Biliary Colic Mimics: What you don’t want to miss
- Jun 27th, 2017
- Kristen Whitworth
Author: Kristen Whitworth, DO (EM Resident Physician, Lakeland Health) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)
A 43-year-old female with a history of obesity and diabetes comes to the emergency department complaining of right upper quadrant abdominal pain for the past two hours. The pain started approximately 45 minutes after her lunch today and is associated with nausea and vomiting.
Vitals: T 37.8C, HR 109, BP 132/68, RR 22, SpO2 93% on room air.
Exam is notable for an uncomfortable looking female holding her epigastric area in pain. She is slightly diaphoretic and is mildly tender to palpation in the right upper quadrant. You suspect her pain is related to gallstones and begin an appropriate workup for cholecystitis including an ultrasound. One hour later, her ultrasound report returns with no evidence of cholelithiasis or other gallbladder pathology. What is your next move?
Cholelithiasis is the term used to refer to the presence of gall stones in the gallbladder. In the United States, 8% of men and 17% of women have gallstones.1 Many people with gallstones are asymptomatic, however the risk for having complications or developing symptoms is 1-4% per year.2 Gallstones are classified based on composition with brown stones forming from cholesterol and pigmented stones produced from calcium bilirubinate. Increasing concentration of these components in the bile results in crystallization and stone formation. Gallbladder dysmotility can also play a role in this process. Risk factors for cholesterol stone formation include increased age, female gender, obesity, bariatric surgery and rapid weight loss, parity, and familial tendency. Pigmented stones are more common in patients with chronic intravascular hemolysis (i.e. sickle cell disease, spherocytosis). Pigmented stones can also result from infection.
Cholelithiasis is responsible for many disease processes. Biliary colic is the term used to describe pain secondary to gallstones causing an obstruction of bile flow. This pain dissipates when the stone is displaced resolving the obstruction. The term “colic” is misleading however as the pain is usually steady and not intermittent. Patients usually complain of right upper quadrant or epigastric pain that may radiate to the shoulder. Associated symptoms include nausea and vomiting. Classically this pain occurs after eating a fatty meal, however pain can occur remotely from eating.
In patients presenting to the ED with biliary colic, it is important to rule out complications arising from cholelithiasis including obstruction and infection. Patients with fevers, jaundice, or peritoneal signs on exam indicate a more serious process. Laboratory tests in biliary colic should be relatively normal. Leukocytosis should raise concern for infection while elevation in liver enzymes or bilirubin suggest an obstruction along the biliary tract. Ultrasound is the preferred imaging modality in evaluation for biliary pathology secondary to its convenience, low cost, lack of exposure to radiation, sensitivity for visualization of gall stones, and ability to elicit tenderness over the gallbladder. Gallbladder wall thickening, pericholecystic fluid, and common bile duct dilation should be absent in pure biliary colic. If these abnormalities are present, further investigation is warranted to rule out infection or obstruction. X-ray is of little value in evaluation of biliary colic as the stones will not be visualized. Gallstones only become opaque when greater than 4% calcium by weight.3
Treatment of biliary colic in the ED includes symptom control with antiemetics and analgesia. Patient symptoms should resolve within the initial few hours of treatment in the ED. Pain lasting more than a few hours suggests a more severe disease process, and further investigation is warranted. Upon discharge from the emergency department, patients should be referred to a general surgeon to discuss definitive treatment with a cholecystectomy.
When evaluating a patient for biliary pathology, emergency physicians must consider other mimics. There are several biliary colic mimics including acute coronary syndrome, pneumonia, pulmonary embolism, acute hepatitis, bowel perforation, hepatic abscess, right sided diverticulitis, mesenteric ischemia, aortic catastrophe, portal vein thrombosis, and Fitz-Hugh-Curtis syndrome. Identifying the origin of patients’ pain can be difficult, as abdominal pain can have components of visceral and parietal pain, as well as referred. Visceral pain is experienced secondary to stretching of unmyelinated fibers innervating the walls or capsules of organs and follows a segmental distribution relating to the embryologic origin of the organ. It is usually midline secondary to the bilateral innervation. This pain is usually described as cramp-like or achy. Irritation of the parietal peritoneum is responsible for parietal pain which localizes to the corresponding dermatome superficial to the affected organ. Referred pain is pain appreciated at a site distant to the source. The patterns of referred pain are secondary to embryological development. Referred pain is usually located on the same side as the involved organ.
When considering the most likely cause of a patient’s symptoms, it is important to keep in mind that certain disease processes are more prominent in older populations, while others are more likely in younger patients. Cholecystitis is the most common surgical entity in elderly patients with abdominal pain.5 Younger patients would be more likely to present with appendicitis. When narrowing the differential, it is helpful to take into account patient risk factors that make a certain disease process more likely. It is also crucial to consider risk factors for atypical presentations. Factors such as old age and diabetes mellitus may mask patients’ pain or cause a less severe presentation. Cognitive impairment in older populations can hinder history taking and make physical exam less accurate. However, in this older population, it is even more imperative for ED physicians to correctly identify the cause of patient’s symptoms upon presentation because for patients over 80 years of age, the mortality rate doubles if their diagnosis is incorrect at the time of admission.6
Cholecystitis is inflammation of the gallbladder, usually from an obstructing stone. When a stone obstructs the flow of bile, the gallbladder becomes distended, leading to inflammation and sometimes infection. Gangrenous cholecystitis is a subtype of cholecystitis in which there is necrosis of the gallbladder wall. Emphysematous cholecystitis describes infection of the gallbladder with gas producing organisms and has increased mortality. Pain related to cholecystitis presents similar to biliary colic. Patients usually complain of right upper quadrant or epigastric abdominal pain with nausea and vomiting. Pain elicited on exam by palpating the right upper quadrant may be more severe than that seen with biliary colic, and guarding and rebound may be appreciated. Murphy’s sign on physical exam is 65% sensitive and 87% specific for cholecystitis.7 Jaundice is usually absent; however, fever may be present in one third of cases.7 Leukocytosis can be helpful in evaluation of cholecystitis. A leukocyte count of >10,000/mm3 has a 63% sensitivity and 57% specificity for cholecystitis, with a 1.5 positive likelihood ratio and a 0.6 negative likelihood ratio.7 Liver enzymes are usually normal in cholecystitis.
Ultrasound is the imaging modality of choice for cholecystitis with a sensitivity of 81% and a specificity of 83%.8 Key findings include presence of gallstones and Murphy’s sign. The presence of both has a positive predictive value of 92% for cholecystitis, while the absence of both findings has a negative predictive value of 95%.9 Ultrasound findings of pericholecystic fluid and gallbladder wall thickening are nonspecific and can result from other conditions. While ultrasound is the preferred imaging, sometimes it is limited secondary to poor visualization of the biliary tract secondary to patients’ body habitus and compliance with the exam. Computerized tomography (CT) scan has lower sensitivity and specificity for cholecystitis, however it may reveal complications including emphysematous cholecystitis, gangrenous cholecystitis, or gallbladder perforation. In instances where a patient has an equivocal ultrasound, but there is high suspicion for cholecystitis, cholescintigraphy or an MRI can be performed. Technetium-99m hepatobiliary iminodiacetic acid cholescintigraphy, more commonly referred to as a HIDA scan, is 96% sensitive and 90% specific for cholecystitis.8 The use of HIDA scans in the ED is limited as these studies take hours to perform. Magnetic resonance cholangiopancreatography (MRCP) has similar sensitivity and specificity for cholecystitis as ultrasound imaging; additionally, it is beneficial when adequate images cannot be obtained.8
Treatment for acute cholecystitis is early cholecystectomy. Fluid resuscitation, anti-emetics and pain control are key to management in the ED. Choices for antibiotic coverage include second and third generation cephalosporins, carbapenems, β-lactam/β-lactamase inhibitor combinations, or the combination of metronidazole and a fluoroquinolone. Recently there has been debate on the utility of antibiotics in early/mild cholecystitis.
Choledocholithiasis refers to a gallstone in the common bile duct, usually causing an obstruction. This pain presents similar to that of biliary colic and cholecystitis. Jaundice on exam should raise suspicion for obstruction. Key lab abnormalities that differentiate choledocholithiasis are elevated liver enzymes including bilirubin, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transpeptidase. While stones are not usually visualized on US or CT, the combination of cholelithiasis and a dilated common bile duct suggests choledocholithiasis. The common bile duct should measure <4mm in diameter for patients 40 and younger. One millimeter is added for every decade after 40 years of age. For those patients with equivocal studies or in which the diagnosis is not completely certain, MRCP can be considered for better visualization of the biliary tree. Stone extraction with ERCP is the treatment of choice. If there is evidence of ascending infection, a gastroenterologist should be contacted emergently to perform this procedure.
Cholangitis is an infection of the biliary tree. It usually occurs secondary to choledocholithiasis but can also be iatrogenic after an ERCP or occur idiopathically. Charcot’s triad describes the classic presentation of cholangitis: fever, right upper quadrant abdominal pain and jaundice. All three criteria are present in slightly over half of cases.11 The addition of altered mental status and shock make up Reynold’s’ pentad, though all five are present less than 10% of the time. Ascending cholangitis has a high mortality and requires aggressive treatment with prompt administration of broad spectrum antibiotics, fluid resuscitation, and ERCP. Percutaneous drainage is a treatment option for patients too ill to undergo surgical intervention.
Pancreatitis is inflammation of the pancreas that can present as spectrum of disease from local inflammation to multi-organ dysfunction. While 80% of cases resolve with symptomatic care, severe cases of pancreatitis can lead to life threatening complications of pancreatic necrosis and organ dysfunction, with a related 30% mortality rate.12,13 Gallstones and alcohol are the most common causes of pancreatitis in the United States. Pancreatitis can also occur secondary to hypertriglyceridemia, abdominal trauma, iatrogenic causes such as ERCP, and some pharmaceutical drugs. The most common drug classes to cause pancreatitis are antiretrovirals, chemotherapy agents, and immunosuppressants.
Pancreatitis classically presents as severe epigastric pain that radiates to back. It is usually associated with nausea and vomiting, and symptoms are worsened with oral intake. Patients typically appear uncomfortable with tenderness to palpation isolated to the epigastric region. Tachycardia, hypotension, tachypnea, and diaphoresis may be present as well. Two physical exam findings that signify severe disease are Cullen’s sign (bluish discoloration around the umbilicus) and Grey Turner sign (reddish brown discoloration along the flanks). These are both late findings of necrotizing or hemorrhagic pancreatitis.
Formal diagnosis requires two out of the three following clinical criteria: 1. Clinical presentation consistent with pancreatitis. 2. Lipase levels elevated above the upper normal limit. 3. Imaging findings consistent with pancreatic inflammation. There is debate regarding the exact elevation in lipase required for diagnosis. Some guidelines state the cut off is three times the upper limit of normal, while others state any elevation in lipase is diagnostic. However, it is important to keep in mind that patients with chronic pancreatitis may not have enough pancreatic reserve for elevated lipase in the setting of inflammation.
Laboratory testing helps evaluate the severity of the disease. It is important to evaluate renal function as well as electrolytes, glucose, WBC, and hemoglobin/hematocrit. Liver enzymes are helpful if the cause of the pancreatitis is unknown, as elevation may point to gallstones as the cause. An ALT level >150 U/L in the first 48 hours has an 85% positive predictive value for gallstone pancreatitis.14 Imaging is not indicated in patients with uncomplicated disease. However, it can be helpful if the etiology of pancreatitis is unknown or there is concern for complications. If biliary pancreatitis is suspected, an abdominal ultrasound should be obtained to evaluate for cholelithiasis. A chest x-ray should be obtained in patients with associated respiratory complaints to evaluate for pleural effusions or infiltrates, as this signifies severe disease. If the diagnosis of pancreatitis is in doubt, a CT with IV contrast is helpful to evaluate for pancreatic inflammation, surrounding fluid collections, or pancreatic pseudocyst.
Treatment for pancreatitis is largely supportive with symptom management. Patients should be made NPO and receive IV antiemetics as needed. IV opioids are often needed for pain control. IV fluid resuscitation has been shown to decrease morbidity and mortality from pancreatitis.15 Patients are prone to fluid loss from emesis, third spacing, increased insensible losses and decreased oral intake. Classically, it has been taught that patients should receive aggressive IV fluid hydration with 250-500mL crystalloid solution per hour for the first 12-24 hours.16 More recent guidelines from the International Association of Pancreatology and the American Pancreatic Association recommend 2,500-4000mL total in the first 24 hours of hospitalization, closer to 250 mL/hr.17 A more gradual and less aggressive approach can help avoid volume overload and associated complications including pulmonary edema and abdominal compartment syndrome. Vital signs and urine output can help guide resuscitation.
There is a one percent mortality rate overall for acute pancreatitis, however for severe disease, the mortality rate is as high as 30%.18,19 There are many scoring systems to help classify the severity, though most require data obtained at 48 hours after onset and are not helpful for use in the ED. Some studies have found the presence of SIRS at admission that persists for the first 48 hours is predictive of severe disease.20,21 Admission should be considered for patients with pancreatitis in the following circumstances: a first-time episode, need for IV medications, inability to tolerate oral intake, persistent abnormal vital signs, and signs of organ insufficiency. Patients should also be admitted if their pancreatitis is biliary in origin as they need surgical evaluation for future cholecystectomy or an ERCP if there is evidence of obstruction.
Hepatitis is inflammation of the liver that can be caused by infection, toxins, or metabolic injury. Viruses and toxins such as alcohol and acetaminophen are the most common causes. Social history is key when hepatitis is suspected. Recent travel outside the US is a risk factor for Hepatitis A. Hepatitis B should be considered in patients participating in unprotected sexual intercourse. IV drug users are at risk for Hepatitis C. Other potential toxins include antibiotics, statins, herbal remedies, and dietary substances. Amanita phalloides, the “death cap mushroom”, is also important to keep in mind. Patients often present with RUQ pain associated with nausea and vomiting. Fever, jaundice, and/or hepatomegaly may be present on examination. Bilirubin, both direct and indirect, is helpful to assess if the cause of jaundice is intravascular or hepatic in origin. Elevation of LFT’s indicates hepatocyte injury. A ratio of AST:ALT < 1 points towards a viral or toxic cause of injury, while AST:ALT > 2 is associated with alcohol hepatitis. Other helpful labs include PT/INR, albumin, and ammonia to assess liver function. Work up should include viral studies as well as an acetaminophen level. With the exception of administering N-acetylcysteine in acetaminophen toxicity, treatment for hepatitis is mainly supportive with avoidance of hepatotoxic agents. If any toxins are suspected, the Poison Control Center should be notified.
Hepatic abscesses can be either pyogenic or amebic in nature. They both present similarly, though different treatment. Pyogenic abscesses are caused by both anaerobic and aerobic bacteria. The most commonly isolated pathogens from a pyogenic abscess are E. coli, Klebsiella, Pseudomonas, and Enterococcus.22 Patients will usually present with right upper quadrant pain, high fever, chills, nausea, and vomiting. Pyogenic abscesses have a more acute presentation. Physical exam is remarkable for tenderness to palpation in the RUQ, hepatomegaly, fever, and/or jaundice. These patients tend to appear ill. Workup is significant for leukocytosis, hyperbilirubinemia, elevated ALP, and elevation of aminotransferase levels. In the ED, both ultrasound and CT scan can be used to evaluate for hepatic abscess which appear as large cystic masses in the live parenchyma, usually in the right upper lobe. Treatment of pyogenic abscess starts with stabilization of the patient in the ED prior to admission to the hospital. Broad spectrum, triple coverage antibiotics should be started with an aminoglycoside or 3rd generation cephalosporin to cover gram negative bacteria, metronidazole or clindamycin for anaerobic coverage, and ampicillin for streptococcus coverage. Definitive treatment is drainage of the abscess, usually percutaneously.
Amebic abscesses are the most common extra-intestinal complication of amebiasis. Amebic infection is transmitted via fecal oral route and is more common in travelers, manifesting as intestinal disease. Entamoeba histolytica is responsible for invasive disease. E. histolytica invades the intestinal mucosa and follows the portal vein to the liver. Amebic abscess presents similarly to pyogenic abscess, though patients may report a history of diarrhea weeks prior. Work up is similar to that of pyogenic abscess. Identification of the protozoan pathogen in the stool helps differentiate amebic abscess from pyogenic. Stool microscopy, antigenic testing of the stool, as well as enzyme linked immunosorbent essay (ELISA) can be used to detect the organism. These tests can be low yield, and history is key to diagnosis. Treatment includes metronidazole 750mg PO/IV for 7-10 days followed by treatment of intraluminal cysts with paromomycin 25-35mg/kg/day divided into 3 doses for 5-10 days. Patients with mild disease and adequate follow up may be treated as an outpatient. Percutaneous drainage is only required in refractory or complicated cases.
Bowl perforation should be considered in patients presenting with sudden onset upper abdominal pain. The most common cause is peptic ulcer disease. The ulcer erodes through the wall of the bowel or stomach, allowing gastric contents and air to spill into the peritoneal cavity. The anterior wall of the duodenum is the most common site. There are numerous other causes of bowel perforation that need to be considered including iatrogenic from recent surgery or endoscopy, blunt trauma to the abdomen, and violent emesis. Even rarer causes include foreign body, neoplasms, ingestion of corrosive agents, and medications. Perforation can also occur in areas of constant irritation, such as from the end of a nasogastric tube. The typical presentation is abrupt onset of severe abdominal pain at the site of perforation, followed by a generalized constant abdominal pain as the spilled contents spread. Patients may have a more chronic presentation in situations where a fistula has formed and contents are now beginning to leak into the peritoneal cavity. Peritoneal signs are often common on abdominal exam.
Upright chest and abdominal x-rays should be obtained to evaluate for free air under the diaphragm. X-ray has a 50-70% sensitivity for free air.24 If x-ray is inconclusive and there is a high suspicion for bowel perforation, a CT scan of the abdomen and pelvis should be obtained. CT not only has increased sensitivity for pneumoperitoneum, but it can also aid in identifying the source of the perforation. General surgery should be consulted from the ED. Patient should be made NPO and started on broad spectrum antibiotics along with IV fluid resuscitation.
Acute Coronary Syndrome (ACS) is a spectrum of disease ranging from unstable angina to acute myocardial infarction. Patients with the classic “elephant sitting on my chest” presentations make ACS hard to miss. It is the patient who presents with atypical symptoms that make diagnosing ACS a challenge. Patients presenting with symptoms such as epigastric pain, nausea, and vomiting could easily take a physician down the biliary workup pathway. Atypical presentation of ACS is more common in older patients, diabetics, and women. It is important to consider all of patient risk factors for ACS including age > 65, known coronary artery disease, family history of coronary artery disease, hypertension, diabetes, hyperlipidemia, and history of tobacco use. Patients with ACS may have an unremarkable physical exam which makes the diagnosis even more challenging. Patients with diaphoresis, tachycardia, hypotension, JVD, pulmonary edema, or a new murmur should make ACS higher up on the differential. Workup for patients presenting with atypical symptoms should be guided by suspicion. If the patient has risk factors for ACS or an unclear diagnosis, an electrocardiogram (EKG) and troponin should be obtained along with other labs and imaging ordered for a biliary workup. If the end of the workup for biliary pathology is unremarkable, extending the workup to include serial troponins and EKGs should be considered. No physician wants to diagnose a STEMI with an EKG after a negative biliary workup.
Right Lower Lobe Pneumonia
Pneumonia is an infection of the alveoli of the lungs that can be caused by bacteria, viruses, and fungi. It is important to consider a right lower lobe pneumonia in the differential when evaluating for right upper quadrant pain, especially if the pain is pleuritic in nature. Pleuritic chest pain is present in 39-49% of patients with pneumonia.26 Associated symptoms include cough, fever, weakness, and fatigue. Physical exam may reveal decreased or abnormal breath sounds in the right lower lung base, tachypnea, fever, or low SpO2. Chest x-ray should reveal an infiltrate or consolidation in the right lower lobe. Blood work is only indicated if there is concern for sepsis or severe illness. Disposition and antibiotic treatment are based on severity of the infection and suspected pathogen. There are many risk stratifying scores that can aid in clinical decision making, including CURB-65 and the Pneumonia Severity Index.
Unfortunately, not all cases of appendicitis present in text book fashion. Sub-hepatic appendix is a rare anatomic variant that occurs in 0.08% of patients with appendicitis.27 Inflammation of a sub-hepatic appendix does not have a classic presentation and remains a diagnostic challenge. Diagnosis requires a high index of suspicion. If you don’t consider it, you can’t diagnosis it.
Diverticuli are small herniations through the mucosal and submucosal layers of the wall of the colon. Their presence increases with age, with one study finding 70% of people have diverticulosis by the age of 85, 30% by 60 years of age, and 5% at the age of 40.28 They are primarily located along the descending and sigmoid colon; however, right sided diverticulosis occurs in 2-5% of the population.29 Diverticulitis occurs when the diverticuli become inflamed. Complications include abscess, perforation, and fistula formation. Right sided diverticulitis should be considered in the differential for patients presenting with RUQ pain and fever. They may complain of change in bowel habits with either constipation or diarrhea. Nausea, vomiting, and anorexia may also be present. Physical exam can range from mild tenderness to palpation to guarding and rigidity consistent with peritonitis. Leukocytosis will often be present. For patients who are stable with known diverticulitis and similar presentations in the past, no imaging is indicated. If patient has no previous history of diverticulitis or there is concern for a complication related to diverticulitis, diagnostic imaging should be obtained. CT abdomen/pelvis with IV and oral contrast is 97% sensitive and almost 100% specific for diverticulitis.30 However, newer technology with IV contrast provides similar sensitivity and specificity. Treatment is based on the presence of complications. Uncomplicated patients who appear well can be treated with oral antibiotics as an outpatient with close follow up. Ill appearing patients or those with medical comorbidities require admission for IV antibiotics. For patients with complications such as abscess, perforation, or fistula formation, general surgery should be consulted along with admission and IV antibiotics.
Mesenteric ischemia is a rare condition, occurring in 0.1% of hospitalizations.31 It is a diagnostic challenge as it mimics other pathology and requires a high index of suspicion from providers. Unfortunately, even with rapid diagnosis, it has a mortality rate of 60-80%.32 It results from insufficient blood supply to the small bowel or right colon and rarely affects the left side of the colon secondary to increased collateral blood flow. Causes of mesenteric ischemia include occlusion of the superior mesenteric artery (SMA) by thrombus or embolus, mesenteric vein thrombus, or low flow state through the SMA secondary to vasospasm.
Presentation often depends on the cause of the ischemia. Pain is often poorly localized and acute in onset in SMA occlusion. For mesenteric venous thrombus, symptom onset may be more gradual in nature and have progressed over a span of days before the patient seeks evaluation. Many of these patients have a history of a prior embolism or thrombotic event. Nonocclusive mesenteric ischemia is usually found in patients who are already critically ill secondary to low flow state through the SMA (such as sepsis). Patients often have pain out of proportion to examination. While the patient may be writhing in pain, their abdomen is often soft to palpation. Peritonitis does not present until ischemia progresses to infarction. Initial lab work in the emergency department is very nonspecific. Lactic acid is key in the work up as sensitivity approaches 100%, though it may be normal within the first several hours.33 CT angiography is the imaging study of choice from the ED.
Treatment focuses on restoring mesenteric blood flow, preventing further thrombus formation, and preventing vasospasm. Patients should be hemodynamically stabilized and started on broad spectrum antibiotics. General or Vascular Surgery should be consulted. Regardless of the cause of the ischemic event, patients with intestinal infarction or perforation require emergent laparotomy.
Acute Portal Vein Thrombosis
Portal vein thrombosis (PVT) is the development of a thrombus in the portal vein, including the right and left intrahepatic branches. The thrombus may even extend into the superior mesenteric vein or splenic vein. PVT is usually incited by inherited or acquired hypercoagulable states (i.e. polycythemia vera, Factor 5 Leiden Mutation, hepatocellular CA). Other causes include hepatic stasis from cirrhosis and infection. PVT can present either acutely or chronically with complications. Acute PVT usually presents with severe RUQ abdominal pain, nausea, and/or fever. Ascites, hepatomegaly, or splenomegaly may be present on examination. Liver enzymes are usually normal or minimally elevated, unless there is underlying hepatic disease. First line imaging is ultrasound with duplex doppler. There is absence of flow through the portal vein in PVT. CT with IV contrast and MRI/MRA can aid in diagnosis. Early diagnosis and treatment is key to prevent extension of the thrombus and complications such as intestinal ischemia. Treatment options include anticoagulation, thrombolysis, and thrombectomy. A systematic review in 2011 found that early anticoagulation resulted in a complete recanalization of the portal vein in 38.3% of patients.34 Thrombolysis was found to be associated with significant complications in up to 60% of patients.34 It is also important to treat the underlying etiology responsible for thrombus formation.
Perihepatitis, also known as Fitz-Hugh-Curtis Syndrome, is inflammation of the liver capsule and RUQ peritoneal surfaces that occurs as a complication from pelvic inflammatory disease (PID). It occurs in approximately 4% of patients with mild to moderate PID.36 Patients typically present with RUQ pain, often with a pleuritic component. Their RUQ pain can distract from the diagnosis of PID, so a detailed sexual history is important. Physical exam may reveal RUQ tenderness, jaundice, and/or fever in addition to pelvic exam findings consistent with PID. Gonorrhea and chlamydia are the most common cause; however, the infection may be polymicrobial with aerobic and anaerobic vaginal flora. Workup should include testing for gonorrhea and chlamydia as well as other STDs (i.e. syphilis, trichomonas, HIV) and pregnancy. LFTs are typically normal. Diagnosis is made on history and clinical exam findings. Imaging is not indicated unless the diagnosis is in question. If patient has asymmetric pelvic exam findings, a pelvic ultrasound is needed to rule out a tubo-ovarian abscess. Treatment of Fitz-Hugh-Curtis syndrome focuses on treating the underlying infection with antibiotics. Patients with mild disease and adequate follow up may be treated with oral antibiotics as an outpatient. Patients with more severe disease, inadequate follow up, or questionable compliance should be admitted for IV or PO antibiotic treatment.
Abdominal aortic aneurysms (AAA) can present in a variety of ways. The classic triad of abdominal/back pain, pulsatile abdominal mass, and hypotension is only present in 1/3 of patients.37 Patients may complain of flank pain, back pain, or abdominal pain. It can be associated with nausea and vomiting, which could make AAA easy to overlook in the diagnosis. Risk factors for AAA are age >60 years old, male, history of hypertension, and history of smoking. It is also important to consider this diagnosis in patients with connective tissue disorder. Physical exam may or may not reveal a pulsatile mass. Sensitivity increases along with the size of the aneurysm. Palpation is 29% sensitive for an aortic diameter of 3.0-3.9 cm, 50% for 4-4.9 cm, and 76% for > 5 cm.37 Patients with AAA may present in shock with tachycardia and hypotension or have stable vitals, especially if there is a retroperitoneal hematoma. Flank ecchymosis on exam is a sign of retroperitoneal hemorrhage.
Ultrasound is the ideal screening tool for AAA, as it can be performed at bedside with a sensitivity of 90%.38 An aorta < 3cm in diameter excludes this diagnosis. US can also evaluate for fluid in the abdomen but is limited in accessing for retroperitoneal hemorrhage. It can also be limited by bowel gas and obesity. CT scan with IV contrast allows for better visualization of the aneurysm; however, it can only be performed in stable patients. Patients with AAA need emergent surgery consultation. Do not delay consult for imaging. A symptomatic aneurysm of any size is emergent. Goal of ED care is stabilization until surgery. Type and cross-match several units of blood and consider mass transfusion protocol. If the patient is hypotensive, transfuse to goal systolic blood pressure of 90 until definitive treatment of surgical correction.
Pulmonary emboli (PE) in the basilar segment of the right lung can refer pain to the right shoulder, mimicking biliary colic. It is important to include this diagnosis in the differential when evaluating a patient for RUQ pain. Consider the patient’s risk factors for thromboembolism (i.e. hypercoagulable state, immobilization, recent surgery, pregnancy, use of oral contraceptives, malignancy). Physical exam may reveal tachycardia, tachypnea, decreased SpO2, and even fever. Be sure to assess both lower extremities for edema, swelling, or size discrepancy. The workup for PE starts with deciding if the patient is high or low risk. There are multiple algorithms that follow this decision and should be followed in a workup for RUQ if there is any suspicion for PE.
Pyelonephritis is an infection of the upper urinary tract that presents with flank pain and/or costovertebral angle tenderness. Associated symptoms can include fevers, chills, nausea, and vomiting. Right sided pyelonephritis could present similarly to biliary colic, especially if the patient is a poor historian or has difficulty localizing the pain. Patients may or may not endorse urinary symptoms. If there is any concern for pyelonephritis, a urinalysis should be included in the workup. Imaging is not indicated in healthy female patients with acute pyelonephritis. Imaging should be considered in males, the elderly, diabetics, history of neurologic disease, structural abnormalities of the urinary system, and those who are acutely ill. Renal ultrasound may show evidence of obstruction (i.e. hydronephrosis, hydroureter) or parenchymal abnormalities such as an abscess. A CT should be obtained if there is concern for ureteral stone or emphysematous pyelonephritis. Stable patients who are able to tolerate PO and have adequate follow up may be discharged with PO antibiotics for 10-14 days. Fluoroquinolones are first line treatment; however, consider your local antibiotic resistance when selecting an antibiotic. Patients who are unstable, pregnant, immunocompromised, unable to tolerate PO, have urinary tract abnormalities, an infected urinary stone, or have significant comorbidities should be admitted for IV antibiotics.
Take Home Points
-It is difficult to distinguish between Cholelithiasis and Acute Cholecystitis by history and physical alone. Use an ultrasound!
-Remember an ultrasound demonstrating gallstones with a positive “sonographic” Murphy’s sign is often enough to nail the diagnosis of Acute Cholecystitis.
–The older the patient, the broader the differential. CT imaging may be more useful in select patients.
-Don’t forget the lipase!
–Fear the Fever! Consider Acute Cholecystitis or Cholangitis, but don’t forget about intraabdominal abscess or a right-sided pneumonia.
References / Further Reading
- Everhart JE, Khare M, Hill M, Maurer KR: Prevalence and ethnic differences in gallbladder disease in the United States. Gastroenterology117: 632, 1999.
- Portincasa P, Moschetta A, Palasciano G: Cholesterol gallstone disease. Lancet368: 230, 2006.
- Oyama L. Rosen’s Emergency Medicine. 8th ed. Elsevier; 2014:Chapter 90 Disorders of the Liver and Biliary Tract.
- Tintinalli J, Stapczynski J, Ma O, Cline D, Yealy D, Meckler G. Tintinalli’s Emergency Medicine. 8th ed. [New York]: McGraw-Hill Education; 2016:Chapter 71: Acute Abdominal Pain.
- van Geloven AA, Biesheuvel TH, Luise JS et al.: Hospital admissions of patients aged over 80 with acute abdominal complaints. Eur J Surg 166: 866, 2000.
- Trowbridge RL, Rutkowski NK, Shojania KG: Does this patient have acute cholecystitis? JAMA289: 80, 2003
- Kiewiet JJS, Leeuwenburgh MMN, Bipat S, Bossuyt PMM et al.: A systematic review and meta-analysis of diagnostic performance of imaging in acute cholecystitis. Radiology264: 708, 2012.
- Ralls PW, Colletti PM, Lapin SA, et al.: Real-time sonography in suspected acute cholecystitis. Prospective evaluation of primary and secondary signs. Radiology155: 767, 1985.
- Wada K, Takada T, Kawarada Y et al.: Diagnostic criteria and severity assessment of acute cholangitis: Tokyo guidelines. J Hepatobiliary Pancreat Surg14: 52, 2007.
- Singh VK, Bollen TL, Wu BU, et al.: An assessment of the severity of interstitial pancreatitis. Clinical Gastroenterol Hepatol9: 1098, 2011.
- Petrov MS, Shanbhag S, Chakraborty M, Phillips AR, Windsor JA: Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology139: 813, 2010.
- Moolla Z, Anderson F, Thomson SR: Use of amylase and alanine transaminase to predict acute gallstone pancreatitis in a population with high HIV prevalence. World J Surg37: 156, 2013.
- Wall I, Badalov N, Baradarian R, Iswara K, Li JJ, Tenner S: Decreased morbidity and mortality in patients with acute pancreatitis related to aggressive intravenous hydration. Pancreas40: 547, 2011.
- Tenner S, Baillie J, DeWitt J, Vege S. American College of Gastroenterology Guideline: Management of Acute Pancreatitis. The American Journal of Gastroenterology. 2013;108(9):1400-1415. doi:10.1038/ajg.2013.218.
- IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4):e1-e15. doi:10.1016/j.pan.2013.07.063.
- Peery AF, Dellon ES, Lund J: Burden of gastrointestinal disease in the United States: 2012 update. Gastroenterology143: 1179, 2012.
- Talukdar R, Clemens M, Vege SS: Moderately severe acute pancreatitis: prospective validation of this new subgroup of acute pancreatitis. Pancreas41: 306, 2012.
- Mofidi R, Duff MD, Wigmore SJ, Madhavan KK, Garden OJ, Parks RW: Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis. Br J Surg93: 738, 2006.
- Papachristou GI, Muddana V, Yadav D et al.: Comparison of BISAP, Ranson’s, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis. Am J Gastroenterol105: 435, 2010.
- Lederman ER, and Crum NF. Pyogenic liver abscess with a focus on Klebsiella pneumoniae as a primary pathogen: an emerging disease with unique clinical characteristics. Am J Gastroenterol 2005; 100: pp. 322-331.
- Furukawa A, Sakoda M, Yamasaki M et al. Gastrointestinal tract perforation: CT diagnosis of presence, site, and cause. Abdominal Imaging. 2005;30(5):524-534. doi:10.1007/s00261-004-0289-x. https://commons.wikimedia.org/wiki/File:FreeairXray.png
- Fine MJ, Stone RA, Singer DE, et al. Processes and outcomes of care for patients with community-acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study.Arch Intern Med159: 970, 1999.
- Palanivelu C, Rangarajan M, John SJ, et al.Laparoscopic appendectomy for appendicitis in uncommon situations: the advantages of a tailored approach. Singapore Med J 2007;2013:737–40.
- Hughes LE: Postmortem survey of diverticular disease of the colon. Gut10: 336, 1969.
- Miura S, Kodaira S, Shatari T, et al.: Recent trends in diverticulosis of the right colon in Japan: a retrospective review in a regional hospital. Dis Colon Rectum43: 1383, 2000.
- Jacobs DO: Diverticulitis. N Engl J Med357: 2057, 2007.
- Klein HM, Lensing R, Klosterhalfen B, Töns C, and Günther RW: Diagnostic imaging of mesenteric infarction.Radiology1995; 197: pp. 79-82.
- Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, and Burger CD: Acute mesenteric ischemia: A clinical review. Arch Intern Med 2004; 164: pp. 1054-1062
- Lange H, and Jäckel R: Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease. Eur J Surg 1994; 160: pp. 381-384
- TC, Garcea G, Metcalfe M, et al: Management of acute non-cirrhotic and non-malignant portal vein thrombosis: A systematic review. World J Surg 2011; 35: pp. 2510-2520
- Risser WL, Risser JM, Benjamins LH, et al.: Incidence of Fitz-Hugh Curtis syndrome in adolescents who have pelvic inflammatory disease. J Pediatr Adolesc Gynecol20: 179, 2007.
- Lederle FA, Simel DL: The rational clinical examination. Does this patient have abdominal aortic aneurysm? JAMA281: 77, 1999.
- Emergency ultrasound imaging criteria compendium. Ann Emerg Med48: 487, 2006