Acute Complication of Acute Complication of HemodialysisHemodialysis

Dr.Alaa Mohammed Fouad MousliSurgical Demonstrator

ObjectiveObjectiveIn this presentation we will review

briefly the causes, diagnosis and treatment of the common acute complications that we face during hemodyalysis.

Acute complication Acute complication HHCCBNFHHCCBNF

Hypotension — 25 to 55 %Cramps — 5 to 20 % Nausea and vomiting — 5 to 15 % Headache — 5%Chest pain — 2 to 5 %Back pain — 2 to 5 %Itching — 5 %Fever and chills — Less than 1 %

Hypotension Hypotension Usual manifestation of

hemodynamic instability during ultrafiltration dialysis (in which fluid removal is the primary goal)

Why is it important?Whatever the underlying cause,

patients with hemodialysis-associated hypotension appear to have increased mortality.

Clinical PatternsClinical PatternsThere are TWO clinical patterns of

dialysis-associated hypotension:

Episodic hypotension, which typically occurs during the latter stages of dialysis; this is associated with vomiting, muscle cramps, and other vagal symptoms (such as yawning).

Clinical Patterns – Con’tClinical Patterns – Con’t

Chronic persistent hypotensionin long-term patients with predialysis systolic blood pressures of less than 100 mmHg.

EtiologyEtiologyRapid reduction in plasma osmolality,

which causes extracellular water to move into the cells .

Rapid fluid removal in an attempt to attain "dry weight"

Inaccurate determination of true "dry weight".

Autonomic neuropathy (the role of baroreceptors and a subsequent increase in efferent sympathetic activity).

Diminished cardiac reserve.

Use of acetate rather than bicarbonate as a dialysate buffer. (Acetate accumulation in the blood has vasodilator activity).

Intake of antihypertensive medications that can impair cardiovascular stability.

Use of a lower sodium concentration in the dialysate

Arrhythmias or pericardial effusion with tamponade, which are volume-unresponsive causes of hypotension.

Reactions to the dialyzer membrane, which may cause wheezing and dyspnea as well as hypotension.

Increased synthesis of endogenous vasodilators, such as nitric oxide.

Sudden release of adenosine during organ ischemia

High magnesium concentrations in the dialysate.

Failure to increase plasma vasopressin levels.

Keep it in MindKeep it in Mind

Plasma osmolality.True dry wight.Autonomic Neuropathy.Acetate & Nitric Oxide.Na & Mg.Cardiac Diseases.

Be patient in your management

DIAGNOSIS AND DIAGNOSIS AND TREATMENTTREATMENTAlthough occasionally

asymptomatic, patients with hypotension may suffer from :◦light-headedness. ◦muscle cramps. ◦Nausea & vomiting.◦dyspnea.

The acute management of low blood pressure associated with hemodialysis includes the following:

Ultrafiltration should either be stopped or the rate decreased.

The patient should be placed in the Trendelenburg position.

The blood flow rate should be reduced.

Intravascular volume may be replaced with mannitol or saline. Currently the use of an intravenous bolus of saline is the first-line therapy for hypotension.

PREVENTIONPREVENTIONAccurate setting of the "dry

weight"Steady, constant ultrafiltration Increased dialysate sodium

concentration and sodium modeling 

Bicarbonate dialysate buffer Temperature control 

Prevention – Con’tPrevention – Con’tImprovement in cardiovascular

performance in cardiac patients.Midodrine (the selective alpha-1

adrenergic agonist) in patients with autonomic neuropathy and perhaps others with severe hemodialysis hypotension not responsive to the above measures.

Carnitine .Avoidance of food.Adenosine receptor antagonist. Vasopressin infusion. 

Muscle CrampsMuscle CrampsA cramp is a prolonged involuntary muscle

contractioncommon complication of hemodialysis

treatments and mostly involves the muscle of the lower extremities in old non diabetic anxious patient resulting in early termination of a hemodialysis session.

Usually occur near the end of hemodialysis treatments.

Low PTH Values and high serum Creatin phosphokinase is frequent finding

EtiologyEtiologyPlasma volume contraction.Tissue hypoxiaHyponatremia.Hypomagnesemia.Carnitine deficiency.

Treatment.Treatment.

Treatment is directed at two goals:◦Reducing the frequency of cramps.◦Relieving symptoms when they

occur.

Interventions to reduce the Interventions to reduce the frequency of crampsfrequency of cramps

◦Prevention of dialysis-associated hypotension.

◦The use of high concentrations of sodium in the dialysate.

◦Carnitine supplementation◦Administration of quinine that decrease the

excitability of the motor end-plate to nerve stimulation and increase muscle refractory period, thereby preventing prolonged involuntary muscle contraction.

All these may reduce the frequency of dialysis-associated cramps.

Minimize inter-dialytic weight Minimize inter-dialytic weight gains gains 

◦will avoid plasma volume contraction and hypo-osmolality that occurs with high rates of ultrafiltration required to achieve the patient's dry weight during a brief dialysis session.

OthersOthersThese include short acting

benzodiazepines (eg, oxazepam), nifidepine, phynetoin, creatine monohydrate, carbamezapine, amitryptalyin, and gabapentin.

Headach, Nausea & Headach, Nausea & VomitingVomitingThe longer treatment times

together with large degree of urea removal and/or ultra filtration significantly enhance the incidence of headache, nausea, and vomiting during dialysis.

Longer dialysis time alone doesn’t cause these side effects.

These symptoms may be apart of dialysis disequilibrium Syndrome (DDS) will be discussed later.

Patients who have headaches on dialysis in the absence of hypotension and suspected dialysis disequilibrium should be questioned about :◦ Caffien use, which can sometimes

precipitate headache ◦ Metabolic disturbances (eg, hypoglycemia,

hypernatremia, hyponatremia), ◦ Uremia◦ Subdural hematoma◦ Medication-induced headaches.

Dialysis disequilibrium Dialysis disequilibrium Syndrome DDSSyndrome DDScentral nervous system disorder

described in dialysis patients characterized by neurological symptoms of varying severity that are thought to be due primarily to cerebral edema.

Usually occure in new patient started on hemodialysis especially with hign BUN.

Other risk factor , sever metabolic acidosis , extremes of age , presence of other CNS diseases like seizure disorders.

PathogenesisPathogenesisThe symptoms of DDS are

caused by water movement into the brain, leading to cerebral edema. Two theories have been proposed to explain why this occurs: ◦a reverse osmotic shift induced by

urea removal .◦fall in intracellular pH.

Clinical ManifestationClinical ManifestationThe classic DDS develops during or

immediately after hemodialysis. Early findings include ◦Headache◦Nausea ◦Disorientation ◦Restlessness ◦Blurred vision ◦Asterixis ◦More severely affected patients progress

to confusion, seizures, coma, and even death.

Differential DiagnosisDifferential DiagnosisUremiaSubdural hematomaCVAMeningitisMetabolic disturbances Drug induced encephalopathy

TreatmentTreatment  In general, symptoms of DDS are self-limited and

usually resolve within several hours. The management of mild nonspecific

disequilibrium symptoms, such as nausea, vomiting, restlessness, and/or headache, is symptomatic; however, in the acutely uremic patient with such symptoms who is undergoing dialysis, the blood flow rate should be slowed and consideration should be given to stopping the dialysis session.

Dialysis is stopped in the patient with seizures, coma, and/or obtundation. Patency of the airway should be ensured.

Severe DDS with seizures can be reversed more rapidly by raising the plasma osmolality with either 5 mL of 23 percent saline or 12.5 g of hypertonic mannitol.

CHEST PAINCHEST PAINChest pain that occurs during dialysis

could be: associated with hypotension DDSAnginaHemolysisAir or pulmonary embolism (rare). The decision to continue or stop the

dialysis treatment because of chest pain is based upon clinical findings, such as hemodynamic stability, and the results of the history and physical examination.

AnginaAngina should always be considered as those patients at

an increased risk of coronary disease. The appropriate history, physical examination, and, if clinically indicated, electrocardiogram and cardiac enzyme evaluation should therefore be performed.If dialysis is continued, the administration of oxygen and aspirin, reduction of the desired ultrafiltration and/or blood pump speed, and administration of nitrates or morphine should be considered on an individual basis.

Angina during dialysis may be prevented with the administration of nitrates and/or beta blockers prior to the treatment. However, the efficacy of these agents is diminished since they commonly result in hypotension, thereby reducing the ability to effectively remove extracellular fluid.

HemolysisHemolysis May present as chest pain and tightness, or back pain and If

it is not recognized early, severe hyperkalemia may happen and lead to death.

Findings highly suggestive of hemolysis include: A port wine appearance of the blood in the venous line Complaints of chest pain, shortness of breath, and/or back

pain A falling hematocrit A pink color of the plasma in centrifuged specimens. The etiology of hemolysis in hemodialysis patients is usually

related to problems with the dialysis solution These include: Overheating Hypotonicity due to an insufficient concentrate-to-water ratio Red blood cell trauma like in kinking of the blood lines.

Con’t hemolysisCon’t hemolysisThe initial treatment is to: stop dialysis immediatelyClamp the blood lines (do not return the

blood to avoid hyperkalemia)prepare to treat hyperkalemia and the

potentially severe anemia investigate the causehospitalization for observation since life-

threatening hyperkalemia may develop after dialysis has been terminated.

Air embolismAir embolism Rare but fatal cause of chest pain and dyspnea during

dialysis. (Foam in the venous blood line should rise the suspicion that air is entering the dialysis system). Disconnection of connecting caps and/or blood lines can also lead to air embolism in patients being dialyzed with central venous catheters.

Symptoms of the air embolism depend upon the patient's position at the time of the event. In the seated patient, air tends to migrate into the cerebral venous system without entering the heart leading to loss of consciousness and seizure while in those who are recumbent, air tends to enter the heart and then the lungs leading to dyspnea, cough, and perhaps chest tightness.

Con’t- Air embolismCon’t- Air embolism Treatment of suspected air embolism includes: Clamping the venous line and stopping the blood

pump Positioning of the patient on the left side in a supine

position with the chest and head tilted downward. Cardiorespiratory support The administration of 100 percent oxygen by either

mask or endotracheal tube The most important aspect of air embolism is

prevention by the adequate function of monitoring devices on dialysis machines

THANK YOUTHANK YOU