https://orcid.org/0000-0002-2122-9889
Abstract
Air emboli are a life-threatening diagnosis, which may form through a range of mechanisms. In this case, we describe the case of extensive multi-territory air emboli in a patient with a history of intravenous drug abuse.
This case describes a 41-year-old male who presented with confusion following fall with long lie. He was diagnosed with hyperkalaemia, renal failure, rhabdomyolysis, and compartment syndrome, and he developed extensive multi-territory air emboli. Air embolism was identified in arterial, venous, subcutaneous, and mediastinal territories. Echocardiography demonstrated right ventricular dilation and dysfunction, consistent with air visualized in the right coronary artery on computed tomography. The patient was transferred to the intensive care unit for close cardiac and neurological monitoring and supportive organ care, and ultimately made an uneventful recovery by 6 weeks without apparent complications from the air emboli.
The presence of multi-territory air emboli has previously been described in the setting of surgery, manipulation of intravascular catheters, pulmonary barotrauma, and in sepsis with gas-forming organisms. It has not previously been reported in intravenous drug use or sterile rhabdomyolysis. Computed tomography imaging and echocardiography are useful to diagnose air emboli and their haemodynamic impact. Our patient’s case provides a novel example of multi-territory air emboli in a unique scenario.
Air emboli are life-threatening events and may result from surgery, instrumentation, and accessing large-bore intravascular cannulae or from sepsis with gas-forming organisms.
Air emboli in intravenous drug users or sterile rhabdomyolysis have not been reported previously.
Primary specialities involved other than cardiology
Emergency medicine, internal medicine, intensive care medicine.
Introduction
Air emboli are a life-threatening diagnosis, which may form through a range of mechanisms.1,2 They present in the venous or arterial system, subcutaneous tissues, or, more rarely, across multiple bodily territories.3 Depending on location, they may present incidentally, with chest pain, visceral ischaemia, altered neurology, or cardiac arrest.4 Imaging, particularly, computed tomography (CT), is very useful for identification.3
Summary figure
Case summary
A 41-year-old man was brought to the emergency department with confusion following a fall with long lie on his left side. His medical history was notable for longstanding intravenous heroin use, utilizing a range of injection sites over his body. There was no surgical history.
A bystander had found that the patient collapsed on the floor and phoned for an ambulance. The patient was able to convey to paramedics that he had injected heroin ‘at sunrise’ but was disoriented as to which day that might have been. He believed he had fallen to the floor, but had no recollection of any exact events or how long he might have been lying there. On arrival to the emergency department, the patient was in a state of shock with a blood pressure of 75/50 mmHg, heart rate of 75 b.p.m., and temperature of 35.5°. Oxygen was provided in the ambulance at 4 L/min via nasal prongs, maintaining oxygen saturations of 94%. A clinical examination indicated a tense painful left arm but no other focal abnormalities. No murmurs were auscultated and no specific signs of right heart failure were identified.
Arterial blood gas analysis demonstrated severe metabolic acidosis and hyperkalaemia with pH 6.9 (normal 7.35–7.45), lactate of 10, and potassium of 7.8 mmol/L (normal 3.5–5.0 mmol/L). Electrocardiogram (ECG) indicated typical changes of severe hyperkalaemia, with near-sinusoidal appearance of the QRS complex (Figure 1). Laboratory results indicated an extremely elevated creatine kinase value of 100 240 U/L (normal 45–250 U/L) indicative of rhabdomyolysis, acute kidney injury, and likely ischaemic liver injury (Table 1). Calcium gluconate, insulin/dextrose, and sodium bicarbonate were administered according to hyperkalaemia guidelines.5 Following this, the patient’s ECG evolved to show ST elevation in leads V1 and V2 (Figure 2A), and then, normal sinus rhythm with an incomplete right bundle branch block (Figure 2B).
Initial arterial blood gas values and electrocardiogram of the patient.
Electrocardiogram following treatment for hyperkalaemia with (A) ST elevation in leads V1 and V2 and (B) subsequent resolution of ST-segment changes.
Biochemical parameters on arrival to emergency department
| Parameter | Patient value | Laboratory reference range |
|---|---|---|
| Haemoglobin | 141 | 130–180 g/L |
| White cell count | 25.3 | 4.0–11.0 × 109/L |
| Platelets | 214 | 150–400 × 109/L |
| Sodium | 135 | 135–145 mmol/L |
| Potassium | 7.9 | 3.5–5.2 mmol/L |
| Chloride | 99 | 95–110 mmol/L |
| Anion gap | 32 | 5–15 |
| Creatinine | 310 | 60–110 µmol/L |
| Urea | 12.8 | 2.1–7.1 mmol/L |
| ALP | 114 | 30–110 U/L |
| GGT | 48 | 0–50 U/L |
| ALT | 2225 | 0–40 U/L |
| AST | 2706 | 0–35 U/L |
| Creatinine kinase | 100 240 | 45–250 U/L |
| Parameter | Patient value | Laboratory reference range |
|---|---|---|
| Haemoglobin | 141 | 130–180 g/L |
| White cell count | 25.3 | 4.0–11.0 × 109/L |
| Platelets | 214 | 150–400 × 109/L |
| Sodium | 135 | 135–145 mmol/L |
| Potassium | 7.9 | 3.5–5.2 mmol/L |
| Chloride | 99 | 95–110 mmol/L |
| Anion gap | 32 | 5–15 |
| Creatinine | 310 | 60–110 µmol/L |
| Urea | 12.8 | 2.1–7.1 mmol/L |
| ALP | 114 | 30–110 U/L |
| GGT | 48 | 0–50 U/L |
| ALT | 2225 | 0–40 U/L |
| AST | 2706 | 0–35 U/L |
| Creatinine kinase | 100 240 | 45–250 U/L |
Bold text indicates abnormal values. ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, gamma glutamyltransferase.
Biochemical parameters on arrival to emergency department
| Parameter | Patient value | Laboratory reference range |
|---|---|---|
| Haemoglobin | 141 | 130–180 g/L |
| White cell count | 25.3 | 4.0–11.0 × 109/L |
| Platelets | 214 | 150–400 × 109/L |
| Sodium | 135 | 135–145 mmol/L |
| Potassium | 7.9 | 3.5–5.2 mmol/L |
| Chloride | 99 | 95–110 mmol/L |
| Anion gap | 32 | 5–15 |
| Creatinine | 310 | 60–110 µmol/L |
| Urea | 12.8 | 2.1–7.1 mmol/L |
| ALP | 114 | 30–110 U/L |
| GGT | 48 | 0–50 U/L |
| ALT | 2225 | 0–40 U/L |
| AST | 2706 | 0–35 U/L |
| Creatinine kinase | 100 240 | 45–250 U/L |
| Parameter | Patient value | Laboratory reference range |
|---|---|---|
| Haemoglobin | 141 | 130–180 g/L |
| White cell count | 25.3 | 4.0–11.0 × 109/L |
| Platelets | 214 | 150–400 × 109/L |
| Sodium | 135 | 135–145 mmol/L |
| Potassium | 7.9 | 3.5–5.2 mmol/L |
| Chloride | 99 | 95–110 mmol/L |
| Anion gap | 32 | 5–15 |
| Creatinine | 310 | 60–110 µmol/L |
| Urea | 12.8 | 2.1–7.1 mmol/L |
| ALP | 114 | 30–110 U/L |
| GGT | 48 | 0–50 U/L |
| ALT | 2225 | 0–40 U/L |
| AST | 2706 | 0–35 U/L |
| Creatinine kinase | 100 240 | 45–250 U/L |
Bold text indicates abnormal values. ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, gamma glutamyltransferase.
Given the unclear presentation with a fall, shock, and severe metabolic derangement, a CT ‘pan-scan’ (whole-body multi-slice CT) was organized. This demonstrated gas within the venous system (left axillary vein, main pulmonary trunk), arterial system [right ventricular (RV) pneumatosis], subcutaneous tissues (supraclavicular subcutaneous tissues), and within cavities (superior and anterior mediastinum). No arteriovenous shunts or fistulae were identified on the scan (Figure 3).
Air in (A) the right ventricular free wall (pneumatosis, bracket), (B) pulmonary trunk (arrow), (C) mediastinum adjacent to the RV (arrow), and (D) subcutaneous emphysema (arrows).
Blood cultures were negative, specifically for any anaerobic gas-forming organisms. Transthoracic echocardiography (TTE) revealed a small compressed left ventricle and a moderately dilated right ventricle with moderately severe systolic dysfunction. The anterior RV free wall was thinned and akinetic. Right ventricular fractional area change was 25% (normal 32–60%), tricuspid annular plane systolic excursion was 8 mm (normal >15 mm), and RV Sʹ was 4 cm/s (normal >11 cm/s). The tricuspid valve leaflets were mildly thickened, particularly the septal leaflet, raising suspicion for previous episodes of endocarditis (Figure 4).
Initial echocardiography demonstrated a dilated right ventricle with moderate systolic dysfunction and heavy trabeculation (arrow and bracket). (A) Right ventricular inflow view. (B) Right ventricle–focused apical four-chamber view.
The patient subsequently developed evolving compartment syndrome of the left forearm and leg and was transferred to the operating theatre for left arm and glutaeal fasciectomy. All three compartments of the glutaeus medius were released, with the muscle reported to be necrotic at surgery. Given the patient’s renal failure, surgical issues, and the uncertainty regarding the air emboli, he was subsequently transferred to the intensive care unit for assessment.
No surgical intervention was undertaken for the air emboli, and the patient was managed supportively in the left lateral decubitus position with dialysis, diuresis, and wound care. He was transferred to the ward after 5 days in the intensive care unit, with normalization of rhabdomyolysis. A repeat TTE performed 2 weeks later showed normalized RV size and function. As indicated in the timeline, he was ultimately transferred to rehabilitation and then discharged home with normalized renal and hepatic function. Medications at discharge were opioid replacement therapy (monthly buprenorphine), analgesia, and thiamine.
Discussion
The presence of multi-vessel air emboli has previously been described in the setting of surgery, manipulation of intravascular catheters, pulmonary barotrauma, and in sepsis with gas-forming organisms.1,2,6–8 Mortality is quoted at up to 80%,2 and a volume of 250 mL of air infused into the body at a rate of 100 mL/s is considered to be clearly lethal.3 In previously described cases, there has been a clear precipitant and confinement to one territory of the body. Our patient’s case is highly unusual in several ways and raises several unanswered questions.
The precipitant for our patient’s air emboli was presumed to be frequent intravenous drug use. However, air emboli have never previously been reported in the literature in people who inject drugs, presumably because there is no sustained venous access, and any amount of air injected with drugs would be presumed to be miniscule and should be resorbed within the pulmonary circulation.
An alternative possibility could be that the patient’s air emboli arose from myonecrosis at the site of the evolving compartment syndrome. Massive air emboli have previously been reported in the context of fungal cavitating lesions and gangrene.7,8 They have not, however, been linked to rhabdomyolysis or sterile acute compartment syndrome in the literature. Our patient’s blood culture test results remained negative, and no organisms were grown from excised tissue to explain the multi-territory embolic air.
The second unexplained element of our patient’s presentation is the multi-territory nature of their air emboli. Air injected into the left axillary vein could have travelled to the pulmonary trunk, explaining two of the identified sites. However, the air identified in the RV free wall was presumed to be in the right coronary artery, demanding arterial air presence. The ECG recorded in Figure 2A could be consistent with right precordial strain in the setting of right coronary arterial air emboli. However, the air in the mediastinum and the subcutaneous tissues is not immediately explicable. Our patient was known to have challenging intravenous access, and whether frequent rotation of sites resulted in inadvertent arterial and intra-thoracic air injections is a possibility. It is intriguing that air was identified only within thoracic structures, as the patient was also known to inject blindly into his groin on regular occasions.
As detailed previously in the case summary, no arteriovenous fistula was identified on comprehensive imaging to explain the multi-territory character of the air emboli. Cases of multi-territory air emboli including arterial emboli, subcutaneous emphysema, and pneumomediastinum have previously been described in the context of higher volumes of infused gas (for example, when oxygen tubing was connected to an intravenous cannula at 3 L/min) in the absence of a pathological shunt.3 In such cases, it was presumed that physiological intrapulmonary shunts resulted in passage of air from the venous to the arterial systems.3 However, the mechanism by which the required large volume of gas would have entered our patient’s vasculature remains highly uncertain.
The time course over which these air emboli occurred is also opaque. Typically, injected air will be resorbed into the circulation relatively rapidly.9 The patient was profoundly acidotic and in a low-flow state when brought to the emergency department, and this may have facilitated persistence of air emboli within the circulation. In animal studies, it has been demonstrated that air transit and disappearance times within the heart may be affected by multiple factors, including semi-upright position and larger volumes of air.4
Importantly, CT is highly sensitive for the detection of small amounts of intravascular air,9 but it is not routinely performed in intravenous drug users or patients with compartment syndrome. A closer evaluation of CT imaging performed in high-frequency intravenous drug users or patients with compartment syndrome may lead to the identification of subacute air emboli as being more common than previously recognized.
Conclusion
This is the first reported case of apparent massive gas embolism in a high-frequency intravenous drug user with compartment syndrome. The cause and mechanism of our patient’s air embolism remains uncertain as they did not exhibit any classical risk factors for air emboli. Consideration of CT imaging and a detailed history of injecting patterns may help explain critical organ pathology due to massive air embolism.
Lead author biography
Dr Elizabeth D. Paratz is a cardiologist with particular expertise in sudden cardiac arrest and cardiac imaging. She is based in Melbourne, Victoria.
Consent: The patient provided informed consent for their case to be published in a de-identified form, compliant with COPE guidelines.
Funding: E.D.P. is supported by the Wilma Beswick Senior Research Fellowship at Melbourne University.
Data availability
The data underlying this article cannot be shared publicly due to the issue of identifiability of the patient. De-identified data will be shared on reasonable request to the corresponding author.
References
Author notes
Conflict of interest: None declared.
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