الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
 |  | from | 135 |  |  |
| | | from | 135 | | |
Abstract
S
pinal hypotension is common in pregnant female who receive spinal anaesthesia for Caesarean delivery. Spinal hypotension can occur precipitously and, if severe, can result in important perinatal adverse outcomes, such as maternal nausea and vomiting, fetal acidosis and may be an important contributory factor for maternal death related to regional anaesthesia.
Mothers with pre-delivery hypovolaemia may be at risk of cardiovascular collapse because the sympathetic blockade may severely decrease venous return. As a consequence, prevention of spinal hypotension has been a key research area within the field of obstetric anaesthesia
To prevent spinal hypotension, a number of approaches have been investigated, notably fluid loading, vasopressors, or both. Despite early enthusiasm, the efficacy of fluid loading for preventing spinal hypotension has been called into question. In contrast, the use of vasopressors has gained increasing prominence as the primary technique for the prevention and treatment of spinal hypotension during Caesarean delivery
Ketamine, is a non- competitive antagonist at the N-Methyl-D-Aspartic Acid (NMDA) receptor, stimulating the cardiovascular system with high blood pressure, heart rate, and cardiac output. These changes are not related to the dose of ketamine but related to time of administration.
The mechanism by which ketamine stimulates the cardiovascular system seems to be the central reason rather than peripheral. Ketamine attenuates the baroreceptor effect by blocking the NMDA receptors in the nucleus tractus solitarius. This effect results in a centrally mediated sympathetic response.
The Purpose of this study was to find out the effectiveness of prophylactic administration of intravenous ketamine for attenuation of spinal anesthesia induced hypotension in obstetric spinal anesthesia surgeries.
Therefore, A prospective double-blind, placebo-controlled, randomized study was found to be the most suitable design in order to achieve the study objectives. A total of 60 patients females included in the study, aged 18-45 years, and were divided equally into two groups:
group A received 0.5 mg/kg ketamine diluted in volume of 3 ml normal saline immediately after spinal anesthesia.
group B received a placebo of 3 ml normal saline 5 minutes immediately after spinal anesthesia.
Vital signs including. Heart Rate (HR) and Mean Arterial Blood Pressure (MAP) were recorded at baseline 5 minutes prior to the intrathecal injection and 5 minutes, 10 minutes, 15 minutes, and 20 minutes after the injection and then every 15 minutes till the end of the operation. Also, recorded total dose of ephidren, sedation score on Modified Ramsay Sedation Score at 5 min, 10 min, 15 min, 30 min and 45 min since induction. APGAR score was recorded at 1min and 5min. Shivering, hallucination and nystagmus were also recorded.
Results showed that:
The study revealed that ketamine didn’t prevent hypotension, it only delayed it for 10 min compared to control group 5 min. Also, observed that total ephidren dose significantly decreased in ketamine group compared to control group. And sedation scores in the first 30 min were higher in ketamine group. HR was’t affected. No changes in APGAR score were noticed between the two groups. No side effects from ketamine except for nystagmus.