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Opioid Epidemic and Pulmonary Hypertension, What Do They Have in Common?
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A3721 - Opioid Epidemic and Pulmonary Hypertension, What Do They Have in Common?
Author Block: M. Berrou1, M. Chaker2, P. Almalouf1; 1Department of Medicine and Center for Lung Biology, Univ of S Alabama College of Medicine, Mobile, AL, United States, 2Department of Oncology, Wayne State University, School of Medicine, Detroit, MI, United States.
Introduction: The opioid epidemic has a heavy impact on public health. Pulmonologists and intensivists are tasked with taking care of patients who overdose on opioids and require respiratory support. We also observe the opioids effects on CO2 homeostasis. On the other hand, pulmonary hypertension is not usually thought of when opioids are mentioned. We present a case of talc induced acute and transient pulmonary hypertension in a patient who was injecting crushed hydromorphone tablets intravenously.
Case Description: This case is of a 33 y/o female with history of recent soft tissue infection receiving home IV antibiotics via PICC line, she also has chronic pain managed with oral hydromorphoe. She was sent to the ER by her visiting nurse due to abnormal vitals: HR 150, SpO2 78% on RA. Upon evaluation in the ED she declined having any symptoms. Her tachycardia improved but she remained hypoxemic with SpO2 of 85% on RA, ABG 7.39/40/47 on RA. Her exam was remarkable for +JVD, LE edema and loud S2. Her CBC and CMP were unremarkable. CXR showed a full AP window, chest CT showed ground glass with nodular opacities. Echocardiogram showed EF 65-70%. D-shaped LV, dilated RV with normal wall thickness, RVSP was estimated at 55 mmHg. She clinically improved with diuresis and was easily weaned off O2. She was discharged with follow up in pulmonary hypertension center. The PICC line was discontinued. Workup showed: FEV1: 69%, FEV1/FVC: 0.8, TLC: 65%, DLCO: 48%, ABG: 7.47/34/90 on RA. V/Q scan low probability, HIV/hepatitis, ANA, ANCA, anti-CCP were negative. RHC was performed few weeks following the echo evaluation. It showed PCWP 7 mmHg, PA pressure 33/17 (mean 23) mmHg, and no evidence of intracardiac shunting. The quick normalization of the patient's vitals and RHC pressures was puzzling. We then learned from the patient's family she was crushing her hydromorphone tables and injecting them via the PICC line at the time of our initial evaluation. We concluded that she developed an acute and transient pulmonary hypertension from foreign body granulomatosis.
Discussion: Foreign body granulomatosis is caused by intravenous injection of pulverized tablets. Talc embolization causes an initial arteritis leading to acute pulmonary hypertension. This is followed by the development of foreign body granulomas. PFTs usually show low DLCO, TLC. HRCT: nodular opacities and diffuse GGO. There are no clearly established treatments for this disease. Cessation of smoking and intravenous drug use is essential.
Author Block: M. Berrou1, M. Chaker2, P. Almalouf1; 1Department of Medicine and Center for Lung Biology, Univ of S Alabama College of Medicine, Mobile, AL, United States, 2Department of Oncology, Wayne State University, School of Medicine, Detroit, MI, United States.
Introduction: The opioid epidemic has a heavy impact on public health. Pulmonologists and intensivists are tasked with taking care of patients who overdose on opioids and require respiratory support. We also observe the opioids effects on CO2 homeostasis. On the other hand, pulmonary hypertension is not usually thought of when opioids are mentioned. We present a case of talc induced acute and transient pulmonary hypertension in a patient who was injecting crushed hydromorphone tablets intravenously.
Case Description: This case is of a 33 y/o female with history of recent soft tissue infection receiving home IV antibiotics via PICC line, she also has chronic pain managed with oral hydromorphoe. She was sent to the ER by her visiting nurse due to abnormal vitals: HR 150, SpO2 78% on RA. Upon evaluation in the ED she declined having any symptoms. Her tachycardia improved but she remained hypoxemic with SpO2 of 85% on RA, ABG 7.39/40/47 on RA. Her exam was remarkable for +JVD, LE edema and loud S2. Her CBC and CMP were unremarkable. CXR showed a full AP window, chest CT showed ground glass with nodular opacities. Echocardiogram showed EF 65-70%. D-shaped LV, dilated RV with normal wall thickness, RVSP was estimated at 55 mmHg. She clinically improved with diuresis and was easily weaned off O2. She was discharged with follow up in pulmonary hypertension center. The PICC line was discontinued. Workup showed: FEV1: 69%, FEV1/FVC: 0.8, TLC: 65%, DLCO: 48%, ABG: 7.47/34/90 on RA. V/Q scan low probability, HIV/hepatitis, ANA, ANCA, anti-CCP were negative. RHC was performed few weeks following the echo evaluation. It showed PCWP 7 mmHg, PA pressure 33/17 (mean 23) mmHg, and no evidence of intracardiac shunting. The quick normalization of the patient's vitals and RHC pressures was puzzling. We then learned from the patient's family she was crushing her hydromorphone tables and injecting them via the PICC line at the time of our initial evaluation. We concluded that she developed an acute and transient pulmonary hypertension from foreign body granulomatosis.
Discussion: Foreign body granulomatosis is caused by intravenous injection of pulverized tablets. Talc embolization causes an initial arteritis leading to acute pulmonary hypertension. This is followed by the development of foreign body granulomas. PFTs usually show low DLCO, TLC. HRCT: nodular opacities and diffuse GGO. There are no clearly established treatments for this disease. Cessation of smoking and intravenous drug use is essential.
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