Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + ADDISON DISEASE Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Chronic renal insufficiency1 Hypocortisolism1 +++ ICD-9-CM CODES2 ++ 255.41 Glucocorticoid deficiency PT diagnoses/treatment diagnoses that may be secondary adrenal gland disorders 315.4 Developmental coordination disorder 719.70 Difficulty in walking involving joint site, unspecified 728.2 Muscular wasting and disuse atrophy, not elsewhere 728.89 Other disorders of muscle, ligament, and fascia classified 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES3 ++ E27.1 Primary adrenocortical insufficiency E27.2 Addisonian crisis E27.40 Unspecified adrenocortical insufficiency +++ PREFERRED PRACTICE PATTERNS4 ++ 4B: Impaired Posture 4C: Impaired Muscle Performance ++ PATIENT PRESENTATION A 25-year-old female referred with significant sarcopenia and a BMI of 16. Her gait is unstable and she demonstrates coordination deficits. She is mildly short of breath on exertion. She describes little interest in food, but does have self-described craving for potato chips at times. Of late, she is too tired to exercise and she thinks it is because she is depressed. Her history reveals that she menstruates infrequently over the past year and that her skin tone has changed. ++ FIGURE 19-1 Clinical features of Addison disease. Note the hyperpigmentation in areas of increased friction including (A) palmar creases, (B) dorsal foot, (C) nipples and axillary region, and (D) patchy hyperpigmentation of the oral mucosa. (From Longo DL, Fauci A, Kasper D, et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012.) Graphic Jump LocationView Full Size||Download Slide (.ppt) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ KEY FEATURES +++ Description ++ Insufficient production or release of glucocorticoids (cortisol),1 androgens, and mineralocorticoids from the adrenal glands These hormones play a role in Conversion of food to energy Inflammatory response Response to stress Maintaining sodium–potassium balance for blood pressure regulation and production of androgens in males and women, involved in maintaining libido +++ Essentials of Diagnosis ++ May be insidious onset or sudden onset as in Addisonian crisis May cause pathology in multiple organ systems or be caused by pathology in other organ systems Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary system Confirmation of suspected disease through blood testing +++ General Considerations ++ Clinic should have carbohydrates available if needed for drop in blood sugar Orange juice, sugar packets, or similar May result in secondary problems such as Aerobic capacity and muscle endurance impairment Sarcopenia Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems Weight loss indicating the need for PT intervention depending on severity ++ FIGURE 19-2 Addison disease A. Hyperpigmentation representing an accentuation of normal pigmentation of the hand of a patient with Addison disease. B. Note the accentuated pigmentation in the palmar creases. (From Wolff K, Johnson RA. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology. 6th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Demographics ++ Males and females equally Can develop at any age May be familial5 +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS It is not the purview of a PT to medically diagnose hypothyroid, but rather to recognize the possibility in the differential diagnosis process, especially when the findings are not consistent with conditions commonly treated such as musculoskeletal, neuromuscular, integumentary, and cardiopulmonary. PTs may, however, treat conditions caused by adrenal disorders or treat patients with Addison disease for other pathologies that are unrelated. Hypotension Fatigue Weight loss,1 loss of appetite Decreased activity tolerance Fainting/loss of consciousness Headaches Sweating Anorexia Muscle weakness1 Darkening/hyperpigmentation of skin Craving for salt Hypoglycemia Nausea Diarrhea Vomiting Irritability Depression Pain Joint pain Low back pain Abdominal pain Leg pain Hyperkalemia Loss of libido Oral lesions Metabolic acidosis Personality changes Amenorrhea Sparseness of hair in axilla +++ Functional Implications ++ Severe symptoms such as immediacy of need to defecate and diarrhea may be disabling and result in the inability to leave home. Decreasing weight with inability to exercise or move well. Sarcopenia resulting in weakness, muscle mass loss, inability to ambulate or perform self-care, and aerobic capacity limitation secondary to inactivity. Decreased exercise tolerance. Limitations in ADLs, or IADLs. +++ Possible Contributing Causes ++ Damage to the adrenal glands Autoimmune dysfunction Tuberculosis Infections of the adrenal glands Metastatic cancer Adrenal tumors Surgery Bleeding into the adrenals, as in trauma Illness Systemic infection Hypoparathyroidism Type 1 diabetes mellitus Celiac sprue Primary ovarian failure Testicular failure Pernicious anemia Trauma Anticoagulation therapy Heredity Such as polyglandular syndrome, familial glucocorticoid deficiency, congenital adrenal hypoplasia or hyperplasia, X-linked adrenal leukodystrophy Secondary adrenal disease may be caused by Pituitary disease, inadequate adrenocorticotropic hormone (ACTH) production which leads to inadequate production of adrenal hormones Abrupt stopping of corticosteroids, which may be taken for a variety of conditions including, but not limited to, asthma, arthritis, and inflammatory conditions ++ FIGURE 19-3 A. This patient with Addison disease demonstrates the characteristic hyperpigmentation of the skin with accentuation in sun-exposed areas. B. Palmar creases are also hyperpigmented compared with a normal hand. (Goldsmith LA, Katz SI, Gilchrest BA, et al. Fitzpatrick’s Dermatology in General Medicine. 8th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 19-4 Management of the patient with suspected adrenal insufficiency. PRA, plasma renin activity. (From Longo DL, Fauci A, Kasper D, et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Differential Diagnosis ++ Anorexia nervosa Appendicitis Benign prostatic hypertrophy Bladder infections, urinary tract infections, kidney pathology Bowel disorders Celiac disease Endocrine disorders Gastroenteritis Gynecologic problems in females such as Endometriosis Menses, amenorrhea Ovarian cysts, ovarian dysfunction, or ovarian disease Fibroids Menopause Hyperpigmentation from other causes Hypoaldosteronism Hypotension from other causes Infections in the abdomen Kidney disease Nonmalignant tumors in the abdomen or organs Organ dysfunction as a result of cancer or malignancy Pelvic inflammatory disease Perforated ulcers anywhere in GI system Peritonitis Pituitary dysfunction Prostatitis +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Blood tests/lab tests: Complete blood count (CBC) Levels of: Sodium, potassium, antibodies associated with Addison disease Cortisol levels ACTH levels ACTH stimulation test Insulin-induced hypoglycemia test +++ Imaging ++ Ultrasound Chest X-rays CT scans MRIs +++ FINDINGS AND INTERPRETATION ++ Low cortisol levels Elevated ACTH levels +++ TREATMENT ++ Pharmacologic management Hormone replacement Oral corticosteroids: Fludrocortisones for aldosterone, hydrocortisone, prednisone Corticosteroid injections if vomiting is present Androgen replacement Other Sodium supplements especially with exercise or during episodes of stress Sugar (if Addisonian crisis) Saline (if Addisonian crisis) ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not considered to be appropriate for PT, refer to the appropriate physician. If an emergency is identified, refer to an ER. If the patient’s history and reactions to PT indicate possible adrenal gland dysfunction and or symptoms, refer to a physician. Interprofessional Physician: Smoking cessation Physician: Weight management Nutritionist: Dietary counseling Optometry Ophthalmology Audiology Psychological intervention Occupational therapy +++ IMPAIRMENTS ++ Muscle weakness Muscle atrophy, sarcopenia Gait abnormality/difficulty walking Shortness of breath, fatigue Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries that may be causative of diverticula. Striae pink or purplish may be indicative of Cushing syndrome, and dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Abdominal contour: Roundedness, concavity/hollowness, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus, which may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen; Grey Turner sign which is a sign of hemorrhagic pancreatitis. Bulging in groin or other areas of abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in the area of the navel may be abdominal aortic aneurysm. Palpable abdominal tenderness on left/right or generalized. Psoas sign: Provide resistance over patient’s right knee as they flex the hip. Pain is indicative of appendicitis or possible inflammation of the abdomen. Obturator sign: Internal rotation of right lower extremity (RLE) and flexion may be indicative of appendicitis or pelvic inflammation. Rovsing sign: Pain on right side of the abdomen when pressure is put on the left may be indicative of appendicitis. As differential diagnosis includes GI as well as other endocrine and UG pathologies, the following tests and measures are presented: Palpation of back Skin changes: Turgor, dryness, hairlessness, pigmentation Kidneys: In supine, place one hand under client between ribs and iliac crest and other hand on abdomen below ribs pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder Not usually palpable unless it is distended and rises above pubic bone. In supine, place hand above pubis and press down: + = tenderness, reproduction of pain, or ability to feel the bladder: __+ __−. Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus. Liver: In supine, with left hand under trunk parallel to 11th and 12th rib, lift upward; right hand lateral to rectus and press in and up: + = reproduction of symptoms with deep breath. Ascites: With the fingers, percuss outward from center, if sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate an enlarged spleen (only palpable if enlarged) because of the potential of rupture. Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: + = sudden pain and muscle tensing with deep breath. +++ INTERVENTION ++ Carbohydrates, available if needed for drop in blood sugar Orange juice, sugar packets, or similar PT intervention is consistent with the movement-related problems that may occur secondary to weakness and hormone deficiencies Gait training Therapeutic exercise: All relevant categories, energy conservation Assess for orthostasis, hypotension As hypoglycemia may occur, ensure blood sugar levels are in appropriate ranges May require supplemental sodium during exercise, as sodium deficiency is characteristic, and cramping, nausea should be prevented PT should inquire about medications taken Self-care management training, including skin care/moisturizing, lifestyle management Neuromuscular re-education: Balance and postural training Wound management as indicated +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve adequate functional aerobic capacity and the ability to talk during activity in order to achieve functional gait and activity tolerance for work, play, school, self-care; ADLs and IADLs. Functional gait in the home and community (with or without a device), allowing for work, play, self-care; ADLs and IADLS; up to ___ feet based on patient need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, and transferring in and out of a car. Tolerate 30 minutes of continuous moderate exercise three times a week in ___ weeks, and five times a week in ___ weeks, depending on the severity of disease. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, the physician establishes the medical prognosis. Most are able to maintain active lifestyles with normal life expectancy. It can, however, be life threatening, especially in sudden onset as in an Addisonian crisis. PT prognosis should be good to return to premorbid function if condition is adequately managed. ++ PATIENT RESOURCE Adrenal Insufficiency and Addison’s Disease. National Institute of Diabetes and Digestive and Kidney Diseases. NIH Publication No. 09-3054. National Endocrine and Metabolic Diseases Information Service. http://www.endocrine.niddk.nih.gov/pubs/addison/addison.aspx#symptoms. Accessed March 13, 2013. +++ REFERENCES +1. +Dutton M. Adrenal disorders. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/56510071. Accessed January 25, 2013. +2. +ICD9Data.com. http://www.icd9data.com. Accessed March 13, 2013. +3. +ICD10Data.com. http://www.icd10data.com. Accessed March 13, 2013. +4. +The American Physical Therapy Association. Interactive Guide to Physical Therapist Practice. Alexandria, VA: The American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org/. Accessed March 13, 2013. +5. +Hay WW, Levin MJ, Deterding RR, Abzug MJ, Sondheimer JM. Adrenal cortex. In:Hay WW, Levin MJ, Deterding RR, Abzug MJ, Sondheimer JM CURRENT Diagnosis & Treatment: Pediatrics. 21st ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/56829956. Accessed January 25, 2013. +++ ADDITIONAL REFERENCES + +Adams R, Hinkebein MK, McQuillen M, Sutherland S, El Asyouty S, Lippmann S. Prompt differentiation of Addison’s disease from anorexia nervosa during weight loss and vomiting. South Med J. 1998;91(2):208–211. [PubMed: 9496878] CrossRef + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +de Herder WW, van der Lely AJ. Addisonian crisis and relative adrenal failure. Rev Endocr Metab Disord. 2003;4(2):143–147. doi:10.1023/A:1022938019091. [PubMed: 12766542] CrossRef + +Nieman LK, Chanco Turner ML. Addison’s disease. Clin Dermatol. 2006;24(4):276–280. doi:10.1016/j.clindermatol.2006.04.006. [PubMed: 16828409] CrossRef + +Reisch N, Arlt W. Fine tuning for quality of life: 21st century approach to treatment of Addison’s disease. Endocrinol Metab Clin North Am. 2009;38(2):407–418, ix–x. doi: 10.1016/j.ecl.2009.01.008. [PubMed: 19328419] CrossRef + +Ten S, New M, Maclaren N. Clinical review 130: Addison’s disease 2001. J Clin Endocrinol Metab. 2001;86(7):2909–2922. doi: 10.1210/jc.86.7.2909. [PubMed: 11443143] + +Winqvist O, Karlsson FA, Kämpe O. 21-Hydroxylase, a major autoantigen in idiopathic Addison’s disease. Lancet. 1992;339(8809): 1559–1562. doi: 10.1016/0140–6736(92)91829-W. [PubMed: 1351548] CrossRef + ADRENAL GLAND HYPERFUNCTION Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Hyperadrenalism Hyperadrenocorticism Adrencorticalhyperfunction +++ ICD-9-CM CODES ++ 255.0 Cushing syndrome 255.3 Other corticoadrenal overactivity 255.6 Medulloadrenal hyperfunction Associated physical therapy diagnoses 315.4 Coordination disorder (clumsiness, dyspraxia and/or specific motor development disorder) 718.45 Contracture of joint, pelvic region, and thigh 719.70 Difficulty in walking 728.2 Muscular wasting and disuse atrophy 728.89 Disorders of muscle, ligament, and fascia 729.9 Other disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait: Ataxic, paralytic, spastic, staggering 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E24.0 Pituitary-dependent Cushing disease E24.2 Drug-induced Cushing syndrome E24.3 Ectopic ACTH syndrome E24.8 Other Cushing syndrome E24.9 Cushing syndrome, unspecified E27.5 Adrenomedullary hyperfunction +++ PREFERRED PRACTICE PATTERNS ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction1 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation2 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning3 7B: Impaired Integumentary Integrity Secondary to Superficial Skin Involvement4 ++ PATIENT PRESENTATION A 60-year-old male is referred to PT for generalized muscle weakness, back pain, and complaints of fatigue. His history reveals type 2 diabetes, hypertension, and illegal drug use in his somewhat remote past. He complains of being sweaty most of the time, even without exertion, and is drinking a lot of water. The back pain is constant and he describes it as dull. His lower back is tender to touch, and the pain is not relieved with rest or change in activity. He states his wife is complaining about his decreased libido. Although he used to be an avid exerciser, he complains of being too tired and his legs are getting “skinny.” +++ KEY FEATURES +++ Description ++ Excessive production and release of adrenal hormones, glucocorticoids (cortisol), androgens, mineralocorticoids from the adrenal glands Adrenal glands are critical in regulating inflammation and cardiovascular function Insidious or sudden onset High cortisol levels +++ Essentials of Diagnosis ++ Fatigue Weight gain Decreased activity tolerance Hypertension Confirmation of suspected disease through blood testing ++ FIGURE 20-1 Moon (round, full, puffy) facies and facial flushing in Cushing syndrome. (From Wolff K, Johnson RA. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology. 6th ed. New York, NY: McGraw-Hill; 2009.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 20-2 Approach to the renal workup of hematuria. (Exclude UTI, lithiasis, trauma, bleeding disorders, sickle cell disease.) Complement is depressed in acute poststreptococcal type of glomerulonephritis (about 30 days), chronic glomerulonephritis (persistent), and lupus. ANA, antinuclear antibody; ASO, antistreptolysin antibody; BP, blood pressure; BUN, blood urea nitrogen; C3, complement; Ca, calcium; CBC, complete blood count; Cr, creatinine; IgA, immunoglobulin A; RBC, red blood cell; SLE, systemic lupus erythematosus; U/A, urinalysis. (From Hay WM, Levin MJ, Deterding RR, et al. Current Diagnosis & Treatment: Pediatrics. 21st ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ General Considerations ++ Diagnosis for more occult problems may take time and require intensive diagnostic testing May cause or be caused by pathology in multiple organ systems Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems needing physical therapy intervention depending on severity: Such as aerobic capacity/muscle endurance impairment, weakness/impaired muscle performance, musculoskeletal problems, neuromuscular problems, weight gain +++ Demographics ++ Males and females equally affected Can develop at any age +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Fatigue Weight loss or gain Libido changes Pallor Flushed face Chest pain Rapid breathing Tachycardia Palpitations Hypertension Excessive thirst Sweating Increased heat sensitivity Headaches Decreased gastrointestinal motility Tingling Increased or decreased muscle bulk Muscle weakness Paralysis Increased frequency of urination Increased bowel frequency Darkening/hyperpigmentation of skin Stretch marks Acne Hyperglycemia or diabetes Inability to absorb calcium Water retention, edema Thinning of skin Easy bruising Poor wound healing Abdominal pain Diarrhea Vomiting Nausea Depression, irritability, personality changes Tremors Low-back pain in area of kidneys Hypokalemia Increased sodium levels Hallucinations Amenorrhea, menstrual irregularities Reduced uterus or breast size Infertility Increased body or facial hair Deepened voice Baldness Growth deficiency, short stature Round face, moon face Increased excess body fat in trunk and thoracic back Osteoporosis Increased infection risk Kidney stones Goiter Sleep disturbances Cushing syndrome Adrenal crisis Coma Shock Seizures Death ++ FIGURE 20-3 Diagram depicts the approximate contribution of the adrenal glands and ovaries to levels of androgens, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS). (From Hoffman BL et al. Williams Gynecology. 2nd ed. New York: McGraw-Hill, 2012.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Functional Implications ++ Decreased libido in males Eating disorders Fatigue, weakness, muscle-mass loss Inability to ambulate or perform self-care Infertility Limited ADLs, IADLs Limited aerobic capacity or decreased exercise tolerance secondary to inactivity Onset of diabetes Psychological changes, anxiety, depression, irritability Severe symptoms may be disabling, causing inability to leave home Sleep disturbances +++ Possible Contributing Causes ++ Adrenal tumor (pheochromocytoma) Alcohol Autoimmune dysfunction Bleeding into the adrenals (i.e., from trauma) Cancer of adrenal glands Cushing syndrome Damage to adrenal glands Diabetes mellitus type 1 Dietary stimulants such as caffeine Excessive production of pituitary hormones (causing over stimulation of adrenal glands) Excessive stimulation of adrenal glands Heredity Hyperparathyroidism Hypothalamic disorders Illegal drugs: Cocaine, heroin Illness Impending adrenal failure Infection of adrenal glands Medications: Prescription stimulants, ephedrine Metastatic cancer Obesity Oral corticosteroids Pituitary gland pathology/disorder Systemic infection +++ Differential Diagnosis ++ Autoimmune disease affecting upper and lower GI tracts or cardiovascular system (involve multiple organs and have fatigue component) Crohn disease or irritable bowel syndrome Rheumatoid arthritis Cardiovascular disease Celiac disease Cushing syndrome Endocrine disorder Gynecologic problems in females Hyperaldosteronism Hyperpigmentation from other cause Hypertension from other cause Kidney disease Nonmalignant tumor in abdomen or organs Organ dysfunction from cancer or malignancy Pituitary dysfunction +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Complete blood count (CBC) Levels of sodium, potassium, cortisol, adrenocorticotropic hormone (ACTH), antibodies Dexamethasone suppression test Corticotropin-releasing hormone (CRH) stimulation test to determine adrenal versus pituitary cause Urinalysis 24-hour urine test Saliva tests Biopsy +++ Imaging ++ CT MRI X-ray +++ FINDINGS AND INTERPRETATION ++ Excessive production and release of adrenal hormones Glucocorticoids (cortisol) Androgens Mineralocorticoids +++ TREATMENT +++ Medication ++ Diabetes medication as indicated Cardiac medications as indicated Management of hypertension as indicated (Diuretics, Vasodilators, Ace inhibitors, etc.) Drug therapy: Nizoral (Ketoconazole), Lysodren (Mitotane), Metopirone (Metyrapone) Hormone-replacement therapy +++ MEDICAL PROCEDURES ++ Surgery: Tumor removal as indicated from adrenal glands, pancreas, pituitary, lungs Radiation therapy: Gamma knife or small doses over several weeks ++ REFERRALS/ADMITTANCE If the patient history, symptoms, reactions to PT indicate possible adrenal gland dysfunction, refer to physician If causative problem is not considered appropriate for PT intervention, refer to appropriate physician Refer to ER if emergency identified +++ IMPAIRMENTS ++ Muscle weakness Gait abnormality, difficulty walking Balance impairment Shortness of breath, fatigue Inability to perform self-care Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries causative of diverticula. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundness, concavity, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, signals hemorrhagic pancreatitis. Bulging in groin and abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in navel area may be abdominal aortic aneurysm. Left lower quadrant pain, often following a meal. Palpable abdominal tenderness: On left side or generalized. Psoas sign: Provide resistance over patient’s right knee as they flex the hip; pain indicates appendicitis, possible inflammation of abdomen. Obturator sign: Internal rotation and flexion of right lower extremity may indicate appendicitis, pelvic inflammation. Rovsing sign: Pain on right side of abdomen when pressure applied to left may indicate appendicitis. Palpation Appendix (McBurney’s): Apply vertical pressure halfway between right ASIS and umbilicus; −/+ may indicate appendicitis. Liver: In supine, with left hand under trunk parallel to 11th and 12th ribs, lift upward; right hand lateral to rectus, press in and up: +/= reproduction of symptoms with deep breath, indicates liver involvement. Ascites: Percuss outward from center with fingers; if sound is dull, ascites may be present. Spleen: Not recommended for PT to palpate enlarged spleen secondary to possible rupture (only palpable if enlarged). Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. Kidneys: In supine, place one hand under client between ribs and iliac crest, other hand on abdomen below ribs and ribs pointing in opposite direction; +/− tenderness or reproduction of symptoms. Bladder: Not usually palpable unless distended and raised above pubic bone; in supine, place hand above pubis and press down; +/= tenderness, reproduction of pain, ability to feel the bladder: __+ ___−. +++ INTERVENTION ++ Gait training Therapeutic exercise: All relevant categories, energy conservation If stoma from a colostomy or ileostomy, PT must avoid activities that cause retraction. If insulin pump, take care not to interfere in any way. As hypoglycemia may occur, ensure blood sugar levels in appropriate range. May require supplemental sodium during exercise; cramping, nausea should be prevented. PT should inquire about medications taken. Therapeutic activities for bed mobility, transfer and transitional movement. Wheelchair management. Self-care training, including skin care and moisturizing, lifestyle management. Neuromuscular re-education: Balance and postural training. Wound management as indicated; skin inspection. +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve functional aerobic capacity, ability to talk during activity so as to achieve functional gait and activity tolerance for ADLs/IADLs. Achieve 600 m or greater in a 6-minute walk test for initiation of safe, functional gait in the community. Tolerate 30 minutes of continuous, moderate exercise three times a week in ______weeks, and five times a week in ____________weeks, depending on the severity of the disease. +++ PROGNOSIS ++ Most patients respond to treatment and can maintain active lifestyles. Poor prognosis if condition is caused by cancerous tumor or metastatic disease. Physician establishes the medical prognosis, as pathology is primarily medical in nature. Prognosis from a PT perspective is good if condition is adequately managed; patient should return to premorbid level of function. ++ PATIENT RESOURCE Hyperfunction of the adrenal cortex and social security disability. http://www.disabilitybenefitscenter.org/social-security-disabling-conditions/hyperfunction-of-adrenal-cortex. Accessed April 14, 2014. +++ REFERENCES +1. +The American Physical Therapy Association. Pattern 4D: impaired joint mobility, motor function, muscle performance, and range of motion associated with connective tissue dysfunction. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide. 3.1_4. http://guidetoptpractice.apta.org/content/1/SEC11.short. Accessed January 20, 2013. +2. +The American Physical Therapy Association. Pattern 4E: impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide.3.1_5. http://guidetoptpractice.apta.org/content/1/SEC12.short. Accessed January 20, 2013. +3. +The American Physical Therapy Association. Pattern 6B: impaired aerobic capacity/endurance associated with deconditioning. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide. 3.3_2. http://guidetoptpractice.apta.org/content/1/SEC28.extract?sid=16923df1-6a2d-4480-a71c-6f9e6453b9ad. Accessed January 20, 2013. +4. +The American Physical Therapy Association. Pattern 7B: impaired integumentary integrity associated with superficial skin involvement. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide.3.4_2. http://guidetoptpractice.apta.org/content/1/SEC36.extract?sid=ec1eaf5a-4c10-4b04-ae93-465180eb5e64. Accessed January 20, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +David RR. Adrenal virilism in childhood. Ann N Y Acad Sci. 1967;142(3):787–793. [PubMed: 4291824] CrossRef + +Dutton M. Adrenal disorders. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/5402409. Accessed January 20, 2013.+ +Elte JW. Diagnosis of Cushing’s syndrome. Eur J Intern Med. 2006;17(5):311–312. [PubMed: 16864002] CrossRef + +Goodman CC, Fuller KS. Pathology Implications for the Physical Therapist. 3rd ed. St. Louis, MO: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Adrenal cortex. In:Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/content/6588287. Accessed January 20, 2013.+ +ICD9DATA. http://www.icd9data.com. Accessed January 20, 2013.+ +ICD10DATA. http://www.icd10data.com. Accessed January 20, 2013.+ +Makras P, Toloumis G, Papadogias D, Kaltas GA, Besser M. The diagnosis and differential diagnosis of endogenous Cushing’s syndrome. Hormones (Athens). 2006;5(4):231–250. [PubMed: 17178699] CrossRef + +Magiakou MA, Smyrnaki P, Chrousos GP. Hypertension in Cushing’s syndrome. Best Pract Res Clin Endocrinol Metab. 2006;20(3):467–482. [PubMed: 16980206] CrossRef + +Newell-Price J, Bertagna X, Grossman AB, Nieman LK. Cushing’s syndrome. Lancet. 2006;367(9522):1605–1617. [PubMed: 16698415] CrossRef + +Quinkler M, Lepenies J, Diederich S. Primary hyperaldosteronism. Exp Clin Endocrinol Diabetes. 2002;110(6):263–271. [PubMed: 12373629] CrossRef + +Riddick DH, Hammond CB. Adrenal virilism due to 21-hydroxylase deficiency in the postmenarchial female. Obstet Gynecol. 1975; 45(1):21–24. [PubMed: 163016] + +Shibli-Rahhal A, Van Beek M, Schlechte JA. Cushing’s syndrome. Clin Dermatol. 2006;24(4):260–265. [PubMed: 16828407] CrossRef + +Storr HL, Chan LF, Grossman AB, Savage MO. Paediatric Cushing’s syndrome: epidemiology, investigation and therapeutic advances. Trends Endocrinol Metab. 2007;18(4):167–174. [PubMed: 17412607] CrossRef + CUSHING SYNDROME Download Section PDF Listen Eric Shamus, PhD, DPT, PT, CSCS, Debra F. Stern, DPT, DBA, MSM, PT, Marangela Obispo, MSPT, GCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Hyperadrenocorticalism Hypercortisolism +++ ICD-9-CM CODES ++ 255.0 Cushing syndrome Associated physical therapy diagnoses 315.4 Developmental coordination disorder 718.45 Contracture of joint, pelvic region, and thigh 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy, not elsewhere classified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E24.0 Pituitary-dependent Cushing disease E24.2 Drug-induced Cushing syndrome E24.3 Ectopic ACTH syndrome E24.8 Other Cushing syndrome E24.9 Cushing syndrome, unspecified +++ APTA PRACTICE PATTERNS ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction1 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning 7B: Impaired Integumentary Integrity Associated with Superficial Skin Involvement +++ PREFERRED PRACTICE PATTERN ++ 5F: Impaired Peripheral Nerve Integrity and Muscle Performance Associated with Peripheral Nerve Injury ++ FIGURE 21-1 Typical findings in Cushing syndrome. (From McPhee SJ, Hammer GD. Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 21-2 Clinical features of Cushing syndrome. A. Note central obesity and broad, purple stretch marks (B close-up). C. Note thin and brittle skin in an elderly patient with Cushing. D. Hyperpigmentation of the knuckles in a patient with ectopic ACTH excess. (From Longo DL, Fauci A, Kasper D, et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ PATIENT PRESENTATION A 38-year-old female who works as a certified nurse assistant in a nursing home arrived complaining of upper and lower back pain which started 3 years ago after transferring a patient from wheelchair to bed. Patient reports that she has been suffering from back pain since then for which she has received all kinds of conservative treatment, including prior physical therapy for which she specifies hot packs and massage about 8 months ago. She reports having received multiple corticosteroids injections as well as oral corticosteroids for multiple periods of time prescribed by different physicians for pain control. The past medical history includes hypertension. Patient denies any history of osteoporosis and has never received a bone density test. In addition, patient reported that she feels very depressed because she has been unable to get pregnant. Upon observation, patient appears with central obesity and thin extremities (all four), kyphotic posture, thick neck, and round moon like face. During examination, patient presents pain upon palpation at C7-T2 and L3-S1 paraspinals with tender points, diminished ROM in the lumbar and cervical spines, and mild decreased strength in all four extremities. Patient presents with difficulty with IADLs and job related duties. Laboratory tests showed abnormally high urine cortisol levels. CT scan of the brain was normal. Bone density test showed osteopenia. +++ KEY FEATURES +++ Description ++ Pituitary gland releases excessive adrenocorticotropic hormone (ACTH) The adrenals play a critical role in regulating inflammation and cardiovascular function High cortisol levels Tumor or increased growth of the pituitary gland Can be drug induced +++ Essentials of Diagnosis ++ Noniatrogenic1 ACTH dependent Cushing disease (ACTH-secreting pituitary adenoma Ectopic ACTH syndrome ACTH independent Functional adrenocortical tumor Iatrogenic1 Exogenous glucocorticoid administration in high doses Round, full face (moon face)1 24-hour urine cortisol test Confirmation of suspected disease through blood testing, blood-ACTH level +++ General Considerations ++ May cause pathology in multiple organ systems or be caused by pathology in other organ systems Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary system Mnemonic for each letter of CUSHING May result in secondary problems such as Aerobic capacity and muscle endurance impairment Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems Weight gain May indicate a need for physical therapy intervention depending on severity +++ Demographics ++ Cushing disease (ACTH-secreting pituitary adenoma1 More common in women (female–male ratio of approximately 8:1) Age at diagnosis, 20 to 40 years Ectopic ACTH syndrome1 More common in men (male–female ratio of approximately 3:1) Age at diagnosis, 40 to 60 years Functional adrenocortical tumor1 More common in women Adrenal carcinoma occurs in about two per million population per year Age at diagnosis, usually 35 to 40 years. +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Growth retardation in children (85%)1 Psychiatric effects: Depression (50% to 80%)1 Round face: Moon face (80%)1 Thick neck (80%)1 Thin extremities (80%)1 Atrophy of skin and dermal connective tissue (70%)1 Easy bruising (50%)1 Muscle wasting and weakness (70%)1 Weight gain: Increased body fat in trunk and thoracic back (80%)1 Pallor Flushed face Chest pain Fatigue Rapid breathing Tachycardia Palpitations Hypertension Skin changes: Striae on the abdomen and chest Darkening/hyperpigmentation of skin Stretch marks Acne Excessive thirst Sweating Increased heat sensitivity Decreased gastrointestinal motility Increased frequency of urination Increased bowel movement frequency Poor healing of wounds Abdominal pain Irritability Low back pain in kidney area Decreased libido Infertility Increased body and facial hair Growth deficiencies: Short stature Osteoporosis Increased infection risk Sleep disturbances Adrenal crisis Coma Shock Seizures Death ++ FIGURE 21-3 Diagnostic evaluation of Cushing syndrome and procedures for determining the cause. Boxes enclose clinical diagnoses, and ovals enclose diagnostic tests. (Redrawn with permission from Baxter JD, Tyrrell JB. The adrenal cortex. In: Felig P, Baxter JD, eds. Endocrinology and Metabolism. 2nd ed. McGraw-Hill; 1987.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Functional Implications ++ Severe symptoms such as immediacy of need to urinate may be disabling, resulting in an inability to leave home Ability/inability to afford testing and medications or other treatment Fatigue Weakness, muscle-mass loss, inability to ambulate or perform self-care, aerobic capacity limitation, secondary to inactivity Decreased exercise tolerance Sleep disturbances Changes in lifestyle Psychological changes Eating disorders Inappropriate self-medication Anxiety and depression Irritability Limitations in ADLs or IADLs Skin changes Infertility Decreased libido in males In females, abnormal hair growth Increase in male characteristics for females +++ Possible Contributing Causes ++ Adrenal tumors Cancer of the adrenal glands Excessive stimulation of the adrenal glands Excessive production of pituitary hormones, which stimulate the adrenals Drug use; glucocorticoids2 +++ Differential Diagnosis ++ Organ dysfunction as a result of cancer or malignancy Kidney disease Cardiovascular disease Hypertension from other causes Hyperaldosteronism Hyperpigmentation from other causes Celiac disease Pituitary dysfunction Nonmalignant tumors in the abdomen or organs Malignancies in other organs/systems Type 1 diabetes mellitus Endocrine disorders Bleeding into the adrenals, often due to trauma Systemic infection Medications: Prescription stimulants, ephedrine Alcohol Illegal drugs: Cocaine, heroin Gynecologic problems in females Autoimmune diseases that affect the upper and lower gastrointestinal tracts as well as the cardiovascular system Crohn or irritable bowel syndrome Rheumatoid arthritis RA +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Complete blood count (CBC) Levels of: Sodium, potassium, cortisol, ACTH, antibodies ACTH (Cosyntropin test) stimulation test Dexamethasone suppression test Corticotropin-releasing hormone (CRH) stimulation test to determine adrenal versus pituitary Urinalysis: Urinary free cortisol and 17-hydroxycorticosteroid excretion 24-hour urine test Saliva tests Biopsy +++ Imaging ++ CT scans MRI of the brain X-ray of rib and spine to check for thinning of the bones +++ FINDINGS AND INTERPRETATION ++ Confirmation of suspected disease through blood testing, blood-ACTH level Excessive production and release of adrenal hormones Glucocorticoids (cortisol)2 Androgens +++ TREATMENT +++ Medications ++ Cardiac medications as indicated Medications for management of hypertension as indicated Cortisol replacement therapy +++ MEDICAL PROCEDURES ++ Surgery: Tumor removal as indicated from adrenals, pancreas, pituitary, lungs Radiation therapy: Small doses over several weeks or gamma knife ++ REFERRAL/ADMITTANCE If the patient’s history and reactions to PT indicate possible adrenal gland dysfunction and or symptoms, referral to a physician should be made. +++ IMPAIRMENTS ++ Muscle weakness Gait abnormality/difficulty walking Shortness of breath/fatigue Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries causative of diverticula. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundness, concavity, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, signals hemorrhagic pancreatitis. Bulging in groin and/or abdomen especially apparent with contraction of musculature in area; may be hernia. Pulsing in navel area; may be abdominal aortic aneurysm. Left lower quadrant pain, often following a meal. Palpable abdominal tenderness on left side or generalized. Psoas sign: Provide resistance over patient’s right knee as they flex the hip; pain indicates appendicitis, possible inflammation of abdomen. Obturator sign: Internal rotation and flexion of right lower extremity; may indicate appendicitis, pelvic inflammation. Rovsing sign: Pain on right side of abdomen when pressure applied to left may indicate appendicitis. Palpation Appendix (McBurney’s): Apply vertical pressure halfway between right ASIS and umbilicus; −/+ may indicate appendicitis. Liver: In supine, with left hand under trunk parallel to 11th and 12th ribs, lift upward; right hand lateral to rectus, press in and up: +/= reproduction of symptoms with deep breath, indicates liver involvement. Ascites: Percuss outward from center with fingers; if sound is dull, ascites may be present. Spleen: Not recommended for PT to palpate enlarged spleen secondary to rupture (only palpable if enlarged). Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. Kidneys: In supine, place one hand under client between ribs and iliac crest, other hand on abdomen below ribs and ribs pointing in opposite direction; +/− tenderness or reproduction of symptoms. Bladder: Not usually palpable unless distended and raised above pubic bone; in supine, place hand above pubis and press down; +/= tenderness, reproduction of pain, ability to feel the bladder: __+ ___−. +++ INTERVENTION ++ Gait training Therapeutic exercise: All relevant categories, energy conservation Therapeutic activities for bed mobility training, transfer and transitional movement training Self-care management training including skin care/moisturizing, lifestyle management Neuromuscular re-education; balance and postural training Wound management as indicated; skin inspection +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve adequate functional aerobic capacity and the ability to talk during activity, in order to achieve functional gait and activity tolerance for work, play, school, and self-care; ADLs and IADLS. Functional gait in the home and community (with or without a device), allowing for work, play, and self-care; ADLs and IADLS, up to __________ feet based on patient need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Tolerate 30 minutes of continuous moderate exercise three times a week in ______weeks, and five times a week in ____________, depending on the severity of the disease. Increase score levels of a standardized balance test (Berg, Tinetti’s, etc.) from _____ to _____, depending on the severity of the patient’s balance. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, it is the physician who establishes the medical prognosis. Most are able to maintain active lifestyles and respond to treatment. The prognosis is not as good if tumors are cancerous or a result of metastatic disease and are not treated. PT prognosis if condition is adequately managed; patient should be good to return to premorbid functioning with tumor removal. ++ PATIENT RESOURCES Cushing’s Support & Research Foundation. http://csrf.net/. Accessed May 6, 2013. Cushing’s Understanding Support & Help Organization. http://www.cush.org. Accessed May 6, 2013. +++ REFERENCES +1. +McPhee SJ, Hammer GD. Pathophysiology of selected adrenocortical disorders. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371816. Accessed May 6, 2013. +2. +Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ. Immunosuppressive agents. In:Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ Pharmacology for the Physical Therapist. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6095411. Accessed May 6, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +David RR. Adrenal virilism in childhood. Ann NY Acad Sci. 1967;142(3):787–793.CrossRef+ +Dutton M. Pathology, gynecology, and psychology. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/5402409. Accessed January 26, 2013.+ +Elte JW. Diagnosis of Cushing’s syndrome. Eur J Intern Med. 2006;17:311–312. [PubMed: 16864002] CrossRef + +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. St. Louis, MO: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Kita M, Sakalidou M, Saratzis A, Ioannis S, Avramidis A. Cushing’s syndrome in pregnancy: report of a case and review of the literature. Hormones (Athens). 2007;6(3):242–246. [PubMed: 17724009] + +Makras P, Toloumis G, Papadogias D, Kaltsas GA, Besser M. The diagnosis and differential diagnosis of endogenous Cushing’s syndrome. Hormones (Athens). 2006;5(4):231–250. [PubMed: 17178699] CrossRef + +Magiakou MA, Smyrnaki P, Chrousos GP. Hypertension in Cushing’s syndrome. Best Pract Res Clin Endocrinol Metab. 2006;20(3):467–482. [PubMed: 16980206] CrossRef + +Newell-Price J, Bertagna X, Grossman AB, Nieman LK. Cushing’s syndrome. Lancet. 2006;367(9522):1605–1617. [PubMed: 16698415] CrossRef + +Quinkler M, Lepenies J, Diederich S. Primary hyperaldosteronism. Exp Clin Endocrinol Diabetes. 2002;110(6):263–271. [PubMed: 12373629] CrossRef + +Riddick DH, Hammond CB. Adrenal virilism due to 21-hydroxylase deficiency in the postmenarchial female. Obstet Gynecol. 1975;45(1):21–24. [PubMed: 163016] + +Shibli-Rahhal A, Van Beek M, Schlechte JA. Cushing’s syndrome. Clin Dermatol. 2006;24(4):260–265. [PubMed: 16828407] CrossRef + +Storr HL, Chan LF, Grossman AB, Savage MO. Paediatric Cushing’s syndrome: epidemiology, investigation and therapeutic advances. Trend Endocrinol Metab. 2007;18(4):167–174.CrossRef+ +Zeitler PS, Travers SH, Nadeau K, Barker J, Kelsey MM, Kappy MS. Endocrine disorders. In:Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/content/6588287. Accessed January 26, 2013. + DIABETES MELLITUS Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Juvenile diabetes Diabetes type 1 Diabetes type 1.5 Diabetes type 2 Gestational diabetes +++ ICD-9-CM CODES ++ 249.91 Secondary diabetes mellitus with unspecified complication, uncontrolled 250 Diabetes mellitus +++ ICD-10-CM CODES ++ E08.65 Diabetes mellitus due to underlying condition with hyperglycemia E08.8 Diabetes mellitus due to underlying condition with unspecified complications E09.8 Drug or chemical-induced diabetes mellitus with unspecified complications +++ PREFERRED PRACTICE PATTERNS ++ As of June, 2014, the APTA Guide to Physical Therapist Practice does not include practice patterns for organ system pathology; therefore, the associated or secondary musculoskeletal, cardiovascular/pulmonary, or potential neuromuscular patterns would be indicated. ++ PATIENT PRESENTATION A 30-year-old woman presents to the physician’s office with the chief complaint of a “yeast infection that I can’t seem to shake.” She also has noticed that she has been urinating more frequently, but thinks that it is related to her yeast infection. Over the last several years she has noticed that she has gained more than 40 lb. She has tried numerous diets, most recently a low-carbohydrate, high-fat diet. The patient’s only other pertinent history is that she was told to watch her diet during pregnancy because of excessive weight gain. Her baby had to be delivered by cesarean because he weighed more than 9 lb. Her family history is not known, as she was adopted. On physical examination, her blood pressure is 138/88 mm Hg, her pulse is 72 beats/min, and her respiratory rate is 16 breaths/min. Her height is 65 in and her weight is 190 lb (body mass index [BMI] = 31.6). Her physical examination reveals darkened skin that appears to be thickened on the back of her neck and moist, reddened skin beneath her breasts. Her pelvic examination reveals a thick, white, vaginal discharge. A wet preparation from the vaginal discharge reveals branching hyphae consistent with Candida. A urine dipstick is performed that is negative for leukocyte esterase, nitrites, protein, and glucose.1 ++ FIGURE 22-1 Diabetes mellitus: atrophy of skin (necrobiosis diabeticorum) of legs with coronary disease. (From Fuster V, Walsh RA, Harrington RA. Hurst’s The Heart. 13th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ KEY FEATURES +++ Description ++ Diabetes mellitus Primary diabetes mellitus Type 1: Inability of the body to produce insulin, formerly referred to as juvenile diabetes Type 1.5: Latent autoimmune diabetes in adults (LADA), signs of both type 1 and type 2 diabetes where the body can initially produce some insulin but ultimately cannot Type 2: Insulin resistance; inability of the body to produce adequate insulin or inability for adequate insulin uptake by the body to sufficiently regulate insulin/glucose, some insulin is produced by the pancreas Impaired glucose tolerance (IGT) Gestational diabetes mellitus Secondary diabetes mellitus Destructive pancreatic disease Endocrine diseases Drug-induced diabetes Stress diabetes +++ Essentials of Diagnosis ++ Frequent urination Unexplained weight loss, especially with Type 1 Excessive thirst Increased hunger Inappropriate sweating Dizziness Nausea Decreased activity tolerance Hyperosmolar Hyperglycemic Nonketotic Syndrome Rare condition in which blood sugar is 600 mg/dL or above and can result in death; in those who may have diagnosed or undiagnosed diabetes can result in coma and death. +++ General Considerations ++ May cause pathology in multiple organ systems Kidney and urinary tract GI: Liver, pancreas Cardiovascular: Heart, peripheral circulation Neuromuscular: Neuropathy Integumentary Vision Reproductive system May result in secondary problems, such as aerobic capacity and muscle endurance impairment, sarcopenia, weakness/impaired muscle performance, musculoskeletal problems, neuromuscular problems, weight loss or weight gain—indicating the need for physical therapy intervention depending on severity Increased incidence of tendonitis Increased incidence of frozen shoulder Exercise may cause hypoglycemia Exercise may interfere with timed insulin uptake if performed in the area of injection site soon after injecting Metabolic syndrome: Presence of High blood pressure High cholesterol Belly fat Elevated blood sugar Hyperlipidemia +++ Demographics ++ Occurs in males and females. Higher incidence in African Americans and Hispanics. Type 2 is more common in individuals who are obese, and is on the rise in children secondary to sedentary lifestyle and obesity. During 2002 to 2005, 15,600 children were newly diagnosed with type 1 diabetes annually, and 3600 youth were newly diagnosed with type 2 diabetes annually.2 Among children younger than 10 years, the rate of new cases was 19.7 per 100,000 each year for type 1 diabetes and 0.4 per 100,000 for type 2 diabetes. Among children ages 10 years or older, the rate of new cases was 18.6 per 100,000 each year for type 1 diabetes and 8.5 per 100,000 for type 2 diabetes.2 Non-Hispanic White youth had the highest rate of new cases of type 1 diabetes: 24.8 per 100,000 per year among those younger than 10 years and 22.6 per 100,000 per year among those ages 10 to 19 years.2 Type 2 diabetes was extremely rare among youth ages younger than 10 years. Although still infrequent, rates were greater among youth ages 10 to 19 years than in younger children, with higher rates among US minority populations than in non-Hispanic Whites.2 Among non-Hispanic White youth ages 10 to 19 years, the rate of new cases was higher for type 1 than for type 2 diabetes. For Asian/Pacific Islander Americans and American Indian youth ages 10 to 19 years, the opposite was true; the rate of new cases was greater for type 2 than for type 1 diabetes. Among non-Hispanic Black and Hispanic/Latino youth ages 10 to 19 years, the rates of new cases of type 1 and type 2 diabetes were similar.2 There is a 4% incidence rate during pregnancy.2 In people under the age of 20 years, 0.22% have diabetes.2 In people over the age of 20 years, 10.7% have diabetes.3 In people over the age of 60 years, 23.1% have diabetes.3 Twelve million men in the United States over the age of 20 years have diabetes.3 In the United States 11.5 million women aged 20 years or older have diabetes.3 African Americans have a 70% higher chance of getting diabetes than Caucasian Americans.3 ++ FIGURE 22-2 Spectrum of glucose homeostasis and diabetes mellitus (DM). The spectrum from normal glucose tolerance to diabetes in type 1 DM, type 2 DM, other specific types of diabetes, and gestational DM is shown from left to right. In most types of DM, the individual traverses from normal glucose tolerance to impaired glucose tolerance to overt diabetes (these should be viewed not as abrupt categories but as a spectrum). Arrows indicate that changes in glucose tolerance may be bidirectional in some types of diabetes. For example, individuals with type 2 DM may return to the impaired glucose tolerance category with weight loss; in gestational DM, diabetes may revert to impaired glucose tolerance or even normal glucose tolerance after delivery. The fasting plasma glucose (FPG), the 2-hour plasma glucose (PG) after a glucose challenge, and the A1C for the different categories of glucose tolerance are shown at the lower part of the figure. These values do not apply to the diagnosis of gestational DM. The World Health Organization uses an FPG of 110 to 125 mg/dL for the prediabetes category. Some types of DM may or may not require insulin for survival. *Some use the term “increased risk for diabetes” (ADA) or “intermediate hyperglycemia” (WHO) rather than “prediabetes.” (Adapted from the American Diabetes Association: Clinical Practice Recommendations 2007. Diabetes Care. 2007;30:S4.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Insulin necessary in treatment Type I: Almost always Type 2: Sometimes Abnormal metabolism Lethargy after consuming large amounts of carbohydrates Nausea Emesis Frequent urination Increased hunger Thirst Type 1: Common Type 2: Rare Weight loss Type 1: Common Type 2: Rare Irritability Shakiness following physical activity Unexplained weight loss Peripheral neuropathy Fever Skin infections Skin tags UTIs Gum infections Heart disease Chronic complications with the organ systems Circulatory problems that may lead to amputation (i.e., peripheral artery disease) Sudden changes in mental status or behavior Sweet smelling or alcohol-like smelling breath Vision impairment: Retinopathy, blurred vision Hearing impairment Kidney disease: Nephropathy Hypoglycemia: When awake Hunger Shakiness Nervousness Sweating Dizziness or light headedness Sleepiness Confusion Difficulty speaking Anxiety Weakness Hypoglycemia: When asleep Crying out Nightmares Damp sleep clothing from perspiration Tiredness, irritability or confusion upon wakening Hyperglycemia early signs Frequent urination Increased thirst Blurred vision Fatigue Headache Hyperglycemia (later signs): Medical emergency; persistent blood sugar 240+ Toxic acids (ketones) build up in blood and urine Fruity-smelling breath Nausea and vomiting Abdominal pain Shortness of breath Dry mouth Weakness Confusion Coma Ketoacidosis Common in type 1 diabetes Rare in type 2 diabetes Condition in which there is too little insulin Body produces very high levels of blood acids (ketones), in which the body is breaking down fats Blood sugar 300+, medical emergency Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Loss of appetite Weakness or fatigue Shortness of breath Fruity-scented breath Confusion High blood sugar level High ketone levels in urine (home test) +++ Functional Implications ++ Severe symptoms such as immediacy of need to urinate, may be disabling and result in the inability to leave home Need to check blood sugar levels on regular basis and appropriately discard needles Challenges with travel relative to managing medication, especially insulin; time changes, possible need for refrigeration Sarcopenia, resulting in weakness, muscle-mass loss, inability to ambulate or perform self-care, as well as aerobic capacity limitation secondary to inactivity Decreased exercise tolerance although indicated for management of type 2 and health lifestyle for type 1 Sleep disturbances Changes in lifestyle to accommodate dietary changes such as counting carbohydrates and medication regiments: Oral, injected, or pump Eating disorders Fatigue Inappropriate self-medication Noncompliance with dietary recommendations or medication regiments Possible management of insulin pump Anxiety and depression Can be indicative of serious medical conditions such as pancreatitis, cancer of the pancreas Limitations in ADLs, or IADLs Infection; systemic Skin lesions Neuropathy; increased risk for falls Vision impairment; most often retinal Prone to infections (i.e., bacteria in the skin, fungal, UTIs, kidney) Potential for kidney problems Gastroparesis +++ Possible Contributing Causes ++ Type 1: Body stops production of insulin; autoimmune Not usually associated with obesity Type 1.5: Most probably a genetic type of slowly progressing Type 1 Type 2 Obesity Lack of exercise Pancreatic disease Secondary effect of other illnesses such as pancreatitis, cancer of the pancreas Genetic disposition Type 1: Weak, polygenic Type 2: Strong, polygenic Pregnancy (gestational diabetes) 4% incidence May disappear following the pregnancy Increased chance for development of diabetes later in life with a history of gestational diabetes Metastatic cancer Cushing syndrome Infections (i.e., congenital rubella and cytomegalovirus Cystic fibrosis Down syndrome Prader–Willi syndrome Leprechaunism Chemical inducement +++ Differential Diagnosis ++ Organ dysfunction as a result of cancer or malignancy, especially the pancreas Non-malignant tumors in the abdomen or organs Endocrine disorders Gastroparesis Gynecologic problems in females Autoimmune diseases that affect the upper and lower gastrointestinal tracts Crohn or irritable bowel syndrome SLE Rheumatoid arthritis (RA) Appendicitis Peritonitis Prostitis Benign prostatic hypertrophy Pelvic inflammatory disease Gastroenteritis Perforated ulcers anywhere in GI system Bladder infections, urinary tract infections, kidney pathology Infections in the abdomen Bowel disorders +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Blood tests, complete blood test Kidney function: Creatinine, protein Screening for microalbuminuria Blood glucose levels: HbA1C; average over 3 months, not fasting, fructosamine; average over 1 month Glucose tolerance testing Fasting plasma glucose (FPG) test Random plasma glucose test: Based on when last food was taken +++ Imaging ++ Ultrasound Intravenous urinary pyelogram using dye for kidneys CT scans MRIs +++ FINDINGS AND INTERPRETATION ++ Glucose Before meals: Between 70 and 130 mg/dL (4 and 7 mmol/L) 1 to 2 hours after meals: Lower than 180 mg/dL (10 mmol/L) Type 1: Severe intolerance Type 2: Mild glucose intolerance Serum insulin level Type 1: Reduced Type 2: Normal to high Fasting plasma glucose test 99 or below: Normal 100 to 125: Prediabetes 126 or above: Diabetes Hemoglobin AIC >6.5 5.7 to 6.4 = prediabetes +++ TREATMENT +++ Medication ++ Pharmacologic management Sulfonylureas: Glyburide (DiaBeta®), glipizide (Glucotrol®), and glimepiride (Amaryl®) Increases insulin production Biguanides: Metformin Decreases liver glucose production Thiazolidinediones Mostly removed from market, stimulate insulin receptors Alpha-glucosidase inhibitors: Acarbose (Precose®) and miglitol (Glyset®) Blocks the action of alpha-glucosidase enzymes at the brush border of the intestine. The inhibition slows the breakdown of dietary oligosaccharides and disaccharides. Meglitinides: Repaglinide (Prandin®) and nateglinide (Starlix®) are Rapid lowering of postprandial glucose Insulin Type 1 is managed strictly with insulin and diet Type 2 may be managed with or without a combination of diet, oral medications, and insulin Insulin: Short acting, medium acting, long acting +++ MEDICAL PROCEDURES ++ Hospitalization if severe, with IV insulin if glucose is high and not controlled with regular medication Insertion of insulin pumps Bariatric surgery: Gastric bypass, lap bands, sleeves for weight loss for management of type 2 ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not considered to be appropriate for PT, referral to the appropriate physician must be made. If an emergency is identified, referral to an ER may be necessary. If the patient’s history and reactions to PT indicate possible diabetes signs and/or symptoms, referral to a physician should be made immediately. +++ IMPAIRMENTS ++ Muscle weakness Muscle atrophy Gait abnormality/difficulty walking Shortness of breath Inability to perform self-care Peripheral neuropathy Balance impairment Impaired skin integrity Vision impairment +++ TESTS AND MEASURES ++ Palpation Hemosiderin in lower extremities Open skin lesions, especially distally Skin changes: Turgor, dryness, flakiness, redness, shininess, hairlessness Increase capillary refill >3 seconds for fingers and toes +++ INTERVENTION ++ Physical therapy intervention is consistent with the movement-related problems that occur secondary to diabetes and includes (as indicated). Gait training. Therapeutic exercise: All relevant categories, energy conservation. Therapeutic exercise: Aerobic, strengthening, flexibility. If there is an insulin pump, care must be taken not to interfere with it in any way. PT should inquire if medication is taken, when, and where (if insulin is injected) to avoid facilitating rapid uptake if patient has eaten appropriately; if patient has glucose testing monitor with them for monitoring. If glucose >300, exercise should be avoided. If glucose 250 to 300, exercise should be performed with caution. Patients with diabetes should be instructed in alternative methods of monitoring exertion as they may not experience chest pain or other pain secondary to neuropathy. Snacks high in carbs, juice, or sugar cubes should be available for patients in care of blood sugar lows during PT. Therapeutic activities: Bed-mobility training, transfer- and transitional-movement training. Therapeutic activities: Posture, breathing, functional training, pelvic floor retraining as applicable. Self-care management training including skin care, lifestyle management. Neuromuscular re-education: Balance and postural training. Wound management. Shoe wear training. Relaxation training. Lifestyle modification. Smoking cessation. Weight management. Dietary counseling. Support group participation. Psychological intervention. Surgical management. Spiritual support. Palliative care or instruction to caretakers in end stages of kidney disease. +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve adequate functional aerobic capacity, and the ability to talk during activity, in order to achieve functional gait and activity tolerance for work, play, school, self-care; ADLs and IADLs. Functional gait in the home and community, (with or without a device) allowing for work, play, self-care; ADLs and IADLs, up to __________ feet based on patient need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, transferring in and out of a car. Determine location, if patient has an insulin pump. Determine time and injection site, if patient has taken insulin. Determine when patient last ate and if medication is taken as directed. Clinics should have carbohydrates available if needed for drop in blood sugar. Orange juice, sugar packets, or similar. Tolerate 30 minutes of continuous moderate exercise three times a week in ______ weeks, and five times a week in ____________ weeks, depending on the severity of the disease. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, it is the physician who establishes the medical prognosis. If untreated or poorly managed, the prognosis is poor, resulting in limb amputation, stroke, heart disease, skin infections/ulcers, chronic infections, vision and hearing loss, and kidney failure. If type 2 can be managed with dietary changes and weight loss, the prognosis is good. PTs do not specifically manage diabetes, but may be managing conditions secondary to diabetes in which compensatory behaviors are being taught, as in proprioceptive loss. If the individual can effectively learn compensatory behaviors, the prognosis would be good. PTs may be involved in teaching foot care, skin inspection, and exercise programs for which the prognosis should be good. ++ PATIENT RESOURCE American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2010;33(suppl 1):S62–S69. +++ REFERENCES +1. +Toy EC. Diabetes Mellitus, Case 72. LANGE Case Files. http://www.accessmedicine.com/casecontent.aspx?aid=510023498&tabid=1. Accessed June 20, 2013. +2. +National Diabetes Statistics, 2011. National Diabetes Information Clearinghouse (NDIC); a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the National Institutes of Health (NIH). http://diabetes.niddk.nih.gov/dm/pubs/statistics. Accessed June 20, 2013. +3. +Demographics of Diabetes in America. DefeatingDiabetes.com. http://www.defeatingdiabetes.com/diabetes-demographics.htm. Accessed June 20, 2013. +++ ADDITIONAL REFERENCES + +Chandrasoma P, Taylor CR. The endocrine pancreas (islets of Langerhans). In:Chandrasoma P, Taylor CR Concise Pathology. 3rd ed. New York, NY: McGraw-Hill; 1998. http://www.accessphysiotherapy.com/content/190198. Accessed June 20, 2013.+ +Chase HP, Eisenbarth GS. Diabetes mellitus. In:Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/content/6588451. Accessed June 20, 2013.+ +Colcher A, Hurtig HI. Endocrine disorders. In:Watts RL, Standaertt DG, Obeso JA Movement Disorders. 3rd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/55806123. Accessed June 20, 2013.+ +Dutton M. Pharmacology for the physical therapist. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/5406725. Accessed June 20, 2013.+ +Fainardi V, Scarabello C, Cangelosi A et al.. Physical activity and sedentary lifestyle in children with type 1 diabetes: a multicentre Italian study. Acta Biomed. 2011;82(2):124–131. [PubMed: 22480067] + +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. St. Louis, MO: Saunders; 2009.+ +Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders; 2007.+ +Kamboj MK, Draznin MB. Diabetes mellitus. In:Patel DR, Greydanus DE, Baker RJ Pediatric Practice: Sports Medicine. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6975753. Accessed June 20, 2013.+ +Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ. Pancreatic hormones and antidiabetic drugs: introduction. In:Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ Pharmacology for the Physical Therapist. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6093568. Accessed June 20, 2013.+ +Patel P, Macerollo A. Diabetes mellitus: diagnosis and screening. Am Fam Physician. 2010;81(7):863–870. [PubMed: 20353144] + +Sakurai T, Iimuro S, Sakamaki K et al.. Risk factors for a 6-year decline in physical disability and functional limitations among elderly people with type 2 diabetes in the Japanese Elderly Diabetes Intervention Trial. Geriatr Gerontol Int. 2012;12 (Suppl 1):117–126. doi: 10.1111/j.1447–0594.2011.00819.x. [PubMed: 22435947] CrossRef + DIABETIC NEUROPATHY Download Section PDF Listen Mollie Venglar, DSc, MSPT, NCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Diabetic polyneuropathy Metabolic polyneuropathy +++ ICD-9-CM CODES ++ 250.60 Diabetes mellitus with neurological manifestations type 2 or unspecified type not stated as controlled 357.2 Polyneuropathy in diabetes +++ ICD-10-CM CODE ++ E13.40 Diabetes, diabetic (mellitus) with neuropathy +++ PREFERRED PRACTICE PATTERN ++ 5G: Impaired Motor Function and Sensory Integrity Associated with Acute or Chronic Polyneuropathies1 ++ PATIENT PRESENTATION A 59-year-old man was brought begrudgingly to outpatient physical therapy by his wife. She reports that he has been complaining that his ankle hurts. She also reports noticing that he constantly holds on to the wall, furniture, or other objects whenever he is walking. The man reports having fallen about 2 weeks ago when his toe caught the edge of the sidewalk, and his right ankle has hurt since then. On examination, the right ankle is discolored and demonstrates excessive inversion on passive testing. Grossly, manual muscle testing of the upper and lower extremities is within normal limits. The man does not have two-point discrimination in his feet, ankles, and up to mid-calf bilaterally. Proprioception is impaired in bilateral feet and ankles. Balance testing reveals loss of balance with feet together and eyes closed on a stable surface and with feet together and eyes open on a compliant surface. He is able to maintain single-leg stance on the left for 2 seconds with eyes open. His right ankle is too painful to perform single-leg stance. Past medical history includes: diabetes mellitus, morbid obesity, and coronary artery disease. +++ KEY FEATURES +++ Description ++ Damage to peripheral sensory (most common) and/or motor neurons Three major types Distal, primarily sensory, symmetric polyneuropathy (most common) Autonomic neuropathy Transient asymmetric neuropathies Most likely due to demyelination, inflammation, ischemia, or infarction from as yet poorly understood metabolic abnormality ++ FIGURE 23-1 Diabetic foot and diabetic neuropathy. Data from Physical activity/exercise in diabetes. Diabetes Care. 2004;27(suppl 1):S58–S62. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Essentials of Diagnosis ++ Distinct clinical syndromes include Distal, symmetrical, primarily sensory polyneuropathy affecting feet and legs in a chronic, slowly progressive manner (most common) Usually unnoticed by patient until fairly progressed Most common complaint is persistent numbness or tingling, worse at night Acute ophthalmoplegia affecting cranial nerve III (oculomotor) and less often cranial nerve VI (abducens) on one side Acute mononeuropathy of limbs or trunk, including painful thoracolumbar radiculopathy Acute or subacute painful, asymmetrical, predominantly motor multiple neuropathy affecting upper lumbar roots and proximal leg muscles (diabetic amyotrophy) Symmetrical, proximal motor weakness and wasting, usually without pain, with variable sensory loss, pursing subacute or chronic course Autonomic neuropathy involving bowel, bladder, sweating, circulatory reflexes +++ General Considerations ++ Sensory loss puts patient at risk for skin tears, skin breakdown Sensory and motor loss can result in loss of normal forces on joints, particularly foot and ankle, causing joint deformity over time Sensory and motor loss puts patient at higher risk for injury, acute and repetitive Peripheral nerve damage most common in lower extremities, but may occur in the upper extremities +++ Demographics ++ In patients with diabetes, 15% have symptoms of polyneuropathy In cross-sectional sample of people with diabetes, 50% have evidence of peripheral nerve damage on nerve conduction velocity testing Less than 10% have clinical neuropathy on diagnosis of diabetes Infrequent in people under 30 years of age +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Numbness Tingling Weakness, muscle atrophy Loss or impairment of deep tendon reflexes, vibration, proprioception Pain, burning, stabbing Impaired balance Altered gait Impaired vision Orthostatic hypotension +++ Functional Implications ++ Fall risk with mobility on uneven or unpredictable surfaces Injury risk with items of unknown sharpness or temperature Impaired driving due to lower-extremity neuropathy or ophthalmoplegia Difficulty with fine motor tasks (writing, grooming, cooking, feeding, bathing) Difficulty with gross motor tasks (transfers, gait, stair climbing, dressing) +++ Possible Contributing Causes ++ Cardiovascular risk factors associated with “metabolic syndrome” thought to be risk factors for diabetic polyneuropathy: Triglyceride levels, body mass, hypertension Poorly controlled diabetes results in higher likelihood of developing polyneuropathy +++ Differential Diagnosis ++ Spinal cord injury Guillain–Barré syndrome (GBS) Tabes dorsalis Lumbar radiculopathy Peripheral vascular disease Lyme disease Leprosy HIV-related neuropathy Lupus erythematosus Sarcoidosis Polyarteritis nodosa Rheumatoid arthritis ++Table Graphic Jump LocationTABLE 23-1General Guidelines for Exercise Based on Preexercise Blood GlucoseView Table||Download (.pdf) TABLE 23-1 General Guidelines for Exercise Based on Preexercise Blood Glucose Preexercise Blood Glucose Recommended Action Less than 100 mg/dL Ingest 15 g of carbohydrates snack with protein Between 250 and 300 mg/dL Test urine for ketonesExercise if urine negative for ketonesIf urine positive for ketones, delay exercise until negative More than 300 mg/dL May exercise with caution if urine negative for ketonesIf urine positive for ketone, delay exercise until negative Source: Data from Physical activity/exercise in diabetes. Diabetes Care. 2004;27(suppl 1):S58–S62 +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ CSF +++ Imaging ++ Nerve conduction velocity testing Electromyography +++ FINDINGS AND INTERPRETATION ++ CSF: Elevated protein concentration +++ TREATMENT +++ Medication ++ Pharmacologic management Sulfonylureas: Glyburide (DiaBeta®), glipizide (Glucotrol®), and glimepiride (Amaryl®) Increase insulin production Biguanides: Metformin Decreases liver glucose production Thiazolidinediones Mostly removed from market, stimulate insulin receptors Alpha-glucosidase inhibitors: Acarbose (Precose®) and miglitol (Glyset®) Blocks the action of alpha-glucosidase enzymes at the brush border of the intestine. The inhibition slows the breakdown of dietary oligosaccharides and disaccharides. Meglitinides: Repaglinide (Prandin®) and nateglinide (Starlix®) are Rapid lowering of postprandial glucose Insulin Type 1 is managed strictly with insulin and diet Type 2 may be managed with or without a combination of diet, oral medications, and insulin Insulin: Short acting, medium acting, long acting ++Table Graphic Jump LocationTABLE 23-2Onset, Peak, and Duration of Action of Insulin PreparationsView Table||Download (.pdf) TABLE 23-2 Onset, Peak, and Duration of Action of Insulin Preparations Insulin Onset of Action (hours) Peak of Action (hours) Duration of Action (hours) Rapid acting Lispro Aspart Glulisine 0.25–0.5≤0.20Rapid 0.5–2.51–30.9 ≤53–5Not listed Short acting Regular 0.5–1 2–3 3–6 Intermediate acting NPH (Isophane) 2–4 4–10 10–16 Long acting Glargine 2–4 Peakless 20–24 Source: American Diabetes Association. Tools of therapy: Exercise. In: BW Bode, ed. Medical Management of Type I Diabetes Mellitus. 4th ed. Alexandria, VA; American Diabetes Association. LEVEMIR Insulin detemir [rDNA origin] injection; Product insert; Robinson, DM, Wellington, K. Insulin glulisine. Drugs. 2006;66(6):861–869. +++ MEDICAL PROCEDURES ++ Hospitalization if severe, with IV insulin if glucose is high and not controlled with regular medication Insertion of insulin pumps ++ REFERRALS/ADMITTANCE To endocrinologist for regular management of diabetes To neuroendocrinologist for management of more severe neuropathy To occupational therapist for fine motor compensation, ADL modification To orthotist for appropriate footwear, custom bracing as needed To wound care specialist for foot ulcers if needed +++ IMPAIRMENTS ++ Peripheral nerve integrity Cranial nerve integrity Gait training Balance Static standing Dynamic standing Moving base of support Muscle strength Muscle recruitment Coordination Posture, postural control ROM Reflexes: Deep tendon reflexes reduced or absent Muscle tone Bed mobility Transfers Endurance Aerobic capacity Self-care Home management Decreased fine motor control in people who have upper-extremity involvement +++ TESTS AND MEASURES ++ Blood pressure (test specifically for orthostatic hypotension) Vascular examination (particularly blood flow to feet) Heart rate Sensory testing Reflex testing Cranial nerve testing Manual muscle test Active and passive ROM testing, muscle length testing Functional assessment (assist, device, environment) Bed mobility Transitions Sitting balance Standing balance Transfers Gait Stairs Pain assessment Postural assessment Cardiovascular endurance ++Table Graphic Jump LocationTABLE 23-3Chronic Complications of Diabetes MellitusView Table||Download (.pdf) TABLE 23-3 Chronic Complications of Diabetes Mellitus Microvascular disease Nephropathy Neuropathy Sensorimotor distal symmetric neuropathy Autonomic neuropathy Focal and multifocal neuropathies Vascular Nonvascular (entrapment) Macrovascular disease Coronary artery disease Cerebrovascular disease Peripheral vascular disease Associated complications Foot ulcers Infections Source: McPhee SJ, Hammer GD. Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved. +++ INTERVENTION ++ Lifestyle modification Postural correction Mobility: Walking or wheelchair Include devices, bracing, shoe selection Balance strategies Compensatory strategies for lost sensory feedback Pain management Diet modifications to control weight gain, glycemic index, hydration Cardiovascular exercise with glucose monitoring Orthotic or bracing as needed for joint support/deformity Total contact casting for patients with significant or chronic diabetic foot ulcers +++ FUNCTIONAL GOALS ++ Specific to individual’s lifestyle, glycemic control, type of neuropathy. Geared toward individuals with lower-extremity sensory neuropathy. Patient will show written evidence of appropriate insulin use in conjunction with home exercise program for 2 weeks. Patient will demonstrate accurate, consistent stepping strategy with unanticipated balance perturbations from all directions with eyes open, feet shoulder-width apart. Patient will tolerate 15 minutes of aerobic exercise at 65% to 80% maximum heart rate with appropriate blood pressure response. +++ PROGNOSIS ++ Life expectancy reduced by 7 to 9 years for those who control diabetes appropriately; reduced further for those who do not appropriately control the disease. Causes of death related to diabetes include: Myocardial infarction, renal failure, cerebrovascular accident, infection, ketoacidosis, hyperosmolar coma, hypoglycemia. ++ PATIENT RESOURCES Neuropathy. American Diabetes Association. http://www.diabetes.org/living-with-diabetes/complications/neuropathy. Accessed June 19, 2013. Peripheral Neuropathy. The Neuropathy Association. http://www.neuropathy.org/site/PageServer?pagename=Type_Diabetic. Accessed April 28, 2014. +++ REFERENCE +1. +The American Physical Therapy Association. Pattern 5G: impaired motor function and sensory integrity associated with acute or chronic polyneuropathies. Interactive Guide to Physical Therapist Practice. 2003. http://guidetoptpractice.apta.org/content/1/SEC24.extract. Accessed April 28, 2014. +++ ADDITIONAL REFERENCES + +Chandrasoma P, Taylor CR. Chronic complications. In:Chandrasoma P, Taylor CR Concise Pathology. 3rd ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/content/190262. Accessed June 19, 2013. + +Dutton M. Signs and symptoms of DM. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/5402380. Accessed June 19, 2013. + +ICD9DATA. http://www.icd9data.com. Accessed June 19, 2013. + +ICD10DATA. http://www.icd10data.com. Accessed June 19, 2013. + +McPhee SJ, Hammer GD. Microvascular complications. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371165. Accessed June 19, 2013. + +Ropper AL, Samuels MA. Adams and Victor’s Principles of Neurology. 9th ed. New York, NY: McGraw-Hill; 2009:1277–1280. + GOITER Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS, Wendy Song, DO ++ +++ CONDITION/DISORDER SYNONYM ++ Enlarged thyroid +++ ICD-9-CM CODES ++ 240.9 Goiter, unspecified 241.0 Nontoxic uninodular goiter 241.1 Nontoxic multinodular goiter 241.9 Unspecified nontoxic nodular goiter 242 Thyrotoxicosis with or without goiter 242.0 Toxic diffuse goiter 242.00 Toxic diffuse goiter without mention of thyrotoxic crisis or storm 242.01 Toxic diffuse goiter with mention of thyrotoxic crisis or storm 242.1 Toxic uninodular goiter 242.10 Toxic uninodular goiter without mention of thyrotoxic crisis or storm 242.11 Toxic uninodular goiter with mention of thyrotoxic crisis or storm 242.2 Toxic multinodular goiter 242.20 Toxic multinodular goiter without mention of thyrotoxic crisis or storm 242.21 Toxic multinodular goiter with mention of thyrotoxic crisis or storm 242.3 Toxic nodular goiter unspecified type 242.30 Toxic nodular goiter, unspecified type, without mention of thyrotoxic crisis or storm 242.31 Toxic nodular goiter, unspecified type, with mention of thyrotoxic crisis or storm 242.40 Thyrotoxicosis from ectopic thyroid nodule without mention of thyrotoxic crisis or storm +++ ICD-10-CM CODES ++ E01.1 Iodine-deficiency related multinodular (endemic) goiter E01.2 Iodine-deficiency related (endemic) goiter, unspecified E03.0 Congenital hypothyroidism with diffuse goiter E03.1 Congenital hypothyroidism without goiter E04 Other nontoxic goiter E04.0 Nontoxic diffuse goiter E04.2 Nontoxic multinodular goiter E04.8 Other specified nontoxic goiter E04.9 Nontoxic goiter, unspecified E05.00 Thyrotoxicosis with diffuse goiter without thyrotoxic crisis or storm E05.0 Thyrotoxicosis with diffuse goiter E05.2 Thyrotoxicosis with toxic multinodular goiter E07.1 Dyshormogenetic goiter P72.0 Neonatal goiter, not elsewhere classified ++ FIGURE 24-1 Goiter with hyperthyroidism symptoms: Patient has large solitary toxic adenoma on the left lobe. (From Tintinalli JE, Stapczynski JS, Ma JA, Cline DM, Cydulka RK, Meckler GD. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 24-2 Axial contrast-enhanced CT scan of the neck in an elderly woman with a gradually enlarging neck mass demonstrates massive enlargement of a heterogeneously enhancing thyroid gland (arrowheads). There is maintenance of a smooth margin; however, no evidence of any invasion of adjacent structures. No abnormal lymph nodes are identified. Adjacent structures are displaced and compressed by this large mass, notably, the trachea (Tr), esophagus (E), and carotid (C) and jugular (J) vessels. The surgical pathology confirmed diffuse goiter. (From Lalwani AK. Current Diagnosis & Treatment in Otolaryngology-Head & Neck Surgery. 3rd ed. www.accesssurgery.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ PREFERRED PRACTICE PATTERNS ++ 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation1 6A: Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary Disorders2 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning3 ++ PATIENT PRESENTATION A 35-year-old female presents with low back pain and fatigue from standing at work for 4 hours. The patient reports feeling fatigue despite of getting 9 hours of sleep daily. She also experiences constipation, a 15 lb weight gain over the last year and a “lump” above her Adam’s apple. Family history is positive for a “thyroid problem” in her mother. Vitals are: Temperature: 97.8°F, Pulse: 64, Respirations: 16, Blood pressure: 136/78, and SpO2% of 97%. Physical examination shows an overweight woman with dry flaky skin. Her thyroid gland is uniformly enlarged, but nontender to palpation. A blood test for thyroid stimulating hormone (TSH) is elevated at 17.4. +++ KEY FEATURES +++ Description ++ Enlarged thyroid gland, can result in decreased production of thyroid hormone Prolonged elevation of TSH Weight gain or loss May range from single or small nodules to significant enlargement Multinodular goiter4 Enlargement can limit neck mobility and swallowing +++ Essentials of Diagnosis ++ Fatigue Decreased activity tolerance Sensitivity to cold Abnormal thyroid function tests Thyroid enlargement +++ General Considerations ++ Diagnosis for more occult problems may take time and require intensive diagnostic testing, inability to afford testing and medications, noncompliance with medication regimen May cause pathology in multiple organ systems GI: Liver Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems indicating need for PT intervention: Aerobic capacity and muscle endurance impairment, sarcopenia, weakness, musculoskeletal problems, neuromuscular problems, weight gain Hyperlipidemia Can result in hyperthyroidism +++ Demographics ++ Can occur in anyone throughout lifespan, beginning at birth (1 in 4000 infants affected) Estimated five million people affected in the United States, and an equal number undiagnosed Higher incidence in women and people aged 60 years and older +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Nausea Vomiting Diarrhea Coughing Sweating Shaking agitation Hoarseness Dizziness with arms overhead Difficulty swallowing Sensitivity to cold Slowed or rapid heart rate Constipation Joint or muscle pain Paleness Dry skin Thinning hair, including eyebrows Brittle fingernails Weakness Unexplained weight gain Depression Heavy menstruation Decreased sense of smell or taste Swollen hands, feet, face Slowed speech Thickened skin Liver dysfunction Heart disease In severe cases Below-normal body temperature Depressed breathing Low blood pressure Low blood sugar Unresponsiveness +++ Functional Implications ++ Severe symptoms, such as immediacy of need to urinate, may cause inability to leave home Swelling in throat Fatigue Infertility, miscarriage Heart disease Weight gain from inability to exercise or move well Sarcopenia resulting in weakness, muscle-mass loss, inability to ambulate or perform self-care, limited aerobic capacity secondary to inactivity Decreased exercise tolerance Sleep disturbance Lifestyle changes Eating disorders Difficulty swallowing Dizziness with neck extension Limited ROM in neck Inappropriate self-medication Anxiety, depression Liver problems Limited ADLs, IADLs Infection (systemic) Skin lesions from dryness Neuropathy, increased risk for falls Vision impairment (most often retinal) Risk for infection (bacterial, fungal) of skin, urinary tract, kidney +++ Possible Contributing Causes ++ Autoimmune or Hashimoto thyroiditis5 Viral thyroiditis Congenital Grave disease Overexposure to radiation, as in CT scan or radiation therapy to neck or brain Inflammation of thyroid Pregnancy Cancer, metastatic Chemical inducement Radioactive iodine to treat hyperthyroidism Surgical removal of part or whole thyroid gland to treat other thyroid problems Drugs: Amiodarone, drugs to treat hyperthyroidism, lithium Low or excess iodine4 Pituitary dysfunction +++ Differential Diagnosis ++ Organ dysfunction from cancer or malignancy, especially the liver Pituitary dysfunction Non-malignant tumor in the abdomen, organs, or thyroid Endocrine disorder Thyroiditis Hashimoto thyroiditis Grave disease Hypo- or hyperthyroidism Autoimmune disease, causing bowel inflammation or dysfunction Gastroparesis Autoimmune disease affecting upper and lower GI tracts Appendicitis Peritonitis Prostatitis Benign prostatic hypertrophy Pelvic inflammatory disease Gastroenteritis Perforated ulcer in GI system Bladder or urinary tract infection, kidney pathology Throat infection Bowel disorders +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Blood tests, complete blood count (CBC) Thyroid function test: TSH and T4 Cholesterol Liver enzymes Prolactin, normal value: 1.6 to 18.8 ng/mL Sodium levels +++ Imaging ++ Ultrasound Chest x-ray CT Thyroid scan MRI +++ Diagnostic Procedure ++ Biopsy +++ FINDINGS AND INTERPRETATION ++ Prolactin (may be elevated in women) Sodium levels (low in hypothyroidism) Normal range: 135 to 145 milliequivalents per liter (mEq/L) +++ TREATMENT +++ Medication ++ If hyperthyroid Thyroid hormone replacement : Levothyroxine Lifelong, with levels checked annually at least If hyperthyroid: Methimazol (Tapazole) or propylthiouracil If inflammation: Aspirin If iodine deficiency: Iodine +++ MEDICAL PROCEDURES ++ Surgical removal may be indicated if hyperthyroidism results Surgical removal (full or partial) may also be indicated if vessel or esophageal compression Surgery may also be considered for cosmesis ++ REFERRALS/ADMITTANCE If patient history and reactions to PT indicate possible hypo- or hyperthyroidism, refer to appropriate physician If causative problem is not considered appropriate for PT intervention, refer to appropriate physician Refer to ER if emergency identified +++ IMPAIRMENTS ++ Muscle weakness Muscle atrophy Gait abnormality, difficulty walking Shortness of breath, fatigue Inability to perform self-care Balance impairment, dizziness with neck extension Impaired skin integrity +++ TESTS AND MEASURES ++ Palpation Appendix (McBurney’s): Apply vertical pressure halfway between right ASIS and umbilicus: −/+ may indicate appendicitis. Liver: In supine, with left hand under trunk parallel to 11th and 12th ribs, lift upward; right hand lateral to rectus, press in and up: +/= reproduction of symptoms with deep breath, indicates liver involvement. Ascites: Percuss outward from center with fingers; if sound is dull, ascites may be present. Spleen: Not recommended for PT to palpate enlarged spleen secondary to ease of rupture (only palpable if enlarged). Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. Kidneys: In supine, place one hand under client, between ribs and iliac crest, other hand on abdomen below ribs and ribs pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder: Not usually palpable unless distended and raised above pubic bone; in supine, place hand above pubis and press down: +/= tenderness, reproduction of pain, ability to feel the bladder: __+ ___−. +++ INTERVENTION ++ Gait training Therapeutic exercise: All relevant categories, energy conservation Self-care training: Skin care, moisturizing, lifestyle management Neuromuscular re-education: Balance and postural training +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve functional aerobic capacity, ability to talk during activity so as to achieve functional gait and activity tolerance for ADLs/IADLs. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, transferring in and out of car. Tolerate 30 minutes of continuous, moderate exercise three times a week in ______ weeks, and five times a week in ____________ weeks, depending on disease severity. +++ PROGNOSIS ++ Physician establishes the medical prognosis, as pathology is primarily medical in nature. May be lifelong condition unless viral, transient type. Asymptomatic in some cases. Can usually be managed with medication. If thyroid hormones get too low, myxedema coma and ensuing death may result. Prognosis for return to premorbid function is good with adequate medical management. ++ PATIENT RESOURCE American Thyroid Association. Goiter. http://www.thyroid.org/what-is-a-goiter. Accessed June 12, 2013. +++ REFERENCES +1. +The American Physical Therapy Association. Pattern 4E: impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide.3.1_5. http://guidetoptpractice.apta.org/content/1/SEC12.extract?sid=108e960a-5e95-419c-90f2-4a47ca50d8f4. Accessed April 28, 2014. +2. +The American Physical Therapy Association. Pattern 6A: primary prevention/risk reduction for cardiovascular/pulmonary disorders. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide.3.3_1. http://guidetoptpractice.apta.org/content/1/SEC27.extract?sid=e04b1cce-7657-4a83-80cb-fa2d2d550f4a. Accessed April 28, 2014. +3. +The American Physical Therapy Association. Pattern 6B: impaired aerobic capacity/endurance associated with deconditioning. Interactive Guide to Physical Therapist Practice. 2003. doi: 10.2522/ptguide.3.3_2. http://guidetoptpractice.apta.org/content/1/SEC28.extract?sid=52429ec2-d21c-46d5-90f7-038735671158. Accessed April 28, 2014. +4. +Bauer DC, McPhee SJ. Thyroid disease: introduction. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371499. Accessed June 12, 2013. +5. +Chronic thyroiditis (Hashimoto’s disease). NIH National Institutes of Health. MedlinePlus. http://www.nlm.nih.gov/medlineplus/ency/article/000371.htm. Online June 4, 2012. Accessed June 12, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Bauer DC, McPhee SJ. Thyroid diseases. In:McPhee SJ, Hammer GD Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371561. Accessed June 12, 2013.+ +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician. 2005;72(4):623–630. [PubMed: 16127951] + HASHIMOTO THYROIDITIS Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Chronic lymphocytic thyroiditis Autoimmune thyroiditis +++ ICD-9-CM CODES ++ 244.0 Postsurgical hypothyroidism 244.1 Other postablative hypothyroidism 244.2 Iodine hypothyroidism 244.3 Other iatrogenic hypothyroidism 244.8 Other specified acquired hypothyroidism 244.9 Unspecified acquired hypothyroidism 245.0 Acute thyroiditis 245.2 Chronic lymphocytic thyroiditis Associated ICD-9-CM PT diagnoses/treatment diagnoses that may be directly related 315.4 Developmental coordination disorder 718.45 Contracture of joints of pelvic region and thigh 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy, not elsewhere specified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E06.0 Acute thyroiditis E06.3 Autoimmune thyroiditis E89.0 Postprocedural hypothyroidism +++ PREFERRED PRACTICE PATTERNS1 ++ 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation 6A: Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary Disorders 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning ++ FIGURE 25-1 The human thyroid. (Redrawn with permission from Ganong WF. Review of Medical Physiology. 22nd ed. McGraw-Hill; 2005.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 25-2 Thyroid cell. Left: normal pattern. Right: after TSH stimulation. The arrows on the right show the secretion of thyroglobulin into the colloid. On the right, endocytosis of the colloid and merging of a colloid-containing vacuole with a lysosome are also shown. The cell rests on a capillary with gaps (fenestrations) in the endothelial wall. (From Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ PATIENT PRESENTATION A 46-year-old female has been referred to PT for sarcopenia and fatigue. She is a high school teacher, and describes barely being able to get through a day. She complains of generalized achiness and has been treated for depression over the past 3 months but has not seen any improvement. Up until about a year ago she was an avid walker, and walked with colleagues at least three to four times a week. Her history indicates weight gain without change in diet. During postural assessment, the PT notes what appears to be a swelling in her neck, which she attributes to the weight gain. There is a nontender palpable mass in her neck. When tested, her muscle performance demonstrated extremity and core weakness, with easy fatigability. +++ KEY FEATURES +++ Description ++ Autoimmune disease Thyroid gland is gradually destroyed Results in hypothyroidism Enlargement of the thyroid +++ Essentials of Diagnosis ++ Thyroid gland becomes lobulated Decreased activity tolerance Sensitivity to cold Abnormal thyroid function tests Often misdiagnosed as fibromyalgia and depression +++ General Considerations ++ Diagnosis for more occult problems may take time and require intensive medical diagnostic testing May cause pathology in multiple organ systems Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems indicating the need for PT intervention depending on severity Aerobic capacity and muscle endurance impairment Sarcopenia Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems Weight gain, indicating the need for physical therapy intervention depending on severity Gradual onset Hyperlipidemia +++ Demographics ++ Can occur in anyone Higher incidence in women, primarily middle aged Tends to run in families Between 0.1% and 5% of all adults +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Asymptomatic in some cases Clinical findings for hypothyroidism Constipation Hair loss Fatigue Weight gain Slowed heart rate Dry skin Depression Infertility Goiter Panic attacks Memory loss Joint stiffness Facial swelling (lion mask) ++ FIGURE 25-3 The human thyroid. (From Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Functional Implications ++ Severe symptoms such as immediacy of need to urinate may be disabling, resulting in the inability to leave home Inability to afford testing and medications Fatigue Drowsiness Infertility Miscarriage Heart disease Decreased sex drive Increasing weight with inability to exercise or move well Sarcopenia resulting in Weakness Muscle-mass loss Inability to ambulate or perform self-care Aerobic capacity limitation secondary to inactivity Decreased exercise tolerance Sleep disturbances Changes in lifestyle Eating disorders Anxiety and depression Can lead to problems with liver Limitations in ADLs or IADLs Systemic infection Skin lesions from dryness Neuropathy, increased risk for falls Vision impairment, most often retinal Prone to infections such as bacterial and fungal in the skin, urinary tract (UT), kidney Potential for liver problems Difficulty thinking clearly Birth defects in newborns of mothers with Hashimoto In severe cases Below-normal body temperature Depressed breathing Low blood pressure Low blood sugar Unresponsiveness: Myxedema coma ++ FIGURE 25-4 Thyroid anatomy. A. Anterior view B. Lateral view. *The recurrent laryngeal nerve runs in the tracheoesophageal groove on the left and has a slightly more oblique course on the right before it enters the larynx just posterior to the cricothyroid muscle at the level of the cricoid cartilage. (From Doherty GM. Current Diagnosis & Treatment: Surgery. 13th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Possible Contributing Causes ++ Inappropriate self-medication Noncompliance with medication regiments/inability to pay Inflammation of the thyroid Family history Hypoparathyroidism Adrenal insufficiency Fungal infections, mouth and nails Goiters Environmental Pregnancy Cancer Metastatic cancer Other autoimmune disorders Chemical inducement Radiation treatments to the neck Viral thyroiditis Older than age 50 Being female Congenital birth defects Low iodine Pituitary dysfunction as the pituitary signals production of thyroid-stimulating hormone (TSH) ++ FIGURE 25-5 Palpation of the thyroid gland and adjacent structures. A. Palpation from behind. B. Frontal palpation of the thyroid gland. (From LeBlond RF, DeGowin RL, Brown DD. DeGowin’s Diagnostic Examination. 9th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Differential Diagnosis ++ Organ dysfunction as a result of cancer or malignancy, especially the liver Goiter Euthyroid sick syndrome Fibromyalgia Pituitary dysfunction Thyroid lymphoma Non-malignant tumors in the abdomen or organs Other forms of thyroiditis Endocrine disorders, diabetes Cardiac disorders Gynecologic problems in females Autoimmune diseases that affect the upper and lower GI tracts Crohn disease Irritable bowel syndrome Bladder infections UTIs Kidney pathology Fatigue syndromes such as Epstein–Barr Infections in the abdomen Bowel disorders +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Complete blood count (CBC) Total cholesterol Thyroid function: TSH, T3, and Free T42 Serum prolactin Sodium levels, low in hypothyroid Cell pathology Thyroid autoantibodies Antithyroid peroxidase antibody Antithyroglobulin antibody +++ Imaging ++ Ultrasound Chest X-ray CT scans MRIs Radioactive iodine uptake +++ FINDINGS AND INTERPRETATION ++ Thyroid function: TSH and free T4 (low)2 T3 (low or normal)2 +++ TREATMENT +++ Medication ++ Thyroid hormone replacement therapy, most commonly levothyroxine, lifelong, with levels checked at least annually Bone density monitoring required when on levothyroxine ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not appropriate for PT, refer to the appropriate physician. If an emergency is identified, refer to an ER. If the patient’s history and reactions to PT indicate possible hypothyroidism and/or symptoms, refer to a physician. +++ IMPAIRMENTS ++ Muscle weakness/cramps Muscle atrophy Gait abnormality/difficulty walking Shortness of breath, fatigue Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries causative of diverticula. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundness, concavity, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, signals hemorrhagic pancreatitis. Bulging in groin and abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in navel area may be abdominal aortic aneurysm. Left lower quadrant pain, often following a meal. Palpable abdominal tenderness on left side or generalized. Psoas sign: Provides resistance over patient’s right knee as they flex the hip; pain indicates appendicitis, possible inflammation of abdomen. Obturator sign: Internal rotation and flexion of right lower extremity may indicate appendicitis, pelvic inflammation. Rovsing sign: Pain on right side of abdomen when pressure applied to left may indicate appendicitis. Palpation Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus: −/+ may indicate appendicitis. Liver: In supine, with left hand under trunk parallel to 11th and 12th ribs, lift upward; right hand lateral to rectus, press in and up: +/= reproduction of symptoms with deep breath, indicates liver involvement. Ascites: Percuss outward from center with fingers. If sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate enlarged spleen secondary to rupture issues (only palpable if enlarged). Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. Kidneys: In supine, place one hand under client between ribs and iliac crest, other hand on abdomen below ribs pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder Not usually palpable unless distended and raised above pubic bone. In supine, place hand above pubis and press down: +/= tenderness, reproduction of pain, ability to feel the bladder: ____ + ____ −. +++ INTERVENTION ++ PT intervention is consistent with the movement-related problems that occur secondary to diabetes. Therapeutic exercise, all relevant categories, energy conservation If there is a stoma from a colostomy or ileostomy, PT must be aware that activities are avoided if they cause retraction. If there is an insulin pump, take care not to interfere with it in any way. PT should inquire if medication is taken. If glucose >300, exercise should be avoided. Monitor heart rate. Cardiac monitoring with possible MET calculation if history of angina. Therapeutic activities for bed-mobility training, transfer-, and transitional-movement training. Wheelchair management (in severe cases). Self-care management training including skin care/moisturizing, lifestyle management. Neuromuscular re-education: Balance and postural training. +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve adequate functional aerobic capacity and the ability to talk during activity in order to achieve functional gait and activity tolerance for work, play, school, self-care, ADLs, and IADLs. Achieve functional gait in the home and community (with or without a device), allowing for work, play, self-care ADLs, and IADLs, up to _____ feet based on patient’s need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, transferring in and out of a car. Determine when patient last ate and if medication taken as directed. Tolerate 30 minutes of continuous moderate exercise three times a week in _____ weeks, and five times a week in _____ weeks, depending on disease severity. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, the physician establishes the medical prognosis. Prognosis is usually good and the condition may be asymptomatic. From a PT perspective, the prognosis to return to premorbid functional status is good. Outcome is usually very good. ++ PATIENT RESOURCE Hashimoto’s disease. National Endocrine and Metabolic Diseases Information Service. http://www.endocrine.niddk.nih.gov/pubs/hashimoto. Accessed July 5, 2013. +++ REFERENCES +1. +APTA. Guide to Physical Therapy Practice. Atlanta, GA: American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org. Accessed July 5, 2013. +2. +McPhee SJ, Hammer GD. Formation & secretion of thyroid hormones. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371509. Accessed July 5, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Bauer DC, McPhee SJ. Thyroid disease. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371611. Accessed July 5, 2013.+ +Chandrasoma P, Taylor CR. The thyroid gland. In:Chandrasoma P, Taylor CR Concise Pathology. 3rd ed. New York, NY: McGraw-Hill; 1998. http://www.accessphysiotherapy.com/content/192117. Accessed July 5, 2013.+ +Fazio S, Palmieri EA, Lombardi G, Biondi B. Effects of thyroid hormone on the cardiovascular system. Recent Prog Horm Res. 2004;59:31–50. [PubMed: 14749496] CrossRef + +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician. 2005;72(4):623–630. [PubMed: 16127951] + +Staii A, Mirocha S, Todorova-Koteva K, Glinberg S, Jaume JC. Hashimoto thyroiditis is more frequent than expected when diagnosed by cytology which uncovers a pre-clinical state. Thyroid Res. 2010;3(1):11. doi:10.1186/1756–6614–3–11. [PubMed: 21172028] CrossRef + +Wémeau JL. Hashimoto’s thyroiditis (hypertrophic chronic lymphocytic thyroiditis): the centennial of a discovery. Presse Med. 2012;41(12 P 2):e609–e610. doi: 10.1016/j.lpm.2012.10.004. [PubMed: 23177645] CrossRef + +Zeitler PS, Travers SH, Nadeau K, Barker J, Kelsey MM, Kappy MS. Endocrine disorders. In:Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www. accessphysiotherapy.com/content/6588008. Accessed March 5, 2013. + HYPERPARATHYROIDISM Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYM ++ Primary Hyperparathyroidism +++ ICD-9-CM CODES ++ 252.0 Hyperparathyroidism 252.00 Hyperparathyroidism, unspecified 252.01 Primary hyperparathyroidism 252.08 Other hyperparathyroidism 252.02 Secondary hyperparathyroidism, nonrenal 588.81 Secondary hyperparathyroidism (of renal origin) Associated ICD-9-CM PT diagnoses/treatment diagnoses that may be directly related 315.4 Developmental coordination disorder 718.45 Contracture of joint, pelvic region and thigh 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy not elsewhere classified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath ++ FIGURE 26-1 Skeletal changes of hyperparathyroidism. A. Subperiosteal resorption of the phalanges and calcification of the digital arteries. B. Erosion of the distal clavicle and soft tissue calcification. C. “Rugger jersey” spine. (From Imboden J, Hellmann DB, Stone JH. Current Rheumatology Diagnosis & Treatment. 2nd ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ICD-10-CM CODES ++ E21 Hyperparathyroidism and other disorders of parathyroid gland E21.0 Primary hyperparathyroidism E21.1 Secondary hyperparathyroidism, not elsewhere classified E21.2 Other hyperparathyroidism E21.3 Hyperparathyroidism, unspecified N25.81 Secondary hyperparathyroidism of renal origin R19.2 Hyperperistalsis +++ PREFERRED PRACTICE PATTERNS1 ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning ++ PATIENT PRESENTATION A 66-year-old male referred to physical therapy with cervical pain. In his history, he stated that he was recently diagnosed with low Vitamin D and was put on a supplement. His doctor told him his circulating calcium levels were a bit elevated, but that he was not concerned and would check it again in 6 months. He complains of some mild loss of appetite, but is happy about it because he needs to lose a few pounds. Most surprising to him was when his bone density was tested at a recent health fair and he was told he had osteopenia. He also complains of recent onset of constipation. Cervical assessment demonstrated mild limitation in ROM and muscles pulling especially with forward flexion. In addition, when actively forward flexing, he described feeling like “maybe there was lump in his throat.” +++ KEY FEATURES +++ Description ++ Excess of systemic hyperparathyroid hormone (PTH) (hypersecretion) from one or more of the four parathyroid glands Hormone regulates calcium in the bloodstream, producing hypercalcemia and hyperphosphatemia May be primary or secondary to another disease process Primary hyperparathyroidism (HPT) (most common) Enlargement of one of the glands Excess production of the hormone Increased calcium in the blood/hypercalcemia Secondary hyperthyroidism Secondary disease causing low levels of calcium in the body Chromic renal insufficiency Calcium malabsorption Osteomalacia Tertiary hyperparathyroidism Glandular hyperfunction and hypersecretion even after correction of abnormality Caused by chronic renal failure Quartary hyperthyroidism After surgical removal of primary hyperparathyroidism Familial hypocalciuric hypercalcemia (FHH) Autosomal inheritance ++ FIGURE 26-2 Transverse image from a B-mode ultrasound image of the thyroid bed demonstrating a large, ovoid hypoechoic lesion consistent with a parathyroid adenoma (white arrow). Also seen are the carotid artery (CA) and the thyroid gland (Thy). (From Lalwani AK. Current Diagnosis & Treatment in Otolaryngology-Head & Neck Surgery. 3rd ed. www.accesssurgery.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 26-3 Images from a 99mtechnetium-sestamibi scan 2 hours after injection in a patient with renal hyperparathyroidism showing uptake in each of four hyperplastic parathyroid glands. Note that the right inferior parathyroid gland has descended into an ectopic location in the anterior mediastinum. (From Lalwani AK. Current Diagnosis & Treatment in Otolaryngology-Head & Neck Surgery. 3rd ed. www.accesssurgery.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Essentials of Diagnosis ++ Usually diagnosed before symptoms occur via complete blood count (CBC) test Elevated calcium in the blood Elevated parathyroid hormone Decreased phosphorus in the blood Vitamin D deficiency +++ General Considerations ++ May cause pathology in multiple organ systems Gastrointestinal (GI): Liver Cardiovascular: Heart, peripheral circulation, blood pressure Integument Decreased calcium in the bones May result in secondary problems such as aerobic capacity and muscle endurance impairment, sarcopenia, weakness/impaired muscle performance, musculoskeletal problems, neuromuscular problems, indicating the need for physical therapy intervention depending on severity +++ Demographics ++ Primary type in adults: 1:1000 in the Unites States2 More common in individuals with Columbia descent More common over age 50 More common in females after menopause2 +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Signs and symptoms of primary hyperparathyroidism Abdominal pain Abdominal pain Blood in urine Bone cysts Bone pain Cardiovascular disease (usually as a result of high calcium): Small-vessel necrosis Depression Excessive urination Fatigue Forgetfulness Frequent complaints of illness, unknown etiology Hypercalcemia Hypertension Impaired muscle function Joint pain Kidney stones Loss of appetite/anorexia Mental changes, confusion Nausea Osteoporosis/osteomalacia Pancreatitis (rare) Pseudogout Skin necrosis Urinary tract infections (UTIs) Vomiting Weakness Weight loss +++ Functional Implications ++ Anxiety and irritability Decreased exercise tolerance Fatigue Inability or reluctance to leave home secondary to excessive urination, not feeling well Inability to focus Kidney disease Limitations in activities of daily living (ADLs) or instrumental activities of daily living (IADLs) Muscle performance deficits, inability to ambulate or perform self-care as well as aerobic capacity limitation secondary to inactivity Neuropathy, increased risk for falls Osteoporosis Pathological fractures Shortness of breath Sleep disturbances Systemic infection Untreated hyperparathyroidism in pregnant women may cause dangerously low levels of calcium in newborns +++ Possible Contributing Causes ++ Solitary adenomas causes primary hyperparathyroidism 85%2 Parathyroid hyperplasia causes primary hyperparathyroidism 10%2 Parathyroid Carcinoma causes primary hyperparathyroidism 2% to 5%2 Multiple adenomas causes primary hyperparathyroidism 2%2 Noncompliance with medication regiments/inability to pay Changes in lifestyle Inappropriate self-medication Vitamin D deficiency Benign parathyroid tumors Enlargement of two or more parathyroid glands Heredity, genetic disorder Multiple endocrine neoplasia: Type 1 Calcium deficiency Chronic kidney/renal failure Menopause Multiple endocrine neoplasia Radiation to the neck Lithium use +++ Differential Diagnosis ++ Autoimmune diseases (i.e., sarcoidosis) Bladder infections, UTIs, kidney pathology Bowel disorders Corticosteroid therapy Differential diagnosis of hypercalcemia Endocrine disorders Hypercalcemia Hypercalcemia Hyperthyroidism Infections in the abdomen Multiple myeloma Non-malignant tumors in the abdomen or organs Prolonged bed rest Renal dysfunction as result of cancer or malignancy Tuberculosis Vitamin D deficiency Vitamin D toxicity +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ CBC 24-hour urine collection Urinalysis Thyroid function test +++ Imaging ++ Ultrasound X-rays CT scans Sestamibi scan (CT scan with radioactive compound) MRI Imaging of kidneys Bone mineral density test ECG +++ FINDINGS AND INTERPRETATION ++ Laboratory findings in hypercalcemia from various causes Elevated calcium in the blood Elevated parathyroid hormone Decreased phosphorus in the blood Vitamin D deficiency +++ TREATMENT +++ Medication ++ Hormone replacement therapy Bisphosphonates Calcimimetic agents Calcium supplements Vitamin D supplements +++ MEDICAL PROCEDURES ++ Surgery, removal of one to three glands ++ REFERRALS/ADMITTANCE If patient is referred for PT and causative problem is not considered appropriate for PT, refer to appropriate physician. If an emergency is identified, refer to ER. If patient’s history and reactions to PT indicate possible hyperthyroid and/or symptoms, refer to a physician. +++ IMPAIRMENTS ++ Muscle weakness Muscle spasm Gait abnormality/difficulty walking Shortness of breath, fatigue Limited aerobic capacity Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundedness, concavity/hollowness, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus, which may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, a sign of hemorrhagic pancreatitis. Bulging in groin or other area of abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in area of the navel may be abdominal aortic aneurysm. Palpable abdominal tenderness: On left/right or generalized. Psoas sign: Provides resistance over patient’s right knee as patient flexes hip. Pain is indicative of appendicitis or possible inflammation of abdomen. Obturator sign: Internal rotation of right lower extremity and flexion may be indicative of appendicitis or pelvic inflammation. Rovsing sign: Pain on right side of abdomen when pressure is put on the left may be indicative of appendicitis. Because there may be GI signs associated with hypoparathyroidism, the following tests and measures are necessary: Palpation of thyroid/neck Test for enlargement of thyroid or any abnormalities Skin changes Vital signs Chvostek sign: Tap on the face at a point just anterior to the ear and just below the zygomatic bone; positive response in hypoparathyroid; twitching of the ipsilateral facial muscles, suggests neuromuscular excitability caused by hypocalcemia. Trousseau sign: Inflate a sphygmomanometer cuff above systolic blood pressure for several minutes; positive response in hypoparathyroid, muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggesting neuromuscular excitability. Abdominal palpation, may be enlargement of ovaries. Kidneys: In supine position, place one hand under patient between ribs and iliac crest, other hand on abdomen below ribs and pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder: Not usually palpable unless it is distended and rises above pubic bone; in supine position, place hand above pubis and press down: +/= tenderness, reproduction of pain, or ability to feel the bladder: __ + __ −. Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus. Liver: In supine position, with left hand under trunk parallel to 11th and 12th rib, lift upward; right hand lateral to rectus and press in and up: +/= reproduction of symptoms with deep breath. Ascites: With the fingers, percuss outward from center; if sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate an enlarged spleen (only palpable if enlarged) because of the potential of rupture. Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. +++ INTERVENTION ++ PT intervention is consistent with movement-related problems that occur secondary to hypoparathyroidism and include Gait training Therapeutic exercise: All relevant categories, energy conservation Stretching if contractures present in neck postsurgery Therapeutic activities for bed mobility, transfer-, and transitional-movement training Self-care management training including skin care/moisturizing, lifestyle management Neuromuscular re-education: Balance and postural training Soft tissue mobilization if contractures present in neck postsurgery +++ FUNCTIONAL GOALS ++ Patient will be able to Extend and rotate head and neck left and right with adequate functional range in all directions to safely use mirrors while driving (if postsurgical). Achieve adequate functional aerobic capacity and ability to talk during activity to achieve functional gait and activity tolerance for work, play, school, self-care; ADLs, and IADLs. Achieve functional gait in the home and community (with or without a device), allowing for work, play, self-care; ADLs, and IADLs, up to _____ feet, based on patient’s need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, and transferring in and out of a car. Tolerate 30 minutes of continuous moderate exercise three times a week in _____ weeks, and five times a week in _____ weeks, depending on disease severity. +++ PROGNOSIS ++ As this pathology is primarily medical, physician establishes medical prognosis. Prognosis from a PT perspective is based on effective medical management to return to healthy level of function, prior to onset of disease, if individual is receiving care secondary to problems related to hyperparathyroidism. ++ PATIENT RESOURCE American Thyroid Association. http://www.thyroid.org. Accessed August 8, 2014. +++ REFERENCES +1. +The American Physical Therapy Association. Interactive Guide to Physical Therapist Practice. Alexandria, VA: The American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org/. Accessed July 5, 2013. +2. +Shoback DM, Sellmeyer DE. Disorders of the parathyroids & calcium & phosphorus metabolism. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5370820. Accessed July 5, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Bryant LR, Wulsin JH, Altemeier WA. Hyperparathyroidism and hypoparathyroidism. Ann Surg. 1964;159:411–415. [PubMed: 14129389] CrossRef + +Colcher A, Hurtig HI. Systemic illnesses that cause movement disorders. In:Watts RL, Standaert DG, Obeso JA Movement Disorders. 3rd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/55806123. Accessed July 5, 2013.+ +Dutton M. Parathyroid disorders. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/56510065#56510065. Accessed July 5, 2013.+ +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Habib Z, Camacho P. Primary hyperparathyroidism: an update. Curr Opin Endocrinol Diabetes Obes. 2010;17(6):554–560. [PubMed: 20890202] CrossRef + +Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/resource/14. Accessed July 5, 2013.+ +Ng SM, Anand D, Weindling AM. High versus low dose of initial thyroid hormone replacement for congenital hypothyroidism. Cochrane Database Syst Rev. 2009;21:CD006972. doi: 10.1002/14651858.CD006972.pub2.+ +Parathyroid.com. Norman Parathyroid Center. Hyperparathyroidism: Disease of the parathyroid glands. http://www.parathyroid.com/parathyroid-disease.htm. Accessed July 5, 2013.+ +Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ. Growth, thyroid, and gonadal pharmacology. In:Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ Pharmacology for the Physical Therapist. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6093102. Accessed July 5, 2013.+ +Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician. 2005;72(4):623–630. [PubMed: 16127951] + +Tahmi AS, Saunders J, Sinha P. A parathyroid adenoma: benign disease presenting with hyperthyroid crisis. Case Report Med. 2010:596185. doi: 10.1155/2010/596185. + HYPERTHYROIDISM Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS, Marangela Obispo, MSPT, GCS ++ +++ CONDITION/DISORDER SYNONYM ++ Overactive thyroid +++ ICD-9-CM CODES ++ 242.20 Toxic multinodular goiter without mention of thyrotoxic crisis or storm 242.90 Thyrotoxicosis without mention of goiter or other cause, and without mention of thyrotoxic crisis or storm PT diagnosis codes that may be secondary to thyroid disorders 315.4 Developmental coordination disorder 709.2 Scar conditions and fibrosis of the skin 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy, not elsewhere classified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E05.20 Thyrotoxicosis with toxic multinodular goiter without thyrotoxic crisis or storm E05.90 Thyrotoxicosis, unspecified without thyrotoxic crisis or storm +++ PREFERRED PRACTICE PATTERNS1 ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning ++ FIGURE 27-1 Algorithm for thyroid function tests. This algorithm does not apply in patients with hypothalamic–pituitary disease, serious illness, or those who are taking certain medications such as amiodarone, glucocorticoids, and dopamine. (From McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. Principles and Practice of Hospital Medicine. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 27-2 Hyperthyroidism: laboratory evaluation. FT4, free thyroxine; T3, 3,5,3’-triiodothyronine; TSH, thyroid-stimulating hormone. (Modified with permission from Gardner DG, Shoback D, eds. Greenspan’s Basic & Clinical Endocrinology. 9th ed. Originally published by Appleton & Lange. Copyright © 2011 by the McGraw-Hill Companies, Inc.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ PATIENT PRESENTATION A 47-year-old female has been suffering from bilateral shoulder pain for the last 2 months, which increases with dressing her upper body and washing her head. She reports a decreased ability to perform her job as an administrative assistant for a lawyer’s firm because of pain, difficulty in concentrating which she attributes to being concerned about her shoulder pain, and increased frequency of urination requiring her to leave her workstation several times during the day. She reports that she enjoys running; however, was unable to finish her last 5K because of heat intolerance and palpitations. She has noticed weight loss, however, reports feeling hungry at all times. Upon examination patient presents with clammy skin and mild exophthalmos. Vital signs were normal except heart rate of 110 bpm at rest. ROM was limited in bilateral shoulders. MMT was decreased in bilateral shoulders and bilateral hip flexors. Gait was normal. Endurance was impaired by demonstrating abnormally increased vitals after a gait assessment on short distance. Patient presents with limited ability to perform ADLs, specifically dressing and showering. +++ KEY FEATURES +++ Description ++ Increased thyroid gland activity Characterized by increased basal metabolic rate The thyroid regulates metabolism and produces thyroid hormones (thyroxine [T4] and triiodothyronine [T3]) Hyperthyroidism is a cause of thyrotoxicosis2 +++ Essentials of Diagnosis ++ It is not the purview of a PT to medically diagnose hypothyroid but rather to recognize the possibility in the differential diagnosis process, especially when findings are not consistent with conditions commonly treated such as musculoskeletal, neuromuscular, integumentary, and cardiopulmonary. PTs may treat conditions caused by hyperthyroid or treat patients with hyperthyroidism for other unrelated pathologies. +++ General Considerations ++ May cause pathology in multiple organ systems GI: Liver Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems Aerobic capacity and muscle endurance impairment Sarcopenia Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems Weight gain, indicating the need for PT intervention depending on severity ++ FIGURE 27-3 Hypothalamic–pituitary-thyroid axis. T4, thyroxine; T3, triiodothyronine; TRH, thyrotropin-releasing hormone; TSH, thyroid-stimulating hormone. (Redrawn and modified with permission from Greenspan FS, Gardner DG, eds. Basic and Clinical Endocrinology. 8th ed. McGraw-Hill; 2007.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Demographics ++ Higher incidence in women2 More difficult to diagnose in the elderly +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Graves ophthalmopathy, red or swollen eyes, bulging or protruding eyeballs, impaired vision, inflammation, light sensitivity Tachycardia Cardiac: Atrial fibrillation, arrhythmias, palpitations Heart disease Racing/rapid pulse High blood pressure Hyperactivity Difficulty concentrating and focusing Heat intolerance Sweating, clammy skin Confusion, disorientation Diuresis Weakness Tremors Neck pain Unexplained weight loss with inability to gain weight Difficulty swallowing Change in voice Fatigue2 Decreased activity tolerance Sensitivity to cold Dyspnea, shortness of breath Airway obstruction Enlarged thyroid Increased appetite Menstrual disturbance, irregularity2 Increased bowel frequency Breast development in men Clammy skin Diarrhea Hair loss Hand tremor Itching Nausea and vomiting Skin blushing or flushing Difficulty sleeping Osteoporosis ++ FIGURE 27-4 Hyperthyroidism: exophthalmos and atrial fibrillation manifestations of hyperthyroidism. (From Fuster V, Walsh RA, Harrington RA. Hurst’s The Heart. 13th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Functional Implications ++ Severe symptoms such as immediacy of need to urinate, increased volume of urine, and an increase in bowel frequency may be disabling and result in the inability or reluctance to leave home. Sarcopenia resulting in weakness, muscle-mass loss, inability to ambulate or perform self-care as well as aerobic capacity limitation secondary to inactivity. Decreased exercise tolerance Limitations in ADLs or IADLs Neuropathy, increased risk for falls Vision impairment, driving issues Voice changes, hoarseness ++ FIGURE 27-5 Clinical features of hyperthyroidism. The patient shows (A) ophthalmopathy with exophthalmos (proptosis), and (B) pretibial myxedema. (From Brunicardi CF, Andersen DK, Billiar TR, et al. Schwartz’s Principles of Surgery. 9th ed. New York, NY: McGraw Hill; 2009.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Possible Contributing Causes ++ Autoimmune or Hashimoto thyroiditis Body production of too much thyroid hormone Cancer Chemical inducement Congenital birth defects Female Getting too much iodine Graves disease Older than age 50 Growths/tumor of the thyroid or pituitary gland Heredity Inflammation of the thyroid Metastatic cancer Pituitary dysfunction/tumors as the pituitary signals production of thyroid stimulating hormone (TSH) Plummer disease (toxic multinodular goiter) Radiation to the brain Radiation treatments to the neck Taking large amounts or overdoses of thyroid hormone Testicular or ovarian tumors Thyroiditis Toxic adenoma Viral thyroiditis +++ Differential Diagnosis ++ Organ dysfunction as a result of cancer or malignancy, especially the liver Severe anemia2 Pituitary dysfunction Non-malignant tumors in the abdomen or organs Pheochromocytoma2 Testicular tumors Endocrine disorders Gastroparesis Gynecologic problems in females Autoimmune diseases that affect the upper and lower GI tracts, Crohn or irritable bowel syndrome, systemic lupus erythematosus, rheumatoid arthritis (as they involve organs and have a fatigue component) Bladder infections, urinary tract infections, kidney pathology Chronic infections in the abdomen2 Bowel disorders +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Blood tests/lab tests: Complete blood count (CBC) Thyroid function: TSH, T3, T4 (usually high) Abnormal thyroid function tests2 Cholesterol Liver enzymes Prolactin Sodium levels low (normal range: 135 to 145 mEq/L) ++ FIGURE 27-6 Hyperthyroidism with thyroid dermopathy in a classic location on the anterior shins. Note that infiltrated plaques extend to the calf and are partially hyperkeratotic. An isolated nodule is also present on the dorsum of the foot. (From Goldsmith LA, Katz S, Gilchrest B, Paller A, Leffefl DJ, Wolff K. Fitzpatrick’s Dermatology in General Medicine. 8th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Imaging ++ Ultrasound Chest X-ray CT scans MRIs +++ FINDINGS AND INTERPRETATION ++ Thyroid function: TSH (usually low) and T3 and T4 (usually high) Abnormal thyroid function tests Prolactin (may be elevated in women) Sodium levels low in hypothyroid Radioactive iodine uptake by the thyroid is increased2 +++ TREATMENT +++ Medication ++ Antithyroid medications Methimazole (tapazole) Propylthiouracil (PTU) Beta-blockers (to control the cardiac symptoms and anxiety) Other Radioactive iodine to destroy the thyroid Surgical removal of thyroid (making thyroid hormone a lifelong necessity) Newer treatment options under investigation include Endoscopic subtotal thyroidectomy Embolization of the thyroid arteries Plasmapheresis Percutaneous ethanol injection of toxic thyroid nodules Autotransplantation of cryopreserved thyroid Nutritional supplementation with L-carnitine ++ FIGURE 27-7 A. and B. Lymph nodes in the neck can be divided into six regions. Upper mediastinal nodes constitute level VII. m., muscle; n., nerve. (From Brunicardi CF, Andersen DK, Billiar TR, et al. Schwartz’s Principles of Surgery. 9th ed. New York, NY: McGraw Hill; 2009.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not considered appropriate for PT, refer to the appropriate physician. If an emergency is identified, refer to ER. If the patient’s history and reactions to PT indicate possible hyperthyroidism and or symptoms, refer to a physician. Lifestyle modification Physician: Smoking cessation Physician/nutritionist for weight management Nutritionist for dietary counseling Optometry Ophthalmology Audiology Psychological intervention Occupational therapy Speech language pathology +++ IMPAIRMENTS ++ Balance impairment Gait abnormality/difficulty walking Impaired skin integrity Inability to perform self-care Limited aerobic capacity Muscle atrophy Muscle weakness Shortness of breath, fatigue +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Abdominal contour: Roundedness, concavity/hollowness, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus, which may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, which is a sign of hemorrhagic pancreatitis. Bulging in groin or other areas of abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in the area of the navel may be abdominal aortic aneurysm. Palpable abdominal tenderness on left/right or generalized. Psoas sign: Provides resistance over patient’s right knee as they flex the hip; pain is indicative of appendicitis or possible inflammation of the abdomen. Obturator sign: Internal rotation of right lower extremity and flexion may be indicative of appendicitis or pelvic inflammation. Rovsing sign: Pain on the right side of abdomen when pressure is put on the left may be indicative of appendicitis. Because there may be GI signs associated with hyperthyroid, GI tests and measures are included in this section. Palpation of thyroid/neck for enlargement of thyroid or any abnormalities. Skin changes: Turgor, dryness, hairlessness with hyperthyroid, sweaty, clammy. Abdominal palpation, may be enlargement of ovaries. Kidneys: In supine, place one hand under client between ribs and iliac crest, and other hand on abdomen below ribs and pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder Not usually palpable unless it is distended and rises above pubic bone. In supine, place hand above pubis and press down: +/= tenderness, reproduction of pain, or ability to feel the bladder: __+ __−. Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus. Liver: In supine, with left hand under trunk parallel to 11th and 12th rib, lift upward; right hand lateral to rectus and press in and up: +/= reproduction of symptoms with deep breath. Ascites: With the fingers, percuss outward from center; if sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate an enlarged spleen (only palpable if enlarged) because of the potential of rupture. Gallbladder (Murphy’s): Place fingers right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. +++ INTERVENTION ++ PT intervention is consistent with the movement-related problems that occur secondary to diabetes and include Gait training. Therapeutic exercise: All relevant categories, energy conservation. Stretching if contractures present in neck postsurgery. PT should inquire about the medication taken. If glucose >300, exercise should be avoided. Therapeutic activities for bed mobility training, transfer, and transitional movement training. Self-care management training including skin care/moisturizing, lifestyle management. Neuromuscular re-education; balance and postural training. Soft tissue mobilization if contractures present in neck postsurgery. +++ FUNCTIONAL GOALS ++ Patient will be able to Extend and rotate head and neck left/right with adequate functional range in all directions to safely use mirrors while driving (if postsurgery). Achieve adequate functional aerobic capacity, and the ability to talk during activity, in order to achieve functional gait and activity tolerance for work, play, school, and self-care as well as ADLs and IADLs. Functional gait in the home and community (with or without a device), allowing for work, play, and self-care as well as ADLs and IADLs, up to __ feet, based on patient’s need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, and transferring in and out of a car. Tolerate 30 minutes of continuous moderate exercise three times a week in __ weeks, and five times a week in __ weeks, depending on disease severity. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, the physician establishes the medical prognosis. The condition is lifelong unless it is the viral transient type. It can usually be managed with medication. In general, medical prognosis is good unless there is a surgical complication or inappropriate medication management. Hyperthyroidism spontaneously disappears in some cases, but the disease does carry a risk of thyrotoxicosis. If the hyperthyroidism is caused by Graves disease, the prognosis is not as good. Prognosis from a PT perspective: Based on effective medical management, patient is good to return to a healthy level of functioning before onset of disease if individual receives care secondary to the problems related to hyperthyroid. ++ PATIENT RESOURCE American Thyroid Association. http://www.thyroid.org. Accessed July 5, 2013. +++ REFERENCES +1. +APTA. Guide to Physical Therapy Practice. Atlanta, GA: American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org. Accessed July 5, 2013. +2. +Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Thyroid gland. In:Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/content/6588008. Accessed July 5, 2013. +++ ADDITIONAL REFERENCES + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Dutton M. Thyroid disorders. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/56510055. Accessed July 5, 2013.+ +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician. 2005;72(4):623–630. [PubMed: 16127951] + +Watts RL, Standaert D, Obeso JA. Other neurological and systemic diseases. In:Watts RL, Standaert D, Obeso JA Movement Disorders. 3rd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/55801578. Accessed July 5, 2013. + HYPOPARATHYROIDISM Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Acquired Hypoparathyroidism Autoimmune Hypoparathyroidism Congenital Hypoparathyroidism Idiopathic Hypoparathyroidism Familial isolated hypoparathyroidism (FIH) +++ ICD-9-CM CODES ++ 252.1 Hypoparathyroidism Associated ICD-9-CM PT diagnoses/treatment diagnoses that may be directly related 315.4 Developmental coordination disorder 718.45 Contracture of joint, pelvic region and thigh 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy not elsewhere classified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E20.0 Idiopathic hypoparathyroidism E20.1 Pseudohypoparathyroidism E20.8 Other hypoparathyroidism E20.9 Hypoparathyroidism, unspecified E89.2 Postprocedural hypoparathyroidism P71.4 Transitory neonatal hypoparathyroidism +++ PREFERRED PRACTICE PATTERNS1 ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated With Connective Tissue Dysfunction 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated With Localized Inflammation 6B: Impaired Aerobic Capacity/Endurance Associated With Deconditioning ++ PATIENT PRESENTATION A 30-year-old female marathon runner referred to physical therapy with complaints of lower extremity (LE) cramping and tingling in her feet, limiting her ability to compete. She also described feeling short of breath as she struggles to increase distances again. There is no history of injury. In the course of casual conversation, she also complains of her nails breaking more than usual with her manicures not lasting more than a few days. Her boyfriend told her that her “legs were looking skinny” and observation reveals sarcopenia in her calves. The skin on her feet is dry and pealing, but she stated they have a tendency to be dry. She has started a reconditioning program in PT which is not responding well. Although referred by an orthopedist to PT, she is scheduled for an annual physical with her primary doctor in the next few weeks. The PT has suggested discussing her signs and symptoms with her physician and has offered to give her a summary of her PT to be brought to him. ++ FIGURE 28-1 Levels of immunoreactive parathyroid hormone (PTH) detected in patients with primary hyperparathyroidism, hypercalcemia of malignancy, and hypoparathyroidism. Boxed area represents the upper and normal limits of blood calcium and/or immunoreactive PTH. (From SR Nussbaum, JT Potts, Jr, in L DeGroot, JL Jameson, eds. Endocrinology. 4th ed. Philadelphia, PA: Saunders; 2001, with permission.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 28-2 Anatomic relations of the thyroid gland, anterior view. The blue structures are the thyroid gland and the course of the obliterated thyroglossal duct. (From LeBlond RF, DeGowin RL, Brown DD. DeGowin’s Diagnostic Examination. 9th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ KEY FEATURES +++ Description ++ Insufficient hyperparathyroid hormone from four parathyroid glands resulting in low calcium and high phosphorus Muscle cramps Low calcium +++ Essentials of Diagnosis ++ Muscle spasms as severe as tetany Abdominal cramps Low calcium High phosphorus levels Decreased calcium in urine Positive Chvostek sign Positive Trousseau phenomenon +++ General Considerations ++ Can be congenital or acquired2 Can have autoimmune bias2 Diagnosis for more occult problems may take time and require intensive medical diagnostic testing May cause pathology in multiple organ systems GI: Liver Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems indicating the need for PT intervention depending on severity Aerobic capacity and muscle endurance impairment Sarcopenia Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems +++ Demographics ++ Considered rare Lifespan +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Abdominal pain Anxiety Arrhythmias Breathing difficulties secondary to throat spasms Brittle nails Calcium deposits in the brain Depression, mood swings Dry, coarse, scaly skin Fatigue Headaches Heart failure Hyperphosphatemia2 Kidney disease Loss of consciousness, fainting Malformations of teeth Memory problems Muscle aches/pain Muscle cramps in LEs, abdomen, or face Nervousness Painful menstruation Paresthesias in lips Patchy hair loss (e.g., eyebrows) Peripheral paresthesias Seizures Short stature Signs and symptoms of hypocalcemia2 Slow mental development in children Twitching or spasms in muscles and throat Vision impairment, cataracts Weakness +++ Functional Implications ++ Inability or reluctance to leave home secondary to not feeling well or impaired mental status Fatigue Inability to focus Kidney disease Shortness of breath Muscle performance deficits, inability to ambulate or perform self-care, and aerobic capacity limitation secondary to inactivity Decreased exercise tolerance Sleep disturbances Changes in lifestyle Inappropriate self-medication Anxiety and irritability Limitations in ADLs or IADLs Neuropathy, increased risk for falls Low mentation, need for special schooling considerations +++ Possible Contributing Causes ++ Inability to afford testing and medications and noncompliance with medication regiments/inability to pay Damage/trauma to the parathyroid glands Heredity Autoimmune disease Radiation for cancer Low magnesium levels Recent neck surgery Addison disease Removal of the parathyroid glands +++ Differential Diagnosis ++ Autoimmune diseases Bladder infections, urinary tract infections, kidney pathology Bowel disorders Brain tumor Candidiasis Differential diagnosis of hypocalcemia Endocrine disorders Hypermagnesemia Hyperphosphatemia Hyperthyroidism Hyperventilation syndrome Hypocalcemia secondary to other pathology Hypomagnesemia Hypoparathyroidism Infections in the abdomen Malignant tumors in the neck Metabolic alkalosis Non-malignant tumors in neck Organ dysfunction as a result of cancer or malignancy Renal failure +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Complete blood count (CBC) 24-hour urine collection Urinalysis Thyroid function test, T-cell dysfunction2 +++ Imaging ++ Ultrasound X-rays CT scans MRIs Bone mineral density test Other ECG +++ FINDINGS AND INTERPRETATION ++ Hypocalcemia Laboratory findings of hypocalcemia Hypophosphatemia Hypomagnesemia Laboratory findings of magnesium depletion +++ TREATMENT +++ Medication ++ Calcium carbonate Vitamin D Other Low-phosphorus diet Diet rich in calcium ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not considered appropriate for PT, refer to the appropriate physician. If an emergency is identified, refer to an ER. If the patient’s history and reactions to PT indicate possible hyperthyroidism and or symptoms, refer to a physician. +++ IMPAIRMENTS ++ Muscle weakness Muscle spasm Gait abnormality/difficulty walking Shortness of breath, fatigue Limited aerobic capacity Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries. Pink or purplish striae may be indicative of Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundedness, concavity/hollowness, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around umbilicus, which may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, which is a sign of hemorrhagic pancreatitis. Bulging in groin or other areas of abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in the area of the navel may be abdominal aortic aneurysm. Palpable abdominal tenderness: On left/right or generalized. Psoas sign: Provides resistance over patient’s right knee as they flex the hip. Pain is indicative of appendicitis or possible inflammation of the abdomen. Obturator sign: Internal rotation of right LE and flexion may be indicative of appendicitis or pelvic inflammation. Rovsing sign: Pain on the right side of abdomen when pressure is put on the left may be indicative of appendicitis. Because there may be GI signs associated with hypoparathyroidism, the tests and measures listed here are included. Palpation of thyroid/neck For enlargement of thyroid or any abnormalities Skin changes Vital signs Chvostek sign: Tap on the face at a point just anterior to the ear and just below the zygomatic bone. Positive response in hypoparathyroidism: Twitching of the ipsilateral facial muscles suggestive of neuromuscular excitability caused by hypocalcemia. Trousseau sign: Inflate a sphygmomanometer cuff above systolic blood pressure for several minutes. Positive response in hypoparathyroidism: Muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggestive of neuromuscular excitability. Abdominal palpation, may be enlargement of ovaries. Kidneys: In supine, place one hand under client between ribs and iliac crest, and other hand on abdomen below ribs and pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder Not usually palpable unless it is distended and rises above pubic bone. In supine, place hand above pubis and press down: +/= tenderness, reproduction of pain, or ability to feel the bladder: __ + __ −. Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus. Liver: In supine, with left hand under trunk parallel to 11th and 12th rib, lift upward; right hand lateral to rectus and press in and up: +/= reproduction of symptoms with deep breath. Ascites: With the fingers, percuss outward from center, if sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate an enlarged spleen (only palpable if enlarged) because of the potential of rupture. Gallbladder (Murphy’s): Place fingers to the right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. +++ INTERVENTION ++ PT intervention is consistent with the movement-related problems that occur secondary to hypoparathyroidism and include Gait training Therapeutic exercise: All relevant categories, energy conservation Stretching if contractures present in neck postsurgery Therapeutic activities for bed mobility, transfer-, and transitional-movement training Self-care management training including skin care/moisturizing, lifestyle management Neuromuscular re-education: Balance and postural training Soft tissue mobilization if contractures present in neck postsurgery +++ FUNCTIONAL GOALS ++ Patient will be able to Extend and rotate head and neck left and right with adequate functional range in all directions to safely use mirrors while driving (if postsurgical). Achieve adequate functional aerobic capacity and the ability to talk during activity in order to achieve functional gait and activity tolerance for work, play, school, self-care; ADLs, and IADLs. Achieve functional gait in the home and community (with or without a device), allowing for work, play, self-care; ADLs, and IADLs, up to _____ feet based on patient’s need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, and transferring in and out of a car. Tolerate 30 minutes of continuous moderate exercise three times a week in _____ weeks, and five times a week in _____ weeks, depending on disease severity. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, the physician establishes the medical prognosis. It can usually be kept under control, although changes in dentition, cataracts, and calcium deposits in the brain are not reversible. Prognosis from a PT perspective, based on effective medical management, to return to prior level of function is good if individual is receiving care secondary to the problems related to hypoparathyroidism. ++ PATIENT RESOURCES American Thyroid Association. http://www.thyroid.org. Accessed August 8, 2014. The National Academy of Hypothyroidism. http://nahypothyroidism.org. Accessed August 8, 2014. +++ REFERENCES +1. +APTA. Guide to Physical Therapy Practice. Alexandria, VA: American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org. Accessed July 2, 2013. +2. +Dutton M. Thyroid disorders. In:Dutton M McGraw-Hill’s NPTE (National Physical Therapy Examination). 2nd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/56510055. Accessed July 2, 2013. +++ ADDITIONAL REFERENCES + +American Academy of Pediatrics, et al. Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics. 2006;117:2290–2303. doi: 10.1542/peds.2006-0915. [PubMed: 16740880] CrossRef + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Colcher A, Hurtig HI. Systemic illnesses that cause movement Disorders. In:Watts RL, Standaert DG, Obeso JA Movement Disorders. 3rd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/55806123. Accessed July 2, 2013.+ +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/resource/14. Accessed July 2, 2013.+ +LaFranchi SH, Austin J. How should we be treating children with congenital hypothyroidism? J Pediatr Endocrinol Metab. 2007;20(5):559–578. [PubMed: 17642417] CrossRef + +Ng SM, Anand D, Weindling AM. High versus low dose of initial thyroid hormone replacement for congenital hypothyroidism. Cochrane Database Syst Rev. 2009;21:CD006972. doi: 10.1002/14651858.CD006972.pub2.+ +Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ. Growth, thyroid, and gonadal pharmacology. In:Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ Pharmacology for the Physical Therapist. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6093102. Accessed July 2, 2013.+ +Powers J, Joy K, Ruscio A, Lagast H. Prevalence and incidence of hypoparathyroidism in the USA using a large claims database. J Bone Miner Res. 2013;28:2570–2576. doi: 10.1002/jbmr.2004. [PubMed: 23737456] CrossRef + +Rovet JF. Children with congenital hypothyroidism and their siblings: do they really differ? Pediatrics. 2005;115:e52–e57. doi: 10.1542/peds.2004-149. [PubMed: 15629966] + +Shoback DM, Sellmeyer DE. Disorders of the parathyroids & calcium & phosphorus metabolism. In:McPhee SJ, Hammer GD Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5370820. Accessed July 2, 2013. + HYPOTHYROIDISM Download Section PDF Listen Debra F. Stern, DPT, DBA, MSM, PT, Eric Shamus, PhD, DPT, PT, CSCS ++ +++ CONDITION/DISORDER SYNONYMS ++ Hypothyreosis Underactive thyroid +++ ICD-9-CM CODES ++ 244 Acquired hypothyroidism 244.0 Postsurgical hypothyroidism 244.1 Other postablative hypothyroidism 244.2 Iodine hypothyroidism 244.3 Other iatrogenic hypothyroidism 244.8 Other specified acquired hypothyroidism 244.9 Unspecified acquired hypothyroidism Associated ICD-9-CM PT diagnoses/treatment diagnoses that may be directly related 315.4 Developmental coordination disorder 718.45 Contracture of joint, pelvic region and thigh 719.70 Difficulty in walking involving joint site unspecified 728.2 Muscular wasting and disuse atrophy not elsewhere classified 728.89 Other disorders of muscle, ligament, and fascia 729.9 Other and unspecified disorders of soft tissue 780.7 Malaise and fatigue 781.2 Abnormality of gait 782.3 Edema 786.0 Dyspnea and respiratory abnormalities 786.05 Shortness of breath +++ ICD-10-CM CODES ++ E03.9 Hypothyroidism, unspecified E89.0 Postprocedural hypothyroidism +++ PREFERRED PRACTICE PATTERNS1 ++ 4D: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction 4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation 6B: Impaired Aerobic Capacity/Endurance Associated with Deconditioning ++ PATIENT PRESENTATION A 65-year-old female presents to the clinic feeling tired and fatigued all the time. She has also noticed an increasing problem of constipation despite adequate fiber intake. She is frequently cold when others are hot. Her skin has become dry, and she has noticed a swelling sensation in her neck area. On examination she is afebrile with a pulse of 60 beats per minute. She is in no acute distress and appears in good health. She has an enlarged, nontender thyroid noted on her neck. Her reflexes are diminished, and her skin is dry to the touch.2 +++ KEY FEATURES +++ Description ++ A deficiency of thyroid gland activity Characterized by decreased basal metabolic rate, fatigue and lethargy, sensitivity to cold, and menstrual disturbances In infants, severe hypothyroidism leads to cretinism Thyroid regulates metabolism and produces three types of thyroid hormone3 ++ FIGURE 29-1 Hypothyroidism: diagnostic approach. FT4, free thyroxine; TPOAb+, thyroid peroxidase antibodies positive; TPOAb–, thyroid peroxidase antibodies negative; TSH, thyroid-stimulating hormone. (From Nicoll D, Lu CM, Pignone M, Mcphee SJ. Pocket Guide to Diagnostic Tests. 6th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Essentials of Diagnosis ++ Gradual onset Palpation of thyroid/neck for enlargement of thyroid or any abnormalities Thyroid function test Three types of hypothyroidism Primary: Thyroid gland dysfunction Secondary: Pituitary gland dysfunction Tertiary: Hypothalamus dysfunction +++ General Considerations ++ Can progress to myxedema if untreated Thyroid needs iodine as a critical element3 May cause pathology in multiple organ systems GI: Liver Cardiovascular: Heart, peripheral circulation, blood pressure Integumentary May result in secondary problems indicating the need for PT intervention depending on severity Aerobic capacity and muscle endurance impairment Sarcopenia Weakness/impaired muscle performance Musculoskeletal problems Neuromuscular problems Weight gain, indicating the need for PT intervention depending on severity Hyperlipidemia +++ Demographics ++ Affects individuals throughout the lifespan, starting at birth (1 in 4000 infants) Estimated five million in the United States and possibly double that are undiagnosed Higher incidence in women Higher incidence in those older than age 60 +++ CLINICAL FINDINGS ++ SIGNS AND SYMPTOMS Cold sensitivity Fatigue Weight gain Slowed heart rate Constipation Joint pain Muscle pain Muscle cramps Paleness Dry skin Hair thinning, including eyebrows Brittleness of fingernails Weakness Unexplained weight gain with inability to lose it Depression Heavier menstrual periods Decreased ability to smell Decreased taste Puffiness of hands, feet, and face Peripheral neuropathy/numbness Slowness of speech Thickening of skin Liver dysfunction Heart disease Worsening of angina if history of angina Anemia In severe cases Below normal body temperature Depressed breathing Low blood pressure Low blood sugar Unresponsiveness ++ FIGURE 29-2 Clinical features of hypothyroidism. The patient shows a lack of facial expression, together with pallor, dry skin, loss of hair in the lateral eyebrows, facial puffiness, broadening of the nose, and drooping eyelids. (From Wolff K, Goldsmith LA, Katz, Gilchrest BA, Paller A, Leffel DJ. Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York, NY: McGraw-Hill; 2007.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Functional Implications ++ Severe symptoms such as immediacy of need to urinate may be disabling, resulting in the inability to leave home Fatigue Infertility Miscarriage Heart disease Decreased sex drive Increasing weight with inability to exercise or move well Sarcopenia resulting in Weakness Muscle-mass loss Inability to ambulate or perform self-care Aerobic capacity limitation secondary to inactivity Decreased exercise tolerance Sleep disturbances Changes in lifestyle Eating disorders Inappropriate self-medication Anxiety and depression Can lead to problems with liver Limitations in ADLs or IADLs Infection (systemic) Skin lesions from dryness Neuropathy, increased risk for falls Vision impairment, most often retinal Prone to infections such as bacterial or fungal in the skin, urinary tract (UT), kidney Potential for liver problems Difficulty in thinking clearly +++ Possible Contributing Causes ++ Acquired (juvenile hypothyroidism) causes Autoimmune or Hashimoto thyroiditis Cancer Chemical inducement Congenital birth defects Congenital causes Drugs: Amiodarone, drugs used for hyperthyroidism, lithium Female Goiters Older than age 50 Inflammation of the thyroid Iodine deficiency Low iodine Metastatic cancer Pituitary dysfunction as the pituitary signals production of thyroid stimulating hormone (TSH) Pregnancy Radiation to the brain Radiation treatments to the neck Radioactive iodine to treat hyperthyroidism Surgical removal of part or all of the thyroid gland to treat other thyroid problems Viral thyroiditis +++ Differential Diagnosis ++ Autoimmune diseases that affect the upper and lower GI tracts Bladder infections, UTIs, kidney pathology Bowel disorders Cardiac disorders Crohn or irritable bowel syndrome Endocrine disorders, diabetes Gastroparesis Gynecologic problems in females Infections in the abdomen Non-malignant tumors in the abdomen or organs Organ dysfunction as the result of cancer or malignancy, especially the liver Pituitary dysfunction +++ MEANS OF CONFIRMATION OR DIAGNOSIS +++ Laboratory Tests ++ Complete blood count (CBC) Thyroid function: TSH, T3, T43 Cholesterol Liver enzymes Prolactin Sodium levels +++ Imaging ++ Ultrasound Chest X-ray CT scans MRIs +++ FINDINGS AND INTERPRETATION ++ Prolactin (may be elevated in women and men) Sodium levels, low in hypothyroidism The normal range: 135 to 145 milliequivalents per liter (mEq/L) ++ FIGURE 29-3 Some of the major signs of hypothyroidism. (From Murray RK, Bender DA, Botham KM, Kennelly PJ, Rodwell V, Weil PA. Harper’s Illustrated Biochemistry. 29th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TREATMENT +++ Medication ++ Thyroid hormone replacement therapy, most commonly levothyroxine, lifelong, with levels checked at least annually Bone density monitoring is required on levothyroxine ++ FIGURE 29-4 Diagnosis of hypothyroidism. (From Gardner DG, Shoback D. Greenspan’s Basic & Clinical Endocrinology. 9th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ REFERRALS/ADMITTANCE If a patient is referred for PT and the causative problem is not considered appropriate for PT, refer to the appropriate physician. If an emergency is identified, refer to an ER. If the patient’s history and reactions to PT indicate possible hypothyroidism and/or symptoms, refer to a physician. +++ IMPAIRMENTS ++ Muscle weakness/cramps Muscle atrophy Gait abnormality/difficulty walking Shortness of breath, fatigue Inability to perform self-care Balance impairment Impaired skin integrity +++ TESTS AND MEASURES ++ Observation Scars may indicate adhesions or abdominal surgeries causative of diverticula. Pink or purplish striae may indicate Cushing syndrome. Dilated veins may indicate hepatic pathology or inferior vena cava obstruction, not diverticulitis. Contour: Roundness, concavity, asymmetry, distension, pregnancy signs. Cullen sign: Bluish discoloring around the umbilicus may be a sign of retroperitoneal bleeding. Bluish discoloration in lower abdomen: Grey Turner sign, signals hemorrhagic pancreatitis. Bulging in groin/abdomen especially apparent with contraction of musculature in area may be hernia. Pulsing in navel area may be abdominal aortic aneurysm. Left lower quadrant pain, often following a meal. Palpable abdominal tenderness on left side or generalized. Psoas sign: Provides resistance over patient’s right knee as they flex the hip. Pain indicates appendicitis, possible inflammation of abdomen. Obturator sign: Internal rotation and flexion of right lower extremity (LE) may indicate appendicitis, pelvic inflammation. Rovsing sign: Pain on the right side of abdomen when pressure applied to the left may indicate appendicitis. The following list of tests and measures are included for a variety of pathology from a differential diagnosis perspective. Palpation of thyroid/neck For enlargement of thyroid or any abnormalities. Skin changes: Turgor, dryness, hairlessness. Kidneys: In supine, place one hand under client between ribs and iliac crest and other hand on abdomen below ribs and pointing in opposite direction: +/− tenderness or reproduction of symptoms. Bladder Not usually palpable unless it is distended and rises above pubic bone. In supine, place hand above pubis and press down: +/= tenderness, reproduction of pain, or ability to feel the bladder: __ + __ −. Appendix (McBurney’s): Apply vertical pressure halfway between right anterior superior iliac spine (ASIS) and umbilicus. Liver: In supine, with left hand under trunk parallel to 11th and 12th rib, lift upward; right hand lateral to rectus and press in and up: +/= reproduction of symptoms with deep breath. Ascites: With the fingers, percuss outward from center, if sound is dull, ascites may be present. Spleen: It is not recommended for PT to palpate an enlarged spleen (only palpable if enlarged) because of the potential of rupture. Gallbladder (Murphy’s): Place fingers to the right of rectus abdominus below rib cage: +/= sudden pain and muscle tensing with deep breath. ++ FIGURE 29-5 Thyroid histology. The appearance of the gland when it is inactive (left) and actively secreting (right) is shown. Note the small, punched-out “reabsorption lacunae” in the colloid next to the cells in the active gland. (From Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ INTERVENTION ++ PT intervention is consistent with the movement-related problems that occur secondary to diabetes and include Gait training Therapeutic exercise: All relevant categories, energy conservation If there is an insulin pump, take care not to interfere with it in any way. PT should inquire about medication taken; if glucose >300, exercise should be avoided. Monitoring heart rate. Cardiac monitoring with possible metabolic equivalent (MET) calculation if history of angina. Therapeutic activities for bed-mobility training, transfer-, and transitional-movement training. Self-care management training including skin care/moisturizing, lifestyle management. Neuromuscular re-education: Balance and postural training. Wound management. +++ FUNCTIONAL GOALS ++ Patient will be able to Achieve adequate functional aerobic capacity and the ability to talk during activity in order to achieve functional gait and activity tolerance for work, play, school, self-care, ADLs, and IADLs. Achieve functional gait in the home and community (with or without a device), allowing for work, play, self-care, ADLs, and IADLs, up to _____ feet based on patient’s need and prior functional level. Achieve 600 m or greater in a 6-minute walk test for initiation of safe functional gait in the community. Perform active verbalization with increasing taxonomy for safety during gait, including negotiation of even and uneven surfaces, opening and closing doors, and transferring in and out of a car. Tolerate 30 minutes of continuous moderate exercise three times a week in _____ weeks, and five times a week in _____ weeks, depending on disease severity. +++ PROGNOSIS ++ As this pathology is primarily medical in nature, the physician establishes the medical prognosis. The condition is lifelong, unless it is the viral transient type. It can usually be managed with medication. If thyroid hormones are too low, myxedema coma can result with ensuing death. +++ ADDITIONAL INFORMATION ++ See problem-oriented patient study on AccessPhysiotherapy.com for more information. ++ PATIENT RESOURCES American Thyroid Association. http://www.thyroid.org. Accessed August 8, 2014. The National Academy of Hypothyroidism. http://nahypothyroidism.org. Accessed August 8, 2014. +++ REFERENCES +1. +The American Physical Therapy Association. Interactive Guide to Physical Therapist Practice. Alexandria, VA: The American Physical Therapy Association; 2003. http://guidetoptpractice.apta.org/. Accessed July 5, 2013. +2. +Toy EC. Hypothyroidism, Case 48. LANGE Case Files. http://www.accessmedicine.com/casecontent.aspx?aid=8651335&tabid=1. Accessed July 3, 2013. +3. +McPhee SJ, Hammer GD. Formation & secretion of thyroid hormones. In:McPhee SJ, Hammer GD Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill; 2010. http://www.accessphysiotherapy.com/content/5371509. Accessed July 5, 2013. +++ ADDITIONAL REFERENCES + +American Academy of Pediatrics, et al. Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics. 2006;117:2290–2303. doi: 10.1542/peds.2006–0915. [PubMed: 16740880] CrossRef + +Baskin HJ, Cobin RH, Duick DS et al.. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457–469. [PubMed: 15260011] + +Colcher A, Hurtig HI. Systemic illnesses that cause movement disorders. In:Watts RL, Standaert DG, Obeso JA Movement Disorders. 3rd ed. New York, NY: McGraw-Hill; 2012. http://www.accessphysiotherapy.com/content/55806123. Accessed July 5, 2013.+ +Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2009.+ +Goodman CC, Snyder TK. Differential Diagnosis for Physical Therapists: Screening for Referral. 4th ed. St. Louis, MO: Saunders Elsevier; 2007.+ +Hay WW, Levin MJ, Sondheimer JM, Deterding RR CURRENT Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011. http://www.accessphysiotherapy.com/resource/14. Accessed March 5, 2013.+ +LaFranchi SH, Austin J. How should we be treating children with congenital hypothyroidism? J Pediatr Endocrinol Metab. 2007;20(5):559–578. [PubMed: 17642417] CrossRef + +Ng SM, Anand D, Weindling AM. High versus low dose of initial thyroid hormone replacement for congenital hypothyroidism. Cochrane Database Syst Rev. 2009;21:CD006972. doi: 10.1002/14651858.CD006972.pub2.+ +Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ. Growth, thyroid, and gonadal pharmacology. In:Panus PC, Jobst EE, Masters SB, Katzung B, Tinsley SL, Trevor AJ Pharmacology for the Physical Therapist. New York, NY: McGraw-Hill; 2009. http://www.accessphysiotherapy.com/content/6093102. Accessed July 5, 2013.+ +Rovet JF. Children with congenital hypothyroidism and their siblings: do they really differ? Pediatrics. 2005;115:e52–e57. doi: 10.1542/peds.2004–149. [PubMed: 15629966]