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Acute lung injury secondary to intra-abdominal hypertension and abdominal decompression in a burn patient
Injury Extra 40 (2009) 106–108
Contents lists available at ScienceDirect
Injury Extra journal homepage: www.elsevier.com/locate/inext
Case report
Acute lung injury secondary to intra-abdominal hypertension and abdominal decompression in a burn patient Jun Oda *, Katsuyuki Yamashita, Takuya Inoue, Yoshiki Aoki, Kazuharu Mega, Mitsuhiro Noborio, Nobuyuki Harunari, Masashi Ueyama Department of Trauma, Critical Care Medicine and Burn Center, Social Insurance Chukyo Hospital, Nagoya, Aichi, Japan
A R T I C L E I N F O
Article history: Accepted 19 January 2009
1. Introduction Secondary abdominal compartment syndrome (ACS) is known as a lethal complication after resuscitation from burn shock due to the large volume of resuscitation fluid and fluid shift.7,14 Although several cases successfully treated by surgical decompression,4,8 and percutaneous drainage3,9 have been reported, the prognosis of severely burned patients is generally very poor once ACS develops. ACS has been identified to be an independent predictor,1 and could be a second hit for multiple organ dysfunction.11,15 We report here a burn patient with ACS who developed acute lung injury (ALI) shortly after abdominal decompression even though hemodynamic parameters immediately improved. Ischaemia–reperfusion injury was suspected of being involved in the development of ALI. 2. Case The patient (55-year-old male) was admitted after being severely burned (87% TBSA with 41% full thickness) except for the head and part of the right upper limb by accidental falling into a scalding hot water (90 8C) tank at work. Admission occurred 1 h after injury. Prior to the accident the patient was healthy, and his weight was 67 kg before the accident and he was not taking any medication. During the first 24-h post-burn after admission, Lactated Ringer’s solution was administered to meet the resuscitation endpoint for urine output (UO) of 0.5–1 mL/(kg h). Haemoconcentration was prolonged (hematocrit = 58%, at 12 h). The total
* Corresponding author at: Department of Emergency and CCM, Tokyo Medical University, 6-7-1 Nishishinjuku, Tokyo 160-0023, Japan. Tel.: +81 3 3342 6111; fax: +81 3 3342 5687. E-mail addresses: [email protected] (J. Oda), [email protected] (K. Yamashita), [email protected] (T. Inoue), [email protected] (Y. Aoki), [email protected] (K. Mega), [email protected] (M. Noborio), [email protected] (N. Harunari), [email protected] (M. Ueyama). 1572-3461/$ – see front matter ß 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2009.01.119
volume of crystalloid administered during the first 20 h, already exceeded the expected 4 mL/(kg %TBSA): 27,500 mL (4.7 mL/ (kg %TBSA 20 h)). At 20 h PB, the peak inspiratory pressure (PIP) exceeded 50 cmH2O, and tense abdomen was noted (Fig. 1). One hour later, the patients developed severe intra-abdominal hypertension (IAH) with an intra-abdominal pressure (IAP) of 60 cmH2O. Decompression was performed, resulting in an immediate decrease in IAP from 60 cmH2O to 35 cmH2O, PIP from 64 cmH2O to 43 cmH2O, and increase of abdominal perfusion pressure (APP) from 42 mmHg to 62 mmHg, cardiac output (CO) from 4.5 L/(min m2) to 7.5 L/ (min m2), central venous pressure (CVP) from 20 cmH2O to 9 cmH2O, pulmonary artery wedge pressure (PAWP) from 38 mmHg to 21 mmHg, pulmonary static compliance calculated as the tidal volume divided by (PIP minus positive end-expiratory pressure (PEEP)) of 7 mL/cmH2O to 13 mL/cmH2O. On arterial blood gas analysis, PaO2/FIO2 ratio increased from 148 to 181. Decompression led to improvement in ventilatory and hemodynamic parameters. However, through 12 h after decompression, severe hypoxemia rapidly progressed with slightly increased PIP although IAP did not become elevated again. Hypoxemia worsened with an even higher PEEP as the P/F ratio became 52.8 24 h after decompression, and chest radiograph showed bilateral infiltration, indicating acute respiratory dysfunction syndrome (ARDS). Central venous pressure remained within the normal range (4–10 cmH2O). Sivelestat sodium hydrate, a selective inhibitor of neutrophil elastase treatment was intravenously started at 4.8 mg/(kg h) from 25 h after decompression, and oxygenation was gradually improved as serial values of the PaO2/FIO2 ratio reached 150 (48 h after decompression) and 290 (72 h after decompression). Pulmonary compliance also improved from 13 mL/cmH2O to 27 mL/cmH2O. Later the patient underwent four allograft/autograft and developed renal failure requiring renal replacement therapy several times due to sepsis during the hospital course. He left our burn critical care unit on 117-day post-burn, have improved to moving by himself with a wheel chair, and transferred from our hospital on 260-day post-burn to other hospital for rehabilitation.
J. Oda et al. / Injury Extra 40 (2009) 106–108
Fig. 1. Tense abdomen 20-h post-burn.
3. Discussion Secondary ACS is a lethal complication after resuscitation from burn shock and is caused by the effects of massive resuscitation fluid and fluid shift. Regarding ACS in burn patients, several case reports,3,4,8,17 as well as reported of changes of physiologic parameters before and after decompression,13,16 and a correlation between IAP and total fluid volume,7,14 have been published. Deterioration of the ventilation status due to IAH was examined in both primary2 and secondary ACS,10 in which PIP,5 PaO2,16 PaCO2,3 PaO2/FIO2 ratio and pulmonary compliance2 were evaluated. High PIP in patient with IAH is caused by increased pleural pressure, no change in lung tissue compliance. In our other burn patients, few changes in PIP were observed by escharotomy on the thoracic wall,13 suggesting that the diaphragm may be most responsible for the elevated pleural pressure in patients with IAH. Therefore, it is possible that the parameter ‘‘pulmonary compliance’’ should be described by the term ‘‘thoracic compliance.’’ Clinically measured PAWP is clearly thought to be the total of the left atrial enddiastolic pressure and pleural pressure. In this case, it does not indicate the true pressure under IAH, which makes PAWP an unreliable index of preload or intravascular volume. After decompression, recovered pleural pressure decreased PIP, restored CVP and PAWP to an indication of ‘‘true pressure,’’ and normalised venous return, which improved cardiac output. In several reports of burned patients with IAH, decompression improves not only hypercarbia but also oxygenation evaluated with PaO2 or PaO2/FIO2 ratio.2,16 In this case, however, PaO2/FIO2 ratio increased temporally after decompression. Twelve hours after decompression, the patient showed progressive hypoxia which was thought to indicate acute lung injury even though ventilation maintained PaCO2 within the normal range. It is necessary to consider the fluid shift to the intravascular refilling phase with normalised capillary permeability after the burn shock period as the cause of hypoxia. Timing is also an important factor to describe respiratory function. Extensively burned patients are at risk of developing IAH/ACS because of fluid shift of large amount of resuscitation fluid to tissue oedema or ascites due to capillary leakage. As IAH during the resuscitation period occurs within 24-h post-burn in many cases, the refilling phase generally follows decompression. The present patient had no history of heart disease before injury, CO remarkably increased and cardiothoracic ratio did not change, urinary output increased and CVP was maintained within the normal range after decompression. Several authors described that inflammatory response in IAH/ ACS model because an excessive level of inflammatory cytokines are associated with morbidity and mortality in critically ill patients, and that it could be a second hit for multiple organ
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dysfunction.12,15 It can be speculated that IAH itself or decompression after IAH following severe burn injury could play a role through splanchnic hypoperfusion or splanchnic reperfusion. In the present case, serial plasma levels of IL-8 were 132.5 pg/mL 6 h PB, 24.8 pg/mL after decompression, and 231.4 pg/mL 1 day after decompression. These serial values are not thought to substantially exceed those of other extensively burned patient described previously;19 however, it is interesting that the plasma IL-8 level after decompression was higher than that before decompression although hemodynamic and respiratory parameters improved after decompression and the patient did not show any septic symptoms or signs. Is the intra-abdominal volume proportional to IAP? Based on compliance of the abdominal wall, IAP is likely to be low enough that increase of the IAP with increased intra-abdominal volume remains mild during the early phase. However, once the intraabdominal volume exceeds a critical point at which elasticity is lost, IAP rapidly increases. Additionally, it becomes a vicious cycle whereby gut oedema is enhanced because of the affected venous return. In this case, the reevaluated IBP prior to performing decompression was 60 cmH2O, which rapidly elevated as a result, while a short time later the patient showed a high PIP and IAP greater than 30 cmH2O. Extremely high IAP might be associated with abdominal hypoperfusion and reperfusion, which caused severe lung injury as noted above. A large proportion of patients with IAH generally have a poor prognosis after ACS, especially severely burned patients, even though abdominal decompression improves physiologic parameters at the time it is performed. Close monitoring is important to avoid delayed treatment and seriously impaired abdominal perfusion. Additionally, we suggested using hypertonic lactated saline solution (HLS) as a resuscitation fluid in the burn shock period to reduce the risk of developing to IAH with a resuscitation fluid volume sparing effect.12 It is also protective for a risk of pulmonary oedema in the refilling period after the burn shock period, however, it cannot be applied safely to elderly persons or children due to risks of dehydration or hyperosmorality. Neutrophil elastase has been discussed recently as playing central role in development of acute lung injury.18 Neutrophil elastase promotes damage to lung tissue, increases vascular permeability, and induces neutrophil migration to the alveoli. Sivelestat, a selective inhibitor of neutrophil elastase, was developed to reduce acute lung injury caused be systemic inflammatory response syndrome.6,18 However, the efficacy of the sivelestat as treatment for acute lung injury remains controversial.20 We also speculate that sivelestat sodium effectively improved respiratory function in the present case of acute lung injury, because acute lung injury was a inflammatory response induced by hypoperfusion due to IAH or ischaemia– reperfusion of splanchnic perfusion following IAH and decompression, and was not caused by sepsis. Our patient showed rapid progression of acute lung injury after decompression for secondary ACS, although decompression did effectively improve physiologic parameters. We speculate that abdominal hypoperfusion itself with secondary ACS after severe burn injury or splanchnic reperfusion injury was important to the induction of acute lung injury. References 1. Balogh Z, McKinley BA, Holcomb JB, Miller CC, Cocanour CS, Kozar RA, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003;54:848–59. 2. Chang MC, Miller PR, D’Agostino Jr R, Meredith JW. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma 1998;44:440–5. 3. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma 2001;51:1062–4.
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4. Greenhalgh DG, Warden GD. The importance of intra-abdominal pressure measurements in burned children. J Trauma 1994;36:685–90. 5. Hobson KG, Young KM, Ciraulo A, Palmieri TL, Greenhalgh DG. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002;53:1129–33. 6. Inoue Y, Seiyama A, Tanaka H, Ukai I, Akimau P, Nishino M, et al. Protective effects of a selective neutrophil elastase inhibitor (sivelestat) on lipopolysaccharide-induced acute dysfunction of the pulmonary microcirculation. Crit Care Med 2005;33:1814–22. 7. Ivy ME, Atweh NA, Palmer J, Possenti PP, Pineau M, D’Aiuto M. Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 2000;49:387–91. 8. Ivy ME, Possenti PP, Kepros J, Atweh NA, D’Aiuto M, Palmer J, et al. Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 1999;20: 351–3. 9. Latenser BA, Kowal-Vern A, Kimball D, Chakrin A, Dujovny N. A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002;23:190–5. 10. Maxwell RA, Fabian TC, Croce MA, Davis KA. Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma 1999;47:995–9. 11. Oda J, Ivatury RR, Blocher CR, Malhotra AJ, Sugerman HJ. Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia –reperfusion. J Trauma 2002;52:625–31. 12. Oda J, Ueyama M, Yamashita K, Inoue T, Noborio M, Ode Y, et al. Hypertonic lactated saline resuscitation reduces the risk of abdominal
compartment syndrome in severely burned patients. J Trauma 2006;60: 64–71. [13] Oda J, Ueyama M, Yamashita K, Inoue T, Harunari N, Ode Y, et al. Effects of escharotomy as abdominal decompression on cardiopulmonary function and visceral perfusion in abdominal compartment syndrome with burn patients. J Trauma 2005;59:369–74. 14. Oda J, Yamashita K, Inoue T, Harunari N, Ode Y, Mega K, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns 2006;32:151–4. 15. Rezende-Neto JB, Moore EE, Melo de Andrade MV, Teixeira MM, Lisboa FA, Arantes RM, et al. Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure. J Trauma 2002;53: 1121–8. 16. Tsoutsos D, Rodopoulou S, Keramidas E, Lagios M, Stamatopoulos K, Ioannovich J. Early escharotomy as a measure to reduce intraabdominal hypertension in full-thickness burns of the thoracic and abdominal area. World J Surg 2003;27:1323–8. 17. Wilson MD, Dziewulski P. Severe gastrointestinal haemorrhage and ischaemic necrosis of the small bowel in a child with 70% full-thickness burns: a case report. Burns 2001;27:763–6. 18. Yamazaki T, Ooshima H, Usui A, Watanabe T, Yasuura K. Protective effects of ONO-5046*Na, a specific neutrophil elastase inhibitor, on postperfusion lung injury. Ann Thorac Surg 1999;68:2141–6. 19. Yeh FL, Lin WL, Shen HD, Fang RH. Changes in levels of serum IL-8 in burned patients. Burns 1997;23:555–9. 20. Zeiher BG, Artigas A, Vincent JL, Dmitrienko A, Jackson K, Thompson BT, et al. Neutrophil elastase inhibition in acute lung injury: results of the STRIVE study. Crit Care Med 2004;32:1695–702.
Contents lists available at ScienceDirect
Injury Extra journal homepage: www.elsevier.com/locate/inext
Case report
Acute lung injury secondary to intra-abdominal hypertension and abdominal decompression in a burn patient Jun Oda *, Katsuyuki Yamashita, Takuya Inoue, Yoshiki Aoki, Kazuharu Mega, Mitsuhiro Noborio, Nobuyuki Harunari, Masashi Ueyama Department of Trauma, Critical Care Medicine and Burn Center, Social Insurance Chukyo Hospital, Nagoya, Aichi, Japan
A R T I C L E I N F O
Article history: Accepted 19 January 2009
1. Introduction Secondary abdominal compartment syndrome (ACS) is known as a lethal complication after resuscitation from burn shock due to the large volume of resuscitation fluid and fluid shift.7,14 Although several cases successfully treated by surgical decompression,4,8 and percutaneous drainage3,9 have been reported, the prognosis of severely burned patients is generally very poor once ACS develops. ACS has been identified to be an independent predictor,1 and could be a second hit for multiple organ dysfunction.11,15 We report here a burn patient with ACS who developed acute lung injury (ALI) shortly after abdominal decompression even though hemodynamic parameters immediately improved. Ischaemia–reperfusion injury was suspected of being involved in the development of ALI. 2. Case The patient (55-year-old male) was admitted after being severely burned (87% TBSA with 41% full thickness) except for the head and part of the right upper limb by accidental falling into a scalding hot water (90 8C) tank at work. Admission occurred 1 h after injury. Prior to the accident the patient was healthy, and his weight was 67 kg before the accident and he was not taking any medication. During the first 24-h post-burn after admission, Lactated Ringer’s solution was administered to meet the resuscitation endpoint for urine output (UO) of 0.5–1 mL/(kg h). Haemoconcentration was prolonged (hematocrit = 58%, at 12 h). The total
* Corresponding author at: Department of Emergency and CCM, Tokyo Medical University, 6-7-1 Nishishinjuku, Tokyo 160-0023, Japan. Tel.: +81 3 3342 6111; fax: +81 3 3342 5687. E-mail addresses: [email protected] (J. Oda), [email protected] (K. Yamashita), [email protected] (T. Inoue), [email protected] (Y. Aoki), [email protected] (K. Mega), [email protected] (M. Noborio), [email protected] (N. Harunari), [email protected] (M. Ueyama). 1572-3461/$ – see front matter ß 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2009.01.119
volume of crystalloid administered during the first 20 h, already exceeded the expected 4 mL/(kg %TBSA): 27,500 mL (4.7 mL/ (kg %TBSA 20 h)). At 20 h PB, the peak inspiratory pressure (PIP) exceeded 50 cmH2O, and tense abdomen was noted (Fig. 1). One hour later, the patients developed severe intra-abdominal hypertension (IAH) with an intra-abdominal pressure (IAP) of 60 cmH2O. Decompression was performed, resulting in an immediate decrease in IAP from 60 cmH2O to 35 cmH2O, PIP from 64 cmH2O to 43 cmH2O, and increase of abdominal perfusion pressure (APP) from 42 mmHg to 62 mmHg, cardiac output (CO) from 4.5 L/(min m2) to 7.5 L/ (min m2), central venous pressure (CVP) from 20 cmH2O to 9 cmH2O, pulmonary artery wedge pressure (PAWP) from 38 mmHg to 21 mmHg, pulmonary static compliance calculated as the tidal volume divided by (PIP minus positive end-expiratory pressure (PEEP)) of 7 mL/cmH2O to 13 mL/cmH2O. On arterial blood gas analysis, PaO2/FIO2 ratio increased from 148 to 181. Decompression led to improvement in ventilatory and hemodynamic parameters. However, through 12 h after decompression, severe hypoxemia rapidly progressed with slightly increased PIP although IAP did not become elevated again. Hypoxemia worsened with an even higher PEEP as the P/F ratio became 52.8 24 h after decompression, and chest radiograph showed bilateral infiltration, indicating acute respiratory dysfunction syndrome (ARDS). Central venous pressure remained within the normal range (4–10 cmH2O). Sivelestat sodium hydrate, a selective inhibitor of neutrophil elastase treatment was intravenously started at 4.8 mg/(kg h) from 25 h after decompression, and oxygenation was gradually improved as serial values of the PaO2/FIO2 ratio reached 150 (48 h after decompression) and 290 (72 h after decompression). Pulmonary compliance also improved from 13 mL/cmH2O to 27 mL/cmH2O. Later the patient underwent four allograft/autograft and developed renal failure requiring renal replacement therapy several times due to sepsis during the hospital course. He left our burn critical care unit on 117-day post-burn, have improved to moving by himself with a wheel chair, and transferred from our hospital on 260-day post-burn to other hospital for rehabilitation.
J. Oda et al. / Injury Extra 40 (2009) 106–108
Fig. 1. Tense abdomen 20-h post-burn.
3. Discussion Secondary ACS is a lethal complication after resuscitation from burn shock and is caused by the effects of massive resuscitation fluid and fluid shift. Regarding ACS in burn patients, several case reports,3,4,8,17 as well as reported of changes of physiologic parameters before and after decompression,13,16 and a correlation between IAP and total fluid volume,7,14 have been published. Deterioration of the ventilation status due to IAH was examined in both primary2 and secondary ACS,10 in which PIP,5 PaO2,16 PaCO2,3 PaO2/FIO2 ratio and pulmonary compliance2 were evaluated. High PIP in patient with IAH is caused by increased pleural pressure, no change in lung tissue compliance. In our other burn patients, few changes in PIP were observed by escharotomy on the thoracic wall,13 suggesting that the diaphragm may be most responsible for the elevated pleural pressure in patients with IAH. Therefore, it is possible that the parameter ‘‘pulmonary compliance’’ should be described by the term ‘‘thoracic compliance.’’ Clinically measured PAWP is clearly thought to be the total of the left atrial enddiastolic pressure and pleural pressure. In this case, it does not indicate the true pressure under IAH, which makes PAWP an unreliable index of preload or intravascular volume. After decompression, recovered pleural pressure decreased PIP, restored CVP and PAWP to an indication of ‘‘true pressure,’’ and normalised venous return, which improved cardiac output. In several reports of burned patients with IAH, decompression improves not only hypercarbia but also oxygenation evaluated with PaO2 or PaO2/FIO2 ratio.2,16 In this case, however, PaO2/FIO2 ratio increased temporally after decompression. Twelve hours after decompression, the patient showed progressive hypoxia which was thought to indicate acute lung injury even though ventilation maintained PaCO2 within the normal range. It is necessary to consider the fluid shift to the intravascular refilling phase with normalised capillary permeability after the burn shock period as the cause of hypoxia. Timing is also an important factor to describe respiratory function. Extensively burned patients are at risk of developing IAH/ACS because of fluid shift of large amount of resuscitation fluid to tissue oedema or ascites due to capillary leakage. As IAH during the resuscitation period occurs within 24-h post-burn in many cases, the refilling phase generally follows decompression. The present patient had no history of heart disease before injury, CO remarkably increased and cardiothoracic ratio did not change, urinary output increased and CVP was maintained within the normal range after decompression. Several authors described that inflammatory response in IAH/ ACS model because an excessive level of inflammatory cytokines are associated with morbidity and mortality in critically ill patients, and that it could be a second hit for multiple organ
107
dysfunction.12,15 It can be speculated that IAH itself or decompression after IAH following severe burn injury could play a role through splanchnic hypoperfusion or splanchnic reperfusion. In the present case, serial plasma levels of IL-8 were 132.5 pg/mL 6 h PB, 24.8 pg/mL after decompression, and 231.4 pg/mL 1 day after decompression. These serial values are not thought to substantially exceed those of other extensively burned patient described previously;19 however, it is interesting that the plasma IL-8 level after decompression was higher than that before decompression although hemodynamic and respiratory parameters improved after decompression and the patient did not show any septic symptoms or signs. Is the intra-abdominal volume proportional to IAP? Based on compliance of the abdominal wall, IAP is likely to be low enough that increase of the IAP with increased intra-abdominal volume remains mild during the early phase. However, once the intraabdominal volume exceeds a critical point at which elasticity is lost, IAP rapidly increases. Additionally, it becomes a vicious cycle whereby gut oedema is enhanced because of the affected venous return. In this case, the reevaluated IBP prior to performing decompression was 60 cmH2O, which rapidly elevated as a result, while a short time later the patient showed a high PIP and IAP greater than 30 cmH2O. Extremely high IAP might be associated with abdominal hypoperfusion and reperfusion, which caused severe lung injury as noted above. A large proportion of patients with IAH generally have a poor prognosis after ACS, especially severely burned patients, even though abdominal decompression improves physiologic parameters at the time it is performed. Close monitoring is important to avoid delayed treatment and seriously impaired abdominal perfusion. Additionally, we suggested using hypertonic lactated saline solution (HLS) as a resuscitation fluid in the burn shock period to reduce the risk of developing to IAH with a resuscitation fluid volume sparing effect.12 It is also protective for a risk of pulmonary oedema in the refilling period after the burn shock period, however, it cannot be applied safely to elderly persons or children due to risks of dehydration or hyperosmorality. Neutrophil elastase has been discussed recently as playing central role in development of acute lung injury.18 Neutrophil elastase promotes damage to lung tissue, increases vascular permeability, and induces neutrophil migration to the alveoli. Sivelestat, a selective inhibitor of neutrophil elastase, was developed to reduce acute lung injury caused be systemic inflammatory response syndrome.6,18 However, the efficacy of the sivelestat as treatment for acute lung injury remains controversial.20 We also speculate that sivelestat sodium effectively improved respiratory function in the present case of acute lung injury, because acute lung injury was a inflammatory response induced by hypoperfusion due to IAH or ischaemia– reperfusion of splanchnic perfusion following IAH and decompression, and was not caused by sepsis. Our patient showed rapid progression of acute lung injury after decompression for secondary ACS, although decompression did effectively improve physiologic parameters. We speculate that abdominal hypoperfusion itself with secondary ACS after severe burn injury or splanchnic reperfusion injury was important to the induction of acute lung injury. References 1. Balogh Z, McKinley BA, Holcomb JB, Miller CC, Cocanour CS, Kozar RA, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003;54:848–59. 2. Chang MC, Miller PR, D’Agostino Jr R, Meredith JW. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma 1998;44:440–5. 3. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma 2001;51:1062–4.
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4. Greenhalgh DG, Warden GD. The importance of intra-abdominal pressure measurements in burned children. J Trauma 1994;36:685–90. 5. Hobson KG, Young KM, Ciraulo A, Palmieri TL, Greenhalgh DG. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002;53:1129–33. 6. Inoue Y, Seiyama A, Tanaka H, Ukai I, Akimau P, Nishino M, et al. Protective effects of a selective neutrophil elastase inhibitor (sivelestat) on lipopolysaccharide-induced acute dysfunction of the pulmonary microcirculation. Crit Care Med 2005;33:1814–22. 7. Ivy ME, Atweh NA, Palmer J, Possenti PP, Pineau M, D’Aiuto M. Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 2000;49:387–91. 8. Ivy ME, Possenti PP, Kepros J, Atweh NA, D’Aiuto M, Palmer J, et al. Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 1999;20: 351–3. 9. Latenser BA, Kowal-Vern A, Kimball D, Chakrin A, Dujovny N. A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002;23:190–5. 10. Maxwell RA, Fabian TC, Croce MA, Davis KA. Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma 1999;47:995–9. 11. Oda J, Ivatury RR, Blocher CR, Malhotra AJ, Sugerman HJ. Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia –reperfusion. J Trauma 2002;52:625–31. 12. Oda J, Ueyama M, Yamashita K, Inoue T, Noborio M, Ode Y, et al. Hypertonic lactated saline resuscitation reduces the risk of abdominal
compartment syndrome in severely burned patients. J Trauma 2006;60: 64–71. [13] Oda J, Ueyama M, Yamashita K, Inoue T, Harunari N, Ode Y, et al. Effects of escharotomy as abdominal decompression on cardiopulmonary function and visceral perfusion in abdominal compartment syndrome with burn patients. J Trauma 2005;59:369–74. 14. Oda J, Yamashita K, Inoue T, Harunari N, Ode Y, Mega K, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns 2006;32:151–4. 15. Rezende-Neto JB, Moore EE, Melo de Andrade MV, Teixeira MM, Lisboa FA, Arantes RM, et al. Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure. J Trauma 2002;53: 1121–8. 16. Tsoutsos D, Rodopoulou S, Keramidas E, Lagios M, Stamatopoulos K, Ioannovich J. Early escharotomy as a measure to reduce intraabdominal hypertension in full-thickness burns of the thoracic and abdominal area. World J Surg 2003;27:1323–8. 17. Wilson MD, Dziewulski P. Severe gastrointestinal haemorrhage and ischaemic necrosis of the small bowel in a child with 70% full-thickness burns: a case report. Burns 2001;27:763–6. 18. Yamazaki T, Ooshima H, Usui A, Watanabe T, Yasuura K. Protective effects of ONO-5046*Na, a specific neutrophil elastase inhibitor, on postperfusion lung injury. Ann Thorac Surg 1999;68:2141–6. 19. Yeh FL, Lin WL, Shen HD, Fang RH. Changes in levels of serum IL-8 in burned patients. Burns 1997;23:555–9. 20. Zeiher BG, Artigas A, Vincent JL, Dmitrienko A, Jackson K, Thompson BT, et al. Neutrophil elastase inhibition in acute lung injury: results of the STRIVE study. Crit Care Med 2004;32:1695–702.