Tracheal-innominate artery fistula caused by the endotracheal tube tip: case report and investigation of a fatal complication of prolonged intubation.

CASE REPORT: A patient with extensive burns was intubated with an 8.0 mm internal diameter endotracheal tube (ETT) equipped with a subglottic suction port (Mallinckrodt HiLo Evac). The ETT was secured to a left upper molar with wire sutures throughout the hospitalization course to ensure airway stability. On the 40th day of intubation, the patient exsanguinated and died from a tracheo-innominate artery fistula. Postmortem examination revealed a 1 cm lesion of the left anterior tracheal wall at the position of the ETT tip. The prolonged stationary position of the ETT was considered the primary factor responsible for the fistula. Yet tracheo-innominate artery fistula normally is associated with high cuff pressures rather than with the tube tip. The special ETT construction required for the subglottic suction feature was suspected to have increased tube rigidity and may have played a contributory role. METHODS: The rigidity of the Mallinckrodt HiLo Evac was measured with a mechanical model and compared to 5 other commercially-available ETTs. Rigidity was expressed as the force generated by the ETT tip when the tube curvature was altered by 5 cm and 10 cm of flexion from its resting position. RESULTS: The mean force exerted by the Mallinckrodt HiLo Evac was 10.1 +/- 2.8 g at 5 cm of flexion and 17.7 +/- 5.1 g at 10 cm of flexion. This was significantly greater than all other ETT brands tested (by one-way analysis of variance and Student-Newman-Kuels test, p < 0.05). CONCLUSION: This case of fatal tracheo-innominate artery fistula formation associated with an ETT tip was unusual because of the extended duration of endotracheal intubation and the complexity of the patient's airway management problems. Our data suggest that the higher rigidity of the HiLo Evac ETT may have contributed to fistula development at the tube tip. However, we do not believe that the higher rigidity of the HiLo Evac ETT necessarily poses any greater risk than other ETTs under normal circumstances, in which the tube tip is not fixed in a stationary position for an extended period.

Lung collapse during low tidal volume ventilation in acute respiratory distress syndrome.

BACKGROUND: Current ventilator management for acute respiratory distress syndrome (ARDS) incorporates low tidal volume (V(T)) ventilation in order to limit ventilator-induced lung injury. Low V(T) ventilation in supine patients, without the use of intermittent hyperinflations, may cause small airway closure, progressive atelectasis, and secretion retention. Use of high positive end-expiratory pressure (PEEP) levels with low V(T) ventilation may not counter this effect, because regional differences in intra-abdominal hydrostatic pressure may diminish the volume-stabilizing effects of PEEP. CASE SUMMARY: A 35-year-old man with abdominal compartment syndrome (intra-abdominal pressure > 48 cm H2O developed ARDS and was treated with V(T) of 4.5 mL/kg and PEEP of 20 cm H2O. Despite aggressive fluid therapy, appropriate airway humidification and tracheal suctioning, the patient developed complete bronchial obstruction, involving the entire right lung and left upper lobe. After bronchoscopy the patient was placed on a higher V(T) (7.0 mL/kg). Intermittent PEEP was instituted at 30 cm H2O for 2 breaths every 3 minutes. This intermittently raised the end-inspiratory plateau pressure from 38 cm H2O to 50 cm H2O. With the same airway humidity and tracheal suctioning practices bronchial obstruction did not reoccur. CONCLUSION: Low V(T) ventilation in ARDS may increase the risk of small airway closure and retained secretions. This adverse effect highlights the importance of pulmonary hygiene measures in ARDS during lung-protective ventilation.

Measuring intra-esophageal pressure to assess transmural pulmonary arterial occlusion pressure in patients with acute lung injury: a case series and review.

BACKGROUND: Positive end-expiratory pressure (PEEP) may interfere with accurate assessment of cardiac function. PEEP may decrease left ventricular volume by lowering the transmural gradient between ventricular and pleural surface pressure (P(PL)) around the heart while raising the absolute pulmonary arterial occlusion pressure (PAOP). Clinical formulas used to predict the transmural PAOP (PAOP(TM)) require subtracting 25-50% of the PEEP level from the PAOP. However, both PAOP and P(PL) are influenced by transmitted PEEP and transmitted intra-abdominal pressure (IAP). We compared PAOP(TM) calculated by measuring intra-esophageal pressure (P(ES)) with PAOP(TM) estimated by clinical formulas. METHODS: Twenty-two P(ES) measurements were made with a bedside pulmonary mechanics monitor (BICORE CP-100) on 11 patients with acute lung injury who had an elevated PAOP (mean +/- standard deviation) of 21.1 +/- 6.2 mm Hg and PEEP of 13.0 +/- 3.8 mm Hg. Paired comparisons were made with the Wilcoxon signed-rank test and multiple comparisons were made using one-way analysis of variance (ANOVA) and the Student-Newman-Keuls test. Pearson product-moment correlation coefficients were calculated. A MEDLINE literature search was done to survey the reported range of PEEP transmitted to P(PL). RESULTS: P(ES) (14.6 +/- 5.0 mm Hg) exceeded PEEP; 9 of 11 patients had clinical evidence of increased IAP. PAOP(TM) predicted by clinical formulas were 13.5-17.7 mm Hg, whereas PAOP(TM) calculated by P(ES) was 6.2 +/- 3.6 mm Hg (p < 0.05). Linear regression revealed a moderate correlation between PAOP and PEEP (r = 0.49, p = 0.02). In contrast, there was a strong correlation between PAOP and P(ES) (r = 0.83, p < 0.0001). A review of data derived from the literature did not show a consistent pattern of PEEP transmission. CONCLUSION: PAOP(TM) calculated by P(ES) may reflect transmitted IAP to the pleural surface. Using P(ES) to calculate PAOP(TM) may provide a more accurate assessment of hemodynamic status than predicting PAOP(TM) using clinical formulas based solely on estimated PEEP transmission.

The rise and fall of i-STAT point-of-care blood gas testing in an acute care hospital.

In response to a $350,000 laboratory budget cut and closure of an intensive care unit-based laboratory and a desire to maintain turnaround times of 10 minutes or less, a multidisciplinary group developed and implemented point-of-care (POC) testing. Only blood gases (pH, PO2, and PCO2) and ionized calcium values were deemed essential stat tests. Three commercially available POC blood gas devices were evaluated; all yielded results comparable to in-house reference methods. The 1 device with a US Food and Drug Administration-approved method for ionized calcium testing and with an existing interface for laboratory information systems was selected. Fiscal analysis predicted annual savings of approximately $225,000. POC blood gas analysis was implemented in April 1996 coincident with closure of the intensive care unit-based laboratory. Clinical laboratories and POC blood gas test volumes remained constant through August 1998; in contrast, the number of ionized calcium tests decreased dramatically after April 1996. In August 1998, clinically significant (i.e., artificial ventilation parameters would have been altered based on test results) discrepant PCO2 values were observed sporadically and noted only with patient specimens, not with commercial controls or electronic simulators. Because investigation failed to identify the cause, use of the POC device was discontinued in September 1998.