Quotation 1. Headline 2. Headline 3. Headline 4. Friday, June 19, Andres Felipe Cardenas Maria Paula Ardila Edema pulmonar. Edema pulmonar: la descripción general exhaustiva comprende los síntomas, las causas y el tratamiento de esta afección pulmonar. El edema pulmonar neurogénico es un diagnóstico de exclusión, cuya frecuencia de presentación no ha sido establecida, dada la falta de.
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Neurogenic pulmonary edema NPE is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system CNS insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction.
A myriad of CNS events, including spinal cord injury, subarachnoid hemorrhage SAHtraumatic brain injury TBIintracranial hemorrhage, status epilepticus, meningitis, and subdural hemorrhage, have been associated with this syndrome [ 1 – 5 ].
Although NPE was identified over years ago, it is still underappreciated in the clinical arena. Its sporadic and relatively unpredictable nature and a lack of etiologic-specific diagnostic markers and treatment modalities may in part be responsible for its poor recognition at the bedside. In this manuscript, we will review the anatomical origin of NPE, outline the various possible pathophysiologic mechanisms responsible for its development, and propose a clinical framework for the classification of NPE.
The syndrome of NPE has been recognized for over a century. Shanahan reported 11 cases of acute pulmonary edema as a complication of epileptic seizures [ 7 ]. Francois Moutier described the sudden onset of pulmonary edema among soldiers shot in the head in World War I [ 8 ].
Similar reports exist of observed alveolar edema and hemorrhage in the lungs of 17 soldiers dying after isolated bullet head wounds in the Vietnam War [ 1 ].
Because much of the clinical information on NPE has been derived from case reports phlmonar autopsy series, the true incidence of NPE is unknown and is likely underreported. Any acute CNS insult, including spinal cord trauma, can result in pulmonary edema.
Clinically, the likelihood of developing NPE following SAH correlates with increasing age, delay to surgery, vertebral artery origin, and the severity of clinical and radiographic presentation e. In other series, close to one-third of patients with status epilepticus also developed NPE [ 14 ].
The pathophysiology linking the neurologic, cardiac, and pulmonary conditions in NPE has been subject to debate and controversy since the recognition of NPE as a clinical entity. Neurologic conditions that cause abrupt, rapid, and extreme elevation in intracranial pressure ICP appear to be at greatest risk of being associated with NPE [ 1819 ].
The abrupt increase in ICP leading to neuronal compression, ischemia or damage is believed to give rise to an intense activation of the sympathetic nervous system and the release of catecholamines [ 221 ].
In addition to pharmacologic intervention, anatomical interruption of the nervous system pathway e. In one animal model, NPE was prevented by removal of one lung followed by reimplantation. Deema was in contrast to the pulmonary edema that developed in the innervated intrinsic lung [ 24 ]. In a human example, NPE has been reported in soldiers who died suddenly after gunshot wounds edemx the head. The soldiers with concomitant cervical spinal cord injury and presumably severed neuronal connection did not have evidence of pulmonary edema on post-mortem exam [ 1 ].
Pulmonary edema has also been reported in patients with pheochromocytoma, presumably from catecholamine surge [ 25 ]. Animal studies assessing possible therapeutic interventions for neurogenic pulmonary edema NPE. Although the exact source of sympathetic outflow has not been identified, certain centers in the brain have been implicated. These ‘NPE eema zones’ include the hypothalamus and the medulla, specifically area A1, A5, nuclei of neurpgenico tract and the area postrema [ 5 ].
Area A1 is located in the ventrolateral aspect of the medulla and is composed of catecholamine neurons which project into the hypothalamus neueogenico 5 ]. The neurons from area A5, located in the upper portion of the medulla, pulmonra into the preganglionic centers for spinal cord sympathetic outflow [ 5 ].
Injury to Area A1 or disruption of the efferent pathway between A5 and the cervical cord has been shown to result in the formation of pulmonary edema [ 26 ]. Stimulation of area A5 also causes increases in systemic blood pressure [ 27 ]. The nuclei of solitary tract and the area postrema of the medulla have also been linked to the formation of NPE.
These areas are related to respiratory regulation and receive input from the carotid sinus.
In animal models, bilateral irritation of the nuclei solitary tract causes severe hypertension and NPE [ 23 ]. Unilateral stimulation of the area postrema also results in profound hemodynamic changes, including increased cardiac output, peripheral vascular resistance, and hypertension [ 5 ].
Finally, NPE was shown to develop after lesions were induced in the hypothalamus of laboratory animals [ 28 ]. In a case series of 22 patients suffering from NPE, 11 of the patients had significant radiographic abnormalities in the hypothalamus. The presence of hypothalamic lesions among these NPE patients conferred a worse prognosis [ 29 ]. It is the prevailing view that the autonomic response to elevated ICP plays an important role in the pathogenesis of NPE. However, what occurs mechanistically at the level of the pulmonary vascular endothelium remains enigmatic and theoretical.
Several clinicopathologic paradigms have been proposed to explain the clinical syndrome of NPE: Whereas NPE has traditionally been described as a ‘non-cardiogenic’ form of pulmonary edema, there is evidence that, in at least a subset of patients, neurologic insult leads to direct myocardial injury and the development of pulmonary edema.
Takotsubo’s cardiomyopathy is a reversible condition characterized by depressed cardiac contractility following a neurologically ‘stressful’ event. The transiently diminished lusitropy, diastolic dysfunction, and global hypokinesis of the Takotsubo heart can render these patients susceptible to cardiogenic pulmonary edema [ 30 ].
Connor was one neurogenicco the first investigators to describe the myocytolysis and contraction-band necrosis on myocardial biopsies of neurosurgical patients with pulmonary edema pulkonar 31 ]. Since this original report, several cases of cardiac injury associated with pulmonary edema following a CNS event have been described.
Neurogeenico a retrospective analysis, patients with no previous cardiac history developed acute onset of pulmonary edema in association with a SAH. The patients all demonstrated segmental wall motion abnormalities on echocardiogram, mildly elevated cardiac enzymes, electrocardiogram EKG abnormalities, and elevated pulmonary artery occlusion pressures PAOPs.
These patients were noted to have focal myocardial necrosis, yet had no evidence of infarction and had normal coronary arteries [ 32 ]. As with all forms of NPE, massive sympathetic discharge following CNS insult is thought to be the precipitating factor. More specifically, in this subset of patients with ‘neuro-cardiac’ NPE, it is catecholamines that induce direct myocyte injury. This is supported by the fact that the wall motion abnormalities seen on echocardiogram in patients with neurogenic stunned myocardium follow a pattern of sympathetic nerve innervation [ 33 ].
Similarly, myocardial lesions have deema shown in patients with pheochromocytoma, supporting the role of catecholamine surge in the pathogenesis of stunned myocardium [ 34 ]. Unlike the direct toxic effects to edems myocardium as detailed above, the ‘neuro-hemodynamic’ theory posits that ventricular compliance is indirectly altered by neurobenico abrupt increases in systemic and pulmonary pressures following CNS injury.
In the original studies by Sarnoff and Sarnoff, substantial increases in aortic and pulmonary pressures were observed following the injection of thrombin into the intracisterna magna of dogs and rabbits [ 35 ]. The authors noted that following the sympathetic surge, the left ventricle had reached its workfailure pulmpnar and failed to effectively pump against the systemic pressures.
A translocation of blood flow from the highly resistant systemic circulation to the low resistance pulmonary circuit subsequently ensued, leading to a hydrostatic form of pulmonary edema.
The increased sizes of the left atrium and pulmonary veins in the animals were well documented in this study, and the authors subsequently coined the term “neuro-hemodynamic pulmonary edema” [ 35 ]. Several other animal models have documented large elevations in left atrial, systemic and pulmonary pressures associated with Phlmonar [ 182236 ].
One study induced graded levels of ICP in chimpanzees. All of the animals developed systemic hypertension, but only those with a marked increase in left atrial pressure and a decrease in cardiac output developed pulmonary edema [ 18 ]. The neuro-cardiac and neuro-hemodynamic theories outlined above both suggest pulmonaar alterations in hydrostatic and Starling forces are central to the formation of pulmonary edema following CNS injury.
Although hydrostatic pressures may play a role in the pathogenesis, neurogeniico mechanism alone cannot explain the presence of red blood cells RBCs and protein observed in the alveolar fluid in many NPE subjects [ 3738 ]. The exudative properties of the pulmonary fluid imply that alterations in vascular permeability play a role in the pathogenesis of NPE.
In order to explain the presence of both hydrostatic factors and vascular leak, Theodore and Robin introduced the “blast theory” of NPE [ 39 ]. Similar to the neuro-hemodynamic model, the “blast theory” posits that the severe abrupt increases in systemic and pulmonary pressures following the catecholamine surge result in a net pulmoar of blood volume from the systemic circulation to the low resistance pulmonary circulation. This increase in pulmonary venous pressure leads to the development of transudative pulmonary edema.
The “blast theory” further posits that the acute rise in capillary pressure induces a degree of barotrauma capable of damaging the capillary-alveolar membrane. The structural damage to the pulmonary endothelium ultimately leads to vascular leak and persistent protein-rich pulmonary edema [ 39 ].
The pulmonary edema according to the “blast theory” is thus the result of two mechanisms which act synergistically: A high-pressure hydrostatic influence and pulmonary endothelial injury. Several pre-clinical models support this mechanism [ 4041 ].
Maron showed that barotrauma and vascular permeability neurkgenico when pulmonary pressures exceeded 70 torr following CNS injury in dogs [ 40 ].
In another study, EVLW was observed when pulmonary artery pressures reached 25 torr or greater in rabbits [ 41 ]. The authors concluded that some degree of pulmonary hypertension is required for the development of pulmonary edema, and that the degree of permeability is “pressure dependent” [ 41 ]. Theodore and Robin in the “blast theory” acknowledged that it is rare to pulmonarr elevated systemic and pulmonary pressures in human cases of NPE.
According to their theory, this can be explained by the fact that the sympathetic pulmonarr and subsequent hemodynamic instability occurs at the time of the inciting event when hemodynamic monitoring is rare [ 39 ]. During the later pulmonaf of NPE, systemic and pulmonary pressures can return to normal, whereas the endothelial injury and vascular leak may persist [ 39 ]. A few case reports have been edemaa to document this sequence of events in human subjects, lending credence to the “blast theory”.
One case study described a patient who had hemodynamic monitoring at the time of a seizure that led to NPE.
Within minutes of the seizure, marked increases in systemic, pulmonary and pulmonary artery occlusion pressures were recorded. The hemodynamics quickly normalized and two hours later, pulmonary edema developed, which was determined to be high in protein content [ 37 ]. This was followed by a dramatic decrease in the patient’s oxygen levels.
The patient’s pulmonary edema did not clear on radiograph for 72 hours following the last episode of transient systemic and pulmonary hypertension. The authors eddma that persistent vascular leak was the basis for these findings [ 42 ]. Many reports of NPE fail to consistently demonstrate the hypertensive surges and changes in left atrial pressures nerogenico described in the theories above. This suggests that systemic hypertension and its effect on cardiac contractility may not always contribute to the development of NPE.
An alternative hypothesis is that the massive sympathetic discharge following CNS injury directly affects the pulmonary vascular bed, and that the edema develops regardless of any systemic changes. We refer to this as the ‘pulmonary venule adrenergic hypersensitivity’ theory.
In a well designed study by McClellan et al. Autonomic activation following the CNS insult was evidenced by pumlonar increase in systemic and pulmonary vascular pressures. The pulmonary edema developed in the dogs and was proven to be exudative in content.
When the same degree of pulmonary hypertension and increased left atrial pressure was induced with a left atrial balloon in the control group, pulmonary edema did not develop.
Neurogehico authors concluded that neurologic insult resulted in acute lung injury ALIwhich could not be explained by hemodynamic changes, but rather by direct neurological influences on the pulmonary endothelium [ 44 ].
In other studies of intracranial lesions induced in sheep, pulmonary edema developed despite normal or only mildly increased left atrial and systemic pressures [ 3845 ]. In human examples, continuous cardiac monitoring during the development of NPE in neurogenio with SAH and brain tumor resection failed to demonstrate preceding hemodynamic changes [ 46 – 48 ]. These findings suggest that isolated pulmonary venoconstriction or endothelial disruption following CNS injury may be responsible for the formation of pulmonary edema [ 4748 ].
Two distinct clinical forms of NPE have been described. The early form of NPE is most common and is characterized neudogenico the development of symptoms within minutes to hours following neurologic injury.
In contrast, the delayed form develops 12 to 24 hours after the CNS insult [ 5 nneurogenico.