Neurogenic Pulmonary Edema Research Articles

Successful Microsurgical Clipping under Extracorporeal Membrane Oxygenation Treatment for a Poor-Grade Subarachnoid Hemorrhage Patient with Severe Pulmonary Neurogenic Lung

AbstractHemorrhagic strokes are considered as contraindications of extracorporeal membrane oxygenation (ECMO) therapy because of anticoagulant administration and ECMO-associated coagulopathy. We present a rare case of successful microsurgical clipping under ECMO for a poor-grade subarachnoid hemorrhage (SAH) patient with severe neurogenic pulmonary edema (NPE). A 50-year-old man presenting with the sudden loss of consciousness was diagnosed with poor-grade SAH with severe NPE, and was intubated. Because of severe hypoxemia refractory to conventional treatment, venovenous ECMO was used 6 hours after admission. To avoid thrombosis inside the ECMO circuit despite no anticoagulants, a heparin-bonded ECMO was maintained at a comparatively high blood flow rate. Subsequently, the patient underwent a microsurgical clipping under ECMO. Intraoperatively we had difficulty in bleeding control, and therefore the multiple transfusions were necessary to correct anemia and ECMO-associated coagulopathy. The aneurysmal clipping was accomplished without hemorrhagic intracranial complications. After 2 years from onset, his activities of daily life were independent. To our knowledge, this is the first report of successful microsurgical clipping for poor-grade SAH under ECMO without any anticoagulants. The use of a heparin-bonded ECMO tubing, maintenance of a slightly higher ECMO pump speed, and multiple transfusions to correct ECMO-associated coagulopathy could make the micro-neurosurgical procedures under ECMO possible. This report demonstrated the possibility to extend the range of application of microsurgical clipping for poor-grade SAH patients requiring ECMO treatment.

Seized by Blood: A Case of Neurogenic Pulmonary Edema Presenting As Diffuse Alveolar Hemorrhage

Seized by Blood: A Case of Neurogenic Pulmonary Edema Presenting As Diffuse Alveolar Hemorrhage

Massive Flash Neurogenic Pulmonary Edema after Subarachnoid Hemorrhage

Neurogenic pulmonary edema is a rare condition associated with subarachnoid hemorrhage secondary to intracranial aneurysm rupture posing high mortality rate. Management of flash pulmonary edema immediately after ictus of spontaneous subarachnoid hemorrhage is very challenging. Here, we reported a rare case of a 47- year-old lady who had massive immediate pulmonary edema following spontaneous subarachnoid hemorrhage.

Neurogenic Pulmonary Edema Associated with Hyponatremia, Primary Polydipsia, and Cannabis Use: A Case Report.

Neurogenic pulmonary edema is a rare and potentially life-threatening condition that can present as severe pulmonary edema after significant neurologic insults. This is the first documented instance that shows a plausible causal link between cannabis consumption, psychogenic polydipsia, and the subsequent development of neurogenic pulmonary edema associated with status epilepticus secondary to acute hyponatremia. We report a case of a 34-year-old female who presented to the emergency department altered and postictal after a witnessed new-onset seizure. She developed significant respiratory distress that required intubation. Her sodium was 121 millimoles per liter (mmol/L), from 137 mmol/L 36 hours prior on routine outpatient labs. Further history revealed excessive water ingestion after eating a cannabis edible prior to the seizure. This case highlights the importance of recognizing neurogenic pulmonary edema in connection with psychogenic polydipsia, severe hyponatremia, and status epilepticus subsequent to cannabis consumption.

Successful management of pulmonary edema secondary to accidental electrocution in a young dog

BackgroundHuman records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes.Case presentationA 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits.ConclusionsWe present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Interaction between Neurogenic Pulmonary Edema and Thoracic 3 DRG Degeneration Following Spinal Subarachnoid Hemorrhage: First Experimental Study.

Neurogenic pulmonary edema (NPE) following subarachnoid hemorrhage (SAH) is still one of the most catastrophic complications with high morbidity and mortality rates. Systemic sympathetic hyperactivity has been considered in the pathogenesis, but it has not been clarified. In this study, we investigate the relationship between the degeneration of the T3 dorsal root ganglion (DRG) and the development of NPE following spinal SAH. The study was conducted on 23 rabbits. Five rabbits were used as the control group, 5 as the sham group (n = 5), and 13 as the study group. The correlation between the degenerated neuronal densities of the T3 nerve axons and neurons in the DRG and NPE scores was analyzed statistically. A correlation between the neuronal degeneration of the T3 nerve, its DRG, and high NPE scores was found in the study group and the sham group. Massive NPE was detected in the study group along with neural degeneration of T3 axons and ganglia. The present study indicates that NPE and pulmonary artery vasospasm can be prevented by reducing T3 DRG degeneration.

Preventing Fluid Retention After Subarachnoid Haemorrhage During Administration of Endothelin Receptor Antagonist.

Prevention of delayed cerebral infarction (DCI) due to cerebral vasospasm after subarachnoid haemorrhage (SAH) has been done with intravenous Rho kinase inhibitors (ROCKI), ozagrel sodium (TXA2I), selective ROCKI infusion (ROCKI i.a.), and cerebrospinal fluid (CSF) drainage. The endothelin receptor antagonist (ERA, clazosentan) became available in 2022 and is said to be highly recommended for DCI prevention, while fluid retention such as pleural effusion and pulmonary oedema accumulation is often experienced. We investigated the relationship between patient background, fluid retention, and ERA. Ten consecutive SAH patients treated with ERA from July to December 2022 were included. We examined the results of blood sampling on admission, echocardiography, chest computed tomography (CT), with postoperative DCI, and hydrocephalus requiring cerebrospinal fluid shunt (hydro), and symptomatic fluid retention requiring albumin and furosemide (third fluid space). Two males and eight females, mean age 63years, mean preoperative World Federation Neurosurgical Surgeons (WFNS) grade 3.5, mean creatinine 0.94, mean brain natriuretic peptide (NT-proBNP). In 1883, two patients with Takotsubo cardiomyopathy and four patients with neurogenic pulmonary oedema are present. All patients underwent coil embolisation, and postoperative CSF drainage, ROCKI, TXA2I systemic administration, and ROCKI i.a. There were one DCI, three hydro, and five third fluid cases. Concerning the third fluid, the only significant difference was found in the age. An improvement in fluid retention after ERA discontinuation in old patients was shown. Our experience suggests that age may be the most influential factor. Based on these results, we have also found that by avoiding the use of ERA in patients older than 80years, strictly limiting the infusion volume when using ERA, and actively using the drugs for heart failure early on, the frequency of suffering from third fluid space is reduced.

Acute brain injury increases pulmonary capillary permeability via sympathetic activation-mediated high fluid shear stress and destruction of the endothelial glycocalyx layer

Neurogenic pulmonary edema secondary to acute brain injury (ABI) is a common and fatal disease condition. However, the pathophysiology of brain-lung interactions is incompletely understood. This study aims to investigate whether sympathetic activation-mediated high fluid shear stress after ABI would damage pulmonary endothelial glycocalyx thus leading to increased pulmonary capillary permeability. The tricuspid annular plane systolic excursion (TAPSE) was detected in a rat model of controlled cortical impact (CCI) and CCI + transection of the cervical sympathetic trunk (TCST). Changes in pulmonary capillary permeability were assessed by analyzing the Evans blue, measuring the dry/wet weight ratio of the lungs and altering protein levels in the bronchoalveolar lavage fluid (BALF). The parallel-plate flow chamber system was used to simulate the fluid shear stress in vitro. Western blotting and immunofluorescence staining were used to determine the expression levels of hyaluronan-binding protein (CEMIP), syndecan-1 and tight junction proteins (TJPs, including claudin-5 and occludin). TCST could restrain cardiac overdrive and sympathetic activation in a rat model of CCI. Compared to the CCI group, the CCI + TCST group showed a reduction of CEMPI (which degrades hyaluronic acid), along with an increase of syndecan-1 and TJPs. CCI + TCST group presented decreasing pulmonary capillary permeability. In vitro, high shear stress (HSS) increased the expression of CEMIP and reduced syndecan-1 and TJPs, which was coordinated with the results in vivo. Our findings show that sympathetic activation-mediated high fluid shear stress after ABI would damage pulmonary endothelial glycocalyx thus leading to increased pulmonary capillary permeability.

Insufficiency of plasmatic arginine/homoarginine during the initial postoperative phase among patients with tumors affecting the medulla oblongata heightens the likelihood of neurogenic pulmonary oedema following surgery.

This prospective clinical study aims to investigate the fluctuations of neurotransmitters in peripheral venous blood during the perioperative period and to identify independent predictors for postoperative neurogenic pulmonary oedema (NPE) in patients with medulla oblongata-involved tumours. Peripheral venous blood samples of the enroled patients at seven perioperative time points, as well as their medical records and radiologic data were collected. High-performance liquid chromatography-tandem mass spectrometry was utilized to detect the concentrations of 39 neurotransmitters in these samples. The study applied univariate and multivariate generalized estimating equation (GEE) logistic regression analyses to explore independent predictors of postoperative NPE, and one-way repeated-measures ANOVA to compare the concentrations of the same neurotransmitter at different perioperative time points. The study included 36 patients with medulla oblongata-involved tumours from January to December 2019, and found that 13.9% of them experienced postoperative NPE. The absence of intraoperative use of sevoflurane ( P =0.008), decreased concentrations of arginine ( P =0.026) and homoarginine ( P =0.030), and prolonged postoperative tracheal extubation ( P <0.001) were identified as independent risk factors for postoperative NPE in medulla oblongata-involved tumour patients. Pairwise comparison analysis revealed that the perioperative decreases in arginine and homoarginine concentrations mainly occurred within the postoperative 8 h. This study demonstrates that NPE is not uncommon in patients with medulla oblongata-involved tumours. The absence of intraoperative use of sevoflurane, decreased concentrations of plasmatic arginine and homoarginine, and prolonged postoperative tracheal extubation are independent predictors of postoperative NPE. These two neurotransmitters' concentrations dropped mainly within the early postoperative hours and could serve as potential early warning indicators of postoperative NPE in clinical practice.

Inhibition of S100A9 alleviates neurogenic pulmonary edema after subarachnoid hemorrhage

Background and PurposeNeurogenic pulmonary edema (NPE) frequently arises as a complication subsequent to subarachnoid hemorrhage (SAH). Heterodimers of S100A8 and S100A9 are commonly formed, thereby initiating an inflammatory reaction through receptor binding on the cell surface. Paquinimod serves as a specific inhibitor of S100A9. The objective of this investigation is to assess the impact of Paquinimod administration and S100A9 knockout on NPE following SAH. MethodsIn this study, SAH models of C57BL/6J wild-type (WT) and S100A9 knockout mice were established through intravascular perforation. These models were then divided into several groups, including the WT-sham group, S100A9-KO-sham group, WT-SAH group, WT-SAH + Paquinimod group, and S100A9-KO-SAH group. After 24 h of SAH induction, pulmonary edema was assessed using the lung wet-dry weight method and Hematoxylin and eosin (HE) staining. Additionally, the expression levels of various proteins, such as interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), occludin, claudin-3, Bax, Bcl-2, TLR4, MYD88, and pNF-κB, in lung tissue were analyzed using western blot and immunofluorescence staining. Lung tissue apoptosis was detected by TUNEL staining. ResultsFirstly, our findings indicate that the knockout of S100A9 has a protective effect on early brain injury following subarachnoid hemorrhage (SAH). Additionally, the reduction of brain injury after SAH can also alleviate neurogenic pulmonary edema (NPE). Immunofluorescence staining and western blot analysis revealed that compared to SAH mice with wild-type S100A9 expression (WT-SAH), the lungs of S100A9 knockout SAH mice (S100A9-KO-SAH) and mice treated with Paquinimod exhibited decreased levels of inflammatory molecules (IL-1β and TNF-α) and increased levels of tight junction proteins. Furthermore, the knockout of S100A9 resulted in upregulated expression of the apoptotic-associated protein Bax and down-regulated expression of Bcl-2. Furthermore, a decrease in TLR4, MYD88, and phosphorylated pNF-κB was noted in S100A9-KO-SAH and Paquinimod treated mice, indicating the potential involvement of the TLR4/MYD88/NF-κB signaling pathway in the inhibition of the protective effect of S100A9 on NPE following SAH. ConclusionThe knockout of S100A9 not only ameliorated initial cerebral injury following subarachnoid hemorrhage (SAH), but also mitigated SAH-associated neurogenic pulmonary edema (NPE). Additionally, Paquinimod was found to diminish NPE. These findings imply a correlation between the central nervous system and peripheral organs, highlighting the potential of safeguarding the brain to mitigate harm to peripheral organs.

Plants and their Bioactive Compounds as a Possible Treatment for Traumatic Brain Injury-Induced Multi-Organ Dysfunction Syndrome.

Traumatic brain injury is an outcome of the physical or mechanical impact of external forces on the brain. Thus, the silent epidemic has complex pathophysiology affecting the brain along with extracranial or systemic complications in more than one organ system, including the heart, lungs, liver, kidney, gastrointestinal and endocrine system. which is referred to as Multi-Organ Dysfunction Syndrome. It is driven by three interconnected mechanisms such as systemic hyperinflammation, paroxysmal sympathetic hyperactivity, and immunosuppression-induced sepsis. These multifaceted pathologies accelerate the risk of mortality in clinical settings by interfering with the functions of distant organs through hypertension, cardiac arrhythmias, acute lung injury, neurogenic pulmonary edema, reduced gastrointestinal motility, Cushing ulcers, acute liver failure, acute kidney injury, coagulopathy, endocrine dysfunction, and many other impairments. The pharmaceutical treatment approach for this is highly specific in its mode of action and linked to a variety of side effects, including hallucinations, seizures, anaphylaxis, teeth, bone staining, etc. Therefore, alternative natural medicine treatments are widely accepted due to their broad complementary or synergistic effects on the physiological system with minor side effects. This review is a compilation of the possible mechanisms behind the occurrence of multiorgan dysfunction and reported medicinal plants with organoprotective activity that have not been yet explored against traumatic brain injury and thereby, highlighting the marked possibilities of their effectiveness in the management of multiorgan dysfunction. As a result, we attempted to respond to the hypothesis against the usage of medicinal plants to treat neurodegenerative diseases.

Initial Treatment of Subarachnoid Hemorrhage

The re-rupture of a subarachnoid hemorrhage(SAH)due to a ruptured cerebral aneurysm is a poor prognostic factor, and initial treatment to prevent re-rupture is important in the acute phase of SAH. Prevention of re-rupture is performed by reducing blood pressure, by sedation, and by analgesia until the patient undergoes radical surgery. It is recommended that the systolic blood pressure be lowered to below 120-140 mmHg. When SAH is suspected, a head CT scan should be obtained after the initial treatment. If the SAH is not clearly visible on CT but is strongly suspected, MRI should be performed. Once a SAH is diagnosed, three-dimensional CT angiography should be performed to search for cerebral aneurysms. SAHs may also cause breathing and circulation problems due to neurogenic pulmonary edema and Takotsubo cardiomyopathy. Clipping is more curative than coil embolization, but coil embolization has been shown to have better long-term survival and independence rates than clipping for aneurysms that can be treated with either technique. Ideally, ruptured cerebral aneurysms should be treated at institutions that offer both clipping and coil embolization, and the choice of treatment should be based on a comprehensive assessment of the patient's age; the severity, location, size and shape of the aneurysm; the clipping and coil embolization techniques of the treating physician; and the wishes of the patient and family.

Fluid therapy in the acute brain injured patient.

Adequate fluid therapy in the acute brain injured (ABI) patient is essential for maintaining an adequate brain and systemic physiology and preventing intra- and extracranial complications. The target of euvolemia, implying avoidance of both hypovolemia and fluid overloading (or "hypervolemia," by definition associated with fluid extravasation leading to tissue edema) is of key importance. Primary brain injury can be aggravated by secondary brain injury and systemic deterioration through diverse pathways which can challenge appropriate fluid management, e.g. neuroendocrine and electrolyte disorders, stress cardiomyopathy (also known as cardiac stunning) and neurogenic pulmonary edema. This is an updated expert opinion aiming to provide a practical overview on fluid therapy in the ABI patient, partly based on more recent work and stressing the fact that intravenous fluids should be regarded as drugs, with their inherent potential for both benefit and (unintended) harm.

A Case of Aneurysmal Sub Arachnoid Hemorrhage Complicated by Nstemi and Acute Pulmonary Edema

Aneurysmal SAH is a life threatening event which can cause permanent disability, the mortality and morbidity will be increased with associated complications like ACS and Acute pulmonary edema, which are rare complications of aneurysmal SAH. The combination of these three conditions imposes important treatment dilemmas. These patients tend to have electrocardiographic changes along with elevated cardiac biomarkers and neurogenic stress cardiomyopathy and pulmonary edema.

Extensive bilateral anterior and posterior circulation ischemic stroke caused by severe vasospasm (Delayed cerebral ischemia) due to aneurysmal subarachnoid haemorrhage (aSAH) - A case report

Aneurysmal subarachnoid haemorrhage (aSAH) is a disease with high morbidity and mortality even in this modern era. Since treating vasospasm is a challenging task, we emphasize in developing newer aganets for the treatment of vasospasm. In the hyper acute phase, patients with SAH can have catecholamine surge-related arrhythmia, neurogenic pulmonary edema, and irreversible damage to the hypothalamus and brainstem. Delayed cerebral ischemia (DCI) is a serious complication of aneurysmal subarachnoid haemorrhage (aSAH). Though there are many clinical trials to look upon the therapies for DCI and vasospasm in aSAH, none have led to an improvement in outcome of the patient.The prognosis of patients with SAH is grave even with the recent advancements in medical treatments. One of the main cause for this situation, that there are no usable neuroprotective drugs that can be used as soon as SAH is diagnosed. We report a case of ruptured Post Communicating Artery (PCOM) aneurysm with diffuse SAH causing severe vasospasm leading to extensive bilateral anterior and posterior ischemic stroke causing severe morbidity. Since there is no therapeutic breakthrough in treatment of aneurysmal SAH, we emphasize in developing a same.

Edema Paru Neurogenik Perioperatif

Neurogenic pulmonary edema (NPE) is one of the leading causes of death in the intensive care unit. These events are often disguised as diseases or disorders that originate purely from the respiratory system. Diagnostic examination of NPE needs to be done, both radiologically and in the laboratory. Several things are useful in determining the estimated incidence of NPE, including the causes of neurological events, supporting examinations, length of stay, and preconditions for comorbidities owned by the patient or his family. Patients who are about to undergo a surgical procedure and have previous respiratory problems, a recent history of neurological disorders, or even both have a special note about the risk of perioperative NPE events. Management of NPE can be appropriate if it is managed comprehensively and always considers possible differential diagnoses of causes because if it is wrong to make a diagnosis, then of course it will result in an error in therapy. Effective and efficient management of NPE, based on diagnosis that is strengthened by the support of laboratory and supporting examinations, to rule out ambiguous causes of NPE, both purely neurological and non-neurological cases. Postoperative patients who are indicated to have NPE, during treatment in the intensive care unit or post anesthesia care unit (PACU), need to receive temporary special attention so that the patient does not experience aggravation.

Emergency Medical Management of Aneurysmal Subarachnoid Hemorrhage

Aneurysmal subarachnoid hemorrhage is a medical emergency that necessitates direct transfer to a tertiary referral center specialized in the diagnosis and treatment of this condition. The initial hours after aneurysmal rupture are critical for patients with aneurysmal subarachnoid hemorrhage, both in terms of rebleeding and combating the effect of early brain injury. No good treatment options are available to reduce the risk of rebleeding before aneurysm occlusion. Lowering the blood pressure may reduce the risk of rebleeding but carries a risk of inducing delayed cerebral ischemia or aggravating the consequences of early brain injury. Early brain injury after aneurysmal rupture has an important effect on final clinical outcome. Proper cerebral perfusion is pivotal in these initial hours after aneurysmal rupture but threatened by complications such as neurogenic pulmonary edema and cardiac stunning, or by acute hydrocephalus, which may necessitate early drainage of cerebrospinal fluid.

SUDEP as Endpoint of SARS-CoV-2 Associated Encephalitis with Status Epilepticus

With interest we read the article by Farias et al. on a 31 year-old, previously healthy male with SARS-CoV-2 related meningo-encephalitis who died suddenly and unexpectedly during a status epilepticus on the intensive care unit (ICU) [1]. Because the patient was co-infected with influenza-A, it was suspected that meningoencephalitis was due to infection with both viruses [1]. No autopsy was performed. The study is excellent, but has limitations that are cause of concerns and should be discussed. The main limitation of the study is that the patient did not undergo autopsy. To clarify whether SARS-CoV-2 or influenza-A was truly present inside neurons and glial cells, it is critical to have the results of histological, immune-histological, and electron microscopy examinations of the brain. Autopsy is also critical to assess whether the lung was affected or not since no CT of the lungs had been done intra vitam. Another limitation of the study is that no cerebral MRI with contrast medium had been done intra vitam to document the extension and localisation of encephalitis. It would have been also interesting to know whether the patient had developed cerebral edema or brainstem herniation with progression of encephalitis. Another limitation is that RT-PCR for SARS-CoV-2 and influenza-A in the CSF was not repeated and the initial test results were not confirmed by using a different kit to rule out a false positive result on the first test. It is speculative to assume that the patient had both, SARS-CoV-2 encephalitis and influenza-A encephalitis. Since presence of the influenza-A virus was not documented in the CSF, it is rather unlikely that the patient also had influenza-A encephalitis. A cause of death not discussed in the report is sudden unexpected death in epilepsy (SUDEP). SUDEP has been repeatedly reported as a complication of witnessed and unwitnessed seizures [2]. Because the patient died suddenly and unexpectedly during a status epilepticus on the ICU, it cannot be ruled out that SUDEP was responsible. SUDEP is assumed due to neurogenic pulmonary edema, autonomic dysreflexia, or acute cardiac disease, such as Takotsubo syndrome (TTS), acute heart failure, or ventricular arrhythmias. Therefore, we should know whether the ECG shortly before or during resuscitation on the ICU was abnormal or not and whether a bedside echocardiography was done during CPR. We disagree with the statement that the patient had only neurological symptoms [1]. Figure 1 clearly shows that the patient also had coughing, fever, and running nose, which are all non-neurological. Meningo-encephalitis, myelitis, and ADEM are neither neurological symptoms nor neurological syndromes, as stated in the introduction [1]. All of them are simply central nervous system (CNS) diseases. At the beginning of 2022 anti-SARS-CoV-2 vaccinations were already available. We therefore should know if the patient was vaccinated and had a breakthrough SARSCoV-2 infection or if she was unvaccinated. There is no mention of the anti-seizure drugs the patient received for the initial tonic clonic seizure and for status epilepticus. There is also no mention of the reference limits of the blood and CSF values reported. Overall, the interesting study has limitations that call the results and their interpretation into question. Addressing these issues would strengthen the conclusions and could improve the status of the study. Before claiming that encephalitis was due to SARS-CoV-2 and influenza-A, repeated documentation of the presence of both viruses is warranted. This can be achieved by autopsy, or repeated CSF investigations, both of which were not carried out in the index patient.

Neurogenic Pulmonary Edema : A Rare Presentation of Traumatic Brain Injury

Neurogenic Pulmonary Edema : A Rare Presentation of Traumatic Brain Injury

Noncardiogenic pulmonary edema in small animals.

To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs. NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be dueto changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature,or a combination thereof.Possiblecausesinclude inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post-obstructive pulmonary edema), neurologic disease such as headtraumaor seizures (neurogenic pulmonary edema), electrocution,after re-expansion of a collapsed lung orafter drowning. Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left-sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis. The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases. Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE.