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Hepato Renal Syndrome : 

Hepato Renal Syndrome Dr.J.Rajesh., DNB.,D.A.,

Definition : 

Definition HRS is defined as the development of renal failure in patients with advanced liver failure (acute or chronic) in the absence of any identifiable causes of renal pathology

Introduction : 

Introduction Usually occurs in patients with advanced liver disease and portal hypertension characterized by Renal failure, with creatinine level more than 1.5mg/dl Marked decrease in GFR and renal plasma flow (RPF) in the absence of other identifiable cause of renal failure Marked abnormality in systemic hemodynamics Activation of endogenous vasoactive systems

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HRS occurs predominantly in the setting of cirrhosis, but it may also develop in other types of severe chronic liver diseases, such as alcoholic hepatitis, or in acute liver failure.

HRS can occur with…. : 

HRS can occur with…. Cirrhosis - Predominant Alcoholic hepatitis Fulminant hepatic failure Infection Bleeding in the gastrointestinal tract Overuse of diuretic medications

HRS - Pathophysiology : 

HRS - Pathophysiology Hepatorenal syndrome is associated with critically low perfusion and blood flow to the kidneys due to deteriorating liver function This cause changes in the circulation that supplies the intestines altering the blood flow and blood vessel tone in the kidneys.

HRS : 

HRS The renal failure in HRS is a consequence of changes in blood flow rather than direct damage to the kidney Kidneys themselves are normal in form when viewed grossly and under the microscope Kidneys function normally in a normal environment, such as if transplanted into a person with a healthy liver

Pathophysiology : 

Pathophysiology Factors involved in the pathogenesis of HRS are: Disturbance in systemic hemodynamics (VD mainly splanchnic) Increased activity of vasoconstrictor systems Reduced activity of vasodilator factors

Pathophysiology : 

Pathophysiology Vasodilators Prostaglandins Nitric oxide Atrial natriuritic peptide Vasoconstrictors RAAS and SNS ADH , Endothelin Adenosine, leukotrienes

Pathophysiology : 


Pathophysiology : 


Arterial vasodilation theory : 

Arterial vasodilation theory Effect of vasoconstrictor systems acting on the renal circulation Homeostatic mechanisms to improve the extreme underfilling of the arterial circulation Decreased renal perfusion and glomerular filtration rate (GFR) but tubular function is preserved.

Underfill theory : 

Underfill theory The renal failure arise from abnormalities in blood vessel tone in the kidneys Blood vessels in the renal circulation are constricted due to the dilation of blood vessels in the splanchnic circulation (supplies the intestines), which is mediated by factors released by liver disease (NO, Pg) Decrease in the "effective" volume of blood sensed by the juxtaglomerular apparatus, leading to the secretion of renin and the activation of the renin-angiotensin system

Underfill theory : 

Underfill theory Activation of RAS ? vasoconstriction of vessels systemically and in the kidney Insufficient to counteract the mediators of vasodilation in the splanchnic circulation ? persistent "underfilling" of the renal circulation and worsening renal vasoconstriction ? renal failure

Types : 

Types There are two well-differentiated clinical patterns of HRS Type 1 HRS Type II HRS In both categories, the deterioration in kidney function is quantified either by an elevation in creatinine level in the blood, or by decreased clearance of creatinine in the urine

Type I HRS : 

Type I HRS Characterized by rapid and progressive impairment of renal function (doubling of the initial serum creatinine to a level greater than 2.5 mg/dl or a 50% reduction of the initial 24-hour creatinine clearance to a level lower than 20 ml/min in less than 2 weeks) Usually occur in severe liver failure (Jaundice, encephalopathy, and coagulopathy) Occur frequently after precipitating factor (e.g. GI bleeding)

Type 2 HRS : 

Type 2 HRS Characterized by a less severe and non-progressive reduction of GFR Associated with relatively preserved liver function The main clinical consequence of this type of HRS is refractory ascites, due to a lack of response to diuretics

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Type 1 HRS Rapid decline in renal function, defined as a doubling of serum creatinine to a level > 2.5 mg/dL or Halving of the creatinine clearance to < 20 mL/min within 2 weeks. The clinical presentation is that of acute renal failure Type 2 HRS Renal function deteriorates more slowly, with serum creatinine increasing to > 1.5 mg/dL or a creatinine clearance of < 40 mL/min The clinical presentation is that of stable renal failure in a patient with refractory ascites

Diagnosis of HRS - Problems : 

Diagnosis of HRS - Problems The presence of renal dysfunction is often missed in patients with cirrhosis. Because of a reduction in muscle mass in these patients, serum creatinine may be within the normal range, even with a very low GFR. The use of blood urea nitrogen (BUN) concentration as a measure of renal function is even less reliable, because BUN levels can be affected by the presence of gastrointestinal bleeding or by the amount of protein in the diet.

Diagnosis of HRS : 

Diagnosis of HRS HRS should only be diagnosed in patients with decreased renal function in the presence of advanced cirrhosis, chronic liver disease with severe liver failure and portal hypertension, or acute liver failure. Other forms of organic renal disease must be ruled out.

Diagnosis of HRS : 

Diagnosis of HRS Some patients with primary liver diseases are at higher risk for developing certain forms of kidney diseases While some systemic processes can affect both the liver and the kidney The International Ascites Club requires major criteria to be fulfilled for the diagnosis of HRS Despite the existence of these criteria, arriving at an accurate diagnosis can be challenging.

Renal Disease Associated With Major Types of Liver Disease : 

Renal Disease Associated With Major Types of Liver Disease

Systemic Diseases Involving Both Liver and Kidney : 

Systemic Diseases Involving Both Liver and Kidney Drug toxicity -- acetaminophen, acetylsalicylic acid, carbon tetrachloride, etc. Granulomatous diseases (sarcoidosis, drug-induced) Infectious -- malaria, leptospirosis Infiltrative – amyloidosis Inflammatory -- lupus, Sjogren's syndrome

Systemic Diseases Involving Both Liver and Kidney : 

Systemic Diseases Involving Both Liver and Kidney Nonalcoholic fatty liver disease and diabetic nephropathy Preeclampsia/HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome Polycystic kidney/liver disease (autosomal dominant/autosomal recessive forms) Sickle cell disease Shock states (congestive heart failure, sepsis, hypovolemia

Hepatorenal Syndrome: Diagnostic Criteria (International ascites club) : 

Hepatorenal Syndrome: Diagnostic Criteria (International ascites club) Major criteria (all must be present) Chronic or acute liver disease with advanced hepatic failure and portal hypertension Low GFR as indicated by a 24-hr creatinine clearance of < 40 mL/min or serum creatinine > 1.5 mg/dL Absence of shock, sepsis, volume depletion, exposure to nephrotoxins. No sustained improvement in renal function (to creatinine > 1.5 mg/dL or 24-hr CrCl to > 40 mL/min) following diuretic withdrawal and plasma volume expansion with 1.5 L of normal saline Proteinuria < 500 mg/dL. No ultrasonographic findings of obstructive uropathy or parenchymal renal disease.

Hepatorenal Syndrome: Diagnostic Criteria : 

Hepatorenal Syndrome: Diagnostic Criteria Additional criteria (not necessary but would support diagnosis) Urine volume < 500 mL/day Urine sodium < 10 mEq/L Urine osmolality greater than plasma osmolality Urine red blood cells < 50 per high-power field Serum sodium < 130 mEq/L

Work-up for Patients With Suspected HRS : 

Work-up for Patients With Suspected HRS History Fluid losses -- vomiting, diarrhea, diuretic use Gastrointestinal bleeding Infection -- fever, cough, dysuria, abdominal discomfort Exposure to nephrotoxins -- drugs (aminoglycosides, NSAIDs), radiocontrast agents

Physical exam : 

Physical exam Heart rate, blood pressure (including orthostatic), temperature Signs of infection (pulmonary, abdominal, cellulitis, etc.) Other causes of renal failure -- purpuric rash may suggest cryoglobulinemia

Investigations : 

Investigations Complete blood count, electrolytes, creatinine level Urine sodium, osmolality Urinalysis for protein, cells, and casts Renal ultrasound

Differentiating HRS From Other Forms of Renal Failure in Liver Disease : 

Differentiating HRS From Other Forms of Renal Failure in Liver Disease

Management of HRS -- Prevention : 

Management of HRS -- Prevention Prophylaxis Against Bacterial Infections Prophylaxis with antibiotics is recommended in patients presenting with gastrointestinal bleeding or those with a history of SBP Volume Expansion Postparacentesis circulatory dysfunction is not always spontaneously reversible, it then follows that albumin should be able to prevent the development of HRS after large-volume paracentesis. Albumin seems to be the best plasma expander to prevent this complication.

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Judicious Use of Diuretics Diuretic-induced renal impairment occurs in 20% of patients with ascites The renal failure is nearly always reversible with cessation of the diuretics Avoidance of Nephrotoxic Agents Patients with cirrhosis and ascites are predisposed to ATN with use of aminoglycosides NSAIDs should also be avoided Angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists result in arterial hypotension and cause prerenal failure in cirrhotic patients

Management of HRS -Initial : 

Management of HRS -Initial Search for precipitating factors Nephrotoxic drugs should be removed Fluid challenge to assess response and to treat subclinical hypovolemia Managed in intensive care units to protect effective circulating blood volume and renal perfusion In patients with cirrhosis and SBP, treatment with intravenous albumin in addition to an antibiotic has been shown in one study to reduce the incidence of renal impairment and death compared with treatment with an antibiotic alone.

Management of HRS : 

Management of HRS Pharmacologic Therapy The aim of pharmacologic therapy is to increase renal blood flow - accomplished either by improving the renal perfusion pressure or by inducing renal vasodilatation. Splanchnic vasoconstriction redistributes some of the intravascular volume to the systemic circulation and improves circulatory function and effective arterial volume, thereby improving renal perfusion and GFR.

Management of HRS : 

Management of HRS Dopamine Noradrenaline Midodrine and octreotide Endothelin antagonists

Management of HRS : 

Management of HRS Terlipressin Synthetic analogue of vasopressin, with intrinsic vasoconstrictor activity, nonselective V1 vasopressin agonist Improve systemic hemodynamics and to improve renal function in patients with type 1 HRS In addition to improving renal function, this agent has been associated with improved survival. One suggested protocol consists of 0.5 mg every 4 hours with a titration upward by 0.5 mg every 3 days up to 2 mg every 4 hours

Management of HRS : 

Management of HRS Renal Support Dialysis Should only be offered in select cases if there is a real chance of liver transplantation in the short term Dialysis in these patients is fraught with difficulties because of coagulopathy and hemodynamic instability, as well as risk of sepsis The effectiveness of dialysis in the treatment of HRS has not been proven.

Management of HRS - Procedural : 

Management of HRS - Procedural Transjugular Intrahepatic Portosystemic Shunt TIPS has been shown to improve renal function in patients with hepatorenal syndrome Involves the decompression of the high pressures in the portal circulation by placing a small stent between a portal and hepatic vein The main limitation to using TIPS in HRS includes Worsening encephalopathy Liver failure from reduced liver venous perfusion, thereby causing relative liver ischemia.

Other procedures : 

Other procedures Liver dialysis - extracorporeal dialysis to remove toxins from the circulation, usually through the addition of a second dialysis circuit that contains an albumin-bound membrane MARS – Molecular adsorbents recirculation system - removes some of the vasoactive substances that mediate the hemodynamic changes that lead to HRS, thereby improving systemic hemodynamics and, hence, renal perfusion.

Liver Transplantation : 

Liver Transplantation The only effective and permanent treatment for end-stage cirrhosis and HRS is liver transplantation Patients who are transplanted with HRS have a lower probability of both graft and patient survival after liver transplantation compared with patients without HRS

Whats Anaesthesiologist’s role in HRS? : 

Whats Anaesthesiologist’s role in HRS?

HRS – Anaesthesiologist’s view.. : 

HRS – Anaesthesiologist’s view.. 3 major complications of advanced liver disease Portal hypertension – variceal haemorrhage Intractable fluid retention – Ascites, HRS Hepatic encephalopathy

Hepatorenal syndrome : 

Hepatorenal syndrome Functional renal deficit in patients with advanced liver disease Follows GI bleed, Diuretics, Sepsis, Major surgery Features – Progressive oliguria, ? Na+ retention, Azotemia, Ascites

Preoperative preparation : 

Preoperative preparation Avoid preoperative diuresis Maintain adequate hydration - IV hydration for 12 hours before surgery Intravascular volume deficit correction with Colloids Loop diuretics only after bed rest,sodium restriction Daily body weight measurement during diuresis Hyponatremia – Water retention Potassium supplementation Mannitol Infusion

Allowed Weight loss : 

Allowed Weight loss Ascites + Peripheral edema ? < 1 kg/day loss allowed Ascites ? < 0.5 kg/day loss allowed

Intraoperative considerations : 

Intraoperative considerations Monitors 5 lead ECG ABP CVP,PAC Pulse oximetry ABG Urine output Others – Temperature, PNS

Intraoperative considerations : 

Intraoperative considerations Anaesthetic technique ? Regional Vs General anaesthesia Avoid hypotension with regional anaesthesia Preferred technique is General anaesthesia - RSI

Intraoperative considerations : 

Intraoperative considerations Maintain adequate intravascular volume status with colloids Colloid replacement for ascites removal Blood transfusion as indicated Prophylactic Mannitol Avoid Halothane – ISOFLURANE is DOC Vigilent monitoring – CVP, ABP, U.O

Postoperative considerations : 

Postoperative considerations Maintain adequate intravascular volume status CVP, U.O guided fluid resuscitation Mannitol infusion

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