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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
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
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?
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:
Clin J Am Soc Nephrol 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.
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)
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
Compartments
RBCs~1.5L
Intravascular8% TBW~3.5 L Ex
tracellualr 1/3 TBW (14L)
Intracellular 2/3 TBW
~28L
Interstitial25% TBW~10.5 L
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
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
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
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
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
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
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
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
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.
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 Soc Nephrol 2009) Studied medicare beneficiaries with AKI.
AKI requiring HD were at a 28X risk for advanced CKD (Lo et al. Kidney Int 2009)
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
Etiology of AKI
Prerenal AKI- 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.
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
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
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.
Pathogenesis of Acute Tubular Necrosis
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.
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.
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.
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?
Questions??