A 77-Year-Old Man With Suddenly Worsened Abdominal Pain

Background

　A 77-year-old man presents to the emergency department (ED) in the early morning
　with a 4-hour history of severe, generalized abdominal pain.
　He describes some “cramp-like” abdominal pain and bilious vomiting yesterday,
　but states he simply “got on with things”.
　His condition had worsened considerably by late evening.
　He describes the sudden onset of generalized, constant,
　intense abdominal pain necessitating an ambulance call.
　On presentation to the ED, he has no current vomiting.
　He complains of episodic “indigestion” that has occurred off and on for the past few months.
　On further questioning,
　the patient reports experiencing infrequent but quite painful episodes of upper abdominal pain
　after meals which sometimes feel as if it is ”going to his right upper back”
　and is associated with intermittent vomiting.
　This lasts for minutes to hours after the intake of meals.
　He states that antacid preparations do little good in controlling these symptoms,
　but he takes them anyway.
　His past medical history includes hypertension, ischemic heart disease,
　chronic obstructive pulmonary disease (COPD), and gout.
　He has no significant past surgical history and
　his currently prescribed medications include aspirin, atenolol,
　furosemide, a glyceryl trinitrate spray,
　and 2 inhalers for his COPD (the names of which the patient does not know).

　On examination, the patient is lying quite still.
　He does not appear cachectic, but does seem clinically dehydrated.
　His heart rate is 80 bpm, his blood pressure is 102/65 mm Hg,
　his capillary refill time is prolonged, and cool extremities are noted. He is afebrile.
　His lungs are clear to auscultation and his heart sounds are normal, with no added sounds.
　His abdomen is mildly distended, without visible scars, and there is no discoloration of the skin.
　When asked to cough, the patient winces in pain.
　No hernias are appreciated on examination.
　Palpation of the abdomen reveals generalized, diffuse tenderness and board-like rigidity.
　The abdomen is tender to percussion throughout all 4 quadrants,
　with a tympanitic note that is associated with loss of liver dullness.
　A rectal examination reveals a small amount of normal stool.
　Both femoral pulses are palpable and equal.
　The neurologic examination reveals no abnormalities.
　The peripheral examination is normal except for cool extremities.

　A fluid challenge of 500 mL 0.9% saline is given along with analgesia, and his vital signs improve.
　Laboratory investigations yield the following information:
　a white blood cell (WBC) count of 15.8 × 103/μL (15.8 × 109/L),
　C-reactive protein is 247 mg/L, sodium is 148 mEq/L (148 mmol/L),
　potassium is 3.1 mEq/L (3.1 mmol/L), urea is 28.6 mg/dL (10.2 mmol/L),
　creatinine is 1.5 mg/dL (131μmol L). Blood gas analysis reveals
　a pH of 7.31, HCO3 of 20 mEq/L (20 mmol/L), PCO2 4.1 kPa, and lactate of 23.4 mg/dL (2.6 mmol/L).
　Erect chest and supine abdominal radiographs are obtained (see Figures 1 and 2).
　A nasogastric tube is inserted and instructions are given for the patient to remain ‘nil by mouth’.
　He is catheterized and the urinary output is monitored along with the vitals.
　A further 1000 mL of 0.9% is initiated.
　Cefuroxime and metronidazole are started intravenously,
　and after urgent surgical consultation the patient is taken to the operating room
　for an emergency laparotomy.

Discussion

　This patient was suffering from mechanical small-bowel obstruction
　complicated by perforation and subsequent peritonitis.
　The patient’s history and examination findings were consistent with this sequence of events.
　Further support for this was found on the erect chest and supine abdominal radiographs;
　the presence of a large amount of free intraperitoneal air and dilated loops of small bowel were noted.
Regardless of the underlying etiology,
　the initial treatment for intra-abdominal free air with peritonitis is emergency laparotomy.

　After resuscitation,
　the patient was transferred to the operating room for an exploratory laparotomy.
　During the procedure,
　it was revealed that the peritoneal cavity was grossly contaminated with
　intestinal contents spilling out from a small hole in the distal ileum.
　The cause of the obstruction was found to be a gallstone of 1.18 in (30 mm) in diameter
　that was impacted in the terminal ileum.
　The gallbladder was adherent to the duodenum.
　The entire length of the bowel was examined for other stones, but none were found.
　The stone was gently massaged in order to move it proximally and it was removed via an enterolithotomy.
　The perforation was closed with interrupted sutures and, after copious lavage, the abdomen was closed.

　Cholelithiasis is a common disorder prevalent in 10% of the population,
　with symptomatic manifestation in 20-30% of those affected.[1,2]
　Gallstone disease may present with an assortment of complications
　that are usually the result of stones within the gallbladder and biliary tree,
　with the most common presentation being biliary colic.
　Extrabiliary problems are rare;
　however, some 3-5% of patients with cholelithiasis have a cholecystenteric fistula
　as part of the spectrum of their disease,
　most commonly occurring between the gallbladder and duodenum (71.4%),
　followed by a fistula with the stomach (14.3%) and, lastly, with the colon (6.3%).[3]
　In addition,
　fistulae may arise between the common bile duct and the intestinal tract,
　and other organs and the abdominal wall have also been reported as being involved.
　The possibility of concurrent Mirizzi syndrome
　(a rare condition in which gallstones lodged in the Hartmann pouch or cystic duct
　externally compress the common hepatic duct) should be ruled out
　because an association between these has been suggested.
　Gallstones may migrate into the gastrointestinal tract through such a fistula
　(as in the case of this patient), but the majority of such cases pass without incident.
　Stones larger than 0.7-1.0 in (2-2.5 cm), however, are at risk of becoming impacted.[4]
　Gallstones can grow in diameter as they pass through the intestinal lumen and sediment
　from the bowel contents is deposited onto them.
　In a series of 40 patients,
　the site of impaction was found to be the ileum in 25 patients, jejunum in 9,
　duodenum in 3, and colon in 1.[5]
　A further review of 1001 patient cases delineated these sites further,
　with the terminal ileum and ileocecal valve reportedly being most commonly involved,
　followed by the ligament of Treitz and the pylorus,
　whereas the duodenum and sigmoid colon were relatively rare locations
　for impaction of a gallstone within the enteric tract.[6]
　It should be noted that these sites represent regions of anatomically smaller luminal diameter.
　Colonic obstruction would likely only occur if a pre-existing pathology,
　such as a colonic stricture, were present.

　Mechanical intestinal obstruction with a gallstone was first described by Bartholin in 1654,
　with the term “gallstone ileus”; however, this is a misnomer.
　The symptoms are variable depending on the site of impaction and
　mirror those of intestinal obstruction resulting from any etiology.
　Classically,
　the patient will present with subacute episodes of obstruction
　resulting in abdominal pain and vomiting that subside as the stone spontaneously disimpacts.
　The symptoms will then recur as the stone becomes larger
　(because of accrued bowel sediment) and reobstructs the bowel lumen.
　On a side note, high duodenal or pyloric impaction will produce a clinical picture
　more akin to gastric outlet obstruction and is known as Bouveret syndrome.
　Of all the causes of mechanical intestinal obstruction, gallstones account for 1-4%
　(up to 25% if we consider only patients over 65 with nonstrangulated obstruction) and
　occur more commonly in women.[6]
　The diagnosis is notoriously difficult to make,
　with up to 50% of diagnoses being made at laparotomy.[4]
　Patients often have no previous history of biliary symptoms and
　other causes of obstruction are more common, which can lead to this condition being overlooked.
　Radiographic clues are responsible for the majority of early diagnoses.
　On abdominal radiography,
　the Rigler triad (pneumobilia, small-bowel obstruction, and
　a gallstone usually seen in the right iliac fossa) is considered highly suggestive of gallstone ileus.
　It should be remembered here that only 10% of gallstones are visible on radiographs,
　and gas in the biliary tree and gallbladder has many causes and is most commonly iatrogenic.
　This can be extended to other imaging modalities.
　Current evidence indicates that the Rigler triad can be seen in 15% of patients
　on abdominal radiography, 11% on ultrasonography, and with computed tomography (CT) scans
　demonstrating the triad in 78% of cases;
　in fact, CT scanning was often able to show the fistula itself.[7]
　Further studies support the role of CT scanning in the evaluation of patients
　with gallstone ileus by highlighting its ability to detect the size,
　location, and exact number of ectopic stones, and
　they also laud its overall value in the diagnoses of many cases of acute abdomen.[8]
　Contrast studies of the upper gastrointestinal tract have also been used,
　albeit less frequently, and
　have had some success in defining the site of obstruction and
　demonstrating the fistula via retrograde flow into the biliary tree.
　The success of CT scanning at demonstrating additional ectopic stones raises the issue of recurrence.
　Additional ectopic stones may be present and, rarely,
　may be overlooked, possibly leading to a second episode of obstruction after operation.
　Attention should be paid to the fistula itself;
　determining its presence is essential, as is planning for its remediation.
　This lends credence for the use of CT scanning in the investigations for this condition.
　Although ultrasonography fairs worse than plain films in demonstrating the Rigler triad,
　it remains excellent at demonstrating biliary pathology overall.

　In this case,
　a further complication had occurred, namely ileal perforation proximal to the site of obstruction.
　Only a handful of cases of gallstone ileus report such a complication,
　which normally arises as a result of the pressure of the stone
　causing necrosis of the bowel wall at the site of obstruction,
　or increased wall tension caused by distention proximal to the obstruction.[9]
　Although this patient’s complication occurred because of a delay in presentation,
　it is important to bear in mind that a delay in the diagnosis
　also adds to the already significant mortality and morbidity of this condition
　by allowing the development of further complications and
　decreasing the physiologic reserve of the patient prior to therapeutic management,
　which often includes surgery.
　Typical patients are also elderly and more likely to have comorbidities;
　all of these factors combine to give an overall perioperative mortality of 12-17%.[6]

　Whatever methods are used to guide the clinician, prompt resuscitation and surgery
　are pivotal in offering the best prospects of survival to the patient with gallstone ileus.
　There is significant disagreement over how to surgically approach these patients
　to relieve the obstruction.
　Some favor a laparoscopic approach and argue that it is a diagnostic tool
　in the acute abdomen with the potential for definitive treatment,
　and that the smaller incisions and reduced recovery time suit the patient population better;
　in addition,
　there is also the ability to convert to an open procedure
　if the operation is technically too difficult.
　Laparoscopy, however, can result in decreased venous return as a result of the increase
　in intra-abdominal pressure;
　this can translate into hypotension in a patient who is already hemodynamically unstable.
　This being said, there are numerous case reports of laparoscopic enterolithotomy
　and disimpaction procedures being carried out successfully,
　with patients going on to have uneventful hospital stays and discharge.[10,11]
　The choice of open versus laparoscopic surgery should be based on the surgeon’s skill
　and the anesthesiologist’s opinion.
　Another issue is whether or not definitive biliary surgery,
　namely closure of the fistula and cholecystectomy, should be undertaken and,
　if so, when. Relief of the intestinal obstruction is the first priority and,
　in general, enterolithotomy alone is believed to be the best course of action
　in the typical patient with gallstone ileus.[12,13]
　Closure of the fistula and cholecystectomy can then be performed electively at a later date
　(the so-called “2-stage procedure”).
　Performance of a “1-stage procedure” should only take place in
　a highly select group of low-risk patients,
　as a small but significant increase in perioperative mortality has been observed
　(from 11% to 16.7% in general populations).[12,14]
　Although surgery is the treatment of choice, endoscopic sphincterotomy
　and common bile duct stone extraction have been shown to cause spontaneous healing of fistulas.
　Extracorporeal and electrohydraulic lithotripsy of stones has also been described in cases
　where gas-containing bowel loops were not in the way.
　Finally,
　endoscopic procedures for removing stones from the duodenum and colon
　can also be employed at specialized centers.
　Such procedures are reserved for the treatment of patients
　who are unable to undergo surgery to correct the fistula.[15,16]
　A fact that needs to be stressed is that at the time of surgery the entire length of bowel
　should be examined for further ectopic stones or fragments.

　In conclusion,
　mechanical obstruction of the intestine with a gallstone
　is an uncommon complication of stone disease in the biliary system,
　occurring in less than 0.5% of patients.[6]
　The diagnosis is difficult to make given the lack of antecedent history
　in a large proportion of patients and its relative infrequency as a cause of obstruction.
　A careful history-taking and physical examination,
　in particular excluding adhesion and external hernia,
　and the use of imaging such as CT scanning can expedite the establishment of the diagnosis.
　This should be undertaken when resuscitative measures are being done,
　and should not delay operative intervention when perforation and peritonitis are present.
　The procedure of choice should be chosen bearing in mind
　that obstruction relief is the first priority.