Senior Report 6.20

Case Presentation by Dr. Jeanise Butterfield


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


 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




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:


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.


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



1)  b

2)  a

3)  a


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


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.


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….


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:


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.


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



c, d, d



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%.


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


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.


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.



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.


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



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.


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

Laos Senior Report 6.16

Case Presentation by Dr. Ryan Doss

Pic 4

The following patient presents to your emergency department complaining of pain in his left hand radiating up his left arm after messing around with a friend’s pet snake and getting bitten. He does not know the species of snake. The bite occurred approximately 6 hours ago. (After contacting the friend in question, he denies knowledge of the species of snake as well, stating that he purchased it from a charming stranger 1 week ago who has since left town. In addition, he spent the last several hours destroying the snake by means of blade and fire in retaliation and is unable to recall any patterns or really even any overall general color of the snake. In addition, everybody involved in this story is super drunk. Probably even the snake was.)

You decide to discard the issue of speciation.

The patient is rating his pain as 9/10 and is also reporting a sensation of difficulty breathing and pleuritic discomfort in the left side of his chest. He denies any past medical history, allergies, or previous exposure to snake venom or antivenom.

Pic 1

1)  Initial treatment, select as many as appropriate (there are 5 correct answers):

A. ETOH level, TCU, sobriety, firm talking to

B. Proximal limb tourniquet

C. Generate a tincture composed of monkey ladder, cat’s claw, wild gri gri root, and  mashed Battus polydamas caterpillars aged in alcohol for 4-6 weeks, then apply to the wound and/or/especially the GI tract

D. Ceftriaxone

E. Floor Admission

F. 4 vials of FabAV antivenom

G. ICU admission

H. Local suction. Mechanism: Dealer’s Choice.

I. ED amputation

J. Elevate and immobilize the limb

K. Methylprednisolone

L. Tetanus booster

M. Get a non-venomous creature to bite the patient on the opposite arm and wait for the venom and non-venom to duke it out near the patient’s heart? I just thought of this one

N. Immediate discharge. D/C Instructions: New Pregnancy. He’s not going to read it anyway.

2)  30 minutes after initiating the non-crazy treatments above, the patient develops a fever, generalized urticarial rash, and begins complaining of pain in his knees and wrists. You administer prednisone to treat his serum sickness (I’m not going to waste a question on this, plebs). He is one of the approximately 5% of patients who are unlucky enough to develop serum sickness from the modern FabAV – a much more rare occurrence than with the previous horse serum-based antivenoms. He improves and is granted admission to the [ICU/Floor/TCU/His mom’s house] depending on your answers to the previous question. 4 hours later, the [ICU fellow/floor grunt/Hamidou/patient’s mom] calls you stating that the patient has begun bleeding out of orifices that rarely, if ever, express blood.

Good God, what have you done?

A. The serum sickness has resulted in an autoimmune thrombocytopenia, give more steroids

B. He’s developed sepsis and DIC from a localized wound infection, give broad spectrum antibiotics and for pity’s sake use the sepsis order set

C. Millennia of evolution have resulted in venom components which are highly potent activators of coagulation factors as well as fibrinolytics, causing syndromes similar to DIC; administer blood products and continue scheduled FabAV dosing

D. Did you ever see that movie Outbreak with Captain Hook? Shut down the circulation systems, hijack a helicopter, and whatever you do don’t take off your spacesuit helmet thing even if you have to puke into it.

3)  Oh man are you guys getting sick of this yet? Because I’m just getting warmed up. Astutely realizing that FabAV is formulated specifically for North American venomous snakes and, for all you know, this patient’s friend purchased an Asian snake from Beelzebub over there (get it? Charming, itinerant, deals in snakes) and, furthermore, resigning yourself to the fact that your patient is getting worse instead of better, you begin to worry. Or continue to worry. (Also, forget that we admitted the patient previously…there’s no beds or something).

What’s the next step?

A. Surgical consultation. Debridement of the local wound and close monitoring for compartment syndrome may be the difference between limb and not-limb.

B. Poison control. Even without speciation, polyvalent antivenoms (meaning in this context created from multiple species) exist for the most popular Asian or African venomous snakes that can be used in a last-ditch effort.

C. Family conference. Venomous injuries, especially those involving neurotoxin, can progress rapidly and unpredictably, resulting in respiratory arrest, coma, and death.

D. All of those sound pretty good.


Answers and Discussion:

1)  Answers: D, F, G, J, L

The mainstays of treatment are antivenom, admission to the ICU for close monitoring, elevation and immobilization of the affected limb, and a tetanus booster. Empiric antibiotics are also recommended and are standard of care, but there is little data to support their use.

Tourniquets and suction (especially with an incision made at the bite site) have fallen out of favor. They do not appear to be effective and are potentially harmful.

Steroids have been shown to be of no benefit. In the real world they are sometimes used for severe cases in a practice I have just decided to call “kitchen sink”-ing. Probably won’t help, though.

The tincture described in answer C is really a collage of various real-life local treatments (from random localities), some of which may be somewhat effective (but nowhere near as effective as antivenom). Tobacco is another popular option. However, the answer is impractical unless you have a tincture prepared ahead of time.

Answer M awaits randomized controlled trials.

2)  Answer: C

Much of the hypotheses regarding the evolution of venom are speculative. This is because being an evolutionary biologist is the easiest job in the world and you can basically make stuff up. (Semi-aquatic human ancestors, humbug). However, based on the anatomical structures involved, it can be assumed that the evolutionary progenitors of modern venom were digestive proteins and enzymes – a sort of pre-digestion. Then, when you managed to catch up with your meal, you could finish the job internally. However, some prey animals are very quick. So an evolutionary arms race resulted in chemicals that had the effect of immobilizing the prey in various ways. One of these ways is by breaking down all the various cell walls and basement membranes that interfere with the spread of your venom. This has the added benefit of turning a springy muscular limb into a “I ran out of my Lasix one month ago” limb, which is less effective at propelling your lunch away from you. Another method is to turn your prey into a giant blood clot or cause them to leak all their oxygen- and nutrient-carrying substrate out their eyeballs. Or BOTH, or all of the above plus paralysis via neurotoxin. The treatment is to stay the antivenom course and to replace what’s being used up (with blood, platelet, and FFP transfusions). If your patient is unlucky enough to have been injected with neurotoxin, the treatment is supportive (intubation and sedation).

3)  Answer: D

There’s got to be at least one “all of the above.” Probably the most helpful thing you can do in this case is contact poison control. If you had a picture or description of the snake to begin with, this should have been one of the things you did right away. In this case, without speciation, you can describe to them the symptoms and effects of the venom at least. They have access to the local zoo’s stores of antivenom which may include polyvalent options as described above. It’s worth a shot.

Tissue necrosis necessitating debridement may be a direct result of the venom or a secondary effect of compartment syndrome. See below for some pictures of a Lao patient with untreated tissue necrosis of the leg after a snake bite.

As an aside, if you have a patient who comes in with a wild snakebite in the United States the most likely offenders would be coral snakes or pit vipers (rattlesnakes, massasauga, copperheads, or water moccasins). For pit vipers, think of symptoms similar to the patient described above. These include local tissue damage, progressive worsening edema, nausea, vomiting, etc. Treatment is essentially as described above. Administer FabAV if the edema and pain are moderate to severe, and provide supportive care. Coral snakes are less predictable. Whereas a potential victim of a pit viper bite should be treated with antivenom based on the severity of symptoms and edema, ANY patient with a confirmed coral snake bite should be given coral snake-specific Antivenin. Coral snakes kill primarily with neurotoxins, and the effects of these toxins are difficult to predict and somewhat variable in their time of onset. They may be delayed up to 12 hours and the patient may require prolonged ventilatory support. Pit viper bites should be observed for 8 hours, potentially in the ED. ALL coral snake bites should be admitted, potentially to the ICU. You will want to closely monitor coagulation profiles, basic labs, and various measures of pulmonary function (pulse ox, peak flow, respiratory status, chest x-rays) for either type of snake bite throughout their stay.

Finally, here are a picture of a real patient in Laos with a snake envenomation who ended up being discharged home due to lack of funds for transfer to a tertiary care facility. He came back after watching his leg decay for one week. The medical system here is (obviously) quite different than in the United States, and the framework is simply too rickety to support socialistic excesses such as EMTALA. Here, if a patient or patient’s family cannot pay up front for a treatment, transfer, or sterile glove, the patient is denied treatment or discharged. Patients in Detroit also present with advanced pathology secondary to lack of access to primary care, but that’s a bit of a different problem than being sent home to watch your leg fall off because of a lack of Kip. Perspective!

Pic 2