Acute Hemodialysis Prescription

I. THE HEMODIALYSIS PRESCRIPTION. All patients are different, and the circumstances eventuating in the need for acute hemodialysis vary widely. The prescription for hemodialysis will change accordingly. As a teaching tool only, we present a “typical” prescription for an acute hemodialysis in a 70-kg adult.
Rx: Acute hemodialysis (not for initial treatment)
Session length: Perform hemodialysis for 4 hours
Blood flow rate: 350 mL/min
Dialyzer:

Dialyzer membrane: your choice

Dialyzer K_UF: your choice

Dialyzer efficiency: usually a dialyzer with a K₀A of 800–1200 is used

Dialysis solution composition (variable):

Base: bicarbonate 25 mM

Sodium: 145 mM

Potassium: 3.5 mM

Calcium: 1.5 mM (3.0 mEq/L)

Magnesium: 0.375 mM (0.75 mEq/L)

Dextrose: 5.5 mM (100 mg/dL)

Phosphate: none

Dialysis solution flow rate: 500 mL/min

Dialysis solution temperature: 35°C–36°C

Fluid removal orders:

Remove 2.2 L over 4 hours at a constant rate

Anticoagulation orders:

See Chapter 14

A. Determining dialysis session length and blood flow rate. The dialysis session length together with the blood flow rate is the most important determinant of the amount of dialysis to be given (dialyzer efficiency is also a factor).

1. Reduce the amount of dialysis for the initial one or two sessions. 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. A longer initial dialysis session or use of excessively high blood flow rates in the acute setting may result in the so-called disequilibrium syndrome, described more fully in Chapter 12. This neurologic syndrome, 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 session, the patient can be reevaluated and should generally be dialyzed again the following day. 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). 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.

2. Dialysis frequency and dose for subsequent treatments and dialysis adequacy. It is difficult to deliver a large amount of dialysis in the acute setting. Most intensive care unit patients are fluid overloaded, and urea distribution volume is often much greater than 50%–60% of body weight. True delivered blood flow rate through a venous catheter rarely exceeds 350 mL/min and is often substantially lower. Recirculation occurs in venous catheters and is greatest with catheters in the femoral position owing to the low pericatheter venous flow rate. Often, the treatment is interrupted owing to hypotension. Furthermore, the degree of urea sequestration in muscle may be increased, as such patients are often on pressors, reducing blood flow to muscle and skin, which contain a substantial portion of urea and other dissolved waste products. Concomitant intravenous infusions, which are often given to patients in an acute setting, dilute the urea level in the blood and reduce further the efficiency of dialysis.

A typical 3- to 4-hour acute-dialysis session will deliver a single-pool Kt/V of only 0.9, with an equilibrated Kt/V of 0.7. Dialysate-side urea removal may be even lower (Evanson, 1999). This low level of Kt/V, if given three times per week, is associated with a high mortality in chronic, stable patients. One option is to dialyze sick patients with acute renal failure on a daily (six or seven times per week) basis. Each treatment is then approximately 3–4 hours in length. Data by Schiffl (2002) suggest that mortality is reduced in patients with acute renal failure dialyzed six times per week as opposed to those receiving dialysis every other day. If every-other-day dialysis is to be given, the treatment length should probably be set at 4–6 hours, to deliver a single-pool Kt/V of at least 1.2–1.3, as recommended for chronic therapy. The VA/NIH (2008) study compared outcomes in acute patients dialyzed either 3 or 6 times per week and found absolutely no difference in outcomes. The intensity of dialysis in the 3-times-per-week group was substantially higher (Kt/V of 1.3 or more) than in the Schiffl article. For this reason, the KDIGO workgroup on acute kidney injury (2012) recommends that when attempting to maintain acute patients on a 3-times-per-week schedule, each treatment should have a Kt/V of ≥1.3. When there is a concern that there is inconsistent dialysis delivery (e.g., catheter flow or hollow-fiber thrombosis problems), one can verify HD adequacy by assessing the URR using blood tests or devices that measure real-time solute clearance (ionic conductance or UV-absorption technologies).

The amount of dialysis may need to be adjusted upward in hypercatabolic patients. A low predialysis SUN level should not be used as a justification to reduce the amount of dialysis unless substantial residual renal urea clearance is documented; many acute renal failure patients tend to have decreased urea generation rates due to lack of protein ingestion and/or to impairment of urea synthesis by the liver. Therefore, in such patients a low SUN does not necessarily reflect low levels of other uremic toxins.

B. Choosing a dialyzer

1. Membrane material. A Cochrane report has suggested that no firm conclusions could be drawn as of 2006 regarding the benefits of any one group of modern dialysis membranes over another for acute or chronic dialysis. The best dialyzer to select for acute dialysis, therefore, remains unclear. No recommendation favoring use of high-flux membranes for acute dialysis can be made at this time, as membrane flux has not been studied as a separate factor in any randomized study of acute dialysis.

a. Anaphylactoid reactions. These can occur and depend on both membrane material and sterilization mode. See Chapter 12 for details.

2. Ultrafiltration coefficient (K_UF). Ultrafiltration controllers are now available on all modern dialysis machines, and these accurately control the ultrafiltration rate by means of special pumps and circuits. Machines with volumetric ultrafiltration controllers are designed to use dialyzers of high water permeability (e.g., K_UF > 6.0) and may lose accuracy if a high fluid removal rate is attempted using a dialyzer that is relatively impermeable to water.

In the unlikely event that a dialysis machine with an ultrafiltration controller is not available, then a membrane with a relatively low water permeability (K_UF) should be chosen so that the transmembrane pressure (TMP) will have to be set at a relatively high level to remove the amount of fluid desired; then the inevitable errors in maintaining the desired TMP will have less impact on the rate of fluid removal. When close monitoring of the fluid removal rate is required and a machine with advanced ultrafiltration control circuitry is not available, the fluid removal rate can be monitored by placing the patient on an electronic bed or chair scale and continuously following the weight during dialysis.

3. Dialyzer urea clearance. For the first couple of dialysis sessions, it is best to avoid using very high-efficiency dialyzers, although these can be used as long as the blood flow is low. A dialyzer with an in vitro K₀A urea of about 500–600 mL/min is recommended for the initial session to minimize the risk of inadvertent overdialysis and of developing the disequilibrium syndrome, although even with such lower efficiency dialyzers, a markedly shortened dialysis session is required to prevent overdialysis. When heparin-free dialysis is used, there is less risk (theoretically) of clotting when a lower blood flow rate is used with a smaller dialyzer, as the blood velocity through a small fiber bundle will be higher. After the initial one or two sessions, particularly if a high blood flow rate is being used, normal-sized dialyzers can be chosen.

C. Choosing the dialysis solution. In our example, we have chosen a bicarbonate level of 25 mM with a sodium level of 145 mM, a potassium level of 3.5 mM, a calcium level of 1.5 mM (3.0 mEq/L), a magnesium level of 0.375 mM (0.75 mEq/L), a dextrose level of 5.5 mM (100 mg/dL), and no phosphorus. Depending on the circumstances, this prescription may have to be altered in a given patient. It is important to recognize that for acute patients the dialysis solution composition should be tailored. The “standard” composition designed for acidotic, hyperphosphatemic, hyperkalemic, chronic dialysis patients is often inappropriate in an acute setting.

1. Dialysis solution bicarbonate concentration. In the sample prescription mentioned earlier, we have chosen to use a 25 mM bicarbonate level. Intensive care unit patients are often relatively alkalotic for reasons described in what follows, and so prescriptions for “standard” bicarbonate dialysis solution, containing 35–38 mM, should not be used without first carefully evaluating the patient’s acid–base status.

If the predialysis plasma bicarbonate level is 28 mM or higher, or if the patient has respiratory alkalosis, a custom dialysis solution containing an appropriately lower bicarbonate level (e.g., 20–28 mM, depending on the degree of alkalosis) should be used. One should remember that many dialysis solutions provide an additional 4–8 mEq/L of bicarbonate-generating base from acetate or citrate as discussed in Chapter 5. In machines where the dialysate bicarbonate level can be adjusted by changing the proportioning ratio between the acid and base concentrates, final dialysate bicarbonate levels shown on the display screen often correspond to bicarbonate after mixing with the acid concentrate, and so the value shown may not incude the added base content coming from acetate or citrate.

a. Dangers of metabolic alkalosis. A dialysis patient with even a mild metabolic alkalosis (e.g., plasma bicarbonate level of 30 mmol/L) requires very little hyperventilation to increase blood pH to dangerous levels. Alkalemia (blood pH > 7.50) may be more dangerous than acidemia. Dangers of alkalemia include soft tissue calcification and cardiac arrhythmia (sometimes with sudden death), although documentation of the latter risk in the literature is not easy to find. Alkalemia has also been associated with such adverse symptoms as nausea, lethargy, and headache.

In dialysis patients, the most common causes of metabolic alkalosis are a reduced intake of protein, intensive dialysis for any reason (e.g., daily dialysis), and vomiting or nasogastric suction. Another common cause is administered lactate or acetate with total parenteral nutrition (TPN) solutions, or citrate due to citrate anticoagulation.

b. Predialysis respiratory alkalosis. Many patients who are candidates for acute dialysis have preexisting respiratory alkalosis. The causes of respiratory alkalosis are the same as in patients with normal renal function and include pulmonary disease (pneumonia, edema, embolus), hepatic failure, and central nervous system disorders. Normally, compensation for respiratory alkalosis is twofold. There is an acute decrease in the plasma bicarbonate level owing to release of hydrogen ions from body buffer stores. In patients with normal renal function, there is a further delayed (2–3 days) compensatory fall in the plasma bicarbonate level because of excretion of bicarbonate in the urine. Renal bicarbonate excretion obviously cannot occur in dialysis patients.

The therapeutic goal should always be to normalize the pH rather than the plasma bicarbonate level. In patients with respiratory alkalosis, the plasma bicarbonate level at which the blood pH will be normal may be as low as 17–20 mmol/L; the dialysis solution to use should contain less than the usual amount of bicarbonate to achieve a postdialysis plasma bicarbonate level in the desired subnormal range.

c. Achieving an appropriately low dialysis solution bicarbonate level. In certain machines, the proportioning ratio of concentrate to product water is fixed, and as a result, the dialysis solution bicarbonate level can be reduced only by changing the concentrate bicarbonate level. With such machines, the bicarbonate cannot be reduced below about 32 mM. In machines where the concentrate-to-product water ratio can be changed, bicarbonate levels as low as 20 mM usually can be delivered, but not lower, and this does not include the 4-8 mEq/L from acetate or citrate. When attempting to provide a low-base-content dialysate, sodium diacetate-containing concentrate should not be used, as this will increase the base content by 8 mEq/L.

d. Patients with severe predialysis acidosis

1. Dangers of excessive correction of metabolic acidosis. Excessive correction of severe metabolic acidosis (starting plasma bicarbonate level <10 mmol/L) can have adverse consequences, including lowering of the ionized calcium level and a paradoxical acidification of the cerebrospinal fluid and an increase in the tissue production rate of lactic acid. Initial therapy should aim for only partial correction of the plasma bicarbonate level; a target postdialysis plasma bicarbonate value of 15–20 mmol/L is generally appropriate; and for such severely acidotic patients, a dialysis solution bicarbonate level of 20–25 mM is normally used.

2. Respiratory acidosis. The normal compensation to respiratory acidosis is an acute buffer response, which can increase the plasma bicarbonate level by 2–4 mmol/L, followed by a delayed (3–4 days) increase in renal bicarbonate generation. Because the second response is obviated in dialysis patients, respiratory acidosis will have a more pronounced effect on blood pH than in patients with normal renal function. For such patients, dialysis solution bicarbonate levels should be at the higher range, targeted to keep their pH in the normal range.

2. Dialysis solution sodium level. The dialysis solution sodium level in the sample prescription is 145 mM. This level is generally acceptable for patients who have normal or slightly reduced predialysis serum sodium concentrations. If marked predialysis hypernatremia or hyponatremia is present, the dialysis solution sodium level will have to be adjusted accordingly.

a. Hyponatremia. Hyponatremia is common in seriously ill patients requiring acute dialysis, primarily because such patients have often received large amounts of hyponatric intravenous solutions with their medications and parenteral nutrition. Hyponatremia is frequently seen accompanying severe hyperglycemia in diabetic dialysis patients. For every increase of 100 mg/dL (5.5 mmol/L) in the serum glucose concentration, there is a corresponding initial decrease of 1.6 mmol/L in the serum sodium concentration as a result of osmotic shift of water from the intracellular to the extracellular compartment. Because osmotic diuresis secondary to the hyperglycemia does not occur, the excess plasma water is not excreted, and hyponatremia is maintained. Correction of hyperglycemia by insulin administration reverses the initial water shift and thereby corrects the hyponatremia.

1. Predialysis serum sodium level .130 mmol/L. Intensive care patients often tend to be slightly hyponatremic, as they often are given various intravenous drugs in 5% dextrose and water. The goal should be to keep serum sodium at or above 140 mmol/L, and dialysis solution sodium should be in the range of 140-145 mM. The potential benefits of keeping dialysis solution sodium <10 mM above the serum level in patients with possible brain edema and/or hypotension have been reviewed by Davenport (2008).

2. Predialysis serum sodium level ,130 mmol/L. When the degree of predialysis hyponatremia is moderate to severe, and especially if the hyponatremia is of long duration, it is dangerous to achieve normonatremia quickly. Rapid correction of hyponatremia has been linked to a potentially fatal neurologic syndrome known as osmotic demyelination syndrome (Huang, 2007). The maximum safe rate of correction of the serum sodium concentration in severely hyponatremic patients is controversial but probably is in the range of 6-8 mmol/L per 24 hours. At this stage of incomplete knowledge, it seems prudent when treating patients with severe hyponatremia to set the dialysis solution sodium level as low as possible (with most machines one can go no lower than 130 mM, although with the Dialog Plus machine from B.Braun one can get down to a dialysate sodium of ~123 mM), and to dialyze at a slow (50-100 mL/min) blood flow rate, and for not longer than 1 hour at a time, alternating with isolated ultrafiltration as needed for volume control. One can check the serum sodium after each 30–60 min of dialysis to ensure that the desired rate of sodium increase is not being exceeded. In one case report, use of a 50 mL/min blood flow over 3 hours resulted in the desired increase in the serum sodium of 6 mmol/L over the 3-hour dialysis period (Wendland and Kaplan, 2012). Another approach is to delay dialysis for a few days if possible and to treat hyponatremia with hypertonic saline, removing excess fluid by isolated ultrafiltration as needed. If continuous hemodialysis or hemofiltration is available, use of one of these modalities with an appropriate sodium-reduced dialysis solution/replacement fluid is another good option and allows for the greatest control of the rate of serum sodium increase (Yessayan, 2014).

b. Hypernatremia. Hypernatremia is less common than hyponatremia in a hemodialysis setting but does occur, usually in a context of dehydration, osmotic diuresis, and failure to give sufficient electrolyte-free water. It is somewhat dangerous to attempt to correct hypernatremia by hemodialyzing against a low-sodium dialysis solution. Whenever the dialysis solution sodium level is more than 3–5 mM lower than the plasma value, three complications of dialysis occur with increased incidence:

1. Osmotic contraction of the plasma volume occurs as water shifts from the dialyzed blood (containing less sodium than before) to the relatively hyperosmotic interstitium, causing hypotension.

2. The propensity to develop muscle cramps is increased.

3. Water from the dialyzed, relatively hyponatremic blood enters cells, causing cerebral edema and exacerbating the disequilibrium syndrome.

The risk of disequilibrium syndrome is the most important one; use of low-sodium dialysis solution should certainly be avoided in situations in which the predialysis SUN level is high (e.g., >100 mg/dL [36 mmol/L]). The safest approach is to first dialyze a patient with a dialysis solution sodium level close to that of plasma and then correct the hypernatremia by slow administration of slightly hyponatric fluids.