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![Hemodialysis prescription
• Determining dialysis Session length and Blood Flow Rate.
• For the initial treatment, especially when the predialysis serum urea
nitrogen (SUN) level is very high (e.g., >125 mg/dL [44 mmol/L]), the
dialysis session length and blood flow rate should both be reduced. A
urea reduction ratio of <40% should be targeted.
• This usually means using a blood flow rate of only 200 mL/min (150
mL/min in small patients) for adults along with a 2-hour treatment time
and a relatively low-efficiency hemofilter.
• The length of the second dialysis session can usually be increased to 3
hours, provided that the predialysis SUN level is <100 mg/dL (36 mmol/L).](https://image.slidesharecdn.com/hemodialysis-250802015248-d2ea56ee/85/Hemodialysis-Lecture-for-Nephro-Rotation-21-320.jpg)
![Hemodialysis prescription
• Determining dialysis Session length and Blood Flow Rate.
• For the initial treatment, especially when the predialysis serum urea
nitrogen (SUN) level is very high (e.g., >125 mg/dL [44 mmol/L]), the
dialysis session length and blood flow rate should both be reduced. A
urea reduction ratio of <40% should be targeted.
• This usually means using a blood flow rate of only 200 mL/min (150
mL/min in small patients) for adults along with a 2-hour treatment time
and a relatively low-efficiency hemofilter.
• The length of the second dialysis session can usually be increased to 3
hours, provided that the predialysis SUN level is <100 mg/dL (36 mmol/L).](https://image.slidesharecdn.com/hemodialysis-250802015248-d2ea56ee/75/Hemodialysis-Lecture-for-Nephro-Rotation-21-2048.jpg)
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Hemodialysis Lecture for Nephro Rotation
- 1. HEMODIALYSIS Dr. Don JayricV. Depalobos 2nd year IM Resident Nephro Rotator Dr. Ruel Agni IM-Nephro Consultant
- 2. Objectives • Discuss Indicationsof Hemodialysis • Discuss Principles of Hemodialysis • Identify Goals of Dialysis • Hemodialysis Prescription (Duration, BFR, DFR, UF) • Identify Complications During Hemodialysis
- 3. DIalysis • It isa process whereby the solute composition of a solution, A, is altered by exposing solution A to a second solution, B, through a semipermeable membrane. • Mechanisms of Solute Transport: • Diffusion • Ultrafiltration • Removal of Protein-bound Compounds
- 4. HEMODIALYSIS • It relieson the principles of solute diffusion across a semipermeable membrane. • The rate of diffusive transport increases in response to several factors, including the magnitude of the concentration gradient, the membrane surface area, and the mass transfer coefficient of the membrane. • A small molecule, such as urea (60 Da), undergoes substantial clearance, whereas a larger molecule,
- 5. Indications of Dialysis •Presence of uremic symptoms • Presence of hyperkalemia unresponsive to conservative measures • Persistent extracellular volume expansion despite diuretic therapy • Acidosis refractory to medical therapy • Bleeding diathesis • Creatinine clearance or estimated glomerular filtration rate (GFR) <10 mL/min per 1.73 m2
- 6. Indications of dialysis(KDIGO) • Symptoms or signs attributable to kidney failure • Inability to control volume status or blood pressure; • Progressive deterioration in nutritional status refractory to interventions.
- 7. Components of hemodialysis •The dialyzer • The composition and delivery of the dialysate • The blood delivery system
- 8. Dialyzer • It isa plastic chamber with the ability to perfuse blood and dialysate compartments simultaneously at very high flow rates. • It is where the blood and dialysis solution circuits interact and where the movement of molecules between dialysis solution and blood across a semipermeable membrane occurs. • Basically, the dialyzer shell is a box or tube with four ports. Two ports communicate with a blood compartment and two with a dialysis solution compartment. The mem- brane within the dialyzer separates the two compartments.
- 9. Dialyzer • Low-Flux Dialyzer- low permeability for water • High-Flux Dialyzer - non-celluloses membrane with increased permeability, which is capable of removing moderate-sized molecules between 10000 to 15000 Dalton
- 10. DIalysate • Patients areexposed to 120 200 L of dialysis solution − during each dialysis treatment. • Dialysis Solution Preparation • Proportioning Machine • Dual-concentrate system for bicarbonate-based solutions. • Dry concentrates
- 11. DIalysate • Potassium • Thepotassium concentration of dialysate may be varied from 0–4 mmol/L depending on the predialysis serum potassium concentration. • The use of 0- or 1-mmol/L potassium dialysate is becoming less common owing to data suggesting that patients who undergo treatments with very low potassium dialysate have an increased risk of sudden death, perhaps due to arrhythmias in the setting of potassium shifts.
- 12. dialysate • Calcium • Theusual dialysate calcium concentration is 1.25 mmol/L (2.5 mEq/L), although modification may be required in selected settings (e.g., higher dialysate calcium concentrations may be used in patients with hypocalcemia associated with secondary hyperparathyroidism or with “hungry bone syndrome” following parathyroidectomy).
- 13. Dialysate • Sodium • Theusual dialysate sodium concentration is 136–140 mmol/L. In patients who frequently develop hypotension during their dialysis run, “sodium modeling” to counterbalance urea-related osmolar gradients may be employed. • With sodium modeling, the dialysate sodium concentration is gradually lowered from the range of 145–155 mmol/L to isotonic concentrations (136–140 mmol/L) near the end of the dialysis treat- ment, typically declining either in steps or
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- 15. Blood delivery system Itis composed of the extracorporeal circuit and the dialysis access. The dialysis machine consists of a blood pump, dialysis solution delivery system, and various safety monitors. The blood flow rate typically ranges from 250–450 mL/min, depending on the type and integrity of the vascular access.
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- 18. Goals of dialysis •The hemodialysis procedure consists of pumping heparinized blood through the dialyzer at a flow rate of 250– 450 mL/min, while dialysate flows in an opposite counter- current direction at 500–800 mL/min. • Current targets include a urea reduction ratio of >65–70% and a body water–indexed clearance × time product (Kt/V) >1.2 or 1.05, depending on whether urea concentrations are “equilibrated.” • For the majority of patients with ESKD, 9–12 h of dialysis are required each week, usually divided into three equal
- 19. Hemodialysis prescription • Allpatients are different, and the circumstances eventuating in the need for acute hemodialysis vary widely.
- 20. Hemodialysis prescription • Determiningdialysis Session length and Blood Flow Rate. • The blood flow rate (BFR) refers to the speed at which blood is pumped from the patient’s body through the dialyzer. It is typically measured in milliliters per minute (mL/min). Common BFR values range from 300 to 500 mL/min. Adequate BFR is crucial for efficient clearance of waste products and optimal dialysis treatment.
- 21. Hemodialysis prescription • Determiningdialysis Session length and Blood Flow Rate. • For the initial treatment, especially when the predialysis serum urea nitrogen (SUN) level is very high (e.g., >125 mg/dL [44 mmol/L]), the dialysis session length and blood flow rate should both be reduced. A urea reduction ratio of <40% should be targeted. • This usually means using a blood flow rate of only 200 mL/min (150 mL/min in small patients) for adults along with a 2-hour treatment time and a relatively low-efficiency hemofilter. • The length of the second dialysis session can usually be increased to 3 hours, provided that the predialysis SUN level is <100 mg/dL (36 mmol/L).
- 22. Hemodialysis prescription • UltrafiltrationOrders • The ultrafiltration rate (UFR) is the rate at which excess fluid is removed from the blood during hemodialysis. It is usually measured in milliliters per hour (mL/hr). UFR is critical for managing fluid overload in patients.
- 23. Hemodialysis prescription • UltrafiltrationOrders • Guidelines for ultrafiltration orders: • Even patients who are quite edematous and in pulmonary edema rarely need removal of more than 4 L of fluid during the initial session. Remaining excess fluid is best removed during a second session the following day. • If the patient does not have pedal edema or anasarca, in the absence of pulmonary congestion, it is unusual to need to remove greater than 2–3 L over the dialysis session. In fact, the fluid removal requirement may be zero in patients with little or no jugular venous distention. Fluid removal rates of 10 mL/kg per hour are usually well tolerated in volume overloaded patients. • The fluid removal plan during dialysis should take into account the 0.2 L that the patient will receive at the end of dialysis in the form of saline to rinse the dialyzer and any other fluid ingested or administered during the hemodialysis session.
- 24. Hemodialysis prescription • UltrafiltrationOrders • Guidelines for ultrafiltration orders: • If it is the initial dialysis, the length of the dialysis session should be limited to 2 hours. However, if a large amount of fluid (e.g., 4.0 L) must be removed, it is impractical and dangerous to remove such an amount over a 2-hour period. In such instances, the dialysis solution flow can initially be shut off, and isolated ultrafiltration can be performed for 1–2 hours, removing 2–3 kg of fluid. Immediately thereafter, dialysis can be performed for 2 hours, removing the remainder of the desired fluid volume. (If severe electrolyte abnormalities, such as hyperkalemia, are present, dialysis may have to be performed prior to isolated ultrafiltration.) • In general, it is best to remove fluid at a constant rate throughout the dialysis treatment. If the dialysis solution sodium level has been set lower than the plasma value (e.g., in the treatment of hypernatremia), the ultrafiltration rate can initially be reduced to compensate for the osmotic contraction of blood volume that will occur as the plasma sodium concentration is being lowered.
- 25. Hemodialysis prescription • DialysateFlow Rate • The dialysate flow rate (DFR) is the rate at which dialysate (the cleansing fluid) flows through the dialyzer. DFR is also measured in mL/min, with typical values ranging from 500 to 800 mL/min. Proper DFR ensures effective diffusion of waste products from the blood into the dialysate. • 500-800 ml/min (typically 1.5-2 times the Qb is sufficient)
- 26. Hemodialysis prescription • Anticoagulation •Routine or Tight Heparin, single or repeated-bolus Administer the initial bolus dose (e.g., 4,000 units). Then give an additional 1,000- to 2,000-unit bolus dose if necessary. • Low Molecular Weight Heparin
- 27. Hemodialysis dose and adequacy •Indicesof Urea Removal • Urea Reduction Ratio • The current primary measure of dialysis adequacy. • This is computed as follows: • Assume that predialysis SUN is 60 mg/dL and postdialysis SUN is 18 mg/dL. The relative reduction in SUN (or urea) level is (60 18)/60 = 42/60 = 0.70. By − convention, URR is expressed as a percentage, so the value of the URR in this example would be 70%. • SI units: Assume that predialysis serum urea is 21 mmol/L and postdialysis is 6.4 mmol/L. The relative reduction in SUN (or urea) level is (21 6.4)/21 = 14.6/21 = − 0.70.
- 28. Hemodialysis dose and adequacy •Indices of Urea Removal • Kt/V • The Kt/V urea was popularized by Gotch and Sargent in their reanalysis of the National Cooperative Dialysis Study (1985). • Recommended a minimum Kt/V value of at least 1.2 for hemodialysis patients being dialyzed three times per week. • The Kt/V urea is a dimensionless ratio representing volume of plasma cleared of urea (Kt) divided by the urea distribution volume (V). K is the dialyzer blood water urea clearance (L/hr), t is dialysis session length (hours, hr), and V is the distribution volume of urea (liters, L), which is close to total body water. • K 3 t = L/hr 3 hr = L V=L • (K 3 t)/V = L/L = dimensionless ratio • The Kidney Disease Outcomes Quality Initiative (KDOQI) group has adopted the Kt/V of 1.2 as the standard for dialysis adequacy.
- 29. Complications of hemodialysis I.Intradialytic Hypotension • Intradialytic hypotension (IDH) is important not only because it can cause distressing symptoms, but because it is associated with poor long-term outcomes. • There are various definitions for IDH, including a nadir (lowest) systolic BP less than 90 mm Hg, a fall in systolic BP of 20 or 30 mm Hg, or a fall in some percentage of the starting blood pressure.
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- 32. Complications of hemodialysis II.MUSCLE CRAMPS • The pathogenesis of muscle cramps during dialysis is unknown. • The four most important predisposing factors are hypotension, hypovolemia (patient below dry weight), high ultrafiltration rate (large weight gain), and use of low-sodium dialysis solution. • Hypertonic Solution may be more effective in dilating muscle blood vessels • Nifedipine (10 mg) sometimes can reverse cramping. Though reportedly not causing a notable fall in blood pressure, nifedipine should be reserved for cramping in hemodynamically stable patients.
- 33. Complications of hemodialysis III.NAUSEA AND VOMITING • Nausea or vomiting occurs in up to 10% of routine dialysis treatments. • The cause is multifactorial. Most episodes in stable patients are probably related to hypotension. • Nausea or vomiting can also be an early manifestation of the disequilibrium syndrome • Predialysis single dose Metoclopramide 5-10mg
- 34. Complications of hemodialysis IV.HEADACHE • Headache occurs in as many as 70% of patients during dialysis • Acetaminophen can be given during dialysis • Preventive measures can be given depending on probable cause.
- 35. Complications of hemodialysis V.CHEST PAIN AND BACK PAIN • Mild chest pain or discomfort (often associated with some back pain) occurs in 1%–4% of dialysis treatments • The occurrence of angina during dialysis is common and must be considered in the differential diagnosis, along with numerous other potential causes of chest pain.
- 36. Complications of hemodialysis VI.ITCHING • Common problem in dialysis patients, is sometimes precipitated or exacerbated by dialysis • General moisturizing and lubrication of the skin using emollients is recommended, and this should be the first line of therapy • Standard symptomatic treatment using antihistamines is useful • Gabapentin (or pregabalin), UVB (ultraviolet light B) therapy, oral charcoal, or nalfuralfine might be the next line of therapy, followed by naltrexone or tacrolimus ointment
- 37. Complications of hemodialysis VII.DISEQUILIBRIUMSYNDROME • It is a set of systemic and neurologic symptoms often associated with characteristic electroencephalographic findings that can occur either during or following dialysis. • Early manifestations include nausea, vomiting, restlessness, and headache. More serious manifestations include seizures, obtundation, and coma.
- 38. Complications of hemodialysis VII.DISEQUILIBRIUMSYNDROME • Mild disequilibrium. • Symptoms of nausea, vomiting, restlessness, and headache are nonspecific; when they occur, it is difficult to be certain that they are due to disequilibrium. Treatment is symptomatic. If mild symptoms of disequilibium develop in an acutely uremic patient during dialysis, the blood flow rate should be reduced to decrease the efficiency of solute removal and pH change, and consideration should be given to terminating the dialysis session earlier than planned. Hypertonic sodium chloride or glucose solutions can be administered as for treatment of muscle cramps.
- 39. Complications of hemodialysis VII.DISEQUILIBRIUMSYNDROME • Severe disequilibrium. • If seizures, obtundation, or coma occur in the course of a dialysis session, dialysis should be stopped. • The differential diagnosis of severe disequilibrium syndrome should be considered. • The management of coma is supportive. The airway should be controlled and the patient ventilated if necessary. • Intravenous mannitol may be of benefit. If coma is due to disequilibrium, then the patient should improve within 24 hours.
- 40. Complications of hemodialysis VIII.DIALYZERREACTIONS • Severe disequilibrium. • Management is supportive. Nasal oxygen should be given. Myocardial ischemia should be considered, and angina pectoris, if suspected, can be treated. Dialysis can usually be continued, as symptoms invariably abate after the first hour. • Prevention. Trying a different dialyzer membrane may be of value.
- 41. Complications of hemodialysis IX.HEMOLYSIS • The symptoms of hemolysis are back pain, tightness in the chest, and shortness of breath. • The blood pump should be stopped immediately and the blood lines clamped. The hemolyzed blood has a very high potassium content and should not be reinfused.
- 42. Complications of hemodialysis X.AIR EMBOLISM • These depend to an extent on the position of the patient. • In seated patients, infused air tends to migrate into the cerebral venous system without entering the heart, causing obstruction to cerebral venous return, loss of consciousness, convulsions, and even death. • In recumbent patients, the air tends to enter the heart, generate foam in the right ventricle, and pass into the lungs, producing dyspnea, cough, and chest tightness and arrhythmias. Further passage of air across the pulmonary capillary bed into the left ventricle can result in air embolization to the arteries of the brain and heart, with acute neurologic and cardiac dysfunction. • The first step is to clamp the venous blood line and stop the blood pump. The patient is immediately placed in a recumbent position on the left side with the chest and head tilted downward. Further treatment includes cardiorespiratory support, including administration of 100% oxygen by mask or endotracheal tube. Aspiration of air from the atrium or ventricle with a percutaneously inserted needle or cardiac catheterization may be needed if the volume of air warrants it.
- 43. References • Harrison’s Principlesof Internal Medicine 21st Edition • Handbook of Dialysis Therapy 5th Edition • KDIGO Executive Conclusions • Kidney International, Vol. 58, Suppl. 76
- 44.
Editor's Notes
- #3 Conceptually, one can view the semi- permeable membrane as a sheet perforated by holes or pores. Water molecules and low-molecular-weight solutes in the two solutions can pass through the membrane pores and intermingle, but larger sol- utes (such as proteins) cannot pass through the semipermeable bar- rier, and the quantities of high-molecular-weight solutes on either side of the membrane will remain unchanged. MECHANISMS OF SOLUTE TRANSPORT. Solutes that can pass through the membrane pores are transported by two different mecha- nisms: diffusion and ultrafiltration (convection). A. Diffusion. The movement of solutes by diffusion is the result of random molecular motion. The larger the molecular weight of a solute, the slower will be its rate of transport across a semipermeable membrane. Small molecules, moving about at high velocity, will collide with the membrane often, and their rate of diffusive transport through the membrane will be high. Large molecules, even those that can fit easily through the membrane pores, will diffuse through the membrane slowly because they will be moving about at low velocity and collid- ing with the membrane infrequently (Fig. 3.1). Diffusion is the net movement of anything (for example, atoms, ions, molecules, energy) generally from a region of higher concentration to a region of lower concentration. B. Ultrafiltration. The second mechanism of solute transport across semipermeable membranes is ultrafiltration (convec- tive transport). Water molecules are extremely small and can pass through all semipermeable membranes. Ultrafiltration occurs when water driven by either a hydrostatic or an osmotic force is pushed through the membrane (Fig. 3.1). Those sol- utes that can pass easily through the membrane pores are swept along with the water (a process called “solvent drag”). The water being pushed through the membrane is accompa- nied by such solutes at close to their original concentrations. Analogous processes are wind sweeping along leaves and dust as it blows and current in the ocean moving both small and large fish as it flows. Larger solutes, especially those that are larger than the membrane pores, are held back. For such large solutes, the membrane acts as a sieve. Ultrafiltration is a process that removes excess fluid from the blood during dialysis by using pressure to filter blood through a semipermeable membrane: Ultrafiltration is used when regular hemodialysis is unable to remove excess fluid easily. The ultrafiltration rate and the length of the dialysis treatment determine how much fluid is removed. The dialysis staff sets the ultrafiltration rate based on the patient's fluid weight gain since their last treatmen C. Removal of protein-bound compounds. The normal kidney detoxifies protein-bound organic acids and bases. Being protein bound, they are filtered to only a small extent and so bypass the glomerulus (Sirich, 2013). However, in the peritubular capillary network, these substances are removed from albumin and are taken up by proximal tubular cells. Then they are secreted into the tubular lumen, to be excreted in the urine. Other protein-bound compounds (bound to albumin and small proteins) are filtered in the glomerulus along with their carrier proteins. In the proximal tubule, the filtered proteins are catabolized along with their bound compounds. The plasma concentration of such protein-bound sub- stances is markedly elevated in dialysis patients (Sirich, 2013), but the association between high blood levels of these compounds and mortality is not completely clear (Melamed, 2013). Removal of protein-bound compounds by hemodialysis depends on the percentage of the “free” fraction of the com- pound in plasma (the fraction that is exposed to dialysis). Also, removal depends on how quickly the free fraction is replenished by the protein-bound pool. Substances that are tightly bound to proteins with a low free fraction in the plasma will be removed to a small extent by conventional hemodialysis.
- #4 According to laws of diffusion, the larger the molecule, the slower its rate of transfer across the membrane. In addition to diffusive clearance, movement of waste products from the circulation into the dialysate may occur as a result of ultrafiltration. Convective clearance occurs because of solvent drag, with solutes being swept along with water across the semipermeable dialysis membrane.
- #5 Timely referral to a nephrol- ogist for advanced planning and creation of a dialysis access, education about ESKD treatment options, and management of the complications of advanced CKD, including hypertension, anemia, acidosis, and sec- ondary hyperparathyroidism, is advisable.
- #6 Initiation of dialysis is usually considered when one or more of the following are present: symptoms or signs attributable to kidney failure (e.g., neurological signs and symptoms attributable to uremia, pericarditis, anorexia, medically resistant acid-base or electrolyte abnormalities, reduced energy level, weight loss with no other potential explanation, intractable pruritus, or bleeding); Inability to control volume status or blood pressure; progressive deterioration in nutritional status refractory to interventions. Depending on the patient’s preferences and circumstances, an aggressive trial of medical nondialytic management of advanced CKD symptoms may be warranted before initiating maintenance dialysis.
- #8 These dialyzers are composed of bundles of capillary tubes through which blood circulates while dialysate travels on the out- side of the fiber bundle. Virtually all dialyzers now manufactured in the United States are “biocompatible” synthetic membranes derived from polysulfone or related compounds (vs older cellulose “bioincompatible” membranes that activated the complement cascade). The frequency of reprocessing and reuse of hemodialyzers and blood lines varies across the world. In general, as the cost of disposable supplies has decreased, their use has increased. In the United States, reprocessing of dialyzers is now extremely rare. Formaldehyde, peracetic acid–hydrogen peroxide, glutaraldehyde, and bleach have all been used as reprocessing agents.
- #9 The principle of hemodialysis involves the clearance of solutes across a semi-permeable membrane through diffusion and ultrafiltration mechanisms. The utilized membranes are classified into two main groups: low-flux, which is based on using dialyzers with low permeability for water (5); and high-flux, non-celluloses membrane with increased permeability, which is capable of removing moderate-sized molecules between 10000 to 15000 Dalton, including many of the inflammatory proteins, ß₂ microglobulin and lipoproteins (6). Some studies have suggested that high‐flux membrane improves the removal of moderate-sized molecules such as lipid profiles or homocysteine (7, 8) while other studies have concluded it has no significant impact on these molecules such as homocysteine levels (9).
- #10 Any small molecular weight contaminants in the dialysis solu- tion can enter the blood unimpeded and accumulate in the body in the absence of renal excretion. Therefore, the chemical and microbiologic purity of dialysis solution is important if patient injury is to be avoided. Dialysis solution is prepared from puri- fied water (product water) and concentrates, the latter contain- ing the electrolytes necessary to provide dialysis solution of the prescribed composition. Most concentrates are obtained from commercial sources and their purity is subject to regulatory over- sight. The purity of the water used to prepare dialysis solution or to reconstitute concentrates from powder at a dialysis facility, is the responsibility of the dialysis facility. Dialysis Solution Preparation: Proportioning machines. To reduce bulk and shipping costs, dialysis fluid is manufactured in concentrated form and machines proportion it with water before delivering it to the dialyzer. The dialysis machine incorporates pumps and one-way valve systems that make the final dialysis solution by taking fixed volumes of dialysate concentrates and mix- ing them with a fixed volume of heated purified water, or by using conductivity-based servocontrol systems to mix the concentrates and water. As discussed in the previous chapter, the ionic composition of the final dialysis solution is checked by conductivity, which is kept in a very tight range. As long as the solution remains in the target conductivity range, the dialysis solution is allowed to pass on to the dialyzer. If con- ductivity gets outside the range, an alarm sounds and dialysis stops. Dual-concentrate system for bicarbonate-based solutions. Almost all dialysis solution used today is bicarbonate based, and this engenders a solubility issue. When making a bicarbonate solution of about 30 mM, the pH will be close to 8.0. At this pH, calcium and magnesium will precipitate out from solution, reducing their diffusible concentration and also contributing to scaling on dialysis machine lines and passages. To circum- vent the problem of calcium and magnesium precipitation, a bicarbonate-based dialysis solution–generating system utilizes two concentrates: a “bicarbonate” concentrate and an “acid” concentrate. The “acid” concentrate contains a small amount of acetic or citric acid plus sodium, potassium (as needed), calcium, magnesium, chloride, and dextrose (optional). The low pH of the acid concentrate keeps the calcium and magnesium in solution, even in concentrated form. Dry Concentrates Bicarbonate. In some machines, a cartridge containing dry sodium bicarbonate is used in place of a liquid “bicarbonate” concentrate. Use of dry bicarbonate cartridges obviates the problem of bacterial growth in “bicarbonate” concentrate and the concern of subsequent contamination of the final dialysis solutions. 2. Acid (citric acid or sodium diacetate). While acetic acid is a liq- uid, dry “acid” concentrates can be made using either citric acid or sodium diacetate. The low concentration of citrate generated in citric acid–based dialysis solution may che- late plasma calcium that is adjacent to the dialysis mem- brane, impeding coagulation, improving dialyzer clearance slightly, and increasing the dialyzer reuse number. In dry
- #14 The acetate or citrate is added in the form of acetic acid, sodium diacetate, or citric acid to the “acid concentrate.” When mixed with the “bicarbonate concentrate,” the hydrogen ion from either of these acids reacts with bicarbonate to form CO2 (i.e., carbonic acid) to establish a buffer system. The concentrations of sodium, potassium, and calcium can be varied by choosing different “acid” concentrates or by adding salts of these cations to the appropriate “acid” concentrates prior to use. In addition, some dialysis machines allow the concentra- tion of sodium in the dialysis solution to be varied during the course of an individual treatment—a practice known as so- dium profiling. Sodium profiling may help reduce the tendency to intradialytic hypotension and the postdialysis washed-out feeling in some patients, but whenever the average dialysis solution sodium level is increased, this may predispose to in- creased thirst, excessive fluid intake, and hypertension (see Chapter 12). Most dialysis machines allow the bicarbonate level to be varied without changing to a different concentrate by altering the proportioning pump ratio. This allows use of dialysis solution bicarbonate levels from 20 to 40 mM, and such a feature is particularly useful when more frequent di- alysis is employed, when dialyzing nonuremic patients (e.g., to treat poisoning) or to treat alkalemic patients. Minor changes in calcium, magnesium, and potassium (if present) will take place whenever dialysate bicarbonate level is altered. Sodium modeling can quantitate the impact of profiles, that is, it can quantitate changes in the plasma sodium concentration and in the sodium balance. This may help us to understand the clinical effect of sodium profiling.
- #15 The blood pump moves blood from the access site, through the dialyzer, and back to the patient. Negative hydrostatic pressure on the dialysate side can be manipulated to achieve desirable fluid removal or ultrafiltration. Dialysis membranes have different ultrafiltration coefficients (i.e., mL removed/min per mmHg) so that along with hydrostatic changes, fluid removal can be varied. The dialysis solution delivery system dilutes the concentrated dialysate with water and monitors the temperature, conductivity, and flow of dialysate.
- #18 The efficiency of dialysis is determined by blood and dialysate flow through the dialyzer as well as dialyzer characteristics. The dose of dialysis, which is currently defined as a derivation of the fractional urea clearance during a single treatment, is further governed by patient size, residual kidney function, dietary protein intake, the degree of anabolism or catabolism, and the presence of comorbid conditions. Several studies have suggested that longer hemodialysis session lengths may be beneficial (independent of urea clearance), although these studies are confounded by a variety of patient characteristics, including body size and nutritional status.
- #20 Importance: Higher BFR can enhance the clearance of urea and other toxins, improving dialysis efficiency. However, excessively high BFR can lead to complications such as vascular access issues
- #21 A longer initial dialysis session or use of excessively high blood flow rates in the acute set- ting may result in the so-called disequilibrium syndrome, described more fully in Chapter 12. This neurologic syn- drome, which includes the appearance of obtundation, or even seizures and coma, during or after dialysis, has been associated with excessively rapid removal of blood solutes. The risk of disequilibrium syndrome is increased when the predialysis SUN level is high. After the initial dialysis ses- sion, the patient can be reevaluated and should generally be dialyzed again the following day. The length of the sec- ond dialysis session can usually be increased to 3 hours, provided that the predialysis SUN level is <100 mg/dL (36 mmol/L). Subsequent dialysis sessions can be as long as needed. The length of a single dialysis treatment rarely exceeds 6 hours unless the purpose of dialysis is treatment of drug overdose. Slow low-efficiency hemodialysis (SLED) uses low blood and dialysis solution flow rates and longer treatment sessions in order to more safely remove fluid. SLED is described in Chapter 15.
- #24 In patients with acute renal failure, it is extremely important to avoid hypotension at all times, including during dialysis. In a rat model of acute renal failure, Kelle- her (1987) showed that the renal autoregulatory response to systemic hypotension is greatly impaired. They found that transient episodes of hypotension caused by blood withdrawal caused further renal damage and delay of functional renal recovery.
- #25 Importance: An optimal DFR maximizes the concentration gradient for toxin removal. Inadequate DFR can result in suboptimal dialysis and poor clearance of waste products.
- #26 Importance: An optimal DFR maximizes the concentration gradient for toxin removal. Inadequate DFR can result in suboptimal dialysis and poor clearance of waste products.
- #28 In that study, a urea Kt/V value <0.8 was found to be associated with a high likelihood of morbidity and/or treatment failure, while a Kt/V >1.0 was associated with a good outcome. Largely because of this study, guide- lines groups have recommended a minimum Kt/V value of at least 1.2 for hemodialysis patients being dialyzed three times per week. If we deliver a Kt/V of 1.0, this implies that K × t, or the total volume of blood cleared during the dialysis session, is equal to V, the urea distribution volume.
- #29 Patients with IDH show increased mortality and also an increased rate of cardiac wall motion abnormalities during di- alysis, the so-called myocardial stunning For quality assurance purposes, a definition of nadir systolic BP less than 90 mm Hg might be most useful as this has the strongest association with increased mortality The incidence of IDH is highest in patients with low predialysis blood pressure. A low predialysis blood pressure may be a marker of cardiac disease, and hearts with functional or structural abnormalities may be less able to compensate hemodynamically for fluid removal. IDH is also associated with an increased risk of access thrombosis
- #30 Patients with IDH show increased mortality and also an increased rate of cardiac wall motion abnormalities during di- alysis, the so-called myocardial stunning For quality assurance purposes, a definition of nadir systolic BP less than 90 mm Hg might be most useful as this has the strongest association with increased mortality The incidence of IDH is highest in patients with low predialysis blood pressure. A low predialysis blood pressure may be a marker of cardiac disease, and hearts with functional or structural abnormalities may be less able to compensate hemodynamically for fluid removal. IDH is also associated with an increased risk of access thrombosis
- #32 The pathogenesis of muscle cramps during dialysis is unknown. The four most important predisposing factors are hypotension, hypovolemia (patient below dry weight), high ultrafiltration rate (large weight gain), and use of low-sodium These factors all tend to favor vasoconstric- tion, resulting in muscle hypoperfusion, leading to second- ary impairment of muscle relaxation. Muscle cramps most commonly occur in association with hypotension, although cramps often persist after seemingly adequate blood pressure has been restored. Cramping is more common during the first month of dial- ysis than in subsequent periods. It is more common in patients with a low cardiac index. Diagnostically obscure elevations in serum creatinine phosphokinase levels on routine monthly laboratory tests may result from intradialytic muscle cramp- ing. Hypomagnesemia may cause treatment-resistant muscle cramping during dialysis. Hypocalcemia should also be con- sidered as a potential cause, especially in patients treated with relatively low-calcium dialysis solution (1.25 mM) and calcium- free phosphate binders and/or cinacalcet. Predialysis hypoka- lemia will be exacerbated by the usual level of dialysis solution potassium (2 mM) and may precipitate cramping as well. C. Prevention. Prevention of hypotensive episodes will eliminate most cramping. 1. Stretching exercises. A program of stretching exercises tar- geted at the affected muscle groups may be useful and should be the first-line treatment for both dialysis-related cramps and nocturnal cramps (Evans, 2013). Dialysate sodium. The frequency of cramping is inversely related to the dialysis solution sodium level. Raising so- dium levels to just below the threshold for induction of postdialysis thirst will be beneficial, and use of sodium gradient dialysis can definitely reduce cramps, although sometimes at the expense of increasing IDWG and blood pressure. Dialysate magnesium. Avoiding low predialysis levels of mag- nesium, calcium, and potassium may also be helpful. In one preliminary study, use of 0.5 mM (1 mEq/L) dialysis solu- tion magnesium was associated with a lower incidence of cramps than when 0.375 mM (0.75 mEq/L) solution was used (Movva, 2011). Magnesium supplements have not been shown to be useful in nonuremic subjects, and magnesium should be given with great caution to dialysis patients. The use of Osvaren (calcium acetate/magnesium carbonate) as a phosphate binder compared with sevelamer showed no change in the incidence of cramps. Biotin. Biotin, in a dose of 1 mg per day, has been reported to improve intradialytic cramps, despite baseline serum levels being higher than in control subjects (Oguma, 2012). This study needs to be confirmed before biotin use can be more widely recommended. Carnitine, oxazepam, and vitamin E. Carnitine supplementation of dialysis patients may reduce intradialytic muscle cramps (Ahmad, 1990) as may oxazepam (5–10 mg, given 2 hours prior to dialysis) and vitamin E. See Evans (2013) for a review. Compression devices. A type of sequential compression device may be of benefit (Ahsan, 2004). Quinine. Quinine sulfate before dialysis, though effective in pre- venting intradialytic cramps, is now considered inadvisable because of its association with thrombocytopenia, hypersen- sitivity reactions, and QT prolongation. The FDA has issued a number of guidance documents aimed at counseling health professionals against use of quinine for leg cramps.
- #33 III. NAUSEA AND VOMITING Etiology. Nausea or vomiting occurs in up to 10% of routine dialysis treatments. The cause is multifactorial. Most epi- sodes in stable patients are probably related to hypotension. Nausea or vomiting can also be an early manifestation of the disequilibrium syndrome described below. Both type A and type B varieties of dialyzer reactions can cause nausea and vomiting. Gastroparesis, very common in diabetes but also seen in nondiabetic patients, is exacerbated by hemo- dialysis and may play a role in some patients. Contaminated or incorrectly formulated dialysis solution (high sodium, calcium) may cause nausea and vomiting as part of a con- stellation of symptoms. Dialysis patients appear to develop nausea and vomiting more readily than other patients (e.g., with an upper respiratory infection, narcotic usage, hyper- calcemia); dialysis may precipitate these symptoms in such a predisposing setting. Management. The first step is to treat any associated hypoten- sion. Vomiting may be particularly problematic when asso- ciated with a hypotension-induced reduction in the level of consciousness owing to the risk of aspiration. Antiemetics can be administered for other causes of vomiting as needed. Prevention. Avoidance of hypotension during dialysis is of prime importance. Persistent symptoms unrelated to hemodynam- ics may benefit from metoclopramide. Sometimes a single predialysis dose of 5–10 mg is sufficient.
- #34 IV. HEADACHE Etiology. Headache occurs in as many as 70% of patients during dialysis; its cause is largely unknown. It may be a subtle manifestation of the disequilibrium syndrome (see section VII, below). In patients who are coffee drinkers, headache may be a manifestation of caffeine withdrawal as the blood caffeine concentration is acutely reduced during the dialysis treat- ment. Dialysis may precipitate migraine headaches in those with a history of the disorder. With atypical or particularly severe headache, a neurologic cause (particularly a bleeding event precipitated by anticoagulation) should be considered. Management. Acetaminophen can be given during dialysis. Prevention. Decreasing dialysis solution sodium may also be help- ful in patients being treated with high sodium levels. A cup of strong coffee may help prevent (or treat) caffeine withdrawal symptoms. Patients suffering from headache during dialysis may be magnesium deficient (Goksel, 2006). A cautious trial of magnesium supplementation may be indicated, keeping in mind the risks of giving magnesium to patients with renal failure.
- #35 CHEST PAIN AND BACK PAIN. Mild chest pain or discomfort (often as- sociated with some back pain) occurs in 1%–4% of dialysis treat- ments. The cause is unknown. There is no specific management or prevention strategy, though switching to a different variety of dialyzer membrane may be of benefit. The occurrence of angina during dialysis is common and must be considered in the differ- ential diagnosis, along with numerous other potential causes of chest pain (e.g., hemolysis, air embolism, pericarditis). The man- agement and prevention of angina is discussed in Chapter 38.
- #36 ITCHING. Itching, a common problem in dialysis patients, is some- times precipitated or exacerbated by dialysis. Itching appearing only during the treatment, especially if accompanied by other minor allergic symptoms, may be a manifestation of low-grade hypersensitivity to dialyzer or blood circuit components. More often than not, however, itching is simply present chronically, and is noticed in the course of the treatment while the patient is forced to sit still for a prolonged period of time. Viral (or drug- induced) hepatitis and scabies should not be overlooked as potential causes of such itching. Chronically, general moisturizing and lubrication of the skin using emollients is recommended, and this should be the first line of therapy. One should make sure that dialysis is adequate, and that a Kt/V of at least 1.2 and possibly higher is being delivered, though the evidence that higher Kt/V improves pruritus is not strong. Pruritus is often found in patients with elevated serum cal- cium or phosphorus levels and/or substantially elevated parathy- roid hormone (PTH) level; reductions in phosphorus, calcium (to the lower end of the normal range), and PTH levels are indicated. Standard symptomatic treatment using antihistamines is useful. Gabapentin (or pregabalin), UVB (ultraviolet light B) ther- apy, oral charcoal, or nalfuralfine might be the next line of ther- apy, followed by naltrexone or tacrolimus ointment (Figure 12.1) (Mettang and Kremer, 2014).
- #37 Definition. The disequilibrium syndrome is a set of systemic and neurologic symptoms often associated with characteristic elec- troencephalographic findings that can occur either during or following dialysis. Early manifestations include nausea, vomit- ing, restlessness, and headache. More serious manifestations include seizures, obtundation, and coma (see also Chapter 40). Etiology. The cause of the disequilibrium syndrome is contro- versial. Most believe it is related to an acute increase in brain water content. When the plasma solute level is rapidly lowered during dialysis, the plasma becomes hypotonic with respect to the brain cells, and water shifts from the plasma into brain tissue. Others incriminate acute changes in the pH of the cere- brospinal fluid during dialysis as the cause of this disorder. The disequilibrium syndrome was a much larger problem two or more decades ago, when acutely uremic patients with very high serum urea nitrogen values were commonly subjected to prolonged dialysis. However, milder forms of the syndrome may still occur in long-term dialysis patients, manifesting as nau- sea, vomiting, or headache. The full-blown disequilibrium syn- drome, including coma and/or seizures, can still be precipitated when an acutely uremic patient is dialyzed too energetically. Management 1. Mild disequilibrium. Symptoms of nausea, vomiting, restless- ness, and headache are nonspecific; when they occur, it is difficult to be certain that they are due to disequilibrium. Treatment is symptomatic. If mild symptoms of disequilib- rium develop in an acutely uremic patient during dialysis, the blood flow rate should be reduced to decrease the effi- ciency of solute removal and pH change, and consideration should be given to terminating the dialysis session earlier than planned. Hypertonic sodium chloride or glucose solu- tions can be administered as for treatment of muscle cramps. 2. Severe disequilibrium. If seizures, obtundation, or coma oc- cur in the course of a dialysis session, dialysis should be stopped. The differential diagnosis of severe disequilib- rium syndrome should be considered (see Chapter 40). Treatment of seizures is discussed in Chapter 40. The man- agement of coma is supportive. The airway should be con- trolled and the patient ventilated if necessary. Intravenous mannitol may be of benefit. If coma is due to disequilib- rium, then the patient should improve within 24 hours. Prevention 1. In an acute dialysis setting. When planning dialysis for an acutely uremic patient, one should not prescribe an overly aggressive treatment session (see Chapter 10). The target reduction in the plasma urea nitrogen level should initially be limited to about 40%. Use of a low-sodium dialysis solu- tion (more than 2–3 mM less than the plasma sodium level) may exacerbate cerebral edema and should be avoided. In hypernatremic patients, one should not attempt to correct the plasma sodium concentration and the uremia at the same time. It is safest to dialyze a hypernatremic patient initially with a dialysis solution sodium value close to the plasma level and then to correct the hypernatremia slowly postdialysis by administering 5% dextrose. 2. In a chronic dialysis setting. The incidence of disequilibrium syndrome can be minimized by use of a dialysis solution with a sodium concentration of at least 140 mM. Intra- dialytic symptom frequency has been shown to be simi- lar with a dialysate glucose concentration of 200 versus 100 mg/dL (11 vs. 5.5 mM) (Raimann, 2012). Using a high dialysis solution sodium concentration (145–150 mM) that declines over the course of treatment for patients has been advocated in this setting: the initially high dialysis solution sodium results in a rising plasma sodium that may counteract the osmotic effects of the initially rapid removal of urea and other solutes from plasma. There is evidence that use of this approach reduces the incidence of disequilibrium-type intradialytic symptoms, but it may increase IDWG and blood pressure because of diffusive entry of sodium from dialysis solution to blood during the treatment session.
- #38 Definition. The disequilibrium syndrome is a set of systemic and neurologic symptoms often associated with characteristic elec- troencephalographic findings that can occur either during or following dialysis. Early manifestations include nausea, vomit- ing, restlessness, and headache. More serious manifestations include seizures, obtundation, and coma (see also Chapter 40). Etiology. The cause of the disequilibrium syndrome is contro- versial. Most believe it is related to an acute increase in brain water content. When the plasma solute level is rapidly lowered during dialysis, the plasma becomes hypotonic with respect to the brain cells, and water shifts from the plasma into brain tissue. Others incriminate acute changes in the pH of the cere- brospinal fluid during dialysis as the cause of this disorder. The disequilibrium syndrome was a much larger problem two or more decades ago, when acutely uremic patients with very high serum urea nitrogen values were commonly subjected to prolonged dialysis. However, milder forms of the syndrome may still occur in long-term dialysis patients, manifesting as nau- sea, vomiting, or headache. The full-blown disequilibrium syn- drome, including coma and/or seizures, can still be precipitated when an acutely uremic patient is dialyzed too energetically. Management 1. Mild disequilibrium. Symptoms of nausea, vomiting, restless- ness, and headache are nonspecific; when they occur, it is difficult to be certain that they are due to disequilibrium. Treatment is symptomatic. If mild symptoms of disequilib- rium develop in an acutely uremic patient during dialysis, the blood flow rate should be reduced to decrease the effi- ciency of solute removal and pH change, and consideration should be given to terminating the dialysis session earlier than planned. Hypertonic sodium chloride or glucose solu- tions can be administered as for treatment of muscle cramps. 2. Severe disequilibrium. If seizures, obtundation, or coma oc- cur in the course of a dialysis session, dialysis should be stopped. The differential diagnosis of severe disequilib- rium syndrome should be considered (see Chapter 40). Treatment of seizures is discussed in Chapter 40. The man- agement of coma is supportive. The airway should be con- trolled and the patient ventilated if necessary. Intravenous mannitol may be of benefit. If coma is due to disequilib- rium, then the patient should improve within 24 hours. Prevention 1. In an acute dialysis setting. When planning dialysis for an acutely uremic patient, one should not prescribe an overly aggressive treatment session (see Chapter 10). The target reduction in the plasma urea nitrogen level should initially be limited to about 40%. Use of a low-sodium dialysis solu- tion (more than 2–3 mM less than the plasma sodium level) may exacerbate cerebral edema and should be avoided. In hypernatremic patients, one should not attempt to correct the plasma sodium concentration and the uremia at the same time. It is safest to dialyze a hypernatremic patient initially with a dialysis solution sodium value close to the plasma level and then to correct the hypernatremia slowly postdialysis by administering 5% dextrose. 2. In a chronic dialysis setting. The incidence of disequilibrium syndrome can be minimized by use of a dialysis solution with a sodium concentration of at least 140 mM. Intra- dialytic symptom frequency has been shown to be simi- lar with a dialysate glucose concentration of 200 versus 100 mg/dL (11 vs. 5.5 mM) (Raimann, 2012). Using a high dialysis solution sodium concentration (145–150 mM) that declines over the course of treatment for patients has been advocated in this setting: the initially high dialysis solution sodium results in a rising plasma sodium that may counteract the osmotic effects of the initially rapid removal of urea and other solutes from plasma. There is evidence that use of this approach reduces the incidence of disequilibrium-type intradialytic symptoms, but it may increase IDWG and blood pressure because of diffusive entry of sodium from dialysis solution to blood during the treatment session.
- #39 Definition. The disequilibrium syndrome is a set of systemic and neurologic symptoms often associated with characteristic elec- troencephalographic findings that can occur either during or following dialysis. Early manifestations include nausea, vomit- ing, restlessness, and headache. More serious manifestations include seizures, obtundation, and coma (see also Chapter 40). Etiology. The cause of the disequilibrium syndrome is contro- versial. Most believe it is related to an acute increase in brain water content. When the plasma solute level is rapidly lowered during dialysis, the plasma becomes hypotonic with respect to the brain cells, and water shifts from the plasma into brain tissue. Others incriminate acute changes in the pH of the cere- brospinal fluid during dialysis as the cause of this disorder. The disequilibrium syndrome was a much larger problem two or more decades ago, when acutely uremic patients with very high serum urea nitrogen values were commonly subjected to prolonged dialysis. However, milder forms of the syndrome may still occur in long-term dialysis patients, manifesting as nau- sea, vomiting, or headache. The full-blown disequilibrium syn- drome, including coma and/or seizures, can still be precipitated when an acutely uremic patient is dialyzed too energetically. Management 1. Mild disequilibrium. Symptoms of nausea, vomiting, restless- ness, and headache are nonspecific; when they occur, it is difficult to be certain that they are due to disequilibrium. Treatment is symptomatic. If mild symptoms of disequilib- rium develop in an acutely uremic patient during dialysis, the blood flow rate should be reduced to decrease the effi- ciency of solute removal and pH change, and consideration should be given to terminating the dialysis session earlier than planned. Hypertonic sodium chloride or glucose solu- tions can be administered as for treatment of muscle cramps. 2. Severe disequilibrium. If seizures, obtundation, or coma oc- cur in the course of a dialysis session, dialysis should be stopped. The differential diagnosis of severe disequilib- rium syndrome should be considered (see Chapter 40). Treatment of seizures is discussed in Chapter 40. The man- agement of coma is supportive. The airway should be con- trolled and the patient ventilated if necessary. Intravenous mannitol may be of benefit. If coma is due to disequilib- rium, then the patient should improve within 24 hours. Prevention 1. In an acute dialysis setting. When planning dialysis for an acutely uremic patient, one should not prescribe an overly aggressive treatment session (see Chapter 10). The target reduction in the plasma urea nitrogen level should initially be limited to about 40%. Use of a low-sodium dialysis solu- tion (more than 2–3 mM less than the plasma sodium level) may exacerbate cerebral edema and should be avoided. In hypernatremic patients, one should not attempt to correct the plasma sodium concentration and the uremia at the same time. It is safest to dialyze a hypernatremic patient initially with a dialysis solution sodium value close to the plasma level and then to correct the hypernatremia slowly postdialysis by administering 5% dextrose. 2. In a chronic dialysis setting. The incidence of disequilibrium syndrome can be minimized by use of a dialysis solution with a sodium concentration of at least 140 mM. Intra- dialytic symptom frequency has been shown to be simi- lar with a dialysate glucose concentration of 200 versus 100 mg/dL (11 vs. 5.5 mM) (Raimann, 2012). Using a high dialysis solution sodium concentration (145–150 mM) that declines over the course of treatment for patients has been advocated in this setting: the initially high dialysis solution sodium results in a rising plasma sodium that may counteract the osmotic effects of the initially rapid removal of urea and other solutes from plasma. There is evidence that use of this approach reduces the incidence of disequilibrium-type intradialytic symptoms, but it may increase IDWG and blood pressure because of diffusive entry of sodium from dialysis solution to blood during the treatment session.
- #40 This is a broad group of events that includes both anaphylactic and less well-defined adverse reactions of un- known cause (Jaber and Pereira, 1997). In the past, many of these reactions were grouped under the term “first-use” syndrome be- cause they presented much more often when new (as opposed to reused) dialyzers were employed. However, similar reactions occur with reused dialyzers, and we now discuss them under the more general category used here. There appear to be two variet- ies: an anaphylactic type (type A) and a nonspecific type (type B). The occurrence of type B reactions appears to have diminished considerably during the past several decades. A. Type A (anaphylactic type) 1. Manifestations. When a full-blown, severe reaction occurs, the manifestations are those of anaphylaxis. Dyspnea, a sense of impending doom, and a feeling of warmth at the fistula site or throughout the body are common presenting symptoms. Cardiac arrest and even death may supervene. Milder cases may present only with itching, urticaria, cough, sneezing, coryza, or watery eyes. Gastrointestinal manifestations, such as abdominal cramping or diarrhea, may also occur. Patients with a history of atopy and/or with eosinophilia are prone to develop these reactions. Symptoms usually be- gin during the first few minutes of dialysis, but onset may occasionally be delayed for up to 30 minutes or more. 2. Etiology Ethylene oxide. Most type A (anaphylactic) reactions in the past were due to hypersensitivity reactions to eth- ylene oxide, which was widely used by manufacturers to sterilize dialyzers. It tended to accumulate in the potting compound used to anchor the hollow fibers, hampering efforts to remove it by degassing prior to sale. These reactions were observed exclusively dur- ing first use of dialyzers. Manufacturers currently use a variety of methods of sterilization (gamma radiation, steam, electron beam) , and when ethylene oxide is used, little residual compound is left in the dialyzers. As a result, ethylene oxide reactions are now uncommon. AN69-associated reactions. These were initially reported in patients dialyzed with the AN69 (acrylonitrile-sodium methallyl sulfonate) membrane who were also taking angiotensin-converting enzyme (ACE) inhibitors. The reactions are thought to be mediated by the bradyki- nin system. The negatively charged AN69 membrane activates the bradykinin system with the effects mag- nified because ACE inhibitors block bradykinin inacti- vation. Plasma bradykinin levels, higher at baseline in patients treated with AN69 dialyzers, rise substantially during reactions. The bradykinin effect should be less pronounced with angiotensin receptor blockers than with ACE inhibitors (Ball, 2003). It is unclear to what extent ACE inhibitor–associated reactions occur with other PAN (polyacrylonitrile)-based membranes or with other non–PAN-based membranes. c. Contaminated dialysis solution. Type A dialyzer reactions may be accounted for in some instances by dialysis solution contamination with high levels of bacteria and endotoxin, particularly with the use of high-flux 230 Part II / Blood-Based Therapies dialyzers. Such reactions are likely to occur promptly (within 2 minutes) of initiating dialysis; complement- mediated reactions are more delayed (15–30 minutes) in onset. Fever and chills are particularly common symp- toms with these reactions. The higher the bacteria and endotoxin levels are, the greater the risk is of a reaction. Reuse. Clusters of anaphylactic-type dialyzer reactions have occurred in a reuse setting. The problem has often been linked to inadequate dialyzer disinfection during the reuse procedure, but in many cases the cause is un- known. Half of Centers for Disease Control and Preven- tion (CDC) investigations of outbreaks of bacteremia or pyrogenic reactions in dialysis patients over a 20-year period were ascribed to dialyzer reuse problems (Roth and Jarvis, 2000). Heparin. Heparin has occasionally been associated with allergic reactions, including urticaria, nasal conges- tion, wheezing, and even anaphylaxis. When a patient seems to be allergic to a variety of different dialyzers re- gardless of the sterilization mode, and dialysis solution contamination also has been reasonably excluded, a trial of heparin-free dialysis or citrate anticoagulation should be considered. Low-molecular-weight hepa- rins are not a safe substitute in such patients owing to cross-reactivity with heparin, which may result in ana- phylactic reactions. Complement fragment release. Acute increases in pulmo- nary artery pressure have been documented in both animals and humans during dialysis with unsubsti- tuted cellulose membranes. However, there is no good evidence that complement activation causes type A dialyzer reactions. Several studies have found no dif- ference in type A reaction rates between membranes that readily activate complement (cuprophane) and those that do not (polysulfone, AN69). Eosinophilia. Type A reactions tend to occur more read- ily in patients with mild to moderate eosinophilia. Very severe reactions to dialysis or plasmapheresis were reported in patients with very high eosinophil counts; these were thought to be due to sudden eosin- ophil degranulation with release of bronchoconstric- tive and other mediators. Management. Identifying the actual cause of a dialyzer reaction frequently is not possible. It is safest to stop dialysis imme- diately, clamp the blood lines, and discard the dialyzer and blood lines without returning the contained blood. Immediate cardiorespiratory support may be required. According to the severity of the reaction, treatment with intravenous antihis- tamines, steroids, and epinephrine can be given. Prevention. For all patients, proper rinsing of dialyzers prior to use is important to eliminate residual ethylene oxide and Chapter 12 / Complications during Hemodialysis 231 other putative allergens. In a patient with a history of type A reaction to an ethylene oxide–sterilized dialyzer, the dialyzer type can be changed to a γ-irradiated, steam-sterilized, or electron beam–sterilized dialyzer (see Table 4.1). The neces- sity of using non–ethylene oxide–sterilized blood lines when switching to a dialyzer sterilized by some alternate method has not been established. For patients whose mild type A symptoms persist following a switch to equipment free of ethylene oxide, predialysis administration of antihistamines may be of benefit. Placing the patient on a reuse program and subjecting even new dialyzers to the reuse procedure prior to first use may be of benefit because of enhanced washout of potential noxious substances or allergens. Changing or stop- ping heparin, trying a less complement-activating mem- brane, and substituting an angiotensin receptor–blocking agent for an ACE inhibitor may also be tried. A role for latex exposure during dialysis initiation in a sensitized patient should be considered as well. B. Nonspecific type B dialyzer reactions 1. Symptoms. The principal manifestations of a type B reac- tion are chest pain, sometimes accompanied by back pain. Symptom onset is usually 20–40 minutes after starting di- alysis. Typically, type B reactions are much less severe than type A reactions. 2. Etiology. The cause is unknown. Complement activation has been suggested to be a culprit, but its etiologic role in the development of these symptoms is uncertain. Chest and back pain may occur less frequently with reused dialyzers than with new dialyzers, though this is controversial. Any beneficial effects may be due to increased biocompatibility from protein coating of the membrane (not seen with bleach reprocessing) or to washout of potentially toxic substances from the dialyzer. Other causes of chest and back pain must be excluded, and the diagnosis of a type B dialyzer reaction is one of exclusion. In particular, subclinical hemolysis must be ruled out. A syndrome of acute respiratory distress as- sociated with heparin-induced thrombocytopenia has been described (Popov, 1997), which may superficially resemble a type B dialyzer reaction. 3. Management. Management is supportive. Nasal oxygen should be given. Myocardial ischemia should be consid- ered, and angina pectoris, if suspected, can be treated as discussed in Chapter 38. Dialysis can usually be continued, as symptoms invariably abate after the first hour. 4. Prevention. Trying a different dialyzer membrane may be of value.
- #41 HEMOLYSIS. Acute hemolysis during dialysis may be a medical emergency. A. Manifestations: The symptoms of hemolysis are back pain, tightness in the chest, and shortness of breath. A dramatic deepening of skin pigmentation may occur. Common are a port-wine appearance of blood in the venous blood line, a pink discoloration of the plasma in centrifuged blood samples, and a marked fall in the hematocrit. If massive hemolysis is not detected early, then hyperkalemia can result owing to re- lease of potassium from the hemolyzed erythrocytes, leading to muscle weakness, electrocardiographic abnormalities, and, ultimately, cardiac arrest. Etiology. Acute hemolysis has been reported in two primary set- tings: (a) an obstruction or narrowing in the blood line, catheter, or needle or (b) a problem with the dialysis solution. The possibil- ity of hemolysis induced by the combination of G6PD deficiency and predialysis quinine sulfate therapy should be considered. Blood line obstruction/narrowing. Kinks may develop in the ar- terial blood line (Sweet, 1996). An epidemic of hemolysis also has been reported owing to manufacturing defects in the link between the dialyzer outlet blood line and the ve- nous air trap chamber (CDC, 1998). Hemolysis (usually sub- clinical) may also appear when blood flow rate is high and relatively small needle sizes are used (De Wachter, 1997). Routine blood line pressure monitoring will call attention to many, but not all, such problems. Problems with dialysis solution. These are as follows: a. Overheateddialysissolution Hypotonicdialysissolution(insufficientconcentrate-to- water ratio) Dialysis solution contaminated with formaldehyde, bleach, chloramine (from city water supply), copper ( from copper piping), fluoride, nitrates ( from water sup- ply), zinc, or hydrogen peroxide (see Chapter 5). Management. The blood pump should be stopped immediately and the blood lines clamped. The hemolyzed blood has a very high potassium content and should not be reinfused. One should be prepared to treat the resultant hyperkalemia and possible drop in hematocrit. The patient should be observed carefully, and hospitalization should be considered. Delayed hemolysis of injured erythrocytes may continue for some time after the di- alysis session. Severe hyperkalemia may occur, and this may re- quire additional dialysis or other measures (e.g., administration of an Na/K ion exchange resin by mouth or rectum) to control. A complete blood count, reticulocyte count, and levels of hap- toglobin, free hemoglobin, lactate dehydrogenase (LDH), and methemoglobin should be obtained. Dialysis solution water (chloramine, nitrates, metals) and, if reprocessed, the dialyzer (residual sterilant) need to be assessed as well. Prevention. Unless the problem is an obstruction in the blood path or faulty roller pump causing excessive blood trauma, the cause of the hemolysis must be assumed to be in the dialysis solution, and samples of dialysis solution must be investigated to determine the cause.
- #42 AIR EMBOLISM. Air embolism is a potential catastrophe that can lead to death unless detected and treated quickly. A. Manifestations 1. Symptoms. These depend to an extent on the position of the patient. In seated patients, infused air tends to migrate into the cerebral venous system without entering the heart, causing obstruction to cerebral venous return, loss of con- sciousness, convulsions, and even death. In recumbent patients, the air tends to enter the heart, generate foam in the right ventricle, and pass into the lungs, producing dys- pnea, cough, and chest tightness and arrhythmias. Further passage of air across the pulmonary capillary bed into the left ventricle can result in air embolization to the arteries of the brain and heart, with acute neurologic and cardiac dysfunction. 2. Signs. Foam is often seen in the venous blood line of the dialyzer. If air has gone into the heart, a peculiar churning sound may be heard on auscultation. Etiology. The predisposing factors and possible sites of air entry have been discussed in Chapter 4. The most common sites of air entry are the arterial needle, the prepump arterial tubing segment, and an inadvertently opened end of a central venous catheter. Management. The first step is to clamp the venous blood line and stop the blood pump. The patient is immediately placed in a recumbent position on the left side with the chest and head tilted downward. Further treatment includes cardiore- spiratory support, including administration of 100% oxygen by mask or endotracheal tube. Aspiration of air from the atrium or ventricle with a percutaneously inserted needle or cardiac catheterization may be needed if the volume of air warrants it. Prevention. See Chapters 4 and 10. XI. OTHER COMPLICATIONS: Arrhythmia and cardiac tamponade are discussed in Chapter 38. Severe disequilibrium syndrome, sei- zures, and intracerebral bleed are discussed in Chapter 40.