Ariana Alejandra Chacón-Aponte, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, Tariq Janjua
Acute Crit Care. 2022;37(1):35-44. Published online February 11, 2022
The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.
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The clinical course is described in this article.
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Reexpansion pulmonary edema (RPE) is a rare but sometimes fatal complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis.
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Hysteroscopy is utilized for making the diagnosis and treating a series of uterine disease. It's advantages are more accurate removal of lesion, a short operating time, low morbidity and rapid postoperative recovery. However, serious complications can happen following hysteroscopic surgery.
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Cardioversion used for the treatment of various cardiac arrhythmias is a safe and effective procedure with infrequent complication. The restoration of sinus rhythm is followed by a improvement in hemodynamics, but acute pulmonary edema has been reported as a rare complication following successful electrical reversion of various tachyarrhythmia to normal sinus rhythm. This report describes a 42-year-old woman with a history of schizophrenia who experienced pulmonary edema after cardioversion for torsade de pointes. She had taken chlorpromazine and haloperidol for schizophrenia. The antipsychotic drugs were suspected to induce QT interval prolongation and resultant torsade de pointes. Two hours after cardioversion, pulmonary edema developed on chest X-ray and chest computed tomography. She responded to conservative treatment including oxygen therapy and the pulmonary edema improved on the second hospital day. The mechanism of pulmonary edema after cardioversion is still uncertain and remains controversial.
Hunter syndrome is one of the mucopolysaccharidoses, characterized by abnormal accumulation and deposition of mucopolysaccharides in the tissues of several organs which are known to complicate anaesthetic and airway management.
We experienced a case of pulmonary edema which developed during induction of general anesthesia of Hunter syndrome after several attempts of intubation and airway obstruction.
Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. Post anesthetic laryngospasm has been implicated as the most frequent cause of this syndrome. Risk factors for development of post laryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. We report a case that developed acute bilateral pulmonary edema after laryngospasm induced by failed intubation.
Post obstructive pulmonary edema (POPE) after anesthesia is a rare, but potentially dangerous pulmonary edema during or after relief of severe total or partial upper airway obstruction. The formation of POPE is believed to be the generation of negative intrapleural and intraalveolar pressures which increase the pulmonary transvascular hydrostatic pressure gradient and cause fluid movement to the interstitium and alveoli. Because of both the rapidity and severity with which POPE can develop, prompt recognition and management are essential. A case of POPE after anesthesia in a 23 year-old healthy male undergoing the primary repair of T12 fracture was presented. The patient was extubated without problem after operation. Arrived at the ICU, the patient showed laryngospasm and low oxygen saturation (around 50%). After the intubation with PEEP and the suction of the big amount of pinky frothy transudates through endotracheal tube, oxygen saturation was kept mid 70 s for over 30 minutes. After about 10 times chest compression with suctioning through endotracheal tube, the patient's oxygen saturation showed mid 90 s. This chest compression for the POPE was not recognized by the reference. Even though I can not tell the advantage or disadvantage of this treatment, I report this case for the future reference. After reviewing the reference, the risk factors, differential diagnosis, management and prevention of POPE are discussed.
BACKGROUND This study was to clarify the influence of collapse and re-ventilation of lung on the development of pulmonary edema in rabbit. METHODS: Animals were randomly assigned to one of three groups: Sham group receiving two lung ventilation (n=14), Collapse group receiving collapse of right lung (n=14), Reventilation group receiving collapse of right lung for 3 hours followed by reventilation of collapsed right lung for 3 hours (n=14). The lung of rabbits were ventilated with 50% oxygen through the tracheostomy.
Right main bronchus was secured by thoracotomy in all animal. Collapse and reventilation were performed using by bulldog forcep. Mean arterial pressure, heart rate, arterial oxygen tension (PaO2), peripheral blood leukocyte and platelet counts were recorded at 0, 1, 2, 3, 4, 5 and 6 hour after the start of experiment. The wet to dry (W/D) weight ratio of lung, lung injury score and leukocyte counts, percentage of polymorphonuclear leukocyte (PMNL), concentration of albumin, and interleukin-8 (IL-8) in bronchoalveolar lavage fluid (BALF) were measured 6 hour after the start of experiment in both lung. RESULTS: W/D weight ratio of lung, lung injury score and leukocyte counts, percentage of PMNL, concentration of albumin and IL-8 in BALF were significantly increased in both lung of reventilation group. And the degree of increases is more significant in right than left lung. CONCLUSIONS: These findings suggest that reventilation of collapsed lung causes the bilateral pulmonary edema in rabbit mainly by activating neutrophil and IL-8 responses, which may play a central role in non cardiogenic pulmonary edema.
Because the emergence from anesthesia may be delayed in the patient with the cerebral palsy, extubation must be delayed until consciousness is recovered completely. Postoperative pulmonary edema has several causes and one of them, upper airway obstruction is rare. We had experienced pulmonary edema due to upper airway obstruction after neck mass excision in the patient with cerebral palsy, who was 21-year-old, 50 kg, male and normal preoperative laboratory data. There was no significant change in blood volume during operation for 1 hour. After operation, the patient breathed spontaneously and the endotracheal tube was extubated in the operating room. When the patient was transfered to the recovery room, he had cyanosis, intercostal and substernal retraction, and the pulse oximeter showed very low oxygen saturation. We supplied oxygen to the patient and reintubated him, and recognized the pinkish frothy sputum by suction of the endotracheal tube. On the portable chest X-ray film of the patient at the moment, hazy increased density on both lung fields indicating pulmonary edema, but the heart size was not increased. By routine treatment for pulmonary edema, the symtoms and signs of the patient were improved. He had stayed for 1 day in the SICU and then transfered to the general ward.
Peripartum cardiomyopathy (PPCM) is defined as the onset of acute heart failure without demonstrable cause in the last trimester of pregnancy or within the first 6 months after delivery. Mortality from PPCM ranges from 25% to 50% and cause of death is usually chronic congestive heart failure or thromboembolic complications. We experienced 2 patients with PPCM. One was a twin pregnant woman and PPCM was developed after cesarean section. In the other case, PPCM was combined with aspiration pneumonia in the preterm labor patient. They were treated with diuretics and cardiotonic drugs and recovered to normal cardiac function within 7 to 10 days. Prognosis is related to recovery of left ventricular function, which usually occurs within 6 months postpartum. Early diagnosis and appropriate treatment of PPCM improve outcome.