acute n chronic complication of hd.yenny.ppt

8/11/2019 acute n chronic complication of hd.yenny.ppt

1/77

enny kandarini


2/77

0

10

20

30

4050

60

70

80

90

1stQtr

2ndQtr

3rdQtr

4thQtr

East

West

North


3/77

George Haas used acollodion tubearrangement to

successfully dialyzehuman subjects

Allergic reactions toimpurities in Hirudin

led him to abandon hisexperiments


4/77

1937:Nils Alwall usedthe Alwall Kidney toperform the first ever

hemodialysistreatment at theuniversity of Lund,Sweden


5/77


6/77

Patient Complications

Hypotension (20-30%) Muscle Cramps

Disequilibrium Syndrome

Nausea and Vomiting

. bleeding

Headache Hemolysis

Chest Pain

Itching

Fever and Chills

Pyrogen reaction Hypertension


7/77

Clotting Blood leak

Power failure

Hemolysis

Air EmbolismAir in bloodlines

Exsanguination

Dialyzer reactions


8/77

Dysequilibrium

Cramps

Hypotension

bleeding


9/77

Hypotension 20-30% Cramps 5-20%

Nausea and vomiting 5-15%

Headache 5-10%

Chest pain 2-5% Pruritus 5%

Fever and chills


10/77

Definition: A decrease in systolic BP 20 mm

Hg or a decrease in MAP 10 mm Hg frompredialysis 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


11/77

Gradual or sudden decrease in B/PIncrease 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


12/77

Complication: cardiac arrhythmias, coronaryand/or cerebral ischemic events

Long-term side effects: volume overload dueto suboptimal ultrafiltration, LVH, and

interdialytic hypertension


13/77

Low body mass Poor nutritional status and hypoalbuminemia

Severe anemia

Advancedage (Age > 65 years old)

Cardiovascular disease

Large interdialysis weight gain

Low blood pressure (predialysis systolic BP


14/77

Excessive rate and degree of

ultrafiltration

Inappropriate peripheral venodilation Autonomic dysfunction

Inadequate vasoconstrictor secretion


15/77

Acetate dialysate

Low calcium dialysate

Eat shortly before dialysis

Antihypertensive medications

LV dysfunction


16/77

Ultrafiltration

OsmolalityFall

Warm

Dialysate

Bio-incom-

patibility

Endotoxin

Acetate

Infusion

Volume

Vasopressors

Vasodilatator

Cell

Dysfunction

ComplementActivation,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


17/77

Treat the symptomsPay 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 correctReview medication list for BP meds


18/77

Switch to CAPD

Hyperoncotic albumin

Nasal oxygen

Mannitol infusion


19/77

L-Carnitine therapy

Sertraline

Midodrine Blood transfusion or erythropoietintherapy

Volume expansion

Vasoconstrictor


20/77

0

0,2

0,40,6

0,8

1

1,2

1,4

1,6

1,8

Pre-Sertraline Sertraline

Numberof

Hypotensiveepi

sodes

Fig. Number of hypotensive episodes per hemodialysis

session in the sertraline and pre-sertraline periods.

Dheenan S. AJKD 31:624, 1998.

p < 0.005


21/77

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.


22/77

Etiology : Hypotension

Disequilibrium

Gastroparesis

Management: Treat and avoid hypotension

Slow blood pump during first hours

Antiemetics/prokinetic agents


23/77

Manifestation of disequilibrium

Caffeine withdrawl

Idiopathic

Management Ramped Na dialyzer

Reduced BP during first hours

Analgetic

B blocker


24/77

Alkali attenuate hyperventilation

Acetate dialysate

Complement activation Pulmonary leukosequestration

Actin polymerization

Biocompatible hollow fiber


25/77

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


26/77

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


27/77

Table. Clinical relevance of cytokine production in hemodialysispatients

Acute Chronic

Fever Anemia

Sleep disorders Bone diseaseHypotension Malnutrition

Immunological dysfunction

Pertosa G KI 58 suppl 76:S104, 2000.


28/77

50-90% of dialysis patients

Risk: male, high serum BUN, Ca, P, 2-

microglobulin, duration of dialysis

Diagnositc criteria


29/77

Pruritogenic substancemast cell releasehistamine, IL-2, cascade of nerve conduction

to induce in perception of itch


30/77


31/77

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 mexiliti(d) Opioid antagonists(e) Activated charcoal(f) Cholestyramine(g) Serotonin antagonists(h) Parathyroidectomy(i) Nalfurafine


32/77

30-48% of dialysis patients

Risk factor:

Compromised myocardium: CAD,Intermyocardiocytic fibrosis,

Pericarditis

Increased QT interval or dispersion


33/77

Electrolyte imbalance: hypokalemia,hyperkalemia, hypercalcemia,

hypermagnesemia

Anemia Increased LV mass

Advanced age

Acetate dialysate


34/77

Platelet dysfunction

Impaired dense granule release of ATP and

serotonin

Reduced synthesis of thromboxane A2

Elevated platelet cytosolic cAMP and calcium

Impaired aggregation response


35/77

Altered adhesive fibrinogen and vWf

Impaired fibrinogen receptor (GPIIbIIIfunction

Uremic toxin or inhibitors

Erythropoietin augments GPIIbIIIa


36/77

Pack RBC

Cryoprecipitate, FFP(VIII/vWF)


37/77

1 ml/kg air may be fatal Occlude RV outflow tract and pulmonary vascula

bed

Thromboxane B2, endothelin Trendelenburg position with left side down

Withdrawal of air from RA

Hyperbaric oxygen


38/77

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


39/77

Precordial pain, hypotension, dyspnea,

fever, weight gain

Heparin free dialysis

Intensive dialysis

Subxiphoid pericardiostomy

ialysis Pericarditis II


40/77

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


41/77

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


42/77

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


43/77

prevention1. Early detection of uremia, early intervention with

dialysis2. 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 notrecommended


44/77

6. Assess new patients

electrolyte levels7. Use a smaller dialyzer, lower

BFR and shorter dialysis timefor first few treatments

8. Ramped hypertonic Na+dialysate

9. Dont correct hypernatremia

during dialysis


45/77

Water intoxication

Hyperkalemia

Metabolic acidosis Tx:

Correction of hyponatremia

Drink water, 5% G/W for hypernatremia


46/77

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


47/77

Dietary intake GI bleeding

Overheated or hypotonic dialysate

Chloramine, sodium hypochlorite,

fluoride

Medications

Metabolic acidosis


48/77

Intensive dialysis

Phosphorus binders

Reduced intake

Dysfunction of erythrocytes, CNS,

skeletal and cardiac muscle

Phosphorus rich food


49/77

Liberation of calcium from bone

Intradialytic gain

Phosphorus binders

Widespread use of calcitriol

Aluminum poisoning


50/77

Low dialysate calcium

Phosphorus binders during meals

Discontinue vitamin D Therapy

Treat aluminum toxicity

Pamidronate


51/77

Faulty RO and deionization

Bring down calcium and magnesium

Vomiting, abdominal pain, cardiac irritability

Muscle twitching, tetany, petechiae bleeding

Respiratory failure, hypotension, cardiac arres

Metabolic, respiratory acidosis


52/77

Less than 0.1 mg/L

Oxidize hemoglobin to form

methemoglobin

Appropriate charcoal filters

Vitamin C


53/77

Bacterial infections

Bicarbonate dialysate conc.

Endogenous pyrogens

Header syndrome

Disinfection of the O rings

Backfiltration with high flux dialysis


54/77

Paradoxical, hypertensive response

Rise in plasma catecholamine

Activation of renin-angiotensin system

Antihypertensive withdrawal

Sublingual captopril and nifedipine


55/77

Abdominal pain, acute diarrhea Dialysis hypotension

Digitalis, bblockers Occlusive and non-occlusive infarction (25 to

60%) Congestive heart failure Cardiac arrhythmia (esp. AF) Hyperkalemia, acidemia, leukocytosis

elevated LDH and CPK

T bl L ti f M t i I f ti


56/77

Table. Location of Mesenteric Infarction

Location No. of Patients (n=12)

Small bowel 1Colon 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, 198


57/77

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


58/77

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


59/77

Treat the symptoms:

HypotensionAngina pain with Nitroglycerin

MI pain requires analgesics

Anxiety/stress

Prevention

Accurate fluid removal and weight assessment


60/77


61/77

the most frequent long-termcomplications occurring in HD patientsrelate to cardiovascular disease,

2-microglobulin (2M) amyloidosis,

renal osteodystrophy and

the effects of malnutrition.


62/77

the major cause of death in ESRD patients

atherosclerosis is present in all long-term dialysispatients.

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


63/77

Increasing numbers of dialysis patients are

requiring coronary artery bypass surgery, but thepost-operative mortality with this is more thanthree times that of patients who do not have ESRD.

Hypertension is a major risk factor for

cardiovascular disease

and is often poorlycontrolled.

Some of the other risk factors include


64/77

hyper-phosphatemia

elevated calcium-phosphorus product with calcium

deposition in the coronary arteries, the cardiac conductionsystem,heart valvesand 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]
http://www.sjkdt.org/article.asp?issn=1319-2442;year=2001;volume=12;issue=4;spage=487;epage=493;aulast=Blagghttp://www.sjkdt.org/article.asp?issn=1319-2442;year=2001;volume=12;issue=4;spage=487;epage=493;aulast=Blagg


65/77

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 ofreducing oxidative stress and cardiovascularmortality.

An interesting ongoing study is a multicentercontrolled trial of a new statin, Cerivastatin, thatlowers LDL-cholesterol and may have anti-

inflammatory and other effects.

Preventions of bone mineral ds:


66/77

Preventions of bone mineral ds: using low calcium dialysate,

selective vitamin D analogues,

calcium-free phosphate binders and otherimprovements in the management of bone diseaseand vascular disease.

The use of erythropoietin to correct anemia in

dialysis patients and thus improve cardio-vascular dynamics and exercise tolerance.


67/77

The importance of hyper-homocysteinemia is

uncertain. Tx : dialysis using synthetic membranes,and

supplementation with folic acid, vitamins B6and B12, betaine and serine.

lowering homocysteine not shown to affectendothelial dysfunction, but because folic acid ischeap and harmless, its use might be consideredlarge doses are required because high-flux and

high-efficiency dialyzers remove folic acid.


68/77

a major cause of the physical handicaps affecting

the quality of life of patients who have been ondialysis for ten or more years, and is occasionallylife threatening if it results in severe cervical spinalcord compression.

Deposits begin a few months of starting HD,although clinical and radiological findings do notbegin to appear for five years or more.

Any or all joints may be affected, but especially thesternoclavicular joint and hips.

Clinical features


69/77

Clinical features periarthritis of the shoulders, carpal

tunnel syndrome, flexor tenosynovitisof the hands, stiffness, pain andswelling of other joints, depositsbeneath the skin and

spondyloarthropathy

The pathogenesis of Mamyloidosis is complex and poorly

understood.


70/77

There is no specific treatment for 2M--

amyloidosis. Transplantation will lower 2M levels and may

halt progression of amyloidosis and easesymptoms.

no modality of dialysis can remove more 2Mthan is generated, although removal is greaterwith biocompatible membranes and withhemofiltration and hemodiafiltration


71/77

the other major cause of serious morbidityin longterm dialysis patients.

is the increase in parathyroid hormonewith time on dialysis, an increase that issignificant even after adjusting for calcium

and phosphorus concentrations and otherfactors

f


72/77

hip fractures in dialysis patients ~ osteo-dystrophy

management of calcium and phosphorusmetabolism and availability of newphosphate binders and other drugsosteo-dystrophy and complications related to

calcification may be better controlled in thefuture.


73/77

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 beginsto decline during the second decade of treatment.

might relate to chronic mild metabolic acidosis orto reduced physical activity as a result of 2M-amyloidosis.


74/77

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 ofbody weight per day

Recommended daily energy intake:


75/77

g 35 kcal/kg of body weight per day for people aged

60 years

30 to 35 kcal/kg of body weight per day for peopleaged 60 years

Increased resting energy expenditure

Amino acid losses in dialysate:

5 to 8 g of free amino acids per dialysis session withlow-flux dialyzers

30% greater amino acid losses withigh-flux dialyzers


76/77

Initiation of hemodialysis (can increase

serum albumin and IGF-1 levels and bodymass)

Oral nutritional supplementation

Intradialytic parenteral nutrition

Vitamin and trace elementsupplementation


77/77

acute n chronic complication of hd.yenny.ppt

Documents