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* From the Departments of Anesthesia and Critical Care, and
Surgery, Sunnybrook and Women’s College Health Sciences Centre, and
the Department of Surgery, Ross Tilley Burn Centre, Toronto, Ontario, Canada.
Address correspondence to: Dr. Robert Cartotto, Ross Tilley Burn Centre, Sunnybrook and Women’s College Hospital, Room D712, 2075 Bayview Avenue, Toronto, Ontario M4N 3M5, Canada. Phone: 416-480-6706; Fax: 416-480-6708; E-mail: Robert.Cartotto{at}swchsc.on.ca
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Abstract |
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Clinical features: A 19-yr-old male with smoke inhalation and flame burns to 50% total body surface area was admitted to the Ross Tilley Burn Centre. High frequency oscillatory ventilation (HFOV) was initiated on day three for treatment of severe hypoxemia. By day four, the patient met consensus criteria for acute respiratory distress syndrome. On day nine, alveolar ventilation was severely compromised and was characterized by hypercapnea (PaC02 136 mmHg) and acidosis (pH 7.10). Attempts to improve CO2 elimination by a decrease in the HFOV oscillatory frequency and an increase in the amplitude pressure failed. An intentional orotracheal tube cuff leak was also ineffective. A 6.0-mm nasotracheal tube was inserted into the supraglottic hypopharynx to palliate presumed expiratory upper airway obstruction. After nasotracheal tube placement, an intentional cuff leak of the orotracheal tube improved ventilation (PaCO2 81 mmHg) and relieved the acidosis (pH 7.30). The improvement in ventilation (with normal oxygen saturation) was sustained until the patient’s death from multiple organ dysfunction four days later.
Conclusion: During HFOV in burn patients, postresuscitation edema of the supraglottic upper airway may cause expiratory upper airway obstruction. The insertion of a nasotracheal tube, combined with an intentional orotracheal cuff leak may improve alveolar ventilation during HFOV in such patients.
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Introduction |
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While it has become commonplace to adopt a lung protective ventilation approach to patients with thermal and inhalation injury, clinical experience with HFOV in adult burn patients is not well documented in the literature. Evidence in this population is limited to improvements in oxygenation in small case series of adult burn patients.5,6 Complications associated with HFOV in the above studies included hypotension, barotrauma (pneumothorax, pneumomediastinum), desiccation of secretions and equipment failure. While alveolar hypoventilation (hypercapnic respiratory failure) may occur during initial management of HFOV,7 carbon dioxide elimination has been found to be superior compared to conventional ventilation.5 We present an adult burn patient in whom, to the contrary, severe alveolar hypoventilation was encountered and we discuss our management of this unusual clinical problem.
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Case report |
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On day three at 07:00, pressure control ventilation (PCV) settings were peak inflation pressure (PIP) 34 cm H2O, PEEP 10 cm H2O, tidal volume 540 mL, rate 18 min-1 with a PaO2/ FIO2 ratio of 103. The chest x-ray showed mild interstitial pulmonary edema, pleural fluid tracking superiorly and left lower lobe atelectasis. At 12:00 hr, HFOV was initiated to improve oxygenation within the context of evolving hypoxemic respiratory failure. HFOV settings were FIO2 1.0, mean airway pressure 35 cm H2O, frequency 4 Hz, I: E 33%. Amplitude was set to obtain oscillations to mid-thigh level. The patient subsequently underwent staged excision and grafting of his burn wounds. On day four the patient’s hypoxemia, bilateral airspace consolidation and the lack of evidence for congestive heart failure satisfied consensus criteria for ARDS.8
On day five the patient had developed abdominal compartment syndrome, manifested by worsening oliguria, and intra-abdominal pressures > 30 mmHg by bladder transduction, and was taken urgently to the operating room for a decompressive laparotomy. Following laparotomy, there was no further evidence of abdominal hypertension based on daily measurements of intra-abdominal pressure by bladder transduction.
On day seven, operative debridement and temporary allografting of the face and neck was performed. On arrival in the operating room the patient became impossible to ventilate due to an apparent obstruction of the tracheostomy tube. Fibreoptic endoscopy did not disclose the cause of the obstruction. The patient was orally re-intubated with an 8.0 oral endotracheal tube by the anesthesiologist. Postoperatively the patient developed hypercapnic ventilatory failure and at 21:00 hr ventilation was briefly changed to PCV mode. With PIP 48 cm H2O, PEEP 20 cm H2O, tidal volume 800 mL and rate 16 min-1 the arterial blood gases were pH 7.23 pCO2 68 pO2 145 HCO3- 29. The patient’s subsequent ventilation and oxygenation course are presented in graphic form in Figure 1
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Hypercapnic ventilatory failure continued on day nine. The endotracheal tube cuff leak was sealed because of concerns about oxygenation. This resulted in a zenith of hypoventilation at 18:00 hr, while oscillator settings were FIO2 1.0, mean airway pressure 48 cm H2O, frequency 3 Hz, I: E 33%, with 
P power set as before. Blood gases then were pH 7.10 pCO2 136 pO2 139 HCO3- 44, PaO2/ FIO2 ratio 278. After much reflection, we entertained the possibility that massive edema of the upper airway might have prevented egress of CO2 after initiation of the endotracheal tube cuff leak. To create an effective upper airway, a 6.0 endotracheal tube was gently inserted through the left naris into the hypopharynx (Figure 2). The orotracheal cuff leak was re-instituted at 21:00 hr. There was free gas flow through the lumen of the nasotracheal tube and a change in the pitch of the oscillation of the ventilator diaphragm was noted. CO2 elimination immediately and dramatically improved; at 22:00 pH 7.30 pCO2 85 pO2 82 HCO3- 42, PaO2/ FIO2 ratio 170. The improvement in alveolar ventilation persisted until the patient’s death (Figure 1
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Discussion |
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P) is centered over the Pmean and oscillates above and below the Pmean with each short breath. Thus, the Pmean is only exceeded by P/2 at the peak of each brief inspiratory phase. However, it is estimated that only 10% of the P/2 is transmitted to the alveoli.11 Hence, during HFOV, alveolar recruitment is achieved with sustained mean airway pressures, while avoiding significant or prolonged over-distending peak pressures. During HFOV, expiration is active and CO2 elimination is manipulated by adjusting the oscillatory frequency, and the P. At the bedside, the initial P is empirically adjusted so that the chest wall vibrations are transmitted as far as the mid-thigh, to create thigh "wiggle".5 This usually correlates with a P that is adequate for effective CO2 removal. However, the P may need to be adjusted thereafter based on the PaCO2 . We describe an adult patient with cutaneous burns and ARDS in whom a reduction in HFOV frequency setting to 3 Hz (with adequate oscillatory amplitude) failed to improve alveolar ventilation. A common practice when this measure fails is to create an intentional cuff leak in the oral endotracheal tube. This usually improves CO2 elimination and is recommended by the manufacturer’s training manual.5,12
When the change in HFOV settings and an intentional cuff leak failed to improve ventilation, we first satisfied ourselves that there was no malfunction of the ventilator circuit or endotracheal tube. It was acknowledged that the patient’s burn could be expected to result in increased carbon dioxide production. However, the deterioration occurred acutely and minute ventilation had previously been adequate which suggested that an acute increase in carbon dioxide production was unlikely to be the cause of the problem. The smoke inhalation injury he sustained had previously resulted in clinically minor alveolar hypoventilation, without an excessive volume of secretions from the lower airway. There was no evidence of lower airway obstruction clinically, and chest x-rays did not show hyperinflation consistent with gas trapping. The possibility of an acute increase in physiological deadspace resulting from pulmonary embolism was considered. However, a concurrent deterioration in oxygenation had not occurred and the patient remained hemodynamically stable. The patient had received prophylactic anticoagulation with subcutaneous heparin since admission. He was judged to have an intermediate probability (20–79%) of pulmonary embolism based on clinical criteria.13 Because of the risk involved in transporting the patient to the computed tomography (CT) suite in his unstable condition, a decision was made to investigate pulmonary embolism with CT angiography only if measures to improve ventilation failed to be effective. Systemic anticoagulation with therapeutic-dose heparin was considered inadvisable in view of the patient’s risk factors for surgical bleeding.
Carbon dioxide elimination during HFOV was studied extensively in animal models during the 1980’s. During HFOV CO2 excretion is essentially independent of lung volume above functional residual capacity, up to high transpulmonary pressures.14 Log - log plots show that arterial PCO2 decreases linearly as a function of the product of frequency and the square of tidal volume. Carbon dioxide transport during HFOV depends on an inefficient diffusion mechanism, dependent on frequency and tidal volume, and a more efficient convective mechanism that is dependent on tidal volume.15 At the bedside, improved alveolar ventilation is achieved by increasing the amplitude and reducing the frequency.16 The common clinical observation of improved CO2 elimination with a reduction in oscillatory frequency probably results from reduced impedance and increased tidal volume as oscillation approaches the natural frequency of the patient’s respiratory system (Slutsky A, personal communication). There had been no observed decrease in our patient’s oscillatory amplitude at the time of the ventilatory crisis. In contrast to conventional ventilation modes, alterations in the ratio of inspiratory to expiratory time have little effect on carbon dioxide elimination during HFOV.17
Physical examination of the patient during the crisis was revelatory. The patient was in supine position, and the chest was oscillating freely. Oscillations could also be seen to mid-thigh level. Auscultation of the chest was positive only for the expected transmitted sounds of the ventilator’s oscillating diaphragm. Severe edema of the visible upper airway (nose, tongue, and lips) was associated with an increased neck circumference (Figure 2). These features of the patient’s condition together with alveolar hypoventilation crisis suggested an analogy with the obstructive sleep apnea syndrome (OSAS). Increased neck circumference in OSAS is highly correlated with patient symptoms and objective evidence of sleep-disordered breathing.18 Magnetic resonance imaging studies of the upper airway anatomy of patients with OSAS have demonstrated thickened lateral pharyngeal walls as the substrate for upper airway obstruction.19 Nocturnal noninvasive ventilation (bilevel positive airway pressure) improves alveolar ventilation by stenting the obstructed upper airway, thereby increasing airway caliber.20 Although occurring in a very different clinical setting from OSAS, upper airway obstruction due to edema was a probable cause for the failure of an intentional endotracheal tube cuff leak to improve our patient’s alveolar ventilation during HFOV. The immediate and sustained improvement in carbon dioxide elimination (PaCO2 136–85 mmHg) that occurred after insertion of a nasopharyngeal airway, we believe, is consistent with this mechanism of ventilatory failure.
In summary, we feel this case emphasizes important principles of ventilator management that are applicable to any patient, regardless of mode of mechanical ventilation. During an acute ventilatory crisis it is important to ensure adequacy of the airway and to exclude technical failure of the mechanical ventilator. A thorough and systematic review of the physiology of the acute problem with consideration of the impact of the patient’s unique pathophysiology may suggest an intervention. In the case presented, the unusual problem of expiratory upper airway obstruction during HFOV was identified and successfully treated by following the steps described.
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Footnotes |
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Revision received May 13, 2002. Accepted for publication January 14, 2002.
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References |
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2 The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301–8.
3 Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338: 347–54.
4 Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome. A randomized controlled trial. JAMA 1999; 282: 54–61.
5 Mehta S, Lapinsky SE, Hallett DC, et al. Prospective trial of high-frequency oscillation in adults with acute respiratory distress syndrome. Crit Care Med 2001; 29: 1360–9.[Medline]
6 Cartotto R, Cooper AB, Esmond JR, Gomez M, Fish JS, Smith T. Early clinical experience with high-frequency oscillatory ventilation for ARDS in adult burn patients. J Burn Care Rehabil 2001; 22: 325–33.[Medline]
7 Fort P, Farmer C, Westerman J, et al. High-frequency oscillatory ventilation for adult respiratory distress syndrome - a pilot study. Crit Care Med 1997; 25: 937–47.[Medline]
8 Bernard GR, Artigas A, Brigham KL, et al., and the Consensus Committee. The American-European consensus conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Resp Crit Care Med 1994; 149: 818–24.[Abstract]
9 Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med 1995; 23: 1638–52.[Medline]
10 Innes M, Cartotto RC, Cooper AB, Fish JS, Gomez, M. The multiple organ dysfunction score (MODS) in burn patients. J Burn Care Rehabil 2001; 22: 109.
11 Brambrink AM, Brachlow J, Weiler N, et al. Successful treatment of a patient with ARDS after pneumonectomy using high-frequency oscillatory ventilation. Intensive Care Med 1999; 25: 1173–6.[Medline]
3100A High Frequency Oscillatory Ventilator Training Manual. 1997.
13 Hyers TM. Venous thromboembolism. Am J Respir Crit Care Med 1999; 159: 1–14.
14 Slutsky AS, Kamm RD, Rossing TH, et al. Effects of frequency, tidal volume, and lung volume on CO2 elimination in dogs by high frequency (2–30 Hz), low tidal volume ventilation. J Clin Invest 1981; 68: 1475–84.
15 Boynton BR, Hammond MD, Fredberg JJ, Buckley BG, Villanueva D, Frantz ID 3rd. Gas exchange in healthy rabbits during high-frequency oscillatory ventilation. J Appl Physiol 1989; 66: 1343–51.
16 Morgan C, Dear PR, Newell SJ. Effect of changes in oscillatory amplitude on PaCO2 and PaO2 during high frequency oscillatory ventilation. Arch Dis Child Fetal Neonatal Ed 2000; 82: F237–F42.
17 Venegas JG, Yamada Y, Custer J, Hales CA. Effects of respiratory variables on regional gas transport during high-frequency ventilation. J Appl Physiol 1988; 64: 2108–18.
18 Flemons WW, Whitelaw WA, Brant R, Remmers JE. Likelihood ratios for a sleep apnea clinical prediction rule. Am J Respir Crit Care Med 1994; 150: 1279–85.[Abstract]
19 Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995; 152: 1673–89.[Abstract]
20 Schwab RJ, Pack AI, Gupta KB, et al. Upper airway and soft tissue structural changes induced by CPAP in normal subjects. Am J Respir Crit Care Med 1996; 154: 1106–16.[Abstract]
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