Hematoma intraparenchimatos

Hematoma intraparenchimatos Intraparenchimatos hematoma develops in the parenchyma of the cerebral hemispheres as a result of head trauma. The hematoma is characterized by a restricted blood spilled, located in the white matter of cerebral hemispheres. Contents hematoma is the blood clot and a small amount of liquid blood. Source of bleeding is usually venous nature and rarely result from a ruptured artery. Cerebral hematoma appears in an isolated context, it is associated with other traumatic injuries as fractures and contusions. This type of hematoma is a lower frequency than other types of intracranial hematomas. Causes Conditions that can lead to a hematoma intraparenchimatos are multiple, from cranio-cerebral trauma to flare-ups hypertensive cerebral aneurysm rupture or rupture of a cerebral vascular malformation and even bleeding from the primary or metastatic brain tumors. Risk factors are favoring hypertension, diabetes mellitus, or aspirin treatment trombostop abusive consumption of cigarettes, alcohol, drugs.
Intraparenchimatos hematoma formation mechanism consists of three ways: - Rupture of a cerebral vessel arterial or venous nature (most common vein) following a traumatic event. - After a head trauma microhemoragii outbreaks can occur. These outbreaks may conflict and result in a hematoma intraparenchimatos. - Intraparenchimatos hematoma can occur after brain dilacerarii, evolving either from rupture of a cerebral vessel, or hemorrhagic foci of the confluence.
Headquarters intraparenchimatos hematoma is usually temporal or fronto-temporal region. In evolution, this type of hematoma tends to expand. If the bleeding does not close source, increase in hematoma volume by pressing on surrounding structures, creating a mass effect. Sometimes it happens that the component of blood to flood the lateral ventricles hematoma or subdural space, with adverse consequences and prognosis. In terms of pathology, intraparenchimatos hematoma consists of blood clots and gelatinous consistency and integrity of blood lactate. In the case of a subacute hematoma intraparenchimatos, its structure is represented mainly by blood clots.
Clinical There are several ways to onset of symptoms. The onset may be abrupt, immediately after trauma, manifesting in a comatose state and hemiplegia. Or may occur after a period of several days, in which case disturbances associated with hemiplegia and focal intracranial hypertension. Based outbreak disorders depend on the hematoma, thus being able to meet language disorders, sensitivity problems, mental disorders, hemianopsia. Clinical manifestations depend on the intensity of the trauma that caused the hematoma, bleeding and mechanism of brain lesions associated. Craniocerebral trauma which produces an intraparenchimatos hematoma is usually moderate or high. For mild injuries, usually do not develop intraparenchimatoase hematoma. Outbreaks occur immediately after the injury bleeding in brain parenchyma, smaller or larger, confluence or to produce a intraparenchimatoasa massive bleeding from the very beginning. After producing injury, the immediate symptoms of the clinical evidence is dominated by contusion. Hematoma evolution depends on many factors: the flow of bleeding, type of vessel injured, head injury. Thus, after a certain time (several hours or several days, depending on the speed of evolution of the hematoma), the compressive phenomena occurs hematoma and perifocal edema develops. The effect of weight you carry (around nerve compression) is a profound alteration of consciousness with the entry into coma in severe cases and nedispensarizate on time. Then develop autonomic disorders and focal neurological signs appear. If surgical intervention was not in time, will show signs of impairment of the brainstem and exitus. There are several forms of clinical manifestation of intraparenchimatos hematoma. In the acute form, the outcome is very fast, consciousness begins to alter a few minutes or hours after the causal injury. Vegetative disorders and neurological signs of outbreaks, also early. Subacute form has a slower evolution as the acute form. From production to injury and impaired consciousness may take several days, usually 3-10 days. After this time it alters consciousness suddenly. In the chronic form of evolution covers a long period of time from production to injury and impaired consciousness can be of three weeks. Altered consciousness is slower in this case.
Diagnostic Laboratory Diagnosis is on account of certain brain imaging examination, represented by CT, which identifies the hematoma as a high density area. Additional tests must be carried out to identify factors favoring: Doppler examination and cross examination for carotid and vertebral arteries to identify ateromatoase disease. Atherosclerotic vascular disease can lead to cerebral vascular wall rupture with hematoma formation intraparenchimatos. It also performs cardiac ultrasound examination and electrocardiography. Haematological examination aims to determine total cholesterol, triglycerides, homocysteine and the coagulation tests.
Treatment Intraparenchimatos hematoma is a surgical emergency. Surgical hematoma evacuation should be done as soon as possible after diagnosis. Any delay may jeopardize the patient's life, and the recovery period will be longer. Neurosurgical intervention involves both hematoma evacuation, and identify the source of bleeding to be sutured. The complexity of surgery and postoperative prognosis depends on the topographic location of the hematoma. If it comes to flooding of the lateral ventricles, the prognosis is usually reserved.
Evolution and prognosis Evolution depends on the size of the hematoma, the lesions, the patient's neurological status. The highest mortality is seen in acute forms if more than one third of patients dying in the first days after hematoma formation. Recovery depends largely on the precocity of treatment discharge of the brain affected and the preoperative condition of the patient. Small hematomas recover in short period. Massive hematoma that large areas of the cerebral hemispheres are interested recovers in months and sometimes years (depending on lot and hemispheric area affected). Some skills will no longer be recovered.