A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
Management of renal vein thrombosis by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of renal vein thrombosis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This lecture is for undergraduates and post graduates. It is a case based discussion, taking the audience from definition of ascites and spontaneous bacterial sepsis to its symptomatology, physical findings, diagnostic algorithm and management of ascites and bacterial peritonitis
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
Management of renal vein thrombosis by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of renal vein thrombosis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This lecture is for undergraduates and post graduates. It is a case based discussion, taking the audience from definition of ascites and spontaneous bacterial sepsis to its symptomatology, physical findings, diagnostic algorithm and management of ascites and bacterial peritonitis
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
2. SBP- Definition
Ascitic fluid infection without evident intra-abdominal
surgicically treatable source
Usually occurs in patients with cirrhosis and ascites
3. SBP - Pathogenesis
Overgrowth of intestinal flora (usually E. coli) and spread outside
into mesentery and lymph nodes (translocation)
Cirrhosis decreases intestinal motility
Increased permeability
OR from other infections (e.g. UTI, cellulitis)
Lymphatic rupture of contaminated lymph d/t portal hypertension
(bacteriascites)
Microbes overwhelm host defenses
Cirrhosis = acquired immune deficiency (decreased compliment
capability)
9. SBP - Treatment
Ascitic PMN <250 cells/mm3 +
Signs/symptoms of infection:
Empiric antibiotic therapy, e.g. ceftotaxime 2 g IV q8h, while
awaiting cultures
American Association for the Study of Liver Disease (2012)
10. SBP - Treatment
Ascitic PMN ≥250 cells/mm3 +
Community-acquired setting + absence of β-lactam antibiotic exposure:
Empiric antibiotic therapy, e.g. IV third generation cephalosporin, preferably
cefotaxime 2 g IV q8h
Nosocomial setting ± in the presence of recent β-lactam antibiotic
exposure:
Empiric antibiotic therapy based on local susceptibility testing of bacteria in
patients with cirrhosis
Can substitute with ofloxacin 400 mg PO BID in inpatients without prior
exposure to quinolones, vomiting, shock, grade ≥II hepatic
encephalopathy, or SCr >3 mg/dL
American Association for the Study of Liver Disease (2012)
11. SBP - Treatment
Ascitic PMN ≥250 cells/mm3 +
High suspicion of secondary peritonitis
Test for protein, LDH, glucose, gram stain, carcinoembryonic antigen and
alkaline phosphatase (distinguish between SBP and secondary peritonitis)
Computed tomographic scanning
Nosocomial setting ± recent β-lactam antibiotic exposure ± atypical
organism or atypical clinical response to treatment
Follow-up paracentesis after 48 hours of treatment
Clinical suspicion of SBP, SCr >1 mg/dL, BUN >30 mg/dL or tBili >4
mg/dL
Albumin 1.5 g/kg within 6 hours and 1 g/kg on day 3
American Association for the Study of Liver Disease (2012)
12. SBP - Prophylaxis
Cirrhosis and GI bleeding
IV ceftriaxone or norfloxacin BID x 7 days
Survived an episode of SBP
Long-term norfloxacin 400 mg QD (or SMX/TMP)
Cirrhosis and ascites but no GI bleeding + ascitic fluid protein
<1.5 g/dL + renal insufficiency (SCr ≥1.2 mg/dL, BUN ≥25 mg/dL
or serum Na+ ≤130 mE/L) or hepatic failure (Child-Pugh ≥9 points
+ bilirubin ≥3 mg/dL)
Long-term norfloxacin (or SMX/TMP)
Daily (vs. intermittent) antibiotic dosing recommended
American Association for the Study of Liver Disease (2012)
16. Hepatic Encephalopathy – Classification
Underlying Disease
Hepatic encephalopathy occurring in the setting of…
Type A Acute liver failure
Type B Portal-systemic bypass with no intrinsic hepatocellular disease
Type C Cirrhosis with portal hypertension or systemic shunting
Severity of Manifestations
Minimal Abnormal results on psychometric or neurophysiologic testing without
clinical manifestations
Grade I Changes in behavior, mild confusion, slurred speech, disordered
sleep
Grade III Marked confusion (stupor), incoherent speech, sleeping but arousable
Grade IV Coma, unresponsive to pain
17.
18.
19. Hepatic Encephalopathy - Diagnosis
History and physical exam
Cognitive and neuromuscular impairments
Laboratory tests
Ammonia, glucose, urea, electrolytes
Psychometric tests
Changes in mental function
Number connection test (NCT; Reitan Test), Psychometric Hepatic
Encephalopathy Score (PHES)
Electrophysiology tests
E.g. electroencephalogram (EEG)
Imaging
MRI, CT
20. Hepatic Encephalopathy – Differential
Diagnosis
Reye syndrome
GI bleeding
Renal disease
UTI with urease-producing microbe (e.g. P. mirabilis)
Shock
Severe muscle exertion
Metabolic abnormalities
Salicylate intoxication
24. References
Runyon BA. Pathogenesis of spontaneous bacterial peritonitis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016.
Runyon BA. Spontaneous bacterial peritonitis in adults: Clinical manifestations. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April
2016.
Runyon BA. Spontaneous bacterial peritonitis in adults: Diagnosis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016.
Runyon BA. Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27
April 2016.
Runyon BA. Practice Guideline: Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012. American Association for the Study of Liver
Diseases. (2012). p. 1-96.
Ferenci P. Hepatic encephalopathy: Pathogenesis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016.
Ferenci P. Hepatic encephalopathy in adults: Clinical manifestations and diagnosis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 28
April 2016.
Leise MD, Poterucha JJ, Kamath PS, et al. Management of Hepatic Encephalopathy in the Hospital. Mayo Clin Proc. 2014; 89(2): 241-253. PMC4128786
Editor's Notes
SBP bacteria require phagocytosis via opsonization (complement) and/or Ig
Ascitic fluid 10-fold more dilute than serum (less compliment factors)
Serum complement deficient common in liver disease patients advanced enough to produce ascites
SBP bacteria require phagocytosis via opsonization (complement) and/or Ig
Ascitic fluid 10-fold more dilute than serum (less compliment factors)
Serum complement deficient common in liver disease patients advanced enough to produce ascites
SBP bacteria require phagocytosis via opsonization (complement) and/or Ig
Ascitic fluid 10-fold more dilute than serum (less compliment factors)
Serum complement deficient common in liver disease patients advanced enough to produce ascites
SBP bacteria require phagocytosis via opsonization (complement) and/or Ig
Ascitic fluid 10-fold more dilute than serum (less compliment factors)
Serum complement deficient common in liver disease patients advanced enough to produce ascites
SBP bacteria require phagocytosis via opsonization (complement) and/or Ig
Ascitic fluid 10-fold more dilute than serum (less compliment factors)
Serum complement deficient common in liver disease patients advanced enough to produce ascites
“Widespread use of quinolones to prevent SBP in high-risk subgroups of patients as well as frequent hospitalizaions and exposure to broad-spectrum antbiotics have led to a change in flora with more gram-positives and extended spectrum B-lactamase producing Enterobacteriaceae in recent years. Risk factors for multireisstant infections include: nosocomial origin of infection, long-term norfloxacin prophylaxis, recent infection with multiresistant bacteria, and recent use of B-lactam antibiotics.”
LOLA = L-ornithine L-aspartate
BCCA = branch chain amino acids
MARS = Molecular Adsorbent Recirculating System
LOLA = L-ornithine L-aspartate
BCCA = branch chain amino acids
MARS = Molecular Adsorbent Recirculating System
