renal failure complicatio1

BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014

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

1 MAGDI AWAD SASI 2014 RF COMPLICATIONS


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

DepressionAnxietyUncooperative behaviorSuicidal behaviorPsychosis---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----



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 eveningBurning 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 pericardiumFactors contributing to it in pts with renal failure:

1. 1Late start or inadequate H.D.2. Retained uremic toxins3. loss of residual renal function4. Parathyroid hormone



5. Underlaying systemic disease6. Infection ,viral ,bacterial ,TB7. Platelet dysfunction with pericardial bleeding8. 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



PREVENTION :

1. Analgesic (aspirin should be avoided )2. Intrapericardial injection of NSAIDS3. 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 failure2. Myocardiac infarction/angina3. 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



MANAGEMENT:

A. Risk factor intervention:1. Blood pressure control2. Reduction in serum lipid3. Cessation of smoking 4. LV hypertrophy intervention

B. Uremia related intervention:1. Erythropoietin2. Prevention and treatment of hyperparathyroidism3. Adequate dialysis4. Prevention of malnutrition5. 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.



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/minAnemia in CRF precipitate many of the symptoms previously attributed to uremia and is more disabiling than is generally appreciated.

Pathophysiology:

1. Relative erthropiotein deficiency2. Shortened RBC survival3. Bone marrow inhibition4. Bleeding with platelet dysfunction

TREATMENT:

1.Folic acid ,Iron , Androgen -----------mild anemia2.Packed RBCs -----------------------------severe anemia3.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:-



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 bagsEffect –start 1hr over , maximum 4-12 hr ,24-36hr

2. DSMOPRESSIN—dose 0.3 micgm/kg IV , 3MICGM/KG INTRANASALSTART 1hr ,maximum 2-4 hr , end 6-8hr

Conjugated estrogen : 3mg/kg IV in 5 daily infusionStart – 6 hours , max 5-7 days and 21 – 30 daysThis 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 :



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:



In CRF , nephrogenic or idiopathic dialysis ascitis

6. Metabolic and endocrine complication:I. Glucose and insulin metabolism:

Characteristic features:1. Normal fasting blood suger2. Spontanous hypoglycemia3. Fasting hyperinsulinemia4. Normal , elevated or decrease blood insulin in response to hyperglycemia. 5. Impaire insulin secretion by pancreatic cells6. 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. Hyperphosphatemia2. Hypocalcemia3. Secondary hyperparathyroidism4. Defective intestinal absorption of calcium5. Altered vit D metabolism6. Bone disease



7. Soft tissue calcification8. Pruritis9. Proximal myopathy10. Skin ulceration and soft tissue necrosis

CRF---almost always have secondary hyperplasia of parathyroids (PTH)due to hypocalcemia.

1. Hyperphostemia2. Bone resistant to PTH

3. Abnormal vit D metabolismBone disease -----Two major types of bone disease are:1. Enhanced bone resorption2. 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 adultC. 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 ,clavicleNo specific changes in s.ca , po4 ,or ALPOsteosclerosis can be induced by excess PTH as pt with primary hyperparathyroidism display radiological evidence of osteosclerosisOsteoporosis---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 toA. Increase in CA , PO4 production in serumB. Secondary hyperparathyroidismC. Local tissue injuryD. Rise in local PH of tissue

8. Pruritis :Is common in patient with CRFIT USUALLY IMPROVES OR DISSAPPEAR WITH ADEQUTE HEMODIALYSIS.Resistant pruritis

Preventation:



The goals of therapy in pt with osteodystrophy w RF are:1. Maintain blood concentration of CA &PO4 as near normal as possible2. To prevent the development of 2ry hyperparathyroidism3. To heal bone disease 4. To prevent and reverse soft tissue calcification

Therapeutic approaches to be done are:

A. Supplementation of CAB. Treatment with VIT DC. Control of phosphate retention and hyperphosphatemia

Diet ,use of phosphate binder , increase frequency of dialysis.


renal failure complicatio1

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