COVID-19-Related Spontaneous Aortic Arch Thrombus With Delayed Embolization.

Presentation of a 62-year-old man with baseline chronic obstructive pulmonary disease admitted to the hospital with dyspnea and newly diagnosed COVID-19 infection. CT scan of the chest was obtained to rule out pulmonary embolism. This revealed a mural thrombus of the inner curvature of the aortic arch with a floating component. Therapeutic full dose anticoagulation was initiated in combination with close clinical observation and treatment for modest hypoxia. He did well for 1 month and then returned with ischemic rest pain of the right foot. Angiography revealed thrombosis of all 3 tibial arteries in the right leg. Percutaneous mechanical thrombectomy with tissue plasminogen activator injection and angioplasty was performed with success in 1 tibial artery to achieve in line flow to the foot. After continued anticoagulation, the remainder of the tibial arteries autolysed and the aortic thrombus was noted to be resolved 4 months later. A brief pathophysiology discussion is included.

Orbital cellulitis and cavernous sinus thrombosis with contralateral sinus disease in a COVID-19 positive adolescent patient.

Patients with COVID-19 have been reported to have elevated coagulation factors, which is a well-documented cause of venous thromboembolism events such as deep vein thrombosis and pulmonary embolism. Other venous thrombotic events, however, such as cavernous sinus thrombosis (CST) have been less commonly observed, specifically in combination with primary orbital cellulitis. Due to its unique anatomic location, the cavernous sinus is susceptible to thrombophlebitis processes including septic thrombosis and thrombosis most commonly from sinusitis. Many studies have shown that in the antibiotic era thromboembolic events of the cavernous sinus are less common due to infection spread from the orbit or facial region. This case report describes a 17-year-old COVID-19 positive male who presented with a left-sided primary orbital cellulitis with CST without radiographic evidence of ipsilateral sinus disease.

Possible consequences of Covid-19 on the nervous system

OBJECTIVES: The aim of the survey was to find out what the possible consequences are of the COVID-19 disease on the nervous system and to propose a method of using artificial intelligence. MATERIAL AND METHODS: Recent research has shown that the risks to patients due to severe acute coronavirus 2 respiratory syndrome (SARS-COV-2) differ most significantly depending on age and the presence of underlying comorbidities such as: cardiovascular disease, hypertension, diabetes and others. The consequences of COVID-19 on the nervous system are especially important. We performed a detailed selection of articles describing the effects of COVID-19 on the nervous system. RESULT(S): We made a clear summary of the main consequences of COVID-19 on the nervous system and suggested a way to use artificial intelligence. CONCLUSION(S): We confirmed research that artificial intelligence methods have the potential to accelerate prediction, especially for the possible consequences of COVID-19 on the nervous system.Copyright © 2020 Neuroendocrinology Letters

Thromboelastography Parameters do not Discriminate for Thrombotic Events in Hospitalized Patients With COVID-19.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with a prothrombotic state; leading to multiple sequelae. We sought to detect whether thromboelastography (TEG) parameters would be able to detect thromboembolic events in patients hospitalized with COVID-19. METHODS: We performed a retrospective multicenter case-control study of the Collaborative Research to Understand the Sequelae of Harm in COVID (CRUSH COVID) registry of 8 tertiary care level hospitals in the United States (US). This registry contains adult patients with COVID-19 hospitalized between March 2020 and September 2020. RESULTS: A total of 277 hospitalized COVID-19 patients were analyzed to determine whether conventional coagulation TEG parameters were associated with venous thromboembolic (VTE) and thrombotic events during hospitalization. A clotting index (CI) >3 was present in 45.8% of the population, consistent with a hypercoagulable state. Eighty-three percent of the patients had clot lysis at 30 min (LY30) = 0, consistent with fibrinolysis shutdown, with a median of 0.1%. We did not find TEG parameters (LY30 area under the receiver operating characteristic [ROC] curve [AUC] = 0.55, 95% CI: 0.44-0.65, P value = .32; alpha angle [α] AUC = 0.58, 95% CI: 0.47-0.69, P value = .17; K time AUC = 0.58, 95% CI: 0.46-0.69, P value = .67; maximum amplitude (MA) AUC = 0.54, 95% CI: 0.44-0.64, P value = .47; reaction time [R time] AUC = 0.53, 95% CI: 0.42-0.65, P value = .70) to be a good discriminator for VTE. We also did not find TEG parameters (LY30 AUC = 0.51, 95% CI: 0.42-0.60, P value = .84; R time AUC = 0.57, 95%CI: 0.48-0.67, P value .07; α AUC = 0.59, 95%CI: 0.51-0.68, P value = .02; K time AUC = 0.62, 95% CI: 0.53-0.70, P value = .07; MA AUC = 0.65, 95% CI: 0.57-0.74, P value < .01) to be a good discriminator for thrombotic events. CONCLUSIONS: In this retrospective multicenter cohort study, TEG in COVID-19 hospitalized patients may indicate a hypercoagulable state, however, its use in detecting VTE or thrombotic events is limited in this population.

SARS-CoV-2 vaccines are not associated with hypercoagulability in apparently healthy people.

Background: SARS-CoV-2 adenoviral-vector-DNA vaccines have been linked to the rare but serious thrombotic post-vaccine complication vaccine-induced immune thrombotic thrombocytopenia (VITT). This has raised concerns regarding the possibility of increased thrombotic risk after any SARS-CoV-2 vaccines. Objectives: To investigate whether SARS-CoV-2 vaccines cause coagulation activation leading to a hypercoagulable state. Methods: This observational study included 567 healthcare personnel, 521 were recruited post-vaccination after a first dose of adenoviral vector ChAdOx1-S (Vaxzevria®, AstraZeneca) vaccine, and 46 prospectively before vaccination with an mRNA vaccine, either Spikevax® (Moderna, n=38) or Comirnaty® (Pfizer-BioNTech, n=8). In the mRNA group, samples were acquired before and 1-2 weeks after vaccination. In addition to pre-vaccination samples, 56 unvaccinated blood donors were recruited as controls (total n=102). Thrombin generation, D-dimer and free tissue factor pathway inhibitor (TFPI) were analyzed. Results: No participant experienced thrombosis, VITT or thrombocytopenia (platelet count <100·109/L) one week to one month post-vaccination. There was no increase in thrombin generation, D-dimer or TFPI in the ChAdOx1-S vaccine group compared with controls, or after the mRNA vaccines compared with baseline values. Eleven of 513 vaccinated with ChAdOx1-S (2.1%) had anti-PF4/polyanion antibodies without concomitant increase in thrombin generation. Conclusion: In this study, SARS-CoV-2 vaccines were not associated with thrombosis, thrombocytopenia, increased thrombin generation, D-dimer or TFPI levels compared with baseline or unvaccinated controls. These findings argue against subclinical activation of coagulation post-COVID-19 vaccination.

Cerebral venous thrombosis secondary to ulcerative colitis: A case report with a literature review.

Ulcerative colitis is an idiopathic inflammatory bowel condition that may be worsened by thromboembolic events such deep vein thrombosis, cerebral venous thrombosis, and pulmonary embolism. Cerebral venous thrombosis is a rare but critical consequence of ulcerative colitis characterized by high mortality and morbidity rate. It is thought to be caused by the hypercoagulable state that occurs during ulcerative colitis relapse. Cerebral venous thrombosis is a reversible condition with good outcomes when detected early and treated properly. In this study, we describe the case of a young woman who presented with cerebral venous thrombosis secondary to ulcerative colitis complicated by venous infarction with petechial cerebral hemorrhage.

[Utility of probability scores for the diagnosis of pulmonary embolism in patients with SARS-CoV-2 infection: a systematic review]. / Utilidad de las escalas de predicción diagnósticas de embolia de pulmón en pacientes con infección por SARS-CoV-2: una revisión sistemática.

BACKGROUND AND OBJECTIVE: Clinical prediction models determine the pre-test probability of pulmonary embolism (PE) and assess the need for tests for these patients. Coronavirus infection is associated with a greater risk of PE, increasing its severity and conferring a worse prognosis. The pathogenesis of PE appears to be different in patients with and without SARS-CoV-2 infection. This systematic review aims to discover the utility of probability models developed for PE in patients with COVID-19 by reviewing the available literature. METHODS: A literature search on the PubMed, Scopus, and EMBASE databases was carried out. All studies that reported data on the use of clinical prediction models for PE in patients with COVID-19 were included. Study quality was assessed using the Newcastle-Ottawa scale for non-randomized studies. RESULTS: Thirteen studies that evaluated five prediction models (Wells score, Geneva score, YEARS algorithm, and PERC and PEGeD clinical decision rules) were included. The different scales were used in 1,187 patients with COVID-19. Overall, the models showed limited predictive ability. The two-level Wells score with low (or unlikely) clinical probability in combination with a D-dimer level <3000 ng/mL or a normal bedside lung ultrasound showed an adequate correlation for ruling out PE. CONCLUSIONS: Our systematic review suggests that the clinical prediction models available for PE that were developed in the general population are not applicable to patients with COVID-19. Therefore, their use is in clinical practice as the only diagnostic screening tool is not recommended. New clinical probability models for PE that are validated in these patients are needed.

Late diagnosis of COVID-19 in a 34-year-old man in a hypercoagulable state: A case report.

Background: Late diagnosis of COVID-19 in young patients in a hypercoagulable state can cause a high mortality rate. Clinical manifestations of COVID-19 include respiratory and extrapulmonary symptoms such as a hypercoagulable state, increased transaminase enzymes, and multiple-organ failure. Case and outcomes: A 34-year-old male presented to the emergency room after 3 days of high fever, weakness, and flatulence. The patient had thrombocytopenia and elevated liver transaminase enzymes and was initially diagnosed with dengue hemorrhagic fever. He was given hydration intravenous fluids, oxygen, antipyretic, and hepatoprotector. On day 4, the patient was diagnosed with COVID-19 and received therapy to decrease the Alanine transaminase and Aspartate transaminase levels. While waiting for outsourced D dimer and prothrombin time results, the patient was given low molecular weight heparin (LMWH) on day 5. On day 13, his condition deteriorated with cephalgia and shortness of breath, but the patient's family refused intubation. The chest CT scan revealed large ground-glass opacities in both lungs. The patient was given additional medications, such as Meropenem, Dexamethasone, and Remdesivir. On day 15, the patient passed away. Discussion: Intermediate LMWH dosage seems to be associated with a lower mortality incidence than standard Deep Vein Thrombosis (DVT) prophylaxis in hospitalized COVID-19 patients. However, due to the late COVID-19 diagnosis, the patient was not given LMWH at the beginning of treatment. Conclusion: A hypercoagulable state is partly responsible for the high mortality rate of COVID-19 patients. Early detection and management of the hypercoagulable state, including the use of LMWH, can decrease the severity of COVID-19 symptoms.

Utility of probability scores for the diagnosis of pulmonary embolism in patients with SARS-CoV-2 infection: A systematic review.

BACKGROUND AND OBJECTIVE: Clinical prediction models determine the pre-test probability of pulmonary embolism (PE) and assess the need for tests for these patients. Coronavirus infection is associated with a greater risk of PE, increasing its severity and conferring a worse prognosis. The pathogenesis of PE appears to be different in patients with and without SARS-CoV-2 infection. This systematic review aims to discover the utility of probability models developed for PE in patients with COVID-19 by reviewing the available literature. METHODS: A literature search on the PubMed, Scopus, and EMBASE databases was carried out. All studies that reported data on the use of clinical prediction models for PE in patients with COVID-19 were included. Study quality was assessed using the Newcastle-Ottawa scale for non-randomized studies. RESULTS: Thirteen studies that evaluated five prediction models (Wells score, Geneva score, YEARS algorithm, and PERC and PEGeD clinical decision rules) were included. The different scales were used in 1,187 patients with COVID-19. Overall, the models showed limited predictive ability. The two-level Wells score with low (or unlikely) clinical probability in combination with a D-dimer level <3000 ng/mL or a normal bedside lung ultrasound showed an adequate correlation for ruling out PE. CONCLUSIONS: Our systematic review suggests that the clinical prediction models available for PE that were developed in the general population are not applicable to patients with COVID-19. Therefore, their use is in clinical practice as the only diagnostic screening tool is not recommended. New clinical probability models for PE that are validated in these patients are needed.

Global Hemostasis Potential in COVID-19 Positive Patients Performed on St-Genesia Show Hypercoagulable State.

BACKGROUND: At the dawn of the pandemic, severe forms of COVID-19 were often complicated by thromboembolisms. However, routine laboratory tests cannot be used to predict thromboembolic events. The objective of this study was to investigate the potential value of the thrombin generation test (TGT) in predicting hypercoagulability and thrombotic risk in the aforementioned set of patients. METHODS: The study panel comprised 52 patients divided into two groups (26 COVID-19 positive and 26 COVID-19 negative); COVID-19-positive patients were further grouped in "severe" (n = 11) and "non-severe" (n = 15) categories based on clinical criteria. The routine blood tests and TGT of these patients were retrospectively analyzed. RESULTS: All 26 COVID-19-positive patients showed decreased lymphocyte, monocyte and basophil counts and increased lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine transaminase (ALT) compared with control patients. Conversely, we did not observe statistically significant differences between severe and non-severe patients despite anecdotal variations in the distribution patterns. TGT without thrombomodulin (TM) addition showed statistically significant differences in the thrombin peak heights between COVID-19-positive and negative patients. After addition of TM, peak height, Endogenous Thrombin Potential (ETP) and velocity index were increased in all COVID-19-positive patients while the percentage of inhibition of ETP was reduced. These trends correlated with the severity of disease, showing a greater increase in peak height, ETP, velocity index and a drastic reduction in the percentage of ETP inhibition in more severely affected patients. CONCLUSIONS: Our data suggest that all COVID-19 patients harbor a hypercoagulable TGT profile and that this is further pronounced in severely affected patients.

COVID-19 and Acute Pulmonary Embolism: A Case Series and Brief Review.

The SARS-CoV-2 virus, or COVID-19, is responsible for the current global pandemic and has resulted in the death of over 400,000 in the United States. Rates of venous thromboembolism have been noted to be much higher in those infected with COVID-19. Here we report a case-series of COVID-19 patients with diverse presentations of pulmonary embolism (PE). We also briefly describe the pathophysiology and mechanisms for pulmonary embolism in COVID-19. These cases indicate a need to maintain a high index of suspicion for PE in patients with COVID-19, as well as the need to consider occult COVID-19 infection in patients with PE in the right clinical circumstance.

A Case of Deep Vein Thrombosis After Recovery From COVID-19 and Its Association With Elevated D-dimers.

The coronavirus disease 2019 (COVID-19) continues to be a devastating disease for the elderly population, especially in long-term care facilities, and it presents with varying clinical presentations. We have ample evidence that COVID-19 can predispose to deep vein thrombosis (DVT) and pulmonary embolism (PE) during an active infection. Still, very few cases of DVT have been reported after recovery from COVID-19. The imbalance of the coagulation cascade and the increased release of certain coagulation factors play an essential role in promoting hypercoagulability and vascular endothelial dysfunction. It leads to a rise in the level of fibrin degradation products, D-dimers, which can remain elevated for up to several weeks, even after recovery. It has been suggested that the risk of DVT occurring after recovering from COVID-19 remains high for up to three months. We report a case of a 77-year-old long-term care female resident at a nursing facility, ambulatory at baseline, who was noted to be COVID-19 positive upon routine facility-wide testing per department of health guidelines. She was asymptomatic during her 10-day quarantine period. D-dimer levels during routine labs were high (initial D-dimer level of 1.87 mg/L FEU {normal value: 0.19-0.52 mg/L FEU}), but the patient had no clinical signs and symptoms of DVT. Ultrasound of the bilateral legs was not performed due to low clinical suspicion. The patient received an enoxaparin DVT prophylaxis dose during the quarantine period. Follow-up D-dimer levels were done at frequent intervals after recovery, but D-dimer levels continued to remain elevated up till six weeks after her 10-day quarantine period ended. Based on previous experience with other long-term care residents who suffered from COVID-19, bilateral lower extremity ultrasound was performed, which showed bilateral DVT. Elevated D-dimer levels are a predictor of hypercoagulation complications in COVID-19. Patients with persistently elevated D-dimer levels after recovery from COVID-19 should be screened for thromboembolic complications, even if they are asymptomatic. DVT can occur up to three months post-recovery from COVID-19 infection.

Implications of COVID-19 to Stroke Medicine: An Epidemiological and Pathophysiological Perspective.

The neurological complications of Coronavirus 2019 (COVID-19) including stroke have been documented in the recent literature. COVID-19-related inflammation is suggested to contribute to both a hypercoagulable state and haemorrhagic transformation, including in younger individuals. COVID-19 is associated with a heightened risk of ischaemic stroke. Haemorrhagic stroke in COVID-19 patients is associated with increased morbidity and mortality. Cerebral venous sinus thrombosis (CVST) accounts for <1% of stroke cases in the general population but has come to heightened public attention due to the increased risk associated with adenoviral COVID-19 vaccines. However, recent evidence suggests the prevalence of stroke is less in vaccinated individuals than in unvaccinated COVID-19 patients. This review evaluates the current evidence of COVID-19-related ischaemic and haemorrhagic stroke, with a focus on current epidemiology and inflammatory-linked pathophysiology in the field of vascular neurology and stroke medicine.

COVID-19 Infection: A Sparked Ignition to a Thrombotic Storm.

Thrombotic storm (TS) is a rare yet life-threatening condition that requires aggressive thrombolytic or anticoagulant therapy. Clinical manifestation of TS can be disastrous as it amplifies thrombotic pathways causing widespread organ ischemia. We present a patient who developed TS following a COVID-19 infection. He was simultaneously diagnosed with an ST-elevation myocardial infarction, multiple pulmonary emboli, aortic thrombi, and bilateral limb ischemia. Further workup was positive for a spindle cell neoplasm, which combined with the prothrombotic nature of COVID-19 infection likely produced an exaggerated response leading to a diffuse thrombotic event. Through this case, we would like to highlight the importance of having a collective field of expertise in making the most appropriate medical decision under critical situations.

Gastrointestinal System: COVID-19 and Potential Mechanisms Associated with Coagulopathy.

SARS-CoV-2 is a novel coronavirus that expanded worldwide, generating a pandemic of acute respiratory syndrome called "coronavirus disease 2019" (COVID-19), which resulted in a global health crisis. The spectrum of COVID-19 manifestations ranges from none or mild symptoms to severe respiratory failure associated with systemic manifestations, mostly gastrointestinal symptoms. Hypercoagulability is an important feature of COVID-19 disease, which can potentially influence patients' prognosis. Therefore, gastroenterologists should focus on subjects with concomitant hypercoagulable gastrointestinal disorders as they may display a higher risk of thrombotic complications during SARS-CoV-2 infection. The aim of this review is to summarize the available evidence regarding the interplay of the prothrombotic pathogenetic mechanisms of both COVID-19 and hypercoagulable digestive diseases and the possible clinical implications. We summarized the potential interplay of prothrombotic mechanisms of both COVID-19 and hypercoagulable digestive diseases in the graphical abstract.

Acute Limb Ischemia due to Arterial Thrombosis in a Patient with COVID-19 Pneumonia: A Case Report.

The COVID-19 pandemic has caused more than 4 million deaths worldwide to date. During the course of the COVID-19 pandemic, thrombotic complications due to hypercoagulable state have emerged as an important issue. Acute limb ischemia is one of emergency cases in vascular disease caused by a sudden decrease in arterial limbs perfusion. Here, we report a 53-year-old male patient with severe COVID-19 and a history of uncontrolled type 2 diabetes mellitus (T2DM) who developed extensive arterial thrombosis and limb ischemia despite being on therapeutic-dose anticoagulation, requiring surgical intervention. Right and left leg open thrombectomy was performed at day 7 after admission due to the excruciating pain and the worsening of the limb conditions. The patient was transferred to intensive care unit in emergency room because of the unstable hemodynamic and passed away a few hours after the surgery. For critically ill patients with COVID-19, special attention should be paid to abnormal coagulation dysfunction and microcirculatory disorders.

Incidental and Asymptomatic Splenic Infarction and Infrarenal Thrombus in a COVID-19 Patient.

The cytokine storm associated with coronavirus disease 2019 (COVID-19) triggers a hypercoagulable state leading to venous and arterial thromboembolism. Lab findings associated with this phenomenon are elevated D-dimer, fibrinogen, C-reactive protein (CRP), ferritin, and procalcitonin. We present the case of a 66-year-old male with dyslipidemia who was diagnosed with COVID-19 with worsening shortness of breath, myalgia, and loss of taste. Physical examination was remarkable for crackles with diminished lung sounds and use of his accessory muscles. Labs showed normal white blood cell count, D-dimer of 1.42 mg/L, ferritin of 961 ng/mL, lactate dehydrogenase (LDH) of 621 U/L, and CRP of 2.1 mg/dL. Chest X-ray showed atypical pneumonitis with patchy abnormalities. He required oxygen supplementation with fraction of inspired oxygen of 100% proning as tolerated. He received remdesivir, ceftriaxone, azithromycin, dexamethasone, prophylactic enoxaparin, and a unit of plasma therapy. His D-dimer had increased from 1.65 to 3.51 mg/L with worsening dyspnea. At this time, computed tomography angiogram (CTA) of the chest showed extensive ground-glass opacities and a 2.4 × 1.9 × 1.3 cm distal thoracic aortic intraluminal thrombus. He was started on a heparin drip. A follow-up CTA of the aorta showed thrombus or hypoattenuation within the splenic artery and wedge-shaped areas extending from the hilum with possible infarction and a 6 mm thrombus in the infrarenal abdominal aorta. He was transitioned to enoxaparin 1 mg/kg twice daily. He remained asymptomatic from his splenic infarction. This case adds more insight to splenic infarction associated with COVID-19 in addition to the 32 reported cases documented thus far. Management of thromboembolism includes a therapeutic dose of anticoagulation. To prevent thromboembolism, prophylactic anticoagulation is recommended for those hospitalized with COVID-19.

Dementia in a patient with autoimmune disease and hypercoagulable state worsened by COVID-19 vaccination: A case report.

Background: Systemic autoimmune disorders are associated with an increased risk of hypercoagulability. The hypercoagulable state in people with systemic autoimmune disorders has lately gained attention. Presentation of case: We presented a 44-year-old male with a chief complaint of progressive difficulty concentrating, memory impairment, and weakness in all limbs. Seven months before admission to our Memory Clinic, the patient began to have infrequent short-term memory loss and sometimes got lost when he went for a drive. Three months later, he complained of feeling dizzy when in a crowd, being unable to watch television for a long time, and easily forgetting. Computed tomography (CT) scan showed brain infarction. After receiving the first dose of COVID-19 vaccine (Sinovac), the patient had difficulty communicating verbally and could only point at objects, as well as tetraparesis. These conditions severely intervened in his daily activities. The patient was then referred to an immunologist and diagnosed with autoimmune disease. In our Memory Clinic, his performances of attention, memory, language, visuospatial, and executive function were very poor. We diagnosed him with autoimmune dementia. The administration of methylprednisolone, mycophenolate mofetil, vitamin D3, donepezil, and memantine could improve his condition. Discussion: Autoimmune disease can cause microvascular thrombosis and microembolism at the central nervous system level, which would cause vascular damage and cognitive impairment leading to brain infarction and dementia. Conclusion: There seems to be a link between autoimmune disease, hypercoagulable state, and dementia, although the magnitude of this link and the underlying processes are not fully understood.

COVID myocardial involvement presenting as left ventricular aneurysm and clot associated with normal coronary anatomy, deep vein thrombosis, and abnormal brachial artery flow-mediated dilatation.

A 40-year-old non-diabetic, non-hypertensive male patient presented with complaints of dyspnea of a few days duration and coronavirus -19 disease (COVID) pneumonia. The electrocardiography (ECG) revealed sinus tachycardia with T inversion in V1 only. The ECG revealed a left ventricular aneurysm with a clot and severe left ventricular dysfunction. He had deep vein thrombosis involving the left lower leg. The cardiac magnetic resonance imaging revealed a left ventricular posterodorsal aneurysm with a large clot. Computed tomography angiography revealed normal coronaries and no evidence of pulmonary embolism or aortitis. The d-dimer was raised. A brachial artery Doppler revealed severe impairment of flow-mediated dilatation, suggesting endothelial dysfunction. He was stabilized with anti-platelets and anticoagulants, and diuretics.

A Case Report of a Young Female With Renal Infarction Secondary to Breakthrough COVID Infection.

COVID-19 infection is a disease that induces a hypercoagulable state that appears to be more aggressive than other conditions related to endothelial damage. The kidney, a highly vascularized organ rich in Angiotensin-Converting Enzyme 2 (ACE2) receptors, is commonly affected by COVID-19 infection. Acute kidney injury (AKI) is common in these patients and has been linked to worse outcomes. Furthermore, kidney infarction, although uncommon, has also been reported. We present the case of a 21-year-old otherwise healthy female presenting with flank pain who was found to have renal infarction in the setting of breakthrough COVID-19 infection and Oral contraceptive pill (OCP) use. Despite getting appropriate vaccination, the patient was infected. She was not hypoxic, and her kidney function was preserved. CT angiography demonstrated peripheral hypoattenuation in the right kidney compatible with infarct but no evidence of a thrombus. The patient was medically managed with anticoagulation, and supportive therapy was offered for pain control. She had clinical improvement. The follow-up at three weeks showed normal renal function. She was continued with novel oral anticoagulation (NOAC). This case demonstrates that COVID-19 infection may present renal infarction in otherwise healthy young individuals even after appropriate vaccination. Early recognition is essential so that appropriate therapy can be given. Long-term anticoagulation and outcomes of this entity must be studied.