ACUTE ABDOMEN IN THE ELDERLY – A DIAGNOSTIC DILEMMA
Assoc Professor Nasser Amjad MS, FRCS@
INTRODUCTION:
The evaluation of abdominal pain in elderly patients poses a difficult challenge for surgeons. It also is destined to become an increasingly common problem as the population ages. Almost 50% of elderly patients presenting with acute abdominal pain need hospitalization and of these, at least a third eventually require surgery for their underlying condition. Approximately 40% of elderly patients presenting with abdominal pain initially are misdiagnosed, contributing to the overall mortality rate of approximately 10%.
Even in the presence of serious intra-abdominal, elderly patients are more likely than younger patients to present with vague symptoms and have non-specific findings on examination. This is compounded by the fact that elderly patients have a diminished sensorium, allowing pathology to advance to a very dangerous state prior to developing symptoms.
A careful history and physical examination as well as a high index of suspicion are crucial to prevent missed diagnoses. We present this patient to highlight these important points when confronted with an elderly patient presenting with abdominal pain.
THE PATIENT
Mr. A, s Malay man aged 81 presented with a 2 day history of sudden onset generalized abdominal pain, which according to him was a continuous aching pain, gradually increasing in severity. It was aggravated on taking food but had no associated nausea or vomiting. He has had no bowel motions for 2 days prior to admission but was passing flatus. On further questioning he did complain of similar type of pain on and off for the last one year which was precipitated on taking food. The attacks were becoming more frequent lately. He also has a history of bronchial asthma of several years duration and did mention about an admission to hospital for a ‘heart disease’ 6 months ago. An ultrasound scan of abdomen which was done during that admission showed gallstones and “swelling of vessels”. He was on several medications for his asthma but was not on steroids
On examination he was ill looking, dehydrated and pale. Examination of the cardiovascular system revealed a pulse rate of 96/minute but irregularly regular. BP was 110/90. No cardiomegaly was noted. Examination of the abdomen revealed generalized distension with diffuse tenderness and guarding more marked in the hypogastrium. No obvious masses were palpable. Bowel sounds were sluggish. Hernial orifices were normal. Rectal examination revealed an empty rectum.
Our initial diagnosis was Peritonitis due to perforated viscus (perforated peptic ulcer disease or perforated appendix). Differential diagnoses were acute pancreatitis and large bowel obstruction
Investigations were carried out and revealed the following. Full blood count: Hg 11g/dl, PCV 34.4, and platelets 124 x 103 /uL. Differential count: Total 20.6, Differential N 92.8, L 3.3. Random blood sugar 5.7m.mol/l. BUSE: Blood urea11.8, Na 145, K + 4.5, and Cl 111. SGOT: 25 u/l, SGPT 19 u/l, ALP 132 u/l, Creatine kinase 440 u/l, LDH 653 u/l. Abdominal x-ray showed marginally dilated large bowel loops (Non-specific). Chest x-ray showed no subphrenic gas shadow but cardiomegaly was noted. The echocardiogram indicated ischaemic dilated cardiomyopathy with AF and poor LV function. Ultrasound examination of abdomen showed abdominal aortic aneurysm with a mural thrombus seen. There were no signs of a leak
The possibility of bowel ischemia as an alternative diagnosis was suspected due firstly to the presence of atrial fibrillation and secondly the presence of an abdominal aortic aneurysm. A decision was made to proceed with a laparotomy which was done about 36 hours after admission. Laparatomy revealed a gangrenous colon extending from the splenic flexure to the distal sigmoid and the inferior mesenteric artery was completely occluded. The infracted segment was resected and both ends exteriorized. Post operatively the patient was in intensive care but succumbed to multi-organ failure on the 5th post operative day.
DISCUSSION OF MESENTERIC ISCHAEMIA
Although mesenteric ischemia accounts for no more than 2% of hospitalizations for gastrointestinal conditions, it must be included in the initial differential diagnosis of abdominal pain. Timely diagnosis minimizes the risk of a disastrous bowel infarct. The nonspecific symptoms and the potential for catastrophic outcomes require the physician to be deliberately mindful of this diagnostic possibility and to perform the appropriate investigations in a timely fashion
Anatomy: The blood supply to the colon is via the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA) as shown in the figure.

Acute mesenteric ischemia (AMI) accounts for less than 1% of cases of abdominal pain in elderly patients but is an important cause. It is associated with 50% mortality but this can rise to 90 % if infarction is present. The risk factors for mesenteric ischaemia are age and
Co-morbidities like atherosclerotic disease, arrhythmia, acute myocardial infarction, renal failure, patients on haemodialysis, hypercoagulability states, patients on vasoactive medications (digoxin, pressors, cocaine, diuretics), and recent hypoperfusive state (e.g. major surgery, cardiac arrest)
It is the clinical syndrome resulting from a decrease in blood flow to the small intestine, usually involving the circulation of the superior mesenteric artery (SMA) but can affect the inferior mesenteric artery (IMA) as well resulting in ischaemia to the left colon as in our patient. Emboli are responsible for almost half of all cases of AMI. Emboli result from disruption of a thrombus in the left atrium in the setting of atrial fibrillation as in this patient but can also follow myocardial infarction. Another possible source in this patient could have been from the aortic aneurysm
Classification:Mesenteric ischaemia is classified as follows:

Manifestations of mesenteric artery occlusion may range from transient episodes of visceral pain to irreversible infarction. Past history of similar episodes of pain of milder nature in our patient could have been due to chronic ischaemia which is characterized by intermittent insufficiency provoked by increase demand for perfusion during digestion. These recurrent episodes of postprandial abdominal pain sometimes termed ‘intestinal angina.’
If unattended it can lead to sustained insufficiency, a condition that invariable lead to actual ischaemic injury. This will ultimately manifest as infarction which could be either partial or full thickness.
Clinical presentation: Patients classically present with severe abdominal pain despite having little tenderness on examination. Abdominal pain is disproportionate to the findings on physical examination. Many patients initially complain of vague symptoms such as lower abdominal pain, abdominal distension, diarrhoea, nausea with vomiting, or anorexia.
The patient can also present with chronic ischaemia of bowel. Intestinal angina is a recognized presentation with a history of an aching pain which is poorly localized, being referred to the anterior abdomen. Useful clue is that it seems to be precipitated by meals.
Patients may also present with chronic weight loss due to decreased intake and not decreased absorption. The decrease intake is due more to the fear of precipitating abdominal pain than other factors.
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Death
This algorithm shows the pathophysiology of mesenteric ischaemia
Another mode of presentation is with disturbances in bowel function which may be non- specific like a bloated feeling of the abdomen, generalized abdominal discomfort and a tendency towards diarrhoea or constipation
Most are elderly and have other evidence of obliterative artheromatous disease. Some patients are found to have multiple shallow antral gastric and duodenal ulcers which are resistant to the usual therapy which should make you suspect that ischaemia could be a cause. Thrombosis of the origin of the celiac or mesenteric arteries is the end result of severe occlusive arterial disease
Clinical evaluation:
As mentioned above symptoms are non specific and in established infarction, diagnosis becomes more obvious but survival is unusual as it is too late. In some situation other pathologies detected, may delay the diagnosis of mesenteric ischaemia (e.g. peptic ulcer disease, gallstones). Therefore careful history depends on characteristics of the pain and weight loss.
Diagnosis: The clinician should have a high index of suspicion and must look for clues to suggest a vascular event. Lack of reliable, accurate, early clinical diagnostic findings is a factor responsible for late diagnosis. With regard to abdominal pain or discomfort, may not necessarily be sudden in onset, not necessarily be constant or colicky, Bloody stool or diarrhoea may be present but absence of these symptoms like in our patient does not exclude mesenteric ischaemia. Nausea and/or vomiting may or may not be an associated feature.
Lack of reliable, accurate, early physical examination findings is another contributing factor for late diagnosis.
As shown in the table below, elderly patients over 50y with acute abdominal pain are more likely to have a significant structural explanation

Features consistent with, but not diagnostic of mesenteric ischaemia are:
Blood may be hemoconcentrated (Hct ³ 50)
White cell count may be elevated
Serum amylase may be elevated
Metabolic acidosis may be present at an early stage
Imaging: Plain X-ray abdomen /KUB may help in establishing an alternative process. Non-specific gas distribution in an abdominal x-ray is a common finding like what was noted in our patient. “Pathognomonic” findings if seen are usually late and may point to a poor prognosis. They are Pneumatosis intestinalis (Fig.1), Portal venous gas (Fig.2) and Intestinal “thumbprinting” (Fig.3) which are shown below.
Colonoscopy, abdominal ultrasonography, and barium radiography are not useful in the diagnostic workup of acute mesenteric ischaemia. Barium enema is contraindicated if the condition is suspected
Abdominal computed tomography (CT) scans are valuable in distinguishing not only the possible causes of AMI but also very useful for evaluation of alternative diagnoses in cases where mesenteric ischemia is not the sole consideration.
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| Fig.1 Pneumatosis intestinalis | Fig. 2 Portal venous gas |
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| Fig 3 Intestinal “thumbprinting”of the transverse colon. Note the accentuated focal thickening that indents the contrast in the bowel as if a thumb were pressing on the contrast column. This finding is not specific to ischemic disease |

Dilated loops of bowel
Abdominal CT with intravenous contrast has a sensitivity of 64-71% and a specificity of 73-92%. CT findings supportive of mesenteric ischemia are bowel wall abnormalities like dilated loops of bowel, regional bowel wall thickening, presence of pneumatosis intestinalis and / or portal venous gas. Mesenteric streaking and vascular thrombosis or cut-off may be additional findings.
Angiography
Mesenteric angiography is the “gold standard” for the diagnosis of arterial causes of AMI. It serves as a diagnostic test to identify emboli and thrombi, localize vascular obstructions, and characterize the collateral circulation. It is not only diagnostic but may be useful for therapeutic options like intra-arterial injection of papaverine or thrombolytic agents and also in angioplasty and insertion of stents.
Relative risk is low compared to mortality of delayed diagnosis of mesenteric ischemia

Superior Mesenteric angiogram
CT angiograms, Duplex ultrasonography and Magnetic resonance angiography are newer imaging techniques that are been studied extensively.
Treatment: Initially the primary focus should be basic supportive resuscitative measures like correction of fluid and electrolyte imbalance, stabilization of cardiac function and broad spectrum antibiotic therapy.
If there is evidence of peritonitis, laparatomy is indicated. If there is a doubt about the viability of the nonresected bowel, a "second look" laparatomy should be performed in 24 to 48 hours after the first surgery.
Early diagnosis is essential to reduce morbidity and mortality. If diagnosed early, an embolic episode can be treated by minimally invasive surgical procedures to restore intestinal blood flow. They are intra-arterial thrombolysis, intra-arterial vasodilation, and systemic anticoagulation. If laparatomy is done then a surgical embolectomy should be carried out. Thrombolysis has a higher probability of success when performed within 12 hours of onset of symptoms. Postoperative anticoagulation is used to prevent recurrence. In acute thrombosis, minimally invasive procedures like thrombolytic infusion and angioplasty has been recommended but is not yet accepted as standard practice. In patients with no evidence of infarction intra-arterial infusion of papaverine has been successful but anticoagulation alone is the mainstay of treatment for these patients.
Lesson of the day: Think of mesenteric ischemia if an elderly patient presents with an acute abdomen. Take a proper history and if the abdominal pain is disproportionate to the findings on physical examination think of mesenteric ischaemia. Inquire about other co-morbid factors like heart disease which may contribute to the patient’s condition. Non-specific abdominal examination findings may be unhelpful in establishing a diagnosis. No specific investigation is available. So a high index of suspicion is vital to detect them earlier and minimize morbidity and mortality.
REFERENCES:
· Kumar S, et al.: Mesenteric venous thrombosis. N Engl J Med 345:1683, 2001
· Ho K, Walls R. “Mesenteric ischemia and infarction.” The Clinical Practice of Emergency Medicine. Ed. Harwood-Nuss A, Lippincott Williams-Wilkins 2001; 219-222
· Lock G and Scholmerich J: Non-occlusive mesenteric ischemia. Hepato-Gastroenterology 42:234, 1995.
· Lange H, Jackel R. “Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease.” Eur J Surg 1994; 160:381-4. “Mesenteric Ischemia.” Surg Clin. North Am.