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Renal failure complicatio1


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Renal failure complicatio1

  1. 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. 2. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 2 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 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. 3. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 3 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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
  4. 4. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 4 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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. 5. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 5 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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
  6. 6. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 6 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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.
  7. 7. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 7 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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. 8. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 8 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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. 9. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 9 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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. 10. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 10 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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
  11. 11. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 11 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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 , 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:
  12. 12. BY DR . MAGDI AWAD SASI RF COMPLICATIONS 2014 12 MAGDI AWAD SASI 2014 RF COMPLICATIONS 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.