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Pregnancy in SCD patients presents a clinical challenge as maternal mortality is 1–2% and perinatal mortality is 5–6% [289, 290]. Maternal mortality is rare in pregnant nonsickler patients with AA (see Sect. 15.10.3.1), similar to SCD patients [286]. The fetal loss and premature delivery rates were 9 and 18%, respectively, con­sistent with other reports [15, 21]. The variability of complications [291] may be due to the milder form of SCD in the Al-Hassa area (high levels of HbF). The high HbF levels protect against several clinical features associated with SCD, but the association between HbF levels and the severity of the disease process is complex [289].

The overall AE complication rate is higher than with AA, especially during the third trimester, partly because the incidence is the highest during the third trimester. Intra-appendiceal decidual cells induce a higher inammatory response resulting in a higher occurrence of transmural lesions, which increase the risk of perforation [314]. Approximately 27% of cases during preg­nancy were perforated, all cases during the third trimester. There were no maternal or fetal com­plications in 45% of the cases [302].

unstable inner boundary of the abscess, increas­ing the possibility of rupture [48]. The highest risk of rupture occurs during labor when the uterus contracts, later shrink, and has a signi­cant impact on disseminating pus with the possi­bility of contamination of the genital tract. An abscess can be drained by radiology interven­tional techniques. The patient is in the left lateral decubitus position. MRI-guided puncture through the right psoas muscle is the only safe access to the lesion without other interposing structures. (Fig.15.26). After a successful puncture, pus is aspirated and sent to microbiology. The resolu­tion of an abscess can be re-evaluated with MRI [334].

The unique consideration in the postpartum patient is the presence of a healing abdominal incision after CS.There are no studies on out­comes for recent abdominal incisions subjected to early pneumoperitoneum. Commonly, pneu­moperitoneum is limited to 10 mmHg in CS patients. This prevents undue mechanical strain on the healing wound, though there were no controls for comparison with the standard pres­sures (15–16mmHg). It seems prudent to uti-

220, 337]. Up to 1908, the perforation rate was

64% [338]. When the operation is delayed >24h, a perforation rate is 66% compared to 0% with the operation <24h after the presentation [45]. The timing of intervention varies by trimester: 90% in the rst trimester undergo the operation within 24h of the onset of symptoms. In the third trimester, up to 64% have symptoms >48h before operation [109, 339]. Diagnostic and therapeutic delay >48h is more common during labor and the early puerperium [50, 340–342]. Perforation increases the risk of generalized peritonitis because the omentum cannot isolate the infection [46]. Diagnostic and therapeutic delay is more common during the early puerperium due to the following:

The trend in the perforation rate is decreasing from 25–29% [80, 345] to 15–20% during the last several decades [24, 34]. The perforation rate through the trimesters increases: 6–8.7%, 10–12.5%, and 13–26.1%, respectively [24, 47]. In summary, the causes for the treatment delay include [50, 109, 229, 339, 340] the following:

• Atypical clinical picture when observa­tion delays the intervention,

(patients since 1949 included), maternal mortal­ity was 17% [124]. In all deceased patients, MD perforation was present [124]. The likelihood of maternal death in the USA is higher in the non­Hispanic black population compared to the non­Hispanic white population and Hispanics (OR:

• Maternal temperature>38°C,

• Non-Hispanic black population (USA).

Increased maternal morbidity associated with AA was partly due to the increased peritonitis rate [207]. Maternal morbidity with LA is the same [195] or less [233] compared to OA.The advan­tages of laparoscopy include (1) decreased surgi­cal trauma with lesser use of analgesics, especially opioids that can lead to fetal depression, (2) decreased gravid uterine manipulation, (3) mini­mal use of electrosurgery in the proximity of the uterus, (4) earlier recovery of bowel function with shorter time to oral intake and therefore less nutri­tional stress to the fetus, (5) early mobilization with a lesser risk of thromboembolic risk associ­ated with pregnancy, (6) shorter postoperative length of stay in the hospital, and (7) faster return to daily activities [151, 195, 225, 227, 236, 352–

does not inuence the type of delivery at term, with half of the patients having CS and another half having vaginal delivery in both non­perforated and perforated groups [93]. However, the rate of CS is almost doubled in the presence of peritonitis. This likely reects the increased severity of maternal illness and possible fetal compromise requiring (1) an appendectomy with simultaneous delivery or preterm delivery early after appendectomy [74, 207]. Approximately 12% underwent CS as the mode of delivery and 7% at the time of appendectomy [24].

Surgery (appendectomy) and general anes­thesia are not signicant risk factors for spontaneous abortion and do not increase the risk of major birth defects, even during the rst trimester.

from the literature and stated that the fetal mor­tality in cases of perforative AA during preg­nancy, even when operated upon without delay, was up to 90% [56]. Until 1908, fetal mortality was 40%. Edmund Adam Babler concluded that “the mortality of appendicitis complicating pregnancy is the mortality of delay” [348]. This statement was published several years earlier by Heaton [53]. Until 1973, fetal mortality was 20% (perforated AA 30% and non-perforated AA 3%) and seemed to be related to the severity of the disease rather than the period of gestation [244].

28, 69, 80, 93, 351]. For a comparison, fetal mor-

The risk of appendiceal perforation increases with gestational age, and perforation in the third trimester often results in preterm labor [46]. Patients with peritonitis are more likely to deliver preterm and by CS [207]. Appendectomy in the third trimester has a 1.6× greater risk of preterm birth than in the rst or second trimesters and a

• The increase in preterm delivery: – During the rst week after appendec-

and CS between LA, OA, and conservative treat­ment was observed [194]. Conservative treatment was associated with a lower risk of preterm labor by 60% compared to OA [194]. Another population- based study showed that infants of patients with AA were less likely to be growth restricted at the time of birth, which is in contrast to previous reports of the increased risk of fetal weights <3000g [22] or even <2500g [13]. The study evaluated only patients who delivered in the context of an AA.There was no opportunity for placental insufciency to develop or for the fetus to be exposed to the inammatory environ­ment and develop possible associated sequelae, such as growth restriction over the remainder of the pregnancy. If the authors had been able to fol­low patients who developed AA and delivered later, the fetal weight at birth would be more helpful in determining the impact of AA on intra­uterine growth. Furthermore, as only 1% of preg­nancies with AA were complicated by growth restriction, this raises the possibility of a coding error and missing data.

If there was an effect of surgical trauma on the fetoplacental-uterine elements, it should have ceased approximately 1week after the appendec­tomy of uncomplicated cases [22, 27]. In one study with NA, those without further surgery were considerably more likely to continue their pregnancy undisturbed than those who proceeded with appendectomy (89% versus 57%, respec­tively) [244]. The week following surgery, this increased risk of delivery was present when per­formed after 23 weeks of gestation [26]. Any complication and increased risk of preterm deliv­ery after that period in a patient without surgical complications should not be related to the opera­tion itself [22, 27]. The premature delivery rate was often omitted in reports on AA, but it ranges from 15–45% [21, 108, 364]. It is now believed that subclinical IAI is a cause of preterm prema­ture rupture of membranes or preterm labor and, as such, contributes to the leading cause of infant morbidity and mortality complications from pre­maturity (see Chap. 4).