... konulu sunumlar: "YBÜ’DE SEPSİS DIŞI AKI NEDENLERİ"— Sunum transkripti:
1 YBÜ’DE SEPSİS DIŞI AKI NEDENLERİ Doç Dr Serhan TuğlularMarmara Üniversitesi Tıp FakültesiNefroloji BD
2 ABY- TANI ALGORİTMASI Prerenal Fonksiyonel ABY Intrensek renal Hipotansiyon, ESVİlaçlar, İdrar göstergeleriIntrensekrenalOrganik ABYKlinik özellikler, US Normal, İdrar göstergeleriCauses of acute renal failure can be broadly divided into three categories (figure 1). In the prerenal form there is a reversible increase in serum creatinine and blood ureaconcentrations; it results from decreased renal perfusion, which leads to a reduction in glomerular filtration rate (GFR). Postrenal acute renal failure is due to obstruction of the urinary collection system by either intrinsic or extrinsic masses. The remaining patients have the renal form, in which structures of the nephron, such as the glomeruli, tubules, vessels, or interstitium, are affected.PostrenalObstrüktif ABYAğrı, Hematüri, Anüriİdrar yolu dilatasyonu
3 Eff Dolaşım hacminde mutlak azalma Renal arter Trombozu ya da stenozu Prerenal ABYEff Dolaşım hacminde mutlak azalmaKanamaVolüm EksikliğiKan Hacminde görece ↓KKYDekompanse KC SirozuRenal arter Trombozu ya da stenozuHemodinamik TipNSAIDACEI/ARB: RAS ya da KKY’de
5 Eff Dolaşım hacminde mutlak azalma Renal arter Trombozu ya da stenozu Prerenal ABYEff Dolaşım hacminde mutlak azalmaKanamaVolüm EksikliğiKan Hacminde görece ↓KKYDekompanse KC SirozuRenal arter Trombozu ya da stenozuHemodinamik TipNSAIDACEI/ARB: RAS ya da KKY’de
11 GFR Düşmeden BUN ve Kreatinin Yükselme Nedenleri Üre sentezinde GİS kanamaKortikosteroidlerTetrasiklinProtein alımında artışAmino asit uygulanmasıKatabolizmada artış ve ateşli hastalıkKreatinin yapımında RabdomiyolizTubuler Kr sekresyonunda CimetidineTrimethoprim
12 RADYOKONTRAST NEFROPATİSİ (1) Kontrasttan saat sonra Kr ↑Kr günde zirve yapar7-10. günde bazale geri dönerÇoğunlukla nonoligurikİdrar analizi: granüler silendirler, tubuler epitel hücreleri, minimal proteinüriFE Na ↓Patients with CN typically present with an acute rise in serum creatinine anywhere from 24 to 48 hafter the contrast study. Serum creatinine generally peaks at 3 to 5 d and returns to baseline value by 7 to 10 d (2– 4). The acute renal failure is nonoliguric in most cases (5,6). Urinalysis often reveals granular casts, tubular epithelial cells, and minimal proteinuria, but in many cases may be entirely bland. Most, but not all, patients exhibit low fractional excretion of sodium (5,7). The diagnosis of CN is frequently obvious if the typical course of events follows the administration of contrast.
13 Doğrudan hücresel toksisite RKN: PATOGENEZDoğrudan hücresel toksisiteRenalMedüller iskemiCN appears to be the result of a synergistic combination of direct renal tubular epithelial cell toxicity and renal medullary ischemia (8). Direct cytotoxicity in CN is suggested by histologic changes of cell injury and enzymuria after contrast administration (9). The nature of the contrast, associated ions, concentration, and concomitant hypoxia are all important to the degree of cellular damage, while the osmolality of the solution seems to be of secondary importance (8). The injection of contrast induces a biphasic hemodynamic change in the kidney, with an initial, transient increase and then a more prolonged decrease in renal blood flow (2). The mediators of these changes are still unknown. Alterations in the metabolism of prostaglandin, nitric oxide, endothelin,or adenosine may play a role.Kontrastın tipiEşlik eden hipoksiRisk faktörleri
14 RKN: RİSK FAKTÖRLERİ Önceden varolan BY >2ml/kg kontrast dozu Diyabetes MellitusEffektif arteriyel volümde↓KKYDehidratasyonNefrotik sendromSiroz>2ml/kg kontrast dozuYaş>60Eş zamanlı nefrotoksik ilaç:NSAIDACEI/ARBPreexisting renal impairment Diabetes mellitusDecrease in effective arterial volumecongestive heart failure dehydration nephrosis cirrhosis High doses of contrast Concurrent use of nephrotoxic drugs nonsteroidal anti-inflammatory drugs angiotensin-converting enzyme inhibitors
15 ALINMASI GEREKLİ ÖNLEMLER RKNALINMASI GEREKLİ ÖNLEMLERGerekliliğinin sorgulanmasıÖncesinde Kr. KontolüNon-Nefrotoksik ajan tercihiKontrast dozu YETERLİ HİDRASYON :%0.45 SF → 1ml/kg/saat1-2 saat öncesinden24 saat sonrasına kadarA reasonable starting protocol might use intravenous0.45% saline at a rate of 1 ml/kg per h, beginning 1 to2 h before contrast and continuing for up to 24 h, depending on the duration of the attendant diuresis. The protocol should beflexible to allow an increase in rate if a negative fluid balanceseems to be developing.
16 ALINABİLECEK ÖNLEMLER RKN:ALINABİLECEK ÖNLEMLEROral theophylline (5mg/kg)1 saat öncesinden-48 saat >N-acetylcystein (600mg; 2x1)1 gün öncesinden-48 saat >Ca Kanal blokerleriİdrarın alkalinizasyonuThese studies suggest that theophylline prevents some of the contrast-associated changes in renal function, but a benefit over saline hydration alone has not been convincingly demonstrated. This is particularly true with respect to patients with preexisting renal impairment. Nevertheless, there may be somevalue to the use of theophylline for reduction of CN in those at risk. Although the dose, duration, and route of administration of theophylline differed in each study, it seems likely that a dose of ,5 mg/kg for less than 2 d, starting before contrast, would suffice. The Renal Insufficiency Following ContrastMedia Administration Trial (REMEDIAL) was a randomized trial comparing 3 strategies for the prevention of contrast-induced AKI in patients with CKD (as defined by a serum creatinine 2.0 mg/dL [177 mol/L] or eGFR 40 mL/min/1.73 m2 [0.67 mL/s/1.73 m2]) undergoing coronary or peripheral angiography and/or angioplasty.6 Patient were randomly assigned to prophylactic administration of either (1) intravenous 0.9% normal saline (1
17 iv NaH2CO3+%5 Dx 3mL/kg/saat RKN- REMEDİAL (Renal Insufficiency Following Contrast Media Administration Trial)AKIiv SF 1mL/kg/saat<12 saat>NAC 1200mg 2x1%9.9iv NaH2CO3+%5 Dx 3mL/kg/saat<1 saat1mL/kg/saat6 saatNAC 1200mg 2x1%1.9The Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL) was a randomized trial comparing 3 strategies forthe prevention of contrast-induced AKI in patients with CKD (as defined by a serum creatinine 2.0 mg/dL [177 mol/L] or eGFR 40 mL/min/1.73 m2 [0.67 mL/s/1.73 m2]) undergoing coronary or peripheral angiography and/or angioplasty.6 Patient were randomly assigned to prophylactic administration of either (1) intravenous 0.9% normal saline (1mL/kg/h for 12 hours before and 12 hours after the procedure) plus NAC (1,200 mg orally twice daily before and after) (n 111); (2) intravenous sodium bicarbonate (154 mEq/L [154 mmol/L] in dextrose and H2O, 3 mL/kg bolus for 1 hour before and 1 mL/kg/h for 6 hours after the procedure) plus NAC (as above) (n 108); or (3) normal saline (as above) plus ascorbic acid (3 g intravenously before and 2 g intravenously for 2 doses afterwards) plus NAC (as above) (n 107). Based on thisdefinition, AKI developed in 11 of 111 patients (9.9%) in the saline plus NAC group, in 2 of 108 (1.9%) in the bicarbonate plus NAC group(P v saline plus NAC), and in 11 of 107 (10.3%) in the saline plus ascorbic acid plusNAC group (P v saline plus NAC group).Ascorbic asit3giv –önce2giv-sonra x2iv SF 1mL/kg/saat<12 saat>%10.3
18 RKN: EPİDEMİYOLOJİK BİLGİLER Hastanede yatan hastalarda 3.sık ABY nedeniOlguların %7’si geçici diyaliz ya da SDBYHastanede yatış süresini ve maliyeti ↑Ölüm riskini ↑Acute radiocontrast nephropathy is the third most common cause of acute renal failure in patients admitted to a hospital (1). Up to 7% of patients with thiscondition need temporary dialysis or progress to end-stage renal disease (2). Radiocontrast nephropathy does not only cause extended hospitalization and increased cost (3), but is also associated with an increased risk of death
19 Contrast- Induced Nephropathy (CIN) ConsensusWorking Panel: Executive Summary. Rev Cardiovasc Med 7: , 2006Consensus Statement 1Patients and clinicians should be aware that contrast-induced AKI is a common and potentially serious complicationfollowing the administration of contrast media in patients at risk for AKI.Consensus Statement 2The risk of contrast-induced AKI is elevated and of clinical importance in patients with CKD (particularly when diabetes isalso present), recognized by an eGFR of less than 60 mL/min/1.73 m2.Consensus Statement 3When serum creatinine or estimated glomerular filtration rate is unavailable, then a medical history (inquiring about riskfactors for CKD) may be used to identify patients at higher risk for contrast-induced AKI than the general population.Consensus Statement 4In the setting of emergency procedures, where the benefit of very early imaging outweighs the risk of waiting, theprocedure can be performed without knowledge of serum creatinine or eGFR.Consensus Statement 5Clinicians should recognize the presence of multiple contrast-induced AKI risk factors in the same patient or high-riskclinical scenarios can create a very high risk (approximately 50%) for contrast-induced AKI and (approximately 15%) forneed for dialysis after contrast exposure.Consensus Statement 6In patients at increased risk for contrast-induced AKI undergoing intra-arterial administration of contrast, nonionic, isoosmolarcontrast (iodixanol) is associated with the lowest risk of contrast-induced AKI.Consensus Statement 7Iodinated contrast volumes should be minimized. Higher contrast volumes (100 mL) are associated with higher rates ofcontrast-induced AKI in patients at risk. However, even small (approximately 30 mL) volumes of iodinated contrast invery high-risk patients can cause contrast-induced AKI and need for dialysis, suggesting the absence of a thresholdeffect.Consensus Statement 8Intra-arterial administration of iodinated contrast appears to pose a greater risk of contrast-induced AKI above that withintravenous administration, thus when possible, intravenous studies are preferred.Consensus Statement 9Adequate intravenous volume expansion with isotonic crystalloid ( mL/kg/h) for 3 to 12 hours before the procedureand continued for 6 to 24 hours afterwards can lessen the probability of contrast-induced AKI in patients at risk.Consensus Statement 10No adjunctive medical or mechanical treatment has been proven to be effective in reducing the risk of AKI after exposureto iodinated contrast. Hence use of a prophylactic agent is at the discretion of the treating physician. Prophylactichemodialysis or hemofiltration has not been validated as an effective strategy.
20 İLACA İKİNCİL ABY Akut Tubuler Hasar Otoregülasyon bozukluğu AminoglikozidlerBazı sefalosporinlerAmfoterisin BOtoregülasyon bozukluğuACE inhibitörleriAII reseptör blokerleriNSAIDRadyokontrast ajanlarAkut Interstisyel nefritTüm ilaçlar
21 İlaç Dozunun Ayarlanması İdrar çıkışı <400ml/gün ise, serum kreatinindeğeri ne olursa olsun, klirens <10ml/dk>60 yaşta klirens 10-50ml/dkOLARAK KABUL EDİLMELİDİRYÜKLEME DOZU DEĞİŞMEZİDAME DOZU:DOZ AZALTILABİLİRDOZ ARASI UZATILABİLİR
23 HEPATORENAL SENDROM TANI KRİTERLERİ MAJÖR KRİTERLER1-Scr >1.5 mg/dl ve/veya GFR <40 ml/dk2-Şok, Bakteriyel infeksiyon, sıvı kaybı venefrotoksik ilaç kullanımı olmaması3-1,5 L sıvı verilmesine / diüretiklerinKesilmesine rağmen Scr’nin düşmemesiEK KRİTERLERİdrar volümü <500ml/günİdrar Na <10 mEq/Lİdrar osm>plasma osmHematüri <50/HPFSerum Na<130mEq/L
25 INTRA-ABDOMİNAL HYPERTENSION & COMPARTMENT SYNDROME IAHT: Batın içi basınçta artışACS: IAHT’a ikincil organ disfonksiyonu“Intra-abdominal hypertension”, the presence of elevated intra-abdominal pressure, and “abdominalcompartment syndrome”, the development of pressure-induced organ-dysfunction and failure, havebeen increasingly recognized over the past decade as causes of significant morbidity and mortalityamong critically ill surgical and medical patients. Although initially recognized over 150 years ago, the pathophysiologic implications of elevated intraabdominalpressure (IAP) have essentially been rediscovered only within the past two decades [1-3].An explosion of scientific investigation and accumulation of clinical experience has confirmed thesignificant detrimental impact of both “intra-abdominal hypertension” (IAH) (see figure 1), thepresence of elevated intra-abdominal pressure, and “abdominal compartment syndrome” (ACS), thedevelopment of IAH-induced organ-dysfunction and failure, among the critically ill [4,5].Mortalite ↑Morbiditeyi ↑
26 IAH ve ACS ve BÖBREK Renal kan akımı ve fonksiyon↓ IAP >15 mmHg OliguriIAP > 30 mmHg AnuriRenal arteryel kan akımı ↓Renal ven basıncı ve RVR↑Renal Kortexte kan akımı↓Glomeruler ve tubuler fonksiyon ↓IAH-induced reductions in renal blood flow and function have been demonstrated in both animal andhuman models [33,35,42,51,77]. These changes occur in direct response to increasing IAP witholiguria developing at an IAP of 15 mmHg and anuria at 30 mmHg [32,33,42]. Renal artery blood flowhas been demonstrated to be preferentially diminished in comparison to both celiac and superiormesenteric artery blood flow . Renal vein pressure and renal vascular resistance are both significantly elevated [35,42,48]. All of these changes shunt blood away from the renal cortex and functioning glomeruli leading to impaired glomerular and tubular function and significant reductions in urinary output. IAH decreases glomerular filtration rate causing a rise in both blood urea nitrogen and serum creatinine and a reduction in creatinine clearance [33,35,42,48,51,79]. Osmolar clearance is similarlydecreased and fractional excretion of sodium increased . Urinary sodium and chloride concentrations decrease and urinary potassium concentrations increase . Plasma renin activity and aldosterone levels increase significantly [33,48]. Antidiuretic hormone levels have been demonstrated to increase to more than twice basal levels . All of these pathophysiologic changesappear to be potentially reversible if the patient’s IAH is recognized and treated appropriately beforesignificant organ dysfunction has developed [32,48].BUN ve Kreatinin ↑Ozmoler klirens ↓Fe Na ↑İdrarda Na ve Cl ↓; K ↑PRA ve aldosterone ↑ADH↑
27 APB: Abdominal perfüzyon basıncı World Society of the Abdominal Compartment Syndrome 2004 Consensus Conference (WSACS) (www.wsacs.org)IAP: Batın içi basınçAPB: Abdominal perfüzyon basıncıAPB= MAP - IAPViseral perfüzyonResusitason hedefidefined as MAP minus IAP, has been demonstrated to be an accurate predictor of visceralperfusion and an endpoint for resuscitation APP is also superior to other commonresuscitation endpoints such as arterial pH, base deficit, arterial lactate, and hourly urinary output.Failure to maintain an APP of at least 60 mmHg by day 3 of critical illness has been demonstrated topredict survival from IAH and ACS [64,105,106]. APP thus figures prominently in the resuscitationstrategy recommended by the WSACS.Filtration GradientArteryel pHBaz defisitiArteryel laktatSaatlik idrar çıkışıAPBScandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009
28 IAP için Normal ve Patolojik Değerler Normal IAP :Sub-atmosferik- 0 mmHgTipik YBÜ hastası : 5-7 mmHgYeni Batın cerrahisi geçirmişSepsisOrgan yetmezliğiDehidratasyon>25 mmhg – mortalite ↑IAHT: >12mmHg (persistan)ACS: > 20 mmHg10-20 mmhgNormal IAP ranges from sub-atmospheric to zero mmHg [109,113,116]. In the typical intensive careunit patient, however, IAP is commonly elevated to a range of 5-7 mmHg while patients with recentabdominal surgery, sepsis, organ failure, or need for volume resuscitation may demonstrate IAPs of mmHg [11,15]. Prolonged elevation in IAP to such levels can result in organ dysfunction andfailure while pressures above 25 mmHg are associated with significant potential mortalityScandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009
29 ACS Belirti ve Bulguları Abdominal distentionElevated IAPOliguria refractory to volume administrationRefractory metabolic acidosisElevated PIPHypercarbiaHypoxemia refractory to increasing FiO2 and PEEPElevated ICPScandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009
30 Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009
31 IAB ÖLÇÜM YÖNTEMİCurrent Opinion in Critical Care 2005, 11:156—171
32 Current Opinion in Critical Care 2005, 11:156—171
33 Current Opinion in Critical Care 2005, 11:156—171
34 ‘Kronik’ zeminde ‘Akut’ Olgusu KBY zemininde araya giren ek bir sorun nedeniyle renal işlevde Akut kötüleşmeHipovolemiNefrotoksik ilaç kullanımıInfeksiyonObstrüksiyonKalp yetersizliğiAkselere hipertansiyon
38 Böbrek yetersizliğinin İlaç kullanımına etkisi Oral alımda biyoyararlanım düşeri.v. yol tercih edilmeliProteine bağlanma oranı azalırİlaç toksisite riski artarDağılım hacmi etkilenirMetabolizması etkilenirAtılımı etkilenirBöbrek yetersizliğinde ilaç kullanımrehberlerinden yararlanılmalıdır
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