Senior Report 8.23

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Case Presentation by Aditee Jodhani, MD

 

History of Present Illness:

A 45 year old female presents to the ED with shortness of breath worsening for the past 2 weeks. She states for the last several days she has also been experiencing fatigue, subjective fever, and chills. The patient denies any productive cough, hemoptysis or chest pain. She does have a history of HIV and intermittently follows up with a physician for treatment. She denies any current or past tobacco use. The patient has been living at a homeless shelter for the past 2-3 months and doesn’t know if she’s had contact with sick individuals.

 

Physical Exam:

Vital Signs:

BP 112/76, HR 102, RR 22, T 37.7, pulse ox 91% on RA

General: mildly uncomfortable, sitting upright

HEENT: no pharyngeal erythema, no palpable cervical lymphadenopathy

Cardiovascular: RRR, normal S1 and S2, no murmurs

Respiratory: Clear breath sounds bilaterally, mildly tachypneic speaking in short sentences, no wheezing or rales

GI: abdomen soft, nontender, +BS

Neurological: Alert and oriented x3, moving all four extremities spontaneously.

 

A chest xray and ABG was obtained. ABG: pH 7.46, C02 28, p02 68

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Questions:

1. Based on the information given above what is the most likely cause for the patient’s presentation?

A. bacterial pneumonia

B. COPD exacerbation

C. Pneumocystis jiroveci pneumonia

D. Pneumothorax

 

2. What is the most appropriate treatment for this patient?

A. Nebulized beta agonists with oral steroids

B. Ceftriaxone and doxycycline

C. Trimethoprim-sulfa

D. Trimethoprim-sulfa and corticosteroids

 

3. The patient states she has an allergy Bactrim, what other medications can be used to treat the patient’s condition?

A. Dapsone and trimethoprim

B. Clindamycin and primaquine

C. Lower dose Bactrim 10mg/kg daily

D. Caspofungin aerosolized pentamidine

 

Answers:

1. C
2. D
3. B

 

Explanation:

1. The best answer is C, Pneumocystis jiroveci pneumonia. The patient is immunocompromised with unknown CD4 count and should be treated as Pneumocystis jiroveci pneumonia until further workup (bronchoscopy) can prove otherwise. The chest xray represents early Pneumocystis jiroveci pneumonia, which can look normal instead of the classical diffuse bilateral infiltrates seen in image 1:

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Based on the patient’s symptoms, vital signs and ABG, treatment should not be postponed. Pneumocystis jiroveci pneumonia is an opportunistic infection seen mostly in immunocompromised patients. HIV patients not on antiretroviral treatment have a 75-90% risk of developing Pneumocystis jiroveci pneumonia, mostly when CD4 counts fall below 200. Patients begin prophylaxis either when CD4 counts fall below 200 or when an AIDS defining illness like oral-pharyngeal candidiasis occurs.

The patient has a normal respiratory physical exam, no significant history of tobacco use or risk factors such as trauma to indicate pneumothorax or COPD as a possible diagnosis. Although bacterial pneumonia is a possibility the patient’s personal medical history and mild hypoxia are concerning and more consistent with Pneumocystis jiroveci pneumonia. Increased morbidity and mortality due to infection require emergent treatment until the diagnosis can be confirmed. Mortality rates ranged between 20-40% but have since gone down to 10-20% with appropriate treatment survival rates are as high as 60-90%.

 

2. The answer is D. The ABG results show the patient requires treatment with antibiotics and steroids. Although Pneumocystis jiroveciis classified as both protozoan and fungal first line treatment is trimethoprim-sulfa. Dosage is 15-20mg/kg daily.

Steroid treatment has been shown to decrease alveolar exudates and inflammation, reduce intubation by 50% and proven beneficial in HIV patients with Pneumocystis jiroveci pneumonia. Use of steroids has not been proven effective in immunocompromised patients with Pneumocystis jiroveci pneumonia. Steroid therapy is initiated when 1 of 2 criteria are met with a high suspicion of Pneumocystis jiroveci pneumonia. 1.) Arterial pO2 < 70 mmHg or 2.) A-a gradient >35mmHg on room air. Some studies indicate that steroid therapy should be started within 72 hours of antibiotic therapy. Steroids help decrease the toxins responsible for worsening pulmonary inflammation after antibiotic therapy is initiated. However for severe disease starting steroid therapy after 72 hours has not shown a clear benefit in many studies.

 

3. The correct answer is B. The patient has moderate to severe disease which can be treated with clindamycin and primaquine. IV pentamidine can also be used for severe disease however is considered less effective and more toxic. Mild to moderate disease can be treated with dapsone and trimethoprim for patients requiring alternate therapy, however this patient is characterized as having severe disease.

Severe disease is characterized by use of steroids in conjunction with antibiotics. Aerosolized pentamidine is considered an ineffective treatment associated with frequent relapses and is not used as a second line agent for Pneumocystis jiroveci pneumonia. Lower dose Bactrim at 10mg/kg has shown efficacy, Thomas et al, and is associated with fewer side effects however at this time is not currently recommended by the CDC or for patients with intolerance to bactrim.

 

References:

Thomas M, Rupali P, Woodhouse A, Ellis-Pegler R. Good outcome with trimethoprim 10 mg/kg/day-sulfamethoxazole 50 mg/kg/day for Pneumocystis jirovecii pneumonia in HIV infected patients. Scand J Infect Dis. Aug 17 2009;1-7. [Medline].

[Guideline] Siberry GK, Abzug MJ, Nachman S, Brady MT, Dominguez KL, Handelsman E, et al. Guidelines for the prevention and treatment of opportunistic infections in HIV-exposed and HIV-infected children: recommendations from the National Institutes of Health, Centers for Disease Control and Prevention, the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics. Pediatr Infect Dis J. Nov 2013;32 Suppl 2:i-KK4.

Spach, David MD. OIs: Treatment: A 40 year old with fever and Respiratory Symptoms. HIV web study. http://www.hivwebstudy.org/cases/ois-treatment/40-year-old-fever-and-respiratory-symptoms. March 2015.

Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP; Chief Editor: Michael Stuart Bronze, MD. Pneumocystis jiroveci Pneumonia Overview of Pneumocystis jiroveci Pneumonia. Medscape. http://emedicine.medscape.com/article/225976-overview#aw2aab6c17. Sept 2014.

Constance A. Benson, M.D., Jonathan E. Kaplan M.D., Henry Masur, M.D. Treating Opportunistic Infections Among HIV-Infected Adults and Adolescents. Recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association/Infectious Diseases Society of America. MMWR. December 17, 2004 / 53(RR15);1-112.

Cindy Meng Hou, DO, MBA and Sindy Paul, MD, MPH, FACPM. PREVENTING AND TREATING PCP AND MAC: A CONTINUING CHALLENGE IN HIV/AIDS CARE (11HC08). Rutgers, Center for continuing outreach and education. http://ccoe.rbhs.rutgers.edu/online/ARCHIVE/11HC08/article2.htm. 2015.

Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents. http://www.aidsinfo.nih.gov. 2015

Senior Report 8.22

seniorreport

Case Discussion by Eric Malone, MD

Visual Stimulus Case:

A 26 year old male with a past medical history of schizophrenia presents after jumping out of a second story window in a possible suicide attempt. He was brought to the emergency department on petition and was originally taken to the crisis center, where, in addition to intramuscular haloperidol and lorazepam, he also received a foot X-ray, which is provided below.

He has no other injuries and complains only of right foot pain. Examination shows deformity of the dorsal aspect of the right foot with tenderness and soft tissue edema over the midfoot. Range of motion in the right ankle is intact, as are peripheral pulses and neurologic function.

8.2228.22

 

Questions:

  1. Based on the above X-ray, which of the following is the most appropriate course of management:

A. Order more haloperidol and lorazepam because the patient is clearly malingering and there is nothing wrong with his foot.

B. Posterior mold right leg splint (with stirrups), non-weight bearing on the right leg, crutches, adequate analgesia and rapid orthopedic outpatient follow up (following completion of psychiatric evaluation)

C. Pain control, preoperative laboratory studies, and emergency department orthopedic consultation

D. Post-op shoe, pain control, PRN orthopedic or podiatric follow up.

 

  1. In addition to the findings that you identified on the above x-ray, which of the following other injuries is also likely present:

A. Occult talar dome fracture

B. Disruption of the ligamentous structure of the midfoot at the tarsometatarsal joint

C. Disruption of the vascular supply of the fifth metatarsal head

D. Calcaneal tendon rupture

 

  1. Failure to diagnose and appropriately manage this injury pattern is most commonly associated with which of the following:

A. Midfoot instability and collapse, severe arthritis

B. Avascular necrosis of the fifth metatarsal head

C. Atrophic degeneration of musculature of the dorsal foot including extensor digitorum brevis

D. Fracture non-union

 

Answers:

  1. C
  2. B
  3. A

Discussion:

The radiographs demonstrate a fracture through the base of the second metatarsal. In addition, there is widening of the joint space between the base of the first and second metatarsals and inferolateral subluxation of the first and second metatarsals relative to their respective cuneiforms. As with seemingly all orthopedic injuries, this pattern has an eponymous description. This injury pattern is known as a Lisfranc injury.

Lisfranc injuries refer more generally to a pattern of injury that involves disruption of the Lisfranc joint. As shown below, the Lisfranc joint is described anatomically as the articulation between the bases of the metatarsals and cuneiform bones.

This joint extends across the midfoot. Any disruption with or without fracture can be described as a Lisfranc injury. Notably, not all such injuries involve obvious metatarsal fractures; some are subtle and involve only ligamentous injury. Note that in the normal anatomical relationships of the midfoot, the proximal metatarsal articulates with the tarsal bones such that the borders of each are aligned, as shown below. The medial border of the second metatarsal aligns with the medial border of the middle cuneiform on the AP view. Presence of an avulsion fragment within the joint space between the first and second metatarsals is known as a Fleck sign (because you can never have enough eponymous ortho descriptors).

Mechanistically, Lisfranc injuries occur as a result of either direct (i.e. blunt) or indirect trauma. With an indirect traumatic injury, the Lisfranc joint undergoes excessive pronation or supination in an already plantar flexed foot, resulting in ligamentous injury. Examination will show midfoot tenderness, soft tissue swelling, potential ecchymosis, and difficulty or inability to bear weight. Plantar ecchymosis is an exam finding specific for Lisfranc injury.

Radiographic evaluation for Lisfranc injuries should focus on the relationships of the midfoot structures described above. In reviewing the x-rays in this case, note the abnormal relationship of the base of the second metatarsal to the cuneiform (red), the widening of the space between the first and second metatarsals (yellow), and the Fleck sign (blue).

Some Lisfranc injuries can be subtle. If history and exam is suggestive of more severe injury than demonstrated by x-ray, weight bearing radiographs or CT should be considered. Failure to diagnose and obtain appropriate early fixation is associated with increased complication rates.

All suspected Lisfranc injuries warrant ermegency department orthopedic consultation, and most will undergo operative fixation and extensive casting as an outpatient. Even when appropriately diagnosed and managed, there is a high degree of post-operative complications, primarily residual pain.

References:

Ross G,Cronin R,Hauzenblas J,Juliano P. Plantar ecchymosis sign: a clinical aid to diagnosis of occult Lisfranc tarsometatarsal injuries. J Orthop Trauma 1996;10(2):119–22.

Rosen’s Emergency Medicine: Concepts And Clinical Practice. Marx J, Hockberger R, Walls RM, Adams J, Rosen P. Philadelphia. Mosby

M.J. Welck et al. / Injury, Int. J. Care Injured 46 (2015) 536–541

Hatem SF. Imaging of Lisfranc injury and midfoot sprain. Radiol Clin North Am 2008;46(6):1045–60.

DeOrio M, Erickson M, Usuelli FG, Easley M. Lisfranc injuries in sport. Foot Ankle Clin 2009;14(2):169–86.vier, 2010

Senior Report 8.21

seniorreport

Case Presentation by Dr. Sean Michael, MD

Visual Stimulus Case:

A 59-year-old man with COPD presents with acute dyspnea. His breath sounds are nearly inaudible. He is tripoding with accessory muscle use and suprasternal retractions. Temperature is 37.7°C, heart rate 112, respiratory rate 36, blood pressure 168/92, and oxygen saturation 89% on 2 liters via nasal cannula. Glucocorticoids and nebulized bronchodilators are administered. Bedside thoracic ultrasound is performed and demonstrates the following M-mode image in the right second intercostal space:

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Questions: 

  1. The most likely etiology of the ultrasonographic finding above is:

A. Emphysematous bulla or apical bleb

B. Iatrogenic pneumothorax

C. Lobar pneumonia

D. Primary spontaneous pneumothorax

 

Additional images are obtained of the right chest at the level of the fifth intercostal space:

 

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  1. Given the new information obtained in this image, which of the following is the best course of action:

A. CT Thorax

B. Intravenous antibiotics

C. Non-invasive positive pressure ventilation

D. Tube thoracostomy

 

  1. The findings in the second ultrasound image serve mostly to:

A. Increase diagnostic sensitivity (ie. have a high negative predictive value)

B. Increase diagnostic specificity (ie. have a high positive predictive value)

C. Predict a decreased risk of mortality

D. Predict an increased risk of treatment failure

 

Answers and explanation:

1. A
2. D
3. B

(Note: This explanation assumes that you understand the basics of lung ultrasound. If you need a refresher, there are lots of great online resources.)

This patient presented with an apparent moderate to severe COPD exacerbation with hypoxia and poor air exchange on lung auscultation. Bedside lung ultrasound (image 1) demonstrates absence of pleural sliding on M-mode. In the setting of COPD (or many other critical illness states), the absence of lung sliding may be caused by any number of pathophysiologic conditions. While the absence of lung sliding is quite sensitive for pneumothorax of any etiology, in comparison to patients with traumatic pneumothorax, patients with non-traumatic dyspnea may have numerous other causes of poor lung sliding, which may increase the false-positive rate for ultrasound exams (Slater 2006, Lichtenstein 2008).

In this clinical presentation, the most likely reason for the absence of lung sliding is an emphysematous bulla/apical bleb (question 1, answer A). Bullae are common in COPD, especially in advanced disease, and a ruptured apical bleb is a common cause of secondary spontaneous pneumothorax (Noppen 2008). While iatrogenic pneumothorax (question 1, answer B) is a known complication of a number of procedures, this patient did not undergo any high-risk interventions, such as transthoracic needle aspiration, central venous access, thoracentesis, transbronchial or pleural biopsy, or positive pressure ventilation (Sassoon 1992). Lobar pneumonia (question 1, answer C) on ultrasound is characterized mostly by an A-B profile or by the absence of lung sliding with a B profile (Lichtenstein 2008). Primary spontaneous pneumothorax (question 1, answer D) typically occurs in young male smokers with thin body habitus and (by definition) is not secondary to underlying pulmonary disease, such as COPD, cystic fibrosis, or malignancy (Noppen 2008).

The second ultrasound image shows a lung point, which is much more specific for pneumothorax (Lichtenstein 2008). Given the patient’s dyspnea, hypoxia, and the size of the pneumothorax (from at least the second through the fifth intercostal spaces, but more likely from the apex through the fifth), the correct intervention is tube thoracostomy (question 2, answer D). This can be accomplished with either a small bore surgical chest tube or via percutaneous small-bore catheter (aka “a pigtail”) (Contou 2012, Tsai 2006). There is already enough clinical information to diagnose pneumothorax, and CT Thorax (question 2, answer A) is not required. Intravenous antibiotics (question 2, answer B) might be indicated in suspected bacterial pneumonia, but the second ultrasound image is not diagnostic of pneumonia. Non-invasive positive pressure ventilation (question 2, answer C) may be required for this patient, which is an even more compelling reason to perform thoracostomy. The ultrasound does not predict need for NIPPV, however.

As mentioned previously, lung point dramatically increases specificity (question 3, answer B) for pneumothorax (Lichtenstein 2008 and lots of other papers—this isn’t a comprehensive review). The most sensitive (question 3, answer A) finding is absence of lung sliding (or perhaps absence of sliding with augmented color power Doppler) (Cunningham 2002, Lichtenstein 2008, etc). Lung ultrasound has not yet been shown to predict either treatment failure (question 3, answer C) or mortality (question 3, answer D) in the setting of secondary spontaneous pneumothorax.

In this case, a small-bore chest tube was placed, the patient placed on bi-level NIPPV, and he did well.

References:

Contou D, Razazi K, Katsahian S, et al. Small-bore catheter versus chest tube drainage for pneumothorax. American Journal of Emergency Medicine. 2012;30(8):1407–1413. doi:10.1016/j.ajem.2011.10.014.
Cunningham J, Kirkpatrick AW, Nicolaou S, et al. Enhanced recognition of “lung sliding” with power color Doppler imaging in the diagnosis of pneumothorax. J Trauma. 2002;52(4):769–771.
Lichtenstein DA. Relevance of Lung Ultrasound in the Diagnosis of Acute Respiratory Failure*. Chest. 2008;134(1):117. doi:10.1378/chest.07-2800.
Noppen M, De Keukeleire T. Pneumothorax. Respiration. 2008;76(2):121–127. doi:10.1159/000135932.
Sassoon CS, Light RW, OHara VS, Moritz TE. Iatrogenic pneumothorax: etiology and morbidity. Respiration. 1992;4:215–20.
Slater A, Goodwin M, Anderson KE, Gleeson FV. COPD can mimic the appearance of pneumothorax on thoracic ultrasound. Chest. 2006;129(3):545–550. doi:10.1378/chest.129.3.545.
Tsai W-K, Chen W, Lee J-C, et al. Pigtail catheters vs large-bore chest tubes for management of secondary spontaneous pneumothoraces in adults. The American journal of emergency medicine. 2006;24(7):795–800. doi:10.1016/j.ajem.2006.04.006.
Ultrasound for Detection of Pneumothorax. Rebel EM (http://rebelem.com/ultrasound-detection-pneumothorax). Accessed 3/20/2015.