Acute Complication of
Hemodialysis
Dr.Alaa Mohammed Fouad Mousli
Surgical Demonstrator
Objective
In this presentation we will review briefly
the causes, diagnosis and treatment of the
common acute complications that we face
during hemodyalysis.
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 %

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:
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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’t

Chronic persistent hypotension
in long-term patients with predialysis
systolic blood pressures of less than 100
mmHg.
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.
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 Mind
Plasma osmolality.
 True dry wight.
 Autonomic Neuropathy.
 Acetate & Nitric Oxide.
 Na & Mg.
 Cardiac Diseases.
Be patient in your management

DIAGNOSIS AND
TREATMENT

Although occasionally asymptomatic,
patients with hypotension may suffer from
:
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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.

PREVENTION
Accurate setting of the "dry weight"
 Steady, constant ultrafiltration
 Increased dialysate sodium concentration
and sodium modeling
 Bicarbonate dialysate buffer
 Temperature control

Prevention – Con’t
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.
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Treatment is directed at two goals:
◦ Reducing the frequency of cramps.
◦ Relieving symptoms when they occur.
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 dialysisassociated cramps.
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.
Others
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These include short acting
benzodiazepines (eg, oxazepam),
nifidepine, phynetoin, creatine
monohydrate, carbamezapine,
amitryptalyin, and gabapentin.
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 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 :
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◦ Caffien use, which can sometimes precipitate
headache
◦ Metabolic disturbances (eg, hypoglycemia,
hypernatremia, hyponatremia),
◦ Uremia
◦ Subdural hematoma
◦ Medication-induced headaches.
Dialysis disequilibrium Syndrome
DDS
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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.
Pathogenesis
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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.
Clinical Manifestation
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The classic DDS develops during or
immediately after hemodialysis. Early findings
include
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Headache
Nausea
Disorientation
Restlessness
Blurred vision
Asterixis
More severely affected patients progress to
confusion, seizures, coma, and even death.
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
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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 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
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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 embolism
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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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