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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
Catheter-associated Peritonitis
Catheter-associated peritonitis (CAP) is seen in ESRD patients on peritoneal dialysis (PD) and often presents with fever, diffuse abdominal pain
with peritoneal signs and cloudy dialysate effluent. Treatment consists of
peritoneal lavage followed by the administration of intraperitoneal
antibiotics (see Table 1). Patients with severe peritonitis or sepsis despite
antibiotic treatment may require PD catheter removal and possibly
conversion to HD until a new PD catheter can be placed. Of note, polymicrobial peritonitis is not typical and other diagnoses (e.g. bowel perforation,
abscess) should be considered.
Volume Overload
Many ESRD patients are either anuric or have minimal residual renal
function. Noncompliance with dietary salt and water restriction or the
dialysis prescription may lead to life-threatening pulmonary edema, a
common cause for hospital admission or presentation to the Emergency
Department in ESRD. Pulmonary edema in ESRD is diagnosed clinically. An elevated brain naturetic peptide (BNP) level is of little use
unless the “cut-off” value is adjusted upward to account for its
decreased clearance in ESRD.
4
However, a normal BNP level has a
high negative predictive value in virtually excluding heart failure in
ESRD. Treatment typically involves emergent HD or ultrafiltration for
volume removal.
Treatment of volume overload in ESRD patients on PD involves multiple short exchanges (1–2 hour dwells) with the dialysate containing a
high dextrose concentration (4.5%) to maximize ultrafiltration and allow
rapid volume removal.
Routine treatments for pulmonary edema, such as nitroglycerin and
high-dose IV diuretics, in addition to oxygen therapy and/or BiPap, may
be administered to ESRD patients — especially patients initiating dialysis
who may still retain a significant degree of residual renal function — if
hemodialysis therapy cannot be provided immediately.
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A. Reddy, S. R Allam and B. Radbill
Vascular Access Issues
An arteriovenous fistula (AVF) is formed by creating an anastomosis
between an artery and a vein in a patient’s arm. An arteriovenous graft
(AVG) uses a synthetic graft to connect the artery and the vein in patients
with suboptimal vasculature. Complications of AVFs and AVGs may
occur immediately postoperatively due to the sudden alteration in peripheral blood flow or later due to the repeated cannulations involved with
chronic use. These complications include steal syndrome, venous hypertension, high-output heart failure, pulmonary hypertension, access thrombosis, aneurysm or pseudoaneurysm formation, hemorrhage or access
rupture, and infection.
Steal Syndrome
Placement of an AV access can result in distal hypoperfusion due to shunting (“steal”) of arterial blood flow into the fistula. Acute ischemic symptoms characterized by an absent pulse or a cold extremity warrant
immediate surgical correction to prevent the development of permanent
injury. The treatment of choice is a distal revascularization with interval
ligation (DRIL).
5
In this procedure, the artery is ligated distal to the arteriovenous anastomosis (thus preventing retrograde flow) and additional
distal blood flow is provided by the bypass.
Aneurysms
Aneurysms and pseudoaneurysms develop in AVFs and AVGs, respectively. Multiple or large aneurysms or pseudoaneurysms may limit
available cannulation sites and thereby risk functional access loss; however, the more serious concern is the risk of access rupture and subsequent
catastrophic hemorrhage in the setting of a rapidly expanding or unstable
lesion. Changes in the overlying skin (such as thinning, a shiny appearance, or eschar formation) signify an increased risk of access rupture and
require immediate surgical evaluation.
405
Management of Hospitalized Patients with End-Stage Renal Disease
Hyperkalemia
Potassium excretion is impaired in ESRD and hyperkalemia frequently
develops. In addition to a low potassium diet, dialysis is considered the
definitive treatment for hyperkalemia in patients with ESRD. However,
because the initiation of acute hemodialysis may be delayed due to logistical reasons, a variety of temporizing measures must often be employed.
These include:
• Cardiac membrane stabilization with intravenous calcium
• Potassium redistribution with insulin (with dextrose to prevent
hypoglycemia)
• Potassium elimination with sodium polystyrene sulfonate (SPS;
Kayexalate, Kionex).
SPS is a cation exchange resin that exchanges sodium for potassium in the large intestine and is excreted in the stool. Although SPS is
frequently used to treat hyperkalemia in an inpatient setting, there are
numerous reports of patients who have developed intestinal necrosis
and bowel perforation after exposure to SPS in sorbitol as an enema
and as an oral agent.
6
Therefore, this medication should be used judiciously, especially in patients with impaired bowel function (e.g. postoperatively).
Tips for Managing Hospitalized ESRD Patients
Orders
Daily Weights
The post-dialysis weight at which the patient is not volume overloaded
(e.g. minimal or no edema) is termed the “dry weight.” It is important to
weigh ESRD patients daily so that the correct amount of ultrafiltrate may
be removed when the patient is dialyzed.
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A. Reddy, S. R Allam and B. Radbill
Renal Diet
Despite the significant amount of solute removal achieved with chronic
dialysis therapy, most ESRD patients must adhere to a strict diet and limited free water intake in order to prevent electrolyte imbalances such as
hyperkalemia, hyperphosphatemia and hyponatremia. In addition, phosphorus binders are often required in order to reduce ingested phosphorus
absorption. Lastly, when ESRD patients are NPO, maintenance IV fluids
should not be routinely ordered as they can result in volume overload.
Labs
Because most dialysis patients have poor venous access and obtaining
bloodwork is often challenging, physicians routinely ask that labs be drawn
when the patient receives dialysis. However, while pre-dialysis chemistries
may aid in prescribing the correct dialysis bath, drawing electrolytes postdialysis can be misleading. Low potassium levels which may be observed
immediately after dialysis increase over the next several hours, and immediate repletion may result in hyperkalemia.
7
This effect is more pronounced
in patients with high pre-dialysis serum potassium concentration and in
patients with massive intracellular release of potassium as seen in tumor
lysis syndrome and rhabdomyolysis. In these instances, it is recommended
to check serum potassium six hours after hemodialysis as these patients can
develop rebound hyperkalemia and may require more frequent dialysis.
Medications
All medications that require renal excretion must be dosed properly in
patients with ESRD in order to ensure efficacy and avoid toxicity. HD
and PD offer variable drug clearance according to the size of the drug and
degree of protein binding, and physicians should consult with a pharmacist before prescribing drugs which may require special dosing considerations. Commonly used outpatient medications in ESRD patients, such as
phosphate binders, erythropoiesis stimulating agents, vitamin D derivatives and calcimimetics, should be continued during hospitalization if
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Management of Hospitalized Patients with End-Stage Renal Disease
they were adminstered prior to admission unless there are reasons to hold
(see Table 2).
Some medications, such as low molecular weight heparin (LWMH),
should be avoided altogether as serious bleeding complications have been
reported. Certain opioids, including morphine, codeine and meperidine,
should not be used because of the risk of accumulation of the parent drug
or metabolites. Hydromorphone, fentanyl and methadone are better
options for pain control in ESRD. Furthermore, because it is now recognized that preserving residual renal function in ESRD may be of significant benefit, nephrotoxic agents such as NSAIDs, aminoglycosides, and
IV contrast dye should ideally be used sparingly or avoided when possible for patients who maintain any degree of urinary output.
Ancillary Studies
CT scans routinely require the use of hypersomolar intravenous contrast
agents which may lead to volume overload in an under-dialyzed ESRD
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A. Reddy, S. R Allam and B. Radbill
Table 2. Reasons to Hold Commonly Used Outpatient Medications in ESRD
Patients*
Medication Indication for Use When to Hold
Erythropoiesis-stimulating Anemia of chronic Hemoglobin >13 g/dL (consider
agents, (ESAs) (epoetin kidney disease when hemoglobin > 11 g/dL)
alfa, darbepoetin alfa etc.)
Phosphate binders (calcium Hyperphosphatemia Serum phosphate < 3.5 mg/dL or
carbonate, calcium acetate, when patient is NPO as these
sevelamer, lanthanum etc.) agents only act by binding
to phosphate present in food
Vitamin D derivatives Hyperparathyroidism Intact PTH <150 or corrected
(calcitriol, paricalcitol, total calcium >10.2 mg/dL
doxercalciferol etc.) or serum phosphate > 6 mg/dL
Calcimimetics (cinacalcet) Hyperparathyroidism Corrected total calcium
< 8.4 mg/dL
*Adapted from the National Kidney Foundation Kidney Disease Outcomes Quality Initiative
(NKF KDOQI).
patient. Cardiac catheterizations, in particular, often use a large volume of
contrast dye, especially when evaluating left ventricular function.
Therefore, such procedures should be done in coordination with the
nephrology team so that dialysis may be provided after the procedure in a
timely fashion if necessary.
Gadolinium-containing contrast agents, used in magnetic resonance
imaging, have been linked to a rare condition characterized by cutaneous
and visceral fibrosis called nephrogenic systemic fibrosis (NSF) in
patients with advanced kidney disease. There is currently no cure for NSF
and use of gadolinium should be avoided in ESRD. If gadolinium is used,
prompt dialysis post-procedure and then daily for the following 1–2 days
should be considered, but whether aggressive hemodialysis prevents NSE
is unknown.
8
Opportunity for Renal Replacement Therapy Preparation and Re-Evaluation During Inpatient Hospitalization
Hospitalized patients with advanced CKD should be educated about the
various types of chronic renal replacement therapy so that preparations may
be made for future progression to ESRD. Arranging pre-emptive kidney
transplantation may take several months or even years if a suitable donor
cannot be identified. AVFs take several weeks to mature and the primary
failure rate is significant. Furthermore, choosing between HD and PD is
often a difficult decision for a patient. Initiating the conversation early,
before an emergent situation develops, may help avoid significant morbidity later. In addition, establishing goals of care before an urgent indication
for renal replacement therapy manifests is important so as to prevent initiating or continuing dialysis in a patient for whom there is no benefit.
References
1. Plantinga LC, Jaar BG. (2009) Preventing repeat hospitalizations in
dialysis patients: A call for action. Kidney Int 76(3): 249–251.
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Management of Hospitalized Patients with End-Stage Renal Disease
2. Naqvi SB, Collins AJ. (2006) Infectious complications in chronic
kidney disease. Adv Chronic Kidney Dis 13(3): 199–204.
3. Allon M. (2009) Treatment guidelines for dialysis catheter-related
bacteremia: An update. Am J Kidney Dis 54(1): 13–17.
4. Dhar S, Pressman GS, Subramanian S, et al. (2009) Natriuretic pep-
tides and heart failure in the patient with chronic kidney disease: A
review of current evidence. Postgrad Med J 85(1004): 299–302.
5. Schanzer H, Eisenberg D. (2004) Management of steal syndrome
resulting from dialysis access. Semin Vasc Surg 17(1): 45–49.
6. Watson M, Abbott KC, Yuan CM. (2010) Damned If You Do, Damned
If You Don’t: Potassium Binding Resins in Hyperkalemia. Clin J Am
Soc Nephrol 5(10): 1723–1726.
7. Blumberg A, Roser HW, Zehnder C, Muller-Brand J. (1997) Plasma
potassium in patients with terminal renal failure during and after
haemodialysis; relationship with dialytic potassium removal and total
body potassium. Nephrol Dial Transplant 12(8): 1629–1634.
8. Leiner T, Kucharczyk W. (2009) NSF prevention in clinical practice:
Summary of recommendations and guidelines in the United States,
Canada, and Europe. J Magn Reson Imaging 30(6): 1357–1363.
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A. Reddy, S. R Allam and B. Radbill
Acute Kidney Injury
Tonia K. Kim*
Key Pearls
• Specific laboratory tests, including the BUN/creatinine ratio, frac-
tional excretion of sodium (FeNa), and the examination of the urinary
sediment, can help distinguish between the different types of acute
kidney injury (AKI) and determine the appropriate management.
• Recognizing risks of developing contrast-induced nephropathy (CIN)
and employing strategies to help prevent CIN are important for mini-
mizing renal damage.
• Anticipating some of the commonly seen electrolyte disturbances in
AKI can help avert emergency situations.
• Certain medications and procedures should be avoided in AKI to
prevent complications.
• Medications should be reviewed and adjusted throughout the course
of AKI.
Introduction
Acute kidney injury (AKI) is defined as renal function deterioration
over hours to days as measured by at least a 0.5 mg/dL creatinine increase
over the baseline value or a >50% increase in creatinine over the baseline.
AKI represents a compelling spectrum of disease, owing to the
frequency of its occurrence and the mortality with which it is associated.
411
35
Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
AKI is the current term for acute renal failure. AKI is very common in the
hospital setting. One percent of patients have AKI at the time of hospital
admission, 2%–5% develop AKI during hospital stay, and 4%–15% sustain
AKI post-cardiopulmonary-bypass. The mortality rates for AKI can be staggering — as high as 80% in some postoperative patients. Prerenal AKI at
hospital admission has been associated with approximately 7% mortality.
1
All creatinine clearance calculations assume that the patient is in the
steady state with regard to creatinine handling. In AKI, patients are not in
the steady state. Therefore, the calculated creatinine clearance can be an
overestimation of the patient’s true glomerular filtration rate (GFR). If the
patient’s serum creatinine is rising every day, it is correct to assume that
the patient’s creatinine clearance is <10 mL/min.
The relationship between the GFR and plasma creatinine is not linear.
• When the plasma creatinine is below 2 mg/dL, even a 0.5 mg/dL
increase in creatinine represents a large decrease in the GFR.
• When the plasma creatinine is above 2 mg/dL, increases in it repre-
sent smaller decreases in the GFR.
Initial Workup of AKI
The primary tests to order upon recognition of AKI are:
• Chemistry panel including calcium, phosphorus, and liver function tests
• Urinalysis
• Random urine electrolytes, creatinine, osmolarity, and urea (if there is
exposure to diuretics)
All from the same urine sample.
• Random urine protein/creatinine (urine P/C)
The urine P/C is an estimation of proteinuria and assumes there is
a 1 g excretion of creatinine per day.
A random urine P/C of 1 is equivalent to 1 g of protein per day in
a 24 hr urine collection.
Ensure that the units are identical in the numerator and denominator
(either both are g/L or mg/dL). Otherwise, conversion is necessary
for meaningful interpretation of the urine P/C.
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T.K. Kim
The upper limit of normal is 0.2.
The nephrotic range is 3 or 3.5 or higher.
In AKI, the urine P/C can overestimate the true amount of protein-
uria, because the amount of creatinine excreted can be significantly
decreased.
The random urine microalbumin to creatinine ratio can also be used
if the patient has relatively low levels of proteinuria. Microalbumin
is measured in µg/dL and creatinine in mg/dL, resulting in the units
of µg/mg.
• Renal and bladder ultrasound
The results of these initial tests will help guide the clinician in determining what further tests are needed. They will also lay the groundwork
for discussion between the referring physician and the renal consultant in
navigating the management of the patient.
Categories of AKI
• Prerenal AKI
• Intrarenal (intrinsic) AKI
• Postrenal AKI
Prerenal AKI
Definition
Prerenal AKI is AKI in which glomerular and tubular function remains
intact but there is a problem in renal perfusion. The pathophysiology of
prerenal AKI is reviewed in Fig. 1.
The clinical settings in which prerenal AKI is commonly seen are:
• Absolute decrease in effective arterial volume
GI or renal losses
Hemorrhage
• Relative decrease in effective arterial volume
Congestive heart failure
Cirrhosis (hepatorenal syndrome)
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Acute Kidney Injury