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  • Pulmonary Edema in Severe Falciparum Malaria: Udomsak Silachamroon M.D

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    Pulmonary edema is a known complication of severe falciparum malaria, occurring in approximately 0.1% of cases but in up to 21% of cases of cerebral malaria. Pulmonary edema can result from an increase in pulmonary capillary pressure due to heart failure or volume overload, or from an increase in alveolar-capillary membrane permeability due to lung injury from sepsis or shock. Clinical signs include rapid onset of tachypnea, cough, dyspnea, and basal lung rales. Treatment involves antimalarial drugs, careful fluid management to avoid volume overload while maintaining cardiac and renal function, supplemental oxygen or mechanical ventilation for hypoxemia, and management of any associated complications. Mortality from pulmonary edema in

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    Malaria

    Original Title

    PE in Malaria

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    Pulmonary edema is a known complication of severe falciparum malaria, occurring in approximately 0.1% of cases but in up to 21% of cases of cerebral malaria. Pulmonary edema can result from an increase in pulmonary capillary pressure due to heart failure or volume overload, or from an increase in alveolar-capillary membrane permeability due to lung injury from sepsis or shock. Clinical signs include rapid onset of tachypnea, cough, dyspnea, and basal lung rales. Treatment involves antimalarial drugs, careful fluid management to avoid volume overload while maintaining cardiac and renal function, supplemental oxygen or mechanical ventilation for hypoxemia, and management of any associated complications. Mortality from pulmonary edema in

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    14 views15 pages

    Pulmonary Edema in Severe Falciparum Malaria: Udomsak Silachamroon M.D

    Uploaded by

    amincelo
    Pulmonary edema is a known complication of severe falciparum malaria, occurring in approximately 0.1% of cases but in up to 21% of cases of cerebral malaria. Pulmonary edema can result from an increase in pulmonary capillary pressure due to heart failure or volume overload, or from an increase in alveolar-capillary membrane permeability due to lung injury from sepsis or shock. Clinical signs include rapid onset of tachypnea, cough, dyspnea, and basal lung rales. Treatment involves antimalarial drugs, careful fluid management to avoid volume overload while maintaining cardiac and renal function, supplemental oxygen or mechanical ventilation for hypoxemia, and management of any associated complications. Mortality from pulmonary edema in

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    of 15

    Pulmonary Edema in Severe

    Falciparum Malaria
    Udomsak Silachamroon M.D.

    Pulmonary Edema
    Leakage of fluid into alveoli
    Incidence in malaria
    Pf ~ 0.1%
    21% in cerebral malaria

    Associated factors:

    Hyperparasitemia
    Cerebral malaria
    Pregnancy
    Renal failure

    Mechanisms
    Increase pulmonary capillary pressure
    Heart failure (cardiogenic PE), volume
    overload

    Increase alveolar-capillary membrane


    permeability (non- cardiogenic PE)
    Lung injury: sepsis, shock
    Decrease threshold of increase pressure PE

    Combination of both mechanisms

    Clinical Characteristics
    Onset
    acute
    at presentation or delayed (1-2 days after
    treatment)
    at the time of recovery of cerebral malaria,
    clearing of parasitemia

    Progression: rapid

    Clinical Characteristics
    Symptoms & signs:

    tachypnea (most early)


    cough, dyspnea, respiratory distress
    bilateral basal rales
    cyanosis (severe case)

    DDx of tachypnea in severe falciparum


    malaria: metabolic acidosis, basal atelectasis,
    pneumonia (aspiration, infection)

    Laboratory Findings
    Radiographic findings:
    bilateral alveolar edema
    no cardiac enlargement in non-cardiogenic PE

    Arterial blood gas analysis:


    Hypoxemia: various degree depending on
    severity
    Respiratory alkalosis (hyperventilation,
    metabolic acidosis)

    Day1

    Day 3

    Day 4

    Day 6

    Day 13

    CVP & PCWP


    Central venous pressure (CVP)
    elevated in volume overload
    normal in non-cardiogenic PE

    Pulmonary capillary wedge pressure


    (PCWP): Swan-Ganz catheter
    elevated in volume overload
    normal in non-cardiogenic PE
    cut point - 18 mmHg

    Severity
    Respiratory failure may occur
    Cardiogenic PE: no severity classification
    Non-cardiogenic PE
    P/F ratio = PaO2/FiO2
    Acute lung injury (ALI): P/F <300
    Acute respiratory distress syndrome (ARDS):
    P/F <200
    a part of Multiple Organ Dysfunction
    Syndrome (MODS)

    Treatment
    Specific treatment: antimalarial drugs
    Fluid balance:
    Keep the lungs dry, diuretic in volume
    overload
    Not compromising cardiac & renal function

    Treatment for hypoxemia:


    Supplemental oxygen: volume overload, ALI
    Mechanical ventilation with positive end
    expiratory pressure (PEEP): ARDS

    Prognosis
    Mortality: varies (as high as 70% in the
    past)
    Depending on:

    Severity: ARDS
    Reversibility of mechanisms; volume
    Level of intensive care
    Associated complication; intractable shock,
    acidosis

    Survivors: good recovery

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