Correlation liver disfunction and infection disease (dengue typhoid fever)01
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Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever)

Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever)
Dr Erwin, SpPD, FINASIM
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013

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Correlation liver disfunction and infection disease (dengue typhoid fever)01 Correlation liver disfunction and infection disease (dengue typhoid fever)01 Presentation Transcript

  • Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever) Dr Erwin, SpPD, FINASIM
  • Functions of the Liver  Metabolic  Carbohidrat metabolism  Protein and lipoprotein metabolism  Fatty acid metabolism  Biotransformation of drugs  Storage  Glycogen  Vitamins A, D, E, and K  Iron and copper
  • Functions of the Liver  Immunological function s       Synthesis of immunoglobulins Phagocytosis by Kupffer cells Filtration of bacteria Degradation of endotoxins Excretion of bilirubin and urea formation Haematological functions   Blood reservoir Haematopoiesis in the foetus
  • Major Determinants of Disease  The metabolic consequences of liver disease are serious & include  toxic accumulations of           metabolic waste (ammonia & bilirubin) drugs & toxins endogenous hormones (estrogen) Bleeding  a deficiency of coagulation factors Edema  a deficiency of albumin failure to absorb intestinal fat because of a deficiency of bile acids Viral hepatitis is a common contagious disease Cirrhosis is the final endpoint for many liver diseases Portal HTN is the most important consequence of cirrhosis & can be associated with liver failure & severe hemorrhage Stones often form in the gallbladder & may pass into & obstruct the bile duct
  • Response to Injury   Responds well as it has a functional reserve that must suffer a large loss before become symptomatic Liver function tests (LFTs)  enzymes          Lactic dehydrogenase (LDH) Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Alkaline phosphatase (ALKP) bilirubin albumin PT & PTT viral antigens & antibodies autoimmune antibodies
  • Anatomic Patterns of Injury  Inflammation   Degeneration    hydropic fatty Necrosis    hepatitis infarct Councilman bodies Fibrosis  cirrhosis
  • Hepatic Failure     Die within a few weeks or months May be sudden injury or chronic injury Loss of 90% of function Clinically              jaundice ascites fetor hepaticus hypoalbuminemia hypoglycemia palmar erythema spider angiomata testicular atrophy balding gynecomastia bleeding disorders hepatorenal syndrome hepatic encephalopathy
  • LIVER FAILURE  Classification. Acute - no pre-existing liver disease. Chronic - pre-existing liver disease  Causes. Acute - viral hepatitis, drugs, toxins, severe fatty change (eg fatty liver of pregnancy, Reye syndrome), vascular. Chronic - cirrhosis, chronic hepatitis.  Morphology. Acute - varying degrees of necrosis up to massive liver necrosis (zonal to panacinar histologically). Chronic - that of cirrhosis or chronic hepatitis. Chronic liver failure is more common than acute liver failure. Mortality from liver failure without liver transplantation is 75% to 90%. Drugs and viruses account for about 80% & 15% of cases of acute liver failure respectively; figures vary according to geographical area.
  • FEATURES OF LIVER FAILURE  - - - Hepatic encephalopathy a neuropsychiatric disturbance leading to coma. The cardinal feature of acute liver failure, progressing over hours to days. More insidious in chronic liver failure when it is a sign of worsening liver failure. Pathogenesis:- nitrogenous compounds derived from bacterial action in the colon are not metabolised in the failing liver; in addition shunting of portal blood to systemic circulation by-passes the liver. Compounds involved - ammonia and derivatives of aromatic amino acids (eg mercaptans, a cause of foetor hepaticus) false neurotransmitters (eg octopamine) neuroinhibitors, eg gammaaminobutyric acid (GABA), endogenous benzodiazepines. Morphology of brain - oedema; Alzheimer type 2 astrocytic reaction.
  • FEATURES OF LIVER FAILURE - hyperbilirubinaemia; deep jaundice = worse prognosis.  - decreased clotting factors (II,VII,IX,X) results in a bleeding tendency.  Cardiovascular - hyperkinetic circulation.  Respiratory - hepatopulmonary syndrome.  Renal - hepatorenal syndrome.  Endocrine - in chronic failure - gonadal atrophy, gynaecomastia, amenorrhoea.  Skin changes - in chronic failure - spider naevi, palmer erythema.  Others - impaired metabolism of amino acids, carbohydrates (hypoglycaemia) and drugs; impaired protein synthesis (low albumin), systemic infections and endotoxaemia. Laboratory investigations - bilirubin (>300umol/l = poor prognosis). - prothrombin (>50sec.= poor prognosis). - transaminases. - albumin. Possible factors precipitating liver failure in chronic liver disease: - increase in liver injury due to virus or alcoholic binge, infection, GIT haemorrhage (which can precipitate encephalopathy, as can excess dietary protein,constipation, drugs, uraemia, hypokalaemia).  Jaundice Haematological
  • FEATURES OF LIVER FAILURE        Infections. Toxins and drugs. Viral hepatitis, other infection (dengue and typhoid) Alcohol. Therapeutic drugs. Autoimmune. Hepatitis. Primary biliary cirrhosis. Metabolic. Haemochromatosis. Wilson disease. Alpha-1-antitrypsin deficiency. Glycogen storage disease and many others. Biliary obstruction. Congenital atresia. Sclerosing cholangitis. Hepatic outflow obstruction. Cryptogenic. The etiology of cirrhosis varies throughout the world. In the Western world, alcohol is the most common factor at 60% and viral hepatitis 10%. Viral hepatitis is the most common factor in Asia and Africa. Cryptogenic cirrhosis (cause unknown) forms 10%. Once cirrhosis has developed, it is usually not possible to determine the aetiology by morphology alone and results of other investigations are required.
  • FEATURES OF LIVER FAILURE Liver Injury Chronic Inflamation Hepatic Stellete Cells Portal Hypertension Activation Kupffer Cell Cytokines Liver Cell Damage
  • Acute Liver Failure
  • The mortality rate for acute liver failure ranges between 56% and 80%
  • Formal diagnosis of acute liver failure  An increase in PT by 4-6 seconds (INR>1.5)  And the development of hepatic encephalopathy (HE).  In a patient without pre-existing cirrhosis and with an illness of less than six months duration.
  • Etiology Cause Agent Responsible Viral Hepatitis Hep. A, B, D, E, CMV, HSV, seronegative hepatitis (14-25% in UK) Drug-related Dose-related, e.g.paracetamol; idiosyncratic reactions, e.g. anti-TB, statins, recreational drugs, anticonvulsants, NSAIDs, many others Toxins Vascular events Other Carbon tetrachloride, amanita phalloides Iscahemic hepatitis, veno-occlusive disease, BuddChiari, heatstroke Pregnancy-related liver disease, Wilson’s disease, lymphoma, carcinoma, trauma, Dengue, Ty phoid Fever
  • Epidemiology of Dengue Fever
  • Transmission Infected mosquito Healthy person Infected person Incubation Period: 3 to 14 days Most commonly 4 to 7 days 20
  • Circulation of Dengue Infected       Hiperbilirubinemia Hipoalbuminemia Glukoneogenesis Hipoglikemia Asidosis Laktat Decreased synthesis of Clotting factor
  • TYPHOID FEVER
  • Epidemiology strongly endemic endemic sporadic cases
  • Transmission fecal-oral route close contact with patients or carriers contaminated water and food flies and cockroaches.
  • liver、spleen、gall、 S.Typhi. 2nd bacteremia BM ,ect early stage&acme stage (1-3W) stomach (mononuclear phagocytes ) Bac. In gall Bac. In feces Lower ileum S.Typhi eliminated convalvescence stage (4-5w) peyer's patches & mesenteric lymph nodes LN Proliferate,swell necrosis defervescence stage Enterorrhagia,i ntestinal perforation (3-4w) thoracic duct 1st bacteremia (Incubation stage) 10-14d
  • Pathology  essential lesion: proliferation of RES (reticuloendothelial system ) specific changes in lymphoid tissues and mesenteric lymph nodes. "typhoid nodules“  Most characteristic lesion: ulceration of mucous in the region of the Peyer’s patches of the small intestine
  • Complications Intestinal hemorrhage Commonly appear during the second-third week of illness difference between mild and greater bleeding often caused by unsuitable food, diarrhea et al serious bleeding in about 2~8% a sudden drop in temperature、 rise in pulse、and signs of shock followed by dark or fresh blood in the stool.
  • Intestinal perforation:  The more serious .Incidence,1-4%  Commonly appear during 2-3 weeks.  Take place at the lower end of ileum.  Before perforation,abdominal pain or diarrhea,intestinal bleeding .  When perforation, abdominal pain, sweating, drop in temperature, and increase in pulse rate, then, rebound tenderness when press abdomen, abdomen muscle entasia, reduce or disappear in the sonant extent of liver, leukocytosis .  Temperature rise .peritonitis appear.  celiac free air under x-ray.
  •  Toxic hepatitis: common,1-3 weeks hepatomegaly, ALT elevated get better with improvement of diseases in 2~3 weeks  Toxic myocarditis. seen in 2-3 weeks, usually severe toxemia.  Bronchitis, bronchopneumonia. seen in early stage
  • ILUSTRASI KASUS          Pasien Laki-laki 34Thn, Keluhan utama demam 5 hr smrs, disertai sakit kepala, mual, muntah, nyeri ulu hati, diare dan nyeri sendi. PF : KU : sakit sedang, CM, TD : 110/70 N 98X/mnt suhu 39O C RR 18X/mnt, lidah kotor C/P DBN nyeri tekan epigastrium hepar 1 jari BAC limfa tidak teraba
  • Masalah pada pasien ini ? a. b. c. d. e. Febris Dispepsia Cephalgia Diare Hepatomegali
  • Pemeriksaan Lab HB :16,7. HT : 49 L : 4.700 Tr : 98.000 Widal : O 1/320 H 1/160 Analisa pada pasien ini : a. DHF b. DF c. Typhoid d. A dan C e. B dan C
  • Observasi Selanjutnya   S : Demam mulai berkurang, mual O : TD 100/70 N 96x/mnt suhu 38,2OC NT ulu hati lab HB :15,9 HT: 48 L :4.900 Tr : 72rb SGOT/PT 198/114 TUBEK T skala 6 GDS 104 Ur/Cr 40/1,2 Na 133 K 3,4
  • Masalah pada pasien ini a. b. c. d. DHF dan Typhoid Gangguan fungsi hati DHF, typhoid, inbalance elektrolit B dan C
  • Planning         RL 40 tts/mnt DPL/hari DL III 1700 kal Pct 3x1 Antasida 3x1 Omeprazole inj 1x1 amp Ceftriaxon 1x2 g Hepatoprotector
  • Diskusi     Apakah infeksi virus bisa bersamaan dengan infeksi bakteri? Apakah gangguan fungsi hati sering bersamaan dengan penyakit infeksi atau gangguan fungsi hati oleh karena penyebab lain? Perlukah gangguan fungsi hati pada penyakit infeksi diobati ? Kapan gangguan fungsi hati menjadi normal pada penyakit infeksi?