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Identify ARF earlier and eliminate the cause to avoid the spread of damage Prevention is the key!! in developed ARF, patients should receive therapy to prevent occurrence and reduce its severity avoid nephrotoxins as much as possible. Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR)
Identify ARF earlier and eliminate the cause to avoid the spread of damage Prevention is the key!! in developed ARF, patients should receive therapy to prevent occurrence and reduce its severity avoid nephrotoxins as much as possible. Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR)
Identify ARF earlier and eliminate the cause to avoid the spread of damage Prevention is the key!! in developed ARF, patients should receive therapy to prevent occurrence and reduce its severity avoid nephrotoxins as much as possible. Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR)
MEDAN 2011 Dosen Prof. Dr. Urip Harahap, Apt. 21 Oktober 2011 KELOMPOK 4 PSP APOTEKER 2011
Rogabe Roma Anita Rosfianita Santaria Sri Dewi Sri Kurniasih Sri Rahmadani Sri Dewi Handayani T. Azma Ulya Tonny Setiawan
Wahyuni Widya Akarina Wilson Yuliana Zulkifli Zulhamidah Layani Pransiska N Yustina Samosir Yensi Zahara Tamba T. Pasaribu
Identify ARF earlier and eliminate the cause to avoid the spread of damage Prevention is the key!! In developed ARF, patients should receive therapy to prevent occurrence and reduce its severity Avoid nephrotoxins as much as possible Once the cause of ARF is identified and eliminated, supportive therapy is the only remaining option, as we can hasten the recovery of developed ARF
RENAL BLOOD FLOW Effective Circulating Volume Normal RBF/RPF Intrarenal Autoregulation GFR, FF Renal Perfusion Pressure Cardiac out put Mean Arterial Pressure Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR) despite large changes in the systemic blood pressure RBF - blood perfusing the kidneys each minute (1200 ml/min) Renal Plasma Flow (RPF) - plasma flowing to kidneys each minute (670 ml/min or 55-60% of RBF) GFR - amount of plasma filtered each minute by the glomeruli. (Normal GFR -125 ml /min for men and 100 ml/min for women) Filtration Fraction (FF) - the ratio of GFR to RPF (Normal - .18 - .22)
F = P R
RAP RBF R aff + R eff ~ F = Flow P = Pressure Changes R = Resistance RBF = Renal blood flow Raff = Afferent arteriolar resistance RAP = Renal arterial pressure Reff = Efferent arteriolar resistance Major sites of renal vascular resistance -> Glomerular afferent (R aff )
and efferent (R eff ) arterioles
Changes in R aff and R eff affect RBF Vasoconstrictors Renin Angiotensin II Endothelin ADH Vasodilators PGs Kinins NO ANP RBF GFR Figure : RBF / GFR is maintained by a balance between vasodilators and vasoconstrictors of Afferent and Efferent arterioles Afferent Arteriole PGC GFR. Glomerulus Efferent Arteriole Tubule Figure - shows normal conditions normal renal perfusion pressure and a normal GFR. RBF Reff / Raff ratio =N N Engl J Med 357;8 August 23, 2007 RBF Afferent Arteriole PGC GFR. Efferent Arteriole PGE Ang II Figure: shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction. MAP Reff / Raff ratio = N Engl J Med 357;8 August 23, 2007 Reff / Raff ratio Figure: Loss of vasodilatory PGs increases afferent resistance causing drop in the glomerular capillary pressure below normal values and the fall in GFR RBF PGC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE NSAID
Reduced perfusion pressure with a NSAID. N Engl J Med 357;8 August 23, 2007 PGC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE ACEIs /ARB
Figure: Loss of angiotensin II action reduces efferent resistance; this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease. Reff / Raff ratio RBF N Engl J Med 357;8 August 23, 2007 Sudden and sustained decrease in GFR which is occuring over hours to days, sometimes over weeks, that associated with an accumulation of waste products, including urea and creatinine (Cr).
Acute renal failure is an acute loss of kidney function that occurs over days to weeks and results in an inability to appropriately excrete nitrogenous wastes and creatinine.
ARF is a common condition in the general population, with an annual incidence of approximately 200 cases per million population per year. The incidence rate is higher in hospitalized patients (1-5%). The highest incidence of ARF is in hospitalized patients in the intensive care unit (15-20%), reported mortality rates range from 50-70%. Am Fam Physician 2005;72:1739-46. Copyright 2005 American Academy of Family Physicians Infection and cardiorespiratory complications are the most common causes of death in patients with acute renal failure. Am Fam Physician 2005;72:1739-46. Copyright 2005 American Academy of Family Physicians Based on Severity (RIFLE classification).
RIFLE : Risk, Injury, Failure, Loss, and End-stage Kidney Disease STAGE I
RISK (R) STAGE II
INJURY (I)
STAGE V ESRD (E) STAGE III
FAILURE (F) STAGE IV LOSS (L) Severity Outcome increasing in the serum creatinine level of 0.5 mg per dL (44.2 mol per L) or a 50 percent increase in the creatinine level above the baseline value, a 50 percent decrease in the baseline-calculated glomerular filtration rate (GFR), or the need for acute kidney replacement therapy. Oliguria : a urine output of less than 400 mL in 24 hours. Anuria : a urine output of less than 100 mL in 24 hours.
Catt : Nilai Normal GFR = 120-125 ml/menit Am Fam Physician 2005;72:1739-46. Copyright 2005 American Academy of Family Physicians
CAUSES OF ARF Generalized or localized reduction in RBF Hypovolaemia Haemorrhage Volume depletion ( vomiting, diarrhoea, inappropriate diuresis, burns)
Hypotension Cardiogenicshock Distributive shock (sepsis, anaphylaxis) Oedema states Cardiac failure Hepatic cirrhosis Nephrotic syndrome Renal Hypoperfusion NSAIDs ACEI / ARBs AAA RAS /occlusion Hepatorenal syndrome Reduced GFR PRE-RENAL (Hemodynamic) PRERENAL RENAL TUBULAR Ischemia, Nefrotoxins (Table 2) tubular cells begin to die ATN (Acute Tubular Necrosis)
GLOMERULAR Glomerulonefritis : fever, rash, and arthritis, urine findings include red blood cell casts, hematuria, and proteinuria.
Red blood cell cast MARKER OF GLOMERULAR INJURY Granular cast Am Fam Physician 2005;72:1739-46. Copyright 2005 American Academy of Family Physicians INTERSTITIAL Acute Interstitial Nephritis results from an allergic reaction to a drug (Table 3) Sign : fever, rash, serum and urine eosinophil counts may be elevated.
VASCULAR microvascular macrovascular
Am Fam Physician 2005;72:1739-46. Copyright 2005 American Academy of Family Physicians MARKER OF ACUTE INTERSTITIAL NEPHRITIS POST RENAL Obstruction of the outflow tracts of the kidneys Prostatic hypertrophy, Catheters, Tumors, Strictures, Crystals Neurogenic bladder obstruction The following symptoms may occur with acute Renal failure. Some people have no symptoms, at least in the early stages. The symptoms may be very subtle. Hyperkalemia Nausea/Vomiting Pulmonary edema Oliguria or non oliguria Swelling, especially of the legs and feet Ascites Asterixis Encephalopathy Decrease urine output Mental changes Heart failure Pruritus Anemia Tachypenic Pale and moist skin
Identify and correct pre-renal, renal and post- renal factors Optimise cardiac output and RBF Review drugs: Stop ACEIs, NSAIDs Adjust doses / monitor drug concentrations Avoid aminoglicoside Maintaining adequate intravascular volume and mean arterial pressure
Discontinuing all nephrotoxic drugs Eliminating exposure to any other nephrotoxins Accurately monitor fluid balance and daily body weight Identify and treat acute complications Hyperkalaemia Acidosis Oedema Optimise nutritional support
Prinsip Terapi Pengetahuan dan perjalanan klinik dari tahap- tahap GGA, dengan cairan:
1. Terapi Konservatif a. Preventif b. Suportif c. Substitusi
2. Terapi ginjal pengganti/dialisa Dilakukan apabila terapi konservatif gagal
Mencegah faktor risiko yg ada baik akibat tindakan di dalam Rumah sakit maupun yang memang sudah ada sebelumnya
Memperingan keadaan GGA dan mengusahakan agar perfusi renal seoptimal mungkin (oliguri menjadi non-oliguri).
Volume efektif tubuh diusahakan normal, bila hipovolemi ditambah, bila hipervolemi harus dikurangi.
Catt : Volume urine normal = 600-1800 mL
1. Perdarahan, diberi transfusi 2. Plasma expander bila ada luka peritonitis 3. Air dan elektrolit yang sesuai a. Muntah-muntah : NaCl 0,45% + Kalium 10-20 mmol/l b. Kehilangan cairan/gangguan pankreatitis : NaCl 0,9 % + HCO3 c. Diare : D5% ditambah HCO3 + Kalium 4. Bila masih terjadi oliguri, diberi diuresis osmotik berupa:
a. Mannitol 12,5 g iv/5 menit diulang 30 menit kemudian bila produksi urin <20cc/jam. Bila produksi urin >20cc/jam teruskan Mannitol 100 grdalam D5% liter/24 jam. b. Furosemid 40-80 mg iv. Bila dalam 1-2jam diuresis tidak timbul, dilakukan diuresis paksa dengan dosis 250-500 mg drip dalam 150cc D5%/jam. 5. Bila tetap oliguri, berikan vasoaktif untuk memperbaiki perfusi ginjal yaitu: dopamin dosis rendah 2-5mg per kg/menit dalam 12 jam. 6. Bila semua tindakan 1-5 gagal, diperlukan terapi aktif/dialisa agar tidak terjadi oliguri menetap.
Fase gawat dalam GGA
Biasanya disertai komplikasi : Hiperkalemia, infeksi/sepsis, koma, kardiovaskuler, gastrointestinal, respirasi, dan asidosis metabolik.
Tujuan : untuk menjaga agar pasien tetap dpt bertahan hidup sehingga ada kesempatan ginjal pulih.
Terapi suportif adalah dengan mengatasi gangguan keseimbangan. 1. Cairan a. Bila ada overhidrasi, berikan furosemid 40-80 mg/iv. Dapat dilakukan diuresis paksa dosis 250 mg dalam 600cc D5%. Bila gagal lakukan dialisa. b. Pemberian cairan dibatasi 500 cc c. Bila penderita panas dpt ditambah 10cc/jam tiap kenaikan 1derajat C.
Catt : pedoman kebutuhan cairan dipantau dari kadar Na, bila turun, berarti terjadi overhidrasi, sehingga asupan cairan lebih dibatasi.
2. Elektrolit Asam Basa a. Hiperkalemi Penyebab kematian yang paling sering pada GGA. Bila <6 mg/L, hiperkalemi ringan, berikan resin exchange 25-50 gr/3-4 hari Bila >6mg/L, hiperkalemi sedang + berat, dapat dilakukan pilihan pengobatan hiperkalemia sbb :
2. Hiponatremia Sering terjadi karena hidrasi berlebihan akibat pemberian cairan yg sangat banyak Terapi : pembatasan cairan atau pemberian 2g NaCl 0,9% atau 34 mEq. 3. Hipokalsemia Akibat kegagalan absorbsi di GI, asidosis, dan rhabdomiolisis Terapi : pemberian Ca Gkukonat 10-30 cc/hari 4. Hipermagnesia Sering berupa gejala paralisis otot, depresi pernapasan, hipotensi bahkan koma Terapi : preparat Kalsium, insulin + D5%.
5. Asidosis metabolik Terjadi pernapasan Kussmaul, kadar bikarbobat sering 15mg/l Jumlah bikarbonat = 0,5 x BB x 15 serum HCO3 6. Nutrisi 1. Kalori : diberikan kalori 35-50 kal/kg BB 2. Protein : ditentukan oleh hiperkatabolisme pasien, sebaiknya 0,5 gr/kgBB/hari 3. Lemak : jumlah kecil (maksimal 1/3 jumlah kalori) 7. Pemakaian obat-obatan Hindari pemakaian obat-obatan yang nefrotoksik Jika memang sangat dibutuhkan, atur lama dan interval dosis Perlu diperhatikan adanya poliuri (4000-5000 cc/hari) yang mungkin berakibat dehidrasi, asidosis, bahkan hipokalemi.
Terapi substitusi cairan, garam, bikarbonat, kalium, dicoba per oral, bila tidak mungkin dapat secara parenteral 3-5 hari.
Indikasi dilakukan dialisa pada GGA : 1. Secara Klinis overload cairan, perdarahan hebat, sindrom ureum, asidosis metabolik, koma yang tidak teratasi dengan terapi konservatif
2. Secara Laboratoris HCO3 < 12 mEq , K > 6,0 mEq , Na < 120 mEq , BUN > 100 mg/dl
ARF is common worldwide
Occurs in all clinical & community settings
It carries a high morbidity and mortality risks, involves high cost of management.
ARF is increasingly common, particularly among hospital inpatients, elderly people, and critically ill patients.
It carries a high mortality
Patients at risk are - elderly people; patients with diabetes, hypertension, or vascular disease; and those with pre -existing renal impairment
ARF is often preventable.
Rapid recognition of incipient ARF and early treatment of established ARF may prevent irreversible loss of nephrons.
No drug treatment has been shown to limit the progression of, or speed up recovery from, ARF.
Advice from a nephrologist should be sought for all cases of ARF.