“Acute” here doesn’t mean “the acute abdomen” (i.e. surgical). It refers to chronology, pain less than a couple of weeks’ duration, often just a few days’. Also, many conditions may cause abdominal pain, but present primarily with another complaint, such as vomiting or diarrhea. These aren’t listed; we’re dealing with the patient with pain as the chief complaint.
Lots of possibilities — see the tables. First step: have the patient stand, point to their umbilicus, & then to the area of maximal pain. It may be hard to tell exactly where they’re pointing while sitting. Sometimes I even have to ask at the outset, “Show me your bellybutton.”
TABLE — ACUTE ABDOMINAL PAIN
? = can overlap into this area, but mostly felt in another area
||Periumbilical / Diffuse
We’ll add links to the lower tables when we come to those postings.
Some brief preliminary comments about Abdominal Examination.
Auscultation — Rarely useful. The only time I ever auscultate is to R/O a bowel obstruction, when bowel sounds are hyperactive. “Hyperactive” is not a subjective finding (“Wow, there’s sure a lot of noise in there”). Rather, it means you hear “tinkles” (like tapping crystal) or “rushes” (like a jet take-off).
“Absent” bowel sounds, as in peritonitis, require 5 minutes of silence, for which I’ve never had patience. There are usually other findings to alert me. If I suspect an Aortic Aneurysm, I may listen for a bruit.
Palpation for tenderness is the main parameter we seek. Avoid the area of maximal pain at first; sneak in there later. Begin lightly, then go deeper. Never inquire, “Does this hurt?” Rather, ask about the patient’s kids, or talk about sports, or the weather. Tenderness is defined by a grimace. If an area seems tender, move on to another area, & return later a few times to confirm it.
Our goal is actually to try as hard as possible to be able to chart, “No Tenderness.” If one spot is consistently tender every time, we can’t distract or get around it, then we have a bona fide and significant finding. Serious intra-abdominal pathology is always tender. This is especially important in children. If even one time out of five I’m able to palpate without reaction, I chart my “No Tenderness.”
Involuntary guarding, a reflex muscle contraction while we palpate, is worse than tenderness. “Rebound” is best elicited by shaking the pelvis, or pounding axially on the patient’s heels as they lie supine. The reaction is nothing subtle. A “board-like” abdomen is the worst of all. A normal ambulatory gait rules out advanced peritonitis.
I never check for Obturator or Psoas Signs. They’re for surgeons face-to-face with a boardlike abdomen, who want a better idea of what’s going on before they cut. If a person walks normally, hops on & off the exam table, any “peritonitis” findings are ridiculously false-positives.
As a student practicing on a friend, I pushed a finger into his RLQ, and released it. He responded, “Ow!” I thought, “Appendicitis???” On a healthy guy volunteering for a dumb student’s PE practice?!?!?!?!?! Give me a break!!!!!
DO NOT perform a fecal occult blood test (FOBT)!!! NEVER EVER in the office!!! The test is a marvelous screen for colon cancer, for anybody ≥50 (shown to save lives), but has NO PLACE in diagnosis. Specificity is dismal. Then what do you do with your 25 y.o. and a positive FOBT? Get laughed at by GI (who will still conclude their report-back “thank you for this interesting patient”)? Ignore it, & not tell your lawyer? For persons ≥50 not up-to-date on screening, have them do it at home (more false positives when obtained via anal manipulation on exam).
A word of caution about Abdominal Pain — no matter what the presentation, always BEWARE unusual presentations, often of lethal diseases, in the COMPROMISED HOST. Who is a compromised host? Includes:
I had a 75-year-old patient with 2 days of LLQ pain. She didn’t look ill, but I had no diagnosis, and sent her to an E.D. based on age alone. Her labs & CT were normal, so they discharged her as “gastroenteritis.” Next day, Zoster lesions appeared. I didn’t feel bad in the least.
Also beware the Severely Mentally Ill, who have very high pain thresholds. So if they present with new type of abdominal pain, have a high index of suspicion for something serious.
Onward, to the geography of the abdomen. Remember, of course, that our focus is on out-patient diagnosis, not the guy clutching his belly and vomiting non-stop, or other obvious E.D. candidates. So, starting today with…
EPIGASTRIC & UPPER ABDOMINAL PAIN
Before anything else, make sure it’s not an MI. Age alone may rule, if they’re young. But determine if the pain is exertional, if there are other “angina equivalents.” See our postings about “Chest Pain” and “Dyspnea.”
STOMACH — Assuming we’re not suspecting cardiac disease, most Epigastric Pain will emanate from the stomach. It might be an Ulcer, Gastritis, Esophageal Reflux (GERD), or even better, “Dyspepsia NOS.” “N.O.S.” is an ‘interesting’ abbreviation [click if uncertain].
Before identifying and treating these “stomach” diseases, make sure you haven’t missed another entity in the mid-upper column of our table. Note that diseases usually felt in the LUQ or RUQ may occasionally present with primarily epigastric pain instead. They include:
PANCREATITIS — Pain usually extends to the LUQ, but sometimes not. Suspect it if there’s prominent nausea/vomiting, recent heavy alcohol. Another risk factor: very high Triglycerides (at least >500, usually >1,000). Many patients describe radiation to the back, or gain relief by leaning forward. The rarely-detected flank ecchymosis implies hemorrhage & very poor prognosis.
Serum lipase is more sensitive and specific than an amylase, even on day #1, and is the test-of-choice. Since most patients with acute pancreatitis deserve admission for n.p.o. and hydration, ER referral is appropriate. They’ll do a CT to look for complications.
ACUTE HEPATITIS — Consider it if (gentle) punch-percussion of the liver elicits tenderness (in contrast to contralateral side). Also seek a history of anorexia, nausea, or malaise. Check the eyes for jaundice (in viral hepatitis, onset of jaundice occurs as symptoms abate). If still wondering, order LFTs — a high ALT is the definition of “hepatitis” (technically acute “transaminitis”, until you identify the exact etiology).
The ALT will range from 200 in alcoholic hepatitis to >1,000 in acute Hep A. A very high ALT means nothing in terms of severity; only the prothrombin time is prognostic (INR >1.5 is bad). See posting Acute Hepatitis for etiologic diagnosis.
BILIARY COLIC — Pain often radiates to the right, especially to the right shoulder or back. Other clues: abrupt onset of pain, prominent nausea / vomiting, and especially a history of prior episodes lasting less than a day, which began abruptly over 30-60 minutes, & terminated similarly (stone stuck in duct, then passed). Physical exam may reveal a “Murphy’s Sign” — inspiratory arrest plus a gasp of pain as patient takes slow deep breaths during deep RUQ palpation under the costal margin.
The above description is classic, but most patients with uncomplicated Biliary Colic simply describe recurrent severe upper abdominal pain lasting <12 hours, with some component of nausea. Quality of pain & onset after fatty meal are neither sensitive nor specific. If the patient is symptomatic during presentation, LFTs may be elevated. Diagnosis is made by image (preferably ultrasound). Fever or jaundice suggest frank cholecystitis or choleangitis (send to E.D.).
MUSCLE STRAIN — a commonly missed cause of abdominal pain. Sometimes you get a history of recent or new culprit physical activity (“just joined a gym,” etc.).
First evaluate the presence or absence of tenderness while the patient is relaxed supine. Then have them do a sit-up, maybe even push on the patient’s clavicles as resistance [alert them first], and palpate the muscles while they’re tense. If that maneuver elicits more tenderness, you may have a diagnosis. It’s called “Carnett’s Sign,” though no clinician, including me, would have heard of it.
HERNIAS can occur in any incision, including those for laparoscopy ports. Suspect this in patients with compatible surgical histories, & compatible localization of pain. Palpate for a mass, with patient supine, also while flexing the abdomen and standing, if necessary. Have the patient strain, which can bring out the mass.
Don’t forget EARLY APPENDICITIS, which begins with 1-2 days of low-grade epigastric or periumbilical pain, before localizing in the RLQ. You might even elicit subtle RLQ tenderness to palpation, even though pain hadn’t been felt there. So I always warn patients, “If you get worse, come back.”
A few additional comments about Upper Abdominal Pain. In terms of RUQ PAIN, the most notorious error is to miss a right lower lobe Pneumonia. Always consider the possibility in febrile patients. On Day #1, pleuritic “abdominal” pain may predominate over a cough. Pity the poor surgeons who performed emergent cholecystectomies on patients dying from Pneumococcus [pity the patients].
LUQ PAIN has to be due to gastric conditions or pancreatitis [see prior posting]. Pneumonia isn’t as much of a concern (though MI might be). And splenic [more properly splanchic] infarcts are quite rare outside of sickle cell disease; you’d suspect them by a very tender spleen on exam.
Then there’s Herpes Zoster (shingles), discussed under “Chest Pain”, which can obviously present in a RUQ or LUQ dermatome. Pain may present before skin lesions. No way to tell for another day or two.
NOT “Gastroenteritis” — Why is this in the Table? Acute gastroenteritis causes nausea & vomiting (the “gastro” component) or diarrhea (“enteritis”). It doesn’t present with a chief complaint of “Pain.” Of course, repetitive vomiting like with Staphylococcal “food poisoning” (from a toxin, not the Staph per se) can wind up painful, & some diarrheal pathogens cause gas accumulation. But “pain” isn’t primary.
- PEARL: If vomiting began first, perhaps secondary pain may develop. But if Abdominal Pain begins before the emesis, strongly suspect a visceral origin (gall bladder, pancreas, appendix, etc.) & DO NOT DIAGNOSE “gastroenteritis.”
But let’s say we decide against these above entities, and are convinced the STOMACH is the source. How to distinguish among ulcer, gastritis, GERD, & dyspepsia? It’s very hard. Studies show that symptomatology offers poor correlation with endoscopy.
In one sense, it almost doesn’t matter, because H2-Receptor-blockers (H2RBs) or proton pump inhibitors (PPIs) work for all. We’d advise “no alcohol, no NSAIDs,” no matter what. I refer for endoscopy if a patient doesn’t respond to high doses of a PPI. For age >45, I’m cautious with PPIs, because they can mask the pain of gastric cancer, as opposed to H2RBs. An older patient requiring ongoing PPIs should be scoped.
I don’t test for Heliobacter pylori. Heresy !?!?!?! Once a patient feels better, I certainly test and treat for H. pylori if I think a patient had had a peptic ulcer or non-NSAID-induced erosive gastritis, because of:
- Recent hematemesis or melena (follow hematocrits as well);
- Significant nausea, vomiting, or weight loss resolved with PPI Tx;
- Past History of GI bleed.
- Recurrent episodes of daily upper abdominal pain lasting >3 weeks.
I also test and treat for H. pylori if patients have a family history of gastric cancer.
But the effect of H. pylori eradication on non-ulcer dyspepsia is minimal. For GERD, H. pylori may even be protective [!!!!]. In the U.S., rates of positive serology range from 10% among young adults to 50% among those over 60. Prevalence is higher among the poor and among immigrants. But you don’t find 10% of young adults getting ulcers (nor 50% of seniors)! Interestingly, a colleague’s patient got H. pylori treatment elsewhere, and subsequent rhabdomyalysis from clarithromycin plus the simvastatin that nobody knew he was on.
I got disgusted with H. pylori in the 1990s, when countless free “educational” dinners were promoted by manufacturers of PPI and/or macrolide antibiotic brand names before they’d gone generic (and perhaps lab test vendors too). Various professional societies recommend “test-and-treat,” but that strategy is mainly to reduce endoscopies. Sorry, but I remain a skeptic of the eradication crusade. Address H. pylori for patients you truly think have ulcers or gastritis, not dyspepsia or GERD.