1 / 41

Perioperative Considerations for the Patient at Risk for Altered R enal P erfusion

Perioperative Considerations for the Patient at Risk for Altered R enal P erfusion . John P. Maye CRNA PhD CAPT USN Associate Professor Graduate School of Nursing Uniformed Services University Bethesda, Maryland. Objectives .

bishop
Télécharger la présentation

Perioperative Considerations for the Patient at Risk for Altered R enal P erfusion

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Perioperative Considerations for the Patient at Risk for Altered Renal Perfusion John P. Maye CRNA PhD CAPT USN Associate Professor Graduate School of Nursing Uniformed Services University Bethesda, Maryland

  2. Objectives • Develop an appreciation for the numerous perioperative factors which influence renal perfusion • Review the physiology of the renal system with regard to perfusion, elimination of fluid and waste and the maintenance of homeostasis. • Review the renin angiotensin aldosterone system as it relates to renal perfusion and the influence of ACE Inhibitors on perioperative events • Understand the importance of perfusion as it relates to renal physiology and the occurrence of Acute Kidney Injury and Tubular Necrosis

  3. Clinical Questions • What is intraoperative hypotension? • When intraoperative hypotension occurs at what point should anesthesia providers become concerned with postoperative outcomes? • Is intraoperative hypotension associated with Acute Kidney Injury (AKI)? • Is ACE inhibitor therapy associated with the development of AKI ? • Should ACE Inhibitors be continued until the day of surgery in all patients?

  4. Non-cardiac surgical patients in a database of more than 33,000 patients at the Cleveland Clinic. Two main outcomes AKI and Myocardial injury • Acute Kidney Injury developed in 2478 patients • The MAP threshold where the risk was increased was less than 55mmHg • MAP less than 55mmHg for 1-5 min, 6-10 min, and 11-20 min and more than 20 min had graded increases in their outcomes. Anesthesiology 2013:

  5. Clin J Am SocNephrol 2007 • Retrospective analysis of 504 patients who underwent gastric bypass procedures between 2003 and 2005 at University of Cincinnati Medical Center. • AKI was defined as a greater than 50% increase from baseline serum creatinine during the first three postoperative days • A total of 42 patients (8.5%) developed postoperative AKI. • Hyperlipidemia, preoperative use of ACE-Inhibitors, ARB’s, intraoperative hypotension and higher BMI’s were all associated with increased frequency of AKI.

  6. Hospital for Special Surgery Journal (2011) • 65 year old female bilateral knee prosthesis under spinal anesthesia. (HTN, Obesity, hypercholesterolemia, CAD) on Lisinopril, beta blocker • MAP greater than 60mmHg throughout the case. 1200ml of lactated ringers with 100ml blood loss. • Intraoperative urine output 250ml over the 2 hour case • POD1 Serum creatinine doubles 0.9mg/dl to 1.9 mg/dl (AKI as defined by the RIFLE Criteria)

  7. 57 year old male elective hip arthroplasty with a hx of rheumatoid arthritis, obesity, and hypertension. • Medications: olmesartan 20mg combined with hydrochlorothiazide 12.5 mg daily (did take on the morning of surgery) • Preoperative vital signs 140/70 heart rate of 70. • Combined spinal/epidural with 2.2ml of 0.5% bupivicaine. • Shortly after induction became profoundly hypotensive and bradycardic which rapidly progressed to asystole • Atropine 2mg, Epinephrine 5mg, and Vasopressin 40 units. Restoration of pulse and blood pressure after 9 minutes

  8. Compartments

  9. Major Functions of the Nephron • Filtration of water soluble substances from the blood • Reabsorption of filtered nutrients, water, and electrolytes • Secretion of wastes or excess substances into the filtrate

  10. Functions of the Nephron segments Glomerulus • Filters fluid from blood into Bowman capsule • Prevents passage of blood cells (erythrocytes, leukocytes, platelets) and plasma proteins • Proteins and blood are not usually present in urine

  11. Functions of the Nephron segments Proximal Convoluted Tubule • Transports two thirds of filtered water and electrolytes for reabsorption by the peritubular capillaries • Transports all of the filtered bicarbonate, glucose, amino acids, and vitamins from the filtrate to the interstitium

  12. Functions of the Nephron segments Descending loop of Henle • Transports water and delivers a concentrated filtrate to ascending loop of henle • Permeable to water • Water drawn out by extra ions pumped into the Interstitium by ascending limb

  13. Functions of the Nephron segments Ascending loop of Henle • Actively transports NA. K and CL • Not permeable to water • Results in hypoosmotic filtrate and a high interstitial osmolality

  14. Functions of the Nephron segments Distal convoluted tubule • Filtrate that reaches the distal tubule is hypoosmotic (100mOsm/L) in comparison with plasma (280mOsm/L) • Only 10% of the original glomerular filtrate remains • Further reabsorption is under hormonal control

  15. Functions of the Nephron segments Collecting duct • Distal tubules of several nephrons empty into a single collecting tubule • Merge into larger and fewer collecting ducts • Collecting ducts travel through high interstitial gradient of the medulla on the way to the renal pelvis • Cells in the collecting duct under the influence of ADH

  16. Acute Kidney Injury • Acute kidney injury is the sudden reduction of kidney function causing disruptions in fluid, electrolyte, and acid base balances • Retention of nitrogenous waste products • Increased serum creatinine levels • Decreased glomerular filtration rates

  17. RIFLE classification for staging Acute Kidney Injury • R Risk of injury (serum creatinine increased X 1.5 or GFR decreased by 25%) • I Injury (serum creatinine increased x2 or GFR decreased by 50%). • F Failure (serum creatinine increased by x3 or GFR decreased by 75%) or (serum creatinine greater than 4mg/dl with acute rise of 0.5mg/dl) • L Loss persistent acute kidney failure complete loss of kidney function greater than 4 weeks • E End stage complete loss of kidney function greater than 3 months.

  18. Epidemiology of AKI • Incidence is 2 to 7% of hospitalized patients may be higher in the elderly • 40-60% of patients in the ICU( rates increase with length of stay) • Once diagnosed mortality rates range from 40-90% • Risk of ESRD 8X compared to normal (Ishani et al J Am SocNephrol 2009) Studied medicare beneficiaries with AKI. • AKI requiring HD were at a 28X risk for advanced CKD (Lo et al. Kidney Int 2009)

  19. Risk factors for AKI • Age (greater than 75 years) • CKD (GFR less than 60ml/min/1.73m 2) • Cardiac failure • Peripheral vascular disease • Liver disease/cirrhosis-impairment of liver blood flow • Diabetes mellitus • Sepsis • Hypovolemia • Nephrotoxic medications

  20. Etiology of AKI • PrerenalAKI- hypovolemic states, CHF, Liver disease, blood loss, cardiogenic shock( use of NSAIDS, ACE Inhibitors, AII receptor blockers may precipitate prenal AKI in the absence of hypoperfusion) • Intrinsic/Intrarenal AKI- further classified by the specific anatomic area involved: vascular, interstitial, glomerular, tubular. (most common cause is acute tubular necrosis) (nephrotoxins with contrast medium the most offending agent) • Postrenal AKI: Obstruction of the renal pelvis or ureters of both kidneys, of the bladder outlet, the urethra will result in discernible kidney disease. (obstruction increases retrograde pressure will result in ATN and AKI.

  21. Acute Tubular Necrosis ATN • Acute tubular necrosis (ATN) is the death of tubular cells, which may result when the tubular cells do not get enough oxygen (ischemic ATN) or when they have been exposed to a toxic drug or molecule (nephrotoxic ATN). • New tubular cells can replace those that have died. • The tubular cells of the kidneys undergo a continuous cycle of cell death and renewal, much like the cells of the skin

  22. Acute Tubular Necrosis ATN • ATN accounts for nearly half of all cases of AKI in hospitalized patients • Sepsis is the most common cause of ischemic ATN and may develop in about 50% of critically ill patients (profound vasodilation leads to hypoperfusion within the kidney) • Elderly about 30% of ischemic cases are due to sepsis and another third are related to surgical interventions • Prolonged prerenal kidney injury, perioperative and postoperative hypotension, hemorrhage and perioperative cardiac complications may also contribute

  23. Acute Tubular Necrosis ATN Pathophysiologic processes • Vascular process: As renal blood flow is decreased flow is shunted from the medulla to the cortex and medullary cells are further compromised. Local vasoconstrictors are released ( prostaglandins, leukotrienes) and stimulation of the SNS all produce further vasoconstriction. Tubular damage and hypoxia activate the inflammatory mediator cascade • Tubular process: A reflection of the ischemia and inflammatory process. Damaged tubular epithelial cells are shed from the basement membrane and accumulate in the tubular filtrate where they eventually obstruct filtrate flow.

  24. Pathogenesis of Acute Tubular Necrosis

  25. Phases of Acute Tubular Necrosis ATN • Prodromal phase: Normal or declining urine output, serum BUN and creatinine levels begin to rise (injury has occurred and duration of this phase is dependent upon cause and severity of injury) • Oliguric phase: Most patients with ATN will develop oliguria. Accumulation of metabolic waste products, retained fluid, edema, HTN, pulmonary edema, heart failure, metabolic acidosis (impaired ability to excrete hydogen ions) accumulation of urea • Postoliguric Phase: Marked by renal recovery. Full recovery may take up to 1 year and is indicated when serum creatinine returns to normal range. 31% of elderly may not regain renal function.

  26. ACE Inhibitors: provide end organ protection independent of their blood pressure lowering properties in diseases such as congestive heart failure, post myocardial infarction, diabetes mellitus, and renal insufficiency • Drenger et al. 2012 Circulation: Withdrawal of an ACEI preoperatively is associated with an increase number of cardiovascular events mainly CHF and Postoperative MI. • Observational nature of the study does not allow for definitive recommendations regarding perioperative ACEI use. Randomized clinical trials are recommended.

  27. So what do we do? • Pay attention to those patients who are taking ACEI and ARB’s. • Question them as to when the last dose was administered. • Be aware of other antihypertensive medications that may be being administered concurrently (HCTZ) • Maintain mean arterial blood pressures greater than 55mmhg at all times if possible • Consider vasopressin when patients on ACEI have hypotension that appears refractory to traditional vasopressors.

  28. Clinical Questions • What is intraoperative hypotension? • When intraoperative hypotension occurs at what point should anesthesia providers become concerned with postoperative outcomes? • Is intraoperative hypotension associated with Acute Kidney Injury (AKI)? • Is ACE inhibitor therapy associated with the development of AKI ? • Should ACE Inhibitors be continued until the day of surgery in all patients?

  29. Questions??

More Related