Intern Report 5.10

Posted on January 23, 2012 by kjones100

Case Presentation by Dr. Vit Kraushaar

A 38 year old African American female presents to the ED with a chief complaint of shortness of breath.  She began feeling ill 3 days ago with cough, myalgias, severe chills, fever and progressively worsening shortness of breath.  This morning she coughed up some blood streaked sputum, which prompted her to come to the emergency department.  The patient complains that her shortness of breath is associated with sharp, non-radiating midsternal chest tightness that is pleuritic in nature.  She informs you that several of her co-workers are also feeling ill, with one admitted to the ICU yesterday with a diagnosis of pneumonia.  The patient works at a coffee shop that you recall is located across the street from the local university’s newly constructed bioterrorism research lab.

ROS: Positive for fevers, chills, myalgias, nausea, cough/hemoptysis, and shortness of breath.

PMH: Hypertension.  Denies CAD, CHF, COPD, cancer.

PSH: None

Social Hx: Drinks alcohol rarely.  Denies tobacco or illicit drug use.

Medications:  amlodipine

Allergies: Seasonal allergies

Physical Exam:

General appearance:  Patient is ill-appearing, diaphoretic, and only able to speak in half-sentences because of dyspnea.

Vitals: BP 120/55, HR 115 bpm, RR 28, T 38.6, 97% O2 saturation on room air

Eyes: No scleral icterus or conjunctival pallor

HEENT: Mucous membranes are moist, no oropharyngeal swelling, erythema, or tonsillar exudates, no oral thrush

Neck:  Trachea midline. No nuchal rigidity, no jugular venous distension.

Heart: S1 and S2 were heard.  Tachycardic rate and regular rhythm.  No murmurs or gallops.

Lungs: Inspiratory rales and diminished breath sounds auscultated bilaterally.  No wheezing.

Abdomen: Soft, non-tender, no guarding.

Skin: No rashes or bruising noted

Neurologic: Alert and oriented with no motor or sensory deficits.

Labs:

CBC: Hb 15, Hct 46, WBC 11.5, Plt 130

Electrolytes: Na 134, K 3.5, Cl 96, CO2 26, BUN 18, Cr 0.8

Troponin: Negative x 1

Blood and sputum cultures are pending

EKG: Sinus tachycardia, 116 bpm.  PR, QRS, QTc intervals normal.  Normal axis, no LVH.  No ST-T changes.

Imaging:

Chest x-ray (see image below)

Formal read of the CT demonstrates “Mediastinal hemorrhagic lymphadenopathy (white arrowhead), with additional involvement of the paratracheal, subaortic, and azygoesophageal recess nodes. A high-density hemorrhagic pericardial effusion is also present.”

The patient continues to develop worsening respiratory distress and eventually she is intubated in the ED for acute respiratory failure.

As an astute ED physician, you think that there is a connection between this patient’s symptoms and the fact that she works across the street from a bioterrorism research facility, especially considering her reports of several sick coworkers.  Though you are still considering more common diagnoses on your differential, you consider that this patient may have been exposed to a bioterrorism agent.

1)     This patient’s history and clinical presentation is typical of inhalational exposure to which of the following possible bioterrorism agents?

  1. anthrax (Bacillus anthracis)
  2. Q fever (Coxiella burnetii)
  3. ricin toxin (from Ricinus communus)
  4. smallpox (Variola major)
  5. tularemia (rabbit fever) (Francisella tularensis)

2)     You call the hospital laboratory and state that you are concerned that your patient may have been exposed to a biologic weapons agent.  They send a blood sample to a state public health lab.  In the meantime, you request that they perform a peripheral blood smear on one of the blood samples that you sent to their lab.  They call you back in half an hour stating that the sample contained large gram positive bacilli.  Having tentatively confirmed your diagnosis (from question 1), which of the following antibiotics should you initiate?

  1. cefepime
  2. ceftriaxone
  3. ciprofloxacin
  4. gentamicin
  5. trimethoprim/sulfamethoxazole

3)     The patient was accompanied to the ED by one of her coworkers.  You are worried that he may have been exposed to the same bioterrorism agent.  He states that he generally feels fine, but he does have a skin lesion on his arm (see picture below).  The patient states that this lesion is painless.


What is the appropriate treatment?

a)     incision and drainage

b)     observation and follow-up

c)     oral antibiotics

d)     topical antibiotics

e)     topical steroids

 

Answers:

1)     Correct answer: A (Inhalational anthrax)

This case mimics a real life incident where anthrax spores were accidentally vented from a bioweapons facility in the town of Sverdlovsk, in the former Soviet Union in 1979.  This led to 77 cases of inhalational anthrax and many deaths, with many cases occurring in workers from a nearby factory.  The appearance of multiple cases of previously healthy patients who develop a rapidly fulminant pneumonia should raise the suspicion for a bioterrorism incident.  Inhalational anthrax has classically been described as following a two stage course.  In the first stage, symptoms are nonspecific and often flu-like (e.g. fever, dyspnea, cough, headache, vomiting, chills, weakness, abdominal pain, and chest pain).  This first stage can last from hours to days.  The second stage is marked by abrupt onset of high fever, dyspnea, diaphoresis, and shock.  Chest x-ray will show multiple abnormalities, most classically a widened mediastinum, but also including infiltrates and a pleural effusion.  CT Thorax will show enlarged hyperdense mediastinal and hilar lymph nodes.  Cyanosis and hypotension eventually develop, and death follows soon.  This second stage can occur within hours.  Mortality rate is estimated at between 50 – 90% for inhalational anthrax.   (Note: Pneumonic plague caused by Yersinia pestis can present very similarly to this case, with flu like symptoms progressing to respiratory failure, shock, and death within days.  Pneumonic plague, unlike inhalational anthrax, can be transmitted from person to person).   Ricin toxin inhalation would cause symptoms within hours of exposure, leading rapidly from flu like symptoms to respiratory distress and then shock and death.  Inhaled aerosolized F. tularensis, or C. burnetii could both cause initial flu-like symptoms progressing to pneumonia, though the course in both of these diseases would be slower, milder and less likely to be fatal than inhalational anthrax (especially for C. burnetii infection).  Neither ricin, tularemia, nor Q fever are associated with widened mediastinum on chest x-ray.  Variola major infection (Smallpox), starts off with a flu-like prodrome and then produces a characteristic pustular rash and is not consistent with this patient’s clinical picture.

2)     Correct answer: C (ciprofloxacin)

Anthrax is described as a large, gram positive bacilli that can be seen on a blood smear or CSF stain later on in the disease course.  Blood cultures should be drawn prior to antibiotic initiation, and will grow B. anthracis in 6-24 hours.  The recommended initial IV therapy for inhalational anthrax is ciprofloxacin, 400 mg Q12 hours or alternately doxycycline 100mg Q12 hours.   Naturally occurring B. anthracis have shown resistance to extended spectrum cephalosporins as well as TMP/SMX.

3)     Correct answer: C (oral antibiotics)

This picture shows the characteristic painless black eschar of cutaneous anthrax.  There were 11 cases of cutaneous anthrax following the 2001 anthrax mail attacks.  Cutaneous anthrax starts as a pruritic macule or papule, progresses to ulcer and vesicles, and finally leads to a black painless eschar with local edema.  Without treatment, cutaneous anthrax can progress to systemic disease with a mortality rate as high as 20%.  The appropriate treatment is oral ciprofloxacin or doxycycline.  Treatment does not alter the course of the eschar but does prevent the development of systemic disease.

 

 

Take Home Message:

-        ED physicians play an instrumental role in health surveillance in the event of a possible bioterrorism attack

-        Suspect inhalational anthrax in the presentation of multiple cases of a severe acute febrile illness progressing to pneumonia with a fulminant course in previously healthy individuals

-        Chest x-ray will commonly show a widened mediastinum and pleural effusions, and CT will show enlarged mediastinal and hilar lymph nodes

-        Large gram positive bacilli can be identified in blood smears and CSF gram stains, and in blood cultures in 6 – 24 hours

-        The initial IV antibiotics of choice are ciprofloxacin or doxycycline

-        Any case of inhalational anthrax should be regarded as a bioterrorism incident until proven otherwise.  Suspicions of anthrax infection should be reported immediately to local or state public health departments.


Anthrax (Bacillus anthracis)

 

Natural anthrax infections  - Natural cases of B. anthracis infection occur in herbivores that ingest the bacteria from the soil.  Human infection occurs mainly from exposure to infected animals, historically in goat hair mill workers and leather tanners.  No natural cases of inhalational anthrax have been reported in the U.S. since 1976 due to vaccination of livestock.

Anthrax as a weapon – Multiple countries including the U.S., former Soviet Union, and Japan historically investigated the use of anthrax as a biological weapon.  Unintentional release of anthrax from a Soviet bioweapons facility occurred in Sverdlovsk in the former Soviet Union in 1979 leading to many infections and deaths.  The Aum Shinrikyo cult, known better for releasing sarin nerve gas in a Tokyo subway station in the 1990s, attempted to disperse anthrax spores through Tokyo multiple times, but were unsuccessful.  In 2001, anthrax was used as a terror weapon through delivery of spores through U.S. mail to multiple locations, resulting in 22 anthrax cases, 11 cases of inhalational anthrax, and 5 deaths.

 

Pathogenesis

Humans can develop cutaneous, inhalational, and gastrointestinal anthrax.  In inhalational anthrax, spores are inhaled into the alveoli, where they are phagocytosed by macrophages and transported to the mediastinal lymph nodes.  There, the spores hatch into vegetative cells, which release cytotoxic factors leading to cell death, edema, and ultimately mediastinal hemorrhage and bloody pleural effusions.  In cutaneous anthrax, spores gain entry into the skin, often through abrasions or cuts.  The spores hatch and again the vegetative cells release cytotoxins leading to cell necrosis.  Gastrointestinal anthrax is mainly caused by ingestion of undercooked meat contaminated with vegetative B. anthracis, and is not generally associated with bioterrorism.

 

Clinical Manifestations

Inhalational anthrax classically has been described as following a two stage course.  In the first stage, symptoms are nonspecific and include fever, dyspnea, cough, headache, vomiting, chills, weakness, abdominal pain, and chest pain.  This first stage can last from hours to days.  The second stage is marked by abrupt onset of high fever, dyspnea, diaphoresis, and shock.  Mediastinal lymph node enlargement can be so severe that it leads to airway obstruction.  Cyanosis and hypotension eventually develop, and death follows soon.  This second stage can occur within hours.

Cutaneous anthrax starts as a pruritic macule or papule, progresses to ulcer and vesicles, and finally leads to a black painless eschar with local edema.  Without antibiotics, cutaneous anthrax can often lead to systemic disease with a mortality rate as high as 20%.

 

Lab/Microbiology

General lab tests – May show leukocytosis, hemoconcentration, and/or elevated transaminases.

Specific identification –    B. anthracis cells appear as large gram positive bacilli. They can be seen in blood smears and in CSF.  Blood cultures will grow B anthracis in all media in anywhere from 6 to 24 hours.  Suspected anthrax should be confirmed by a local or state public health laboratory.

Imaging

Chest x-ray: Multiple abnormalities are usually present, including mediastinal widening (secondary to mediastinal lymphadenopathy), pulmonary infiltrates, and pleural effusion

CT: Hyperdense hilar and mediastinal lymph nodes, edema, infiltrates, and pleural effusion

 

Treatment

Suspicion or confirmation of inhalational anthrax should lead to immediate notification of the local or state public health department, local or hospital epidemiologist, and local or state public health laboratories. It is important to treat suspected cases of inhalational anthrax even before there is laboratory confirmation.  It is also important to draw cultures before antibiotics are initiated.

The following tables show recommended treatments for inhalational anthrax in a contained casualty situation, as well as the treatment regimen for cutaneous anthrax.

 

Inglesby TV, O’Toole T, Henderson DA, Bartlett JG, Ascher MS, Eitzen E, et al. Anthrax as a biological weapon 2002: updated recommendations for management. Jama. 2002;287:2236–2252.

Inglesby TV, O’Toole T, Henderson DA, Bartlett JG, Ascher MS, Eitzen E, et al. Anthrax as a biological weapon 2002: updated recommendations for management. Jama. 2002;287:2236–2252.

Bibliography:

“CDC | Bioterrorism Agents/Diseases (by Category) | Emergency Preparedness & Response.” CDC Emergency Preparedness & Response Site. Centers for Disease Control and Prevention. Web. 13 Jan. 2012. <http://www.bt.cdc.gov/agent/agentlist-category.asp>.

Cutaneous Anthrax picture was taken from: http://www.freeinfosociety.com/media.php?id=1298

Inglesby TV, O’Toole T, Henderson DA, Bartlett JG, Ascher MS, Eitzen E, et al. Anthrax as a biological weapon 2002: updated recommendations for management. Jama. 2002;287:2236–2252.

Mina B, Dym JP, Kuepper F, Tso R, Arrastia C, et al. Fatal inhalational anthrax with unknown source of exposure in a 61-year old woman in New York City. JAMA. 2002;287:858–862.

 

 

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Case 5.9

Posted on January 16, 2012 by dwseitz

Case Presentation by Dr. Andrew Klutman

CC:  “My chest hurts and the left side of my body is tingling and numb”

HPI: 82 yo female was otherwise normal until 10am this morning when her family stated that she kind of passed out. She did not hit her head as she was sitting on the couch. When she came to she complained of tingling and numbness in her left arm and leg along with rather severe chest pain. She was brought in by EMS and they stated that she was in minor distress and sitting in a chair when they arrived on seen. She also complains of a sharp chest pain she describes as below the sternum that was worse when it first started but is more mild but constant now. She has been eating and drinking without issues, and has been feeling just fine previously. She denies any fevers or chills, nausea/vomiting/diarrhea, cough, or problems urinating. However she does provide that she has feels a little SOB since being picked up by EMS when asked.

ROS: Negative otherwise noted in HPI

PMH: TIA last year, Hypertension, aortic valve replacement in 2007

PSH: Cholecystectomy in 2001

MEDS: Metoprolol

SH: Quit smoking 15 years ago. Denies drinking or elicit drug use. Lives at home with her husband.

EXAM:

Vitals: T- 37.6 oral  HR- 95 BP- 148/68 RESP- 22

GEN: In mild distress. Is alert and oriented and answers questions appropriately

CV:  Regular rate and rhythm, no murmurs noted. Upper ext pulses are 3+ and the lower ext pulses are 2+.

RESP: CTAB

GI: Non tender, non distended, positive bowel sounds

EXT: 5+ strength in both upper and lower extremities.

HENT: Normal cephalic, no facial droop or asymmetry noted.

NEURO: All extremities are intact to soft touch

Labs: Abnormalities: WBC – 12, electrolytes are WNL, INR – 1.6

EKG:

CXR:

QUESTIONS:

What is the most likely diagnosis?
a) Cardiac tamponade
b) PE
c) Stroke
d) Aortic dissection

What subjective finding helps most in delineating MI from the above diagnosis?
a) Tingling/numbness on the left side of the body
b) Substernal chest pain
c) Sudden severe chest pain that was worse upon onset
d) Radiation up into the jaw

Roughly what percentage of patients with this diagnosis are initially confused for MI or something else upon initial presentation?
a) None
b) 100%
c) 72.655 %
d) 38 %

 

 

Discussion & Answers

1)    D

2)    C

3)    D

 

What is the most likely diagnosis?
a) Cardiac tamponade
b) PE
c) Stroke
d) Aortic dissection

Aortic dissection is a great imitator.  There are several physical exam findings is this case that help guide you toward the diagnosis. First, she is hypertensive which is a common finding and also cause of a dissection. The hypertension is related to a combination of the underlying factors that led to the dissection, a resulting catecholamine surge and/or the false lumen compressing and narrowing the true lumen. The narrowing, for all intent and purposes, “stenosis” the true lumen increasing the overall pressure proximal to the involved portion of the aorta. It’s important to note that dissections can also present with hypotension which should make you think tamponade, rupture or MI from involvement of the coronaries if the diagnosis of dissection is being considered. The narrowing also causes the difference in peripheral pulses which makes sense. I like to kind of think of it as being similar to a coarctation where the blood pressure is less distally to the dissection making it less easily palpated in the lower extremities. Next, the wide pulse pressure is likely due to the tear extending into the aortic valve resulting in aortic regurgitation. Remember she previously had a valve replaced? Valve replacement can help precipitate the dissection.  The CXR shows widening of the mediastinum. An estimated 62 percent of patients with a dissection have a widened mediastinum. However, nearly 12% are read as normal.

As far as the subjective findings, the patient “passed out.” 5% of patients with aortic dissection will experience a syncopal episode. She also states that she is short of breath which can be a result of the dissection compressing a main stem bronchus. Other symptoms to look for include dysphagia from the esophagus being compressed, flank pain from renal artery involvement in the dissection, and of course stomach pain from a descending dissection occluding a mesentery vessel.

 

What subjective finding helps most in delineating MI from the above diagnosis?
a) Tingling/numbness on the left side of the body
b) Substernal chest pain
c) Sudden severe chest pain that was worse upon onset
d) Radiation up into the jaw

Dissection can look like an MI. The classical substernal ripping/tearing sensation that radiates to the back is not always the case. In fact, 10% of patients with dissection present with no pain at all, while others present with more mild symptoms that look like musculosketal pain. As far as MI vs dissection, they both can cause substernal chest pain (aortic root) and both can even radiate into the neck or jaw (aortic arch). In addition to all this, dissections into the cardiac vessels can an STEMI with elevated troponins.  So, the fact that the pain is more severe at onset is a clue that the patient is likely dissecting. This subjective finding was highlighted by several sources as being a focal finding during initial presentation that should clue us in that dissection needs to be considered.

 

Roughly what percentage of patients with this diagnosis is initially confused for MI or something else upon initial presentation?
a) None
b) 100%
c) 72.655 %
d) 38%

 

MI and musculoskeletal pain are not the only contributors to the confusion. In fact, 38% dissections are missed upon initial presentation. 20% of dissections have neurological manifestations which can make you think stroke. Patients can present with hemiparesis, hemianesthesia or weakness. If the cervical ganglion is affect, dissection patients can present with Horner’s syndrome. If that was not enough, peripheral nerve ischemia may manifest with numbness and tingling, pain, or weakness in the extremities. The bottom-line is to keep dissection in your differential when working up chest pain as it has a very high morbidity and mortality and has a high probability of being initially missed.

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Senior Case Report 5.8

Posted on January 14, 2012 by dwseitz

Case Presentation by Dr. Katie Dobratz

CC: “I fell”

HPI: Patient is a 49 yo male who states he fell off a ladder about 3 feet. He believes he landed on his left side, mostly on the left elbow and left side of his body and back.  He states that his head hit last and he did not sustain any loss of consciousness and has no acute headache.  He is complaining of acute pain in the left elbow.  He states he looked at his back and noticed a swelling and is having pain there as well. He drove himself here to the hospital and currently is standing at the side of the bed complaining of pain in the left lower back, left elbow, and left flank pain.  The pain in the back has not radiated.  It stays on the left side near the swelling and is described as a sharp pinching movement that is deep inside.  He states movement makes it worse.  Nothing makes it better.  Rates it an 8/10.

ROS:

CONSTITUTIONAL:  No fevers, chills or weakness.

EYES:  No visual changes.

ENT:  No facial trauma.

CARDIOVASCULAR:  Some left-sided upper back, chest pain.

RESPIRATORY:  Some pain with deep breaths on the left.  No shortness of breath.

GI:  No abdominal pain.

GENITOURINARY:  No hematuria.  Positive left flank pain.

SKIN:  Positive laceration over the left elbow.

MUSCULOSKELETAL:  Left lower lumbar pain, left rib pain.  Left elbow pain.

NEUROLOGIC:  No loss of consciousness, numbness, tingling or weakness.

PAST MEDICAL HISTORY:  None.

PAST SURGICAL HISTORY:  Vasectomy

MEDICATIONS:  NONE

ALLERGIES:  None.

SOCIAL HISTORY:  Denies alcohol, tobacco, and illicit drug abuse.  The patient works as a UPS driver and deliveryman.

PHYSICAL EXAM:

VITAL SIGNS:  On arrival 161/89 with pulse 64, respirations 16, temperature 36.6 and pulse oximetry is 98% on room air, which is within normal limits.

GENERAL:  This is a 49-year-old, well-nourished, well-developed, well-hydrated male standing at the side of an ER cart in mild to moderate distress.

PSYCHIATRIC:  Awake, alert, and cooperative, with normal memory, mood and judgment.

HEAD:  Normocephalic, atraumatic.

EYES:  Reveal no conjunctiva injection.  No scleral icterus.

ENT:  His oropharynx is clear with moist mucous membranes.

NECK:  Trachea is midline, no tenderness in the cervical spine to palpation

CARDIOVASCULAR:  Heart has a regular rate and rhythm.  There is no S3, S4.

RESPIRATORY:  Normal respiratory effort. He has equal and clear breath sounds bilaterally.  No rales, rhonchi or wheezes.  No obvious splinting.     GI:  His abdomen is soft, nontender.  There is no rebound, rigidity or guarding.

SKIN:  Warm and dry. There is a laceration and abrasion over the left elbow.  There is a contusion over L1.  No other obvious sites of bruising or injury.  No further abrasions or lacerations.

MUSCULOSKELETAL:  He has some tenderness over the superior SI joint on the left and over the paraspinal musculature of the lumbar area.  He has contusion and swelling over L1 but no acute tenderness to palpation in this area.  He has some tenderness over the left posterior ribs profusely.  There is no point tenderness.  Extends from the midaxillary to the midscapular line.  He has no tenderness over the C-spine or T-spine.  Examination of the right upper extremity, left lower and right lower extremity shows no gross abnormalities or tenderness to palpation.  The pelvis is nontender.  The left upper extremity reveals a 2-cm laceration over the elbow.  However, he has full range of motion of the elbow.  No acute bony tenderness to palpation is noted up and down the left upper extremity.

Neruologically: A&O x 3, GCS of 15, no facial droop, normal speech, ambulates with a steady gait and has symmetrical strength upper and lower extremities

XRAY:

QUESTIONS:

1) What abnormality is seen in the radiologic study seen above?

2) Based on the radiologic study, what laboratory study must be ordered to rule out an important associated injury?

a) electrolytes

b) CPK

c) lactate

d) U/A

3) What other imaging study can be of use in further diagnosing this injury or associated injuries

a) Intravenous pyleogram

b) Angiography

c) Ultrasound

d) Computed tomogram

————————————————————

Answers and Discussion:

1)   Transverse process fracture of the lumbar spine

2)   Urinalysis

3)   Computed Tomography

1)   Transverse Process fractures put the patient at risk for ureteral injuries.  Ureteral injuries due to external trauma are rare. It composes less than 1% of all genitourinary injuries caused by external trauma.   The ureter is well protected by the bony pelvis, psoas muscle and vertebrae.  If the ureter is damaged, it is generally due to a significant trauma with associated injuries to other abdominal organs.  The presentation and management is generally dictated by the severity of associated injuries.  Penetrating trauma is more likely the cause of ureteral injury than blunt trauma accounting for 91%.  Ureteral injuries associated with blunt trauma generally occur at the pelviureter junction.  With blunt trauma the mechanism of injury is generally hyperextension with overstretching or compression of the ureter against the transverse process of the lumbar spine.  These injuries generally result from high speed MVCs, a fall from a significant height, or a direct blow to L2-L3 region   In this case, the transverse processes were actually fractured off the vertebral body, increasing the risk of penetrating ureteral injury.  Penetrating ureteral injuries generally occur in the upper portion greater than the distal portion, although this is generally due to penetrating trauma from a projectile or stab wound.  Ureteral injuries can range from a simple contusion to partial tear to full transection.

2)   In patients with external trauma a high level of suspicion must be maintained.  The diagnostic laboratory test of choice to assess for ureteral injury is a urinalysis.  This is to assess for microscopic hematuria or gross hematuria.  There is controversy related to the evaluation of ureteral injuries, by means of urinalysis.  Hematuria is found in 74% of cases (either gross or microscopic.) Failure to see hematuria may be due to complete transection of the ureter or partial transection of an adynamic segment. There have been studies that show absent hematuria in patients with penetrating trauma, but operatively found to have disruption of the ureter (Brandes et al.)  This has made the evaluation of ureteral trauma with urinalysis not completely reliable.

3)   CT is the most reliable means to diagnosis an ureteral injury in blunt trauma with a stable patient.  If the clinician has a high index of suspicion for ureteral injury, a CT scan should be performed with images in the excretory phase to visualize the opacified collecting system and ureters.  This means having delayed imaging of at least 10-15 minutes after contrast injection in order to see urine extravasation. The integrity of the ureter can be determined whether iodinated urine is present in the ureter below the level of the injury.  If it is this may be indicative of a partial disruption or contusion.  This type of injury, particularly a partial tear, may be repaired by ureteral stenting versus a laparotomy.  Intravenous pyleograms maybe considered if a patient is unstable and unable to be taken to the CT scanner.  IVP’s can be done in the operating room, but there have been documented cases where IVP has failed to diagnosis a ureteral injury, making this an unreliable test as well.  Findings that suggest an injury include delayed renal function or excretion, ureteral dilatation or deviation, extravasation of contrast or non-visualization of the ureter.

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Case 5.7

Posted on December 19, 2011 by kjones100

Case Presentation by Dr. Tim Scott

CC: Fatigue

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

ROS:  Positive for fatigue

PMH: Denies

PSH: Denies

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

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

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

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

CV: RRR, S1 S2

Lungs: CTAB

Abd: Soft, NT/ND, BS +

Extr: normal pulses, strength and ROM

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

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

Lytes: WNL

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

You order a CXR because he has an elevated white count

Questions:

1) What is the likely Diagnosis in this patient?

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

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

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

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

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

 

Answers:

  1. A.  This patient likely has Hodgkins Lymphoma.  HL arises from germinal center or post-germinal center B cells and has a unique cellular composition, containing a minority of neoplastic cells (Reed-Sternberg cells and their variants) in an inflammatory background and can cause anemia and elevated white counts. HL has a bimodal age distribution curve. In the US and other economically advantaged countries, there is one peak in young adults (approximately age 20 years) and one in older age (approximately age 65 years); the majority of patients are young adults and there is a slight male predominance.  AML and ALL are close second options here due to similar early presentations, however, with AML, the median age at diagnosis is 65 years old and with ALL the vast majority of cases present between 2-5 years of age.  Bleeding disorders are more likely to be present and the cause of an initial presentation with these patients.

 

  1. D.  The incidence of HL is increased in a number of settings associated with immunodeficiency and infection. Among patients infected with HIV, the relative risk of HL is increased in various studies from fivefold to 25-fold. There also appears to be an increased risk of HL in patients with a history of infectious mononucleosis caused by Epstein Barr virus.  Interestingly, other childhood infectious illnesses including chickenpox, measles, mumps, rubella, and pertussis are negatively associated with the risk of HL.

 

  1. C.  A, B and D are all true.  Though a mediastinal mass discovered on routine chest x ray is a common presentation in an HL patient, it is NOT common to have any symptoms associated with it. The mass may be fairly large without producing local symptoms. Less commonly, the mass produces nonspecific symptoms such as retrosternal chest pain, cough, or shortness of breath. Small pericardial or pleural effusions are rare except in patients with bulky mediastinal disease. Superior vena caval obstruction is also rare.  Painless lymphadenopathy is present in as much as 80% of patients with HL.  Fever, weight loss and night sweats (the classic B symptoms), though not specific to HL, are present in less than 20 percent of patients with stage I/II Hodgkin lymphoma and up to 50 percent of patients with advanced disease.  Pruritus and fatigue, though not specific, can be early symptoms of the disease.  Pruritus specifically may be an important early symptom, preceding the diagnosis of HL by months or even a year or more. Pruritus occurs early in approximately 10 to 15 percent of patients, but the great majority of patients experience pruritus at some time during the course of illness. It is usually generalized and occasionally severe enough to cause intense scratching and excoriations.

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Case 5.6

Posted on December 12, 2011 by kjones100

Case Presentation by Dr. Erin Murphy

CC: Snakebite

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

ROS:

Constitutional: no fever, +malaise.

Head:  no headache

Eyes: no blurry vision

Ears: no earache or tinnitus

Nose: no discharge

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

Cardiovascular: no palpitations

Respiratory: no breathing difficulty

GI: no abdominal pain, + nausea, no vomiting

Musculoskeletal: + left lower extremity pain & swelling

Skin: + puncture marks on left foot

Neurological: + slight perioral numbness/tingling

PMHx: None

PSHx: None

Allergies: None

Meds: children’s multivitamins

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

 

Physical Exam:

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

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

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

Neck: no swelling

Cardiovascular: regular rhythm, S1/S2, no murmurs

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

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

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

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

http://en.wikipedia.org/wiki/File:Snake_Bite_injury.jpg

http://www.flickr.com/photos/25268283@N06/3150819625#/photos/michiganherper/3150819625/

QUESTIONS:

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

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

(b) immobilization of the affected limb

(c) immersion of the affected extremity in ice water

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

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

(a) septic shock

(b) neuromuscular blockade

(c) increased capillary membrane permeability

(d) cell death secondary to apoptosis

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

(a) 1-3 vials

(b)  4-6 vials

(c) 7-10 vials

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

BONUS QUESTION:

Michigan’s only venomous snake is:

(a) Eastern massasauga rattlesnake (Sistrurus catenatus)

(b) Cottonmouth water moccasin (Agkistrodon piscivorus)

(c) Timber rattlesnake (Crotalus horridus)

(d) Eastern diamondback rattlesnake (Crotalus adamanteus)

 

 

Answers:

1. B

2. C

3. B

4. A

 

Pit Vipers

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

 

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

 

Clinical Presentation of Pit Viper Bites

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

 

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

 

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

 

Treatment

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

 

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

 

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

 

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

 

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

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Case 5.5

Posted on December 5, 2011 by kjones100

Case Presentation by Dr. Megan Dougherty

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

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

PMH: none

PSH: none

Allergies: no known drug allergies

Family History: no history of hypertension or diabetes

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

Physical Exam

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

HEENT: NC/AT. EYES: Sclera clear.

CVS: RRR.  Good S1, S2.  NO S3 or S4.

Respiratory: Clear to auscultation bilaterally. No wheezes

Abdomen: Soft, non tender, non distended.

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

Labs:

WBC: 16.8, Hgb: 14.1, Platelets: 275

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

Radiology:

Questions:

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


    ANSWERS:
    1. d
    2. c
    3. f

    DISCUSSION:

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

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

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

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

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

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

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

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

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

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

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

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

    References:

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

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

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Case 5.4

Posted on November 28, 2011 by kjones100

                                  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.
ROS:

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
PMHx:  HTN

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

.

.
Questions: 

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

Answers:

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.

 

 

Management: 

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.

 

References:

Rosen’s Emergency Medicine:  Pelvic Trauma.  Ch 52


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Case 5.3

Posted on November 21, 2011 by kjones100

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.

FH:  DM, HTN

INITIAL EXAMINATION:

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

ED COURSE and STUDIES:

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:

.

Questions:

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

http://www.youtube.com/watch?v=Xxdedx1HtHo

A good ACEP resource for Ultrasound Pneumothorax:  http://www.acep.org/Content.aspx?id=43362

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.

TREATMENT STRATEGIES:

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.

STEPS:

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.

TROUBLE SHOOT YOUR CHEST TUBES:

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.

PEARLS OF WISDOM:

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.

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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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