**3.6 Myocardiac infarction**

An increase is observed in the prevalence of coronary incidences in patients with end-stage renal failure and in mortality following a myocardial infarction (MI) (Herzog et al., 1998; Winkelmayer et al., 2006). A cardiac-related death is seen 10 to 20 times as much in this patient group as compared to the normal population (Foley et al., 1998).

We come across pericarditis in hemodialysis patients in two ways. The first is in the form of a uremic pericarditis. This type of pericarditis can be seen before starting the dialysis or in the first 8 weeks of dialysis. It is usually associated with uremia. The other type of pericarditis is a dialysis-related pericarditis that can be seen any time after the patient starts the dialysis. Although its definite cause is not known, insufficient dialysis and excess volume are the most blamed factors in pathogenesis (Rostand&Rutsky,1990; Rutsky& Rostand, 1987). Prevalence of pericarditis in dialysis patients is reported to be between 2 and

They can be clinically present as complaints such as a nonspecific chest pain, muscle weakness and coughing, but they can also come in as a hypotension and heart failure. A reduction of heart sounds and pericardial rubbing, and in serious cases, hypotension can be observed depending on the intensity of effusion during a physical examination. Classical ECG changes may not appear in uremic pericarditis. A final diagnosis is made using an

The treatment depends on the symptoms and the diameter of the effusion. A small scale asymptomatic effusion does not usually necessitate taking urgent measures. Those having a large amount of pericardial fluid may need to undergo an urgent drainage by way of pericardiotomy if it is hemodynamically unstable or an intensive hemodialysis therapy for 7 to 14 days and avoidance of heparinization during hemodialysis if it is hemodynamically stable. Glucocorticoid and non-steroidal anti-inflammatory drugs are usually ineffective (Banerjee& Davenport,2006; Shastri &Sarnak,2010). In uremic pericarditis, a response can be obtained from an intensive hemodialysis therapy in >85% (76-100%) of the patients and in dialysis-related pericarditis, in <60% (12.5-66%) of the patients (Alpert & Ravenscraft,2003).

Sudden cardiac death is held responsible for 62% of the cardiac-related deaths and is usually attributed to arrs (Herzog et al.,2008). The first year of hemodialysis is significant in terms of sudden cardiac deaths and a sudden death was reported in 93 of 1000 patients in the first

Ischemic heart diseases, cardiomyopathy, fast ion change and electrolyte during hemodialysis, changes in PH, microvascular diseases or endothelial dysfunction are blamed

It is the same as in the normal population. It is advisable that an external defibrillator is made available in hemodialysis units and the staff is trained in using it (K/DOQI Workgroup, 2005). There is not adequate data on the use of B blockers (Pun et al.,2007) and

An increase is observed in the prevalence of coronary incidences in patients with end-stage renal failure and in mortality following a myocardial infarction (MI) (Herzog et al., 1998; Winkelmayer et al., 2006). A cardiac-related death is seen 10 to 20 times as much in this

patient group as compared to the normal population (Foley et al., 1998).

**3.4 Pericarditis** 

21% (Lange& Hillis,2004; Banerjee& Davenport,2006).

ECHO (Shastri &Sarnak,2010).

**3.5 Sudden cardiac death** 

year (Shastri &Sarnak,2010).

**3.6 Myocardiac infarction** 

**Treatment** 

in its pathogenesis (Shastri &Sarnak,2010).

internal defibrillators (de Bie et al.,2009).

**Treatment** 

Acute MI is diagnosed in the normal population at the presence of a high cardiac enzyme level, classical chest pain and ECG changes. However, there are some differences in MI presentation and laboratory findings of hemodialysis patient group. This situation causes a delay in diagnosing MI in this group and thus a less frequent use of the thrombolytic and early coronary angiography/coronary stent applications for treatment of MI as compared to the normal population.

For example, MI-associated classical chest pain is seen less in patients with renal failure in correlation with the intensity of such renal failure. The cause of this is thought to be the impairment of sensory and autonomic nerve functions seen in patients with renal failure. It was demonstrated in a study made by Komukai et al that as the renal function disorders increased, the prevalence of painless MI also increased (Komukai et al., 2007). In another study conducted by Pitsavos C et al, it was shown that MI patients with renal failure admitted to the hospital late and the possible reason for such late admission was thought to be the less occurence of alerting symptoms such as chest pain in this patient group (Pitsavos et al., 2007). Late admissions certainly mean that coronary interventions are less and mortality is more.

Cardiac troponin T (cTnT) and creatine kinase-MB, which are two of the enzymes used in the verification of a myocardial infarction diagnosis, were seen in high levels in the hemodialysis patient group without the presence of coronary ischemia. cTnT in particular was shown to be as high as 17 to 23.8% in this patient group (Chew, 2008). This situation leads to controversies in diagnosing MI in the hemodialysis patient group. Researches are still in progress to find an ideal marker that supports an MI diagnosis. For the time being, it is advisable to monitor the cardiac enzyme levels in patients clinically suspected of having an MI.

Another point to take into consideration is that 15 to 40% of the patients are seen to have ST depression during hemodialysis (Abe et al., 1996; Conlon et al., 1998). Dialysis therapy itself may cause subclinical myocardial ischemia in this patient group which is prone to atherosclerosis and left ventricular hypertrophy (Selby& McIntyre, 2007).

There is not sufficient data about the reliability of conducting a dialysis within 48 hours after a myocardial infarction (MI). In such a case, the volume status of the patient should be assessed together with its biochemical parameters and the hemodialysis therapy should be adjusted in a way to avoid hypotension (Coritsidis et al., 2009). The treatment of acute MI is recommended to be the same as in the normal population (K/DOQI Workgroup, 2005).

#### **4. Neurologic complications**

Neurologic complications may develop in the patients of end-stage renal failure due to a multiple metabolic disorder caused by a chronic kidney disease and due to the dialysis procedure. These complications may appear in the form of variations in consciousness, headache, nausea, vomiting, myoclonus, tremor, focal and generalized seizures, cerebrovascular events (infarct and bleeding) and disequilibrium syndrome.

#### **4.1 Disequilibrium syndrome**

Dialysis Disequilibrium syndrome (DDS) was first defined by Kennedy AC (Kennedy ,1970, Chen et al.,2007). Although the pathogenesis of DDS is controversial, the first theory blamed in etiology is the fast urea removal theory. According to this theory, the fast removal of urea from plasma in patients who newly started a hemodialysis therapy creates an osmotic gradient between the brain cells and plasma and the fluid enters the brain cells due to this osmotic gradient (Kennedy,1970; Attur et al.,2008; Chen et al.,2007; Trinh-Trang-Tanet

Acute Complications of Hemodialysis 273

After making sure that there is no migraine, cerebrovascular event or intracranial mass, the first step in treatment is to investigate if there is a hemodialysis headache. If a hemodialysis headache is suspected, the factors that are thought to trigger the headache should be reviewed and the necessary electrolyte replacements or a modification in the treatment

A cerebrovascular event constitutes the 3rd most common cause of death in the normal population. Patients with chronic kidney failure have an increased rate of cerebrovascular event risk as compared to the normal population (K/DOQI Workgroup, 2005). Although there is not any clear information on its prevalence, a study made in Japan revealed that cerebrovascular events were seen at a rate of 8% and cerebral hemorrhage was seen more frequently (Kawamura et al.,1998). According to the American data, the rates of hemorrhagic stroke and ischemic stroke were found equal, which were 5 to 10 times more than those seen in the normal population (Selinger et al.,2003). It was found in another study made in 2009 that ischemic stroke was seen more frequently (Sozio et al.,2009). There are just a few studies make on the etiologic risk factors of cerebrovascular event. Hypertension was defined as a risk factor in a study conducted in Japan (Iseki&Fukiyama,1996). In a study made by Selinger SL et al, the risk factors for cerebrovascular event were determined to be hypertension, low hemoglobin level and indicators of malnutrition (low weight, low level of albumin) (Selinger et al.,2003). The frequency of carotid artery atherosclerosis increased in patients with end-stage renal failure. This in turn may increase the rate of ischemic strokes. Hypertension, routine heparin use during dialysis therapy and tendency to bleeding diathesis in this patient group may

Since subclinical vascular disease is common in the dialysis population, ultrasonographic measurement of carotid artery elasticity during screening may be helpful (Pascazio et al.,1996). Likewise, since an increase in the thickness of carotid intima media is attributed to the increase in cardiovascular events, this can also be used during screening (Benedetto et al.,2001). Screening is not recommended in asymptomatic patients (K/DOQI Workgroup,2005). Screening of patients for cerebrovascular event is the same as recommended for the normal population. It only differs from the normal population in that it should be remembered to educate the patients who are planned to be given a heparinisation or thrombolytic therapy about the increased bleeding diathesis. Differentiation between the hemorrhagic and ischemic stroke should also be made before initiating the hemodialysis therapy (because heparinisation will be wrong in hemorrhagic

Heparin is frequently used as an anticoagulant in hemodialysis therapy due to its low cost and short half life, but a heparin-induced thrombocytopenia (HIT) is a situation restricting the use of heparin and resulting in a significant amount of mortality. HIT is classified as

result in an increase in hemorrhagic strokes (Selinger et al.,2003).

**5. Complications associated with use of anticoagulant therapy** 

**Treatment** 

modality should be made.

**4.3 Cerebrovascular event** 

**Screening and treatment** 

stroke) (K/DOQI Workgroup).

Type-I and Type-II.

**5.1 Heparin-induced thrombocytopenia** 

al.,2005). Another theory is the idiogenic osmole effect. According to this theory, the diffusion of bicarbonate from the dialysate to plasma increases PH. Bicarbonate transforms into carbon dioxide (CO2) outside the cell. Blood with CO2 penetrates the brain barrier and enters the brain cells, causing an intracellular acidosis. This event then causes the cell proteins to break down to form idiogenic osmoles. An increase of idiogenic osmoles in the cell in turn results in an osmotic gradient and eventually causes the fluid to enter the cell (Arieff et al.,1976). DDS usually develops as a result of fast reduction of urea in patients with severe uremia. Risk factors include young age, a history of head trauma or cerebrovascular event, and an electrolyte imbalance such as a malign hypertension and hyponatremia (Trinh-Trang-Tanet al.,2005; Patel et al.,2008).

DDS is a diagnosis of exclusion, because its clinical signs resemble other neurologic complications. DDS is an acute neurologic complication of dialysis. It generally starts towards the end of dialysis or after it ends. Its symptoms and signs can be fatigue, slight headache, HT, nausea, vomiting, blurred vision, and muscle cramps, and it can cause arrhythmia, confusion, tremor, seizure, and coma. DDS may rarely result in death due to a brain edema (Patel et al.,2008).

To prevent a Dialysis Disequilibrium syndrome, the initial dialysis session may be performed using a slow flow and in a shorter time, sodium level may be raised in the dailysate and osmotic active compounds may be administrated. In a slow-flow shortened dialysis, it may be useful to limit the time to 2 hours and the blood flow rate to 200 ml/min and to use a dialyzer with a small surface area (Levin&Goldstein,1996; Sang et al.,1997). The target rate of urea reduction may be 0.4 to 0.45 for the first session. There are studies showing that adding urea to the dialysate is useful in preventing DDS (Hampl et al.,1983, Patel et al.,2008, Levin&Goldstein,1996; Sang et al.,1997). The aim in raising the level of Na in the dialysate is to reduce the osmolarity difference resulting from a fast urea removal by an increase in plasma Na. Na profile applications and use of fixed high-Na dialysate can be attempted in this respect, but they are not evidenced to be effective. Therefore, use of dialysate containing 143-146 mmmol/L is recommended in patients under DDS risk (Patel et al.,2008; Levin&Goldstein,1996, Sang et al.,1997). Administration of osmotic active compounds follows the same logic. Various studies showed that osmolarity change and DDS were reduced by administering a dialysate with high glucose content and 1 gr/kg mannitol (Rodrigo et al.,1977; Rosa et al.,1981).

### **4.2 Headache**

The International Headache Society (ICHD, 2004) included the hemodialysis headache in the headache classification. To be able to mention a hemodialysis headache, the headache should prevail in at least half of the hemodialysis sessions, there should be 3 acute headache attacks meeting at least two criteria and the headache should be relieved within 72 hours after the hemodialysis (Gladstone& Dodick,2004,; Goksel et al.,2006). Although its prevalence is not certain, it was found to be 30% by Goksel et al and 48% by Göksan et al (Goksel et al.,2006; Göksan et al.,2004). Jesus AC et al, on the other hand, found a much lower prevalence of 6.7% in 2009 (Jesus et al.,2009).

Although its physiopathology is not fully clear, the factors triggering headache may be hypertension, hypotension, low level of sodium, decreased serum osmolarity, low level of plasma rennin, pre- and post-dialysis Bun values and low levels of magnesium (Bana et al.,1972; Bana& Graham,1976; Göksan et al.,2004; Goksel et al.,2006).

#### **Treatment**

272 Technical Problems in Patients on Hemodialysis

al.,2005). Another theory is the idiogenic osmole effect. According to this theory, the diffusion of bicarbonate from the dialysate to plasma increases PH. Bicarbonate transforms into carbon dioxide (CO2) outside the cell. Blood with CO2 penetrates the brain barrier and enters the brain cells, causing an intracellular acidosis. This event then causes the cell proteins to break down to form idiogenic osmoles. An increase of idiogenic osmoles in the cell in turn results in an osmotic gradient and eventually causes the fluid to enter the cell (Arieff et al.,1976). DDS usually develops as a result of fast reduction of urea in patients with severe uremia. Risk factors include young age, a history of head trauma or cerebrovascular event, and an electrolyte imbalance such as a malign hypertension and hyponatremia

DDS is a diagnosis of exclusion, because its clinical signs resemble other neurologic complications. DDS is an acute neurologic complication of dialysis. It generally starts towards the end of dialysis or after it ends. Its symptoms and signs can be fatigue, slight headache, HT, nausea, vomiting, blurred vision, and muscle cramps, and it can cause arrhythmia, confusion, tremor, seizure, and coma. DDS may rarely result in death due to a

To prevent a Dialysis Disequilibrium syndrome, the initial dialysis session may be performed using a slow flow and in a shorter time, sodium level may be raised in the dailysate and osmotic active compounds may be administrated. In a slow-flow shortened dialysis, it may be useful to limit the time to 2 hours and the blood flow rate to 200 ml/min and to use a dialyzer with a small surface area (Levin&Goldstein,1996; Sang et al.,1997). The target rate of urea reduction may be 0.4 to 0.45 for the first session. There are studies showing that adding urea to the dialysate is useful in preventing DDS (Hampl et al.,1983, Patel et al.,2008, Levin&Goldstein,1996; Sang et al.,1997). The aim in raising the level of Na in the dialysate is to reduce the osmolarity difference resulting from a fast urea removal by an increase in plasma Na. Na profile applications and use of fixed high-Na dialysate can be attempted in this respect, but they are not evidenced to be effective. Therefore, use of dialysate containing 143-146 mmmol/L is recommended in patients under DDS risk (Patel et al.,2008; Levin&Goldstein,1996, Sang et al.,1997). Administration of osmotic active compounds follows the same logic. Various studies showed that osmolarity change and DDS were reduced by administering a dialysate with high glucose content and 1 gr/kg

The International Headache Society (ICHD, 2004) included the hemodialysis headache in the headache classification. To be able to mention a hemodialysis headache, the headache should prevail in at least half of the hemodialysis sessions, there should be 3 acute headache attacks meeting at least two criteria and the headache should be relieved within 72 hours after the hemodialysis (Gladstone& Dodick,2004,; Goksel et al.,2006). Although its prevalence is not certain, it was found to be 30% by Goksel et al and 48% by Göksan et al (Goksel et al.,2006; Göksan et al.,2004). Jesus AC et al, on the other hand, found a much

Although its physiopathology is not fully clear, the factors triggering headache may be hypertension, hypotension, low level of sodium, decreased serum osmolarity, low level of plasma rennin, pre- and post-dialysis Bun values and low levels of magnesium (Bana et

(Trinh-Trang-Tanet al.,2005; Patel et al.,2008).

mannitol (Rodrigo et al.,1977; Rosa et al.,1981).

lower prevalence of 6.7% in 2009 (Jesus et al.,2009).

al.,1972; Bana& Graham,1976; Göksan et al.,2004; Goksel et al.,2006).

**4.2 Headache** 

brain edema (Patel et al.,2008).

After making sure that there is no migraine, cerebrovascular event or intracranial mass, the first step in treatment is to investigate if there is a hemodialysis headache. If a hemodialysis headache is suspected, the factors that are thought to trigger the headache should be reviewed and the necessary electrolyte replacements or a modification in the treatment modality should be made.

## **4.3 Cerebrovascular event**

A cerebrovascular event constitutes the 3rd most common cause of death in the normal population. Patients with chronic kidney failure have an increased rate of cerebrovascular event risk as compared to the normal population (K/DOQI Workgroup, 2005). Although there is not any clear information on its prevalence, a study made in Japan revealed that cerebrovascular events were seen at a rate of 8% and cerebral hemorrhage was seen more frequently (Kawamura et al.,1998). According to the American data, the rates of hemorrhagic stroke and ischemic stroke were found equal, which were 5 to 10 times more than those seen in the normal population (Selinger et al.,2003). It was found in another study made in 2009 that ischemic stroke was seen more frequently (Sozio et al.,2009). There are just a few studies make on the etiologic risk factors of cerebrovascular event. Hypertension was defined as a risk factor in a study conducted in Japan (Iseki&Fukiyama,1996). In a study made by Selinger SL et al, the risk factors for cerebrovascular event were determined to be hypertension, low hemoglobin level and indicators of malnutrition (low weight, low level of albumin) (Selinger et al.,2003). The frequency of carotid artery atherosclerosis increased in patients with end-stage renal failure. This in turn may increase the rate of ischemic strokes. Hypertension, routine heparin use during dialysis therapy and tendency to bleeding diathesis in this patient group may result in an increase in hemorrhagic strokes (Selinger et al.,2003).

#### **Screening and treatment**

Since subclinical vascular disease is common in the dialysis population, ultrasonographic measurement of carotid artery elasticity during screening may be helpful (Pascazio et al.,1996). Likewise, since an increase in the thickness of carotid intima media is attributed to the increase in cardiovascular events, this can also be used during screening (Benedetto et al.,2001). Screening is not recommended in asymptomatic patients (K/DOQI Workgroup,2005). Screening of patients for cerebrovascular event is the same as recommended for the normal population. It only differs from the normal population in that it should be remembered to educate the patients who are planned to be given a heparinisation or thrombolytic therapy about the increased bleeding diathesis. Differentiation between the hemorrhagic and ischemic stroke should also be made before initiating the hemodialysis therapy (because heparinisation will be wrong in hemorrhagic stroke) (K/DOQI Workgroup).
