Non-invasive positive pressure ventilation for severe thoracic trauma

M. J. Garfield1,* and R. M. Howard-Griffin

Intensive Care Unit, Ipswich Hospital NHS Trust, Heath Road, Ipswich IP4 5PD, UK 1Present address: Anaesthetic Department, Norfolk and Norwich Hospital, Brunswick Road, Norwich NR1 3SR, UK

Accepted for publication: May 27, 2000


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 35-year-old man was admitted to the intensive care unit (ICU) following a road traffic accident. He had sustained severe trauma to the left side of his chest, as well as other musculoskeletal injuries. After a short initial period of ventilation of the lungs via a tracheal tube, he was managed using a combination of continuous positive airway pressure and non-invasive positive pressure ventilation. He avoided ventilator-associated pneumonia, and spent a large part of his time on the ICU without any invasive monitoring lines, another potential focus of infection. He was discharged from the ICU after 25 days without having suffered any septic complications. The role of non-invasive positive pressure ventilation in severe thoracic trauma is discussed.

Br J Anaesth 2000; 85: 788–90

Keywords: ventilation, non-invasive; complications, trauma; complications, nosocomial pneumonia


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Victims of thoracic trauma are often referred to critical care services for assistance with analgesia and ventilation. Some of these patients have historically required long periods of ventilatory support, and have therefore been at high risk of acquiring nosocomial pneumonia. We report a case in which a patient with severe thoracic trauma (Abbreviated Injury Scale score 5/6 for thoracic injury (where 0 represents no injury, and 6 represents an unsurvivable injury1)) was managed mainly using non-invasive positive pressure ventilation (NIPPV), an approach which, we postulated, would be as effective as conventional ventilation, but expose him to a lower risk of nosocomial pneumonia.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 35-year-old pedal cyclist was hit by, and trapped under, a heavy goods vehicle. He was extricated by the emergency services, and brought to the accident and emergency department on a spinal board. His Glasgow coma score was 15 throughout. He was complaining of severe left-sided chest pain and marked shortness of breath. He had a respiratory rate of 40 b.p.m., and the clinical features of a left flail chest. His oxygen saturation by pulse oximeter was 85% on a fractional inspired oxygen concentration (FIO2) of 0.6. This was thought to be accurate as the probe was on an uninjured limb, there was a good trace on the monitor, and the patient was centrally cyanosed. He was tachycardic, with a heart rate of 140 beats min–1, and hypotensive, with an initial systolic blood pressure of 55 mm Hg. He was resuscitated initially with crystalloid solution, followed by blood when it was available. He received a total of 5.5 litres of crystalloid, followed by 9 units of packed red blood cells. His blood pressure responded well, if transiently, to intravascular filling.

A chest x-ray (Fig. 1) showed fractures of the second–ninth ribs on the left, with disruption of the costovertebral joints, resulting in a large flail segment. There was severe contusion of most of the left lung and contusion of the right lower lobe. He had a disruption of his left shoulder joint, a large laceration over his left iliac crest, and a fractured left ankle. His Revised Trauma Score was 6.0, which represents an expected mortality of approximately 10%, and his Trauma Score – Injury Severity Score (TRISS) expected mortality was 18%.1



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Fig 1 Admission chest x-ray, showing multiple left-sided rib fractures, massive left, and right lower lobe pulmonary contusion. A left intercostal drain is in situ.

 
In view of his injuries and cardiorespiratory instability, his trachea was intubated and his lungs ventilated. A left chest drain drained initially 500 ml of blood, but the loss quickly decreased. A right chest drain was inserted prophylactically, in accordance with current Advanced Trauma Life Support (ATLS) teaching for a patient with severe thoracic injury requiring positive pressure ventilation.2 This approach has arisen in view of the high risk of an occult pneumothorax in such patients.3 4

Computed tomography (CT) of the chest, cervical and thoracic spine, performed after stabilization confirmed the initial chest x-ray findings, as well as revealing bilateral small pneumothoraces and fractures of many of the spinous processes of the thoracic vertebrae. The neural arches were, however, intact and there was no evidence of spinal cord injury. The cervical spine appeared normal.

The patient’s lungs were ventilated using volume controlled ventilation, with a positive end-expiratory pressure (PEEP) of 6 cm H2O, and an FIO2 of 0.35 (Servo 900C ventilator, Siemens-Elema, Sweden). This resulted in an arterial oxygen partial pressure (PaO2) of 13.7 kPa. He was thought not to require an open lung strategy as his peak airway pressure was acceptable (<25 cm H2O), and oxygenation was not problematic. His initial cardiovascular instability was such that high levels of PEEP were thought inadvisable.

After a 48-h period of stabilization, and once his coagulopathy (a result of the massive transfusion) had been treated by infusion of fresh frozen plasma and cryoprecipitate, a thoracic epidural was inserted at the T7/8 level, and infusion of bupivacaine commenced. The epidural provided good analgesia for the thoracic injuries, but the shoulder fracture continued to produce a lot of pain. A patient-controlled analgesia infusion of morphine was therefore also commenced. These infusions resulted in good analgesia, ventilatory support was weaned off, and his trachea was extubated on the fourth day after admission.

On day 5, increasing oxygen requirement was treated with periods of intermittent positive pressure breathing (IPPB) via a Bird ventilator and continuous positive airway pressure (CPAP) by facemask. IPPB is a form of treatment, usually administered by the physiotherapists, which is designed to reinflate collapsed pulmonary segments and so reduce shunting of deoxygenated blood. The patient uses a mouthpiece; the lungs are ventilated with a constant pressure. Despite this, by day 7 his FIO2 had risen to 0.6, giving a PaO2 of only 9 kPa. Facial CPAP at a level of 7.5 cm H2O was continued and negative fluid balances were obtained by fluid restriction and forced diuresis by loop diuretics. Fluid balance was monitored in the usual way by detailed input/output charts and urethral catheterization. These treatments resulted in reduction of his FIO2 to 0.45.

On day 9, after internal fixation of his ankle, the patient’s lungs were ventilated overnight. Following tracheal extubation the next morning, he was given CPAP at a level of 7.5 cm H2O by facemask. At this stage he still had a large flail segment, and radiological and clinical evidence of continuing contusion in his left lung. The right basal contusion had now resolved.

Over the next 72 h, the patient developed increasing respiratory distress, with an increasing respiratory rate (up to 50 b.p.m.), shallow breathing and an uneven respiratory pattern, and the FIO2 had increased to 0.6, in order to maintain a PaO2 of 10 kPa. On day 12, NIPPV was commenced via a nasal mask (NIPPY2 ventilator, Aeromed, UK), with an immediate reduction in his oxygen requirements. He remained on continuous nasal NIPPV for a further 9 days, with a reducing level of pressure support and CPAP; the NIPPV was tolerated extremely well throughout. His invasive lines were all removed on day 18.

By day 20, he was receiving only intermittent NIPPV, and otherwise had an oxygen saturation (SaO2) of 98% on 3 litres min–1 of oxygen via nasal cannulae. On day 22, he was given NIPPV overnight only, and the NIPPV was discontinued on day 24. Nocturnal CPAP by facemask continued for a further night, and he was discharged to the ward on day 26.

Apart from a 5-day course of flucloxacillin to treat a Staphylococcus aureus infection in a laceration, the patient required no antibiotics during his stay on the intensive care unit (ICU). At no stage was there any evidence of systemic or pulmonary infection.


    Discussion
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Ventilator-associated pneumonia represents a major subgroup of nosocomial pneumonia, a condition that is associated with a mortality of 30%.5 In those patients who survive, ventilator-associated pneumonia is associated with increased morbidity, longer ICU stays, and hence increased costs.6 The pathogenesis of this condition involves bacterial colonization of the upper aerodigestive tract, and hence oropharyngeal secretions. These contaminated secretions pool above the cuff of the tracheal tube, and are aspirated into the trachea during patient movement, coughing, tracheal suctioning and many other manoeuvres.79 Tracheal intubation has indeed been shown to be an important risk factor for the development of ventilator-associated pneumonia,10 and so it would seem sensible to avoid this if at all possible.11

NIPPV has been shown to be as effective as conventional ventilation in a variety of settings, including exacerbations of chronic obstructive pulmonary disease12 and acute respiratory failure.13 The causes of the acute respiratory failure in the latter paper ranged from infection and pulmonary oedema to acute respiratory distress syndrome. To date, there have been no reports of the use of NIPPV in severe chest trauma.14

Nava et al.12 allocated random patients with exacerbations of chronic obstructive pulmonary disease to either NIPPV or conventional ventilation, after an initial period of 48 h conventional ventilation. Seven out of 25 patients in the conventionally ventilated group developed ventilator- associated pneumonia, compared to none of the NIPPV group (P=0.009). Antonelli et al.13 allocated random patients to either NIPPV or conventional ventilation from the outset. Again, the patients ventilated non-invasively had a significantly lower incidence of ventilator-associated pneumonia and sinusitis. While this study had some minor methodological flaws, it demonstrates a clear difference in infective complications between the two groups, and adds further evidence to the hypothesis discussed above, that avoidance of tracheal intubation reduces the incidence of ventilator-associated pneumonia, and thus decreases length of ICU stay and other variables.6

Thoracic injury consists of a spectrum of disease, ranging from rib fractures with mild pulmonary contusion to disruption of the thoracic cage and acute respiratory distress syndrome. Although many of the less severely injured patients are now managed without ventilatory support, with a thoracic epidural and aggressive chest physiotherapy,14 there will always be a number for whom this is not sufficient. These patients, usually with significant hypoxaemia, often require an extended period of invasive ventilation,15 and the risk of ventilator-associated pneumonia is thus high. We believe that in this group, avoidance of tracheal intubation and hence avoidance of ventilator-associated pneumonia may be a major step in reducing ICU stay, morbidity and mortality. NIPPV is safe, effective, and, we believe, may be the mode of choice for managing patients with thoracic trauma who have no contraindications to its use. We have since used NIPPV in a further two patients with bilateral flail chest and lesser degrees of pulmonary contusion, and had very similar results with regard to effectiveness of the ventilatory support, and avoidance of ventilator-associated pneumonia.


    Footnotes
 
* Corresponding author Back


    References
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Boyd CR, Tolson MA, Copes WS. Evaluating trauma care: the TRISS method. J Trauma 1987; 27: 370–8[ISI][Medline]

2 American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors, 6th edition. Chicago, Illinois: American College of Surgeons, 1997; 127–41

3 Hill SL, Edmisten T, Holtzman G, Wright A. The occult pneumothorax: an increasing diagnostic entity in trauma. Am Surg 1999; 65: 254–8[ISI][Medline]

4 Collins JA, Samra GS. Failure of chest X-rays to diagnose pneumothoraces after blunt trauma. Anaesthesia 1998; 53: 74–8

5 Crabtree TD, Gleason TG, Pruett TL, Sawyer RG. Trends in nosocomial pneumonia in surgical patients as we approach the 21st century: a prospective analysis. Am Surg 1999; 65: 706–9

6 Kelleghan SI, Salemi C, Padilla S, et al. An effective continuous quality improvement approach to the prevention of ventilator-associated pneumonia. Am J Infect Control 1993; 13: 322–330

7 Bonten MJ, Gaillard CA, de Leeuw PW, Stobberingh EE. Role of colonisation of the upper intestinal tract in the pathogenesis of ventilator-associated pneumonia. Clin Infect Dis 1997; 24: 309–19[ISI][Medline]

8 Greene R, Thompson S, Jantsch HS, et al. Detection of pooled secretions above endotracheal-tube cuffs: value of plain radiographs in sheep cadavers and patients. Am J Roentgenol 1994; 163: 1333–7[Abstract]

9 Kingston DW, Phang PT, Leathley MJ. Increased incidence of nosocomial pneumonia in mechanically ventilated patients with subclinical aspiration. Am J Surg 1991; 161: 589–92[ISI][Medline]

10 Craven DE, Steger KA. Epidemiology of nosocomial pneumonia. New perspectives on an old disease. Chest 1995; 108: 1S–16S[Free Full Text]

11 Kollef MH. Avoidance of tracheal intubation as a strategy to prevent ventilator-associated pneumonia. Intensive Care Med 1999; 25: 553–5[ISI][Medline]

12 Nava S, Ambrosino N, Clini E, et al. Non-invasive mechanical ventilation in the weaning of patients with respiratory failure due to chronic obstructive pulmonary disease. Ann Intern Med 1998; 128: 721–8[Abstract/Free Full Text]

13 Antonelli M, Conti G, Rocco M, et al. A comparison of non-invasive positive pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. New Eng J Med 1998; 339: 429–35[Abstract/Free Full Text]

14 Mazuski JE, Durham RM. Management of the chest injury. In: Webb AR, Shapiro MJ, Singer M, Suter PM, eds. Oxford Textbook of Critical Care. Oxford: Oxford University Press, 1999; 715–8

15 Jackson J. Management of thoracoabdominal injuries. In: Capan LM, Miller SM, Turndorf H, eds. Trauma Anesthesia and Intensive Care. Philadelphia: Lipincott, 1991; 481–3





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