Uso da ventilação não invasiva em síndrome do desconforto respiratório agudo grave por inalação acidental de cloro: um relato de caso / Use of noninvasive ventilation in severe acute respiratory distress syndrome due to accidental chlorine inhalation: a case report

RESUMO A síndrome do desconforto respiratório agudo é caracterizada por lesão pulmonar inflamatória difusa, classificada em leve, moderada e grave. Clinicamente observam-se hipoxemia, opacidades bilaterais na imagem pulmonar e diminuição da complacência pulmonar. A sepse está entre as causas mais prevalentes (30 - 50%). Dentre as causas diretas de síndrome do desconforto respiratório agudo, a inalação de cloro é uma causa incomum, gerando, na maior parte dos casos, irritação de mucosas e vias aéreas. Apresentamos um caso de síndrome do desconforto respiratório agudo grave após inalação acidental de cloro em piscina, sendo utilizada ventilação não invasiva como tratamento com boa resposta neste caso. Classificamos como síndrome do desconforto respiratório agudo grave baseado na relação pressão parcial de oxigênio/fração inspirada de oxigênio < 100, embora a classificação de Berlin seja limitada em considerar pacientes com hipoxemia grave manejados exclusivamente com ventilação não invasiva. A taxa de falha da ventilação não invasiva nos casos de síndrome do desconforto respiratório agudo está em torno de 52%, estando associada à maior mortalidade. As possíveis complicações do uso da ventilação mecânica não invasiva com pressão positiva na síndrome do desconforto respiratório agudo seriam o atraso para a intubação orotraqueal sendo a mesma realizada em uma condição clínica pior e um alto nível de pressões de suporte, somados a esforços inspiratórios profundos, gerando elevados volumes correntes e pressões transpulmonares excessivas, que contribuem para injúria pulmonar associada à ventilação. Apesar disto, alguns estudos mostraram diminuição nas taxas de intubação orotraqueal em pacientes com síndrome do desconforto respiratório Agudo com baixos escores de gravidade, estabilidade hemodinâmica e ausência de outras disfunções orgânicas.

ABSTRACT Acute respiratory distress syndrome is characterized by diffuse inflammatory lung injury and is classified as mild, moderate, and severe. Clinically, hypoxemia, bilateral opacities in lung images, and decreased pulmonary compliance are observed. Sepsis is one of the most prevalent causes of this condition (30 - 50%). Among the direct causes of acute respiratory distress syndrome, chlorine inhalation is an uncommon cause, generating mucosal and airway irritation in most cases. We present a case of severe acute respiratory distress syndrome after accidental inhalation of chlorine in a swimming pool, with noninvasive ventilation used as a treatment with good response in this case. We classified severe acute respiratory distress syndrome based on an oxygen partial pressure/oxygen inspired fraction ratio <100, although the Berlin classification is limited in considering patients with severe hypoxemia managed exclusively with noninvasive ventilation. The failure rate of noninvasive ventilation in cases of acute respiratory distress syndrome is approximately 52% and is associated with higher mortality. The possible complications of using noninvasive positive-pressure mechanical ventilation in cases of acute respiratory distress syndrome include delays in orotracheal intubation, which is performed in cases of poor clinical condition and with high support pressure levels, and deep inspiratory efforts, generating high tidal volumes and excessive transpulmonary pressures, which contribute to ventilation-related lung injury. Despite these complications, some studies have shown a decrease in the rates of orotracheal intubation in patients with acute respiratory distress syndrome with low severity scores, hemodynamic stability, and the absence of other organ dysfunctions.

Continuous blood purification treatment for endotoxin-induced acute respiratory distress syndrome

This study aimed to explore the effects of continuous blood purification (CBP) treatment in pigs affected with acute respiratory distress syndrome (ARDS). A total of 12 healthy male pigs, weighing 12±1.8 kg, were randomly and equally assigned to the control and experimental groups. The ARDS pig model was prepared by intravenous injections of endotoxin (20 µg/kg). The control group was given conventional supportive therapy, while the experimental group was given continuous veno-venous hemofiltration therapy. During the treatment process, the variations in dynamic lung compliance, oxygenation index, hemodynamics, and urine volume per hour at different times (Baseline, 0, 2, 4, and 6 h) were recorded. The levels of tumor necrosis factor (TNF-α), interleukin 6 (IL-6), and IL-10 in serum and bronchoalveolar lavage fluid (BALF) were measured using the enzyme-linked immunosorbent assay. The histomorphological changes of the lung, heart, and kidney were visualized using a light microscope. The nuclear factor κB p65 protein content of the heart, lung, and kidney tissues was also detected using western blot. The experimental group outperformed the control group in both respiratory and hemodynamic events. CBP treatment cleared TNF-α, IL-6, and IL-10 partially from serum and BALF. The pathological examination of the heart, lung, and kidney tissues revealed that the injury was less severe in the experimental group. CBP treatment can improve the organ functions of pigs affected with endotoxin-induced ARDS and protect these organs to some extent.

Acute Respiratory Distress Syndrome after the Use of Gadolinium Contrast Media

Acute respiratory distress syndrome (ARDS) is a medical emergency that threatens life. To this day, ARDS is very rarely reported by iodine contrast media, and there is no reported case of ARDS induced by gadolinium contrast media. Here, we present a case with ARDS after the use of gadobutrol (Gadovist) as a magnetic resonance imaging (MRI) contrast medium. A 26 years old female without any medical history, including allergic diseases and without current use of drugs, visited the emergency room for abdominal pain. Her abdominopelvic computed tomography with iodine contrast media showed a right ovarian cyst and possible infective colitis. Eighty-three hours later, she underwent pelvis MRI after injection of 7.5 mL (0.1 mL/kg body weight) of gadobutrol (Gadovist) to evaluate the ovarian cyst. She soon presented respiratory difficulty, edema of the lips, nausea, and vomiting, and we could hear wheezing upon auscultation. She was treated with dexamethasone, epinephrine, and norepinephrine. Her chest X-ray showed bilateral central bat-wing consolidative appearance. Managed with mechanical ventilation, she was extubated 3 days later and discharged without complications.

Characterization of oleic acid-induced acute respiratory distress syndrome model in rat.

Animal studies using oleic acid (OA) model to produce acute respiratory distress syndrome (ARDS) have been inconsistent. Therefore, the present study was undertaken to establish an acute model of ARDS in rats using OA and to characterize its effect on cardio-respiratory parameters and lethality. The trachea, jugular vein and femoral artery of anesthetized adult rats were cannulated. A dose of OA (30-90 µL; iv) was injected in each animal and changes in respiratory frequency (RF), heart rate (HR) and mean arterial pressure (MAP) were recorded. Minute ventilation and PaO2/FiO2 (P/F) ratio were also determined. At the end, lungs were excised for determination of pulmonary water content and histological examination. At all doses of OA, there was immediate decrease followed by increase in RF, however at 75 and 90 µL of OA, RF decreased abruptly and the animals died by 63 ± 8.2 min and 19 ± 6.3 min; respectively. In all the groups, HR and MAP changes followed the respiratory changes. The minute ventilation increased in a dose-dependent manner while the values of P/F ratio decreased correspondingly. Pulmonary edema was induced at all doses. Histological examination of the lung showed alveolar damage, microvascular congestion, microvascular injury, infiltration of inflammatory cells, pulmonary edema and necrosis in a dose-dependent manner. With these results, OA can be used to induce different grades of ARDS in rats and OA doses of 50, 60 and 75 µL resemble mild, moderate and severe forms of ARDS respectively. Hence, OA model serves as a useful tool to study the pathophysiology of ARDS.

Reported survival with severe mixed acidosis and hyperlactemia after toluene poisoning

Lactic acidosis is a recognized complication of the inhalant abuse such as toluene, especially in patients with renal insufficiency. We report a case of severe metabolic acidosis and hyperlactemia due to toluene sniffing. The favorable outcome, despite extremely poor clinical symptoms, signs, laboratory and radiological findings, was unexpected. Specific aspects of the clinical course are addressed. Toluene sniffing should be considered in evaluating sever metabolic acidosis. Favorable outcome could be achieved with early diagnosis and proper interventions

Induction of acute respiratory distress syndrome in rats by lipopolysaccharide and its effect on oxidative stress and antioxidant status in lung.

Acute lung injury (ALI) or its severe form, acute respiratory distress syndrome (ARDS) is an important cause of mortality in the human population. Despite significant advances made, the mortality associated with ALI remains unchanged. The objective of the present study was to evaluate the role of oxidative stress, alveolar antioxidant status and multiple organ injury in ARDS induced by lipopolysaccharide (LPS) in rats. Rats were divided into 4 groups, group I control rats were given saline intraperitoneally, whereas groups II, III and IV (LPS-treated) rats received an intraperitoneal injection of LPS (10 mg/kg body weight) and sacrificed after various time intervals. In LPS-treated rats, we observed increased levels of oxidative products, decreased levels of antioxidants in lung tissues and increased levels of serum marker enzymes, suggesting multiple organ injury. Bronchoalveolar lavage fluid (BALF) neutrophil content and protein concentration in LPS-treated rats were significantly elevated in a time-dependent manner. Histological studies revealed neutrophil influx and diffused alveolar damage in LPS-administered rats. These results clearly suggested that increased oxidant levels led to oxidative stress, antioxidant deficiency attenuating lung inflammation and tissue damage. LPS administration resulted in multiple organ failure, leading to increased mortality.

Variable positive end-expiratory pressure can maintain oxygenation in experimental acute respiratory distress syndrome induced by oleic acid in dogs

The use of positive end-expiratory pressure (PEEP) or lung recruitment maneuvers (RM) to improve oxygenation in acute respiratory distress syndrome (ARDS) is used but it may reduce cardiac output (CO). Intermittent PEEP may avoid these complications. Our objective was to determine if variable PEEP compared with constant PEEP is capable of maintaining arterial oxygenation and minimizing hemodynamic alterations with or without RM. Eighteen dogs with ARDS induced by oleic acid were randomized into three equal groups: group 1, low variable PEEP; group 2, high variable PEEP, and group 3, RM + high variable PEEP. All groups were submitted to constant PEEP, followed by variable PEEP (PEEP was increased from 5 to 10 cmH2O in group 1, and from 5 to 18 cmH2O in the other two groups). PaO2 was higher in group 3 (356.2 ± 65.4 mmHg) than in group 1 (92.7 ± 29.7 mmHg) and group 2 (228.5 ± 72.4 mmHg), P < 0.05. PaO2 was maintained during variable PEEP except in group 2 (318.5 ± 82.9 at constant PEEP to 228.5 ± 72.4 at variable PEEP). There was a reduction in CO in group 3 after RM (3.9 ± 1.1 before to 2.7 ± 0.5 L·min-1·(m2)-1 after; P < 0.05), but there was not any difference between constant and variable PEEP periods (2.7 ± 0.5 and 2.4 ± 0.7 L·min-1·(m2)-1; P > 0.05. Variable PEEP is able to maintain PaO2 when performed in combination with RM in dogs with ARDS. After RM, CO was reduced and there was no relevant difference between the variable and constant PEEP periods.

Intoxicación por Paraquat: descripción de un caso clínico / Paraquat poisoning: a case report

El paraquat es el herbicida más vendido en todo el mundo. Se absorbe por las vías digestiva e inhalatoria. Si llega a los pulmones, produce congestión, edema alveolar con aumento de macrófagos que progresa a fibrosis y edema pulmonar, los cuales se presentan hasta 14 días después de la exposición si el afectado no recibió tratamiento oportuno y correcto. El paraquat se dirige fundamentalmente a los pulmones y genera allí radicales libres oxidantes; por eso, en los casos de intoxicación aguda está totalmente contraindicado usar oxígeno excepto cuando la presión parcial de oxigeno en sangre arterial sea inferior a 50 mmHg. Se presenta un caso clínico de un paciente quien desarrolló un síndrome de distress respiratorio del adulto (SDRA) secundario a ingesta intencional de paraquat. El manejo inicial se realizó con lavado gástrico y tierra de Fuller en solución acuosa al 30%. Posteriormente, el paciente desarrolló compromiso pulmonar y renal, los cuales fueron manejados con pulso de ciclofosfamida a 15 mg/kg/día por 2 días, metilprednisolona 1g/día por 3 días y posteriormente dexametasona 5 mg IV cada 6 horas por 5 días con una evolución clínica satisfactoria.

Paraquat is the best-selling herbicide throughout the world. It is absorbed by the digestive and inhalatory routes. If it reaches the lungs, congestion with swelling is developed, increased alveolar macrophages that progresses to fibrosis and pulmonary edema, which occur until 14 days after exposure if not treated timely and correct. Paraquat is directed primarily to the lungs and therefore generates free radicals oxidants, which is why, in cases of acute poisoning is absolutely forbidden to use oxygen except where arterial blood partial pressure of oxygen in is less than 50 mm Hg. A patient who developed an adult respiratory distress syndrome (ARDS) secondary to deliberate ingestion of paraquat is presented. Initial patient management was performed with gastric lavage and land Fuller in aqueous solution at 30%. Subsequently developing pulmonary and renal failure were handled with cyclophosphamide pulse of 15 mg/kg/day for 2 days, methylprednisolone 1g/día for 3 days, then dexamethasone 5 mg IV every 6 hours for 5 days, with favourable outcome.

Relationship between Pulmonary Surfactant Protein and Lipid Peroxidation in Lung Injury due to Paraquat Intoxication in Rats

BACKGROUND: Pulmonary damage resulting from lipid peroxidation is a principal effect of paraquat intoxication. The host-defense functions of surfactant are known to be mediated by the surfactant proteins A and D (SP-A and SP-D, respectively). The primary objective of this study was to evaluate the variations over time in levels of surfactant protein and lipid peroxidation (LPO) in lung tissue following free-radical-induced injury. METHODS: 42 adult, male, Sprague-Dawley rats were administered intraperitoneal injections of paraquat (35 mg/kg body weight). SP-A and SP-D levels were determined via Western blot. LPO in the left lung homogenate was measured via analyses of the levels of thiobarbituric acid-reactive substances. RESULTS: LPO levels peaked at 6 hours, with no associated histological changes. SP-D levels increased until hour 12 and declined until hour 48; SP-D levels subsequently began to increase again, peaking at hour 72. SP-A levels peaked at hour 6, declining thereafter. CONCLUSIONS: We suggest that in the early phase of paraquat injury, SP-D levels reflect alveolar damage and that de novo synthesis of SP-D takes 72 hours. Levels of SP-A, on the other hand, reflect abnormalities in the surfactant system in the late stage of paraquat intoxication. Surfactant proteins may play a role in protecting the lungs from reactive oxygen injury. A time-dependent variation has been observed in the levels of surfactant proteins A and D following paraquat injury, and it has been suggested that these proteins play a role in the protection of lung tissue against ROS-induced injuries.

Las lecciones derivadas del ASA Closed Claims Project (ASACCP). Proyecto de la ASA acerca de las razones que promovieron demandas contra anestesiólogos cuyos casos estaban ya archivados (2a parte): La paciente obstétrica. Una actualización / Lessons learned from the ASA Closed Claims Project (ASACCP). ASA Project about the reasons for wich claims against anesthesiologists were rewed in cases that had already been close (part 2): The obstetric patient. An update

El análisis de los últimos casos relacionados con el tema fue publicado en el año 1996 cuando en la base de la ASACCP constaban 3533 demandas terminadas. De éstas, 434 estuvieron relacionadas con la anestesia obstétrica. De las 434 demandas relacionadas con la anestesia obstétrica, 310 correspondieron a la operación cesárea y 124 al parto por vía vaginal con anestesia regional. Las muertes maternas (n=83) y el daño cerebral del recién nacido (n=82) continúan siendo las injurias más frecuentes en las pacientes obtétricas. La muerte materna estuvo más comúnmente relacionada con la anestesia general y con la operación cesárea. A pesar de que el número de muertes maternas consecutivas a la anestesia general se mantuvo estable a través de los años, el número de muertes asociadas a la anestesia regional declinó en forma marcada. Este decremento de muertes maternas bajo anestesia regional ocurrió sobre todo en los años 80, coincidiendo con la prohibición del uso de bupivacaína al 0,75 por ciento. Además, esta declinación se debe, sin duda, a la solución de los problemas creados por la vía aérea, la cual es más difícil de acceder en la mujer embarazada (1:270 en la paciente obstétrica, contra 1:2.230 de la no obstétrica). La necesidad de controlar la vía aérea es crucial para reducir los casos de muerte durante anestesia general. Lo mismo sucede con la anestesia regional cuando la altura del bloqueo es muy elevada o por cualquier otra razón que obligue a convertir una anestesia regional en una general. Siempre existe el temido problema de la aspiración de contenido gástrico, que sigue siendo la primera causa de muerte materna durante la anestesia y casi siempre asociada con una intubación dificultosa o fallida. El daño cerebral del recién nacido se produjo en el 19 por ciento de las demandas estudiadas por la ASACCP. En una Unidad de Cuidados Intensivo de recién nacidos en EE.UU se realizó un estudio retrospectivo, como los estudios de la ASACCP, para analizar el número de demandas relacionadas con los casos internados en dicha unidad. El estudio comprendió el período 1972-1992 durante el cual se produjeron 31 demandas por mala praxis sobre 9367 internaciones, con una incidencia de 0,33 por ciento. Según los autores, la frecuencia de juicios contra los anestesiólogos por problemas vinculados con el recién nacido se incrementó del 0,19 por ciento entre los años 1772-1974 al 0,39 entre 1980 y 1992...

Antituberculous therapy-induced toxicity.

Antituberculous drugs are generally safe but can occasionally be associated with life-threatening complications. This is a case report of neurotoxicity, acute respiratory distress syndrome (ARDS) and drug fever, occurring in a patient after initiation of antituberculous therapy (ATT).

Neuroleptic-induced acute respiratory distress syndrome

CONTEXT: A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests. CASE REPORT: A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50 percent (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome

Fatal paraquat poisoning: report of two cases.

Paraquat, a dipyridium compound is widely used as a herbicide. It is available in India as a liquid concentrate for agricultural use and is highly toxic if ingested. It leads to renal, hepatic, cardiac and pulmonary toxicity and also causes burns of oral mucosa and esophagus as it is caustic in nature. We describe two cases of paraquat poisoning who developed serious toxicity following its ingestion and died of respiratory failure.

Acute respiratory distress syndrome following nitrogen dioxide exposure.

A young laborer was accidentally exposed to toxic nitrogen dioxide fumes following an accidental explosion at work place. He developed acute respiratory distress within few hours of exposure and manifested with severe hypoxemia and permeability edema. Assistance with mechanical ventilation and corticosteroid therapy could be instituted only after 24 hours of exposure. He had shown remarkable recovery and could be weaned off after seven days. At three weeks after discharge, his lung function tests were normal.

Mercury inhalation poisoning and acute lung injury

Acute mercury inhalation poisoning is a rare cause of acute lung injury. It is usually fatal because of progressive pulmonary failure. We experienced a patient with acute respiratory distress syndrome (ARDS) after illicit use of mercury vapor for hemorrhoid treatment; he developed acute chemical pneumonitis following exposure to mercury vapor. Prompt treatment with corticosteroids and penicillamine for acute chemical pneumonitis was instituted; radiologic pulmonary infiltrates disappeared within a week, but late phase neurologic sequelae and pulmonary interstitial fibrosis progressed.

Adult respiratory distress syndrome following aluminium phosphide ingestion. Report of 4 cases.

Four cases of adult respiratory distress syndrome (ARDS) following aluminium phosphide ingestion (ALP) are being reported. The dose of the intoxicant varied from 2 tablets (6.0 gm) to 3 tablets (9.0 gm). All patients had shock at admission and developed ARDS within 6 hours. The exhalation of Phosphine, (PH3) detected by positive silver nitrate paper test, was the possible noxious triggering factor in our cases. The cases are being reported because of their rare occurrence.

Avances obtenidos como modelos experimentales del síndrome de distress respiratorio del adulto / Advances in experimental models of adult respiratory distress syndrome

El presente artículo tiene el propósito de discutir los principales logros en el conocimiento de los mecanismos etiopatogénicos del síndrome de distress respiratorio del adulto obtenidos con el empleo de diferentes modelos experimentales que simulan este síndrome. La participación de elementos celulares, como macrófagos, neutrófilos, plaquetas y diferentes mediadores humorales y locales como el complemento, los derivados del ácido araquidónico, del metabolismo del oxígeno, del sistema de la coagulación y otros, son analizados como probables factores involucrados en la patogenia de este daño pulmonar agudo