1. Acute Complications of Hemodialysis

2. Intradialytic hypotension★
Intradialytic hypotension
Definition: A decrease in systolic BP ≥20 mm Hg or a decrease in MAP ≥ 10 mm Hg associated with symptoms.
Complication: cardiac arrhythmias, coronary and/or cerebral ischemic events
Long-term side effects: volume overload due to suboptimal ultrafiltration, LVH, and interdialytic hypertension
K-DOQI guildline

3. Risk Factors of Dialysis Hypotension
A third of dialysis patients
Low body mass
Poor nutritional status and hypoalbuminemia
Severe anemia
Advanced age (Age > 65 years old)
Cardiovascular disease
Large interdialysis weight gain
Low blood pressure (predialysis systolic BP <100 mm Hg)

4. Etiology of Dialysis Hypotension (I)
Excessive rate and degree of ultrafiltration
Inappropriate peripheral venodilation
Autonomic dysfunction
Inadequate vasoconstrictor secretion

5. Etiology of Dialysis Hypotensoin (II)
Acetate dialysate
Low calcium dialysate
Eat shortly before dialysis
Antihypertensive medications
LV dysfunction

6. CARDIAC OUTPUT PERIPHERAL RESISTANCE HYPOTENSiON
PATHOGENESIS
MEDIATORS
PATHOPHYSIOLOGY
PATIENT
CARDIAC
OUTPUT
Heart Disease
Volume
Ultrafiltration
Vascular
Disease
Osmolality
Fall
Vasopressors
Autonomic
Dysfunction
Vasodilatator
Warm
Dialysate
PERIPHERAL
RESISTANCE
Hormonal
Dysfunction
Cell
Dysfunction
Bio-incom-
patibility
Medications
Complement
Activation,
Cytokine release
Endotoxin
Sepsis
Infection
HYPOTENSiON
Acetate
Infusion
Hypoxemia
Vasovagal stim.

7. Table. Results of four tests of autonomic function in normotensive and hypotensive patients on maintenance hemodialysis
Before Dialysis After Dialysis
Test Normotensive Hypotensive Normotensive Hypotensive
Orthostasis (standing up)
∆SBP (mmHg) ± ± 2.6* -6.0 ± ± 3.1†
∆DBP (mmHg) ± ± 1.4* -4.3 ± ± 1.7†
30:15 ratio (normal ≥ 1.04) ± ± ± ± 0.011
Valsalva quotient (normal ≥ 1.21) ± ± ± ± 0.029†
Sustained handgrip (normal ≥ 15)
∆DBP (mmHg) 5.8 ± ± ± ± 0.7
Cutaneous cold
∆SBP (mmHg) 6.8 ± ± ± ± 0.8
∆DBP (mmHg) 5.1 ± ± ± ± 0.7
Lin YF, Wang JY et al., ASAIO 39: , 1993.

8. BV (%)  cGMP (pmol/ml) 
Fig. Correlation between changes in blood volume and plasma cGMP throughout HD.
Wann GL. Lin YF. ASAIO 44:M569, 1998.

9. Plasma NO2- + NO3- (mM/l)
Fig. Plasma levels of nitrite and nitrate in hypotensive and normotensive patients on hemodialysis.
Lin SH. ASAIO J 42:M895, 1996.

10. Accurate Estimation of Dry Weight
cGMP, ANP
IVCD
Continuous monitoring of BV
Bioimpedence ECF/TBW

11. Prevention and Management of Dialysis Hypotension (I)
Limiting sodium intake
Minimize interdialytic weight gain by education
Blood sugar control
Slow ultrafiltration
Sodium modeling
Raise dialysate calcium
Lower dialysate temperature

12. Prevention and Management of Dialysis Hypotension (II)
Switch to CAPD
Hyperoncotic albumin
Nasal oxygen
Mannitol infusion

13. Prevention and Management of Dialysis Hypotension (III)
L-Carnitine therapy
Sertraline
Midodrine
Blood transfusion or erythropoietin therapy
Volume expansion
Vasoconstrictor

14. p < 0.005
Number of Hypotensive episodes
Fig. Number of hypotensive episodes per hemodialysis session in the sertraline and pre-sertraline periods.
Dheenan S. AJKD 31:624, 1998.

15. Figure. Serial changes in MAP HD before ( ) and after ( )midodrine therapy.
YF Lin et al. Am J Med Sci 2003;325:

16. Conclusion and clinical application
Midodrine improves chronic hypotensin in HD patients by modulating autonomic function and its direct effects on peripheral vessels.

17. Table. Carnitine levels in patients with (n=8) and without (n=23)
Table. Carnitine levels in patients with (n=8) and without (n=23) intra-dialytic hypotension
Without hypotension With hypotension
Total carnitine (mml/l) ± ± 2.2*
Free carinitine (mmol/l) ± ± 1.7**
Acyl/free carnitine ratio ± ± 0.15
Values are mean ± SEM, * p < 0.05, ** p < 0.01 vs without hypotension
Riley S. Clin Nephrol 48:392, 1997.

18. Hypoxemia Alkali attenuate hyperventilation Acetate dialysate
Complement activation
Pulmonary leukosequestration
Actin polymerization
Biocompatible hollow fiber

19. Muscle Cramps 35-86% of hemodialysis patients Lower extremities
Mechanisms: Rapid ultrafiltration, Intradialytic hypotension, tissue hypoxia
Treatment: Quinine, Vit E, L-carnitine, Creatine monohydrate, Sodium modeling, hypertonic solution

20. ★

21. Acute Allergic Reaction
First use syndrome
Burning retrosternal pain
Diffuse heat, cold perspiration, urticaria, pruritus, laryngeal strider, bronchospasm, loss of consciousness
Polyurethane function as a reservoir for ethylene oxide

22. ** *
Serum C3a (ng/ml) **
Fig. Comparisons of serum C3a levels during hemodialysis
procedure with different dialysis membrane.
(* p< 0.05, ** p<0.01 vs baseline)

23. * * ** WBC (/cumm) Fig. Comparisons of WBC levels during hemodialysis
procedure with different dialysis membrane.
(* p< 0.05, ** p<0.01 vs baseline)

24. TNF-a (pg/ml/2 x 106 monocytes)
Fig. Comparisons of TNF-a production by zymoxan-stimulationed
Monocytes between Cuprophan and PMMA hollow fiber before, at the 15th minute of and at the end of dialysis. NC= Normal control.
** p<0.01 between two hollow fibers, +++ p<0.001 among three time periods.
YF Lin. Am J Nephorl 16:293, 1996.

25. Sleep disorders Bone disease Hypotension Malnutrition
Table. Clinical relevance of cytokine production in hemodialysis patients
Acute Chronic
Fever Anemia
Sleep disorders Bone disease
Hypotension Malnutrition
Immunological dysfunction
Pertosa G KI 58 suppl 76:S104, 2000.

26. Fig. Relationship between interleukin-6 (IL-6) production by peripheral blood mononuclear cells (PBMC) and erythropoietin (EPO) requirements in 34 hemodialysis subjects (r=0.384, p=0.039)
Goicoechea M KI 54:1337, 1998.

27. * * * * Serum b2 microglobulin (mg/L)
Fig. Comparisons of serum b2M during hemodialysis procedure with different dialysis membrane. (* p< 0.05 vs baseline)

28. ★ Uremic Pruritus (I) 50-90% of dialysis patients
Risk: male, high serum BUN, Ca, P, β2-microglobulin, duration of dialysis
Diagnositc criteria

29. Pathogenesis ★
Pruritogenic substancemast cell release histamine, IL-2, …cascade of nerve conduction to induce in perception of itch

30. Causes of itching in ESRD★

31. ★ Uremic Pruritus (II) Optimize the dialysis dose Treat anemia
Treat 2nd hyperparathyroidism
Ultraviolet B phototherapy
Topical emollients
Capsaicin
Antihistamine
Anti-serotonin agents
Topical treatment
(a) Skin emollients
(b) Capsaicin
(c) Topical steroids
Physical treatment
(a) Phototherapy
(b) Acupuncture
(c) Sauna
Systemic treatment
(a) Low-protein diet
(b) Primrose oil
(c) Lidocaine and mexilitine
(d) Opioid antagonists
(e) Activated charcoal
(f) Cholestyramine
(g) Serotonin antagonists
(h) Parathyroidectomy
(i) Nalfurafine

32. Table. Degree of pruritus on capsaicin therapy
Degree of pruritus None Mild Moderate Severe
Before treatment
After treatment *
8 weeks postreatment

33. κ-opoid receptor agonist-Nalfurafine★
κ-opoid receptor agonist-Nalfurafine

34. ★ Arrhythmia (I) 30-48% of dialysis patients Risk factor:
▲ Compromised myocardium: CAD, Intermyocardiocytic fibrosis, Pericarditis
▲ Increased QT interval or dispersion

35. ★
Arrhythmia (II)
▲ Electrolyte imbalance: hypokalemia, hyperkalemia, hypercalcemia, hypermagnesemia
▲ Anemia
▲ Increased LV mass
▲ Advanced age
▲ Acetate dialysate

36. 350
400
450
500
P < 0.001
Fig. Distribution of QTc values among hemodialysis patients and controls.
The mean value of QTc was significantly increased in hemodialysis patients
(432.6 ± 24.9 ms) compared controls (402.0 ± 21.0 ms) (p<0.01)
Suzuki R. Clin Nephrol 49:240, 1998.
Contol
(n=30) HD
(n=42)

37. Table. Independent predictors of QTc interval by multivariate
stepwise regression analysis
Variable Coefficient Standard error T value P value
Diabetes mellitus
Ejection fraction
(Constant)
Independent factor: QTc interval R2 = 0.497
Suzuki R. Clin Nephrol 49:240, 1998.

38. Results of 24-Hour Holter ECG Monitoring
Arrhythmias Seen No. of Tapes (%)
Ventricular ectopic beats (> 20/hr) 15 (24)
Ventricular ectopic beats (> 100/hr) 2 (3)
Episodes of ventricular tachycardia 5 (8)
Epidoses of supraventricular tachycardia 2 (3)
Episodic atrial fibrillation (11)
Heart block (intermittent) 1 (1.6)
Jassal SV AJKD 30:219, 1997.

39. Bleeding During Dailysis (I)
Platelet dysfunction
Impaired dense granule release of ATP and serotonin
Reduced synthesis of thromboxane A2
Elevated platelet cytosolic cAMP and calcium
Impaired aggregation response

40. Bleeding During Dialysis (II)
Altered adhesive fibrinogen and vWf
Impaired fibrinogen receptor (GPIIbIIIa) function
Uremic toxin or inhibitors
Erythropoietin augments GPIIbIIIa

41. Bleeding During Dialysis (III)
Pack RBC
Cryoprecipitate, FFP(VIII/vWF)
dDAVP
Estrogen

42. Air Embolism 1 ml/kg air may be fatal
Occlude RV outflow tract and pulmonary vascular bed
Thromboxane B2, endothelin
Trendelenburg position with left side down
Withdrawal of air from RA
Hyperbaric oxygen

43. Dialysis Pericarditis I★
Uremic pericarditis: pericarditis before RRT or within 8 weeks of its initiation.
Dialysis pericarditis: ≥ 8 weeks after initiation of RRT.
Incidence of dialysis pericarditis: 2-12%
Etiology: inadequate dialysis, volume overload, infection, autoimmune, drugs

44. Dialysis Pericarditis II
Precordial pain, hypotension, dyspnea, fever, weight gain
Heparin free dialysis
Intensive dialysis
NSAID
Subxiphoid pericardiostomy

45. Dialysis Disequilibrium (I)
Headache, vomiting, seizure, delirium
Rapid correction of marked azotemia
Cerebral swelling
Reverse urea effect
Acidosis of the CSF

46. Dialysis Disequilibrium (II)
Inefficient dialysis
Shorten the duration
Lower dialyzer blood flow
Less efficient dialyzer
Osmotic agents, high sodium
IV diazepam

47. Metabolic Disorders Metabolic alkalosis Sodium citrate
Falty delivery of a buffer base
Fluoride poisoning
Acute cupper intoxication

48. Sodium Disorders Conductivity limits are not adjusted
Water intoxication
Hyperkalemia
Metabolic acidosis
Correction of hyponatremia
Drink water, 5% G/W for hypernatremia

49. Hypokalemia Loss into dialysate, alkali therapy
Renal or extrarenal losses
Arrhythmia, hypotension, fatigue, weakness, paralysis
CAD, digitalis, hypercalcemia, hypomagnesemia, meta alkalosis
Adjust dialysate potassium and buffer

50. Hyperkalemia Dietary intake GI bleeding
Overheated or hypotonic dialysate
Chloramine, sodium hypochlorite, fluoride
Medications
Metabolic acidosis

51. Hypophosphatemia Intensive dialysis Phosphorus binders Reduced intake
Dysfunction of erythrocytes, CNS, skeletal and cardiac muscle
Phosphorus rich food

52. Hypercalcemia (I) Liberation of calcium from bone Intradialytic gain
Phosphorus binders
Widespread use of calcitriol
Aluminum poisoning

53. Hypercalcemia (II) Low dialysate calcium
Phosphorus binders during meals
Discontinue vitamin D Therapy
Treat aluminum toxicity
Pamidronate

54. Fluoride Contamination
Faulty RO and deionization
Bring down calcium and magnesium
Vomiting, abdominal pain, cardiac irritability
Muscle twitching, tetany, petechiae bleeding
Respiratory failure, hypotension, cardiac arrest
Metabolic, respiratory acidosis

55. Chloramine Contamination
Less than 0.1 mg/L
Oxidize hemoglobin to form methemoglobin
Appropriate charcoal filters
Vitamin C

56. Endotoxin Bacterial infections Bicarbonate dialysate conc.
Endogenous pyrogens
Header syndrome
Disinfection of the O rings
Backfiltration with high flux dialysis

57. Hypertensive Emergencies
Paradoxical, hypertensive response
Rise in plasma catecholamine
Activation of renin-angiotensin system
Antihypertensive withdrawal
Sublingual captopril and nifedipine

58. Bowel Ischemia Abdominal pain, acute diarrhea Dialysis hypotension
Digitalis, b blockers
Occlusive and non-occlusive infarction (25 to 60%)
Congestive heart failure
Cardiac arrhythmia (esp. AF)
ESRD
Hyperkalemia, acidemia, leukocytosis
elevated LDH and CPK

59. Table. Location of Mesenteric Infarction
Location No. of Patients (n=12)
Small bowel 1
Colon 1
Cecum 2
Sigmoid 3
Ileocecal and distal transverse
colon 1
Diffuse involvement
Large bowel 1
Small and large bowel 1
Distal ileum and right colon 1
Diamond SM. JAMA 256:2545, 1986.

60. Table. Pertinent History and Medications (I)
Clinical Characteristic Bowel Infarction Controls
Heart disease
Coronary artery disease 7 8
By conornary angiography 4 3
Angina
Myocardial infarctions 2 1
Congestive heart failure 2 1
Atrial arrhythmias 3 2
Diabetics with heart disease 2 3
Diamond SM. JAMA 256:2545, 1986.

61. Table. Pertinent History and Medications (II)
Clinical Characteristic Bowel Infarction Controls
Cardiac medications, No. of patients 6 5
Digoxin
b-Blockers 2 1
Calcium antagonists
Episodes of hypotension when
undergoing dialysis
Frequent and/or severe hypotension 4 1
when undergoing dialysis *
Diagnosis of severe atherosclerosis 3 1
Diamond SM. JAMA 256:2545, 1986.

62. Table. Laboratory Values in Bowel Infarction Group
Findings No. of Patients (n=12)
White blood cell count
> mm3 ( >15 x 109 /L) 2
> mm3 ( > 20 x 109 /L) 6
Hematocrit
Increase by 10% (0.10) 1
Increase by 20% (0.20) 3 pH
<
<
Potassium, mEq/L (mmol/L)
>
>
Bicarbonate, mEq/L(mmol/L)
<
<
<
Diamond SM. JAMA 256:2545, 1986.