patients with sepsis ( Bagshawet al. 2009). The need for rapid identification of the cause of AKI and those patients at highest risk is essential so that the correct course of treatment can be adopted ( DuBose et al. 1997). Therefore it is vital for the nurse to play a major role in assisting physicians in the treatment options available for this fragile group of patients. The development of new biochemical markers may enable a diagnosis to be made before changes are seen in either serum creatinine or the urine output.

6. Prerenal Aetiology Stage Major causes Aetiology Prerenal Cardiovascular Vasodilation Hypovolemia Congestive cardiac failure Myocardial infarction Cardiogenic shock Cardiac tamponade Pulmonary embolism Sepsis Anaphylaxis Haemorrhage , including blood loss due to surgery Burns Gastrointestinal loss Renal loss

7. Intrarenal Aetiology Stage Major causes Aetiology intrarenal Glomerulonephritis Vascular Intratubular Pigment Protein Crystal Poststreptococcal infection Systemic lupus erythematosus Haemolytic-uraemic syndrome Wegener’s granulomatosis Goodpasture’s syndrome Vasculitis Hypertension Eclampsia of pregnancy Renal artery stenosis Renal vein thrombosis Myoglobin ( rhabdomyolysis ) Myeloma Nephrotoxin

8. Postrenal Aetiology Stage Major causes Aetiology Postrenal Obstruction of lower urinary tract Obstruction of upper urinary tract Prostatic hypertrophy Ureteric obstruction (clots, extrinsic compression, calculi)

9. Classification Prerenal – relates to the ineffective perfusion of the kidneys, which are structurally normal Renal (intrinsic) – damage to the renal parenchyma, sometimes secondary to Prerenal problems Postrenal – disordered urinary drainage of both kidneys or of a single functioning kidney .

10. 1.Prerenal failure Prerenal causes of AKI are directly related to hypoperfusion states or a decline in the blood supply to the kidneys. The structure of the kidneys is normal. However, when the renal blood supply is restricted, glomerular filtration is reduced, causing decreased perfusion of the kidneys. The net effect is a decreased blood flow to the glomeruli, which therefore leads to ineffective filtration because of inadequate blood flow. Without an effective renal plasma flow rate the glomeruli are unable to filter waste from the blood but the structure of the renal tubules remains intact . In this prerenal state, urine osmolarity is high and sodium low, which is consistent with renal hypoperfusion and well-preserved renal function. If, at this stage, renal blood flow can be restored, then normal renal function will return.

11. 2.Renal failure This cause is sometimes referred to as intrinsic or intrarenal failure and is associated with structural damage to the glomeruli and renal tubules. The difference between pre- and post renal failure and intrinsic failure is that in intrinsic failure the correction of the aetiology will not guarantee the complete recovery of renal function because of damage to the nephron itself. Here the episode of AKI may have a lengthy duration and can often lead to CKD . The clinical course of intrinsic renal failure is often complex and, depending upon underlying disorders, the recovery may be prolonged for up to six weeks.

12. 3.Postrenal failure Postrenal conditions obstruct the flow of urine, so the obstruction has to be bilateral in order to cause failure. The rapidity of recovery will depend on the duration and completeness of the obstruction. The urinary tract may be obstructed by three mechanisms: obstruction from within (e.g. ureteric stones ) disease of the wall obstruction from outside (e.g. prostatic hypertrophy).

13. AKIN-Classification Category Serum creatinine Urine output Stage-1 Serum creatinine ≥ 150–200% from baseline <0.5 ml/kg/h for > 6 h Stage-2 Serum creatinine ≥ 200–300% from baseline <0.5 ml/kg/h for > 12 h Stage-3 Serum creatinine ≥ 300% from baseline OR serum creatinine ≥ 54 μmol /l with an acute rise of at least 44 μmol /l < 0.3 ml/kg/h for > 24 h or anuria for >12 h

14. Diagnostic test History and physical examination Identification of precipitating cause Serum creatinine and BUN level Serum electrolyte Renal ultrasound Renal scan as indicated CT scan and MRI as indicated Retrograde pylogram as indicated

15. Management of Acute Kidney Injury Since normal kidney function is essential to homeostasis of the body, particularly with regard to volume, electrolyte balance, acid-base balance and excretion of nitrogenous waste products, loss of these functions can lead to hyperkalaemia , volume overload, acidosis and uraemia .

16. Continue… Prevention is better than a cure, so early detection and treatment of AKI will prevent rapid deterioration. Some people are at a greater risk of AKI – these include patients who have chronic kidney disease, cardiac failure and liver disease, diabetes and those who are over 60 years of age. The clinical management goals for patients with AKI can be divided into three main categories: restoration of renal perfusion minimizing toxic effects correction of metabolic derangements.

17. Hyperkalemia Hyperkalaemia is often a fatal complication in AKI. The failing kidney is unable to excrete potassium effectively when the patient is oliguric (<400 ml urine day) or, worse, anuric (no urine). It is further complicated by the very complex treatment of an individual who is often septic, hypoxic and requiring blood transfusions and potassium containing drugs .

18. Fluid overload Successful volume homeostasis permits maintenance of a constant internal circulatory and extracellular volume despite consumption of varying quantities of water and salt intake and variable invisible losses of water . The presence of oedema may be seen in the feet, legs and sacral area. This is often pitting in nature. The skin is particularly at risk at this stage and extra care must be taken.

19. Fluid overload continue… Each patient in AKI should have an individual prescription for fluid and sodium intake . As a generalization, the fluid intake volume should equal the daily urine output plus 300–500 ml. Patients with a large insensible loss, such as happens with burns, obviously need a larger fluid intake and special care should be taken. It is important that the patient and family are involved in accurate fluid balance.

20. Metabolic acidosis The presence of AKI must not lead the nurse to think that it is the only cause of acidosis until other causes have been eliminated, for example ketoacidosis, lactic acidosis. Acidosis in kidney injury occurs when the renal tubules fail to regenerate bicarbonate and secrete hydrogen ions into the urine, which in turn causes an acid-base imbalance. As most acid comes from the breakdown of dietary protein, it is possible to reduce the level of acidosis by limiting the level of intake of protein. Another alternative is to infuse sodium bicarbonate but one has to be aware of fluid overload and hypernatremia. The most efficient way of treating acute acidosis via RRT.

21. Uremia The accumulation of nitrogenous waste products will produce acute uremia and symptoms of uremia often include nausea, vomiting, hiccups, increasing bleeding, infection risks , neurological problems, irritability , confusion and twitching. As previously mentioned, it is necessary to begin appropriate dialysis.

22. Nutrition The aims of nutritional support are to: Prevent protein energy wasting Preserve lean body mass/prevent or minimize malnutrition Avoid further metabolic arrangements Stimulate immunocompetence Repair tissue damage Preserve organ function Maintain biochemistry/fluid balance Enhance recovery.

23. Nutrition continue.. Adequate protein intake (0.6-2 mg/kg/day) depending on the degree of catabolism Potassium restriction Phosphate restriction Sodium restriction

24. RRT In Acute Kidney Injury The purpose of RRT is to prevent morbidity and to support the kidney during its recovery phase . The amount, type and frequency of RRT are dictated by the severity of the patient’s condition. Indications for RRT are: Uraemic symptoms, such as pericarditis Volume overload Hyperkalemia Metabolic acidosis space-making ’ – for example, nutrition, transfusions;

25. RRT There are a variety of treatment options available for AKI and the choice will depend on physician preference, nurse expertise and availability of the appropriate equipment. The options fall broadly into two categories : Intermittent treatments (acute haemodialysis and haemodiafi ltration ) and continuous renal replacement therapies, of which there are three basic types: continuous haemofiltration , and continuous haemodialysis and continuous haemodiafiltration . Treatments performed continuously over long periods of time allow optimal values to be obtained for urea and fluid exchange control,and electrolyte and acid-base balance.

26. Clinical course of AKI 1. Initiating stage This occurs when the kidneys are injured and when diagnosis is made and treatment established . It can last anything from hours to days.

27. Clinical course of AKI 2. Oliguric stage This can last from 5 days to over 15 days. When AKI persists for weeks, endocrine problems, such as reduced erythropoietin production, are noticed. Functional renal changes occur , such as decreased tubular transport, reduced urine formation and lowered glomerular filtration . Renal healing will begin to occur, with the basement membrane being replaced with fibrous scar tissue and the nephron clogged with inflammatory products. The patient is particularly susceptible to bleeding and infection during this stage.

28. Clinical course of AKI 3. Diuretic stage With continued healing the kidney begins to regain most of its lost function, but this depends on the severity of the initial injury. The signs and symptoms of the original condition begin to disappear. Urine output can begin to increase back to normal levels of up to 3 L day.

29. Clinical course of AKI 4. Recovery stage: The recovery stage can last from several months to over a year. The basement membrane is restored to its previous structure; scar tissue will remain but is not clinically significant . The kidneys respond in a regulatory excretory function to the body’s needs.

30. Nursing assessment Obtain subjective data and Subjective data History and physical examination Intake output chart monitoring Hemodynamic monitoring Prevention of infection

31. Nursing diagnosis Excess fluid volume related to renal failure and fluid retention. Risk for infection related to invasive line, uremic toxins and altered immune repose secondary to kidney failure. Imbalanced nutrition less than body requirement related to altered metabolic star and dietary restriction.

32. Thank you…