Pneumothorax due to Ball-Valve Obstruction of an Endotracheal Tube in a Mechanically Ventilated Patient

Pneumothorax due to Ball-Valve Obstruction of an Endotracheal Tube in a Mechanically Ventilated Patient· john H . Russomanno . M .D.; and Lee K. Brown. M .D.• F.C.C.P.

Barotrauma is a well-known complication of mechanical ventilation, thought to be related to alveolar rupture from localized hyperinflation. Mishaps related to endotracheal intubation can lead to barotrauma such as inadvertent intubation of the right mainstem bronchus. In this report, we describe pneumothorax as a consequence of ball-valve occlusion, a previously undescribed endotracheal tube malfunction. (Chest 1992; 101:1444-45)

=

Flo. fractional concentration of inspired oxygen; Pco,

=

partial pressure of CO.; PEEP = positive end-expiratory pressure; Po. = partial pressure of 0.

pneumothorax. suhcutaneous emP neumomediastinum. physema, and interstitial emphysema are well-known

complications of mechanical ventilation, thought to be associated with regional or localized alveolar hyperinflation. I Alveolar hyperinflation can result from the use of positive pressure ventilation alone. from the use of excessive levels of PEEp, from inadvertent endobronchial intubation and from failure to allow for adequate expiratory time, especially in the presence of airway obstruction CautoPEEP" effect). In this communication we describe a previously unreported cause of hyperinflation and pneumothorax: one-way Chall-valve") endotracheal tube ohstruction. CASE REPORT

A 60-year-old white woman with a history of stage 3 ovarian carcinoma was admitted seven days after chemotherapy with complaints of weakness. anorexia. nausea. vomiting, cough, sweats and chills. Physical examination revealed a tachypneic patient in respiratory distress. Vital signs included respiratory rate of 44 hreaths per minute. systolic blood pressure of 60 mm H~ and a temperature of 37 .5°C . There were rales and rhonchi at the right lung base. A chest roentgenogram showed slight right costophrenie angle blunting. The hemoglobin value was 9.3 g percent and the white blood cell count was 400 cu mm . She was treated with intravenously administered ceftuzidime, gentamicin. metronidazole. and Ruids for presumed right lower lobe pneumonia with sepsis. On the second hospital day. she suffered a pulseless respiratory arrest and an oral endotracheal tube was inserted . Volume-eycled ventilation was at an assist/control rate of 16 breaths per minute: Fto., 0 .35; and tidal volume. 0.6 L. No PEEP was administered . Arterial blood gas values revealed a pH of 7.44; Pco, of 44 mm Hg; and Po, of lOS mm H~ . Hypotension improved with administration of dopamine after further volume repletion. By the third hospital day; a chest roentgenogram revealed evidence of right lower and middle lobe pneumonia. and hl'Nxl cultures grew Escherichia coli. Peak inspiratory pressure remained between 15 and 30 cm H,O with ventilator settings maintained as mentioned before. *From the Division of Pulmonarv and Critical Care Medicine. Mount Sinai Medical Center. Ne~ York. Reprint requests: Dr. Brown. Pulmonary Division. Box 12.32, Mt . Sinai Medical Center; New York 10029

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FIGURE 1. Mass of dried secretions and coagulated blood adherent over the Murphy eye with the d istal endotracheal tube port "ope n." as would occur during inspiration. On the seventh hospital day the patient developed respiratory distress and a sudden increase in peak inspiratory pressures to 90 cm H,o. Manual ventilation resulted in no improvement. Catheter suctioning of the endotracheal tube using a small amount of saline lavage yielded moderate amounts of tenacious secretions and some improvement of respiratory status. Breath sounds were equal bilaterally: Several minutes after the patient was reconnected to the ventilator. respiratory distress and high peak inspiratory pressures recurred. along with hypotension and bradycardia. Manual ventilation with the patient disconnected from the ventilator circuit was a~ain difficult even ufter deRating the endotracheal tube culf. Breath sounds over the right hemithorax were greatly diminished. with hyperresonance to percussion. jugular venous distension was present. Passage of a suction catheter appeared to meet SOIllI' resistance . The patient was treated with epinephrine and dopamine and was emergently extubated and reintubated . A chest tube also was inserted into the right side of the chest for a suspected tension pneumothorax . The patient responded with a prompt return to baseline vital signs and peak inspiratory pressures. A chest roentgl'noj!;ram taken during the acute event and viewed later confirmed the presence of a right tension pneumothorax, as well as marked subcutaneous emphysema. The patient's leukopenia and sepsis resolved. she was weaned from mechanical ventilation. and eventually was discharged from the hospital. Examination of the removed endotracheal tube revealed a mass of dried secretions and coagulated blood adherent to the internal wall of the endotracheal tube. adjacent to. and occluding, the Murphy eye . The mass extended beyond the e nd of the tube in a mobil e fashion capable of intermittently occluding the distal endotracheal tube port in a hall-valve manner (Fig 1 aud 2). COMMENT

Endotracheal tube ohstruction can occur from a wide variety of mechanisms. These include tube kinking! cuff herniation! and tube delamination, especially with the use

FI(:tIIlE 2. Mass of dried secretions and coagulated blood in the "d osed " position occluding the distal endotracheal tube port during expiration.

Pneumothorax due to BalI·VaIve Obstruction (Rossumanno, Brown)

of nitrous oxide in laminated, wire-reinforced endotracheal tubes.' A wide variety of foreign bodies also have been reported to cause endotracheal tube obstruction, including nasal turbinates avulsed during nasotracheal .intubation, 4 surgical tape," dried lubricant," a broken endotracheal tube stylet sheath" and retained plastic debris from the manufacturing of the Murphy eye." Another common complication of endotracheal tube use is right mainstem bronchus intubation which has been reported, in one series, to occur in 9.6 percent of all cases of intubation. 7 Alveolar hyperinflation, atelectasis and rightsided tension pneumothorax can result from right mainstem bronchus intubation. We are unaware, however, of any previously reported cases of tension pneumothorax resulting from ball-valve endotracheal tube obstruction. As demonstrated by the removed specimen (Fig 1 and 2) obstruction of an endotracheal tube by such a ball-valve mechanism requires both endotracheal tube ports to be involved in the occlusion. In this case, a mass of dried secretions and clotted blood was adherent inside the tube, completely occluding the Murphy eye. The remainder of the dried secretions and clot extended beyond the tip of the endotracheal tube. The large diameter and mobility of this mass allowed it to open and close over the distal endotracheal tube port. Inspiratory pressure would move the mass away from the distal port allowing inspiratory flow to occur; expiratory pressure distal to the endotracheal tube would push the mass into the distal port, occluding expiratory flow. The repeated ball-valve action of this mass resulted in pulmonary hyperinflation and consequent barotrauma, as manifested by a tension pneumothorax and subcutaneous emphysema. Whenever airway obstruction is suspected in an intubated patient, prompt, thoughtful intervention is necessary to locate and relieve the obstruction. By utilizing physical examination findings, manual ventilation, a suction catheter, and by deflating the endotracheal cuff the problem should be localizable to either the patient, the endotracheal tube, the cuff or the ventilator circuit. In this patient, difficult passage of the suction catheter suggested a problem related to the endotracheal tube. Urgent extubation and rein tubation revealed the nature of the endotracheal tube obstruction, while the physical findings allowed prompt recognition and treatment of the tension pneumothorax. REFERENCES

1 Petersen G~ Baier H. Incidence of pulmonary barotrauma in a medical I.C. U. Crit Care Med 1983; 11:67-69 2 Hosking M~ Lennon RL, \Varner MA, Gray JR, Masley ~ De Luca LA, et al. Endotracheal tube obstruction: recognition and management. Milit Med 1989; 154:489-91 3 Munson ES, Stevens OS, Redfern RE. Endotracheal tube obstruction by nitrous oxide. Anesthesiology 1980; 52:275-76 4 Ripley JF, McAnear JT, Tilson HB. Endotracheal tube obstruction due to impaction of the inferior turbinate. J Oral Maxillofac Surg 1984; 42:687-88 5 Zmyslowski W~ Kam 0, Simpson GT. An unusual cause of endotracheal tube obstruction [letter). Anesthesiology 1989; 70:833 6 Harrington JF. An unusual cause of endotracheal tube obstruction [letter]. Anesthesiology 1984; 61:116-17 7 Petty TL. Complications occurring during mechanical ventilation. Heart Lung 1976; 5:112-13

Deterioration of Ventricular Tachycardia to Ventricular Fibrillation after Rapid Intravenous Administration of Magnesium Sulfate* Sand Viskin, M.D.; Bernard Belhassen; M.D.; and Shlomo Laniado, M.D.

We report the case of a patient who had development of ventricular fibrillation following rapid intravenous administration of magnesium sulfate (2 g over 5 s) for treatment of sustained monomorphic ventricular tachycardia. Initial slowingof the tachycardia was followed by gradual widening of QRS complexes and electrical alternaDS, leading to ventricular fibrillation within 3 min of magnesium admin(Che.t 1992; 101:1445-41) istration.

vr =ventricular

=

tachycardia; VF ventricular 8brillation; LVEF = left ventricular ejection fraction; RBBB = right bundle

branch block

magnesium sulfate is a well-established treatI ntravenous ment of polymorphic ventricular tachycardia (VT) asso-

ciated with QT prolongation. I Recently, the use of magnesium was proposed as an alternative therapy for sustained monomorphic W. 2 Reservations concerning rapid administration of magnesium sulfate have been expressed, mainly relating to possible cardiac arrest:" however, electrocardiographic documentation of the sequence of events leading to cardiac arrest is not available. ~.5 We report the case of a patient who had development of ventricular fibrillation (VF) following rapid administration of magnesium sulfate for treatment of sustained monomorphicW. CASE REPORT

A 65-year-old man was hospitalized with an extensive anterior myocardial infarction complicated by severe left ventricular dysfunction (left ventricular ejection fraction [LVEF] = 21 percent, right hundle branch block [RBBB], and left anterior hemiblock). Two weeks later, he developed multiple episodes of sustained VI: The tachycardia was of monomorphic configuration, with rates ranging from 160 to 180 heats/min. VI' resulted in hemodynamic deterioration and invariably required electrical cardioversion for termination. Spontaneous deterioration of VT to VF, however, was never ohserved. Successive treatment with intravenous lidocaine, procainamide, hretylium tosylate, amiodarone, and magnesium sulfate (6 g over 24 h) failed to terminate or to prevent the episodes of sustained VI'. Nonoliguric renal failure occurred (with gradual increase of serum creatinine levels up to 4.5 mg/dl) and led to discontinuation of magnesium sulfate infusion. The last serum magnesium level, obtained shortly before discontinuation of treatment, was 3.7 mg/dl, Three days later, during a new episode of sustained monomorphic VI', which occurred while the patient was receiving a continuous infusion of procainamide and amiodarone (2 mglmin and 0.5 mgl min, respectively), a bolus of 2 ~ of magnesium sulfate (as a 10 percent solution) was administered over a period of 5 s (Fig 1). Progressive slowing of the VI', from 160 to 130 heats/min, was *From the Department of Cardiology, Ichilov Hospital, Tel Aviv Medical Center and Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. CHEST I 101 151 MA'f. 1992

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