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    Pathophysiology of Neonatal Sepsis Secondary To Neonatal Pneumonia

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    paul andrew laranjo asuncion
    This document summarizes the pathophysiology of neonatal sepsis secondary to neonatal pneumonia. [1] Streptococcus pneumoniae is a virulent microorganism that enters the lungs through the nasal passages and causes an immune response and inflammation. [2] As the bacteria multiplies in the alveoli, it releases toxins that damage lung tissue leading to consolidation and impaired gas exchange. [3] Untreated, it can cause systemic infection, multiple organ dysfunction syndrome, and death.

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    Pathophysiology of Neonatal Sepsis Secondary To Neonatal Pneumonia

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    paul andrew laranjo asuncion
    11K views4 pages
    This document summarizes the pathophysiology of neonatal sepsis secondary to neonatal pneumonia. [1] Streptococcus pneumoniae is a virulent microorganism that enters the lungs through the nasal passages and causes an immune response and inflammation. [2] As the bacteria multiplies in the alveoli, it releases toxins that damage lung tissue leading to consolidation and impaired gas exchange. [3] Untreated, it can cause systemic infection, multiple organ dysfunction syndrome, and death.

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    Pathophysiology of Neonatal Sepsis secondary to Neonatal Pneumonia

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    This document summarizes the pathophysiology of neonatal sepsis secondary to neonatal pneumonia. [1] Streptococcus pneumoniae is a virulent microorganism that enters the lungs through the nasal passages and causes an immune response and inflammation. [2] As the bacteria multiplies in the alveoli, it releases toxins that damage lung tissue leading to consolidation and impaired gas exchange. [3] Untreated, it can cause systemic infection, multiple organ dysfunction syndrome, and death.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    11K views4 pages

    Pathophysiology of Neonatal Sepsis Secondary To Neonatal Pneumonia

    Uploaded by

    paul andrew laranjo asuncion
    This document summarizes the pathophysiology of neonatal sepsis secondary to neonatal pneumonia. [1] Streptococcus pneumoniae is a virulent microorganism that enters the lungs through the nasal passages and causes an immune response and inflammation. [2] As the bacteria multiplies in the alveoli, it releases toxins that damage lung tissue leading to consolidation and impaired gas exchange. [3] Untreated, it can cause systemic infection, multiple organ dysfunction syndrome, and death.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    of 4
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    The document outlines the pathophysiology of neonatal sepsis secondary to pneumonia including risk factors, the process of infection and inflammation in the lungs, and systemic effects. It also discusses signs/symptoms, treatment approaches, and potential complications.

    The microorganism enters the lungs through the nasal passages and airways, causes inflammation and damage in the alveoli, and can spread systemically. This leads to fever, difficulty breathing, impaired gas exchange, and potential organ dysfunction.

    In the initial phase there is systemic infection, fever, increased work of breathing and heart rate to compensate. In the late phase signs include poor perfusion, hypotension, hypothermia as the hyperinflammatory response takes over.

    Pathophysiology of Neonatal Sepsis secondary to Neonatal Pneumonia

    Non-modifiable Modifiable
    Age: 0-5 yrs old – their Diet: Poor (poor
    immune system is still breastfeeding by mother)
    immature
    Infections: Streptococcus
    Pneumoniae

    Virulent Microorganism
    Streptococcus Pneumoniae
    Microorganism enters the
    nose (nasal passages)

    Passes through the larynx,


    pharynx, trachea
    Microorganism enters lung
    parenchyma

    Passes through the larynx,


    pharynx, trachea
    Microorganism enters lung
    parenchyma

    Activation of Immune response


    Cough
    (mucus production)
    • inflamation
    • vasodilation
    • leukocyte and macrophage

    Bacteria multiplies in the alveoli


    Fever Release of endotoxins and exotoxins from the bacteria
    (toxins are directly causing the damage to the tissues)

    Antibiotics
    Continuous mucus production
    Narrowing of air passage

    1
    Lung consolidation (region of lung tissue
    filled with liquid) due to cellular exudates Difficulty of breathing
    (fluid, pus, and blood) from inflammation

    Impaired 02 and C02 exchange


    due to lung consolidation
    Increased respiratory
    rate
    Increase oxygen demand

    O2 administration Increased pulse rate


    Hypoxia

    Necrosis of pulmonary tissue

    Failure of immune response in


    the pulmonary tissues

    The bacterium goes with the blood and


    release toxins

    Whole-body inflammatory state

    Inflammatory response Systemic Reaction


    • Neutrophils –
    marks the
    pathogen as
    foreign then
    Pro-Inflammatory Response Anti-Inflammatory Response
    signals
    (Cytokines) Interleukin 10 (IL-10) – and
    phagocytes for
    anti-inflammatory cytokine
    ingestion of
    bacteria

    Antibiotic Therapy
    Failure of
    Whole-body inflammatory state 2
    Systemic Infection
    (Septicemia)

    Initial Phase (1-3 days)

    Body compensates from systemic inflammatory response by slowing


    things down in order for body to recover.

    Decrease systemic Hypometabolism


    vascular resistance

    Decreased energy
    Warm, bounding
    expenditure
    pulses, with brisk
    capillary refill, edema

    Decrease o2
    Antibiotic therapy consumption
    broad spectrum
    cephalosporin
    Vasoconstriction

    Cool extremities, poor


    peripheral pulses, and Late Phase
    hypotension Compensatory
    mechanism:
    • Increase BP
    Hyperdrive (Compensatory mechanism)
    • Increase PR
    (If the body doesn’t recover it goes into hyperdrive)
    This is partly due to the • Increase RR
    Exaggerated inflammatory response • Increase TEMP

    End of compensatory mechanism Negative Feedback:


    (negative feedback mechanism) • sudden decrease BP
    • deminished PR
    • decrease body TEMP
    Poor perfusion

    3
    Lactic acidosis
    Inadequate 02 delivery
    and nutrients to tissues

    Metabolic acidosis
    Fluid Replacement
    therapy

    Shock or septic shock

    MODS
    Multiple Organ Dysfunction
    Syndrome due to inability to
    maintain homeostasis

    Hepatic Acute renal Impaired Disseminated intravascular coagulation


    dysfunction failure pulmonary (DIC) -also known as consumptive
    function coagulopathy a pathological
    activation of coagulation
    (blood clotting) mechanisms

    Hyperbilirubinemia
    DEATH

    LEGEND
    AAAAAAAA - Pathophysiology

    AAAAAAAA - Signs and symtoms

    AAAAAAAA - Treatment, medical interventions


    4

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