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Cyanosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Amandeep Singh M.D.[3], Chandrakala Yannam, MD [4]

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]

Overview

Cyanosis is the condition that there is inadequate oxygen delivery to peripheral tissue. Oxygen in the blood is carried in two physiologic states. Approximately 2% is dissolved in plasma and the other 98% is bound to hemoglobin. In central cyanosis there is increased level of deoxyhemoglobin around 3-5 g/dl. In peripheral cyanosis there is increased oxygen extraction by the peripheral tissues. Several factors can affect the appearance of cyanosis including skin pigmentation,Hemoglobin (Hb) levels, oxygen affinity to the hemoglobin (Hb). Cyanosis was first described by deSenac who was the physician for King Louis XV in 1749. He described it as the mixture of arterial and venous blood due to an abnormal connection between the two sides of the heart. In 1761, Morgagini showed association of cyanosis with pulmonary stenosis due to stasis of blood. Cyanosis was described by Sandifort, a European, in 1777 as a “blue boy” with tetralogy of Fallot. In 1892, Vaquez described the first case of polycythemia, as a cause of cyanosis. In 1919, Christen Lundsgaard quantified the amount of blood required to be deoxygenated to give the bluish discoloration of cyanosis. Blalock and Taussid performed the first anastomosis of subclavian to pulmonary artery on November 9, 1944 to lessen the cyanosis in tetralogy of Fallot. United States’ Olympian and gold medalist Shaun White was born with tetralogy of Fallot and had cyanosis because of that. Cyanosis may be classified into two groups including central cyanosis and peripheral cyanosis. Right to left shunt in congenital heart disease causes central cyanosis. Secondary erythrocytosis (increased red blood cell mass due to hypoxia) and polycythemia (neoplastic proliferation of red blood cell) are different conditions and need different evaluation. Two mechanisms involved in the development of cyanosis including systemic arterial oxygen desaturation and increased oxygen absorption by tissues. Cyanosis is evident when arterial oxygen saturation falls below 85% or the concentration of deoxygenated hemoglobin (Hb) exceeds 5 gm/dl. Common causes in the development of cyanosis include congenital heart diseases with right to left shunt, presence of abnormal hemoglobin, carbon monoxide poisoning, respiratory disorders associated with impaired gas exchange, impaired gas diffusion via the alveoli, embolism, pulmonary arteriovenous malformations, cold exposure, and raynaud’s phenomenon. Different causes of cyanosis may include pulmonary, cardiovascular, hematological, neurological, and vascular diseases. Prenatal echocardiography and genetic testing are useful methods for early detection of cyanotic congenital heart disease. Postnatal pulse oximetry is recommended for diagnosis of cyanotic congenital heart disease. Central cyanosis in the first hours or days of life in the neonate may happen and implies life-threatening conditions such as congenital cardiac abnormalities , airway obstruction , central nervous system problem, hemoglobinopathy. Peripheral cyanosis may happen in neonate called acrocyanosis. Prognosis is generally good if the underlying causes of cyanosis are determined and treated. Peripheral cyanosis improves with oxygen therapy. Conversely, central cyanosis does not respond to oxygen therapy because of the underlying intrapulmonary or intracardiac shunt which is responsible for mixing the nonoxygenated venous blood and oxygenated arterial blood. All causes of central cyanosis may cause peripheral cyanosis. cyanosis is a symptom of a disease process, then physical examination may include tachypnea, tachycardia, abnormal heart sounds or murmurs, wheezing, crackles, fever, clubbing, edema. In every neonate presented with cyanosis and shock, congenital heart disease dependent on patency ductus arteriosus should be considered. The physiologic constriction of ductus arteriosus after birth in a neonate whose pulmonary blood flow or aortic blood flow is dependent on PDA leads to shock and collapse in the neonate. Infusion of prostaglan E1 is life-saving and keeps patency ductus arteriosus. Treatment of underlying causes of cyanosis such as tamponade or cardiogenic shock due to low cardiac output state or peripheral vasoconstriction is considered. Cardiac defects causing central cyanosis include Transposition of the great arteries, Tetralogy of fallot, Tricuspid atresia, Truncus arteriosus,Total anomalous pulmonary venous connection, Ebstein anomaly, critical Pulmonary stenosis or atresia, functional single ventricle. The palliative surgical shunt maybe done in such lesions to increase pulmonary blood flow even in the presence of cyanosis. Complete repair procedure leads to relief of cyanosis and shunt and also causes long-term complications. Effective measures for primary prevention in neonatal cyanosis include prenatal echocardiography and genetic testing for detecting congenital heart defects and prenatal corticosteroid therapy for prevention of neonatal respiratory distress syndrome and development of lung maturation. Secondary prevention in cyanotic congenital heart disease includes obtaining EKG Exercise stress test, Holter monitoring, Transthoracic echocardiography, Cardiac MRI, Cardiac CT Scan, Pulse oximetry every 12-60 months based on the stage of disease.

Historical Perspective

Cyanosis was first described by deSenac who was the physician for King Louis XV in 1749. He described as admixture of arterial and venous blood due to an abnormal connection between two sides of the heart. In 1761, Morgagini showed association of cyanosis with pulmonary stenosis due to stasis of blood. Cyanosis was described by Sandifort, a European, in 1777 as a “blue boy” with tetralogy of Fallot. In 1892, Vaquez described the first case of polycythemia, as a cause of cyanosis. In 1919, Christen Lundsgaard quantified the amount of blood required to be deoxygenated to give the bluish discoloration of cyanosis. Blalock and Taussid performed the first anastomosis of subclavian to pulmonary artery on November 9, 1944 to lessen the cyanosis in tetralogy of Fallot. United States’ Olympian and gold medalist Shaun White was born with tetralogy of Fallot and had cyanosis because of that.

Classification

Cyanosis is classified into central cyanosis and peripheral cyanosis.

Pathophysiology

Cyanosis is a bluish or purplish discoloration of the skin and mucous membranes. Two mechanisms involved in the development of cyanosis, Systemic arterial oxygen desaturation and increased oxygen absorption by tissues. Cyanosis is evident when arterial oxygen desaturation falls below 85% or the concentration of deoxygenated hemoglobin (Hb) exceeds 5 gm/dl. Several factors can affect the appearance of cyanosis including skin pigmentation, Hemoglobin (Hb) levels, oxygen affinity to the hemoglobin (Hb).

Causes

In central cyanosis, saturation of oxygen is less than 85% when there is reduced hemoglobin more than 5g/dl following intrapulmonary shunt or intracardiac shunt leading to mixing of arterial and venous oxygen content. In peripheral cyanosis, saturation of oxygen is normal and there is peripheral capillary bed vasoconstriction due to low cardiac output state or sepsis.

Differentiating Cyanotic diseases from Other Diseases

The underlying causes of cyanosis are classified based on the type of cyanosis (central cyanosis or peripheral cyanosis). Different causes of cyanosis include pulmonary, cardiovascular, hematological, neurological, and vascular diseases.

Epidemiology and Demographics

The prevalence of congenital heart disease is approximately 1,000 per 100,000 individuals worldwide. Data about the incidence of cyanotic congenital heart disease is inadequate. Congenital cyanotic heart disease is more commonly observed among neonates. Congenital cyanotic heart disease affects men and women equally. There is no racial predisposition for cyanotic congenital heart disease.

Risk Factors

Cyanosis is the sign of underlying disease. Risk factors related to the presence of underlying conditions should be noticed. Common risk factors in the development of congenital heart diseases with the right to left shunt include maternal age >35 years, no intake of the multivitamin, febrile illness in the first trimester, obesity, paternal age> 25 years.

Screening

Prenatal echocardiography and genetic testing are useful methods for early detection of cyanotic congenital heart disease. Postnatal pulse oximetry is recommended for diagnosis of cyanotic congenital heart disease.

Natural History, Complications, and Prognosis

Central cyanosis in the first hours or days of life in the neonate may happen and implies life-threatening conditions such as congenital cardiac abnormalities , airway obstruction , central nervous system problem, hemoglobinopathy. Peripheral cyanosis may happen in neonate called acrocyanosis. If the underlying causes of cyanosis are determined and treated, the prognosis is generally good.

Diagnosis

Diagnostic Study of Choice

Echocardiography is the gold standard test for the diagnosis of cyanotic congenital heart diseases

History and Symptoms

The hallmark of cyanosis is blue discoration of skin and mucous membranes. Obtaining the history is most important aspect because of its association with wide variety of disorders (cardiac, pulmonary, vascular, neurologic and neuromuscular disorders). History taking also provides clues to specific causes, precipitating factors and associated comorbid conditions.

Physical Examination

Physical examination of patients with cyanosis will show bluish discoration of lips, tongue, oral mucosa, nose tip, ear lobules, hands and feet. Because cyanosis is a symptom of disease process careful physical examination for associated symptoms include tachypnea, tachycardia, abnormal heart sounds or murmurs, wheezing, crackles, fever, clubbing, edema of extremities will be necessary to identify underlying disease process.

Laboratory Findings

Laboratory findings consistent with the diagnosis of central cyanosis include Polycythemia due to secondary erythrocytosis, Elevated prothrombin time and partial thromboplastin time , decreased levels of factors 5,7,8,9 (qualitative and quantitative),Platelet disorder, increased fibrinolysis and paradoxical thrombotic tendency, Proteinuria, Hyperuricemia, Renal failure and nephrolithiasis.

Electrocardiogram

An ECG may be helpful in the diagnosis of congenital cyanotic heart disease and helps differentiate the causes of cyanotic heart disease.

X-ray

A chest x-ray may be helpful in the diagnosis of congenital heart diseases leading central cyanosis and other life-threatening causes of cyanosis such as pneumothorax, tamponade, pulmonary edema.

Echocardiography

Echocardiography is the gold standard test for the diagnosis of cyanotic congenital heart diseases

CT scan

A cardiac CT scan plays an important tool in the assessment of cyanotic congenital heart disease and determines the volume and size of cardiac chambers and determines the relation between the cardiac chambers and great arteries and veins.

MRI

A cardiac MRI is a noninvasive imaging for evaluation of cyanotic congenital heart disease and determines myocardial function and the area of fibrosis, the direction of flow and velocity across the palliative shunt and valves, the anomaly of connection of arteries and veins and correlation of anatomic and morphologic ventricles with great arteries in complex congenital heart disease.

Other Imaging Findings

Cardiac catheterization is an invasive study for the anatomic and physiological assessment of patients with cyanotic congenital heart disease.

Other Diagnostic Studies

Pulse oximetry may be helpful in the diagnosis of the type of cyanosis. Findings suggestive of hypoxia following central cyanosis include low oxygen saturation.

Treatment

Medical Therapy

In every neonate that presents with cyanosis and shock, congenital heart disease dependent on patency ductus arteriosus should be considered. The physiologic constriction of ductus arteriosus after birth in a neonate whose pulmonary blood flow or aortic blood flow is dependent on PDA leads to shock and collapse in the neonate. Infusion of prostaglandin E1 in such a neonate is life-saving and keeps patency ductus arteriosus. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock due to low cardiac output state and peripheral vasoconstriction lead to disappearing of cyanosis.

Surgery

Cardiac defect causing central cyanosis include transposition of the great arteries, tetralogy of fallot, tricuspid atresia, truncus arteriosus,total anomalous pulmonary venous connection, Ebstein anomaly, critical pulmonary stenosis or atresia, functional single ventricle. The palliative surgical shunt maybe done in such lesions to increase pulmonary blood flow even in the presence of cyanosis. Complete repair procedure leads to relief of cyanosis and shunt and also has long term complications.

Primary Prevention

Effective measurement for primary prevention includes prenatal echocardiography and genetic testing for detecting cyanotic congenital heart disease and prenatal corticosteroid therapy for the prevention of neonatal respiratory distress syndrome and the development of lung maturation.

Secondary Prevention

Secondary prevention in cyanotic congenital heart disease includes obtaining EKG Exercise stress test, Holter monitoring, Transthoracic echocardiography, Cardiac MRI, Cardiac CT Scan, Pulse oximetry every 12-60 months based on the stage of disease.

References

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

Overview

Cyanosis was first described by deSenac who was the physician for King Louis XV in 1749. He described it as the admixture of arterial and venous blood due to abnormal connection between two sides of the heart. In 1761, Morgagini showed association of cyanosis with pulmonary stenosis due to stasis of blood. Cyanosis was described by Sandifort, a European, in 1777 as a “blue boy” with tetralogy of Fallot. In 1892, Vaquez described the first case of polycythemia, as a cause of cyanosis. In 1919, Christen Lundsgaard quantified the amount of blood required to be deoxygenated to give the bluish discoloration of cyanosis. Blalock and Taussid performed the first anastomosis of subclavian to pulmonary artery on November 9, 1944 to lessen the cyanosis in tetralogy of Fallot. United States’ Olympian and gold medalist Shaun White was born with tetralogy of Fallot and had cyanosis because of that.

Historical Perspective

Discovery

  • Cyanosis was first described by deSenac who was the physician for King Louis XV in 1749.[1] He described it as the admixture of arterial and venous blood due to abnormal connection between two sides of the heart.[2][3]
  • In 1761, Morgagini showed association of cyanosis with pulmonary stenosis due to stasis of blood.[4]
  • Cyanosis was described by Sandifort, a European, in 1777 as a “blue boy” with tetralogy of Fallot.[5]
  • In 1785, William Hunter described cyanosis as “When the fit  was coming..he grew oppressed at his heart, became weak or faint, grew dark in his color, and at last almost black, fell down and seemed insensible….a very small quantity of blood (instead of the whole) passed through the lungs to receive the benefit of respiration and that with a small force too.”
  • In 1892, Vaquez described the first case of polycythemia, as a cause of cyanosis.[6]
  • In 1919, Christen Lundsgaard quantified the amount of blood required to be deoxygenated to give the bluish discoloration of cyanosis.[2][7]

Landmark Events in the Development of Treatment Strategies

Famous Cases

  • United States’ Olympian and gold medalist Shaun White was born with tetralogy of Fallot and had cyanosis because of that.

References

  1. ↑ de Senac, J. B., Trait6 de la structure ducoeur, desonacfionetdesesmaladies, Paris, 1749.
  2. ↑ 2.0 2.1 Lundsgaard C (September 1919). “STUDIES ON CYANOSIS : I. PRIMARY CAUSES OF CYANOSIS”. J. Exp. Med. 30 (3): 259–69. PMC 2126682. PMID 19868357.
  3. ↑ McGee, Steven (2012). Evidence-based physical diagnosis. Philadelphia: Elsevier/Saunders. ISBN 978-1437722079.
  4. ↑ Morgagni, J. B., De sedibus et causis morborum per anatomen indagatis libri quinque, Venice, 1761.
  5. ↑ Chopra, H. K. (2012). Textbook of cardiology : a clinical & historical perspective. New Delhi London: Jaypee Medical. ISBN 978-9350900819.
  6. ↑ Vaquez, H., Compt. rend. Soc. biol., 1892, iv, series 9, 384.
  7. ↑ Lundsgaard C (September 1919). “STUDIES ON CYANOSIS : II. SECONDARY CAUSES OF CYANOSIS”. J. Exp. Med. 30 (3): 271–93. PMC 2126678. PMID 19868358.
  8. ↑ Blalock, Alfred (1945). “THE SURGICAL TREATMENT OF MALFORMATIONS OF THE HEART”. Journal of the American Medical Association. 128 (3): 189. doi:10.1001/jama.1945.02860200029009. ISSN 0002-9955.
Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Amandeep Singh M.D.[3]

Overview

Cyanosis is defined as bluish discoloration of the skin and or mucous membrane resulting from insufficient oxygenation of the blood and the presence of at least 5g/dl unsaturated hemoglobin in tissue. Anemia may lead to hypoxia but is not the cause of cyanosis. Right to left shunt in congenital heart disease causes central cyanosis. Secondary erythrocytosis (increased red blood cell mass due to hypoxia) and polycythemia (neoplastic proliferation of reb blood cell) are different conditions and need different evaluation. Cyanosis may be classified into central cyanosis and peripheral cyanosis.

Classification

  • Cyanosis may be classified into two groups:[1]

References

  1. ↑ McMullen, Sarah M.; Patrick, Ward (2013). “Cyanosis”. The American Journal of Medicine. 126 (3): 210–212. doi:10.1016/j.amjmed.2012.11.004. ISSN 0002-9343.
Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]

Overview

Cyanosis is a bluish or purplish discoloration of skin and mucous membranes. Two mechanisms are involved in the development of cyanosis, systemic arterial oxygen desaturation and increased oxygen absorption by tissues. Cyanosis is evident when arterial oxygen desaturation falls below 85% or the concentration of deoxygenated hemoglobin (Hb) exceeds 5 gm/dl. Several factors can affect the appearance of cyanosis which include: skin pigmentation, Hemoglobin (Hb) levels, oxygen affinity to the hemoglobin (Hb).

Pathophysiology

Genetics, Associated Conditions, Gross Pathology, Microscopic Pathology

Hand with cyanosis – By James Heilman, MD – Own work, CC BY-SA 3.0,[17]

For detailed information on the genetics, associated conditions, gross and microscopic pathological features associated with conditions causing cyanosis, click the links below.

References

  1. ↑ Blount SG (May 1971). “Cyanosis: pathophysiology and differential diagnosis”. Prog Cardiovasc Dis. 13 (6): 595–605. PMID 4933007.
  2. ↑ GERACI JE, WOOD EH (July 1951). “The relationship of the arterial oxygen saturation to cyanosis”. Med. Clin. North Am. 1: 1185–1202. PMID 13098533.
  3. ↑ Sarkar M, Niranjan N, Banyal PK (2017). “Mechanisms of hypoxemia”. Lung India. 34 (1): 47–60. doi:10.4103/0970-2113.197116. PMC 5234199. PMID 28144061.
  4. ↑ Lundsgaard C (September 1919). “STUDIES ON CYANOSIS : I. PRIMARY CAUSES OF CYANOSIS”. J. Exp. Med. 30 (3): 259–69. PMC 2126682. PMID 19868357.
  5. ↑ Snider HL, Roy TM (October 1988). “Deoxyhaemoglobin concentrations in the detection of central cyanosis”. Thorax. 43 (10): 801. PMC 461518. PMID 3206391.
  6. ↑ Adeyinka A, Kondamudi NP. PMID 29489181. Missing or empty |title= (help)
  7. ↑ Lundsgaard C (September 1919). “STUDIES ON CYANOSIS : II. SECONDARY CAUSES OF CYANOSIS”. J. Exp. Med. 30 (3): 271–93. PMC 2126678. PMID 19868358.
  8. ↑ Steinhorn RH (September 2008). “Evaluation and management of the cyanotic neonate”. Clin Pediatr Emerg Med. 9 (3): 169–175. doi:10.1016/j.cpem.2008.06.006. PMC 2598396. PMID 19727322.
  9. ↑ Whelan JF (May 1984). “Methemoglobin as a cause of cyanosis”. Can Med Assoc J. 130 (10): 1260. PMC 1483499. PMID 6722683.
  10. ↑ Ananthakrishna R, Moorthy N, Rao DP, Nanjappa MC (2015). “An adult with central cyanosis and differential pulmonary vascularity”. Ann Pediatr Cardiol. 8 (3): 253–4. doi:10.4103/0974-2069.150701. PMC 4608209. PMID 26556978.
  11. ↑ Stadie WC (September 1919). “THE OXYGEN OF THE ARTERIAL AND VENOUS BLOOD IN PNEUMONIA AND ITS RELATION TO CYANOSIS”. J. Exp. Med. 30 (3): 215–40. PMC 2126679. PMID 19868355.
  12. ↑ Bailliard F, Anderson RH (January 2009). “Tetralogy of Fallot”. Orphanet J Rare Dis. 4: 2. doi:10.1186/1750-1172-4-2. PMC 2651859. PMID 19144126.
  13. ↑ Martins P, Castela E (October 2008). “Transposition of the great arteries”. Orphanet J Rare Dis. 3: 27. doi:10.1186/1750-1172-3-27. PMC 2577629. PMID 18851735.
  14. ↑ Jain A, Patel A, Hoppe IC (2016). “Benzocaine-Induced Cyanosis”. Eplasty. 16: ic18. PMC 4879862. PMID 27257469.
  15. ↑ Baranoski G, Van Leeuwen SR, Chen TF (July 2017). “On the detection of peripheral cyanosis in individuals with distinct levels of cutaneous pigmentation”. Conf Proc IEEE Eng Med Biol Soc. 2017: 4260–4264. doi:10.1109/EMBC.2017.8037797. PMID 29060838. Vancouver style error: initials (help)
  16. ↑ Das S, Maiti A (November 2013). “Acrocyanosis: an overview”. Indian J Dermatol. 58 (6): 417–20. doi:10.4103/0019-5154.119946. PMC 3827510. PMID 24249890.
  17. ↑ https://commons.wikimedia.org/w/index.php?curid=17978808
Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]

Overview

In central cyanosis saturation of oxygen is less than 85% when there is reduced hemoglobin more than 5g/dl following a intrapulmonary shunt or intracardiac shunt leading to mixing of arterial and venous oxygen content. In peripheral cyanosis, the saturation of oxygen is normal and there is peripheral capillary bed vasoconstriction due to low cardiac output state or sepsis.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Central Cyanosis

There following are some of the common causes of central cyanosis:

Peripheral Cyanosis:

There following are some of the common causes of peripheral cyanosis: [34][35]

Pseudocyanosis:

Causes by Organ System

Cardiovascular Aberrant subclavian artery, acrocyanosis, air embolism, Al Gazali-Aziz-Salem syndrome, alveolar capillary dysplasia , aortic arch defects, aortic coarctation, aortic stenosis, arterial occlusion, atrial myxoma, atrial septal defect, Bindewald-Ulmer-Muller syndrome, Blalock-Taussig shunt, Bland-White-Garland syndrome, blue baby syndrome, Buergers disease, cardiac tamponade, cardiomyopathy, Cassirer disease, cholesterol emboli syndrome, cholesterol pneumonia, congenital heart disease, congestive heart failure, cor biloculare, cor triatriatum, coronary artery anomaly, critical valvular aortic stenosis, Crocq disease, cyanotic congenital heart disease, deep vein thrombosis, double inlet left ventricle, double outlet right ventricle, Ebstein anomaly, Eisenmenger syndrome, familial pulmonary capillary hemangiomatosis, heart attack, hemothorax, hypocalcemia, hypoplastic left heart syndrome, hypovolemia, hypoxemia, idiopathic pulmonary hypertension, intermittent claudication, ischemic heart disease, isolated ventriculoarterial discordance, Ivemark syndrome, Jervell and Lange-Nielsen syndrome, Kugel-Stoloff syndrome, laryngeal edema, malignancy-related superior vena cava syndrome, Marfan syndrome, Meadows syndrome, mitral atresia in infants, myocardial infarction, partial atrioventricular canal, patent ductus arteriosus, patent foramen ovale, peripartum cardiomyopathy, peripheral arterial disease, persistent pulmonary hypertension of the newborn, persistent truncus arteriosus, phlegmasia cerulea dolens, pseudocyanosis, pulmonary arteriovenous fistula, pulmonary arteriovenous malformation, pulmonary embolism, pulmonary hypertension, pulmonary stenosis, pulmonary veno-occlusive disease, pulmonary venous return anomaly, right ventricle hypoplasia, right ventricular outflow tract obstruction, shock, Sneddon syndrome, subpulmonary stenosis, superior vena cava syndrome, TAPVC, Taussig-Bing syndrome, tetralogy of Fallot, total anomalous pulmonary venous connection, transposition of the great vessels, tricuspid atresia, tricuspid stenosis, truncus arteriosus, vascular malposition, vascular rings, velocardiofacial syndrome, ventricular septal defect
Chemical / poisoning 2,4,6-trinitrotoluene, 4-Nitrophenol, anchovy poisoning, aniline, anisidine, antifreeze, apple seed poisoning, apricot seed poisoning, arsine gas, bird cherry seed poisoning, bitter almond seed poisoning, brown snake poisoning, carbamates, chlorate salts, chlorobenzene, chronic mercury exposure, clupeotoxin, cyanide poisoning, demeton-S-methyl, diazinon, dichlorvos, dicrotophos, dinitrocresol, dioxathion, disulfoton, endosulfan, epichlorohydrin, ethion, ethylene glycol, ethylene oxide, ethylene, fensulfothion, fenthion, herring poisoning, hydrogen sulfide, iron poisoning, lantana poisoning, lead, malathion, methidathion, methiocarb, methomyl, organophosphate poisoning, paraquat, parathion, phosdrin, profenofos, propane, sea snake venom, silver iodide, silver nitrate, silver, smoke inhalation, snakebites, stachybotrys chartarum exposure, strychnine, sulfur dioxide, terbufos, tetraethyl pyrophosphate, tetrodotoxin, thioglycolic acid, trichloroethylene
Dermatologic Acrodynia, Al Gazali-Aziz-Salem syndrome, angioneurotic edema, chromhidrosis
Drug Side Effect Acetaminophen and hydrocodone, amiodarone, amyl nitrite, benzocaine, benzodiazepines, beta blockers,bicisate dihydrochloride, bufotenin, chloramphenicol, chloroquine, clonazepam, clorazepate, codeine, dapsone, desmopressin, diazepam, dilaudid, gray baby syndrome, hydrocodone, hydroquinone, ibuprofen, Imipenem-Cilastatin,lorazepam, lortab, maternal sedation, meperidine, methadone, metoclopramide, midazolam, morphine, narcotics, nitrates, nitrazepam, nitrites, nitroglycerin, oxazepam, phenazopyridine, phenol, phenothiazines, primaquine , ribavirin, rifampin, sedatives, sulfonamides
Ear Nose Throat Choanal atresia, epiglottitis, laryngomalacia, laryngotracheomalacia, lethal chondrodysplasia Moerman type, Ludwig’s angina, macroglossia, microcephalic osteodysplastic primordial dwarfism type 1, micrognathia, Pierre Robin syndrome, retrognathia, syndromic microphthalmia type 9, vocal cord paralysis, Weinstein Kliman Scully syndrome
Endocrine Adrenal hemorrhage, congenital hyperinsulinism, hypoadrenalism, hypocalcemia, hypoglycemia, hypomagnesemia, pseudoaldosteronism, type 1 pseudohypoaldosteronism, Waterhouse-Friederichsen syndrome, Weinstein Kliman Scully syndrome
Environmental Asbestosis, berylliosis, coal worker’s pneumoconiosis, cold exposure, hypersensitivity pneumonitis, insect sting allergy, pneumoconiosis, Shaver’s disease, silicosiderosis, silicosis
Gastroenterologic Boerhaave syndrome, Cast syndrome, cirrhosis of liver, congenital diaphragmatic hernia, cystic fibrosis, duodenal atresia, esophageal atresia, tracheal agenesis without tracheoesophageal fistula, tracheoesophageal fistula
Genetic 1p36 deletion syndrome, acrocephalopolysyndactyly, acrofacial dysostosis, benign familial neonatal convulsions, chromosome 22q11 deletion, cystic fibrosis, DiGeorge syndrome, HMG-CoA lyase deficiency, Jervell and Lange-Nielsen syndrome, Marfan syndrome, microcephalic osteodysplastic primordial dwarfism type 1 , Sakati syndrome, Sakati-Nyhan-Tisdale syndrome, Shprintzen syndrome, velocardiofacial syndrome, VLCAD deficiency, Werdnig-Hoffman disease
Hematologic Blood transfusion, cystic hygroma, deep vein thrombosis, disseminated intravascular coagulation, hemoglobinopathy, methemoglobinemia, Osler-Vaquez disease, phlegmasia alba dolens, phlegmasia cerulea dolens, polycythemia vera, pulmonary embolism, sulfhemoglobinemia, Vaquez disease
Iatrogenic Mendelson’s syndrome
Infectious Disease Acute histoplasmosis, anthracosis, bacterial tracheitis, bordetella pertussis, epiglottitis, legionellosis, legionnaire’s disease, Ludwig’s angina, melioidosis, meningitis, pertussis, sepsis, streptococcal group B invasive disease , Waterhouse-Friederichsen syndrome, western equine encephalitis, whooping cough
Musculoskeletal / Ortho Adams–Oliver syndrome, Al Gazali-Aziz-Salem syndrome, Bindewald-Ulmer-Muller syndrome, Isaac’s syndrome, lethal chondrodysplasia Moerman type, microcephalic osteodysplastic primordial dwarfism type 1, neuromyotonia, thoracic dystrophy
Neurologic Adams-Oliver syndrome, benign familial neonatal convulsions, Bindewald-Ulmer-Muller syndrome, birth asphyxia, cerebral hypoxia, congenital central hypoventilation syndrome, encephalitis, head trauma, hypoxic ischemic encephalopathy, intracranial hemorrhage, intraventricular hemorrhage, Isaac’s syndrome, meningitis, monomelic amyotrophy, mountain sickness, neonatal myasthenia gravis, neuromyotonia, obstructive sleep apnea, perinatal asphyxia, phrenic nerve injury, seizure, sleep apnea, sudden infant death syndrome, suffocation, tonic-clonic seizures, vein of Galen aneurysm, vocal cord paralysis, Werdnig-Hoffman disease, western equine encephalitis
Nutritional / Metabolic Dehydration, diphosphoglycerate mutase deficiency, HMG-CoA lyase deficiency
Obstetric/Gynecologic Meadows syndrome, Mendelson’s syndrome, peripartum cardiomyopathy
Oncologic Cystic hygroma, malignancy-related superior vena cava syndrome, Osler-Vaquez disease, Pancoast tumor, polycythemia vera, Vaquez disease
Opthalmologic Matthew-Wood syndrome, Sneddon syndrome, Weinstein Kliman Scully syndrome
Overdose / Toxicity Drug overdose, heroin, phosdrin
Psychiatric Congenital central hypoventilation syndrome, shaken baby syndrome
Pulmonary Acrocyanosis, acute interstitial pneumonitis, air leak syndromes, airway obstruction, alveolar capillary dysplasia, angioneurotic edema, apnea of prematurity, aspiration, asthma, atelectasis, bacterial tracheitis, Besnier-Boeck-Schaumann disease, bronchiectasis, bronchiolitis, bronchopulmonary dysplasia, bronchospasm, Cassirer disease, cholesterol pneumonia, chronic bronchitis, chronic obstructive pulmonary disease, chylothorax, community-acquired pneumonia, congenital central hypoventilation syndrome, congenital cystic adenomatoid malformation, congenital pulmonary lymphangiectasia, Crocq disease, croup, cystic fibrosis, diaphragmatic paralysis, emphysema, empyema, epiglottitis, erythrocyanosis, exercise-induced asthma, extrinsic allergic alveolitis, familial interstitial fibrosis , familial pulmonary capillary hemangiomatosis, fibrosing alveolitis, flail chest, foreign body aspiration, Hamman-Rich syndrome , hemothorax, hyaline membrane disease, hypersensitivity pneumonitis, hypoventilation, hypoxemia, hypoxia (medical), idiopathic diffuse interstitial pulmonary fibrosis, idiopathic pulmonary fibrosis, idiopathic pulmonary hemosiderosis, idiopathic pulmonary hypertension, idiopathic subglottic tracheal stenosis , infant respiratory distress syndrome, infantile apnea, interstitial lung disease, laryngeal cleft, laryngeal edema, laryngomalacia, laryngotracheomalacia, lethal chondrodysplasia Moerman type , lobar emphysema, lung abscess, Matthew-Wood syndrome, meconium aspiration syndrome, Mendelson’s syndrome, mountain sickness, obstructive sleep apnea, Pancoast tumor, perinatal asphyxia, Pickwickian syndrome, Pierre Robin syndrome, pleural effusion, pneumoconiosis, pneumonia, pneumothorax, pseudocyanosis, pulmonary alveolar proteinosis, pulmonary arteriovenous fistula, pulmonary arteriovenous malformation, pulmonary artery sling, pulmonary atresia, pulmonary edema, pulmonary embolism, pulmonary fibrosis, pulmonary hemorrhage, pulmonary hypertension, pulmonary hypoplasia, respiratory depression, respiratory distress syndrome, respiratory failure, respiratory muscle paralysis, sarcoidosis, Shaver’s disease, sleep apnea, smoke inhalation, spontaneous pneumothorax, sudden infant death syndrome, suffocation, surfactant metabolism dysfunction, tension pneumothorax, tracheal agenesis without tracheoesophageal fistula, tracheal stenosis, tracheoesophageal fistula, transient tachypnea of the newborn, unilateral pulmonary agenesis, unilateral pulmonary hypoplasia, whooping cough
Renal / Electrolyte Cholesterol emboli syndrome, dehydration, Goodpasture syndrome, hypermagnesemia, hypocalcemia, hypomagnesemia
Rheum / Immune / Allergy Angioneurotic edema, Besnier-Boeck-Schaumann disease, Buergers disease, DiGeorge syndrome, extrinsic allergic alveolitis, Goodpasture syndrome, hypersensitivity pneumonitis, insect sting allergy, laryngeal edema, lupus, neonatal myasthenia gravis, Raynaud’s disease, Raynaud’s phenomenon, sarcoidosis, Shprintzen syndrome, velocardiofacial syndrome
Sexual Weinstein Kliman Scully syndrome
Trauma Flail chest, head trauma, hemothorax, penetrating chest wounds, shaken baby syndrome, thermal injury,
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Choking, drowning, hanging, high altitude, hypothermia, immobility

Causes in Alphabetical Order

Causes of Cyanosis Based on Classification

Causes of Central Cyanosis


Causes of peripheral cyanosis

References

  1. ↑ Olson K, Smollin C (July 2008). “Carbon monoxide poisoning (acute)”. BMJ Clin Evid. 2008. PMC 2907971. PMID 19445736.
  2. ↑ Parker-Cote JL, Rizer J, Vakkalanka JP, Rege SV, Holstege CP (February 2018). “Challenges in the diagnosis of acute cyanide poisoning”. Clin Toxicol (Phila): 1–9. doi:10.1080/15563650.2018.1435886. PMID 29417853.
  3. ↑ 3.0 3.1 Zoorob RJ, Campbell JS (November 2003). “Acute dyspnea in the office”. Am Fam Physician. 68 (9): 1803–10. PMID 14620600.
  4. ↑ Just-Viera JO, Norwood T, Yeager GH (April 1967). “Importance of shock and cyanosis in pulmonary embolism”. Ann. Surg. 165 (4): 528–35. PMC 1617449. PMID 6021453.
  5. ↑ Barton ED (July 1999). “Tension pneumothorax”. Curr Opin Pulm Med. 5 (4): 269–74. PMID 10407699.
  6. ↑ Wang RF, Hung TY, Chong CF, Wang TL, Chen CC (February 2008). “Central cyanosis due to severe pulmonary hypertension combined with pericarditis as the initial manifestation of systemic lupus erythematosus”. Am J Emerg Med. 26 (2): 248.e1–2. doi:10.1016/j.ajem.2007.04.007. PMID 18272123.
  7. ↑ Costello RA, Nehring SM. PMID 28722864. Missing or empty |title= (help)
  8. ↑ 8.0 8.1 8.2 Bailliard F, Anderson RH (January 2009). “Tetralogy of Fallot”. Orphanet J Rare Dis. 4: 2. doi:10.1186/1750-1172-4-2. PMC 2651859. PMID 19144126.
  9. ↑ Bodson L, Bouferrache K, Vieillard-Baron A (October 2011). “Cardiac tamponade”. Curr Opin Crit Care. 17 (5): 416–24. doi:10.1097/MCC.0b013e3283491f27. PMID 21716107.
  10. ↑ Komine S (February 1964). “In vitro studies on the degradation and synthesis of serum proteins in placentae. I. Synthesis of serum proteins”. Nippon Juigaku Zasshi. 26 (1): 15–23. PMID 4173631.
  11. ↑ Steinhorn RH (September 2008). “Evaluation and management of the cyanotic neonate”. Clin Pediatr Emerg Med. 9 (3): 169–175. doi:10.1016/j.cpem.2008.06.006. PMC 2598396. PMID 19727322.
  12. ↑ 12.0 12.1 Kaur K, Bhardwaj M, Kumar P, Singhal S, Singh T, Hooda S (2016). “Amniotic fluid embolism”. J Anaesthesiol Clin Pharmacol. 32 (2): 153–9. doi:10.4103/0970-9185.173356. PMC 4874066. PMID 27275041.
  13. ↑ Dueñas-Laita A, Burillo Putze G, Alonso JR, Bajo A, Climent B, Corral E, Felices F, Ferrer A, Hernández Frutos MP, Nogué S, Puiguriguer J (December 2010). “[Basis for the clinical management of fire smoke poisoning “Docohumo Madrid 2010″]”. Med Intensiva (in Spanish; Castilian). 34 (9): 609–19. doi:10.1016/j.medin.2010.07.007. PMID 21051109.
  14. ↑ Costumbrado J, Ghassemzadeh S. PMID 29083723. Missing or empty |title= (help)
  15. ↑ Gossman WG, Burns B. PMID 29261942. Missing or empty |title= (help)
  16. ↑ Jain S, Bakshi N, Krishnamurti L (December 2017). “Acute Chest Syndrome in Children with Sickle Cell Disease”. Pediatr Allergy Immunol Pulmonol. 30 (4): 191–201. doi:10.1089/ped.2017.0814. PMC 5733742. PMID 29279787.
  17. ↑ Kondamudi NP, Dulebohn SC. PMID 28722923. Missing or empty |title= (help)
  18. ↑ Kondamudi NP, Wilt AS. PMID 28722998. Missing or empty |title= (help)
  19. ↑ Memon J, Manganaro SN. PMID 28722938. Missing or empty |title= (help)
  20. ↑ Bergeron M, Cohen AP, Cotton RT (2017). “The Management of Cyanotic Spells in Children with Oesophageal Atresia”. Front Pediatr. 5: 106. doi:10.3389/fped.2017.00106. PMC 5430373. PMID 28555179.
  21. ↑ Maitre B, Similowski T, Derenne JP (September 1995). “Physical examination of the adult patient with respiratory diseases: inspection and palpation”. Eur. Respir. J. 8 (9): 1584–93. PMID 8575588.
  22. ↑ Hermansen CL, Mahajan A (December 2015). “Newborn Respiratory Distress”. Am Fam Physician. 92 (11): 994–1002. PMID 26760414.
  23. ↑ Bishop NB, Stankiewicz P, Steinhorn RH (July 2011). “Alveolar capillary dysplasia”. Am. J. Respir. Crit. Care Med. 184 (2): 172–9. doi:10.1164/rccm.201010-1697CI. PMC 3172887. PMID 21471096.
  24. ↑ Justice NA, Le JK. PMID 28722988. Missing or empty |title= (help)
  25. ↑ Reuter S, Moser C, Baack M (October 2014). “Respiratory distress in the newborn”. Pediatr Rev. 35 (10): 417–28, quiz 429. doi:10.1542/pir.35-10-417. PMC 4533247. PMID 25274969.
  26. ↑ Woods WA, McCulloch MA (November 2005). “Cardiovascular emergencies in the pediatric patient”. Emerg. Med. Clin. North Am. 23 (4): 1233–49. doi:10.1016/j.emc.2005.07.003. PMID 16199347.
  27. ↑ Driscoll DJ (February 1990). “Evaluation of the cyanotic newborn”. Pediatr. Clin. North Am. 37 (1): 1–23. PMID 2407997.
  28. ↑ Martínez de Zabarte Fernández JM, García Íñiguez JP, Domínguez Cajal M (February 2018). “Metahemoglobinemia in infants over one year”. Med Clin (Barc). doi:10.1016/j.medcli.2017.12.009. PMID 29439874.
  29. ↑ Günal E, Akkuş Y, Çığşar G, Çiftçi H, Kahramanca Ş, Özdemir M (October 2017). “Methemoglobinemia incidence after the application of lidocaine for small surgical procedures”. Agri. 29 (4): 173–176. PMID 29171648.
  30. ↑ Hilbert P, Zur Nieden K (September 2004). “[Suicidal fatal beta-blocker intoxication]”. Anaesthesist (in German). 53 (9): 826–9. doi:10.1007/s00101-004-0721-1. PMID 15249969.
  31. ↑ Hifumi T, Sakai A, Kondo Y, Yamamoto A, Morine N, Ato M, Shibayama K, Umezawa K, Kiriu N, Kato H, Koido Y, Inoue J, Kawakita K, Kuroda Y (2015). “Venomous snake bites: clinical diagnosis and treatment”. J Intensive Care. 3 (1): 16. doi:10.1186/s40560-015-0081-8. PMC 4393627. PMID 25866646.
  32. ↑ Kondamudi NP, Virji M. PMID 28722926. Missing or empty |title= (help)
  33. ↑ Jensen JD, Vincent AL. PMID 28613569. Missing or empty |title= (help)
  34. ↑ Fardoun MM, Nassif J, Issa K, Baydoun E, Eid AH (2016). “Raynaud’s Phenomenon: A Brief Review of the Underlying Mechanisms”. Front Pharmacol. 7: 438. doi:10.3389/fphar.2016.00438. PMC 5110514. PMID 27899893.
  35. ↑ Das S, Maiti A (November 2013). “Acrocyanosis: an overview”. Indian J Dermatol. 58 (6): 417–20. doi:10.4103/0019-5154.119946. PMC 3827510. PMID 24249890.
Differentiating Cyanosis from other Diseases

Differentiating Cyanosis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Overview

Differential Diagnosis of Cyanosis

Differential Diagnosis of Central Cyanosis

To review the differential diagnosis of central cyanosis, click here.

To review the differential diagnosis of central cyanosis and dyspnea, click here.

To review the differential diagnosis of central cyanosis and fever, click here.

To review the differential diagnosis of central cyanosis and chest pain, click here.

To review the differential diagnosis of central cyanosis and clubbing, click here.

To review the differential diagnosis of central cyanosis, dyspnea, and fever, click here.

To review the differential diagnosis of central cyanosis, dyspnea, and chest pain, click here.

To review the differential diagnosis of central cyanosis, dyspnea, and clubbing, click here.

To review the differential diagnosis of central cyanosis, fever, and chest pain, click here.

To review the differential diagnosis of central cyanosis, fever, and clubbing, click here.

To review the differential diagnosis of central cyanosis, chest pain, and clubbing, click here.

To review the differential diagnosis of central cyanosis, dyspnea, fever, and chest pain, click here.

To review the differential diagnosis of central cyanosis, fever, chest pain, and clubbing, click here.

To review the differential diagnosis of central cyanosis, dyspnea, fever, and clubbing, click here.

To review the differential diagnosis of central cyanosis, dyspnea, fever, chest pain, and clubbing, click here.

Differential Diagnosis of Peripheral Cyanosis

To review the differential diagnosis of peripheral cyanosis, click here.

To review the differential diagnosis of peripheral cyanosis and dyspnea, click here.

To review the differential diagnosis of peripheral cyanosis and fever, click here.

To review the differential diagnosis of peripheral cyanosis and chest pain, click here.

To review the differential diagnosis of peripheral cyanosis and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, and fever, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, and chest pain, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, fever, and chest pain, click here.

To review the differential diagnosis of peripheral cyanosis, fever, and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, chest pain, and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, fever, and chest pain, click here.

To review the differential diagnosis of peripheral cyanosis, fever, chest pain, and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, fever, and clubbing, click here.

To review the differential diagnosis of peripheral cyanosis, dyspnea, fever, chest pain, and clubbing, click here.

Abbreviations: ABG= Arterial blood gas, ANP= Atrial natriuretic peptide, BNP= Brain natriuretic peptide, CBC= Complete blood count, COPD= Chronic obstructive pulmonary disease, CRP= C-reactive protein, CT= Computed tomography, CXR= Chest X-ray, DVT= Deep vein thrombosis, ESR= Erythrocyte sedimentation rate, HRCT= High Resolution CT, IgE= Immunoglobulin E, LDH= Lactate dehydrogenase, PCWP= Pulmonary capillary wedge pressure.

Diseases Cyanosis Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging
Peripheral Central Dyspnea Fever Chest pain Clubbing Peripheral edema Auscultation CBC ABG Electrolytes Other X-ray CT scan Other
Pulmonary diseases Airway disorder Severe croup[1] + – + +/- – – – Stridor Lymphocytosis Normal Normal – Steeple sign Normal Distended hypopharynx during inspiration Clinical findings Intercostal and subcostal retraction, Barking cough
Epiglottitis[2] + – + + – – – Stridor Leukocytosis with neutrophilia Normal Normal – Thumb sign Normal – Laryngoscopy Muffled voice, Drooling
Foreign body aspiration[3] + – + – +/- – – Decreased breath sounds, Wheezing Normal Normal Normal – Hyperinflation, Atelectasis, Objects Foreign body entrapment with edema or granulation tissue – Bronchoscopy Mediastinitis
Bacterial tracheitis[4] + – + + + – – Inspiratory stridor Leukocytosis Normal Normal Blood culture, Gram stain Irregular tracheal margin Normal Steeple sign (confusing) Laryngotracheobronchoscopy Brassy cough, Hoarseness
Sleep apnea[5] – + + – – – – Normal Polycythemia ↓O2, ↑CO2 Normal – Normal Normal Polysomnography Polysomnography Nightmares, Snoring
Chronic bronchitis[6] – + + +/- +/- + – Rales, crackles, Wheeze Leukocytosis ↓O2, ↑CO2, Respiratory acidosis Hypokalemia, Hypernatremia Gram stain of sputum Elongated heart, Flattened diaphragms, Prominent hilar vasculature Bronchial wall thickening with increased bronchovascular markings – HRCT Productive cough, Chest tightness
Atelectasis[7] – + + – + – – Localized diminished breath sounds, Wheeze Leukocytosis ↓O2, ↑CO2, Respiratory acidosis Normal – Localized increased opacity, Deviation toward the atelectasis Local crowding of pulmonary vessels and bronchi MRI for distinguishing obstructive from non-obstructive HRCT Cough, Shallow breathing
Parenchymal disorder Alveolitis[8] +/- + + + + +/- – Wheeze, Crackles Leukocytosis, Eosinophilia ↓O2, ↑CO2 Normal ↑ESR, ↑CRP Scattered opacities, Fine reticulation Homogeneous ground-glass opacity – HRCT PLUS Clinical findings Malaise, Chills, Headache
Pneumonia[9] – + + + + +/- – Rales, Crackles, Wheeze, Pleural friction rub Leukocytosis with neutrophilia Normal Hyponatremia – Entire lobe consolidated, Air bronchograms Focal ground-glass opacity – HRCT Tachycardia, Bradycardia (Legionella)
Asthma (Late)[10] – + + – +/- +/- – End expiratory wheeze Eosinophilia ↓O2, ↑CO2 Normal ↑ IgE Atelectasis Allergic bronchopulmonary aspergillosis, Bronchiectasis – Spirometry before and after bronchodilator Triad of asthma, nasal polyps, and rash is indicative of aspirin sensitivity.
Cystic fibrosis[11] + – +/- +/- + – Wheeze, Crackles Normal ↓O2, ↑CO2 Increased sweat chloride Sweat chloride test Hyperinflation, Nodules Peribronchial thickening, Bronchiectasis – Sweat chloride test Absent vas deferens
COPD

(Severe emphysema)[12]

+ – + +/- + +/- +/- Reduced breath sounds, Wheeze, Inspiratory crackles Polycythemia ↓O2, ↑CO2 Normal Alpha 1-antitrypsin test Elongated heart, Flattened diaphragms, Prominent hilar vasculature Bullae – HRCT Pulmonary hypertension, Right heart failure
Tuberculosis[13] – + + + + +/- – Reduced breath sounds, Wheeze, Inspiratory crackles Leukocytosis, ↑Lymphocyte ↓O2, ↑CO2 Hyponatremia, Hyperkalemia, Hypochloremia PPD, interferon-gamma release assay (IGRA) Dense, homogeneous parenchymal consolidation Nodules with low-density centers and rim enhancement Fluorodeoxyglucose positron emission tomography/CT (FDG PET/CT) Sputum culture, QuantiFERON-TB Gold (QFT) Loss of appetite, Night sweats
Pulmonary fibrosis[14] – + + – + + – Inspiratory crackles Anemia ↓O2, ↑CO2 Normal Matrix metalloproteinases (MMPs) Honeycombing Traction bronchiectasis,

Interlobular septal thickening

HRCT HRCT Fatigue, Weight loss
Pneumoconiosis[15] – + + – +/- +/- – End expiratory wheeze Leukocytosis, Anemia ↓O2, ↑CO2, Respiratory acidosis Hyper/Hypocalcemia,

Hypermagnesemia

– Small to large round nodular opacities Diffuse distribution of small nodules MRI and PET-CT scan CT/HRCT scan Tightness in the chest
Lung cancer[16] – + + – +/- + – Absence of breath sounds, Stridor, Wheezing Leukocytosis, Anemia ↓O2, ↑CO2 Hyponatremia ↑CRP, ↑ESR Pulmonary nodule or mass,

Mediastinal widening

Hilar lymphadenopathy

Massive lymphadenopathy, Direct mediastinal invasion MRI, PET-CT scan, Bronchoscopy Low dose computed tomography scan (LDCT) Weight loss, Loss of appetite
Acute respiratory distress syndrome[17] – + + +/- + – – Inspiratory crackles Leukopenia/Leukocytosis ↓O2, ↓CO2, Respiratory alkalosis Hyponatremia, Hyperkalemia ↑BNP, ↑Von Willebrand factor (VWF) Bilateral pulmonary infiltrates (patchy to diffuse) Emphysema, Pneumothorax and pneumomediastinum, Mediastinal lymphadenopathy Invasive Hemodynamic Monitoring (PCWP), Bronchoscopy Chest CT scan Tachypnea, Muscle weakness
Pulmonary vascular disorders Massive pulmonary embolism[18] + – + +/- + – +/- Reduced breath sounds, Crackles, Loud P2 Leukocytosis ↓O2, ↑CO2, Respiratory acidosis Normal D-dimer, BNP Fleischner sign, Hampton hump, Westermark sign, Pleural effusion  Filling defects in the pulmonary vasculature Spiral CT pulmonary angiogram Spiral CT pulmonary angiogram Tachycardia, Shock, Pulmonary hypertension
Pulmonary arterio-venous malformation[19][20][21] – + + – + + – Pulmonary bruit Normal ↓O2, ↑CO2, Respiratory acidosis Normal – One or more rounded or multilobular opacities Connecting vessel in hilum Magnetic resonance angiography, Echocardiography Contrast enhanced magnetic resonance angiography  Cerebral arteriovenous malformation
Pulmonary hypertension[22] – + + – +/- +/- – Tricuspid regurgitation murmur, Pulmonic insufficiency murmur Mild anemia ↓O2, ↑CO2 Hypernatremia ↑BNP, ↑ANP Right deviated cardiac apex,

Prominent pulmonary artery

Ill-defined nodules, Interlobular septal thickening CT pulmonary angiography (CTPA), MRA Cardiac catheterization (PCWP) Fatigue, Inability to exercise
Chest wall disorders Flail chest[23] + – + – + – – Normal Normal ↓O2, ↑CO2 Normal – ≥3 adjacent ribs with segmental fractures, >5 adjacent rib fractures Normal – CXR Bruises over chest
Pneumothorax[24] + – + – + – – Diminished breath sounds Normal ↓O2, ↑CO2 Normal – No lung marking on one side, Collapsed lung Loculated air in thoracic cavity M-mode ultrasonography Chest CT scan Tachypnea
Disease Peripheral Central Dyspnea Fever Chest pain Clubbing Peripheral edema Auscultation CBC ABG Electrolytes Other X-ray CT scan Other Gold standard Additional findings
Cardiac diseases Congenital disorders Atrioventricular canal defect[25] +/- + + – +/- +/- – Wheezing,Holosystolic or systolic ejection murmur Normal Normal Normal Pulse oximetry Cardiomegaly, Increased pulmonary vascular markings Normal Echocardiography, MRI Echocardiography Tachypnea, Lack of appetite, Pale skin color, Excessive sweating
Ebstein anomaly[26] – + +/- – +/- – – Loud S1 Normal Normal Normal Pulse oximetry Cardiomegaly, “Box shape” heart Apical displacement of the septal and posterior leaflets of the tricuspid valve “Atrialisation” of the right ventricle in MRI, Tricuspid regurgitation in echocardiography Echocardiography Fatigue, Palpitations
Tetralogy of Fallot[27] – + +/- – +/- – – Harsh systolic murmur Normal Normal Normal Pulse oximetry “Boot-shaped” heart with an upturned cardiac apex Aortopulmonary collateral vessels Peripheral pulmonary stenosis and atresia in echocardiography Echocardiography Fainting, Palpitation
Pulmonic stenosis[28] – + + – + +/- – Crescendo-decrescendo ejection murmur Schistocyte ↓O2 Normal Pulse oximetry Right ventricular hypertrophy, Dilated main pulmonary artery Stenotic segment, Post stenotic dilatation Severity of the stenosis by velocity encoded phase contrast (VEC) cine sequences Echocardiography Fainting, Palpitation
Total anomalous pulmonary venous connection[29] – + + – +/- +/- – Systolic murmur over the pulmonary area Normal ↓O2 Normal Pulse oximetry Snowman sign Anomalous venous return Blind ended left atrium with no connecting veins in echocardiography Echocardiography Pounding heart, Weak pulse, Extreme sleepiness
Transposition of the great vessels[30] – + + – +/- +/- – Diastolic and Systolic murmur Normal ↓O2 Normal Pulse oximetry Cardiomegaly with narrow superior mediastinum (egg on a string sign) Abnormal great vessel anatomy Flow dynamics on Steady-state free precession (SSFP) MRI Echocardiography Lack of appetite, Poor weight gain
Truncus arteriosus[31] – + +/- – +/- +/- – Holosystolic or ejection type murmur Normal ↓O2 Normal Pulse oximetry Moderate cardiomegaly, pulmonary plethora, Widened mediastinum Single cardiac trunk Anomalous anatomy in MRI Echocardiography Fatigue, Sweating, Pale or cool skin
Patent ductus arteriosus[32] – + +/- – +/- +/- – Continuous machinery murmur Normal ↓O2, ↑CO2 Normal Pulse oximetry Cardiomegaly, Aortopulmonary window obsecuration Tortuous morphology of ductus (Krichenko classification) Spiral CT pulmonary angiogram Echocardiography Failure to thrive, Respiratory distress
Acquired disorders Heart failure[33] + – + +/- + – + Coarse crackles, S3 Anemia ↓O2, ↑CO2 Hyponatremia, Hypokalemia, Hypomagnesemia Elevated BNP Pleural effusion, Cardiomegaly Kerley B lines Normal Radioisotope scan Echocardiography Generalized edema, Hepatomegaly
Valvular heart disease[34] + – + – – – + Murmurs Schistocyte Normal Normal Hyperthyroidism Valve calcification Normal Valvular dysfunction in echocardiography Echocardiography Syncope, Palpitation
Myocardial infarction[35] – + + +/- + – – S3 and S4 Normal Normal Hyponatremia, Hypokalemia Elevated troponin I and CKMB Rolling out other causes Coronary luminal narrowing in CT perfusion scan Wall motion abnormality in echocardiography Cardiac troponin I Dizziness, Fatigue, Lightheadedness, Cold sweat
Cardiogenic shock[36] +/- + + – – – + Muffled heart sound Anemia ↓O2, ↑CO2 Hyperkalemia ↓PaO2 in pulse oximetry Normal Normal Echocardiography  Clinical findings Tachypnea, Palpitation, Hypotension, Weak pulse
Cardiomyopathy[37] – + + – + + + S3 and S4 Lymphocytosis ↓O2, ↑CO2 Normal ↓PaO2 in pulse oximetry Enlarged left ventricle and atria, Pulmonary edema Normal MRI Endomyocardial biopsy Arrhythmia, Bloating
Heart tumors[38] – + + – +/- +/- +/- Early diastolic tumor plop Normal Normal Normal Mild ↓PaO2 in pulse oximetry Calcification in lateral view Intracardiac mass Echocardiography  Histologic diagnosis (biopsy) Syncope, Weight loss
Mitral Stenosis[39] – + + – +/- +/- +/- Diastolic murmur Normal Normal Normal Mild ↓PaO2 in pulse oximetry Left atrial enlargement, Mitral annular calcification Secondary pulmonary hemosiderosis Velocity-encoded cine-magnetic resonance imaging (VEC-MRI) Echocardiography Dizziness, Hemoptysis
Vascular disease Arterial disorders Acrocyanosis[40] + – +/- – – + – Normal Anemia, Leukocytosis ↓O2, ↑CO2 Hypercalcemia ↓PaO2 in pulse oximetry Normal Normal – Clinical findings Brittle nails, Telangiectasia
Arterial embolism[41] + – + – + +/- – Normal Normal Normal Hyperkalemia ↓PaO2 in pulse oximetry Normal Normal Transesophageal echocardiography (TEE) Clinical findings Headache, Decreased sensation
Raynaud’s Phenomenon[42] + – – – – + – Normal Polycythemia ↓O2 Normal Mild ↓PaO2 in pulse oximetry Normal Normal – Clinical findings Sensitivity to cold, Decreased sensation
Venous disorders Superior vena cava obstruction[43] + – +/- – +/- +/- + Normal Polycythemia ↓O2 Normal ↓PaO2 in pulse oximetry Superior mediastinal widening, Right hilar prominence  Thrombosis, Mediastinal mass or lymphadenopathy, Associated lung mass – Chest CT scan Headache,

Facial swelling

Venous stasis[44] + – – – – +/- + Normal Polycythemia ↓O2 Hypercalcemia Normal Normal Normal Color-flow duplex ultrasound Color-flow duplex ultrasound Leg swelling, Pain during walking,

Leg ulcers

Disease Peripheral Central Dyspnea Fever Chest pain Clubbing Peripheral edema Auscultation CBC ABG Electrolytes Other X-ray CT scan Other Gold standard Additional findings
Hematologic diseases Methemoglobinemia[45] – + + +/- + – – Wheezing Anemia, Methemoglobinemia Normal PaO2, ↑SaO2, “Saturation gap” Normal ↓SaO2 in pulse oximetry Normal Normal Echocardiography for ruling out other causes Co-oximetry, ABG paired with pulse oximetry. Serum methemoglobin levels Headache, Altered mental status, Delirium, Seizure, Coma
Polycythemia[46] + + + +/- +/- + – Normal ↑RBC, ↑WBC, ↑HGB, ↑Plt ↓O2 Hyperkalemia ↑Leukocyte alkaline phosphatase, ↑Ferritin, ↑Erythropoietin AVM, COPD, pulmonary hypertension Normal Abdominal ultrasound or renal vascular studies for ruling out renal artery stenosis RBC mass (RCM) and plasma volume measurement Itchiness, Headache. Dizziness. Blurred vision
Neurological disease Breath-holding spells[47] – + + – +/- – – Wheezing Hypochromic microcytic anemia ↓O2 Hypocalcemia, Hypokalemia Iron deficiency Ruling out foreign body aspiration Normal EEG monitoring Clinical findings Fainting, Twitching muscles, Seizure
Seizure[48] – + + +/- – – – Normal Normal ↓O2, ↑CO2 Hyponatremia, Hypo/Hypercalcemia ↑CPK, ↑LDH, Normal Normal EEG EEG Fainting, Tonic-clonic movements
Coma[49] – + – – – – +/- Wheezing Normal ↓O2, ↑CO2 Normal – Underlying disease Underlying disease – Glasgow Coma Scale (GCS) Depressed brainstem reflexes, Agonal breathing
Head trauma[50] – + + – – – – Normal Normal ↓O2, ↑CO2 Normal – Skull fracture Intracranial hemorrhage MRI CT scan Nausea, Hypertension, Bradycardia,Tachypnea
Miscellaneous High altitude exposure[51] +/- + + – +/- + – Wheezing Polycythemia ↓O2, ↓CO2, Respiratory alkalosis Hyperphosphatemia, Hypercalcemia, Hyponatremia, Hypokalemia, Hypomagnesemia Decreased bicarbonate Central interstitial edema Pulmonary consolidation – Hypoxic challenge test Dizziness, Coma, Death
Septic shock[52] + – + + +/- – – Rales, crackles, Wheeze, Pleural friction rub Leukocytosis with neutrophilia ↓O2, ↑CO2, Metabolic acidosis Hyperkalemia ↑ESR, ↑CRP Consolidation Pulmonary infiltration Echocardiography Blood culture Chills, Hypothermia, Loss of consciousness
Smoke inhalation[53] +/- + + – + – – Wheezing Anemia, Carboxyhemoglobin ↓O2, ↑CO2, Respiratory acidosis Normal CO-oximetry Diffuse opacities Pulmonary infiltration Pulmonary function testing Bronchoscopy Cough, Hoarseness, Hemoptysis, Headache, Fainting
Cold exposure[54] + – +/- – – – – Normal Leukopenia, ↑RBC ↓O2, ↑CO2, Metabolic acidosis Hypokalemia, Hypocalcemia Hyperglycemia, ↑CK Normal Normal – Clinical findings Confusion, Tachycardia/Bradycardia, Coma

References

  1. ↑ Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  2. ↑ Abdallah C (2012). “Acute epiglottitis: Trends, diagnosis and management”. Saudi J Anaesth. 6 (3): 279–81. doi:10.4103/1658-354X.101222. PMC 3498669. PMID 23162404.
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  45. ↑ Ashurst J, Wasson M (July 2011). “Methemoglobinemia: a systematic review of the pathophysiology, detection, and treatment”. Del Med J. 83 (7): 203–8. PMID 21954509.
  46. ↑ Spivak JL (February 2002). “The optimal management of polycythaemia vera”. Br. J. Haematol. 116 (2): 243–54. PMID 11841424.
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  52. ↑ Hotchkiss RS, Moldawer LL, Opal SM, Reinhart K, Turnbull IR, Vincent JL (2016). “Sepsis and septic shock”. Nat Rev Dis Primers. 2: 16045. doi:10.1038/nrdp.2016.45. PMC 5538252. PMID 28117397.
  53. ↑ Rehberg S, Maybauer MO, Enkhbaatar P, Maybauer DM, Yamamoto Y, Traber DL (2009). “Pathophysiology, management and treatment of smoke inhalation injury”. Expert Rev Respir Med. 3 (3): 283–297. doi:10.1586/ERS.09.21. PMC 2722076. PMID 20161170.
  54. ↑ Marriott, Bernadette (1996). Nutritional needs in cold and in high-altitude environments : applications for military personnel in field operations. Washington, D.C: National Academy Press. ISBN 0-309-05484-2.
Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]

Overview

Cyanosis is the sign of underlying disease. Risk factors related to the presence of underlying conditions should be noticed. Common risk factors in the development of congenital heart diseases with the right to left shunt include maternal age >35 years, No intake of the multivitamin, febrile illness in the first trimester, obesity, paternal age> 25 years.

Risk Factors

The risk factors for cyanosis include:


References

  1. ↑ Blumenthal I (June 2001). “Carbon monoxide poisoning”. J R Soc Med. 94 (6): 270–2. PMC 1281520. PMID 11387414.
  2. ↑ Dueñas-Laita A, Burillo Putze G, Alonso JR, Bajo A, Climent B, Corral E, Felices F, Ferrer A, Hernández Frutos MP, Nogué S, Puiguriguer J (December 2010). “[Basis for the clinical management of fire smoke poisoning “Docohumo Madrid 2010″]”. Med Intensiva (in Spanish; Castilian). 34 (9): 609–19. doi:10.1016/j.medin.2010.07.007. PMID 21051109.
  3. ↑ Zoorob RJ, Campbell JS (November 2003). “Acute dyspnea in the office”. Am Fam Physician. 68 (9): 1803–10. PMID 14620600.
  4. ↑ Ranjit MS (March 2000). “Cardiac abnormalities in birth asphyxia”. Indian J Pediatr. 67 (3 Suppl): S26–9. PMID 11129917.
  5. ↑ Kondamudi NP, Dulebohn SC. PMID 28722923. Missing or empty |title= (help)
  6. ↑ Kondamudi NP, Virji M. PMID 28722926. Missing or empty |title= (help)
  7. ↑ Choi WI (March 2014). “Pneumothorax”. Tuberc Respir Dis (Seoul). 76 (3): 99–104. doi:10.4046/trd.2014.76.3.99. PMC 3982243. PMID 24734096.
  8. ↑ FRASER RS, SPROULE BJ, DVORKIN J (December 1963). “HYPOVENTILATION, CYANOSIS AND POLYCYTHEMIA IN A THIN MAN”. Can Med Assoc J. 89: 1178–82. PMC 1922100. PMID 14091905.
  9. ↑ Garvey C, Ortiz G (2012). “Exacerbations of chronic obstructive pulmonary disease”. Open Nurs J. 6: 13–9. doi:10.2174/1874434601206010013. PMC 3282915. PMID 22393337.
  10. ↑ Wang RF, Hung TY, Chong CF, Wang TL, Chen CC (February 2008). “Central cyanosis due to severe pulmonary hypertension combined with pericarditis as the initial manifestation of systemic lupus erythematosus”. Am J Emerg Med. 26 (2): 248.e1–2. doi:10.1016/j.ajem.2007.04.007. PMID 18272123.
  11. ↑ Grech V, Goldman A (November 2001). “Acute respiratory distress syndrome due to cyanotic spell in an infant with tetralogy of Fallot”. Pediatr. Pulmonol. 32 (5): 406–7. PMID 11596167.
  12. ↑ Kosacka M, Brzecka A, Jankowska R, Lewczuk J, Mroczek E, Weryńska B (2009). “[Combined pulmonary fibrosis and emphysema – case report and literature review]”. Pneumonol Alergol Pol (in Polish). 77 (2): 205–10. PMID 19462358.
  13. ↑ Stadie WC (September 1919). “THE OXYGEN OF THE ARTERIAL AND VENOUS BLOOD IN PNEUMONIA AND ITS RELATION TO CYANOSIS”. J. Exp. Med. 30 (3): 215–40. PMC 2126679. PMID 19868355.
  14. ↑ Muhe L (1996). “Managing pneumonia”. Child Health Dialogue (3–4): 13. PMID 12292168.
  15. ↑ Angerio AD, Kot PA (November 1994). “Pathophysiology of pulmonary edema”. Crit Care Nurs Q. 17 (3): 21–6. PMID 8000933.
  16. ↑ Martins P, Castela E (October 2008). “Transposition of the great arteries”. Orphanet J Rare Dis. 3: 27. doi:10.1186/1750-1172-3-27. PMC 2577629. PMID 18851735.
  17. ↑ POTTS WJ (February 1953). “[Congenital heart disease cyanotic children]”. Calif Med (in Undetermined). 78 (2): 101–3. PMC 1521678. PMID 13019603.
  18. ↑ Just-Viera JO, Norwood T, Yeager GH (April 1967). “Importance of shock and cyanosis in pulmonary embolism”. Ann. Surg. 165 (4): 528–35. PMC 1617449. PMID 6021453.
  19. ↑ Whelan JF (May 1984). “Methemoglobin as a cause of cyanosis”. Can Med Assoc J. 130 (10): 1260. PMC 1483499. PMID 6722683.
  20. ↑ George A, Goetz D (2017). “A case of sulfhemoglobinemia in a child with chronic constipation”. Respir Med Case Rep. 21: 21–24. doi:10.1016/j.rmcr.2017.03.009. PMC 5358970. PMID 28348950.
  21. ↑ Engelhart M, Seibold JR (June 1990). “Cyanosis and Raynaud’s phenomenon: the relation to underlying disease and venous abnormalities”. Angiology. 41 (6): 432–8. doi:10.1177/000331979004100603. PMID 2375536.
  22. ↑ Weatherald J, Marrie TJ (May 2008). “Pseudocyanosis: drug-induced skin hyperpigmentation can mimic cyanosis”. Am. J. Med. 121 (5): 385–6. doi:10.1016/j.amjmed.2008.01.029. PMID 18456031.
  23. ↑ Hess W, Eberlein HJ, Pöthe H (March 1983). “[Cyanosis as a result of drug-induced methemoglobinemia. A case report]”. Anaesthesist (in German). 32 (3): 124–6. PMID 6859496.
  24. ↑ Peng T, Hu Z, Yang X, Gao Y, Ma C (February 2018). “Nitrite-induced acute kidney injury with secondary hyperparathyroidism: Case report and literature review”. Medicine (Baltimore). 97 (8): e9889. doi:10.1097/MD.0000000000009889. PMID 29465577.
  25. ↑ Jensen JD, Vincent AL. PMID 28613569. Missing or empty |title= (help)
  26. ↑ Busardò FP, Frati P, Zaami S, Fineschi V (March 2015). “Amniotic fluid embolism pathophysiology suggests the new diagnostic armamentarium: β-tryptase and complement fractions C3-C4 are the indispensable working tools”. Int J Mol Sci. 16 (3): 6557–70. doi:10.3390/ijms16036557. PMC 4394548. PMID 25807263.
  27. ↑ Hifumi T, Sakai A, Kondo Y, Yamamoto A, Morine N, Ato M, Shibayama K, Umezawa K, Kiriu N, Kato H, Koido Y, Inoue J, Kawakita K, Kuroda Y (2015). “Venomous snake bites: clinical diagnosis and treatment”. J Intensive Care. 3 (1): 16. doi:10.1186/s40560-015-0081-8. PMC 4393627. PMID 25866646.
  28. ↑ Lepper PM, Ott SR, Hoppe H, Schumann C, Stammberger U, Bugalho A, Frese S, Schmücking M, Blumstein NM, Diehm N, Bals R, Hamacher J (May 2011). “Superior vena cava syndrome in thoracic malignancies”. Respir Care. 56 (5): 653–66. doi:10.4187/respcare.00947. PMID 21276318.
Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]

Overview

Prenatal echocardiography and genetic testing are useful methods for early detection of cyanotic congenital heart disease.Postnatal pulse oximetry is recommended for diagnosis of cyanotic congenital heart disease

Screening

References

  1. ↑ Liu, Xiwang; Xu, Weize; Yu, Jiangen; Shu, Qiang (2019). “Screening for congenital heart defects: diversified strategies in current China”. World Journal of Pediatric Surgery. 2 (1): e000051. doi:10.1136/wjps-2019-000051. ISSN 2516-5410.
Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]

Overview

Central cyanosis in the first hours or days of life in the neonate may happen and implies life-threatening conditions such as congenital cardiac abnormalities , airway obstruction , central nervous system problem, hemoglobinopathy. Peripheral cyanosis may happen in neonate called acrocyanosis. If the underlying causes of cyanosis are found and treated, the prognosis is generally good.

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

  • Prognosis is generally good and dependent on the diagnosis and treatment of underlying causes.
  • The 10-year survival rate of children with severe congenital heart disease is approximately 90%.

References

  1. ↑ Sasidharan P (August 2004). “An approach to diagnosis and management of cyanosis and tachypnea in term infants”. Pediatr Clin North Am. 51 (4): 999–1021, ix. doi:10.1016/j.pcl.2004.03.010. PMID 15275985.
Diagnosis

Diagnosis

Diagnostic Study of Chocie | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | Echocardiography or Ultrasound | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case #1

Case #1


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