ACUTE COMPLICATIONS

OF

HEMODIALYSIS

Dr Farid Ghalli

Thursday Morning Teaching

26/10/2017

UHW

HYPOTENSION IN HD

Am J Nephrol 2015;42:337-350

Pattern of intradialytic BP Behaviour

*Definition Ι: Minimum SBP <90 or <100 mmHg.

Definition ΙΙ: The combination of minimum SBP <90 or <100 mmHg and

ocurrence of symptoms.

Definition ΙΙΙ: SBP fall of at least 20 or 30 mmHg.

Definition IV: The combination of SBP fall of at least 20 or 30 mmHg and

of minimum SBP <90 mmHg .

*J Am Soc Nephrol. 2015 Mar;26(3):724-34

Definition of hypotension in HD

The abrupt fall in blood pressure which is typically

accompanied by symptoms and requires medical or nursing

intervention.

Renal Association Clinical Practice Guidelines: Hemodialysis Guideline 8.1, 2012

• Frequency: 15-20% of HD sessions1.

• It is an independent prognostic factor for 2-year mortality in

HD2.

• It has been associated with increased comorbidity.

1Hemodial Int 2014;18: 415–4222Kidney Int. 2004; 66:1212-1220

Clinical epidemiology of hypotension

Residual renal function

loss

Vascular access

thrombosis

Cognitive

dysfunction

Myocardial stunning

J Am Soc Nephrol 2011; 22: 1526 –1533

Clin J Am Soc Nephrol. 2009 May;4(5):914-20

Kidney Int. 2002; 62, 1046–1053

Am J Kidney Dis. 2014 Sep;64(3):434-42

HYPOTENSION

Hypovolemia

Defective vasoconstriction

1. Dialysate settings (↑T, ↓Ca+2)

2. Autonomic neuropathy

3. Antihypertensive drugs

4. Eating during treatment

5. Anemia

6. Sepsis

Cardiac causes

1. Diastolic dysfunction

2. Acute coronary syndromes

3. Arrhythmias

Uncommon causes

1. Hemolysis

2. Dialysis reactions

3. Air embolism

4. Hemorrhage

5. Pericardial tamponade

↑ Ultrafiltration

rate

Inadequate plasma refilling

↓ DialysateNa+

Hypotension etiology is multifactorial

Hypovolemia

Decreased venous return

Decreased filling pressures in right heart chambers

Cardiac ouput decrease*

(Bezold-Jarisch reflex)

HYPOTENSION

Blood Pressure =

*ASAIO Trans. 1989;35(3):245-7

Inadequate vasoconstriction

(De Jager-Krogh phenomenon, ↑adenosine secretion)

Diastolic dysfunction

Cardiac Output

x

Systemic Vascular Resistance

±

±

Which factors determine UFR?

Sodium consumption

1.

2.

3. 4.

↓DialysateNa+

↑DialysateNa+

Dialysate Νa+ must be individualized

Optimally, dialysate Νa+ = pre-HD serum Νa+

• Dizziness

• Nausea - vomiting

• Muscle cramps

• Sweating

• Tachycardia (or rarely bradycardia)

• Angina pectoris

• Drowsiness

• Loss of consciousness

• Seizures

In some patients, there are no symptoms whatsoever until the blood

pressure falls to extremely low levels. For this reason, blood pressure

must be monitored on a regular basis throughout the HD session.

Clinical manifestations

Acute management

1. Patient placement in Trendeleburg position.

2. Ultrafiltration pause and administration of 100-200 cc N/S

0,9% i.v. bolus.

3. Ο2 administration.

4. Diagnostic workup for hemorrhage, sepsis, cardiac or

uncommon causes of hypotension.

Prevention of hypotension in HD

• Cool temperature dialysate (35,5o C).

• Increased duration and/or frequency of HD.

• Dietary sodium restriction.

• Dry weight reassessment.

• Avoidance of eating during HD.

• Avoidance of antihypertensive drugs before HD.

• Maintenance of residual diuresis with furosemide.

• Use of real time blood volume monitoring.

• Use of ↑Ca++ dialysate.

• Midodrine administration (a-adrenergic agonist).

Am J Nephrol 2015;42:337-350

Mean BP was significantly higher with dialysate

temperature 35οC versus 37οC

CJASN 2006;1:1216-1225

Nephrol. Dial. Transplant. 2006 21 (7): 1883-1898

In a meta-analysis of 22 studies, cool temperature

dialysate was effective at preventing hypotension

Kidney Int. 2006; 69, 1222–1228.

Kidney Int. 2011; 80, 1080-91

N Engl J Med 2010; 363:2287-2300

• UFR > 10 ml/kg/h is associated with increased risk for

intradialytic hypotension (OR: 1,30, p=0,045).

•

•

Increased duration and/or frequency of HD reduces intradialytic

hypotension in the two FHN randomized trials.

Intradialytic

hypotensive

episodes

Standard HD 4h

9.5%

Nocturnal HD > 6h

3.1% p<0.001

Intradialytic

hypotensive

episodes

Standard HD 3/wk

13,6%

Frequent HD 6/wk

10,9% p=0,04

MUSCLE CRAMPS

• Frequency: 5-20%1.

• Common cause of premature termination of HD

sessions.

• Unexplained CPK elevations may be due to

frequent or prolonged cramping.

1Semin Dial.1992; 5:299-304.

Muscle cramps pathogenesis is still unknown

Hypotension -

hypovolemia

↓DialysateΝα+

↑ Ultrafiltration

rate

↓Plasma osmolality

Vasoconstriction Muscle ischemiaMuscle fiber relaxation

impairment

Risk factors:

↓Serum

K+, Mg+2, Ca+2

?

The acute management is directed at increasing

plasma osmolality

1. Hypertonic Na+ solution (15%).

2. Hypertonic glucose solution (35-50%) in non-diabetics.

3. In concomitant hypotension, N/S 0,9% administration.

4. Forced stretching of the muscle involved.

Muscle cramps prevention

1. Dry weight increase.

2. ↑Dialysate Na+.

3. ↓K+, Mg+2, Ca+2 correction before HD.

4. Stretching exercises.

DIALYSIS DISEQUILIBRIUM SYNDROME (DDS)

• Definition: A combination of neurologic and systemic symptoms observed

due to rapid urea removal during HD initiation.

• Risk factors: Young age, severe uremia, ↓ dialysate Να+, CNS disease

history.

• It occurs towards the end of HD session or even 24h afterwards.

DDS remains a clinical diagnosis

Symptoms - signs Benna et al.1Al-Hilali

et al.2Sadowski

et al.3Agraharkar

et al.4

Nausea/vomiting 76% – 23% 3.3%

Headache 60% 37.5% 20% –

Tremor/convulsion

s6% – – –

Psychomotor

agitation29% – – –

Altered sensorium 13.6% – – –

1Ital J Neurol Sci 2:53–57, 19812Transplant Proc 36:1827–1828, 20043J Am Soc Nephrol 4:1192–1198, 19934Nephron Clin Pract 97:c54–c60, 2004

Increased intracranial pressure is the final result of

DDS.

BMC Nephrol. 2004; 5: 9.

Greater fall of plasma urea

compared to CSF

Osmotic gradient between plasma

and brain

Water shift from plasma to brain

CEREBRAL EDEMA

Acute management of DDS

• Mild:

1. Symptomatic treatment (acetaminophen, metoclopramide).

2. Blood flow rate decrease + hypertonic Νa+, Glu.

• Severe:

1. HD termination.

2. Treatment of ↑ICP (mannitol, hyperventilation).

DDS PREVENTION

M I L D HD

1. Blood flow rate ≤ 200 ml/min.

2. Treatment time ≤ 2h.

3. Small surface, low-flux dialyzer.

4. Dialysate Na+ ≥ serum Na+.

AIM: Urea reduction ratio ~ 30-40%.

ACUTE HEMOLYSIS

• It is rarely seen today with modern HD equipment and better

water purification process.

• Clinical manifestations:

➢ Back pain.

➢ Chest tightness.

➢ Nausea – vomiting.

➢ Hypotension.

➢ Shortness of breath.

➢ Cyanosis.

➢ Grossly translucent hemolysed blood in the tubing.

Causes of intradialytic hemolysis

Comprehensive Clinical Nephrology, 5th ed, 2015.

BEWARE of hyperkalemia!

Massive hemolysis causes K+ release from lysed blood cells

Diagnostic workup:

• Complete blood count

• Reticulocyte count

• Haptoglobin levels

• Lactate dehydrogenase (LDH)

• Methemoglobin

• Coombs test

Management of acute hemolysis

1. Blood pump should be stopped and lines clamped.

2. Hemolysed blood should not be reinfused because of the ↑Κ+

content.

3. Anemia – hyperkalemia should be treated.

4. Dialysate samples should be collected for chemical analysis to

identify the cause of hemolysis.

ARRHYTHMIAS

• Etiology: Left ventricular hypertrophy, myocardial ischemia, uremic

pericarditis, conduction system calcifications, rapid electrolyte

shifts.

• QTc dispersion has been suggested as a prognostic factor for

severe cardiac events1.

• ↓ Κ+ in the dialysate (<2 mmol/l) has been associated with

fatal arrhytmias2 and should be avoided, especially in patients on

digoxin or those with residual diuresis.

• Management is done as in the general population.

1Nephrology (Carlton). 2005; 10(2):113-82CJASN 2012; 7:765-74

SUDDEN DEATH

• Frequency: 45% of all deaths in HD patients are caused

from cardiac events; 60% of them are sudden deaths. The

incidence of intradialytic cardiac arrest is 7/100.000

sessions1.

• Risk factors: Old age, DM, permanent catheters1.

• In thrice-weekly HD, it is more commonly observed at the

end of the long interdialytic interval2.

1Kidney Int. 2001;60(1):350-72N Engl J Med. 2011;365(12):1099-107

SUDDEN DEATH II

• 80% of cardiac arrests during HD are caused by ventricular

fibrillation/ventricular tachycardia.

• When cardiopulmonary arrest occurs during HD, an

immediate decision must be made as to whether the collapse

is the result of an intrinsic disease or technical errors.

• The management of cardiopulmonary arrest during HD

should follow the standard principles of cardiopulmonary

resuscitation.

AIR EMBOLISM

• Sources of entry: IV fluid administration during HD, air bubbles in the

dialysate, HD catheters, pre-pump tubing segment.

• Clinical manifestations depend upon patient position, volume and speed

of air entry:

1. Sitting position: Seizures - coma (cerebral circulation embolism).

2. Supine position: Dyspnea – cough – chest pain (pulmonary

vasculature embolism).

3. Trendeleburg position: Acrocyanosis – pain - paresthesias (lower

extremity venous embolism).

Clamp blood lines

Stop blood pump

Place patient in left Trendeleburg

position

Cardiorespiratory support:

100% Ο2 -Intubation

Percutaneous air aspiration from right ventricle

Hyperbaric O2

Air embolism management

DIALYSIS REACTIONS

• Blood exposure to the components of the extracorporeal circuit

(dialyzer membrane, lines etc.) may lead to various adverse reactions.

• They are classified as:

➢ Anaphylactic – anaphylactoid reactions (type Α).

Onset of symptoms occurs 5 – 20 min after HD initiation

and they vary from subtle to severe.

➢ Non specific reactions (type Β).

Onset of symptoms occurs 20 – 40 min after HD

initiation and they are generally mild.

Etiology – pathogenesis of dialysis reactions

Formaldehyde

IgE releaseAnaphylactic

reaction

ACE inhibitors

± ΑΝ69membrane

Bradykinin

Anaphylactoidreaction

Cellulose membranes

Complement activation

Non specific reactions

HistamineIron dextrane

Heparin

Ethylene oxide(ΕΤΟ)

Clinical manifestations of dialysis reactions

• Dyspnea.

• Chest tightness.

• Burning sensation – paresthesias.

• Angioedema – laryngeal edema.

• Rhinorrhea – lacrimation.

• Coughing – sneezing.

• Urticaria – pruritus.

• Abdominal cramps.

• Nausea – vomiting.

• Diarrhea.

❖ Risk factors: History of atopy, ↑IgE, eosinophilia, ACE-inhibitors

use.

Anaphylactic – anaphylactoid reactions (type Α):

1. Immediate cessation of HD without returning the blood from the

extracorporeal circuit to the patient.

2. Antihistamines, corticosteroids, epinephrine, cardiorespiratory support.

Non specific reactions (type Β):

1. HD can be continued because symptoms usually abate after the first

hour.

2. Symptomatic treatment (analgesics, Ο2).

Dialysis reactions treatment

Dialysis reactions prevention

Anaphylactic – anaphylactoid reactions (type Α):

1. Good rinsing of the dialyzer.

2. Use of dialyzer/lines sterilized with irradiation.

3. Avoidance of AN69 membrane in patients on ACE-inhibitors.

4. Replacement of dialyzer/lines/heparin preparation.

5. Antihistamines administration before HD.

Non specific reactions (type Β):

1. Replacement of cellulosic membranes with synthetics.

PYROGEN REACTIONS

• Definition: The occurrence of fever during HD due to increased bacterial

load or bacterial products (eg. endotoxins) entry in the circulation.

• Etiology: Contamination of dialysate or bicarbonate, improperly

sterilized dialyzers, high-flux dialyzers (backfiltration), bacterial entry

during vascular access cannulation or catheter manipulation.

• In every case of fever during HD, localized or systemic infection should

be searched for. The diagnosis of pyrogen reaction is made after

infection has been ruled out.

Fever management during HD

1. Protection of hemodynamic stability (fluid administration,

cessation of ultrafiltration – HD).

2. Investigation for infection (blood cultures, vascular access

examination etc.).

3. Broad spectrum antibiotics administration, antipyretics.

DIALYZER – EXTRACORPOREAL CIRCUIT THROMBOSIS

• Etiology: Inadequate or avoidance of heparin dose, ↓ blood flow,

air in the extracorporeal circuit due to inadequate rinsing, ↑

hematocrit, ↑ ultrafiltration rate.

• Diagnosis: ↑ venous – transmembrane pressure, visible clots in

dialyzer- extracorporeal circuit.

• Prevention: Adequate heparin dose, proper dialyzer –

extracorporeal circuit rinsing, vascular access correction (in case

of ↓ blood flow).

DIALYZER MEMBRANE RUPTURE – BLOOD LEAK

• The ↑ of hydrostatic pressure in the blood compartment of the dialyzer can

cause membrane rupture and blood leak to the dialysate.

• Membrane rupture activates the machine alarm and blood pump stops.

• Blood leak must be confirmed with a positive result in dipstick test and then

the patient is reconnected to the machine using a new dialyzer.