scholarly journals Eventratio diaphragmatica

1973 ◽  
Vol 13 (1) ◽  
pp. 35
Author(s):  
Subagjo Martodipuro ◽  
Nurjono Sunarjo ◽  
Pitono Suparto ◽  
L. Partana

A diaphragmatic eventration is a displacement of abdominal structures into the thoracic cavity, due to weakness and balooning of the diaphragm (Nelson, 1969). In several aspects it has similarities with a diaphragmatic hernia, i.e. the space occupying effects to the lungs, and the sequences of it. An eventration can be divided in 2 groups, the congenital eventration, where the diaphragm is devoid of mucles and only a membrane is separating the abdominal from the pleural cavity; and the acquired one where the phrenic nerve is damaged, usually due to birth injury; but it can also be caused by any other trauma (Bernado et aI., 1961; Bisono et aI., 1970) such as surgical procedures at the time of thoracotomy, the so called iatrogenic  eventration (Jewett et aI., 1964).

2018 ◽  
Vol 47 ◽  
Author(s):  
Bruna Marquardt Lucio ◽  
Rafael Almeida Fighera ◽  
Saulo Tadeu Lemos Pinto Filho ◽  
Mariana Martins Flores

Background: Diaphragmatic eventration is characterized by weakness of the diaphragmatic muscle, which leads to cranial dislocation of the affected diaphragm and, ultimately, in dyspnea. This condition is rare in humans and even rarer in animals, and may be congenital or acquired. The acquired form is less commom and may be induced by trauma or inflammation and neoplastic invasion of the phrenic nerve. Here, we report a case of acquired diaphragmatic eventration in a dog, with the aim of increasing the knowledge of this condition in animals and helping others to recognize and treat future cases.Case: A 12-year-old male dachshund presented with severe dyspnea, exercise intolerance and episodes of coughing. Based on a physical examination and imaging, the main suspicion was a diaphragmatic hernia, and surgery was performed. When the surgeon entered the thoracic cavity, an extremely thin - yet, intact - right hemidiaphragm was observed. The left side of the diaphragm was normal. A polypropylene mesh was sutured to the affected diaphragm in an attempt to strengthen the hemidiaphragmatic muscles and prevent further insinuations of viscera into the thoracic cavity. The dog developed bronchopneumonia, postoperatively, and was hospitalized and treated with antibiotics, analgesics and support medication. However, the dog died five days after surgery. A postmortem examination revealed that the right side of the diaphragm was markedly thin and flaccid. Diaphragm samples were collected for histopathological examination. For comparison, a sample of normal diaphragm was collected from a same age, matched dachshund that died due to an unrelated condition. This tissue was called “diaphragm control”, and it was collected in order to compare the histologic features of a normal diaphragm muscle with the affected one. Histopathology revealed a marked reduction of muscle fibers. In the affected sample, replacement of these fibers by fibrous connective tissue and a marked infiltration of fat were seen among the remaining muscle fibers.  Multifocal areas of necrosis were also observed affecting some muscles fibers. Microscopic comparisons of both diaphragm samples (affected vs. control) revealed a drastic difference in the amount of muscle fibers and fat, corroborating the intense diaphragmatic atrophy observed in the diaphragm from the affected dog. Based on clinical presentation, the gross lesions observed during surgery and later during the post mortem examination, and histopathological findings, a definitive diagnosis of acquired diaphragmatic eventration was established.Discussion: Diaphragmatic eventration is rarely reported in small animal clinics and thus may be confused with other conditions. It must be mainly differentiated from diaphragmatic hernia and should be considered as a differential diagnosis when an animal, regardless of age, presents with dyspnea, apathy and coughing episodes.  On suspecting diaphragmatic eventration, surgical intervention should be carried out as soon as possible. The recommended treatment is plication of the affected hemidiaphragm. However, in the present case, a polypropylene mesh was sutured to the affected area to support the atrophic muscles. It is thought that, trauma injured the dog’s phrenic nerve, affecting right hemidiaphragmatic innervation, and generating progressive atrophy of diaphragmatic muscle fibers. Subsequently, the dog developed diaphragmatic eventration due to diaphragmatic fragility. Diaphragmatic eventration is a very rare disorder in small animals and can be difficult to diagnose based solely on physical and radiographic examinations.


1983 ◽  
Vol 4 (8) ◽  
pp. 244-266

In spite of the availability of almost immediate surgery and neonatal intensive care, congenital diaphragmatic hernia is a life-threatening anomaly in the newborn. It is the result of early embryologic malformation or failure of fusion of the components of the diaphragm allowing for the displacement of the abdominal contents into the thoracic cavity. There is consequent compression of the lung which may result in pulmonary hypoplasia or compression of the cardiovascular structures resulting in deleterious hemodynamic changes. Hypoxia and acidosis result in the presentation of respiratory distress and cyanosis. This is frequently associated with pulmonary arterial hypertension with right to left shunting through fetal circuits.


Author(s):  
N.V. Mashinets

Objectives. To assess the effectiveness of the use of prenatal ultrasound indexes in congenital diaphragmatic hernia of the fetus to determine the postnatal prognosis. Materials. The analysis of 95 observations of left-sided congenital diaphragmatic hernia of the fetus was carried out. In the prenatal period, the composition of organs displaced into the pleural cavity was determined, the heart compression index (HCI), O/E LHR according to Jani and DeKoninck, and QLI were calculated. Results. Survival rate of newborns was 57.9%, mortality rate was 42.1%. The newborns were divided into two groups depending on the outcome of the disease. Group I — surviving newborns (n = 55), group II — deceased patients (n = 40). In the analyzed groups, there were no statistical differences in the timing of delivery, birth weight of newborns, the severity of asphyxia after birth and the type of hernia. In group I, the intestinal loops and stomach were significantly more often identified in the pleural cavity in isolation, less often the liver. HCI corresponded to 1.3, Jani O/E LHR 45.7%, DeKoninck O/E LHR 38.7%, QLI 0.7. In group II, concomitant malformations, polyhydramnios and displacement of the liver into the pleural cavity were significantly more frequent. HCI was 1.5, Jani O/E LHR 38.6%, DeKoninck O/E LHR 32.0%, QLI 0.6. Conclusions. In predicting the outcome of the disease for a newborn, the most effective is a comprehensive assessment of the location of the liver, the heart compression index and the index of lung hypoplasia (O/E LHR according to Jani). The diagnostic accuracy of the method is 80%, the sensitivity is 74.4%, and the specificity is 83.3%.


2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Alqasem Fuad H. Al Mosa ◽  
Mohammed Ishaq ◽  
Mohamed Hussein Mohamed Ahmed

Chest tube malpositioning is reported to be the most common complication associated with tube thoracostomy. Intraparenchymal and intrafissural malpositions are the most commonly reported tube sites. We present a case about a 21-year-old patient with cystic fibrosis who was admitted due to bronchiectasis exacerbation and developed a right-sided pneumothorax for which a chest tube was inserted. Partial initial improvement in the pneumothorax was noted on the chest radiograph, after which the chest tube stopped functioning and the pneumothorax remained for 19 days. Chest computed tomography was done and revealed a malpositioned chest tube in the right side located inside the thoracic cavity but outside the pleural cavity (intrathoracic, extrapleural). The removed chest tube was patent with no obstructing materials in its lumen. A new thoracostomy tube was inserted and complete resolution of the pneumothorax followed.


CHEST Journal ◽  
2015 ◽  
Vol 148 (4) ◽  
pp. 780A
Author(s):  
John Bishara ◽  
Sathyaprasad Burjonrappa ◽  
Melodi Pirzada ◽  
Claudia Halaby

Author(s):  
Jagroop Mavi ◽  
Anne C. Boat ◽  
Senthilkumar Sadhasivam ◽  
Catherine P. Seipel

Congenital diaphragmatic hernia is an embryologic defect in diaphragm formation that allows abdominal contents to enter into the fetal pleural cavity, resulting in ipsilateral lung compression, pulmonary hypoplasia, and abnormal pulmonary vasculature. Though diagnosis is frequently made on prenatal imaging, the diagnosis should be considered in any newborn with respiratory distress. Prenatal predictors of defect severity include evaluation of observed-to-expected lung volumes on fetal magnetic resonance imaging and lung-to-head ratio on fetal ultrasound. Treatment focuses on medical stabilization, including optimization of oxygenation and ventilation, followed by surgical repair. Anesthetic considerations for these patients include management of coexisting cardiac disease and ventilatory parameters, in addition to standard neonatal anesthetic considerations.


1997 ◽  
Vol 83 (2) ◽  
pp. 338-347 ◽  
Author(s):  
Douglas W. Allan ◽  
John J. Greer

Allan, Douglas W., and John J. Greer. Pathogenesis of nitrofen-induced congenital diaphragmatic hernia in fetal rats. J. Appl. Physiol. 83(2): 338–347, 1997.—Congenital diaphragmatic hernia (CDH) is a developmental anomaly characterized by the malformation of the diaphragm and impaired lung development. In the present study, we tested several hypotheses regarding the pathogenesis of CDH, including those suggesting that the primary defect is due to abnormal 1) lung development, 2) phrenic nerve formation, 3) developmental processes underlying diaphragmatic myotube formation, 4) pleuroperitoneal canal closure, or 5) formation of the primordial diaphragm within the pleuroperitoneal fold. The 2,4-dichloro-phenyl- p-nitrophenyl ether (nitrofen)-induced CDH rat model was used for this study. The following parameters were compared between normal and herniated fetal rats at various stages of development: 1) weight, protein, and DNA content of lungs; 2) phrenic nerve diameter, axonal number, and motoneuron distribution; 3) formation of the phrenic nerve intramuscular branching pattern and diaphragmatic myotube formation; and 4) formation of the precursor of the diaphragmatic musculature, the pleuroperitoneal fold. We demonstrated that previously proposed theories regarding the primary role of the lung, phrenic nerve, myotube formation, and the closure of pleuroperitoneal canal in the pathogenesis of CDH are incorrect. Rather, the primary defect associated with CDH, at least in the nitrofen rat model, occurs at the earliest stage of diaphragm development, the formation of the pleuroperitoneal fold.


2019 ◽  
Vol 95 (1) ◽  
pp. 143-152 ◽  
Author(s):  
Shin-ichi Sekiya ◽  
Honami Oota ◽  
Yukari Maruyama ◽  
Mitsuo Sakaihara ◽  
Yoko Takashima

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