Left Upper Quadrant Abdominal Pain

I. Problem/Condition.

Left upper quadrant (LUQ) pain has a wide and varied differential diagnosis. This differential is driven by the overlying structures (skin) as well as the internal organs that populate the LUQ of the abdomen. It is important to understand the quality of the pain (constant versus colicky, dull versus sharp) and consider the time course over which the pain developed.

LUQ pain results more acutely from trauma, infection, and perforation. Subacute and chronic LUQ pain results from inflammation, lymphatic, and vascular complications. Careful consideration of these structures coupled with labs, imaging, and a thorough examination will allow the hospitalist to narrow the broad differential.

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

The most common diagnoses for LUQ pain relate to intestinal (small/large), splenic, pancreatic, and renal processes. Small bowel causes include obstruction, Crohn’s disease, irritable bowel xyndrome (IBS), mesenteric ischemia, and mesenteric adenitis – an inflammatory process of mesenteric lymph nodes that often mimics appendicitis.


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Large bowel causes include colitis, diarrhea, diverticulitis, volvulus, mesenteric ischemia, and obstipation/constipation. Splenic etiologies include trauma, infarct, and splenomegaly secondary to neoplasms, lymphoma, portal vein thrombosis, Gaucher’s disease, portal hypertension, and endocarditis. Pancreatic causes include both acute and chronic pancreatitis, and pancreatic abscesses/cysts and malignancy. Finally, most common diseases of the renal system include pyelonephritis, nephrolithiasis, and perinephric abscess. In addition to intra-abdominal causes of abdominal pain, extra-abdominal and referred causes of LUQ pain to consider are dermatologic, musculoskeletal, and cardio/pulmonary.

B. Describe a diagnostic approach/method to the patient with this problem.

A thorough history, as detailed in the section below, is critical to define acuity of LUQ pain, as several surgical emergencies may present with LUQ pain. By understanding the acuity, severity, and characterization of the pain, a targeted physical exam can be performed.

There are several approaches to generating a differential diagnosis list for LUQ pain. One approach is to separate superficial or extra-abdominal causes of LUQ pain, and then focus on intra-abdominal causes of pain. Extra-abdominal causes include dermatologic diseases such as Herpes Zoster or cellulitis, musculoskeletal causes such as bone fractures and neuropathies, and referred pain from other organs that lay adjacent to the peritoneum such as pleuritis, pneumonia, acute coronary syndrome, and pericarditis.

1. Historical information important in the diagnosis of this problem

After considering the location of the pain and the systems involved, it is critical to get a detailed history from the patient that involves the following: frequency of pain, associated symptoms, radiation, characterization, time of onset, location of pain, duration of symptoms, exacerbating and relieving factors. These descriptors will dictate which organs are most likely to be involved. Key questions would highlight the following:

Constant pain versus colicky pain – Colicky pain indicates a luminal obstruction. The most common luminal tracts in this region include the large bowel, small bowel, and ureters. Conversely, constant pain might suggest disease of a solid organ (i.e. splenomegaly).

Pain out of proportion to exam – Acute/chronic mesenteric ischemia, functional abdominal pain.

Recent trauma – Perforation of bowel, splenic laceration, pancreatitis, developing obstruction, hematoma.

Recent sick contacts – Abscess formation, infectious causes of colitis, Crohn’s flare.

Recent travel – Increased risk of infection such as hepatitis, malaria, CMV (cytomegalovirus).

Surgical history – 70-80% of small bowel obstructions are secondary to post-operative adhesions.

Social factors such as drug use – Cocaine can cause mesenteric ischemia.

Smoking history and alcohol intake – Risk factors increase risk of nearly all diseases including mesenteric ischemia and pancreatitis.

Sexual history and history of sexually transmitted diseases – patient at higher risk of pyelonephritis and abscess formation. A variety of viruses can also cause splenomegaly.

Environmental exposure to carcinogenic agents – increased risk of neoplasm formation.

Family history of diseases including colon cancer, inflammatory bowel disease.

Urinary habits – Dysuria, nocturia, hematuria, incontinence, incomplete voiding are associated with nephrolithiasis, urinary tract infection, and risk of pyelonephritis.

Bowel habits – Frequency of bowel movements, pain, or pain relief with defecation, size, consistency, color, and association with food intake may elucidate diseases such as IBS, Crohn’s, pancreatitis, obstruction/obstipation, malignancy.

Menstrual history including concerns for endometriosis and referred pains.

Systemic symptoms – Constitutional symptoms, such as fever, chills, and night sweats, suggest an infectious or inflammatory cause. Symptoms such as weight loss and appetite change suggest more chronic problems such as Crohn’s, mesenteric ischemia, or malignancy.

Nutritional habits – What kinds of food does the patient eat? Do they refrain from certain types of food or eat high amounts of other food? Post-prandial pain may indicate mesenteric ischemia or peptic ulcer disease.

Cancer screening history – Colon cancer, breast cancer.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

When performing a physical exam, the patient must be undressed to expose the abdomen, laying supine on the bed with their knees bent, and feet flat in order to relax their abdominal muscles.

Visually inspect the abdomen for trauma, lesions, bruises, and surgical scars. Bruising (Cullen’s sign around the umbilicus or Grey Turner’s sign around the flanks) may indicate pancreatic or retroperitoneal hemorrhage. Recent surgical scars may indicate an area of adhesions and obstruction.

Second, auscultate the abdomen – listen for absence/presence of bowel sounds. If high pitched sounds, like tinkles and rushes, are present, this is a sign of obstruction as the peristaltic action of the intestine pushes against a small bowel obstruction.

Next, lightly palpate the abdomen in a step wise fashion. Start with a quadrant of the abdomen that is not painful, and move either clockwise or counter-clockwise until you palpate the painful LUQ. If any masses are appreciated, proceed with deep palpation to characterize the size. Pay close attention to the facial response of the patient as you palpate. Assess for guarding – both involuntary and voluntary. With involuntary guarding, the patient still has abdominal pain as they exhale while your hand is palpating that area. Assess for rebound tenderness – pain that is elicited, or worsens, as the pressure from the examiner’s hand is removed.

Both involuntary guarding and rebound tenderness are signs of peritonitis, and may require immediate surgical consultation. The spleen may be challenging to palpate, even if enlarged. Since the spleen is very mobile, you must push lightly in the LUQ and ask the patient to inhale. As they inhale, the diaphragm pushes the spleen caudally and toward the umbilicus. A normal spleen should not be palpable. Palpating the kidneys is not always possible; however, you can assess if they are edematous or swollen by forming a fist and lightly tapping on the costovertebral angle (CVA) on the left-side of the flank. If CVA tenderness is present, this may suggest pyelonephritis.

Finally, percuss the abdomen; tympanic sounds indicate air in the bowel or stomach. A dull sounding abdomen is consistent with stool filled bowel, ascites, or an abdominal mass.

3. Laboratory, radiographic, and other tests that are likely to be useful in diagnosing the cause of this problem

Labs:

Complete blood count (leukocytosis for infection, thrombocytopenia for platelet sequestration, hemoglobin/hematocrit – blood loss anemia or hemolysis)

Basic metabolic profile (renal insufficiency, BUN:Creat ratio may help differentiate volume status), electrolyte abnormalities

Liver function test (elevated protein gap suggesting HIV, hepatitis, or multiple myeloma; hyperbilirubinemia suggesting possible pancreatohepatobiliary obstruction; elevated transaminases suggesting parenchymal injury or biliary obstruction; and liver synthetic function when considering causes of splenomegaly)

Lactic acid (mesenteric ischemia secondary to vascular or toxic [cocaine] causes)

Lactate dehydrogenase (LDH) (pancreatitis, mesenteric ischemia)

Amylase (mesenteric ischemia, pancreatitis)

Lipase (pancreatitis)

Urine toxicity screen (cocaine induced mesenteric ischemia)

Blood alcohol level, fasting lipid profile, fecal fat studies (acute and chronic pancreatitis)

Stool studies – fecal leukocytes, ova and parasites, gram stain and culture, Clostridium difficile

Anti-saccharomyces antibody (Crohn’s disease)

Fecal calprotectin level (inflammatory bowel disease)

Imaging:

  • Total abdominal ultrasound with Doppler imaging (gallstone pancreatitis, nephrolithiasis with hydronephrosis, splenic masses, splenic vein thrombosis, perinephric abscess, portal vein thrombosis)

  • Computed tomography (CT) scan with kidney stone protocol (nephrolithiasis)

  • CT Abdomen/ Pelvis (pancreatitis, pancreatic abscess, perinephric abscess, pyelonephritis, obstruction, diverticulitis)

  • Barium contrast enema (Crohn’s disease, volvulus)

  • MRA or CT Angiogram or Mesenteric Angiography (mesenteric ischemia)

  • Abdominal X-Ray (obstruction, Crohn’s disease, nephrolithiasis, colitis)

  • CXR flat and upright (perforated lumen with free intraperitoneal air)

  • MRCP/ ERCP +/- EUS (pancreatitis, pancreatic abscess/cyst, pancreatic malignancy)

  • Colonoscopy – (Crohn’s disease, colitis, diverticulosis)

Other Tests: Intra-abdominal pressure/bladder pressure (if concerned for abdominal compartment syndrome secondary to pancreatitis or peritonitis)

C. Criteria Suggestive of Each Diagnosis in the Method Above

Splenic infarct/trauma:

  • Sx: LUQ Pain, fever, chills, nausea, vomiting, left shoulder pain

  • Tests: leukocytosis possible

  • Imaging: Abdominal ultrasound – good sensitivity and specificity for trauma or abscess; CT abdomen with IV contrast (delayed phase), Angiography when a vascular lesion is suspected

Splenomegaly:

  • Sx: LUQ Pain with occasional left shoulder pain, early satiety, nausea, vomiting, fever, chills

  • Labs: leukocytosis or leukopenia, thrombocytopenia, and anemia due to sequestration

  • Imaging: Abdominal ultrasound or CT abdomen

Mesenteric ischemia:

  • Sx:

    Acute – Pain out of proportion to physical exam, colicky or constant pain, abdominal distension, GI bleeding, fever, diarrhea, nausea, and vomiting

    Chronic – postprandial pain, fear of eating, weight loss

  • Labs: if infarction – hyperamylasemia, lactic acidosis, leukocytosis, elevated LDH

  • Imaging:

    Abdominal X-ray – Flat and erect (thumb-printing)

    CT Angiogram / MR Angiography – sensitive and specific for venous thrombosis but not peripheral arterial occlusion and non-occlusive mesenteric ischemia

    Angiography – gold standard for arterial and venous occlusion

Small bowel obstruction:

  • Sx: LUQ pain, tinkling bowel sounds, abdominal distension, nausea, and vomiting

  • Labs: not helpful unless infarction present – then hyperamylasemia, lactic acidosis, elevated transaminase levels

  • Imaging:

    Abdominal X-ray – (dilated loops of bowel); upright and decubitus (air-fluid levels)

    CT abdomen – defines location and presence of transition point with obstruction as well as suggests inflammatory or neoplastic etiologies

    Contrast enema radiography (water soluble) – upper / lower GI tract

Crohn’s disease:

  • Sx: abdominal pain, fatigue, malaise, fever, chills, nausea, vomiting, diarrhea (bloody and non-bloody), fistula formation, extra-intestinal manifestations including: arthritis, hepatobiliary complications, erythema nodosum, uveitis, oral ulcers, DVT/PE, recurrent UTIs

  • Labs: nonspecific CBC/CMP; elevated ESR, low albumin, anti-saccharomyces antibody positive (60% of patients), pANCA negative (10% of Crohn’s patients are positive)

  • Imaging:

    Colonoscopy with tissue biopsy – confirmatory test

    Air contrast barium enema, small bowel follow through, enteroclysis – confirm location

    Abdominal ultrasound or EUS, CT abdomen, MRI – can discriminate intra-abdominal masses/abscesses

Irritable bowel disease

Rome III criteria:

Irritable Bowel Syndrome can be diagnosed based on at least 12 weeks (which need not be consecutive) in the preceding 12 months, of abdominal discomfort or pain that has two out of three of these features:

1. Relieved with defecation

2. Onset associated with a change in frequency of stool

3. Onset associated with a change in form (appearance) of stool

Mesenteric adenitis:

  • Sx: abdominal pain (usually RLQ), fever, diarrhea, anorexia, peripheral lymphadenopathy

  • Labs: leukocytosis, blood cultures, urinalysis – signs of infection

  • Imaging:

    CT abdomen – definitive

    Abdominal ultrasound – useful in excluding other diagnoses; may be preferred initial imaging test

Colitis:

  • Sx: acute diarrhea, abdominal pain

  • Labs: electrolyte abnormalities (dehydration), leukocytosis, CBC (anemia), liver function tests, fecal leukocytes, fecal fat, ova and parasites, occult blood, fecal gram stain and culture, C difficile, HIV, ESR

  • Imaging:

    Sigmoidoscopy or colonoscopy with biopsy

    Further imaging tests may be warranted for chronic causes of diarrhea

Diverticulitis:

  • Sx: abdominal pain, nausea and vomiting, ileus, possible palpable mass

  • Labs: leukocytosis

  • Imaging: Abdominal X-ray – rule out ileus, free air, constipation

    CT abdomen – preferred modality to evaluate for abscess and perforation

    Ultrasound – useful detecting and draining pericolonic fluid collections

Volvulus:

  • Sx: abdominal pain, distention, obstipation, nausea, and vomiting

  • Labs: lactic acid (if evidence of ischemia)

  • Imaging:

    Abdominal X-ray (inverted U shaped loop)

    Barium or gastrografin enema radiography (diagnostic and therapeutic)

Obstipation/constipation:

  • Sx: Abdominal pain, borborygmi, abdominal distension, nausea, vomiting, abdominal mass

  • Labs: electrolyte abnormalities (calcium, potassium, magnesium), thyroid function tests

  • Imaging:

    Abdominal X-ray – (dilated loops of bowel proximal to obstruction)

    Contrast enema radiography – upper / lower GI tract

Acute pancreatitis:

  • Sx: abdominal pain with radiation to back, increased pain in supine position, nausea, vomiting, fever, decreased bowel sounds, diarrhea, tachycardia, periumbilical or flank ecchymoses

  • Labs: elevated amylase, lipase (more specific), leukocytosis, electrolyte abnormalities (hypocalcemia), low hematocrit (retroperitoneal hemorrhage), hyperbilirubinemia (biliary causes), blood alcohol level, fasting lipid panel

  • Imaging:

    Abdominal ultrasound with Doppler – sensitive for detecting gallstones, biliary tract dilation, gallbladder sludge

    CT abdomen with arterial phase protocol – superior to U/S for imaging pancreatic bed- Reserved for patients with severe disease or evidence of necrosis

    MRCP – can detect choledocholithiasis down to 3 mm in diameter and pancreatic duct disruption

Chronic pancreatitis:

  • Sx: abdominal pain with possible radiation to the back, increased pain in supine position, nausea, vomiting, intensity of pain increases with food intake, steatorrhea

  • Labs: leukocytosis, vitamin B12 deficiency, amylase/lipase usually normal, fecal fat studies (Sudan stain or 72 hour), secretin/CCK stimulation test

  • Imaging:

    Abdominal ultrasound – 70% sensitive and 90% specific for detecting chronic pancreatitis

    CT abdomen – 70% sensitive and 90% specific; can also differentiate chronic pancreatitis from pancreatic neoplasm

    ERCP +/- EUS – gold standard for diagnosing chronic pancreatitis

Pancreatic cyst/abscess/malignancy:

  • Sx: Indolent onset of abdominal pain, jaundice, malnourishment, weight loss

  • Labs: Leukocytosis, amylase/lipase – mildly elevated; CEA and CA19-9 are elevated in >75% of pancreatic adenocarcinoma

  • Imaging:

    Abdominal ultrasound

    CT abdomen (spiral or standard dynamic)

    ERCP +/- EUS

Pyelonephritis (symptoms usually persist for <5days):

  • Sx: dysuria, hematuria, flank pain, abdominal pain, fever, urinary urgency/frequency, nausea, vomiting

  • Labs: leukocytosis with left shift, positive urinalysis (+ nitrites, + leukocyte esterase, WBC casts), urine culture, and blood cultures

  • Imaging:

    Abdominal ultrasound to evaluate for hydronephrosis

    Abdominal CT with IV contrast (after 72 hours if failure to improve)

Perinephric abscess (symptoms usually persist >5 days):

  • Sx: fever, flank pain, dysuria

  • Labs: leukocytosis with left shift, positive urinalysis (+ nitrites, + leukocyte esterase, WBC casts) urine culture, and blood cultures.

  • Imaging: Abdominal CT with IV contrast – modality of choice

Nephrolithiasis:

  • Sx: colicky flank pain, nausea and vomiting, pain may refer to different areas as it progresses down the ureter including the groin, hematuria

  • Labs: electrolyte abnormalities (Ca, Phos, uric acid), urinalysis (hematuria, pH)

  • Imaging:

    Abdominal X-ray – may diagnose most stones except uric acid or struvite

    Renal Ultrasound with Doppler (check for hydronephrosis)

    Spiral CT non-contrast – modality of choice as it visualizes all stones except rare calculi due to indinavir therapy

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem

Ultrasound imaging may have limited value in morbidly obese patients due to limitations of image quality with body habitus.

Amylase and lipase are not predictors of severity of acute pancreatitis; amylase is less specific compared to lipase in diagnosing acute pancreatitis and can be elevated in other disorders of the small and large bowel.

Although abdominal X-rays can detect renal calculi, there is only a 50% concordance between renal calculi on AXR and spiral CT of the abdomen.

MRI offers no additional diagnostic capabilities compared to CT scan in the workup of mesenteric ischemia.

III. Management while the Diagnostic Process is Proceeding

A. Management of Left-Upper Quadrant Abdominal Pain

Initial management of the patient consists of:

Airway protection (if indicated)

IV fluids if signs of dehydration or prolonged nausea and vomiting

Electrolyte management due to GI losses

IV antibiotics (covering gram-negative bacteria including Pseudomonas) if infection is suspected

Early goal directed therapy with fluid resuscitation and cardiovascular stabilization

All patients should remain NPO

Nasogastric tube may be useful to decompress or assess stomach contents

Assess if patient has an acute/surgical abdomen. The most life-threatening causes of LUQ abdominal pain include acute mesenteric ischemia, pyogenic nephrolithiasis, pyelonephritis, acute pancreatitis, complicated diverticulitis, and perforated viscera

Emergent imaging if concerned for acute abdomen must include chest X-ray to rule out perforation as demonstrated by free air under the diaphragm, abdominal CT which may demonstrate air-fluid levels indicative of bowel obstruction, evidence of perforation, or intra-abdominal processes causing peritonitis

Subspecialist consultation for suspected emergent surgery or procedures

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Immunocompromised and elderly patients can present atypically for many of the diagnoses described above. Given their weakened immune system and their inability to mount a sufficient response to infection, the physician must always consider this when suspecting a diagnosis.

IV antibiotic choices for LUQ pain should initially include broad coverage for gram-positive (including MRSA), if skin flora is the likely source, gram-negative, and anaerobic bacteria. Once a source is identified and speciated, the regimen can be de-escalated.

IV. What's the evidence?

Anand, N, Park, JH, Wu, BU. “Modern management of acute pancreatitis”. Gastroenterol Clin North Am.. vol. 41. 2012 Mar. pp. 1-8.

Tenner, S, Baillie, J, DeWitt, J, Vege, SS. “American College of Gastroenterology Guideline: Management of Acute Pancreatitis”. Am J Gastroenterology. vol. 108. 2013. pp. 1400-1415.

Antopolsky, M, Hiller, N, Salameh, S, Goldshtein, B, Stalnikowicz, R. “Splenic infarction: 10 years of experience”. Am J Emerg Med. vol. 27. 2009. pp. 262-265.

Greenberger, NJ, Blumberg, RS, Burakoff, R. Current Diagnosis & Treatment: Gastroenterology, Hepatology, & Endoscopy. 2012.

Knudson, MP. “Evaluation of acute abdominal pain in adults”. Am Fam Physician. vol. 77. 2008 Apr 1. pp. 971-8.

Lees, C, Ho, GT, Satsangi, J, Bloom, S. “Guidelines for the management of inflammatory bowel disease in adults”. Gut.. vol. 60. 2011 May. pp. 571-607.

Lewiss, RE, Egan, DJ, Shreves, A.. “Vascular abdominal emergencies”. Emerg Med Clin North Am.. vol. 29. 2011 May. pp. 253-72.

Longo, DL, Fauci, AS, Kasper, DL. Harrison's Principles of Internal Medicine. 2015.

McGee, S.. Evidence-based Physical Diagnosis. 2007.

Sleisenger, MH, Feldman, M, Friedman, LS, Brandt, LJ. Sleisenger & Fordtran's Gastrointestinal and liver disease: pathophysiology, diagnosis, management. 2010.