bilateral tension pneumothorax and massive surgical emphysema

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221 Indian J. Anaesth. 2004; 48 (3) : 221-223 BILATERAL TENSION PNEUMOTHORAX AND MASSIVE SURGICAL EMPHYSEMA DURING ANAESTHESIA Dr. (Mrs) Geeta A. Patkar 1 Dr. (Mrs) S. R. Jagtap 2 SUMMARY A ten year old male child presented for tonsillectomy, developed bilateral tension pneumothorax and massive surgical emphysema under general anaesthesia. Prompt treatment saved the patient from fatality. This report highlights the possible mechanisms, clinical and radiological features and treatment of tension pneumothorax. Keywords : Bilateral tension pneumothorax, Surgical emphysema, Nonrebreathing circuit, Fish mouth valve. 1. M.D., D.A., Associate Professor 2. M.D., D.A., Professor Dept. of Anaesthesiology Lokmanya Tilak Muncipal Medical College and General Hospital, Sion, Mumbai – 400022, Maharashtra. Correspond to : Dr. (Mrs) G. A. Patkar 74, Anant Nivas Keluskar Road, Shivaji Park, Mumbai – 400 028, Maharashtra. E-mail : [email protected] (Accepted for publication on 20-02-2004 ) Introduction Bilateral pneumothorax and surgical emphysema are rare during the course of anaesthesia. However failure to recognise it and to provide prompt treatment may result in fatality. Pneumothorax can occur due to number of mechanisms. 1 Malfunctioning or misuse of equipment used for intermittent positive pressure ventilation can cause high airway pressure resulting in lung damage. We present a case of bilateral tension pneumothorax with surgical emphysema associated with the use of a fish mouth non rebreathing valve incorporated in a non rebreathing circuit. Case report A 10 year old male child, weighing 25 kgs, presented for tonsillectomy under general anaesthesia. Patient had no serious medical history and was clinically stable. His investigations were within normal limits, Hb of 11.8 gm%, BT 4 min 5 sec and CT 3 min. The child was premedicated with inj. glycopyrolate 0.1 mg intramuscularly half hour prior to surgery. The preinduction pulse rate was 110 min -1 and the blood pressure was 120 mmHg systolic. After adequate preoxygenation, anaesthesia was induced with inj. thiopentone sodium 150 mg and inj. succinylcholine 50 mg intravenously. The patient was ventilated with 100% oxygen and intubated with no. 6 portex oral cuffed endotracheal tube. Air entry was confirmed bilateraly and the cuff was inflated. Further anaesthesia was maintained using 60% nitrous oxide in oxygen, with intermittent halothane and vecuronium bromide. Ventilaton was carried out using a non rebreathing circuit with a fish mouth valve on a Drager anaesthesia machine. The patients ECG, oxygen saturation and blood pressure were monitored. The surgery was completed uneventfully in the next 45-50 mins. During confirmation of surgical hemostasis, the patients pulse suddenly dropped from 110 min -1 to 50 min -1 . This was associated with severe resistance to ventilation and the oxygen saturation dropped from 99% to 74%. Inj. atropine 0.3 mg was given IV immediately. We suspected an accidental extubation of the endotracheal tube and reconfirmed its position. The patient was then ventilated with 100% oxygen, however the resistance to ventilation persisted. The surgical drapes were removed, which revealed massive surgical emphysema extending from the eyelids, to the scrotum, cyanosis, and absent breath sounds bilaterally though the pulse was palpable. Bilateral tension pneumothorax was suspected from the above findings. Intermittent positive pressure ventilation was suspended and 18G needles were introduced bilaterally in the 2 nd intercostal space and connected to an under water seal drainage. Air leaked out under pressure and air entry improved. The patient had gained spontaneous respiration by now and was allowed to breathe 100% oxygen through a Magill’s circuit. The patients parameters improved. The oxygen saturation increased to 90%, pulse rate to 150 min -1 and the blood pressure was 110 mmHg systolic. Portable radiograph of the chest revealed bilateral pneumothorax (fig.1). Surgical help was summoned. Bilateral intercostal drainage (ICD) with underwater seal were placed in the 5 th intercostal space in the axilla. Air entry improved considerably with oxygen saturation of 100%. There was no resistance to ventilation. The water

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Page 1: bilateral tension pneumothorax and massive surgical emphysema

PATKAR, JAGTAP : TENSION PNEUMOTHORAX AND SURGICAL EMPHYSEMA DURING ANAESTHESIA 221Indian J. Anaesth. 2004; 48 (3) : 221-223

BILATERAL TENSION PNEUMOTHORAX AND MASSIVESURGICAL EMPHYSEMA DURING ANAESTHESIA

Dr. (Mrs) Geeta A. Patkar1 Dr. (Mrs) S. R. Jagtap2

SUMMARYA ten year old male child presented for tonsillectomy, developed bilateral tension pneumothorax and massive surgical emphysema undergeneral anaesthesia. Prompt treatment saved the patient from fatality. This report highlights the possible mechanisms, clinical andradiological features and treatment of tension pneumothorax.Keywords : Bilateral tension pneumothorax, Surgical emphysema, Nonrebreathing circuit, Fish mouth valve.

1. M.D., D.A., Associate Professor2. M.D., D.A., Professor

Dept. of AnaesthesiologyLokmanya Tilak Muncipal Medical Collegeand General Hospital, Sion, Mumbai – 400022, Maharashtra.Correspond to :Dr. (Mrs) G. A. Patkar74, Anant Nivas Keluskar Road,Shivaji Park, Mumbai – 400 028, Maharashtra.E-mail : [email protected](Accepted for publication on 20-02-2004 )

IntroductionBilateral pneumothorax and surgical emphysema

are rare during the course of anaesthesia. However failureto recognise it and to provide prompt treatment mayresult in fatality. Pneumothorax can occur due to numberof mechanisms.1 Malfunctioning or misuse of equipmentused for intermittent positive pressure ventilation cancause high airway pressure resulting in lung damage.We present a case of bilateral tension pneumothoraxwith surgical emphysema associated with the use of afish mouth non rebreathing valve incorporated in anon rebreathing circuit.

Case reportA 10 year old male child, weighing 25 kgs,

presented for tonsillectomy under general anaesthesia.

Patient had no serious medical history and wasclinically stable. His investigations were within normallimits, Hb of 11.8 gm%, BT 4 min 5 sec and CT 3 min.The child was premedicated with inj. glycopyrolate 0.1mg intramuscularly half hour prior to surgery. Thepreinduction pulse rate was 110 min-1 and the bloodpressure was 120 mmHg systolic.

After adequate preoxygenation, anaesthesia wasinduced with inj. thiopentone sodium 150 mg andinj. succinylcholine 50 mg intravenously. The patientwas ventilated with 100% oxygen and intubated with

no. 6 portex oral cuffed endotracheal tube. Air entry wasconfirmed bilateraly and the cuff was inflated. Furtheranaesthesia was maintained using 60% nitrous oxide inoxygen, with intermittent halothane and vecuroniumbromide. Ventilaton was carried out using a non rebreathingcircuit with a fish mouth valve on a Drager anaesthesiamachine. The patients ECG, oxygen saturation and bloodpressure were monitored.

The surgery was completed uneventfully in thenext 45-50 mins. During confirmation of surgical hemostasis,the patients pulse suddenly dropped from 110 min-1 to50 min-1. This was associated with severe resistance toventilation and the oxygen saturation dropped from 99% to74%. Inj. atropine 0.3 mg was given IV immediately. Wesuspected an accidental extubation of the endotracheal tubeand reconfirmed its position. The patient was then ventilatedwith 100% oxygen, however the resistance to ventilationpersisted. The surgical drapes were removed, which revealedmassive surgical emphysema extending from the eyelids, tothe scrotum, cyanosis, and absent breath sounds bilaterallythough the pulse was palpable.

Bilateral tension pneumothorax was suspected fromthe above findings. Intermittent positive pressure ventilationwas suspended and 18G needles were introducedbilaterally in the 2nd intercostal space and connected toan under water seal drainage. Air leaked out underpressure and air entry improved. The patient had gainedspontaneous respiration by now and was allowed tobreathe 100% oxygen through a Magill’s circuit. Thepatients parameters improved. The oxygen saturationincreased to 90%, pulse rate to 150 min-1 and the bloodpressure was 110 mmHg systolic. Portable radiograph ofthe chest revealed bilateral pneumothorax (fig.1). Surgicalhelp was summoned.

Bilateral intercostal drainage (ICD) with underwaterseal were placed in the 5th intercostal space in the axilla.Air entry improved considerably with oxygen saturation of100%. There was no resistance to ventilation. The water

Page 2: bilateral tension pneumothorax and massive surgical emphysema

INDIAN JOURNAL OF ANAESTHESIA, JUNE 2004222

column in the intercostal drains was moving well withrespiration. The patient was haemodynamically stable. Inj.dexamethasone 8 mg and inj. mannitol 50 ml were given toprevent cerebral edema.

Subcutaneous emphysema disappeared in the next 36 hours.The ICD drains were removed on the 2nd and 3rd

postoperative days. Check radiograph of the chest showedfull expansion of the lungs. The patient was weaned oftracheostomy and discharged after one week.

DiscussionBilateral tension pneumothorax under anaesthesia has

been reported in the past.2,3,4 We reexamined its cause inour case. The non-rebreathing fish mouth valve is a verypopular device which was used in this case to provideintermittent positive pressure ventilation. However manyoperators are unaware of the potential for barotrauma,that may result from improper use of this common device.

Specifically high flow rates or use of emergencyoxygen flush must have made the reservoir bag tense,keeping the fish mouth valve open during expiration andoccluding the expiratory port (fig. 3. a,b,c.). This exposedthe lungs to an intrinsic PEEP and also preventedexpiration. Thus high airway pressure was generated, leadingto barotrauma. A similar mechanism of tensionpneumothorax with a self inflating bag valve device hasbeen described by Robert Silberghat et al.5A repeat radiograph revealed full expansion of both

the lungs with inter costal drains (fig. 2). The blood gasanalysis done at the point was normal.

In the next half an hour a tracheostomy was performedin view of the massive surgical emphysema.

Patient started responding to verbal commands andhis respiration and hemodynamic parameters were stable.Blood gas analysis was normal and the patient was shiftedto the post anaesthesia care unit breathing humidified oxygenthrough T-piece. The postoperative course was uneventful.

Fig. 3a : Normal function of fish mouth valve - Inspiratory Phase.

Fig. 3b : Normal function of fish mouth valve Expiratory phase.

Fig. 3B

Fig. 3A

Fig.2

Fig.1

INSPIRATORY PHASE

Exhalation port closed

Exhalation flapPatientFish mouth valveopen to patient

Inspiratory Port

Valve Body

Exhalation port open

Exhalation flapPatient

Fish mouth valveclosed to patient

Inspiratory Port

Valve Body

EXPIRATORY PHASE

Page 3: bilateral tension pneumothorax and massive surgical emphysema

PATKAR, JAGTAP : TENSION PNEUMOTHORAX AND SURGICAL EMPHYSEMA DURING ANAESTHESIA 223

Further, use of a cuffed endotracheal tube robbedthe airway of a relief value. In case a pressure relief valvewas incorporated in the circuit it would have prevented arise in the intra circuit pressure. Nitrous oxide used duringthe case could have aggravated the condition further.

Barotrauma occurs most commonly in patients withunderlying obstructive lung disease and is associated withhigh airway pressure.6

However in normal lungs it is most likely in themarginal alveoli as compared to the partitional alveoli.7

Partitional alveoli are supported by neighboring alveoli anddo not rupture with an increase in intraluminal pressure.However marginal alveoli which are adjacent to nonaeratedstructures are unsupported. Once an endotracheal tube is inposition and its cuff is inflated, excessive pressure in theanaesthesia circuit is transmitted to these alveoli resultingin their rupture.

Experimental alveolar distension in cats alwayscauses bilateral pneumothorax, as air tracks along bloodvessels to the hilum and the mediastinum. The pressurerequired to cause alveolar rupture is quite low. In dogseven 24 mmHg pressure is enough.8 Air tracks along theperivascular and peribronchiolar spaces to the mediastinum,it produces tension pneumomediastinum, which causes ruptureof the friable mediastinal pleura producing bilateralpneumothorax. As the pressure in the mediastinum increasesair seeps into the subcutaneous tissue to produce surgicalemphysema.1,6

This was the probable mechanism of tensionpneumothorax and surgical emphysema. As the pneumothorax

Fig. 3c : High fresh gas flows (FGF) occluding the expiratory port during expiration

came under tension, the patients condition deterioratedrapidly. Early clinical diagnosis and treatment with simplemeans saved the patient till radiology and surgicalintervention was available. Retrospectively a tracheostomycould have been avoided and an endotracheal tube couldhave served the purpose of an airway till the surgicalemphysema subsided.

ConclusionUse of a non rebreathing circuit is generally safe,

but minor deviations in their recommended use can exposepatients to barotraumas and sudden tension pneumothorax.The following cautions should be kept in mind,

1. Gas flows used for anaesthesia should be just highenough to keep the reservoir bag loosely filled.

2. A relief valve should always be incorporated in thecircuit.

3. When pressure is increasing in the bag, the firstmaneuver should be to disconnect the circuit fromthe endotracheal tube.

References1. John T Martin, Robert T Patrick, Rochester Minnesta

Pneumothorax. Its significance to the anaesthesiologist.Anesth Analg 1960; 39(5): 420-429.

2. Rastogi PN, Wright JE. Bilateral tension pneumothorax underanaesthesia. Anaesthesia 1969; 24(2): 249-252.

3. Doctor NH, Hussain Z. Bilateral pneumothorax associatedwith laproscopy. Anaesthesia 1973; 28: 75-81.

4. Spence M. Surgical emphysema during anaesthesia: Its natureand management. Anaesthesia 1955; 10: 50.

5. Robert Silbergliet, David C Lee, Cynthia Blank-Reid, RobertNamara. Sudden severe barotraumas from selfinflating BagValve devices. J Trauma 1996; 40(2): 320-322.

6. Pierson DJ. Alveolar rupture during mechanical ventilation:Role of peep, peak airway pressure and distending volume.Respiratory Care 1988; 33: 472-484.

7. Macklin MT, Macklin CC. Malignant interstial emphysema ofthe lungs and mediastinum as an important occult complicationin many respiratory diseases and other conditions: Aninterpretation of clinical literature in the light of laboratoryexperiment. Medicine, Baltimore 1944; 23: 281.

8. Marcotte RJ, Philips FJ, Adams WE, Livingstone H. Differentialintrabronchial pressures and mediastinal emphysema.J Thoracic Surg 1940; 9: 346.

Fig. 3C

INSPIRATORY PHASE Exhalation port closed

Exhalation flap closedPatient

Fish mouthvalve open

High FGF

Valve Body

Tenseresevoir

bag