Sliding inguinal hernias have a much higher risk of colonic injury during repair than other hernias. This is because the posterior wall of the hernia sac is formed by a retroperitoneal organ (colon or bladder). A clue to the presence of a sliding hernia is the finding of a thickened posterior wall of the hernia sac at surgery, in association with a large indirect hernia (D) that has descended into the scrotum (direct hernias rarely descend into the scrotum). Attempting to completely excise the hernia sac (A) (which is otherwise normally done), or to divide the sac completely at the internal ring (E) (which is again normally recommended), would result in dividing the bowel or bladder. Sliding hernias are more common on the left side (C) (the sigmoid colon is less fixed and more likely to slide down than the right colon). A sliding hernia is an indirect inguinal hernia (D).

Multigravida causes stretching of the abdominal musculature and increases the risk of femoral hernia. Femoral hernias occur in the femoral canal, inferior to the inguinal ligament traversing the empty space medial (C) to the femoral vein (recall the mnemonic “NAVEL” {from lateral to medial: femoral nerve, artery, vein, empty space, lymphatic}). The most common type of hernia in women, and in men, is an indirect inguinal hernia (A). Although femoral hernias appear infrequently (10 % of all hernias), they occur more commonly in females and have the highest risk of strangulation (B). Because of the high risk of strangulation, surgical repair of a femoral hernia is indicated (D) once diagnosed, regardless of whether the patient is having symptoms.

Always consider a nonmechanical postoperative ileus in patients that have had a recent surgery. This occurs in up to 50 % of patients that have undergone abdominal surgery. Although the exact cause has not been elucidated, it most likely involves impaired peristalsis of intestinal contents. Inflammatory mediators (e.g., recent surgery) and opioid analgesics are thought to contribute to the development of postoperative ileus. Initial management should begin with changing pain medication to a non-opiate analgesic. Encouraging ambulation (A) should also be done for all postoperative patients, but is not as imperative as discontinuing opiates. If the patient’s postoperative ileus continues with worsening symptoms (e.g., emesis), bowel decompression including a NGT (B) can be considered. Returning to the OR for exploration (E) is inappropriate for postoperative ileus. Neostigmine is used in patients with pseudo-obstruction (Ogilvie’s syndrome).

With a Richter’s hernia, only one wall of the bowel protrudes into the hernia sac (A). That segment of bowel is prone to incarceration and strangulation but does so without associated symptoms, signs, or radiologic evidence of SBO (C). Therefore, it may easily mislead clinicians into thinking that the hernia is not incarcerated (B). Manual reduction of hernias (including Richter’s) should not be attempted if strangulation is suspected as dead bowel will be reduced into the peritoneum. Strangulation should be suspected in the presence of fever, leukocytosis, acidosis, severe pain, or marked erythema overlying the skin of the hernia. It is often difficult to palpate a Richter’s hernia, and it should be reduced in the operating room (E).

This patient has evidence (on history, physical, and radiologic imaging) of a small bowel obstruction (SBO) that is most likely secondary to adhesions from prior surgery (scar in RUQ). SBO from adhesions can present many years after surgery. The initial management of SBO includes placing the patient NPO, aggressive intravenous fluid resuscitation (the patient is tachycardic and likely very dehydrated), and NG tube placement. Aside from the salutatory effect of NG decompression on the distended bowel, patients with SBO are at risk of aspiration. Once the patient has been adequately resuscitated, CT scan (E) with oral contrast is recommended as it is useful in confirming the diagnosis of SBO, determining if the SBO is partial or complete, and ruling out other diagnosis. Most patients with SBO due to adhesions improve with these maneuvers, and do not require surgery. Operative management (C) with laparotomy and lysis of adhesions should be considered in the following conditions: if the patient demonstrates evidence of clinical deterioration as manifest by increasing pain, tenderness, fever, leukocytosis, or acidosis. Operative management can be achieved either via open laparotomy or laparoscopy (B). Evidence of a complete SBO is a relative indication for surgery, but recent studies suggest that some of these patients resolve with nonoperative management as well. Intravenous erythromycin acts as a prokinetic agent and has some utility for gastroparesis, but not for a SBO (D).

This patient has an umbilical hernia, which is a common finding in newborns. It is recommended that repair be delayed (A) until after the child is 4 years old, unless the defect is larger than 2 cm, the defect is growing, or there is evidence of strangulation. Umbilical hernias are not associated with the VACTERL (vertebral, anal, cardiac, tracheoesophageal fistula, renal, limb) complex of anomalies (B). Defects smaller than 2 cm will likely close spontaneously (C). It is very rare for umbilical hernias in children to incarcerate (D).

This patient likely has ischemic orchitis secondary to damage to or thrombosis of the pampiniform plexus. This is most likely to occur in patients with large or densely adhesed hernia sacs. The condition is usually self-limited (E), so urgent exploration (B) is not indicated. Ischemic orchitis is more commonly caused by injury to the pampiniform plexus than to the testicular artery (C). Testicular torsion (D) is less likely than a vascular injury in this case, although both would present with acute testicular pain and decreased or absent Doppler signal.

The genital branch of the genitofemoral nerve provides sensation to the scrotum and the cremaster reflex. The femoral branch of the genitofemoral nerve (B) provides sensation to the proximal medial thigh. The ilioinguinal nerve (C) provides sensation to the lower abdomen and medial thigh. The lateral femoral cutaneous nerve (D) provides sensation to the lateral thigh as low as the knee. The iliohypogastric nerve (E) supplies the gluteal region.

This patient has a SBO with evidence of ischemic or gangrenous bowel most likely secondary to adhesions from past surgery (e.g., sigmoidectomy). Necrotic bowel generally does not occur in association with a SBO unless there is a closed-loop obstruction. A closed-loop obstruction is a particularly dangerous form of bowel obstruction in which a segment of intestine is obstructed both proximally and distally. Gas and fluid accumulate within this segment of bowel, and cannot escape. This progresses rapidly to strangulation with risk of ischemia, gangrene, and subsequent perforation. Clues to ischemic bowel include the presence of acidosis, fever, leukocytosis, and severe localized pain (unusual for SBO). As such the patient will need exploratory laparotomy, and any bowel that is obviously nonviable needs to be resected. Most patients with SBO (without necrotic bowel) due to adhesions improve with conservative management, and do not require surgery. Observation is not appropriate for this patient (B). Upper GI studies (C–D) would not be indicated since this patient has strong evidence of necrotic bowel and requires urgent surgical intervention. RUQ ultrasound (E) is appropriate in the workup for cholelithiasis.

Although bloody nipple discharge should raise concern for cancer, intraductal papilloma is the most common cause of bloody nipple discharge. This is a benign breast tumor arising from the proliferation of mammary duct epithelium that classically occurs in females 20–40 years of age. Treatment includes excision, which is diagnostic as well as curative. Fibrocystic changes (A) are a common cause of breast pain in young females. Patients report painful breast tissue before menses with improvement during menstruation. Physical exam reveals fibrotic tissue and cystic, lumpy tissue. It may be associated with bilateral serous discharge. DCIS (C) and infiltrating ductal carcinoma (E) are more common in older women. DCIS most often presents as suspicious calcifications on mammography, and not with bloody nipple discharge. Although breast cancer can present with bloody nipple discharge, it is less common than intraductal papilloma, especially in a young woman. Paget’s disease of the breast (D) causes an eczematous lesion on the breast that is associated with an underlying breast carcinoma. Given that this patient’s skin exam is normal, this diagnosis is unlikely.

The patient most likely has inflammatory breast carcinoma, an especially aggressive type of breast cancer. Inflammatory breast cancer can be easily confused with mastitis, as there is usually no palpable breast mass and ultrasound and mammography similarly are often negative. As such, it is imperative to perform a biopsy of the skin, which may show cancer cells invading the subdermal lymphatics. Additional workup should include a breast MRI (which is more likely to show the breast cancer in this setting than ultrasound and mammogram), as well as consideration for needle biopsy of the lymph nodes. Antibiotics (B–C) or NSAIDs (D) would be inappropriate. Incision and drainage (E) would be appropriate if there was an indication on physical examination or evidence of a breast abscess on ultrasound. Inflammatory breast carcinoma typically presents as swelling of the breast and with edematous skin due to obstruction of subdermal lymphatics by tumor (termed peau d’orange, meaning orange peel in French). At presentation, positive lymph node involvement is frequent, and approximately one-third of patients have distant metastases. Inflammatory breast carcinoma can present during pregnancy and should be suspected if suspected mastitis does not respond to appropriate antibiotic treatment.

A diagnostic mammogram should be ordered in a woman over the age of 30 who presents with a new breast mass. Mammography helps to look for suspicious calcifications in other areas of the affected breast, characterize the mass, as well as evaluate the contralateral breast. It is important to note that the mammogram may be normal despite the presence of a palpable breast cancer. For this reason, a tissue biopsy is recommended for palpable breast masses regardless of the mammogram results. Tissue sampling is best performed via ultrasound-guided core needle biopsy. Ultrasound also provides more information about the mass (cystic vs. solid). Fine-needle aspiration (B) is rarely used as it relies on cytology rather than histology. MRI (C) is not routinely needed. Follow-up examination in 3 months (D) without a biopsy would be inappropriate. Genetic testing (E) would be indicated if this patient had a strong family history of breast or ovarian cancer, but would not be done until tissue diagnosis of breast cancer is confirmed.

The patient most likely has lactation mastitis. Lactation mastitis is a localized, painful inflammation of the breast accompanied by fever and malaise occurring in breastfeeding women. The diagnosis of mastitis is made clinically based on an erythematous, tender, swollen area of one breast associated with fever in a nursing mother. Other symptoms may include muscle pain (myalgias) and malaise. Transmission occurs via introduction of bacteria in small breaks in the skin caused by the trauma of breastfeeding. Most cases of lactation mastitis are a result of an infection by Staphylococcus aureus. Treatment consists of antibiotics to cover skin flora, symptomatic relief with analgesics including anti-inflammatory agents such as ibuprofen, and cold compresses to reduce local pain and swelling. Patients should be encouraged to continue breastfeeding (C) as this helps relieve any ductal obstruction that might be contributing to the infection. Biopsy (A) would be appropriate if the patient has suspected inflammatory breast carcinoma. Although very rare, inflammatory breast carcinoma can occur during pregnancy. If mastitis fails to resolve after antibiotics, then consideration should be given to performing a biopsy of the skin. Diagnostic mammography (D) would not be indicated at this time. Incision and drainage (E) is appropriate if there was evidence of a localized abscess with fluctuance. Ultrasound can help differentiate mastitis from a breast abscess.

The history and physical exam is most consistent with a diagnosis of fibrocystic changes of the breast, which is considered a normal variant of the breast in adolescents and young adults. Patients will present with painful breast tissue before menses that improves during menstruation. On examination, fibrotic tissue may be palpated and is generally found in the upper outer quadrants of the breast. This patient should be counseled and instructed to look for these changes with a follow-up appointment in a month. Persistent cystic breast lesions can be evaluated and treated with fine-needle aspiration (E), although this is not be needed in children and adolescents. Cystic lesions that resolve with aspiration should be reevaluated with ultrasonography 3 months after aspiration (C). Excisional biopsy (B) may be warranted for cystic lesions that do not resolve with aspiration or for suspicious solid lesions. Diagnostic mammography (A) is not indicated for adolescents and should be reserved for females >30 years old who present with a breast mass.

The most important risk factors for breast cancer are female gender, increasing age, and a family history of premenopausal breast cancer. A new breast mass in a woman over the age of 50 should be considered cancer until proven otherwise, as it carries the highest relative risk of being cancer. A family history of breast cancer (B) can also significantly increase the risk of breast cancer, particularly if diagnosed in a premenopausal woman. The majority of inherited breast cancers are associated with BRCA1 or BRCA2 gene mutations. Other important risk factors associated with a slightly higher risk of developing breast cancer include early menarche (A), nulliparity or older age at first full-term pregnancy (D), and/or late menopause (E).

This patient is diagnosed with infiltrating ductal carcinoma. Treatment for stage I and II breast cancers includes the option of breast conserving therapy (BCT), which consists of excision of the primary tumor (lumpectomy), sentinel lymph node biopsy (SLNB), followed by radiation therapy to the remaining breast. Studies have shown that breast conserving therapy leads to survival rates that are equivalent to that of mastectomy (though a higher local recurrence rate), while providing a more aesthetically pleasing surgical result. Triple negative breast cancers (ER, PR and Her2/neu receptor) are thought to have a worse prognosis as it is insensitive to some of the best therapies (tamoxifen and aromatase inhibitors for hormone positive, and trastuzumab for Her2/neu positive). As such, chemotherapy is recommended postoperatively.

The presentation is concerning for Paget’s disease of the breast. This presents as an eczematous, scaling, and ulcerating lesion around the areola. Paget’s disease of the breast is a type of DCIS that extends into the ducts to involve the skin of the nipple. Patients are initially misdiagnosed with a skin condition, including eczema and psoriasis, and receive a variety of ointments that do not resolve the lesion. Paget’s disease of the breast is almost always associated with an underlying carcinoma and must be diagnosed via biopsy of the lesion. Trying different regimens of steroids and antibiotics is inappropriate given the high likelihood that she has cancer (B–E).

Trastuzumab is a monoclonal antibody that blocks the HER-2 receptors. The medication is used in the treatment of HER-2-positive breast cancers to help reduce recurrence and improves survival. Since there is a high risk of cardiomyopathy in patients receiving trastuzumab, it is recommended that all patients receive an echocardiogram prior to initiating therapy with trastuzumab. An alternative is to obtain a MUGA scan (multigated acquisition scan), which is a nuclear study that evaluates ventricular function. Trastuzumab-related cardiotoxicity is most often manifested by an asymptomatic decrease in ejection fraction. The optimal surveillance for trastuzumab-related cardiotoxicity is not well defined. The remaining answer choices are not needed prior to starting trastuzumab (A–B, D–E).

DCIS is characterized by malignant epithelial cells within the mammary ductal system, without invasion into the surrounding stroma. Comedo-type DCIS is typically high grade and associated with a worse prognosis (C). DCIS lesions have a high risk of subsequent invasive carcinoma at the site of the DCIS. As such if left unresected, it will often progress to invasive ductal cancer. Thus the mainstay of DCIS treatment is lumpectomy (excision of entire lesion with negative margins). Lobular carcinoma in situ is considered a marker for malignancy in either breast (B). Breast cancer in males is rare (1 % of all breast cancers) with most cases identified as invasive ductal carcinoma. DCIS can occur in men but is even more rare, as DCIS most often presents as abnormal calcifications on mammogram (D). Radiation therapy can be used in combination with surgical excision, but cannot replace it (E).

Proceeding with elective surgery 1 week after an acute MI is inappropriate (A–D). Patients with a recent MI are at significantly increased cardiac risk during noncardiac surgery, particularly within the first month after MI. Since the proposed operation is elective, options A–D would place the patient under unnecessary risk. Although performing the operation under local anesthesia with sedation (B) seems appealing, there is still considerable stress and cardiac risk with such an approach. The best recommendation for this patient is to postpone surgery for at least 4 weeks. At that point, consideration should still be given to cardiac stress testing prior to surgery or even further surgical delay, as the cardiac risk persists for at least 6 months after an MI.

Major predictors of adverse postoperative cardiac events must be identified prior to elective noncardiac surgery. These include recent (within 1 month) MI, unstable or severe angina, decompensated CHF, and significant arrhythmias. Such cardiac conditions require postponing surgery and performing further cardiac workup. A systolic, crescendo-decrescendo murmur at the sternal border of the right second intercostal space radiating into the neck is highly suggestive of aortic stenosis and would require an echocardiogram to rule out severe aortic stenosis. Aortic stenosis impairs coronary perfusion, which can become further exacerbated during induction of anesthesia. From all the choices listed, it portends the highest operative risk. Lee’s revised cardiac risk index identifies intermediate risk factors; these include known coronary artery disease (B) history of CHF, history of stroke or TIA, insulin-dependent diabetes (C), creatinine > 2.0 mg/dl (possibly D), and high-risk surgery (i.e., aortic). Adding a point for each factor and a assigning a score (from 0 to 6) are highly effective in stratifying cardiac risk. Interestingly, smoking (E) has not been shown to be an independent risk factor for adverse perioperative cardiac events in most studies.

The patient has suffered a postoperative NSTEMI. Most NSTEMI (as opposed to a STEMI) in the postoperative setting are managed without percutaneous coronary intervention (PCI) with a combination of oxygen, morphine for pain relief, aspirin, and a beta-blocker. Optimally, an additional antiplatelet agent (such as clopidogrel) and intravenous heparin are also given, but this depends on how recent the operation was and the potential for postoperative bleeding. Consideration should be given to stress testing at 4–6 weeks after surgery, and depending on the results, PCI is then considered. Urgent PCI (B,C) is indicated in the setting of a STEMI, and in certain high-risk NSTEMIs (continued rise in troponins, ongoing chest pain), but will require clopidogrel (again may not be desirable so soon after surgery) if a stent is placed. The patient described has a down trend of troponins and relief of symptoms, further supporting medical management. Emergent CABG (D) would be considered if PCI fails or is not technically feasible with severe three-vessel disease. Emergent operations for acute MI continue to have a high mortality despite many technological advances in myocardial protection. Thrombolytic therapy (A) is an alternative when PCI is not available but would be contraindicated within 2–3 weeks of major surgery.

The patient likely has hypertrophic obstructive cardiomyopathy, an asymmetric thickening of the ventricular septum that creates a narrowing of the left ventricular outflow tract. Vigorous exercise places him at increased risk of sudden cardiac death. T wave inversion (A) would be found in ischemic heart disease, very unlikely in an otherwise healthy 17-year-old. Laterally displaced PMI (B) would be found in patients with congestive heart failure, also very unlikely in this patient. Weak femoral pulses compared to brachial pulses (C) is a finding in coarctation of the aorta, and would not create the characteristic murmur. Murmurs due to aortic regurgitation, mitral regurgitation, and ventricular septal defect (VSD) increase in intensity with squatting (E).

Acute pericarditis is inflammation in the pericardial sac accompanied by pericardial effusion. It can occur following post-MI (termed Dressler’s syndrome), chest radiation, or recent heart surgery. Patients present with pleuritic chest pain that lessens when leaning forward, friction rub heard on auscultation, global ST elevation, and PR depression. Patients with myocarditis (A) usually present with signs and symptoms of acute decompensating heart failure (e.g., tachycardia, gallop, mitral regurgitation, and edema). Chest pain accompanied with MI (C) would not be expected to lessen with leaning forward. Furthermore, global ST elevation would not be expected. Cardiac tamponade (C) can occur once the effusion reaches a critical mass in which cardiac output is compromised. Pulmonary embolism (E) can present with pleuritic chest pain, but it will not be influenced by positioning and is more likely to have ECG findings suggestive of right heart failure.

It is important to know the timing of causes of death after MI. In the first 48 h after MI, death is likely due to ventricular arrhythmia. If arrhythmia occurs after 48 h, an implantable defibrillator should be placed. Ruptures of the myocardium, either as a ventricular septal rupture or free wall rupture (A), usually do not occur until 4–5 days after MI, at which point the dead myocardium has been weakened by the body’s inflammatory response. Post-MI pericarditis, also known as Dressler’s syndrome, (D) usually occurs weeks or months after MI or cardiac surgery. An embolic stroke (B) would present with sudden onset of numbness on one side of the body, cranial nerve deficits, and/or aphasia. It is unlikely to cause death so quickly. There is no reason to believe the patient has sustained an overwhelming infection (E).

The MUGA scan is the most accurate test in measuring ejection fraction. It is a noninvasive nuclear test that uses a radioactive isotope called technetium to evaluate the function of the ventricles. Though not as accurate, an echocardiogram (B) is used more commonly because it is cheaper and more readily available and can look for valve function as well as focal areas of wall motion abnormality. Electrocardiogram (C) and exercise stress test are unable to measure a patient’s ejection fraction. Coronary angiography (D) is considered the gold standard in identifying coronary artery disease and can estimate ejection fraction, but is not as accurate.

It is important to rapidly identify Stanford type A dissections, as they require urgent surgical intervention due to the fact that they can lead to cardiac tamponade, acute aortic valve insufficiency, acute MI, and stroke. A Stanford A dissection involves the ascending aorta and/or the aortic arch. Thus an aortic dissection involving the innominate artery is a Stanford type A. Stanford type B aortic dissection is more common. A Stanford type B dissection begins in the descending aorta, distal to the takeoff of the left subclavian artery (A–D). Stanford Type B dissections are much less likely to cause acute complications since the ascending aorta/aortic arch are not involved. A type B dissection may involve the mesenteric, renal, or iliac arteries, but not occlude them, as blood may continue to flow normally (either though the true or the false lumen). Most can be managed medically with blood pressure control (beta-blockers). Surgical intervention is needed if the involvement of these vessels leads to malperfusion (such as leg ischemia, bowel ischemia, or renal failure).

Based on the description of the site of the dissection, this is a type B aortic dissection. These are usually managed medically (A) unless the patient has evidence of malperfusion. Since her peripheral pulses are all 2+ and her abdomen is soft and non-tender, there is no evidence of malperfusion. The goal is to maintain a relatively low blood pressure in order to minimize stress on the aorta. Aggressive IV fluids (B) will not reduce blood pressure and may actually raise it. Nicardipine (E) will lower blood pressure, but intravenous beta-blocker is the treatment of choice because it also reduces the rate of pressure increase with each beat of the heart, which lowers the stress on the aortic wall. Endovascular therapy (D) is not routinely needed for most type B dissections.

Patients with a recent history of myocardial infarction are at risk of thrombus formation on the scarred endocardium, which can then embolize to the brain and cause a stroke. Patients with a recent history of MI and evidence of thrombus on echocardiography should be treated with warfarin to maintain an INR of 2–3 and followed up within 3 months. Thromboembolism from the left atrial appendage (D) is a concern in patients with atrial fibrillation. Paradoxical venous thromboembolism (E) is a concern in patients with an atrial septal defect or patent foramen ovale, wherein a deep venous thrombus can travel through the defect into the left heart and ultimately to the brain. Septic embolism (B) is a concern in IV drug abusers and can lead to cerebral abscess. Type A dissection (C) would usually present with severe chest pain radiating to the back.

This patient has a postoperative right-sided MI, resulting in compromised cardiac output secondary to decreased preload. One of the steps in management of right-sided MI is to administer fluids to help increase filling of the heart. Avoid nitrates (B, C) in these patients as it may further reduce preload. Acutely, patients with MI need oxygen, aspirin, analgesics, and beta-blockers. Dihydropyridine calcium channel blockers, such as nifedipine (D), are contraindicated in MI because of the associated peripheral vasodilation that may lead to reactive tachycardia and subsequently result in even more stress on the heart. ACE inhibitors (E) should be considered for long-term treatment after the acute episode has resolved.

This patient’s presentation is most concerning for acute mediastinitis. This is a life-threatening infection of the mediastinum with a very high mortality rate that is most commonly associated with cardiac surgery. The incidence rate is 1–2 % following CABG. The source of infection may be a sternal wound infection, combined with instability of the sternum that permits bacteria to enter the mediastinum. Hamman’s sign is a crunching sound heard with a stethoscope over the precordium during systole and is suggestive of acute mediastinitis. Patients will frequently present with chest pain, increased drainage from sternal wound, fevers, and leukocytosis. Chest radiograph findings include pneumomediastinum and/or air-fluid levels within the mediastinum. A CT scan can also support the diagnosis by demonstrating dehiscence of the sternum and stranding, fluid and air pockets within the anterior mediastinum. Management includes surgical debridement, drainage, antibiotics, and rewiring the sternum. Acute pericarditis (A) will present with pleuritic chest pain that lessens when leaning forward, friction rub heard on auscultation, and characteristic ECG findings (global ST elevation). Pneumonia (E) would present with shortness of breath, productive cough, and abnormal lung sounds. Postoperative MI (B) would not be expected to present with evidence of systemic inflammation. Empyema (C) is defined as pus in the pleural space, and would not explain the physical exam findings of sternal instability and Hamman’s sign. CT scan would demonstrate a loculated fluid collection within the right or left pleural cavity.

The classic signs of severe aortic stenosis are angina (A), syncope (C), and congestive heart failure (which may manifest as swollen legs). Of the three, congestive heart failure portends the worst prognosis, with median survival as low as 2 years. A loud mid-systolic murmur (D) indicates hemodynamically significant obstruction but is a better prognostic sign than an absent murmur, which indicates low blood flow across the valve. Small head nodding movements with each heartbeat (E) are known as de Musset’s sign and is found in aortic regurgitation.

All of the above are risk factors for aortic dissection (A–C, E). However, the most significant risk factor for aortic dissection is systemic hypertension.

In cardiac tamponade, fluid (blood or effusion) in the pericardial space externally compresses the heart, which limits diastolic filling and reduces stroke volume. Since pericardial fluid is free flowing, the pressure is distributed equally along the pericardium. As this continues the rising pressure in the pericardium is transmitted to all four cardiac chambers resulting in equalization of central pressures. Pulsus bisferiens (A), also known as a biphasic pulse, refers to two strong systolic pulses with a mid-systolic dip, in other words, two pulses during systole. It can be seen in aortic regurgitation with or without aortic stenosis and hypertrophic cardiomyopathy. Watson’s water hammer pulse (B) is a pulse with a rapid upstroke and descent seen in patients with aortic regurgitation. Peaked T waves (C) is most often associated with hyperkalemia. It is unlikely to be seen in patients with cardiac tamponade since their ECG findings are characteristically low voltage. Pulsus alternans (E) is a physical exam finding wherein the amplitude of a peripheral pulse changes from beat to beat associated with changing systolic blood pressure. It is most commonly caused by left ventricular failure.

Sudden onset of severe abdominal pain in association with an aortic dissection should always raise suspicion for malperfusion of the bowel which can lead to bowel gangrene and death. This most likely would occur if the dissection extends into, and suddenly occludes, the superior mesenteric artery, which supplies blood to the bowel from the ligament of Treitz to the mid-transverse colon. It is also important to recognize that bowel ischemia early on causes excruciating pain in the absence of peritonitis (“pain out of proportion to physical exam”). He has not been on broad-spectrum antibiotics, and has no reason to have C. difficile infection (A), which most often presents with vague abdominal pain and diarrhea. Pancreatitis (C) presents with epigastric pain radiating to the back, nausea, vomiting, anorexia, fever, and tachycardia and is most commonly associated with cholelithiasis and alcohol abuse. Aortoenteric fistula (D) is a possible long-term sequela in patients who have had an intra-aortic synthetic graft placed. Diverticulitis (E) is a common cause of left lower quadrant abdominal pain in elderly patients, and does not typically cause such sudden severe pain.

Wide mediastinum on chest X-ray is concerning for aortic dissection. Patients with type A aortic dissection can present with coronary artery malperfusion and thus have a similar presentation as an acute MI. Suspected aortic dissection is considered an absolute contraindication to thrombolysis in patients with myocardial infarction. The remaining choices (A–B, D–E) are all relative contraindications for intravenous thrombolytics.

This patient presents with the rare but classic presentation of pheochromocytoma during pregnancy. The preferred imaging modality in pregnancy is an MRI, due to the risks of exposing the fetus to radiation with other types of imaging (A, D). In men and non-pregnant women, CT with contrast can also be considered a first line imaging study. Pheochromocytoma is usually hyperintense on T2-weighted images due to its high water content. Failing to work up and treat a potential pheochromocytoma in pregnancy exposes the fetus and mother to a very high risk of morality during the pregnancy and delivery (B, E).

Patients with pheochromocytoma are volume depleted due to intense alpha-mediated vasoconstriction. Hypertension is controlled with alpha-blockade (e.g., phenoxybenzamine) for 10–14 days before surgery. This allows for volume expansion, and the patient is encouraged to liberally intake salt and fluids. The dose is titrated until hypertensive episodes are controlled, often resulting in mild orthostatic hypotension. Beta-blockers (B) can be used to decrease reflex tachycardia once appropriate alpha-blockade has been established. Initiating beta-blocker therapy prematurely can precipitate a hypertensive crisis due to unopposed alpha-adrenergic vasoconstriction. Octreotide (A) is a somatostatin analogue that may have minimal efficacy in the palliation of symptoms from malignant pheochromocytoma, but it has no role in preparing a patient for surgery. Metyrosine (D) inhibits catecholamine production and is a secondary agent for pheochromocytoma, though now rarely used. Diuresis (E) would be contraindicated as these patients are volume depleted.

This patient was incidentally found to have an adrenal mass. Guidelines for surgical resection include tumors > 6 cm, features on CT suspicious for malignancy (high attenuation, irregular borders, inhomogeneous), and those that are hormonally active. Most adrenal carcinomas are hormonally active. Thus the patient described has several indications for adrenalectomy. Open adrenalectomy is preferred when malignancy is suspected, as this allows for a wider resection with en bloc resection if adjacent structures are involved and eliminates the possibility of seeding the port sites that may occur with laparoscopic adrenalectomy (C). Laparoscopic adrenalectomy is preferred for benign lesions. Radiation therapy (D) is not the mainstay of treatment for adrenal cortical carcinoma. Percutaneous biopsy (E) is not recommended as there are no histologic features that diagnose adrenal cortical carcinoma and a biopsy may risk seeding the biopsy tract.

Osteitis fibrosa cystica is a skeletal disorder that results from a surplus of parathyroid hormone. Patients experience increased bone pain, bone fractures, and skeletal deformities with bowing of the bones. Radiographs show thin bones, fractures, and cysts with a moth-eaten appearance. Osteoporosis (A) usually occurs in elderly patients and is characterized by decreased bone density with normal mineralization. It does not have any associated cyst-like features. Similarly, osteopetrosis (B) would not have any cysts seen on plain films. Paget’s disease (E) results from overactive osteoclasts and osteoblasts leading to excessive bone turnover and is characterized by tibial bowing, kyphosis, increased cranial diameter, and deafness. Patients with Paget’s disease and osteoporosis have normal serum calcium, while patients with osteomalacia (C) would be expected to have decreased serum calcium.

The first step in the evaluation of an incidentally discovered adrenal mass is to perform a biochemical workup to determine if the tumor is functional or nonfunctional (E). In practice, it is common to order a single battery of tests: serum aldosterone, plasma renin activity, and a 24-h urine collection to simultaneously measure catecholamines, metanephrines, and cortisol. Given that this patient is normotensive, the suspicion for pheochromocytoma and hyperaldosteronism is low. In addition, adrenal masses < 6 cm are unlikely to be malignant. If the mass is found to be a hormonally active adrenal adenoma, then laparoscopic adrenalectomy (D) would be recommended. If biochemical testing reveals a nonfunctioning mass, this small lesion may be observed with interval CT scanning (A). Percutaneous needle biopsy (B) cannot readily distinguish between benign and malignant primary adrenal tumors.

Hypercalcemia can cause abdominal pain, constipation, mental status changes, and depressed mood (stones, bones, moans and groans). Prolonged immobilization is a known cause of hypercalcemia and is seen in adolescents and in other patients with increased bone turnover such as Paget’s disease. Certain diuretics (thiazide) also cause hypercalcemia by increasing renal calcium resorption.

Patients with hyperaldosteronism have hypertension and hypokalemia – not hyperkalemia (B). Aldosterone acts on the kidney to increase sodium reabsorption, and potassium is excreted to balance the positively charged sodium ions. Hyperglycemia, hirsutism, and abdominal striae (A) are more consistent with Cushing’s syndrome. Elevated plasma metanephrine, hypertension, and increased vanillylmandelic acid excretion (D, E) are all consistent with pheochromocytoma.

Elevated serum calcium combined with elevated PTH is consistent with primary hyperparathyroidism. Rarely, it can be associated with MEN-1 which includes parathyroid, pituitary, and pancreatic pathology (3Ps). Pancreatic tumors include gastrinoma, insulinoma, VIPoma, and glucagonoma. Glucagonoma should be suspected in a patient with new-onset diabetes mellitus (even if thin), diarrhea, and the classic rash: annular, erythematous erosions with blisters over the lower abdomen (necrolytic migratory erythema). The patient’s symptoms of polyuria and polydipsia are highly suggestive of diabetes mellitus. Insulinoma (A) is characterized by hypoglycemia, headache, visual changes, confusion, weakness, and diaphoresis. Prolactinomas (B) are excess prolactin-producing anterior pituitary tumors that may result in amenorrhea, galactorrhea, decreased libido, and gynecomastia. A VIPoma (C) (also called WDHA syndrome: watery diarrhea hypokalemia achlorhydria) presents with profuse diarrhea, but will not have any skin manifestations of the disease. An adrenal adenoma (E) is oftentimes benign, nonfunctional, and incidentally found on imaging (incidentalomas).

Severe hypertension in a young patient should raise suspicion for surgically correctable causes such as aldosteronoma, Cushing’s disease, coarctation of the aorta, fibromuscular dysplasia of the renal arteries, and pheochromocytoma. Her symptoms, combined with an elevated plasma metanephrine level, make pheochromocytoma the most likely cause. The addition of labs consistent with primary hyperparathyroidism (elevated calcium and PTH) suggests she has MEN-2A which is characterized by primary hyperparathyroidism, pheochromocytoma, and medullary thyroid cancer. Calcitonin is a reliable tumor marker for medullary thyroid cancer and should always be ordered to rule out this very aggressive cancer in this patient population. Fasting blood glucose (A) (insulinoma), prolactin levels (prolactinoma) (B), MRI of the sella turcica (C) (pituitary adenoma), and serum gastrin level (E) (gastrinoma) are all associated with MEN-1.

A sudden rise in blood pressure after anesthetic induction raises concern for an undiagnosed pheochromocytoma, malignant hyperthermia, and thyrotoxicosis (thyroid storm). For each of these situations, cessation of anesthesia is recommended. There are several clues that point to pheochromocytoma as the cause. The administration of beta-blockers without alpha-blockade first leads to worsening hypertension due to unopposed alpha-mediated vasoconstriction as in the case above. Pheochromocytoma is associated with neurofibromatosis-1 which may present with skin neurofibromas (rubberlike discolored skin lesions) and cataracts. Malignant hyperthermia (B) presents with muscle rigidity (most often the masseter), a rapid increase in core body temperature, a rise in end tidal CO₂, arrhythmia, and a mixed metabolic and respiratory acidosis at anesthetic induction. Treatment is immediate cessation of surgery and dantrolene. Thyrotoxicosis (C) presents in a similar fashion to malignant hyperthermia (fever, hypertension, tachycardia); however, it is not associated with muscle rigidity or rising end tidal CO₂. The associated hypertension and tachycardia respond to the administration of beta-blockade. It is due to a hypermetabolic state caused by excess thyroid hormone. Inadequate anesthetic agents (D) may lead to hypertension and tachycardia, but would not lead to high fevers. An undiagnosed pituitary tumor resulting in excess ACTH production can cause hypertension, but this will be accompanied with symptoms consistent with Cushing’s disease (e.g., truncal obesity, abdominal striae, muscle wasting, hirsutism).

This patient has a thyroglossal duct cyst, which is the most common midline congenital malformation of the neck. Though present at birth, these do not often appear until age 2 as baby fat recedes. During embryological development, the thyroid originates at the base of the tongue and travels down the thyroglossal duct to the anterior neck, where it normally involutes. However, if a persistent duct remains, it may undergo cystic dilation later in life and present as a well-defined anterior neck mass, located midline and above the cricoid cartilage. Unlike a brachial cleft cyst, this elevates with tongue protrusion or swallowing. Ectopic thyroid gland may be associated with thyroglossal duct cysts so it’s necessary to confirm the thyroid gland is in its correct anatomic location prior to surgical intervention. The definitive management involves thyroglossal duct cyst excision or the Sistrunk procedure. Reassurance and observation (C) are inappropriate as thyroglossal duct cysts have a high rate of recurrent infections and a small risk of progressing to malignancy. FNA biopsy (A) is appropriate for a thyroid nodule, but not for suspected thyroglossal duct cyst. He does not have symptoms suggestive of hyper- or hypothyroidism so a thyroid panel would not be indicated (D). CT scan (E) is unnecessary for the diagnosis, and additionally should not be performed in such a young patient secondary to significant radiation exposure.

Plasma free metanephrine is highly sensitive for pheochromocytoma but is more prone to false-positive results. Plasma chromogranin A is released from neuroendocrine cells and is elevated in the majority of patients with pheochromocytoma. It is nonspecific (i.e., it is elevated in other neuroendocrine tumors) but can help confirm the diagnosis. Superoxide dismutase and malondialdehyde (B, C) are both markers for oxidative stress, and neither has been shown to be associated with pheochromocytoma. CA 19–9 (D) may be elevated in some patients with pancreatic cancer. Increased level of 5-hydroxyindoleacetic acid (HIAA) (E) would be expected in a patient with carcinoid syndrome.

Patients with MEN-2A can develop pheochromocytoma, hyperparathyroidism, and medullary thyroid cancer. The definitive management for pheochromocytoma consists of medical conditioning with alpha-blockade and sometimes beta-blockade for at least 2 weeks, followed by an adrenalectomy (B). This should be performed first (A, D–E) because a pheochromocytoma can increase the risk of complications during the surgical management of other endocrine tumors. Although he is asymptomatic with respect to his hyperparathyroidism, parathyroid surgery is generally recommended for most patients with inherited forms, as it tends to be more aggressive and presents at a much younger age. Age less than 50 is an indication for parathyroid surgery for sporadic forms as well, as the patient is more likely to suffer one of the sequelae of hyperparathyroidism.

If a patient that has undergone bilateral adrenalectomy presents postoperatively with severe hypotension and hypoglycemia, suspect Addisonian crisis (acute adrenal insufficiency) and check a cortisol level. This is considered to be a life-threatening condition caused by insufficient levels of cortisol, which is responsible for maintaining blood pressure and glucose homeostasis. Patients will present with nausea, vomiting, weakness, blurry vision, and mild abdominal pain. Laboratory exam would be expected to show hypoglycemia, hyperkalemia, and mild hyponatremia. Plasma ACTH levels will be low, and a Cortrosyn (synthetic ACTH) stimulation test will demonstrate a low cortisol response. This patient should receive immediate fluid resuscitation (normal saline) and intravenous corticosteroids. Acute adrenal insufficiency does not respond to vasopressors. Additionally, it can mimic sepsis. However, he does not meet SIRS criteria. Similarly, sepsis (B) is unlikely to present with this patient’s lab abnormalities. Patients that have had major surgery should always be monitored for signs of internal hemorrhaging. Although his serum calcium is shown to be low (C), this should be corrected for hypoalbuminemia. His corrected serum calcium is 8.7 mg/dL, is within the normal range, and would not explain the hypotension (B). Although he may be volume depleted (A), this would not cause hypoglycemia or hyperkalemia. Loss of catecholamine production (E) may accompany Addisonian crisis and is also seen after removing a pheochromocytoma. It is associated with hypotension and hypoglycemia; however, it will not cause hyperkalemia and hyponatremia.

The patient most likely has hypocalcemia. Temporary hypoparathyroidism occurs in up to 30 % of patients after total thyroidectomy and generally lasts a few weeks. It is thought to be related to temporary ischemia to the adjacent parathyroid glands. Patients will complain of numbness and tingling in their hands and feet, as well as around the mouth. These patients should be managed with prompt oral calcium supplementation. Oral calcitriol may be added to increase calcium absorption from the gut. Some centers routinely check the postoperative PTH level for the purposes of anticipating hypocalcemia. Left untreated, hypocalcemic symptoms may progress to muscle twitching (including Chvostek’s sign) and ultimately tetany, which is an emergency. IV calcium (gluconate or chloride) may be given in these circumstances, but its use can generally be avoided when patients are carefully monitored postoperatively. Symptoms of hypomagnesemia (A) are indistinguishable from hypocalcemia; however, low magnesium levels are not associated with thyroidectomy. Disturbances in potassium (C) and thyroid hormone (D) would not cause the symptoms described. Carotid ultrasound (E) would be indicated if the patient developed symptoms of a stroke or transient ischemic attack (one-sided arm and leg weakness/numbness).

This patient most likely has an ectopic production of erythropoietin leading to high levels of hemoglobin and hematocrit. This paraneoplastic syndrome, termed polycythemia vera, is classically associated with pheochromocytoma, renal cell carcinoma, hepatocellular carcinoma, and hemangioblastoma (A, D–E).

Paragangliomas arise from extra-adrenal chromaffin tissue, with the most common location being in the abdomen (organ of Zuckerkandl). They are essentially identical on a cellular level to intra-adrenal pheochromocytomas. However, they are more likely to have a hereditary basis (30–50% of cases) and to be malignant (15–35%). The diagnosis is made by biochemical analysis followed by imaging localization. It is particularly important to consider a whole body functional scan due to the higher propensity for multifocal and metastatic disease.

There is currently no way to establish the diagnosis of malignancy in pheochromocytoma based on histopathologic evaluation (A). However, there are tumor characteristics that are associated with higher risk (e.g., larger size, extra-adrenal location, certain genetic mutations, and a high tumor proliferative index). Malignancy is determined by the development of metastatic disease, defined by a recurrence in an area that normally does not have any chromaffin tissue (lymph nodes or a distant site such as the liver or lungs). MIBG scanning (B) can be useful to identify metastatic disease, but positivity of the primary tumor on MIBG does not determine whether it is malignant. Biomolecular markers (D) can differentiate a functional tumor from nonfunctional, but is unable to rule out malignancy. Similarly, intractable hypertension (E) is not a characteristic of malignancy.

The most important step in the diagnostic workup of a thyroid nodule is to obtain a tissue sample. This is best obtained via fine-needle aspiration and is best done under ultrasound guidance. Thyroid nodules greater than 1 cm in size, nodules with ultrasound characteristics suggestive of malignancy (internal microcalcifications, e.g.), or those with a history of growth should undergo ultrasound guided FNA. CT (A) or MRI (B) would be appropriate for patients found to have clinical or sonographic evidence of locally advanced thyroid cancer that may extend into the aerodigestive tract or substernal region. Open biopsy (D), done by removing an entire thyroid lobe, should be done next if FNA results are suspicious for a follicular neoplasm. Nuclear scanning (E) has a very limited role in the preoperative setting. It is more beneficial in the postoperative setting to look for recurrent or metastatic malignancy.

Don’t forget the ABCs. This patient has a compromised airway and is in moderate respiratory distress. Normally, the first step to ensure an airway is via endotracheal intubation (B). However, a neck hematoma is in a closed space that leads to compression of the airway that may render safe intubation difficult or impossible. As such, the first step is to immediately open the neck wound at the bedside to decompress the hematoma. This will typically relieve the airway obstruction. The patient can then be transported emergently to the operating room for intubation, wound exploration, adequate hemostasis, and subsequent wound closure (C). Although thyroidectomy is considered a safe procedure, one well-known complication is airway obstruction following bleeding and hematoma formation which occurs within the first 24 h after thyroidectomy. Checking oxygen saturation (D) or waiting for labs (E) is never appropriate for a patient with a compromised airway.

The superior laryngeal nerve lies adjacent to the superior thyroid artery and is thus at high risk of being injured during mobilization of the thyroid, particularly the superior pole. The external branch of the superior laryngeal nerve permits singing in a high pitch. This nerve may be injured in up to 25 % of cases but is usually asymptomatic unless the patient is a singer or voice professional. Damage to the recurrent laryngeal nerve on one side results in a paralyzed vocal cord in a median or paramedian position. This manifests as hoarseness (A) and sometimes aspiration. The rate of permanent unilateral recurrent laryngeal nerve injury during thyroidectomy should be less than 2 % in expert hands. If both recurrent laryngeal nerves were injured during a total thyroidectomy, then both vocal cords could be paralyzed, and this may lead to a compromised airway which may necessitate a permanent tracheostomy (E). A droop in the corner of the mouth results from injury to the marginal mandibular branch of the facial nerve. Swallowing is controlled by multiple nerves (C) including the glossopharyngeal, vagus, and/or hypoglossal nerves.

The surgical treatment of hyperparathyroidism depends on whether the pathology is a single adenoma (most common, remove single gland), more than one adenoma (remove abnormal ones), or four gland hyperplasia (remove 3.5 glands). Distinguishing these entities is not always obvious. Because of the short half-life of PTH (about 4 min), intraoperative rapid PTH testing aids in determining the completeness of parathyroid resection. The most commonly used protocol involves drawing PTH levels at the time of gland excision and again 10 min post-excision. A fall of >50 % in the PTH level is associated with a 98 % long-term cure rate. Given the small size of the parathyroid glands, it is generally not recommended to biopsy all of them for frozen section (B), as such a biopsy may render all the glands ischemic. Transient hypocalcemia is expected following parathyroidectomy so postoperative serum calcium level (D) is not indicative of cure. Oral calcium supplementation can help alleviate minor symptoms. Intraoperative ultrasound (A) is sometimes used when the abnormally enlarged gland cannot be found. Sestamibi (E) may be used if recurrent or persistent hyperparathyroidism develops, but is not routinely used for confirmation of successful surgery.

Sestamibi scanning involves using a radioisotope, technetium-99 m, which is taken up by cells with high mitochondrial activity. It is more accurate for single adenomas than for four gland hyperplasia. Sestamibi scanning and to a lesser extent ultrasound (B) are the most frequently used imaging tests to localize the involved gland(s) in primary hyperparathyroidism. Localizing studies are generally not indicated in secondary or tertiary hyperparathyroidism, since multiple-gland hyperplasia is the expected underlying pathology. Preoperative FNA (D) is not helpful in the workup of primary hyperparathyroidism. In about 85 % of patients, imaging will localize the abnormal parathyroid gland, and a great majority will have a single parathyroid adenoma. If localizing scans are negative, yet the diagnosis of primary hyperparathyroidism is clearly established, surgery is still performed at which time intraoperative exploration of all four glands (E) is performed.

With the increasing use of routine laboratory testing, most patients with primary hyperparathyroidism are currently discovered incidentally in asymptomatic patients. Although the patients may be asymptomatic, long-standing hyperparathyroidism can lead to kidney injury and osteoporosis. Evidence of such should be sought out via bone mineral density testing as well as calculation of creatinine clearance. For patients with asymptomatic hyperparathyroidism diagnosed through laboratory screening, a 2008 consensus statement recommended the following indications for surgery:

The patient described meets the age criterion for surgical intervention. The surgical treatment of primary hyperparathyroidism due to four gland hyperplasia is to remove 3.5 glands. An acceptable alternative is to remove all four glands and to reimplant half of a gland within the muscles of the forearm. That way if the patient develops recurrent hyperparathyroidism, additional parathyroid tissue can be removed from the forearm under local anesthesia as opposed to re-operative neck surgery with the attendant risk of cranial nerve injury. Removal of all four glands (B) is not recommended as it will render the patient permanently hypocalcemic with a lifelong need for calcium supplementation. Observation (A) would not be appropriate for patients meeting criteria for surgery. Patients not selected for surgical therapy require biochemical monitoring of serum calcium and serum creatinine annually (D). Bone mineral density should be measured every 1–2 years. Cinacalcet (E), a calcimimetic, is mainly used to treat secondary hyperparathyroidism (seen in patients with renal failure). It may be considered to reduce the serum calcium in patients who are not candidates for surgery.

A chest X-ray is routinely performed to rule out a concurrent primary lung cancer or pulmonary metastases. This is important as a majority of laryngeal and lung cancers are attributed to smoking. In addition, the most common location for distant metastasis of head and neck squamous cell carcinoma is the lungs. Additional imaging such as MRI (B), PET (C), or bronchoscopy (D) is not considered necessary for early stage laryngeal cancer.

This patient most likely has malignant otitis externa secondary to otomycosis. Aspergillus niger is the most common cause of otomycosis and can present very similarly to otitis externa. However, patients with otomycosis will complain of an intense fullness in the ear and pruritus, and physical exam will be significant for a gray exudate from the affected ear. Unlike otitis media, patients with otomycosis will have a normal-appearing tympanic membrane as this typically affects the external ear canal. The two high-risk populations for malignant otitis externa secondary to otomycosis include patients with acute myeloid leukemia and/or diabetic ketoacidosis. Depending on the extent of local spread, patients can present with a myriad of symptoms including blindness, headache, seizure, and coma. CT scan of the head will help evaluate the extent of damage and infiltration and help guide surgical management (e.g., debridement, washout). Answer choices A–C are all common causes of otitis media with Streptococcus pneumoniae being the most common organism. Mycoplasma (D) has been associated with bullous myringitis, which is characterized by vesicular inflammation of the tympanic membrane and is seen most commonly with untreated otitis media. Patients will present with very tender ear canals, and otoscopy shows large red vesicles on the tympanic membrane.

Ludwig’s angina is characterized by a progressive cellulitis in the floor of the mouth and often involves the submandibular space (which is divided by the mylohyoid muscle). It can present with fevers, neck pain, neck swelling, dental pain, dysphagia, and drooling. This can be life threatening as it can lead to airway obstruction. The majority of cases follow dental procedures which allow bacteria from a tooth infection to migrate into the submandibular space. Patients with labored breathing and marked swelling require an immediate airway. This may be achieved via endotracheal intubation or alternatively via a surgical airway (cricothyroidotomy or tracheostomy). The neck infection will then need immediate surgical drainage, (A) but this is best accomplished in the operating room. Broad-spectrum antibiotics (C) and IV fluids (D) are also necessary, but should not be prioritized over the airway. Laryngoscopy (B) is not recommended as it will only delay establishment of the airway and any potential trauma/gagging may further compromise the airway.

A solitary enlarged lymph node that persists beyond 3 weeks particularly in a middle-aged male smoker should be considered a metastatic lymph node until proven otherwise. Oftentimes, the patient will have symptoms (such as hoarseness, persistent sore throat, ulcerative lesions) that will guide the workup. But if no symptoms are present, a flexible nasopharyngoscopy is used initially to evaluate the nasal cavities, nasopharynx, oropharynx, hypopharynx, and glottis to look for a site of primary tumor. FNA is subsequently performed for to confirm that the solitary neck mass is a metastatic lymph node. Once FNA confirms this, CT scan of the neck may identify the primary. If the primary is still not evident, the next step is to try to identify the location of the primary tumor using a panendoscopy (also termed triple endoscopy) with random biopsies. This involves a complete endoscopic evaluation of the upper aerodigestive track, including laryngoscopy (C), esophagoscopy, and bronchoscopy under general anesthesia in the operating room. A neck dissection (B) would not be considered until after panendoscopy. Radiation and chemotherapy (D) may be used as adjuncts depending on the stage and grade of the primary tumor.

Mastoiditis usually occurs days to weeks after an episode of acute otitis media. Patients present with fevers and complaints of a red, swollen, and tender area behind the ear (mastoid process). Physical exam may reveal a displaced ear on the affected side. The diagnosis can be confirmed with a CT scan of the mastoid process and is recommended for patients suspected of having mastoiditis. Patients with CT-confirmed acute surgical mastoiditis are candidates for mastoidectomy with insertion of a tympanostomy tube (E). Observation (A) is not an appropriate management for patients with mastoiditis. Oral corticosteroids (B) are not considered part of the management of acute mastoiditis. Augmentin (D) would be an appropriate choice for patients with acute otitis media suspected of having a resistant strain.

This patient most likely has torus palatinus, a bony benign mass located on the hard palate of the mouth. The cause is unknown. It occurs more frequently in women and those of Asian descent. There is no associated malignant transformation. Biopsy (C) is not warranted and patients only need reassurance. Operative management (A) with surgical removal would be indicated only for symptomatic patients (e.g., interference with denture placements, pain, trouble swallowing). There is no medical management (B) available for torus palatinus. Nasopharyngeal carcinoma, a rare tumor arising from the epithelium of the nasopharynx, occurs more frequently in patients of Asian descent and those infected with EBV (E). However, a bony outgrowth of the hard palate would not be expected in these patients.

Although it occurs infrequently, brain abscesses are a complication of acute otitis media. It shows many of same manifestations as a brain tumor (space occupying) but with a much shorter timetable (week or two). Patients typically have a fever, acute onset of headache, focal neurologic findings (e.g., weakness in the right arm), seizure, and an obvious source, such as otitis media or mastoiditis. A MRI or CT of the head will find ring enhancing lesions. Treatment is open drainage (by a neurosurgeon). All these patients should also be started on empiric antibiotics. Although controversial, some clinicians also administer corticosteroids as it may have some benefit in decreasing the growth of the abscess and preventing cerebral edema. Ring-enhancing lesions and seizures can also be found in patients with CNS lymphoma, toxoplasmosis, or neurocysticercosis. CNS lymphoma primarily occurs in patients with AIDS. Pyrimethamine and sulfadiazine (A) would be the appropriate choice to treat patients with toxoplasmosis. Seizures secondary to neurocysticercosis (Taenia solium) can occur in patients with a recent travel history to Mexico, but this patient’s temporal relation of her acute condition and a recent episode of otitis media make this less likely. Patients with neurocysticercosis should be started on antiparasitics, such as albendazole, and corticosteroids (B). Antiepileptics (D) can be used to manage her acute condition, but it is unlikely that she also has a concurrent seizure disorder obviating the need for long-term antiepileptic therapy. Chemotherapy and radiation (E) would be considered in patients with brain malignancies.

Laryngeal papillomas or recurrent respiratory papillomatosis is a condition caused by human papilloma virus (HPV) types 6 and 11. Infection with the virus can lead to benign papillary tumors of the larynx (cauliflower-like growths) and presents primarily with hoarseness. It rarely gives rise to laryngeal carcinoma. Laser fulguration can be performed to destroy the papillary growths. Laryngectomy (D) would not be appropriate. HIV (B) can present with various AIDS-defining malignancies including Kaposi’s sarcoma, non-Hodgkin’s lymphoma, and cervical cancer. EBV (C) has been associated with nasopharyngeal carcinoma and Burkitt’s lymphoma. Antiviral agents (e.g., cidofovir) are used as an adjunct to laser ablation to prevent recurrence, but they are not the primary treatment modality.

Sialolithiasis (salivary ductal stones) can increase the risk of developing a tumor of the gland. Lemon drops will stimulate saliva production and help facilitate passage of the stone. Pleomorphic adenoma is benign and considered the most common neoplasm of the parotid gland. The greater auricular nerve is a branch of the cervical plexus (C2–C3) and provides cutaneous sensation to the lower portion of the ear, including the earlobe. The facial nerve (A), which traverses through the two lobes of the parotid gland, can also be injured and will present with facial droop. Injury to the trigeminal nerve (C) can cause widespread numbness in the face. However, this type of injury occurs rarely because of the deep location, immediate branching, and redundancy of these nerves. An injured spinal accessory nerve (D) will present with partial paralysis of the trapezius and sternocleidomastoid muscles. The auricular branch of the vagus nerve (E) provides cutaneous sensation to the ear canal, not the earlobe.

The most appropriate recommendation for a young patient presenting with a newly discovered, isolated, and enlarged cervical node is observation with follow-up and reexamination in 3 weeks. If the node disappears, it most likely was inflammatory in nature. However, if this patient presented with any red-flag symptoms (e.g., dysphagia, odynophagia, dysphonia, hoarseness, and weight loss), additional workup would be required to rule out malignancy. CT scan (B, C) with contrast is the initial preferred imaging modality for a solitary neck mass that is concerning for malignancy (following a careful head and neck examination). FNA (A) is indicated for neck masses that are persistent, enlarging, or suspicious for malignancy. Panendoscopy (E) is performed in the operating room in the setting of a metastatic neck lymph node (when the primary is occult).

Croup, also known as laryngotracheobronchitis, is caused by the parainfluenza virus and primarily affects young children. The cough associated with this condition is described as a low-pitched seal-like bark. The diagnosis can be confirmed by looking for the classic “steeple sign” on posteroanterior X-ray of the neck, which is indicative of subglottic narrowing. Patients are at risk for airway obstruction and will require intubation if they appear to be in respiratory distress. Management includes steroids and aerosolized racemic epinephrine. Respiratory distress syndrome of the newborn (A) is caused by surfactant deficiency. It occurs within 2 days of birth and presents with cyanosis, nasal flaring, crackles, and expiratory grunting. Epiglottitis (C) is a rapidly progressive infection of the epiglottis, most commonly due to Haemophilus influenzae type B. Patients with epiglottitis may require intubation or even tracheostomy due to airway compromise from the swollen epiglottis. Bronchiolitis (D) is characterized by a viral infection of the bronchioles and occurs most commonly in patients < 2 years old. Laryngomalacia (E) is a congenital abnormality of the laryngeal cartilage and can result in collapse of the supraglottic structures in newborns, leading to airway obstruction. Infants with laryngomalacia should be fed upright and remain in this position for at least 30 min after each feed.

The larynx is the most common site for foreign body aspiration in children younger than 1, while the trachea (C, D) and right mainstem bronchus (A) are the most common sites in older children. The left mainstem bronchus (B) is a less frequent site for foreign body aspiration owing to its acute angle as it enters the lung versus an obtuse angle in the right. Patients with foreign body aspiration may have wheezing, but using a bronchodilator increases the risk of further pushing the foreign body down the airway. Order a chest X-ray if there is a suspicion for a foreign body obstruction. Bronchoscopy is recommended for definitive diagnosis. Extracting the foreign body requires a rigid bronchoscopy.

Most salivary gland tumors are in the parotid gland, and the majority are benign (80 %). The most common type of parotid gland tumor is a pleomorphic adenoma. Although benign, it does have a known risk of malignant transformation that becomes as high as 10–25 % when present beyond 15 years. Warthin’s tumor (B) is the second most common benign salivary tumor and is strongly related to smoking. Mucoepidermoid carcinoma (C) is the most common malignant salivary gland tumor. Facial nerve involvement is more suggestive of malignant transformation. The second most common malignancy is adenoid cystic carcinoma (D). Oncocytoma (E) is a rare (1–2%) salivary gland tumor and most often involves the parotid gland.

The triad of dysphagia, esophageal webs (e.g., feeling of choking with solid foods), and iron-deficiency anemia is highly suggestive of Plummer-Vinson syndrome. The pathophysiology still remains unclear but is most likely multifactorial. Barium esophagram is one of the most sensitive methods and diagnostic tests of choice to confirm the presence of esophageal webs, which appears as a thin projection off the postcricoid, anterior esophageal wall. If esophagram is equivocal, esophagoscopy (D) can be used next. Laryngoscopy (A–B) or bronchoscopy (C) is not typically required in the workup for Plummer-Vinson syndrome. However, if there is any concern for head and neck cancer (e.g., neck mass in patient with smoking history), a panendoscopy can be considered in the workup.

In an older (>50) male patient with a history of smoking, presenting with persistent laryngitis and recent difficulty in projecting his voice, laryngeal cancer must be ruled out. The initial test is to evaluate the larynx and vocal cords with indirect laryngoscopy in the office (with administration of local anesthetic spray to the back of the throat). It is termed indirect, as it has a mirror that permits indirect visualization of the vocal cords. Structural abnormalities, such as masses, ulcers, or mucosal irregularities, may be noted, as well as motion of the vocal cords. Direct laryngoscopy (E) is done in the OR under general anesthesia. It involves insertion of a rigid metal tube directly into the larynx and allows for biopsies to be taken. Given the high likelihood of cancer, antibiotics (B) or reassurance (C) would be inappropriate.

This patient’s presentation is concerning for mucormycosis, most commonly caused by Rhizopus or Mucor fungi. Patients with poorly controlled diabetes and/or neutropenia are the most common groups affected with mucormycosis. They most often present with local invasion of the fungi into the facial sinuses and eventually the brain (e.g., sudden onset or worsening of headache), as in this patient. Black eschar on the nose and discharge from the nares is characteristic of mucormycosis. Management consists of immediate antifungal therapy with liposomal amphotericin B and surgical debridement. Antifungal therapy alone would be inappropriate, as well as antibiotics (A,C–D). Hyperbaric oxygen (E) is currently being investigated as an adjunctive therapy for select patients with mucormycosis. Mortality for mucormycosis ranges from 50 % to 75%.

Acalculous cholecystitis is a condition seen in patients that are critically ill such as those with multiorgan trauma, burns, or recent major surgery. The exact mechanism is unclear, but it is thought to be secondary to a combination of biliary stasis (from being NPO) and gallbladder ischemia as a result of hypovolemic and/or septic shock. The diagnosis can be difficult for several reasons. Patients are critically ill so a history may be unobtainable and physical exam may be unreliable. The imaging test of choice is ultrasound (US). Findings suggestive of acalculous cholecystitis include gallbladder wall thickening and pericholecystic fluid; however, such findings are not consistent. If US is not definitive, HIDA scan is the next test and is considered positive if the gallbladder is not visualized. However, false positives are seen in patients who have been NPO for a prolonged period (which many of these critically ill patients have). Gallstones are not implicated in this condition, and will not be seen on ultrasonography. Treatment of acalculous cholecystitis includes broad-spectrum antibiotics followed by urgent percutaneous cholecystostomy (if the patient is critically ill) or cholecystectomy (laparoscopic vs. open cholecystectomy) if the patient is stable enough to undergo general anesthesia. Acute pancreatitis (A) is in the differential; however, the patient’s lipase is normal (more specific than amylase), and the amylase is only mildly elevated (acute pancreatitis requires an elevation 3x above normal). Mild hyperamylasemia can be seen with many intra-abdominal conditions including cholecystitis or bowel ischemia. Burn victims are at risk for stress-related mucosal damage (Curling ulcer) secondary to an inability to maintain the integrity of the gastrointestinal mucosal barrier. This may subsequently lead to perforated viscus (D) which will present with an acute abdomen and a plain film demonstrating free air under the diaphragm. Cholangiohepatitis (C) is associated with biliary parasites such as Clonorchis sinensis and is characterized by brown pigment stones that result from biliary sludge and dead bacterial cell bodies. Acute cholangitis (E) would present with evidence of cholestasis (jaundice and/or elevated liver enzymes) and biliary obstruction (dilated bile ducts on ultrasound).

The most likely diagnosis is acute pancreatitis secondary to gallstones. More than half of all cases of pancreatitis are associated with either gallstones or alcohol. Patients with gallstone pancreatitis have extremely high serum amylase (sometimes in the thousands) and ALT (greater than 3x the upper limit of normal) as compared to other etiologies. A biliary etiology of pancreatitis is further supported by the elevated bilirubin and alkaline phosphatase which suggest at least a temporary obstruction of the common bile duct by a gallstone. Most gallstones only transiently obstruct the common bile duct and pass on their own. Pancreatitis due to alcohol is seen in patients with long-standing heavy alcohol abuse (which is not suggested by the history in this patient), and not following a onetime binge. Chronic pancreatitis is rare with gallstones. It is most often seen in association with long-standing alcohol abuse. Patients present with chronic epigastric pain, steatorrhea, and/or diabetes. Amylase and lipase levels are often not elevated.

The patient is presenting with painless jaundice, which should be considered as due to malignancy until proven otherwise. Courvoisier’s sign is a term used to describe a palpable non-tender gallbladder that markedly distends as a result of a gradual common bile duct obstruction, most often by a pancreatic adenocarcinoma at the head of the pancreas (distal common bile duct and ampullary cancer are also in the differential). Gallstones typically cause sudden obstruction of the biliary tree and often harbor bacteria. They are almost always associated with pain and often trigger an inflammatory response. Charcot’s triad (B) (RUQ pain, fever, and jaundice) and Reynold’s pentad (C) (the triad plus hypotension and altered mental status) are associated with acute cholangitis most often secondary to a gallstone obstructing the distal common bile duct. Murphy’s sign (E) (RUQ tenderness on palpation that stops inspiration) is associated with acute cholecystitis due to a gallstone obstructing the cystic duct. Cullen’s sign (A) is a blue-red discoloration at the umbilicus, and the appearance is a result of digested blood products in the retroperitoneum, forming methemalbumin, that then travel towards the anterior abdominal wall. It is associated with retroperitoneal bleeding, as seen with hemorrhagic pancreatitis.

The presentation is most consistent with pancreatitis secondary to alcohol. Lipase is more specific for pancreatitis than amylase. The vast majority of acute pancreatitis cases are due to peripancreatic inflammation, not infection. Antibiotics (A) are therefore not beneficial. CT scan (B) is not necessary to establish the diagnosis and should be reserved for situations where the diagnosis is in question or if the patient clinically deteriorates during the subsequent hospitalization. The most appropriate management is to make the patient NPO, aggressively hydrate, and administer analgesics. Routine use of an NG tube is unnecessary. ERCP (C) is utilized in gallstone pancreatitis, specifically if the patient demonstrates evidence of concomitant cholangitis or obstructive jaundice. Librium (E) may be utilized for alcohol withdrawal, but should not be prioritized ahead of aggressive hydration. The majority of patients resolve the episode of pancreatitis within 3–5 days using conservative management.

Gallstones are commonly discovered incidentally in asymptomatic patients after imaging studies that are performed for unrelated reasons. Only 2–3% of asymptomatic patients develop biliary colic per year, and only a small fraction of those patients progress to complications from gallstones (such as acute cholecystitis, pancreatitis, acute cholangitis). For this reason, the vast majority of asymptomatic gallstones should not receive prophylactic cholecystectomy (A). Prophylactic cholecystectomy might be considered in patients who are planning extended travel to areas without healthcare access (Antarctica in the winter). Because patients with diabetes are at greater risk of developing complications from gallstones, some authors have recommended prophylactic cholecystectomy in diabetics. However, even in the diabetic population, it is reasonable to wait to see if symptoms develop. Ursodeoxycholic acid (B) can dissolve gallstones. However, it is completely successful in only about 1/3 of cases, only for cholesterol stones, is associated with side effects (diarrhea), and is costly. In addition, the stones may recur once the medication is stopped. ERCP (C) is an invasive procedure utilized for choledocholithiasis and acute cholangitis. Extracorporeal shock wave lithotripsy (E) is effective in breaking stones into small particles, but does not prevent stone recurrence.

The patient is manifesting evidence of systemic inflammatory response syndrome (SIRS); the presentation is most concerning for a pancreatic abscess. When SIRS is diagnosed, the first steps include fluid administration, blood cultures, and prompt institution of intravenous antibiotics (within 1 h), preferably imipenem. This should be followed by a CT scan (B) with contrast looking for necrotic tissue (non-enhancing areas) and a possible pancreatic abscess. In the past, such a finding on CT would warrant immediate exploration for pancreatic debridement (D). However the current approach is termed a “step-up” approach, which consists of a series of increasingly more invasive interventions. This begins with a percutaneous attempt at drainage of any infected pancreatic collections. If that fails, the next step is laparoscopic drainage (E). Finally open surgical pancreatic debridement is recommended. ERCP (C) would be indicated for suspected acute cholangitis, usually in association with gallstones.

Persistent abdominal pain, fevers, and nausea beyond a few days following laparoscopic cholecystectomy should raise suspicion of a bile duct injury or a bile leak from the cystic duct stump (due to the surgical clip inadvertently coming off). Imaging by CT scan should be obtained to look for a fluid collection. Abdominal ultrasound is also an acceptable imaging modality, but CT provides more information about the amount of fluid and its location. Additionally, findings on CT will guide subsequent management. Endoscopic ultrasound (A) is primarily used in the setting of pancreatic or bile duct cancer to help determine resectability and look for adjacent enlarged lymph nodes. If the patient has evidence of infection, and a large fluid collection is found, a percutaneous drain should be placed. Bilious output suggests that bile has leaked (from the stump of the ligated cystic duct or worse from an injury to the common hepatic/bile duct). A HIDA scan (E) should be obtained next. If the common bile duct or common hepatic duct were inadvertently transected, the HIDA will show extravasation of tracer in the RUQ without tracer filling the small bowel. Such a finding would mandate exploratory laparotomy (B), and a loop of small bowel would need to be anastomosed to the proximal bile duct (hepaticojejunostomy). If on the other hand, the HIDA scan shows extravasation of tracer in the RUQ but tracer is seen in the small bowel, this confirms that the integrity of the main bile ducts. The most common cause for this latter finding is a cystic duct stump leak (as in the present case). Management is to perform ERCP with stenting (D) of the ampulla. This lowers the pressure in the biliary tree, creating a path of least resistance for the bile, thus permitting the cystic duct stump to seal.

Patients with mild pancreatitis can often be managed being NPO along with intravenous hydration alone since recovery occurs rapidly, within 5–7 days, at which time oral intake can resume. However, patients with moderate-severe pancreatitis are unlikely to resume oral intake within 5–7 days, prompting the need for nutritional support. The most appropriate management is enteral nutrition. Enteral nutrition is provided through a nasojejunal tube, ideally placed past the ligament of Treitz as to not stimulate and irritate the pancreas. Enteral nutrition is preferred for those with a prolonged course of pancreatitis because it helps maintain the intestinal barrier and prevents bacterial translocation from the gut. In addition, enteral nutrition avoids the complications associated with parenteral nutrition including those secondary to venous access and blood stream infections. A 2010 meta-analysis of eight trials demonstrated that enteral nutrition significantly reduced mortality, multiorgan failure, infections, and the need for surgery as compared with those who received parenteral nutrition. Parental nutrition should only be initiated in patients who do not tolerate enteral feeding. In moderate-severe pancreatitis, oral feeding is not tolerated due to pain, nausea, or vomiting related to inflammation and edema causing gastric outlet obstruction, and should not be used.

Gallbladder polyps are usually incidental findings, most are asymptomatic, and the vast majority are benign. Risk of malignancy is related to polyp size. Polyps <10 mm can be observed, whereas laparoscopic cholecystectomy is recommended for those ≥10 mm. Open cholecystectomy (B) is not necessary for a polyp. Percutaneous gallbladder drainage (C) is indicated for the management of acalculous cholecystitis. Endoscopic ultrasound (D) would not provide any additional information. A follow-up ultrasound (E) would be appropriate for small polyps.

The patient has severe pancreatitis as evidenced by having five Ranson’s criteria. Mortality is markedly increased with three or more such criteria. Mortality in the first week is due to multisystem organ failure (pulmonary, renal, cardiac). ARDS occurs in a variety of settings, including severe pancreatitis. The classic presentation is severe hypoxia, with an associated respiratory alkalosis and a CXR that shows bilateral infiltrates that is often symmetrical. Therapy includes starting mechanical ventilation with positive end-expiratory pressure (PEEP). The overall mortality is very high (>50 %). Although a pulmonary embolism (B) may also present with hypoxia and a respiratory alkalosis, it is unlikely to present with bilateral infiltrates (the CXR is usually negative). Hospital-acquired pneumonia (C) would present with a productive cough, dyspnea, chills, pleuritic chest pain, decreased breath sounds, wheezing, and a CXR showing lobar consolidation. A patient with pulmonary edema (D) would have a CXR showing cephalization of vessels and Kerley B lines (i.e., prominent horizontal interstitial markings in lower lung fields), as well as an elevated CVP (>18 mmHg). Atelectasis (E) would appear as a white out of a lobe.

Obstructive jaundice is an elevation of serum conjugated bilirubin due to inability to excrete it into the intestines via the biliary system. Thus there would be decreased available bilirubin in the intestine for intestinal bacteria to convert to urobilinogen and subsequently stercobilin. Although indirect and direct bilirubin are both elevated in obstructive jaundice, the direct component should be higher. Unconjugated bilirubin is bound to protein, and not filtered by the kidney. In patients with jaundice, conjugated bilirubin is elevated in the urine. The elevation in urine conjugated bilirubin gives it the brown (“tea-colored”) discoloration. Elevation of transaminases out of proportion to alkaline phosphatase (E) would suggest hepatocellular injury.

Smoking is a risk factor for pancreatic cancer. Pancreatic cancer is also more common in men, advanced age, in the obese, and in African Americans. Chronic pancreatitis is the strongest risk factor pancreatic cancer, although alcohol consumption (A) per se is not. A family history of prostate cancer (C) is not a risk factor for pancreatic cancer. Although malabsorption (D) and pancreatic enzyme supplementation (E) is frequently associated with patients that have chronic pancreatitis, they are not themselves directly linked to an increased risk for pancreatic cancer.

UGI bleeding from varices most often are the result of alcohol-related liver cirrhosis with subsequent portal hypertension. This leads primarily to esophageal varices and less commonly to concomitant gastric varices. Isolated gastric varices are uncommon. They often arise in association with splenic vein thrombosis (SVT), which forces all the venous drainage of the spleen to travel through the short gastric veins resulting in large gastric varices that are at risk for rupture and bleeding. The most common cause of SVT is pancreatitis (acute and chronic). The most common cause of chronic pancreatitis is alcohol abuse. Peripancreatic inflammation can lead to occlusion of the splenic vein, which is posterior to the pancreas. SVT does not lead to esophageal varices because the collaterals do not involve the esophageal vasculature. Diagnosis of SVT can be made by duplex ultrasound of the splenic vein. It can also be detected on a venous phase CT scan. Splenectomy effectively eliminates the enlarged short gastric veins and thus cures the gastric varices. Gastric varices are particularly dangerous as they tend to cause massive bleeding. In addition, they do not respond well to standard treatment for esophageal varices such as banding (B) or sclerotherapy (C). Both liver transplantation (A) and TIPS (D) would reduce portal hypertension and thus help remedy esophageal varices but would be ineffective for isolated gastric varices in the setting of SVT.

The first step in working up a pancreatic leak is to test the drained fluid for amylase. In addition, serum amylase level should be checked as well. If fluid amylase level is high and output levels are high (>50 cm³/day), patient can be made NPO to decrease secretion of pancreatic fluid that accompanies oral intake. Imaging (A–B) can be done at a later time to evaluate adequacy of drainage. Octreotide (D) can be given to decrease pancreatic secretions, but it is not used routinely, and there is no evidence-based data that demonstrate cost-effective efficacy of octreotide use in this setting. TPN (E) is not routinely needed in this setting.

At this time CA 19–9 is not recommended for screening pancreatic cancer, and is also not a diagnostic test. However, many surgeons use CA 19–9 to monitor for recurrence following surgery.

The patient presented has RUQ pain and tenderness, nausea, and an ultrasound demonstrating gallstones with a thickened gallbladder wall suggestive of acute cholecystitis. Mild elevations in ALT and AST can be expected with acute cholecystitis, as well as leukocytosis with a left shift. The patient should be admitted to the hospital, made NPO, given IV fluids, and IV antibiotics with gram negative, enterococcus, and anaerobic coverage. She should undergo laparoscopic cholecystectomy, ideally within 48 h (C–E). Multiple studies have shown that delaying surgery is of no benefit and, in fact, makes the operation technically more challenging due to more scarring. Elective outpatient laparoscopic cholecystectomy is appropriate for patients with biliary colic (A).

This patient has acute pancreatitis, most likely secondary to gallstones (most common cause). She has had prior episodes of pain after eating fatty food, which is characteristic of symptomatic gallstones. In addition, the lipase and amylase are elevated (3× greater than the upper limit of normal). Cholecystectomy is considered the standard of care in patients with gallstone pancreatitis because there is a high risk of recurrent pancreatitis. Although most centers have traditionally waited until all laboratory values have normalized for patients with mild disease (may take 5–7 days) (B), recent randomized studies have demonstrated that cholecystectomy can be safely performed within 48 h of admission (in patients with mild pancreatitis) regardless of whether laboratory values have normalized (D). Thus this patient should proceed with LC with IOC since she demonstrates no evidence of severe pancreatitis. On the other hand, with severe pancreatitis, such as necrotizing pancreatitis, delaying gallbladder removal until complete resolution of the pancreatitis is recommended. The gallstones that cause pancreatitis are usually small, and as such, in the majority of cases, the stone remains impacted very briefly, only transiently obstructing the ampulla of Vater, and soon after passes into the duodenum. As such persistent of a CBD stone is uncommon, and therefore ERCP is not usually needed (C, E).

A diabetic patient presenting with symptoms suggestive of acute cholecystitis with high fevers, high WBC with left shift, and RUQ ultrasound demonstrating gas bubbles within the wall of the gallbladder should be suspected of having emphysematous cholecystitis, which is generally considered a surgical emergency. It is generally caused by gas-forming organisms, such as Clostridia and E. coli. Compared to acute cholecystitis, emphysematous cholecystitis is associated with a much higher mortality due to severe sepsis as the gallbladder becomes gangrenous. Broad-spectrum antibiotics (include high-dose penicillin or clindamycin to cover Clostridia) and fluid replacement are started immediately to stabilize the patient (B), but because of the risk of gangrene, these patients should undergo an immediate cholecystectomy. The diagnosis can be supported with CT scan of the abdomen (D) which will also demonstrate gas within the gallbladder wall. ERCP (E) is not indicated. Cholecystostomy (C) would not be an appropriate intervention for emphysematous cholecystitis as the necrotizing tissue infection would not be removed.

A heavy calcified gallbladder is termed a porcelain gallbladder and is most commonly found incidentally on imaging for unrelated reasons. Patients are often asymptomatic. However, it is important to recognize that a porcelain gallbladder is associated with an increased risk of gallbladder adenocarcinoma. As such, the recommendation is that patients should undergo surgical management with laparoscopic cholecystectomy. Reassurance (A) or “watchful waiting” with annual CT scan (B) is not appropriate, even for asymptomatic patients, because of the risk for malignancy. There is no reason to suspect hyperparathyroidism, and so a serum calcium and PTH level would not be appropriate (D). ERCP with brushings is useful for suspected bile duct cancer, but not for suspected gallbladder cancer (E).