Diagnostic Methods in Forensic Pathology: Autoptic Findings and Immunohistochemical Study in Cases of Sudden Death Due to a Colloid Cyst of the Third Ventricle.

The colloid cyst is a non-malignant tumor growth made of a gelatinous material covered by a membrane of epithelial tissue. It is usually located posterior to the foramen of Monro, in the anterior aspect of the third ventricle of the brain. Due to its location, it can cause obstructive hydrocephalus, increased intracranial pressure, and sudden cardiac death, catecholamine-mediated, through hypothalamus compression. All the mechanisms are still controversial, but the role of catecholamine has been confirmed with histological findings that highlighted myocardial injury (coagulative myocytolysis and contraction band necrosis, CBN). This study presents a case of sudden death in a previously healthy 22-year-old male due to a colloid cyst of the third ventricle. A complete autopsy was performed, highlighting in the brain an abundant quantity of cerebrospinal fluid (CSF) and a 2 cm pale grayish-green rounded cyst formation partially filling and distending the third ventricle. The diagnosis was confirmed through immunohistochemical investigation: positivity for Periodic acid-Schiff (PAS) staining and CK7 expression. In cases such as the one reported here, a combined approach of autopsy, histology, and immunohistochemistry is mandatory in order to identify the neoformation's location and morpho-structural characteristics for a correct differential diagnosis, as well as to identify the cause of death.

Neurogenic pulmonary edema and Takotsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage.

PURPOSE: Neurogenic pulmonary edema (NPE) combined with Takotsubo cardiomyopathy (TCM) is a rare condition associated with aneurysmal subarachnoid hemorrhage (aSAH). Although several mechanisms have been proposed, the pathophysiology and management strategies are not yet fully established. We aimed to determine the radiological and clinical outcomes of patients with NPE and with TCM after aSAH to propose management strategies. METHODS: We analyzed the data of 564 patients with aSAH recorded at a single medical center from February 2015 to July 2022. This study retrospectively investigated the incidence and demographics of SAH combined with both NPE and TCM and the clinical outcomes of the patients. Correlating factors, independently associated with NPE-TCM, were also investigated. RESULTS: During the 7 years, 11 (2.0%) of 564 patients had NPE complicated with TCM after aSAH. Seven of 11 (63.6%) patients had poor-grade SAH (Hunt-Hess Grade 4 to 5). Three of 11 patients had a posterior circulation in the NPE-TCM group. The most prevalent treatment option was endovascular coil embolization, except for one case of clip. Long-term outcomes were favorable in 6 of 11 patients, and there was one case of mortality. Age, troponin I level, and alveolar-arterial oxygen gradient were correlating factors of NPE-TCM. CONCLUSION: Although NPE-TCM represents a rare complication associated with aSAH, achieving active resolution of underlying neurological causes through early and appropriate treatment may contribute to a favorable prognosis. Considering the limited incidence of SAH complicated with NPE-TCM, a multi-center study may be needed.

Cerebral arterial gas embolism and neurogenic stunned myocardium in a previously healthy freediver.

Cardiomyopathy is a known but rare sequelae of diving-related cerebral arterial gas embolism (CAGE). In previously reported cases, patient findings have been consistent with takotsubo cardiomyopathy (TCM) per the revised Mayo Clinic's diagnostic criteria. A lesser-known variant of stress-related cardiomyopathy is neurogenic stunned myocardium (NSM), which occurs after a neurological event such as subarachnoid hemorrhage and typically presents in younger patients. Presentation tends to differ slightly to TCM with non-specific left ventricular dysfunction and T wave inversions. This case adds to the rare numbers of reported cardiomyopathy from diving and is the first reported case of suspected NSM associated with CAGE.

Role of the protein kinase A signaling pathway and identification of mediators in the cardioprotective effects of enteral lactoferrin for ischemia-reperfusion injury in an isolated rat heart model.

OBJECTIVE: Lactoferrin is an iron-binding glycoprotein. Enteral lactoferrin attenuates myocardial ischemia-reperfusion (IR) injury, but the underlying mechanism remains unknown. The aim of this study was to investigate protein kinase A (PKA) signaling pathway activation and levels of serum glucagonlike peptide-1 (GLP-1), secreted by intestinal endocrine L cells, and adiponectin, secreted by adipose tissue, after enteral lactoferrin administration. METHODS: Hearts (N = 32) were excised from Wistar rats and perfused using a Langendorff system. To assess the role of the PKA pathway in the cardioprotective effects of lactoferrin, an inhibitor of PKA (H89) was applied before no-flow ischemia. Rats were randomly divided into four groups: control, lactoferrin (LF), control+H89, and LF+H89. The control and control+H89 groups were administered normal saline by gavage, and the LF and L +H89 groups were administered bovine lactoferrin (1000 mg/kg) by gavage 15 min before intraperitoneal pentobarbital injection. Muscle sampling was performed at the end of reperfusion. When rats were sacrificed, blood was sampled to measure hormone levels. The primary outcome was maximum left ventricular pressure derivative (LV dP/dt max) 15 min after reperfusion. RESULTS: LV dP/dt max at 10 and 15 min after reperfusion was significantly higher in the LF group than in the control group (P < 0.05), and the effect was diminished by H89. The PKA pathway was significantly activated in the LF group. Enteral lactoferrin increased serum GLP-1 but not serum adiponectin levels. CONCLUSIONS: Enteral lactoferrin induces cardioprotective effects against myocardial IR injury via the PKA signaling pathway and increases serum GLP-1 levels.

Takotsubo Cardiomyopathy in a Polytrauma Patient With Subarachnoid Hemorrhage.

Takotsubo cardiomyopathy (TCM) is a sudden, transient myocardial stunning precipitated by severe emotional or physical stress. It is characterized by left ventricular apical ballooning and elevated cardiac enzymes without significant coronary artery stenosis. Stress-induced catecholamine surge has been proposed to be the likely mechanism of TCM. We report the case of a 23-year-old female who presented to the emergency department unconscious and in respiratory distress following a motor vehicle accident. The point-of-care ultrasonography showed prominent B lines in bilateral lung fields and a dilated inferior vena cava (IVC). An x-ray and computed tomography (CT) scan of the chest revealed bilateral diffuse ground glass opacities. A CT scan of the brain showed a subarachnoid hemorrhage (SAH). Electrocardiography (ECG) showed normal sinus rhythm, but troponin I was elevated. Echocardiography revealed left ventricular apical hypokinesia. The coronary angiogram was normal. A diagnosis of TCM with SAH was made. Appropriate emergent care was provided, and at follow-up, she made a complete cardiologic recovery. TCM is a puzzling condition in an emergency setting and accurate and timely diagnosis is imperative in the management. Early prevention of hypoxemia and maintenance of mean arterial pressure and cerebral perfusion pressure is critical in determining the long-term outcome of the patient in the setting of co-existing CNS pathologies.

Hematomyelia Presenting with Neurogenic Stunned Myocardium.

Various neurological disorders and emotional stress may cause left ventricular dysfunction, known as a neurogenic stunned myocardium. A previously healthy 71-year-old woman collapsed immediately after experiencing left arm numbness and pain. Thereafter, the patient complained of anterior chest pain and became comatose. An electrocardiogram showed ST-segment elevation of I, aVL, and V2-3 and depression of II, III, and aVF. Echocardiography revealed anteroseptal hypokinesis of the left ventricle. Emergency coronary angiography revealed no significant stenosis in the coronary arteries; however, left ventriculography revealed obvious anteroseptal hypokinesis. When the patient regained consciousness the following day, tetraplegia was observed. Spinal computed tomography and magnetic resonance imaging revealed an intramedullary spinal cord hemorrhage from the medulla to the conus. The cardiac function recovered, but the patient remained tetraplegic with poor spontaneous respiration. Although its incidence is extremely rare, hematomyelia should be recognized as a potential cause of neurogenic stunned myocardium.

Acute neurogenic stunned myocardium in a patient with Guillain-Barré syndrome: case report.

Autonomic dysfunction is a prevalent symptom of Guillain-Barré syndrome (GBS); cardiovascular involvement in this scenario has been mentioned infrequently in the literature. Case Presentation: A 65-year-old man with GBS presented with reversible left ventricular systolic failure. On first presentation, our patient had no history or indications of heart malfunction. During the clinical manifestation of his autonomic dysfunction, he had electrocardiographic alterations, modestly increased cardiac enzymes, significant left ventricular systolic dysfunction, and segmental wall motion irregularity. Once the initial episode was over, these anomalies and his symptoms resolved quickly. Discussion: We believe the reversible left ventricular dysfunction was caused by the toxic impact of elevated catecholamines as well as transiently injured sympathetic nerve endings in the myocardium, which was apparently caused by GBS. We recommend that echocardiography be performed in patients who exhibit clinical signs of autonomic dysfunction, particularly if they are associated with abnormal electrocardiographic findings, cardiac enzyme elevation, or hemodynamic instability, so that appropriate medical therapy can be instituted as soon as possible. Conclusion: GBS is a not a very rare situation in our context. Thus, doctors are supposed to know the life-threatening complications such as neurogenic stunned myocardium and be prepared to dodge it.

Cardiac patterns for differentiation of neurogenic stunned myocardium in aneurysmal subarachnoid hemorrhage versus acute ischemic stroke.

AIMS: Neurogenic stunned myocardium (NSM) has heterogeneous presentations for acute ischemic stroke (AIS) and aneurysmal subarachnoid hemorrhage (SAH). We sought to better define NSM and differences between AIS and SAH by evaluating individual left ventricular (LV) functional patterns by speckle tracking echocardiography (STE). METHODS: We evaluated consecutive patients with SAH and AIS. Via STE, LV longitudinal strain (LS) values of basal, mid, and apical segments were averaged and compared. Different multivariable logistic regression models were created by defining stroke subtype (SAH or AIS) and functional outcome as dependent variables. RESULTS: One hundred thirty-four patients with SAH and AIS were identified. Univariable analyses using the chi-squared test and independent samples t-test identified demographic variables and global and regional LS segments with significant differences. In multivariable logistic regression analysis, when comparing AIS to SAH, AIS was associated with older age (OR 1.07, 95% CI 1.02-1.13, p = 0.01), poor clinical condition on admission (OR 7.74, 95% CI 2.33-25.71, p < 0.001), decreased likelihood of elevated admission serum troponin (OR .09, 95% CI .02-.35, p < 0.001), and worse LS basal segments (OR 1.18, 95% CI 1.02-1.37, p = 0.03). CONCLUSION: In patients with neurogenic stunned myocardium, significantly impaired LV contraction by LS basal segments was found in patients with AIS but not with SAH. Individual LV segments in our combined SAH and AIS population were also not associated with clinical outcomes. Our findings suggest that strain echocardiography may identify subtle forms of NSM and help differentiate the NSM pathophysiology in SAH and AIS.

The Incidence of Takotsubo Cardiomyopathy in Patients with Intracerebral Hemorrhage: A US Nationwide Study.

BACKGROUND: Takotsubo cardiomyopathy (TC) is a commonly observed complication among patients with intracerebral hemorrhage (ICH); however, the incidence of TC in patients with ICH have not been investigated yet. The goal of this study was to examine the incidence of TC in ICH and identify its risk factors, incidence rate, and outcomes of TC in patients with ICH in a US nationwide scale. METHODS: Data for patients with ICH between the years of 2015 and 2018 were extracted from the Nationwide Inpatient Sample and stratified based on the diagnosis of TC. RESULTS: Our results showed that the incidence rate of TC in ICH discharges was 0.27% (95% confidence interval [CI] 0.24-0.31). The mean age of patients with ICH developing TC was 66.28 years ± 17.11. There were significantly more women in the TC group, with an odds ratio (OR) of 3.65 (95% CI 2.63-5.05). Acute myocardial infarction (OR 7.91, 95% CI 5.80-10.80) was significantly higher in the TC group. The mortality rate of patients with ICH who had TC was significantly higher (33.48%, p < 0.0001). Length of stay (mean days; 15.72 ± 13.56 vs. 9.56 ± 14.10, p < 0.0001) significantly increased in patients with ICH who had TC. Patients with intraventricular ICH (OR 2.46, 95% CI 1.88-3.22) had the highest odds of TC. CONCLUSIONS: Takotsubo cardiomyopathy is associated with a higher mortality, longer hospitalization period, and more acute myocardial infarctions in patients with ICH. It is illustrated that intraventricular ICH is associated with higher odds of TC.

Diagnosis and Management of Takotsubo Syndrome in Acute Aneurysmal Subarachnoid Hemorrhage: A Comprehensive Review.

Takotsubo syndrome (TS) is a frequent complication of subarachnoid hemorrhage (SAH), especially in massive SAH with severe neurological damage. The initial presentation of TS is similar to acute coronary syndrome, causing differential diagnostic issues. Unnecessary diagnostic steps and uncertainty in therapy may delay the definitive treatment of the aneurysm, therefore increasing the risk of rebleeding. The purpose of this review is to summarize the latest knowledge on the diagnosis and therapy of TS in SAH and to provide a diagnostic and therapeutic algorithm for the acute phase, promoting the early definitive treatment of the aneurysm. Rapid hemodynamic stabilization and early aneurysm securing are key points in reducing the risk of delayed cerebral ischemia and improving outcomes. In acute SAH noninvasive bedside diagnostic methods are preferred and securing the aneurysm is the priority. The combination of electrocardiography, cardiac biomarkers, and echocardiography is of great importance in differentiating TS from acute myocardial infarction. The risk-benefit ratio of coronary angiography should be carefully and individually considered and its use should be limited to patients with strong evidence of myocardial ischemia, after the successful endovascular treatment of the aneurysm. Invasive hemodynamic monitoring may be beneficial in cases of cardiogenic shock or pulmonary edema. In patients with hemodynamical instability secondary to TS, the use of non-catecholamine inotropes, especially levosimendan is recommended. In refractory hypotension, mechanical support should be considered. The left ventricular function improves within days to months after the acute event, low initial ejection fraction may predispose to delayed recovery.

Cardioprotective effects of enteral vs. parenteral lactoferrin administration on myocardial ischemia-reperfusion injury in a rat model of stunned myocardium.

BACKGROUND: Lactoferrin, an iron-binding glycoprotein, is known to have protective effects against intestinal and cerebral ischemia-reperfusion (IR) injuries; however, its cardioprotective effects against the stunned myocardium are unknown. This study aimed to test the hypothesis that lactoferrin has cardioprotective effects against stunned myocardium. METHODS: Using isolated rat hearts (Langendorff system), we determined the effects of lactoferrin administered enterally and by direct cardiac perfusion. Rat hearts were perfused using the Langendorff system, and two experiments were performed. In experiment 1, the hearts were divided into the enteral lactoferrin (E-LF) 7.5 m, 15 m, 30 m, and 60 m groups, where lactoferrin (1000 mg/kg) was administered enterally 7.5, 15, 30, and 60 min, respectively, before perfusion; and a control group, where saline was administered 30 min before perfusion. In experiment 2, hearts were allocated to the perfusate lactoferrin (P-LF) 15 and 100 groups, where 15 mg/L and 100 mg/L lactoferrin were respectively added to the perfusate, and a control group. Each group was perfused for 20 min prior to 15 min of no-flow ischemia with pacing, followed by 20 min of reperfusion. The primary outcome was the maximum left ventricular derivative of pressure development (LV dP/dt max) 15 min after reperfusion. Myocardial phospho-protein kinase B (p-Akt) was assayed using western blotting. RESULTS: The LV dP/dt max 15 min after reperfusion in the E-LF 15 and 30 m groups was significantly higher than that in the control group. However, the effects disappeared in the E-LF 60 m group. In the second experiment, there were no significant differences in LV dP/dt max. Myocardial p-Akt was not significantly activated in any lactoferrin group. CONCLUSION: Cardioprotection was observed 15-30 min after enteral lactoferrin but not by direct cardiac perfusion with lactoferrin. Myocardial p-Akt was not associated with the cardioprotective effect. The cardioprotective effect may be induced by enteral lactoferrin-induced substances.

A Rare Case of Postoperative Extradural Hematoma in the Posterior Fossa Complicated by Both Stunned Myocardium and Neurogenic Pulmonary Edema.

Acute neurological insult can trigger a cascade of events in other organ systems such as the heart and lung. Neurogenic stunned myocardium (NSM) and Neurogenic pulmonary edema (NPE) are mostly reported after stroke, subarachnoid hemorrhage, or seizures whenever sympathetic storm and autonomic dysregulation occurs. We report here for the first time, a case of postoperative infratentorial extradural hematoma in a patient triggering NSM and NPE at the same time. The challenges involved in the management of such a patient are described in this case report. The patient was successfully managed and discharged home with no new neurological deficits.

Takotsubo cardiomyopathy following a simple partial seizure.

A 67-year-old woman presented to the emergency department for a simple partial seizure of her left upper and lower limbs that lasted for 1 hour and ultimately resolved before her presentation. She had no history of coronary artery disease, and her neurological exam was normal. Five hours later, she complained of chest pain. An electrocardiogram showed ST segment elevation in the lateral leads, and her troponin level was increased. She was diagnosed with takotsubo cardiomyopathy. This case reflects the brain-heart connection and is the first reported case of takotsubo cardiomyopathy following a simple partial seizure.

Neurogenic stunned myocardium resulting from surgical brainstem handling during resection of paediatric recurrent medulloblastoma-a possible brain heart interaction.

BACKGROUND: Neurogenic stunned myocardium (NSM) is characterised by an acute onset cardiac dysfunction following an acute neurological insult which mimics acute coronary syndrome. CASE DETAILS: A 12-year-old male child was admitted to the neuro-intensive care unit (NICU) following midline suboccipital craniotomy and resection of recurrent medulloblastoma. Postoperatively, in NICU, he developed tachycardia and hypotension, which was unresponsive to fluid challenge requiring norepinephrine infusion. Intraoperatively, during tumour resection from the dorsal medulla, episodes of hypertension and bradycardia were observed. Intraoperative blood loss was adequately managed with a stable hemodynamic profile without postoperative anaemia. An electrocardiogram showed sinus tachycardia with T wave inversion, and blood investigation revealed elevated cardiac troponin T levels. Point of care ultrasound (POCUS) of heart and lung showed features of NSM. Infusion dobutamine was added to achieve a target mean arterial pressure of 65 mm Hg with concomitant furosemide infusion and fluid restriction. Daily POCUS assessment of cardiac contractility and volume status was done. The patient was weaned from vasoactive drugs and ventilator following improvement of cardiac function and was discharged from NICU after 17 days. CONCLUSION: NSM results from the excessive release of catecholamines following stimulation of trigger zones in the brain. To date, a handful of cases of pediatric NSM following primary brain tumour are reported where hydrocephalus resulted in trigger zone activation. In this presented case, direct brain stem stimulation during tumour resection might have triggered NSM. Irrespective of the cause, timely diagnosis and execution of supportive management in our patient resulted in a positive outcome.

Atrio-ventricular block and takotsubo syndrome: A review illustrated with two case reports.

Takotsubo syndrome (TS) can be complicated by life-threatening arrhythmias. Data on the association of AV-block, pacemaker implantation, and TS are scarce. We describe two cases of AV-block associated with TS. AV-block persisted despite the recovery of left ventricular dysfunction during follow-up. A review of AV-block and TS association is provided.

"Broken Heart" and "Broken Brain": Which Connection?

The interconnections between brain and heart are increasingly recognized. Takotsubo cardiomyopathy, also known as "broken heart syndrome", is characterized by a cardiovascular dysfunction provoked by an emotional or stressful situation. Similar events can trigger a neurological pathology called transient global amnesia. These conditions can occur simultaneously, although their precise connection is not well understood. We aim to present the case of a patient who experienced them and to review the relevant literature.

Takotsubo cardiomyopathy in post-traumatic brain injury: A systematic review of diagnosis and management.

OBJECTIVE: Myocardial dysfunction is a known complication in patients who experience severe stressful events, such as traumatic brain injuries (TBI). One common manifestation is Takotsubo Cardiomyopathy (TC) which can appear concomitantly in patients with haemorrhagic brain injuries. There is often a management dilemma when two conditions with conflicting treatment regimens arise in the same individual. Previous systematic review had highlighted the importance of accurate diagnosis but there is no algorithm to aid decision-making in an emergency trauma setting. A systematic review was performed with the aim of establishing a new algorithm to aid in the diagnosis and management of TC patients with concurrent TBI. METHODS: We performed a comprehensive search of Pubmed, google scholar, Embase and Cochrane databases using keywords 'traumatic brain injury' and 'head injury' associated with keywords of 'Takotsubo cardiomyopathy,' 'Tako-tsubo cardiomyopathy,' 'stress cardiomyopathy,' 'stunned myocardium,' 'transient-left-ventricular ballooning syndrome,' 'apical ballooning syndrome,' 'myocardial dysfunction' or 'heart failure'. Non traumatic brain injury, blunt cardiac injury or cardiac events from chest trauma were excluded. The search was done between 1st to 4th October 2020 and only articles published after the year 2000 in English were included. Articles were then analysed in-depth. No articles were excluded after analysis to remove reporting bias. RESULTS: A total of 11 case reports and 7 cohort studies were analysed, giving a total number of 382 patients, with 36% of the patients analysed presenting with subdural haematoma, 27% with subarachnoid haemorrhage and 5% with extradural haematoma. Of the patients who underwent surgical interventions for traumatic brain injuries, 75% survived. 9% of patients in total were reported to have an EF of less than 55% whereas 51% had an EF of equal to or more than 55%. TTE details were not reported in a total of 35% of patients. All case reports which had followed up on their patient's cardiac status with repeated echocardiography had demonstrated a resolution of cardiac function independent of cardiac intervention. DISCUSSION: Our analysis was limited by the fact that not all papers analysed had reported the parameters we required. However, based on our review, we conclude that most patients with TC demonstrate a resolution of cardiac function independent of cardiac interventions from as fast as a few hours to as long as 6-12 weeks. Therefore, despite high cardiac risks, if neurosurgical intervention is needed, it should be offered to improve the chance of survival as transient cardiomyopathy can be supported with inotropes. We have developed a new algorithm for management of cases of concurrent TBI and TC.

Regression of Q waves and clinical outcomes following primary PCI in anterior STEMI.

BACKGROUND: Pathological Q waves are correlated with infarct size, and Q-wave regression is associated with left ventricular ejection fraction improvement. There are limited data regarding the association of Q-wave regression and clinical outcomes. Our main objective was to assess the association of pathological Q wave evolution after reperfusion with clinical outcomes after anterior STEMI. METHODS: Standard 12-lead electrocardiograms (ECGs) were recorded in 780 anterior STEMI patients treated with primary percutaneous coronary intervention (PCI) from the CIRCUS trial. ECGs were recorded before and 90 min following PCI, as well as at hospitalization discharge and 12 months of follow-up. The number of classic ECG criteria Q waves was scored for each ECG. Patients were classified in the Q wave regression group if they had regression of at least one Q wave between the post-PCI, the discharge and/or one year ECGs. Patients were classified in the Q wave persistent group if they had the same number or greater between the post-PCI, the discharge and/or 1 and one year ECGs. All-cause death and heart failure events were assessed for all patients at one year. RESULTS: There were 323(43%) patients with persistent Q waves (PQ group), 378(49%) patients with Q wave regression (RQ group) and 60(8%) patients with non-Q wave MI (NQ group). Infarct size as measured by the peak creatine kinase was significantly greater in the PQ group compared to the RQ and NQ groups (4633 ±â€¯2784 IU/l vs. 3814 ±â€¯2595 IU/l vs. 1733 ±â€¯1583 IU/l respectively, p < 0.0001). At one year, there were 22 deaths (7%) in the PQ-group, 15 (4%) in the RQ-group and none in the NQ-group (p = 0.04). There was a 4-fold increase in the risk of death or heart failure in the PQ compared to the NQ group (HR 4.7 [1.1; 19.3]; p = 0.03), but there was no significant difference between NQ and RQ groups (HR 3.3 [0.8; 13.8]; p = 0.09). CONCLUSION: In a population of anterior STEMI patients, persistent Q waves defined according to the classic ECG criteria after reperfusion was associated with a 4-fold increase in the risk of heart failure or death compared to non-Q-wave MI, while Q-wave regression was associated with significantly lower risk of events.

Aneurysmal subarachnoid hemorrhage as a trigger for Takotsubo syndrome: a comprehensive review.

Takotsubo syndrome (TTS) can result in acute heart failure and lead to a potentially life-threatening complication of aneurysmal subarachnoid hemorrhage (aSAH). The incidence of TTS in aSAH is less than 10% of all patients with aSAH, with a preponderance of postmenopausal women. Early indicators of TTS include elevated serum troponin levels and electrocardiographic abnormalities. The key finding is left ventricular wall motion abnormality. Echocardiography and coronary angiography help to establish the diagnosis. Vasopressors, milrinone, levosimendan, insulin, and anticoagulation may be required. The value of beta-blockers is a matter of controversy. TTS must not delay the treatment of a ruptured aneurysm. The clinical outcome in patients with aSAH and TTS is mostly determined by the aSAH and not the TTS.

Neurogenic Stunned Myocardium Following an Attempt to Pass a Drug Test.

Ingestion of a large volume of free water or other hypotonic solution can cause acute hyponatremia, leading to multiorgan dysfunction. Individuals may attempt to generate a false-negative urine drug screen through increased free water consumption leading to acute hyponatremia requiring emergency medical care. We present the case of a 19-year-old male who presented to a community emergency department for altered mental status after an attempt to generate a false-negative urine drug screen. He ingested a large volume of free water and multiple detoxification solutions, causing acute hyponatremia with resultant cerebral edema and neurogenic stunned myocardium. He required extracorporeal membrane oxygenation therapy with complete recovery of neurologic and cardiac function. Acute hyponatremia from excess free water consumption is a well-documented phenomenon that all emergency providers should be aware of. Prompt identification and management of acute hyponatremia are essential to prevent potentially severe, devastating sequelae, including cerebral edema and cardiopulmonary failure.In addition, extracorporeal membrane oxygenation may be considered in patients with cardiopulmonary failure in the setting of reversible cardiomyopathy, as evidenced in our case.