INTRODUCTION: There is a documented association between critically ill patients who are in refractory shock and adrenal insufficiency. The underlying pathophysiology may be related to ischemia, necrosis, reperfusion, or resuscitative dilution. We hypothesize this blunted adrenal response is due to ischemia and necrosis of the adrenal parenchyma. METHODS: Thirty Sprague-Dawley rats were intravascularly catheterized and hemorrhagic shock induced to a mean arterial pressure of 65 mm Hg. After 4 hours of hypotension, fluid resuscitation was initiated with a crystalloid solution (Lactated Ringers). A control group underwent catheterization without hemorrhage. Serum corticosterone levels were measured and adrenal glands harvested for histologic evaluation of hemorrhagic necrosis. RESULTS: Baseline corticosterone was 30.8 ng/mL in control animals and 35.3 ng/mL in hemorrhagic animals (P = 0.10). One hour after hemorrhage, corticosterone was maximally stimulated at 406.2 ng/mL and in control animals was 35.0 ng/mL (P = 0.0001). In experimental animals after 4 hours of hypovolemia, corticosterone dropped to 308.9 ng/mL (P = 0.0001). At 6 hours, corticosterone levels dropped to 149.0 ng/mL in experimental animals (P = 0.0001). Adrenal microscopy showed 1.5+ hemorrhagic necrosis in experimental animals compared with 0.0+ in controls (P = 0.004). CONCLUSION: Our model suggests that ischemia and necrosis of the adrenal glands may be responsible for the adrenal insufficiency seen in patients with hemorrhagic shock. Further research may enable clinicians to discern earlier which patients will benefit from adrenal corticoid replacement.
INTRODUCTION: There is a documented association between critically ill patients who are in refractory shock and adrenal insufficiency. The underlying pathophysiology may be related to ischemia, necrosis, reperfusion, or resuscitative dilution. We hypothesize this blunted adrenal response is due to ischemia and necrosis of the adrenal parenchyma. METHODS: Thirty Sprague-Dawley rats were intravascularly catheterized and hemorrhagic shock induced to a mean arterial pressure of 65 mm Hg. After 4 hours of hypotension, fluid resuscitation was initiated with a crystalloid solution (Lactated Ringers). A control group underwent catheterization without hemorrhage. Serum corticosterone levels were measured and adrenal glands harvested for histologic evaluation of hemorrhagic necrosis. RESULTS: Baseline corticosterone was 30.8 ng/mL in control animals and 35.3 ng/mL in hemorrhagic animals (P = 0.10). One hour after hemorrhage, corticosterone was maximally stimulated at 406.2 ng/mL and in control animals was 35.0 ng/mL (P = 0.0001). In experimental animals after 4 hours of hypovolemia, corticosterone dropped to 308.9 ng/mL (P = 0.0001). At 6 hours, corticosterone levels dropped to 149.0 ng/mL in experimental animals (P = 0.0001). Adrenal microscopy showed 1.5+ hemorrhagic necrosis in experimental animals compared with 0.0+ in controls (P = 0.004). CONCLUSION: Our model suggests that ischemia and necrosis of the adrenal glands may be responsible for the adrenal insufficiency seen in patients with hemorrhagic shock. Further research may enable clinicians to discern earlier which patients will benefit from adrenal corticoid replacement.
Authors: Nikolai S Tolstoy; Majid Aized; Morgan P McMonagle; Daniel N Holena; Jose L Pascual; Seema S Sonnad; Carrie A Sims Journal: J Surg Res Date: 2012-05-25 Impact factor: 2.192
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Authors: Juan A Llompart-Pou; Joan M Raurich; Jon Pérez-Bárcena; Antonia Barceló; Jordi Ibáñez; José I Ayestarán Journal: Neurocrit Care Date: 2008 Impact factor: 3.210