 | smeyering@atsu.edu |
Stefan H. Meyering, MS-III, CNMT
A.T. Still University- School of Osteopathic Medicine
President - SOSA Surgical Chapter 2009-10
Vice President - LMSA SOMA Chapter
Duke Research Assistant, ResearcherID: A-3312-2012
A.T. Still University- School of Osteopathic Medicine
President - SOSA Surgical Chapter 2009-10
Vice President - LMSA SOMA Chapter
Duke Research Assistant, ResearcherID: A-3312-2012
Journal articles | |
2011 |
 Abstract: 60 yr. old male with a history of non-compliance in relation to control of diabetes mellitus and psoriasis. Presenting with a previous
diagnosis of onychomycosis, found to have fulminant onychgryphosis, with Rams horn nail curvature and profuse hyperkeratosis in the
Emergency Department setting. In light of a rapidly growing number of onychogryphosis conditions presenting to community
Emergency Departments, this case report illustrates the need for intervention. In addition, it reviews the clinical aspects of
onychogryphosis, as well as its pathomechanisms and treatment options. Notes: Onychogryphosis is a severe deformation of the nail, most often affecting the great toes. Onychogryphosis occurs when the nail plate
thickens, the nail bed is hyperkeratotic, and uneven growth occurs at the matrix. The thick nail grows spirally, like a ‘ram’s horn’.
Onychogryphosis occurs commonly in the elderly but can occur in younger patients seen with onychomycosis or due to matrix injury.
Grossly, the onychogryphotic nail is severely distorted, thickened, brownish, possibly spiraled, and unattached to the nail bed
The nail plate is composed of 3 distinct layers: a dorsal thin layer, a thick intermediate layer, and a ventral layer4,5 . The healthy nail
plate appears as a smooth, convex, nearly rectangular, translucent structure that has a pink color when light is reflected from its
surface; the color is due to the underlying vascular-enriched nail bed. The nail matrix is the germinative portion of the nail complex,
giving rise to the nail plate1,4,5. The matrix is at the most proximal point of the nail bed and is seated deep beneath the PNF. Nail
thickness is directly related to the length or the size of the nail matrix, thus, the nail matrix allows hypertrophy in cases of
onychogryphosis.
To help in diagnosing or differentiating from mycotic nail dystrophies such as onychomycosis, biopsy of the nail plate and the
hyponychium may be performed, such as and other dermatoses affecting the nail plate. Biopsy of the nail plate usually involves
removing a piece of the distal plate along with a portion of the underlying hyponychium by using scissors, a bone rongeur, or a scalpel .
At the target site, the punch is applied with moderate pressure against the nail plate, passing through the nail bed until it contacts the
periosteum5,7,9. The punch is withdrawn, and the specimen is removed for histopathologic examination.
A technique that can be used to rule out onychomycosis is the noninvasive keratin biopsy. This biopsy technique has the added benefit
of helping differentiate between hemosiderin versus melanic pigment in cases in which the nail has black or brown discoloration
First-line treatment of onychogryphosis is to trim the deformed nails. If blood supply is satisfactory, urea ointment may be used to
debride and avulse dystrophic nails in onychogryphosis, onychomycosis, and psoriasis, candidal and bacterial infections.
Complete excision of the viable nail matrix results in loss of the nail plate1,6,8. Therefore, a new nail plate cannot be regenerated.
Relative contraindications to performing surgery in the nail unit include the presence of established peripheral vascular disease,
collagen vascular disease, diabetes mellitus, and disorders of hemostasis. Patients presenting with acute infection or inflammation of
the nail unit, including the surrounding paronychial tissues, are considered to have relative contraindications to nail surgery. When
possible, surgery in these patients should be postponed until the acute event has resolved3,5,10.
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2009 |
S Meyering, H Lomas (2009) Effects of adenosine A2A receptor low affinity agonist Regadenoson in patients with obstructive pulmonary disease, at risk for adenosine-induced bronchoconstriction mediated via A2B and/or A3 adenosine receptors The Internet Journal of Cardiovascular Research 6: 2. Abstract: The pharmaceutical Regadenoson (Lexiscan TM) Produced by Astellas Inc. Is currently in use as a pharmacological stress agent for myocardial perfusion imaging within the field of Nuclear Cardiology. Regadenoson is a selective A2A adenosine receptor agonist, and also has a low affinity for adenosine receptors which cause bronchoconstriction in patients with reactive airways mediated via A 2B and A3 adenosine receptors. In a study of 42 patients with mild to moderate asthma and/or moderate to severe COPD who had a positive adenosine monophosphate test, Regadenoson proved to be relatively safe and well tolerated by most patients (90%). Notes: Trademarks
1. Marketed by: Astellas Pharma US, Inc. Deerfield, IL 60015. Vials Manufactured by: Baxter Pharmaceutical Solutions LLC, Bloomington, IN 47403. Syringes Manufactured by: Hospira, Inc. Lake Forest, IL 60045 USA. FDA Rev date: 4/10/2008
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2008 |
S Meyering (2008) Spinal cord compression and vertebral body metastasis diagnosed in correlation with TC-99m H/MDP scan ( Prostate Cancer) The Internet Journal of Nuclear Medicine 5: 1. Abstract: 69 yr old male with history of previously diagnosed prostatic carcinoma 5 years earlier presenting with elevated PSA levels and lower extremity weakness. Serum calcium and alkaline phosphatase were found to be elevated. No abnormalities were noted on plain film, however there were degenerative changes found on MRI to be highly suspect for metastatic disease significantly in the thoracic spine. Utilization of nuclear medicine bone scan was found to confirm suspicions of widespread bony metastatic disease . There is a significant expansile process encroaching upon the spinal cord at the T4 level with spinal cord compression explaning possible neurological affects to lower extremities. Prompt recognition of central canal encroachment caused by metastatic disease was lead to treatment and effective reduction of cord edema post diagnosis. Notes: Compression of the spinal cord and nerve roots is found to be only second in prevalence to metastatic disease found in the brain. Neurological complications most commonly arrive from brain metastases.[1] Each year in the United States, approximately 20,000 persons with cancer develop SCC; this group represents 5% to 10% of the general cancer population.[2,3] Because of improved treatments and prolonged survival in various cancers, the incidence of SCC may be increasing.[4]
Neoplastic spinal cord compression usually follows hematogenous dissemination of malignant cells to the vertebral bodies, with subsequent expansion into the epidural space. Spread into the epidural space may occur by means of tumor extension through the intervertebral foramina or hematogenous spread by way of the Batson venous plexus. Generally, metastatic seeding appears in the thoracic spine (accounting for about 70% of cases), with the lumbar spine being the next most involved site (20% of cases). The cervical spine is affected in approximately 10% of cases. Multiple spinal levels are affected in about 30% of patients.[1] Malignant SCC can yield compressive indentation, displacement, or encasement of the spinal cord / thecal sac .[1] Spinal cord compression produces edema, inflammation, and mechanical compression, which causes direct neural injury to the cord, as well as vascular damage and impairment of oxygenation.[4] Prognosis of SCC also depends on the functional status and length of survival after treatment. Spinal cord compression has demonstrated to be fatal only if it occurs in the cervical region of the spinal cord (C4 and above) and if it results in respiratory paralysis that is uncompensated by mechanical ventilation.[5] Tumor tissue type must be considered when the treatment plan is being determined. SCC in this case requires immediate treatment with either localized radiation , and or surgical intervention to prevent cord injury.[2,4,5] Subsequently, the patient underwent resection of encroaching tissue and vertebroplasty of multiple thoracic vertebrae to relieve the spinal cord compression and help relieve neurological symptoms. In vertebroplasty, a cement mixture consisting mostly of polymethylmethacrylate is injected through a needle into porous bone, with the porosity commonly caused by osteoporosis but also by malignancy as seen here .This cement reinforces the bone to reduce further fracture. [3] In this case, Bone scan was used in correlation with other modalities to confirm differential diagnosis of metastatic disease with spinal cord compression.
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Book chapters | |
2009 |
S Meyering (2009) Vertebral Metastatic Disease and Spinal Cord Compression secondary to Invasive Prostate Cancer 18 Encyclopedia Britannica 34385203 Abstract: Notes:
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2006 |
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Conference papers | |
2011 |
D Hernandez, S Meyering, J Taitano (2011) Aneurysmal bone cyst in the right greater trochanter of a 6 year old child seen 2 months post trauma In: Musculoskeletal Sarcoma Conference Duarte Abstract: Notes:
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V Call, L DeLaPortilla, C Jenkins, M Johnston, S Meyering, E Murphy, K Patel, S Singh (2011) 'Self-Aware', Sexual health awareness in Low-country college students In: National Association of Community Health Centers Conference NACHC San Diego Abstract: Beaufort Jasper Hampton Comprehensive Health Services (BJHCHS), Inc. offered the Self Aware! program to students enrolled at University of South Carolina Beaufort Hilton Head Gateway (USCB) and Technical College of the Lowcountry (TCL) from Sept 1, 2010 - January 31, 2011. The program was designed to provide sexual health education and pregnancy prevention strategies via condom distribution and birth control education to college students. Free condoms and sexual health information were offered to the students. The patient population served by the eight BJHCHS clinics consists of young adults including 58% African American, 24% Hispanic, 14% Caucasian, and 4% others (including American Indian, Asian, Chinese and Filipino). The target population for the Self Aware! project was aimed at 18 to 19 year-olds, which represent the highest risk group of unplanned pregnancies in the Beaufort, Jasper, Hampton tri-county region of South Carolina’s Lowcountry.
Notes: Conclusions:
Based on the statistics and age range of the participants in the survey, the target age range demographic of 18 and 19 year-olds was reached. Eighteen and nineteen year-olds are considered the highest risk group for unplanned pregnancies in the Beaufort, Jasper, Hampton tri-county area of South Carolina’s Lowcountry. Condom use was the most common prior birth control method amongst surveyed individuals. Birth control pills were the second most popular contraception choice. Depo-provera was the third most prevalent form of birth control and had a greater representation at the TCL campus. STD and Birth Control brochures were the most distributed among both campuses. More students were interested in HPV prevention information at the TCL campus. Information regarding medical care utilizing a sliding fee scale was widely sought at both campuses. There were more student revisits at the USCB campus, and males comprised the majority of that population. The target age group for this project was represented better at the USCB campus. The twenty-one and older age group was more predominant at the TCL campus.
Sustainability:
Partnerships created by BJHCHS, A.T. Still University, Technical College of the Low Country and USC Beaufort will provide access to health care for 18-19 year olds beyond family planning services. Staff will also be able to continue implementing preventive health education with sexually active 18 to 19 year-old patients after the project is completed.
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2008 |
S Meyering, N Hanna (2008) Incidence of spinal cord compression in vertebral body metastatic disease. Case studies on patients exhibiting spinal cord compression, and treatment using interventional polymethylacrylate In: WSU Radiological Sciences Department Weber State University Ezekiel R. Dumke College of Health Professions Abstract: 69 year old male patient presented upon routine followup with elevated PSA levels, elevated serum calcium and alkaline phosphatase upon consultation. Also noted was patients bilateral lower extremity weakness and recent history of fall. Initial plain film imaging proved to be non diagnostic, with further analyzation of MRI of the t-spine without contrast yielding abnormal findings from various vertebral bodies. Results were highly concerning for metastatic disease and positive findings of cord compression at the T4 level. MRI scan of the T-spine noted for an expansile process within the left pedicle of the vertebral T4 causing significant cord compression at that level. (Fig.1). Resultant abnormal signal at that level is suggestive of cord edema . Notes: Compression of the spinal cord and nerve roots is found to be only second in prevalence to metastatic disease found in the brain. Neurological complications most commonly arrive from brain metastases.[1] Each year in the United States, approximately 20,000 persons with cancer develop SCC; this group represents 5% to 10% of the general cancer population.[2,3] Because of improved treatments and prolonged survival in various cancers, the incidence of SCC may be increasing.[4]
Neoplastic spinal cord compression usually follows hematogenous dissemination of malignant cells to the vertebral bodies, with subsequent expansion into the epidural space. Spread into the epidural space may occur by means of tumor extension through the intervertebral foramina or hematogenous spread by way of the Batson venous plexus. Generally, metastatic seeding appears in the thoracic spine (accounting for about 70% of cases), with the lumbar spine being the next most involved site (20% of cases). The cervical spine is affected in approximately 10% of cases. Multiple spinal levels are affected in about 30% of patients.[1] Malignant SCC can yield compressive indentation, displacement, or encasement of the spinal cord / thecal sac .[1] Spinal cord compression produces edema, inflammation, and mechanical compression, which causes direct neural injury to the cord, as well as vascular damage and impairment of oxygenation.[4] Prognosis of SCC also depends on the functional status and length of survival after treatment. Spinal cord compression has demonstrated to be fatal only if it occurs in the cervical region of the spinal cord (C4 and above) and if it results in respiratory paralysis that is uncompensated by mechanical ventilation.[5] Tumor tissue type must be considered when the treatment plan is being determined. SCC in this case requires immediate treatment with either localized radiation , and or surgical intervention to prevent cord injury.[2,4,5] Subsequently, the patient underwent resection of encroaching tissue and vertebroplasty of multiple thoracic vertebrae to relieve the spinal cord compression and help relieve neurological symptoms. In vertebroplasty, a cement mixture consisting mostly of polymethylmethacrylate is injected through a needle into porous bone, with the porosity commonly caused by osteoporosis but also by malignancy as seen here .This cement reinforces the bone to reduce further fracture. [3] In this case, Bone scan was used in correlation with other modalities to confirm differential diagnosis of metastatic disease with spinal cord compression.
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C Pastore MD, FACC, FSCAI, S Meyering CNMT, H Lomas IV PA-C, MPAS (2008) Application and side effects of the new FDA approved ‘Lexiscan’ (Regadenoson) in Nuclear Stress Testing In: University of South Florida College of Medicine Abstract: Regadenoson is chemically described as adenosine, 2-[4-[(methylamino) carbonyl]-1H-pyrazol-1-yl]-, monohydrate. The molecular formula for regadenoson is C15H18N8O5• H2O and its molecular weight is 408.37.4,5
The solution is clear and colorless. Each 1 mL in the 5-mL vial or pre-filled syringe contains 0.084 mg of regadenoson monohydrate, corresponding to 0.08 mg regadenoson on an anhydrous basis, 10.9 mg dibasic sodium phosphate dihydrate or 8.7 mg dibasic sodium phosphate anhydrous, 5.4 mg monobasic sodium phosphate monohydrate, 150 mg propylene glycol, 1 mg edetate disodium dihydrate, and Water for Injection, with pH between 6.3 and 7.7.5 The recommended intravenous dose of Regadenoson is 5 mL (0.4 mg regadenoson). 5
Regadenoson has a 2-3 minute biological half-life, as compared with adenosine (predecessor’s) 30 second half life.4,5 Regadenoson stress tests are not affected by the presence of beta blockers, as regadenoson acts as a vasodilator but does not stimulate beta adrenergic receptors.4,9 Oral ingestion of caffeine, a nonselective competitive A2A receptor antagonist, is usually contraindicated before vasodilator MPI9,8 because it attenuates the coronary hyperemia caused by the nonselective adenosine receptor agonists adenosine and dipyridamole in a dose-dependent manner .3 It has this effect on regadenoson, and was withheld in this clinical trial.
Patients with reactive airways are at risk for adenosine-induced bronchoconstriction, mediated via A(2B) and/or A(3) adenosine receptors.7,3 Since patients who have these conditions are being treated and tested with MPI (Myocardial Perfusion Imaging) using Regadenoson currently post-FDA approval, it is significant to note which precautions should be used with patients with prior lung conditions, and outcomes post MPI stress testing using Regadenoson. Benefits include statistical data on the safety and optimal use of the new pharmaceutical Regadenoson in populations of patients who have clinically stable COPD, asthma, or emphysema, in which the predecessor vasodilator Adenosine could not be used effectively without inducing bronchospasm.4 Effectiveness and ability to use Regadenoson in this population of patients, reduces patients further risk by potentially eliminating the need for cardiac catheterization in the event that a non-invasive cardiac stress test may be performed for analysis of coronary stenosis.
To examine the effects of regadenoson on airway resistance, a randomized, double-blind, placebo-controlled crossover trial was conducted with asthmatic and/or COPD patients with a positive adenosine monophosphate challenge test. Subject population comprised of patients with moderate to severe, yet clinically stable chronic obstructive pulmonary disease (COPD), and known asthmatics. Patients receiving glucocorticoids or oxygen and those with pretreatment wheezing were included2. Short-acting bronchodilators were withheld for approximately 4 hours before treatment, with the exception of patients who presented with pre-test wheezing, who were administered a nebulized albuterol solution. A forced expiratory volume test was conducted as a baseline for each patient, with a mean forced expiratory volume in 1 second (FEV(1)) of 1.67 +/- 0.50 L . Approximately 40% of the patient population in the study complained of dyspnea during daily activities. A forced expiration volume test was conducted approximately 5 mins and 45 mins post Regadenoson administration. The mean ratio of the forced expiratory volume in 1 second (FEV1) at each tested time point relative to the baseline FEV1 gives an inclination the level of bronchoconstriction in these patients post administration of the pharmaceutical Regadenoson 9. This was compared with placebo from 5 to 45 minutes after treatment.
No differences emerged between regadenoson and placebo on multiple lung function parameters, including repeated FEV(1) and forced vital capacity, respiratory rate and oxygen saturation1. The most common adverse events with regadenoson were hypotension and tachycardia (58%), dizziness (53%), headache (44%), and dyspnea (26%). The mean heart rate increased with regadenoson (maximum of +10.4 beats/min) compared to placebo. The mean maximum decline in FEV(1) was 0.11 +/- 0.02 L with Regadenoson. On placebo the mean maximum decline was 0.12 +/- 0.02 L . Wheezing post Regadenoson was observed in 19% of the assessed patients. Wheezing post placebo was observed to be 9%. No patients required acute treatment with oxygen post Regadenoson, however 14% of patients actively wheezing pre-Regadenoson were administered a bronchodilator consisting of 2.5 mg nebulized albuterol. Out of the 14% of patients which developed acute wheezing, half of those patients were administered aminophylline intravenously, which alleviated bronchoconstrictive symptoms2. The other half were administered a nebulizer treatment similar to treatment pre regadenoson, post FEV analysis. The aminophylline vs. albuterol challenge post onset of acute wheezing showed aminophylline to cause a reduction in acute symptomology an average of 4.8 minutes faster than albuterol. The mean ratio of the forced expiratory volume in 1 second (FEV1) at each tested time point relative to the baseline FEV1 was shown to be significantly higher after treatment with regadenoson as compared with placebo from 5 to 45 minutes after treatment. Three patients had a significant but asymptomatic FEV1 reduction (−39.6%) after regadenoson that reversed spontaneously. Notes:
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2006 |
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