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Tension pneumothorax in asthma
Resuscitation (2006) 69, 525—527
LETTER TO THE EDITOR
Tension pneumothorax in asthma Several definitions exist of what exactly comprises a tension pneumothorax but one suggested clinical definition is ‘‘pneumothorax with significant respiratory or haemodynamic compromise that reverses on decompression (needle or finger) alone’’1 i.e. the improvement occurs before one way valve drainage is connected. Castle’s series of three patients correctly highlights an area for improvement of care and training in the sphere of potentially reversible cardiac
arrest.2,3 It adds to the already substantial evidence base showing that a lack of hiss on needle thoracocentesis does not have a 100% negative predictive value. Finger thoracostomy, feeling the lung with ones finger and making a thoracostomy big enough to hear air ingress and egress is a superior technique in an emergency to rule out/treat a tension pneumothorax (TPT).1 This can be done (even bilaterally) without waiting for a chest tube in the ventilated patient.4 We support the recommenda-
Figure 1 0300-9572/$ — see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2005.10.011
526
Letter to the Editor
Figure 2
tions that this be performed following unsuccessful needle thoracocentesis in all high risk patients—– which includes arrest secondary to chronic respiratory disease and traumatic arrest. These recommendations need consideration by all who teach ALS, ATLS or similar courses. A recent review on TPT emphasizes the fact it is a hypoxic condition,1 that presents with symptoms of hypoxic compensation in the spontaneously ventilating (awake) patient that may precede respiratory arrest and eventual cardiovascular collapse.1,5—7 The differential diagnosis between TPT and asthma may be difficult as both present with respiratory distress, wheeze, tachycardia, tachypnoea, desaturation, hyper-expansion, agitation and decreased air entry. Tracheal deviation and venous distension are unreliable signs and hypotension is extremely rare in the unventilated patient.1 This leaves just chest pain and ipsilateral hyper-resonance to point towards a diagnosis of TPT. The former may be difficult to differentiate in an anxious hypoxic patient and even the latter may be difficult to detect.1 Hyper-expansion would be expected to be bilateral in asthma whereas in TPT there will be ipsilateral hyper-expansion with hypo-mobility and contralateral hyper-mobility but this is a subtle distinction to make.
A recent case is believed to be the first confirmed report of TPT in a spontaneously ventilating asthmatic patient. A 16-year-old male with mild asthma presented to the emergency department 5½ h after sudden onset of dyspnoea associated with rightsided pleuritic chest pain. On arrival at hospital he was dyspnoeic but talking in sentences. He had a respiratory rate of 40 per minute, arterial oxygen saturation of 98% on FiO2 0.6, heart rate of 90 beats per minute, blood pressure of 130/80 mmHg and Glasgow coma score of 15. He had a central trachea, ipsilateral increased percussion note and decreased breath sounds with contralateral vesicular breath sounds. Immediate chest X-ray showed a large pneumothorax, splayed ribs, a depressed diaphragm and a contralaterally distorted mediastinum (Figure 1). Needle thoracocentesis in the 2nd inter-costal space, mid-clavicular line, produced partial improvement in his condition but an intercostal drain in the 6th inter-costal space midaxillary line resulted in dramatic improvement of his clinical condition. Repeat CXR demonstrated full lung re-inflation (Figure 2). The patient’s rapid improvement on pleural decompression along with radiological signs indicating high right-sided pleural pressure (that resolved after treatment) suggests that this was under tension1 .
Letter to the Editor Although most asthma deaths occur in chronic severe asthmatics some occur suddenly in patients with only moderate or minor background disease8 . Unless post mortem examination includes chest radiology or monitors pleural pressure before opening the thoracic cavity, tension pneumothorax as cause of death may be missed9,10 . This raises the question as to whether some asthma deaths may be due to tension pneumothorax and are hence avoidable. In the ventilated patient the time course is accelerated and TPT presents with signs of decompensation including early cardiovascular collapse. In three cases reported by Castle it is difficult to say at exactly what point a TPT occurred and whether this was initially unilateral or bilateral. The possibilities include: (1) unilateral TPT whilst unventilated becoming bilateral on intermittent positive pressure ventilation (IPPV), (2) bilateral TPT whilst unventilated (unlikely) and (3) bilateral TPT developing only on IPPV. It is thus possible that TPT was the primary condition leading to respiratory arrest with cardiac arrest secondary to severe hypoxia1,5—7 . All three cases exhibited deterioration of respiratory disease known to cause raised airway pressures and pneumothorax. They illustrate cases who present with respiratory distress followed by respiratory arrest (cases 1 and 3) or peri-respiratory arrest (case 2) that precedes a cardiac arrest. The time of onset of TPT is an important issue as not only is it fundamental to understanding the condition but effective pleural decompression at an early stage may restore cardiac output.
References 1. Leigh-Smith S, Harris T. Tension pneumothorax—–time for a re-think? Emerg Med J 2005;22:8—16.
527 2. Castle N, Tagg A, Owen R. Bilateral tension pneumothorax. Resuscitation 2005;65:103—5. 3. ALSG. Advanced Life Support Manual. 4th ed. London: Resuscitation Council (UK); 2001. 4. Deakin CD, Davies G, Wilson A. Simple thoracostomy avoids chest drain insertion in prehospital trauma. J Trauma 1995;39(2):373—4. 5. Subotich D, Mandarich D. Accidentally created tension pneumothorax in patient with primary spontaneous pneumothorax—–confirmation of the experimental studies, putting into question the classical explanation. Med Hypotheses 2005;64(1):170—3. 6. Crocker HL, Ruffin RE. Patient-induced complications of a Heimlich flutter valve. Chest 1998;113(3):838—9. 7. Spouge AR, Thomas HA. Tension pneumothorax after reversal of a Heimlich valve. Am J Roentgenol 1992;158(4): 763—7. 8. British Thoracic Society and Scottish Intercollegiate Guidelines Network, British guideline on the management of asthma. Revised April 2004. http://www.britthoracic.org.uk/c2/uploads/asthmafull.pdf (accessed 11 august 2005). 9. Ludwig J, Kienzle GD. Pneumothorax in a large autopsy population. A study of 77 cases. Am J Clin Pathol 1978;70(1): 24—6. 10. Saltet JF. Pneumothorax. Lancet 1979;1(8117):671.
a Defence b Trauma
Simon Leigh-Smith∗ Medical Services, UK
Grant Christey Department, Liverpool Hospital, Sydney, Australia
∗ Corresponding
author at: Institute of Naval Medicine, Monckton House, Alverstoke, Gosport, Hants PO12 2DL, UK. Tel.: +44 7718 926590.
E-mail address: [email protected] (S. Leigh-Smith) 12 August 2005
LETTER TO THE EDITOR
Tension pneumothorax in asthma Several definitions exist of what exactly comprises a tension pneumothorax but one suggested clinical definition is ‘‘pneumothorax with significant respiratory or haemodynamic compromise that reverses on decompression (needle or finger) alone’’1 i.e. the improvement occurs before one way valve drainage is connected. Castle’s series of three patients correctly highlights an area for improvement of care and training in the sphere of potentially reversible cardiac
arrest.2,3 It adds to the already substantial evidence base showing that a lack of hiss on needle thoracocentesis does not have a 100% negative predictive value. Finger thoracostomy, feeling the lung with ones finger and making a thoracostomy big enough to hear air ingress and egress is a superior technique in an emergency to rule out/treat a tension pneumothorax (TPT).1 This can be done (even bilaterally) without waiting for a chest tube in the ventilated patient.4 We support the recommenda-
Figure 1 0300-9572/$ — see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2005.10.011
526
Letter to the Editor
Figure 2
tions that this be performed following unsuccessful needle thoracocentesis in all high risk patients—– which includes arrest secondary to chronic respiratory disease and traumatic arrest. These recommendations need consideration by all who teach ALS, ATLS or similar courses. A recent review on TPT emphasizes the fact it is a hypoxic condition,1 that presents with symptoms of hypoxic compensation in the spontaneously ventilating (awake) patient that may precede respiratory arrest and eventual cardiovascular collapse.1,5—7 The differential diagnosis between TPT and asthma may be difficult as both present with respiratory distress, wheeze, tachycardia, tachypnoea, desaturation, hyper-expansion, agitation and decreased air entry. Tracheal deviation and venous distension are unreliable signs and hypotension is extremely rare in the unventilated patient.1 This leaves just chest pain and ipsilateral hyper-resonance to point towards a diagnosis of TPT. The former may be difficult to differentiate in an anxious hypoxic patient and even the latter may be difficult to detect.1 Hyper-expansion would be expected to be bilateral in asthma whereas in TPT there will be ipsilateral hyper-expansion with hypo-mobility and contralateral hyper-mobility but this is a subtle distinction to make.
A recent case is believed to be the first confirmed report of TPT in a spontaneously ventilating asthmatic patient. A 16-year-old male with mild asthma presented to the emergency department 5½ h after sudden onset of dyspnoea associated with rightsided pleuritic chest pain. On arrival at hospital he was dyspnoeic but talking in sentences. He had a respiratory rate of 40 per minute, arterial oxygen saturation of 98% on FiO2 0.6, heart rate of 90 beats per minute, blood pressure of 130/80 mmHg and Glasgow coma score of 15. He had a central trachea, ipsilateral increased percussion note and decreased breath sounds with contralateral vesicular breath sounds. Immediate chest X-ray showed a large pneumothorax, splayed ribs, a depressed diaphragm and a contralaterally distorted mediastinum (Figure 1). Needle thoracocentesis in the 2nd inter-costal space, mid-clavicular line, produced partial improvement in his condition but an intercostal drain in the 6th inter-costal space midaxillary line resulted in dramatic improvement of his clinical condition. Repeat CXR demonstrated full lung re-inflation (Figure 2). The patient’s rapid improvement on pleural decompression along with radiological signs indicating high right-sided pleural pressure (that resolved after treatment) suggests that this was under tension1 .
Letter to the Editor Although most asthma deaths occur in chronic severe asthmatics some occur suddenly in patients with only moderate or minor background disease8 . Unless post mortem examination includes chest radiology or monitors pleural pressure before opening the thoracic cavity, tension pneumothorax as cause of death may be missed9,10 . This raises the question as to whether some asthma deaths may be due to tension pneumothorax and are hence avoidable. In the ventilated patient the time course is accelerated and TPT presents with signs of decompensation including early cardiovascular collapse. In three cases reported by Castle it is difficult to say at exactly what point a TPT occurred and whether this was initially unilateral or bilateral. The possibilities include: (1) unilateral TPT whilst unventilated becoming bilateral on intermittent positive pressure ventilation (IPPV), (2) bilateral TPT whilst unventilated (unlikely) and (3) bilateral TPT developing only on IPPV. It is thus possible that TPT was the primary condition leading to respiratory arrest with cardiac arrest secondary to severe hypoxia1,5—7 . All three cases exhibited deterioration of respiratory disease known to cause raised airway pressures and pneumothorax. They illustrate cases who present with respiratory distress followed by respiratory arrest (cases 1 and 3) or peri-respiratory arrest (case 2) that precedes a cardiac arrest. The time of onset of TPT is an important issue as not only is it fundamental to understanding the condition but effective pleural decompression at an early stage may restore cardiac output.
References 1. Leigh-Smith S, Harris T. Tension pneumothorax—–time for a re-think? Emerg Med J 2005;22:8—16.
527 2. Castle N, Tagg A, Owen R. Bilateral tension pneumothorax. Resuscitation 2005;65:103—5. 3. ALSG. Advanced Life Support Manual. 4th ed. London: Resuscitation Council (UK); 2001. 4. Deakin CD, Davies G, Wilson A. Simple thoracostomy avoids chest drain insertion in prehospital trauma. J Trauma 1995;39(2):373—4. 5. Subotich D, Mandarich D. Accidentally created tension pneumothorax in patient with primary spontaneous pneumothorax—–confirmation of the experimental studies, putting into question the classical explanation. Med Hypotheses 2005;64(1):170—3. 6. Crocker HL, Ruffin RE. Patient-induced complications of a Heimlich flutter valve. Chest 1998;113(3):838—9. 7. Spouge AR, Thomas HA. Tension pneumothorax after reversal of a Heimlich valve. Am J Roentgenol 1992;158(4): 763—7. 8. British Thoracic Society and Scottish Intercollegiate Guidelines Network, British guideline on the management of asthma. Revised April 2004. http://www.britthoracic.org.uk/c2/uploads/asthmafull.pdf (accessed 11 august 2005). 9. Ludwig J, Kienzle GD. Pneumothorax in a large autopsy population. A study of 77 cases. Am J Clin Pathol 1978;70(1): 24—6. 10. Saltet JF. Pneumothorax. Lancet 1979;1(8117):671.
a Defence b Trauma
Simon Leigh-Smith∗ Medical Services, UK
Grant Christey Department, Liverpool Hospital, Sydney, Australia
∗ Corresponding
author at: Institute of Naval Medicine, Monckton House, Alverstoke, Gosport, Hants PO12 2DL, UK. Tel.: +44 7718 926590.
E-mail address: [email protected] (S. Leigh-Smith) 12 August 2005