Amantadine-Induced Cardiac Arrest in a Patient With COVID-19.

Amantadine, which is known for its antiviral activity, is presently used as therapy for Parkinson's disease. Adverse effects, such as cardiac arrhythmias, have been described in patients after ingestion of amantadine. Here, we present a patient who suffered a cardiac arrest following ingestion of a low dose of amantadine. A 71-year-old man was admitted to the emergency department for a witnessed cardiac arrest. He had developed an upper respiratory tract infection the preceding week and was prescribed 100 mg of amantadine. Within half an hour of taking the first dose, the patient collapsed. He was found to be in asystole by emergency medical services, and advanced cardiac life support protocols were initiated, including cardiopulmonary resuscitation and intubation for airway protection. However, he sustained multiple recurrences of cardiac arrest, and despite all resuscitation efforts, the patient expired.

Double Valve Infective Endocarditis Complicated by Systemic Arterial Embolization.

A 26-year-old male with a past medical history of intravenous opioid abuse was admitted with the diagnosis of double valve infective endocarditis and methicillin-resistant Staphylococcus aureus bacteremia. Imaging, excluding the head, was indicative of systemic arterial embolization, as abscesses had developed in the retroperitoneum and prostate. There was evidence of splenic infarct, and the presence of extensive pulmonary infiltrates indicative of showering septic foci from the heart. Antibiotic therapy was started and a transesophageal echocardiogram demonstrated mitral and tricuspid valve vegetations with a preserved ejection fraction. Fortunately, the valvular repair was successful and artificial valves were not needed. The patient had an uncomplicated postoperative course in the intensive care unit and was transferred back to the ward in stable condition. He remained on the ward for six weeks due to his unfunded status until his antibiotic course and physical rehabilitation were completed.

Heroin Relapse "Strikes a Nerve": A Rare Case of Drug-Induced Acute Myelopathy.

Opioid addiction is a major public health problem. Through a commitment to individualized treatment plans meant to help patients meet personal goals, behavioral therapy can encourage abstinence and help prevent relapses that can have debilitating consequences. This case describes a 31-year-old male with heroin relapse who presented with flaccid quadriparesis as well as loss of sensation below the T2-3 spinal level, loss of rectal tone, and urinary retention. A urine drug screen (UDS) was positive for opiates and amphetamines. Autoimmune serologies were negative. Cerebrospinal fluid (CSF) analysis was negative for any acute ongoing infectious process. Magnetic resonance imaging (MRIs) of the cervical and thoracic spine showed increased intramedullary signals with spinal cord expansion from C2-T2, indicating acute transverse myelitis. Upon completion of the aforementioned work-up, idiopathic transverse myelopathy (TM) was diagnosed, and the patient was started on intravenous (IV) methylprednisolone; he also received five sessions of plasmapheresis. By process of elimination, suspicion remained of a diagnosis of opioid-induced myelopathy. The patient showed mild improvement in his original sensory deficits and flaccid quadriplegia.

What Is Uncommon Can Be Critical: A Case of Quinolone-Induced Acute Liver Failure.

Many drugs are known to potentially cause liver injury; however, only a few reports investigate the association between levofloxacin and acute liver failure (ALF).  The case describes a 65-year-old man who was admitted with primary diagnoses of cerebrovascular accident (CVA) and acute coronary syndrome (ACS) who developed an upper respiratory tract infection for which he was started on levofloxacin. Following its administration, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increased more than 100-fold above the upper limit of normal. Over the next 24 hours, AST peaked at 9334 U/L, ALT at 4525 U/L, prothrombin time to 24.6 seconds, international normalized ratio (INR) to 2.22, and serum ammonia to 157 µmol/L. The patient developed signs and symptoms of decompensated liver disease, namely hepatic encephalopathy (HE). Levofloxacin was discontinued immediately, and evidence-based treatment per society guidelines from The American Association for the Study of Liver Diseases consisting of IV n-acetylcysteine as well as lactulose and rifaximin was initiated. Such medical management resulted in clinical resolution of his ALF, but he had a poor overall prognosis and eventually succumbed to critical illness.

More than Meets the Eye: Aspergillus-Related Orbital Apex Syndrome.

The patient is a 67-year-old Caucasian male with a past medical history of diabetes mellitus type 2, coronary artery disease (CAD) status post stent placement, renal cell carcinoma (RCC) status post left nephrectomy and bilateral adrenalectomy secondary to metastatic disease, and aspergillus pneumonia who was transferred from an outside hospital for evaluation of progressively worsening pulsating right temple and retrobulbar headache. Initial studies ruled out glaucoma, giant cell arteritis, and stroke, or aneurysmal pathology. The only positive finding was right sphenoid sinus disease on imaging that had caused bony destruction and infiltration of the right orbital apex. Broad-spectrum antibiotics were started for bacterial versus fungal sinusitis and the patient was admitted to the medical floor with consultations to Neurology, Otolaryngology (ENT), and Ophthalmology. ENT took the patient emergently to the OR. The final diagnosis was chronic aspergillus sinusitis and right-sided orbital apex syndrome (OAS). Antibiotics and antifungals were optimized by the infectious disease team. ENT also ordered steroid washouts post-operatively with budesonide and saline as well as sinus debridements every couple of weeks.

Hypertension With Brachydactyly Syndrome: A Case Report.

We describe the case of a 23-year-old African American male who presented to the emergency department complaining of unremitting dyspepsia for the last four months. His blood pressure was incidentally found to be 230/157 mm Hg. The initial admitting diagnosis in the intensive care unit was hypertensive "emergency" as he had also displayed acute kidney injury that was deemed to be superimposed on chronic kidney disease. While the diagnostic work-up of his hypertension was inconclusive, physical examination was impressive for the presence of brachydactyly of the bilateral hands, especially the fourth digits. His feet appeared grossly normal. X-rays (XRs) of the bilateral hands revealed absent distal phalanges and fused middle and distal phalanges of the second digits. XRs of the bilateral feet showed similar findings in addition to the absence or hypoplasia of the lateral cuneiform bones. His family medical history was unknown as the patient was adopted and did not have contact with his biological parents. Given these findings in the setting of uncontrolled hypertension in a young adult, he was diagnosed with hypertension with brachydactyly syndrome.

An Asymptomatic Case of Radiologically Active Neurocysticercosis.

The case describes an 82-year-old right-handed Hispanic male with multiple chronic comorbidities complaining of upper and lower extremity weakness as well as paresthesias that had been worsening over the last two weeks. He had bilateral upper and lower extremity weakness that was worse on the right and he complained of not being able to walk on his own with several falls preceding admission because of this. There were no overt signs of spinal cord compression or cauda equina syndrome. Laboratory work-up was unremarkable with exception to mildly elevated acute phase reactants. Computed tomography (CT) and magnetic resonance (MR) imaging later showed critical cervical compressive myelopathy at the C3-C4 level and multiple parenchymal and extra-axial enhancing lesions in the frontal lobes with associated calcifications suspicious for neurocysticercosis. Antihelminthic therapy was started and the patient underwent spinal fusion surgery with neurosurgery with an uncomplicated post-operative course - also lacking seizure activity of any kind.

A Flare-up of Systemic Lupus Erythematosus with Unusual Enteric Predominance.

Enteritis associated with systemic lupus erythematosus (SLE) is a rare and unusual manifestation of the gastrointestinal (GI) consequences of SLE itself. Complications of the enteritis component include mesenteric vasculitis, intestinal pseudo-obstruction, and protein-losing enteropathy. Lupus enteritis is very responsive to treatment with pulse steroids in almost 70% of the patients, but it is critical to diagnose it early to prevent devastating organ damage. The case describes a 21-year-old Caucasian female with a past medical history of uncomplicated laparoscopic appendectomy (one month prior to the time of presentation), major depressive disorder, asthma, iron deficiency anemia, pelvic inflammatory disease secondary to sexually transmitted Chlamydia trachomatis infection, and SLE (diagnosed two weeks prior to presentation). She had been transferred from an outside facility with complaints of severe right upper quadrant (RUQ) abdominal pain for one day. The patient had run out of her prescription for steroids and hydroxychloroquine two days prior to the presentation. Her abdominal pain was accompanied by nausea, bilious vomiting, non-bloody diarrhea, a photosensitive facial rash, left-sided pressure-type periorbital headache, diplopia, oral ulcers, inappetence, joint stiffness, and muscle weakness. A CT of the abdomen and pelvis from an outside facility showed enteritis involving the proximal jejunum with associated mesenteric edema and ascites, suggesting infectious versus inflammatory or autoimmune etiology. A repeat CT scan a few days later confirmed these findings along with adjacent mesenteric fat stranding. Her autoimmune workup confirmed the serological diagnosis of SLE, and assessment of the SLE Disease Activity Index (SLEDAI) confirmed the diagnosis of a severe SLE flare. Upper endoscopy detected edematous mucosa in the duodenum and jejunum without active bleeding, gastropathy, or ulceration. No surgical intervention was required. Her symptoms resolved with supportive care, pulse steroids, and hydroxychloroquine. She was discharged with instructions for outpatient follow-up with gastroenterology and rheumatology.

Glycemic Disturbances in Pheochromocytoma and Paraganglioma.

In this review article, we aimed to analyze the available data on pheochromocytomas and paragangliomas as it pertains to their not as well-recognized association with significant glycemic abnormalities in the preoperative, perioperative, and postoperative settings as well as how they should be managed clinically. Pheochromocytomas are rare adrenal tumors that account for about 0.1% of hypertension. Paragangliomas, on the other hand, are even less common and have fewer clinical manifestations. Both types of tumors may have unusual modes of presentation which can challenge even the most experienced clinicians and are easy to overlook, resulting in post-mortem diagnosis. We wish to draw further attention to the life-threatening effects on glucose and insulin homeostasis that can occur in the form of hyperglycemic and hypoglycemic states. Hyperglycemia is a result of a glucose intolerant state created in the setting of catecholamine excess, which can present in the form of resistant diabetes, diabetic ketoacidosis (DKA), or even hyperglycemic hyperosmolar states (HHS). In many reported cases, these abnormalities resolve with resection of the tumor. However, past clinicians have also described a state of "reactive hypoglycemia" that can occur following tumor resection, further emphasizing the need for very close perioperative and postoperative monitoring. Severe hypoglycemia may also occur with inherited diseases linked to pheochromocytoma such as von Hippel-Lindau (VHL) disease as well as predominantly epinephrine-producing tumors, given some of the dramatic downstream effects of alpha and beta adrenoceptor agonization. While much of the data remains anecdotal, clinicians will benefit from the awareness of the protean manifestations of these tumors and the varied and lesser-known effects on glucose and insulin homeostasis.

Early Accreta and Uterine Rupture in the Second Trimester.

The differential diagnosis of third trimester bleeding can range from placenta abruptia to placenta previa to uterine rupture and the placenta accreta spectrum (PAS). However, patients with risk factors such as multiple cesarean sections (c-sections), advanced maternal age (AMA), grand multiparity, and single-layer uterine closure are at greater risk of developing these complications earlier than we would traditionally expect. This case recounts a 38-year-old gravida 6 preterm 3 term 1 abortus 1 live 4 (G6P3114) at 23 weeks and five days gestational age (GA) with a past medical history of preterm pregnancy, pre-eclampsia, chronic abruptia, three previous c-sections, and low-lying placenta who presented to the emergency department (ED) with vaginal bleeding. Initial workup revealed placenta accreta and possible percreta. The patient was placed on intramuscular (IM) corticosteroids in anticipation of preterm delivery. As soon as the patient was stable, she was discharged home. She presented to a different hospital the next day with the same complaints. Imaging was consistent with accreta and her presentation with abruption. During the hospital stay, the patient went into threatened preterm labor (PTL). At first, we suspected preterm premature rupture of membranes (PPROM) due to apparent pooling of amniotic fluid in the vaginal canal. Upon further work up, the diagnosis was consistent with chronic abruption oligohydramnios sequence (CAOS). Before this could be investigated, her hospital course was complicated by acute abruption and Category III/nonreassuring fetal heart rate (FHR) tracing. The patient underwent an emergency c-section at 26 weeks GA as well as a planned supracervical hysterectomy for desired permanent sterilization. During the operation, the patient suffered a postpartum hemorrhage (PPH) of 4500 mL. She was later discharged home on postoperative day (POD) eight.

Intracranial Atherosclerosis Versus Primary Angiitis of the Central Nervous System: a Case Report.

Primary angiitis of the central nervous system (PACNS) is a rare disease with various clinical presentations. It is the preferred name for vasculitis that is confined to the central nervous system (CNS) and is often considered a diagnosis of exclusion in vascular or inflammatory CNS diseases. This case describes a 46-year-old right-handed female with a past medical history of hypertension (HTN), hyperlipidemia (HLD), diabetes mellitus type two (DM2), obesity, and hemorrhagic stroke who was transferred from an outside facility after a one-month hospitalization to be evaluated for CNS vasculitis. Emergency medical personnel who brought the patient to the receiving hospital endorsed dysarthria and fluctuating level of cognition. Before she was transferred, the patient underwent a series of computed tomography (CT) and magnetic resonance imaging and angiographies (MRI/MRA) as well as four-vessel angiography. The studies revealed multiple bilateral striatal and cortical infarcts, scattered narrowing and occlusion of major cerebral vasculature, as well as other signs initially more suggestive of intracranial atherosclerosis than CNS vasculitis. Before she was transferred, imaging demonstrated a new cortical stroke. Hypercoagulable studies were positive for protein C deficiency although ensuing echocardiograms with normal ejection fractions were negative for a source of cardioembolism. Having undergone extensive rheumatological, radiological, and neurosurgical evaluation in the receiving facility, recommendations were made for the patient to undergo leptomeningeal biopsy to confirm the diagnosis of vasculopathy and to specifically rule out intracranial atherosclerosis and reversible cerebral vasoconstriction syndrome (RCVS).