Case Reports in Critical Care最新文献

Background: Primary 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 presentation: We 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.

Discussion: Cardiac 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.

Conclusion: This 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.

We present the case of a 68-year-old male who experienced presyncope and was found to have a large, free-floating thrombus in the right atrium, accompanied by a concurrent pulmonary embolism. Given the high risk of a massive pulmonary embolism, a multidisciplinary team recommended surgical thrombectomy under cardiopulmonary bypass. However, shortly after the treatment decision, the thrombus spontaneously disappeared, most likely having embolized into the pulmonary arteries. As the patient exhibited minimal hemodynamic compromise, the team opted for thrombolytic therapy with rt-PA instead of surgery. The patient was discharged 10 days later following an uneventful recovery from infarct pneumonia. This case highlights the unpredictable behavior of intracardiac thrombi and emphasizes the importance of ongoing reassessment and imaging in guiding clinical management.

The management of acute respiratory distress syndrome (ARDS) in a patient suffering from a severe brain injury may be difficult, especially when hypercapnia occurs. The rise of PaCO₂ may compromise cerebral hemodynamics and increase intracerebral pressure (ICP). We describe herein a case of a 41-year-old man with a severe subarachnoid haemorrhage who develops a severe ARDS consequent to an inhalation pneumonia. Despite optimisation of mechanical ventilation, respiratory mechanics worsened and led to a major hypercapnic acidosis associated with an ICP rise. Because of concomitant ICP elevation and hemodynamic instability, prone positioning was considered too high-risk. We therefore opted for an extracorporeal carbon dioxide removal (ECCO₂R) technique first. PaCO₂ rapidly decreased, as well as ICP, and the patient could finally be proned while in ECCO₂R. ECCO₂R was kept for a total of 77 h with no complications. Thereafter, the patient progressively improved and could be weaned from the ventilator after 27 days. He was evaluated 3 months later during an outpatient visit. He was doing well with no sequelae and has resumed previous activities. While the use of extracorporeal decarboxylation techniques is being studied in ARDS, specific investigation in severely brain-injured patients deserves to be conducted.

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.

A 37-year-old man had a cardiac arrest. His colleagues started CPR and called an ambulance to our emergency department. The ECMO team assessed him and initiated ECPR. Coronary, left ventricular, and pulmonary angiography showed no abnormalities. The patient had pupil dilation, prompting a bilateral decompressive craniectomy under heparin-free ECMO support. Postoperatively, pupils remained dilated until cerebral angiography revealed venous sinus thrombosis, prompting anticoagulation therapy, which led to pupil constriction and partial neurological recovery. The patient was weaned off ECMO and was transferred to a rehabilitation hospital. Successful resuscitation after prolonged cardiac arrest using ECPR, bilateral decompressive craniectomy, and CVST treatment is rare.

Background: High 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 presentation: We 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.

Conclusion: These 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.

We present the case of a 29-year-old female who ingested a 60 g dose of hydroxychloroquine in a suicide attempt. This report details the acute clinical presentation, successful management strategies, and prolonged sequelae of severe hydroxychloroquine toxicity, including recurrent and delayed episodes of Torsades de Pointes (TdP) and profound metabolic derangements. Early recognition, intensive supportive care, and the use of targeted interventions-including activated charcoal administration, meticulous electrolyte correction, and vasoactive support-were critical to successful management. This case underscores the importance of prompt intervention in hydroxychloroquine overdoses and provides a review of the pathophysiology and therapeutic strategies informed by current literature and our clinical experience.

Methemoglobinemia is defined as an increase in methemoglobin of > 2% of hemoglobin. Ketamine is increasingly used for severe depression. To our knowledge, a patient with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) who died suddenly and unexpectedly 1-12 h after ketamine infusion with high postmortem methemoglobin has not yet been reported. The patient was a 32-year-old woman with MELAS, manifesting as migraine, deafness, diabetes, bloating, and a seizure, due to the mtDNA variant m.3243A>G who received a single infusion of ketamine for the treatment of depression and posttraumatic stress disorder. Presumably, 1-12 h later, the patient died in her apartment, initially with no apparent cause for her demise. The autopsy revealed a methemoglobin level of 71% (normal: 0-2%). Whether ketamine was responsible for the death remains speculative, but ketamine has a mitochondrial toxic effect by reducing ATP production and impairing methemoglobin reductase, which may have led to methemoglobinemia. In conclusion, ketamine should be administered with caution in MELAS patients, particularly those with a history of seizures, and if unavoidable, these patients should be carefully monitored during and after ketamine infusion.

Background: Lung ultrasound is increasingly used in critical care medicine to identify pneumothorax, usually by the absence of lung sliding and identification of the lung point. Heart point is a less recognized but specific sign in cardiac ultrasound indicating pneumothorax.

Case presentation: A 20-year-old Caucasian male presented with a pneumothorax after a traumatic resuscitation to the emergency room upon bilateral chest decompression being initiated. Upon presentation to the intensive care unit, there were no clinical signs of pulmonary compromise on mechanical ventilation. Performance of transthoracic echography at the ICU identified heart point, and the subsequent diagnosis of pneumothorax was made. A thoracic drain was inserted and resulted in the re-expansion of the lung. The chest tube was removed after 2 days.

Conclusion: The utility of point-of-care ultrasound in the diagnosis of pneumothorax is aided by awareness of heart point. Recognition is imperative to ensure prompt therapeutic measures and ensure improved patient outcomes. Knowledge of mimicking appearances such as pseudo heart point and air gap sign is essential to assure diagnostic accuracy.

Background: Supratherapeutic 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 summary: We 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.

Discussion: Medication 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.

Conclusions: Serum alkalinization from sodium bicarbonate administration has implications in the length of stay and need for adjunctive therapies in the treatment of flecainide toxicity.