Cardiac herniation is a significant and potentially fatal complication of BTPR. This is by no means a new problem [1, 2] and its occurrence in severe blunt trauma is in the order of 0.4% [3, 4]. Despite literature experience dating back to 1864 [5], it is an injury that frequently results in pre/early hospital death and diagnosis at autopsy, probably owing to a combination of diagnostic difficulties, lack of familiarity and associated polytrauma [3, 6]. Of those who make it to hospital, and are later diagnosed with BTPR, the survival rate is 36.4% - 42.9% [7]. The high mortality rate is probably a reflection of not only BTPR and cardiac herniation but also the associated injuries [3].

Here, we present two interesting cases of both left and right pleuropericardial ruptures and cardiac herniation. Despite the delay in initial diagnosis, both patients survived, though with varying degrees of disability secondary to related traumatic injuries. The second patient is one of the few reported cases of cardiac herniation and a delayed penetrating cardiac injury secondary to rib fractures.

The common issue echoed throughout our experience and those of others is that of missed or delayed diagnosis. With these cases and literature review we hope to provide further awareness of this injury and clues which can be sought from the clinical presentation and investigations to aid diagnosis.

A 21-year-old male was admitted to a district general hospital accident and emergency department following a moderate speed motorbike accident with the predominant vector of force through the chest and head. Initially when seen by the local ambulance service he was noted to be GCS 15/15, have a high Alveolar-arterial gradient but was cardiovascularly stable. Of note, he could not move or feel his legs.

Management in the district general accident and emergency department followed standard Advanced Trauma Life Support (ATLS) practices. Chest radiograph showed pulmonary contusions on the left but nothing else of significance. He became increasingly agitated and hypoxic and was intubated prior to transfer for computed tomography (CT) scan.

Head CT scans showed an interventricular haemorrhage. Spinal images showed T8/T9 fracture/dislocation with a normal cervical CT. Initial chest CT scans were reported as showing dextracardia and bilateral pneumothoraces; on the left side, the pneumothorax was reported as a possible tension pneumothorax. The possibility of a pneumopericardium was later attributed to an anterior pneumothorax. Abdominal and pelvis CT scans were essentially normal.

As time progressed, persistent hypotension developed despite bilateral tube thoracostomies, fluid challenges and inotropes. The initial working diagnosis of spinal shock was made and a referral was made for further management and neurosurgical intervention for stabilisation of the T8-9 fracture/dislocation.

On transfer to our trauma centre, the patient's condition deteriorated; on arrival in our department, he was found to be on a FiO₂ of 1.0 with PaO₂ around 10 kPa and requiring high dose norepinephrine and epinephrine to sustain his mean arterial pressure. He was re-trauma called at this stage and plain radiographs were obtained to further ascertain and clarify his injuries (Figure 1).

The finding of dextracardia had been noted previously at the district general hospital and was not thought to be pathological at this stage. A further tube thoracostomy did not improve the hemodynamic status of the patient. The patient was transferred for CT scan where the following images were obtained (Figure 2 and 3).

The CT showed a multitude of head and thoracic injuries. A number of rib fractures and bilateral haemopneumothacaces as well as the aforementioned neuroaxial injuries were all noted. The presence of pericardial air with herniation of the heart into the right hemithorax was also causing concern. At this stage the patient's condition had not improved and, on balance, it was agreed to take the patient to theatre to investigate his thoracic injuries. The patient underwent a clamshell thoracotomy where a 10 cm tear in the right of the pericardium (along the path of the phrenic nerve) was noted with a cardiac herniation through the defect. The heart was noted to be large and dilated. The heart was relocated and the pericardium repaired with interrupted non-absorbable sutures. An intracranial pressure (ICP) bolt was also inserted for monitoring and further management of his traumatic brain injury.

There was an almost immediate reduction in inotrope requirement and the patient was transferred to ICU. His post-op care was complicated by a chest infection and frequent episodes of fast atrial fibrillation secondary to a myocardial contusion, requiring DC cardioversion. He was discharged from ICU after 14 days. Although he was left with a permanent disability from his T8/T9 fracture dislocation, he recovered a good cognitive neurological status and arm strength. With no ongoing cardiovascular problems, he is currently awaiting transfer to a rehabilitation centre.

The second case is that of a 45-year-old male brought into our regional trauma centre by air ambulance. He was the driver in a road traffic collision in which the force vector came through the passenger/left side of the car; unfortunately, the passenger was pronounced life extinct on the scene. On scene, the patient was agitated, moving all limbs and complaining of difficulty in breathing. As a result, he underwent tracheal intubation with drug assistance, bilateral thoracostomies, 750 ml crystalloid and application of a pelvic splint and usual spinal precautions.

On arrival in the department, the initial concern was that of multiple rib fractures, left-sided flail and a large amount of surgical emphysema. Bilateral tube thoracostomies were inserted with 300 mls of blood from the left tube; ventilation/oxygenation improved adequately. Of note, cardiac pulsations were felt when there was a finger sweep of the left pleural cavity.

The chest radiograph showed pneumopericardium, extensive surgical emphysema and improvement in the left-sided haemopneumothorax/right-sided pneumothorax (Figure 4). The evolving problem quickly became that of cardiovascular instability which remained fluid/packed red blood cell responsive throughout. A Focused Assessment with Sonography in Trauma (FAST) scan was negative on two occasions and a pelvic radiograph showed a stable pelvic pubic ramus fracture. Given the negative FAST scans and a period of stability, the patient was taken for a full body CT. The CT chest showed a multitude of injuries, resulting in two further tube thoracostomies being sited (Figure 5). The CT head/spine showed multiple facial and base of skull fractures but no evidence of parencymal or extra-axial bleeds and no fracture or mal-alignment of C/T/L spine. CT abdomen showed a small anterior spleenic laceration with no free fluid in the peritoneal cavity.

Following a joint review of the CT scans and the now-stable patient, no surgical intervention was felt to be needed. The patient had an ICP bolt inserted and was taken to the ICU for further resuscitation and stabilisation.

Sixteen hours post-injury on the ICU, the blood output from the left basal tube thoracostomy started to climb, finally reaching 600 ml/Hr. This was associated with a transfusion requirement, haemodynamic compromise and climbing lactates. At this point, the patient was taken to theatre for a thoracotomy to establish the cause of a likely complex chest bleed.

The following injuries were found and repaired through a left anterior lateral thoracotomy: left-sided longitudinal rupture of the pericardium and cardiac herniation; left ventricular laceration secondary to overlying rib fractures; multiple lung lacerations; and multiple flail ribs. Following insertion of a pericardial and further tube thoracostomies (on suction), the patient was transferred back to ICU for further care.

An eighteen day ICU admission followed, the main issues being that of recurrent atrial flutter and a slow respiratory wean. The respiratory wean was protracted as a result of adult respiratory distress syndrome caused by the primary polytrauma and ventilator-acquired pneumonia.

Over 6 weeks after his initial accident, the patient was discharged home and, all things considered, was doing well in follow up clinic one month later.

BTPR and cardiac herniation is a complex and often fatal injury that usually presents under the umbrella of multisystem trauma. The majority of patients will be non-salvageable; where, despite best efforts, the severity of the initial injury results in death prior to arrival in hospital. In the polytrauma patients with severe blunt chest injuries who survive to hospital arrival, the clinician must maintain a high index of suspicion for BTPR. Even with a high index of suspicion, the diagnosis is still fraught with difficulty. However, patients with blunt chest trauma and any of the following signs are exceptionally high risk for BTPR and the need for an urgent operative intervention should be considered:

Personal experience and a review of past literature show that, in the majority of cases, it is still an injury diagnosed at autopsy or thoracotomy. Potentially, with increasing awareness of the injury and improved use and availability of imaging modalities, the survival rates will improve and cardiac H erniation could even possibly be considered the 5^th 'H' of reversible causes of blunt traumatic PEA arrest.

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.