Risk Of Brain Edema Research Articles

Evaluation of the Use of Antihypertensive Agents in Ischemic Stroke Patients Hospitalized in West Nusa Tenggara Hospital, Indonesia

Antihypertensive agents are one of the drugs recommended on ischemic stroke patients as a secondary therapy for prevention of occurrence repeated stroke and reduce the risk of brain edema. If the management of hypertension is incorrect on ischemic stroke patient can worsen the patient's condition and affect mortality. The use of antihypertensive drugs must be evaluated accordingly with rational use of drugs. This study aims to examine the accuracy of the use of antihypertensive drugs in ischemic stroke patients which includes right indication, right patient, right medicine, right dose and right frequency. This research is a cross sectional descriptive study using medical record data of 19 ischemic stroke patients. The inclusion criteria of the study were all ischemic stroke hospitalization patients and receiving antihypertensive drugs therapy. The evaluation of accuracy was done descriptively by comparing research data to the literature which includes JNC VII & VIII, PERDOSSI 2011, PIONAS 2015, FORNAS and Revised RSUDP Formulary 6th. The results showed the accuracy of use antihypertensive agents is 100% that is 100% precise indication; 100% right patient; 100% right dose; and 95% right frequency. The type of inaccuracy encountered is frequency imprecision drug administration, therefore the role of a pharmacist in hospital are needed as part of efforts to improve the accuracy of the use of drugs in ischemic stroke patients.

Protecting the Brain During Pediatric DKA Treatment.

The most feared complication when treating diabetic ketoacidosis (DKA) is sudden onset of neurologic deterioration, which may include central herniation. Clinical brain swelling complicates 0.5% to 1% of pediatric DKA episodes, and when it occurs, permanent morbidity and mortality are common. However, children in DKA are known to have subclinical brain edema.1 Factors that lead to clinical edema and neurologic abnormalities are not clear. The key issue is to determine the best way to manage these patients, who are dehydrated, severely hyperglycemic, and may have hypo or hypernatremia and severe acidosis.In this issue of Pediatrics, Glaser et al2 provide clinically helpful and reassuring findings in a comparison of 4 intravenous infusion protocols, with varying sodium concentrations and differing rates of rehydration.2,3 There was no difference in rates of neurologic dysfunction or clinically apparent brain swelling in any of the groups.1,2 Even more reassuring, there were no significant differences in these outcomes among those whose serum sodium remained stable or increased versus those whose sodium fell during the first 12 hours of therapy. An important clinical lesson is that this study prospectively demonstrated that rehydration over 1.5 to 2 days does not increase the risk of neurologic injury.2Prevention of DKA is difficult because just over half of episodes are the initial presentation of diabetes.3 Assessment of sensorium can be challenging because headache, throat pain, difficulty waking, and cooperation in infants and younger children can be difficult to judge. The primary study from which Glaser used data included 1389 episodes of DKA in 1255 children. There were 48 episodes (3.5%) when the Glasgow Coma Score was <14 for 2 assessments, and clinically apparent brain injury occurred in 12 episodes (0.9%).3 However, they did not find a significant difference in depression of Glasgow Coma Score or in clinically apparent brain injury among the 4 rehydration protocols.2,3Neuroimaging with MRI and apparent diffusion coefficient (ADC) of water, diffusion weighted images, and spectroscopy reveal that DKA is associated with increased water content in brain tissues supplied by the anterior and middle cerebral arteries with increased perfusion; however, the mean ADCs are abnormally elevated. This differs from what would be predicted by the osmotic disequilibrium theory because the ratio of extracellular volume to total tissue volume determines in part the ADC and should decrease.4,5 Clinical features that were significantly associated with severity of ADC increases during DKA were hypocarbia and elevated serum urea nitrogen but not glucose, sodium, or osmolality.6–8Previous studies with serial neuroimaging of children receiving faster versus slower rehydration during DKA did not differ significantly in the risk of brain edema.9 This previous work, also conducted by Glaser, helped to establish the foundation for this current study to assess different strategies for rehydration.What other pathophysiology occurs that might lead to neurologic injury and brain edema? The brain autoregulates blood flow to meet metabolic needs across a wide range of blood pressure but cerebral blood flow is highly responsive to partial pressure carbon dioxide (paco2). Acute hyperventilation causes vasoconstriction and severe hypocarbia can cause brain ischemia. Although the hypocarbia during DKA causes a compensatory respiratory alkalosis to increase blood pH, the cerebrospinal fluid (CSF) pH typically is normal before treatment. As blood ketosis decreases and the blood paco2 increases, the CSF becomes acidotic. It is important to remember that administration of bicarbonate exacerbates the CSF acidosis associated with DKA treatment. Likewise, a sudden relative increase in paco2 will increase intracranial pressure and CSF acidosis. Airway manipulation should include targeting the child’s baseline paco2 rather than normal values.The current state-of-the-art method to prevent neurologic abnormalities and clinical brain swelling in DKA is not dependent on specific fluid administration but instead on earlier recognition and treatment to avoid profound acidosis and hyperventilation. Current imaging data do not implicate rehydration regimens or changes in blood glucose or sodium with progression to clinical brain edema. The astute clinician will need to rehydrate carefully while paying attention to neurologic status, sustained ventilation, and acid–base status to protect the brain from worsening edema.

The great fluid debate: saline or so-called "balanced" salt solutions?

BackgroundIntravenous fluids are commonly prescribed in childhood. 0.9 % saline is the most-used fluid in pediatrics as resuscitation or maintenance solution. Experimental studies and observations in adults suggest that 0.9 % saline is a poor candidate for fluid resuscitation. Although anesthesiologists, intensive care specialists, perioperative physicians and nephrologists have been the most active in this debate, this issue deserves some physiopathological considerations also among pediatricians.ResultsAs compared with so-called “balanced” salt crystalloids such as lactated Ringer, administration of large volumes of 0.9 % saline has been associated with following deleterious effects: tendency to hyperchloremic metabolic acidosis (called dilution acidosis); acute kidney injury with reduced urine output and salt retention; damaged vascular permeability and stiffness, increase in proinflammatory mediators; detrimental effect on coagulation with tendency to blood loss; detrimental gastrointestinal perfusion and function; possible uneasiness at the bedside resulting in unnecessary administration of more fluids. Nevertheless, there is no firm evidence that these adverse effects are clinically relevant.ConclusionsIntravenous fluid therapy is a medicine like insulin, chemotherapy or antibiotics. Prescribing fluids should fit the child’s history and condition, consider the right dose at the right rate as well as the electrolyte levels and other laboratory variables. It is unlikely that a single type of fluid will be suitable for all pediatric patients. “Balanced” salt crystalloids, although more expensive, should be preferred for volume resuscitation, maintenance and perioperatively. Lactated Ringer appears unsuitable for patients at risk for brain edema and for those with overt or latent chloride-deficiency. Finally, in pediatrics there is a need for new fluids to be developed on the basis of a better understanding of the physiology and to be tested in well-designed trials.

EFFECT OF GIVING ANTIHYPERTENSIVE DRUG AGAINST REDUCTION OF BLOOD PRESSURE IN ACUTE ISCHEMIC STROKE PATIENTS WHO HOSPITALIZED IN RSUP DR. SARDJITO YOGYAKARTA

Incidence of ischemic stroke 10 times more often than haemorrhagic stroke in the the west countries, but haemorrhagic stroke has a higher risk of mortality than ischemic stroke. One focus of acute stroke management is the management of hypertension. Blood pressure reduction in ischemic stroke patients could potentially reduce the risk of brain edema, the risk of hemorrhage, and prevent further vascular damage. However, an aggressive blood pressure reduction can cause a decrease in perfusion pressure to the ischemic area. Most hypertensive patients require two or more antihypertensive medications to achieve blood pressure targets. This study used observational study design with retrospective data collection on medical records of acute ischemic stroke patients and performed in RSUP Dr. Sardjito Yogyakarta period January 2010-December 2010. Data were analyzed with descriptive analysis and chi-square evaluative analysis on the relationship between the type of therapy with a reduction in blood pressure of acute ischemic stroke patients. Initial antihypertensive medication use in patients with acute ischemic stroke in RSUP Dr. Sardjito were 13 types of five classes of antihypertensive drugs. After getting a single antihypertensive medication, patients who experienced a decrease in systolic blood pressure on day-3 was 60%, while 17% fixed and 23% up and after getting a combination of antihypertensive medications, patients who experienced a decrease in systolic blood pressure on day-3 was 75%, while 10% fixed and 15% rise. Antihypertensive drug therapy alone or in combination had the same ability to lower systolic blood pressure (p = 0.260) and diastolic (p = 0.567) in patients with acute ischemic stroke in RSUP Dr. Sardjito Yogyakarta. Keywords : Hypertension, acute ischemic stroke, single antihypertensive drug, antihypertensive drug combinations, RSUP Dr.Sardjito Yogyakarta

The use of radiosurgery for the treatment of mesial temporal lobe epilepsy and long‐term results

To determine the efficacy of gamma knife radiosurgery in the treatment of mesial temporal lobe epilepsy due to mesial temporal sclerosis. Between November 1995 and May 1999, 14 patients underwent radiosurgical entorhinoamygdalohippocampectomy with a marginal dose of 18, 20, or 25 Gy to the 50% isodose following a standard preoperative epilepsy evaluation. One patient was classified as Engel Class Ib, three were Engel Class IIc, one was Engel Class IIIa, and two were Engel Class IVb in a subgroup of seven patients who were unoperated 2 years prior to the last visit and at least 8 years after irradiation (average 116 months). The insufficient effect of irradiation led us to perform epilepsy surgery on another seven patients an average of 63.5 months after radiosurgery. The average follow-up period was 43.5 months after the operation. Four patients are seizure-free; one is Engel Class IIb and one is Engel Class IId. One patient cannot be classified due to the short period of follow-up. The frequency of seizures tended to rise after irradiation in some patients. Collateral edema was observed in nine patients, which started earlier and was more frequent in those irradiated with higher doses. It had a marked expansive character in three cases and clinical signs of intracranial hypertension were present in three cases. We found partial upper lateral quadrant anopia as a permanent side effect in two patients. Repeated psychotic episodes (two patients) and status epilepticus (two patients) were also seen after treatment. No significant memory changes occurred in the group as a whole. Radiosurgery with 25, 20, or 18-Gy marginal dose levels did not lead to seizure control in our patient series, although subsequent epilepsy surgery could stop seizures. Higher doses were associated with the risk of brain edema, intracranial hypertension, and a temporary increase in seizure frequency.