Infectious Diseases Of The Liver - Emergency Room Procedures

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Presentation, diagnosis, and treatment of infectious diseases of the liver in the emergency room setting.

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  • Although the viral hepatitides have a very similar presentation, the subtypes can sometimes be differentiated by the time course, suspected source, host differences, environment and characteristic clinical syndromes. A diligent history best narrows the diagnosis. 5 different hepatitis virus agents have been recognized: A, B, C, D and E/an additional 4% of acute cases may be due to a viral agent not yet identified and are currently classified as “G” or “X” Other viral agents such as CMV, EBV, HSV, HIV, can produce similar clinical syndrome but these are rarely seen in the immunocompetent patients. Yellow fever: due to a flavivirus which causes hepatocellular and tubular(renal) necrosis. Hepatic manifestations include: jaundice, albuminuria, coagulopathy which produces the characteristic black vomit, epistaxis, gum bleeding, petechial & purpuric hemorrhages. Present in South America & Sub-Saharan Africa
  • to a polycyclic waxing and waning of sx to the abrupt onset of fulminant hepatitis In a “classic” presentation, 4 phases of infection can be characterized Asymptomatic phase of viral replication where serologic & enzyme markers can be measured Prodromal phase occurs next. One interesting symptom is aversion to cigarette smoke even in smokers. Patients who present during this phase are often diagnosed with “Viral Syndrome”, “URI” or “Viral Gastroenteritis” Icteric phase: that’s the phase when most patients present, GI symptoms and malaise predominate and the patient may complain of RUQ pain with corresponding hepatomegaly on exam. Before becoming jaundiced the patient may c/o darkening of the urine and then lightening of the stool, a historic finding that should always be sought. Final phase is a convalescent phase, where sx subside, icterus abates and LFT’s normalize, unless the infection becomes chronic. In chronic viral infection, the acute phases of infection are not frequently recalled and the patient seeks care for abnormal liver tests found on routine testing or for gradual onset of chronic fatigue.
  • abdo pain: especially in RUQ Rash can be macular, papular, urticarial or a serum sickness syndrome Magnitude of transaminases elevation is not a good indicator of severity of disease Imaging: rarely indicated unless there are atypical signs such as high fevers, rigors, colicky pain, high alk phosph, high amylase
  • Early signs of encephalopathy: changes in sleep/wake cycle Anxiety/agitation Personality change Altered mental status
  • The virus is also present in saliva & serum but only serum has been implicated in the rare transmission of HAV via transfusion. You cant get it by kissing, sneezing, coughing or needlestick!
  • Infection with hep B virus results in a broad spectrum of liver disease ranging from subclinical infection, to acute self-limited hepatitis to fulminant hepatic failure. Exposure to HBV especially in infancy may result in an asymptomatic carrier state that progresses to chronic active hepatitis, cirrhosis of the liver and eventually hepatocellular CA. Complex viral and host factors determine the variable clinical outcome More than 1 million HBV related deaths worldwide secondary to hepatocellular CA or cirrhosis 90% of children become carriers that is why it is so crucial to vaccinate babies at birth.
  • 36
  • The hepatitis Be antigen is a more sensitive gauge of ongoing viral replication than HBSAg and is indicative of high infectivity. Detection of HBeAg for >10 weeks suggest chronic infection. IgM anti HBc is usually not detected in patients with chronic HBV infection and can therefore be used to differentiate a chronic from an acute infection in the HBsAg + patient
  • 31
  • Prognosis: 6% risk of dying from hepatocellular CA
  • Hep B Vaccine: EngerixB/ RecombivaxHB TwinRix: hep A + hep B vaccine >18 years age
  • Interferon blocks the production or release of virus from infected cells.
  • Hep C discovered on 1989 (HIV 1983) Rates of infection in some prisons > 80%
  • - Most patients asymptomatic and discovered to have high LFT’s on routine labs
  • Risk from percutaneous injury: HCW have a prevalence of HBV infection 10X higher than the general population Because it can survive at room temp >1 week, infections can occur in HCW with no hx of percutaneous injury, but could have resulted from direct or indirect blood or body fluid exposures that inoculated HBV into scratches, abrasions, burns, other lesions or mucosal surfaces HCV: not transmitted efficiently thru occupational exposures to blood with one study indicating that transmission occurred only from hollow-bore needles compared with other sharps.
  • 1 1 1
  • But Hep C is more virulent with 50% chance of developing significant liver disease
  • Hygiene and hand washing
  • Flush with 2-3 L/ no vigorous scrubbing Human bites: possible exposure of both the person bitten and the person who inflicted the bite must be considered. If a bite results in blood exposure to either person involved, PEP should be provided SE of vaccine: pain at injection site Anaphylaxis: none died HBIG: screened and prepared by cold ethanol extraction eliminating HIV from the final product. Other methods inactivate HCV and other viruses.
  • Available data suggest that an established infection might need to be present before Interferon can be an effective treatment Data from studies outside the US suggest that a short course of Interferon started early in the course of acute Hep C is associated with a higher rate of resolved infection than if begun after chronic Hep C has been well established In the absence of PEP for HCV, recommendations are intended to achieve early identification of chronic disease
  • 1 million deaths a year/10-30 million new cases a year
  • Age: when seen in children & adolescents, underlying immune deficiency and trauma frequently exist
  • Pathophysiology: Appendicitis was the leading source of PLA in the preantibiotic era, but has been eliminated in recent times. Biliary Tract disease accounts for 60% of case. Obstruction of bile flow allows for bacterial proliferation. Biliary obstruction need not be from stone disease: patients with Caroli’s disease have a particularly high rate of pyogenic liver abscess formation (rare congenital cystic dilatation of intrahepatic bile ducts) Pylephlebitis: suppurative pylephlebitis usually arises from infection in the female genital tract but may result from infection elsewhere in the peritoneal cavity such as diverticulitis, pancreatitis, IBD. This occurs via septic thrombophlebitis of any tributary of the portal venous system. Septic emboli are released in the portal circulation, trapped by the hepatic sinusoids and become the nidus for microabscess formation. Initially, abscesses are multiple but usually they coalesce into a solitary lesion. Contiguous spread from empyema of the Gallbladder, subphrenic or perinephric abscess. About 4% develop in this manner. Cryptogenic cause: we don’t know Trauma: Penetrating via direct inoculation or Blunt Secondary infection can also be a complication of liver transplantation
  • Fever: especially in the elderly, FUO may be the presenting complaint Chills: the only patient I saw with this was having severe RIGORS Abdo pain can be localized to the RUQ or you can have referred pain to the right shoulder Cough due to diaphragmatic irritation may be present Exam: General: Patients are generally systemically unwell especially if they have multiple abscesses with signs of systemic toxicity but individuals with solitary lesions have a more insidious course with weight loss and anemia. 30% have a pleural effusion
  • Ultrasound: allows for close eval. of biliary tree and simultaneous aspiration of cavity/benefits include portability and diagnostic utility in patients too critical/operator dependent CT scan: peripheral enhancement is seen when IV contrast is given, gas can be seen in as many as 20% of lesions, Ct scan is superior in its ability to detect lesions less than 1 cm, also enables the eval. Of concurrent pathology throughout abdomen and pelvis
  • usually is the rule When the biliary tree is the source of infection, enteric gram – bacilli and enterococci are common isolates. Abscesses involving Klebsiella pneumonia has been associated with multiple cases of Endophthalmitis Antibiotics: 2 nd or 3 rd generation ceph, beta-lactam or beta-lactamase inhibitor + anaerobic coverage: flagyl or clinda. Carbapenems for PCN allergies. Duration: Multiple abscesses are more problematic and can require up to 12 weeks of therapy. Both the clinical and radiographic progress of the patient should guide the length of therapy Drainage introduced in the 70’s as an alternative to surgery, overall success rate equal or superior to surgery, taken out when output < 10 cc/ day or cavity collapse is documented by serial CT scanning/ Good even for multiple abscesses.
  • GI: after successful drainage to evaluate any underlying gastointestinal disease using colonoscopy or ERCP ID: in complicated case or unusual pathogens
  • - Starry sky seen on sono can be seen in disseminated mycobacterial disease, disseminated pneumocystis carinii or CMV infection
  • Fascioliasis Schistosomiasis (blood fluke) Ascariasis: round worm that causes the most common helminthic infection in the world/can cause biliary obstruction & cholangitis
  • Source: the infective cysts reach humans thru water and vegetables contaminated with feces, thru food contaminated by night soil fertilizers or by hands of infected food handlers or by direct transmission of the cyst
  • Pain is constant dull aching CXR: abnomal in 50% of patients, elevation of the right hemidiaphragm, pleural effusion, atelectasis, Sono: rounded or oval lesion that is hypoechoic and homogeneous in appearance with an absence of wall echoes; lesion near or contiguous with the liver capsule CT: Is highly sensitive but not specific. It reveals detailed margins of the lesion and info re: blood supply that help differentiate an amebic abscess from a hepatic cyst, solid tumor or hemangioma. MRI of the liver is considered the most sensitive imaging technique but not specific Tc Nuclear Scan is useful in differentiating an amebic abscess from a pyogenic abscess. Because amebic abscesses do not contain leukocytes, they appear as “cold” lesions
  • Flagyl is efficacious against both the systemic and intestinal manifestations of amebiasis. Luminal agent: iodoquinol, paromomycin, diloxanide/failure to use luminal agents can lead to relapse of infection in 10% of patients Aspiration should be considered in patients with a high risk of abscess rupture as defined by a cavity size >5cm, left lobe liver abscess which is associated with higher mortality and higher frequency of leak or rupture into the pericardium Pus is odorless and sterile on routine culture
  • Pleural cavity rupture can cause a large pleural effusion, empyema, severe dyspnea or pleuritic pain IVC obstruction can occur secondary to mechanical compression from the abscess ARDS + sepsis can also develop in severe cases of extraintestinal amebiasis
  • Liver is the commonest organ involved but lung, brain and bone can also be infected
  • Clinical: symptoms are generally non-specific, may be asymptomatic Aspiration: previously contraindicated in patients with Echinococcal disease because it is associated with risk of dissemination or anaphylaxis, nowadays it is gaining acceptance. Percutaneous Rx entails drainage & instillation of a sclerosing scolicidal agent. Pretreatment with mebendazole preferred. Precautions to prevent allergic & anaphylactic reactions are necessary. Surgery: liver is packed off with hypertonic saline soaked swabs, cysts are then decompressed with trocar and cannula, Scolicidal agent (hypertonic saline or 0.5% silver nitrate) can be injected into cyst cavity to kill residual daughter cysts in the germinal membrane before unroofing and pericystectomy
  • Infectious Diseases Of The Liver - Emergency Room Procedures

    1. 1. Infectious Diseases of the Liver Josyann Abisaab, MD Department of Emergency Medicine New York Presbyterian Hospital – Weill Cornell Medical Center
    2. 2. Overview <ul><li>Viral infections </li></ul><ul><li>Pyogenic Liver Abscess </li></ul><ul><li>Fungal and mycobacterial infections </li></ul><ul><li>Parasitic infections </li></ul>
    3. 3. Viral Hepatitis <ul><li>Hepatitis A, B, C, D, E, G, “X” </li></ul><ul><li>CMV </li></ul><ul><li>EBV </li></ul><ul><li>HSV </li></ul><ul><li>VZV </li></ul><ul><li>HIV </li></ul><ul><li>Yellow Fever </li></ul>
    4. 4. Clinical Presentation <ul><li>Very mild, asymptomatic to intermittent sx to fulminant hepatic failure </li></ul><ul><li>4 phases of infection </li></ul><ul><ul><li>Asymptomatic phase of viral replication </li></ul></ul><ul><ul><li>Prodromal phase: N/V, fatigue, malaise, anorexia, arthralgias, urticaria, pruritus, altered sense of taste </li></ul></ul><ul><ul><li>Icteric phase: dark urine + light stools, jaundice, RUQ pain & hepatomegaly </li></ul></ul><ul><ul><li>Final phase: convalescence </li></ul></ul><ul><li>Chronic viral infection </li></ul>
    5. 5. Typical ED patient with Hepatitis <ul><li>Hx: young male, c/o fatigue, anorexia, abdo pain, dark urine, light stool, transient rash, arthralgia and pruritus </li></ul><ul><li>Exam: Jaundiced, dehydrated, with an enlarged tender liver, possibly a rash + low grade fever </li></ul><ul><li>Labs: nl WBC, nl alkaline phosphatase, bili 9.0, AST 700, ALT 1200, Gluc 60. </li></ul><ul><li>Imaging: sono or CT rarely indicated </li></ul><ul><li>Rx: supportive </li></ul>
    6. 6. Indications for Admission <ul><li>Encephalopathy </li></ul><ul><li>PT > 15 </li></ul><ul><li>Fluid or electrolyte imbalance </li></ul><ul><li>Intractable vomiting </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Bili > 20mg/dl </li></ul><ul><li>Severe underlying disease </li></ul><ul><li>Age > 50 years </li></ul><ul><li>Immunosuppression </li></ul>
    7. 7. Hepatitis A <ul><li>Epidemiology </li></ul><ul><li>125,000-200,000 cases/yr in U.S. </li></ul><ul><li>100 deaths/yr from fulminant hepatitis A </li></ul><ul><li>15% of infected individuals develop prolonged or relapsing disease </li></ul><ul><li>Accounts for 20-25% of clinical hepatitis </li></ul><ul><li>Most often affects persons 5-14 years-old </li></ul><ul><li>Causes acute hepatitis, no chronic state </li></ul><ul><li>Transmission: fecal-oral route </li></ul>
    8. 9. Risk Factors for Hepatitis A <ul><li>Close personal contact with an infected individual </li></ul><ul><li>Association with daycare centers or young children </li></ul><ul><li>International travel </li></ul><ul><li>Water borne outbreaks with raw oysters and clams </li></ul><ul><li>IV drug use & transfusion (rare) </li></ul>
    9. 10. Hepatitis A <ul><li>Clinical course </li></ul><ul><li>Most cases asymptomatic, esp. children </li></ul><ul><li>If symptomatic fatigue, nausea, myalgias, jaundice, fever </li></ul><ul><li>More severe presentation in adults vs. children </li></ul><ul><li>Diagnosis </li></ul><ul><li>Elevated ALT>AST, total bilirubin, hepatitis A IgM + </li></ul><ul><li>Prognosis </li></ul><ul><li>Complete recovery in almost all patients </li></ul><ul><li><1% develop fulminant liver failure </li></ul>
    10. 11. Hepatitis A <ul><li>Prevention </li></ul><ul><li>Early recognition and isolation of infected patients </li></ul><ul><li>Hygiene- Hand washing </li></ul><ul><li>Vaccination- recombinant vaccine/Havrix,Vaqta </li></ul>
    11. 12. Hepatitis B <ul><li>Epidemiology </li></ul><ul><li>350 million carriers worldwide </li></ul><ul><li>More than 1 million HBV related deaths annually (WHO) </li></ul><ul><li>10% of adults and 90% of children become carriers </li></ul><ul><li>Transmission: parenterally, sexually, vertical transmission </li></ul><ul><li>Risk factors: IV drug use, prostitutes, homosexual men, Asian population, hemodialysis patients, health care workers </li></ul>
    12. 13. Geographic Distribution of Chronic HBV Infection HBsAg Prevalence  8% - High 2-7% - Intermediate <2% - Low
    13. 14. Hepatitis B
    14. 15. Hepatitis B <ul><li>Clinical course </li></ul><ul><li>Symptoms of fatigue, myalgias, jaundice, nausea, vomiting, rash </li></ul><ul><li>Jaundice for 1-2 months, elevated ALT, AST, T. bili </li></ul><ul><li>Fulminant hepatitis- rapid clinical decline, marked elevation of liver function tests, encephalopathy </li></ul><ul><li>Extrahepatic manifestations- polyarteritis, glomerulopathy, Guillain Barre </li></ul>
    15. 16. Hepatitis B Anatomy Surface DNA Core
    16. 17. Hepatitis B <ul><li>Diagnosis </li></ul><ul><li>Laboratory findings: </li></ul><ul><ul><li>HepBsAg positive </li></ul></ul><ul><ul><li>HepBcore IgM positive </li></ul></ul><ul><ul><li>HepBeAg positive </li></ul></ul><ul><ul><li>HBVDNA positive </li></ul></ul><ul><li>Hep B surface antibody confers immunity </li></ul>
    17. 18. Acute Hepatitis B Virus Infection with Recovery Total anti-HBc IgM anti-HBc anti-HBs HBsAg 0 4 8 12 16 20 24 28 32 36 52 100 Typical Serologic Course Titer Weeks after exposure Symptoms HBeAg anti-HBe
    18. 19. Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course Weeks after Exposure Titer IgM anti-HBc Total anti-HBc HBsAg Acute (6 months) HBeAg Chronic (Years) anti-HBe 0 4 8 12 16 20 24 28 32 36 52 Years
    19. 20. Hepatitis B <ul><li>Prognosis </li></ul><ul><li><1% develop fulminant hepatic failure </li></ul><ul><li>5-10% develop chronic hepatitis </li></ul><ul><li>30% of chronically infected develop cirrhosis </li></ul>
    20. 21. Hepatitis B <ul><li>Prevention </li></ul><ul><li>Early recognition and education </li></ul><ul><li>Adequate hygiene and universal precautions </li></ul><ul><li>Vaccination- health care workers, high risk groups, children born to infected mothers (HBIG) </li></ul><ul><li>Vaccine- recombinant vaccine given at 0, 1, 6 months, ?booster at year 7 </li></ul>
    21. 22. Hepatitis B <ul><li>Chronic Hepatitis B </li></ul><ul><li>Failure to clear Hep B s Ag after 6 months </li></ul><ul><li>Cause of cirrhosis and hepatocellular carcinoma </li></ul><ul><li>Treatment includes interferon 5 million units daily for 16 weeks </li></ul><ul><li>~30% sustained response </li></ul><ul><li>Lamivudine 100mg daily- high relapse rate once discontinued </li></ul><ul><li>Liver transplantation for patients with cirrhosis </li></ul>
    22. 23. Hepatitis D <ul><li>Only occurs with hepatitis B~10% of cases </li></ul><ul><li>Superinfection vs. coinfection </li></ul><ul><li>Highest incidence in IV drug users </li></ul><ul><li>Results in greater morbidity and decreased response to interferon </li></ul><ul><li>Prevented with vaccination against hepB </li></ul>
    23. 24. Hepatitis C (the silent epidemic) <ul><li>“ We stand at the precipice of a grave threat to our public health… It affects people from all walks of life, in every state, in every country. And unless we do something about it soon, it will kill more people than AIDS.” </li></ul><ul><li>C. Everett Koop </li></ul><ul><li>Former US Surgeon </li></ul><ul><li>General </li></ul>
    24. 25. Hepatitis C <ul><li>Epidemiology </li></ul><ul><li>200 million carriers worldwide, 4.5 million in US </li></ul><ul><li>80% of infected patients develop chronic infection </li></ul><ul><li>Transmission: parenterally, low vertical and sexual transmission </li></ul><ul><li>Risk factors- IV drug use, blood transfusion history, hemophiliacs, dialysis, prison, inhalational cocaine?, tatoos? </li></ul><ul><li>#1 indication for liver transplantation </li></ul><ul><li>1-4% incidence of hepatocellular carcinoma </li></ul>
    25. 26. Hepatitis C <ul><li>Clinical course </li></ul><ul><li>Only 25% of infected individual report symptoms </li></ul><ul><li>10-20 years may elapse from infection to diagnosis </li></ul><ul><li>80% of infected individuals develop chronic hepatitis and 20% develop cirrhosis </li></ul><ul><li>Diagnosis </li></ul><ul><li>Measure ALT </li></ul><ul><li>Hepatitis C antibody </li></ul><ul><li>Hepatitis C viral titer (HCVRNA) </li></ul><ul><li>Liver biopsy if elevated ALT and candidate for therapy </li></ul>
    26. 27. Hepatitis C
    27. 28. Hepatitis C <ul><li>Therapy </li></ul><ul><li>Interferon plus ribavirin for 6-12 months </li></ul><ul><li>35% sustained response </li></ul><ul><li>Side effects </li></ul><ul><li>Interferon- flu like symptoms, lowering blood counts, thyroid disease, depression, hair loss </li></ul><ul><li>Ribavirin- teratogenicity, hemolytic anemia </li></ul>
    28. 29. Hepatitis E and G <ul><li>Hepatitis E </li></ul><ul><li>RNA virus similar to hepatitis A </li></ul><ul><li>Spread by fecal oral route, 2 week incubation </li></ul><ul><li>Rare in U.S. , more common in Africa and India </li></ul><ul><li>Severe course in pregnancy, no chronic state </li></ul><ul><li>Hepatitis G </li></ul><ul><li>0.2% acute hepatitis, 900-2000 infections/yr </li></ul><ul><li>Exact role not known, probably not a pathogen </li></ul>
    29. 30. Review of Viral Hepatitis A B C E genome RNA DNA RNA RNA age young all all adults onset abrupt insidious insidious abrupt incubation 15-50 28-160 14-160 15-45 rash no yes no yes fever yes no no yes jaundice yes possible no yes Pregnancy mild mod mild severe
    30. 31. Review of Viral Hepatitis A B C E chronic no yes yes no liver cancer no yes yes no Transmission oral yes unlikely no yes IV rare yes yes no sexual uncommon yes yes no perinatal no yes low no
    31. 32. Markers of viral hepatitis Marker Significance HAV IgM acute hepatitis A infection HAV IgG prior hepatitis A infection, immunity HBVsurface antigen acute or chronic hepatitis B HBV core IgM acute hepatitis B HBV core IgG prior hepatitis B infection HBV surface antibody immunity to hepatitis B HBV e antigen infectious hepatitis B HCV Ig G antibody infection with hepatitis C HBVDNA viral titer of HBV HCVRNA viral titer of HCV
    32. 33. Risk for Occupational Transmission <ul><li>HBV </li></ul><ul><ul><li>If HBsAg & HBeAg + : 22-33% </li></ul></ul><ul><ul><li>If HBsAg + only: 1-6% </li></ul></ul><ul><ul><li>HCW with antibodies have no risk </li></ul></ul><ul><ul><li>Risk less with body fluids </li></ul></ul><ul><ul><li>HBV can survive in dried blood at room temp on environmental surfaces for at least 1 week </li></ul></ul><ul><li>HCV </li></ul><ul><ul><li>Needlestick: 1.8% </li></ul></ul><ul><ul><li>Rarely from mucous membrane exposures to blood </li></ul></ul><ul><ul><li>No transmission from intact or nonintact skin exposures to blood </li></ul></ul><ul><ul><li>Exposure to body fluids not quantified but expected to be low </li></ul></ul>
    33. 34. High Moderate blood semen urine serum vaginal fluid feces wound exudates saliva sweat tears breastmilk Concentration of Hep B virus in Body Fluids Low/Not Detectable
    34. 35. Blood Transfusion Risk <ul><li>Hep B : 1/66,000 units of blood </li></ul><ul><li>Hep C : 1/103,000 units of blood </li></ul>
    35. 36. Post Exposure Prophylaxis <ul><li>Hep A </li></ul><ul><li>Household & sexual contacts of known cases </li></ul><ul><li>Exposure to contaminated water or food before cases begin to appear </li></ul><ul><li>All staff and attendees of daycare centers caring for children in diapers with any known case among children or staff </li></ul><ul><li>Hygiene </li></ul><ul><li>Dose: IG 0.02 ml/Kg IM </li></ul>
    36. 37. Post Exposure Prophylaxis <ul><li>Hep B </li></ul><ul><li>Wash wound or skin with soap & water/flush mucosa </li></ul><ul><li>Human Bites: reciprocal exposure </li></ul><ul><li>Rape victims: Rx has to be <14 days </li></ul><ul><li>Pregnancy & Lactation: HBIG + vaccine safe </li></ul><ul><li>Efficacy of HBIG + Hep B vaccine > 90% (preferably within 24 hours) </li></ul><ul><li>Side effect of vaccine: pain + mild fever/anaphylaxis 1 in 600,000 doses </li></ul><ul><li>HBIG prepared from pooled human plasma: no transmission of HBV, HCV or HIV </li></ul><ul><li>Side effect of HBIG: local pain,urticaria, angioedema, rarely anaphylaxis </li></ul><ul><li>Testing of needles or sharps is not recommended </li></ul>
    37. 38. Source: CDC
    38. 39. Hepatitis B vaccine schedule <ul><li>1 st dose in ED or UC </li></ul><ul><li>2 nd dose: 1-2 months </li></ul><ul><li>3 rd dose: 4-6 months </li></ul>
    39. 40. Postexposure Management of HCV <ul><li>Prevention of HCV by IG is not indicated </li></ul><ul><li>No clinical trials conducted to assess use of Interferon </li></ul><ul><li>Antivirals are not FDA approved </li></ul><ul><li>Early identification of chronic disease </li></ul><ul><li>Source: check anti-HCV </li></ul><ul><li>Person exposed: baseline anti-HCV + ALT, f/u at 4-6 weeks, 4-6 months </li></ul>
    40. 42. Pyogenic Liver Abscess <ul><li>Background </li></ul><ul><ul><li>Relatively rare </li></ul></ul><ul><ul><li>Described since the time of Hippocrates (400 BC) </li></ul></ul><ul><li>Frequency </li></ul><ul><ul><li>8-16 cases per 100,000 hospitalized patients </li></ul></ul><ul><ul><li>Increased rates in specific populations eg. Crohn’s Disease </li></ul></ul><ul><li>Age </li></ul><ul><ul><li>Most common toward the sixth and seventh decades of life </li></ul></ul>
    41. 43. Anatomy of the Liver
    42. 44. <ul><li>Pathophysiology </li></ul><ul><li>Most common source is Biliary Tract Disease (60%) </li></ul><ul><ul><li>Cholecystitis, ascending cholangitis, stricture, malignancy, congenital diseases </li></ul></ul><ul><li>Portal pylephlebitis (24%) </li></ul><ul><li>Hematogenous dissemination (15%) </li></ul><ul><ul><li>Endocarditis, pyelonephritis </li></ul></ul><ul><li>Contiguous spread </li></ul><ul><li>Cryptogenic </li></ul><ul><li>Trauma </li></ul><ul><li>Secondary infection </li></ul><ul><ul><li>Amebic abscess, hydatid cystic cavities, metastatic and primary hepatic tumors </li></ul></ul>Pyogenic Liver Abscess
    43. 45. Pyogenic Liver Abscess <ul><li>History </li></ul><ul><ul><li>Fever (90%) </li></ul></ul><ul><ul><li>Chills </li></ul></ul><ul><ul><li>Anorexia + malaise </li></ul></ul><ul><ul><li>Weight loss </li></ul></ul><ul><ul><li>Abdo pain (50%) </li></ul></ul><ul><ul><li>Cough or hiccoughs </li></ul></ul><ul><li>Exam </li></ul><ul><ul><li>General appearance </li></ul></ul><ul><ul><li>Jaundice (25%) </li></ul></ul><ul><ul><li>Tender hepatomegaly </li></ul></ul><ul><ul><li>Hypochondrial or epigastric mass </li></ul></ul><ul><ul><li>Decreased breath sounds at the RLL </li></ul></ul>
    44. 46. Pyogenic Liver Abscess <ul><li>Lab studies </li></ul><ul><ul><li>High WBC (77%) </li></ul></ul><ul><ul><li>High ESR </li></ul></ul><ul><ul><li>High Alkaline Phosphatase is the most common abnormality </li></ul></ul><ul><ul><li>Elevations of AST, Tbili variable </li></ul></ul><ul><ul><li>Blood cultures + (50%) </li></ul></ul><ul><li>Imaging studies </li></ul><ul><ul><li>CXR: raised right hemidiaphragm & pleural effusion (50%) </li></ul></ul><ul><ul><li>Ultrasound (sensitivity 80-90%): hypoechoic masses with irregularly shaped borders </li></ul></ul><ul><ul><li>CT scan (sensitivity 95-100%): well demarcated hypodense areas, gas seen in 20% </li></ul></ul>
    45. 48. Pyogenic Liver Abscess <ul><li>Microbiology </li></ul><ul><li>Polymicrobial involvement with aerobes and anaerobes </li></ul><ul><li>Biliary tree: enteric gram – bacilli and enterococci </li></ul><ul><li>Pelvic or colonic source: mixed flora incl. Aerobic and anaerobic especially B. fragilis </li></ul><ul><li>Hematogenous spread: Staph aureus or Strep milleri </li></ul>
    46. 49. Pyogenic Liver Abscess <ul><li>Management </li></ul><ul><li>Antibiotics: cephalosporin and flagyl </li></ul><ul><li>Duration: </li></ul><ul><ul><li>4-6 weeks for solitary lesions with adequate drainage </li></ul></ul><ul><ul><li>Up to 12 weeks for multiple abscesses </li></ul></ul><ul><li>Procedures: </li></ul><ul><ul><li>Percutaneous needle aspiration under ultrasound guidance </li></ul></ul><ul><ul><li>Percutaneous catheter drainage </li></ul></ul><ul><li>Surgery: peritonitis, diverticular abscess, failure of drainage attempts, complicated multiloculated, thick walled abscess </li></ul>
    47. 50. Pyogenic Liver Abscess <ul><li>Consultations </li></ul><ul><ul><li>Diagnostic interventional radiology </li></ul></ul><ul><ul><li>General surgery </li></ul></ul><ul><ul><li>GI </li></ul></ul><ul><ul><li>ID </li></ul></ul><ul><li>Prognosis </li></ul><ul><ul><li>Mortality: 5-30% </li></ul></ul><ul><ul><li>Indicators of poor prognosis: </li></ul></ul><ul><ul><ul><li>Multiple lesions </li></ul></ul></ul><ul><ul><ul><li>Severity of underlying medical conditions </li></ul></ul></ul><ul><ul><ul><li>Presence of complications </li></ul></ul></ul><ul><ul><ul><li>Delay in diagnosis </li></ul></ul></ul><ul><ul><ul><li>Hgb < 11, bili > 1.5, WBC >15, alb < 2.5, elevated PTT </li></ul></ul></ul>
    48. 51. Fungal & Mycobacterial Infections <ul><li>Fungal </li></ul><ul><ul><li>Immunocompromised patients </li></ul></ul><ul><ul><li>Hematogenous dissemination </li></ul></ul><ul><ul><li>Most occur in leukemic patients: Candida albicans </li></ul></ul><ul><ul><li>Aspergillus, Actinomyces, Cryptococcus, Histoplasma </li></ul></ul><ul><li>Mycobacterial </li></ul><ul><ul><li>Usually a miliary process </li></ul></ul><ul><ul><li>High suspicion if multiple 1cm or less liver lesions, especially in HIV + patient </li></ul></ul>
    49. 52. Parasitic infections <ul><li>Amebic Liver Abscess </li></ul><ul><li>Echinococcal or Hydatid Disease </li></ul><ul><li>Liver Flukes </li></ul><ul><ul><li>Clonorchis sinensis </li></ul></ul><ul><ul><li>Opisthorchis species </li></ul></ul><ul><ul><li>Fasciola hepatica (Fascioliasis) </li></ul></ul><ul><ul><li>Schistosoma species (Schistosomiasis) </li></ul></ul><ul><li>Ascariasis </li></ul><ul><li>Toxoplasmosis </li></ul><ul><li>Strongyloides </li></ul><ul><li>Malaria </li></ul>
    50. 53. Amebic Liver Abscess <ul><li>Pathogenesis </li></ul><ul><li>- Protozoan parasite: </li></ul><ul><ul><li>Entamoeba histolytica </li></ul></ul><ul><li>Exposure via fecal-oral route </li></ul><ul><li>Humans are the principal host </li></ul><ul><li>Source of infection is the cyst-passing chronic patient or asymptomatic carrier </li></ul>
    51. 54. Amebic Liver Abscess <ul><li>Epidemiology </li></ul><ul><li>Highest endemic activity in Mexico, India, East and South Africa, portions of Central & South America. </li></ul><ul><li>40 to 50 million people worldwild become symptomatic with amebic colitis or ALA (WHO 1995) </li></ul><ul><li>40,000 to 100,000 deaths /year </li></ul><ul><li>Increase in male homosexuals with/without HIV </li></ul>
    52. 55. Amebic Liver Abscess <ul><li>Typical patient in US: young hispanic male with a travel hx to an endemic area or emigration from Mexico or Southeast Asia </li></ul><ul><li>Age: 20-40 </li></ul><ul><li>Male:Female ratio = 10:1 </li></ul><ul><li>Liver is the commonest extraintestinal site of infection </li></ul><ul><li>10% of affected patients develop liver abscesses </li></ul><ul><li>80% of abscesses develop in the right lobe </li></ul><ul><li>Hx of Alcohol abuse is common </li></ul>
    53. 56. Amebic Liver Abscess <ul><li>Clinical </li></ul><ul><li>Most common: fever, chills, nausea, weakness, malaise and RUQ or epigastric pain </li></ul><ul><li>Diarrhea (20%) </li></ul><ul><li>Jaundice is uncommon </li></ul><ul><li>Exam: RUQ tenderness, hepatomegaly, decreased BS in the Right lung base or a pleural rub </li></ul><ul><li>Labs: </li></ul><ul><ul><li>High WBC + ESR, hct < 35, abnormal LFT’s </li></ul></ul><ul><ul><li>Latex agglutination assay + (90%) </li></ul></ul><ul><ul><li>Stool microscopy or stool antigen tests helpful only in < 30% </li></ul></ul><ul><ul><li>Imaging: CXR, Sono, CT, MRI, A99m Tc nuclear hepatic scan </li></ul></ul>
    54. 58. Amebic Liver Abscess <ul><li>Management </li></ul><ul><li>Metronidazole 750mg po tid for 10 days (90% cure rate) </li></ul><ul><li>Luminal agent for Rx of asymptomatic colonization state </li></ul><ul><li>Ultrasound guided aspiration: </li></ul><ul><ul><li>Cavity size > 5cm </li></ul></ul><ul><ul><li>Left lobe liver abscess </li></ul></ul><ul><ul><li>No response to drug Rx within 5-7 days </li></ul></ul><ul><li>Aspiration produces a typical “anchovy sauce” appearing pus </li></ul>
    55. 59. Amebic Liver Abscess <ul><li>Complications </li></ul><ul><li>Rupture into peritoneum, pleural cavity, pericardium </li></ul><ul><li>Peritonitis, paralytic ileus, fulminant colitis, colonic perforation or toxic megacolon </li></ul><ul><li>Compression of biliary tree causing obstructive jaundice </li></ul><ul><li>Inferior vena cava obstruction </li></ul><ul><li>Bacterial superinfection </li></ul><ul><li>ARDS & sepsis </li></ul><ul><li>Brain abscess </li></ul>
    56. 60. Amebic Liver Abscess <ul><li>Prognosis </li></ul><ul><li>Good in uncomplicated cases (<1% mortality) </li></ul><ul><li>Bad if pulmonary complications (20% mortality) </li></ul>
    57. 61. Echinococcal disease <ul><li>Due to infection with the helminth Echinococcus Granulosa </li></ul><ul><li>Man is an accidental intermediate host </li></ul><ul><li>Adult worm found normally in the dog and sheep intestine </li></ul><ul><li>Seen in Mediterranean areas, Australia and South America </li></ul><ul><li>Liver is the commonest organ involved </li></ul><ul><li>Cysts are unilocular, can be up to 20cm in diameter and may be multiple </li></ul>
    58. 63. Echinococcal Disease <ul><li>Clinical </li></ul><ul><ul><li>RUQ pain (60%) </li></ul></ul><ul><ul><li>Jaundice (15 %) </li></ul></ul><ul><ul><li>Skin rashes, pruritus, allergic reactions </li></ul></ul><ul><ul><li>Cysts can rupture causing bronchobiliary fistula </li></ul></ul><ul><ul><li>Eosinophilia (30%) </li></ul></ul><ul><ul><li>Dx confirmed by indirect haemagglutinin assay </li></ul></ul><ul><ul><li>Cyst can be imaged by sono or CT </li></ul></ul><ul><li>Management </li></ul><ul><ul><li>Aspiration/high failure rate </li></ul></ul><ul><ul><li>Pharmacological treatment is not curative: albendazole, mebendazole </li></ul></ul><ul><ul><li>Surgical removal is preferred </li></ul></ul><ul><ul><li>Recurrence rate 5% at 5 years </li></ul></ul>

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