It has been close to a year since my cousin passed away from complications involving a fibrocartilaginous embolism (FCE) in her upper cervical spine. Sadly, after 14 years of learning about an FCE, it is still listed as a rare disorder with most research being performed by Veternarians due to the high occurrence rate in dogs. Currently, there is still very little published about the impact of an FCE on human lives.
Why are we not hearing about the impact of FCE on human lives? Well, one reason is it usually occurs in young people (under age 30). Best restorative prognosis is in the very early years of life, but there are too few documented occurrences in older patients to encourage further study. The second reason is the lack of immediate, effective treatment as it does not respond to "clot busters" or methylprednisone, making it one of those issues with little evidence based data and a small cohort. The third reason is its misdiagnosis as another nasty neurologic issue such as Transverse Myelitis (TM), Guillian Barre (GB) or Arterio-Venous Malformation (AVM). And finally, the fourth reason being the inaccurate characterization as "death by unknown cause", further minimizing the actual occurrence rate of an FCE.
The sad, but typical scenario of an upper cervical FCE is the onset of severe headache/arm symptoms, eventual weakening and finally the shutting down of one's ability to breath or vocalize. Many of these patients simply pass away quietly; toxicology, cardiac and cerebral screens all appearing negative. Many of these cases continuing to fall into the category of "death by unknown cause". The challenge for the future is to help educate and expose the incidence of this nasty disorder, learning to question and identify it early so there can be a movement towards an effective and immediate treatment plan. This amount of suffering needs to come to an end soon..........and this diagnosis needs to be UN-cloaked.
Monday, November 26, 2018
Sunday, March 25, 2018
I saw very interesting signs while attending the March for our Lives on 3/25/18. It was absolutely amazing listening to the young speakers, raw with emotion yet hopeful for the future. The most eye opening sign was the fact that a young person can purchase a gun with greater ease than purchasing Sudafed, a "behind the counter" product. Thinking it is time to change up some laws.........
Posted by lit'l duck at 6:10 AM
Tuesday, March 21, 2017
Skin infections encompass many specialty groups, ranging from infectious disease and lymphology societies to wound care specialists and emergency room clinicians, all uniquely aware of the huge personal and financial cost incurred when infections are not handled in a prompt and effective manner. The collaborative management and treatment of cellulitis, an acute and rapidly progressing bacterial skin infection, is critically important as 2.5% of the general population is impacted by this disorder and its high level of recurrence when not addressed promptly and effectively (Nguyen, Rowland & Mounsey, 2014).
Cellulitis is a rapidly spreading inflammatory skin infection that specifically affects subcutaneous tissues and is characterized by erythema (redness), swelling and localized tenderness (Goodman & Fuller, 2009). These authors further defined a sub-category of cellulitis called erysipelas, a surface cellulitis that primarily affects the skin and upper dermis, although it may involve lymphatic vessels with an appearance of redness and sharply defined borders with occasional red colored streaking. Cellulitis presents as warm and painful to touch, reddened and edematous in appearance, but with smooth and ill-defined borders except in severe cases where it may contain pustules or areas of necrosis (Sambrano, Gordon, Mays, Lapolla & Scheinfeld, 2012). According to Mortimer and Rockson (2014), cellulitis and erysipelas are among the most common conditions seen in emergency departments.
Erysipelas, usually caused by group A Streptococcus, results in the sudden onset of fever, pain and redness (Koster, Kullberg & Van der Meer, 2007). The typical scenario that creates a predisposition to infection is the interaction between high bacteria colonization and circulation of the blood, compounded by increased vulnerability in moist areas of the body and on the lower extremities (Erbil et al., 2014). The predisposition to cellulitis or erysipelas, is increased by the presence of skin disruptions or lymphedema, an abnormal accumulation of fluid in the interstitial space (Koster, Kullberg & Van der Meer, 2007). This interstitial edema occurs when the capillary filtration rate exceeds the capability of the lymphatic drainage mechanism (Trayes, Studdiford, Pickle & Tully, 2013). The lymphatic system tends to be one of the most poorly understood body systems, however it has been identified as having three specific functions that include fluid balancing, fatty absorption and host defense (Mortimer & Rockson, 2014). Their feeling is the lymphatic system maintains volume homeostasis and creates an adaptive immunity through its immune surveillance of antigen and immune cell transport, all important aspects in the maintenance of a healthy body.
Cellulitis and erysipelas are definitely more prevalent in patients with lymphedema and skin disruptions, but other risk factors include diabetes mellitus, chronic venous insufficiency and skin ulcerations (Perello-Alzamora, Santos-Duran, Sanchex-Barba, Canueto, Marcos & Unamumo, 2012). These authors feel that rendering a diagnosis of cellulitis is often difficult to provide or problematic in differentiating from other conditions such as an abscess, as gathering cultures for microbiologic analysis or isolating a pathogen is not always accessible or available.
When the diagnosis of erysipelas is rendered, studies have found these bacteria respond well to narrow spectrum penicillins, such as benylpenicillin (penicillin G), or to macrolides such as erythromycin, for patients allergic to penicillin (Koster, Kullberg & Van der Meer, 2007). According to Ciccone (2013), penicillin G is classified as an anti-infective and falls within the pharmacologic category of penicillins. The anti-infective mechanism is the occurrence of cellular death through its binding action to specific enzymes within the cell wall, making the cellular membrane unable to act as a selective barrier and unable to handle the high internal osmotic pressure of the bacterial cell (Ciccone, 2007, p. 504). This anti-infective mechanism makes it very effective in treating most gram-positive organisms, some gram-negative organisms and a few anaerobic bacteria and spirochetes (Ciccone, 2013). Ciccone (2013) further states that Penicillin G, known as a natural occurring penicillin, is particularly helpful with streptococci and staphylococci, as well as some penicillin-susceptible strains of N. gonorrhoeae as it gets widely distributed throughout the body, although poorly distributed in the central nervous system (CNS).
A common adverse drug reaction (ADR) for penicillin is the frequency of allergic reactions that may include hives, skin rashes, itching and difficulty breathing, although in some cases it may even progress to life-threatening anaphylactic shock (Ciccone, 2007, p. 505). Other ADRs mentioned were the possibility of seizures, with some milder gastrointestinal side effects like colitis, nausea, vomiting and diarrhea, as well as nephritis, eosinophilia and leukopenia.
In the presence of an allergic sensitivity to penicillin, a macrolide antibiotic such as erythromycin is the alternative of choice for treatment of erysipelas and cellulitis (Koster, Kullberg & Van der Meer, 2007). The role of the macrolide antibiotic is to corrupt the peptide bonding between adjacent amino acids thus disrupting structural and functional features at specific areas of the ribosomes, resulting in the inhibition of bacterial synthesis (Sothiselvam et al., 2014).
As with penicillin, erythromycin is an anti-infective that is very effective with gram-positive streptococci and staphylococci, and gets widely distributed throughout the body, although poorly perfused throughout the CNS (Ciccone, 2013). According to this author there are several strong ADRs that include ventricular arrhythmias, QT prolongation characterized by palpitations, seizures or syncope, as well as pseudomembranous colitis. Other side effects mentioned were gastrointestinal issues like nausea, vomiting, cramping and diarrhea, as well as rashes, drug induced hepatitis and on rare occasion, drug induced pancreatitis. Both penicillin and erythromycin cross the placenta and enters into the breast milk (Ciccone, 2013).
The diagnosis of cellulitis tends to be based mainly on clinical findings versus microbiologic results from needle aspirations due to an issue of unreliable accuracy with organism identification that is common in healthy hosts (Sambrano, Gordon, Mays, Lapolla & Scheinfeld, 2012). These authors found the most common cause of cellulitis was S. aureus and streptococci, treated initially with beta-lactam, administered intravenously in severe cases. Ciccone (2007) characterizes beta-lactam antibiotics as cephalosporin drugs that utilize a penicillin-like anti-infective mechanism to adversely impact the integrity of cellular membrane (p. 505). He states that cephalosporin is commonly used as an alternative for patient’s having difficulty tolerating penicillins, although it should not be used in those having allergic reactions to penicillin.
The treatment of cellulitis varies in response to the specific causative agent, as methicillin-resistant S. aureus (MRSA) will typically require interventions with vancomycin, linezolid or daptomycin (Sambrano, Gordon, Mays, Lapolla & Scheinfeld, 2012). These authors feel that vancomycin should be used with MRSA cellulitis, especially in the presence of a penicillin allergy, but promptly switched to linezolid, an oxazolidinone, if there is a vancomycin-resistant infection. But they all believe that cellulitis, especially those atypical in nature or in the presence of MRSA, should be treated in an empirical manner utilizing patient history, anatomic site and clinical presentation for the most appropriate antibiotic choice.
Vancomycin, an anti-infective, also has an action of binding to the cell wall, resulting in cell
death (Ciccone, 2013). He highlighted the most severe ADRs as being hypersensitivity and anaphylaxis, with lesser side effects being ototoxicity, hypotension, nausea, rash, chills and neck or back pain. This author feels vancomycin is also widely distributed throughout the body and crosses the placenta, but it also allows some permeation into the cerebral spinal fluid (CSF).
Linezolid, an oxazolidinone, has an anti-infective action that inhibits bacterial protein synthesis at the ribosomal level (Ciccone, 2013). This author feels it serves as a very effective treatment against streptococci, as well as having a bacteriostatic action against staphylococci. Side effects of linezolid include headache, insomnia, diarrhea, nausea, lactic acidosis, thrombocytopenia, as well as optic and peripheral neuropathies (Ciccone, 2013).
Recurrent episodes of cellulitis or erysipelas manifest in spite of antibiotic treatment, whether curative or preventive in nature. An analysis by Koster, Kullberg and Van der Meer (2007) reported patient noncompliance, incorrect selection of antibiotics, insufficient dosages or antibiotic concentrations, as well as the possibility of other causative agents as reason for recurrence. According to Cox (2005), 40% of cellulitis cases currently have recurrences. However, in a study summary by Nguyen, Rowland and Mounsey ( 2014), they found the prophylactic use of lower dose penicillin effective in reducing recurrence of leg cellulitis, but feel that more trials are needed to determine if this lower recurrence rate persists upon its discontinuation.
In a study by Morgan and McGuckin (2013), they found that collaboration between dermatology and lymphedema services created a multi-specialist approach that provided prompt and effective management of cellulitis. The treatment plan they identified began with intravenous antibiotics that progressed to oral antibiotics for 14 days, or until the cellulitis resolved, topical steroids and wound dressings/soaks, if needed, followed by compression. From there they highlighted the progression to multilayer compression wrapping using short stretch bandages, followed by thorough instruction in self-care strategies for good nutrition, hydration, proper skin care and manual lymphatic drainage techniques. The final phase of this treatment plan was the progression to custom or over-the-counter compression garments and the incorporation of appropriate self-care strategies.
Physical therapists treating patients with lymphedema must always be aware of the potential for cellulitis or erysipelas, carefully monitoring the skin on a daily basis. Once cellulitis is diagnosed it is important to monitor the involved area of redness, either by measurement or photography, observing the impact and effectiveness of the empiric antibiotic. Those therapists specialized in complex lymphedema management will work with bandaging, skin care, compression garments, manual lymphatic drainage and exercises. However, caution must be utilized during the performance of an active physical therapy (PT) program as these antibiotics possess ADRs ranging from anaphylaxis and seizures to pseudomembranous colitis (Ciccone, 2013). Side effects may include nausea, fatigue, hypotension and neuropathies to name just a few, but all require astute clinical observation for safety while attending the PT appointment (Ciccone, 2013).
In conclusion, the benefits of the collaborative management of cellulitis are clearly presented in many studies similar to Morgan and McGuckin (2013), with the education of healthcare professionals being an essential aspect to insuring early antibiotic intervention or early referral to appropriate dermatology or lymphedema services. Early intervention provides significant patient benefits by limiting tissue damage and medical complications, as well as significant cost savings through shorter hospital stays and less frequent recurrences.
Ciccone, C. D. (2007). Pharmacology in rehabilitation (4th ed). Philadelphia, PA: F. A. Davis
Ciccone, C. D. (2013). Drug guide for rehabilitation professionals. Philadelphia, PA: F. A.
Cox, N. H. (2006). Oedema as a risk factor for multiple episodes of cellulitis/erysipelas of the
lower leg: a series with community follow-up. Br J Dermatol, 155(5), 947-50.
Erbil, B., Ersoy, G., Ozkutuk, A., Akarca, F. K., Korkmaz, T., Demir, O. F. & Kiyan, S. (2014).
The effects of oral antibiotics on infection prophylaxis in traumatic wounds. Ulus Travma
Acil Cerrahi Derg, 20(4), 231-235.
Koster, J. B., Kullberg, B. J. & Van der Meer, J. W. M. (2007). Recurrent erysipelas despite
antibiotic prophylaxis: An analysis from case studies. The Netherlands Journal of
Medicine, 65(3), 89-94.
Mortimer, P. S. & Rockson, S. G. (2014). New developments in clinical aspects of lymphatic
disease. The Journal of Clinical Investigation, 124(3), 915-921.
Nguyen, L., Rowland, K. & Mounsey, A. (2014). Low dose penicillin for recurrent cellulitis?
The Journal of Family Practice, 63(1), E10-E12.
Perello-Alzamora, M. R., Santos-Duran, J. C., Sanchex-Barba, M., Canueto, J., Marcos, M. &
Unamumo, P. ( 2012). Clinical and epidemiological characteristics of adult patients
hospitalized for erysipelas and cellulitis. Eur J Clin Microbiol Infect Dis, 31, 2147-2152.
Sambrano, V., Gordon, R., Mays, R., Lapolla, W. & Scheinfeld, N. ( 2012). Intravenous
antibiotics used in dermatology. Dermatologic Therapy, 25, 70-81.
Sothiselvam, S., Liu, B., Han, W., Ramu, H., Klepacki, D., Atkinson, G. C.,.….
Mankin, A. S. (2014 ). Macrolide antibiotics allosterically predispose the ribosome for
translation arrest. PNAS, 11(27), 9804-9808. 10.1073/pnas.1403586111
Trayes, K. P.,. Studdiford, J. S., Pickle, S. & Tully, A. S. (2013). Edema: Diagnosis and
Management. Am Fam Physician, 88(2), 102-110.
Posted by lit'l duck at 7:22 AM
Sunday, January 31, 2016
USE OF MANUAL LYMPHATIC DRAINAGE THERAPY FOR THE RESOLUTION OF POST-INFLAMMATORY HYPERPIGMENTATION: A CASE REPORT
Background: Literature suggests that manual lymphatic drainage therapy (MLDT) can positively impact general skin complexion. MLDT was selected as treatment for dark skin discolorations caused by post inflammatory hyperpigmentation (PIH). Purpose: The purpose of this study is to observe MLDT in reducing PIH. Methods: MLDT was performed on two adult women for more than 2 ½ months. Skin was observed each session with photographs taken pre/post treatment. Patient 1 had PIH related to leg flea bites and familial predisposition; Patient 2 had PIH from cystic acne at inner thighs. Each received 60-65 minute MLDT sessions, performed full body and locally on hyperpigmented areas. Instruction in diaphragmatic breathing began day 1, with each educated about diet and water intake. The Dermatology Life Quality Index (DLQI) was provided pre/post treatment. Frequency of treatment was individualized, patient 1 coming twice monthly for 4 months and patient 2 was weekly for 2 ½ months. Outcomes: Patient 1 had noticeable improvement in skin discoloration at 2 ½ months, with near complete resolution at 4 months. Patient 2 had partial resolution of skin discoloration at 2 ½ months. Discussion: Observable improvement in skin discoloration was seen in both cases, but longer duration treatment and habitual use of class 1 compression socks may explain the more complete resolution of PIH in patient 1. The DLQI deemed unnecessary by one patient, demonstrated improvement in the other, particularly in areas of clothing choice and intimacy. Conclusion: These findings suggest that MLDT may be a feasible non-invasive alternative for reducing PIH.
Chakraborty, S., Zawieja, S., Wang, W. Zawieja, D. C., & Muthuchamy, M. (2010). Lymphatic system acts as a vital link between metabolic syndrome and inflammation. Ann NY Acad Sci, 1207(Suppl 1). doi: 10.1111/j.1749-6632.2010.05752.x
Chikly, B. (2001). Silent waves: Theory and practice of lymph drainage therapy. Palm Beach Gardens, FL: Upledger Institute, Inc.
Durai, P. C. T., & Nair, D. G. (2015). Acne vulgaris and quality of life among young adults in south India. Indian Journal of Dermatology, 60(1), 33-40. doi: 10.4103/0019-5154.147784
Jerajani, H. R., Mizoguchi, H., Li, J., Whittenbarger, D. J., & Marmor, J. J. (2010). The effects of daily facial lotion containing vitamins B3 and E and provitamin B5 on the facial skin of Indian women: A randomized, double-blind trial. Indian J Dermatol Venereol Leprol, 76(1), 20-26. doi: 10.4103/0378-6323.58674
Lévesque, M., Feng, Y., Jones, R. A., & Martin, P. (2013). Inflammation drives wound hyperpigmentation in zebrafish by recruiting pigment cells to sites of tissue damage. Disease Models & Mechanisms, 6(2), 508–515. doi:10.1242/dmm.010371
Lynde, C. B, Kraft, J. N., & Lynde, C. W. (2006). Topical treatments for melasma and postinflammatory hyperpigmentation. Skin Therapy Letter, 11(9), 1-6. Retrieved from http://www.skintherapyletter.ca
Negrini, D., & Moriondo, A. (2011). Lymphatic anatomy and biomechanics. J Physiol, 589(12), 2927-2934. doi:10.1113/physiol.2011.206672
Olczyk, P., Mencner, L., & Komosinska-Vassev, K. (2014). The role of the extracellular matrix components in cutaneous wound healing. Biomed Research International, 2014, 1- 8. doi: 10.1155/2014/747584
Pyke, C. (2010). Massage: A helping hand for the people with chronic oedema and lymphoedema. Br J Community Nurs, 15(4), S28-30. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20559174
Rohl, J., Zaharia, A., Rudolph, M. & Murrary, R. Z. (2015). The role of inflammation in cutaneous repair. Wound Practice and Research, 23(1), 8-15. Retrieved from http://www.awma.com.au
von der Weid, P.-Y.,& Zawieja, D. C. (2004). Lymphatic smooth muscle: The motor unit of lymph drainage. IJBCB, 36, 1147-1153. doi:10.1061/j.biocel.2003.12.008
Williams, A. (2010). Manual lymphatic drainage: Exploring the history and evidence base. British Journal of Community Nursing, 15(4), S18-24. doi: 10.12968/bjcn.2010.15.Sup3.47365
Posted by lit'l duck at 5:36 AM
Monday, January 5, 2015
According to Sweeney, Stewart and Gaitonde (2014), HT is fairly routine to diagnose, usually characterized by a painless goiter, elevated thyroid peroxidase (TPO) antibodies with presenting symptoms of low thyroid such as cold hands, weight gain and hair loss (p. 389). In some hypothyroid cases there is no goiter, considered a atrophic form, and may correlate with extensive fibrosis of the thyroid and increased susceptibility of overt hypothyroidism (p. 390). Occasionally other unusual diagnostic findings may present, such as suppression of the thyroid-stimulating hormone (TSH), a finding more commonly seen in hyperthyroidism (p. 389). An understanding of the management of hypothyroidism offers great insight into clinical presentations, enabling early detection and appropriate symptom monitoring in the rehabilitation setting for improved thyroid health.
The typical mechanism for hypothyroidism is still not fully understood, but appears to be the byproduct of the interplay between susceptibility genes and environmental factors that produce high levels of antithyroid peroxidase (anti-TPO) and antithyroglobulin (anti-Tg) antibodies (Thompson, 2014, p. 152). Although some studies show that 10-15% of HT patients may actually test antibody negative, demonstrating the need for greater clinical surveillance (Caleo et al. 2013). A clinical correlation between high rates of HT with family history, as well as, a personal history of type 1 diabetes mellitus, Addison disease, Turner syndrome or untreated hepatitis C seems to exist (Sweeney et al., 2014, p.391).According to Sweeney et al. (2014), initial clinical complaints present as fatigue, fullness in the neck, intolerance to cold, increases in body weight and diffuse muscle aches (p. 392). A careful examination should not only include serum TSH and TPO antibody levels, but also a thorough history and palpation of the thyroid (p 392). The palpation of the thyroid gland usually reveals a firm, bumpy surface with symmetrical gland enlargement (p.392). If pain is present in the thyroid region, then a diagnosis of subacute thyroiditis (SAT) may be rendered if associated with fever, elevated serum makers for acute inflammation such as C reactive protein (CRP) and decreased radioactive iodine uptake on thyroid scan (Ipekci, Ozturk and Cakir, 2011, p. 125). In some cases a fine needle aspiration may be indicated formulate a differential diagnosis between painful HT and SAT, as lymphocytic infiltration and fibrosis is seen in HT and granulomatous changes in SAT (p. 127). A thyroidectomy may be considered in cases of unrelenting HT pain, as the causal pain mechanism is still unknown (p. 127). Ipekci et al. (2011) further states the incidence for converting to a permanent form of hypothyroidism is quite high in HT but only 5% in SAT (p.127).
SAT is known as a transient thyrotoxic state that may be caused by an upper respiratory virus that disrupts thyroid follicles via an inflammatory reaction (Sweeney et al, 2014, p. 395). SAT tends to be self-limiting and the thyroid gland can spontaneously resume normal functioning within a few months of diagnosis (p. 395). First line treatment for SAT is aimed at the reduction of anterior neck and jaw pain through the use of high dose nonsteroidal anti-inflammatory or acetylsalicylic acid agents, with prednisone being a pharmacologic alternative (p. 395). Interestingly, in a study of twins living in separate geographic locations, diagnosed with SAT years apart, suggests the pathogenesis of SAT may be a genetic predisposition, specifically in those possessing the human leukocyte antigen (HLA)-B35 (Hamaguchi, Nishimura, Kaneko and Takamura, 2005, p. 562).
Sweeney et al. (2014) found patients with overt hypothyroidism showed elevated TSH and low free T4 levels, with typical treatment consisting of T4 or levothyroxine (Synthroid) to achieve a goal of TSH levels of 1 to 3 mlU per L (p.392). Thompson (2014) went further to state that laboratory findings for hypothyroidism may include decreased T4, possibly decreased T3 and the presence of antibodies for an array of thyroid antigens (p. 152). HT is considered an autoimmune disorder that is part of an organ-specific autoimmune subgroup, best known as autoimmune thyroid disease (AITD) (Nada and Hammouda, 2014, p. 575). Findings show that T lymphocytes and regulatory T cells get down regulated in AITD, compromising the body’s ability to control autoimmune processes (p. 579). Apoptosis or cellular death of thyroid cells was first observed in 1995, a probable result of the dysfunctional immune response (Asik et al., 2013, p. 54). Of significance, it is suspected that apoptosis could take many years to occur, suggesting that early diagnosis and appropriate treatment is a necessary step in preserving overall thyroid health (p. 54).
Pharmacologic treatment of HT typically consists of a T4 hormone called levothyroxine (Synthroid), starting at a low initial dose of 1.6 mcg per kg daily, with incremental changes made every three months, as needed (Sweeney et al., 2014, p. 392). Levothyroxine’s action replaces endogenous thyroid hormones, causing an increased metabolic rate in body tissues (Ciccone, 2013, p. 618). It promotes gluconeogenesis, mobilizes glycogen stores, stimulates protein synthesis, promotes cellular growth and aids in brain and central nervous system (CNS) development (p. 618-619). However, excessive T4 dosing may result in iatrogenic hyperthyroidism and other side effects include insomnia, headache, cardiac arrhythmias, angina, abdominal cramping, vomiting, diarrhea, menstrual issues, sweating, weight loss and heat intolerance (p. 619).
Levothyroxine has variable absorption in the gastrointestinal (GI) tract and is distributed to most tissues with the exception of the placenta and breast milk (Ciccone, 2013, p. 619). Levothyroxine is best taken on an empty stomach, 30 minutes to one hour before breakfast and four hours before or after taking an antacid to obtain the best absorption (NIH, 2013). Ciccone (2013) reports that levothyroxine gets metabolized into active T3 by the liver and other body tissues, with excretion occurring in the feces through the bile (p. 619). It is contraindicated in patients with a history of a recent myocardial infarction, hypersensitivity or hyperthyroidism, and should be used cautiously in the presence of severe renal or adrenal insufficiency and during use with infants or the geriatric population (p. 619).
Drug to drug interactions that reduce effectiveness of levothyroxine include bile acid sequestrants used for high cholesterol or concurrent estrogen therapy (Ciccone, 2013, p. 619). It may minimize the anti-clotting efforts with warfarin, reduce effectiveness of insulin or other oral hypoglycemic agents but may potentiate cardiovascular effects when combined with adrenergic agents such as bronchodilators or vasopressors (p. 619). Drug to food interactions occur with items containing high levels of calcium, iron, magnesium or zinc as it may bind to levothyroxine thus limiting overall absorption (p. 619). Drug formulations for levothyroxine are available in tablet, soft gels and powder form for injections, with dosing routes being oral, intramuscular or through an intravenous application (p. 620).
Thyroid (Armour thyroid) is a desiccated thyroid hormone preparation used for treatment of hypothyroidism through a T3/T4 combination therapy of levothyroxine and liothyronine (Cytomel) that compensates for hormone deficiencies and helps restore hormonal balance (Gaitonde, Rowley, and Sweeney, 2012, p. 249). Ciccone (2013) not only indicates its use in thyroid supplementation and treatment of euthyroid goiters, but also as suppression testing to differentiate mild hypothyroidism from thyroid gland autonomy (p. 1072). According to Vigneri et al. (1993), autonomous thyroid nodules may develop as a result of iodine deficiency, independent of TSH, with a clinical diagnosis determined by the presence of negative suppression of nodular iodine uptake and scan imaging upon T3 administration.
The drug action of thyroid (Armour thyroid) increases the metabolic rate of body tissues, a similar mechanism to those mentioned for levothyroxine, although it also possesses T3 in addition to T4 activity (Ciccone, 2013, p. 1072). The adverse reactions, drug to drug and drug to food interactions are similar to those mentioned for levothyroxine, however, there is an additional contraindication listed with hypersensitivity to beef (p. 1073). These thyroid formulations are limited to oral tablet use, with each 1gr being equivalent to 100 mcg of T4 or 25 mcg of T3 ; T3 being well absorbed and T4 having variable absorption (p. 1073).
In cases of persistent hypothyroidism, combination T3/T4 therapy with dessicated hormone preparations of Amour thyroid or levothyroxine (Synthroid) plus Liothyronine (Cytomel) may be the treatment of choice, although the use of dessicated preparations made from domesticated animals is not recommended by the American Association of Clinical Endocrinologists (Gaitonde et al., 2012, p. 249). According to Antonio Bianco, MD in an interview with Gustafson (2014), he suggested genetic testing of type 2 deiodinase polymorphism known as a disruption in the enzymatic conversion of T4 into T3 and necessary for the appropriate management of persistent hypothyroidism associated with unsuccessful T4 replacement therapy. Gaitonde et al. (2012) states although T3 is a biologically active form, its short half-life and dependency upon the peripheral conversion of T4 into T3 by deiodinase enzymes may result in impaired serum concentration levels, creating a hormone imbalance.
Liothyronine (Cytomel) is a T3 supplement used for treatment of hypothyroidism and in suppression testing to differentiate hyperthyroid from thyroid gland autonomy, and as an intravenous formulation for treatment of myxedema coma (Ciccone, 2013, p. 624). As with the other thyroid hormones, it has an action that increases the metabolic rate of body tissues and aims to restore hormonal balance (p. 624). It is contraindicated in patients with a history of a recent myocardial infarction, hypersensitivity or hyperthyroidism, and should be used cautiously in the presence of severe renal and adrenal insufficiency or during use with infants or the geriatric population (p. 625). The pharmokinetics demonstrate good absorption that gets distributed to most body tissues, although it does not tend to cross the placenta and may sparingly enter into breast milk (p. 625). It is metabolized by the liver and other tissues, getting excreted in the feces through the bile (p. 625).
Drug to drug interactions that reduce effectiveness of liothyronine include bile acid sequestrants used to control high cholesterol or concurrent estrogen therapy (Ciccone, 2013, p. 625). Liothyronine may limit the anti-clotting effect of warfarin, reduce effectiveness of insulin or other oral hypoglycemic agents, but may potentiate cardiovascular effects when combined with adrenergic agents such as bronchodilators or vasopressors (p. 625). Drug to food interactions were not common although care should be taken with iodine containing products such as seaweed.
When reviewing studies on HT, Nada et al. (2014) found patients with HT had variability in presentation, either high or suppressed TSH along with positive tests for anti-TPO and anti-Tg (p.575). A study by Sahin et al. (2012) revealed TSH seemed closely associated with vitamin D levels with their findings showing TSH levels of 3.88 mlU/l when vitamin D levels were above 30ng/ml with 25(OH)D testing (p. 318). Their animal studies revealed that low dose vitamin D and cyclosporine A, a powerful immunosuppressant, correlated with a reduction in experimental autoimmune thyroiditis (p. 317). Their conclusion was that vitamin D deficiency may be involved in the primary pathogenesis of HT and not simply an adverse result of HT (p. 319).
A review of studies concerning complications related to HT revealed evidence of Hashimoto’s encephalopathy first documented in 1966 following a patient presentation of aphasia, seizures, disorientation and hemiparesis (Yong, Soule and Hunt, 2014). They felt it was a rare diagnosis of exclusion, factoring in the seizures and neurologic symptoms, positive thyroid autoantibodies and responsiveness to steroids. Myeloneuropathy, a complication of HT, is also a rare diagnosis of exclusion, looking carefully at the autoimmune factors including anti-thyroid antibodies in order to not mistake it for a B12 deficiency (Kayal, Basumatary, Dutta, Mahanta, Islam and Mahanta, 2013, pp. 427-428). The myeloneuropahty presentation is characterized by scattered weakness and spasticity along with peripheral neuropathy, and it also is highly responsive to steroid therapy (p. 427).
Studies revealing risks from HT included a report by Thompson (2014), stating HT has an increased risk for developing lymphoma, making careful monitoring of long term laboratory levels a necessity (p. 152). Dhanwal (2011) found that thyroid hormones play a role in balancing bone mineral and bone density, noting increased fracture risk in both clinical presentations with hypothyroidism or hyperthyroidism (p. S111). Hypothyroidism, to a lesser extent, did reveal some reduction in bone mineral density (BMD) in qualitative ultrasound studies, and showed poor bone quality that directly correlated with increased TSH (p. S111).
Issues necessary to consider in physical therapy (PT) that are associated with hypothyroidism, specifically HT, include aiding in the diagnosis of an occult thyroid disorder or monitoring for medication trends or tolerances. Caution needs to be used during the performance of aerobics and conditioning exercises due to the increased risk of angina or cardiac arrhythmias. The incidence of increased sweating may heighten the risk of skin issues such as rashes, infections and blisters, making certain heat generating activities less tolerable. It is important to stay aware of the patient’s mental clarity, motor coordination, pain complaints and fatigue level as a way to assist in monitoring their medication response or effectiveness of their thyroid dose. Querying the patient about the timing of their thyroid medication and foods ingested may reveal absorption issues or possible interactions with concurrent drugs such as lithium or amiodarone.
In conclusion, it is clear that HT has a multifactorial origin, with causation ranging from increased stress, infection and pregnancy to limited iodine absorption, genetic issues, radiation exposure and abnormal hormone levels (Sahin et al., 2012, p. 319). Time is crucial, as minimizing the duration of symptoms is necessary to limit the permanent, long term thyroid damage that may occur from persistent abnormal thyroid hormone levels that enables autoimmune thyroid destruction. The rehabilitation setting is a perfect venue for closely monitoring the physical, emotional and spiritual issues associated with disease states, with time provided for patient education regarding stress management and physical therapy treatment for the associated risks and comorbidities of HT.
Asik, M., Sahin, M., Anaforoglu, I, Ankan S., Haydardedeoglu, F. I., Ertugrul T. D., & Tutuncu,
N. B. (2013). The antibody response to endoplasmic reticulum stress in Hashimoto’s thyroiditis. Turk Jen, 17, 53-56. Doi: 10.4274/Tjem.2151
Caleo, A., Vigliar, E., Vitale, M., Di Crescenzo, V., Cinelli, M., Carlomagno, C.,…Zeppa, P. (2013). Cytological diagnosis of thyroid nodules in Hashimoto thyroiditis in elderly patients. BMC Surgery, 13(Suppl 2), S41. Retrieved from http://www.biomedcentral.com/1471-2482/13/S2/S41
Ciccone, C. D. (2013). Drug guide for rehabilitation professionals. Philadelphia, PA: F. A. Davis Company.
Dhanwal, D. K. (2011). Thyroid disorders and bone mineral metabolism. Indian J Endocrinol
Metab, 15(Suppl2), S107-S112. Doi: 10.4103/2230-8210.83339
Gaitonde, D. Y., Rowley, K. D. & Sweeney, L. B. (2012). Hypothyroidism: An Update. Am
Fam Physician, 86(3):244-251. Retrieved from http://www.aafp.org/afp/2012/0801/p244.html
Hamaguchi, E., Nishimura, Y., Kaneko, S.& Takamura, T. (2005). Subacute Thyroiditis
Developed in Identical Twins Two Years Apart. Endocrine Journal, 52(5), 559–562.
Retrieved from https://www.jstage.jst.go.jp/article/endocrj/52/5/52_5_559/_pdf
Ipekci, S., Ozturk, K. & Cakir, M. (2011). A difficult decision—Hashimoto’s thyroiditis or
subactue thyroiditis? Turk Jem, 15, 125-127. Retrieved from www.researchgate.net
Kayal, A. K., Basumatary, L. J., Dutta, S., Mahanta, N., Islam, S. & Mahanta, A. (2013).
Myeloneuropathy in a case of Hashimoto’s disease. Neurology India, 61(4), 426-428.
National Institutes of Health (NIH) (2013). Levothyroxine. Medline Plus. Retrieved from
Nada, A. & Hammoda, M. (2014). Immunoregulatory T cells, LFA-3 and HLA-DR in
autoimmune thyroid diseases. Indian Journal of Endocrinology and Metabolism, 18(4),
574-581. Doi: 10.4103/2230-8210.137524
Sahin, M., Taslipinar, A., Keapcilar, L., Yilmaz, H., Akgul, E. O., Beyhan, Z.,….Delibasi, T.
(2012). Low vitamin D3 levels in euthyroid Hashimoto thyroiditis. International Medical
Journal, 19(4), 317-320. Retrieved from
Sweeney, L. B., Stewart, C. & Gaitonde, D. Y. (2014). Thyroiditis: An integrated approach.
American Family Physician, 90(6), 389-396. Retrieved from http://www.aafp.org/afp/2014/0915/p389.html
Thompson, L. D. R. (2014). Chronic lymphocytic thyroiditis (Hashimoto thyroiditis). Ear, Nose
& Throat Journal, 93(4-5), 152-153. Retrieved from www.entjournal.com/article/chronic-lymphocytic-thyroiditis-hashimoto-thyroiditis
Vigneri, R., Catalfamo, R., Freni, V., Giuffrida, D., Gullo, D., Ippolito, A.,… Regalbuto C.
(1993). Physiopathology of the autonomous thyroid nodule. Minerva Endocrinol, 18(4),
143-145. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8190053
Yong, K. W., Soule, S. & Hunt, P. (2014). Endocrine encephalopathy. NZMJ, 127(1394).
Retrieved from http://journal.nzma.org.nz/journal/127-1394/6132/
Posted by lit'l duck at 8:16 AM