Intern Case Report 2.2

Posted on February 1, 2010 by ajrosh

intern-report

Presented by Bao Dang, MD

Case

A 34-yo-female with PMH of DM and symptomatic L5-S1 disc herniation, presents to the ED with a chief complaint of fever and back pain.  Pt states she was involved in a MVC 7 months prior that left her with a L5-S1 disc herniation with L foot drop and tingling and numbness on dorsum of L foot.  Pt states she received a “back steroid injection” from a pain specialist 7 days ago.  Since the injection, the pain has not subsided but instead she is experiencing worsening pain.  The back pain is described as being midline of lower back.  Pain is 8/10, constant even when pt is lying still, which is different from pt’s prior back pain.  Pt has trouble sleeping over last few days because of pain.  Pt also notes she’s been febrile with a max temperature of 102.1 taken at home.  Pt has no c/o of urinary or fecal incontinence, N/V, HA, neck stiffness, photophobia, weight loss, dysurea, BM changes, weightloss, history of cancer.

PMH: DM
PSH:None
Allergies: None
Social Hx: No tobaco, Occasional Drinker, No Illicit drug use
Physical Exam:

Vitals:BP134/75, HR105, RR19, T38.9.
Generally the pt appeared uncomfortable lying in her stretcher.  Pt was unable to ambulate from triage to Module.
HEENT: WNL
Pulmonary: CTA
Cardiovascular: S1 S2, no murmur, rubs or gallops
Neuro exam: Strength is 5/5 proximal and distally and FROM in bilateral upper extremities and right lower extremity.  Left lower extremity showed decreased strength of dorsiflexion of L ankle, other wise strength is normal.  Normal finger to nose examination.  Decreased pin prick and light touch sensation was also noted over dorsum of left foot relative to right foot.  Left leg raise produces sharp pain radiating down to lower leg.  Palpation of lower back revealed slight tenderness of midline of lower back.
Abdominal examination: soft, nondistended, no tenderness, BS present.
Rectal: good rectal tone, guaiac negative, intact touch sensation perianally.

Lab Results: CBC:WBC(16),Hgb(13),Hct(34), Platelets(155), ESR:50(high), UA: Negative for UTI and hematuria

Questions

1.  Considering the above presentation, what is the most likely diagnosis?
a.  AAA
b.  Primary or Secondary Carcinoma
c.  Renal Colic
d.  Spinal Epidural Abcess
e.  Vertebral fracture

2.  What is the diagnostic test of choice for this patient in the ED?
a.   CT scan
b.   Emergent MRI
c.   Lumbar Puncture
d.   Ultrasound
e.   X-ray spine

3.  Which organism is the most likely cause of the above diagnosis?
a.   Anaerobes
b.   Gram-negative bacilli
c.   Mycobacterium
d.   Staphylococcus aureus
e.   The diagnosis is not due to an infection

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

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Answer radER Vol. 1.6

Posted on January 31, 2010 by kjones100

radER Winners:

Allison Loynd

Answer to Case 1.6

A 49-year old man fell off a ladder 4 days ago and continues to have pain in his right wrist. He denies pain in other parts of his body.  On examination, there is tenderness and swelling at the dorsal medial aspect of his wrist.  The patient receives a dose of oral analgesic medication.  The following radiograhs are obtained.

Questions

1.  What is the radiographic diagnosis?

2.  What is the most appropriate ED treatment and follow up?

Answers

1.  Acute triquetral dorsal chip fracture.
2.  Volar splint and follow up with an orthopedic or hand surgeon within 7-10 days



The above radiographs show a small dorsal chip on the lateral radiograph.  This is pathognomonic for a triquetral fracture.  The triquetrum is the second most commonly fractured carpal bone.  The mechanism of injury can either be forced hyperextension, hyperflexion or a direct blow.  Patients typically have pain and swelling on the dorsal medial aspect of the wrist.  Tenderness is often palpated just distal to the distal ulna and ulna styloid.  The triquetrum has a very rich vascular supply and non-union is usually not an issue.  All patients should be splinted and given orthopedic or hand surgeon follow-up.

Wrist radiographs can be difficult to interpret and missed injuries are common.  Radiograph interpretation is aided by knowing which injuries are common, which can be easily missed, and the findings on physical examination.  In the wrist, distal radius fractures are by far most common and, although usually obvious, the radiographic findings are occasionally subtle or the radiographs are normal (an occult fracture).

Among carpal injuries, scaphoid fractures account for 60%.  The radiographs may have subtle findings or be normal.  The second most commonly fractured carpal is the triquetrum – a dorsal chip fracture that is seen on the lateral view.  (The triquetrum is the most dorsally projecting carpal bone on the lateral view.)  When a patient with a wrist injury presents with pain and swelling on the dorsum of the wrist, a dorsal chip triquetrum fracture should be suspected and the lateral view examined for this injury.  In this patient, there is also soft tissue swelling over the dorsal surface of the wrist on the lateral view.  Dorsal chip fractures of the triquetrum account for 20% of carpal injuries.

Most of the remaining 20% of carpal injuries are “perilunate injuries,” a spectrum of ligmentous injuries, subluxations, dislocations and fractures in proximity to the lunate.  Injuries of other carpals are uncommon, but can also be difficult to detect radiographically.  Therefore, any patient with significant wrist pain following an injury should be splinted and referred to an orthopedist or hand surgeon for further evaluation.  This may entail repeat radiographs, a bone scan (no longer used), MRI or possibly MDCT.

trquetrum

References:

Schwartz DT: Emergency Radiology: Case Studies, McGraw-Hill, 2008, pp.249-256, 257-266.

radER is a weekly contest, hosted by Dr. Kerin Jones’ “Fracture”,  consisting of a radiograph selected from various areas of emergency medicine that are central to the education of medical students and residents in training.

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Intern Report Case Discussion 2.2

Posted on January 31, 2010 by ajrosh

intern-report

Presented by Sarah Albers, MD

CC: FeverHPI: A 23-month-old female presents to the ED with fever for the last 2-3 days.  Recently finished antibiotics for an ear infection.  Mom said she was doing well until 2-3 days ago, when she developed some nausea, non bloody, nonbilious vomiting, loose stools, and a fever as high as 104 at home.  She was seen at another hospital last night, diagnosed with a virus and told her to take Motrin and Tylenol, 10 cc of each alternating.

Apparently, there was some miscommunication between mom and the previous hospital.  She has been giving 10 cc of Tylenol and Motrin Infant Drops instead of the child formula and so there is a concern for overdose.  She has had 2 doses of each, last dose of Motrin was about an hour and a half ago, Tylenol was about three and half hours ago.  The patient is eating and drinking, awake, interactive, slightly decreased urine output.  Mom said the urine is very foul smelling and darker than normal.

PAST MEDICAL HISTORY: Reflux.

HOSPITALIZATIONS: None.

PAST SURGICAL HISTORY: None.

MEDICATIONS: Zantac.

ALLERGIES: None

IMMUNIZATIONS: Up to date.

FAMILY HISTORY: None

SOCIAL HISTORY: Positive for sick contacts.

BIRTH HISTORY: Full term, no complications.

Physical Exam and Vitals

BP 97/52, P 148, RR 32, Temp 39.0 (temporal), repeat 40.2 axillary.

HEENT:

Head:  Normocephalic, atraumatic.

Eyes:  Extraocular movements intact.  Pupils are equal, round, and reactive.  No conjunctival pallor or scleral icterus.

Mouth:  Mucous membranes pink, moist.  No intraoral lesions.

NECK:  Supple.

CARDIOVASCULAR:  S1, S2 regular.  No murmurs, rubs, or gallops.

RESPIRATORY:  Clear bilaterally.  No wheezing, rales, or rhonchi.

ABDOMEN:  Soft, nontender, nondistended.

MUSCULOSKELETAL:  No gross deformity.

EXTREMITIES:  No cyanosis, clubbing, or edema.

SKIN:  Warm, dry, and intact.

NEUROLOGIC:  The patient is awake, alert, interactive, and has a normal gait

Labs:

WBC: 18

Hgb: 12.2

Hct: 36.5

Plts: 243

Fecal leukocytes: negative

Ova and parasites: negative

Stool culture: negative

C diff: negative

Blood culture: negative

UA:

pH 7.5

sp gr 1.009,

blood 1+

LE 3+

Nitrites neg

WBC’s 50-100

Bacteria 1+

UCx: >100,000 E Coli

Abd U/S Final Read:

1.  Unremarkable ultrasound examination of the kidneys.

2.  Two splenules in the left upper quadrant.

Side note:

This is a 23-month-old who had fever for 2 days.  She was seen previously at another hospital, and no urine was obtained.   Also, she had approximately 2 g of Tylenol over 2 hours.  Her 24 hour dose calculates to be approximately 80 mL/kg per dose which is below the toxic level.  The patient has also had approximately 400 mg of Motrin which calculates about 30 mg/kg which is below the toxic level as well.  Toxicology should be (and was) consulted (with no acute intervention).

Questions:

1)    What is the most common source of UTI in Pediatrics?

  1. E coli
  2. b. Fungi (Candida species)
  3. Staphylococcus saprophyticus
  4. Streptococcus group B
  5. Adenovirus

Answer Aa)    E coli is the most frequent pathogen, causing 75-90% of UTI’s.

b)    Fungi (Candida) occurs especially after instrumentation of the urinary tract.

c)    Staphylococcus saprophyticus, occurs especially among sexually active females

d)    Streptococcus group B occurs especially among neonates

e)    Adenovirus (rare)

2)    How should the urine analysis be obtained in this non toilet trained child?

  1. Sterile bag collection
  2. Bladder catheterization
  3. Suprapubic catheterization
  4. Wring out the diaper
  5. Wait for the child to urinate

Answer BA urine specimen for urinalysis and culture in a non-toilet trained child should be obtained by bladder catheterization or suprapubic aspiration, before treatment is started.  Sterile bag collection has a notoriously high false positive rate (up to 85%).

3)    What is the concentration/dosage of Children’s Tylenol?

  1. 80 mg / 0.8mL
  2. 160 mg  /5 mL
  3. 100 mg / 5mL
  4. 50 mg / 1.25 mL
  5. 150 mg / L

Answer: Ba) Tylenol – infant drops concentration with calibrated dropper, c) children’s Motrin, d) Motrin – infant drops with calibrated dropper,  e)  Toxic dose of tylenol at the 4 hour mark.  If the Tylenol level is at or above this level, it must be treated!

UTI Pathophysiology

Almost all urinary tract infections are ascending in origin. Disturbance of the normal periurethral flora, which is part of the host defense against colonization by pathogenic bacteria, predisposes a person to a urinary tract infection. Bacteria of the periurethral flora also inhabit the distal urethra. Urine in the proximal urethra, urinary bladder, and other proximal sites in the urinary tract is normally sterile. Uropathogens must gain access to the urinary bladder and proliferate for infection to occur. Uropathogens in the distal urethra may gain access to the bladder because of turbulent urine flow during normal voiding or because of dysfunctional voiding. Successful urinary bladder colonization is unlikely unless bladder defense mechanisms are impaired because normal voiding usually results in an essentially complete washout of contaminating bacteria.

After birth, the periurethral area, including the distal urethra, becomes colonized with aerobic and anaerobic microorganisms that appear to function as a defense barrier against colonization by uropathogens. In early childhood, enterobacteria and enterococci are part of the normal periurethral flora. Escherichia coli is the dominant gram-negative species in young girls, whereas E coli and Proteus species predominate in boys. Children as old as about 5 years are predisposed to have urinary tract infections, partly because of periurethral colonization by E coli, enterococci, and Proteus species. These potential uropathogens usually diminish in the first year of life and are rarely found in children older than 5 years. Studies of girls and women prone to urinary tract infection showed that periurethral colonization occurs with the specific bacterium that causes the next infection.

Causes

Proliferation of bacteria in the urinary tract is the cause of urinary tract infection.

  • Infections are almost always ascending in origin and caused by bacteria in the periurethral flora and the distal urethra. These bacteria inhabit the distal GI tract and colonize the perineal area. E coli usually causes a child’s first infection, but other gram-negative bacilli and enterococci may also cause infection.
  • Staphylococcal infections, especially those due to Staphylococcus saprophyticus, are common causes of urinary tract infection among female adolescents.
  • Entry of bacteria into the urinary bladder may be the result of turbulent flow during normal voiding, voiding dysfunction, or catheterization. In addition, sexual intercourse or genital manipulation may foster the entry of bacteria into the urinary bladder. More rarely, the urinary tract may be colonized during systemic bacteremia (sepsis); this usually happens in infancy.
  • Risk factors for urinary tract infection include the following:
    • Children who receive broad-spectrum antibiotics (eg, amoxicillin, cephalexin) that are likely to alter GI and periurethral flora are at increased risk for urinary tract infection because these drugs disturb the natural defense against colonization by pathogenic bacteria.
    • Prolonged incubation of bacteria in bladder urine due to incomplete bladder emptying or infrequent voiding compromises an important bladder defense against infection. Symptoms of voiding dysfunction, such as urgency, frequency, hesitancy, dribbling, or incontinence may occur in the absence of infection or local irritation because of uninhibited detrusor contractions. When the child attempts to prevent incontinence during a detrusor contraction by posturing (eg, obstructing the urethra), bacteria-laden urine in the distal urethra may be milked back into the urinary bladder (urethrovesical reflux). This mode of bacterial access is a common risk factor for urinary tract infection among pediatric patients who use posturing or pelvic withholding procedures to prevent incontinence.
    • Voiding dysfunction is not usually encountered in a child without neurogenic or anatomic abnormality of the bladder until the child is in the process of achieving daytime urinary control. Children with voiding dysfunction may attempt to prevent incontinence during an uninhibited detrusor contraction by voluntarily increasing outlet resistance. This may be achieved by using various posturing maneuvers, such as tightening of the pelvic-floor muscles, applying direct pressure to the urethra with the hands, or performing the Vincent curtsy, which consists squatting on the floor and pressing the heel of one foot against the urethra.
    • Constipation, with the rectum chronically dilated by feces, is an important cause of voiding dysfunction. Neurogenic or anatomic abnormalities of the urinary bladder may also cause voiding dysfunction.
    • Neonatal circumcision decreases the risk of urinary tract infection by about 90% in male infants during the first year of life. The risk of urinary tract infection in a circumcised infant is about 1 in 1000 during the first year, whereas an uncircumcised male infant has a 1 in 100 risk of developing a urinary tract infection. Given this risk, 111 healthy male infants must be circumcised to prevent 1 urinary tract infection. The risk and long-term effect of scarring due to 1 preventable urinary tract infection in a male infant are not known.

This case discussion presented by Dr Sarah Albers

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Intern Case Report 2.1

Posted on January 25, 2010 by ajrosh

intern-report

Presented by Sarah Albers, MD

CC: FeverHPI: A 23-month-old female presents to the ED with fever for the last 2-3 days.  Recently finished antibiotics for an ear infection.  Mom said she was doing well until 2-3 days ago, when she developed some nausea, non bloody, nonbilious vomiting, loose stools, and a fever as high as 104 at home.  She was seen at another hospital last night, diagnosed with a virus and told her to take Motrin and Tylenol, 10 cc of each alternating.

Apparently, there was some miscommunication between mom and the previous hospital.  She has been giving 10 cc of Tylenol and Motrin Infant Drops instead of the child formula and so there is a concern for overdose.  She has had 2 doses of each, last dose of Motrin was about an hour and a half ago, Tylenol was about three and half hours ago.  The patient is eating and drinking, awake, interactive, slightly decreased urine output.  Mom said the urine is very foul smelling and darker than normal.

PAST MEDICAL HISTORY: Reflux.

HOSPITALIZATIONS: None.

PAST SURGICAL HISTORY: None.

MEDICATIONS: Zantac.

ALLERGIES: None

IMMUNIZATIONS: Up to date.

FAMILY HISTORY: None

SOCIAL HISTORY: Positive for sick contacts.

BIRTH HISTORY: Full term, no complications.

Physical Exam and Vitals

BP 97/52, P 148, RR 32, Temp 39.0 (temporal), repeat 40.2 axillary.

HEENT:

Head:  Normocephalic, atraumatic.

Eyes:  Extraocular movements intact.  Pupils are equal, round, and reactive.  No conjunctival pallor or scleral icterus.

Mouth:  Mucous membranes pink, moist.  No intraoral lesions.

NECK:  Supple.

CARDIOVASCULAR:  S1, S2 regular.  No murmurs, rubs, or gallops.

RESPIRATORY:  Clear bilaterally.  No wheezing, rales, or rhonchi.

ABDOMEN:  Soft, nontender, nondistended.

MUSCULOSKELETAL:  No gross deformity.

EXTREMITIES:  No cyanosis, clubbing, or edema.

SKIN:  Warm, dry, and intact.

NEUROLOGIC:  The patient is awake, alert, interactive, and has a normal gait

Labs:

WBC: 18

Hgb: 12.2

Hct: 36.5

Plts: 243

Fecal leukocytes: negative

Ova and parasites: negative

Stool culture: negative

C diff: negative

Blood culture: negative

UA:

pH 7.5

sp gr 1.009,

blood 1+

LE 3+

Nitrites neg

WBC’s 50-100

Bacteria 1+

UCx: >100,000 E Coli

Abd U/S Final Read:

1.  Unremarkable ultrasound examination of the kidneys.

2.  Two splenules in the left upper quadrant.

Side note:

This is a 23-month-old who had fever for 2 days.  She was seen previously at another hospital, and no urine was obtained.   Also, she had approximately 2 g of Tylenol over 2 hours.  Her 24 hour dose calculates to be approximately 80 mL/kg per dose which is below the toxic level.  The patient has also had approximately 400 mg of Motrin which calculates about 30 mg/kg which is below the toxic level as well.  Toxicology should be (and was) consulted (with no acute intervention).

Questions:

1)    What is the most common source of UTI in Pediatrics?

  1. E coli
  2. b. Fungi (Candida species)
  3. Staphylococcus saprophyticus
  4. Streptococcus group B
  5. Adenovirus

2)    How should the urine analysis be obtained in this non toilet trained child?

  1. Sterile bag collection
  2. Bladder catheterization
  3. Suprapubic catheterization
  4. Wring out the diaper
  5. Wait for the child to urinate

3)    What is the concentration/dosage of Children’s Tylenol?

  1. 80 mg / 0.8mL
  2. 160 mg  /5 mL
  3. 100 mg / 5mL
  4. 50 mg / 1.25 mL
  5. 150 mg / L

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

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radER vol. 1.6

Posted on January 18, 2010 by kjones100

Case 1.6

A 49-year old man fell off a ladder 4 days ago and continues to have pain in his right wrist. He denies pain in other parts of his body.  On examination, there is tenderness and swelling at the dorsal medial aspect of his wrist.  The patient receives a dose of oral analgesic medication.  The following radiograhs are obtained.



Questions

1.  What is the radiographic diagnosis?

2.  What is the most appropriate ED treatment and follow up?

radER is a weekly contest, hosted by Dr. Kerin Jones’ “Fracture”,  consisting of a radiograph selected from various areas of emergency medicine that are central to the education of medical students and residents in training.

Filed under: radER | 2 Comments »

case 1.2 answer

Posted on January 11, 2010 by ajrosh

morrisons-pouch-redo2

Presented by Dr. Debia Kim

NICE JOB

Dan Seitz

Kyle Perry

Richard Gordon

47 y/o woman presents with pain and swelling in her right underarm for the past few days.  She says she first noticed an itchy “bug bite” in her armpit which gradually became larger but never “came to a head.”  She has not tried anything at home to relieve the pain, and her strength and range of motion are unaffected by the swelling.  No fevers/chills.  The patient has a history of DM2 and is a cigarette smoker.

Her physical exam reveals normal vital signs, and a 6cm x 4cm very tender, raised erythematous area of induration in the R axilla.  Peripheral pulses and neuro exam are normal.  No fluctuance.  You decide to do an ultrasound examination of the right (abnormal) underarm and also the left (normal) for comparison.

Image 1

Image 2

Image 3

Image 4

Questions:

  1. What is the diagnosis?
  2. Which images show pathology?
  3. What are the structures highlighted in the color-flow images?case

Answers:

  1. Celluitis and abscess
  2. Images 1 and 3
  3. Lymph nodes

This case prepared by Dr Debia Kim, PGY-1 Emergency Medicine Resident, Detroit Receiving Hospital

“Morrison’s Pouch” is an educational module that utilizes ultrasound video clips from case presentations in the Emergency Department.

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Case 1.2

Posted on January 4, 2010 by ajrosh

morrisons-pouch-redo2

Presented by Dr. Debia Kim

47 y/o woman presents with pain and swelling in her right underarm for the past few days.  She says she first noticed an itchy “bug bite” in her armpit which gradually became larger but never “came to a head.”  She has not tried anything at home to relieve the pain, and her strength and range of motion are unaffected by the swelling.  No fevers/chills.  The patient has a history of DM2 and is a cigarette smoker.

Her physical exam reveals normal vital signs, and a 6cm x 4cm very tender, raised erythematous area of induration in the R axilla.  Peripheral pulses and neuro exam are normal.  No fluctuance.  You decide to do an ultrasound examination of the right (abnormal) underarm and also the left (normal) for comparison.

Image 1

Image 2

Image 3

Image 4

Questions:

  1. What is the diagnosis?
  2. Which images show pathology?
  3. What are the structures highlighted in the color-flow images?

Please post your answer in the “reply box” or click on the “comments” link  You will not see your answer post until next week when all of the submitted answers will be posted.  Good luck!

This case prepared by Dr Debia Kim, PGY-1 Emergency Medicine Resident, Detroit Receiving Hospital

“Morrison’s Pouch” is an educational module that utilizes ultrasound video clips from case presentations in the Emergency Department.

Filed under: Morrison's Pouch | 4 Comments »

Case 3.3

Posted on December 13, 2009 by ajrosh

critical-care2

Prepared by Dr Maria Pak

Case Presentation

A 19-year-old man presented to the ED.  The patient is an employee in a nutritional supplement store.  He states that he took an herbal supplement intended for energy and weight loss.  He states that he only ingested a single pill.  Shortly after ingestion, he began experiencing palpitations and chest pain.  His chest pain is pleuritic in nature, severity of 5/10, diffusely located over his chest with no radiation, and exacerbated by movement and breathing.

Hospital course: The patient was admitted to the ICU service.  He was started on an esmolol drip, which was later switched to propanolol.  It was found that the ingested supplements contained clenbuterol and tamoxifen. His CPK was elevated to the level of rhabdomyolysis.  Rhabdomyolysis was treated with IVF hydration. CPK and creatinine gradually trended down.  Lactic acidosis also resolved.  Cardiology was consulted for the elevated troponin, and 2D-echo showed mild LVH and impaired relaxation.  He was continued on beta-blocker therapy and troponin gradually trended down.  His hypotension and tachycardia resolved by hospital day 6.  He was discharged on hospital day 8.

Discussion

Anabolic steroids have been used by strength athletes for almost five decades in order to improve performance by increasing muscle mass and strength.  Among the numerous documented toxic and hormonal effects of AAS, attention has been focused especially on the cardiovascular effects during recent years. Increases in blood pressure and peripheral arterial resistance are known from experimental studies, but there are also effects on the heart muscle, primarily left ventricular hypertrophy with restricted diastolic function.  Severe cardiac complications such as cardiac insufficiency, ventricular fibrillation, ventricular thromboses, myocardial infarction, or sudden cardiac death in individual strength athletes with acute steroid abuse have also been reported.

More recently, beta-agonists have been used as anabolic agents to increase body weight and build muscle strength. Clenbuterol [4-amino-(t-butylamino)methyl-3,5-dichlorobenzyl alcohol] is a β2-adrenergic receptor agonist that has been shown to have a significant effect on muscle metabolism in a variety of muscle atrophy models, including hind-limb suspension atrophy, starvation induced atrophy, and denervation induced atrophy. Additionally, clenbuterol is known to induce a significant repartitioning effect by increasing the growth of skeletal muscle at the expense of fat tissues in most livestock species.  It is licensed as a bronchodilator for use in human medicine in Spain and other countries in the European Community. It is also used as bronchodilator and tocolytic for the treatment of respiratory disease in horses and cattle and to relax the uterus in cows at parturition. Clenbuterol  causes regression in body lipids, muscle growth, and weight gain and has been illegally used in the past as a growth promoter in young cattle.

β1-adrenoceptors are found in many areas of the body including the heart, kidney, white adipose tissue and the brain, where, in particular, high concentrations are found in the pineal gland. Receptors in the heart mediate positive chronotropic and inotropic responses; those in the kidney control renin release from the  juxtaglomerular apparatus, whereas those in adipose tissue control lipolysis. In the brain, β1-adrenoceptors control the secretion of melatonin from the pineal gland and also appear to have a role in mood alterations. In blood vessels, β2-adrenoceptors have classically been considered to be dominant but in a number of arteries, including the coronary, mesenteric and saphenous, β1-adrenoceptors also mediate vasodilatation

Prolonged activation of β1-adrenoceptors has deleterious effects on the heart.  For example, the use of xamoterol as an inotropic agent is associated with increased mortality, and transgenic mice with relatively mild cardiac over expression of β1- adrenoceptors rapidly develop cardiac failure.  Chronic activation of cardiac β1- adrenoceptors is associated with apoptosis of cardiomyocytes. This may be a significant factor in the greatly increased risk of heart failure in people taking cocaine or amphetamines and in the success associated with the use of β-adrenoceptors antagonists for the treatment of cardiac failure.

β2-adrenoceptors have a wider distribution than β1-adrenoceptors and control a wide variety of functions in the body. They also mediate positive inotropic and chronotropic effects in the heart. The human heart has a significant (up to 40% of total β- adrenoceptors) population of β2-adrenoceptors. In the lung, the activation of β2- adrenoceptors causes not only a bronchodilator effect but also reduces the release of bronchoconstrictor mediators and increases the release of surfactants and mucus. β2- adrenoceptors mediate a powerful vasodilator effect in small coronary blood vessels and skeletal muscle blood vessels. Other effects seen in skeletal muscle include increased growth and speed of contraction, glycogenolysis and tremor. In the pancreas, there is an increase in both insulin and glucagon secretion, and glycogenolysis in the liver is increased.

The β3- adrenoceptor is widely distributed in the gut, brain, genitourinary tract, uterus and white and brown adipose tissue.  The presence of the receptor in fat stimulated activity in the pharmaceutical industry to develop anti-obesity and anti-diabetic β3- adrenoceptor agonists that has so far been a success in rodents but not in humans.

A major  target for many illicitly used drugs in sport is the β2-adrenoceptor that is found in the heart, lungs and skeletal muscle where it controls rate and force, relaxes tone and stimulates growth. β2-adrenoceptor agonists are powerful bronchodilators, anabolic agents and, in combination with corticosteroids, powerfully enhance their anti-inflammatory actions.

A survey of 113 cases of clenbuterol poisoning cases in Spain in 1992 showed that more than half of those afflicted presented symptoms of tachycardia, muscle tremors, nervousness, myalgia, and headache.  Exposure and onset ranged from 15 minutes to 6 hours . The duration of symptoms varied between 90 minutes and 6 days.

Clenbuterol influences cell metabolism by combining with β2-adrenergic receptors and by increasing the cAMP concentration in cells. In adipocytes, stimulation of β-adrenergic receptors increases cyclic AMP levels and activates protein kinase A (PKA), which stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin.

Adipose accumulation decreases dramatically by clenbuterol administration.  In this study pigs treated with clenbuterol had a lean meat percentage increase by 2%, the back fat thickness was reduced by ~0.2 cm, and the loin muscle area was reduced by 4.7 cm2.  This effect increased with the age of the pigs. Clenbuterol produces specific protein anabolic effects in skeletal muscle in addition to lipolysis in adipose tissue. The clenbuterol thickened the pig muscle fibers and reduced the sizes of the pig adipocyte cells. Histological sections and global evaluation of gene expression after administration of clenbuterol in pigs identified profound changes in adipose cells. With clenbuterol stimulation, adipose cell volumes decreased and their gene expression profile changed, which indicate some metabolism processes have been also altered.  These findings indicate that some metabolic processes, such as DNA transcription, protein translation and protein translocation, were enhanced in the adipose cells by clenbuterol stimulation.

However, data has revealed that clenbuterol is also capable of inducing significant myocyte apoptosis  and necrosis in the heart and slow-twitch soleus muscle of rats. Furthermore, the onset of myocyte death occurs at doses lower than those commonly used to demonstrate the hypertrophic effects of this agent

The skeletal myocyte death induced by administration of clenbuterol to whole animals in vivo is mediated by overstimulation of the myocyte β2-AR4.  When administered in vivo, clenbuterol also stimulates the β2-AR of the sympathetic nerve terminals, which augments their release of norepinephrine, and the β2-AR of the peripheral vasculature, which results in a reflex tachycardia. These neuromodulatory effects may act synergistically, increasing the release of norepinephrine from the sympathetic varicosities, which induces cardiomyocyte death through the β1-AR pathway

Administration of clenbuterol induced significant and clearly discernible myocyte death in the heart and slow-twitch soleus muscle. Bolus injection of doses as low as 10 μg.kg-1 of clenbuterol induces significant myocyte death in the heart and soleus muscle of rats. In response to sustained exposure to an agonist, β-AR desensitization and downregulation occur resulting in tachyphylaxis. However, because of clenbuterol’s long plasma half-life and the fact that it accumulates in specific tissue compartments, particularly the heart, it is difficult to predict whether chronic administration would be more or less myotoxic than a bolus injection.

The patient above was treated with beta-blocker therapy. Mcclennan et al performed a study on the effects of clenbuterol and propanolol n muscle mass.  They found that in animals treated with clenbuterol and propranolol, the changes in body weight and body composition observed in animals treated with clenbuterol alone were abolished. The Beta-blocking agent also abolished the effects of clenbuterol on both muscle growth and protein synthesis rate. However, the study showed that the effects of clenbuterol on muscle cyclic AMP, lactate and glycogen concentrations were still detectable after twice-daily injection of the drug for 7 days. The dose of propranolol employed in the study was able to inhibit the effects of clenbuterol on cardiac, fat and liver mass and on energy expenditure.

References

Zhang J,  He Q, Liu QY, Guo W, Deng XM, Zhang W, Hu X and Li N. Differential gene expression profile in pig adipose tissue treated with/without clenbuterol.  BMC Genomics 2007, 8:433

Baker JS,  Graham M, Davies B. Gym users and abuse of prescription drugs. Journal of the Royal Society of Medicine (2006)  9 9:331-332.

Maclennan PA, Edwards RHT. Effects of clenbuterol and propranolol on muscle mass. Biochem. J. (1989) 264, 573-579.

Spurlock DM, McDaneld TG and McIntyre LM.  Changes in skeletal muscle gene expression following clenbuterol administration.  BMC Genomics 2006, 7:320

Burniston JG, Clark WA,, Tan LB, Phil D, andGoldspink DF. Dose-dependent separation of the hypertrophic and myotoxic effects of the β2-adrenergic receptor agonist clenbuterol in rat striated muscles. Muscle Nerve. 2006 May ; 33(5): 655–663.

Burniston JG, Clark WA,, Tan LB, and Goldspink DF.   Relative myotoxic and haemodynamic effects of the β-agonists fenoterol and clenbuterol measured in conscious unrestrained rats.  Exp Physiol. 2006; 91(6): 1041–1049.

Davis E, Loiacono R and Summers RJ.  The rush to adrenaline: drugs in sport acting on the b-adrenergic system.  British Journal of Pharmacology (2008) 154, 584–597.

Salleras L, Dominguez A, Mata E, Taberner JL, Moro I, Salva P. Epidemiologic Study of an outbreak of Clenbuterol Poisoning in Catalonia, Spain.  Public Health Reports 1995, 110(3):338-342.

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radER 3.2 Answer

Posted on December 7, 2009 by ajrosh

rader new

Winners

David Mishkin

Marjan Siadat

Claire Jensen

Richard Gordon

Ayse Avcioglu

Case

A 23-year-old man presents to the ED complaining of left thumb pain after he collided with another player during a rugby match. There is swelling and tenderness at the base of the thumb.  You think the patient may have sustained a fracture of his proximal thumb so you order radiographs.  One of the radiographs is seen below:

thumb 2

Questions

1. What is the eponym for this fracture?

2. What is the ED management for this fracture?

3. Is the prognosis better or worse than the fracture seen in radER 3.1

Answers

1. Rolando Fracture – This is a  Y-shaped fracture of the base of the thumb metacarpal.  It can be considered an intraarticular, comminuted Bennett fracture.

thumb2a

2. ED Management requires a thumb spica splint and referral to a Hand specialist

3. The prognosis of a Rolando fracture is worse than a Bennett fracture, and operative fixation is usually necessary.

radER is a weekly contest consisting of a radiograph selected from various areas of emergency medicine that are central to the education of medical students and residents in training.

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radER 3.2

Posted on November 30, 2009 by ajrosh

rader new

Case

A 23-year-old man presents to the ED complaining of left thumb pain after he collided with another player during a rugby match. There is swelling and tenderness at the base of the thumb.  You think the patient may have sustained a fracture of his proximal thumb so you order radiographs.  One of the radiographs is seen below:

thumb 2

Questions

1. What is the eponym for this fracture?

2. What is the ED management for this fracture?

3. Is the prognosis better or worse than the fracture seen in radER 3.1

Please click on the “comments” link or post your answer in the “reply box”. You will not see your answer post until next week when all of the submitted answers will be posted. Good luck!

radER is a weekly contest consisting of a radiograph selected from various areas of emergency medicine that are central to the education of medical students and residents in training.

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