Department of Anaesthesiology, Geetanjali Medical College and Hospital Udaipur 313 001, Rajasthan, India
ABSTRACT
This article deals with the anatomic changes that occur in the different organ systems of a parturient at term. Changes in the respiratory, cardiovascular, gastrointestinal, nervous system, musculoskeletal, and renal systems have been highlighted. The anesthesiologist should be well versed with these changes as along with the physiological changes of pregnancy they tend to profoundly alter the maternal responses to anesthesia, which have been discussed with each system. The anatomical changes in pregnancy induced hypertension and obesity are discussed in brief, along with special emphasis on cardiopulmonary resuscitation in parturient.
INTRODUCTION
The common physical complaints in pregnancy are a reflection of the anatomical and physiological changes that occur through the course of pregnancy. For example, back pain accompanies increased lumbar vertebral lordosis and weight bearing strain; ankle edema, leg varices and hemorrhoids indicate lower extremity venous engorgement and stasis while breathlessness, repeated respiratory infections and acidity, nausea and vomiting are related to the changes in the respiratory and gastrointestinal (GI) system.
Early in pregnancy, the rising levels of hormones especially progesterone, estrogen, human chorionic gonadotropin and prostaglandin play a primary role in these changes. As pregnancy advances, the enlarging uterus plays a more important role in the alteration of respiratory, circulatory, GI, renal and skeletal functions. These anatomical and physiological changes of pregnancy tend to profoundly alter 316the maternal response to anesthesia. This article will deal with the anatomical changes and their practical implications for the anesthesiologist.
CHANGES IN RESPIRATORY SYSTEM
Airway management may be challenging during pregnancy. Capillary dilatation occurs throughout the respiratory tract, leading to engorgement of the nasopharynx, larynx, trachea and bronchii. This leads to frequent nasal blockage, laryngitis and change in voice. The condition is further worsened following respiratory infections, fluid overload and preeclampsia. Pregnant women often have difficulty with nasal breathing. There is friability of the mucous membranes during pregnancy, which can cause severe bleeding, especially on airway instrumentation. These changes are caused by increase in extracellular fluid and vascular engorgement. Thus, nasal intubation should be avoided, as it can lead to brisk epistaxis.
Bag-mask ventilation may be more difficult due to increased soft tissue in the neck. It may also be difficult to perform laryngoscopy in obese, short-necked parturient with enlarged breasts. The enlarged breasts tend to project upwards to fill in the space in which the laryngoscope handle is placed. Thus standard laryngoscopy will not be possible unless measures are taken to displace the breasts or special equipment is used, such as a short-handled laryngoscope or a polio blade.
Swelling of the false vocal cords due to increased capillary permeability decreases the glottic opening, which can hinder intubation and increase the risk of bleeding. Thus when endotracheal intubation is performed, a 6–7 mm cuffed endotracheal tube is recommended. Similarly insertion of airways, suctioning of the oropharynx and laryngoscopy may further cause edema and bleeding. This may make further attempts at intubation more difficult and increase the incidence of failed intubation. Airway edema may be particularly severe in pregnant women with preeclampsia, those in the Trendelenburg position for prolonged periods, and those with concurrent use of tocolytic agents.
The airway is classified according to the anatomical structures seen by Mallampati scoring1 into grades I–IV (Figure 1). This scoring is further correlated with the view of the laryngeal structures visible on laryngoscopy according to Cormack and Lehane classification2 from grades 1 to 4 (Figure 2). Grades 3 and 4 views on laryngoscopy are considered difficult to intubate. Data suggests that Mallampati scores change during gestation with an increase in class IV scores among patients between 12 weeks and 38 weeks gestation3 which is further exacerbated by a prolonged II stage of labour.4 This worsening Mallampati score has been attributed to pharyngeal edema and fatty infiltration of the pharyngeal tissue.
Elevation of the diaphragm occurs, by as much as 4 cm in later pregnancy, with increase in the size of the uterus (Figure 3). However, the internal volume of the thoracic cavity is unchanged.317
Figure 1: Modified Mallampati classification for difficult laryngoscopy and intubation (Class I–IV).
The external diameter of the chest increases by 12.5–17.5 cm, as there is a compensatory increase in the transverse and anteroposterior diameters of the thorax.5 Other changes in the thorax include flaring of the ribs and an increase in the substernal angle. Splinting of the diaphragm may occur in the anesthetized pregnant woman in the Trendlenberg or horizontal position.
CHANGES IN THE CARDIOVASCULAR SYSTEM
During pregnancy, numerous changes occur in the cardiovascular system (CVS) of the mother, which prepares her for the demands of her fetus and forthcoming delivery. The enlarging uterus pushes up the diaphragm and shifts the position of the heart leftward and anteriorly, so that the apex beat is shifted outward and upward. At term, there is an increase in the end-diastolic chamber size as compared to the nonpregnant females (4.86 cm vs. 4.67 cm) and an increase in the left ventricular wall thickness (2.01 cm vs. 1.69 cm).6 Asymptomatic pericardial effusion, innocent grade I and II systolic murmurs, a third and occasionally a fourth heart sound may be heard. They appear due to an increase in plasma volume and cardiac output along with annular dilatation of the tricuspid valve, which initiates a mild regurgitant flow. These changes lead to common electrocardiogram (ECG) findings of left axis deviation, sagging ST segments and frequently inversion or flattening of the T wave in lead III.
From the second trimester, aortocaval compression by the enlarged uterus becomes progressively more important, reaching its maximum effect at 36–38 weeks, after which it may decrease as the fetal head descends into the pelvis. Cardiac output may decrease when patients are in the supine position but not in the lateral decubitus position. Venous occlusion by the growing fetus causes supine hypotensive syndrome in 20% of pregnant term women, who have inadequate collateral circulation of intervertebral venous plexus, vertebral azygous and portal system, and abdominal veins.
It manifests as maternal tachycardia, arterial hypotension, sweating, nausea, vomiting, pallor and changes in cerebration. In the supine position, the gravid uterus partially or completely compresses the lower aorta and inferior vena cava, leading to decreased venous return, cardiac output, maternal hypoxia and decrease in uteroplacental perfusion with fetal asphyxia (Figure 4).7 In the third trimester, when the mother is supine, the contracting uterus obstructs its own blood supply to the level of L3-4 (Poseiro effect). Thus, aortocaval compression must be prevented, and parturient with a 20-week or longer gestation should not assume a supine position without left uterine displacement. Uterine displacement or lateral pelvic tilt should be applied routinely with a wedge (>15°) under the right hip (Figure 5), especially during anesthetic management of the pregnant patient.319
Figure 5: Aortocaval compression in A, supine position B, following left uterine displacement with wedge.
CHANGES IN THE GASTROINTESTINAL SYSTEM
The risk of regurgitation on induction of general anesthesia depends, in part, on the gradient between the lower esophageal sphincter (LOS) and intragastric pressures. In parturient with “heartburn,” the lower esophageal sphincter tone is greatly reduced. Circulating progesterone reduces the LOS tone, increasing the incidence of esophageal reflux. This is further exacerbated by anatomical changes. The gravid uterus is displaced upwards and to the left pushing the intra-abdominal part of the esophagus into the thorax in most pregnant women. There is also a gradual cephalad displacement of stomach and intestines. This often makes the LOS incompetent and lowers the barrier pressure. These factors, along with a lowered stomach pH, increase the risk and severity of aspiration pneumonitis under general anesthesia. It is recommended that from 16 weeks gestation patients undergoing general anesthesia should be given prophylaxis against aspiration pneumonitis. This ideally includes a nonparticulate antacid, such as sodium citrate 0.3 M 30 ml and an H2 receptor antagonist, e.g., ranitidine 150 mg orally or 50 mg intravenously. However, the efficacy of prophylactic nonparticulate antacids is diminished by inadequate mixing with gastric contents, improper timing of administration, and the tendency for antacids to increase gastric volume; hence its use in obstetrics is slowly but surely waning. Administration of histamine (H2) receptor antagonists, such as cimetidine and ranitidine, requires careful timing. The administration of intravenous (IV) metoclopramide before elective Cesarean section delivery, hastens gastric emptying and increases resting lower esophageal sphincter tone in both nonpregnant and pregnant women.
Induction of anesthesia should be by a rapid sequence induction with cricoid pressure and a short-acting muscle relaxant, followed by intubation with a cuffed endotracheal tube. Extubation should be done in a fully awake parturient in the lateral position. These important steps during general anesthesia will ensure against regurgitation and aspiration of gastric contents.321
CHANGES IN NERVOUS SYSTEM
During pregnancy, obesity and edema frequently obscure anatomical landmarks, the interspinal ligament is hormonally softened, and in homogeneous tissue can cause false loss of resistance. These changes may make neuraxial anesthesia technically more difficult with more complications. Ultrasonography (USG)8 has shown that the distance from the skin to the epidural space was longer and the epidural space was narrower. Therefore, the “safety zone” between transfixation of the ligamentum flavum and inadvertent dural puncture was smaller.
Neural blockade with local anesthetics occurs at lower concentrations, as obstruction of the vena cava by the enlarging uterus distends the epidural venous plexus and increases epidural blood volume. This reduces the volume of the epidural space and cerebrospinal fluid (CSF), which increases the cephalad spread of local anesthetics. Thus lower doses of local anesthetic are needed per dermatome for epidural or spinal block. This has been attributed to an increased spread of local anesthetic in the epidural and subarachnoid spaces as a result of epidural venous engorgement and enhanced sensitivity to local anesthetic block due to progesterone. Increase in the epidural space pressures results in higher incidence of dural puncture during epidural anesthesia, while engorgement of the epidural veins results in increased possibility of intravascular placement of epidural catheters during labor analgesia. Due to a combination of anatomic variables, the spinal cord and its meninges are also more vulnerable to needle trauma.9
CHANGES IN THE MUSCULOSKELETAL SYSTEM
Anatomical changes in the pelvis around delivery include softening of the cervix, inhibition of uterine contractions and relaxation of pubic symphysis and pelvic joints. The placenta produces relaxin, a hormone that causes widespread relaxation of ligaments and increased mobility of the pubis and sacroiliac joints to allow passage of the fetus through the birth canal. Ligamentous laxity can make it technically difficult to identify the epidural space with loss of resistance (LOR). This laxity of the spine also makes parturient more susceptible to back injury and pain in the postpartum period, which is often blamed on regional anesthesia.
During spinal anesthesia, positioning in the parturient is a challenge as the exaggerated lumbar lordosis interferes with flexion of the spine, along with the abdominal bulge due to the gravid uterus. Progressive lumbar lordosis also tends to alter the surface anatomy in parturient. The pelvis tends to rotate on the long axis of the spinal column, causing the intercristal line (Tuffier's line)9 joining the highest points of the iliac crest to be displaced more cephalad (Figure 6). This line normally crosses the interspace at L4-5 or the L4 vertebral body, while in parturient, due to lateral tilting of the broad female pelvis (Figure 7), this line may appear to cross at L3-4 interspace.6322
Figure 7: Differences in slant of spine in lateral decubitus position A, female patient B, male patient.
Consequently, cephalad errors in the vertebral level of needle insertion are very common. Due to limited flexion, there is also reduced interspace between the spinous processes (Figure 8).5 Magnetic resonance imaging has shown that the apex of the lumbar lordosis is shifted caudad and the typical thoracic kyphosis is reduced.10 The increased lumbar lordosis of pregnancy may enhance the cephalad spread of local anesthetic solutions placed in the CSF.
CHANGES IN THE RENAL SYSTEM
After the 12th week of gestation, progesterone can induce dilation and atony of the renal calyces and ureters. As gestation advances, the enlarging uterus can compress the ureters as they cross the pelvic brim and cause further dilatation by obstructing flow. These changes can lead to frequency of urinary tract infections during pregnancy.323
The enlarging uterus displaces the urinary bladder upwards and flattens it with resultant decrease in bladder capacity and increased frequency of micturition. Obstruction of lower aorta by the gravid uterus can diminish blood flow to the kidneys at term, leading to a markedly lower maternal renal function in the supine than in the lateral position. This is another important reason why parturient beyond 20-week gestation, should not assume a supine position, while lying down.
SPECIAL SITUATIONS
Parturients, who suffer from pregnancy induced hypertension (PIH) or obesity, develop airway related changes which have major implications for the anesthesiologist in terms of maintenance of the airway both during elective surgery as well as in an emergency.
Preeclampsia
Adequate extension and flexion during positioning of the parturient for intubation is hampered by the significant tissue edema and soft tissue deposition in the neck 324region of parturient with PIH. They also have a narrower upper airway than nonpregnant women. The tongue is larger and less mobile due to the reduced plasma proteins consequent to proteinuria and marked fluid retention (especially in the head and neck region), causing more difficult identification of landmarks in these parturients. In severe preeclampsia, there could be edema of the face and neck which should alert the anesthesiologist to the possibility of a difficult intubation, while if there is edema of the tongue it may indicate immediate airway compromise. Further, in preeclamptic parturient, the edematous soft tissue is more friable and along with coagulopathy, can lead to laceration and catastrophic bleeding, on repeated attempts at direct laryngoscopy, thus complicating the management of a difficult airway. Upper respiratory tract infection can further compromise the edematous airway in preeclampsia. Laryngeal edema, facial edema, enlarged tongue, voice change, or stridor can rapidly develop in a pre-eclamptic patient without any warning signs; therefore, caution should be exercised even during extubation.
Morbid Obesity
Morbid obesity in pregnancy is associated with increased risk for diabetes, hypertension, preeclampsia, and primary Cesarean section. The incidence of partially obliterated oropharyngeal anatomy among obese parturients is double than among nonobese parturients. There is not only an increased risk of difficult intubation but also increased difficulty in maintaining adequate mask ventilation. Mask ventilation tends to be difficult because of low chest wall compliance and increased intra-abdominal pressure.11
Atlanto-occipital flexion and extension may be impeded by thoracic and breast fat whereas mouth opening may be restricted by numerous chins.12 Fleshy cheeks, a large tongue, high anterior larynx, flaps of intra-airway tissue all make laryngoscopy and intubation more difficult in the obese parturient.13 During general anesthesia, positioning is of paramount importance in the obese parturient and adequate time should be spent on preparing the patient for intubation. The shoulders should be elevated and occiput supported by placing folded towels (Figure 9). This allows the breasts to fall away from the neck and chin and places the head in a sniffing position.
During regional anesthesia, establishing an epidural or spinal block can be complicated by technical difficulties. The depth of epidural space from the skin depends on patient weight and the degree of obesity. Long length of needle (15 or 20 cm) may be required, along with a paramedian approach. Unintentional dural puncture, vascular placement of catheter is also common. However, incidence of postdural puncture headache is less common in the morbidly obese parturient.14325
Cardiopulmonary Resuscitation
Cardiopulmonary resuscitation (CPR) in a parturient following cardiac arrest is one of the most challenging situations that anesthesiologists can face, in their professional career. Advanced cardiovascular life support (ACLS) guidelines are the gold standard for CPR, but these have to be modified in a pregnant woman, considering that two lives need to be saved. The major modifications advocated by ACLS guidelines15 due to anatomical and physiological changes, include the following:
- Leftward displacement of uterus during chest compressions
- Perimortem Cesarean section in 4–5 minutes of arrest
- IV access in upper limbs only, in view of caval compression
- Early endotracheal intubation.
During cardiac arrest, in order to minimize the effects of the gravid uterus on venous return and cardiac output, a maternal pelvic tilt to the left of greater than 15° is recommended. The tilt needs to be 27–30°, using a firm wedge to support the pelvis (Figure 10), for effective closed chest compression to take place. An alternative technique is manual displacement of uterus to the left with a one hand (Figure 11) or two-hand technique (Figure 12), in the supine position, from patient's left side or right side respectively. If chest compressions are ineffective, after the above steps, then an immediate emergency Cesarean section should be done. This would relieve the aortocaval compression, increase the cardiac output by 30%, decrease the demand of uteroplacental circulation on the cardiac output, improve thoracic compliance and allow neonatal resuscitation.326
CONCLUSION
- The mucous membrane of the upper airway is edematous and friable with more chances of bleeding and difficulty during intubation. Careful assessment of the airway in all parturients should be mandatory before subjecting to anesthesia. A difficult airway cart should be kept ready in the operation theater
- Aortocaval compression caused by the enlarging uterus starts from the 20th week of gestation and is maximum at 36–38 weeks gestation. Always place the patient with a left lateral tilt of 15–30° with a wedge under the right hip, to avoid aortocaval compression
- There is gradual cephalad displacement of the stomach which makes the LOS incompetent and makes the parturient more prone to regurgitation and aspiration of gastric contents. Aspiration prophylaxis should be routinely given before anesthesia
- During regional anesthesia, one should remember that anatomic variations following lumbar lordosis, cephalad shift of intercristal line, reduced interspace between spinous processes, can all pose technical difficulties in the success of the procedure.
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