Diagnosis of Neonatal Respiratory Distress Syndrome
Neonatal Respiratory Distress Syndrome Diagnosis: Book Excerpts
Diagnosis of Neonatal Respiratory Distress Syndrome: medical news summaries:
The following medical news items
are relevant to diagnosis and misdiagnosis issues for Neonatal Respiratory Distress Syndrome:
Diagnostic Tests for Neonatal Respiratory Distress Syndrome: Online Medical Books
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Review excerpts from medical books online, free, without registration,
for more information about diagnostis of Neonatal Respiratory Distress Syndrome.
Cyanotic Newborn:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Transposition of the great vessels (TGV)
–The most common cardiac cause of cyanosis in the newborn
–Aorta connected to RV and pulmonary artery
connected to LV
–PE, ECG normal
–CXR: Normal or egg-on-string
- Tetralogy of Fallot
–Most common cyanotic heart disease
–Right ventricular hypertrophy, pulmonary stenosis, VSD, and an overriding aorta
–Associated with 22q11 deletion
–Murmur; reduced PVM; R-axis deviation,
RVH
- Critical pulmonary valve stenosis
–Thickened pulmonary valve
–Murmur; reduced PVM; RVH
- Pulmonary atresia
–No flow from RV to pulmonary artery, so pulmonary blood flow depends on ductus arteriosus
–PE normal; reduced PVM; reduced R-sided forces with normal axis
- Tricuspid atresia
–No inflow into R ventricle, causing R ventricular hypoplasia
–With or without murmur; reduced PVM; reduced R-sided forces with L-axis deviation
- Truncus arteriosus
–Single outlet to ventricles divides into aorta and pulmonary arteries
–VSD always present
–PE normal; possibly increased PVM; ECG
normal
- Total anomalous pulmonary venous return
–Cardiac cause of cyanosis that mimics respiratory disease with respiratory distress and “white-out” of lungs
–Consider for patients who appear to have bad respiratory disease
–With or without murmur; increased PVM; ECG normal
- Ebstein anomaly
–The tricuspid valve is displaced down into the R ventricle, usually with severe tricuspid regurgitation with R-to-L atrial level shunting
–Murmur; huge heart; R atrial enlargement (tall P waves)
- Other: Respiratory most common, polycythemia, hypoglycemia
Workup and Diagnosis
- History
–Sometimes a family history of congenital heart disease
–Usually presents on second day of life rather than in
the delivery room
- Physical exam
–Almost all patients with cyanotic heart disease have single S2, however, splitting of S2 difficult to appreciate in babies due to fast heart rate
–See Differential Diagnosis for findings by lesion
- Hyperoxia test
–Used to differentiate cardiac from respiratory causes
–Administration of 100% O2 for 10 minutes
–PaO2 improves with respiratory causes of cyanosis, but not cardiac causes, because oxygenated blood in the lungs is not transported systemically
–Arterial blood gas PaO2 >200 is more indicative of respiratory disease; <100 consistent with cyanotic heart disease or very severe respiratory disease
-
Chest X-ray shows PVM, cardiac silhouette
-
Electrocardiogram
–Evaluates the presence/absence of R ventricle
–Normal newborns have a dominant R wave in lead V1
with a QRS axis of 60–180
Echocardiogram
–Definitive test for cardiac anatomy and function
Cardiac catheterization is rarely needed except in some instances with very complicated anatomy
>
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Source: In A Page: Pediatric Signs and Symptoms, 2007
Accessory muscle use:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient’s condition allows, examine him more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, or fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; also inquire about neuromuscular disorders, such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function tests or received respiratory therapy. Ask about smoking and occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting an abnormal respiratory rate, pattern, or depth. Assess the color, temperature, and turgor of the patient’s skin, and check for clubbing.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Infant respiratory distress syndrome:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
CONFIRMING DIAGNOSIS Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest IRDS, a chest X-ray and arterial blood gas (ABG) analysis are necessary to confirm the diagnosis.
❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with IRDS), but 24 hours after birth it will show the characteristic ground-glass appearance and air bronchograms.
❑ ABG analysis shows decreased partial pressure of arterial oxygen; normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).
❑ Chest auscultation reveals normal or diminished air entry and crackles (rare in early stages).
When a cesarean delivery is necessary before 36 weeks’ gestation, amniocentesis enables the determination of the lecithin/sphingomyelin (L/S) ratio and the presence of phosphatidylglycerol. An L/S ratio of more than 2:1 and the presence of phosphatidylglycerol decrease the likelihood of IRDS.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Accessory muscle use:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s condition allows, examine him more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, and fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; also inquire about neuromuscular disorders, such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function tests or received respiratory therapy. Ask about smoking and about occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting abnormal respiratory rate, pattern, or depth. Assess the color, temperature, and turgor of the patient’s skin, and check for clubbing. (See Accessory muscle use: Causes and associated findings, page 30.)
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Respirations, grunting:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Epigastric Distress:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Pain is the usual presentation of epigastric distress. First priority is to ask questions about the onset, intensity, frequency, pattern, and location of the pain. Onset: When did the pain start? Is there any prior history of similar pain?
B. Intensity and quality. Can you describe the pain? (sharp, dull, burning, radiating, pressure). Burning pain is often used to describe GERD. Pressure sensation “like an elephant sitting on me” suggests cardiac ischemia (Chapter 7.1).
C. Frequency and pattern. Does the pain occur at any particular time of day? Is there anything that makes the pain better or worse? Pain that is worse at night when lying down suggests GERD. Pain that occurs after a high fat meal increases the likelihood of gallbladder disease (Chapter 9.1).
D. Location. Where is the pain? Does the pain radiate anywhere? Radiation to the back suggests pancreatitis. Pain radiating to the scapula can indicate gallbladder disease.
E. Associated symptoms. Has there been any nausea, vomiting, or hematemesis? The previous symptoms can indicate a Mallory-Weiss tear or PUD. If diarrhea is present, is there bright red blood or melena in the stool? The presence of blood or melena in the stool requires further workup for GI bleed.
F. Past medical history. Has the patient had any prior GI problems? Obtain a drug history, including the use of aspirin, nonsteroidal antiinflammatory drugs, alendronate sodium (Fosamax), steroids, antibiotics. Is there a history of tobacco or alcohol use? Both tobacco and alcohol use are associated with an increased incidence of GERD and PUD. Multiparity and obesity increase the risk of gallbladder disease. Are there risk factors for sexually transmitted diseases? Hepatitis B and human immunodeficiency virus can be transmitted sexually and can be causative factors in epigastric distress.
Physical examination
A. General assessment. Obtain vital signs. Is the patient febrile—indicating an infectious cause? Tachycardia and hypotension can indicate dehydration or GI bleed. Is the patient in acute distress? Jaundiced?
B. Cardiopulmonary assessment. Evaluate the heart and lungs to rule out any cardiac or pulmonic process that could present with epigastric distress. Is there evidence of an arrhythmia, myocardial infarction, or congestive heart failure? Are there crackles or rales suggesting a pneumonia?
C. Abdominal examination. Are bowel sounds present? Decreased or absent bowel sounds can indicate a small bowel obstruction, acute surgical abdomen (appendicitis, perforated ulcer), or pancreatitis. Rebound tenderness should prompt consideration of an acute surgical abdomen. The right upper quadrant (RUQ) should be palpated. A palpable liver warrants evaluation for other signs of liver disease—jaundice, ascites, skin changes. Murphy’s sign—sudden cessation of the patient’s inspiratory effort during deep palpation of the RUQ—is suggestive of acute cholecystitis (3). Tenderness to palpation of the left upper quadrant can indicate splenic infarct such as seen with sickle cell disease. Tenderness of the midepigastric area can represent peptic ulcer disease, dyspepsia, “nonclassical” presentation of acute appendicitis, or any other of the above-mentioned conditions. A rectal examination with testing for occult blood should be a part of the examination, particularly with any concern about GI bleeding (Chapter 9.7).
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Respiratory distress syndrome:
Diagnosis
(Handbook of Diseases)
Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest respiratory distress syndrome, the following tests are necessary to confirm the diagnosis:
❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with respiratory distress syndrome) but later shows a fine reticulonodular pattern.
❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (Pao2); normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).
❑ Pulmonary function studies may be necessary.
When a cesarean section is necessary before the 36th week of gestation, amniocentesis allows determination of the lecithin-sphingomyelin ratio, which helps to assess prenatal lung development and the risk of respiratory distress syndrome.
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Source: Handbook of Diseases, 2003
Acuterespiratory distress syndrome:
Diagnosis
(Handbook of Diseases)
On room air, arterial blood gas (ABG) analysis initially shows a decreased partial pressure of arterial oxygen (Pao2) — less than 60 mm Hg — and a decreased partial pressure of arterial carbon dioxide (Paco2) — less than 35 mm Hg. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG levels indicate respiratory acidosis (a Paco2 greater than 45 mm Hg) and metabolic acidosis (a bicarbonate level less than 22 mEq/L) as well as a decreasing Pao2, despite oxygen therapy.
Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema: It allows evaluation of pulmonary artery wedge pressure (PAWP); collection of PA blood, which shows decreased oxygen saturation, indicating tissue hypoxia; measurement of PA pressure; and measurement of cardiac output via thermodilution.
Serial chest X-rays initially show bilateral infiltrates; in later stages, the X-rays show ground-glass appearance and, eventually (as hypoxemia becomes irreversible), “whiteouts” of both lung fields. This is seen more clearly by the use of computed tomography of the chest.
A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause of ARDS, laboratory work should include a sputum Gram stain, culture and sensitivity tests, and blood cultures to detect infections; a toxicology screen for drug ingestion; and, when pancreatitis is a consideration, a serum amylase determination.
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Source: Handbook of Diseases, 2003
Respirations, grunting:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. Is he usually healthy with normal growth and development? If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Physical examination
Begin the physical examination by inspecting the rate, depth, and ease of respirations and any signs of respiratory distress. Auscultate the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Also, characterize the color, amount, and consistency of discharge or sputum. Note the characteristics of the cough, if any. Observe for abrupt behavior changes and lowered level of consciousness.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Accessory muscle use:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If the patient’s condition allows, question him thoroughly. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, or fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders such as heart failure, which may lead to pulmonary edema; also inquire about neuromuscular disorders such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function testing or received respiratory therapy. Ask about smoking and occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the patient’s family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Respirations, grunting:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Respiratory Distress and Apnea:
Clinical Features and Diagnosis: Respiratory Distress (Neonatal)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Upper Respiratory Tract Obstruction
Disorders that cause upper respiratory tractobstruction are discussed in Chap.63, Stertor, Stridor, and Airway Obstruction. Lower Respiratory Tract Disorders
Transient Tachypnea of the Newborn
Delayedresorption of lung fluid or mild immaturity of surfactant systemare most probable explanations for this disorder, which usuallyoccurs in term infants soon after birth.Respiratory rate is commonly 60–80breaths/min but sometimes is >100 breaths/min.Mild intercostal retractions and expiratory grunting also may occur.Characteristic chest radiographic findingsare prominent perihilar markings, hyperaeration, widening of interlobarfissures, and evidence of interstitial and pleural fluid.Most infants require <40% supplementaloxygen. Tachypnea usually resolves in 3 or 4 days. Respiratory Distress Syndrome (Hyaline Membrane Disease)
Respiratorydistress syndrome, which is most common cause of respiratory distress inpreterm infants, is due to inadequate amount of surfactant. Someinfants experience intrapartum asphyxia and fail to expand theirlungs at birth, whereas others develop tachypnea and expiratorygrunting within first 1–2 hrs of life.Spectrum of disease varies from mild(tachypnea and minimal oxygen requirement) to severe (apnea andrespiratory failure). Crackles may be heard on chest exam.Characteristic chest radiograph showsdiffuse reticulogranular infiltrates, atelectasis, and air bronchograms.Diagnosis is clinical and radiographic. Meconium Aspiration and Other Aspiration Syndromes
Neonateswho aspirate meconium are usually those who have had intrapartumasphyxia.Thick meconium in upper airway andmeconium staining of skin and nails are usual findings. Airway obstruction,pneumonia, and respiratory failure can occur.Chest radiography shows irregular distributionof coarse, patchy infiltrates and hyperaeration.Clinical and radiologic findings arediagnostic.Aspiration of feedings sometimes occursin normal infants but is more frequent in those with sucking andswallowing disorders (see Chap.65, Sucking and Swallowing Difficulty). Pneumonia
Pneumoniamay be caused by infections acquired transplacentally, during birthprocess, and postnatally. Viral infections transmitted by transplacentalroute include enteroviruses, adenoviruses, influenza viruses, rubellavirus, varicella-zoster virus, herpes simplex virus, cytomegalovirus,and HIV. Transplacental bacterial infections caused by L. monocytogenes,M. tuberculosis, or T. pallidum are less common than viral infections.Neonatal pneumonia is most commonlyacquired during birth process. Group B Streptococcus is most commonpathogen; other pathogens (e.g., gram-negative enteric bacteria)are less common. Most common viral agents acquired during birthprocess are herpes simplex virus and cytomegalovirus. C. trachomatisis also acquired during delivery and usually presents at 2–8wks of age with staccato cough and wheezing. History of conjunctivalinfection may or may not exist.Inadequate hand washing and exposureto respiratory equipment or humidified incubators may contributeto infection, especially with S. aureus and gram-negative entericbacteria.Other causes of postnatal infectionsinclude respiratory syncytial virus, parainfluenza viruses, influenzaviruses, herpes simplex virus, cytomegalovirus, and fungi (C. albicans).Infants with pneumonia present withrespiratory distress. Chest radiography shows interstitial or alveolarinfiltrates or consolidation. With suspected bacterial pneumoniain newborns, blood and spinal fluid cultures should be performed,and treatment begun immediately while awaiting culture results.Diagnosis of viral infections is discussedin other chapters. Pulmonary Air Leaks
Extrapulmonaryair can accumulate in interstitial spaces of lung (pulmonary interstitialemphysema), mediastinum (pneumomediastinum), pleural space (pneumothorax),and pericardium (pneumopericardium).Common cause of pulmonary interstitial emphysemais positive-pressure mechanical ventilation.Pneumomediastinum results from dissectionof air from interstitial space into mediastinum.Pneumothorax results from mediastinalair rupture into pleural space or rupture of air blebs on surfaceof lung. Most common causes of pneumothorax are respiratory distresssyndrome, meconium aspiration, and high-pressure mechanical ventilation.Pneumopericardium is produced fromdissection of mediastinal air into pericardium. Clinical presentation depends on sizeand location of air leak. Significant unilateral pneumothorax collapsesipsilateral lung and shifts heart and mediastinum to opposite sidewith diminished breath sounds on affected side. Significant pneumopericardiummay compromise cardiac filling and cause diminished cardiac output.Chest radiography is diagnostic ofdifferent types of air leak. Pulmonary Hemorrhage
Predisposingfactors in neonatal period include perinatal asphyxia, septicemia,and mechanical ventilation, especially in those with respiratorydistress syndrome.Accompanying respiratory distress isbloody fluid, which oozes from nose, mouth, or endotracheal tube.Depending on how severe bleeding is,chest radiography may show spectrum of findings ranging from patchyinfiltrates to opacification of lungs. Bronchopulmonary Dysplasia
This form of chronic lung disease developsin neonates treated with prolonged oxygen therapy and positive-pressureventilation for primary lung disorders. Most infants improve duringfirst 1–2 yrs of life, and with time chest radiograph becomesnormal. However, some of these children continue to have abnormalpulmonary function in childhood. Others with severe disease developcor pulmonale and succumb to their illness. Congenital Malformations of Lungs, Bronchi, Diaphragm, andRib Cage
Lung Agenesis and Aplasia
Lung agenesisis complete absence of lung or lobe and its branches, whereas lung aplasiais complete absence of lung tissue except for presence of smalllobar bronchus.Respiratory distress often occurs atbirth with decreased breath sounds on affected side.Chest radiography shows opaque hemithoraxwith displacement of mediastinum and normal lung toward involvedside.Bronchoscopy shows absence of mainbronchus in agenesis and presence of small bronchus in aplasia. Pulmonary Hypoplasia
Pulmonaryhypoplasia refers to smaller than normal lungs. Can be isolatedmalformation or occur in association with space-occupying lesionsof thorax (congenital diaphragmatic hernia, cystic adenomatoid malformation,large pleural effusion), oligohydramnios (renal agenesis, polycystickidney disease), and thoracic and abdominal wall abnormalities (asphyxiatingthoracic dystrophy, large omphalocele).Respiratory distress, chronic cough,and recurrent infection may occur with unilateral hypoplasia. Thoraxis asymmetric because of underdevelopment of 1 side.Chest radiography shows small hemithoraxwith displacement of mediastinum toward affected side. When bilateralhypoplasia occurs as isolated malformation, respiratory distressoccurs at birth and chest radiography shows small but clear lungfields. Pulmonary Sequestration
Mass ofnonfunctioning pulmonary tissue that receives its blood supply fromsystemic circulation.May occur within or outside a lobe.Intralobar sequestration usually occurs in lower lobe of eitherlung, whereas extralobar sequestration usually occurs just aboveor below diaphragm on left side. Whereas intralobar sequestrationis usually isolated malformation, extralobar sequestration is commonly associatedwith other malformations (e.g., diaphragmatic hernia and pulmonaryhypoplasia).Clinical findings include respiratorydistress, hemoptysis, and recurrent pneumonia.Chest radiography shows mass lesion.Chest CT or MRI is usually diagnostic. Lobar Emphysema
Overdistensionof lobe of lung (usually upper lobe). Usually congenital but alsomay be acquired secondary to extrinsic or intrinsic airway obstruction.Respiratory distress occurs with decreasedbreath sounds and hyperresonance on involved side.Chest radiography shows large distendedlobe or lobes with displacement of mediastinum to opposite sideand compression of contralateral lung. Extension of pulmonary vesselsto periphery of hyperexpanded lung almost always distinguishes lobaremphysema from lung cyst or pneumothorax. Cystic Lung Lesions
Bronchogenic Cyst
Abnormalbudding or branching of tracheobronchial tree produces bronchogenic cysts,which are found incidentally or because they are infected. Locationcan be above or at carina or adjacent to 1 of main lobar bronchi.They usually do not communicate withtracheobronchial tree and are usually fluid-filled, but if theycommunicate with airway or esophagus, they may contain air. Airwayor lung compression can cause respiratory distress.CT or MRI is usually diagnostic. Congenital Cystic Adenomatoid Malformation
Usuallyconsists of multiple cysts, frequently within 1 lobe of lung.Size of lesion determines age of presentationand degree of respiratory distress.Chest CT is usually diagnostic. Intrapulmonary Cysts
Can be singleor multiple and involve ≥1 lobes of lung.Respiratory distress may occur duringneonatal period. Older children may develop chronic cough or persistentinfiltrate.Chest radiography usually shows ovalor round translucent area or areas within pulmonary parenchyma containingair or combination of fluid and air.Chest CT usually confirms diagnosis. Congenital Pulmonary Lymphangiectasia
Is the dilatationof lung lymphatics. Can occur as isolated defect, with congenital heartlesions that cause obstruction of pulmonary venous drainage, orwith generalized lymphangiectasia.Respiratory distress usually beginsat birth.Chest radiography shows reticular appearanceof lungs with nodular infiltrates and hyperinflation.Localized form of this disorder, whichis less common, may only involve 1 or 2 lobes of lung and presentlater in life with mild respiratory distress or abnormal chest radiograph.Lung biopsy confirms diagnosis. Chylothorax
Presenceof chylous fluid in the thorax. Usually attributed to trauma fromdelivery or congenital abnormalities of thoracic duct system.Lymph does not become chylous untilingestion of formula or breast milk. If large amount of chyle accumulates,respiratory distress occurs, with decreased breath sounds over affectedthorax.Chest radiography shows large fluidcollection and shift of mediastinum.Thoracentesis reveals chyle, whichappears milky and has high protein and fat content. Bronchial Malformations
Bronchialstenosis usually involves main bronchus with narrowing just distalto carina. Narrowing of lobar bronchus usually results in recurrentinfection or atelectasis of involved lobe. Usual presenting featuresare respiratory distress and recurrent lung infection.Chest radiography may show hyperinflationof involved lung and evidence of recurrent infection or atelectasis.Chest CT or bronchoscopy is usuallydiagnostic. Diaphragm Lesions
Congenital Diaphragmatic Hernia
Congenitaldefect in diaphragm allows herniation of abdominal organs into hemithorax,producing varying degrees of lung hypoplasia. Nearly 90% areon left side.Severe respiratory distress beginsat birth.Diagnostic chest radiograph shows air-filledloops of bowel and occasionally liver in thoracic cavity. Diaphragmatic Eventration
Abnormalhigh position of diaphragm or portion of diaphragm, which is dueto congenital defect of muscularization of diaphragm.Most children are asymptomatic, butmild respiratory distress can occur.Diagnosis is usually made by chestradiography or fluoroscopy. Diaphragmatic Paralysis or Paresis
Occurrenceis usually due to phrenic nerve injury from thoracic surgery.Respiratory distress and asymmetricchest movement can occur.Fluoroscopy or U/S that showsparadoxic movement of affected hemidiaphragm during respirationis diagnostic. Rib Cage Anomalies
Thoracicrib cage anomalies that reduce amount of intrathoracic volume maycause respiratory distress. These include asphyxiating thoracicdystrophy, thanatophoric dysplasia, achondrogenesis, and chondroectodermaldysplasia.Structural anomalies of rib cage andthorax usually are obvious on physical exam.Physical exam, chest radiograph, andskeletal survey are usually diagnostic of specific disorder. Persistent Fetal Circulation
Is the persistenceof high pulmonary vascular resistance after birth with resultinghypoxemia and cyanosis. Affected infants are usually near term,and many have history of perinatal asphyxia.Soon after birth, respiratory distressoccurs. Hyperoxia test with exposure to 100% oxygen for5–10 mins shows small, if any, increase in partial pressureof arterial oxygen (PaO2)(<20 mm Hg). Simultaneous preductal-postductal measurementsof PaO2 inright arm and umbilical artery reveal PaO2 inright arm that is >15 mm Hg higher than in umbilical artery,which is consistent of right-to-left shunt across patent ductusarteriosus2-D echocardiogram with Doppler methodsshould be performed to rule out any form of structural cardiac disease. Cardiac Disorders
Disorders that cause cardiac failure or cyanosismay produce respiratory distress. See Chap.7, Cardiac Failure, and Chap. 12, Cyanosis. Hematologic Disorders
Anemia
Severe acute or chronic anemia may causerespiratory distress. Pallor usually is evident. Low Hct or Hgbconfirms presence of anemia. Diagnostic approach to anemia is discussedin Chap. 45, Pallor (Anemia). Polycythemia
Common occurrence in infants who have haddelayed clamping of umbilical cord or in infants of diabetic mothers.Venous Hct is greater than 65%, and mild respiratory distressmay occur. Metabolic Disorders
Hypothermia
May occur in preterm low-birth-weight infantswho are otherwise normal, or in ill newborns who have bacterialmeningitis, septicemia, or intracranial hemorrhage. Oxygen consumptionis significantly increased, and hypoxemia as well as metabolic acidosismay occur. Hypoglycemia
Irregularrespirations, apnea, seizures, and alteration of consciousness mayoccur in infants with hypoglycemia.Low blood glucose is diagnostic (see Chap. 59, Seizures). Metabolic Acidosis
Increase in minute ventilation is compensatoryresponse to metabolic acidosis and lowered blood pH. Normal aniongap with reduced bicarbonate may occur with diarrhea or renal tubularacidosis. Increased anion gap with accumulation of fixed acid occurswith lactic acidosis (lactate), diabetic ketoacidosis (beta-hydroxybutyrate,acetoacetate), and organic acidemias (organic acids). Neurologic and Muscle Disorders
Brain Disorders
Respiratory distress and apnea may occurwith intracranial hemorrhage or cerebral edema as consequence ofperinatal asphyxia or birth trauma. Other causes of depressed respirationand apnea include cerebral malformations (Chiari, Dandy-Walker),bacterial meningitis, viral encephalitis, and brain tumors. Spinal Cord Injury
Injury tospinal cord in neonates may occur with vaginal breech delivery orshoulder dystocia.Fractures of vertebrae with transectionof the cord may result in irregular respirations and apnea, as wellas absence of spontaneous movements.Neurologic findings depend on locationand severity of lesion. Neuromuscular Disorders
Disorders affecting neuromuscular system(spinal muscular atrophy, myasthenia gravis, congenital myopathies)may produce slow and shallow respirations with hypoventilation andrespiratory failure (see Chap.33, Hypotonia and Weakness). Drugs
Drugs (e.g., magnesium sulfate, morphine,and meperidine) that are given to some mothers during labor cancause neonatal respiratory depression. Neonatal drug withdrawalsyndrome may produce tachypnea as 1 of its manifestations. >>
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Accessory muscle use:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's condition allows, examine him more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, sputum production, or fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; inquire about neuromuscular disorders, such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function tests or received respiratory therapy. Ask about smoking and occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting an abnormal respiratory rate, pattern, or depth. Assess the patient's chest for equal expansion during inspiration. Check the trachea for midline position. Assess the color, temperature, and turgor of the patient's skin, and check for clubbing. Auscultate the lungs for adventitious breath sounds.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Respirations, grunting:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After addressing the child's respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child's activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any. Note the respiratory rate. Assess accessory muscle use for breathing and cyanosis.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
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