Cerebral Arterial Gas Embolism Research Articles

Effect of a helium and oxygen mixture on physiological parameters of rats with cerebral arterial air embolism.

Introduction: Cerebral arterial air embolism (CAE) is a serious and potentially dangerous condition that can interrupt the blood supply to the brain and cause stroke. One of the promising gas mixtures for emergency treatment of air embolism is an oxygen-helium mixture. Methods: We modeled CAE in awake rats by injecting air into the common carotid artery. Immediately after CAE, animals were either untreated or underwent hyperbaria, oxygen inhalation, heated air inhalation, or helium-oxygen mixture inhalation. Body temperature, locomotor activity, respiratory and cardiovascular parameters were monitored in the animals before CAE modeling, and 3 and 24h after CAE modeling. Results: After 3 hours of CAE modeling in awake rats, depression of the nervous, cardiovascular and respiratory systems, as well as decreased body temperature were observed. 24h after CAE modeling multifocal cerebral ischemia was observed. Normobaric helium-oxygen mixture inhalation, on par with hyperbaric treatment, restored body temperature, locomotor activity, respiratory volume, respiratory rate, and blood pressure 3 hours after CAE, and prevented the formation of ischemic brain damage lesions 24h after CAE. Discussion: Thus, inhalation of a heated oxygen-helium gas mixture (O2 30% and He 70%) immediately after CAE improves the physiological condition of the animals and prevents the foci of ischemic brain damage formation.

Computer tomography perfusion patterns in iatrogenic cerebral arterial gas embolism: A retrospective cohort study

PurposeCerebral arterial gas embolism (CAGE) occurs when air or medical gas enters the systemic circulation during invasive procedures and lodges in the cerebral vasculature. Non-contrast computer tomography (CT) may not always show intracerebral gas. CT perfusion (CTP) might be a useful adjunct for diagnosing CAGE in these patients. MethodsThis is a retrospective single-center cohort study. We included patients who were diagnosed with iatrogenic CAGE and underwent CTP within 24 h after onset of symptoms between January 2016 and October 2022. All imaging studies were evaluated by two independent radiologists. CTP studies were scored semi-quantitatively for perfusion abnormalities (normal, minimal, moderate, severe) in the following parameters: cerebral blood flow, cerebral blood volume, time-to-drain and time-to-maximum. ResultsAmong 27 patient admitted with iatrogenic CAGE, 15 patients underwent CTP within the designated timeframe and were included for imaging analysis. CTP showed perfusion deficits in all patients except one. The affected areas on CTP scans were in general located bilaterally and frontoparietally. The typical pattern of CTP abnormalities in these areas was hypoperfusion with an increased time-to-drain and time-to-maximum, and a corresponding minimal decrease in cerebral blood flow. Cerebral blood volume was mostly unaffected. ConclusionCTP may show specific perfusion defects in patients with a clinical diagnosis of CAGE. This suggests that CTP may be supportive in diagnosing CAGE in cases where no intracerebral gas is seen on non-contrast CT.

Pneumothorax during manned chamber operations: A summary of reported cases

In-chamber pneumothorax has complicated medically remote professional diving operations, submarine escape training, management of decompression illness, and hospital-based provision of hyperbaric oxygen therapy. Attempts to avoid thoracotomy by combination of high oxygen partial pressure breathing (the concept of inherent unsaturation) and greatly slowed rates of chamber decompression proved successful on several occasions. When this delicate balance designed to prevent the intrapleural gas volume from expanding faster than it contracts proved futile, chest drains were inserted. The presence of pneumothorax was misdiagnosed or missed altogether with disturbing frequency, resulting in wide-ranging clinical consequences. One patient succumbed before the chamber had been fully decompressed. Another was able to ambulate unaided from the chamber before being diagnosed and managed conventionally. In between these two extremes, patients experienced varying degrees of clinical compromise, from respiratory distress to cardiopulmonary arrest, with successful resuscitation. Pneumothorax associated with manned chamber operations is commonly considered to develop while the patient is under pressure and manifests during ascent. However, published reports suggest that many were pre-existing prior to chamber entry. Risk factors included pulmonary barotrauma-induced cerebral arterial gas embolism, cardiopulmonary resuscitation, and medical or surgical procedures usually involving the lung. This latter category is of heightened importance to hyperbaric operations as an iatrogenically induced pneumothorax may take as long as 24 hours to be detected, perhaps long after a patient has been cleared for chamber exposure.

Bronchoscopy-Associated Cerebral Arterial Air Embolism Presenting with Acute Ischemic Stroke and Status Epilepticus (P12-5.013)

<h3>Objective:</h3> To describe a rare cause of iatrogenic air embolism, causing acute ischemic stroke complicated by status epilepticus. <h3>Background:</h3> The incidence of vascular air embolism during bronchoscopy is estimated to be 2.65 per 100,000 hospitalizations, with 30% of these involving endovascular procedures. A recent case report and literature review identified only 5 cases of cerebral arterial air embolism following bronchoscopy. A small minority of acute ischemic strokes present with seizures, even fewer with status epilepticus. <h3>Design/Methods:</h3> NA <h3>Results:</h3> An 81-year-old woman with past medical history significant for hypertension and CREST syndrome presented to an outside hospital for elective bronchoscopy with biopsy of pulmonary nodules. Post-procedurally, she was noted to have new left-sided hemiparesis. Non-contrast CT head demonstrated a small arterial air embolism in the right frontal lobe. She was brought to the Emergency Department and sustained a bilateral tonic-clonic seizure lasting 30 seconds, resolving with intravenous lorazepam. Prior to returning to her mental status baseline, she had recurrent seizure activity, refractory to benzodiazepines, requiring an intravenous phenytoin load, intubation for airway protection, and sedation with propofol. She was transferred to our institution’s neurocritical care unit where repeat CT head exhibited sulcal effacement and she was treated with hypertonic saline for cerebral edema. Continuous EEG did not reveal any epileptiform patterns but the patient was started on levetiracetam for her acute symptomatic seizures. MRI later revealed small infarcts in multiple vascular territories. She was ultimately extubated and at the time of discharge to short-term rehabilitation, her only deficit was 4+/5 strength throughout the left arm, which normalized by 1-month follow-up. She was eventually weaned off of levetiracetam in the outpatient setting. <h3>Conclusions:</h3> This case adds to our understanding of this rare procedural complication and, given the complications of her stroke by status epilepticus and cerebral edema, highlights the potential severity of these injuries. <b>Disclosure:</b> Dr. Sutherland has received personal compensation in the range of $0-$499 for serving as a Consultant for McGraw-Hill. Dr. Gummerson has nothing to disclose. Dr. Sharma has nothing to disclose.

Case report of CT-guided lung biopsy complicated by air embolism

Rationale: Cerebral arterial air embolism is a rare but potentially fatal complication of Computed Tomography (CT)-guided lung biopsy. Hyperbaric oxygen (HBO2) is the first line of treatment for arterial gas embolism and needs to be administered immediately after the event. Early HBO2 can reduce the mortality rate of cerebrovascular air embolism. Patient concerns: A 65-year-old woman was diagnosed with a pulmonary nodule with a diameter of approximately 0.8 cm in the right lower lung. The patient developed consciousness, convulsions, and arrhythmia after CT-guided lung biopsy. Diagnosis: Cranial CT revealed arborizing/linearly distributed gas in the right temporal, parietal, and occipital lobes and left frontal and parietal lobes. Chest CT showed a small amount of pneumothorax. Interventions: The patient was administered HBO2 twice and also received other medical treatments and bone flap decompressive craniectomy. Outcomes: The patient developed multiple acute cerebral infarctions and even brain herniation complicated with acute myocardial infarction. Three months after the event, the patient’s consciousness was still “open eyes coma” and GCS score was 8t points (E4VtM4). Head CT showed multiple cerebral infarctions and softening lesions. ECG showed sinus rhythm, normal range of the electrocardiogram axis, T wave change, and low voltage on the limb leads. Lessons: Cerebral arterial air embolism is a serious complication of CT-guided lung biopsy. The recommended standard HBO2 should be used as early as possible. However, too severe injury caused by severe arterial air embolism may not be significantly improved by one to two sessions of HBO2.

Case report of CT-guided lung biopsy complicated by air embolism

Rationale: Cerebral arterial air embolism is a rare but potentially fatal complication of Computed Tomography (CT)-guided lung biopsy. Hyperbaric oxygen (HBO2) is the first line of treatment for arterial gas embolism and needs to be administered immediately after the event. Early HBO2 can reduce the mortality rate of cerebrovascular air embolism. Patient concerns: A 65-year-old woman was diagnosed with a pulmonary nodule with a diameter of approximately 0.8 cm in the right lower lung. The patient developed consciousness, convulsions, and arrhythmia after CT-guided lung biopsy. Diagnosis: Cranial CT revealed arborizing/linearly distributed gas in the right temporal, parietal, and occipital lobes and left frontal and parietal lobes. Chest CT showed a small amount of pneumothorax. Interventions: The patient was administered HBO2 twice and also received other medical treatments and bone flap decompressive craniectomy. Outcomes: The patient developed multiple acute cerebral infarctions and even brain herniation complicated with acute myocardial infarction. Three months after the event, the patient’s consciousness was still “open eyes coma” and GCS score was 8t points (E4VtM4). Head CT showed multiple cerebral infarctions and softening lesions. ECG showed sinus rhythm, normal range of the electrocardiogram axis, T wave change, and low voltage on the limb leads Lessons: Cerebral arterial air embolism is a serious complication of CT-guided lung biopsy. The recommended standard HBO2 should be used as early as possible. However, too severe injury caused by severe arterial air embolism may not be significantly improved by one to two sessions of HBO2.

Cerebral arterial gas embolism and neurogenic stunned myocardium in a previously healthy freediver

Cardiomyopathy is a known but rare sequelae of diving-related cerebral arterial gas embolism (CAGE). In previously reported cases, patient findings have been consistent with takotsubo cardiomyopathy (TCM) per the revised Mayo Clinic’s diagnostic criteria. A lesser-known variant of stress-related cardiomyopathy is neurogenic stunned myocardium (NSM), which occurs after a neurological event such as subarachnoid hemorrhage and typically presents in younger patients. Presentation tends to differ slightly to TCM with non-specific left ventricular dysfunction and T wave inversions. This case adds to the rare numbers of reported cardiomyopathy from diving and is the first reported case of suspected NSM associated with CAGE.

Cerebral arterial air embolism after bag-valve-mask ventilation

Cerebral Arterial Gas Embolism (CAGE) is a serious condition, which tends to occur as an iatrogenic complication of numerous invasive medical and surgical procedures performed in an esthesia and intensive care

Electroencephalographic findings after convulsive seizures due to cerebral arterial air embolism secondary to lung cancer: a case report

BackgroundCerebral arterial air embolism is often associated with an invasive iatrogenic etiology and a high rate of convulsive seizures. There are only a few descriptions of electroencephalogram findings in convulsive seizures due to cerebral arterial air embolism of noniatrogenic etiology. Herein, we describe the case of a patient with lung cancer and convulsive seizures with abnormalities detected on electroencephalogram caused by cerebral arterial air embolism of noniatrogenic etiology.Case presentationA 55-year-old Japanese man underwent radiotherapy and chemotherapy for cancer in the hilum of the left lung that was diagnosed after hemoptysis. One year after the diagnosis, he developed fever and chest pain that required hospitalization. At admission, he was in shock, and chest computed tomography revealed invasion of the left atrium and left main bronchus by the hilar cancer. Chest and abdominal computed tomography revealed small low-density areas within the tumor and around the intestinal membrane, which were interpreted as the presence of air due to invasion of the lung cancer. He was diagnosed with septic shock due to necrotic infection secondary to cancer invasion into the left atrium. The following day, he complained of difficulty in speaking and weakness in the left side of his body. A head computed tomography scan revealed multiple small low-density areas in the right cortex and bilateral subcortex, which were interpreted as air emboli. On day 3, he experienced generalized tonic–clonic seizures for approximately 1 minute, followed by myoclonus-like convulsions in the left lower limb and a right-sided gaze. The electroencephalogram findings after the convulsive seizures revealed partial epilepsy-like waves with intermittent spikes in the bilateral cerebral hemispheres and a diffuse slow wave in the left frontal lobe. He recovered from sepsis without recurrence of convulsive seizures; however, he died of hemoptysis on day 50 after discharge.ConclusionsElectroencephalogram findings of focal spike activities and diffuse slow waves were detected in early seizures due to cerebral arterial air embolism of noniatrogenic etiology associated with lung cancer. Additional case descriptions are warranted to establish patterns in electroencephalogram findings specific to cerebral arterial air embolism.

A rare but lethal complication: Post-endoscopic retrograde cholangiopancreatography cerebral arterial gas embolism

A rare but lethal complication: Post-endoscopic retrograde cholangiopancreatography cerebral arterial gas embolism

Paradoxical and Retrograde Air Embolism from Pressurized Peripheral Bolus

Introduction Cerebral air embolism is a rare, yet serious neurological occurrence with unclear incidence and prevalence. Here, we present a case of fatal cerebral arterial and venous cerebral gas embolism in a patient with infective endocarditis and known large right-to-left shunt and severe tricuspid regurgitation following pressurized fluid bolus administration. Case Presentation. A 32-year-old female was admitted to the medical intensive care unit from a long-term acute care facility with acute on chronic respiratory failure. Her medical history was significant for intravenous heroin and cocaine abuse, methicillin-sensitive Staphylococcus aureus tricuspid valve infective endocarditis on vancomycin, patent foramen ovale, septic pulmonary embolism with cavitation, tracheostomy with chronic ventilator dependence, multifocal cerebral infarction, hepatitis C, nephrolithiasis, anxiety, and depression. After intravenous fluid administration, she became unresponsive with roving gaze, sluggish pupils, and hypotensive requiring vasopressors. CT of the brain showed diffuse arterial and venous cerebral air embolism secondary to accidental air administration from fluid bolus. Magnetic resonance imaging of the brain showed diffuse global anoxic injury and flattening of the globe at the optic nerve insertion. Given poor prognosis, her family chose comfort measures and she died. Conclusions Fatal cerebral air embolism can occur through peripheral intravenous routes when the lines are inadequately primed and fluids administered with pressure. Caution must be exercised in patients with right-to-left shunting as air may gain access to systemic circulation.

Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Seizures in Iatrogenic Cerebral Arterial Gas Embolism

Iatrogenic cerebral arterial gas embolism occurs when gas enters the cerebral arterial circulation during a medical procedure and is considered a severe complication. Seizures have been described in these patients, but information on clinical characteristics, treatment, and outcome is lacking in current literature. The aim of the study was to explore seizures in patients with iatrogenic cerebral arterial gas embolism and to evaluate management strategies. Retrospective single-center observational study. The only university hospital in the Netherlands with a hyperbaric oxygen therapy facility. All patients presenting at or referred to our center with iatrogenic cerebral arterial gas embolism between May 2016 and December 2020. Not applicable. Fifteen patients with iatrogenic cerebral arterial gas embolism were identified, of whom 11 (73%) developed seizures. Five patients developed their first seizure prior to hyperbaric oxygen therapy, three during hyperbaric oxygen therapy, and three after hyperbaric oxygen therapy. Of the 11 patients with seizures, all but one were treated with anti-epileptic drugs. With a median follow-up time of 5 months (range, 1-54 mo), five patients showed complete neurologic recovery, five had minor neurologic deficit, two had moderate to severe neurologic deficit, and three had died. Four patients still used anti-epileptic drugs at follow-up. No patients had recurrent seizures after hospital discharge. `Seizures are a common symptom in iatrogenic cerebral arterial gas embolism. They are often treated with anti-epileptic drugs and do not seem to lead to chronic epilepsy.

Cerebral arterial air embolism after endobronchial electrocautery: a case report and review of the literature

BackgroundEndobronchial electrocautery is a common and safe therapeutic endoscopic treatment for malignant airway obstruction. Cerebral arterial air embolism (CAAE) is a rare but potentially fatal complication of endobronchial electrocautery.Case presentationWe present the first case of cerebral arterial air embolism after endobronchial electrocautery. A 56-year-old male with a pulmonary tumour in the right upper lobe received repeated endobronchial electrocautery. During the procedure, he experienced unresponsiveness, hypoxemia and bradycardia, and he developed tetraplegia. Brain computed tomography showed several cerebral arterial air emboli with low-density spots in the right frontal lobe. He received hyperbaric oxygen therapy with almost full recovery, except for residual left-sided weakness.ConclusionsGeneral physicians should realize that CAAE may be a possible complication of endobronchial electrocautery. Several measures, including avoiding positive pressure, lowering ventilatory pressures if possible, avoiding advancing the bronchoscope to occlude the bronchus and using the non-contact technique, should be used to prevent this devastating complication.

Cerebral arterial air embolism with anterior spinal cord syndrome after CT-guided hook-wire localization of Lung mass and pulmonary nodule

Systemic arterial air embolism (SAAE) is a rare but serious complication of CT-guided hook wire localization of pulmonary nodule usually with catastrophic and poor outcome. Hook wire needle localization is done pre-operatively by placing wire around or into the pulmonary nodule to provide the thoracic surgeon accurate location guidance of the target nodule for Video-Assisted Thoracoscopic Surgery (VATS) wedge resection with safety margins. Physicians should be aware of this possible complication during the procedure in order to rescue the patient promptly as it requires rapid diagnosis and management. We describe a 55-year-old male who underwent a CT-guided hook wire needle localization of left upper lobe lung cancer and left lower lobe pulmonary nodule prior to planned VATS wedge resection who developed altered mental status and bilateral lower extremities paralysis after wire placement was completed. His CT head demonstrated small air embolism in the left occipital area, confirming the diagnosis of cerebral air embolism and follow up CT and MRI of the head revealed multiple areas of brain infarction. In addition, he was diagnosed with anterior spinal cord syndrome (ACS), most likely due to anterior spinal artery ischemia from micro air embolism on the basis of clinical findings but with negative ischemic changes on MRI of the spinal cord. His mental status recovered but he remained paraplegic and transferred to inpatient rehabilitation service.

Tactical Combat Casualty Care Scenario: Management of a Gunshot Wound to the Chest in a Combat Swimmer.

Tactical Combat Casualty Care (TCCC) has always emphasized the need to consider the tactical setting in developing a plan to care for wounded unit members while still on the battlefield. The TCCC Guidelines provide an evidence-based trauma care approach to specific injuries that may occur in combat. However, they do not address what modifications might need to be made to the basic TCCC guidelines due to the specific tactical setting in which the scenario occurs. The scenario presented below depicts a combat swimmer operation in which a unit member is shot while in the water. The unit casualty response plan for a combat swimmer who sustains a gunshot wound to the chest while on a mission is complicated by the inability to perform indicated medical interventions for the casualty while he is in the water. It is also complicated by the potential for ballistic damage to his underwater breathing apparatus and the need to remain submerged after wounding for at least for a period of time to avoid further hostile fire. Additionally, there is a potential for a cerebral arterial gas embolism (CAGE) and/or a tension pneumothorax to develop while surfacing because of the decreasing ambient pressure on ascent. The tactical response may be complicated by limited communications between the mission personnel while submerged and by the vulnerability of the mission personnel to antiswimmer measures if their presence is compromised.

Effect of antiplatelet and/or anticoagulation medication on the risk of tympanic barotrauma in hyperbaric oxygen treatment patients, and development of a predictive model.

Middle ear barotrauma (MEBt) is a common side effect of hyperbaric oxygen treatment (HBOT) and can result in pain, hearing loss, tinnitus and otorrhagia. The use of antiplatelet/anticoagulant drugs is thought to increase the risk and severity of MEBt during HBOT. Single centre, retrospective observational cohort study of all patients treated with HBOT over a 4-year period (between 01 January 2015 to 31 December 2018) looking at the incidence of MEBt and the concurrent use of antiplatelet and/or anticoagulant drugs. MEBt was assessed by direct otoscopy of the tympanic membrane post-HBOT and scored using the modified Teed classification. Multivariate modelling assessed the relationship between antiplatelet and/or anticoagulation drug use, age, sex, and MEBt during HBOT. There was no evidence that antiplatelet and/or anticoagulation drugs increase the risk of tympanic barotrauma in HBOT patients. The prevalence of MEBt was higher in female patients than in males (χ2 P = 0.004), and increased with age (χ2 P = 0.048). No MEBt was recorded in patients undergoing recompression therapy for decompression sickness or cerebral arterial gas embolism. In this retrospective single-centre study, antiplatelet and/or anticoagulation drugs did not affect the risk of MEBt, but both age and sex did, with greater prevalence of MEBt among older patients and females compared with younger patients and males. A predictive model, requiring further validation, may be helpful in assessing the likelihood of MEBt in patients undergoing HBOT.

Cerebral arterial gas embolism proven by computed tomography following transthoracic echocardiography using bubble contrast

A 75 year-old male developed features of an acute stroke following bubble contrast echocardiography, which was shown on emergent computed tomography scanning to be a result of cerebral arterial gas embolism (CAGE) to the left middle cerebral artery. Ischaemic stroke symptoms have previously been reported as a rare complication of bubble contrast echocardiography. Radiologically proven CAGE from bubble contrast echocardiography had not been reported at the time this case occurred. Immediate provision of 100% oxygen and administration of hyperbaric oxygen are recommended treatments for CAGE and were associated with a substantial recovery for this patient.

Medical conditions in scuba diving fatality victims in Australia, 2001 to 2013.

This study identified pre-existing medical conditions among scuba diving fatalities in Australia from 2001 to 2013, inclusive, and assessed whether these conditions likely contributed to the deaths. The National Coronial Information System (NCIS) was searched for scuba diving-related cases during 2001-2013, inclusive. Coronial findings, witness and police reports, medical histories, and autopsy and toxicology reports were scrutinised for pre-existing medical conditions and autopsy findings. Predisposing factors, triggers, disabling agents, disabling injuries and causes of death were analysed using a validated template. There were 126 scuba diving-related fatalities identified during the study period. Forty-six (37%) divers were identified as having a significant medical condition which may have contributed to their incident. The most common condition was ischaemic heart disease (IHD) which had been diagnosed in 15 of the divers. Thirty-two (25%) deaths were attributed to cardiac disabling injuries (DI) such as ischaemic heart disease and arrhythmias, although a cardiac DI was thought likely in another six. Respiratory conditions were implicated in eight (6%) deaths, at least four associated with cerebral arterial gas embolism. At least 14 (11%) divers who had contributory pre-existing medical conditions had been cleared to dive by a medical practitioner within the year prior. Chronic health-related factors played a major role in almost half of these deaths; primarily cardiac conditions such as IHD and cardiac arrhythmias. Although fitness-to-dive (FTD) assessments have limitations, the high incidence of cardiac-related deaths indicates a need for 'older' divers to be medically assessed for FTD.

A diver\u2019s dilemma \u2013 a case report on bronchopulmonary sequestration

BackgroundAn asymptomatic SCUBA (Self-contained underwater breathing apparatus) diver was discovered to have an intralobar bronchopulmonary sequestration during routine pre-course screening. This is the first reported case of a diver who, having previously completed several recreational and military diving courses, was subsequently diagnosed with a congenital lung condition, possibly contraindicating diving. Presently, there is no available literature providing guidance on the diving fitness of patients with such a condition.Case presentationAn asymptomatic 26-year-old male diver was nominated to attend an overseas naval diving course. Prior to this, he had been medically certified to participate in, and had successfully completed other military and recreational diving courses. He had also completed several hyperbaric dives up to a depth of 50 m and 45 recreational dives up to a depth of 30 m. He did not have a history of diving-related injuries or complications. He had never smoked and did not have any medical or congenital conditions, specifically recurrent respiratory infections. As part of pre-course screening requirements, a lateral Chest X-ray was performed, which revealed a left lower lobe pulmonary nodule. This was subsequently diagnosed as a cavitatory left lower lobe intralobar bronchopulmonary sequestration on Computed Tomography Thorax. The diver remains asymptomatic and well at the time of writing and has been accepted to participate in another overseas course involving only dry diving in a hyperbaric chamber, with no prerequisites for him to undergo surgery.ConclusionAlthough bronchopulmonary sequestrations lack communication with the tracheobronchial tree, they may still contain pockets of air, even if not radiologically visible. This can be attributed to anomalous connections which link them to other bronchi, lung parenchyma and/or pores of Kohn. As such, there is a higher theoretical risk of pulmonary barotrauma during diving, leading to pneumothorax, pneumomediastinum, or cerebral arterial gas embolism. Taking these into consideration, the current clinical consensus is that bronchopulmonary sequestrations and all other air-containing lung parenchymal lesions should be regarded as contraindications to diving. Patients who have undergone definitive and uncomplicated surgical resection may be considered fit to dive.