Acute Complication of Hemodialysis

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Acute Complication of Hemodialysis

• Dr.Alaa Mohammed Fouad Mousli
• Surgical Demonstrator

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Objective

• In this presentation we will review briefly the
  causes, diagnosis and treatment of the common
  acute complications that we face during
  hemodyalysis.

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Acute complication HHCCBNF

• 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

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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.

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Clinical Patterns

• There 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).

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Clinical Patterns Cont

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

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Etiology

• Rapid 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.

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• 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.

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• 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.

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Keep it in Mind

• Plasma osmolality.
• True dry wight.
• Autonomic Neuropathy.
• Acetate Nitric Oxide.
• Na Mg.
• Cardiac Diseases.
• Be patient in your management

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DIAGNOSIS AND TREATMENT

• Although 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

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• 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.

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PREVENTION

• Accurate setting of the "dry weight"
• Steady, constant ultrafiltration 
• Increased dialysate sodium concentration and
  sodium modeling 
• Bicarbonate dialysate buffer 
• Temperature control 

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Prevention Cont

• Improvement 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. 

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Muscle Cramps

• A cramp is a prolonged involuntary muscle
  contraction
• common 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

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Etiology

• Plasma volume contraction.
• Tissue hypoxia
• Hyponatremia.
• Hypomagnesemia.
• Carnitine deficiency.

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Treatment.

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

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Interventions to reduce the frequency 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.

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Minimize inter-dialytic weight 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.

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Others

• These include short acting benzodiazepines (eg,
  oxazepam), nifidepine, phynetoin, creatine
  monohydrate, carbamezapine, amitryptalyin, and
  gabapentin.

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Headach, Nausea Vomiting

• The 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 doesnt cause these
  side effects.

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• 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.

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Dialysis disequilibrium Syndrome DDS

• central 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.

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Pathogenesis

• The 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.

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Clinical Manifestation

• The 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.

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Differential Diagnosis

• Uremia
• Subdural hematoma
• CVA
• Meningitis
• Metabolic disturbances
• Drug induced encephalopathy

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Treatment

•  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.

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CHEST PAIN

• Chest pain that occurs during dialysis could be
• associated with hypotension
• DDS
• Angina
• Hemolysis
• Air 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.

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Angina

• 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.

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Hemolysis

• 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.

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Cont hemolysis

• The initial treatment is to
• stop dialysis immediately
• Clamp the blood lines (do not return the blood to
  avoid hyperkalemia)
• prepare to treat hyperkalemia and the potentially
  severe anemia
• investigate the cause
• hospitalization for observation since
  life-threatening hyperkalemia may develop after
  dialysis has been terminated.

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Air 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.

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Cont- 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

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Thank you