Overview of acute liver failure in emergency department.pptx

Acute liver failure overview

1. Presented by DR.AlaaAdeen sadeq Supervised by DR.Ahmed Hadi

2. definition : Acute liver failure is an uncommon condition in which rapid deterioration of liver function results in coagulopathy, usually with an international normalized ratio (INR) of greater than 1.5, and alteration in the mental status (encephalopathy) of a previously healthy individual. Acute liver failure often affects young people and carries a very high mortality.

3. (1) Synthetic liver failure (INR > 1.5) with hepatic encephalopathy. Coagulopathy alone (without encephalopathy) is termed acute liver injury (2) No underlying cirrhosis. (3) Hepatic encephalopathy beginning within roughly <12weeks.

4. subclassification of acute liver failure based on speed of disease progression Hyperacute liver failure (HALF) : <1 week from jaundice to encephalopathy. Common causes include acetaminophen or viral hepatitis. Carries a higher risk of cerebral edema and multiorgan dysfunction. If patients can survive the immediate illness, they may have a greater likelihood of experiencing hepatic recovery and thus avoiding transplantation.

5. Acute liver failure : 1-4 weeks from jaundice to encephalopathy. Subacute liver failure (SALF) : 4-12 weeks from jaundice to encephalopathy. Indicates a  smouldering  disease process. This is less likely to cause cerebral edema or cause immediate death.  Clinically this disease process may mimic  cirrhosis  (e.g., a gradual process with ascites and splenomegaly). There is a much lower likelihood of hepatic recovery, so patients are more likely to ultimately require transplantation .

6. causes of acute liver failure most common causes Acetaminophen . Other drugs & toxins : Numerous drugs are implicated.   Occasional clues to idiosyncratic drug-induced hepatitis may include rash, fever, and/or eosinophilia . Non-acetaminophen drug-induced liver injury often doesn't resolve, so transplantation may be an earlier consideration

7. Antimicrobials account for ~50% (e.g., isoniazid, beta-lactams). Chemotherapy. NSAIDs. Statins. Carbamazepine. Phenytoin.

8. L ess common causes Wilson's disease. Budd-Chiari syndrome (hepatic vein thrombosis). Pregnancy-associated: Acute fatty liver of pregnancy. Preeclampsia/HELLP syndrome. Ischemic hepatitis: May especially occur in presence of biventricular dysfunction, causing congestion and poor perfusion; frank hypotension isn't always noted. Most patients improve with supportive management.  Liver transplant is rarely, if ever, indicated. Hyperthermia (including heat stroke). Malignant infiltration of the liver (e.g., lymphoma or metastatic adenocarcinoma). Veno -occlusive disease following bone marrow transplantation. Hemophagocytic lymphohistiocytosis (HLH). Reye's Syndrome.

9. Substance use , including cocaine and MDMA (“ecstasy”). Amanita phalloides mushroom poisoning. ( Note: Alcohol does not cause acute liver failure; rather, this is classified as acute-on-chronic liver failure ). Viral hepatitis  (mostly HAV and HBV): HAV is usually self-limited, but an cause ALF. HBV can cause ALF, especially reactivation of chronic HBV in the context of chemotherapy or immunosuppression. HEV is more common in some areas, especially in the context of pregnancy. Herpesviruses: HSV can occur in immunocompetent patients CMV, EBV, or VZV in immunosuppression . Autoimmune hepatitis.

10. signs & symptoms Jaundice, although this may not be prominent. Encephalopathy, graded as follows: Grade I: Patient shows altered behavior with normal level of consciousness, reduced attention span. Grade II: Patient displays altered behavior with disorientation, drowsiness. Grade III: Patient is confused, incoherent, mostly sleeping but arousable to painful stimuli. Grade IV: Patient is comatose and unresponsive to pain.

11. Cerebral edema: May lead to signs of increased intracranial pressure (ICP) ( eg , papilledema, hypertension, bradycardia) Jaundice: Often present but not always Ascites: Potential for hepatic vein thrombosis with rapid development in the presence of fulminant hepatic failure accompanied by abdominal pain Right upper quadrant tenderness: Variably present Change in liver span: May be small due to hepatic necrosis or may be enlarged due to heart failure, viral hepatitis, or Budd-Chiari syndrome Hematemesis or melena: Due to upper gastrointestinal (GI) bleeding Hypotension and tachycardia: Due to reduced systemic vascular resistance

12. laboratory indications of hepatic failure Complete blood count: May reveal thrombocytopenia Coagulation studies: PT and/or international normalized ratio (INR) Liver function tests: Often elevated levels of aspartate aminotransferase (AST)/serum glutamic- oxaloacetic transaminase (SGOT), alanine aminotransferase (ALT)/serum glutamic-pyruvic transaminase (SGPT), alkaline phosphatase (ALP) Serum bilirubin level: Elevated Serum ammonia level: May be dramatically elevated (accuracy: arterial > venous level) Serum glucose level: May be dangerously low

13. Serum (arterial) lactate level: Often elevated Arterial blood gas: May reveal hypoxemia Serum creatinine level: May be elevated Serum free copper and ceruloplasmin levels: Low levels in Wilson disease Serum phosphate level: May be low Acetaminophen and acetaminophen-protein adducts levels Drug screening: Consider in patients who are intravenous drug abusers Blood cultures: For patients with suspected infection

14. Viral serologies : Consider for hepatitis A virus immunoglobulin M (IgM), hepatitis B surface antigen ( HBsAg ), hepatitis B virus anticore IgM; hepatitis C viral load testing; hepatitis D virus IgM if HBsAg is positive; in post transplantation or immunosuppressed setting, consider studies for cytomegalovirus viremia, cytomegalovirus antigenemia , and herpes simplex virus Autoimmune markers (for autoimmune hepatitis diagnosis): Antinuclear antibody (ANA), anti-smooth muscle antibody (ASMA), and immunoglobulin levels

15. Other studies may include the following: Electroencephalography Intracranial pressure monitoring Percutaneous (contraindicated in the presence of coagulopathy) or transjugular liver biopsy Imaging studies Hepatic Doppler ultrasonography Abdominal computed tomography (CT) scanning or magnetic resonance imaging without contrast Cranial CT scanning

16. Management The most important aspect of treatment for acute liver failure is to provide good intensive care support, including the protection of the airways.    Specific therapy is also dependent on the cause of the patient’s liver failure and the presence of any complications. Pay careful attention to the patient’s fluid management and hemodynamics. It is crucial to monitor their metabolic parameters, assess for infection, maintain nutrition, and promptly recognize GI bleeding.

17. Pharmacotherapy Various medications may be necessary because of the variety of complications that may occur from fulminant hepatic failure. In specific cases, antidotes that effectively bind or eliminate toxins are essential. The following medications may be used in the management of acute liver failure: Antidotes ( eg , penicillin G, silibinin , activated charcoal ,) N-acetylcysteine can given IV 150mg/kg over 1 hr ,then 50mg/kg for 4 hr then 100mg/kg for 60 hr,there is oral dose 140mg/kg PO once then 70mg/kg PO every 4 hr for total 17 doses Osmotic diuretics ( eg , mannitol) Barbiturate agents ( eg , pentobarbital, thiopental) Benzodiazepines ( eg , midazolam) Anesthetic agents ( eg , propofol )

18. Anorectal Disease

19. The anorectal is formed by the 12-15cm rectum and the 4cm anal canal. The columnar intestinal epithelium of the rectum changes to stratified squamous epithelium at the dentate or pectinate line, which is where the anal glands and crypts lie The  anorectum  is supplied by the haemorrhoidal arteries and drained by the internal haemorrhoidal plexus of veins. Sphincteric support is provided by the internal sphincter, puborectalis muscle and the external sphincter

20. Patients with benign anorectal disease tend to present to primary care, although many present to the emergency department (ED), particularly when suffering from significant pain or rectal bleeding

21. Anorectum detailing the internal sphincter, external sphincter and Puborectails The  external sphincter  is made up of three parts: Deep Superficial Subcutaneous and is a continuation of the puborectalis muscle.

22. Detailed int sphincter, anal columns, dentate line, ext sphincter and puborectais These form a ring of muscle in the anus which have an important function in the maintenance of continence. Several tissue spaces lie between the muscles and become sites of potential abscess and fistula formation

23. Hemorrhoids are vascular cushions that become enlarged and distally displaced within the anal canal. 1 Consequently, the downward displacement of these cushions causes the internal and external hemorrhoidal plexuses to become excessively engorged. .Hemorrhoids may become inflamed, thrombosed, prolapsed, ulcerated, or ischemic . Internal hemorrhoids originate proximal to the dentate line Internal hemorrhoids are not readily palpable and can best be visualized through an anoscope . . External hemorrhoids , distal to the dentate line , form as a result of dilatation of veins at the anal verge, and can be seen at external inspection .

24. Haemorrhoids They can also be classified in terms of their degree of prolapse, which helps to aid treatment decisions: 1st degree: completely internal 2nd degree: prolapse but reduce spontaneously 3rd degree: prolapse but reduce manually 4th degree: cannot be reduced once prolapsed

25. Hemorrhoids

26. Other Anorectal Disease

27. Anal fissures Are superficial tears of the anal mucosa Anorectal abscesses Form a spectrum of disease that can affect various areas of the anorectum . The abscesses can be defined by their anatomic location Pilonidal disease Covers a spectrum of conditions from pilonidal sinuses, in the natal cleft to the formation of a laterally placed pilonidal abscess. Rectal prolapse Occurs when protrusion of all or part of the rectal canal takes place

28. BLEEDING PAIN Tend to cause bright red blood on stool or pan Normally painless, unless thrombosed Haemorrhoids Tend to cause small amount of bright red blood on paper Severe pain on defecation lasting for 1-2 hours after Anal Fissure Small amounts of blood or pus PR may occur if fistula present Pain worse on defecation or sitting, a tender swelling, deep pain or buttock pain depending on location of absces Anorectal abscess Blood stained mucus PR Largely painless unless strangulated Rectal prolapse   symptoms include : Itch Discharge Swelling

29. Mangment 1-Resuscitate any patient with signs of sepsis or haemodynamic instability Involve senior ED physician High concentration oxygen delivered via a variable deliver mask with reservoir bag Two large bore peripheral intravenous cannulae Bloods Intravenous fluids crystalloid administer 1-2 litres immediately and reassess IV broad spectrum antibiotics if signs of sepsis Urinary catheter and measure urine volumes Urgent referral to senior Surgeon and Critical Care

30. 2- Analgesia as required Patients that do not require urgent surgical intervention can generally be discharged for either GP or surgical follow up. Haemorrhoids Most patients can be discharged to either GP care or with surgical follow-up; some patients may require urgent surgical referral or admission, these include: Patients with profuse haemorrhoidal bleeding [4] Thrombosed haemorrhoids although these are acutely painful most patients can be treated conservatively at home with analgesia, ice, bed rest, stool softeners. Symptoms usually settle within 2 weeks [3] If the external haemorrhoid is necrotic or gangrenous then surgery may be needed to excise the haemorrhoid [4, 7] Patients with 4th degree haemorrhoids (NHS) Suspected malignancy (NHS)

31. Anal fissure Patients can normally be discharged home with analgesia, stool softeners and surgical follow-up.

32. Anorectal abscesses All require surgical intervention. There is no role for the treatment of a closed abscess with antibiotics, incision and drainage is required and failing to ensure that this happens in a timely fashion risks worsening sepsis, fistula formation and serves only to delay surgery

33. Rectal prolapse All should be referred to the admitting surgical team

34. Rectal prolapse All should be referred to the admitting surgical team

35. The end