Yenny kandarini

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George Haas used a
collodion tube
arrangement to
successfully dialyze
human subjects
Allergic reactions to
impurities in Hirudin
led him to abandon his
experiments


1937:Nils Alwall used
the Alwall Kidney to
perform the first ever
hemodialysis
treatment at the
university of Lund,
Sweden
Patient Complications
Hypotension (20-30%)
Muscle Cramps
Disequilibrium Syndrome
Nausea and Vomiting
. bleeding
Headache
Hemolysis
Chest Pain
Itching
Fever and Chills
Pyrogen reaction
Hypertension

Clotting
Blood leak
Power failure
Hemolysis
Air Embolism
Air in bloodlines
Exsanguination
Dialyzer reactions
Dysequilibrium
Cramps
Hypotension
bleeding
Hypotension 20-30%
Cramps 5-20%
Nausea and vomiting 5-15%
Headache 5-10%
Chest pain 2-5%
Pruritus 5%
Fever and chills <1%

Definition: A decrease in systolic BP 20 mm
Hg or a decrease in MAP 10 mm Hg from
predialysis pressure associated with symptoms.

Etiology: excessive decreased in blood volume,
lack of vasoconstriction, cardiac cause

Rare cause : pulmonary embolus, tamponade,
hemorrhage, septicemia, dialyzer reaction, air
embolism, hemolysis

K-DOQI guildline
Gradual or sudden decrease in B/P
Increase in pulse
Cold, clammy skin (diaphoresis)
Nausea/Vomiting
Cramping
Chest pain/angina
Yawning, feeling dizzy, sleepy or weak
Pallor
Decreasing mental status to loss of consciousness
Seizure
Complication: cardiac arrhythmias, coronary
and/or cerebral ischemic events

Long-term side effects: volume overload due
to suboptimal ultrafiltration, LVH, and
interdialytic hypertension

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)
Excessive rate and degree of
ultrafiltration
Inappropriate peripheral venodilation
Autonomic dysfunction
Inadequate vasoconstrictor secretion
Acetate dialysate
Low calcium dialysate
Eat shortly before dialysis
Antihypertensive medications
LV dysfunction
Ultrafiltration
Osmolality
Fall
Warm
Dialysate
Bio-incom-
patibility
Endotoxin
Acetate
Infusion
Volume
Vasopressors
Vasodilatator
Cell
Dysfunction
Complement
Activation,
Cytokine release
Hypoxemia
Heart Disease
Vascular
Disease
Autonomic
Dysfunction
Hormonal
Dysfunction
Medications
Sepsis
Infection
Vasovagal stim.
HYPOTENSiON
CARDIAC
OUTPUT
PERIPHERAL
RESISTANCE
PATHOGENESIS MEDIATORS PATHOPHYSIOLOGY PATIENT
Treat the symptoms
Pay attention to how the patient feels
NS bolus
Place patient in trendelenburg position
Use Sodium modeling
Prevention
- determine the cause
Evaluate target and pre-weight for accuracy
Evaluate that fluid goal was correct
Review medication list for BP meds
Switch to CAPD
Hyperoncotic albumin
Nasal oxygen
Mannitol infusion
L-Carnitine therapy
Sertraline
Midodrine
Blood transfusion or erythropoietin
therapy
Volume expansion
Vasoconstrictor
0
0,2
0,4
0,6
0,8
1
1,2
1,4
1,6
1,8
Pre-Sertraline Sertraline
N
u
m
b
e
r

o
f

H
y
p
o
t
e
n
s
i
v
e

e
p
i
s
o
d
e
s

Fig. Number of hypotensive episodes per hemodialysis
session in the sertraline and pre-sertraline periods.
Dheenan S. AJKD 31:624, 1998.
p < 0.005
Without hypotension With hypotension

Total carnitine (mml/l) 27.0 2.7 18.4 2.2*

Free carinitine (mmol/l) 18.8 2.0 10.9 1.7**

Acyl/free carnitine ratio 0.58 0.06 0.78 0.15

Table. Carnitine levels in patients with (n=8) and without (n=23)
intra-dialytic hypotension
Values are mean SEM, * p < 0.05, ** p < 0.01 vs without hypotension
Riley S. Clin Nephrol 48:392, 1997.
Etiology :
Hypotension
Disequilibrium
Gastroparesis

Management:
Treat and avoid hypotension
Slow blood pump during first hours
Antiemetics/prokinetic agents

Manifestation of disequilibrium
Caffeine withdrawl
Idiopathic

Management
Ramped Na dialyzer
Reduced BP during first hours
Analgetic
B blocker
Alkali attenuate hyperventilation
Acetate dialysate
Complement activation
Pulmonary leukosequestration
Actin polymerization
Biocompatible hollow fiber
35-86% of hemodialysis patients
Lower extremities
Mechanisms: Rapid ultrafiltration,
Intradialytic hypotension, tissue hypoxia,
low (Na+) dialysate, hypocalcemia
Treatment: Quinine, Vit E, L-carnitine,
Creatine monohydrate, Sodium modeling,
hypertonic solution
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
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.
50-90% of dialysis patients
Risk: male, high serum BUN, Ca, P, 2-
microglobulin, duration of dialysis
Diagnositc criteria
Pruritogenic substancemast cell release
histamine, IL-2, cascade of nerve conduction
to induce in perception of itch
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
30-48% of dialysis patients
Risk factor:
Compromised myocardium: CAD,
Intermyocardiocytic fibrosis,
Pericarditis
Increased QT interval or dispersion
Electrolyte imbalance: hypokalemia,
hyperkalemia, hypercalcemia,
hypermagnesemia
Anemia
Increased LV mass
Advanced age
Acetate dialysate
Platelet dysfunction
Impaired dense granule release of ATP and
serotonin
Reduced synthesis of thromboxane A2
Elevated platelet cytosolic cAMP and calcium
Impaired aggregation response
Altered adhesive fibrinogen and vWf
Impaired fibrinogen receptor (GPIIbIIIa)
function
Uremic toxin or inhibitors
Erythropoietin augments GPIIbIIIa
Pack RBC
Cryoprecipitate, FFP(VIII/vWF)
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
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
Precordial pain, hypotension, dyspnea,
fever, weight gain
Heparin free dialysis
Intensive dialysis
Subxiphoid pericardiostomy

Dialysis Pericarditis II
A set of systemic and neurologic symptoms with onset
during or soon after dialysis, with characteristic EEG
changes
Headache, nausea, vomiting, seizure, delirium, and coma
Cause :
Acute increase in brain water contens
Slower transfer of urea from the brain tissue to the blood
Fluid shift into the brain due to removal of wastes
from the blood stream causing cerebral edema
Rapid changes in serum electrolytes, especially in new patients
Rapid correction of marked azotemia
Elevated BUN > 150
BFR to high
Treatment time too long
Dialyzer to big for first treatments (too efficient)
Acidosis of the CSF
Treat the symptoms:
Monitor new patients carefully for hypertension
Decrease BFR
Treat N/V and headache per protocol
Be alert for restlessness, speech/mental changes
Osmotic agents, high sodium
IV diazepam
Consider DD


prevention
1. Early detection of uremia, early intervention with
dialysis
2. First few treatments should aim to achieve
modest reduction in serum urea concentration (
30% or less)
3. Sodium modeling, use of Bicarbonate dialysis,
slow QB
4. Prophylactic use of Mannitol is not
recommended
6. Assess new patients
electrolyte levels
7. Use a smaller dialyzer, lower
BFR and shorter dialysis time
for first few treatments
8. Ramped hypertonic Na+
dialysate
9. Dont correct hypernatremia
during dialysis
Water intoxication
Hyperkalemia
Metabolic acidosis
Tx:
Correction of hyponatremia
Drink water, 5% G/W for hypernatremia
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
Dietary intake
GI bleeding
Overheated or hypotonic dialysate
Chloramine, sodium hypochlorite,
fluoride
Medications
Metabolic acidosis
Intensive dialysis
Phosphorus binders
Reduced intake
Dysfunction of erythrocytes, CNS,
skeletal and cardiac muscle
Phosphorus rich food
Liberation of calcium from bone
Intradialytic gain
Phosphorus binders
Widespread use of calcitriol
Aluminum poisoning
Low dialysate calcium
Phosphorus binders during meals
Discontinue vitamin D Therapy
Treat aluminum toxicity
Pamidronate
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
Less than 0.1 mg/L
Oxidize hemoglobin to form
methemoglobin
Appropriate charcoal filters
Vitamin C
Bacterial infections
Bicarbonate dialysate conc.
Endogenous pyrogens
Header syndrome
Disinfection of the O rings
Backfiltration with high flux dialysis
Paradoxical, hypertensive response
Rise in plasma catecholamine
Activation of renin-angiotensin system
Antihypertensive withdrawal
Sublingual captopril and nifedipine
Abdominal pain, acute diarrhea
Dialysis hypotension
Digitalis, b blockers
Occlusive and non-occlusive infarction (25 to
60%)
Congestive heart failure
Cardiac arrhythmia (esp. AF)
Hyperkalemia, acidemia, leukocytosis
elevated LDH and CPK
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
Small bowel 1
Large bowel 1
Small and large bowel 1
Distal ileum and right colon 1
Diamond SM. JAMA 256:2545, 1986.
Angina:
Chest pain
Caused from ischemia
(lack of oxygen to tissue)
Resolved by Nitroglycerin
Myocardial Infarction.
Chest pain
Caused from ischemia that results in tissue death
Not resolved by Nitroglycerin
Ischemia to heart muscle (Coronary Artery
Disease)
Anemia
Hypotension from fluid depletion
Hypovolemia
Anxiety-stress, physical exertion, illness
Blood flow rate increased too rapidly on
patient with known cardiac disease
Treat the symptoms:
Hypotension
Angina pain with Nitroglycerin
MI pain requires analgesics
Anxiety/stress
Prevention
Accurate fluid removal and weight assessment
the most frequent long-term
complications occurring in HD patients
relate to
cardiovascular disease,
2-microglobulin (2M) amyloidosis,
renal osteodystrophy and
the effects of malnutrition.
the major cause of death in ESRD patients
atherosclerosis is present in all long-term dialysis
patients.
Premature cardiac death
has reached epidemic levels in the world's dialysis
populations,
occurring five to ten times as commonly as in the age-
matched general population and
accounting for at least half of all patient deaths
Increasing numbers of dialysis patients are
requiring coronary artery bypass surgery, but the
post-operative mortality with this is more than
three times that of patients who do not have ESRD.

Hypertension is a major risk factor for
cardiovascular disease

and is often poorly
controlled.
Some of the other risk factors include
hyper-phosphatemia
elevated calcium-phosphorus product with calcium
deposition in the coronary arteries, the cardiac conduction
system
,
heart valves

and vessels elsewhere,
anemia,

hypertriglyceridemia,

low HDL-cholesterol,

increased lipoprotein[a],

insulin deficiency or resistance,

hyper-homocysteinemia,

endothelial dysfunction,

inflammation and elevated C-reactive protein,
and smoking.
[16]

stop smoking
control of DM , hypertension, hypercholesterolemia.
Lowering cholesterol levels with medications,
particularly the LDL-cholesterol concentration
Vitamin E has been suggested as a means of
reducing oxidative stress and cardiovascular
mortality.
An interesting ongoing study is a multicenter
controlled trial of a new statin, Cerivastatin, that
lowers LDL-cholesterol and may have anti-
inflammatory and other effects.

Preventions of bone mineral ds:
using low calcium dialysate,
selective vitamin D analogues,
calcium-free phosphate binders and other
improvements in the management of bone disease
and vascular disease.
The use of erythropoietin to correct anemia in
dialysis patients and thus improve cardio-
vascular dynamics and exercise tolerance.




The importance of hyper-homocysteinemia is
uncertain.
Tx : dialysis using synthetic membranes,

and
supplementation with folic acid, vitamins B
6
and B

12
, betaine and serine.
lowering homocysteine not shown to affect
endothelial dysfunction, but because folic acid is
cheap and harmless, its use might be considered
large doses are required because high-flux and
high-efficiency dialyzers remove folic acid.

a major cause of the physical handicaps affecting
the quality of life of patients who have been on
dialysis for ten or more years, and is occasionally
life threatening if it results in severe cervical spinal
cord compression.
Deposits begin a few months of starting HD,
although clinical and radiological findings do not
begin to appear for five years or more.
Any or all joints may be affected, but especially the
sternoclavicular joint and hips.
Clinical features
periarthritis of the shoulders, carpal
tunnel syndrome, flexor tenosynovitis
of the hands, stiffness, pain and
swelling of other joints, deposits
beneath the skin and
spondyloarthropathy

The pathogenesis of M
amyloidosis is complex and poorly
understood.


There is no specific treatment for 2M--
amyloidosis.
Transplantation will lower 2M levels and may
halt progression of amyloidosis and ease
symptoms.

no modality of dialysis can remove more 2M
than is generated, although removal is greater
with biocompatible membranes and with
hemofiltration and hemodiafiltration
the other major cause of serious morbidity
in longterm dialysis patients.
is the increase in parathyroid hormone
with time on dialysis, an increase that is
significant even after adjusting for calcium
and phosphorus concentrations and other
factors



hip fractures in dialysis patients ~ osteo-
dystrophy
management of calcium and phosphorus
metabolism and availability of new
phosphate binders and other drugs osteo-
dystrophy and complications related to
calcification may be better controlled in the
future.
time on dialysis is a strong predictor of
malnutrition.

Even in patients who are well dialyzed and have an
adequate protein intake, body weight often begins
to decline during the second decade of treatment.
might relate to chronic mild metabolic acidosis or
to reduced physical activity as a result of 2M-
amyloidosis.
Highly prevalent in hemodialysis patients
Associated with increased morbidity and mortality

Pathogenesis of Malnutrition
Inadequate protein and/or calorie intake
Recommended daily dietary protein 1.2 g/kg of
body weight per day
Recommended daily energy intake:
35 kcal/kg of body weight per day for people aged
60 years
30 to 35 kcal/kg of body weight per day for people
aged 60 years
Increased resting energy expenditure
Amino acid losses in dialysate:
5 to 8 g of free amino acids per dialysis session with
low-flux dialyzers
30% greater amino acid losses withigh-flux dialyzers
Initiation of hemodialysis (can increase
serum albumin and IGF-1 levels and body
mass)
Oral nutritional supplementation
Intradialytic parenteral nutrition
Vitamin and trace element
supplementation