When Should You Evaluate Lymphadenopathy?

Patient Presentation
A 10-year-old female came to clinic with “swelling in her armpit.” She was healthy except for eczema flares, but noted the swelling about 6 days ago and it is described as somewhat painful. She also had a low grade fever about the same time.
On her review of systems she had no weight loss, night sweats, or malaise. She did have some red bumps on her arm recently that were bigger than her normal eczema flares. She has no recent travel history, she has a pet cat and guinea pigs at school.
The pertinent physical exam shows normal vital signs and growth parameters. She has shoddy anterior and inguinal adenopathy. She has a 1.5 cm solitary left axillary node that is firm, and mobile with minimal overlying induration and pain. She has a mild lichenified rash medially on her elbow that is somewhat excoriated, red and raised appearing. The rest of her examination is normal.
The patient was treated for mild impetigo with Cephalexin antibiotic. After 2 weeks she returned and the axillary lymph node had not decreased in size. She had no fever and the impetigo had resolved.
The work-up at that time included complete blood count which showed a white blood cell count of 14 X 1000/mm2, erythrocyte sedimentation rate of 15 mm/hr and liver function tests which were normal. Additionally she had a tuberculosis skin test placed that was negative. An immunofluorescence antibiody assay eventually returned positive for Bartonella henselae and the diagnosis of Cat Scratch Disease was made.
She was treated with Azithromycin antibiotics and was to return in two weeks for re-evaluation.

Discussion
Cat Scratch Disease is caused by Bartonella henselae, a slow-growing, gram-negative bacillus. It commonly occurs in people younger than 20 years of age. Cats are common reservoirs especially kittens. Cat fleas transmit the organism between cats but there is no known person-to-person transmission.
Diagnosis is generally made by immunofluorescence antibody. Treatment is primarily symptomatic with resolution usually within 2-4 months. Antibiotics may speed resolution, but painful supprative nodes may need drainage for relief.

Almost everyone has a few palpable lymph nodes at any time. Palpable lymph nodes are normal in anterior cervical, axillary and inguinal regions in healthy children.
Lymphadenopathy is enlargement of the lymph nodes beyond this normal state. Practically this is any node >1.0 cm in greatest diameter, but certain nodes should be considered enlarged at different sizes (i.e. epitrochlear nodes > 0.5 cm, inguinal nodes > 1.5 cm, submandibular nodes > 1.5 cm).
The history and physical examination are particularly important in determing the differential diagnosis and ultimately the timing, workup and treatment of lymphadenopathy.

History

  • Duration
    • Short (< 2 weeks) – likely to be infectious
    • Long (> 2 weeks but < 1 year) – likely to be infectious, malignancy, autoimmune, drug reaction
    • Very long (> 1 year) likely to be pathologic but not malignancy
  • Location
    • Localized – likely to be infectious
    • Regional – likely to be infectious
    • Generalized – more likely pathologic (e.g. malignancy, autoimmune, etc.)
    • Head and Neck – likely infectious
    • Mediastinal – likely pathologic
    • Abdominal – likely pathologic
    • Inguinal – likely infectious
  • Associated symptoms – each may be associated with infectious, malignant, autoimmune, or immunodeficiency diseases
    • Pain
    • Fever
    • Weight loss (> 10% over 6 months)
    • Night sweats
    • Pruritis
    • Myalgia/arthralgia
    • Rashes
    • Malaise
  • Other history
      Pets – especially cats for Cat Scratch Disease

    • Travel – including Tuberculosis exposure
    • Possible immunodeficiency such as HIV
    • Family history of similar problems
    • Previous treatments such as antibiotics and how patient responded
    • What do parents think might be going on? What are parents most worried about?

Physical Examination

  • Nodes themselves
    • Location – local, regional, generalized lymphadenopathy
    • Size
    • Character – e.g. firm, rubbery, etc. is subjective and may or may not be helpful
    • Fixed or non-fixed may be more helpful
    • Erythema and tenderness – likely infectious

      Note:
      Generalized, firm, discrete, non-tender, fixed tend to be more ominous causes such as malignancy
      Localized, warm, tender, matted, erythematous – tend to be associated with infections

  • Other Signs
    • Signs of anemia – tachycardia, pale conjunctiva – may be associated with malignancy, autoimmune diseases
    • Dermatological changes – petechiae, bruising, bleeding – may be associated with malignancy
    • Weight/growth – poor growth may be associated with malignancy

The differential diagnosis of lymphadenopathy is large. Common categories include:

  • Infectious
    • Bacterial – Staphylococcus, Streptococcus, Cat Scratch Disease, Toxoplasmosis, Syphilis, Tuberculosis, Atypical mycobacterium, Brucellosis, Tularemia, Leptospirosis

    • Viral – Epstein Barr Virus, Cytomegalovirus, HIV, Rubella, Hepatitis B
    • Fungal – Aspergillosis, Candida, Histoplasmosis
  • Malignant – Leukemia, Lymphoma, Metastatic
  • Autoimmune – Rheumatoid arthritis, Systemic Lupus Erythematosis, Serum Sickness, Sarcoidosis
  • Immunodeficiency – HIV
  • Drug reactions – Phenytoin, Hydralazine, Allopurinol
  • Endocrine – Hyperthyroidism
  • Other benign/pathologic processes – Storage diseases, Embryological cysts

Learning Point
When should lymphadenopathy be evaluated depends on the history, physical examination, differential diagnosis, level of suspicion of serious underlying pathology and the anxiety of the patient, parent and health care provider. There is not one single approach.

A general approach is outlined below.


Figure 14 – Diagram showing an algorighm for evaluation of lymphadenopathy

Patients generally should be considered for referral if:

  • Unexplained generalized lymphadenopathy

  • Any supraclavicular or popliteal node that is palpable
  • Significant constitutional symptoms
  • Hepatic or splenic enlargement
  • Anemia or bleeding
  • Unresponsiveness to antibiotic treatment
  • Not decreasing in size after appropriate period of observation

The evaluation of lymphadenopathy may include a number of tests as indicated by the history, physical examination, differential diagnosis, index of suspicion and the anxiety of the patient, parent and health care provider.
These may include:

  • Laboratory – complete blood count with differential, erythrocyte sedimentation rate or C-reactive protein, lactate dehydrogenase, uric acid, liver function tests
  • Purified Protein Derivative skin test for Tuberculosis
  • Viral titers
  • Other titers – Toxoplasmosis, Bartonella henselae
  • Chest radiograph
  • Consultation with surgery, oncology, rheumatology, infectious disease, radiology
  • Biopsy

Questions for Further Discussion
1. What are the indications for a fine needle aspiration?
2. What are the indications for an incisional or excisional biopsy?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Cat Scratch Disease.

Morland B. Lymphadenopathy. Arch Dis Child 1995;74(5):476-479.

Perkins SL, Segal GH, Kjeldsberg CR. Work-up of Lymphadenopathy in Children. Sem Diag Pathol. 1995;12(4):284-287.

Twist CJ, Link MP. Assessment of Lymphadenopathy in Children. Ped Clin North Amer. 2002:49;1009-25.

American Academy of Pediatrics. Cat-Scratch Disease, In Pickering LD, ed. Red Book: 2003 Report of the Committee on Infectious Diseases. 26th edit. Elk Grove Village, IL: American Academy of Pediatrics; 2003;232-234.

Umapathy N, De R, Donaldson I. Cervical Lymphadenopathy in Children. Hospital Medicine. 2003;64(2):104-7.

Leung AKC, Robson WLM. Childhood Cervical Lymphadenopathy. J Pediatr Health Care. 2004;18:3-7.

Nield LS. Lymphadenopathy in Children: When and How to Evaluate. Clin Pediatr. 2004;43:25-33.

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
April 25, 2005

What are the Grades for Ankle Sprains?

Patient Presentation
A 19-year-old female came to to the emergency room complaining of spraining her right lateral ankle while playing basketball one hour ago. She has a history of multiple ankle sprains in the past. She was going up to catch a ball and inverted her foot after striking the foot of another player.
She states that it immediately swelled differently than previous sprains and she is unable to walk which is also unusual from her other sprains. She also says “it just feels different.”The past medical history reveals that she is otherwise a healthy active athlete.
Her review of systems shows no other injuries.
Her pertinent physical exam shows her entire right ankle is markedly swollen with the lateral > medial aspect. She is markedly tender over the anterior and lateral ligaments of the lateral ankle (i.e. anterior talofibular ligament and fibulocalcaneal ligament). She has a positive anterior drawer sign.
The radiologic evaluation showed no associated fracture.
The patient was diagnosed with a grade 3 ankle sprain of the anteriolateral ligament and grade 2 ankle sprain of the fibulocalcaneal ligament.
Her clinical course was uncomplicated. She placed ice on it and elevated her ankle at every opportunity. She was placed into an air cast immobilization device with crutches for mobility for 6 weeks. After that time, she underwent aggressive, supervised physical therapy to increase range of motion and muscle strengthening to facilitate proprioception sense in the ankle joint.
She was able to run without hesitation or pain after 5 months and was returned to sports.

Discussion
Ankle injuries are one of the most common sports-related injuries. Ankle fractures are more common in young children and preadolescents because the ligaments are much stronger than the bones or growth plates in this area. Ankle sprains are more common in adolescents and adults as the reverse is true.

Ankle sprains result from force around the ankle that exceeds the tensile strength of the supporting ligaments of the ankle but less than that which breaks the ankle bones.

The ankle capsule-ligament complex has 5 primary ligaments:

  • Medial ankle – the deltoid is the strongest ligament in the ankle and has two parts:
    • Superficial deltoid ligament – runs from the medial malleolus to the calcaneus posteriorly
    • Deep deltoid ligament – runs from medial malleolus to the talus
  • Lateral ankle – these ligaments act like 3 guidewires to the lateral ankle and are generally injuried in the following order:
    • Anterior talofibular ligament – runs anteriorly to the lateral malleolus

    • Fibulocalcaneal ligament- runs laterally to the lateral malleolus
    • Posterior talofibular ligament – runs posterior to the lateral malleolus

Most ankle injuries involve an inversion of the ankle. The ability to walk generally excludes a fracture. People with third-degree ankle sprains often give a history of an audible snap.
The physical examination revels intact skin with swelling. Pain upon motion is common as is point tenderness over the ligaments. An anterior drawer sign indicates anterior talofibular ligament rupture.

Luckily most ankle sprains are self-limited and can be treated conservatively with
ice, rest, immobilization and elevation being early mainstays. Ice and elevation help to decrease the swelling and reduce the danger of long-term postswelling fibrosis.
Once acute swelling and pain are reduced, therapy to increase the range of motion should be instituted to prevent recurrence of an ankle sprain. Desired range of motion is 90 degrees plantar flexion and 10-15 degrees of dorsiflexion.
Muscle strengthening also helps. Regular walking is often all that is needed. Additionally, specific muscle strengthening and proprioreceptive exercises may be done by the patient themselves or under the direction of a physical therapist.

Surgery is indicated for complete rupture of the distal talofibular ligament. Surgery is also indicated if the deltoid ligament is entrapped in the joint itself. Surgery for anterior talofibular ligament ruptures does not improve the outcome for most patients. Surgery indications for patients with with double ruptures (i.e. anterior talofibular and fibulocalcaneal ligament ruptures) is debated.

Patients can return to sports when they have no limp, hesitation or pain. Lack of swelling in the ankle is not a good indicator of readiness to return. Protective strapping and/or supportive footwear may help reduce recurrance rates.

Learning Point
The staging of ankle sprains is:

  • Grade 1 – symptomatic stretching of the ligaments without rupture or failure of the ligament fibers
  • Grade 2 – partial rupture or failure of the ligament fibers
  • Grade 3 – complete rupture or failure of the ligament fibers

Ankle sprains are primarily staged or graded clinically. The amount of swelling and bruising and the clinical stability of the ankle determines whether the ankle ligaments are stretched without significant tear, partially torn, or completely torn.

Questions for Further Discussion
1. How useful is magnetic resonance imaging in ankle sprains?
2. What are the indications for an ankle arthrogram?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Sprains.

Fleisher GR, Ludwig S. Synopsis of Pediatric Emergency Medicine. Williams and Wilkins. Baltimore, MD. 1996:123-126.

Foster R. Acute Ankle Sprains. eMedicine.
Available from the Internet at http://www.emedicine.com/orthoped/topic373.htm (rev. 7/20/04, cited 3/28/05).

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
April 11, 2005

Is this Kawasaki Disease?

Patient Presentation
A 6-year-old male came to clinic with new rash and a 5 day history of recurrent fevers. The morning of day 1 he woke up with right eye conjunctivitis that was non-purulent. A family member was a healthcare provider and began him on antibiotic ophthalmic ointment. That evening his fevers began and were 103.5 degrees F axillary. They responded to acetaminophen and ibuprofen but recurred every 4 hours.
On day 2, he was seen in clinic because of the fever, sore throat, mild abdominal pain and a sibling who was being treated for strep throat. His lips were noted to be slightly dry but not cracked, the papillae of the tongue were slightly prominent. He also had shotty cervical adenopathy. The rapid strep test was negative, and he was diagnosed with a viral syndrome.
On day 3, his left eye also had non-purulent conjunctivitis and his fevers continued.
On day 4, his fevers continued as did his conjunctivitis and dry lips. On day 5 he broke out in a rash on his trunk, palms and soles.
The past medical history revealed him to be a healthy child.
The review of systems showed he had recently travelled within the U.S. and family members were sick with strep throat or bronchitis. He inconsistently complained of photophobia and also a sore foot. He had no other medications.
The pertinent physical exam showed him to be tired appearing with a fever to 39.5 degrees C. His eyes showed scleral and palpebral injection and increased tearing without exudate. His lips were dry without cracking or bleeding. Posterior pharynx was quite red, but without ulcers, petechiae or exudate present. Tongue papillae were prominent. Tympanic membranes were normal. He had general anterior cervical adenopathy and a 1 cm anterior cervical node on the left side. His skin showed a red, macular, blanching rash, that was slightly lacy appearing on his trunk, arms, legs, palms and soles.
His heart, lung, abdominal, genital and extremity examinations were normal.
His laboratory evaluation included a hemoglobin = 14.4 mg/dl, hematocrit = 38%, platelets = 188 x 1000/mm2, WBC = 7.4 x 1000/mm2 with 924 bands, C-reactive protein = 2.51mg/dl and ESR = 28 mm/hr.
The diagnosis of a febrile illness and possible Kawasaki Disease was made. The plan was to follow him clinically and consider beginning intravenous gamma globulin. His antibiotic ointment was also stopped.
The patient’s clinical course the following day (day 6), showed him to be having fevers around 102 degrees F axillary, his rash was also fading slightly. That night he had two drenching night sweats, but no fever was documented at that time. The plan was to continue to monitor him and treat
On day 7, his fevers were around 100-101 degrees F axillary. That night he also had another drenching night sweat.
On day 8 he returned to clinic, having had no fever for ~20 hours. On physical examination he was still tired appearing with bilateral conjunctivitis, a 1 cm anterior cervical node, dry lips, and prominent tongue papillae. The rash was gone.
A full work-up to decide if he needed intrvenous gamma globulin was made. Laboratory testing and consultation with cardiology and infectious disease specialists were obtained concurrently. The laboratory evaluation revealed hemoglobin = 13.9 mg/dl, hematocrit = 39%, platelets = 332 x 1000/mm2, WBC = 7.1 x 1000/mm2 with 144 bands, C-reactive protein = 1.1mg/dl and ESR = 30 mm/hr. Urinanalysis was normal. A chest radiograph and electrocardiogram were normal.
It was the opinion of the consultant specialists and the general pediatrician that this was unlikely to be Kawasaki Disease because the fevers were decreasing and the laboratory evaluation showed decreased markers of inflammation. Therefore, he was sent home with a diagnosis of an unknown viral syndrome to be monitored and again return if the symptoms worsened or returned.
His final viral culture for adenovirus, influenza virus, parainfluenza virus, respiratory syncytial virus as well as a blood and urine cultures. did not grow an organism. He remained fever free with resolution of his symptoms over the next 3 days. He did not have any later symptoms such as peeling fingers or toes.

Discussion
Kawasaki Disease (KD) is an acute, self-limited vasculitis of unknown etiology. It was first described in Japan in 1967 by Tomisaku Kawasaki. It occurs in children of all races and more commonly occur more in late winter and spring months. Boys have it more commonly than girls and ~75% are in children < 5 years old.
The etiology is unknown but data strongly suggests an infectious cause or trigger of the patient’s immune system.

KD is is defined as:

  • Fever of at least 5 days

  • Plus 4 or more of the following:
    • Polymorphous exantham

    • Bilateral bulbar conjunctival injection without exudate
    • Changes in lips and oral cavity – erythema, cracked lips, strawberry tongue, diffuse injection
    • Cervical lymphadenopathy – more than 1.5 cm, usually unilateral
  • Exclusion of other diseases with similar findings
    • Viral infections – especially adenovirus, entervirus, Epstein-Barr virus and measles

    • Scarlet fever
    • Staphylococcal scalded skin syndrome
    • Toxic Shock Syndrome
    • Bacterial cervical lymphadenitis
    • Drug hypersensitivity reactions
    • Stevens-Johnson syndrome
    • Juvenile rheumatoid arthritis
    • Rocky Mountain spotted fever
    • Leptospirosis
    • Mercury hypersensitivity reaction

Coronary artery aneurysm or ectasis occurs in 15-25% of untreated patients which can lead to ischemic heart disease, myocardial infarction, and possibly death.

As this constellation of symptoms is commonly seen, simple laboratory investigations are undertaken. Laboratory findings associated with KD include:

  • Leukocytosis with neutrophilia and immature forms

  • Elevated C-reactive protein
  • Elevated erythrocyte sedimentaiton rate
  • Thrombocytosis after week 1
  • Sterile pyuria

Treatment for KD involves giving intravenous gamma globulin and aspirin (or other anti-platelet medications) plus follow-up with echocardiograms.

Learning Point
Some patients do not fulfill the full criteria for KD and/or have unusual presentations of the findings. The American Heart Association states that patients with incomplete KD are those patients who “???lack sufficient clinical signs of the disease to fulfill the classic criteria; they do not demonstrate atypical clinical features.” They argue that ‘atypical KD’ should be “??? reserved for patients who have a problem, such as renal impairment, that generally is not seen in Kawasaki disease.” Suspected incomplete KD often makes healthcare providers and families very uncomfortable because one is balancing the risks of potentially serious cardiac morbidity and mortality against the risks of intravenous gamma globulin (i.e. potential anaphylaxis) that may not even be needed. In 2004 the American Heart Association released a scientific statement with an algorithm outlining the evaluation of suspected incomplete KD.
The algorithm outlines when to obtain laboraory tests, cardiac echocardiogram and subspecialty consults.

Algorithm for the Evaluation of Incomplete Kawasaki Disease is available from the American Heart Association.

The current patient’s symptoms were consistent with incomplete KD. He had the criteria for fever and exclusion of other diseases. He had the rash and conjunctivitis. But, he only had dry lips, and papillae on his tongue were prominent. Neither finding was described as classic for KD. He also did not have lymphadenopathy that was sufficiently large enough to meet criteria. He was followed closely and his work-up generally followed this algorithm. Luckily this patient did not have KD as the fevers decreased, the laboratory evaluation showed decreased inflamamtion markers and during follow-up he did not show other symptoms. The etiology of this patient’s symptoms was not identified.

Questions for Further Discussion
1. What other clinical findings are associated with KD?
2. What other laboratory findings are associated with KD?
3. What are the criteria for high dose or low dose aspirin therapy for patients with KD?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Kawasaki Disease.

Newberger JW, Takahasi M, Gerber MA, et. al. Diagnosis, Treatment and Long-term Management of Kawasaki Disease. Circulation 2004;110:2747-2771. Available from the Internet at: Available from the Internet at: http://circ.ahajournals.org/cgi/content/full/110/17/2747 (cited 3/28/05).

Scheinfeld NS, Silverberg N, Jones EL. Kawasaki Disease. eMedicine.
Available from the Internet at http://www.emedicine.com/ped/topic1236.htm (rev. 6/6/03, cited 3/28/05).

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
April 11, 2005

What is the Most Effective Treatment for Primary Nocturnal Enuresis?

Patient Presentation
A 7.5-year-old male comes to clinic because of enuresis.
He wets 5 nights out of the week and has never been dry at night in the past. He was toilet trained at 3.5 years for bowel and daytime bladder with no difficulty. He voids 5 times/day.
He restricts fluids after mealtime at night. He takes no medications and is a second grader doing well.
His past medical history shows he is healthy with no other complaints.
For the family history his mother says that father denies bedwetting problems but that dad’s brother had problems.
The review of systems reveals no frequency, urgency, pain, daytime urinary problems such as stream problems, incontinence, or dribbling. He also has no stooling problems and no developmental/neurological problems.
The pertinent physical exam shows normal growth. His abdominal, rectal and genitourinary examinations are normal. Additionally his back shows no dimples or abnormal hair patterns. His neurological examination is normal including bilateral cremasteric reflexes and anal winks.
The laboratory evaluation included a urinalaysis and urine culture which also were normal.
The diagnosis of primary nocturnal enuresis was made. The family was counseled regarding the unlikelihood of an organic underlying cause of the enuresis and told his enuresis was most likely due to neurodevelopmental maturation.
They were counseled as to the natural history and treatment options. The boy was very motivated to try to become dry at night and a bed alarm system was prescribed. He was to return to clinic after two weeks of using the alarm.

Discussion
Enuresis comes from the Greek – Enourein – to void urine. It functionally means voiding urine where it should not be urinated either day or night. In contrast, nocturia means voiding urine at night in the proper place and its cause is commonly habitual.
Primary Nocturnal Enuresis (PNE) is persistent bedwetting in the absence of any urologic, medical or neurological anomaly in a child beyond the age when over 75% of children are normally dry. A practical definition of PNE
is bedwetting more than 2x/month after the age of 6 years for females or after 7 years for males.

PNE is very common. Depending on the study, approximately 7% of 7 years olds have PNE. PNE in the adult population is about 0.5-1%, again depending on the study. It is more common among males and also appears to have a genetic predisposition as the incidence increases with the number of parents who also had PNE and in monozygotic twins.

The exact cause of PNE is not entirely know but appears to be a neurodevelopmental problem which is probably multifactorial.

  • Psychosocial – no relationship to social background, life stresses, family constellation, or number of residencies has been shown. Enuresis may be a symptom seen in people with underlying psychological problems but is not a psychological problem itself.
  • Caffeine – has a well-documented diuretic activity. Generally enuretics ingest a moderate amount of caffeine.
  • Genetics – associated with the genes 13q and 12q (possibly 5 and 22 also). As noted above there is in increased incidence in families and monozygotic twins.
  • Anti-diuretic hormone (ADH) production – Normally ADH increases at night. This increase doesn’t occur in child enuretics, but does occur in adolescent enuretics. The diurnal change may not be seen until ~age 10.
  • Sleep disturbance – Currently data cannot support that there is a definitive sleep disturbance, i.e. enuretics sleep “harder” or are more difficult to wake. However, there is some evidence that the change in ADH may also be linked to some difficulties in light sleep to awake transition. For instance, enuretics do not awaken to sound as easily as non-enuretics. This may be related to changes in delta wave activity between enuretics and non-enuretics.
  • Decreased bladder capacity – Current data does support increased bladder tone in some enuretics, which functionally would decrease bladder capacity.

Prognosis of PNE is excellent with ~15% of enuretics having spontaneous resolution per year.

Learning Point
The most effective treatment for PNE depends on the particular child. The most important variables being the age of the child, and the motivation of the child and family.
All treatment options should include discussion of the cause and natural history. PNE is not the child’s fault but some studies report that 20-36% of parents punish their children for bed-wetting. Punishment has been shown to decrease the success of treating the problem. Doing nothing also is always an option as the spontaneous resolution rate is approximately 15% per year and the child may truly outgrow the problem.

Other treatment options include

  • Bed Alarms – These have the highest success rate at 75-85% with only 10-20% relapse. Retreatment has even higher success rates. These work by conditioning where the child learns to waken to the urge to urinate.
    Most children are generally dry in 6-8 weeks. Use of the alarm can stop after 1 month of being continually dry. This usually takes 2-3 months total of using the alarm.
    Realistic goals should be set such as only waking to the alarm the first week, waking and getting up without help the second week, etc.
    Success is measured by smaller and smaller urine puddles before the first dry night. The cost is ~$50-75. The side effects are the distruptions of noise waking family members, having to wake up/change bedclothes, etc.

  • Medication – These generally work well while the medication is being taken but the relapse rate is high once the medications are stopped. The medications also may have side effects.
    • DDAVP (i.e. ADH or Desmopressin) works by increasing urine concentration and decreasing volume. It has a ~22% long term success rate. It is often very good for short term use such as sleep overs or camp. The cost is approximately $50-150 per month.
      Oral medication dosing is 0.2 milligrams at bedtime. This may be increased to 0.6 milligrams.
      Intranasal medication is also available.
      Side effects include possible water intoxication and some people recommend no more than 8 ounces of fluid to be drunk when DDAVP has been taken.

    • Oxybutynin chloride is an anticholinergic, antispasmodic used to decrease contractions.
      The success rate is 33% for polysymptomatic nocturnal enuresis while on the medication. It costs ~$10 per month.
      Oral dosing is 5 milligrams twice a day which may be increased to 20 milligrams a day.

    • Imipramine (Tofranil) is a tricyclic Antidepressant with anticholinergic properties that relax the detrusor muscle and increase the tone of the bladder neck. It has a small therapeutic window and can cause death with an overdose.
      It is generally used when co-morbid conditions exist such as attention deficit disorder or depression. Success rates are 10-60% and the relapse rate is ~90%.
      The cost is $8 per month.
  • Simple Behavioral Interventions such as sticker charts may be useful when used with alarms or other treatments. By themselves they have an 18% success rate. Overlearning (i.e. giving children extra fluids at bedtime after successfuly becoming dry using the alarm system) decreases the relapse rate of bed alarms.
  • Complex Behavioral Interventions such as dry bed training may or may not be helpful.
  • Psychotherapy – enuresis is a symptom not a cause of psychiatric problems. Treatment should be directed toward underlying psychological problems and data does not support this as primary treatment for enuresis.

Questions for Further Discussion
1. Whaat are the causes of diurnal enuresis?
2. What are the treatment options for diurnal enuresis?
3. What questions are important in the history?
4. What areas of the physical examination are important and why?

Related Cases

To Learn More

To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Bedwetting (Enuresis).

Neveus T, Lackgren G, Tuvemo T, Hetta J, Hjalamas K, Stenberg A. Scand J Urolo Nephrolo Suppl 2000;206:1-44.

Jalkut MW, Lerman SE, Churchill BM. Enuresis. Ped Clin North America 2001;48: 1461-1488.

Thiedke, CC. Noctural Enuresis. American Family Physician. 2003;67;1499-106, 1509-10.

Glazener CMA, Evans JHC, Peto RE. Alarm Interventions for Noctural Enuresis in Children. Cochrane Database of Systematic Reviews. Available from the Internet at http://www.cochrane.org/cochrane/revabstr/AB002911.htm (rev.2/26/05, cited 3/24/05).

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
April 4, 2005