Probable positive effects of the photobiomodulation as an adjunctive treatment in COVID-19: A systematic review.

BACKGROUND: COVID-19, as a newly-emerged viral infection has now spread all over the world after originating in Wuhan, China. Pneumonia is the hallmark of the disease, with dyspnea in half of the patients and acute respiratory distress syndrome (ARDS) in up to one -third of the cases. Pulmonary edema, neutrophilic infiltration, and inflammatory cytokine release are the pathologic signs of this disease. The anti-inflammatory effect of the photobiomodulation (PBM) has been confirmed in many previous studies. Therefore, this review study was conducted to evaluate the direct effect of PBM on the acute lung inflammation or ARDS and also accelerating the regeneration of the damaged tissues. The indirect effects of PBM on modulation of the immune system, increasing the blood flow and oxygenation in other tissues were also considered. METHODOLOGY: The databases of PubMed, Cochrane library, and Google Scholar were searched to find the relevant studies. Keywords included the PBM and related terms, lung inflammation, and COVID-19 -related signs. Studies were categorized with respect to the target tissue, laser parameters, and their results. RESULTS: Seventeen related papers were included in this review. All of them were in animal models. They showed that the PBM could significantly decrease the pulmonary edema, neutrophil influx, and generation of pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1ß), interleukin 6 (IL-6), intracellular adhesion molecule (ICAM), reactive oxygen species (ROS), isoform of nitric oxide synthase (iNOS), and macrophage inflammatory protein 2 (MIP-2)). CONCLUSION: Our findings revealed that the PBM could be helpful in reducing the lung inflammation and promoting the regeneration of the damaged tissue. PBM can increase the oxygenation indirectly in order to rehabilitate the affected organs. Thus, the infra-red lasers or light-emitting diodes (LEDs) are recommended in this regard.

The unknown known: non-cardiogenic pulmonary edema in amlodipine poisoning, a cohort study.

Context: Amlodipine is the most common calcium channel blocker (CCB) on the Swedish market, and poison center (PC) consultations for amlodipine overdoses are increasing. The clinical picture is dominated by vasodilation with relative preservation of cardiac function. CCBs selectively dilate vessels on the afferent side of the capillary network which, in states of preserved or increased blood flow may lead to edema formation, including non-cardiogenic pulmonary edema (NCPE). This complication has been considered rare in CCB poisoning. In this cohort study of nineteen amlodipine poisonings with high amlodipine blood levels, the incidence and clinical significance of NCPE in severe amlodipine poisoning are explored.Methods: During 2017-2018 the Swedish PC prospectively encouraged the gathering of blood samples in amlodipine poisonings with symptoms requiring treatment with inotropes or vasopressors. Samples were sent by mail to the Forensic Toxicology Division at the Swedish National Board of Forensic Medicine for screening and quantification of relevant toxicants. Patients with blood amlodipine levels >0.25 µg/mL were included in a cohort whose case details were gathered from medical records and PC-case notes with a special focus on signs of NCPE.Results: Nineteen patients met the blood amlodipine inclusion criteria. Four (21%) died and one patient was treated with VA-ECMO. Nine patients developed NCPE defined as a need for positive pressure ventilation (PPV) while having an echocardiographically normal left ventricular function.Conclusion: In this prospective cohort study of consecutive and analytically confirmed significant amlodipine poisonings NCPE was a common finding occurring in 47% of the whole cohort and in 64% of patients who did not go on to develop complete hemodynamic collapse.

HSP-70-Mediated Hyperbaric Oxygen Reduces Brain and Pulmonary Edema and Cognitive Deficits in Rats in a Simulated High-Altitude Exposure.

High-mountain sickness is characterized by brain and pulmonary edema and cognitive deficits. The definition can be fulfilled by a rat model of high-altitude exposure (HAE) used in the present study. This study aimed to investigate the protective effect of hyperbaric oxygen therapy (HBO2T) and to determine the underlying mechanisms. Rats were subjected to an HAE (9.7% O2 at 0.47 absolute atmosphere of 6,000 m for 3 days). Immediately after termination of HAE, rats were treated with HBO2T (100% O2 at 2.0 absolute atmosphere for 1 hour per day for 5 consecutive days) or non-HBO2T (21% O2 at 1.0 absolute atmosphere for 1 hour per day for 5 consecutive days). As compared to non-HAE+non-HBO2T controls, the HAE+non-HBO2T rats exhibited brain edema and resulted in cognitive deficits, reduced food and water consumption, body weight loss, increased cerebral inflammation and oxidative stress, and pulmonary edema. HBO2T increased expression of both hippocampus and lung heat shock protein (HSP-70) and also reversed the HAE-induced brain and pulmonary edema, cognitive deficits, reduced food and water consumption, body weight loss, and brain inflammation and oxidative stress. Decreasing the overexpression of HSP-70 in both hippocampus and lung tissues with HSP-70 antibodies significantly attenuated the beneficial effects exerted by HBO2T in HAE rats. Our data provide in vivo evidence that HBO2T works on a remodeling of brain/lung to exert a protective effect against simulated high-mountain sickness via enhancing HSP-70 expression in HAE rats.

Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report.

Hyperbaric oxygen therapy (HBOT) for carbon monoxide (CO) poisoning is widely performed to prevent delayed neuropsychiatric syndrome. Although HBOT can generally be performed with safety, the appropriate management of HBOT still remains unestablished. A 31-year-old man was transferred to our facility to undergo HBOT in a multiplace chamber with a diagnosis of CO poisoning. The first HBOT session ended uneventfully. During the second HBOT session, the patient suddenly experienced convulsive seizures. The accompanying doctor administered intravenous propofol to stop the convulsion and terminated the HBOT. Soon after the convulsion, the patient developed frothy secretions through the endotracheal-tube with impaired oxygenation. Head computed tomography scan showed no abnormalities, suggesting the seizure was associated with complications of HBOT. A chest X-ray revealed bilateral pulmonary edema, and echocardiography revealed normal cardiac function, indicating that the pulmonary edema resulted from HBOT or neurogenic mechanism secondary to the seizure. The patient's respiratory status improved without recurrence of the seizure and no delayed neurological sequelae was seen afterwards. Here we report unexpected rare adverse events during HBOT. Hyperbaric oxygen therapy for acute indications should be performed in multiplace chambers, with appropriate preparation and medical equipment. J. Med. Invest. 65:286-288, August, 2018.

Fatal Pulmonary Edema in a Child After Jellyfish Stings in Korea.

Jellyfish have been increasing at a global scale in recent years. These blooms not only have deleterious effects on marine ecosystems, they also increase the risk of jellyfish stings and accompanying envenomation. Here, we report a fatal case of pulmonary edema caused by jellyfish envenomation in a child in Korea. The patient died 4 h after envenomation despite cardiopulmonary resuscitation. Nemopilema nomurai was the suspected species of jellyfish encountered by the patient, although we are unable to confirm this. With this case report, we aim to inform on the serious issue of toxicity associated with jellyfish species that bloom mainly along Korean, east Chinese, and Japanese shores and to discuss appropriate first aid methods in case of jellyfish stings.

Curcumin ameliorated ventilator-induced lung injury in rats.

BACKGROUND: Curcumin (CUR) is a Chinese medicine monomer with antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects and mechanisms of CUR treatment on ventilator-induced lung injury (VILI) in rats. METHODS: Total 50 SD rats were divided into five groups: sham, VILI, VILI+CUR-50 (CUR 50?mg/kg pretreated intraperitoneal), VILI+CUR-200 (CUR 200?mg/kg pretreated intraperitoneal) and VILI?+?DXM (5?mg/kg pretreated intraperitoneal). The morphology and ultrastructure were observed by microscope and transmission electron microscope. The wet to dry ratio, protein concentration in bronchoalveolar lavage fluid (BALF), evans blue dye (EBD) content, nuclear factor kappa B (NF-?B) activity, myeloperoxidase (MPO), malondialdehyde (MDA), xanthine oxidase (XO) and total antioxidative capacity (TAOC) levels were measured. RESULTS: Histological studies revealed that inflammatory cells infiltration and alveolar edema were significantly severe in VILI as compared to other groups. CUR-200 and DXM treatment reversed lung injury significantly. The wet to dry ratio, protein concentration in BALF, EBD content, MPO activity, tumor necrosis factor (TNF)-? level and NF-?B activity were significantly increased in VILI group as compared to other groups. CUR-200 and DXM treatment significantly suppressed permeability and inflammation induced by ventilation. Furthermore, the significantly higher MDA content in VILI could be markedly decreased by CUR-200 and DXM treatment while the levels of XO and TAOC were markedly recovered only by CUR (200?mg/kg) treatment after VILI. CONCLUSION: CUR could inhibit the inflammatory response and oxidative stress during VILI, which is partly through NF-?B pathway.

Revascularization of atherosclerotic renal artery stenosis for chronic heart failure versus acute pulmonary oedema.

AIM: The aim of the study is to determine whether the apparent benefit of revascularization of renal artery stenosis for 'flash' pulmonary oedema extends to heart failure patients without a history of prior acute pulmonary oedema. METHODS: A prospective study of patients with renal artery stenosis and heart failure at a single centre between 1 January 1995 and 31 December 2010. Patients were divided into those with and without previous acute pulmonary oedema/decompensation. Survival analysis compared revascularization versus medical therapy in each group using Cox regression adjusted for age, estimated glomerular filtration rate, blood pressure and co-morbidities. RESULTS: There were 152 patients: 59% male, 36% diabetic, age 70 ± 9 years, estimated glomerular filtration rate 29 ± 17 mL/min per 1.73 m2 ; 52 had experienced previous acute pulmonary oedema (34%), whereas 100 had no previous acute pulmonary oedema (66%). The revascularization rate was 31% in both groups. For heart failure without previous acute pulmonary oedema, the hazard ratio for death after revascularization compared with medical therapy was 0.76 (0.58-0.99, P = 0.04). In heart failure with previous acute pulmonary enema, the hazard ratio was 0.73 (0.44-1.21, P = 0.22). For those without previous acute pulmonary oedema, the hazard ratio for heart failure hospitalization after revascularization compared with medical therapy was 1.00 (0.17-6.05, P = 1.00). In those with previous acute pulmonary oedema, it was 0.51 (0.08-3.30, P = 0.48). CONCLUSION: The benefit of revascularization in heart failure may extend beyond the current indication of acute pulmonary oedema. However, findings derive from an observational study.

Effect of chronic khat (Catha edulis, Forsk) use on outcome of Plasmodium berghei ANKA infection in Swiss albino mice.

BACKGROUND: The objective of this study was to explore effects of khat (Catha edulis) on outcome of rodent malaria infection and its anti-plasmodial activities on Plasmodium berghei ANKA (PbA). METHODS: Female Swiss albino mice were orally treated with crude khat (Catha edulis) extracts (100, 200 and 300 mg/kg) on a daily basis for 4 weeks prior to PbA infection. Physical, clinical, hematological, biochemical and histo-pathological features of the mice were assessed. In addition, in vivo anti-plasmodial activities of khat were evaluated. RESULTS: The finding of this study showed that khat use was strongly associated with increment of levels of liver and kidney biomarkers, leucopenia, severe anemia, rise in level of inflammation biomarkers: C-reactive protein (CRP), uric acid (UA), increased monocyte-lymphocyte count ratio (MLCR), manifestation of cerebral malaria symptoms such as ataxia, paralysis and deviation of the head but with no pulmonary edema. Significantly lower level of parasitemia (P<0.05), rectal temperature, but, high level of hemoglobin were observed at the early stage of the PbA infection in khat treated mice than the control. With extension of the treatment period, however, drastic increments were observed in parasite load and rectal temperature although there was reduction in hemoglobin (Hb) level. Moreover, khat showed poor anti-plasmodial activity with <10% parasite suppression activity and lack protection against major malaria symptoms. The significant reduction (P<0.01) of hematological parameters during PbA infection strengthen the notion that hematological parameters could be good predictors of severe malaria complications in human. CONCLUSIONS: In mice model treated with khat prior to infection with the rodent malaria parasite, khat was found to worsen manifestation of most malaria complications. Furthermore, the same plant showed poor in vivo anti-plasmodial activity and protection against major malaria symptoms.

Postinfection A77-1726 treatment improves cardiopulmonary function in H1N1 influenza-infected mice.

Acute respiratory disease is associated with significant morbidity and mortality in influenza. Because antiviral drugs are only effective early in infection, new agents are needed to treat nonvaccinated patients presenting with late-stage disease, particularly those who develop acute respiratory distress syndrome. We found previously that the de novo pyrimidine synthesis inhibitor A77-1726 reversed the influenza-induced impairment of alveolar fluid clearance. Patients with acute respiratory distress syndrome and intact alveolar fluid clearance demonstrate lower mortality than those with compromised fluid clearance. We therefore investigated the effects of treatment with nebulized A77-1726 (67.5 mg/kg) on indices of cardiopulmonary function relevant to the diagnosis of acute respiratory distress syndrome. BALB/cAnNCr mice (8-12 wk old) were inoculated intranasally with 10,000 plaque-forming units/mouse influenza A/WSN/33 (H1N1). Pulse oximetry was performed daily. Alveolar fluid clearance, lung water, and lung mechanics were measured at 2 and 6 days after inoculation in live, ventilated mice by BSA instillation, magnetic resonance imaging, and forced-oscillation techniques, respectively. A77-1726 treatment at 1 day after inoculation delayed mortality. Treatment on Days 1 or 5 reduced viral replication on Day 6, and improved alveolar fluid clearance, peripheral oxygenation, and cardiac function. Nebulized A77-1726 also reversed influenza-induced increases in lung water content and volume, improved pulmonary mechanics, reduced bronchoalveolar lavage fluid ATP and neutrophil content, and increased IL-6 concentrations. The ability of A77-1726 to improve cardiopulmonary function in influenza-infected mice and to reduce the severity of ongoing acute respiratory distress syndrome late in infection suggests that pyrimidine synthesis inhibitors are promising therapeutic candidates for the management of severe influenza.

Device monitoring strategies in acute heart failure syndromes.

Acute heart failure syndromes (AHFS) represent the most common discharge diagnoses in adults over age 65 and translate into dramatically increased heart failure-associated morbidity and mortality. Conventional approaches to the early detection of pulmonary and systemic congestion have been shown to be of limited sensitivity. Despite their proven efficacy, disease management and structured telephone support programs have failed to achieve widespread use in part due to their resource intensiveness and reliance upon motivated patients. While once thought to hold great promise, results from recent prospective studies on telemonitoring strategies have proven disappointing. Implantable devices with their capacity to monitor electrophysiologic and hemodynamic parameters over long periods of time and with minimal reliance on patient participation may provide solutions to some of these problems. Conventional electrophysiologic parameters and intrathoracic impedance data are currently available in the growing population of heart failure patients with equipped devices. A variety of implantable hemodynamic monitors are currently under investigation. How best to integrate these devices into a systematic approach to the management of patients before, during, and after AHFS is yet to be established.

Prevention and treatment of high-altitude pulmonary edema.

We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high-altitude pulmonary edema (HAPE). Individual susceptibility is the most important determinant for the occurrence of HAPE. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressure 36-51 mm Hg), caused by an inhomogeneous hypoxic pulmonary vasoconstriction which leads to an elevated pulmonary capillary pressure and protein content as well as red blood cell-rich edema fluid. Furthermore, decreased fluid clearance from the alveoli may contribute to this noncardiogenic pulmonary edema. Immediate descent or supplemental oxygen and nifedipine or sildenafil are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent, average gain of altitude not exceeding 300 m/d above an altitude of 2500 m. If progressive high altitude acclimatization would not be possible, prophylaxis with nifedipine or tadalafil for long sojourns at high altitude or dexamethasone for a short stay of less then 5 days should be recommended.

Effect of core body temperature on ventilator-induced lung injury.

OBJECTIVE: Ventilator-induced lung injury is a risk in patients requiring elevated ventilatory support pressures. We hypothesized that thermal stress modulates the development of ventilator-induced lung injury. DESIGN: Experimental study. SETTING: University laboratory. SUBJECTS: Anesthetized rabbits. INTERVENTIONS: Two experimental studies were designed to determine the role of temperature as a cofactor in ventilator-induced lung injury. In the first study, three groups of anesthetized rabbits were randomized to be ventilated for 2 hrs at core body temperatures of 33, 37, or 41 degrees C while ventilated with pressure control ventilation of 15/3 cm H2O (noninjurious settings-control) or 35/3 cm H2O (potentially injurious settings-experimental). To exclude effects arising from cardiac output fluctuations or from extrapulmonary organs, an isolated lung model was used for the second study, perfused at a fixed rate and studied at either 33 degrees C or 41 degrees C. MEASUREMENTS AND MAIN RESULTS: In the first study, the hyperthermic group compared with the hypothermic animals had significantly reduced mean PaO2 (-114 vs. + 14 mm Hg, p <.05), increased lung edema formation (mean wet weight/dry weight ratio of 8.1 vs. 5.7), and altered pressure-volume curves. The hyperthermic isolated, perfused lungs had an increased ultrafiltration coefficient, formed more edema, and experienced greater alveolar hemorrhage than hypothermic lungs. CONCLUSIONS: In two studies of ventilator-induced lung injury in rabbits, maintaining hyperthermia compared with hypothermia augmented the development of lung injury. Similar results from both the in vivo and isolated, perfused lung studies suggest that the observed effects were not due to cardiovascular factors or consequences of heating nonpulmonary organs.

The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure.

OBJECTIVE: Conventional hemodynamic indexes (cardiac index (CI), and pulmonary capillary wedge pressure) are of limited value in the diagnosis and treatment of patients with acute congestive heart failure (CHF). PATIENTS AND METHODS: We measured CI, wedge pressure, right atrial pressure (RAP) and mean arterial blood pressure (MAP) in 89 consecutive patients admitted due to acute CHF (exacerbated systolic CHF, n=56; hypertensive crisis, n=5; pulmonary edema, n=11; and cardiogenic shock, n=17) and in two control groups. The two control groups were 11 patients with septic shock and 20 healthy volunteers. Systemic vascular resistance index (SVRi) was calculated as SVRi=(MAP-RAP)/CI. Cardiac contractility was estimated by the cardiac power index (Cpi), calculated as CIxMAP. RESULTS AND DISCUSSION: We found that CI<2.7 l/min/m(2) and wedge pressure >12 mmHg are found consistently in patients with acute CHF. However, these measures often overlapped in patients with different acute CHF syndromes, while Cpi and SVRi permitted more accurate differentiation. Cpi was low in patients with exacerbated systolic CHF and extremely low in patients with cardiogenic shock, while SVRi was increased in patients with exacerbated systolic CHF and extremely high in patients with pulmonary edema. By using a two-dimensional presentation of Cpi vs. SVRi we found that these clinical syndromes can be accurately characterized hemodynamically. The paired measurements of each clinical group segregated into a specific region on the Cpi/SVRi diagnostic graph, that could be mathematically defined by a statistically significant line (Lambda=0.95). Therefore, measurement of SVRi and Cpi and their two-dimensional graphic representation enables accurate hemodynamic diagnosis and follow-up of individual patients with acute CHF.

High-altitude illness.

High-altitude illness is the collective term for acute mountain sickness (AMS), high-altitude cerebral oedema (HACE), and high-altitude pulmonary oedema (HAPE). The pathophysiology of these syndromes is not completely understood, although studies have substantially contributed to the current understanding of several areas. These areas include the role and potential mechanisms of brain swelling in AMS and HACE, mechanisms accounting for exaggerated pulmonary hypertension in HAPE, and the role of inflammation and alveolar-fluid clearance in HAPE. Only limited information is available about the genetic basis of high-altitude illness, and no clear associations between gene polymorphisms and susceptibility have been discovered. Gradual ascent will always be the best strategy for preventing high-altitude illness, although chemoprophylaxis may be useful in some situations. Despite investigation of other agents, acetazolamide remains the preferred drug for preventing AMS. The next few years are likely to see many advances in the understanding of the causes and management of high-altitude illness.

Pulmonary functions in patients with epidemic dropsy.

Pulmonary functions were performed in thirteen patients with epidemic dropsy. The epidemic occurred in Delhi in 1998 during which 102 patients with epidemic dropsy reported to our medical unit. Other investigations included chest radiograph, ECG, liver and renal function tests. There was a restrictive ventilatory defect with diminution of diffusion capacity for carbon monoxide in these patients. Echocardiogram was done in seven of these patients and was normal. The cause of breathlessness and restrictive ventilatory defect is likely to be non-cardiogenic pulmonary oedema.

Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management?

Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same. Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the long-term neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.

Deformation of the ventrolateral medulla oblongata by subarachnoid hemorrhage from ruptured vertebral artery aneurysms causes neurogenic pulmonary edema.

The occurrence of neurogenic pulmonary edema (NPE) associated with subarachnoid hemorrhage (SAH) due to ruptured aneurysm was analyzed in 48 consecutive patients. Correlations of the location of the aneurysm, clinical grade, amount of subarachnoid clot, and severity of NPE were examined. NPE was observed in 29.4% of all SAH cases, but the incidence was significantly higher in cases of ruptured vertebral artery (VA) aneurysm. Clinical grade, severity of NPE, and deformation of the medulla oblongata were studied in the five cases of ruptured VA aneurysm. Deformation of the ventrolateral medulla oblongata was observed in all patients. Asymmetry index of the medulla oblongata measured on the axial computed tomography scan was correlated with the severity of NPE. Severity of NPE tended to correlate with deformation of the medulla oblongata. NPE associated with ruptured VA aneurysm is caused by deformation of the ventrolateral site of the medulla oblongata by the localized hemorrhage.