Obesity
Ashraf S. Habib MBBCh, MSc, MHSc, FRCA, Robert D’Angelo MD
Chapter Outline
Obesity is a worldwide health problem, with the prevalence in the general population growing at an alarming rate and reaching epidemic proportions. Data from the National Center for Health Statistics show that in 2010, 69% of Americans were overweight and 36% were obese; 56% of women of reproductive age (20 to 39 years old) were overweight, and 32% were obese.1 Although no definition of obesity specific to pregnancy exists, a pregnant woman is generally considered overweight when her body mass index (BMI) is 25.0 to 29.9 kg/m2, and obese when her BMI is 30 kg/m2 or greater. The World Health Organization defines three grades of obesity: class I (BMI 30.0 to 34.9 kg/m2), class II (BMI 35.0 to 39.9 kg/m2), and class III (BMI 40 kg/m2 or greater).
Obesity is associated with an increased risk for maternal morbidity and mortality. The care of obese parturients poses significant challenges to the anesthesia provider as a result of common comorbidities, an increased cesarean delivery rate, and technical difficulties associated with both neuraxial and general anesthesia. Understanding the pathophysiologic changes and comorbidities associated with obesity and pregnancy is crucial for the safe conduct of anesthesia in these high-risk patients.
Physiologic Changes of Obesity
Pulmonary Changes
Obesity increases the demands on the pulmonary system. As energy expenditure increases proportionate to the increase in body mass,2 oxygen consumption and carbon dioxide (CO2) production also increase proportionate to the increase in work performed.3 Minute ventilation is increased owing to the elevated respiratory demand, except in the 5% to 10% of patients with Pickwickian syndrome, who display a reduced sensitivity to CO2.4 Obesity affects the body’s ability to meet these demands by changing pulmonary mechanics, altering lung volumes, and impairing oxygen consumption. The combined effects of obesity and pregnancy on the respiratory system are summarized in Table 50-1.
TABLE 50-1
Physiologic Changes in the Respiratory System Induced by Pregnancy and Obesity
↑, increase; ↓, decrease, ↔, no change; more than one arrow represents the degree of intensity; FEV, forced expiratory volume in 1 sec; VC, vital capacity; 
, ventilation/perfusion.
Modified from Saravanakumar K, Rao SG, Cooper GM. Obesity and obstetric anaesthesia. Anaesthesia 2006; 61:36-48.
Pulmonary Mechanics
Obesity increases the weight of the chest wall; thus, greater energy expenditure is required during ventilation to move this greater mass. Several prospective studies have demonstrated that morbidly obese patients, in comparison with controls, expend a disproportionately high percentage of total oxygen consumption on respiratory work, even during quiet breathing.5 The weight gain associated with pregnancy further increases the work of breathing in obese patients. In obese individuals, frequent shallow respirations may represent a more efficient breathing pattern than a pattern characterized by large tidal volumes. This pattern of frequent shallow respirations contrasts to the increased tidal volumes that typically accompany pregnancy. Although the PaCO2 in most morbidly obese pregnant women is not different from that in nonobese pregnant women, pulmonary reserve is reduced.
Lung Volumes
Greater abdominal weight restricts diaphragm movement, especially in the supine or Trendelenburg position, thus encouraging smaller tidal volumes. Functional residual capacity (FRC) decreases at the expense of expiratory reserve volume and may be less than closing capacity. In morbidly obese patients, this difference can result in airway closure during tidal ventilation. Similarly, expiratory reserve volume, vital capacity, inspiratory capacity, total lung capacity, and maximum minute ventilation all decrease in morbidly obese patients. Both chest wall and lung compliance decrease, but airway resistance increases.6,7
Pregnancy also alters lung volumes, and these changes may modify some of the normal effects of obesity on respiratory function. In nonobese pregnant women, expiratory reserve volume and FRC both decline 20% to 25% by term. Eng et al.,8 examining a series of pregnant women whose estimated prepregnancy weights ranged from 50% to 140% above normal, measured lung volumes during the third trimester and again at 2 months postpartum. With the exception of FRC, the lung volume changes resembled those that occur in nonobese pregnant women. However, FRC decreased less in obese pregnant women than in nonobese pregnant women.
Oxygenation
Pulmonary diffusion typically remains normal in most women with morbid obesity. Decreased chest wall compliance and greater abdominal weight promote airway closure in the dependent portion of the lung.9 Ventilation preferentially occurs in the more compliant, nondependent portion of the lung. In contrast, pulmonary blood flow preferentially occurs in the dependent portion of the lung, resulting in ventilation-perfusion mismatch and hypoxemia.9
Consistent with the positional deterioration of lung volumes, oxygenation worsens in obese persons in the supine and Trendelenburg positions. Both term pregnant and obese patients are prone to rapid oxygen desaturation during induction of general anesthesia.10 Although oxygenation does not necessarily correlate linearly with weight,11 massive weight loss improves PaO2 and expiratory reserve volume. Weight loss does not, however, improve forced expiratory volume in 1 second, forced vital capacity, or maximum mid-expiratory flow.12
Cardiovascular Changes
Cardiovascular changes associated with pregnancy and obesity are summarized in Table 50-2. Both obesity and pregnancy increase blood volume and cardiac output. The latter increases by 30 to 50 mL/min for every 100 g of fat.13 This change occurs as a result of increases in both stroke volume and heart rate. In addition to the elevated preload observed in obese parturients, left ventricular afterload is also increased owing to the high peripheral resistance and greater arterial wall stiffness. These changes result in both eccentric and concentric left ventricular hypertrophy. Messerli et al.14 documented a 30-fold increase in premature ventricular contractions in obese patients with eccentric left ventricular hypertrophy in comparison with lean subjects. The increase in heart rate limits the time available for diastolic filling. Diastolic relaxation is impaired, leading to diastolic dysfunction.15 In contrast, ventricular systolic function is usually normal in obese individuals.16
TABLE 50-2
Physiologic Changes in the Cardiovascular System Induced by Pregnancy and Obesity
↑, increase; ↓, decrease, ↔, no change; more than one arrow represents the degree of intensity.
Modified from Saravanakumar K, Rao SG, Cooper GM. Obesity and obstetric anaesthesia. Anaesthesia 2006; 61:36-48.
Pulmonary blood volume increases in proportion to increases in cardiac output and total blood volume. Pulmonary hypertension can occur and may be position dependent. Paul et al.17 observed an 11% increase in oxygen consumption and a 44% increase in pulmonary capillary wedge pressure when morbidly obese patients were placed in a supine position. Hypoxemia, if present, increases pulmonary vascular resistance. Airway obstruction may also increase pulmonary artery pressure.
Hypertension occurs more frequently among obese pregnant women than lean women. A BMI of 30 kg/m2 or more is associated with a threefold higher incidence of hypertension during pregnancy than a BMI less than 30 kg/m2.18 BMI and left ventricular mass are directly related, even after controlling for age and blood pressure, especially in patients with a BMI greater than 30 kg/m2.19 Among morbidly obese pregnant women, left atrial size, left ventricular thickness, interventricular septal thickness, and left ventricular mass are increased compared with nonobese pregnant women.13 Fatty infiltration of the heart can occur, especially in the right ventricle and perhaps in the conduction system.20
Aortocaval compression of the great vessels in the supine position may be greater in obese parturients, particularly those with a large fat panniculus.21 Tsueda et al.22 reported two cases of cardiac arrest in morbidly obese patients who had been placed in the supine position. The authors speculated that the sudden circulatory changes associated with this change in position accounted for the sudden death of these patients.
Gastrointestinal Changes
It is unclear whether obesity in pregnancy is associated with an increase in gastric volume and a decrease in gastric pH. Vaughan et al.23 observed that 88% of obese nonpregnant patients presenting for surgery had a gastric pH less than 2.5 and 86% had a gastric volume exceeding 25 mL. These findings resemble those in a cohort of healthy pregnant women who presented for elective cesarean delivery.24 Roberts and Shirley25 reported that gastric volumes aspirated from obese laboring women undergoing cesarean delivery were significantly higher than those obtained from lean controls.
Other studies, however, did not confirm these findings and reported conflicting evidence regarding gastric volume and pH in obese patients.26,27 Similarly, studies have reported conflicting data regarding gastric emptying in the obese population; studies have reported delayed, unchanged, or more rapid rates of gastric emptying in obese subjects compared with lean subjects.28 In a nonobstetric obese population, Maltby et al.29 reported that drinking 300 mL of clear fluid 2 hours before surgery had no effect on gastric fluid volume and pH compared with fasting after midnight. Similarly, Wong et al.30 found that gastric emptying in obese, nonlaboring term pregnant volunteers was not delayed after ingestion of 300 mL of water compared with ingestion of 50 mL of water. The gastric volume was similar to baseline 60 minutes after ingestion of water. It should be remembered, however, that obesity is a risk factor for diabetes,18 which may cause delayed gastric emptying.
Both gastroesophageal reflux and hiatal hernia are more common in obese than in nonobese patients.31 Obesity is also associated with a higher risk for difficult airway management, which is a known risk factor for aspiration.32 Therefore, it seems likely that morbidly obese patients are at higher risk for pulmonary aspiration of gastric contents.
Coagulation Changes
Obesity is associated with a higher risk for thromboembolic complications.33 Venous thromboembolism was the leading cause of direct maternal mortality in the United Kingdom from 1985 to 2005.34 Although the most recent report of the Confidential Enquiries into Maternal Deaths in the United Kingdom covering the triennium 2006 to 2008 showed a reduction in deaths from venous thromboembolism, 12 of the 16 women who died were obese.34 Obesity is associated with changes in coagulation, venous stasis, and endothelial injury that contribute to the pathogenesis of venous thromboembolism. For instance, adipose tissue secretes the following: (1) adipokines such as plasminogen activator inhibitor-1 (PAI-1), which results in impaired fibrinolysis; (2) leptin, which promotes platelet aggregation; and (3) interleukin-6, which stimulates the liver to produce coagulation factors.35,36 C-reactive protein levels are also elevated in obese women, leading to platelet activation.37 Venous stasis is compounded in obese women by increased intra-abdominal pressure, which leads to increased iliofemoral venous pressure.38 Endothelial injury may also be increased in obese patients; obesity was shown to be associated with endothelial dysfunction in the nonpregnant population.39 Therefore, all risk factors that contribute to the pathogenesis of thromboembolic complications are likely to be exacerbated by obesity.
Endocrine Changes
Gestational diabetes and diabetes mellitus occur more frequently in obese patients.18 The pathologic process is attributed to the following: (1) peripheral insulin resistance as a result of augmentation of free fatty acids by visceral obesity,40 (2) increased proinflammatory cytokine levels,41 (3) relative gonadotropin resistance, and (4) a low sex hormone–binding globulin concentration, which leads to hyperandrogenism and decreased insulin sensitivity.42 The concentration of adiponectin, an adipokine with insulin-sensitizing properties, is also decreased in obesity, which leads to decreased insulin sensitivity.43
CoMorbidities Associated with Obesity
Sleep Apnea
Obesity is a significant risk factor for obstructive sleep apnea (OSA), which is characterized by repeated episodes of complete or partial upper airway collapse, leading to hypoxemia and hypercarbia. Those repeated periods of hypoxemia and reoxygenation lead to significant endocrine and metabolic disturbances, which result in an increased risk for hypertension, myocardial infarction, stroke, diabetes, and metabolic syndrome.44 There is no consensus on the definition of OSA in pregnancy, and therefore the prevalence is unknown.
The changes of pregnancy may both worsen and protect against OSA. For instance, weight gain45 and estrogen-induced hyperemia and edema of nasal mucosa46 might promote OSA, whereas sleeping in the lateral position,47 reduced rapid eye movement (REM) sleep, and the progesterone-induced increase in minute ventilation might protect against it. Obesity does not seem to be as strongly correlated with OSA in pregnancy as in the nonpregnant population.45
The risks for gestational hypertension, preeclampsia, and gestational diabetes are increased with OSA.48,49 Some studies have examined the potential impact of maternal OSA on poor perinatal outcomes, but most of the studies have been small with conflicting results. For instance, Sahin et al.50 simultaneously performed polysomnography and a nonstress test to assess the impact of hypoxemia due to OSA on the fetus. OSA was found in 4 of the 35 women evaluated; in 3 of these women fetal heart rate (FHR) decelerations accompanied maternal oxyhemoglobin desaturation. Olivarez et al.51 performed simultaneous polysomnography and at least 3 hours of continuous FHR monitoring on 100 pregnant women (including 19 with a diagnosis of OSA), and they found no association between FHR abnormalities and OSA parameters. Louis et al.52 reported an increased risk for preeclampsia (odds ratio [OR], 3.54; 95% confidence interval [CI], 1.26 to 9.92), neonatal intensive care unit admission (OR, 3.39; 95% CI, 1.23 to 9.32), and cesarean delivery (OR, 3.04; 95% CI, 1.14 to 8.1) among obese pregnant women with OSA compared with those with no OSA after adjusting for age, race, and BMI.
Other Comorbidities
Obesity is associated with an increased risk for a number of disease states compared with lean controls (Table 50-3).31,33,53 These comorbidities complicate the care of obese parturients.
TABLE 50-3
Relative Risk or Odds Ratio of Comorbidities in Obese Women
| Comorbidity | Relative Risk | 95% CI of Relative Risk |
| Type 2 diabetes* | 12.41 | 9.03, 17.06 |
| Hypertension* | 2.42 | 1.95, 3.67 |
| Coronary artery disease* | 3.10 | 2.81, 3.43 |
| Congestive heart failure* | 1.78 | 1.07, 2.95 |
| Pulmonary embolism* | 3.51 | 2.61, 4.73 |
| Stroke* | 1.49 | 1.27, 1.74 |
| Asthma* | 1.78 | 1.36, 2.32 |
| Gallbladder disease* | 2.32 | 1.17, 4.57 |
| Osteoarthritis* | 1.96 | 1.88, 2.04 |
| Chronic back pain* | 2.81 | 2.27, 3.48 |
| Odds Ratio | 95% CI of Odds Ratio | |
| Depression† | 1.55 | 1.22. 1.98 |
| Gastroesophageal reflux disease‡ | 1.89 | 1.70, 2.09 |
* Data from Guh DP, Zhang W, Bansback N, et al. The incidence of co-morbidities related to obesity and overweight: a systematic review and meta-analysis. BMC Public Health 2009; 9:88.
† Data from Luppino FS, de Wit LM, Bouvy PF, et al. Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies. Arch Gen Psychiatry 2010; 67:220-9.
‡ Data from Eslick GD. Gastrointestinal symptoms and obesity: a meta-analysis. Obes Rev 2012; 13:469-79.
CI, confidence interval.
Impact of Obesity on Pregnancy
Maternal and Fetal Complications
Obesity results in greater use of health care resources. Chu et al.54 reported that obese pregnant women receive significantly more prenatal tests, ultrasonographic examinations, medications, and prenatal visits with a physician, and they are at greater risk for having a high-risk pregnancy, cesarean delivery, and prolonged hospitalization than pregnant women of normal weight.
Obesity is associated with a significantly increased incidence of maternal, fetal, and neonatal complications. These include a higher risk for spontaneous abortion (miscarriage), thromboembolic complications, gestational diabetes, hypertensive disorders of pregnancy, dysfunctional labor, shoulder dystocia, operative vaginal delivery, cesarean delivery, postpartum hemorrhage, wound infection, fetal macrosomia, fetal congenital anomalies, stillbirth, and neonatal death.18,55,56 In a prospective multicenter cohort study of more than 16,000 unselected pregnant women in the United States, Weiss et al.18 assessed obstetric complications in 1473 obese women (BMI 30.0 to 34.9 kg/m2), 877 morbidly obese women (BMI ≥ 35 kg/m2), and 3752 lean controls (BMI < 30.0 kg/m2). The odds of gestational diabetes, gestational hypertension, preeclampsia, macrosomia, preterm delivery, and operative vaginal and cesarean delivery were all greater in morbidly obese pregnant women compared with lean women (Table 50-4).
TABLE 50-4
Obstetric Complications in Obese and Morbidly Obese Women
| Outcome | Odds Ratio (95% Confidence Interval) | |
| OBESE VERSUS CONTROL | MORBIDLY OBESE VERSUS CONTROL | |
| Gestational diabetes | 2.6 (2.1, 3.4) | 4.0 (3.1, 5.2) |
| Gestational hypertension | 2.5 (2.1, 3.0) | 3.2 (2.6, 4.0) |
| Preeclampsia | 1.6 (1.1, 2.3) | 3.3 (2.4, 5.5) |
| Birth weight > 4500 g | 2.0 (1.4, 3.0) | 2.4 (1.5, 3.8) |
| Birth weight > 4000 g | 1.7 (1.4, 2.0) | 1.9 (1.5, 2.3) |
| Preterm delivery | 1.1 (0.9, 1.5) | 1.5 (1.1, 2.1) |
| Operative vaginal delivery | 1.0 (0.8, 1.3) | 1.7 (1.2, 2.2) |
| Cesarean delivery* | 1.7 (1.4, 2.2) | 3.0 (2.2, 4.0) |
* Nulliparous women.
Data from Weiss JL, Malone FD, Emig D, et al. Obesity, obstetric complications and cesarean delivery rate—a population-based screening study. Am J Obstet Gynecol 2004; 190:1091-7.
Most importantly, obesity increases the risk for death during pregnancy. The latest report of Confidential Enquiries into Maternal Deaths in the United Kingdom for the 2006 through 2008 triennium showed that 49% of women who died were overweight or obese.34 Similarly, in the previous report that covered the 2003-2005 triennium, 52% of the mothers who died were overweight or obese.57 The impact of obesity on maternal mortality was even greater among women who died of thromboembolism or cardiac disease; of the mothers who died of these two disease entities, 78% and 61%, respectively, were overweight or obese.34 Because of the high risk for thromboembolism in obese pregnant women and the significant probability of subtherapeutic anticoagulation with fixed-dose low-molecular-weight heparin regimens, the Royal College of Obstetricians and Gynaecologists (RCOG) added weight-based recommendations for thromboprophylaxis to their 2009 guidelines.58
Obesity has also been identified as a risk factor for anesthesia-related maternal mortality. Six of the 13 direct maternal deaths attributed to anesthesia in the last two triennial reports from the United Kingdom occurred in obese parturients.34,57 In the United States, Mhyre et al.59 reported that six of eight pregnant women who died of anesthesia-related deaths in Michigan between 1985 and 2003 were obese. Because of the increased risk for complications, in 2010 the United Kingdom Centre for Maternal and Child Enquiries (CMACE) and the RCOG published joint guidelines on the management of women with obesity in pregnancy.60 Both these guidelines and the American College of Obstetricians and Gynecologists (ACOG) guidelines61 recommend a multidisciplinary approach to the care and treatment of obese pregnant women, including (1) evaluation of all women for obesity by calculating BMI, (2) offering preconception counseling to obese women, (3) screening for gestational diabetes, (4) providing guidelines for prenatal weight gain, and (5) referring obese women for antepartum consultation with an anesthesiologist.
Progress of Labor and Method of Delivery
The progress of labor appears to be impacted by BMI. A large multicenter study involving 118,978 patients, whose labor management reflected current practice in the United States, reported that labor progressed more slowly with increasing BMI for both nulliparous and parous women.62 The median time to progress from 4 to 10 cm cervical dilation increased from 5.4 hours to 7.7 hours for lean and morbidly obese nulliparous women, respectively, and from 4.6 hours to 5.4 hours for lean and morbidly obese parous women, respectively. These findings were independent of gestational age and induction of labor. Entry into the active phase of labor was also delayed in parous women as a function of BMI. Possible explanations include increased fetal size, higher induction rates, and/or decreased responsiveness to oxytocin.62 Poor uterine contractility has also been demonstrated in obese parturients. Zhang et al.63 found that myometrium obtained from obese women at cesarean delivery contracted with less force and frequency and had less calcium flux than that from normal-weight women. This observation may be attributable to the inhibitory effect of cholesterol63 and/or adipokines (e.g., leptin, ghrelin, apelin), which were shown to inhibit human uterine contractility in vitro.64
Obesity is also associated with a higher risk for failed medical induction of labor. In a secondary analysis of data from a large labor induction trial involving 1273 patients (in which patients were stratified according to BMI), the duration of labor, oxytocin requirements, and cesarean delivery rates were significantly higher in women with a greater BMI.65 In a large series from Sweden involving 233,887 deliveries, Cedergren66 found a fourfold increase in the risk for cesarean delivery in parturients with a BMI greater than 40 kg/m2, primarily because of failed or obstructed labor, despite attempts at augmentation.
Operative vaginal delivery, with its associated maternal and fetal morbidity, is more likely in the obese parturient.18 One study examining maternal anthropometric parameters associated with shoulder dystocia reported a 2.7-fold increase in risk for shoulder dystocia in obese compared with lean parturients after adjustment for potential confounders such as macrosomia and diabetes.67 Risk for fetal macrosomia is also higher with obesity, which, in addition to increasing the risk for shoulder dystocia and its associated birth trauma, predisposes to perineal lacerations, newborn infant injury, and postpartum hemorrhage.18,67,68
Higher BMI, increased prepregnancy weight, and excessive maternal weight gain increase the risk for both elective and emergency cesarean delivery.69,70 This risk is further increased by obesity-related pregnancy complications such as macrosomia, fetal growth restriction (also known as intrauterine growth restriction), diabetes mellitus, and hypertensive disorders of pregnancy.55,71 In a meta-analysis of 33 trials,56 the unadjusted odds ratios (95% CI) of cesarean delivery were 1.46 (1.34 to 1.60), 2.05 (1.86 to 2.27), and 2.89 (2.28 to 3.79) among overweight, obese, and severely obese women, respectively, compared with normal-weight pregnant women.
Anesthetic Management
The high incidence of comorbid conditions among obese pregnant women necessitates early, careful preanesthetic assessment. There are also a number of technical matters that should be considered when caring for an obese parturient.
An appropriate-sized blood pressure cuff must be used for noninvasive blood pressure measurements. Unless the length of the sphygmomanometer cuff exceeds the circumference of the arm by 20%, systolic and diastolic blood pressure measurements may overestimate true maternal blood pressure. Forearm blood pressure measurement is sometimes used if an appropriate-sized blood pressure cuff is not available or if the upper arm cuff continues to slide from its position owing to the shape of the obese patient’s upper arm. There is a good correlation between upper arm and forearm noninvasive measurements, but forearm pressures exceed upper arm pressures by 10 ± 10 mm Hg (mean ± SD).72 In selected cases, invasive monitoring of blood pressure with an intra-arterial catheter may be desirable.57
Intravenous access may be difficult in some obese patients. Ultrasonographic guidance may be useful; however, if peripheral intravenous access remains unsuccessful, central venous cannulation may be necessary.
Appropriately sized labor beds, transportation gurneys, and operating tables, and sufficient personnel to assist with patient transport, are imperative. Although standard operating tables are generally rated for persons weighing up to 500 pounds (227 kg), this rating may be insufficient for morbidly obese patients, especially when the table is articulated. Regardless of the weight rating of the table, it is critical that the obese patient be centered over the operating table pedestal at all times. Special equipment for positioning the patient, and longer spinal/epidural needles, may be needed (see later discussion).
Labor and Vaginal Delivery
Options for analgesia are the same as those for nonobese patients. Using the McGill pain questionnaire, Melzack73 reported a positive correlation between BMI and the severity of labor pain. A later study, however, did not confirm these findings.74
Many of the options for labor analgesia have limitations in the obese parturient. For example, obese parturients with OSA may be more susceptible to the respiratory depressant effect of systemic opioids, leading to episodes of apnea and oxyhemoglobin desaturation. Pudendal nerve block may be more difficult technically in obese patients. Inhalation analgesia is useful in some patients; however, nitrous oxide has limited effectiveness and is not available in many birthing rooms. Further, inhalation analgesia may lead to loss of consciousness, which can be very dangerous in an obese woman with a difficult airway.
Neuraxial analgesia represents the best option for pain relief and is particularly desirable in the obese parturient. Given the greater risks for fetal macrosomia and shoulder dystocia in obese patients, adequate analgesia is often needed to facilitate an atraumatic vaginal delivery. The use of epidural analgesia during labor allows the anesthesia provider to extend epidural analgesia to surgical anesthesia for cesarean delivery and thus avoid the need for general anesthesia with its associated risks. Given the increased likelihood for cesarean delivery and the greater risks of general anesthesia in the obese parturient, the early administration of neuraxial labor analgesia is recommended in the obese parturient.
When performing a neuraxial anesthetic technique in the obese parturient, technical difficulties may include (1) inability to palpate the spinous processes or identify the midline75; (2) greater depth of the epidural space,76 which may exaggerate minor needle directional errors and increase the likelihood of identifying a lateral portion of the epidural space77; and (3) the presence of fat pockets as well as hormonal softening of the ligaments, which may result in a false loss of resistance and/or a higher risk for unintentional dural puncture.78
