Baseline electrolyte disorders predict disease severity and mortality in patients with COVID-19.

Distinguishing critical laboratory biomarkers for disease severity at the time of hospital presentation is important for early identification of patients who are most likely to have poor outcomes and effective use of health resources. This study aimed to evaluate whether electrolyte imbalances on hospital admission predict severe disease and mortality in patients with coronavirus disease 2019 (COVID-19). We retrospectively collected data on the blood electrolyte concentrations of 286 COVID-19 patients at admission. The correlations between electrolyte imbalances, inflammation, and thrombosis markers in COVID-19 patients were also evaluated. We assessed the predictive performance of baseline blood electrolyte concentrations for severe disease and death using receiver operating characteristic curve analysis and multivariate logistic regression methods. Abnormalities in serum sodium, calcium, and potassium levels at admission were found at 20.6%, 14%, and 4.2%, respectively in this study. In the receiver operating characteristic curve analyses, hypocalcemia and hyponatremia effectively predicted disease progression to hospitalization (area under the curve 0.82, P < .001 and 0.81, P < .001, respectively) and 30-day mortality (area under the curve 0.85, P < .001 and 0.91, P < .001, respectively). In the multivariate logistic regression analysis, baseline hypocalcemia was identified as an independent risk factor associated with the risk of hospitalization (ß = 2.019, P = .01; odds ratio: 7.53). Baseline hypocalcemia and hyponatremia effectively predicted disease progression toward hospitalization and 30-day mortality in patients with COVID-19. Clinicians should closely follow up or reevaluate COVID-19 patients with baseline electrolyte disorders.

Evaluation of the effect of hyperchloremia on the prognosis and mortality of medical intensive care patients: a single-center study.

BACKGROUND: While chloride (Cl) is the most abundant anion in the serum, it is unfortunately one of the most commonly disregarded laboratory test results routinely drawn upon admission into the medical intensive care unit (MICU). We aimed to investigate the relation between in-hospital mortality, different pathologies requiring admission to the MICU, serum Cl levels, and other biochemical tests in a tertiary center. METHODS: The prospective study included data from 373 patients admitted to the ICU of a tertiary care center between 2017 and 2019. Data of patients under 18, pregnant patients or patients who were in the MICU for under 48 h were excluded. Comorbidity status, complete blood count, biochemistry tests, and blood gas analysis results of all patients included in the study were collected and recorded. Univariate and multivariate analyses were performed with the obtained data. RESULTS: : Of the patients included in the study, 158 (42.4%) were discharged, and 215 (57.6%) died. In the receiver operator characteristics curve analysis performed to determine the discriminating power of Cl levels with a cut-off value of >98 mEq/L in relation to mortality, its sensitivity was found to be 84% and specificity 60%. According to Kaplan-Meier analysis results, mortality rate was higher (60% vs 46%) and survival time was lower (19.0 ± 1.46 vs. 23.0 ± 4.36 days; p = 0.035) in the patient group with high Cl levels compared to the patient group with normal or low Cl levels. In the Cox regression analysis, it was found that the survival time of the patients hospitalized in the MICU was associated with the variables of Cl, presence of cancer diagnosis and pCO2 (hazard ratio: 1.030 (1.008-1.049), 2.260(1.451-3.500), and 1.020 (1.003-1.029); p < 0.05, respectively). DISCUSSION: Mortality in MICU patients were found to increase in association with higher Cl levels at admission, presence of cancer disease, and higher pCO2 levels. In addition, it should not be ignored that there may be an important relationship between renal failure and hyperchloremia in MICU patients.

Effect of Electrolyte Imbalance on Mortality and Late Acute Kidney Injury in Hospitalized COVID-19 Patients.

INTRODUCTION: As a multisystem illness, Coronavirus disease 2019 (COVID-19) can damage different organs. This study investigated the effect of electrolyte imbalance (EI), with or without concomitant renal dysfunction, on the prognosis of COVID-19 in hospitalized patients. METHODS: We evaluated 499 hospitalized patients with confirmed COVID-19, without a history of chronic kidney disease. The patients' demographic data, laboratory values, and outcomes were retrospectively collected from the hospital information system. Serumelectrolytes including sodium, potassium, magnesium, calcium, and phosphorus abnormalities were analyzed on admission and during the hospitalization period. The outcomes of this study were the occurrence of acute kidney injury (AKI) after the first week of hospitalization and in-hospital mortality rate. Multivariate analyses were carried out to obtain the independent risk of each EI on mortality, by adjusting for age, gender, and AKI occurrence. RESULTS: Among the 499 COVID-19 patients (60.9% male), AKI occurred in 168 (33.7%) and mortality in 92 (18.4%) cases. Hypocalcemia (38%) and hyponatremia (22.6%) were the most prevalent EIs, and all EIs were more common in the AKI group than in the non-AKI group. Hyponatremia (Adjusted Odds ratio [AOR] = 2.34, 95% CI: 1.30 to 4.18), hypernatremia (AOR = 8.52, 95% CI: 1.95 to 37.32), and hyperkalemia (AOR = 4.63, 95% CI: 1.65 to 13) on admission were associated with poor prognosis. Moreover, hyponatremia (AOR = 3.02, 95% CI: 1.28 to 7.15) and hyperphosphatemia (AOR = 5.12, 95% CI: 1.24 to 21.09) on admission were associated with late AKI occurrence. CONCLUSION: This study highlights the role of hyponatremia, hypernatremia, hyperkalemia, and hyperphosphatemia in poor prognosis of COVID-19. According to the independent effect of EI on late AKI and mortality, we recommend physicians to raise awareness to closely monitor and correct EI during hospitalization.  DOI: 10.52547/ijkd.6904.

Fluid balance neutralization secured by hemodynamic monitoring versus protocolized standard of care in critically ill patients requiring continuous renal replacement therapy: study protocol of the GO NEUTRAL randomized controlled trial.

BACKGROUND: Fluid overload is associated with worse outcome in critically ill patients requiring continuous renal replacement therapy (CRRT). Net ultrafiltration (UFNET) allows precise control of the fluid removal but is frequently ceased due to hemodynamic instability episodes. However, approximately 50% of the hemodynamic instability episodes in ICU patients treated with CRRT are not associated with preload dependence (i.e., are not related to a decrease in cardiac preload), suggesting that volume removal is not responsible for these episodes of hemodynamic impairment. The use of advanced hemodynamic monitoring, comprising continuous cardiac output monitoring to repeatedly assess preload dependency, could allow securing UFNET to allow fluid balance control and prevent fluid overload. METHODS: The GO NEUTRAL trial is a multicenter, open-labeled, randomized, controlled, superiority trial with parallel groups and balanced randomization with a 1:1 ratio. The trial will enroll adult patients with acute circulatory failure treated with vasopressors and severe acute kidney injury requiring CRRT who already have been equipped with a continuous cardiac output monitoring device. After informed consent, patients will be randomized into two groups. The control group will receive protocolized fluid removal with an UFNET rate set to 0-25 ml h-1 between inclusion and H72 of inclusion. The intervention group will be treated with an UFNET rate set on the CRRT of at least 100 ml h-1 between inclusion and H72 of inclusion if hemodynamically tolerated based on a protocolized hemodynamic protocol aiming to adjust UFNET based on cardiac output, arterial lactate concentration, and preload dependence assessment by postural maneuvers, performed regularly during nursing rounds, and in case of a hemodynamic instability episode. The primary outcome of the study will be the cumulative fluid balance between inclusion and H72 of inclusion. Randomization will be generated using random block sizes and stratified based on fluid overload status at inclusion. The main outcome will be analyzed in the modified intention-to-treat population, defined as all alive patients at H72 of inclusion, based on their initial allocation group. DISCUSSION: We present in the present protocol all study procedures in regard to the achievement of the GO NEUTRAL trial, to prevent biased analysis of trial outcomes and improve the transparency of the trial result report. Enrollment of patients in the GO NEUTRAL trial has started on June 31, 2021, and is ongoing. TRIAL REGISTRATION: ClinicalTrials.gov NCT04801784. Registered on March 12, 2021, before the start of inclusion.

Overhydration Assessed Using Bioelectrical Impedance Vector Analysis Adversely Affects 90-Day Clinical Outcome among SARS-CoV2 Patients: A New Approach.

BACKGROUND: COVID-19 has taken on pandemic proportions with growing interest in prognostic factors. Overhydration is a risk factor for mortality in several medical conditions with its role in COVID-19, assessed with bioelectrical impedance (BI), gaining research interest. COVID-19 affects hydration status. The aim was to determine the hydration predictive role on 90 d survival COVID-19 and to compare BI assessments with traditional measures of hydration. METHODS: We studied 127 consecutive COVID-19 patients. Hydration status was estimated using a 50 kHz phase-sensitive BI and estimated, compared with clinical scores and laboratory markers to predict mortality. RESULTS: Non-surviving COVID-19 patients had significantly higher hydration 85.2% (76.9-89.3) vs. 73.7% (73.2-82.1) and extracellular water/total body water (ECW/TBW) 0.67 (0.59-0.75) vs. 0.54 (0.48-0.61) (p = 0.001, respectively), compared to surviving. Patients in the highest hydration tertile had increased mortality (p = 0.012), Intensive Care Unit (ICU) admission (p = 0.027), COVID-19 SEIMC score (p = 0.003), and inflammation biomarkers [CRP/prealbumin (p = 0.011)]. Multivariate analysis revealed that hydration status was associated with increased mortality. HR was 2.967 (95%CI, 1.459-6.032, p < 0.001) for hydration and 2.528 (95%CI, 1.664-3.843, p < 0.001) for ECW/TBW, which were significantly greater than traditional measures: CRP/prealbumin 3.057(95%CI, 0.906-10.308, p = 0.072) or BUN/creatinine 1.861 (95%CI, 1.375-2.520, p < 0.001). Hydration > 76.15% or ECW/TBW > 0.58 were the cut-off values predicting COVID-19 mortality with 81.3% and 93.8% sensitivity and 64 and 67.6% specificity, respectively. Hydration status offers a sensitive and specific prognostic test at admission, compared to established poor prognosis parameters. CONCLUSIONS AND RELEVANCE: Overhydration, indicated as high hydration (>76.15%) and ECW/TBW (>0.58), were significant predictors of COVID-19 mortality. These findings suggest that hydration evaluation with 50 kHz phase-sensitive BI measurements should be routinely included in the clinical assessment of COVID-19 patients at hospital admission, to identify increased mortality risk patients and assist medical care.

COVID-19 and Cardiac Arrhythmias.

Since the coronavirus disease (COVID-19) pandemic spread unrelentingly all over the world, millions of cases have been reported. Despite a high number of asymptomatic cases, the course of the disease can be serious or even fatal. The affection of the myocardium, called myocardial injury, is caused by multiple triggers. The occurrence of cardiac arrhythmias in COVID-19 patients with myocardial involvement and a critical course is common. In this review, potential mechanisms, incidence, and treatment options for cardiac arrhythmias in COVID-19 patients will be provided by performing a literature research in MESH database and the National Library of Medicine. Common cardiac arrhythmias in COVID-19 patients were sinus tachycardia, atrial fibrillation (AF), ventricular tachycardia (VT), ventricular fibrillation (VF), atrioventricular block, sinusoidal block or QTc prolongation. AF was the most common heart rhythm disorder. About 10% of COVID-19 patients develop new-onset AF and 23 to 33% showed recurrence of AF in patients with known AF. One retrospective trial revealed the incidence of VT or VF to be 5.9% in hospitalized patients. Both AF and VT are clearly associated with worse outcome. Several mechanisms such as hypoxia, myocarditis, myocardial ischemia, or abnormal host immune response, which induce cardiac arrhythmias, have been described. The effect of QT-prolonging drugs in inducing cardiac arrhythmias has become mitigated as these medications are no longer recommended. Acute management of cardiac arrhythmias in COVID-19 patients is affected by the reduction of exposure of health care personnel. More prospective data are desirable to better understand pathophysiology and consecutively adapt management.

Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective.

In Covid-19, systemic disturbances may progress due to development of cytokine storm and dysregulation of and plasma osmolarility due to high release of pro-inflammatory cytokines and neuro-hormonal disorders. Arginine vasopressin (AVP) which is involve in the regulation of body osmotic system, body water content, blood pressure and plasma volume, that are highly disturbed in Covid-19 and linked with poor clinical outcomes. Therefore, this present study aimed to find the potential association between AVP serum level and inflammatory disorders in Covid-19. It has been observed by different recent studies that physiological response due to fever, pain, hypovolemia, dehydration, and psychological stress is characterized by activation release of AVP to counter-balance high blood viscosity in Covid-19 patients. In addition, activated immune cells mainly T and B lymphocytes and released pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells, which in a vicious cycle trigger release of pro-inflammatory cytokines. Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit AVP-induced hyponatremia and release of pro-inflammatory cytokines in Covid-19. In conclusion, release of AVP from hypothalamus is augmented in Covid-19 due to stress, high pro-inflammatory cytokines, high circulating AngII and inhibition of GABAergic neurons. In turn, high AVP level leads to induction of hyponatremia, inflammatory disorders, and development of complications in Covid-19 by activation of NF-κB and NLRP3 inflammasome with release of pro-inflammatory cytokines. Therefore, AVP antagonists might be novel potential therapeutic modality in treating Covid-19 through mitigation of AVP-mediated inflammatory disorders and hyponatremia.

Hydroelectrolytic Disorder in COVID-19 patients: Evidence Supporting the Involvement of Subfornical Organ and Paraventricular Nucleus of the Hypothalamus.

Multiple neurological problems have been reported in coronavirus disease-2019 (COVID-19) patients because severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) likely spreads to the central nervous system (CNS) via olfactory nerves or through the subarachnoid space along olfactory nerves into the brain's cerebrospinal fluid and then into the brain's interstitial space. We hypothesize that SARS-CoV-2 enters the subfornical organ (SFO) through the above routes and the circulating blood since circumventricular organs (CVOs) such as the SFO lack the blood-brain barrier, and infection of the SFO causes dysfunction of the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON), leading to hydroelectrolytic disorder. SARS-CoV-2 can readily enter SFO-PVN-SON neurons because these neurons express angiotensin-converting enzyme-2 receptors and proteolytic viral activators, which likely leads to neurodegeneration or neuroinflammation in these regions. Considering the pivotal role of SFO-PVN-SON circuitry in modulating hydroelectrolyte balance, SARS-CoV-2 infection in these regions could disrupt the neuroendocrine control of hydromineral homeostasis. This review proposes mechanisms by which SARS-CoV-2 infection of the SFO-PVN-SON pathway leads to hydroelectrolytic disorder in COVID-19 patients.

New onset adrenal insufficiency in a patient with COVID-19.

SARS-CoV-2 is the cause of COVID-19. Since the outbreak and rapid spread of COVID-19, it has been apparent that the disease is having multi-organ system involvement. Still its effect in the endocrine system is not fully clear and data on cortisol dynamics in patients with COVID-19 are not yet available. SARS-CoV-2 can knock down the host's cortisol stress response. Here we present a case of a 51-year-old man vomiting for 10 days after having confirmed COVID-19 infection. He had hypotension and significant hyponatraemia. Work-up was done including adrenocorticotropic hormone stimulation test. He was diagnosed as suffering from adrenal insufficiency and started on steroids with subsequent improvement in both blood pressure and sodium level. COVID-19 can cause adrenal insufficiency. Clinicians must be vigilant about the possibility of an underlying relative cortisol deficiency in patients with COVID-19.

Electrolyte imbalance in COVID-19 patients admitted to the Emergency Department: a case-control study.

In patients visiting the emergency department (ED), a potential association between electrolytes disturbance and coronavirus disease 2019 (COVID-19) has not been well studied. We aim to describe electrolyte disturbance and explore risk factors for COVID-19 infection in patients visiting the ED. We carried out a case-control study in three hospitals in France, including adult ED inpatients (≥ 18 years old). A total of 594 ED case patients in whom infection with COVID-19 was confirmed, were matched to 594 non-COVID-19 ED patients (controls) from the same period, according to sex and age. Hyponatremia was defined by a sodium of less than 135 mmol/L (reference range 135-145 mmol/L), hypokalemia by a potassium of less than 3.5 mmol/L (reference range 3.5-5.0 mmol/L), and hypochloremia by a chloride of less than 95 mmol/L (reference range 98-108 mmol/L). Among both case patients and controls, the median (IQR) age was 65 years (IQR 51-76), and 44% were women. Hyponatremia was more common among case patients than among controls, as was hypokalemia and hypochloremia. Based on the results of the multivariate logistic regression, hyponatremia, and hypokalemia were associated with COVID-19 among case patients overall, with an adjusted odds ratio of 1.89 [95% CI 1.24-2.89] for hyponatremia and 1.76 [95% CI 1.20-2.60] for hypokalemia. Hyponatremia and hypokalemia are independently associated with COVID-19 infection in adults visiting the ED, and could act as surrogate biomarkers for the emergency physician in suspected COVID-19 patients.

Acute intermittent porphyria: A case report / [Porfiria intermitente aguda: reporte de caso].

The term 'porphyria' comes from the Greek 'porphyra'. It refers to a heterogeneous group of metabolic disorders caused by the enzymatic deficiency in the biosynthesis of the heme group. Acute intermittent porphyria is caused by a deficiency of the porphobilinogen deaminase enzyme. A 40-year-old woman presented with abdominal pain for ten days (which required laparotomy that evidenced no surgical pathology), severe hydroelectrolytic disorder due to hyponatremia and resistant hypokalemia, persistent tachycardia and hypertension. Seven days later, she developed acute flabby quadriparesis and presented a single generalized tonic-clonic convulsive crisis. Neurophysiological studies supported mixed axonal polyneuropathy and urine results of porphobilinogen and porphyrins were elevated. After acute intermittent porphyria was diagnosed, hemin was administered, which stabilized the patient's clinical signs and normalized the porphobilinogen. The prevalence of this entity is 1 in 2,000 people. It is an autosomal dominant disease, which affects mainly women between 20 and 40 years of age. This entity manifests with neurological and visceral symptoms. Management consists of hematin and dextrose administration avoiding hypotonic solutions because of the risk of exacerbating hyponatremia.

El término 'porfiria' proviene del griego 'porphyra' y alude a un grupo heterogéneo de trastornos metabólicos causados por una deficiencia enzimática en la biosíntesis del grupo hemo. La causa de la porfiria intermitente aguda es la deficiencia de la enzima deaminasa del porfobilinógeno. Se presenta el caso de una mujer de 40 años que presentó dolor abdominal de 10 días de evolución, trastorno hidroelectrolítico grave debido a hiponatremia e hipopotasemia, taquicardia e hipertensión arterial sistémica persistentes, por lo cual fue sometida a una laparotomía en la que no se encontró ninguna afección de origen quirúrgico, A los siete días del examen inicial, la paciente desarrolló cuadriparesia flácida aguda y presentó una crisis convulsiva tónico-clónica generalizada. Los estudios neurofisiológicos evidenciaron una polineuropatía axonal mixta, y los valores de porfobilinógeno y porfirinas en orina eran elevados. Tras diagnosticarse porfiria intermitente aguda, esta se trató con hemina, lo que estabilizó los signos clínicos y normalizó el porfobilinógeno. La prevalencia de esta enfermedad es de 1 en 2.000 personas. Tiene un patrón de herencia autosómico dominante y se manifiesta principalmente en mujeres con edades entre los 20 y los 40 años. La enfermedad cursa con síntomas neurológicos y viscerales, y se trata con la administración de hemina y dextrosa, evitando las soluciones hipotónicas por el riesgo de exacerbar la hiponatremia.

COVID-19 and the burning issue of drug interaction: never forget the ECG.

The coronavirus disease of 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), has been rapidly escalating, becoming a relevant threat to global health. Being a recent virus outbreak, there are still no available therapeutic regimens that have been approved in large randomised trials and so patients are currently being treated with multiple drugs. This raises concerns regarding drug interaction and their implication in arrhythmic burden. In fact, two of the actually used drugs against SARS-CoV2, such as chloroquine and the combination lopinavir/ritonavir, might determine a QT (the time from the start of the Q wave to the end of the T wave) interval prolongation and they show several interactions with antiarrhythmic drugs and antipsychotic medications, making them prone to an increased risk of developing arrhythmias. This brief review focuses the attention on the most relevant drug interactions involving the currently used COVID-19 medications and their possible association with cardiac rhythm disorders, taking into account also pre-existing condition and precipitating factors that might additionally increase this risk. Furthermore, based on the available evidence and based on the knowledge of drug interaction, we propose a quick and simple algorithm that might help both cardiologists and non-cardiologists in the management of the arrhythmic risk before and during the treatment with the specific drugs used against SARS-CoV2.

Renal complications in COVID-19: a systematic review and meta-analysis.

PURPOSE: Emerging data suggest that coronavirus disease 2019 (COVID-19) has extrapulmonary manifestations but its renal manifestations are not clearly defined. We aimed to evaluate renal complications of COVID-19 and their incidence using a systematic meta-analysis. DESIGN: Observational studies reporting renal complications in COVID-19 patients were sought from MEDLINE, Embase and the Cochrane Library from 2019 to June 2020. The nine-star Newcastle-Ottawa Scale was used to evaluate methodological quality. Incidence with 95% confidence intervals (CIs) were pooled using random-effects models. RESULTS: We included 22 observational cohort studies comprising of 17,391 COVID-19 patients. Quality scores of studies ranged from 4 to 6. The pooled prevalence of pre-existing chronic kidney disease (CKD) and end-stage kidney disease was 5.2% (2.8-8.1) and 2.3% (1.8-2.8), respectively. The pooled incidence over follow-up of 2-28 days was 12.5% (10.1-15.0) for electrolyte disturbance (e.g. hyperkalaemia), 11.0% (7.4-15.1) for acute kidney injury (AKI) and 6.8% (1.0-17.0) for renal replacement therapy (RRT). In subgroup analyses, there was a higher incidence of AKI in US populations and groups with higher prevalence of pre-existing CKD. CONCLUSIONS: Frequent renal complications reported among hospitalized COVID-19 patients are electrolyte disturbance, AKI and RRT. Aggressive monitoring and management of these renal complications may help in the prediction of favourable outcomes. Systematic review registration: PROSPERO 2020: CRD42020186873 KEY MESSAGES COVID-19 affects multiple organs apart from the respiratory system; however, its renal manifestations are not clearly defined. In this systematic meta-analysis of 22 observational cohort studies, the prevalence of pre-existing chronic kidney disease (CKD) in COVID-19 patients was 5.2%. The most frequent renal complication was electrolyte disturbance (particularly hyperkalaemia) with an incidence of 12.5% followed by acute kidney injury (AKI) with an incidence of 11.0%; US populations and groups with higher prevalence of CKD had higher incidence of AKI.

New onset acute symptomatic seizure and risk factors in coronavirus disease 2019: A retrospective multicenter study.

Our aim was to clarify the incidence and risk of acute symptomatic seizures in people with coronavirus disease 2019 (COVID-19). This multicenter retrospective study enrolled people with COVID-19 from January 18 to February 18, 2020 at 42 government-designated hospitals in Hubei province, the epicenter of the epidemic in China; Sichuan province; and Chongqing municipality. Data were collected from medical records by 11 neurologists using a standard case report form. A total of 304 people were enrolled, of whom 108 had a severe condition. None in this cohort had a known history of epilepsy. Neither acute symptomatic seizures nor status epilepticus was observed. Two people had seizurelike symptoms during hospitalization due to acute stress reaction and hypocalcemia, and 84 (27%) had brain insults or metabolic imbalances during the disease course known to increase the risk of seizures. There was no evidence suggesting an additional risk of acute symptomatic seizures in people with COVID-19. Neither the virus nor potential risk factors for seizures seem to be significant risks for the occurrence of acute symptomatic seizures in COVID-19.

Incidental COVID-19 in a heart-kidney transplant recipient with malnutrition and recurrent infections: Implications for the SARS-CoV-2 immune response.

The clinical course and outcomes of immunocompromised patients, such as transplant recipients, with COVID-19 remain unclear. It has been postulated that a substantial portion of the disease burden seems to be mediated by the host immune activation to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, we present a simultaneous heart-kidney transplant (SHKT) recipient who was hospitalized for the management of respiratory failure from volume overload complicated by failure to thrive, multiple opportunistic infections, and open non-healing wounds in the setting of worsening renal dysfunction weeks prior to the first case of SARS-CoV-2 being detected in the state of Connecticut. After his third endotracheal intubation, routine nucleic acid testing (NAT) for SARS-CoV-2, in anticipation of a planned tracheostomy, was positive. His hemodynamics, respiratory status, and ventilator requirements remained stable without any worsening for 4 weeks until he had a negative NAT test. It is possible that the immunocompromised status of our patient may have prevented significant immune activation leading up to clinically significant cytokine storm that could have resulted in acute respiratory distress syndrome and multisystem organ failure.