Maternal History Maternal and Fetal Risks and Complications

Maternal History Maternal and Fetal Risks and Complications Delivery and Stabilization Admission exam and diagnostics Primary admission diagnoses Etiology and Pathophysiology of Primary Admission Diagnoses Initial Plan of Care Hospital Course by Symptoms Medications Pertinent Theories and Evidence Based Practice Family Interactions Discharge Plan and Follow Up

37 yo, married Hispanic G 6 now P 5 1 SAB 1994 -39 weeks 1997 -40 weeks 2004 -39 weeks 2009 -39 weeks EDD 6/10/14 A+, GBS-, RPR NR, Rubella Immune, HIV NR, HBUnremarkable Medical history Denies alcohol, tobacco, and illicit drug use

Advanced maternal age 37 year old U/S 12/16/14 Nuchal thickness of 3. 1 Low AFP 12/31/14 + Trisomy 21 U/S 2/28/14 Suspected Coarctation of the aorta

Scheduled induction at 39 weeks Due to suspected Coarctation of the aorta Spontaneous labor 38 1/7 weeks GA SROM 2 ½ hours prior to delivery Clear fluid Vertex presentation NSVD No maternal medications prior to delivery Apgars 8 at 1 minute 8 at 5 minutes Delivery summary Lusty cry at delivery, cord clamped and cut. Infant taken to radiant warmer. Dried and stimulated. Infant dusky, BBO 2 (40%) provided at 5 minutes of life for pre-ductal saturations below 85%. Continued to dry and stimulate. Improvement in color and saturations noted. O 2 discontinued at 8 minutes of life. Infant placed skin to skin with mother prior to transfer to NICU for transition.

Echocardiogram 5/28/2014 - 1 hour of life FISH chromosomes 5/29/2014 - results pending High resolution chromosomes 5/29/2014 - results pending Bedside chemstrip 51 @ 1426 (admit)

38. 1 week AGA male infant, 3078 gms Suspected Coarctation of the aorta Suspected Trisomy 21

Narrowing of the aorta Constricted segment of the aorta that comprises localized medial thickening. 5 -8% of all congenital heart defects May also occur with bicuspid aortic valve and VSD (Cates, 2009)

Increased afterload on the left ventricle Increased wall stress resulting in ventricular hypertrophy As the PDA closes (may cause rapid CHF and shock) Causes increased left ventricular pressures, increased left atrial pressure, and opening of the foramen ovale Resulting in left-to-right shunting and dilation of the right atrium and right ventricle When the foramen ovale doesn’t open the pulmonary venous and artery pressures increase Resulting in right ventricular dilation (Gholampour, et al. , 2006)

(Gomella, 2013) (Syamasundar, 2012)

(Cates, 2009)

Surgical Treatment Goal is to bypass the narrowed section of the aorta Left subclavian aortoplasty Resection and end-to-end anastomosis Angioplasty with Dacron patch Stenting Balloon angioplasty (Gholampour, et al, 2004).

(Blackburn, 2007) (Gomella, 2013)

(Bajaj & Gross, 2011)

Physical findings Hypotonia, poor or absent moro reflex, flat facial profile, protruding tongue, up slanting palperbral fissures, Brushfield spots, anomalous auricles, joint hyperextensibility, excess nuchal skin, fifth-digit brachydactyly/clinodactyly, and single transverse palmar crease. Associated Anomalies Congenital heart defects in 40% of infants (most common ASD or VSD), PDA, endocardial cushion defect, aberrant subclavian artery. Hirschsprung disease, duodenal or esphageal atresia, imperforate anus, (Gomella, 2013) (Jones, 2006)

Treatment There is no cure for Down’s syndrome Supportive care Early intervention is essential to assist in the progression of developmental milestones. (Heyn & Perlstein, 2014)

Vitamin K IM injection, 1 mg x 1 within 1 hour of birth Erythromycin ophthalmic eye ointment to both eyes x 1 within 1 hour of birth D 10 W @ 10 cc/hr (80 ml/kg/day) Hepatitis B vaccine 5 mcg IM x 1 Little noses Q 4 hours x 24 hours

COARCTATION OF THE AORTA Until surgery can be performed PGE is needed. Surgical correction has the lowest risk of restenosis then any other treatment. Although surgical correction reduces the morbidity and mortality rate. These infant’s still have a decreased life expectancy related to poor blood pressure control. Outcome is worse when there is also a hypoplastic arch present. If the ECHO is performed by someone whom is not experienced in neonates and small children a CT or cardiac MRI should be performed to officially adequately assess the aortic arch. Surgical intervention is the preferred method of treatment because those whom have a balloon dilation will almost always need a repeat dilation and/or surgery.

TRISOMY 21 Currently there is no cure for Down’s syndrome. Genetic studies are focuses on finding therapies to improve learning and potential therapies. Early intervention programs, physical therapy, occupational therapy, and speech therapy can improve outcomes. At greater risk for hearing, vision, and learning deficits. Leukemia is more common with Trisomy 21 patients then those without.

Mother and father were concerned immediately after birth, questions answered and plan of care explained. Infant skin to skin with mother prior to transfer to NICU for further evaluation. Father accompanied infant to NICU and further questions answered. After recovery mother visited infant in the NICU, asked appropriate questions regarding suspected Coarctation and Trisomy 21.

Coarctation is a constricted segment of the aorta that comprises localized medial thickening and can be life threatening if not diagnosed and treated. A prenatal diagnosis of Coarctation of the aorta can assist the medical professionals in the preparation for treatment. Trisomy 21 is a genetic defect that may have multiple associated anomalies. Confirmation of a prenatal diagnosis is important to assist the family in the acceptance of a child with a chronic disorder and/or a genetic disorder. Although it is common for a Trisomy 21 infant to have an associated heat defect it is not commonly associated with coarctation of the aorta.