The novel COVID-19 virus has been found to be associated in a wide variety of complications most commonly involving the lungs namely by pneumonia with resultant ARDS. We present a case of COVID19 related extensive pulmonary emboli. CASE PRESENTATION: A previously well 47-year-old male presented with an 8 day history of fever, cough & dyspnea. He tested positive for COVID-19 as an outpatient. Four days later, he developed left sided pleuritic chest pain & presented to hospital. On examination, blood pressure was 119/89mmHg, HR 124beats/min & RR 44breaths/min. Despite this, he was saturating 93% on room air. On examination, he had diminished breath sounds and faint crackles bilaterally. Significant laboratory investigations revealed, leucocytosis of 18 (4.00-11.00 K/ul), troponin of 3.13 (0.00-0.03ng/ml), C-reactive protein was 236 (<10mg/l) , Ddimer was >20 UG/ml FEU (0.00-0.04 ug/ml) and BNP of < 5 (0-100pg/ml). Electrocardiogram revealed sinus tachycardia with no ST segment changes. Plain chest radiograph had subsegmental airspace disease in the left lower lobe. CT pulmonary angiography revealed a saddle pulmonary embolus with filling defects throughout right upper middle and lower lobe and left upper and lower lobe pulmonary arteries, and evidence of right heart strain. There were airspace opacities in the left and right lungs. A transthoracic echocardiogram study confirmed right heart strain. He underwent emergent catheter directed thrombolysis and was placed on heparin infusion. Two days later, an IVC filter was placed. He was discharged on day 7 with a six month course apixaban. He received five days of hydroxychloroquine, thiamine, vitamin C and zinc. He was also given 5 days of ceftriaxone. At 2 month follow up, he continues to do well and no longer has any respiratory symptoms or further hypoxia
INTRODUCTION: Severe Gestational Hypertriglyceridemia (HTG) is a rare but potentially life-threatening condition, which can lead to devastating complications, including acute pancreatitis (AP), hyperviscosity syndrome, preeclampsia, maternal & fetal morbidity & mortality. CASE PRESENTATION:A 33-year-old female G3P1þ1 at 37-week gestation, presented with acute abdominal pain nausea & vomiting. She admitted consuming a high fat high carb diet for a few weeks before presentation. Family history significant for her mother was diagnosed with familial Chylomirconemia & AP in pregnancy due to HTG. On presentation her vital signs were stable, physical exam consistent with early labor & negative for eruptive xanthomas. Labs showed Lipase 1,106 U/L, Amylase 750 U/L, TG 5,531 mg/dl, Cholesterol 702 mg/dl, ALP 163 U/L & glucose 82 mg/dl. She underwent C-section after which she was admitted to ICU for treatment of AP with aggressive fluid resuscitation, insulin drip with dextrose infusion & Gemfibrozil. Abdominal US revealed no biliary stones with CT abdomen revealing edematous pancreas & a region of hypoattenuation suspicious for necrotizing pancreatitis & was started on IV antibiotics. Insulin Drip was stopped once TG were less than 700 mg/ dl & symptoms resolved. She was discharged on Gemfibrozil & fish Oil.DISCUSSION: Plasma TG level normally increases 2-4 folds in pregnancy secondary to hormonally driven changes in the liver & adipose tissue with the most profound increase in the 3rd trimester as high estrogen enhances hepatic TG synthesis. Concomitantly, insulin resistance caused by human placental lactogen decreases lipoprotein lipase activity which increases adipose tissue lipolysis & free fatty acids needed for TG synthesis(1). Gestational HTG is defined as fasting plasma TG level above the age-adjusted 95th percentile for the non-pregnant population. Severe HTG defined as TG levels greater than 1000 mg/dl as it's associated with an increased risk of AP which represents a diagnostic challenge in pregnancy due to nonspecific presentation & imaging limitation(1,2). Severe Gestational HTG is typically seen in patients with underlying genetic abnormalities in TG metabolism which most likely what our patient has given her family history & poorly controlled diabetes considered the most common secondary risk factor(1). Insulin infusion is used to treat severe HTG if associated with AP or hyperglycemia. Low fat diet remains the cornerstone of maintenance management with oral administration of medium chain fatty acid or omega-3 acid ethyl esters has become part of management. Though safety for fibrates has not been well established yet; they may still be used in the later stages of gestation when benefits outweigh the risks(1,2). CONCLUSIONS:Severe gestational HTG is a rare but serious condition that can cause AP which can be challenging to diagnose & treat in pregnancy.
INTRODUCTION: Noncardiogenic pulmonary edema from naloxone is a rare adverse effect; but even more uncommon is the development of Takotsubo Cardiomyopathy (TCM).CASE PRESENTATION: A 75-year-old woman with a history of breast cancer s/p bilateral mastectomy & post-herpetic neuralgia on chronic opioids, presented with clostridium colitis. On day 3 of admission, she was noted to have decreased responsiveness, pinpoint pupils & an empty bottle of Hydrocodone/acetaminophen was found at bedside. She was given IV naloxone 0.4mg. Two hours after naloxone admission, RR 32, HR 115 bpm, BP 133/86mmHg, SpO2 97% on RA. Physical exam revealed normal pupils, hyperdynamic apex with no murmurs, basilar crackles throughout, BNP 1,170 pg/ml (normal 0-100PG/ ML). EKG sinus tachycardia, CXR showed pulmonary edema and ABG 7.49/<16.1/65.8/CNC. She was initiated on BIPAP but subsequently intubated due to continued respiratory distress. She remained intubated for 2 days where she received IV Lasix with improvement of pulmonary congestion. ECHO showed LVEF 20-25 % with mid-ventricle extending to apex is akinetic in a circumferential pattern, sparing the base which was hyperdynamic, consistent with TCM. Cardiac catherization showed 30% occlusion of mid-LAD & 20% occlusion of mid LCX with severely elevated LVEDP 34mmhg with wall motion abnormality consistent with TCM. She was discharged on daily metoprolol 25mg, losartan 25 mg, ASA 81 mg & lasix 20mg.DISCUSSION: Though undoubtedly an important tool in addressing the magnitude of opioid overdose cases both in & outside of hospitals, naloxone is not without its own concerns; many of which are related to the heart. It has been demonstrated in animal & human models that naloxone induces catecholamine release which has direct positive inotropic effects on the heart (2). It reverses the usual inhibitory effects that endogenous opioids have in regulating catecholamine release in peripheral sympathetic nerves & adrenal medullae(2). This mechanism results in hypertension including at the level of the pulmonary vasculature leading to pulmonary vasoconstriction & increased capillary permeability, (1) decreased gaseous exchange and subsequent translocation of fluid into the alveoli. This results in the pulmonary edema as well as the resultant hypoxia with eventual acute hypoxic respiratory failure.Similarly, it is plausible that this same mechanism of acute surge in plasma catecholamine levels leads to direct toxicity on cardiomyocytes. Acute catecholamine surge is purported to result in stunning of the myocardium leading to characteristic changes noted in TCM. The findings of TCM are transient and are the main distinguishing feature of this condition from other cardiomyopathies.
Introduction: Primary hyperparathyroidism (PHPT) is rarely diagnosed in pregnancy and if left untreated has the potential to lead to serious maternal and neonatal complications. We describe a case of PHPT with associated complicated pre-eclampsia. Clinical Case29-year-old primigravida admitted at 33 + 6 weeks with fatigue, 10lbs weight gain and elevated BP. Labs revealed potassium 2.9 (3.5-5.2mmol/L), corrected serum calcium (Ca)11.62 (8.4-10.2mg/dL), ionized calcium 1.69 (1.15-1.33mmol/L), PTH 163.9 (15-65pg/mL) and vitamin D 24.6 (30-100ng/mL). Other labs were normal. Urine studies showed 315mg/24h proteinuria and urine calcium of 129.5 mg/24hrs (100-300mg/24hrs). She was started on magnesium sulphate along with labetalol for BP control, given betamethasone for stimulation of fetal lung maturity as well as potassium repletion. Hypercalcemia (HCa) was initially managed with fluids and Lasix intravenously. At 34 + 2 weeks she developed SOB, orthopnea, headaches with new 9lbs weight gain over 5 days and sustained BP elevation. Urgent C-section was done for pre-eclampsia with severe features. Post-operatively, she suffered from postpartum hemorrhage, managed with transfusion of packed red cells and transient placement of a Bakri balloon. Her HCa worsened with Ca 12.56 and cinacalcet was started after delivery. This coincided with gradual improvement of her BP and Ca to 10.8. She declined additional work-up and was discharged in stable condition. Clinical LessonPHPT often goes undiagnosed in pregnancy, with symptoms of fatigue and constipation mimicking common complaints of pregnancy. Studies have also suggested that up to 25% of patients with PHPT during pregnancy present with hypertension and pre-eclampsia and that there is an association between preeclampsia and the presence of parathyroid adenomas. The pathophysiology is unclear but is thought to be due to endothelial dysfunction triggered by hypercalcemia as well as abnormal placentation. No clear guidelines exist for the management of PHPT during pregnancy, with observation and rehydration being the preferred initial options. The use of cinacalcet as well as curative surgical parathyroidectomy when Ca levels persist >11 in the second trimester have also been described. Our patient presented similarly, with severe pre-eclampsia needing urgent C-section, further complicated by persistent severe HCa. Early diagnosis of PHPT, along with treatment including cinacalcet improved her Ca. It is therefore important that PHPT be considered in patients presenting like ours, progressing to severe pre-eclampsia as early reduction of serum calcium may reduce morbidity and mortality. ReferencesMcCarthy, A., Howarth, S., Khoo, S., Hale, J., Oddy, S., Halsall, D., ... & Samyraju, M. (2019). Management of primary hyperparathyroidism in pregnancy: a case series. Endocrinology, diabetes & metabolism case reports, 2019(1).
INTRODUCTION: Corona Virus Disease (COVID-19) main presenting feature is hypoxia which coincidentally is a feature of Pulmonary Embolism (PE) that can be life-threatening if not diagnosed early. COVID-19 causes excessive inflammation that can induce expression tissue factors, which is a major coagulation activator1,2. Therefore, PE should also be a consideration for those presenting with COVID-19 with worsening hypoxia. CASE PRESENTATION: 79-year-old a man with non-ischemic cardiomyopathy with Ejection Fraction (EF) 45-50% presented with worsening shortness of breath, dry cough, and bilateral lower limb edema for 2 weeks. On presentation, he was afebrile normotensive with tachypnea, tachycardia, and hypoxia. On physical examination, he was in respiratory distress with faint bilateral crackles and bilateral lower limb edema. Lab Investigations showed elevated Brain Natriuretic Peptide to 1830 pg/ml (normal range 0-100 PG/ml), troponin level to 6.89 ng/ml (normal range 0.00-0.03 ng/ml) and the D-dimer level was >20.00 UG/ ml FEU (normal range 0.00-0.40 UG/ml FEU). Viral PCR confirmed COVID-19. No ischemic changes noted in EKG. Echocardiography (Echo) revealed EF (Ejection Fraction) at 10-15%, dilated right ventricle with reduced function, and left ventricular thrombus. In CT chest with contrast noted to have acute segmental right middle lobe pulmonary arterial embolus. He was therapeutically anti-coagulated with enoxaparin. He received antibiotics, systemic steroids, and diuresis On day 3 of admission, he had worsening hypoxia and dyspnea while on 100% oxygen therapy. The patient opted for no escalation in care with ventilation or resuscitation. As he had no clinical improvement, the family agreed on comfort care. He died on day 5 of admission. No relevant relationships by Fausto Lisung, source¼Web Response No relevant relationships by Rani Sittol, source¼Web Response
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