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Year : 2014 Month : February Volume : 3 Issue : 8 Page : 1915-1919

SPINAL ANESTHESIA IN PREECLAMPTIC PARTURIENTS

Ashok V. Deshpande1, Sanjivani A. Deshpande2

1. Intensivist, I. C. U, Department of Anaesthesia, Bharti Vidyapeeth, Deemed University Medical College and Hospital, Sangli.
2. Associate Professor, Department of Obstetrics and Gyanaecology, Bharti Vidyapeeth, Deemed University Medical College and Hospital, Sangli.

CORRESPONDING AUTHOR

Dr. Ashok V. Deshpande,
Email : drashokvdeshpande@yahoo.co.in

ABSTRACT

CORRESPONDING AUTHOR:
Dr. Ashok V. Deshpande,
Sanjivan Hospital,
S. T. Colony Road,
Vishrambag, Sangli – 416415, India.
E-mail: drashokvdeshpande@yahoo.co.in

ABSTRACT: In this prospective cohort study, we compared the incidence and severity of spinal anesthesia (SA) associated hypotension in pre eclamptics (n=50) versus healthy parturients (n=50) undergoing caesarean delivery before due date to avoid the effects of pre eclampsia on mother and baby. After proper preloading, SA was administered with 0.5% hyperbaric bupivacaine. Blood pressure (BP) was recorded before performing SA(baseline BP), and then after SA, every 2 minutes for 30 minutes, and thereafter, every 5 minutes up to completion of surgery. The pre eclamptic patients had a less frequent incidence of clinically significant hypotension, which was less severe and required less ephedrine. The risk of hypotension was significantly less in pre eclamptic patients than that in healthy patients. Spinal anesthesia seemed to be a useful and safe option, and alternative to epidural anesthesia, in pre eclamptic patients in setting of large patient turn up for caesarean deliveries.

KEYWORDS: Preeclampsia, Caesarean delivery, Spinal anesthesia, Hypotension, Ephedrine, Bupivacaine.

INTRODUCTION: Cesarean delivery is a common method of terminating pregnancy in preeclamptic patients, more common when the later becomes severe. Anesthesiologists are more likely to encounter a difficult airway in a severely preeclamptic patient. Furthermore the hazards related to the hemodynamic consequences of laryngoscopy and tracheal intubation in a severely preeclamptic patient are very much obvious1. So, general anesthesia in such patients may be resorted to only when regional anesthesia is contraindicated. Although spinal anesthesia has been usually avoided in these patients because of the risk of precipitous fall in BP and severe hypotension, and epidural anesthesia preferred, several studies are now available that show that the hemodynamic effects of spinal and epidural anesthesia are almost similar1- 4. Recent studies have indicated that SA may be an appropriate anesthetic choice for women with severe preeclampsia having a cesarean delivery before due date5. Furthermore, owing to its simplicity, reliability and rapidity, SA may be considered as an alternative to GA for emergency cesarean delivery in preeclamptic women who have been adequately prepared with judicious amount of IV preload.5

METHODS: After informed consent from the patients, the study was conducted in Bharti Vidyapeeth Deemed University Medical College and Hospital December 2006 to June 2007. The study included 50 preeclamptic patients posted for routine and emergency LSCS before due date. Another 50 normal patients were studied as control. Severe preeclampsia was defined as per criteria of Davy and MacGillivary6, as systolic blood pressure (SBP) greater than 160 mmHg, and diastolic blood pressure (DBP) greater than 110 mm Hg, or both. After each case enrollment, the next normotensive patient scheduled for LSCS was administered spinal anesthesia and selected as a control. Patients with chronic hypertension, diabetes or coagulopathy were not included in the study.

All patients were preloaded with lactated Ringer's solution, about 1000 ml before the anesthesia was administered. The preloading was done with patient in left lateral position and continuous monitoring of heart rate (HR) and blood pressure (BP). Baseline BP and HR were calculated as mean of 3 consecutive measurements 2 minutes apart. Spinal anesthesia was administered, with patient in sitting position, after skin infiltration with 1ml of 2% lignocaine, with a 25 gauge spinal needle in L3-4 vertebral interspace. Hyperbaric bupivacaine, 0.5% (2.5ml to 2.8 ml) was injected intrathecally and the patient returned to supine position with left uterine displacement. A 10-15 degree head down tilt was used to facilitate upward spread of local anesthetic.

We recorded maternal BP and HR every 2 minutes for first 30 minutes, and every 5 minutes thereafter up to completion of surgery. we defined spinal hypotension as fall of greater than 30% mean arterial pressure (MAP) from baseline, considering that a decrease of 20% in MAP is usually a therapeutic goal in severe hypertension1, and used IV ephedrine in installments of 5-6 mg to treat hypotension, the dose was repeated after 2-3 min if necessary. We also studied variables including demographic data, gestational age and Apgar scores.

RESULTS: We studied 50 pre eclamptic patients and 50 health controls. The results of the comparative study are depicted in table A. Demographic variables, gestational age an Apgar score in two study groups are compared in table B.

The statistical analysis of the data was done by using test statistics student's t-test for difference of means.

These tests were further referenced for p-values for their significance. All tests were two sided, and p-value less than 0.05 were considered statistically significant.

Variable

Healthy

(n =50)

Preeclamptic

(n =50)

p-value

SBP

 

 

 

Baseline (mmHg)

130+/- 7.5

165.0 +/ -18.0

<0.001

Lowest after SA (mmHg)

100.5 +/- 15.2

124.6 +/- 20.0

<0.001

Decrease from baseline at

 the lowest value (%)

- 22.62+/- 12.1

- 24.48 +/- 11.0

0.456

DBP

-           

 

 

Baseline (mmHg)

88.5+/- 9.5

106.7 +/ -11.2

<0.001

Lowest after SA (mmHg)

62.5 +/- 15.2

82.7 +/- 12.9

<0.001

Decrease from baseline

at the lowest value (%)

- 29.4+/- 15.3

- 21.0 +/- 11.5

0.010

IAP

 

 

 

Baseline (mmHg)

101.2+/- 7.6

122.8 +/ -10.0

<0.001

Lowest after SA (mmHg)

72.5 +/-15.0

95.5 +/- 16.5

<0.001

Decrease from baseline

at the lowest value (%)

-28.06+/- 13.4

- 22.23 +/- 12.5

0.045

H R

 

 

 

Baseline (bpm)

90.6 +/-16.3

100.7+/- 19.9

0.061

Lowest after SA (bpm)

74.6+/- 12.3

80.6+/-16.6

0.064

Decrease from baseline

at the lowest value (%)

--19.44 +/--9.3

-- 19.2+/-11.7

0.964

Highest after SA (bpm)

105.2 +/-15.8

109.8+/-19.4

0.378

Increase from the baseline at the highest value

17.1+/- 12.1

9.9 +/- 12.1

0,047

Table A: Changes in BP and HR after spinal anesthesia

 

Variable

Healthy

Preeclamptic

P - value

Age

32.50+/-6.5

30.70+/-5.8

0.394

Weight (Kg)

73.80 +/- 12.40

75.80+/-11.50

0.584

Gestational Age  (Wks.)

37 +/- 2

33.2+/- 1.9

<0.001

Height (Cms)

162+/- 6.3

162+/- 4.2

0.870

Ephedrine Dose mg

11.7+/-6.5

6.5+/- 1.2

0.0007

Apgar score (5 Min) median range

10(8-10)

10(8-10)

0.486

Table B: Maternal and neonatal characteristics

 

Mean baseline values of SBP, DBP, and MAP were more in preeclamptic group. There was a significant decrease in all the 3 variables in both groups following administration of spinal anesthesia. It is evident from table A that magnitude of decrease in SBP was similar in both groups, whereas that of decrease in SBP and MBP was significantly smaller in preeclamptic patients. Preeclamptic patients had significantly less incidence of clinically significant hypotension that made use of IV ephedrine necessary than normal patients (table A). Baseline values of HR were similar in the 2 groups and the incidence of HR changes did not differ significantly among the study groups, albeit, the magnitude of increase in HR was larger in healthy patients.

DISCUSSION: It is obvious from this study that preeclamptic patients experience less hypotension following spinal anesthesia than healthy parturients posted for LSCS before date . Though magnitude of fall in SBP was similar in the 2 study groups that of fall in DBP and MAP was significantly less in preeclamptic patients, including severe preeclamptic parturients, than healthy controls.

As changes in MAP reflect changes in both SBP and DBP over a course of time and because it is usually used in study of patients with severe preeclampsia to evaluate the effects of regional anesthesia on BP in these patients2- 4, we did chose MAP as primary study variable instead of SBP. However special attention was paid when SBP decreased significantly from baseline and IV ephedrine used immediately to avoid any harmful effect of hypotension on uteroplacental blood flow in healthy parturients.

It has been believed that severely preeclamptic patients may carry a high risk with use of spinal anesthesia owing to possibility of severe hypotension with maternal and fetal consequences12 because of reduced plasma volume13 and of need to limit IV fluids to avoid iatrogenic pulmonary edema14, so use of spinal anesthesia has not been popular in preeclampsia. At present several prospective and retrospective studies are available that clearly show that properly administered spinal anesthesia induces a similar incidence and severity of hypotension in patients with severe preeclampsia as epidural anesthesia.2- 4 In our study, we administered spinal anesthesia safely in preeclamptic parturients, including severe preeclamptics. Furthermore incidence and severity of hypotension were less in preeclamptic patients compared to healthy controls in our study. We didn't encounter any case of iatrogenic pulmonary edema with judicious preloading in preeclampsia in this study.

Several factors might have contributed to our observed findings. One obvious factor should be significantly decreased gestational age in preeclamptics at the time of LSCS before date. Indeed, healthy parturients, at term or near term, carrying a larger fetus may be at increased risk of aortocaval compression. One more contributing factor may be altered physiology regarding regulation of BP in preeclampsia. BP is regulated via vascular tone by sympathetic and endothelial pathways. Sympathetic activity increases the vascular tone. As sympathetic over activity has been suggested in preeclampsia7, this may contribute to their hypertension. The sympathetic outflow to vessels may be altered in both preeclamptic and healthy parturients by spinal anesthesia. Regarding the endothelial pathway, the endothelium regulates the vascular tone via endothelium-related vasodilator system that is altered in preeclampsia, decreasing the role of endothelial-dependent relaxation of small resistance vessels.8- 10

Furthermore, preeclampsia is characterized by an increased production of numerous circulating factors with a potent presser effect on one hand, and by an increased sensitivity of blood vessels to presser drugs because of endothelial damage, on the other hand. These two phenomena contribute to the widespread vasoconstriction seen in preeclamptic patients11, are not altered by spinal anesthesia, and could maintain a vascular tone that, ultimately, contributes to limit decrease in BP following intrathecal block in preeclamptic patients. The increased sensitivity of blood vessels to the vasoconstrictor effect of presser agents in preeclampsia may explain easy restoration of BP to baseline with smaller doses of ephedrine in preeclamptics compared to healthy patients in our study.

Although MAP decreased more in healthy parturients, 5-minute Apgar score didn't differ significantly between the study groups. This shows that even though MAP did fall to a larger extent, uteroplacental blood flow was not impaired significantly in healthy parturients.

CONCLUSION: From our this prospective study, we draw the conclusion that incidence and severity of hypotension following spinal anesthesia is less in preeclampsia compared to healthy parturients, and use of spinal anesthesia, when properly administered and monitored, is a safe alternative to epidural anesthesia in preeclamptic patients including severe preeclampsia. spinal anesthesia owing to its simplicity, reliability and quicker onset may save lot of time and so may be more practical method of anesthesia in preeclamptic parturients in such a setting.

REFERENCES:

  1. Antoine G M, Roselin M, Nathalie V, Ferrer JM, Robert C, Ripart J, Coussy JE. Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesarean delivery than healthy parturients. Anesth Analg 2003; 97:867-872.
  2. Wallace D H, Leveno K J, Cunningham FG, et al. Randomized comparison of general and regional anesthesia for cesarean deliveries in pregnancies complicated by severe preeclampsia. Obstet Gynecol 1995; 86:193-9.
  3. Karien J, Rasanen J, Alahuhta S, et al. Maternal and uteroplacental hemodynamic state in preeclamptic patients during spinal anesthesia for cesarean section. BJA 1996; 76: 616-20.
  4. Hood DD, Curry R. Spinal versus epidural anesthesia for caesarean section in severely preeclamptic patients. Anesthesiology 1999; 90: 1276-82.
  5. Santos AC, Birnbach DJ. Spinal anesthesia in the parturients with severe preeclampsia: time for reconsideration. Anesth Analg 2003; 97: 621-22.
  6. Davy DA, Mac Gillivary I. The classification and definition of hyprertensive disorders of pregnancy. Am J Obstet Gynecol 1988; 158: 892-8.
  7. Schobel HP, Fischer T, Heusezer K, et al. Preeclampsia : a state of sympathetic hyperactivity. N Engl J Med 1996; 335: 1480-5.
  8. Ashworth JR, Warren AY, Baker PN, Johnson IR. Loss of endothelium-dependent relaxation in myometrial resistance arteries in preeclampsia . BJ Obstet Gynecol 1997; 104: 152-58.
  9. Bosio PM, Wheeler T, Anthony F, et al. Maternal plasma vascular endothelial growth factor in normal and hypertensive pregnancies and their relationship to peripheral vascular resistance. Am J Obstet Gynecol 2001; 184:146-52.
  10. Vederniko YP, Belfort MA, Saade GR, Garfield RE. Inhibition of cox but not NO synthase influences effects on human omental artery of the thromboxane A2 mimetic U46619 & 17 beta estradiol. Am J Obstet Gynecol 2001; 185: 182-89.
  11. Visser W, Wallenbreg HC. Central hemodynamic observations in untreated preeclamptic patients. Hypertension 1991; 17: 1072-7.
  12. Cunningham FG, Mac Donald PC, Gant NF. Hypertension disorders in pregnancy. Williams’s obstetrics 18th. Ed.,1989: 653-94.
  13. Hays PM, Cruikshank DP, Dunn LM. Plasma volume determination in normal and preeclamptic pregnancies. Am J Obstet Gynecol 1985;151:958-66.
  14. Sibai BM, Mabie BC, Harvey CJ, Gonzalez AR. Pulmonary edema in severe preeclampsia-eclampsia. Am J Obstet Gynecol 1997; 104: 1152-58.

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