prof.barmawi.....kuliah 7 thyphoid ,pancreatitis fever 1
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Typho id Fever
pancreat i t is
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Typhoid Fever
Typhoid fever is a systemic infection with the
bacterium Salmonella enterica serotype
typhi.
A subset of Salmonel laserotypes thatincludes S. typhiand S. paratyphicauses
enteric (typhoid) fever and is restricted to
growth in human hosts.
Clinically S. typhi > S. paratyphi
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Salmonella
Genus enterobacteriaceae
" S. enter i t id is"
including var. t yph imur ium,paratyphi& bongor i
200 serovarian
S. chol erae-su is, 1 serovar
S. typh i, 1 serovar
gram-negative bacilli
Motil & pathogenic
Salmonel lacan be further divided into serovars
based on the detection of three major antigenicdeterminants:
the somatic O antigen
[lipopolysaccharide (LPS) cell-wall
components]
the surface Vi antigen (restricted to S.
typhiand S. paratyph iC), the flagellar H antigen.
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Nomenklatur
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Epidemiology
Endemic in developing contries
Incubation period : 3 d3 m (1-3 wk)
Transmission : most cases of disease result from
ingestion of contaminated food or water
anal-oral transmission health care workers
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Pathogenesis
The bacteria traverse the gastrointestinal tract, including the acidic environment of the
stomach, to colonize the small intestines. Salmonellae cross the intestinal barrier, where
phagocytosis by macrophages results in their dissemination throughout the
reticuloendothelial system.
Once salmonellae reach the small intestine, the bacteria resist a variety of innate immune
factors before penetrating the mucus layer. The organisms enter the intestines through
phagocytic microfold or M cells overlying the Peyer's patches. Salmonellae (S. typhior S. paratyphi) undergo phagocytosis by macrophages after crossing
the epithelial layer of the small intestine.
Once phagocytosed, the bacteria are protected from PMNs) the complement system, and
antibodies.
After phagocytosis, salmonellae disseminate throughout the body in macrophages via the
lymphatics and colonize reticuloendothelial tissues (liver, spleen, lymph nodes, and bone
marrow).
Signs and symptoms, including fever and abdominal pain, probably result from secretion of
cytokines by macrophages when a critical number of organisms have replicated..
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Patofisiologi
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Rose spot
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Relative bradicardia
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Laboratorium
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Widal Test
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Treatment
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Complications
Complications occur in 10 to 15 percent of patients
Gastrointestinal bleeding, intestinal perforation, and
typhoid encephalopathy are the most important.
Gastrointestinal bleeding is the most common,
occurring in up to 10 percent of patients. It results
from erosion of a necrotic Peyers patch through the
wall of an enteric vessel.
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CarrierTyphoid
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Typhoid FeverPrevention Safe water supplies sanitary disposal of humanfeces and hygienic food handle are essentialsteps to Typhoid control. Sanitation improvements demand high publicinvestments. For this reason achieving realgains in sanitation coverage has been achallenge in developing countries. Whether a rapid reduction in the incidence ofTyphoid could be brought about by mass
vaccination has been a matter of discussion. Thecurrently licensed Vi polysaccharide vaccinesare not very effective. In Brazil vaccines havenot been used so far.
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Acute Pancreatitis
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Associated Structures of theGall Bladder and Pancreas
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Acute Pancreatitis
Epidemiology Second most common principal
inpatient GI diagnosis aftercholelithiasis and acute
cholecystitis Unreliable data due to misdiagnosis Estimated yearly incidence of 5-
40/100,000
1998 data from the U.S. aboutpancreatic diseases 327,000 inpatient stays 78,000 outpatient hospital visits 195,000 ER visits 531,000 office visits
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Natural History
80% of cases are mild
20% are severe with organ failure andlocal complications
Estimated 25-33% mortality Overall mortality estimates range from 2%
to 10%
Half of death occur within the first week,perhaps 25% to 33% of deaths occur withinthe first 48 hours
Obese patients have higher rates of localcomplications, respiratory failure, severeacute pancreatitis and death from sterile
necrosis than non-obese patients
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Definition
Acute inflammation of thepancreas
Varying degree of regionaltissue involvement and remoteorgan systems
Classified as acute unless thereis evidence of chronicpancreatitis, otherwise
considered as exacerbation of
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Pathology
Initial injury to peripheral acinarcells, fat necrosis and autodigestion
Interstitial (edematous) pancreatitis: Interstitial edema associated with
inflammatory cells in the parenchyma
Parenchymal necrosis is microscopic
Necrotizing pancreatitis Focal macroscopic or diffuse necrosis
Hemorrhage, vascular thrombosis
Involvement of the main pancreatic duct
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Pathogenesis of AcutePancreatitis
Trypsinogen to trypsinconversion in acinar cells
overwhelms neutralizationmechanisms
Proenzymes (trypsinogen,
elastase, phospholipase A2(PLA2) and carboxypeptidase)are activated by trypsin
Activation of complement and
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Etiologies of AcutePancreatitis
Obstructive
Toxic
Metabolic Infectious
Vascular
Trauma
Iatrogenic
Hereditary
Controversial etiologies
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Toxic and MetabolicEtiologies
Toxic
Ethanol
Methyl alcohol Scorpion venom (hyperstimulation of
pancreas)
Organophosphate insecticides
(hyperstimulation of pancreas) Drugs
Metabolic
Hypertriglyceridemia
Hypercalcemia
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Other Causes
Cardiovascular
Small vessel vasculitis
Emboli to pancreatic vessels Hypotension
Blunt and penetrating
abdominal traumas Iatrogenic
ERCP
Surgery
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Gallstone/BiliaryPancreatitis
40% of all cases of AP
Risk of AP due to existing
gallstones is greater in men, butoverall incidence is lower asgallstones are more common in
women Small stones (< 5 mm) are more
likely to cause pancreatitis
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Biliary Sludge
Viscous suspension of gallbladderbile that may contain tiny stones (< 3mm)
Usually composed of cholesterolmonohydrate crystals, but alsooccurs with ceftriaxone-bilecomplexes
Appears as a mobile, low-amplitudeecho without shadow
Biliary sludge often develops inacute pancreatitis
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Alcohol
Causes 30% of cases
Most but not all patients also havesome degree of underlying chronicpancreatitis
Proposed mechanisms: Sphincter of Oddi relaxation & duodenal
reflux
Increased pancreatic duct permeability
Sudden release of pancreatic enzymeswith inappropriate activation
Increased protein concentration in
pancreatic juice leading to obstruction
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Hypertriglyceridemia
Third most common identifiablecause of AP
Serum triglycerides > 1000mg/dL
Median serum TG concentration
~ 3-4K Mechanism?
Possibly, release of free fatty
acids may cause pancreatic acinar
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Hypertriglyceridemia
Associated conditions in adults
Diabetes mellitus
Alcohol abuse (chicken or theegg?)
Obesity
Hypothyroidism Pregnancy
Estrogen therapy
Types I & V hyperlipoproteinemia
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Hypercalcemia
Rare, proposed mechanism is due todeposition of calcium in the pancreaticduct with activation of trypsinogen in thepancreatic parenchyma
Chronic hypercalcemia less likely toinduce pancreatitis than acute increases(animal data)
Hyperparathyroidism causes < 0.5% of allcases of acute pancreatitis
Incidence of acute pancreatitis inhyperparathyroidism is reportedly 02%-1.5%
Rarely after metastatic cancer with boneinvolvement, TPN, sarcoidosis, vitamin D
toxicity and following parenteral
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Tumors
Probably cause AP due toobstruction of the pancreatic duct
Usually in older patients Most common with intraductal
papillary mucinous neoplasm/tumor(IPMN/IPMT) of the pancreas
Also possible with ampullaryneoplasms
Less commonly due to pancreatic
adenocarcinoma
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DrugsGeneralConsiderations
Over 80 drugs implicated based onunconvincing anecdotal reports
Usually mild and self-limited afterstopping drug
Reliable causative etiology requires:
Exclusion of other etiologies
Appropriate interval (usually 4-8 weeks)since initiation of therapy
Clear mechanism of drug-inducedpancreatitis
Reproducible recurrence of pancreatitis
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Drugs Implicated
-Methyldopa Mesalamine Cimetidine
Cytosinearabinoside Dexamethasone Ethinylestradiol/
lynestrenol
Furosemide Isoniazid 6-Meraptopurine Metronidazole
Norethindrone/mestranol
Pentamidine Perindopril Pravastatin
Procainamide Stibogluconate Sulfamethizole Sulfasalazine Sulindac Tetracycline TMP/SMX Didanosine Valproic acid
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Potential Mechanisms(Contd)
Accumulation of toxicmetabolites
Onset typically occurs afterseveral months
E.g. valproic acid, didanosine
Hypertriglyceridemia Thiazides, tamoxifen, isotretinoin
Intrinsic toxicity
Pancreatitis can occur with
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Diagnosis of AP
Clinical findings
Laboratory findings
Radiological findings
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Clinical Findings
Usually acute onset of severe pain
Epigastric, upper quadrants
Radiation to back and chest (DDxmyocardial ischemia)
Nausea, vomiting, hematemesis
Bowel obstruction
Fever, tachypnea, shock
Ecchymoses on the flanks (Turners
sign)
Periumbilical ecch mosis Cullens
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Laboratory findings
2-3 fold elevations of pancreatic enzymesamylase and/or lipase
Amylase
Cheap, fast and widely available Not 100% sensitive or specific (normal values in
mild attacks, in the setting of chronicpancreatitis or even with fatal pancreatitis havebeen reported)
False positive (as far as AP Dx is concerned)with:
Macroamylasemia (e.g. IG-bound amylase notcleared by kidneys)
Parotitis (can also be EtOH induced, look forhamster cheeks!)
Salpingitis/ectopic pregnancy Bowel obstruction and erforation
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Lipase
Sensitivity similar to amylase(85%-100%)
Probably more specific (allpancreatic except a smallamount of gastric lipase)
Usually remains elevated longerthan amylase
False positive values in: Renal insufficiency
Macrolipasemia
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Other PancreaticEnzymes
Generally speaking, no significant clinicaladvantage over routine tests due to: Similar dynamics Expense
Unavailability Phospholipase A2 Trypsin Caboxypeptidase A
Colipase Elastase Ribonuclease Trypsin Activation Peptide (TAP)
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Other Lab Findings
Nonspecific findings include
Leukocytosis
LFT abnormalities CRP and other acute reactants
Serum triglycerides
Azotemia Hyperglycemia
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Radiological Findings
Plain Films: Localized segment of small intestine
(sentinel loop)
Generalize ileus Calcifications (stones, or pancreas with
chronic calcific pancreatitis)
Pneumobilia following stone passage
and/or bilioenteric fistula formation Severe ascites
Retroperitoneal gas (pancreaticabscess)
30% with CXR abnormalities (elevatedhemidiaphragm, pleural effusion, basal
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CT and US
Cross-sectional imaging withmore specific pancreaticchanges (i.v. contrast is neededfor detecting necrosis andtumors)
US may show biliary dilation,
stones, pancreaticcalcifications, hypoechoicappearance of the pancreaswith edema, pseudocysts and
eri ancreatic fluid collections
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Differential Diagnosis
Biliary pain and acute cholecystitis
Epigastric distress syndrome/non-
ulcer dyspepsia Peptic ulcer disease and perforated
hollow viscus
Small bowel obstruction
Inferior myocardial infarction
Aortic dissection
Ruptured ectopic pregnancy
Acute a endicitis
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Range of Severity
Mild Minimal or no organ dysfunction
Full recovery withoutcomplications
Severe Local complications
Organ failure
death
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Predictors of Severity
Ransons Score 2: Mortality
2.5%*
Ransons Score 3: Mortality62%*
Limitations of Ransons Score:
Cumbersome Takes 48 hours to compute
Not validated beyond 48 hours
Cutoff of 3 has sensitivity of 40%-* Obtained within the first 48 hours
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Atl t C it i f
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Atlanta Criteria forSevere AP
ORGAN FAILUREShock SBP < 90 mm Hg
Pulmonary insufficiency pO2 60 mm Hg
Renal failure Serum creatinine > 2 mg/dL
GI bleeding >500 mL/24 hr
LOCAL COMPLICATIONSNecrosis
Abscess
PseudocystUNFAVORABLE EARLY PROGNOSTIC SIGNS 3 Ransons criteria
APACHE II score 8
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Approach to Patient
Triage Prognosis
Placement
Etiology Could affect the acute management
Supportive care I.v. fluid resuscitation
Nutritional support
Analgesia
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Further care
Observation for early detectionof potential complications
Treatment of complication Nutritional support (10% rate of
TPN line infections in patients
with severe pancreatitis)
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Nutritional Support
TPN disadvantages Expensive
High complication rate
Generally associated with highermorbidity and longer lengths of staythan enteral feeding via nasoenterictubes
In mild to moderate AP, enteral feedingwas started within 48 hours ofadmission and was associated withfaster improvement and shorter LOSthan TPN
In severe/necrotizing pancreatitis, LOS,
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