During pregnancy and postpartum women often have gastrointestinal discomforts such as nausea, vomiting and heartburn, but the most troublesome thing is defecation disorders.
Recently, Grace et al. from the Gastroenterology Department of Temple University School of Medicine in the United States reviewed the research on bowel disorders during pregnancy and postpartum. The article was published in AM J GASTROENTEROL.
Common bowel disorders during pregnancy and postpartum mainly include constipation and fecal incontinence, which are important causes of stress and health burden for pregnant women.
The muscle groups that play a major role in the defecation process are the levator ani muscle and anal sphincter complex. Its structure and function may be affected by chronic strain, age, physical condition, and increased intra-abdominal pressure (such as obesity and pregnancy).
Anatomy and physiological function of pelvic floor and anorectum
1. Pelvic floor anatomy
The levator ani muscle complex constitutes most of the pelvic floor and mainly includes three groups of muscles: iliococcygeus, pubococcygeus and puborectalis (Figure 1). The main function of the levator ani muscle complex is to support the pelvic organs, form a right angle to help control defecation and play a role in sexual function.
The levator ani muscle complex is innervated by the pudendal nerve, inferior rectal nerve, perineal nerve and sacral nerve, and it cooperates with the internal and external anal sphincter to control defecation. The genitourinary tract divides the female pelvic floor into two parts, the front pelvic floor damage mainly leads to urinary incontinence, and the rear pelvic floor damage mainly leads to defecation disorders.
Figure 1. The levator ani muscle complex forms most of the pelvic floor
2. Controlled bowel physiology
Defecation can be divided into four physiological processes: (1) static period (2) pre-defecation period (3) discharge period (4) defecation termination. Stool is transported to the rectum through the migration compound movement of the colon, and after reaching the rectum, it promotes rectal expansion and the activation of the rectal anus inhibition reflex. The rectal expansion is sensed by the brain and forms the meaning of stool.
If the environment does not allow defecation, the pelvic floor and the external anal sphincter will contract and inhibit defecation; when the environment is suitable, defecation will proceed: the puborectalis muscle becomes loose and the anorectal angle increases and the anorectal tube becomes straight.
Then the external sphincter loosens, the anterior abdominal wall muscles, diaphragm and rectum contract, which promotes the excretion of feces by increasing intra-abdominal pressure. Finally, the internal sphincter and puborectalis muscle return to their resting state.
3. The effects of pregnancy
During pregnancy, progesterone levels continue to rise, which can lead to decreased gastrointestinal motility (delayed gastric emptying and constipation), reduced sphincter tension (affecting the lower esophageal sphincter can lead to esophageal reflux and heartburn), and affect the state of anal sphincter .
Progesterone can also cause ligaments to relax and promote the extension of the pubic symphysis. At the same time, intra-abdominal pressure and uterine weight increase during pregnancy, which further induces changes in the conformation of the pelvic floor, which ultimately leads to changes in defecation patterns.
The main cause of postpartum fecal incontinence is the damage of the anal sphincter and pudendal nerve during delivery, which may be caused by perineal tear or perineal incision during normal labor. Tool-assisted labor (such as the use of forceps and fetal suction) can aggravate the injury.
Overweight during pregnancy, prolonged second stage of labor, and passing through the birth canal for babies older than gestational age can cause pelvic muscle damage. However, due to weight loss and pelvic floor muscle healing after delivery, these injuries can be improved in the postpartum period.
The pathophysiological mechanisms of constipation during pregnancy are diverse. In the first 3 months of pregnancy, the action of progesterone weakens the movement of the small intestine and colon, followed by slow transit constipation. In the later stages of pregnancy, the pressure of the pregnant uterus on the rectosigmoid colon can lead to obstructive constipation (Figure 2).
Studies have found that the cause of constipation in some women during pregnancy may be the lack of response to progesterone in the gastrointestinal tract, rather than excessive progesterone.
Figure 2. Obstructive symptoms caused by pregnant uterus
(2) Risk factors
Whether the mode of delivery is related to postpartum constipation remains controversial. In addition, other possible factors associated with constipation during pregnancy include pre-existing gastrointestinal disorders (IBS, Hirschsprung's disease, Hirschsprung's disease, Hirschsprung's disease and pseudo-obstruction), and suffering from extraintestinal metabolic diseases (hypothyroidism) And the side effects of some drugs.
If pregnant women have functional intestinal disorders before pregnancy, they often take antiemetics (such as ondansetron, promethazine, and prochlorazine) and antihistamines (such as anti-allergy, diphenhydramine, and chlorbenzyl) Azine), and the side effects of these drugs include constipation.
In addition, iron supplement formulas can cause constipation in pregnant women, and the degree of constipation is directly proportional to the amount of elemental iron intake. At this time, you can alleviate constipation by switching to a formula with a low elemental iron content. Finally, the use of magnesium sulfate to inhibit preterm birth or treat preeclampsia may also cause constipation.
The treatment of pregnancy-related constipation is similar to the treatment of constipation in the normal population. The purpose of treatment is to eliminate the patient’s doubts, encourage patients to take in adequate fluids, supplement dietary fiber (20-35g/day), and use osmotic laxatives (such as polyethylene glycol, 8-25g/day) and lactulose (15 -30ml/day).
However, the FDA has not approved the use of polyethylene glycol for pregnant women and defines it as a Class C drug for pregnant women. Polyethylene glycol can increase the water content of feces and has the characteristics of low system absorption, so it is unlikely to cause fetal malformations.
Lactulose is a class B drug for pregnant women classified by the FDA, which can promote colonic peristalsis and has a low systemic absorption. Although the above two drugs are widely used and seem to be safe, patients should still be informed of the theoretical risks.
Hemorrhoids are a common complication of pregnant women with constipation, mainly due to excessive force in defecation and the thrust of the second stage of labor. The main clinical manifestations of internal hemorrhoids are anal discomfort and bleeding, while external hemorrhoids are mainly pain and itching outside the anus.
At this time, the main treatment is conservative treatment such as increasing dietary fiber and drinking water or using stool softeners. Hydrocortisone suppositories and sitz baths may reduce swelling, discomfort, and itching associated with external hemorrhoids.
If conservative treatment fails and symptomatic internal hemorrhoids persist, surgery or endoscopic treatment can be performed after delivery. Endoscopic apron ligation, injection of sclerotherapy, infrared coagulation and surgical hemorrhoidectomy are all safe treatments in the postpartum period.
The grade of hemorrhoids determines the treatment method; grade I hemorrhoids can be treated conservatively; drug-resistant grade I or II hemorrhoids can be treated with endoscopic therapy, and the success rate of skin band ligation is 80%; symptomatic grade III hemorrhoids can be treated with skin Strap ligation or surgical resection; grade IV hemorrhoids or grade III hemorrhoids with significant prolapse are best treated with surgery.
It should be noted that any operation that requires sedation or prone position during the first 3 months and the last 3 months of pregnancy should be avoided as much as possible.
2. Fecal incontinence
Fecal incontinence is related to factors such as anal sphincter, innervating anorectal nerves and anal cushion. The main mechanism of postpartum fecal incontinence is sphincter weakness and loss of bowel movement.
Anal sphincter weakness can be caused by structural damage to the muscles, pudendal nerve damage, or both, and the loss of feces is caused by damage to the nerves that innervate the anorectal sensory function.
After the parturient has experienced a high degree of tear during complex delivery, fecal incontinence secondary to the injury often occurs, and surgical intervention is required at this time.
Since most women of childbearing age can compensate for the impaired bowel control caused by acute structural and nerve damage through other bowel control mechanisms, acute onset fecal incontinence is not common, but most patients will experience fecal incontinence in later life. Treatment is also mainly for patients with delayed fecal incontinence.
(2) Risk factors:
Recent studies have found that the causes of fecal incontinence in the postpartum days include forceps delivery, prolongation of the second stage of labor for more than 5 hours, expulsion period of more than 20 minutes, and a perineal laceration; the main risk factor for fecal incontinence in the 6-8 weeks postpartum is shoulder dystocia , The distance between the anus and the vulva is less than 2cm, the perineal scar and the waist diameter are greater than 105mm. Third-degree or fourth-degree sphincter injury was significantly associated with fecal incontinence at 12 months postpartum (Figure 3).
Figure 3. Classification of clinically significant perineal tears: a. Third degree tear; b. Fourth degree tear
Although common sense tells us that selective caesarean section may have a preventive effect on subsequent fecal incontinence, the existing literature is not sufficient to support this view. Evaluation of anatomical damage to the anal sphincter showed that fetal suction is less likely to cause damage than forceps, which may cause unrecognizable vaginal damage, and the degree of damage is directly related to the symptoms of incontinence.
Recent studies have shown that the occurrence of fecal incontinence is related to the increase in maternal age and birth frequency.
The treatment of fecal incontinence includes conservative treatment (such as dietary adjustment and supplementation of dietary fiber), drug treatment (loperamide), pelvic floor muscle exercise, and surgical treatment. Surgical treatment is the last choice for patients who are ineffective in non-surgical treatment.
Pelvic floor muscle exercises and surgery can be used for the treatment of urinary incontinence and fecal incontinence of pregnant women. Recent systematic reviews have shown that pelvic floor muscle exercise has a certain preventive and therapeutic effect on postpartum urinary incontinence, but there is no relevant research on the long-term effect of pelvic floor muscle exercise on urinary incontinence or fecal incontinence.
Surgical treatment for fecal incontinence has progressed rapidly in recent years. Sphincteroplasty is an invasive procedure and may cause complications, but some patients have continuous improvement.
Studies have reported that bulking agent injection therapy may be a safe short-term method to relieve incontinence, and it may improve symptoms and quality of life, but the heterogeneity of the study makes the certainty of its conclusion questionable.
Comparing the use of sacral nerve stimulation and transcutaneous tibial nerve stimulation to treat fecal incontinence, it was found that both methods reduced the symptom score after treatment, but the effect of transcutaneous tibial nerve stimulation was poor.
The development of treatment methods brings hope to patients with fecal incontinence, but it is still necessary to study whether these methods can improve the quality of life of patients.