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SAN FRANCISCO – Multiple organ dysfunction syndrome is "underappreciated" by many of today’s clinicians, as optimal ways to treat it remain elusive, said Dr. Larry H. Hollier.
At the Vascular Annual Meeting, Dr. Hollier, professor of surgery and chancellor of the Louisiana State University Health Sciences Center, New Orleans, defined multiple organ dysfunction syndrome (MODS) as altered organ functions in an acutely ill patient requiring intervention to achieve homeostasis. "That’s a pretty broad definition, but it’s one of the most common causes of death in surgical intensive care units," he said. "Numerous precipitating factors classically described in multiple organ dysfunction syndrome include sepsis, trauma, cardiac arrest, visceral ischemia, burns, pancreatitis, shock, and major surgery with postoperative instability."
The pathophysiology of MODS "is fairly straightforward," he continued. "Some events result in ischemia and tissue hypoxia. Reperfusion occurs with the activation of cytokines, and an exaggerated inflammatory response generates oxygen free radicals, tissue damage, and then organ dysfunction." said Dr. Hollier, the invited speaker for the John Homans Lectureship of the SVS.
The major underlying issue in MODS stems from uncorrected oxygen debt in tissues. In fact, the level of perioperative tissue debt has a direct relationship on postoperative morbidity and mortality. According to Dr. Hollier, the predicted outcome by acutely accumulated oxygen debt in the first 4 hours post injury works like this: 8 L/m2 leads to a severe flulike syndrome (mild SIRS); 26 L/m2 leads to multiple organ dysfunction syndrome; and 33 L/m2 or more leads to death. "The uncorrected oxygen debt in tissues that is initiated is not the end of it," he said. "There’s an accumulating oxygen debt that amasses to keep biomass viable during low oxygen delivery. After resuscitation, there’s increased oxygen required above the basal rate, because explosive oxygen needs occur in order to fuel the inflammation of reperfusion injury."
Conventional therapies for MODS include volume resuscitation, ionotropic agents to improve cardiac performance and increase oxygen delivery, and ventilator support to improve oxygen input. Multiple experimental therapies have also been used, but no universal treatment has been found that reverses MODS, he said. "Early diagnosis and prompt treatment of organ hypoperfusion and hypoxia are of utmost importance. The major goal is to increase oxygen delivery as soon as possible."
Vascular surgeons are most likely to encounter MODS in cases of extensive blunt trauma, aortic transection/dissection, crush injury, severe ischemia following acute aortic occlusion, mesenteric infarction, and thoracoabdominal aortic surgery, both with extensive direct repair and with hybrid repair. The "hypoxia cascade" can occur without progression to the full multiple organ dysfunction syndrome. "The cascade can occur in refractory hypotension following repair of ruptured aortic aneurysm or other major vascular procedure, during brain ischemia, visceral ischemia, delayed onset paraplegia following repair of thoracoabdominal aortic aneurysms, and during the compartment syndrome."
Recommendations for intraoperative management of thoracoabdominal aortic aneurysms include maintaining visceral perfusion with a pump or a bypass or using visceral perfusion catheters, and perioperative CSF drainage "to allow reduction in the pressure around the spinal cord," he said.
Dr. Hollier said that management of serious injury in the commercial diver in the field has afforded two observations. First, high-dose hyperbaric oxygen, used very early in acute resuscitation of the severely injured, "effectively reduces oxygen debt." Second, the quick reduction of the oxygen debt by high-dose hyperbaric oxygen leverages chances of recovery. "What we do know is that there is only one variable that consistently predicts both mortality and multiple organ dysfunction syndrome following traumatic shock. That is oxygen debt."
Dr. Hollier had no disclosures.
SAN FRANCISCO – Multiple organ dysfunction syndrome is "underappreciated" by many of today’s clinicians, as optimal ways to treat it remain elusive, said Dr. Larry H. Hollier.
At the Vascular Annual Meeting, Dr. Hollier, professor of surgery and chancellor of the Louisiana State University Health Sciences Center, New Orleans, defined multiple organ dysfunction syndrome (MODS) as altered organ functions in an acutely ill patient requiring intervention to achieve homeostasis. "That’s a pretty broad definition, but it’s one of the most common causes of death in surgical intensive care units," he said. "Numerous precipitating factors classically described in multiple organ dysfunction syndrome include sepsis, trauma, cardiac arrest, visceral ischemia, burns, pancreatitis, shock, and major surgery with postoperative instability."
The pathophysiology of MODS "is fairly straightforward," he continued. "Some events result in ischemia and tissue hypoxia. Reperfusion occurs with the activation of cytokines, and an exaggerated inflammatory response generates oxygen free radicals, tissue damage, and then organ dysfunction." said Dr. Hollier, the invited speaker for the John Homans Lectureship of the SVS.
The major underlying issue in MODS stems from uncorrected oxygen debt in tissues. In fact, the level of perioperative tissue debt has a direct relationship on postoperative morbidity and mortality. According to Dr. Hollier, the predicted outcome by acutely accumulated oxygen debt in the first 4 hours post injury works like this: 8 L/m2 leads to a severe flulike syndrome (mild SIRS); 26 L/m2 leads to multiple organ dysfunction syndrome; and 33 L/m2 or more leads to death. "The uncorrected oxygen debt in tissues that is initiated is not the end of it," he said. "There’s an accumulating oxygen debt that amasses to keep biomass viable during low oxygen delivery. After resuscitation, there’s increased oxygen required above the basal rate, because explosive oxygen needs occur in order to fuel the inflammation of reperfusion injury."
Conventional therapies for MODS include volume resuscitation, ionotropic agents to improve cardiac performance and increase oxygen delivery, and ventilator support to improve oxygen input. Multiple experimental therapies have also been used, but no universal treatment has been found that reverses MODS, he said. "Early diagnosis and prompt treatment of organ hypoperfusion and hypoxia are of utmost importance. The major goal is to increase oxygen delivery as soon as possible."
Vascular surgeons are most likely to encounter MODS in cases of extensive blunt trauma, aortic transection/dissection, crush injury, severe ischemia following acute aortic occlusion, mesenteric infarction, and thoracoabdominal aortic surgery, both with extensive direct repair and with hybrid repair. The "hypoxia cascade" can occur without progression to the full multiple organ dysfunction syndrome. "The cascade can occur in refractory hypotension following repair of ruptured aortic aneurysm or other major vascular procedure, during brain ischemia, visceral ischemia, delayed onset paraplegia following repair of thoracoabdominal aortic aneurysms, and during the compartment syndrome."
Recommendations for intraoperative management of thoracoabdominal aortic aneurysms include maintaining visceral perfusion with a pump or a bypass or using visceral perfusion catheters, and perioperative CSF drainage "to allow reduction in the pressure around the spinal cord," he said.
Dr. Hollier said that management of serious injury in the commercial diver in the field has afforded two observations. First, high-dose hyperbaric oxygen, used very early in acute resuscitation of the severely injured, "effectively reduces oxygen debt." Second, the quick reduction of the oxygen debt by high-dose hyperbaric oxygen leverages chances of recovery. "What we do know is that there is only one variable that consistently predicts both mortality and multiple organ dysfunction syndrome following traumatic shock. That is oxygen debt."
Dr. Hollier had no disclosures.
SAN FRANCISCO – Multiple organ dysfunction syndrome is "underappreciated" by many of today’s clinicians, as optimal ways to treat it remain elusive, said Dr. Larry H. Hollier.
At the Vascular Annual Meeting, Dr. Hollier, professor of surgery and chancellor of the Louisiana State University Health Sciences Center, New Orleans, defined multiple organ dysfunction syndrome (MODS) as altered organ functions in an acutely ill patient requiring intervention to achieve homeostasis. "That’s a pretty broad definition, but it’s one of the most common causes of death in surgical intensive care units," he said. "Numerous precipitating factors classically described in multiple organ dysfunction syndrome include sepsis, trauma, cardiac arrest, visceral ischemia, burns, pancreatitis, shock, and major surgery with postoperative instability."
The pathophysiology of MODS "is fairly straightforward," he continued. "Some events result in ischemia and tissue hypoxia. Reperfusion occurs with the activation of cytokines, and an exaggerated inflammatory response generates oxygen free radicals, tissue damage, and then organ dysfunction." said Dr. Hollier, the invited speaker for the John Homans Lectureship of the SVS.
The major underlying issue in MODS stems from uncorrected oxygen debt in tissues. In fact, the level of perioperative tissue debt has a direct relationship on postoperative morbidity and mortality. According to Dr. Hollier, the predicted outcome by acutely accumulated oxygen debt in the first 4 hours post injury works like this: 8 L/m2 leads to a severe flulike syndrome (mild SIRS); 26 L/m2 leads to multiple organ dysfunction syndrome; and 33 L/m2 or more leads to death. "The uncorrected oxygen debt in tissues that is initiated is not the end of it," he said. "There’s an accumulating oxygen debt that amasses to keep biomass viable during low oxygen delivery. After resuscitation, there’s increased oxygen required above the basal rate, because explosive oxygen needs occur in order to fuel the inflammation of reperfusion injury."
Conventional therapies for MODS include volume resuscitation, ionotropic agents to improve cardiac performance and increase oxygen delivery, and ventilator support to improve oxygen input. Multiple experimental therapies have also been used, but no universal treatment has been found that reverses MODS, he said. "Early diagnosis and prompt treatment of organ hypoperfusion and hypoxia are of utmost importance. The major goal is to increase oxygen delivery as soon as possible."
Vascular surgeons are most likely to encounter MODS in cases of extensive blunt trauma, aortic transection/dissection, crush injury, severe ischemia following acute aortic occlusion, mesenteric infarction, and thoracoabdominal aortic surgery, both with extensive direct repair and with hybrid repair. The "hypoxia cascade" can occur without progression to the full multiple organ dysfunction syndrome. "The cascade can occur in refractory hypotension following repair of ruptured aortic aneurysm or other major vascular procedure, during brain ischemia, visceral ischemia, delayed onset paraplegia following repair of thoracoabdominal aortic aneurysms, and during the compartment syndrome."
Recommendations for intraoperative management of thoracoabdominal aortic aneurysms include maintaining visceral perfusion with a pump or a bypass or using visceral perfusion catheters, and perioperative CSF drainage "to allow reduction in the pressure around the spinal cord," he said.
Dr. Hollier said that management of serious injury in the commercial diver in the field has afforded two observations. First, high-dose hyperbaric oxygen, used very early in acute resuscitation of the severely injured, "effectively reduces oxygen debt." Second, the quick reduction of the oxygen debt by high-dose hyperbaric oxygen leverages chances of recovery. "What we do know is that there is only one variable that consistently predicts both mortality and multiple organ dysfunction syndrome following traumatic shock. That is oxygen debt."
Dr. Hollier had no disclosures.
EXPERT ANALYSIS FROM THE VASCULAR ANNUAL MEETING
