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CONTENTS
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A Look at Chapman Reflex Points
Beena Iype, MS-III; Bahram Madari, MS-III
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A Look at the Galbreath Techniques
Beena Iype, MS-III; Bahram Madari, MS-III
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Respiratory Distress Syndrome in a Term Newborn
Meghan Lynch, OMS-III; Carl Backes, DO
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A Look at Chapman Reflex Points
Beena Iype, MSIII
Lake Erie College of Osteopathic Medicine
Erie, PA
Bahram Nadari, MSIII
Lake Erie College of Osteopathic Medicine
Erie, PA
Chapman’s points are viscerosomatic reflexes discovered by Frank Chapman D.O. (1) Frank Chapman was a student of Andrew Taylor Still, and graduated from the American School of Osteopathy in 1897. As a student of Dr. Still, Chapman learned the importance of the role of fascia and how lymphatics play a part in health and disease.
Chapman’s work was published posthumously in the 1930’s by his wife and brother-in-law.
There are about 50 Chapman reflexes ranging from the eyes to the prostate. The points are bilateral, and are located on the front and the back of the body. Chapman reflexes are points of excess tissue congestion and reflect visceral dysfunction that is mediated by sympathetic division of the autonomic nervous system. Irritated, diseased, or stressed organs produce sympathetic tone that leads to lymphatic stasis producing myofascial nodules called Chapman points. An acute reflex point may feel boggy or edematous. A chronic point may feel ropy or stringy. These points exhibit pain on palpation.
When the physician is ready to proceed to treatment, a gentle rotatory motion is applied to each point using the pad of the finger for about 15 seconds. Treatment may take 15 seconds or up to 2 minutes. The pressure exerted should be firm, but not hard enough to produce a sustained grimace from the patient. The end point of treatment is determined by a release of tension from the myofascial tissues.
Although Chapman reflexes are well known by osteopathic physicians, they are not commonly used. (2) One of the reasons for infrequent utilization of Chapman reflexes is the lack of evidence of potential diagnostic and therapeutic benefit. However, one study published in the Journal of The American Osteopathic Association did show a statistically significant relationship between the presence of Chapman reflex points and pneumonia in hospitalized patients.
Chapman reflexes are excellent diagnostic tools that osteopathic physicians can use and also may be used to break positive feedback cycles that could result in health restoration. (1) Chapman’s work has influenced many osteopathic physicians, and will hopefully help osteopathic physicians in the future diagnose and treat viscerosomatic reflexes that manifest at Chapman points.
Foundations for osteopathic medicine 2nd edition page 1053-1054
References:
- Capobianco, John D. Chapman Reflex Points. An Osteopathic Approach to Diagnosis and Treatment. 2005: 113-115.
- Washington K. D.O., Mosiello R. D.O., Venditto M. D.O., Simerlo J. D.O., Coughlin P. PhD, Crow W.T. D.O., Nicholas A. D.O. Presence of Chapman Reflex Points in Hospitalized Patients with Pneumonia. Journal of American Osteopathic Association. 103 (10): 479.
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A Look at the Galbreath Technique
Beena Iype, MSIII
Lake Erie College of Osteopathic Medicine
Erie, PA
Bahram Nadari, MSIII
Lake Erie College of Osteopathic Medicine
Erie, PA
Because of the long-term morbidity of otitis media, medical journals and the popular press publish many articles annually on the treatment and prevention of this disorder. (1). Even with high attention directed towards otitis media, few articles discuss about how osteopathic manipulative treatment can help.
Otitis media is inflammation of the middle ear that is usually due to a viral or bacterial infection. The pathogenesis of otitis media is as follows:
- Patient has an upper respiratory infection
- Eustachian tube becomes congested due to inflammation of upper respiratory tract
- Secretions accumulate in the middle ear
- Bacteria proliferate in the pool of secretions leading to symptoms
The Galbreath technique is a non-invasive and simple technique that can be performed by physicians to help quicken resolution of otitis media. This technique was first described in 1929 by William Otis Galbreath, D.O. and involves mandibular manipulation that aids in drainage of the middle ear
The physician can perform this technique one of two ways: with the patient supine or with the patient sitting upright in the physician’s or parent’s lap. The physician turns the child head so that the affected ear is away and the unaffected ear is near, and uses the hand that is opposite the affected ear. (ex. otitis media of right ear, physician uses left hand). The hand is placed on the mandible of the affected side and exerts a downward, transverse, mild force that crosses the face. This act is repeated in a slow rhythmic fashion, about 3-5 seconds for each action for a total of 30-60 seconds. This technique can also be taught to parents or guardians to be performed at home approximately three times daily.
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Patient sitting upright |
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Patient Supine |
By performing the Galbreath technique, the physician increases blood flow to the pterygoid plexus of veins and lymphatics that make up the primary path of drainage for the middle ear and eustacian tube. In addition, the pumping action created by the slow rhythmic motion of the technique may also cause alternating pressures in the middle ear and eustacian tube, enhancing drainage of the middle ear into the pharynx.
Poorly treated otitis media can lead to conductive hearing loss and, if not treated, can lead to abnormalities in speech, language, and behavioral and cognitive development in children. Although antibiotics, immunizations, and surgeries are very effective for otitis media, the Galbreath technique is a quick and easy tool for physicians and parents to use as an adjunct to help resolve cases of otitis media.
References
- Pratt-Harrington D.O., Dale. Galbreath technique: a manipulative treatment for otitis media revisited. Journal of American Osteopathic Association. 100 (10): 635-639.
- Nicholas, Alexander S. and Evan A. Mandibular Drainage: Galbreath Technique. Atlas of Osteopathic Techniques. 2008: 418.
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Respiratory Distress Syndrome in a Term Newborn
Meghan Lynch, OMS-III; Carl Backes, DO
Ohio University College of Osteopathic Medicine, Athens, OH;
OhioHealth, Nationwide Children’s Hospital; Columbus, OH
Introduction
Respiratory distress syndrome (RDS) is primarily a diagnosis seen in preterm infants due to lung immaturity. In the premature infant this condition is typically fatal if there is a complete lack of surfactant. The presence and persistence of RDS in a term infant can be less severe and due to a genetic abnormality. Here we present a term infant who presented with respiratory distress syndrome shortly after birth which persisted for several months. The presence and persistence of RDS in this term newborn warranted genetic testing which revealed a mutation in the ABCA3 gene causing a surfactant dysfunction mutation.
Case Presentation
A term male infant was born vaginally at 39 weeks 2 days gestation with normal Apgar scores. He then had an increasing oxygen requirements and eventual respiratory failure. He was treated with endotracheal surfactant, cycled ventilatory support for 18 days and nasal CPAP. Initial and repeat imaging studies done in the first days of life revealed a diffuse fine granular appearance of the lungs indicating respiratory distress syndrome. He was discharged from the NICU at 14 weeks of age. Multiple diagnostic studies were done with genetic testing showing no mutation in the SFTPC gene but mutations in the ABCA3 gene confirmed congenital surfactant dysfunction.
His initial chest CT scan is shown (fig A) as well as a recent repeat chest CT scan (fig B); chest radiographs from the first days of life (fig C & D) and a recent picture of the patient and his mother (Fig E). Presently at 25 months of age he continues to have intermittent episodes of respiratory distress and is on chronic preventative inflammatory medications including inhaled steroids, montelukast and an inhaled bronchodilator as needed.
Conclusion
Congenital surfactant deficiency with an ABCA3 gene mutation is typically fatal in the newborn period. There is, however, increasing evidence that certain gene mutations cause a dysfunction of the ABCA3 gene rather than a deficiency. Our patient has been found to have 2 gene mutations on separate alleles causing his respiratory symptoms. The Nt875Aà T mutation (also known as the E292V mutation) has previously been reported in children with interstitial lung disease. The other, Nt3997delA, was a previously unreported mutation. Fortunately this child is doing relatively well despite having diffuse interstitial lung disease. He continues to require medications and close monitoring for disease progression.
Discussion
Respiratory distress syndrome is primarily a diagnosis seen in preterm infants due to lung immaturity. In the premature infant this condition is typically fatal due to a lack of surfactant. It is most commonly seen in infants born before 28 weeks gestation but can persist up to 34 weeks gestation. This condition presents with grunting, retractions, hypoxia and cyanosis occurring immediately after birth. Chest radiographs will reveal homogenous opaque infiltrates. Improvement can be seen after 2-4 days of treatment with cycled ventilatory support or nitric oxide however death is another possibility in days 2-7 of life. This condition can also be present in term newborns due to genetic mutation causing a surfactant deficiency. Lethal respiratory failure has been seen in infants with a recessive loss of function mutation of the SFTPB gene leading to a loss of the protein making up the structure of surfactant or the ABCA3 gene causing a loss of lipid transport in lamellar bodies located in the alveolar type II cells. There is increasing research suggesting the role of ABCA3 gene mutation leading to a non-lethal surfactant dysfunction and pediatric interstitial lung disease which is illustrated in this case. The infant presented with increasing and persistent respiratory distress. Radiologic findings suggested interstitial lung disease which warranted genetic testing revealing two mutations in the ABCA3 gene causing a surfactant dysfunction. The first mutation is E292V, a missense mutation that has been documented in multiple cases of pediatric interstitial lung disease. The second is Nt3997delA; a frameshift mutation located in exon 27 causing a premature stop codon and a truncated protein. Many mutations of the ABCA3 gene have been documented in association with interstitial lung disease and neonatal respiratory distress syndrome; however this is the first time the Nt3997delA mutation has been seen in a patient.
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Figure A |
Figure C |
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Figure B |
Figure D |
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Figure E |
References:
- Bullard J, Wert S, Whitsett J, et al. ABCA3 Mutations Associated with Pediatric Interstitial Lung Disease. Am J Respir Crit Care Med 2005; 172; 1026-31.
- Hamvas A, Nogee L, Wegner D, et al. Inherited Surfactant Deficiency Caused by Uniparental Disomy of Rare Mutations in the Surfactant Protein-B and ATP Binding Cassette, Subfamily A, Member 3 Genes. The Journal of Pediatrics 2009; 155: 854-59.
- Hermensan C, Lorah K. Respiratory Distress in the Newborn. American Family Physician 2007 Oct 1; 76 (7): 987-94.
- Shunlenin S, Nogee L, Annilo T, et al. ABCA3 Gene Mutations in Newborns with Fatal Surfactant Deficiency. The New England Journal of Medicine 2004; 350: 1296-303.
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