<i>Introduction</i>. Trazodone is a serotonin receptor antagonist and reuptake inhibitor commonly used to treat major depression disorder (MDD), anxiety, and sleep disorders. It is considered safe for the heart due to minimal anticholinergic effects. Prolonged QT intervals can cause polymorphic ventricular tachycardia, known as torsades de pointe (TdP). We present a case of a 67-year-old female with a history of MDD who developed trazodone-induced TdP. <i>Case Presentation</i>. The patient was referred to a tertiary hospital with a ten-hour history of nausea and vomiting. Trazodone (50 mg daily) was started for her six days ago due to her past medical history of MDD. The initial electrocardiography (ECG) revealed a prolonged corrected QT interval (<span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="33.198pt" style="vertical-align:-2.15716pt" id="M1" height="10.9105pt" version="1.1" viewBox="-0.0498162 -8.75334 33.198 10.9105"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g190-82" d="M720 -138C627 -96 538 -41 476 2C594 39 703 153 703 331C703 532 552 665 384 665C170 665 44 499 44 315C44 215 87 129 147 73C211 11 298 -11 355 -14C476 -99 554 -136 584 -144S664 -160 712 -159L720 -138ZM348 25C231 49 146 172 146 342C146 533 249 629 360 629C497 629 601 510 601 302C601 142 523 51 443 28C434 34 425 41 416 47L348 25Z"/></g><g transform="matrix(.013,0,0,-0.013,9.607,0)"><path id="g190-85" d="M592 498C586 556 582 629 581 675H560C545 656 537 650 510 650H115C87 650 74 652 60 675H40C38 620 33 555 28 495H57C69 539 77 568 89 585C102 607 122 616 205 616H267V123C267 44 259 34 168 28V0H454V28C360 34 352 44 352 123V616H422C498 616 514 608 531 584C542 568 552 543 562 495L592 498Z"/></g><g transform="matrix(.013,0,0,-0.013,16.349,0)"><path id="g190-100" d="M390 111C344 68 312 56 269 56C212 56 118 102 118 241C118 346 175 401 241 401C277 401 312 388 342 360C350 352 355 349 361 349C372 349 394 371 394 392C394 403 391 411 378 422C362 436 329 449 288 449H287C250 449 190 432 138 392C71 341 37 274 37 197C37 90 112 -12 238 -12C297 -12 363 32 407 90L390 111Z"/></g><g transform="matrix(.013,0,0,-0.013,25.567,0)"><path id="g117-34" d="M535 323V373H52V323H535ZM535 138V188H52V138H535Z"/></g></svg><span class="irelop"/><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.918pt" style="vertical-align:-2.15716pt" height="10.9105pt" version="1.1" viewBox="36.780183799999996 -8.75334 18.918 10.9105"><g transform="matrix(.013,0,0,-0.013,36.83,0)"><path id="g113-54" d="M153 550H386L412 615L406 623H120L82 318C104 327 142 338 184 338C294 338 347 275 347 187C347 112 305 39 221 39C160 39 119 71 97 89C88 97 80 96 71 90C59 80 50 67 49 57C48 45 52 36 66 23C80 9 123 -12 169 -12C221 -11 288 15 342 59C403 109 431 165 431 225C431 308 366 395 238 395C212 395 165 379 127 364L153 550Z"/></g><g transform="matrix(.013,0,0,-0.013,43.07,0)"><path id="g113-57" d="M249 635C141 635 70 555 70 471C70 401 114 353 179 316C143 294 106 267 90 252C68 231 45 202 45 157C45 50 130 -12 237 -12C322 -12 435 52 435 169C435 256 372 304 303 343C349 374 375 398 383 407C401 429 411 458 411 487C411 569 344 635 249 635ZM238 603C285 603 337 567 337 482C337 422 310 385 276 358C205 393 145 426 145 500C145 552 179 603 238 603ZM248 20C183 20 125 70 125 163C125 218 158 268 206 300C284 261 355 217 355 143C355 66 308 20 248 20Z"/></g><g transform="matrix(.013,0,0,-0.013,49.31,0)"><path id="g113-55" d="M137 343C167 482 260 545 321 574C357 591 397 603 429 609L423 641C382 634 335 622 295 608C189 570 37 457 37 238C37 84 125 -12 242 -12C362 -12 447 89 447 209C447 311 374 393 267 393C247 393 226 386 204 376L137 343ZM227 337C318 337 361 256 361 173C361 105 336 22 258 22C176 22 126 120 126 240C126 266 127 291 132 310C155 323 189 337 227 337Z"/></g></svg></span> ms) due to a long ST segment and generalized T wave inversion. A few moments after admission to the intensive care unit, she suddenly lost consciousness. ECG monitoring showed a TdP, which terminated immediately with the asynchronous defibrillation. A temporary pacemaker was implanted due to repeated arrhythmias and bradycardia. Arrhythmia did not recur for hours and days later. After four days of stopping trazodone, all abnormal ECG findings were resolved, and she was discharged with a normal ECG. She was followed up six months later; the ECG was normal, and she had no complaints. <i>Conclusion</i>. Trazodone may lead to QTc prolongation and TdP, potentially fatal even without risk factors for QTc prolongation. Close monitoring is essential to prevent adverse complications in trazodone users.

Hamid Khederlou

Vanoushe Azimi Pirsaraei

Torsades de Pointe Associated with Trazodone Consumption

Clostridium botulinum produces the most potent bacterial toxin, botulinum toxin A (BTXA), which has various therapeutic and cosmetic indications. Intragastric BTXA injection is a new obesity treatment method that was argued to be safe due to the inactivation of BTXA through the liver or metabolization within the gastric wall. However, a 36-year-old woman was admitted to the intensive care unit (ICU) due to developing botulism as a result of an intragastric injection of BTXA. The diplopia, headaches, ptosis, decreased muscle force, and respiratory distress two days after injection were her first chief complaints, and also, she experienced significant dysphagia, hoarse voice, thick tongue, constipation, hyposmia, and hypogeusia after two weeks. This case report highlights the necessity for physicians to have sufficient information about this method and consider possible life-threatening adverse effects including botulism.

Mojtaba Mojtahedzadeh

Farhad Najmeddin

Elham Pourheidar

Atabak Najafi

Reza Bahman

Ehsan Yousefi-Mazhin

Hossein Karballaei-Mirzahosseini

Rezvan Hassanpour

Intragastric Botulinum Toxin Injection and Botulism: An Alarm for Clinicians

<i>Background</i>. Mitral valve prolapse (MVP) is a common condition with an estimated prevalence of 1-3%, in which there is systolic displacement of a morphologically redundant mitral valve towards the left atrium. Mitral annular disjunction (MAD) is a separation of the MV attachment with the left ventricle, with hypermobility of the leaflets, and with systolic “curling” of the basal LV (left ventricle) myocardium. It is frequently associated with MVP and may confer an increased arrhythmic risk. <i>Case Description</i>. A 28-year-old male had ventricular fibrillation leading to out-of-hospital cardiac arrest, which was successfully resuscitated. His coronary arteries were unobstructed on invasive coronary angiography. Transthoracic echocardiogram (TTE) demonstrated MAD, confirmed by cardiac magnetic resonance (CMR) imaging and transoesophageal echocardiogram (TOE). The LV was severely dilated with reduced EF (ejection fraction), and the QTc interval was also prolonged. His father had died suddenly aged 50 years. <i>Conclusions</i>. This report describes the clinical dilemma of identifying and treating a patient with multiple potential causes of cardiac arrest. Despite being relatively common, the clinical significance of MAD is still uncertain and the extent to which it may be linked with complications such as ventricular arrhythmias and sudden cardiac death. MAD appears to confer an increased risk of ventricular arrhythmias, particularly when associated with MVP, particularly nonsustained VT.

James Ainsworth

Adrian Ionescu

Sudden Cardiac Arrest in a Youth with Multiple Arrhythmic Substrates

<i>Introduction</i>. Extracorporeal membrane oxygenation (ECMO) support for severe acute respiratory distress syndrome (ARDS) is nowadays widely used with notable results on the overall survival as reported in the ELSO registry near to 55% at 90 days. This is the reason why ECMO teams force the use of this extreme technique to several populations, even though there is still a lack of data about its use on hematological patients. <i>Case Report</i>. A 39-year-old woman without a history of previous diseases, but a new diagnosis of acute myeloblastic leukemia (AML) was admitted to intensive care unit (ICU) for worsening hypoxia and respiratory acidosis, presenting an ARDS with <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="32.838pt" style="vertical-align:-3.18147pt" id="M1" height="12.4698pt" version="1.1" viewBox="-0.0498162 -9.28833 32.838 12.4698"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g190-81" d="M46 650V622C120 617 128 613 128 525V125C128 42 120 34 40 28V0H311V28C221 34 212 39 212 124V281L286 262C297 261 316 261 331 263C429 275 526 338 526 468C526 533 501 579 462 609C422 638 364 650 293 650H46ZM212 559C212 588 215 600 223 606C230 613 251 618 279 618C361 618 430 572 430 464C430 337 350 302 285 302C252 302 225 309 212 314V559Z"/></g><g transform="matrix(.013,0,0,-0.013,7.032,0)"><path id="g190-98" d="M433 39L423 65C413 59 399 54 387 54C370 54 352 69 352 114V299C352 352 342 392 307 422C285 440 255 449 225 449C168 437 102 399 75 379C56 365 44 353 44 339C44 315 69 296 87 296C101 296 111 303 116 319C124 349 133 371 145 385C156 397 171 404 190 404C241 404 275 364 275 291V274C253 256 180 229 120 209C65 190 39 159 39 110C39 47 88 -12 159 -12C189 -12 237 25 277 52C282 35 288 21 301 8C312 -3 333 -12 348 -12L433 39ZM275 84C256 65 221 48 195 48C164 48 124 73 124 124C124 161 146 180 185 198C206 208 254 229 275 240V84Z"/></g><g transform="matrix(.013,0,0,-0.013,12.788,0)"><path id="g190-80" d="M381 665C170 665 44 498 44 318C44 125 188 -15 369 -15C552 -15 703 117 703 333C703 534 550 665 381 665ZM359 629C491 629 601 517 601 306C601 114 502 21 390 21C249 21 146 158 146 346S248 629 359 629Z"/></g><g transform="matrix(.0091,0,0,-0.0091,22.535,3.132)"><path id="g50-51" d="M414 144C384 79 371 75 317 75H135L276 221C367 316 408 376 408 465C408 570 327 635 237 635C179 635 131 609 100 575L42 494L67 471C94 510 138 565 205 565C277 565 321 517 321 435C321 348 258 270 195 195C146 137 88 81 33 26V0H411C423 44 433 88 446 135L414 144Z"/></g><g transform="matrix(.013,0,0,-0.013,27.482,0)"><path id="g113-48" d="M368 703H309L44 -163H104L368 703Z"/></g></svg><span class="isep"/><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="36.356pt" style="vertical-align:-3.18147pt" height="12.4698pt" version="1.1" viewBox="32.7931838 -9.28833 36.356 12.4698"><g transform="matrix(.013,0,0,-0.013,32.843,0)"><path id="g190-71" d="M493 503C489 551 484 614 483 650H43V622C120 616 128 611 128 525V126C128 40 120 34 40 28V0H312V28C221 34 213 40 213 126V307H316C407 307 412 296 424 227H453V420H424C412 355 407 346 316 346H213V584C213 613 216 616 246 616H322C398 616 419 607 436 579C449 559 455 539 464 499L493 503Z"/></g><g transform="matrix(.013,0,0,-0.013,39.72,0)"><path id="g190-106" d="M135 536C164 536 186 560 186 587C186 617 164 639 136 639C109 639 85 617 85 587C85 560 109 536 135 536ZM252 0V26C188 32 181 38 181 106V451C138 433 90 420 39 412V388C99 379 102 374 102 312V106C102 38 95 32 32 26V0H252Z"/></g><g transform="matrix(.013,0,0,-0.013,43.243,0)"><use xlink:href="#g190-80"/></g><g transform="matrix(.0091,0,0,-0.0091,52.99,3.132)"><use xlink:href="#g50-51"/></g><g transform="matrix(.013,0,0,-0.013,61.568,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g></svg><span class="irelop"/><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.933pt" style="vertical-align:-3.18147pt" height="12.4698pt" version="1.1" viewBox="72.78118380000001 -9.28833 18.933 12.4698"><g transform="matrix(.013,0,0,-0.013,72.831,0)"><path id="g113-50" d="M384 0V27C293 34 287 42 287 114V635C232 613 172 594 109 583V559L157 557C201 555 205 550 205 499V114C205 42 199 34 109 27V0H384Z"/></g><g transform="matrix(.013,0,0,-0.013,79.071,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.013,0,0,-0.013,85.311,0)"><use xlink:href="#g113-49"/></g></svg></span> in spontaneous breathing treated with noninvasive ventilation via full-face mask. Meanwhile, chemotherapy was started leading to a severe bone marrow aplasia that was managed with multiple blood and platelet transfusions. These conditions did not allow physicians to start any invasive approaches. After 14 days, ARDS worsened whereas bone marrow recovered, making possible the beginning of an invasive mechanical ventilation, with low positive end-expiratory pressure and a low tidal volume. Moreover, an immediate extracorporeal CO<sub>2</sub> removal (ECCO<sub>2</sub>R) therapy was added. Despite these efforts, no improvement was achieved, and that is why venovenous ECMO throughout femoral-jugular cannulation was applied. A full protective lung ventilation by ultralow tidal volumes was guaranteed. After 2 weeks of ECMO, a gradual weaning from ECMO support was started and completed after two days. No ECMO-related complications were registered. In the end, the patient started her weaning from the mechanical ventilation and reached 12 hours of spontaneous ventilation in oxygen therapy. <i>Discussion</i>. ECMO is used as a rescue therapy in patients affected by severe respiratory failure with life-threatening hypoxia and respiratory acidosis nonresponsive to other maneuvers. However, immunosuppression and coagulopathies of hematological malignancies are considered relative contraindications for ECMO, while long-lasting respiratory failure represents another relative contraindication to extracorporeal support. ECMO could be a valid option to improve the survival of hematological patients with severe ARDS and thrombocytopenia, and management could change case by case, even if high incidence of recurrency.

Martina Cuccarelli

Lorenzo Schiavoni

Felice Eugenio Agrò

Giuseppe Pascarella

Fabio Costa

Rita Cataldo

Massimiliano Carassiti

Alessia Mattei

Extracorporeal Membrane Oxygenation in Acute Respiratory Failure due to Hemorrhagic Alveolitis in a Patient with Acute Myeloblastic Leukemia

Ketamine, initially developed as an anesthetic, has shown versatility in medical applications, including pain management, treatment-resistant depression, and sedation in the intensive care unit (ICU). While generally well-tolerated, long-term use at high doses raises concerns about potential toxicities, particularly in the liver. We present a case of a 27-year-old female with a complex medical history who received ketamine infusion for ICU sedation and experienced a sudden rise in liver function tests (LFTs), indicating possible ketamine-induced liver injury (KILI). The patient’s liver function normalized after ketamine discontinuation. KILI is infrequent with short-term ketamine use, but emerging case reports suggest it may be associated with chronic or intermittent exposure. The underlying mechanisms for KILI are not fully understood but may involve the accumulation of ketamine metabolites, causing direct toxic effects on the liver. As ketamine’s use expands, especially in critical care settings, clinicians should be vigilant for the potential development of KILI. Further research is needed to better understand its risk factors and mechanisms, as early detection and management of KILI are crucial to ensuring patient safety and optimizing ketamine’s therapeutic benefits.

Noah Yoo

Sarun Thomas

Michael Bender

Xian Jie Cindy Cheng

A Case of Hepatotoxicity Induced by Therapeutic Ketamine Use for Sedation

A 56-year-old woman was transferred to the intensive care unit (ICU) two days after an allogeneic stem cell transplantation (ASCT) when she presented acute respiratory distress due to the relapse of a SARS-CoV-2 infection. Following that, she received two intravenous doses of 100 mg remdesivir. Subsequently, the patient developed multiple instances of diarrhea, progressing to oliguria and acute kidney injury, necessitating continuous venovenous hemofiltration (CVVH). Despite the absence of signs of hypoxemia or cardiocirculatory failure requiring vasopressor intervention, a progressive lactic acidosis emerged. Two days after the onset of lactic acidosis, a significant rise in aminotransferases and lactate dehydrogenase occurred, in the absence of encephalopathy and coagulation disorders. Remdesivir therapy had been interrupted upon the initial signs of lactic acidosis. Despite an improvement in liver function tests and lactic acidosis, the patient’s condition deteriorated, ultimately leading to her demise on day 29 due to newly arising hematological complications.

Elise André

Florian Lemaitre

Marie-Clémence Verdier

Vincent Haufroid

João Pinto Pereira

Philippe Hantson

Transient Lactic Acidosis and Elevation of Transaminases after the Introduction of Remdesivir in a Patient with Acute Kidney Injury

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<p><em>Case Reports in Critical Care</em> publishes case reports and case series in all areas of critical care medicine, including anesthesiology, perioperative and critical care medicine, and postoperative critical care management and recovery.</p>


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Case Reports in Critical Care - Table of contents 2024

title

Case Reports in Critical Care publishes case reports and case series in all areas of critical care medicine, including anesthesiology, perioperative and critical care medicine, and postoperative critical care management and recovery.

Case Reports in Critical Care