EM@3AM – Ankle Sprains

Authors: Jared Cohen, MD, MHA (EM Resident Physician, SAUSHEC, USA) and Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


An 18-year-old male, without significant past medical history, presents to the ED for a lower extremity injury. The young man reports “twisting his ankle” during basketball practice one hour prior to arrival.  He describes his lower extremity pain as constant (8/10), localized to the lateral aspect of his right ankle, and limiting his ambulation. He denies alterations in extremity sensation and previous ankle injury/trauma.

Pertinent physical examination findings:
MSK (Right lower extremity):
Hip: Full, painless ROM. No obvious trauma. No erythema/induration.
Knee: No evidence of joint effusion (patellar ballottement test negative). No joint ecchymosis, erythema, or induration. No TTP of the fibular head. Negative anterior and posterior drawer. Negative Apley Compression.
Ankle: Significant ecchymosis localized to the lateral malleolus extending to the lateral midfoot. Significant Edema. TTP anterior to the lateral malleolus. Positive anterior drawer test. Negative talar tilt test. Negative squeeze test.

Meets Ottawa Ankle criteria.

What do you suspect as a diagnosis? What’s the next step in your evaluation and treatment?


Answer: Ankle Sprain1-7

  • Epidemology: Greater than 5 million ankle injuries occur annually in the U.S.1 Ankle sprains account for 40% of all sports-related injuries.2
  • Classification of Sprains:
    • Anatomic Location:
      • Lateral ankle sprain: most common ankle injury; results from inversion mechanism.3 The lateral ligament complex consists of the anterior talofibular ligament (ATFL; most frequently injured), calcaneofibular ligament (CFL), and the posterior talofibular ligament.3
        • Maffulli classification for lateral ankle sprains => performed only after rest, ice, compression, and elevation (RICE) therapy for 48 hours + early ROM exercises:2
          • Grade I: Partial tear
          • Grade II: ATFL tear
          • Grade III: ATFL + CFL tear
      • Medial ankle sprain: given the tensile strength of the deltoid ligament, this is a rare ankle eversion injury that may result in avulsion of the medial malleolus.3
      • High ankle sprain: injury to the anterior tibiofibular ligament, posterior tibiofibular ligament, transverse tibiofibular ligaments, or interosseous membrane (syndesmosis) due to forces which rotate the talus within the mortise (separating the tibia and fibula, and injuring the syndesmotic fibers).3
        • Note: Both medial and high ankle sprains are classified according to the following:2
          • Grade I: Strain
          • Grade II: Partial tear
          • Grade III: Complete tear
          • Note: Grade II and III deltoid and syndesmotic injuries assigned following MRI.2
  • Evaluation:
    • Perform a thorough H&P. The mechanism of injury should direct a focused examination.
    • Examination:
      • Assess for signs of neurovascular compromise. (More often encountered in the setting of posterior ankle dislocation. Dislocation + neurovascular compromise or skin tenting = immediate reduction and orthopedic consultation).2
      • Assess gait
      • Examine the ipsilateral knee: palpate the fibular head => Maisonneuve fracture.2
      • Evaluate the syndesmosis:
        • Most reliable test = external rotation:4
          • Patient seated with hip and knee flexed, and the foot and ankle in the neutral position. With the knee facing forward, external rotation is applied to the foot. The test is positive if the pain is reproduced at the anterior syndesmosis.
      •  Evaluate for Achilles tendon injury = Thompson’s test:
        • Patient in the prone position with the feet hanging off the table, or with the knees flexed and the feet hanging over the end of a chair. As the examiner squeezes the patient’s calf muscle, plantar flexion of the ankle should occur if the Achilles tendon is intact. The test is positive if the foot remains in the neutral position or if there is minimal plantar flexion of the ankle compared with the unaffected side.
      •  Evaluate the for lateral ankle sprain as applicable:
        • ATFL injury assessment = anterior drawer test:2
          • Patient seated and the distal tibia stabilized with one hand of the examiner while the other hand grasps the heel and the foot is anteriorly translated (repeat on contralateral limb for comparison). Complete ATFL tear => the talus subluxates anteriorly and a dimple forms on the anterolateral joint area.
        • CFL injury assessment = talar tilt test:2
          • Patient seated and the leg secured with the examiner’s hand while the heel is grasped with the opposite hand and an inversion force is administered to cause talar tilt (repeat on contralateral limb for comparison).
      •  Evaluate for medial ankle injury by assessing for deltoid insufficiency:2
        • Patient should be asked to lower himself or herself to a squatting position with the feet flat on the floor => if insufficiency: medial malleolus becomes overtly prominent as compared with the other ankle (a positive medial malleolar pointing sign).
      •  Clinical Decision Tool: Ottawa Ankle Rules:
        • Systematic review of 27 studies (n =15,581) => highly sensitive for the exclusion of ankle fracture (96.4-99.6%).5
    •  Imaging:
      • Ottawa ankle positive:
        • AP, lateral, and mortise views recommended for lateral, medial, and high ankle sprains:
          • Lateral radiograph: allows assessment of medial joint space.
          • Mortise view: allows for measurement of the lateral displacement of the lateral malleolus and the width of the syndesmosis.
        • Suspicion for Grade II or III lateral ankle sprain => bilateral stress views (talar tilt): allows calculation of the difference in the angle between the distal tibial articular surface and dome of the talus.
        • Assessment of medial ankle sprains and high ankle sprains => weight-bearing films recommended.2
        • High ankle sprain: imaging should include the entire tibia and fibula (Maisonneuve).2
        • Non-emergent MRI indicated if concern for Grade II or III deltoid ligament or syndesmotic injury.2
  •  Treatment:2
    • Lateral ankle sprains => aircast, RICE, early ROM, progressive weight bearing.
    • Medial ankle sprains =>
      • Grade I: aircast, RICE, rehab/ROM exercises, return to activity within 3 weeks.
      • Grade II and Grade III: Orthopedic consult: complete deltoid insufficiency may require surgical repair vs. boot/orthotic immobilizer, physical therapy, and orthopedic follow-up for graduated return to activity.
    • Syndesmotic injuries =>
      • Grade I: aircast, RICE, rehab/ROM exercises, return to activity within 3-6 weeks under ortho supervision.
      • Grade II and Grade II: Orthopedic consult for surgical repair.
  • Pearls:
    • As many as 30% of patients with ankle sprains develop chronic ankle instability.6
    • False negative Thompson’s tests may occur following delayed patient presentation: hematoma may cause reconstitution of the tendon.7


References:

  1. Daly PJ, Fitzgerald RH, Jr., Melton LJ, Ilstrup DM. Epidemiology of ankle fractures in Rochester, Minnesota. Acta Orthop Scand 1987;58:539-44.
  2. Molloy A, Selvan D. Ligamentous Injuries of the Foot and Ankle. In DeLee & Drez’s Orthopaedic Sports Medicine. 4th ed. Philadelphia, Saunders. 2015; 116:1392-1407.e2.
  3. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med 2007;35:1197-207.
  4. Alonso A, Khoury L, Adams R. Clinical tests for ankle syndesmosis injury: reliability and prediction of return to function. J orthop Sports Phys Ther. 1998; 27:276-284.
  5. Jenkins M, Sitler M, Kelly J. Clinical usefulness of the Ottawa Ankle Rules for detecting fracutres of the ankle and midfoot. J Athl Train. 2010; 45(5):480-482.
  6. Konradsen L, Bech L, Ehrenbjerg M, Nickelsen T. Seven years follow-up after ankle inversion trauma. Scand J Med Sci Sports 2002;12:129-35.
  7. Gravlee J, Hatch R, Galea A. Achilles tendon rupture: a challenging diagnosis. J Am Board Fam Pract. 2000; 13(5):371-373.

 

For Additional Reading:

Diagnostic accuracy of ankle x-rays: How often do we miss fractures?

How can we improve?

Diagnostic accuracy of ankle x-rays: How often do we miss fractures? How can we improve?

The post EM@3AM – Ankle Sprains appeared first on emDOCs.net - Emergency Medicine Education.

EM@3AM – Calcium Channel Blocker Toxicity

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) and Daniel Sessions, MD (EM Associate Program Director, SAUSHEC, USA / Medical Toxicologist, South Texas Poison Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 78-year-old female, with a previous medical history of hypertension (diltiazem) and dementia (donepezil), presents to the ED with the chief complaint of weakness. The woman’s husband, her sole caregiver, reports the patient as “increasingly fatigued” since her morning awakening. Per the husband, the patient was without complaints prior to the onset of symptoms. The caregiver denies the observance of facial droop, motor difficulties, and slurred speech. He reports his spouse as without recent febrile illness, sick contacts, and changes in pharmaceutical therapy.

Initial VS: BP 124/88, HR 63, T 99.7F Oral, RR 14, SpO2 97% on room air.

Physical examination:
General: Thin, frail female appearing as stated age.
Neuro: GCS 15, no focal deficits.
CV: Regular rate and rhythm, no murmurs, rubs or gallops.
Pulm: Lungs CTAB.
Abdomen: Soft, non-tender, non-distended; no guarding, or rebound.

Upon completion of the physical examination, the patient suddenly slumps backwards on the stretcher.

Repeat VS: 82/64, HR 38, T 99.7F Oral, RR 14, SpO2 97% on room air.
Accucheck: 327 mg/dL

EKG: Sinus bradycardia, rate 37 bpm, QRS 200 msec, no acute ST-T wave changes

Bedside electrolyte assessment: Sodium 137 mmol/L, potassium 3.3 mmol/L, ionized calcium 0.8 mmol/L

What do you suspect as a diagnosis? What’s the next step in your evaluation and treatment?


Answer: Calcium Channel Blocker (CCB) Toxicity1-7

  • Epidemology:1 In 2015, the American Association of Poison Control Centers identified 1,253 persons with confirmed exposures to calcium channel blockers. Of these individuals, 958 required treatment at a healthcare facility, and 18 perished.
  • Pathophysiology and Clinical Presentation: Calcium is vital to a number of physiologic processes – an understanding of which yields insight regarding patient presentation and subsequent treatment:2
    • Cardiac:
      • Sinoatrial nodal and atrioventricular nodal tissue: slow inward calcium channels (and to a lesser extent, sodium channels) responsible for action potential generation.
      • Cardiac myocyte: calcium entry by L-type or voltage-gated calcium channels => calcium induced calcium release from intracellular organelles => excitation-contraction coupling.
    • Vascular:
      • Calcium required for the maintenance of vascular smooth muscle tone.
    • Metabolic:
      • Shock state induced by cardiac calcium insufficiency => increased free fatty acid metabolism and liver glycogenolysis.
      • Pancreatic β-islet cells: require calcium for insulin release. Insulin required for glucose uptake (cell specific: skeletal muscle, etc.). Lack of insulin => Krebs cycle shift to anaerobic metabolism (pyruvate production).
    • Presentation: bradycardia, conduction abnormalities, hypotension, possible shock, hyperglycemia, acidosis. (Note: patients with dihydropyridine CCB toxicity frequently present with reflex tachycardia – see below.)
  • Calcium Channel Blocker Classification:
    • Phenylalkylamine CCBs (verapamil) and benzothiazepine CCBs (diltiazem): bind to receptor sites in the pores of calcium channels and block them.3
      • Verapamil and diltiazem are responsible for the majority of cases of severe cardiovascular compromise.  These medications are commonly ingested in sustained release (SR) formulations => peak toxicity may be delayed for several hours, and the duration of toxicity prolonged secondary to continued GI absorption. Patients can appear clinically well for an extended period of time prior to sudden deterioration.
    • Dihydropyridine CCBs (amlodipine, nifedipine, etc.): enhance or inhibit the activation of voltage-gated calcium channels in heart and vascular smooth muscle by acting at allosteric modulatory sites outside of calcium channel pores.
      • As compared to verapamil and diltiazem, dihydropyridines display a lesser effect on cardiac myocytes: negative resting potential of cardiac myocytes => dihydropyridine dissociation.
      • Affect on vascular smooth muscle => vasodilatory shock and reflex tachycardia (compensation).
    • Summary of hemodynamic effects:4

  • Evaluation and Treatment:
    • Assess the ABCs and obtain vital signs.
    • Obtain an EKG and initiate continuous cardiac monitoring.
    • Perform a thorough H&P: Question regarding specific medication(s) ingested (number of capsules/tablets and dose), sustained release formulations, time of ingestion, co-ingestions, and intent.
    • Laboratory evaluation and imaging:
      • ABG/VBG: acidosis demonstrated to worsen myocardial dysfunction secondary to calcium channel antagonism (hypothesis: increased drug binding at calcium channels).5
      • Accucheck: assess for hypoglycemia; essential evaluation for hyperinsulinemia euglycemia therapy (HIET) (detailed below).
      • BMP: evaluate renal function in the setting of hemodynamic compromise/hypoperfusion state. Hypokalemia is frequently present.
      • Consider serum acetaminophen, serum salicylates, serum ETOH, and a UDS if concern for co-ingestions.
      • Bedside ultrasound: useful adjunct for the evaluation cardiac function.2
  • Treatment:
    • Source control:
      • Gastric lavage: not routinely employed. Consult toxicology => may be considered in patients presenting within 1-2 hours of a “life threatening” ingestion.2
      • Activated charcoal: consider a single dose for patients presenting within 4 hours of the ingestion of a potentially toxic dose (immediate release formulations).4
      • Whole bowl irrigation: initiate following the ingestion of SR formulations in asymptomatic patients.
        • Symptomatic patients (bradycardia and/or hypotension) = not indicated given association with depressed GI function and ileus.4
    •  Hemodynamic support:
      • Consider initial therapy with IVF and atropine.
        • IVF therapy: 1-2 L titrated to response (avoid additional fluids as the majority of patients are euvolemic (iatrogenic pulmonary edema)).4
          • Note: IVR and atropine often fail to improve heart rate and blood pressure in significant overdose.2
        • Atropine: 0.02mg/kg (min 0.1mg, max 0.5mg)4
      • Hypotension, cardiogenic shock, or vasodilatory shock:
        • HIET:4 insulin 1 U/kg IV bolus
          • Follow with an insulin infusion of 1-10 U/kg/hr + 50% glucose infusion to maintain euglycemia (requires frequent accuchecks). May increase infusion by 0.5-1 U/kg/hr every 30-60 minutes.
        • Calcium:4,6 6-mL/kg (3-6g) bolus of 10% calcium gluconate, or 0.2 mL/kg (1-2g) 10% calcium chloride administered over 5 to 10 minutes.
          • Follow with a calcium gluconate infusion at 0.6-1.2 mL/kg/hour (0.2–0.4 mL/kg/hour 10% calcium chloride). Titrate to improved blood pressure or contractility.
          • Assess ionized calcium levels q 30 mins. Goal = 2x normal.
        • Epinephrine: 0.05-1 μg/kg/min to increase heart rate and contractility; titrated to effect.4,6
        • Norepinephrine to increase blood pressure.4,6
    •  Toxicity refractory to initial treatment:
      • Incremental increase in HIET up to 10U/kg/hr.
      • Lipid emulsion therapy:6    1.5 mL/kg of 20% lipid emulsion administered as a bolus; repeat up to two times as needed to achieve clinical stability.
        • Followed by infusion of 0.25mL/kg/min for 30-60 min.
      • In the absence of myocardial contractility dysfunction, consider pacemaker if bradycardia or high grade AV block.6
      • Consult for venoarterial extracorporeal membrane oxygenation (VA-ECMO) if available.6 
  • Disposition:
    • Symptomatic patients required ICU-level care. All asymptomatic patients in whom concern for ingestion of SR formulations exist = admission for 24 hour monitoring.4
  • Pearls:
    • Consult Poison Control at 1-800-222-1222 for expert opinion given low level of evidence for management.6
    • The extent of hyperglycemia and metabolic acidosis serve as a marker of the degree of calcium channel toxicity.7

 References:

  1. Mowry J, Spyker D, Brooks D, Zimmerman A, Schauben J. 2015 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 33rd Annual Reports. Available from: https://aapcc.s3.amazonaws.com/pdfs/annual_reports/2015_AAPCC_NPDS_Annual_Report_33rd_PDF.pdf
  2. Kerns W. Management of B-adrenergic blocker and calcium channel antagonist toxicity. In Emergency Medicine Clinics of North America. Philadelphia, Elsevier. 2007; 25(2):309-331.
  3. Catterall W, Swanson T. Structural basis for pharmacology of voltage-gated sodium and calcium channels. Mol Pharmacol. 2015; 88(1):141-150.
  4. Graudina A, Lee H, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. Br J Pharmacol. 2016; 81(3):453-461.
  5. Smith H, Briscoe M. The relative sensitization by acidosis of five calcium channel blockers in cat papillary muscles. J Mol Cell Cardiol. 1985; 17:1709-1716.
  6. St. Onge M, Anseeuw K, Cantrell FL, et al. Experts consensus recommendations for the management of calcium channel blocker poisoning in adults. Crit Care Med 2017 Mar;45(3):e306-315.
  7. Kine J, Raymond R, Schroeder J, et al. The diabetogenic effects of acute verapamil poisoning. Toxicol Appl Pharmacol 1997; 145: 357-362.

 

For Additional Reading:

Core EM: Hyperinsulinemia Euglycemia Therapy (HIET) for BB and CCB Toxicity

Core EM: Hyperinsulinemia Euglycemia Therapy (HIET) for BB and CCB Toxicity

 

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Fever of Unknown Origin

Originally published at Pediatric EM Morsels on September 17, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Fever is one of the most common chief complaints in the Peds ED.  We are all very accustomed to the common considerations (ex, UTI, Croup, Bronchiolitis, Appendicitis, and Sinusitis).  We also know there are “zebras” that may try to trample us (ex, Kawasaki’s, Myocarditis, Osteomyelitis, Acute Rheumatic Disease, Lemierre’s, and Cat Scratch Disease). Additionally, we are aware of how important it is to avoid the “It’s Just a Virus” statement. On occasion though, the cause of the fever will not be clear, but the prolonged fever warrants concern. Let us, now, look at Fever of Unknown Origin.

 

Fever of Unknown Origin: Basics

  • Often confused with “Fever Without a Source
    • Fever of Unknown Origin involves a prolonged duration of fever.
    • Fever Without a Source may become Fever of Unknown Origin, if it lasts long enough.
  • The exact incidence of Fever of Unknown Origin is not well defined.
    • There is no standard definition.
    • The ability to determine etiologies has improved over time.
    • If a diagnosis is eventually determined, then it is no longer of “Unknown Origin.”
  • Definition:
    • Generally requires a duration of fever that is deemed to be excessively long for what was expected.
      • Historically, up to 3 weeks of fever was used. [Petersdorf, 1961]
      • Now, fever lasting longer than 8 days without a source is often cited.
    • Ideally, there are documented fevers (38.0 C; 100.4 F).
  • The Big Categories of Potential Causes to Consider:
    • Infectious – ~30%
      • The proportion of infectious causes has decreased in recent years, likely due to improved diagnostic testing.
    • Rheumatologic / Autoimmune– ~20%
    • Oncologic – ~10%
    • Other Zebras – ~5%
      • Familial Dysautonomia
      • Periodic Fever Syndromes
      • Cyclic Neutropenia
    • Drug Fever – ~5%
      • Often overlooked [Antoon, 2015]
      • First step in evaluation is stopping all nonessential medications [Antoon, 2015]
      • Many agents, including ibuprofen and acetaminophen, can be a source of drug fever.
    • Undiagnosed (often spontaneously resolved) – ~30%

 

Fever of Unknown Origin: ED Considerations

  • Do not under-appreciate the family’s concern
    • Once we hear that the fever has been present for “2 weeks straight” we may “roll our eyes” internally and immediately think that this is no longer an emergency.  Refrain from this (particularly if you tend to show your inner thoughts readily on your face).
    • This goes along with never saying that it is “just a virus.”
  • General Appearance: Is the child sick or not sick?
    • Sick – Higher risk for badness and you should have lower threshold for hospitalizing.
    • Not Sick – Lower risk for badness (not no risk), but likely more appropriately evaluated as an outpatient.
  • The diagnosis is likely hiding in the History and Physical[Tolan, 2010]
    • Instead of ordering a ton of random tests, ask more questions... even the same ones over again (we have all witnessed “historic alternans”).
    • Additional historic details to obtain:

      • Ethnic Background 
      • Travel history and prophylaxis
      • Animal exposurescats? petting zoos? etc.
      • Vector exposuresticks?
      • HIV and TB risk factors
      • Pica and Dietary exposures
    • Physical exam aspects to include:

  • Look first for Disguised Horses rather than Zebras
    • More likely to be dealing with an unusual presentation of a common condition than a common presentation of an unusual condition. [Antoon, 2015]
    • Consider Pseudo-Fever of Unknown Origin
      • Series of benign, self-limited illnesses over a short period of time [Tolan, 2010]
      • Kids love to get another viral illness just as they are getting rid of one.  This can create the appearance of the child being sick over a protracted course.

 

Fever of Unknown Origin: Work-up

  • The differential for Fever of Unknown Origin is vast, but resist the urge to order every test available in your hospital.
    • Broad laboratory testing is often more harmful than helpful.
    • The history and physical are the foundation for your Ddx development and subsequent testing strategy.
  • There are some basic tests that are supported by experts and may be useful in your ED to help sort through the Ddx: [Antoon, 2015]
    • CBC w/ Diff – yes, I know that the WBC count is the “last bastion of the intellectually destitute” (Amal Matt, MD), but ensuring that it is not 125,000 is helpful… plus Hgb and platelet counts are helpful. [Chow, 2011]
    • U/A and UCx
    • CMP
    • Radiographs as indicated
  • Additional testing:
    • Well-appearing
      • Likely appropriate for outpatient evaluation
      • Limit unnecessary testing
      • Arrange for serial examinations and have family keep fever journal.
    • Ill-Appearing
      • Admit
      • Blood Cultures
      • CSF Cultures – if neurologic symptoms present
      • ESR and CRP – have limited value in isolation, but may be helpful to track over time. Normal values do NOT rule-out serious conditions.
      • Categorical Based Evaluations: (likely to be ordered by inpatient team)
        • Infectious
          • Serial Cultures if considering endocarditis
          • Specific antibody and viral testing (ex, EBV)
        • Oncologic
          • Uric Acid
          • LDH
          • Peripheral Smear
        • Rheum/Autoimm
          • ANA, RF
          • C3, C4, CH50
          • Thyroid function panel
          • CRP, ESR, ferritin
        • Immunodeficiency
          • Immunoglobins
          • Lymphocyte markers
          • Antibody titers

 

Fever of Unknown Origin: Empiric Antibiotics?

  • Ill Appearing?
    • Then have a lower threshold for obtaining cultures and starting empiric antibiotics.
  • Well Appearing?
    • DO NOT give antibiotics!
    • In developed countries, the rates of infectious etiologies of Fever of Unknown Origin have been decreasing.
    • Empiric antibiotics can delay the diagnosis of many conditions like osteomyelitis and endocarditis. [Antoon, 2015; Chow, 2011]

 

References

Antoon JW1, Potisek NM2, Lohr JA3. Pediatric Fever of Unknown Origin.Pediatr Rev. 2015 Sep;36(9):380-91. PMID: 26330472. [PubMed] [Read by QxMD]

Tezer H1, Ceyhan M, Kara A, Cengiz AB, Devrim İ, Seçmeer G. Fever of unknown origin in children: the experience of one center in Turkey.Turk J Pediatr. 2012 Nov-Dec;54(6):583-9. PMID: 23692783. [PubMed] [Read by QxMD]

Chow A1, Robinson JL. Fever of unknown origin in children: a systematic review. World J Pediatr. 2011 Feb;7(1):5-10. PMID: 21191771. [PubMed] [Read by QxMD]

Tolan RW Jr1. Fever of unknown origin: a diagnostic approach to this vexing problem. Clin Pediatr (Phila). 2010 Mar;49(3):207-13. PMID: 20164070. [PubMed] [Read by QxMD]

PETERSDORF RG, BEESON PB. Fever of unexplained origin: report on 100 cases. Medicine (Baltimore). 1961 Feb;40:1-30. PMID: 13734791. [PubMed] [Read by QxMD]

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