Modern Resident - The newsletter of AAEM/RSA
December 2015/
January 2016
Volume 8: Issue 2 | Facebook  Twitter  LinkedIn

Inside This Issue


Acute Cholangitis
Danielle Goodrich, MD
Stanford/Kaiser Emergency Medicine

A 50-year-old male with a history of a common bile duct stone presented to the emergency department (ED) with three days of epigastric pain, nausea and vomiting. On arrival to the ED, he was febrile to 39.7°C and tachycardic to 117. On exam, he appeared jaundiced with tenderness and guarding in his right upper quadrant. His laboratory studies revealed an elevated alkaline phosphatase to 326, an elevated total bilirubin of 9.2 and an elevated white blood cell count to 17. He underwent an ultrasound that showed a massively dilated common bile duct (2.5cm) with a stone. He previously had a failed ERCP and therefore the decision was made to undergo placement of a percutaneous drain by interventional radiology. He was admitted for IV antibiotics. Biliary cultures grew Serratia Marcescens, E.Coli and Klebsiella.

Acute cholangitis is an ascending bacterial infection resulting from biliary obstruction. The normal barrier mechanisms of the bowels are disrupted and bacteria translocate and spread retrograde from the portal system or duodenum. The most common cause of biliary obstruction is an obstructing gallbladder stone followed by malignancy and stenosis.2 Clinically the patient presents with fever, abdominal pain and jaundice; the constellation of symptoms is known as Charcot’s triad. The triad of symptoms is only seen in 50-75% of patients.2 Hypotension and mental status changes combined with Charcot’s signs constitutes Reynauld’s pentad and suggests a significant morbidity and mortality.2

In choledocholithiasis, more than 90% of patients will have elevations in serum alkaline phosphatase and GGT levels.1 Obstruction of the common bile duct will lead to an elevation of total and conjugated bilirubin. E.Coli, Klebsiella, Streptococcus, Clostridium and Bacteroides are common organisms inciting the infection.1 Ultrasound has a low sensitivity but high specificity for the detection of bile duct stones.1 Greater than 6mm of dilation of common bile duct on ultrasound suggests the presence of a calculus. A CT scan may be useful to demonstrate biliary dilation. Treatment includes antibiotics and biliary drainage. Endoscopic sphincterotomy with stone extraction and/or stent insertion is the treatment of choice for biliary drainage. Common bile duct stones can be removed successfully in most patients with sphincterotomy. If ERCP is not feasible, percutaneous transhepatic cholangiography or open surgical decompression is necessary.

Practice Questions:

1. Which lab abnormality is most commonly seen in patients with acute cholangitis?
A. Elevated indirect bilirubin
B. Elevated alkaline phosphatase
C. Elevated AST
D. Elevated INR

2. Which of the following are common risk factors for cholangitis?
A. Biliary stent placement
B. Recent ERCP or cholangiogram
C. Gallstones
D. All of the above.

3. What is the gold standard for diagnosis of common bile duct stone?
A. Ultrasound
B. CT scan of the abdomen
C. Cholescintigraphy (HIDA scan)
D. Magnetic Resonance Cholangiopancreatography (MRCP)

Answers:
1. B
2. D
3. D

References:

  1. Adams J. Biliary tract disorders. Emergency Medicine: Clinical Essentials. Philadelphia, PA: Elsevier/Saunders, 2013. 361-69. Print
  2. Afdhal NH. Acute Cholangitis. In: Uptodate, Post TW, Uptodate, Waltham, MA. (Accessed on August 15, 2015.)


 

TXA Literature Review
Alexandra Murray, DO PGY1
Mercy St. Vincent Medical Center Emergency Medicine

What is tranexamic acid (TXA)?
When the body experiences vascular injury, the hemostatic system tries to maintain circulation by balancing the formation and degradation of blood clots. In response to severe blood loss, this balance is challenged and hyper-fibrinolysis can occur. The conversion of plasminogen to plasmin plays a large role in fibrin binding and degradation. Tranexamic acid is a synthetic derivative of lysine that reversibly blocks binding sites on plasminogen and inhibits fibrinolysis.1 TXA has been approved by the FDA since 1986 as an antifibrinolytic and has been marketed for menorrhagia (Lysteda) and dental hemorrhage in hemophiliacs (Cyklokapron).2,3 More recently, TXA has been investigated as a treatment for posttraumatic hemorrhage, postpartum hemorrhage and prevention of surgical blood loss.

CRASH-2 Trial (2010)
The CRASH-2 (Clinical Randomization of an Antifibrinolytic in Significant Haemorrhage-2) Trial was published in the Lancet in 2010. This double-blinded, randomized, placebo-controlled trial examined 20,211 adult trauma patients in 274 hospitals in 40 countries.4 The study was designed to assess effects of early administration of TXA (within eight hours of injury) on death, vascular occlusive events and the receipt of blood transfusion in trauma patients. The results showed that all-cause mortality was significantly reduced with TXA (RR 0.91, p=0.0035).4 The risk of death due to bleeding on Day Zero was also significantly reduced (RR 0.80, p=0.003) with the greatest benefit of TXA administration being within the first hour of injury (RR 0.68, p=0.0001).4 There was concern that TXA would increase the formation of pathologic blood clots; however, there was no apparent increase in fatal or nonfatal vascular occlusive events between treatment and control groups. Based on the results, the number needed to treat with TXA was 67 patients.4

MATTERs Study (2012)
The MATTERs (Military Application of Tranexamic Acid in Trauma Emergency Resuscitation) Study was published in Archives of Surgery in 2012 as a retrospective observational cohort study that examined 896 military combat injuries.5 The study was designed to characterize contemporary use of TXA in combat injury and to assess the effect of its administration on total blood product use, thromboembolic complications and mortality.5 There was a significant reduction in 48 hour (ARR 7.6%, p=0.004) and in-hospital (ARR 6.5%, p=0.004) all-cause mortality with TXA administration, but not 24 hour all-cause mortality (ARR 2.8%, p=0.20).5 The benefit of TXA was greatest in those patients who received massive transfusion of >10 units PRBC per 24 hours (<24h: ARR 5.2%, p=0.17; <48h: ARR 13.1%, p=0.003; In-hospital: ARR 13.7%, p=0.004).5 The number of venous thrombotic events in the study was too small to assess any independent risk of TXA for vascular occlusive events. Based on the results, the number needed to treat with TXA was seven patients.5

Cochrane Review: Antifibrinolytic Drugs for Acute Traumatic Injury (2015)
In 2015, the Cochrane Collaboration published a review of randomized controlled trials of antifibrinolytic agents (aprotinin, TXA, epsilon-aminocaproic acid and aminomethyl-benzoic acid) to assess the effect of antifibrinolytic drugs in patients with acute traumatic injury.6 Three trials were included; however, 99% of the data was contributed by the CRASH-2 trial. Two trials (n=20,451) assessed the effect of TXA (CRASH-2 2010, Yutthakasemsunt 2013) and one trial (n=77) assessed aprotinin (McMichan 1982). The pooled data show that antifibrinolytic drugs reduce the risk of death from any cause by 10% (RR 0.90, p=0.002). There is no evidence that antifibrinolytics have an effect on the risk of vascular occlusive events, need for surgical intervention or receipt of blood transfusion.6 The authors recommend that TXA should be given as early as possible and within three hours of injury for trauma patients with bleeding. They give no recommendations concerning the effect of TXA in patients with isolated traumatic brain injury; however, there are two ongoing trials that should help guide future management.6

References:

  1. Okamoto S, et al. Enzyme-controlling medicines: Introduction. Semin Thromb Hemost. 1997;23(6):493-501.
  2. Wilton JM. Tranexamic acid: A new option for heavy menstrual bleeding. Nurs Womens Health. 2012 Apr-May;16(2):146-50.
  3. Nuvvula S, Gaddam KR, and Kamatham R. Efficacy of tranexamic acid mouthwash as an alternative for factor replacement in gingival bleeding during dental scaling in cases of hemophilia: A randomized clinical trial. Contemp Clin Dent. 2014 Jan;5(1):49-53.
  4. CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): A randomized, placebo-controlled trial. Lancet. 2010 Jul 3;376(9734):23-32.
  5. Morrison JJ1, Dubose JJ, Rasmussen TE, and Midwinter MJ. Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study. Arch Surg. 2012 Feb;147(2):113-9.
  6. Ker K, Roberts I, Shakur H, and Coats TJ. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev. 2015 May 9;5:CD004896.


Journal Club: Steroids for Everything?
Linda Sanders, MD PGY3
Temple University Hospital

Back Pain
A randomized controlled trial (RCT) in which 269 patients with lumbar radiculopathy on MRI and low back pain were given a 15-day course of prednisone versus placebo demonstrated an improved disability score at three weeks after receiving steroids.3 By comparison, a RCT of 67 patients presenting to the ED with musculoskeletal pain from a twisting or bending injury not thought to be radicular in nature demonstrated no benefit in pain or disability with prednisone at one week.2 Thus, steroids may benefit patients with lumbar radiculopathy but have no demonstrated benefit in those with musculoskeletal back pain.

Pharyngitis
A Cochrane review of eight RCTs comparing steroids to placebo demonstrated that patients given oral or intramuscular steroids for pharyngitis were three times more likely to have resolution of pain within 24 hours with a number needed to treat of 3.7.4 Most trials used a single dose of dexamethasone and all eight studies gave both groups antibiotics. Thus there is no data demonstrating the benefit of steroids without antibiotics.

Meningitis
In an attempt to identify a subgroup of patients with bacterial meningitis that benefit from steroids, van de Beek, et al. performed a meta-analysis of 2,029 patients from five RCTs comparing the use of dexamethasone versus placebo for bacterial menigitis.6 Patients of all ages were included and received dexamethasone for two to four days. There was no significant reduction in mortality but there was some reduction in hearing loss among survivors. This study had surprisingly negative results compared to two prior meta-analyses from 2004 and 2011, which demonstrated a mortality benefit and hearing loss reduction.7,8 A large multinational RCT is still needed to answer this question.

Pneumonia
The inflammatory response in pneumonia may account for worsening pulmonary dysfunction leading to ARDS and treatment failure. A previous Cochrane review investigated the use of steroids for pneumonia, demonstrating a mortality benefit. However, this study had a small sample size and used studies of low quality.1 In an expansion of this review, Siemieniuk, et al. published a meta-analysis of 13 RCTs comparing the use of steroids versus placebo for hospitalized adults with community acquired pneumonia.5 This study demonstrated a mortality benefit for those patients with severe pneumonia and a reduction in the cases of mechanical ventilation and ARDS in cases of less severe pneumonia. It is unclear which patients with pneumonia would derive the most benefit from steroids.

References:

  1. Chen Y, Li K, Pu H and Wu T. Corticosteroids for pneumonia. Cochrane Database Syst Rev 2011: CD007720.
  2. Eskin B, Shih RD, Fiesseler FW, Walsh BW, Allegra JR, Silverman ME, Cochrane DG, Stuhlmiller DF, Hung OL, Troncoso A and Calello DP. Prednisone for emergency department low back pain: A randomized controlled trial. J Emerg Med 2014 Jul; 47(1): 65-70.
  3. Goldberg H, Firtch W, Tyburski M, Pressman A, Ackerson L, Hamilton L, Smith W, Carver R, Maratukulam A, Won LA, Carragee E and Avins AL. Oral steroids for acute radiculopathy due to a herniated lumbar disk: a randomized clinical trial. JAMA 2015 May 19; 313(19):1915-23.
  4. Hayward G, Thmopson MJ, Perera R, Glasziou PP, Del Mar CB and Heneghan CJ. Corticosteroids as standalone or add-on treatment for sore throat. Cochrane Database Syst Rev 2012 Oct 17;(10): CD008268.
  5. Siemieniuk RA, Meade MO, Alonso-Coello P, Briel M, Evaniew N, Prasad M, Alexander PE, Fei Y, Vandvik PO, Loeb M and Guyatt GH. Corticosteroid therapy for patients hospitalized with community-acquired pneumonia: A systematic review and meta-analysis. Ann Intern Med 2015 Oct 6;163(7)519-28.
  6. van de Beek D. Farrar JJ, de Gans J, Mai NT, Molyneux EM, Peltola H, Peto TE, Roine I, Scarborough M, Schultsz C, Thwaites GE, Tuan PQ and Zwinderman AH. Adjunctive dexamethasone in bacterial meningitis: A meta-analysis of individual patient data. Lancet Neurol 2010 Mar;9(3):254-63.
  7. van de Beek D, de Gans J, McIntyre P and Prasad K. Steroids in adults with acute bacterial meningitis: a systematic review. Lancet Infect Dis 2004; 4: 139-43.
  8. van de Beek D, de Gans J, McIntyre P and Prasad K. Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev 2007; 1: CD004405.


SCUBA and Diving Injuries, Part 1
Daniel F. Leiva, MS OMSIV
Nova Southeastern University

SCUBA, an acronym for self-contained underwater breathing apparatus, is a system for recreational diving practiced by hundreds of thousands of people across the world, but is not without its risks. In 2012, the incidence of SCUBA-related injuries ranged from seven to 35 per 10,000 divers and from five to 152 injuries per 100,000 dives. Insufficient training and preexisting medical conditions were common factors that played a role in injury, and drowning was the most common cause of death.1 While risks of trauma, hypothermia and submersion injury also exist, those more specific to diving including barotrauma, decompression sickness and nitrogen narcosis will be discussed in this piece and the next.

Boyle’s law describes the relationship between pressure and volume of a system: as pressure increases (for example: descent), the volume of gas decreases. The opposite occurs during ascent. An example of this mechanism is the discomfort felt by divers and swimmers within their ears when descending and ascending in water. During descent, the increase in external water pressure causes a decrease in middle ear volume, a space enclosed by the tympanic membrane and the Eustachian tube. This causes pain in the form of middle ear squeeze or otic barotrauma, and is why divers and swimmers must frequently perform maneuvers to open their Eustachian tube. This is done by yawning, swallowing, jaw thrusting, head tilting and performing the Valsalva maneuver. For people who have trouble achieving equilibrium, advanced techniques employing a combination of moves may be necessary. Without equalization divers run the risk of tympanic membrane rupture or inner ear barotrauma leading to a perilymph fistula, which requires a referral to an otolaryngologist.

Other air spaces can also experience painful disequilibrium. The air space created inside of a diver’s mask can lead to face squeeze, which is remedied simply by exhaling through the nose. Trapped air within a tooth secondary to decay, a filling or an abscess can lead to tooth squeeze (barodontalgia) with either an increase or decrease in external pressure. If the external ear is occluded with cerumen, the area between this plug and the tympanic membrane can become squeezed. This is called external ear squeeze, which can also lead to pain and tympanic membrane rupture. Finally, if any of the openings to the sinuses are occluded or become occluded while diving, sinus barotrauma can occur. This can lead to hemorrhage or paresthesia in the distribution of the infraorbital nerve. Thus, it is recommended not to dive if taking decongestants due to the risk of occlusion as the medication begins to wear off.

The majority of injuries caused by barotrauma of descent, excluding inner ear trauma, heal spontaneously. Decongestants, as mentioned previously, and antihistamines may help promote opening of the occluded airspaces. If there is concern for contamination after tympanic membrane rupture, antibiotics can be considered.

References:

  1. Buzzacott PL. The epidemiology of injury in scuba diving. Medicine and Sport Science (2012): 57-79. Web. 15 Sept. 2015.
  2. Tintinalli JE and Stapczynski JS. Chapter 208 Dysbarism and complications of diving. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 2011. 1410-413. Print.
  3. Chandy D and Weinhouse Gl. Complications of SCUBA diving. UpToDate, 10 Nov. 2014. Web. http://www.uptodate.com/contents/complications-of-scuba-diving. Accessed 07 Sept 2015.


Board Review: Neutropenic Fever
Phillip Fry, OMSIV
Midwestern University - Arizona College of Osteopathic Medicine

Neutropenic fever is a hematological emergency associated with significant morbidity and mortality. The latest guidelines suggest neutropenia be defined as an absolute neutrophil count (ANC) of <500 cells/microL or an ANC expected to decrease to <500 cells/microL during the next 48 hours. Fever criteria is a single measurement >38.3°C or a temperature of >38.0 C sustained over a one hour period.1 This commonly develops in oncologic patients receiving cytotoxic antineoplastic therapy, which affects myelopoiesis and decreases the body’s ability to combat infection. These cytotoxic agents also disrupt the developmental integrity of the gastrointestinal mucosa, putting these patients at risk for invasive infection due to the organism’s greater ability to translocate across intestinal mucosa.

When evaluating these patients, a thorough history is needed to determine comorbid conditions and to assess if there is a noninfectious cause of fever, such as a blood transfusion or the underlying malignancy. The multinational association for supportive care in cancer (MASCC) score can be utilized to help differentiate which patients require inpatient versus outpatient treatment.2 A thorough physical exam is also required, evaluating specifically sites that are most likely to be infected. Due to neutrophils being absent in these patients, signs of inflammation may be extremely subtle. These individuals are more likely to have catheter sites, biopsy and bone marrow aspirate sites that are also possible sources of infection. The examination should also include inspection of the perianal area. Erythema, pain on palpation and tender hemorrhoids are important signs of infection. However, digital rectal examination and rectal temperatures must be avoided so that one does not seed infection by traumatizing the fragile mucosa.

Treatment should be started as soon as possible, as early studies documented mortality rates of up to 70 percent if initiation of antibiotics was delayed.3 Broad-spectrum antibiotics should be given as soon as possible (within 60 minutes of triage) and at full doses, adjusted for renal and/or hepatic function with the aim of treating the most likely and most virulent organism the patient is susceptible to. Patients who remain febrile after the initiation of empiric antibiotics should be re-evaluated for possible infectious sources, and there is a current recommendation of adding antifungal agents to the treatment regimen if the patient is high risk with prolonged fever greater than four days.1

References:

  1. Freifeld AG, Bow EJ, Sepkowitz KA, Boeckh MJ, Ito JI, Mullen CA, Raad II, Rolston KV, Young JA and Wingard JR. Infectious Diseases Society of America. Clinical Infectious Disease. 2011;52(4):e56
  2. Klastersky J and Paesmans M. The Multinational Association for supportive care in cancer (MASCC) risk index score: 10 years of use for identifying low-risk febrile neutropenic cancer patients. Support Care Cancer. 2013 May;21(5):1487-95. Epub 2013 Feb 27.
  3. Schimpff S, Satterlee W, Young VM and Serpick A. Empiric therapy with carbenicillin and gentamicin for febrile patient with cancer and granulocytopenia. N Engl J Med. 1971;284(19):1061


Tox Talks: Lithium Toxicity
Kaitlin Fries, DO PGY1
Doctors Hospital

Lithium is often a first line treatment for bipolar disorder and major depressive disorder, and is commonly present on many emergency department patients’ medication lists. Studies have shown that as many as 75-90% of patients taking lithium long-term develop toxicity at some point throughout their treatment.5 This is primarily due to the fact that lithium has a very narrow therapeutic index. In 2008, the American Association of Poison Control Centers received over 6,000 reports of potential lithium toxicities and four reported deaths.5 While lithium toxicity is not as commonly seen as some other toxidromes in the emergency department, it is still very relevant to daily practice.

Lithium carbonate is a monovalent cation whose mechanism of action is not well understood.4 It is thought to modify intracellular second messenger systems as well as affect neurotransmitters.2,5 Lithium is absorbed rapidly and will reach peak serum concentrations as quickly as two to four hours after ingestion.2 It is cleared exclusively by the kidneys with a half-life around 20 hours.2

There are three classes of lithium toxicity: acute, acute on chronic, and chronic, all of which differ in their presentations.

  • Acute toxicity is seen in patients who are often not on long-term lithium treatment. These patients will present with gastrointestinal symptoms, typically nausea, vomiting and diarrhea.1,3 Lithium levels will be extremely elevated, but will not correlate with the degree of their symptoms. Even without intervention, as lithium equilibrates throughout the tissues, the serum level will fall, thus only exposing the body to elevated serum levels for a short time.
     
  • Acute on chronic toxicity occurs in those who are on chronic lithium treatment and consume additional amounts of the drug. These individuals will also have markedly elevated lithium levels. However, since they have been on lithium long-term, less tissue reabsorption can occur, thus serum levels will remain elevated without intervention. These patients will present with varying degrees of neurological symptoms.
  • Chronic toxicity is seen in individuals on lithium therapy whose renal function decreases. These patients will present with neurologic symptoms such as a fine tremor and can progress to fasciculations, dysarthria, nystagmus, ataxia, hyperreflexia, clonus, agitation, lethargy, seizures and even coma.1,3

Studies have shown that the serum lithium level does not accurately correlate with the severity of toxicity. In 2007, Waring, et al. reviewed five years of lithium toxicities reported to the Scottish Poison Information Bureau, and concluded that regardless of the serum level, acute on chronic and chronic toxicities are the most severe due to the body’s inability to quickly redistribute the drug into the tissues.3 In addition to a serum lithium level, diagnostic testing should include renal function tests, electrolytes, calcium and magnesium levels, complete blood count and studies looking for additional co-ingestants.

Since there is no specific antidote for lithium, management focuses on reducing the amount of time the body is exposed to toxic levels. Activated charcoal does not bind lithium and is therefore only useful if co-ingestants are suspected. Whole bowel irrigation is shown to have some efficacy if done promptly, however it is only useful if the patient ingested sustained release capsules.1 Fluid resuscitation should be the initial main focus, to correct any underlying renal failure or dehydration while maximizing urinary excretion of the drug.1-3 It is important to closely monitor sodium levels, as hypernatremia can lead to worsening neurologic symptoms. Diuretics are not recommended.1 The most effective detoxification method is hemodialysis as lithium is extremely dialyzable. Guidelines of when to initiate dialysis in these patients have not been universally standardized, but dialysis is commonly initiated with lithium levels greater than 4mmol/l.1,2 Patients with levels greater than 2.5mmol/l and renal insufficiency, severe neurologic symptoms or contraindications to aggressive fluid rehydration (heart failure) should also undergo emergent dialysis.2 It is important to realize these patients may require multiple hemodialysis treatments as lithium can cause a rebound effect as it continues to slowly be released from the central nervous system and tissues.1,2

References:

  1. Betten D. Lithium. In Toxicology Handbook. American Academy of Emergency Physicians Resident & Student Association.
  2. Haussmann R, Bauer M, Bonin S, Grof P and Lewitzka U. (2015). Treatment of lithium intoxication: Facing the need for evidence. Int J Bipolar Disord International Journal of Bipolar Disorders.
  3. Mattu A. (2011). Acute lithium toxicity is more dangerous in individuals already taking lithium than in those who are lithium naive. In Avoiding common errors in the emergency department (pp. 743-744). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health.
  4. Rotella J. (2012, April 18). Acute lithium toxicity cased-based Q&A. Retrieved November 16, 2015, from http://lifeinthefastlane.com/toxicology-conundrum-048/
  5. Tintinalli J. (2011). Lithium. In Tintinalli's emergency medicine: A comprehensive study guide (7th ed., pp. 1211-1213). New York: McGraw-Hill.


Chest X-Ray Findings in Pulmonary Embolism
Jorge Luis Aceves, MSIII; Sachin Allahabadi, MSIII; Veronica Tucci, MD JD
Baylor College of Medicine

A 61-year-old male with a prior pulmonary embolism not currently on anticoagulation presents with two weeks of progressive right-sided chest pain, worse with deep inspiration, and non-productive cough. The patient denies hemoptysis, fever, chills, nausea, vomiting, diaphoresis or abdominal pain. The patient reports he has not had lower extremity edema, swelling or pain. He works as a taxi driver and is seated throughout the day.

He is afebrile, with a heart rate of 59, blood pressure 141/97, respiratory rate of 20 breaths per minute and he is saturating 100% on room air. His physical exam is unremarkable. The below chest X-ray is obtained.

Click to enlarge.

What is the name of the finding shown on this chest X-ray? Is it a sensitive or specific sign for pulmonary embolism?
The focal wedge-shaped density on the periphery of the lung is classically called the “Hampton Hump,” named after Dr. Otis Hampton who described his findings in a 1940 publication. It is most commonly seen in patients experiencing a pulmonary embolism (PE). The wedge opacity forms as a result of hemorrhaging from bronchial arteries, which attempt to compensate for occluded distal branches of the pulmonary artery.

Various studies including the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) Study, which analyzed over 400 chest radiographs of patients diagnosed with PE, have highlighted a low sensitivity of classic radiograph findings, such as the Hampton Hump. The Hampton Hump was calculated to have a sensitivity of only 22% for detecting pulmonary embolism. The Westermark sign, another classic X-ray sign of PE caused by vessel collapse distal to the embolus, similarly had a sensitivity of 22%. Thus neither sign is an accurate tool to specifically include or exclude PE as a diagnosis.5

Patients presenting similarly to the one in this case should be approached with a broad differential diagnosis. Other causes of chest pain, such as acute coronary syndrome, pneumonia, pneumothorax or cholecystitis should be considered. Therefore, the chest radiograph is still recommended to rule out other dangerous causes of chest pain, especially in patients with low probability of PE. Decision rules including the Pulmonary Embolism Rule-Out Criteria, Geneva Score and Wells Criteria may be used to determine whether additional laboratory testing such as a D-Dimer or additional radiographic studies such as lower extremity Doppler ultrasounds or pulmonary angiography is indicated.6-12 Despite the existence of several validated decision-making rules, one retrospective analysis concluded that clinical gestalt was superior in ascertaining the presence or absence of PE because of the selection of patients with low and high clinical probability.13 CT Pulmonary Angiography (CTPA) is commonly the definitive diagnostic imaging of choice, due to its high sensitivity and specificity. If necessary, physicians can also use the contrast-enhanced pulmonary angiography or ventilation/perfusion scans in conjunction with clinical assessment and pretest probability.14

References:

  1. Hampton AO and Castleman B. Correlation of postmortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction. Am. J. Roentgenol 43.305 (1940): 1040.
  2. Karwinski B and Svendsen E. Comparison of clinical and postmortem diagnosis of pulmonary embolism. Journal of clinical pathology 42.2 (1989): 135-139.
  3. Tsao MS, Schraufnagel D and Wang NS. Pathogenesis of pulmonary infarction. The American Journal of Medicine 72.4 (1982): 599-606.
  4. Frazier AA, et al. From the rchives of the AFIP: Pulmonary Vasculature: Hypertension and Infarction 1 (CME available in print version and on RSNA Link). Radiographics 20.2 (2000): 491-524.
  5. Worsley D F, et al. Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study. Radiology 189.1 (1993): 133-136.
  6. Kline JA, et al. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2004; 2: 1247–55.
  7. Kline JA, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 2008; 6: 772–80.
  8. Le Gal G, Righini M, Roy PM, Sanchez O, Aujesky D, Bounameaux H and Perrier A. Prediction of pulmonary embolism in the emergency department: The revised Geneva score. Ann Intern Med. 2006 Feb 7;144(3):165-71.
  9. Ceriani E, Combescure C, Le Gal G, Nendaz M, Perneger T, Bounameaux H, Perrier A and Righini M. Clinical prediction rules for pulmonary embolism: A systematic review and meta-analysis. J Thromb Haemost. 2010 May;8(5):957-70.
  10. Klok FA, Kruisman E, Spaan J, Nijkeuter M, Righini M, Aujesky D, Roy PM, Perrier A, Le Gal G and Huisman MV. Comparison of the revised Geneva score with the Wells rule for assessing clinical probability of pulmonary embolism. J Thromb Haemost. 2008 Jan;6(1):40-4.
  11. Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D, Forgie M, Kovacs G, Ward J and Kovacs MJ. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001 Jul 17;135(2):98-107.
  12. Wolf SJ, McCubbin TR, Feldhaus KM, Faragher JP and Adcock DM. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary embolism. Ann Emerg Med. 2004 Nov;44(5):503-10.
  13. Penaloza A, Verschuren F, Meyer G, Quentin-Georget S, Soulie C, Thys F and Roy PM. Comparison of the unstructured clinician gestalt, the wells score, and the revised Geneva score to estimate pretest probability for suspected pulmonary embolism. Ann Emerg Med. 2013 Aug;62(2):117-124.
  14. Thompson T. Clinical Presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism. Up to Date. Version 48.0. Accessed via the web at uptodate.com on November 1, 2015.


International Corner Featured Case: Dengue Fever
Aaron Tyagi, MD
EW Sparrow Hospital - Michigan State University

Case Description:
A 25-year-old Asian female presented to the ED with several days of fever, severe retro-orbital headache and myalgias. She also reported nausea and vomiting with joint pain bilaterally in her knees. She became alarmed and came to the ED when the symptoms did not resolve after a few days. The patient stated that she has had frequent mosquito exposure, sustaining a large number of bites to her arms and legs on a recent hike. She denied any past medical or surgical history. She was not on any medications and denied any sick contacts. Physical exam revealed a febrile female in moderate distress who was warm to the touch. No rash or petechia were appreciated. Serologic testing confirmed the diagnosis of dengue fever. The patient was treated with paracetamol and fluids and discharged with instructions for bed rest, paracetamol and to maintain fluid intake.

Discussion:
Dengue fever, also known as “breakbone fever,” is an arboviral illness transmitted by the mosquito vectors Aedes aegypti and albopictus. It exists in four serotypes: 1-4. It is one of the most common arboviral diseases and is endemic to Dominica and the Caribbean, as well as Central and South America, parts of Africa and Asia. As many as 2.5 million people (approximately 40% of the world’s population) live in areas that have a high risk of dengue transmission. The WHO estimates 50-100 million cases occur worldwide each year, with roughly 22,000 deaths, predominantly in children under the age of 15.

Recognizing the signs and symptoms of dengue is important in making the diagnosis. One must have a high index of suspicion and serologic testing of serum IgM will aid in confirming the diagnosis. Look for a history of a patient moving from or with recent history of traveling to a country where dengue is known to be endemic. The incubation time after being bitten by a vector is typically three to seven days but can be as long as 14 days so questions should be targeted at travel within that time frame. Any prodromal symptoms that fall outside that time window are highly unlikely to be dengue. Symptoms may include fever (as high as 40°C or 104°F), severe myalgias, arthralgias and headache with retro-orbital features. Patients may also present with nausea and vomiting, anorexia and a maculopapular rash.

Dengue hemorrhagic fever (DHF) is a potentially disastrous sequelae of the disease. It largely occurs in patients under the age of 15 and may present with petechia, altered mental status, epistaxis, hematuria, gastrointestinal bleeding and bleeding from sites of trauma. If untreated, it can progress to dengue shock syndrome (DSS). This must be addressed quickly, with rapid fluid resuscitation. Platelets and FFP may be indicated in severe cases.

Dengue itself is a self-limiting disease process. Treatment and management are largely supportive, with bed rest, pain and fever control with analgesics and antipyretics, and maintenance of adequate fluid intake.

References:

  1. Soni H, Gandhi V, Varma S, Kaur D, Epelbaum O. A 47-year-old returning traveler with shock. Chest. 2015 Jan;147(1):e8-12. doi: 10.1378/chest.14-0615. PMID: 25560874
  2. Kyle JL, Harris E. Global spread and persistence of dengue. Annu Rev Microbiol. 2008. 62:71-92.
  3. Osterwell N. Dengue 'Under-recognized' as source of febrile illness in US. Medscape Medical News. Jan 23 2014.
  4. Shepherd SM, Hinfey PB and Schoff WH. Dengue Treatment and management. Medscape: eMedicine. Updated: March 14, 2014


Impact of Angiotensin II Receptor Neprilysin Inhibitors on the Emergency Physician
Megan Litzau, MD and Stefanie Ellison, MD
Indiana University

Most EM residents will not work a single shift without seeing a patient who carries a diagnosis of heart failure (HF). Though the use of Brain-type Natriuretic Peptide (BNP) does vary by institution, if you are using BNP you need to be aware of a new medication called LCZ696, now referred to as Entresto. This medication is a combination of sacubitril and valsartan and is used to reduce the risk of cardiovascular death and hospitalization for patients with chronic HF and is indicated for NYHA Class II-IV chronic heart failure.

Sacubitril is a prodrug that when activated inhibits angiotensin II receptor neprilysin (a neutral endopeptidase). The inhibition of neprilysin results in increased bioavailability of BNP resulting in increased natriuretic and vasodilatatory effects, which lead to powerful cardiac ventricular unloading and antihypertensive response. The outcome of this medication is that serum BNP levels will be falsely elevated. In order to obtain a natriuretic level on a patient on this medication, you will need to order a NT-proBNP level instead of a conventional BNP. The use of this medication is currently limited due to expense but it will likely increase in the future.

Also of note, this medication contains valsartan and therefore additional ACE/ARB medications should not be added. Likewise, complications from traditional ACE/ARB medications can be seen with the valsartan component of this medication including angioedema, hyperkalemia, hypotension and a decline in renal function. This medicine contains a valsartan component that has increased bioavailability than other formulations and therefore doses for the valsartan are lower in the combination drug than standard doses. The doses of valsartan in this medication (all in mg) are 26, 51 and 103 corresponding to 40, 60 and 160 respectively for standard dosing. Be aware of this medication as it enters clinical practice. Consult your clinical laboratory, pharmacist and prescribing cardiologist for additional assistance when these patients begin arriving in your emergency department.

References:

  1. McMurray JJ, Packer M, Desai AS, et al. PARADIGM-HF investigators and committees. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014;371(11):993-1004.[PubMed 25176015]10.1056/NEJMoa1409077.

 

 

Notes from the Night Shift: Single Parents as Patients
Heather Boynton, MD
UC San Diego Health System

With pediatric cases, we often say that we have two patients: the child and the parent. How does our approach change when the parent is the patient, and the kids are in the room too?

On a recent string of overnight shifts, I noticed I was seeing a lot of single parents who told me they decided to come to the ED at night so that their children would sleep through most of the visit. My first patient was a young, single, working mother with two small children. In tears she told me how she had been having rectal bleeding for over a week. During the day she worked at a new job, and was afraid to take time off to go to a clinic; at night she had no one to watch her kids, and money was tight, making a babysitter feel like a sacrifice. Her toddler had been outfitted with headphones and was deeply engrossed in a cartoon; the older child, a girl maybe five or six years old, looked at her shoes. My sexual history taking, usually easy with frank, plain language, halted and stumbled. I put off a bimanual exam. When I returned with a pelvic cart and someone to watch the kids, they were asleep in the bed I wanted to use for my patient, and she was in a chair.

Another patient, also a single mother, was roomed with her two young children around 11:00pm while her two older children waited in the waiting room. She, too, had been having symptoms for about a week, complaining of a bad headache with nausea. I sent labs and started fluids. I decided to order Compazine without Benadryl, concerned that the combination would be too sedating. When I checked on my patient twenty minutes later, she was standing on her bed, screaming and pulling her clothes off. Now all four children were in the room, and the youngest two were crying. Fortunately, more fluids and a small dose of benztropine resolved things.

A few pearls:

  • Make sure your patient is in the right room. A room with a door helps keep young children calm in an otherwise chaotic environment. A small family camped out for the night can wreak havoc on department flow, so think early about your plan for discharge or admission.
  • Identify up-front what parts of your assessment would be best completed without children. Ask your ancillary staff for help when you need a sexual history, pelvic or rectal exams. Twenty minutes may be hard to come by, but five minutes is usually doable.
  • Use the equipment available to you. Paper, pens, warm blankets and small containers of milk from the patient food refrigerators go a long way to smooth over a late-night visit. If your ED has reclining chairs, try to get one into your patient’s room. Encourage the patient to tuck a child into a soft chair or cot instead of the patient bed.

Your 2015-2016 Leaders:

President
Victoria Weston, MD

Vice President
Michael Gottlieb, MD

Secretary-Treasurer
Nicole Battaglioli, MD

Immediate Past President
Meaghan Mercer, DO

At-Large Board Members
Phillip Dixon, MD
Mary Haas, MD
Nathan Haas, MD
Amy Ho, MD
Megan McKay, MD
Gregory Wanner, DO

Medical Student Council President
Michael Wilk

Copy Editor:
Nathan Haas, MD

Managing Editor:
Madeleine Montony,
AAEM/RSA Staff

Modern Resident Contributors

Special thanks to this issue's contributors:

Sachin Allahabadi, MSIII; Jorge Luis Aceves, MSIII; Heather Boynton, MD; Stefanie Ellison, MD; Kaitlin Fries, DO; Phillip Fry, OMSIV; Danielle Goodrich, MD; Daniel Leiva, MS OMSIV; Megan Litzau, MD; Alexandra Murray, DO; Linda Sanders, MD; Veronica Tucci, MD JD; Aaron Tyagi, MD.

Interested in writing?
Email submissions to: info@aaemrsa.org

Please submit articles by January 15th for the February/March edition.

Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles may not be duplicated or distributed without the explicit permission of AAEM/RSA.

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