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Dr. Chinsky is in practice with Chest Diseases of Northwestern Pennsylvania.
Correspondence to: Kenneth Chinsky, MD, FCCP, 3580 Peach St, Suite 103A, Erie, PA 16508; e-mail: LChinsky{at}aol.com
Positive pressure ventilation has been used for hundreds of years since Vesalius demonstrated its benefit in dying animals in 1543. Mechanical ventilation (MV) may be employed to improve pulmonary gas exchange, to relieve respiratory muscle fatigue, to allow lung and airway healing, and to avoid complications. Nonetheless, complications associated with MV were described as far back as 1827 when Leroy observed that pneumothorax could result from overaggressive bellows inflation.1
Physicians are aware of multiple complications associated with MV. There may be problems related to the acts of intubation and extubation. Many problems are directly related to the ventilator itself, and they include machine malfunction, alarm failure, inadequate humidification, and volutrauma/ventilator-induced lung injury. Ventilator-associated pneumonia and hemodynamic alterations caused by MV represent major challenges as well.2 3
Some problems, however, may be indirectly related to MV. In this issue of CHEST, Mutlu et al (see page 1222) review various GI complications associated with MV. The authors discuss topics including stress-related mucosal damage, esophagitis, motility problems, diarrhea, and acalculous cholecystitis. The underlying pathophysiologic mechanisms are likely multifactorial and are not always clearly known. For reasons discussed in the article, the GI system is at increased risk for ischemic events. MV may precipitate hemodynamic changes resulting in hypoperfusion. There can be hormonal changes, including activation of the renin-angiotensin axis and increased catecholamines. This too can result in vasoconstriction and vascular redistribution. Inflammatory mediators, including several cytokines, can initiate a cascade of events with multiple downstream effects resulting in splanchnic hypoperfusion and activation of the immune system.
We should not be surprised that other extracorporeal mechanical devices also have both direct and indirect complications. We should also not be surprised since many of the same pathophysiologic mechanisms are invoked. Cardiopulmonary bypass (CPB) has been implicated in a whole-body inflammatory response with complement activation, cytokines, free radicals, and the arachidonic acid cascade.4 The postpump syndrome is probably the most well-known complication of CPB, but other organ systems, including the GI tract, can be involved. CPB has been associated with alterations in mucosal perfusion, epithelial permeability, edema formation, and vascular regulation in the GI tract. Complement 5a has been implicated as causal in regard to neutrophil-mediated impairment of ileal microvascular regulation.5 Fitzgerald et al6 reviewed GI complications associated with CPB. Similar to the study of Mutlu et al on MV, they described complications including pancreatitis, gastritis or ulcers, cholecystitis, colonic perforation, bleeding, bowel obstruction, diverticulitis, and visceral ischemia. They concluded that patients with risk factors including end-stage renal disease, female sex, noncoronary artery bypass graft surgery, and longer pump times should undergo endoscopic colon examination early in the postoperative period to try to prevent these adverse effects.
Renal dialysis represents another intervention with both direct and indirect complications. Hemodialysis-induced hypoxemia is well-characterized. Similar to MV and CPB, inflammatory mediators have been implicated because the dialysis membrane can activate the complement cascade. Dialysis also may lead to hypoventilation with subsequent hypoxemia.7 Paradoxically, high-volume hemofiltration can remove certain inflammatory cytokines, and there is a porcine sepsis model demonstrating hemodynamic improvement when hemofiltration is applied early.8 Although provocative, there are no human survival data yet to support this approach. Like MV and CPB, GI complications have been described in dialysis as well. Flobert et al9 found right-sided ischemic colitis in patients with chronic renal failure requiring hemodialysis. Another study demonstrated that the risk of acute pancreatitis is increased in patients receiving long-term peritoneal dialysis.10
MV has been associated with several non-GI complications in other organ systems. For example, the CNS may be affected. The positive end-expiratory pressure (PEEP) necessary to ensure adequate oxygenation may result in decreased venous blood return to the heart, decreased mean arterial pressure, and subsequently, diminished cerebral perfusion. Studies show conflicting results of the effects of PEEP on intracranial pressure (ICP).11 Hyperventilation, long used to cause vasoconstriction and decrease ICP, may induce cerebral ischemia. On the other hand, permissive hypercapnea employed to avoid volutrauma may increase cerebral blood flow and may lead to elevated ICP. Pulmonary venous air embolism is a rare but potentially serious complication in patients with ARDS who are receiving MV.12
Ventilator-associated pneumonia is the most common infectious complication of MV, but patients appear to have an increased risk for eye infections as well.13
Neuromuscular dysfunction may complicate MV in critically ill patients. Muscle atrophy is common. Myopathy associated either with critical illness itself or pharmacologic paralysis is well-known. There may be muscle breakdown due to catabolism and anterior horn loss due to hypoxic myelopathy.14
Critically ill patients, especially those receiving MV, are at risk for dermatologic complications including pressure ulcers.15 They are immobile, may have reduced tissue perfusion exacerbated by hypoxemia, and poor nutritional status. All of these factors may contribute to the development of pressure ulcers.
As Mutlu et al point out in their review, and as these further examples illustrate, it is difficult to discern which complications in patients receiving MV are due to the ventilator itself and which are complications associated with critical illness in general. It would be difficult to design human clinical trials to answer these questions. The authors also admit that some of the data remain theoretic or have been demonstrated in animals but not humans and may not necessarily be extrapolated. In fact, a rat model recently was published16 specifically to study the effects of MV on distant organ systems. A group of rats was ventilated at different tidal volumes, and their hepatic and renal tissues were analyzed. These data, although preliminary, suggest that various ventilator strategies may result in different effects in organs other than the lung.
As pulmonary and critical-care physicians, we understand that the daily use of life-sustaining devices may have unintended consequences. These complications may be indirect and may occur in organ systems distant from the ones for which the mechanical device is intended. Information concerning the pathophysiology is complex, multifactorial, and ever-expanding. There are both cellular and humoral mechanisms as well as inflammatory mediators, including complement and the arachidonic acid cascade. Even a patient with single-system dysfunction who needs these machines requires vigilance in physical and laboratory evaluations to prevent or to diagnose these complications.
References
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