**6. Electrolyte disorders**

#### **6.1 Impaired potassium balances**

Chronic hemodialysis patients are usually predisposed to hyperkalemia at the beginning of dialysis sessions. The first reason for such tendency to hyperkalemia is this patient group does not have residual urine whose major duty is to remove potassium (K) from the body. Another reason is that K passes from inside the cells to outside to correct the acid-base balance and an increase being present in nitrogenous catabolites and inhibition of these Na / K ATPase (Weiner & Wingo, 1998). K is normally in balance inside and outside the cells. A small change in K in the extracellular area causes big changes in resting membrane potential (RMP). The myocardial tissue is affected the most from this situation. A decline in RMP may result in fetal arrhythmias. For this reason, if there is a change in ECG, hyperkalemia should be treated urgently (Browning & Channer, 1981). To prevent a cardiac interaction, iv calcium may be administered. It generally starts affecting in 1 to 3 minutes; if not, a second dose may be given (Schwarts, 1978). K starts dropping after dialysis therapy begins in the hemodialysis patient group, but if the interdialytic hyperkalemia persists, dietary compatibility should be questioned in these patients. Potassium binding resins may also be given to these patients (Acker et al., 1998).

During dialysis, potassium is removed 85% by diffusion and 15% by convection. Hypokalemia is seen more often in dialysis patients and especially in those whose predialysis K levels are normal and who are administered a sodium profile technique (Buemi et al., 2009). Hypokalemia creates tendency to arrhythmia just like hyperkalemia. In order to avoid hypokalemia, the level of K in the dialysate should be arranged for each patient and the intracellular and extracellular shifts of K should be borne in mind. It is especially

Acute Complications of Hemodialysis 277

the dialysate is kept between 139 and 144 mEq/L to prevent development of hyponatremia or hypernatremia in patients (Henrich et al., 1982, Swartz et al., 1982). An Na modeling is made today in some patient groups (high level of Na at the beginning of dialysis and low levels in later hours). Such modeling is particularly made for patients with intradialytic hypotension, cramps or severe uremia or for those whose hemodynamics is not stable. However, modeling will not be appropriate for patients with hypernatremia or intradialytic hypertension (Palmer, 2001). Finally, preparation of individual HD prescriptions should be

Hemolysis was observed at a level of 2% in the initial years of the chronic dialysis program (Maher&Schreiner, 1965), and this has now declined considerably. Various factors lead to hemolysis. These include those arising through oxidizing agents and reducing agents, osmolar insults, thermal and mechanical injury or excessive uremia at initiation of dialysis (Abtahi et al., 2007; Sweet et al., 1996) Oxidizing agents result from contamination of the dialysate with copper, zinc, chloramine or nitrate. These agents lead to hemolysis by establishing oxidant damage in erythrocytes (Kjellstrand et al., 1974; Carlson&Shapiro 1970; Calderaro & Heller 2001; Blomfield et al., 1969). Reducing injury generally arises because of the formaldehyde used in the dialyzer sterilization process (Fonseca et al., 2004). Osmolar injury generally develops secondary to hypotonic dialysate use (Said et al., 1977). Thermal injury is observed when dialysate temperature reaches levels higher than body temperature (Berkes et al., 1975). Mechanical injury may develop in association with maloccluded blood pumps, arterial line collapse, kinked or obstructed hemodialysis tubing of the use of

Acute hemolytic reaction symptoms include malaise, nausea, chest pain, shortness of breath, abdominal pain, back pain, emesis, cyanosis and headache. A positive pink test (pinkappearing serum) is seen in massive hemolysis. Pink test positivity is due to the almost total loss of haptoglobin, elevated levels of serum lactate dehydrogenase and the presence of free hemoglobin (Malinauskas, 2008; Murcutt, 2007). Acute hemolysis is a life-threatening condition that may lead to such complications as anemia, hyperkalemia, vasoconstriction in

In treatment, dialysis must be brought to a conclusion and patients should not be given blood in sets. Emergency resuscitation should be performed depending on the patient's clinical condition, electrolyte imbalance and hemoglobin decrease evaluated, and appropriate treatments administered. The etiological factors leading to hemolysis must

Neutropenia may be observed in correlation with membrane biocompatibility during hemodialysis. It generally begins within 2-3 min of the start of dialysis and reaches a maximum 10-15 min subsequently (Cheung et al., 1994; Deppisch et al.,1990; Twardowski, 2006). It generally reverts to normal levels after dialysis. Neutropenia observed during hemodialysis is associated with neutrophils accumulating on the hemodialysis membrane surfaces and with sequestration in the lungs in particular (Dodd et al., 1983). C5 and C5ades Arg binding to specific receptors and alterations to various receptors on the neutrophil

subclavian hemodialysis catheter (Abtahi et al., 2007; Sweet et al., 1996)

remembered in adjusting the Na balance.

**7. Hematological complications** 

plasma hemoglobin and pancreatitis.

**7.2 Neutropenia** 

subsequently be investigated and eliminated.

**7.1 Hemolysis** 

recommended in recent years to avoid using dialysates with very low levels of K during dialysis in order to prevent excessive decrease of K. For example, it is recommended to use a dialysate containing 2 mEq/L of K in patients whose serum K level is 4-6 mEq/L at the beginning of dialysis (Zehnder et al., 2001), and a dialysate containing 3 mEq/L of K in patients whose pre-dialysis K is in normal intervals (Weisberg& Rachoin, 2010).

#### **6.2 Impaired calcium balances**

Calcium plays an important role in the contraction of skeletal, smooth and cardiac muscle. The major factors causing increases and decreases in the Ca level in the hemodialysis patient group are secondary hyperparathyroidism and vitamin D used in treating it or its analogs, calcimimetics, and phosphorus binders containing calcium and magnesium. Since there is no urination in these patients, the excess calcium taken through diet may also cause increases in the serum calcium. In addition to these factors, the changes in Ca level are also associated with the concentration of calcium in the dialysate during hemodialysis therapy (Saha et al., 1996). Dialysates containing 3.5 mEq/L of Ca have been used for many years to help treat secondary hyperparathyroidism. However, this approach resulted in an increase both in hypercalcemia and adynamic bone disease. The relationship between a high serum calcium and mortality has been demonstrated in many studies conducted over years (Block et al., 2004; Kalantar-Zadeh et al., 2006). Due to the relationship between hypercalcemia and mortality, K-DOQI recommended that the target for serum Ca should be 8.4-9.5 mg/dl and for dialisate Ca to be 2.5 mEq/l (Hemodialysis Adequacy 2006 Work Group,2006). A tendency to hypocalcemia is seen in the hemodialysis patient group in recent years as a result of decreases in the use of calcimimetics, phosphorus binders with no Ca content and dialisates with low levels of Ca, and in the dietary intakes of Ca (Hemodialysis Adequacy 2006 Work Group,2006; Kalantar-Zadeh et al., 2006; Stevens et al.,2010). It was demonstrated in the study carried out recently by Miller JE and associates that the Ca values of < 9 mg/dl and >10 mg/dl were associated with increased mortality (Miller et al., 2010). Hypercalcemia causes mortality through tendency to arrhythmia, hypertension and vascular calcification, and hypocalcemia through tendency to arrhythmia. As a result, both hypercalcemia and hypocalcemia can cause an increase in mortality. The most important approach in the prevention and treatment of this electrolyte imbalance will be to assess each patient individually and prescribe hemodialysis accordingly.

#### **6.3 Impaired sodium balances**

The Na balance in the hemodialysis patient group is closely associated with the Na level in the dialysate and the volume situation. The Na balance in the HD patient group, on the other hand, is mainly maintained by the balance between the amount taken through the diet and the amount removed through dialysis. Various studies showed that HD patient group has been taking salt as much as taken by the normal population (Maduell& Navarro, 2000; Lambie et al., 2005). Intake of excessive salt in turn leads to an increase in thirstiness and interdialytic weight gain (Santos&Peixoto, 2010).

In a study made by Peixoto AJ and associates, 100 stable HD patients were observed for a period of 12 months and it was seen that the patients had lower pre-dialysis levels of salt, but they were stable in the 12-month period (Peixoto&Santos, 2010).

During hemodialysis, Na is removed mainly through diffusion and in fewer amounts through convection (Lambie et al., 2005). The level of Na being high or low in the dialysate directly affects the level of Na in patients. It is recommended, therefore, that the Na level in the dialysate is kept between 139 and 144 mEq/L to prevent development of hyponatremia or hypernatremia in patients (Henrich et al., 1982, Swartz et al., 1982). An Na modeling is made today in some patient groups (high level of Na at the beginning of dialysis and low levels in later hours). Such modeling is particularly made for patients with intradialytic hypotension, cramps or severe uremia or for those whose hemodynamics is not stable. However, modeling will not be appropriate for patients with hypernatremia or intradialytic hypertension (Palmer, 2001). Finally, preparation of individual HD prescriptions should be remembered in adjusting the Na balance.
