Infectious Diseases Of The Liver - Emergency Room Procedures
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Infectious Diseases Of The Liver - Emergency Room Procedures
- 1. Infectious Diseases of the Liver Josyann Abisaab, MD Department of Emergency Medicine New York Presbyterian Hospital – Weill Cornell Medical Center
- 13. Geographic Distribution of Chronic HBV Infection HBsAg Prevalence 8% - High 2-7% - Intermediate <2% - Low
- 14. Hepatitis B
- 16. Hepatitis B Anatomy Surface DNA Core
- 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
- 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
- 27. Hepatitis C
- 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
- 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
- 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
- 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
- 38. Source: CDC
- 43. Anatomy of the Liver
Editor's Notes
- 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