Continue Renal Replacement Therapy in liver parenchymal disease.pptx

This presentation show help of continuous renal replacement therapy in patients of liver parenchymal disease

1. Renal Replacement Therapy in Patients of liver parenchymal disease Under guidance of – Dr Pranjal Modi (Prof and head of urology & Abdominal organ transplantation.) Present by- Dr Rahul Amin (fellow ,Abdominal organ transplantation)

2. Acute liver failure Acute liver failure (ALF) is defined by the American Association for the Study of Liver Disease (AASLD) as a new coagulopathy (with International Normalized Ratio [INR] ≥ 1.5) and any degree of encephalopathy without any changes of Cirrhosis

3. Renal Replacement Therapy required in patients of liver parenchymal disease Hyperammonemia Renal impairment

4. Hyperammonemia

5. Case A 12 years/ Female , history of Nausea, vomiting and fever since 28/5/2024 then admitted private hospital Diagnosed viral Hepatitis A, on Day 1 bilirubin 3.3 and SGPT -1854, SGOT -3468, INR -2.07 within 3 days of admission patient’s Enzymes was improving, with mild coagulopathy and mild increased bilirubin, at that time there is no clear cut indication for liver transplant, unfortunately patient develop alter behaviour , Slurred speech, confusion ( hepatic encephalopathy grade 2 lethargy and moderate confusion) since morning 1/6/2024 hence patient referred to IKD for further management and liver transplantation.

6. The shorter the time interval between the start of symptoms and the onset of encephalopathy Greater risk of cerebral edema With Acute kidney injury in ALF Reduced ammonia excretion by Kidneys leads further worsens hyperammonemia .

7. Intestine Liver

8. Hyperammonemia is a fundamental driver of hepatic encephalopathy (HE) Its accumulation in the astrocytes ↓ lead to cerebral edema ↓ intracranial hypertension ↓ and brain stem herniation How increased level of serum ammonia affect brain in liver failure patients?

9. CRRT started Day 1 Day 2 Day 3 Day 4 Day 5 CRRT stopped Day 6 Shift in ward CNS Hepatic encephalopathy grade 2 HE Grade 2 Conscious, mild drowsy Conscious, Oriented Taking orally Conscious,
Oriented
Taking orally Conscious, Oriented Taking orally Bp 104/78 1 episode of hypotension,ini NORAD for 18 hours 100/60 102/66 102/68 100/70 Ammonia 110 55 40 38 Not done Not done SGPT 1338 1272 852 617 436 125 SGOT 1038 1008 565 239 142 104 Bilirubin 4.7/2.9/1.8 5.6/3.7/1.9 5.6/3.4/2.2 4.9/2.8/2.1 5.0/3.2/1.8 7.8/4.5/3.3 Lactate 3.2 2.8 1.1 Not done Not done Not done Creatinine 0.3 0.23 0.18 Not done Not done Not done

10. “ Any extracorporeal blood purification therapy intended to substitute for impaired renal function over an extended period of time and applied for 24 hours/day.” CRRT: Continue Renal Replacement Therapy

11. Indication of CRRT Renal Indications ARF with Oliguria(<400- 500 ml of Urine per 24 Hours in Adults) or Anuria (Absence of Urine production or <100ml per day in Adults) Uremic complications Fluid overload/ pulmonary edema Electrolyte imbalance Metabolic acidosis Non- renal Indications Hyperammonemia in ALF Fluid management in congestive heart failure & multiorgan failure Cerebral edema Metabolic disorders Crush injuries Sepsis Drug overdose

12. PRINCIPLES OF CRRT ULTRAFILTRATION DIFFUSION CONVECTION ADSORPTION |

13. High molecular weight, high protein bound, so high volume of distribution ↓ Poorly dialyzable Cordoba et al. described clearance of ammonia by intermittent HD. An ammonia clearance of 225 ml/min was obtained at a blood flow ( Qb ) of 350 ml/min and a dialysate flow ( Qd ) of 500 ml/min Under the optimal condition NH3 can extracted >80%

14. Intermittent Hemodialysis QB ( blood flow) is high, so can achieve maximum clearance within short time But can not control on Ammonia when patient is not on dialysis Davenport et al. postulated that, in with liver failure ↓ Already increased intracranial pressure, ↓ rapid fluid shifts associated with HD may, in fact, worsen cerebral edema, CRRT Ammonia is continuously being produced & that ammonia can clear each and every minute although if QB is low. No rapid shift as IHD, as CRRT is slow process Better tolerated Great cardiovascular stability Allowing slower correction of hyponatremia decreasing the risk of disequilibrium syndrome

15. Cardoso et al, This was the multi center cohort study Among 340 patients with Acute liver failure with serial ammonia levels, 61 (18%) were on continuous RRT (CRRT), 59 (17%) were on intermittent RRT (IRRT), 220 (65%) no RRT for the first 2 days. From days 1 to 3, median ammonia decreased by 38% CRRT 23% IRRT 19% No RRT

16. Chronic liver disease patient & hyperammonemia Hyperammonemia because of loss of hepatic functional metabolic capacity Other factors : Constipation: bowel colonization with urease containing bacteria enhanced absorption of ammonia secondary to the increased splanchnic blood flow associated with portal hypertension ; decreased ammonia metabolism in muscle because of loss of muscle mass increased renal production of ammonia secondary to the respiratory alkalosis commonly seen in these patients which is due to primary hyperventilation and hypokalaemia .

17. Renal impairment

18. Case 58 years / male known case of Diabetes mellitus since 2012 on oral hypoglycemic agent, index presentation was Ascites in October 2023 ,Diagnosed as Chronic liver disease , Was on Diuretic and Albumin therapy, non bleeder, with small esophageal varices, with gross ascites, then in 3/6/2024 on Diuretic treatment patient develop Abdominal distension for that 4L Ascitic Fluid tapping done in private hospital, then after 3-4 days patient had complain of deceased urine output and pedal edema, patient referred to IKD

19. At that time patient creatinine was 7.5 , with serum potassium 7.1,no proteinurea , hematuria, mean blood pressure was 78, no any inotropes,no any sign of Sepsis, TC,CRP,PCT normal, patient received volume explanations as albumin therapy but no response diagnosed as most probably Acute kidney injury hepatorenal syndrome (HRS-AKI)

20. What is HRS ( Hepato -renal syndrome) HRS has been defined as ‘‘a functional renal failure caused by intrarenal vasoconstriction in patients with end-stage liver disease / acute liver failure / alcoholic hepatitis”. HRS-AKI in cirrhosis is a diagnosis of exclusion HRS-AKI are often precipitated by bacterial infection, diarrhoea , bleeding, diuretics, large volume paracentesis, Virus (HBV flare-up) alcohol Hepatitis

21. Definition of AKI in Cirrhotic patients Increase serum creatinine ≥0.3mg/dl (≥26.5lmol/L) within 48h; or percentage increases S Cr≥50% Stage 1 : increase in sCr≥0.3mg/dl or an increase in sCr≥ 1.5 -fold to 2 -fold from baseline;- Stage 2 : increase in sCr > 2 -fold to 3 -fold from baseline;- Stage 3 : increase of sCr > 3 -fold from baseline or sCr≥4.0mg/dl (353.6lmol/L) or initiation of renal replacement therapy

22. CRRT started Day 1 Day 3 Day 5 Day 7 Urine output 150 ml 150 ml 100 ml 80 ml Creatinine 7.5 3.17 2.4 1.76 Sodium 134 134 135 135 Potassium 7.1 3.9 4.2 4.3 On Day 7 CRRT stopped and started inj Terlipressin infusion as 3 amp in 50 CC NS 2.2 ml/ hr with inj albumin 20 % -10 ml/ hr

23. https://www.journal-of-hepatology.eu/article/S0168-8278(24)00214-9/fulltext#:~:text=The%20following%20diagnostic%20criteria%20for,absence%20of%20improvement%20in%20serum

24. Urinary neutrophil gelatinase associated lipocalin (NGAL)is the most promising for diagnosis of Acute Tubular Necrosis. STOP DIURETIC
STOP BETA BLOCKER
STOP other NEPHROTOXIC DRUG Antibiotics if Urosepsis Replace volume if volume loss
20% albumin solution at the dose of 1g of albumin/kg weight For HRS There should be No Signs of renal parenchymal damage (proteinuria/haeamturia / ultrasongraphy )

25. Terlipressin ( splanchnic vasoconstictor ) was initially proposed to be administered by i.v. boluses at a starting dose of 0.5–1 mg every 4–6 h, progressively increased to a maximum of 2mg every 4–6h Noradrenaline can be analternative to terlipressin . However, limited data is available. The indications for RRT in cirrhotic patient : severe and/or refractory electrolyte or acid-base imbalance or refractory volume overload, and/or symptomatic azotaemia . Pharmacological treatment and RRT serve as a “bridge” to transplant to improve the patient’s prognosis. For HRS AKI

26. Recent data suggest that in patients with HRS-AKI as part of the ACLF syndrome, improving renal function with RRT may decrease 28-day mortality by decreasing the number of organ failure. Liver transplantation is the only curative treatment of HRS-AKI

27. Reference Thummaporn Naorungroj , Fumitaka Yanase , Glenn M. Eastwood, Ian Baldwin, Rinaldo Bellomo ; Extracorporeal Ammonia Clearance for Hyperammonemia in Critically Ill Patients: A Scoping Review. Blood Purif 20 July 2021; 50 (4-5): 453–461. https://doi.org/10.1159/000512100 Gupta S, Fenves AZ, Hootkins R. The Role of RRT in Hyperammonemic Patients. Clin J Am Soc Nephrol . 2016 Oct 7;11(10):1872-1878. doi : 10.2215/CJN.01320216. Epub 2016 May 19. PMID: 27197910; PMCID: PMC5053785. EASL Clinical Practice Guidelines on the management of hepatic encephalopathy :Journal of Hepatology 2022 vol. 77 j 807–824