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A 24-Year-Old Man with Spontaneous Right Tension Pneumothorax Presenting with Abdominal Pain with an Initial Symptomatic Diagnosis of Acute Pancreatitis
Unusual clinical course, Challenging differential diagnosis, Clinical situation which can not be reproduced for ethical reasons
- 1 Department of General Surgery, Urology and Anesthesia, Faculty of Medicine, The Hashemite University, Zarqa, Jordan
- A Study design/planning
- B Data collection/entry
- C Data analysis/statistics
- D Data interpretation
- E Preparation of manuscript
- F Literature analysis/search
- * Corresponding author: [email protected]
- 2 Department of Thoracic Surgery, Hirslanden Clinic Beau Site Bern and Lindenhof Hospital, Bern, Switzerland
- 3 Division of Thoracic Surgery, University of Bern, Bern, Switzerland
DOI: 10.12659/AJCR.939036
Am J Case Rep 2023; 24:e939036
- * Corresponding Author: Mohammad Al-Hurani, e-mail: oj.ude.uh@om_fdammahom
- Submitted: 22 November 2022
- Accepted: 01 March 2023
- In Press: 08 March 2023
- Published: 09 April 2023
This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International ( CC BY-NC-ND 4.0 ) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
BACKGROUND: Tension pneumothorax (TP) is a medical emergency resulting in air accumulation in the pleural cavity of the affected side. Later, this air applies pressure on the mediastinal structures, leading to a shift of these structures toward the contralateral side. This shift results in a picture of obstructive shock with a possibly fatal consequence if not detected and treated early. Treatment should not await radiological confirmation, and the red flags in the history and physical examination are enough to proceed with decompressing the affected hemithorax with a large-bore needle. Usually, patients with TP present to the Emergency Department with pleuritic chest pain and shortness of breath, but rare presentations are still possible.
CASE REPORT: We report a case of a 24-year-old male patient with TP who presented to the Emergency Department with severe epigastric abdominal pain with a clinical picture of acute pancreatitis. X-ray showed a right-sided TP. Immediately, we performed a needle decompression followed by chest tube insertion. Four days later, the patient was discharged home uneventfully.
CONCLUSIONS: In this case report, we aim to draw the attention of physicians in the Emergency Department to the need to consider the possibility of upper abdominal pain elicited by chest pathologies. Furthermore, we need to investigate the effect of TP on coronary perfusion.
Keywords: Chest Pain, Pneumothorax, Thoracic Surgery, Male, Humans, young adult, Adult, Acute Disease, Pancreatitis, Thorax, Abdominal Pain
Pneumothorax is an accumulation of air in the pleural cavity. It can result from trauma to the chest cavity (traumatic pneumothorax) or underlying disease (secondary spontaneous pneumothorax), while in cases of no identifiable underlying etiology, it is called primary spontaneous pneumothorax (PSP) [1]. PSP is a common cause of pleuritic chest pain and dyspnea in tall young men [2]. It usually results from a ruptured lung bullae or bleb [2].
All pneumothoraces, regardless of the etiology, can present without mediastinal displacement (simple pneumothorax) or with mediastinal displacement (tension pneumothorax [TP]), which is considered a fatal condition if left untreated [1,3].
Usually, we diagnose pneumothorax using radiological imaging, including X-ray and computed tomography, except for tension pneumothorax, which is a clinical diagnosis that should be managed initially with needle decompression and then chest tube insertion.
We report the case of a 24-year-old healthy male patient who presented to the Emergency Department (ED) complaining of acute onset of severe epigastric abdominal pain due to right-sided TP.
Case Report
A 24-year-old male patient, with unremarkable medical or surgical history except for heavy smoking, presented to the ED with severe epigastric abdominal pain of a 4-h duration. The pain started suddenly in the epigastric area of the abdomen, with radiation to the back. The pain was continuous and increasing in intensity over time, with mild pain relief when leaning forward. Additionally, it was associated with dyspnea but without any chest pain. On arrival, the patient’s vital signs were within normal limits, except for his heart rate, which was 130 beats per min. His temperature was 37.2°C, blood pressure was 100/70 mmHg, and oxygen saturation was 92%. On examination, he had tenderness in the epigastric area; otherwise, his abdominal examination was unremarkable. After the history taking and physical examination, blood samples were sent to the biochemistry laboratory. The laboratory tests included complete blood count, kidney function test, lipase, liver function test, serum glucose, C-reactive protein, and cardiac enzymes. All his laboratory tests were within normal ranges except for a slight elevation in white blood count (14×109/L) (reference range: 4–11×109/L). Furthermore, an electrocardiogram was performed and did not show any abnormality. Subsequently, an abdominal X-ray was ordered to rule out any free air under the diaphragm due to perforated viscus. Surprisingly, right tension pneumothorax was obvious on his X-ray (Figure 1). Immediately, the decision to decompress the right pleural cavity with a large-bore needle was made. Later, definite treatment with a chest tube was performed in the right triangle of safety. After that, complete resolution of his symptoms was observed, and his right lung regained full expansion (Figure 2). Then, the patient was admitted to the surgical ward in the hospital. Four days later, he was discharged home free of any symptoms.
In this report, we aim is to draw the attention of physicians to the need to never neglect pathologies originating from the chest, neither during history taking nor in physical examination of patients presenting with acute upper abdominal pain. Acute abdominal pain is among the most frequent causes of ED visits. Abdominal pain located in the upper abdomen can result from gastrointestinal pathologies of foregut embryological origin or pathologies related to the cardio-thoracic organs, like inferior myocardial infarction (MI) or lower lobe pneumonia. Upper abdominal pain as the main symptom of pneumothorax has only rarely been described in the international literature, and although 3 hypotheses attempt to explain this rare presentation [4], no hypothesis has been proven yet. The first hypothesis claims that the pain originates from depression of the diaphragm on the affected side in patients with TP [5]. The second hypothesis attributes the pain to a small pleural effusion on the affected side [2]. Furthermore, the third hypothesis relates this pain to traction applied to the pulmonary ligament due to lung collapse [6].
However, we hypothesize another explanation that depends on understanding the pathophysiology of TP; namely, displacement of mediastinal structures will affect the filling of the heart, leading to obstructive shock. Consequently, this can also affect cardiac muscle perfusion, giving a clinical picture of inferior MI that presents as epigastric pain [7]. Since we already considered MI in the differential diagnosis, an electrocardiogram and cardiac enzymes were performed, and all were normal.
PSP is a common disease in tall young men. Its etiology relates to a rupture of a lung bulla or lung blebs, which results in the accumulation of air in the pleural cavity leading to pneumothorax [2]. If the volume of leaking air is significant, this can lead to the development of TP.
TP is considered a red flag that should be caught during the primary assessment of any patient. Postponing the treatment of this condition until radiological confirmation can result in fatal consequences due to the obstructive shock that could develop. Subsequently, there is no rule for conservative treatment in patients with TP; the conservative treatment is preserved for those with uncomplicated PSP [8]. In our case, the initial treatment consisted of needle decompression of the affected side, followed by chest tube insertion once the patient was stabilized.
We searched PubMed and have identified 5 cases of SP presenting with abdominal pain as the main symptom [2,4–6]. All except 1 were treated only with chest tube insertion, without any need for further surgical intervention [2,4–6]. Only 1 case presented as right upper quadrant pain mimicking acute cholecystitis [2], while the other 4 cases presented as epigastric abdominal pain. Furthermore, only 2 cases were documented to have TP, while the other case reports did not mention the development of TP. Additionally, all the reported patients were at young ages with no underlying cause except in the case reported by Mizumoto, in which the patient was a known case of COPD [4]. Interestingly, the patient was treated conservatively [4].
Conclusions
TP rarely presents as epigastric abdominal pain, especially in the case of SP. The differential diagnosis of upper abdominal pain should always include cardiothoracic pathologies. Therefore, careful history taking and examination performance are crucial as they lead to the correct diagnosis in most cases. Moreover, further studies are needed to investigate the effect of TP on coronary perfusion.
References:
1.. Jalota Sahota R, Sayad E, Tension pneumothorax: StatPearls [Internet], 2022, Treasure Island (FL), StatPearls Publishing [Updated 2022 Nov 28]
2.. Lien WC, Yuan A, Tsai KC, Primary spontaneous pneumothorax with clinical manifestation mimicking acute cholecystitis: J Emerg Med, 2004; 26(3); 354-56
3.. Rojas R, Wasserberger J, Balasubramaniam S, Unsuspected tension pneumothorax as a hidden cause of unsuccessful resuscitation: Ann Emerg Med, 1983; 12(6); 411-12
4.. Mizumoto J, Pneumothorax presenting as epigastric pain: J Gen Fam Med, 2021; 22(5); 291-92
5.. Hollins GW, Beattie T, Harper I, Little K, Tension pneumothorax: Report of two cases presenting with acute abdominal symptoms: J Accid Emerg Med, 1994; 11(1); 43-44
6.. Ogawa R, Yamamoto Y, Haraguchi N, Spontaneous pneumothorax presenting as epigastric pain: Am J Emerg Med, 2005; 23(4); 572-74
7.. Culić V, Mirić D, Eterović D, Correlation between symptomatology and site of acute myocardial infarction: Int J Cardiol, 2001; 77(2–3); 163-68
8.. Brown SGA, Ball EL, Perrin K, Conservative versus interventional treatment for spontaneous pneumothorax: N Engl J Med, 2020; 382(5); 405-15
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Pneumothorax
Author: Doug Franzen, MD, M.Ed., University of Washington School of Medicine
Edited by: Benjamin J. Sandefur, MD, Mayo Clinic College of Medicine and Science
Updated: November 2019
A 29-year-old male presents to the ED complaining of the sudden onset of left sided chest pain and dyspnea that started while he was playing basketball. He denies any medical problems and takes no medications. He speaks in short sentences as he answers your questions. You note his vital signs: BP 124/68, HR 94, RR 18, sPO2 99% on room air. You have been working on focusing your assessments and considering the questions:. What are the main concerns in this patient? How do you focus your history and exam? What tests will help make the diagnosis? Should any treatments be started prior to definitive diagnostic testing?
- Discuss pneumothorax as part of the differential diagnosis of chest pain and/or shortness of breath
- Recognize the common exam findings in patients with a pneumothorax
- Recognize both the radiographic and ultrasonographic findings associated with pneumothorax
- Describe different treatment options for a pneumothorax
Introduction
A pneumothorax occurs when a pleural defect allows the potential space between the parietal and visceral pleura of the lung to fill with air, which subsequently collapses the lung. Pneumothoraces can occur spontaneously or as the result of trauma. They are also a potential complication of multiple procedures and positive pressure ventilation.
Pneumothoraces can be classified as “simple” or “tension.” A simple pneumothorax is non-expanding. In a tension pneumothorax, a “one way valve” defect allows air into but not out of the pleural space. If left untreated, increasing pressure starts to collapse vascular structures within the mediastinum. As pressure builds, venous return to the heart decreases, eventually leading to an obstructive shock state, with hemodynamic collapse and cardiac arrest. Prompt diagnosis and treatment of a pneumothorax is essential.
Spontaneous pneumothorax should be considered in non-trauma patients who complain of dyspnea and/or chest pain. Symptom onset is usually sudden. Other diagnoses that may present similarly to a spontaneous pneumothorax include acute coronary syndrome, thoracic aortic dissection, and pulmonary embolism, as well as pneumonia, pleurisy, and pericarditis. Traumatic pneumothoraces (including iatrogenic) will also present with chest pain and dyspnea, but in temporal proximity to a traumatic event or invasive procedure.
For further discussion of traumatic pneumothorax, see the Chest Trauma section.
Initial Actions and Primary Survey
Before performing a lengthy history and physical examination, the clinician must first consider, diagnose, and treat a tension pneumothorax. Chief complaints of chest pain or shortness of breath suggest pneumothorax. Vital sign abnormalities that increase suspicion for tension pneumothorax include tachycardia, tachypnea, hypoxia and hypotension. Decompensation shortly after the initiation of positive pressure ventilation is highly concerning for an expanding pneumothorax. Breath sounds and respiratory status should be assessed as part of the primary survey. Findings that suggest tension pneumothorax include unequal breath sounds (diminished or absent on the side of the pneumothorax), tracheal deviation (away from the side of the pneumothorax), distended neck veins, and/or signs of respiratory distress. In intubated patients, additional signs of tension pneumothorax include high airway pressures or difficulty bagging.
If signs suggestive of a tension pneumothorax are found, immediate decompression is indicated. Most of the findings noted above are late findings – do not wait for them to appear before taking action.
Presentation
Spontaneous pneumothorax should be considered in patients presenting with dyspnea and/or chest pain. The pain usually begins suddenly and is described as sharp and unilateral, with associated shortness of breath. Patients may also complain of a cough. The pain is often initially pleuritic but may become dull and aching with time. Occasionally the pain is more prominent in the back and shoulder. The degree of dyspnea may increase over time as the pneumothorax increases in size.
A thorough past medical history is important in the evaluation of spontaneous pneumothorax. A spontaneous pneumothorax can be classified as either primary or secondary. A primary pneumothorax occurs in patients that have no underlying pulmonary disease. It is most common in thin, young males with a history of tobacco use. Smoking increases the risk of primary pneumothorax 9-fold in women and 22-fold in men. Cannabis smoking also increases the risk of pneumothorax. A secondary pneumothorax occurs as a result of other underlying disease, most commonly COPD, but also including cystic fibrosis, lung cancer or Marfan syndrome. If the patient has had any recent procedures, iatrogenic pneumothorax should be considered. The most common procedures to cause a pneumothorax include central line placement, thoracentesis, pacemaker placement, tracheostomy, or biopsy. Other causes include CPR and positive-pressure ventilation.
Vital sign abnormalities in patients with pneumothorax can include tachycardia, tachypnea and, depending on the severity, hypoxia and hypotension. Sinus tachycardia is the most common early finding.
In addition to the findings suggestive of tension pneumothorax discussed above, other physical exam findings that can be seen in patients with pneumothorax include diminished or absent breath sounds, hyperresonance with percussion (the side with the pneumothorax will resonate more), asymmetric chest wall excursion (decreased excursion on the affected side), and loss of tactile fremitus on the affected side of the chest. The chest wall should be palpated and any crepitus or signs of trauma should be noted. In addition to a thorough lung exam, look for signs of respiratory distress (nasal flaring, accessory muscle use) and findings suggestive of potential contributing causes, such as nail clubbing.
Diagnostic Testing
As noted above, if tension pneumothorax is suspected and the patient is unstable, proceed immediately to decompression – do not wait for imaging to confirm the diagnosis.
Pneumothorax is classically diagnosed with a chest x-ray. The sensitivity of plain films varies from study to study, from well below 50% to a high of about 80%. Supine films are less likely to detect pneumothorax; upright films improve the sensitivity. A lateral decubitus film is the most sensitive view, able to detect as little as 5mL of air in the pleural space. The classic findings of pneumothorax on chest radiography are a white, visceral pleural line that is parallel to the chest wall, with a loss of vascular lung markings distal to the line, i.e. between the chest wall and the pleural line.
Figure 1a – chest x-ray with pneumothorax. Image used with permission of Joel Gross, MD
Figure 1b – pleural line highlighted in red, demonstrating left pneumothorax
On a supine film, air layers out across the anterior chest wall and the classic findings above are not seen. Instead, a “deep sulcus” suggests pneumothorax. A deep sulcus is a large, lucent costophrenic angle, extending more inferiorly than expected on the affected side.
Figure 2 – Deep Sulcus Sign due to right pneumothorax.
Multiple studies have shown that ultrasound is more sensitive than plain films in diagnosing pneumothorax, with the sensitivity of ultrasound approaching that of CT. To evaluate for pneumothorax with ultrasound, have the patient lay supine. Place a linear (vascular/soft tissue) probe in the most anterior point of the chest wall, usually at about the 3rd or 4th intercostal space. The probe should be oriented perpendicular to the ribs (usually marker dot towards the head). A bright white pleural line will be visible just deep to the ribs. In a normal lung you will see the sliding movement of the pleura and a “comet tail” artifact as the patient breathes. These findings are due to the apposition of the two pleural layers. Because air separates the two pleural layers in pneumothorax, absence of these normal findings is diagnostic for pneumothorax.
Figure 3 – ultrasound of the anterior chest wall using a linear probe. Note the bright white pleural line visible between and just deep to the ribs. Image used by permission of Doug Franzen, MD
Figure 3a
M-mode can also be used to diagnose pneumothorax. In a normal lung, ultrasound passes through the pleura and the multiple air/tissue interfaces of the alveoli result in a “seashore” appearance. A pneumothorax creates a reverberation artifact beneath the bright pleural line, creating a “bar code” appearance due to multiple bright A-lines.
Figure 4 – M-Mode: Seashore (normal - left image) vs. Barcode (pneumothorax - right image)
Images used by permission of Doug Franzen, MD
CT scan is the gold standard for detecting pneumothorax, but is rarely necessary in evaluating spontaneous pneumothorax, as a pneumothorax too small to be detected by other modalities is unlikely to need intervention. More often, a pneumothorax is seen on a CT that has been ordered to evaluate for other processes such as pulmonary embolism when an initial chest x-ray is non-diagnostic. CT can be useful to differentiate between a large bulla and pneumothorax in patients with underlying lung disease.
Figure 5 – Pneumothorax as seen on CT
Tension pneumothorax should be treated immediately. Needle decompression can be rapidly achieved in most settings. A large-bore (14g) angiocatheter can be placed in either a) the 2nd or 3rd intercostal space at the midclavicular line or b) the 4th or 5th intercostal space at the anterior axillary line. Lateral placement is recommended in obese patients, as the catheter may not be long enough to pierce the pleura in an anterior placement. If needle decompression is performed, the patient will need definitive treatment with chest tube placement.
Once tension pneumothorax has been excluded, the goal of treatment for simple pneumothorax is relief of dyspnea. Management depends on multiple factors, including the degree of symptoms, size and cause of the pneumothorax, and whether this is the first or a recurrent pneumothorax. Multiple different methods have been proposed to estimate the size of a pneumothorax. One of the simplest is measuring the distance from the chest wall to the visible pleural line.
A simple pneumothorax will spontaneously resolve as the air is absorbed. Supplemental oxygen increases the rate of resorption. For small primary spontaneous pneumothoraces (pleural line < 1-2cm from the chest wall) with minimal symptoms, treatment may consist of 100% oxygen applied for a brief period of observation (3-6 hours), a repeat x-ray to ensure the pneumothorax is not enlarging, and close outpatient follow-up. If the patient is symptomatic, treatment options include aspiration, insertion of a pigtail catheter, or insertion of a small-bore standard chest tube. Aspiration is performed in a manner similar to thoracentesis. Pigtail catheters are smaller and more comfortable for patients than even a small chest tube. If a catheter is placed with a Heimlich or other one-way valve and the patient is reliable, discharge with close outpatient follow-up is a reasonable plan.
Figure 6 –A commercial pigtail catheter, compared to a 24Fr chest tube.
Image used by permission of Doug Franzen, MD
A larger primary spontaneous pneumothorax (pleural line >2-3cm from the chest wall) or any secondary pneumothorax will usually require admission in addition to drainage via catheter or chest tube. Research has shown that patients with secondary spontaneous pneumothorax frequently fail conservative management such as observation or simple aspiration. Caution is advised before draining a secondary pneumothorax, to ensure it truly is a pneumothorax and not a large bleb. Patients with a recurrent pneumothoraces may require a more aggressive management plan such as thoracoscopy and pleurodesis.
Figure 7 – Pigtail catheter placement. Note that the pneumothorax is still present. This patient (the same patient from Figure 1) ultimately required surgical intervention to treat his pneumothorax. Image used with permission of Joel Gross, MD.
Figure 8 – The patient from figure 7, with a chest tube in place. The pneumothorax has resolved. Image used with permission of Joel Gross, MD.
Figure 9 – Resolution of deep sulcus sign after chest tube placement. (This is the patient from Figure 2). Image used with permission of Joel Gross, MD.
Pearls and Pitfalls
- Pneumothorax should be considered in all patients with chest pain and/or shortness of breath
- The classic findings of a tension pneumothorax are late findings.
- Do not wait for a chest x-ray to decompress a suspected tension pneumothorax
- Remember that pneumothorax can be a cause of decompensation in intubated patients, especially after CPR
- Ultrasound is more sensitive than chest x-ray in diagnosing pneumothorax, especially in a supine patient.
A targeted history decreased your concern for most of the items on your differential, other than pneumothorax. Physical exam was notable for decreased breath sounds and hyperresonance to percussion of the left chest. There was no JVD and the trachea was midline. Because the patient was stable, a bedside ultrasound was performed, which demonstrated absence of pleural sliding or comet tails on the left. M-mode ultrasound showed a “bar code” appearance on the left. An upright chest x-ray showed a moderate pneumothorax, with a pleural line approximately 3cm from the chest wall. The patient did not have insurance or a primary care provider. Due to all of these factors, a pigtail catheter was placed, and the patient was admitted for observation with resultant improvement in his symptoms. Repeat x-ray after pigtail placement showed marked improvement in the pneumothorax.
- Alrajab S, Youssef AM, Akkus NI, Caldito G. Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: review of the literature and meta-analysis. Crit Care. 2013 Sep 23;17(5):R208
- Carr JJ, Reed JC, Choplin RH, et al. Plain and computed radiography for detecting experimentally induced pneumothorax in cadavers: implications for detection in patients. Radiology 1992; 183:193.
- Kosowsky J and Kimberly H. Pleural Disease. In: Walls R, Hockberger R, Gausche-Hill M, editors. Rosen's Emergency Medicine: Concepts and Clinical Practice. 9th Ed. Philadelphia: Elsevier. 2018. pp 881-889.
- Nicks BA, Manthey D. Pneumothorax. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com/content.aspx?bookid=1658§ionid=109429615. Accessed April 9, 2019
- Wong A, Galiabovitch E, Bhagwat K. Management of primary spontaneous pneumothorax: a review. ANZ J Surg. 2019 Apr;89(4):303-308.
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Case In Point: Spontaneous Pneumothorax in a Teenage Boy
A 17-year-old Asian male with no significant medical history presented to the emergency department (ED) with acute shortness of breath and associated left-sided chest pain. Symptoms began while the patient was at rest: the pain was sharp and worsened with inspiration. He denied a history of fever, trauma, cough, or any other constitutional complaints.
In the ED, the patient's temperature was 37.8°C (100°F); heart rate was 100 beats per minute; respiratory rate, 28 breaths per minute; and blood pressure, 124/96 mm Hg. Oxygen saturation was 100% on room air. He had no nasal flaring but used accessory respiratory muscles. The trachea was in midline. Breath sounds were markedly diminished on the left side, with good air entry on the right. No crepitus, wheezing, stridor, or crackles were appreciated. Cardiac examination revealed a normal S 1 and S 2 , without any murmurs, rubs, or gallops. Mediastinal shift could not be detected clinically. Chest films showed a left-sided tension pneumothorax ( Figure 1 ).
A chest tube was placed, and symptoms resolved ( Figure 2 ). The patient underwent surgery to resect an apical pleural bleb.
SPONTANEOUS PNEUMOTHORAX
A spontaneous pneumothorax (SP) is a collection of air or gas between the visceral and parietal pleura that causes the lung to collapse in the absence of a traumatic injury to the chest or lung. Primary spontaneous pneumothorax (PSP) occurs in persons with no previously known lung disease. Typically, the cause of this type of pneumothorax is the rupture of a subpleural bleb or cyst in the lung.
A secondary spontaneous pneumothorax (SSP) occurs in persons with known lung disease--most often chronic obstructive pulmonary disease in adults. In pediatric patients, cystic fibrosis, pneumonia, and asthma are the most common causes of SSP. Other conditions less commonly associated with SSP are tuberculosis, cystic adenomatoid malformation, Marfan syndrome, and certain types of interstitial lung disease.
SSP is generally more severe than PSP--and is often life threatening. Mortality associated with SSP is about 15%. 1
Smoking greatly increases the risk of SP. 2 Men who smoke a pack a day or less have a 20-fold increased risk of SP; in women, the risk rises by 10-fold. In men who smoke more than a pack per day, the risk of SP increases more than 80-fold; in women, the risk increases more than 40-fold.
SP also can be an inherited disorder, although this is not common. One literature review described 61 cases of familial SP in 22 families. 3
The major symptom is sudden-onset chest pain with breathlessness. This pain may be dull, sharp, or stabbing; it typically begins suddenly while the patient is at rest. Pain can be associated with dyspnea, tachypnea, and hypoxia; typically, it is exacerbated by breathing deeply or by coughing.
Patients with SSP may also experience dyspnea disproportional to the size of the pneumothorax as well as tachycardia, hypotension, and cyanosis.
DIAGNOSIS AND MANAGEMENT
The diagnosis usually can be made after a detailed history and physical examination. Chest radiographs can confirm the diagnosis and determine the size of the pneumothorax. A recent randomized controlled trial found no advantage for inspiratory/expiratory films. 4
The objectives of management are to eliminate the intrapleural air collection, to facilitate pleural healing, and to prevent recurrence. The treatment of SP is multifactorial and depends on its size, course, and classification. A small pneumotho-rax may resolve spontaneously. Needle decompression or chest tube placement may be needed to facilitate reexpansion when air accumulation is relatively large. Strong- ly consider therapeutic interventions for patients with recurrent pneumo- thorax.
While the treatment options for PSP and SSP are the same, the conditions are managed differently. In asymptomatic patients with PSP who have less than 15% air accumulation, simple observation and administration of 100% oxygen have been successfully used as a treatment option. 1 Oxygen increases the resorption rate of the pneumothorax 3-fold to 4-fold; the greatest increases occur in patients with larger pneumothoraces. The application of oxygen creates a gas pressure gradient between the pleural space and the tissue capillaries that surround the pleural space. This enhances the absorption of nitrogen and other gases within this space. 5
If the pneumothorax is smaller than 15% and if the patient is symptomatic but hemodynamically stable, needle aspiration is considered the treatment of choice. Advantages include its relative simplicity and lack of invasiveness. 6
SSP, on the other hand, can be life-threatening. Most patients are treated with a chest tube. Tube thoracostomy has been advocated for patients with PSP in whom simple aspiration fails--and for most patients with SSP. 1,6 Other more invasive management options include pleural sclerosis (pleurodesis) and video-assisted thoracic surgery (VATS).
Recurrence rates can be high, espeically if SP is untreated. Recurrence rates as high as 30% at 6 months and 50% at 2 years have been reported. 1 More specifically, recurrence rates have been reported at 28% for PSP and 53% for SSP. 1 There is a 15% rate of recurrence on the contralateral side in patients with PSP. Recurrence is more likely in patients who are tall and thin and who smoke; however, there is no relationship with the number or size of apical blebs on CT. Once a recurrence has occurred, the risk for repeated pneumothoraces exceeds 50%. 7
Chest tube insertion helps relieve the pneumothorax and improve symptoms. However, it does not reduce the risk of recurrence as significantly as VATS or pleurodesis. One randomized trial compared simple needle aspiration with tube thoracostomy in the management of first-time PSP. 8 Recurrence rates were measured at 1 week (11% vs 12%), at 3 months (15% vs 8%), at 1 year (22% vs 42%), and at 2 years (31% vs 25%). There were no statistically significant differences between the 2 treatment modalities.
LONG-TERM CARE
Patients who have had SP need to stop smoking and to avoid high altitudes, scuba diving, or flying in an unpressurized aircraft in attempt to limit the risk of a recurrent pneumothorax.
TAKE-HOME MESSAGE
Cardiac causes of pediatric chest pain are uncommon. If the pain is associated with shortness of breath, especially in a thin adolescent who smokes, consider spontaneous pneumothorax (SP). When SP is diagnosed, it is important to differentiate between a primary and secondary cause because management differs.
References:
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1996;166:313-316. 5. Chada TS, Cohn MA. Noninvasive treatment of pneumothorax with oxygen inhalation.
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- CASE HISTORY
A 24-yr-old Caucasian female was evaluated in May, 2003 at the San Martino hospital, Genoa, Italy, for the presence of “sudden onset” chest pain and nonproductive cough. Past medical history was only characterised by the presence of frequent headaches. The patient had been playing competitive tennis from the age of 6–20 yrs and, after retirement from competitions, had been smoking cigarettes (0.5 pack·day −1 ) for the last 4 yrs. The patient was nulliparous and reported the use of oral contraceptive in the last 3 yrs. Any suggestion of respiratory symptoms, including cough, shortness of breath or physical limitations during exercise were denied.
On admission, the patient had no dyspnoea, and physical examination demonstrated a slight decrease in breath sounds over the left hemithorax. Heart sounds were normal and there was no cyanosis, clubbing or oedema. The abdomen was nondistended, nontender, and without bruits, hepatosplenomagaly or masses. There were no focal neurological findings. The patient had normal body temperature with normal values of blood pressure, pulse and respirations and transcutaneous blood gas determination in room air showed normal arterial oxygen and carbon dioxide tension.
A chest radiograph demonstrated the presence of a left-sided pneumothorax. Blood tests were within normal values. After successful chest drainage, the patient was discharged.
After a period of 2 weeks, in June 2003, the patient was evaluated in the outpatient clinic at the G. Gaslini Institute, Genoa, Italy, complaining of a persistent mild pain on the left hemithorax. High-resolution computed tomography (HRCT) scans (figs 1a ⇓ and b) and pulmonary function tests (fig. 3 ⇓ ; table 1 ⇓ ) were performed and a follow-up re-evaluation was planned after 6–7 months. The patient did not complain of any symptoms until mid-December 2003, when a sudden onset left-sided chest pain was again experienced along with mild dyspnoea, but a chest radiograph failed to demonstrate the presence of a pneumothorax or any detectable lung abnormality. Both the chest pain and mild dyspnoea resolved without any treatment in 24 h. As previously planned in June 2003, chest HRCT scans (figs 2a ⇓ and b) and pulmonary function tests (fig. 4 ⇓ ; table 2 ⇓ ) were again obtained in January, 2004 at the G. Gaslini Institute. A lung biopsy was performed and the surgical specimens were sent for morphological evaluation (fig. 5a–d ⇓ ).
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High-resolution computed tomography (CT) scans of the chest at two different levels of thoracic CT cuts performed on first admission to the outpatient clinic.
High-resolution computed tomography (CT) scans of the chest at two different levels of thoracic CT cuts performed on the second admission to the outpatient clinic, 7 months later.
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–volume curves performed on the first admission
–volume curves performed on the second admission, 7 months later
BEFORE TURNING THE PAGE, INTERPRET THE PULMONARY FUNCTION TEST DATA, COMPUTER TOMOGRAPHY SCANS AND LUNG BIOPSY RESULTS AND SUGGEST A DIAGNOSIS.
- INTERPRETATION
HRCT and pulmonary function tests on first admission to the outpatient clinic
Figures 1a ⇑ and b show bilateral small cystic lesions of varying size, although regularly shaped, that are diffusely distributed throughout the lungs. The cystic walls are faintly perceptible. No evidence of interstitial involvement, hilar lymph node enlargement and pleural thickening or effusions was present.
Figure 3 ⇓ shows the flow–volume curve, which demonstrates normal lung volumes, including forced vital capacity (FVC) and forced expiratory volume in one second (FEV 1 ), and a slight decrease in forced mid-expiratory flow (FEF 25–75%).
Flow–volume curve on first admission to the outpatient clinic.
HRCT and pulmonary function tests on the second admission to the outpatient clinic
Figures 2a ⇑ and b show HRCT scans of the chest performed 7 months later, clearly demonstrating a progression of the cystic lesions, and an increase in their number and/or size.
Figure 4 ⇓ shows the flow–volume curve demonstrating normal volumes and flows, including FVC and FEV 1 , and a decrease in FEF 25–75% , with increased values, as compared to those obtained in June, 2003. Carbon monoxide diffusing capacity of the lung ( D L,CO ) and the D L,CO to alveolar volume ratio ( D L,CO / V A ) were also within normal values.
Flow–volume curve on the second admission to the outpatient clinic, 7 months later.
Diagnostic considerations
In the differential diagnosis of the present case, the authors considered the following diagnosis: a) lymphangioleiomyomatosis; b) tuberous sclerosis (TS); and c) Langerhans cell histiocytosis or eosinophilic granuloma (LCH).
Surgical procedure and interpretation of surgical specimens
A left-sided mini-thoracotomy was performed, and multiple subpleural cystic lesions were highlighted. Biopsies of the lingula were obtained and sent to the pathologist for morphological evaluation of lung tissues.
Macroscopic features
The resected lung tissue showed a variety of small cystic lesions with thickened walls in subpleural tissue.
Microscopic features
At low magnification, ill-defined cystic lesions with thickened walls were detected in the lung parenchyma (fig. 5a ⇓ ). At higher magnification, the cyst walls appeared to be infiltrated by proliferating smooth muscle-like cells, which are also present in the alveolar interstitium (fig. 5b ⇓ ). These smooth muscle-like cells stain positive with monoclonal antibodies reacting against anti-smooth muscle actin and show a benign appearance (fig. 5c ⇓ ). A significant proportion of the smooth muscle cells infiltrating the lung parenchyma and the cyst walls show reactivity for the HMB-45 antigens (fig. 5d ⇓ ).
Histological preparations of lung biopsy specimen: a) haematoxylin and eosin staining at lower magnification (scale bar=100 μm); b) haematoxylin and eosin staining at higher magnification (scale bar=100 μm); c) immunostaining with monoclonal antibodies reacting against antismooth muscle action (scale bar=10 μm); and d) immunostaining with the antimelanomaassociated antigen (HMB45) monoclonal antibody (Mab; scale bar=10 μm).
Diagnosis: lymphangioleiomyomatosis.
Clinical course
Staging procedures, including abdomen computed tomography (CT) scans and ultrasonography, failed to demonstrate the presence of renal masses ( e.g. angiomyolipomas) or dilatations of the abdominal lymph vessels due to lymphatic obstruction ( e.g. lymphangioleiomyomas) and chylous ascites.
The patient was then referred to J. Moss, at the Pulmonary-Critical Care Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health (NIH), Bethesda, MD, USA, for further evaluation and follow-up.
The patient had two admissions at the NIH, the first in April 2004, confirming the diagnosis of lymphangioleiomyomatosis (LAM), and lack of pulmonary function abnormalities, also during cardiopulmonary exercise testing. The second visit was in September 2004, when only a mild decrease in the D L,CO values ( D L,CO SB: from 91 to 80%; D L,CO / V A : from 102 to 91%) were detected. The patient was well and did not complain of any symptoms at the time of writing this case study.
LAM is an uncommon parenchymal lung disease characterised by progressive cystic lung lesions, lymphatic tumours, and angiomyolipomas, primarily affecting females of childbearing age 1 – 3 . Onset of symptoms is most common in the 4th decade of life but may occur in late teenage yrs or those aged >60 yrs 1 , 2 , 4 . Diagnosis is made between 8 months and 22 yrs after onset of symptoms 1 , 2 , 4 . The present patient was 24-yrs old, and the diagnosis was established <1 yr after the initial symptoms. Only a small proportion of LAM patients appear to be smokers (as was the patient of the present study) or ex-smokers 2 – 5 .
The presence of proliferating immature-appearing smooth muscle cells (referred to as LAM cells) in the lungs and in the axial lymphatic in the thorax and abdomen is considered the typical pathological hallmark of LAM 5 . Overgrowth of LAM cells may induce compression of conducting airways (leading to obstruction of airflow, air trapping, alveolar disruption, and cystic changes), pulmonary venules (causing pulmonary haemorrhage and haemosiderosis) and of lymphatic vessels (producing chylothorax and chylous ascites) 1 – 3 , 5 . As a result of these changes, the clinical manifestations of LAM include, almost always, pleuro-pulmonary symptoms, such as chylothorax, haemoptysis, nonproductive cough, slowly progressive dyspnoea and recurrent spontaneous pneumothorax 1 – 3 . This latter complication occurs in ∼40–50% of cases 1 – 5 . In the presented case, spontaneous pneumothorax occurred in a very early stage of the disease, when the subject had no respiratory symptoms, normal pulmonary function and limited cystic lung changes. In addition to airway obstruction by proliferating smooth muscle cells, other factors may induce air leaking in the pleural space in LAM patients. These include metalloproteinases expressed and released by proliferating LAM cells, which degrade the extracellular matrix components of the lung and may contribute to the development and, possibly, the rupture of the cysts 6 , 7 .
The cystic lesions are characteristically round and thin-walled, of various sizes, and symmetrically and uniformly distributed throughout the lungs. The appearance of LAM examined by HRCT is quite characteristic, but two disorders should be considered in the differential diagnosis: TS and LCH. Pulmonary involvement in TS is indistinguishable from LAM 8 . However, isolated pulmonary TS, without extrathoracic manifestations, is rare and in the vast majority of cases, other clinical (mental status, skin, family history) and radiology (cranial CT) features are present to help make the correct diagnosis. In contrast, in LCH, a disorder found predominantly in smokers, there are a number of radiographic features (pulmonary nodules, the irregular shape of the cysts, and their uneven distribution, prevalent in the upper and middle lung, with little or no involvement of the lower lobes), which are not present in LAM 9 .
The profusion of cysts may be quantified by CT scans and seem to correlate with impairment of clinical conditions and functional test values 1 , 4 , 5 . Indeed, in LAM, evaluation of pulmonary function typically demonstrates chronic, progressive airway obstruction with increased lung volume and decreased carbon dioxide diffusion 5 , leading to dyspnoea, hypoxaemia and finally to respiratory failure 4 . Since the severity of lung function impairment often closely reflects the structural/functional lung abnormalities, it was not surprising to find normal function values and no exercise-limiting symptoms in a patient with early stage disease, like the patient described in the current study 4 , 5 .
In addition to the lung structures, LAM frequently involves other organs, such as the kidneys ( e.g. angiomyolipomas) and retroperitoneal lymph nodes 3 , 10 . No extrathoracic alterations were detectable in the presented patient.
Light microscopy examination of lung tissue in LAM is characterised by diffuse interstitial proliferation of “immature” smooth muscle cells, frequently located in the wall of enlarged air cavities and, to a larger or lesser degree, making up part of the wall 11 . The proliferating cells are morphologically heterogeneous in shape and size, have a benign appearance and react with antibodies against smooth muscle actin, desmin, and vimentin 11 , 12 . However, in contrast to normal smooth muscle cells, LAM cells and smooth muscle cells of angiomyolipomas react with the anti-melanoma-associated antigen monoclonal antibody (HMB45 Mab), which recognises a 100 kDa glycoprotein (gp100) found in human melanoma cells 11 . Immunohistochemical study with this Mab may useful in the diagnosis, especially when evaluating very early stage disease (as in the patient presented here) or a biopsy specimen containing small numbers of these cells (as in transbronchial biopsy samples) 11 , 12 . LAM cells are heterogeneous with respect to their expression of melanoma antigens; those actively proliferating, which are probably more relevant to the progression of LAM, are more likely to be negative for reactivity with the HMB45 Mab 12 . Haemosiderin deposition in the lung interstitium and the presence of haemosiderin-laden alveolar macrophages are other typical findings of LAM, the degree of these abnormalities being associated with the degree of myomatosis 13 . These changes were not detectable in the lung biopsy of the patient in the current study, possibly due to the early stage of the disease.
The overall prognosis of LAM is not good, due to the lack of effective treatment, other than lung transplantation, and death usually occurs from respiratory failure 1 – 5 , 13 . However, the clinical course of LAM is highly variable. Indeed, in some patients pulmonary function tests show only a slow decline (primarily impaired D L,CO and FEV 1 ) whilst in others, loss of respiratory function is rapid, and the time from the first symptoms to onset of respiratory failure and lung transplantation may only be a few years 1 – 5 .
Numerous strategies have been described to treat LAM 1 – 5 , 8 . As a result of evidence of clinical worsening of the disease during pregnancy and with use of exogenous oestrogens, hormone manipulation has been extensively applied 13 – 15 . However, careful evaluation of studies aimed to evaluate the effects of these therapeutic approaches revealed improvement in chylothorax or chylous ascites, but no changes on the progression of pulmonary involvement and no beneficial effect on the overall course of the disease 1 – 5 , 8 , 15 .
New hopes for LAM patients are based on molecular biology approaches aimed at understanding the molecular signalling pathways responsible for aberrant LAM cell growth and tissue remodelling 16 . These studies have led to the identification of promising molecular targets for therapy, which form the basis for pilot trials now underway in Europe and the USA 17 , 18 .
The patient presented in this case study clearly shows that early lung changes in lymphangioleiomyomatosis may not be detected by plain chest radiography. The availability of new drugs, such as rapamycyn, able to inhibit (at least in vitro ) lymphangioleiomyomatosis cell proliferation 18 , will give rise to questions on the opportunity to perform computed tomography scans in females of reproductive age in case of spontaneous pneumothorax, to detect early stage disease.
- Acknowledgments
The authors would like thank J. Moss, the Pulmonary-Critical Care Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA, for critically reviewing the manuscript.
- Received June 8, 2004.
- Accepted October 13, 2004.
- © ERS Journals Ltd
- ↵ NHLBI Workshop Summary. Report of workshop on lymphangioleiomyomatosis. National Heart, Lung, and Blood Institute. Am J Respir Crit Care Med 1999 ; 159 : 679 –683. OpenUrl PubMed
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- ↵ Taveira-DaSilva AM, Stylianou MP, Hedin CJ, et al. Maximal oxygen uptake and severity of disease in lymphangioleiomyomatosis. Am J Respir Crit Care Med 2003 ; 168 : 1427 –1431. OpenUrl CrossRef PubMed Web of Science
- ↵ Kitaichi M, Nishimura K, Harumi I, Izumi T. Pulmonary lymphangioleiomyomatosis: a report of 46 patients including a clinicopathologic study of prognostic factors. Am J Respir Crit Care Med 1995 ; 151 : 527 –533. OpenUrl CrossRef PubMed Web of Science
- ↵ Hayashi T, Fleming MV, Stetler-Stevenson WG, et al. Immunohistochemical study of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in pulmonary lymphangioleiomyomatosis (LAM). Hum Pathol 1997 ; 28 : 1071 –1078. OpenUrl CrossRef PubMed Web of Science
- ↵ Matsui K, Takeda K, Yu ZX, et al. Downregulation of estrogen and progesterone receptors in the abnormal smooth muscle cells in pulmonary lymphangioleiomyomatosis following therapy. An immunohistochemical study. Am J Respir Crit Care Med 2000 ; 161 : 1002 –1009. OpenUrl CrossRef PubMed Web of Science
- ↵ McCormack F, Brody A, Meyer C, et al. Pulmonary cysts consistent with lymphangioleiomyomatosis are common in women with tuberous sclerosis: genetic and radiographic analysis. Chest 2002 ; 121 : Suppl. 3 61S OpenUrl CrossRef PubMed Web of Science
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- ↵ Maziak DE, Kesten S, Rappaport DC, Maurer J. Extrathoracic angiomyolipomas in lymphangioleiomyomatosis. Eur Respir J 1996 ; 9 : 402 –405. OpenUrl Abstract / FREE Full Text
- ↵ Kaiserling E, Krober S, Xiao JC, Schaumburg-Lever G. Angiomyolipoma of the kidney: immunoreactivity with HMB-45: light- and electronmicroscopic findings. Histopathology 1994 ; 25 : 41 –48. OpenUrl PubMed Web of Science
- ↵ Matsumoto Y, Horiba K, Usuki J, Chu SC, Ferrans VJ, Moss J. Markers of cell proliferation and expression of melanosomal antigen in lymphangioleiomyomatosis. Am J Respir Cell Mol Biol 1999 ; 21 : 327 –336. OpenUrl CrossRef PubMed Web of Science
- ↵ Rossi GA, Balbi B, Oddera S, Lantero S, Ravazzoni C. Response to treatment with an analog of the luteinizing-hormone-releasing hormone in a patient with pulmonary lymphangioleiomyomatosis. Am Rev Respir Dis 1991 ; 143 : 174 –176. OpenUrl PubMed Web of Science
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- ↵ Taylor JR, Ryu J, Colby TV, Raffin TA. Lymphangioleiomyomatosis: clinical course in 32 patients. N Engl J Med 1990 ; 323 : 1254 –1260. OpenUrl CrossRef PubMed Web of Science
- ↵ Usuki J, Horiba K, Chu SC, Moss J, Ferrans VJ. Immunohistochemical analysis of proteins of the Bcl-2 family in pulmonary lymphangioleiomyomatosis: association of Bcl-2 expression with hormone receptor status. Arch Pathol Lab Med 1998 ; 122 : 895 –902. OpenUrl PubMed Web of Science
- ↵ Carsillo T, Astrinidis A, Henske EP. Mutations in the tuberous sclerosis complex gene TSC2 are a cause of sporadic pulmonary lymphangioleiomyomatosis. Proc Natl Acad Sci USA 2000 ; 97 : 6085 –6090. OpenUrl Abstract / FREE Full Text
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Posttraumatic Pneumothorax in Sport: A Case Report and Management Algorithm
Sherwood, David H. DO 1 ; Gill, Benjamin D. DO, MBA 2 ; Schuessler, Bradley A. MD 3 ; Smith, David MD 4
1 Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, TN
2 Department of Physical Medicine and Rehabilitation, University of Missouri‐Columbia, Columbia, MO
3 Department of Rehabilitation Medicine, University of Kansas Medical Center, Kansas City, KS
4 Sports Medicine, Department of Family Medicine, University of Kansas Medical Center, Kansas City, KS
Address for correspondence: David H. Sherwood, DO, Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, 2201 Children’s Way, Suite 1318, Nashville, TN 37212; E-mail: [email protected] .
Introduction
A pneumothorax is the collection of extrapleural intrathoracic air due to an interruption in either the parietal or visceral pleura ( 1 ). The three types with which a sideline physician should be the most familiar are the following: tension, spontaneous, and traumatic pneumothorax. These are not mutually exclusive, because one could have a tension pneumothorax following trauma, although this classification allows for categorical understanding of the pathology. Tension type is the result of a visceral pleural laceration that leads to the creation of a one-way valve, allowing air to travel into the pleural space but not back out. Eventually, this accumulation of air in the pleural space can lead to venous congestion and acute decompensation of the patient. Spontaneous pneumothorax is an accumulation of air in the pleural space that happens acutely and without traumatic etiology or in the absence of a disease process ( 2 ). Finally, a traumatic pneumothorax, the focal concern for this manuscript, is usually created in the setting of a displaced rib that lacerates the parietal pleura, allowing extra-pleural air to exit.
The theory of the traumatic pneumothorax in the setting of nondisplaced rib fracture is that there is an acute increase in intrathoracic pressure secondary to trauma, which is responsible for a small rupture in the pleura or bronchial tree ( 2 ). Based on cadaveric studies, it has been demonstrated that the force with which ribs can be fractured ranges from 5.45 to 11.2 kN ( 3,4 ). Football hits can reach 1600 lbs of force or just over 7 kN, which would suggest that a portion of the hits, which occur on a football field place the athlete at risk for this diagnosis ( 5,6 ). Whether in the clinic or on the sideline, the physician should always be mindful of symptoms, which may suggest pneumothorax, because the necessary treatment from such a diagnosis can vary from urgent needle decompression to watchful observation without intervention.
The presentation of an athlete with posttraumatic chest pain to a clinician's musculoskeletal or sports medicine clinic is not an uncommon occurrence. The initial diagnosis is often a “chest contusion” before a definitive diagnosis is made ( 1,7,8 ). Overwhelmingly, chest pain is the presenting symptom in the setting of a pneumothorax, but other symptoms may include dyspnea or tachycardia ( 2,7,9–12 ). In around 10% of cases the patient will be asymptomatic at the time of evaluation, thus making an accurate history and physical examination of the utmost importance ( 2,8,10,13 ). Hyperresonance to percussion and decreased breath sounds on the affected side are consistently described ( 2,14,15 ). However, it should be noted that the sideline physician would likely encounter difficulty auscultating on the sideline given crowd noise. Consequently, the immediate sideline examination is of variable benefit ( 9 ). If the sideline physician's index of suspicion for traumatic pneumothorax is high enough to consider imaging, the most often used study per literature review is the chest radiograph. Despite this, the chest computed tomography is the “criterion standard” for diagnosis ( 8,16 ). There is developing evidence to suggest the utility of ultrasound for pneumothorax evaluation. Given the portability and immediate evaluation capabilities of the imaging modality, it may serve a larger role in the future ( 17–19 ).
Case Report
An 18-year-old man presented to an off-site ambulatory sports medicine clinic at a large academic institution for evaluation of a traumatic thoracic injury that occurred in a high school football game 3 d prior. He described an impact event to his left posterior lateral inferior chest wall, which resulted in localized sharp pain. He denied dyspnea, abdominal pain, hematuria, nausea, emesis, headaches, or dizziness. He denied antecedent cough, chest pain, or back pain. He denied trauma to chest or back, aside from aforementioned impact, or previous occurrence of pneumothorax. An athletic trainer saw the patient at the time of injury and recommended physician evaluation for definitive diagnosis.
Physical examination revealed a 79-kg man measuring 188 cm in no acute distress. There was normal chest excursion bilaterally with an absence of palpable subcutaneous emphysema. Auscultation of the chest was notable for decreased breath sounds on the left apex when compared with the right. Lungs were otherwise clear. Tenderness was noted over the posterior aspect of the left lower ribs with pain greatest at the 11th rib. The athlete demonstrated full active range of motion of the bilateral upper extremities without thoracic or lumbar spine pain. Three-view radiographs of the chest wall with rib focus were obtained and revealed a left-sided pneumothorax with 3.2-cm pleural parenchymal separation in the lung apex ( Fig. 1 ). There was a subtle lucency through the posterolateral aspect of left 11th rib related to a faint nondisplaced fracture ( Fig. 2 ).
Because of the presence of the pneumothorax, the athlete was ordered not to participate in any exertional physical activities. An over-the-counter NSAID one to two times daily for 14 days for pain control and deep breathing with a pillow at affected side was recommended. The attending physician projected 6 weeks for healing the rib fracture but explained that the pneumothorax would be the rate limiting step with regard to return-to-play (RTP). Moreover, it was recommended that this athlete return to clinic in 1 week for follow-up imaging. If symptoms were to worsen, he was instructed to return to clinic as soon as possible.
The patient returned to clinic 7 days later as scheduled. He described the development of a nonproductive cough, which he attributed to allergies and improved with cetirizine. His left-sided low back pain was resolving but exacerbated by left lateral side bending and twisting. On examination, tenderness was noted over the posterior aspect of the 11th rib with mild 12th rib tenderness. Lungs were clear and equal at the apices. Interval imaging showed complete resolution of the pneumothorax. The patient was instructed to perform light, noncontact exercise throughout the following week under the care of the team's athletic trainer. He was released to contact activity with a flak jacket 1 week later following no return of symptoms or pain at the rib fracture site with noncontact exercise. The patient was ordered to halt RTP protocol if he experienced shortness of breath or pain associated with nondisplaced fracture. No follow-up imaging was performed with regard to the nondisplaced rib fracture given resolution of rib pain symptoms. The athlete was able to successfully and safely RTP roughly 3 to 4 weeks postinjury following this protocol.
Traumatic pneumothorax is a potentially dangerous sports injury that requires prompt and accurate diagnosis for appropriate treatment. However, there is a lack of consistent guidelines to advise physicians through the diagnostic process and subsequent RTP management.
If traumatic injury occurs to the chest wall or back, the athlete should be evaluated promptly. These authors suggest examination in a quiet room to optimally appreciate auscultatory findings in the setting of a potential pneumothorax ( 9 ). Moreover, following such injury, an athlete should be required to demonstrate ability to run along the sideline without dyspnea or splinting away from the injury ( 1 ). If either symptom is present, we suggest immediate removal from the game and advancement to definitive evaluation.
If the index of suspicion is high for traumatic pneumothorax, patients should be provided supplemental oxygen expeditiously with frequent monitoring of vitals until further imaging can be obtained ( 9,20 ). Transportation to a facility and prompt chest radiograph is often the fastest and most appropriate starting point in diagnostic work-up ( 20 ).
If a pneumothorax is identified on imaging in the setting of a posttraumatic event, we have elected to classify the immediate management of the patients based on the size of the pneumothorax. Patients with a small pneumothorax, defined as less than 15% of total lung volume, can be observed and do not require admission ( 1–3,14 ). However, these authors suggest a repeat chest radiograph be obtained 3 hours to 6 hours after the initial diagnosis to rule out enlargement of the pneumothorax ( 21 ). If the follow-up image does not demonstrate progression and the patient persists with stable vitals, it is appropriate to safely discharge home. Weekly radiographs should be obtained until full resolution of the pneumothorax. Most can expect spontaneous resolution within 2 weeks ( 1,2 ).
If a pneumothorax is identified as greater than 20% of the total lung volume initially via the Collins method of measurement, or the patient has unstable vitals, or if repeat imaging demonstrates progression of the pneumothorax, then hospital admission is most appropriate with likely evacuation by tube thoracostomy ( 1,6,21 ). The patient should receive at least one chest radiograph a week following hospital discharge to ensure resolution of the diagnosis.
The question every athlete will ask is: “When can I get back on the field?” Currently, there are no consensus guidelines regarding RTP after pneumothorax. Most providers posit that RTP should be goal-oriented rather than a defined timetable ( 21,22 ). It is recommended that the athlete should not participate in exertional physical activity until complete resolution of the pneumothorax is demonstrated on imaging ( 1–3,7,8,21 ). Under the supervision of a physician or athletic trainer, the athlete should undergo gradual RTP guided by symptoms with return-to-contact activities 3 to 4 weeks after resolution on imaging ( 2 ). A flak jacket for rib protection has been shown to ease RTP symptoms in this population ( 21 ).
Finally, air travel restrictions should be established following pneumothorax. It is recommended that no air travel should occur for at least 14 days after imaging shows resolution of the pneumothorax because of the possibility of respiratory distress and exacerbation of pneumothorax, as seen in a small prospective study of travelers who waited 14 or more days compared with those who did not ( 2,3,14 ).
Conclusions
The current body of literature regarding the management of traumatic pneumothorax in sports is scarce. These authors consolidated available recommendations and provided an algorithm to guide practitioners who may encounter this injury on the field or in the clinic ( Fig. 3 ). While our outcome in the clinic was successful, there is need for future well-designed studies to validate this treatment algorithm.
The authors would like to thank Mitch Cain for his artistic support on this manuscript.
The authors declare no conflict of interest and do not have any financial disclosures.
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A 24-year-old man presented to the ED with unilateral chest pain that began about six hours earlier.
The pain was initially “sharp” in quality and began abruptly. The pain had been persistent since it began and was now dull and aching. It was worse with deep inspiration. There was no associated shortness of breath, diaphoresis, nausea, cough, fever, or chills. The pain was not relieved by ibuprofen.
The patient had no risk factors for coronary artery disease aside from a history of smoking one pack of cigarettes per day for the past six years. He denied using cocaine or other drugs.
On examination, he was a healthy appearing young man in no apparent distress.
Vital signs—blood pressure 120/80 mm/Hg, pulse 84 beats/ min, respirations 18 breaths/min, temperature 99.°F rectal, SO 2 97% on room air
Lungs—equal bilateral breath sounds without wheeze or râles; there was no chest wall tenderness
Heart—regular rhythm without murmur, rub, or gallop.
Abdomen—soft and nontender
• What does his chest radiograph show ( Figure 1 )?
See patient outcome .
Chest radiography is often not a helpful test in the evaluation of patients with chest pain; however, when pneumonia, malignancy, thoracic aortic aneurysm, or pneumothorax is suspected, radiography can be diagnostic. An upright chest radiograph can confirm or exclude a pneumothorax in nearly all patients, although in some cases, the findings can be subtle and must be specifically sought when examining the chest radiograph.
A spontaneous pneumothorax (not due to trauma or iatrogenic) can be either primary or secondary, i.e., associated with an underlying pulmonary disorder. Such disorders include chronic obstructive pulmonary disease (COPD), cysts or cavities due to necrotizing pneumonia (staphylococcus aureus), malignancies, tuberculosis, or pneumocystis pneumonia, and interstitial lung diseases such as sarcoidosis, collagen vascular diseases, pneumoconiosis, or idiopathic pulmonary fibrosis.
Primary spontaneous pneumothorax occurs in patients without underlying lung disease. It is most common in young adults, predominantly males in their third or fourth decades, who almost invariably have histories of cigarette smoking. There is rupture of an apical bleb (air-containing cyst within the visceral pleura) or subpleural bulla (enlarged airspace due to degeneration of alveoli). The precipitating event may be increased intrathoracic pressure due to physical exertion, although most cases occur at rest.
Clinical Manifestations
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Unexpected Fatal Tension Pneumothorax: A Case Report Regarding a Patient With Multiple Traumas on Air Medical Transportation
Affiliations.
- 1 Aerospace and Sub-Aquatic Medical Faculty, Aja University of Medical Sciences, Tehran, Iran.
- 2 Medical Faculty, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: [email protected].
- PMID: 33637277
- DOI: 10.1016/j.amj.2020.12.004
A 45-year-old male driver was assessed by the road rescue team after a car crash. He was in shock and had a deep second-degree burn, multiple bone fractures, and chest wounds. After stabilization, he was delivered to the nearest local clinic by an ambulance. The doctor decided to refer him via air transportation due to the lack of sufficient facilities and the urgent need for an intensive care unit after coordination with the nearest hospital and air medical team. A Bell 214C medical helicopter was called, and transfer was initiated after patient preparation by the air medical team. A few minutes later, his clinical condition deteriorated, and because of the suspicion of a tension pneumothorax, needle thoracostomy was performed. Crosswind and frequent helicopter movements interfered with tube thoracostomy, leading the air medical crew's decision to land. After completion of tube thoracostomy and during endotracheal intubation, his heart rhythm converted to bradycardia and then asystole. Unfortunately, despite 30 minutes of cardiopulmonary resuscitation, the patient died. The forensic report stated that a glassy foreign body led to penetrating chest wall injury and left lung perforation, possibly causing the tension pneumothorax, cardiopulmonary arrest, and death.
Copyright © 2021 Air Medical Journal Associates. Published by Elsevier Inc. All rights reserved.
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“Someone’s been shot": An EMS case study
There are critical decisions made in the prehospital emergency care of unstable patients with penetrating trauma.
The crew heard a “Pop, pop, pop” nearby, and knew it wasn’t just a car backfiring. The dispatch was for “someone shot,” and they were two blocks away. Law enforcement worked quickly to secure the area, and asked that EMS approach quickly. A young man was on the ground, unconscious. He was warm. There was no blood. A rapid assessment found multiple wounds in his chest, and he would respond to painful stimuli. He had a weak pulse, and agonal respirations.
The trauma protocol called for a rapid removal, and the police were nervous because a high powered automatic weapon was used and the perpetrator might still be in the area.
The patient was strapped on a backboard and moved to the ambulance, where the paramedic could do a full secondary assessment. The injured man had no head wounds, but there was blood in the mouth and coming up from the airway. The neck veins were distended. The victim was breathing in a very shallow fashion, and the paramedic noted that the right side of the chest “felt like a full balloon.”
He carefully removed the muscular man’s shirt, making sure he did not cut through the bullet holes. There was no air moving into that side of the chest on auscultation. He had two wounds on that side of his chest: there was an additional open wound to his left anterior chest, which caused a 4x4cm open area to be blown away. This was covered initially with a large trauma dressing. There was an additional wound to his upper left thigh. He had no other wounds to the extremities or his back, and he withdrew all four extremities from painful stimuli. The paramedic was able to barely palpate a carotid artery pulse, so he moved immediately to primary interventions.
As the ambulance began to move on a 20-minute transport to the trauma center, the crew communicated a “trauma alert,” critical in the case of an unstable penetrating trauma patient. The paramedic arranged equipment for a quick set of life-saving interventions.
The trauma protocol called for the paramedic to “restore perfusion,” which is an important concept. In penetrating trauma, this means performing techniques that will allow the most important organs to have adequate blood supply, but not accelerating hemorrhage or fulfilling any specific numbers for blood pressure or pulse or oxygen saturation.
To do this, the paramedic would need to:
- Control the airway and ventilate using a bag-valve-mask
- Apply a seal to the chest wound, and decompress any tension pneumothorax
- Infuse enough fluid to restore critical perfusion
- To infuse fluids in a patient with open chest wounds, the paramedic would try to get intravenous access above and below the diaphragm. This is usually done below the diaphragm using an intraosseous infusion device .
- Use pressure infusers to give rapid fluid boluses
The important first interventions are to ventilate and secure an airway. The EMT inserted an oral airway and started bagging the patient with high flow oxygen. It was very difficult to ventilate, so the paramedic knew he would have to seal the chest wound quickly and decompress the chest. He needed an occlusive dressing to the left chest wound that would seal it, and that would adhere to the skin despite the blood, sweat, and hair on the man’s chest. A new generation of occlusive dressings is available for that purpose, and one version of the dressing is available with a pressure relief valve system that would allow air to escape from the open wound, but would not allow it to get sucked back into the chest. These dressings have been used in recent war zones, and have been designed to be quickly applied and transparent, so that the trauma team can visualize the wounds once the patient arrives at the hospital.
The SAM Chest Seal is the self-adherent occlusive dressing that the paramedic applied to the open left chest wound. The hydrogel adhesive was strong and flexible, so it adhered to the skin in the presence of blood, hair, and diaphoresis. With the cap removed, the dressing functions as a valve chest seal with one-way outward flow. Once in place, the paramedic performed a needle decompression of the right chest, due to the EMT’s ongoing difficulty trying to ventilate the patient, the lack of air flow and chest wall movement on that side, and the feeling that the chest “was like a tight balloon.” The man had a muscular chest wall, so the paramedic inserted one of the three inch long needle and catheter devices into the second intercostal space, and had to almost bury the needle to the hub before he could get into the pleural space. He heard a large rush of air, followed by a “thank you” from the EMT that is was now much easier to bag the patient.
The patient had a large antecubital vein in the right arm, so a large catheter was inserted and a normal saline infusion started with the bag put in a pressure infusion cuff. The paramedic then inserted an intraosseous needle into the patient’s right tibia, away from the injured left leg. He started another infusion of normal saline with a pressure infusion cuff.
The patient continued to have blood coming up from his mouth, so the paramedic quickly performed an endotracheal intubation. The blood was coming from the patient’s lungs, so the paramedic relayed that information to the trauma center, and the crew suctioned the airway on a regular basis to keep the blood from occluding the tube and compromising ventilation.
After about 2 liters of fluid, the patient developed a regular pulse on the pulse oximeter, with a saturation of about 94%. His diaphoresis disappeared, and the wound on his left thigh began to bleed more profusely. The paramedic considered applying a tourniquet, but instead started with direct pressure, and the bleeding was controlled. The victim started to stir around a little.
With these signs of improving perfusion, he takes the pressure infusers off the bags, and cuts the fluid administration rate back to about 100cc per hour. As they arrive in the trauma center Emergency Department, the victim has a pulse rate of 110, an oxygen saturation of 96%, and is moving all four extremities. The trauma team assumes care of the patient, with a plan for rapid transport to the operating room.
After weeks of treatment, and multiple operations the patient was able to leave the hospital.
Decision making in cases of critical penetrating trauma There are critical decisions made in the prehospital emergency care of unstable patients with penetrating trauma. The key assessments and interventions are summarized as:
Integrity of the body and important body portions : Penetrating wounds to the face, neck and chest create immediate and profound airway problems. Where possible, the patient should be positioned to control his or her own airway. Spine immobilization should be dictated by mechanism of injury and evidence of trauma to the spine. Many patients with penetrating wounds away from the spinal column can be managed without immobilizing the spine, and that may simplify airway management. Chest and neck integrity is necessary for preventing major bleeding, and allowing the patient to both ventilate and perfuse. Loss of integrity, particularly with major bleeding, can be addressed by direct pressure, the new adherent dressings, or another occlusive dressing.
Airway : Where needed, airways using oral, nasal, or cricothyroid routes are lifesaving. With some facial injuries, before bleeding and swelling progress, the EMT can perform an oral or digital intubation to secure the airway. In some cases, the patient will need a needle or surgical cricothyrotomy, which can be performed by paramedics in some systems. Crews that are managing critical airways across long prehospital care timelines must be prepared with a number of options for airway management.
Ventilation : The chest wall must be intact for the patient to breathe, and the pleural space cannot be filled with air or blood. Filling those spaces with air creates a life threat to the patient, and the air must be removed with a needle or a chest tube. A tension pneumothorax also creates filling problems for the heart, and perfusion will decrease.
Oxygenation : Lung integrity is important for oxygenation. Supplemental oxygen is usually helpful. Perfusion is the ability of the body to provide critical oxygenation to cells and remove waste products, and the compromise of perfusion is called “shock”. Enhancing both volume and oxygen delivery to the patient is needed to restore or maintain perfusion in the traumatized patient.
Surgical intervention : EMS providers should be experienced in their work with local hospitals or the trauma center, and capable of “making the call” in a timely manner that a crisis is en route and will need to be managed at the ED.
James J. Augustine is an emergency physician and Fire/EMS medical director, and a clinical professor in the Department of Emergency Medicine at Wright State University in Dayton, Ohio. He is chair of the National Clinical Governance Board for US Acute Care Solutions, based in Canton, Ohio. Dr. Augustine currently serves a medical director role with fire rescue agencies in Ohio and Florida.
In addition, he has been a member of national groups and organizations overseeing emergency medical services, emergency service quality improvement, benchmarking and best practices and disaster preparation.
Case Study: Pneumothorax
Introduction, the patient, history of present condition.
- To treat the pneumothorax he had a chest tube inserted with 20cm dry suction water-seal drainage ordered. The patient endured no complications as a result of this procedure.
- To treat the dislocated joint he had his arm placed in a sling to stabilize the sternoclavicular joint.
- The scalp laceration was closed with staples.
- For his pain the patient had a thoracic epidural placed (10mg Dilaudid , 2 mL q4min).
Course of Action: Day #3 Patient received another chest x-ray to monitor the status of the chest tube placement and pneumothorax . Results showed that the right lung remained fully expanded. He also converted back to normal sinus rhythm at 2200.
Course of Action: Day #5-10 Patient's lung remains reexpanded . Copious amounts of drainage collected in water-seal system. He also completed his round of IV antibiotics for the pneumonia.
Course of Action: Day #11 Patient's chest tube removed as well as the staples from his scalp laceration.
Course of Action: Day #12 Patient was dismissed home. Went home with sling for his arm to stabilize the sternoclavicular joint.
Pathophysiology
Past Medical History
Assessment findings, relevant labs, diagnostic tests, relevant medications, multiple choice questions.
- http://www.mollymarkham2.blogspot.com
- Hart, J.P. (2005, June 10). Chest tube insertion-series: Procedure. Retrieved April 30, 2007 from Medline Plus Medical Encyclopedia: http://www.nlm.nih.gov/medlineplus/ency/presentations/100008_3.htm
- Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. (2004). Medical-surgical nursing: Assessment and management of clinical problems. (6th ed). St. Louis MO: Mosby.
- Morton, P.G., et al. (2005). Critical care nursing: A holistic approach.. (8th ed). Philadelphia, PA: Lippincott.
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- Volume 17, Issue 9
- Management of a rare case of lymphangioleiomyomatosis complicated by recurrent pneumothorax
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- Kyle Jordan Fletke 1 ,
- Nicole Taylor 2 and
- Nirev Shah 3
- 1 Family and Community Medicine , University of Maryland School of Medicine , Baltimore , Maryland , USA
- 2 University of Maryland Medical Center , Baltimore , Maryland , USA
- 3 Division of Pulmonary and Critical Care , University of Maryland School of Medicine , Baltimore , Maryland , USA
- Correspondence to Dr Kyle Jordan Fletke; kfletke{at}som.umaryland.edu
A female of reproductive age presents to the emergency department with progressive dyspnoea due to pneumothorax. She has a history of lymphangioleiomyomatosis (LAM) diagnosed by lung biopsy 15 years ago following incidental finding of pneumothorax. Despite various procedural and medicinal treatments, she continued to have recurrent pneumothorax, with three hospital admissions over the preceding 3 months. LAM is a rare cystic lung disease affecting the lymphatic system, which most commonly affects women of childbearing age. It can be diagnosed via imaging or tissue biopsy (gold standard). Treatment can be difficult, and it often requires highly specialised care by pulmonologists and often confers significant limitations to patients’ independence and quality of life. Family physicians are often part of multidisciplinary team to provide care to patients with rare chronic conditions.
- Respiratory system
- General practice / family medicine
- Pneumothorax
- Respiratory medicine
This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .
https://doi.org/10.1136/bcr-2024-260369
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Lymphangioleiomyomatosis (LAM) is a rare cystic lung disease, which can occur sporadically or in conjunction with tuberous sclerosis complex (TSC). 1 The estimated prevalence of LAM is 3–7 cases per million women, with an estimated 15% of cases associated with tuberous sclerosis complex. 2 Tuberous sclerosis complex can be diagnosed with the identification of either a TSC1 or TSC2 pathogenic mutation or from clinical diagnostic criteria. 3 LAM primarily affects the lung parenchyma but can affect other organs, including the kidneys, brain and liver. 4 The most common presenting symptom is dyspnoea, which can easily be mistaken for more common diagnoses like asthma or Chronic Obstructive Pulmonary Disease (COPD) in the emergency department or primary care setting. 5 Interdisciplinary management of rare diseases, such as LAM, is required to assist primary care physicians in the diagnosis and treatment of such illnesses.
Case presentation
A female in her 30s presented to the emergency department experiencing progressive dyspnoea, non-productive cough and left-sided chest pain. This was her third presentation during a 3-month period, with multiple prior pneumothoraxes resolved following chest tube placement over the past 15 years. She has a medical history of sporadic-LAM (S-LAM) and allergic rhinitis, and no significant family history of cardiopulmonary disease. Her social history includes one alcoholic unit per week and no history of tobacco, vaping or other inhaled substances. Her vital signs were significant for tachycardia with a pulse of 112 beats per minute, tachypnoea of 22 breaths per minute and an oxygen saturation (SpO2) of 89% in room air. Her physical exam was notable for diminished breath sounds on the left side without wheezes, rales or crackles. Chest radiograph demonstrated a new left-sided pneumothorax and stable loculated pneumothorax on the right side with underlying cystic lung disease. An interventional pulmonologist was consulted for acute management of her spontaneous pneumothorax. CT chest after placement of left-sided pigtail catheter showed small residual left-sided pneumothorax in the medial posterior pleural space with stable loculated right pneumothorax ( figure 1 ). Cardiac enzymes were negative, and ECG demonstrated normal sinus rhythm with right atrial enlargement.
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Coronal view CT chest.
Investigations
The patient was first diagnosed with sporadic LAM 15 years ago. A CT abdomen and pelvis without contrast was suggested to evaluate abdominal pain and it showed a haemorrhagic exophytic left renal mass and incidental finding of right pneumothorax. Subsequent CT chest showed diffuse scattered cystic changes with well-defined walls. No other lung abnormalities were noted. Given the persistence of the patient’s pneumothorax and concern for LAM, a lung biopsy was performed during a video-assisted thoracic surgery (VATS) procedure. Immunostaining was focally positive for HMB-45 and Desmin and negative for Mart-1, which is consistent with the diagnosis of LAM. An ophthalmologist evaluated the patient during initial hospitalisation and did not find stigmata of TSC. Brain MRI was also obtained to evaluate intracranial tumours and was found to be normal other than a non-specific right frontal subcortical white matter hyperintense focus.
Pulmonary function tests demonstrated a forced expiratory volume in one second/forced vital capacity (FEV1/FVC) ratio of 71%, FVC of 2.91 L (69% predicted), FEV1 of 2.05 L (61% predicted and decreased from 2.5 L previously), total lung capacity of 4.4 L (83% predicted) and a diffusion capacity of carbon monoxide of 18.9 mL/mm Hg/min (71% predicted).
An echocardiogram revealed that the left ventricle was found to be decreased in size (consistent with decreased filling), with normal wall thickness, wall motion and left ventricular diastolic filling. The left ventricular ejection fraction was 70%. The right ventricle was normal in size, with normal systolic function and trace tricuspid regurgitation. Right ventricular systolic pressure was not calculated.
The patient has not undergone genetic testing for TSC. However, she does not have additional clinical stigmata of TSC. The left renal mass present on the CT on initial presentation 15 years ago was consistent with angiomyolipoma (a finding in LAM) versus clear cell – cell carcinoma. The patient underwent embolisation of this lesion. This lesion was never biopsied but remained stable in size on subsequent imaging, confirming the presence of malignancy less likely. The diagnostic criterion for LAM requires the presence of ≥2 angiomyolipoma, which this patient does not meet. Additionally, a combination of two major clinical features (LAM and angiomyolipomas) without other features does not meet the criteria for definite diagnosis of TSC. Therefore, the patient does not meet the clinical diagnostic criteria for definite diagnosis of TSC. 3
Differential diagnosis
Although the patient’s history of LAM was the most likely cause for her pneumothorax, it is imperative to consider other causes of her pneumothorax to prevent future events. Typically, the differential for pneumothorax is divided into three categories. 6 The first is trauma, often from blunt or penetrating chest trauma such as a motor vehicle accident. The second is iatrogenic, caused by a healthcare procedure such as a central line insertion. The third is spontaneous, in which no specific cause is identified. A subcategory of spontaneous pneumothorax is secondary in which the patient has an underlying lung condition. Cystic lung diseases, such as LAM, pulmonary Langerhans cell histiocytosis, Birt-Hogg-Dube syndrome, amyloidosis and lymphocytic interstitial pneumonia, can increase risk of spontaneous pneumothorax. 7
The absence of recent trauma or healthcare procedures, no smoking or vaping history and imaging studies negative for other lung pathologies make pathology other than LAM to be the unlikely cause of this patient’s recurrent pneumothorax. This is supported by the definitive diagnoses of LAM by positive biopsy and CT findings of multiple thin-walled cysts, consistent with LAM.
The patient was managed in the acute setting with placement of an anterolateral left-sided chest tube. The chest tube was slowly transitioned from suction to water seal and then removed following resolution of her pneumothorax. No significant changes were made to her medication regimen at the time of discharge.
Outcome and follow-up
The patient underwent a doxycycline pleurodesis and later a betadine pleurodesis with resolution of her pneumothorax. She was able to return to her daily life, though with continued reduced exercise tolerance. 2 months after hospitalisation, repeat pulmonary function tests demonstrated reduced lung function. She was unable to join clinical trials for LAM due to her recent pneumothoraxes. Sirolimus, an established pharmacotherapy for LAM, was suggested by the pulmonology team to stabilise her pulmonary function though it was initially deferred per patient’s preference due to the concerns for side effects. After experiencing a recurrent spontaneous pneumothorax (the fifth one of the year), sirolimus, an established therapy for LAM which affects the mTOR pathway, was initiated. 8 Follow-up pulmonary function testing and CT scan demonstrated that her pulmonary disease was stable following initiation of the daily sirolimus. She has not had a recurrent pneumothorax in over 1 year.
LAM is a rare cystic lung disease affecting the lungs and lymphatic system. It can occur either in combination with tuberous sclerosis or alone. 1 It mainly affects women of childbearing age and is characterised by pulmonary cystic changes, recurrent spontaneous pneumothorax and chylous pleural effusions, and can proceed to progressive respiratory failure. 9 It can also include abdominal manifestations such as lymphadenopathy, lymphatic masses and angiomyolipomas, which may cause abdominal pain. Throughout the disease process, LAM cells (smooth muscle) accumulate in the lungs, resulting in cystic changes and progressive loss of healthy lung tissue. LAM cells also accumulate in the lymphatics, resulting in the thickening of lymphatic vessel lumen and cystic dilation. 10 Diagnosis is often delayed but can be achieved by obtaining pulmonary function tests and CT scan imaging of the chest. Pulmonary function tests typically demonstrate airflow obstruction (often with a bronchodilator response), normal total lung capacity and decreased diffusion capacity. 11 CT scans will demonstrate many thin-walled cysts throughout the lungs. 10 If CT findings and other typical manifestations of LAM are present, then tissue biopsy is often not needed for diagnosis. The diagnostic gold standard is a lung/lymphatics biopsy demonstrating LAM cells or nodular infiltration by abnormal smooth muscle cells and specific immunohistochemical staining for smooth muscle marker and melanoma-related antigen HMB45. 12 Treatment includes managing acute symptoms of pneumothorax, typically with chest tube placement. It can also include pleurodesis to help reduce spontaneous pneumothorax frequency. Sirolimus, an immune modulator acting on the mTOR pathway which is responsible for part of the pathophysiology of LAM, has been shown to be an effective therapy for stabilising lung function. 8 Ultimately, some patients require lung transplant.
Patient’s perspective
Living with Llymphangioleiomyomatosis (LAM) for the past 14 years has been a profound journey, one that has tested my resilience as an individual. Throughout this journey, my spiritual connection with God has deepened, providing me with strength and comfort as I navigate the challenges of this chronic illness.
Despite the lifestyle changes and uncertainties, I am immensely grateful and feel blessed to be alive today. I am incredibly thankful for the exceptional care and support provided by the medical professionals. Their collaborative approach and dedication to my well-being have played a pivotal role in managing my condition and achieving the best possible outcomes.
Acknowledgement is also due to the LAM Foundation, whose tireless efforts in research, fundraising, and information dissemination have significantly contributed to advancing understanding and treatment options for LAM. Their commitment to organizing conferences and forums has been instrumental in fostering a supportive community and providing access to valuable resources.
Lastly, I want to express my heartfelt gratitude to my family and friends for their unwavering love and support throughout this journey. Their encouragement and presence have been invaluable in helping me face the challenges of LAM with courage and optimism.
Learning points
It is important for primary care physicians to be aware of rare diseases as to be able toso they can direct patients to appropriate specialists and ongoing clinical trials to improve outcomes.
Lymphangioleiomyomatosis is a rare cystic lung disease that should be considered in young women of childbearing agoe who have spontaneous pneumothorax or progressive pulmonary decline of unclear origin.
Sirolimus can be considered for the treatment of LAM in patients with recurrent respiratory symptoms, including pneumothorax.
Ethics statements
Patient consent for publication.
Consent obtained directly from patient(s).
- Barnes PM , et al
- Harknett EC ,
- Chang WYC ,
- Byrnes S , et al
- Northrup H ,
- Krueger DA , International Tuberous Sclerosis Complex Consensus Group
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Contributors All the authors participated in the clinical care of the patient, contributed to the writing of the manuscript and edited clinical images. They also gave final approval of the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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Case Study: Pneumothorax | |||
Pneumothorax
Case Presentation
John, a healthy twenty-eight year old electrical engineer, was driving home from work one evening when he experienced sudden stabbing pain in his right pectoral and right lateral axillary regions. He began to feel out of breath and both his respiratory rate and heart rate increased dramatically. As luck would have it, John passed a hospital each day on his way home and was able to get himself to the hospital’s emergency room. The emergency room physician listened to John's breathing with a stethoscope and requested blood gas analysis and a chest x-ray. John answered a few of the doctor's questions. The doctor noted that John had no history of respiratory problems but was a heavy smoker.
After viewing the chest radiograph, the doctor informed John that he had experienced a spontaneous pneumothorax, or what is commonly called a collapsed lung. The doctor explained that a hole had opened in John's right lung and that this hole had allowed air to leak into the cavity surrounding the lung. Then, as a result of the lung's own elastic nature, the lung had collapsed. The doctor said he could not be certain of the cause of the pneumothorax, but smoking cigarettes had certainly increased the likelihood of it happening. He told John he was fortunate the pneumothorax was small, which meant that relatively little air had escaped from the lung into the surrounding cavity, and it should heal on its own. He instructed John to quit smoking, avoid high altitudes, flying in nonpressurized aircraft, and scuba diving. He also had John make an appointment for a re-check and another chest x-ray.
Case Background
Spontaneous pneumothorax occurs when a blister on the surface of the lung opens, allowing air from the lung to move into the pleural cavity. This occurs because alveolar pressure is normally greater than the pressure in the pleural cavity. As air escapes from the lung, the lung tissues will recoil, and the lung will begin to collapse. The lung will continue to collapse until the difference between the alveolar pressure and pleural pressure disappears or until the collapsing of the lung causes the opening to seal.
The pneumothorax decreases the efficiency of the respiratory system, which in turn results in decreased blood oxygen concentration, increased respiratory rate, and increased heart rate. If the pneumothorax is small, the air that escapes into the pleural cavity can be reabsorbed into the lung once the opening has sealed shut. If the pneumothorax is large, a needle or chest tube may have to be inserted into the pleural cavity to draw the air out and allow for the reexpansion of the lung.
Define the following terms and explain how they may have been affected by John’s spontaneous pneumothorax.
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IMAGES
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Pneumothorax is an accumulation of air in the pleural cavity. It can result from trauma to the chest cavity (traumatic pneumothorax) or underlying disease (secondary spontaneous pneumothorax), while in cases of no identifiable underlying etiology, it is called primary spontaneous pneumothorax (PSP) [1]. ... A Case Study with Surgical ...
A 36-year-old man was brought to the emergency department with suspected COVID-19, following a 3-week history of cough, fevers and shortness of breath, worsening suddenly in the preceding 4 hours. On presentation he was hypoxaemic, with an SpO 2 of 88% on 15 L/min oxygen, tachycardic and had no audible breath sounds on auscultation of the left ...
Acknowledge that some events (labs, imaging) may happen in compressed time compared to reality. Inform group that labs and imaging data may change in the course of the simulation. Scenario brief: Patient involved in MVA three blocks from hospital is currently en route to trauma bay. You may perform any essential team preparation now (give team ...
For example, in a patient with worsening respiratory status or hypotension that is out of proportion to findings on chest radiography, appropriate diagnostic imaging is warranted, as was the case ...
The classic findings of pneumothorax on chest radiography are a white, visceral pleural line that is parallel to the chest wall, with a loss of vascular lung markings distal to the line, i.e. between the chest wall and the pleural line. Figure 1a - chest x-ray with pneumothorax. Image used with permission of Joel Gross, MD.
1. Introduction. Pneumothorax is an abnormal collection of air in the pleural space between the lung and chest wall. Pneumothorax is classified as either traumatic or spontaneous. Traumatic pneumothorax is a consequence of blunt or sharp trauma to the chest, mechanical ventilation, and diagnostic or therapeutic procedures.
A spontaneous pneumothorax (SP) is a collection of air or gas between the visceral and parietal pleura that causes the lung to collapse in the absence of a traumatic injury to the chest or lung. Primary spontaneous pneumothorax (PSP) occurs in persons with no previously known lung disease.
Our patient had a massive pneumothorax that was timely solved, but still she had a fatal outcome. However, we cannot state that the size of the pneumothorax had a defining role in the patient's evolution as there are studies with COVID-19 patients experiencing small pneumothorax and still a poor prognosis [9,10].
Repeat chest x-ray revealed early left tension pneumothorax, and the next emergency physician on duty confirmed the x-ray findings of an acute left-sided tension pneumothorax because the pigtail catheter attached to the Heimlich valve had failed. A left lateral chest tube thoracostomy was performed using a 28French tube, which yielded immediate ...
A 24-yr-old Caucasian female was evaluated in May, 2003 at the San Martino hospital, Genoa, Italy, for the presence of "sudden onset" chest pain and nonproductive cough. Past medical history was only characterised by the presence of frequent headaches. The patient had been playing competitive tennis from the age of 6-20 yrs and, after retirement from competitions, had been smoking ...
Case Report. An 18-year-old man presented to an off-site ambulatory sports medicine clinic at a large academic institution for evaluation of a traumatic thoracic injury that occurred in a high school football game 3 d prior. He described an impact event to his left posterior lateral inferior chest wall, which resulted in localized sharp pain.
Case Study of Pneumothorax in a 27-year-old Male as a Possible Post- COVID 19 Infection Complication Vince Thomas 1 iD , Meraj Alam 1 , Zohaer Muttalib 1 , Nalin Ranasinghe 2 , Leonard Ranasinghe 3*
Spontaneous pneumothorax occurs when a blister on the surface of the lung opens, allowing air from the lung to move into the pleural cavity. This occurs because alveolar pressure is normally greater than the pressure in the pleural cavity. As air escapes from the lung, the lung tissues will recoil, and the lung will begin to collapse.
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Case Study Progress A. recovers uneventfully and is discharged home 4 days later with a chest tube and Heimlich valve. The physician connects the one-way (Heimlich) valve between the distal end of the chest tube and a drainage pouch. 14. Discuss the purpose of this device.
The management of pneumothorax depends on the severity of symptoms, its size, and the presence of underlying lung disease. According to British Society Guidelines 2010, the size between the lung edge and chest wall is used to estimate the size of pneumothorax, i.e., <2 cm for small pneumothorax and ≥2 cm for large pneumothorax.
A 45-year-old male driver was assessed by the road rescue team after a car crash. He was in shock and had a deep second-degree burn, multiple bone fractures, and chest wounds. After stabilization, he was delivered to the nearest local clinic by an ambulance. The doctor decided to refer him via air t …
James J. Augustine, MD, FACEP. The crew heard a "Pop, pop, pop" nearby, and knew it wasn't just a car backfiring. The dispatch was for "someone shot," and they were two blocks away. Law ...
Case Study: Pneumothorax Introduction. This is a blog devoted completely to the discussion of pneumothorax. Here you will find an actual case study of a patient who experienced a pneumothorax, as well as pictures, external links, and a short quiz comprised of NCLEX like questions. Please, look around and let me know if you have any questions.
A female of reproductive age presents to the emergency department with progressive dyspnoea due to pneumothorax. She has a history of lymphangioleiomyomatosis (LAM) diagnosed by lung biopsy 15 years ago following incidental finding of pneumothorax. Despite various procedural and medicinal treatments, she continued to have recurrent pneumothorax, with three hospital admissions over the ...
Case Background. Spontaneous pneumothorax occurs when a blister on the surface of the lung opens, allowing air from the lung to move into the pleural cavity. This occurs because alveolar pressure is normally greater than the pressure in the pleural cavity. As air escapes from the lung, the lung tissues will recoil, and the lung will begin to ...
Most pediatric thoracic injuries (80% to 85%) are the result of blunt trauma, with falls, sports-related injuries, and high-speed crashes accounting for most blunt traumatic injuries in older children and teenagers. 2. Thoracic trauma is one of the leading causes of tension pneumothorax. Chest X-rays can be obtained if diagnosis of pneumothorax ...
The objective of the Integrated Approaches for Testing and Assessment (IATA) Case Studies Project is to increase experience with the use of IATA by developing case studies which constitute examples of predictions that are fit for regulatory use. The aim of this project is to create common understanding of using novel methodologies and the generation of considerations/guidance stemming from ...
Scaling platform development often means absorbing cognitive burdens, but empathy is key. Understanding users beyond their immediate issues leads to better solutions. Platforms help manage growth ...
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