Acute complications during hemodialysis

INTRODUCTION — Patients treated with hemodialysis (HD) may experience acute complications during dialysis. These include cardiac arrhythmias, intradialytic hypotension or hypertension, dialysis disequilibrium syndrome, reactions to the HD membrane, air embolism, bleeding, and seizures. However, some of these acute complications, such as air embolism, hemolysis, vascular access hemorrhage, and major allergic reactions, are now rare due to advances in the safety features on HD machines, meticulous treatment of dialysis water, adherence to strict safety protocols, and extensive training of the dialysis staff.

Compared with these rarer complications, symptoms such as cramps, nausea and vomiting, and headache occur more frequently. These symptoms can be debilitating and can lead to nonadherence or partial adherence to dialysis (shortened treatment sessions or missed sessions), which can be associated with hospitalizations and death. In addition, physical complications of HD can negatively affect health-related quality of life and can exacerbate mood disorders. Understanding and alleviating HD-related symptoms may, therefore, have an immediate impact on patient well-being.

This topic will discuss the epidemiology, causes, brief evaluation, and management of the most common acute complications that occur during HD. Some of these complications are discussed in more detail elsewhere:

●Intradialytic hypotension (see "Intradialytic hypotension in an otherwise stable patient")

●Intradialytic hypertension (see "Hypertension in patients on dialysis", section on 'Hypertension during hemodialysis')

●Dialyzer reactions (see "Reactions to the hemodialysis membrane")

●Seizures during HD (see "Seizures in patients undergoing hemodialysis")

●Dialysis disequilibrium syndrome (see "Dialysis disequilibrium syndrome")

IMPACT OF THE CLINICAL SETTING ON EVALUATION AND MANAGEMENT — In patients on HD who are experiencing an acute complication, the extent of the initial assessment and management depends in part on the location of the patient. This is because of differences in the availability of on-site clinical staff and resources across different levels of care. Typically, freestanding outpatient HD units are usually staffed by nurses and technicians, unlike dialysis units located within hospitals, which have clinicians, in addition to nurses and technicians, on site.

In the outpatient setting, the initial assessment and management are usually communicated by telephone between the clinician (who is remote) and an HD nurse (who is on site). In addition, resources such as electrocardiogram and stat laboratory testing are usually not available. Thus, outpatients with severe symptoms (eg, dyspnea, chest pain, hypotension) that do not promptly respond to corrective interventions should be transported to an emergency department or inpatient setting for evaluation without delay. Patients with less severe symptoms that respond to initial corrective measures (eg, fluid resuscitation) can generally be managed as outpatients.

COMMON COMPLICATIONS

Intradialytic hypotension — Hypotension during HD is discussed at length elsewhere. (See "Intradialytic hypotension in an otherwise stable patient", section on 'Clinical presentation' and "Intradialytic hypotension in an otherwise stable patient", section on 'Acute management' and "Intradialytic hypotension in an otherwise stable patient", section on 'Prevention of recurrent episodes'.)

Intradialytic hypertension — Hypertension during HD is discussed elsewhere. (See "Hypertension in patients on dialysis", section on 'Hypertension during hemodialysis'.)

Chest pain and/or dyspnea — Chest pain and dyspnea are relatively common complications during HD and may result from a variety of causes. The causes of chest pain and dyspnea are overlapping, and therefore these symptoms, when they occur, often coexist.

●Initial management of patients with chest pain – The resources available to evaluate patients with chest pain differ according to whether the patient is receiving dialysis in the outpatient setting (the most common scenario) or in a hospital. Our immediate general approach to acute chest pain occurring during HD is as follows (algorithm 1):

•Turn off the ultrafiltration

•Reduce the blood flow rate to ≤200 mL/min

•Lay the patient flat

•Administer oxygen

•Record vital signs

•Visually inspect the venous line blood for air or foam

•Visually inspect the venous line blood for a port-wine appearance

•Determine if other patients concurrently receiving dialysis in the unit are experiencing similar symptoms

•Obtain a 12-lead electrocardiogram (ECG), if available

•Draw blood from the arterial line; send for electrolytes, troponin levels, and complete blood count (and save extra tubes for additional possible assays)

If the patient is hypotensive:

•Raise their legs or place them in Trendelenburg position and give an intravenous bolus of isotonic fluid (200 to 300 mL).

•If both the hypotension and chest pain resolve, dialysis can be continued (initially without ultrafiltration) and a subsequent chest pain evaluation (eg, cardiology referral, stress testing, echocardiography) should be arranged if not recently performed.

•If the patient has persistent chest pain and/or persistent hypotension, then dialysis should be discontinued and, if in the outpatient setting, the patient should be transferred to a hospital setting (eg, emergency department) for a chest pain evaluation.

In patients with chest pain without hypotension, dialysis should be discontinued and, if in the outpatient setting, the patient should be transferred to a hospital setting (eg, emergency department).

The evaluation and initial management (of cardiac and other causes) are as follows:

•In all cases of chest pain occurring in the outpatient HD setting that do not resolve with cessation of ultrafiltration, a reduction in the blood flow rate, and management of hypotension, arrangements should be made for transportation to a hospital setting (eg, by ambulance).

•In general, aspirin (ie, 81 mg orally) should be administered to patients with suspected cardiac pain. We typically avoid the use of nitrates, especially among hypotensive or hypovolemic patients, in patients undergoing HD because they precipitously reduce venous tone and can induce or exacerbate hypotension. In addition, nitrates should be avoided after dialysis has been discontinued (ie, when the dialysis needles have been removed or the dialysis tubing detached from an HD catheter); in this setting, an episode of hypotension could not be managed quickly. Some experts do use nitrates for suspected cardiac pain in patients without hypotension who still have venous access (since an episode of hypotension could be managed with intravenous saline). Further analgesia can be managed by emergency personnel once they arrive to transfer the patient to the emergency department.

Although angina is usually a manifestation of obstructive coronary artery disease, patients receiving HD may also experience angina in the absence of obstructive coronary artery disease. This may be due to mismatched perfusion from inadequate capillary density in hypertrophied cardiomyocytes that are often present among patients on dialysis. In addition to the physiologic stress of the HD procedure, angina may be provoked by other states with high cardiac output such as anemia, sepsis, and high outflow from an arteriovenous fistula.

•If intravascular hemolysis is suspected (eg, port-wine appearance in the venous blood line, similar symptoms occurring in other patients concurrently receiving dialysis in the same unit, pink color of plasma in centrifuged blood specimen, falling hematocrit) [1,2], then, when discontinuing dialysis, clamp both blood lines and do not return the blood to the patient. Patients with hemolysis require hospitalization for observation since severe anemia and life-threatening hyperkalemia may develop after HD has been terminated.

Hemolysis in patients on HD may result from problems with the dialysis solution, such as overheating, hypotonicity due to a low solute-to-water ratio, or contaminants in the dialysis water (eg, formaldehyde, bleach, chloramine, copper) (table 1). Red blood cell trauma and hemolysis can also occur due to improperly functioning roller clamps on dialysis machines, kinking of the blood lines, and poorly constructed blood tubing [1,3,4].

•If air embolism is suspected (eg, neurologic symptoms such as altered mentation, seizures, focal neurologic deficits, or if air or foam is visible in the venous blood line), then, when discontinuing dialysis, clamp the venous blood line, provide 100 percent oxygen by face mask, assure that the patient is lying on their left side with their feet up (eg, Trendelenburg), provide cardiorespiratory support, and consult emergency personnel for potential airway management. (See "Air embolism".)

Among patients who are recumbent, the air generally travels to the right side of the heart and then into the pulmonary circulation. Symptoms can include chest tightness or pain, dyspnea, cough, tachycardia, hypotension, and syncope. Among patients who are seated, air may enter directly into the cerebral circulation and cause seizures, blurry vision, altered mental status, or ischemic stroke.

Air can inadvertently enter the HD circuit from an uncapped or damaged central venous catheter, from various connection points in the circuit, or from incomplete priming of the circuit (figure 1) [5]. The introduction of air traps and detector alarms in modern HD machines has greatly reduced the risk of significant air accumulation and embolism, and now this is a rare complication [6-8]. The risk of air embolism can be minimized by keeping the arterial luer lock tightened, adequately priming the HD circuit and tubing system before initiation of HD, and maintaining a high blood level in the venous air catcher (figure 1) [5].

●Initial management of patients with dyspnea – Patients with dyspnea during dialysis may also have chest pain. In such patients, the immediate management is the same as in patients with chest pain mentioned above (algorithm 1).

The management of those patients presenting only with dyspnea depends upon whether or not they had dyspnea prior to the start of the HD treatment or if dyspnea onset occurred after the initiation of HD:

•Dyspnea prior to initiation of HD – Patients who report dyspnea prior to initiation of HD most likely have hypervolemia. In such cases, ultrafiltration during the HD procedure will often lead to resolution of symptoms. If the patient also has hypoxemia, supplemental oxygen should be provided.

If the dyspneic patient did not have an unusually large interdialytic weight gain or reports dyspnea when presenting for HD, then their dry weight should be challenged (eg, by approximately 0.5 kg).

If a patient receiving outpatient HD has persistent dyspnea despite adequate ultrafiltration, they should be transferred to a higher level of care (eg, emergency department) for further evaluation. However, if the patient is hemodynamically stable and not hypoxemic, then transfer to the emergency department or hospital can often be delayed until after completion of the HD treatment.

•Acute dyspnea beginning after the initiation of HD – Patients who have acute onset of dyspnea occurring after initiation of HD may have angina, acute coronary syndrome, or bacteremia (often associated with catheter infection). Isotonic saline is frequently administered at the onset of HD and, even with small volumes, may precipitate dyspnea. Uncommon causes include acute severe hypertension, pericardial effusion with or without tamponade, pulmonary embolism (particularly in a patient who recently underwent treatment of a thrombosed vascular access) and, rarely, intravascular hemolysis, an air embolism, or an allergic reaction to intravenous iron or heparin [9-12].

Patients with hypoxia should be administered supplemental oxygen. If acute severe hypertension is suspected to be the cause of acute dyspnea, then the patient should be treated with additional ultrafiltration. (See "Hypertension in patients on dialysis", section on 'Assessment of volume status' and "Hypertension in patients on dialysis", section on 'How to reduce target dry weight'.)

If the dyspnea occurs at the onset of HD, just after administration of isotonic saline, then hypervolemia is the likely cause, and the dyspnea should improve with ultrafiltration. As with patients who present repeatedly with hypervolemia and dyspnea, the dry weight should be challenged.

In outpatients with acute onset of dyspnea who have unstable vital signs or hypoxemia, or if there is concern for a life-threatening cause, dialysis should be stopped, and arrangements should be made for transportation to a hospital setting (eg, by ambulance). In hemodynamically stable patients without hypoxemia, the dialysis treatment can often be continued.

The management of patients with suspected intravascular hemolysis or air embolism is described above (algorithm 1). The management of suspected allergic reactions to intravenous iron or heparin is presented elsewhere. (See "Treatment of iron deficiency anemia in adults", section on 'Treatment or allergic and infusion reactions' and "Heparin and LMW heparin: Dosing and adverse effects", section on 'Systemic allergic reactions'.)

Dialyzer reactions — There are two types of reactions to the dialysis membrane: type A and type B; the clinical presentations of these reactions are variable. Both are rare. As an example, type A reactions (the more severe type) occur in approximately 0.004 percent of HD treatments [13]. Dialyzer reactions are presented in detail separately. (See "Reactions to the hemodialysis membrane".)

Cramps — A muscle cramp is a prolonged involuntary muscle contraction [14]. The origin of a cramp is neural, not muscular [14]. Muscle cramps are a common complication of HD treatments [15-19] and are among the top three physical symptoms prioritized by patients as needing attention [18]. Muscle cramps often result in the early termination of an HD session and are, therefore, a significant cause of inadequate dialysis and hypervolemia. The exact etiology of cramps in patients on dialysis is unknown. Since cramps tend to occur most frequently near the end of HD treatments, changes in plasma osmolality and/or extracellular fluid volume have been implicated.

Some etiologies of HD-associated cramps, alone or in combination, may include [14,15,20]:

●Change in plasma osmolality

●Plasma volume contraction

●Tissue hypoxia

●Hypomagnesemia, hypokalemia, and electrolyte shifts

Of these, volume contraction and electrolyte shifts, either alone or in combination, are most commonly implicated; however, supporting data are sparse, and these explanations may be oversimplified.

Cramps occurring with dialysis treatment most commonly involve the muscles of the lower extremity, but the muscles of the hands, arms, and abdomen may also be affected. The modality of HD (eg, high-flux HD, hemodiafiltration) may also have an impact on the frequency of cramps [21].

Treatment is directed at two goals: reducing the frequency of cramps and relieving symptoms when they occur. Interventions that may be attempted to reduce the frequency of cramps include:

●Slowing the rate of ultrafiltration – The rate of ultrafiltration should be slowed to as low as possible without leaving the patient hypervolemic. This can be achieved by:

•Counseling patients to avoid excess interdialytic weight gains (eg, by restricting dietary sodium and fluid intake) and to remain adherent to dialysis  

•Extending the dialysis treatment duration while maintaining the same ultrafiltration goal for the session

•Achieving the ultrafiltration goal over additional dialysis sessions rather than in a single session (ie, adding an additional session)

•Allowing the dry weight to be higher

●Sodium modeling – Sodium modeling may be helpful in young patients with no known cardiovascular disease. In one study of 16 young patients on HD [22], compared with a dialysis using a fixed sodium of 138 mEq/L, sodium modeling with a gradual reduction in sodium from 148 mEq/L to 138 mEq/L reduced the frequency of dialytic cramps. However, many sodium modeling approaches can result in a net positive sodium balance placing patients at risk for volume expansion and hypertension over time. Thus, although sodium modeling is a useful technique in some cases (eg, to prevent dialysis disequilibrium), some experts avoid sodium modeling specifically to manage cramps. (See "Dialysis disequilibrium syndrome".)

●Raising plasma osmolality – Raising the plasma osmolality with hypertonic saline, dextrose, or mannitol at the beginning of the HD session may help reduce the frequency of cramps. In one trial of 20 patients, compared with injection of 5 percent dextrose, injection of hypertonic saline or 50 percent dextrose were equally effective in relieving cramps [23]. Mannitol infusion, given at a dose of 12.5 to 37.5 g/dialysis, is also effective in the management of dialysis-associated cramps [15]. However, mannitol may accumulate in the extracellular space, particularly when administered near the end of an HD session.

Some of our contributors use sodium modeling to raise plasma osmolality, and some have used hypertonic saline or mannitol.

●Switching dialysis modality – In a patient who is incapacitated by cramps, switching dialysis modalities to nocturnal HD, peritoneal dialysis, or home HD can be used when other approaches are infeasible or have failed.

●Other methods – A variety of additional medications (eg, gabapentin, amitriptyline, vitamin E, vitamin C) have been used to prevent dialysis-associated cramps. They are of variable efficacy and have rarely been tested in controlled trials in patients on dialysis. Leg massage of the affected muscle and/or application of warm compresses during HD may also be beneficial [24,25]. Exercise, such as intradialytic cycling or walking after dialysis for 20 minutes, and performing stretching exercises can also be beneficial for cramping on dialysis that may have been exacerbated by muscle fatigue.

Syncope — Syncope during HD may occur in the setting of severe hypotension, arrhythmia, myocardial infarction, or stroke. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

If a patient has syncope during HD, the following approach is appropriate:

●Turn off the ultrafiltration

●Raise their legs

●Administer oxygen

●Obtain vital signs

●If hypotensive, administer an intravenous bolus of isotonic fluid (200 to 300 mL)

●Obtain a 12-lead ECG, if available

●Draw blood from the arterial line; send for electrolytes, troponin levels, and complete blood count

●Refer for syncope evaluation

Outpatients who have syncope during HD should be transferred to a higher level of care.

Seizures — Seizures during HD are uncommon. They are typically generalized (rather than focal).

The causes, evaluation, and management of seizures in patients undergoing HD are presented in detail elsewhere:

●(See "Seizures in patients undergoing hemodialysis", section on 'Causes'.)

●(See "Seizures in patients undergoing hemodialysis", section on 'Evaluation'.)

●(See "Seizures in patients undergoing hemodialysis", section on 'Immediate management of seizures'.)

●(See "Seizures in patients undergoing hemodialysis", section on 'Maintenance antiseizure therapy'.)

Headache, nausea, and vomiting — Headache, nausea, and vomiting are nonspecific symptoms commonly experienced by patients during HD [17,19,26-30].

These symptoms may occasionally occur in the setting of a severe underlying disorder (eg, cardiac or pulmonary disease, hypotension, accelerated/severe hypertension [31], infection). Prompt treatment is typically required. (See 'Chest pain and/or dyspnea' above and 'Intradialytic hypotension' above and 'Intradialytic hypertension' above and 'Fever' below.)

However, if there are no concerning features that would indicate discontinuation of the dialysis treatment, then dialysis is continued and analgesics and/or antiemetics are given (most outpatient dialysis clinics stock acetaminophen and promethazine).

Other causes of headache, nausea, and vomiting in patients on HD include metabolic disturbances (eg, hypoglycemia, hyponatremia, hypernatremia), common headache syndromes (eg, migraine headache, tension headache), or psychologic factors [32,33]. They may also be caused by various dialysis-related factors (eg, caffeine withdrawal due to dialytic removal) [30,34-37]. These potential etiologies should be evaluated and managed appropriately.

Apart from these more common causes, there is a specific syndrome of dialysis-associated headache that is characterized by a bifrontal or temporal headache starting after initiation of dialysis, worsening over the duration of the treatment, with resolution over 72 hours. This may be due to dialysis-associated changes in vasoactive substances such as nitric oxide [34,38,39]. In patients with recurrent and severe dialysis-associated headache, some experts perform a trial of reduced HD duration in an attempt to alleviate symptom burden combined with an increase in dialysis frequency to maintain adequate dialysis [40].

In one study, for example, the rate of symptom occurrence was lower when patients received HD for two hours at a blood flow rate of 400 mL/min compared with four hours at 200 mL/min (19 versus 32 percent) [37]. Similarly, in the Frequent Hemodialysis Network trial, patients randomly assigned to more frequent but shorter duration of dialysis had a lower physical burden of symptoms compared with those assigned to conventional dialysis, despite a higher weekly solute clearance and longer total weekly dialysis time in the frequent dialysis group.  

The relationship between longer dialysis sessions, higher solute removal per session, and intradialytic symptoms suggests that dialysis disequilibrium syndrome may underlie the symptoms in some of these patients. Details regarding dialysis disequilibrium syndrome are presented separately. (See "Dialysis disequilibrium syndrome", section on 'Pathogenesis' and "Dialysis disequilibrium syndrome", section on 'Clinical manifestations'.)

Fever — Patients receiving HD are at high risk for infection. A fever that develops during HD (ie, after initiation of the treatment) should raise suspicion for a vascular access infection. The evaluation of such patients is presented elsewhere. (See "Tunneled hemodialysis catheter-related bloodstream infection (CRBSI): Epidemiology, pathogenesis, clinical manifestations, and diagnosis" and "Arteriovenous fistula creation for hemodialysis and its complications", section on 'Infection' and "Arteriovenous graft creation for hemodialysis and its complications", section on 'Graft infection'.)

Febrile patients on HD may also require evaluation for other sources of infection, depending upon the clinical presentation. (See "Non-access-related infections in patients on chronic dialysis".)

Nonfunctioning hemodialysis access — Complications related to dialysis access occur frequently and include both arteriovenous access (fistula or graft) and catheter dysfunction.

●Inability to use the arteriovenous access – In cases where access dysfunction prevents HD treatment, patients may require temporary vascular access (with a catheter) to correct metabolic disarray or hypervolemia. An interventional radiologist, interventional nephrologist, or a surgeon should be contacted promptly to formulate a plan to address the nonfunctioning arteriovenous access.

If the patient's electrolytes and acid-base status are known, and if these and the volume status are in an acceptable range, then it may be possible to delay HD until definitive treatment of the access is performed. This decision is based upon clinical judgement and depends in large part on the clinician's knowledge of the patient (eg, their typical interdialytic weight gain or their typical interdialytic potassium increase). Often, the patient will need dialysis within one to two days. If the delay to definitive treatment is too long, then the interventionalist, surgeon, or nephrologist should plan to establish temporary vascular access with a catheter.

Conversely, if the patient has a significant electrolyte or volume disturbance, or if the electrolyte and acid-base status is unknown, then a catheter should be placed (and HD performed that same day). This typically requires hospitalization.

Arteriovenous fistula and graft dysfunction are presented in detail elsewhere. (See "Arteriovenous fistula creation for hemodialysis and its complications", section on 'Complications of AV fistula placement' and "Arteriovenous graft creation for hemodialysis and its complications", section on 'Complications of AV graft placement'.)

●Inability to use the hemodialysis catheter – HD catheters may provide no blood flow, intermittent flow, or a blood flow rate insufficient to conduct adequate dialysis without significantly lengthening the treatment.

Early dysfunction (ie, when the catheter could never be successfully used after its placement) results from technical issues during the catheter placement procedure or catheter malposition. A replacement catheter is typically required.

Late dysfunction (ie, when a previously functioning catheter can no longer be used to provide adequate dialysis) is typically due to intrinsic thrombus (ie, intraluminal, tip, or fibrin sheath) or extrinsic thrombus (ie, extending beyond the catheter tip into the vessel).

Evaluation of late dysfunction often involves Doppler ultrasound imaging of the vessel. Intrinsic thrombus is frequently treated with forceful saline flushes, guidewire catheter exchange, or catheter replacement.

Details of the evaluation and management of catheter dysfunction are presented separately. (See "Malfunction of chronic hemodialysis catheters".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Hemodialysis (The Basics)")

●Beyond the Basics topic (see "Patient education: Hemodialysis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Overview – In patients on HD who are experiencing an acute complication, the extent of the initial assessment and management depends in part on the location of the patient. In the outpatient setting, the initial assessment and management are usually communicated by telephone between the clinician (who is remote) and an HD nurse (who is on site). In addition, resources such as electrocardiogram and stat laboratory testing are usually not available. Thus, outpatients with severe symptoms (eg, dyspnea, chest pain, hypotension) that do not promptly respond to corrective interventions should be transported to an emergency department or inpatient setting for evaluation without delay. Patients with less severe symptoms that respond to initial corrective measures (eg, fluid resuscitation) can generally be managed as outpatients. (See 'Impact of the clinical setting on evaluation and management' above.)

●Common complications – Common complications occurring during HD include the following:

•Intradialytic hypotension – Hypotension during HD is discussed in another topic. (See "Intradialytic hypotension in an otherwise stable patient".)

•Intradialytic hypertension – Hypertension during HD is discussed in another topic. (See "Hypertension in patients on dialysis", section on 'Hypertension during hemodialysis'.)

•Chest pain – Our immediate general approach to acute chest pain occurring during HD is presented in the algorithm (algorithm 1). (See 'Chest pain and/or dyspnea' above.)

•Dyspnea – The causes of dyspnea and chest pain are overlapping, and therefore these symptoms, when they occur, often coexist. If the patient also has chest pain, the initial approach is presented in the algorithm (algorithm 1). (See 'Chest pain and/or dyspnea' above.)

The management of those patients presenting only with dyspnea (and not concurrent chest pain) depends upon whether or not they had dyspnea prior to the start of the HD treatment or if dyspnea onset occurred after the initiation of HD.

-Patients who report dyspnea prior to initiation of HD most likely have hypervolemia and are treated with ultrafiltration.

-If a patient receiving outpatient HD has persistent dyspnea despite adequate ultrafiltration, or if they develop acute dyspnea after the start of the HD procedure, then the management depends in part on whether or not they are hemodynamically stable or hypoxemic. If there are unstable vital signs or hypoxemia, or if there is concern for a life-threatening cause, dialysis should be stopped and arrangements should be made for transportation to a hospital setting (eg, by ambulance). In hemodynamically stable patients without hypoxemia, the dialysis treatment can often be completed; further ultrafiltration may alleviate the symptoms.

•Dialyzer reactions – There are two types of reactions to the dialysis membrane: type A and type B. Both are rare. Dialyzer reactions are discussed in another topic. (See 'Dialyzer reactions' above.)

•Cramps – Muscle cramps often result in the early termination of an HD session and are, therefore, a significant cause of inadequate dialysis and hypervolemia. The exact etiology of cramps in patients on dialysis is unknown. Treatment is directed at two goals: reducing the frequency of cramps and relieving symptoms when they occur. Interventions that may be attempted to reduce the frequency of cramps include (see 'Cramps' above):

-Slowing the rate of ultrafiltration (while maintaining adequate ultrafiltration by extending the length of treatments or adding additional treatments)

-Sodium modeling or raising the plasma osmolality by other means

-Switching dialysis modality (eg, to nocturnal HD, peritoneal dialysis, or home HD)

•Syncope – Syncope during HD may occur in the setting of severe hypotension, arrhythmia, myocardial infarction, or stroke. In addition to immediate measures to take in the HD unit (eg, discontinuing ultrafiltration, raising the legs, administering isotonic fluid if hypotensive, and administering oxygen), outpatients who have syncope during HD should be transferred to a higher level of care. (See 'Syncope' above.)

•Seizures – Seizures during HD are discussed in another topic. (See "Seizures in patients undergoing hemodialysis".)

•Headache, nausea, vomiting – Headache, nausea, and vomiting are nonspecific symptoms commonly experienced by patients during HD. If they occur in the setting of a severe underlying disorder (eg, cardiac or pulmonary disease, hypotension, accelerated/severe hypertension, infection), prompt treatment is typically required. (See 'Headache, nausea, and vomiting' above.)

However, if there are no concerning features that would indicate discontinuation of the dialysis treatment, then dialysis is continued and analgesics and/or antiemetics are given.

•Fever – A fever that develops during HD (ie, after initiation of the treatment) should raise suspicion for a vascular access infection. The evaluation and management of such patients are presented elsewhere. (See 'Fever' above.)

•Nonfunctioning hemodialysis access – Complications related to dialysis access occur frequently and include both arteriovenous access (fistula or graft) and catheter dysfunction. The causes and evaluation of such patients depend upon the type and age of the access. However, in the acute setting, patients may require temporary vascular access (with a catheter) to correct metabolic disarray or hypervolemia. If so, this typically requires hospitalization. (See 'Nonfunctioning hemodialysis access' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jean Holley, MD, FACP, who contributed to earlier versions of this topic review.