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PedsConditions
Peds Conditions Barry
| Question | Answer |
|---|---|
| 2 factors cause intraventricular hemorrhage: | 1. Loss of cerebral autoregulation 2. Abrupt alterations in cerebral blood flow and pressures |
| When is the highest occurrence of intraventricular hemorrhage? | Highest occurrence in first 72 hours of life. |
| Increased incidence of intraventricular hemorrhage in what population? | Incidence up in infants < 32 weeks gestation and with birth weight < 1500 grams. |
| To prevent intraventricular hemorrhage, avoid conditions that: | -Interfere with autoregulation (hypocarbia, hypercarbia,hypoxia, acidosis) -Overwhelm autoregulation abilities (Hypertension) -Contribute to rapid fluctuations of cerebral blood flow or pressure |
| Primary cause of respiratory distress syndrome (RDS): | Primary Cause: surfactant deficiency secondary to immature type II alveolar cells in the preterm lung. |
| When does surfactant appear, when is it mature? | Surfactant appears in amniotic fluid 28-32 weeks and mature levels by 34-35 weeks. |
| What can cause earlier release of surfactant? | Maternally administered steroids. |
| Tell me the story of what happens after hypoxia in the infant (RDS)? | Increase work of breathing-> hypercarbia-> pulmonary arterial vasoconstriction->R to L shunting and ischemic injury to cells producing surfactant. |
| On an RDS Xray you will see: | Bell shaped thorax with diffuse symmetrical ground glass infiltrates. |
| Treatment for RDS: | -Supplemental Oxygen for target -PaO2 of 55 – 70 mm Hg -CPAP up to 10 cmH2O -Mechanical ventilation -Avoid oxygen toxicity and pulmonary barotrauma -Artificial surfactant |
| PDA = Failed closure or reopening after functional closure. What happens? | -Left to right shunt occurs and may be asymptomatic or result in CHF and failure to thrive if large -If PVR remains high the R to L shunt results in hypoxemia -Obligatory PDA occurs in 10% of infants with CHD |
| Physical signs of R to L shunt: | -Hyperdynamic precordium -Wide pulse pressures -Bounding arterial pulses -Increased oxygen requirements -Metabolic acidosis |
| Diagnosis or R to L shunt is by: | ECHO. |
| Treatment for PDA: | Indomethacin Fluid restriction Diuretics for CHF Surgery Mechanical ventilation |
| Hypoglycemia in a neonate = | less than 40 |
| Hyperglycemia in term and preterm infants: | over 125 and over 150 |
| To maintain normoglycemia, what is required? | Neonates require 3-5 mg/kg per minute and preterm neonates 5-6 mg/kg per minute of glucose to maintain euglycemia. |
| What are 4 neonate thermoregulatory disadvantages? | -Increased surface are relative to metabolic mass -Smaller heat sink reserve -Less insulating fat -Decreased skin keratinization = more evaporative heat loss -Inability to shiver |
| To create heat, neonates rely on 2 metabolically costly mechanisms: | -Brown fat metabolism -Shunting of hepatocyte oxidative phosphorylation to the thermogenic proton leak pathway |
| Neonates creating heat results in what bad stuff? | Acidosis, hypoxia, hypoventilation and hypotension |
| Postoperative apnea - who is at greatest risk? | Infants 55weeks of post-conceptual age & younger are at greatest risks. |
| Retinopathy of prematurity - who is at greatest risk and why? | PRETERM INFANTS <1500 G AND 34 WEEKS GESTATION @RISK - RETINAL VASCULATURE NOT FULLY MATURE. |
| What happens in retinopathy of prematurity - in caps, please? | VESSELS CAN VASOCONSTRICT, HEMORRHAGE, AND VASOPROLIFERATE IN RESPONSE TO HYPEROXIA. |
| When is vascularization of the eye complete? | 44 weeks. |
| Blindness can result from retinal detatchment - what has been implicated in causing retinopathy of prematurity? | HYPOXEMIA, ACIDOSIS, HYPOTENSION, AND SEPSIS HAVE BEEN IMPLICATED IN CAUSING ROP. |
| You should measure O2 where? | Preductal (Rt hand or ear). |
| To avoid ROP, where should you keep your O2 during GETA? | 93-96% |
| How much type 1 fibers in diaphragm? | 10-25% |
| What is most common laryngeal disorder of newborn? | Laryngomalacia. |
| What is laryngomalacia? | Inward collapse of epiglottis and aryepiglottic folds during inspiration. |
| What are signs of laryngomalacia? | Stridor especially when infant lying supine, crying, or feeding. |
| What other condition is associated with laryngomalacia? | Possible association of gastroesophageal reflux. |
| Can you easily PPV a child with laryngomalacia? | Yes. |
| Is laryngomalacia relieved with an oral airway? | No. |
| What's associated with OSA? | -Habitual snoring, daytime somnolence, behavioral problems, school problems, developmental delay -Failure to thrive -Hypoxemia, hypoventilation, PHTN, CHF and death |
| Can OSA cause Cor Pulmonale? | Hell yeah it can. |
| Many patients with craniofacial abnormalities can also have: | OSA. |
| What is the most common acquired anomaly of the larynx in children and most common cause of tracheostomy for children younger than 12 months? | Subglottic Stenosis |
| What sadly causes subglottic stenosis? | Chronic inflammation and scarring from the presence of an endotracheal tube. |
| Is it easy to PPV a patient with subglottic stenosis? | PPV may be difficult. |
| Tracheomalacia is: | Defined as a softening of the tracheal cartilage. |
| Tracheomalacia causes airway collapse during: | Forceful coughing or exhalation ventilation. |
| Patients with tracheomalacia have these symptoms: | Long term mechanical ventilation, noisy breathing, “barky” cough, wheezing and respiratory distress. |
| Asthma is a chronic disease of reversible airway obstruction and characterized by: | Bronchial hyperreactivity, inflammation, & mucous secretion. |
| Asthma pharmacotherapy: | -Beta adrenergic agonists -Corticosteroids -Cromolyn sodium -Anticholinergics -Leukotriene pathway modifiers |
| Unfortunately, for intraoperative bronchospasm, Intraoperative bronchospasm efficiency of MDI of albuterol through 3.0 – 6.0 mm ID tracheal tubes is: | Low. |
| What is cystic fibrosis? | A hereditary disease of exocrine glands primarily affecting the pulmonary and GI systems. |
| Cystic fibrosis causes exocrine pancreatic... | Insufficiency. |
| Cystic fibrosis causes GI... | Obstruction. |
| In a patient with cystic fibrosis, how does sweat change? | They lose an excess of sodium and chloride. |
| Sinopulmonary disease is found in... | Cystic fibrosis patients. |
| Cystic fibrosis patients' sbnormal thick and viscous secretions coupled with decreased ciliary activity lead to... | Pneumonia, wheezing and bronchiectasis |
| What does cystic fibrosis do to pulmonary function? | Increases residual volume and airway resistance with decreased vital capacity & expiratory flow rate. |
| Cystic fibrosis may lead to malabsorption syndrome which may lead to... | Malabsorption syndrome may lead to dehydration, electrolyte disorders and Vitamin K deficiencies (Clotting factors). |
| Cystic fibrosis patients have a higher incidence of this cardiac condition: | Right ventricular hypertrophy. |
| Common surgical procedures for the patient with cystic fibrosis: | -Endoscopic sinus surgery (Nasal Polyps) -CVP catheter placement -Bronchoscopy -Lobectomy -Pneumonectomy -Abdominal exploration -Colostomy |
| N2O in a patient with cystic fibrosis? | NO! Avoid N2O; increase FiO2; Inhalational uptake prolonged. Rapid emergence good. |
| Do cystic fibrosis patients have issues with hyperactive airway? | Uh, yeah. |
| In a patient with meconium aspiration, what is believed to be responsible for the violent inflammatory response? | Bile salts. |
| Can pulmonary hemorrhage occur in meconium aspiration? | Yes. |
| Therapy for patients with meconium aspiration | -Amnioinfusion -Tracheal Intubation and suctioning -Antibiotics -Surfactant Replacement -ECMO for severe MAS with PPHN |
| Bronchopulmonary dysplasia is: | BPD is a chronic disease of lung parenchyma and small airways with chronic respiratory insufficiency in prematurely born infants. |
| Bronchopulmonary dysplasia is oxygen dependence at when? | BPD is oxygen dependence at 36 weeks postconceptual age. |
| What is cerebral palsy? | It is an abnormality of posture and movement caused by brain injury occurring before 2 years of age. |
| What causes cerebral palsy? | Prematurity, LBW, prenatal infections (rubella), congenital malformations of the brain, meningitis, brain tumors, and intracranial hemorrhage. |
| Describe pyramidal type of cerebral palsy: | Pyramidal type: damage to cerebral cortex usually produces spasticity, contractures and bony deformities. |
| Describe extra-pyramidal type of cerebral palsy: | Extra-pyramidal type: damage to the basal ganglia or cerebellum tens to produce athetosis or ataxia. |
| Can pyramidal and extra-pyramidal type of cerebral palsy co-exist? | Yes, and do, often. |
| What is baclofen? | Baclofen is a GABA receptor agonist with action in the dorsal horn of the spinal cord. It is used to reduce pain with muscle spasms and delay development of contractures. Abrupt withdrawal issues. |
| What does botox do/anesthesia issues? | Botox produces reversible muscle denervation & temporary reduction in muscle tone. No anesthesia issues. |
| Why do patients with cerebral palsy have hypothermia issues? | Hypothalamus issues. |
| Do CP patients have latex allergy issues? | Yes. |
| What is the inherited, sex-linked recessive disease that presents in early childhood between 2 and 6 years of age? | Duchennes's Muscular Dystrophy. |
| T or F: Duchenne's patients look like they're wasting away? | F: they LOOK very muscular. |
| S/S of Duchenne's: | -Symmetric skeletal muscle wasting -Wasting of pelvics – Gower’s sign Hypertrophy of skeletal muscles Kyphoscoliosis EKG changes: tall R in V1, deep Q in limb leads, short P-R interval, tachycardia Mitral valve prolapse Intestinal hypomobility and d |
| Sux and muscular dystrophy? | Hyperkalemia Massive rhabdomyolysis Cardiac arrest. Good God no don't do it! |
| Non-depolarizing muscle relaxants and MD: | OK: prolonged recovery time. |
| What can't you give to patients with congenital myotonic dystrophy? | No succinylcholine – induces intense generalized myotonic contraction. |
| Heart and congenital myotonic dystrophy? | Fifty to ninety % have myocardial conduction defects, bradycardia and 1st degree AV block are common. |
| In patients with congenital myotonic dystrophy, reversal? | Reversal of muscle relaxation with anticholinesterase drugs may precipitate or enhance myotonia. |
| Osteogenesis imperfecta: | Congenital connective tissue disorder that causes a generalized decrease in bone mass and bones that break easily. |
| Clinical manifestations of osteogenesis imperfecta: | Blue sclera, dental abnormalities and brittle bones. Deafness, abnormal platelet function, increased BMR & O2 consumption, cleft palate, vascular fragility, hydrocephalus, spina bifida and aortic and mitral regurgitation. |
| Scoliosis and osteogenesis imperfecta? | About 20% of the time. |
| Sux and osteogenesis imperfecta? | No - spasms will break their bones. |
| Scoliosis and PVR: | Elevated Pulmonary vascular resistance from chronic hypoxia causes Pulmonary HTN and Right ventricular hypertrophy. |
| What does scoliosis do to lung numbers? | Reduced lung volumes and chest wall compliance. PaO2 is reduced as a result of V/Q mismatch and increased PaCO2 signals severe disease. |
| Down Syndrome is an extra what? | Chromosome 21. |
| Down and catecholamines? | Decreased stores. |
| Obesity is an independent risk factor for: | DVT. |
| Obesity is associated with pseudotumor cerebri, which is what? | Benign intracranial hypertension. |
| What is maturity onset diabetes of youth? | Inherited form of NIDDM. |
| What's the most common childhood abdominal malignancy? | Wilm's tumor. |
| What is WAGR syndrome? | Airidia, genital anomalies, mental retardation, 30% chance of developing Wilm's tumor. |
| What causes prune belly syndrome? | It is caused by agenesis of the abdominal musculature, which results in a thin walled, protrudent abdomen. |
| Anesthetic implications for prune belly? | -Mult pulm complications with inability to cough effectively -High risk of asp -Controlled ventilation is necessary to prevent hypoventilation & hypoxemia -Skeletal muscle relaxants are not needed -Avoid overhydration -Postop pulm complications |
| Phenylketonuria (PKU) is: | Disorder of amino acid metabolism. |
| PKU patients have: | -Most significant consequence is mental retardation -At least ¼ of the patients have seizures -Eczema is common -Increased incidence of pyloric stenosis |
| PKU patients and drugs: | Very sensitive to narcotics and CNS depressants |
| Sickle cell results from: | Hemoglobin S results from the substitution of a valine molecule for a glutamate in position 6 of the beta chain. |
| What happens with hemaglobin S cells? | Altered hemoglobin readily forms polymers when deoxygenated producing the pathognomonic sickled RBC’s. |
| Genetic cause of sickle cell: | SCD – autosomal recessive sickling gene. |
| Full sickle cell patients have 90% HgbS and 10%: | HgbF. |
| People with sickle cell trait have up to how much HgbS? | 45%. |
| Infants under how many months will have false positive for sickle cell test? | 6 months. |
| What organ disorders in hemophilia? | Splenomegaly Abnormal liver function Joint disease related to hemarthrosis |
| Adequate clotting usually occurs with what percentage of clotting factors? | 30% |
| In patients with hemophilia and moderate bleeding, we should raise their clotting factors to what? | 40% |
| What do you give to Von Willebrand patients? | Factor 8 or DDAVP. |
| Intracellular C is primarily controlled by: | The sarcoplasmic reticulum and more specifically the ryanodine receptor. |
| MH is triggered by: | ALL the agents (except N2O) and sux. |
| MH specific signs: | Muscle Rigidity Increased CO2 Production Rhabdomyolysis Marked Temperature Elevation |
| MH nonspecific signs: | Tachycardia Tachypnea Acidosis (Resp/Metabolic) Hyperkalemia |
| What drugs for MH crisis? | Treat hyperkalemia (bicarbonate 1-2 mg/kg PRN) Give dantrolene 2.5mg/kg push. Repeat PRN |
| CHD: Obstructive lesions: | Obstruction to blood flow is present. Obstruction may be intracardiac e.g. pulmonary or aortic stenosis or may be extracardiac e.g. Coarctation of the aorta. |
| What happens with increased pulm blood flow? | L to R shunting occurs (no cyanosis). |
| Typical L to R shunting patient and conditions? | These patients usually present with failure to thrive, pulmonary hypertension, recurrent chest infections or congestive cardiac failure(CCF). Examples include ASD, VSD or PDA. |
| Decreased pulm blood flow: | Right to left shunting occurs with some type of obstruction to normal pulmonary blood flow. |
| Presentation/examples of R to L shunting: | This results in cyanosis, polycythemia, and systemic emboli. Examples include tetralogy of Fallot, tricuspid atresia, and pulmonary atresia. |
| Shunting and inhalational induction: | R to L = DELAY uptake into blood occurs more slowly L to R = minimal to no effect |
| Shunting and IV induction: | R to L = response is faster L to R = minimal effect if systemic perfusion is preserved |
| 4 things in tet. of fallot: | VSD Pulm stenosis Overriding aorta RVH |
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