Diagnosis of Hantavirus
Hantavirus Diagnosis: Book Excerpts
Diagnostic Tests for Hantavirus: Online Medical Books
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AUSCULTATORY SIGNS OF PULMONARY DISEASE:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Clinically, the grouping together of signs provides the best way of narrowing the differential diagnosis.
Rales
- Bilateral crepitant rales, lack of dullness, and normal breath sounds suggest pulmonary edema or pneumonitis.
- Focal crepitant rales, reduced alveolar breathing, dullness to percussion, and increased tactile and vocal fremitus suggest lobar pneumonia or pulmonary infarction.
- Bilateral sibilant and sonorous rales without dullness and with increased bronchial breathing suggest asthma, chronic bronchitis and emphysema, acute bronchitis or bronchiolitis, and cardiac asthma.
- Focal crepitant rales and amphoric breathing with dullness below and hyperresonance above suggest a lung abscess or cavitation
Hyperresonance
- Hyperresonance bilaterally with diminished breath sounds bilaterally and sibilant rales suggests pulmonary emphysema or asthma.
- Focal hyperresonance with diminished or absent breath sounds and no rales suggests pneumothorax.
- Focal hyperresonance with normal or only diminished breath sounds suggests a large bulla.
Dullness or Flatness
- Dullness with diminished breath sounds and no rales suggests atelectasis or pleural effusion from empyema, CHF, or pulmonary infarct. In atelectasis, there is no hyperresonance or egophony above the dullness.
- Dullness with diminished breath sounds and crepitant rales suggests pneumonia or pulmonary infarct. If there is bronchophony as well, there is probably no associated effusion. If there is no bronchophony but hyperresonance and egophony above the dullness, then an associated pleural effusion should be considered.
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Source: Differential Diagnosis in Primary Care, 2007
Hantavirus pulmonary syndrome:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Despite ongoing efforts to identify clinical and laboratory features that distinguish Hantavirus pulmonary syndrome from other infections with similar features, diagnosis currently is based on clinical suspicion along with a process of elimination developed by the Centers for Disease Control and Prevention (CDC) with the Council of State and Territorial Epidemiologists. (See Screening for Hantavirus pulmonary syndrome.) Serologic testing for hantavirus can be performed.
Laboratory tests usually reveal an elevated white blood cell count with a predominance of neutrophils, myeloid precursors, and atypical lymphocytes; elevated hematocrit; decreased platelet count; elevated partial thromboplastin time; and a normal fibrinogen level. Usually, laboratory findings demonstrate only minimal abnormalities in renal function, with serum creatinine levels no higher than 2.5 mg/dl.
Chest X-rays eventually show bilateral diffuse infiltrates in almost all patients (findings consistent with acute respiratory distress syndrome).
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Source: Professional Guide to Diseases (Eighth Edition), 2005
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
Solitary Pulmonary Nodule:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Obtain a complete history, including smoking, occupational exposure, immigration, and travel. Check previous chest x-ray studies to establish prior presence of a nodule, as well as growth on an existing nodule. An absence of growth over a period of 2 years is generally accepted as a sign of the benign nature of a SPN.
Physical examination
should include a search for evidence of weight loss, chronic obstructive pulmonary disease, and primary or metastatic disease of other organs.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
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
Hantavirus pulmonary syndrome:
Diagnosis
(Handbook of Diseases)
Despite efforts to identify clinical and laboratory features that distinguish Hantavirus pulmonary syndrome from other infections with similar features, diagnosis is based on clinical suspicion along with a process of elimination developed by the Centers for Disease Control and Prevention (CDC) with the Council of State and Territorial Epidemiologists. (See Screening for Hantavirus pulmonary syndrome.)
Laboratory tests usually reveal an elevated white blood cell count with a predominance of neutrophils, myeloid precursors, and atypical lymphocytes; elevated hematocrit; decreased platelet count; prolonged partial thromboplastin time; and a normal fibrinogen level.
Usually, laboratory findings demonstrate only minimal abnormalities in renal function, with serum creatinine levels no higher than 2.5 mg/dl.
Chest X-rays eventually show bilateral diffuse infiltrates in almost all patients (findings consistent with adult 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
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
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. >>
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
AUSCULTATORY SIGNS OF PULMONARY DISEASE:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Clinically, the grouping together of signs provides the best way of
narrowing the differential diagnosis.
Rales
-
Bilateral crepitant rales, lack of dullness, and normal breath
sounds suggest pulmonary edema or pneumonitis.
-
Focal crepitant rales, reduced alveolar breathing, dullness to
percussion, and increased tactile and vocal fremitus suggest lobar pneumonia
or pulmonary infarction.
-
Bilateral sibilant and sonorous rales without dullness and with
increased bronchial breathing suggest asthma, chronic bronchitis and
emphysema, acute bronchitis or bronchiolitis, and cardiac asthma.
-
Focal crepitant rales and amphoric breathing with dullness
below and hyperresonance above suggest a lung abscess or cavitation.
Hyperresonance
-
Hyperresonance bilaterally with diminished breath sounds
bilaterally and sibilant rales suggests pulmonary emphysema or asthma.
-
Focal hyperresonance with diminished or absent breath sounds
and no rales suggests pneumothorax.
-
Focal hyperresonance with normal or only diminished breath
sounds suggests a large bulla.
Dullness or Flatness
-
Dullness with diminished breath sounds and no rales suggests
atelectasis or pleural effusion from empyema, CHF, or pulmonary infarct. In
atelectasis, there is no hyperresonance or egophony above the dullness.
-
Dullness with diminished breath sounds and crepitant rales
suggests pneumonia or pulmonary infarct. If there is bronchophony as well,
there is probably no associated effusion. If there is no bronchophony but
hyperresonance and egophony above the dullness, then an associated pleural
effusion should be considered.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
Hantavirus:
Hantavirus - DIAGNOSIS
(The 5-Minute Pediatric Consult)
Pitfalls:
- Recognizing the prodrome of hantavirus pulmonary syndrome is difficult and requires a careful history, evaluation of the risk of exposure, and rapid access to testing:
- The diagnosis depends on serologic testing, which can take some time.
- Lacking serologic confirmation, one mostly depends on clinical history and serial hematologic tests.
- In anticipation of the rapid progression of the cardiopulmonary phase, it is preferable to have the patient closely observed in the hospital.
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
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