May 2023 Medical Image of the Month: Methamphetamine Inhalation Leading to Cavitary Pneumonia and Pleural Complications

Figure 1. Two axial images from a thoracic CT angiogram with intravenous contrast upon admission demonstrates ground-glass opacities in the left upper and bilateral lower lobes.

Figure 2.  Axial images from noncontrast CT 19 days later show progression with necrosis and cavitation with areas of pleural dehiscence and loculated hydropneumothorax formation.

A 31-year-old man with a self-reported history significant for active methamphetamine and OxyContin use (last use of methamphetamine the same day with confirmation on urine drug screen) presented to the hospital with several hours of dyspnea. Having gone into cardiac arrest shortly after, he received several rounds of epinephrine and CPR and was intubated before spontaneous circulation returned. Bedside ultrasound revealed global hypokinesis with left ventricular ejection fraction of 10 to 15%, trivial pericardial effusion, and a moderate left pleural effusion. Chest CT (Figure 1) revealed segmental to subsegmental pulmonary emboli in the left lower lobe and ground-glass opacities in the left upper and bilateral lower lobes. He was treated as septic shock with Vancomycin and Cefepime, eventually speciating methicillin-sensitive Staphylococcus aureus in respiratory culture. Due to difficulty liberating the patient from the ventilator, he underwent tracheostomy tube placement. Chest x-ray on hospital day 18 showed a large left partially loculated hydropneumothorax, for which a left thoracostomy tube was placed. The next day repeat CT chest without contrast (Figure 2) showed persistent moderate left lung volume loss with tethering of the lateral and separate anterior margin of the left upper lobe to the costal pleural margin. A dense consolidation of the left lung base had progressed to developing irregular cavitary spaces with air-fluid level. There was a dehiscence of the cavitary space with the posterior left pleura.  The right upper lobe showed extensive tree-in-bud ground-glass opacities and consolidation. The right lower lobe showed necrosis with intrapulmonary cavitary spaces/air-fluid levels. There was associated focal dehiscence of the parenchyma along the posterior cavity with the pleura. Patient had developed bilateral cavitary lung lesions with persistent bilateral hydropneumothoraces.

Typical findings of amphetamine induced lung injury can include ground-glass opacities as seen here. Worldwide prevalence of amphetamine use ranged between 0.3-1.3% for those aged 15-64 in 2009 (1). Crystal meth refers to the pure form of d-methamphetamine hydrochloride that can be smoked and inhaled as heated vapor as well. It can also be administered intravenously. Other amphetamines include MDMA, methyl methcathinone (commonly referred to as bath salts), and methylenedioxyamphetamine. Neural catecholamine reuptake is blocked, and neurotransmitter is expunged into the synaptic cleft. Additionally, serotonin and dopamine reuptake blockade and increased release take place.

With inhalation, there is higher percentage uptake, faster peak time, and slower clearance in the lungs compared to other organs as evidence by data from positron emission tomography. Time to peak concentration is the same between inhalation and intravenous use. Laboratories that produce amphetamines in the United States of America reduce L-ephedrine or D-pseudoephedrine either over red phosphorous with hydrochloric acid or with liquid ammonia and lithium. Therefore, they pose risks of contamination. Red phosphorous is flammable and causes smoke inhalation injury. Other solvents used also contribute to respiratory illness including pulmonary edema and mucous membranes irritation (1).

Typical respiratory symptoms from illicit drug use, including amphetamine use, include dyspnea, cough, dark sputum, and chest pain. Mechanisms include toxic effects on the respiratory system, coronary artery constriction, and impaired coronary artery oxygen delivery leading to chest pain. Dyspnea is a primarily a result of ventilation-perfusion mismatch from vasospasm. Bronchospasm is precipitated by airway mucosal irritation. Mucosal ulceration and burns as well as subsequent diffuse alveolar capillary injury lead to hemoptysis.  Cardiogenic pulmonary edema stems from the same causes of chest pain as well as acute hypertension and myocardial ischemia. Noncardiogenic pulmonary edema is a result of alveolar epithelial and endothelial damage.

As compared to cocaine, amphetamines have lower rates of barotrauma including pneumothorax, pneumopericardium, and pneumomediastinum, however these are still significant. There have been reports of MDMA-related epidural pneumatosis and retropharyngeal emphysema (1). Air dissects along fascial planes when alveoli are injured and travels up the pulmonary vascular sheath into the mediastinum, pericardium, and between the parietal and visceral layers.  When inhaled, coughing, and performing a Valsalva maneuver predispose the patient to this complication (2). Additionally, pneumothorax is more common with exertion shortly after consumption. Attempts at intravenous administration along the chest, supraclavicular regions, and internal jugular veins increase risk of pneumothorax (3). Hemothorax and pseudoaneurysm have been documented as well (2).

Kia Ghiassi DO¹, Colin Jenkins MD¹, Prateek Juneja DO²

^1,2University of California Riverside, Riverside, CA USA

²Inspira Health, Vineland, NJ USA

References

1. Tseng W, Sutter ME, Albertson TE. Stimulants and the lung : review of literature. Clin Rev Allergy Immunol. 2014 Feb;46(1):82-100. [CrossRef] [PubMed]
2. Nguyen ET, Silva CI, Souza CA, Müller NL. Pulmonary complications of illicit drug use: differential diagnosis based on CT findings. J Thorac Imaging. 2007 May;22(2):199-206. [CrossRef] [PubMed]
3. Gotway MB, Marder SR, Hanks DK, et al. Thoracic complications of illicit drug use: an organ system approach. Radiographics. 2002 Oct;22 Spec No:S119-35. [CrossRef] [PubMed]

Cite as: Ghiassi K, Jenkins C, Juneja P. May 2023 Medical Image of the Month: Methamphetamine Inhalation Leading to Cavitary Pneumonia and Pleural Complications. Southwest J Pulm Crit Care Sleep. 2023;26(5):80-82. doi: https://doi.org/10.13175/swjpccs010-23 PDF

April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease

Figure 1. ECG demonstrating sinus bradycardia and T-wave inversion in lead III and aVF.

Figure 2.  Transthoracic echo apical four-chamber view (zoomed) demonstrating 2.3 x 2.6 cm echogenic mass of the left atrium. LV = left ventricle. RA = right atrium. LA = left atrium.

Figure 3.  Transesophageal echo, midesophageal long axis view demonstrating 2.5 x 1.71 cm echogenic left atrial mass attached to upper dome of the left atrium. LA = left atrium. LV = left ventricle.

A 43-year-old woman presents to the Emergency Department (ED) with right-sided weakness and numbness for several hours. Medical history is significant for Raynaud’s Phenomenon (RP), initially presenting six months prior to presentation, manifesting as intermittent episodes of painless discoloration of multiple fingers.  Cardiac exam was unremarkable with regular rhythm and no discernable murmur. Neurological exam demonstrated right arm pronator drift. Other examination findings were unremarkable. Labs demonstrated a troponin of 0.00 ng/mL, C-reactive protein of 2.28 mg/dL, and an erythrocyte sedimentation rate of 40 mm/hr. The electrocardiogram (ECG) demonstrated sinus bradycardia and notable for T-wave inversion in lead III and aVF, but without any ST-segment deviations (Figure 1).  Magnetic Resonance Imagining (MRI) of the brain demonstrated acute ischemic left frontal, left parietal, and right parietal infarcts along with mild subcortical left parietal infarct, concerning for venous or watershed distal embolic arterial infarct. MRI Angiogram of the brain showing diminutive bilateral, lateral transverse dural venous sinuses, consistent with thrombus. The patient’s neurological deficits resolved within five hours of ED arrival. Given the background diagnoses of RP and new thrombosis, a complete autoimmune and hypercoagulability workup was pursued and was otherwise negative.

As part of acute stroke work-up, the patient also underwent transthoracic echocardiogram (TTE) with a bubble study, which was significant for left atrial (LA) echogenic intracardiac structure attached to the superior part of the LA (Figure 2). Transesophageal Echocardiogram (TEE) was performed which demonstrated a large, 2.5 x 1.71 cm mass, consistent with an atrial myxoma, not appearing to involve the interatrial septum but instead thought to originate from the upper dome of the atrium immediately adjacent to the pulmonary veins (Figure 3). Patient was also evaluated by neurology and started on anticoagulation with parental continuous unfractionated heparin infusion given the dural venous sinus thrombosis and a possible hypercoagulable state due to the underlying myxoma. Patient underwent surgical resection of the atrial mass Histopathological examination of the resected mass was consistent with the diagnosis of atrial myxoma.

Although atrial myxomas are the most common primary cardiac tumor, clinical presentation ranges from incidental imaging findings to profound life-threading cardiovascular manifestations (1). This range of presentation is closely associated with size, mobility, and location (2). Pinede et al. studied 112 cases of atrial myxomas and reported that signs of cardiac obstruction were the primary manifestation of LA myxoma. Approximately, 67% of patients presented with signs of cardiac obstruction, such as heart failure, syncope, or myocardial infarction, while embolic signs were only present in 29% of patients. Systemic signs including fever and weight loss were only reported in 34% of patients with only 5% of patients having associated connective tissue disease (3). Rarely, RP has been described as the primary presenting symptom of atrial myxoma (4,5), underscoring the utility of maintaining a high degree of suspicion when symptomatology coexists.

RP is a vascular response to stress or cold temperature that appears as color changes in the digits (6). Although primary RP has no known underlying etiology, it is more commonly seen in female patients with a history of smoking, migraine headaches, and cardiovascular disease (6). This is in contrast to secondary RP, which presents in patient with an underlying autoimmune rheumatic disease including, but not limited, to Systemic Sclerosis, Mixed Connective Tissue Disease, Systemic Lupus Erythematosus, Sjogren’s Syndrome, and hematologic disorders such as Cryoglobulinemia, Cold Agglutinins Disease, and Paraproteinemia (7).

Atrial myxoma may rarely make its initial appearance under the guise of RP (4). This phenomenon is likely attributable to overproduction of IL-6 by the myxoma (9-11). Our patient presented with RP six months prior to her presentation to the ED with right-sided weakness and numbness and a complete autoimmune and hypercoagulability workup was negative; this may suggest that the underlying pathophysiology of her RP is the associated overproduction of IL-6 by the atrial myxoma.

TTE may be considered in the initial diagnostic evaluation of a patient presenting with RP without additional findings suggestive of secondary etiologies. Given that myxomas are typically localized within the atrial lumen, transthoracic echocardiography is a highly sensitive modality for diagnosis, whereas CT and MRI may also help in diagnostics in uncertain cases. Once suspicion of a cardiac myxoma has been supported by imaging modalities, surgical removal of the tumor should be performed as soon as possible due to the risk of myxoma associated embolic episodes (5).  Post intervention, long term prognosis is excellent with an approximated 5% rate of recurrence (3). Long-term follow-up with serial TTE are recommended, particularly in younger patients (3) but there is no specific guideline regarding the frequency of TTE surveillance post atrial myxoma resection.

Ali A. Mahdi MD, Chris Allahverdian MD, Vishal Patel MD, Serap Sobnosky MD

Dignity Health, St. Mary Medical Center, Department of Internal Medicine, Long Beach, CA

References

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3. Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases. Medicine (Baltimore). 2001 May;80(3):159-72. [CrossRef] [PubMed]
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7. Prete M, Favoino E, Giacomelli R, et al. Evaluation of the influence of social, demographic, environmental, work-related factors and/or lifestyle habits on Raynaud's phenomenon: a case-control study. Clin Exp Med. 2020 Feb;20(1):31-37. [CrossRef] [PubMed]
8. Khouri C, Blaise S, Carpentier P, Villier C, Cracowski JL, Roustit M. Drug-induced Raynaud's phenomenon: beyond β-adrenoceptor blockers. Br J Clin Pharmacol. 2016 Jul;82(1):6-16. [CrossRef] [PubMed]
9. Jourdan M, Bataille R, Seguin J, Zhang XG, Chaptal PA, Klein B. Constitutive production of interleukin-6 and immunologic features in cardiac myxomas. Arthritis Rheum. 1990 Mar;33(3):398-402. [CrossRef] [PubMed]
10. Saji T, Yanagawa E, Matsuura H, Yamamoto S, Ishikita T, Matsuo N, Yoshirwara K, Takanashi Y. Increased serum interleukin-6 in cardiac myxoma. Am Heart J. 1991 Aug;122(2):579-80. [CrossRef] [PubMed]
11. Parissis JT, Mentzikof D, Georgopoulou M, Gikopoulos M, Kanapitsas A, Merkouris K, Kefalas C. Correlation of interleukin-6 gene expression to immunologic features in patients with cardiac myxomas. J Interferon Cytokine Res. 1996 Aug;16(8):589-93. [CrossRef] [PubMed]

Cite as: Mahdi AA, Allahverdian C, Patel V, Sobnosky S. April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease. Southwest J Pulm Crit Care Sleep. 2023;26(4):56-58. doi:https://doi.org/10.13175/swjpccs006-23 PDF