Diagnosis of Blue baby
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CYANOSIS:
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Is there a history of drug ingestion? Potassium chlorate, sulfanilamide, and coal tar products are only a few of the drugs that may cause methemoglobinemia and sulfhemoglobinemia.
- Is the cyanosis limited to one extremity? If the cyanosis is limited to one extremity, one should suspect an arterial embolism or phlebothrombosis.
- Is the cyanosis limited to the extremities or is it generalized? Cyanosis that is limited to the extremities only suggests Raynaud's disease, Raynaud's phenomena, shock, and acrocyanosis.
- Is there associated dyspnea? If there is significant dyspnea, one should consider a pulmonary or cardiac origin for the cyanosis such as cyanotic congenital heart disease, pulmonary emphysema, pulmonary fibrosis, or pulmonary embolism.
- Is the patient a child or an adult? Certain causes of cyanosis are limited to children, such as laryngismus stridulus, laryngotracheitis, and acute subglottic laryngitis.
- Is there a heart murmur or cardiomegaly? A heart murmur or cardiomegaly suggests rheumatic carditis, congenital heart disease, or congestive heart failure.
DIAGNOSTIC WORKUP
It is wise to order a cardiology consult at the outset. Arterial blood gases, EKG, chest x-ray, and pulmonary function studies will diagnose most cases that are due to pulmonary or cardiac causes. If there is a history of drug ingestion, the blood should be drawn for methemoglobin and sulfhemoglobin testing. If a pulmonary embolism is suspected, a ventilation-perfusion scan and pulmonary arteriography may need to be done. If a peripheral embolism is suspected, angiography of the vessel involved will be diagnostic. Sputum or nose and throat cultures will be useful in diagnosing the infectious diseases associated with cyanosis.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Cyanosis:
Differential Diagnosis
(In a Page: Signs and Symptoms)
Central cyanosis (cyanosis of lips and mucous membranes)
-
Pulmonary disease
–Severe pneumonia
–Pulmonary edema
–Pulmonary arteriovenous fistulas
–Tension pneumothorax
–Severe COPD or asthma
–Adult respiratory distress syndrome
–Lung cancer
–Obstruction (e.g., tracheal foreign body or
stenosis)
–High altitude exposure
–Decreased respiration with oversedation
–Sleep apnea
Congenital heart disease with shunting
–Tetralogy of Fallot
–Transposition of the great vessels (most
common cause of cyanosis in the
immediate newborn period)
–Tricuspid atresia
–Truncus arteriosus
-
Cardiovascular disease
–Cardiogenic shock (e.g., massive MI)
–Severe valvular heart disease
–Cor pulmonale
–Massive pulmonary embolus
-
Abnormal hemoglobin
–Methemoglobinemia: Usually caused by drugs or chemicals (e.g., sulfa, nitrites, benzene derivatives) or genetic defects
–Hemoglobin Kansas
–Sickle cell disease
-
Toxins/poisons (e.g., carbon monoxide, nitroprusside, cyanide)
Peripheral cyanosis (cyanosis of phalanges, earlobes, and nose)
-
Increased resistance to blood flow
–Raynaud's phenomenon
–Acrocyanosis
–Superior vena cava obstruction
–Venous hypertension
–Arterial embolism
–Exposure to cold air or water
-
Decreased cardiac output
–Shock
–Congestive heart failure
–Mitral stenosis
-
Increased blood viscosity
–Polycythemia vera
Workup and Diagnosis
-
History and physical examination
–Clubbing of the fingers or toes may indicate congenital heart disease or chronic pulmonary disease
–Blood pressure, capillary refill, and heart and lung exam are always indicated
–Pulses and neurologic function in all involved extremities must be evaluated in peripheral cyanosis
Initial labs include pulse oximetry, CBC, electrolytes, BUN/creatinine, glucose, arterial blood gas (to assess oxygenation, CO level, and presence of methemoglobin), and ECG
Chest X-ray and/or CT scan to evaluate for lung pathology and heart size
Echocardiogram will assess ventricular function and valves, and rule out structural abnormalities
Pulmonary function tests
Cardiac enzymes may be indicated to rule out MI
Hemoglobin electrophoresis may be indicated to evaluate hemoglobin structure
For peripheral cyanosis isolated to one limb, arterial Doppler studies or angiogram may be indicated to rule out embolus
Pulmonary angiogram may be indicated to rule out an arteriovenous fistula or massive pulmonary embolism
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Source: In a Page: Signs and Symptoms, 2004
Cyanosis:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Recall the pathway for oxygen, from the air to the tissue; etiology is often multifactorial
-
Reduced O2 availability: High altitude (>6,000 feet), e.g., air travel, ski resort, mountain travel
-
Reduced O2 transport to alveoli: Respiratory failure/arrest, air flow obstruction (usually compensate for large obstruction unless complete); restrictive chest wall disease (e.g., kyphosis, weakness, or obesity)
-
Abnormal gas exchange or V/Q mismatch: Most common physiologic pulmonary cause of hypoxia
- Abnormal ventilation
–Alveolar diseases: Pneumonia, pulmonary edema, diffuse alveolar damage, alveolar proteinosis
–Conducting airway diseases: Asthma,
bronchiolitis
–Combined pathology: ARDS,
bronchopulmonary dysplasia, HMD
-
Abnormal perfusion
–Pulmonary hypertension, pulmonary embolus, abnormal anatomy (e.g., pulmonary sequestration)
-
Shunt
–Intrapulmonary shunt (or “total” V/Q mismatch), e.g., AV malformations
–Extrapulmonary shunt, e.g., TOF, TAPVR, TGA
- Abnormal transport to tissue
–Abnormal hemoglobin: β-thalassemia, sickle cell disease, CO poisoning
–Decreased hemoglobin: Anemia, blood loss
–Decreased blood flow: Dysrhythmia,
bradycardia, cardiac arrest, hypotension
-
Abnormal O2 delivery at tissue
–Abnormal hemoglobin affinity for O2
–End-organ failure (e.g., mitochondrial
disease, cyanide poisoning)
-
Chronic cyanosis starting at birth suggests either congenital lesion or neonatal injury (e.g., meconium aspiration, group B streptococcus sepsis, HMD)
Workup and Diagnosis
- History
–Birth history
–Past medical history including respiratory, cardiac and
hematologic disorders, acute or chronic onset, and accompanying features
- Physical exam
–Patency of the airway, adequate air movement, distribution of air flow, symmetry of breath sounds, crackles, dullness to percussion, chest wall movement
–Auscultate heart, feel all pulses, obtain BP, seek signs of chronicity (e.g., clubbing of nail beds)
–Examine well-perfused soft tissue (e.g., gums) to assess for cyanosis, not fingertips
-
Oximetry is useful but may not help during shock or hemoglobinopathies; may not be accurate with dark skin
-
If O2 does not help, consider shunt (cardiac disease is more common than intrapulmonary shunt)
-
Arterial blood gases
–Disparate PaO2 and SaO2 suggests possibility of abnormal hemoglobin affinity for O2
-
Chest film and CT for parenchymal disease
-
MRI/MRAfor vascular anatomy
-
V/Q scan
-
ECG, Echo, or catheterization for cardiac disease
-
PFT for obstructive or restrictive disease
-
Sleep studies, EEG for CNS causes
-
Muscle biopsy for tissue or mitochondrial diseases
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Source: In A Page: Pediatric Signs and Symptoms, 2007
CYANOSIS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup of cyanosis includes pulmonary function studies before and after bronchodilators, arterial blood gases, routine and before and after breathing 100% oxygen, venous pressure and circulation times, chest x-rays, ECGs, and ventilation–perfusion scans. It is unusual not to be able to pinpoint the cause.
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Source: Differential Diagnosis in Primary Care, 2007
Cyanosis:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If cyanosis accompanies less-acute conditions, perform a thorough examination. Begin with a history, focusing on cardiac, pulmonary, and hematologic disorders. Ask about previous surgery. Then begin the physical examination by taking the patient's vital signs. Inspect the skin and mucous membranes to determine the extent of cyanosis. Ask the patient when he first noticed the cyanosis. Does it subside and recur? Is it aggravated by cold, smoking, or stress? Is it alleviated by massage or rewarming? Check the skin for coolness, pallor, redness, pain, and ulceration. Also note clubbing.
Next, evaluate the patient's level of consciousness. Ask about headaches, dizziness, or blurred vision. Then test his motor strength. Ask about pain in the arms and legs (especially with walking) and about abnormal sensations, such as numbness, tingling, and coldness.
Ask about chest pain and its severity. Can the patient identify aggravating and alleviating factors? Palpate peripheral pulses, and test the capillary refill time. Also, note edema. Auscultate heart rate and rhythm, especially noting gallops and murmurs. Also auscultate the abdominal aorta and femoral arteries to detect any bruits.
Does the patient have a cough? Is it productive? If so, have the patient describe the sputum. Evaluate his respiratory rate and rhythm. Check for nasal flaring and use of accessory muscles. Ask about sleep apnea. Does the patient sleep with his head propped up on pillows? Inspect the patient for asymmetrical chest expansion or barrel chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for shifting dullness or fluid wave. Percuss and palpate for liver enlargement and tenderness. Also, ask about nausea, anorexia, and weight loss.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Cyanosis:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If cyanosis accompanies less acute conditions, perform a thorough examination. Begin with a history, focusing on cardiac, pulmonary, and hematologic disorders. Ask about previous surgery. Then begin the physical examination by taking vital signs. Inspect the skin and mucous membranes to determine the extent of cyanosis. Ask the patient when he first noticed the cyanosis. Does it subside and recur? Is it aggravated by cold, smoking, or stress? Is it alleviated by massage or rewarming? Check the skin for coolness, pallor, redness, pain, and ulceration. Also note clubbing.
Next, evaluate the patient’s level of consciousness. Ask about headaches, dizziness, or blurred vision. Then test his motor strength. Ask about pain in the arms and legs (especially with walking) and about abnormal sensations, such as numbness, tingling, and coldness.
Ask about chest pain and its severity. Can the patient identify any aggravating or alleviating factors? Palpate peripheral pulses, and test capillary refill time. Also, check for edema. Auscultate heart rate and rhythm, especially noting gallops and murmurs. Also auscultate the abdominal aorta and femoral arteries to detect any bruits.
Does the patient have a cough? Is it productive? If so, have the patient describe the sputum. Evaluate respiratory rate and rhythm. Check for nasal flaring and use of accessory muscles. Ask about sleep apnea. Does the patient sleep with his head propped up on pillows? Inspect the patient for asymmetrical chest expansion or barrel chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for shifting dullness or a fluid wave. Percuss and palpate the abdomen for liver enlargement and tenderness. Also, ask about nausea, anorexia, and weight loss.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Cyanosis:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. When did the cyanosis appear? Is cyanosis of recent onset or has it been present since birth? A history of “squatting” episodes in childhood and congenital cyanosis suggest congenital heart disease. Chronic cyanosis caused by methemoglobinemia can be congenital or acquired. Other causes of chronic cyanosis include chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and pulmonary atrioventricular fistula. Acute and subacute cyanosis is caused by acute myocardial infarct, pneumothorax, pulmonary embolus, pneumonia, or upper airway obstruction.
B. Is the patient symptomatic or asymptomatic? Asymptomatic patients may have methemoglobinemia (congenital or drug-induced), or sulfhemoglobinemia. Exposure to drugs (prescribed and illicit) or environmental factors are important in these patients. Intermittent cyanosis, skin color changes, and pain with cold exposure suggests Raynaud’s phenomenon. Symptomatic patients, especially with chest pain and respiratory distress, are more likely to have a cardiac or pulmonary cause of cyanosis.
C. Does the patient have known risk factors for cardiac or pulmonary disease, including smoking, hyperlipidemia, asthma, drug abuse (especially methamphetamines), severe obesity (sleep apnea), neuromuscular disease, or autoimmune disease? Does the patient have chest pain or intermittent cyanosis with exercise, suggesting angina? Chest pain can be present with acute pulmonary emboli or pneumothorax. Is there a cough and fever suggesting pneumonia? Has the patient had any occupational or environmental exposures that might cause pulmonary problems?
D. Other. Is there a family history of abnormal hemoglobins or pulmonary disease? Has the patient suffered an episode of hypotension that could produce adult respiratory distress syndrome (ARDS), such as sepsis or heart failure?
Physical examination
A. Initial assessment. Vital signs are very important: tachycardia suggests cardiac arrhythmia, shock, volume depletion, anemia, or fever (Chapter 7.12). An increased or decreased respiratory rate and use of accessory musculature suggests hypoxia from any cause. Hypotension can signal vascular collapse from myocardial infarction, septic shock, or pulmonary embolus.
B. Additional physical examination. Stridor suggests upper airway obstruction. Examine the pharynx for evidence of obstruction. If epiglottitis or foreign body is suspected, be prepared to intubate the patient. Check the neck for evidence of jugular venous distention (JVD). Auscultate the chest for rales, suggesting pulmonary edema; wheezing and rhonchi consistent with reactive airway disease; or absence of breath sounds, suggesting pneumonia or pneumothorax. Auscultate the heart for murmurs, arrhythmias, and abnormal heart sounds. Feel the pulses in the extremities to assess for arterial embolus or venous thrombosis, especially if cyanosis is localized to one extremity. Examine the abdomen for evidence of intraabdominal catastrophe or aneurysm. Examine the nails for evidence of clubbing, suggesting chronic pulmonary disease.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Cyanosis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Asthma
❑ Chronic obstructive pulmonary disease
❑ Raynaud phenomenon
❑ Hypoventilation
❑ Pulmonary embolism
❑ Cardiac right-to-left shunt
❑ Pulmonary edema
❑ Low cardiac output/shock
❑ Polycythemia vera
❑ Arterial insufficiency
❑ Intrapulmonary shunts
❑ Tracheal obstruction
❑ Tricuspid insufficiency
❑ Superior vena cava obstruction
❑ Pneumonitis
❑ Methemoglobinemia
❑ Patent ductus arteriosus
❑ Pseudocyanosis
Diagnostic Approach
Central cyanosis is best seen in the nailbeds or mucous membranes in good natural light. Peripheral cyanosis (due to increased capillary oxygen extraction) is seen in exposed areas such as the fingers, earlobes, and the tip of the nose. Massage or heat, which increase blood flow, will abolish peripheral but not central cyanosis.
The minimal amount of deoxyhemoglobin to cause central cyanosis is 2.38 g/dL. This is an absolute amount, so is dependent upon the hemoglobin concentration. For example, at a hemoglobin of 12 g/dL, cyanosis appears at SaO2 of 80%, while at a hemoglobin of 6 g/dL, cyanosis appears at SaO2 of 60%.
“Harlequin cyanosis” with one arm pink and the other blue can occur with aortic dissection, embolic arterial occlusion, or patent ductus arteriosis with pulmonary hypertension. Blue fingers and pink toes suggest complete transposition of the great vessels, preductal coarctation with a patent ductus arteriosis, or pulmonary hypertension with reversed flow through a patent ductus.
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Source: Field Guide to Bedside Diagnosis, 2007
Cyanosis:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Ask the patient about cardiac, pulmonary, and hematologic disorders or previous surgeries. Ask whether he’s experiencing chest pain; if so, ask him to rate its severity using a standardized pain rating scale. Note precipitating, aggravating, or alleviating factors and whether the pain radiates. Determine when the patient first noticed the cyanosis and precipitating, aggravating, or alleviating factors; ask whether it’s intermittent or constant. Does the patient have a history of headaches, dizziness, blurred vision, or pain or abnormal sensations in the extremities ? Does he have a cough and if so, is it productive? Ask him to describe sputum. Inquire about a history of sleep apnea. Document the patient’s medication history, including over-the-counter medications.
Physical examination
Obtain the patient’s vital signs. Inspect the skin and mucous membranes to determine the extent of cyanosis. Assess the skin for coolness, pallor, redness, pain, and ulceration. Note the presence of clubbing.
Evaluate the patient’s level of consciousness and test motor strength. Palpate peripheral pulses and test capillary refill time. Auscultate heart rate and rhythm, especially noting gallops and murmurs. Auscultate the abdominal aorta and femoral arteries to detect bruits.
Evaluate respiratory rate and rhythm. Check for nasal flaring and accessory muscle use. Inspect the patient for asymmetrical chest expansion or barrel chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for shifting dullness or fluid wave. Percuss and palpate for liver enlargement and tenderness.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Cyanosis:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Begin with a history, focusing on cardiac, pulmonary, and hematologic disorders. Ask about previous surgery. While taking the patient’s history, evaluate his mental status and level of consciousness. Ask the patient when he first noticed the cyanosis. Does it subside and recur? Is it aggravated by cold, smoking, or stress? Is it alleviated by massage or rewarming? Check the skin for coolness, pallor, redness, pain, and ulceration. Also note clubbing. Ask about headaches, dizziness, or blurred vision. Ask the patient about pain in the arms and legs (especially with walking) and about abnormal sensations, such as numbness, tingling, and coldness.
Ask about chest pain and its severity. Can the patient identify any aggravating and alleviating factors? Also, ask about nausea, anorexia, and weight loss. Does the patient have a cough? Is it productive? If so, have the patient describe the sputum. Ask about sleep apnea. Does the patient sleep with his head propped up on pillows?
CULTURAL CUE:The lips of some black people have a bluish hue making it difficult to assess cyanosis. Establishing a baseline color of the patient’s skin and mucous membranes will help you detect color changes.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Cyanosis:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Peripheral Cyanosis
When peripheralvasoconstriction results in decreased peripheral perfusion, moreoxygen is extracted from peripheral blood. Decrease in oxygen contentof venous blood produces bluish discoloration.Cold temperature, fever, hypovolemia,septicemia, and cardiac failure may cause peripheral vasoconstriction.Polycythemia is another cause of peripheralcyanosis. Increase in blood viscosity impairs capillary blood flow,producing excessive amount of reduced Hgb. Venous Hct of >65–70% isdiagnostic.Common cause of polycythemia is delayedcord clamping at birth. Central Cyanosis
Respiratory Disorders
See Chap.56, Respiratory Distress and Apnea.
Cardiovascular Disorders
3 mechanismsor their combination can produce central cyanosis: right-to-leftshunts at atrial, ventricular, or ductal levels (congenital heartdisease, persistent pulmonary artery hypertension of the newborn,pulmonary vascular disease); alveolar hypoventilation (cardiac failure);and V/Q inequality (pulmonary arteriovenous malformation).The congenital heart lesions can bedivided into 2 groups: lesions with either decreased or increasedpulmonary blood flow.Chest radiography can show decreaseor increase in pulmonary vascular markings, which indicates amountof pulmonary blood flow. Congenital Heart Lesions with Decreased Pulmonary Blood Flow
Tricuspid Atresia with Intact Ventricular Septum and NormalOrigin of Great Arteries
RV is hypoplastic,and pulmonary arteries may be small.Right-to-left shunting occurs at atriallevel, and cyanosis often occurs during first 24 hrs of life.Usual findings include prominent apicalimpulse and loud single S2. Continuous murmur of patent ductus maybe heard at upper left sternal border, but sometimes no murmursare heard.Chest radiograph shows normal-sizedheart, decreased pulmonary vascular markings, and absent pulmonaryartery segment.ECG usually shows right atrial hypertrophy,LV hypertrophy, and left axis deviation.2-D echocardiography is diagnostic.Cardiac catheterization and angiographyare usually performed prior to surgery. Ebstein Malformation of Tricuspid Valve
Septal andinferior leaflets of tricuspid valve are displaced into RV. Dependingon specific anatomy, wide spectrum of clinical presentations canoccur. Severe RV dysfunction and increased pulmonary vascular resistancecan produce intense cyanosis and cardiac failure in neonates.Usual physical findings are wide splittingof S1 and S2, prominent S3 and S4, murmur of tricuspid incompetence,and hepatomegaly.Chest radiograph shows marked cardiomegalyand decreased pulmonary vascular markings.ECG commonly shows right atrial hypertrophy,prolonged PR interval, right bundle branch block, and evidence ofWolff-Parkinson-White syndrome.2-D echocardiography is diagnostic.Cardiac catheterization and angiographyare performed when specific anatomic details need to be evaluated. Pulmonary Atresia with Intact Ventricular Septum
Consistsof atresia of pulmonary valve and, occasionally, infundibulum of RV.Tricuspid valve and RV are usuallysmall.Right-to-left shunting occurs at atriallevel.Blood flow to lungs depends on patentductus arteriosus and bronchial circulation.Cyanosis usually appears during first24 hrs of life. As ductus closes, cyanosis becomes more severe.Palpable apical impulse, absence ofRV impulse, and single S2 are usual physical findings. Murmurs ofpatent ductus arteriosus and tricuspid incompetence may or may notbe heard.Chest radiograph shows variable heartsize, diminished pulmonary vascular markings, and flat or concavepulmonary artery segment.ECG usually shows absence of RV predominancepattern of newborns, but normal R waves occasionally are seen inright precordial leads. Tall P waves indicative of right atrialenlargement develop within first month of life.2-D echocardiography shows small RVwith absence of pulmonary valve.Cardiac catheterization and angiographyare performed to demonstrate coronary artery anatomy and prior toany procedure. Ventricular Septal Defect with Pulmonic Stenosis or PulmonaryAtresia (Tetralogy of Fallot)
VSD withpulmonic stenosis usually presents with cyanosis but depends onseverity of RV obstruction. Pulmonary valvar stenosis, infundibularstenosis, or both may occur.With VSD and severe pulmonary valvarstenosis, cyanosis usually occurs in newborns.With infundibular stenosis alone, cyanosisusually occurs later in infancy.Some children with mild stenosis have left-to-rightshunt at rest and no cyanosis, but as infundibular narrowing becomesmore severe, cyanosis appears.Usual physical findings are prominentRV impulse, narrowly split or single S2, and grade II–III/VIsystolic ejection murmur heard with maximum intensity in secondand third left intercostal spaces.The more severe the outflow tract obstruction,the less intense the murmur. With VSD and pulmonary atresia, cyanosisoccurs during first week of life and becomes more severe as ductusbegins to close.Ifductus stays open or large collateral vessels supply pulmonary vascularbed, cyanosis is less pronounced.Usual findings are single S2 and continuousmurmur from patent ductus or large collateral circulation. Chest radiograph shows typical boot-shapedheart of normal size, diminished pulmonary vascular markings, absentpulmonary artery segment, and sometimes right aortic arch.ECG shows RV hypertrophy.2-D echocardiography confirms diagnosis.Cardiac catheterization and angiographyare performed to demonstrate levels of stenosis in pulmonary outflowtract and pulmonary arteries, presence of multiple VSDs, and anycoronary artery anomalies. Critical Pulmonary Stenosis with Patent Foramen Ovale
Neonateswith critical pulmonary valvar stenosis develop severe cyanosisand cardiac failure during first few days of life.Usual physical findings are prominentRV impulse; normal, diminished, or inaudible pulmonary componentof S2; grade II–IV/VI systolic ejection murmurwith maximum intensity at upper left sternal border; and hepatomegaly.Occasionally, continuous murmur of patent ductus arteriosus or pansystolicmurmur of tricuspid incompetence is heard.Chest radiography shows cardiomegalyand decreased pulmonary vascular markings.ECG usually shows RV hypertrophy, unlessRV is hypoplastic. T-wave inversion sometimes is seen in right precordialleads.2-D echocardiography confirms diagnosis.Cardiac catheterization and angiographyare performed prior to any procedure. Complex Lesions
Transpositionof great arteries and pulmonic stenosis ± VSD, double-outletright ventricle with pulmonic stenosis, and univentricular heartwith pulmonic stenosis are complex lesions that may present withcyanosis.Degree of cyanosis depends on degreeof intracardiac mixing and severity of pulmonic stenosis. With severestenosis, usually S2 is single and grade II–III/VIsystolic ejection murmur is heard at left second intercostal space.With pulmonary atresia, S2 is always single, and continuous murmurfrom patent ductus or large collateral circulation may be heard.These lesions cannot be distinguishedfrom each other by physical exam.Chest radiograph shows normal or mildlyenlarged heart with decreased pulmonary vascular markings.2-D echocardiography is usually diagnostic.Cardiac catheterization with angiographyis performed prior to surgery. Congenital Heart Lesions with Normal or Increased PulmonaryBlood Flow
Transposition of Great Arteries with Intact Ventricular Septum
Aorta arisesfrom RV, pulmonary artery arises from LV, and ventricular septumis intact. Mixing of blood occurs at atrial or ductal level or atboth levels.Severe cyanosis and respiratory distressusually appear within 24 hrs of birth.Prominent RV impulse, narrowly splitor single S2, and either no murmur or grade I–II/VI systolicejection murmur along left sternal border are usual physical findings.Chest radiograph shows oval or egg-shaped,mildly enlarged heart, mild increase in pulmonary vascular markings,and absent pulmonary artery segment.ECG shows normal RV predominance ofnewborn.2-D echocardiography is diagnostic.Balloon septostomy can be performedto increase atrial mixing and improve oxygenation as temporizingmeasure.Cardiac catheterization and angiographyare performed before surgical intervention. Tricuspid Atresia with Ventricular Septal Defect and NormalOrigin of Great Arteries
Most childrenwith tricuspid atresia and normal origin of great arteries have VSD.Commonly presents with cyanosis andcardiac failure at 2–3 wks of age.Prominent LV impulse, normally splitS2, and typical murmur of VSD are usual physical findings.Chest radiograph shows enlarged heartwith increased pulmonary vascular markings.ECG usually shows right atrial andLV hypertrophy as well as left axis deviation.2-D echocardiography confirms diagnosis. Tricuspid Atresia with Transposition of Great Arteries
Usuallypresents during first month of life with mild cyanosis and cardiacfailure.Usual physical findings are grade II–III/VIsystolic ejection murmur along left sternal border and narrowlysplit S2.Chest radiograph shows enlarged heart,increased pulmonary vascular markings, and narrow vascular pedicle.ECG shows right atrial enlargement,LV hypertrophy, and left axis deviation.2-D echocardiography is diagnostic. Other Lesions
Hypoplasticleft-heart syndrome, transposition of great arteries with ventriculardefect or large patent ductus arteriosus, double-outlet right ventricle,truncus arteriosus, univentricular heart, total anomalous venousreturn ± obstruction, and other pulmonary venous obstructivelesions may produce cyanosis.Cardiac failure is common manifestation.See Chap.7, Cardiac Failure. Persistent Pulmonary Artery Hypertension of Newborn (PersistentFetal Circulation)
Can be dueto pulmonary vasoconstriction, prenatal increase in pulmonary vascular smoothmuscle development, or decrease in cross-sectional area of pulmonaryvascular bed.Right-to-left shunting occurs at atrialor ductal levels or both.Clinical spectrum depends on amountof pulmonary blood flow.Severe cyanosis and respiratory distressusually develop soon after birth.Usual physical findings are prominentRV impulse and narrowly split S2 with loud pulmonary component.Grade I–II/VI systolic ejection murmur sometimesis heard along middle and upper left sternal borders. Liver alsomay be enlarged.Chest radiography shows enlarged heartwith decreased, normal, or increased pulmonary vascular markings.ECG shows RV hypertrophy.Partial pressure of arterial oxygen (PaO2)is slightly higher in right arm than in umbilical artery becauseof right-to-left ductal shunting. Placing infant in 100% oxygenusually increases this difference.2-D echocardiography that demonstratesright-to-left or bidirectional shunting at atrial or ductal levelsin structurally normal heart confirms diagnosis.Sometimes difficult to distinguishthis lesion from total anomalous pulmonary venous return with obstruction.In this circumstance, cardiac catheterization and angiography shouldbe performed. Pulmonary Vascular Disease
Pulmonaryvascular resistance is greater than systemic vascular resistance.Common causes includeCardiac lesionswith high pulmonary blood flow or pressure or both (e.g., VSD, patentductus arteriosus, AV canal, transposition of great arteries withVSD, truncus arteriosus)Cardiac lesions with decreased pulmonaryflow requiring systemic-pulmonary artery shunting procedures, resultingin pulmonary artery hypertensionPrimary pulmonary hypertension Physical findings include increasedRV impulse, loud single or narrowly split S2, often murmur of pulmonaryregurgitation, and clubbing of digits.Chest radiograph usually shows normalheart size, but in advanced cases heart may be enlarged.Main pulmonary artery and branchesare prominent with tapering of more distal branches.ECG shows RV hypertrophy.2-D echocardiography can demonstrateright-to-left shunting at atrial, ventricular, or ductal levels.Cardiac catheterization evaluates pulmonaryvascular resistance and reactivity. Pulmonary Arteriovenous Malformation
Pulmonaryarteries communicate directly with variable number of pulmonaryveins to produce pulmonary arteriovenous fistula. Bypass of pulmonarycapillary bed produces mixing of oxygenated and unoxygenated blood,arterial desaturation, and cyanosis.Usual presentation in childhood oradolescence is cyanosis, clubbing of fingers and toes, and exerciseintolerance. Grade II–III/VI systolic or continuousmurmur may be heard on chest wall over the fistula.Chest radiograph shows ≥1 opacitiesof variable size in 1 or both lung fields. Vascular nature of lesioncan be demonstrated by contrast-enhanced CT or MRI.Pulmonary angiography is definitive. Abnormal Hemoglobin: Methemoglobinemia
Decreasescapacity of blood to deliver oxygen to tissues.Color of blood is reddish-brown ratherthan bright red; however, PaO2 isnormal.When measured by blood oximetry, oxygensaturation is low, but when measured by pulse oximetry, oxygen saturationis normal. Blood oximetry measures oxyhemoglobin as percentage oftotal Hgb, whereas pulse oximetry measures oxygen saturation ofonly the Hgb available for saturation.Congenital causes are NADH-dependentmethemoglobin reductase deficiency (autosomal-recessive trait) andhemoglobin M disease (autosomal-dominant trait). Intense cyanosismay occur soon after birth in both disorders.Mass spectrometry of blood sample confirmspresence of methemoglobinemia, whereas Hgb electrophoresis confirmsdiagnosis of hemoglobin M disease.Acquired methemoglobinemia may be dueto ingestion of specific drugs (sulfonamides, phenytoin) or chemicals(naphthalene, nitrates, cyanides, benzene, aniline).Usual presentation is intense cyanosis1–2 hrs after ingestion. In mild cases, no other distress occurs.In severe cases, respiratory distress and shock may occur. Diagnostic Approach
First taskis to decide whether cyanosis is peripheral or central. This isusually accomplished by history and physical exam.Presence of central cyanosis must beinvestigated immediately because of possibility of life-threateningheart or lung disease.Certain findings favor diagnosis oflung disease: respiratory distress or apnea in extreme prematureinfants in whom most common cause of lung disease is respiratorydistress syndrome; significant increase in PaO2 afteradministration of 100% oxygen (usually >150 mmHg); and elevated partial pressure of carbon dioxide (PCO2).Certain findings suggest heart disease:significant murmur, cardiomegaly, hepatomegaly, chest radiographwith decreased or increased pulmonary vascular markings, abnormalECG, marked generalized cyanosis with PaO2 thatdoes not improve significantly with 100% oxygen (usually <100mm Hg), and normal or decreased PaCO2.Absence of murmur does not rule outpossibility of heart disease.Examples of life-threatening cardiaclesions that may not be associated with murmurs include transpositionof great arteries with intact ventricular septum, pulmonary atresiawith intact ventricular septum, and total anomalous pulmonary venousreturn with obstruction.Infants with cyanotic heart diseasedo not usually have increased PaCO2,unless severe cardiac failure exists.Cardiac lesions causing decrease inblood flow or lack of adequate mixing (transposition of great arteriesand intact ventricular septum) present with severe cyanosis ± mildrespiratory distress. Cardiac lesions causing increase in pulmonaryblood flow present with respiratory distress, cardiac failure, andmild cyanosis.Chest radiographic findings of decreaseor increase in pulmonary vascular markings provide evidence of decreaseor increase in pulmonary blood flow, respectively, except in transpositionof great arteries with intact ventricular septum. In this lesion,pulmonary vascular markings may be mildly increased, but severecyanosis occurs because of parallel systemic and pulmonary circulationswith inadequate mixing of oxygenated blood.Degree of cyanosis, presence of respiratorydistress, and chest radiographic findings (increase or decreasein pulmonary vascular markings) can be used to categorize lesionsto help make a diagnosis.With suspected persistent pulmonaryartery hypertension in newborn, measurement of simultaneous PaO2 orarterial oxygen saturation (SaO2)at pre- and postductal sites (right radial and umbilical arteryor right finger and toe, respectively) may reveal right-to-leftductal shunt if preductal PaO2 or SaO2 ishigher. This finding also may be seen with severe coarctation ofaorta and interruption of aortic arch, but 2-D echocardiographycan usually confirm these diagnoses.When severe generalized cyanosis occursin infants who do not appear to have septicemia, certain tests shouldbe performed: CBC with differential, chest radiography, ECG, pulseoximetry in room air and in 100% oxygen, and 2-D echocardiography.In most cases, diagnosis can be made based on test results.If diagnosis is still uncertain andlife-threatening cyanotic congenital heart disease is possible,cardiac catheterization and angiography should be performed. >
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Cyanosis:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If cyanosis accompanies less-acute conditions, perform a thorough examination. Begin with a history, focusing on cardiac, pulmonary, and hematologic disorders. Ask about previous surgery. Then begin the physical examination by taking the patient's vital signs and pulse oximetry. Inspect the skin and mucous membranes to determine the extent of cyanosis. Ask the patient when he first noticed the cyanosis. Does it subside and recur? Is it aggravated by cold, smoking, or stress? Is it alleviated by massage or rewarming? Check the skin for coolness, pallor, redness, pain, and ulceration. Also note clubbing.
Next, evaluate the patient's level of consciousness. Ask about headaches, dizziness, or blurred vision. Then test his motor strength. Ask about pain in the arms and legs (especially with walking) and about abnormal sensations, such as numbness, tingling, and coldness.
Ask about chest pain and its severity. Can the patient identify aggravating and alleviating factors? Palpate peripheral pulses, and test the capillary refill time. Also, note edema. Auscultate heart rate and rhythm, especially noting gallops and murmurs. Also auscultate the abdominal aorta and femoral arteries to detect any bruits.
Does the patient have a cough? Is it productive? If so, have the patient describe the sputum. Evaluate his respiratory rate and rhythm. Check for nasal flaring and use of accessory muscles. Ask about sleep apnea. Does the patient sleep with his head propped up on pillows? Inspect the patient for asymmetrical chest expansion or barrel chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for shifting dullness or fluid wave. Percuss and palpate for liver enlargement and tenderness. Also, ask about nausea, anorexia, and weight loss.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
CYANOSIS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup of cyanosis includes pulmonary function studies before and
after bronchodilators, arterial blood gases, routine and before-and-after
breathing 100% oxygen, venous pressure and circulation times, chest
x-rays, ECGs, and ventilation–perfusion scans. It is unusual not to be able
to pinpoint the cause.
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Source: Differential Diagnosis in Primary Care, 2007
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