Edema pulmonar agudo no cardiogénico secundario a hidroclorotiazida: reporte de un caso y revisión de la literatura / Hydrochlorothiazide induced non-cardiogenic acute pulmonary edema: a case report

Las tiazidas son fármacos frecuentemente usados en la terapia de la hipertensión arterial. Las reacciones adversas de riesgo vital como shock y edema pulmonar agudo son raros. Comunicamos el caso de una mujer de 55 años de edad atendida en Hospital de Puerto Montt, quien tras dos horas de ingerir hidroclorotiazida presentó disnea. Los exámenes de laboratorio generales e imágenes muestran cuadro concordante con edema pulmonar agudo no cardiogénico. Además de la suspensión del fármaco, se realizó soporte hemodinámico y ventilatorio no invasivo, evidenciándose resolución del cuadro a las 48 h. La paciente fue dada de alta 3 días después de su ingreso sin sintomatología.

Thiazides are drugs often used in management of high arterial blood pressure. Shock and acute pulmonary edema are rarely described as adverse reactions related to this drug. We report the case of a 55 years-old woman admitted at Hospital de Puerto Montt, Chile. Two hours after having her first dose of hydrochlorothiazide she presented dyspnea. Laboratory tests and images support the diagnosis of non-cardiogenic pulmonary edema. Resolution of her clinical picture was observed 48 hours after hydrochlorothiazide administration was discontinued and hemodynamic and non invasive ventilation support were supplied. The patient was discharged without symptoms, 3 days after entering to hospital.

Edema pulmonar agudo por hidroclorotiazida: una reacción adversa poco conocida / Hydrochlorothiazide-induced acute pulmonary edema: a rare adverse reaction

In Chile, hydrochlorothiazide is frequently prescribed as first line antihypertensive therapy. Among it’s well known adverse reactions are: electrolytic disorders, hyperuricemia, dyslipidemia, agranulocytosis and azotemia. Acute pulmonary edema is a rare and potentially lethal adverse effect. Only 50 cases have been reported since 1968. In this article, we discuss a case of a 70 year old woman who, one hour after the ingestion of hydrochlorotiazide, presented acute and progressive dyspnea. Her clinical and radiologic findings are compatible with non-cardiogenic acute pulmonary edema.

En Chile, la hidroclorotiazida se utiliza ampliamente como terapia de primera línea en la hipertensión arterial esencial. Entre los efectos adversos más conocidos destacan: trastornos hidroelectrolíticos, hiperuricemia, dislipidemia, azotemia, entre otros. El edema pulmonar agudo es un efecto adverso infrecuente y potencialmente grave. Desde 1968, se han reportado 50 casos clínicos en la literatura. En este artículo presentamos el caso clínico de una mujer de 70 años atendida en el Hospital Santiago Oriente quien, una hora posterior a la ingesta de hidroclorotiazida, presenta disnea aguda progresiva. El estudio clínico y radiológico es compatible con edema pulmonar agudo no cardiogénico.

Toxicidad pulmonar por inyección intravenosa de eugenol / Pulmonary toxicity due to an intravenous administration of eugenol

Se presenta el caso clínico de una paciente que instaló edema pulmonar no cardiogénico, luego de la inyección intravenosa de eugenol requiriendo un tratamiento agresivo de soporte de las funciones vitales en una Unidad de Cuidados Intensivos.

It is presented the case of a patient, who developed a non-cardiogenic pulmonary edema, after the intravenous administration of eugenol, requiring aggressive supportive measures in an Intensive Care Unit.

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.

The dose of cyclophosphamide for treating paraquat-induced rat lung injury

BACKGROUND/AIMS: Cyclophosphamide (CP) is a promising treatment for severe cases of paraquat (PQ) poisoning. We investigated the effective dose of CP for mitigating PQ-induced lung injury. METHODS: Adult male Sprague-Dawley rats were allocated into five groups: control, PQ (35 mg/kg, intraperitoneal injection), and PQ + CP (1.5, 15, or 30 mg/kg). The dimensions of lung lesions were determined using X-ray microtomography (micro-CT), and histological changes and cytokine levels were recorded. RESULTS: The micro-CT results showed that 15 mg/kg CP was more effective than 1.5 mg/kg CP for treating PQ-induced lung injury. At a dose of 1.5 mg/kg, CP alleviated the histological evidence of inflammation and altered superoxide dismutase activity. Using 15 mg/kg CP reduced the elevated catalase activity and serum transforming growth factor (TGF)-beta1 level. CONCLUSIONS: A CP dose of > 15 mg/kg is effective for reducing the severity of PQ-induced lung injury as determined by histological and micro-CT tissue examination, possibly by modulating antioxidant enzyme and TGF-beta1 levels.

Injuria pulmonar aguda en la intoxicación por ácido acetilsalicílico: Caso clínico y revisión bibliográfica / Acute lung injury due to acetylsalicylic acid poisoning: Case report and review

La intoxicación por salicilatos frecuentemente no es tenida en cuenta como causa de edema pulmonar no cardiogénico y de alteración del sensorio en pacientes adultos. Se describe el caso de una mujer de 52 años de edad, la cual presentó dos episodios de edema pulmonar no cardiogénico habiendo requerido para su manejo, asistencia ventilatoria mecánica. La presentación clínica de la intoxicación fue reconocida al ingreso al servicio de urgencias y llevó al diagnóstico correcto. Se le realizó hemodiálisis y alcalinización urinaria llevando a una rápida resolución del edema pulmonar. Varios aspectos de la presentación clínica sugirieron que la paciente tenía una intoxicación crónica, una condición que a menudo no es diagnosticada oportunamente, lo que contribuye al aumento de la morbi-mortalidad en estos pacientes. Frente a un caso de edema pulmonar agudo no cardiogénico debe considerarse la posibilidad de intoxicación con salicilatos, porque la institución rápida de una terapia apropiada, incluyendo la hemodiálisis, una vez establecido el diagnóstico, es un factor determinante de los resultados en esta grave intoxicación.

Salicylate intoxication is frequently overlooked as a cause of noncardiogenic pulmonary edema and altered mental status in adult patients. We described the case of a 52 years-old woman who presented two episodes of recurrent non-cardiogenic pulmonary edema requiring intubation. On admission, recognition of the clinical syndrome in the emergency department led to the correct diagnosis of salicylate intoxication. The patient was successfully treated with hemodialysis and urinary alkalinization, leading to rapid resolution of pulmonary edema and extubation. Several aspects of the clinical presentation suggest that the patient suffered from chronic salicylism, a condition often misdiagnosed or diagnosed late in the course of disease, contributing to substantial morbidity and mortality in these patients. This poisoning should be considered in the differential diagnosis of acute pulmonary edema not cardiogenic and altered sensorium because rapid institution of appropriate therapy, including hemodialysis, once the diagnosis is established is an important determinant of outcome in this serious disorder.

Naloxone-induced pulmonary edema: a potential cause of postoperative morbidity in laparoscopic donor nephrectomy.

A 28-year-old patient operated for laparoscopic donor nephrectomy (LDN) developed overdose effect of fentanyl leading to poor postoperative recovery. Naloxone (200 microg) treatment was used to reverse fentanyl effects, but it was associated with hypertension. The patient developed pulmonary edema after 2 hours and required overnight mechanical ventilation with positive end-expiratory pressure. Volume overload prescribed in the management of LDN to overcome the immediate poor renal graft functioning probably predisposed this healthy young patient to develop cardiac failure during sympathetic surge associated with naloxone administration. The authors feel that the reversal of overdose effect of opioid by naloxone after intravascular blood volume expansion puts the patient at risk to develop pulmonary edema.

Edema pulmonar agudo por uso de tiazidas, ¿existe falla cardíaca?: Comunicación de un caso / Thiazide induced acute pulmonary edema: Report of one case

Acute pulmonary edema caused by thiazides is uncommon and of difficult diagnosis. It is considered an idiosyncratic reaction and the physiopathology or cardiac function changes are not well known. We report a 60 year-old female with a thiazide induced acute pulmonary edema who was followed with serial measurements of type B n-terminal natriuretic peptide fraction as marker for cardiac dysfunction. There was a significant elevation of the peptide, not associated to evidences of ventricular dysfunction. Its normalization paralleled the resolution of the clinical picture.

Acute pulmonary oedema following oxytocin administration: a life threatening complication.

Water Intoxication is not a common complication of oxytocin infusion. A 26 years primigravida developed acute onset severe pulmonary oedema in postpartum period to whom oxytocin was infused for the induction of labour and to prevent postpartum haemorrhage. The relative role of oxytocin and of electrolyte-free fluids in the pathogenesis of this problem is discussed.

Fatal pulmonary oedema following laparoscopic chromopertubation.

The body of a 30-year-old woman was received for autopsy. The available medical case records mentioned that she had been married for the past 3 years and had had primary infertility. She had undergone a diagnostic-cum-operative laparoscopy under general anaesthesia in a private nursing home. On laparoscopy, the internal genital organs were normal except for a fimbrial cyst on each side. Chromopertubation was done using methylene blue dye along with diagnostic dilatation and curettage. The patient was extubated and shifted to the recovery room. About 15 minutes later she developed cyanosis and became unconscious. She died despite sustained efforts at resuscitation.

Pulmonary Edema following Phenylephrine Intranasal Spray Administration during the Induction of General Anesthesia in a Child

Topical phenylephrine, an agent used to facilitate nasotracheal intubation and prevent nasal mucosal bleeding, can cause severe hypertension in some patients, secondary to its stimulation of alpha-adrenergic receptors. Moreover, a high incidence of pulmonary edema is found in patients whose phenylephrine administration is followed by treatment with beta-blocking agents. We report a case of acute pulmonary edema in a pediatric patient who developed severe hypertension after the inadvertent administration of a large dose of topical nasal phenylephrine, followed by beta-adrenergic antagonists (esmolol).

Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema

Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

Near-fatal amlodipine poisoning.

Amlodipine poisoning is very rare and only few cases have been reported in English literature. We report here a case of severe amlodipine poisoning with non-cardiogenic pulmonary edema.

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.

Acute pulmonary edema as a complication of anti-snake venom therapy.

Polyvalent Anti-snake Venom (ASV) is a life-saving antivenin for severe envenomation due to snake bite in India. ASV infusion is occasionally associated with severe allergic reactions, i.e. anaphylaxis and death. We report a rare instance of non-cardiogenic pulmonary edema due to ASV infusion in an eleven years old boy.

Prazosin therapy and scorpion envenomation.

BACKGROUND: 25-30% fatality due to acute pulmonary oedema in victims of Indian red scorpion (Mesobuthus tamulus) sting have been reported from Western Maharashtra, India. The advent of prazosin in recent years has revolutionized the management of severe scorpion sting cases. Majority of cases developed acute pulmonary oedema in 4-8 hours in a hospital setting irrespective of control of their arterial blood pressure with six hourly oral prazosin regimen, these cases recovered with extra dose of prazosin. We developed a standardised protocol for acute phase of treatment of these cases with the aim of preventing the development of pulmonary oedema. METHOD: We compared scorpion sting cases managed by non-protocol conventional (NPC) treatment and those by standardised protocol (SP) that included three hourly dose of oral prazosin. SP group included severe scorpion sting cases admitted to general hospital at Mahad in the year 1998 (Jan.-Dec.). While those admitted in the year 1997 (Jan.-Dec.) before the SP was implicated were the NPC group. FINDING: Characteristics on arrival of severe scorpion sting patients SP (n-17) and NPC (n-15) groups were similar that more case 6 (35%) from SP group had several hypertension on arrival. On arrival two cases from SP group and one from NPC group had pulmonary oedema. 16 (94.11%) patients from SP group recovered uneventfully, compared with 8 (53.33%) in NPC group (p-0.05). 0% Vs 5 (38.46%) developed acute pulmonary oedema (p < 0.0001) from SP and NPC group respectively, three (one had on arrival two patients during hospitalization) from NPC group had massive pulmonary oedema recovered with i.v. nitroprusside drip (SNP). While from SP group one had massive pulmonary oedema on arrival recovered with i.v. SNP, other one had pulmonary oedema recovered with oral prazosin. Cool extremities (vasoconstriction) persisted 11.5 (5-20) VS 18 (12-26) hours in SP and NPC group respectively. INTERPRETATION: Compared with NPC management; development of acute pulmonary oedema prevented by standardised protocol regimen at rural setting.

The Mexican poppy poisons the Indian mustard facts and figures.

Argemone seeds are mixed with mustard seeds either accidentally or purposefully, and, ingestion of this contaminated oil can lead to often fatal "epidemic dropsy". The liver, heart, kidney and lungs are the major target organs of the toxins (the alkaloids, sanguinarine and dihydrosanguinarine) and damage is mostly caused by free radical (singlet oxygen and hydroxyl radical) to the cell membranes. Treatment at present is mainly symptomatic but therapy with anti-secretory agents for glaucoma and anti-oxidants/free radical scavengers for systemic manifestations appear to be logical.

Edema pulmonar: Una complicación del empleo de terbutalina como tratamiento tocolítico / Plmonary edema: a complication in the use of terbutaline as a tocolytic therapy

Los agentes tocolíticos han demostrado tener una variedad de efectos indeseables. Los betamiméticos principalmente conllevan riesgo para edema pulmonar en la madre. Se reporta una paciente en quien se presentó edema pulmonar agudo 24 horas después de tratamiento con terbutalina por vía intravenosa. La paciente presentaba estenosis mitral que no había sido reconocida. El mecanismo por el cual el edema pulmonar se desarrolla en la mujer embarazada es desconocido, siendo más comúnmente multifactorial. Las medidas para disminuir el riesgo de edema pulmonar deben incluir medición estricta de ingresos y egresos de líquidos, evitar esteroides con alto poder mineralcorticoide y frecuentes determinaciones de electrólitos séricos y hematócrito