RESPIRATORY 211-PEDIATRICS AND NEONATOLOGY
Fetal and Transitional Circulation
The Fetal Respiratory SystemThermoregulation of the Newborn
Evaluation and Delivery Room Care of the Newborn
Neonatal Diseases--Birth Asphyxia, RDS, BPD, MAS
Neonatal Diseases--Pulmonary Dysmaturity, Apnea, TT, the Pneumo's
Neonatal Diseases--Pulm Hem., PPHN
Neonatal Diseases--EA, TEF, Choanal Atresia, CDH, NEC
Pediatric Diseases--Epiglottitis, Croup, FBA
Pediatric Diseases--Asthma, Bronchiolitis
Pediatric Diseases--CF, Pneumonia
Pediatric Diseases--Near Drowning, Orthopedic problems, Neuromuscular Diseases, Poisoning
Equipment--Infant Ventilators, Capnographers
1) FETAL AND TRANSITIONAL CIRCULATION--Part 1
The development of the placenta begins as a zygote (fertilized egg) that implants itself into the lining of the uterine wall (endometrium). After three weeks the villi have developed allowing placental/fetal circulation to begin. By six weeks the spiral arteries are in the intervillous space, and by twelve weeks all the arterioles are developed. Dilatation of the existing arteries continues until birth.
1. Maternal Side of the circulation--Uterine Arteries--Endometrial Arteries--Spiral Arteries--Blood enters the intervillous space. Blood flow is pulsitile (propelled in jet-like streams) as maternal blood pressure (BP) is very high compared to fetal BP (intervillous space). The arterial oxygenated maternal blood flows over and around the villi allowing metabolic gaseous exchange to take place. The maternal deoxygenated blood carrying fetal waste products makes its way back to the endometrial veins--uterine veins--systemic circulation.
Analogy between the Alveolar/Capillary Membrane--the Maternal/Fetal blood never comes in contact with each other.
2. Fetal Side of the Circulation--Fetus--Umbilical Arteries (carrying deoxygenated blood from the fetus--similar to PA) into fetal capillaries in the anchoring villi. Maternal blood in the intervillous space flows over and around the villi--metabolic/gaseous products exchanged--fetal oxygenated blood returns to the placenta via the Umbilical Vein.
The rate of blood flow through the placenta is determined by the interaction of Maternal/Fetal blood pressure and Maternal Systemic Vascular Resistance (SVR).
REMEMBER--THE UMBLICAL ARTERIES CARRY DEOXYGENATED FETAL BLOOD TO THE PLACENTA (MOM) WHILE THE UMBLICAL VEIN CARRIES OXYGENATED BLOOD FROM THE PLACENTA (MOM) TO THE FETUS.
Pathway-A) The single Umbilical Vein carrying oxygenated blood from the maternal side of the placenta enters the fetal umbilical area .The Vein then splits into two sections. The first one half of the blood goes directly to the liver via the Portal Vein. Metabolism takes place then the blood is drained via the Hepatic Veins directly into the Inferior Vena Cava (IVC). The second half of the blood is shunted directly into the IVC via the Ductus Venosus (DV) when both halves of the blood enter the Right Atrium via the IVC, the blood is still very well oxygenated.
B. In the RA, two streams of blood are traveling across each other's paths without mixing. The Blood from the IVC shoots across the RA through the Foramen Ovale (FO) into the Left Atrium (LA). It then proceeds through the Left Ventricle (LV) into the Aorta and into the Internal Carotids, the Vertebral and the Subclavian arteries. The result is that the fetal brain and upper thorax receive well-oxygenated blood from the mother. This is critical as the fetal brain has extremely high oxygen demands. The second stream of blood in the RA comes from all the venous drainage in the head. The Internal Jugular, the Vertebral and the Subclavian veins all drain via the Superior Vena Cava (SVC) into the RA. This blood drains into the Right Ventricle (RV) and goes into the Pulmonary Artery (PA). When it tries to drain into the Right and Left PA's, this venous blood meets a huge resistance (high back pressure) from the fluid filled lungs. It therefore takes the path of least resistance by shunting across the Ductus Arteriosus (DA) into the Aorta after oxygenated blood has been delivered to the head.
C. After the oxygenated blood goes to the brain and deoxygenated blood (venous) from the head have mixed after the DA, this mixed blood proceeds down the fetal thorax, abdomen, etc., via the aorta. Eventually, the aorta divides into the Iliac Arteries--Hypogastric Arteries--and finally two Umbilical arteries. The two umbilical arteries take the deoxygenated blood from the fetus back to the maternal side of the placentas.
VERY IMPORTANT--IF A NEONATE BECOMES HYPOXIC SHORTLY AFTER BIRTH, THE DUCTUS ARTERIOSUSU WILL REOPEN TO REESTABLISH FETL CIRCULATION. THIS IS CALLED A PDA (PATENT DUCTUS ARTERIOSUS).
Once Steps a--e have occurred, adult circulation is established.
***26-28 weeks--The alveolar Capillary Membrane is sufficiently developed to support extrauterine life.
***35-36 weeks--Full maturation of the respiratory system.
Remember that MOM is the best incubator. When trying to delay labor of a premature infant, give beclamethasone.
L:S ratio of 2:1 correlates with a gestational age of 35-36 weeks. Prior to 35-36 weeks, the L:S ratio is <= 2:1, thus IRDS is much more common. Postnatally, an L:S ratio can be obtained via gastric aspirate.
This technique withdraws a sample of the chorionic tissue from the placenta using needle aspiration and ultrasound. Recent controversy centers on doing this procedure prior to ten weeks gestation as an increased incidence of deformity of the extremities has been noted.
The negative intrathoracic pressures required by the first breath are -70 cwp. By the 3-4th extrauterine breath, these pressures have dropped to -20 cwp. These large pressures are applied for only .5-1 second, and after the first few breaths, the infant has established both his Vt and FRC.
The premature infants had rate compensation only due to: 1) the Hering Breuur deflation reflex-inhibits inspiration once a certain title volume is reached. This is much stronger in the premature than the full term infants: 2) decreased neuromuscular development in premies-they lack gamma fibers in their striated muscle. Remember that when gamma fibers are stimulated, the patient experience dyspnea; 3) decreased chest wall stability due to very little ossification.
2. Secondary Apnea--does not respond to pain, cold or bagging. Resuscitative efforts must begun immediately.
3. Premature Apnea--seen in 30% of all premature infants. This is apnea of >= 30 seconds duration accompanied by decreasing O2 saturations. We know they have decreasing saturations by Pulse Ox, but what do you see if you're a parent?
RULE #1--THE LONGER THE DURATION OF APNEA, THE LONGER THE RESUSCIATION WILL BE!
RULE #2--NEVER LEAVE A GASPING INFANT
b) Causes of Apnea--1) Upper Airway occlusion due to formula or secretions;
Note: Premature Apnea does not respond particularly well to O2 bagging
c)Rx of Apnea--1) Tactile Stimuli;
2) Rocking Beds H20 or IPPB
3)Theophylline--CNS Stimulant
a) Newborns have an enormous surface area compared to their mass, and they lack the insulating layer of fat adults have. Infants lose heat by four mechanisms:
1. This is a recent innovation in the field of neonatology. In the 1890's Budin (MD) noted a striking difference in mortality of infants weighing <=2000 gms at birth. If their rectal temperature was <= 32 0 C--98 % died, but if their rectal temperature was >= 35 0C, only 23% died. He proceeded to build the first modern incubator with the Director of the Paris Zoo.
1. Warm baby slowly so that the temperature gradient between the skin and the room is <= 1.5 0 C. This prevents further metabolic stress.
Equipment used to RX Hypothermia
Part IV--Evaluation and Delivery Room Care of the Newborn
What do the numbers mean? If the infant scores between 7-10, maintain an NTE and observe.
Remember ABC--Airway--place the infant in the sniffing position, do not hyper extend the neck.
Breathing--Laryngoscope, tube, aspiration of secretions via suctioning, intubate, bag with 100% O2 at a RR of 40-60 per minute.
Circulation--Chest massage--Hand position-one finger below the nipple line at a rate of 100-120 per minute depressing the sternum 1/2 to 1 inch using the two thumbs or two finger technique.
Retractions (intercostal and xiphoid), audible wheezing, nasal flaring, grunting and respiratory pattern. In this case, the higher the score, the worse is the respiratory distress the infant has.
14. Why does an infant end up with an Apgar score of 1-3?
a) Maternal factors
1. Uterine/Placental factors
a) Placenta Abruptio--the partial or complete detachment of the placenta from the uterine wall prenatally. The mother is at risk for hemorrhage and the baby is at risk for death. This condition is an indication for immediate delivery.
b) Placenta Previa--the placenta is attached to the cervix instead of the uterine wall, i.e., the placenta is preceding the baby. A vaginal delivery is impossible or hemorrhage results. A mother may have a total or partial placenta previa. 6/10 women with a partial placenta previa still need a C-section.
c) Postmaturity of the Placenta--an old placenta deteriorates in function. (limit is two weeks overdue, then labor is induced).
d) Toxemia (pre-eclampsia)--complication that usually happens at the 20-24th week of pregnancy. Originally, we thought it was brought about by two rapid weight gain during pregnancy, but now poor nutrition especially decreased protein in the diet
appears to be the cause.
Stage 1 of Toxemia-edema, increased BP, and proteinuria
Stage 2-vision disturbance, headaches, mental dullness due to cerebral edema, abdominal pain.
Stage 3-convulsions, coma
Toxemia affects the baby negatively (poor placental function, SGA [small or gestational age], increased incidence of prematurity, placenta Abruptio, therefore increased likelihood of C-section.
e) PROM (Premature Rupture of the Membranes)--delivery must occur in <= 24 hours to prevent infection to the fetus. Umbilical Cord Compression and Prolapse are often associated with PROM--MEDICAL EMERGENCY-O2 is cut off to the fetus--Knee/Chest Position.
f) Erythroblastosis fetalis--Hemolytic anemia of the newborn--Blue Baby--We know that in a normal placenta fetal and maternal blood are prevented from mixing. During the birth of the first child, the placenta may tear, so that some fetal blood cells enter the maternal circulation.
Rh- mother Rh+ father
Rh+ fetus
If the second child is Rh+, maternal antibodies pass easily through the placenta and destroy the fetal circulation; this results in a Blue Baby at birth. This condition can be prevented by giving RHOGAM(anti Rh gamma globulin) during the 7th month and
right after birth.
g) Diabetes Mellitus--There are more then ten million diabetes in the U.S.-1/2 are unaware of their condition.
1. Diabetic women who become pregnant are more prone to toxemia, infections and congenital malformations. All diabetic pregnancies should be considered high risk. The earlier the onset of diabetes in a women's life, the worse the prognosis for the pregnancy. The risk is greatest for insulin dependent diabetics.
2. The risks to a fetus of a diabetic women are: hypoglycemia, decreased serum Ca++ levels, increased Bilirubin levels, increased size of the heart and adrenals, decreased brain size. The risk of RDS is 5.6% greater in a diabetic pregnancy compared to a normal one. The safest time for delivery is 36 weeks when the L:S ratio is 2:1 or >. The fetus of a diabetic women is at greatest risk during the last several weeks before labor especially is the women is insulin dependent. Doctors will normally induce labor at week 36-37 in the diabetic Mom to prevent maternal strain. If a diabetic pregnant women becomes toxemic, this is an immediate indication for delivery.
3. Gestational diabetes--Dx via High carbohydrate meal and Glucola. TX-high protein, low carbohydrate diet during pregnancy.
2. Drugs administered to Mom during Labor and Delivery
a) Inhalation Anesthetics--70% N20/30% O2
b) Local anesthetics--epidural block
c) Parenteral Medications--given to block the pain of L/D-ex. Narcotics.
d) Substance Abuse--ETOH, Cocaine, Lithium, Reserpine all depress the neonate.
3. CardioPulmonary Problems
a) Hypotension due to Aortic IVC Compression--"Supine
Hypotension Syndrome" or hypotension due to sympathetic block from regional anesthetics (epidural) or hemorrhaging.
b) To prevent Aspiration Pneumonia, Mom is not allowed to eat until several hours after labor.
4. Trauma during delivery
a) Intrauterine obstetric manipulation
b) Cephalopelvic disproportion (CDD)
c) Fetal presentation--breech, brow, face
2. Fetal Problems
a) Abnormal Fetal Heart Rate- A decreased rate indicates the fetus is not tolerating labor well. Normal Fetal Heart Rate (FHR) is 120-160 BPM. During contractions, the FHR slows and quickly returns to normal when the contraction is completed. An increase
or decrease of 20 beats/min abruptly indicates that the fetus is not receiving enough O2.
Part V--Pharmacology of the Neonate
Because of placental transfer, a woman is advised to take as few drugs as possible during pregnancy. Review of Placental Circulation-- Deoxygenated blood from the fetus makes its way to the fetal capillaries via the umbilical veins. Remember that the
fetal capillaries are in the tip of the placental villi. At this point the maternal blood spurts via the spiral arteries into the intervillous space--gas and drug exchange can take place.
1. Mechanisms drugs use to cross the placenta
a) Simple diffusion-a substance moves from an area of high to lower concentration. O2, CO2, fatty acids and some drugs are transported this way.
b) Facilitated diffusion-simple diffusion with an added push (membrane proteins guide and expedite materials moving through the membrane.) Glucose and other CHO's travel this way.
c) Active Transport-This is an energy requiring process when substances move against a concentration gradient. Amino acids and H2O soluble vitamins use this route.
d) Pinocytosis-substances are transported across the membrane via small vesicles, ex. IgE.
e) Abnormal breaks in the placental architecture such as the transfer of drugs or fetal blood cells as in Erythroblastosis Fetalis.
2. Factors that will help a drug get across the Placenta
a) High Lipid Solubility--remember that the cell membrane is made up of lipoproteins.
b) Low Molecular Weight--the lower the weight, the more easily a substance can traverse the placenta via simple diffusion.
c) High Placental Blood Flow--If you want to get a drug into Mom but not the fetus during L&D, give it during a uterine contraction when blood flow to the placenta is decreased.
3. How to get drugs in and out of the neonate
The safety and efficacy of any drug is dependent on four processes:
a) ABSORPTION-This is required for a drug to reach its site of action.
1. Oral Route--the drug is well absorbed this way, but many infants have vomiting or an active spitting reflex, so we may not be successful this way.
2. Subcutaneous--only very small volumes can be administered this route as it can compromise blood flow to the skin and tissues. In addition, poorly perfused areas will not receive this medication.
The opposite situation can also occur. Absorption of drugs through the skin of the neonate is>= adults as infants have a thin stratum corneum, therefore systemic absorption can easily occur. This is especially true of infants undergoing
phototherapy as the heated skin vasodilates.
3. Parenteral-anyway but the abdomen-#1,2,4,5,6
4. Intramuscular-ex.deltoid, gluteus maximus
5. Intravenous-most effective as it enters the circulation directly, but not all drugs can be given this way. In addition, many combinations of drugs can't be given this way.
6. Inhalation-how much is reaching the targeted area--
2nd most effective way to give a drug.
b)DISTRIBUTION--the passage of drugs across the membranes through the circulation and out into the tissues. The initial distribution of a drug is related to the perfusion of a specific tissue or organ.
1. Drugs in the circulation become bound to plasma proteins. When this happens they on longer have a pharmacological effect. Therefore the level of plasma proteins can have a significant effect on the distribution of drug. Review oncotic vs. Hydrostatic pressure.
c)BIOTRANSFORMATION--This is the rate limiting step in many neonates. Most drugs are highly lipid soluable and easily cross into the renal tubules. However, in order to exit in the urine, they must be converted into a H2O soluable form. Due to the immature kidneys in infants, this may cause an increased half-life of the drug.
d)RENAL EXCRETION THROUGH URINE--In the newborn renal blood flow and Glomerular Filtration Rate (GFR) are about 30% of adult values. There is also decreased tubular secretion, but fortunately there is a very rapid maturation of the kidney in the first week of life. The above differences are even more pronounced in the premature baby.
There are two basid types of drugs used during L&D--Analgesics which relieve by raising your threshold to it, and anesthesia. Anesthesia can either be regional (to a particular area of the body) or general (block consciousness).
a) Analgesics
1. Tranquilizers-ex. Valium, Miltown,Vistaril. These are good for a long labor to reduce anxiety, but Mom tends to lose alertness and may lose control over contractions.
2. Barbiturates--ex, Seconal, Nembutal. Sedate and produce sleep. Unfortunately, they easily cross the placenta and are stored in the infants midbrain for >= 1 week postpartum.
3. Narcotics--
a) Nistenil-allows Mom to relax without losing control of contractions. It is short-acting and has little depressive effect on the infant.
b)Demerol (Merperidine)-used to bring blood pressure down during toxemia that develops during labor. It's so effective that it can produce hypotension thus compromising the O2 supply to the fetus. It can also bring about loss of control as Mom feels sleepy and drunk. If given, IV is the quickest way not cross the placenta (protein bound), but it does effect labor. It is administered into the epidural space surrounding the spinal cord after Mom is 6 cm dilated.
Disadvantages--1. An experienced anesthesiologist must do the procedure otherwise the meninges will be punctured.
2. It takes 10-15 minutes to take effect unlike a Spinal that takes only 3-4 minutes.
3. It may decrease maternal BP significantly and therefore
O2to the fetus, thus BP must be monitored religiously.
4. It may make the following chain of events probable:
a) Episiotomy and/or forceps delivery
b) IV hydrating solution with oxytocin (to increase the contractions that may have slowed down).
c) Artificial rupture of the membranes to make sure the baby is positioned head down. The uterus may relax post-epidural letting the baby position himself sideways. d) Fetal Monitoring-(noninvasive or invasive)-to check thebaby's reaction to the epidural.
c) How much do L&D drugs result in Neonatal Depression?
Research studies correlating maternal sedation with the clinical condition of the newborn indicate that the drugs given during L&D do not have a profound depressive effect on the infant. But, if fetal asphyxia is present, the added effects of the drug create a prolonged recovery from CNS depression for the newborn.
1. Signs of Fetal/Neonatal Depression
a) Bradycardia-most frequent
b) hypotonia, hyporeflexia
c) hypotension, apnea, seizures
d) mydriasis-pupils dilated
5. Drugs of Resuscitation
a) The most important resuscitative effort is adequat ventilation and oxygenation as hypoxia is the greatest threat to the infant's survival and normalcy.
b) Plasma Volume Expanders--many infants especially the premature ones become volume depleted at birth secondary to in utero asphyxia. We can correct this by giving large volumes of fluids. The best fluids to give are:
1. Whole Blood--Cross type and match--In the past, placental blood has been used, but sepsis was a real problem. Universal donor vs. universal receiver.
2. Colloids--Blood Substitutes--these replace or add blood protein, increase oncotic pressure and draws fluid into the vessels. Albumin or Salt Poor Albumin (SPA) are given. What if you have leaky capillaries?
3. Isotonic Crystalloids--These are used to increase Hydrostatic pressure, but they can leak into the extravascularspace easily (Third Spacing), and also cause hypernatremia.
Examples are NaHCO3, D5W and NaCl solutions.
Remember that infants have immature kidneys that are not adept at handling fluids, therefore edema and overload are very common problems.
c) Narcotic Antagonists-Neonatal Depression due to maternal narcotic administration can be reversed by giving Nalorphine or Naloxone (both are better known as Narcan). Drug elimination in the newborn is best if it can wear off naturally, but methods to expedite this are: 1) forced diuresis with Lasix; or 2) if renal failure is present, gastric lavage or exchange transfusion is possible.
d) Sodium Bicarbonate for Metabolic Acidosis--If ventilation is adequate, give 1 ml/kg through a Umbilical Artery (UA) catheter. Commercially available preparations are 1 ampule = 44 meq. In the last fifteen years we have become much more conservative with the administration of Na HCO3 in both adults and infants. In premature infants there is a greater risk of intraventricular hemorrhage (IVH) if too much
NaHCO3 is given too fast.
e) If good ventilation is established but bradycardia persists, give Calcium Gluconate-The HR should pick up immediately, if not stop drug instantly.
f) Unresponsive Asystole- 1-3 ml of 1:10,000 dilution of Epinephrine IV or Intracardiac injection. Remember that sympathomimetics work best in a normal pH range, thus expect a rebound effect post code.
g) Other drugs likely to be found on the Code Cart--What are their functions?
1. Atropine
2.Diazepam (Valium)
3.Digoxin
4. Dopamine
5. Epinephrine
6. Furosemide (Lasix)
7. Heparin
8. Hydrocortisone
9. Lidocaine
10. Racemic Epinephrine
11. Phenobarbital
6. Drugs used to Rx Infections and Apnea in the Newborn
a) Infections especially bacterial are very common in the newborn period. Many times the specific causative agent is not isolated. The Penicillin's are a group of drugs that are effective against most gram positive and negative organisms. Anaphylactic reactions to penicillin are fairly uncommon. Penicillin G is the prototype drug used in newborns. It is excreted unchanged in the urine therefore the rate of excretion not biotransformation controls the serum levels. It's expensive. Both birth weight and age correlate with clearance of penicillin from the plasma, therefore the dosage and drug interval change rapidly with age and weight. In the hospital the drug is normally given IM or IV. Other examples of Penicillin antibiotics are: Ampicillin, Methicillin, Naficillin and the
Semi-synthetic Penicillin's (several generations for organisms that are resistant to the original).
b) Aminoglycosides (ex. Kanamycin, gentamicin, streptomycin, neomycin, tobramycin and amikacin). These drugs act by inhibiting protein synthesis in bacteria (bacteriostatic). They are given parenterally as they are not absorbed by the GI tract, i.e., IM or IV. Aminoglycosides are toxic to the 8th cranial nerve
(Vestibular-Cochlear) and the kidney, therefore hearing loss, vertigo, proteinuria and azotemia (increased uric acid) result. The limiting factor is the total dose not the duration of the Rx. Neonatal sepsis is often a mixed infection (gram - or +) so penicillin and aminoglycosides are given together for complete coverage.
c) Chloramphenicol is a bacteriostatic drug against gram - and + organisms, Rickettsia and Chlamydia. This drug is reserved for infections that have not responded to to the previous drugs "gray baby syndrome"--vomiting, diarrhea, abdominal distention, poor feeding, respiratory distress and cardiovascular collapse. The drug side effects may be difficult to distinguish from the underlying disease
d) Theophylline, Caffeine, Theobromine and other Xanthines for Apnea and Bradycardia--Direct stimulus to the medullary center, the CNS, a bronchodilator, increases heart rate and is a diuretic. Can be administered orally, rectally, or IV. Rectal
absorption through suppositories can be erratic. Serum levels are the most accurate way to judge the dosage and drug interval(peak and trough levels). The therapeutic range is 10-20 ug/ml.
Part VI--Resuscitation of the Neonate--ABC
1. Differences between an Adult and Infant Airways--see Handouts
2. Tracheal Intubation--This is seldom an emergency. Bag and Mask ventilation is more than adequate while all the equipment is being assembled and tested.
a) Equipment needed:
1. Laryngoscope handle with bulbs, blades, batteries- test bulbs to make sure working. Straight Blade (Miller) Size 0 for premature infants, size 1 for full term newborns vs. Curved Blades (MacIntosh). In infants, the straight blade is more popular as it gently covers the epiglottis for visualization vs. the curved blade that rubs up against the vallecula causing further airway edema.
2. Endotracheal tubes--see chart (Premature Infants 2.5 or 3. Full terms 3.5)--always have several sizes available.
3. Water soluble lubricant--KY jelly or lubrifax
4. Local anesthetic--ex. Cetacaine or Benzocaine
5. Tincture of Benzoin and Tape or the Dale trach tube holders (velcro) or the Neobar.
6. Bag and Mask with Manometer and O2 source
7. Suction source with the appropriate size catheters, Yankeur if needed.
3. Procedure for Intubation
a) Infant's head should be slightly extended in the sniffing position. Hold laryngoscope in the left hand, insert near the midline of the mouth and move to the left side gently deflecting the tongue. A second person should be stabilizing the infant's
head as this is done.
b) Suction with a regular suction catheter or Yankeur the oro and laryngopharynx thoroughly. Advance the blade. Don't try to pick up the epiglottis with the laryngoscope blade as it may cause hemorrhage and edema.
c) Lift the jaw and tongue up (pull up on the blade) as the third person applies pressure over the hyoid bone/laryngeal cartilage. This pushes the larynx posteriorly and exposes the vocal cords. Insert the ETT alongside the laryngoscope through the cords and about 2 cm beyond. In adults, insert until the cuff disappears.
d) Withdraw the laryngoscope carefully while holding onto the ETT with the right hand. Connect the tube to a 100% O2 source and ventilate the infant at 40-60 BPM at a pressure of 20-25 cwp. Evaluate breath sounds in bilateral lower lobes, if decreased BS, increase the ventilating pressure.
e)The maximum allowable time for one intubation try is 30 seconds. Do not wait until bradycardia and hypotension develop. If an attempt at intubation fails, ventilate >= 2 minutes before another attempt is made.
f) Correct placement of the tube is verified by checking Bilateral BS, listening over the stomach to make sure the ETT is in the trachea. Look for symmetrical chest movement on inspiration and get an X-Ray.
4. Practical Points for Tracheal Intubation
A) Bag and Mask Therapy--Two types of bags used in the newborn:
1) Flow Inflating (Mapleson) Bag is a thin walled anesthesia bag with a soft blob face mask to prevent pressure necrosis. The pressure is adjusted by a valve and read with a manometer. The Peep is adjusted by changing the flow. A tight fit around the nose and mouth is essential.
2) Self-Inflating Bag--Recoil characteristics of the bag allow for reinflation following a manual deflation. It doesn't require source gas to work, unlike a flow inflating bag. Pressure popoffs and PEEP devises are available for these self inflating bags. An ADVANTAGE of the flow-inflating bag is that the therapist can feel the compliance of the lungs.
3) Complications of Bag and Mask Therapy
a) Pneumothorax--always check the pressure limit or popoff before using it on a baby.
b) corneal lacerations, pressure necrosis
c) aspiration of vomit
d) dependence of assisted ventilation
4) ETT-- should be made of non-toxic polyvinyl chloride which will conform to the shape of the trachea when warmed to body temperature. It should be implant tested (Z-79), sterile and have a radiopaque line to facilitate location. As children's tubes are uncuffed up until they are 10-12 years old, we can't use the minimal leak technique of adults. We use the "Pressure Leak" Technique,i.e., we listen for a small leak on inspiration and note the pressure that occurs at. See Handout for tube sizes.
Cut the tube if extra-long, but leave enough in case we have to change the position post-XRay. In order to fix the tube, dry mouth and lips, paint cheekbones with benzoin, allow to dry and secure the tube with adhesive or umbilical tape. Newer methods for securing tubes include the Dale ETT or Tracheostomy holder and the Neobar. Tape will have to be changed often depending upon the amount of secretions and salvia.
a) Nasotracheal intubation--This is an elective procedure for greater patient comfort and long term stability. The tube is introduced through the nares; the cords are
visualized as usual, and then the McGill forceps are used to direct the nasal tube through the cords while the oral tube is being removed. Nasal trauma and necrosis can occur if not done carefully.
5) External Cardiac Massage--A,B,C (Airway, Breathing
Circulation and Compressions)
a) Check Pulse--Infant <= 1 yr.-Brachial
Child 1-8 yrs-Carotid
Remember that Infants have no necks, thus to find a brachial pulse, go halfway between the shoulder and the elbow and press against the humerus.
b) Compressions--In the Infant go one finger below the nipple line in the mid-sternum. The heart is higher in the Infant compared to the child or adult. Use two-three fingers to compress 1/2 to 1 inch at a rate of >= 100 minute. Count
1,2,3,4,5. Alternative method is to use two thumbs with hands encirculating the chest. As with adults, the infant must have firm back support for the compressions to be effective. A child's compressions have the same hand position as an adult, but
only one hand is used to compressed. The rate is 80-100 a minute compressing 1-1 1/2 inches with the count of 1 and 2 and 3...With Infants and Children, 1 man OR 2 man CPR, the ratio of Compressions/Breaths is 5:1. Remember, in adults one man CPR
ratio of compressions/breaths is 15:2 while two man CPR is 5:1.
1. Asphyxia Neonatorum--term used to describe the hypoxia,
hypercapnia and acidosis in the newborn. All neonates experience varying degrees of asphyxia as a result of delivery. How do we assess if it is clinically dangerous?
a) Factors that produce Birth Asphyxia
1. prolonged severe contractions
2. uteroplacental insufficiency
3. multiple births
4. umbilical cord prolapse or entanglements
5. maternal sepsis or hemorrhage
6. maternal analgesics and anesthetics
b) Fetus will demonstrate asphyxia via
1. passage of meconium
2. tachycardia (>= 180 beats/min) or bradycardia (<=100 beats/min)
c) Fetal Asphyxia is monitored by:
1. Fetal Heart Rate (FHR)-Internal or External
Monitoring-see Handout
2. Fetal scalp gases-drawn in utero during labor after
ROM
ABG's Early labor Just before delivery
pH 7.33 pH 7.2
PaCO2 41 PaCO2 55
PaO2 24 PaO2 17
d) Respiratory Complications from Birth Asphyxia
1. Meconium Aspiration Syndrome (MAS)
2. Respiratory Distress Syndrome (RDS)
3. Neurological damage due to cerebral edema, seizures and respiratory depression.
2. RDS, IRDS, Hyaline Membrane Disease (HMD)
a) most clinically significant disease of the newborn
period. Full term infants-1/6000 births vs. Premature Infants-
600/6000 or 10%.
b) Factors that cause RDS
1. weight <= 1.5 kg
2. diabetic mother
3. C-section-no vaginal squeeze
4. intrapartum and postpartum asphyxia
c) Clinical Signs and Symptoms of RDS
1. Cyanosis in Rm Air
2. Tachypnea (60-120 BPM)
3. Flaring Nares
4. Intercostal Retractions
5. Expiratory Grunt
Numbers 3-5 are often abbreviated in a chart as GFR.
Expiratory Grunt-infant exhales against a partially closed glottis. This maintains back pressure on the airways and prevents the alveoli from collapsing, thus increasing physiological PEEP. Severely affected infants will grunt with every breath.
d) Breath sounds-decreased aeration, fine rales-Why?
What are the alterations in lung function?
1. decreased Vt-ling compliance is 20% of normal-"Cement
Block Lung"
2. Massive Atelectasis-decreased V/Q ratio-this is followed
by decreased perfusion to the collapsed areas. decreased due to increased VD, therefore increased WOB
4. right to left shunt-PDA-cyanosis due to hypoxia, increased PVR.
e) Etiology RDS-
1)Theory 1--decreased surfactant production-->atelectasis-->alveolar hypoperfusion-->ischemic lung tissue-->change in alveolar permeability "leaky"-->formation of hyaline membranes
2) Theory 2--intrauterine hypoxia-->pulmonary vasoconstriction-->alveolar hypoperfusion-->decreased surfactant production-->increased alveolar wall permeability-->formation of hyaline membranes
f) Histological Section of the lung--hyaline membranes lining the lung made up of blood and fibrin results in dilated alveolar ducts and atelectasis--> major diffusion defect
g) Differential Diagnosis-RDS resembles other neonatal diseases such as D-Hernia, Pneumothorax, etc. but the key is the Chest X-Ray (CXR). It resembles "ground glass" (diffuse bilateral reticulogranular densities) with air bronchograms and
cardiomegaly.
h) Treatment
1. Rx hypoxia and prevent return to fetal circulation. Normally at birth the increasing PaO2 and the decreasing Pulmonary Vascular Resistance close the Ductus Arteriosus(DA), but if the infant is hypoxic as in RDS both the DA and the
Foramen Ovale (FO) reopen This causes a R-->L shunt which makes the hypoxia, hypercapnia and acidosis worst. The infant ends up cyanotic with refractory hypoxemia.
2. Give O2 to stop the hypoxia but prevent the Flip-Flop phenomena. If one decreases the FIO2 too rapidly in an infant, there is a dramatic and disproportional drop in the PaO2. Then in order to get the PaO2 back up to where it was before, we have to go way up on the FIO2. The rule of thumb is that in weaning FIO2 on stable neonates decrease it <= 5% at one time. On unstable neonates, decrease it <= 2% at one time. Monitor their reactions via pulse ox saturations and vital signs.
REMEMBER- Increased PaO2 in the lungs--vasodilation of vessels
Increased PaCO2 in the lungs-vasoconstriction of the vessels
Increased PaO2 in the head--vasoconstriction of the vessels
Increased PaCO2--vasodilatation of the vessels
3. The infant must be maintained in a Neutral Thermal
Environment (NTE), therefore any O2 must be warm and humidified to 32-34 oC. Remember that the temperature sensors for an infant are located on his forehead and around the eyes and nose, thus if the infant's head is warm, the whole body will believe it is warm. Increased or decreased head temperature will lead to increased O2 consumption and WOB.
4. Infants with the expiratory grunt will benefit from CPAP (nasal or oral). CPAP will stabilize the alveoli by increasing the FRC and decreasing atelectasis, therefore the PaO2 will increase. Infants with respiratory/ventilatory failure and/or apnea will require mechanical ventilation. ABG's--pH <=7.2, PaCO2>= 70, PaO2 <=40 on 100% O2--"buy a tube"
5. Prolonged O2 therapy in RDS may cause O2 toxicity (depends on the level of FIO2 and the duration of hyperoxia). If the hyperoxia is short, retinal vasoconstriction will occur, but this is reversible. If the hyperoxia is prolonged, new capillaries and fibrous tissue grow causing hemorrhage. This causes retinal detachment and blindness. This process is known as Retrolental Fibroplasia (RLF)orRetinopathyof Prematurity (ROP). To prevent this we try to keep the premature infant's PaO2 in the 50-80 mm Hg range. In addition, prolonged O2 therapy may also cause pulmonary hemorrhage and BPD.
3. Bronchopulmonary Dysplasia (BPD)-See the Spitzer article
a) Pulmonary Interstitial Emphysema (PIE) Air Leak Syndrome-during stage III and IV, the alveoli develop leaks due to tissue breakdown from increased FIO2 and PIP. The CXR becomes fuzzy as air leaks into the interstitium.
4. Meconium Aspiration Syndrome (MAS)-see handout and case study with ECMO
5. Pulmonary Dysmaturity or Wilson-Mikety Syndrome
a)Etiology-this affects premature infants <= 1.5 kg. It normally occurs 1-5 weeks afterbirth. It is caused by alveoli that have failed to grow and multiply, not due to RDS.
b)Symptoms-Cyanosis, dyspnea, wheezing, hyperinflation, cor pulmonale. The respiratory distress and Cor Pulmonale retard the growth of the infant.
c) CXR-Cysts, diffuse infiltrates, hyperinflated lungs, flattened diaphragms
d)RX-is supportive. Give O2, diuretics and digitalis to relieve resp. distress and Cor Pulmonale while waiting for alveoli to grow.
6. Apnea-the more premature the infant is, the more likely apnea is to occur. >= 75% of infants that weight <= 1.25 kg have apnea.
a) Primary apnea occurs at birth. It is defined as no breath for >= 30 seconds with bradycardia and acidosis. It responds to touch and O2. Gasping follows primary Apnea
that turns into normal breathing or secondary apnea. Secondary apnea produces severe cyanosis and bradycardia that do not respond to touch or O2. Full resuscitation is required.
b) Etiology-1.immature respiratory center or brain damage
2. RDS, Pulmonary hemorrhage, asphyxia, fever or infection can
precipitate apnea.
c) Rx-tactile stimuli, rocking beds, theophylline or caffeine, apnea monitors (HR and RR), CPAP (2-4 cwp to increase FRC and cerebral oxygenation), MV.
7. Transient Tachypnea-RDS II-hard to differentiate Transient
Tachypnea(TT) from RDS in the early stages.
a) Etiology-This occurs in full term infant with slow absorption of amniotic fluid from the lungs. C-section babies are at risk due to no vaginal squeeze. Normally, this disease clears up spontaneously within 3-5 days as the lymphatics removed excess fluid.
b) Symptoms-infants breath up to 120/minute. ABG's are normal, CXR-lung fields streaky, cardiomegaly.
c) Rx-supportive
8. Pneumothorax, Pneumomediastinum, Pneumopericardium
a) Pneumothorax-usually associated with other problems of
prematurity
1. Types-A) Spontaneous-resolves without Rx or resp. distress, in communication with air leak-usual cause is contact sports.
B) Loculated-sealed off-resolves without Rx.
C)Tension-positive pressure creates a ball/valve mechanism.
2. Causes-A) MV, resuscitation, intubation-increased incidence of pneumothorax.
B) Aspiration of foreign material into the lungs such as meconium, blood, amniotic fluid, formula.
C) generated by taking the first breath.
3.Clinical Symptoms/Diagnostic procedures
A)Irritability, deterioration in appearance.,
B) Cyanosis, dyspnea, tachycardia.
C) Decreased breath Sounds and hyperresonance on the affected side. This will be difficult to assess in a premature infant as breath sounds are transmitted all over the chest, therefore a change in the point of maximal impulse (PMI) is diagnostic. Remember that an infant's PMI is further to the right than an adult due to the increased size of the RV.
D) CXR-what would you see?
E) Nasal Flaring, intercostal retractions
F) Transillumination-turn out the lights and view both sides of the chest with a high intensity LED. The side with the pneumothorax will transmit more light (light up) as air is translucent. The normal side will not transmit as much light.
4. Rx-aspirate the air via needle, insert a chest tube to reexpand the lung. Chest tube placement-for an apical pneumothorax, place at the level of the second rib at the MCL (midclavicular line): for a basal pneumothorax place at the sixth to eighth rib at the
MAL (Midaxillary line).
b) Pneumomediastinum-How does the air get there? Positive Pressure causes weakened alveoli blebs to rupture. Free air travels along the perivascular sheath or into the interstitial spaces. Air ends up at the lung hilum, and can cause PIE in infants. At the hila, air dissects between the fascial sheaths and moves into the mediastinum and/or the pericardium. Air can also dissect between the parietal and visceral pleura at the
hila, and can cause a pneumothorax.
1. RX-Pneumomediastinum is assymptomatic and will resolve by itself. A lateral CXR is diagnostic for a retrosternal air pocket.
c) Pneumopericardium is LIFE THREATENING due to cardiac
tamponade. Clinically, the patient has muffled heart sounds, decreased systolic blood pressure (the heart is an ineffectual pump), cyanosis and rapid deterioration.
1. CXR-a halo of air around the heart is pathonomonic. Rx includes needle aspiration and chest tube.
9. Pulmonary Hemorrhage-is interstitial or intraalveolar bleeding occurring in two or more pulmonary lobes that are free of infection.
a) Etiology-This condition can be seen with several newborn diseases such as RDS, Beta Streptococci pneumonia, aspiration of foreign material or hypothermia. The present theory is that birth asphyxia/trauma causes LV failure--> increased pulmonary capillary hydrostatic pressure-->fluid moves into the alveoli.
b) Clinical Symptoms-peripheral vasoconstriction,
bradycardia, gasping several minutes prior to the hemorrhage. In
intubated infants and children, blood pours into the ETT occluding it, while in the non-intubated infant or child blood pours out of the oropharynx.
c) Rx-frequent suctioning, MV with increased I.T., reverse I:E ratio's and PEEP to improve oxygenation, but the patient doesn't usually live.
10. PPHN (Persistent Pulmonary Hypertension of the Newborn) or
PFC (Persistent Fetal Circulation)(0riginal lecture A. Levin,
M.D. 10/4/84
"Is there Life After Meconium" song by the Doctones, 1984
In the DR, the baby's coming out green
It's just disgusting, to have to suck him clean
Don't get MEC on me
But got to stop that PFC
My tube, my tube
Putting in my tube
"One of the critical guidelines is early intervention to prevent the progressive worsening of the right to left shunt...The primary objective is to lower the PaCO2." W. Fox, M.D. J.
Pediatrics 10/83
a) Etiology-PPHN is 1. Marked increased in pulmonary
vacuslar resistance (above systemic) resulting in right to left shunts across the PDA and FO which leads to a vicious cycle of hypoxia, hypercarbia and acidosis.
b) Diagnosis-Recognize the clinical picture, the sooner the better!
1. associated with MAS, MAS and asphyxia, MAS with group B Streptococcus Pneumonia GBS), Postmaturity (>= 32weeks), myocarditis, Pulmonary Hypoplasia, CDH (Congenital Diaphragmatic Hernia) TT.
2. Immediate (at birth), Delayed (4-12 hours postnatal), or Late (12-24 hours postnatal)
3. Extreme lability of PaO2, severe cyanosis, acidosis, hypercarbia, +/- low apgars, RV Heave.
c) Use the A-a gradient to calculate shunting (quickie version) [(760-47)FIO2-PaCO2] - PaO2
Normal Newborn 20-30 mm Hg Stable Newborn <= 100 mm Hg Shunting
Newborn >= 400 mm Hg
d) Clinical Tests
1. Hyperoxia Test-give 100% O2 via BM. If increase in
PaO2, then a Parenchymal lung disease (ex, RDS). If no changes, either CHD or PFC.
2. Pre/Postductal ABG's >= 50% change in PFC, no changes in RDS or CHD.
3. Hyperoxia/Hyperventilation Test--give 100% O2 with
ETT placed at rates up to 150/minute. PIP's up to 50 cwp.
RESULT: we drive down the PaCO2 until we reach the CRITICAL
PaCO2-suddenly (from 5 minutes up to two hours) baby turns pink/Transcutaneous PaO2 jumps up/ arterial blood gas changes color from blue to red. A positive response to this
hyperventilation is diagnostic for PFC. No change from this test indicates CHD.
4. Ancillary Tests (least helpful)
a) CBC to R/O Infection, polycythemia, low platelets with pulmonary hemorrhage. Do Blood Cultures and push Amp and Gent.
c)Management
1. Airway-intubate as PFC'ers do two things very frequently just to make you angry> If the PaCo2 skyrockets think:
a) Plugged ETT-Change with new tube at chords before
pulling old.
b) Pneumothorax-don't be afraid to needle and place chest tube. At PIPS >= 40 cwp, it bound to happen.
2. Breathing
a) Ventilate fast and hard to keep the PaCo2 below the
CRITICAL PaCO2 you have diagnosed above.
rates of 80-150 Don't wean on transport or once the baby
PIP of 30-50 is pink or stable
PEEP of 2-4 only
FIO2 100% always
3. Circulation-Can't let systemic pressure fall below pulmonary. Give IV and/or UV fluids, Dopamine if necessary.
a)Dopamine-start at 2-5 mcg/kg/min and keep raising up to 25 mcg/kg/min, then as needed to kept systolic BP > 50 mm Hg.
b) Last Ditch Effort Only = Tolazoline (Priscoline) start with 15 mg/kg over 10 minutes preferably through a vein draining into the SVC if available. Follow this by an infusion of 1-2 mg/kg/hr.
1. Adverse Side Effects-all babies flush, and some may get hypotensive, thus get ready to up the Dopamine. Other problems include NG tube needed for increased secretions or GI Bleeding, oliguria.
4. Don't forget these additional Rx's--Glucose, Antibiotics, Morphine for sedation and Pavulon for paralysis.
d) Talking to the Parents/Prognosis
1. Poor prognostic factors:
a) Outborn babies have increased mortality (>= 50%).
b) PIP > 35-40 cwp
c) CRITICAL PaCO2 < 20 mm Hg to keep PaO2 > 50 mm Hg
d) Rate > 150/min
e) Severe PaO2 lability
f) Pulmonary Hypoplasia
g) Underlying disease (CDH, GBS)
Most predictive of prognosis is pulmonary hypoplasia and least predictive is the rate.
2. Iatrogenic Risks:
a) IVH (not as much as mature but still a risk)
b) ROP (not as much as premature but still a risk)
c) Pneumothorax
d) BPD
e) Sepsis
f) Death (especially if Tolazoline has to be given)
However, if the child survives, the neurologic prognosis tends to
be very good.
11. Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF)
a) Etiology-During the second month of embryonic life the septum that divides the trachea from the esophagus forms. Any interruption in this septal formation causes a TEF.
After this septum is formed, the esophagus is obliterated by cellular proliferation, but later the esophagus is recanilized. Any interruption in this recanalization results in EA, i.e., an esophagus without a lumen.
There are seven variations of these abnormalities, but two are the most common:
1. esophageal atresia plus a TEF between the distal portion of the esophagus and the trachea above the carina
2. pure EA.
b) Clinical symptoms-Infants will be asymptomatic at birth with increased oral secretions, but the first time the child is feed, severe choking, cyanosis and coughing will result-Why?
1. If a TEF is present, formula,secretions and gastric contents will be aspirated into the lungs.
2. As soon as this happens, try to pass an NG tube.
Will you be successful in TEF or EA?
c) Diagnosis-on CXR
1. EA-- no air in the stomach or intestines.
2. TEF--air in the stomach and intestines via the trachea
3. Definitive Diagnosis of EA-pass a size 10 or 12
French catheter through the noses or mouth until you meet resistance. On CXR (AP or lateral), the coiled catheter can be seen in the EA blind pouch.
d) Rx
1. For a TEF-surgery to separate the trachea and esophagus-patch the trachea
2. for an EA-cut and anastomosis of the two atretic ends. For a combination TEF/EA-do both
3. Post Surgery for all conditions-very careful oral suctioning to prevent esophageal trauma. If aspiration has occurred pre-surgery, place infant in the sitting up position, give supplemental O2, check ABG's.
12. Choanal Atresia-
a) Etiology-blockage of one or both nares by a membranous or bony closure.
b) Physiological consequences-Infants are obligate nose breathers up to six months of age, therefore if both nares are blocked, severe respiratory distress, cyanosis, intercostal and sternal retractions will be seen immediately after birth. If one nare is blocked, the condition may not become evident until a catheter is passed down the "good" nare.
c) Diagnosis-Contrast medium is injected into the nares and
a lateral CXR is taken.
d) Rx-insert an oral airway and secure (ETT may be necessary). Place the infant in the prone position to allow the tongue to fall forward. This can be followed by surgery. Snip the membranous or bony plates in the nare; place an nasal ETT in for several days to keep the nares open (An NP airway may also be used).
13. Congenital Diaphragmatic Hernia (CDH)
a) Etiology-Between the 8th and 10th gestation week the diaphragm is formed by the fusion of approximately 10 different pieces of connective tissue. At the same time, the embryo is undergoing major GI development, therefore if the diaphragm dopes
not fuse correctly, the stomach and intestines can herniate into the thorax.
The most common site of herniation is on the left side, the posterior lateral segment (Foramen of Bodechek).
b) Clinical Signs and Symptoms-The extent of herniation will determine how hypoplastic the lungs are. The patient will exhibit respiratory distress, cyanosis, flaring nostrils, retractions.
The CXR will show air filled bowel loops and the stomach in the thorax, the heart and lungs are displaced toward the unaffected side.
c) Rx-Surgery ASAP. The Bowel and stomach are pushed back into the abdomen and the hernia hole is patched. The hypoplastic lung is allowed to expand gradually. We want to use very low levels of positive pressure, thus the High Frequency Jet
Ventilator or the Oscillator are perfect. EMCO may also be necessary to alleviate the respiratory distress while the hypoplastic lung is expanding.
14. NEC (Necrotizing Enterocolitis)
a) Etiology-The large and small bowel disintegrate during the first few weeks of life as a complication of early aggressive feeding.
b) Conditions that place an infant at risk for NEC
1. Prematurity (<= 37 weeks gestation)
2. Term infants with cyanotic heart disease, short bowel syndrome, severe asphyxia
3. RDS
4. Hypotension, Hypothermia, Acidosis
5. Exchange transfusion
6. Low Apgar scores
7. Umbilical catheters
8. Sepsis
9. PROM(> 24 hours before delivery)
10. Erythroblastosis fetalis
11. Hyperosmolar formula
c) Signs and Symptoms of NEC
1. abdominal distention
2. vomiting
3. increased gastric aspirates (bile stained)
4. bloody or mucoid stools
5. apnea, hypothermia
6. lethargy, hypotension
7. guaiac positive stools
d) Rx-Gavage feeding. This means that the NG or OG tube is placed in the stomach (The position is checked--How?) Feeding volume plus the residual in the stomach are kept track of (How?) The infant is feed slowly using gravity feed. At the end of the
feeding, the infant is placed in the sitting up position-Why? No vigorous suctioning, CPT is done for an hour.
Introduction-The most serious pediatric diseases all have in common acute upper airway obstruction. In fact, the majority of time when we give children CPR, it is because of a respiratory arrest. Acute airway obstruction begins with a barking cough or
stridor and can progress to death in as little as half an hour.
a) Causes of Acute Upper Airway Obstruction
1. Epiglottitis
2. Croup-Laryngotracheobronchitis
3. Head and Neck Trauma-bleeding into the airways
4. Diphtherial Croup-the thick gray-white membrane produced by diphtheria is aspirated into the airway. This disease is on the rise as many children are not receiving their immunization shots.
5. Foreign Body Obstruction
1. Epiglottitis-
a) Etiology. This is a bacterial infection and inflammatory edema of the supraglottic laryngeal structures. Complete Airway obstruction can easily occur. This disease is always considered a pediatric emergency!
Hemophilus Influenza virus Type B-H. Flu is a very common organism that spreads in day care centers or public places. Children who attend daycare normally receive a vaccination against H. flu at 18 or 24 months.
b) Epidemiology-10-15% of all systemic H. Flu infections are Epiglottitis. The most common ages are between 2-8 years, the most common time is winter/spring, and males and females have equal incidence.
c) Clinical Manifestations
1. Acute Febrile Illness-temp >= 39 0C, onset <= 24 hours
2. Mild to Moderate Respiratory distress
3. Hoarse-c/o sore throat
4. Drooling
5. Inspiratory Stridor
6. Moderate to Severe suprasternal and intercostal retractions
7. hypoxemia may cause decreased mental status and agitation.
8. As the swelling of the epiglottis becomes worse, the child assumes a sitting position with the chin thrusting forward. This position maintains an open airway.
d) Dx
1. The clinical history should arouse suspicion.
2. Position the child on the parent's lap and do no anxiety producing procedures such as ABG's. Hold an O2 mask near the child's face but not covering it.
3. CXR-the lateral neck will show the "thumb sign"-a swollen protuberant epiglottis-usually don't bother with as going straight to the OR. Never go to radiology alone-take the Doc.
e) Rx
1. In the OR, the ENT attending or the anesthesiologist will do a direct visualization of the epiglottis-either a Naso or oral ETT or Tracheostomy (preferred)
2. transfer to ICU. Mechanical ventilation is rarely necessary, but humidified warm or cool O2 via ETT or Trach is usually adequate.
3. the duration of intubation/trach is usually between 12 hours and 5 days. What clinical sign would indicate to you the infection was passing? Extubation usually occurs within 36-48 hours. Before extubation, we get a everything (equipment and drugs) ready for reintubation.
4. How important is an airway? Research studies show up to a 25% mortality rate without an airway and <= 1% mortality rate with an airway.
5. Lab studies show that H, flu can normally be recovered from the blood or by swabbing the epiglottis, but IV ampicillin and/or chloramphenicol is given prophylactically pending C and S results.
2. Croup
a) Definition and Etiology-This is normally a subglottic inflammation of the lower airway. Children can also acquire Croup from a congenital narrowing of the airway or previous intubations. Viral Croup can be life threatening!
The organisms that normally cause croup are parainfluenza viruses (Type I and II), RSV (Respiratory Syncytial Virus), Adenoviruses.
b) Epidemiology-Age 8-30 months, more common in males than females, repeat episodes are common.
c) Clinical Manifestations
1. febrile, barking stridorous cough
2. URI symptoms for several days before the croupy cough.
3. Symptoms become worse at night when the child is asleep.
4. runny nose is common, WBC's are normal or slightly elevated (compare to Epiglottis).
5. Mild to moderate respiratory distress with suprasternal retractions.
6. lower airway edema results in V/Q abnormalities, thus hypoxia may be seen in ABG's. The child is tachycardiac, cyanotic and anxious.
d) CXR-subglottic narrowing
e) Rx
1. The majority of children can be managed at home with cool humidified air via vaporizer (really a nebulizer) or the shower. Children normally improve dramatically when taken out in the night air-Why?
2. Only 10% of children with croup need to be hospitalized(i.e., only if mild to moderate respiratory distress is present).
3. Rx includes a croup tent with Air or O2, IV hydration, close observation. These kids will not normally tolerate an O2 mask. All laboratory procedures such as ABG's and
Physical Exam should be postponed.
4. Frequent monitoring of VS is necessary to prevent hypoxemia. We feed the child normally or via IV's if PO intake is inadequate.
5.Corticosteriods may be given to decrease airway inflammation. and also Racemic Epinephrine (Vaponephrin or Micronephrin) .25 or .5 ml diluted in 2.5 ml NS as needed. How does this drug work? What are its dangers? Careful as there may be rebound effect several hours later?
6. <= 5% of children with croup require intubation, but for example, allergic croup may cause anaphylactic shock (insect bite, allergy to a specific food) and require a tube.
3. Foreign Body Aspiration
a) Hx-Although kids put everything in their mouths, aspiration is uncommon as the object is normally expelled by coughing. Adults are much more prone to aspirate food and have a Cafe Coronary due to decreased gag reflex from ingestion of alcohol.
b) Immediate Rx-the Heimlich Maneuver-Complete Airway Obstruction-"Can you speak?-clasp hands in the epigastric area midway between the xiphoid process and the umbilicus-for adults and children >= 1 year age.
1. No Heimlich maneuver infants as it would cause serious abdominal lacerations, therefore four back blows followed by four chest thrusts (same as CPR). Inspect mouth for foreign body, and only put your fingers or forceps in if you can see the object.
2. In complete airway obstruction, after the child becomes unconscious, the pharyngeal muscles relax, and the object normally comes out easily. Mouth to mouth resuscitation may be required.
c) Long Term Effects-Dx
1. Ask parents if there was a choking episode with cyanosis. Kids may remain assypmtomatic for weeks.
2. Symptoms-Recurrent lobar pneumonia, wheezing that doesn't respond to bronchodilators. The foreign body acts like a valve in the airway; air can enter easily during inspiration when the airways are expanded, but on expiration, air trappingoccurs behind the foreign that obstructs the airway. The affected lung tends to be overexpanded, and there is a mediastinal shift away from the affected side.
d) Rx-Rigid Bronchoscopy historically, more likely replaced with Fibroptic Bronchoscopy today in the OR environment. CPT sometimes may be an alternative. "Foods of Death" = Hot Dogs, Hard Candy, Popcorn, Peanuts, and Steak.
a) Definition-Pathological Triad-Bronchospasm due to smooth muscle reactivity, mucosal edema, retained secretions.
1. Differences between Extrinsic vs. Intrinsic Asthma
b) Why do kids die of Asthma? Bronchial obstruction due to
V/Q mismatch. In Stage 1, decreased PaCO2 (hyperventilating) and decreased PaO2. By Stage 3, increased PaCO2 and decreased PaO2 due to acute impending ventilatory failure.
c) Epidemiology
1. 80% of children develop asthma prior to age five.
2. Factors that consistently mean a worse prognosis are severe illness at onset and a family Hx of atopic disease.
3. Every Asthma study comes to a different conclusion about prognosis, age of onset, contributing factors, but most children show remission between 6-10 years of age. Asthma may return with avengence at puberty or during pregnancy.
d) Differential Dx-"All that wheezes is not asthma"
c) Clinical Presentation
1. Mild Asthma can be controlled at home via administration of syrup (Ventolin or Alupent), Sprinkles placed on food (Theophylline) Oral Bronchodilators or MDI's
Review-How do they work? Side Effects?
a) Ventolin, Proventil, Albuterol
b) Atropine, Atrovent
c) Aerobid, Vanceril (Beclamethasone)
d) Cromolyn Sodium (Intal)
e) Mucomyst (Aceytlcysteine) for CF only
f) Flovent, Servent
g) Combovent
What problems arise if MDI's or nebulizer's are overused?
Author's personal opinion-If parents purchase and give their children their medications, the vast majority can stay out of the ER. Patient education is the key.
If also helps to know who your child's MD is and to show up for clinic appointments. Dysfunctional ill-educated families are the major reason Asthma is growing in the urban, lower socioeconomic groups. Another problem is with the MD's. All the scientific research in the last five years has shown that Asthma is much more of an inflammatory disease than we earlier understood. Yet physicians routinely refuse to prescribe low doses because of the past specter of corticosteriods side effects.
2. What does an acute Asthma attack look like in the ER?
a) Tachycardia, tachypnea, cyanosis
b) Sensorium clear unless profound drop in PaO2 and increase in PaCO2 (Stage 3)
c) Anxiety, fear due to dyspnea
d) Retractions, Nasal Flaring, Uses of Accessory Muscles on percussion due to air trapping
f) Auscultation-Initially, scattered rhonchi, rales and expiratory wheezing throughout the lung fields. As the attack gets worse, inspiratory and expiratory wheezing throughout the lungs fields is heard followed by now wheezing and marked respiratory distress. At this point the patient is in severe bronchospasm (no air entry)-"going to die"
g) Laboratory findings-
1.ABG'S Stage 1-decreases PaO2 and PaCO2 vs. Stage 3 decreased PaO2 and increased PaCO2 (silent chest)
2. CXR-Hyperinflation due to air trapping, Atelectasis due to underlying pneumonia
d) Rx
1. Humidified O2 at an FIO2 that relieves hypoxia.
Allow the parents or patient to hold face mask or B&M to decrease anxiety.
2. Administer nebulized Sympathomimetics with O2. If the respiratory distress is severe, a shot of subcutaneous epinephrine can be given (older method). Any child who is old enough to cooperate should use a mouthpiece instead of a mask as they will get better aerosol distribution.
3. In the past IV Xanthines were administered at the same time (Theophylline, Aminophylline), however, these have fallen out of favor due to chronic cardiac arrhythmias. Also, Ventolin alternating with Isoproterenol was also tried(why do we
no longer use this?). Today continuous nebulization of ventolin 2-4 cc/hrs tried for several hours to prevent mechanical ventilation. Corticosteriods are given at the same time.
***Review the Heart Nebulizer and math.
4. If mechanical ventilation is required, the ideal situation is to use a volume ventilator with large tidal volumes and long IT's. This will improve oxygenation and allow a better
distribution of flow. The problem is that adequate expiratory time must also be available to prevent air trapping and pneumothorax. Neuromuscular paralysis may also be necessary to synchronize the patient with the vent (Pavulon). Continuous ventolin may also be given through the ventilator with filters in the expiratory lines.
5. Weaning can begin when there is decreased hyperaeration and atelectasis and the heart is a normal size. The ABG's should show a PaCO2 <= 45 mm Hg and a PaO2 >= decreasing the mode of ventilation (A/C, SIMV, PC, and PRVC). IV corticosteriods should be continued for at least 6-8 hours post extubation.
***Review Resp. assessment Sheet for ACU.
5. Bronchiolitis-
a) Definition and Etiology-This is the most common infection of the lower respiratory tract during the first few years of life. This disease closely resembles asthma, thus we must develop a differential diagnosis. Respiratory Syncytial causes it
Virus (RSV) which is a RNA virus found in Nasopharyngeal secretions.
b) Epidemiology-All age groups are affected, but the majority of illness occurs between 3 weeks and 24 months. Reinfection is common and immunity is incomplete. RSV begins in
December and lasts through March.
c) Clinical Manifestations
1. In all ages this illness usually begins as a cold with cough. As the symptoms get worse, wheezing becomes prominent. Respiratory distress severe enough to interfere with feeding and fever follow. This is what usually brings parents to the MD's or ER. Only 1% of the infants <= 2 years of age require hospitalization. Mortality in this group is 1-3%, but 20% in neonates.
2. Infants <= 3 months may experience apnea.
3. Laboratory Tests
a) RSV slide-taken as soon as the child is hospitalized-Nasopharyngeal secretions sucked into a viral growth medium. In the lab, a slide is prepared and stained with
Immunofluoresecent Assay. Under microscope, antibodies to RSV stand out as green or orange spots. Children suspected of RSV on admission should be placed in isolation rooms.
b) CXR will show hyperinflation and ABG's will show hypoxemia. This disease is normal self limiting within a few days, although a severe pneumonia can develop.
d) RX-Most infants do well at home without medical intervention. Cool Mist and slow frequent feedings to improve hydration usually work. Meds that don't work-Antibiotics,
Corticosteriods, Xanthines.
1. For the 1% that require hospitalization-Mist tents or hoods to Rx hypoxemia, IV hydration if necessary. Drugs that may work-Ventolin, Racemic epinephrine, Ribovarin.
***See Bronchiolitis Pathway-Why was it developed?
2. Children who are most severely ill will require Ribovarin (Viruzole). The Pharmacist prepares this by diluting 6 gms in 300 ml of sterile H2O. This is given for 12 hours for five days (best-time-during sleep). Every hospital uses a slightly different protocol
a) Children at high risk for severe RSV are those with a chronic underlying disease (ex. neurological or metabolic disorder, multiple congenital abnormalities) or congenital heart disease (CHD), BPD, Immunodeficiency or neonates. New vaccine available for this type of child.
4. Infants <= 3 months old may require mechanical ventilation may require mechanical ventilation to respiratory and ventilatory failure. The infection normally subsides within a few days, but the high PIPS and FIO2's need may lead to O2
toxicity, barotrauma and BPD.
6. Cystic Fibrosis (Mucoviscidosis)
a) Etiology/Epidemiology-This is a hereditary disease of the exocrine glands involving the lungs, liver and pancreas. It is inherited via a simple autosomal recessive gene, thus the risk of a child being born to a couple is 25% for each pregnancy.
The male/female incidence is equal and the "sweat test" is our most important diagnostic tool. The drug Pilocarpine is administered and increased levels of Cl- (>= 60 meg/l) is considered a positive test.
b) Intestinal problems-Pancreatic Replacement enzymes and vitamin supplements must be given to compensate for a poorly functioning pancreas. The child must eat as high protein, low fat diet (has a hard time digesting the fat) in order to prevent FTT (Failure to Thrive).
c) Lungs-CF is the most common life threatening chronic disease of childhood. Death usually results from airway obstruction from viscous secretions leading to respiratory and
ventilatory failure. The only treatment is early intensive pulmonary hygiene.
1. The Mucociliary Escalator (part of the exocrine glands) is abnormal leading to increased thick viscous mucus production; the Cl can't escape the cells and this leads to a change in the cells electrical charge. This mucus obstructs airways leading to atelectasis and overinflation. In addition, this viscous mucus can not be coughed up easily, therefore it sits around becoming infected with gram negative organisms such as Staphylococcus aureus and Pseudomonas aeruginosa. At first, patchy areas of the lung are involved, but soon all the lobes are infected.
2. The problem list for CF includes: Bronchitis, Bronchiectasis, Overinflation, Atelectasis, Bleb formation, Fibrosis, Cor Pulmonale, Respiratory and Ventilatory Failure and death.
d) Rx
1. O2 mask, Mist tent, or Nasal Cannula for hypoxia.
We must be careful that aerosol particles do not help the spread of infection, therefore humidifiers are normally used with these patients.
2. Nebulized medications and MDI's
a) Bronchodilators-Ventolin
b) Mucolytic Agents-Mucomyst
c) Cromolyn Sodium-Intal
d) Steroids-Aerobid, Beclamethasone
e) Pulmozyme (Dornase Alfa) or DNAase-run off Rm Air
3.CPT/PD with vibrations to all lobes. In order to do this properly, approximately 45 minutes will be required.
4. Pneumothoraces are especially common in the upper lobes due to bleb formation. We do a chest tube placement. If this is a recurring problem, we do a thoracotomy and instill an irritating agent onto the pleural surface (pleuradesis). Scar tissue forms thus decreasing the incidence of Pneumothoraces.due to the erosion of blood vessels from infection. The bleeding may be minimal such as a few streaks in the sputum or a massive life-threatening hemorrhage. Vitamin K is given (to increase
prothrombin time) and antibiotics. CPT is put on hold. As a last ditch effort, we do a Bronchoscopy and use a laser to localize and cauterize areas of bleeding. A bronchial artery embolization or lobectomy may be necessary.
6. Cor Pulmonale may develop secondary to elevated PVR, hypoxia and acidosis. A salt restricted diet, diuretics and digitalis are prescribed.
7. Mechanical Ventilation is a last resort. Weaning must be slow with no hypoxia or hypercapnia present. Many patients and their families may elect not to intubate. Getting the CF patients off is very difficult as they are usually in fatal respiratory/ventilatory failure.
Tracheostomy is contradicted in these patients as it will decrease the effectiveness of their cough post-extubation. IPPB before or after intubation is also contradicted as it only makes air trapping worse.
8. Newest Rx's Gene Therapy via genetically altered adenovirus and Lung or Heart/Lung transplants.
7. Pneumonia
a) Definition-This is a diverse group of diseases in childhood involving inflammation of the bronchi down to the alveoli. It can be a sharply localized infection such as a classic lobar pneumonia or a diffuse disease such as bronchopneumonia, viral or aspiration pneumonia. It can be a primary disease itself (Ex. Staphylococcal or Pneumococcal), or it can be secondary to a primary disease such as CF or asthma.
b) Pathophysiology-Mucosal edema and secretions lead to decreased V/Q ratio, shunt and hypoxemia.
c) Rx
1. Humidified O2, Antibiotics, IV Hydration,
Brochodilators if relieve SOB. MV is only required in overwhelming infection,.
a) Possible Sequelae-1. Death due to asphyxia
2. long range metabolic abnormalities due to aspiration of
salt, fresh water, organisms 3. pneumonia
b) Aspiration Pneumonia-If it is a fresh water near- drowning, water moves from the lungs to the blood causing hemodilution. If it is a salt water near-drowning, the NaCl in
the lungs moves into the blood causing hemoconcentration. These are really academic matters as survival depends upon the length of asphyxia and how fast/effective the resuscitative efforts are. Pre-existing respiratory problems such as asthma make the
prognosis worse.
If the patient vomits during resuscitation, we have regular aspiration pneumonia in addition to either fresh or salt water aspiration pneumonia.
c) Rx-
1.ABC's of Resuscitation
2.Correction of electrolyte imbalance--> possible cardiac arrhythmias
3. NG tube and antibiotics for aspiration pneumonia
4. Humidified O2 with ABG's to prevent hypoxemia
5. IPPB or MV for hypercarbia and pulmonary edema
6. Bronchodilators and Corticosteriods for Bronchospasm
7. Check for possible suicide attempt (refuses therapy) vs. ETOH in adults
8. Discussion of DNR status, termination of MV.
9. Orthopedic Problems associated with Respiratory Disease
a) Definition-Skeletal Diseases bring about progressive deformity of the thoracic cage and inefficient use of the respiratory muscles. This leads to impaired ventilation, cough and recurrent infections.
b) Scoliosis as a primary disease or as secondary to poliomyelitis, neurofibromatosis will require vertebral fusion's if progressing rapidly. ABG's and PFT's pre-op will assess the degree of resp/vent. impairment. The patient should be educated beforehand about tracheotomies, IPPB and MV as these all may be necessary. Post-operatively, recurrent infections due to a compromised cough will be the main pulmonary problem.
10. Neuromuscular Diseases (ex. Muscular Dystrophy, Werdnig-
Hoffman, Guillain Barre, Infant Botulism)
a) all patients in this group have decreased Vital
Capacities, which we normally measure, bid to decide if MV is necessary. These patients also have recurrent pulmonary infections due to a decreased cough.
b) Rx-This will vary according to the type of disease and how far along it has progressed. Acute flare-ups will require humidified O2, bronchodilator Rx's, CPT/PD with vibration, much like COPD acute exacerbation's. Atelectasis and respiratory failure may require IPPB and MV. As with the orthopedic patients, education about all the equipment and procedures that may be required is very important.
***# 9 and 10-IPPB Alert
11. Acute Poisoning with and without Corrosive Substances
a) Should vomiting be induced with Ipecac?
b) Always bring to the hospital what your child has swallowed.
1. Bourns BP2001-Bear Cub
a) This machine is a pneumatically powered, electronically controlled, Time cycled, Time limited continuous flow ventilator. It produces a square wave and is
pressure relief preset.
b) The modes of ventilation available are only two:
1. IPPB/IMV-(control mode) What happens it that the machine provides a certain number of positive pressure breaths per minute that we have dialed in. If the baby wants additional breaths, he/she takes spontaneous breaths from the continuous flow in between machine breaths. Really, in today's terms, it's SIMV.
2. CPAP-Spontaneous Breathing with PEEP
b) Drive Mechanism and Flow Characteristics
1. When the Pressure limit is not reached during the I.T.
2. When the Pressure limit is reached during the I/T.(pressure hold)
c) Preset Pressure Limit-PIP-seen on Pressure manometer adjustable between 0-80 cwp.
d) Flowmeter 0-30 lpm-good for PPHN
e) Oxygen percent-precision metering devise. 50 psig O2 and
Air enters, regulators inside drop the pressure to 10 psig-->patient
f) PEEP/CPAP System-Opposing Flow-the more gas is sent to the venturi, the more pressure is exerted against the patient's exhaled gas, the greater is the PEEP.
g) Heated Modified Passover or Wick Humidifiers used.
h) How to estimate the VT being delivered to the Baby?
Vt = Inspiratory Time (secs) x Flow (lpm)
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60
An infant's VT will be affected by his compliance resistance and the size of the ETT. Can we do a lost volume calculation on an infant?
i) Rate with toggle switch (so typical of Bear) 1-75. 75-
150. Why is the rate not allowed to go above 150? The Rate and
I.T. control are separate. Expiratory time is what is left over.
The I:E ratio is determined when the Rate and I.T. controls are set.
j) I.T. control .1-3 secs
k) MAP display-not very accurate-good for trending
l) Audiovisual Alarms-Low Inspiratory Pressure, Loss of
PEEP/CPAP, Prolonged Inspiratory Time (10 cwp above PEEP for 3.5
secs), Ventilator Inoperative, Low Air and O2 pressure.
m) External; Spring loaded pressure relief-in case the normal pressure limit fails or the expiratory limb is kinked or blocked.
2. End Tidal CO2 Monitoring-Capnography
a) Definition-Capnography is recording the changing levels of expired CO2. CO2 and water absorb infrared light, therefore we remove the water via filter. The higher the level of CO2, the more infrared light will be absorbed.
b) Factors that affect the EtCO2
1. cellular production of CO2-varies with the patient's metabolism.
2. Transport of CO2 from the cells to the lungs-varies
with the patient's circulation
3. Elimination from the lungs-central/peripheral chemorecptors
c) Physiology
1. Any disease/event that causes alveolar hypoventilation will increase the EtCO2, Ex. Neurological trauma, drugs, Asthma, Diffusion Defect
2.decreased EtCO2= decreases pulmonary blood flow-Suspect
Emboli!
d) Instrumentation
1. Aspirating devises (Sidestream)-Novametrix-older models
2. Mainstream devises (non-aspirating)-Hewlett Packard, Nellcor-all recent ones are of this type.
e) Math-How to convert % to torr
1. Normal EtCO2 is 5.6% .056 x 713= 40 mm Hg
f) Normal waveform-Similar to the Single Breath N2 Washout Curve, but the patient doesn't exhale to RV
A-dead space gas B-Deadspace plus alveolar gas C-Alveolar
gas D-Peak expired CO2-plateau F-rebreathing-curve does not
return to base line
g) ABG Correlation with EtCO2-should be within 3-10 mm Hg.
If greater, don't use monitor (see factors under b for explanation).
h) Technique-Chest Squeeze-Watch out for recent feeding, surgical sites, chest tubes, CVP or arterial lines
1. How do you get a Newborn Vital Capacity-Cry
2. Whether on or off the vent-squeeze the chest at the end of inspiration.