Paroxysmal Sympathetic Hyperactivity Research Articles

Bispectral Index Monitoring in the Nursing of Patients With Paroxysmal Sympathetic Hyperactivity.

To investigate the clinical nursing effect of bispectral index (BIS) monitoring for paroxysmal sympathetic hyperactivity (PSH) patients in the neurosurgical intensive care unit (NICU). From January 2022 to June 2023, a total of 30 patients with PSH secondary to moderate to severe craniocerebral injury in the NICU were monitored for BIS. The patients' paroxysmal sympathetic hyperactivity-assessment measure (PSH-AM) scores were recorded. PSH patients generally appear in 3 states: calm state, seizure state, and postmedication state. Thirty PSH patients' BIS values were recorded during the calm period, during the seizure state, and postmedication state, and these 3 different stages' BIS values were divided into groups A, B, and C, using the Kruskal-Wallis H test to compare groups. The Kruskal-Wallis H test yielded a value of H=22.599, P<0.001. H0 was rejected against the test standard of α=0.05, and the BIS values of groups A, B, and C differed. The BIS values of group A and group B differed after a pairwise comparison, and the difference was statistically significant (adjusted P=0.001). Group B and group C had different BIS values, and the difference was statistically significant (adjusted P=0.001); group A and Group C had no difference in BIS values, and the difference was not statistically significant (adjusted P=1.00). Taking BIS value as the nursing observation index for PSH patients can make nursing work more objective, reasonable, and accurate, reduce the inducing factors of PSH attack, further reduce the attack of PSH, save nursing resources, and help guide the safety assessment of sedative use.

Decreased levels of hydrogen sulfide in the hypothalamic paraventricular nucleus contribute to sympathetic hyperactivity induced by cerebral infarction.

Paroxysmal sympathetic hyperactivity (PSH) is a common clinical feature secondary to ischemic stroke (IS), but its mechanism is poorly understood. We aimed to investigate the role of H2S in the pathogenesis of PSH. IS patients were divided into malignant (MCI) and non-malignant cerebral infarction (NMCI) group. IS in rats was induced by the right middle cerebral artery occlusion (MCAO). H2S donor (NaHS) or inhibitor (aminooxy-acetic acid, AOAA) were microinjected into the hypothalamic paraventricular nucleus (PVN). Compared with the NMCI group, patients in the MCI group showed PSH, including tachycardia, hypertension, and more plasma norepinephrine (NE) that was positively correlated with levels of creatine kinase, glutamate transaminase, and creatinine respectively. The 1-year survival rate of patients with high plasma NE levels was lower. The hypothalamus of rats with MCAO showed increased activity, especially in the PVN region. The levels of H2S in PVN of the rats with MCAO were reduced, while the blood pressure and renal sympathetic discharge were increased, which could be ameliorated by NaHS and exacerbated by AOAA. NaHS completely reduced the disulfide bond of NMDAR1 in PC12 cells. The inhibition of NMDAR by MK-801 microinjected in PVN of rats with MCAO also could lower blood pressure and renal sympathetic discharge. In conclusion, PSH may be associated with disease progression and survival in patients with IS. Decreased levels of H2S in PVN were involved in regulating sympathetic efferent activity after cerebral infarction. Our results might provide a new strategy and target for the prevention and treatment of PSH.

Magnetic Resonance Imaging Lesions Associated With Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

Magnetic Resonance Imaging Lesions Associated With Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

Beyond the brain: General intensive care considerations in pediatric neurocritical care

Managing children with critical neurological conditions requires a comprehensive understanding of several principles of critical care. Providing a holistic approach that addresses not only the acute interactions between the brain and different organ systems, but also critical illness-associated complications and recovery is essential for improving outcomes in these patients.The brain reacts to an insult with autonomic responses designed to optimize cardiac output and perfusion, which can paradoxically be detrimental. Managing neuro-cardiac interactions therefore requires balancing adequate cerebral perfusion and minimizing complications. The need for intubation and airway protection in patients with acute encephalopathy should be individualized following careful risk/benefit deliberations. Ventilatory strategies can have profound impact on cerebral perfusion. Therefore, understanding neuro-pulmonary interactions is vital to optimize ventilation and oxygenation to support a healing brain. Gastrointestinal dysfunction is common and often complicates the care of patients with critical neurological conditions. Kidney function, along with fluid status and electrolyte derangements, should also be carefully managed in the acutely injured brain. While in the pediatric intensive care unit, prevention of critical illness-associated complications such as healthcare-associated infections and deep vein thrombosis is vital in improving outcomes. As the brain emerges from the acute injury, rehabilitation and management of delirium and paroxysmal sympathetic hyperactivity is paramount for optimal recovery. All these considerations provide a foundation for the care of pediatric patients with critical neurological conditions in the intensive care unit.

Takotsubo syndrome linked to paroxysmal sympathetic hyperactivity as a postoperative complication after brain tumor removal: a case report and literature review.

Paroxysmal sympathetic hyperactivity (PSH) is a relatively common syndrome typically observed following traumatic brain injury (TBI). It manifests through a combination of non-specific symptoms that collectively define its presentation. Linked to sympathetic hyperactivity, takotsubo syndrome is a cardiomyopathy marked by left ventricular dysfunction and may coincide with PSH. While various factors can lead to the simultaneous occurrence of these syndromes, a notably rare scenario involves their manifestation after brain tumor removal. The nonspecific nature of PSH symptoms and of the cardiac dysfunction in takotsubo syndrome pose challenges in accurately diagnosing these conditions in an intensive care unit (ICU) setting. They often overlap with more prevalent diagnoses like sepsis, pulmonary embolism, and acute heart failure. Thus, it is crucial for clinicians dealing with these patients to be aware that symptoms indicating sympathetic activity surge and left heart failure might prompt consideration of takotsubo syndrome and PSH. This study presents the case of an 8-year-old girl who developed takotsubo syndrome associated with sympathetic hyperactivity following the surgical removal of a bulbar tumor. To the best of our knowledge, this is the tenth case of PSH following brain tumor removal in a pediatric patient and the first reported case of occurrence of takotsubo linked to PSH after brain tumor removal. We offer a detailed account of the patient's clinical journey in the ICU, accompanied by a comprehensive review of relevant literature to identify similar cases. The significance of this case study lies in emphasizing the potential occurrence of takotsubo syndrome due to PSH and underscores the importance of early diagnosis and management due to their association with unfavorable clinical outcomes.

Role of Gabapentin in Traumatic Brain Injury: A Prospective Comparative Study.

Traumatic brain injury (TBI) is a major cause of mortality among young individuals, accounting for 65% of deaths in road traffic accidents. Paroxysmal sympathetic hyperactivity (PSH) is a common syndrome associated with TBI. This study represents the first prospective investigation aimed at assessing the impact of gabapentin on TBI patients, focusing on the prevention of secondary brain injury and brain edema while enhancing the Glasgow Coma Scale (GCS). The study was conducted from September 2019 to July 2021 after receiving ethical committee approval. It included adult ICU patients (≥18 years) with moderate and severe GCS. Patients below 18 years, death within 48 hours, non-consenting, pregnant females, and individuals allergic to gabapentin were excluded from the study. Patients were randomly allocated in two groups: study group received 300 mg of gabapentin orally twice daily and control group received multivitamin tablets twice daily. The treatment period spanned 2 weeks. Follow-up occurred in the ICU and continued for up to 3 months post-discharge, including telephonic conversations. About 60 patients were involved for analysis. Significant differences were found in GCS change from admission to discharge, Glasgow Outcome Scale (GOS) at 30 and 90 days, PSH episodes, and sedation bolus per day. Glasgow Coma Scale change was 53% in the study group compared with 25% in the control group (p = 0.009). Mortality was significantly lower in the study group. Glasgow Outcome Scale change between 30 and 90 days showed a 25% improvement in cases and no change in controls (p = 0.001). This pioneering study underscores the potential of gabapentin in managing traumatic brain injuries. Singh R, Ambasta S, Bais PS, Azim A, Kumar S, Upreti B, et al. Role of Gabapentin in Traumatic Brain Injury: A Prospective Comparative Study. Indian J Crit Care Med 2024;28(2):120-125.

Medical comorbidities in patients with prolonged disorder of consciousness: A narrative review.

A few studies specifically addressed medical comorbidities (MCs) in patients with severe acquired traumatic or non-traumatic brain injury and prolonged disorders of consciousness (pDoC; i.e., patients in vegetative state/unresponsive wakefulness syndrome, VS/UWS, or in minimally conscious state, MCS). To provide an overview on incidence of MCs in patients with pDoC. Narrative review on most impacting MCs in patients with pDoC, both those directly related to brain damage (epilepsy, neurosurgical complications, spasticity, paroxysmal sympathetic hyperactivity, PSH), and those related to severe disability and prolonged immobility (respiratory comorbidities, endocrine disorders, metabolic abnormalities, heterotopic ossifications). Patients with pDoC are at high risk to develop at least one MC. Moderate or severe respiratory and musculoskeletal comorbidities are the most common MCs. Epilepsy and PSH seem to be more frequent in patients in VS/UWS compared to patients in MCS, likely because of higher severity in the brain damage in VS. Endocrine metabolic, PSH and respiratory complications are less frequent in traumatic etiology, whereas neurogenic heterotopic ossifications are more frequent in traumatic etiology. Spasticity did not significantly differ between VS/UWS and MCS and in the three etiologies. MCs are associated with higher mortality rates, worse clinical improvement and can impact accuracy in the clinical diagnosis. The frequent occurrence of several MCs requires a specialized rehabilitative setting with high level of multidisciplinary medical expertise to prevent, appropriately recognize and treat them. Comprehensive rehabilitation could avoid possible progression to more serious complications that can negatively impact clinical outcomes.

ACTH Secreting Pituitary Microadenoma Presenting with Acute Psychosis, Delirium and Paroxysmal Sympathetic Hyperactivity

ACTH secreting pituitary adenomas are known to be associated with behavioral changes but acute presentation including psychosis and delirium are less common. We report the case of a 42-year-old lady with a known medical history of hypertension and diabetes mellitus, presenting with acute onset behavioral changes suggestive of psychosis. Further evaluation revealed an ACTH dependent Cushing’s disease with a pituitary microadenoma. The patient was admitted for endoscopic resection of the adenoma. During the peri-operative period, she experienced worsening of psychosis along with delirium. She also developed episodes of unresponsiveness, posturing, severe diaphoresis and dyspnea accompanied by tachycardia and hypertension which were managed with Midazolam and Levetiracetam. A seizure work-up and CT brain were unremarkable. At follow-up, she showed full resolution of symptoms with good blood pressure and glycemic control. ACTH secreting pituitary microadenoma presenting with acute psychosis, delirium and paroxysmal sympathetic hyperactivity.&#x0D; Keywords: Cushing’s disease, neuropsychiatric, dysautonomia.

A digital solution for determining the severity of paroxysmal sympathetic hyperactivity syndrome in patients with brain injury

Paroxysmal sympathetic hyperactivity syndrome is a frequent complication of acute severe brain injury, so with severe traumatic brain injury, it develops in 30 % of patients. Despite a large number of publications, the issues of diagnosis, prevention and treatment of this syndrome remain unresolved. To date, the assessment of the syndrome of paroxysmal sympathetic hyperactivity takes, with proper training of the doctor, from 8 to 15 minutes, taking into account the calculation of points using a calculator. With the digitalization of this process, a single assessment will take about 2–3 minutes to enter the indicators. In this case, the calculation will occur automatically. Subsequently, when using «wearable gadgets for measurement», the process of filling in indicators can also occur automatically. The application allows to register and store basic data about users who can have three roles: patients, specialist doctors, administrators. The creation of a database of patients with sympathetic hyperactivity syndrome will significantly improve diagnostic methods and assess the adequacy of therapy. Medical data is only useful if it can be turned into meaningful information. This requires high-quality data sets, uninterrupted communication between IT systems, and standard data formats that can be processed by humans and machines.

Paroxysmal Sympathetic Hyperactivity: Development of a Pediatric Clinical Practice Guideline.

Paroxysmal Sympathetic Hyperactivity: Development of a Pediatric Clinical Practice Guideline.

Paroxysmal Sympathetic Hyperactivity After Acquired Brain Injury: An Integrative Review of Diagnostic and Management Challenges.

Paroxysmal sympathetic hyperactivity (PSH) mainly occurs after acquired brain injury (ABI) and often presents with high fever, hypertension, tachycardia, tachypnea, sweating, and dystonia (increased muscle tone or spasticity). The pathophysiological mechanisms of PSH are not fully understood. Currently, there are several views: (1) disconnection theory, (2) excitatory/inhibitory ratio, (3) neuroendocrine function, and (4) neutrophil extracellular traps. Early diagnosis of PSH remains difficult, given the low specificity of its diagnostic tools and unclear pathogenesis. According to updated case analyses in recent years, PSH is now more commonly observed in patients with stroke, with tachycardia and hypertension as the main clinical manifestations, which is not fully consistent with previous data. To date, the PSH Assessment Measure tool is optimal for the early identification of PSH and stratification of symptom severity. Clinical strategies for the management of PSH are divided into three main points: (1) reduction of stimulation, (2) reduction of sympathetic excitatory afferents, and (3) inhibition of the effects of sympathetic hyperactivity on target organs. However, use of drugs and standards have not yet been harmonized. Further investigation on the relationship between PSH severity and long-term neurological prognosis in patients with ABI is required. This review aimed to determine the diagnostic and management challenges encountered in PSH after ABI.

Plants and their Bioactive Compounds as a Possible Treatment for Traumatic Brain Injury-Induced Multi-Organ Dysfunction Syndrome.

Traumatic brain injury is an outcome of the physical or mechanical impact of external forces on the brain. Thus, the silent epidemic has complex pathophysiology affecting the brain along with extracranial or systemic complications in more than one organ system, including the heart, lungs, liver, kidney, gastrointestinal and endocrine system. which is referred to as Multi-Organ Dysfunction Syndrome. It is driven by three interconnected mechanisms such as systemic hyperinflammation, paroxysmal sympathetic hyperactivity, and immunosuppression-induced sepsis. These multifaceted pathologies accelerate the risk of mortality in clinical settings by interfering with the functions of distant organs through hypertension, cardiac arrhythmias, acute lung injury, neurogenic pulmonary edema, reduced gastrointestinal motility, Cushing ulcers, acute liver failure, acute kidney injury, coagulopathy, endocrine dysfunction, and many other impairments. The pharmaceutical treatment approach for this is highly specific in its mode of action and linked to a variety of side effects, including hallucinations, seizures, anaphylaxis, teeth, bone staining, etc. Therefore, alternative natural medicine treatments are widely accepted due to their broad complementary or synergistic effects on the physiological system with minor side effects. This review is a compilation of the possible mechanisms behind the occurrence of multiorgan dysfunction and reported medicinal plants with organoprotective activity that have not been yet explored against traumatic brain injury and thereby, highlighting the marked possibilities of their effectiveness in the management of multiorgan dysfunction. As a result, we attempted to respond to the hypothesis against the usage of medicinal plants to treat neurodegenerative diseases.

Overlapping Physiologic Signs of Sepsis and Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury: Exploring A Clinical Conundrum.

Paroxysmal sympathetic hyperactivity (PSH) occurs in a subset of patients with traumatic brain injury (TBI) and is associated with worse outcomes. Sepsis is also associated with worse outcomes after TBI and shares several physiologic features with PSH, potentially creating diagnostic confusion and suboptimal management of each. This is the first study to directly investigate the interaction between PSH and infection using robust diagnostic criteria. We performed a retrospective cohort study of patients with TBI admitted to a level I trauma center intensive care unit with hospital length of stay of at least 2weeks. From January 2016 to July 2018, 77 patients diagnosed with PSH were 1:1 matched by age and Glasgow Coma Scale to 77 patients without PSH. Trauma infectious diseases subspecialists prospectively documented assessments corroborating diagnoses of infection. Extracted data including incidence, timing, classification, and anatomical source of infections were compared according to PSH diagnosis. We also evaluated daily PSH clinical feature severity scores and systemic inflammatory response syndrome (SIRS) criteria and compared values for patients with and without confirmed infection, stratified by PSH diagnosis. During the first 2weeks of hospitalization, there were no differences in rates of suspected (62%) nor confirmed (48%) infection between patients with PSH and controls. Specific treatments for PSH were initiated on median hospital day 7 and for confirmed infections on median hospital day 8. SIRS criteria could identify infection only in patients who were not diagnosed with PSH. In the presence of brain injury-induced autonomic nervous system dysregulation, the initiation and continuation of antimicrobial therapy is a challenging clinical decision, as standard physiologic markers of sepsis do not distinguish infected from noninfected patients with PSH, and these entities often present around the same time. Clinicians should be aware that PSH is a potential driver of SIRS, and familiarity with its diagnostic criteria as proposed by the PSH assessment measure is important. Management by a multidisciplinary team attentive to these issues may reduce rates of inappropriate antibiotic usage and misdiagnoses.

Clonidine safety and effectiveness in the management of suspected paroxysmal sympathetic hyperactivity post-traumatic brain injury: A retrospective cohort study.

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. In addition, TBI may cause paroxysmal sympathetic hyperactivity (PSH), which is associated with poor clinical outcomes. This study aimed to evaluate the safety and effectiveness of clonidine in patients with TBI and suspected PSH. A retrospective cohort study for critically ill patients with TBI with suspected PSH admitted to intensive care units (ICUs) from 1 May 2016 to 31 January 2020 at a tertiary academic medical center. Eligible patients were categorized based on clonidine use during their ICU stay (Clonidine group vs. Control group). The primary outcome was the improvement in functional outcomes during ICU stay, defined by a delta Glasgow Coma Score (GCS). Secondary outcomes included ICU and hospital length of stay, heart rate variation, and 90-day mortality. A total of 2915 patients were screened, of which 169 were included. Based on multiple regression analysis, patients who received clonidine showed better improvement in functional outcomes by a higher mean delta GCS than patients who did not (Beta Coeff. 0.41; CI: 0.07 - 0.74; P = 0.02). In addition, the patient's GCS upon ICU discharge and IV opioids requirement on day three were higher in the clonidine group than control (beta coefficient (95% CI): 0.18 (0.03, 0.32); p = 0.02 and beta coefficient (95% CI): 1.38 (0.24, 2.52); p = 0.02, respectively). No statistical differences were observed in any of the other secondary outcomes after adjusting for confounders. This study found that patients who received clonidine had better functional outcomes during their ICU stay, as shown by their delta GCS than those who did not. Other outcomes were similar between the groups. More data are needed to explore the role of clonidine in patients with TBI with suspected PSH.

Treatment of non-epileptic episodes of anxious, fearful behavior in adolescent juvenile neuronal ceroid lipofuscinosis (CLN3 disease).

Recurrent non-epileptic episodes of frightened facial and body expression occur in more than half of post-adolescent patients with juvenile neuronal ceroid lipofuscinosis (JNCL, CLN3 disease). Clinically, the episodes look similar to the attacks of paroxysmal sympathetic hyperactivity (PSH) commonly seen following traumatic brain injury (TBI). The episodes occur when the patients are exposed to separation, hear loud sounds or are otherwise bothered by discomfort and as in PSH following TBI, the attacks are difficult to prevent and/or treat. Based on present knowledge of triggering factors, the neural anxiety/fear circuit, its afferent and efferent pathways and documented CLN3 disease-impact on these tracks, the current study discusses a rational approach how to prevent and/or treat the attacks. Patients with JNCL have a disturbed somatosensory modulation leading to a reduced threshold of pain; a degeneration within the neural anxiety/fear circuit leading to an imbalance of central network inhibition and excitation pathways; and finally, an, with advancing age, increasing autonomic imbalance leading to a significant dominance of the sympathetic neural system. Theoretically, there are three points of attack how to prevent or treat the episodes: (1) increase in threshold of discomfort impact; (2) modulation of imbalance of central network inhibition and excitation, and (3) restoring the balance between the sympathetic and parasympathetic neural systems prompted by a parasympathetic withdrawal. As to (1) and (2), prevention should have the greatest priority. As regards (3), research of transcutaneous vagal stimulation treatment in JNCL is warranted.

Assessment of Risks for Gastrointestinal Bleeding in Patients with Brain Injury

The aim of the study was to develop a risk model for upper gastrointestinal tract (GIT) bleeding in patients with brain injury of various etiologies.Material and methods. Case histories of 33 patients were included into a retrospective descriptive study: 22 patients had severe brain injury of various etiologies, and 11 patients after elective surgery for cerebral aneurisms with uneventful postop period were taken for comparison. The patients were grouped in two arms: Group 1 included patients with obvious signs of GIT bleeding (N=11) and Group 2 had no obvious signs of bleeding (N=22). Complaints, life and medical history, comorbidities, specialists’ exams data, results of laboratory and instrumental examinations, therapeutic regimens were analyzed. Presence of disproportionate pathologic sympathetic overreaction to acute brain injury, i.e., paroxysmal sympathetic hyperactivity (PSH), was assessed on admission and on Days 1, 3 and 5 after brain injury. Results. A model for upper GIT bleeding risk assessment was designed using logistic regression. The resulting model gains high quality rating: χ²=33,78, 3; p&lt;0,001; OR=315. The risk of upper GIT bleeding exceeded 95% in patients having combination of 4 symptoms in their medical history (presence of PSH on Day 1 after acute brain injury; Karnofsky performance scale index 75; lack of neurovegetative stabilization in the acute period of brain injury; gastric and/or duodenal ulcer).Conclusion. Determining the risk factors thresholds enables stratification of patients by the risk for upper GIT bleeding. Modification of the identified four risk factors (presence of PSH on Day 1after acute brain injury; Karnofsky performance scale index 75; lack of neurovegetative stabilization in the acute period of brain injury; gastric and/or duodenal ulcer) will probably reduce the occurrence of upper GIT bleeding in patients with acute brane injury of various etiology.

The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review.

The objective was to evaluate the efficacy and safety of dexmedetomidine in the treatment and prophylaxis of paroxysmal sympathetic hyperactivity (PSH). A review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria and queried Embase, MEDLINE (PubMed), Cochrane CENTRAL, Web of Science, SciELO, Korean Journal Index (Clarivate), Global Index Medicus, and CINAHL Plus for results through June 2023. Studies providing efficacy or safety data associated with dexmedetomidine with a reported diagnosis of PSH were included. Exclusion of studies in pediatric populations, without quantitative and qualitative outcome data, and not readily translatable to English was adhered to. Thirteen observational studies of 178 patients were included in the qualitative analysis. Reductions in PSH frequency or symptom severity were reported in 44 of 48 patients who received dexmedetomidine for acute treatment. Prophylactic use of dexmedetomidine was associated with reductions in PSH-Assessment Measure (PSH-AM) scores in postsurgical patients with traumatic brain injuries (TBIs). Adverse events associated with dexmedetomidine were either absent or reported as none. This review supports the safe and effective use of dexmedetomidine in the treatment and prophylaxis of PSH. Further investigation is required to determine optimal dosing strategies and the extent to which PSH etiology correlated to the efficacy of dexmedetomidine. The use of dexmedetomidine appears to be both efficacious and safe for the treatment and prevention of PSH in patients experiencing a TBI. Additional research is needed to elucidate dosing strategies, titration parameters, and duration of therapy.

Improving Traumatic Brain Injury Outcomes: Early Identification and Management of Paroxysmal Sympathetic Hyperactivity

Improving Traumatic Brain Injury Outcomes: Early Identification and Management of Paroxysmal Sympathetic Hyperactivity

Paroxysmal sympathetic hyperactivity in a child with stroke: a case report

BackgroundParoxysmal sympathetic hyperactivity (PSH) is the result of dysregulated autonomic function with sympathetic symptoms characterised by increased heart rate, respiratory rate, blood pressure and temperature with abnormal posture, which predominately occur periodically but can be persistent in severe cases. Common causes that present in similar fashion such as infectious process (bacteremia, meningitis, etc.); non-PSH neurological deterioration (increased intracranial pressure, intracranial haemorrhage, intracranial oedema, seizures, encephalitis); pulmonary embolism; thyrotoxicosis, alcohol or drug withdrawal; neuroleptic malignant syndrome; serotonin syndrome; and malignant hyperthermia need to be excluded before diagnosing PSH. The earlier the diagnosis made, the better the prognosis.Case presentationWe report a case of a 3-year-old male child who was a diagnosed case of Tetralogy of Fallot presented with left focal seizure with secondary generalisation. Child also had respiratory complaints prior to convulsion. He had developed signs of raised intracranial pressure. Blood culture sent to rule out infective endocarditis was negative. CT brain showed bilateral diffuse cortical infarct. Child developed signs and symptoms of PSH such as fever, tachycardia, tachypnoea, hypertension, diaphoresis, dystonia and bilateral completely dilated pupils. Other common causes such as infective endocarditis, increased intracranial pressure, intracranial oedema, intracranial haemorrhage, seizure, encephalitis and infectious processes (bacteremia, meningitis and infective endocarditis) were ruled out. The diagnosis of PSH was made and started on propranolol along with clonidine. Child responded well to the treatment.ConclusionThe complex pathophysiology of PSH warrants extensive work-up to rule out other common causes. The outcome of our patient shows the importance of early diagnosis and multidisciplinary treatment for better outcome.

Highlighting Paradoxical Cerebral Fat Embolism: Potentially Fatal Sequela of Road Traffic Accident. (P9-7.006)

<h3>Objective:</h3> We present a case of severe neurologic decline secondary to paradoxical cerebral fat embolism (CFE) following bilateral femur fractures after a road traffic accident (RTA). <h3>Background:</h3> Fat embolism syndrome (FES) is a triad of petechial rash, deteriorating mental status and progressive respiratory insufficiency, caused by embolization of fat particles into multiple organs. When neurological signs and symptoms predominate, cerebral fat embolism must be kept high in differential. It usually occurs within 24–72 hours of trauma with traumatic long-bone fractures or an orthopedic surgery. Its incidence ranges from 0.9–11% with a mean mortality rate around 10%. Pathophysiology involves either paradoxical embolism or lung filtration. <h3>Design/Methods:</h3> Case report. <h3>Results:</h3> 17-year-old, boy with type 1 diabetes mellitus, presents after having a RTA resulting in bilateral femoral and L1 spine burst fractures with mesenteric contusions. On scene, he had a self-resolving loss of consciousness followed by GCS 14 in ER with some confusion and unremarkable CT head. Had gradual improvement throughout the day, being more conversant within 24 hours. Later, he suddenly developed paroxysmal sympathetic hyperactivity with GCS 7 and normal CT head, followed 2 hours later by episodes concerning for decorticate posturing, requiring Lorazepam and Levetiracetam load with maintenance. He underwent internal fixation and intubated subsequently the next day. MRI brain obtained within 48 hours showed “starfield pattern” on DWI sequence, characteristic for CFE. Echocardiography showed patent foramen ovale. Mental status improved gradually over two-weeks with ability to follow simple commands. Managed supportively, underwent tracheostomy and peg-tube placement and transferred to a rehab hospital. <h3>Conclusions:</h3> FES complicated with CFE is an uncommon, but fatal sequela of RTA. A missed diagnosis of neurologic dysfunction due to CFE may inappropriately guide assessment of patient’s prognosis and subsequently decisions regarding escalation or even withdrawal of care. <b>Disclosure:</b> Dr. Asif has nothing to disclose. Evan Fields has nothing to disclose. Dr. Mahmoud has nothing to disclose. Dr. Shoaib has nothing to disclose. Dr. Anadani has nothing to disclose.