Small Bowel Intussusception

Small Bowel IntussusceptionIntussusception is a common concern that we manage when faced with a child with abdominal pain and/or vomiting. We have discussed multiple aspects of the evaluation and management of intussusception (ex, Intussusception, Intussusception and HSP, Change in Mental Status, and Disposition). Obviously, the use of ultrasound has dramatically improved our ability to expeditiously evaluate these children, but what do you do when the ultrasound finds something unexpected? What do you do with Small Bowel Intussusception?

 

Small Bowel Intussusception: Basics

  • Any segment of bowel can develop intussusception.
    • Most often (~80%) it is located at the ileocecal junction or in the ileocolic region.
    • Small Bowel Intussusception is more rare.
  • Can occur in any age, but more rare in children compared to adults. [Koh, 2006]
  • Small Bowel Intussusception presents in non-specific fashion:
    • Irritability
    • Vomiting
    • Abdominal Pain
    • Fever (~50% in one case series) [Ko, 2002]

 

Small Bowel Intussusception: The Benign and The Bad

The Benign

  • Small Bowel Intussusception can be transient and of no clinical consequence. [Mateen, 2006]
  • Can be seen incidentally on other studies performed for other reasons (ex, Pelvic U/S, Abd CT). [Strouse, 2003]
  • Thought to be due to “momentary dysrhythmic contractions.” [Mateen, 2006]
  • Often will reduce spontaneously… many times during the ultrasound study.

 

The Bad

  • Small Bowel Intussusception can also lead to intestinal necrosis.
    • More likely to be associated with underlying pathologic process like:
      • Post-surgical adhesions or Jejunal Tubes
      • Malabsorption syndromes
      • Inflammatory processes (ex, Crohn’s Disease, HSP)
    • Even with underlying pathology, observation has been shown to be appropriate in some cases. [Sonmez, 2002]
  • Require surgical correction, as air-contrast enema is less effective in treating small bowel. [Koh, 2006]
  • More difficult to diagnose than large bowel associated intussusception. [Ko, 2002]
    • Delays in diagnosis and surgical correction are common.
    • These delays are associated with higher complication rates. [Ko, 2002]

 

Small Bowel Intussusception: Will it be Transient?

  • So, if the condition can be either “no big deal” or a “real big deal,” what can be done to differentiate between these two extremes?
    • Obviously it would be best to avoid unnecessary surgery for those that will have spontaneous reduction of their benign small bowel intussusception.
    • Equally important, it is necessary to limit ischemic time and not delay surgical intervention for those with pathologic small bowel intussusception.
  • Several studies have determined that U/S characteristics can help with this determination:
    • Likely to spontaneously reduce:
      • Length < 1.8 cm, Mean diameter < 1.5 cm, No Wall Swelling, Preserved Wall Motion, No Lead Point [Kim, 2004]
      • Length < 3.5 cm, No Lead Point, Normal Wall Thickness, No Proximal Dilation, Normal Blood Flow [Mateen, 2006]
    • Likely to need a surgeon to reduce:
      • Length > 3.5 cm [Munden, 2007]
      • Length ≥ 4.2 cm, Diameter ≥ 2.1 cm, Outer Rim Thickness ≥ 0.04 cm [Zhang, 2011]

 

Moral of the Morsel

  • Small Bowel Intussusception can be Benign… but it can also lead to Badness!
  • U/S Characteristics can help distinguish which ones will likely reduce on their own… and which ones will not.
    • Smaller is better.
    • Motion is marvelous.
    • Lead Points are bad.
  • Pay attention to the patient!  Persistent symptoms may warrant repeat U/S and/or surgical consultation.
  • If the intussusception does not spontaneously reduce during the U/S study, even if it has low risk findings, have low threshold for repeating the U/S. [Kornecki, 2000]

 

References

Rajagopal R, Mishra N1, Yadav N, Jhanwar V, Thakur A, Mannan N. Transient versus surgically managed small bowel intussusception in children: Role of ultrasound. Afr J Paediatr Surg. 2015 Apr-Jun;12(2):140-2. PMID: 26168754. [PubMed] [Read by QxMD]

Lioubashevsky N1, Hiller N, Rozovsky K, Segev L, Simanovsky N. Ileocolic versus small-bowel intussusception in children: can US enable reliable differentiation? Radiology. 2013 Oct;269(1):266-71. PMID: 23801771. [PubMed] [Read by QxMD]

Zhang Y1, Bai YZ, Li SX, Liu SJ, Ren WD, Zheng LQ. Sonographic findings predictive of the need for surgical management in pediatric patients with small bowel intussusceptions. Langenbecks Arch Surg. 2011 Oct;396(7):1035-40. PMID: 21274558. [PubMed] [Read by QxMD]

Munden MM1, Bruzzi JF, Coley BD, Munden RF. Sonography of pediatric small-bowel intussusception: differentiating surgical from nonsurgical cases. AJR Am J Roentgenol. 2007 Jan;188(1):275-9. PMID: 17179377. [PubMed] [Read by QxMD]

Mateen MA1, Saleem S, Rao PC, Gangadhar V, Reddy DN. Transient small bowel intussusceptions: ultrasound findings and clinical significance. Abdom Imaging. 2006 Jul-Aug;31(4):410-6. PMID: 16944032. [PubMed] [Read by QxMD]

Koh EP1, Chua JH, Chui CH, Jacobsen AS. A report of 6 children with small bowel intussusception that required surgical intervention. J Pediatr Surg. 2006 Apr;41(4):817-20. PMID: 16567200. [PubMed] [Read by QxMD]

Kim JH1. US features of transient small bowel intussusception in pediatric patients. Korean J Radiol. 2004 Jul-Sep;5(3):178-84. PMID: 15467415. [PubMed] [Read by QxMD]

Strouse PJ1, DiPietro MA, Saez F. Transient small-bowel intussusception in children on CT. Pediatr Radiol. 2003 May;33(5):316-20. PMID: 12695864. [PubMed] [Read by QxMD]

Ko SF1, Lee TY, Ng SH, Wan YL, Chen MC, Tiao MM, Liang CD, Shieh CS, Chuang JH. Small bowel intussusception in symptomatic pediatric patients: experiences with 19 surgically proven cases. World J Surg. 2002 Apr;26(4):438-43. PMID: 11910476. [PubMed] [Read by QxMD]

Sönmez K1, Turkyilmaz Z, Demirogullari B, Karabulut R, Aral YZ, Konuş O, Başaklar AC, Kale N. Conservative treatment for small intestinal intussusception associated with Henoch-Schönlein’s purpura. Surg Today. 2002;32(12):1031-4. PMID: 12541018. [PubMed] [Read by QxMD]

Kornecki A1, Daneman A, Navarro O, Connolly B, Manson D, Alton DJ. Spontaneous reduction of intussusception: clinical spectrum, management and outcome. Pediatr Radiol. 2000 Jan;30(1):58-63. PMID: 10663512. [PubMed] [Read by QxMD]

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Dental Trauma

Dental TraumaWe all know that kids like to test gravity and sometimes suffer the consequences (ex, Tongue Laceration, Eyelid Laceration, and Concussions). One of the most common consequences of testing gravity (or general poor coordination) is dental trauma.  This is true for adults and older children also, but what needs to be done when the trauma involves a young child’s primary dentition?

What follows is based on info from www.dentaltraumaguide.com (which has some excellent graphics) as well as other references, like [Keels, 2014].

 

Dental Trauma Basics

  • Toddlers and Pre-Teens!
    • Dental trauma often occurs in Toddlers (2-4 years) and school-aged children (8-10 years). [Ritwik, 2015]
      • Toddlers – they like to toddle and fall down
      • Pre-Teens – like to partake in activities (like sports), yet often are not as coordinated as their older counterparts.
        • Sports (39%) and Accidental Falls (33%) comprise the majority of cases. [Bruns, 2008]
    • Primary dentition involved in close to half of the cases (~47%). [Ritwik, 2015]
  • While often seen in the Emergency Department, a Dental Clinic is the most efficient venue for treating routine dental trauma. [Mitchell, 2014; Wagle, 2014]
  • As with all trauma, do not get distracted by/focus only on the obvious injury.
    • It is always best to consider “worse first” and proceed in a organized fashion.
    • Many dental injuries will be isolated, but make sure that there is not evidence of more significant trauma (ex, Raccoon Eyes, Battle Sign, Hemotympanum, Mid-face instability, etc).
  • When dealing with children and trauma, always ask whether the mechanism makes sense for the injury.

 

Primary Dentition Basics

  • Primary teeth are identified by letters rather than numbers.
    • “A” through “T”
    • Starting with Right Maxillary Second Molar and ending with Right Mandibular Second Molar.
  • Primary incisors are smaller than adult incisors.
  • Management decisions are different between Primary and Adult dentition, so it is important to know which your patient has injured.
    • In GENERAL (not all patients abide by these generalities):
      • Children < 5 years of age have primary teeth.
      • Children 6 – 12 years have mixed dentition.
        • Most incisors are adult teeth by age 8 or 9 years.
        • Continue to have mixture of primary canine and molars until ~12 years of age.
      • Children > 13 years of age, typically, have lost all of their primary teeth.
    • Ask the patient/parent whether it was a “baby tooth” or an adult one: they will likely know best.

 

Primary Tooth Trauma: Management

  • Most common primary teeth injured are the primary incisors.
  • Most common type of injury to primary teeth is luxation. [Flores, 2002]
  • Must consider the un-erupted permanent tooth’s health during management of primary tooth.
  • With respect to trauma to a tooth, decide whether there is displacement or pulp involvement. [Keels, 2014]
  1. Concussion and Subluxation
    • Similar to adult tooth care. No immediate care required.
    • Potential risk for discoloration of tooth or development of gingival abscess – recommend monitoring.
  2. Lateral luxation
    • If displacement is minor, can gently reposition. Often will reposition spontaneously.
    • Ensure tooth position does not interfere with bite. If it does, it needs to be repositioned.
  3. Extrusive Luxation/Partial Avulsion
    • Vertical displacement of the tooth from its socket.
    • If minor, gentle repositioning is fine.
    • If > 3mm, extraction of tooth is preferred.
  4. Intrusive Luxation
    • Tooth is forced into the alveolus.
    • It will appear shortened and may even appear to be missing!
      • If you are unsure whether the tooth in avulsed or intruded, x-rays are warranted.
    • Primary teeth that are intruded will typically re-erupt without intervention.
    • Observation and follow-up is warranted to ensure the tooth re-erupts, as rarely it will become fused to the bone.
    • Families should be informed about the potential damage to the developing permanent tooth (only time will tell).
  5. Avulsion
    • Unlike an permanent tooth, an avulsed primary tooth should not be replaced!
    • Most important question to ask: “Where is it?” If location isn’t know, consider Intrusion or Aspiration of it.

 

  1. Infraction / Crack and Enamel Only Fractures
    • No immediate care needed.
    • Rough edges may need to be resurfaced by dentist.
  2. Uncomplicated Enamel and Dentin Fracture
    • Referral to dentist in a few days for possible restorative care.
    • May have discoloration and/or gingival abscess formation – needs monitoring.
  3. Crown Fracture with Exposed Pulp
  4. Root Fracture
    • The closer the fracture is to the apex of the root the better the prognosis.
    • The closer to the crown the fracture is the worse the prognosis.
    • This requires specialized case (see video).

 

Dental Trauma Basic Home Care

  • Oral hygiene is important after (and yes, even before) dental trauma.
  • Soft Diet is recommended for the first ~10 days after injury.
  • Pacifier or digit sucking should be restricted.
    • If a tooth is extracted / avulsed, patients who suck pacifiers/fingers may require a spacer.
  • Antibiotics are NOT needed empirically for most patients.
  • Monitor for signs of discoloration, gingival swelling, and/or facial swelling.

 

References

Ritwik P1, Massey C, Hagan J. Epidemiology and outcomes of dental trauma cases from an urban pediatric emergency department. Dent Traumatol. 2015 Apr;31(2):97-102. PMID: 25425231. [PubMed] [Read by QxMD]

Goldberg BE1, Sulman CG, Chusid MJ. Group A beta streptococcal infections in children after oral or dental trauma: a case series of 5 patients. Ear Nose Throat J. 2015 Jan;94(1):E1-6. PMID: 25606837. [PubMed] [Read by QxMD]

Keels MA; Section on Oral Health, American Academy of Pediatrics. Management of dental trauma in a primary care setting. Pediatrics. 2014 Feb;133(2):e466-76. PMID: 24470646. [PubMed] [Read by QxMD]

Mitchell J1, Sheller B2, Velan E2, Caglar D3, Scott J4. Managing pediatric dental trauma in a hospital emergency department. Pediatr Dent. 2014 May-Jun;36(3):205-10. PMID: 24960386. [PubMed] [Read by QxMD]

Wagle E1, Allred EN2, Needleman HL3. Time delays in treating dental trauma at a children’s hospital and private pediatric dental practice. Pediatr Dent. 2014 May-Jun;36(3):216-21. PMID: 24960388. [PubMed] [Read by QxMD]

Hatef DA1, Cole PD, Hollier LH Jr. Contemporary management of pediatric facial trauma. Curr Opin Otolaryngol Head Neck Surg. 2009 Aug;17(4):308-14. PMID: 19528801. [PubMed] [Read by QxMD]

Cornwell H1. Dental trauma due to sport in the pediatric patient. J Calif Dent Assoc. 2005 Jun;33(6):457-61. PMID: 16060338. [PubMed] [Read by QxMD]

Flores MT1. Traumatic injuries in the primary dentition. Dent Traumatol. 2002 Dec;18(6):287-98. PMID: 12656861. [PubMed] [Read by QxMD]

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Aplastic Anemia

 

Aplastic CrisisPreviously, the Ped EM Morsels have requested that we remove the phrase “it’s just a virus” from our lexicons. One simple reason is that viruses can lead to significant illness also (ex, myocarditis, Guillain-Barre). While ordering a million tests and admitting everyone is not the answer, remaining vigilant can help you find subtle, ominous clues (ex, Derm Exam). That odd rash in the setting of fatigue may lead you to diagnose an Aplastic Anemia.

 

Aplastic Anemia: Basics

  • The diagnosis, evaluation, and treatment of aplastic anemia varies between institutions. [Williams, 2014]
  • “Aplastic Anemia” = tri-lineage peripheral blood cytopenia due to reduced or absent production of hematopoietic cells without cellular infiltration. [Barone, 2015]
    • Bone marrow failure leads to:
      • Severe anemia
      • Thrombocytopenia
      • Neutropenia
  • Mortality rates have improved with improved supportive care and anti-microbial management.
  • Majority of cases are idiopathic (~70-80%), but can be due to inherited conditions.
    • Fanconi Syndrome is the most common inherited bone marrow failure syndrome
    • Dyskeratosis congenita and Schwachmai-Diamond Syndrome also cause aplastic anemia.
  • Can be acquired from:
    • Viral illness (ex, EBV, Hepatitis)
    • Graft-vs-host disease
    • Systemic lupus erythematous
    • Radiation exposure
    • Chemical exposure

 

Aplastic Anemia: Severity

  • Based on  [Barone, 2015]
  • Non-Severe
    • Neutrophils > 0.5 x10^9/L, but < 1.0 x10^9/L
    • Marrow cellularity < 30%
  • Severe
    • At least 2 of the following:
      • Neutrophils < 0.5 x10^9/L
      • Platelets < 20 x10^9/L
      • Reticulocytes < 20 x10^9/L
    • Marrow cellularity < 30%
  • Very Severe
    • Neutrophils < 0.2 x10^9/L

 

Aplastic Anemia: Evaluation

  • Family history is important
    • Can help distinguish patients with an inherited condition
    • Ask about family history of:
      • Bleeding disorders
      • Malignancy
      • Congenital abnormalities
      • Consanguinity
  • Drug and Environmental Exposure history can also offer clues, even if you aren’t a toxicologist!
    • Some offending drugs:
      • Linezolid, Chloramphenicol
      • Indomethacin, naproxen, sulfasalazine, diclofenac
      • Phenytoin, carbamazepine
      • Chloroquine
      • Thiazide diuretics, allopurinol
  • Thorough (and purposeful) physical exam can also find clues!
    • Physical findings may help alert us to the presence of aplastic anemia:
      • Pallor, petechiae
      • Tachycardia, hepatomegaly, systolic flow murmur
    • Physical findings can also highlight possible inherited condition:
      • Ex, dystrophic nails, oral leukoplakia, and reticular skin pigment consistent with congenital dyskeratosis
        • 2nd most common inherited cause of bone marrow failure
      • Cafe au last spots, microcephaly, hypogonadism, mucosal abnormalities? [Barone, 2015]
  • Lab Tests useful in the Emergency Department:
    • CBC with Differential
      • Usually shows normochromic, normocytic anemia
      • In early stages, only one or two cell lines may be effected (usually thrombocytopenia).  [Barone, 2015]
    • Reticulocyte Count
      • Always reduced.  [Barone, 2015]
    • Blood Type and Crossmatch
    • Peripheral Smear
      • Presence of dysplastic cells or blast cells may suggest leukemia instead!

 

Aplastic Anemia: Treatment

  • Non-severe cases may not require transfusions. Discuss with hematologist.
  • Transfuse Packed Red Blood Cells
    • Transfuse indications:
      • Symptomatic anemia
      • Asymptomatic anemia with Hgb < 8 g/dL [Barone, 2015]
    • Need to be leukoreduced and CMV-negative
    • Consult hematologist prior to transfusing. A period of observation is often used first.  [Barone, 2015]
  • Transfuse Platelets
    • Need to be leukoreduced and CMV-negative
    • Indications:
      • Platelet count < 10,000/microL
      • Platelet count < 20,000 /microL in setting of fever, sepsis, or bleeding
  • Consider bacterial infections, especially if neutropenic!
    • Empiric antibiotics should be given if patient is febrile and neutropenic.
    • Often regimen to include anti-pseudomonal coverage in addition to gram-negative and gram-postivive coverage.
    • If persistent fevers, consider fungal coverage.
  • Other disease specific regimens:
    • Immunosuppressants
    • Matched unrelated donor Stem Cell Transplant

 

References

Barone A1, Lucarelli A2, Onofrillo D3, Verzegnassi F4, Bonanomi S5, Cesaro S6, Fioredda F7, Iori AP8, Ladogana S9, Locasciulli A10, Longoni D5, Lanciotti M7, Macaluso A11, Mandaglio R12, Marra N13, Martire B14, Maruzzi M9, Menna G13, Notarangelo LD15, Palazzi G16, Pillon M17, Ramenghi U18, Russo G19, Svahn J7, Timeus F20, Tucci F21, Cugno C22, Zecca M22, Farruggia P11, Dufour C23, Saracco P18. Diagnosis and management of acquired aplastic anemia in childhood. Guidelines from the Marrow Failure Study Group of the Pediatric Haemato-Oncology Italian Association (AIEOP). Blood Cells Mol Dis. 2015 Jun;55(1):40-7. PMID: 25976466. [PubMed] [Read by QxMD]

Williams DA1, Bennett C, Bertuch A, Bessler M, Coates T, Corey S, Dror Y, Huang J, Lipton J, Olson TS, Reiss UM, Rogers ZR, Sieff C, Vlachos A, Walkovich K, Wang W, Shimamura A. Diagnosis and treatment of pediatric acquired aplastic anemia (AAA): an initial survey of the North American Pediatric Aplastic Anemia Consortium (NAPAAC). Pediatr Blood Cancer. 2014 May;61(5):869-74. PMID: 24285674. [PubMed] [Read by QxMD]

Young NS1, Calado RT, Scheinberg P. Current concepts in the pathophysiology and treatment of aplastic anemia. Blood. 2006 Oct 15;108(8):2509-19. PMID: 16778145. [PubMed] [Read by QxMD]

Guinan EC1. Aplastic anemia: management of pediatric patients. Hematology Am Soc Hematol Educ Program. 2005:104-9. PMID: 16304366. [PubMed] [Read by QxMD]

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Intussusception Discharge

Intussusception Discharge

The Ped EM Morsels have discussed several medical myths (ex, Atropine, Morphine for Appendicitis, IV Fluids for rehydration), but remember that “myths” were not born from madness.  Previously, physicians were not maliciously inventing erroneous plans; they were doing what was deemed most appropriate based on the available information.  This, thus, means that it is incumbent upon all of us to continually reassess management strategies as newer data becomes available.  Along that line of thinking, let us consider the appropriate disposition of a child with intussusception: Intussusception Discharge from the ED to Home.

 

Intussusception Basics

  • Intussusception is the most common cause of gastrointestinal obstruction in children.
  • Abdominal pain is the most common complaint in children with intussusception. [Mandeville, 2012]
  • Once diagnosed, Hydrostatic / Pneumatic Reduction is first choice to treat.
    • Air enema or saline enema success rates reported as 80 to 95%
    • Should not be done if there is concern for bowel perforation.
  • Occasionally, surgical intervention is required if:
    • Evidence of peritonitis / Free air present / Patient clinically unstable
    • Hydrostatic/pneumatic reduction unsuccessful
    • Pathologic lead point present
    • Multiple recurrences of intussusception

 

Intussusception Recurrence

  • Recurrence rates after successful reduction:
    • Overall: 5-15%. [Beres, 2014; Whitehouse, 2010]
    • In the first 24 hours: 2-5%. [Gray, 2014; Chien, 2013]
    • In the first 48 hours: 2-5%. [Gray, 2014; Chien, 2013]
  • The recurrence rates do not differ significantly between those children discharged from the ED and those who were hospitalized. [Beres, 2014; Whitehouse, 2010]

 

Intussusception Disposition

  • Historically, after successful reduction a patient would be hospitalized to monitor for:
    • Possible recurrence
    • Possible complication of the reduction
    • Possible ischemic changes of the intussusceptum via serial exams
  • How long is long enough though? – 6hrs? “Overnight?” 24 hours? 48 hours?
    • The practice variance for disposition amongst hospitals is vast:
      • For patients successfully reduced the percent discharged the same day ranged from 0% to 83.8%. [Rice-Townsend, 2012]
      • Overall rate of same day discharge after successful reduction was 15.2%. [Rice-Townsend, 2012]
  • Based on low recurrence rates and low rates of complications, many are recommending discharge from the ED following successful reduction. [Raval, 2015; Beres, 2014; Whitehouse, 2010]
    • Whitehouse, 2010 proposed discharging patients after successful reduction if:
      • Patient is afebrile
      • Patient is hemodynamically stable
      • Patient is tolerating oral hydration (requires period of observation in the ED).
    • Additional considerations should include:
      • Patient should be pain-free
      • Patient requires good social situation and easy access to transportation

 

Moral of the Morsel

  • There is evidence to support a change in some of our practice… or at least a prospective study evaluating the safety of discharge from the ED .
  • Recurrence happens, but hospitalization does not appear to alter the rate of recurrence or the rate of complications.
  • The management of intussusception is multi-disciplinary and it is necessary for us to understand how the surgeons and radiologists interpret this data.
  • If your local practice is to discharge appropriate patients after successful reduction, ensure you have a system to reinforce appropriate anticipatory guidance and return precautions.

 

References

Raval MV1, Minneci PC2, Deans KJ2, Kurtovic KJ3, Dietrich A4, Bates DG5, Rangel SJ6, Moss RL2, Kenney BD2. Improving Quality and Efficiency for Intussusception Management After Successful Enema Reduction. Pediatrics. 2015 Nov;136(5):e1345-52. PMID: 26459654. [PubMed] [Read by QxMD]

Beres AL1, Baird R2, Fung E3, Hsieh H1, Abou-Khalil M1, Ted Gerstle J3. Comparative outcome analysis of the management of pediatric intussusception with or without surgical admission. J Pediatr Surg. 2014 May;49(5):750-2. PMID: 24851762. [PubMed] [Read by QxMD]

Gray MP1, Li SH2, Hoffmann RG2, Gorelick MH3. Recurrence rates after intussusception enema reduction: a meta-analysis. Pediatrics. 2014 Jul;134(1):110-9. PMID: 24935997. [PubMed] [Read by QxMD]

Chien M1, Willyerd FA, Mandeville K, Hostetler MA, Bulloch B. Management of the child after enema-reduced intussusception: hospital or home? J Emerg Med. 2013 Jan;44(1):53-7. PMID: 22555056. [PubMed] [Read by QxMD]

Rice-Townsend S1, Chen C, Barnes JN, Rangel SJ. Variation in practice patterns and resource utilization surrounding management of intussusception at freestanding Children’s Hospitals. J Pediatr Surg. 2013 Jan;48(1):104-10. PMID: 23331801. [PubMed] [Read by QxMD]

Mandeville K1, Chien M, Willyerd FA, Mandell G, Hostetler MA, Bulloch B. Intussusception: clinical presentations and imaging characteristics. Pediatr Emerg Care. 2012 Sep;28(9):842-4. PMID: 22929138. [PubMed] [Read by QxMD]

Whitehouse JS1, Gourlay DM, Winthrop AL, Cassidy LD, Arca MJ. Is it safe to discharge intussusception patients after successful hydrostatic reduction? J Pediatr Surg. 2010 Jun;45(6):1182-6. PMID: 20620317. [PubMed] [Read by QxMD]

Bajaj L1, Roback MG. Postreduction management of intussusception in a children’s hospital emergency department. Pediatrics. 2003 Dec;112(6 Pt 1):1302-7. PMID: 14654601. [PubMed] [Read by QxMD]

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Microscopic Hematuria

Microscopic Hematuria

Obtaining a urinalysis is often part of the management plan in the Ped ED to screen for a condition.  Often it is obtained to look for possible infection.  Sometimes we are evaluating unusual swelling with concern for proteinuria. What, however, do we need to consider when we encounter Microscopic Hematuria?

 

Hematuria

  • Blood, obviously, should not be in the urine, but it is relatively commonly encountered. [Davis, 2015]
  • Hematuria, strictly defined, is the presence of 5 or more RBCs per HPF. [Massengill, 2008]
    • Officially, this requires three successive samples obtained over several weeks
    • So, keep this in mind as many times the most appropriate next step is to have the urinalysis repeated later by the Primary Physician.
      • The prevalence of asymptomatic microscopic hematuria decreases from ~6% to ~0.5% upon repeating the screening specimen. [Massengill, 2008]
  • It can be further described as:
    • Persistent vs Transient
    • Symptomatic vs Asymptomatic
    • Gross vs Microscopic
      • Gross hematuria, unlike microscopic, is more likely to be associated with an identifiable cause.
      • Gross hematuria considerations = UTI, trauma, nephrolithiasis, coagulopathies, crystalluria, and renal disease.
      • Gross hematuria associated with edema/proteinuria and/or hypertension warrants concern for renal disease, like Post-Infectious Glomerulonephritis. [Davis, 2015]
      • Gross hematuria with abdominal pain and/or rash? Think HSP.
  • It can also be described based on pathologic origin:
    • Glomerular vs ExtraGlomerular
      • Glomerular hematuria
        • RBCs inappropriately cross the glomerular capillary wall.
        • Due to inflammation, structural defects, or toxic effects on nephron.
        • U/A findings – RBC, WBC Casts, dysmorphic RBCs, 2+ or > Proteinuria
        • Urine Protein / Creatinine ratio > 0.2 is suggestive of glomerular source.
      • ExtraGlomerular
        • Bleeding source at any other location of the urinary tract.
        • No Casts, normal RBC morphology, <2+ Proteinuria
  • Different from adults, hematuria in children is often not urologic issue and kids rarely need cystoscopy. [Massengill, 2008]

 

Hematuria: Mimics

  • Before we get carried away with a large work-up for “blood in the urine,” consider…
  • False positive results are common.
  • Substances can alter urine dipstick results:
    • Myoglobin
      • Confirm + Heme result on dipstick with microscopy.
      • + Heme without RBCs? Think Rhabdomyolysis!
  •  Several substances can alter the appearance of the urine, but there is no true blood present:
    • Drugs
      • ex, Nitrofurantoin, sulfonamides, and salicylate
    • Toxins
      • ex, Lead and benzene
    • Foods
      • ex, Beets, food coloring, blackberries, rhubarb, paprika
    • Urate crystals 
      • Often seen in neonates diapers

 

Hematuria: “HEMATURIA” History

  • Important historic factors that should be considered when evaluating hematuria can be recalled with the pneumonic “HEMATURIA.” [Davis, 2015]
    • Headaches
    • Edema
    • Myalgias
    • Arthralgias
    • Time course
    • Urinary symptoms
    • Recent sore throat
    • Infection (ex, UTIs)
    • Abdominal pain

 

Hematuria: Microscopic

  • Microscopic hematuria often generates the biggest questions.
  • First ask, is this Symptomatic or Asymptomatic?
  • Symptomatic Microscopic Hematuria
    • Naturally, requires the greatest attention. [Massengill, 2008]
    • Symptoms are often not specific – i.e., fever, malaise
    • Symptoms may point toward diagnosis – ex, abdominal pain, edema, oliguria
  •  Asymptomatic Microscopic Hematuria
    • Rarely found to have significant renal disease and is often transient.
      • Extensive evaluation is not necessary. [Massengill, 2008]
      • Close follow-up, however, is necessary! [Davis, 2015]
    • Family history is particularly important to help risk stratify these patients.
      • Family history of hematuria or renal impairment?
      • Family history of hearing or ocular abnormalities?
    • Be mindful of concurrent proteinuria, even if asymptomatic!
      • Finding both does not diagnose a pathologic condition, but it is more concerning for a glomerular process. [Massengill, 2008]

 

Hematuria: Initial Evaluation

  1. Obtain microscopy to confirm that it is hematuria.
  2. Evaluate for infection.
  3. Pay attention to RBC morphology and presence of casts or crystals.
  4. Consider close follow-up and further evaluation as outpatient.
    • Repeating test 2 to 3 times over the course of 2 weeks is advocated prior to further testing.
  5. If history or exam inspires you to evaluate further in the ED (ex, edema, hypertension, symptomatic) consider:
    • Bun/Cr
    • Hemoglobin and platelet counts
    • If concern for acute Post-Infectious Acute Glomerulonephritis, consider:
      • ASO titer
      • C3 level
  6. Emergent imaging is usually not required for microscopic hematuria.

 

References

Davis TK1, Hmiel P2. Pediatric Hematuria Remains a Clinical Dilemma. Clin Pediatr (Phila). 2015 Aug;54(9):817-30. PMID: 25253774. [PubMed] [Read by QxMD]
Pade KH, Liu DR. An evidence-based approach to the management of hematuria in children in the emergency department. Pediatr Emerg Med Pract. 2014 Sep;11(9):1-13; quiz 14. PMID: 25296518. [PubMed] [Read by QxMD]

Quigley R1. Evaluation of hematuria and proteinuria: how should a pediatrician proceed? Curr Opin Pediatr. 2008 Apr;20(2):140-4. PMID: 18332708. [PubMed] [Read by QxMD]

Massengill SF1. Hematuria. Pediatr Rev. 2008 Oct;29(10):342-8. PMID: 18829770. [PubMed] [Read by QxMD]
Youn T1, Trachtman H, Gauthier B. Clinical spectrum of gross hematuria in pediatric patients. Clin Pediatr (Phila). 2006 Mar;45(2):135-41. PMID: 16528433. [PubMed] [Read by QxMD]

The post Microscopic Hematuria appeared first on Pediatric EM Morsels.

Microscopic Hematuria

Microscopic Hematuria

Obtaining a urinalysis is often part of the management plan in the Ped ED to screen for a condition.  Often it is obtained to look for possible infection.  Sometimes we are evaluating unusual swelling with concern for proteinuria. What, however, do we need to consider when we encounter Microscopic Hematuria?

 

Hematuria

  • Blood, obviously, should not be in the urine, but it is relatively commonly encountered. [Davis, 2015]
  • Hematuria, strictly defined, is the presence of 5 or more RBCs per HPF. [Massengill, 2008]
    • Officially, this requires three successive samples obtained over several weeks
    • So, keep this in mind as many times the most appropriate next step is to have the urinalysis repeated later by the Primary Physician.
      • The prevalence of asymptomatic microscopic hematuria decreases from ~6% to ~0.5% upon repeating the screening specimen. [Massengill, 2008]
  • It can be further described as:
    • Persistent vs Transient
    • Symptomatic vs Asymptomatic
    • Gross vs Microscopic
      • Gross hematuria, unlike microscopic, is more likely to be associated with an identifiable cause.
      • Gross hematuria considerations = UTI, trauma, nephrolithiasis, coagulopathies, crystalluria, and renal disease.
      • Gross hematuria associated with edema/proteinuria and/or hypertension warrants concern for renal disease, like Post-Infectious Glomerulonephritis. [Davis, 2015]
      • Gross hematuria with abdominal pain and/or rash? Think HSP.
  • It can also be described based on pathologic origin:
    • Glomerular vs ExtraGlomerular
      • Glomerular hematuria
        • RBCs inappropriately cross the glomerular capillary wall.
        • Due to inflammation, structural defects, or toxic effects on nephron.
        • U/A findings – RBC, WBC Casts, dysmorphic RBCs, 2+ or > Proteinuria
        • Urine Protein / Creatinine ratio > 0.2 is suggestive of glomerular source.
      • ExtraGlomerular
        • Bleeding source at any other location of the urinary tract.
        • No Casts, normal RBC morphology, <2+ Proteinuria
  • Different from adults, hematuria in children is often not urologic issue and kids rarely need cystoscopy. [Massengill, 2008]

 

Hematuria: Mimics

  • Before we get carried away with a large work-up for “blood in the urine,” consider…
  • False positive results are common.
  • Substances can alter urine dipstick results:
    • Myoglobin
      • Confirm + Heme result on dipstick with microscopy.
      • + Heme without RBCs? Think Rhabdomyolysis!
  •  Several substances can alter the appearance of the urine, but there is no true blood present:
    • Drugs
      • ex, Nitrofurantoin, sulfonamides, and salicylate
    • Toxins
      • ex, Lead and benzene
    • Foods
      • ex, Beets, food coloring, blackberries, rhubarb, paprika
    • Urate crystals 
      • Often seen in neonates diapers

 

Hematuria: “HEMATURIA” History

  • Important historic factors that should be considered when evaluating hematuria can be recalled with the pneumonic “HEMATURIA.” [Davis, 2015]
    • Headaches
    • Edema
    • Myalgias
    • Arthralgias
    • Time course
    • Urinary symptoms
    • Recent sore throat
    • Infection (ex, UTIs)
    • Abdominal pain

 

Hematuria: Microscopic

  • Microscopic hematuria often generates the biggest questions.
  • First ask, is this Symptomatic or Asymptomatic?
  • Symptomatic Microscopic Hematuria
    • Naturally, requires the greatest attention. [Massengill, 2008]
    • Symptoms are often not specific – i.e., fever, malaise
    • Symptoms may point toward diagnosis – ex, abdominal pain, edema, oliguria
  •  Asymptomatic Microscopic Hematuria
    • Rarely found to have significant renal disease and is often transient.
      • Extensive evaluation is not necessary. [Massengill, 2008]
      • Close follow-up, however, is necessary! [Davis, 2015]
    • Family history is particularly important to help risk stratify these patients.
      • Family history of hematuria or renal impairment?
      • Family history of hearing or ocular abnormalities?
    • Be mindful of concurrent proteinuria, even if asymptomatic!
      • Finding both does not diagnose a pathologic condition, but it is more concerning for a glomerular process. [Massengill, 2008]

 

Hematuria: Initial Evaluation

  1. Obtain microscopy to confirm that it is hematuria.
  2. Evaluate for infection.
  3. Pay attention to RBC morphology and presence of casts or crystals.
  4. Consider close follow-up and further evaluation as outpatient.
    • Repeating test 2 to 3 times over the course of 2 weeks is advocated prior to further testing.
  5. If history or exam inspires you to evaluate further in the ED (ex, edema, hypertension, symptomatic) consider:
    • Bun/Cr
    • Hemoglobin and platelet counts
    • If concern for acute Post-Infectious Acute Glomerulonephritis, consider:
      • ASO titer
      • C3 level
  6. Emergent imaging is usually not required for microscopic hematuria.

 

References

Davis TK1, Hmiel P2. Pediatric Hematuria Remains a Clinical Dilemma. Clin Pediatr (Phila). 2015 Aug;54(9):817-30. PMID: 25253774. [PubMed] [Read by QxMD]
Pade KH, Liu DR. An evidence-based approach to the management of hematuria in children in the emergency department. Pediatr Emerg Med Pract. 2014 Sep;11(9):1-13; quiz 14. PMID: 25296518. [PubMed] [Read by QxMD]

Quigley R1. Evaluation of hematuria and proteinuria: how should a pediatrician proceed? Curr Opin Pediatr. 2008 Apr;20(2):140-4. PMID: 18332708. [PubMed] [Read by QxMD]

Massengill SF1. Hematuria. Pediatr Rev. 2008 Oct;29(10):342-8. PMID: 18829770. [PubMed] [Read by QxMD]
Youn T1, Trachtman H, Gauthier B. Clinical spectrum of gross hematuria in pediatric patients. Clin Pediatr (Phila). 2006 Mar;45(2):135-41. PMID: 16528433. [PubMed] [Read by QxMD]

The post Microscopic Hematuria appeared first on Pediatric EM Morsels.