Module 2: Vinod Flashcards
Transition: Cardiovascular changes
Review Cardiovascular system in utero and post utero
- constriction of the ductus arteriosus is a gradual process permitting bidirectional shunting of the blood
- PVR may be higher than the SVR, allowing right to left shunting until SVR rises above the PVR and blood flow is directed left to right.
- Most neonates have a patent ductus arteriosus in the first 8 hrs of life
- spontaneous closure occurs about 42% in the 1st 24 hrs
- 90 % and 48 hrs-96 hours
- Permanent anatomic closure of the ductus arteriosus occurs 3wks to 3 months after birth
Transition: Respiratory changes
- at birth clamping of cord signals end of oxygenated blood flow to fetus
- for respirations to be established, fetus must clear lungs of fluid, establish regular pattern of breathing and match pulmonary perfusion to ventilation
- other factors: pulmonary flow, surfactant production, and respiratory musculature also influence respiratory adaptation.
- Catecholamine surge experienced prior to birth helps to remove fluid from fetal lungs
- infants that do not experience labor and are born via c-section are more likely to have residual fluid in the lungs and develop TTN (Transient Tachypnea of the Newborn) because of the lower levels of catecholamine.
Transition: Thermal and metabolic adaptation
-Newborns are predisposed to heatless because: a large surface area in relation to body weight, limited body fat, and a decreased ability to shiver. Newborns attempt to stay warm by increasing muscle activity and by burning brown fat (non-shivering thermogenesis), which increases metabolic rate. Peripheral vasoconstriction also decreases heat loss to the skin surface. The production of heat requires oxygen and glucose and produces lactic acid; therefore persistent hypothermia may result in metabolic acidosis, hypoglycemia, decreased surfactant production, and over the longer term, poor growth.19
Maternal glucose readily crosses the placenta and, under normal circumstances, supplies the fetus with enough energy to grow appropriately and to store glycogen in the liver for use after birth. The release of catecholamines occurring during labor and birth mobilizes glycogen; however, blood glucose levels decline after birth, reaching their lowest point at one hour of age.
Normal Transitional findings of the Newborn
-most of the transition occurs 4-6 hours after birth while cardiovascular changes may take up to 6 weeks.
During the initial hours after birth, the majority of fetal lung uid is reabsorbed, a normal functional residual capacity is estab- lished in the lungs, and the cardiovascular system redistrib- utes blood ow to the lungs and tissues. The infant moves through a fairly predictable series of events, mediated by the sympathetic nervous system, that results in changes in heart rate, respirations, gastrointestinal function, and body tem- perature. In a classic description still used today, Desmond and colleagues organized these changes into three stages:21 • The rst period of reactivity (0–30 minutes) is character-
ized by an increase in heart rate, irregular respirations, and
ne crackles in the chest with grunting and nasal aring
• A period of decreased responsiveness (30 minutes to 3 hours) with rapid shallow respirations, lower heart rate, and decreased muscle activity interspersed with jerks and
twitches and sleep
• A second period of reactivity (2–8 hours) in which exagger-
ated responsiveness, tachycardia, labile heart rate, abruptchanges in tone and color, and gagging and vomiting are commonly seen
Residual symptoms of transition such as crackles in the lungs, a soft cardiac murmur, and acrocyanosis may persist for periods up to 24 hrs in otherwise healthy infants.
Red flags in Transition
-Symptoms of greater than 2 hours duration
• Worsening distress
• Congenital anomalies
• Abnormal muscle tone
• Central cyanosis
• Apnea in a near-term or term infant
• Moderate-to-severe respiratory distress:
grunting
nasal flaring
marked retractions
need for supplemental oxygen beyond two hours of age
What is PPHN
persistent pulmonary hypertension of the newborn
PPHN is a special case of a cardiopulmonary disorder occurring in term or near-term infants that is triggered by an insult such as hypoxia, hypotension, or hypercarbia. PPHN develops when the expected drop in pulmonary vascular resistance does not occur after birth. Pressure within the pul- monary vasculature remains elevated, leading to continued shunting of blood away from the lungs and across the foramen ovale and ductus arteriosus.
Risk factors for problems in Transition: Maternal
Diabetes Hypertension Cardiac or respiratory disease Severe anemia Shock Infection or febrile illness
Risk factors for problems in Transition: Antepartum
Intrauterine growth restriction Placenta previa, Abruptio placenta Fetal-maternal hemorrhage Malpresentation, Multiple gestation Pregnancy-induced hypertension Illicit or prescription drug exposure
Risk factors for problems in Transition: Intrapartum
Chorioamnionitis
Fetal distress
Prolapsed cord
Premature or prolonged rupture of membranes Narcotic or magnesium sulfate administration Malpresentation
Shoulder dystocia
Vacuum forceps or cesarean delivery
Presence of meconium-stained amniotic fluid
Risk factors for problems in Transition: Neonatal Complications
Prematurity
Congenital malformations
Postmaturity
Birth trauma
TTN
Transient tachypnea of the newborn
Retained fetal lung fluid
due to
Late preterm infant Delivery by cesarean section, especially with no labor
Infants of diabetic mothers
Respiratory distress syndrome (RDS)
Surfactant deficiency and anatomic immaturity
Due to:
Prematurity
Meconium aspiration
Chemical pneumonitis secondary to meconium
Surfactant deactivation
Ball and valve obstruction leading to air trapping
Due to:
Term or postterm
History of meconium-stained amniotic fluid
May accompany signs of fetal intolerance of labor
Pneumonia
Initiation of inflammatory cascade
Secondary surfactant deficiency
Systemic illness
Due to:
Preterm
Prolonged rupture of membranes
Maternal Group B Streptococcus colonization
Maternal urinary tract infection or febrile illness
Persistent pulmonary hypertension
of the newborn (PPHN)
Failure of pulmonary vascular resistance to lower after birth, leading to continued right-to-left shunting, severe hypoxemia, and acidosis
Due to:
Late preterm/term infant
History of meconium aspiration, sepsis, RDS, congenital diaphragmatic hernia, and congenital heart disease
What is the PO2 of the fetus (intrauterine) compared to the newborn (extrauterine)?
fetus: 30
Newborn: 60-80
What is the organ of gas exchange for the fetus compared to the newborn?
fetus: placenta
newborn: lungs
What is the % of CO to the lungs in fetus compared to newborn?
fetus: 10%
newborn: 50%
What is the pulmonary vascular resistance in fetus compared to the newborn?
fetus: high
newborn: low
What is the systemic vascular resistance in fetus compared to newborn?
fetus: low
newborn: high
What is the pressure gradient in fetus compared to the newborn?
fetus : right > left
newborn: left > right
How is the foramen ovale presented in fetus compared to newborn?
fetus: patent
newborn: closed
How is the ductus arteriosus presented in fetus compared to newborn?
fetus: patent
newborn: closed
What is the direction of shunting in fetus compared to a newborn?
fetus: right to left
newborn: none or left to right
What is perinatal asphyxia?
Perinatal asphyxia occurs during the perinatal period. It is a life-threatening disorder that occurs when a fetus or newborn doesn’t adequately exchange gases. Asphyxia, as it is characterized by hypoxia, threatens successful transition.
What are the results of impaired gas exchange?
impaired gas exchange –> decreased blood oxygen levels–> increased CO2 levels –> Multisystem organ effects (MSOE)
Asphyxia can happen for a variety of reasons. About ninety percent of asphyxia occurs prenatally when gas exchange through the placenta decreases as a result of problems such as:
- pregnancy induced hypertension (PIH)
- abruptio placenta
- cord compression
Fetal monitoring will often reveal an infant’s response to antenatal asphyxia:
- fetal heart rate decelerations suggest asphyxia
- passage of meconium is also a clue to the presence of asphyxia
Post-natally gas exchange can also be interrupted and this accounts for approximately 10% of asphyxia. Some disorders that affect gas exchange in a newborn are:
congenital diaphragmatic hernia
sepsis
meconium aspiration
some congenital heart defects
Alteration of blood flow is an attempt to provide those organs necessary for immediate survival. Where is the blood shunted to?
the brain and the heart — with as much oxygen as possible. In order to do this, blood is shunted away from non-vital organs such as the lungs, intestines, kidneys, and peripheral vessels. The longer those organs receive less blood, the more damage they sustain. Unless the cause of the asphyxia is remedied, the heart and brain eventually also succumb to hypoxia and are damaged
Why is tachycardia present during times of hypoxia?
Reflects the heart’s effort to increase cardiac output to respond to the decrease in blood oxygen levels
How does hypoxia and asphyxia alter glucose production?
Hypoxia and asphyxia alter glucose production and utilization by requiring an increase in glycogeolysis to meet the increased metabolic and energy demands. Because oxygen availability is compromised, the infant switches from aerobic to anaerobic metabolism. Anaerobic metabolism is less efficient than aerobic metabolism and requires significantly more glucose to create energy. This rapidly depletes the glucose reserves; this decreased energy production is often inadequate to maintain normal cell processes and leads to the accumulation of lactic acid which causes metabolic acidosis. Hypoxia will also lead to hypercapnia (CO2) due to the body’s attempt to bring in more oxygen and will result in respiratory acidosis. Left uncorrected, these problems (hypoxia, hypercapnia, and acidosis) worsen. The result can be tissue and cell damage in all organ systems, and if enough cells in an organ are damaged organ failure will result. In addition if enough organs fail, death may ensue.
There are 4 criteria for asphyxia:
- Arterial cord blood sample < 7
- Apgar score of 0-3 for more than 5 minutes
- Seizures, hypotonia, coma, or hypoxic-ischemic encephalopathy in the early postnatal period
- Multiple organ dysfunction in the early postnatal period
Conditions Contributing to Asphyxia: Antepartum
- Placental insufficiency
- Maternal pulmonary disease
- Maternal cardiac disease
- Congenital fetal abnormalities
- Prematurity
Conditions Contributing to Asphyxia: Intrapartum
- Rotational maneuvers
- birth trauma
- abnormal presentation
- placental abruption
- prolapsed umbilical cord
- maternal hypotension
- infection
Conditions Contributing to Asphyxia: Postnatal
- severe lung disease
- severe apnea
- congenital heart disease
- persistent fetal circulation
- sepsis
- shock
Adjusting to extrauterine life, the newly born infant experiences a complex series of…
biologic, physiologic, and metabolic changes
When delivery is complicated and perinatal depression is suspected what is the aim of resuscitation?
to reverse
- hypoxia
- hypercarbia
- acidosis
Resuscitation begins with…
- thermal control
- clearing of the airway if needed
- stimulation of breathing
primary apnea
respiratory movements cease after a brief period of rapid breathing.
Asphyxia
Asphyxia is a process characterized by inadequate gas exchange leading to progressive hypoxia, hypercapnia, and acidosis which may occur in utero or shortly after an infant is born. Events such as pregnancy induced hypertension (PIH), abruptio placenta, cord compression, apnea at birth, or meconium aspiration can cause inadequate gas exchange. If the cause of the problem is not corrected, the infant shunts blood away from the periphery, lungs, intestines, and kidneys to try to preserve blood supply to the heart and the brain. If no intervention occurs to stop and reverse the process of increasing hypoxia, hypercapnia, and acidosis, organs become damaged (including the heart and brain), the infant stops gasping/breathing, the heart stops beating, and the infant dies.
What responses has Vinod displayed that lead you to suspect that he has been asphyxiated?
- meconium present in amniotic fluid suggests two things: -one, that Vinod has been hypoxic in utero and two, that he is at risk for postnatal asphyxia via meconium aspiration
- late heart rate decelerations during labor
- need for resuscitation
- spontaneous respirations not established until 2½ minutes of age
- color didn’t improve until 2½ minutes of age
- not moving arms and legs until 2½ minutes of age
- low Apgar score — especially at one minute
- still pale after resuscitation
Identify at least one negative response in each of the following systems that could occur as result of Vinod having been asphyxiated.
pulmonary system
respiratory distress, meconium aspiration, persistent pulmonary hypertension, atelectasis, and pneumonia
cardiovascular system
congestive heart failure, cardiogenic shock, hypotension, and disseminated intravascular coagulation (DIC)
gastrointestinal system
feeding intolerance and necrotizing enterocolitis (NEC)
renal system
decreased urine output, hyperkalemia, and renal failure
central nervous system
hypoxic ischemic encephalopathy (HIE), periventricular leukomalacia PVL, seizures, and sometimes long-term neurological problems such as spasticity, ataxia, and cognitive deficits
What nursing measures could you implement in order to prevent further asphyxia and to prevent the complications associated with asphyxia?
Some of the nursing measures you could implement to prevent further asphyxia and prevent complications associated with asphyxia include:
- immediate effective resuscitation with provision of warmth, ventilatory support, and maintenance of adequate circulation. Establishing spontaneous respirations, a normal heart rate, and correcting acidosis will prevent further brain injury
- assess for the effects of asphyxia — hypoxia, hypercarbia, acidosis, and hypoglycemia which may show up in many ways — seizures, apnea, respiratory distress, intolerance of feeds (when started), and temperature instability
- closely monitor the infant’s vital signs (including blood pressure), oxygen saturation, blood work results, and urine output
-maintain the infant’s warmth — prevent cold stress
ensure sufficient glucose intake — usually the infant is NPO, so an IV is initiated. Fluid intake may be restricted to 50–70 ml/kg/hr to prevent fluid overload (since renal function may be impaired due to hypoxia) and to prevent cerebral edema
- keeping the infant NPO will give the gut an opportunity to recover
- apply ACoRN framework to evaluate and/or guide the care the team is providing
Meconium aspiration
Meconium aspiration is a common feature of perinatal asphyxia for full- and post-term infants. Preterm infants, particularly those less than 32 weeks gestation, rarely experience meconium aspiration as their gut contain very little meconium. Full- and post-term infants, in contrast, have large amounts of meconium in their colons.
When full- and post-term fetuses experience hypoxia, their gastrointestinal wall relaxes and meconium is expelled into the amniotic fluid. The hypoxia will cause the fetus to gasp. When the fetus is delivered, aspiration of the meconium occurs during the first breath, severe respiratory distress can result from the meconium blocking small airways, trapping air, and initiating an inflammatory response.
Post-term infants are at particular risk for meconium aspiration for several reasons:
- they have large amounts of meconium in their gut
- these infants can be quite large (if they continue to grow in utero) and consequently suffer second stage problems arising from their larger size
- if they have not been growing — because the placenta has been deteriorating — they will likely be stressed and may already be experiencing hypoxia, causing meconium passage
Meconium aspiration causes hypoxia in the neonate by:
airway obstruction
-physically obstructing the glottis, trachea, and smaller airways resulting in atelectasis, air trapping and alveolar collapse
surfactant dysfunction
-meconium deactivates surfactant and may inhibit surfactant synthesis
chemical pneumonitis
-an inflammatory response to meconium in the airways and parenchyma
increased pulmonary vascular resistance
-which results in the ductus arteriousus staying open (right to left shunting) and the maintenance of fetal circulation
The following diagrams compare normal and impaired pulmonary blood flow.
In the presence of hypoxia, pulmonary vasoconstriction continues, which in turn will maintain a patent ductus arteriosus leading to pulmonary hypoperfusion. This will continue the cycle of hypoxia and PPHN, a cycle that is difficult to break.
It is extremely difficult to treat this cycle and infants with PPHN can experience profound ongoing hypoxia that can lead to significant multi-system organ damage. In addition to the added multi-system effects of asphyxia infants like Vinod can result in increased illness. (see diagram)
Persistent Pulmonary Hypertension of the Newborn
Full- and post-term infants are particularly vulnerable to PPHN because the muscles in the walls of their pulmonary vessels are well developed and are highly sensitive to hypoxia. Preterm infants, while they can and do experience asphyxia, are less likely to develop PPHN as their pulmonary vessels are less muscularized and less sensitive to hypoxia. The development of PPHN significantly adds to an infant’s vulnerability, morbidity, and mortality.
Very briefly, this is why: a rising blood oxygen level is critical to successful transition. Recall that in utero, low pO2 levels help to keep the ductus arteriosus open and cause pulmonary vasoconstriction. Together, a patent ductus arteriosus and pulmonary vasoconstriction shunt blood away from the lungs (right-to-left shunting). During transition, a rising pO2 begins to close the duct and causes pulmonary vasodilation, lung fluid is absorbed and the lungs take over the process of gas exchange (which was previously done by the placenta).
NRP incorporates the ABC’s of resuscitation:
airway – position and clear
breathing – stimulate to breath
circulation – assess heart rate and color
Most newborns will require only the initial steps in resuscitation (stimulating and assessment); however, a very small number will require increased resuscitation efforts (chest compressions and medications).
Practice apgar
heart rate, resp effort, muscle tone, irritability and color.
Management of perinatal asphyxia involves every organ system. Why is that so?
Management of perinatal asphyxia involves every organ system because perinatal asphyxia has multiple organ system sequelae. Every organ system is vulnerable as a result of perinatal asphyxia and must, therefore, be supported.
How, in general, would you approach assessment for Vinod?
Assessment during resuscitation is based on the NRP sequences of: airway, breathing, and circulation. In these sequences position, color, HR, respiratory rate, and effort are important parameters.
Assessment must also be multi system. Once an infant is resuscitated and stabilized, a baseline assessment must be done with a view to collecting key information in each system. This can be done by a systems approach or from a head to toe approach. Whichever approach you chose, ensure that you are always doing a thorough assessment of the infant and family.
Blood Gas Analysis
Blood gas analysis assesses three interrelated, but separate processes: oxygenation, ventilation, and acid-base homeostasis. normal blood gas values: pH: 7.35-7.45 pCO2: 35-45 PaO2:50-80 P02 (cap): 40-60 HCO3-:20-26 BE: -4 - +4
Oxygenation
Oxygenation is assessed by how much oxygen the lungs are delivering to the bloodstream, told by the pO2 and oxygen saturation.
pO2 measures dissolved oxygen (3% of total oxygen)
normal values for pO2 are: arterial sample = 50–80 mmHg, capillary sample = 40–60 mmHg
Arterial pO2 values are much more accurate than capillary pO2 values
O2 sat measures oxygen carried on hemoglobin (97% of total oxygen)
normal range for O2 saturation is 88–95%
pulse oximetry should be used instead of capillary pO2 values (as they are not as accurate as arterial values)
Ventilation
Alveolar ventilation is determined by the pCO2 level. Carbon dioxide is very sensitive to minute ventilation, which is the volume of air inspired and exhaled in a minute. Minute ventilation (tidal volume x rate), and in particular, tidal volume (volume of air moved with each breath) is affected by the functioning of the pulmonary system.
-normal values for pCO2 are 35–45 mmHg
-hypoventilation leads to a buildup of CO2
A high amount of CO2 in the bloodstream, such as when ventilation is impaired, decreases the pH as excess carbon dioxide combines with water to form carbonic acid, creating respiratory acidosis
-hyperventilation leads to a decrease in CO2
A low amount of CO2 in the bloodstream, usually caused by over ventilation, will cause a respiratory alkalosis
Acid-Base Homeostasis
Acid-base homeostasis is the balance of acid to base necessary to keep the blood pH level normal.
Respiratory acidosis
caused by too much CO2, which combines with water to form carbonic acid, which in turn drops the pH
commonly caused by hypoventilation
Metabolic acidosis
caused by too much lactic acid
occurs with hypoxia and/or poor perfusion
anaerobic metabolism produces a lot of lactic acid as a byproduct, which lowers the pH
caused by failure of the kidneys to eliminate the hydrogen ions they normally eliminate from the body via urine
caused by failure of the kidneys to reabsorb the bicarbonate they normally recycle back into the body
Respiratory alkalosis
alkalosis (state of too much base or too little acid) is caused by too little carbon dioxide
occurs with hyperventilation
Metabolic alkalosis
caused by loss of acid through gastric suctioning
Alkalosis is a far less common neonatal response to illness than is acidosis. Both respiratory and metabolic acidosis are common neonatal blood gas abnormalities.
Occasionally, respiratory alkalosis is seen in an infant who is hyperventilating, either spontaneously or by a mechanical ventilator set with too high of a rate.
Metabolic alkalosis will rarely be seen.
pH 7.17
This pH is decreased, indicating acidosis. It is actually quite low. When a pH is this low, it suggests that the acid-base imbalance might be a mixed problem: that is, both metabolic and respiratory in origin.
source of acid-base problem
pCO2: 61 , bicarb: 17, base excess: -5
The high pCO2 suggests respiratory acidosis.
The low bicarb and low base excess suggest metabolic acidosis.
Therefore, this is a mixed — respiratory and metabolic — acidosis.
oxygenation
pO2: 35
This pO2 is low for a capillary sample. When assessing pO2, it is important to know whether the sample
is arterial or capillary. If capillary, it is not useful. Pulse oximetry is better.
ventilation
pCO2 61
This indicates hypoventilation, usually the result of lung disease. In Vinod’s case, I would suggest the meconium aspiration and resultant air trapping are to blame for the hypoventilation and elevated pCO2.
Why does Vinod have the blood gas results that he has?
Vinod’s blood gases reflect his asphyxia and his failure to adequately exchange gases. The high CO2 leads to respiratory acidosis. The low O2 leads to anaerobic metabolism, production of lactic acid, and a metabolic acidosis. This is a typical picture of asphyxia: hypoxia, hypercapnia, and mixed acidosis.
What should Sharon do with the results of the blood gas?
Sharon should inform Debra. She should give oxygen to keep oxygen saturation above 88% and repeat a blood gas in two hours. If Vinod is not already intubated and ventilated, it may be necessary to intubate and ventilate him. Mechanical ventilation will blow off Vinod’s CO2 by increasing his minute ventilation.
A common neurologic problem due to asphyxia is ?
seizures
In addition to differentiating seizure activity from jitteriness and other abnormal non-seizure movements, it is very important that you describe the seizure activity accurately. Aspects to consider are:
time of onset and duration of seizure
preceding activity, e.g., at the end of a feed
type of movement, e.g., cycling, twitching
body parts involved, e.g., right arm
change in level of consciousness/alertness
change in vital signs
post seizure status — alertness, vital signs, tone
Causes of seizures are:
- intracranial hemorrhage (IVH) is responsible for up to 16% of seizures in infants. Intraventricular hemorrhage is also often caused by asphyxia and/or hypoxia and is common in preterm infants
- metabolic disturbances — hypoglycemia, hypocalcemia, hypomagnesemia, and hyperphosphatemia
- bacterial meningitis (often group B Strep)
- viral encephalitis
- the most common cause of seizures in term infants is hypoxic-ischemic encephalopathy (HIE), accounting for 60–65% of seizures. Hypoxicischemic encephalopathy is often caused by asphyxia and is characterized by decreased blood flow to the brain, resulting in areas of ischemic damage.
Primary nursing interventions involve the identification of those infants who are at risk for developing seizures and observing those infants closely for subtle seizure activity.
If you suspect that an infant is having a seizure:
- stay with the infant and observe him/her closely
- if the infant is apneic or shows signs of respiratory distress, provide oxygen and ventilation as necessary
- attempt to stop the movement by gently touching or flexing the involved extremity — this will distinguish seizures from jitteriness
- document the seizure noting: preceding events or disturbances, exact description and type of seizure activity, duration of seizure, and condition of infant during and following the seizure
- report the seizure activity, specifying why you felt this was a seizure and not a normal movement or jitteriness
- review results of diagnostic tests to determine the cause of seizures
- give medications as ordered to control the seizures
- ensure the parents are informed of the seizure and provide support to them
- support and comfort the infant during and after the seizure
Explain hypoxic-ischemic encephalopathy, in your own words.
Hypoxic-ischemic encephalopathy (HIE) is a neurologic condition often experienced by full- and post-term infants who have been asphyxiated. The hypoxia associated with the asphyxia leads initially to increased cerebral blood flow. Over time, as hypoxia worsens and acidosis develops, cardiac performance is decreased, and cerebral blood flow decreases. Diminished perfusion with hypoxemic blood causes damage to vulnerable brain cells. In term and post-term infants, the most vulnerable area of the brain is the cerebral cortex. The extent of damage caused by HIE is best diagnosed by MRI, 48 to 72 hours after the insult. Long-term neurologic outcome can range from mild to severe.
Note: When the hypoxia associated with asphyxia leads to increased cerebral blood flow, this is the time that a preterm infant can experience an intraventricular hemorrhage.
Vinod’s birth weight is 3,850 grams. What is the correct loading dose of phenobarbital for Vinod?
(Loading dose is 10 – 20mg/kg).
3,850 gm = 3.85 kg
3.85 kg ´ 10–20 mg/kg = 38.5–77 mg
What is the most common side effect of phenobarbital seen in infants
The most common side effect of phenobarbital seen in neonates is respiratory depression. Therefore, close monitoring and availability of oxygen and bag and mask ventilation equipment are important.
Given the information provided, what do you think is the most probable cause of Vinod’s seizures?
- His blood glucose was normal, suggesting hypoglycemia is not to blame, but perhaps this should be rechecked.
- Metabolic disturbances probably aren’t the cause of Vinod’s seizures — but, to rule this out, we need to know the calcium, potassium, and magnesium levels.
- Sepsis may be a possibility; we don’t have enough information to determine this. The preliminary blood culture results won’t be available until 48 hours after collection. We do know that Ranjeet’s membranes ruptured within 18 hours of delivery, which does not present a high possibility of sepsis due to prolonged rupture of membranes. We do not know if Ranjeet’s cervix was swabbed for group B Strep (a frequent cause of sepsis in newborn infants). We do know that, so far, Vinod’s temperature has been within normal limits and there has been no sign of apnea or bradycardic episodes (these are frequent signs of sepsis). His WBCs were normal from the preliminary blood work.
- Given the information provided, the most likely cause of Vinod’s seizure is hypoxic ischemic encephalopathy secondary to asphyxia.
Describe how you would explain seizures to Ranjeet and Jason.
This question could be answered in a variety of ways. Some things to think about are:
language — are the words you use easily understood by non-health professionals?
tone — are you conveying concern, panic, reassurance?
pacing — is there ample opportunity for parents to ask questions?
amount — how much information is too much? too little?
How do you think Ranjeet and Jason might be feeling?
Anxious, fearful, confused, panic, bewilderment, overwhelmed, sad, guilty … there is a wide range of emotional responses that parents display when their newborn is ill. We can only speculate. If you were actually caring for this family it would be important to try to find out from them how they are feeling, what they are concerned about, and what they need.
If you were the nurse caring for Vinod, what would you do to facilitate family-centered care for Vinod and his family as they await transport to the tertiary hospital?
- provide the parents with emotional support and factual information about what is happening with Vinod. Keep in mind you may need to repeat the information several times
- offer to contact family members/friends who can provide support for the parents
- provide Ranjeet and Jason with information about where Vinod is going: the specific address of the hospital, the phone number of the NICU he is being transferred to, directions as to how to get to the new hospital, any information about the unit (e.g., give them an information brochure/pamphlet about the unit if available)
- talk with Ranjeet’s postpartum nurse and discuss the feasibility and appropriateness of obtaining a discharge order for Ranjeet so she can accompany Vinod to the tertiary center
- discuss with the physician in charge of transferring Vinod or the infant transport team the possibility of Ranjeet accompanying Vinod in the ambulance
-encourage Ranjeet and Jason to touch/stroke/talk to Vinod, and possibly hold him while awaiting transfer
acknowledge any feelings of fear, anxiety, grief, etc. expressed by Ranjeet and Jason, and encourage them to express their feelings if they want. Validate that their feelings are normal
- provide a private place in NICU (through the use of screens, curtains, etc.) where Vinod and his parents can be without the curious eyes of other parents, etc. observing their every move during this stressful time
- provide Ranjeet and Jason with a photograph of Vinod (many units have a camera available for just this purpose)
- discuss with Ranjeet her plans for feeding Vinod — i.e., is she planning to breast-feed Vinod. Hopefully Sharon or her postpartum nurse has already talked with her about this and if she is planning to breast-feed, she is starting to express her milk (pump)
What are some of the factors that remove control from parents who have a baby admitted to an intensive care nursery? What are some of the nursing measures that you as a neonatal nurse can do to return control back to the parents?
Some of the factors that remove control from parents who have babies admitted to NICU include:
the environment of a typical NICU — the equipment, the noise, the number of people
the lack of a normal typical routine that occurs with a newborn who doesn’t have any special needs — infants usually are in the room with their mothers, the main focus is on how to care and feed the infant, there is lots of happiness, etc. In contrast, holding, caring for, and feeding the infant in NICU is often limited.
fear of death and disability of the infant — the loss of the perfect infant
lack of knowledge about what is happening to their infant
Some of the ways to return control to the parents include:
find out what they need
provide factual, honest information
encourage contact with the infant — talking, touching, and holding if possible
involve parents in decision making — e.g., treatment decisions, feeding times, etc.
involve the parents in the infant’s care — dressing or providing clothing for the infant, changing the infant’s diaper, taking the infant’s temperature, etc. — as soon as it is medically safe and reasonable
encourage the parents to spend as much time as possible with their infant
encourage parents to ask questions
Anaerobic metabolism:
- uses copious amounts of glucose to create energy
- Is less efficient than aerobic metabolism
- leads to lactic acid production
Oxygenation can be assessed by:
measuring pO2 in the blood and pulse ox
Aerobic metabolism refers to cellular respiration in the presence of oxygen
True
Meconium aspiration is common in preterm infants
false
In order for successful transition to occur the pO2 must:
increase
Meconium Aspiration causes hypoxia in the neonate by:
- obstructing the airway
- chemical pneumonitis
- increasing pulmonary vascular resistance
- deactivating surfactant
Perinatal asphyxia is when a fetus or newborn does not adequately exchange gases:
True
If an infant’s hand is twitching and you hold/flex the limb the twitching stops it is…
they are having jitteriness
After the first breath is taken an infants’ pulmonary vascular resistance will increase
False
In utero the infants lungs are:
collapsed and fluid filled
