Escolar Documentos
Profissional Documentos
Cultura Documentos
Anatomi ginjal
BEAN SHAPE RETROPERITO NEAL
NEPHRON
A.aFFEREN
A.eFFEREN
Kidney function
Regulation of body fluid Regulation of electrolyte balance Regulation of acid base balance Regulation of blood pressure Excretion of nitrogenous waste product Regulation of erytropoiesis Metabolism of vitamin D Synthesis of prostaglandin
Kosinski (2009), acute renal failure is a sudden decline in both glomerular and tubular function, resulting in the failure of the kidneys to excrete nitrogen and waste products with a corresponding failure to maintain fluid, electrolyte and acid-base balance ARF may be associated with decreased urinary output of less than 30 ml/h.
ARF: the sudden decline in GFR, resulting in retention of nitrogenous waste products (azotemia). Usually accompanied by oliguria (uop < 400mL/24 hr)non oliguric (> 400mL/24hr)
AKI
Decrease in renal function not limited to ARF, but broad clinical syndrome encompassing various etiologies: including specific kidney disease (ex acute interstitial nephritis, acute glomerular, and vasculitic renal diseases), non specific conditions (ischemia, toxic injury), and extrarenal pathology.
AKI
An abrupt (within 48hr) reduction in kidney function currently defined as an absolute increase in serum creatinine of either >0.3 mg/dL or a percentage increase of >50% or a reduction in urin out put (documented as oliguria of <0.5 ml/kg/hr for >6hr)
------------------------------------------------------------------------------------------------------------------ AKI stage II Increase of serum creatinine to > 200% 300% from baseline < 0.5 ml/kg/hour for > 12 hours
------------------------------------------------------------------------------------------------------------------ AKI stage III increase of serum creatinine to > 300% from baseline or serum creatinine 4.0 mg/dl 354 mol/L) after a rise of at least 44 mol/L or treatment with renal replacement therapy < 0.3 ml/kg/hour for > 24 hours or anuria for 12 hours
Epidemiology
Prevalence 1% all patients admitted to hospital 10-30% patients admitted to ICU Etiology Hemodynamic 30% Parenchymal 65% Acute tubular necrosis 55% Acute glomerulonephritis 5% Vasculopathy 3% Acute interstitial nephritis 2% Obstruction 5%
Mortality
Dialysis requiring 40-90% Increased mortality even in patients not requiring dialysis
25% increase in creatinine associated with a mortality rate of 31% compared with 8% for matched patients without renal failure
GFR
Chemotherapy drugs: Cisplatin, 5-FU, mitomycin C, streptozocin Antiviral: Acyclovir, indinavir, Ritonavir, Adenovir
Optimal Volume Status Low-osmolality contrast media Evaluate Creatinine 24 72hr after contrast exposure Adequate IV volume expansion with isotonic crystalloid for 3 12hr before the procedure and continue for 6 24hr afterward. Oral fluid data is insufficient No adjunctive medical or mechanical treatment has been proved to be efficacious Prophylactic hemodialysis and hemofiltration not validated
1.BPH 2. Blood clots 3. Renal stones or crystals 4. Tumors 5. Post operative edema 6. Drugs Tricyclic antidepressants Ganglionic blocking agents 7. Foley cathether obstruction 8. Ligation of ureter during surgery
Symptoms:
Dyspnea heart failure. Hemoptysis Preceding bloody diarrhea Preceding pharyngitis post-Strep, post-infectious
From the occurrence of the precipitating event to the beginning of the change in urine output. 1. Several hours-2 days 2. Normal renal process begin to deteriorate 3. INTRINSIC RENAL DAMAGE IS NOT YET ESTABLISHED Potentially reversible
- Intrinsic renal damage is well established - GFR 5-10 mL/mnt - Last 8-14 days 1-11 months - Anuric Condition oliguric (uop > 400 mL/mnt) - Complication: hyperkalemia, infection
- Renal tissue recovers and repairs itself (4-6 months) - Gradual increase in uop & improvement in laboratory value - Diuresis happen caused of: 1. salt and water accumulation in ECF 2. osmotic diuresis from retained waste product 3. Diuretic agents DANGER????
Assessment
Physical Exam.
Skin new rashes.
Petechiae Malar rash
Eye
Papilledema
Cardio
Rub Gallop
Pt. may be edematous (low albumin) or have significant right sided heart disease.
BUN/Creatinine ratio.
> 20:1 suggest prerenal or obstruction. Can be elevated by anything leading to increased urea production/absorption.
GI bleed TPN Steroids Drugs Tigecycline.
Nursing Dx
1. Excess fluid volume related to sodium and water retention and excess intake 2. Risk for infection r.t depressed immune response secondary to uremia and impaired skin integrity 3. Imbalanced nutrition: less than body requirements related to uremia, altered oral mucous membranes, and dietary restriction
Nursing Dx
4. Anxiety r.t diagnosis, treatmen plan, prognosis, and unfamiliar environment 5. Deficient knowledge r.t disease process and theraeutic regimen
NOC, NIC
Its for your home work
Nurse competencies
AACN Synergy Model. The eight nursing competencies of the Synergy Model are as follows: clinical judgment, advocacy and moral agency, caring practice, collaboration, systems thinking, response to diversity, facilitator of learning, and clinical inquiry.
Nutrition
- low in protein and sodium and - high in fats and carbohydrates to prevent the protein burden on the patients kidneys (Campbell, 2003). - Fluids are generally restricted to the amount of the patients urine output plus 500 to 700 ml. - Parental nutrition is recommended if the gastrointestinal tract is not functional.
Complication
1. Renal 1. The primary effect of ARF is a decrease in urinary output that leads to fluid retention and edema. 2. The decrease in filtration leads to BUN and creatinin build up in the blood as the kidney loses its ability to remove waste products. 3. metabolic acidosis, hypercalemia, hyponatremia, hyperphosphatemia, hypocalcemia, and hypermagnesemia.
3. Cardiovascular - In general, the fluid volume overload experienced in ARF may lead to hypertension, pulmonary edema, peripheral edema, and arrhythmias. - The kidneys fail to excrete excess potassium which may lead to the following: muscle weakness, neuromuscular irritability, bradycardia, heart block, asystole, or other arrhythmias (Campbell, 2003).
4. Respiratory
Dyspnea may result from the decrease in oxygenation either from associated anemia or from fluid volume overload and pulmonary edema associated with ARF.
Auscultation of lung field may reveal crackles.
5. Hematologic Anemic secondary to the impaired RBC production, hemolysis, bleeding, hemodilution, and decrease RBC survival.
Damaged kidneys produce less erythropoietin to stimulate RBC production and the damaged red blood cells are not replaced.
The decrease in hemoglobin leads to insufficient oxygenation manifested by dyspnea.
6. Gastrointestinal
Uremia may cause nausea, vomiting, anorexia, gastric ulcers and colitis which places the patient at risk for GI bleeding.
The increase in urea may also cause the patients breath to smell like foul urine.
Diagnostic Tools
Conventional Biomarkers
1. urine output 2. creatinin 3. urea.
New Biomarkers
Cystatin C, Interlukin 18 (IL 18), Neutrophil Gelatinas-Associated Lipocalin (NGAL), and Kidney injury Molecule (KIM-1).
Diagnostic Imaging
1. X rays, 2. computed tomography scan (CT), 3. magnetic resonance imaging (MRI), ultrasound, 4. arteriogram, 5. renal biopsy.
Refferences
1. KDIGO Clinical prctice guideline for acute kidney injury. 2012. 2 (1). http://www.kdigo.org/clinical_practice_guidelines/p df/KDIGO%20AKI%20Guideline.pdf 2. So Yoon Jang, S.Y. Renal Fellow. UNC Kidney Center At the Courtesy of Dr. Hladik and Dr. Derebail. 3. Sole, Klein & Moseley. 2009. Introduction to Critical care Nursing. Fifth Edition. Saunders. Elsevier. 4. Stroud, B. 2013. Acute Renal Failure. http://rnjournal.com/journal-of-nursing/acuterenal-failure