How Does Transverse Myelitis Present?

Patient Presentation
An 8-year-old female came to clinic for back pain and fevers. She complained of thoracic back and chest pain for two weeks.
The pain increased over the two weeks with shooting pains into her hands and feet. During one of these episodes, three days prior, she complained of severe chest pain and was taken to the local emergency room where she was diagnosed with pneumonia and pleurisy but was not begun on any medications.
She had intermittent fevers to 101º Fahrenheit. The fevers and pain improved with acetaminophen or ibuprofen, but would return when the medication wore off.
Over the previous week, she had several episodes of urinary incontinence, intermittent headache and several episodes of emesis.
The parents also noted that the pupils of her eyes seem to be different sizes in the morning which prompted the return visit.
The patient also says that she has been dizzy at times and the parents said that she seemed disoriented occasionally. She had an upper respiratory infection about 3 weeks ago but has had no trauma or other illnesses.
The past medical history was non-contributory.
The family history is positive for seizures in a cousin.
The review of systems revealed no weakness, sore throat, rhinorrhea, constipation, diarrhea, dysuria, rashes or heart palpitations. She had not been eating or drinking well.
The pertinent physical exam shows normal vital signs and the patient was not experiencing pain. Eyes showed a right pupil of 4 mm and left pupil of 2 mm in size; both were reactive to light.
Ears, nose and throat were negative.
Neck was supple with shoddy anterior cervical lymphadenopathy and no change in symptoms with motion.
Heart, lungs and abdomen were normal. No pain could be elicited on palpation or motion of the spine or chest.
Neurological examination showed cranial nerves were normal other than her anisocoria. Deep tendon reflexes were 2+/2+ throughout. She had no motor or sensory abnormalities. She had a normal Romberg test and normal gait but was somewhat hesitant to move much for fear of the pain.
Tone was normal as was cerebellar testing.
The laboratory evaluation included normal electrolytes and glucose, erythrocyte sedimentation rate of 6 mm/hr, and C-reactive protein of 0.5 mg/dl.
Her complete blood count had a hemoglobin of 15 mg/dl, hematocrit of 40%, platelets of 239 x 1000/mm2 and a white blood cell count of 8.3 x 1000/mm2 with 5204 neutrophils, no bands, and 2117 lymphocytes.
Because of the concerning neurological examination and a differential diagnosis that included diseases which required neurosurgical intervention, the radiologic evaluation of a magnetic resonance imaging study of her spinal cord and head was ordered.
The head was normal but the spine showed extensive T2 signal involving the cervical spine that was consistent with transverse myelitis.
The diagnosis of transverse myelitis was made and the patient was begun on methylprednisolone intravenously for 3 days and then discharged home on oral prednisone.
She had some improvement of her symptoms at discharge.
Mycoplasma pneumoniae titres were positive during her hospitalization and she was treated with a 5 day course of oral azithromycin.
The patient’s clinical course over the next 2 months showed her to improve with occasional episodes of mild back pain but with no radiation. The family has also noticed a few episodes of short duration anisocoria. Both of these symptoms are decreasing in frequency.
The patient was to continue tapering the prednisone and follow-up in another month.



Figure 46 – Magnetic resonance imaging including sagittal (left) and axial (right) T2-weighted images through the thoracic spine demonstrate bright signal intensity in the center of the thoracic spinal cord throughout its length. The thoracic spinal cord showed no enhancement after the administration of intravenous gadolinium contrast.

Discussion
Transverse myelitis is a segmental spinal cord disease that usually has both sensory and motor abnormalities at and below the lesion.
The onset of symptoms is hours to days and is often associated with respiratory infections or viral illnesses such as Epstein-Barr, mumps or varicella viruses.
Mycoplasma pneumoniae is also a known cause of transverse myelitis.

Differential diagnosis includes:

  • Intraspinal problems
    • Abscess
    • Hematoma
    • Intraspinal cyst
    • Necrosis, idiopathic
    • Neoplasm
    • Syringomyelia
    • Vascular occlusion or accident
  • Extraspinal problems
    • Arteriovenous malformation
    • Epidural abscess
    • Hematoma
    • Neoplasm

Other flaccid paralyses that should be distinguished from transverse myelitis include poliomyelitis, Guillian-Barré and traumatic neuritis following injections.

Evaluation usually includes magnetic resonance imaging to look for a surgically-treatable condition.
Cerebrospinal fluid testing may be necessary but should be done only after consultation with neurology and neurosurgery because of the risk of further damage from a mass lesion.
If performed, it may be normal or show mild inflammatory changes.
Nerve conduction velocities and electromyograms usually are normal.

Treatable causes of transverse myelitis should be given specific appropriate treatment.
Treatment for idiopathic transverse myelitis is usually steroid medications but sometimes intravenous immunoglobulin is used. Both are used for their immunomodulatory effects.

Outcome for children is better than adults with often complete recovery.

Learning Point

The level of the spinal lesion determines the clinical symptoms of transverse myelitis.

Above the lesion – no abnormalities

At the level of the lesion

  • Paraesthesias that are usually painful. They begin at the back and circumferentially radiate.
  • Cranial nerves are often not involved unless the lesion is cervical.

Below the level of the lesion

  • Motor abnormalities – flaccid paralysis is common, but this depends on the extent of the lesion
  • Sensory abnormalities – loss of pain but depends on the extent of the lesion. Posterior columns are usually spared.
  • Autonomic abnormalities – loss of temperature control
  • Reflex loss

Questions for Further Discussion
1. What clinical features distinguish poliomyelitis and Guillian-Baré from transverse myelitis?
2. What are the treatment options for recurrent transverse myelitis?

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 MedlinePlus for this topic: Spinal Cord Diseases.

To view current news articles on this topic check Google News.

Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1061, 2315.

Lucchinetti CF, Pittock SJ. Inflammatory tranverse myelitis: evolving concepts. Current Opinion in Neurology. 2006;19:362-368.

ACGME Competencies Highlighted by Case

  • Patient Care
    1. When interacting with patients and their families, the health care professional communicates effectively and demonstrates caring and respectful behaviors.
    2. Essential and accurate information about the patients is gathered.
    3. Informed decisions about diagnostic and therapeutic interventions based on patient information and preferences, up-to-date scientific evidence, and clinical judgment is made.
    4. Patient management plans are developed and carried out.
    5. Patients and their families are counseled and educated.
    7. All medical and invasive procedures considered essential for the area of practice are competency performed.
    8. Health care services aimed at preventing health problems or maintaining health are provided.
    9. Patient-focused care is provided by working with health care professionals, including those from other disciplines.

  • Medical Knowledge
    10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
    11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

  • Practice Based Learning and Improvement

    13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.
    14. Knowledge of study designs and statistical methods to appraisal clinical studies and other information on diagnostic and therapeutic effectiveness is applied.

  • Systems Based Practice
    23. Differing types of medical practice and delivery systems including methods of controlling health care costs and allocating resources are known.
    24. Cost-effective health care and resource allocation that does not compromise quality of care is practiced.
    25. Quality patient care and assisting patients in dealing with system complexities is advocated.

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

    Date
    February 19, 2007

  • What Treatments are Recommended for Head Lice?

    Patient Presentation
    A 4-year-old male came home with a note from school that stated that head lice was being seen in the classroom and that he had been found with some nits in his hair (see Figure 41).
    The school health department and local public health agency recommended over-the-counter Permethrin 1% to be used once and then again one week later.
    Additionally, they recommended combing the wetted, shampooed hair with a nit comb nightly for 1-2 weeks after shampooing (see Figure 42 for an example, note the very fine teeth). Other control measures for the household were recommended such as treating the rest of the household members with the same medication and washing bedding, cleaning toy animals and other household items the child had contact with.
    The parents noted on their physical exam of the child that he had several white spots stuck to the shaft of the hair but no obvious lice.
    The work-up included the sibling and parents being inspected and they did not have any spots or lice noted by the parents.
    The diagnosis of head lice was made. The child was treated according to the school’s recommendations and he had no recurrences of infestation.


    Figure 44 – Photograph of head lice.


    Figure 45 – Example of nit comb.

    Discussion
    Pediculosis capitis or head lice is a common human infestation. Patients often are asymptomatic but itching is a common symptoms. Adult lice may be seen and nits (eggs) are found on the hair shafts.
    Lice lay eggs within 3-4 mm of the scalp and so the time since infestation can be approximated because hair grows at a rate of ~1 cm/month.

    Parents often worry that infestation is a sign of poor hygiene but all socioeconomic groups are affected. Lice do not spread disease and therefore are not a health hazard.

    Transmission is by direct contact with the hair of infested persons or objects such as hats, combs and brushes. The incubation period is 10-14 days but can be lengthened in cold climates and shortened in warm climates. Adult lice can produce eggs after 2 weeks.

    Learning Point
    According to the American Academy of Pediatrics, first line pediculicide treatment should be with Permethrin 1% over-the-counter topical medication, noting there is resistance to it commonly.
    Treatment failure should then be treated with Malathion 0.5% topically. If there is treatment failure with Malathion, then oral Ivermectin is recommended.
    All medications should be used as directed. The major safety risk is the medication itself as the infestation does not cause disease.

    Permethrin 1% is an over-the-counter topical medication that is applied to the hair for 10 minutes after regular washing and towel drying. One treatment is thought effective since it last for 2 weeks but some people recommend a second treatment at 7-10 days. Permethrin 5% is available by prescription for treatment of scabies but not for lice.

    Malathion 0.5% is available by prescription and is an organophosphate pesticide. It is approved for children 6 years and older. It is contraindicated in children < 2 years. It is applied to dry hair and left for 8-12 hours. It is reapplied at 7-10 days only if lice are still present.

    Ivermectin is not currently approved by the FDA as a pediculicide. It is given as a single oral dose of 200 micrograms/kilogram with a second dose at 7-10 days. It should not be given to children less than 15 kilograms in weight.

    Other medications that are used include various Pyrethrin products, Lindane, Crotamiton, and oral Trimethoprim-sulfamethoxazole.

    Efficacy by suffocation of occlusive agents such as petroleum jelly or mayonnaise has not been determined. One recent study showed that hot air was effective.

    Manual removal of nits is not necessary to prevent spreading. If nits are still visible, particularly close to the scalp, manual removal may increase success.

    Household contacts and other close contacts should be treated prophylactically with a pediculicide. Combs, brushes, etc. should be treated with a pediculicide shampoo or in hot water (> 53.5 degrees Celsius or 128.3 degrees fahrenheit) for more than 5 minutes. Bedding and clothing should be washed in hot water and dried on the hot cycle. Dry cleaning or storing items in sealed plastic bags for 2 weeks also is an effective environmental control. Vacumning is also effective.
    Pets do not need to be treated.

    Questions for Further Discussion
    1. How do you treat Pediculosis corporis or Pediculosis pubis?

    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 MedlinePlus for these topics: Head Lice and Parasitic Diseases
    and at Pediatric Common Questions, Quick Answers for this topic: Head Lice

    To view current news articles on this topic check Google News.

    American Academy of Pediatrics. Pediculosis Capitis, In Pickering LD, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th edit. Elk Grove Village, IL: American Academy of Pediatrics; 2006;488-492.

    Goates BM,
    Atkin JS,
    Wilding KG,
    Birch KG,
    Cottam MR,
    Bush SE,
    Clayton DH. An effective nonchemical treatment for head lice: a lot of hot air. Pediatrics. 2006 Nov;118(5):1962-70.

    Centers for Disease Control. Head Lice Infestation.
    Available from the Internet at http://www.cdc.gov/ncidod/dpd/parasites/lice/factsht_head_lice.htm (rev. 8/12/2005, cited 1/22/07).

    National Pediculosis Association. Licemeister Nit Comb.
    Available from the Internet at http://www.headlice.org/ (rev. 2007, cited 1/22/07).

    ACGME Competencies Highlighted by Case

  • Patient Care

    3. Informed decisions about diagnostic and therapeutic interventions based on patient information and preferences, up-to-date scientific evidence, and clinical judgment is made.
    4. Patient management plans are developed and carried out.
    5. Patients and their families are counseled and educated.

    9. Patient-focused care is provided by working with health care professionals, including those from other disciplines.

  • Medical Knowledge
    10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
    11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

  • Practice Based Learning and Improvement

    13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.

  • Systems Based Practice

    26. Partnering with health care managers and health care providers to assess, coordinate, and improve health care and how these activities can affect system performance are known.

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

    Date
    February 12, 2007

  • What Causes SIDS?

    Patient Presentation
    A 74-day-old premature twin male stopped breathing while on his father’s lap. His father was doing computer work and stated that he looked down and the baby was no longer alive. The baby was lying on his back and not swaddled in a blanket.
    His father states that there were no sounds or struggling. The father also said that he had no idea how long it had been since he had noted the baby to be alive. The baby was not revived with cardiopulmonary resuscitation.
    The past medical history revealed a twin male who had been in the neonatal intensive care unit with some episodes of apnea after birth. He did not go home with an apnea/bradycardia monitor and had been otherwise healthy.
    The twin had also been healthy.
    The review of systems revealed that the father said that the infant’s breathing was labored but that it seemed like a cold.
    A full work-up included an investigation by the local police department for possible child abuse. The diagnosis of sudden infant death syndrome was made. The father later was told that the most likely cause was acid reflux leading to heart and respiratory failure.

    Discussion
    Sudden Infant Death Syndrome (SIDS) is a clinical diagnosis with the sudden death of an under one year of age infant that remains unexplained after a thorough case investigation, including examination of the scene of death, a complete autopsy, and review of the clinical history.
    Cases not meeting these standards, should not be classified as SIDS, such as those without an autopsy.

    SIDS is the most common cause of death in the postneonatal period (i.e., in infants aged 1 month to 1 year).
    Most occur in infants 2-4 months, with 90% of cases occuring in &lt; 6 month old infants, and 95% of deaths occuring in < 8 month old infants.
    The male-to-female ratio is 3:2 in most population studies, and SIDS is higher in African Americans and Native Americans for unknown reasons.

    After studies completed in multiple developed countries internationally, the U.S. began recommending placing infants on their back for sleeping, i.e. the “Back to Sleep” campaign in 1994.
    SIDS rates have fallen approximately ~75% since then. In 2002, a total of 2295 SIDS deaths were reported nationwide.

    An ALTE (apparent life-threatening event) is different than SIDS and is defined as an event “???that is frightening to the observer and is characterized by some combination of apnea (central or obstructive), change in muscle tone (usually diminished), and choking or gagging.”ALTE frequency in healthy term infants is estimated to be 1-3%. The subsequent death among infants with an ALTE is 1-2%. The rate increases to 4% if the infant had respiratory syncytial virus, and goes up to 8% if the infant had the ALTE during sleep or required cardiopulmonary resuscitation. Thus, there may be a relationship between ALTE and SIDS.

    Learning Point
    The cause or causes of SIDS is not currently known. Many people believe that SIDS is multifactorial. Potential causes of SIDS include:

    • Triple risk model – where an infant with intrinsic abnormalities of cardiorespiratory control is in a critical period of homeostatic cardiorespiratory development, and then has external stressors that cause the infant to have inadequate cardiorespiratory homeostasis and results in cardiorespiratory failure.
      • Critical developmental period – the peak time period for SIDS is also the time when the brain undergoes rapid developmental change for sleep, arousal, cardiorespiratory homeostasis and metabolism.
      • Stressors could include the concentration of oxygen and carbon dioxide in the infant’s microenvironment, temperature, and infections. This may explain why smoking, especially maternal smoking, appears to increase the risk of SIDS.
        Additionally, asphyxiation though co-sleeping and prone sleeping may also be explained though this mechanism.
        This may also explain why the father of the patient in the case above was told that acid reflux may have been the cause of his son’s death (e.g. possibly through aspiration leading to asphyxia).
    • Neurodevelopmental pathology – various studies have found differences in neurotransmitters and neuropathways in various parts of the brain. These include dopamine, tyrosine and serotonin. Potentially involved areas include the medulla, cerebellum, and pre-frontal cortex.
      A recently study found medullary sertonin pathology to be more extensive in SIDS than previously thought.
      An increased risk of SIDS in premature infants may possibly be explained through this mechanism.

    • Long QT Syndrome – may contribute to some cases of SIDS. It appears that certain sodium channel mutations, such as SCN5A, may contribute to arrhythmias and thus potentially death.
    • Fatty acid oxidation defects – At autopsy some infants have fatty changes in their liver. Medium-chain acyl-CoA dehydrogenase deficiency (MCADD) is a proposed cause.
    • Child abuse – is estimated to cause 1-10% of all unexplained, sudden deaths in infancy. Most SIDS cases do not have any risk factors for child abuse, but it does emphasize the need for a through death investigation to be completed.

    Questions for Further Discussion
    1. What are current indications for using an apnea/bradycardia monitor?
    2. What are the recommendations for using pacifiers, bundling of infants and side-lying sleeping position?

    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 MedlinePlus for this: Sudden Infant Death Syndrome (SIDS).

    To view current news articles on this topic check Google News.

    Carolan PL. Sudden Infant Death Syndrome. eMedicine.
    Available from the Internet at http://www.emedicine.com/ped/topic2171.htm (rev. 6/8/2006, cited 1/22/07).

    Paterson DS,
    Trachtenberg FL,
    Thompson EG,
    Belliveau RA,
    Beggs AH,
    Darnall R,
    Chadwick AE,
    Krous HF,
    Kinney HC. Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA. 2006 Nov 1;296(17):2124-32.

    Wang DW, Desai RR, Crotti L, Arnestad M, Insolia R, Pedrazzini M, Ferrandi C, Vege A, Rognum T, Schwartz PJ, George AL Jr.
    Cardiac Sodium Channel Dysfunction in Sudden Infant Death Syndrome.
    Circulation. 2007

    ACGME Competencies Highlighted by Case

  • Patient Care

    5. Patients and their families are counseled and educated.

    9. Patient-focused care is provided by working with health care professionals, including those from other disciplines.

  • Medical Knowledge
    10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
    11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

  • Practice Based Learning and Improvement
    12. Evidence from scientific studies related to the patients’ health problems is located, appraised and assimilated.
    13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.

  • Professionalism
    20. Respect, compassion, and integrity; a responsiveness to the needs of patients and society that supercedes self-interest; accountability to patients, society, and the profession; and a commitment to excellence and on-going professional development are demonstrated.

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

    Date
    February 5, 2007

  • What Organisms Cause Neonatal Sepsis?

    Patient Presentation
    A female infant was born at 38 4/7 week gestation to a 34 year old gravida 2, para 1 mother. The mother was positive on Group B streptococcus screening 2 weeks prior to delivery.
    Labor was induced because of late-term maternal hypertension. The mother received antibiotics during labor and delivery was by emergent cesarean section for fetal bradycardia.
    The baby was vigorous at delivery but then became cyanotic at 4 minutes of age and received blow-by oxygen. Apgar scores were 4 at 1 minute, 6 at 2 minutes, and 7 at 5 minutes.
    Her initial capillary blood gas was pH = 7.13, CO2 = 77, and base excess of +2. She was given oxygen by hood, 2 intravenous boluses of normal saline, and ampicillin and gentimicin after blood cultures were drawn.
    She continued to have respiratory distress and was intubated and sedated before transfer
    to a regional hospital. She was later extubated on day of life 1.
    The pertinent physical exam on arrival showed a term infant with temperature of 35.6 degrees Celsius, heart rate = 106, respiratory rate = 40, and blood pressure = 69/40 with no evidence suggesting of coarctation of the aorta on 4 extremity blood pressures.
    Her oxygen saturation was 100% on 40% oxygen. She did not appear dysmorphic. Skin showed a few red, blanching 3 mm macules on the face. Lungs were normal. Heart had a regular rate and rhythmn with no murmurs. Upper extremity pulses were equal to lower extremity pulses.
    Abdomen had no organomegaly, normal bowel sounds and a 3 vessel cord. She had a good tone, strength, and appropriately reacted to handling.
    The work-up included a complete blood count that showed a hemoglobin of 15.0, hematocrit of 45%, platelets of 233 with segmented neutrophils of 7889, lymphocytes of 5474 and bands of 483.
    A C-reactive protein was &lt;0.5 mg/dl. Her chest radiograph showed some mild hyperexpansion and general haziness of the lung fields (see below).
    Over the next day, the patient’s clinical course showed her to be more awake, her respiratory distress resolved and she was extubated. She had no glucose instability.
    Her blood cultures locally did not grow an organism.
    The diagnosis of presumed neonatal sepsis was made and she received a 7 day course of ampicillin and gentimicin therapy. Her complete blood count was normal at discharge.


    Figure 43 – AP radiograph of the chest on the first day of life demonstrates normally positioned tubes and lines along with diffuse fine interstitial infiltrates. The differential diagnosis for this finding would include transient tachypnea of the newborn versus neonatal pneumonia due to Group B Strep.

    Discussion

    Neonatal sepsis is an important contributor to neonatal morbidity including poor neurodevelopmental outcomes and neonatal death.
    Early in the 20th century, group A streptococcus was the leading cause, but in the 1970s group B streptococcus (GBS) emerged.
    In the 1990’s universal antenatal screening was recommended at 35-37 weeks gestation with recommendations for intrapartum prophylaxis for colonized women.
    These guidelines decreased the rate of early GBS infection from 1.7/1000 live births to 0.34/1000 live births.
    Although the rate of GBS infection has declined, the proportion of mothers exposed to intrapartum antibiotics has more than doubled.
    Concerns of antibiotic-resistance have also been raised.

    Early-onset neonatal sepsis is defined as occuring within the first 7 days of life. Most (85%) infants present in the first 24 hours. Overall GBS neonatal sepsis has decreased with the use of antibiotic protocols, but the overall incidence of early-onset sepsis has remained stable mainly because of increased sepsis resulting from Escherichia coli.
    This is especially true for premature infants and the onset may be extremely rapid.
    The organisms are acquired as an ascending infection from the cervix or transplacentally from the mother.
    Most early-onset neonatal sepsis is not culture-proven and many infants are defined as having “clinical sepsis” such as the infant described above.

    Late-onset neonatal sepsis is defined as occuring between 8-90 days. It is acquired from the environment by colonization of the conjunctiva, skin, gastrointestinal tract, respiratory tract, or umbilicus.

    Pneumonia is a common early-onset sepsis presentation, whereas bacteremia and meningitis are more common in late-onset sepsis.
    Other presentations include metabolic acidosis, hyper- or hypo-glycemia, jaundice, pulmonary hypertension, decrease cardiac output, necrotizing enterocolitis, thrombocytopenia, neutropenia, or disseminated intravascular coagulation.

    Workup often includes complete blood count with differential, C-reactive protein, cerebrospinal fluid analysis and culture, urinalysis and culture, blood culture, chest radiograph, and possibly head imaging and/or other infectious disease markers.

    Learning Point

    Early-onset neonatal sepsis commonly is associated with GBS (most commonly), Escherichia coli, Haemophilus influenzae, and Listeria monocytogenes.

    Late-onset sepsis syndrome is associated with Staphylococcus epidermidis (most commonly), coagulase-negative staphylococcus, Staphylococcus aureus, E. coli, Klebsiella, Pseudomonas, Enterobacter, Candida, GBS, Serratia, Acinetobacter, and anaerobes.

    Empiric treatment for early-onset neonatal sepsis is usually begun with and includes combined IV aminoglycoside and expanded-spectrum penicillin antibiotic therapy in the U.S. and Canada. Clinical situation and local pathogen sensitivities must be considered when selecting antibiotic coverage.

    Questions for Further Discussion
    1. What are the local pathogens that cause neonatal sepsis?
    2. What are the local pathogens’ sensitivities to antibiotics?
    3. How long should treatment be given for presumed neonatal sepsis, i.e. culture-negative sepsis?

    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 MedlinePlus for these topics: Sepsis, Streptococcal Infections and Infections and Pregnancy.

    To view current news articles on this topic check Google News.

    Schrag SJ, Stoll BJ. Early-onset neonatal sepsis in the era of widespread intrapartum chemoprophylaxis.
    Pediatr Infect Dis J. 2006 Oct;25(10):939-40.

    American Academy of Pediatrics. Group B Streptococcal Infections, In Pickering LD, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th edit. Elk Grove Village, IL: American Academy of Pediatrics; 2006;620-627.

    Anderson-Berry AL, Bellig LL. Neonatal Sepsis. eMedicine.
    Available from the Internet at http://www.emedicine.com/ped/topic2630.htm (rev. 8/18/06, cited 1/16/07).

    ACGME Competencies Highlighted by Case

  • Patient Care
    1. When interacting with patients and their families, the health care professional communicates effectively and demonstrates caring and respectful behaviors.
    2. Essential and accurate information about the patients is gathered.
    3. Informed decisions about diagnostic and therapeutic interventions based on patient information and preferences, up-to-date scientific evidence, and clinical judgment is made.
    4. Patient management plans are developed and carried out.
    7. All medical and invasive procedures considered essential for the area of practice are competency performed.
    8. Health care services aimed at preventing health problems or maintaining health are provided.
    9. Patient-focused care is provided by working with health care professionals, including those from other disciplines.

  • Medical Knowledge
    10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
    11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

  • Practice Based Learning and Improvement
    13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.
    14. Knowledge of study designs and statistical methods to appraisal clinical studies and other information on diagnostic and therapeutic effectiveness is applied.

  • Systems Based Practice
    23. Differing types of medical practice and delivery systems including methods of controlling health care costs and allocating resources are known.
    24. Cost-effective health care and resource allocation that does not compromise quality of care is practiced.

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

    Date
    January 29, 2007