Symptoms

Signs

Pt appears severely ill, often diaphoretic, sitting bolt upright, tachypneic, and cyanosis may be present. Bilateral pulmonary rales; third heart sound may be present. Frothy, blood-tinged sputum may occur.

Laboratory Tests

 

Early arterial blood gases show reductions of both PaO2 and PaCO2.

With progressive respiratory failure, hypercapnia develops with acidemia.

Chest X-Ray

CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields with perihilar “butterfly” appearance.

 

Life-threatening, acute development of alveolar lung edema due to one or more of the following:

  1. Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis).

  2. Specific precipitants, resulting in cardiogenic pulmonary edema in pts with previously compensated heart failure or without previous cardiac history.


    PRECIPITANTS OF ACUTE PULMONARY EDEMA

    Acute tachy- or bradyarrhythmia
    Infection, fever
    Acute MI
    Severe hypertension
    Acute mitral or aortic regurgitation
    Increased circulating volume (Na+ ingestion, blood transfusion, pregnancy)
    Increased metabolic demands (exercise, hyperthyroidism)
    Pulmonary embolism
    Noncompliance (sudden discontinuation) of chronic CHF medications
  3. Increased permeability of pulmonary alveolar-capillary membrane (noncardiogenic pulmonary edema). For common causes, see Table 13-2.


    COMMON CAUSES OF NONCARDIOGENIC PULMONARY EDEMA

    Direct Injury to Lung
    Chest trauma, pulmonary contusion Pneumonia
    Aspiration Oxygen toxicity
    Smoke inhalation Pulmonary embolism, reperfusion
    Hematogenous Injury to Lung
    Sepsis Multiple transfusions
    Pancreatitis IV drug use, e.g., heroin
    Nonthoracic trauma Cardiopulmonary bypass
    Possible Lung Injury Plus Elevated Hydrostatic Pressures
    High-altitude pulmonary edema Reexpansion pulmonary edema
    Neurogenic pulmonary edema  

 

 

 

 

 

Pulmonary edema results from transudation of fluid, first from pulmonary capillaries into interstitial spaces and then from the interstitial spaces into alveoli as a result of an alteration in one or more of Starling's forces.

The alveolar epithelial membrane is usually permeable to water and gases but is impermeable to albumin (and other proteins).

A net movement of water from the interstitium into alveoli occurs only when the normally negative interstitial pressure becomes positive (relative to atmospheric pressure). Fortunately, because of the lung’s unique ultrastructure and its capacity to increase lymph flow, the pulmonary interstitium usually accommodates large increases in capillary transudation before interstitial pressure becomes positive. When this reserve capacity is exceeded, pulmonary edema develops.

Pulmonary edema is often divided into four stages:

  • Stage I: Only interstitial pulmonary edema is present. Patients often become tachypneic as pulmonary compliance begins to decrease. The chest radiograph reveals increased interstitial markings and peribronchial cuffing.
  • Stage II: Fluid fills the interstitium and begins to fill the alveoli, being initially confined to the angles between adjacent septa (crescentic filling). Near-normal gas exchange may be preserved.
  • Stage III: Many alveoli are completely flooded and no longer contain gas. Flooding is most prominent in dependent areas of the lungs. Blood flow through the capillaries of flooded alveoli results in a large increase in intrapulmonary shunting. Hypoxemia and hypocapnia (the latter due to dyspnea and hyperventilation) are characteristic.
  • Stage IV: Marked alveolar flooding spills into the airways as froth. Gas exchange is compromised due to both shunting and airway obstruction, leading to progressive hypercapnia and severe hypoxemia.

 

 

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Vascular Fluid and Protein Exchange

The essential factors that govern fluid exchange in the lungs are expressed in the Starling equation for the microvascular barrier:

Image not available.
where
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The Starling equation predicts the development of two different kinds of pulmonary edema. Increased pressure pulmonary edema occurs when the balance of the driving forces increases, forcing fluid across the barrier at a rate that can no longer be accommodated by lymphatic drainage. Increased permeability pulmonary edema occurs in the presence of ARDS that damages the normal barriers to fluid filtration and allows increased flux of liquid and protein into the extravascular compartments of the lungs. Congestion, atelectasis, and pulmonary edema were features of the original description of the syndrome.4

Thus, pulmonary edema results from increases in either hydrostatic driving pressures (increased pressure edema) or barrier conductance (increased permeability edema), or both. What distinguishes the two types is barrier permeability, which is normal in increased pressure edema, but abnormal in increased permeability edema. Fluid flow into the lungs is driven across the barrier in both types of edema by the balance of pressures. ARDS results primarily from an increase in lung vascular permeability, although some cases may be made worse by the presence of elevated lung vascular hydrostatic pressures.

Increased Permeability Pulmonary Edema

Increased permeability pulmonary edema is caused by an increase in liquid and protein conductance across the barriers in the lungs. The essential feature is that the integrity of the barrier to fluid and protein flow into the lung interstitium and alveoli is altered. Increased permeability edema is sometimes called noncardiogenic pulmonary edema, and the resulting clinical syndromes in humans are commonly lumped together as ALI or ARDS.

Accumulation of fluid and protein increases when the lung endothelial and epithelial barriers are injured. If the rate of fluid accumulation exceeds the rate at which it can be removed, increased permeability edema occurs. Large animal models employing measurements of hemodynamics and lung lymph flow demonstrate that clinically relevant causes of ARDS, including live bacteria, endotoxin, and microemboli, induce an increase in lung vascular permeability that causes protein-rich lung edema.57 Because the barriers limiting fluid and protein flow into the lungs do not function normally when the lungs are injured, the lungs are not protected against edema by the usual safety factors. Although increases in fluid and protein filtration across the lung endothelium can be removed by lymphatics and drained away from the alveolar walls as in increased pressure edema, much more fluid and protein are filtered at any given sum of driving pressures, since the barriers to flow are much less restrictive than normal.

Edema formation in injured lungs is sensitive to hydrostatic driving pressures. Driving pressures are often increased when the lungs are injured because of the vasoconstrictive effects of inflammatory mediators, such as thromboxanes. Thromboxanes may shift the main site of vascular resistance to postcapillary venules, thus increasing hydrostatic pressure at the microvascular fluid exchange sites, or may exert cardiac effects. For example, elevated left atrial pressure, pulmonary venoconstriction, or an increase in cardiac output in sepsis may increase hydrostatic pressure at the microvascular fluid exchange sites. Although a primary event in ARDS is an increase in lung vascular permeability, the magnitude of lung edema formation in ARDS may be substantially increased when lung vascular pressures and volume are elevated, consistent with the effects of elevated hydrostatic pressure on transvascular flux of fluid and protein.

Because the lung endothelial and epithelial barriers are injured in ARDS, the protective effects of protein osmotic pressure differences across them are lost; driving pressure is unopposed by protein osmotic pressure, and even normal hydrostatic pressure results in significant fluid and protein extravasation into the interstitial and alveolar spaces. The ability of the lymphatics to pump the excess filtrate away is increased when the lungs are injured. If the alveolar epithelial barrier is damaged, edema may accumulate readily in alveoli, since most of the resistance to fluid and protein flow into the alveoli is in the epithelial barrier.

To summarize, the majority of patients with ARDS have normal or low hydrostatic pressures and increased alveolar-capillary permeability. However, up to 30% of patients with ARDS may have an elevated left atrial pressure.8 Lung fluid balance is a dynamic concept that incorporates both formation and removal of edema fluid in the interstitium and airspaces.

Lung Physiology

The effects of increased permeability edema on lung mechanics and gas exchange depend, in part, on the magnitude of edema accumulation. As with increased pressure edema, the major effects on pulmonary mechanics occur with alveolar flooding.

About 20% to 30% of the extravascular water of the lungs is in the extravascular interstitial tissue. This volume can more than double before alveolar flooding occurs. In experimental lung injury, functional residual capacity (FRC) is decreased as a consequence of alveolar flooding; the loss of units that can be ventilated accounts for most of the decrease in static lung compliance.9 Computed tomography has provided new insights into structure–function relationships in human ARDS. In the early stage of lung injury, when alveolar edema predominates, the lungs are characterized by a more homogeneous alteration of vascular permeability, and edema may accumulate evenly in all lung regions, with a nongravitational distribution. Later in the exudative phase of ARDS, the consolidation is more gravity-dependent. In the organizing phase, lung reticulation appears.

Measurements of pulmonary mechanics in mechanically ventilated patients with ARDS show a decrease in static lung compliance as a consequence of loss of ventilated lung units. In addition, airflow resistance is increased as a result of decreased lung volume.10Bronchospasm may add to the increase in airflow resistance and may be partially reversed in some patients by administration of inhaled bronchodilators. Chest wall compliance is reduced, probably because of alterations in the intrinsic mechanical properties of the chest wall by abdominal distention, chest wall edema, and pleural effusion. Respiratory mechanics and responses to positive end-expiratory pressure (PEEP) during mechanical ventilation in patients with ARDS originating from pulmonary disease (e.g., pneumonia and associated lung consolidation) and that arising from extrapulmonary disease may differ.11

The injured lung in ARDS may release biologically active substances that can interfere with the normal state of low surface tension in the alveoli. In addition, activated neutrophils may reduce surfactant function in vitro and degrade major surfactant apoproteins through a combination of proteolysis and oxidant radical–mediated mechanisms. Human lung surfactant obtained from bronchoalveolar lavage (BAL) fluid in patients at risk for ARDS and from those with established ARDS are abnormal in chemical composition and functional activity.12 Abnormalities may also be caused by interactions between surfactant and edema proteins, since plasma proteins interfere with surfactant function.

Gas exchange is severely compromised in increased permeability edema, because of both intrapulmonary shunting of blood and ventilation–perfusion inequalities. Clinical evidence indicates that patients with early ARDS have a marked increase in pulmonary dead space fraction.13 This finding indicates that many ventilated lung units are not well perfused, although intrapulmonary shunting may also contribute to the elevated dead space. Minute ventilation is typically twice normal (approximately 12 L/min) at the onset of ARDS.

Pathologic Findings

Based on several studies that included a preponderance of postmortem pathology, the light and electron microscopic appearances of human and animal lung tissue in ARDS have been described.14 The earliest changes are marked by widespread alveolar and interstitial edema, inflammation, and hemorrhage. Hyaline membranes, composed of precipitated plasma proteins, fibrin, and necrotic debris, are frequently found and constitute the footprint of a pathologic finding termed diffuse alveolar damage (DAD), which pathologists use to define ARDS microscopically (Fig. 140-1).15

 

 

 

 

Pulmonary edema is caused by:

cardogenic

non cardiogenic conditions

The distinction between cardiogenic and noncardiogenic causes is not always possible, since the clinical syndrome may represent a combination of several different disorders.

The diagnosis is important, however, because treatment varies considerably depending upon the underlying pathophysiologic mechanisms.

 

 

 

 

 

 

 

Occurs in approximately 25% of intubated ICU patients; overall mortality, 20–50%.

 

Needs immediate, aggressive therapy

Measures instituted simultaneously as possible for cardiogenic pulmonary edema:

  1. Administer 100% O2 by mask to achieve PaO2 >60 mmHg;

    if inadequate, use positive-pressure ventilation by face or nasal mask, and if necessary, proceed to endotracheal intubation.

  2. Reduce preload:

    1. Seat patient upright to reduce venous return, if not hypotensive.

    2. Intravenous loop diuretic (e.g., furosemide, initially 0.5–1.0 mg/kg); use lower dose if pt does not take diuretics chronically.

    3. Nitroglycerin (sublingual 0.4 mg × 3 q5min) followed by 5–20 μg/ min IV if needed.

    4. Morphine 2–4 mg IV; assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.

    5. Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.

    6. Consider nesiritide (2-μg/kg bolus IV followed by 0.01 μg/kg per min) for refractory symptoms—do not use in acute MI or cardiogenic shock.

  3. Inotropic agents are indicated in cardiogenic pulmonary edema and severe LV dysfunction: dopaminedobutaminemilrinone.
  4. The precipitating cause of cardiogenic pulmonary edema should be sought and treated, particularly acute arrhythmias or infection. For refractory pulmonary edema associated with persistent cardiac ischemia, early coronary revascularization may be life-saving. For noncardiac pulmonary edema, identify and treat/remove cause.

 

 

Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.

 

Content 3

Content 13

Content 11

 

A

A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

Complete Quiz and View Results
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The correct answer is A. You answered A.

Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.

 

Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?

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The correct answer is A. You answered A.

The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.

 


 

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