Covid-19 is known to cause both lung and endovascular dysfunction. Calcium channel blockers (CCBs) have been proposed as a potential treatment for COVID-19. The use of calcium channel blockers such as amlodipine, diltiazem, and nifedipine are among first-line therapy for treating systemic and pulmonary hypertension. CCBs have also been used in high altitude pulmonary edema. The utilization of the ACE2 receptor by SARS-CoV-2 can cause diffuse pulmonary vasoconstriction. In this study, we seek to investigate whether the use of CCBs has a beneficial influence on mortality and the rate of intubation among hospitalized COVID-19 patients.METHODS: This is a retrospective review of electronic medical records for 865 patients admitted from 3/1/2020 to 4/30/2020 who tested positive for SARS-CoV-2. Patients were divided into two groups based on whether they were prescribed CCBs or not. We examined baseline characteristics including comorbidities. The two primary outcomes measured were all-cause mortality and intubation. We used t-test for analysis of age. Pearson's chi-squared test was used for primary outcome as well as comorbidities.RESULTS: In this study, We identified 298 patients on CCBs and 568 not on CCBs. Mean age, sex, comorbidities, and prescribed hypertension medications were compared between patients on CCBs and those not on CCBs. The data shows patients on CCBs had a mean age of 70.4 AE 13.8 compared to the non-CCB group had a mean age of 65.27 AE 18.22 (p<0.001). Male patients comprised 61% of the CCB group compared to the 56% of males in the non-CCB group (p<0.162). Patients in the CCB group were seen to have a higher incidence of underlying comorbidities compared to the non-CCB group (p<0.003). Patients in the CCB group were seen to have higher rates of being on other antihypertensive medications compared to the non-CCB group (p<0.035). Patients treated with CCBs had a higher incidence of intubation (37% vs 26%) with an odds ratio of 1.72 (CI¼1.269 -2.32, P<0.001). There was no significant difference in terms of mortality between the two groups (34% vs 39%) with an odds ratio of 0.791 (CI¼0.590-1.061, p¼0.118) CONCLUSIONS: In this analysis of COVID-19 patients treated with either CCBs or non-CCBs, it was found that CCBs demonstrated a significantly elevated rate of intubation compared to the non-CCB group. We also found that the use of CCBs did not demonstrate a significant improvement to mortality, potentially due to the CCB group being older in age, having a higher number of comorbidities, and using a relatively small sample size.CLINICAL IMPLICATIONS: CCBs should be used with caution due to its association with increased intubation. There is no demonstrated benefit of using CCBs at this time as there was no difference in mortality between patients treated with and without CCBs. Further research using clinical trials and studies with a larger group of patients is needed.

Introduction: Previous studies have suggested that SARS-CoV-2 causes microvascular inflammation and thrombosis, leading to microvascular angiopathy. A downstream sequela of microvascular angiopathy is AKI. Literature extensively describes the renoprotective effects of ACEI and ARB. Hypothesis: We hypothesize that using an ACEI/ARB in patients with SARS-CoV-2 is negatively associated with AKI. Methods: We conducted a retrospective chart review of patients 18 years and older who tested positive for SARS- CoV-2 using a polymerase chain reaction test between March 2020 and April 2021. Patients were divided into two groups, AKI, and non-AKI. The primary outcomes were all-cause mortality and hospitalization rate. The secondary outcomes were myocardial infarction, hypotension, intubation, use of vasopressors and ventricular tachycardia (VT). We used multivariate logistic regression to adjust for baseline characteristics. Results: We identified a total of 1,212 patients with AKI and 21,887 without AKI who tested positive for SARS-CoV-2. Incidence was 539 (44%) for all-cause mortality, 1144 (94.2%) for hospitalization, and 413 (34.6%) for patients taking ACEI/ARB. After logistic regression analysis, OR was 3.006 (95% Confidence Interval [CI]: 2.342-3.858; p<0.001) for hospitalization, 7.359 (95% CI:5.191-10.433, p <0.001) for all-cause mortality, and 1.034 (95% CI: 0.784-1.365; p< 0.810) for patients taking ACEI/ARB. The AKI group had significantly increased adjusted OR for hypotension (p< 0.001), calcium channel (p<0.001) and beta-blocker (p<0.038) use. Adjusted OR for all other secondary outcomes were not increased but not significant, including myocardial infarction (p<0.697), VT (p<0.184), vasopressor use (p<0.113), and intubation (p<0.096). Conclusions: This study suggests that ACEI/ARB use was not positively associated with AKI in patients with SARS-CoV-2, while calcium channel blocker and beta-blocker use were. A positive association between BB and CCB with AKI suggests that there should be a preference for ACEI/ARB in patients where all three medications are possible therapy options. Further studies are needed to confirm the association between ACE/ARB and AKI and rule out potential confounding variables.

The management of patients with symptomatic rectal masses can be challenging and is further complicated in cases of advanced age, comorbidities, prior surgeries, and acute hemorrhage. In this report, we describe a patient who presented with massive hemorrhage from a 7 cm low rectal tumor with subsequent cardiac arrest. After return of spontaneous circulation, emergent pelvic angiography identified extensive tumor enhancement and blush off the anterior division of the right internal iliac artery from multiple parasitized vessels. The right internal iliac artery was embolized with multiple microcoils to decrease the tumor blood supply and slow the rate of bleeding. The patient was then taken directly from the angiography suite to radiation oncology for planning CT, and within several hours, underwent his first session of radiation. In conjunction with angioembolization, short-course radiation therapy can be an effective treatment modality for advanced bleeding rectal tumors not amenable to surgical resection.

Introduction:Vasopressin is an antidiuretic hormone analog that has become an important drug in the treatment of vasodilatory shock through its vasoconstrictive and water retention properties to maintain blood pressure. We present two cases of vasodilatory shock where intravenous access was limited and intramuscular (IM) vasopressin was used for management.CASE PRESENTATION: Patient 1: An 85 year old female with a medical history of hypertension and colon cancer presented with septic shock. She received dopamine via midline on the upper left arm to maintain blood pressure, with the patient's healthcare proxy refusing a central line. Multiple attempts to obtain venous access for a blood transfusion were unsuccessful. The dopamine drip could not be held due to severe hypotension. The decision was made to administer IM vasopressin (10 Units) to maintain blood pressure while stopping dopamine during the blood transfusion. The transfusion was completed over two hours and the blood pressure improved from 76/39 -123/63. Patient 2: A 63 year old male with a medical history of smoking and peripheral vascular disease was admitted for tachycardia and hypoxia. He had necrotizing pneumonia and was in septic shock. He continued to be volume unresponsive despite intravenous fluid resuscitation. He was placed on a dopamine drip to maintain blood pressure and became tachycardic and remained in shock. Bedside ultrasound showed signs of volume overload. Twenty units of intramuscular vasopressin was given and blood pressure improved within 15 minutes and was maintained between 120/ 76-105/69 for 1.5 hours.DISCUSSION: Very frequently we encounter difficulties obtaining intravenous access while resuscitating a patient. Such situations pose an immense challenge in managing shock. Vasopressin is unique in its ability to be utilized intramuscularly. [1] Utilizing medications intramuscularly for urgent situations has a significant impact on management when there is limited, or lack of, intravenous access for hemodynamically unstable patients. The onset of action for vasopressin is approximately two hours, however our patient showed response within 15 minutes, demonstrating its potential.[1] After the initial onset of shock, endogenous stores of antidiuretic hormone are consumed and the vasodilatory mechanisms of shock may propagate.[3] Vasopressin itself may reverse some of the vasodilatory changes induced in shock, and in combination with other pressors may prove to be of greater benefit than that of pressors alone. [2] CONCLUSIONS: In the setting of shock with limited intravenous access, intramuscular vasopressin may be an effective option for initial stabilization until IV access is obtained.

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