Intracranial Hemorrhage: A Case Study

According to Teleanu and Constantinescu (2014), spontaneous intracerebral hemorrhage can occur from sudden small vessel bleeding secondary to hypertension or angiopathy, which is called primary spontaneous intracerebral hemorrhage, or from arteriovenous malformations, coagulopathies, vasculitis, tumors, or trauma, which is called secondary spontaneous intracerebral hemorrhage. The recommended treatment plan for patients with an intracranial hemorrhage includes blood pressure management, increased intracranial pressure management, seizure prevention and management, and, depending on the severity and location of the hemorrhage, surgery (Teleanu & Constantinescu, 2014). Other complications the nurse practitioner should be aware of for patients
with intracranial hemorrhage includes an expansion of the bleeding, cerebral edema around the hemorrhage site, hydrocephalus, coagulopathies, hyperglycemia, fever, and infection (Balami & Buchan, 2012). In fact, according to Balami and Buchan (2012), patients with bleeding expansion, hydrocephalus, and focal cerebral edema have an increased risk for poor outcomes with neurological decline.
For those with a systolic blood pressure greater than 180 mmHg, the goal for blood pressure management should be a systolic blood pressure of 160 mmHg. However, if the patient has increased intracranial pressure and a systolic blood pressure at least 180 mmHg, then the blood pressure should be lowered to reach a cerebral perfusion pressure 61 to 80 mmHg. One should be aware that some medications that lower systemic blood pressure can actually increase cerebral perfusion, which could further increase intracranial pressure. Teleanu and Constantinescu (2014) suggest using short acting alpha and beta blocking agents, such as labetalol, or vasodilators like hydralazine. Angiotensin-converting-enzyme inhibitors and calcium channel blockers are also appropriate choices for blood pressure management in this cohort. Venous vasodilators should not be used, for they will increase intracranial pressure. Increased intracranial pressures can be managed by elevating the head of bed to 30 degrees and intravenous sedatives and analgesics. If the patient has a Glasgow Coma Scale score of less than 8, have symptoms of herniation, large intraventricular
hemorrhage, or hydrocephalus, invasive monitoring is recommended. Intracranial pressure should be no more than 20 mmHg, and if it is higher than 20, then mannitol should be administered. Hyperventilation via mechanical ventilation can also reduce the PaCO2 to 25-30 mmHg which can reduce a high intracranial pressure temporally. Other options to reduce intracranial pressure include a ventriculostomy drain, which drains cerebrospinal fluid to reduce the pressure, paralytics, or a craniectomy to alleviate the pressure. Intravenous anticonvulsants should be administered prophylactically to prevent seizure activity secondary to neuron irritability from the hemorrhage (Teleanu & Constantinescu, 2014). With these recommendations, the nurse practitioner can prevent complications associated with increased intracranial pressure, such as brain stem herniation, and complications associated with hypertension, such as an increase in the hemorrhagic space or another hemorrhage in a different location. Seizure prevention, infection prevention, and glycemic control are also important in the comprehensive care for the patient with intracerebral hemorrhage.