Isolated Left Atrial Cardiac Tamponade Caused by Pleural Effusion.

A localized left atrial tamponade caused by left side pleural effusion is a rare finding that leads to hemodynamic instability. Here, we describe left atrial systolic and diastolic collapse resulting from left pleural effusion. An increase in intrapleural pressure by a pleural effusion can compress the pericardial space and lead to impaired cardiac filling and tamponade physiology. Here, we present a case of a 79-year old African American female who presented with shortness of breath and dry cough for a duration of one week. Chest radiograph and CT scan of the chest showed left pleural effusion. The echocardiogram revealed left atrial systolic and diastolic collapse due to pleural effusion, which triggered cardiac tamponade physiology. With the guidance of a bedside thoracic ultrasound, she underwent a diagnostic and therapeutic thoracentesis which resolved her symptoms. Repeat echocardiogram revealed resolution of the cardiac tamponade with no further indication of left atrial diastolic collapse. In conclusion, pleural effusions can cause tamponade physiology and can be resolved by thoracentesis. Early recognition by a bedside point-of-care ultrasound may help provide prompt relief of tamponade.

A 44-Year-Old Hispanic Man with Loss of Taste and Bilateral Facial Weakness Diagnosed with Guillain-Barré Syndrome and Bell's Palsy Associated with SARS-CoV-2 Infection Treated with Intravenous Immunoglobulin.

BACKGROUND This case report is of a patient who presented with loss of taste and facial weakness and was diagnosed with Guillain-Barre syndrome (GBS) and Bell's palsy, associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. GBS is a neurological emergency defined as acute inflammatory demyelinating polyneuropathy. The patient responded to intravenous immunoglobulin (IVIG) treatment. CASE REPORT We present the case of a 44-year-old Hispanic man who came for evaluation of bilateral facial weakness and lack of taste sensation. He had lower motor neuron facial weakness. His head computed tomography and brain magnetic resonance imaging scans did not show any pathological abnormalities. He tested positive for SARS-CoV-2 by a nasopharyngeal swab reverse transcription polymerase chain reaction (RT-PCR) test. Cerebrospinal fluid (CSF) analysis via lumbar puncture revealed elevated protein levels, no leukocytes, and a negative Gram stain. The CSF RT-PCR test for SARS-CoV-2 was negative. PCR tests of the CSF for other viral infections were negative. A diagnosis of GBS was made, and he was treated successfully with IVIG. After the fourth dose of IVIG, the patient was able to close his eyes, frown, show his teeth, and smile. CONCLUSIONS Our case is rare because the patient did not present with lower extremity weakness, but only with bilateral Bell's palsy. Physicians should be aware of GBS because it is a neurological emergency for which COVID-19 can be a risk factor. Early diagnosis and treatment of GBS can prevent neurological disability.

Diclofenac-induced thrombotic thrombocytopenic purpura with concomitant complement dysregulation: a case report and review of the literature.

BACKGROUND: Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are two forms of thrombotic microangiopathies. They are characterized by severe thrombocytopenia, microangiopathic hemolysis, and thrombosis, leading to a systemic inflammatory response and organ failure. Plasmapheresis is used to treat thrombotic microangiopathies. A different entity known as atypical hemolytic uremic syndrome has garnered more clinical recognition because reported cases have described that it does not respond to standard plasmapheresis. Diclofenac potassium is a non-steroidal anti-inflammatory drug that is used to treat pain. CASE REPORT: A 35-year-old Hispanic man presented to our emergency department with complaints of generalized malaise, fever, and an evanescent skin rash. During admission, he reported the use of diclofenac potassium for back pain on a daily basis for 1 week. He was noted to have peripheral eosinophilia, so he was admitted for suspected drug reaction involving eosinophilia and systemic symptoms. His initial laboratory work-up showed microangiopathic hemolytic anemia and thrombocytopenia. He also experienced a seizure, encephalopathy, and had a PLASMIC score of 7, thus raising concerns for thrombotic thrombocytopenic purpura. He underwent emergent plasmapheresis, which improved his clinical condition. The diagnosis was confirmed by assessing the levels of disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13, which was less than 3%. In addition, his skin biopsy was positive for patchy complement deposition, demonstrating complement dysregulation. CONCLUSION: Thrombotic thrombocytopenic purpura is a rare condition that can be acquired. Our case is rare because it represents the first report of diclofenac potassium-induced thrombotic thrombocytopenic purpura with subjacent complement activation and dysregulation. Early recognition and aggressive management led to a favorable outcome.

Acute Colonic Pseudo-Obstruction Caused by Dexmedetomidine: A Case Report and Literature Review.

BACKGROUND Acute colonic pseudo-obstruction (ACPO) is an infrequent entity characterized by non-toxic, non-mechanical, abrupt, functional dilation of the colon. Clinically patients present with abdominal distention, anxiety, severe abdominal pain, nausea, and vomiting. This rare entity can lead to a fatal outcome if not recognized early. A high level of suspicions is paramount for early diagnosis and prompt intervention. CASE REPORT A 50-year-old male was admitted to the intensive unit care due to acute hypoxic respiratory failure, pneumonia, and septic shock requiring mechanical ventilation and intravenous vasopressors. Two weeks after admission, his clinical course deteriorated and was complicated with acute abdominal distension, pain, and ileus. Imaging confirmed acute onset of ileus and after ruling out metabolic and infectious causes, the diagnosis of ACPO was made. Aggressive medical and surgical management resulted in a favorable outcome. CONCLUSIONS Critically ill patients on ventilator are commonly sedated; therefore, usual symptoms of ACPO can be missed or misinterpreted leading to late diagnosis with increased morbidity and mortality. Clinicians must be aware of potential harm and side effects from common sedatives used in the intensive care unit and should be current on medical literature. Alpha-2 agonists, i.e., dexmedetomidine, is increasingly been used in critical care setting and there are few reports of a possible association with ACPO. We present here a case of a patient with dexmedetomidine-induced ACPO, and we provide a review of the existing literature and pathophysiology of the condition.

Multiorgan Failure and Refractory Lactic Acidosis due to Pasteurella multocida Septicemia in a Patient with No Animal Exposure.

INTRODUCTION: Pasteurella multocida is a gram-negative coccobacillus pathogenic to animals. It can cause infection in humans by a bite, scratch, or lick from a cat or dog. P. multocida can cause a variety of infections in humans, including cellulitis, osteomyelitis, endocarditis, peritonitis, and septic shock. CASE PRESENTATION: A 56-year-old male presented to our hospital with a 2-day history of fever, abdominal pain, nausea, and vomiting. He denied exposure to cats, dogs or other pets. He had severe respiratory distress requiring ventilator support, profound septic shock requiring multiple vasopressors, severe lactic acidosis, and renal failure requiring emergent hemodialysis. Blood cultures confirmed the presence of P. multocida. The patient subsequently died of cardiopulmonary arrest due to multiorgan failure with refractory shock. CONCLUSION: P. multocida septicemia can lead to septic shock. Early identification of this organism may decrease mortality. Although our patient had no known cat or dog exposure, physicians should enquire about a history of animal exposure when a patient presents with an infection with no obvious cause.