TO THE SOUL OF THE PEOPLE WHO DREAMS BETTER DAYS AND PERFECT FUTURE WHO DIED THINKING THAT LIBYA IS WORTHY NOT THE LIBYAN HOPPING OUR ALLAH ACCEPT THIS SMALL WORK

1. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
1 MAGDI AWAD SASI 2014 RF COMPLICATIONS
Renal failure complication
ARF:
METABOLIC:-
 Hyponatremia
 Hyperkalemia
 Hypocalcemia, hyperphosphatemia
 Hypermagnesemia
 Hyperuricemia
CARDIO VASCULAR:
 Pulmonary edema
 Arrhythmia hypertension
 Pericarditis
NEUROLOGIC
 Asterixis
 Neuromuscular irritability
 Somnolence
 Coma
 Seizures
HEMATOLOGIC
 Anemia
 Coagulopathies
 Hemorrhagic diathesis
GASTROINTESTINAL
 Nausea
 vomiting
INFECTIOUS
Pneumonia UTI
Wound infection septicemia

2. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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1.CENTRAL AND PERIPHERAL N. S. IN UREMIA:
A.PSYCHATRIC COMPLICATION:
Organic mental disorder----
Affect cognitive function or delirium ,dementia or pure psychiatric illness
Differentiated from other psychiatric illness
This is known metabolic problem with impaired intellectual (cognitive)function
Depression
Anxiety
Uncooperative behavior
Suicidal behavior
Psychosis---mainly in dialysis but not more than other medical/surgical
problems.
Sexual disorder ----more than other medical or surgical
PREVENTIVE MEASURES:
 Discussion with the patient
 Use of psychotropic medication:
Metabolism (lithium, barbiturate) , dose ,anxylotic, antidepresent
 Psychotherapy—
B.BRAIN ABNORMALITIES:
 Uremic encephalopathy- acute symptoms and signs of confusion due to
dialysis after the first session due to disequilibrium
 Dialysis dementia ----progressive ,frequently fatal , chronic dialysis more
than 2 years .
 Disequilibrium :
Most common among younger patient.
More common in patient with preexsisting neurologic disease as head
trauma ,recent stroke, malignant HTN.
TREATMENT----

3. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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Preventive –by adding osmotically active solute or exchange of
bicarbonate for acetate.
Hem filtration , slow hemodialysis ,peritoneal dialysis
C. PERIPHERAL NEUROPATHY:
 sensory motor neuropathy, upto 65%
 cant be differentiated fro other causes of peripheral neuropathy i.e.
diabetes mellitus ,alcoholic , vitamins deficiencies
 No relation to type of underlying renal disease.
 Mainfestation:
Restless leg syndrome—prickling sensation, pruritis, worse distally,
prominent at evening
Burning food syndrome—10%, swelling and tenderness of distal L.L.
O/E:
 Loss of deep tendon reflexes ((knee ,ankle ))
 Impaired vibration sense
 Stoking glove anesthesia
Cranial nerve neuropathy---nerves of eye muscles ,miosis ,nystagmus ,7th
8th
palsy
D. AUTONOMIC NEUROPATHY---
 Defection sweat GIT
 Orthostatic hypotension
 Impotence
 Arrhythmia
 Dysfunction of GIT motility
2. CARDIOVASCULAR COMPLICATIONS:
A. Percarditis--- inflammation of pericardium
Factors contributing to it in pts with renal failure:
1. 1Late start or inadequate H.D.
2. Retained uremic toxins
3. loss of residual renal function
4. Parathyroid hormone

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5. Underlaying systemic disease
6. Infection ,viral ,bacterial ,TB
7. Platelet dysfunction with pericardial bleeding
8. Anticoagulants
Clinical features:
Symptoms –chest pain ,dyspnea ,irregular heart beats ,loss of pulse in fistula
,orthostatic dizziness ,decrease urine out put ,rapid weight gain.
Signs --------- fever ,mental confusion ,pericardial friction ,edema ,anasarca ,
hypotension ,pulsus paradoxus ,distention of neck veins
Lab results-----enlarged cardiac size ((CXR)) ,leucocytosis , ECG arrhythmia,
pericardial effusion (aspiration) ,cardiac tamponade.
Complication: Constrictive pericarditis
Treatment : UREMIC PERICARDITIS
No effusion or only minimal effusion Significant effusion
Initiate dialysis Hemodynamically stable H. unstable
If on dialysis ,increase frequency/duration
Intensive dialysis
Resolution unchanged 10 -14 dialysis
PERICARDIOTOMY

5. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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PREVENTION :
1. Analgesic (aspirin should be avoided )
2. Intrapericardial injection of NSAIDS
3. Percardiotomy
B. Cardiomyopathy:
Cardiac disease has a major impact on both morbidity and mortality.
Chronic uremia –its manifestation are often present when patient begins
dialysis therapy.
Manifestation of cardiac disease on starting drug therapy
1. Congestive cardiac failure
2. Myocardiac infarction/angina
3. Dysarrhythmia requiring treatment
ECG changes--- Q wave ,ST-T wave changes
ECHO----Abnormal cardiac dimension ,cardiac myopathy ,systolic failure .L.V. hypertrophy.
POTENTIAL RISK FACTORS PREDISPOSING TO CMP & IHD IN DIALYSIS PATIENTS
 HTN HYPERPARATHYRODISM
HYPERLIPIDEMIA
 ANEMIA SMOKING HTN
 FISTULA UREMIA LVH
 UREMIA ANEMIA
LVH DILATED CRDIOMYOPATHY IHD
CCF , ARRHYTHMIA ,CARDIAC ARREST MI
DEATH

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MANAGEMENT:
A. Risk factor intervention:
1. Blood pressure control
2. Reduction in serum lipid
3. Cessation of smoking
4. LV hypertrophy intervention
B. Uremia related intervention:
1. Erythropoietin
2. Prevention and treatment of hyperparathyroidism
3. Adequate dialysis
4. Prevention of malnutrition
5. Choice of ESRD treatment modality
DILATED CMP L.V. hypertrophy ,normal systolic function
 DIGOXIN , ACEI BP control
 Vasodilators EPO Avoid digoxin & vasodilator w increase contract
 salt & H2O removal
3.PULMONARY COMPLICATIONS OF UREMIA:
Uremic lung
Effect of uremia on PFT—
 Decrease in vital capacity – mild restriction in vital capacity ---mild restriction
 No evidence of obstruction features , negative correlation between diffusion capacity
(DL co) and blood urea.
 Pulmonary infection ----major cause of death in ARF
 IN CRF -----------------------pulmonary infection increase mobidity & mortality
 Uremic pleuritis---------- PLEURAL EFFUSION 20% --DX by exclusion
Usually clear ,occasionally bloody especially in dialysis pt. we may use surgical
decortications.
 Chronic pulmonary changes---increased incidence of interstitial fibrosis ,pleural
fibrosis ,pulmonary arteriosclerosis &calcification.

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4. Hemopoietic system in uremia:
Anemia ,bleeding , echymosis
A. Anaemia:
Is the most common complication of R.F.
Anemia developed when creatinine clearance dropped to 30ml/min
Anemia in CRF precipitate many of the symptoms previously attributed to uremia and
is more disabiling than is generally appreciated.
Pathophysiology:
1. Relative erthropiotein deficiency
2. Shortened RBC survival
3. Bone marrow inhibition
4. Bleeding with platelet dysfunction
TREATMENT:
1.Folic acid ,Iron , Androgen -----------mild anemia
2.Packed RBCs -----------------------------severe anemia
3.Recombinent Erythropoietin (r Hu EPO –185a.a ) –no allergy
 Clear dose- response relation ship – IV ,SC ,IM
 Target HCT ---30%---- higher level is better .
 Positive response –lead to dramatic change in CRF TR .
 Few show failure to response to EPO ---initially and then acquire refractory
response and need increasing dosages.
 Mostly , those patients are iron deficient & respond probably after transfusion.
 If iron store repletedand no response , other factors should be searched for like severe
hyperparathyroidism ,inflammatory diseases.
 Side effects:
Increase blood volume , myalgia , flu like syndrome, accelerated HTN , seizure.
B. Bleeding and coagulation abnormalities:
Usually mild ----ecchymosis , purpura
Sometimes severe –epistaxis ,hemorrhagic pericarditis ,GIT hemorrhage or intracranial.
Causer:-

8. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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Platelets dysfunction ,anemia ,abnormal platelets vessels interaction.
Management----- two approaches:
a.prevention of bleeding in pt at high risk B/C of invasive punctures or surgery.
By ---1. RBC transfusion
Dose ---depend on severity of anemia
Effect --- continue till RBC life span
Aim----PCV 30% more
2. R Hu ERP
Dose ---50u/kg IV
Start when PCV 27%
Pts with ACTIVE BLEEDI NG:
1. CRYOPRECIPITATE – dose 10 bags
Effect –start 1hr over , maximum 4-12 hr ,24-36hr
2. DSMOPRESSIN—dose 0.3 micgm/kg IV , 3MICGM/KG INTRANASAL
START 1hr ,maximum 2-4 hr , end 6-8hr
Conjugated estrogen : 3mg/kg IV in 5 daily infusion
Start – 6 hours , max 5-7 days and 21 – 30 days
This is used when long lasting effect is required or major surgery.
5. Gastrointestinal complication:
A. Oropharynx and esophageal :
Candidiasis ,esophageal infection ,herpes ( TR , TR OF rejection)
B.Stoamch and duodenum :
Gastritis ,duodenitis ,edema ,moility disorder ,PUD 60%
C.Small intestine :

9. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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Decrease villous height ,increase inflammatory cells ,no effect on absorption.
Changes due to toxin ,bacteria of moutha and intestine , VIT D deficiency
D.Large intestine :
Uremic colitis is rare now
Now ,non specific ulcers ,fecal impaction ,angiodysplastic ,diverticulosis—80%
E.Liver :
Hepatic dysfunction is common . it is due to viral hepatitis , hypervolemia, drug
intoxication ,hypoxia
Hepatitis ---
It is of interist B/C patient with ESRD vulnerable to suffer from acute or chronic
hepatitis .
Causes – different causes especially viral cause . It may be source for transmission to
other PATIENTS OR STAFF.
Common viruses-----A B C D E , EBV , CMV or drugs and toxins
HAV---- no risk for patients and staff
HBV—from a significant risk for the patients and staff. Patients with HBV should have
a separate machine for dialysis.
HDV --- usually with HBV infection
HCV--- a common problem now days (( non A non B hepatitis )) . It is a cause of
chronic liver disease .
F.Pancrease:
Changes occur and correlate with duration of CRF.
Pancreatitis –occur more frequently in dialysis patients due to hyperparathyroidism ,
hypercalcemia ,elevted choleytokinin
G. Ascitis:

10. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014
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In CRF , nephrogenic or idiopathic dialysis ascitis
6. Metabolic and endocrine complication:
I. Glucose and insulin metabolism:
Characteristic features:
1. Normal fasting blood suger
2. Spontanous hypoglycemia
3. Fasting hyperinsulinemia
4. Normal , elevated or decrease blood insulin in response to hyperglycemia.
5. Impaire insulin secretion by pancreatic cells
6. Decrease peripheral sensitivity to insulin action.
7. Decrease insulin requirement in diabetic
II. Lipid metabolism:
Present even with only moderate degree of renal failure –not correlate by H.D.
1.Hypertriglycedemia:--most common ,due to accumulation of VLDL 80%
Decrease GFR ====== increase TG
2.S.cholestrol :-- in contrast to TG , total amount normal or slightly increased but
fractions of cholesterol LDL normal but HDL is decreased.
III. Thyroid hormone metabolism:
A.Hypothyrodism-------------------------9.5%
B.Hyperthyrodism-------- similar to general population
Therapy should be reserved for patient with documented hypothyroidism.
7. Divalent Iron metabolism and renal osteodystrophy:
Major disorder in renal failure:
1. Hyperphosphatemia
2. Hypocalcemia
3. Secondary hyperparathyroidism
4. Defective intestinal absorption of calcium
5. Altered vit D metabolism
6. Bone disease

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7. Soft tissue calcification
8. Pruritis
9. Proximal myopathy
10. Skin ulceration and soft tissue necrosis
CRF---almost always have secondary hyperplasia of parathyroids (PTH)due to hypocalcemia.
1. Hyperphostemia
2. Bone resistant to PTH
3. Abnormal vit D metabolism
Bone disease -----
Two major types of bone disease are:
1. Enhanced bone resorption
2. Defective mineralization
A. Osteoclastic process due to increase PTH ----lead to excess resorption ---- marked
fibrosis in bone marrow ------OSTEITIS FIBROSA CYSTICA
B. Defective mineralization & osteitis leads to rickets in children &osteomalacia in adult
C. Osteosclerosis -----increase bone density in x rays due to accumulation of mineralized
trabecular bone with total increase in bone mass.
So , mostly seen in vertebrae ,pelvis ,ribs ,clavicle
No specific changes in s.ca , po4 ,or ALP
Osteosclerosis can be induced by excess PTH as pt with primary hyperparathyroidism
display radiological evidence of osteosclerosis
Osteoporosis---decrease in the mass of normally minerailized bone.
It is a frequent in renal failure.
Immbolization & CA deficiency & chronic protein depletion may be the cause of
osteoporosis.
Soft tissue calcification--- due to
A. Increase in CA , PO4 production in serum
B. Secondary hyperparathyroidism
C. Local tissue injury
D. Rise in local PH of tissue
8. Pruritis :
Is common in patient with CRF
IT USUALLY IMPROVES OR DISSAPPEAR WITH ADEQUTE HEMODIALYSIS.
Resistant pruritis
Preventation:

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The goals of therapy in pt with osteodystrophy w RF are:
1. Maintain blood concentration of CA &PO4 as near normal as possible
2. To prevent the development of 2ry hyperparathyroidism
3. To heal bone disease
4. To prevent and reverse soft tissue calcification
Therapeutic approaches to be done are:
A. Supplementation of CA
B. Treatment with VIT D
C. Control of phosphate retention and hyperphosphatemia
Diet ,use of phosphate binder , increase frequency of dialysis.