Senior Report 6.22

Case Presentation by Dr. Dan Paling

HPI: 3 year-old female presents to the emergency department accompanied by her parents with complaints of worsening rash. The mother states that her child developed the rash 2 days ago. She states that it acutely worsened overnight. The patient reportedly developed a fever overnight of 102.6. She states that she is currently being treated for acute bilateral otitis media. The patient was taken to her pediatrician when the rash was first noticed on the patient’s legs and feet. The pediatrician told the patient’s mother to discontinue using amoxicillin and to start trimethoprim-sulfamethoxazole. The pediatrician stated that the rash should go away after stopping the amoxicillin. The mother states that she gave the first dose of the new antibiotic the evening before the rash worsened. The mother denies any coughing or difficulty in breathing. She denies nausea, vomiting, and diarrhea. The mother states that the patient has not had this type of rash in the past.

The mother attempted Benadryl without any improvement of the rash.

PMH: none

Allergies: NKDA

Immunizations: UTD

Physical Exam:

Constitutional: no acute distress

Vitals: Temp 39.2, BP 107/67, HR 130, RR 14, O2 Sat 99%

HEENT: PERRL, no conjunctival or scleral injection, few intraoral lesions

Respiratory: CTAB, no wheezing, no retractions

Cardiovascular: tachycardic with regular rhythm, normal S1 S2

Skin: Diffuse blanching papular rash not involving palms and soles. Mucous membrane involvement. Majority of lesions in acral distribution however scattered lesions on face, chest, abdomen, and back. Less than 10% BSA skin desquamation.

6.21-1 copy

 Questions:

1) What is the diagnosis?

a) Urticaria

b) Erythema Nodosum

c) Erythema Multiforme Minor

d) Erythema Multiforme Major

2) What is the probable etiology for this child’s condition?

a) Virus

b) Post-Group A Strep infection

c) Amoxicillin

d) Food Allergy

3) What is the most common cause of Erythema Multiforme?

a) Penicillins

b) Sulfonamides

c) Herpes Simplex Virus

d) Group-A Streptococcal infection

 

Discussion & Answers:

1)  Correct answer D

Erythema Multiforme Major constitutes painless blanching target-like papular rash that is usually first noticed on the extremities. This rash spares the palms and soles. Rashes involving the mucous membranes are considered Erythema Multiforme (EM) Major with total BSA desquamation less than 10%. Desquamation rash involving mucous membranes that involves more than 10% but less than 30% total BSA is considered SJS. More than 30% BSA is considered TEN.

(A)  This rash is not an annular urticarial rash because urticaria usually resolves within 24 hours of its onset. Urticaria will not form target-type lesions. Urticaria most often resolves with antihistamines.

(B)  Erythema Nodosum lesions are painful erythematous nodules most often occurring on patient’s lower extremities that do not exhibit central clearing.

(C)  This rash involves at least one mucous membrane therefore is considered EM Major. EM Minor primarily exhibits acral distribution. EM Minor typically will not involve the face, trunk, chest, or back

2) Correct answer C

In this case, it is probable that Amoxicillin was the cause of this EM Major rash. HSV is most often the cause EM however the child does not have any vesicular lesions suggesting HSV infection. Common pharmacologic causes of EM are penicillins, sulfonamides, phenytoin, barbiturates, and aspirin. EM does not occur as a result of a Group-A Streptococcal infection. Erythema Nodosum is noted to be a post-streptococcal complication. Urticaria can be a result of an allergic reaction to food however EM has not been linked.

3) Correct answer C

Herpes Simplex Virus-1 and Mycoplasma are the most common predisposing factors that lead to the development of EM. Penicillins and sulfonamides result in fewer total cases of EM however the majority of the most severe cases are medication induced. Group-A Steptococcal infections have not been linked to the development of EM.

Erythema Multiforme is considered a Type IV delayed hypersensitivity reaction.

Senior Report 6.21

Case Presentation by Dr. Deepa Japra

Questions:

1.) A 19 year old female presents with decreased hearing from her right ear since going diving earlier today. Otoscopic exam reveals the findings in the picture, which of the following is an acceptable treatment?

6.21-1

a) oral ciprofloxacin

b) topical neomycin

c) hydrogen peroxide

d) ciprofloxacin otic solution

2.) Your next patient arrives with a chief complaint of ear pain and with 45 minutes left in your shift, you know it’s bad form to push it off for the next resident to see. You are dreading having to see yet another cerumen impaction, and are startled to observe the following findings on physical exam. Which of the following is central to management of this condition?

6.21-2

a) admission for IV antibiotics

b) emergent bedside incision and drainage

c) ENT consult for emergency mastoidectomy

d) outpatient antibiotics with urgent ENT follow up

3) Your next patient presents with a foreign body in the ear. You grab your alligator forceps with 10 minutes left in your shift, but which of the following findings should prompt an ENT evaluation instead of attempted removal by the ED physician?

a) disk-shaped battery

b) live insect

c) cotton ball

d) object present more than 8 hours

Answers & Discussion

1) d

2) a

3) b

Question 1 –  d

The picture above is of a perforated tympanic membrane. This can occur through various mechanisms, including a direct blow to the ear, blast injury, scuba diving, air travel while having an upper respiratory infection, and more commonly from the traumatic usage of cotton swabs to clean the ear. In the case of this patient, TM perforation occurred during a diving injury. Topical antibiotics, such as d) ciprofloxacin otic solution, can be safely prescribed, especially in this case since the perforation likely occurred in a contaminated setting while the patient was in water. It is important to note, however, that usage of topical anitbiotics in TM perforation is not proven by evidence, but can also be given in cases of external puncture or canals occluded with blood or drainage.  Most cases of tympanic membrane perforation heal spontaneously. Larger, more central lesions such as those greater than 25% of the total drum surface area may require operative repair, especially in patients that do not heal spontaneously in 4 weeks. Lesions in elderly patients are also less likely to heal on their own. Topical ototoxic agents should be avoided in perforated TM and includes aminoglycosides like, b) neomycin, and antiseptics and compounds with low pH including c) hydrogen peroxide and acetic acid. Alcohol is also ototoxic and should not be applied.  If the clinician cannot fully visualize the tympanic membrane and is unsure of whether it is disrupted and there is an index of suspicion for perforation, it is best to avoid these ototoxic agents. After the diagnosis is made, patients with small isolated tympanic membrane perforation with minimal hearing loss can be managed with avoidance of water exposure for 4 to 6 weeks, possible topical antibiotics in contaminated settings as described above, the recommendation for audiometry within 24 hours, and follow up with ENT within 4 weeks to ensure the perforation is closed and the hearing deficit has resolved. There is no indication for oral antibiotics, a), in a perforated TM with no signs of infection.  Patients with more marked hearing loss, vestibular signs such as nystagmus, vomiting, and ataxia, or those with findings consistent with facial nerve injury should have emergent ENT evaluation if possible or within 48 hours of injury.

If the mechanism for perforation is secondary to barotrauma, such as air travel with a URI, diving, or blast injury, making the diagnosis of perforated TM can give insight to other injuries. The tympanic membrane is sensitive to changes in pressure and more likely to be injured at lower pressures than any other organ. Some studies suggest that it can be used as a triage tool in blasts with multiple victims, especially with patients that are initially healthy appearing, in order to identify patients that have a higher risk of delayed sequelae including pulmonary or gastrointestinal injury.

Question 2 – a

The picture represents acute mastoiditis, which occurs most likely as a complication of acute otitis media. Acute mastoiditis is more common in children than adults, and the incidence has declined with the use of antibiotics for the treatment of otitis media, and is now relatively rare. The mastoid air cells are connected to the distal end of the middle ear through the antrum. While most episodes of acute otitis media are associated with some inflammation of the mastoid, mastoiditis occurs when the mucous lining of the middle ear lining the mastoid becomes persistently inflamed and purulent material accumulates in the mastoid air cells.

The clinical presentation of mastoiditis can include fever, posterior ear pain, local erythema and tenderness over the mastoid bone, edema of the pinna, and posterior and downward displacement of the auricle. If mastoiditis is suspected, the patient should be a) admitted for IV antibiotics and a CT scan of the temporal bone should be performed.  CT scan can demonstrate air-fluid levels and identifies the extent of the disease, but it is important to note that the isolated or incidental finding of mastoid air-fluid levels on CT should not prompt a change in treatment in a well appearing patient without other clinical signs of mastoiditis. IV antibiotics should be directed against streptococcus pneumoniae, the most common pathogen, with consideration for broader coverage against pseudomonas, staphylococcus aureus, and enteric gram negative rods when mastoiditis presents as a complication of a more chronic disease. A third-generation cephalosporin is acceptable as an initial antibiotic choice, and other recommendations include vancomycin, clindamycin, or imipenem. Answer d) outpatient antibiotics with ENT follow up is inappropriate as acute mastoiditis can lead to further intracranial spread and neurological sequelae if not appropriately diagnosed and treated. Choice b) emergency bedside incision and drainage is not an appropriate treatment option for acute mastoiditis. Though an emergency ENT consult is warranted, choice c), an emergency mastoidectomy for debridement of necrotic bone, is not an initial intervention performed and is sometimes indicated if the patient does not respond to conservative therapy with IV antibiotics. A myringotomy by ENT for aspirate and fluid cultures is an appropriate initial treatment choice in order to guide antibiotic therapy and may include placement of a tympanostomy tube for drainage.

Question 3 – a

When removing a foreign body in the ear in the emergency department, the clinician should remember that smaller instruments are more likely to cause damage to the canal so one should use the largest, bluntest instrument that has the capacity to grasp the object or pass a hook behind it.  Choice b) live insect, can be safely removed by the ED physician, and the insect should be killed first with solutions such as lidocaine (2% gel or liquid) or mineral oil prior to removal. Though some studies suggest that ethanol causes the most rapid killing of insects, this should not be routinely used because alcohol is ototoxic and contraindicated unless the TM is intact, which is difficult to assess with an insect blocking visualization.

Choice a) disk-shaped battery should prompt an ENT evaluation because of its ability to cause burns or liquefactive necrosis of the external auditory canal. The battery’s electrical potential is damaging and does not need to leak or rupture in order to cause damage. Choice c) cotton ball, can be safely removed as long as the object is easily visualized and accessible. Choice d) object present more than 8 hours, is not a definite ENT referral. Some studies suggest that primary ENT referral should be performed for any sharp-edged or spherical object, any vegetable matter or disk-shaped battery, location adjacent o the TM, age less than 4 years, previous unsuccessful removal attempts, and time in ear exceeding 24 hours, all of which were associated with increased complications. Other studies suggest that there is no increase in complication rates related to patient age or the time object is present in the ear.

After removal of any foreign body, the physician should perform appropriate inspection of the ear canal for signs of damage to the external canal, TM perforation, or infection, and treat these conditions appropriately.

Senior Report 6.20

Case Presentation by Dr. Jeanise Butterfield

Case:

An 18 year old girl was riding her horse when the horse stopped suddenly and put his head down.  She slid off the front of her horse landing on the posterior aspect of her left should and neck, rolling onto her back (think somersault).  She complains of severe back pain.  There is tenderness of the thoracic and lumbar spine diffusely with no neurologic deficits. CT of the cervical spine was within normal limits.  Radiographs of the thoracic and lumbar spine are shown below.

6.19-1j        6.19-2j    6.19-3j                           6.19-4j

Questions: 

 1) By mechanism of her injury, which type of spinal column injury do you suspect?

a) Flexion

b) Extension

c) Compression

2) Is there deformity visible on radiograph?

a) Yes

b) No

c) More information required

 3) Which of the following is a stable spinal fracture?

a) Flexion teardrop fracture

b) Unilateral facet dislocation

c) Hangman’s fracture

d) Jefferson fracture

4) If this patient was uncooperative and combative, the following treatment would be appropriate?

a) Have an individual hold patient’s head in alignment with spine

b) Sedation

c) Drug induced paralysis

d) All of the above

 

Answers and Discussion:

1.  a

2.  a

3.  b

4.  d

 

 

6.19-mri

Spinal column injuries are classified according to the mechanism of trauma: flexion, flexion-rotation, extension and vertical compression.  When assessing stability of a spinal injury (meaning the spinal cord is protected) it is helpful to view the spine as an anterior and a posterior column.  The anterior column consists of alternating vertebral bodies, intervertebral disks, anterior and posterior longitudinal ligaments.  The posterior column contains the spinal canal, pedicles, transverse processes, articulating facets, laminae and spinal processes with nuchal ligament complex, capsular ligaments and ligamentum flavum.  In a very basic sense you can imagine that if both columns are disrupted, the spine will move as two separate entities whereas if only one column is disrupted the other will resist movement.  This can only be applied to injuries below C2.

Unstable flexion injuries

-        Flexion teardrop fracture: avulsion of anteroinferior corner of a vertebral body by anterior longitudinal ligament causing anterior displacement of a wedge shaped fragment resembling a teardrop.  It commonly involves ligamentous disruption and is often associated with neurologic injury.  Of note, this can also occur with extension injury (see below).

-        Bilateral facet dislocation: Forces of flexion cause disruption anterior to the annulus fibrosis and anterior longitudinal ligament.  This causes anterior displacement of the spine above the level of injury as the upper vertebra passes over superior facets of the lower vertebra

-        Alanto-occipital dislocation: This occurs more often in children, partly due to larger relative head size and ligamentous laxity, can also occur non-traumatically in Down syndrome and rheumatoid arthritis.

-        Odontoid fracture with lateral displacement: need I say more?

-        Subluxation is also potentially unstable

Unstable flexion-rotation injuries

-        Rotary atlantoaxial dislocation: In trauma, may occur with forced rotation of the neck with some element of lateral tilt.  There are several ways this can occur with respect to placement of atlas on axis including rotation on odontoid or on one of the lateral articular process

Unstable extension injury

-        Hangman’s fracture: traumatic spondylolysis of C2.  Fracture-dislocation of atlas and axis, specifically of pars interarticularis of C2 and disruption of C2-3 junction.

-        Extension teardrop fracture: Same as above flexion teardrop fracture, usually occurs in lower cervical vertebra from diving accidents.

-        Posterior atlantoaxial dislocation

-        Posterior neural arch fracture (C1): results from compression of the posterior elements between occiput and spinous process of the axis during forced extension.  This is unstable primarily due to location.

Unstable vertical compression

-        Jefferson fracture: Axial loading results in shattering of the ring of the atlas, associated with disruption of transverse ligament.

Always think of spinal injury in patients presenting with trauma, especially motor vehicle collisions, falls from heights and sports related injuries.  Obtain radiographs in patients with suspected injury but don’t let distracting injury prevent you from performing complete physical exam and maintain spinal immobilization until spinal injury has been excluded.

Senior Report 6.19

Case Presentation by Dr. Sarah Hyatt

Chief complaint: “I can’t see.

HPI:  A 23 year old African American female comes into the ER because of a sudden loss of vision. She was working out in the gym when she accidentally hit herself in the eyes with an exercise band about one half hour prior to her arrival in the ED. She is very concerned because her eyes were open when this occurred. She states that she instantly experienced sudden loss of vision in her left eye. She denies any pain currently or foreign body sensation but states that she cannot see any light or movement out of her left eye. She denies any visual changes in her right eye.

PMH: asthma, sickle cell anemia

PSH: none

meds: albuterol prn

allergies: none

family history: hyperlipidemia, hypertension, sickle cell trait

Physical Exam:

Vitals: blood pressure 119/73, heart rate 75, respirations: 18,  temp. 36.3

General: well nourished, well developed 23 year old female in no acute distress.

HEENT: there are no abrasions to the face. The facial bones are non-tender to palpating without palpable crepitus. When you look at the patient’s left eye you see the following:

6.18-1

Pupils are equally round and reactive to light, although there is pain with constriction of the left pupil. Fluorecein stain does reveal some linear uptake around 5 o’clock on the left iris, with a negative Seidel’s test. There is no uptake in the right eye. Patient has 20/30 vision on the right but sensitivity to light only on the left, without detection of motion. Slit lamp exam is unremarkable on the right and reveals an anterior chamber with a large amount of blood on the left that has a small amount settled on the bottom and without any lenticular dislocation. Ocular pressure is 12 on the right and 16 on the left.

Neuro: extra ocular movements are intact and pain free. Face is symmetric. Patient spontaneously moves all 4 extremities.

Questions:

1)  What treatment should you initiate for this patient?

a) Analgesia, prompt ophthalmology consultation

b) Timolol, homatropine, eye patch, analgesia, prompt ophthalmology consultation

c) Timolol, homatropine, outpatient follow up with ophthalmology in 3-5 days

d) Timolol, homatropine, prednisolone, eye shield, follow up with ophthalmology in one week

2)  What treatment should be avoided in this patient?

a) Carbonic anhydrase inhibitors

b) Topical beta blockers

c) Analgesics

d) homatropine

3)  After speaking with ophthalmology and arranging follow up, we are preparing to discharge the patient. Her hyphema has started to settle and she is encouraged as she is now starting to see shapes and movement. Although it looks like the hyphema will eventually take up less than 1/3 of the anterior chamber, and she will likely do well, we counsel her that it is very important that she follow closely with an ophthalmologist as there are certain complications that she needs monitored for. What is the most common complication?

a) Re-bleeding

b) Corneal blood staining

c) Traumatic glaucoma/elevated intraocular pressure

d) Vision loss

 

Answers:

1)  b

2)  a

3)  a

Discussion:

Question 1:

Treatment of a hyphema usually involves prompt consultation with ophthalmology. Previously these patients had been admitted and followed in-patient, although ophthalmologists now often follow most uncomplicated cases as outpatients. Treatment typically consists of things to lower the intraocular pressure – topical beta blockers and sometimes oral carbonic anhydrase inhibitors; cycloplegics to prevent papillary movement (so long as the patient’s intraocular pressures are not elevated); an eye patch to avoid movement during the daytime; shield at night to avoid further injury; and instructions to keep the head of the bed >45 degrees while resting to allow the blood to settle and avoid clogging the trabecular meshwork. Although topical steroids may prevent re-bleeds and treat iridocyclitis, this is best left to the discretion of the treating ophthalmologist as these patients will require frequent eye exams to make sure there is no corneal infection or perforation.  Additionally, NSAIDS such as aspirin should be avoided for treatment of pain as they have platelet inhibiting properties and could, in theory, place patients at a higher risk of re-bleeding. Most small hyphemas will reabsorb on their own, but larger ones may require surgical intervention.  Care should be taken to look for an irregular pupil or positive Seidel’s Test (oozing of fluorescien stain secondary to leakage of fluid from the anterior chamber) on exam as these can be signs of globe rupture.

Question 2:

Sickle cell patients should not receive carbonic anhydrase inhibitors as they can lead to increased sickling and blockage of the trabecular meshwork with resultant elevated intraocular pressures. Because of the possiblility of sickling, patients with sickle cell disease are at increased risk of increased ocular pressure and significant vision loss, and should be monitored closely or admitted. Patients with sickle cell disease are also more susceptible to elevated intraocular pressures (ie- 24mm Hg as opposed to 50mm in patients without hemoglobinopathy). Because of this they are at increased risk of ischemic damage, and are also at increased risk of re-bleeding, both of which can contribute to increased vision loss.

It is also important to remember to question patients about personal or family histories of other blood dyscrasias and to check a CBC, PT/PTT/INR on these patients. Those with increased bleeding tendencies (i.e. – hemophilia) may need treatment to normalize their clotting capabilities, as increased bleeding can put them at risk for complications such as glaucoma and vision loss. Hyphemas can also occur secondary to retinoblastoma or melanoma of the iris and so cancer should remain in the differential as well, especially if there is no traumatic cause of the hyphema. This is especially important since hyphemas, in the absence of significant trauma, can be a symptom of ocular cancers or abuse in young children.

Question 3:

The most common complication of hyphemas is a re-bleed.  This typically occurs 3-5 days after the initial bleed and can happen in up to 30% of patients. With a re-bleed there is increased risk for visual loss and elevations of intraocular pressure, sometimes so much that these patients require surgical washout of the hyphema. Usually patients whose hyphema occupies 1/3 or less of the anterior chamber are at lower risk of this complication, and often have resolution of their hyphema in 4-5 days. Patients are at increased risk of a rebleed if their visual acuity is < 20/200; have a hyphema that occupies more than 1/3 of the anterior chamber, are delayed > 1 day in seeking medical attention, or have elevated intraocular pressures on exam.

Other complications include elevated intraocular pressure/glaucoma from blockage of the trabecular meshwork, corneal blood staining, and formation of synechia.  It is important to instruct patients not to lay flat, to keep the head of their bed >45 degrees, and to avoid video games, reading or other activities with frequent eye movement as this can put them at risk for increased complications (such as glaucoma). Patients should have follow up arranged with opthamology prior to their discharge and should return to the ED should they notice decreased vision or increased pain.

Morrison’s Pouch V 2.2

morrisons-pouch-redo2

Case Presented by: Dr. Meredith Hill

CC: “My Stomach Hurts”

HPI: 18-year-old man presents to the emergency department complaining of abdominal pain.  He states last night his older brother who weights 400 lbs jumped on his back driving his knee into his left upper chest.  This took place around 11 pm.  At that time he did not feel significant pain but since then he has had pain in his left upper quadrant of his abdomen.  He feels there is a “bump” which is growing in size and is also painful to the touch.

ROS: unremarkable

PMH/PSH: asthma

Medications: none

Family History: CAD Allergies: none

Social history: +tobacco, denies alcohol and drug use

VS: Temp: 36.7  BP: 137/67 HR: 64 RR: 20

General: Patient is resting in bed.  He appears to be in some pain.

Head: Normocephalic, atraumatic

Eyes: Pupils are equal, round and reactive to light and accomidation. Extraoccular movements are intact bilaterally, no conjunctiva pallor, no sclera icterus    

Throat: Moist oral mucosa without intraoral lesions. No tonsilar exudate.

Neck: Supple, no lymphadenopathy. Trachea midline.

Lungs: Breath sounds clear to auscultation bilaterally without rhonchi, wheezes or rales.

Cardiovascular: Regular rate and rhythm, S1 and S2 auscultated. No murmur, rubs or gallops to auscultation. No peripheral edema, radial and dp pulses present and equal bilaterally

Abdomen: The abdomen is tender in the left upper quadrant just below the costal margin. Patient also has tenderness to palpation of the ribs on left anterior chest.  Appears to be rib 8 or 9. There is a slight amount of swelling here.  There is no rebound of the abdomen appreciated. Normal bowel sounds.

Extremity: Normal muscle strength and tone.  Full range of motion of upper and lower extremities.

Neurologic: Awake, alert and oriented to person, place and time.

Let’s review the information: 18-year-old male with history of trauma complaining of abdominal pain. +LUQ tenderness and pain as well as point tenderness over left anterior ribs with some swelling. Although patient’s mechanism of injury was from behind, he may have sustained either a significant abdominal injury as well as possible a skeletal injury.  With concern for a splenic injury a FAST exam was performed which was negative. A trauma panel was sent and chest x-ray was obtained. Patient was given pain medication.

Chest Radiograph

It was read as normal by radiology. An abdominal series was also obtained which did not show evidence of free air. There was still concern for bony injury versus possible splenic injury. Surgery was consulted.

A musculoskeletal ultrasound was performed to evaluate for rib fracture and a FAST exam repeated which was still negative. The ultrasound of patient’s ribs on his left anterior lower chest is pictured below.

There is an obvious cortical disruption. This is rib 9 on the left anterior chest toward the auxiliary line. Because of this finding, a CT abdomen was ordered to rule out splenic injury as patient continued to complain of pain. There was, however, no change in his abdominal exam. He did not have peritoneal signs. The Surgical team was able to view the ultrasound in real time and agreed with the plan to CT. A member of the on call surgical team also placed a rib block, which significantly improved patient’s pain.

CT scan read as negative for splenic injury. No acute intra-abdominal process was noted.

In this case, ultrasound was key in identifying patient’s diagnosis. Ultrasound has long been known as a more sensitive modality for identifying rib fractures as compared to a standard chest X-ray.  The exam is easy to learn and not painful for the patient. It can also be used in conjunction with the initial FAST exam.

Musculoskeletal Scan for Rib Fracture

This is a limited exam. You start by asking the patient where the point of maximal tenderness is located. Using the linear probe, place the transducer on the patient’s thorax with the indicator facing caudally. Locate the rib you want to scan and then turn the probe 90 degrees so the indicator is to the patients right or operators’ left.  Keeping the prop perpendicular to the long axis of the rib (see below) scan the rib for signs of cortical disruption. Remember that the rib will curve along the back so you will want to pay attention that you stay on the same rib. It does take some practice but ultrasound was found to be 78-80% sensitive as compared with X-ray, which is only 12-23% sensitive. In the case above, both X-ray and CT scan were read as normal.

A Few Pearls You Want to Remember:

-   The area will be tender, so use a copious amount of gel to avoid placing pressure over a painful area.

-   Keep the probe perpendicular to the rib and remember the angle of the rib will require you to angle the probe as you move from anterior to posterior.

-   Scan multiple ribs around the point of maximal tenderness to look for other fractures.

Below is a video showing how to scan for rib fractures using ultrasound. This video uses a slightly different technique. The initial scan over the point of maximal tenderness is done in the transverse plane then rotated 90 degrees when a cortical disruption is visualized.

Ultrasound Use in the Diagnosis of Rib Fracture from HQMedEd on Vimeo.

Sources

Sonoguide.com

Vimeo.com

Senior Report 6.18

Case Presentation by Dr. Sam Sadler

41 yo female presents to the ARC with chief complaint of “rash and not feeling well.” She says her symptoms have been present for 7 days consisting of malaise initially and today she developed a rash on her bilateral upper and lower extremities. She had a few episodes of chills associated with tactile fevers. No sick contacts. No runny nose, cough, abdominal pain, vomiting or diarrhea.

Since this is the ARC you quickly go to your physical exam expecting of course to find a whole lot of nothing since obviously this patient cant possibly be sick as they have been triaged to the “low acuity” area….

ROS:

constitutional: tactile fevers

skin: rash

PCP: None

PMH: No HTN or illnesses

PSH: None

Alg: None

FH: HTN, DM, Rheumatoid Arthritis

SH: Smokes, drinks etoh, smokes marijuana denies other illicits, multiple partners

PE: BP: 145/88, HR: 72, RR: 20, Temp: 37.9

Constitutional: Anxious appearing obese female.

Skin: Non blanching rash as seen below:

6.18-1

Resp: CTA b/l

Card: S1S2 no abnormal heart sounds

Gastro: Soft, Nondistended

Neurologic: Smiles symmetrically, protrude the tongue is midline, 5 out of 5 strength in the upper and lower extremities, no loss of feeling in a dermatomal distributions of the upper or lower extremities.  Normal cerebellar testing and normal gait.

Just as you are about to walk out of the room and re-triage this patient she drops her cell phone and shrieks “my arm is numb!!” You examine her right upper extremity and notice that her strength is 0/5 on grip testing, bicep/tricep testing and shoulder girdle the rest of her neuro exam is unchanged.

You race to your attending and share the history. When the attending evaluates the patient the neurologic exam is completely normal. Fully aware that petechia are bad and something must be done your transfer your patient to module 4 where Tabby and the intern are working… When you call module 4 Tabby says “We are in the weeds over here can you put some orders in for that patient?” You agree thinking to yourself I have no idea what orders to put in…. but send a CBC, lytes and coagulation studies.

Questions:

1)  If you could only order one study to make a definitive diagnosis which would it be?

a.  CT Scan

b.  CBC alone

c.  CBC with peripheral smear

d.  Urine electrolytes

e.  Comprehensive metabolic panel

The nurse informs you of a panic value plt count of 8,000.

2)  Which symptoms are the most common in the presentation of this disease?

a.  petechia and fever

b.  thrombocytopenia, hemolytic anemia, and acute renal failure

c.  thrombocytopenia, fever, hemolytic anemia, and acute renal failure

d.  thrombocytopenia, microangiopathic hemolytic anemia, and neurologic deficit

The patients other labs return showing normal basic metabolic profile, hemoglobin of 6.2 mg/dL and .  She now has abdominal pain and her arm isn’t working again.

3) Which of the following therapies is an absolute contraindication to the definitive therapy for this disease?

a.  FFP

b.  Steroids

c.  2L D5W 0.9 NaCL bolus

d.  Platelets

e.   PRBC

 

Answers

c, d, d

 

Discussion:

The diagnosis for this patient is TTP. distinguishing this from say ITP important as the prognosis is significantly different. Thrombotic thrombocytopenia purpura is rare however if left untreated mortalitity is 100% but with proper treatment it is reduced to 10-20% It is a true hematologic emergency, one of very few. So it must be on the radar and we must know what to do for these patients. ITP an autoimmune disease that targets platelets on the otherhand is relatively benign. They are generally going to have a drop in platelets to less than 50,000/mm3 with associated petechia or purpura. It is associated with other autoimmune diseases. These patients should get basic labs including coags but they will essentially have a isolated thrombocytopenia. ITP treatment in the emergency department is simple with steroids and admission only necessary when patients are actively bleeding or cannot arrange timely outpatient follow up.

The diagnosis of TTP is mostly based on history and physical but you will likely need labs to get a hematologist out of bed…

The textbook will say that there is a pentad of findings: some neurologic finding, thrombocytopenia, fever, hemolytic anemia, and acute renal failure however these are only all present 1/3 of the time. However ¾ of the time a triad is present: thrombocytopenia, microangiopathic hemolyctic anemia (MAHA) and neurologic deficit.  Thrombocytopenia is commonly defined as anything below 50/ml. MAHA is the presents of schistocytes on smear. And the neurologic symptoms are usually focal and transient almost like TIA they may not be active at the time of presentation so it is important to ask about it in the history. On physical exam you will find the petechia, jaundice and most patients have splenomegaly as the spleen tries to sequester all of the schistocytes. Risk factors are obesity, african american, female, rheumatologic diseases, HIV and taking plavix.

For labs you are going to need a CBC for platelet count a smear, Lytes for renal failure although not always present at time of presentation, unconjugated bilirubin, UA for hematuria. The CBC with smear is most important because it will demonstrate the schistocytes and low platelets confirming microangiopathic hemolytic anemia and thrombocytopenica. Bonus points from your hematologist if you send off an ADAMTS13 study to included level, activity level and function. This is a protease which is key in the pathophysiology of TTP. It’s job is to cleave vWF therefor the lack and/or decreased function of it forms long chains in the middle of capillaries which the platelets adhere to resulting in platelet aggregation which leads to consumption and clotting.

Definitive treatment is plasma exchange transfusion which will remove the bad proteases (ADAMTS13) and replace them with functional proteases. However this needs to be initiated usually by the hematologist or really by the blood bank so in a bind you could call them directly. Regardless early consult with the hematologist is imperative. In the meantime steroids and fluids are really the mainstay of treatment in the emergency department. FFP can also be given as this will provide ADAMTS13 but again the definitive treatment is exchange transfusion. Patients who are anemic are going to need PRBC’s as well. Any blood product containing platelets is absolutely contraindicated as more platelets will only fuel the fire. With appropriate treatment mortality goes from 100% to 10-20%.

References:

Kessler et al. Thrombotic thrombocytopenic purpura: a hematological emergency. J Emerg Med. 2012 Sep;43(3):538-44.

Rosen’s Emergency Medicine. 7th ed. 2010. Marx.

Senior Report 6.17

Case Presentation by Dr. Daniel Helzer

6.17-1

A pleasant 43 year old female from Royal Oak presents to the ED ARC complaining of a bite wound.  She is embarrassed to tell you but eventually the truth reveals itself.  She enjoys feeding the hordes of black squirrels that reside in her backyard.  She gets a kick out of letting them eat out of her hand and was feeding them freshly baked oatmeal cookies.

6.17-2

While taking part in this extraordinary event, a black squirrel with a white tail gets into a scuffle with another over the last morsel of cookie.  Mistakenly the squirrel bit your patient on her right foot during the scuffle.  The patient, visibly shaken, thought she should come in to get checked out. She is otherwise healthy, takes no medication, no allergies, has no clue when her last tetanus update was, and has normal vital signs on presentation.  PE demonstrates below on dorsum of foot, wound exploration reveals superficial wounds with no deep puncture wounds.

6.17.3

Questions:

1)   Initial management of this patient would include?

A)  Reassure and discharge home.

B)  Wound irrigation, bacitracin dressing and discharge with wound care instructions.

C)  Wound irrigation, bacitracin dressing, Tdap and discharge with wound care instructions.

D)  Wound irrigation, bacitracin dressing, Tdap, Human rabies diploid cell vaccine and discharge with wound care instructions.

E)  Wound irrigation, bacitracin dressing, Tdap, Human rabies diploid cell vaccine, Human rabies immune globulin and discharge with wound care instructions.

Unfortunately you pick choice A.  The patient returns to the ED 9 days later complaining of Flu like symptoms x 2 days that keep getting worse despite Tylenol.  She has been having headaches, fevers, arthralgias particularly in her knees, runny nose, and 1 episode of vomiting. Brief initial PE was nonspecific, neuro exam was normal.

VS:  BP 115/85, HR 112, RR 21, Temp 39.4

The sepsis bug fires and while you are trying to figure out how to make it disappear you remember seeing the patient for a squirrel bite and run over to see how it healed up.  The wound has completely healed but you note this rash on BOTH of her feet and hands upon inspection.

6.17-4J

2)   The causative organism is?

A)  Rickettsia rickettsii

B)  Neisseria meningitidis

C)  Rabies virus

D)  Streptobacillus moniliformis

E)  Leptospira Icterohaemorrhagiae

3)   The patient receives 1g Tylenol for fever and vital signs normalize in ED. Proper treatment and disposition of this patient would be?

A)  Oral Augmentin 875 mg x 10 days and D/C home

B)  IV Penicillin G 600,000 IU/day and medicine admission

C)  Rabies vaccine and Ig (you failed last time), MICU admission, and cross your fingers

D)  Oral doxycycline 100mg Q12 and observation admission

E)  IV ceftriaxone, vancomycin, and decadron and Neuro ICU admission

 

Discussion

The Final Diagnosis??  Rat Bite Fever.

The first question deals more with basic management of animal bites.  Obviously basic wound management should include wound irrigation and bandaging.  Life saving tetanus should be given.  Rabies vaccination is the next important consideration in management. After a bite wound/ exposure proper post exposure rabies management includes providing the rabies diploid vaccine and possibly the rabies immune globulin.  It is a time consuming and expensive process so it is important to know who needs it and who does not.

Previously unvaccinated people should receive the vaccine intramuscularly at 0, 3, 7, and 14  days. For adults the vaccine is given in the deltoid area; for children, it may be given in the anterolateral aspect of the thigh. In addition to rabies vaccine, these people should also receive rabies immune globulin (HRIG) at the same time as the first dose of the vaccine to provide rapid protection that persists until the vaccine works.

Previously vaccinated people should receive two doses of the vaccine intramuscularly—the first immediately, the other three days later. HRIG is unnecessary and should not be given.

HRIG is given in a weight based dosage and is calculated in Units.  Average cost for a 70 kg adult is $1500. The entire dose of HRIG should be injected directly into and around the bite wound if feasible and if a wound is evident; the remainder of the dose should be given intramuscularly in the upper arm, lateral thigh, or gluteal muscle.

So who needs this?? It can get a little complicated but here is the CDC algorithm.

Helzer

Keep in mind for stray dogs in Wayne County the recommendation is to initiate rabies post exposure prophylaxis and to not wait for apprehension of the animal.

As you can see small rodents including our crazy black squirrel is low risk and does not require rabies post exposure prophylaxis.

 

Answer to Question #1 is C

Antibiotic prophylaxis is also not recommended for rodent bites.  Animal bites that may require antibiotics prophylaxis include dog bites to hand, cat bites to hand, camel bites, pig bits, and monkey/primate bites.

Now onto the diagnosis.  Rat Bite Fever, caused by Streptobacillus moniliformis bacteremia, is a systemic illness classically characterized by fever, rigors, and polyarthralgias.

 

Answer to Question #2 is D

 Historically transmission occurs via rat bits hence its name but can occur via other rodents including mice, squirrels, guinea pigs, hamsters, ferrets, ect.   The bite wound is typically healed by the time rat bite fever sets in and signs of local cellulitis or abscess formation at the bite site should steer one away from the diagnosis.

Systemic onset usually occurs in 7 – 10 days.  Fever is the most common manifestation usually intermittent and above 38.0 with rigors. Other nonspecific complaints are present with the fever as well.

50% of patients develop migratory polyarthitis typically in knees and hips.

75% of patients develop a rash that may appear maculopapular, petechial, or purpuric. Hemorrhagic vesicles may also develop on the peripheral extremities, especially the hands and feet, and are very tender to palpation.  Note the hemorrhagic vesicles in the image above. Appearance of this rash, especially the hemorrhagic vesicles, in the setting of an otherwise nonspecific set of disease signs and symptoms should strongly suggest the diagnosis of rat bite fever.

Complications involve endocarditis, myocarditis, polyateritis nodosa, meningitis, abscess, ect. 10% of untreated cases lead to death.

Treatment is with IV penicillin, there is very little resistance.

 

Answer to Question #3 is B

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