Acute Cholangitis: Diagnostic Criteria and Management.pptx

This presentation describe the diagnostic criteria, risk factors and management if acute cholangitis.

1. Acute Cholangitis Diagnostic Criteria & Severity Assessment Dr Monkez M Yousif MD, AGAF Professor of Internal Medicine Zagazig University 2023

2. Definition Inflammation of the biliary tree This inflammation is more commonly caused by enteric bacteria in the instance of biliary stasis or obstruction

3. Epidemiology Acute cholangitis is not uncommon Occurs in patients with gallstones (0.3-1.6%) 12% of these cases fit the Tokyo guidelines for severe disease Median age of presentation is between 50-60 y

4. Etiology

5. Etiology - Choledocolithiasis Gallstones lodged in the CBD are the most common cause They obstruct the flow of bile This stasis of bile permits the ascent of enteric bacteria via Ampulla of Vater from the duodenum resulting in inflammation Elevated pressure in the CBD may also result in infection spreading to the bloodstream via the bile canaliculi, hepatic veins, and perihepatic lymphatics leading to bacteremia

6. Etiology - ERCP ERCP can cause cholangitis where endoscopes and accessories introduce infection into the biliary tree if not adequately sterilized Risk factors for ERCP infection include: Incomplete drainage of the biliary tree Presence of jaundice Placement of a stent in malignant bile duct strictures (such as those caused by pancreatic cancer)

7. Etiology – Obstructive tumors Carcinoma of head of pancreas causing narrowing of CBD

8. Etiology – Obstructive tumors Choloangiocarcinoma – these most commonly present in the seventh decade of life The position of these tumors can vary There are 3 main classifications based on the site of these tumors Intrahepatic tumors of the left and right hepatic ducts Extrahepatic tumors Hilar (occur near the junction of Rt and Lt hepatic ducts Distal (can present from the ampulla of Vater upwards)

9. Etiology – Obstructive tumors Porta hepatis mass The porta hepatis is a groove on the inferior surface of the liver where various structures pass-through A wide array of conditions can cause a mass to develop at this point, impeding bile flow This could include for example, thrombosis, stenosis or aneurysm of the portal triad vessels , or even a rare mass from nerves that pass through a neurofibrosarcoma

10. Etiology – Benign Bile Strictures The majority of these strictures (80%) are iatrogenic , caused by procedures such as ERCP Other causes of benign biliary strictures include: Primary sclerosing cholangitis Pancreatitis

11. Etiology – Malignant Bile Strictures Malignant bile strictures are strictures secondary to malignancy: Choloangiocarcinoma Pancreatic carcinoma Ampullary carcinoma Hepatocellular carcinoma Lymphoma Metastasis

12. Etiology – Mirizzi Syndrome This is where the CBD is obstructed by a large gallstone in the cystic duct

13. Pathogenesis Normally, there are different defensive mechanisms to prevent cholangitis. The bile salts have bacteriostatic activity The biliary epithelium secretes IgA and mucous which probably act as anti-adherent factors. Kupffer cells on the biliary epithelium and the tight junction between the cholangiocytes prevent translocation of bacteria from the hepatobiliary system into the portal venous system. Normal bile flow flushes out any bacteria into the duodenum. The sphincter of Oddi also prevents any migration of bacteria from the duodenum into the biliary system.

14. Pathogenesis Biliary obstruction → Bile stasis in the biliary system → ↑ intraductal pressure → Widening of the tight junction between cholangiocytes Malfunction of Kupffer cells Decreased IgA secretion cholangiovenous and cholangiolymphatic reflux leading to bacteremia and endotoxemia Systemic release of inflammatory mediators like: TNF, IL- 1,6, 10 leading to hemodynamic instability

15. Diagnosis

16. Jean-Martin Charcot 1877

17. Reynolds BM, Dargan EL (August 1959). "Acute obstructive cholangitis; a distinct clinical syndrome". Ann Surg. 150 (2): 299–303.

18. Lab workup Initial blood tests include: CBC, CRP, PT, LFTs, KFTs Specifically for diagnostic criteria purposes: Inflammation WBC < 4k or > 10K or CRP ≥ 10 mg/L Jaundice T Bill ≥ 2 Abnormal liver chemistries ALP > 1.5 × ULN AST > 1.5 × ULN GGT > 1.5 × ULN ALT > 1.5 × ULN

19. Imaging Ultrasound Typically, the initial test performance due to accessibility and the noninvasive nature Can evaluate for bile duct dilatation and bile duct stones with high specificity (94-100%), but varying sensitivity (38-91%) Abdominal CT scan High sensitivity for bile duct dilatation and biliary stenosis High radiation MRI/MRCP Imaging of choice when indeterminate CT or US findings Highly specific (98%) and sensitive (100%) for evaluation of biliary duct dilatation

20. Endoscopic Ultrasound (EUS) Best imaging test Only takes 5 minutes Can perform ERCP at the same time Invasive

21. Diagnostic criteria for AC adapted from TG18/ 13 A. Systemic inflammation B. Cholestasis C. Imaging A-1. Fever and/or shaking chills (T >38°C) B-1. Jaundice. T. bilirubin ≥2 mg/dl C-1. Biliary dilatation A-2 . Evidence of inflammatory response. WBC <4 k or >10 k/mm 3 , CRP>/10mg/L B-2. Abnormal LFTs ALP (>1.5 × ULN) GGT (>1.5 × ULN) AST (>1.5 × ULN) ALT (>1.5 × ULN) C-2. Evidence of etiology on imaging stricture, stone, stent, and others Suspected diagnosis: one item in A + one item in either B or C; Definite diagnosis: one item in A, one item in B + one item in C Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholangitis (with videos). J Hepatobiliary Pancreat Sci. 2018 Jan;25(1):17-30.  Note: Other factors which are helpful in diagnosis of acute cholangitis include abdominal pain (right upper quadrant or upper abdominal) and a history of biliary disease such as gallstones, previous biliary procedures, and placement of a biliary stent.

22. Severity assessment criteria for AC adapted from TG18/TG13 Grade Clinical Features Laboratory Findings I- Mild Does not meet the criteria of ”grade III (severe)” or ”grade II (moderate)” AC at initial diagnosis II- Moderate AC + any 2 of the following conditions: 1. Abnormal WBC count (>12k/mm 3 or <4k/mm 3 ) 2. Fever (≥39°C) 3. Age (≥75 years) 4. Hyperbilirubinemia (total bilirubin ≥5 mg/ dL ) 5. Hypoalbuminemia ( < 0.7 x ULN) III- Severe AC + one dysfunction at least in any of the following systems: 1. Cardiovascula r— hypotension requiring vasopressors (dopamine >5 ug/kg per min or any dose of norepinephrine) 2. Neurologica l — disturbance of consciousness 3. Respiratory — PaO 2 /FiO 2 <300 4. Renal — oliguria, serum creatinine >2.0 mg/ dL 5. Hepatic — INR >1.5 6. Hematologic — platelet count <100k/mm 3

23. Differential Diagnosis Acute cholecystitis Biliary leak Acute pancreatitis Liver abscess Acute hepatitis

24. Triage Disposition Mild AC Regular floor Will need access to endoscopic surfaces for biliary drainage if no response to treatment within 24 hours or choledocholithiasis suspected Moderate AC Regular floor or step down Will need access to endoscopic surfaces for biliary drainage Severe AC ICU level care Emergent biliary drainage

25. Overall Treatment Approach Disease severity may help guide the treatment plan Mortality can exceed 50% if cholangitis is not treated General management approach Supportive treatment and hemodynamic stabilization Antibiotic therapy Biliary decompression

26. Supportive Therapy Volume resuscitation with IV fluids Analgesics for pain control Antiemetics Correction of electrolyte disturbances Treatment of end-organ dysfunction Pressors for septic shock Intubation for respiratory support NPO for potential biliary drainage procedures Discontinuation and reversal of anticoagulation

27. Antibiotic Therapy Antibiotic selection should target the most common intra-abdominal bacteria Initial choice can be piperacillin-tazobactam , cephalosporin plus metronidazole, or ampicillin-sulbactam depending on severity Tailor antibiotic selection to culture and susceptibility results Duration of antibiotic treatment is usually 7 days after source control is achieved and longer if bacteremia is present

28. Isolated microorganisms from bile cultures Proportions of isolated organisms (%) Gram-negative organisms Escherichia coli Klebsiella  spp. Pseudomonas  spp. Enterobacter  spp. Gram-positive organisms Enterococcus  spp. Streptococcus  spp. Staphylococcus  spp. Anaerobes 31–44 9–20 0.5–19 5–9 3–34 2–10 in bile but 3.6 in blood culture 4–20 Common microorganisms isolated from bile cultures among patients with acute biliary infections (endorsed from the TG13)

29. Endoscopic Intervention ERCP is the primary modality of choice Stone Extraction Endoscopic drainage with or without biliary stent

30. Percutaneous Transhepatic Biliary Drainage Performed when endoscopic drainage is unavailable, unsuccessful, or the patient is too unstable for anesthesia Can be done by IR via intrahepatic approach into the bile duct

31. Alternative Intervention EUS-guided biliary drainage in patients with moderate-severe cholangitis Surgical Drainage Rarely used, when all other methods of source control have failed

32. Timing of Endoscopic Intervention Early biliary drainage via ERCP within 24 h has been associated with decreased hospital stay and recurrent cholangitis, though no significant difference in mortality if done within 72 h

33. Prognosis Early studies from the 1970s show mortality rates exceeding 50% More recent studies show mortality rates of 11% or less for mild to moderate disease Severe disease carries a mortality rate between 20-30%

34. Flowchart for the initial response to acute biliary infection

35. Take-Home Messages AC is an infection of the biliary tree Diagnosis is based on evidence of systemic inflammation, cholestasis, and imaging findings of biliary obstruction Mainstays of treatment are end-organ support, IV antibiotics, and biliary decompression Disease severity can be mild, moderate, or severe, which can help inform the disposition and timing of biliary drainage Mortality rates are decreasing with improvements in patient care and biliary drainage techniques

36. Monkez Yousif