Subacute combined degeneration due to nitrous oxide-induced vitamin B-12 deficiency

Background: Nitrous oxide also known as “laughing gas” is a naturally occurring gas that is colorless, odorless, nonflammable, and nontoxic. It has been used as an inhalant anesthetic in the medical field for more than 150 years for dental and surgical procedures. Due to its wide availability and ability to cause euphoria, recreational use is on the rise.1 Here, I will present a case of subacute combined degeneration in the setting of nitrous oxide induced vitamin B-12 deficiency. Case presentation: 23-year-old right-handed gentleman with no past medical history presented to the ED complaining of 1 week of bilateral lower extremity symmetric paresthesia, weakness, and difficulty with ambulation. He initially experienced paresthesia in the lower extremities. Two days later, he experienced difficulty ambulating which led to multiple falls at home. The patient stated sensation in both legs was reduced in addition to experiencing difficulty with positioning during movement and balance difficulty. Strength in bilateral lower extremities was also markedly reduced as he eventually noticed he was unable to stand by himself and after his most recent fall which prompted his visit to the emergency department. The patient denied trauma, fever, chills, fatigue, weight loss, nausea, vomiting, diarrhea, dizziness, vision changes. He denied alcohol use, tobacco use, or drug use. On neurological examination, the patient was alert and oriented to place, time, and situation, normal 5-minute recollection, normal mood, no aphasia, cranial nerves II-XII intact. Motor strength was 4/5 hip flexion bilaterally with eyes open, decreased to 3/5 with eyes closed. Dorsiflexion 4/5 bilaterally with eyes open, decreased to 3/5 with eyes closed. Deep tendon reflexes were 2+ in bicep reflex bilaterally, 3+ in patellar reflex with cross adductor response bilaterally, 3+ in achilles reflex. No clonus. Absent Babinski. On sensory exam, there was profound impairment in proprioception and vibration in bilateral lower extremities and decreased sensation to vibration in bilateral upper extremities. Proprioception preserved in upper extremities. Finger to nose, normal heal to the shin, normal rapid alternating movements. The patient had no tremor, and he was found to have an ataxic gait. Laboratory studies including complete blood count, complete metabolic panel, thyroid-stimulating hormone, creatine kinase, lactate dehydrogenase, folate levels were within normal limits. Serum vitamin B-12 was low at 78 pg/mL and vitamin D was low at 13.9 ng/mL. MRI of the cervical spine showed an abnormal T2 signal within the cervical spinal cord extending from the level of C2-C6, which appears to be centered posteriorly, without associated abnormal enhancement, potentially indicating evidence of myelopathy. In order to rule out Neuromyelitis Optica Spectrum Disorders, aquaporin 4 antibody and anti-myelin oligodendrocyte antibody were ordered. HIV type 1 and 2 antibodies revealed no reactivity. Immunologic workup with ANA, dsDNA, SSA/Ro Ab, SS-B/La Ab, gastric parietal cell Ab was negative. Lumbar puncture was performed with CSF studies showing normal opening pressure, glucose, and white blood cell count, however, CSF protein was elevated at 243 mg/dL. Infectious workup with CSF culture, CSF acid-fast bacilli, CSF VDRL, CSF West Nile virus was negative. CSF oligoclonal revealed no bands. CSF cytology was negative for malignant cells. Aquaporin 4 antibody and anti-myelin oligodendrocyte glycoprotein antibody were negative. Workup revealed no evidence of infectious or immunologic underlying disease. While waiting for additional laboratory results, the patient was started on IVIG. On day 5 of hospitalization patient reported that he has been inhaling nitric oxide from whipped cream cans for recreational use for approximately a year. The patient was started on vitamin B-12 and vitamin D supplementation. He was also started on methylprednisolone IV 1000mg for 5 days. The patient’s condition improved progressively with vitamin B-12 supplementation and physical therapy enabling him to be transferred to inpatient rehabilitation to continue recovering. Conclusion: Patients presenting with neurological symptoms like paresthesia, numbness, weakness, and ataxic gait along with laboratory studies indicating vitamin B-12 deficiency should be questioned about nitrous oxide recreational use. Unfortunately, there is no test to screen for nitrous oxide use so this shows how essential it is to obtain a thorough complete history in regard to recreational drug use. Nitrous oxide inactivates vitamin B-12 making it unable to function as a cofactor for methionine synthase which normally converts homocysteine to methionine.2 Methionine is a precursor of S-adenosyl methionine which is used as a methyl donor required for the maintenance of the integrity of the neuron sheath. This will result in damaged myelin sheath by impairing the methylation of myelin basic proteins and lipids.3 Treatment consists of cessation of nitrous oxide use and vitamin B 12 supplementation. Vitamin B-12 supplementation should be started immediately upon suspected diagnosis since the response to treatment is associated with severity and duration of symptoms. Patients should be educated on the importance of the cessation of nitrous oxide for recreational use

Renal Artery Stenosis as a Cause of Acute Kidney Injury in a Post-kidney Transplant Patient

Introduction: The most common complication of kidney transplantation is allograft dysfunction, which can present as acute kidney injury (AKI). Here, we report a case of transplant renal artery stenosis (TRAS) presenting with acute elevation in creatinine in concomitant with resistant hypertension. Case Presentation: A 69-year-old African American male with history of end stage renal disease status post living unrelated kidney transplant presented for evaluation of worsening kidney function. Past medical history included hypertension, diabetes mellitus type 2, coronary artery disease. Physical exam was significant for blood pressure 164/85, bilateral crackles, lower extremities edema. Blood work showed creatinine 3..8 mg/dL (up from base line 2 mg/dL), BUN 69 mg/dL. Doppler Ultrasound of transplant kidney showed anastomotic luminal stenosis. His hypertension remained refractory to multiple antihypertensive medications. Patient underwent renal artery angiogram with primary stenting of transplanted renal artery. The creatinine improved to 3.4 mg/dL. His blood pressures were also under-controlled with oral medications. Patient was discharged with creatinine of 3.3 mg/dL and improved to 3.1 mg/dL at his 1-week follow-up with transplant specialist. Discussion: Common causes of allograft dysfunction include acute tubular necrosis, acute rejection, infection, urinary obstruction. TRAS is a less common cause but should be suspected among patients with concomitant hypertension. Renal arteriography with potential angioplasty and stenting is gold-standard diagnosis and treatment of choice for TRAS. However, this procedure involves IV contrast, which can potentially worsen kidney function. Therefore, risk and benefit of pursuing work-up for TRAS should be considered carefully and always start with non-invasive alternatives

Takotsubo Cardiomyopathy, presentation as a cardiac arrest in a 67 year old female with depression and anxiety history

Background: Takotsubo cardiomyopathy also known as broken heart syndrome or stress induced cardiomyopathy is a sudden transient reversible dramatic left ventricular apical akinesis mimicking acute coronary syndrome, making it a diagnostic challenge. Most common mechanism for Taktosubo is stress induced catecholamine release causing sympathetic activation leading to microvascular dysfunction or direct toxicity. Mayo Clinic Criteria for making diagnosis at the time of presentation requires 1) transient hypokinesis, dyskinesis, or akinesis of the LV midsegments with or without apical involvement, and a stressful trigger is often but not always present. 2) absence of obstructive coronary disease or angiographic evidence of acute plaque rupture 3) new ECG abnormalities (either ST segment elevation and or T wave inversion) 4) absence of pheochromocytoma or myocarditis. Case presentation: A sixty-seven year old Hispanic woman with past medical history of depression and anxiety, presented to emergency department with generalized body weakness, chronic severe lower back pain. In emergency department, patient experienced cardiac arrest with return of spontaneous circulation achieved in 5 mins, was intubated for airway protection. Electrocardiogram showed sinus tachycardia with elevated cardiac troponins. Echocardiogram revealed large area of akinesis involving mid anteroseptal, lateral wall, inferoapical; severe left ventricular dysfunction with ejection fraction 30-35%. She was found to have pulmonary edema and was started on vasopressors, heparin drip, and aggressive diuresis for cardiogenic shock. Imaging negative. Eventually she was able to be weaned off vasopressor support and extubated. Her repeat echo three days later revealed improved left ventricular systolic function with ejection fraction of 45-50%. Patient underwent left heart catheterization which demonstrated no significant obstructive coronary disease. Patient improved clinically and was discharged to a skilled nursing facility for rehabilitation on beta blocker and angiotensin receptor blocker. Discussion: The exact etiology of our patient’s arrest remains unknown. Early suspicion and use of Mayo clinic criteria at time of presentation is important especially in patients with a history of psychiatric disorders as there is a high rate of recurrence and complications reported among them. Our patient has a history of anxiety and depression, which can be considered precipitating factors predisposing the patient to a stress induced cardiomyopathy

Primary Pancreatic Mature T-Cell Lymphoma as a Cause of Obstructive Jaundice: A Case Report and Review of the Literature

Primary pancreatic lymphoma (PPL) is an extremely rare type of non-Hodgkin\u27s lymphoma (NHL). It accounts for 0.1% of all lymphomas and less than 1% of pancreatic tumors. Within this subtype, T-cell lymphomas only account for up to 6.7% of pancreatic lymphomas. In this study, we present the case of a 78- year-old Hispanic man who presented with obstructive jaundice associated with a mass within the head of the pancreas; pathologic analysis of the tumor revealed a mature T-cell lymphoma, not otherwise specified (NOS)

Factor V Leiden and its Association with Vascular Disease and Treatment in a Latino patient

Introduction: Factor V Leiden (FVL) is the most common hereditary thrombophilia, and a single amino acid mutation renders Factor V resistant to inactivation by Activated Protein C resulting in a prothrombotic state. The association between FVL and vascular disease has been reported and debated. We present a case of a patient with FVL and its repercussion on medical treatment. Case Description: A 64-year old Hispanic man with a past medical history of coronary artery bypass grafting, Type 2 diabetes mellitus, hypertension and severe peripheral vascular disease with history of left above the knee amputation presented to the emergency department with severe, sharp right upper back pain that radiated to his chest for one day. It was not associated with fever, shortness of breath, or palpitations. He reported taking apixaban for the last three years however he was unsure of the indication. He denied smoking, prolonged inactivity or travel. Vital signs included a temperature of 97.7o F, heart rate of 97 bpm, respiratory rate of 17 breaths/min, blood pressure of 140/86 mmHg, and BMI of 28. Physical exam was remarkable for right paraspinal tenderness of the upper back upon palpation. Coagulation profile showed PT 15.8, INR 1.33, PTT 37.0. Patient was at moderate risk for a pulmonary embolism (PE) using the Wells’ Score. A PE was noted on CT angiography and bilateral non-occlusive proximal deep vein thromboses (DVTs) of the right deep femoral vein, the left common and superficial femoral veins were found on venous doppler. The cardiac echocardiography showed no evidence of right heart strain and troponins were negative. He was initially started on a heparin drip and two liters of oxygen nasal cannula in the emergency room and was transitioned to enoxaparin after admission. On genetic analysis, it was found that the patient was heterozygous for the FVL (R506Q) variant in the Factor V gene. Protein C and Protein S levels were normal. Given failed anticoagulation therapy, an IVC filter was placed. Apixaban was changed to rivaroxaban and the patient was discharged home with close follow up. Conclusion: Our patient with an extensive history of CAD and PAD was found to be heterozygous for FVL after presenting with a PE and bilateral DVTs despite anticoagulation. The EINSTEIN EXT trial found that there was an 82% relative risk reduction in recurrent DVT in patients who received rivaroxaban compared to placebo and acetylsalicylic acid. The AMPLIFY-EXT trial found a 64% relative risk reduction for recurrent VTE in patients who received apixaban compared to placebo. Previous studies have shown that FVL is associated with increased severity of CAD and PAD however the pathophysiology is unclear. It has been hypothesized that long-term anticoagulation may prevent severe progression of PAD and CAD in patients with FVL however it is unknown whether anticoagulation would have prevented progression of vascular disease in our patient. In patients with CAD and PAD with venous thromboembolism despite anticoagulation, screening for FVL may be warranted for appropriate anticoagulation management

Dementia, Delirium, and Depression

Changes in mental status can affect many residents during their stay in a post-acute or long-term care (PA/LTC) facility. Changes in cognition can either be acute as in seen in delirium, subacute as seen in depression, or chronic as seen in dementia. As such assessment by the practitioner can be challenging as one or more of these conditions may occur in the same resident. Understanding the similarities and dissimilarities between the clinical features of dementia, delirium, and depression is paramount when evaluating the resident who presents with a change in mental status. The chapter will emphasize how to differentiate between these three conditions and to describe the common presentations of dementia, delirium, and depression, and review their differential diagnosis and treatment. Screening tools are discussed as well as the pharmacologic, non-pharmacologic and behavioral interventions in the treatment of delirium, depression, and dementia