Cyanosis natural history, complications and prognosis: Difference between revisions

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Latest revision as of 20:16, 29 January 2021

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

The symptoms of neonatal cyanosis usually develop in the first hours or days of life.^[1]
Acrocyanosis or peripheral cyanosis is a physiologic finding limited to extremities and caused by slowing flow through the peripheral capillary bed and large difference between arteriovenous oxygen content.
The symptoms of central cyanosis is presentation as bluish of mucous membranes and tongue.
Early clinical features related to central cyanosis include severe respiratory distress, tachycardia, tachypnea, apnea and need to immediate evaluation.
Central cyanosis implies life-threatening condition in neonate such as congenital cardiac abnormalities , airway obstruction , central nerve system problem, hemoglobinopathy.

Complications

Common complications of the underlying causes of central cyanosis in neonate include airway obstruction, hyporventilation due to CNS disease or apnea and circulatory collapse.

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

↑ 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.

[pmid15275985-1] 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.

[1]

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 {{Cyanosis}}
-{{CMG}}; {{AE}}
+{{CMG}}; {{AE}} {{Sara.Zand}}
 ==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===
-*The symptoms of neonatal cyanosis usually develop in the first few weeks of life and start with symptoms such as [[acrocyanosis]].
+*The symptoms of neonatal cyanosis usually develop in the first hours or days of life.<ref name="pmid15275985">{{cite journal |vauthors=Sasidharan P |title=An approach to diagnosis and management of cyanosis and tachypnea in term infants |journal=Pediatr Clin North Am |volume=51 |issue=4 |pages=999–1021, ix |date=August 2004 |pmid=15275985 |doi=10.1016/j.pcl.2004.03.010 |url=}}</ref>
-* [[Acrocyanosis]] or [[peripheral cyanosis]] is a physiologic finding limited to extremities and causes by slowing flow through the peripheral capillary bed and large difference between arteriovenous [[oxygen]] content.
+* [[Acrocyanosis]] or [[peripheral cyanosis]] is a physiologic finding limited to extremities and caused by slowing flow through the [[peripheral capillary bed]] and large difference between arteriovenous [[oxygen]] content.
-* The [[symptoms]] of [[Central cyanosis]] is present in [[mucous membranes]] and [[tongue]].
+* The [[symptoms]] of [[central cyanosis]] is presentation as bluish of [[mucous membranes]] and [[tongue]].
-* Early clinical features include severe [[respiratory distress]], [[tachycardia]], [[tachypnea]] and need to immediate evaluation.
+* Early clinical features related to [[central cyanosis]] include severe [[respiratory distress]], [[tachycardia]], [[tachypnea]], [[apnea]] and need to immediate evaluation.
-*[[Central cyanosis]] implies  life threatening condition in neonate such as [[cardiac]], [[respiratory system]], [[central nerve system]], [[hemoglobinopathy]].
+*[[Central cyanosis]] implies  life-threatening condition in neonate such as [[ congenital cardiac abnormalities ]], [[ airway obstruction ]], [[central nerve system problem]], [[hemoglobinopathy]].
 ===Complications===
+*Common complications of the underlying causes of  [[central cyanosis]] in neonate include [[airway obstruction]], [[hyporventilation]] due to [[CNS]] disease or [[apnea]] and [[circulatory collapse]].
 ===Prognosis===
-*Most infants with critical CHD are diagnosed either prenatally or upon clinical examination during the birth hospitalization. However, up to 30 percent of infants with critical CHD appear normal on routine examination and signs of critical CHD may not be apparent in the first days of life [15,16]. Cyanosis may not be clinically apparent in patients with mild desaturation (>80 percent saturation) or anemia [17]. In darkly pigmented infants, cyanosis can be especially difficult to appreciate. (See "Identifying newborns with critical congenital heart disease", section on 'Postnatal diagnosis'.) The timing of presentation varies with the underlying lesion and its dependence upon a patent ductus arteriosus (PDA). In patients with ductal-dependent lesions (table 1), closure of the PDA within the first few days of life can precipitate rapid clinical deterioration with potentially life-threatening consequences (ie, severe metabolic acidosis, seizures, cardiogenic shock, cardiac arrest, or end-organ injury) [18]. Other patients may have lesions that are not dependent on the patency of the PDA (eg, total anomalous pulmonary venous return, truncus arteriosus), yet delayed diagnosis can similarly lead to poor outcomes. For infants with critical CHD who are not diagnosed during the birth hospitalization, the risk of mortality is as high as 30 percent [9,11,19].  In a population-based observational study of 3603 infants with critical CHD born in 1998 to 2007 (prior to institution of routine pulse oximetry screening) identified through a state Birth Defects Registry, about one-quarter of patients were not diagnosed during the birth hospitalization [20]. In this group of late detected critical CHD (n = 825), 15 deaths were deemed to be potentially preventable (1.8 percent). In addition, adjusted multivariable analysis showed that infants with late detected critical CHD had a greater number of admissions, more hospitalized days, and higher inpatient costs than those diagnosed prenatally or during the birth hospitalization.  In a simulation model based upon estimates of birth prevalence, prenatal diagnosis rates, late detection rates, and sensitivity of pulse oximetry screening, one study estimated that 875 infants with critical CHD will be detected annually in the United States through newborn screening [16]. An additional 880 false-negative screenings are expected.
+*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==
 {{Reflist|2}}
+[[Category:Primary care]]
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+[[Category:Up-To-Date]]
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