In 1925, G. F. LAUGHLEN, M.D. was the first physician to describe lipoid pneumonia. He first interacted with the disease by routine autopsy at the Toronto, Ontario hospital for sick children. He described grayish red nodules at the autopsy with three types of exudates, found out mononuclear cells which were unexpected in the exudates. In 1949 McDonald et al described endogenous lipoid pneumonia for the first time. He observed so-called “obstructive pneumonia” in patients with lung neoplasms. In September 2019, there was an outbreak of lipoid pneumonia related to vaping. it was then reported to be because of vitamin E soluble in THC e-cigarette juice. Lipoid pneumonia may be classified according to source of the lipid exposure into 2 subtypes: Exogenus, more common type reported, due to aspiration or inhalation of fatty substance, and endogenus, due to obstructive pneumonia.lipoid pneumonia parthenogenesis is different in its two sub-types: Exegenous form:it is understood that exogenus lipoid pneumonia is the result of chronic body reaction to fatty substance in the alveol. Lipid reaches alveoli by aspiration or inhalation. Some mineral oils can cause lung injuries such as gasoline. Mineral oils can enter the tracheobronchial tree without causing cough reflex which will bother mucociliary transport system chronically. Injected lipids mechanism of further producing lipid pneumonia is more complicated. As the lipid goes inside the alveoli, it is trapped and hard to expectorate, this condition may be worsen by associated neurological and gastrointestinal disorders affecting swallowing or cough. Lipids in alveoli form emulsion and then consumed by macrophages via phagocytosis. Since the alveolar macrophages cannot metabolize consumed fatty substance, oil is repeatedly released into alveoli after death of these macrophages. The oil released, illicits a giant-cell granulomatosis reaction. Endogenous form: The pathogenesis of endogenous lipoid pneumonia is still not well understood however there are plenty of suggested mechanisms, endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products. Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason. Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and mono-oxygenases.Infection changes to endogenous lipid pneumonia is generally localized in airways because the souronding lung is already consolidated, limiting the spread of bacteria. On gross and microscopic histology well circumscribed, firm with prominent lymphatics on lung surface in exogenous typelipoid material (or empty spaces), inflammatory cells and young fibroblasts. Reactive endarteritis, marked alveolar lining cell hyperplasia. Lipid-laden foamy macrophages are seen.Vaping is a common cause of lipoid pneumonia. occupationally related lipoid pneumonia is seen in fire-eaters(caused by Kedran oil). some trivial habits such as: use of oil-based laxatives, lip balm, lip gloss petroleum jelly play a role in lipoid pneumonia development. siphoning various mineral oils such as diesel is another common risk factor especially in India may be another causetive factor.Lipod pneumonia must be differentiated from other diseases that cause Cough with basilar infiltrates, such as bacterial pneumonia, viral pneumonia, congestive heart failure, pulmonary fibrosis, and aspiration pneumonia. Exogenous lipoid pneumonia is usually misdiagnosed as community-acquired pneumonia. in patients at risk of aspiration early CT scan is very useful for further diagnosis of lipoid pneumonia. Since lipid-laden pneumonia is is very sensitive but may not be very specific, the diagnosis of exogenous lipoid pneumonia is based on the triad of: History of mineral oil ingestion or vaping, compatible radiological findings, and presence of intra-alveolar lipids and/or lipid-laden macrophages.The incidence and prevalence of lipoid pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonias from each other. In 2019 there was an outbreak of vaping based pulmonary complications.Lipoid pneumonia pathogenicity is because of lipid aspiration. Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.There is insufficient evidence to recommend routine screening for lipoid pneumonia.Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs. Owing to its nonspecific symptoms and radiological features, lipoid pneumonia often remains undiagnosed or diagnosis is delayed. The oil released illicits a giant-cell granulomatous reaction (hence also called lipid granulomatosis), chronic inflammation, and alveolar and interstitial fibrosis. Evolution of lesions with time has been described: Fresh lesions show alveolar infiltration by lipid-laden macrophages and almost normal alveolar walls and septa, and advanced lesions show larger vacuoles and inflammatory infiltrates in alveolar walls, bronchial walls and septa. Diagnostic Study of Choice: lipoid pneumonia is mainly diagnosed based on clinical presentation. The CURB-65 and the eCURB scoring systems are used to evaluate and predict mortality in patients with pneumonia. However, they are not helpful in aspiration pneumonia. History and Symptoms; Patients with exogenous lipoid pneumonia have a positive history of oil contaminating prescription, E-cigarette smoking, vaping, using oily laxative, or other oil related history. in some cases high susceptibility to aspiration must be considered. Common symptoms of aspiration pneumonia include: Chest pain, cough, fever, sweating, and shaking chills.Physical examination of lipoid pneumonia does not reveal any different feature and is usually mistaken with community acquired pneumonia (CAP). may reveal low grade fever or sometimes low body temperature, an increased respiratory rate, low blood pressure, a fast heart rate, or a low oxygen saturation, which is the amount of oxygen in the blood as indicated by either pulse oximetry or blood gas analysis. Patients who have difficulty breathing, who are confused, or who have cyanosis (blue-tinged skin) require immediate attention. Auscultation findings include lack of normal breath sounds, the presence of crackling sounds (rales), or increased loudness of whispered speech (whispered pectoriloquy) with areas of the lung that are stiff and full of fluid, called consolidation. Vital signs are useful in determining the severity of illness and have predictive values. However, a high degree of suspicion should be kept in elderly as the presentation could be subtle in them. Different laboratory tests might be used in patients with aspiration pneumonia. Sputum analysis including lipid laden macrophage, gram stain and culture must be done in patients with cough. ABG may show acute hypoxemia and decreased mixed venous oxygen saturation. CBC shows leukocytosis with left shift or leukopenia, anemia, or thrombocytopenia. There are some non-specific findings on ECG of a patient with lipoid pneumonia which include sinus tachycardia, minor nonspecific ST-segment or T-wave changes, right atrial enlargement, QRS abnormalities like right axis deviation, and presence of S1S2S3.Chest x-rays may be helpful in the diagnosis of aspiration pneumonia. Findings on an chest x-ray suggestive of aspiration pneumonia include lobar pneumonia, areas of opacity, unilateral consolidation, air bronchogram, or cavitation. In some cases, ultrasound is used for the diagnosis and follow-up of a patient with pneumonia, for a guided thoracocentesis and to quantify the amount of pleural effusion, however its benefits are not yet indicated for lipoid pneumonia. Chest CT scan might be used in patients with aspiration pneumonia if a chest x-ray is not conclusive. CT findings may include lobar consolidation, ground-glass opacities, bronchiectasis, atelectasis, pleural effusion, and consolidation. A chest CT can also help to assess reasons for therapy failure and complications, such as lung abscess, and pleural effusions. Chest MRI may be helpful in the diagnosis of lipoid pneumonia. Findings on MRI suggestive of lipoid aspiration pneumonia may differentiate disease from other forms of aspiration pneumonia. Other findings are: atelectasis, consolidation and opacities.Bronchoscopy with bronchoalveolar lavage is useful to obtain samples for finding lipid-laden macrophages. In some cases of lipoid pneumonia, transbronchial lung biopsy or even surgical biopsy may be required to determine the exact cause of lipoid pneumonia, specially in endogenous form. videofluoroscopic swallow study (VFSS) might be used to evaluate swallowing difficulties. Treatment of lipoid pneumonia is not well studied and published experience is only with case reports.Bronchoalveolar lavage (BAL) is both diagnostic and therapeutic procedure in lipoid pneumonia, specially in children. Surgery is not a common treatment for lipoid pneumonia, but if there is a high suspicion of cancer, it would be considered as a therapy plan. video-assisted thoracoscopic surgery (VATS) lobectomy, is the favored method for these interventions. Lipoid pneumonia can be prevented by cessation of underlying cause like E-cigarette smoking or lipid based medications.it is also preventable by preventing aspiration pneumonia. effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol. Lipoid pneumonia can be prevented by cessation of underlying cause like E-cigarette smoking or lipid based medications.it is also preventable by preventing aspiration pneumonia. effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol.

In 1925, G. F. LAUGHLEN, M.D. was the first physician to describe lipoid pneumonia. He first interacted with the disease by routine autopsy at the Toronto, Ontario hospital for sick children. He described grayish red nodules at the autopsy with three types of exudates, found out mononuclear cells which were unexpected in the exudates. In 1949 McDonald et al described endogenous lipoid pneumonia for the first time. He observed so-called “obstructive pneumonia” in patients with lung neoplasms.

Lipoid pneumonia may be classified according to source of the lipid exposure into 2 subtypes: Exogenus, more common type reported, due to aspiration or inhalation of fatty substance, and endogenus, due to obstructive pneumonia.

lipoid pneumonia parthenogenesis is different in its two sub-types: Exegenous form:it is understood that exogenus lipoid pneumonia is the result of chronic body reaction to fatty substance in the alveol. Lipid reaches alveoli by aspiration or inhalation. Some mineral oils can cause lung injuries such as gasoline. Mineral oils can enter the tracheobronchial tree without causing cough reflex which will bother mucociliary transport system chronically. Injected lipids mechanism of further producing lipid pneumonia is more complicated. As the lipid goes inside the alveoli, it is trapped and hard to expectorate, this condition may be worsen by associated neurological and gastrointestinal disorders affecting swallowing or cough. Lipids in alveoli form emulsion and then consumed by macrophages via phagocytosis. Since the alveolar macrophages cannot metabolize consumed fatty substance, oil is repeatedly released into alveoli after death of these macrophages. The oil released, illicits a giant-cell granulomatosis reaction. Endogenous form: The pathogenesis of endogenous lipoid pneumonia is still not well understood however there are plenty of suggested mechanisms, endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products. Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason. Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and mono-oxygenases.Infection changes to endogenous lipid pneumonia is generally localized in airways because the souronding lung is already consolidated, limiting the spread of bacteria. On gross and microscopic histology well circumscribed, firm with prominent lymphatics on lung surface in exogenous typelipoid material (or empty spaces), inflammatory cells and young fibroblasts. Reactive endarteritis, marked alveolar lining cell hyperplasia. Lipid-laden foamy macrophages are seen.

Vaping is a common cause of lipoid pneumonia. occupationally related lipoid pneumonia is seen in fire-eaters(caused by Kedran oil). some trivial habits such as: use of oil-based laxatives, lip balm, lip gloss petroleum jelly play a role in lipoid pneumonia development. siphoning various mineral oils such as diesel is another common risk factor especially in India may be another causetive factor.

Lipod pneumonia must be differentiated from other diseases that cause Cough with basilar infiltrates, such as bacterial pneumonia, viral pneumonia, congestive heart failure, pulmonary fibrosis, and aspiration pneumonia. Exogenous lipoid pneumonia is usually misdiagnosed as community-acquired pneumonia. in patients at risk of aspiration early CT scan is very useful for further diagnosis of lipoid pneumonia. Since lipid-laden pneumonia is is very sensitive but may not be very specific, the diagnosis of exogenous lipoid pneumonia is based on the triad of: History of mineral oil ingestion or vaping, compatible radiological findings, and presence of intra-alveolar lipids and/or lipid-laden macrophages.

The incidence and prevalence of lipoid pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonias from each other. In 2019 there was an outbreak of vaping based pulmonary complications.

Lipoid pneumonia pathogenicity is because of lipid aspiration. Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

There is insufficient evidence to recommend routine screening for lipoid pneumonia.

Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs. Owing to its nonspecific symptoms and radiological features, lipoid pneumonia often remains undiagnosed or diagnosis is delayed. The oil released illicits a giant-cell granulomatous reaction (hence also called lipid granulomatosis), chronic inflammation, and alveolar and interstitial fibrosis. Evolution of lesions with time has been described: Fresh lesions show alveolar infiltration by lipid-laden macrophages and almost normal alveolar walls and septa, and advanced lesions show larger vacuoles and inflammatory infiltrates in alveolar walls, bronchial walls and septa

Lipoid pneumonia is mainly diagnosed based on clinical presentation. The CURB-65 and the eCURB scoring systems are used to evaluate and predict mortality in patients with pneumonia. However, they are not helpful in aspiration pneumonia.

Patients with exogenous lipoid pneumonia have a positive history of oil contaminating prescription, E-cigarette smoking, vaping, using oily laxative, or other oil related history. in some cases high susceptibility to aspiration must be considered. Common symptoms of aspiration pneumonia include: Chest pain, cough, fever, sweating, and shaking chills.

Physical examination of lipoid pneumonia does not reveal any different feature and is usually mistaken with community acquired pneumonia (CAP). May reveal low grade fever or sometimes low body temperature, an increased respiratory rate, low blood pressure, a fast heart rate, or a low oxygen saturation, which is the amount of oxygen in the blood as indicated by either pulse oximetry or blood gas analysis. Patients who have difficulty breathing, who are confused, or who have cyanosis (blue-tinged skin) require immediate attention. Auscultation findings include lack of normal breath sounds, the presence of crackling sounds (rales), or increased loudness of whispered speech (whispered pectoriloquy) with areas of the lung that are stiff and full of fluid, called consolidation. Vital signs are useful in determining the severity of illness and have predictive values. However, a high degree of suspicion should be kept in elderly as the presentation could be subtle in them.

Different laboratory tests might be used in patients with aspiration pneumonia. Sputum analysis including lipid laden macrophage, gram stain and culture must be done in patients with cough. ABG may show acute hypoxemia and decreased mixed venous oxygen saturation. CBC shows leukocytosis with left shift or leukopenia, anemia, or thrombocytopenia.

There are some non-specific findings on ECG of a patient with lipoid pneumonia which include sinus tachycardia, minor nonspecific ST-segment or T-wave changes, right atrial enlargement, QRS abnormalities like right axis deviation, and presence of S1S2S3.

Chest x-rays may be helpful in the diagnosis of aspiration pneumonia. Findings on an chest x-ray suggestive of aspiration pneumonia include lobar pneumonia, areas of opacity, unilateral consolidation, air bronchogram, or cavitation.

In some cases, ultrasound is used for the diagnosis and follow-up of a patient with pneumonia, for a guided thoracocentesis and to quantify the amount of pleural effusion. However its benefits are not yet indicated for lipoid pneumonia.

A chest CT scan might be used in patients with aspiration pneumonia if a chest x-ray is not conclusive. CT findings may include lobar consolidation, ground-glass opacities, bronchiectasis, atelectasis, pleural effusion, and consolidation. A chest CT can also help to assess reasons for therapy failure and complications, such as lung abscess, and pleural effusions.

Chest MRI may be helpful in the diagnosis of lipoid pneumonia. Findings on MRI suggestive of lipoid aspiration pneumonia may differentiate disease from other forms of aspiration pneumonia. Other findings are: atelectasis, consolidation and opacities.

Bronchoscopy with bronchoalveolar lavage is useful to obtain samples for finding lipid-laden macrophages.

In some cases of lipoid pneumonia, transbronchial lung biopsy or even surgical biopsy may be required to determine the exact cause of lipoid pneumonia, specially in endogenous form. videofluoroscopic swallow study (VFSS) might be used to evaluate swallowing difficulties.

Treatment of lipoid pneumonia is not well studied and published experience is only with case reports.

Bronchoalveolar lavage (BAL) is both diagnostic and therapeutic procedure in lipoid pneumonia, specially in children.

Surgery is not a common treatment for lipoid pneumonia, but if there is a high suspicion of cancer, it would be considered as a therapy plan. video-assisted thoracoscopic surgery (VATS) lobectomy, is the favored method for these interventions.

Lipoid pneumonia can be prevented by cessation of underlying cause like E-cigarette smoking or lipid based medications.it is also preventable by preventing aspiration pneumonia. effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol.

Lipoid pneumonia can be prevented by cessation of underlying cause like E-cigarette smoking or lipid based medications.it is also preventable by preventing aspiration pneumonia. Effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol.

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In 1925, G. F. LAUGHLEN, M.D. was the first physician to describe lipoid pneumonia. He first interacted with the disease by routine autopsy at the Toronto, Ontario hospital for sick children. He described grayish red nodules at the autopsy with three types of exudates, found out mononuclear cells which were unexpected in the exudates. In 1949 McDonald et al described endogenous lipoid pneumonia for the first time. He observed so-called “obstructive pneumonia” in patients with lung neoplasms.

• In 1925,G. F. LAUGHLEN, M.D. was the first physician to describe exogenous lipoid pneumonia.^[1]
• He first interacted to the disease by routine autopsy at the Toronto, Ontario hospital for sick children.
• He described grayish red nodules at the autopsy with three types of exudates, found out mononuclear cells which were unexpected in the exudates.
• All of his 4 observed cases underwent laxative and nasal drop therapy regimen.
• In 1949 McDonald et al described endogenous lipoid pneumonia for the first time.^[2]
• He observed so called “obstructive pneumonia” in patients with lung neoplasms.^[3]

Following are important landmark events that shows how aspiration pneumonia became an important entity of critical care:^{[4][5][3][6][7][8]}

Year	Events
460 BC–380 BC	Hippocrates described pneumonia.
1138–1204 AD	Maimonides wrote about pneumonia as “The basic symptoms which occur in pneumonia and which are never lacking are as follows: acute fever, sticking pleuritic pain in the side, short rapid breaths, serrated pulse, and cough.”
1875	Edwin Klebs identified bacteria in the airways of individuals who died from pneumonia.
1848	Carl Friedländer identified the two common bacteria such as Streptococcus pneumoniae and Klebsiella pneumoniae that cause pneumonia.
1893	Veillon was first to write about the role of anaerobic bacteria in aspiration pneumonia.
1896	Roentgen described x-rays.
1918	Sir William Osler, known as “the father of modern medicine,” appreciated the morbidity and mortality of pneumonia, describing it as the “captain of the men of death.”
1927	Smith was first to clearly show anaerobic bacterial growth in animal models suffered from aspiration pneumonia.
1929	Drinker and Shaw announced the invention of the iron lung during the polio epidemic.
1985	Specimens collected from patients with aspiration pneumonia were vastly cultured and it was called anaerobic bandwagon.

• During July and August 2019, five patients were identified at two hospitals in North Carolina with acute lung injury potentially associated with e-cigarette use.
• Patients were adults aged 18–35 years and all experienced several days of worsening dyspnea, nausea, vomiting, abdominal discomfort, and fever.
• All patients demonstrated tachypnea with increased work of breathing on examination, hypoxemia (pulse oximetry <90% on room air), and bilateral lung infiltrates on chest x-ray.
• All five patients shared history of recent use of marijuana oils or concentrates in e-cigarettes.^_MMWR2-9|[9]
• Thirty-three deaths confirmed due to vaping in 24 states of US, but lipoid pneumonia role in those mortalities was not proven.^{_MMWR-10|[10]}
• The higher risk of lipoid pneumonia in THC vaping was then hypothesized to be due to usage of vitamin E in THC juice of e-cigarettes.^[11]
• Vitamin E is a substance added to cannabis products to increase their central effect.
• It’s streaky and high solubility potential is said to be the cause of lipoid pneumonia.

{{#ev:youtube|https://www.youtube.com/watch?v=BtKbUpKeU_Q%7C500}}

Lipoid pneumonia may be classified according to source of the lipid exposure into 2 subtypes: Exogenous, more common type reported, due to aspiration or inhalation of fatty substance, and endogenous, due to obstructive pneumonia.

• Lipoid pneumonia may be classified according to source of the lipid exposure into 2 subtypes:^[1][2]

Lipoid pneumonia classification

Exogenus: More common type reported, due to aspiration or inhalation of fatty substance.

Endogenus: Due to obstructive pneumonia.

Type I

Type II

Type III

• Endogenous pneumonia further divide into 3 subgroups:^[3]
  • Type I: Localized to the lung parenchyma distal to an airway obstructed by a tumor.
  • Type II: Features of type I lipoid pneumonia and consecutively spreading to the adjacent segment whose airway is not affected.
  • Type III: Features of type II lipoid pneumonia and spreading to isolated segments.
    
    

Lipoid pneumonia pathogenesis is different in its two subtypes: Exogenous form is the result of chronic body reaction to fatty substance in the alveoli. Lipid reaches alveoli by aspiration or inhalation. Some mineral oils can cause lung injuries such as gasoline. Mineral oils can enter the tracheobronchial tree without causing cough reflex which will bother mucociliary transport system chronically. Injected lipids mechanism of further producing lipid pneumonia is more complicated. As the lipid goes inside the alveoli, it is trapped and hard to expectorate, this condition may be worsen by associated neurological and gastrointestinal disorders affecting swallowing or cough. Lipids in alveoli form emulsion and then consumed by macrophages via phagocytosis. Since the alveolar macrophages cannot metabolize consumed fatty substance, oil is repeatedly released into alveoli after death of these macrophages. The oil released, elicits a giant-cell granulomatosis reaction. Pathogenesis of endogenous form is still not well understood however there are plenty of suggested mechanisms, one saying that endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products. Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason. Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and monooxygenases. Infection changes to endogenous lipid pneumonia is generally localized in airways because the surrounding lung is already consolidated, limiting the spread of bacteria. On gross and microscopic histology will show well circumscribed, firm with prominent lymphatics on lung surface, inflammatory cells, and young fibroblasts. Reactive endarteritis and marked alveolar lining cell hyperplasia may also be seen. Lipid-laden foamy macrophages are part of pathology.

The important pathophysiology aspects regarding exogenous lipoid pneumonia include:^[1][2]

• It is understood that exogenous lipoid pneumonia is the result of chronic body reaction to fatty substance in the alveoli.
• Lipid reaches alveoli by aspiration or inhalation.
• Some mineral oils can cause lung injuries such as gasoline.
• Mineral oils can enter the tracheobronchial tree without causing cough reflex which will bother mucociliary transport system chronically.
• Injected lipids mechanism of further producing lipid pneumonia is more complicated:
  • It is suggested that the lung is the first capillary bed encountered during circulation, bearing the majority of damage.
• As the lipid goes inside the alveoli, it is trapped and hard to expectorate, this condition may be worsen by associated neurological and gastrointestinal disorders affecting swallowing or cough.
• Lipids in alveoli form emulsion and then consumed by macrophages via phagocytosis.
• Since the alveolar macrophages cannot metabolize consumed fatty substance, oil is repeatedly released into alveoli after death of these macrophages.
• The oil released, elicits a giant-cell granulomatosis reaction:
  • In fresh lesions, lipid-laden macrophages are seen.
  • In advanced lesions larger vacuoles and inflammatory infiltrates are seen in alveolar and bronchial walls and septa.
  • In oldest lesions fibrosis and parenchymal destruction around large lipid-containing vacuoles is seen.
• Staining can help demonstrating whether vacuoles are filled with lipid or not:
  • Oil red O.
  • Sudan black.

The pathogenesis of endogenous lipoid pneumonia is still not well understood however there are plenty of suggested mechanisms:^[3][4][5]

• Most proven mechanisms are:
  • Retained epithelial secretion.
  • Cell breakdown.
  • Leakage from vessels.
  • Prolonged hypoxia.
  • Local oxygen and carbon dioxide tension.
• Endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products.^[6]
• Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason.
• Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and mono-oxygenases.^[7][8][9]
• These enzymes activation in turn cause modification of LDL cholesterol, enhancing lipid uptake by alveolar macrophages similar to atherogenesis.

• Infection changes to endogenous lipid pneumonia is generally localized in airways because the surrounding lung is already consolidated, limiting the spread of bacteria.^[10]
  

There is no genetic predisposition reported with lipoid pneumonia.

• Vaping is associated with exogenous lipoid pneumonia.^[7][4]
• Fire eating is associated with exogenous lipoid pneumonia.
• Using oily laxative is associated with exogenous lipoid pneumonia.
• Pulmonary adenocarcinoma is associated with endogenous lipid pneumonia.
• Long lasting pulmonary granulomatosis diseases is associated with endogenous lipid pneumonia.

• Well circumscribed, firm with prominent lymphatics on lung surface in exogenous type.^[11]
• Parenchymal consolidation in endogenous lipoid pneumonia produce a characteristic yellowish discoloration, hence called “golden pneumonia“.^[12]

• Lipoid material (or empty spaces), inflammatory cells and young fibroblasts.^[14]
• Reactive endarteritis, marked alveolar lining cell hyperplasia.
• Lipid-laden foamy macrophages

{{#ev:youtube|https://www.youtube.com/watch?v=nGi0udE5EI8%7C500}}

Vaping is a common cause of lipoid pneumonia. Occupationally related lipoid pneumonia is seen in fire-eaters(caused by Kedran oil). Some trivial habits such as: Use of oil-based laxatives, lip balm, lip gloss petroleum jelly play a role in lipoid pneumonia development. Siphoning various mineral oils such as diesel is another common risk factor especially in India may be another causetive factor.

• Vaping is a common cause of lipoid pneumonia:^{[1][2]_MMWR-3|[3]}
  • E-cigarets and vapes use an oily juice as their source.
  • Heating the oil makes the smoke.
  • They can be used as THC or other drug smoking material.
  • There is a high association between THC or other highly concentrated oil juice material with lipoid pneumonia.
• Occupationally related lipoid pneumonia is seen in fire-eaters(caused by Kedran oil).^[4][5]

• Some trivial habits such as:^[6][7]
  • Use of oil-based laxatives
  • Lip balm
  • Lip gloss
  • Petroleum jelly
• Siphoning various mineral oils such as diesel is another common risk factor especially in India.
• Forceful animal fat feeding such as ‘Ghee’ is another common cause among Indians.
• Exogenous lipid could be aspirated through these mechanisms

• There is no reported genetic causes for exogenous lipoid pneumonia.^[8]

• Incompetent swallowing mechanism, such as in neurological disease (a common cause being strokes) or while a person is intoxicated.
• Iatrogenic causes such as general anaesthesia for an operation. Patients are therefore instructed to be “not permitted orally” (NPO) for at least four hours before surgery.
  • Exogenous lipoid pneumonia could be an iatrogenic outcome of bronchoscopy with propylidone dye.

• Drug Side Effect:
  • Blinatumomab
  • Belimumab
  • Boceprevir
  • Ceritinib
  • Dornase Alfa
  • Enfuvirtide
  • Ethanolamine oleate
  • Felbamate
  • Iloperidone
  • Interferon alfacon-1
  • Pegylated interferon alfa-2b

• Most common cause of endogenous lipoid pneumonia pre-existing conditions such as:^{[9][10][11][12][13][14][15]}
  • Endogenous lipid pneumonia is a direct consequence of bronchial obstruction:
    • The main reason is non-small cell carcinoma.
  • Endogenous lipid pneumonia can occure as manifestation of infection or other diseases with no obstruction.
  • Endogenous lipoid pneumonia has been observed in association with pulmonary alveolar proteinosis.
    • Alveolar proteinosis is filling the alveoli with protein and lipid resembling surfactant.
    • It manifest as ground-glass capacities and crazy-paving pattern on CT scan
  • Niemann-pick disease
  • Sclerosing cholangitis
  • Bronchiolitis oblitera
  • Nercotizing granulomatosis
  • Connective tissue disease

Cardiovascular	No underlying causes
Chemical/Poisoning	petroleum jelly
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Oil based luxatives
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Oil based prescriptions
Infectious Disease	No underlying causes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	solid tumors
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Vaping with oily juice

Lipod pneumonia must be differentiated from other diseases that cause cough with basilar infiltrates, such as bacterial pneumonia, viral pneumonia, congestive heart failure, pulmonary fibrosis, and aspiration pneumonia. Exogenous lipoid pneumonia is usually misdiagnosed as community-acquired pneumonia. In patients at risk of aspiration early CT scan is very useful for further diagnosis of lipoid pneumonia. Since lipid-laden pneumonia is very sensitive but may not be very specific, the diagnosis of exogenous lipoid pneumonia is based on the triad of: History of mineral oil ingestion or vaping, compatible radiological findings, and presence of intra-alveolar lipids and/or lipid-laden macrophages.

• Lipod pneumonia must be differentiated from other diseases that cause cough with basilar infiltrates, such as bacterial pneumonia, viral pneumonia, congestive heart failure, pulmonary fibrosis, and aspiration pneumonia.^[1]
• Differentiating exogenous lipoid pneumonia from other diseases on the basis of radiologic features and specimen histologic features:^{[2][3][4][5][6][7]}
  • Exogenous lipoid pneumonia is usually misdiagnosed as community-acquired pneumonia.
  • It is considered usually as the initial diagnosis that does not lead to appropriate therapy.
  • In patients at risk of aspiration early CT scan is very useful for further diagnosis of lipoid pneumonia.
  • Diagnosis is confirmed by detecting intra-alveolar lipid and lipid-laden macrophages.
  • Specimens could be brought by:
    • BAL (Broncho Alveolar Lavage)
    • Transthoracic fine-needle aspiration cytology
    • Biopsy from lesion
  • Sputum examination has questionable reliability because lipid-laden macrophages in sputum have been demonstrated in the absence of lipoid pneumonia.
  • BAL is widely available and the choice of specimen taking today.
  • Frozen samples must be stained in order to determine the type of oil.
  • Since lipid-laden pneumonia is is very sensitive but may not be very specific, the diagnosis of exogenous lipoid pneumonia is based on the following triad (based on order):

1. 1. History of mineral oil ingestion or vaping
   2. Compatible radiological findings
   3. Presence of intra-alveolar lipids and/or lipid-laden macrophages

Diseases	Diagnostic tests			Physical Examination			Symptoms							Past medical history	Other Findings
	CT scan and MRI	EKG	Chest X-ray	Tachypnea	Tachycardia	Fever	Chest Pain	Hemoptysis	Dyspnea on Exertion	Wheezing	Chest Tenderness	Nasalopharyngeal Ulceration	Carotid Bruit
Pulmonary embolism	On CT angiography: Intra-luminal filling defect On MRI: Narrowing of involved vessel No contrast seen distal to obstruction Polo-mint sign (partial filling defect surrounded by contrast)	S1Q3T3 pattern representing acute right heart strain	Fleischner sign (enlarged pulmonary artery), Hampton hump, Westermark’s sign	✔	✔	✔ (Low grade)	✔	✔ (In case of massive PE)	✔	–	–	–	–	Hypercoagulating conditions (Factor V Leiden, thrombophilia, deep vein thrombosis, immobilization, malignancy, pregnancy)	May be associated with metabolic alkalosis and syncope
Congestive heart failure	On CT scan: Mediastinal lymphadenopathy Hazy mediastinal fat On MRI: Abnormality of cardiac chambers (hypertrophy, dilation) Delayed enhancement MRI may help characterize the myocardial tissue (fibrosis) Late enhancement of contrast in conditions such as myocarditis, sarcoidosis, amyloidosis, Anderson-Fabry‘s disease, Chagas disease)	Goldberg’s criteria may aid in diagnosis of left ventricular dysfunction: (High specificity) SV1 or SV2 + RV5 or RV6 ≥3.5 mV Total QRS amplitude in each of the limb leads ≤0.8 mV R/S ratio <1 in lead V4	Cardiomegaly	✔	✔	✔	–	–	✔	–	–	–	–	Previous myocardial infarction Hypertension (systemic and pulmonary) Cardiac arrythmias Viral infections (myocarditis) Congenital heart defects	Right heart failure associated with: Hepatomegaly Positive hepato-jugular reflex Increased jugular venous pressure Peripheral edema Left heart failure associated with: Pulmonary edema Eventual right heart failure
Percarditis	On contrast enhanced CT scan: Enhancement of the pericardium (due to inflammation) Pericardial effusion Pericardial calcification On gadolinium-enhanced fat-saturated T1-weighted MRI: Pericardial enhancement (due to inflammation) Pericardial effusion	ST elevation PR depression	Large collection of fluid inside the pericardial sac (pericardial effusion) Calcification of pericardial sac	✔	✔	✔ (Low grade)	✔ (Relieved by sitting up and leaning forward)	–	✔	–	–	–	–	Infections: Viral (Coxsackie virus, Herpes virus, Mumps virus, HIV) Bacteria (Mycobacterium tuberculosis-common in developing countries) Fungal (Histoplasmosis) Idiopathic in a large number of cases Autoimmune Uremia Malignancy Previous myocardial infarction	May be clinically classified into: Acute (< 6 weeks) Sub-acute (6 weeks – 6 months) Chronic (> 6 months)
Pneumonia	On CT scan: (not generally indicated) Consolidation (alveolar/lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO) Abscess Pleural effusion On MRI: Not indicated	Prolonged PR interval Transient T wave inversions	Consolidation (alveolar/lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO)	✔	✔	✔	✔	–	✔	✔	–	–	–	Ill-contact Travelling Smoking Diabetic Recent hospitalization Chronic obstructive pulmonary disease	Requires sputum stain and culture for diagnosis Empiric management usually started before culture results
Vasculitis	On CT scan: (Takayasu arteritis) Vessel wall thickening Luminal narrowing of pulmonary artery Masses or nodules (ANCA-associated granulomatous vasculitis) On MRI: Homogeneous, circumferential vessel wall swelling	Right or left bundle-branch block (Churg-Strauss syndrome) Atrial fibrillation (Churg-Strauss syndrome) Non-specific ST segment and T wave changes	Nodules Cavitation	✔	✔	✔	✔	✔	✔	–	✔	✔	✔	Takayasu arteritis usually found in persons aged 4-60 years with a mean of 30 Giant-cell arteritis usually occurrs in persons aged > 60 years Churg-Strauss syndrome may present with asthma, sinusitis, transient pulmonary infiltrates and neuropathy alongwith cardiac involvement Granulomatous vasculitides may present with nephritis and upper airway (nasopharyngeal) destruction
Chronic obstructive pulmonary disease (COPD)	On CT scan: Chronic bronchitis may show bronchial wall thickening, scarring with bronchovascular irregularity, fibrosis Emphysema may show alveolar septal destruction and airspace enlargement (Centrilobular- upper lobe, panlobular- lower lobe) Giant bubbles On MRI: Increased diameter of pulmonary arteries Peripheral pulmonary vasculature attentuation Loss of retrosternal airspace due to right ventricular enlargement Hyperpolarized Helium MRI may show progressively poor ventilation and destruction of lung	Multifocal atrial tachycardia (atleast 3 distinct P wave morphologies)	Enlarged lung shadows (emphysema) Flattening of diaphragm (emphysema)	✔	✔	–	–	–	✔	✔	–	–	–	Smoking Alpha-1 antitrypsin deficiency Increased sputum production (chronic bronchitis) Cough	Alpha 1 antitrypsin deficiency may be associated with hepatomegaly

The incidence and prevalence of lipoid pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonias from each other. In 2019 there was an outbreak of vaping based pulmonary complications.

• In 2019 there was an outbreak of vaping based pulmonary complications.
• The majority of underlying cause of morbidity was lipoid pneumonia.
• The incidence of cases differentiated based on state can be seen on :“Outbreak of Lung Injury Associated with E-Cigarette Use, or Vaping”.
• The incidence and prevalence of lipoid pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonia from each other.^[1]
• There is no prediction of incidence of lipoid pneumonia but the incidence of lipoid pneumonia is approximately 300,000 to 600,000 individuals annually in the United States.^[2]

• There is no study about prevalence of lipoid pneumonia.

• Prognosis of lipoid pneumonia is usually indolent, however, it may also be progressive.^[3]
• Lipoid pneumonia is not usually a cause of death. Most patients suffer from complications such as superinfection, cor pulmonale or lung cancer which may be mortal.^[4][5][6][7]

• Lipoid pneumonia commonly affects children and elderly.^[8]
• The incidence of lipoid pneumonia increases with age; the median age at diagnosis is 70-80 years.^[9]

• There is no gender preference in lipoid pneumonia.^[10]

​

Lipoid pneumonia pathogenicity is because of lipid aspiration. Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

• Lipoid pneumonia major risk factor is vaping, E-cigarette smoking, occupational (fire eaters) , lipoid laxatives, aspiration pneumonia.
• Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization.^[1][2][3]
• Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

• Common risk factors of developmentin lipoid pneumonia:^{[4][5][6][7][8][9][10][11][12]}
  • The aspiration or inhalation of fatty substances is a central causative factor for exogenous lipoid pneumonia.
  • Trivial habits such as use of oil based laxatives, lip balm, lip gloss and petroleum jelly.
  • Siphoning of various mineral oils (e.g., diesel) from containers.
  • Traditional folk remedies such as the use of oily nasal drops.
  • Forceful animal fat feeding, such as ‘ghee’, in children to establish regular bowel habits.
  • Trans nasal prescriptions of oil based drugs to treat cough and cold.
  • Iatrogenic complication following bronchography using the dye propyliodone.

• Common risk factors in the development of aspiration pneumonia include:
  • Dysphagia from neurologic diseases such as:
    • Dementia
    • Parkinson disease
    • Multiple sclerosis
    • Post-stroke
  • Swallowing dysfunction
  • Chronic obstructive pulmonary disease (COPD)
  • Hyperinflation
  • Altered mental status
  • Acute alcohol abuse
  • Seizures
  • Hospitalization
  • Nursing home residents

• Less common risk factors in the development of aspiration pneumonia include:
  • Medications such as:
    • Sedatives
    • Antipsychotics
    • Proton pump inhibitors
    • Histamine receptor-2 antagonists
    • Systemic antibiotics
  • Esophageal motility disorders such as
    • Achalasia
    • Esophageal strictures
  • Vomiting
  • Anesthesia induction
  • Enteral feeding
  • Oropharyngeal colonization
  • Poor oral hygiene
  • Smoking
  • Diabetes mellitus

There is insufficient evidence to recommend routine screening for lipoid pneumonia.

• There is insufficient evidence to recommend routine screening for lipoid pneumonia..^[1]

Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs. Due to its nonspecific symptoms and radiological features, lipoid pneumonia often remains undiagnosed or diagnosis is delayed. The oil released illicits a giant-cell granulomatous reaction (hence also called lipid granulomatosis), chronic inflammation, and alveolar and interstitial fibrosis. Evolution of lesions with time has been described: Fresh lesions show alveolar infiltration by lipid-laden macrophages and almost normal alveolar walls and septa, and advanced lesions show larger vacuoles and inflammatory infiltrates in alveolar walls, bronchial walls and septa.

• Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs.^[1][2]

• Due to its nonspecific symptoms and radiological features, lipoid pneumonia often remains undiagnosed or diagnosis is delayed.
• The oil released illicits a giant-cell granulomatous reaction (hence also called lipid granulomatosis), chronic inflammation, and alveolar and interstitial fibrosis.
• Evolution of lesions with time has been described:^[3][4][5]

• • Fresh lesions show alveolar infiltration by lipid-laden macrophages and almost normal alveolar walls and septa.
  • Advanced lesions show larger vacuoles and inflammatory infiltrates in alveolar walls, bronchial walls and septa.