INTRODUCTION: Cardiorespiratory disorders usually present with acute respiratory distress; likewise, ureteral rupture usually presents as an acute abdomen [1]. We report a case of ureteral rupture presenting with acute respiratory distress leading to a delayed diagnosis.CASE PRESENTATION: An 82 y/o M with a history of congestive heart failure (CHF), chronic obstructive pulmonary disease, chronic renal failure and recently diagnosed COVID -19 pneumonia, was admitted for progressive dyspnea and abdominal discomfort for 2 days. Arterial blood gas showed hypercapnic hypoxic respiratory failure. Chest computed tomographic (CT) scan without contrast showed moderate right-sided pleural effusion but pulmonary embolism (PE) could not be ruled out. He also had a left leg deep venous thrombosis with worsening renal function and B-type natriuretic peptide (BNP) of 139pg/ml.His symptoms were thought to be due to acute decompensated CHF, COVID-19 pneumonia and possible PE. He failed to improve with intravenous furosemide, bilevel positive airway pressure ventilation and empiric anticoagulation. Due to worsening renal function and abdominal pain, an abdominal CT was done which showed right ureteral rupture with retroperitoneal collection and multiple non-obstructing renal calculi. The patient had placement of a double J stent with prompt resolution of respiratory distress.DISCUSSION: There are very few case reports of ureteral rupture occurring spontaneously and causing marked dyspnea. Respiratory distress may occur if the extravasated urine leads to an urinothorax or abdominal compartment syndrome [1]. Suspicion of non-cardiorespiratory causes of acute dyspnea in patients with underlying congestive heart failure includes respiratory distress disproportionate to the size of pleural effusion, unilateral effusions or effusions of markedly disparate size, absence of pulmonary vascular congestion and cardiomegaly, worsening renal function, ascites, urinary retention or anuria, abdominal pain, failure of the effusion to respond to management of heart failure, fever or pleuritic chest pain, and low or nearnormal natriuretic peptides [2,3].When there are concerns for non-cardiorespiratory causes of respiratory distress, the diagnosis can be made with thoracentesis and imaging such as abdominal ultrasound, or CT [2].CONCLUSIONS: This case illustrates a rare presentation of ureteral rupture causing respiratory distress and the key points that should elicit high clinical suspicion for non-cardiorespiratory causes of acute respiratory distress. When these findings are present, appropriate investigations and urgent intervention may be life-saving.

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.

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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.