Fuad Zeid

Limbic encephalitis (LE) is a rare neurological paraneoplastic complication that occurs secondary to malignant tumors. It is commonly presented as refractory seizures that are resistant to most anti-epileptics. We are presenting a unique case of small cell lung cancer complicated with LE. The challenging part of our case is that the patient had a history of seizure disorder in the past, and she was treated initially as an anti-epileptic treatment failure. A 68-year-old patient with a history of epilepsy was admitted to the ICU with resistant status epilepticus (SE), and respiratory failure secondary to pneumonia. Further workup revealed that the patient has small cell lung carcinoma. An extensive workup done to investigate resistant seizures revealed that she had a rare type of paraneoplastic autoantibodies (Anti-Hu) in the cerebrospinal fluid, which supported the diagnosis of the paraneoplastic autoimmune LE. High dose steroids helped to decrease the seizures episodes, but the family decided to proceed with palliative measures only at the end. Diagnosing LE requires ruling out other common causes of SE. Treatment options include treating underlying cancer as well as means of immunosuppression or antibody removal by tacrolimus and cyclophosphamide and even intravenous immunoglobulin (IVIG) or plasma exchange. It is important to consider LE in the differential diagnosis when managing patients with resistant SE in the ICU, even if the brain imaging and cerebrospinal fluid (CSF) analysis were within normal limits.

We are presenting a case of primary lymphedema (PL) complicated with a repeated need for thoracentesis and pericardiocentesis. Our patient is a 24-year-old male with primary lymphedema that is manifested in the left hand and right lower limb. The patient presented to the emergency department (ED) for recurrent right lower lobe cellulitis that had failed repeated attempts with outpatient antibiotic therapy. The patient was admitted to the intensive care unit due to signs of cardiac tamponade that were discovered on the physical examination. Pericardial tamponade was confirmed by echocardiography. The patient underwent thoracentesis and multiple pericardiocenteses and required a pericardial window. Pericardial and pleural fluids appeared milky and biochemical analysis was consistent with chylopericardium and chylothorax.

Clopidogrel is one of the most commonly prescribed thienopyridines used postcoronary stenting for acute coronary syndrome (ACS). There have been several concerns regarding performing small-bore thoracocentesis on patients on clopidogrel in our practice. We present an 85-year-old male with a history of diabetes, atrial fibrillation, diastolic heart failure, chronic kidney disease (CKD) stage three, who recently had a non-ST elevation myocardial infarction (NSTEMI) requiring a drug-eluting stent (DES) to the left anterior descending (LAD) artery, and was on dual anti-platelet therapy (DAPT). He was admitted with worsening shortness of breath and found to have bilateral pleural effusions. He required several small-bore, ultrasound-guided thoracocentesis on the right side while on clopidogrel. Intensivists or residents did all the procedures. The patient went into a hemorrhagic shock following his third small-bore thoracocentesis, requiring pressors, blood and platelet transfusions, and a surgical intercostal (IC) drain insertion. He eventually became clinically stable. An IC arteriogram within 24 h ruled out IC artery injury. Healthcare professionals perceive small-bore thoracocentesis as a safe procedure done on medical, surgical, intensive care, and interventional radiology (IR) units. The overall consensus is that it is safe to perform it on patients taking clopidogrel. We emphasize through this case report the bleeding risks associated with performing such procedures on patients while on clopidogrel and considering holding clopidogrel when feasible or bridging with an intravenous anti-platelet drug.

Cases of coronary artery spasm secondary to contrast agent use are rarely reported. Herein, we report the case of a 53-year-old woman who developed chest pain, dyspnea, and bradycardia and quickly become unresponsive after magnetic resonance imaging of the brain. A heart monitor showed ST elevation, and an electrocardiogram showed ST elevations in leads II, III, aVF, V3, and V4 and ST segment depression in lead I. Urgent left heart catheterization revealed no evidence of obstructive coronary artery disease or pulmonary embolism. A few days later, she was discharged from the hospital with no symptoms. A type I variant of Kounis syndrome was diagnosed.

Xanthogranulomatous pyelonephritis is a rare form of chronic pyelonephritis that generally afflicts middle-aged women with a history of recurrent urinary tract infections. Its pathogenesis generally involves calculus obstructive uropathy and its histopathology is characterized by replacement of the renal parenchyma with lipid filled macrophages. This often manifests as an enlarged, nonfunctioning kidney that may be complicated by abscess or fistula. This case details the first reported case of xanthogranulomatous pyelonephritis complicated by urinothorax, which resolved on follow-up chest X-ray after robot-assisted nephrectomy.

Empyema thoracis is a serious condition characterized by the accumulation of purulent fluid in the pleural cavity, typically following a pneumonia, subdiaphragmatic abscess, or esophageal rupture. Fungal empyema thoracis is a rare form of this condition with especially high mortality, in which the most frequently isolated fungus is Candida spp. This article presents a 74-year-old female with Candida krusei pneumonia and a complicated hospital course, initially presenting with nausea, vomiting, and dysphagia. She was initially suspected to have community-acquired pneumonia and was started on azithromycin and ceftriaxone. Worsening respiratory function led to the diagnosis of hydropneumothorax. Pleural fluid and an independent sample of pus and pleural tissue grew Candida krusei, giving the diagnosis of fungal empyema. With further respiratory deterioration, the patient was intubated and switched to piperacillin/tazobactam and micafungin. Decortication with extensive pleural peel and removal of foul-smelling pus and food particles within the chest was performed. This further lead to confirmation of esophageal perforation, and she was started on voriconazole and meropenem. After developing septic shock, the patient was managed with phenylephrine and vasopressin. Finally, after improving she was weaned off pressors and extubated, followed by an esophagogastroduodenoscopy (EDG) with pneumatic balloon dilation and WallFlex stent placement. This patient’s case demonstrated an example of empyema thoracis, which required a high index of suspicion since the presentation was with a community-acquired infection. Candida empyema thoracis may be a complication of operation, gastroesophageal fistula, and spontaneous esophageal rupture. On the other hand, the course of this patient’s hospital stay progressed from esophageal perforation to Candida krusei pneumonia, empyema, and pneumothorax. Thus, community-acquired fungal empyema should be considered in patients with respiratory symptoms and suspected esophageal perforation; nevertheless, after a diagnosis of fungal empyema, esophageal perforation should also be ruled out in addition to other causes like pneumonia, subphrenic abscess, and hematogenous spread. Improved communication between clinicians and microbiologists can lead to early diagnosis and a reduction in the morbidity and mortality of this condition.