Costochondritis – Diagnosis and treatment

Diagnosis

During the physical exam, your doctor will feel along your breastbone for areas of tenderness or swelling. The doctor may also move your rib cage or your arms in certain ways to try to trigger your symptoms.

The pain of costochondritis can be very similar to the pain associated with heart disease, lung disease, gastrointestinal problems and osteoarthritis. While there is no laboratory or imaging test to confirm a diagnosis of costochondritis, your doctor might order certain tests — such as an electrocardiograph, X-ray, CT or MRI — to rule out other conditions.

Treatment

Costochondritis usually goes away on its own, although it might last for several weeks or longer. Treatment focuses on pain relief.

Medications

Your doctor might recommend:

• Nonsteroidal anti-inflammatory drugs. Although certain medications, such as ibuprofen (Motrin IB) or naproxen sodium (Aleve) are available over the counter, your doctor might prescribe stronger varieties of these nonsteroidal anti-inflammatory medications. Side effects might include damage to your stomach lining and kidneys.
• Narcotics. If your pain is severe, your doctor might prescribe medications containing codeine, such as hydrocodone/acetaminophen (Vicodin, Norco) or oxycodone/acetaminophen (Tylox, Roxicet, Percocet). Narcotics can be habit-forming.
• Antidepressants. Tricyclic antidepressants, such as amitriptyline, are often used to control chronic pain — especially if it’s keeping you awake at night.
• Anti-seizure drugs. The epilepsy medication gabapentin (Neurontin) also has proved successful in controlling chronic pain.

Therapy

Physical therapy treatments might include:

• Stretching exercises. Gentle stretching exercises for the chest muscles may be helpful.
• Nerve stimulation. In a procedure called transcutaneous electrical nerve stimulation (TENS), a device sends a weak electrical current via adhesive patches on the skin near the area of pain. The current might interrupt or mask pain signals, preventing them from reaching your brain.

Surgical and other procedures

If conservative measures don’t work, your doctor might suggest injecting numbing medication and a corticosteroid directly into the painful joint.

Lifestyle and home remedies

It can be frustrating to know that there’s little your doctor can do to treat your costochondritis. But self-care measures might make you feel more comfortable. They include:

• Over-the-counter nonsteroidal anti-inflammatory drugs pain relievers. Ask your doctor about using ibuprofen (Advil, Motrin IB, others) or naproxen sodium (Aleve, others).
• Heat or ice. Try placing hot compresses or a heating pad on the painful area several times a day. Keep the heat on a low setting. Ice also might be helpful.
• Rest. Avoid activities that make your pain worse.

Preparing for your appointment

You may be referred to a doctor who specializes in disorders of the joints (rheumatologist).

What you can do

• Write down your symptoms, including any that may seem unrelated to the reason why you scheduled the appointment.
• Write down your key medical information, including other conditions and any history of injury to the painful joint.
• Write down key personal information, including any major changes or stressors in your life.
• Make a list of all your medications, vitamins or supplements.
• Ask a relative or friend to accompany you, to help you remember what the doctor says.
• Write down questions to ask your doctor.

Questions to ask your doctor

• What’s the most likely cause of my symptoms?
• What kinds of tests do I need?
• What self-care steps are likely to help improve my symptoms?
• Do I need to restrict any activities?
• What new signs or symptoms should I watch for at home?
• How soon do you expect my symptoms will resolve?
• I have other health conditions. How can I best manage them together?

In addition to the questions that you’ve prepared to ask your doctor, don’t hesitate to ask other questions.

What to expect from your doctor

Your doctor is likely to ask you a number of questions. Being ready to answer them may leave time to go over points you want to spend more time on. You may be asked:

• When did you first begin experiencing these symptoms? Have they worsened over time?
• Where is your pain located?
• Does exercise or physical exertion make your symptoms worse?
• Does anything else seem to make your pain worse or better?
• Are you having any difficulty breathing?
• Have you had any recent respiratory infections?
• Have you had any recent injuries to your chest?
• Have you been diagnosed with any other medical conditions?
• Have you recently experienced a significant amount of stress or change?
• Are you aware of any history of heart problems in your family?

April 22, 2020

Show references

1. Ferri FF. Costochondritis. In: Ferri’s Clinical Advisor 2015: 5 Books in 1. Philadelphia, Pa.: Mosby Elsevier; 2015. https://www.clinicalkey.com. Accessed Feb. 4, 2015.
2. Phillips K, et al. Treatment of musculoskeletal chest pain. http://www.uptodate.com/home. Accessed Feb. 4, 2015.
3. McMahon SB, et al. Thoracic pain. In: Wall & Melzack”s Textbook of Pain. 6^th ed. Philadelphia, Pa.: Saunders Elsevier; 20015. https://www.clinicalkey.com. Accessed Feb. 4, 2015.
4. Wise CM. Major causes of musculoskeletal chest pain in adults. http://www.uptodate.com/home. Accessed Feb. 4, 2015.
5. Frontera WR, et al. Costernal syndrome. In: Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation. 3rd ed. Philadelphia, Pa.: Saunders Elsevier; 20013. https://www.clinicalkey.com. Accessed Feb. 4, 2015.
6. AskMayoExpert. What are the most common causes of chest wall pain? Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2014.
7. McConaghy JR, et al. Outpatient diagnosis of acute chest pain in adults. American Family Physician. 2013;87:177.

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When chest pain is “just” costochondritis – Heart Sisters

by Carolyn Thomas  ♥  @HeartSisters

Many female heart patients become familiar with the word “costochondritis” only while being misdiagnosed with the condition during an actual cardiac event, as in:

• “My MD said it was just costochondritis and a  pinched nerve, because my ribs were sore. ” (LH, age 51, New York: heart attack)

• “At first, we looked at musculoskeletal causes. It had to be costochondritis; my chest wall seemed tender to touch, so I even had steroid injections in my chest wall.” (ZM, age 59, Arizona: heart attack, 12 stents, triple bypass surgery)

• “Pains in chest radiating down arm and up to my chin. My GP reluctantly sent me to a cardiologist who was dismissive, said that my age was a big factor and that it was 99% likely to be just costochondritis as I also have fibromyalgia” (BT, age 42, U.K: heart attack, 90% blocked LAD coronary artery, two stents)  

Costochondritis is an inflammation of the junctions where the upper ribs join with the cartilage that holds them to the breastbone, or sternum. The condition causes localized chest pain that you can often reproduce by pushing on the cartilage in the front of your ribcage.

Costochondritis can be extremely painful yet, mercifully, it’s often relatively benign. Much of the medical literature suggests that it will usually go away on its own within a few days, but some patients report symptoms that can linger for weeks or even months. It can also be a recurring condition that appears to have little or no warning of onset. Pneumonia can be misdiagnosed as costochondritis. Many patients living with fibromyalgia or chronic fatigue syndrome complain of chest wall pain and restriction of movement, often identified by their health care providers as costochondritis.

Chest pain in adults is considered by most doctors to be a potentially serious sign of a heart problem until proven otherwise. Reporting chest pain usually leads to a battery of medical tests to rule out heart disease. If those tests are normal and your physical exam is consistent with costochondritis, your doctor may diagnose costochondritis as the culprit. It may, however, be difficult to distinguish between the two without specific testing. 

Never assume chest pain is “just costochondritis”.

Here’s an example: Emergency physician Dr. Seth Trueger described this study as one that “might be the coolest chest pain study ever done.”

The study found that when rheumatologists using the American College of Rheumatology criteria for diagnosing costochondritis evaluated patients in the E.R. complaining of chest pain:

“Six per cent of the patients the doctors diagnosed with costochondritis actually had an acute myocardiardial infarction (heart attack).”

What rheumatologists were doing in the E.R. was not explained . . .

Most (real) cases of costochondritis seem to have no clear cause. Occasionally, however, the diagnosis might be correlated with:

• Injury. A blow to the chest

• Physical strain. Heavy lifting and/or strenuous exercise

• Arthritis. In some people, costochondritis has been linked to specific problems, such as osteoarthritis, rheumatoid arthritis and ankylosing spondylitis.

• Joint infection. The rib joint itself can become infected by viruses, bacteria or fungi. Examples include tuberculosis, syphilis and aspergillosis.

• Tumours. Non-cancerous and cancerous tumours also can cause costochondritis. Cancer may travel to the joint from another part of the body, such as the breast, thyroid or lung.

Costochondritis may also occur as the result of an infection or as a complication of surgery on your sternum.  Sometimes patients with a severe cough can develop this as a result of continued coughing and rapid expansion/contraction of the rib cage.

In New Zealand, physiotherapists like Steve August (see his detailed comments below) not only suffered himself for seven years with costochondritis after a serious climbing fall, but has been successfully treating the backs of his costochondritis patients manually for the past 30 years with non-drug, non-invasive physiotherapy, as he discusses in his video. Yes, you read that right: it is the back that is treated.

He sees costochondritis as often a straightforward musculoskeletal mechanical problem in which the costovertebral rib joints at the back are somehow jammed. This requires the anterior rib joints around the front to work excessively to compensate, leading to irritation, then to the inflammation that doctors call costochondritis.

Watch Steve’s second video in which he describes:

• exercises and treatments recommended by New Zealand physiotherapists to unlock the rib hinges in the back to ease the symptoms of costochondritis
• massage therapy for affected shoulder muscles
• how to stretch tight, scarred muscles in between the ribs
• gentle stretching exercises you can do at home to help open up the ribcage
• use of anti-inflammatory gel to apply on the rib hinges at the front of your chest

If you are a physiotherapist or massage therapist, please watch this video and read this 2017 research paper from Zaruba and Wilson.

This condition affects females more than males (70% versus 30%).

Kelly Young is a patient advocate, blogger, and president of the Rheumatoid Patient Foundation. She described costochondritis like this in her blog RA Warrior:

“As early as 1964, the journal ‘Radiology’ published a study explaining that the effects of Rheumatoid Arthritis on the rib joints “have not been adequately described in the literature.”[1] Mayo Clinic’s description of costochondritis makes it clear the word describes a symptom, pain or inflammation of the rib joints that can be caused by various illnesses.[2,3]

“The term is also confusing because there can be varying diagnoses with similar symptoms.”

But Kelly says that she has also read some skeptical articles about costochondritis symptoms, considered by some physicians as the garbage can diagnosis of hypochondriacs.

Costochondritis is not associated with swelling, as opposed to Tietze’s syndrome, where swelling is characteristic.  Tietze’s syndrome is an inflammation of the costochondral cartilages of the upper front of the chest that involves swelling around the joint, the ribs or cartilage near the breastbone. Redness, tenderness, and warmth can also be present, but a localized swelling is the distinguishing finding, although even swelling can be variable from patient to patient. The pain can cause difficulty with sleeping, and even rolling over in bed is sometimes painful.

READER COMMENT:  “Thanks for this article. I did have “just” costochondritis, but wound up in the ER four times feeling like I was having a heart attack. Turned out my diabetes medication was inhibiting my body’s production of DAO enzyme, thus giving me histamine intolerance. My body was inflamed head to toe with multiple symptoms. I switched to insulin and went on a low histaine diet and am getting better. Also, most of my “menopause” symptoms went away too. Take good care!” Melinda (August 15, 2021)

Besides physiotherapy as New Zealand physiotherapists treat this condition, possible treatments include heat or ice, and medications like NSAIDs to relieve pain and reduce inflammation*. 

And until there is improvement in your symptoms, avoid unnecessary exercise or contact sports activities. 

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*  CAUTION:  Studies have found that, among those who had already had one heart attack, people who took the painkillers called NSAIDs (non-steroidal anti-inflammatory drugs) such as Vioxx, Bextra, Aleve, Advil, Motrin, etc. were at >40% higher risk of having a second heart attack compared with those who did not take them. If you’re in this group, do NOT take NSAIDS before talking with your physician.

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NOTE FROM CAROLYN:   I wrote much more about diagnosis and misdiagnosis in my book, “A Woman’s Guide to Living with Heart Disease” . You can ask for it at your local library or favourite bookshop, or order it online (paperback, hardcover or e-book) at Amazon, or order it directly from my publisher, Johns Hopkins University Press (use the JHUP code HTWN to save 20% off the list price).

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1  Alpert M, Feldman F. The rib lesions of rheumatoid arthritis. Radiology. 1964 May 82: 872-875

2  Mayo Clinic. Costochondritis. 2012 May 6.

3  HealthHype.com. Severe costochondritis – causes, symptoms, treatment. 2010 May 9.

4  Flowers LK. Medscape. Costochondritis. 2012 Apr 13.

Q:  Have you ever experienced costochondritis?

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Pediatric Costochondritis Treatment & Management: Medical Care, Consultations, Activity

Author

Joseph P Garry, MD, FACSM, FAAFP Associate Professor, Department of Family Medicine and Community Health, University of Minnesota Medical School

Joseph P Garry, MD, FACSM, FAAFP is a member of the following medical societies: American Academy of Family Physicians, American Medical Society for Sports Medicine, Minnesota Medical Association, American College of Sports Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Barry L Myones, MD Co-Chair, Task Force on Pediatric Antiphospholipid Syndrome

Barry L Myones, MD is a member of the following medical societies: American Association of Immunologists, American Heart Association, American Society for Microbiology, Clinical Immunology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

David D Sherry, MD Chief, Rheumatology Section, Director, Amplified Musculoskeletal Pain Program, The Children’s Hospital of Philadelphia; Professor of Pediatrics, University of Pennsylvania School of Medicine

David D Sherry, MD is a member of the following medical societies: American College of Rheumatology, American Pain Society

Disclosure: Nothing to disclose.

Chief Editor

Lawrence K Jung, MD Chief, Division of Pediatric Rheumatology, Children’s National Medical Center

Lawrence K Jung, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Rheumatology, Clinical Immunology Society, New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

James M Oleske, MD, MPH François-Xavier Bagnoud Professor of Pediatrics, Director, Division of Pulmonary, Allergy, Immunology and Infectious Diseases, Department of Pediatrics, Rutgers New Jersey Medical School; Professor, Department of Quantitative Methods, Rutgers New Jersey Medical School

James M Oleske, MD, MPH is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Allergy Asthma and Immunology, American Academy of Hospice and Palliative Medicine, American Association of Public Health Physicians, American College of Preventive Medicine, American Pain Society, Infectious Diseases Society of America, Infectious Diseases Society of New Jersey, Medical Society of New Jersey, Pediatric Infectious Diseases Society, Arab Board of Family Medicine, American Academy of Pain Management, National Association of Pediatric Nurse Practitioners, Association of Clinical Researchers and Educators, American Academy of HIV Medicine, American Thoracic Society, American Academy of Pediatrics, American Public Health Association, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Update on the Diagnosis and Treatment of Caustic Ingestion

Ochsner J. 2009 Summer; 9(2): 54–59.

, MD,^*,^†, MD,^‡ and , MD^‡

Michael Lupa

^*Department of Otolaryngology, Head and Neck Surgery, Tulane University School of Medicine, New Orleans, LA

Jacqueline Magne

^†Tulane University School of Medicine

J. Lindhe Guarisco

^‡Department of Otolaryngology, Head and Neck Surgery, Ochsner Clinic Foundation, New Orleans, LA

Ronald Amedee

^‡Department of Otolaryngology, Head and Neck Surgery, Ochsner Clinic Foundation, New Orleans, LA

^*Department of Otolaryngology, Head and Neck Surgery, Tulane University School of Medicine, New Orleans, LA

^†Tulane University School of Medicine

^‡Department of Otolaryngology, Head and Neck Surgery, Ochsner Clinic Foundation, New Orleans, LA

Address correspondence to: Ronald Amedee, MD, Department of Otolaryngology-Head & Neck Surgery, Ochsner Clinic Foundation, 1514 Jefferson highway, New Orleans, LA 70121, (504)-842-4080, (504)-842-3979, e-mail: gro. renshco@eedemarCopyright Academic Division of Ochsner Clinic FoundationThis article has been cited by other articles in PMC.

Abstract

Caustic ingestion is a serious medical problem with a variety of clinical presentations and a complicated clinical course. This article reviews the epidemiology and pathophysiology of caustic ingestion as well as the most current approaches to diagnosis and treatment. Finally, a recent case will be presented that highlights the difficulty this problem poses to a medical team.

Keywords: Caustic ingestion, caustic substance, corrosive injury, corrosive substance, endoscopy, esophageal stricture

INTRODUCTION AND EPIDEMIOLOGY

Caustic injury remains an important public health problem in the United States and the world despite various education and regulatory efforts to reduce its occurrence. In the United States, an estimated 5,000 to 15,000 caustic ingestions occur per year.1–3 The age of occurrence of these ingestions shows a bimodal pattern. 1 The first peak is seen in children aged 1 to 5 years, with most of these ingestions being accidental, though reports of child abuse have been reported in the literature.1,4,5 The problem of caustic ingestion in children is spreading in developing countries, as these agents become more available, with much of the recent research coming from that part of the world.6 The other peak age for caustic ingestion is seen among adults aged 21 years and older. Most of the ingestions seen in this population are intentional suicide attempts.1,4,5

Caustic ingestions may cause widespread injury to the lips, oral cavity, pharynx, and the upper airway. The effect that these agents have on the esophagus accounts for most of the serious injuries and long-term complications seen among both children and adults.3 Short-term complications include perforation and death. Long-term complications include stricture and increased lifetime risk of esophageal carcinoma.7 In children, 18% to 46% of all caustic ingestions are associated with esophageal burns. This number may be higher in adults who often consume larger amounts of the caustic substance as part of a suicide attempt.7,8 Because of its importance, a large portion of the discussion will be concerned with esophageal injuries.

ETIOLOGIC AGENTS AND TYPES OF INJURIES

The nature of the injury caused by caustic ingestion is determined by a number of factors including the identity of the agent, the amount consumed, the concentration, and the length of time the agent is in contact with a given tissue.5,9

Caustic materials cause tissue injury by chemical reaction. These materials are generally acidic or alkali. Usually, acids with pH less than 3 or bases with pH greater than 11 are of the greatest concern for caustic injury.10 Alkalis contain bases dissolved in water.5 Examples are such agents as sodium hydroxide and potassium hydroxide (for complete list see ). Lye is a general term for alkali found in cleaning products.7 Caustic alkaline materials are also found in drain cleaners, various cleaning agents, hair relaxers, dishwasher detergents, and disk batteries. 4,11

Table 1

Commonly Ingested Caustic/Corrosive Agents

In liquid form, bases are tasteless and denser than water, resulting in pronounced distal injuries1,9 Alkali ingestion causes liquefactive necrosis with diffusion into deeper layers of the injured mucosa. Saponification of fats, denaturation of proteins, and blood vessel thrombosis will occur during the injury process.1,4,5,11 This injury occurs quickly, with a 30% solution of sodium hydroxide being able to produce full thickness injury in 1 second.7 Even lower concentrations can produce extensive injury. A recent animal study from Brazil12 showed that a low concentration solution (1.83%) was able to produce esophageal epithelial necrosis in 1 hour.

Like their liquid counterparts, solid strong alkali substances can produce deep injuries although they tend to adhere to the mucosa of the mouth and esophagus, thus sparing the stomach. Weaker alkalis that are powdered or granular, such as dishwater detergents, tend to injure the upper airway and can cause laryngeal edema and airway compromise. 1,8,13

Alkaline disk batteries contain a 45% solution of potassium hydroxide or sodium hydroxide. Their ingestion will result in damage and leakage within 1 hour and in perforation in 8 to 12 hours if they lodge in the esophagus; this event mandates the immediate removal.4,5 If they are ingested and become lodged in the esophagus, an emergency situation arises.

Hair straighteners and relaxers containing calcium or lithium hydroxide are highly alkaline. Despite this, they rarely cause severe injury or sequelae; thus, treatment is largely conservative with overnight observation and management.4

Acids, in contrast to alkali substances, have a poor taste and are irritating, which may lead to a child’s choking and gagging. This may predispose the patient to aspirate the caustic material, with subsequent airway compromise.1,4,9 Examples of acids in commercial products include hydrochloric acid, sulfuric acid, and silver nitrate.4,11 They are found in toilet bowl cleaners, swimming pool cleaners, and rust removers. 4

Acids are conventionally thought to cause coagulation necrosis that forms an eschar, preventing deep tissue penetration.1,4,11 This eschar is thought to decrease the rate of esophageal burn, though pooling of these agents in the stomach is thought to predispose patients to gastric perforation and stricture.1,9 One recent caustic ingestion series from Israel3 questions this protective eschar theory, showing increased rates of esophageal perforation in patients who ingested acid.

Bleaches such as chloride bleach, peroxide, and mildew remover are also considered caustic esophageal irritants, though pH is typically neutral in commercial preparations.1,5,9 Because of the low concentrations and the neutral pH, bleaches do not cause extensive esophageal damage, though they may cause laryngeal edema and airway compromise in the short-term setting.1

STAGING AND PATHOPHYSIOLOGY

As mentioned above, the esophagus is the site of most long-term sequelae from caustic ingestion. The esophagus is a 10 to 12 cm tube at birth, which increases to from 25 to 30 cm in the adult. It has 3 primary layers. The innermost is the mucosa, consisting of squamous epithelium, lamina propria, and muscularis mucosa. A deeper layer is the submucosa, which consists of fibrous connective tissue with blood vessels, nerves, and numerous mucous glands. Finally, there is a muscular layer divided into inner and outer muscle layers.11 The anatomic layers of the esophagus are of particular importance because most staging systems for injury are based on findings seen on endoscopy that correlate with the depth of injury (see ). Multiple staging systems for injuries are described in the literature, with older systems characterizing injury severity according to different degrees, similar to that used for burns of the skin. The system shown in correlates findings seen on endoscopy. Eighty percent of patients with grade 3 burns develop stricture, while only one third of those with grade 2 burns will eventually develop stenosis. 7

Table 2

Injury to the esophagus is rapid, as described above, for both acids and alkalis, but this acute tissue disintegration and deep tissue penetration may continue for hours.1 Injury progresses within the first week after ingestion, with inflammation and vascular thrombosis. A developing ulcer with fibrin crust will be seen in a few days. Granulation tissue develops between 2 to 4 days and is revealed under shed necrotic tissue by days 15 to 20. This is clinically relevant to healing because collagen deposition may not begin until the second week after injury; thus, the healing tissue will be less strong. This weakness may increase risk during endoscopy performed between 5 to 15 days after injury and may predispose the esophagus to spontaneous rupture during this period.4,14

PRESENTATION AND TREATMENT

After caustic ingestion, patients may present with a combination of many symptoms or none at all depending on the nature of the agent, the specifics of the ingestion (quantity, intent, timing), and what tissues were affected. Patients may have obvious burns to the lips, mouth, and oropharyx. The presence or absence of these lesions does not correlate with the presence of injury to the esophagus or stomach.1,5 Patients with significant laryngeal or epiglottic edema may present with stridor, aphonia, hoarseness, or dyspnea.1 More nonspecific presenting symptoms include nausea, recurrent emesis, hematemesis, dysphagia, odynophagia, and drooling. The presence of abdominal pain or rigidity as well as substernal/chest or back pain may be a sign of severe burn or perforation.1,5,11 Some authors10,14 claim that presentation with 2 or more symptoms may suggest esophageal injury, but there is no 100% accurate sign or group of symptoms that indicates esophageal injury.

The adequacy of the patient’s airway must first be addressed. Fiberoptic laryngoscopy can be useful in this regard. If the airway is unstable, intubation under direct visualization is required. “Blind” intubation can lead to bleeding and additional injury and make additional attempts more difficult. If it is impossible to secure the airway through intubation, a surgical airway may be required.1,4,5 When the airway is secured, a thorough physical examination should be completed and a thorough history taken, with particular attention to the timing of the ingestion, identity of the agent, and amount ingested.1,4,5,9 Chest and abdominal radiographs should be obtained to detect free air in the mediastinum (esophageal perforation) or under the diaphragm (gastric perforation) as well as to provide a baseline if aspiration pneumonia develops.5 Furthermore, oral food and fluids should be withheld from the patient, who should, however, receive aggressive hydration. Laboratory results and vital signs should be assessed for signs of acidosis and shock. Induction of emesis should be avoided to prevent further injury as the agent is vomited.11 Neutralization of the caustic material should be avoided because of the potential for causing an exothermic injury, which may worsen an existing injury.1 When the patient is stable, the pH of any unknown liquid or agent should be obtained, and the poison control center should be contacted. 4,5,9

Multiple modalities exist to assess the extent of injury to the esophagus, including barium esophagram, technetium-labeled sucralfate, and endoscopy.1 Barium esophagram assesses mild to moderate esophageal burns with a 30% to 60% false-negative rate and is therefore of little use in the short-term setting.1 It is, however, quite useful for following the development of late complications and strictures. Technetium-labeled sucralfate swallow has high sensitivity and specificity but limited ability to show extent of injury. Endoscopy, specifically flexible esophagoscopy, is the most effective method for visualizing the extent of esophageal injury.4 Rigid esophagoscopy may be used but should not be extended beyond the site of caustic burn because of an increased risk of perforation. The flexible endoscope may be advanced past a site of mild injury but should only be stopped at the site of circumferential grade 2 or 3 burns.1,7 Additionally, the flexible esophagoscope provides important information about the stomach and duodenum. Rigid endoscopy is recommended for nasogastric tube placement and airway management.1

The timing of endoscopy and the circumstances for its use, as recommended in the literature, are controversial. In the past, there was a tendency to wait at least 24 hours to allow time for the injury to mature.5 Most authors4,7 are recommending earlier endoscopy and suggesting a wait of only 12 hours and a total wait of no more than 24 hours after ingestion for early assessment and treatment. Endoscopy past 48 hours is discouraged because of progressive wall weakening and increased risk of perforation.1 Most agree that strong alkali ingestion mandates endoscopy, while asymptomatic or questionable ingestions may be observed, according to some sources.1,4

Treatment schemes for caustic injuries vary and no consensus exists. Multiple protocols have been formulated on the basis of documented success in preventing impending complications, though a paucity of randomized trials have assessed any of these interventions. Nasogastric tube placement under endoscopic guidance has been suggested for grade 2b and 3 injuries to stent the injured area and to provide nutritional support.2 Stent placement has shown success in some series,6 though timing and type vary. Stents should be left in place for 14 to 21 days to allow for epithelization.4 Early dilation has been proposed, but has been found to increase rate of perforation.8 Regardless of the intervention, pain control is essential. Antibiotics are often used and have been shown to increase epithelization in animal models though they do not change stricture formation rate or infection rate in numerous series.1,4 Antacids decrease pepsin and acid exposure, which may delay healing of the esophagus, though again, rigorous trials are lacking. Larythrogenic drugs, such as N-acetylcysteine and penicillamine, and mitomycin, an antibiotic and antineoplastic agent, decrease rate of collagen crosslinking and inhibit protein synthesis, respectively, and decrease scarring and stricture formation in animal models. 1,5 Data from human trials are lacking.4

Steroids have been a controversial treatment since they were first shown to decrease granulation and stricture formation in animal models.4 Some prospective and retrospective reports have shown that steroids decrease stricture formation in grade 2 injuries in humans.1,9,10 Recent meta-analyses have revealed conflicting results. One recent analysis in 2005 included a total of 10 studies15 in which 572 patients showed no decreased incidence of stricture, with steroids used for second and third-degree (grade 2 and grade 3) burns. In contrast, a meta-analysis of 362 children showed a 40% rate of stricture in the no-steroid group versus a 19% rate of stricture in the steroid-treated group.14

The landmark randomized trial by Anderson et al2 found no difference in the incidence of stricture formation with the use of steroids, though the number of patients in the study was relatively low. A definitive study on the value of steroids is lacking but, if used, most resources suggest the concurrent use of antibiotics. 2,4,7 Dosing is controversial and recommendations vary widely.1,8 Side effects of steroids, especially vulnerability to infection, should be considered.2

CASE REPORT

The following case highlights the complexities of treating patients who experience caustic ingestion.

A 2-year-old boy presented to a local hospital after ingesting an unknown amount of hair and grease remover. The patient’s past medical and surgical history were unremarkable. The patient underwent intubation at the outside emergency department because of respiratory distress and was transferred to our facility. He had obvious burns to the lips and mouth, though not severe. The patient received flexible endoscopy within the 24 hours following injury. He was found to have erythema and small ulcerations in both the esophagus and stomach. His injuries were deemed grade 2a.

The patient received a nasogastric tube over a guide wire and was given multiple broad spectrum antibiotics without steroids. Our service was consulted to evaluate the patient’s upper airway to assess if the patient could be extubated on posttrauma day 4 (). As can be seen, the patient’s upper airway was grossly edematous with white exudates (grade 2) and we recommended the patient remain intubated. Tube feedings were started and the patient remained afebrile. The patient was finally extubated on posttrauma day 11 after a repeated laryngoscopy/bronchoscopy ().

Endoscopic view of the epiglottis and vocal cords 4 days after ingestion.

Endoscopic view of the epiglottis and vocal cords 11 days after ingestion.

After extubation the patient had persistent difficulty with secretions. A barium swallow on day 12 revealed mild irregularity and narrowing of the proximal esophagus with normal distention. Most importantly, there was no evidence of a perforation. The patient never tolerated oral intake. He had repeated endoscopy on day 14 with replacement of the nasogastric tube that had been previously removed.

On day 19, during a planned open jejunostomy tube placement, the patient was found to have a walled off area of gastronecrosis and perforation. Throughout his previous stay at the pediatric intensive care unit, he had remained afebrile. The patient’s clinical course remained complicated. He was found to have a stricture involving from 15 to 25 cm of his esophagus, and balloon dilations were performed under fluoroscopic guidance 32 days after his initial injury.

This case highlights the unpredictability of these injuries. This is made most apparent by the gastric perforation despite only low-grade findings on initial endoscopy. Furthermore, the patient had a relatively unremarkable barium swallow; yet, he developed an extensive stricture, which currently still requires dilations, despite all the efforts (antibiotics, nasogastric tube, endoscopies) taken by the team providing his medical care. Although the indications and descriptions of standard of care are useful, the unpredictable nature of these injuries continues to trump expectations for patient outcomes and for complications.

COMPLICATIONS

As evidenced by the above case, complications can occur even in “low-grade” injuries, though most long-term sequelae are seen in injuries that are more severe. Esophageal stricture may be seen as early as 3 weeks after ingestion.2,15 It occurs in 10% to 20% of caustic injuries, most commonly at the level of the cricoid cartilage, the region of the aortic arch, and below the left main stem bronchus, as well as the esophageal hiatus, all of which are anatomic regions of narrowing in the esophagus.1,11 Stricture can lead to severe dysphagia, with approximately 80% of strictures causing obstructive symptoms 2 months after their formation.8 Of children ingesting alkalis, 30% will develop esophageal burns; of these, 50% will develop strictures.5 Severe and recalcitrant strictures may require esophageal replacement with colon or jejunum interpositional grafts, while less severe strictures are managed with dilation.1,2,5,11,15 Balloon dilation is the procedure of choice for management of most strictures in children.4 The literature suggests a baseline barium esophagram 3 to 4 weeks after ingestion to establish baseline for future stricture formation. 1 Complications of stricture include nutritional compromise, hospitalization, chronic anemia, and repeated dilations.1

Other sequelae may occur that require surgical management. Perforation of the esophagus can lead to tracheoesophageal fistula, mediastinitis, pneumonia, and sepsis, requiring immediate esophagectomy with resultant cervical esophagostomy and gastrostomy.1,4,9,11 Perforation of the stomach or duodenum may lead to peritonitis, shock, and death.4 Such injuries require surgical interventions such as exploratory laparotomy.4,5 Burns to the larynx result in airway loss and strictures; treatment includes tracheostomy and further reconstructive surgeries.16 Some authors1 suggest early reconstruction for grade 3 and some grade 2 injuries to prevent stricture and perforation complications.

Mortality and morbidity for caustic ingestion is most severe for extensive injuries. Transmural burns to the esophagus may be associated with up to 20% mortality.1,9 Injury and stricture formation predispose to esophageal carcinoma, with an estimated increase in risk by a factor of 1000, which continues for 10 to 25 years after injury and requires careful follow-up. 1,4,11 Routine screening, however, is not currently recommended.10 Morbid functional complications include nasopharyngeal reflux, hypopharyngeal and laryngeal stenosis, and tongue fixation.1

CONCLUSION

The epidemiology and pathophysiology of caustic ingestion has been thoroughly described in the literature. Despite this, medical teams continue to have difficulty managing the injuries and complications created by this problem. The current available treatment options strive to treat immediate injury and prevent later complications.

Our hope is that this review of literature and this case report demonstrate the unpredictable nature of these injuries as well as the need for more definitive research into treatment. More importantly, we hope it shows the need for treating caustic ingestion on a case by case basis, with great attention given to even low-grade injuries because of the devastating complications that can occur.

REFERENCES

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Consultation Report Samples (3) – MTinformation

Consultation Report Sample #1

CHIEF COMPLAINT: Chest pain.

HISTORY OF PRESENT ILLNESS: This is a 55-year-old white female referred today for chest pain. She was recently evaluated for a typical chest pain and had exercise stress testing. She exercised for 9 minutes and 26 seconds and the test was clinically negative. She continues to have atypical chest pain complaints. She has no orthopnea, no lower extremity edema, no palpations, or dyspnea on exertion.

PAST MEDICAL HISTORY: Hypothyroidism.

PAST SURGICAL HISTORY: Partial hysterectomy, lumbar laminectomy, and benign bony tumor removed from sinus cavity.

SOCIAL HISTORY: She is married and has a 28-year-old son. She is self-employed. She makes custom draperies.

FAMILY HISTORY: Father is deceased from congestive heart failure and mother is still living at age 86 with history of hypertension and CVA. She has three sisters who are healthy. She smokes cigarettes one-half pack per day for 25 years. She quit 10-15 years ago. She drinks on a social basis, one to two mixed drinks per week. Caffeine intake, two to three diet Rite Cola’s per day. Three to five eight-ounce glasses of water per day. She exercises regularly and walks one to one-and-one-half miles per day, five day a week. She follows a regular diet with no restrictions.

REVIEW OF SYSTEMS: She has lost 16 pounds since January. She is positive for easy bruising. She does experience occasional seasonal allergies symptoms, occasional nocturia, urinary urgency, and hyperkeratosis.

CURRENT MEDICATIONS: Premarin everyday, Synthroid everyday, and oxybutnin p.r.n.

ALLERGIES: SULFA DRUGS CAUSE RASH.

PHYSICAL EXAMINATION: Weight 169 pounds, height 5’8” tall.

VITAL SIGNS: In the right arm blood pressure 140/80 and in the left arm 130/80. She has an applicable respiratory rate at 16.

GENERAL: A 56-year-old white female in no acute distress.

SKIN: Warm and dry.

PHYSICAL EXAM: Unremarkable.

EKG: Normal sinus rhythm.

IMPRESSION:
1. A typical chest pain with negative exercise stress testing on 09/11/02.
2. Reform smoker.
3. Unknown lipid status.
4. Hypertension.

DISCUSSION: At this time, chest pain appears to be caustic chondritis, will treat with Motrin. Check fasting lipids. I will see the patient back in the office in four weeks and reevaluate blood pressure readings at that time, as to whether or not medical therapy will be necessary.

Consultation Report Sample #2

CHIEF COMPLAINT: Low back pain, bilateral lower extremity pain of 4-5 weeks duration.

HISTORY OF PRESENT ILLNESS: This is a 70-year-old male with chief complaint of low back pain and bilateral lower extremity pain. The patient denies any recent trauma to the low back. He states that he has been a body builder for the past 30 years and has worked out at the gym on a regular basis. He has entered in one multiple body building contests. He states that approximately 3 years ago, he was a using a machine at the gym doing crunches and felt a pop in his low back. He states that his back has not been the same since then. However, he was able to continue working out until about 4-5 weeks ago when he states he was unable to get out of bed due to bilateral lower extremity burning in his legs. He went to see a chiropractor and had some manipulation, which helped somewhat. He has taken multiple pain medications, NSAID’s and narcotics. At present, he is taking Percocet. He states that this has not helped much at all. He has not been able to return to the gym. The patient also gives a history of taking a growth hormone that was a black market product from China for an entire year, approximately 4-5 years ago. He denies any change in bladder or bowel movements.

ALLERGIES: NO KNOWN DRUG ALLERGIES.

PAST MEDICAL HISTORY: Significant for depression and anxiety.

PAST SURGICAL HISTORY: The patient had a right knee arthroscopy in January of 2002.

SOCIAL HISTORY: The patient denies any alcohol use, denies any smoking history. He is presently retired. Prior to retiring, he worked as a massage therapist. He does this occasionally for friends at the present time. He is married. He lives with his wife. There is no litigation involved in this pain management case.

FAMILY HISTORY: Parents are deceased. Mother died of cancer in 2001. Father died of cardiac disease.

PHYSICAL EXAM: The patient is a 70-year-old well developed, well nourished male in moderate distress secondary to low back pain, as well as bilateral lower extremity pain. His blood pressure is slightly elevated today at 130/90. The patient’s pulse is 70. He is 5’6” tall and weighs 223 lbs HEENT: Normocephalic. Atraumatic. Extraocular muscles are intact. Pupils are equal and reactive to light and accommodation. Neck: Supple without masses or adenopathy. Lungs: Clear to auscultation and percussion bilaterally. No rales, rhonchi or wheezing is appreciated. Heart: Negative S4, positive S1, positive S2, negative S3. No murmurs or ectopy is appreciated. Abdomen: Soft and non-tender to palpation. Bowel sounds are present in all four quadrants. GU: Deferred. Skin: Clear. Pulses: Bilaterally symmetric in the upper and lower extremities. No clubbing, cyanosis or edema is noted in the lower extremities. Sensory Evaluation: No sensory deficits are noted in the upper or lower extremities. Motor strength function: The patient ambulates with a normal gait. Transfers on and off the exam table are fluid. There is no motor weakness noted in the lower extremities. Motor strength testing is bilaterally symmetric and 5/5. The patient has well defined musculature. Reflexes are bilaterally symmetric in the upper and lower extremities.

Focus examination of the lumbar spine reveals the patient ambulating with a normal gait. Transfers on and off the exam table are fluid. There is no abnormal list or posturing. Lumbar lordosis is maintained. The patient has full range of motion of the lumbar spine in all planes. He is able to toe-heel walk without difficulty. Straight leg raise is negative. Motor strength testing of the lower extremities is 5/5 and symmetric. The lower extremities are without muscle atrophy. Skin is warm and dry to touch. Pulses are intact. Deep tendon reflexes are bilaterally symmetric.

DIAGNOSTIC TESTING: The patient had an MRI done on 07/14/08. MRI findings reveal HNP L4-L5 on the right minimally compressing the thecal sac. There is an HNP at L3-L4, again, mildly flattening the thecal sac. There is degenerative disc disease at multiple levels.

CURRENT MEDICATIONS:Celexa 10 mg one daily, Ativan 2 mg one daily, Ambien 12. 5 mg one daily, and Percocet 5 mg t.i.d./q.i.d.

DIAGNOSTIC IMPRESSION:

1. Degenerative disc disease.
2. Chronic low back pain.
3. Lumbar radiculopathy.
4. HNP L3-L4 and L4-L5.

PLAN: The patient is in an acute state of pain secondary to a lumbar radiculopathy. After careful review of his medications and disease status, the patient would most likely benefit from a lumbar epidural steroid injection. He was advised no aspirin products or NSAID’s products 3-5 days prior to his injections. At present, he is taking Percocet for pain. He also understands that the injections may or may not relieve any or all of his pain and the risks include, but are not limited to injection site tenderness, redness, infection, nerve damage or injury, exacerbation of his pain, as well as death. He has been advised to remain NPO 8-10 hours prior to the injections and to have a driver available to transport him to and from the facility. He understands the risks and benefits of the procedure and is willing to undergo a lumbar epidural steroid injection tomorrow. He has been advised of conscious sedation and what that entails. His questions regarding the procedures were answered to his satisfaction.

History And Physical Report Sample #3

HISTORY OF PRESENT ILLNESS: This is a 43-year-old black man with no apparent past medical history who presented to the emergency room with the chief complaint of weakness, malaise and dyspnea on exertion for approximately one month. The patient also reports a 15-pound weight loss. He denies fever, chills, and sweats. He denies cough and diarrhea. He has mild anorexia. Past Medical History: Essentially unremarkable except for chest wall cysts which apparently have been biopsied by a dermatologist in the past, and he was given a benign diagnosis. He had a recent PPD which was negative in August 1994.

MEDICATIONS: Advil and Ibuprofen.

ALLERGIES: NO KNOWN DRUG ALLERGIES.

SOCIAL HISTORY: He occasionally drinks. He is a nonsmoker. The patient participated in homosexual activity in Haiti during 1982, which he described as “very active.” He denies intravenous drug use. The patient is currently employed.

FAMILY HISTORY: Unremarkable.

PHYSICAL EXAMINATION:
General: This is a thin, black cachectic man speaking in full sentences with oxygen.
Vital Signs: Blood pressure 96/56, heart rate 120. No change with orthostatics. Temperature 101.6 degrees Fahrenheit. Respirations 30.
HEENT: Funduscopic examination normal. He has oral thrush.
Lymph: He has marked adenopathy including right bilateral epitrochlear and posterior cervical nodes.
Neck: No goiter, no jugular venous distention.
Chest: Bilateral basilar crackles, and egophony at the right and left middle lung fields.
Heart: Regular rate and rhythm, no murmur, rub or gallop.
Abdomen: Soft and nontender.
Genitourinary: Normal.
Rectal: Unremarkable.
Skin: The patient has multiple, subcutaneous mobile nodules on the chest wall that are nontender. He has very pale palms.

LABORATORY: Sodium 133, potassium 5.3, BUN 29, creatinine 1.8, hemoglobin 14, white count 7100, platelet count 515, total protein 10, albumin 3.1, AST 131, ALT 31, urinalysis shows 1+ protein, trace blood, total bilirubin 2.4, and direct bilirubin 0.1.

X-RAYS: Electrocardiogram shows normal sinus rhythm. Chest x-ray shows bilateral alveolar and interstitial infiltrates.

IMPRESSION:
1. Bilateral pneumonia; suspect atypical pneumonia, rule out Pneumocystis carinii pneumonia and tuberculosis.
2. Thrush.
3. Elevated unconjugated bilirubin.
4. Hepatitis.
5. Elevated globulin fraction.
6. Renal insufficiency.
7. Subcutaneous nodules.
8. Risky sexual behavior in 1982 in Haiti.

PLAN:
1. Induced sputum, rule out Pneumocystis carinii pneumonia and tuberculosis.
2. Begin intravenous Bactrim and erythromycin.
3. Begin prednisone.
4. Oxygen.
5. Nystatin swish and swallow.
6. Dermatologic biopsy of lesions.
7. Check HIV and RPR.
8. Administer Pneumovax, tetanus shot, and Heptavax if indicated.

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Management of Subglottic Stenosis and Subglottic Stenosis in Systemic Disease

Etiology and Pathogenesis

During the first decades of the twentieth century, infection and external airway trauma were the primary causes for SGS. In the late 1960s, the incidence of acquired SGS began to increase as a result of long-term intubation and other invasive procedures of the airway. Currently, common etiologies resulting in SGS are endotracheal intubation, tracheotomy, previous airway surgery, neoplasms, and radiation for oropharyngolaryngeal tumors. Other causes, while rare, are important to consider when evaluating SGS of unclear etiology (Table 40.1).

Table 40.1

Causes for subglottic stenosis

SGS can be classified as congenital and acquired. The acquired form is much more frequent than the congenital type and can be subdivided into traumatic, inflammatory, infectious, and tumoral. An additional inadequately characterized female population suffers from idiopathic SGS (ISGS).

Congenital SGS

Even though this type of stenosis is uncommon, it is the third most frequent congenital airway problem. A malformation of the cricoid cartilage is linked to inadequate recanalization of the laryngeal lumen upon conclusion of the normal epithelial fusion at the end of the third month of gestation. Different degrees of atresia, stenosis, or webbing can be found in these patients (Fig. 40.2). Histopathologically, congenital SGS can be subdivided into cartilaginous and membranous. The cartilaginous type results from a thickened or distorted cricoid cartilage, creating an anterior subglottic shelf that extends to the posterior region. It is frequently more severe than the membranous stenosis and is rarely managed successfully with endoscopic techniques. The membranous form is more common, circumferential, often involving the true vocal cords, and is characterized by fibrous soft tissue thickening.

Fig. 40.2

Congenital subglottic web with Myer-Cotton grade I cricoid cartilage stenosis. This thin web was mechanically broken

Laryngeal Trauma

Trauma is the most frequent cause of acquired laryngeal stenosis in children and adults. Internal subglottic trauma is usually iatrogenic (e.g., endotracheal intubation, tracheotomy, or prior tracheal instrumentation). External trauma can be originated by contusion, penetrating wound, or inhalation injury.

In SGS caused by intubation, several risk factors have been identified such as prolonged intubation, large-caliber endotracheal tube, traumatic intubation, numerous re-intubations, local infection while intubated, frequent displacement of the endotracheal tube, and the concomitant existence of a nasogastric tube (Fig. 40.3a). The pathogenesis of this form of acquired SGS is not fully understood. The more widely accepted theory proposes that high pressure from a tube or cuff exceeds the capillary pressure of the airway wall and contributes to ischemia of the mucosa and cartilage (Fig. 40.3b). The three overlapping phases of wound repair are inflammation (initial injury generates edema and vascular congestion with recruitment of cells and mediators, occasionally ulceration and infection can occur), proliferation (reepithelialization, neovascularization, increased fibroblast activity, granulation tissue), and airway remodeling (collagen deposition, scar formation, contracture, and loss of structural integrity leading to stenosis).

Fig. 40.3

CT reconstruction of a 78-year-old female with subglottic stenosis caused by prolonged endotracheal intubation (a). Multiple comorbidities, high position of the tube, excessive cuff pressure, and the presence of a nasogastric tube contributed to an extensive mucosal and cartilage damage (b). A straight silicone stent 12/40 mm was deployed (c)

Postsurgical SGS may occur as a complication of previous tracheotomy, percutaneous tracheotomy, cricothyroidotomy, and surgical treatment for airway neoplasms. Stenosis following tracheotomy may be above the stoma, at the same level as the stoma, at the cuff site, and at the tip of the cannula. In addition to ischemic mucosal injury and chondritis, fracture of the cartilage is an important factor for SGS in these patients. Damage to the cartilage above the stoma is the most frequent cause of stenosis after emergency tracheotomy performed with a poor technique.

The incidence of traumatic SGS can be radically reduced if high tracheotomy and cricothyroidotomy are only performed in extreme emergencies; aggressive endoscopic manipulation for benign laryngeal lesions is avoided; intubation and endoscopy are done gently on calm patients; factors contributing to laryngeal trauma secondary to intubation are recognized and prevented when possible.

Infection

Acute laryngotracheobronchitis, an acute viral respiratory disease commonly seen in children, can cause subglottic narrowing. Croup most commonly occurs in children 6–36 months of age, and it is rare beyond the age of 6. Acute bacterial tracheitis can also originate thick, purulent secretions and mucosal edema that may cause symptoms of upper airway obstruction.

SGS secondary to chronic infection is rare, except in certain endemic geographic areas, and it has been described in patients with tuberculosis, syphilis, diphtheria, typhoid fever, scarlet fever, leprosy, and laryngeal scleroma.

Though infrequent, subglottic and endotracheal tuberculosis may result in significant obstruction related to the initial lesion or subsequent stricture formation. Some degree of stenosis may still develop despite appropriate antituberculosis chemotherapy.

Laryngeal scleroma is also an uncommon chronic disease originated by an aerobic gram-negative bacteria, Klebsiella rhinoscleromatis. It is prevalent in certain regions such as Africa, Asia, Central and South America, and Central and Eastern Europe. It typically involves the nose but can also affect other parts of the respiratory system. Subglottic involvement is reported in 23% of cases. Following the initial infection, three sequential phases are described: exudative stage, with active inflammation, edema, congestion, and necrosis; proliferative stage characterized by multiple reddish nodules; and fibrotic stage with cicatricial tissue. Clinical suspicion is important in order to achieve the diagnosis. The CT scan normally shows concentric irregularities and narrowing in the subglottic space. Biopsy specimens are needed for the definitive diagnosis, usually obtained during the proliferative phase. There is a recognizable histological pattern with clusters of vacuolated histiocytes – Mikulicz cells. Treatment should be directed according to clinical stage, severity, and anatomic location. In the proliferative phase, long-term antibiotics are the treatment of choice. In the fibrotic stage, if the patient is symptomatic and there is mild subglottic involvement, endoscopic procedures can be valid therapeutic options. Open surgical techniques have been attempted for extensive SGS.

Wegener’s Granulomatosis

Wegener’s granulomatosis (WG) is a multisystemic disease characterized by necrotizing vasculitis and granuloma formation that has a predilection for the upper and lower respiratory tracts and kidneys. Its etiology is unknown and affects both males and females with a peak around 40–55 years old. The course of WG varies widely, from localized to multisystemic, from mild to life-threatening disease. Nasal and sinus findings are present in a high percentage of cases (e.g., chronic sinusitis, epistaxis, septal perforation, saddle nose deformity). SGS may occur either as a presenting characteristic or as a late-stage manifestation of the disease and is reported in 12–23% of WG patients (Fig. 40.4). It often occurs independently from other features of disease activity and frequently does not improve with systemic treatment. Laboratory studies may show a positive anti-neutrophil cytoplasmic autoantibodies (ANCA-c) test, although it should be interpreted cautiously because ANCA-c may be positive in other diseases and WG may be present in face of a negative ANCA test. Chest radiographs and CT scans may show pulmonary infiltrates and/or cavitary nodules. Biopsy remains the gold standard for the diagnosis, but specimens from the larynx and trachea often do not exhibit the characteristic inflammatory infiltrates with multinucleated giant cells, granuloma formation, and vasculitis of the small and medium vessels. Systemic immunosuppressive therapy is the mainstream treatment in WG. The endoscopic management of subglottic lesions (laser resection, serial dilatations, topical corticosteroids, local mitomycin-c) is an important aspect in those who remain symptomatic despite appropriate medical management.

Fig. 40.4

Subglottic stenosis in Wegener’s granulomatosis. One can notice the red inflammatory friable tissue circumferentially narrowing the subglottis

Amyloidosis

Amyloidosis is a disorder characterized by extracellular tissue deposition of fibrillar proteins and can involve virtually any organ or system. It can be idiopathic or associated to inflammatory, hereditary, or neoplastic diseases. Respiratory tract amyloidosis may be part of a widespread or local process. Sites in the larynx that show predilection for nodular or polypoid amyloidosis include the ventricles, false cords, aryepiglottic folds, and the subglottis. Pulmonary manifestations comprise tracheobronchial infiltration, persistent pleural effusions, and parenchymal nodules. There may be diffuse narrowing and wall thickening, circumferential airway involvement, often with ossification of the amyloid deposits (Fig. 40.5). Bronchoscopy displays multiple plaques or localized tumor-like masses. Tissue biopsy stained with Congo red and examined under polarized light shows the characteristic submucosal extracellular deposits of amyloid protein that confirms the diagnosis. Bronchoscopy-based techniques (laser therapy, stenting) have been suggested as a possible method for dealing with subglottic obstructing lesions. There is no effective medical treatment and excision, when possible, remains the treatment of choice in localized forms of amyloidosis.

Fig. 40.5

Bronchoscopic appearance of laryngotracheal amyloidosis in a 37-year-old female patient. Amyloid deposits infiltrate the mucosa reducing airway caliber

Relapsing Polychondritis

Relapsing polychondritis (RP) is a multisystemic immunemediated disease characterized by recurrent episodes of inflammation of cartilaginous structures. RP is most likely between age 40 and 60, although it can occur in younger patients. One-third of cases develop in association with another recognizable condition, particularly systemic vasculitis or connective tissue diseases. Auricular chondritis represents the usual initial presentation, but the disease may involve the nose, laryngotracheobronchial tree (malacia and/or stenosis), peripheral joints, and other organs. In the active stage, there is a red, warm, painful swelling of the cartilage. After the inflammatory episode, significant destruction may occur. The definitive diagnosis is based on the presence of three of the following criteria or at least one along with a confirmatory biopsy showing inflammatory changes in the cartilage: recurrent bilateral auricular chondritis, nonerosive inflammatory polyarthritis, nasal cartilage chondritis, ocular inflammation, respiratory tract chondritis, and cochlear or vestibular damage. CT and bronchoscopic findings include diffuse smooth thickening of the larynx, trachea, and proximal bronchi; thickened, densely calcified cartilaginous rings with spared posterior tracheal membrane; tracheal wall nodularity; diffuse narrowing of the tracheobronchial lumen, major airway collapse caused by destruction of cartilaginous rings (Fig. 40.6). It is difficult to predict the clinical path of the disease because it can have an indolent course or fulminating consequences. This means that it is important to perform a prompt diagnosis and treatment plan before irreversible damage occurs. Medical management of RP focuses on suppressing the acute inflammatory process. Ernst and coworkers have shown that it is feasible to treat these patients by endoscopic procedures (dilatation, stenting). The majority experience improvement of respiratory symptoms although on occasion, involvement of glottis and subglottic regions may necessitate a tracheotomy.

Fig. 40.6

Firm thickening of the subglottis in a patient with relapsing polychondritis (Courtesy of Armin Ernst, M.D.)

Tumor

Direct extension of a locally advanced tumor and/or extrinsic compression may cause SGS (e.g., laryngeal cancer, thyroid tumors). Primary laryngeal and tracheal tumors are extremely rare in children, with papillomas, hemangiomas, and granular cell tumors being the most common. In adults, squamous cell carcinomas followed by adenoid cystic carcinomas are the most frequent and in some instances may cause SGS. Other less common tumors in adult patients include hemangiomas, neurogenic tumors, and papillomas.

Recurrent papillomatosis results from infection of the upper respiratory tract by the human papilloma virus (HPV). HPV6 and 11 are most commonly involved, while HPV16 has been reported and may be associated with an increased risk of malignant degeneration. This disease is most common in children but may also occur in adults, as previously stated. Infection frequently occurs during birth, and laryngeal papillomas may lead to contamination of the trachea and lungs. At bronchoscopy, the papillomas have a polypoid appearance and may involve the larynx, trachea, or bronchi (Fig. 40.7). Endoscopic interventions are crucial since repeated treatment is usually required because recurrence is quite common.

Fig. 40.7

Glottic and subglottic cauliflower-like tumors with smooth surface corresponding to recurrent papillomatosis in a 42-year-old (a). There was a marked improvement in airway caliber after laser treatment (b)

Idiopathic Subglottic Stenosis

ISGS is a rare inflammatory process of unknown cause, usually limited to the subglottic region and the first two tracheal rings. It is an exclusion diagnosis based on the absence of recent intubation or trauma, and other rare diseases that can affect the subglottis. Some reports advance a hormonal cause, since most patients are females with preponderance in the 20–50 age range, although no major causal factor was identified. Mark et al., in 63 tracheal resections performed in patients with the diagnosis of ISGS, found an extensive fibrosis, dilation of mucus glands, a relatively normal cartilage, and in most cases, a positive staining for estrogen and progesterone receptors in fibroblast cells. The theory of laryngopharyngeal reflux as a possible etiological factor seems to be excluded by recent reports given the poor responses to anti-gastroesophageal reflux medication. A new hypothesis suggests that severe coughing episodes may cause mechanical trauma, intermittent disruption of blood supply to the cricoid, and scarring in the subglottic area leading to ISGS. Dilatation, laser incisions, intralesional steroids, mitomycin-c, and airway stenting have all been used for the initial management of ISGS.

Other Causes

Gastroesophageal reflux has been proposed as a medical condition that may exacerbate the pathogenesis of SGS, be the single cause for stenosis, or cause restenosis after repair. Roh and colleagues have induced subglottic injury in a rabbit model demonstrating that the inflammation scores, fibrosis, thickening, and luminal stenosis were greatest in the acid reflux group compared to the nonacid reflux group, suggesting that subglottic wound healing is significantly affected by acidic conditions. Active empirical treatment is recommended for this condition in patients undergoing SGS treatment.

Additional systemic factors may also increase the risk of subglottic injury and decrease the rate of wound healing (e.g., diabetes mellitus, immunodeficiency, and chronic infections).

Russian translations, synonyms, antonyms, pronunciation, example sentences, transcription, meaning, collocations

Surgical dentistry – Page 49

burn areas use the nines rule and the palm rule.The severity of the patient’s condition is largely determined by the age of the victim and the severity of the burn of the respiratory tract. In practical work, the same patient may have superficial and deep burns in combination with respiratory tract damage and without it. The severity of the burn injury helps to assess the injury severity index (ITP). According to him, 1% of II-III degree burns corresponds to 1 unit, 1% of deep burns (III-VI degree) – 3 units. I degree burns are not counted. In the presence of burns of the respiratory tract, 30 units are added to the ITP.

Burn disease develops with relatively extensive thermal trauma: with deep burns, which occupy more than 15% of the body surface in adults and 10% in children and the elderly. Superficial and limited in area deep burns are not accompanied by burn disease. With isolated burns of the head, face and neck, burn disease develops extremely rarely. There are 4 periods of burn disease: I – burn shock; II – acute burn toxemia; III – burn septicotoxemia; IV – convalescence.

The name of each period predetermines its pathogenetic orientation.

Features of burns to the head, face and neck. The surface of the face makes up 3.12% of the total body area. Good innervation and vascularization of the face, the unfavorable mental state of the victim with disfigurement of the face determine the severity of his condition even with isolated burns of the face of the II-IV degree. The relief of the face is uneven, the skin is thin and of unequal thickness in different areas of it. Therefore, on the face, even in areas close to each other, when exposed to the same thermal agent, burns of different depths can occur – from the most superficial to the deepest.Deep burns occur more often on the higher parts of the face: brow ridges, ears, nose, zygomatic region, lips, chin, and often the tissues of the forehead and eyelids are affected. Burns of the face are often combined with burns of the respiratory tract and hands (Fig. 124). They are accompanied by severe soreness and significant tissue edema, which appears in the first hours after the injury and grows rapidly. The brow ridges are often affected. With deep burns, a thin scar forms at the site of the eyebrows, which increases the eversion of the upper eyelid.There is no hair growth.

Burns of the auricles are often deep, up to charring with damage to the cartilage. The developing chondritis is accompanied by significant edema, hyperemia of the tissues of the auricle, and severe pain. Above the areas of suppuration, fluctuation appears due to the accumulation of exudate. After the rejection of the dead cartilage sections, defects and deformities of the auricles occur. With total damage to the auricles, they are hard to the touch, painless, white or dark in color.

The nose (external) has a complex anatomy. The skin on the back of the nose is thin. Under it is a small layer of loose connective tissue and there is no subcutaneous adipose tissue. In the area of ​​the wings of the nose, there are thin cartilages. More often burns suffer

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tip and wings of the nose, sometimes its entire surface. Often, wing and triangular cartilage is damaged, which leads to the development of chondritis, followed by their necrosis. There are defects in the tissues of the nose, persistent deformation of it.

In case of tissue burns in the zygomatic region and cheeks, tissues up to the parotid fascia may die, exposing the parotid salivary gland. Scarring of the tissues of these areas leads to eversion of the lower eyelid and displacement of the corner of the mouth outward. Zygomatic bone necrosis is possible.

Lips – the movable part of the face. They play a large role in food intake. The red border of the lips does not contain sweat and mucous glands, hair follicles. Its integumentary epithelium is thin and transparent. With burns of the lips, the red border is often necrotic and not restored.The crusts that form are injured, bleed, the cracks that form cause pain and create significant difficulties in eating. As a result of edema, the red border turns inside out, a “fish mouth” is formed. Burns of the lips can lead not only to a violation of the shape of the oral area, but also to the formation of a microstomy and difficulty in eating through the mouth.

Chin tissues are affected along with the lower lip. In men, the crusts of the burn wound are firmly connected to the hair, which causes significant inconvenience to the victim and contributes to the formation of a scar with an uneven surface in this area.

Deep burns of the forehead can lead to damage to the frontal bone, followed by necrosis of the outer compact plate, the development of frontal sinusitis. The possibility of the spread of the inflammatory process to the dura mater is not excluded.

The eyelids are less affected, because with a burn of the face, reflex muscle contraction reduces the area of ​​the skin of the eyelids exposed to thermal effects. Under the influence of a strong thermal agent, total damage to the eyelids is possible with exposure of the sclera and cornea of ​​the eye and even their burns.Swelling of the eyelids is always significant and decreases only by the 5-6th day. The ciliary margins are often necrotic and covered with purulent crusts. Incorrect position of the preserved eyelashes leads to corneal trauma and the development of keratitis. Cicatricial eversion of the eyelids is accompanied by deformation of the cartilaginous plate, even if it has not been subjected to thermal action. In case of burns of the eyelids, it is necessary to assess the condition of the eyes. In case of damage to the tissues of the eye, the participation of an ophthalmologist is necessary in the treatment of the patient.

Scalp burns are limited and deep, less common.Often there is an alternation of deep and superficial lesions. The scalp can persist for a long time even with third-degree burns. With deep burns, necrosis of the skull bones is possible. Rejection of the dead

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areas of the bone are extremely slow, so they are shown to be operatively removed with subsequent skin grafting of the resulting defect.

Burns to the neck are often combined with burns to the lower third of the face and chest. Burns of the anterior surface of the neck are more often observed, less often – lateral, relatively rarely – of the posterior surface and circular.Their depth may be different in different parts of the neck. Burns of the neck are accompanied by the development of deep scars, leading to significant deformation of it even with III degree burns. This is due to the defeat of the subcutaneous muscle of the neck located under the thin skin. In severe cases, fusion of the chin with the chest is possible, which excludes head movement. The lower lip is pulled downwards, turns inside out, the mouth does not close, there is constant salivation.

Thus, the features of facial burns include pronounced tissue edema and severe soreness in the affected area, the formation of burns of varying degrees in nearby areas.The degree (depth) of the burn when exposed to the same thermal factor on the face will be greater than on other parts of the body. Burns to the face are often associated with burns to the upper respiratory tract.

Burns of the mucous membrane of the mouth, nasopharynx, and less often the larynx are caused by hot gases. They are always superficial. Burnt hairs of the nasal openings, hyperemia and edema of the mucous membrane are clinically determined. Against this background, there may be areas with a grayish-white bloom. Violation of the sonority of the voice is possible.Deep burns of the mucous membrane of the larynx, mouth, trachea and bronchi are possible only in case of prolonged exposure to high temperatures when the victim is in a closed room, in the foci of forest fires. The mucous membrane of the trachea and bronchi, less often the lung tissue can be affected by inhalation of combustion products. Such patients develop a cough with phlegm, which contains soot, there are signs of impaired external respiration. The most difficult manifestations are combined lesions of the respiratory system with hot gas (air), combustion products and their toxic effects.

Treatment of patients with burns, including the face, includes a complex of general and local effects on the body of the victim and the affected area.

First aid is provided at the scene. It is necessary to stop the effect of the thermal agent on the fabric in any way possible in this situation [pour water, throw snow, sand, cover with a tarpaulin or blanket until the flame disappears (for a short time – danger of asphyxiation!), Knock down the flame, etc.].Do not leave the victim in an upright position, as it promotes the spread of flame to the face. It should be laid on its side. When clothes catch fire, you must not run, as the movement of air inflates the flame. To reduce the heating of the underlying tissues in the first 15-20 minutes 470 after a thermal injury, cold on the burnt surface is effective (cold water, an ice pack, a towel moistened with water, etc.).

With immediate cooling of the burnt surface, the subcutaneous temperature at a depth of 1 cm reaches the initial temperature after 20 s, and without cooling – after 14 minutes.In addition, after the termination of the effect of the thermal agent on the skin, the temperature of the underlying tissues continues to rise. If it is not possible to apply cold, the fired surface should be left open for air cooling. Before transporting the victim, it is advisable to close the wound with an aseptic bandage. If indicated, cardiopulmonary resuscitation is performed.

D o r e d h e r h e r. The paramedical worker can administer non-narcotic or narcotic analgesics, cardiovascular drugs, tetanus toxoid, or toxoid.It is necessary to give the patient a drink, giving from 0.5 to 2 liters of water in which 1 teaspoon of sodium chloride and 0.5 teaspoon of baking soda (per 1 liter of water) or 5.5 g of sodium chloride and 4 g of baking soda are dissolved … Reception of more than 0.5 liters of pure water is contraindicated due to the risk of developing water intoxication. If indicated, continue cardiopulmonary resuscitation. If necessary, transportation is applied to the burned face with an aseptic dressing with holes for the eyes. For superficial burns, the skin is lubricated with petroleum jelly.When providing first aid and first aid, do not use fat-based ointments, as well as tanning agents, methylene blue or brilliant green. All this complicates the treatment of the burn wound and the determination of the depth of the burn.

Patients with I-II degree burns of more than 10% of the body surface, with deep burns, burns of the face, neck, respiratory system, hand, foot, large joints, perineum with combined injuries are subject to hospitalization. In a hospital setting, life-saving measures may be needed by patients with burns of the face, whose respiratory organs are affected.It should not be applied to a tracheostomy patient if there are no signs of asphyxia, in case of damage to the trachea and bronchi by combustion products, as this significantly aggravates the condition of the burned one. These lesions are treated conservatively (use of heart drugs and bronchodilators, corticosteroid hormones, oxygen inhalation, etc.). The oral cavity is irrigated with 3-5% sodium bicarbonate solution, antiseptic solutions. If anti-tetanus serum has not been previously administered, then it is administered. Antibiotic therapy is started.Carefully and gently treat the burn wound. Healthy skin around the affected areas is wiped with gasoline, 96% ethyl alcohol or 0.5% ammonia solution, you can wash the skin with soap and water. Existing blisters are irrigated with a solution of furacilin or other antiseptic. Scraps of the epidermis are removed. The bubble is undercut to remove fluid from it. The exfoliated epidermis (bladder lining), adhering to the wound surface, acts as a biological dressing that accelerates the epithelialization of the wound. Therefore, the bubble cannot be excised.This is done only when its contents become “thick” or fester. Burns of the face are treated in an open, less often – in a closed way. Topical preparation

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treatment of burns should create conditions for the growth of the epithelium and have bacteriostatic properties, not irritate the tissue. The main requirement for him: he should not inhibit the epithelialization of the wound. For burns of the first degree, a moisturizing cream of lanolin, peach oil and distilled water is used in equal amounts; 2% boric petroleum jelly; prednisolone or other ointment containing corticosteroid hormones.You can use a mixture of zinc oxide, talc, equal parts glycerin and distilled water. It is allowed to treat burnt skin with alcohol or alcohol-containing liquids (cologne), baby cream. Wounds on the face, if they are treated openly, are lubricated with ointment or emulsion 3-4 times a day. To do this, you can use 10% synthomycin emulsion, 1% gentamicin, 0.5% furacilin, 10% anesthetic or 10% sulfamilone ointment. A 1% solution of silver sulfadiazine (cream on a water-soluble basis) has a good effect.

In the treatment of III-IV degree burns, accompanied by necrosis of the dermis, the main task is first to form a dry scab, and then to accelerate its rejection. This creates optimal conditions for epithelialization of the wound with a burn of Ilia degree or the development of healthy granulations on the wound surface, which makes it possible to carry out autodermoplasty (for burns of III6-IV degree). This task is better and faster achieved if the wound is treated in a closed way (under a wet-drying dressing with antiseptics or antibiotics).After rejection of the scab with a burn of Ilia degree, to accelerate epithelialization, oil-balsamic dressings can be applied, and UV irradiation of the wound can be performed. With deep burns of the face, primary and early necrectomy is not used, since engraftment of a free graft is possible only if the necrotic tissue is excised within absolutely intact. On the face, it is not possible to comply with this condition. In addition, there is a real danger of damage to the facial and other nerves, as well as severe bleeding.Therefore, the wound surface with deep burns is prepared for plastic closure gradually in the course of conservative treatment. The areas of the scab that are rejected during the treatment are carefully cut off with scissors, without injuring the viable tissues. A granulating wound on the face is ready for autodermoplasty, if the necrotic tissue is completely rejected, there are no signs of purulent inflammation in it, the granulation is fine-grained and pink in color with a narrow border of young epithelium along the edges. The thickness of the skin graft should be 0.3-0.4 mm.For burns of the face, only continuous skin flaps taken with a dermatome from any accessible area of ​​the body are used. Perforations on the flap are not done, as they impair the cosmetic effect.

For I-II degree burns of the eyelids and cornea, the affected areas should be washed with 1% novocaine solution, 30% albucide solution should be instilled into the eyes, 2 drops every 3-4 hours. In addition, hydrocortisone, tetracycline , chloramphenicol eye ointment.

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For pain, instill 0.25% dicaine solution. Special eye films are applied to the cornea, which have analgesic and antibacterial properties.

In case of ear burns, when the effusion between the perichondrium and cartilage has not yet suppurated and the cartilage remains viable, the effusion can be aspirated with a syringe and needle and thereby prevent the development of acute chondritis. If the effusion suppurates, then the abscess must be opened and the wound drained. This most often leads to a pronounced deformation of the auricle, sometimes to its complete loss.It is possible that the external auditory canal becomes infected, which is associated with hearing loss.

In the presence of deep scalp burns, the hair around the wound is clipped and shaved within a radius of 5-7 cm. After 1-2 days, the dead periosteum of the skull is excised. If she is not

died, it is covered with wet dressings to prevent it from drying out. The skin over the exposed and viable periosteum should be restored as soon as possible. With deep burns, the outer compact plate of the skull bones may be affected.It should be removed without waiting for the self-rejection of the dead area. The cancellous bone is covered over time with granulation tissue, onto which a skin autograft is transplanted.

In case of deep burns of the lips, chin region, cheeks, when the formation of a tissue defect is expected, the plastic material should be prepared and moved in advance for faster (later) elimination of it. To prevent cicatricial contractures, functional methods of treatment and the correct position of the patient in bed are of great importance.The most severe consequences are IV degree burns, especially with damage to the facial bones. Eliminating them requires multistage reconstructive surgery. Only burns of I and II degrees heal without a trace.

Mortality from burns depends on their size, depth and age of the victim. To predict the outcome of a burn, they use the rule of hundreds. The total area of ​​the burn as a percentage should be added to the patient’s age. The prognosis is unfavorable if the sum is 101 or more, doubtful – 81-100, relatively favorable – 61-80, favorable – 60.This rule applies only to adults.

ELECTRIC BURNS

Electric burns occur at the point of contact of tissues with a source of electric current, where electrical energy is converted into heat, creating a temperature of up to 3000-4000 ° C. Along with local changes, the functions of various organs are disrupted, primarily the cardiovascular system and respiration. Even with short-term exposure to electric current, respiratory arrest and fibrillation of the heart muscle can occur. Electrical trauma is accompanied by convulsive muscle contraction without loss or with

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loss of consciousness (I and II degree of severity, respectively), loss of consciousness and impaired heart function (III degree) and leads to clinical death (IV degree).

If a burn occurs during an electric shock, the severity of the electrical injury may not be as pronounced, since the charred tissue becomes an insulator.

Atmospheric electricity (lightning) has greater strength and tension and causes more severe damage than conventional “electricity”.

Electric burns of the face account for 1.3% of burn wounds. They differ from the usual thermal ones and, depending on the area of ​​contact of the skin with the source of electricity, they can be pointlike (in the form of “current marks and signs”) or have significant dimensions.”Current signs” are represented by dry, shiny, painless areas of the skin of a whitish-gray or brown color. They contour well, rising above the surface of unaffected skin. Subsequently, these areas turn into a dense scab. In case of lightning strikes, “current signs” look like branchy red lines. Electric burns are often deep, affecting not only the subcutaneous fatty tissue, but also the muscles and even the bones of the facial skeleton. Their feature is also the fact that skin lesions can be local, and the underlying tissues – more widespread in area.This is due to the unequal electrical conductivity of various tissues and developing circulatory disorders. It is known that facial skin has the highest electrical resistance. The wound process proceeds in the same way as with thermal burns. However, due to the significant destruction of the underlying tissues, there are signs of severe intoxication. In the case of the addition of a purulent infection, deep abscesses (abscess, phlegmon) may develop. Possible erosive bleeding from large vessels 2-4 weeks after electrical injury.The burned surface of the face, formed as a result of the contact effect of an electric current, is painless or not very painful. There is no tissue edema and skin hyperemia around the burn. The wound is resistant to the action of purulent microflora. Expressed trophic disorders, which predetermines a slowdown in tissue regeneration (Fig. 125).

First aid is primarily to stop the action of electric current on the victim in any way possible, excluding the damage to the one who is providing assistance.In the absence of spontaneous breathing and heart contractions, cardiopulmonary resuscitation should be performed (closed heart massage, artificial respiration using the mouth-to-mouth or mouth-to-nose method). Transport the victim to

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Fig. 125. Electric burn of the right half of the face (IV degree).

, the hospital should be in a horizontal position and, regardless of the severity of the electrical injury, be hospitalized in the intensive care unit. Local treatment of electric burns and deep thermal burns does not differ significantly from those already stated.

CHEMICAL BURNS

Chemical burns as a result of accidents at home or at work occur when acids (nitric, sulfuric, hydrochloric, hydrofluoric), alkalis (caustic soda, caustic potash, quicklime), heavy metal salts (silver nitrate, zinc chloride) come into contact with the skin … The depth of the burn depends on the concentration of the chemical, its temperature, and the duration of its contact with the skin.

Chemical burns are different from thermal burns. Their features depend on the nature of the chemical agent.Acids are coagulants and alkalis are thinners. Acids and alkalis disrupt microcirculation and trophism in healthy tissues surrounding the burn area. Therefore, with chemical burns, wound healing proceeds much slower than with thermal. Burns with acids and salts of heavy metals proceed as coagulation (dry) necrosis. They cause the breakdown of proteins and a sharp dehydration of tissues, which leads to the formation of areas of coagulated tissues. In case of burns with sulfuric acid, affected

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leather turns brown or black, salty yellow, hydrofluoric dirty gray or white.With alkali burns, colliquation (wet) necrosis develops. Alkalis break down proteins to form alkaline proteins and saponify fats. When in contact with the skin, they destroy the epidermis first, which causes the appearance of bright pink erosions on it. Then alkalis penetrate into deep-lying tissues, damaging them. Tissues that have undergone necrosis contain alkali for several days, forming highly absorbable toxic albuminates. Alkalis act more slowly, last longer and penetrate deeper into tissues than acids.Therefore, the depth of burns with alkalis can be established at a later date than with thermal burns or burns with acids.

When providing assistance, it is necessary to remove the chemical from the skin as quickly as possible, reduce its concentration, and cool the damaged tissue area. The simplest, most accessible and quite effective is the washing of the damaged area with running water for at least 20-30 minutes. The exception is burns with quicklime, concentrated sulfuric acid.These substances, when in contact with water, give a chemical reaction with the release of heat, which can cause additional thermal damage to tissues. Do not use water for burns with diethylaluminum hydride and triethylaluminum, which, when combined with it, ignite.

When providing first aid, it is not always possible to wash the burn surface with neutralizing solutions (weak sodium bicarbonate solutions, 0.01% hydrochloric acid solution, 1-2% acetic acid solution), since their preparation leads to a loss of time.In this situation, the time factor is of decisive importance for the outcome: the earlier the chemical is removed, the less tissue will undergo destruction. In addition, the first aid provider and the victim himself are often unaware of the chemical nature of the substance that has come into contact with the skin. It also makes it difficult to use neutralizing solutions outside the hospital.

In a hospital, when the nature of the chemical agent is known, it must be neutralized. This is due to the partial penetration of acid or alkali (more often) into the thickness of the skin and into the subcutaneous fatty tissue, even with jet washing with water during first aid.To neutralize acids, use a 2-5% solution of sodium bicarbonate in the form of a lotion, to neutralize alkalis – weak solutions of acids (1-2% solution of acetic, citric, etc.). If the victim is delivered late, pastes made of appropriate substances are applied to the burn surface.

If there are signs of intoxication with chemical substances due to their resorptive action, deintoxication therapy is carried out, appropriate antidotes are prescribed.

Topical treatment of chemical burns does not differ from therapy for thermal burns.

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FROST

Frostbite is caused by low temperatures. On the face, frostbite is most often exposed to the nose, ears, tissues of the zygomatic region, and cheeks. Cartilage suffers from the action of low temperature even with minor skin lesions. Perichondritis may develop, which last for a long time and lead to deformation of the auricles or nose. The bones of the facial skeleton are rarely affected by frostbite. There are frostbites of the tongue and lips (more often in children) as a result of contact of these tissues with metal in the cold (an attempt to lick a metal object).In case of violation of natural and artificial thermoregulation, frostbite of tissues is possible in conditions of high humidity at moderately low temperatures. When exposed to low temperatures, the lesion spreads deep into the tissues, and not over the surface. Frostbite of facial tissues is rarely an indication for hospitalization. In outpatient practice, they are observed in half of patients with frostbite. During the Great Patriotic War, 0.69% of those treated for frostbites in hospitals had single frostbite of the face.Severe frostbite of the face is extremely rare as a result of prolonged contact exposure to low temperatures on the tissues.

There are two periods in the development of pathological changes in tissues during frostbite: a) pre-reactive, or the period of tissue hypothermia, b) reactive, which occurs after tissue warming. It is the second period that determines the nature of the clinical manifestations of the disorders that have arisen, caused first by spasm, and then by thrombosis of the blood vessels.

In the pre-reactive period, patients note tingling, burning, pain in the area of ​​the face that has been exposed to low temperatures, then anesthesia in these areas.Victims most often do not notice the onset of frostbite. Objectively, in this period, one can note a sharp pallor of the skin, a decrease in local temperature at the affected area, and the disappearance of pain sensitivity.

After warming the frostbitten tissues, severe pain and other objective signs appear, the severity of which depends on the severity of the injury.

Depending on the depth of the lesion, 4 degrees of frostbite are distinguished.

I degree. Tissue death does not occur, all changes are reversible.Patients complain of itching, stitching, severe pain intensity, burning, feeling of numbness and crawling creeps (paresthesia). The skin is hyperemic, with a bluish tinge (marbled). Swelling of tissues is pronounced. Pain sensitivity is reduced. These changes are eliminated within 3-7 days, after which the epidermis peeling is noted for some time.

II degree. The epidermis dies. Complaints are the same as in 1st degree frostbite, but the pain intensifies at night and persists for 2-3 days.The dead epidermis exfoliates, and single or multiple blisters are formed. They are filled with

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Star Hunter – Express News

An EN correspondent met with a Belarusian stalker.

When you see a shooting star in the sky, it is customary to make a wish. Not only lovers know about this. Peering into the blazing horizon, people ask for health, fame, or money. The hero of our story addresses the sky with similar requests.But he looks at the meteorites with a notebook and a compass in his hands.

FROM SANITATION TO THE STARS

Andrey Bubnov is a unique person in his own way. He is not a scientist or an inventor, he is an ordinary plumber. Have you ever seen a plumber who dreams of the stars? Andrey has been dreaming about them since childhood. But he is ready to be content with even a small piece of his dream.

During the day, Andrei fiddles with German plumbing, and in the evening he wanders through the woods. A simple Orsha plumber is a stalker.The one that the Strugatsky brothers once dreamed of. Meteorites are something of a hobby for Bubnov.

– In order to get rich, desire alone is not enough. You also need experience and patience. And that, and the other, I sipped pretty well. I gained experience in Russian institutes, and patience came in a forest ditch.

The universe for a stalker begins in the Orsha forest. The place is wondrous and mysterious. In these forests lies a huge boulder Semigayun. He became famous for his healing properties in the Middle Ages, allegedly curing seven brothers from the plague.According to legend, the patients went down to Orsha by boat, along the course of the Dnieper. They decided not to go to the city, but to spend the night in the forest. There was a heavy downpour at night. The brothers woke up to find that the huge boulder remained miraculously dry. The brothers warmed up near the stone, and when they got up in the morning, they felt that the deadly disease was gone. Since then, the sick, the crippled and the wretched go to the stone. In summer, not a drop of rain will fall on Semigayun, while in winter the snow is afraid of the stone, lying at a distance.

While walking through the woods, Andrey came across mossy boulders.A map was engraved on them. Who and when created it is a mystery. This common forest clearing, where our ancestors worshiped pagan gods, is a kind of anomalous zone. Psychics, who have been in the clearing for several years, have always seen the same picture – black monks wandering south. In addition, outlandish boulders literally attract small things. Every time Andrei comes to the clearing, something disappears from him. Lighter, pen, or copper coins.

But all this does not frighten Andrey.A forest clearing is an ideal place to watch the starry sky. The stalker brings with him a metal detector and a special tripod with two LEDs. An unusual device is used to calculate the trajectory of a meteorite fall. Simple formulas of the hunter for the stars were taught in Moscow institutes. Andrey did not graduate from any faculties and courses. And sometimes natural flair helps. He says that if it hovers over your head, it means that it is your meteorite that is flying, it will fall nearby. And after what he struck on the horizon, it’s useless to chase.All the same – it will collapse in 200-300 kilometers.

EXACT CALCULATION

In Russia, all those falling from the sky are dealt with by a special Committee on meteorites. The Committee knows about the Belarusian stalker firsthand. At one time, a boy from Orsha brought dozens of poods of selected Belarusian stones to Russian scientists. I thought I had found a meteorite. Someone from local ethnographers put forward a theory according to which it turned out that the Vitebsk land was simply crammed with meteorites. The land was turned into a “treasury” by a glacier that stopped at the Dnieper floodplain more than two thousand years ago.While it was melting, all the meteorites falling to it, along with the flowing waters, rolled down to the Dnieper. Andrey Bubnov checked the theory. He took a shovel and went to dig in the mud. From time to time I went to Moscow – to show the found stones. Two months later, the Russian professors howled and happily taught Andrey to do the primary chemical test on his own. In order to confirm the cosmic origin of an object, it is necessary to identify at least the slightest signs of iridium in its body. Iridium is a rare earth metal (it was discovered in 1803, it occurs in nature in the form of osmous iridium – grains of white color and great hardness, has the color of polished steel, is fragile, does not dissolve in any acid – approx.auth.). It’s harder to find than gold or even platinum. Iridium is almost always found in meteorites. In very small proportions. From one kilogram of space stone, two or three thousandths of a gram can be scraped off at most. Hunters use iridium as a reference point, a kind of quality mark. Fortunately, it is not difficult to identify the metal. It is enough to drop a special cheap chemical on the meteorite. In Moscow, “candidates” for meteorites go through a more complex and careful selection. Naturally, not free. You have to pay for all tests out of your own pocket.

– I have never come across rare meteorites for eight years. – Andrey says with annoyance. – As well as other hunters. That’s why they are rare. Belarus is unlucky. The best meteorites fall in America, Mexico. But if I am ever lucky, I will immediately become a millionaire and for the rest of my days I will forget about the current toilet bowls and sinks.

If the stalker brings a rare meteorite, scientists can offer the hunter an exchange: donate a quarter of a stone. You share – you get a special quality certificate.Selling a meteorite is not a problem with him. You can even list it on the E-bay online auction.

DREAM PRICE

Belarusian meteorites cannot be called running. Mostly chondrites – the cheapest and most widespread meteorites – fall from the sky onto the long-suffering earth. They are an incredible alloy of all the elements of Mendeleev’s periodic table. Unfortunately, chondrites do not live long in the earth’s atmosphere. Oxygen and water destroy the cosmic structure in a matter of years.A kilogram traveler can last ten years at most. Now chondrites are littered with storage facilities of space museums around the world. So at auction for a puny meteorite body will not give more than a hundred dollars.

Fragments of solid lunar rocks sometimes reach the Earth. In the classification of meteorites in terms of price and quality, they occupy an honorable third place. The second got to the moon dust.
Belarusians are not interested in debris of stars. The small collection of meteorites possessed by the National Academy of Sciences does not match what the Russians managed to collect.They even have moon dust. It was brought in by American astronauts. Lunar dust has recently come on sale when NASA sold a portion of the “lunar” stock to selected museums. The Russians got it too. The price of one gram of dust fluctuated around 160-200 thousand dollars.

Most meteorites fall to the ground in August and September each year. At this time, the Earth passes through small asteroid belts. Most of the space stones do not reach the ground – they melt in the atmosphere. Units capable of withstanding temperature extremes and impact on the ground are landing.The “sweetest” time for stellar stalkers comes when a large comet wanders into the solar system.

By the way, the ISS, dangling in orbit, regularly throws its “meteorites” to the hunters. Pieces of rubbish, excrement and other junk in a melted state look very attractive. Some Western collectors offer very substantial sums for the excrement of astronauts. Unfortunately, most of it burns out in the atmosphere, and stalkers get very small specimens that are not worth a dime.

STARS FOR SALE

Selling a meteorite in our country is not easy. Stalkers deal mainly with resellers. Only two or three people buy meteorites in Belarus. Andrei Bubnov keeps their names in the strictest confidence. Underground trade in meteorites is a punishable occupation. But the stalker has no other choice. In order to legally put a find up for auction, you need to shell out several hundred dollars. Simple chondrite will not pay off such costs. On the E-bay, a maximum of $ 50-100 will be given for it.And even then only with a certificate and a heap of references. The buyer does not ask unnecessary questions and does not require documents. The necessary analyzes are carried out in the presence of a stalker on an ordinary kitchen table. The black price of chondrite is $ 3 per gram. Minor, of course, but you don’t have to choose. It is problematic to take a meteorite abroad on your own. Customs is on guard. A stone in a travel bag will attract more attention at the border than a kilogram of drugs.

CARRIERS OF LIFE?

Some Western biologists swear that meteorites are potential carriers of alien life.The pores of the same chondrites contain scraps of amino acids. They are so small that there is no need to talk about full-fledged genetic material. But everything is possible in the Universe. Scientists are aware of several types of microorganisms that are able to travel in conditions of space cold and vacuum. Andrei Bubnov says that he found an unusual reservoir near Borisov, in which a lungfish lives. A small swamp was formed allegedly from the fall of a multi-ton meteorite. It’s hard to say when he fell.Despite the absence of underground springs and waterways, the lake breeds new life with enviable constancy. Even during a drought, when the lake dries up completely. After the first rain, a fish appears in the meteorite reservoir. Now, says Andrei, local residents have begun to use the reservoir for washing. The pungent powders almost finished off the unique fishy look. Bubnov did not agree to name the exact location of the lake. He is ready to reveal the secret only to scientists and only in exchange for a place in the research group.The stalker dreams of using modern scientific equipment. Now Andrey has only an old Soviet metal detector in his hands. There is a sticker on its body: “Radiation control”. Andrey laughs:

– I pasted it on for the district police officer. We have a strict search work here. The police are furious, they are looking for all black diggers.

For eight years of walking in the woods, Andrei Bubnov found only four meteorites. For star hunters, this is a good result. By the way, about ten years ago, a fragment of a star almost finished off a young Orsha citizen.A red-hot meteorite swept a meter away from the man and went into the forest thicket. A stunned eyewitness found a stone. It got stuck in the resinous trunk of a spruce. Andrey says that the meteorite went to one of the school’s museums in the city. Bubnov is still going to examine the old find. Suddenly it turns out that the schoolchildren are keeping a priceless treasure behind the glass. But the stalker does not really count on chance. He says happiness with your own hands and then you need to get it. Museums are for visual aid. To know what and when fell on the Earth.And so, there are enough stars in the sky for everyone …

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