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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
268 T. Sorrentino and F. M. Pieracci
{ Dialysate is a specially formulated solution containing electrolytes and
minerals such as potassium, calcium, and bicarbonate. The concentrations
of each solute are determined such that by diffusion of solutes across a
semipermeable membrane, the patient’s blood more closely resembles
normal physiologic blood.
{ A flow-driven system, such as intermittent HD, uses high dialysate flow-
rates (>800 ml/min) to maximize the concentration gradient on either side
of the semipermeable membrane at any given moment.
{ A pressure-driven system, such as in HF, uses a high transmembrane pres-
sures (hydrostatic pressure) to push large volumes across the membrane.
These pressures are generated either by mechanical pumps, or the
patient’s blood pressure as in AV systems.
{ Solvent drag refers to transport of solute particles small enough to pass
through the filter pores in pressure-driven systems such as HF.
{ SLED is an intermittent technique that uses faster flow-rates than
continuous modalities, but is run for less than 12 hours per day.
{ SCUF, like HF, uses convection to clear solutes but generates lower
ultrafiltrate volumes than HF, which typically do not need to be replaced.
Hemodialysis versus hemofiltration: Mechanisms
• The driving force in HD is diffusion of solutes down their concentration
gradients from higher concentration to lower concentration solutes. Thus, the
limiting factor in HD is the size of the solute; larger molecules will diffuse
across the semipermeable membrane, but only at a much slower rate than
smaller molecules.
{ Large: albumin, inulin, tumor necrosis factor
{ Medium: glucose, uric acid, creatinine, phosphate
{ Small: urea, potassium, phosphorus, sodium
• Advantages of HD include rapid solute and volume removal (per-minute
solute clearance), thus it is most useful in the setting of hemodynamically
stable patients with hyperkalemia, or toxin ingestion.
• The main disadvantage HD is hypotension, which occurs in 20–30% of all
HD treatments, and is caused by rapid solute and volume removal. This can
result in renal hypoperfusion and delayed return of function.
• In contrast to IHD, CVVH accomplishes large volume filtration without
major adverse effects on hemodynamic status. HF utilizes convection, thereby
mimicking the function of the glomerulus. Conceptually this means that the
concentration of solute on either side of the membrane is the same, while
Renal Replacement Therapy 269
volume is pushed across the filter, carrying with it dissolved solutes. Due to
the slow, continuous solute drag, CVVH more closely approximates physiological clearance. For the above reasons, CVVH is of considerable use in ICU
patients who are often hemodynamically unstable.
• Pressure, determined by flow rate, is the determining factor of effective
volume removal in HF. Because an extracorporeal pump generates the
pressure necessary for HF, the risk of hypotension is considerably reduced
with CVVH.
• However, CVVH is not without its disadvantages. The filter is prone to clot-
ting, and thus requires anticoagulation.
Indications for CRRT and clinical considerations
• Indications for CRRT:
{ oliguric renal failure with associated hemodynamic instability
{ severe academia without a clear and quickly reversible cause
{ electrolyte disturbances (hyperkalemia)
{ ingestion (toxins)
{ volume overload (iatrogenic fluid resuscitation, intravenous medication
administration, congestive heart failure)
{ uremia
{ multiorgan failure
{ hypercatabolism
{ sepsis and SIRS, even in the absence of acute renal failure (removal
of inflammatory cytokines may improve outcomes, though the data is
limited).
• Specific Clinical Considerations and Modality of Choice
{ Head injury or cerebral edema — CRRT due to decreased association
with wide swings in cerebral perfusion pressure.
{ The current data do not show a long-term survival benefit for CRRT over
IHD. Instead, the benefits are demonstrated in short-term outcomes
including renal recovery and length of stay.
{ Data do not support the superiority of any particular mode of RRT in
patients with AKI.
{ The availability of specific resources greatly influences the practical use
of the various modalities. HD requires a trained nurse. CVVH requires
hourly attention from nursing staff. CRRT machines are expensive and not
ubiquitously available.
270 T. Sorrentino and F. M. Pieracci
{ RRT can be discontinued when renal function returns as evidenced by
urine production, even if serum creatinine levels are still elevated.
Dosing
• In IHD, the “delivered dose” is equal to Kt/V, where K is the clearance of
urea, t is dialysis time, and V is the volume of distribution of urea (approximated by total body water, TBW).
• With respect to dosing of RRT, IHD should be provided three times per week,
alternating days, with a goal delivery of a Kt/V of ≥1.2 per treatment.
• If using CRRT, the delivered effluent rate (HF rate + dialysate flow rate)
should be ≥20 ml/kg/hr.
• The Nephrology care team is a valuable resource in managing complex
patients requiring CVVH. However, the primary team should understand the
basic goals of therapy; for example, maintaining euvolemia verses net negative
fluid balance. This can best be reported through hourly and daily goals for
fluid removal (i.e. 60 ml/hr for a total of 1.5 L removed by CVVH per day).
Practical Algorithm(s) / Diagrams
Table 1. Diagnostic classification and staging of AKI: RIFLE and AKIN criteria.
RIFLE
Criteria
Risk 1.5-fold increase 25% decrease < 0.5 ml/kg/hr for >6 hr Stage 1
Injury 2-fold increase 50% decrease < 0.5 ml/kg/hr for >12 hr Stage 2
Failure 3-fold increase 75% decrease < 0.5 ml/kg/hr for >24 hr;
Loss Complete loss of kidney function for more than 4 weeks.
ESRD** Complete loss of kidney function for more than 3 months.
* Glomerlar Filtration Rate
** End-Stage Renal Disease
*** Acute Kidney Injury Network Criteria
Serum
Creatinine GFR* Urine Output
or anuria for >12 hr
AKIN
Criteria***
Stage 3
Renal Replacement Therapy 271
Fig. 1. Continuous venovenous hemodiafiltration set up.
Blood from the patient is run countercurrent to the dialysate. At the filter, solutes and
fluids are exchanged across the membrane according to their respective concentration
gradients and transmembrane hydrostatic pressure. Excess fluid and waste products are
drawn off as effluent. The filtered blood mixes with a physiologic replacement fluid to
account for the volume removed.
Fig. 2. Hemodialysis versus hemofiltration.
Hemodialysis and hemofiltration differ mechanistically. Hemodialysis uses diffusion,
allowing high concentration solutes in the patient’s blood to passively cross a semipermeable membrane into the dialysate. In contrast, hemofiltration uses positive hydrostatic
pressure to drive both water and solutes across a semipermeable membrane, thereby clearing
both using convection (John, Stefan and Eckardt, Kai-Uwe. CHEST 2007; 132, 4).
272 T. Sorrentino and F. M. Pieracci
Fig. 3. Choosing a renal replacement modality decision tree.
Hemodynamically stable patients with acute kidney injury can be treated with intermittent
modalities, using either hemodialysis for solute removal, or hemofiltration for fluid
removal. Hemodynamically unstable patients requiring solute, toxin, or cytokine removal
should receive continuous venovenous hemofiltration (CVVHF), or continuous peritoneal
dialysis if access is established. If the resources for CVVH are otherwise unavailable, slow
continuous ultrafiltration (SCUF) or slow low-efficiency dialysis (SLED) settings can be
used instead.
Review of Current Literature with References
• The CONVINT trial is a single-center prospective randomized control trial that
randomized critically ill patients with ARF to either continuous or intermittent
HD (n = 252). They found no difference between study groups with respect to
their primary and secondary endpoints, including 14-day, 30-day-, ICU-, and
intrahospital mortality, as well as course of disease severity/biomarkers and
need for organ-support therapy (Scheforld et al. Crit Care 2014; 18, R11).
Renal Replacement Therapy 273
• On review of a 17-year trauma database, Denver Health’s group noted that
the develop-ment of AKI in trauma patients is significantly associated with
multiorgan failure (incidence 78%) and mortality (27%). Furthermore, they
noted that these data exceeded those associated with early heart, lung or liver
failure (Wohlauer et al. J Trauma 2011; 72, 2).
• PICARD study demonstrated an increased risk of death associated with initiation of RRT with a BUN >76 mg/dL in comparison to <76 mg/dL, showing
that earlier initiation of RRT is better (Mehta et al. Kidney International
2004; 66).
• Suggested Reading: Liu F, Mehta R. Chapter 52. Continuous Renal
Replacement Therapy. In: Lerma EV, Berns JS, Nissenson AR. eds. CURRENT
Diagnosis & Treatment: Nephrology & Hypertension. New York, NY:
McGraw-Hill; 2009. http://accessmedicine.mhmedical.com.liboff.ohsu.edu/
content.aspx?bookid=372&Sectionid=39961194. Accessed October 20, 2014.
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Chapter 7-(iv)
Electrolytes
Daniel Lollar, MD*
* Fellow, Trauma and Acute Care Surgery, Denver Health Medical Center
Take Home Points
• Evaluation of acid/base status begins with pH. The pCO2 reflects the
contribution of volatile acid (respiratory response). The serum bicarbonate
and base deficit reflect alterations in fixed acids (metabolicresponse).
• Evaluation of metabolic acidosis begins with determination of the anion gap.
Anion gap acidoses are caused by excess accumulation of acids (lactic acid,
urea); non-anion gap acidoses are caused by increased production/accumulation of chloride or decreased excretion of bicarbonate.
• Evaluation of metabolic alkalosis begins with assessment of urine chloride
(UCl). Chloride sensitive alkalosis (UCl < 20 mEq/L) reflects chloride loss due
to gastrointestinal or renal wasting and should be treated with normal saline
fluid repletion. Chloride resistant alkalosis (U
by diverse physiology but can be categorized into normotensive versus
hypertensive etiologies.
> 40 mEq/L) can be caused
Cl
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Email: daniel.lollar@
ucdenver.edu
275
276 D. Lollar
• Calculation of the appropriate compensatory response to a given acid/
base problem helps identify deviations from a predicted compensation.
This practice prevents overlooking a second derangement or mixed process
(Fig. 1).
• A mixed acid base disorder must be suspected with a normal pH but abnormal
anion gap or bicarbonate level. For instance, salicylate toxicity is marked by
a lactic acidosis combined with a respiratory alkalosis frequently resulting in
a normal pH.
• Always check the anion gap and serum chloride concentration in every critically ill patient with a metabolic acidosis. This practice will avoid unnecessary
and potentially dangerous volume expansion.
• A thorough evaluation of hyponatremia requires four pieces of information:
the serum osmalarity, the urine osmolarity, the urine sodium, and the overall
fluid status.
• Hyperkalemia can be a life-threatening disorder, as a widened QRS complex
signals impending ventricular dysrhythmias. This should be recognized and
treated immediately with administration of calcium chloride 1–2 g IV to stabilize cardiac myocyte membranes and 20 mg of inhaled albuterol to shift
potassium out of plasma and into cells. Concomitant administration of insulin
10 units and dextrose 50 g both IV and sodium bicarbonate are also useful
modalities.
• Hypercalcemia with symptoms of altered mentation or seizures should be
treated with fluid resuscitation and loop diuretics such as furosemide. Severe
hypocalcemia with symptoms of altered mental status or tetany should be
treated with IV calcium supplementation. Calcium chloride via central
venous line is the most efficient means of calcium repletion in the emergency
scenario.
Background
• Homeostasis requires the excretion of acid produced by physiologic processes. Excretion of fixed acid is accomplished by the kidneys in the form of
bicarbonate while volatile acids are excreted through the lungs in the form of
carbon dioxide.
• Physiologic pH is accomplished by multiple buffering agents including the
bicarbonate system, albumin, phosphate, hemoglobin and other weak acids.
• The Henderson-Hasselbach Equation, pH = pKa + log([HCO
0.0301), describes the relationship between the metabolic and respiratory
components.
−
] / [pCO2] ×
3
Electrolytes 277
• The kidney handles changes in fixed acid via three mechanisms: resorption of
filtered bicarbonate, creation of bicarbonate and excretion of ammonium (NH
+
).
4
• The anion gap represents the unmeasured anions in plasma, and an elevated
anion gap indicates increased amounts of acid anions, produced endogenously
or absorbed exogenously. Under normal situations, albumin contributes most
significantly to the anion gap.
• L-lactic acid is produced from the anaerobic metabolism of pyruvate in tissue
beds. Lactic acidosis accounts for 60% of anion gap acidoses in the ICU and
can be of two types. Type 1 is due to increased production of lactate, most
frequently from either global hypoperfusion (shock) or locally ischemic tissue beds (e.g., myonecrosis). Type 2 lactic acidosis is due to decreased
clearance of lactate from the blood, typically due to impaired liver function.
• Anti-diuretic hormone (ADH) increases water reabsorption in the collecting
ducts and distal convoluted tubule by increasing the number aquaporin channels thus decreasing the loss of free water. ADH is potently stimulated by
dehydration and hypernatremia.
• The Na/K ATPase exchange pump moves 3 Na+ ions outside the cell for 2 K+
ions into the cell. This difference creates a voltage gradient in excitable tissue
such as nerve and muscle.
• Potassium is exchanged for hydrogen ions via the H+/K+ exchanger on the
cellular membrane. Thus, excess serum hydrogen ions (acidosis) will be
brought into the cell in exchange for potassium ions. As a result, the body
protects itself from the detrimental effects of acidosis in exchange for hyperkalemia. Conversely, alkalosis will decrease hydrogen/ potassium exchange
and produce plasma hypokalemia.
• Potassium excretion is determined by flow of filtrate to the distal nephron and
maintenance of the negativity of filtrate by the epithelial sodium channel
(ENaC). Decreased flow of filtrate simulates the renin-angiotensin axis.
Aldosterone secretion causes sodium retention and potassium wasting.
Main Body
• Acidosis
{ The diagnosis of acidosis is made with an arterial blood gas showing a pH
level less than 7.40. Respiratory acidosis is diagnosed by a low pH in
conjunction with a pCO2 > 40. Metabolic acidosis is diagnosed by a low
pH in conjunction with a pCO2 < 40. A low bicarbonate level or elevated
anion gap aid in the diagnosis of a metabolic acidosis.