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Pulmonary Pathology Online

Complications of Neonatal Respiratory Distress Syndrome

Dr Sampurna Roy MD

 

                                                                                                                      

 

Infants who recover are at risk for developing :

(i) Retinopathy of prematurity ;

(ii) Retrolental fibroplasias, and

(iii) Bronchopulmonary dysplasia as a direct consequence of high-concentration oxygen therapy.

Infants are also at risk for developing-

(iv) Patent ductus arteriosus ;

(v) Intraventricular hemorrhage ;

(vi) Necrotizing enterocolitis.

 

Major complications of the idiopathic respiratory distress syndrome of the neonate are intraventricular cerebral hemorrhage, persistence of the patent ductus arteriosus  and necrotizing enterocolitis.

These pathologic changes are consequences of anoxia, hypercapnea and acidosis.

Periventricular germinal matrix :  The periventricular germinal matrix in the brain is especially susceptible to injury in neonates with respiratory distress.

Dilated thin-walled veins in this area rupture rupture easily, leading to extravasation of blood into the brain and destruction of nerve cells.

Hematocephalus : Bleeding often extends into the ventricles and causes hematocephalus.

Factors invoked to explain the pathogenesis of this injury include:

(i) the lack of connective support of the germinal matrix blood vessels, 

(ii) impaired vascular autoregulation, hypoxia leading to venous sludging

(iii) thrombosis, and direct injury to periventricular capillaries, and

(iv) increased fibrinolytic activity in the fetal brain that allows the formation of large hematomas.

None of these theories provides a full explanation for the occurrence of this complication.

The clinical diagnosis may be suspected on the basis of an acute onset of hypotension, acidosis, flaccidity, hypoventilation, and a sudden drop in hematocrit in an otherwise stable infant.

The mortality of intracerebral and intraventricular hemorrhage exceeds 50%.

However, this serious complication is not invariably lethal, and many children recover without significant neurologic deficits.

Posthemorrhagic hydrocephalus is found in 20% of survivors.

Persistence of the ductus arteriosus is a serious consequence of the respiratory distress syndrome that is due to the partial preservation of the fetal circulation.

Blood is shunted from right to left through the foramen ovale and the ductus, thus bypassing the lungs.

In many neonates who survive the syndrome, the ductus remains patent.

Circulatory recovery reverses the shunt and forces blood from the arterial side into the pulmonary circulation.

Pulmonary congestion and right-sided heart failure may ensue and are clinically apparent in almost one-third of all infants recovering from the respiratory distress syndrome.

Necrotizing enterocolitis, a less common but serious complication, is the most common acquired gastrointestinal emergency in neonates.

The pathogenesis of this condition is not fully understood.

It has been suggested that the lesion is initiated by anoxic necrosis of intestinal mucosal cells, leading to ulceration, perforation, and finally peritonitis.

Bacterial infection is always evident but is thought to be superimposed on the initial injury caused by anoxia.

Necrotizing enterocolitis occurs in neonates who have been fed formula fluids.

It is thought that various components or the hypertonicity of the formulas may potentiate the effects of ischemia and facilitate bacterial overgrowth.

Penetrating ulcers are usually localized to the ileum and caecum.

                                                                  

Bronchopulmonary dysplasia is a late complication of the respiratory distress syndrome that usually occurs in infants who weigh less than 1500g and were maintained on a respirator for more than 6 days.

Radiographically the lungs show focal emphysema  and atelectasis .

Exudative inflammation in the alveoli leads to the formation of granulation tissue, which progresses to fibrosis.

In final stages the lungs show focal fibrosis and bullous emphysema.

Pulmonary Hypertension and eventually cor pulmonale develop.

In order to prevent bronchopulmonary dysplasia, respirator treatment should be as short as possible, and attempts to close the patent ductus arteriosus should be made.

Despite precautions, bronchopulmonary dysplasia will develop in some infants.

 

 

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

 

 


 

 

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