Answers Case 5.2

Posted on November 18, 2011 by kjones100

Answers

1)     B

2)     D

3)     D

Discussion:

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.

Treatment

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.

References

Erowid Crew. “Cocaine Adulterated with Levamisole on the Rise: Status as of September 2009″ Erowid.org. Oct 1,    2009. http://www.erowid.org/cocaine/cocaine_article2.shtml

Farnier, C. Agranulocytosis Associated with Cocaine Use. Morbidity and Mortality Weekly Report, Dec. 8, 2009. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5849a3.htm

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.  http://www.time.com/time/health/article/0,8599,1955112,00.html

  

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Intern Report Case 5.2

Posted on November 14, 2011 by kjones100

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”

PMH:  CAD, MI

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

Labs/EKG:

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

 

Questions

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

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Answers Case 5.1

Posted on November 10, 2011 by kjones100

Answers

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.

Management

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.

Misc.

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

Pearls

  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.

Sources:

Skull Fracture.http://emedicine.medscape.com/article/248108-overview.accessed[11/02/2011]

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

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Intern Report Case 5.1

Posted on November 8, 2011 by dwseitz

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.

QUESTIONS

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.

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Intern Report Case 4.3

Posted on November 2, 2011 by dwseitz

Case Presentation by Dr. Dan Helzer

HPI
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.
PE
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?
SourceURL:file://localhost/Users/adamrosh/Desktop/Syncope%20Case.doc
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.
Questions: 
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 

 

 

Discussion:

 

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.   emedicine.medscape.com/article/811669

Carotid Sinus Hypersensitivity: E-Medicine. emedicine.medscape.com/article/153312

Approach to adult patient with syncope:  UpToDate.  www.uptodate.com

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Intern Report Case 4.2

Posted on November 2, 2011 by dwseitz

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
Questions:
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
Discussion:
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

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Intern Report Case 4.1

Posted on November 2, 2011 by dwseitz

Case Presentation by Dr. Sarah Hyatt

Case
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
      10.2
13.5        451  MCV 81.7       Fetal heart tone 150’s
          32.6
 
Questions
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?
A.diabetes
B.hypertension
C.anemia
D. idiopathic thrombocytopenic purpura
E. all of the above
Answers: 1. D, 2. B, 3. E
Discussion:
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
Migraine
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
Migraine
Vertebral basilar insufficiency
Cerebrovascular disease
Toxins (methanol, salicylates, quinine, ergot)
Optic or retrobulbar neuritis
Hysteria
Malingering
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
References:
1.Retinopathy, Valsalva, eMedicine http:emedicine.medscape.com/article/1228106
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

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Intern Report Case 4.0

Posted on November 2, 2011 by dwseitz

Case Presentation by Dr. Stephanie Wise

A 42-year-old man presents to the Emergency Department with a 2-day history of coughing up blood. His symptoms started about 5 days after he returned from a week-long business trip in South Africa. He has not had any fevers or weight loss. He does have chest pain, however, on the left antero-lateral side. He describes this pain as sharp, worse with a deep breath. He denies any shortness of breath. No nausea or vomiting or diarrhea. Appetite has been normal.

PMH: Asthma
Medications: albuterol HFA PRN
Allergies: None
Surgeries: Appendectomy, age 19
FH: HTN, “blood problem” in two uncles
SH: Smokes 1/2 pack daily for 12 years; occasional alcohol, denies ilicit drugs

Physical exam:

BP 134/85, HR 108, RR 21, Temp 37.1
General: Well-developed overweight male, sitting up on stretcher, mild distress
HEENT: PERRL, EOMI; trachea midline, no LAD
CV: Regular rhythm, tachycardic, no murmurs
Resp: Breath sounds decreased at the left base with mild crackles; otherwise clear to auscultation, no wheezing
ABD: soft, non-tender, non-distended; normal active bowel sounds
Extremities: pulses equal, no deformities seen
Neuro: AOx3, normal strength and sensation in all extremities; no facial droop or other focal deficits; gait normal; reflexes 2+ in all extremities

Labs:
143 105 12
4.1 21 0.9 Glucose 88
WBC 9.9
Hb 14.2
Platelets 248
EKG shows sinus tachycardia, rate of 112, no ST elevations or depressions
CXR:

______________________________
Questions:

1. What is the most common inherited hypercoagulable state?
a. Factor V Leiden
b. Protein C deficiency
c. Anti-thrombin III deficiency
d. von Willebrand disease
e. Sticky platelet syndrome

2. In the presence of acute pulmonary embolism, what is true of ECG findings:
a. “S1Q3T3″ is the most sensitive finding
b. Anterior T wave inversions are the most specific finding
c. Typically no abnormality is seen on ECG
d. Sinus tachycardia is an uncommon finding

3. Which statement is correct about the diagnosis of pulmonary embolism?
a. Lower extremity Doppler studies that are positive for DVT are present in 70% of PE patients
b. The chest x-ray is typically normal
c. Pulmonary angiography is the gold standard
d. A D-dimer’s value is in its positive predictive value

4. What percentage of ambulatory patients who present with PE have no identifiable clinical risk factors?
a. 10%
b. 30%
c. 50%
d.80%

Discussion

Answers

1) A. The most common inherited hypercoagulable state is Factor V Leiden. This is characterized by the production of a “rogue clotter” protein, which is also resistant to proteolysis by protein C. It is inherited in an autosomal recessive fashion, and is most common in people of northern European descent.  Von Willebrand disease is the most common genetic cause of excessive bleeding. The other options are other inherited hypercoagulable disorders.
2) B. Of the options provided, the correct statement is that T wave inversions are the most specific finding (81%) in the presence of pulmonary embolism. This has been the most common finding in some studies (68%).
S1Q3T3 is an indicator of cor pulmonale, which makes it less specific of a finding, and it is also not considered sensitive as it is only present in approximately 50% of cases.
Typically an ECG of a PE patient is abnormal; the difficulty is that the abnormalities are non-specific. The value of the ECG is more in ruling out other causes of the patient’s symptoms, especially myocardial infarction.
Sinus tachycardia is a common finding, but again, very non-specific.
3) C. Pulmonary angiography is the gold standard for diagnosis of pulmonary embolism. Doppler imaging can indicate a source of PE, but up to 60% of ambulatory patients (the people we’ll be seeing in the ED) do not have DVT.
In the presence of pulmonary embolism, the chest x-ray typically has some abnormality, but the abnormalities are usually both non-sensitive and non-specific. The findings more specific to PE (Hampton’s hump, Westermark sign and Fleischner’s lines) are rare. If you see them, however, you should be able to recognize them. Also, if you suspect PE, you should at least be aware of these findings so that you can identify them when present.
The value of D-dimer in diagnosis of PE is to rule it out. If clinical suspicion is low and the D-dimer is normal, PE is rare (2% or less). Thus, the value is in its negative predictive value.
4) C. Half of patients who present to the ED with a pulmonary embolism will have no identifiable clinical risk factors. Work-up will ultimately try to identify previously unidentied risk factors, but for the ED physician, a high index of suspicion needs to be present even if there is not a “convenient” history like what our patient in this case provided. Otherwise cases will be missed, which could be detrimental to our patients.

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Intern Report Case 3.9

Posted on November 2, 2011 by dwseitz

Case Presentation by Dr. Deshon Moore
A 67-year-old man with a significant medical history of COPD, CAD requiring many interventions, CHF, sustained ventricular tachycardia, and diverticulosis came to the emergency department with a 2-week history of generalized abdominal pain non positional and not related to food. He also complained of general weakness over the past several months.  No c/o weight loss, no changes in urination volume.
Physical exam showed no pertinent findings.
Initial laboratory values were drawn and showed a serum sodium concentration of 117 mEq/L (normal 135-145 mEq/L). The patient’s medical records indicated that almost 3 months earlier his serum sodium concentration was 134 mEq/L. Three weeks after that visit, his serum sodium concentration was 126 mEq/L.
On presentation the patient stated he was on amiodarone, Aspirin, Metoprolol, Nitroglycerin, lisinopril, furosemide, spironolactone, and simvastatin. The majority of his meds were started 3 mos ago.
Further Labs:
Serum osmolality 264 mOsm/kg,
U osm-730 mOsm/kg
Glu 120 mg/dl,
BUN 11 mg/dl,
Cr 1.0 mg/dl,
K- 4.4 mEq/L
Complete blood count and thyroid-stimulating hormone and thyroxine levels were normal; corticotropin stimulation test result was negative; chest radiograph showed no infiltrates or masses; and thoracic CT revealed no evidence of malignancy. An abdominal CT scan was normal.
Despite fluid restriction (< 1000 ml/day), serum sodium concentrations were 118-120 mEq/L over the next 2 days after admission.
Amiodarone was discontinued based on a publications suggesting that this drug can cause SIADH-induced hyponatremia. The patient’s serum sodium concentration began to rise within 3 days of discontinuation and was 129 mEq/L at discharge the next day. At an internal medicine follow-up visit the patient’s serum sodium concentration was within normal limits at 136 mEq/L. Symptoms of abdominal pain and general weakness improved as serum sodium levels increased.
Questions:
An 80-year-old woman who presented to the emergency department with weakness and dizziness had labs reveal a serum osmolality of 260 mOsm/kg, serum sodium of 125 mEq/L (normal 135–154 mEq/L), Urine sodium level of 50 mEq/L (normal, 0–300 mEq/L) and urine osmolality of 200 mOsm/kg. She takes furosemide for peripheral edema. Her PCP prescribed HCTZ for htn 1 week ago. The patient denies fevers, chills, nausea, or vomiting. She claims to be more thirsty than usual and has been drinking apple juice in response. BP is 100/60 mm Hg lying down and 84/40 mm Hg sitting. She weighs 60 kg.

1. Which of the following is this patient’s most likely diagnosis?
(A) Adrenal insufficiency
(B) Furosemide-induced hyponatremia
(C) Hydrochlorothiazide-induced hyponatremia
(D) Syndrome of inappropriate antidiuretic hormone
(SIADH)
(E) Thyroid disease
2. How should this patient be managed?
(A) Give intravenous (IV) normal saline (0.9%) at
125 mL/hr
(B) Give IV 5% dextrose in half-strength normal
saline at 50 mL/hr
(C) Restrict free water intake orally
(D) Provide salt tablets orally
 3. 50-year-old man admitted to the CCU with a MI has a sodium level of 124 mEq/L. There are no other laboratory abnormalities; however, the sample is lipemic. The patient is resting  comfortably and denies any symptoms. Which of the following is most likely to establish the  diagnosis?

(A) Serum osmolality
(B) Serum uric acid
(C) Urine osmolality
(D) Urine sodium
4.  You have a type 2 diabetic with ESRD on HD who presents with weakness. He missed dialysis and ran out of his long-acting insulin 2 days ago. No other complaints. Physical Examination is unremarkable, including a normal neurologic examination. CXR negative. 12 lead ECG-NSR w no T wave abnormality

Labs: Sodium-125 mEq/L, K-5.2 mEq/L, Serum Glu- 700 mg/dL, Serum Osm 310 mOsm/kg
Which of the following is the most appropriate
next step in this patient’s management?

(A) Immediate hemodialysis
(B) Initiate IV short-acting insulin therapy
(C) Restart subcutaneous insulin therapy for dosing
at home
(D) Restrict free water to correct hyponatremia
5. How many oz of water do you drink a day?
(A)  <16 oz/ day
(B)  16-32 oz/day
(C)  48 oz/day
(D)  >54 oz/day
(E)  Only coffee
Discussion
1. (C) Hydrochlorothiazide-induced hyponatremia. In the elderly, diuretic use has been associated with hyponatremia and usually occurs within 1 to 2 weeks of starting the drug. Diuretics can cause volume depletion and stimulate the release of antidiuretic hormone (ADH), which acts on the collecting duct to cause water reabsorption. However, this movement of water depends on a medullary concentration gradient. Loop diuretics like furosemide impair this gradient, and therefore water reabsorption is diminished even with adequate ADH levels. Thiazide
diuretics have no effect on the medullary gradient and water reabsorption is sustained. Diuretics
can also cause a heightened thirst response leading to increased fluid intake and further elevations of plasma free water. Older women in particular have been found to be most susceptible to thiazide related hyponatremia (reference below by Clark). Although thyroid disease and adrenal insufficiency can be associated with hyponatremia, there is nothing in the patient’s history to support these conditions as the reason for an acute presentation. A high urine sodium level may be caused by SIADH, but in this case, the elevated urinary sodium level is due to diuretic use. SIADH is characterized by an inappropriately concentrated urine (urine osmolality > serum osmolality), which
is not the case here.2. (A) Give IV normal saline (0.9%). This woman has chronic hypovolemic hyponatremia as a result of diuretic use, and the hyponatremia must be corrected slowly. In cases in which hyponatremia is not life-threatening (sodium > 120 mEq/L), the goal is to replace about a 3rd of the sodium deficit over the first 12 to 24 hours (not to exceed 12mEq/ day) and the remainder over the next 2 to 3 days. IV normal saline can correct hyponatremia because the stimulus for ADH release in this case (volume depletion) is inhibited. This patient’s total sodium deficit is 450 mEq/L (Weight kg x 0.5 x (desired NA- current NA)), which equals approximately 3 L of normal saline (154 mEq/L). One liter of normal saline should be given over the first 8 to 12 hours (at 125ml/hr) with a subsequent infusion rate reduction. Using hypotonic saline at a slow rate is not indicated in severe hypovolemic hyponatremia. Although restriction of free water may have initially prevented the development of hyponatremia, it will not play a role in its correction or in raising blood pressure. Salt tablets, which can play a role in treatment of SIADH, would not be used for immediate treatment in this case.

3. (A) Serum osmolality. This is a case of pseudohyponatremia Secondary to high triglycerides. With high triglycerides, plasma gets expanded. When this happens, the assays we use that employ plasma dilution while measuring serum sodium levels may report an abnormally low value. However, these lipids and proteins do not contribute to serum osmolality (2 × plasma Na + [glucose/18] + [blood urea nitrogen/2.8]). Therefore, pseudohyponatremia is diagnosed when serum osmolality is normal. Pseudohyponatremia can also be seen with multiple myeloma and the production of paraproteins. Urine osmolality, urine sodium, and serum uric acid can vary and have no role in diagnosing pseudohyponatremia.

4. (B) Initiate IV short-acting insulin therapy. Because glucose is an effective osmole, hyperglycemia leads
to hyponatremia by causing an osmotically driven shift of water from cells into the extracellular compartment,
resulting in dilution of serum sodium. This osmotic shift can be estimated by a correction
factor that predicts a 1.6 mEq/L decrease in sodium for every 100 mg/dL rise in glucose above 100 mg/dL.
Thus, in this patient, the corrected sodium would be 135 mEq/ based on the correction factor : Na+ (0.016 x (Glu-100)). In patients with intact renal function, the osmotic shift in water to the extracellular compartment caused by glucose is somewhat balanced by an osmotic diuresis also driven by glucose. These pts usually have a mild decrease
in serum sodium. A patient on dialysis cannot respond with diuresis, and therefore hyponatremia tends to be more pronounced. In this case, the treatment is to remove the osmotic driving force, which will require immediate IV insulin. Subcutaneous insulin is not recommended for managing critical hyperglycemia. Free water intake will likely worsen the underlying hyponatremia. Although the patient missed his hemodialysis, hyponatremia is not a primary indication for urgent dialysis; correction of hyperglycemia is the first line of treatment. In addition, this patient has no other indications for receiving immediate hemodialysis, such as critical hyperkalemia or volume overload.

5. This is for you to realize your water intake. Stay hydrated, but remember that too much of a good thing can actually be bad! For my purposes I’m just referring to water…

REFERENCES
1. Rosen’s Emergency Medicine. Electrolyte Disturbance. Ch 123 p 1615
2.Clark BA, Shannon RP, Rosa RM, Epstein FH. Increased
susceptibility to thiazide-induced hyponatremia in the
elderly. J Am Soc Nephrol 1994;5:1106–11.
3. Douglas I. Hyponatremia: why it matters, how it presents,
and how we can manage it. Clev Clin J Med 2006;73
4. Hillier TA, Abbott RD, Barnett EJ. Hyponatremia: evaluating
the correction factor for hyperglycemia. Am J Med
1999;106:399–403.

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Intern Report Case 3.8

Posted on November 2, 2011 by dwseitz

Case Presentation by Dr. Dan Paling

History and Physical
61-year-old obese male was sent to the local Emergency Department by his primary care physician with a complaint of low back pain. He reported a history of intermittent, worsening low back pain over the past 2 months. The patient experienced pain with movement of his low back.  The pain was characterized as dull, aching, and rated 6-7/10 in intensity located at the level of L3-L5. He patient denied any radiation of the pain down his legs, but admitted that sitting and standing for long periods aggravated his pain. He denied recent or remote falls and/or trauma to this region of his back. The patient denied urinary or fecal incontinence. He stated that he had similar pain about one year ago and was treated for a lumbar muscular strain. The patient felt that he has had fevers intermittently over the past 3 months for which he took acetaminophen. He denied any complaint of chest pain or shortness of breath. He also reported having occasional epigastric abdominal pain with nausea, but no vomiting. He attributed this to a history of heartburn.
Past Medical History:  hypertension and peripheral artery disease.  No surgical history
Medications:  hydrochlorothiazide and metoprolol, but has been noncompliant.
Social History:  40-pack-year tobacco, currently smoking 4 to 5 cigarettes a day.
Physical Examination:  BP is 184/112, HR 78, RR 15, Temp 38.2 (oral), O2 Sat 95% on RA.
General appearance:  mild distress secondary to pain.
HEENT: AT/NC, PERRL, EOMI
CV: RRR, S1 S2, no m/r/g
Resp: CTAB/L, equal breath sounds, no wheezes or ronchi appreciated
ABD: obese, soft, diffuse tenderness to palpation worse in the umbilical region, no rebound or guarding, no CVA tenderness
Extremities: 2+ distal pulses present in all extremities, no cyanosis, clubbing, or edema
Rectal exam:  guaiac negative, normal tone, no masses
Neuro: strength 5/5 bilaterally in all extremities, no sensory or motor deficits, straight leg test positive bilaterally at 60 degrees of hip flexion, reflexes 2+ b/l
Musculoskeletal:  point tenderness over spinous processes of L3, L4, and L5, no soft tissue pain
Laboratory Results
WBC 21, Hb 13.6, Platelets 426, Na 134, K 4.5, Cl 102, CO2 content 23, BUN 28, Cr 1.1
ALT 35, AST 38, Alk Phos 98, Lipase 23, Lactate 0.8
Diagnostic Studies
EKG: 


Acute abdominal Series is unremarkable. No free air. No evidence of obstruction
MRI Lumbar Spine:  as shown…
Interpretation:  Osteomyelitis of L3 and L4 vertebral bodies. Inflammation extends into adjacent structures including the abdominal aorta. Marked dilation of the abdominal aorta at approximately 4 cm in diameter showing inflammatory changes of the vessel wall.
Questions

1.  Which of the following is a modifiable risk factor for developing an abdominal aortic aneurysm?
    1. alcohol abuse
    2. diabetes mellitus
    3. stress
    4. insomnia
    5. tobacco smoking

2.  Which of the following cases requires medical management ONLY?

    1. AAA that has enlarged from 3.0 to 3.7cm over the past 6 months
    2. AAA that has enlarged from 4.7 to 5.0cm in the past 6 months
    3. 55 YOM with newly diagnosed symptomatic 4.5cm infrarenal AAA
    4. 65 YOM with asymptomatic 5.7cm infrarenal AAA
    5. 71 YOM with ruptured 5.0cm AAA exhibiting good mentation and stable vital signs

3.  Which is the most important predictor of AAA rupture?

    1. advanced age
    2. aneurysm diameter
    3. expanding AAA
    4. family history of AAA rupture
    5. female gender
Discussion
Abdominal Aortic Aneurysm (AAA) is a potentially life-threatening condition that is frequently diagnosed incidentally when working up various abdominal complaints, and is often undiagnosed until the time of rupture. It is important for EM physicians to know that elderly  white males are at the highest risk of having an AAA. High risk patients complaining of abdominal or back pain should receive a bedside ultrasound to screen for the possibility of AAA as the cause of their clinical presentation.
Managing patients with an AAA in the emergency department is primarily focused on heart rate and blood pressure control as well as appropriate surgical consultation. Once an AAA is diagnosed (normally with u/s), a CT angiogram should be performed to determine the AAA’s location and potential involvement with other vessels including the SMA, IMA, renal and iliac arteries. Patients with asymptomatic AAAs less than 5.5 cm can be watched and followed by a vascular surgeon. The patient should undergo abdominal ultrasonography every 6 to 12 months to assess the extent of further dilation if the aneurysm is less than 5.5 cm, is completely infrarenal, and only involves the aorta.
A CT angiogram should be performed every 6 to 12 months in patients with SMA, renal and/or iliac artery involvement.
Symptomatic patients may present with vague or sharp abdominal pain, low back pain, and/or the sensation of an abdominal pulsation. Patients with AAA not complaining of pain may present with syncope, nausea, vomiting, or early satiety. Patients with AAA that complain of abdominal tenderness (usually epigastric) are likely to have an expanding or infected AAA. These patients should receive an immediate surgical consultation as rupture can be spontaneous and imminent. Blood pressure control is the goal in these patients. Intravenous beta blockers are the drug of choice for acutely reducing blood pressure and heart rate. Goals of treatment include a heart rate of 55 to 65 bpm and a systolic blood pressure of 100 to 120mmHg or a MAP of 60 to 65 mmHg. If this SBP range is not achieved with a beta blocker alone and the patient has good mentation, nitroprusside can be added at 0.5mcg/kg/min until the blood pressure is controlled.
A ruptured AAA can present similarly to a myocardial infarction with syncope, hypotension, epigastric pain, nausea, vomiting, and diaphoresis. As many as 30% of AAAs are misdiagnosed on presentation, therefore ED physicians should have a high level of suspicion in patients with h/o AAA or that fall into the high risk categories (ie., white males of advanced age, patients with MCTD (spell out), or smokers with PVD). Rapid diagnosis, resuscitation and surgical consultation are required for treating these patients.
Answers to Questions
  1. “(e) tobacco smoking” is the correct answer. There are several risk factors, both unmodifiable and modifiable, for developing an AAA. Smoking is the leading modifiable risk factor. It is hypothesized to increase a patient’s risk by 8-fold over a nonsmoker of similar age and comorbidities. (c) stress and (d) insomnia are not risk factors for the development of an AAA.  (a) alcohol abuse and (b) diabetes mellitus are modifiable risk factors for the development of many other disorders including cardiovascular disease, but have not been linked to an increased incidence of AAA.
  1. “(b) AAA that has enlarged from 4.7 to 5.0cm in the past 6 months” is the correct answer. Many AAAs are medically managed while being monitored by a vascular surgeon. Asymptomatic AAAs that are less than 5.5cm in diameter are managed medically until they become (a) symptomatic (regardless of size), (b) rapidly expanding (>0.5 cm in a 6 month period), (c) larger than 5.5 cm in diameter, or (e) ruptured, at which time surgical intervention is necessary.
  1. “(b) aneurysm diameter” is the correct answer. The three main predictors of AAA rupture are size (aneurysm diameter), (c) rapid expansion (>0.5cm in 6 month period), and (e) female gender (18 vs 12% in males with aneurysms > 5.5cm), but the most important predictor for AAA rupture is aneurysm diameter. (d) Family history of AAA rupture and (a) advanced age are risk factors for AAA development, not rupture.
Clinical Pearls
  • AAA rupture is misdiagnosed in nearly 30% of patients upon presentation. Have a high level of clinical suspicion for the high risk groups!
  • Heart rate (<65 bpm) and systolic blood pressure (100 to 120 mmHg) control are the keys to managing symptomatic / acutely expanding AAAs. Intravenous beta blockers are the drug of choice for HR and BP control.
  • Patients should be counseled on smoking cessation and proper follow-up once an AAA is diagnosed.

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