What is the Current Treatment for Uncomplicated Urethritis?

Patient Presentation
A 15-year-old previously healthy male comes to the clinic complaining of “somthing blocking my urine” occurring daily for the past two months. He describes it as more discomfort than pain. There is occasionally burning with urination. There is no other pain or discomfort.
On his review of systems he denies discharge, sores, lesion, fever, or hematuria. There is no history of conjunctivitis, joint pain or catheterization in the past.
His social history shows his last sexual activity was 4 months previous. He has had 2 lifetime partners and uses condoms sporatically.
His pertinent physical examination reveals he is afebrile with normal vital signs. His genitourinary examination reveals a circumcized male, Tanner stage 5. His testes are both in the scrotal sack without masses. His penis also has no masses. He states he has slight internal tenderness to palpation approximately 1 cm proximal to the corona. There is no deformity of the penis. He has no rashes, skin lesions or musculoskeletal abnormalities.
The laboratory evaluation shows a normal urinanalysis. Urethal cultures for Chlamydia trachomatis and Neisseria gonorrhoeae were sent. He was sent to the laboratory for Syphilis, HIV and Hepatitis B which were not completed because he left.
A presumed diagnosis of a sexually transmitted infection was made and he was treated with one dose of Azithromycin and Rocephin. His culture for chlamydia later was positive and he was followed-up by the public health department.

Discussion
Sexually transmitted infections (STIs) are the most frequent cause of genital related complaints in teenagers. Adolescents are at greater risk for STIs because they frequently have unprotected intercourse, are more susceptible to infection biologically, are engaged in more partnerships, and face multiple obstacles to utilization of health care. All adolescents in the United States can consent to the confidential diagnosis and treatment of STIs with few exceptions. Medical care for STIs can be provided to adolescents without parental consent or knowledge.

Urethritis is caused by an infection characterized by urethral discharge of mucopurulent or purulent material and sometimes by dysuria or urethral pruritis. Asymptomatic infections are common. The common pathogens are Neisseria gonorrhoeae and Chlamydia trachomatis.

Urethritis should be documented on the basis of any of the following signs:

  • Mucopurulent or purulent discharge.

  • Gram stain of urethral secretions demonstrating >5 WBCs per oil immersion field. The gram stain is the preferred rapid diagnostic test.
  • Positive leukocyte esterase test on first-void urine or microscopic examination of first-void urine demonstrating >10 WBCs per high power field.

Patients should be treated for both infections because of the high rate of co-infection if diagnostic tools (e.g., a gram stain and microscope) are unavailable or urethritis cannot be documented and the patient is at high risk of infection and unlikely to return for follow-up. Non-gonococcal urethritis is diagnosed if gram-negative intracellular diplococci cannot be identified on urethral smears.
If none of these criteria is present, then treatment should be deferred, and the patient should be tested for N. gonorrhoeae and C. trachomatis and followed closely if test results are negative. If the results demonstrate infection with either N. gonorrhoeae or C. trachomatis, the appropriate treatment should be given and sex partners referred for evaluation and treatment.
Common etiologies for non-gonococcal, non-chlamydial urethritis include Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis and Herpes simplex.

Chlamydia trachomatis is an obligate intracellular bacteria. It is one of the most common reportable sexually transmitted infections in the US, especially in teens and young adults. Genital infection in adolescents is sexually transitted but the possibility of sexual abuse should be considered in prepubertal children. The incubation period is variable but is usually at least 1 week. Testing for Chlamydia usually is done by tissue culture or detecting chlamydial antigen. Antigen testing of urethal, endocervical, or conjunctival swab specimens are common. Additionally, polymerase chain reaction and ligase chain reactions tests are useful for evaluating urine specimens. Positive antigen tests need to have a second test confirm the diagnosis because of the potential adverse implications of a false-positive test.
Patients do not need to be retested after completing treatment unless symptoms persist or reinfection is suspected.

Learning Point
Uncomplicated chlamydial genital tract infection in adolescents or young adults can be treated by:

Recommended Regimens:
Azithromycin 1 g orally in a single dose
OR
Doxycycline 100 mg orally twice a day for 7 days.

Alternative Regimens:

Erythromycin base 500 mg orally four times a day for 7 days
OR
Erythromycin ethylsuccinate 800 mg orally four times a day for 7 days
OR
Ofloxacin 300 mg twice a day for 7 days
OR
Levofloxacin 500 mg once daily for 7 days
Note: Doxycycline and ofloxacin are contrindicated during pregnancy.

Patients should be instructed to abstain from sexual intercourse until 7 days after therapy is initiated. Patients should refer for evaluation and treatment all sex partners within the preceding 60 days. Because a specific diagnosis may facilitate partner referral, testing for both gonorrhea and chlamydia is encouraged.

Uncomplicated gonococcal infections of the cervix, urethra and rectum may be treated by:

Recommended Regimens:

Cefixime 400 mg orally in a single dose
OR
Ceftriaxone 125 mg IM in a single dose
OR
Ciprofloxacin 500 mg orally in a single dose*
OR
Ofloxacin 400 mg orally in a single dose*
OR
Levofloxacin 250 mg orally in a single dose*

*These medications have specific uses. Additional information should be obtained from the Centers for Disease Control prior to using these regimens (see To Learn More below).

Questions for Further Discussion
1. What are the current options for male STI/birth control?
2. Potentially, how could a latex-allergic patient use a latex condom?
3. What STIs are considered reportable to public health officials?

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: Sexually Transmitted Diseases (STDs)

Centers for Disease Control. Morbity and Mortality Weekly Report. Sexually Transmitted Diseases Treatment Guidelines 2002. 2002;51:RR-6. Available from the Internet at: http://www.cdc.gov/STD/treatment/TOC2002TG.htm (rev. 5/10/02, cited 11/8/04)

American Academy of Pediatrics. Chlamydia trachomatis and Gonococcal Infections. 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;238-243, 285-291.

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

Date
November 29, 2004

What Causes Chronic Chest Pain?

Patient Presentation
An 8-year-old male came to clinic complaining of left sided intermittent chest pain for 2 months. The pain is in the anterior or slightly lateral chest. It lasts for ~2-3 seconds coming on abruptly and then leaving abruptly. It occurrs at any time including rest or mild exercise (like walking) but not during sleep. The episodes happen 3-4 times/week and ~ 1-3 times/day. There was no radiation, palpitations, racing heart, shortness of breath, dizziness or fainting. The episodes possibly occurr with inhalation. He is alert during the episodes and they frightened him at first but now they are just bothersome.
His past medical history reveals that he has attention deficit disorder for which he was begun on a long acting stimulant medication about 2 months ago. He had no recent illnesses.
His family history reveals no hypercholesterolemia and a grandfather with myocardial infarction after age 50.
On physical examination his weight and height are normal. Pulse = 72, blood pressure = 92/65. His cardiac examination shows a normal S1, S2, no murmurs. He has no jugular venous distention and normal cardiac waves in his neck. No bruits are heard in the neck or abdomen. Lungs are clear. There is no organomegaly. Peripheral pulses in the upper extremities are equal to the lower extremities in intensity and timing. His nailbeds showed no clubbing or cyanosis.
Laboratory evaluation of an electrocardiogram was normal.
A clinical diagnosis of precordial catch syndrome was made. The patient was instructed to maintain a symptom diary and was to report any changes especially if there was a change in the character, intensity, location, or associated symptoms.

Discussion
The cause of precordial catch syndrome (Texidor’s twinge or a stitch in the side) is unknown but it is a benign illness with no significant side effects. It usually occurs in teens and pre-teens. It has a sudden onset of intense, sharp pain in the chest or back usually with inhalation. It can occur for a few seconds to minutes and generally resolves spontaneously. It is not associated with exertion.
Several episodes may occur per day and the frequency of the episodes decreases with time.

Stimulant medication for Attention Deficit Disorder has some potential side effects. The most common ones are anorexia, weight loss and sleep disturbances. Additionally, stimulant medication may also potentially cause the unmasking of tic disorders or lower seizure thresholds. Tachyarrhythmias can be seen with stimulant medication but by themselves generally do not cause chest pain. Tachyarrhythmias also usually respond to decreasing the medication dosing or interval. Other possible side effects include rash, nausea, emesis, abdominal pain, changes in blood pressure, restlessness, headaches, fever, tremor, mood changes, abnomral liver function tests and scalp hair loss.

Learning Point
The differential diagnosis of chest pain in a child is very different then that of an adult. Chest pain is more often a presenting symptom of a pulmonary or musculoskeletal problem in children rather than a cardiac problem.
The differential diagnosis of chest pain may include:

  • Cardiac

    • Ischemic ventricular dysfunction
      • Hypertrophic obstructive cardiomyopathy
      • Severe pulmonic stenosis
      • Severe aortic stenosis
      • Mitral valve prolapse
      • Myocardial infarction
      • Aortic aneurysm or dissection
      • Anomylous coronary arteries
      • Kawasaki disease
    • Inflammatory conditions
      • Myocarditis
      • Pericarditis
      • Kawasaki disease
      • Postpericardiotomy syndrome
    • Arrhythmias
      • Supraventricular tachycardia
      • Premature ventricular tachycardia
  • Gastrointestinal

    • Esophageal foreign body
    • Gastroesophageal reflux
  • Hematologic/Oncologic

    • Tumors
    • Sickle cell disease with acute chest syndro,e
  • Infections

    • Herpes zoster
    • Coxsackie virus with pleurodynia
  • Musculoskeletal

    • Musculoskeletal trauma
    • Costochondritis
    • Strain – overuse including coughing
  • Pulmonary

    • Pneumonia
    • Pleuritis
    • Spontaneous pneumothorax/pneumomediastinum
    • Asthma
    • Pleural effusion
    • Pulmonary embolism
  • Psychogenic

    • Anxiety
    • Hyperventilation
    • Drug abuse
    • Conversion symptoms
    • Depression
    • Somatization
  • Other

    • Breast tenderness

This child had an electrocardiogram performed because of the timing of initiation of stimulant medication and the chest pain. The electrocardiogram was normal and although the patient was somewhat young, he had a history that was consistent with precordial catch syndrome. The family was reassurred that it was unlikely there was significant underlying pathology as a cause of this child’s chest pain. They were asked to monitor him closely and return if any changes did occur in the future.

Questions for Further Discussion
1. How common is a myocardial infarction in a healthy child?
2. What health problems would increase the likelyhood of a myocardial infaction for a child?

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: Chest Pains.

Park MK. Pediatric Cardiology for Practitioners. 3rd edition. Mosby, St. Louis, MO. 1996;443-451.

Gunn VL, Nechyba C. The Harriet Land Handbook. 16th edition. Mosby, St. Louis, MO. 2002:756.

Woodhead JC. Pediatric Clerkship Guide. Mosby., St. Louis MO, 2003. pp. 183-185.

Cincinnati Children’s Hospital. Chest Pain. Available from the Internet at: http://www.cincinnatichildrens.org/health/heart-encyclopedia/signs/chest.htm (rev.2004, cited 11/1/04)

Perry P, Kuperman S. Attention-Deficit Hyperactivity Disorder Pharmacotherapy. Available from the Internet at: http://www.vh.org/adult/provider/psychiatry/CPS/39.html (rev. 5/04, cited 11/1/04)

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

Date
November 22, 2004

What Causes Different Colored Stool ?

Patient Presentation
A 2.5-year-old boy is brought to the clinic because of flecks of blood in his stool. He had two stools this morning that had red colored specks mixed throughout the stool. There were previously normal bowel movements and there has been no mucous in the stool. He has no recent painful or large bowel movements and he has been playing, eating and acting normally. His family history and review of systems are negative. On physicial examination his abdomen is soft and non-tender with no organomegaly and normal bowel sounds. His anus shows normal tissue without fissures. His genitourinary examination is normal. The laboratory evaluation showed the stool to have 1-2 mm bright red speaks throughout the formed stool. Hemoccult was negative. With further questioning, the mother remembers the boy coloring yesterday. During clean-up she wasn’t able to find all the crayons including a red one. A clinical diagnosis of red crayon ingestion was made. The mother is told that the flecks will clear with additional bowel movements. She is instructed to monitor the boy and call if any problems arise.

Discussion
Most stool color changes are harmless. They often are due to eating particular food or drugs. The changes can also be caused by dyes in foods such as brightly colored breakfast cereal or children’s art supples such as non-toxic crayons, markers, and paint. Usually parents can be reassurred that that once the child stops ingesting the offending agent, the stool will return to normal in a short time. A patient or caregiver factitious disorder can also present with different colored stools because of ingested agents or colorings added to the stool.

Sometimes infections or other medical problems cause changes. It is important to exclude potential problems such as upper or lower gastrointestinal bleeding as the cause of a red stool. Rectal fissures caused by hard stools are a common cause of “bloody stools.” Blood from a rectal fissure is usually streaked on the stool, diaper or underpants and not mixed in the stool.

Learning Point
The causes of stool color changes are listed below by body/cell contents, diseases, drugs, foods, infections and other causes.

  • Red/Pink Stool

    • Blood
    • Diazepam syrup
    • Ampicillin
    • Viprynium
    • Phenophthalein
    • Red Jell-O
    • Dioralyteoral rehydration solution
  • Yellow Stool
    • Normal in formula-fed babies
  • Green/Greenish Gold Stool
    • Normally in fully breastfed babies
    • Stomach infection
  • Black Stool
    • Blood
    • Iron
    • Pepto-Bismol
    • Black licorice
    • Blueberries
    • Green-leafy vegetables
    • Lead
    • Charcoal
    • Coal
    • Dirt
  • White/Clay Colored Stools
    • Malabsorption
    • Biliary system blockage
    • Barium
    • Aluminum Hydroxide

Questions for Further Discussion
1. What are common causes of bright red blood by rectum?

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: Stool and Urine Color Changes.

Sheldon SH Levy HB. Pediatric
Differential Diagnosis, Second Edition. Raven Press: New
York. 1985. pp. 22, 156.

Schiff D, Shelov SP. American
Academy of Pediatrics. The Official, Complete Home Reference:
Guide to Your Child’s Symptoms. Villard: New York. 1997. pp. 587.

Illingworth RS. Common Symptoms of Disease in
Children. Blackwell Scientific Publications: Oxford. 1998. pp. 95, 97.

Gunn VL, Nechyba C. The
Harriet Lane Handbook. 16th. Mosby Publications: St. Louis. 2002. pp. 387-98.

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

Date
November 15, 2004

What Causes Hypotonia in Infants?

Patient Presentation
A 36 week premie infant female is transferred to an academic medical center for persistent hypotonia and poor feeding for one week. She is a dichorionic-diamnionic twin gestation. The pregnancy was complicated by decreased fetal movement, polyhydraminios and amniotic fluid reduction. Chromosomes on the amniontic fluid were normal. Her family history is negative.
She was delivered by cesarean section with Apgar scores of 41 and 85 and had hypotonia and a weak suck by report. She had some apnea without bradycardia on day of life #1 and required nasogastric feedings of breastmilk. She had a normal head CT. Her physical examination upon transfer shows her to be generally emaciated with a weight of 2136 grams, respiratory rate of 48 and shallow breathing, generalized hypotonia with no suck or swallow reflexes. Her gag reflex is normal. Her DTRs are 1+/2+ and are slow to recoil. She has no clonus. The rest of her physical examination is unremarkable.
Her laboratory evaluation includes a normal newborn screening test, TORCH titres, creatinine kinase, T4 and TSH, and electrolytes. Genetic testing for inherited metabolic problems, including a chromosome methylation test, confirms the diagnosis of Prader Willi Syndrome.

Discussion

Prader Willi is an autosomal dominant genetic syndrome most commonly caused by a paternal deletion on chromosome 15 (~70%). A mneumonic for the clinical syndrome is H3O = hyptonia, hypogonadotropic hypogonadism, hypomentation and obesity.
Patients also often have decreased fetal activity in utero. At birth, patients often have diminished suck and swallowing. Feeding improves by ~ 6 months but from 12-18 months onward there is uncontrolled hyperphagia and decreased linear growth. Patients also often have cryptorchidism with hypoplastic penis and scrotum in boys and hypoplastic labiae in girls. There is normal size of hands and feet in the first year of life which become smaller later in life.
The face is often characterized by strabismus, almond-shaped eyes, triangular mouth and a narrow bifrontal diameter. Plethoric obesity is striking feature. Hypotonia improves with time but the hypomentation becomes more apparent.
The syndrome was first described by Langsdon-Down in 1887 and later by Prader in 1956.

Hypotonia is a common diagnostic problem. It may occur with or without weakness. Decreased fetal movements in utero, persistant hypotonia and difficulty feeding are more consistant with congenital rather than an acquired hypotonia. Common treatable conditions such as hypothyroidism, electrolyte abnormalities and metabolic problems can often be ruled in or out relatively quickly. Supportive treatment while the evaluation progresses is important. The differential diagnosis can be long but often can be identified with an anatomical location:

  • Central Nervous System

    • Perinatal hypoxia, birth trauma
    • Metabolic disorders – mucopolysaccaridosis, lipidoses
    • Chromosomal disorders – Down Syndrome
  • Spinal Cord
    • Spinal cord injury
    • Spinal muscle atrophy – Werdnig-Hoffmann
    • Poliomyelitis
  • Neuromuscular Junction
    • Botulism
    • Congenital myasthenia
    • Neonatal myasthenia
  • Skeletal muscle
    • Congenital muscular dystrophy
    • Congenital myotonic dystrophy
    • Metabolic myopathies – glycogenoses, mitochondrial
    • Structural congenital myopathies – nemaline, central core, myotubular
  • Connective Tissue
    • Ehler-Dahlos Syndrome
    • Marfan Syndrome
  • Other
    • Prader-Willi Syndrome
    • Benign Congenital Hypotonia
    • Metabolic – hypocalcemia, hypermagnesemia
    • Nutritional
    • Endocrine – hypothyroidism
    • Maternal drugs – narcotics near or at time of birth
    • Organophosphate intoxication

Learning Point
This patient had persistant hypotonia and difficulty feeding. She also had decreased fetal movements antenatally. Both of these are consistent with a congenital rather than acquired hypotonia and the patient was evaluated accordingly.This patient received aggressive nutritional support during evaluation and after. Her parents also received parental education and were scheduled for a formal genetic counseling session after discharge.

Questions for Further Discussion
1. What are the elements of the physical examination that can help narrow the differential diagnosis?
2. How would nerve conduction or electromyelogram tests be helpful?
3. What follow-up is necessary for a patient with Prader Willi Syndrome?
4. Although each patient and family are different, what are some of the basic tenets of delivering bad news to families?

Related Cases

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

National Center for Biotechnology Information, U.S. National Library of Medicine. Online Mendelian Inheritance of Man. Prader-Willi Syndrome;PWS. Available from the Internet at: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176270 (rev. 10/14/04, cited 10/18/04)

Rudolph CD, et.al. Rudolph’s Pediatrics 21st edit. McGraw-Hill, New York, NY. 2003. pp. 2303-2304.

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

Date
November 8, 2004