Medic 61, a BLS ambulance with three personnel, and EMS 60, a rapid response vehicle staffed with a paramedic, are dispatched to a rural address for a male patient with difficulty breathing. A chief officer is added after the communication operator updates that the “patient is on the floor ‘changing color,'” suggesting that the patient may be in cardiac arrest.
The EMS crew finds the patient lying on the bathroom floor, mottled and trying to talk, but without enough tidal volume to speak. He’s immediately moved to the living room floor and a nasopharyngeal airway is placed before a crew member begins assisting respirations with a bag-valve mask. The patient’s heart rate is 94, noting atrial fibrillation on the monitor and an oxygen saturation of 53%.
To the crew’s surprise, the patient’s blood pressure is noted at 160/100 manually, and confirmed at 163/111 on the monitor, despite delayed capillary refill, mottling, cold and visually looking sick. It’s suspected the patient is in the compensatory phase of shock.
Lung sounds are clear bilaterally near the apex and diminished or absent at the bases. The patient is quickly ventilated to an oxygen saturation of 92%.
The patient is determined to have an altered level of consciousness (ALOC) and, after a correction in his hypoxia, the crew proceeds down the algorithm for ALOC. An IV is placed with a large bore catheter and a 300 mL fluid bolus is initiated. A blood sugar is taken with a reading of 60 mg/dL. A dextrose dose of 25 g is then given IV without a change in the patient’s condition.
The company officer collecting the history and medications reports that the son conveyed a history of a small cerebrovascular accident (CVA) over a month ago without neurological impairment, and a stent placement over a year ago. The son says he found his father bracing himself against the sink this morning, adding his dad had complained of nausea and vomiting for the past four days. After returning from calling 9-1-1, his father collapsed on the floor.
A history of hypertension is also relayed, along with numerous antihypertensive medications including a beta-blocker. The crew members question the beta-blocker’s influence on the patient and whether the heart rate of 94 is another indicator of shock.
Percocet is also discovered in the patient’s current medications, and naloxone 1 mg is administered via IV with minimal improvement.
Progression down the ALOC algorithm fails to change the patient’s status and he remains with poor respiratory effort, experiencing another fall in oxygen saturation below 90% despite assistance with respirations. It’s decided to facilitate an intubation.
Versed 5 mg is administered and the patient is moved to the ambulance. A size 7.5 endotracheal tube is placed on first attempt with the aid of a video laryngoscope.
Oxygen saturation immediately improves to 100% and end-tidal carbon dioxide is at 28 mmHg. During the 20-minute emergent return to the regional medical center, the compensatory phase of shock becomes more evident as the patient’s blood pressure drops to 108/74.
EMS crews bring the patient into the resuscitation room. After receiving the report from the paramedic, lungs sounds are checked and an absence of breath sounds on the right is noted. The patient is obtunded but with spontaneous over-breathing of the ventilator. His blood pressure is difficult to obtain and inconsistent with both automated and manual cuff readings. His heart rate is rapid with irregularly irregular rhythm and weak peripheral pulses. His skin is pale and cool.
A normal saline bolus is initiated by EMS and continued with a second liter rapidly infused. Ketamine is administered for its sedative and analgesic properties in an effort to avoid causing further hypotension.
A portable chest X-ray confirms the placement of the endotracheal tube in the trachea and shows that the right hemithorax is completely opacified and shows a slight shift of the mediastinum to the left. (See Figure 1.) Point-of-care laboratory data shows a lactate of 12.9 mmol/L and venous blood gas pH of 7.07-both confirming the patient’s state of poor perfusion that had been in progress for some time.
Figure 1: An X-ray shows the right hemithorax completely
opacified and a slight shift of the mediastinum to the left
After a rapid bolus of 2 L normal saline without improvement in his hemodynamic state, a central line is placed in the right internal jugular vein under ultrasound guidance. Norepinephrine is infused with improvement of his perfusion and he’s deemed stable enough to undergo a CT scan.
Upon returning, the patient’s blood pressure has trended downward despite maximum infusion rates of norepinephrine. The CT of the abdomen reveals he has a tension pneumothorax with evidence of pneumomediastinum and pneumoperiotneum. (See Figure 2.)
Figure 2: Patient’s CT scan of the abdomen reveals a tension
pneumothorax with evidence of pneumomediastinum and pneumoperiotneum
Given these findings, the diagnosis of Boehaave’s syndrome is made. An emergent tube thoracostomy is placed in the fifth intercostal space. A liter of foul, bilious, fecal material is drained. Soon after the tube placement, the patient’s hemodynamic state improves.
Boerhaave’s syndrome was first described by the Dutch physician Herman Boerhaave in 1724 when, during an autopsy of a patient whom he had treated, he found a tear in the esophagus along with stomach contents filling the chest cavity.1 The condition is caused by a rapid increase in esophageal pressure as the result of retching or vomiting in the setting of the cricopharyngeus muscles contracting against a closed pyloric sphincter. This results in a perforation in a weak point of the esophageal wall, usually the distal portion near the gastroesophageal junction.
The classic triad of findings includes violent vomiting and retching followed by sudden onset of chest pain along with subcutaneous emphysema.2 In reality, the presence of this triad is rare. As the pressure increases within the mediastinum, the stomach contents may enter into the pleural space. This in turn may lead to trapping of air and digestive fluid into the thorax, resulting in hemodynamic compromise from a tension pneumothorax.
Mortality rates in all cases of Boerhaave’s syndrome are 35% and, if left untreated for 24 hours, range upwards to 50%.3 Immediate decompression with tube thoracostomy is necessary to relieve the pressure in the pleural cavity. Once stabilized and a definitive diagnosis of esophageal rupture is confirmed, the patient requires surgical intervention.
In the case presented above, the diagnosis of Boerhaave’s syndrome wasn’t suspected until the results of the CT were viewed. On arrival to the ED, the patient was intubated and the only history available was what the patient’s son had relayed to the paramedics: the patient was found on the bathroom floor earlier in the day, after reporting frequent nausea and vomiting over the prior four days. Paramedics found a bottle of Percocet near the patient.
Hypoglycemia had been treated with D50 and possible opiate overdose had been treated with naloxone. With this limited information, a wide differential diagnosis included altered mental status due to head trauma, sepsis, myocardial infarction, hypoxia from aspiration pneumonia or chest trauma.
The absence of lung sounds on the right and initial portable chest X-ray pointed toward the cause of the hemodynamic compromise, but the emergency physician didn’t fully appreciate the shifting of the mediastinum.
Higher on the list of possible causes of shock was sepsis, hence the placement of the central line and infusion of norepinephrine after the patient didn’t respond to the fluid bolus.
The CT findings of air and fluid within the right hemithorax prompted the emergent tube thoracostomy, which resulted in immediate improvement of the patient’s cardiopulmonary status.
Due to the patient’s underlying cardiovascular disease now combined with multiple organ system failure, the family decided on comfort measures only due to the near impossibility of meaningful recovery.
1. Venø S, Eckardt J. Boerhaave’s syndrome and tension pneumothorax secondary to Norovirus induced forceful emesis. J Thorac Dis. 2013;5(2):E38-E40.
2. Onyeka WO, Booth SJ. Boerhaave’s syndrome presenting as tension pneumothorax. J Accid Emerg Med. 1999;16(3):235-236.
3. de Schipper JP, Pull ter Gunne AF, Oostvogel HJ, et al. Spontaneous rupture of the oesophagus: Boerhaave’s syndrome in 2008. Literature review and treatment algorithm. Dig Surg. 2009;26(1):1-6.