Mr. C

Stacey Moenter

Margaret Michaud

Laura Baughman

Review of Medical Conditions

Fibular head dislocation Peroneal nerve damage Diabetes HIV Nummular eczema Chronic renal failure Anemia Benzene toxicity

Proximal Tibiofibular Joint Dislocation

Types of instability:– Subluxation – Anterolateral– Posteromedial– Superior

Fibular Head Dislocation

Signs and Symptoms of the Types of Instability:– Subluxation- Pain along the lateral side of the knee and

lower limb during palpation over the fibular head.– Anterolateral- Pain in the lateral popliteal fossa along the

course of the bicep tendon and pain usually occurs when the pt DF and everting their ankle. The pt may lack a few degrees of knee extension. The fibular head may become prominent laterally, the surrounding tissue may be swollen or bruised or effusion of the joint may occur but is rare.

– Posteromedial, and Superior Dislocation- A mass may appear on the lateral side of the proximal tibiofibular joint.

Fibular Head Dislocation cont.

Mechanism of Injury:– Anterior Dislocation

Sudden inversion and PF of the foot that causes tension in the peroneal muscles, extensor digitorum longus, and extensor hallicus longus, applying the forward dislocation.

Simultaneous flexion of the knee, relaxing the bicep tendon and fibular collateral ligament

Concomitant twisting of the body, torque of the tibia on the foot, which is already fixed in inversion.

– Posterior Dislocation Severe blow to the knee in which the proximal part of the fibula

is pushed posteriorly and medially– Superior Dislocation

Usually associated with tibial shaft fx.

Fibular Head Dislocation cont.

Causes of Fibular Head Dislocation:– Anterior Dislocation:

Twisting Slipping injury Parachute landing Falls- Knee flexed, adducted with inversion of the foot. Multiple trauma Sports- soccer, skiing, wrestling, football, rugby, gymnastics,

judo, and broad jumping.– Posterior Dislocation

Osteomyelitis BKA Osteochondroma Ligament hyperlaxity

Fibular Head Dislocation

Complication from Fibular Head Dislocation:– Peroneal palsy- foot drop– Chronic instability

Dx of Fibular Head Dislocation:– Roentgenogram (Radiograph)– CTs– MRIs

Rx for Fibular Head Dislocation

Arthrodesis of the joint- pt still experience significant pain and instability at the ankle.

– Bone graft– Screw fixation

Resection of the proximal end of the fibula Close reduction with the knee flexed at 90 to 110 degrees, the foot

externally rotated, and direct pressure was applied to the fibular head. Followed by immobilization for approximately 3 wks. (Anterior Dislocation)

Open reduction in which the capsule and fibular collateral ligament are repaired and temporary internal fixation with Steinmann pins are used to correct the posterior dislocation. Kirschner wires may also be used.

Immobilization Pts are usually NWB approximately 2 wks after a close reduction and then

are allowed to WBAT and then finally full WB without a limp. Full activity should occur 6-8 weeks. Usually performed on anterior dislocations.

Pts who have a open reduction will be in a short leg cast for 6 weeks and then the cast and the wires are able to be removed. Usually performed on posterior dislocations.

Peroneal Nerve Damage

Peroneal nerve: a branch of the sciatic nerve, splits into superficial and deep branches

Winds around lateral fibular head Superficial branch:

– Innervates peroneus longus and brevis– Supplies sensation to skin on front lower leg, dorsum of

foot, and toes– If injured, results in decreased foot eversion

Deep branch:– Innervates dorsiflexors– Supplies sensation to skin on first and second toes– If injured, results in decreased ankle dorsiflexion

Peroneal Nerve Cont.

Most common causes of nerve damage:– Acute or chronic compression– Ischemia– Traction

Initial symptoms after injury don’t determine prognosis, so need to look at mechanism of injury

Peroneal Nerve Cont.

Complications:– Plantarflexion contractures– Inversion contractures– Steppage gait with foot slap

Peroneal Nerve Cont.

Therapeutic Implications– Need to maintain ROM of muscles innervated by peroneal

nerve – Stretch antagonistic muscles to prevent contracture– Joint mobilization to adjacent joints to prevent joint

restrictions– Strengthen agonisitic and synergistic muscles– Be careful not to fatigue the muscles– Use dorsiflexion assist orthotic during early treatment when

muscles are at their weakest to prevent contractures

Diabetes Mellitus (DM)

Definition: Is a disease in which the body does not produce or properly use insulin.

Insulin: Is a hormone that is needed to convert sugar, starches and other food into energy needed by cells for daily life

Cause:- Genetic- Environmental (obesity)

Cardinal Signs of DM:- Polyuria - Polydipsia -Polyphagia -Asymptomatic

- Weight loss -Recurrent blurred vision - Kenonuria -Weakness, fatigue & dizziness

DM cont.

Complication from DM:

- Heart disease and stroke

- Kidney disease

-Retinopathy

-Neuropathies

-Foot ulcers

-Skin issues

-Gastroparesis

DM cont.

Hemoglobin A1c: - Measures glucose levels over time to how well the pt’s DM is controlled.- helps to minimize the complications caused by chronically elevated glucose levels, such as progressive damage to the body organs like kidneys, eyes, cardiovascular system, and nerves.- A1c of 1% = an average change of 30 mg/dL in blood glucose

- A1c of 6% = an average glucose of 135 mg/dL- A1c of 9% = an average glucose of 240 mg/dL

The closer to 6% the better the diabetes is in control and as the A1c increase from here so does the risk of complications.

Type I vs Type II DM

Features Type I Type II

Age at onset Usually < 20yr Usually > 40 yr

Proportion of all cases 10% 90%

Type of onset Abrupt Gradual

Etiologic factors Possible viral/ autoimmune, resulting in destruction of pancreatic beta cells

Obesity-associated insulin receptor resistance

HLA association Yes No

Insulin antibodies Yes No

Body weight at onset Normal or thin Majority are obese (80%)

Endogenous insulin production

Decreased (little or none) Variable (above of below normal)

Ketoacidosis May occur Rare

Treatment Insulin, diet, and exercise Diet, oral hypoglycemic agents, exercise, insulin, and weight control

Hypoglycemia vs. Hyperglycemia

Variable Hypoglycemia Hyperglycemia

Onset Rapid (minutes) Gradual (days)

Mood Labile, irritable, nervous, weepy Lethargic

Mental status Difficulty concentrating, speaking, focusing, coordination

Dulled sensorium, confused

Inward feeling Shaky, hungry, headache, dizziness Thirst, weakness, nausea/vomiting, abdominal pain

Skin Pallor, sweating Flushed, signs of dehydration

Mucous Membrane Normal Dry, crusty

Respiration Shallow Deep, rapid

Pulse Tachycardic Less rapid, weak

Breath Odor Normal Fruity, acetone

Neurologic Tremors; late: dilated pupils, convulsion, headache, blurred vision, numbness of the lips and tongue, coma

Diminished reflexes, paresthesias

Glucose Level Low: < 50 mg/dL High ≥ 250 mg/dL

DM cont.

Signs of Ketoacidosis (DKA): Blood glucose over 249mg/dL Acetone breath Nausea and/or vomiting Abdominal pain Dry, warm skin Confusion Frequent urination Dehydration Weak and rapid pulse Deep and rapid respirations (Kussmaul’s) Loss of consciousness in bad cases. Causes: Failure to take medications, stress, dietary changes without

medication adjustments, eating disorders, and illness or injury. Rx: administering insulin to lower blood glucose levels and restoring fluid

balance to the bloodstream with an intravenous saline drip. Electrolytes may also be given via IV.

Exercise and DM

Exercise Dos Exercise DON’Ts

Give fruit juice or honey to your patient if he/she becomes hypoglycemic or if you are unsure if he/she is in hypo or hyperglycemic state give he/she fruit juice or honey anyways.

Avoid exercise if blood glucose is > 250 mg/dL with evidence of ketosis (type I) or near 300mg/dL with or without urinary ketones (type II)

Drink at leat 17 ounces of fluid before exercise

Avoid exercise during peak insulin times

Exercise about 1 hr after a meal is best

Avoid exercise without eating at least 2 hrs before exercise

Exercise and DM cont.

Benefits of Exercise in People with DM:– Improves cardiovascular function – Improves maximum oxygen uptake– Improves insulin binding and sensitivity– Lowers insulin requirements (type II DM)– Improves sense of well-being and quality of life– Promotes other healthy lifestyle activities– Increase carbohydrate metabolism– Improves blood glucose control– Reduces hypertension– Weight loss– Improves lipid profile– Reduces stress

Exercise and DM cont.

Risk of Exercise in People with DM:– Hypoglycemia– Hyperglycemia– Cardiovascular disease (myocardial infarction,

arrhythmias, excessive increase in blood pressure, post exercise orthostatic hypertension, or sudden death)

– Microvascular disease ( retinal hemorrhage or increased proteinuria

– Degenerative joint disease– Orthopedic injury related to neuropathy

Exercise and DM cont.

Contraindications to Exercise in People with DM: – Unable to control blood glucose– Recent photocoagulation or surgery for retinopathy– Dehydration– Extreme environmental temperatures (hot or cold) – Unevaluated or poorly controlled associated conditions– Retinopathy– Hypertension– Neuropathy (autonomic or peripheral)– Nephropathy

Exercise and DM cont.

Proper Equipment for People with DM:– Proper fitting running shoes for walking or running with frequent

foot exams before and after activity.– Proper shoes for swimming such as boat shoes to prevent

abrasions on the pool bottom and gently drying feet after swimming.

– Avoid intermittent high intensity activities such as racquetball, basketball, baseball or soccer which may cause trauma to the feet and eyes.

– High resistance should be limited to young diabetic patients with no diabetic complications, avoid in older diabetics.

– Low resistance should be encouraged unless retinopathy is present

– Exercise involving jarring or rapid head motion may precipitate hemorrhage or retinal detachment

– Stationary indoor equipment may be best overall choice.

Medications for Type II DM

Diabinese, Glucotrol and Glucotrol XL, Micronase, Glynase, and Diabeta and Amaryl, Prandin, Starfix- Stimulates Beta cells to increase insulin.

Glucophage, Avandia, Rezulin, ACTOS- Decrease glucose produced by the liver to make muscle more sensitive to insulin, so glucose can be absorbed:

Precose, Glyset- Block the breakdown of starches in intestine to slow the absorption of glucose:.

Symlin- works with insulin to help with absorption of glucose.

Byetta- works to increase insulin secretion

HIV

HIV (human immunodeficiency virus) develops into AIDS (acquired immunodeficiency syndrome)

Classification– Based on CD4 (T-helper cell) count:

Asymptomatic HIV: >500 μL Symptomatic HIV: 201-499 μL AIDS: <200 μL

HIV Cont.

Pathogenesis: – Genetic material is RNA instead of DNA– Infects lymphocytes, mostly macrophages and

CD4 cells, also some B cells– Fuses with and enters lymphocytes– HIV releases reverse transcriptase so a DNA

copy of the virus can be made and becomes part of the host cell genetic material

– Virus replicates rapidly for ~3 months (patient is asymptomatic or has flu-like symptoms: fever, fatigue, etc.)

HIV Cont.

Asymptomatic Phase– Symptoms: generalized lymphadenopathy– Emotionally dealing with disease: denial, grief,

depression, anger, etc.– Normal physically, except when affected by

depression

HIV Cont.

Symptomatic Phase– Symptoms: night sweats, fevers, peripheral

neuropathy– Begin taking medications (antiretroviral drugs and

prophylaxis for other infections)– Often still working– Same emotional symptoms, increasing with the

appearance of symptoms– Physically: decreased energy, pain, wasting

HIV Cont.

AIDS– Symptoms: opportunistic infections (meningitis),

Kaposi’s sarcoma, TB, pneumonia, lymphomas, etc.

– On antiretroviral drugs, chemotherapy, antibiotics– Similar emotional symptoms, fluctuates with

symptoms and dealing with facing death– Changes in family and friend relationships– Often not able to work– Physically: fatigue, wasting, debilitated from

infections, may have cognitive deficits

HIV Cont.

Kaposi’s sarcoma– Purple cutaneous or visceral lesions– Most commonly found on skin and mucus

membranes– Most common in homosexual men, rare in women

and IV drug users– Linked to lymphatic system (altered lymphatic

transport, tumors, and dysfunctional nodes), causes lymphedema in extremities

– Treatment: range of treatment options from cryotherapy to chemotherapy

Kaposi’s Sarcoma

HIV Cont.

HIV medications:– Nucleoside reverse transcriptase (RT) inhibitors: keeps the

virus from replicating early in the cycle, delays the disease process

AZT (Azidothymidine), ddC (zalcitabine), ddI (dideoxyinosine), d4T (stavudine), 3TC (lamivudine), Abacavir (ziagen)

– Protease inhibitors: stops replication later in the cycle Ritonavir (Norvir), Saquinivir (Invirase), Indinavir (Crixivan),

Amprenivir (Agenerase), Nelfinavir (Viracept)

– Fusion inhibitors: keeps virus from entering cells Fuzeon (enfuvirtide or T-20)

HIV Cont.

HAART: highly active antiretroviral therapy – When ≥3 drugs are used together– Necessary since people can become resistant to

drugs– Often associated with the decline in deaths

related to AIDS (slows down the progression) Side effects of medication:

– Nausea, diarrhea, decrease of red or white blood cells, pancreatitis, painful nerve damage, pneumonia, trouble breathing, chills and fever, skin rash, blood in urine, and low blood pressure

HIV Cont.

Therapeutic Implications– Exercise is only known way to fight wasting and

lipodystrophy– Exercise has been shown to improve strength and

aerobic capacity– Mixed data on effect of exercise on CD4 and

neutrophil levels– Barriers: decreased motivation, periods of illness

(exercise is contraindicated during these times), poverty, physicians not recommending exercise

Nummular Eczema

Definition (Eczema): A superficial inflammation of the skin caused by irritant exposure, allergic sensitization (delayed hypersensitivity), or genetically determined idiopathic factors.

Stages of Eczema:1. Acute- Extensive erosions with serous exudates or by intensely pruritic, erythematous papules and vesicles on a background of erythema.2. Subacute- Erythematous, excoriated (scratched or abraded), scaling papules or plaques that are either grouped or scattered over erythematous skin. The skin may acquire a slivery sheen.3. Chronic- Thickened skin and increased skin marking secondary to rubbing and scratching; excoriated papules, fibrotic papules, and nodules; and postinflammatory hyperpigmentation and hypopigmentation.

Nummular Eczema cont.

Definition (Nummular): Nummular Eczema: A stubborn, itchy rash that forms coin-shaped patches on the skin. It may appear as ringworm or as psoriasis. Nummular eczema is usually chronic in nature

Signs and Symptoms:– Itching – Skin redness or inflammation – Scaly or excoriated (raw) skin – Skin lesions that may be macules, papules, vesicles, or patches

Nummular (coin shaped) Primarily located on the arms and legs Spreading to the trunk Oozing, crusting over

Nummular Eczema cont.

Nummular Eczema cont.

Causes: Nummular Eczema is usually unknown, but may be caused by an allergic reaction to medications. Nummular eczema is not contagious.

Complications: Secondary infections may occur to the skin from scratching.

Prognosis: Chronic and there is no real cure.

Topical Steroids for Nummular Eczema

Topical Steroids- anti-inflammatory cream or ointments available by prescription which may reduce irritation. The cream or ointment is applied 1-2x/day.

– Class 1: Very potent (up to 600 times as potent as hydrocortisone) Clobetasol propionate Betamethasone dipropionate

– Class 2: Potent (I50-100 times as potent as hydrocortisone) Betamethasone valerate Betamethasone dipropionate Diflucortolone valerate Fluticasone valerate Hydrocortisone 17-butyrate Mometasone furoate Methylprednisolone aceponate

Topical Steroid for Nummular Eczema cont

– Class 3: Moderate (2-25 times as potent as hydrocortisone)

Aclometasone dipropionate Clobetasone butyrate Fluocinolone acetonide Triamcinolone acetonide

– Class 4: MildHydrocortisone 0.5-2.5% Topical steroids are also available in

combination with salicylic acid to enhance penetration, and with antibacterial and antifungal agents.

Skin Absorption of Topical Steroids

Steroids are absorbed at different rates from different parts of the body. A steroid that works on the face may not work on the palm. But a potent steroid may cause side effects on the face. For example:

– Forearm absorbs 1% – Armpit absorbs 4% – Face absorbs 7% – Eyelids and genitals absorb 30% – Palm absorbs 0.1% – Sole absorbs 0.05%

Other Rx for Nummular Ezcema

Treatment:– Emollients- bath oils, soap substitutes, and moisturizing

creams, which are used to help decrease itching, scaling and dryness

– Oral or topical antibiotics- antibiotics such as flucloxacillin in cases those are sticky or crusty.

– Oral antihistamines– Phototherapy- ultraviolet light treatment several times

weekly– Systemic steroids- can be taken by mouth or may be

injected. This is only used in severe cases– Avoid- multiple showers in one day, hot water, rubbing dry,

soaps that may causes irritations, wool or rough clothing, fabric softeners, dryer sheets, and avoid dry air such as winter.

Chronic Renal Failure

What is it? AKA Renal Insufficiency or Kidney Failure Caused by a variety of conditions that result in

permanent loss of nephrons  Loss of nephrons leads to progressive deterioration

of glomerular filtration, tubular reabsorption, and endocrine functions of the kidneys

Etiology of CRF

Two leading causes:   Diabetes mellitus   High blood pressure (controlled or uncontrolled)Other risk factors:    Urinary tract obstruction and infection    Glomerular disorders    Systemic lupus erythematosus    Heavy use of OTC analgesics    Age

CRF: How Does It Happen?

Kidneys’ job is to remove metabolic waste products from the blood and regulate fluid, electrolyte, and pH balance of ECF

4 Progressive stages:1.  Diminished renal reserve2.  Renal insufficiency3.  Renal failure4. End Stage Renal Disease (ESRD)

CRF: Stage 1

Glomerular Filtration Rate (GFR) ~50% of normal

Normal BUN and Creatinine levels

CRF: Stage 2

GFR 20-35% of normal Appearance of anemia, HTN, azotemia (high

levels of nitrogenous waste in the blood)

CRF: Stage 3

GFR <20-25% of normal Appearance of edema, metabolic acidosis,

hypercalcemia Neurologic, gastrointestinal, and

cardiovascular complications

CRF: Stage 4

~90% of kidney function lost GFR <5% of normal Magnification of already existing

complications Uremia- urea and other waste products in the

blood Survival dependent on dialysis or

transplantation

CRF: Clinical Presentation

General: Fatigue, weakness, decreased alertness, inability to concenctrate

Skin: Pallor, ecchymosis, pruritus, dryskin and mucous membranes, thin/brittle fingernails, urine odor on skin

Hematologic: Anemia, tendency to bleed easily Body Fluids: Polyuria, nocturia, dehydration,

hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia

CRF: Clinical Presentation

Eye, ear, nose, throat: Metallic taste in mouth, nosebleeds, urinous breath, pale conjunctiva

Pulmonary: Dyspnea, rales, pleural effusion Cardiovascular: Dyspnea on exertion, HTN, friction

rub,retrosternal pain on inspiration Gastrointestinal: Anorexia, nausea, vomiting,

hiccups, GI bleeding

CRF: Clinical Presentation

Genitourinary: Impotence, amenorrhea, loss of libido

Skeletal: Osteomalacia, osteoporosis, bone pain, fracture, metastatic calcification of soft tissues, edema

Neurologic: Recent memory loss, coma, seizures, muscle tremors, parasthesias, muscle weakness, restless legs, cramping

CRF: Treatment

Conservative: aims to slow the deterioration of the remaining renal function and to assist the body in its fight to compensate for the existing condition

Wide variety of interventions: e.g. renal artery angioplasty, carefully managed nutrition and supplements, treatment of hypertension, oral or IV calcitriol to suppress parathyroid hormone, recombinant human erythropoietin

Renal Replacement Therapy

  Hemodialysis: Requires 3 tx per week with 3-4hrs per session Blood flows from an artery, through the dialysis

machine chambers, then back to the body’s venous system, with the waste products and excess electrolytes diffusing into the dialyzing solution

Patient travels to a renal center for treatment and remains immobile during the treatment

Renal Replacement Therapy

Peritoneal Dialysis: Performed at home with a catheter implanted in the

peritoneal cavity Sterile dialyzing solution is instilled and drained over

a specific period Performed 4x/day Fewer diet restrictions and symptom swings than HD Complications: infection, catheter malfunction,

dehydration, hyperglycemia, hernia

Kidney Transplantation

Kidney transplantation with renal allografts is often the treatment of choice, but limited by donor availability

CRF and Physical Therapy

Challenges to treating patients with CRF: Malnutrition Side effects of meds Number of body systems involved Decreased alertness

Inability to concentrate Short-term memory deficits*All of the above interfere with following instructions

with transfers, exercises, and body mechanics

CRF and Physical Therapy Cont’d

Rest periods may be necessary due to fatigue/weakness

Osteoporosis education Renal transplantation complications: HTN,

lipid disorders, hepatitis, CA, tendinopathies, osteopenia

CRF: Lab Values

Metabolic waste accumulates in the blood Two most commonly measured: serum creatinine

and BUN; usually they shouldn’t affect PT– BUN: concentration of urea nitrogen reflects glomerular

filtration and urine concentrating capacity– Creatinine: represents balance between production by

muscles and clearance by kidneys

Monitor serum albumin levels; may indicate poor nutrition if low

CRF and Exercise

Impaired oxygen transport Functional capacity of patients on dialysis is

often 2 S.D.’s below the age and gender-predicted norm

Autonomic dysfunction may limit max age-predicted HR better to use perceived exertion to monitor exercise

CRF and Exercise cont’d

Exercise is important for patients on dialysis improves QOL, endurance, and functional abilities

Some sources recommend exercise during and after dialysis due to a greater risk of instability before dialysis

Risk of exercise related to exacerbation of comorbid conditions BP and blood glucose should be monitored

CRF Research Article

Resistance training improved the following compared to controls:-Type I and Type II muscle fiber cross-sectional area increased-Muscle strength improved and body weight maintained-Total body potassium increased

Anemia

What is it? Reduced oxygen-carrying capacity of blood

secondary to abnormality in quality or quantity of erythrocytes

Hematocrit:– Adult Males: < 41%– Adult Females: < 37%

Hemoglobin:– Females: Hgb <12g/100mL– Males: Hgb <14g/100mL

Anemia Classification

Classification (according to etiologic factors): Excessive Blood Loss: e.g. trauma, GI Cancers Increased destruction of erythrocytes: e.g. SLE, leukemia,

lymphoma Decreased production of erythrocytes: e.g. chronic diseases

such as RA, systemic lupus erythematosus, TB, Cancer, HIV– Decreased RBC life span; bone marrow fails to compensate– Nutritional deficiency- iron, protein, Vitamin B12 and other vitamins

and minerals– Folic acid deficiency– Bone marrow disorders aplastic anemia, marrow replacement

with fibrotic tissue or tumor, acute leukemia, infiltrative disease– Kidney Failure- kidneys responsible for producing EPO, a hormone

that acts on the bone marrow to increase production of RBCs

Anemia: Clinical Manifestations

Anemia just presents as mild fatigue until values fall below 1/2 of normal

Symptoms with progression: – Weakness– DOE– Easily fatigued– Pallor or yellowness of skin (especially palms of hands, fingernails,

mucosa, conjunctiva)– Tachycardia, increased angina in pre-existing CAD– Leg ulcers– Koilonychias (spoon-shaped nails)

CNS symptoms in severe pernicious anemia

Anemia: Complications

Complications depend on type of anemia: Severe anemia can cause heart failure and

hypoxic damage to the liver and kidneys Anemia in the presence of coronary obstruction

results in low blood oxygen levels Oxygen perfusion of the heart causes increased

angina

Anemia: Treatment

Identification and treatment of underlying cause Examples of Tx:

Bone marrow transplantation to replace damaged marrow Vitamin B12, Folic acid, or iron supplemental therapy for

nutritional deficits or in the case of chronic blood loss Oxygen therapy to prevent hypoxia Corticosteroids and androgens to stimulate marrow to

produce RBCs Splenectomy to decrease destruction of RBCs Anti-T lymphocyte antibodies and other immunosuppressive

agents for the tx of aplastic anemia Recombinant human erythropoietin for tx of anemia related

to chronic disease

Anemia

Implications for Rehab: Expect decreased exercise tolerance, easy fatigability Pace activity over time to allow patient to accomplish more

with adequate rest Patients with CRF and severe anemia must exercise at a

lower intensity than the normal population VO2 max at least 20% less than normal population Exercise with caution and proceed gradually Monitor vital signs: HR, BP, chest pain, confusion,

concentration, skin color, etc.

Benzene Toxicity

Benzene: colorless, sweet smelling chemical found naturally occurring in the environment and also used in several man-made products, such as solvents, paints, dyes, and a number of chemical and household products

Linked to several health problems, including aplastic anemia and leukemia

Aplastic Anemia: reduced production of RBCs, WBCs, and platelets

Aplastic Anemia: Symptoms

Pale skin coloring Blood in stools Nose bleeds Tender sinuses Enlarged liver or spleen Oral thrush symptoms Bleeding gums

Fever HA Dizziness Nausea SOB Increased bruising Fatigue

Subjective

Additional Questions– How much help does his partner need?– Does he have first floor set-up?– Are there steps to get into the house?– Is his Diabetes under control?– What medications is he on?– Is he receiving dialysis?– Does he have any DME? – Is he having any pain?– Has his fibula ever dislocated before?

Physical Exam

Observation (edema, erythema, etc.) Palpation: 1/3 of fibular head dislocation

cases go unnoticed Sensation: LE dermatomes MMT: Hip, Knee, Ankle AROM/PROM: Knee, Ankle Fibular Head Mobility

Physical Exam Cont’d.

Special Tests:– Varus and Valgus Stress Tests– Anterior and Posterior Drawer

Assess wound; Request wound care order if nedded

Gait: Observe with crutches

Assessment/Prognosis

Patient is a 43 y.o. male presenting with fibular head dislocation with peroneal nerve damage and multiple comorbidities, including: DM, CRF, HIV, anemia. Recommend surgical repair of fibular head dislocation prior to initiating rehab. Crutch training will be performed prior to surgery.

Fair – Good prognosis secondary to multiple comorbidities listed above.

Intervention

Crutch Training- Assess for safety and issue walker if needed

AAROM and PROM at ankle Knee and Hip Strengthening Wound care if needed Ace wrap for Dorsiflexion assist Gait training for normalized gait once WB status

increased Develop HEP due to limited medical coverage

References

Hall, C.M. and L.T. Brody. Therapeutic Exercise, Moving Toward Function. Magee, D.J. Orthopedic Physical Assessment. Neumann, D.A. Kinesiology of the Musculoskeletal System, Foundations for

Physical Rehabilitation. Roubenoff, R. Exercise and HIV Infection. Nutrition in Clinical Care. 3(4) 230-

236, 2000. Saidoff, D.C. and A.L. McDonough. Critical Pathways in Therapeutic

Intervention, Extremities and Spine. Umphred, D.A. Neurological Rehabilitation. www.cdc.gov http://www.nlm.nih.gov/medlineplus/ency/article/000870.htm http://dermnetnz.org/dermatitis/nummular-dermatitis.html www.aocd.org/skin/dermatologic_disease/nummular_eczema.htm Ogden, J. Subluxation and Dislocation of the Proximal Tibiofibular Joint.

Journal of Bone and Joint Surgery. 56:145-154, 1974. Parkes, J II; Russel, Z. Isolated Acute Dislocation of the Proximal Tibiofibular

Joint: Case Report. Journal of Bone and Joint Surgery. 55:177-180, 1973 Class notes from Dennis (Diff dx)