Mr Bala. clinicalcases3

Transcription

1 Mr Bala clinicalcases3

2 AKI & CKD Nigel Fong

3 Practical approach to AKI 1. Is this AKI (vs CKD)? 2. What is (are) the causes? 3. What are the complications? 4. Is dialysis emergent?

4 Scenario Q1 Mr Bala is a 67-year old Indian gentleman. One month ago, he was diagnosed with type 2 diabetes, hypertension, and hyperlipidemia, after presenting to the polyclinic with osmotic symptoms. On diagnosis his HbA1c was 9.2%, and he was found to have retinopathy and peripheral neuropathy. He was started on losartan, atorvastatin, metformin, and glipizide. Two weeks ago he complained of muscle aches and saw a GP, who prescribed etoricoxib (arcoxia) with good relief. He presents to the A&E with non-specific complaints of lethargy and malaise for the past week. In the past 2 days he has also become more breathless. You look through the bloods done in A&E and notice that the creatinine is 340 (egfr 15)

5 Scenario - Q1 Q1. Regarding Mr Bala s Acute Kidney Injury (AKI), all of the following are correct EXCEPT (Choose 2 of 7) Mr Bala may not have AKI. Oliguria conveys a worse prognosis for renal recovery. Mr Bala s diabetes does not predispose him to AKI. A rise in creatinine is expected after initiation of candesartan and may not constitute AKI. Unlike COX-1 (traditional) NSAIDs, COX-2 NSAIDs are less likely to cause AKI. In identifying the etiology of AKI, an abdominal examination is critical. A urine formed element microscopy (UFEME) may reveal muddy brown granular casts

6 Scenario - Q1 Q1. Regarding Mr Bala s Acute Kidney Injury (AKI), all of the following are correct EXCEPT (Choose 2 of 7) Mr Bala may not have AKI. Oliguria conveys a worse prognosis for renal recovery. Mr Bala s diabetes does not predisposes him to AKI. A rise in creatinine is expected after initiation of candesartan and may not constitute AKI. Unlike COX-1 (traditional) NSAIDs, COX-2 NSAIDs are less likely to cause AKI. In identifying the etiology of AKI, an abdominal examination is critical. A urine formed element microscopy (UFEME) may reveal muddy brown granular casts

7 Staging of AKI

8 Scenario - Q1 Q1. Regarding Mr Bala s Acute Kidney Injury (AKI), all of the following are correct EXCEPT (Choose 2 of 7) Mr Bala may not have AKI. Oliguria conveys a worse prognosis for renal recovery. Mr Bala s diabetes does not predisposes him to AKI. A rise in creatinine is expected after initiation of candesartan and may not constitute AKI. Unlike COX-1 (traditional) NSAIDs, COX-2 NSAIDs are less likely to cause AKI. In identifying the etiology of AKI, an abdominal examination is critical. A urine formed element microscopy (UFEME) may reveal muddy brown granular casts

9 Etiology

10 Etiology Pre renal Renal Post renal AKI Hypotension Intravascular hypovolemia (including third spacing) Renal artery stenosis Acute tubular necrosis > Ischaemia,drugs, toxins Glomerulonephritis Microangiopathiese,g, TTP/HUS Acute interstitial nephritis Others Urinary obstruction, acute CKD Third spacing e.g. CCF (cardiorenal), cirrhosis (hepatorenal) DM HTN Glomerulonephritis Vasculitis Polycystic kidney Other interstitial Urinary obstruction, chronic CKD predisposes to AKI; AKI accelerates CKD progression

11 Practical approach to AKI 1. Is this AKI (vs CKD)? 2. What is (are) the causes? Look at the vitals chart and clinical hx Look at the medication list Examine hydration status Palpating for bladder / inserting IDC Looking at the urea / creatinine ratio UFEME +/- phase contrast microscopy US kidneys Urinary protein excretion Renal biopsy 3. What are the complications? 4. Is dialysis emergent?

12 Scenario - Q1 Q1. Regarding Mr Bala s Acute Kidney Injury (AKI), all of the following are correct EXCEPT (Choose 2 of 7) Mr Bala may not have AKI. Oliguria conveys a worse prognosis for renal recovery. Mr Bala s diabetes does not predisposes him to AKI. A rise in creatinine is expected after initiation of candesartan and may not constitute AKI. Unlike COX-1 (traditional) NSAIDs, COX-2 NSAIDs are less likely to cause AKI. In identifying the etiology of AKI, an abdominal examination is critical. A urine formed element microscopy (UFEME) may reveal muddy brown granular casts

13 Scenario Q2 Q2. Which of the following, if present, BEST suggests a diagnosis of acute kidney injury over chronic kidney disease? (Choose 2 of 7) Patient with fatigue and pruritus for the past 3 months Well patient incidentally discovers elevated creatinine during health screening Blood tests: Hb 9.7, MCV 85.6, Fe sat 19%, Ferritin 287 Blood tests: Hb 9.7, low platelets, low haptoglobin, LDH, and bilirubin. Blood tests: Hb 9.7, calcium 3.5, and new vertebral fracture. Ultrasound scan showing a normal kidney Bland urinary sediment

14 Practical approach to AKI 1. Is this AKI (vs CKD)? Baseline creatinine Renal ultrasound: size, parenchymal echogenicity Long-term complications of CKD > Anaemia > Mineral bone disease Symptom duration or overt precipitant for AKI 2. What is (are) the causes? 3. What are the complications? 4. Is dialysis emergent?

15 Scenario Q2 Q2. Which of the following, if present, BEST suggests a diagnosis of acute kidney injury over chronic kidney disease? (Choose 2 of 7) Patient with fatigue and pruritus for the past 3 months Well patient incidentally discovers elevated creatinine during health screening Blood tests: Hb 9.7, MCV 85.6, Fe sat 19%, Ferritin 287 Blood tests: Hb 9.7, low platelets, low haptoglobin, LDH, and bilirubin. Blood tests: Hb 9.7, calcium 3.5, and new vertebral fracture. Ultrasound scan showing a normal kidney Bland urinary sediment

16 Scenario Q3 You look through Mr Bala s records and discover that at last month s polyclinic visit, his creatinine was 163 (egfr 37). On examination, he is breathless, requiring oxygen (2L nasal prongs), with bilateral pitting edema and basal lung crackles. Available investigations are: Hb 8.7, TW 12, Plt 320 Urea 23, Cr 340, Na 136, K 6.2, HCO3 14, Cl 105, Glucose 7.0

17 Scenario Q3 Q3. All of the following will be helpful for Mr Bala EXCEPT (Choose 2 of 7): Serial cardiac enzymes IV calcium gluconate IV hydration IV furosemide SC actrapid 10 units Suspend losartan Renal ultrasound scan

18 Scenario Q3 Q3. All of the following will be helpful for Mr Bala EXCEPT (Choose 2 of 7): Serial cardiac enzymes IV calcium gluconate IV hydration IV furosemide SC actrapid 10 units Suspend losartan Renal ultrasound scan

19 Scenario Q4 Mr Bala is diuresed and his hyperkalaemia is corrected. He remains afebrile and blood pressure is stable, but he fails to pass any urine despite a total of 160mg furosemide boluses. The next morning, he becomes confused and increasingly breathless. His oxygen requirement has gone up to 8L via face mask. Repeat investigations reveal: - Troponin ph 7.13, po2 103, pco Urea 30, Cr 400, Na 132, K 5.6, HCO3 7, Cl Calcium / Phosphate / Magnesium unremarkable.

20 Scenario Q4 Q4. The BEST management for Mr Bala is (Choose 1 of 5): Add IV albumin to IV furosemide Change IV furosemide to an infusion, titrated to maintain SBP >90 mmhg IV sodium bicarbonate infusion Insertion of femoral vascular catheter and hemodialysis Intubation and ventilation

21 Scenario Q4 Q4. The BEST management for Mr Bala is (Choose 1 of 5): Add IV albumin to IV furosemide Change IV furosemide to an infusion, titrated to maintain SBP >90 mmhg IV sodium bicarbonate infusion Insertion of femoral vascular catheter and hemodialysis Intubation and ventilation

22 Indications for urgent dialysis A E I O U Severe acidosis Electrolytes: hyperk refractory to medical Rx Intoxication with dialysable toxin Overload: refractory pulmonary edema Uremia: uremic encephalopathy, pericarditis

23 Scenario Q5 Mr Bala undergoes one session of slow low efficiency dialysis in high dependency and is thereafter able to wean off oxygen. His subsequent renal panels are: 4h post dialysis: Cr 262, Na 139, K 3.6, HCO3 15, Cl 96 Next morning: Cr 250, Na 142, K 3.9, HCO3 14, Cl 97 Following am: Cr 241, Na 138, K 4.0, HCO3 17, Cl 97 He is transferred out of high dependency.

24 Scenario Q5 Q5. Regarding Mr Bala s subsequent progress and management, which of the following statements is FALSE? (Choose 1 in 5) Creatinine may never return to baseline Over the next few days, Mr Bala may develop hypernatremia Over the next few days, Mr Bala may develop hypokalaemia Candesartan should not be restarted, regardless of creatinine level The temporary dialysis catheter should be removed.

25 Scenario Q5 Q5. Regarding Mr Bala s subsequent progress and management, which of the following statements is FALSE? (Choose 1 in 5) Creatinine may never return to baseline Over the next few days, Mr Bala may develop hypernatremia Over the next few days, Mr Bala may develop hypokalaemia Candesartan should not be restarted, regardless of creatinine level The temporary dialysis catheter should be removed.

26 Management of AKI Oliguric phase Remove inciting agent (sepsis, toxin, etc) Supportive management especially that for complications Polyuric phase Balance I/O Correct electrolyte losses Recovery phase But creatinine may never return to baseline

27 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD? 3. How can I retard disease progression? 4. What complications do I have to manage? 5. Is it time to start renal replacement therapy? 6. If on RRT, what are the issues with RRT? 7. What are the comorbids?

28 Practical approach to CKD

29

30 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD?

31 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD? 3. How can I retard disease progression? Treat the cause Inhibit proteinuria Avoid further insults 4. What complications do I have to manage? 5. Is it time to start renal replacement therapy? 6. If on RRT, what are the issues with RRT? 7. What are the comorbids?

32 The crucial role of ACE inhibition

33 Scenario Q6 Over the new few days, Mr Bala receives IV hydration and electrolyte corrections. His vascular catheter is removed and he is discharged. At his follow up visit 2-weeks after discharge, he is well and back to his usual daily activities with good effort tolerance. BP is 160/93, HR 79, SpO2 97% on room air. He has slight pedal edema. Laboratory results are:

34 Scenario Q6 BP is 160/93, HR 79, SpO2 97% on room air. He has slight pedal edema. Laboratory results are: Hb 8.3, Ferritin 200 ng/ml, transferrin saturation 18% Cr 201 (GFR 28), Urea 16, Na 134, K 4.5, Cl 105, HCO3 14 cca 2.1 ( ), PO ( ), vit D 23 ng/nmol, ipth 29.5 (1-6) Urine protein/creatinine ratio 1.7 g/g (= proteinuric) US: shrunken kidney, loss of norm parenchymal echogenicity HbA1c 8.5% Meds: PO losartan 50mg OM, PO atorvastatin 40mg ON, PO metformin 500mg BD, PO glipizide 5mg BD

35 Scenario Q6 Q6. All of the following medication changes should be made at THIS visit EXCEPT (Choose 3 in 10): Increase metformin to 850mg BD Increase PO glipizide to 10mg BD Add PO furosemide 40mg OM Add PO calcium acetate 667mg TDS Add PO alphacalcidol ( one alpha ) 0.25mcg 3 times a week Add PO cholecalciferol 1000 unit OM Add PO sodium bicarbonate 500mg TDS Add PO nifedipine LA 30mg OM Add PO ferrous fumarate 400mg BD Add SC recormon (recombinant erythropoietin) 4000 units alternate weeks

36 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD? 3. How can I retard disease progression? 4. What complications do I have to manage? A: Anaemia B: Blood pressure C: Calcium / Phosphate D: Vitamin D / PTH / Bone disease E: Electrolytes - Hyperkalaemia - Acidosis F: Fluid overload 5. Is it time to start renal replacement therapy? 6. If on RRT, what are the issues with RRT? 7. What are the comorbids?

37 Anaemia in CKD Anemia in CKD should be investigated before concluding that it is due to renal disease alone. Target Hb: (avoid <9 or >13) Management 1. Ensure adequate iron stores PO or IV (Aim ferritin >500, transferrin saturation >30%) 2. Prescribe erythropoietin stimulating agent Beware risks: HTN, risk of thrombolic event

38 Blood pressure in CKD Most guidelines: aim <140/90 (KDIGO guideline: <130/80 for proteinuric CKD) Management 1. Use an ACE/ARB 2. Adjust dry weight 3. Add antihypertensives as needed to meet target

39 Ca/PO4 / Bone disease in CKD Pathophysiology

40 Ca/PO4 / Bone disease in CKD Importance: phosphate is a modifiable risk factor in vasculopathy and cardiovascular death. Management: stepwise 1. Bring down the phosphate - Diet: phosphate restriction - Phosphate binder > Calcium-based initially > Non-calcium based if hypercalcemia 2. When phosphate controlled, supplement vitamin D

41 Ca/PO4 / Bone disease in CKD Management: stepwise 1. Bring down the phosphate 2. When phosphate controlled, supplement vitamin D Need an activated form of vitamin D. Note the difference between > Ergocalciferol / cholecalciferol > One alpha calcidol --- the one for CKD > Calcitriol

42 Ca/PO4 / Bone disease in CKD Management: stepwise 1. Bring down the phosphate 2. When phosphate controlled, supplement vitamin D 3. If becomes hypercalcaemic, patient may have developed tertiary hyperparathyroidism. Options: - Cinacalcet - Parathyroidectomy.

43 Electrolytes & Fluid in CKD Hyperkalaemia Diet Resonium Acidosis: Usually NAGMA initially, then NAGMA + HAGMA Associated with mortality Give sodium bicarbonate tab to keep bicarb in normal range Fluid status: Fluid restrict Furosemide

44 Other tasks in CKD Look through all medications: doses often need to be changed Treat comorbids Psychosocial support

45 Scenario Q6 BP is 160/93, HR 79, SpO2 97% on room air. He has slight pedal edema. Laboratory results are: Hb 8.3, Ferritin 200 ng/ml, transferrin saturation 18% Cr 201 (GFR 28), Urea 16, Na 134, K 4.5, Cl 105, HCO3 14 cca 2.1 ( ), PO ( ), vit D 23 ng/nmol, ipth 29.5 (1-6) Urine protein/creatinine ratio 1.7 g/g (= proteinuric) US: shrunken kidney, loss of norm parenchymal echogenicity HbA1c 8.5% Meds: PO losartan 50mg OM, PO atorvastatin 40mg ON, PO metformin 500mg BD, PO glipizide 5mg BD

46 Scenario Q6 Q6. All of the following medication changes should be made at THIS visit EXCEPT: Increase metformin to 850mg BD Increase PO glipizide to 10mg BD Add PO furosemide 40mg OM Add PO calcium acetate 667mg TDS Add PO alphacalcidol ( one alpha ) 0.25mcg 3 times a week Add PO cholecalciferol 1000 unit OM Add PO sodium bicarbonate 500mg TDS Add PO nifedipine LA 30mg OM Add PO ferrous fumarate 400mg BD Add SC recormon (recombinant erythropoietin) 4000 units alternate weeks

47 Scenario Q7 Over the next 3 years, he suffers another 2 episodes of acute kidney injury, both precipitated by infections. He also complains of a change in bowel habit, and is discovered to have T3N1M0 colon cancer for which he undergoes an open right hemicolectomy. His creatinine has increased gradually to 342 (GFR 15) and he feels generally lethargic. Despite furosemide doses of 80mg TDS, he still has bilateral pedal edema but is not dyspneic. He remains normokalaemic. Mr Bala is counselled for dialysis initiation.

48 Scenario Q7 Q7. With regards to dialysis initiation, which of the following options is BEST for Mr Bala? (Choose 1 in 5) He should be offered peritoneal dialysis, which better preserves residual urine output He should be considered for renal transplant. A tunneled catheter (permcath) should be inserted for urgent dialysis initiation He should be referred for early vascular access creation, and hemodialysis initiated thereafter. He should receive an arteriovenous graft as first-choice vascular access.

49 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD? 3. How can I retard disease progression? 4. What complications do I have to manage? 5. Is it time to start renal replacement therapy? Hemodialysis Peritoneal dialysis Transplant 6. If on RRT, what are the issues with RRT? 7. What are the comorbids?

50 Renal replacement therapy Hemodialysis Types: HD, SLED, CRRT Access permanent: AVF (RC, BC, BB) AVG - temporary: Permcath Vascath Peritoneal dialysis Types: Continuous ambulatory PD Automated (night) PD Access: Insertion of tenckoff catheter

51 Renal replacement therapy APD CAPD

52 Renal replacement therapy

53 Renal replacement therapy Complications Adequacy of dialysis Access issues Infection - Line / access sepsis - PD peritonitis Intra-dialysis issues: e.g. hypotension, angina, disequilibrium

54 Scenario Q7 Q7. With regards to dialysis initiation, which of the following options is BEST for Mr Bala? He should be offered peritoneal dialysis, which better preserves residual urine output He should be considered for renal transplant. A tunneled catheter (permcath) should be inserted for urgent dialysis initiation He should be referred for early vascular access creation, and hemodialysis initiated thereafter. He should receive an arteriovenous graft as first-choice vascular access.

55 Practical approach to AKI 1. Is this AKI (vs CKD)? 2. What is (are) the causes? 3. What are the complications? 4. Is dialysis emergent?

56 Practical approach to CKD 1. How bad is the CKD? 2. Why does this patient have CKD? 3. How can I retard disease progression? 4. What complications do I have to manage? A: Anaemia B: Blood pressure C: Calcium / Phosphate D: Vitamin D / PTH / Bone disease E: Electrolytes - Hyperkalaemia - Acidosis F: Fluid overload 5. Is it time to start renal replacement therapy? 6. If on RRT, what are the issues with RRT? 7. What are the comorbids?