BackgroundPrimary cardiac sarcomas are rare and aggressive tumors that often present with nonspecific symptoms, typically diagnosed at advanced stages. Obstruction of the left ventricular outflow tract (LVOT) due to these tumors is an exceptionally rare and life‐threatening complication.Case PresentationWe describe the case of a previously healthy 33‐year‐old male who presented with progressive exertional dyspnea, orthopnea, and hemoptysis. Upon admission, he quickly developed hemodynamic instability and respiratory failure. Point‐of‐care transthoracic echocardiography revealed a large intracardiac mass causing dynamic LVOT obstruction. During intubation, the patient experienced cardiac arrest, necessitating advanced cardiopulmonary resuscitation. Urgent surgical intervention confirmed the presence of an infiltrative cardiac sarcoma with positive margins. The postoperative recovery was favorable, enabling extubation and withdrawal of vasoactive agents within 24 h.DiscussionCardiac sarcomas often mimic other cardiovascular conditions, complicating early diagnosis. Imaging techniques such as echocardiography and cardiac MRI are essential for detection and characterization. The prognosis for patients with cardiac sarcomas remains poor due to the tumors′ infiltrative nature and high rates of recurrence; however, complete surgical resection is the cornerstone of treatment.ConclusionThis case underscores the necessity for clinical vigilance in patients presenting with unexplained cardiopulmonary symptoms. The early application of bedside echocardiography facilitated prompt diagnosis and timely surgical intervention, proving life‐saving in this instance of obstructive shock due to a primary cardiac sarcoma.

The use of left ventricular assist devices (LVADs) is now commonplace in the management of nonischemic cardiomyopathy. LVADs are preload‐dependent and afterload‐sensitive, meaning rapid changes in a patient′s volume status can significantly impact device function. Cerebral salt‐wasting syndrome (CSWS), a rare cause of hyponatremia, is characterized by an acute increase in urine output and low serum sodium. Here, we present the case of a 43‐year‐old man with end‐stage heart failure supported by an LVAD, who experienced refractory low‐flow alarms due to CSWS. The patient initially presented with a new‐onset headache. Brain computed tomography (CT) scan revealed an acute subdural hematoma with midline shift, requiring emergency craniotomy, which was performed without complications. After discharge from the intensive care unit (ICU), he returned with multiple low‐flow alarms on his LVAD (flow less than 1.5 L/h), despite high mean arterial pressures and normal perfusion indexes. Laboratory evaluation showed a serum sodium of 130 mmol/L, a urine osmolality of 522 mmol/kg, a serum osmolality of 282 mmol/kg, and a urine sodium of 147 mEq/day. His urine output was 4 L/day. A diagnosis of CSWS was made. Treatment included normal saline drip for 1:1 volume replacement, daily fludrocortisone, low‐dose desmopressin, and intermittent 3% hypertonic saline boluses. Salt tablets were prescribed to maintain a serum sodium goal of 135–140 mmol/L and a urine output of 2.5–3.5 L/day. Over time, the frequency of low‐flow alarms decreased significantly, and the patient was discharged. CSWS is an unlikely cause of hyponatremia in the ICU. Aggressive fluid hydration and sodium supplementation are necessary for positive clinical outcomes. This is especially true in patients with LVADs, who are both preload‐dependent and afterload‐sensitive. Failure to rapidly treat CSWS can lead to respiratory arrest, brainstem herniation, and even death.

BackgroundHigh anion gap metabolic acidosis (HAGMA) is common in critical illness. The GOLD MARK mnemonic summarizes conventional etiologies, but a subset of cases remain unexplained and refractory to standard therapy.Case PresentationWe report two ICU patients with severe, refractory HAGMA. Case 1 was a 67‐year‐old man with profound lactic acidosis and an anion gap of 46 mmol/L, unresponsive to CRRT and supportive care. Case 2 was a 50‐year‐old man with cardiogenic shock who developed persistent HAGMA despite CRRT. In both cases, metabolic workup excluded standard etiologies. Laboratory testing revealed abnormalities in amino acids and acylcarnitines. In Case 1, low albumin electrophoresis was observed despite normal serum albumin levels. Each patient underwent three sessions of plasma exchange with albumin replacement, resulting in rapid and sustained resolution of metabolic acidosis.ConclusionThese cases highlight plasma exchange as a potential rescue therapy for refractory HAGMA, possibly mediated by protein‐bound acids. While causality cannot be established, our findings support further study into the role of plasma exchange in unexplained or treatment‐resistant HAGMA.

BackgroundSupratherapeutic flecainide concentrations may result in wide complex cardiac dysrhythmias, which are normally treated with hypertonic sodium bicarbonate therapy. Previous cases have suggested that in acute toxicity, serum alkalinization may impair the elimination of flecainide.Case SummaryWe present a single case of chronic flecainide toxicity. A 69‐year‐old patient began taking oral flecainide 1 month prior and developed recurrent wide complex tachycardia (WCT) that was refractory to treatment with sodium bicarbonate and repeated defibrillations. Further arrhythmias stopped after the resolution of alkalosis and treatment with lidocaine. Serum flecainide concentrations were notable for an apparent rise from initial levels following serum alkalinization.DiscussionMedication interactions and pharmacodynamic testing could not account for increasing serum flecainide concentrations following treatment. No evidence of supratherapeutic ingestion was identified. Tissue redistribution as a result of serum alkalinization likely contributed to impaired elimination in a patient with chronic flecainide toxicity.ConclusionsSerum alkalinization from sodium bicarbonate administration has implications in the length of stay and need for adjunctive therapies in the treatment of flecainide toxicity.

Gastroesophageal variceal bleeding is a life‐threatening complication of portal hypertension in patients with cirrhosis. Endoscopic cyanoacrylate injection is an established therapy for variceal hemorrhage, but it may lead to rare systemic complications, including glue embolization. The authors report the case of a patient with decompensated cirrhosis who developed acute gastroesophageal variceal bleeding, managed with endoscopic variceal ligation and cyanoacrylate injection. Postprocedural investigations revealed multiple emboli involving the cerebral, pulmonary, coronary, and renal vascular territories. The present case report and review of the literature highlight the need for increased awareness of glue embolization as a potential adverse effect of cyanoacrylate therapy. Careful patient selection, refined endoscopic technique, and close postprocedure monitoring are essential to minimizing the risks of embolization, reducing complications and optimizing outcomes.

Severe anaphylaxis is an acute allergic reaction that can be life‐threatening if not managed rapidly. Its clinical manifestations are diverse, typically including hypotension, respiratory failure, and skin manifestations. However, seizures are an uncommon presentation and may easily be overlooked. We report a case of severe anaphylaxis following intrathecal injection of a contrast agent used in the evaluation of brachial plexus injuries. The initial manifestations were seizures and hypotension, occurring 15 min after injection. The patient survived following appropriate treatment and was subsequently discharged.

Central venous catheters (CVCs) are commonly placed in patients in critical care units (CCUs) for a variety of reasons. Indications for CVC placement include rapid volume resuscitation, central venous pressure monitoring, venous access in patients with severe vascular disease, hemodialysis, and the need for the administration of vasoactive/bioactive medications. The placement of a CVC, however, does not come without risks to the patient, and one must keep these complications in mind. A 66‐year‐old male with Stage IV chronic kidney disease was admitted for dehydration secondary to diarrhea and was started on intravenous fluid resuscitation. During his eventful hospital course, the patient was transferred to the CCU, where a right internal jugular CVC was placed with eventual removal. A few minutes after removal, the patient was found to be poorly responsive, diaphoretic, and noted to have neurologic findings. A computed tomography scan of the head and a computed tomography angiogram of the head and neck revealed air within the subarachnoid space, subtle parenchymal hypodensity along the right cerebral cortex, and air inside the jugular and vertebral venous system. Magnetic resonance imaging of the brain revealed air within the cavernous sinuses, cortical veins, and dural sinuses. The patient was treated with aspirin and statin therapy given stroke‐like symptoms, with eventual improvement and discharge. Air embolism (AE) is an uncommon and dangerous complication that can result from various reasons, such as trauma, surgery, septal defects, or barotrauma. In this case, the AE was a devastating complication of a CVC. They can occur at various portions of the insertion and removal process. AE may cause cardiopulmonary distress and/or neurologic symptoms. Given the clinical context, a high level of suspicion is required to diagnose cerebral AE. This unfortunate event highlights the dangerous complications of a routine procedure. Early diagnosis and clinical suspicion of AE decrease morbidity and mortality.

Urine discoloration is a frequent clinical observation that often indicates underlying pathological or pharmacological conditions. Pink urine syndrome (PUS) is a rare phenomenon characterized by the sudden appearance of pink‐colored urine, typically attributed to the excretion and crystallization of propofol metabolites. Factors such as obesity, dehydration, and critical illness may exacerbate this condition. Although rare, PUS should be considered in critically ill patients receiving propofol sedation in the intensive care setting. This case report describes the occurrence of PUS in a 29‐year‐old male with a body mass index of 27.31 kg/m2, who was sedated with propofol following an overdose. The urine discoloration resolved after discontinuation of propofol and initiation of hydration therapy, emphasizing the importance of early recognition and prompt intervention. While PUS is benign, generally self‐limiting, and resolves without specific treatment, careful monitoring is essential to mitigate potential complications due to precipitation of uric acid crystals, such as urolithiasis, obstructive uropathy, and acute kidney injury, if exposure continues.

We present the case of a 58‐year‐old woman with fibrotic hypersensitivity pneumonitis, without significant comorbidities, who developed posterior reversible encephalopathy syndrome (PRES) 7 days after a bilateral lung transplant. Initial symptoms included hypertension, headache, nausea, vomiting, and cortical blindness. Although no seizures were observed, the electroencephalogram revealed occipital epileptic discharges. Brain magnetic resonance imaging confirmed the diagnosis of PRES, showing a typical pattern of vasogenic edema in the corticosubcortical occipital regions. Tacrolimus was discontinued, and antihypertensives and anticonvulsants were initiated, resulting in complete neurological recovery within 4 days. After 16 days without calcineurin inhibitor, cyclosporine was introduced with no recurrence of the neurological condition.

We report the case of a 37‐year‐old female patient admitted to our hospital with unstable bradyarrhythmia, abdominal cramping, vomiting and visual disturbances including xanthopsia and diplopia. Ten hours prior to admission, she reported ingestion of four seeds of Cerbera odollam and four crushed nutmegs with suicidal intent. The patient was hypotensive and suffered from hyperkalemia (serum potassium > 5.5 mmol/L), leucocytosis and acute kidney injury. Her heart rate ranged between 28 and 40 bpm, and electrocardiogram (ECG) revealed a second‐degree atrioventricular (AV) block and ST‐depressions. The patient developed a third‐degree AV block requiring vasopressors and transvenous pacing, which she remained completely dependent upon for 56 h. After a total of 3 days, the patient remained hemodynamically stable, and the pacemaker was removed. ECG still featured downsloping ST‐depressions, first‐degree AV block and sinus bradycardia. The patient survived. Her clinical course was typical and severe. Cerbera odollam poisoning is a potentially fatal condition associated with arrhythmia, abdominal symptoms and electrolyte disturbances. It remains a rarity in Europe and hardly known to Western physicians. Given its potentially lethal effects and increasing availability of its seeds, Cerbera odollam poisoning must be included in the differential diagnosis of unknown intoxications. With this case report, we hope to raise awareness among physicians for Cerbera odollam intoxications in Europe.