Mendelson’s Syndrome
Presenter: Yuvetha , Soon Yong Hao, Poh Elaine
Prepared by: Hemirah, Meenambeegai
Introduction
According to Curtis Lester Mendelson’s,
“Mendelson syndrome” was initially
described as aspiration of gastric
contents causing a chemical pneumonitis
characterized by fever, cyanosis, hypoxia,
pulmonary edema, and potential death.
Lower esophageal sphincter pressure is higher
than intragastric pressure, which creates a
barrier pressure to prevent the reflux of gastric
contents
Loss of Lower esophageal sphincter barrier
pressure is caused by:
Peristalsis
Pathophysiology Vomiting
During pregnancy (a progesterone effect)
Achalasia
Various drugs (anticholinergics, propofol,
thiopentone, opioids)
Pathophysiology
Increased intragastric pressure will increase the risk of Mendelson syndrome.
Increased intragastric pressure is caused by:
Gastric volume exceeds 1000ml
Raised intra-abdominal pressure such as that occurring with pneumoperitoneum during laparoscopy
Etiology
Risk of Medelson syndrome increased during
pregnancy due to increased intra-abdominal
pressure because:
I. Minute ventilation, oxygen consumption, and carbon
dioxide production are increased in early pregnancy
II. Gravid uterus displaces the diaphragm upward in late
pregnancy, substantially reducing functional residual
capacity
III. Cardiac output, heart rate, stroke volume and
circulating blood volume are all increased
IV. Progesterone-mediated relaxation of the lower
esophageal sphincter (LES)
V. Prolonged gastric emptying time due to progesterone
PREDISPOSI
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FACTORS
CLASSIFICATION FOR PULMONARY
ASPIRATION OF GASTRIC CONTENTS
1) Aspiration/Chemical Pneumonitis (Mendelson’s Syndrome)
• This condition involves lung tissue damage as a result of aspiration of non-infective but very acidic
gastric fluid.
• Clinically either asymptomatic or present as tachypnoea, bronchospasm, wheeze, cyanosis and
respiratory insufficiency, it may mimic pulmonary edema in its presentation with dyspnea, cough, fever,
and profuse frothy pink sputum.
• On physical examination there is crackles on auscultation of chest mostly on the right lower part which
is the most dependent area for the aspirated contents.
• Pulse oximetry can show oxygen desaturation and tachycardia.
2) Aspiration Pneumonia 3) Particulate-Associated Aspiration
This occurs either as a result of inhaling infected • If particulate matter is aspirated, acute
material or secondary bacterial infection following obstruction of small airways will lead to distal
chemical pneumonitis. atelectasis.
It is associated with typical symptoms of • If large airways are obstructed, immediate
pneumonia (tachycardia, tachypnoea, cough and arterial hypoxaemia may be rapidly fatal.
fever).
• Mendelson syndrome may • On physical examination
History & mimic pulmonary edema in the patient is
Physical its presentation with an acute
onset following aspiration.
tachypneic,
tachycardia
Examination Patients present with
dyspnea, crackles on auscultation of
of cough,
chest mostly on the right
lower part which is the
Mendelson fever, most dependant area for
the aspirated contents.
profuse frothy pink sputum.
Syndrome Symptoms may be indolent or
can progress to pulmonary
necrosis with lung abscess or
empyema.
DIAGNOSIS OF MENDELSON
SYNDROME
• witnessed aspiration
• risk factors
• characteristic chest radiography findings, although X-
rays may initially be negative.
• Radiographic films may reveal irregular densities in the
dependent pulmonary segments, primarily on the right
side, which is at greater risk of aspiration due to the
larger diameter and more vertical orientation of the
right mainstem bronchus.
• Pulse oximetry can show oxygen desaturation and
tachycardia.
• A computed tomography scan of the chest can reveal
consolidation.
PREVENTION & TREATMENT
DIFFERENTIAL DIAGNOSIS
COMPLICATION
PROGNOSIS
Prepared by : V.Meenambeegai 10
Prevention of Mendelson Syndrome.
1) Preoperative fasting
- Current guidelines are 2 hours for clear fluids, 4 hours for breast milk, and 6 hours for a
light meal, sweets, milk (including formula) and non clear fluids.
2) Reducing gastric acidity
- Histamine (H2) antagonists and proton pump inhibitors (PPIs) are commonly used to increase gastric
pH, although they do not affect the pH of fluid already in the stomach.
- H2 antagonists act by blocking H2 receptors of gastric parietal cells, thereby inhibiting
the stimulatory effects of histamine on gastric acid secretion. It should be given 1-2 hours before anesthesia.
- PPIs blocks the ‘proton pump’ of the same cell, inhibiting the stimulatory actions of histamine, gastrin and acetylcholine.
It should be given 12 hours before anesthesia.
3)Rapid Sequence Induction (RSI)
-It has been shown that most cases of aspiration occur on induction and laryngoscopy
-For patients at high risk of aspiration, a RSI is the induction of choice unless presented with a sufficiently difficult airway
to warrant an awake fibreoptic intubation
-The patient should be on a tilting trolley, with suction to hand. Three minutes of pre-oxygenation
precede the administration of an induction agent, cricoid pressure and the rapidly acting muscle relaxant succinylcholine.
This avoids the need for bag-mask ventilation and thepossibility of gastric insufflation.
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4) Cricoid pressure
- The aim is to compress the oesophagus between the cricoid ring cartilage and the sixth cervical vertebral body
thus preventing reflux of gastric contents.
-The force recommended is 30N, or that required to close the oesophagus without distorting the airway.
-This latter complication is the greatest limiting feature of the manoeuvre, causing malalignment, distortion
of the cricoid ring and possible closure of the vocal cords. Even when applied correctly there is doubt
as to its efficacy, simply causing anatomical displacement of the oesophagus in some people, and non
compression in others.
-Cricoid pressure should be released in the case of active vomiting to avoid oesophageal rupture.
5) Airway device
-A cuffed endotracheal tube is considered the gold standard device used for airway protection.
-However, it has disadvantages - cardiovascular and respiratory instability, postoperative hoarseness,
sore throat, increased length of stay in recovery to name but a few.
-Alternative supraglottic devices include the classic Laryngeal Mask Airway(LMA) and the Proseal LMA, the
latter providing a higher seal pressure (up to 30cmH20) and a drainage channel for gastric contents. These
have excellent safety records, and can be used for positive pressure ventilation although the main contraindication
to their use is an increased risk of regurgitation.
Management of Mendelson Syndrome
1) Initial management
Initial management involves the recognition of aspiration by way of visible gastric contents in the oropharynx, or more
subtle indications such as hypoxia, increased inspiratory pressure, cyanosis, tachycardia or abnormal auscultation, when a
list of differentials must be thought through.
Once the diagnosis is suspected, the patient should be positioned head-down to limit pulmonary contamination, and
suctioning performed to clear the oropharynx. Oxygen (100%) must be administered, followed by immediate RSI and
securing of the airway with an endotracheal tube. At this point, tracheal suctioning should ideally precede positive pressure
ventilation to avoid any aspirate being forced further down the bronchial tree. Early bronchoscopy is recommended if
aspiration of particulate matter is suspected to prevent distal atelectasis. Symptomatic treatment of bronchospasm with
bronchodilators may be necessary.
Complications of Mendelson’s syndrome
Mendelson syndrome can lead to serious complications and these include:
1) Bacterial pneumonia
2) Lung abscess
3) Airway obstruction
4) Bronchopleural fistula
5) Respiratory failure
6) Acute respiratory distress syndrome
7) Pleural effusion
8) Empyema
9) Shock
10) Sepsis Enter title Enter title Enter title
Prognosis
The prognosis of Mendelson syndrome depends upon the comorbid disease, the severity of aspiration,
complications, and the patient's underlying health status.
In Mendelson's 1946 original series, 66 obstetric patients aspirated gastric acid during their anesthetic, and almost
all had a complete clinical recovery.
Subsequent studies have included elderly patients with the comorbid disease, with a reported mortality rate of 30
to 62%, as chemical pneumonitis can lead to ARDS. The mortality rate for chemical pneumonitis can be up to
70%. If pneumonia develops and does not receive prompt treatment, it can lead to the development of a lung
abscess or a bronchopleural fistula. The mortality rate for empyema that complicates aspiration pneumonia is
approximately 20%, while that of uncomplicated pneumonia is about 5%.
References
1.Mendelson Syndrome - StatPearls - NCBI Bookshelf (nih.gov)
2. https://medscape.com/search/?q=mandelson%20syndrome
THANKS
3.
https://www.ncbi.nlm.nih.gov/books/NBK539764/#article-24955.
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