7-9 Flashcards

1
Q
  1. Pulmonary pathology in the neonatal period: Hyaline-membrane disease, aspiration syndrome, bronchopulmonary dysplasia.
    - pulmonary pathology in the neonatal period
A

refers to diseases affecting the pulmonary system from birth to 28 days as respiratory distress

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2
Q

respiratory distress defiend as:

A
  • tachypnoe less than 60 breaths a minute
  • laboured breathing, with chest wall recession and nasal flaring
  • expiratory grunting
  • cyanosis
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3
Q

transient tachypnea of the newborn

  • definition
  • cause
A
  • Is a benign self-limitid condition that can present in any infants of any gestational age shotly after birth
  • it is caused by a delay in the clearance of fetal lung fluid after birth that leads to ineffective gas exchange, respiratory distress and tachypnea.
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4
Q

transient tachypnea of the newborn

  • Etiology
  • History and physical
A
  • Delivery before completion of 39 weeks gestation, a cesarean section without labour, gestational diabetes, and maternal asthama
  • tachypnea less than 60 breaths per minute, nasal flaring, grunting, intercostal/subcostal/supracostal retractions.
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5
Q

transient tachypnea of the newborn

  • Evaluation
  • Treatment
A

-complete blood count, blood culture, C-reactive protein, lactate to rule out neonatal sepsis
Arterial blood gas may show hypoxemia (less than 85mmhg) and hypocapnia - low carbondioxide in the blood.( pco2 less than 45mmhg)
-treatment is supplemental oxygen and rule of two, or CPAP

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6
Q

Hyaline membrane disease

-overview

A

-Also known as respiratory distress, and is the result of insufficient surfactant which is responsible for keeping the alveoli open

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7
Q

Hyaline membrane disease

-etiology

A

caused by lack of surfactant, surfactants is made by type 2 alveolar cells that produce a lipiprotein complex knows as sufractant
the mother starts producing surfactant around the 24th week of gestation, and it is a slow process in the start, but around the 34-35 th week of gestation when the mother stars producing cortisol is when the surfactant production increses.
-surfactant decreases the surface tension in the lungs by binding to the water molecules and not making them stuck on the bottom of the alveoli, thus decreasing the surface tension and making it easier for the alveoli to expand.
-Hyline membrane disease is a type of of hypoplasia ( a lack of cells in an organ or tissue) with type 2 alveolar cells failing to develop.
-premature birth

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8
Q

Hyaline membrane disease

  • Diagnosis
  • Treatment
A

diagnosis is usally via clinical picture tachypnea, tachycardia cyanosis, and x-ray will show decresed lung volume and ground glass infiltrates uniform through the lungs
ABG will show lowered amount of oxygen less than 85mmhg and increased amount of co2.
-treatment include oxygen supplementation, with CPAP with iv fluids and exogenous surfactant through the breathing tube into the lungs.

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9
Q

Aspiration syndrome

  • general
  • meconium
A

-also known as meconium aspiration, in which the fetus pass meconium in the amniotic fluid, where it can put itself in a risk of aspiration that can have serious consequences
-meconium is a thick green brownish, blackish, substance that makes up the fetal stool, and is made up of bile, bile acids, mucus, pancreatic fluid, blood and cellular debris.
meconium is usally not found in the amniotic fluid, instead its usally passed within the first 24.72 hours after birth.

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10
Q

Aspiration syndrome

  • etiology
  • diagnosis
A
  • post term neonates less than 42 weeks of gestational age, umbilical cord/ plancetal pathology as they can put stress on the fetus in utero.
  • staining of the amniotic fluid, the fetus has meconium stains, tachycardia, x-ray.
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11
Q

Aspiration syndrome

  • complications 1-5
  • treatment
A

complications include 1-5

  1. mechanical obstruction
  2. surfactant wash
  3. pneumonitis occurs in 50% of meconium aspiration, defined as inflammation of the airways due to irritants found in the meconium , leads to inflammatory response in the alveoli causing stifness and fibrosis.
  4. pulmonary vasoconstriction/pulmonary hypertension as meconium has vasoconstrictive properties.
  5. damage to umbilical cord by inflammation and fibrosis, widespread vasoconstriction that can lead to umbilical cord ischemia that can turn in umbilical necrosis.
    - treatment includes mechanical ventilation and nitric oxide for vasodilation.
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12
Q

bronchopulmonary dysplasia

  • generall
  • etiology
A

-Infants who have an oxygen requirement at a postmenstrual age of 36 weeks are
described as having ​bronchopulmonary dysplasia (aka chronic lung disease).
Often a complication of Respiratory Distress Syndrome
-the lung damage is due to delay in lung maturation and possibly from pressure and volume trauma from atrifical ventilation.
-has a multifactoral etiology, significant risk factors include prolonged mechanical ventilation, high concentrations of inspired oxygen and infections

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13
Q

bronchopulmonary dysplasia

  • symptoms
  • treatment
A
  • symptoms include rapid breathing, labored breathing, wheezing, repeted lung infections
  • the focus of the treatment is to minimize further lung damage and provide support to the infants lung allowing them to heal and grow.
  • diuretics: decrease the amount of fluid in alveloi.
  • bronchodilators: relax muscles around air passage
  • cortical steroids: reduce inflammation within the lungs
  • cardiac medications: relaxing the blood vessles around the lungs and reduce the strain on the heart.
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14
Q

Infections of the neonatal infant:

  • common causes
  • ealry symptoms of infections
A

neonatal infections can be acquired during prenatal development or the first four weeks of life
-preterm infants are at an increased risk of infections as IgG is mostly transferred across the placenta in the first trimester, additionally infections around the cervix is often a cause of preterm labor and may cause postpartum infection. such infections are called congenital infections
-common causes include toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus, varcicella zoster, syphilis and others.
when the infection is intrauterine we can see growth restrictions and infants deformities.
-early symptoms of infections include: respiratory distress with transient apnea, lethargy, increase in liver and spleen size, WBC can be both elevated or decreased.

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15
Q

Infections of the neonatal infant: neonatal sepsis,

-general

A

Sepsis is the bodys response to a systemic infection, sepsis can be early onset or late onset.
sepsis can be confused with bacterimia, bacterimia is defined as the presence of bacteria in the blood, while sepsis is the response to the bacteria.
-the response include vasodilation leading to hypertension leading to tachycardia.
-sepsis is casued usally to a primary infection somwhere else in the body, which makes sepsis a complication of the primary infection.

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16
Q

Infections of the neonatal infant: neonatal sepsis,

  • early onset sepsis
  • late onset sepsis
A
  • early onset sepsis: is generally caused by transmission of pathogens from the female genitourinary system to the newborn or fetus, these pathogens can ascend the vagina, the cerviz and the uterus and can also infect the amniotic fluid, Neonates can also be infected in utero or during delivery as they pass through the vaginal canal.
  • typical pathogens include group B streptococcus, E,coli, H.influenza and listeria monocytogenes.

-late onset sepsis: transmission from pathogens from the surrounding environment after delivery.

17
Q

Infections of the neonatal infant: neonatal sepsis,

  • lab analysis
  • treatment
  • complications
  • diffrential diagnosis
A

-lab analysis: CBC, differential smear, blood culture, urine culture and lumbar culture.

  • treatment: IV-benzylpencicillin with gentamicin as first choice
  • Benzylpenicillin dose 25mg/kg every 12 hours
  • Gentamicin 5mg/kg, single dose, only give second after 36 hours
  • complications: meningitis, chronic lung disease,
  • In the community, if you suspect meningitis give IM Benzylpenicillin
  • diffrential diagnosis: congenital heart disease, transient tachypnea of the newborn, meconium aspiration syndrome, and metabolic disease.
18
Q

necrotizing enterocolitis

  • General
  • Etiology
A

necrotizing enterocolitis is the most common gastrointestinal medical/surgical emergency in neonates.
-is an acute inflammatory disease with a multifactorial etiology.

-Etiology: occurs in preterm infants, prematurity is a constant contributor to the disease, the cause is thought to be multifactorial cause, the combination of a genetic predisposition, intestinal immaturity and an imbalance in microvascular tone (lack of blood flow), accompanied by abnormal microbial colonization in the intestine and a highly reactive intestinal mucosa.

19
Q

necrotizing enterocolitis

  • clinical signs
  • management
  • treatment
A

-clinical signs: abdominal distention, feeding intolerance, emesis (vomiting), rectal bleeding, and occasional dairrhea, patients can also present with electrolyte imbalance.

radiographic imaging is the gold standard for diagnosis.

-management: discontinuation of enteral feeding, GI decompression, electrolyte correction, septic work up, and antibiotic course.
Regular x-rays, slow return to feeding,
50% of infants require surgical intervention, this decision is based on presence of pneumoperitoneum, and can be complicated by and infection from clostridium perfringens.

antibiotics should be: Ampicillin, Gentamicin, cefotaxime for gram negative and Metronidazole, clindamycin and vancomyacin for gram negative.

20
Q

neonatal Pneumonias

  • general
  • types
  • etiology
A

-Pneumonia is swelleing (inflammation) in the tissue in one or both lungs due to infection
-early onset pneumonia: is part of generalized sepsis, that manifests at or within hours of birth.
-late onset pneumonia: usally occurs efter 7days of age, most common in neonatal intensive care units, among infants that require prolonged endotracheal intubation, becuse of a lung disease (ventilator associated pneumonia)
-Etiology: pathogens are aquired from the maternal genital tract, or the nursery.
these organism include gram positive cocci, both methicillin-sensitive and methicillin-resistant pathogens
and gram negative bacili as E.coli, klebsiella, proteus.
-in infants who have received broad spectrum antibiotics there can be many other pathogens as :pseudomonas , citrobacter, bacillus and serratia, viruses and fungi cause some cases.

21
Q

neonatal Pneumonias

  • Symptoms
  • Diagnosis
  • Treatment
A

-symptoms: late onset hospital acquired pneumonia manifests with unexplained worsening of the patients respiratory status, thick and brown respiratory secretions, temperature instability and neutropenia (low netruphils count).
-diagnosis: chest x-ray, blood cultrue, gram stain, and culture of tracheal aspirate.
new persistent infiltrates should be visible on chest x-ray but may be difficult if the infants has severe bronchopulmonary dysplasia.

-Treatment: vancomyacin and a broad spectrum beta-lactam drugs.

22
Q

Osteoarthritis (septic arthritis)

  • general
  • Diagnosis
A
  • Septic arthritis in children is most often a hematogenous infection, the increased blood flow in the metaphyseal capillaries makes growing bones susceptible to infections from hematogenous seeding from any trauma or infection.
  • most commonly affected locations in the body are the large joints of the lower limb
  • Staphylococcus aureus and respiratory pathogens are the most common causative agents.
  • Kingella kingae is a regional pathogen that has been increasingly identified as a common causative agent especially in children between 6-36 months.
  • Diagnosis: classic presentation is an acutely swollen, red, painful joint with limited motion, and fever
  • fever is especially high in cases caused by MRSA
  • cases caused by kingella kingae are milder and fever may even be absent.
  • diganosis is via CPR, ESR and joint punture to detect pus and obtain a sample for labs.
23
Q

Osteoarthritis (septic arthritis)

  • Treatment
  • Differential diagnosis
  • complications and monitoring
A
  • Treatment: for MRSA cephalosporins or clindamyacin and for Kingelle kingae any penicillin and cephalosporin
  • Differential diagnosis: Aseptic synovitis of the hip, viral arthritis, osteomyelitis, juvenile rheumatoid arthritis, legg-calve perthes disease.
  • complications and monitoring: surgery for drainage of pus, and keep monitering with CPR.
24
Q

9.Nervous system disorders in neonatal infant: neonatal seizures, hypoxia-ischemic encephalopathy, intracranial hemorrhage, periventricular leukomalacia.
-Neonatal seizures
Clinical types of neonatal seizures

A
  • Focal clonic​ - repetitive rhythmic contractions of muscle groups of the limbs, face or trunk. May be unilateral or multifocal and cannot be suppressed
  • Focal tonic​ - sustained posturing of single limbs, sustained asymmetric posturing of
    the trunk with sustained eye deviation.
  • Myoclonic ​- arrhythmic contractions of muscle groups of limbs, face, or trunk. Typical not repetitive and may be provoked by stimulation
  • Generalised tonic​ - sustained symmetric posturing of limbs, trunk and neck.
  • Ocular signs​ - random and roving eye movements of nystagmus
  • Orobuccolingual movements ​- sucking, chewing or tongue protrusions
  • Progression movements - rowing/swimming of arms, pedaling of legs, may be
    suppressed unlike tonic and clonic movements
25
Q

Neonatal seizures

  • general
  • etiology
A
  • Seizures occur in 1.4% of infants and 20% of preterm infants, seizures may be related to as serious neonatal problem and require immediate evaluation.
  • most neonatal seizures are focal, becuse electrical activity is impended in neonates by lack of myelination and incomplete formation of dendrites and synapses in the brain.
  • Etiology: the abnormal central nervous system electrical discharge may be casued by:
  • primary inter-cranial process as meningitis, ischemic stroke, encephalitis, intracrainal hemorrhage, tumor, malformation.
  • systemic problems such as hypoxia-ischemia, hypoglycemia, hypocalcemia, hyponatremia and other disorders of metabolism.
26
Q

Neonatal seizures

  • Symptoms
  • diagnosis
  • Treatment
  • Antizeure Drugs
A
  • Symptoms: neonatal seizures are usally focal and can be difficult to distinguish from normal neontal activity, because they manifest as chewing and bicycling movements.
  • diagnosis: Electroencephalogram EEG, lab tests (serum glucose, electrolytes, CSF, urine and blood culture)
  • Evaluation begins with a detailed family history and a physical examination.
  • Treatment: treatment focuses primarily on the underlying disorder and secondarily on the seizures themselfs.
  • Drugs: phenobarbital , levetiracetam and lorazepam.
27
Q

hypoxia-ischemic encephalopathy

  • general
  • etiology
A
  • hypoxia-ischemia encephalopathy occurs when both oxygen and blood supply to the babys brain is restricted or interrupted during child birth (perinatal asphyxia) that causes brain cells to die efter short period.
  • Etiology labour and delivery complications, placental abruption, low maternal BP, umbilical cord complications, uterine rupture, maternal infections, placenta blood circulation issues and fetal strokes.
28
Q

hypoxia-ischemic encephalopathy

  • symptoms
  • diagnosis
  • complication
  • treatment
A
  • symptoms: the symptoms after birth will vary significantly based on the severity of the underlying brain damage, and the areas of the brain that are affected,
  • the specific symptoms will depend on the stage of the injury, genarally symptoms include: reduced conscienceless, seizures, respiratory difficulties and depression of muscle tone, infants presents with low APGAR score.
  • diagnosis: if you suspect Hypoxic-ischemic encephalopathy the best way to find out is via MRI scan that will show cerebral edema, cortical necrosis and involvement of the basal ganglia, head ultra sound scan.
  • complication: after reperfusion, hypoxic-ischemic injury is complicated by cell necrosis and vascular endothelial edema, that reduces blood flow to the affected area.
  • Treatment: the primary treatment is body and head cooling (therapeutic hypothermia) slows cellular decay and damage process within the brain, it aims to minimize the long term effect of hypoxic-ischemic encephalopathy.
29
Q

intracranial hemorrhage

  • general
  • types
A
  • intracranial hemorrhage refers to bleeding and accumulation of blood and may be confined to one anatomic are of the brain.
  • There are three categories of neonatal intracranial hemorrhage
  • ​subdural, subarachnoid and periventricular​
  • intraparenchymal or cerebellar region
30
Q

subural hemorrhage

  • Etiology
  • symptoms
  • Treatment
A

Etiology: subdural hemorrhage are seen in association with birth trauma, cephalopelvic disproportion, forceps delivery, large for gestional age infants, skull fractures, and postnetal head trauma.
-occasionally a massive subdural hematoma can be caused by a rupture of the veins of galen, or by an inherited coagulation disorder such as hemophilia.
-Symptoms: subdural hematomas does not always cause symptoms immediately after birth, but with time red blood cells undergo hemolysis and water is drawn into the hemorrhage because of the high oncotic pressure of protein leading to an expanding symptomatic lesion ssymptoms include: Anemia, vomiting seizures and macrocephaly.
Treatment for all the symptomatic subdural hematomas is sugical evacuation.

31
Q

Subarachnoid hemorrhage

  • General
  • Treatment
A
  • Subarachnoid hemorrhage may be spontaneous and are associated with hypoxia or caused by bleeding from a cerebral arteriovenous malformation.
  • seizures are a common presenting manifestation, the prognosis depends on the underlying injury.
  • Treatment is directed at the seizures and at the rare occurrence of post hemorrhagic hydrocephalus.
32
Q

Periventricular hemorrhage

  • General
  • Pathogenesis
  • Clinical manifestation
A
  • Periventricular hemorrhage and intraventricular hemorrhages are common in very low birth weight infants, with the risk decreasing with increasing gestational age, as many as 50% of infants weighing less than 1,5 kg have evidence of intracranial bleeding.
  • The exact pathogenesis os not known, but the vessels rupture and hemorrhage due to passive change in cerebral blood flow occurring with the variation of blood pressure that sick premature infants often exhibits due to failure of auto-regulation.

-most of these kinds of hemorrhage occurs in the first 3 days of life, Clinical manifestations include: Bradycardia, lethargy, coma, hypotension, metabolic Acidosis, anemia, bulging fontanelle.

  • periventricular/intraventricular hemorrhage are grades 1-4 with 4 the most severe.
  • upon resolution cysts/gliosis may occur causing periventricular leukomalacia, a precursor to cerebral palsy.
33
Q

periventricular leukomalacia

  • generall
  • symptoms
  • treatment
A
  • PVL is a type of white matter hypoxic brain injury, histologically characterised by white matter necrosis ner the lateral ventricles, significantly more common amongs premature infants, and can lead to neonatal encephalopathy, one of the causes for cerebral palsy.
  • PVL undergoes there pathogenic stages, necrosis, resorption, and formation of gliosis scars or cysts.
  • PVL is incredibly hard to distinguish clinically in newborn infants.
  • Symptons include hypotonia, respiratory distress, vision defects, apnea, seizures and bradycardia.
  • Later motor development is invariably affected and it is later in childhood as patients miss developmental milestones that they are diagnosed.
  • Treatment: there are no clear treatments methods for PVL, management is largely supportive.