Introduction

A diaphragmatic hernia (DH) is defined as a protrusion of abdominal viscera into the thoracic cavity through a defect within the diaphragm. Most commonly the disorder is congenital in nature, arising due to the failure of complete diaphragmatic fusion during embryologic development. The less common acquired variant is secondary to blunt or penetrating trauma to the abdomen / thorax or iatrogenic causes [1, 2], and generally termed as posttraumatic diaphragmatic hernias (PTDHs). The presentation may be acute with haemodynamic and respiratory instability or else, they may go undiagnosed at the initial trauma at all and manifest months or years later as a diaphragmatic hernia [3]. They can present a diagnostic and therapeutic challenge and have an overall mortality rate of up to 31% [4].

In this retrospective analysis, we describe our experience with patients who reported to the general surgical unit of a medical college in the Kashmir Valley with delayed presentations of PTDH.

Materials and Methods

A retrospective study was conducted at the Department of Surgery, SKIMS Medical College, Srinagar, Kashmir, India. The medical records of all the patients treated for delayed presentation of PTDH from June 2010 to May 2024 were retrieved from the databank.

Carter’s classification criteria [5] concern the temporal parameter of the development of PTDH and recognize three phases: the acute phase (up to 14 days after injury), the interval or latent phase when patients may be asymptomatic, and the obstructive phase when symptoms start appearing. The latter two phases are collectively referred to as delayed PTDH, and in this study, presentation in these phases was the single inclusion criterion to be fulfilled. The exclusion criteria included acute PTDH and congenital diaphragmatic hernia.

This study did not involve any invasive interventions but relied on a retrospective analysis of stored data and was approved by the departmental review committee. Proper informed consent was sought from the patients for publication the data and the accompanying images, after assuring them of privacy and confidentiality, under the Declaration of Helsinki.

Results

The patient characteristics are depicted in Table 1 .

There were 5 (71.4%) females and 2 (28.6%) males, ranging in age from 14 years to 58 years (mean 37.7 years). The clinical presentations of the patients included abdominal pain (n = 7; 100%), nausea/vomiting (n = 2; 28.6%), abdominal bloating (n = 2; 28.6%), chest discomfort/breathlessness (n = 1; 14.3%), and shoulder pain (n = 1; 14.3%). Physical examination revealed diminished breath sounds (n-2; 28.6%) and audible bowel sounds (n-1; 14.3%) over the affected hemithorax. Five cases (71.4%) had chronic symptoms ranging from 3 months to 2 years. 2 (28.6%) cases presented acutely with symptoms for 1 and 2 days, respectively. The mechanism of index injury was blunt in 6 (85.7%) cases who had been managed conservatively, and 1 (14.3%) case had a history of penetrating trauma, managed by laparotomy with splenectomy. The interval between index injury and presentation of PTDH ranged from 5 months to 7 years (mean 4.6 years). Hernia was left sided in 5 (71.4%) and right sided in 2 (28.6%) cases.

X-ray chest (with or without plain X-ray abdomen) and CT scan chest/abdomen were undertaken in all cases (Figures 1A & 1B). CT scan was contrast enhanced in 6 (85.7%) cases and non-contrast enhanced in 1 (14.3%). These imaging modalities revealed features suggestive of herniation of viscera/bowel loops into the thorax. Once the diagnosis of PTDH was confirmed, all the patients underwent surgical operation, which entailed reduction of hernia, repair of diaphragmatic defect primarily with non-absorbable sutures (n = 5; 71.4%) or with mesh (n = 2; 28.6%), excision of gangrenous omentum (n = 1; 14.3%), and tube thoracostomy (n = 2; %). All the cases went through an uneventful postoperative phase, and the only postoperative complication was superficial surgical site infection in 1 (14.3%) case. The approach was laparoscopic in 6 (85.7%) cases, and in 1 (14.3%) case, due to technical difficulties, conversion to an open approach was undertaken. One case was lost to follow-up, and there was no recurrence in the remaining six cases at follow-up ranging from 1 year to 7 years (3.7 years) as determined by physical examination and imaging ( Figure 2).

Figure 1: (A) CXR Chest: Raised left diaphragm, air fluid levels projecting into lower half of left hemithorax & left lower lung atelectasis (red arrow). (B) Contrast enhanced CT scan Chest: Intrathoracic herniation of hollow viscera (white arrow) (C) Herniated splenic flexure of colon (yellow star). (D) Diaphragmatic defect after reduction of herniated contents (white star).

Figure 2: Posttraumatic right diaphragmatic hernia A: Preoperative Chest Xray B : Chest Xray at one year follow up after surgical operation.

Discussion

Traumatic diaphragmatic injury (TDI) is a rare condition that occurs in approximately 0.5% to 5% of abdominal trauma cases, with a ratio of 2:1 for penetrating to blunt trauma [6]. They occur mostly in the areas of potential weakness along embryological points of fusion by a sudden increase in the pleuroperitoneal pressure gradient in thoracoabdominal trauma and result in the entry of an abdominal viscera into the pleural cavity [1, 7].

Historically, Sennertus described it for the first time in 1541 when he performed an autopsy on a patient who had died eight months after being shot and found strangulation of the colon that had herniated through the diaphragmatic defect [8]. Ambroise Pare later documented PTDH in an artillery commander in 1579, and Riolfi made the first successful repair in 1886 [9]. The delay in presentation can be explained because of the pattern of emergence as below:

i. After being devitalized due to trauma, the diaphragmatic muscle becomes inflamed and heals by developing a weak scar that eventually breaks down, resulting in a defect that progressively extends in size through radial pulling during breathing. [10].

ii. Sometimes a defect is produced at the time of injury, but because there hasn't been a herniation of intra-abdominal viscera into the chest cavity, the symptoms don't show up right away, or they get masked up by more serious, potentially fatal injuries [11].

The symptoms with which the patients presented in this series included abdominal pain (n = 7; 100%), nausea/vomiting (n = 2; 28.6%), abdominal bloating (n = 2; 28.6%), chest discomfort/breathlessness (n = 1; 14.3%), and shoulder pain (n = 1; 14.3%). None of the cases reported with hemodynamic instability or respiratory compromise, though cases are reported in literature where missed hernias had manifested many months or even years later as complications such as intestinal obstruction, perforation, or ischemia with morbidity and mortality rates as high as 30% and 10%, respectively [12-13]. Acute tension viscerothorax is a manifestation where herniated viscera into the thoracic cavity produces hemodynamic compromise but without perforation [14-15]. Tension faecopneumothorax (TFP) is a rare and potentially lethal presentation of PTDHs. It is a condition where herniated gut perforates, releasing gas and feces-contaminated fluids into the pleural cavity, creating an intrapleural pressure that exceeds the atmospheric pressure, thereby leading to adverse effects, which include mediastinal shift, kinking of the great vessels, reduced venous return, and cardiovascular collapse [16-18].

The interval between the initial trauma and the clinical presentation with PTDH ranged from 5 months to 7 years (mean 4.6 years) in this series. When a patient presents years or decades later, it may be challenging to diagnose them because they may have forgotten the episode of trauma, particularly if managed conservatively, or else the healthcare provider may not have enough awareness to connect the acute symptoms to the index injury of the past [16]. Singh et al. [19] and Faul [20] have reported cases of PTDH that presented 50 years and 40 years, respectively, after the traumatic event. Hariharan et al. [21] reported a 65-year-old male with splenic herniation into the left hemithorax, causing fundal varices leading to hematemesis and melena 28 years after the penetrating injury. Popovic et al. [22] have presented a case where symptoms due to PTDH appeared 26 years after the index injury. The symptoms (epigastric pain, meteorism, nausea, and vomiting) were interpreted as acute alcoholic gastritis. The condition of the patient, however, deteriorated, and on evaluation, the diagnosis of gastrothorax was made.

In this series, PTDH was left sided in 5 (71.4%) and right sided in 2 (28.6%) cases. This proportion concurs with the data in the literature that shows the predominance of hernias on the left side and is attributed to the protective nature of the liver on the right, the increased strength of the right part of the diaphragm, and the weakness of the left hemidiaphragm at embryonic points of fusion [23-24]. The location of hernia influences the nature of clinical features. Left-sided hernias tend to present with obstructive gastrointestinal symptoms, recurrent thoracoabdominal pain, dyspnea, postprandial fullness, and vomiting [24]. Right-sided hernia is commonly limited to respiratory difficulties, and the liver tends to hinder the further visceral herniation due to its bulk [25].

X-ray chest and CT scan were the major imaging modalities utilized in all the patients in this series. Imaging has a significant role in the management of PTDH by revealing features including elevation of the hemidiaphragm, radiopacities in the hemithorax, and displacement of the mediastinum towards the contralateral side [8, 25]. Successful diagnosis requires a high index of suspicion, but if visceral herniation has occurred, diagnosis can be made from the chest radiograph in 90% of the patients [26-27].

In this series, the approach adopted for surgical management was laparoscopic in 6 (85.7%) cases, and in 1 (14.3%) case, due to technical difficulties, conversion to an open approach was undertaken. In literature, different approaches have been reported, including laparotomy, thoracotomy, combined laparotomy and thoracotomy, laparoscopy, and video-assisted thoracic surgery, depending on the type of injury (acute or chronic), the laterality of the injury, the surgeon's experience, and the availability of equipment [8]. The literature recommends the use of nonabsorbable suture material and that the running or interrupted sutures can be used to repair diaphragmatic abnormalities with comparable efficacy [28]. The laparoscopic approach has been found to be a safe treatment by several authors due to its minimally invasive nature.

Conclusion

Post-traumatic diaphragmatic hernias with delayed presentation are rarely encountered and can be challenging for surgeons. A high index of suspicion is required for diagnosis in patients who have a past history of thoracoabdominal trauma. Wrong diagnosis and delay in management can lead to morbidity and mortality .The patients discharged after thoracoabdominal trauma need radiographical follow-ups to detect diaphragmatic hernias at an earlier stage. Management is surgical, and laparoscopic approach is successful in most situations, though the approach depends upon the patient characteristics, skill of the surgeons, and the availability of equipment.

Acknowledgements

The patients' consent to the use of their photos for scholarly purposes is acknowledged by the authors. This study does not have any financial sources, and there are no conflicts of interest. The article was prepared with input from each author.

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