ABSTRACT
Background: An emerging finding about COVID-19 is its effect on nutrition and weight loss. The COVID-19 symptoms of fatigue, altered taste or smell, and lack of appetite are well known. But COVID-19 may have a more profound effect on clinical nutrition status. Two recent studies have identified that approximately one-third of ambulatory COVID-19 patients are at risk of experiencing weight loss >= 5% (Anker, et al;di Filippo, et al). The case study presented here discusses home start total parenteral nutrition (TPN) in a patient recently diagnosed with COVID-19 at high risk for refeeding syndrome. Method(s): N/A Results: Case Study: A 92-year-old patient was diagnosed with COVID-19 on June 8, 2022. Over the next week, she was hospitalized twice to manage symptoms of acute mental status changes, lethargy, aphasia, hypotension, and loss of appetite. The patient received nirmatrelvir/ritonavir, remdesivir, and bebtelovimab to treat COVID-19 at different times between June 9, 2022, and June 18, 2022. She remained COVID positive and continued to deteriorate clinically. On June 20, 2022, the patient began receiving 24/7 homecare, including intravenous (IV) fluids of dextrose 5% in normal saline (D5NS) 1000 mL daily for three days. She continued to experience loss of appetite and had no bowel movement for 3 days. On June 23, 2022, she was referred to this specialty infusion provider to initiate TPN therapy in the home setting. The patient's BMI was 18.2 kg/m2. Lab results revealed potassium 3.0 mmol/L, phosphate 1.6 mg/dL, and magnesium 1.6 mg/dL. High risk of refeeding syndrome was identified by the level of hypophosphatemia and hypokalemia. The specialty infusion provider's registered dietitian recommended to discontinue D5NS and begin NS with added potassium, phosphate, and magnesium. Thiamine 200mg daily was added to prevent Wernicke's encephalopathy. The patient's clinical status and lab values were monitored closely each day until her electrolyte levels stabilized (Table 1). Home TPN therapy was initiated on June 28, 2022, with <10% dextrose and 50% calorie requirement with 85% protein and 1.0 g/kg lipids. Three-day calorie count and nutrition education were performed four days post TPN initiation. Oral intake met only 25% of estimated needs. Over several days, theTPN formula was gradually increased to goal calories and the infusion cycle was slowly decreased. The following week, the patient's oral intake improved to 60%-75% of estimated needs. Her constipation resolved, and she showed improvement in functional status and mobility. Her appetite drastically improved when the TPN was cycled. Another three-day calorie count was performed when TPN calories reached goals. Oral intake demonstrated 100% estimated calorie and protein needs. TPN therapy was ultimately discontinued on July 14, 2022. As of September 30, 2022, the patient has stabilized at her pre-COVID weight of 45 kg with full recovery of appetite, function, and cognition. Discussion(s): The ASPEN Consensus Recommendations for Refeeding Syndrome (da Silva, et al) describe the repletion of electrolyte levels before introducing calories to prevent end-organ damage associated with refeeding syndrome (respiratory muscle dysfunction, decreased cardiac contractility, cardiac arrhythmias, and encephalopathy). Conclusion(s): This case study highlights the successful initiation of home TPN therapy in a patient at high risk of refeeding syndrome post COVID-19 infection. Although home start TPN and the risk of refeeding syndrome are not new concepts, they must be considered in the setting of COVID-19. Given the effects COVID-19 has on taste, smell, and appetite and the recent finding that one-third of patients with COVID infection may experience weight loss of >= 5%, nutrition support and patient education are vital components of overall patient care. (Figure Presented).
ABSTRACT
Case Presentation: Term male infant born to SARS-CoV-2 positive mother with infant testing negative. ECG for perinatal bradycardia revealed ventricular pre-excitation. Echocardiogram showed asymmetric LV hypertrophy with prominent trabeculations, subaortic narrowing with no pressure gradient, and normal biventricular systolic function. Rapid increase in RV pressure estimates and NT-proBNP in first week if life concerning for diastolic dysfunction. Anti-arrhythmic therapy initiated for SVT with subsequent resolution. Later, developed progressive LV dilation and systolic dysfunction. Myocardium showed regions resembling non-compaction and others concerning for infiltrative process. Cardiac MRI showed no obvious tumors, but rhabdomyomas could not be ruled out given similar appearance to myocardium. Due to worsening heart failure, everolimus therapy initiated to target potential rhabdomyomas while awaiting genetic testing for tuberous sclerosis. Subaortic narrowing and LV hypertrophy improved within days, and LV appearance became more consistent with non-compaction. Genetic testing revealed a TSC2 gene variant consistent with tuberous sclerosis. Systolic function improved, and patient discharged on afterload reduction. Echocardiogram 6 months post-discharge shows continued LV dilation and mild systolic dysfunction. Discussion(s): Although outflow obstruction and arrhythmias are common with cardiac rhabdomyomas and can cause dysfunction, our patient developed progressive dysfunction in the absence of outflow tract gradient or prolonged arrhythmia. As rhabdomyomas subsided, it became clearer that he had an underlying cardiomyopathy. We suspect that rhabdomyomas in the setting of abnormal myocardium led to abnormalities in myocardial contractility and compliance causing combined systolic and diastolic dysfunction. After complete resolution of rhabdomyomas, cardiac function has improved. However, he continues to have ventricular dilation and mild dysfunction attributable to cardiomyopathy. It is unlikely that mother's SARS-CoV-2 infection played a role as infant tested negative and clinical picture was not consistent with myocarditis.
ABSTRACT
CASE: An 84-year-old woman with atrial fibrillation on Digoxin presented with acute onset of confusion associated with a week history of abdominal pain, vomiting, and poor fluid intake. A few days prior, Amiodarone was added to her drug regimen which included Lasix. Additionally, she received the COVID-19 booster vaccine which led to a viral-like syndrome resulting in dehydration. The patient was afebrile, normotensive, but bradycardic. EKG showed a prolonged PR interval and scooped ST segments. Labs showed hyperkalemia, pre-renal acute kidney injury (AKI), and a Digoxin level of 4.3 ng/mL (therapeutic range: 0.8-2.0 ng/mL). Digoxin and Lasix were held and Digoxin antidote, Digibind, was administered with normalizing heart rate, potassium, and clinical improvement. IMPACT/DISCUSSION: Digoxin is used to slow conduction in atrial fibrillation and increase cardiac contractility in heart failure. It inhibits the membrane sodium-potassium-adenosine triphosphatase pump (Na/K ATPase), resulting in increased cytosolic calcium and subsequent cardiac contractility and automaticity. In turn, this can also cause premature ventricular contractions and tachycardia. In the carotid sinus, increased baroreceptor firing and subsequent increased vagal tone occurs which can cause bradycardia, atrioventricular blocks, hypotension, and GI symptoms. In skeletal muscle, hyperkalemia can result due to the abundance of Na/K ATPase pumps. Digoxin has a narrow therapeutic index with serum levels easily affected by many commonly prescribed drugs by way of decreasing renal clearance, inhibiting P-glycoprotein, and inducing secondary electrolyte disturbances. That said, drug dosing should be individualized with close monitoring to avoid potentially life-threatening effects that may result with even mildly increased digoxin levels. Acute toxicity manifests as non-specific GI, and neurologic symptoms (confusion, lethargy, visual changes), hyperkalemia, and brady or tachy-arrhythmias. Treatment is with digoxin specific fragment antigen binding (Fab) antibody, Digibind, which binds digoxin, inactivating it within 6-8 hours. Postadministration, digoxin serum testing cannot distinguish free verse bound drug;therefore, drug levels remain elevated for days to weeks until the FabDigoxin complex is excreted. In the case above, the viral-like-syndrome after the booster vaccine with subsequent AKI secondary to dehydration likely precipitated Digoxin toxicity. Accompanying drug interactions of diuretics causing dehydration and hypokalemia, P-glycoprotein inhibitors (Amiodarone, Verapamil, Diltiazem, Quinidine), and ACE inhibitors can further worsen renal clearance and culminate in Digoxin toxicity. CONCLUSION: Given Digoxin's narrow therapeutic index, small clinical changes such as post COVID-19 vaccine flu-like symptoms, dehydration, and medication changes can manifest drug toxicity. Therefore, attentive monitoring of accompanying comorbidities and drug interactions is imperative at preventing catastrophic toxic effects.
ABSTRACT
Introduction: Multisystem inflammatory syndrome in children (MISC), or paediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 (PIMS-TS), is a newly described pediatric syndrome, partially overlapping with Kawasaki Disease (KD) and Macrophage Activation Syndrome. According to the literature, MIS-C requires ICU admission in 73,3% of cases, with 1.9% overall mortality. Patients may develop coronary artery anomalies (CAA), either dilatations (11,6%) or aneurysms (10,3%). Most physicians have been treating MIS-C like KD, so far. Conversely, based on our experience, since April 2020 we have been treating MIS-C patients with IV methylprednisolone (MP) as a first-tier monotherapy: herein, we present the outcome of the first 23 consecutive patients treated according to our treatment protocol. Objectives: To evaluate the outcome (ICU admission, inotropic support, coronary abnormalities) of a cohort of consecutive MIS-C patients treated with MP as first-line monotherapy. Methods: Patients satisfying the WHO preliminary case definition of MIS-C, with no need of inotropic support at admission, have been treated with fluid restriction and MP monotherapy, the dose depending on the presence/absence of myocardial involvement: if hypotension according to age, gender, and height adjusted chart, or Ejection Fraction (EF) <50%, or NT-proBNP ≥1500 pg/ml are present, the patient receives high-dose pulse IV MP 10 mg/ Kg/day for 3-5 days, otherwise low dose IV MP 2 mg/Kg/day is administered. After 48 hours, if CRP increases and/or fever persists, the treatment is intensified either with a MP dose increase or with subcutaneous Anakinra 5 mg/ Kg/day. IVIG is reserved for patients with suspected CAA at any ultrasound evaluation (defined according to American Heart Association 2017 Guidelines for KD), or presenting persistent symptoms despite defervescence and CRP reduction. We retrospectively collected and analyzed clinical data of a cohort of consecutive MIS-C patients treated with MP mono-therapy between the 1st of April and the 31st of January 2021, at Regina Margherita Children Hospital (Turin, Italy). Clinical data were retrospectively collected;as primary outcomes we considered: rate of ICU admission, rate of inotropic support need, and incidence of CAA. As secondary outcomes we evaluated: CRP halving time, MP and NT-proBNP halving time, and days between first pathological echocardiogram and EF normalization. Results: Twenty-three MIS-C patients were included. 18 patients (78,3%) showed myocardial involvement and were treated with highdose pulse MP (Group A), 4 needed anakinra due to persistent fever. 5 patients with no cardiac damage (21,7%) were treated with low dose MP (Group B), in 2 of these (40,0%) MP dose was intensified due to persistent fever. All of the patients recovered;1 (4.3%) needed ICU admission with inotropic support, 1 developed a CAA six days after MP start. Median CRP halving time was 2 days (2 days in Group A and 5 days in Group B), NT-pro-BNP halved in 3 days in Group A, while EF normalized in 4.5 days. One patient needed ICU admission and inotropic support (4.3%), 1 patient of group A developed a small coronary aneurysm (5 mm, z score 4). Conclusion: Despite some limitations, including the sample size and the absence of a control group treated with IVIG, our data suggest that early administration of MP together with fluid restriction can rapidly decrease the inflammation and restore myocardial contractility in MIS-C, considerably reducing the need of ICU admission and/or inotropic support. Encouragingly enough, the incidence of CAA in our cohort is low compared to published cohorts (4.3% vs 20%). Further studies in bigger cohorts are needed to confirm our findings.