CARDIAC ARREST AFTER A CEREBRAL GAS EMBOLISM – CASE REPORT 
Ferreira E., Ferraz S., Panzina A., Francisco E., Pereira A.I., Teixeira R.

INTRODUCTION
Cerebral arterial gas embolism (CAGE) is a serious and often iatrogenic fatal event associated to invasive procedures.1,2 Correct diagnosis is only possible upon suspicion. We report a case of a cardiac arrest (CA) after a CAGE, successfully managed with Hyperbaric Oxygen Therapy (HBOT).
CASE REPORT
A 63-year-old male, ASA II, underwent a CT-guided Transthoracic Needle Aspiration Biopsy (CT-TNAB) of a nodule in the apex of the left lung without immediate complications. The patient was transferred to the recovery room and was monitored according to ASA standards. One hour later he lost consciousness and CA in pulseless electrical activity was diagnosed. Advanced life support was initiated and recovery of spontaneous circulation achieved after one cycle. He was admitted to the emergency room (ER) with a Glasgow coma scale (GCS) 7 (E4M2V1). The neurological examination revealed conjugate eye deviation, isochoric photorreactive pupils and bilateral decerebrate posture. The ECG disclosed no signs of ischemia. A brain CT-scan showed a fronto-parietal cerebral gas embolism in the territory of the right middle cerebral artery (MCA). The chest x-ray and CT were normal. A transthoracic echocardiogram revealed a likely patent foramen ovale, but more investigation is required. A left chest tube was placed. The patient was transferred, intubated and ventilated with FiO2 1, to a Hyperbaric Center. After a HBOT session, significant recovery was observed: GCS 15, central facial palsy on the left side and a left hemiparesis (muscle strength grade 2 in the upper limb and 4+ in the lower limb). The brain CT scan showed a complete resolution of the CAGE. He was then admitted into an Intensive Care Unit and, given the hemodynamic stability, he was discharged to the neurology nursery the day after. During the hospitalization, physical rehabilitation was started. He was discharged home 9 days after the event, with an improved neurological condition.
DISCUSSION
Air embolism is mainly a iatrogenic clinical problem that can result from many surgical and medical procedures, including central line placement, positive pressure ventilation, hemodialysis, pacemaker placement, cardiac ablation, laparoscopic surgery, trauma and decompression sickness.2 
There are two types of gas embolism, venous and arterial, depending of the mechanism of gas entry and the site where the emboli ultimately lodge. However, there may be some overlap between them. In fact, in arterial gas embolism, gas may enter the arteries as a result of overexpansion of the lung by decompression barotrauma or as a result of paradoxical embolism - that occurs when air or gas that has entered the venous circulation manages to enter the systemic arterial circulation and causes symptoms of end-artery obstruction. Every venous gas embolism has the potential to evolve into an arterial gas embolism.1
In this case, TNAB might have caused a fistula allowing the air to reach the pulmonary veins, the systemic circulation through the left heart.3 
Another mechanism includes arterialization of venous bubbles via a patent foramen ovale (an example of paradoxical embolism).1,3 
In this case, the etiology remains poorly understood and further investigation is needed. 
Cerebral arterial gas embolization cause pathologic changes by two mechanisms: a reduction in perfusion distal to the obstruction and an inflammatory response to the bubble (endothelial injury)1,2 which determines a wide variability in the clinical presentation and difficult diagnosis with a possible delay in the treatment. 2
Most of the times, air embolism does not cause hemodynamic  complication, but there are a few cases reported followed by cardiac arrest. Some studies suggest that there may be a pathological connection between   brain and heart. When the brain is subjected to ischemic stroke, its ability to control heart rhythm is disrupted, directly compromising the heart. The insular cortex of the brain is the region primarily responsible for controlling the heart rate, so, there may be a crosstalk between the heart and insular cortex shortly after cerebral ischemia.4
In the case of suspected CAGE, it is recommended to administer pure oxygen and refer the patient to a hyperbaric center as soon as possible.3 HBOT accelerates nitrogen reabsorption and improves oxygenation of ischemic tissue 1,3, by raising the ambient pressure and by causing systemic hyperoxia. The hyperoxia produces enormous diffusion gradients for oxygen into the bubble and for nitrogen out of the bubble. It also allows oxygen to be dissolved in the plasma and increases the extent of oxygen diffusion in tissues. The improvements in the oxygen-carrying capacity of plasma and in the delivery of oxygen to tissues offset the embolic insult to the microvasculature. Other benefits of hyperbaric oxygen are prevention of cerebral edema by reducing the permeability of blood vessels while supporting the integrity of the blood–brain barrier.1
Furthermore, experiments have suggested that hyperbaric oxygen diminishes the adherence of leukocytes to damaged endothelium.
In our case HBOT was the key for an improved outcome of our patient. 
LEARNING POINTS
The diagnosis of CAGE is challenging and must be sought off following some invasive procedures. It’s a possible cause of a CA. HBOT can be a successful treatment for this condition.

REFERENCES
1.	Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000; 342:476-82.
2. Rahman ZU, et al. Cardiac Arrest as a Consequence of Air Embolism: A Case Report and Literature Review. Case Rep Med. 2016; 2016 (4)
3. Rocco M, et al. Successful Treatment of Cerebral Arterial Gas Embolism Following Uneventful TBNA. J Pulm Respir Med. 2015; 5:302
4. Ghanekar S, Corey S, Lippert T, Borlongan C.V. Pathological links between stroke and cardiac arrest. Chinese Neurosurgical Journal. 2016; 2:40
5. Ishikawa H, et al. Ischemic stroke brain sends indirect cell death signals to the heart. Stroke; a journal of cerebral circulation. 2013;44(11):10.1161/STROKEAHA.113.001714. doi:10.1161/STROKEAHA.113.001714.


05 / Cardiac arrest after a cerebral gas embolism - case report