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Mendelssohn syndrome
Last reviewed: 23.04.2024
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Mendelssohn's syndrome is the aspiration of chemically aggressive substrate with subsequent burn and the development of hyperergic respiratory tract reaction. The development of a chemical burn of the mucosa of the respiratory tract can be caused by the action of acidic, enzyme-rich gastric juice.
[What causes Mendelssohn's syndrome?
Mendelssohn syndrome can develop if you get into the respiratory tract even a small amount of gastric juice with a low pH (20-30 ml or less). The worst prognosis is observed in cases of aspiration of a large volume (> 0.4 ml / kg) of acidic contents (pH <2.5). Damage to the epithelium of the trachea, bronchi, bronchioles, alveolar wall and endothelium of pulmonary capillaries can occur at higher pH values (> 5.9), especially if there is a parallel occurrence of bile, gastric enzymes and other biologically active substrates.
Mendelssohn's syndrome can develop if mineral oils, fat and other lipophilic agents get into the respiratory tract, which leads to the development of noninfectious inflammation in the lungs - "fatty pneumonia."
This term refers to the alveolar infiltration that developed with the aspiration of oils or fatty substances. It can occur with the use of oily or nasal agents to soften the mucous membranes of the upper respiratory tract.
The severity of the lesion is directly dependent on the acidity of the amount of aspirated gastric juice.
Acid burn leads to the development of hyperergic respiratory tract epithelium, increased permeability of the alveolocapillary membranes, the release of the plasma portion of the blood into the pulmonary interstitium and the cavity of the alveoli, to the development of interstitial edema and to acute damage to the lungs. There is pronounced edema of the mucous and submucous layers of the bronchi, bronchiolospasm, bronchial obstruction, damage to the surfactant system, atelectasisation of part of the lung, reduction in pulmonary perfusion, the discovery of intrapulmonary arteriovenous shunts and direct damage to the alveoli.
An important role is played by the local effect of the chemically active substrate on the pulmonary parenchyma.
There is a release of biologically active substances, complement systems are activated, tumor necrosis factor, various cytokines and substances that determine leukocyte chemotaxis are released. Systemic endothelial damage occurs. Reflex development of laryngo- and bronchiolospasm aggravates the severity of the patient's condition and may be accompanied by severe cardiac disorders.
What are the symptoms of Mendelssohn syndrome?
The Mendelssohn syndrome is characterized by a sharp onset (usually immediately after aspiration).
It is the development of hypoxemia in the first 10 minutes after aspiration is the most important sign.
As a rule, there is a growing anxiety of the patient, signs of a violation of breathing (laryngospasm, bronchospasm, expiratory dyspnoea as an asthmatic condition).
Mendelssohn syndrome is characterized by a triad of symptoms:
- tachycardia;
- tachypnea;
- cyanosis.
There are reflex disorders from the cardiovascular system (primarily the drop in blood pressure). At the time of aspiration of acidic gastric contents, bronchiolospasm occurs.
Against the backdrop of urgent medical interventions, there is a temporary improvement in the condition - a light period (it can last several hours). But later there are signs of obstructive (bronchiolitis) and restrictive (pneumonitis) disorders.
Cyanosis and low values of Sp O2 do not decrease even when 100% oxygen is supplied (hypoventilation with a saved blood flow leads to shunting of venous blood).
How to recognize Mendelssohn's syndrome?
With auscultation of the lungs, wheezing rales are heard in all fields (creping rales can be heard in the lower parts). Chryps on exhalation indicate obstruction of small caliber bronchi.
With the progression of respiratory disorders, PaO2 decreases to 35-45 mm Hg. Increased pulmonary vascular resistance and pressure in the pulmonary artery. There is a decrease in lung elongation, aerodynamic resistance of the respiratory tract increases, acute lung damage develops.
Radiographic examination reveals areas of reduced airiness and diffuse darkening of lung tissue (a picture of "shock lung"). Often there is a diffuse spotted blackout with a predominant lesion usually of the right lung, as there is more frequent gastric contents.
In mild cases, the process is resolved in the coming days (sometimes even without special treatment). But after the apparent improvement in some patients. After 2-5 days, signs of respiratory failure appear again. Fever, cough, leukocytosis. That is, there are symptoms of secondary bacterial pneumonia with radiographic foci of infiltration.
Since pneumonitis can be caused by aspiration of various biologically aggressive liquids, Mendelssohn syndrome (chemical burn caused by gastric juice) and aspiration pneumonitis (due to any chemically aggressive substance) should not be considered synonyms. Figuratively speaking, any Mendelssohn syndrome is essentially an aspiration pneumonitis, but not every aspiration pneumonitis can be called this disease.