RENAL FAILURE

1. RENAL FAILURE Melissa Greer, Ylise Dobson, Megan Stacey, Melissa Terpstra, & Emily Peterson

2. The Radical Renal Team Dr. McCurly

3. The Radical Renal Team The Nurses McTall & McShorty

4. The Radical Renal Team The Nurses McSmall & McGiant

5. Case Study Tia Smith is a 26 year old female patient who is 10 hours post-partum following an emergency C-section for twins. She was 33.5 weeks pregnant and had a difficult pregnancy with PIH (pregnancy induced hypertension) and frequent urinary tract infections. On admission Tia was diagnosed with HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) which necessitated immediate delivery of her babies. During the C-section Tia became hypovolemic resulting from massive hemorrhaging and required blood products and fluid replacements. Tia eventually developed hypovolemic shock and remained unstable for 2 hours. For the past nursing shift Tia has been hypotensive with blood pressures ranging from 59/47 to 95/52. Tia’s urinary output has been 2-12cc/hr of brown cloudy foul smelling urine. During your morning assessment you discover the following:

6. Case cont’d • VS: T: 37.4 P: 125bpm R: 33 BP: 96/62 • Respiratory: Chest is clear fine crackles heard throughout all lung fields, there is diminished A/E at the bottom of the R & L lobes • CV: S1, S2 audible with pericardial friction, bounding rapid pulse • Mental Status: drowsy and with assistance will orient slowly to PPT, pt c/o persistent hiccups • Neurovascular: edema, skin cool & pale, bruises observed throughout extremities, skin turgor poor, bilateral decreased sensation in feet • GI: pt c/o N&V • Genitourinary: pt has foley catheter draining brown cloudy foul smelling urine at 2-12cc/hr • Psychosocial: pt very emotional and crying at times because she cannot be with her newborn babies and is unable to breastfeed, she is concerned for their health, and does not understand how this happened to her

7. So… What is Tia’s diagnosis? Acute Renal Failure

8. Anatomy of the Kidney http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html

9. Nephron http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html

10. 10 Functions of the Kidney’s • Urine Formation: Formed in the nephrons through a complex three-step process: GF, tubular reabsorption, and tubular secretion • Excretion of waste products: eliminates the body’s metabolic waste products (urea, creatinine, phosphates, sulfates) • Regulation of electrolytes: volume of electrolytes excreted per day is exactly equal to the volume ingested • Na – allows the kidney to regulate the volume of body fluids, dependent on aldosterone (fosters renal reabsorption of Na) • K – kidneys are responsible for excreting more than 90% of total daily intake • RETENTION OF K IS THE MOST LIFE-THREATENING EFFECT OF RENAL FAILURE

11. Renin-Angiotensin System http://en.wikipedia.org/wiki/Image:Renin-angiotensin-aldosterone_system.png

12. Kidney Function con’td • Regulation of acid-base balance: elimination of sulphuric and phosphoric acid

13. Kidney function cont’d • Control of water balance: Normal ingestion of water daily is 1-2L and normally all but 400-500mL is excreted in the urine • Osmolality: degree of dilution or concentration of urine (#particles dissolved/kg urine (glucose & proteins are osmotically active agents) • Specific Gravity: measurement of the kidney’s ability to concentrate urine (weight of particles to the weight of distilled water) • ADH: vasopressin – regulates water excretion and urine concentration in the tubule by varying the amount of water reabsorbed.

14. Still talking about kidney function… • Control of blood pressure: BP monitored by the vasa recta. • Juxtaglomerular cells, afferent arteriole, distal tubule, efferent arteriole http://www.wisc-online.com/objects/AP2204/AP2204.swf • Renal clearance: ability to clear solutes from plasma • Dependent on… rate of filtration across the glomerulus, amount reabsorbed in the tubules, amount secreted into the tubules • CREATININE • Regulation of red blood cell production: Erythropoeitin is released in response to decreased oxygen tension in renal blood flow. This stimulates the productions of RBCs (increases amount of hemoglobin available to carry oxygen)

15. Kidney function cont’d • Synthesis of vitamin D to active form: final conversion of vit D into active form to maintain Ca balance • Secretion of prostaglandins: important in maintaining renal blood flow (PGE & PGI). They have a vasodilatory effect

16. Timeline of Events EMERGENCY C-SECTION PIH HELLP HEMORRHAGE HYPOVOLEMIC SHOCK HYPOVOLEMIA ACUTE RENAL FAILURE

17. HELLP SYNDROME • A syndrome featuring a combination of "H" for hemolysis (breakage of red blood cells), "EL" for elevated liver enzymes, and "LP" for low platelet count (an essential blood clotting element). • PREGNANCY COMPLICATION - occurring in 25% of pregnancies with toxemia or pre-eclampsia. • Symptoms include- • Shortness of breath • H/A • Dimmed vision • Nausea • Dizziness & Fainting • Edema • Pain in the upper abdomen

18. Effects of HELLP on Mom & Baby • Mothers with HELLP are at increased risk for: • Liver rupture, DIC, abruptio placentae, and acute renal failure, stroke, seizure, ARD, pulmonary edema • 1st order of tx is management of blood clotting issues • Women with a hx of HELLP are considered at risk for future pregnancies • After delivery, mothers vitals are CLOSELY monitored to observe for complications

19. Acute Renal Failure

20. Definition • Acute renal failure (ARF) is an abrupt and sudden reduction in renal function resulting in the inability to excrete metabolic wastes and maintain proper fluid & electrolyte balance • It is usually associated with oliguria (urine output <30cc/hr or <400cc/day), although urine output may be normal or increased • BUN & creatinine values are elevated

21. Statistics of ARF • Frequency: condition develops in 5% of hospitalized patients and 0.5% patients require dialysis • Elderly are at high risk • Post-op patients • Mortality: the mortality rate estimates vary from 25-90% • Race: no racial predilection is recognized

22. Pathophysiology • ARF may occur in 3 clinical settings: • As an adaptive response to severe volume depletion and hypotension, with structurally and functionally intact nephrons (Prerenal) • In response to cytotoxic or ischemic insults to the kidney, with structural and functional damage (Intrinsic or Intrarenal) • Obstruction to the passage of urine (Postrenal)

23. Phases of Acute Renal Failure • Clinical progression of reversible RF occurs in four phases: • Initiation phase • Begins with initial insult and ends when oliguria develops • Oliguric phase • Accompanied by rise in serum concentrations of substances usually excreted by kidneys (urea, creatinine, ua, organic acids, intracellular cations [K+ & Mg]) • urinary output <400cc/day • May last 1-3 weeks • Diuretic phase • The kidneys begin to recover • Initially produce hypotonie urine d/t increase in GFR • Recovery phase • Tubular function restored • Diuresis subsides and kidney begins to function normally again

24. Prerenal acute renal failure • Is the most common cause of ARF occurring in 60-70% of cases • It is caused by impaired blood flow as a result of intravascular depletion, which leads to decreased effective circulating volume to the kidneys • In patients with prerenal ARF, the parenchymal is undamaged, and the kidneys respond as if volume depletion has occurred.

25. Prerenal ARF • Causes include: • Secondary to renal hypoperfusion which occurs in setting of extracellular fluid loss • Diarrhea • Vomiting • Diuretics • Impaired/inadequate cardiac output • Drugs • NSAIDs • ACE Inhibitors • Hypovolemia • Hemorrhage • Renal vasoconstriction

26. Intrinsic acute renal failure • Is the result of actual parenchymal damage to the glomeruli or kidney tubules • A physiologic hallmark is failure to maximally concentrate urine • Is divided into 4 categories: • Acute tubular disease • Glomerular disease • Vascular disease • Interstitial disease

27. Intrinsic ARF • Acute Tubular Necrosis • most common type of ARF, a more ischemic insult to the kidneys, usually induced by ischemia or toxins • Caused by: • Burns, and crush injuries – myoglobin & hemoglobin are liberated causing renal toxicity or ischemia • Drugs – NSAIDs, ACE inhibitors, aminoglycosides • Infections • Nephrotoxic agents – contrast agent • Glomerulonephritis • uncommon cause, most associated with CRF • Caused by: • Can be a primary disorder or can occur secondary to systemic disease • Systemic lupus erythematosus

28. Intrinsic ARF • Acute Interstitial Nephritis • Interstitial disturbance that leads to ARF • Caused by: • Allergic reaction to drugs • Vascular Disease • Can occur on microvascular and macrovascular • Caused by: • Microvascular • Hemolytic anemia • ARF secondary to small vessel thrombosis or occlusion • Macrovascular • Suspected in elderly • Renal artery stenosis or thrombosis • Atheroembolism secondary to atrial fibrillation and aortic disease

29. Postrenal acute renal failure • Is rare and occurs with urinary tract obstruction that affects the kidneys bilaterally • Pressure rises in the kidney tubules, eventually the GFR decreases

30. Postrenal ARF • Causes include: • Bladder tract obstruction • Prostatic hypertrophy • Catheters • Neurogenic bladder • Postrenal causes are typically reversible

31. Assessment • History • Observe for disorder that predisposes pt to ARF • Ask questions about recent illness, infections, or injuries • Medication history • Urinary patterns • History of GI problems • Psychosocial • Anxious • Family members

32. Cardiovascular Arrhythmias BP, N, high or low Anemia P, rapid, bounding, or N Pericardial-type chest pain Respiratory Dyspnea Crackles Tachypnea Kussmaul’s respirations Mental Status Lethargy Tremors Memory loss Confusion Musculoskeletal Muscle spasms Weakness Genitourinary Oliguria Anuria abN urine colour, clarity, smell GI Moist tongue & increased saliva Dry tongue & mucous membranes N&V Integumentary Moist, warm skin & pitting edema Decreased skin turgor bruises Pallor Thin, brittle hair & nails Clinical Manifestations of ARF

33. Nursing Care Plan • Fluid volume deficit related to hemorrhage (hypovolemic shock) • Priority to restore fluid balance and circulation • The patient will: • show stable vital signs • have adequate urine output >30cc/hr • have strong peripheral pulses indicating tissue perfusion • display LOC normal for patient

34. Interventions Bleeding reduction, fluid resuscitation, blood product administration, IV therapy Monitor VS q2h Monitor weight daily Skin & tongue turgor Monitor and document I&O Monitor CBC, ABG, urinalysis, ECG Rationales Early intervention can prevent progression of hypovolemia to hypovolemic shock that may result in renal damage S&S correlate with the approximate percentage of volume loss Medullary vasomotor center stimulation via the baroreceptor reflex ADH Foley catheter facilitates monitoring of urine output Shock pt hemodynamically unstable with compromised compensatory mechanisms, volume admin may cause fld overload Nursing Care Plan

35. Nursing Care Plan • Electrolyte imbalance related to decreased electrolyte excretion, and metabolic acidosis • Priority to prevent complications of electrolyte imbalance • Within 24h of admission and then continuously, the pt will: • Maintain serum electrolyte levels within acceptable limits • Have normal sinus rhythm

36. Interventions Monitor & document electrolyte levels q8-12h, especially: K+, P, Ca, Mg Monitor ABG Monitor ECG especially: High tented T waves, prolonged PR interval or widened QRS complex Limit dietary & drug intake of potassium Rationales Kidneys’ ability to regulate electrolyte excretion & reabsorption may result in high K+ & P, low Ca, & high/low Mg levels. ARF causes metabolic acidosis which may increase the release of K+ from cells in exchange for H+ ions Electrolyte abN can trigger arrhythmias & cardiac arrest When kidneys cannot excrete K+, excess intake can increase serum K+ to dangerous levels Nursing Care Plan

37. Nursing Care Plan • Knowledge deficit of acute renal failure related to lack of exposure to information on management of complex condition • Priority to provide in depth information on acute renal failure • Upon discharge the patient will: • Be able to identify signs and symptoms to report to nurse or physician • Commitment to comply with treatments, including dialysis, dietary modifications, and activity restrictions

38. Interventions Provide as appropriate information on the severity of ARF & dialysis Stages of ARF Medications including action and adverse effects S&S Procedures such as dialysis including schedule and adverse effects Dietary modifications including limitations of proteins (catabolism), electrolytes and fluids Rest and activity restrictions Rationales The patient and family need assistance, explanation, and support during this time. Teaching may decrease anxiety and fear, and enhance recovery to patient and family members. Continued assessment of the patient for complications of ARF and of its precipitating cause is essential. Nursing Care Plan

39. Acute Renal Failure LAB VALUES

40. Medications for ARF Pharmacologic treatment of ARF has been attempted on an empirical basis, with varying success rates. Several promising experimental therapies in animal models are awaiting human trials It is critical to adjust (decrease or discontinue) medication dosages for patient in acute renal failure. Administering the average dose to patient in renal failure can kill a patient.

41. Medications for ARF continued Immediate goal is to retain fluid volume deficit through use of blood products and crystalloids • Normal Saline (0.9% Na) – only one that is compatible with blood transfusions • Restores fluid loss • Provides electrolytes resembling those of plasma • Packed RBC • To increase blood volume • To restore blood to kidneys

42. Medications for ARF continued • Diuretics • Furosemide (Lasix) only given with severe fluid overload • Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the thick ascending loop of Henle and the distal renal tubule • Adult dose: 20-80 mg PO/IV once; repeat 6-8h prn or dose may be increased by 20-40 mg no sooner than 6- 8h after previous dose until desired effect • Nursing Assessments: Watch for hypokalemia, assess BP before and during therapy can cause hypotension

43. Medications for ARF continued • Vasodilators • Dopamine • In small doses causes selective dilatation of the renal vasculature, enhancing renal perfusion. • Reduces sodium absorption, thereby decreasing the energy requirement of the tubules. This enhances urine flow, which, in turn, helps prevent tubular cast obstruction. • Adult dose: 2-5 mcg/kg/min • Nursing Assessments: Monitor BP during administration, stop infusion if BP drops 30mm Hg, Monitor I&O

44. Medications for ARF continued • Alkalinizer • Sodium Bicarbonate • Increases plasma bicarbonate, which buffers Hydrogen ion concentration; reverses acidosis • Adult Dose: Initial dose IV bolus 1 mEq/kg, then infuse 2-5 mEq/kg over 4-8 hr depending on CO2, pH • Dilute with equal amounts of NS, 2-5 mEq/kg • Nursing assessments: Assess resp. and pulse rate, rhythm, depth, lung sounds, monitor I&O, electrolytes, blood pH, PO2, HCO3, monitor urine pH, and UO during beginning of treatment, monitor for alkalosis, monitor ABGs and blood studies

45. 13 have passed and now Tia is diagnosed with… Chronic Renal Failure • 13 years have passed  Tia is now 39 years of age and has been experiencing declining renal function over the past 13 years. Tia has lost 15lbs on her already small frame, she feels generally ill most of the time with frequent N&V, she suffers from fatigue, muscle twitching & cramps decreased sensation in her hands and feet and generalized puritus. The Physician has diagnosed Tia with ESRD and has determined that long term dialysis will be required.

46. Chronic Renal Failure ESRF

47. Definition • Also known as End-Stage Renal Failure (ESRF), is a progressive deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia (retention of urea and other nitrogenous wastes in the blood). • decreased kidney glomerular filtration rate (GFR) of <60 mL/min/1.73 m2 for 3 or more months

48. Statistics • In the U.S. The US Renal Data System (USRDS) has shown a dramatic increase in patients with CRF who require chronic dialysis or transplantation. In 1999, there were 340,000 such patients, but, by 2010, this number is projected to reach 651,000. • Internationally: The incidence rates of end-stage renal disease (ESRD) have increased steadily internationally since 1989. The United States has the highest incident rate of ESRD, followed by Japan. Japan has the highest prevalence per million population, with the United States taking second place.

49. Statistics Cont’d • Mortality /Morbidity: CRF is a major cause of morbidity and mortality, particularly at the later stages. The 5-year survival rate for a patient undergoing chronic dialysis is approximately 35%. This is approximately 25% in patients with diabetes. The most common cause of death in the dialysis population is cardiovascular disease. • Race: Affects all races

50. Pathophysiology • As renal function declines, the end products of protein metabolism (which are normally excreted in the urine), accumulate in the blood. Uremia develops and adversely effects every system in the body. • The greater the buildup of waste products, the more severe the symptoms. • Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. Regardless of the etiology of renal injury, with progressive destruction of nephrons, the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons. • This nephron adaptability allows for continued normal clearance of plasma solutes such that substances such as urea and creatinine start to show significant increases in plasma levels only after total GFR has decreased to 50%, when the renal reserve has been exhausted. The plasma creatinine value will double with a 50% reduction in GFR.