31/10/2016. Acute renal failure in dogs and cats: do they survive?? Eric Zini PD, PhD, Dipl. ECVIM-CA (Internal Medicine) Italy.

Transcription

1 Acute renal failure in dogs and cats: do they survive?? Eric Zini PD, PhD, Dipl. ECVIM-CA (Internal Medicine) Italy Switzerland 1

2 Acute kidney injury (AKI)...but before? Definition Acute kidney disease represents a spectrum of disease associated with a sudden onset of renal parenchymal injury most typically characterized by generalized failure of the kidneys to meet the excretory, metabolic, and endocrine demands of the body. 2

3 ...but before? Blood work Blood work Renal functions Excretion Reabsorption Endocrine 3

4 Blood work Blood work Hematology 4

5 Hematology Hematology Hematology Non regenerative anemia, normocytic and normochromic Causes Decreased erythropoietin Nutritional imbalance due to anorexia Reduced half-life of erythrocytes GI bleeding Only anemia??? 5

6 Hematology Hematology Hematology...and leukocytes?...and platelets? 6

7 Biochemistry Biochemistry Biochemistry Urea 1) Synthesized in the liver 2) From catabolism of aminoacids 3) Inversely correlated with renal function (GFR), absorbed-secreted 7

8 Biochemistry Biochemistry Biochemistry Urea (NON RENAL) Increased urea -dietary (high) protein content -increased catabolism -GI bleeding Decreased urea -dietary (low) protein content -liver dysfunction Creatinine Degradation of muscular phosphocreatine Not affected by diet Creatinine excreted through kidneys, but not secreted (..) or reabsorbed Young animals (lower creatinine) Male, muscular masses, Greyhound (higher creatinine) Phosphate GI absorption and renal excreation 8

9 Biochemistry Biochemistry Biochemistry Phosphate Initially... - compensation from functioning nephrons - compensation due to increased PTH But when GFR < 20%... - compensation is not enough - hyperphosphatemia contributes to progression of renal disease Calcium Hypocalcemia due to: - decreased GFR leading to hyperphosphatemia - ethylene glycol - pancreatitis Hypercalcemia... maybe it is the cause of... 9

10 Blood gas Biochemistry Biochemistry Kalium Hypokalemia or hyperkalemia.....depending on output of urine Kalium Hyperkalemia oliguric or anuric AKI obstruction urine tract rupture 10

11 20%, >10 5 cfu 20%, cystitis after catheter Nitrites ph Proteins Glucose Ketons Urobilinogen Bilirubin Erythrocytes/Hgb/Mgb Leukocytes Specific gravity 11

12 After 12 hours at room temperature and at 4 C, the proteinuria significantly increases Proteinuria does not change during 3 months at -20 C 12

13 cutoff Is the ph reliable? Are ketons reliable? 13

14 And glucose? And bilirubin? Hb catabolism of tubuli Abnormal!!! Low renal threshold 1+ paraphysiologic (male) And nitrites? Gram negative bacteria (riduce nitrates to nitrites) False positive: old urines, contaminated False negative: short time allowed to reduce nitrates 14

15 And erythrocytes/hgb/mgb? How to differentiate them? And urobilinogen? What does the color of urine say? 15

16 Causes of AKI Granular Hyaline Waxy Lipidic Cellular 16

17 Causes of AKI Causes of AKI Blood work Pre-renal insufficient blood supply to allow adequate clearance of solutes and uremic toxins...examples: dehydration hypovolemia hypotension hypoadrenocorticism drugs 17

18 Blood work Causes of AKI Which one? Renal Intrinsic renal damage...examples: ischemia electrolyte imbalance infectious nephrotoxins primary renal disorders systemic disorders Pre-renal + intrinsic renal 70-75% of all causes of acute kidney injury Nephrotoxins 18

19 Which one? Which one? Causes of AKI Nephrotoxins Aminoglycosides Sulfonamide Tetracycline Penicillin NSAIDs Diuretics Nephrotoxins Lilium Grapes Post-renal Any obstruction in any part of the urinary tract 19

20 Causes of AKI AKI AKI Post-renal Urine leakage from any part of the urinary tract Phases Initial Progression Maintenance Healing Initial phase Often without obvious clinical signs Until renal damage is detected... Reduced urinary output or increased creatinine and urea 20

21 AKI AKI Staging Progression and maintenance phases Extension of renal damage... Renal cortex very sensitive because: - receives 90% of renal blood flow - has high metabolic activity Healing phase Is it possible? 21

22 IRIS RIFLE and AKIN Diagnosis Clinical picture Acute onset of... 22

23 Diagnosis Diagnosis Diagnosis Clinical picture Acute onset of... Anorexia Polydipsia Lethargy/weakness Nausea/vomiting Diarrhea Abnormal urine output (polyuria or oliguria or anuria) Central nervous system signs Physical examination Physical examination Dehydration Body Condition Score, good Uremic halitosis Oral ulcers (if severe uremia) Painful kidney palpation Nephromegaly Tachycardia Bradycardia 23

24 Diagnosis Diagnosis Tests for specific causes Blood work Increased creatinine and urea Hyperphosphatemia Metabolic acidosis Hypokalemia or hyperkalemia Hypocalcemia Anemia (if GI bleeding) (NGAL/SDMA) Isosthenuria/hyposthenuria/hypersthenuria Proteinuria Glycosuria Cylindruria Crystalluria Bacteriuria Rapid test for ethylene glycole (false positive and negative) Rapid test for Leptospirosis 24

25 Diagnosis Diagnosis Diagnosis Abdominal ultrasonography Renal cytology or histology To identify the underlying cause and the amount of damage Renal cytology or histology To identify the underlying cause and the amount of damage?...risks, depending on expertise 25

26 Treatment The ship Ob, with the sixth Soviet Antarctic expedition on board, sailed from Leningrad on 5 November One of the expedition s members was the 27 year old Leningrad surgeon Leonid Ivanovich Rogozov. 26

27 Treatment Treatment Their task was to build a new Antarctic polar base. After nine weeks, on 18 February 1961, the new base was opened. They finished just in time. The polar winter was descending, bringing months of darkness, and extreme frosts... The ship had sailed and would not be back for a year. Contact with the outside world was no longer possible. Aims - Limiting the progression of renal damage Strategy - Improving renal distribution of blood - Keep urine output Fluid therapy 27

28 Treatment Treatment Fluid therapy 28

29 Treatment Treatment Treatment Potassium Hyperkalemia Emergency condition: Calcium gluconate (slow IV) and ECG monitoring Insulin + glucose (IV) Controlling of metabolic acidosis Metabolic acidosis Fluid therapy Sodium bicarbonate if ph <7.2 or HCO3 <12 meq/l Hypertension 29

30 Treatment Treatment Treatment Anemia??? Gastroenteric signs VERY COMMON!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! Treatment H + -blockers Antiemetics Prokinetics Sucralfate Urine output normal: anuria: oliguria: polyuria: 1-2 ml/kg/hr <1 ml/kg/h 1-2 ml/kg/h >2 ml/kg/h 30

31 9 April 1961 After several weeks Rogozov fell ill. He noticed symptoms of weakness, nausea, and, later, pain in the upper part of his abdomen. His temperature rose to 37.5 C. Rogozov wrote in his diary: -It seems that I have appendicitis. I am keeping quiet about it, even smiling. Why frighten my friends. Who can help me?- 10 April 1961 He started with antibiotics but his clinical condition got worse during the following 10 days, with more frequent nausea and fever. He realized that to save him self from peritonitis...there was only one solution: he had to perform surgery on his own. 30 April 1961 Rogozov started surgery with a meteorologist and a mechanic....after 2 hours of pain and suffering the surgery was completed. 31

32 Prognostic factors Prognostic factors After 2 weeks he was working again at the Antarctic polar base. Rogozov V, Bermel N. Auto-appendectomy in the Antarctic: case report. BMJ Dec 10;339:b4965. Outcome predictors 32

33 Prognostic factors Prognostic factors Treatment Outcome predictors Dogs with creatinine < 1.6 mg/dl having an increase > 0.3 mg/dl within 3 days 3-fold chances of death within days Cats with creatinine < 1.6 mg/dl that have an increase > 0.3 mg/dl within 3 days 3-fold chances of death within 90 days Outcome predictors 33

34 Contact Eric Zini Istituto Veterinario di Novara, Novara (Italy)