Cyanosis medical therapy

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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] Mohammed Abdelwahed M.D [3]

Overview[edit | edit source]

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 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.

Medical therapy[edit | edit source]

The mainstay of therapy for cyanosis is the treatment of underlying causes of cyanosis.
In cyanotic congenital heart disease whether the flow is dependent on patency ductus arteriosus, infusion of prostaglandin E1 is recommended.
In the setting of pulmonary disease such as pneumonia, pleural effusion, treatment of underlying disease and oxygen therapy are advised.
In the setting of low cardiac output state such as pulmonary thromboembolism and cardiogenic shock, management of thrombotic events and oxygen supplement therapy is recommended.
In methemoglobinemia discontinuing the medications related disorder and administration of methylene blue is recommended.

Medical therapy of Cyanosis[edit | edit source]

The mainstay of therapy is treatment of underlying causes of cyanosis.^[1] ^[2]^[3]^[4]^[5]^[6]

Abbreviations: d-TGA: dextro-Transposition of great arteries; PDA: Patent ductus arteriosus ; ASD: Atrial septal defect; VSD: Ventricular septal defect; TOF: Tetralogy of fallot; CHD: Congenital heart disease; PS: Pulmonary stenosis; PTE: Pulmonary thromboembolism; AS: Aortic stenosis; ARDS: Acute respiratory distress syndrome; PFO: Patent foramen ovale; PVR: Pulmonary vascular resistance; SpO2: Peripheral capillary oxygen saturation.; FiO2: Fraction of inspired oxygen; PEEP: Positive end-expiratory pressure;

Causes of cyanosis	CHD with severe restriction of pulmonary blood flow	CHD with severe restriction of systemic blood flow	CHD due to bidirectional shunt	Methemoglobinemia	PTE	Cardiogenic shock	ARDS	Acute mountain sickness
Note	Pulmonary atresia Tricuspid atresia Tetralogy of Fallot with pulmonary atresia	Severe AS Coarctation aorta Interrupted aortic arch Hypoplastic left heart syndrome	TGA Truncus arteriosus Double outlet right ventricle	Complication of exposue to some drugs such as nitrites and aniline leading to dizziness , coma, chocolate-brown discoloration of blood samples, respiratory distress seizures and myocardial ischemia	Hypoxia due to V/Q mismatch, low cardiac out-put state, acute right ventricular dilation and increased pulmonary vascular resistance	Cyanosis, olyguria, altered mental status	SpO2/FiO2 <315, No PEEP requirement Complication of pneumonia, non cardiogenic shock, drug overdose, trauma	Leakage of large molecules into alveolar space leading rich protein pulmonary edema
Mechanism of cyanosis	Hypoxia and cyanosis due to constriction of the ductus arteriosus after birth and dependency of the Pulmonary circulation on the patency of the ductus arteriosus	Cyanosis,systemic hypoperfusion, circulatory collapse, metabolic acidosis, shock due to constriction ductus arteriosus and dependency systemic circulation on PDA after birth	Constriction of PDA after birth leading decreased systemic circulation due to mixing of pulmonary and systemic blood flow via PDA	Oxidative sresss , methemoglobin level > 10 % total hemoglobin Cyanosis refractory to oxygen therapy,	V/Q mismatches due to small airway constriction in both nonperfused and nonembolized areas of lung, reduced surfactant production, pulmonary edema, atelectasis Right to left shunt via PFO leading central cyanosis Low cardiac output state due to right ventricular dilation and increased PVR leading to peripheral cyanosia	Low cardiac output state due to myocardial infarction and pump failure leading to vasoconstriction and peripheral cyanosis	Increased alveolar vascular permeability Interstitial and alveolar pulmonary edema	Central cyanosis due to alveolar hypoxia , pulmonary vasoconstriction, pulmonary hypertension
Treatment	Prostaglandin E1	Prostaglandin E1	Prostaglandin E1	Methylenblue infusion Hyperbaric oxygen therapy Ascorbi:c acid	Anticoagulant therapy Fibrinolytic therapy in case of collapse and shock Mechanical thrombectomy	Coronary revascularization	Extracorporeal membrane oxygenation High-frequency oscillatory ventilation Neuromuscular blocking agents Intravenous β-2 agonist (Salbutamol)	Descent Supplement oxygen therapy Portable hyperbaric chamber Nifedipine

References[edit | edit source]

↑ Cucerea, Manuela; Simon, Marta; Moldovan, Elena; Ungureanu, Marcela; Marian, Raluca; Suciu, Laura (2016). "Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit". The Journal of Critical Care Medicine. 2 (4): 185–191. doi:10.1515/jccm-2016-0031. ISSN 2393-1817.
↑ Henretig, Fred M.; Gribetz, Bruce; Kearney, Thomas; Lacouture, Peter; Loveiov, Frederick H. (2011). "Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia". Journal of Toxicology: Clinical Toxicology. 26 (5–6): 293–301. doi:10.1080/15563658809167094. ISSN 0731-3810.
↑ Tisi, G M; Wolfe, W G; Fallat, R J; Nadel, J A (1970). "Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion". Journal of Applied Physiology. 28 (5): 570–573. doi:10.1152/jappl.1970.28.5.570. ISSN 8750-7587.
↑ Austin, John H. M. (1973). "Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs". Investigative Radiology. 8 (5): 315–321. doi:10.1097/00004424-197309000-00003. ISSN 0020-9996.
↑ . doi:10.1164/rccm.201503-0584OC. Check |doi= value (help). Missing or empty |title= (help)
↑ Smedley, Tom; Grocott, Michael PW (2013). "Acute high-altitude illness: a clinically orientated review". British Journal of Pain. 7 (2): 85–94. doi:10.1177/2049463713489539. ISSN 2049-4637.

[CucereaSimon2016-1] Cucerea, Manuela; Simon, Marta; Moldovan, Elena; Ungureanu, Marcela; Marian, Raluca; Suciu, Laura (2016). "Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit". The Journal of Critical Care Medicine. 2 (4): 185–191. doi:10.1515/jccm-2016-0031. ISSN 2393-1817.

[HenretigGribetz2011-2] Henretig, Fred M.; Gribetz, Bruce; Kearney, Thomas; Lacouture, Peter; Loveiov, Frederick H. (2011). "Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia". Journal of Toxicology: Clinical Toxicology. 26 (5–6): 293–301. doi:10.1080/15563658809167094. ISSN 0731-3810.

[TisiWolfe1970-3] Tisi, G M; Wolfe, W G; Fallat, R J; Nadel, J A (1970). "Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion". Journal of Applied Physiology. 28 (5): 570–573. doi:10.1152/jappl.1970.28.5.570. ISSN 8750-7587.

[Austin1973-4] Austin, John H. M. (1973). "Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs". Investigative Radiology. 8 (5): 315–321. doi:10.1097/00004424-197309000-00003. ISSN 0020-9996.

[5] . doi:10.1164/rccm.201503-0584OC. Check |doi= value (help). Missing or empty |title= (help)

[SmedleyGrocott2013-6] Smedley, Tom; Grocott, Michael PW (2013). "Acute high-altitude illness: a clinically orientated review". British Journal of Pain. 7 (2): 85–94. doi:10.1177/2049463713489539. ISSN 2049-4637.

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