Atherosclerosis is a condition in which fatty material collects along the walls of arteries.

This
fatty material thickens, hardens (forms calcium deposits), and may eventually block the arteries.

Atherosclerosis is a type of arteriosclerosis. The two terms are often used to mean the same
thing.

Causes

Atherosclerosis is a common disorder that specifically affects the medium and large arteries. It
occurs when fatfat, cholesterol, and other substances build up in the walls of arteries and form
hard structures called plaques.

Eventually, the plaques can make the artery narrow and less flexible, making it harder for blood
to flow. If the coronary arteries become narrow, blood flow to the heart can slow down or stop.
This can cause chest pain (stable anginastable angina), shortness of breath, heart attackheart
attack, and other symptoms.

Pieces of plaque can break off and move through the affected artery to smaller blood vessels,
blocking them and causing tissue damage or death (embolization). This is a common cause of
heart attack and stroke. Blood clots can also form around a tear (fissure) in the plaque leading to
blocked blood flow. If the clot moves into an artery in the heart, lungs, or brain, it can cause a
stroke, heart attack, or pulmonary embolism. In some cases, the atherosclerotic plaque is
associated with a weakening of the wall of an artery leading to an aneurysm.

Risk factors for atherosclerosis include:

• DiabetesDiabetes
• Heavy alcohol use
• High blood pressure
• High blood cholesterolHigh blood cholesterol levels
• High-fat diet
• Increasing age
• ObesityObesity
• Personal or family history of heart diseaseheart disease
• Smoking

Atherosclerosis can affect many different organ systems, including the heart, lungs, brain,
intestines, kidneys, and limbs (extremities).

Symptoms

Symptoms

Symptoms usually do not occur until blood flow becomes restricted or blocked.

See the specific condition for more details on symptoms:

• Abdominal aortic aneurysmAbdominal aortic aneurysm

• Coronary artery diseaseCoronary artery disease
• Kidney diseaseKidney disease
• Mesenteric artery ischemiaMesenteric artery ischemia
• Peripheral artery disease
• Renal artery stenosis
• HypertensionHypertension
• StrokeStroke (cerebrovascular disease)
• Thoracic aortic aneurysm

Aspiration Pneumonitis and Pneumonia

Buy the Book
PDA
Download

Update Me

E-mail alerts
The Merck Manual
Minute
Print This Topic
Email This Topic

Aspiration pneumonitis and pneumonia are caused by inhaling toxic substances,

usually gastric contents, into the lungs. Chemical pneumonitis, bacterial
pneumonia, or airway obstruction can occur. Symptoms include cough and
dyspnea. Diagnosis is based on clinical presentation and chest x-ray findings.
Treatment and prognosis differ by aspirated substance.

Aspiration can cause lung inflammation (chemical pneumonitis), infection

(bacterial pneumonia or abscess), or airway obstruction. However, most episodes
of aspiration cause minor symptoms or pneumonitis rather than infection or
obstruction, and some patients aspirate with no sequelae. Drowning is discussed
in Drowning; airway obstruction is discussed in Respiratory Arrest: Etiology.

Risk factors for aspiration include impaired cognition, impaired swallowing,

vomiting, GI and respiratory devices and procedures (eg, nasogastric or
endotracheal tube placement, dental work), and gastroesophageal reflux disease.

Pathophysiology

Chemical pneumonitis: Multiple substances are directly toxic to the lung or

stimulate an inflammatory response when aspirated; gastric acid is the most
common such aspirated substance, but others include petroleum products
(particularly of low viscosity, such as petroleum jelly) and laxative oils (such as
mineral, castor, and paraffin oil), all of which cause lipoid pneumonia. Aspirated
gasoline and kerosene also cause a chemical pneumonitis (see Poisoning:
Hydrocarbon Poisoning).

Gastric contents produce damage mainly from gastric acid, although food and
other ingested material (eg, activated charcoal as in treatment of overdose) are
injurious in quantity. Gastric acid causes a chemical burn of the airways and lung
leading to rapid bronchoconstriction, atelectasis, edema, and alveolar
hemorrhage. Symptoms include acute dyspnea with cough that is sometimes
productive of pink frothy sputum, tachypnea, tachycardia, fever, diffuse crackles,
and wheezing. Chest x-ray shows diffuse infiltrates frequently but not
exclusively in dependent segments, while pulse-oximetry and ABGs demonstrate
hypoxemia. Treatment is supportive, often involving supplemental O2 and
mechanical ventilation. Antibiotics often are given to patients with witnessed or
known gastric aspiration. The syndrome may resolve spontaneously, usually
within a few days, or may progress to acute respiratory distress syndrome.
Sometimes bacterial superinfection occurs.

Oil or petroleum jelly aspiration causes exogenous lipoid pneumonia, which is

characterized histologically by chronic granulomatous inflammation with
fibrosis. It is often asymptomatic and is detected incidentally on chest x-ray or
may manifest with low-grade fever, gradual weight loss, and crackles. Chest x-
ray findings vary; consolidation, cavitation, interstitial or nodular infiltrates,
pleural effusion, and other changes may be slowly progressive. Treatment is
avoidance of the toxic substance. Anecdotal reports suggest systemic
corticosteroids may be beneficial.

Aspiration pneumonia: Healthy people commonly aspirate small amounts of oral

secretions, but normal defense mechanisms usually clear the inoculum without
sequelae. Aspiration of larger amounts, or aspiration in a patient with impaired
pulmonary defenses, often causes pneumonia and/or abscess (see also Lung
Abscess). Elderly patients tend to aspirate because of conditions associated with
aging that alter consciousness, such as sedative use and disorders (eg, neurologic
disorders, weakness). Empyema (see Mediastinal and Pleural Disorders: Pleural
Effusion) also occasionally complicates aspiration.

Anaerobes often can be cultured from sputum, but it is unclear whether they are
primary infecting organisms to which treatment should be directed or whether
they are simply one of several organisms causing infection.

Symptoms and Signs

Symptoms and signs of pneumonia and abscess are similar and include chronic
low-grade dyspnea, fever, weight loss, and cough productive of putrid, foul-
tasting sputum. Patients may have signs of poor oral hygiene.

Diagnosis

Chest x-ray shows an infiltrate, frequently but not exclusively, in the dependent
lung segments, ie, the superior or posterior basal segments of a lower lobe or the
 posterior segment of an upper lobe.

Treatment

Abscess: Treatment of lung abscess is with clindamycin Some Trade Names

CLEOCIN
Click for Drug Monograph
450 to 900 mg IV q 8 h followed by 300 mg po qid once fever and clinical
symptoms subside. An alternative is a combination of penicillin (either penicillin
G Some Trade Names
BICILLIN
WYCILLIN
Click for Drug Monograph
1 to 2 million units q 4 to 6 h or amoxicillin Some Trade Names
AMOXIL
TRIMOX
Click for Drug Monograph
0.5 to 1 g po tid) plus either metronidazole Some Trade Names
FLAGYL
Click for Drug Monograph
500 mg po tid, amoxicillin-clavulanate Some Trade Names

875/125 mg po tid, or imipenem. Treatment is continued for 6 wk to 3 mo.

Pneumonia: Treatment of aspiration pneumonia can be with clindamycin Some

Trade Names
CLEOCIN
Click for Drug Monograph
, but other antibiotics with lower risk of adverse effects may be effective,
because it is not clear that all the anaerobes cultured from the infection require
specific treatment. Duration of treatment is usually 1 to 2 wk.

Pathophysiology
Aspiration causes an inflammatory reaction called pneumonitis. This can result in damage to the
lung parenchyma. Damage to lung parenchyma causes an inflammatory reaction that can lead to
symptoms such as fever, cough or elevation of white cell count. A secondary bacterial infection
can occur owing to this damaged parenchyma leading to aspiration pneumonia.

The basal segments of the lower lobes are more commonly affected in a patient who aspirates
while sitting upright. [2] The posterior segments of the upper lobes or the apical segments of the
lower lobes are affected in a patient who aspirates while recumbent.
Pathophysiology Concepts

Aspiration is the introduction of a foreign substance into the lungs, but the mere instillation of
foreign substance into the subglottic airway is not sufficient to produce disease. Damage to the
pulmonary tree, which ranges from mild to fatal, depends on the nature, volume and pH of the
aspirated contents, and the pathogenicity of the organisms. Physiologic changes resulting from
aspiration of acidic fluid or gastric contents include a decline in arterial blood oxygen tension,
increased alveolar capillary membrane permeability, and a decrease in intravascular volume. The
lungs can become edematous and gas exchange abnormalities are the result. Histologic
examination shows tracheal mucosal desquamation, damage to the cells of the alveolar lining and
capillary inflammation 24 to 36 hours after aspiration.

Aspiration of nonacidic solutions containing food particles results in a foreign-body reaction of

cell inflammation with granuloma formation. Even aspiration of distilled water or normal saline
can result in damage to the alveolar capillary membrane as detected by electron microscope.

Gastric acid aspirant results in chemical burns that destroy alveoli, which results in acute onset of
respiratory distress secondary to widespread bronchospasm, hypoxemia, and parenchymal
infection. The lower the pH (less than or equal to 2.5) the more severe the injury. There is a 30%
incidence of subsequent development of adult respiratory distress syndrome (ARDS) after acidic
aspiration.

Plasma concentrations of hydrochloric acid administered tracheally to anesthetized dogs reached

peak concentrations in two to three minutes. The pulmonary absorption is immediate, which
suggests that any attempts to neutralize aspirated material would be futile.

Normally, micro-aspirates are cleared by several mechanisms or lines of defense. The materials
are entrapped and removed by filtration, coughing, or by action of the cilia. At the cellular level,
the immune system clears by using inactivation, IgA antibodies, or opsonization, and subsequent
phagocytosis. Loss of these defense mechanisms results in infection and colonization by
pathogenic organisms.

Clinical Manifestations

Aspiration pneumonia is diagnosed clinically by noting its manifestations: a predisposition for

aspiration; recovery of oropharyngeal, gastric or exogenous secretions from the pulmonary bed;
and radiographic evidence of an infiltrative process, usually in a gravity-dependent section of the
lung. The clinical manifestations of aspiration pneumonia are acute and cover a spectrum from
asymptomatic, also known as silent aspiration, to exhibiting a cough, fever, sputum production,
chest pain, increased white blood cell production, acute respiratory distress, tachypnea,
tachycardia, wheezing, and transient hypoxemia with cyanosis. Aspiration pneumonia can
progress to necrotizing lung infections, abscess formation and empyema. Shaking chills are
uncommon in aspiration pneumonia.
Signs of tachypnea, cough, rales, cyanosis, wheezing, fever, leukocytosis and, occasionally,
apnea develop, usually, within two hours of the aspiration. In addition, pulmonary infiltrates in
dependent lung segments - such as posterior segments of upper lobes, superior segments of lower
lobes and basilar segments of lower lobes - are evident on radiographic examination.