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The airways that connect your windpipe to your lungs are called bronchi. Sometimes the muscles that line your bronchi tighten and cause your airways to narrow. This is called a bronchospasm, and it limits the amount of oxygen your body receives.


While bronchospasm affects your bronchi, laryngospasm affects your vocal cords. With laryngospasm, your vocal cords suddenly close up when you take a breath, blocking the flow of air into your lungs. This rare condition can be scary, but it usually goes away on its own within one or two minutes.

Bronchospasm is a symptom of asthma and other medical conditions. People with asthma can get bronchospasm, but not everyone with bronchospasm gets asthma. Both conditions are the result of irritated or inflamed airways.

Anytime your airways are irritated or swollen, it can cause bronchospasm. Asthma is the most common cause of bronchospasm, but there are several other things that can result in the condition, including:

In very rare instances, bronchodilators commonly used to treat bronchospasm can actually make the condition worse. This is called paradoxical bronchospasm. If this happens, you should stop using your bronchodilator immediately and seek alternative treatment.

Exercise-induced bronchospasm (EIB) happens when the airways in your lungs narrow when you exercise. This makes it hard to breathe. If you have EIB, it may be hard to exercise for more than 30 minutes at a time.

Working closely with your pulmonologist, and sometimes an otolaryngologist, you will be able to develop a plan of care that reduces your risk for having repeat bronchospasms. If you have environmental risk factors, such as smoking, allergies, or fragrances that are shown to exacerbate bronchospasms, then eliminating these substances from around you will be key to reducing your risk.

Paradoxical bronchospasm is when a person's airways constrict instead of relax after using a bronchodilator. This is a type of medication that relaxes muscles surrounding the airways to make breathing easier. It's called "paradoxical" because the treatment worsens symptoms rather than relieving them.

Bronchospasm and laryngospasm can both make it hard for you to speak or breathe. While bronchospasm happens when your airways narrow, laryngospasm happens when the muscles in your vocal cords contract. Laryngospasms are uncommon and usually only last for a minute or so.

Nearly 1.5% of the tests met the criteria for paradoxical bronchospasm, which refers to airway constriction that may rapidly occur after inhalation of a short-acting beta2 agonist (SABA) such as albuterol.

However, none of those reports alluded to paradoxical bronchospasm, said investigator Malvika Kaul, MD, fellow in the department of pulmonary and critical care at the University of Illinois at Chicago and the Jesse Brown Veterans Affairs Medical Center, also in Chicago.

If paradoxical bronchospasm occurs, the patient should discontinue the medication immediately and start on alternative therapy, according to the available prescribing information for albuterol sulfate.

Results of this study emphasize the need to recognize potential cases paradoxical bronchospasm in clinical practice, as well as a need for more research, according to Allen J. Blaivas, DO, FCCP, chair of the CHEST Airway Disorders NetWork.

Further research could focus on breaking down whether patients with suspected paradoxical bronchospasm are using metered-dose inhalers or nebulizers, whether or not they are also taking inhaled corticosteroids, and whether prospective testing can confirm paradoxical bronchospasm in patients who report tightness after using a SABA, he said in an interview.

Between 8 - 20% of adult asthmatics experience bronchospasm following ingestion of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). Termed aspirin-induced asthma, this reaction is potentially fatal. Asthmatics with chronic rhinitis or a history of nasal polyps are at greater risk. The reaction rarely occurs in children.Patients initially present with an acute episode of vague malaise, sneezing, nasal obstruction, rhinorrhoea and often a productive cough. Persistent rhinitis and nasal polyps may then develop. Asthma and aspirin sensitivity may appear in the following months. Within 20 minutes to 3 hours of taking a NSAID, aspirin-sensitive asthmatics can develop respiratory symptoms (e.g. bronchospasm, rhinorrhoea, respiratory arrest), urticaria/angiodema or, rarely, a combination of the two.NSAIDs (systemic or topical) should be used with caution in asthmatics and avoided in asthmatics with nasal polyps. Tell asthmatics to seek medical help if symptoms worsen on initiation of a NSAID.

To October 1998, the Centre for Adverse Reactions Monitoring had 81 reports of bronchospasm following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) and 6 reports of exacerbation of asthma symptoms. This includes one fatality following aspirin administration.

Aspirin and other NSAIDs can induce bronchospasm and, in rare cases, this reaction can lead to death in aspirin-sensitive asthmatics.1-4 This reaction is generally referred to as aspirin-induced asthma. The reported incidence varies widely affecting between 8% and 20% of adult asthmatics.5,6 The incidence is increased in asthmatics who also have chronic rhinitis or a history of nasal polyps.4 Aspirin-induced asthma is most likely to be encountered in the third or fourth decade of life although it may occur in childhood, albeit rarely.5,6

A report of worsening asthma, necessitating hospital admission, following the use of NSAID ophthalmic drops serves to warn that all routes of administration can precipitate bronchospasm in sensitive asthmatics.7

NSAID-induced bronchospasm should be suspected in any patient whose asthma control worsens on initiation of a NSAID. Patients with a history of asthma should be warned of this reaction and to seek medical help if symptoms worsen on initiation of a NSAID.

Background: Silent lung is a rare and potentially fatal disease. It is a critical sign of strong bronchospasm or extensive mucus plug blockage, which can result in the obvious weakening of breathing sounds or even disappearance of breathing sounds. Silent lung has an acute onset and rapid progress, which seriously threatens the life of patients. It needs early diagnosis, timely and effective treatment to reverse the persistent severe bronchospasm of patients. If not handled in time, silent lung can cause rapid onset of severe hypoxemia, hypoxic brain injury, and even cardiac arrest. Few studies have been reported on the causes and specific treatments for silent lungs.

Conclusions: Both patients had severe bronchospasm; that is, silent lung. The 2 patients improved after hand-controlled ventilation and the administration of adrenaline and methylprednisolone, and ultimately recovered ventilation.

For severe bronchospasm, existing reports mostly focus on the treatment of bronchospasm in asthmatic patients. There are many reasons for the silent lung in the perioperative period, and most of the time it is not caused by asthma. The use of salbutamol cannot effectively relieve the silent lung. Once delayed, it will lead to catastrophic results. There is no report on the specific treatment measures for the silent lung of severe bronchospasm in the perioperative period.

Anesthesia related bronchospasm itself may manifest as an event or may be a component of another event, such as an allergic reaction (2). It is characterized by prolonged expiratory time and complete silence during lung auscultation in severe cases. Most types of less severe bronchospasm can be relieved by appropriate treatment; however, once silent lung occurs, it can cause severe hypoxemia due to its acute onset and rapid progress. Thus, the timely diagnosis and treatment of patients can save lives.

In relation to the 2 patients, 1 displayed rapid remission from silent lung after the administration of low-dose adrenaline, and underwent surgery on schedule. While the other patient experienced severe bronchospasm during surgery and cardiac arrest after silent lung and was sent to the intensive care unit (ICU) after cardiopulmonary resuscitation (CPR). After 6 days, the tracheal tube was successfully extubated, and the patient underwent further rehabilitation treatment. Both patients were successfully treated after suffering from silent lung. We present the following case in accordance with the CARE reporting checklist (available at -22-617/rc).

Silent lung is a rare and potentially fatal clinical crisis. Due to severe bronchospasm or extensive mucus obstruction, wheezing and inaudible breathing may occur and develop into silent lung. If the rescue is not timely, the condition can easily evolve into hypoxic-ischemic encephalopathy and even cardiac arrest. Silent lung generally has 2 causes: (I) airway hyperresponsiveness, such as a history of asthma, chronic obstructive pulmonary disease, smoking, respiratory tract infection (3); (II) perioperative trigger factors, including the stimulation of endotracheal intubation, irritant inhalation anesthetics (e.g., desflurane), the stimulation of airway secretions and blood, histamine releasing drugs (e.g., muscle relaxants and morphine), non-steroidal anti-inflammatory drugs, and cholinesterase inhibitors (e.g., neostigmine). Another cause of silent lung is severe bronchospasm caused by an allergic reaction (4). When silent lung occurs during the perioperative period, anesthesiologists must be familiar with the inducing factors, identify the signs, and quickly exclude other factors, such as tracheal tube displacement, sputum blockage, anesthesia machine failure, and too shallow anesthesia.

In Case 2, the patient had a history of asthma, high airway reactivity and suffered from severe bronchospasm after endotracheal intubation. After administering a small dose of adrenaline, the patient was relieved without any sequelae. After the operation, the endotracheal tube was successfully removed, and the patient was returned to the ward. The duration of silent lung in both Cases 1 and 2 was about 10 minutes. Compared to Case 1, Case 2 experienced no serious consequences. This may be because Case 2 was oxygenated and denitrified before intubation. Sufficient pre-oxygenation can maintain SPO2. When ventilation is impossible, the time of hypoxia is greatly reduced when the patient had pre-oxygenation. In Case 1, the inhaled oxygen concentration was 50%, and the SPO2 decreased rapidly after silent lung. When silent lung occurs clinically, the pure oxygen flow should be immediately increased to 8 L/min, manual ventilation should be performed, oxygenation should be maintained, and lung compliance should be evaluated. Increasing the concentration of volatile anesthetics (sevoflurane and isoflurane) can relax the smooth muscle and reduce airway resistance (7). 350c69d7ab


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