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A venous air embolism occurs when gas enters a venous structure that is under negative pressure. This arises most frequently through central venous catheterization. We report the case of a man in his 70s who underwent computed tomography (CT) guided biopsy of a 14 millimeter nodule in the left upper lobe of the lung. This procedure was complicated by an anterior left-sided pneumothorax as well as pulmonary hemorrhage due to nicking of the left superior pulmonary vein. This nicking is believed to have introduced an air embolism, which then circulated to the heart as visualized on CT. The patient required bilevel positive airway pressure (BiPAP) for about twelve hours, as well as placement of a thoracostomy tube for three days. Following the event an echocardiogram and CT head were performed in order to track the air embolism, however the embolism was not visualized. The patient continued to have pleuritic chest pain and hemoptysis at the time of discharge, and was followed closely outpatient by pulmonology.

AMA Research Challenge 2023

Introduction of air embolism during a lung biopsy - a case report

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Background 
Diffuse large B cell lymphoma (DLBCL) is a common subtype of non-Hodgkin lymphoma. Rarely, it presents with lactic acidosis, a paraneoplastic phenomenon associated with high mortality. Lactic acidosis is caused by the Warburg effect, resulting in lactate production even in the presence of oxygen. Few cases of lactic acidosis in DLBCL have been reported. Prompt diagnosis and management are crucial. Treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemo-immunotherapy is standard for DLBCL. We present a case of lactic acidosis in a 60-year-old female with DLBCL, emphasizing the importance of timely recognition and treatment of this condition in hematologic malignancies due to its poor prognosis. 

Case Presentation 
We present the case of a 60-year-old woman with a complex medical history, including obesity, hypothyroidism, chronic low back pain, adrenal insufficiency, anemia, thrombocytopenia, hyponatremia, and psychogenic polydipsia. She was admitted due to confusion, gait imbalance, dyspnea, leg edema, and hypotension. Elevated lactate levels indicated potential metabolic issues related to her comorbidities. Multiple specialties were consulted. Diagnostic procedures included laparoscopy, negative AAT stool results, liver and bone marrow biopsies, and discontinuation of antibiotics after negative cultures. Despite continuous monitoring, her lactate level remained elevated. Abnormal light chain ratio and albumin-predominant proteinuria suggested amyloidosis. Imaging revealed lung abnormalities, and a thoracentesis showed lymphocytic exudates. A biopsy of the abdominal fat pad confirmed diffuse large B cell lymphoma (DLBCL). Kidney function worsened, requiring pressure support. Treatment with Rituxan and Rasburicase, followed by R-CHOP chemotherapy, was initiated. This case underscores the challenges in managing a patient with multiple comorbidities, leading to metabolic abnormalities, lung findings, and a diagnosis of DLBCL. Prompt treatment initiation was vital. 

Discussion 
Lactic acidosis, an uncommon manifestation of hematologic malignancies, is associated with poor prognosis. Lactic acidosis occurs when there is an imbalance between lactic acid production and hepatic metabolism. It is classified into types A, B, and D based on the underlying causes. Type B lactic acidosis is linked to malignancies, including hematologic cancers, where tumor cells rely on glycolysis for energy production. The Warburg effect explains this phenomenon, where tumor cells preferentially metabolize glucose to lactate even in the presence of oxygen. Treatment involves addressing the underlying malignancy, while supportive measures like hemodialysis and thiamine supplementation may be used. Malignancy-associated lactic acidosis is a grave prognostic marker. 


Lactic Acidosis Unveiled: A Hidden Clue to Diffuse Large B Cell Lymphoma

Throughout the pandemic, many COVID-19 patients were treated with therapeutic anticoagulation due to the increased risk of thrombotic events. Spontaneous Lumbar Artery Rupture (SLAR) is an uncommon vascular phenomenon typically associated with trauma and even less frequently in the setting of anticoagulation therapy. While Enoxaparin can increase bleeding risk, fatal hemorrhage is a rare occurrence. In this case, we describe a unique presentation of a patient with COVID-19 and NSTEMI on therapeutic Enoxaparin who developed SLAR and widespread catastrophic hemorrhaging at multiple sites resulting in hemorrhagic shock, cardiac arrest, and ultimately death. 
A 64-year-old male with a history of type II diabetes, hypertension, and coronary artery disease status post coronary artery bypass grafting was admitted for Acute Hypoxic Respiratory Failure due to COVID-19 Pneumonia and found to have Non-ST Elevation Myocardial Infarction. Given his COVID-19 infection, cardiac catheterization was postponed and was instead treated medically with therapeutic dose Enoxaparin. On day six, he became intermittently hypotensive without any other vital sign changes, physical complaints, or worrisome changes on physical exam or Point of Care Ultrasound. Labs showed an unchanged Hemoglobin of 14.5 and his blood pressure stabilized with one liter of normal saline. Several hours later, his hypotension returned, now unresponsive to fluids requiring pressor initiation and transfer to ICU. He now complained of lower abdominal and back pain and had developed left flank and left lower abdominal ecchymoses. Shortly after transfer, the patient suffered four cardiac arrests and post-arrest blood gas showed a base deficit of -26 and hemoglobin of 5.0 prompting administration of Protamine. Post-arrest pelvic angiography showed a SLAR and coil embolization was performed. Post-procedure CTA revealed multiple areas of active hemorrhage and large hematoma development throughout the chest, mediastinum, abdomen, and pelvis. Over the next two days, he received massive blood transfusion and maximum doses of pressors before ultimately succumbing to multi-system organ failure.
A PubMed search revealed only two case reports of SLAR in the setting of therapeutic anticoagulation, no case reports of SLAR in setting of COVID-19, and one case series of four cases of localized hemorrhage in the setting of COVID-19 with concomitant therapeutic anticoagulation. This case illustrates the potential for hemorrhage in the setting of COVID-19 possibly due to endothelial dysfunction compounded by therapeutic anticoagulation. It also highlights an unusual presentation of an actively developing hemorrhagic event without obvious exam or vital sign changes.

A Rare Case of Atraumatic Spontaneous Lumbar Artery Rupture and Widespread Hemorrhage in the setting of COVID-19 and Therapeutic Anticoagulation

Background: Linezolid has gained increased use for multi-drug-resistant gram-positive bacteria in recent years. It inhibits bacterial as well as human mitochondrial protein synthesis by binding to specific ribosomes. Therefore, linezolid can cause rare, but potentially life-threatening lactic acidosis. To date, little is known about Linezolid-induced lactic acidosis (LILA). Here, we presented a case report of LILA who presented with the signs and symptoms of acute cholecystitis.

Case Presentation: A 55-year-old male with a history of obesity, tobacco use, and uncontrolled diabetes mellitus complicated by osteomyelitis of the left foot came to the emergency department with complaints of epigastric and left upper quadrant pain for 1 day associated with nausea and vomiting. Vitals signs were as follows: Temperature 35.5, heart rate 123, blood pressure 174/105, Oxygen saturation of 97% on room air. He was producing good urine output. Relevant labs are as following: WBC count 14.3 k/cumm, lactate level 7.3 mmol/L, pH 7.22, anion gap 18 mmol/L, creatinine 1.39 mg/dl. No other abnormalities were noted on the rest of the complete metabolic panel. On a CT scan, the patient had an enlarged gall bladder. Initially, the patient was diagnosed and treated for sepsis due to acute cholecystitis with broad-spectrum antibiotics and intravenous fluids per protocol. Despite additional 2-liter fluid bolus, lactate level continues to be elevated.
On review of his medication, the patient has a previous history of chronic diabetic left foot osteomyelitis and MSSA septicemia requiring hospitalization for 3 days. He was treated with oral linezolid due to his inability to tolerate any adhesives required for a PICC line. After 6 weeks of treatment with Linezolid, the patient developed sudden abdominal pain, nausea and vomiting. 
After investigating alternative differentials such as hypoperfusion, tissue necrosis or liver failure, Linezolid-induced lactic acidosis (LILA) was suspected. Linezolid was discontinued and transitioned to doxycycline. After 12 hours of discontinuation, his lactate level went down to 1.8 mmol/L and his pH improved to 7.32.

Discussion: Linezolid is likely associated with lactic acidosis with high mortality. Moreover, Patients can have divergent presentations. We should have high suspicion and check serum lactate regularly for the patients who are on Linezolid therapy. 


Linezolid-Induced Lactic acidosis mimics symptoms of Acute Cholecystitis: A Case Report

Background:
Prolonged walking can occur in various settings, ranging from amusement and national parks to marathon races. When performed in hot climates, prolonged walking can induce ExerciseInduced Purpura (EIP), a form of small-vessel vasculitis that primarily affects the lower extremities. Purpura in adults typically indicates an underlying platelet disorder or multi-system disease requiring urgent attention. We seek to raise awareness of EIP, a benign condition, among primary care health professionals.

Case Presentation:
A 55-year-old post-menopausal woman from Europe with a sedentary lifestyle traveled to Las Vegas for vacation. She noticed a purpuric rash with mild soreness and edema on her lower extremities, extending from the ankles to the mid-legs. There was no prior history of petechial rashes or bruisability. She drank a few glasses of wine daily and denied recent consumption of raw fish or meat. The only change was prolonged walking for four consecutive days with a daily step count of 20-30 thousand, as documented on a lifestyle device. Sneakers and ankle-socks
were worn throughout. She was afebrile and the physical exam was unremarkable apart from the lower-extremity, palpable petechial and purpuric rash. Areas covered by socks were spared. Based on her history of prolonged walking, coupled with the absence of systemic symptoms, a presumptive diagnosis of EIP was made. The patient recovered with supportive treatment.

Discussion:
Typically affecting healthy females in their 50s, EIP has been labeled in multiple contexts in the literature as Disney Rash, golfer’s rash/vasculitis, hikers’ dermatitis/purpura, jogger’s petechiae, sport-induced vasculitis, marathon runner’s vasculitis, and exercise-induced vasculitis (EIV). Initial cases of EIV are documented in the early 2000’s dermatology literature, exhibiting a common presentation of pruritic and burning lower extremity rash after prolonged walking in
warm climates. These clinical findings are often coupled with a histopathological analysis of small vessel leukocytoclastic vasculitis. Prior studies have suggested that the vasculitis is driven by cytokine release and circulating immune complex deposition. Potential EIV risk factors include chronic venous disease and lipedema due to an impairment in venous return and heat regulation. EIV is commonly misdiagnosed for stasis dermatitis, cellulitis, and systemic vasculitis. To avoid this, patients with bilateral lower extremity purpura after prolonged walking in warm weather should raise clinical suspicion for a diagnosis of benign EIV or EIP. Increased
awareness and knowledge of EIV/EIP is critical for preventing unnecessary diagnostic work-up, improper empirical treatment, or hospitalization.

Disney to Las Vegas: Benign Lower Extremity Purpura Following Prolonged Walking

Resistant hypertension is defined as uncontrolled blood pressure (BP) despite treatment with three or more medications at optimal doses. Hypertensive urgency is characterized by a severe elevation in BP without evidence of end organ damage. Ultimately, this can lead to hypertensive emergency manifesting as neurologic deficit, hypertensive retinopathy, intracranial hypertension, aortic dissection, myocardial ischemia, or hypertensive nephrosclerosis. 
A 55-year-old female with a medical history of longstanding hypertension, hypertensive cerebrovascular accident, CKD IV, hyperparathyroidism status post parathyroidectomy, and left ICA aneurysm presented to the emergency department after an office visit where her systolic BP was 260. She experienced intermittent headache, diaphoresis, and blurry vision for several months prior to presentation. Despite adherence to diet, exercise, and a regimen of losartan 50mg, carvedilol 25mg, isosorbide dinitrate/hydralazine 20-37.5mg, and nifedipine 90mg, her BP remained uncontrolled for years. Family history included accelerated hypertension, kidney disease, and stroke before age 50.
On exam, the patient was comfortable, but diaphoretic with BP 267/140, heart rate 68, respirations 16, and oxygen saturation of 99% on room air. Cardiac exam revealed S3 and S4. Extraocular movements were intact and fundoscopic exam was limited. Laboratory values revealed a creatinine 1.8mg/dL, 2+ urine protein, parathyroid hormone of 367.2 pg/mL and a calcium of 9.1mg/dL. Other values were within normal limits. Nicardipine infusion improved BP to 182/114, and she was restarted on her home regimen with continued improvement over the next several days.
Further work up for secondary hypertension revealed normal TSH and aldosterone. Abdominal imaging showed normal adrenal glands and moderate-to-severe left renal artery stenosis. Serum metanephrines were 1.2 times the upper limit of normal, and urine metanephrines were 1.4 times the upper limit of normal. 
Renal angiogram revealed proximal left renal artery stenosis and was less suggestive of fibromuscular dysplasia. A stent was placed in the left renal artery, resulting in a reduction of systolic pressure from 150-200 during hospitalization to below 130 at outpatient follow-up. 
A hypertension workup for etiologies was essential for this patient, and ultimately revealed several possibilities including MEN IIA, fibromuscular dysplasia, and renovascular hypertension. This underscores the importance of comprehensive assessment of resistant hypertension and hypertensive urgency to mitigate complications. In this patient with chronic, multi-organ injury due to hypertension, we were able to identify a reversible cause with potential benefits to morbidity. Identifying causes of hypertension can help avoid unnecessary pharmacotherapy and long-term sequelae associated with severely elevated blood pressure.

When to dig deeper: Unraveling Secondary Hypertension in the Context of Hypertensive Urgency

Kikuchi-Fujimoto disease is a form of benign necrotizing lymphadenitis also known as histiocytic necrotizing lymphadenitis. While Kikuchi disease is a globally prevalent disease, it is predominantly seen in the Asian population. Etiology can be traced back to dysregulated immune responses triggered by viral or autoimmune factors. Here we present a case report to emphasize the importance of considering Kikuchi disease and possible etiologies, highlighting the need for increased awareness and recognition of this rare condition. A 28-year-old female with a history of hypothyroidism, IBS, and GERD complained of sore throat, intermittent epigastric pain, mild heartburn, and fever and was taking PPIs without any improvement. Abdominal USG was negative for any pathology. She presented with bilateral enlarged cervical lymph nodes and worsening of symptoms 1.5 months later. Ciprofloxacin was prescribed which failed to improve the symptoms. CT scan of the neck showed an enlarged thyroid gland with diffuse lymphadenopathy. Labs showed elevated TSH, for which the levothyroxine dose was increased, despite that she still continued to have symptoms. LDH and CRP were normal. Rheumatology, oncology, and infectious disease specialists were called upon for further evaluation. Excisional Lymph node biopsy showed areas of extensive necrosis with karyorrhectic debris, surrounded by histiocytes and small lymphocytes, suggestive of necrotizing lymphadenitis, specifically consistent with Kikuchi disease. Immunophenotyping by flow cytometry demonstrated normal CD4+ and CD8+ T cell populations without any evidence of clonal lymphoid expansion. AFB and GMS stains were negative for infection. Hydroxychloroquine 200 mg twice daily was given, which resulted in the resolution of her symptoms. Kikuchi disease’s origins can be traced back to Japan, where it was initially documented. More prevalent in the young female Asian population under the age of 30. It presents as tender, enlarged nodes, primarily in the cervical region along with lymphadenopathy, fever, erythematous rash, joint pain, fatigue, arthritis, and hepatosplenomegaly. It becomes important to consider Kikuchi disease in patients presenting with symptoms that can be attributed to sore throat related to GERD, followed by the development of fever with cervical lymph node enlargement.

Unusual presentation of sore throat with bilateral lymphadenopathy in a hypothyroid patient: Kikuchi Fujimoto Disease, A case report.

Background: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary early-onset vascular disease causing recurrent ischemic subcortical infarcts. Common presentations include transient ischemic attacks (TIA) and strokes (74.36%), cognitive impairment (69.23%), psychiatric disturbance (25.64%),(25.64%) and migraines (15.38%). In the realm of medical mysteries, CADASIL stands as a perplexing and devastating hereditary disease. This case aims to highlight the unique presentation of CADASIL with facial palsy and the need for a multidisciplinary approach to management. 
Case: A 52-year-old male with a family history of strokes at a young age in his father and paternal grandfather, presented to a neurology clinic for left facial droop and drooling. Brain MRI showed extensive periventricular and subcortical white matter disease, including the external capsule and subcortical white matter of the temporal lobe. Findings were suggestive of small vessel vasculopathy. A cerebral angiogram showed that all large extra and intracranial vessels were patent without evidence of aneurysm formation. There was no obvious evidence of beading of the distal intracranial vessels. CSF studies were normal. The NOTCHNOTCH 3 mutation was sent to test for CADASIL, which came back positive. The patient was started on aspirin (aspirin 81 mg) and atorvastatin (20 mg) daily. The patient was counselled on the possibility of getting an ischemic or hemorrhagic stroke. Aspirin and atorvastatin were continued, a neuropsychological evaluation was ordered and CADASIL genetic counselling and testing was offered to him and his children. Over several years, the patient developed several strokes and seizures due to infarcts. He also developed Intraparenchymal haemorrhage complicated by dysphagia requiring a feeding tube. Due to his severe physical debility, he was discharged to a nursing home for rehabilitation, where he did not improve with therapy and remained bedbound. He was discharged home with his family.
Conclusion: CADASIL can present as a diagnostic challenge due to its common presentation with migraines, TIA, and strokes with or without risk factors. This unique presentation of CADASIL with facial palsy highlights the importance of emerging atypical presentations and the need for a detailed history of neuroimaging, family history, and personal history of neurovascular events. By accurately diagnosing the condition, patients and families can be counselled on the disease course and genetics. Management requires a multidisciplinary approach with neurology, genetic counselling, physical therapy, psychology, and psychiatry to improve the patient’s quality of life.


CADASIL Presenting With Facial Palsy –A Case Report and Comprehensive Review


Introduction: Posterior reversible encephalopathy syndrome (PRES) is a distinct clinical syndrome with characteristic radiographic abnormalities on imaging. Although the pathogenesis of PRES is not fully understood, abnormal cerebral blood flow regulation likely contributes to its development. As arterial blood pressure rises in the cranium, the blood-brain barrier is disrupted. Efflux of fluid into the brain parenchyma, producing vasogenic edema. Many factors can lead to the development of PRES including and not limited to: hypertension, acute kidney injury, sepsis, illicit drug use, and pharmacological agents. Toxins and substances that increase the sympathetic activity of the CNS system can drastically potentiate the effects of PRES. We report a case of PRES secondary to these conditions.

Case: 64-year-old female with PMHx of hypertension, atrial fibrillation, and recurrent UTI who presented to the hospital due to altered mental status. On the morning of admission, the patient was found confused, nonverbal, and tremulous in her left arm by the patient’s daughter. Furthermore, the patient's daughter noticed empty bottles of tramadol and kratom around the patient. On ED presentation, the patient was hypertensive and afebrile. Urinalysis revealed heavy pyuria, and urine culture showed 100,000+ ESBL-positive E.coli. The patient was started on IV antibiotics. CT head was negative for hemorrhages/infarct. On day 2, the patient was found confused, ANOx1, and unable to follow commands. Bedside EEG was inconclusive for seizures. CT Head Stroke w/o contrast significant for no acute intracranial hemorrhage and mild to moderate vasogenic edema involving the bilateral frontal lobes. The patient loaded on Kreppa. On day 3, the patient was observed at the bedside to have multiple seizures. MRI head was remarkable for vasogenic and cortical edema within the bilateral, occipital, and parietal subcortical white matter suggesting PRES. On day 4, the patient was transferred to ICU. She was intubated, sedated, and placed on mechanical ventilation. The patient started on IV seizure medication and prophylaxis. Continuous EEG is remarkable for ninety-three focal seizures, the majority are from proper posterior quadrant onset during the next twenty-four hours. On the subsequent days, the patient was detected to be actively seizing on continuous EEG despite anti-seizure medications, being intubated, sedated, and on mechanical ventilation.


Discussion/Conclusion: Case reports and studies have been reported to link multiple agents causing seizures and PRES. Though not fully understood, toxins that increase the sympathetic activity of the CNS system can drastically potentiate the effects of PRES. Identifying, treating, and managing the underlying etiology, in addition to careful treatment of hypertension and seizure management is crucial for the management of PRES. The prognosis of PRES is typically favorable if recognized and treated early, with symptom improvement or resolution in a few days to several weeks.

A Multifactorial Analysis of Posterior Reversible Encephalopathy Syndrome 

Acute pancreatitis is a common condition with various possible etiologies. The most common causes include gallstones and alcohol, followed by metabolic, structural, and iatrogenic causes accounting for 20 – 25% of the cases. Hyperlipidemia in the form of hypertriglyceridemia and chylomicronemia accounts for 15-20% of the total cases attending lipid clinics in US. The conventional methods of treatment of severe hypertriglyceridemia are dietary restriction and lipid lowering medications, mainly fibric acid derivatives. In the medical literature, use of insulin infusion to treat hypertriglyceridemia induced acute pancreatitis is still under reported.

Hypertriglyceridemia induced acute pancreatitis treated with parenteral insulin; a possible alternative to plasmapheresis in resource limited setting: a case report

Introduction:
Purple Urine Bag Syndrome (PUBS) is a rare manifestation of bacteriuria that results in a pathognomonic purple discoloration of the urine catheter and collection bag. The accepted hypothesis for this phenomenon is bacterial production of pigment molecules in alkalotic urine. It is historically associated with females with prolonged indwelling urinary catheterization and chronic constipation. Here, we describe an atypical case of PUBS. 

Case Presentation:
A 73-year-old female with prior ischemic stroke, atrial flutter, and urinary retention presented to the emergency department with decreased urine output and lower abdominal pain. She had an indwelling foley catheter exchanged one month prior to presentation. She denied fevers, chills, and constipation. Physical exam revealed a confused woman with dry mucous membranes and suprapubic tenderness. Dark brown urine was present in a purple foley bag and tubing. Labs were significant for serum creatinine of 2.72 mg/dL, BUN of 51.4 mg/dL, and leukocytosis of 13.3 TH/cmm. Foley catheter was exchanged. Urinalysis revealed elevated protein, pH of 8.5, bacteria, and leukocytes. Ceftriaxone and vancomycin were started for treatment of sepsis secondary to urinary tract infection (UTI). Urine culture grew Citrobacter freundii and Escherichia coli, so antibiotics were deescalated to ceftriaxone alone. Her suprapubic pain and mental status improved, and her acute kidney injury resolved after intravenous fluids. Upon discharge, she was scheduled for follow up with Urology for further testing for possible neurogenic bladder and recommendations regarding indwelling foley catheter.

Conclusion:
Much about the manifestation of PUBS is still unknown. It is thought that constipation creates an environment where dietary tryptophan is increasingly produced, converted into indole by intestinal bacteria, and then absorbed by the portal circulation to be conjugated into indoxyl sulfate. Bacteria with phosphatase and sulfatase enzymes convert this compound into indoxyl which oxidizes in alkaline urine to pigmented indirubin and indigo. These pigments interact with the plastic in the catheter bags to produce a violet hue. However, this has not been uniformly proven in all cases. Additionally, many studies have shown that constipation is not always present either. The only true requirements are an indwelling catheter and UTI. Because PUBS is typically observed in patients with recurrent UTIs, it is important to consider modifiable risk factors to prevent future infections, such as prompt replacement of indwelling catheters and bowel regimens. Healthcare workers and patients can be assured that although unusual, the purple discoloration of PUBS is generally benign and not indicative of any underlying pathology except bacteriuria or UTI.

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Introduction of air embolism during a lung biopsy - a case report

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Lactic Acidosis Unveiled: A Hidden Clue to Diffuse Large B Cell Lymphoma

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