Abstract
Respiratory failure after thermal injury is common, but the etiologic roles of high volume crystalloid resuscitation, hypoproteinemia, inhalation injury, or sepsis have not been specifically defined in human studies. We used the thermal-green dye double indicator dilution measurement of extravascular lung water (EVLW) to follow daily lung water changes in seven severly burned adult patients, resuscitated with only crystalloid solutions. An average weight gain of 21.3 kg, a 30% increase (p < 0.001), was present two to three days after admission. Admission EVLW for all patients was 7.9 +/- 1.2 ml/kg, (means +/- SD), and EVLW at the time of maximal weight gain was 5.9 +/- 1.4 ml/kg, a 25% decrease (p < 0.05). Admission pulmonary artery wedge pressure (PAWP) was 8 +/- 3 mmHG, which was not significantly different from PAWP of 13 +/- 4 mmHg at the time of maximal weight gain. In the three patients who died of sepsis, their terminal weight averaged 17.8 kg (27%) above their admitting weight (p < 0.01) and EVLW was 26.4 +/- 4.4 ml/kg, a 200% increase (p < 0.02) from admission. Their terminal PAWP averaged 22 +/- 2 mmHg, a 170% increase (p < 0.005). None of these patients had an increase in EVLW until clinical signs of sepsis occurred and the rise in EVLW preceded the rise in PAWP. Calculated mean plasma colloid osmotic pressure (PCOP) on admission was 20.7 +/- 4.9 mmHg; at the time of maximal weight gain, it was 8.6 +/- 1.7 mmHg (p < 0.001). The PCOP-PAWP gradient fell to -4 +/- 4 mmHg (p < 0.001) at the time of maximal weight gain and remained less than +4 mmHg throughout the study period in all patients. We conclude that massive crystalloid resuscitation while maintaining PAWP below 15 mmHg does not cause an increase in EVLW during the first four days after thermal injury. EVLW actually decreases slightly in all patients despite marked weight gain, hypoproteinemia and a negative PCOP-PAWP gradient. EVLW does not correlate with the PCOP-PAWP gradient in either septic or nonseptic periods. Three patients had severe inhalational injury and normal EVLW for the first four postburn days. It therefore appears that significant interstitial edema does not result from inhalational injury. There is also no evidence that thermal injury causes an early increase in pulmonary capillary permeability. The occurrence of sepsis, however, results in rapid accumulation of lung water, without any change in hydrostatic or osmotic forces. This study supports the primary role of sepsis in altering pulmonary capillary permeability with resulting pulmonary edema.
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- Achauer B. M., Allyn P. A., Furnas D. W., Bartlett R. H. Pulmonary complications of burns: the major threat to the burn patient. Ann Surg. 1973 Mar;177(3):311–319. doi: 10.1097/00000658-197303000-00012. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Anderson R. R., Holliday R. L., Driedger A. A., Lefcoe M., Reid B., Sibbald W. J. Documentation of pulmonary capillary permeability in the adult respiratory distress syndrome accompanying human sepsis. Am Rev Respir Dis. 1979 Jun;119(6):869–877. doi: 10.1164/arrd.1979.119.6.869. [DOI] [PubMed] [Google Scholar]
- Baxter C. R., Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci. 1968 Aug 14;150(3):874–894. doi: 10.1111/j.1749-6632.1968.tb14738.x. [DOI] [PubMed] [Google Scholar]
- Birke G., Liljedahl S. O., Plantin L. O. Distribution and losses of plasma proteins during the early stage of severe burns. Ann N Y Acad Sci. 1968 Aug 14;150(3):895–904. doi: 10.1111/j.1749-6632.1968.tb14739.x. [DOI] [PubMed] [Google Scholar]
- Brigham K. L., Bowers R., Haynes J. Increased sheep lung vascular permeability caused by Escherichia coli endotoxin. Circ Res. 1979 Aug;45(2):292–297. doi: 10.1161/01.res.45.2.292. [DOI] [PubMed] [Google Scholar]
- Brigham K. L., Woolverton W. C., Blake L. H., Staub N. C. Increased sheep lung vascular permeability caused by pseudomonas bacteremia. J Clin Invest. 1974 Oct;54(4):792–804. doi: 10.1172/JCI107819. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Brouhard B. H., Carvajal H. F., Linares H. A. Burn edema and protein leakage in the rat. I. Relationship to time of injury. Microvasc Res. 1978 Mar;15(2):221–228. doi: 10.1016/0026-2862(78)90020-1. [DOI] [PubMed] [Google Scholar]
- Carvajal H. F. A physiologic approach to fluid therapy in severely burned children. Surg Gynecol Obstet. 1980 Mar;150(3):379–384. [PubMed] [Google Scholar]
- Cope O., Moore F. D. A STUDY OF CAPILLARY PERMEABILITY IN EXPERIMENTAL BURNS AND BURN SHOCK USING RADIOACTIVE DYES IN BLOOD AND LYMPH. J Clin Invest. 1944 Mar;23(2):241–257. doi: 10.1172/JCI101487. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Demling R. H., Niehaus G., Perea A., Will J. A. Effect of burn-induced hypoproteinemia on pulmonary transvascular fluid filtration rate. Surgery. 1979 Mar;85(3):339–343. [PubMed] [Google Scholar]
- Demling R. H., Will J. A., Belzer F. O. Effect of major thermal injury on the pulmonary microcirculation. Surgery. 1978 Jun;83(6):746–751. [PubMed] [Google Scholar]
- Esrig B. C., Stephenson S. F., Fulton R. L. Role of pulmonary infection in the pathogenesis of smoke inhalation. Surg Forum. 1975;26:204–206. [PubMed] [Google Scholar]
- Hill S. L., Elings V. B., Lewis F. R. Changes in lung water and capillary permeability following sepsis and fluid overload. J Surg Res. 1980 Feb;28(2):140–150. doi: 10.1016/0022-4804(80)90157-2. [DOI] [PubMed] [Google Scholar]
- Holleman J. H., Gabel J. C., Hardy J. D. Pulmonary effects of intravenous fluid therapy in burn resuscitation. Surg Gynecol Obstet. 1978 Aug;147(2):161–166. [PubMed] [Google Scholar]
- Lewis F. R., Elings V. B., Sturm J. A. Bedside measurement of lung water. J Surg Res. 1979 Oct;27(4):250–261. doi: 10.1016/0022-4804(79)90138-0. [DOI] [PubMed] [Google Scholar]
- Lewis F. R., Jr, Elings V. I. Microprocessor determination of lung water using thermal-green dye double indicator dilution. Surg Forum. 1978;29:182–184. [PubMed] [Google Scholar]
- Lowe R. J., Moss G. S., Jilek J., Levine H. D. Crystalloid versus colloid in the etiology of pulmonary failure after trauma--a randomized trial in man. Crit Care Med. 1979 Mar;7(3):107–112. doi: 10.1097/00003246-197903000-00005. [DOI] [PubMed] [Google Scholar]
- Martyn J. A., Burke J. F. Is there a selective increase in pulmonary capillary permeability following cutaneous burns? Chest. 1979 Oct;76(4):374–375. doi: 10.1378/chest.76.4.374. [DOI] [PubMed] [Google Scholar]
- Morgan A., Knight D., O'Connor N. Lung water changes after thermal burns. An observational study. Ann Surg. 1978 Mar;187(3):288–293. doi: 10.1097/00000658-197803000-00013. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Morissette M., Weil M. H., Shubin H. Reduction in colloid osmotic pressure associated with fatal progression of cardiopulmonary failure. Crit Care Med. 1975 May-Jun;3(3):115–117. doi: 10.1097/00003246-197505000-00007. [DOI] [PubMed] [Google Scholar]
- Oppenheimer L., Elings V. B., Lewis F. R. Thermal-dye lung water measurements: effects of edema and embolization. J Surg Res. 1979 May;26(5):504–512. doi: 10.1016/0022-4804(79)90041-6. [DOI] [PubMed] [Google Scholar]
- Pruitt B. A., Jr, Erickson D. R., Morris A. Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. J Trauma. 1975 May;15(5):369–379. [PubMed] [Google Scholar]
- Rackow E. C., Fein I. A., Leppo J. Colloid osmotic pressure as a prognostic indicator of pulmonary edema and mortality in the critically ill. Chest. 1977 Dec;72(6):709–713. doi: 10.1378/chest.72.6.709. [DOI] [PubMed] [Google Scholar]
- Robin E. D., Carey L. C., Grenvik A., Glauser F., Gaudio R. Capillary leak syndrome with pulmonary edema. Arch Intern Med. 1972 Jul;130(1):66–71. [PubMed] [Google Scholar]
- Skillman J. J., Parikh B. M., Tanenbaum B. J. Pulmonary arteriovenous admixture. Improvement with albumin and diuresis. Am J Surg. 1970 Apr;119(4):440–447. doi: 10.1016/0002-9610(70)90147-9. [DOI] [PubMed] [Google Scholar]
- Staub N. C. Pulmonary edema due to increased microvascular permeability to fluid and protein. Circ Res. 1978 Aug;43(2):143–151. doi: 10.1161/01.res.43.2.143. [DOI] [PubMed] [Google Scholar]
- Stein L., Beraud J. J., Morissette M., Luz P. D., Weil M. H., Shubin H. Pulmonary edema during volume infusion. Circulation. 1975 Sep;52(3):483–489. doi: 10.1161/01.cir.52.3.483. [DOI] [PubMed] [Google Scholar]
- Stephenson S. F., Esrig B. C., Polk H. C., Jr, Fulton R. L. The pathophysiology of smoke inhalation injury. Ann Surg. 1975 Nov;182(5):652–660. doi: 10.1097/00000658-197511000-00020. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Virgilio R. W., Rice C. L., Smith D. E., James D. R., Zarins C. K., Hobelmann C. F., Peters R. M. Crystalloid vs. colloid resuscitation: is one better? A randomized clinical study. Surgery. 1979 Feb;85(2):129–139. [PubMed] [Google Scholar]
- Weil M. H., Henning R. J., Puri V. K. Colloid oncotic pressure: clinical significance. Crit Care Med. 1979 Mar;7(3):113–116. doi: 10.1097/00003246-197903000-00006. [DOI] [PubMed] [Google Scholar]
- Zarins C. K., Rice C. L., Peters R. M., Virgilio R. W. Lymph and pulmonary response to isobaric reduction in plasma oncotic pressure in baboons. Circ Res. 1978 Dec;43(6):925–930. doi: 10.1161/01.res.43.6.925. [DOI] [PubMed] [Google Scholar]
- Zikria B. A., Ferrer J. M., Floch H. F. The chemical factors contributing to pulmonary damage in "smoke poisoning". Surgery. 1972 May;71(5):704–709. [PubMed] [Google Scholar]
- Zikria B. A., Weston G. C., Chodoff M., Ferrer J. M. Smoke and carbon monoxide poisoning in fire victims. J Trauma. 1972 Aug;12(8):641–645. doi: 10.1097/00005373-197208000-00001. [DOI] [PubMed] [Google Scholar]


