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| CASE REPORT |
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| Year : 2019 | Volume
: 9
| Issue : 2 | Page : 91-95 |
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Acute severe asthma complicated with tension pneumothorax and hemopneumothorax
Ayman Anis Metry
Assistant Professor of Anesthesia, ICU and Pain Management, Faculty of Medicine, Ain Shams University, Cairo, Egypt; Anesthesia and ICU Consultant, Kalba Hospital, MOHAP, Sharjah, UAE
| Date of Web Publication | 26-Jun-2019 |
Correspondence Address:
Prof. Ayman Anis Metry
Kalba Hospital, Kalba, Sharjha
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/IJCIIS.IJCIIS_83_18
 Abstract | | |
A 47-year-old patient presented to the emergency room with an attack of acute severe asthma. In spite of all primary measures, the patient was deteriorating. Arterial blood gases showed hypercarbia and acidemia. The patient was shifted to the intensive care unit connected to noninvasive ventilation for 3 h, without any obvious improvement. Decision was taken to intubate, ventilate, and keep her deeply sedated. On the 4th day of ventilation, the patient developed sudden tension pneumothorax and she was near to arrest. Management for tension pneumothorax was immediate and successful. After that, chest X-ray and computerized tomography scan showed hemopneumothorax, for which a chest tube was inserted in both chest sides and blood transfusion was initiated immediately. After this incidence, the patient's parameters improved dramatically. Four days later, the patient was extubated and kept in intensive care unit till the chest tubes were removed and then shifted to the ward and discharged on day 15 from admission.
Keywords: Acute severe asthma, air trapping, hypercarbia, hyperinflation, tension pneumothorax, ventilation
How to cite this article:
Metry AA. Acute severe asthma complicated with tension pneumothorax and hemopneumothorax. Int J Crit Illn Inj Sci 2019;9:91-5 |
How to cite this URL:
Metry AA. Acute severe asthma complicated with tension pneumothorax and hemopneumothorax. Int J Crit Illn Inj Sci [serial online] 2019 [cited 2021 Feb 28];9:91-5. Available from: https://www.ijciis.org/text.asp?2019/9/2/91/261464 |
| Introduction | |  |
Asthma is a disease of global health importance. According to the World Health Organization, between 100 and 150 million people around the world suffer from asthma, and this number is rising. Worldwide, deaths from this condition have reached 180,000.[1] Asthma is a cause of severe morbidity and mortality all over the world. Acute severe asthma represents an emergency seeking immediate medical interference.[2] Most of the patients suffering from acute asthma can be successfully managed with α2-agonist bronchodilators, corticosteroids, and oxygen, but 1%–3% of patients with severe asthma may require endotracheal intubation and mechanical ventilation during their hospital course,[3] in spite of maximal medical therapy.
This case report is an example of severe acute asthma with hyperinflated chest and air trapping, necessitating intubation and ventilation, comorbid with tension pneumothorax, chest tube insertion, then sudden improvement, extubation, and discharge to home.
| Case Report | | |
This case was only presented after approval from the hospital's ethical committee and obtaining an informed consent from the concerned patient. A 47-year-old female patient with a known history of bronchial asthma presented to the emergency room complaining of shortness of breath with 3–4 days' duration, but severely exacerbated today. She is diabetic on insulin, her body weight 72 kg, and height 163 cm.
Tympanic temperature was 36.5°C, peripheral pulse rate 106 beats/min, respiratory rate (RR) 38 breaths/min, and blood pressure 170/100 mmHg.
Arterial blood gases (ABGs) on a 6-L oxygen mask were as follows: pH – 7.13, PO2– 162.0 mmHg, PCO2– 87.0 mmHg, and HCO3– 21.4 mmol/L. Other investigations were within normal levels, except blood sugar which was 3.8 mmol/L.
Rapid management was done with bronchodilators to help alleviate the exacerbation, but in vain.
Portable chest X-ray showed hyperinflated chest without any other pathology as shown below [Figure 1].
On these medications, the patient was still distressed without any improvement in her condition; another ABG on a nasal cannula 2-L oxygen was done, and the results were pH: 7.11, PO2: 84.3 mmHg, PCO2: 139.9 mmHg, and HCO3: 26.7 mmol/L.
The patient was shifted to the intensive care unit (ICU). Methylprednisolone sodium succinate parenteral 500 mg intravenous (IV) was given once. An intramuscular dose of epinephrine 1:1000 at 0.01 mg was administered. Magnesium sulfate 2 g IV was started over 20 min infusion.
The patient became severely dyspneic and restless, so she was connected to continuous positive airway pressure with pressure support (PS) noninvasive ventilation (NIV).
The patient did not respond well to NIV for 3 h, and ABG showed no improvement, so intubation was done and connected to the ventilator, volume controlled and synchronized intermittent mandatory ventilation mode with an inspiratory oxygen fraction (FiO2): 0.5, positive end-expiratory pressure (PEEP): 7 cm H2O, tidal volume (VT): 320 ml, RR: 18 beat/min, PS: 12 cm H2O, and inspiratory time: 1.0. Peak inspiratory pressure (PIP) ranged between 35 and 40 cmH2O and plateau pressure (Pplat) between 26 and 30 cmH2O. Sedation was started in the form of midazolam 2 mg/h + ketamine 15 mg/h.
In spite of ventilation, ABG did not improve. Hence, cisatracurium was started with a bolus dose of 6 mg and maintenance infusion at a rate of 4–6 mg/h. The patient was sedated and kept on mechanical ventilation. She was put on a minimal effective dose of muscle relaxant to avoid myopathy for 2 days because PIP and Pplat were high and also difficulty to wash CO2 and adjust pH.
On the 3rd day, muscle relaxant (cisatracurium) was stopped and sedation was increased with the addition of remifentanil infusion 150–200 ug/h. Midazolam infusion was started at a dose of 2 mg/h in addition to ketamine 10–15 mg/h infusion.
On day 4 after admission, the patient was still ventilated on heavy sedation when she developed a sudden episode of desaturation and severe bradycardia. Ventilator monitor showed VT of zero. AMBU bag ventilation was tried, but was very difficult as pressure was very high. Auscultation of the chest revealed no air entry to both the lungs. Two large bore cannulas (18 G) were inserted in the midclavicular area, second intercostal spaces, 1 cannula on each side, which showed venting of air, and immediately AMBU ventilation became easier, saturation started to improve, and heart rate came back to normal [Figure 2].
Computerized tomography (CT) chest and thorax were done on the next day to tension pneumothorax accident, which showed bilateral pneumothorax, left upper thoracic surgical emphysema, right side pleural effusion, and right fissural effusion [Figure 3].
Chest tubes were inserted for both the chest sides. Right chest tube drained immediately after insertion 650 mL blood. Two units of packed red blood cells were infused after cross-matching.
On day 8, chest X-ray [Figure 4] and ABG were within normal limits, and chest auscultation revealed no abnormalities, so weaning was started gradually with discontinuation of sedation and the patient was extubated successfully. The patient was kept in the ICU under observation for another 3 days till the chest tubes were removed, after that shifted to the female ward and discharged to home on day 15 after admission. All ABGs during admission are shown in [Figure 5], [Figure 6], [Figure 7]. | Figure 4: Portable chest X-ray on extubation day showing chest tubes with clear chest
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 | Figure 5: pH of all arterial blood gas in all days on ventilation till extubation
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 | Figure 6: PCO2 of arterial blood gas in all days on ventilation till extubation
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 | Figure 7: PO2 of arterial blood gas in all days on ventilation till extubation
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| Discussion | | |
Asthma-related airway inflammation is primarily due to the invasion of the airway wall with eosinophils[4] and activated T-lymphocytes, along with spasm of the smooth muscles of the bronchial tree, owing to bronchiolar constriction and mucus plugging of the lumen.[5] The T-helper 2 subtypes of lymphocytes are also present in the bronchial walls, and they can provoke interleukin (IL)-3, IL-4, and IL-5, in addition to granulocyte macrophage colony-stimulating factor.[6]
These pathological changes were the major cause for hyperinflation and high PIP and Pplat in this case with accumulated CO2 which was resistant to wash with ventilation.
The patient was very resistant to all standard measures and medications for treating acute asthmatic attacks even megadose corticosteroids and intramuscular adrenaline.[7]
Since admission, the patient presented with severe chest tightness and blockade of the bronchial tree (mostly mucus plug with muscle spasm) which allowed to some extent inspiration but hindered to a much higher degree the expiration. This condition precipitated air trapping, hyerinflation[8] and hypercarbia with high intrinsic PEEP.
This air trapping with hyperinflation made the ventilation of the patient difficult, as compliance reduced with increase in PIP and Pplat, that is why we preferred to add minimal effective dose of muscle relaxant to maintain ventilation with acceptable pressure levels of PIP and Pplat to avoid lung injury.[9]
All lung protection measures[10] for ventilation were followed for this patient such as low VT, permissive hypercarbia,[11] maintaining PIP <40 cm H2O and Pplat <30 cm H2O, and even to increase expiratory limb to decrease intrinsic PEEP and increase the chance for exhalation. pH ≥ 7.2 was satisfactory, but many attacks of severe spasm occurred which made this target also difficult.
This high intrinsic PEEP with hyperinflation and air trapping with air leak was the main reason for the occurrence of tension pneumothorax, which became more severe when the patient was ventilated.[12]
What makes this case unique is that, after recovery from tension pneumothorax, all lung parameters came back to normal even auscultation which encouraged us to wean and extubate. This picture gives the possibility of hyperinflated lung mimicking pneumothorax, the presence of accumulated cyst from gradual air leak, or emphysematous bolus, which was an obstacle for ventilation of the patient and that is why after its rupture all lung parameters returned normal and ventilation became easy.
Tension pneumothorax is accompanied by severe bradycardia and hypotension due to sudden compression of the mediastinum and cardiovascular collapse.[13] All chest X-rays done after recovery from tension pneumothorax were normal for more than 12 h, which was too much surprising to us, but we kept an eye on the patient to regularly follow-up her with chest X-ray; immediately when we suspected pathology, we shifted her for CT scan which showed hemopneumothorax.
Most probably, pneumothorax was remaining from the event of tension pneumothorax due to incomplete evacuation. The overall success rates for needle thoracostomy in pneumothoraces are only between 68% and 75%,[14] and it has been manifested that needle thoracostomy usually fails to evacuate an ongoing, active air leak.[14]
Hemothorax was possibly a complication of needle thoracostomy, which injured intrapleural or extrapleural blood vessel.[15] The needle itself if inserted more medially may lead to the internal mammary artery or subcostal artery injury. Significant vascular structures located near the second intercostal space include the internal mammary artery and its branches, subclavian vessels, intercostal vessels, and pulmonary arteries.[15] Using the lateral needle thoracostomy placement approach may help avoid major anterior vascular structures.[16]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Acknowledgment
I would like to present my gratitude to Kalba Hospital general and medical director for supporting me to present this case. Great thanks to Prof. Mohammed Magdy, Dr. Usama lotfy, Dr. Faras Azim, Dr. Ahmed Alia and Dr. Volodymyr Babych in addition to ICU nursing staff for supporting me with all data required for publication.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
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