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Sacroiliitis is an inflammatory disorder of the sacroiliac joint in the posterior pelvis. It is a feature of spondyloarthropathies such as ankylosing spondylitis. Patients may present with low back pain or pain in the buttock or leg. There is tenderness to palpation of the sacroiliac joint but no pelvic instability. Patients with ankylosing spondylitis are usually men less than 40 years of age and often report back pain and stiffness that is worse upon waking up and improves with activity throughout the day. Plain films of the spine may demonstrate “squaring” of the vertebral bodies (bamboo spine). Referral to a rheumatologist and treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended. Emergent causes of low back pain (e.g., spinal cord compression, spine infection, trauma) should be considered and screened with directed history and physical examination. Concerning features of back pain include history of trauma, recent surgery, intravenous drug use, old age, history of cancer, fever, focal neurologic deficits (e.g., weakness, numbness), urinary or bowel dysfunction, and unexplained weight loss. Patients with these features should be worked up for emergent causes of back pain such as malignancy, cord compression, or infection with advanced imaging, blood cultures, and potentially consultation to a spine surgeon.

Central cord syndrome (A) is the most common spinal cord syndrome and presents with upper extremity weakness greater than lower extremity weakness. It is caused by extreme neck extension. Pott’s disease (B) is vertebral osteomyelitis. Patients usually present with fever and other signs of infection such as tachycardia, leukocytosis, and erythema overlying the area of infection. A psoas abscess (C) is an infected fluid collection of the iliopsoas muscle compartment. Patients are usually ill-appearing and septic with fever and back pain, flank pain, or lower abdominal pain that does not improve throughout the day.

Fluoroquinolone drugs, including levofloxacin, have been associated with spontaneous tendon ruptures. Fluroquinolones are a commonly prescribed antibiotic class. The class includes ciprofloxacin, moxifloxacin and levofloxacin. The fluoroquinolone class of drugs has a number of side effects, the most serious of which are prolongation of the QTc and spontaneous tendon rupture. Tendon rupture appears to be more common in older patients. The overall risk is between 0.1 – 0.4%. These drugs are discouraged for use in pregnant women and children secondary to their effect on cartilage.

Sciatica is a lumbosacral radiculopathy that is caused by compression of the spinal nerve root(s). 90% of all cases are due to disc herniation, although spinal stenosis, spondylolisthesis, and piriformis syndrome are other notable causes. Symptoms typically develop suddenly during physical activity and consist of back pain radiating down the leg, though the pain may radiate bilaterally. Weakness and numbness in the affected limb may also be present. The straight leg raise (SLR) is a good screening test for sciatica with 92% sensitivity and 28% specificity. The patient’s affected leg is extended and passively elevated. Pain elicited in a sciatic nerve distribution past the knee indicates a positive test. Pain elicited in the back alone is not considered positive. The crossed straight leg raise compliments the straight leg raise well in that it has a sensitivity of 28% and specificity of 90%. The crossed straight leg raise is performed by passively elevating the extended unaffected leg. A positive test is signified by pain evoked in a sciatic nerve distribution in the affected leg. Atraumatic sciatica does not necessitate imaging. Imaging should be sought when there is concern for infection or malignancy or when significant neurologic deficits are present (e.g., marked weakness, numbness, or bowel/bladder dysfunction). MRI is the preferred imaging modality in these cases. Treatment of sciatica is largely symptomatic with the use of non-narcotic analgesics, preferably nonsteroidal anti-inflammatory drugs, and activity as tolerated. Steroids and neuropathic pain medications have not shown significant efficacy in sciatica. With conservative management, most patients’ symptoms resolve after six weeks. Surgical treatment via discectomy is reserved for patients who have failed conservative management. However, while studies have shown short-term improvement in pain control after surgery, no difference in long-term pain control has been found between conservatively and surgically managed patients.

Crossed leg raise alone (A) has good specificity, but poor sensitivity. Crossed straight leg raise and straight leg raise (B) should be used together, however the straight leg test has the highest sensitivity and the crossed straight leg raise has the highest specificity. Straight leg raise alone (C) has good sensitivity, but poor specificity.

This young patient with low back pain and morning stiffness that improves with exercise most likely has ankylosing spondylitis. Ankylosing spondylitis is an inflammatory arthritis that primarily affects the spine and is associated with human leukocyte antigen (HLA-B27). Diagnosis is made using a combination of clinical symptoms, lab testing, and radiographic findings suggestive of sacroiliac joint pathology. Classically, X-ray imaging shows fusion of vertebrae (“bamboo spine”) as the peripheral fibers of the intervertebral annulus fibrosus discs ossify. However, symptoms can be present up to 10 years before radiographic evidence of the disease is apparent. Patients generally present with arthritic symptoms most apparent in the lower back, but can also have enthesopathy (as in this patient’s Achilles tendon pain), uveitis, and fibrosis of the upper lobes of the lung. The sacroiliac joint can be tested by flexing, abducting, and externally rotating one leg (FABER test). If pain is elicited on the posterior, contralateral side, it is suggestive of sacroiliac joint pathology. If pain is elicited on the anterior, ipsilateral side, it is suggestive of pathology within the hip. The mainstay of treatment is nonsteroidal anti-inflammatory drugs (NSAIDs) along with tumor necrosis factor antagonist medications.

Osteoarthritis (B) can also cause back pain, but generally affects older patients and usually improves with rest rather than worsening. The sacroiliac joints are rarely affected. Rheumatoid arthritis (D) can cause arthritic pain in younger individuals with morning stiffness, but usually affects small joints (hands, feet, and cervical spine). Osteofibrous dysplasia (C) is a fibrovascular defect of the long bones that leads to replacement of cortical bone with fibrous tissue. The disease is usually painless and spinal involvement is extremely rare.

Rhabdomyolysis is the result of the breakdown of skeletal muscle releasing the intracellular contents into the bloodstream. In minor cases, patients are asymptomatic but with severe cases the condition is life threatening with severe electrolyte disturbance and renal failure. The ultimate final pathway in rhabdomyolysis is the accumulation of intracellular cytoplasmic calcium which leads to myocyte destruction. This occurs as a result of direct cell membrane damage and ATP depletion. The hallmark of diagnosis is the presence of elevated serum creatine kinase and myoglobinuria. Management of rhabdomyolysis involves treating or removing the underlying cause, correcting electrolyte abnormalities and prevention of renal failure. Intravenous fluid administration is the mainstay of therapy titrating to a goal urine output of 3 mL/kg/hr.

Standard therapy used to include alkalinization of both serum and urine with the administration of sodium bicarbonate. An alkaline pH of the urine (A) above pH of 6.5 is the goal in alkalinization. This is not achieved with intravenous normal saline as described in the vignette. Intravenous fluid should be continued until clearance of the plasma creatine kinase. Precise guidelines do not exist, but the goal CK should be a level less than 1000 U/L, not 15,000 U/L (B). A creatinine less than 1.0 mg/dL (C) is not a standard goal of hydration for rhabdomyolysis. If renal failure is present, hydration will continue until improvement although no specific value is identified as the target.

The subacromial space is an area between the coracoacromial arch and the greater tuberosity of the humerus. It contains the long head of the biceps tendon, the supraspinatus tendon, and the subacromial bursa. Subacromial bursitis is most often an overuse injury due to chronic impingement. Patients who participate in frequent overhead activity are most at risk. The most common complaints are pain with overhead movement and difficulty finding a comfortable position at night due to pain. On physical examination, they likely will have a positive Neer impingement sign (pain with arm in 180 degrees forward flexion, followed by internal rotation) and Hawkins impingement sign (pain with arm in 90 degrees abduction, elbow flexed at 90 degrees, followed by internal rotation). Initial treatment is conservative with rest, nonsteroidal anti-inflammatory drugs and activity modification. Some patients may need additional physical therapy or a subacromial bursa steroid injection. Those with continued pain may proceed to further imaging with ultrasound or MRI and consideration of decompression surgery with orthopedics.

Acromioclavicular separation (A) involves partial or complete tearing of the acromioclavicular and coracoclavicular ligaments. It follows an injury to the shoulder, most often a direct or blunt hit to the shoulder. On examination, there is often a notable deformity at the AC joint along with associated tenderness to palpation. Adhesive capsulitis (B) or “frozen shoulder” is an inflammatory reaction within the capsule and synovium of the glenohumeral joint. It results in significant global loss of active and passive range of motion of the shoulder (forward flexion, abduction, external rotation and internal rotation). It can occur following an injury or spontaneously in those with autoimmune disorders such as diabetes or hypothyroidism. Full-thickness supraspinatus tear (C) most often occurs following an acute injury and presents with an inability to abduct the arm and a positive empty can test (unable to hold arm in 90 degrees of abduction with internal rotation).

auda equina syndrome results from compression of the conus medullaris and nerve roots, most commonly fromherniated discs, bone fragments, hematomas, epidural abscess, tumors, or vascular insufficiency. The compression classically occurs below L1. Patients present with complaints of low back pain, lower extremity pain, paralysis or paresthesia, saddle anesthesia, impotence, and bowel or bladder dysfunction. Urinary retention is the most consistent finding with a sensitivity of 90%. A thorough history about recent spinal procedures, trauma, anticoagulation, intravenous drug use, and malignancy help aide in determining the cause. On physical examination, lower extremity deficits, whether sensory or motor, may be present. Frequently asymmetric and unilateral signs and symptoms are present. Absent or decreased rectal tone and bulbocavernosus reflexes and a palpable bladder due to urinary retention may also be present. Patients with a suspicious history and physical concerning for cauda equina require emergent MRI imaging for evaluation. CT myelogram may be utilized in patients unable to have an MRI performed. Treatment consists on surgical decompression by a spine surgeon.

Fecal incontinence (A), motor deficits (B), and saddle parenthesis (C) all may or may not be present in a patient with cauda equina syndrome, but none of these symptoms are the most sensitive.

Rhabdomyolysis is the breakdown of striated muscle resulting in release of intracellular contents into the extracellular fluid and circulation. This can result in a spectrum of disease severity ranging from asymptomatic elevation of muscle enzymes to life-threatening electrolyte imbalances, acute renal failure, multiorgan failure, and death. There are several causes of rhabdomyolysis such as exertion, drugs and toxins, trauma, infections, electrical current, hypoxia, hyperthermia, or metabolic disorders. However, in the United States, it occurs most often due to prolonged muscle compression in the intoxicated patient who lays motionless or in the elderly with dementia following a fall. Patients classically present with complaints of muscle weakness, myalgias, and tea-colored urine. Physical examination may reveal muscle weakness, tenderness and swelling, or skin color changes, such as blistering or discoloration. Compartment syndrome should be considered if the exam reveals a firm compartment, pain on passive extension, and neurovascular compromise. The diagnosis of rhabdomyolysis can be made with a creatine kinase level greater than five times normal. Other laboratory abnormalities may include an elevated serum myoglobin, myoglobinuria, large blood on urinalysis with the absence of red blood cells, hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and hypoalbuminemia. The mainstay of treatment is with high volumes of normal saline to maintain a urine output of 200 to 300 mL/hr. Urine alkalinization theoretically enhances renal myoglobin clearance and can be achieved by adding bicarbonate to the intravenous fluids to maintain a urine pH greater than 6.5. This can be used as an adjunct, however, there are potential adverse effects such as hypernatremia, fluid overload, and exacerbation of hypocalcemia.

Elevated creatinine (B) may be seen in rhabdomyolysis that is complicated by acute renal failure, however, it is not diagnostic. Hypokalemia (C) is not diagnostic of rhabdomyolysis. Potassium levels are typically elevated in rhabdomyolysis. Large blood on urinalysis with red blood cells present (D) is not diagnostic of rhabdomyolysis, however, large blood on urinalysis with the absence of red blood cells is diagnostic of rhabdomyolysis and is due to myoglobinuria.

Pain with passive stretch of the effected compartment is the most common symptom early in compartment syndrome. Compartment syndrome develops when pressure builds within a confined anatomical space. Increasing pressure leads to decreased perfusion compromising tissue. Tissue ischemia eventually leads to death of muscle, nerve and bone tissue. Although it is typically associated with major trauma and crush injuries, it can develop after a relatively minor injury. Any compartment that is prescribed by fascial planes can develop compartment syndrome. However, the lower extremities are the most common location due to their higher risk for injury and their relatively low-volume compartments. Long-bone fractures account for 75% of all traumatic compartment syndromes. Patients will present with pain that is often out of proportion to examination.

Although pallor (B), parasthesias (C), pulse deficit (D) and paralysis are four of the classic symptoms, pain with passive stretch of the muscles involved is the most common early finding. Early recognition is key as prompt decompression can be limb saving.

Grade IA recommendation is for early activity and to avoid bed rest (by RCT).

The first choice for patients with mild to moderate back pain should be acetaminophen or a nonsteroidal anti-inflammatory drug (NSAID) like ibuprofen or naprosyn. In patients with severe pain, opiate medications may be necessary. However, it is important to note that no studies have demonstrated the superiority of one pain medication (or class of medication) over another in the treatment of back pain. Patients with milder symptoms should initially be treated with acetaminophen or an NSAID. These medications are well tolerated in short courses with minor side effects. NSAIDs have not been shown to be superior to acetaminophen.

The rim sign represents additional overlap between the glenoid and humeral head.
The light bulb sign is due to internal rotation of the humeral head that moves the greater tuberosity out of its normal lateral position on the AP view, causing the head to look more circular.
The trough line sign is an additional line within the humeral head that represents the trough of an impaction fracture (reverse Hill–Sachs deformity).

Clavicle fractures are the most common fracture in children. 80% of clavicle fractures are in the middle third of the clavicle. Most heal without fixation and very rarely require reduction in the ED. A sling is equivalent to a figure-of-eight splint for immobilization of a clavicle fracture

Pseudogout generally affects middle-aged and elderly patients. Pseudogout is a type of crystal-induced synovitis that is caused by calcium pyrophosphate crystals. These crystals are positively birefringent and are rhomboid shaped. Patients will present complaining of joint pain, swelling, and redness. Joints most commonly affected are the knee, wrist, ankle, and elbow. Pseudogout is a type of inflammatory arthritis that is diagnosed and confirmed by synovial fluid analysis. Synovial fluid for an inflammatory arthritis will have a white blood cell count between 200 and 50 000 with a predominance of neutrophils (generally greater than 50%). The appearance of the synovial fluid will be cloudy and yellow with positive birefringent, rhomboid shaped crystals. Treatment includes the use of nonsteroidal anti–inflammatory drugs and opioid analgesics. Corticosteroids are an option in patients with a history chronic kidney disease or patients the provider thinks may be of benefit. Avoid corticosteroids in uncontrolled diabetics given the risk of worsening hyperglycemia. Colchicine is not routinely used due to its side effect profile, however, it may be used in refractory cases or in cases where NSAIDs and corticosteroids cannot be used.

Gout (A) is also a type of inflammatory crystal-induced synovitis, however, it is caused by uric acid crystal deposition. Gout generally affects middle-aged and elderly patients. Uric acid crystals are needle shaped and are negatively birefringent. Patients will present complaining of arthritis, edema, and erythema. The joints most commonly affected are the great toe, tarsal joints, and knee. Synovial fluid analysis will be similar to pseudogout, as both are an inflammatory arthritis. Differentiating the two is based on the characteristic crystal formation. Thus, crystal analysis is imperative to the correct diagnosis. However, treatment remains the same as with pseudogout and so synovial fluid analysis is performed more to rule out septic arthritis. Osteoarthritis (B) is a symmetric and chronic polyarticular joint disease distinguished by the lack of constitutional symptoms. Patients may present with acute exacerbations of monoarticular pain that consists on joint pain and inflammation. Synovial fluid analysis will demonstrate a white blood cell count of less than 200 cells with fewer than 25% neutrophils. The synovial fluid will be have a clear and transparent appearance without crystals. Treatment consists of rest and analgesics. Septic arthritis (D) is a condition that can rapidly lead to irreversible joint destruction if not recognized and treated. Patients will typically present with a monoarticular arthritis and may have associated fever, chills, and malaise. Septic arthritis should be differentiated from periarticular processes such as cellulitis, bursitis, and tendinitis. A true arthritis will produce pain that is exacerbated through active and passive range of motion. Synovial fluid analysis for septic arthritis will demonstrate a significantly elevated white blood cell count typically greater than 50 000 cells with a predominance of neutrophils (greater than 50%). The synovial fluid will be cloudy and yellow in appearance. Admission for parenteral antibiotics and repeated needle aspiration, arthroscopy, or open surgical drainage is required.

The patient in this question is presenting with a history and exam that are consistent with acute-on-chronic osteoarthritis. Osteoarthritis is defined as joint destruction that generally involves the distal interphalangeal joints with polyarticular exacerbations, but patients may present with an acute monoarthritis typically in the knee. Effusions are usually small and difficult to aspirate. Any fluid that is aspirated is noninflammatory. Patients usually do not have other systemic symptoms. Radiographs demonstrate joint space narrowing due to destruction of articular cartilage. Treatment includes joint rest and nonsteroidal anti–inflammatory agents such as ibuprofen.

Opioid medications such as acetaminophen with hydrocodone (A) have been shown to decrease pain in patients with osteoarthritis, however, adverse effects, particularly in older patients, limit opioid use, and in the ongoing opioid epidemic these medications should not be used as first-line therapy. Colchicine (B) is an alternative first-line treatment agent for patients with knee pain and swelling due to gout, a crystal-induced synovitis. The patient in this question is not presenting with a classic gouty flair, as typically gout presents with knee pain, swelling, redness, and sometimes warmth. Additionally, osteoarthritis is not treated with colchicine, as it is not an analgesic medication. Systemic corticosteroids such as prednisone (D) are not indicated for osteoarthritis, but intra-articular corticosteroids such as triamcinolone have been shown to improve pain for months in such patients. The corticosteroid injections can be performed by the patient’s primary physician or an orthopedist.

Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000.

Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence or absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate gouty arthritis versus septic arthritis.

Septic Arthritis

• Patient will be complaining of fever, monoarticular pain with decreased ROM
• Labs will show WBC > 50,000 with > 75% PMNs
• Diagnosis is made by arthrocentesis
• Most commonly caused by:
  • Age < 35: N. gonorrhea, S. aureus overall
• Treatment is IV ABX, surgical washout

Allopurinol therapy should never be initiated until an acute attack has subsided. Allopurinol is a xanthine oxidase inhibitor that decreases uric acid production but also produces a more soluble metabolite. Allopurinol is therefore effective regardless of the cause of the hyperuricemia. Gout is caused by deposition of uric acid crystals in the synovium, bursae, tendon sheaths, skin, heart valves, and kidneys, which can lead to arthritis, tophi, renal stones, and gouty nephropathy. Typically, patients present with acute, exquisitely tender, monoarticular arthritis. The joint is usually warm and erythematous. The first metatarsophalangeal joint (MTP) joint is most commonly affected. Detecting negatively birefringent, needle-like crystals in the synovial fluid from an arthrocentesis confirms the diagnosis. First line treatment are NSAIDs. Indomethacin has traditionally been the NSAID of choice, but any NSAID can be used with similar efficacy.

Ethanol metabolism blocks renal excretion of uric acid which increases the risk for developing gouty arthritis. However, allopurinol is not contraindicated in individuals who consume ethanol (B). Hyperuricemia (C) is present (usually >8 mg/dL) in the gout patient, and when symptomatic, these patients should be treated. Colchicine (D) can be used in combination with allopurinol to help decrease the likelihood of a gouty flare while the uric acid level is decreasing after an acute attack has subsided. Colchicine decreases inflammation associated with lactic acid production and phagocytosis of urate; it terminates most gouty attacks within 6 to 12 hours but is limited by GI side effects.

Gout

• Patient will be a middle-aged man
• Complaining of acute onset of pain in the first MTP (Podagra)
• Labs will show needle-shaped crystal with negative birefringence
• Most commonly caused by uric acid crystals
• Treatment is:
  • Acute: NSAIDs, steroids, colchicine 
  • Chronic: allopurinol or colchicine
• Comments: Can be triggered by loop and thiazide diuretics

With pain along the proximal portion of her arch worse in the morning, plantar fasciitis is the most likely diagnosis. Morton neuroma is a forefoot pain. With a negative Tinel sign, tarsal tunnel syndrome is ruled out. Achilles tendonitis is a posterior heel pain.

Hypothenar Hammer Syndrome: Raynaud sign Hypothenar Hammer Syndrome does not have a specific diagnostic test affiliated with it. Diagnostic maneuvers include tenderness to palpation over the hypothenar area, which may indicate the presence of an ulnar artery aneurysm. The fingers or fingertips may be cold, pale, mottled, atrophic, or ulcerated, and a positive Allen test may suggest an ulnar artery pathology.

A Tinel sign is positive if light tapping over the median nerve at the wrist causes a tingling sensation distally along the median nerve and is useful in the diagnosis of Carpal Tunnel Syndrome.

The Finkelstein test requires that the patient flex the thumb into the palm and then grasp it with the other fingers of the hand. The patient then actively performs ulnar deviation of the wrist. Severe, sharp pain with this maneuver constitutes a positive test and is pathognomonic of de Quervain tenosynovitis.

Froment sign occurs when the adductor pollicis muscle, innervated by the ulnar nerve, is weak. This sign is elicited by having the patient tightly hold a piece of paper between the thumb and the radial side of the index finger while the examiner attempts to pull the paper from the patient. Flexion at the thumb interphalangeal joint (indicating weakness of the adductor pollicis muscle) results in a positive Froment sign. Comparison should be made with the patient’s other hand.

Although disseminated gonococcal disease must be considered, this patient has Reiter syndrome (reactive arthritis), also termed reactive arthritis. These patients are colloquially known to complain they “can’t pee, can’t see, can’t climb a tree.” Conjunctivitis and iritis can be a serious complication that must be actively ruled out.

An elevated hemiscrotum (elevated testicle) with transverse lie is suggestive of testicular torsion, resulting from twisting and foreshortening of the spermatic cord. A palpable bulge in the inguinal region may be present in the case of inguinal hernia, epididymal tenderness in epididymitis, and scrotal ecchymosis in genitourinary trauma.

A positive prehn sign (relief with lifting of the testicle), indicates epidydimitis. NEGATIVE prehn may suggest torsion (no relief).

This patient is presenting in severe sepsis and Fournier’s gangrene. Empiric antibiotics and medical resuscitation should be administered, but this patient requires emergent surgical debridement for definitive treatment. While hyperbaric oxygen has been used in the treatment of necrotizing fasciitis, it is an adjunctive therapy.

When a child presents with abdominal pain, nausea and vomiting, one must perform a testicular/scrotal exam to rule out acute scrotal or testicular pathologies. In this case, the presence of a swollen right testicle and scrotal pain but negative ultrasound findings is concerning for intermittent testicular torsion. It is important to remember that testicular torsion is a clinical diagnosis, requiring a high index of suspicion, even in the face of early, unremarkable ultrasound findings. Blue-dot sign is typically seen in torsion of the appendix testis. Pain alleviation with testicular elevation is seen in epididymitis. The treatment of testicular torsion starts with manual detorsion, followed by timely surgical detorsion and fixation.

The patient in this case has priapism. Given the history of sickle cell disease, and no preceding trauma, this is likely the ischemic, or low-flow type of priapism. All of the above treatment options are appropriate for low-flow priapism, with the exception of angiography with embolization, which is used for high-flow priapism. Other treatment options for low-flow priapism include intracavernosal aspiration and surgical shunt placement. Urology consultation should be obtained for low-flow priapism.

Testicular pain, swelling, and asymmetric hyperemia of epididymis on ultrasound are suggestive of epididymitis. Epididymitis is a clinical diagnosis, combined with ultrasound examination and urinalysis. The choice of antibiotics follows an arbitrary division at age 35. Younger than 35 years of age, patients are treated with ceftriaxone and azithromycin for presumed Chlamydia and Gonorrhea infection. After 35 years of age, patients are treated with fluoroquinolone for presumed E. coli infection. Analgesics and scrotal elevations should be recommended. Prehn’s sign is a relief of pain with scrotal elevation and is seen in epididymitis, as opposed to no changes in pain in testicular torsion. Emergent urology consultation is not required, but patient may follow up with urology as outpatient.

Amiodarone can cause a chemical epididymitis, which is characterized by testicular pain and swelling. This effect is more common with chronic (greater than 4 months) and high dose (more than 400 milligrams per day) amiodarone use. Amiodarone concentrates in the testicle where is causes lymphocytic infiltration and fibrosis. Unlike patients with infectious epididymitis, patients do not experience fever, pyuria, or leukocytosis.

This patient presents with phimosis and evidence of vascular compromise requiring performance of a dorsal slit procedure. Phimosis occurs when the foreskin of an uncircumcised penis becomes constricted preventing retraction of the prepuce from the glans. It results in urinary outlet obstruction, glans ischemia and infarction. Many cases are physiologic resulting from normal development. Patients typically present with an unretractable foreskin and symptoms consistent with urinary obstruction including decreased urinary stream. Management of phimosis can be difficult. Dilation of the prepuce can be performed using forceps but often does not result relief of phimosis. When there are signs of glans vascular compromise (i.e. discoloration) a dorsal split procedure should be performed. During this procedure, the foreskin is anesthetized and incised dorsally allowing for retraction.

The patient presents with balanitis, which results from inflammation of the glans penis or the glans and foreskin (balanoposthitis). The primary cause is infection, most commonly Candida. Treatment consists of  topical antifungal. Balanitis can also be caused by bacterial agents such as group A beta-hemolytic streptococci. Additionally, it may be secondary to irritation, trauma or contact dermatitis. Recurrent balanitis is seen in diabetics from C. albicans. Patients typically complain of pain, discharge, and itching. The glans may appear erythematous and tender to palpation. Systemic symptoms may be present but are unusual. Management of fungal balanitis includes topical antifungal agents such as clotrimazole, adequate hygiene and glycemic control. In patients with no history of diabetes who present with fungal balanitis, diabetes should be considered and a finger stick should be obtained.

Phimosis is the inability to retract foreskin over the glans penis. It is a complication seen in uncircumcised men. About 50% of boys typically are able to retract their foreskin by 1 year of age and 80% by age 3. Topical estrogen therapy has been reported as successful, but no randomized trials support its use. However, low-potency topical corticosteroid therapy combined with daily prepuce retraction appears effective for phimosis. If retraction of foreskin is unsuccessful, the patient will require circumcision.

Testicular torsion usually occurs over an arc of 540 to 720 degrees. Manual detorsion generally requires one to three turns in the medial to lateral direction (“opening a book”) to restore blood flow and relieve pain, and is successful in up to 70% of patients. It is best carried out with the patient supine in a frog leg position.

Although the patient’s examination is consistent with BPH (associated with increased rates in asymptomatic hematuria), he is also at risk for urologic malignancies and needs urgent referral to urology for further evaluation. His urinalysis and lack of symptoms rule out a urinary tract infection as a cause for the hematuria. If urolithiasis is suspected, a noncontrast CT scan should be ordered to confirm the diagnosis.

Acute tubular necrosis accounts for up to 85% of intrinsic renal failure in adults and might occur in the described patient due to the combined renal insults of ischemia secondary to shock and intravenous contrast. Acute interstitial nephritis is a far less common cause of intrinsic renal failure in adults and is usually caused by a drug hypersensitivity reaction. The patient described in this scenario is unlikely to have postrenal azotemia, which is due to obstruction, given the case details. Hemolytic uremic syndrome is classically a disease of children.

Diuresis in an already dehydrated and therefore pre-renal patient may lead to worsening renal function due to renal ischemia. A “trial of diuretics” is not generally advised and is not without risk to the patient. There is no compelling evidence that the combination of diuretics and dopamine helps to prevent progression to end-stage renal disease for oliguric acute renal failure patients. Therefore neither can be considered “routine” therapeutic interventions.

Peritonitis is a fairly common occurrence in patients maintained on CAPD. It is usually initially recognized when peritoneal fluid is noted to be cloudy at the time it is drained for a routine exchange. With prompt medical attention, including microbiologic evaluation of peritoneal fluid, patients can be treated with intraperitoneal antibiotics as outpatients after an initial intraperitoneal dose is given in the ED. The prognosis of uncomplicated peritonitis is generally excellent, and patients are typically asked to follow up in 2 days. Free air seen on abdominal plain film is most often due to air being introduced during a previous fluid exchange. CT scanning is not indicated unless there is severe abdominal pain and tenderness or other findings suggestive of perforation.

Vascular access infections are not uncommon in hemodialysis patients, and patients may present with fever alone, and no local or systemic findings. Although bacteremia is often found, endocarditis is unusual in the absence of prolonged or recurrent fever, or of the usual risk factors for infective endocarditis. The hemodialysis procedure itself rarely causes fever.

A 25-year-old man is brought from the hemodialysis unit because of hypotension that occurred during dialysis. His blood pressure is currently 94/60, pulse is 84, and he is afebrile. Physical examination is otherwise normal. An ECG is unchanged from a previous tracing. Which of the following is most accurate?

Infected obstructing urolithiasis is a urologic emergency. A critical aspect of treatment is prompt decompression of the renal collecting system by percutaneous nephrostomy catheter or retrograde ureteral stent placement. While adjunctive therapy with broad-spectrum intravenous antimicrobials is important, decompression remains the critical intervention. Foley catheter placement and monitoring of urinary output are important adjunctive interventions in patients with a variety of conditions such as sepsis.

Suprapubic catheters are prey to a number of complications including occlusion by debris or mucus. A clogged suprapubic catheter can be flushed with saline as a first attempt to unclog it. Suprapubic catheters should be changed every 4 to 6 weeks. The tract created by a suprapubic catheter may close rapidly if the tube is removed within the first month; thereafter, rapid tract closure is not a concern.

Commonly tested on boards. Calcium oxalate is the most common type of renal stone, accounting for more than 70% of all stones.

Do not miss an infected kidney stone. Calculous pyelonephritis is a urologic emergency and must be excluded in patients presenting with renal colic.

Perilunate dislocations, as well as perilunate fracture dislocations, are among the most devastating closed wrist injuries. They are often missed on initial evaluation and imaging. Most cases involve dorsal dislocation of the capitate and carpus relative to the lunate, while the lunate remains in near-normal alignment with the radius. Volar perilunate dislocations are possible but rare. An important pitfall, besides missing the injury altogether, is misdiagnosing the injury as a lunate dislocation, which can closely mimic a perilunate dislocation, especially on AP projection. The key to not confusing the two is the lateral projection. On a normal lateral wrist X-ray the capitate, lunate, and distal radius articulate with each other and lie in a straight vertical line, like an apple in a cup sitting on a saucer. The radius (the saucer) holds the lunate (the cup), and this cup contains the capitate (the apple). In a perilunate dislocation, the radiolunate articulation is maintained, but the capitate is not sitting within the distal articular “cup” of the lunate. In a lunate dislocation, on the other hand, the radiolunate articulation is disrupted and the lunate is tipped towards the palm, which is known as the “spilled teacup” sign. Although the diagnosis can be made on plain film, CT plays an important role in assessing for commonly associated occult fractures. A scaphoid fracture is found in approximately 60% of perilunate dislocations; this is then called a trans–scaphoid perilunate dislocation. Perilunate dislocations typically occur in young adults who suffered a high energy trauma, such as a motor vehicle collision, a fall from height, or an injury during a sporting event, resulting in loading of a hyperextended, ulnarly deviated hand, with the angle of this hyperextension determining the extent of injury. Patients may present with obvious marked swelling and deformity, or more subtly, complaining simply of a sprained wrist. A thorough trauma survey with assessment for associated injuries of the head, spine, thorax, and extremities is essential, due to the high energy mechanisms. Orthopedic or hand consultation is required. Like other dislocations, the perilunate dislocation is an emergency and should be reduced as soon as possible. If closed reduction cannot be achieved in the ED, the patient must be taken to the operating room for open reduction. Once the fracture is reduced, definitive treatment can be delayed until the patient’s condition allows additional intervention. Despite early and accurate treatment, stiffness, weakness, and degenerative osteoarthritis commonly occur in the long term. Latent carpal instability is one of the most feared complications and is especially difficult to prevent.

Bonus: what is the most feared complication of perilunate dislocation?  => Median nerve palsy

The coronal reconstruction from a cervical spine CT scan pictured above reveals a type III fracture of the second cervical vertebra. There are three common varieties of fracture of the second cervical vertebra involving the dens, or odontoid process, which articulates with the ring of the first cervical vertebra and which are most common seen in the elderly. The characteristic appearance of the fracture which involves the body of the second cervical vertebra is typical for type III fractures. Type II fractures present at the junction of the odontoid process and the vertebral body. Type I fractures involve the tip of the odontoid process.In neurologically intact patients, these fractures are typically initially treated non-operatively with a trial of cervical immobilization in a hard collar.

It is thought that odontoid fractures are more common in older individuals due to age-related bone loss coupled with the fact that there is disproportionate bone loss in the second cervical vertebra at the base of the odontoid process. Since patients who are 1 to 20 years of age (A), 21 to 40 years of age (B), and 41 to 65 years of age (C) are at lower risk of osteoporosis, they are at less risk for a type III odontoid fracture as compared individuals older than 65 years of age.

Nasal bone fractures account for almost half of all facial fracture injuries. Assaults and sports injuries cause the majority of these injuries. The nose is easily exposed to trauma as it is the most anterior and prominent feature of the face. The frontal sinus is protected by a thick cortical bone and is typically more resistant to fracture than other facial bones. Frontal sinus fractures occur only with high impact traumas such as motor vehicle collisions, assaults with weapons, and industrial accidents. Because of the high energy required to fracture the frontal sinus bone, it is rare to find an isolated fracture without other underlying intracranial pathology. Taking this information into consideration the facial bone LEAST likely to fracture is the frontal sinus bone and the facial bone MOST likely to fracture is the nasal bone.  

Mandible fractures are more common in higher impact injuries such as motor vehicle collisions, sports injuries and interpersonal violence. Most fractures occur at the angle of the mandible or the mandibular condyle. A decent blow to the face during a fight is enough to fracture the mandible making it more likely to break than the frontal bone; hence mandible is least likely and maxilla is most likely (B) is incorrect. Fractures of the maxilla are often the result of high energy blunt force from motor vehicle collisions and falls. Because of its relationship with the orbital bones, nasal cavity and oral cavity, maxilla fractures can be life threatening and disfiguring. Zygomatic fractures typically occur secondary to motor vehicle collisions. Due to the thickness of the bone, isolated zygomatic fractures are uncommon. Taken together this information means that the maxilla is LEAST likely and zygoma is MOST likely (C) is incorrect. Orbital fractures commonly occur in men in the third decade of life secondary to motor vehicle collisions or interpersonal violence. Orbital fractures typically do not occur in isolation as the orbits are set back in the facial structure. The weakest portions of the orbit, and therefore the most frequently fractured, include the orbital floor bones, the maxilla and the lamina papyracea. A direct blow to the eye frequently causes a blow out fracture of the orbital bones; however, this fracturing likely helps to prevent globe rupture. It is easier to fracture the orbital bones (D) than many other facial bones, but nasal fractures are still more likely than orbital fractures.

Important historical information when assessing a patient with a hyphema includes a family or personal history of sickle cell disease or trait, which contributes to a higher risk of complications due to sickled erythrocytes becoming stuck within the trabecular mesh through which fluids drain. This results in increasing intraocular pressure and related microvascular occlusions or retinal and ocular nerve ischemia. These patients require aggressive treatment. Also, a history of other bleeding disorders may indicate difficulty in controlling hemorrhage, as does use of anticoagulants, aspirin, other nonsteroidal anti-inflammatory agents, and alcohol. The time of injury is also important because the chance of rebleeding increases when the development of the hyphema occurred over 24 hours prior to evaluation. Rebleeds tend to occur from two to five days after the injury and put the patient at more risk of corneal staining, development of post-traumatic glaucoma, and delay in resolution of the hyphema.

Helmet use with injury (A) is incorrect. Helmet use may be relevant to other possible injuries, but not specifically to determining a patient’s risk of complications related to the hyphema. Loss of consciousness with injury (B) is incorrect. Loss of consciousness may be an indicator of other potential injuries and their acuities, but it does not directly relate to risk of hyphema complications. Use of eyeglasses or contact lenses at time of injury (D) is also incorrect. While this information may be useful in determining whether other ocular or periorbital injuries are likely, it does not directly relate to risk of complications from the hyphema.

Pediatric injuries involving the physis (growth plate) are characterized using the Salter-Harris classification. This classification describes the fracture line relative to the physis. Injuries of the physis may affect normal bone growth and development, so orthopedic intervention may be necessary depending on the severity of the fracture type. Salter-Harris type I fractures occur when the epiphysis slips off the metaphysis with no associated fracture fragment. Type I injuries rarely affect skeletal development. Salter-Harris type II injuries extend into the metaphysis and are the most common of the Salter-Harris injuries. Salter-Harris type III injuries extend into the epiphysis. Salter-Harris type IV injuries involve the metaphysis, the physis, and the epiphysis. Salter-Harris type V injuries result from axial loading mechanisms and crush the epiphysis. These may be radiographically silent but often impact normal bony development.

Fractures with dislocation (B) may not involve the growth plate and are not part of the Salter-Harris classification. Intra-articular compaction (C) is seen in Salter-Harris type V injuries. Metaphyseal extension (D) is seen in Salter-Harris type II injuries.

The patient presents with hemorrhagic shock and an “open-book” pelvic injury and should immediately have an external pelvic binder placed. Unstable pelvic injuries are typically caused by high-energy impact as seen in motor vehicle collisions. The exact fracture pattern depends on the type of injury. Anteroposterior (AP) compression forces causes disruption near the symphysis pubis and sacroiliac joint opening resulting in the “open-book” pelvic injury. This injury can be diagnosed on an AP pelvic X-ray if the diastasis of the pubic symphysis is >2.5 cm. The high-forces from the injuries cause shearing and tearing of blood vessels leading to hemorrhagic shock. Examination of the pelvis will reveal gross instability. “Rocking” of the pelvis is discouraged as this force may dislodge clots that have formed. Instead, the greater trochanters should be grasped with both hands and gently squeezed together. Any movement with this procedure indicates an unstable pelvic fracture. Once an unstable pelvic fracture is recognized, it should immediately be stabilized with either a properly applied sheet and towel clamps or a commercial pelvic binder. Patients who have immediate stabilization have been found to have lower transfusion requirements. Additionally, the AP injury pattern stands to benefit the most from external stabilization.

Angiographic embolization (A) and CT scan of the abdomen and pelvis (B) may be useful in diagnosis and management of pelvic fractures and hemorrhage into the pelvis but the patient should not be transferred until they are more stable. Diagnostic peritoneal lavage (C) plays a role in differentiating between abdominal and pelvic injuries in unstable patients but should be deferred until after external pelvic stabilization has been applied.

In order to fully understand the different syndromes of injuries to the spinal cord, it is imperative to understand the location of the tracts of the cord. The posterior columns carry tracts responsible for ipsilateral position and vibratory sensation. The lateral spinothalamic tract carries fibers for contralateral pain and temperature. The lateral corticospinal tract is responsible for ipsilateral motor function. Syndromes may be incomplete depending on how much of the cord is affected by the injury. In the anterior spinal cord syndrome, just the posterior columns are preserved and so patients lose all pain and temperature sensation as well as motor function. Most cases of anterior cord syndrome follow aortic surgery, but it has also been reported in the setting of hypotension, infection, vasospasm, or anterior spinal artery ischemia or infarct. In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord.

Loss of all motor and sensory function (B) occurs with a complete transection of the spinal cord. Most commonly this occurs after a significant trauma. Isolated motor function loss (A) is not a classic syndrome and would result from a small area of injury on the cord just involving the corticospinal tract. Upper greater than lower motor weakness occurs (D) with a central cord syndrome. Sensory involvement is variable although burning dysesthesias in the upper extremities may occur. Most commonly the syndrome occurs after a fall or motor vehicle accident. Anterior cord syndrome may also be known as ventral cord syndrome.

This patient presents with a myocardial contusion and should have an echocardiogram performed to look for any cardiac damage. Myocardial contusion describes a nebulous condition. It can occur through several mechanisms including a direct blow to the chest and compressive force over a prolonged period of time. Histologically, the disorder has similar findings to those seen after acute myocardial infarction. The majority of contusions heal spontaneously but small pericardial effusions may develop. Delayed rupture after resorption of a hematoma is a feared but rare complication. Patients with myocardial contusion will present after trauma with external signs of trauma and typically have other concomitant thoracic lesions (pulmonary contusion, pneumothorax, hemothorax). Patients will typically have tachycardia (up to 70%). ECG may show dysrhythmia or ST changes but may also be normal. Although myocardial contusion has a very low rate of cardiac complications and it is not effective to admit all patients for workup, in the presence of ECG changes and elevated biomarkers, observation and echocardiography are a reasonable approach. Echocardiogram can be used to diagnose pericardial effusion, thrombi formation, and valvular disruption.

Radial nerve injury is the most common nerve injury seen after humeral shaft fractures. These fractures usually occur from a direct blow to the arm and can be seen in falls and motor vehicle collisions. Patients present with severe pain, arm swelling, and decreased range of motion. The arm can be shortened or rotated in a complete fracture depending on the location of the fracture. A complete neurovascular exam should be performed as with all fractures and dislocations. The radial nerve may be injured during humeral fracture in up to 20% of patients. The injury is usually a neuropraxia and resolves spontaneously in most patients. However, this recovery can take months. Humeral fractures rarely need specific reduction maneuvers for treatment. They should be placed in a sugar tong splint and placed in a sling. Gravity alone is typically successful in fracture reduction.

The anterior cruciate ligament (ACL) is the primary stabilizer of the knee. It resists anterior translation of the tibia on the femur and is the most frequently injured major ligament of the knee. A tear results from deceleration, hyperextension or marked internal rotation of the tibia on the femur. The majority of ACL tears occur during sporting activities such as skiing, football, soccer, and basketball. Clinically, there is usually rapid development of hemarthroses, causing significant swelling. Almost half of individuals report feeling or hearing a pop, which is the most reliable factor. There is usually instability of the knee or a “wobbly” feeling. The Lachman test is the most sensitive test (approximately 98% sensitivity) showing increased anterior tibial displacement and a soft end point. MRI is rarely necessary to make a diagnosis. Rest, ice, crutches, immobilization and NSAIDs are common initial treatment options. Some competitive young patients may choose reconstruction as the best possible chance to return to successful play.

CT scan of the abdomen has rapidly become the imaging modality of choice in diagnosing small bowel obstruction (SBO) as it is both highly sensitive and highly specific. Patients with SBO present with crampy abdominal pain with nausea, vomiting, constipation and abdominal distension. The pain can be generalized and often will come in waves. The rapidity of onset of symptoms depends on how proximal the obstruction is. More proximal obstructions will have a more rapid onset and peak of symptoms. CT scan of the abdomen and pelvis is the diagnostic modality of choice as it has a high sensitivity and specificity and can give additional information including location of obstruction, cause of obstruction and alternative diagnoses.

The acute onset of abdominal pain with minimal tenderness on examination in an elderly patient is concerning for mesenteric ischemia. Patients with ischemia may develop rectal bleeding either with frank blood or hemoccult positive stool. As ischemic time increases, the lactic acid may become elevated. CT angiography is the gold standard for diagnosis. This is a disease of the elderly with a median age of 70. The differential diagnosis of acute severe abdominal pain also includes rupture or leak of an abdominal aortic aneurysm and in this case a 2 cm aorta (normal) was identified. Mesenteric ischemia most commonly involves the small bowel and right colon. Due to the presence of a larger supply of collateral flow, the left colon is rarely involved. The mesenteric vessels include the celiac trunk, superior mesenteric artery and inferior mesenteric artery. The intestines require a constant supply of blood and typically receive 20% of the cardiac output. As a result, injury occurs rapidly in the setting of acute ischemia. More than 50% of cases of mesenteric ischemia result from arterial embolization, most commonly from a cardiac origin (atrial, ventricular or valvular on the left side). Patients with atrial fibrillation are at high risk of developing mesenteric ischemia. The superior mesenteric artery (SMA) is at highest risk because of its large caliber and small angle of takeoff from the aorta. Once the embolus lodges in the SMA the gut becomes ischemic. Jejunum is at highest risk because it receives little collateral flow from the celiac trunk and inferior mesenteric artery.

The presentation of multiple individuals with diarrhea following a shared meal is highly suspicious for foodborne illness. Foodborne pathogens cause illness through a variety of mechanisms. Pathogens like Staph aureus, Bacillus cereus, and Clostridium botulinum (bolulism) exert their toxic effects via a preformed toxin. Toxins present in the food prior to ingestion cause rapid onset of symptoms, typically within 1-6 hours. Bacillus cereus is associated with watery diarrhea and lower abdominal cramping. Foods associated with Bacillus cereus include meats, gravies, stews, and vanilla sauces. Another mechanism by which pathogens cause symptoms is via bacterial production of toxin after ingestion, such as seen withVibrio, Shigella, and Shiga-toxin-producing E. Coli. Some toxins alter fluid and electrolyte movements, causing large volumes of fluid that overwhelms the colon’s ability to absorb them, leading to diarrhea. Other toxins directly disrupt cell membranes leading to cell death. Many pathogens, including enteric viruses, Salmonella,Campylobacter and Shigella directly invade the intestinal epithelium, leading to fever, abdominal cramping, and diarrhea which is sometimes bloody. For acute nonbloody diarrhea without systemic signs of illness, serum and stools studies are not typically required, and patients can be managed supportively.

Epiploic appendagitis is caused by inflammation of the pouches of serosal fat that line the large intestine called epiploic appendages. This is a rare cause of abdominal pain, but its presentation mimics appendicitis and diverticulitis and therefore is sometimes found on CT scan performed in the evaluation of lower abdominal pain. More than half of cases occur in the rectosigmoid colon. Epiploic appendagitis is an inflammatory condition likely caused by autoinfarction of the appendages from torsion. Rarely, colonic bacteria may accumulate in the area causing abscess formation. Most patients present with pain localized to the region of appendagitis. Pain is classically dull and non-radiating. Patients may develop fever and show leukocytosis on laboratory analysis. The condition is most often self-limited and treatment is with pain medication like nonsteroidal anti-inflammatories (NSAIDs).

Sensitivity or the true positive rate measures the proportion of actual positives that are correctly identified as such. It is determined by dividing the number of true positives of the test by the number of true positives + false negatives. Tests with a high sensitivity are good for ruling out disease as the test has very few false negatives. A test with high sensitivity is advantageous as a screening tool as it misses very few people with the disease. The onset of abdominal pain before vomiting has been found to be as high as 100% sensitive in diagnosing acute appendicitis.

The X-ray demonstrates massive dilation of the colon through the cecum consistent with a large bowel obstruction. However, CT scan does not show any obstructing lesion and therefore this is a pseudo-obstruction, also known as Ogilvie’s syndrome. The exact mechanism of the development of pseudo-obstruction is unknown but suspected to result from malfunction of the autonomic control of the bowel. Patients often have multiple other co-morbid conditions and risk factors include nursing home residence, anticholinergic medication, severe electrolyte disturbance, narcotic exposure, or a history of spine or retroperitoneal trauma. This is a diagnosis of exclusion. Patients may first be treated with a rectal tube and sigmoidoscopy and managed conservatively in the hospital. Neostigmine may be used as a pharmacologic intervention as its an acetylcholinesterase inhibitor.

Ischemic colitis is a syndrome caused by inadequate blood flow through the mesenteric vessels, resulting in ischemia and eventual gangrene of the bowel wall. The most important finding is pain that is disproportionate to physical examination findings. The pain is diffuse, and the patient may report frank blood in the stool. These patients typically have a history of atherosclerotic disease at other sites, such as coronary artery disease or cerebrovascular disease. Other risk factors include advanced age and tobacco use. Classic angiography is the diagnostic imaging of choice, however it is invasive and therefore in current clinical practice, computed tomography angiography is ordered much more frequently than classic angiography. Bowel wall edema is the most common finding on imaging. All cases of ischemic colitis with signs of peritonitis or possible bowel infarction, generally warrant immediate surgical intervention for the resection of the ischemic or necrotic bowel. If the ischemia is caused by vasospasm then surgery is not indicated and medical management with anticoagulants and intra-arterial vasodilators is appropriate.

Acute appendicitis is the most common surgical emergency in pregnant women. The rate of acute appendicitis in pregnant patients is the same as seen in nonpregnant patients. Unfortunately, delays in diagnosis lead to an increased rate of perforation, increased morbidity and mortality. Physiologic changes during pregnancy make diagnosis difficult. As the uterus grows, the abdominal organs are more distant from the abdominal wall making it difficult to detect tenderness and peritoneal signs. Additionally, the location of the appendix later in pregnancy is variable as it can rest anywhere between the right lower quadrant to deep within the right upper quadrant. Ultrasound, CT scan and MRI are all viable diagnostic tests depending on availability. However, on occasion, patients will require exploratory laparoscopy.

Octreotide is a useful addition to endoscopic sclerotherapy and decreases rebleeding occurrences. Patients with documented esophageal varices and acute upper GI bleeding should be treated with an intravenous infusion of octreotide at 50 µg/hr for a minimum of 24 hours while being observed in the intensive care unit.

Hives and bronchospasm in this patient point to excessive histamine release. In the setting of diarrhea, histamine release would most likely result from a parasitic infection. This is not common; however, it should be considered in patients presenting with diarrhea and histamine-induced skin changes. Of the choices listed, Giardia lamblia is the only parasite.

Reynolds pentad = Charcots triad (Fever, RUQ pain, and Jaundice), and adds two septic/toxic elements -> Hypotension and AMS!

This answer is tricky, but answers B-D can be ruled out.

Ascending cholangitis is typically treated with urgent biliary decompression and intravenous antibiotics. Reynolds pentad, although classically associated with ascending cholangitis, is rarely present and a high index of suspicion is required for diagnosis. In addition to common duct stones and biliary obstruction, cholangitis should be suspected in patients presenting with sepsis after ERCP.

Although biliary colic in the absence of acute cholecystitis can typically be managed as an outpatient with symptoms control and surgical referral, in special populations such as children and prolonged symptoms in pregnancy may require admission. Acute cholecystitis requires prompt (in ED) surgical consultation and admission.

The presence of this antibody either represents natural immunity from successfully resolved Hepatitis B infection or the desired response to vaccination

While an elevated serum ammonia level is highly indicative of hepatic encephalopathy, a normal level does not rule out the diagnosis. A head CT should always be considered in a patient with altered mental status. An elevated ethanol level may account for this patient’s symptoms, but with his confusion and history of liver disease, other sources must be explored. Blood glucose levels should be checked frequently since this patient with liver disease has likely impaired glucogenesis and reduced glycogen stores.

In severe acute liver failure, transplant is often the only means to improve survival. Thus, transfer to a transplant facility is vital. Oral charcoal is of no real benefit after approximately 3 to 4 hours after ingestion. N-acetylcysteine may still be of some benefit, even up to 48 hours after ingestion.

Despite the potential for pulmonary edema in acute hepatic failure, intravenous fluids should be given as part of the initial resuscitation. Propofol is a recommended agent for the patient requiring sedation. Flumazenil has not been shown to be efficacious in the patient with liver failure and altered mental status. Fresh frozen plasma is necessary to correct the coagulopathy in the liver failure patient with bleeding.

With an incidence of 17% to 28%, biliary complications—bile leaks and instructions to bile flow from strictures, stones, ampullary dysfunction—are the most common and anastomotic complications of orthotopic liver transplant. Hepatic artery thrombosis less commonly complicates orthotopic liver transplant; however, it is more common than portal vein thrombosis or hepatic vein thrombosis.

Hyperparathyroidism can lead to hypercalcemia. This can lead to the inappropriate release of proteolytic enzymes that can lead to acute pancreatitis.

Chronic pancreatitis damages the Islet of Langerhans, impairing the secretion of insulin and glucagon, predisposing the patient to episodes of acute hypoglycemia.

This patient has osteomyelitis of the distal femur. Osteomyelitis, which is a pyogenic infection of the bone, occurs via hematogenous seeding (most common in children), seeding from a contiguous source of infection (eg, diabetic foot ulcer), or direct inoculation (eg, puncture wound, orthopedic procedure). Children will most often present with acute osteomyelitis (< 2 weeks) with signs of systemic infection such as fever and irritability in addition to localized bone pain and swelling. Adults commonly present with subacute or chronic osteomyelitis, and will have pain, swelling, as well as non-healing ulcers more frequently than they will have fever. Plain radiographs are the initial imaging choice in patients with osteomyelitis, though fewer than one third of patients will have any abnormalities in the first seven to ten days of admission. Periosteal reaction is the earliest osseous finding. The most common infecting organism in osteomyelitis for healthy hosts in all age groups except neonates is Staphylococcus aureus. Patients with sickle cell have an increased risk of osteomyelitis overall, especially from Salmonella spp. Additionally, Salmonella spp. are the most common pathogen identified in sickle cell patients with osteomyelitis. Pseudomonas (C) infection should be considered in the setting where osteomyelitis develops following a penetrating injury through a surface colonized with pseudomonas (e.g. the sole of a shoe). Haemophilus spp. (A) used to be the second most common cause of osteomyelitis, however this is no longer true secondary to the advent of the Haemophilus vaccine. Klebsiella spp. (B) and other anaerobes are rarer causes of osteomyelitis and are more frequently associated with chronic osteomyelitis, as in diabetic patients with non-healing foot ulcers.

This patient is presenting with signs and symptoms associated with pyloric stenosis. Pyloric stenosis is caused by the idiopathic hypertrophy and elongation of the pylorus causing gastric outlet obstruction. Pyloric stenosis is best diagnosed with abdominal ultrasound. Risk factors for the development of pyloric stenosis include male sex, being firstborn, and exposure to erythromycin as a neonate. Patients with pyloric stenosis generally present within the first 3 to 6 weeks of life. Signs and symptoms include projectile nonbilious emesis with persistent hunger after vomiting. There may be a palpable olive-shaped mass in the epigastrium or right upper quadrant of the abdomen; however, it is not often palpable due to patient crying during the exam. Management of pyloric stenosis is with surgical pyloromyotomy.

A CT of the abdomen (B) is generally not necessary to make the diagnosis of pyloric stenosis as it is typically easily seen with ultrasound alone. Ultrasound is also more desirable as it does not expose the child to radiation and is non-invasive. An upper GI series (C) is used to diagnose malrotation and midgut volvulus, which presents with bilious emesis. The image produced shows a corkscrew appearance of the oral contrast, revealing the diagnosis. An X-ray of the abdomen (D) is often sufficient to diagnose necrotizing enterocolitis, which presents with pneumatosis intestinalis and feeding intolerance in neonates.

This child is presenting with signs and symptoms associated with Hirschsprung disease, also known as congenital aganglionic megacolon. Hirschsprung disease is caused by the lack of ganglion cells in the colon, leading to increased muscle tone and contractility of the aganglionic segment. The majority (75%) occur in the rectosigmoid segment. The most common presenting complaint is delayed passage of meconium, greater than 48 hours after birth. Other signs and symptoms include diminished stool frequency, abdominal distension, and bilious emesis (late finding). Hirschsprung disease may be diagnosed with barium enema (reveals a cone-shaped transitional zone), rectal manometry (reveals lack of anal sphincter relaxation), or definitively on rectal biopsy. Definitive management of Hirschsprung disease is via resection of the aganglionic segment.

Incomplete rotation of intestine around superior mesenteric artery and abnormal attachment of the abdominal mesentery (A) to the abdominal wall and ligament of Trietz is the mechanism by which malrotation and midgut volvulus occurs. Ectopic gastric mucosa (B) is the most common form of ectopic tissue found within Meckel’s diverticulum and frequently ulcerates causing patients to present with painless rectal bleeding. Pyloric sphincter hypertrophy (D) is the mechanism by which pyloric stenosis occurs.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Management of malrotation with midgut volvulus is with fluid resuscitation, nasogastric tube decompression, and definitively with surgical correction. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 75% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Sepsis and shock may occur with necrotic bowel. Diagnosis of malrotation with midgut volvulus is made on upper GI series, which reveals a “corkscrew” appearance of the contrast.

Air enema (A) is the first-line treatment for intussusception. Broad spectrum intravenous antibiotics (B) would be appropriate if you suspected perforation. Sigmoidoscopy (C) is the treatment of choice for sigmoid volvulus.

Hypoglycemia in neonates and infants should be taken seriously has symptomatic neonatal hypoglycemia is associated with brain injury and poor intellectual performance later in childhood. A high suspicion for hypoglycemia should be maintained as symptoms are nonspecific. Neonates can present with jitteriness, hypotonia, altered mental status, cyanosis, poor feeding, hypothermia, seizures, or coma. Older children may present with tachycardia, tachypnea, diaphoresis, or anxiety. The etiology of hypoglycemia in infants includes decreased oral intake, high ratio of insulin to counter-regulatory hormones including secondary to growth hormone deficiency and adrenal insufficiency, inborn errors of metabolism, and sepsis. Hypoglycemia is diagnosed with rapid bedside glucose testing and treatment should be initiated promptly before other studies are complete. However, when possible, extra tubes of blood should be drawn prior to administration of dextrose for possible further workup by the pediatric endocrinologists. The presence or absence of ketonuria can also help differentiate causes of hypoglycemia. Treatment thresholds for hypoglycemia vary slightly in the first days after birth, but generally are < 45 mg/dL in symptomatic patients and < 35 mg/dL in asymptomatic patients. If the hypoglycemia is thought to be secondary to an inborn error of metabolism, glucose should be maintained above 70 mg/dL. First-line treatment for hypoglycemia is bolus dosing of IV dextrose 0.5 g/kg in any of a number of regimens, with preference for larger volumes of less-concentrated dextrose to reduce venous injury. These regimens can be remembered by the “rule of 50s,” in that the product of the concentration of dextrose and volume per kilogram should equal 50. Neonates and infants should be given 10% dextrose at 5 mL/kg IV bolus, toddlers and children should receive 25% dextrose at 2 mL/kg IV bolus, and adolescents can be given 50% dextrose at 1 mL/kg IV bolus. Maintenance dextrose should the be started with 10% dextrose at 6–8 mL/kg/hr IV. For patients without IV access, glucagon can be given at 0.3 mg/kg intramuscularly. Glucagon is additionally beneficial as it can help determine the etiology of the hypoglycemia. If serum glucose increases with glucagon, there are appropriate hepatic glycogen stores and the problem is likely a hormonal deficiency. A lack of an appropriate increase in serum glucose indicates poor hepatic glycogen stores. Additionally, if there is concern for adrenal insufficiency as the cause of hypoglycemia, hydrocortisone should be given. Lastly, there should be a high index of suspicion for sepsis in hypoglycemic neonates and infants, and broad-spectrum IV antibiotics should be considered in these children if they are ill-appearing or have altered mental status.

25% dextrose at 2 mL/kg IV bolus (B) is an appropriate dose as it meets the “rule of 50s,” however, it is a highly concentrated solution and has a high risk of causing venous injury. Neonates and infants should receive a bolus of 10% dextrose at 5 mL/kg. 5% dextrose at 5 mL/kg IV bolus (C) is too small of a dose and is too dilute to be an effective therapy in this symptomatic hypoglycemic patient. Using the “rule of 50s,” this regimen would only provide half the insulin needed to treat this patient’s hypoglycemia. Additionally, dextrose 5% should not be used for bolus dose treatment of hypoglycemia. It is indicated for maintenance fluids in normoglycemic patients to prevent hypoglycemia, especially while they are being kept NPO in the hospital. Glucagon 0.3 mg/kg intramuscularly (D) can be used to treat hypoglycemia but generally should be reserved for patients without IV access. While there are some benefits to glucagon in that it can be both therapeutic and diagnostic of the etiology of hypoglycemia, IV dextrose remains first-line therapy when IV access is present, as in this patient.

Pediatric patients are at an increased risk of spinal cord injury without radiographic abnormalities (SCIWORA) as compared to adults. SCIWORA was originally defined as clinical evidence of a spinal cord injury (e.g., neurologic deficits, including transient deficits) without abnormalities on cervical spine CT or flexion-extension X-rays. More recently, with the use of MRI, we have found that most SCIWORA patients have visible acute spinal cord injuries, including those with transient symptoms and normal neurologic exams by presentation. Pediatric patients are at higher risk for SCIWORA secondary to larger head-to-body ratios, more elastic spinal ligaments, shallow vertebral facets that predispose to subluxation, as well as higher spinal canal diameter-to-spinal cord diameter, allowing movement of the cord within the canal. As such, it is important to maintain a high index of suspicion for spinal cord injuries in pediatric patients with significant mechanism (e.g., axial loading, high-risk motorized vehicle collision), or those with neurologic symptoms and normal preliminary spine imaging. Pediatric patients are also at higher risk for higher-level cervical spine injuries. As the head-to-body ratio decreases with age, the cervical spine fulcrum moves from C2–C3 at birth to C5–C6 by approximately 8 years of age.

Injury to C6–C7 (B) is more common in adults, as their smaller head-to-body ratio lowers the fulcrum in their cervical spine. Young children, less than 8 years old, are more likely to have higher cervical spinal injuries, as described above. Injury to spinal cord at T4–T5 (C) would cause symptoms at and below that spinal level. The arms are innervated by nerves arising from the brachial plexus, which originates from nerve roots C5–T1. Therefore, an injury below T1 (e.g., T4–T5) would not cause upper extremity paralysis or numbness. Normal MRI (D) would not likely be seen, as this patient had neurologic deficits, albeit transient. As discussed above, the majority of pediatric patients with high-risk mechanisms for cervical spine injury, even transient neurologic deficits and normal cervical spine CT scans, have been found to have cervical spinal cord injuries on MRI.

Child abuse is a common and serious emergency department diagnosis accounting for between 2% and 10% of pediatric ED visits. It is an important diagnosis to recognize, both for the safety of the child and due to mandatory physician reporting in all 50 states. Historical clues as well as injury patterns can help the clinician differentiate unintentional trauma and intentional trauma. Bruising in a child less than 6 months of age has a very high likelihood of being related to intentional trauma. Patients under 6 months are nonmobile and therefore unlikely to fall or pull objects onto themselves. This falls into the TEN-4 mnemonic (bruising to the torso, ears, neck or under 4 months), which has a sensitivity of 97% in detecting intentional trauma. Young age is the most significant risk factor for intentional trauma.

Intentional bruises are more likely to be found in clusters, on the back, and in symmetric patterns versus anterior and isolated bruising such as on the central forehead (B), which can commonly occur from falls during early ambulation. Burns to the face and neck (C) can be seen in children who are cruising (8–16 months) as they unintentionally pull hot objects down. Spiral tibia fracture (D), also known as a toddler fracture, is an unintentional fracture with a twist and fall mechanism in children 9 months to 3 years. Toddler fractures typically present with refusal to bear weight.

This patient presents with signs and symptoms concerning for an obstruction secondary to a volvulus and requires emergent surgical evaluation. Malrotation is a relatively common occurrence (1 in 500 live births) and about 75% of patients with malrotation will develop volvulus. During embryonic development, rotation of the gut arrests. This allows for the small bowel to twist around the superior mesenteric artery causing an acute obstruction. Patients will present with sudden onset of abdominal distension and bilious emesis. These infants will be ill-appearing and possibly toxic on presentation. Although a number of diagnostic modalities can be employed for definitive diagnosis, the priority in an ill-appearing infant with bilious emesis is emergent surgical consultation. All other interventions risk delaying definitive management. While waiting for the surgical consultation, the patient should have an IV placed, fluid resuscitation begun and a nasogastric tube placed for decompression of the stomach. Additionally, broad spectrum antibiotics should be administered. After consultation, an upper GI series may be obtained for definitive diagnosis.

Stool cultures (B) are useful when there is a suspicion for infectious process such as a parasitic or bacterial infection. Laboratory studies (C) will provide limited data and should not delay definitive management by a surgeon. The patient should receive intravenous hydration, not oral rehydration (D) as there is a high likelihood that this patient will be taken to the operating room. As such, the patient should be kept NPO.

Intussusception is when part of the intestine telescopes into itself. Ileocolic intussusception is the most common type which occurs when the small intestine prolapses through the ileocecal valve. It usually occurs in children under the age of 2 years with a peak incidence between 6 and 9 months. It can, however, occur at any age, especially if there is a lead point such as a Meckel’s diverticulum or a polyp. The classic presentation of abdominal pain, bilious emesis, an abdominal mass, and blood in the stool is rare. Most toddlers present with colicky abdominal pain and one or two of the other symptoms to aid in the diagnosis. Infants, in particular, may present with only lethargy and vomiting often being confused with sepsis. In premature neonates it can be easily confused with necrotizing enterocolitis. Most ileocolic intussusception can be successfully treated nonoperatively with an air enema if identified and reduced within 48 hours. Recurrence is rare but typically occurs within the first 48 hours and, if primarily successful, an air enema can be repeated. A small bowel intussusception is treated somewhat differently as it is less likely to respond to an air enema and more likely to spontaneously reduce.

The clinical manifestations of meningitis (B) typically include fever. Vomiting is also a possibility but it is not bilious in nature as seen in our patient. The presence of guaiac positive stool also is not consistent with meningitis. Intracranial subdural hematoma from non-accidental trauma (C) or a toxic ingestion (D) should be considered in patients this age with nonbilious vomiting and lethargy, however findings of bilious vomiting and guaiac positive stool makes intussusception more likely in this patient.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Diagnosis of malrotation with midgut volvulus is made on an upper gastrointestinal series, which reveals a “corkscrew” appearance of the contrast. Abdominal X-ray may show a “double-bubble” sign, but it is not a definitive study as this may also be seen in duodenal atresia. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 90% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Definitive management of malrotation with midgut volvulus is with surgical correction.

Abdominal ultrasound (A) is used in diagnosing intussusception or pyloric stenosis. It can also be used in children to diagnose appendicitis. CT scan of the abdomen (B) is usually a secondary study in children when you are still concerned after a primary (less invasive) study is inconclusive. X-ray of the abdomen (D) is used to evaluate for free air or pneumatosis intestinalis.

This patient is presenting with Boerhaave’s syndrome, which refers to esophageal rupture, usually due to forceful vomiting resulting in a full-thickness tear. Patients present with severe, persistent chest pain. Subcutaneous emphysema may be present on physical examination. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation. This is known as Hamman’s sign. Chest X-ray findings may include a left pneumothorax, a left pleural effusion, mediastinal emphysema, and a widened mediastinum. Diagnosis should be confirmed with an esophagram using water-soluble oral contrast. Emergent surgical consult should be obtained and broad-spectrum antibiotics should be started. Because significant morbidity and mortality occur very rapidly due to sepsis, it is necessary to determine early whether the patient is a surgical candidate. Patients with free perforation likely require emergency surgery, whereas stable patients with a contained perforation may be able to be managed with intravenous antibiotics and maintaining NPO status.
Because Boerhaave’s syndrome is a surgical emergency, surgical consultation should not be delayed to obtain a CT chest with IV contrast (A). Endoscopy (C) could help in diagnosing Boerhaave’s syndrome, but could also worsen the perforation. Therefore, endoscopy is not indicated, and surgical evaluation should be immediate. Nasogastric tube placement (D) is contraindicated with esophageal tears and should be avoided.

The X-ray demonstrates a foreign body in the esophagus that should be removed under direct visualization by an endoscopist. Pediatric patients account for 75% of all ingestions with coins being the most commonly ingested foreign body. The esophagus has four natural areas where it narrows and these are the most likely places for foreign bodies to become stuck. The four areas are at the upper esophageal sphincter, the aortic arch, the left main stem bronchus and the lower esophageal sphincter. Patients are often asymptomatic on presentation if the foreign body is in the esophagus. Anteroposterior and lateral X-rays of the neck and chest should be performed. An esophageal coin can be differentiated from a tracheal coin on X-ray based on orientation. Coins will appear “en face” on anteroposterior X-ray if they are in the esophagus.
Removal under direct laryngoscopy (A) is not recommended as the coin is too deep to be reached this way. Removal with a Foley catheter (C) may be effective in esophageal foreign bodies. If the coin remains in the esophagus, it should be removed and not observed for passage (D).

This patient presents with a perforated peptic ulcer requiring evaluation for emergent surgery. Perforation is one of the serious complications of peptic ulcer disease in addition to hemorrhage and gastric outlet obstruction. Up to 10% of patients with ulcers can develop perforation and it most commonly occurs in the anterior wall of the duodenum. Perforation typically presents with an acute onset of severe abdominal pain and should be preceded by symptoms consistent with peptic ulcer disease (burning or gnawing pain). The acute pain often radiates to the back and the patient may experience referred pain to the shoulder as a result of air sitting under the diaphragm. Upright chest X-ray and abdominal X-ray with decubitus views will often, but not always, show pneumoperitoneum. This finding should prompt immediate surgical consultation as the patient will require operative management.

Clarithromycin, amoxicillin and a proton-pump inhibitor (A) can be used to treat H. pylori. A CT scan of the abdomen and pelvis (B) is helpful in a patient with symptoms suggestive of perforation and negative plain radiographs. Ultrasound of the right upper quadrant (D) is useful in the diagnosis of biliary pathology.

Esophageal varices are dilated veins in the esophagus that result from increased pressure in the portal system usually secondary to liver cirrhosis. They are diagnosed with esophagogastroduodenoscopy and have an increased risk of bleeding. Variceal rupture can cause massive hemorrhaging and be acutely life threatening. The immediate treatment of acute variceal hemorrhage is volume resuscitation, intubation for airway protection if needed, and correction of any underlying coagulopathy. Beyond the immediate resuscitation, there are several pharmacologic treatments for variceal bleeding. However, ceftriaxone and IV antibiotics have shown to decrease mortality by reducing the infectious complications. It is common for patients with variceal bleeding to have concomitant bacterial infections from translocation of gut bacteria. Common antibiotics used are third generation cephalosporins or fluoroquinolones. This should be given as soon as possible and ideally before endoscopy.

Octreotide (C) is an analog of somatostatin that is used to reduce blood flow through the gastric mucosa and cause splanchnic vasoconstriction. The literature shows that octreotide will help achieve hemostasis and prevent rebleeding; however, it has no clear benefit in mortality. Pantoprazole (D) and other proton pump inhibitors are frequently used in undifferentiated upper gastrointestinal bleeding, but benefits are typically seen in patients with peptic ulcer bleeding. Erythromycin (B) is a promotility agent that is used to enhance endoscopic visualization but is not recommended for routine use. All variceal bleeding will need early endoscopy for definitive treatment with ligation or sclerotherapy.

Mallory-Weiss syndrome is characterized by longitudinal mucosal lacerations in the distal esophagus and proximal stomach, commonly associated with violent or repeated vomiting. The lacerations lead to bleeding from submucosal arteries. Mallory-Weiss syndrome is common, representing 8–15% of upper gastrointestinal (GI) bleeding. Symptoms include dysphagia, odynophagia, and upper GI bleeding. Bleeding is usually mild to moderate, often resolving spontaneously. Risk factors include alcoholism, hiatal hernia, and gastritis or esophagitis. The diagnostic study of choice in patients with continued bleeding is endoscopy. All patients with Mallory-Weiss syndrome should be treated with proton pump inhibitors for acid suppression and antiemetics. For patients with actively bleeding, endoscopic therapy (thermal coagulation, hemoclips, or endoscopic band ligation) is indicated.

Boerhaave’s syndrome (A) is a full-thickness esophageal perforation and a surgical emergency. Patients typically present with severe chest pain that begins acutely after vomiting. The patient in this question does not have any pain and is feeling better, making this an unlikely diagnosis. Diverticulosis (B) is a common cause of lower gastrointestinal bleeding but does not cause hematemesis. Peptic ulcer disease (D) is mostly commonly the result of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug usage. Patients will present with vague epigastric pain that may radiate to the back.

Swallowed foreign bodies most commonly obstruct at the level of C6, the cricopharyngeus muscle, one of the four natural areas of luminal narrowing in the esophagus. The cricopharyngeus is the muscle of the upper esophageal sphincter (UES). Depending on the type of material, a plain radiograph may not reveal the object, particularly with food bolus obstructions. Pediatric patients often swallow objects like coins, and it may be difficult to ascertain whether a coin is in the trachea or esophagus. On a soft tissue X-ray, a coin located in the esophagus appears in the coronal plane, “en face,” as opposed to appearing sagitally when in the trachea. Most foreign bodies less than 2 cm x 5 cm will pass spontaneously through the GI tract. If the patient is without severe symptoms, foreign bodies less than this size are observed for 24 hours as only 10-20% require endoscopic removal. Fewer than 1% will require surgical removal. Pediatric patients account for more than 75% of esophageal foreign bodies. Other at risk patients include edentulous persons, those with psychiatric disease and prisoners, and those with underlying structural abnormalities of the esophagus (rings, strictures, diverticula, malignancy).

The aortic arch (A) at the level of T4 is the second most common location for foreign body obstruction in the esophagus. The gastroesophageal junction (C) at T11 is third most common. The tracheal bifurcation (D) at T6 is the fourth most common site, particularly as the left mainstem bronchus pushes against the esophagus. The thoracic inlet at T1 is the least common location for obstruction.

This patient is presenting with peptic ulcer disease secondary to Helicobacter pylori infection. It is estimated that 30%–40% of the US population is infected with H. pylori, although many will never develop peptic ulcer disease. It is usually acquired through the fecal-oral route, typically in childhood. It is estimated that the majority of patients with duodenal and gastric ulcers are infected with H. pylori. Its presence causes mucosal inflammation and disrupts the normal defense mechanism of the stomach lining, leading to ulceration. Methods of testing include urea breath test, urea blood test, blood antibody testing, stool antigen testing, and biopsy during endoscopy. Triple therapy withclarithromycin 500 mg BID, amoxicillin 1 g BID (metronidazole 500 mg BID if allergic to penicillin), and a proton pump inhibitor (such as lansoprazole 30 mg BID) for 10–14 days is currently recommended for all patients with confirmed H. pylori infection.

Amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (A) is incorrect as you need the addition of clarithromycin; clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID for 10–14 days (C) is incorrect as you have not used a PPI; and clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (D) is incorrect as you have treated the patient with too many medications.

Esophageal varices occur in patients with cirrhotic liver disease and portal hypertension. Over time, varices develop in the lower portion of the esophagus and may acutely bleed leading to massive upper GI bleeding. Octreotide is a somatostatin analog which causes splanchnic vasoconstriction when administered intravenously. As a result of splanchnic vasoconstriction, hypertension of the portal system may decrease leading to decreased bleeding. In an acute GI bleed from varices, a bolus of 50 to 100 micrograms is administered followed by a continuous infusion of 50 micrograms/hour.

The placement of a nasogastric tube (A) will not have a therapeutic outcome in the management of upper GI bleeding due to esophageal varices. Nasogastric tubes may be placed to help prevent vomiting in patients with ongoing bleeding. Additionally, in cases where the presence of bleeding is unclear, a tube may be inserted diagnostically although the sensitivity of this limits its usefulness. Some argue that caution must be taken in the presence of variceal bleeding for fear of worsening bleeding from the trauma of tube insertion. Propranolol (C) is a beta-blocker used prophylactically in patients with known esophageal varices in order to maintain blood pressure and heart rate control. The medication has no role in the acute management of a variceal bleeding. Ranitidine (D) is an H2-antagonist used in the suppression of acid production. The pathophysiology of variceal bleeding is not due to increased acid production nor worsened by the presence of acid and these agents are not indicated. In upper GI bleeding due to peptic ulcer disease, proton pump inhibitors may have some benefit in preventing re-bleeding after the initial episode and are often part of the management of those patients.

Gastroesophageal reflux disease (GERD) is caused by damage to the mucosa of the esophagus from reflux of gastric acid. It is further subdivided into erosive and non-erosive GERD based on endoscopic identification of visible esophageal damage. GERD typically manifests as heartburn that occurs after eating and is worse in the supine position. However, it may also present with epigastric pain, indigestion, nausea, and eructation. Reflux may even extend to the oral cavity and lungs, causing sore throat, cough, and wheezing. While GERD can be diagnosed clinically, pharmaceutically refractory cases and those patients in whom alternative diagnoses are a consideration warrant further objective evaluation. Esophageal pH monitoring is appropriate for patients without alarm symptoms. The presence of dysphagia, odynophagia, or other alarming symptoms should be evaluated by endoscopy. Lifestyle changes including weight loss, elevating the head of the bed, and avoiding food triggers (e.g., caffeine, alcohol, and acidic foods) are all important interventions. Mild, intermittent disease can be treated with antacids as needed, whereas patients with more severe disease require treatment with either an H2 blocker or a proton pump inhibitor (PPI). Erosive GERD should be treated with a PPI (e.g., omeprazole and lansoprazole), whereas non-erosive disease can be treated with either an H2 blocker or a PPI. However, studies have shown the use of PPI results in better response as well as faster healing and resolution of symptoms compared to H2 blockers. Accordingly, PPIs are recommended as first-line for gastroesophageal reflux disease where financial issues are not a factor. H. pylori infection is a consideration in patients with peptic ulcer disease, but patients with GERD and a positive H. pylori test should also be treated. Initial triple therapy with lansoprazole, amoxicillin, and clarithromycin for 10 days is one treatment option.

Bismuth subsalicylate, metronidazole, and doxycycline (A) is not a treatment for H. pylori. The substitution of tetracycline for doxycycline would make it appropriate. Continuing famotidine and adding sucralfate (B) is not appropriate as the patient has tested positive for H. pylori. Triple therapy should be offered even in the absence of peptic ulcer disease. Additionally, sucralfate is not recommended for GERD treatment in the non-pregnant patient. Stopping famotidine and starting omeprazole (D) would be appropriate for a patient with objectively diagnosed GERD and a negative H. pylori result.

This patient presents with infectious esophagitis secondary to a candidal infection and can be treated with fluconazole. Esophagitis is defined as inflammation of the esophagus and can be caused by a number of mechanisms including infection, allergy related (eosinophillic) or pills. Infectious esophagitis typically occurs in patients that are immunocompromised (diabetes, HIV/AIDS, chronic steroids etc.). Esophageal candidiasis is common in the HIV/AIDS population and is considered an AIDS-defining illness. In addition to candida, it can be caused by HSV1 and CMV. Patients with infectious esophagitis present with severe odynophagia that may be to solids, liquids or both. They may also have chest pain, nausea and dyspepsia. Dehydration is common secondary to pain. Diagnosis can be made based on clinical presentation but an endoscopy can be performed to confirm the diagnosis. In immunocompromised patients with candidal esophagitis, treatment should be with fluconazole for 14 to 21 days. If they are unable to tolerate oral medications, intravenous fluconazole can be given.

Acylovir (A) is used in the treatment of herpes esophagitis. Clotrimazole troches (B) can be used in the treatment of mild oropharyngeal candidiasis in immunocompetent patients. CT scan of the neck (C) is unnecessary and is unlikely to show the pathology in the esophagus.

Pulmonary emboli most commonly result from deep venous thrombi in the legs that move and pass through the right ventricle into the pulmonary vasculature. The emboli can lodge anywhere across the pulmonary circulation including the main pulmonary arteries or at the smallest subsegmental levels. Traditional chest radiography rarely provides information helpful in identifying pulmonary embolism as the definitive cause of a patient’s symptoms but may suggest alternative causes. Westermark’s sign is a rare finding on chest X-ray representing oligemia of the pulmonary vasculature visualized distal to the site of embolism.

The pulmonary embolism rule-out criteria (PERC) is a decision rule applied to patients with a low pretest probability (< 15%). If none of the criteria are present, the patient’s pretest probability is decreased to < 2% and further diagnostic testing is not recommended.

Well’s Clinical Prediction Criteria is a clinical prediction and risk stratification tool used to quantify a patients pre-test probability of pulmonary embolism (PE). The criteria should be applied only after a history and physical suggests that venous thromboembolism is a diagnostic possibility. It should not be applied to all patients with chest pain or dyspnea or to all patients with leg pain or swelling. While there have been modified versions since its first publication in 2000, the original scoring systems involves 7 risk factors. These factors include: (1) Clinical signs and symptoms of deep vein thrombosis (DVT); (2) An alternative diagnosis is less likely than PE; (3) HR > 100; (4) Immobilization at least 3 days or surgery in the previous 4 weeks, previous;  (5) Objectively diagnosed PE or DVT; (6) Hemoptysis; and (7) Malignancy with treatment within 6 months or palliative. The patient in the above clinical scenario only has a heart rate greater than 100 beats per minute which constitutes a Well’s score of 1.5. She has no further risk factors according to Well’s Criteria. This risk stratification tool has been validated in several studies since its publication and is widely used for stratifying patients who may need further evaluation for PE with a d-dimer or CT angiogram. It is important to note that Well’s criteria have not been validated for use in pregnant females or patients less than eighteen years of age. The scoring system stratifies patients into low risk (1.3% chance of PE), moderate risk (16.2% chance of PE), and high risk (40.6% risk of PE).

This patient presents with a low-risk story for pulmonary embolism but one that cannot be ruled out by history and physical alone. Clinicians can determine low, moderate and high risk based on clinical gestalt or using a scoring system like the Wells’ Criteria seen below.

In patients who are low risk either by clinical gestalt or Wells’ criteria, the PERC rule, seen below, can be applied.

Since the patient takes oral contraceptives so she does not meet the PERC rule criteria. However, since she is low risk according to the Wells’ criteria, a d-Dimer should be obtained.

The correct answer is pulmonary embolism. CXR shows a Hampton’s hump, suggestive of a large infarction due to pulmonary embolism. Further, patients with pulmonary hypertension are at extremely high risk for PE.

Needle thoracostomy and decompression of the tension pneumothorax is indicated prior to any other interventions. COPD increases the prevalence of spontaneous pneumothoraces secondary to ruptured blebs and deformed lung parenchyma. Intubation may be required for the pulseless arrest described, but the most likely cause of this COPD patient’s sudden decompensation is a spontaneous tension pneumothorax which necessitates release via needle thoracostomy

This clinical scenario demonstrates acute pulmonary embolus. With the history of Factor V Leiden disease, this patient is predisposed to thrombotic events. With the acute onset of dyspnea, the presence of DVT in her right leg, tachypnea, and tachycardia, one must suspect PE. The treatment of PE largely depends on the clinical scenario and how stable the patient is. In this case, the patient has hemodynamic instability with evidence of altered mental status. IV thrombolytics should be given immediately. Plasmophoresis is not an indicated treatment in PE.

The correct answer is admission and heparin infusion. This patient has a pulmonary embolism but no right sided heart strain.  Emergent thrombolytic therapy is not indicated, but mortality is significant enough to warrant admission and monitoring. Patients with massive acute pulmonary embolism who have failed thrombolytics or have contraindications to thrombolytics may be considered for embolectomy. However, this patient is hemodynamically stable so embolectomy is not indicated emergently at this time. Thrombolytics are controversial in that limited studies have shown improved hemodynamics but no mortality benefit. That being said, in patients with massive acute pulmonary embolism and persistent and/or worsening hemodynamic instability, many guidelines suggest considering administration of thrombolytics. This patient is stable and so the risk of thrombolytics is too great.

The sensitivity of a single scan is 95%. Thus, 5% are missed.

In moderate- to high-risk patients with an elevated D-dimer level, a single ultrasound examination may be insufficient. A repeated study in 2 to 7 days is often sufficient to confirm the diagnosis. The lack of pulmonary symptoms precludes the need for lung and embolus evaluation at this time. During pregnancy, there is a progressive rise in baseline D-dimer concentration; thus, a “normal” value is useful, but an elevated level is of no discriminatory value.