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

8.23

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:

8.231

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

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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:

8.21

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:

 

8.211

 

 

  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.

Senior Report 8.19

seniorreport

 Case Presentation by Laura Smylie, MD

A 14 year old girl who presents with nausea and vomiting for one day and an abrupt onset of chest pain.
Vitals: BP 100/67, HR 121, RR 25, Temp 36.7, 100% on room air.

1

2

 

Questions:
1. What is the diagnosis based upon the above x-rays?
a) Foreign body
b) Pneumothorax
c)Pneumomediastinum
d)Apical pneumonia

2. What is the likely etiology of the radiographic finding?
a) alveolar rupture secondary to forceful retching
b) esophageal rupture secondary to forceful retching
c) acute PE
d) no abnormality on chest x ray.

3. What is the most appropriate initial management of this patient?
a) place on continuous pulse oximetry, place a left sided chest tube
b) place on continuous pulse oximetry, 4mg ondansetron, NPO.
c) place on a continuous cardiac monitor, start heparin drip, consult cardiology.
d) send blood cultures, start antibiotics, encourage PO intake.

 

Answers and discussion:

1) C
2) A
3) B

1) C – Pneumomediastinum. You can see air tracking in the soft tissues of the neck and the upper aspects of the mediastinum. Although there could potentially be a pneumothorax (B) associated with this this, no pneumothorax can be seen in this study. No foreign body (A) is present and there is no infiltrate to suggest pneumonia (D).

1

 

2) A – Alveolar rupture secondary to forceful retching is the most likely etiology of the pneumomediastinum, although you should also be concerned for possible esophageal rupture secondary to forceful wretching (B) also known as Boerhaave’s esophagus. Review of the literature shows that in similar presentations, esophograms are typically negative for tears in the esophagus. Acute PE (C) has not been shown to present with free air. On a chest xray, the most concerning (and classically pimped) findings for acute PE are Hampton’s Hump and Westermark’s sign. Hampton’s Hump, represented in the first image below, shows a wedge shaped area of hyperdensity along the lung parenchyma periphery, indicative of an infact/PE. Westermark’s sign, as shown in the second image below, shows a focal peripheral hyperlucency secondary to oligemia, with or without dilation of the central pulmonary vessels.

2

 

3) B – Although there is no obvious pneumothorax on the initial chest x ray, you must keep a high level of suspicion for a small pneumothorax. This would not necessitate chest tube placement (A), but a nonrebreather and continuous pulse oximetry are appropriate if a small pneumothorax is present. Given that the retching led to the pneumomediastinum, treat her nausea with ondansetron. She should be kept NPO until an esophagram can be obtained (as an inpatient or in the observation unit) to definitively rule out Boerhaave’s esophagus. As an inpatient, the chest x ray should repeated in 6-8 hours. C is the treatment for a non-massive PE or NSTEMI; D is the treatment for pneumonia, neither of which applies in this case.

3

The percentage of pneumothorax will guide therapy. This picture illustrates that 2 cm pneumo is typically the cut off point for inserting a chest tube with a spontaneous pneumo but not necessarily with a traumatic pneumo.

4

 

References:

Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. Al-Mufarrej F, Badar J, Gharagozloo F, Tempesta B, Strother E and Margolis M. Journal of Cardiothoracic Surgery 2008, 3:59 doi:10.1186/1749-8090-3-59

BMJ Case Rep. 2012 Oct 10;2012. pii: bcr0320091647. doi: 10.1136/bcr.03.2009.1647.

http://radiopaedia.org/articles/westermark-sign

http://usmlepathslides.tumblr.com/post/53392063709/westermarks-sign-cxr-note-the-area-of

Gantner J, Keffeler JE, Derr C. Pulmonary embolism: An abdominal pain masquerader. J Emerg Trauma Shock [serial online] 2013 [cited 2015 Mar 26];6:280-2. Available from: http://www.onlinejets.org/text.asp?2013/6/4/280/120376

Senior Report 8.18

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 Case Discussion by Erin Ge, MD

 

CC: “Nausea”

HPI:

This is an 80 year old female who presents with nausea. She states she has been feeling nauseated and generally unwell for the past week. She denies any significant abdominal pain, vomiting or diarrhea. She has not had any fevers or chills. She reports feeling like she has no energy. She has been refusing to eat. Her family states she has seemed progressively more confused and has been “seeing double”. Today, she started complaining of some episodes of “heart racing” so her family brought her in for evaluation. She denies chest pain or shortness of breath.

ROS:

General: Positive for generalized weakness

Neurological: Positive for confusion

Ear, Nose and Throat: No congestion

Eyes: Positive for diplopia

Cardiovascular: Positive for palpitations

Pulmonary: No shortness of breath

Abdomen: See HPI

Genitourinary: No polyuria

Musculoskeletal: No back pain

Skin: No rashes

 

Past Medical History: Congestive heart failure, hypertension, coronary artery disease

Past Surgical History: Cardiac catheterization, total hysterectomy

Family History: Hypertension

Social History: Lives with her daughter, history of tobacco use but quit over 20 years ago, denies alcohol or illicit drug use

Medications: Aspirin, Lisinopril, Lasix, digoxin, omeprazole

Allergies: NKDA

 

Physical Exam:

General: Overweight, nontoxic

Vitals: Blood pressure 125/92, heart rate 80, respiratory rate 16, temperature 36.8, pulse oximetry 98% on room air

HENT: Normocephalic, atraumatic, mucous membranes moist, trachea midline

Eyes: Sclerae noninjected and nonicteric, pupils 3mm, equal, round and reactive to light, EOMI

Cardiovascular: rate and rhythm regular, normal S1, S2, no murmurs, no JVD, 1+ bilateral lower extremity edema

Respiratory: Clear to auscultation bilaterally with good air entry and equal chest rise

Gastrointestinal: Soft, nontender, non distended, no rebound tenderness, negative Murphy sign, no CVA tenderness

Musculoskeletal: No obvious deformities, extremities nontender, moves all extremities equally

Skin: No erythema, rashes or ulcerations

Neurologic: Alert, oriented x 3, responds slowly, no facial asymmetry, no speech dysarthria, sensation intact to light touch bilateral upper and lower extremities, 5/5 strength bilateral upper and lower extremities

 

EKG:

8.18

 

Laboratory Studies:

CBG – 97

CBC:

5.1           12.0        122

36.0

BMP:

138         97            24            103

6.0           20            2.1

Troponin <0.017

SDS: neg

UDS: neg

Digoxin level: 4.0 ng/mL (nml 0.5-2.0)

 

Questions:

1. In the initial management of an acute digoxin overdose, which of the following should be considered:

A. Gastric lavage

B. Emergent dialysis

C. Activated charcoal

D. High dose insulin

 

2. You are informed by nursing staff that the patient is now tachycardic and a new EKG is obtained:

8.181

What next intervention is indicated?

A. Lidocaine

B. Transvenous pacing

C. Quinidine

D. Procainamide

 

3. What is the appropriate treatment for this patient’s hyperkalemia?

A. Insulin/glucose, sodium bicarbonate, calcium gluconate and kayexalate

B. Fab fragments

C. Emergent dialysis

D. Isotonic fluid hydration

 

Answers:

1. c

2. a

3. b

Digoxin toxicity typically presents with nonspecific symptoms. Generalized weakness, nausea and decreased appetite are often reported.  Visual symptoms are also often seen with the classic being xanthopsia where patients describe yellow halos around lights (think van Gogh’s Starry Night) or other distortions in colors particularly yellow and green. Cardiac dysrhythmias are also typical and the life threatening complications of this overdose.  The patient’s initial EKG should lead the clinician to be suspicious of a dig overdose even prior to receiving the elevated level. The “scooped” appearance of the ST segment or the so called “Salvador Dali” moustache indicates use of digoxin (NOT toxicity).  The multiple PVCs should increase a clinician’s suspicion for toxicity as this is the most common early sign.

1.    The correct answer is C. Activated charcoal.  This can prevent systemic absorption of the drug, although more likely useful in an acute overdose as opposed to a chronic.  Gastric lavage (a.) is contraindicated in this overdose as it can lead to increased vagal stimulation which can produce fatal arrhythmias in this patient.  Emergent dialysis (b.) is also incorrect as digoxin has a wide nonvascular distribution and therefore dialysis does not effectively remove a significant amount of the drug.  High dose insulin is used to treat beta blocker and calcium channel blocker overdoses and does not have a role in digoxin overdose.

2.   A. One the classic (and terrifying looking!) arrhythmias which may be induced by dig toxicity is bidirectional ventricular tachycardia which is demonstrated in the EKG.  The QRS complex axis shifts 180 degrees with each beat (see green arrows).  This is a rare tachyarrhythmia, but classically associated with dig toxicity.  Lidocaine (a.) is the correct answer and has been shown to effectively treat this arrhythmia along with phenytoin. Pacing (b.) or cardioversion should be avoided if possible as they can induce worsening dysrhythmias and if used, low energies are to be used. Both quinidine (c.) and procainamide (d.) are class IA antidysrhythmics and can lead to worsening of the arrhythmia. Quinidine, in particular, has been shown to increase levels of digoxin and therefore worsen toxicity.

3.   B.  The treatment of hyperkalemia in the setting of dig toxicity is treatment of the toxicity itself with administration of digoxin immune Fab (b.). The hyperkalemia itself in this patient would be an indication for use of this, but also the significant dysrhythmia would obviously be another indication. Traditional hyperkalemia treatment (a.) can be used with the exception of calcium.  The “stone heart” theory is the reason calcium in contraindicated in these patients.  Dig toxicity itself causes an elevation of the intracellular calcium concentration and the theory states that further increases in calcium can lead to a “stone heart” or an irreversible noncontractile state.  This is based on case reports and recent studies show evidence that this is likely a false theory, however, the board exam answer is still to avoid calcium in these patients (sorry). Neither emergent dialysis (c.) or IV fluid hydration (d.) are significantly effective in reducing dig levels which is the underlying cause of the hyperkalemia.

As a side note, hyperkalemia is more likely in an acute ingestion (think healthy toddler who got into Grandma’s meds), and less likely in this patient who fits a chronic ingestion picture (known history of taking this medication, potentially induced by decreased renal clearance with an elevated creatinine, although baseline is unknown).

Sources:

Cadogan, Mike, and Nickson Chris. “Life in the FastLane.” Web. http://www.lifeinthefastlane.com

Goldfrank, Lewis R. Goldfrank’s Toxicologic Emergencies. New York: McGraw-Hill Medical Pub. Division, 2002.

“Hippo EM.” Emergency Medicine Board Review, LLSA, & More. Web. <http://www.hippoem.com&gt;

 Mahadevan, Swaminatha V., and Gus M. Garmel. An Introduction to Clinical Emergency Medicine. Cambridge: Cambridge UP, 2005.

Marx, John A., Robert S. Hockberger, Ron M. Walls, James Adams, and Peter Rosen. “Cardiovascular Drugs.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia: Mosby/Elsevier, 2010.

Senior Report 8.15

seniorreport

Case Presentation by Brian Holowecky, MD

CHIEF COMPLAINT  “I have a sore throat and I cannot breathe”

HISTORY OF PRESENT ILLNESS
54-year-old female presents to the emergency department brought by ambulance for sore throat. She states she has had a sore throat since this morning and it has been getting progressively worse. Her throat feels like it is “closing up.” She called the ambulance because she was having increasing difficulty catching her breath. She feels a swelling in her throat which is causing her to be unable to drink or eat anything. She has a history of allergy to lisinopril. She has had angioedema reactions.  She admits to using crack cocaine last night out of a pipe in which she has done many times in the past. No fevers. No upper respiratory symptoms recently. No recent coryza symptoms. On further questioning she states that but used a larger amount of cocaine than usual last night.

REVIEW OF SYSTEMS:  Negative except as in HPI

PAST MEDICAL/SURGICAL HISTORY  History of angioedema, Hypertension, diabetes, asthma, bipolar disorder,
MEDICATIONS:  Albuterol, fluticasone, fluoxetine, clonidine, amlodipine, loratadine, omeprazole.
ALLERGIES:  Lisinopril, anaphylactic.
SOCIAL HISTORY:  Tobacco use, recent crack cocaine use yesterday by a pipe inhalation, heroin abuse. Recently attempted inpatient rehabilitation for drug abuse.

PHYSICAL EXAM
Vitals: BP 166/93 heart rate 58 respirations 16 temp 37.0 saturation 100% on room air.
General: Well nourished patient appearing mildly toxic in respiratory distress. She is hoarse. There is some questionable stridor.

HEENT:  Posterior pharynx is mildly erythematous initially. Mucuous membranes moist. No cobblestoning. Uvula is midline. Mallampati score is 2. Lips are not swollen. No periorbital edema.

Cardiovascular:  S1 S2. RRR. No murmurs. Peripheral pulses equal bilaterally.

Respiratory: Hoarse voice. Stridor. Increased work of breathing. Sitting forward in sniffing position. Breath sounds are equal. No wheeze or crackles. Tolerating secretions initially.

Gastrointestinal:  Soft, NT ND. No rebound, guarding, or rigidity.

MSK/Extremities:  No gross deformities. No joint swelling, erythema. No edema.

Skin:  Warm and dry. No rashes, bruises, or abrasions.

Neurologic:  Alert and Oriented. Follows commands. No facial asymmetry noted. Motor and sensation intact.

Medical Course:  
Initially concerned for anaphylactic reaction in this patient with a known history of anaphylaxis. She was appearing very anxious and beginning not to tolerate her secretions very well. There was slight drooling. I was concerned based on her deterioration for anaphylactic reaction. She began to get more hoarse of voice and to sit forward in the sniffing position. There was questionable stridor.

She received 0.1 mg of epinephrine IM, along with Zantac, 125 mg of Solu-Medrol, 50 mg of IV Benadryl. She did improve somewhat at that time.

The working diagnosis was possible anaphylactic reaction versus anxiety or panic attack. This is a patient with a known psychiatric disorder. She was placed on the cardiac monitors and continuous pulse ox. IV access was established. She began to tolerate her secretions better at that time. Her heart rate remained in the 50s to 60s. Saturation remained 100% on room air.

About 90 minutes into her ER visit, she appears to be worsening and begins tripoding, drooling more profoundly and acting considerably more anxious.  Shas never had any visible airway swelling.

A lateral neck xray is taken:

Epiglottitis.jpg

Questions:  

1) What is the most likely cause for her condition?
A) Anaphylactic reaction from unknown source
B) Thermal pharyngeal Injury
C)Neoplastic transformation of a previously benign lesion
D)That is a normal lateral neck xray. There is no abnormality.

2) What is the treatment for her condition?
A) Urgent intubation in a controlled environment
B) Admission an ICU for close airway monitoring
C) Steroids, antihistamines, and H2 blockers.
D) Antibiotics and ENT consult for drainage.

3) If you suspect anaphylaxis, what is the appropriate initial treatment?
A) 0.3 mg epi subQ, 50mg diphenhydramine, 150 mg ranitidine, steroid
B) 0.3 mg epi IM, 50mg diphenhydramine, 150 mg ranitidine, steroid
C) 0.1 mg epi sub Q, 50mg diphenhydramine, 150 mg ranitidine, steroid
D) 0.1 mg epi IM, 50mg diphenhydramine, 150 mg ranitidine, steroid

Bonus Question 1: Should an epipen be administed into the thigh of the person with the suspected anaphylactic reaction, or into the thumb of the person holding the autoinjector?
A) Thigh
B) Thumb

Bonus Question 2:  Do vaccines cause autism?
A) Yes
B) No

Answers:
1) B
2) A
3) B

Bonus Questions:
4) B
5)B

Discussion:
This patient ended up being found to have crack cocaine induced probable thermal epiglottitis.  It presented atypically, which is how epiglottitis tends to present in adults.  Epiglottitis is a rare finding in the post vaccination world.  Thermal injury is known to cause edema and epiglottitis.  Embers from a pipe or bong may be inhaled and cause thermal burns to epiglottis. In this case no thermal burn was visualized, but patient had clear epiglottitis presumably from cocaine. Imminent airway compromise is possible, if not suspected and treated appropriately.  Crack cocaine is known to cause “crack lung” but crack cocaine epiglottitis has only been reported once before in the early 1990s.

When suspicious for epiglottitis the appropriate course of action is to proceed with intubation with extreme caution.  Laryngeal and epiglottic spasm is very common.  Intubation in the OR with preparation for a surgical airway is desirable.  The diagnosis can be made with lateral neck xray as it was in this case, however another way is by direct visualization with fiberoptic ENT scoping.

Anaphylactic reaction was on the differential and the patient received treatment for anaphylactic reaction, albeit somewhat incorrectly.  Subcutaneous epinephrine has been shown to be less efficacious than intramuscular administration.  In cases of anaphylaxis, the subcutaneous vasculature is constricted and so dissemination of the epinephrine systemically is delayed as compared with intramuscular direct administration.  Remembering dosing and administration is critically important in timely management of anaphylaxis, and epiglottitis too.

Senior Report 8.11

seniorreport

Case Presentation by Alex Weissman, MD

Chief Complaint: “I feel terrible.”

History of Presenting Illness:
The patient is a 32-year-old female presenting with complaint of feeling “terrible and weak.” She states that this has happened to her twice in the last 24 hours. The first episode occurred upon awakening at 3 AM this morning with a sensation of doom, shortness of breath, chest pain, and in a cold sweat with chills. Subsequently she passed out. She ate some corn, felt better, and went back to sleep. Today, prior to arrival, the patient had another episode where she went into a cold sweat with chills and had a sensation of doom with chest pain and shortness of breath; however, this time she did not pass out. She called EMS, who found her capillary blood sugar was 32 mg/dL. The patient denies being sick recently. She denies insulin or sulfonylurea use. She denies abnormal stress in her life. She states that she has been eating normally. Last menstrual period was 3 years ago, the patient has always had irregular menses. The patient denies associated headache, sudden change in vision, abdominal pain, nausea, vomiting, diarrhea, constipation, dysuria, pain or numbness in the extremities, recent illness, or recent travel.

Review of System:
Constitutional: Complains of cold sweats and chills
HEENT: Denies headache
CVS: Complains of substernal chest pain
Lungs: Complains of SOB
Abdomen: Denies abdominal pain
Musculoskeletal: Denies pain in the extremities
Genitourinary: Denies dysuria
Skin: Denies rash
Neurologic: Denies numbness
Psychiatric: Denies depression

 

Past Medical History:
Bronchitis, splenomegaly, anemia, thrombocytopenia

Past Surgical History:
Bone marrow biopsy

Social History:
The patient denies use of tobacco, alcohol, or illicit drugs past or present.

Family Medical History:
Addison’s disease in her mother

Physical Exam:
Vitals: Blood pressure: 100/75, Pulse: 60, Respiratory rate: 18, Pulse Oximetry: Not initially recorded, Temperature: 36.2 degrees Celsius
General: Alert and oriented x3, no acute respiratory distress
Head: normocephalic, atraumatic
Eyes: PERRL, EOMI, bilateral conjunctival pallor, no scleral icterus
ENT: No cervical lymphadenopathy, no pharyngeal edema, mucous membranes moist
Cardiovascular: regular rate and rhythm, no appreciable murmurs, capillary refill <2 seconds
Respiratory: no tachypnea, no retractions, clear to ausculation bilaterally, no appreciable wheezes, rhonchi, or rales
Gastrointestinal: normoactive bowel sounds, nondistended, no tympany to percussion, soft and nontender to palpation
Musculoskeletal: Extremities are atraumatic, dorsalis pedis and radial pulses 2+ and regular bilaterally, no peripheral edema
Skin: no rashes or lesions
Neurological:
MENTAL STATUS: awake, alert, oriented
CRANIAL NERVES: face symmetric, pupils 3mm -> 2mm bilaterally, PERRL, EOMI, visual fields full to confrontation
MOTOR: patient moving all four extremities spontaneously, gait normal
SENSORY: intact to light touch

ECG:
Alex

 

Labs:

Initial CBG – 32 mg/dL

Electrolytes:

132 99 13 9.3 51
5.2 22 0.46 2.1

TSH: 3.586 Micro IU/mL

CBC:

4.7 11.1 109
33.3

Serum pregnancy: negative
Insulin: <0.5 mcUnits/mL
Random cortisol: 2.2 mcg/dL

 

Questions:

1) What are the classic physical exam and laboratory findings in primary adrenal insufficiency (Addison’s Disease)?
a) High blood pressure, high serum potassium, high serum sodium, low random cortisol, low serum glucose
b) Low blood pressure, high serum potassium, low serum sodium, low random cortisol, low serum glucose
c) High blood pressure, high serum potassium, low serum sodium, high random cortisol, high serum glucose
d) Low blood pressure, low serum potassium, low serum sodium, low random cortisol, low serum glucose

2) What laboratory test is used to diagnose adrenal insufficiency, what distinguishes primary versus secondary adrenal insufficiency, and what test value would you expect in primary adrenal insufficiency?
a) ACTH stimulating test; ACTH; low or normal ACTH level
b) Random cortisol; cortisol; low cortisol
c) ACTH stimulating test; ACTH; high ACTH level
d) Random cortisol; ACTH; low or normal ACTH level

3) What are some basic differences in symptomatology between primary and secondary adrenal deficiency?
a) Primary: Hypokalemia, hypernatremia, hypoglycemia, dehydration, hypotension, Cushingoid habitus
Secondary: Hyperkalemia, hyponatremia, normotension, hyperpigmentation, hyperglycemia

b) Primary: Hyperkalemia, hyponatremia, hypoglycemia, dehydration, hypotension, hyperpigmentation,
Secondary: Hypokalemia, hyper/hyponatremia, +/- Cushingoid habitus, hypoglycemia

c) Primary: Hypokalemia, hyponatremia, dehydration, hypotension, +/- Cushingoid habitus, hyperglycemia
Secondary: Hypernatremia, hyperkalemia, hyperpigmentation, normotension
d) Primary: Hyperkalemia, hyponatremia, hyperglycemia, normotension
Secondary: Hypokalemia, hypernatremia, hypoglycemia, hypotension, dehydration, hyperpigmentation, +/- Cushingoid     habitus

 

Bonus Question 1. What is the preferred steroid treatment for adrenal crisis and what vital sign abnormality should raise the ED physician’s clinical suspicion for an adrenal crisis?
a) Hydrocortisone – unexplained hypotension
b) Prednisone – unexplained hypertension
c) Dexamethasone – unexplained hypotension
d) Hydrocortisone – unexplained hypertension

 

Bonus question 2: What is the most common infectious cause of primary adrenal insufficiency in the US?
a) Tuberculosis
b) Meningitis
c) Influenza
d) HIV

Answers & Discussion:

1) Correct answer: B
Primary adrenal insufficiency is characterized by failure of the adrenal gland to produce sufficient steroids including glucocorticoids (namely cortisol), mineralocorticoids (namely aldosterone), and gonadocorticoids (namely estrogen and testosterone). It can be associated with infectious disease states (HIV, tuberculosis, adrenal hemorrhage, sepsis), autoimmunity (polyglandular autoimmune syndrome type I or II), inflammatory diseases (sarcoidosis, hemochromatosis, amyloidosis, lymphoma, etc.), congenital/hereditary causes (congenital adrenal hyperplasia, adrenal hypoplasia, adrenal leukodystrophy, familial glucocorticoid deficiency), or secondary to non-steroid drugs (ketoconazole, mitotane, aminoglutethimide, hemorrhage from warfarin, prolonged IV infusions of etomidate, etc.). It often presents with a shock state due to the body’s inability to produce the stress hormone, cortisol, as well as the lack of aldosterone. Patients typically have low blood pressure, low glucose, low serum sodium, low cortisol levels, and high serum potassium. A random cortisol level less than 3 mcg/dL is diagnostic. The low blood pressure, low serum sodium, and high serum potassium are related to decreased aldosterone levels that are secondary to the adrenal gland failure. Decreased cortisol also leads to decreased blood pressure as well as decreased glucose. Vague GI complaints, salt craving, and postural syncope are common complaints. Another result of adrenal insufficiency is decreased estrogen and testosterone levels.

Secondary adrenal insufficiency occurs when there is failure of the hypothalamus-pituitary-adrenal axis typically at the level of the hypothalamus or pituitary gland, instead of singular failure of the adrenal gland as seen in primary adrenal insufficiency. It is most commonly is due to abrupt withdrawal of long-term high dose steroids. Only cortisol will be low, as opposed to low cortisol and low aldosterone in primary adrenal insufficiency. Other causes of secondary adrenal insufficiency are Sheehan syndrome, head trauma, pituitary disease, infectious diseases affecting the hypothalamus or pituitary (tuberculosis, HIV, meningitis, etc.), or inflammatory diseases affecting the hypothalamus or pituitary (sarcoidosis, cancer, hemochromatosis, etc.).

2) Correct answer: C
Recall that the hypothalamus secretes corticotropin-releasing factor that causes the pituitary to release ACTH, thus resulting in the adrenal gland secreting cortisol. Therefore, the rapid cosyntropin (synthetic ACTH) stimulation test is utilized to diagnose adrenal insufficiency, and the level of plasma ACTH is used to distinguish between primary (a.k.a. adrenal gland failure) and secondary (a.k.a. hypothalamus or pituitary failure) adrenal insufficiency. The cosyntropin test is performed by drawing a baseline cortisol level (18-20 mcg/dL is a normal random cortisol in healthy people), then administering 0.25 mg IV ACTH, and checking plasma cortisol at 30 minutes and 1 hour after administration. In normal people, the plasma cortisol should rise by at least 7 mcg/dL at 30 minutes and peak at >18 mcg/dL at 1 hour.    A high ACTH level is indicative of primary adrenal insufficiency, hence the adrenal glands are not producing sufficient cortisol despite the hypothalamus and pituitary telling them to do so. Since there is no feedback inhibition from circulating cortisol, more and more ACTH is released. A low or normal ACTH level is suggestive of secondary adrenal insufficiency, indicating a problem at the level of the hypothalamus or pituitary gland.

3) Correct answer: B
Primary adrenal insufficiency is characterized by both aldosterone deficiency and cortisol deficiency. Aldosterone deficiency confers hypotension and hyponatremia with hyperkalemia. Cortisol deficiency confers weakness, lethargy, hypotension, hyperpigmentation (due to unopposed ACTH production) and hypoglycemia.

Secondary adrenal insufficiency has intact aldosterone presence, therefore unless the patient is in an adrenal crisis, blood pressure is typically normal. Hypernatremia can result since aldosterone function is intact, unless there is a dilutional hyponatremia secondary to retained water. Hypokalemia results from the unchecked aldosterone effect. There is often hypoglycemia secondary to the lack of ACTH stimulation on cortisol release.

EKG changes can occur secondary to the potassium disturbances: U waves from hypokalemia, or peaked T waves with QT prolongation or even heart block can occur due to hyperkalemia.

Bonus 1: Correct answer: A
High dose steroid administration is the mainstay of therapy for adrenal crisis, regardless of cause or level of dysfunction in the hypothalamic-pituitary-adrenal axis, in addition to supportive care and treatment of the underlying etiology. Hydrocortisone 100 mg IV is the preferred steroid because it has both mineralocorticoid and glucocorticoid effects. If an ACTH stimulating test is going to be ordered, then Dexamethasone 4 mg IV can be used instead because it does not interfere with the test results. Prednisone is not strong enough for a patient with an adrenal crisis. Unexplained hypotension should increase the clinician’s suspicion for an adrenal pathology, especially hypotension refractory to fluids and vasopressors. This occurs secondary to the lack of cortisol. Of course, fluids (dextrose 5% with 0.9% normal saline or hypertonic saline if needed) and vasopressors (norepinephrine, dopamine, or phenylephrine) should absolutely be given in addition to steroids during an adrenal crisis.

Bonus 2 Correct answer: D
HIV (and especially HIV related infections) is the most common cause of primary adrenal insufficiency in the US, but worldwide the most common cause is tuberculosis.

References:

  1. Tintinalli, Judith E, et al. Tintinalli’s Emergency Medicine, 7th Ed. San Francisco: McGraw-Hill, 2011. Print. Chapter 225: Adrenal Insufficiency and Adrenal Crisis, 1453-1456.
  1. Marx, John A, et al. Rosen’s Emergency Medicine, 7th Ed. Philadelphia: Mosby Elsevier, 2010. Print. Chapter 126: Thyroid and Adrenal Disorders, 1671-1675.