CASE 5

A 38-year-old man with altered mental status is brought to the emergency department (ED) by ambulance. The patient had been found sprawled on the stoop of an apartment building when residents called the police. The patient was unresponsive when the paramedics arrived, and they were unable to obtain any additional history from the patient or from any of the onlookers at the scene. The patient was wrapped in blankets and an intravenous (IV) line was inserted, which provided 0.5 L of normal saline during transit to the ED. When the patient was found, the temperature outside was about 35°F (1.7°C), with winds reaching speeds of 10-15 miles per hour (16.1-24.1 kilometers per hour).

On his arrival to the ED, the patient's vital signs are a blood pressure of 88/40 mm Hg, heart rate of 38 bpm, and a respiratory rate of 24 breaths/min. An oral thermometer reading is unsuccessful, but a rectal probe records a temperature of 85.4°F (29.7°C). Repeated attempts to obtain an oxygen saturation measurement via a finger pulse oximeter are not successful. On initial examination, the patient appears to be a homeless, disheveled man with the faint smell of alcohol on his breath. His clothing is stained and extensively worn. He looks older than the stated age on his identification card. In the ED, he is mildly arousable and has trouble following simple commands. He has intact gag and corneal reflexes and does not fight the examiner during the tests. He responds appropriately to painful stimuli. His pupils are equal, round, and reactive to light. No obvious signs of head trauma are noted, and his oropharynx, nares, and ears are unremarkable. His cardiac examination is notable for marked bradycardia of 45 bpm, but no murmurs, rubs, gallops, or extra heart sounds are otherwise noted. A lung examination reveals rhonchi and dullness to percussion in the right lower lung field, but otherwise normal lung sounds. His abdomen is soft, nontender, and nondistended, and normal bowel sounds are heard. The patient's skin is cold and his fingers and toes have a bluish tinge, with a delayed capillary refill time. A brief skin survey reveals some minor abrasions, but no major wounds or erosions. The patient is unable to provide any additional information about his past medical, family, medication, social, or allergy history. His pockets contain an identification card, but no other useful information.

Routine blood work is ordered. The results of his metabolic panel are all within normal limits. His blood glucose level is 104 mg/dL (5.77 mmol/L). His complete blood cell count (CBC) reveals a small elevation in the white blood cell (WBC) count, but it is otherwise unremarkable. A portable chest radiograph shows a small consolidation of the right lower lobe that is consistent with pneumonia.

An electrocardiogram (ECG) is performed

DIAGNOSIS OF CASE 4

This patient's ECG showed atrial fibrillation with a rapid ventricular response, which is a possible cardiac manifestation of thyrotoxicosis. No ischemic changes were noted despite her rapid heart rate. Her laboratory studies confirmed the suspected diagnosis, with findings of a markedly depressed thyroid-stimulating hormone (TSH) of 0.006 mIU/L (normal range, 0.5-5.0 mIU/L) and elevated triiodothyronine (T3) and thyroxine (T4) concentrations of 632 ng/dL (9.73 nmol/L) and 23.7 ug/dL (305.02 nmol/L), respectively (normal ranges, T3: 70-170 ng/dL; T4: 5-11 ug/dL).
Thyrotoxicosis refers to an elevated concentration of thyroid hormone as well as the related clinical manifestations. This is differentiated from thyroid storm, a life-threatening manifestation of thyrotoxicosis in which a markedly hypermetabolic state is present. Hyperthyroidism most commonly results from uncontrolled Graves disease, in which autoantibodies to the TSH receptor are produced. This leads to excessive thyroid hormone production from the thyroid gland and a reflexive inhibition of TSH release from the pituitary gland. Other etiologies can include a solitary thyroid adenoma, toxic multinodular goiter, hypersecretory thyroid carcinoma, thyrotropin-secreting pituitary adenoma, struma ovarii, and iodine or amiodarone administration. A precipitating event, such as surgery, trauma, myocardial infarction, pulmonary embolism, diabetic ketoacidosis, childbirth, severe infection, discontinuation of antithyroid medication, or thyroid surgery on a patient with uncontrolled hyperthyroidism, is often needed to push a patient with hyperthyroidism into thyroid storm.[1,3]
The incidence of hyperthyroidism in the United States is 0.05% to 1.3%, most of which remains undiagnosed. Approximately 1-2% of these patients will progress to thyroid storm at some point. The prevalence is slightly higher in women compared with men and in white and Hispanic populations compared with black populations. Thyroid storm is most common in the third to sixth decades of life, although it can occur at any age.[1]
Thyroid storm is a clinical diagnosis and, considering the acuity of this life-threatening condition, patients with thyrotoxicosis should be treated empirically when the diagnosis is suspected. Symptoms of thyrotoxicosis include weight loss, palpitations, hair loss, diplopia, chest pain, oligomenorrhea, or confusion. The physical examination reveals a hypermetabolic state, with abnormalities involving multiple organ systems. These findings commonly include hyperpyrexia, tachycardia, tachypnea, and hypertension. Other findings may include fine tremor, exophthalmos, ophthalmoplegia, pretibial edema, congestive heart failure, thyromegaly, thyroid bruit, and hyperreflexia.[2] Laboratory studies show a low TSH level and elevated T3 and T4 concentrations. TSH is the most precise indicator of thyroid function because of the very high sensitivity of the thyroid-pituitary feedback loop, and current assays are able to detect levels of 0.02 mIU/L or less. As such, a normal TSH level largely excludes significant thyroid disease. Other laboratory findings seen in thyrotoxicosis may include hyperglycemia, hypercalcemia, leukocytosis, and elevated liver enzymes.[3] Further testing may be indicated as part of a search for the precipitating cause of clinical decompensation, such as infection, myocardial infarction, or diabetic ketoacidosis. Electrocardiography most often reveals sinus tachycardia or atrial fibrillation. Although thyroid storm requires more rapid and aggressive therapy than thyrotoxicosis, differentiating between the two can sometimes be difficult, as it was in this patient. Burch and Wartofsky developed a scoring system to assist in making this distinction that takes into account thermoregulatory dysfunction, central nervous system effects, gastrointestinal dysfunction, the degree of tachycardia, the extent of congestive heart failure, the presence of atrial fibrillation, and the presence or absence of a precipitating event.[4]
Cardiac complications from thyrotoxicosis include arrhythmias, congestive heart failure, and pulmonary hypertension. The most common arrhythmia in thyrotoxicosis is sinus tachycardia; however, atrial fibrillation occurs in 10-20% of patients with thyrotoxicosis, most often in patients who are older than 60 years. Risk factors for atrial fibrillation in these patients include male sex, increasing age, coronary heart disease, heart failure, and structural heart or valvular disease. Congestive heart failure in thyrotoxicosis is predominantly caused by either persistent tachyarrhythmias (tachycardia-induced cardiomyopathy) or uncontrolled hypertension as a consequence of thyrotoxicosis. Systolic dysfunction can occur as a consequence of the persistent cardiac arrhythmias, but it usually resolves once the hyperthyroid state is treated. Pulmonary hypertension can also occur in thyrotoxicosis, either as a result of a primary effect of thyroid hormone on pulmonary arteriolar resistance vessels, decompensated left heart failure, or via increased pulmonary arterial blood flow (high-output).[1]
The differential diagnosis for thyrotoxicosis and thyroid storm may include anxiety, congestive heart failure, heat exhaustion or heatstroke, factitious disorder, neuroleptic malignant syndrome, panic disorder, septic shock, serotonin syndrome, anticholinergic or sympathomimetic toxicity, and alcohol or benzodiazepine withdrawal syndromes.[5] Because infection is a common trigger for thyroid storm, an initial misdiagnosis of sepsis is not uncommon because of similar characteristics, such as tachycardia, fever, and altered mental status.
Management of thyrotoxicosis consists of a 5-pronged, ordered approach, targeting each step in the biosynthetic pathway of thyroid hormone and its activity on target tissues. Treatment begins with administration of propylthiouracil (PTU) or methimazole, both of which act by inhibiting new hormone synthesis. PTU has the added effect of decreasing peripheral T4 to T3 conversion. Beta-blockers are then employed to inhibit target activity of thyroid hormone. Propranolol is the preferred agent because it also blocks peripheral conversion of T4. When cardioselective agents are preferred, atenolol or metoprolol may be used. At least 1 hour after administration of PTU or methimazole, the patient may be given iodide to inhibit further thyroid hormone release. It is imperative that iodine be given only after synthesis of new hormone is blocked because iodide administration can have the undesired effect of increasing new hormone synthesis. Potassium iodide or Lugol solution of iodine is recommended. Peripheral conversion of T4 to T3 is blocked, as noted above, and dexamethasone may be used as well. Further treatment is supportive and may include acetaminophen for fever and hydrocortisone if the patient is hypotensive as a result of adrenal insufficiency. Salicylates are contraindicated because they displace bound thyroid hormone in the blood.[2,3]
With regard to the management of cardiac symptoms related to thyrotoxicosis, treatment is focused on reducing adrenergic drive to the heart and restoring normal cardiac rhythm. As mentioned above, beta-blockers are very effective for rapid hemodynamic improvement. Either propranolol or metoprolol given intravenously can be used to improve heart rate control either in sinus tachycardia or atrial fibrillation. In severe cases, a continuous infusion of esmolol may be required for rate control. Amiodarone should be avoided when treating atrial fibrillation from thyrotoxicosis because of its high iodine content, which may induce or exacerbate thyroid storm. If a patient is hemodynamically unstable from atrial fibrillation, direct current cardioversion should be employed. If symptoms of pulmonary congestion appear, diuretics may be used. Other drugs for heart failure (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and/or aldosterone receptor antagonists) are reasonable agents in patients who have depressed left ventricular systolic function. Anticoagulation is recommended for patients in atrial fibrillation secondary to thyrotoxicosis. The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines recommend anticoagulation with warfarin to an international normalized ratio of 2.0-3.0 until the patient is euthyroid, after which recommendations and risk stratification are the same for atrial fibrillation without thyrotoxicosis.[2] Of note, PTU, methimazole, and iodide solutions are all classified as pregnancy class D and, as such, should not be used in pregnancy.
This patient's clinical presentation bordered between thyrotoxicosis and thyroid storm, and she was hemodynamically stable. She was immediately treated with propranolol and PTU and was admitted to a monitored bed in the medical service. Because her clinical condition improved and she remained stable, the admitting team chose to forgo further therapy with iodine and steroids. Her atrial fibrillation resolved within 12 hours, but an echocardiogram revealed cardiomyopathy with a left ventricular ejection fraction of 45% that was attributed to her long-standing hyperthyroidism. A diagnosis of Graves disease was made. She was continued on methimazole and metoprolol, and anticoagulation was initiated. Five months later, the patient was still taking methimazole. Her thyroid function had normalized, her cardiomyopathy had reversed, and her anticoagulation was discontinued because atrial fibrillation did not recur. Incidentally, she was ruled out for tuberculosis during her admission with 3 induced sputum samples.

CASE 4 Tachycardia in a 61-Year-Old Woman Background

A 61-year-old woman presents to the emergency department (ED) after being referred from her primary care provider's (PCP) office for evaluation of tachycardia. She had been seen by her PCP for routine placement of a purified protein derivative (PPD) tuberculin skin test and was incidentally noted to have a pulse of 160 bpm. The patient currently denies any specific complaints other than occasional palpitations. On review of her systems, however, she notes having night sweats; a 110-lb (50-kg) weight loss over the preceding 12 months; and 2-3 months of anxiety, diarrhea, and occasional diplopia. She denies having any fever, chills, chest pain, dyspnea, or swelling in her extremities. She has a past medical history of an unspecified thyroid problem. She does not take any daily medications and has no medication allergies. She has a 50-pack-year smoking history, with occasional alcohol consumption. She had been homeless for a period of time but is currently living in an apartment.
On examination, the patient is awake and fully oriented. She is diaphoretic but in no apparent distress. Her temperature is 97.0°F (36.1°C); her pulse is 160 bpm; her respiratory rate is 24 breaths/min, with an oxygen saturation of 98%; and her blood pressure is 190/117 mm Hg. She has bilateral exophthalmos with exotropia of the right eye. Her visual acuity and extraocular movements are intact. The neck examination reveals a diffuse, nontender goiter, without nodules or thyroid bruits. The heart is tachycardic, intermittently irregular, and without murmurs. The lungs are clear to auscultation bilaterally. The abdomen is nondistended, soft, and nontender, with no palpable masses. There is no edema of the extremities. The neurologic examination reveals normal mentation, intact cranial nerves, intact motor strength and sensation, and normal reflexes. No tremor is noted.
The initial laboratory studies reveal complete blood count, electrolytes, renal function, and cardiac marker findings that are all within normal limits. A plain chest radiograph is interpreted as normal (not pictured). An electrocardiogram (ECG) is obtained (see Figure 1).

Ankylosing spondylitis

Ankylosing spondylitis (AS) is a type of inflammatory arthritis that targets the joints of the spine. It
particularly affects the sacroiliac (SI) joint where the spine attaches to the pelvis. Symptoms
include back pain, stiffness and reduced mobility. Ankylosing spondylitis is also known as
rheumatoid spondylitis.


Ankylosing spondylitis is more common in Caucasians and affects twice as many men than women.
The condition usually appears between the ages of 14 and 40 years, while onset after the age of 40
is extremely rare. There is no cure for AS, but medical treatment and lifestyle habits such as
regular exercise can improve the person’s outlook.


Damage to the spine
The inflammation causes damage to the vertebrae (backbones). In response, the body grows more
bone tissue to repair the damage. Over time, this process builds abnormal bony outgrowths
(syndesmophytes) that knit together. This fusion of the vertebrae causes pain and reduces
mobility, especially in the lower back. About seven in 10 people with AS will develop some degree
of spinal fusion.


Causes
The exact cause of ankylosing spondylitis is unknown, but genes are thought to play a part.
Studies show that most people with AS have the gene called HLA-B27. Some HLA (human
lymphocyte antigen) genes suggest the person may be more likely to get autoimmune diseases.
Only one in 20 people with this gene develop ankylosing spondylitis. Since the presence of this
gene does not automatically lead to AS, other factors must be involved. Current theory suggests
that a person who has the gene variant must be exposed to certain environmental triggers in order
for the arthritis to develop. These triggers, however, are unknown.


Symptoms in children
In children, ankylosing spondylitis symptoms are commonly ignored or dismissed as ‘growing
pains’. The symptoms particular to children may include:
• Chronic pain in the back or neck
• Chronic pain in the knees, ankles or feet
• Swollen joints
• Increased stiffness after periods of inactivity
• Reduced pain and stiffness during and after exercise.


Symptoms in adults
Ankylosing spondylitis varies widely in its severity and progresses differently from one person to
the next. Generally speaking, the symptoms in adults may include:
• Chronic back pain, particularly in the lower back and hips
• Pain in other joints (such as the knee, shoulder or foot) or tendons (such as those at the
back of the heel or under the foot)
• Poor posture, since standing tall is uncomfortable or even painful
• Back stiffness
• Reduced mobility
• Difficulty standing up from a sitting position
• Difficulty walking
• Increased stiffness after periods of inactivity
• Reduced pain and stiffness during and after exercise
• Fatigue unrelieved by rest or sleep.


Other sites of inflammation
Ankylosing spondylitis
Ankylosing spondylitis may cause inflammation in other areas of the body, including:
• Tendon (enthesitis)
• Eye (uveitis or iritis)
• Bowel (colitis)
• Lung (fibrosis)
• Heart (aortitis).

Complications
Ankylosing spondylitis can cause a range of complications, including:
• Skeletal deformities such as a permanent stoop (in severe cases, the person may be
unable to lift their head from their chest)
• Total fusion of the spine (‘bamboo spine’)
• Increased susceptibility to bone fractures
• Fusion of the rib joints and associated breathing difficulties
• Lung lesions and recurrent lung infections
• Anaemia, as a result of chronic inflammation.

Diagnosis
Research suggests that ankylosing spondylitis may go undiagnosed for years, particularly in
children. It takes an average of seven years for an adult with ankylosing spondylitis to finally get a
diagnosis. This is unfortunate because early diagnosis and prompt treatment can improve the
person’s long-term outlook.
Tests used to diagnose AS may include:
• Medical history
• Physical examination
• X-ray
• Scanning procedures such as CT or MRI
• Blood test
• Genetic testing.

Treatment
There is no cure for ankylosing spondylitis. Medical treatment aims to manage pain, reduce the risk
of complications and improve quality of life. Options include:
• Non-steroidal anti-inflammatory medications (NSAIDs)
• Disease-modifying anti-rheumatic drugs (DMARDs)
• Corticosteroid medications
• Physical therapy, including exercises to improve flexibility and range of motion – either on
land or in the water
• In rare cases, surgery to repair badly damaged joints.

Self-help suggestions
Most people with ankylosing spondylitis develop some degree of spinal fusion. A key aim of
treatment is to encourage good posture so that the spine will fuse in an upright rather than
stooped position. Be guided by your doctor, but general self-help suggestions include:
• The most important management tool is regular exercise (including stretching), which
helps to keep the spine mobile and flexible. Ask your doctor or physiotherapist for further
information.
• Strong abdominal muscles contribute to good posture. Perform exercises to strengthen
your abdominal muscles as recommended by your doctor or physiotherapist.
• Pay careful and daily attention to posture. Remind yourself regularly to ‘stand tall’.
• If you tend to slump when seated, consider buying an ergonomic chair, lumbar support
cushion or other device. Ask your doctor or physiotherapist for recommendations.
• Avoid curling into a ball when in bed. Instead, try to lie straight, either on your back or
stomach.
• Don’t smoke.
Ankylosing spondylitis


Long-term outlook
Ankylosing spondylitis is a progressive disease, which means it tends to get worse over time.
Certain characteristics of AS suggest a poorer outlook, including:
• Earlier rather than later onset of symptoms
• Involvement of one or both sacroiliac joints
• Uveitis or iritis (inflammation of the eye)
• Cigarette smoking
• Sedentary lifestyle
• Failure to consistently manage the condition throughout life.



Things to remember
• Ankylosing spondylitis (AS) is a type of inflammatory arthritis that targets the joints of the
spine, particularly the sacroiliac (SI) joint where the spine attaches to the pelvis.
• There is no cure for AS – medical treatment aims to manage pain, reduce the risk of
complications and improve quality of life.
• The most important management tool is regular exercise (including stretching), which
helps to keep the spine mobile and flexible.

DIAGNOSIS OF CASE 3

THE DIAGNOSIS OF CASE IS ANKYLOSING SPONDYLITIS.

Discussion

The anteroposterior and lateral radiographs of the spine demonstrated the classic "bamboo-spine" finding seen in cases of ankylosing spondylitis. The images showed sclerosis and ankylosis of the vertebral bodies, without loss of disc space. Bone formation extended across the anterior and lateral margins of the intervertebral disks of the lower thoracic and lumbar spine (syndesmophytosis). The sacroiliac joints showed extensive periarticular sclerosis and focal ankylosis.
Ankylosing spondylitis is a chronic inflammatory disorder of multiple articular and para-articular structures that principally involves the axial skeleton. It usually affects the sacroiliac joints and the spinal facet joints of the vertebrae. It sometimes involves the appendicular skeleton as well, such as the joints of the greater trochanter, patella, and calcaneum. Other extraspinal manifestations include iritis/uveitis and pulmonary involvement. The basic pathologic lesion of ankylosing spondylitis occurs at the entheses, which are sites at which ligaments, tendons, and joint capsules attach to bone. In the outer layers of the annulus fibrosis of the intervertebral disks, the condition manifests as a formation of new bone. The name of the disease is derived from Greek; "ankylos" means stiffening of a joint, and "spondylos" means vertebra. The disease is classified as a chronic and progressive form of seronegative arthritis. Ankylosing spondylitis affects men 4-10 times more frequently than women, and the symptoms generally appear in those aged 15-35 years. More than 90% of whites with ankylosing spondylitis have the HLA-B27 gene, but 6-8% of those with this gene do not develop the disease.[2,3]
Symptoms of ankylosing spondylitis include back pain and stiffness, peripheral joint and chest pain, sciatica, anorexia, weight loss, and low-grade fever. The back pain associated with this condition is typically transient at first, but it eventually becomes persistent. It is usually worse in the mornings and resolves with exercise. A typical patient may also complain of waking up with back pain at night. The pain is usually centered over the sacrum, but it may radiate to the groin, buttocks, and down the legs. With time, the back pain usually progresses up the spine and affects the rib cage, resulting in a restriction of chest expansion and diaphragmatic breathing (observed as ballooning of the abdomen during inspiration) as the costovertebral joints become affected. The cervical spine is ankylosed late in the course of the disease, leading to restriction in neck movement and head rotation. Without treatment, the spine eventually becomes completely rigid, with loss of the normal curvatures and movement.[2,3]
On physical examination, the loss of lateral flexion of the lumbar spine is the earliest objective sign of spinal involvement. The sacroiliitis may be detected by eliciting a tenderness response during percussion over the sacroiliac joints. Objective tests to quantify spinal restriction include touching the toes, the Schober test, and measurement of chest expansion. Additional physical findings include restriction of motion in the peripheral joints and tenderness over the enthuses. The physical exam should also include evaluation for signs of potentially serious cardiovascular and pulmonary complications, such as aortic incompetence secondary to aortitis, conduction defects of the heart, cardiomyopathy, pericarditis, apical fibrosis of the lungs, bronchiectasis, cavitation of the chest, and development of a restrictive ventilatory pattern. Other associated conditions include the development of inflammatory bowel disease, uveitis (in up to 20% of patients), radiculitis secondary to inflamed nerves, and, rarely, amyloidosis.[2,3]
Specific criteria for the diagnosis of ankylosing spondylitis include the Rome criteria (developed in 1963) and the New York criteria (developed in 1968). Although these criteria have been generally accepted as useful, limitations are recognized and overlaps exist among the clinical and radiologic features of various seronegative spondyloarthropathies. Sacroiliitis is the hallmark of ankylosing spondylitis and is a requisite for the diagnosis under both sets of criteria. Other conditions, such as psoriasis, Reiter disease, enteropathic arthropathy, hyperparathyroidism, and osteitis condensans ilii, may also result in bilateral symmetric sacroiliac joint disease and should be considered in the differential diagnosis. Ankylosing spondylitis may also present with asymmetric sacroiliitis, which may be more characteristic of other conditions, such as psoriasis, Reiter disease, rheumatoid arthritis, and gouty arthritis. Radiographically, diffuse idiopathic skeletal hyperostosis (DISH) has a similar appearance to ankylosing spondylitis; however, DISH typically occurs at a later age and does not involve the sacroiliac joint.[2,3]
The radiographic changes usually first appear in the sacroiliac joints, followed by the thoracolumbar and lumbosacral spine; this is in line with the natural progression of the disease. The disease then proceeds cephalad up the spine; however, the cervical spine may also be affected without involvement of the thoracic or lumbar spine. Radiographically evident peripheral-joint abnormalities are seen in more than 50% of patients. Abnormalities can also be seen in the symphysis pubis and in the manubriosternal, sternoclavicular, and temporomandibular joints. Spinal findings include osteitis, syndesmophytosis, diskovertebral erosions and destruction (Romanus lesions), and disk calcification. Radiographically, joint involvement appears as joint-space narrowing, periostitis, osseous erosion, and minimal periarticular osteoporosis (less than that seen with rheumatoid arthritis). Sacroiliac joint involvement is usually bilateral and symmetric.[1,3]
Common laboratory findings are an elevated erythrocyte sedimentation rate (during the acute phase), a positive HLA-B27 histocompatibility antigen, mild leukocytosis, normochromic normocytic anemia (anemia of chronic disease), and negative results for rheumatoid factor.[2,3]
The general principles of managing chronic arthritis also apply to ankylosing spondylitis. Among the various nonsteroidal anti-inflammatory drugs (NSAIDs) available to treat the disease, indomethacin may be the most effective. The lowest dose that provides pain relief should be used in order to avoid potentially serious complications, such as gastritis, peptic ulcer disease, and renal insufficiency. Sulfasalazine can be useful if peripheral arthritis is substantial, but it may be less effective when spinal and sacroiliac pain are the most prominent symptoms. In the majority of patients, the symptoms persist for life, although in some cases remission does occur.[5]
Physical therapy and exercise can help prevent axial immobility. Specifically, spinal extension and deep-breathing exercises maintain spinal mobility, encourage erect posture, and promote chest expansion. Maintaining an erect posture and sleeping on a firm mattress with a thin pillow can help reduce thoracic kyphosis. Severe hip or spinal involvement may require surgical repair. Antitumor necrosis factor (anti-TNF) agents, such as infliximab and etanercept, are relatively new but often very effective therapeutic agents that may be considered for patients with pain refractory to other interventions.[4,5]
The patient in this case was started by his primary care provider on a low dose of indomethacin to reduce pain and decrease inflammation. He was referred by the primary care provider to a rheumatologist for further evaluation and management and ongoing medical treatment. He was also referred to a physical therapist to begin a proper exercise and stretching program. Information regarding support groups to provide further education on the disease process and available treatment options were also given to the patient.

CASE 3 Young Man With Lower Back Pain and Low-Grade Fever Background

 
A Young Man With Lower Back Pain and Low-Grade Fever
Background

A 19-year-old man presents to his primary care provider with a 2-month history of lower back pain and stiffness. The pain is intermittent, achy, and usually worse in the morning than it is later in the day or evening. He has also noticed a progressive inability to perform activities that require flexibility in the back, such as bending down to pull on his pants or tying his shoelaces. The pain sometimes awakens him at night. It is improved with exercise. He also reports a several-month history of low-grade fever, malaise, and anorexia, as well as an unintended weight loss of 10 lb (4.5 kg). He has not noted any masses on his testicles with self-examination. The patient has no history of rash. He does not have any known chronic medical conditions. He takes one multivitamin per day. He has never smoked, but he does drink an occasional glass of wine with dinner. There is no significant family history of disease.




On physical examination, the patient has a blood pressure of 125/67 mm Hg and a heart rate of 60 bpm. His respiratory rate is 8 breaths/min and his temperature is normal at 98.0°F (36.7°C). The cardiovascular and respiratory portions of the examination are normal; specifically, no murmurs or rubs are detected. The patient has no photophobia, eye redness, or decreased visual acuity. On examination of the back, flexion of the lumbar spine is clearly decreased when the patient attempts to bend down to touch his toes. He also has pain and limited range of motion with rotation and lateral flexion at the lumbar spine. His chest expansion is mildly diminished. The remainder of the physical examination is within normal limits.
As part of the initial workup of the findings on physical examination, routine laboratory investigations, including a complete blood cell (CBC) count and a basic electrolyte panel, as well as plain radiographs of the back, are performed. The chemistry panel is unremarkable, and the CBC reveals a white blood cell (WBC) count of 4.6 × 103/μL (4.6 × 109/L), a hemoglobin of 13.7 g/dL (137 g/L), a hematocrit of 43% (0.43), and a platelet count of 120 × 103/μL (120 × 109/L). The electrolytes are within normal limits. A rheumatoid factor test is negative, and the erythrocyte sedimentation rate is 64 mm/hr (normal range, <10 mm/hr for men). The patient has a positive finding for human leukocyte antigen (HLA)–B27.
Anteroposterior and lateral radiographs of the lumbar spine are obtained (see Figure 1).


What is the underlying disease process for the radiographic abnormalities?

Hint: The spine and sacroiliac joints show classic findings for the diagnosis.

Ankylosing spondylitis

Spinal stenosis

Psoriatic arthritis

Diffuse idiopathic skeletal hyperostosis