Tuesday, August 18, 2015

Endocrinology and OT!


As promised, here is my next write up - this time, we explore OT's role in endocrinology in order to raise knowledge and awareness in many of the common denominators our patients may share on a metabolic level. I hope you guys get something out of this! It's a lot (I've been typing away at this for the past four hours) to take in, so just take it in small doses! :)

-Dan
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Endocrine and metabolic screening and function: why does it matter to an (outpatient) OT?


Boring stuff first:
Endocrinology is the study of ductless glands that produce hormones, in short. A hormone is a chemical agent that travels via bloodstream to its target tissue, where it either regulates or modifies the activity of the tissue. It is well tied to the neuromusculoskeletal system in function, and is the basis of how we regulate metabolism, electrolyte balance, blood pressure, stress responses, and sexual reproduction. In short, the endocrine system is the office manager of our body.


Briefly, the structures we should be aware of are:
  • Hypothalamus: the master control for the pituitary gland atop the brain stem, secretes the critical neurohormones into the bloodstream directly, such as acetylcholine.
  • Pituitary gland: in charge of secreting hormones for growth, development, and regulation of other glands; at the base of the brain.
  • Thyroid gland: Just like the pituitary gland, it secretes hormones for growth, development, and maintenance of tissue.
  • Adrenal glands: in charge of secretion of epinephrine, norepinephrine, and cortisol, atop the kidneys.
  • Pancreas: in charge of secretion of insulin and glucagon for blood sugar regulation, superior to the liver.
  • Ovaries and testicles: development of sexual gametes and sex hormones internal and external to be pubic cavity respectively.
When you take a peek in a chart or evaluate your patient for the first time, you might see some of these common terms in the past medical history:
  • Hypothyroidism: A depression of thyroid function, creating a similar depression in body metabolism. More common than hyperthyroid. Look for loss of hair, puffy face, cold intolerance, muscle weakness (sarcopenia) and edema.
  • Hyperthyroidism (Grave’s disease; thyrotoxicosis): disorders where the thyroid gland secretes excessive amounts of thyroid hormone. Look for bulging eyes, enlarged thyroid, thin hair tachycardia, mineral deposits and heat intolerance.
  • Hypoparathyroidism: Insufficient secretion of parathyroid hormone, resulting in hypercalcemia, hyperphosphatemia, and serious cardiac instability - look out for muscle spasms/weakness, paresthesias, mineral deposits, tetany and very real and very deadly cardiac arrhythmias.
  • Hyperparathyroidism: Excessive secretion of parathyroid hormone, resulting in demineralization of bone with losses in bone strength and density. Common in those taking lithium for bipolar disorder and those who are postmenapausal. Look for muscle weakness, weight loss, nausea/vomitting, depression, and increased thirst/urination, and sometimes psychotic paranoia.
  • Diabetes Mellitus (I/II): A chronic disorder caused by deficient or eliminated secretion of insulin (or defects in the action of insulin) to manage glucose in the blood - it is the most common cause of end-stage renal disease, lower extremity amputations, blindness, and a major contributor for heart disease and strokes, and may even be share a relationship with dementia and complex regional pain syndrome (CRPS). Look for fatigue and weakness, blurred vision, irritability, recurring infections, numbness and tingling in the hands and feet, and cuts/bruises that stick around.
  • Osteoporosis: Meaning “porous bone”, it is a disorder of bone demineralization that can occur with any of the above conditions (secondary osteoporosis) or just by itself (primary osteoporosis). Look out for back pain, compression fractures of the spine, bone fractures, kyphosis, Dowager’s hump, decreased activity tolerance, and early satiety.
And then some less common terms:
  • Acromegaly: A hyper-pituitary gland disorder resulting in abnormal enlargement of the extremities, face, and jaw, generally from a tumor on the pituitary. Look for deformities of the aforementioned structures, profuse sweating, poor exercise tolerance, diabetes II, and joint pain. A picture for the visually inclined:
  • Adrenal insufficiency (Addison’s Disease): A disorder within the adrenal gland with a decreased production of cortisol and aldosterone, or by understimulation of the adrenal glands by the hypothalamus. Look for dark pigmentation of the skin, hypotension, fatigue, generalized muscle weakness, GI disturbances, anorexia, muscle/joint pain, and tendon calcification.   
  • Cushing’s Syndrome: hyperfunction of the adrenal glands leading to increased production of cortisol, often from long term corticosteroid use. Look for moonface, protuberant abdomen, generalized muscle weakness, osteoporosis, hypertension, psychosocial disorders, diabetes II and slow wound healing. A picture should clarify “moonface”:
  • Goiter: Enlargement of the thyroid; look for dysphagia, increased neck size, difficulty breathing, hoarseness and self feeding deficits. Call up the speech therapist while you’re at it.
  • Gout: Accumulations of uric acid crystals in joints due to errors in purine metabolism. Look for tophi (little lumps under the skin, which may erupt through the skin as chalky crystals), joint pain and swelling, fever and malaise.
  • Psuedogout (chondrocalcinosis): Much like gout, but instead of uric acid, think calcium salts in the cartilage, especially in the knee. The symptoms are relatively the same as gout.
  • Osteomalacia: A softening of the bones precipitated by vitamin D deficiency, impairing bone mineralization, sometimes due to increased vitamin D catabolsim by the endocrine system. Look out for intense bone pain of the spine, pelvis, and lower extremities, fractures, skeletal deformities, severe muscle pain and weakness.


With all of the dry stuff out of the way, lets talk about why this information matters:


As mentioned before, the endocrine system can influence nueromusculoskeletal systems in numerous ways. Some of the most common (and confounding) disorders and symptomatology are as a result of dysregulation of this system:


  • Muscle weakness, myalgia, and fatigue
    • Often, these symptoms are as a result of all of the aforementioned disorders, especially thyroid/parathyroid disease and diabetes II for proximal muscle weaknesses.
    • Diffuse muscle pain and fibromyalgia symptomatology are often related to thyroid dysfunction as well.
    • In the event that proximal muscle weakness or pain does not improve with therapy, consult MD for further endocrine follow up, especially if your patient is diabetic.
  • Bilateral Carpal Tunnel Syndrome (CTS)
    • You’ll see this often in outpatient settings - patients with inexplicable and long standing cases of bilateral UE carpal tunnel syndrome without the occupational history to match it. What gives?
    • There is a high incidence of carpal tunnel for endocrine conditions, especially menopause, post-thyroidectomy, hyperparathyroidism, diabetes II, acromegaly, gout, hypothyroidism and hypercalcemia.
    • If you see bilateral carpal tunnel in clinical practice, assume it's a red flag and get further clarification from an MD before continuing. Your patient may need to be endocrinologically stabilized before therapy will work. There is nearly 40 DIFFERENT CONDITIONS that may cause CTS!
    • As an aside, the role of repetitive activities and occupational factors have been questioned pretty extensively as a direct cause of CTS and remains under further investigation - sufficient evidence to even implicate occupational factors in CTS is still empirically unsubstantiated. Always get a good medical history for CTS patients, every single time.
  • Calcific tendinitis and periarthritis
    • Periarthritis is the fancy term for inflammation of periarticular structures, including tendons, ligaments, and joint capsules.
    • Calcific tendonitis is a brand of tendonitis that develops due to deposits of calcium inside of tendon tissue, most often the supraspinatus tendon (hint: get a script for acetic acid and find an iontophoresis machine).
    • Both of these conditions are often caused by endocrine disorders, especially diabetes II, hypoparathyroidism, and hyperthyroidism. Consult your MD before moving forward - if not properly controlled, treatment may generally only have a temporary palliative effect before invariably relapsing.
  • Hand stiffness
    • Hand stiffness and pain, alongside arthralgias of the hand, can often be caused by hypothyroidism, especially if there is presence of flexor tenosynovitis (pain on power grasp, pincer, oppositional movements).
  • Adhesive Capsulitis (Frozen Shoulder)
    • The dreaded frozen shoulder is a great lesson in compensatory strategies and joint mobilization for any OT. The mechanism for frozen shoulder is not perfectly understood, but it appears to go as such:
      • The posterior capsule (the infraspinatus tendon and teres minor tendon join into a ligamentous-synovial structure at the posterior humeral head) folds inward like an accordion when not in use - little sticky adhesions develop in those folds and prevent the capsule from opening, liming humeral excursion and external rotation of the humeral head.  
      • These adhesions are very incidental with patients with diabetes II - be absolutely sure your patient is controlling their DMII, and don’t be afraid to bring the MD into this as frozen shoulder is easily one of the most severe shoulder conditions orthopaedically, occupationally, and especially psychosocially.
  • Osteoarthritis (and spondyloarthropathy): Inflammation of synovial joint structures (with the latter term specifically referencing spinal joints) is infinitely more common with any individual with hypo and hyperthyroid conditions, with prognosis of treatment heavily dependent on how well medically controlled the arthritis is.. Look for joint inflammation, pain, and decreased activity tolerance.
  • Thyroid Cancer: Thyroid cancer is a slow, lumbering cancer that rarely metastasis; it is more often than not caught unintentionally during examination of the head and neck by therapists and doctors. As OTs, it is critical (especially if you work on the neck very often like myself) that we know what to look for. If you see a nodule on the anterior-medial neck that is irregular, firm, and painless with dyspena, high blood pressure, hoarseness, and sometimes hemoptysis (coughing up blood), refer the patient back to their MD ASAP.
  • Dupuytren's Contracture: A hyperfibrotic growth that joints the flexor digitorum tendon to the palmar fascia, most commonly on the ring finger. It is considerably more likely to develop on those with diabetes II and is a very limiting condition of the hand that may require surgery if chronic (hint: use ionto/phonophresis with typsin/alpha chymotrypsin/hyaluronidase solution coupled with 2.5%lidocaine and yank that bad boy open). Look for poor power grasp, fibrotic grown of the palmar fascia, and flexor contracture of a single digit:


Back to Diabetes - our role as therapists in diabetes management:
  • Our role in educating and enabling our patients to better manage their diabetes cannot be understated. Diabetes is a lifestyle.
  • Our roles in diabetes screening include:
    • Period screenings of diabetic neuropathy via deep tendon reflexes, vibratory and proprioception, sensation testing.
    • Education in hygiene and fingernail/foot care.
    • Monitor blood glucose levels in association with therapeutic activities and exercise.
    • Screen for other neuromusculoskeletal conditions such as carpal tunnel syndrome, complex regional pain syndrome, Dupuytren contracture, frozen shoulder, flexor tenosynovitis, etc.)
    • Monitor blood pressure.
    • Preform occasional upper and lower extremity vascular screens as needed.
    • Screen for alcohol use and depression.
    • Educate your patient on the importance of regular A1C level checks by their MD.
    • Vision screening and encouraging regular eye exams.
    • Educate your patients to carry a source of sugar with them at all times in case of emergency during ADL.
    • Educate and plan with your patients on effective insulin and medication schedules.
    • Educate your patient on safe self testing of glucose if patient is demonstrates cognitive capacity.
    • Alert nursing staff or a physician immediately if there are any changes in mental status with a diabetic patient (especially after therapeutic exercise), and educate patients on personal safety techniques for ensuring medical attention in worst case scenarios.


Questions to ask if in suspicion of endocrine/metabolic disorders
  • Have you ever had any head or neck radiation, or cranial surgery? (Thyroid Cancer, Pituitary Dysfunction)
  • Have you ever had a traumatic brain injury/head injury? (Pituitary Dysfunction)
  • Have you ever been told by your doctor that you have brittle bones, back problems, or osteoporosis? (Cushing’s Syndrome, Osteoporosis)
  • Have you noted any dramatic changes in your muscle strength lately? (Hyper and hypothyroidism)
  • Any changes in your vision lately, including peripheral vision, night vision, or light sensitivity? (Diabetes II, Hyperthyroidism)
  • Have you had an increase in your thirst lately, or have you been urinating more than usual lately? (Diabetes II, Adrenal Insufficiency)
  • Any dramatic increases in appetite lately? (Diabetes II, Hyperthyroidism)
  • Do you bruise easily? (Cushing’s Syndrome)
  • Do you find that your cuts and bruises heal very slowly? (Cushing’s Syndrome, Diabetes II)
  • Do you find yourself more fatigued than usual? If so, what activities are more difficult for you lately? (Cushing’s Syndrome, Adrenal Insufficency, Hypothyroidism)
  • Have you noticed any increases in your collar size, difficulty breathing, changes in your voice, or swallowing problems during self feeding? (Goiter, Hyperthyroidism)
  • Have you noted any changes in your skin color lately, perhaps during bathing or changing your clothes? (Adrenal Insufficiency)


Sources:
Goodman, C.C., Fuller, K.S. (2009). Pathology: implications for the physical therapist (3rd eds.). Philadelphia, PA: Saunders.
Goodman, C. C., Snyder, T. K. (2013). Differential Diagnosis for Physical Therapists: Screening for Referral (5th eds.). Philadelphia, PA: Saunders.
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Next is a toss up between cardiovascular (probably my weakest subject viscerally), gastrointestinal, or musculoskeletal (oh god you thought this endocrinology one was long, just wait).

Neurological Evaluation.

Hey guys! This is Dan - I'm in the process of doing a little bit of compiling of information into protocols/guidelines to better my skillset (and to study up a little for my pain management fellowship testing via the American Academy of Pain Management). I am going to be churning stuff out in fairly rapid succession, so I wanted to share some of my protocols, guidelines, and information with you guys to help on your travels. I'm starting with Neurological Evaluation guidelines for treatment of neuromusculoskeletal conditions - hopefully, you guys get something from it! Many of you guys may find the last part on peripheral nerve injuries particularly useful, I hope!

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Neurological exam outline


The function of the neurological system to coordinate both voluntary and involuntary actions of the human body; this is performed by nervous transmission of signals to and from different parts of the body via nervous tissue and structures. There are two main parts:
  • The Central Nervous system (brain, spinal cord)
  • The Peripheral Nervous system (nerves)


Let’s skip ahead to screening:


RED FLAGS:
  • Sudden and severe headaches with or without head injury.
  • Dizziness/vertigo, nausea and or vomiting.
  • Seizures or tremors.
  • Numbness and tingling without reproducible onset.
  • Difficulty swallowing or speaking.
  • Notable past histories of previous neuropathic disorders.
  • Nystagmus (intentional tremor of the eye)
  • Loss of consciousness.


General tips during the neuro-exam:
  • Explain the tests to your patient. Many of these tests are dependent on command following (such as eyes closed, appropriate responses to give, etc.)
  • Neuro exams are often subjective and can be difficult to interpret.
  • Specifically map out the areas in which the sensory changes are found.
  • Always compare bilateral sides, and distally to proximally.


Mental status:
  • Alertness and orientation.
  • History from family and friends if patient is unreliable or invalid.
  • Memory and concentration: Name the president; three word recall; subtract 7 from 100 five times.


Cranial nerve screening:
  • Smell (I Olfactory)
  • Cardinal fields of gaze (III Occulomotor; IV Trochlear, VI Abducens)
  • Accomodation (III Occulomotor)
  • Peripheral vision (II Optic)
  • Facial Expressions such as smile and frown (VII Facial)
  • Stick out tongue (XII Hypoglossal)
  • Trap/SCM testing (XI Spinal accessory)
  • Consensual light reflex (II Optic, III Occulomotor)
  • Take a peek in the mouth to examine oral mucosa.
  • Say Ahhh test (IX Glossopharyngeal, X Vagus)
  • Bite down on tongue depressor (V Trigeminal)
  • Ophthalmoscopic exam (II Optic)
  • Otoscopic and rhinoscopic exam


Cerebellum screening (RADAR):
  • Rapid alternating movements (hand, finger or foot tapping; rapid supination/pronation)
  • Accessory Movements (intentional tremors or nystagmus [tremor of the eye])
  • Dysmetria (past pointing such as finger to nose, finger to finger)
  • Ataxia (Gait heel to toe, or walking in a circle)
  • Rebound phenomenon (Holme’s sign, elbow flexion MMT in supine causes person to hit themselves upon release)


Spinal cord and nerve screening
Sensory screening (posterior columns):
  • Light touch (fasiculis gracilis (arms); cuneatus (legs))
  • Vibration (128hz C tuning fork)
  • Stereognosis (ID an object with touch only)
  • Graphesthesia (ID a word or number written on skin)
  • Proprioception (Dorsospinocerebellar tract)
Lateral columns (spinothalamic tract)
  • Pain (sharp/dull)
  • Temperature (hot/cold)


Motor testing (myotomes; corticospinal tract)
  • Suboccipital flexors (C1, C2 nerve root)
  • Cervical lateral flexors (C3 nerve root)
  • Shoulder elevators (UT, LS) (C4 spinal nerve root)
  • Deltoid (C5-6 axillary nerve)
  • Brachioradialis (C5-6 radial nerve)
  • Biceps (C5-6 musculocutaneous)
  • Triceps (C6-7-8-T1 radial nerve)
  • Wrist extensors (ECRL/B+ECU C6-7-8 radial nerve)
  • Wrist flexors (FCU, FCR C6-7 median and ulnar nerve)
  • Digit flexors (Flexor digitorums, C7-8, T1 median and ulnar)
  • Innerossei (C7, C8, T1 ulnar nerve)
  • Tibialis anterior (L4-5 deep peroneal nerve)
  • Extensor hallicus longus (L4-5, S1 deep peroneal nerve)
  • Peroneus longus (L5-S1, superficial peroneal)


Reflexes
Note; HYPOreflexia is often from peripheral neuropathy or radiculopathy at LMN level; HYPERreflexia is indicative of UMN level pathology.
  • Deep tendon reflexes (DTR):
    • Biceps (C5-6)
    • Brachioradialis (C5-6)
    • Triceps (C7)
    • Patellar (L4)
    • Hamstring (L5)
    • Achilles (S1)
  • Superficial reflexes:
    • Abdominal (belly button moves to stimulus)
    • Cremasteric, perianal wink
  • Pathological reflexes
    • Hoffman (Clawing of hand on finger flick)
    • Babinski reflex.
  • Nerve root tension testing:
    • SLR, ULLT, Braggards, shoulder depression, brachial stretch, doorbell sign, Tinel’s.


Upper extremity nerve pathology


Radial nerve (C5, 6, 7, 8)
  • Impingement at triangular space (triceps long head, teres major, humerus):
    • Generally due to poorly adjusted crutches, humerus fractures and dislocations, falling asleep on arm a la Saturday Night Palsy.
    • There is often a weakness of elbow and wrist extension (wrist drop)
    • Diminished to loss of triceps reflex
    • Loss of sensation to entire posterior arm and forearm (sans lateral forearm)
    • Loss of sensation to posterior lateral 3.5 fingers to DIP joints.
  • Radial groove impingement:
    • Often due to compression from humerus fractures, or triceps muscle entrapments.
      • Weakness of wrist extension or wrist drop.
      • Loss of sensation to posterior lateral 3.5 fingers to DIP joints.
  • Elbow impingement (at radial tunnel):
    • Deep branch of radial nerve is compressed by either a fracture of the proximal radius or by crush by the supinator (less often the extensor carpi radialis brevis).
      • Expect weakness of thumb and MCP extension.


Musculocutaneous nerve (C5, 6, 7)
  • Only site of impingement is axillary fold of coracobrachialis muscle belly.
    • Generally weakness of elbow flexion.
    • Loss of cutaneous sensation to anterior and lateral forearm (lateral antebrachial cutaneous nerve)
    • Loss of biceps reflex.
Axillary nerve (C5-6)
  • Only site of impingement is Quadrangular Space (Teres major, minor, triceps long head and humerus), most often due to fractures of the humerus, dislocations and poorly adjusted crutches. The Quadrangular Space also contains the posterior humeral circumflex artery.
    • Often weakness in deltoid and teres minor, resulting in poor abduction of arm.
    • Loss of cutaneous sensation to superior posterior and lateral arm (deltoid shield area).
Median Nerve (C5, 6, 7, 8, T1)
  • Elbow compression occasional due to sleeping on the elbow or medial supracondylar fractures.
    • Often weakness of forearm pronation and wrist flexion.
    • Ape hand deformity (atrophy of thenar muscles)
    • Loss of sensation to palm and palmar surface of lateral 3.5 fingers.
  • Impingement at the pronator teres caused by hypertonus of pronator teres (prontaror teres syndrome)
    • Often with throbbing or aching pain in wrist and forearm.
    • Poor grasp strength.
    • Pain with forearm pronation and wrist flexion.
    • Ape hand deformity
    • Loss of sensation to palm and palmar surface of lateral 3.5 fingers.
    • Importantly NOT associated with night pain.
  • Impingement at the transverse carpal ligament at carpal tunnel.
    • Ape hand deformity
    • Loss of sensation to palm and palmar surface of lateral 3.5 fingers, sometimes only the latter!
Ulnar nerve (C7, 8, T1)
  • Cubital tunnel of the elbow (cubital tunnel syndrome), likely from fracture at medial epicondyle, sustained pressure to the ligaments, or anomalies in the anconeus muscle. The cubital tunnel is formed by the tendonous arch jointing the humeral and ulnar heads of the flexor carpi ulnaris - inflammation of the flexor carpi ulnaris may compress the ulnar nerve.
    • Expect claw hand deformity with normal PROM in severe cases.
    • Loss of sensation to medial 1.5 fingers.

  • Dysfunction at the wrist most often stems from defensive wounds from cuts, blunt trauma, or stab wounds.
    • Bishops or claw hand deformity with normal PROM.
    • Loss of sensation to medial 1.5 fingers.

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I haven't decided which topic will be next (read: I am procrastinating on muscle/bone evaluation because it is such a vast yet nuanced topic), so we'll just have to see :) This one is pretty dry, so the next one will also be more candid.