Case 5.4

                                  Case Presentation by Dr. Craig Sharkey

CC: Motorcycle crash

HPI:  A 34yo female presents as a trauma code 2 after a motorcycle crash.  She was traveling approximately 45 mph, not wearing a helmet, when a car turned in front of her.  She was unable to stop in time and ran into the car.  She has amnesia to events, but is alert and speaking appropriately on arrival to the emergency department.  She denies any alcohol or illicit drug use.  She complains of pain in her right shoulder, left forearm, abdomen, and right leg.  She denies any headache, SOB, nausea, or vomiting and does not know the date of her last tetanus vaccination.

Constitutional:  No fever
Eye:  No diplopia

Nose: No discharge

Mouth: No sore throat
Respiratory: No difficulty breathing
Cardiovascular:  No palpitations
Gastrointestinal:  + Abdominal pain

MSK: + joint pains

Skin: + abrasions

Neurological: No Headache

PSHx:  C-section

Allergies: NKDA

Medications: HCTZ
Family Hx: HTN

Social: Denies tobacco/alcohol/street drug usage

Physical Exam:  Vitals:  BP 114/68, P 105 R 22 T 35.8 SpO2 99% on 15 LPM
General:  WD WN female in moderate distress due to pain, but conversant and cooperative
Head:  atraumatic, normocephalic

EENT:  Pupils are equal 3mm, round and reactive to light; Extraocular movements are intact.
Intact hearing to finger rubbing.  No rhinorrhea or epistaxis.  Mouth without injury or lesions.
Neck:  In a cervical collar, no step off deformity.

Respiratory:  Lungs CTA bilaterally, respirations are non-labored.
Cardiovascular:  Regular rhythm, normal S1S2, no murmurs/rubs/gallops
Gastrointestinal:  Soft, Non-distended, diffuse tenderness of abdomen.

Back: no TTP or stepoffs, no spine tenderness

Pelvis: TTP with instability

Rectal: Good tone, no blood, brown stool in vault, no saddle anesthesia
Musculoskeletal:  Upper: deformity of distal left forearm with left hand grip weakness compared to right.  Pain of right shoulder, no distal deformity; 2+ radial pulses, sensation intact in median/radial/ulnar distributions.  Lower:  Degloving of left knee; knee cap loose. 1+  right PT/DP pulse, 2+ left DP/PT.  EHL/FHL/TA/GSC intact.  Sensation intact to light touch in SP/DP/S/S distributions.
Integumentary:  Warm, Dry.
Neurologic:  AAO x 3, Cranial Nerves II-XII intact to H test, face is symmetric with intact sensation, tongue protrudes straight, shoulders shrug equally.

FAST scan: negative for intraperitoneal free fluid



1)  The proper anatomic landmarks for placement of the commercial belt-type pelvic binders are:

a)  not important, as the circumferential pressure is all that is necessary to reduce pelvic volume

b)  anterior superior iliac spines

c)  widest diameter of the soft tissues

d)  greater trochanters of the femurs


2)  Pelvic binders are contraindicated for:

a)  sacral fracture

b)  windswept pelvis

c)  vertical shear pelvis

d)  closed book pelvis


3)  Which of the following injury and clinical finding pairings is correct?

a)  L4, L5 root  :  Loss of ankle plantar flexion

b)  S1-S2 roots  :  Loss of knee extension

c)  S2-S4 roots  :  Loss of voluntary rectal tone

d)  pubic symphysis widening : urethral injury


Question 1 – D

Question 2 – B

Question 3 – C

Stable Pelvic fractures:   Pelvic fractures that do not disturb the architecture of the pelvis, such as avulsion fractures, iliac wing fractures, isolated rami/sacral fractures generally heal with conservative treatment of rest and analgesia.  It is possible for an isolated fracture to be present, but one should always be wary of any other disruption that would indicate the pelvis is not stable.

Unstable fractures: 

Anteroposterior compression:  This patient had an AP compressive force, resulting in open book injury.  These injuries commonly involve the pubic symphysis/rami and, if severe enough, the sacroiliac joint.  Pubic symphysis width of 2.5 cm or greater is considered unstable.  These injuries are associated with the highest crystalloid and blood requirements.  Damage to the bladder or urethra is approximately 6% in all pelvic fractures, which increases drastically with symphysis widening/obturator fracture displacements over 1 cm.

Lateral compression:  Lateral impact is the most common type of motor vehicle crash, and forces transmitted to the pelvis can cause a multitude Windswept pelvis is a combination of internal rotation of a hemipelvis with external rotation of the contralateral hemipelvis after a lateral compression injury.  There are associated pubic rami fractures on either side of the pelvis as well as ligamentous injuries that all contribute to cause rotational instability of the pelvis.  These lateral compression injuries are associated with less blood loss compared to AP compression due to decreased pelvis volume.

Vertical shear:  Vertical shear injuries are caused by force applied vertically to one side of the pelvis, most commonly due to falls from height or motor vehicle crashes.  Fractures of the ischial spine, 5th lumbar vertebrae transverse processes and sacrum are seen.  They represent the most unstable of all pelvic fractures and have a good chance to cause neurologic impairment especially if they sacral fracture extends through the foramina.


Early placement of pelvic binders decreases the transfusion requirements for most pelvic fractures even when compared to embolization or external fixation.  The greater trochanters are the proper landmark for the belt-type binders.   Improper placement across the iliac crests can cause a widening of the pubic symphysis and increase bleeding.  When using sheets instead of belt binders, they can be placed across the entire pelvis without identifying anatomic landmarks.  A windswept pelvis is the only relative contraindication to placing a pelvic binder, where indiscriminant wrapping of this injury can further displace the hemipelvis.  Binding can still be done in order to stabilize the pelvis for movement, but keep in mind that excessive pressure can worsen the injury.


Rosen’s Emergency Medicine:  Pelvic Trauma.  Ch 52

Case 5.3

Case Presentation by Dr. Frankie Civitarese

57 year old female with a history of COPD, DM, HTN, mitral stenosis presented with shortness of breath and was made a medical code for severe dyspnea and hypoxia.  After initial evaluation and attempts at stabilization she required intubation.

ROS:  Unable to be obtained.

PMH:  DM type 2, HTN, COPD, Mitral stenosis

PSH: colonoscopy 2009, EGD 2009, cholecystectomy, tubal ligation, L oophorectomy

Medications:  acetamenophen, tiotroprium bromide, albuterol, azithromycin, amoxicillin, prednisone, isosorbide

Allergies: iodine

Social History:  smokes cigarettes and marijuana.  Denies any other drug use. Denies use of alcohol.



VS: 157/117, HR 102, RR 20, T 37.9, pulse ox 90% RA.

GEN: Acute respiratory distress. Alert and oriented times 3, extremely anxious.

CV:  Regular rhythm.  Tachycardia.  S1, S2.  No murmurs rubs or gallops.

PULM:  Severely tachypneic. Using accessory muscles and having substernal retractions. Speaking in brief words. No crackles/rhonchi.  Prolonged expirations with coarse expiratory nonmusical wheezes.

EXT:  Peripheral pulses are 2+ and symmetric bilaterally.

SKIN:  Warm to the touch and very diaphoretic.

The rest of examination was within appropriate limits


On presentation to the ED, her vital signs were 157/117, HR 102, Temp 37.9.  RR 20 pulse ox 90%.  She was brought to the resuscitation bay from triage as a medical code and was given nebulized breathing treatments.

Labs and Studies:

CXR post intubation:  good tube placement, no infiltrates

CBC, electrolytes, initial troponin were within normal limits.

BNP was 1526.

ABG results returned that revealed:  7.02/61/98/12.3.

The patient was sent to the CT scanner from resuscitation to evaluate for a possible pulmonary embolism.  On the way to the CT scanner, the patient was found to be in PEA, and immediately brought back to resuscitation.  After several rounds of CPR as well as doses of epinephrine and atropine, the patient had return of spontaneous circulation with sinus tachycardia in the 140s.

Subsequently, despite being intubated and maintained on a ventilator, the patient then became increasingly difficult to oxygenate.  A repeat chest xray was done that revealed:



1.  What is the initial evaluation or procedure that should be performed on this patient?

A) needle decompression

B )bedside thoracotomy

C) immediate OR for thoracotomy

D) bedside ultrasound

E) tube thoracostomy 26F tube

F) tube thoracostomy 32F tube


2.  A chest tube was placed on the patient’s right side.  Where should the tube be placed?

A) anterior axillary line at the level of the nipple or inframammary angle

B) behind the lateral edge of pectoralis minor at nipple or inframammary angle

C) mid axillary line at the 6th intercostal space

D) posterior axillary line at the 5th intercostal space


3.  In the case of a hemopneumothorax, what is an indication for the patient to undergo urgent thoracotomy?

A) initial chest tube output of >1000cc after placement

B) consistent chest tube output of 50-100cc/hour for 2-4 hours after placement

C) minimal resolution of pneumothorax on repeat chest xray

D) evidence of tension pneumothorax

E) bronchi/bronchiole occlusion with secretions

F) large bronchus tear or tear of lung parenchyma

Answers and Discussion

1) A

2) A

3) A

Pneumothorax is defined as an accumulation of air in the pleural space, and can be spontaneous or as a result of chest trauma.  It is divided into three different classifications depending on whether or not air has direct access to the thoracic cavity:  simple, communicating, or tension.

A simple pneumothorax is defined when there is no open communication with the thoracic cavity and the atmosphere.  A simple pneumothorax has no mediastinal or tracheal shift.  “small” is defined as 15% or less, “moderate” is 15-60%, and a large pneumothorax is >60%.  Severe symptoms of pneumothorax become evident at a pneumothorax occupying 40% or more of the hemithorax, with a tension pneumothorax, or in a patient with underlying cardiopulmonary disease.

Simple Pneumothorax:

Traumatic pneumothorax can occur with direct penetrating trauma such as a gunshot or stab wound without direct communication with the atmosphere or with blunt trauma.  Chest compressions can fracture ribs that may result in a pneumothorax.  It can also occur without a fracture when the impact or force of the trauma occurs with a closed glottis at full inspiration.

A communicating pneumothorax, or a “sucking chest wound”, is associated with a defect in the chest wall after combat injuries.  This is generally associated with shotgun wounds in the civilian sector.  The loss of chest wall integrity leads to paradoxical collapse of the lung during inspiration.


Tension pneumothorax is defined as the accumulation of air under pressure in the pleural cavity with shift of the mediastinum to the opposite hemithorax and compression of the contralateral lung and great vessels.  A tension pneumothorax occurs when an injury acts as a one way valve, preventing free bilateral communication of air from inside the pleural cavity with the atmosphere.  The increased pressure in the intrapleural cavity results from the air’s inability to exit with expiration.  This results in a shift of the mediastinal structures that can compress the vena cava and may ultimately result in decreased diastolic filling of the chambers of the heart and thus decreased cardiac output.

Patients with tension pneumothorax will present with rapid onset of progressing and severe symptoms such as hypotension, hypoxia, jugular venous distension, tracheal deviation, and shock.  They become rapidly agitated, dyspneic, cyanotic, and display changes in mental status.  Classic physical exam signs of a tension pneumothorax are tachycardia, JVD, and absent breath sounds on the ipsilateral side.  The intubated patient in the emergency department is particularly at risk for developing tension pneumothoracies because they may be receiving positive pressure ventilation thus increasing the intrapleural pressure.  A resistance to ventilation may be the first clinical clue that a tension pneumothorax has developed in such a patient.  Also, those receiving CPR are at risk secondary to the possibility of fractured ribs from the cardiac compressions can puncture the lung parenchyma .

The most common clinical presenting symptoms suggesting pneumothorax are shortness of breath, pleuritic chest pain, and tachycardia.  Severity of symptoms can vary depending on the type of pneumothorax as well as the percentage of the hemithorax involved.  Physical exam will show decreased breath sounds and hyperresonance to percussion on the side of the pneumothorax.

1)  Clinical work up of a pneumothorax also varies depending on the type.  If presenting symptoms suggest that a tension pneumothorax may be the diagnosis, no further workup is required before intervention.  Pressure within the intrapleural cavity should be relieved immediately with needle decompression.  A large bore (14 gauge or larger) catheter, at least 5cm in length (adjusted for those with larger body habitus) should be inserted through the second intercostal space anteriorly in the mid clavicular line, in order to avoid the inframammary vessels that are positioned approximately 3cm on either side lateral to the sternum.  This can also be performed in the 4th or 5th intercostal space laterally on the involved side.  A follow up chest x ray can be then taken to ensure expansion of the lung.

In the case of suspected pneumothorax that does not appear to be a tension pneumothorax, initial diagnositic studies typically begin with an upright full inspiratory film.  To enhance a film if a small pneumothorax is suspected, an expiratory film can be taken that will decrease the lung volume, thus making smaller pneumothoracies more apparent.

In addition to a chest xray, an ultrasound examination as a part of the initial evaluation of the patient can be an important tool during the initial workup.  Some studies compare the accuracy of the bedside ultrasound in the experienced practitioner’s hands to that of a CT scan in detecting occult pneumothoracies.  Sensitivity has been evaluated at 92% (in comparison to 52% in the upright chest xray) with a specificity of 100%.  The clinical clue that a pneumothorax is present is the absence of the “sliding lung” sign.  If both ultrasound and chest xray are unable to detect a pneumothorax, occasionally they can also be revealed on CT scan.

Video from NY Presbyterian US Director on ultrasound of pneumothorax

A good ACEP resource for Ultrasound Pneumothorax:

Occult pneumothorax can be absent from initial chest xray.  Studies have found that pneumothoracies picked up serendipitously on abdominal or chest CT have required tube thoracostomy in 2/3 of cases.  In patients who have experienced penetrating chest trauma, but who are clinically stable, asymptomatic, and have an initial chest xray that is negative, the patient can be observed for a period of 4-6 hours with a chest xray repeated after this time period.  If the repeat chest xray remains negative, the patient can be safely discharged.  Recent data suggest that a period of 3 hours observation is probably effective and safe for reevaluation via chest xray and subsequent discharge of a patient if negative.  If the patient received a CT scan that was negative, a follow up chest xray is unnecessary.


Simple pneumothorax can be treated with a chest tube to relieve respiratory compromise.  However, asymptomatic and small simple pneumothoracies can be safely observed with a  hospital admission.  Pneumothoracies of less than 25% in the hemodynamically stable patient may be observed in patients with penetrating trauma, however this approach is not recommended for multisystem trauma.  Any moderate to large sized pneumothorax should be treated with a chest tube.

2)  Indication for tube thoracostomy:

traumatic cause of pneumothorax

moderate to large size pneumo

symptomatic pneumo regardless of size

increasing size of pneumo

recurrence of pneumo following removal of initial chest tube

pt requires ventilatory support

associated hemothorax

bilateral pneumos regardless of size

tension pneumothorax

Preferred site for chest tube insertion is the fourth or 5th intercostal space at the anterior or midaxillary line at the level of the nipple in males and the inframammary crease in females.  The chest tube position will be beneath the lateral edge of pectoralis major.  The tube should be positioned posteriorly and towards the apex for pneumothorax, and can be positioned posteriorly and laterally for isolated hemothorax.


An oblique incision 1-2cm below the 4th or 5th intercostal space should be made in order to ensure that upon removal of the chest tube, the oblique tunnel that was created will seal, in order to decrease risk of recurrent pneumothorax.  A clamp should then be inserted through the initial skin incision into the intercostal muscles just above the rib and inserted through the intercostals fascia to create a 1.5cm to 2cm space.  A finger should then be inserted into the space to confirm placement within the thorax and to ensure that the lung is not adherent to the chest wall.  Chest tube should be 36-40F in adults and 16-32F in children, especially in trauma when hemothorax is likely to occur simultaneously with pneumothorax.  If the diagnosis is simple pneumothorax, some resources suggest that a 24 or 28 F will suffice.  The vent holes in the chest tube should all be completely positioned well within the chest cavity.  Guidelines suggest that a length of tube at least 2.5cm past the final vent hole should be inserted.  The chest tube should then be placed to water seal and placement confirmed on chest xray.

The chest tube SHOULD NOT be clamped if there is an air leak, and the water seal should be placed 1-2 feet below the level of the patient’s chest.  Chest tubes should be left in place a minimum of 24 hours after all air leaks stop OR if drainage becomes serous and <200cc/24 hours.  All chest tubes should remain in place in the intubated patient.  Recent studies suggest that empiric antibiotics during chest tube placement can be beneficial and can decrease the chances of incurring complications of empyema and pneumonia by 6% and 12% respectively, however there are no guidelines or consensus as to duration or antibiotic choice.


If the chest tube is not functioning properly and the lung has not completely reexpanded, a replacement tube may be placed through the same incision site or another site may be chosen on the affected side.  It is not recommended to irrigate the tube or attempt to recannulate the chest tube with a Fogarty catheter as it will increase the risk of infection.  The practitioner can attempt to “troubleshoot” the chest tube by checking the chest tube’s position on a chest xray, correct any disrupted connections with the water seal, or have a bronchoscopy performed to look for bronchi/bronchiole occlusion secondary to secretions, a tear in the large bronchi, or a tear of the lung parenchyma itself.


3)  Thoracotomy is indicated if there is greater than 1000-1500cc of drainage (or >20cc/kg) after chest tube placement, or if there is 150-200cc/hour for a period of 2-4 hours after initial placement. Persistent bleeding at a rate of >7cc/kg/hr is also an indication for thoracotomy.

Also, other indications include:

the patient requires continuous transfusions to maintain hemodynamic stability

increasing hemothorax on chest xray

patientx remains hypotensive despite adequate blood replacement

patient decompensates after initial response to resuscitation.


1)  Always initially determine sick versus not sick.  If the patient is hemodynamically unstable, anxious, is difficult to oxygenate, and you have suspicion for tension pneumothorax secondary to mechanism, perform a needle thoracostomy immediately.  You do not need an initial chest xray.

2)  Occult pneumothoracies can often be picked up better on CT scan or bedside ultrasound.  Look for the sliding lung sign and comet tail artifacts to be absent on ultrasound.

3)  Tube thoracostomy is indicated for traumatic, large, increasing, tension, symptomatic, or bilateral pneumothoracies.

4)  Emergent thoracotomy is indicated with >1,000 cc of initial drainage from your chest tube or greater than 150cc per hour for 2-4 hours.  Also, thoracotomy is indicated if the patient decompensates, remains hypotensive despite adequate replacement, or a patient requiring continued transfusions.

5) If central venous access is required, placement should occur on the same side as the pneumothorax.

Intern Report Case 5.2

Case Presentation by Dr. Kristi Maso

A 54-year-old woman brought in by EMS presents to the ED with a 2-day history of a painful, enlarging rash over her face, ears, and extremities (rash shown below).  She states the rash started on her left ear and has been spreading to her face and patches of skin on both arms.   She denies any upper respiratory symptoms, shortness of breath, chest pain, abd. pain, nausea, vomiting, diarrhea, or constipation.  Per EMS, who got a minimal history from the patient’s sister, the patient recently moved to Detroit 3 weeks ago to be near family.  She is a known drug user (although her sister doesn’t know of what).  She has a history of a heart attack 5 years ago and at that time “got some stents put in.”

ROS: negative except for current rash and “my heart races sometimes”


Meds: None

Allergies: None

PSH:  s/p stent 5 years ago (unknown how many or what types)

Sexual history : unable to obtain, pt uncooperative

Social history: unable to obtain, pt uncooperative

Family history: unable to obtain, pt uncooperative

Physical Exam with pertinent positives:

Vitals:  BP  168/105,  HR  116,  RR  20,  T  38.1,  Sp02 99% on room air,  Ht 5’6,  Wt 120 lbs

GEN:  Thin, appears malnourished.  Agitated and uncooperative, demanding pain medication

HEENT:  Pupils dilated bilaterally approx. 6 mm, but are equal, round and reactive to light. EOMI.  TM intact.

CVS:  Tachycardic, S1, S2 with regular rhythm, no murmurs, rubs, gallops. 2+ pulses in all 4 extremities.

SKIN:  Well demarcated purpuric area with an erythematous border over the left exterior ear (helix and tragus) and bilateral cheeks, crossing over the nasal bridge.   + Areas of crusted, black plaques, suggesting areas of necrosis.  + Tenderness to palpation over the lesions.  No discharge or draining.

The remainder of the physical exam was unremarkable


12 lead EKG shows sinus tachycardia.  There are Q waves in leads V4-V6. There are no ST changes or T-wave inversions.  PR interval and QT interval are within normal limits.

WBC  4.1,  Hgb 10.6,  Hct 32.1,  Plt 118       ANC  .075,  MCV 87.8

Na 142,  K 4.3,  Cl 103,  HC03 22,  BUN 6,  Cr 1.3, Gluc. 88

PT, INR, AST, ALT, ALP – normal.

Drug screen and ETOH – pending

Muirhead TT, Eid MJ. N Engl J Med 2011; 364:e52



1) Based on the patient’s physical exam and current lab findings, which of the following would be most helpful in determining the likely etiology of the above skin lesion?

a)     Order protein C & S levels

b)     Follow up the urine drug screen

c)     Get a sed rate and CRP

d)     Order a UA

e)     Repeat coags in 1 hour

2)  The patient admits to using cocaine and states she recently moved to Detroit.  She has been buying drugs from wherever she can.  She does not have a “regular” dealer…yet.  You suspect this patient has been exposed to some “bad cocaine” and that her above symptoms are likely due to her exposure to a cutting agent called levamisole. Which of the following laboratory abnormalities is often associated with this agent?

a)     Thrombocytopenia

b)     Elevated creatinine

c)     Proteinuria

d)     Agranulocytosis

e)     Hypoglycemia

3)  What is the treatment for the skin lesions above?

a)     Steroids

b)     Hyperbaric chamber treatment

c)     Skin phototherapy

d)     Cessation of drug use

e)     Skin grafting



1)     B

2)     D

3)     D


The woman above presents with signs and symptoms suggestive of Cocaine Levamisole Toxicity.  Levamisole is a broad spectrum antihelmintic used in the de-worming of primarily sheep and cattle.  It has been used in increasing frequency over the last decade as an adulterant or “cutting” agent in cocaine to increase profits.  “Cutting” agents refer to the mixing or diluting of the illicit drug with another substance.  Common agents used in the past have been rather benign in their side effects when compared to levamisole.  Some of those agents include:

  • Procaine, benzocaine, novacaine
  • Acetaminophen
  • Lactose or Dextrose
  • Quinine
  • Ritalin
  • Baking soda, powdered milk, starch

Levamisole adds bulk and weight to powdered cocaine and also makes the drug appear more pure, making it an appealing adulterant for drug manufacturers trying to sell their product for the highest price.  However, unlike other diluents, levamisole has some very toxic effects.

Toxic effects of levamisole

Levamisole works as a cholinergic agonist.  It can cause nausea, diarrhea, dizziness, dermatitis, taste perversion, fatigue, vomiting, and arthralgias.  However its major toxicity results in profound immune suppression (mechanism unknown).  Severe neutropenia, defined as an absolute neutrophil count (ANC)  <500, and agranulocytosis are serious side effects of patients exposed to cocaine diluted with levamisole.   Agranulocytosis refers to a virtual absence of neutrophils where the ANC is lower than 100/μL (.100).  An ANC less than 100 makes patients extremely vulnerable to chronic bacterial infections.  Patients can present with high fever, chills, swollen glands, painful sores, and wounds that don’t heal.

The dermatitis associated with levamisole has been described as a “dead, dark, skin.” Very early, the purpura may be preceded by erythematous macules.  The lesion is a vasculitis-like rash, well demarcated purpuric area with an erythematous border. There are areas of crusted, black plaques, suggesting areas of necrosis primarily over the ear(s), nose, and cheeks, but can be found on any part of the body.  In dark-skinned individuals, the rash may present with deep red to brown or purple lesions. Purpura is difficult to detect in extremely dark skin people.

“Will I ever even see levamisole toxicity?”

The use of levamisole as a cutting agent in cocaine has been around in the United States since 2003 and has steadily gained popularity in the cocaine-making industry.  In 2005 levamisole was found in less than two percent of all seized cocaine in the US.  However, in 2009, it was found in 73.2 percent of all seized cocaine in the US.  As levamisole becomes more popular, emergency departments will see larger number of patients presenting with these sometimes dangerous signs and symptoms.

Other Differentials

Cocaine Levamisole Toxicity is a diagnosis of exclusion.  And while most of the differential diagnoses are not ones that will be ruled out in the emergency department, we can make an effort to rule out some of the more severe differentials simply by obtaining a good history, paying attention to vital signs that may suggest an infectious process, and review lab studies (especially coagulation studies).   Some differentials include:

  • Cryoglobulinemia – check for serum IgM and IgG cryoglobulins, HCV infection.
  • Cryofibrinogenemia
  • Bacterial sepsis
  • Coumadin necrosis
  • Heparin necrosis
  • Purpura fulminans
  • Acute meningococcemia – the patient is usually systemically ill, but since cocaine use may complicate the neurologic exam, this diagnosis should be considered carefully.
  • Calciphylaxis
  • Vasculitis secondary to viral infections such as hepatitis A, B, C, VZV, parvovirus B19, and CMV, or to medications.
  • Arthropod bites
  • Erythema multiforme minor (EM) – characteristic findings on histology will assist in differentiating EM from LCV. Systemic involvement is rare.
  • Toxic epidermal necrolysis (TEN) – usually larger areas of skin are involved with more skin pain and resulting bullae.
  • Frostbite or chilblains (perniosis) – history of recent cold exposure.
  • Microscopic polyangiitis is ANCA positive and has palpable purpura and constitutional symptoms; look for evidence of pulmonary and renal involvement.
  • Wegener’s granulomatosis is ANCA positive and has necrotizing granulomatous inflammation of the upper and lower respiratory tracts, glomerulonephritis.
  • Churg-Strauss syndrome is ANCA positive and is associated with eosinophilia and asthma.
  • Polyarteritis nodosa – medium vessel vasculitis with subcutaneous nodules, livedo reticularis, ulcers, and gangrene as cutaneous manifestations.
  • Immune thrombocytopenic purpura – look for isolated thrombocytopenia.


Things to avoid

Patients with suspected levamisole toxicity with associated neutropenia (ANC <500) should be advised to avoid contact with people who may have colds, the flu or other contagious illness.  They should not receive live vaccines or be in contact with people who have recently been vaccinated with a live vaccine.

In addition they should be cautioned to avoid the use alcohol as it may cause flushing, nausea, vomiting, headache, and facial swelling.


The only “treatment” of the dermatitis associated with levamisole toxicity is cessation of the drug.  No medications (including steroids) have been associated with any improvement in skin lesions.  In severe cases significant scars have remained even after cessation of drug and skin grafting has been suggested, but for cosmetic reasons only.

ED implications

The blood plasma half life of levamisole is less than 6 hours but the resulting immune suppression may last up to several weeks after the patient’s last use of cocaine.  This makes it difficult to diagnose levamisole toxicity as the cause of a patient’s immune suppression. However, a history of cocaine use or a positive urine drug screen for cocaine in a patient with immune suppression, and a necrotic-looking dermatitis should trigger the consideration of levamisole toxicity and a consult to toxicology.  Patients should receive supportive care and proper analgesia in the ED, and if febrile, should be treated with prophylactic broad spectrum antibiotics (vancomycin and cefepime) and kept isolated as any immunosuppressed patient with febrile neutropenia would be.

Clinical Pearls

  • A history of cocaine use, or a positive cocaine drug screen, in combination with lab abnormalities suggestive of bone marrow suppression and a vasculitic-like rash should trigger the suspicion of Cocaine Levamisole Toxicity.
  • If levamisole toxicity is suspected based on skin lesions and history of drug use, a CBC with differential should be ordered to evaluate ANC and look for severe neutropenia or agranulocytosis.
  • Severe neutropenic patients (ANC <500) with a fever should: 1) wear a mask, 2) be started on broad spectrum antibiotics, and 3) be kept in isolation.
  • Supportive therapy and prophylactic antibiotic therapy (if indicated) are mainstays of treatment in the ED.  Cessation of the drug is the only “cure.”
  • Contact toxicology, as the true incidence of Cocaine Levamisole Toxicity is difficult to track and it’s important from an epidemiology standpoint to get toxicology involved.


Erowid Crew. “Cocaine Adulterated with Levamisole on the Rise: Status as of September 2009” Oct 1,    2009.

Farnier, C. Agranulocytosis Associated with Cocaine Use. Morbidity and Mortality Weekly Report, Dec. 8, 2009.

Muirhead TT, Eide MJ. N Engl J Med 2011;364:e52

Szalavitz, M. “A Common Cut in Cocaine May Prove Deadly.”  Time Magazine, Jan. 10,2010.,8599,1955112,00.html

Intern Report Case 5.1

Case Presentation by Dr. Meredith Hill

50 y/o male brought in by EMS with signs of head trauma.  According to EMS patient had been drinking and was assaulted.  EMS reports that the patient was stuck in the head multiple times with an unknown object.  On presentation the patient is combative, uncooperative and unable to provide any coherent history.

Physical exam:

VS: BP 200/100 HR: 106 RR: 18

Constitutional: Patient is c-collared and back-boarded, disoriented and combative with staff.

HEENT: Patient has significant trauma to the head and face, with a 5 cm laceration noted on the patient’s occiput.  Pupils 4mm, equally round and reactive to light. Right TM is unremarkable, clear fluid is noted behind the left TM.  Clear fluid is noted in the patient’s nares bilaterally.

Neuro: Patient is opening eyes spontaneously.  The patient is moving all four extremities spontaneously and with good strength.  Patient is not answering question appropriately and is not co-operating with examination.

The rest of Physical exam is WNL.


1.  The following image is of the patient’s left ear, what injury is this consistent with?

A.  A skull fracture with a  fracture line communicating with the mastoid air cells, resulting in accumulation of blood in the cutaneous tissue.

B.  A blow directly to the left ear causing bruising over the mastoid bone.

C.  A skull fracture where the fracture line communicates with the auditory canal, resulting in bleeding into the middle ear.

D.  A result of bleeding from a fracture site in the anterior portion of the skull base.

2.  You notice some clear fluid leaking from the patient’s nose.  You are concerned that this is CSF.  What bedside tests can you do to either confirm or refute that this is CSF?

A.  Take a drop of the fluid and place it on filter paper and look for  double ring of clear fluid and blood.

B.  Do an accu check on the fluid and if it is greater than 90 this confirms that it is CSF.

C.  Send a sample to the lab for beta2 transferrin testing to confirm a CSF ottorhea.

D.  Smell a sample of the fluid on your gloove to see if it smells sweet.

3.  The CT of the patient above confirms a basilar skull fracture with a CSF leak.  What is the next best treatment for this patient?

A.  Administer prophylactic broad-spectrum antibiotics and discharge the patient.

B.  Administer prophylactic broad-spectrum antibiotics and admit

C.  No prophylactic antibiotics should be given and patient may be discharges if no other injuries exist

D.  Admit for observation and discuss the patient with neurosurgery regarding starting prophylactic antibiotics

Please submit your answers to the questions in the “leave a reply” box or click on the“comments” link.  Your submission will not immediately post.  Thank you for participating in Receiving’s: Intern Report.



Question 1 – A

Question 2 – A

Questions 3 – D

Basilar skull fracture

In essence, a basilar fracture is a linear fracture at the base of the skull. It is usually associated with a dural tear and is found at specific points on the skull base. Basilar skull fractures represent 19-21% of all skull fractures

Temporal fracture

Temporal bone fracture is encountered in 75% of all skull base fractures. The 3 subtypes of temporal fractures are longitudinal, transverse, and mixed.

Transverse temporal bone fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania)

Longitudinal temporal bone fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania

Longitudinal fracture occurs in the temporoparietal region and involves the squamous portion of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani. These fractures may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells, respectively. Longitudinal fracture is the most common of the 3 subtypes (70-90%).

Transverse fractures begin at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa (5-30%).

Mixed fractures have elements of both longitudinal and transverse fractures.

Yet another classification system of temporal bone fractures has been proposed. This system divides temporal bone fractures into petrous and nonpetrous fractures; the latter includes fractures that involve mastoid air cells. These fractures do not present with cranial nerve deficits.

Occipital condylar fracture

Occipital condylar fracture results from a high-energy blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament. These fractures are subdivided into 3 types based on the morphology and mechanism of injury. An alternative classification divides these fractures into displaced and stable, ie, with and without ligamentous injury.

Type I fracture is secondary to axial compression resulting in comminution of the occipital condyle. This is a stable injury.

Type II fracture results from a direct blow, and, despite being a more extensive basioccipital fracture, type II fracture is classified as stable because of the preserved alar ligament and tectorial membrane.

Type III fracture is an avulsion injury as a result of forced rotation and lateral bending. This is potentially an unstable fracture.

Clivus fractures

Fractures of the clivus are described as a result of high-energy impact sustained in motor vehicle accidents. Longitudinal, transverse, and oblique types have been described in the literature. A longitudinal fracture carries the worst prognosis, especially when it involves the vertebrobasilar system. Cranial nerves VI and VII deficits are usually coined with this fracture type.

Signs and diagnosis

Patients with fractures of the petrous temporal bone present with CSF otorrhea and bruising over the mastoids, ie, Battle sign. Presentation with anterior cranial fossa fractures is with CSF rhinorrhea and bruising around the eyes, ie, “raccoon eyes.” Loss of consciousness and Glasgow Coma Score may vary depending on an associated intracranial pathologic condition.

Longitudinal temporal bone fractures result in ossicular chain disruption and conductive deafness of greater than 30 dB that lasts longer than 6-7 weeks. Temporary deafness that resolves in less than 3 weeks is due to hemotympanum and mucosal edema in the middle ear fossa. Facial palsy, nystagmus, and facial numbness are secondary to involvement of the VII, VI, and V cranial nerves, respectively. Transverse temporal bone fractures involve the VIII cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss.

Occipital condylar fracture is a very rare and serious injury. Most of the patients with occipital condylar fracture, especially with type III, are in a coma and have other associated cervical spinal injuries. These patients may also present with other lower cranial nerve injuries and hemiplegia or quadriplegia.

Vernet syndrome or jugular foramen syndrome is involvement of the IX, X, and XI cranial nerves with the fracture. Patients present with difficulty in phonation and aspiration and ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.

Collet-Sicard syndrome is occipital condylar fracture with IX, X, XI, and XII cranial nerve involvement.

CT showing left sphenoid sinus and an air-fluid level

CT scan: CT scan is the standard modality for aiding in the diagnosis of skull fractures. Helical CT scan is helpful in occipital condylar fractures, but 3-dimensional reconstruction usually is not necessary.  Be careful: fractures can be missed on CT. Always correlate clinically with mechanism of injury and physical exam.

Of  note, patients may have developed Battle sign later, but because the patient in our case presented immediately after his injury, this exam finding was not present.  It takes time for the communicating fracture to accumulate. Therefore, if Racoon and Battle sign are negative, it does not mean you can rule out a basilar skull fracture immediately.  Clinical correlation and the timeline of injury must be considered.  The clinical manifestations of basilar skull fracture may take 6 to 12 hours to fully develop

double-ring sign, comprises blood (inner ring) and CSF (outer ring).

Testing for the double ring sign: take a drop of the fluid and place on filter paper (can be a coffee filter) or a sheet and look for a halo sign. (In our case, a drop of the ottorhea was seen separating on the EMT paper sheets.)  The double “halo” seen when CSF hits filter paper may help to indicate that the pt has an open communicating basilar skull fracture but is not definitive.

Glucose testing of ottorhea: Testing the fluid for glucose level helps distinguish spinal fluid from nasal secretions, which are low in glucose  but contamination of the specimen with blood, serum, tears, or saliva may lead to a false-positive result. State what the glucose of csf from the nose or ear would be expected.

Beta 2 transferrin: This is not a bedside test. Testing for beta2 transferrin, a substance found only in CSF, may identify the substance with a greater degree of certainty. However, the test for beta2 transferrin may not be readily available and the result may not be returned for days to weeks. None of the listed confirmatory tests for CSF ottorhea should hold patient up from CT but can be quick adjunctive tests to help quickly care for a patient.


Call neurosurgery.  Depending patient (if immunosupressed) prophylactic ABX can be started and manitol can laso be used for ICP control. However, these should not be sarted until consulting neurosurgery.


The risk of infection is not high, even without routine antibiotics, especially with CSF rhinorrhea. Facial palsy and ossicular chain disruption associated with basilar fractures are discussed in the Clinical section. However, notably, facial palsy that starts with a 2- to 3-day delay is secondary to neurapraxia of the VII cranial nerve and is responsive to steroids, with a good prognosis. A complete and sudden onset of facial palsy at the time of fracture usually is secondary to nerve transection, with a poor prognosis.

Other cranial nerves also may be involved in basilar fractures. Fracture of the tip of the petrous temporal bone may involve the gasserian ganglion. An isolated VI cranial nerve injury is not a direct result of fracture, but it may be affected secondarily because of tension on the nerve. Lower cranial nerves (IX, X, XI, and XII) may be involved in occipital condylar fractures, as described earlier in Vernet and Collet-Sicard syndromes (vide supra). Sphenoid bone fracture may affect the III, IV, and VI cranial nerves and also may disrupt the internal carotid artery and potentially result in pseudoaneurysm formation and caroticocavernous fistula (if it involves venous structures). Carotid injury is suspected in cases in which the fracture runs through the carotid canal; in these instances, CT-angiography is recommended.

Signs and symptoms


  1. The clinical manifestations of basilar skull fracture may take 6 to 12 hours to fully develop.
  2. Since plain films are unhelpful, there should be a low threshold for head CT in any patient with head trauma, loss of consciousness, change in mental status, severe headache, visual changes, or nausea or vomiting.
  3. The use of filter paper or a dextrose stick test to determine if CSF is present in rhinorrhea is not 100% reliable.
  4. Fracture of the temporal bone could result in temporary conductive hearing loss caused by disruption of the ossicular chain.


Skull Fracture.

The Atlas of Emergency Medicine :Chapter 1. Head and Facial Trauma

Intern Report Case 4.3

Case Presentation by Dr. Dan Helzer

36 year old AA female presents to the emergency department complaining of “passing out.”  Pt states that she was sitting down watching TV when she stood up, became very dizzy and lightheaded but no vertigo and fell to the ground.  She stated that she remembers almost everything but could not stay standing up for some reason.  Family members stated that she was not arousable for a few seconds and then came too.  She felt uneasy as family members helped her up and needed assistance getting into the car to be brought to the ED.  She has felt a little weak over the last few days but has experienced nothing like this recently.  Pt also states that she has had heavy vaginal bleeding for the last 10 days, it began with her normal menses but never stopped.  Her last normal menstruation was a month and a half ago.  Typically she has heavy menses but it only lasts 3-4 days.  She says that currently she is passing large clots and goes through multiple pads daily.  She denies headaches, abdominal pain, chest pain, palpitations, and SOB.  She denies ever being told that she has an abnormal heart beat or problems with her heart.  Her family denies any bladder or bowel incontinence during the event.
Past medical history is significant for anemia and fibroid uterus.  Pt is G3P3 and is sexually active.  Her medications include Fe pills.
Past surgical history positive for C-section x 2.
Social Hx includes a 30 pack/year smoking history.
Vitals:  108/55, HR 104, RR 16, Pulse Ox 99 % on RA, Temp 37.7
General:  Pt is in no acute respiratory distress, appears pale.
HEENT: Normocephalic/atraumatic, PERRLA, EOMI, no nystagmus, conjunctiva pale and non-icteric, mucous membranes moist and pale. Fundoscopy demonstrated no pappiledema.
Neck: No lymphadenopathy, no JVD, no masses
Respiratory and Lungs: Equal excursion bilaterally, CTAB, no wheezes, rales, rhonchi, or stridor.
Cardiovascular and Heart: Tachycardic rate and rhythm, S1/S2 auscultated, no murmurs, gallops, rubs, or thrills.  Pulses palpated in all 4 extremities.
Gastrointestinal and Abdomen: BS +, Abdomen soft, non-tender, non-distended.  No masses.  No CVA tenderness.
Neurological: Patient is alert and oriented to person place and time, CN II-XII intact, sensation to pinprick intact in all 4 extremities, strength 5/5 in all extremities.  No pronator drift was present. Reflexes are 2+.  Heal to shin was normal.  Upon standing pt became lightheaded and dizzy and felt the need to sit back down, therefore gait and Romberg were not properly evaluated. Dix-Hallpike test was normal.
Genitourinary:  External genitalia were normal. Examination of the pelvis and vagina revealed active bleeding from the closed cervical os with pooling of blood and blood clots in the vaginal vault, no tissue like material was present.  The uterus was not enlarged.  CMT was absent.  The adnexa were non-tender and no masses were palpated.
Orthostatic Vital Signs:
-Supine BP 109/60, HR 103
-Sitting BP 100/59, HR 111
-Standing BP 88/52, HR 127  
Lab Results:
Urine pregnancy negative
WBC 11.3, Hemoglobin 2.9, Hematocrit 11.7, Platelets 35
Electrolytes all WNL 
Diagnostic Studies:
12 Lead ECG:  Sinus Tachycardia at 107 BPM.
Ultrasound showed?
Pelvic US with Duplex:
Findings suspicious for adenomyosis.
Nabothian cyst in the cervix largest measuring 0.7 x 0.5 x 0.8 cm
Paraovarian cyst adjacent to left ovary.
1.     What is the most common cause of syncope in adults aged 18-65 who present to the ED?
A.   Postmicturation
B.    Orthostatic
C.    Psychogenic
D.   Unknown or Idiopathic
E.    Cardiac
2.     The same pt is brought in by family members who tell you that when she fell down after standing up her whole body started shaking for at least one minute and she was completely unresponsive during this time. They said it looked just like a seizure that the patient’s cousin with epilepsy has all the time.  Which clue in the HPI can often be the only distinguishing feature between syncope and seizure?
A.   The patient has never had a seizure before
B.    The patient remembers everything
C.    The patient has an abrupt and complete recovery to baseline
D.   The patient has generalized tonic/clonic movements during the episode.
E.    The patient ate 10 tacos from taco bell and drank a liter of cola earlier in the afternoon.
3.     Of the following, which pt with syncope should be discharged from the ED with follow up by PCP and not be admitted.
A.   A 17 year old male with exertional syncope and crushing chest pain.
B.    A previously healthy 37 year old male with 5 seconds of asystole on carotid sinus massage.
C.    Our patient with a hematocrit of 11 and orthostatic hypotension
D.   A 90 year old female with an EF of 22% and enlarged heart borders on CXR
E.    A 52 year old male with SOB on initial presentation.

Answers:  1. D, 2. C, 3. B 





Syncope is the sudden transient loss of consciousness with a loss of postural tone.  The most important defining feature being transient, in that it resolves spontaneously within a small time frame.  It is a common complaint in the ED and presents at a national rate of 2.8 visits per 1000.  Most cases are benign and have a very low morbidity/mortality outcome, although serious underlying disease and trauma following syncope often complicates the clinical picture.

The causes of syncope are numerous, but all causes eventually lead to a final common pathway of dysfunction of either both cerebral hemispheres or the brain stem/reticular activating system.  A 35% reduction in blood flow to the CNS usually results in LOC and can be attributed to changes in CO, SVR, and/or intravascular volume.  Etiologies behind these changes often define the type of syncope that occurs.  With such a large differential the goal of an ED physician handling a patient with syncope is identifying those patients with serious pathology that would result in increased morbidity and mortality if left untreated.  Life threatening causes of syncope that need to be identified include cardiac ischemia, dysrhythmias, cardiac valve lesions, cerebrovascular disease, metabolic and toxicologic derangements, severe hypovolemia, and anemia.

Clearly, syncope is often just a symptom of another disease and often when a patient presents following a syncopal episode they will have no other complaints.  That is why a thorough HPI, PMH, and medication list must be obtained.  It is invaluable in separating benign syncopal events from the more serious.  Combined with a proper physical exam and a few ancillary tests including EKG a serious case of syncope will never be missed.

In our case a middle aged female with past medical hx of anemia and fibroid uterus presented with a case of apparent orthostatic syncope.  The patient reported standing up from a sitting position becoming faint and loosing consciousness.  Family provided details of the actual syncopal event and described the fast return to baseline.  In further questioning she admits to vaginal bleeding for multiple days and feeling weak days leading up to presentation.  Pertinent negatives included the patient not exerting herself before the event, she had no chest pain, SOB, and no history of cardiac arrhythmias or CHF.  Also, no seizure like activity was described.  The patient’s medication list showed no drugs with cardiac effects.

Physical exam also helped narrow the diagnosis.  Vital signs including orthostatics were consistent with anemia or volume depletion.  CV demonstrated no murmurs or thrills and lungs were clear to auscultation leading one away from a diagnosis of valvular disease, MI, of CHF that could be underlying her syncope.  A thorough neuro exam helped rule out stroke and seizure.

Ancillary tests including EKG, CBC, and electrolytes helped clinch the diagnosis. With hemoglobin of 2.9, a hx of sig bleeding and syncope on standing this was most likely a case of volume depletion combined with chronic anemia leading to hypoperfusion of the CNS and syncope.  The patient autocorrected the hypoperfusion on her own by losing postural tone and falling to the ground.  In doing this she was able to increase venous return to the heart, increase CO, and subsequently return proper perfusion to the CNS thereby regaining consciousness and postural tone.

The first question is general epidemiology.  The correct answer is D, unknown or idiopathic.  Most cases of syncope in the age group are related to benign etiologies.  These patients will have a completely negative ED workup and further testing to make a definitive diagnosis like a tilt table test are not within the realm of an ED workup.

The second question brings to light the problem of distinguishing syncope from a seizure which at times can be difficult.  The correct answer is C.  It is not uncommon for generalized tonic/clonic movements to present during syncope.  It is also not completely rare to see new onset seizures in the patients in this age group.  If a patient remembers feeling faint and loosing tone they could have had a “presyncopal” event or a simple/complex partial seizure among other things. If on the other hand, there is no post ictal state with loss of postural tone and a quick return to baseline status no matter what happens in between, this is most likely to be syncope and not a seizure.

The third question brings up disposition of a syncopal pt.  The correct answer is B.  Using the San Francisco Syncope Rule as guidelines, pts with the absence of abnormal ECG findings, SOB, Hypotension (systolic less then 90), anemia (Hematocrit less then 30%), or hx of CHF are low risk and can be followed up outpatient. Furthermore any patients with exertional syncope, chest pain, or valvular disease need hospitalization.   In this question, the correct answer B whom has none of these findings. He does however qualify for carotid sinus sensitivity and carotid sinus syncope which is usually benign and can be followed up as an outpatient.

Rosen’s Emergency Medicine, seventh edition, 2010, pages 142-147, Marx

Syncope: E-Medicine.

Carotid Sinus Hypersensitivity: E-Medicine.

Approach to adult patient with syncope:  UpToDate.

Intern Report Case 4.2

Case Presentation by Dr. Deepa Japra
A 25-year-old woman presents to the emergency department with persistent nausea and vomiting for 6 days. She complains of pain in the lower chest and upper abdomen that she rates as a 6/10.  She describes the pain “like a heart beating real hard”, which is constant and throbbing in character. She is unable to tolerate a regular diet and states she vomits everything she eats.  The vomitus is described as white and yellowish without hematemesis.  The patient had a small bowel movement today, which was soft with no gross blood.  She denies any genitourinary symptoms including no polyuria, dysuria, or hematuria. She does describe a vaginal discharge X 6 days. She is sexually active with one partner, and does not use protection.  Her LMP ended 9 days ago. She has also had subjective fevers and chills, and lightheadedness, but without any syncopal episodes.
Past medical history is significant for genital herpes infection.
VS: BP: 122/75, P: 59, R:18, T: 36.5, O2 saturation 100% on RA
GENERAL:  Pt is conscious, alert, and cooperative
HEENT:  Conjunctivae are pink without pallor, sclera anicteric. Mouth without intraoral lesions.  Pharyngeal soft tissues are normal.
NECK:  Supple. Trachea midline. No thyromegaly or lymphadenopathy.
RESPIRATORY:  Clear symmetric breath sounds. Good air exchange in all lung fields. No accessory muscle use.
CARDIOVASCULAR:  Normal S1 and S2.  No S3 or S4 gallops.  No murmurs or rubs.  CHEST WALL:  Nontender.
ABDOMEN:  Soft, nondistended, bowel sounds present. mild discomfort to palpation in the epigastric and suprapubic areas, but there is no guarding, masses or rebound tenderness.
BACK:  No spinal or paraspinal tenderness. No CVA tenderness.
MUSCULOSKELETAL:  FROM, symmetrical strength, no acutely inflamed joints. SKIN:  No rashes or lesions.
NEUROLOGIC:  No gross focal motor or sensory deficits.
PELVIC EXAM: External genitalia are normal. Slight discharge in vaginal vault, cervical os is closed. Positive cervical motion tenderness. Mild uterine and adnexal tenderness, no masses.
Laboratory Studies are as follows:
CBC: Hb 15.5, Hct 43.1, WBC 9.2, Pl 234
Electrolytes: Na 139, K 3.7, Cl 101, HCO3 26, BUN 21, Cr 1.0, Glu 90, Ca 9.5
Lipase 294
ALT 30, AST 19, Alk Phos 77, TBili .8, DBili .2,
Urine Pregnancy negative
UA: trace glucose, 3+ ketones, 1+ blood, 1+ protein, Positive nitrite, 1+ leukocyte esterase, RBC 2-5, WBC 5-10, 1+ mucus, 1+ bacteria
Rapid HIV negative
Gonorrhea PCR positive, Chlamydia PCR negative
Question 1
Which of the following is the greatest risk factor for development of pelvic inflammatory disease?
a.     age
b.     intrauterine device usage
c.     multiple sexual partners
d.     previous PID
e.     sexually transmitted disease status of sexual partner
Question 2:
According to CDC guidelines, which of the following is essential in the diagnostic criteria for empirical treatment of PID?
a.     abnormal cervical or vaginal mucopurulent discharge
b.     history of Gonorrhea/Chlamydia infection
c.     lower abdominal or pelvic pain with cervical motion tenderness or uterine/adnexal tenderness
d.     numerous WBCs on microscopy of vaginal secretions
e.     oral temperature > 38.3 C
Question 3:
In addition to clinical symptoms and physical exam findings, which of the following criteria suggests a confirmed case of PID?
a.     confirmed N. gonorrhea infection in the past
b.     confirmation of ectopic pregnancy on vaginal ultrasound
c.     demonstration of N. gonorrhea in the genital tract
d.     elevated serum WBC count
e.     positive Pregnancy test
Answers: 1) c, 2) c, 3) c
The patient in this case is suffering from Pelvic inflammatory disease (PID) caused by Neisseria gonorrhoeae infection.  PID includes a spectrum of diseases of the female upper genital tract including endometritis, salpingitis, pelvic peritonitis, and tubo-ovarian abscess. It is an ascending infection most commonly caused by N. gonorrhoeae and Chlamydia trachomatis where the bacteria spread from the cervix and vagina to the upper portions of the female genital tract. PID is responsible for approximately 30% of female infertility and 50% of ectopic pregnancies.
Risk factors for PID include multiple sexual partners, STD status of the sexual partner(s), age, and history of previous PID. Numerous studies have shown that having multiple sexual partners resulted in increased risk of PID ranging from 4.6 to 20 fold. (Question 1c). In one study which compared 712 women hospitalized for PID to 2,719 controls, the risk of PID was increased 3.4 times in patients with four or more sexual partners during the previous six months, and 3.2 times in patients who had intercourse with one partner six or more times per week. Having a partner with symptomatic gonococcal infection including dysuria and urethral discharge also increases a woman’s risk of PID (Question 1e). PID is more common in the 15 to 25 year old age group, with the incidence in women greater than 35 years old being only one-seventh of that in younger women. (Question 1a). Women with previous PID have increased risk of subsequent episodes, with one study citing an increase by a factor of 2.3. (Question 1d). However, caution should be used in diagnosing a woman who presents with abdominal pain in the ED with PID based on a previous diagnosis of PID. IUD usage (Question 1b) causes minimal risk of PID, and risk is usually limited to the first 3 weeks after IUD insertion. There is no evidence indicating that an IUD should be removed in a patient with acute PID.
The clinical features of PID can vary widely, with lower abdominal or pelvic pain being the most common presenting symptom to the ED. Patients may also present with dyspareunia, abnormal bleeding, and/or vaginal/cervical discharge. Physical examination can demonstrate lower abdominal tenderness, cervical motion tenderness, unilateral or bilateral adnexal tenderness on bimanual exam, and/or fever (>38 C).  Though clinical examination has a low sensitivity for the diagnosis of PID, current recommendations by the CDC recommend empirical treatment based on clinical exam due to the long term sequelae, which include risk of ectopic pregnancy and infertility.
The CDC criteria for empirical treatment of PID include a minimum of cervical motion tenderness or adnexal/uterine tenderness in the presence of lower abdominal or pelvic pain (Question 2c). Additional criteria which are used to support a clinical diagnosis of PID includes oral temperature > 38.3 C (Question 2e), abnormal cervical or vaginal mucopurulent discharge (Question 2a), the presence of numerous WBCs on microscopy of a vaginal sample (Question 2d), elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP). These additional criteria, however, are not necessary for empirical treatment. A history of gonorrhea/Chlamydia infection in the past (Question 2b) is not part of the CDC criteria indicating empirical treatment for acute PID.
Findings which confirm a diagnosis of PID in a patient that presents with clinical signs and symptoms suggesting PID include endometritis or acute salpingitis on histological evaluation of a biopsy, demonstration of N. gonorrhoeae in the genital tract (Question 3c), gross salpingitis seen during laparoscopy/laparotomy, isolation of pathogenic bacteria from a clean specimen in the upper genital tract, or inflammatory/purulent pelvic peritoneal fluid without another source of infection.  A confirmed diagnosis of N. gonorrhoeae infection in the past does not confirm acute PID (Question 3a). Though a patient with a positive pregnancy test and clinical symptoms of PID is at increased risk for ectopic pregnancy, a positive pregnancy test or a vaginal ultrasound demonstrating an ectopic pregnancy does not confirm PID (Question 3e and 3b). An elevated serum WBC count may suggest acute inflammation/infection, but is not in the diagnostic criteria to confirm PID (Question 3d).
As discussed above, empiric treatment of acute PID in the ED should be initiated in patients with lower abdominal pain and cervical motion tenderness, uterine tenderness, or adnexal tenderness due to the potential adverse consequences of untreated PID, which include infertility and ectopic pregnancy. Currently, CDC outpatient recommendations include ceftriaxone 250mg IM PLUS doxycycline 100mg BID for 14 days, with or without metronidazole 500mg BID for 14 days. An alternative regimen includes: cefoxitin 2g IM AND probenecid 1g oral PLUS doxycycline 100 mg BID for 14 days with or without metronidazole 500mg BID for 14 days. Metronidazole should be administered in patients with pelvic abscess, proven or suspected infection with Trichomonas vaginalis or bacterial vaginosis, or history of gynecological instrumentation in preceding 2-3 weeks.
Approximately 10 to 25% of women with PID require hospitalization. CDC recommendations for hospitalization include pregnancy, failure to respond to outpatient treatment, inability to tolerate oral medications, nonadherence to outpatient therapy, presence of pelvic abscess, or severe clinical illness including elevated fever, nausea/vomiting, and severe abdominal pain.  Inpatient treatment options include cefoxitin 2g IV q6h OR cefotetan 2g IV q12h PLUS doxycycline 100mg q12h. An alternative regimen is Clindamycin 900mg IV q8h PLUS gentamicin (2mg/kg) loading dose with maintenance dose of 1.5mg/kg q8h.
Clinical Pearls:
–  Pelvic Inflammatory Disease includes a spectrum of diseases of the female upper genital tract including endometritis, salpingitis, pelvic peritonitis, and tubo-ovarian abscess
–  Empiric treatment of acute PID in the ED should be initiated in patients with lower abdominal pain and cervical motion tenderness, uterine tenderness, or adnexal tenderness due to the potential adverse consequences of untreated PID, which include infertility and ectopic pregnancy
– Male sexual partners of women with PID should be treated if they have had sexual contact with the patient during the 2 months prior to patient’s onset of symptoms
– Patients with PID should be tested for other sexually transmitted diseases, including HIV

Intern Report Case 4.1

Case Presentation by Dr. Sarah Hyatt

Chief complaint: “I can’t see”
28 year old female comes to the ER for loss of vision for 2 days, patient states that this happened suddenly after she was vomiting.  Patient is 6.5 months pregnant and has hyperemesis gravidarum that has persisted through her entire pregnancy. She denies any eye pain and the vision has not improved.  She says she is unable to see anything from the left eye. Previous to this she has not had any trouble with her vision, other than wearing reading glasses.  She decided to come to the ER because her vision still has not improved. She has history of hypertension but no longer requires medication. Denies any headache, fever, chills, chest pain, palpitations, shortness of breath, abdominal pain diarrhea, constipation, dysuria, vaginal bleeding or discharge, no recent travel, no sick contacts.
ROS: negative except as noted per HPI.
PMH:  Hx of Hypertension no longer on medication
Surg hx: none
Gyn: G1P0, good prenatal care
Meds:  Prenatal vitamins
Allergies: Vicodin causes “throat to close”
FH: Hypertension and diabetes run in the family
SH: No tobacco/alcohol/drugs
PE:  vitals: T 98.7, HR 76, BP 110/56, RR 18, pulse ox 100% RA,  weight 231, 5’5’’
General:  28 year old, African American female, sitting converses without difficulty
Skin: No rashes or scars
Head: normocephalic, atraumatic
Eyes:  EOMI, PERRLA constricting from 6 to 3 mm bilaterally with light, no afferent pupillary defects, Pt has 20/20 VA in right eye,  left eye able to finger count correctly at 5 ft. In her left eye her vision is more clear in her peripheral fields than centrally, intraocular pressure R eye 12, L eye 13, peripheral fields are intact by confrontation, on fundoscopy there were no distinct optic discs visualized, no pallor, no icterus
Nose: symmetric, no discharge
Mouth, throat: No erythema or exudates
Neck: No tracheal deviation or masses
Heart: RRR, S1, S2 heard no murmurs rubs or gallops
Respiratory: CTA BIL
Abd: gravid uterus above the umbilicus consistent with 26 week gestation, soft NT ND,
CNS: Alert and oriented x 3, cranial nerves:  II, III, IV, and VI  see eye exam above, good eyelid opening bilaterally; V, corneal reflex intact bilaterally facial sensation intact bilaterally in V1,V2, V3, good jaw opening, and bite strength; VII, eyebrow raise, eyelid close, smile, frown, pucker, and taste all intact and equal bilaterally; VIII equal auditory acuity to finger rub bilaterally; IX good swallow reflex, positive gag reflex; XI good lateral head rotation, neck flexion, shoulder shrug bilaterally; XII midline tongue protrusion and equal strength on lateral deviation bilaterally. Equal strength in the upper and lower extremities bilaterally, speech and gait are normal.
Extremities: no peripheral edema, all peripheral pulses are felt, good range of motion, no weakness
Labs:       136    101    5      Glucose 82, Ca 9.1, ALT 13, AST 21, total protein 7.1, albumin 3.4, uric acid 4.2 Alkaline phosphatase 166, negative UDS and UA
13.5        451  MCV 81.7       Fetal heart tone 150’s
1.     After you dilate the pupil this is your fundoscopic exam. Your diagnosis is?
A. acute glaucoma
B. vitreous hemorrhage
C. central retinal vascular occlusion
D. valsava retinopathy
E. central retinal vein occlusion
2. The patient should be advised which of the following?
A. use aspirin
B. sleep in a sitting position
C. decrease fiber intake
D. resume normal physical activity
E . all of the above
3.Which of the following are risk factors for the above diagnosis?
D. idiopathic thrombocytopenic purpura
E. all of the above
Answers: 1. D, 2. B, 3. E
This patient has a Valsava retinopathy. Immediately following a Valsava maneuver, a sudden rise in intraocular pressure causes retinal capillaries to spontaneously rupture. The prognosis for Valsava retinopathy is generally good.
Unilateral manifestations are most commonly seen, but bilateral findings have been reported. Sudden decreased vision occurs in the affected eyes, ranging from complaints of floating spots to complete loss of central vision. Vision often improves over weeks to months, depending on the severity of the retinal findings.
Risk factors for Valsava retinopathy are a history of vascular disease, diabetes, hypertension, sickle cell disease, anemia, idiopathic thrombocytopenic purpura.
Ocular findings are usually described as preretinal hemorrhages. Valsava retinopathy has a predilection for the macula. The ruptured vessels in the perifoveal capillaries usually cause a sudden and painless loss of central vision.
Causes: coughing, weight lifting, vomiting, bungee jumping, aerobic exercise, sexual activity, end-stage labor, colonoscopy procedures, constipation, and blowing musical instruments.
Medical care: patients should be advised to avoid anticoagulants and strenuous activities to prevent a rebleed. Patients should be instructed to sleep in a sitting position to promote blood settling, which may improve visual acuity, stool softeners may need to be considered for those with constipation. A diet rich in fiber is advisable. Physical activity should be limited until the retina has sufficiently healed. The patient should always try to limit activities that cause sudden increases in intrathoracic pressure against a closed glottis. Consultation to ophthalmology is recommended and needed for follow up.
Vision usually returns to normal over a short time period from weeks to months.
Key points:
When testing visual acuity use a Snellen chart at a distance of 20 feet or a Rosenbaum chart at a distance of 14 inches.  If the patient is unable to do this test visual acuity by testing  ability to count fingers (CF), if unable to do this test ability to perceive hand motion (HM), if unable to do this test  ability to perceive light (LP). The result may be recorded as “patient able to count fingers at 5 feet”
Acute angle-closure glaucoma: Pt has a narrow anterior chamber angle; folds of the peripheral iris can block the angle, which prevents aqueous humor outflow. The rapid elevation of intraocular pressure causes optic atrophy if not treated promptly. Patient often complains of nausea, vomiting, and pain. Emergent ophthalmologic consultation is indicated. Acute glaucoma is treated with IV mannitol or glycerol to decrease intraocular pressure by osmotic dieresis, topical miotics (i.e., 2% pilocarpine or 0.5% timolol) to decrease pupil size and increase aqueous outflow, and acetazolamide IV to decrease aqueous production
Vitreous hemorrhage: Suspect if sudden painless monocular loss of vision, more common in diabetics with an obscured red reflex and retinal details. Patients often report seeing flashing lights.  Patients also complain of seeing dark floating spots or floaters, which reflect benign vitreous separations
Central retinal artery and vein occlusion: both occur in middle-aged atherosclerotic patients or elderly hypertensive patients and present as sudden painless loss of vision. Occlusion of the retinal artery or its branches results in a dilated nonreactive pupil with an APD on the affected side. The retina is pale with a cherry-red spot on the macula. Occasionally amaurosis fugax precedes central retinal artery occlusion.
The fundoscopic examination of a central retinal vein occlusion is described as a “blood and thunder fundus” because of the presence of multiple large hemorrhages. Prognosis for both CRAO and CRVO is poor.
Common causes of nontraumatic loss of vision
Transient monocular
Amaurosis fugax
Temporal arteritis
Persistent monocular
Central retinal artery occlusion
Central retinal vein occlusion
Retinal detachment or hemorrhage
Vitreous or macular hemorrhage
Optic or retrobulbar neuritis
Internal carotid occlusion
Acute binocular
Vertebral basilar insufficiency
Cerebrovascular disease
Toxins (methanol, salicylates, quinine, ergot)
Optic or retrobulbar neuritis
Sudden painless loss of vision
Central retinal artery occlusion
Central retinal vein occlusion
Vitreous hemorrhage
Retinal detachment
Ischemic optic neuropathy
Nonarteritic ischemic optic neuropathy
Valsava retinopathy
Functional visual loss, hysterical conversion or malingering
1.Retinopathy, Valsalva, eMedicine
2.Emergency Medicine Secrets, fourth edition, 2006, pages 117-121, Markovchick
3.Rosen’s Emergency Medicine, seventh edition, 2010, pages 870-873, Marx
4.Uptodate, Approach to the adult with acute persistent vision loss, 2010, Leaveque