RESUSCITATION OF NEW BORN

New Born Resuscitation

PURPOSE

l  The main purpose of resuscitation  is to initiate respiration in a newborn,  who is asphyxiated or spontaneous breathing has not been initiated.

What risk factor are associated with the need for neonatal resuscitation?

1, ANTEPARTUM:

l  Maternal Diabetes

l  PIH

l  Bleeding in second & third trimester

l  Post term gestation

l  Maternal age less than 16 or more than 35 year.

l  Multiple pregnancies

l  Severe anemia

l  Pervious still birth

l  Maternal infection

l  Mother on drug therapy (Lithium carbonate)

l  Maternal drug abuse

2, INTRAPARTUM:

l  Abnormal presentation

l  Rupture of membrane more than 24 hrs prior to delivery.

l  Precipitate labour

l  Prolapsed cord

l  Abruptio placenta

l  Meconium stained amniotic fluid

l  Premature labour

l  Foul smell amniotic fluid

l  Prolonged labour either for first or second stage

l  Non reasoning fetal heart pattern

l  Placenta previa

PREPARATION FOR RESUSCITATION:

l  Two trained personnel capable of working together to perform all aspect of resuscitation but one of the two must be skilled in the tracheal intubation.

l  Sources of heat either radiant warmer or 200 watt bulb.

l  Adequate lighting & place to work.

Indication:

·         Asphyxia.

·         Cardiac arest

·         respiratory distress

·         Consider every birth is at risk

·         All resuscitation equipment are kept ready in labour room

·         One person from labour room should be skilled in resuscitation

·         Resuscitation room will be well lighted and warm

·         Essential articles should be good working condition

·         And should be checked by nursing personal at every duty shift.

·         Follow aseptic precaution

·         Universal precaution against HIV ALSO MIAINTAINED

EQUIPMENTS:

SUCTION EQUIPMENT:

1.      mucous aspirator,

2.       meconium aspirator

3.      mechanical suction apparatus,

4.       suction catheters,

5.      feeding tube and 20ml syringes

6.      Oxygen sources,

7.       face mask

INTUBATION EQUIPMENT:

1.      neonatal laryngoscope,

2.      with appropriate blade, (no=0 for preterm, no=1 for term)

3.      extyra bulbs and batteries, e.t tubes,

(SIZE, 2.5, 3, 3.5, 4 MM.DM0)

1.      STYLET

2.      SCISSORS

MEDICATIONS:

1.      Epinephrine

2.      Naloxone hydrochloride

3.      Normal saline

4.      Ringer lactate

5.      Naco2    

6.      Albumin 

7.      Dextrose(5%,10%) 

8.      Sterile water

9.      Ampule of injection, dopamine, slow infusion pump.

MISCELLANEOUS:

1.      Watch with sounds,

2.      Hand prewarmed linen,

3.      Towel shoulder roll

4.      Radient warmer or heat sourses,(bulb 200w)

5.      Stethscope, syringes (1,2,3,5, 10, 20, 50ml)

6.      Needles, umbilical cateters, (3.5fg, 5fg)

7.      Three way stopcocks, gloves, gauze, adhesive tape room thermometer, low radiant thermometer or tele thermometer

8.      Scalp vein set, or iv canula, neonatal airway tube, spot light

TABCs OF RESUSCITATION

T- TEMPERATURE:

1.      Provision of radiant heat sourses

2.      Drying the baby

3.      Removing wet linon

A-ESTABLISNMENT OF OPEN AIRWEY

1.      Position the infant

2.      Suction the mouth, nose and in some instance the trachea,

3.      ET tube if necessary

B-INITIATION OF BREATHING

1.      Tactile stimulation

2.      PPV, using either bag and mask or bag and ET tube

C. MAINTENANCE OF CIRCULATION

1.      Chest compression

2.      Medication

Initial step of resuscitation:

1.      Receive the baby in prewarmed linen.

2.      Dry the baby

3.      Position ther baby (1 inch away from matress, side lying neck slightly extended)

4.      Suctioning( 80mmhg)

5.      Provide tactile stimulation

6.      Using free floe oxygen

Evaluate baby:

1.      Heart rate >100b/m, skin color pink or acrocyanosis, baby need observation and monitoring only.

2.      Spontaneous respiration heart rate >100, with cyanosis at lip or tongue then flow oxygen is administered.

3.      When no spondaneous respiration PPV is started with bag and mask.

4.       spondaneous respiration and heart rate is <100 b/m PPV is started.

Bag and mask ventilation:

1.      It s,b started after tactile stimulation

2.      And the infant is still apnic and gasping and having spondaneous respiration and heart rate is <100 b/m

3.      It s, b done after tracheal suction

4.      Contraindicated in diaphragmatic hernia

5.      Baby head s,b slightly elevated to ensure open airwaymask to be place and seal to be checked by 2 -3 ventilation

6.      Rise of ches to be observed

7.      Ventilation should done at the rate of 40-60 breaths/mitfollow a squeeze ‘one’ ‘two’ squeeze sequence

8. After 15-30 sec of ventilation baby s, b again evaluated.

9. Heart rate is avove 100 and spondaneopus respiration present then provide tactile stimulation monitor heart rate, reap and color.

10. If no breating establishes continue ventilation

11. If heart rate is b/w 60-100 continue ventilation if not increasing start chest compression

Chest compression:

1.      It should be performed always with ventilation and 1005 oxygen

2.      Indicated with 15-30 sec of PPV with 100%oxygen then heart rate is 60to 80b/m and not increasinmg

Techniques:

1.      Thumb techniques

2.      Two finger techniques

Pressure is applied on lower third of the sternum (1/2 to ¾ inches)

Rate is 90 compression with 30 PPV a total of 120 events

Chest complression is 1.5 sec and ½ sec for ventilatiopn

Then carotid and femoral pulse s,b checked to assess effectiveness of chest compression.

ET TUBE INTUBATION:AND MEDICATION:

Medication:

1.       when heart rate is still 80b/m a or above  chest compression s, b discontinued, when 100b/m and have spondaneous respiration ventilation is discontinued.

2.      Umbilical vein is preferable route

3.      No intracardiac injections are recomended for neonates

4.      No direct injection into umbilical card

5.      Some medication given through ET tube

6.      Naco2 is not administetrd still the ventilation is established

7.      . No respiratory stimulant is needed

8.      8. Naco2 is diluted 1:1 with water

9.      9. Metabolic acidosis is corrected with o2 and volume expanders.

Complication of resuscitation:

l  Trauma to the heart

l  Trauma to the lungs

l  Trauma to the liver

l  Broken ribs

l  Laceration of liver and pneumothorax.

INTESTINAL MALROTATION

Intestinal malrotation

Incidence :

•       1 in 500 live births.

•       Approximately 50%of patient with duodenal atresiaa and 33% patient with jejunoileal atresia have maalrotation.

•        Younger patients have higher rates of morbidity and mortality.

•       Infants range from 2 to 24%. Male to female ratio is 2:1

•       No sex discrimination seen in patients with older than one year.

•       40% of malrotattion cases develops during 1^st week of life.

•       50% of cases diagnosed during 1^st month of life, 75% in the 1^st year of life. Remaing 25% will be detected during 1 to 18 years  of life incase of other surgical procedures or at atopsy.

•       50% of cases diagnosed during 1^st month of life, 75% in the 1^st year of life. Remaing 25% will be detected during 1 to 18 years  of life incase of other surgical procedures or at atopsy.

 A report of 25 years' experience demonstrated congenital cardiovascular disease in 27.1% of patients with intestinal malrotation; those patients had a morbidity rate of 61.1% after intestinal malrotation surgery.²

Causes:

•       The exact causes is unknown.

•       It is not associated with a particular gene, but  there is some evidence of recurring in families.

Clinical features.

•       Some time it is asymptomatic

•       Vomitus,

•       Crampy abdominal pain.

•       Abdominal distention.

•       Passage of blood and mucus in the stool

Result of malrotation:

•       the small bowel is found predominantly on the right side of the abdomen

•       the cecum is displaced (from its usual position in the right lower quadrant) into the epigastrium - right hypochondrium

•       the ligament of Treitz is displaced inferiorly and rightward

•       fibrous bands (of Ladd) course over the horizontal part of the duodenum (DII), causing intestinal obstruction.

•       the small intestine has an unusually narrow base, and therefore the midgut is prone to volvulus (a twisting that can obstruct the mesenteric blood vessels and cause intestinal ischemia).

Associated conditions

•       This can lead to a number of disease manifestations such as:

•       Acute midgut volvulus

•       Chronic midgut volvulus

•       Acute duodenal obstruction

•       Chronic duodenal obstruction

•       Internal herniation

Diagnostic evaluation:

History

•       The history of present illness varies in patients with intestinal malrotation according to acute or chronic presentation, as well as according to type of rotational defect.

Acute midgut volvulus

–      Most patients present in the first year of life.

–      The primary presenting sign of acute midgut volvulus is sudden onset of bilious emesis.

Chronic midgut volvulus

–      Chronic midgut volvulus is due to intermittent or partial twisting that results in lymphatic and venous obstruction.

–      Multiple case reports show that 2 of the main presenting features are recurrent abdominal pain and malabsorption syndrome.

–      Several patients presented with acute midgut volvulus, but further history revealed they had had chronic symptoms with misdiagnoses.

–      Other clinical features include recurrent bouts of diarrhea alternating with constipation, intolerance of solid food, obstructive jaundice (1 case),³ and gastroesophageal reflux.

Acute duodenal obstruction

–      This anomaly is usually recognized in infants and is due to compression or kinking of the duodenum by peritoneal bands (Ladd bands).

–      Patients present with forceful vomiting, which may or may not be bile-stained, depending on location of the obstruction with respect to the entrance of the common bile duct (ampulla of Vater).

Chronic duodenal obstruction

–      The typical age at diagnosis ranges from infancy to preschool-age.

–      The most common symptom is vomiting, which is usually bilious.

–      Patients may also have failure to thrive and intermittent abdominal pain (frequently diagnosed as colic).

Internal herniation

–      Internal herniation usually has a chronic picture.

–      Patients have recurrent abdominal pain, which may progress from intermittent to constant.

–      They experience vomiting as well as constipation at times.

–      They are often diagnosed with psychosocial problems.

Physical examination:

•       Physical examination findings may vary depending on the type of rotational defect. Acute and chronic presentations also differ.

•       Acute midgut volvulus

–      Abdominal distention is frequently present, and the infant appears in acute pain.

–      As vascular compromise persists, intraluminal bleeding may occur, which leads to blood per rectum and sometimes hematemesis.

–      Abdominal guarding is usually present and prevents palpation of intestinal loops.

–      Acute midgut volvulus conti.. 

–      As symptoms persist, the infant may develop signs of shock,

including poor perfusion,

decreased urine output, and hypotension.

–      Patients also have signs of peritonitis, including abdominal tenderness and discoloration of the skin.

Chronic midgut volvulus

–      Physical examination results may be completely normal if the patient presents during a period when the obstruction is relieved.

–      If partial twisting is present at the time of examination, the patient may have signs and symptoms equivalent to those of acute midgut volvulus.

–      Abdominal tenderness and guarding is usually present, as well as abdominal distention.

Acute duodenal obstruction

–      Abdominal distention and gastric waves may be present.

–      Passage of meconium or stool can be present.

–      These patients usually do not have signs of peritonitis or shock unless volvulus is also present distal to the obstruction.

Chronic duodenal obstruction

–      Physical examination results may be completely normal at the time of presentation.

–      Abdominal distention and tenderness may be present.

–      Diagnosis is usually made by history and enough suspicion to obtain radiologic studies; physical examination findings are very unreliable.

–      -Intravenous (IV) fluids to help prevent dehydration dopamine at an infusion rate of 3 mcg/kg/min intravenously (IV) and continue it postoperatively even if the patient is not hypotensive.

–      -If the patient is unstable, do not delay surgical intervention for upper GI and laboratory studies. Quick surgical intervention, not prolonged medical management, produces the best results if midgut volvulus is suspected

–      Your child may also be given and antibiotics to prevent infection.

Duodenal obstruction

–      After the volvulus is reduced or if no volvulus was present, identify any extrinsic obstruction to the duodenum.

–      If peritoneal bands crossing the duodenum are found, ligate them with careful attention to protecting the superior mesenteric vessels. The bands may also obstruct the ileum or the jejunum and sometimes run to the gallbladder and liver.

Post operative care and Consultations

•       Pediatric surgeon: The only definitive treatment for malrotation is surgical in nature.

•       Dietary/intravenous nutrition team: In hospitals where available, include a nutritionist in the medical team to monitor total parenteral nutrition to ensure optimal levels are being achieved.

•       Physical therapist

–      A physical therapist can help with range of motion exercises and strength conditioning while patients are bedridden.

–      Frequent repositioning also helps prevent decubitus pressure and head molding (in infants).

•       Occupational therapist

•       An occupational therapist also helps with range of motion exercises.

•       Occupational therapists can also assist with splinting of extremities that contain central lines to prevent contractures.

•       Speech therapist

•       A speech therapist can help with oral stimulation while patients are not being fed. This stimulation can prevent feeding aversion and dyscoordination when oral feeds are restarted.