Symptoms and treatment of pediatric cerebral edema and intracranial hypertension syndrome

  Intracranial hypertension syndrome is a series of clinical manifestations due to increased brain volume and weight caused by increased fluid in the brain parenchyma. In pathology, the accumulation of free fluid in the interstitial space of brain cells is called cerebral edema, while the increase of fluid in brain cells is called cerebral swelling, but in actual clinical work it is difficult to distinguish between the two, or they are different stages of the same pathological process, and often co-exist at a later stage, so they are often collectively referred to as cerebral edema.  I. Symptoms and signs of pediatric cerebral edema and intracranial hypertension syndrome 1. Main symptoms and signs Irregular breathing: Because the development of the central nervous system in children is still immature, brainstem compression can cause irregular respiratory rhythm, pause, sigh-like breathing, double inspiratory breathing, and tidal breathing. It is mostly a prodromal symptom of brain herniation, often suggesting central respiratory failure and brainstem compression.  Hypertension: elevated blood pressure is a compensatory pressor response of the vasomotor center of the medulla oblongata, also called Cushing’s response. It is commonly seen in intracranial hypertension due to traumatic brain injury.  Neuropapillary edema: It is the main clinical manifestation of chronic intracranial hypertension, which is caused by obstruction of venous reflux in the fundus. In children, it is mostly acute intracranial hypertension, so it is less common clinically.  Pupillary changes: It is an important sign of pediatric intracranial hypertension. The pupils may be bilaterally unequal in size, large or small, and irregular in shape. It often indicates the imminent occurrence of brain herniation.  Tight or bulging fontanelle: Intracranial hypertension in newborns is often manifested by tight or bulging fontanelle, cracked bones, increased head circumference, angry superficial veins on the head and face, positive pot-breaking sounds and other signs, which are related to the fact that the bones of the skull have not yet completely closed, and the bones of the skull are soft and have a certain degree of elasticity. This kind of compensatory mechanism often makes the early symptoms atypical.  2. Secondary signs Coma: Children with cerebral edema have varying degrees of impaired consciousness. When only the cerebral cortex is involved, the child shows only mild impairment of consciousness; when both the cerebral cortex and the reticular formation are involved, the child shows severe coma. In general, vasogenic cerebral edema is mildly impaired, while cytotoxic cerebral edema is more severe.  Myotonia changes and convulsions: Intracranial hypertension compression of the brainstem, basal ganglia, cerebral cortex and certain extrapyramidal tracts of the cerebellum can cause a significant increase in myotonia. Most of the symptoms are paroxysmal or persistent internal rotation of upper limbs, extensional tonicity of lower limbs, and sometimes extensional spasm or coracoacusis; all of the above are manifestations of detrusor tonicity.  Jet vomiting: cranial hypertension stimulates the vomiting center at the base of the fourth ventricle and the medulla oblongata and causes jet vomiting, rarely nausea, not related to diet, heavier in the early morning, but jet-like vomiting is less common in clinical practice, often not significantly different from vomiting caused by other diseases.  Headache: caused by pressure on the meninges, blood vessels or nerves involved and inflammatory changes stimulating the nerves. Children with increased intracranial pressure tend to have headaches, often diffuse and nonspecific, which can be aggravated by coughing, straining during defecation, and changes in head position. Younger infants present with irritability, screaming and crying.  The diagnosis can be made by having one major sign and two minor signs.  Treatment Treatment of pediatric cranial hypertension should take comprehensive measures, must be closely guarded, closely observe changes in the condition, while actively treating the original disease, timely and reasonable control of cerebral edema to prevent the formation of brain herniation. Since the most common cause of pediatric cranial hypertension is cerebral edema, treatment is mainly aimed at cerebral edema.  1.General treatment and care The child must rest quietly in bed, and if necessary, sedatives can be used to avoid agitation, coughing and sputum blockage to prevent sudden increase of cranial pressure. The head and shoulders should be elevated 20°~30° when lying in bed to facilitate intracranial blood reflux; when there are prodromal symptoms of brain herniation, the flat position is appropriate; it is also believed that the lateral position of the child can avoid airway obstruction. Do not turn the child’s head, turn over or press on the abdomen and liver during examination or treatment.  Actively correct hypoxia, hypercapnia, electrolyte disturbances and metabolic acidosis. Normal blood pressure and body temperature should also be maintained. Pay attention to eye, ear, mouth, nose and skin care for comatose children to prevent exposure keratitis, otitis media, stomatitis, aspiration pneumonia and bed sores.  2, etiological treatment Removing the cause and stopping the development of lesions is the fundamental measure for treating this disease. Such as anti-infection, correct shock and hypoxia, improve ventilation, prevent carbon dioxide retention, remove intracranial occupying lesions, etc.  3, drug therapy The first-line drugs for the treatment of pediatric acute cerebral edema are currently recognized as mannitol, dexamethasone and furosemide (tachyphylaxis).