Renal Disorders PDF

Renal Disorders Alexis Luigi Lorenzo C. Cresencia, RN, MD  Classification of Renal Disorders Obstructive Disorders vUrolithiasis vPolycystic Kidney Disease vRenal Artery Stenosis Acute Kidney Injury Chronic Kidney Disease ...

Renal Disorders Alexis Luigi Lorenzo C. Cresencia, RN, MD  Classification of Renal Disorders Obstructive Disorders vUrolithiasis vPolycystic Kidney Disease vRenal Artery Stenosis Acute Kidney Injury Chronic Kidney Disease  Urolithiasis Stones (Calculi) 3rd to 5th decade of life Men 2x affected May develop in one or both Depends on site: üNephrolithiasis üUreterolithiasis üCystolithiasis  Pathophysiology Stones are formed due to SUPERSATURATION üDepends on amount of substance, ionic strength, and pH Factors that favor stone formation: üInfection üUrinary Stasis üPeriods of immobility Increased calcium concentrations in serum and urine Causes: Hyperparathyroidism, Renal Tubular acidosis, Cancer, dehydration, Granulomatous diseases, Excess intake of Vit D, Milk, and alkali, Myeloproliferative diseases, and Intestinal bypass surgery  Pathophysiology Uric acid stones (72% in Men) üSeen in gout or myeloproliferative disorders Struvite stones (72% in Women) üAlkaline, ammonia-rich urine üPredisposing factors: Neurogenic bladder, foreign bodies, and recurrent UTIs Other risk factors: Polycystic kidney disease, horseshoe kidneys, chronic strictures, medullary sponge disease, inflammatory bowel disease, and patient with an ileostomy or bowel resection Medications: Antacids, Acetazolamide, Vitamin D, Laxatives and High doses of aspirin  Clinical Manifestations Depends on the presence of obstruction, infection, and edema Renal pelvis – intense, deep ache in CVA üFemales – anteriorly and downward toward the bladder üMale – testes Hematuria, Pyuria Renal colic üAcute pain with CVA tenderness üNausea and vomiting Diarrhea and abdominal discomfort  Ureteral colic üAcute, excruciating, colicky, wavelike pain üRadiates down the thigh and to the genitalia üDesire to void and contains blood Can pass stone if 0.5 cm in diameter Bladder – irritation; assoc. with UTI and hematuria Bladder neck – urinary retention Infection + stone – potential for urosepsis  Assessment and Diagnostic Findings Non-contrast CT Scan Blood chemistries and 24-hour urine test Diet, medication, and family history of renal calculi – predisposing factor Chemical/Stone analysis – determine composition üCalcium Oxalate/Phosphate – oxalate or calcium metabolism disorder üUrate – uric acid/purine metabolism  Medical Management Goals: üEradicate and determine the stone and its type üPrevent nephron destruction üControl infection üRelieve any obstruction In renal/ureteral colic: üOpioid analgesic agents üNSAIDS Increase OFI RTC Nutritional Therapy Fluid intake – mainstay unless CI Eight to ten glasses of water (8 oz) daily Achieve UO > 2L/day  Nutritional Therapy Calcium Stones üRestrict calcium – Patients with Hypercalciuria üLiberal fluid intake üAmmonium chloride üThiazide diuretics – if increase parathormone Uric Acid Stones üLow purine üAllopurinol Cysteine Stones – low-protein diet, potassium alkali, increase OFI Oxalate – limit oxalate intake, increase OFI Interventional Procedures A. Ureteroscopy B. ESWL / Lithotripsy C. Percutaneous Nephrostomy/ Nephrolithotomy  Surgical Management Indicated if no response to other forms of treatment To correct anatomical abnormalities within the kidney Kidney – nephrolithotomy/nephrectomy Renal Pelvis – Pyelolithotomy Ureter – Ureterolithotomy Bladder – Cystotomy; Cystolitholapaxy  Nursing Diagnoses and Interventions Acute Pain Lack of knowledge Potential complications INTERVENTIONS Relieving Pain üOpioid analgesics üIV NSAID üAssume position of comfort üAssisted to ambulate üClose monitoring of pain level  Nursing Interventions Monitoring and managing potential complications Increase OFI IV Fluids I & O monitoring including voiding pattern Ambulation Strain urine Instruct to immediately report any sudden increase in pain intensity Vital signs – especially Temperature  Acute Kidney Injury Deterioration of kidney function over hours or days resulting in the accumulation of toxic wastes and the loss of internal homeostasis Damage is reversible Epidemiology Community-acquired AKI is approximately 100 per 1 million population Hospital-acquired AKI v 4% of hospital admissions v 20% of critical care admissions Mortality rate of approximately 50%  Pathophysiology Normally, the kidney receives 25% of the cardiac output. Decrease in renal blood flow (RBF), glomerular filtration rate is depressed Decreased renal blood flow injures the kidney The kidney tries to adapt by preserving volume that would be lost due to the decreased reabsorptive capacity of the injured tubes Injured renal tubular cells lose their appropriate function, further depressing the glomerular filtration rate During the period of depressed renal blood flow, the kidneys are especially vulnerable to further insults Recovery from AKI is first dependent on restoration of renal blood flow  Ischemic/Prerenal Failure - Conditions that decrease renal blood flow causing a drop in the GFR Volume depletion resulting from: Clinical Manifestations Gastrointestinal losses (vomiting, diarrhea, Nausea nasogastric suction) Vomiting Hemorrhage Diarrhea Renal losses (diuretic agents, osmotic diuresis) Decreased tissue turgor Impaired cardiac efficiency resulting from: Dryness of mucous membranes Cardiogenic shock Somnolence Dysrhythmias Heart failure Myocardial infarction Vasodilation resulting from: Anaphylaxis Antihypertensive medications or other medications that cause vasodilation Sepsis  Intrarenal Failure - Result from ischemic, toxic or immunologic mechanisms; from intrinsic disease of renal parenchyma including glomerular, tubulointerstitial, and vascular diseases Prolonged renal ischemia resulting from: Hemoglobinuria (transfusion reaction, hemolytic anemia) Clinical Manifestations Rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns) Fever Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) Skin Rash Nephrotoxic agents such as: Edema Aminoglycoside antibiotics (gentamicin, tobramycin) Angiotensin-converting enzyme inhibitors Heavy metals (lead, mercury) Nonsteroidal anti-inflammatory drugs Radiopaque contrast agents Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic) Infectious processes such as: Acute glomerulonephritis Acute pyelonephritis  Obstruction/Post-renal Failure - Arise from obstruction of urine flow Urinary tract obstruction, including: Benign prostatic hyperplasia Blood clots Calculi (stones) Strictures Tumors Clinical Manifestations Difficulty in voiding Changes in urine flow Classifications of Acute Kidney Injury  Phases of Acute Kidney Injury PHASE FINDINGS SYMPTOMS Initiation - Oliguria Oliguria/Oliguric Increased BUN Drowsiness, confusion, Inability to excrete metabolic wastes Increased Creatinine coma GI Bleeding Asterixis Pericarditis Inability to regulate electrolytes Hyperkalemia Cardiac dysrhythmias Hyponatremia Kussmaul breathing Acidosis Inability to excrete fluid loads Fluid overload CHF Pulmonary Edema Neck Vein Distention Hypertension  Phases of Acute Kidney Injury PHASE FINDINGS SYMPTOMS Diuresis/Diuretic Hypovolemia Urine output up to 4- Hyponatremia 5L/day Hypokalemia Hypotension Tachycardia Improving mental alertness Weight loss Dry mucus membranes Muscle weakness Constipation Recovery Normal laboratory - values Permanent 1% to 3% GFR reduction  Medical Management Correction of any reversible cause Prerenal Azotemia – optimize renal perfusion Intrarenal Azotemia – supportive therapy Postrenal Failure – relieving the obstruction Attention to and correction of underlying fluid excess or deficits Correction and control of biochemical imbalances— treatment of hyperkalemia Restoration/maintenance of blood pressure Maintenance of nutrition Initiation of hemodialysis, peritoneal dialysis, or continuous renal replacement therapies for patients with progressive azotemia  Nursing Management Monitoring and Managing Hyperkalemia 1. Evaluate for hyperkalemia correlated with ECG changes 2. Administration of sodium bicarbonate or glucose and insulin 3. Administer cation exchange resin (sodium polystyrene sulfonate [Kayexalate, given as retention enema]) 4. WOF cardiac dysrhythmias (cardiac arrest) and congestive heart failure 5. Control potassium balance 6. Prepare for dialysis  Nursing Management Providing Electrolyte Replacement Acidosis: sodium bicarbonate Hyperphosphatemia: aluminum or calcium antacids Monitoring for Gastrointestinal Bleeding Examine all stools for blood Administer H2-receptor antagonist (cimetidine or ranitidine) and/or antacids as prophylaxis Prepare for endoscopy in case bleeding occurs  Nursing Management Correcting Fluid Volume Deficits or Overload WOF signs and symptoms of hypovolemia (dehydration) or hypervolemia vHypovolemia: poor skin turgor, dryness of mucous membranes, hypotension, tachycardia vHypervolemia: dyspnea, tachycardia, distended neck veins, crackles, peripheral edema, pulmonary edema Monitor urinary output and urine specific gravity; measure intake and output Monitor serum and urine electrolyte concentrations. Weigh patient daily; expected weight loss is 0.25-0.5 kg (1/2-1 lb. daily) Provide skin care  Nursing Management Maintain rest/activity balance Provide assistance in ADLs Maintain strict bedrest in the acute phase Prevent injury Keep side rails elevated and pad side rails if necessary Protect patient from bleeding WOF mental status changes Employ seizure precaution  Nursing Management Prevent infection Always maintain aseptic technique Isolate patient from anyone with infection Turn weak or immobile patients frequently Provide meticulous skin care Promote measures to relieve pruritus Improving Nutritional Status Employ moderate protein restriction during oliguric phase Offer high-carbohydrate feedings Restrict foods and fluids containing potassium and phosphorus (bananas, citrus fruits/juices, coffee) Encourage a high-protein, high-caloric diet after diuretic phase  Chronic Kidney Disease Gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes which fatally ends in uremia Damage is irreversible Causes: Chronic systemic diseases (DM, hypertension) Polycystic Kidney Disease Long standing obstruction Chronic glomerulonephritis Obstructive Uropathy Interstitial nephritis Recurrent infections  Pathophysiology Some of the nephrons (including the glomeruli and tubules) are thought to remain intact while others are destroyed The intact nephrons hypertrophy and produce an increased volume of filtrate with increased tubular reabsorption despite a decreased glomerular filtration rate(GFR) This adaptive method permits the kidney function until about three fourths of the nephrons are destroyed The solute load then becomes greater than can be reabsorbed, producing an osmotic diuresis with polyuria and thirst As more nephrons are destroyed, oliguria occurs with retention of waste products  Stages of Chronic Kidney Disease Decreased Renal Reserve (renal End-stage renal disease impairment) v GFR