Obstructive shock in a patient with rib fractures and a flail chest: a case report

Introduction

High velocity, blunt thoracic trauma can be associated with a number of injuries that can cause severe hypotension. These include pulmonary contusions with an associated pneumothorax and tension pneumothorax, direct cardiac contusion causing a decreased ejection fraction, pericardial tamponade with obstructive shock, and hemorrhage from aortic or intercostal injury (1–3). This case report is the first to report obstructive shock due to direct compression of the heart by the rib cage.

Clinical findings

The patient has provided written consent for the publication of this case report. A 35-year-old female patient suffered significant injuries after jumping from a third-floor apartment to escape a fire. The patient had no significant past medical history apart from depression and recreational marijuana use. The patient was stabilized in the Emergency Department and required intubation for smoke inhalation, elevated carboxyhemoglobin levels, and flail chest. Chest CT demonstrated bilateral pneumothoraces. Bilateral chest tubes were placed with re-expansion of the lungs. There was no air leak with mild pulmonary contusions in the upper lobes and some bibasilar atelectasis. There was no aortic injury or hemothorax. There were no intra-abdominal, intracranial, or cervical spine injuries. There were multiple bilateral rib fractures. On the left side, there were anterior fractures of ribs 3–9, lateral fractures of ribs 4–9, and posterior fractures of ribs 1–8 and 10–12, as well as dislocations of the left 8th−10th ribs at the costovertebral joints. There were multilevel rib fractures on the right, with anterolateral fractures of ribs 5–9 and posterior fractures of ribs 2–12 (Figure 1). There was a compression fracture of T11 and T12 and multiple transverse process fractures, T1 and T3–L4 on the left, and T4 and T12–L2 on the right. There was clinical evidence of a spinal cord injury with no leg movement noted. MRI demonstrated a spinal cord contusion from T7 downwards, with epidural hematoma and vertebral fractures of L1 and L2.

The patient was admitted to the Surgical Intensive Care Unit (SICU) and initially ventilated with 100% oxygen due to a carboxyhemoglobin level of 13% and lactic acidosis, with a lactate of 10. The patient was stabilized in the SICU, with improvement in the lactate and carboxyhemoglobin levels. Within 24 h after admission, given MRI findings of a compressive epidural hematoma with spinal cord contusion and clinical findings of absent motor function below the spine lesion, the patient was booked for posterior thoracolumbar decompression and internal fixation for stabilization of the thoracic spine fractures. The patient was brought to the operating room (OR) on an emergency basis at 10:00 PM with the hope of salvaging some neurological function.

On presentation to the OR, the patient was ventilated with 40% oxygen and a positive end-expiratory pressure (PEEP) of 5 cm H₂O, sedated with fentanyl, midazolam, and propofol infusions, and was on no vasopressor or inotropic infusions. Standard Canadian Anesthesiologists Society monitors and invasive blood pressure monitoring were established. The patient’s initial blood pressure upon arrival to the OR was 135/75 mmHg and her heart rate (HR) was 100 bpm. General anesthesia was induced with sufentanil 25 mcg, sevoflurane (Etsev 0.8%), and rocuronium 100 mg, with ongoing hemodynamic stability. A Mayfield device was used to secure the head and the patient was turned prone onto bolsters. Upon proning, the patient became extremely hemodynamically unstable with a blood pressure of 35/15 mmHg and a heart rate of 140 bpm. Airway pressures were slightly elevated, with a peak airway pressure of 25 cm H₂0 and PEEP of 5 cm H₂0. Resuscitative efforts included titrated epinephrine boluses approximately 50 mcg, vasopressin 2–3 U, and intravenous fluids. Simultaneous assessment of the cause of the hypotension included ruling out a tension pneumothorax, arrhythmia, hemorrhagic shock, cardiogenic shock, and anaphylaxis.

Given the emergency nature of the case and the hope of salvaging neurological function, the case proceeded with ongoing hemodynamic support, including norepinephrine and vasopressin infusions. With the placement of the first pedicle screw in the thoracic spine and the surgeon pressing down to insert the screw, the patient again became increasingly unstable, with systolic blood pressure dropping again to 40 mmHg. At this point, it was decided to abort the procedure. After repositioning the patient supine, the patient's hemodynamics improved dramatically and instantaneously. The patient was then brought back to the SICU intubated, ventilated on an FiO₂ of 0.4, and sedated and did not require any vasopressor or inotropic infusion (Figure 2).

After the patient was returned to the SICU, further investigations were conducted. A chest X-ray showed no pneumothorax. A transthoracic ultrasound of the heart demonstrated normal right and left ventricular function and no pericardial effusion. A CT pulmonary angiogram showed no pulmonary embolism and again mild pulmonary contusions. The patient remained intubated and ventilated in the SICU and was nursed with strict log roll precautions. The patient had a significant anterior flail chest component but remained hemodynamically stable. The patient was assessed by the thoracic surgery department for possible rib stabilization but was not thought to be a good candidate because of the number and location of the fractures.

After a week, the patient was brought to the OR for a repeat attempt at stabilization of the thoracic spine fractures. The patient was hemodynamically stable, requiring no vasopressors or inotropes. The patient remained intubated and ventilated on a pressure support mode of ventilation of 12, with a PEEP of 12 cm H₂O and an FiO₂ of 40%. The patient had been started on antibiotics for ventilator-associated pneumonia. Cultures from the endotracheal tube were reported as normal flora. The chest X-ray showed some bibasilar atelectasis.

In discussion with the surgeon, it was decided not to roll the patient prone on bolsters. Instead, the Jackson table was used. After induction of anesthesia, the patient's head was immobilized in a Mayfield frame. Next, while the patient was supine, the base of the Jackson table was placed on top of the patient. The bolsters and padding were situated so that support was primarily on the shoulders and hips of the patient, leaving the chest clear. The base was then compressed onto the patient. The patient’s blood pressure remained stable. The use of the Jackson table allowed for an assessment of the effects of chest wall compression without actually turning the patient supine. Then, the whole Jackson table was flipped via the 180-degree turn-to-prone method, leaving the patient in a prone position for the surgery.

Although the patient remained hemodynamically stable, another problem now occurred. There was an increase in airway pressure with almost complete obstruction of the endotracheal tube, with airway secretions. This resolved with suctioning. Surgery then proceeded and the patient had a T9 to L2 posterior instrumented fusion and stabilization. However, mobilized airway secretions continued to be a problem during the case, with repeated suctioning required. The heat and moisture exchange filter in the anesthetic circuit had to be changed twice during the case when it became clogged with airway secretions. The case was completed, and the patient was returned to the SICU.

The patient subsequently required prolonged ventilation because of the flail chest and eventually had a tracheostomy. The patient was eventually weaned and had the tracheostomy removed approximately 6 weeks after the original injury. The patient's life has been profoundly affected by the injuries she suffered and she remains paraplegic.

Discussion

High velocity, blunt thoracic trauma can be associated with a number of injuries that can cause severe hypotension. These include pulmonary contusions with an associated pneumothorax and tension pneumothorax, direct cardiac contusion causing a decreased ejection fraction, pericardial tamponade with obstructive shock, and hemorrhage from aortic or intercostal injury (1–3).

Rib fractures are commonly seen in blunt thoracic trauma. These may cause pain, impairing respiration, and may also result in a flail chest, with paradoxical indrawing of the chest wall with inspiration. A flail chest impairs the efficiency of breathing and can also result in a poor cough and inability to clear secretions. The presence of a flail chest is not in itself an indication for intubation; however, patients with flail chests often require intubation and ventilation because of poor oxygenation, inadequate ventilation, or increased work of breathing (2, 3).

We believe that this patient had obstructive shock during the first operation from a severe flail chest injury or “floating chest” compressing the heart when the patient was prone. There are no other plausible causes. There was no clinical or imaging evidence of right ventricular contusion and no pericardial effusion. There was no tension pneumothorax, no increase in airway pressures, and chest tubes were in place and functioning. There was no major intrathoracic or intra-abdominal bleeding. A transthoracic ultrasound of the heart and CT pulmonary angiogram conducted within 12 h after the events in the OR were normal. Most importantly, the patient was hemodynamically unstable only when prone in the first OR. There was some stabilization of her blood pressure with vasopressors, but when the surgeon started pressing down with the pedicle screw insertion, her blood pressure again dropped precipitously, suggestive of direct compression of the heart. Once the patient was turned supine, her blood pressure improved and she did not require vasopressors or inotropes.

A limitation of this case report is that there was no real-time ultrasound assessment of the heart. An ultrasound assessment of the heart at the time of the event would have confirmed cardiac compression. However, there was no clinical indication for an ultrasound prior to going for surgery, given the patient's stable hemodynamics. Once the patient was turned onto bolsters, it was not possible to conduct either a transthoracic or transesophageal assessment. The initial surgery took place after hours, with limited help available, and no anesthesiologist certified in transesophageal echocardiography was in-house.

While we could identify no prior reports of a flail chest or flail sternum causing obstructive shock, the mechanism proposed would be similar to the known, rare phenomenon of retrosternal clavicle dislocation causing obstructive shock. In such circumstances, the medial clavicle compresses the innominate vein or superior vena cava, leading to vascular injury or occlusion. We hypothesize that in this case, mediastinal compression that impaired right heart filling created an analogous scenario, resulting in obstructive shock (4).

Patients with severe flail chests and severe hypoxemia can and have been managed successfully by proning in the ICU (5–7). The possibility of direct cardiac compression by a “floating chest” should be considered when proning such patients.

The other problem this patient developed was retained secretions and ventilator-associated pneumonia. These complications are common when patients with unstable spine fractures are ventilated for a prolonged time in an ICU, despite frequent suctioning. Strict log roll precautions impair the ability to position the patient optimally for pulmonary toilet.

In summary, this is a rare but very serious complication in a patient with blunt thoracic trauma who had multiple bilateral rib fractures, bilateral anterior flail chest segments, and thoracic spine fractures. Care must be taken when positioning these patients prone to avoid mechanical compression of the heart by a flail chest segment.

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Supplementary material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fanes.2026.1835888/full#supplementary-material

Supplementary material Supplementary material at the source

Footnotes

Edited by: Mehmet Oğuzhan Özyurtkan, Medicana International İstanbul Hospital, Türkiye

Reviewed by: Andrea De Vico, Azienda Usl Teramo, Italy

Mustafa Kuzucuoğlu, Izmir Kâtip Çelebi University, Türkiye