Sample Write Up #1

Grade: 15/15

Grades Committee Member Comments: Excellent job! Great case, very well-presented. Wonderful details in HPI. PE thorough, well done. Discussion flows very well – my only comment would be that I would not have devoted much (or any) time to discussion of lyme disease, but given the particulars of his presentation, I understand why you did.

Patient: Mr. D.R.

Age 40

Date of Admission: 08/22/2005

Chief Complaint:Mr. D.R. is a 40-year-old Caucasian male presenting with “weakness that I just can’t take anymore,” beginning three weeks prior to admission.

History of Present Illness: Mr. D.R. is a 40-year-old previously healthy computer science administrator presenting to the E.D. with severe weakness in the proximal muscles of his extremities for the past three weeks. Up until three weeks ago, the patient states that he was “perfectly healthy,” and was not taking any medication prescribed by a physician or obtained over-the-counter, including herbal remedies. One month ago, while walking his dog in a wooded area, the patient states that he was stung by an unknown insect on the lateral aspect of his right knee. He developed some localized swelling shortly after being stung, reaching a maximum circumference of roughly 3/4 inches. Other than some mild discomfort, the patient did not have any other symptoms, including pruritis or discharge, and the swelling subsided after two days. However, he developed what he described as “stiffness in his calves” and began to have difficulty walking a week following the sting. When he was asked further about these symptoms, he stated that the “stiffness” was not in his calf muscles as he previously stated, but in his quadriceps, and that the sensation was more of a weakness than stiffness. Two days after noting mild leg weakness, he noticed that his symptoms not only progressed to the point where he became “weaker in his quadriceps”, but that he also began to show signs of “shoulder weakness” after he noted he could not easily lift things he was accustomed to lifting in the past, including plates and jugs of spring water, on top of his already noticeable problems walking even short distances.

Over the course of the last two and a half weeks, the patient has consulted with two physicians. When he visited his primary care doctor, he was prescribed doxycycline because it was believed that the patient may have contracted Lyme disease while in the woods with his dog. After two days of therapy, the patient grew frustrated because his major symptom of proximal muscle weakness seemed to be getting worse. He consulted with a local rheumatologist the following day, and was told to continue treatment with doxycycline. He was also put on a tapering dose of prednisone. Again, the patient states that he “did not benefit” from this treatment, and again saw the rheumatologist three days later. At this visit, the physician increased the patient’s dose of prednisone.

The patient chose to present to the E.D. today because “he couldn’t take it (the muscle weakness) anymore,” following a weekend in which it became difficult for him to even lift himself out of bed, walk, or bathe. A neighbor was asked to drive the patient to the E.D., where he remains to this point.

Mr. D.R. presents as an increasingly anxious individual who is clearly upset about his current health.  He strongly feels that the two physicians he had seen recently “dropped the ball,” and did not listen to his concerns. He is particularly upset because his baseline is normally that of an active, physically fit individual that obtains a yearly physical from his physician and has “never had a health problem of any kind…not even high blood pressure or cholesterol.” The patient states that he “has never been sick in his life” up until the past few weeks, and has “become hysterical” because he leads a very active life which includes walking his dog, working out, and jogging.  When pressed about his symptoms over the last few weeks, he stated he had worsening muscle weakness, and also talked about an erythematous rash that he had on his forehead just prior to visiting his primary care physician. He states he did not share the fact that he had a rash with either of his consults because he “thought it was because he was sweating because (he) was so nervous.” The rash was described to me as red, maculopapular and scaly after a few days.

The patient denies any focal neurological or musculoskeletal complaints other than those described above. Mr. D.R. states he does not have any joint stiffness, pain, swelling, or notice any bony deformity. He has not traveled recently, and denies any recreational drug use, changes in medications, alcohol consumption, or smoking. He also denies fever, chills, night sweats, weight change, chest pain, dyspnea, abdominal pain, nausea, vomiting, change in bowel habits including color or caliber, dysuria, or nocturia. There is not a history of any musculoskeletal diseases in his family, including MS, RA, osteoarthritis, ALS, peripheral neuropathy, or myositis. Mr. D.R. states he usually gets a physical by his primary care physician every year, and has been “perfectly healthy” his entire life.

Past Medical History:

• The patient denies any past medical history, including congenital illnesses such as chickenpox, measles, mumps, rubella, or flu.
• Patient denies any surgical or nonsurgical hospital stays, including tonsillectomy or appendectomy. Patient denies any sort of blood transfusion.
• Patient was asked directly about the following illnesses, and replied “no” to each: CVD, hyperlipidemia, stroke, pneumonia, asthma, COPD, cancer (including colon, lung, and liver), TB, diabetes, hepatitis, kidney disease, myositis, or neurological disease.

Current Medications: (per the patient’s response)

Walmart-brand multivitamin PO QD

No other over-the-counter medications or supplements

No prescription medications

No herbal or “alternative” remedies

Allergies: the patient states that he does not have any allergies to prescription or over-the-counter medications, foods allergies, or seasonal allergies.

Social History: Mr. D.R. is a 40-year-old computer science administrator for a local company in Central New York. The patient moved here from California 2 years ago, where he previously worked for the same company in a similar capacity. He has never been married, and he is not currently in a relationship. Before moving, the patient had a live-in girlfriend for two years, and prior to that, a girlfriend of 6 years. Each of his relationships was monogamous. Mr. D.R. states that he “always used condoms” when he was sexually active in each relationship, because neither of the two women wanted to be prescribed birth control pills. The patient currently lives in a 2 bedroom raised ranch in Liverpool, NY. He does not and has never smoked or used illicit/recreational drugs. His alcohol intake consists only of a glass of wine during Sunday dinner for the last 10 years. The patient is an active outdoorsman. He enjoys taking long walks, hiking, kayaking, and running with his two dogs each night after work. Mr. D.R. feels that he was “in the best shape of his life” prior to his current presentation.

Family History:

See HPI

Father (age 63)- healthy, active individual with no known diseases/illnesses

Mother (age 63)- migraine headaches “since she was a little girl”

Maternal Grandfather (age 84)- essential hypertension, diagnosed July 2002.

Maternal Grandmother (age 81)- diabetes mellitus type II, diagnosed early 1990’s.

Paternal Grandfather (deceased, age 87)- hypertension, diagnosed early 1990’s. Died of “natural causes” according to the patient.

Maternal Grandmother (deceased, age 50)- died following a car accident in 1970’s.

First Cousin (age 40)- history of essential hypertension, diagnosis unknown.

The patient was unaware of the family history of any other members of his extended family, including aunts, uncles, and cousins.

The patient reports no family history of CAD, blood disorders, stroke, COPD, cancer (including lung, GI, GU, or neuro.), GERD, TB, hepatitis, AIDS, autoimmune disease (including SLE, UC, Thyroiditis), or neurological or musculoskeletal disease.

Review of Systems: See HPI. On ROS, the patient had no pertinent positives. The patient stated “no” for the following:

• General: fever, malaise, chills, night sweats, fatigue, unexplained weight change.
• Musculoskeletal: see HPI
• Head and Neck: headache, syncope, head trauma, dizziness, lymphadenopathy, diplopia, blurred vision, change in visual acuity, photophobia, hearing loss, ear pain or discharge, vertigo, tinnitus, change in sense of smell, epistaxis, sinus pain, postnasal drip, sore throat, hoarseness, bleeding gums, tooth or gum pain, ulcers or lesions in the mouth or tongue.
• Endocrine: change in hat or glove size, heat or cold intolerance, thyroid enlargement, polydypsia, polyuria.
• Lungs and Chest: dyspnea, cyanosis, pain on inspiration or expiration, cough or sputum production, wheezing, hemoptysis.
• Cardiovascular: chest pain, palpitations, claudication, edema, orthopnea, hypertension.
• Hematologic: bleeding or bruising easily, anemia, thrombophlebitis.
• GI: change in appetite, food intolerance, dysphagia, nausea or vomiting, heartburn/reflux, hematemesis, change in color or caliber of stool, constipation or diarrhea, hemorrhoids, jaundice, gallstones, polyps.
• GU: dysuria, nocturia, frequency, urgency, dribbling, genital discharge, erectile dysfunction, flank or suprapubic pain, incontinence, STD.
• Neurologic: seizure, syncope, paralysis, decreased sensation, memory loss.
• Psychiatric: anxiety, depression, mood changes, sleep disturbance, difficulty concentrating.

When asked “Is there anything else I may have missed or that you would like to add,” the patient stated “no”.

Physical Examination:

General- 40-year-old Caucasian male. Patient is sitting in hospital bed in some distress and concern over his condition. He is well groomed. The patient is receiving IV normal saline at the time of H&P.

Vitals- T 97F, P 91, R 18, bp 134/80 right arm sitting and 135/77 left arm sitting. Weight 180 lbs. Oxygen saturation 97% on room air. Orthostatic vital signs were not taken in this patient.

Mental Status- oriented to person, place, and time. Mini-mental status exam score= 30. Comprehends and speaks clearly. Seems to be an excellent historian concerning his condition and the days leading up to his admission, although he tended to you “stiffness” and “weakness” interchangeably at the beginning of the interview.

Skin- no lesions, good skin turgor. Some mild edema in extremities. Fingers without clubbing or cyanosis. Brisk capillary refill. No diaphoresis, petechia, or ecchymosis.

Head- no lesions on scalp or face. Male-pattern baldness mild but apparent. Facial features symmetric. No sign of rash patient described as having in the past.

Eyes- conjunctiva pink and moist with no discharge. Accommodation and light reflex equal in each eye. Extraocular movements intact. Red reflex present. Unable to see patient’s retina due to pupillary constriction in well-lit room. 20/20 vision in each eye without corrective lenses or contacts.

Ears- auricles aligned. No lesions or discharge. Tympanic membranes pearly white with no erythema or fluid evident. Able to see bony landmarks.

Nose/Sinuses- no polyps or discharge. Septum midline. No sinus tenderness on palpation in maxillary or frontal sinuses.

Throat- buccal mucosa pink and moist with no lesions. Tongue and uvula midline. No fibrillations of the tongue. Pharynx without erythema. Teeth and gums in excellent condition.

Neck- no lymphadenopathy. Trachea midline. No thyroid enlargement. No JVD.  JVP measured as 6cm.

Lungs/Chest- breathing without use of accessory muscles. Tactile fremitus symmetric. Lungs clear to auscultation anteriorly, posteriorly, and in axilla. No wheezing or rhonchi.

Cardiovascular- apical impulse at midclavicular line, fifth intercostal space. No thrills or heaves. S1 and S2 present. No murmurs, rubs, or bruits. Brachial pulse 2+ bilaterally. Radial pulse 2+ bilaterally. Posterior tibial pulse 2+ bilaterally. Dorsalis pedis pulse 1+ bilaterally.

Abdomen- soft, nontender, no lesions or scars. Bowel sounds present.< Tympanic to percussion. Liver 7cm at left midclavicular line. Spleen tip was not palpable. No pain, rebound, or guarding on palpation. No CVA tenderness.

GU- no lesions or discharge on penis or scrotum, or in rectal area. Rectal exam guaiac negative.

Musculoskeletal- no pedal edema or cyanosis. Muscle strength was significantly diminished, both active and passive, in proximal muscles of the shoulders and hips on extension, flexion, abduction, and adduction. Distal musculature of the hands and feet showed normal strength and resistance. Unable to perform straight leg raises due to weakness. Unable to lift himself up from a seated position, but able to take small steps once someone helped him to his feet. Tremor or atrophy was not evident. Muscle tone equal bilaterally. Following this portion of the exam, the patient felt “out of it” because he was so weak.

Neurologic-

CN II- pupils equal and reactive to light and accommodation.

CN III, IV, VI- intraocular muscles intact. No diplopia or ptosis.

CN V- sensitive to pinprick and light touch bilaterally on forehead, cheek, and chin.

CN VII- facial expressions symmetric on both sides. Able to resist manual opening of eyelids.

CN VII- able to hear whispers and repeat phrases back when I whispered in each ear.

CN IX, X- palate unremarkable. No hoarseness when asked to speak.

CN XI- unable to shrug shoulders.

CN XII- tongue midline.

Sensory- sensitive to vibration (tuning fork), touch (finger) and pinprick (monofilament) on palms and soles, lateral and medial aspects of extremities (including the deltoid and quadriceps areas), and face.

Deep Tendon Reflexes- symmetric bilaterally as follows: Biceps 2+, Brachioradial 2+, Triceps 2+, Patellar 2+, Achilles 2+.

Negative for upper motor neuron (spasticity, hyperactive tendon reflexes, lower facial paralysis) or lower motor neuron (flaccid muscles, weak/absent tendon reflexes, fasciculations) signs.

Cerebellar signs were not tested in this patient. Will test these at a later time.

Labs-

Urinalysis showed trace leukocyte esterase, 2+ proteinuria, 1+ ketonuria, 3-5 WBC’s, 3-5 RBC’s, 3+ hematuria. Positive for urine myoglobin. Urine toxicology negative for narcotics.

White count 25.4, hemoglobin 16.4, hematocrit 48, platelets 206,000. Sodium 129, potassium 4.6, chloride 96, CO2 23, BUN 22, creatinine 0.7, glucose 134, calcium 8.6, albumin 2.5, alkaline phosphatase 175, ALT 800, AST 2483, LDH 2796, CK 72,560, CKMB 407.9. Magnesium 1.8, phosphorus 4.2, uric acid 5.4. CBC differential was pending.

Summary Statement: Mr. D.R. is a 40-year-old male, with no past medical history according to his own account, admitted for severe proximal muscle weakness with myoglobinuria and rhabdomyolysis on urinalysis. Symmetric weakness began in the proximal muscles of the leg, and later included the proximal muscles of the arms. The patient was initially treated for possible Lyme disease due to being stung by an unknown insect while walking his dog prior to onset of symptoms, but other etiologies must be considered in this patient based on his urinalysis and incredible increase in muscle enzymes.

Problem List:

1. Severe proximal muscle weakness in legs and arms
2. Rhabdomyolysis
3. Myoglobinuria
4. Leukocytosis
5. Possible exposure to Lyme disease
6. Health Maintenance- seat belt use, adult immunizations, and tobacco use.

Assessment/Discussion/Plan:

The differential diagnosis for this patient will center around severe proximal muscle weakness and rhabdomyolysis. Many etiologies can cause the breakdown and necrosis of muscle, leading to the “spilling” of muscle enzymes into the circulation, including CK (>72,000 in this patient) and myoglobin (as per myoglobinuria in this patient). Other enzymes, which I will talk about later, further narrow the differential diagnosis in this patient. Possible etiologies of the patient’s presenting symptoms include trauma/compression, exercise, metabolic myopathies including glycogen or lipid storage diseases, certain drugs or toxins, infection, endocrine disorders, and inflammatory myopathies including dermatomyositis and polymyositis (1) as sources of rhabdomyolysis; amyotrophic lateral sclerosis, muscular dystrophy, metabolic myopathy, and inflammatory myopathy as a source of proximal muscle weakness (2).

Prior to the development of severe proximal muscle weakness, the primary care physician taking care of this patient probably believed that Lyme disease was at the top of the differential diagnosis because of the patient’s recent history of being bitten by some sort of insect, in the case of Lyme disease, the Ixodes tick, while walking with his dog through the woods. Lyme disease is the result of a multisystem inflammatory reaction caused by Borrelia bergdorferi, a spirochete. The presentation of Lyme disease usually begins with a localized skin rash that tends to expand, referred to as erythema migrans (3). While this was not noted by the patient, the patient did begin to have some myalgia in his leg one week later, so the chance of Lyme disease was still a possibility. According to his primary care physician’s records, the doctor began a coarse of doxycycline 100mg PO bid. Other symptoms not seen in this patient, but normally evident during the first stage of infection (localized infection), could have included flu-like symptoms, headache, chills, fever, and neck stiffness (3). The primary care physician should have perhaps obtained serologic testing for the disease during the patient’s first visit to better rule Lyme disease in or out. However, both ELISA and immunofluorescence assay, the two methods used to test for Lyme disease, may not be able to detect the disease because it may take up to 2 months for seroconversion to occur (3). When he visited a local rheumatologist due to proximal muscle weakness that was progressing, the patient was put on prednisone “to cut down on the inflammation.” The patient states that he was confused because it was weakness, not inflammation, that he was presenting with, but he continued the treatment nonetheless.

On admission to the hospital, the patient presented with severe proximal muscle weakness. He needed to be lifted into a neighbor’s truck and driven to the hospital because he could not stand or pull himself up out of bed on his own. On admission, we immediately drew blood for a battery of tests, including CBC, BMP, LFT’s, TFT’s, and muscle enzymes, along with urinalysis. While we were told of the patient’s presumed exposure to Lyme disease, his presentation did not fit the typical presentation I alluded to above. For this reason, we had to consider other etiologies that centered around severe proximal muscle weakness. These tests, coupled with the muscle enzyme levels, electrolytes (to rule out electrolyte abnormality-induced myopathy), and thyroid function tests (to rule out hypothyroidism as the possible etiology) would shed some light on the etiology of this disease initially.

Dermatomyositis or polymyositis need to be strongly considered in this patient. Each of these are considered idiopathic inflammatory processes that can present with symmetric proximal muscle weakness (2). Using the Bohan and Peter criteria established in 1975 (2), we can further diagnose the patient based on five clinical manifestations. In each, serum muscle enzymes, including CK, LDH, AST, and ALT, are elevated, usually all at once. As I alluded to before, each presents with symmetric proximal muscle weakness. In dermatomyositis, a rash is typically evident during some point of the presentation. EMG changes occur in each as well.< And finally, muscle biopsy can show characteristic pathology of either dermatomyositis or polymyositis. While not one of the five major criteria, in a percentage of individuals, the detection of distinct autoantibodies may also be seen (UpToDate).

There is significant data that allows us to consider either dermatomyositis or polymyositis as potential etiology of disease in this patient. The appearance of muscle weakness is usually insidious in either of these presentations. However, in a small percentage of individuals, the appearance of proximal muscle weakness may be acute, as seems to be the case in Mr. D.R. In still other patients, proximal muscle weakness may ultimately progress to oropharyngeal muscle weakness of the upper one-third of the esophagus, leading to dysphagia and/or aspiration (2). For this reason, it is important to act quickly in ruling either of these in or out as possible diagnoses.

Perhaps the most striking laboratory manifestation of Mr. D.R.’s presentation is his significant increase in muscles enzymes, including CK (72,560), LDH (2796), AST (2483), and ALT (800). In both dermatomyositis and polymyositis, these enzymes are greatly elevated, usually all at the same time (2). It is also important to point out that the CKMB levels are often elevated, as they are in this patient, because a fraction of this enzyme is found in skeletal muscle. This can at times lead some to believe the patient may be suffering a cardiac episode, when in fact, there etiology is not cardiac in nature. With that said, it may still be a good idea to exclude cardiac events by obtaining troponin I concentrations (2). During the patient’s stay at the hospital, we will continue to monitor all of these enzymes on a daily basis because of the significant increase in all of them. It is important to also consider amyotrophic lateral sclerosis in the differential of this patient because it also may result in significantly higher muscle enzymes and proximal muscle weakness (2). However, because Mr. D.R. did not present with upper motor neuron signs, including hyperreflexic deep tendon reflexes, muscle spasticity, and Babinski’s sign, or lower motor neuron signs, including muscle atrophy or fasciculations, ALS is much lower on our differential diagnosis.

Perhaps most helpful in solving the basis of Mr. D.R.’s symptoms is a muscle biopsy. In the case of polymyositis and dermatomyositis, significant pathology on biopsy serves as the definitive test in diagnosis (2). Normally, biopsy is obtained in one of the larger proximal muscles of the body. In this case, biopsy will be obtained from the patient’s left deltoid. On biopsy, muscle necrosis, inflammatory infiltrate, and muscle degeneration and regeneration are clearly seen (2). However, there are distinctive differences between the two that allow a definitive diagnosis to be made. Polymyositis will show invasion of muscle fibers comprising a fascicle by a cellular infiltrate primarily of CD8+ T cells, with no immune complex deposition. On the other hand, dermatomyositis will histologically show perivascular membrane attack complex-mediated cellular infiltration via B cells and a greater proportion of CD4+ T cells than CD8+ (2). It is important to note that, if the biopsy returns with no evidence of inflammatory myopathy, we would then stain to look for glycogen or lipid storage diseases, which can also result in muscle pain, although usually following exertion (2). Moreover, we would have to strongly consider other elements of the differential diagnosis that I spoke of earlier, even though this patient seems to fit the criteria for inflammatory myopathy.

The presence of autoantibodies may also be detected in patients presenting with symptoms of dermatomyositis or polymyositis. While antinuclear antibodies are found in 80% of people with either of these diseases, they are far from specific (2), and should not be used to definitively diagnose a patient. However, there are some “myositis-specific” autoantibodies, namely anti-Jo-1 (20% of patients) and anti-Mi-2 (7% of patients) that can be used in diagnosis (2). We will be obtaining labs looking for antinuclear antibodies and the anti-tRNA synthetase autoantibody anti-Jo-1, while the anti-helicase autoantibody anti-Mi-2 cannot be tested for clinically at this time. Moreover, we will also look for anti-acetylcholine autoantibodies to rule out myasthenia gravis, which is low on the differential because it normally does not present with increased muscle enzymes, and has a high prevalence of causing facial muscle weakness (2), which this patient did not present with.

Rash is usually a manifestation found in dermatomyositis. Many different types have been documented in this disease, including Gottron’s sign, an erythematous and scaly rash on the extensor surfaces of metacarpophalangeal and interphalangeal joints; heliotrope rash, an eruption on the upper eyelids sometimes with eyelid swelling; “mechanic’s hand,” painful cracking/roughening of the hands; a “shawl-like” rash over the chest and shoulders; and many other rashes (2). While this patient did not present with either of these four rashes, his erythematous and scaly rash on the forehead during the presentation of his symptoms cannot be ignored as a potential manifestation of dermatomyositis.

A few other etiologies may also mimic an inflammatory myopathy. Perhaps the easiest to test for would be myopathy associated with alcohol or cocaine use, which we screened for on urinalysis and during the social history, and hypothyroidism, which has the ability to present with elevated muscle enzymes and subacute weakness of the proximal muscles (2). Hypothyroidism is extremely low on our list because during the primary care office visits, the patient reports that his physician stated his thyroid function was well within normal limits, and he has not presented with cold intolerance, slow thinking, poor memory, dry and thick skin, brittle and coarse hair, and delayed relaxation phase of deep tendon reflexes. We have already added TFT’s to the labs we will obtain, and are awaiting those results.

Rhabdomyolysis results from the release of muscle enzymes into the circulation following muscle necrosis. Clinically, patient’s present with pigmenturia (myoglobinuria) and muscle weakness (1), as was the case with Mr. D.R. It is not myoglobinuria in and of itself that warrants immediate attention when found on urinalysis, but the fact that in large amounts, myoglobin may lead to acute oliguric renal failure due to renal ischemia, pigment casts causing obstruction of the renal tubules, and/or direct tubular injury resulting from free iron (1). With renal dysfunction comes electrolyte abnormalities, including hyperkalemia and hyperphosphatemia (due to release of each from muscle), hypocalcemia (due to calcium deposition in damaged muscles), and/or hyperuricemia (due to significant purine release from muscle breakdown) (1). Fortunately, in this patient, none of this had occurred according to the labs that were drawn, although the patient was in the high normal range for potassium (4.6) and phosphate (4.2). Had the patient had hyperkalemia, he would have been at risk for cardiac arrest, among other respiratory and GI manifestations. If he had had hyperphophatemia, risks may have included symptoms of hypocalcemia, including prolonged QT and possibly arrhythmia.

When looking at the differential diagnoses for both rhabdomyolysis and proximal muscle weakness, coupled with the lab findings, I have narrowed my differential diagnosis to either dermatomyositis or polymyositis. Evidence of a rash prior to admission causes me to lean more toward dermatomyositis, but muscle biopsy will determine which, if any, of these diseases is the etiology of this patient’s symptoms. By narrowing the differential to an inflammatory myopathy, there is one more aspect of such a disease that must be considered, that being the association of both dermatomyositis and polymyositis with malignancy. According to studies, there is a six-fold increase and two-fold increase of malignancy in dermatomyositis and polymyositis, respectively (2,4). Research continues in order to establish the relationship between inflammatory myopathy and malignancy, but some hypotheses include a cancer producing autoantibodies that are sometimes found in inflammatory myopathy, or the therapy of myositis, which is largely immunosuppressive, causing induction of malignancy (4). Regardless of the true mechanism, clinical signs and symptoms of malignancy should warrant investigation of possible cancer in patients with inflammatory myositis. Cancers often associated with inflammatory myopathy include lung, pancreatic, bladder, ovarian, gastric, and Hodgkin’s lymphoma (4). In this patient, occult blood should be and was tested, for possible signs of GI bleed secondary to malignancy. >Ultrasound and CT, if needed, may also be warranted to check for any malignancy based on the patient’s answers to screening questions later on.

Treating this patient will require a two-fold plan of attack. In treating rhabdomyolysis, the primary approach is to protect the kidneys from insults that I spoke of earlier that could ultimately lead to kidney failure. When rhabdomyolysis occurs, the treatment of choice is to expand volume via isotonic saline, followed by mannitol-alkaline or saline-mannitol diuresis (1). Fluids are important in order to increase urine output to protect the kidneys from the adverse effects of myoglobinuria, although this could lead to other complications down the road, including compartment syndrome. Again, monitoring serum electrolytes, BUN, and creatinine will continue to be important in watching for signs of renal failure (1).

Our focus of treatment following volume expansion and diureses for rhabdomyolysis now must turn to what I believe the patient’s underlying disease to be, dermatomyositis or polymyositis. Luckily, the patient already received some treatment for the disease even before he presented with such severe proximal muscle weakness. Initial therapy starts with corticosteroids (5), which the patient was prescribed from his primary care physician when he first presented following possible exposure to Lyme disease. Prednisone is the drug of choice, and is given as a dose of 0.5 to 1.5mg/kg/day. Tapering of the dose begins only when the patient responds to the therapy, seen in this case by a significant decrease in serum muscle enzymes, which can take up to four to six weeks to occur (5). In those patients where prednisone fails, either azathioprine, a purine metabolism antagonist, or methotrexate, a folate antimetabolite that irreversibly binds dihydrofolate reductase to inhibit DNA synthesis, have shown to improve long-term therapy of patients with inflammatory myopathy together with corticosteroids (5). In disease that still proves to be resistant, other therapies have been used and/or are being investigated, including intravenous immune globulin, cyclosporine, cyclophosphamide and other alkylating agents, and others (5). If prednisone itself does prove to produce a significant response in this patient, then there are other problems that could manifest from long-term steroid therapy, including osteoporosis, hyperglycemia, and Cushingoid appearance, that we would have to look out for (5).

Other diagnoses that I alluded to previously, including exercise-induced weakness, drug/toxin induced myopathy, and trauma/compression, are extremely low on my differential based on my initial H&P with the patient. While the patient is an active outdoorsman, he does not lift weights or run for prolonged periods of time, so chances are exercise has not caused his symptoms. The same can be said for drug/toxin-induced myopathy. Nothing in the history, or on urinalysis for that matter, points to this being the culprit. However, I will ask the patient further about possible drug use or exposure to harsh chemicals at a later time during his admission. Finally, and perhaps most obvious, there is nothing that would point to any sort of trauma in this patient.

At the top of the new differential is inflammatory myopathy, namely dermatomyositis or polymyositis. However, we also ordered tests to rule out other diseases, including muscle biopsy of the deltoid muscle, which we used to look for evidence of abnormal glycogen or lipid storage, or inflammatory myopathy; a toxicology screen to screen for cocaine, which can cause increased demand of energy by the muscles; and serology for a host of viral infections. While I strongly believe this patient’s presentation to be the result of inflammatory myopathy, it is my opinion that the following steps should be taken to diagnosis and aid in the treatment of Mr. D.R.’s rhabdomyolysis and proximal muscle weakness:

1. Obtain serology for possible Lyme disease exposure
2. Testing for both antinuclear and anti-Jo-1 autoantibodies (anti-Mi-2 can only be tested in the research, and not clinical, settings at this time according to UpToDate).
3. Muscle biopsy
• Looking for signs of inflammatory myopathy
• Looking for signs of glycogen storage or lipid storage disease
4. Toxicology
• Cocaine
• Alcohol
5. Monitor diagnostic and prognostic information from the patient that may warrant us looking for possible malignancy. Depending on what we learn from the patient, the following studies may be warranted to rule cancer in or out:
• CT
• Colonoscopy
• Endoscopy
• Ultrasound
• other
6. Continue to monitor electrolytes
7. Continue to monitor serum muscle enzymes
8. Continue to monitor kidney function (BUN, creatinine) for signs of renal failure, and urinalysis for myoglobinuria.
9. DVT prophylaxis with heparin
10. GI prophylaxis with Protonix

With that said, I feel we should begin IV normal saline followed by mannitol-alkaline diuresis to protect the patient’s kidneys from myoglobin-induced kidney failure. Moreover, due to my strong suspicion of inflammatory myopathy, prednisone 1.5mg/kg/day should be started.

Once the patient has stabilized, we will introduce the aspect of health maintenance prior to discharge. In a 40-year-old, previously healthy individual that sees his primary care physician on a regular basis, the topics to discuss may include the importance of seat belt use, the importance of refraining from the use of tobacco, and to make sure the patient is up to date on all adult immunizations. Important immunizations of note include tetanus booster (every ten years), hepatitis B, and varicella (especially because the patient has never had chickenpox).

References:

1. Miller, ML. Rhabdomyolysis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2005.
2. Miller, ML. Clinical Manifestations and Diagnosis of Adult Dermatomyositis and Polymyositis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2005.
3. Meyerhoff, J. Lyme Disease. Available from http://www.emedicine.com/med/topic1346.htm. July 2005.
4. Miller, ML. Malignancy in Dermatomyositis and Polymyositis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2005.
5. Miller, ML. Treatment of Adult Dermatomyositis and Polymyositis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2005.