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Dive into the research topics where Maya S. Suresh is active.

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Featured researches published by Maya S. Suresh.


Critical Care Medicine | 2005

Airway problems in pregnancy.

Uma Munnur; Ben de Boisblanc; Maya S. Suresh

Objectives:To provide a current review of the literature regarding airway problems in pregnancy and management. Background:Obstetrical anesthesia is considered to be a high-risk practice that exposes the anesthesiologist to increased medicolegal liability. Anesthetic management of a parturient is a challenge because it involves simultaneous care of both mother and baby. Failure to appropriately manage a difficult or failed intubation increases the risk of hypoxemic cardiopulmonary arrest and/or pulmonary aspiration, resulting in a high probability of maternal morbidity and mortality. Data:Anesthesia is the seventh leading cause of maternal mortality in the United States. Anatomic and physiologic changes during pregnancy place the parturient at increased risk for airway management problems. It is essential to perform a thorough preanesthetic evaluation and identify the factors predictive of difficult intubation. Airway devices such as the laryngeal mask airway, ProSeal, intubating laryngeal mask airway, Combitube, and laryngeal tube are described and have been used during failed intubation in pregnant patients. Conclusion:Teamwork between an anesthesiologist and an obstetrician is absolutely essential for the safety of both the mother and baby. Most of us tend to agree that airway emergencies have a way of occurring at the worst possible times. It is essential that all anesthesia care practitioners must have a preconceived and well thought-out algorithm and emergency airway equipment to deal with airway emergencies during difficult or failed intubation of a parturient.


Obstetrics & Gynecology | 2007

Intrapartum epidural analgesia and maternal temperature regulation.

Laura Goetzl; Jose Rivers; Israel Zighelboim; Ashutosh Wali; Martina Badell; Maya S. Suresh

OBJECTIVE: To examine maternal temperature changes after epidural analgesia. METHODS: A prospective cohort of nulliparas at term was monitored with hourly maternal tympanic temperatures after epidural analgesia (n=99). Temperature response after epidural analgesia was examined in the group as a whole. Subsequently, mean maternal temperature curves were compared between women who remained afebrile throughout labor (n=77) and women who developed intrapartum fever with body temperature greater than 100.4ºF (n=22). Baseline maternal characteristics were assessed. RESULTS: Women who later developed intrapartum fever had a higher mean temperature within 1 hour after epidural analgesia. In contrast, women who remained afebrile had no increase in core temperature. During the first 4 hours after epidural analgesia initiation, women who later develop intrapartum fever have an increase in mean tympanic temperature of 0.33ºF per hour. CONCLUSION: Epidural analgesia is not associated with increased temperature in the majority of women. Hyperthermia is an abnormal response confined to a minority subset, which occurs immediately after exposure. Our findings do not support a universal perturbation of maternal thermoregulation after epidural analgesia. LEVEL OF EVIDENCE: II


American Journal of Obstetrics and Gynecology | 1996

Effects of estradiol-17β and progesterone on isolated human omental artery from premenopausal nonpregnant women and from normotensive and preeclamptic pregnant women

Michael A. Belfort; George R. Saade; Maya S. Suresh; Yuri P. Vedernikov

OBJECTIVE Our purpose was to study the direct vascular effects of estradiol-17 beta and progesterone on isolated omental artery from premenopausal nonpregnant women and from normotensive and preeclamptic pregnant women. STUDY DESIGN Omental artery rings from normotensive premenopausal nonpregnant women and from normal and preeclamptic pregnant women were mounted in Krebs-bicarbonate solution in organ baths for isometric tension recording. The endothelium was removed from some of the rings, and all were contracted with potassium chloride (60 mmol/L) and then exposed to cumulative concentrations of estradiol-17 beta and progesterone. Concentration response curves were constructed and relaxation was expressed as percent change from the reference 60 mmol/L potassium chloride contraction. Data analysis was by repeated-measures analysis of variance, Newman-Keuls test, and the unpaired Student t test as appropriate. A two-tailed p < 0.05 was considered statistically significant. RESULTS Both hormones studied caused vasorelaxation in omental arteries from all three groups of patients. Of the two, estradiol-17 beta was more effective, regardless of the presence or absence of endothelium. Removal of the endothelium shifted the estradiol-17 beta concentration-response curve to the right in the normal pregnant artery but not in nonpregnant or preeclamptic vessels. Removal of the endothelium shifted the progesterone concentration-response curve to the left in arteries from preeclamptic patients. CONCLUSIONS Estradiol-17 beta and progesterone have direct in vitro vasodilator activity that appears to be linked, in part, to the endothelium in human omental artery from normal and hypertensive women in different hormonal states.


Anesthesiology Clinics of North America | 2003

Backache, headache, and neurologic deficit after regional anesthesia

Uma Munnur; Maya S. Suresh

Back pain, chemical backache, PDPH, and neurologic deficit all may be reported after regional anesthesia for childbirth. Back pain is common during pregnancy, but epidural analgesia during labor does not increase the incidence of long-term back pain. Chemical backache caused by 2-chloroprocaine is probably a result of hypocalcemic tetany of paraspinous muscles. The mechanism is presumed to be chelation of calcium by sodium bisulfite, an antioxidant present in nesacaine-MPF. PDPH after dural puncture is caused by leakage of CSF, which causes cerebral hypotension. Cerebral hypotension leads to traction on pain-sensitive intracranial structures and cerebral vasodilation. Initial therapy includes hydration, caffeine, and sumatriptan. EBP is the most effective treatment in severe PDPH. If the first EBP fails, a second blood patch can be performed. Neurologic deficits after regional anesthesia are rare. Meticulous technique and vigilance are the keystones in avoiding major neurologic complications of regional anesthesia. Rapid diagnosis and appropriate treatment are essential to optimize a successful outcome if complications do develop.


Journal of Perinatology | 2004

Prophylactic Acetaminophen Does Not Prevent Epidural Fever in Nulliparous Women: A Double-Blind Placebo-Controlled Trial

Laura Goetzl; Jose Rivers; Tracy Evans; Deborah R Citron; Barbara Richardson; Ellice Lieberman; Maya S. Suresh

OBJECTIVE: Epidural analgesia is associated with a four- to five- fold increase in noninfectious maternal fever in nulliparous women. Fever prophylaxis may safely reduce both unnecessary neonatal sepsis evaluations and the potential effect of fever on the fetus.STUDY DESIGN: We performed a randomized double-blind placebo-controlled study. Immediately after epidural placement, full-term nulliparas with a temperature of <99.5°F received acetaminophen 650 mg or placebo, per rectum, every 4 hours. Tympanic membrane temperatures were measured hourly. Our power to detect an effect of acetaminophen treatment on maternal temperature over time was 90%.RESULTS: In all, 21 subjects were randomized to each arm. Treatment with acetaminophen did not impact maternal temperature curves. Fever >100.4°F was identical in the acetaminophen and placebo groups (23.8%, p=1.0). Neonatal surveillance blood cultures did not reveal occult infection.CONCLUSIONS: Acetaminophen prophylaxis prevented neither maternal hyperthermia nor fever secondary to epidural analgesia, suggesting that the mechanism underlying fever does not include centrally mediated perturbations of maternal thermoregulation.


American Journal of Obstetrics and Gynecology | 1996

Effects of selected vasoconstrictor agonists on isolated omental artery from premenopausal nonpregnant women and from normal and preeclamptic pregnant women

Michael A. Belfort; George R. Saade; Maya S. Suresh; Wayne B. Kramer; Yuri P. Vedernikov

OBJECTIVE Our purpose was to compare the responsiveness of omental resistance arteries from nonpregnant women and from normotensive and preeclamptic pregnant women to selected contractile agonists. STUDY DESIGN Omental artery rings with intact endothelium from normotensive premenopausal nonpregnant women and from normal and preeclamptic pregnant women were mounted in Krebs-bicarbonate solution in organ baths for isometric tension recording. After the presence of endothelium was confirmed, cumulative concentrations of norepinephrine, serotonin, U46619, and endothelin-1 were added. Concentration-response curves were constructed and expressed as percentage of a reference 60 mmol/L potassium chloride contraction. Data analysis was by repeated-measures analysis of variance. Newman-Keuls test, and paired or unpaired Student t test, as appropriate. Statistical significance was by two-tailed p<0.05. RESULTS Endothelin-1 and U46619 increased tension similarly in all three groups. Norepinephrine increased tension in nonpregnant vessels to a greater extent than in either preeclamptic or pregnant vessels (nonpregnant 114.3 +/- 5.42% vs pregnant 65.2 +/- 10.5%, p<0.05). Nonpregnant omental artery developed significantly greater tension than did pregnant tissue at three concentrations of norepinephrine (10(-5) mol/L, 3 x 10(-5) mol/L, 10(-4) mol/L), and preeclamptic vessels developed more tension than that from normal pregnant vessels at 3 x 10(-6) mol/L (p=0.06) and 10(-5) mol/L (p<0.05). There was a negligible change in tension with increasing concentrations of serotonin in the vessels from nonpregnant women; serotonin-induced contraction in the omental arteries from normotensive pregnant women and preeclamptic patients was <6% of the potassium chloride reference contraction, but this was significantly (p<0.05) different from that of the nonpregnant women. CONCLUSIONS Omental artery segments from nonpregnant, normotensive pregnant and preeclamptic women contract similarly to endothelin-1 and U46619 but exhibit variable responses to norepinephrine and serotonin.


American Journal of Obstetrics and Gynecology | 1995

Human umbilical vessels: Responses to agents frequently used in obstetric patients

Michael A. Belfort; George R. Saade; Maya S. Suresh; David Johnson; Yuri P. Vedernikov

OBJECTIVE Our purpose was to study the effects of some drugs frequently used in pregnant women on isolated human umbilical artery and vein segments. STUDY DESIGN Umbilical artery and vein rings from normal term pregnancies were mounted in Krebs-bicarbonate solution in organ baths for isometric tension recording. Rings were contracted with potassium chloride (60 mmol/L) or U46619 (10(-8) mol/L) and then exposed to cumulative concentrations of nimodipine, nifedipine, nicardipine, phenytoin, magnesium sulfate, and hydralazine. Concentration-response curves were constructed by means of the difference in the percent relaxation between test and control vessels. Data analysis was by repeated measures analysis of variance, Newman-Keuls test, and the unpaired Student t test as appropriate. A value of p < 0.05 was considered statistically significant. RESULTS All the agents studied were effective umbilical vasodilators, except for hydralazine, which had minimal effect. The dihydropyridine calcium antagonists were more potent vasodilators than were the other agents studied. Nifedipine was the most potent calcium blocker and was the only dihydropyridine that relaxed the umbilical vein to a greater extent than the umbilical artery. CONCLUSION The most commonly used drugs in preeclampsia have variable effects on the umbilical vessels.


Anesthesiology | 1988

Comparison of Nitroprusside and Hydralazine in Isolated Uterine Arteries from Pregnant and Nonpregnant Patients

Sharon H. Nelson; Maya S. Suresh

The purpose of the present study was to determine the relative potency of nitroprusside and hydralazine with respect to inhibition of norepinephrinc-induced contraction of isolated, uterine arteries from pregnant and nonpregnant patients. The arteries, obtained after hysterectomy, were dissected free from surrounding tissue, and arterial rings were prepared and mounted in tissue chambers filled with Krebs-bicarbonate solution. Isometric tension was recorded. At concentrations of 10-9 M to 10-5 M, both nitroprusside and hydralazine produced concentration-dependent inhibition of the contractile response to norepinephrine. Nitroprusside and hydralazine were more potent in relaxing arteries contracted by a lower concentration (3 X 10-6 M) of norepinephrine than by a higher concentration (10-5 M) of norepinephrine. Regardless of the concentration of norepinephrine, nitroprusside was considerably more potent than hydralazine. The concentrations of nitroprusside that produced 50% inhibition (IC50) of the contractile response to norepinephrine (3 X 10-6 M) in uterine arteries from pregnant and nonpregnant patients were 3.2 ± 0.5 X 10-9 M (n = 5) and 1.2 ± 0.1 X 10-9 M (n = 6), respectively. The IC50 values for hydralazine acting against norepinephrine (3 X 10-6 M) in the uterine arteries from pregnant and nonpregnant patients were 5.1 ± 0.5 X 10-7 M (n = 5) and 4.0 ± 0.5 X 10-7 M (n = 6), respectively. Nitroprusside (10-6 M), compared to hydralazine (10-5 M), produced the greater maximal inhibition of norepinephrine-induced contraction. The results demonstrate that, although both nitroprusside and hydralazine inhibit norepinephrine-induced uterine artery contraction, nitroprusside has a greater potency compared to hydralazine in producing direct vasodilation of the uterine arteries from pregnant and nonpregnant humans.


European Journal of Pharmacology | 1993

Relaxation by calcitonin gene-related peptide may involve activation of K+ channels in the human uterine artery

Sharon H. Nelson; Maya S. Suresh; Deborah J. Dehring; Rebecca L. Johnson

The vasodilatory role of calcitonin gene-related peptide in activating K+ channels was examined in isolated, suffused human uterine arteries. Calcitonin gene-related peptide produced a concentration-dependent relaxation of norepinephrine (1 microM)-induced contractions. Calcitonin gene-related peptide was antagonized by glybenclamide (1-100 microM), an inhibitor of ATP-sensitive K+ channels, but not by tetraethylammonium (1 mM), an inhibitor of calcium(2+)-activated K+ channels. Glybenclamide (10 microM) produced a 6.7 fold and an 11-fold shift to the right of calcitonin gene-related peptide (0.1 to 100 nM) in uterine arteries from pregnant patients (n = 3) and nonpregnant patients (n = 6), respectively. Calcitonin gene-related peptide (10 nM) less effectively (P < 0.05) relaxed contractions produced by KCl (50 mM) (29.4 +/- 1.6%) than by norepinephrine and glybenclamide (10 microM) did not reverse this relaxation (22.2 +/- 6.8%, n = 4 nonpregnant patients). Pinacidil (1 microM), an ATP-sensitive K+ channel opener, relaxed norepinephrine-induced contractions of uterine arteries. Glybenclamide (10 microM) also antagonized pinacidil. These results suggest that calcitonin gene-related peptide relaxes norepinephrine-contracted human uterine arteries, at least in part, by activation of a K+ channel, perhaps of the ATP-sensitive type.


Anesthesiology Clinics | 2008

Maternal Morbidity, Mortality, and Risk Assessment

Ashutosh Wali; Maya S. Suresh

Maternal deaths in developed countries continue to decline and are rare. Maternal mortality statistics are essentially similar in the United States and United Kingdom. However, the situation is completely different in developing countries, where maternal mortality exceeds 0.5 million every year. This article not only assesses morbidity risks in some of the leading causes of maternal death but also highlights strategies to minimize the risks and to prevent maternal morbidity and mortality.

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Dive into the Maya S. Suresh's collaboration.

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Jose Rivers

Baylor College of Medicine

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Uma Munnur

Baylor College of Medicine

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Ashutosh Wali

Baylor College of Medicine

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George R. Saade

University of Texas Medical Branch

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Yuri P. Vedernikov

University of Texas Medical Branch

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David J. Tweardy

Baylor College of Medicine

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Kenneth J. Moise

Memorial Hermann Healthcare System

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