Senior Report 5.23

 

Case Presentation by Dr. Brandon Cheppa

Chief Complaint: “My foot hurts”

History of Present Illness:  This is a 40 year old male with a one day history of sudden right foot pain.  He states that last night he jumped over a fence and upon landing he had sudden onset of pain in his foot.  He states that he has barely been able to put weight on his foot and that walking is difficult.  The pain is constant, worsening, and he has never had pain in his foot like this before.  He denies any knee, hip, or back pain.  He denies any history of pain in any of his other joints.  He denies any head trauma, loss of consciousness, or numbness in any of his extremities.  He has not tried any medications and nothing seems to make it better or worse.

Review of Systems:  As per HPI

Past Medical, Family, and (or) social history:

Past Medical History:  Negative for Hypertension, Negative for diabetes

Past Surgical History: Denies any surgeries

Medications: None

Allergies: No known drug allergies

Social History:  Smokes cigarettes, denies alcohol, drugs, or intravenous drug use.

Family History: Unknown

Examination of organ system and body areas:

Vital signs: BP: 136/97, HR: 88, RR: 18, Temp 36.7 orally

Constitutional:  Patient appears comfortable, sitting in a wheelchair

HEENT:  Head is normocephalic, atraumatic, no tenderness to palpation, PERRLA, EOMI,

Neck:  Soft, supple, no masses, no cervical midlinetenderness

Cardiovascular:  Normal heart sounds

Respiratory:  Normal breathsounds

Gastrointestinal:  Soft, non-tender, non-distended, no palpable masses

Skin: No lacerations, no open lesions, no rashes seen

Neurological:  Patient is AOx3, acting appropriately, No sensory deficits,  grossly moving all extremities well, normal facial symmetry.  He has a hobbling gait favoring his left side and is unable to put weight on his right leg.

Back: No midline tenderness of entire spine

Skin:  No ecchymosis or breaks in skin seen

Musculoskeletal:  Upper extremities and Left lower extremities have full range of motion at all joints with 5/5 strength to flexion and extension and have no swelling or deformities to palpation.  Focused exam of left lower extremity:  Full range of motion of hip and knee with 5/5 strength to flexion and extension.  Patient has no calf tenderness, no Achilles tendon tenderness.  Right ankle has no malleolar tenderness.  He has tenderness of his midfoot, it is red, swollen with no crepetus or fluctuence.  He has good symmetrical pules of both feet with good capillary refill and he is neurovascularly intact.

Labs: None

Images: Complete x-ray of the foot was obtained

Questions:

1) The x-ray obtained is concerning for which type of fracture?

A. Boxer’s fracture

B. Jones’ fracture

C. Lisfranc’s fracture

D. Maisonneuve fracture

E. Salter-Harris type IV fracture

2) What is the appropriate disposition for the patient?

A.  Ace wrap, crutches, non-weight baring, follow-up with orthopedic clinic in 1 week

B.  Ace wrap, “ortho shoe”, weight bare as tolerated, follow-up with orthopedic clinic in 1 week

C.  Immediate orthopedic consultation in the emergency department

D.  Posterior mold splint, crutches, non-weight baring, follow-up with orthopedic clinic the next day

3) What is the most common complication this patient will experience if this injury is not appropriately treated?

A.  Compartment syndrome

B.  Deep Venous Thrombosis

C.  Degenerative Arthritis

D.  Osteomyelitis

E.   Regional Pain Syndrome

Answers:

1)    C

2)    C

3)    C

Discussion:

A Lisfranc fracture is one part of the collective term Lisfranc Injury.  A Lisfranc injury can very in radiographic presentations, but are all centered around any injury to the tarsometatarsal joints, also known as Lisfranc’s joint.

The Lisfranc’s Joint is made up of the five metatarsals and their articulations with the three cuneiforms, the navicular bone, and the cuboid bone.  The biomechanical structure of the foot allows for passage of neurovascular bundles and connective tissues through the foot without being crushed by a person’s weight.  The metatarsal bones have a trapezoid shape and are arranged in an arch configuration using the second metatarsal as the “keystone”.  Under normal physiologic conditions the second metatarsal has very little motion compared to the other four metatarsal bones.

The Lisfranc ligament is the strongest of the tarsometarsal ligaments and connects the lateral surface of the medial cuneiform to the medial base of the fifth metatarsal.  There are no proximal ligaments between the bases of the first and second metatarsals, most likely due to the evolution of the foot from a primitive hand structure where the first metatarsal evolved from a primitive thumb.  There are ligamentous connections between the second through fifth metatarsal bones and all five have distal ligamentous connections.  One to two mm of dorsolateral displacement of the affected base of the second metatarsal can lead to 13-25% reduction of contact at the joint.  The dorsalis pedis artery and deep peroneal nerve can be compromised with this injury due to their locations in the foot.

Patients can injure this structure by many mechanisms and it usually results in a closed fracture.  Motor vehicle collisions, falls, and even pedestrians tripping on curbs can produce this injury.  It stems from forceful abduction of the forefoot of a plantar-flexed foot.  Windsurfers, motorcyclists, and people who get thrown off horses have been historically at risk for this injury.  Patients typically will present with pain, swelling to the midfoot, and difficulty placing weight on the injured extremity.  They may present with ecchymosis to the plantar surface of the midfoot, although not specific, it is suggestive of an injury.  A detailed history and physical exam with attention to other associated injuries such as at the knees, hips, and lower back will guide your work-up.

Complete x-rays of the foot will pick up a Lisfranc injury 90% of the time.  With high clinical suspicion, and a presumptive negative x-ray, you can elect to get “stress” views of the foot which requires the patient to place weight on the injured foot.  Often times this is difficult to accomplish due to significant pain, or lack of ability to interpret a “stressed-view” of a foot x-ray, therefore a CT scan will aid in diagnosis.

With the knowledge of the anatomy combined with the mechanism of force, on radiograph, a fracture at the base of the second metatarsal is pathognomonic of a disruption of the Lisfranc ligamentous complex.  The diagnosis is made radiographically on the anteriorposterior view when there is a gap greater than 1 mm between the bases of the first and second metatarsals.  Other radiographic findings may be present or can lend to the diagnosis such as loss of alignment of the medial edge of the base of the second metatarsal with the medial edge of the middle cuneiform; loss of alignment of the lateral border of the third metatarsal shift with the lateral border of the lateral cuneiform; or loss of alignment of the medial border of the fourth metatarsal with the medial border of the cuboid.  If radiographs are unequivocal, and suspicion is still high, there is a chance of a spontaneously reduced dislocation.

Patient who sustain a Lisfranc injury require an emergency room orthopedic consultation and are to be made non-weight baring until their evaluation.  This is due to the large degree of instability of the joint that could lead to significant disability, and the potential for compartment syndrome and/or neurovascular injury.  Patients typically need to go to the operating room and undergo open or closed reduction with application of hardware.  Patients who have a Lisfranc sprain, will require below-knee casting, crutches, “RICE” therapy, and close orthopedic follow-up due to their potential for operative fixation.

The most common complication of an untreated Lisfranc injury is degenerative arthritis in the form of posttraumatic arthrosis.  Other less common complications include: compartment syndrome in the acute injury setting, deep venous thrombosis due to the amount of immobility, regional pain syndrome.

With early diagnosis and proper orthopedic intervention, 95% of patients at 3.5 years will have an excellent outcome.

The case revisited:

This gentlemen raised our suspicion for a midfoot injury based on his mechanism and physical exam.  We obtained foot radiographs and it showed a fracture of the base of the second metatarsal (circled in green), widening between the bases of the first and second metatarsal (measurement in blue), and a “fleck sign” (circled in red) which is a ligamentous disruption from the base of the second metatarsal.  This radiograph raised our suspicion for a Lisfranc injury and the orthopedic service was consulted.

They requested a CT scan due to the high potential for other associated fractures and it also showed a comminuted fracture of the medial cuneiform bone.

 

They opted to not take him for emergent surgery due to him having an ongoing underlying infection which was unknown during the initial patient encounter.  On reassessment, the patient had been experiencing painless, white discharge from his penis for the last two months.  The orthopedic service felt his infection could complicate his healing due to the chance that hardware will need to be applied during surgery.  They placed him in a cast, made him non-weight baring, and wanted him to follow-up in their clinic when his infection had resolved.  He was swabbed for Gonorrhea and Chlamydia, and treated for both of those infections including Trichomonas.  The results of his cultures were negative making Trichomonas the most likely cause of his infection.  At a follow-up visit in the orthopedic clinic, they felt there was not significant boney displacement and took him to the operating room to achieve “stressed” views of the foot under anesthesia.  They were satisfied with the stability of the joint and did not undergo any surgical intervention.  He was placed him in a non-weight baring cast and will continue to follow-up in the orthopedic clinic.

References:

Rosen’s, 7th edition, pp 681-695

Tintinalli’s, 6th edition, pp 1742-1746

Browner: Skeletal Trauma, 4th edition, 2008, Foot Trauma chapter

Ouzounian T.J., Shereff M.J.: In vitro determination of midfoot motion.  Foot Ankle  1989; 10:140-146.

Lu J., Ebraheim N.A., Skie M., et al: Radiographic and computed tomographic evaluation of Lisfranc dislocation: A cadaver study.  Foot Ankle Int  1997; 18:351-355.

Senior Report 5.22

Case Presentation by Dr. Claire Jensen

CC: “I have a fever.”

HPI: This is a 61 year-old Caucasian female with recently diagnosed squamous cell carcinoma of the base of the tongue who presents to the Emergency Department after noting a fever of 101.9° F at home approximately one hour ago. She is currently undergoing induction chemotherapy with docetaxel, cisplatin, and 5-FU. She completed her third cycle of chemotherapy 8 days ago, which was administered in the inpatient setting. Prior to hospital discharge, she received a dose of pegfilgrastim for anticipated neutropenia. Apparently, her tumor has responded well to chemotherapy and she is tentatively scheduled to undergo neck dissection with tumor resection in the next four weeks. Her chemotherapy course has been complicated by problems with nausea and mucositis.

She states that she has been seen in her oncologist’s office both earlier today and yesterday for complaints of generalized weakness and twice received infusion of intravenous fluids for “low blood pressure.”  She states that she had just returned home from her doctor’s office late this afternoon when she started to feel very cold. She took her temperature, noted the fever, and returned immediately to the hospital on her doctor’s instruction. She has chronic cough since undergoing tracheostomy, but denies changes in sputum. No chest pain or shortness of breath. She denies dysuria or urinary frequency. She reports nausea and diarrhea associated with this most recent round of chemotherapy, but denies melena or hematochezia.

ROS: Per HPI.

PMH: Asthma, T3N2cM0 squamous cell carcinoma of the base of the tongue.

PSH: Hysterectomy, fine-needle aspiration of neck mass, triple endoscopy and tracheostomy, Medi-Port placement.

Allergies: Codeine and shellfish

Medications: Ondansetron, prochlorperazine, acetaminophen/hydrocodone, diazepam, esomeprazole, fluticasone/salmeterol inhaler, docusate, fexofenadine.

FH: Cancer, hypertension, diabetes, “thyroid problems.”

SH: Remote history of tobacco abuse, quit smoking 21 years ago. Denies alcohol or illicit drug abuse.

PE:

General:.This is a well-developed, thin female. She is awake and alert. She answers questions appropriately and speaks in full sentences. She is mildly ill-appearing.

Vitals: BP 132/74, P 128, R 18, T 38.6 C, SpO2 100% on room air

Eyes: There is mild conjunctival pallor, no injections, sclerae anicteric. Pupils and equal and reactive. Extraocular movements are full.

Ear, Nose, Mouth and Throat: Tympanic membranes are normal in appearance bilaterally. There is no nasal drainage, no sinus tenderness. The oropharynx has slightly dry mucous membranes. There is mild mucositis, no candidiasis. Good dentition.

Neck: Supple, no lymphadenopathy, no JVD. Uncuffed tracheostomy tube without purulent secretions, no erythema or drainage at insertion site.

Cardiovascular: Tachycardic, normal S1, S2. No murmurs, rubs, gallops. No lower extremity edema or calf tenderness.

Respiratory: Lungs are clear to auscultation bilaterally with good air entry.

Gastrointestinal: The abdomen is flat, soft, non-tender and non-distended. Bowel sounds are present.

GU: Deferred.

Musculoskeletal: The head is normocephalic and atraumatic. No tenderness over the neck or spine. There is normal muscle bulk and tone. No erythema or swelling of the joints.

Skin: Warm and dry. No rashes, bruising or diaphoresis. The skin over the Medi-port is without induration

Neurologic: Awake and alert. Symmetric facies. Normal speech. Moves all extremities spontaneously. Sensation intact to light touch in all extremities. Normal gait.

Laboratory Studies:

WBC:                                   0.8

Hgb:                                    8.0

Hct:                                    22.8

Plt:                                     104

Myelocytes:                        0%

Metamyelocytes:              4%

Bands:                                0%

Neutrophils:                    14%

Lymphocytes:                 34%

Monocytes:                     46%

Eosinophils:                     2%

Basophils:                         0%

Na:                                   130

K:                                          3.9

Cl:                                      98

CO2:                                  21

BUN:                                15

Cr:                                      1.0

Glu:                               151

Ca:                                    8.4

Mg:                                   1.3

AST:                               27

ALT:                               11

Alk Phos:                      91

Total Protein:                6.1

Albumin:                         3.2

Lactic Acid:                    2.2

Urinalysis

Glucose                        1+

Ketones                        Negative

Blood                             1+

Bilirubin                       Negative

Specific Gravity           1.015

pH                                  6.5

Protein                           Negative

Nitrite                            Negative

LE                                   Negative

RBCs                                    2-5

WBCs                                   <5

Epithelials                          <5

Casts                               None

Crystals                          None

Bacteria                          None seen

Chest X-Ray

Emphesematous lungs. Normal heart size. No active parenchymal disease. Medi-Port and tracheostomy tubes in stable position.

Questions

1.     What is the patient’s absolute neutrophil count?

a) 12

b) 112

c) 1120

d) 11200

2.  Which of the following parenteral antibiotics is considered first-line therapy for the high-risk febrile neutropenia patient?

a) Cefepime

b) Ciprofloxacin

c) Metronidazole

d) Tobramycin

e) Vancomycin

3.  Which factor is associated with “low risk” febrile neutropenia patients, who may be candidates for outpatient antibiotic therapy after careful consideration?

a) Age >60 years

b) Hematologic malignancy

c) Predominance of gastrointestinal symptoms, such as nausea, vomiting, diarrhea, or           abdominal pain.

d) Presence of underlying structural lung disease, such as COPD.

e) Solid tumors

Answers:

1. B, 2. A, 3. E

Discussion:

Febrile neutropenia is a medical emergency that requires a rapid and methodical response from the emergency physician. Prior to the era of empiric antibiotic therapy, infection accounted for almost 75 percent of mortality associated with chemotherapy. The definition of neutropenia varies between institutions, but is typically defined as an absolute neutrophil count of less than 500 cells/microL, or less than 1000 cells/microL with a predicted nadir of less than 500 cells/microL. Profound neutropenia is defined as less than or equal to 100 cells/microL.

The absolute neutrophil count is calculated by multiplying the total white blood cell count by the percentage of neutrophils and bands.

ANC = (WBC count in 1000s) x [(% Neutrophils/100) + (% Bands/100)

So, in our patient:

ANC = (0.8 x 1000) x ((14/100) + (0/100)

= 800 x 0.14

= 112

Multiple factors are used to categorize patients as high-risk or low-risk for severe infection and include presenting signs and symptoms, the type of underlying malignancy, the type of therapy for the underlying cancer, and the presence of medical comorbidities. Significant comorbidities include uncontrolled cancer, COPD, poor functional status, and advanced age. Patients undergoing induction chemotherapy for acute myelogenous leukemia or a chemotherapeutic conditioning regimen in preparation for hematopoeitic stem cell transplantation are at particularly high risk.  Patients with an ANC <100, hemodynamic instability, GI symptoms such as abdominal pain, nausea, vomiting or diarrhea, new-onset neurological symptoms including altered mental status, underlying chronic lung disease, or evidence of hepatic or renal dysfunction are all considered high risk and should be admitted to the hospital for empiric antibiotic therapy. Additionally, it is important to observe neutropenic precautions when the patient is in the emergency department, with placement in a private room if available, use of masks by staff members, and adherence to rigorous hand hygiene. Patients with solid tumors, anticipated short duration of neutropenia (<7 days), and lack of comorbid conditions can be considered for outpatient antibiotic therapy under close supervision, but only after thorough diagnostic evaluation and discussion with their managing oncologist.

Initial evaluation and management of these patients in the emergency department is not tremendously different from that of the septic patient. Emphasis is on immediate and aggressive correction of hemodynamic instability, identification of potential sources using diagnostic studies, early administration of empiric antibiotics, and source control (venous catheters, ports, urinary catheters, etc.). However, it is important to be mindful that severely neutropenic patients are not capable of mounting an immune response the way septic patients are, so a negative chest x-ray or absence of pyuria on urinalysis does not necessarily exclude infection. Standard diagnostic work-up includes CBC with differential, electrolyte studies including renal function, transaminases to assess for hepatic insufficiency, two sets of blood cultures with one from any indwelling catheter if present, chest radiograph, and urinalysis with urine culture. The need for additional studies such as other imaging, lumbar puncture, or fungal cultures are not standard, but should be considered on a case-by-case basis. Neutropenic patients that are afebrile but present with symptoms concerning for infectious illness such as hypothermia, hypotension, abdominal pain, or mental status changes should be treated as high-risk patients.

Early institution of antibiotic therapy is of utmost importance in the setting of febrile neutropenia. Early studies documented mortality rates as high as 70 percent in cases where the administration of empiric antibiotics was delayed. Therapy should be tailored based upon known or suspected sources of infection, the patient’s history as well as any previous culture data or recent antibiotic use, and awareness of institutional nosocomial infection patterns. The Infectious Disease Society of America issued new guidelines in 2010 for the treatment of neutropenic fever, which includes the initiation of monotherapy with an anti-Pseudomonal beta-lactam agent such as cefepime, meropenem, imipenem, or piperacillin-tazobactam. Other antibiotics such as aminoglycosides, fluoroquinolones and/or vancomycin may be added in patients with complicated infections (eg, hypotension or mental status changes) or if antimicrobial resistance is suspected. Vancomycin and other agents that target gram positive organisms are not recommended as part of the standard initial management unless there is suspicion for catheter-related blood stream infection, skin or soft tissue infection, pneumonia or hemodynamic instability is present.

This patient was started on empiric antibiotic therapy with cefepime and vancomycin and admitted to the hospital. She had no further febrile episodes while in the hospital. Her WBC counts started rebounding the next day, and all of her cultures showed no growth. She was discharged in good condition after three days in the hospital and is currently still on schedule to undergo surgical resection of her tumor.

Senior Report 5.21

Case Presentation by Dr. Sarah Albers

CHIEF COMPLAINT(S):

“She has got a fever and is throwing up.”

HISTORY OF PRESENT ILLNESS:

A 16-year-old Caucasian female presents with both of her parents to the emergency department.  The adolescent girl complains of “not feeling well over the past one day.”  She feels dizzy, which she describes further as persistent wooziness that is not positional; there is no sensation that she or the room is spinning. She also feels nauseous, and has a headache – described as a tight band around her temples, with no blurriness of her vision, or change in her vision or hearing. No history of trauma or falls.  She also has generalized myalgias, a sunburn like rash over her trunk, back and upper extremities, redness to her eyes, chills and a fever that started abruptly a couple of hours ago; her temperature was 104 F at home and she took Tylenol, but then vomited it back up.  She states that it hurts her muscles when she takes a deep breath.  She has had no cough or chest pain. She denies shortness of breath or difficulty breathing. No runny nose or sore throat.  No leg pain.  She says she is just feeling “generally weak and my whole body hurts.”

She has had nausea and vomiting today, approximately 10 to 20 episodes of emesis that have been nonbloody, nonbilious.  She has been unable to keep anything down except for a little bit of water and ice chips.  She denies any abdominal pain, blood in her stools, or any black tarry stools.  She states she has bowel movements regularly; her last bowel movement was today with no diarrhea or constipation.  She denies any dysuria, urgency or frequency.  She denies any vaginal discharge, but is currently on her period.

She said she started feeling a little bit “bad” last night with the beginning of a headache; however, today was when everything “hit” her.  She describes as all of these symptoms coming on suddenly.  Mom states she has not been hospitalized nor has she been treated with antibiotics over the past 2 months.  Two months ago she was treated for pneumonia.  She is currently on a homoeopathic medication for Candida called Threelac.  Otherwise, this child is healthy and takes no medications. She has no known sick contacts.

REVIEW OF SYSTEMS:

CONSTITUTIONAL:  Positive fever & chills.

EYES:  No change in vision.  Positive red eyes.

ENT:  No change in hearing, runny nose, or sore throat.

RESPIRATORY:  No wheezing, cough, or hemoptysis.

CARDIOVASCULAR:  generalized muscle soreness of her chest wall when taking deep breaths, otherwise no pain.  No palpitations or edema.

GI:  Positive nausea & vomiting.  No diarrhea or constipation.  No black tarry stools or bright red blood per rectum.

GU:  No dysuria, urgency, or frequency.  She is currently on her menstrual cycle.  She does use tampons, and currently has one in.

MUSCULOSKELETAL:  Positive myalgias.  No injury or trauma.

SKIN:  Positive erythematous rash over her trunk, arms, and back.

CNS:  Generalized weakness, no syncope, numbness, speech deficit, confusion or altered mental status.

PAST MEDICAL, FAMILY, AND(OR) SOCIAL HISTORY:

PAST MEDICAL HISTORY:  None.  However, recent treatment for pneumonia and the patient is currently being treated with a homeopathic medication for a possible candida infection.

PAST SURGICAL HISTORY:  None.

MEDICATIONS:  Include a homeopathic called Threelac to treat Candida.  She is also taking a “digestive enzyme”.

ALLERGIES:  NO KNOWN DRUG ALLERGIES.

FAMILY HISTORY:  negative for hypertension or diabetes

SOCIAL HISTORY:  Negative for tobacco, alcohol, and drugs.  The patient is not currently sexually active.  She has never had sex in the past.  They do have working smoke detectors in the house.  She does always wear a seatbelt in the car.  There are no guns in the house. She does do well in school.

EXAMINATION OF ORGAN SYSTEMS-BODY AREAS:

VITAL SIGNS:  On arrival, her blood pressure 111/90, heart rate of 122, respiratory rate is 18, temperature is 39 orally, pulse ox is 95% on room air.

CONSTITUTIONAL AND GENERAL:  The patient is a tall, thin, well-developed, well-nourished female, in no acute respiratory distress, speaking in full sentences, cooperative for exam, A and O x3. She is nontoxic appearing.  She smiles on exam and converses with her parents and me and jokes around a bit. She is sitting upright on the stretcher with her legs drawn up in front of her with her arms wrapped around her legs.  She is wearing a patient gown.  She does have slightly reddened eyes as well as reddish hue to her arms on observation.

HEENT:  Head is normocephalic, atraumatic.  No acute masses or lesions.  Eyes:  Pupils are 3 mm, round and reactive to light.  Extraocular movements are intact.  No conjunctival pallor.  Sclerae are anicteric.  Sclerae are also injected bilaterally.  No evidence of discharge in her eyes.  Nose: no nasal discharge is noted.  Ears:  Tympanic membranes are clear bilaterally. Landmarks are clearly visualized. Mouth and throat:  Mucous membranes are moist.  No erythema, tonsillar exudates or intraoral lesions.

NECK:  Supple.  No lymphadenopathy.  No thyromegaly.  No tenderness to palpation of the cervical spine.  Trachea is midline.  No meningismus or nuchal rigidity.

LUNGS:  Clear to auscultation bilaterally.  No wheezes, rales or rhonchi.  Good air exchange in all lung fields.

HEART:  S1, S2 are present.  Tachycardic rate and regular rhythm, pulses in all four extremities are equal and 2+.

BACK:  No cervical, thoracic, lumbar or sacral spinal tenderness.  The patient has no CVA tenderness.

EXTREMITIES:  No clubbing, cyanosis or edema.

SKIN: The patient does have an erythematous, first degree sunburn-looking rash on the anterior aspect of her bilateral upper extremities as well as her anterior and posterior chest and abdominal wall.  It is blanching in nature.  There are a few very tiny papules on the area of her anterior forearm.  There is no sloughing of skin or bullae formation.  There is no blistering of the skin.  Skin is not tender to touch.  Skin is warm to touch throughout.  She has no erythema or rash on her palms or soles.  She has no rash or erythema on her bilateral lower extremities.

GU:  Performed in the presence of a female nurse chaperone shows normal, Tanner Stage 5, female external genitalia. On speculum exam a tiny amount of blood in the vaginal vault, patient is currently menstruating.  No tampon is present. There is a closed cervical os.  The patient does have pain on insertion of the speculum.  Swabs were obtained. The patient does have cervical motion tenderness as well as bilateral adnexal tenderness. No masses were palpitated. There are no excoriations or sores on the inside of the vaginal vault. Microscopy was negative for trichomonas or clue cells.

NEUROLOGIC:  The patient is awake, alert, and oriented x3.  Normal speech and hearing to finger rub.  Face is symmetrical.  No nystagmus is present.  Sensation is equal and intact throughout.  Motor strength is 5/5 in all four extremities.  The patient does ambulate with a normal gait.

Questions:

1)    At what point does the accepting hospital assume responsibility for a transfer patient?

  • a.  as soon as the transporting service (ambulance, helicopter) reaches the accepting hospital grounds
  • b.  half-way through transit, when the accepting facility is closer than the  sending facility
  • c.  when the patient arrives inside the accepting facility doors
  • d.  when the patient leaves the sending facility

2)    Which of the following is most likely to predispose a patient to this condition?

  • a.  niacin use
  • b.  recent antibiotic use
  • c.  recent seafood ingestion
  • d.  tampon use

3)    What condition is the patient most likely suffering from?

  • a.  drug-induced dermatitis
  • b.  Stevens-Johnson syndrome
  • c.  toxic epidermal necrolysis
  • d.  toxic shock syndrome

Answers:

1. d

2. d

3. d (Staph Aureus) Toxic shock syndrome from tampon use

Discussion:

Toxic Shock Syndrome (TSS) is characterized by severe prolonged shock and is caused by a toxin produced by S. Aureus. This was originally described by Todd et al. in 1978.  They reported a series of 7 cases of kids 8-17, S. Aureus was cultured from various body sites, but not the blood, in 5 of the 7 cases.  Most of the subsequent cases have occurred in menstruating females often after a menstrual period associated with tampon use.  In the early 1980’s the consistency of tampons were changed to reduce absorbancy due to growing concerns about TSS.  In the late 1980’s group A Streptococcal toxic shock syndrome (strep TSS) was described because it shares so many feature with TSS.

Menstruation and tampon use is the most common setting for TSS, but non-menstruation TSS accounts for just under half of the reported cases.  Of these cases, strep TSS account for just over half of the cases. Nonmenstrual TSS is associated with super infections of skin including burns, surgical sites, dialysis catheters and lung (influenza associated). It can also happened in association with staph respiratory infections or colonization without an obvious infection source. Strep TSS is classically associated with more severe soft tissue infections including necrotizing fasciitis and myositis, as well as pneumonia, peritonitis, myometritis and osteomyelitis. Mortality reaches 30-70% in strep TSS, and in staph TSS it is <3%.

Staph TSS is caused by the colonization or infection with toxigenic strains, specifically TSST-1 (toxic shock syndrome toxin – 1). Because the organism is not invasive, blood cultures are often negative. Strep TSS is caused by invasive infection with toxigenic strains of GAS (Group A Strep).

The clinical presentation of Strep TSS and staph TSS is similar. The primary difference is that an identifiable source is virtually always present with strep TSS and colonization alone may lead to staph TSS.

Clinical presentation:

Patients may present with fever, chills, nausea, vomiting, diarrhea, headache, myalgias, and pharyngitis.  Prodrome may last hours to 2 or 3 days. The fever is usally high and abrupt in onset (although septic patients may be hypothermic).  The classic rash is a nonpuritic, diffuse, blanching, macular erythroderma.  Initially, this may be mistaken as flushing due to fever.  The rash is typically diffuse but may be localized to the trunk, extremities or perineum.  After about a week a fine flaking desquamation occurs of the face, trunk and extremities followed by full thickness peeling of palms, soles and fingers. This classic rash is much more common with staph TSS and is present in less than 10% of patients with strep TSS.

TSS Rash

Toxic shock syndrome. A. Appearance of the rash associated with staphylococcal toxic shock syndrome (TSS). B. Gangrenous toes associated with prolonged hypotension in TSS. C. Desquamation of the skin that occurs during the resolution of TSS.

http://5minuteconsult.com/ViewImage/2027438

The patient’s mental status is frequently abnormal, out of proportion to the hypotension that ensues. Confusion, somnolence, agitiation and combativeness are present in 55% of strep TSS and even more frequent in patients with staph TSS. Other physical findings include pharyngeal and conjunctival erythema, strawberry tongue and peripheral edema. Vaginal mucosal erythema and purulent vaginal discharge may be present in menstrual TSS. As more organ systems become involved a wide range of signs and symptoms may be seen.  GI involvement manifests itself by nausea, vomiting, diarrhea and abdominal pain.  Hepatomegaly may be present. Patients may become hypoxic and develop rales on lung examination.

Comparison for staph and strep TSS

Feature Staph Strep
Age Primarily 15-35 years Primarily 20-50 years
Sex Women > men Women = men
Severe pain Rare Common
Hypotension 100% 100%
Erytheroderma rash Very common Less common
Renal failure Common Common
Bacteremia Low 60%
Tissue necrosis Rare Common
Predisposing factors Tampons, packing, ?NSAID use? Cuts, burns, bruises, varicella, ?NSAID use?
Thrombycytopenia Common Common
Mortality rate 3% 30-70%
  • Risk Factors for TSS
  • tampon use
  • postoperative wound infections
  • postpartum period
  • nasal packing
  • cancer
  • common bacterial infections
  • ETOH abuse
  • infection with influenza A
  • infection with varicella
  • Diabetes
  • HIV
  • Chronic cardiac disease
  • Chronic pulmonary disease
  • NSAID (may mask symptoms rather than be a risk factor)

Diagnosis:

 The case definition for TSS does not require a positive culture for S. Aureus, but a positive culture is required to diagnose strep TSS. Specific tests are not required to rule out other diseases, but if such tests are obtained the results must be negative.

No specific laboratory changes are associated with TSS, but many abnormalities are common including: leukocytosis or leukopenia, bandemia (very common), elevated creatinine and hemoglobinuria, hypoalbuminemia and hypocalcemia. Other abnormailities include anemia, thrombocytopenia, hyperbilirubinemia, elevated transaminase levels and sterile pyuria.

A lumbar puncture should be performed on febrile patients with altered mental status to evaluate for meningitis. It is prudent to wait for the coagulation profile before the LP, as DIC may exist at the time of presentation. The CSF is normal in TSS.

Management:

TSS patients should receive aggressive fluid resuscitation with crystalloids and may require up to 10-20 L a day! Supplemental oxygen should be provided to all septic patients regardless of initial pulse ox. This will allow for maximal tissue oxygenation and reduces acidosis. They should have continuous cardiac and pulse oximetry monitoring.

The source of bacteria (tampons, nasal packs and other foreign bodies) must be removed immediately.  (On our case patient, ROS stated tampon was in and on pelvic exam tampon was out).  Prompt surgical consultation should be obtained to debride wounds. If specimens are sent for culture, the lab should be informed of the suspected diagnosis.

Patients who do not respond to fluids require vasopressors.  Antibiotics (broad spectrum) need to be initiated early in TSS.  Clindamycin is recommended, as it is a potent suppressor of bacterial toxins (dose is 600-900 mg IV q 8h or peds dose is 20-40 mg/kg/day divided every 6-8 hours).


Disposition:

All patients thought to have TSS should be admitted to an ICU!  Again, prompt surgical intervention should be obtained for patients with a wound source.

So back to our patient…

16-year-old adolescent girl presenting with suspected TSS from tampon use.  We had her immediately remove her tampon.  (Note tampon in on ROS, but not during pelvic). On re-evaluation, repeat BP was 70/30-50’s and lab work returned showing:  elevated lactate, acute renal failure, leukocytosis, mild elevation in coags (PT/INR).

ID was consulted and recommended broad spectrum abx including clindamycin, vancomycin and ceftriaxone, which were all started. BP remained at 70’s systolic after 5 L of crystalloid fluids.  Fever and vomiting was controlled with IV NSAIDS and antiemetics.

Patient’s mental status remained AOx3 the entire time, she never looked toxic, continued to smile on exam and wanted to continually walk to the bathroom.  Decision was made to transfer to CHM PICU as a direct admission, CHM requested we not start pressors or a central line at our facility.  They did send PANDA to come get this patient by helicopter.  She ended up on three pressors; dobutamine, Dopamine and vasopressin (all were weaned by hospital day 3) at CHM in the PICU after a femoral line was placed.  Same antibiotics were continued.  Vaginal swab grew Staph Aureus (MSSA), GC and Chlamydia were negative. Blood cultures were negative.  Urine culture grew staph coagulase positive.  After three days in the PICU she was transferred to the ID service and then discharged after one day on the floor.  She was sent out with a 3-week course of clindamycin.  She developed C. Difficile colitis and was treated with oral flagyl and vancomycin.

Intern Report 5.20

Case Presentation by Dr. Jessica Ruffino

HPI: 25y/o female at 36 weeks GA presents to ED via EMS as a trauma code after MVA.  Patient was a restrained driver, airbags were deployed.  Patient states she was rear-ended while stopped at a traffic signal and hit the car in front of her.  Other vehicle was driving about 25mph.  Patient complains of abdominal pain mostly across lower abdomen.  Patient thinks she is having contractions, unsure of frequency.  Denies loss of fluid.  Last felt fetal movement prior to accident.  Patient denies chest pain, SOB, N/V.  Patient states her pregnancy has been uncomplicated, denies high blood pressure or diabetes.  Patient did not lose consciousness, was ambulating at scene per EMS.

ROS:  Negative except for stated in HPI

PMH:  G1P0.  Denies asthma, diabetes, hypertension

PSH:  None

Medications: Prenatal vitamins

Allergies: NKDA

SH:  Denies alcohol, tobacco, drug use.

Physical Examination:

Vital signs: BP 100/75, HR 100, RR 16, Temp. 36.9°, Pulse ox. 98% on RA

Constitutional: Patient is well nourished, gravid uterus.  No respiratory distress.  Appears anxious.

Head:  Normocephalic, atraumatic.  No tenderness to palpation.

Eyes:  Pupils 3mm bilaterally, round and reactive to light.  EOMI.  No conjunctival pallor.  No scleral icterus.

ENMT:  No hemotypmanum bilaterally.  No rhinorrhea or epistaxis.  Mucous membranes are moist.  No erythema or exudates in throat.

Neck:  In cervical collar.  No c-spine tenderness to palpation, no palpable deformities. Cardiovascular:  S1, S2.  Slightly tachycardic.  Regular rhythm.  No murmurs, rubs or gallops.

Respiratory:  Lungs CTAB.  No wheezes, rhonci or rales.  No tenderness over chest wall.  No palpable crepitus over chest wall or neck.

Gastrointestinal:  Gravid uterus.  Uterus is firm.  Fundus palpable about 15cm above umbilicus.  Tenderness to palpation in lower quadrants bilaterally.  Positive seatbelt sign across abdomen.

Genitourinary:  Sterile speculum exam showed small amount of bright red blood in vaginal canal.  Cervix is closed.

Musculoskeletal:  No TTP or deformities palpated along entire spine.  No obvious deformities.  No swelling.  No dependent edema.  2+ DP pulses bilaterally.

Skin:  No lacerations or rashes.  Positive seatbelt sign across abdomen.

Neuro:  Awake, alert and oriented x 3.  Normal speech.  Strength is 5/5 proximally and distally and bilateral upper and lower extremities.  Sensation to light touch intact throughout.  DTR’s 2+ bilaterally.

A FAST exam was performed and was negative.  Transabdominal ultrasound findings shown below.  FHTs in 140s-160s.

Questions:

1.  What is the most sensitive indicator of placental abruption?

a)  Ultrasound findings

b)  Fetal distress

c)  Vaginal bleeding

d)  Uterine tenderness

2.  Which of the following is true of resuscitation of a pregnant patient with uterus palpable at or above umbilicus who is in cardiopulmonary arrest?

a)  No modifications to resuscitative efforts should be made

b)  Chest compressions should be performed higher on sternum

c)  Manual displacement of uterus to the left should be attempted

d)  Defibrillation is contraindicated

3.  A pregnant patient may lose how much circulating blood volume before manifesting hypotension or clinical signs of shock?

a)  30-35%

b)  10-15%

c)  20-25%

d)  40-45%

 

Correct Answers:

  1. B
  2. C
  3. A

 

Discussion:

Trauma occurs in 6 to 7% of all pregnancies.  It is the leading cause of maternal death due to nonobstetric causes, accounting for close to 50% of fatalities in pregnant women.  The most common causes of injury in pregnancy, in order of frequency, that result in emergency department (ED) visits are motor vehicle crashes (MVCs), interpersonal violence, and falls.  Counseling on proper seatbelt and alcohol use and screening for interpersonal violence may help to reduce the morbidity and mortality rates for pregnant patients.  Although the essential principles of trauma management remain unchanged in the pregnant patient, a number of special points need to be considered.  Pregnancy causes alterations in physiology and anatomy that affect multiple organ systems. Although there are two lives involved, maternal life takes priority.

In blunt trauma, 50 to 70% of all fetal losses result from placental abruption.  Placental separation results when the inelastic placenta shears away from the elastic uterus during sudden deformation of the uterus. Because deceleration forces can be as damaging to the placenta as direct uterine trauma, abruption can occur with little or no external sign of injury to the abdominal wall.  Because all gas exchange between the mother and fetus occurs across the placenta, abruption inhibits the flow of oxygen to the fetus and causes in utero CO2 accumulation. Such hypoxia and acidosis can lead to fetal distress.  Sustained uterine contractions induced by intrauterine hemorrhage also inhibit uterine blood flow, further contributing to fetal hypoxia.

 

 

The diagnosis of abruption is a clinical one, and ultrasonography and the Kleihauer-Betke test are of limited value.  Classical clinical findings of abruption may include vaginal bleeding, abdominal cramps, uterine tenderness, maternal hypovolemia (up to 2 L of blood can accumulate in the gravid uterus), or a change in the fetal heart rate. However, in some trauma studies, as many as 63% of cases showed no evidence of vaginal bleeding.

The most sensitive indicator of placental abruption is fetal distress. Hence, prompt fetal monitoring is a very important assessment technique in trauma during pregnancy. There is also a close linkage of abruption to uterine activity. One study reported that if 12 or more contractions occurred in any hour of a 4-hour cardiotocographic monitoring period, the risk of abruption was 14%; abruption did not occur in this study if contractions occurred less than once every 10 minutes.  Ultrasound (US) is less than 50% accurate as a first-line test in detecting placental abruption.  If the abruption bleeds externally, not enough blood collects to be seen sonographically. Even with significant intrauterine blood accumulation, accurate US diagnosis may be difficult because of placental position (i.e., posterior) and confounding uterine or placental structural conditions.

 

Hemodynamic Changes of Pregnancy (Mean Values)

PARAMETER NONPREGNANT TRIMESTER 1 TRIMESTER 2 TRIMESTER 3
Heart rate (beats/min) 70 78 82 85
Systolic blood pressure (mm Hg) 115 112 112 114
Diastolic blood pressure (mm Hg) 70 60 63 70
Cardiac output (L/min) 4.5 4.5 6 6
Central venous pressure (mm Hg) 9.0 7.5 4.0 3.8
Blood volume (mL) 4000 4200 5000 5600
Hematocrit without iron (%) 40 36 33 34
Hematocrit with iron (%) 40 36 34 36
White blood cell (cell/mm3) 7200 9100 9700 9800

 

The relative hypervolemic state can mislead the clinician during maternal resuscitation after trauma and make clinical findings difficult to interpret.  A pregnant patient may lose 30% to 35% of circulating blood volume before manifesting hypotension or clinical signs of shock.  Uterine arteries constrict, which results in diminished fetal blood flow and tissue oxygenation before significant evidence of maternal hypovolemia appears.

Cardiopulmonary arrest in a pregnant patient must be considered under two scenarios: before fetal viability and after fetal viability. The accepted age of fetal viability varies among institutions, but 22 to 26 weeks is generally considered potentially viable. The uterine fundus is palpable at the umbilicus at 20 weeks. After 20 weeks, the gestational age of the fetus can be estimated by measuring the fundus from the pubic symphysis to the top of the fundus. The fundal height in centimeters corresponds roughly to the gestational age in weeks. Before approximately 22 to 24 weeks’ gestation, all efforts should focus on the mother, with no modifications to CPR.  Beyond 22 weeks or if the gravid uterus can be palpated above the umbilicus, several modifications of CPR should be instituted: (1) the patient should be positioned to minimize aortocaval compression, and (2) appropriate preparations for a potential cesarean section and care of a viable fetus should be made.

Limitation of aortocaval compression is achieved by (1) having someone manually displace the uterus to the left, (2) tilting the patient 15 to 30 degrees on a tiltable table, or (3) placement of a roll or a Cardiff wedge, if available, under the patient’s right hip and flank. The Cardiff wedge provides a tilt of 27%, allowing 80% of the compressive force, compared with CPR in the supine position, which maintains 30% or less of normal cardiac output in nonpregnant adults.  The “human wedge” has been advocated for bystander CPR. In this technique, the patient lies across the thighs of the rescuer, who is in a kneeling position. Despite relatively clear current recommendations regarding resuscitation in pregnancy, there is little research in this area.

 

Massive fetomaternal transplacental hemorrhage causes alloimunization in Rh incompatibility but also endangers the fetus by severe fetal anemia and resulting fetal distress and possible exsanguination. ABO incompatibility causes less severe disease.

The Kleihauer-Betke test identifies fetal cells in a maternal blood sample. Most laboratories screen for FMH of 5 mL or more. Unfortunately, the amount of FMH sufficient to sensitize most Rh-negative women is well below this 5-mL sensitivity level. Therefore, all Rh-negative mothers who have a history of abdominal trauma should receive one prophylactic dose of Rhesus immune globulin (RhIG). In the first trimester, one 50-g dose is used because total fetal blood volume is only 4.2 mL by 12 weeks’ gestation and a 50-g dose covers 5 mL of bleeding. During the second and third trimesters, a 300-?g dose of RhIG is given, which protects against 30 mL of FMH. Beyond 16 weeks’ gestation, the total fetal blood volume reaches 30 mL, so it is quite possible that massive FMH may exceed the efficacy of one 300-g dose of RhIG. Therefore, it is unlikely that a Kleihauer-Betke test is useful in the treatment of severely injured pregnant trauma patients.

 

References:

Rosen’s Emergency Medicine. 7th editon. Pages 252-261.

Tintinelli’s Emergency Medicine.  7th edition.