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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
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Chapter 7-(ii)
Approach to the Anuric/Oliguric
Critically Ill Surgical Patient
Robert T. Stovall, MD*
* Assistant Professor of Surgery, University of Colorado School of Medicine
Take Home Points
• Oliguria should be approached in the context of the entire patient and
situation — NEVER in isolation.
• Oliguria has been defined in multiple ways.
• Renal failure does not always present with oliguria.
Background
• Urine output is a commonly followed clinical parameter for information
related to volume status as well as perfusion.
• Urine output may also be followed as a surrogate of kidney function.
• While a critical component of overall patient assessment, urine output must
always be interpreted in the context of the overall patient situation.
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 303-436-4029,
email: robert.stovall@dhha.org
259
260 R. T. Stovall
Main Body
Definition
• Anuria — virtual absence of urine output for six hours.
• Oliguria
{ < 400–500 ml urine output/24 hours
{ < 0.5 ml urine/kg/hour over two hours (This is usually KG of ideal body
weight as its utility is lost for larger patients).
Causes of oliguria
• Categorized into three broad categories for clinical convenience:
{ pre-renal, intra-renal and post renal
• Pre-renal causes
{ Common in the SICU
{ Anything that decreases perfusion to the kidney
Shock — all types
Hypovolemic States
Ö Hemorrhage
Ö GI losses
Congestive Heart Failure
Decompensated liver cirrhosis
Renal artery issues
Ö Stenosis
Ö Aortic Dissection occluding renal artery
Hepato-renal syndrome or other drug or neuro-humeral parameters
affecting normal renal auto regulation (NSAIDS, ACE-I, etc.).
• Intra-renal causes
{ Intrinsic renal pathology
Sequelae of shock
Ischemia Reperfusion
Contrast Nephropathy
Acute tubular necrosis (ATN) reportedly common in ICU patients;
however this pathologic finding is not consistently found when the
clinical diagnosis is given.
Approach to the Anuric/Oliguric Critically Ill Surgical Patient 261
Other drugs toxic to the kidney
Acute interstitial nephritis (AIN) — often from drugs given in ICU
Myoglobinuria
Multiple Organ Failure
Vasculitis
Malignant Hypertension
Abdominal Compartment Syndrome may affect the kidney via pre-
intra or post-renal mechanisms but cannot be forgotten
Other more chronic issues exacerbated in the ICU
• Post-renal causes (obstructed outflow)
{ Iatrogenic
Injured ureter or ureters intra-operatively
Foley occlusion
{ Renal stones causing obstruction
{ Papillary necrosis
{ Prostatic Obstruction of the urethra
{ Other Urethral/ureteral obstruction (strictures/masses)
Work-up of oliguria
• Full history and physical exam should be the first step of the evaluation as
oliguria cannot be assessed in isolation.
{ Review recent events, baseline renal function, all medications adminis-
tered, vitals: current and past, contrast studies, evaluate or place a Foley
catheter
• Labs
{ Consider CBC, Chemistries, urine electrolytes, urinalysis with
microscopy
{ CBC may suggest anemia or ongoing inflammatory process
{ Electrolytes (simultaneous serum and urine) can suggest pre-renal or not
pre-renal but not perfect
Fractional excretion of sodium (FENa)
Ö The sodium clearance divided by the creatine clearance
Ö ((Urine sodium/Plasma sodium)// (Urine Cr/ Plasma Cr)) × 100
Ö FENa < 1 suggests prerenal
Ö Not perfect, some major limitations exist
262 R. T. Stovall
Ö In the setting of diuretics fractional excretion of urea (FEUrea)
may be more useful.
— (FEUrea) = (SerumCr * UUrea ) / (SerumUrea × UCr) %
— Has limitations but
9 FEUrea < 35% consistent with prerenal
9 FEUrea 50–65%consistent with ATN
Ö Other molecules that have been used similarly are lithium and
uric acid.
Suggesting Pre-renal Cause
Ö FENa < 1%
Ö Urine Sodium < 20 mEq/L
Suggesting Intra-renal cause
Ö FENa > 2%
Ö Urine Sodium > 40 mEq/L
{ Urinalysis (UA) with microscopy
Tubular epithelial cells and epithelial cell casts suggests ATN.
WBC casts suggest AIN.
Positive Hansel Stain (urinary eosinophils) suggests AIN but not
highly sensitive; needs to be requested separately.
Hyaline casts suggest pre-renal cause.
Specific gravity is more likely to be high in pre-renal causes.
Pigmented casts suggests myoglobinuria.
• Imaging
{ Renal Ultrasound
Evaluation for dilated ureters or a very distended bladder that suggests
post-renal cause of oliguria/ anuria.
Resistive indices may support intra-renal causes.
Initial management of oliguria
• Identifying and correcting underlying cause is the most important component
of management and is necessary to prevent further injury.
• Goal of fluid supplementation should be to optimize euvolemia and avoid
over or under resuscitation.
• Specific treatments will depend upon the ultimate diagnosis.
Approach to the Anuric/Oliguric Critically Ill Surgical Patient 263
Commonly used medications associated with renal injury (not a comprehensive list)
• Aminoglycosides
• Amphotericin B
• Flouroquinolones
• B-lactam antibiotics
• Sulfonamides
• Vancomycin
• Carbamazepine
• Phenobarbital
• Phenytoin
• NSAIDS
• Furosemide
• Thiazides
• Acetazolamide
• Acetaminophen
• Contrast Dyes
• Ranitidine
• Some chemotherapuetic agents
• Certain immunosuppressant medications
• Angiotensin-converting enzyme inhibitors/ARBs
264 R. T. Stovall
Practical Algorithm(s)/Diagrams
Fig.1. Approach to oliguria.
Review of Current Literature with References
• Prowle JR, Liu YL, Licari E et al. Oliguria as predictive biomarker of acute
kidney injury in critically ill patients. Crit Care 2011; 15(4): R172.
{ Prospective review of relationship between oliguria and the development of
Creatinine defi ned renal failure. 239 patients in multiple centers. Oliguria was
signifi cantly associated with the occurrence of new acute kidney injury but
most episodes of oliguria were not followed by renal injury. They felt that the
occurrence of short periods (1–6 hr) of oliguria lacked utility in discriminating patients with incipient kidney injury. They did note that oliguria accompanied by hemodynamic compromise or increasing vasopressor dose may
represent a clinically useful trigger for other early biomarkers of renal injury.
• Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lancet 2012; 380(9843):
756–766.
{ Review article from pathophysiology to renal replacement therapy.
• McBride WT, Gilliland H. Acute Renal Failure. Surgery 2009; 27: 11.
{ Review article on perioperative renal failure.
Chapter 7-(iii)
Renal Replacement Therapy
Talia Sorrentino, MD* and Fredric M. Pieracci, MD, MPH
* Medical Student, University of Colorado School of Medicine
†
Acute Care Surgeon, Denver Health Medical Center
Take Home Points
• Patients with life-threatening complications from acute kidney injury (AKI)
should receive renal replacement therapy (RRT).
• Patients at high risk for these complications should also receive RRT, before
signs and symptoms of AKI manifest.
• Although the decision to initiate RRT is ultimately clinical, it is generally
accepted that a blood urea nitrogen (BUN) concentration of 80 to 100 mg/dL
mandates initiation of RRT.
• Venovenous access is the preferred modality in any circuit.
• In deciding between continuous renal replacement therapy (CRRT) and inter-
mittent hemodialysis (IHD), current data do not support the superiority of one
over the other.
†
Contact information: (Talia Sorrentino) 12631 E. 17
902-6096, CO 80045; (Fredric M. Pieracci) 777 Bannock Street, MC 0206, A388, Denver,
CO 80206; Email: taliasorrentino@gmail.com; Fredric.Pieracci@dhha.org
265
th
Ave, MCC302, Aurora, Tel.: 303-
266 T. Sorrentino and F. M. Pieracci
• Multiple factors, including resource availability, specific patient needs, and
local expertise, ultimately guide the decision-making process regarding RRT.
Background
• In 1954, the Nobel Prize in Medicine was awarded to Dr. Joseph Murray,
American plastic surgeon, for performing the first human kidney transplant.
• In normal physiology, the kidneys function to control fluid, electrolyte, and
acid-base balance.
• In the setting of severe AKI [Chapter 7-(i)], RRT provides supportive therapy,
thereby promoting renal recovery.
• AKI is a spectrum of disease ranging from subclinical injury to failure.
• On average, 7% of all hospitalized patients develop AKI.
• This number increases significantly to 36–67% in the critically ill, and is
associated with in-hospital mortality rates exceeding 50%.
• Seventy percent of patients with AKI will require RRT of some form.
• Mortality of patients who require RRT is 50–70%.
• Multiple modalities of RRT exist, including IHD, CRRT, mixed therapies,
and organ transplantation.
• The various modalities of RRT can be categorized based upon (1) access —
arteriovenous, venovenous, or peritoneal; (2) what moves — solute versus
volume; and (3) the degree of interruption — intermittent versus continuous.
Main Body
Key concepts of RRT
• The various modalities of RRT (listed below) can be simply categorized
based on:
{ access — arteriovenous (AV), venovenous (VV), peritoneal dialysis (PD)
{ what moves — solute versus fluid (dialysis versus filtration)
{ the degree of interruption — intermittent versus continuous
• List of Modalities
{ Intermittent hemodialysis (IHD)
{ Continuous venovenous hemofiltration (CVVHF)
{ Continuous arteriovenous hemofiltration (CAVHF)
{ Continuous venovenous hemodialysis (CVVHD)
{ Continuous arteriovenous hemodialysis (CAVHD)
Renal Replacement Therapy 267
{ Slow low-efficiency dialysis (SLED)
{ Slow-continuous ultrafiltration (SCUF)
• Access
{ Arteriovenous access is rarely used due to its reliance on the patient’s
vascular pressures to generate a gradient, as well as the need for arterial
cannulation and the associated risks of arterial thrombosis, embolism,
bleeding and limb ischemia [Chapters 5-(vii) and 15].
{ Venovenous access is both the safest and most commonly used technique
in the clinical setting. VV does not rely on the patient’s pressure and
instead uses an external pump to generate the pressure gradient necessary
for solute and water removal.
• Solute and Fluid Removal
{ Hemodialysis (HD) removes solutes such as urea, potassium, phosphate,
creatinine, and toxins.
{ Hemofiltration (HF) is used predominately to remove fluid in the setting
of volume overload. Although fluid removal is part of the treatment goal,
HF requires the patient to receive some replacement fluid.
{ Hemodiafiltration (HDF) represents a combination of dialysis and filtra-
tion and incorporates the benefits of both. HDF will not specifically be
addressed in this chapter, though it should be noted that by adjusting
dialysate, and countercurrent flow rates, the degree of fluid and solute
removal can be individually titrated.
• Intermittent versus Continuous Therapy
{ Intermittent therapies such as IHD and PD have the advantage of rapidly
correcting large metabolic disturbances (a few hours), and thereby freeing
the patient from extracorporeal devices during the interim.
{ The concept behind CRRT is to achieve more physiologic solute clear-
ance over an extended time-period, thereby minimizing wide metabolic or
volume shifts.
{ CVVH is the most commonly used modality of CRRT in the acute care
setting.
• Definitions: Diffusion and Convection
{ Diffusion is the movement of solutes from an area of higher concentration
to an area of lower concentration.
{ Convection relies on a transmembrane pressure gradient to drive
water across a semipermeable membrane, dragging both small and large
molecular weight solutes dissolved in the fluid.