pa tho physiology of sepsis secondary to typhoid ileus

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  • 8/8/2019 Pa Tho Physiology of Sepsis Secondary to Typhoid Ileus

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    PATHOPHYSIOLOGY OF SEPSIS SECONDARY TO TYPHOID ILEUS

    Factors:

    contaminated food and/or drinkno typhoid vaccine

    environment

    gram (-) bacteria

    Salmonella typhi

    Survive gastric pH

    Small intestine (ileus)

    Penetrates mucosa of small intestine to midlayer

    Engulfed by macrophages/ monocytes into the epithelial cells in the Peyers patches

    endotoxin

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    Release of inflammatory cytokines:

    Tumor Necrosis Factor

    Interleukin-1

    others

    Endothelial

    damage

    Peripheral

    vasodilation

    Selective

    vasodilationIncrease

    capillary

    permeability

    microemboli

    fever Maldistribution of

    circulatory blood

    volume

    Decrease cellular

    oxygen supply

    Decrease tissue perfusion

    Reticuloendothelial system

    liver spleen Bone marrow Gall

    bladder

    hapatomegaly

    Blood chem:

    decrease ALT

    and AST

    spleenomegaly

    leukopenia

    lymphocytosis

    anemia

    Ongoing

    exposure

    CBC:WBC- 1.6

    CBC:

    RBC- 3.8

    HGB- 117

    HCT- 0.36

    CBC:

    Lymphocytes-0.64

    Impaired

    cellular

    metabolism

    GI

    Impaired

    immunologic

    function

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    ischemia

    Necrosis and

    ulceration

    Gastric/ intestinal

    bleeding

    Bowel

    perforationAbdominal pain

    SFA:Dilated loop of

    bowel

    Coffee groundgastric aspirate

    constipation Persistence ofprecipitating cause

    Persistent hypotension

    Symphatetic Nervous System stimulation

    Baseline BP: 60/60

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    Alpha adrenergic receptor

    stimulation

    Beta adrenergic receptor

    stimulation

    Widespread vasoconstriction myocardium

    capillaries

    hydrostaticpressure

    Fluid shift

    IV to IT

    Decrease

    circulatoryvolume

    Dry skin

    Slow capillary

    refill

    renal

    RAAS

    Increase

    arteriolear

    constriction

    lungs viscera

    Pulmonary

    arterioles

    constriction

    hypoxemia

    Decrease oxygenavailability

    Crackles

    DOB

    tachypnearetractions

    Decrease

    myocardial

    contractility

    Increase

    heart rate

    Heart rate

    >90

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    Urinalysis:

    (+) Albumin

    Progressive tissue hypoxia Renal tubular ischemia

    Renal dysfunction

    Albumin not reabsorbed

    Pallor

    Cyanosisrestlessness

    Anaerobic metabolism

    Metabolic lactic acidosis Increase capillary

    permeability

    Precapillary spinchterdilation

    Pooling and stasis of blood

    in capillary bed

    Increase capillary hydrostatic

    pressure

    Movement of fluid from IV to IT

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    Blood

    chemistry:

    Albumin- 3.2

    Decrease venous return Movement of plasma

    proteins from IV to IT

    Decrease cardiac output

    hypotension

    Peripheral

    vasoconstriction

    Further tachycardia

    Decrease coronary blood flow

    Myocardial depression

    Decrease cardiac output and heart rate

    Decrease cerebral blood flow

    Severe cerebral ischemiaFailure of vasomotorcenter to stimulate

    sympathetic nervous

    system

    Respiratory

    arrest

    Cardiac

    arrest

    DEATH