On successfully completing this topic, you will be able to:
understand how to assess the pregnant woman with abdominal pain
appreciate how to suspect and promptly diagnose potentially life-threatening conditions
appreciate the changes in anatomy and physiology that occur in pregnancy and understand how these may affect the response to, and presentation of, acute abdominal conditions
understand the investigation and treatment of abdominal pain in pregnancy.
Background and incidence
Abdominal discomfort in pregnancy is common, but any abdominal pain should be taken seriously. Frequently, minor ailments such as urinary tract infections are found to be the cause, but significant serious pathology does occur and can present in subtle ways. This can result in serious diagnoses being missed or delayed which can, in turn, result in death of the mother and/or fetus. In the UK all maternal deaths in pregnancy are reported and there are approximately three deaths each year due to intra-abdominal pathology (Table 21.1).
| Cause of death | 1997–99 | 2000–02 | 2003–05 | 2006–08 | Total |
|---|---|---|---|---|---|
| Intestinal obstruction | 3 (small bowel) | 3 (+1 late death) | 0 | 0 | 7 |
| Pancreatitis | 2 | 1+1 pancreatic cyst | 2 (+2 late deaths) | 0 | 8 |
| Splenic artery aneurysm | 1 | 0 | 0 | 0 | 1 |
| Intra-abdominal bleeding | 1 | 0 | 0 | 0 | 1 |
| Liver failure | 1 | 0 | 3 | 4 | 8 |
| Liver rupture | 1 | 0 | 1 | 0 | 2 |
| Peritonitis | 0 | 1 | 1 appendicitis 1 faecal peritonitis | 0 | 3 |
| Duodenal ulceration | 0 | 0 | 0 | 2 (1 bled; 1 perforated) | 2 |
| Ruptured oesophagus | 0 | 1 | 0 | 0 | 1 |
| Pseudo-membranous colitis | 0 | 0 | 0 | 1 | 1 |
| Crohn’s disease | 0 | 0 | 0 | 2 | 2 |
| Total | 9 | 7 (+1 late death) | 8 (+2 late deaths) | 9 | 36 |
Information for intra-uterine deaths from maternal disease/peritonitis is not systematically collected, so this aspect of mortality is unmeasured. Many of the women who died received substandard care which often included a delay in diagnosis. Recurrent problems highlighted throughout the confidential reports include:
failure to entertain the possibility of a nonobstetric diagnosis
readmission or multiple admissions with no consultant input
repeated doses of pethidine given for analgesia without consultant review or an adequate cause for pain being established
high-risk women being looked after in a disjointed way by junior clinicians with lack of communication between services
anxiety and confusion too readily being attributed to a psychiatric cause rather than the underlying (undiagnosed) organic disease.
Pathophysiology of abdominal pain in pregnancy
Abdominal pain, especially of acute onset, in the pregnant woman is a medical emergency that requires urgent assessment. As pregnancy advances, the assessment of the abdomen becomes more challenging:
areas of maximum pain or tenderness may shift due to organ displacement
the uterus inhibits abdominal palpation
the peritoneum is less sensitive.
The other problem produced by the gravid uterus is that of hampering the omentum from its role as ‘policeman’ of the intra-abdominal contents, with the consequence of an inability to contain local inflammation; in turn, this results in more rampant progression of conditions such as appendicitis or perforation.
Intra-abdominal bleeding can also confuse the clinician as the mother, especially in later pregnancy, tolerates blood loss well. The reader is referred to Chapter 5 (Shock) and Chapter 25 (obstetric haemorrhage), and reminded that the signs of bleeding, including tachycardia, narrowing of the pulse pressure, oliguria and confusion, all occur after significantly more blood is lost in the pregnant than the nonpregnant woman, and that hypotension is an extremely late sign. What does help with assessment in pregnancy is that the fetus tolerates maternal blood loss very badly and is a good ‘monitor’ of maternal hypovolaemia, demonstrating heart rate abnormalities on monitoring. Early fetal heart rate monitoring is therefore extremely useful in women presenting with abdominal pain from the late second trimester onwards.
Clinical approach to diagnosis: history, examination, investigation
History
A detailed history around the nature of the pain is a vital step in beginning the diagnostic process, and is especially important in pregnancy where abdominal examination can be so inhibited by the gravid uterus. The following should be found from general and then direct enquiry.
Pain onset: acute versus gradual
Acute onset with persistent severe pain suggests rupturing or tearing including ruptured ectopic, ruptured uterus, ruptured aneurysm (splenic, renal, epigastric or aortic), rupture of an abscess or perforation of an ulcer. Acute abruption also presents with severe acute abdominal pain and should be the presumptive diagnosis until ruled out. Acute onset with colicky pain suggests either intestinal or ureteric obstruction. Hernial orifices should be checked (sometimes difficult in a heavily pregnant and/or obese woman). If colicky pain becomes constant then the possibility of underlying ischaemia must be considered (e.g. bowel or ovary).
Gradual onset increasing over a comparatively short time is more characteristic of
‘inflammation’ such as might occur with acute appendicitis, acute degeneration of a fibroid, acute cholecystitis, acute pancreatitis and acute diverticulitis.
Other important characteristics
Quality and severity (colicky pain suggests an obstruction or something twisting, while continuous pain is more likely to suggest inflammation/infection).
Location (think uterine, intraperitoneal, retroperitoneal and referred).
Radiation (remembering diaphragm to shoulder, renal to groin and ovary down inner thigh).
Exacerbating or relieving factors (movement, coughing, voiding, position).
Associated symptoms (anorexia, nausea, vomiting, constipation, dysuria, haematuria, frequency).
Location of the pain and its likely cause
Uterine pain: abruption, degeneration of fibroids, chorioamnionitis or uterine contractions
The location of this is usually straightforward and confirmed by tenderness on palpation of the uterus but fibroids can lie posteriorly and be inaccessible to palpation, and a posteriorly located placenta can abrupt without producing local tenderness. Remember to check:
the placental location relative to any uterine pain or tenderness
the fetal heart rate pattern.
Intraperitoneal (abdominal) pain
Visceral peritoneal, compared with parietal peritoneal, irritation stimulates the afferent nerve fibres running within the sympathetic part of the autonomic system back to the sympathetic chain and spinal cord. This, therefore, produces a vague ‘referred pain’, usually in the central region, corresponding to the cutaneous nerves that arise from the corresponding level of the spinal cord. For example, in appendicitis this produces pain in the region of T10, which is around the umbilicus.
Once the parietal peritoneum becomes involved, segmental somatic innervation comes into play and produces sensation in the location of the problem, hence vague pains ‘move’ to localise as the disease process progresses. Inflammation and infection tend to produce constant pain that evolves as described above, but is also usually associated with constitutional upsets of nausea, anorexia, vomiting and fever. In many conditions, initial inflammation leads to subsequent infection, such as in appendicitis and cholecystitis.
Obstruction produces colicky pain that can be severe, and can also be associated with nausea and vomiting if the obstruction is in the small intestine. There may be a change in bowel habit depending if the distal small bowel or colon is involved. Perforation of a viscus usually follows deterioration of the above conditions or more directly from a peptic ulcer, or sigmoid diverticulum. This leads to the severe constant pain of generalised peritonitis, worsened by movement of any sort.
Examples of inflammation without infection include oesophagitis (heartburn) and (simple) peptic ulceration. These lead to epigastric pain, whereas a flare up of either Crohn’s disease or ulcerative colitis leads to more central abdominal pain, which may be colicky and usually associated with diarrhoea. It is worth noting that the administration of steroids, either to promote fetal lung maturation, or as treatment for inflammatory bowel disease, can not only exacerbate peptic ulceration, but also, importantly and dangerously, mask intra-abdominal signs and add to confusion in the diagnostic process.
Examples of inflammation, which lead to infection, include cholecystitis and appendicitis. Both these conditions present with increasing pain that settles into a specific location. The appendix migrates superiorly with advancing gestation, progressing from the right iliac fossa upwards to the right paraumbilical region and can even reach the right hypochondrium.
Examples of obstruction include sigmoid volvulus and pseudo-obstruction, the latter often occurs post-CS. While a sigmoid volvulus is usually associated with absolute constipation, pseudo-obstruction may not be so, and small amounts of liquid stool are not uncommon. Colonic neoplasms, although rare, can also occur.
Perforations from peptic ulceration arise de novo and are rarely associated with any prodromal symptoms of an underlying ulcer. Perforations from appendicitis, sigmoid volvulus or pseudo-obstruction occur due to delay in both diagnosis and management.
Rupture or torsion of an ovarian cyst can also produce a colicky pain, which can progress to a constant pain with constitutional upset once ischaemia develops. While this pain is located in an iliac fossa early in early pregnancy, as with appendicitis, it can occur relatively higher in later pregnancy.
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