Complicati

on
Dialysisinduced
hypotensio
n

Cause

Symptom

Management

Patient related factors

Impaired plasma
volume refilling (too
high ultrafiltration,
autonomic
dysfunction)
Decreased cardiac
reserve (diastolic or
systolic dysfunction)

Impaired venous
compliance

Autonomic
dysfunction
(diabetes, uremia)

Arrhythmias

Anemia

Drug therapy
(vasodilators,
blockers, calcium
channel blockers)

Alteration of
vasoactive
substances in blood
(low NO, high
endothelin-1 and
angiotensin-2)

Eating during
treatment (increased

muscle cramps
abdominal and chest
pain
nausea and vomiting
dyspnea
light-headedness
weakness
anxiety
vertigo
paleness
sweating

stopping or slowing the

rate of ultrafiltration
placing the patient in the
Trendelenburg position
decreasing the blood flow
rate
Restoring intravascular
volume.

Prevention

Patient end strategy

Reduce
intradialytic
weight gain
(dietary and
treatment
compliance)

Avoid antihypertensive
medication on the
morning of the
dialysis day

Avoid missing
dialysis and stay
the entire dialysis
time for
treatment

Avoid eating
during dialysis

splanchnic blood
flow)

Too low target weight

estimation

Procedure related factors

Procedure related
strategy

Rapid decrease in
plasma osmolality
(relatively large
surface area
membrane, high
starting BUN)

Excess absolute
volume and rate of
fluid removal (for
fluid overload)

Change in serum
electrolytes
(hypocalcemia,
hypokalemia)

Dialysate acetate,
warm dialysate

Membrane blood

Dialysate sodiumsodium profiling

and sodium
gradient protocol
but maintaining
zero sodium
balance to the
extent possible1

Modeling fluid
removalsequential
ultrafiltration and
dialysis, blood
volume controlled
hemodialysis2

Cool dialysateisothermic
dialysis3 is well
tolerated and

interaction

clearly reduces
the incidence of
hypotension4

Hypoxia (partially
patient related)
Other less common
causes

Dialyzer
reaction

Reduction of the
ultrafiltration rate
with prolongation
of treatment time

Accurate
estimation of dry
weight
(segmental
bioimpedance,
and others5)

Judiciously
increasing
dialysate calcium
while avoiding
hypercalcemia6

Pericardial
tamponade

Myocardial infarction

Aortic dissection

Internal or external
hemorrhage

Septicemia

Air embolism

Pneumothorax

Hemolysis
Type A
Use of ethylene oxide (ETO)
for sterilization of dialyzer
and polyacrylonitrile
membranes (PAN)
membranes, especially AN69
in patients on ACE-inhibitors

Type B

Type A

Dyspnea
Burning/heat sensation
at the access site or
throughout the body
Angioedema
Urticaria
Rhinorrhea or
lacrimation
Abdominal cramping

Itching
Type B

Symptomatic and
supportive

Discontinue HD and
discard the blood,
oxygen, anti-histamines,
epinephrine and
corticosteroids

HD can be initiated
after stabilization with a

Avoid combination of
PAN membrane and
angiotensin
converting enzyme
inhibitor (ACEI) use

Use of ARBs
(angiotensin receptor
blockers) and
dialysate with 3.5
mEq/L calcium may

Current data do not

support the role of
membrane
biocompatibility in
development of type B
reactions
Air
embolism

Dialysate
reaction

Between patient and

blood pump, due to
high negative
pressure and leaks in
the circuit in this
segment

Air in the dialysate

fluid (uncommon,
mostly gets trapped
in venous chamber)

During central
venous catheter
insertion or removal

Primary symptoms are

chest and back pain

more biocompatible
membrane and a
hemodialyzer not
sterilized with ETO
(ethylene oxide)

Prevent further air

entry by clamping and
disconnecting the circuit

Flat supine position

may be better over
traditionally advocated
left lateral (Durans
position) and
Trendelenburg position1,2

Oxygen with FiO2

100%

Hyperbaric
oxygen3 (prevents
cerebral edema)

Use of Luer-lock
syringes for blood draw
from catheters

lower the risk

Test machine prior

to use to ensure that
the air detector alarm
system is working
effectively

Catheter insertion
or removal should be
in a head low position
(insertion site 5 cm
below right atrium).
Patient can assist by
holding their breath
or doing a Valsalva
maneuver that will
increase central
venous pressure4.

Disease

Hypocalcaemi

Sign & Symptoms

Red or purple spots on
skin
'pins and needles'
sensation in and around
the mouth and lips, and
in the extremities of the
hands and feet.
(unrelieved and strong
contractions of the
hands, and in the large
muscles of the rest of
the body
Latent tetany
Tendon reflexes are
hyperactive
Life-threatening
complications like
Laryngospasm and
Cardiac arrhythmias

Causes
Eating disorders
Prolonged vomiting (e.g.
with a viral illness)
Exposure to mercury,
including infantile
acrodynia
Excessive dietary
magnesium, as with
supplementation.
Excessive dietary zinc,
as with supplementation
(causes rapid
hypocalcemia).
Prolonged use of
medications/laxatives
containing magnesium
Chelation Therapy for
metal exposure,
particularly EDTA

Diagnosis
Because a significant
portion of calcium is bound
to albumin, any alteration
in the level of albumin will
affect the level of calcium is
measured. A corrected
calcium level based on the
albumin level is: Corrected
calcium (mg/dL) =
measured total Ca (mg/dL)
+ 0.8 * (4.0 - serum
albumin [g/dL]). Another
way to determine the
calcium level is to measure
directly the ionized calcium
level.

Management

Intravenous
calcium gluconate
10% can be
administered, or if
the hypocalcaemia
is severe, calcium
chloride is given
instead.
However, in either
circumstance,
maintenance doses
of both calcium and
vitamin-D (often as
1,25-(OH)2-D3, i.e.
calcitriol) are often
necessary to
prevent further

decline.

Hypercalcae
mia

Stones (renal or
biliary)
Bones (bone pain)
Groans (abdominal
pain, nausea and
vomiting)
Thrones (polyuria also looks like Osborn
wave on ECG)
Psychiatric
overtones (Depression
3040%, anxiety,
cognitive dysfunction,
insomnia, coma)
Other symptoms
can include fatigue,
anorexia, and
pancreatitis.
Limbus sign seen
in eye due to
hypercalcemia.
Hypercalcemia has
a negative
chronotropic effect
(decrease in heart

Osteoporosis treatment
or preventive agents,
such as
Bisphosphonates and
Denosumab.
Agents for the
treatment of
hypercalcemia, such as
Calcitonin.
Chronic renal failure
Absent active
vitamin D
Primary
hyperparathyroidism and
malignancy account for
about 90% of cases of
Hypercalcaemia
Other

causes include
Parathyroid function
Cancer
Vitamin-D disorders
High bone-turnover
rates
Kidney failure

Initial therapy

hydration, increasing
salt intake, and
forced diuresis.
after rehydration, a
loop diuretic such as
furosemide can be
given to permit
continued large
volume intravenous
salt and water
replacement while
minimizing the risk of
blood volume
overload and
pulmonary oedema.
In addition, loop
diuretics tend to
depress renal calcium
reabsorption thereby
helping to lower
blood calcium levels

Additional therapy:
bisphosphonates and
calcitonin

rate), and a positive

inotropic effect
(increase in
contractility).

Hyponatremia

nausea and vomiting

headache
short-term memory
loss
confusion
lethargy
fatigue
loss of appetite
irritability
muscle weakness
spasms or cramps
seizures
decreased
consciousness

Bisphosphonates are
pyrophosphate analogues
with high affinity for bone,
especially areas of high
bone-turnover.

Hypervolemic
hyponatremia
Both sodium & water
content increase: Increase
in sodium content leads to
hypervolemia and water
content to hyponatremia.
Total body water and
sodium are regulated
independently.[11]

cirrhosis of the liver

congestive heart
failure

A blood serum test showing

a low sodium concentration
is necessary for diagnosis.
Examination includes taking
vital signs when lying,
sitting, and standing, and
an assessment of how
much blood is in the body.
This determination (i.e.
hypervolemic, euvolemic,
hypovolemic) helps guide
treatment decisions. A full
assessment of other
medical conditions
(comorbidity) is also taken,
because heart and brain

Other therapies :
rarely used, or used in
special circumstances
Plicamycin
inhibits
bone resorption
Gallium nitrate inhibits
bone resorption and
changes structure of
bone crystals
Glucocorticoids
increase
urinary
calcium excretion and
decrease
intestinal
calcium absorption
Dialysis usually used
in
severe
hypercalcaemia
complicated by renal
failure.
The
treatment
of
hyponatremia depends on
the underlying cause and
whether
the
patient's
blood volume status is
hypervolemic, euvolemic,
or hypovolemic.
Hypovolemia
intravenous
administration of normal
saline (salt) is usual, care
being taken not to raise
the serum sodium level
(salt level in the blood)
too quickly.
Euvolemic

nephrotic syndrome
in the kidneys

massive edema of
any cause

Euvolemic hyponatremia
there is volume expansion
in the body, no edema, but
hyponatremia occurs

states of severe pain

or nausea
in the setting of
trauma or other
damage to the brain
SIADH (and its many
causes)
Hypothyroidism
Glucocorticoid
(steroid) deficiency

Hypovolemic
hyponatremia

conditions affect the results

and the treatment
decisions.

Hyponatremia
managed
by
fluid
restriction and treatment
to abolish any stimuli for
ADH secretion such as
nausea. Likewise, drugs
causing
SIADH
are
discontinued if possible.
Patients with euvolemic
hyponatremia
that
persists despite those
measures
may
be
candidates for a so-called
vaptan drug.
Hypervolemic
Hyponatremia
treated by addressing the
underlying heart or liver
failure. If it is not possible
to do so, the treatment
becomes the same as
that
for
euvolemic
hyponatremia (i.e. fluid
restriction and/or use of a
vaptan drug).

The hypovolemia
(extracellular volume loss)
is due to total body sodium
loss. The hyponatremia is
caused by a relatively
smaller loss in total body
water.
any cause of hypovolemia
such as prolonged vomiting,
decreased oral intake,
severe diarrhea
diuretic use (due to the
diuretic causing a volume
depleted state and thence
ADH release, and not a
direct result of diureticinduced urine sodium loss)
Addison's disease and
congenital adrenal
hyperplasia in which the
adrenal glands do not
produce enough steroid
hormones (combined
glucocorticoid and
mineralocorticoid
deficiency)

Hypernatre
mia

Clinical manifestations
of hypernatremia can be
subtle, consisting of
lethargy, weakness,
irritability,
neuromuscular
excitability, and edema.
With more severe
elevations of the sodium
level, seizures and coma
may occur.

Hypovolemic

Inadequate intake of
free water associated
with total body sodium
depletion.
Excessive losses of
water from the urinary
tract,
Water losses associated
with extreme sweating
Severe watery diarrhea
Euvolemic

The
cornerstone
of
treatment
is
administration
of
free
water to correct the
relative
water
deficit.
Water can be replaced
orally or intravenously.
Water alone cannot be
administered
intravenously (because of
osmolarity
issue),
but
rather can be given with

Excessive excretion of
water from the kidneys
caused by diabetes
insipidus, which involves
either inadequate
production of the hormone
vasopressin, from the
pituitary gland or impaired
responsiveness of the
kidneys to vasopressin
Hypervolemic

Hypokalemi
a

Mild hypokalemia is
often without
symptoms, although it
may cause a small
elevation of blood
pressure, and can
occasionally provoke the
development of an

Intake of a
hypertonic fluid
Mineralcorticoid
excess due to a
disease
Salt poisoning (child)

Inadequate potassium
intake
Gastrointestinal or skin
loss
Urinary loss
Distribution away from
ECF
Other

addition to dextrose or
saline infusion solutions.
However, overly rapid
correction
of
hypernatremia
is
potentially
very
dangerous. The body (in
particular
the
brain)
adapts to the higher
sodium
concentration.
Rapidly
lowering
the
sodium
concentration
with free water, once this
adaptation has occurred,
causes water to flow into
brain cells and causes
them to swell. This can
lead to cerebral edema,
potentially resulting in
seizures, permanent brain
damage,
or
death.
Therefore,
significant
hypernatremia should be
treated carefully by a
physician or other medical
professional
with
experience in treatment
of electrolyte imbalance,
specific treatment like
ACE inhibitors in heart
failure and corticosteroids
in nephropathy also can
be used
Severe hypokalemia
improving
the
diet,
treating
diarrhea,
or
stopping an
offending
medication.
May require intravenous
supplementation.
Oral supplementation is

abnormal heart rhythm.

preferred given its safety

profile.

Severe hypokalemia,
may cause muscle
weakness, myalgia,
tremor, and muscle
cramps and constipation

Mild hypokalemia
may be treated with
oral potassium chloride
supplements
otassium-containing
foods may be
recommended, such as
leafy green vegetables,
tomatoes, coconut
water, citrus fruits,
oranges, or bananas

With more severe

hypokalemia, flaccid
paralysis and
hyporeflexia may result.
Hyperkalemia

Symptoms are fairly

nonspecific and generally
include malaise,
palpitations and muscle
weakness

Ineffective elimination

Renal insufficiency
Medication that
interferes with urinary
excretion:
Mineralocorticoid
deficiency or
resistance,
Gordon's syndrome a
rare genetic disorder

Excessive release from

cells
Rhabdomyolysis, burns,
or any cause of rapid
tissue necrosis,
including tumor lysis
syndrome
Massive blood
transfusion or massive
hemolysis
Shifts/transport out of
cells caused by
acidosis, low insulin
levels, Beta-blocker
therapy,
digoxin overdose, or

To gather enough
information for diagnosis,
the measurement of
potassium needs to be
repeated, as the elevation
can be due to hemolysis in
the first sample.
Generally, blood tests for
renal function (Creatinine,
blood urea nitrogen),
glucose and occasionally
creatine kinase and cortisol
will be performed.
Calculating the transtubular potassium gradient
can sometimes help in
distinguishing the cause of
the hyperkalemia.
Also, electrocardiography
(EKG/ECG) may be
performed to determine if
there is a significant risk of
cardiac arrhythmias

the paralyzing agent

succinylcholine
Box jellyfish venom
Acute Digoxin toxicity
may cause
hyperkalaemia
Excessive intake
Excessive intake with
potassium salt-substitute,
potassium-containing
dietary supplements, or
potassium chloride (KCl)
infusion