Pathogenesis of respiratory failure (ARDS) after hemorrhage and trauma

Shoemaker, William C.; Appel, Paul L.; Czer, L.; Bland, Richard; Schwartz, Sandra Kasper; Hopkins, James M.

doi:10.1097/00003246-198009000-00006

Cited by 56 publications

(5 citation statements)

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“…It is characterized by progressive hypoxemia due to alterations in alveolar-capillary dynamics that result in an abnormal pulmonary venoarterial shunt. This process is initiated by yet-undefined systemic insults that have no known relationships to previous disease and is frequently seen in patients with normal cardiopulmonary systems.A spectrum of pulmonary responses has been called ARDS [1][2][3][4]. These range from transient episodes of hypoxemia, which rapidly correct with therapy, to refractory hypoxemia, which is often fatal.…”

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confidence: 99%

“…A spectrum of pulmonary responses has been called ARDS [1][2][3][4]. These range from transient episodes of hypoxemia, which rapidly correct with therapy, to refractory hypoxemia, which is often fatal.…”

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confidence: 99%

“…The frequency of ARDS in other reports is much different. Shoemaker et al studied 152 patients who sustained lifethreatening trauma and hemorrhage [3]. Sixty (39%) patients developed ARDS.…”

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“…ARDS is associated with a high mortality rate (50-70%) [4,7]. A liberal definition of ARDS results in a higher incidence and a lower mortality rate (15-20%) [1,3]. Confusion persists even when ARDS mortality is defined by terminal hypoxemia.…”

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Current concepts in the management of the adult respiratory distress syndrome

Weigelt

1987

World j. surg.

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The adult respiratory distress syndrome is the most severe pulmonary complication that can follow multiple trauma and critical illness. It is caused by an insult to the pulmonary circulation which results in an increased capillary permeability and subsequent interstitial edema. An increased venoarterial shunt occurs resulting in arterial hypoxemia. The mortality rate is at least 50% if treatment is not begun before profound hypoxemia occurs. Recognition of abnormal cardiopulmonary function before overt hypoxemia develops is important. This is best accomplished by attentive monitoring of arterial blood gases. Sequential arterial oxygen tensions obtained on 40% and 100% inspired oxygen concentration are the best guides to selecting patients who have a high probability of pulmonary deterioration. Aggressive cardiovascular monitoring and early treatment with low levels of positive‐end expiratory pressure offer this group of patients an improved change of survival.

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Current concepts in the management of the adult respiratory distress syndrome

Weigelt

1987

World j. surg.

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“…Understanding the mechanisms involved in the tissue damage that follows IR is important in improving the clinical outcome of life-threatening conditions such as trauma/hemorrhagic shock (41), organ transplantation (8), and cardiovascular diseases (46). IR injury may also affect the disease process in patients with autoimmune diseases such as systemic lupus erythematosus (SLE) (1,36,47).…”

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Complement depletion protects lupus-prone mice from ischemia-reperfusion-initiated organ injury

Ioannou

Lieberman

Lucca

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ischemia-reperfusion (IR) injury causes a vigorous immune response that is amplified by complement activation, leading to local and remote tissue damage. Using MRL/lpr mice, which are known to experience accelerated tissue damage after mesenteric IR injury, we sought to evaluate whether complement inhibition mitigates organ damage. We found that complement depletion with cobra venom factor protected mice from local and remote lung tissue damage. Protection from injury was associated with less complement (C3) and membrane attack complex deposition, less neutrophil infiltration, and lower levels of local proinflammatory cytokine production. In addition, complement depletion was able to decrease the level of oxidative stress as measured by glutathione peroxidase 1 mRNA levels and superoxide dismutase activity. Furthermore, blockage of C5a receptor protected MRL/lpr mice from local tissue damage, but not from remote lung tissue damage. In conclusion, although treatments with cobra venom factor and C5a receptor antagonist were able to protect mice from local tissue damage, treatment with C5a receptor antagonist was not able to protect mice from remote lung tissue damage, implying that more factors contribute to the development of remote tissue damage after IR injury. These data also suggest that complement inhibition at earlier, rather than late, stages can have clinical benefit in conditions that are complicated with IR injury.

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