Acute Intracranial Abnormalities Research Articles

7643 Acute blindness due to Metformin associated lactic acidosis

Abstract Disclosure: K.N. Pereira: None. K. Desai: None. T. Khan: None. S. Yong: None. Metformin, one of the most commonly prescribed oral hypoglycemic agents, effectively lowers basal and postprandial blood glucose. However, Metformin carries a black box warning for lactic acidosis, which is more common in setting of liver and kidney dysfunction. With an incidence rate of ∼ 4.3 cases per 100,000 patient-years, Metformin associated lactic acidosis (MALA) can present with nausea, vomiting, diarrhea, encephalopathy, hypothermia, respiratory failure and hypotension. Blindness is a rarely reported outcome of MALA. We present a case of a 48 year old intellectually disabled female with a history of type 2 diabetes (on Metformin) who presented with progressive encephalopathy insetting of intractable nausea and vomiting with poor oral intake, since starting lisinopril & rosuvastatin for newly diagnosed hypertension and hyperlipidemia. She was encephalopathic, hypothermic, hypotensive, tachycardic and tachypneic. Labs were notable for leukocytosis, AKI, hyperkalemia, elevated anion gap metabolic acidosis with a lactate of 13.6 and elevated lipase. She also tested positive for Influenza A. CT head showed no acute intracranial abnormality. CT chest, abdomen & pelvis was concerning for aspiration, multifocal pneumonia or a combination of both as well as acute interstitial pancreatitis. She was admitted to the ICU for further management including hemodialysis. She continued to have improving but persistent lactic acidosis despite multiple dialysis sessions. On day 5 of ICU stay, with resolution of her encephalopathy, she reported new onset complete bilateral painless vision loss. General eye and neurologic exam was unrevealing except for sluggishly reactive pupils to light. MRI brain showed an new acute 2 mm lacunar infarct in the right temporal lobe. Neurology ruled out stroke as the cause for her vision loss. Emergent ophthalmology evaluation revealed no retinopathy, macular edema, acute glaucoma or thromboembolic event. The new onset vision loss was suspected to be due to MALA due to persistent metabolic disturbances. Some animal studies have shown that retinal horizontal cells are sensitive to low pH, resulting in interruption of signal transmission to the visual neurons and consequent blindness. The presence of factors like metformin metabolites may contribute to impaired function of retinal cells.On extensive literature review it was noted that only 5 cases of vision loss associated with MALA have been reported. However, in these cases, vision loss was transient and reversed following correction of acidosis with dialysis. Our case highlights a rare consequence of MALA, which can be irreversible and cause lifelong disability. Presentation: 6/1/2024

5155 Benign Paroxysmal Positional Vertigo as a Potential Manifestation of Hypothyroidism, a Case Report

Abstract Disclosure: M. Ahmad: None. M. Herrera: None. D. Deyar: None. P. Gill: None. Introduction: Benign Paroxysmal Positional Vertigo (BPPV) is a vestibular disorder characterized by recurrent episodes of vertigo triggered by specific head movements. The pathophysiology of BPPV involves the displacement of otoconia within the semicircular canals of the inner ear. However, emerging evidence suggests that BPPV may manifest as a consequence of hypothyroidism. In this case report, we present a clinical case of a patient who exhibited symptoms of BPPV and was subsequently diagnosed with hypothyroidism. We aim to elucidate the relationship between these two seemingly distinct conditions and highlight the importance of considering hypothyroidism as a potential cause of BPPV. Case presentation: A 56-year-old female with a past medical history of migraines presented to the hospital for three days of dizziness. She had multiple bouts of vomiting and right-sided headaches similar to her prior migraine headaches. The patient also noted dry skin, constipation, and hair loss for the past few months. The patient’s vital signs were as follows: temperature: 35.6 C, heart rate: 65 beats per minute, blood pressure: 153/66 mmHg, and respiratory rate: 18 breaths per minute. On physical examination, the Dix-Hallpike maneuver was positive on the right side and the patient was noted to have diffusely dry skin. The patient’s labs were significant for the following: sodium: 137 mmol/L, potassium: 3.7 mmol/L, creatinine: 0.88 mg/dL, thyroid stimulating hormone: 31.2 uIU/ml, free T4 ng/dL, hemoglobin: 10.8 g/dL (MCV of 87), and TPO antibody: 2350 IU/ml. The patient underwent CT and MRI imaging of the brain without contrast, which was negative for any acute intracranial abnormalities. The patient was diagnosed with BPPV and hypothyroidism secondary to Hashimoto’s thyroiditis and subsequently underwent vestibular physical therapy with improvement in her vertigo and was started on 112 mcg of levothyroxine daily. She is set to follow up with her primary care provider as an outpatient. Discussion: BPPV generates significant repercussions to an individual’s quality of life, autonomy, and functionality. Hypothyroidism is a common condition characterized by thyroid hormone deficiency that has been linked with a wide array of clinical manifestations, including vestibular disturbances. Autoimmune dysfunction, anomalies of the endolymphatic flow and low perfusion to the inner ear are potential etiological factors that can explain the relationship between thyroid disorders with BPPV. Some studies mention that thyroid autoantibodies could induce autoimmune-complex deposition in the inner ear, which might change the endolymphatic flow and induce BPPV. Raising awareness regarding this potential manifestation of hypothyroidism can guide clinical and diagnostic decisions that improve patient care, especially in individuals under evaluation for BPPV with other symptoms of hypothyroidism. Presentation: 6/3/2024

Case 324.

A 69-year-old right-handed man with a history of substance use disorder, hypertension, and diabetes presented to the emergency department in an unresponsive state. Upon examination, apart from tachycardia (heart rate, 108 beats per minute), vital signs were within normal ranges (blood pressure, 134/102 mm Hg; temperature, 97.9°F [36.6°C]; respiratory rate, 16 breaths per minute; oxygen saturation, 96%). He had a Glasgow coma scale score of 8. Otherwise, the physical examination revealed no abnormalities. His prior psychiatric and surgical histories were unremarkable. There was no history of recent travel, camping, hiking, or vaccination. No family history could be obtained. Laboratory work-up revealed an elevated creatine kinase level (49 006 U/L [818.4 μkat/L]; normal reference range, 10-205 U/L [0.17-3.42 μkat/L]). An electrocardiogram showed sinus tachycardia without evidence of cardiac ischemia. An echocardiogram was unremarkable. Alanine aminotransferase (126 U/L [2.10 μkat/L]; normal reference range, 0-40 U/L [0-0.67 μkat/L]) and aspartate aminotransferase (488 U/L [8.15 μkat/L]; normal reference range, 3-44 U/L [0.05-0.74 μkat/L]) levels were elevated. Polymerase chain reaction results were negative for HIV-1, HIV-2, syphilis treponemal, and COVID-19 antibodies. The rest of the routine laboratory work-up findings were within normal limits. Urine drug screening was positive for cocaine, marijuana, fentanyl, and benzodiazepines. Naloxone was administered, but the patient remained unresponsive. Intubation was performed for airway protection. Noncontrast and contrast-enhanced CT of the head (Fig 1) and CT angiography were performed in the emergency department to rule out an acute intracranial abnormality. Multisequence MRI of the brain with administration of intravenous contrast material was ordered for further assessment (Figs 2-4). CT of the abdomen and pelvis was unremarkable (images not shown).

Abstract 13710: Cardiac Platypnea-Orthodeoxia Syndrome: How the Stars Aligned

Case description: A 79-year-old man with recurrent falls, dyslipidemia and recent exercise intolerance presented after a fall. He was putting on shoes, lost his balance and fell. There was no pre-syncope, syncope, dyspnea, chest pain, palpitations or dizziness. On admission, vital signs were normal except oxygen saturation (O2 sat) 79% on room air (and no improvement with supplemental O2). An arterial blood gas (ABG) revealed partial pressure of oxygen 42 mmHg with oxygen saturation 80%. He had lower thoracic spine tenderness, normal respiratory and cardiac exam. CT head showed no acute intracranial abnormalities. CTA chest had no pulmonary embolism, arterio-venous malformations or parenchymal lung disease. There was a thoracic aorta aneurysm (4.5cm at aortic root and 5.1cm at posterior arch). Subsequently, O2 sat was 92% supine and 79% standing. He also had a compression fracture of T12 and spinal asymmetry. A transesophageal echocardiogram (TEE) showed an aneurysmal, hypermobile interatrial septum with early right to left shunt with agitated saline due to a large patent foramen ovale (PFO). Right heart catheterization revealed no pulmonary hypertension and confirmed a step down from the pulmonary vein to left atrium (delta O2 sat 6%). A 30mm Gore Cardioform occluder was used to close the defect and immediately supplemental oxygen was removed, and O2 sat on room air was 95%. Follow up echocardiogram showed no residual shunt and exercise intolerance resolved. Discussion: Unexplained positional hypoxemia raised our suspicion for cardiac POS. Hypoxemia is caused by right to left shunting via the PFO, exacerbated by the thoracic aortic aneurysm and spinal changes such as the T12 fracture and spinal asymmetry. Going from being recumbent to erect there is stretching of the atria causing his PFO to enlarge, increasing the shunt. Additionally, the dilated thoracic aorta exerts mechanical pressure on the right atrium (RA) and interatrial septum, increasing PFO patency and augmenting flow from the inferior vena cava through the PFO. The spinal abnormality may cause more aortic distortion and exert forces on the RA, exacerbating shunting. Percutaneous PFO closure is the treatment of choice with closure immediately leading to significant improvement of hypoxemia.

Abstract 018: External carotid artery Pseudo aneurysm induced Internal Carotid Artery compression causing acute ischemic stroke

Introduction Here, we describe a patient in whom ischemic stroke was caused by compression of the Internal Carotid Artery (ICA) by a Pseudoaneurysm (PSA) of the External Carotid Artery (ECA) after Gun Shot injury. Eventually, the PSA of the Internal maxillary artery (IMAX) was embolized, resulting in resolution of the patient's symptoms. Methods Case Report Results A 75‐year‐old male with a history of atrial fibrillation on Eliquis presented to the emergency department after sustaining a gunshot wound to the left face. He had extensive injuries through the left masticator and submandibular space with an inferior orbital wall fracture. A Computed Tomography Angiography (CTA) neck showed injuries to the left proximal IMAX with a small PSA. As the PSA was asymptomatic it was managed with observation. On HOD day 13, CTA was done for a brief period of unresponsiveness, which showed high‐grade narrowing of left cervical ICA due to extrinsic compression from PSA which was supplied by a branch of the left ECA with distal re‐constitution (image A). The next day, patient developed right sided plegia and aphasia with NIHSS of 17. A CT head showed no acute intracranial abnormality. The patient underwent emergent Digital Subtraction Angiography (DSA), which demonstrated occlusion of the left cervical ICA from compression from a left IMAX PSA which was treated with n‐butyl‐cyanoacrylate TRUFILL embolization with resolution of flow limitation in the left cervical ICA (Image B1,B2). After embolization, the patient was oriented and able to lift right arm and leg anti‐gravity. Magnetic Resonance Imaging (MRI) was contraindicated due to retained bullet fragments. Repeat CT head did not show stroke. Conclusion A Pseudo aneurysm is characterized by a rupture of the arterial wall and the formation of an aneurysmal sac by the adjacent structures while the sustaining artery remains intact. The most prevalent causes are penetrating or acute blunt neck trauma, hyperextension injury, and injury to the base of the skull (1). Predisposing factors for PSA include carotid endarterectomy or a late complication of carotid artery dissection, infection, radiotherapy, and malignancy (1‐2). Cox et al. reported 124 patients with significant neck and head penetrating injuries. Eleven patients were found to have thirteen head and neck PSA: two in the ICA, one in the vertebral artery, and ten involving branches of the ECA. Two of seven symptomatic PSAs manifested with episodes of massive hemorrhage (3). There have been case reports describing the consequences of an elongated styloid process causing an ischemic stroke due to subsequent dissection and PSA formation (4). According to our knowledge, this case report is one of the first to describe acute ischemic symptoms resulting from ECA PSA‐induced ICA compression, with resolution of symptoms following PSA embolization. The educational value of our case lies not only in the rarity of the condition but also in the uniqueness of its presentation. This case is a fundamental addition to the existing literature on rare neuro‐vascular anomalies leading to potential catastrophic outcomes.

THU375 A Case Of Right Eye VI Nerve Palsy In A Patient With Uncontrolled Type 2 Diabetes Mellitus

Abstract Disclosure: C. Musurakis: None. A. Havrylyan: None. J.L. Gilden: None. Background: Uncontrolled type 2 diabetes is one of the most common etiologies of acquired VI nerve palsy. Clinical Case: A 40-year-old Mexican female with uncontrolled type 2 diabetes mellitus (DM), diabetic retinopathy and hypertension was admitted to the hospital due to the new onset of diplopia, headache, and right eye pain. Her symptoms started 2 weeks before seeking medical care and had worsened when she looked towards the right. Duration of DM was more than 10 years, with long-standing history of diet and medication non-compliance. She had never taken the prescribed metformin and insulin, nor did she monitor her blood glucose levels at home. Four years previously, she had received laser therapy to both eyes for diabetic retinopathy. Although she denied numbness or tingling of her extremities, she had a left 4th toe amputation in the past, due to infection, which was complicated by chronic osteomyelitis. There was no prior history of cerebrovascular or cardiac disease. Family history was positive for type 2 DM in both parents. Upon hospital admission, HbA1c was 13.2% (n<5.7). BMI 23.7. Vitals: BP 184/104, HR 110. Labs: blood glucose was 439 mg/dL (n=70-99), CO2 23 mEq/L (n=21-31), AG 12 mmol/L (n=4-11), Beta-Hydroxybutyrate/Acetate 2.0 mmol/L (n=0.1-0.3), venous pH 7.36 (n=7.35-7.45). Physical exam: no conjunctival redness, discharge or swelling around the eye, but inability to abduct the right eye laterally. CT head wo contrast: significant atherosclerotic calcifications within the intracranial segment of right vertebral artery and no acute intracranial abnormality. CTA brain w/wo contrast: no obvious mass effect on 6th cranial nerve territories. MRI of brain and orbit w/wo contrast showed no macroscopic anatomic abnormality or impingement on right abducens nerve but showed minimal white matter changes on the centrum bilaterally. She was diagnosed with an isolated VI facial nerve palsy in the setting of longstanding uncontrolled diabetes mellitus and hypertension. She was started with basal-bolus insulin and antihypertensive therapies and recommended to continue this medication regimen after discharge. She was also advised that gradual recovery of vision may be achieved with glycemic control of DM and hypertension. Conclusion: Although the etiology of acquired VI nerve palsy may be idiopathic, or result from hypertension, trauma, multiple sclerosis, neoplasm, CVA, postsurgical complication, or aneurysm, it is also caused by uncontrolled diabetes mellitus combined with hypertension. It is to be noted that when neoplasm or aneurysm is the cause, the history and examination often reveals the presence of other neurologic symptoms or signs. Reference: Patel SV, Holmes JM, Hodge DO, Burke JP. Diabetes and hypertension in isolated sixth nerve palsy: a population-based study. Ophthalmology. 2005 May;112(5):760-3. doi: 10.1016/j.ophtha.2004.11.057. PMID: 15878054. Presentation: Thursday, June 15, 2023

Case 317: Adult-Onset Leukoencephalopathy with Axonal Spheroids and Pigmented Glia.

A 44-year-old previously healthy man with a 9-month history of progressive cognitive decline, depression, urinary incontinence, and inability to perform tasks of daily living presented to the emergency department with worsening cognitive and neuropsychiatric symptoms. He had become more distressed, and his family noticed him departing the house without closing doors, leaving water faucets running, and sending his children to school on Sundays. History taken from the patient's wife revealed that his brother had passed away in his late 30s after a slowly progressing functional and cognitive decline over the course of 5 years. No further detailed family history could be obtained. The review of systems was negative; he had no prior medical, psychiatric, or surgical history; and he denied any history of recent travel, camping, hiking, or vaccination. The patient was not taking any dietary supplements, nor was he taking any over-the-counter or prescription medication. Examination revealed vital signs were within normal limits. Neurocognitive assessment revealed a conscious, coherent, and alert patient with impaired memory and concentration. He showed poor attention, depressed mood, and restricted affect. He was unable to spell the word world forward, nor was he able to understand a request to spell it backward. The rest of the physical and neurologic examination revealed no abnormalities. Extensive laboratory work-up was conducted and included the following: toxicology screening; screening for HIV-1, HIV-2, and syphilis treponemal antibodies; COVID-19 polymerase chain reaction; and measurement of B1 and B12 levels. The results of screening were negative. Cerebrospinal fluid (CSF) assays, including CSF oligoclonal bands and CSF flow cytometry, revealed values within normal limits. CT of the brain without intravenous contrast material was performed in the emergency department to rule out acute intracranial abnormality. Multiplanar multisequence MRI of the brain without and with intravenous contrast material was ordered for further assessment. CT images of chest, abdomen, and pelvis were unremarkable (images not shown).

Unilateral Ptosis Secondary to Pansinusitis in a Pediatric Patient: A Case Report

Introduction: Ptosis or the dropping of an eyelid can affect both the adult and pediatric populations and can be caused by various factors. Ptosis is not very common and in children, the common causes include orbital cellulitis, congenital ptosis, Cranial Nerve III palsy, and Horner’s syndrome. However, unilateral acute ptosis from an infectious disease process is rare and there are only a few documented cases of such occurrences. Acute ptosis is a medical emergency and prompt diagnosis, and management is critical for the resolution of symptoms and prevention of serious complications. Case: We present an interesting case of a 14-year-old female with pansinusitis who experienced unilateral left-sided ptosis. Initially prescribed oral antibiotics for sinusitis, the patient developed ptosis, requiring inpatient hospital admission and intravenous antibiotics. On admission, the patient had leukocytosis, elevated CRP, and ESR levels. CT facial bones showed pansinusitis and ruled out orbital cellulitis, acute intracranial abnormalities, and venous sinus thrombosis. After aggressive treatment with intravenous antibiotics and systemic steroids, the sinusitis resolved, as did her unilateral ptosis and facial swelling. Discussion: This is a unique presentation of ptosis that was treated successfully allowing for prompt and complete resolution. We want to highlight the establishment of a varying diagnosis and treatment courses which led to the final resolution of the acute ptosis. The patient was treated with meropenem and dexamethasone. The adjunctive use of corticosteroids, in this case, was beneficial.

Head computerized tomography in emergency department evaluation of the geriatric patient with generalized weakness.

Weakness in older emergency department (ED) patients presents a broad differential. Evaluation of these patients can be challenging, and the efficacy of head computed tomography (CT) imaging is unclear. This study assesses the usefulness of head CT as a diagnostic study of acute generalized weakness in older ED patients. This retrospective review of patients aged 65 years and older presenting to 2 community EDs included patients with a chief complaint of generalized weakness who received a head CT. Patients presenting with a focal neurologic complaint, altered mental status, or trauma were excluded. Variables evaluated included additional triage chief complaints, dementia diagnosis, and deficits on physical examination. Primary outcome was acute intracranial finding on head CT. Secondary outcomes included neurology consultation, neurosurgical consultation, and neurosurgical intervention. Of 247 patients, 3.2% had an acute intracranial abnormality on head CT. Emergent consultations for neurology and neurosurgery occurred for 1.6% and 2.4% of patients, respectively. None required neurosurgical intervention. Patients with objective weakness or focal neurologic deficits on physical examination were more likely to have acute findings on head CT (8.5% vs. 2.0%, odds ratio 4.56, confidence interval 1.10-18.95). Additional characteristics did not predict acute intracranial abnormality or need for emergent consultation. Few patients with generalized weakness evaluated with head CT had acutely abnormal intracranial findings. Patients with objective weakness or neurologic deficits were more likely to have acute abnormalities. Although head CT is frequently used to evaluate geriatric weakness, its utility is low, especially in patients with normal physical examinations.

539 Contact Burns Associated with Concomitant use of Methamphetamines and Heat Stroke, Resulting in Neurological Sequela

Abstract Introduction On a summer day in the desert southwest, ground surfaces can soar to 180 degrees Fahrenheit, posing significant risk to individuals who sustain contact with such surfaces, particularly if unable to get up. These individuals are also at risk for heat stroke. This summer, an increased number of patients admitted with contact burns were positive for methamphetamine and concomitant heat stroke. The purpose of this case series is to describe the hospital course and outcomes of this subset of patients. Methods A retrospective chart review of patients admitted between June and September 2022 was completed. Criteria for inclusion included contact burn, initial core body temperature > 38.8°C, and a methamphetamine positive drug screen. Outcome measures included length of stay, discharge disposition, number of operations, admission Glasgow Coma Score, neurology work-up and sequela. Results A total of 23 patients were admitted who suffered contact burns and tested positive for methamphetamine. Ten of those patients had core body temperatures greater than 38.8°C upon initial evaluation. The mean age was 36.6 years (24-62), with an average temperature of 42.3°C (40.5-43.1°. All 10 were found down in the community with altered mental status, the average Glasgow Coma Scale was 5.9 (3- 12). CT scans were done on 9, all were negative for acute intracranial abnormalities. Neurology was consulted for 3 patients with 2 having EEGs performed, both displayed slowing and attenuation secondary to hyperthermia. Ten of these patients were concurrently positive for fentanyl. The mean total burn surface area burned was 9.6% (4-17.5%), The average number of operations was 4.1/patient (1-11). Of the 8 patients discharged the average LOS was 30 days (10-61), 2 patients remain hospitalized in the ICU with a current LOS of 61-71 days. Of the 8 patients discharged, all required post-acute care with only 1 meeting rehabilitation criteria. Conclusions Elevated temperatures in the Southwestern United States have been known to cause an increase in surface-related contact burns during the summer months. Historically, the at-risk patient population has been elderly individuals prone to falls with limited physical ability to get up. This summer highlighted a new phenomenon of younger individuals suffering both contact burns and heat stroke secondary to the combination of methamphetamine use and elevated summer temperatures. This patient population suffered significant morbidity, and none were able to be discharged home. This case series highlights the dangers posed by ambiently heated surfaces during the summer months, particularly in combination with illicit drug use. Applicability of Research to Practice This case series, demonstrates the increased risk of sequela associated with burn patients who have comorbid substance abuse disorder.

Case 317

A 44-year-old previously healthy man with a 9-month history of progressive cognitive decline, depression, urinary incontinence, and inability to perform tasks of daily living presented to the emergency department with worsening cognitive and neuropsychiatric symptoms. He had become more distressed, and his family noticed him departing the house without closing doors, leaving water faucets running, and sending his children to school on Sundays. History taken from the patient's wife revealed that his brother had passed away in his late 30s after a slowly progressing functional and cognitive decline over the course of 5 years. No further detailed family history could be obtained. The review of systems was negative; he had no prior medical, psychiatric, or surgical history; and he denied any history of recent travel, camping, hiking, or vaccination. The patient was not taking any dietary supplements, nor was he taking any over-the-counter or prescription medication. Examination revealed vital signs were within normal limits. Neurocognitive assessment revealed a conscious, coherent, and alert patient with impaired memory and concentration. He showed poor attention, depressed mood, and restricted affect. He was unable to spell the word world forward, nor was he able to understand a request to spell it backward. The rest of the physical and neurologic examination revealed no abnormalities. Extensive laboratory work-up was conducted and included the following: toxicology screening; screening for HIV-1, HIV-2, and syphilis treponemal antibodies; COVID-19 polymerase chain reaction; and measurement of B1 and B12 levels. The results of screening were negative. Cerebrospinal fluid (CSF) assays, including CSF oligoclonal bands and CSF flow cytometry, revealed values within normal limits. CT of the brain without intravenous contrast material was performed in the emergency department to rule out acute intracranial abnormality (Fig 1). Multiplanar multisequence MRI of the brain without and with intravenous contrast material was ordered for further assessment (Figs 2-4). CT images of chest, abdomen, and pelvis were unremarkable (images not shown).

Abstract #1408214: Severe Hypernatremia Due to Central Diabetes Insipidus with Adipsia: Challenges in Management

Hypernatremia (serum sodium >145meq/L) is independently associated with increased mortality as high as 40-60%. Mortality correlates with the rapidity of the rise in sodium and the degree of severity. Central Diabetes Insipidus (DI) associated with adipsia pose a unique management challenge, leading to recurrent hospital admissions due to hypernatremia. We report, a patient with Central DI who presented with severe hypernatremia following desmopressin non-compliance and inadequate water intake. A 25-year female with a past history of obstructive hydrocephalous underwent ventriculoperitoneal shunt revision and had a complicated hospital course including new onset Central DI. The patient was discharged on desmopressin and a serum sodium of 148 meq/L. She presented to the hospital 3 days later with altered mentation, dehydration, and a heart rate of 124bmp. Other vital signs were stable. CT head showed no acute intracranial abnormalities. Labs showed: serum sodium 190meq/L, serum osmolality 393mOsm/kg, urine sodium 44mEq/L, and urine osmolality 878mEq/L. She initially received IV isotonic fluid, and IV DDAVP, and later started on hypotonic fluid and oral DDAVP. Labs were monitored every 6 hours. The patient didn’t have a sense of thirst, didn’t like the taste of water, and had a suboptimal response to oral DDAVP. Multiple measures were taken to stabilize her serum sodium: switched to DDAVP Nasal spray, placed alarms on her cell phone as a reminder to drink water, flavored powders were used to make the water palatable, and provided education on the importance of DDAVP, adequate water intake, and outpatient follow-ups. The patient was safely discharged home after demonstrating the ability to maintain normal serum sodium on oral fluid intake and self-administered nasal DDAVP. Thirst is a critical adaptive mechanism to protect against hypernatremia. Intense thirst may be present initially, but it dissipates as hypernatremia progresses and is absent in patients with adipsia. Destruction or improper functioning of osmoreceptors in the hypothalamus that controls the thirst mechanism can result in adipsia; this may result from a congenital malformation or acquired as in the case of stroke, trauma, or infection. It was most likely secondary to multiple intracranial procedures in our patient. This case also highlights cerebral adaptation to chronic hypernatremia. Brain shrinkage is countered by an adaptive response initiated promptly and consists of solute gain (initial uptake of sodium and potassium, followed by the later accumulation of osmolytes; mainly myoinositol and the amino acid glutamine) by the brain that tends to restore lost water. This response leads to the normalization of brain volume and accounts for the milder symptoms of hypernatremia that develops slowly, as seen in this patient. In conclusion, patients with Central DI associated with adipsia can pose a significant management challenge. This case highlights the importance of addressing all the barriers that affect patients’ compliance with DDAVP and ensuring adequate hydration to prevent recurrent hospital admission and associated morbidity and mortality.

COVID-19 Infection Presents as Acute Cerebellar Ataxia (P6-10.003)

<h3>Objective:</h3> To describe a rare case of COVID-19 infection presenting as acute cerebellar ataxia in a pediatric patient. <h3>Background:</h3> The COVID-19 virus is well known to cause respiratory tract infections but other body systems can be affected including the nervous system. Most of the reported neurological manifestations of COVID-19 infection occurred sub-acutely between days to weeks after infection onset. Here, we present a pediatric case of COVID-19 infection presenting with associated cerebellar symptoms. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> A 10-year-old male with no past medical history presented to the emergency department with a new onset fever (Tmax: 104F), headache, odynophagia, rhinorrhea, diarrhea associated with blurry vision, and ataxia. The patient denied any falls, dysarthria, diplopia, paresis, hypoesthesias, bladder or bowel incontinence. On exam T: 98.9F, HR: 65, BP: 107/66, RR: 20. Normal physical exam, on neurological exam patient, was alert and oriented, he did not have paresis, hypoesthesia but had ataxia, bilateral nystagmus, dysdiadochokinesia, dysmetria with finger-to-nose and heel-to-shin testing, he was unable to walk unassisted, had wide-based gait, altered heel, toe, and tandem walking. No papilledema was observed on fundoscopy. CBC, CMP were unremarkable, CT head did not show any acute intracranial abnormality. Infectious workup showed a positive COVID-19 polymerase chain reaction and negative blood cultures. Lumbar puncture revealed normal protein and glucose levels with no pleocytosis, the patient had extensive negative serology testing for autoimmune, demyelinating, and alternative infectious etiologies. Brain and cervicothoracic spine MRIs with and without contrast were normal. The patient was diagnosed with viral cerebellitis secondary to COVID-19 infection, and he was started on intravenous methylprednisolone 1 gram for 5 days with symptomatic improvement, the patient was able to walk with minimal assistance by the end of the hospital stay and was discharged with a prednisone taper. <h3>Conclusions:</h3> Neurological manifestations like cerebellar ataxia can be the presenting symptomatology of acute COVID-19 infection. <b>Disclosure:</b> Dr. Carvajal- Gonzalez has nothing to disclose. Dr. Benjamin has nothing to disclose. Dr. Asghar has nothing to disclose.

Abstract Number ‐ 66: Symptomatic Chronic Internal Carotid Artery Occlusion Managed With Bilateral Common Carotid Angioplasty: A Case Report

Introduction Several guidelines have addressed symptomatic or asymptomatic carotid artery stenosis treatment with intensive medical management and surgical management based on the severity of stenosis [1]. In acute occlusions, endovascular treatment (EVT) and carotid endarterectomy (CEA) with or without prior thrombolytics provide the best recanalization and functional outcomes when compared to intravenous or intra‐arterial thrombolysis alone. There is, however, less robust evidence on management of symptomatic chronic internal carotid artery (ICA) occlusion occurring in tandem with significant contralateral ICA stenosis [2]. In chronic ICA occlusion (ICAO), EVT and carotid endarterectomy (CEA) are technically unfeasible, but indirect procedures have been arising as safe and effective alternatives, notably CEA or stenting of contralateral stenotic ICA [3] and CEA or stenting of ipsilateral external carotid artery (ECA) [4]. We hereby report a case of symptomatic chronic ICAO that was managed with staggered angioplasty and stenting of bilateral common carotid artery (CCA) bifurcations. Methods We hereby present a case report. Results A 62‐year‐old male with atrial fibrillation and hypertension woke up with sudden dysarthria and right upper extremity and facial weakness. NIHSS at presentation was 4. Last seen normal 9 hours prior. Non‐contrast head computerized tomography (CT) did not show acute intracranial abnormality, CT angiogram of head and neck showed severe right ICA stenosis and complete occlusion of the left ICA at cervical, petrous and cavernous segments, with distal reconstitution at the supraclinoid segment with left proximal middle cerebral artery (MCA) thrombus. CT perfusion showed a core infarct volume of 8cc in left MCA territory, mismatch volume of 78cc and ratio of 10.8. Risks of acute neuro‐intervention were deemed to outweigh benefits. Given favorable perfusion imaging, and in concordance with the EXTEND trial [5], tPA was administered. The patient remained stable without hemorrhagic complications with residual deficits of mild right upper extremity weakness and mild expressive aphasia. MRI confirmed left ICA territory ischemic infarcts. Patient underwent stenting of the asymptomatic right ICA at the CCA bifurcation first, followed by left CCA stent after one month with impressive improvement in subsequent perfusion imaging. Conclusions Our case encourages consideration of well‐timed angioplasty and stenting in cases of chronic bilateral carotid artery disease especially when the asymptomatic side is also significantly stenotic

Acute Hyperactive Delirium followed by Excited Catatonia: A case study

Acute Hyperactive Delirium followed by Excited Catatonia: A case studyOluwole A Babatunde, MD, Frank Clark, MD, Jessica Hill, DO, Belynda Veser, MD, Anu Nagar, MDDepartment of Psychiatry, Prisma Health,109 Physicians Drive, Greer, SC 29650.Ms. A. is an 84-year-old Hispanic female with a past psychiatric history of Mild Neurocognitive Disorder due to Frontotemporal lobar degeneration, major depressive disorder (MDD), and one episode of catatonia about six years prior to current presentation. She first presented to the emergency department (ED) for a motor vehicle collision that led to bruising and generalized tenderness. She had four ED visits over the next four weeks. At the fifth visit, she was hospitalized because of concerns of altered mental status (AMS), agitation, and hallucinations. She was noted to have a urinary tract infection (UTI) and bacteremia with positive blood cultures for Escherichia Coli. She was subsequently admitted to the inpatient medical service and the working diagnosis was delirium secondary to UTI/bacteremia, exacerbated by sleep deprivation. Imaging was performed to rule out intracranial abnormalities (e.g., subdural hematoma) following MVC.Psychiatry was consulted for the recent onset of altered mental status (AMS), increasing confusion, and hallucinations. Patient was assessed by consult liaison psychiatry service on day one of admission. Mental status exam was remarkable for the following pertinent positives: oriented to self only, tangential with loose associations, perseveration on her deceased husband, religiously preoccupied and responding to internal stimuli. She was able to recall 0 out of 3 objects in both immediate and delayed recall and having auditory and visual hallucinations. Patient consistently denied suicidal ideation and homicidal ideation. CT scan and MRI were negative and helped rule out acute intracranial abnormalities (e.g., subdural hematoma).Working diagnosis of acute hyperactive delirium secondary to UTI/bacteremia was managed with quetiapine, improving gradually over the subsequent eight days. Medical team managed UTI/bacteremia with 10 days of antibiotics as recommended by the Infectious Disease team and there was clinical evidence of resolved bacteremia and UTI. Quetiapine was titrated to maximum dosage of 100mg QAM, 100mg QPM and 200mg QHS with ongoing gradual improvement. However, she decompensated on day eight with new symptoms of catatonic-like stereotypical hand movements, repetition of words, and general sustained hyperactivity. The Bush Francis score (BFS) was 12. It was at this point that the daughter (a nurse) provided additional collateral history that there was a history of a similar episode of catatonia six years ago. A trial dosage of lorazepam 2mg IV was administered with subsequent improvement of BFS to 6. Over the next four days, lorazepam 1 mg IV was administered daily, and patient continued to improve. During this time, the dosage of Quetiapine was reduced, considering that delirium had improved, and Quetiapine could have been exacerbating the catatonia. However, titrating down of Quetiapine was done slowly to avoid abrupt discontinuation which could cause delirium to re-emerge. After receiving second dose of lorazepam, Montreal Cognitive Assessment (MoCA) score also dramatically improved from 6/30 to 22/30. She was subsequently discharged on day 13 to a nursing home where she was managed for 20 days and discharged home.Two learning objectives.• There is need to ask about history of catatonia in elderly patients as this may help heighten clinical suspicion especially in patients with delirium.• It is possible for a patient who presented with hyperactive delirium with clinical improvement and resolution of delirium to develop excited catatonia in a short time, so clinicians need to have a high index of suspicion especially among patients who have a history of catatonia. Given that hyperactive delirium alone responds excellent to antipsychotics while excited catatonia responds excellent to lorazepam IV, early diagnosis is of utmost important to adjust medications at the earliest time of noticing symptoms of excited catatonia.

Examining four blood biomarkers for the detection of acute intracranial abnormalities following mild traumatic brain injury in older adults.

Blood-based biomarkers have been increasingly studied for diagnostic and prognostic purposes in patients with mild traumatic brain injury (MTBI). Biomarker levels in blood have been shown to vary throughout age groups. Our aim was to study four blood biomarkers, glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), neurofilament light (NF-L), and total tau (t-tau), in older adult patients with MTBI. The study sample was collected in the emergency department in Tampere University Hospital, Finland, between November 2015 and November 2016. All consecutive adult patients with head injury were eligible for inclusion. Serum samples were collected from the enrolled patients, which were frozen and later sent for biomarker analyses. Patients aged 60 years or older with MTBI, head computed tomography (CT) imaging, and available biomarker levels were eligible for this study. A total of 83 patients (mean age = 79.0, SD = 9.58, range = 60-100; 41.0% men) were included in the analysis. GFAP was the only biomarker to show statistically significant differentiation between patients with and without acute head CT abnormalities [U(83) = 280, p < 0.001, r = 0.44; area under the curve (AUC) = 0.79, 95% CI = 0.67-0.91]. The median UCH-L1 values were modestly greater in the abnormal head CT group vs. normal head CT group [U (83) = 492, p = 0.065, r = 0.20; AUC = 0.63, 95% CI = 0.49-0.77]. Older age was associated with biomarker levels in the normal head CT group, with the most prominent age associations being with NF-L (r = 0.56) and GFAP (r = 0.54). The results support the use of GFAP in detecting abnormal head CT findings in older adults with MTBIs. However, small sample sizes run the risk for producing non-replicable findings that may not generalize to the population and do not translate well to clinical use. Further studies should consider the potential effect of age on biomarker levels when establishing clinical cut-off values for detecting head CT abnormalities.

Abstract 11318: A Rare Case of Stretch Syncope of Adolescence Masquerading as Carotid Artery Dissection and Carotid Sinus Syndrome

Introduction: Syncope describes a brief, sudden loss of consciousness and tone, with spontaneous return to baseline. Although episodes arise from a transient interruption of cerebral blood flow, work-up identifying an underlying is critical, as it can determine the proper treatment for cessation of these episodes. In this case, we describe a patient who was later diagnosed with stretch syncope of adolescence (SSA), a rarely reported cause of syncope. Case Presentation A 16-year-old male presented to the E.R. after experiencing a syncopal event immediately after looking up. He endorsed a similar episode one week earlier, after standing and looking up. The patient also revealed that he commonly would crack his neck and would often sleep with his head extended over the arm of his couch. In the E.R., the patient was hypotensive to 107/62 mmHg, but physical exam and lab work-up did not reveal any significant pathology. EKG and a CT head without IV Contrast showed no acute intracranial abnormality. Soon after admission, he became bradycardic, hypotensive, and lightheaded. Due to concern for carotid artery dissection, bilateral carotid duplex scan and CT of the head and neck were completed, and given the reproducibility of the patient’s symptoms with neck dorsiflexion, an MRI to evaluate for carotid sinus syndrome was completed. All imaging, however, returned unremarkable. Given the patient’s age, symptom onset with movement, and exclusion of other etiologies, a diagnosis of SSA was made. The patient was discharged with strict instructions to avoid stretching, especially when standing. Discussion SSA is characterized by episodic loss of consciousness triggered by a combination of stretching and neck hyperextension. It is a rarely reported phenomenon, with only 14 case reports published on SSA as of 2014, and is often confused with more common syndromes, most commonly epileptic seizures. Our case is especially unique because the patient’s presentation was initially most consistent with carotid artery dissection and coronary sinus syndrome, a previously unreported presentation. By continuing to recognize and report cases such as ours, patients with SSA may receive more prompt diagnosis, avoid extraneous work-up, and ultimately, prevent future syncopal events.

UNILATERAL PTOSIS AS A FIRST MANIFESTATION OF SARCOIDOSIS

UNILATERAL PTOSIS AS A FIRST MANIFESTATION OF SARCOIDOSIS

DISSEMINATED LISTERIOSIS: A DEADLY TRIPLICATE

DISSEMINATED LISTERIOSIS: A DEADLY TRIPLICATE

Protocolized management of isolated linear skull fractures at a level 1 pediatric trauma center.

Isolated linear skull fractures without intracranial findings rarely require urgent neurosurgical intervention. A multidisciplinary fracture management protocol based on antiemetic usage was implemented at our American College of Surgeons-verified level 1 pediatric trauma center on July 1, 2019. This study evaluated protocol safety and efficacy. Children younger than 18 years with an ICD-10 code for linear skull fracture without acute intracranial abnormality on head CT were compared before and after protocol implementation. The preprotocol cohort was defined as children who presented between July 1, 2015, and December 31, 2017; the postprotocol cohort was defined as those who presented between July 1, 2019, and July 1, 2020. The preprotocol and postprotocol cohorts included 162 and 82 children, respectively. Overall, 57% were male, and the median (interquartile range) age was 9.1 (4.8-25.0) months. The cohorts did not differ significantly in terms of sex (p = 0.1) or age (p = 0.8). Falls were the most common mechanism of injury (193 patients [79%]). After protocol implementation, there was a relative increase in patients who fell from a height > 3 feet (10% to 29%, p < 0.001) and those with no reported injury mechanism (12% to 16%, p < 0.001). The neurosurgery department was consulted for 86% and 44% of preprotocol and postprotocol cases, respectively (p < 0.001). Trauma consultations and consultations for abusive head trauma did not significantly change (p = 0.2 and p = 0.1, respectively). Admission rate significantly decreased (52% to 38%, p = 0.04), and the 72-hour emergency department revisit rate trended down but was not statistically significant (2.8/year to 1/year, p = 0.2). No deaths occurred, and no inpatient neurosurgical procedures were performed. Protocolization of isolated linear skull fracture management is safe and feasible at a high-volume level 1 pediatric trauma center. Neurosurgical consultation can be prioritized for select patients. Further investigation into criteria for admission, need for interfacility transfers, and healthcare costs is warranted.