Dr. Sandeep Kadam *
DM, MD, Consultant Neonatologist, KEM Hospital, Pune. *
Cyanosis (from the Greek word meaning "dark blue") is a blue to dusky hue in the newborn. Cyanosis is dependent upon the absolute concentration of the reduced hemoglobin and not on the ratio of reduced hemoglobin to oxyhemoglobin.

Central cyanosis is one, which is present throughout the body, including the mucous membranes and tongue. If cyanosis is limited to the extremities, it is called peripheral cyanosis. Oxygen should be given immediately even before analyzing the cause of cyanosis.
  • Mechanism of Central cyanosis:
  • Hypoventilation
  • Significant right-to-left intracardiac or intrapulmonary shunting
  • Ventilation perfusion mismatch
  • Diffusion impairment
  • Inadequate transport of oxygen by the hemoglobin

Peripheral Cyanosis or Acrocyanosis after delivery is common. It should clear in minutes of birth. Tongue and Mucus membranes are pink.

In Differential cyanosis, lower part of body is blue and upper part is pink, which is seen in PPHN, PDA with reversal of shunt or severe left-sided obstructive lesions such as severe AS, Interrupted Aortic Arch syndrome or Coarctation of Aorta.

In Reverse differential cyanosis, the upper part of the body remains cyanotic while the lower part of the body remains pink and this is seen with transposition of the great vessels with pulmonary hypertension and shunt through PDA, and total anomalous pulmonary venous drainage above the diaphragm with shunt through PDA (higher oxygen content in the right ventricular blood).

The essential problem with methemoglobinemia is caused by the altered heme molecule, which is unable to bind oxygen within the red blood cells, and with the increased affinity of the remaining hemoglobin molecules for oxygen, resulting in decreased oxygen release to the tissues. Infants have a slate-gray cyanotic appearance with no respiratory distress.
Steps In The Management Of Cyanotic Newborns
Chest x-ray films:
Chest x-ray films may reveal pulmonary causes of cyanosis. They can also hint at the presence or absence of cardiac defects and the type of defect.

Arterial blood gases in room air:
Arterial blood gases in room air confirm or reject central cyanosis. An elevated PCO2 suggests pulmonary or central nervous system problems. A low pH may be seen in sepsis, circulatory shock, or severe hypoxemia.

Hyperoxia test:
To differentiate between Cardiac from Pulmonary cause. Oxygen should be administered through a plastic hood (such as an Oxyhood) for at least 10 minutes to replace the alveolar air completely with oxygen. With pulmonary disease, arterial PO2 usually rises to > 150 mm Hg. When there is a significant intracardiac right-to-left shunt, the arterial PO2 does not exceed 100 mm Hg, and the rise is not more than 10 to 30 mm Hg. However in Persistent Pulmonary Hypertension of newborn with a normal heart) PaO2 may not have a rise in arterial PO2 to 100 mm Hg. The purpose of positive hyperoxia test helps in ruling out significant cyanotic congenital heart defect but when negative does not differentiate between cyanotic heart and PPHN.

Pre-ductal and Post-ductal saturations:
This helps in differentiating shunting across the ductus in PPHN. The difference of 10% between right upper limb and lower limbs is significant.

ECG may be helpful in cardiac origin of cyanosis. A PaO2 value in a preductal artery (such as the right radial artery) that is 10 to 15 mm Hg higher than that in a post-ductal artery (an umbilical artery line) suggests a right-to-left ductal shunt.

2D Echocardiography and a Doppler examination:
It will reveal the cause of the central cyanosis

Treatment: Administration of oxygen is the cornerstone in the therapy of cyanotic neonate except in cyanotic congenital heart defects.

If perfusion seems compromised, administer 20 ml/kg of normal saline as an intravenous bolus over 15 minutes. Infants who have respiratory distress should have an orogastric tube and need ventilatory support.

If a ductal-dependant congenital heart disease is suspected (e.g., pulmonary atresia with or without VSD, tricuspid atresia, Hypoplastic left heart syndrome [HLHS], interrupted aortic arch, severe Coarctation), it is advisable to start prostaglandin E-1 infusion at a rate of 0.05 mcg/kg/min. The starting dose is 0.05 to 0.1 mcg/kg per minute, administered in a continuous intravenous drip. Three common side effects of intravenous infusion of prostaglandin E 1 are apnea (12%), fever (14%), and flushing (10%). Antibiotic therapy for sepsis if suspected is initiated.

A systematic approach to the diagnosis, starting with the history, physical examination, work-up (including chest radiograph, EKG, echocardiogram, hyperoxia test) and laboratory tests including blood glucose, calcium, CBC, and septic work-up as indicated, is required.

Management is based on clinical diagnosis and requires initial stabilization, assuring hemodynamic stability, oxygen administration, and either referral to a neonatal intensive care unit or continued care in a Level II nursery.

Prognosis depends on the diagnosis, but is generally good with prompt recognition and intervention. Key message:
  • Early detection of cyanosis in a newborn is crucial and oxygen should be started even before analyzing the cause.
  • With improved technology, neonatal ventilation and good supportive care outcome of babies with cyanosis and respiratory distress has improved.
  • PGE1 should be started in duct-dependent cyanotic congenital heart lesions.
  • Cyanosis with normal or higher PaO2 is seen in Methemoglobinemia. The pulse oximetry may be higher than the true level of oxyhemoglobin.
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