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BY PINKY RATHEE
M.Sc. Nursing
CHRONIC RENAL
FAILURE
DEFINITION
CHRONIC RENAL FAILURE (CRF) or
CHRONIC KIDNEY DISEASE (CKD)
Chronic or irreversible renal failure is a
progressive reduction of functioning of renal
tissue such that the remaining kidney mass
can no longer maintain the body’s internal
environment.
ETIOLOGY AND RISK FACTORS OF CRF
CRF may result from an episode or acute
renal failure or it may develop insidiously
over many years.
Obstruction
Nephro-toxins
Acute renal failure
Polycystic kidney disease
CONT…
 Chronic glomerulonephritis
 Repeated episodes of poly-nephritis
 Systemic disease- diabetes mellitus,
hypertension, systemic lupus
erythematous, poly-arteritis
sickle cell disease,
amyloidosis.
STAGES OF CHRONIC KIDNEY DISEASE
STAGES 1 WITH NORMAL
OR HIGH GFR
>90 ml/min.
STAGE 2 MILD CKD 60-90 ml/min.
STAGE 3 A
STAGE 3 B
MODERATE
CKD
45-59ml/min.
30-44ml/min.
STAGE 4 SEVERE CKD 15-29ml/min.
STAGE 5 END STAGE
CKD
<15ml/min.
PATHOPHYSIOLOGY OF
CHRONIC RENAL FAILURE
PATHOPHYSIOLOGY
Decreased renal
blood flow, primary
kidney disease,
damage from other
disease, urine outflow
obstruction
Decreased glomerular
filteration rate
Hypertrophy of
remaining nephrons
Inability to
concentrate urine
Further loss of
nephron function
Loss of excretory
renal function and
non excretory renal
function
LOSS OF EXCRETORY RENAL FUNCTIONS
• DECREASED LIBIDO
• INFERTILITY
DISTURBANCES IN
REPRODUCTION
• DELAYED HEALING
• INFECTION
IMMUNE DISTURBANCES
• ADVANCED ATHEROSCLEROSISINCREASED PRODUCTION
OF LIPIDS
• ERRATIC BLOOD GLUCOSE LEVELIMPAIRED INSULIN ACTION
• ANEMIA, PALLORFAILURE TO PRODUCE
ERYTHROPOIETIN
• DECREASED CALCIUM ABSORPTION:-
OSTEODYSTROPHYAND HYPOCALCEMIA
FAILURE TO CONVERT
INACTIVE FORMS OF
CALCIUM
LOSS OF NON-EXCRETORY RENAL FUNCTIONS
• METABOLIC ACIDOSIS
DECREASED HYDROGEN
SECRETION AND DECREASED
BICARBONATE
REABSORPTION
• HYPERPHOSPHATEMIA→DECREASED CALCIUM ABSORPTION→
HYPOCALCEMIA→ HYPER-PARATHYROIDISM→ DECREASED POTASSIUM
EXCRETION→ HYPERLKALEMIA
DECREASED PHOSPHATE
EXCRETION
• HYPERKALEMIA
DECREASED POTASSIUM
EXCRETION
• WATER RETENTION CAUSING
• HYPERTENSION, HEART FAILURE, EDEMA
DECREASED SODIUM
REABSORPTION IN TUBULE
• UREMIA CAUSING
• INCREASED BUN, CREATININE, URIC ACID, PROTEINURA, PERIPHERAL
NERVE CHANGES, PERICARDITIS, PRURITIS, CNS CHANGES, BLEEDING
TENDENCIES
DECREASED EXCRETION OF
NITROGENOUS WASTE
CLINICAL MANIFESTATION OF
CHRONIC RENAL
FAILURE
 INTEGUMENTORY CHANGES:-
SKIN-VERY DRY BECAUSE OF ATROPHY OF SWEAT GLAND.
PRURITIS-EXCORIATED SKIN.
SKIN COLOR-UROCHROMS PIGMENTS.
MUEHRCKE’S LINE
UREMIC FROST
 MUSCULOSKELETAL CHANGES
• RENAL OSTEODYSTROPHY
OSTEOPOROSIS
OSTEOSCLEROSIS
OSTEOMALACIA
OSTEITIS FIBROSA
 HEMATOLOGIC CHANGES
ANEMIA, FATIGUE,
WEAKNESS, COLD
INTOLERANCE AS KIDNEYS
ARE TO PRODUCE
ERYTHROPOIETIN.
HEMOLYSIS, CLOTTING
ABNORMALITIES.
BLEEDING TENDENCIES AS
ACCUMULATION OF
UREMIC INTERFERE WITH
PLATLET ADHESIVENESS.
 IMMUNOLOGIC CHANGES
MORE
SUSCEPTIBLE TO
INFECTION.
SUPRESSION OF
DELAYED
HYPERSENSITIVITY.
 METABOLIC CHANGES
NORMAL RATIO OF BUN TO CREATININE IS 10:1
HYPOPROTEINURIA
INCREASED SERUM URIC ACID
CARBOHYDRATE INTOLERANCE
METABOLIC ACIDOSIS AS KIDNEYS FAIL TO EXCRETE
HYDROGEN IONS.
 CHANGES IN MEDICATION
TOXICITY
• MEDICATION TOXICITY
 CARDIO-VASCULAR CHANGES
HYPERTENSION
ATHEROSCLEROSIS
LEFT VENTRICULAR DYSTROPHY AND HEART
FAILURE DUE TO VOLUME OVERLOAD.
ACCELERATED DUE TO ABNORMAL LIPID
METABOLISM, ARTERIAL CALCIFICATION.
 RESPIRATORY CHANGES
PULMONARY EDEMA.
UREMIC LUNG
METABOLIC ACIDOSIS AS A RESULT OF
RESPIRATORY CHANGES TO HYDROGEN IONS.
 GASTROINTESTINAL CHANGES
ANOREXIA, NAUSEA, VOMITING
CONSTANT BITTER, METALLIC OR SALTY TASTE
EXPERIENCED.
BREATH- UREMIC FETOR, AMMONIA, FISHY LIKE SMELL.
CONSTIPATION, ULCER.
 REPRODUCTIVE CHANGES
• MENSTURAL IRREGULARITY
• AMENORRORHEA, IMPOTENCE.
ENDOCRINE CHANGES
• HYPOTHYROIDISM
 NEUROLOGIC CHANGES
• PERIPHERAL NEUROPATHY- BURNING
FAT, GAIT CHANGES, PARAPLEGIA.
• IMPAIRED COGNITIVE FUNCTION.
PSYCHOLOGICAL CHANGES
• FINANCIAL STRESS
• LIFE-STYLE CHANGES
DIAGNOSTIC TEST
FOR
CHRONIC RENAL FAILURE
MEDICAL MANAGEMENT
OF CHRONIC RENAL
FAILURE
MEDICAL MANAGEMENT OF CRF
• HYPERKALEMIA
• PERICARDITIS
• HYPERTENSION
• ANEMIA
PREVENT
COMPLICATIONS-
ADMINISTRATION OF:-
ANTI-HYPERTENSIVES
ERYTHROPOIETIN
IRON SUPPLEMENTS
PHOSPHATE BINDING AGENTS
CALCIUM SUPPLEMENTS
ADEQUATE DIALYSIS
DIETARY INTERVENTIONS:-
• FLUID ALLOWANCE 500-600ml MORE
THAN THE PREVIOUS DAY 24hrs. URINE
OUTPUT.
• CARBOHYDRATE & FAT INTAKE 40-
50kcal/kg/day.
• DIET RESTRICTION PROTEIN 1g/kg/day.
• VITAMIN SUPPLEMENTS.
• DIALYSIS
THERAPY
• POTASSIUM
REMOVAL
• POTASSIUM
RESTRICTED
DIET
(KAYEXALATE)
HYPERKALEMIA:-
HYPERPHOSPHATEMIA &
HYPOCALCEMIA PREVENTION &
TREATMENT:-
ALUMINIUM BASED ANTACIDS.
CARBONATE-CARBONATE AND
PHOSPHATE BINDING ANTACIDS.
NEUROLOGICAL ABNORMALITIES
• OBSERVE FOR SLIGHT TWITCHING,
HEADACHE, DELIRIUM, SEIZURES.
• IV DIAZEPAM OR PHENYTOIN.
ANEMIA
• EPOGEN (RECOMBINANT HUMAN
ERYTHROPOIETIN)
SURGICAL
MANAGEMENT
.
1. FLUID VOLUME EXCESS
RELATED TO DECREASED URINE
OUTPUT, DIETARY EXCESS &
RETENSION OF SODIUM AND
WATER SECONDARY TO DISEASE
PROCESS.
2. ALTERED NUTRITION LESS
THAN BODY REQUIREMENT
RELATED TO ANOREXIA, NAUSEA,
VOMITING, DIETARY RESTRICTION,
ALTERED ORAL MUCUS
MEMBRANES SECONDARY TO
DISEASE PROCESS.
3. ACTIVITY INTOLERANCE
RELATED TO FATIGUE,
RETENTION OF WASTE
PRODUCT AND DIALYSIS
PROCEDURES SECONDARY
TO CHRONIC RENAL FAILURE.
4. SELF-ESTEEM DISTURBANCE
RELATED TO DEPENDANCY,
ROLE CHANGE, CHANGE IN
BODY IMAGE AND CANGE IN
SEXUAL FUNCTION SECONDARY
TO DISEASE PROCESS.
5. RISK FOR HYPERKALEMIA,
PERICARDITIS, PERICARDIAL
EFFUSION, PERICARDIAL
TEMPONATE, HYPERTENSION,
ANEMIA, BONE DISEASE,
METASTATIC CALCIFICATION
RELATED TO DISEASE PROCESS.
6. KNOWLEDGE DEFICIT
REGARDING CONDTION
AND TREATMENT
MODALITIES RELATED
TO DISEASE PROCESS.
7. RISK FOR
IMPAIRED SKIN
INTEGRITY RELATED
TO EDEMA, DRY SKIN
AND PRURITIS
8. RISK OF INFECTION
RELATED TO INDEWELLING
PERITONEAL CATHETER,
VENI-PUNCTURE
CONNECTION OF TUBING
DURING HEMODIALYSIS.
,

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Chronic renal failure

  • 1. BY PINKY RATHEE M.Sc. Nursing CHRONIC RENAL FAILURE
  • 2. DEFINITION CHRONIC RENAL FAILURE (CRF) or CHRONIC KIDNEY DISEASE (CKD) Chronic or irreversible renal failure is a progressive reduction of functioning of renal tissue such that the remaining kidney mass can no longer maintain the body’s internal environment.
  • 3. ETIOLOGY AND RISK FACTORS OF CRF CRF may result from an episode or acute renal failure or it may develop insidiously over many years. Obstruction Nephro-toxins Acute renal failure Polycystic kidney disease
  • 4. CONT…  Chronic glomerulonephritis  Repeated episodes of poly-nephritis  Systemic disease- diabetes mellitus, hypertension, systemic lupus erythematous, poly-arteritis sickle cell disease, amyloidosis.
  • 5. STAGES OF CHRONIC KIDNEY DISEASE STAGES 1 WITH NORMAL OR HIGH GFR >90 ml/min. STAGE 2 MILD CKD 60-90 ml/min. STAGE 3 A STAGE 3 B MODERATE CKD 45-59ml/min. 30-44ml/min. STAGE 4 SEVERE CKD 15-29ml/min. STAGE 5 END STAGE CKD <15ml/min.
  • 7. PATHOPHYSIOLOGY Decreased renal blood flow, primary kidney disease, damage from other disease, urine outflow obstruction Decreased glomerular filteration rate Hypertrophy of remaining nephrons Inability to concentrate urine Further loss of nephron function Loss of excretory renal function and non excretory renal function
  • 8. LOSS OF EXCRETORY RENAL FUNCTIONS • DECREASED LIBIDO • INFERTILITY DISTURBANCES IN REPRODUCTION • DELAYED HEALING • INFECTION IMMUNE DISTURBANCES • ADVANCED ATHEROSCLEROSISINCREASED PRODUCTION OF LIPIDS • ERRATIC BLOOD GLUCOSE LEVELIMPAIRED INSULIN ACTION • ANEMIA, PALLORFAILURE TO PRODUCE ERYTHROPOIETIN • DECREASED CALCIUM ABSORPTION:- OSTEODYSTROPHYAND HYPOCALCEMIA FAILURE TO CONVERT INACTIVE FORMS OF CALCIUM
  • 9. LOSS OF NON-EXCRETORY RENAL FUNCTIONS • METABOLIC ACIDOSIS DECREASED HYDROGEN SECRETION AND DECREASED BICARBONATE REABSORPTION • HYPERPHOSPHATEMIA→DECREASED CALCIUM ABSORPTION→ HYPOCALCEMIA→ HYPER-PARATHYROIDISM→ DECREASED POTASSIUM EXCRETION→ HYPERLKALEMIA DECREASED PHOSPHATE EXCRETION • HYPERKALEMIA DECREASED POTASSIUM EXCRETION • WATER RETENTION CAUSING • HYPERTENSION, HEART FAILURE, EDEMA DECREASED SODIUM REABSORPTION IN TUBULE • UREMIA CAUSING • INCREASED BUN, CREATININE, URIC ACID, PROTEINURA, PERIPHERAL NERVE CHANGES, PERICARDITIS, PRURITIS, CNS CHANGES, BLEEDING TENDENCIES DECREASED EXCRETION OF NITROGENOUS WASTE
  • 11.  INTEGUMENTORY CHANGES:- SKIN-VERY DRY BECAUSE OF ATROPHY OF SWEAT GLAND. PRURITIS-EXCORIATED SKIN. SKIN COLOR-UROCHROMS PIGMENTS. MUEHRCKE’S LINE UREMIC FROST
  • 12.  MUSCULOSKELETAL CHANGES • RENAL OSTEODYSTROPHY OSTEOPOROSIS OSTEOSCLEROSIS OSTEOMALACIA OSTEITIS FIBROSA
  • 13.  HEMATOLOGIC CHANGES ANEMIA, FATIGUE, WEAKNESS, COLD INTOLERANCE AS KIDNEYS ARE TO PRODUCE ERYTHROPOIETIN. HEMOLYSIS, CLOTTING ABNORMALITIES. BLEEDING TENDENCIES AS ACCUMULATION OF UREMIC INTERFERE WITH PLATLET ADHESIVENESS.
  • 14.  IMMUNOLOGIC CHANGES MORE SUSCEPTIBLE TO INFECTION. SUPRESSION OF DELAYED HYPERSENSITIVITY.
  • 15.  METABOLIC CHANGES NORMAL RATIO OF BUN TO CREATININE IS 10:1 HYPOPROTEINURIA INCREASED SERUM URIC ACID CARBOHYDRATE INTOLERANCE METABOLIC ACIDOSIS AS KIDNEYS FAIL TO EXCRETE HYDROGEN IONS.
  • 16.  CHANGES IN MEDICATION TOXICITY • MEDICATION TOXICITY
  • 17.  CARDIO-VASCULAR CHANGES HYPERTENSION ATHEROSCLEROSIS LEFT VENTRICULAR DYSTROPHY AND HEART FAILURE DUE TO VOLUME OVERLOAD. ACCELERATED DUE TO ABNORMAL LIPID METABOLISM, ARTERIAL CALCIFICATION.
  • 18.  RESPIRATORY CHANGES PULMONARY EDEMA. UREMIC LUNG METABOLIC ACIDOSIS AS A RESULT OF RESPIRATORY CHANGES TO HYDROGEN IONS.
  • 19.  GASTROINTESTINAL CHANGES ANOREXIA, NAUSEA, VOMITING CONSTANT BITTER, METALLIC OR SALTY TASTE EXPERIENCED. BREATH- UREMIC FETOR, AMMONIA, FISHY LIKE SMELL. CONSTIPATION, ULCER.
  • 20.  REPRODUCTIVE CHANGES • MENSTURAL IRREGULARITY • AMENORRORHEA, IMPOTENCE. ENDOCRINE CHANGES • HYPOTHYROIDISM
  • 21.  NEUROLOGIC CHANGES • PERIPHERAL NEUROPATHY- BURNING FAT, GAIT CHANGES, PARAPLEGIA. • IMPAIRED COGNITIVE FUNCTION. PSYCHOLOGICAL CHANGES • FINANCIAL STRESS • LIFE-STYLE CHANGES
  • 24. MEDICAL MANAGEMENT OF CRF • HYPERKALEMIA • PERICARDITIS • HYPERTENSION • ANEMIA PREVENT COMPLICATIONS-
  • 25. ADMINISTRATION OF:- ANTI-HYPERTENSIVES ERYTHROPOIETIN IRON SUPPLEMENTS PHOSPHATE BINDING AGENTS CALCIUM SUPPLEMENTS ADEQUATE DIALYSIS
  • 26. DIETARY INTERVENTIONS:- • FLUID ALLOWANCE 500-600ml MORE THAN THE PREVIOUS DAY 24hrs. URINE OUTPUT. • CARBOHYDRATE & FAT INTAKE 40- 50kcal/kg/day. • DIET RESTRICTION PROTEIN 1g/kg/day. • VITAMIN SUPPLEMENTS.
  • 27. • DIALYSIS THERAPY • POTASSIUM REMOVAL • POTASSIUM RESTRICTED DIET (KAYEXALATE) HYPERKALEMIA:-
  • 28. HYPERPHOSPHATEMIA & HYPOCALCEMIA PREVENTION & TREATMENT:- ALUMINIUM BASED ANTACIDS. CARBONATE-CARBONATE AND PHOSPHATE BINDING ANTACIDS.
  • 29. NEUROLOGICAL ABNORMALITIES • OBSERVE FOR SLIGHT TWITCHING, HEADACHE, DELIRIUM, SEIZURES. • IV DIAZEPAM OR PHENYTOIN. ANEMIA • EPOGEN (RECOMBINANT HUMAN ERYTHROPOIETIN)
  • 31. .
  • 32. 1. FLUID VOLUME EXCESS RELATED TO DECREASED URINE OUTPUT, DIETARY EXCESS & RETENSION OF SODIUM AND WATER SECONDARY TO DISEASE PROCESS.
  • 33. 2. ALTERED NUTRITION LESS THAN BODY REQUIREMENT RELATED TO ANOREXIA, NAUSEA, VOMITING, DIETARY RESTRICTION, ALTERED ORAL MUCUS MEMBRANES SECONDARY TO DISEASE PROCESS.
  • 34. 3. ACTIVITY INTOLERANCE RELATED TO FATIGUE, RETENTION OF WASTE PRODUCT AND DIALYSIS PROCEDURES SECONDARY TO CHRONIC RENAL FAILURE.
  • 35. 4. SELF-ESTEEM DISTURBANCE RELATED TO DEPENDANCY, ROLE CHANGE, CHANGE IN BODY IMAGE AND CANGE IN SEXUAL FUNCTION SECONDARY TO DISEASE PROCESS.
  • 36. 5. RISK FOR HYPERKALEMIA, PERICARDITIS, PERICARDIAL EFFUSION, PERICARDIAL TEMPONATE, HYPERTENSION, ANEMIA, BONE DISEASE, METASTATIC CALCIFICATION RELATED TO DISEASE PROCESS.
  • 37. 6. KNOWLEDGE DEFICIT REGARDING CONDTION AND TREATMENT MODALITIES RELATED TO DISEASE PROCESS.
  • 38. 7. RISK FOR IMPAIRED SKIN INTEGRITY RELATED TO EDEMA, DRY SKIN AND PRURITIS
  • 39. 8. RISK OF INFECTION RELATED TO INDEWELLING PERITONEAL CATHETER, VENI-PUNCTURE CONNECTION OF TUBING DURING HEMODIALYSIS.
  • 40. ,