Case 5.7

Case Presentation by Dr. Tim Scott

CC: Fatigue

HPI:  19yo W M with no PMH presents to the ED with complaint of fatigue.  He states that over approximately the last 6 months he has noticed that he has decreased energy that has gotten progressively worse.  He is single, lives with a room-mate and is employed.  He has no history or family history of depression.  He denies drug/alcohol abuse.  He denies any hematuria, dark or bloody stools and any other complaints.

ROS:  Positive for fatigue

PMH: Denies

PSH: Denies

Social: Denies smoking or drug use.  Drinks occasionally with friends

PE:  Pulse 86, Respirations 16, Temp 37.1, PaSO2  97% RA

Const: W/D, W/N Appears stated age, NAD

HEENT:  membranes moist, left side painless cervical lymphadenopathy, trachea midline

CV: RRR, S1 S2

Lungs: CTAB

Abd: Soft, NT/ND, BS +

Extr: normal pulses, strength and ROM

At this point you do a CBC with lytes which comes back as follows

CBC:  Hgb 12.1 and WBC 31.1  – the rest was WNL

Lytes: WNL

You go back and press this patient for more information…he says he has felt “the lump” in his neck for a few months now but he denies any cough, fever, vomiting, diarrhea and the only other info you get out of him is that he sometimes feels itchy all over.

You order a CXR because he has an elevated white count


1) What is the likely Diagnosis in this patient?

  1. Hodgkins Lymphoma
  2. Acute Myelogenous Leukemia
  3. Acute Lymphoblastic Leukemia
  4. Pneumonia

2) What current infection (or previous history of infection) would increase the patient’s risk for this disease 5-25 times?

  1. Varicella Zoster
  2. Herpes Zoster
  3. Pertussis
  4. HIV

3) Which one of the following is NOT a common presenting symptom/sign for this disease?

  1. Painless lymphadenopathy of cervical region, axilla or groin
  2. Fever, weight loss and or night sweats
  3. Mediastinal mass causing mass effect symptoms like pain, pleural effusion or superior vena cava syndrome
  4. Pruritis and fatigue


  1. A.  This patient likely has Hodgkins Lymphoma.  HL arises from germinal center or post-germinal center B cells and has a unique cellular composition, containing a minority of neoplastic cells (Reed-Sternberg cells and their variants) in an inflammatory background and can cause anemia and elevated white counts. HL has a bimodal age distribution curve. In the US and other economically advantaged countries, there is one peak in young adults (approximately age 20 years) and one in older age (approximately age 65 years); the majority of patients are young adults and there is a slight male predominance.  AML and ALL are close second options here due to similar early presentations, however, with AML, the median age at diagnosis is 65 years old and with ALL the vast majority of cases present between 2-5 years of age.  Bleeding disorders are more likely to be present and the cause of an initial presentation with these patients.
  1. D.  The incidence of HL is increased in a number of settings associated with immunodeficiency and infection. Among patients infected with HIV, the relative risk of HL is increased in various studies from fivefold to 25-fold. There also appears to be an increased risk of HL in patients with a history of infectious mononucleosis caused by Epstein Barr virus.  Interestingly, other childhood infectious illnesses including chickenpox, measles, mumps, rubella, and pertussis are negatively associated with the risk of HL.
  1. C.  A, B and D are all true.  Though a mediastinal mass discovered on routine chest x ray is a common presentation in an HL patient, it is NOT common to have any symptoms associated with it. The mass may be fairly large without producing local symptoms. Less commonly, the mass produces nonspecific symptoms such as retrosternal chest pain, cough, or shortness of breath. Small pericardial or pleural effusions are rare except in patients with bulky mediastinal disease. Superior vena caval obstruction is also rare.  Painless lymphadenopathy is present in as much as 80% of patients with HL.  Fever, weight loss and night sweats (the classic B symptoms), though not specific to HL, are present in less than 20 percent of patients with stage I/II Hodgkin lymphoma and up to 50 percent of patients with advanced disease.  Pruritus and fatigue, though not specific, can be early symptoms of the disease.  Pruritus specifically may be an important early symptom, preceding the diagnosis of HL by months or even a year or more. Pruritus occurs early in approximately 10 to 15 percent of patients, but the great majority of patients experience pruritus at some time during the course of illness. It is usually generalized and occasionally severe enough to cause intense scratching and excoriations.

Case 5.6

Case Presentation by Dr. Erin Murphy

CC: Snakebite

HPI: A 9yo male from Washington Township, MI presents to the Emergency Department via EMS after sustaining an apparent snakebite to his left lower extremity approximately 25 minutes ago.  His mother states that he had been playing in the backyard barefooted when he came running inside yelling for his mother to come outside and see what had just bitten him. She states that she noticed a puncture wound on her son’s left foot and that the foot quickly began to swell & her son began to complain of pain. When EMS arrived at the scene, they took a picture of the snake with a cell phone. The patient is currently complaining of nausea, slight perioral tingling and severe, burning pain of his left foot & lower leg. Pictures of the snake and child’s foot are shown below.


Constitutional: no fever, +malaise.

Head:  no headache

Eyes: no blurry vision

Ears: no earache or tinnitus

Nose: no discharge

Mouth/Throat: no sore throat, + slight metallic taste

Cardiovascular: no palpitations

Respiratory: no breathing difficulty

GI: no abdominal pain, + nausea, no vomiting

Musculoskeletal: + left lower extremity pain & swelling

Skin: + puncture marks on left foot

Neurological: + slight perioral numbness/tingling

PMHx: None

PSHx: None

Allergies: None

Meds: children’s multivitamins

Social Hx: lives at home with parents and 1 older sibling


Physical Exam:

Vitals: BP 108/70 P 95 RR 20 T 37.2 SpO2 99% RA

General: well-developed, well-nourished male, crying, somewhat anxious and in moderate distress due to pain, otherwise cooperative, alert & oriented

HEENT: head is NC/AT, PERRL, EOMI, vision intact, no facial swelling, intact hearing to finger rub, no eye, ear or nose discharge

Neck: no swelling

Cardiovascular: regular rhythm, S1/S2, no murmurs

Respiratory: non-labored respirations, lungs CTA bilaterally, no stridor

Gastrointestinal: soft, non-distended, minimal discomfort to palpation diffusely

Musculoskeletal: 2 puncture marks are visible superior & lateral to the left heel with minimal oozing of serosanguinous fluid form the puncture wounds, there is tenderness to palpation around the wounds with moderate swelling and some discoloration to the area, as well as minimal swelling of the left ankle & left lower extremity, no blisters are present, patient is able to move all toes of the left foot, there is decreased motion of the left ankle due to pain, otherwise strength is 5/5 in all extremities, pedal pulses present bilaterally, good tone in all 4 extremities

Neurological: A&Ox3, patient unable to walk due to pain, extra-ocular movements are intact, visual fields intact, vision is 20/20 OU, facial sensation & strength intact, hearing intact to finger rub, tongue protrudes in the midline, uvula midline with phonation, shoulder shrug intact, bedside finger to nose intact, rapid alternating movements intact, DTR’s 2 bilaterally

Eastern Massasauga Rattlesnake


1. Proper pre-hospital care of rattlesnake bites includes:

(a) applying a tourniquet on the affected limb proximal to the bite

(b) immobilization of the affected limb

(c) immersion of the affected extremity in ice water

(d) the use of a specialized suction device to remove venom

2. Death from pit viper bites is most often due to:

(a) septic shock

(b) neuromuscular blockade

(c) increased capillary membrane permeability

(d) cell death secondary to apoptosis

3. The initial dose of FabAV (CroFab) is:

(a) 1-3 vials

(b)  4-6 vials

(c) 7-10 vials

(d) None; FabAV is no longer indicated for pit viper bites in the U.S.


Michigan’s only venomous snake is:

(a) Eastern massasauga rattlesnake (Sistrurus catenatus)

(b) Cottonmouth water moccasin (Agkistrodon piscivorus)

(c) Timber rattlesnake (Crotalus horridus)

(d) Eastern diamondback rattlesnake (Crotalus adamanteus)


1. B

2. C

3. B

4. A

Pit Vipers

North America has two snake families with venomous members, the Vipers (subfamily Crotalids) and the Elapids. The Crotalids, or pit vipers are native to every state except Maine, Alaska, and Hawaii and account for 98% of all venomous snakebites in the United States. They include rattlesnakes, copperheads & water moccasins. The eastern massasauga rattlesnake is Michigan’s only venomous snake. The massasauga can be characterized as a shy, sluggish snake that prefers to avoid confrontation. However, if provoked, their short fangs can easily puncture skin and they possess a potent venom. Pit vipers, as their name implies, have a characteristic pit midway between the eye and the nostril on both sides of the head. They also usually have a triangular-shaped head, elliptic pupils, fangs and a single row of subcaudal plates. Also, it is important to keep in mind that rattles are brittle and some adult rattlesnakes may break or lose their rattles.

Marx: Rosen’s Emergency Medicine, 7th ed.

Clinical Presentation of Pit Viper Bites

The signs and symptoms of a venomous snakebite vary considerably and depend on many factors including the location of the bite, the amount of venom injected (up to 25-50% of snake bites are “dry” bites), the size, age & general health of the victim and characteristics of the snake such as size & potency of the venom. Because of these multiple variables, the individual clinical response is the only way to judge the severity of a venomous snakebite.

The most consistent symptom associated with pit viper bites is immediate burning pain in the area of the bite, whereas pain may be minimal with bites of elapids and other exotic snakes. Edema surrounding the bite that gradually spreads proximally is a common finding. This edema is usually subcutaneous, begins early, and may involve the entire extremity. Compartment syndrome is rare but suspicion should be high. Petechiae, ecchymosis, and serous or hemorrhagic bullae are other local signs. Necrosis of skin and subcutaneous tissue is noted later and may result from inadequate doses of antivenin.

Many systemic symptoms, such as weakness, nausea, fever, vomiting, sweating, numbness and tingling around the mouth, metallic taste in the mouth, muscle fasciculations, and hypotension, often occur after pit viper envenomation. Death from pit viper bites is associated with increased capillary membrane permeability & disruption of the coagulation mechanism. Ultimately, these two processes lead to hypovolemia, massive pulmonary edema, shock, and death. Heart and kidney damage occurs secondary to these mechanisms. An allergic type of reaction may add to this process through release of histamine and bradykinin.


Antivenom is the mainstay of therapy for poisonous snakebites and all patients bitten by a pit viper should be taken promptly to a health care facility. First aid measures should never substitute for definitive medical care or delay the administration of antivenom. The patient should be quickly removed from striking range to avoid further bites. Efforts should be made to keep the patient calm and the affected limb should be immobilized & kept below the level of the heart to decrease the rate of venom absorption. Constriction bands may be used if medical care will be delayed (> 30 minutes). The band should be snug but loose enough that a finger can slide comfortably underneath. Jewelry and tight-fitting clothing articles should be removed. First aid measures such as incision & suction, tourniquets, electric shock and ice water immersion of the affected limb are contraindicated and may cause further damage.

Once the patient arrives at a medical facility, a prompt primary survey should be performed to assess ABC’s. IV access should be quickly established and the patient should be placed on continuous cardiac & respiratory monitoring. Supportive therapy should be administered such as IV fluids for hypotension. Laboratory studies should be ordered (see below).

Tintinalli’s Emergency Medicine > Section 16: Emergency Medicine in Unique Environments > Chapter 206. Reptile Bites > Crotalinae (Pit Viper) Bites > Treatment > ED Management >

Antivenom is the mainstay of therapy for poisonous snakebites. Crotalidae Polyvalent Immune Fab (Ovine) (FabAV; commercial name CroFab) is now used in the U.S. It is produced by immunizing herds of sheep with one of four crotaline snake venoms. The equine-derived Antivenin (Crotalidae) Polyvalent [Wyeth] is no longer available, except for certain zoos. All patients with bites that show evidence of progressive signs and symptoms should receive antivenom promptly. Progression is defined as worsening of local injury (e.g., pain, ecchymosis, or swelling), abnormal results on laboratory tests (e.g., worsening platelet count, prolonged coagulation times, decreased fibrinogen level), or systemic manifestations (e.g., unstable vital signs or abnormal mental status). FabAV is administered as a larger “initial control” dose followed by three smaller maintenance doses (see table below).

FYI: DRH pharmacy has 18 vials of CroFab and we still have 7 vials of the expired Wyeth Antivenin (but it can still be used for up to10 years if necessary).

Case 5.5

Case Presentation by Dr. Megan Dougherty

A 43 year old female with a history of IVDU presents to the ED via EMS with a four day history of progressive left upper extremity swelling and pain with subjective fevers.  The patient had a history of a fall off a ladder while she was at work 2 days prior and was unsure of whether she injured the arm, but did not seek medical attention at that time because she thought nothing of it at the time. However, as the pain has increased, the patient sought medical attention.  When asked where she injected drugs, the patient stated that she had injected in the deltoid region of that extremity before, but never in the forearm.

ROS:  Positive for subjective fevers, pain and swelling of left upper extremity in addition to progressive erythema.

PMH: none

PSH: none

Allergies: no known drug allergies

Family History: no history of hypertension or diabetes

Social History: Uses tobacco 1/3 ppd. Uses IV drugs-heroin user for 8 years and cocaine.  Last injection was 3 days prior to presentation.

Physical Exam

Constitutional: T: 36.8, BP: 107/70, HR: 110, Respirations: 16. The patient appears well developed with thin body habitus.  The patient is lying comfortably on stretcher.

HEENT: NC/AT. EYES: Sclera clear.

CVS: RRR.  Good S1, S2.  NO S3 or S4.

Respiratory: Clear to auscultation bilaterally. No wheezes

Abdomen: Soft, non tender, non distended.

Musculoskeletal exam: LEFT UPPER EXTREMITY: 2+ radial pulse, area of fluctuance on the lateral distal part of the forearm, marked tenderness and cellulitis involving the entire left upper extremity with some crepitus, decreased active and passive ROM in the shoulder, elbow and wrist, Nikosky sign negative


WBC: 16.8, Hgb: 14.1, Platelets: 275

Na: 128  K:3.8  CL:93  Bicarb:21  BUN:20 Creatinine: 1.0 Glucose: 110



  1. Based on the patient’s x-ray and physical exam findings, what is the most likely clinical diagnosis?
    1. polymyositis
    2. gas gangrene
    3. necrotizing fasciitis type 1
    4. necrotizing fasciitis type 2
    5. myonecrosis
  1. What are cultures likely to grow?
    1. anaerobes only
    2. non group A streptococcus only
    3. group A beta hemolytic streptococci and staphylococcus aureus
    4. non group A streptococci and anaerobes
    5. staphylococcus aureus
  1. Risk factors for necrotizing fasciitis include:
      1. diabetes
      2. poor circulation
      3. immunocompromise
      4. trauma
      5. IVDA
      6. all of the above

    1. d
    2. c
    3. f


    The patient presents with a history and radiographs highly suggestive of necrotizing fasciitis. Necrotizing fasciitis is infection of the fascia, subcutaneous tissue and skin that is potentially lethal. The CDC reports that there are 500-1000 new cases of necrotizing fasciitis reported yearly in the United States, however this is an underestimate as this only reports those infections caused by group A streptococcal infections.

    Necrotizing Fasciitis Classification:
    Type I infections: The most common type. On average, 4 or more organisms are isolated including non group A streptococci and anaerobes. Diabetes, obesity, PVD, CKD and alcohol abuse are commonly found in patients with this type of infection. The infections are typically found on the abdomen and perineum. Specifically named types include Fournier’s gangrene (involves perineum).

    Type II infections: Typically caused by group A B hemolytic streptococci species, but staphylococcus aureus is increasingly associated with type II infections.

    Typical presentation:
    -Initial presentation is typically pain, degree of pain is typically disproportionate to the physical findings.
    -eventually, blistering, crepitus, bullae or hemorrhagic blebs will develop.

    Direct examination of involved tissues is usually required to make the diagnosis
    Radiographs only demonstrate gas in the soft tissues about 1/3 of the time
    CT has a sensitivity of about 80% for the presence of soft tissue gas but is not specific for necrotizing fasciitis
    MRI: low sensitivity (80-90%), low specificity (50-55%)

    1. Fluid resuscitation and electrolyte/acid/base correction
    -major goal is to restore intravascular volume, which is always depleted in patients due to fluid shifts associated with response to infection
    -Crystalloid fluids are utilized as first line treatment. Lactated Ringers is preferable since there is usually an element of acidemia
    -If anemia is present, the patient should be given blood. Anemia is sometimes caused by hemolysis due to toxins produced by some of the microorganisms present in the infection
    -The most common electrolyte abnormality is hyponatremia and hypocalcemia. The hypocalcemia is caused by precipitation of calcium in necrotic subcutaneous fat.

    2. Initiation of antimicrobial therapy
    -initial broad-spectrum antibiotics should be started. Possible therapies include:
    – clindamycin + PCN
    – 2nd generation cephalosporin + ciprofloxacin

    Based on type of infection
    -Type I-start Piperacillin-tazobactam + Clindamycin + Ciprofloxacin- due to the polymicrobial nature of these infections, multiple antibiotics need to be employed. Clindamycin has been shown to suppress the toxin production by S. aureus, hemolytic streptococci and clostridia and should be included when these organisms are present or suspected and for all patients with hypotension, coagulopathy or organ system failure. If the patient happens to be allergic to clindamycin, then linezolid or vancomycin may be used, but they do not have the same toxin production suppressive properties.

    -Type II-start Clindamycin+Penicillin or Linezolid (if PCN allergy) or Vancomycin (if PCN allergy)
    -Doxycycline should be added when the infection is thought to be due to Vibrio or Aeromonas.

    3. Immediate debridement of necrotic tissues*
    -Need to have early involvement of the surgical team in patient care

    *Single most effective treatment is timely debridement of necrotic tissue
    4. Support of failing organ systems

    Long Term Outcomes:
    Mortality rate ranges from 6-76%, with cumulative mortality rate at about 35%.
    Diabetes mellitus is the most important predictor of mortality
    Other contributors to mortality include: Advanced age, two or more associated comorbidities, a delay before surgery of greater than 24 hours and presence of streptococcal toxic shock syndrome.


    Meizlin, HW and JA Guisto. “Soft Tissue Infections.” in Rosen’s Emergency Medicine Concepts and Clinical Practice 7th edition. 1845. Ed. Marx. Philadelphia: Mosby Elsevier, 2010.

    Ustin, JS and MA Malangoni. Necrotizing soft tissue infections. Critical Care Medicine. 2011; 39(956-62.):21