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The role of early diagnosis in Neurogenic Pulmonary edema.

Acute Neurogenic Pulmonary edema (NPE) is a rare and potentially life-threatening secondary complication of nearly any type of central nervous system (CNS) insult, ranging from an aneurysm to blunt force trauma. Each year it claims the lives of thousands around the world. Patients presenting with a subarachnoidal hemorrhage (SAH) caused by an aneurysmal rupture often develop NPE as a secondary complication. Although NPE has been recognized scientifically since 1908 it is still widely misunderstood and misdiagnosed. There are varying theories on what exactly causes the onset of NPE but each theoretical model reveals conflicting data.

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The most widely recognized theory among researchers suggests that a massive sympathetic discharge, caused by the cerebral insult, increases the body's pulmonary vasomotor tone which leads to constriction of the pulmonary veins and increased pulmonary hydrostatic pressures. Capillary junctions begin to open due to the sympathetic nerves contracting the endothelial cells eventually leading to increased lung water and the occurrence of edema. This particular type of edema often overloads the airways with a protein-rich fluid that resembles plasma.

Due to both its rare nature and largely misunderstood pathophysiology, NPE has a high mortality rate. NPE develops within minutes of the initial insult and is most commonly seen in the emergency room. The mortality rate of early onset NPE associated with cerebral insults can be as high as sixty-percent (60%), although, patients diagnosed early and treated properly usually have a quick recovery time. initial diagnosis is a key component in the successful outcome of a patient presenting with NPE. This can be a difficult task due to a lack of definitive clinical signs and biomarkers and concurrently, NPE is often initially misdiagnosed as aspiration pneumonia, a cardiovascular complication caused by the cerebral Insult or even acute respiratory distress syndrome (ARDS). The purpose of this article will be to look at potential signs and symptoms of NPE, as seen in previous case studies, in order to aid future successful diagnoses.

Patients presenting with an aneurysmal SAH have the highest possibly of developing NPE and should therefore be monitored closely for signs and symptoms of the complication. It is also important to note that patients who develop NPE from an aneuysmal SAH have a higher mortality rate compared to patients who do not present with NPE. This is due to a higher severity of bleeding and subsequent cardiopulmonary failure. A recent case study of 477 patients presenting with SAH over a seven year period revealed that eight-percent (8%) of patients developed NPE secondary to the cerebral insult.

The patients with NPE presented with high intracranial pressure and pathologically high cardiac biomarkers. Researchers noted that these patients had poor neurologic outcomes compared to the patients who did not present with NPE. This case study was reexamined during year eight to better identify the signs and symptoms of patients with NPE. The clinical signs of NPE were the presentation of crackles heard by auscultation and pink tracheal fluid that was shown to be unassociated with cardiac problems, pneumonia or ARDS. Chest X-Rays revealed pulmonary vascular markings with blurring of the perivascular outlines, loss of hilar shadows and sporadic patchy increases in parenchymal density. Serum cardiac biomarkers, creatine kinase (CM-BK) and troponin T were also evaluated in order to better understand the effects of NPE on the cardiovascular system. The patients had abnormally high levels of both CM-BK and troponin T serum biomarkers. It was also noted that cardiac index was pathologically decreased.

It is not uncommon for NPE to be initially misdiagnosed as a cardiovascular complication or cardiogenic pulmonary edema associated with an acute myocardial infarction (AMI) or a variety of central nervous system insults. This misdiagnosis is generally associated with the rise in intracranial pressure (ICP) that often parallels NPE. Intracranial hypertension causes several cardiovascular problems like systemic arterial hypertension, left atrial hypertension, left ventricular hypertension and pulmonary vasoconstriction. Some case studies have revealed that NPE can be misdiagnosed as AMI complicated with cardiogenic pulmonary edema due to misleading ECG readings and initially normal computed tomography (CT) findings. The ECG is read incorrectly because of ST-T changes originally thought to be an AMI. in fact, they are actually caused by left ventricular hypertrophy strains associated with the early onset of both ischaemic stroke and the subsequent NPE. Many physicians believe in these types of cases it is important to evaluate serum levels of cardiac troponin-T in order to make a more definitive diagnosis of a myocardial injury. It is also beneficial to have a second CT scan clone three to six hours after the initial scan in order to better examine possible signs of a stroke or early stages of a major cerebral infarct.

Chest radiography of NPE often shows diffuse bilateral pulmonary infiltrates with a normal heart size; however, these same findings are consistent with aspiration pneumonia. Many patients enter the emergency room in an unconscious state and are at a high risk of aspiration of their gastric contents. NPE is often misdiagnosed as aspiration pneumonia in unconscious patients who have this type of chest radiograph. If NPE is suspected, it is beneficial to perform a bronchoscopy as soon as possible in order to confirm or refute the initial diagnosis of aspiration. It is important to make a definitive diagnosis as quickly as possible due to the increased intracranial pressure caused by NPE. The longer NPE goes untreated, the higher the risk of long term complications or fatality.

In conclusion, NPE is a life-threatening and widely misunderstood complication that claims thousands of lives every year. As these studies show, one of the most important steps in achieving a successful patient outcome is a swift initial diagnosis. Healthcare professionals need to look at the signs and symptoms of NPE and the overall history of the patient in order to properly diagnosis this devastating form of edema. The best way to improve healthcare in the future is to learn from the successes and failures of the past.

by Respiratory Student Wes Johnson

Wes Johnson is a RT student at University of Alabama at Birmingham. His paper was chosen from 7 submitted to Focus for this issue. Mr. Johnson wilt receive a $100 gift certificate and a gratis registration to the 2011 Focus Conference. His school's RT Program will also receive a $100 donation. Students are encouraged to submit their papers for the Nov/Dec issue of Focus by Oct 5th. Papers should be 900 - 1200 words and should be submitted as MS Word files to Focus's Craig Baker at bakerct78@yahoo.com.
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Title Annotation:STUDENT PAPERS
Author:Johnson, Wes
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Date:Jul 1, 2010
Words:1084
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