【持续性肾脏替代治疗CRRT英文精品课件】Acute Kidney Injury(91p)_
合集下载
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
Hallmark:
Red blood cell casts Hematuria, HTN
Intra Renal - Vases:
Malignant HTN Vasculitis Thromboembolic disease
Intra Renal --Acute Tubular Necrosis
85% - intrinsic AKI Histologic changes
Epithelial sloughing Luminal occlusion Common causes Ischemia Toxic
Rhabdomyolysis/myoglobinuria
AKI: Tubules
Anuria - important finding
Common causes of obstruction
Prostatic obstruction Cancer Retroperitoneal disease
Dx = ultrasound
Post Renal AKI
Ureteral and pelvic
Classic presentation
Fever, rash, eosinophilia Eosinophiluria Definitive Dx = renal biopsy
AKI: Interstitial Nephritis
AKI: Interstitial Nephritis
AKI: Post Renal
Tubular obstruction
a) Crystal induced tubular obstructions Allopurinol, sulpha, HIV meds, methotrexate
AKI: Acute Interstitial Nephritis
10% - intrinsic ARF
A. - Blood loss B. - GI or Renal losses
History Dry mucosa, skin turgor Hypotension Oliguria
B. Intravascular Volume Depletion
History
C. Effective circulating volume depletioEndematous states
ATN
a) Neprotoxic agents Drugs: Amphotercin, aminoglycosides Myoglobin, hemoglobin, radio-contrast
b) Ischemic injury Prolonged prerenal state, Shock Arterial cross clamping during AAA and CABG Afferent arteriolar constriction sec to severe hypercalcemia.
AKI: Intra Renal
Glomerular Vascular Tubules Interstitial
Intra Renal- Glomerular Disease
Pathology:
Focal and diffuse glomerulonephritis Cresentic GN
Pre-renal Renal
ATN ARF or CRI GN AIN AED Obstruction
21%
45% 13%
4% 2% 1% 10%
Liano et al. Kidney Int 1996;50:811.
AKI: Prerenal
Prerenal
A. “True” Volume depletion
ligation
• Bladder
• Stones • Blood clots • Prostatic
Intrinsic obstruction
Blood clots Stones/crystals Sloughed papillae Fungus balls
Extrinisic obstruction
Malignancy Retroperitoneal fibrosis Iatrogenic: inadvertent
【持续性肾脏替代治疗CRRT英文精品课件】Acute Kidney Injury(91p)
Diagnostic Criteria for AKI
AKI:
Stage I: Stage II: Stage III:
An abrupt increase in serum creatinine of at least 0.3 mg/dl or 1.5 fold of baseline within 48 hours.
D.
- Congestive heart failure
E.
- Cirrhosis
F.
- Nephrosis
G.
- Sepsis/vasodilated states
Blood Volume
Cardiac Pump dysfunction
Vasodilation
Glomerular autoregulation
Increase in Creatinine 1.5 to 2 fold
Increase in Creatinine > 2.0 to 3 fold
Increase in Creatinine > 3.0 times or Dialysis requirement (or a peak creatinine of > 4.0 mg/dl with at least a 0.5 mg/dl increase)
Acute Kidney Injury Network Consensus Statement, 2007
AKI
Serum Creatinine
Pathophysiology
Pathophysiology
AKI: Pathophysiology
Reasons for AKI Consults (n = 748)
Red blood cell casts Hematuria, HTN
Intra Renal - Vases:
Malignant HTN Vasculitis Thromboembolic disease
Intra Renal --Acute Tubular Necrosis
85% - intrinsic AKI Histologic changes
Epithelial sloughing Luminal occlusion Common causes Ischemia Toxic
Rhabdomyolysis/myoglobinuria
AKI: Tubules
Anuria - important finding
Common causes of obstruction
Prostatic obstruction Cancer Retroperitoneal disease
Dx = ultrasound
Post Renal AKI
Ureteral and pelvic
Classic presentation
Fever, rash, eosinophilia Eosinophiluria Definitive Dx = renal biopsy
AKI: Interstitial Nephritis
AKI: Interstitial Nephritis
AKI: Post Renal
Tubular obstruction
a) Crystal induced tubular obstructions Allopurinol, sulpha, HIV meds, methotrexate
AKI: Acute Interstitial Nephritis
10% - intrinsic ARF
A. - Blood loss B. - GI or Renal losses
History Dry mucosa, skin turgor Hypotension Oliguria
B. Intravascular Volume Depletion
History
C. Effective circulating volume depletioEndematous states
ATN
a) Neprotoxic agents Drugs: Amphotercin, aminoglycosides Myoglobin, hemoglobin, radio-contrast
b) Ischemic injury Prolonged prerenal state, Shock Arterial cross clamping during AAA and CABG Afferent arteriolar constriction sec to severe hypercalcemia.
AKI: Intra Renal
Glomerular Vascular Tubules Interstitial
Intra Renal- Glomerular Disease
Pathology:
Focal and diffuse glomerulonephritis Cresentic GN
Pre-renal Renal
ATN ARF or CRI GN AIN AED Obstruction
21%
45% 13%
4% 2% 1% 10%
Liano et al. Kidney Int 1996;50:811.
AKI: Prerenal
Prerenal
A. “True” Volume depletion
ligation
• Bladder
• Stones • Blood clots • Prostatic
Intrinsic obstruction
Blood clots Stones/crystals Sloughed papillae Fungus balls
Extrinisic obstruction
Malignancy Retroperitoneal fibrosis Iatrogenic: inadvertent
【持续性肾脏替代治疗CRRT英文精品课件】Acute Kidney Injury(91p)
Diagnostic Criteria for AKI
AKI:
Stage I: Stage II: Stage III:
An abrupt increase in serum creatinine of at least 0.3 mg/dl or 1.5 fold of baseline within 48 hours.
D.
- Congestive heart failure
E.
- Cirrhosis
F.
- Nephrosis
G.
- Sepsis/vasodilated states
Blood Volume
Cardiac Pump dysfunction
Vasodilation
Glomerular autoregulation
Increase in Creatinine 1.5 to 2 fold
Increase in Creatinine > 2.0 to 3 fold
Increase in Creatinine > 3.0 times or Dialysis requirement (or a peak creatinine of > 4.0 mg/dl with at least a 0.5 mg/dl increase)
Acute Kidney Injury Network Consensus Statement, 2007
AKI
Serum Creatinine
Pathophysiology
Pathophysiology
AKI: Pathophysiology
Reasons for AKI Consults (n = 748)