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    Pa Tho Physiology of Sepsis Secondary To Typhoid Ileus

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    Phatsee Pangilinan
    1) Salmonella typhi bacteria infect the small intestine during typhoid, penetrating the mucosa and being engulfed by macrophages. 2) This triggers a cytokine release and systemic inflammatory response, causing endothelial damage, increased capillary permeability, and maldistribution of blood flow. 3) Without treatment, ongoing tissue hypoxia and organ dysfunction can occur, potentially leading to shock, multi-organ failure, and death.

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    Pa Tho Physiology of Sepsis Secondary To Typhoid Ileus

    Uploaded by

    Phatsee Pangilinan
    257 views6 pages
    1) Salmonella typhi bacteria infect the small intestine during typhoid, penetrating the mucosa and being engulfed by macrophages. 2) This triggers a cytokine release and systemic inflammatory response, causing endothelial damage, increased capillary permeability, and maldistribution of blood flow. 3) Without treatment, ongoing tissue hypoxia and organ dysfunction can occur, potentially leading to shock, multi-organ failure, and death.

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    Pa Tho Physiology of Sepsis Secondary to Typhoid Ileus

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    1) Salmonella typhi bacteria infect the small intestine during typhoid, penetrating the mucosa and being engulfed by macrophages. 2) This triggers a cytokine release and systemic inflammatory response, causing endothelial damage, increased capillary permeability, and maldistribution of blood flow. 3) Without treatment, ongoing tissue hypoxia and organ dysfunction can occur, potentially leading to shock, multi-organ failure, and death.

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    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
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    257 views6 pages

    Pa Tho Physiology of Sepsis Secondary To Typhoid Ileus

    Uploaded by

    Phatsee Pangilinan
    1) Salmonella typhi bacteria infect the small intestine during typhoid, penetrating the mucosa and being engulfed by macrophages. 2) This triggers a cytokine release and systemic inflammatory response, causing endothelial damage, increased capillary permeability, and maldistribution of blood flow. 3) Without treatment, ongoing tissue hypoxia and organ dysfunction can occur, potentially leading to shock, multi-organ failure, and death.

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    of 6

    PATHOPHYSIOLOGY OF SEPSIS SECONDARY TO TYPHOID ILEUS

    Factors:
    contaminated food and/or drink
    no 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 Peyer’s patches

    endotoxin
    Release of inflammatory cytokines: Endothelial
     Tumor Necrosis Factor damage
     Interleukin-1
     others

    Reticuloendothelial system
    Peripheral Selective Increase microemboli
    vasodilation vasodilation capillary
    permeability

    liver spleen Bone marrow Gall


    bladder
    fever Maldistribution of
    circulatory blood spleenomegaly
    volume
    hapatomegaly lymphocytosis

    Impaired
    immunologic leukopenia anemia
    Decrease cellular
    oxygen supply Blood chem: function
    decrease ALT CBC:
    and AST Lymphocytes-
    0.64
    Decrease tissue perfusion
    CBC:
    CBC: RBC- 3.8
    WBC- 1.6 HGB- 117
    HCT- 0.36
    Impaired GI
    cellular
    metabolism Ongoing
    exposure
    ischemia

    Necrosis and
    ulceration

    Gastric/ intestinal Bowel Abdominal pain


    bleeding perforation

    SFA: Coffee ground


    Dilated loop of gastric aspirate
    bowel

    constipation Persistence of
    precipitating cause

    Persistent hypotension Baseline BP: 60/60

    Symphatetic Nervous System stimulation


    Alpha adrenergic receptor Beta adrenergic receptor
    stimulation stimulation

    Widespread vasoconstriction myocardium

    capillaries renal lungs viscera Decrease Increase


    myocardial heart rate
    contractility

    hydrostatic RAAS Pulmonary


    pressure arterioles Heart rate
    constriction >90
    Increase
    Fluid shift arteriolear
    IV to IT constriction hypoxemia

    Decrease Decrease oxygen Crackles


    circulatory availability DOB
    volume tachypnea
    retractions

    Dry skin
    Slow capillary
    refill
    Progressive tissue hypoxia Renal tubular ischemia

    Pallor Renal dysfunction


    Cyanosis
    restlessness

    Albumin not reabsorbed Urinalysis:


    Anaerobic metabolism (+) Albumin

    Metabolic lactic acidosis Increase capillary


    permeability

    Precapillary spinchter
    dilation

    Pooling and stasis of blood


    in capillary bed

    Increase capillary hydrostatic


    pressure

    Movement of fluid from IV to IT


    Decrease venous return Movement of plasma Blood
    proteins from IV to IT chemistry:
    Albumin- 3.2

    Decrease cardiac output

    hypotension
    Further tachycardia

    Peripheral
    vasoconstriction Decrease coronary blood flow

    Myocardial depression

    Decrease cardiac output and heart rate

    Respiratory Decrease cerebral blood flow


    arrest
    Failure of vasomotor
    center to stimulate Severe cerebral ischemia
    DEATH sympathetic nervous
    system
    Cardiac
    arrest

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