Case Report Lung Ischemia Reperfusion Injury as a Complication of Pulmonary Thrombectomy
by Kushagra Gupta, Diane T Dawley, Praful Schroff*
Division of Pulmonary, Critical Care and Sleep Medicine, East Carolina University, Greenville, North Carolina, USA.
*Corresponding author: Praful Schroff, Division of Pulmonary, Critical Care and Sleep Medicine, East Carolina University, Greenville, North Carolina, USA.
Received Date: 02 April 2024
Accepted Date: 08 April 2024
Published Date: 10 April 2024
Citation: Gupta K, Dawley DT, Schroff P (2024) Lung Ischemia Reperfusion Injury as a Complication of Pulmonary Thrombectomy. Ann Case Report 9: 1751. https://doi.org/10.29011/2574-7754.101751
Abstract
Pulmonary embolism (PE) leads to lung ischemia due to reduced blood flow which can be restored by thrombectomy to prevent infarction. However, this can lead to an under-recognized sequela called lung ischemia reperfusion injury (LIRI), such as in this case. An 86-year-old gentleman in rehabilitation after cervical laminectomy was found to have bilateral PE, right heart strain and newly reduced ejection fraction of 30-35%. He was started on heparin drip and since recent surgery precluded thrombolysis, he underwent emergent thrombectomy. Rapid improvement in perfusion of bilateral pulmonary arteries was noted. However, two hours later, he began to have hemoptysis with shock and hypoxia. He was intubated and bronchoscopy showed blood-tinged frothy secretions but no active bleeding. Despite a stable hemoglobin and improved ejection fraction, shock became progressively refractory to vasopressors. Repeat CTA showed improvement in clot burden but worsening bilateral ground-glass opacities (GGOs), predominant in previous areas of high clot burden. He improved over the next day with supportive care, and was extubated. Restoration of blood flow after thrombectomy to ischemic lung can cause aseptic inflammation and pulmonary edema, known as LIRI. In this, reactive oxygen species cause endothelial dysfunction and increased vascular permeability which presents as non-cardiogenic pulmonary edema in areas with previously obstructed blood flow which can progress to ARDS and death. Our patient’s deterioration into refractory shock after thrombectomy and GGOs in previously ischemic areas can be best explained by LIRI. Therefore, it is imperative to be mindful of this catastrophic outcome when considering thrombectomy for PE.
Keywords: LIRI; Reperfusion Injury; Thrombectomy; Embolectomy; Pulmonary Embolism; Lung Ischemia
Introduction
Pulmonary embolism (PE) leads to lung ischemia as the metabolic needs of the lung cannot be met by reduced blood flow. A novel treatment option in intermediate-high, and high-risk PEs is thrombectomy which can promote rapid resolution of symptoms [1]. Even though this procedure can immediately restore blood flow and thereby, prevent progression of ischemia to infarction, more widespread availability and use of this modality is bringing our attention to a lesser-known physiological complication of this procedure-lung ischemia reperfusion injury (LIRI). LIRI, as the name suggests, is lung injury that occurs due to restoration of blood flow to previously ischemic lung. We present a case of LIRI after thrombectomy along with a review of literature on the topic.
Case Presentation
An 86-year-old African-American male, non-smoker, with hypertension, gastroesophageal reflux disease, arthritis, cervical stenosis, and a remote history of prostate cancer went to our inpatient rehabilitation unit after a C1-C2 and C5-C6 posterior cervical laminectomy. His outpatient medications were amlodipine, pregabalin, valsartan, terazosin, and aspirin.
On post-operative day six, he was noted to be hypoxic (SpO2 79%) and hypotensive (BP 80/50). A stat CT angiogram of the chest showed bilateral pulmonary emboli with evidence of right heart strain. BNP had increased to 764 pg/mL from pre-admission values of 51-83 pg/mL. Troponin (lab reference ≤0.03 ng/mL) increased to 0.23 ng/mL and peaked at 0.24 ng/mL. His pulmonary embolism severity index (PESI) score was 216 and he was upgraded to MICU. Echocardiogram demonstrated a hypokinetic right ventricular free wall (McConnell’s sign) and a newly reduced left ventricular ejection fraction of 30-35%. Vascular surgery was consulted for mechanical thrombectomy as he was not a candidate for thrombolytic therapy for this high-risk PE [2] due to recent spinal surgery.
Patient underwent emergent mechanical thrombectomy and IVC filter placement. During clot evacuation, he was noted to have significant clot burden, right greater than left. He received a 5000-unit heparin bolus during the procedure and was continued on heparin drip after the procedure. The total clot removed from the right main pulmonary artery measured 3.6 cm x 3.1 cm x 0.6 cm. The total clot removed from the left main pulmonary artery measured 2.7 cm x 2.5 cm x 0.4 cm. After removal of these clots, excellent filling of both right and left main pulmonary arteries was confirmed intraoperatively. There was no evidence of dissection or extravasation.
Two hours after the procedure, the patient started having active hemoptysis with worsening shock and hypoxia. The heparin drip was stopped, and PTT level was noted to be supratherapeutic. The patient was intubated for airway protection. His venous sheath, left in after the procedure, was assessed without evidence of bleeding or hematoma. No other bleeding source was identified.
His blood gas after intubation showed combined respiratory and metabolic acidosis with high alveolar-arterial (A-a) gradient (pH 7.28, PaCO2 50, PaO2 291, HCO3- 21 on 100% FiO2). His post-intubation chest x-ray was notable for a left lower lobe opacification. Bedside bronchoscopy showed blood-tinged frothy secretions throughout the airways, more on the left compared to the right, but no focal source of active bleeding. He was started on nebulized tranexamic acid (TXA) every 8 hours. His chemistry panel was unremarkable with mild lactic acidosis of 2.2 mg/dL. His hemoglobin remained stable, however, his hemodynamics continued to worsen, and he went into refractory vasopressor dependent shock for the next twelve hours requiring significant doses of norepinephrine, epinephrine, and vasopressin (Table 1).
|
Date and Time |
9/27 0600 |
9/27 0700 |
9/27 0915 |
9/27 1000 |
9/27 2300 |
9/28 1800 |
9/30 1200 |
|
HR |
99 |
94 |
99 |
91 |
103 |
106 |
95 |
|
BP |
94/63 |
66/54 |
92/50 |
50/33 |
107/64 |
125/61 |
149/52 |
|
MAP |
73 |
58 |
65 |
37 |
79 |
78 |
78 |
|
SpO2 |
93% |
99% |
95% |
80% |
100% |
92% |
91% |
|
RR |
28 |
30 |
25 |
21 |
18 |
23 |
18 |
|
O2 |
HFNC 12L |
HFNC 12L |
HFNC 12L |
100% FiO2 (P-CMV) |
50% FiO2 (P-CMV) |
HFNC 20L, 95% |
HFNC 15L |
|
Norepinephrine (mcg/min) |
- |
- |
- |
80 |
83 |
12 |
2 |
|
Epinephrine (mcg/min) |
- |
- |
- |
4 |
10 |
- |
- |
|
Vasopressin (mcg/min) |
- |
- |
- |
0.04 |
0.04 |
0.04 |
0.03 |
|
Event |
Pre-embolectomy |
Peri-embolectomy |
Hemoptysis |
Peri-Intubation |
Post-intubation |
Post-extubation |
Immediately Prior to Comfort Care |
Table 1: Vital Signs, Oxygen Support and Vasopressors.
Repeat echocardiogram showed improved ejection fraction of 40-45% with dilated IVC concerning for persistently elevated right sided pressures and a small to medium circumferential pericardial effusion. He had a repeat CT angiogram of his chest for hemoptysis and refractory shock which showed improvement in clot burden but residual clot in the segmental and distal subsegmental branches. Worsening patchy ground-glass opacities (GGOs) bilaterally but most severe in the left lower lobe were noted along with a small right pleural effusion and minimal ascites (Figures 1 and 2).
Figure 1: Chest X-ray and CT chest lung windows before (top row) and after (bottom row) thrombectomy.