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Perioperative Considerations for
the Patient at Risk for Altered
Renal Perfusion
Associate Professor
Graduate School of Nursing
Uniformed Services University
Bethesda, Maryland
 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?
Anesthesiology 2013:
 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 1120 min and more than 20 min had graded increases in
their outcomes.
 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
 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%
 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
2/3 TBW
8% TBW
~3.5 L
25% TBW
~10.5 L
Extracellualr 1/3 TBW (14L)
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
 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
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
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
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
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
Collecting duct
 Distal tubules of several nephrons empty
into a single collecting tubule
 Merge into larger and fewer collecting
 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 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
 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
 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
 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
Phases of Acute Tubular Necrosis
 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
 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
 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
 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
 Question them as to when the last dose was
 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
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?

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