Author: Keith Alangaden

Reynolds pentad = Charcots triad (Fever, RUQ pain, and Jaundice), and adds two septic/toxic elements -> Hypotension and AMS!

This answer is tricky, but answers B-D can be ruled out.

Ascending cholangitis is typically treated with urgent biliary decompression and intravenous antibiotics. Reynolds pentad, although classically associated with ascending cholangitis, is rarely present and a high index of suspicion is required for diagnosis. In addition to common duct stones and biliary obstruction, cholangitis should be suspected in patients presenting with sepsis after ERCP.

Although biliary colic in the absence of acute cholecystitis can typically be managed as an outpatient with symptoms control and surgical referral, in special populations such as children and prolonged symptoms in pregnancy may require admission. Acute cholecystitis requires prompt (in ED) surgical consultation and admission.

The presence of this antibody either represents natural immunity from successfully resolved Hepatitis B infection or the desired response to vaccination

While an elevated serum ammonia level is highly indicative of hepatic encephalopathy, a normal level does not rule out the diagnosis. A head CT should always be considered in a patient with altered mental status. An elevated ethanol level may account for this patient’s symptoms, but with his confusion and history of liver disease, other sources must be explored. Blood glucose levels should be checked frequently since this patient with liver disease has likely impaired glucogenesis and reduced glycogen stores.

In severe acute liver failure, transplant is often the only means to improve survival. Thus, transfer to a transplant facility is vital. Oral charcoal is of no real benefit after approximately 3 to 4 hours after ingestion. N-acetylcysteine may still be of some benefit, even up to 48 hours after ingestion.

Despite the potential for pulmonary edema in acute hepatic failure, intravenous fluids should be given as part of the initial resuscitation. Propofol is a recommended agent for the patient requiring sedation. Flumazenil has not been shown to be efficacious in the patient with liver failure and altered mental status. Fresh frozen plasma is necessary to correct the coagulopathy in the liver failure patient with bleeding.

With an incidence of 17% to 28%, biliary complications—bile leaks and instructions to bile flow from strictures, stones, ampullary dysfunction—are the most common and anastomotic complications of orthotopic liver transplant. Hepatic artery thrombosis less commonly complicates orthotopic liver transplant; however, it is more common than portal vein thrombosis or hepatic vein thrombosis.

Hyperparathyroidism can lead to hypercalcemia. This can lead to the inappropriate release of proteolytic enzymes that can lead to acute pancreatitis.

Chronic pancreatitis damages the Islet of Langerhans, impairing the secretion of insulin and glucagon, predisposing the patient to episodes of acute hypoglycemia.

This patient has osteomyelitis of the distal femur. Osteomyelitis, which is a pyogenic infection of the bone, occurs via hematogenous seeding (most common in children), seeding from a contiguous source of infection (eg, diabetic foot ulcer), or direct inoculation (eg, puncture wound, orthopedic procedure). Children will most often present with acute osteomyelitis (< 2 weeks) with signs of systemic infection such as fever and irritability in addition to localized bone pain and swelling. Adults commonly present with subacute or chronic osteomyelitis, and will have pain, swelling, as well as non-healing ulcers more frequently than they will have fever. Plain radiographs are the initial imaging choice in patients with osteomyelitis, though fewer than one third of patients will have any abnormalities in the first seven to ten days of admission. Periosteal reaction is the earliest osseous finding. The most common infecting organism in osteomyelitis for healthy hosts in all age groups except neonates is Staphylococcus aureus. Patients with sickle cell have an increased risk of osteomyelitis overall, especially from Salmonella spp. Additionally, Salmonella spp. are the most common pathogen identified in sickle cell patients with osteomyelitis. Pseudomonas (C) infection should be considered in the setting where osteomyelitis develops following a penetrating injury through a surface colonized with pseudomonas (e.g. the sole of a shoe). Haemophilus spp. (A) used to be the second most common cause of osteomyelitis, however this is no longer true secondary to the advent of the Haemophilus vaccine. Klebsiella spp. (B) and other anaerobes are rarer causes of osteomyelitis and are more frequently associated with chronic osteomyelitis, as in diabetic patients with non-healing foot ulcers.

This patient is presenting with signs and symptoms associated with pyloric stenosis. Pyloric stenosis is caused by the idiopathic hypertrophy and elongation of the pylorus causing gastric outlet obstruction. Pyloric stenosis is best diagnosed with abdominal ultrasound. Risk factors for the development of pyloric stenosis include male sex, being firstborn, and exposure to erythromycin as a neonate. Patients with pyloric stenosis generally present within the first 3 to 6 weeks of life. Signs and symptoms include projectile nonbilious emesis with persistent hunger after vomiting. There may be a palpable olive-shaped mass in the epigastrium or right upper quadrant of the abdomen; however, it is not often palpable due to patient crying during the exam. Management of pyloric stenosis is with surgical pyloromyotomy.

A CT of the abdomen (B) is generally not necessary to make the diagnosis of pyloric stenosis as it is typically easily seen with ultrasound alone. Ultrasound is also more desirable as it does not expose the child to radiation and is non-invasive. An upper GI series (C) is used to diagnose malrotation and midgut volvulus, which presents with bilious emesis. The image produced shows a corkscrew appearance of the oral contrast, revealing the diagnosis. An X-ray of the abdomen (D) is often sufficient to diagnose necrotizing enterocolitis, which presents with pneumatosis intestinalis and feeding intolerance in neonates.

This child is presenting with signs and symptoms associated with Hirschsprung disease, also known as congenital aganglionic megacolon. Hirschsprung disease is caused by the lack of ganglion cells in the colon, leading to increased muscle tone and contractility of the aganglionic segment. The majority (75%) occur in the rectosigmoid segment. The most common presenting complaint is delayed passage of meconium, greater than 48 hours after birth. Other signs and symptoms include diminished stool frequency, abdominal distension, and bilious emesis (late finding). Hirschsprung disease may be diagnosed with barium enema (reveals a cone-shaped transitional zone), rectal manometry (reveals lack of anal sphincter relaxation), or definitively on rectal biopsy. Definitive management of Hirschsprung disease is via resection of the aganglionic segment.

Incomplete rotation of intestine around superior mesenteric artery and abnormal attachment of the abdominal mesentery (A) to the abdominal wall and ligament of Trietz is the mechanism by which malrotation and midgut volvulus occurs. Ectopic gastric mucosa (B) is the most common form of ectopic tissue found within Meckel’s diverticulum and frequently ulcerates causing patients to present with painless rectal bleeding. Pyloric sphincter hypertrophy (D) is the mechanism by which pyloric stenosis occurs.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Management of malrotation with midgut volvulus is with fluid resuscitation, nasogastric tube decompression, and definitively with surgical correction. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 75% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Sepsis and shock may occur with necrotic bowel. Diagnosis of malrotation with midgut volvulus is made on upper GI series, which reveals a “corkscrew” appearance of the contrast.

Air enema (A) is the first-line treatment for intussusception. Broad spectrum intravenous antibiotics (B) would be appropriate if you suspected perforation. Sigmoidoscopy (C) is the treatment of choice for sigmoid volvulus.

Hypoglycemia in neonates and infants should be taken seriously has symptomatic neonatal hypoglycemia is associated with brain injury and poor intellectual performance later in childhood. A high suspicion for hypoglycemia should be maintained as symptoms are nonspecific. Neonates can present with jitteriness, hypotonia, altered mental status, cyanosis, poor feeding, hypothermia, seizures, or coma. Older children may present with tachycardia, tachypnea, diaphoresis, or anxiety. The etiology of hypoglycemia in infants includes decreased oral intake, high ratio of insulin to counter-regulatory hormones including secondary to growth hormone deficiency and adrenal insufficiency, inborn errors of metabolism, and sepsis. Hypoglycemia is diagnosed with rapid bedside glucose testing and treatment should be initiated promptly before other studies are complete. However, when possible, extra tubes of blood should be drawn prior to administration of dextrose for possible further workup by the pediatric endocrinologists. The presence or absence of ketonuria can also help differentiate causes of hypoglycemia. Treatment thresholds for hypoglycemia vary slightly in the first days after birth, but generally are < 45 mg/dL in symptomatic patients and < 35 mg/dL in asymptomatic patients. If the hypoglycemia is thought to be secondary to an inborn error of metabolism, glucose should be maintained above 70 mg/dL. First-line treatment for hypoglycemia is bolus dosing of IV dextrose 0.5 g/kg in any of a number of regimens, with preference for larger volumes of less-concentrated dextrose to reduce venous injury. These regimens can be remembered by the “rule of 50s,” in that the product of the concentration of dextrose and volume per kilogram should equal 50. Neonates and infants should be given 10% dextrose at 5 mL/kg IV bolus, toddlers and children should receive 25% dextrose at 2 mL/kg IV bolus, and adolescents can be given 50% dextrose at 1 mL/kg IV bolus. Maintenance dextrose should the be started with 10% dextrose at 6–8 mL/kg/hr IV. For patients without IV access, glucagon can be given at 0.3 mg/kg intramuscularly. Glucagon is additionally beneficial as it can help determine the etiology of the hypoglycemia. If serum glucose increases with glucagon, there are appropriate hepatic glycogen stores and the problem is likely a hormonal deficiency. A lack of an appropriate increase in serum glucose indicates poor hepatic glycogen stores. Additionally, if there is concern for adrenal insufficiency as the cause of hypoglycemia, hydrocortisone should be given. Lastly, there should be a high index of suspicion for sepsis in hypoglycemic neonates and infants, and broad-spectrum IV antibiotics should be considered in these children if they are ill-appearing or have altered mental status.

25% dextrose at 2 mL/kg IV bolus (B) is an appropriate dose as it meets the “rule of 50s,” however, it is a highly concentrated solution and has a high risk of causing venous injury. Neonates and infants should receive a bolus of 10% dextrose at 5 mL/kg. 5% dextrose at 5 mL/kg IV bolus (C) is too small of a dose and is too dilute to be an effective therapy in this symptomatic hypoglycemic patient. Using the “rule of 50s,” this regimen would only provide half the insulin needed to treat this patient’s hypoglycemia. Additionally, dextrose 5% should not be used for bolus dose treatment of hypoglycemia. It is indicated for maintenance fluids in normoglycemic patients to prevent hypoglycemia, especially while they are being kept NPO in the hospital. Glucagon 0.3 mg/kg intramuscularly (D) can be used to treat hypoglycemia but generally should be reserved for patients without IV access. While there are some benefits to glucagon in that it can be both therapeutic and diagnostic of the etiology of hypoglycemia, IV dextrose remains first-line therapy when IV access is present, as in this patient.

Pediatric patients are at an increased risk of spinal cord injury without radiographic abnormalities (SCIWORA) as compared to adults. SCIWORA was originally defined as clinical evidence of a spinal cord injury (e.g., neurologic deficits, including transient deficits) without abnormalities on cervical spine CT or flexion-extension X-rays. More recently, with the use of MRI, we have found that most SCIWORA patients have visible acute spinal cord injuries, including those with transient symptoms and normal neurologic exams by presentation. Pediatric patients are at higher risk for SCIWORA secondary to larger head-to-body ratios, more elastic spinal ligaments, shallow vertebral facets that predispose to subluxation, as well as higher spinal canal diameter-to-spinal cord diameter, allowing movement of the cord within the canal. As such, it is important to maintain a high index of suspicion for spinal cord injuries in pediatric patients with significant mechanism (e.g., axial loading, high-risk motorized vehicle collision), or those with neurologic symptoms and normal preliminary spine imaging. Pediatric patients are also at higher risk for higher-level cervical spine injuries. As the head-to-body ratio decreases with age, the cervical spine fulcrum moves from C2–C3 at birth to C5–C6 by approximately 8 years of age.

Injury to C6–C7 (B) is more common in adults, as their smaller head-to-body ratio lowers the fulcrum in their cervical spine. Young children, less than 8 years old, are more likely to have higher cervical spinal injuries, as described above. Injury to spinal cord at T4–T5 (C) would cause symptoms at and below that spinal level. The arms are innervated by nerves arising from the brachial plexus, which originates from nerve roots C5–T1. Therefore, an injury below T1 (e.g., T4–T5) would not cause upper extremity paralysis or numbness. Normal MRI (D) would not likely be seen, as this patient had neurologic deficits, albeit transient. As discussed above, the majority of pediatric patients with high-risk mechanisms for cervical spine injury, even transient neurologic deficits and normal cervical spine CT scans, have been found to have cervical spinal cord injuries on MRI.

Child abuse is a common and serious emergency department diagnosis accounting for between 2% and 10% of pediatric ED visits. It is an important diagnosis to recognize, both for the safety of the child and due to mandatory physician reporting in all 50 states. Historical clues as well as injury patterns can help the clinician differentiate unintentional trauma and intentional trauma. Bruising in a child less than 6 months of age has a very high likelihood of being related to intentional trauma. Patients under 6 months are nonmobile and therefore unlikely to fall or pull objects onto themselves. This falls into the TEN-4 mnemonic (bruising to the torso, ears, neck or under 4 months), which has a sensitivity of 97% in detecting intentional trauma. Young age is the most significant risk factor for intentional trauma.

Intentional bruises are more likely to be found in clusters, on the back, and in symmetric patterns versus anterior and isolated bruising such as on the central forehead (B), which can commonly occur from falls during early ambulation. Burns to the face and neck (C) can be seen in children who are cruising (8–16 months) as they unintentionally pull hot objects down. Spiral tibia fracture (D), also known as a toddler fracture, is an unintentional fracture with a twist and fall mechanism in children 9 months to 3 years. Toddler fractures typically present with refusal to bear weight.

This patient presents with signs and symptoms concerning for an obstruction secondary to a volvulus and requires emergent surgical evaluation. Malrotation is a relatively common occurrence (1 in 500 live births) and about 75% of patients with malrotation will develop volvulus. During embryonic development, rotation of the gut arrests. This allows for the small bowel to twist around the superior mesenteric artery causing an acute obstruction. Patients will present with sudden onset of abdominal distension and bilious emesis. These infants will be ill-appearing and possibly toxic on presentation. Although a number of diagnostic modalities can be employed for definitive diagnosis, the priority in an ill-appearing infant with bilious emesis is emergent surgical consultation. All other interventions risk delaying definitive management. While waiting for the surgical consultation, the patient should have an IV placed, fluid resuscitation begun and a nasogastric tube placed for decompression of the stomach. Additionally, broad spectrum antibiotics should be administered. After consultation, an upper GI series may be obtained for definitive diagnosis.

Stool cultures (B) are useful when there is a suspicion for infectious process such as a parasitic or bacterial infection. Laboratory studies (C) will provide limited data and should not delay definitive management by a surgeon. The patient should receive intravenous hydration, not oral rehydration (D) as there is a high likelihood that this patient will be taken to the operating room. As such, the patient should be kept NPO.

Intussusception is when part of the intestine telescopes into itself. Ileocolic intussusception is the most common type which occurs when the small intestine prolapses through the ileocecal valve. It usually occurs in children under the age of 2 years with a peak incidence between 6 and 9 months. It can, however, occur at any age, especially if there is a lead point such as a Meckel’s diverticulum or a polyp. The classic presentation of abdominal pain, bilious emesis, an abdominal mass, and blood in the stool is rare. Most toddlers present with colicky abdominal pain and one or two of the other symptoms to aid in the diagnosis. Infants, in particular, may present with only lethargy and vomiting often being confused with sepsis. In premature neonates it can be easily confused with necrotizing enterocolitis. Most ileocolic intussusception can be successfully treated nonoperatively with an air enema if identified and reduced within 48 hours. Recurrence is rare but typically occurs within the first 48 hours and, if primarily successful, an air enema can be repeated. A small bowel intussusception is treated somewhat differently as it is less likely to respond to an air enema and more likely to spontaneously reduce.

The clinical manifestations of meningitis (B) typically include fever. Vomiting is also a possibility but it is not bilious in nature as seen in our patient. The presence of guaiac positive stool also is not consistent with meningitis. Intracranial subdural hematoma from non-accidental trauma (C) or a toxic ingestion (D) should be considered in patients this age with nonbilious vomiting and lethargy, however findings of bilious vomiting and guaiac positive stool makes intussusception more likely in this patient.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Diagnosis of malrotation with midgut volvulus is made on an upper gastrointestinal series, which reveals a “corkscrew” appearance of the contrast. Abdominal X-ray may show a “double-bubble” sign, but it is not a definitive study as this may also be seen in duodenal atresia. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 90% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Definitive management of malrotation with midgut volvulus is with surgical correction.

Abdominal ultrasound (A) is used in diagnosing intussusception or pyloric stenosis. It can also be used in children to diagnose appendicitis. CT scan of the abdomen (B) is usually a secondary study in children when you are still concerned after a primary (less invasive) study is inconclusive. X-ray of the abdomen (D) is used to evaluate for free air or pneumatosis intestinalis.

This patient is presenting with Boerhaave’s syndrome, which refers to esophageal rupture, usually due to forceful vomiting resulting in a full-thickness tear. Patients present with severe, persistent chest pain. Subcutaneous emphysema may be present on physical examination. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation. This is known as Hamman’s sign. Chest X-ray findings may include a left pneumothorax, a left pleural effusion, mediastinal emphysema, and a widened mediastinum. Diagnosis should be confirmed with an esophagram using water-soluble oral contrast. Emergent surgical consult should be obtained and broad-spectrum antibiotics should be started. Because significant morbidity and mortality occur very rapidly due to sepsis, it is necessary to determine early whether the patient is a surgical candidate. Patients with free perforation likely require emergency surgery, whereas stable patients with a contained perforation may be able to be managed with intravenous antibiotics and maintaining NPO status.
Because Boerhaave’s syndrome is a surgical emergency, surgical consultation should not be delayed to obtain a CT chest with IV contrast (A). Endoscopy (C) could help in diagnosing Boerhaave’s syndrome, but could also worsen the perforation. Therefore, endoscopy is not indicated, and surgical evaluation should be immediate. Nasogastric tube placement (D) is contraindicated with esophageal tears and should be avoided.

The X-ray demonstrates a foreign body in the esophagus that should be removed under direct visualization by an endoscopist. Pediatric patients account for 75% of all ingestions with coins being the most commonly ingested foreign body. The esophagus has four natural areas where it narrows and these are the most likely places for foreign bodies to become stuck. The four areas are at the upper esophageal sphincter, the aortic arch, the left main stem bronchus and the lower esophageal sphincter. Patients are often asymptomatic on presentation if the foreign body is in the esophagus. Anteroposterior and lateral X-rays of the neck and chest should be performed. An esophageal coin can be differentiated from a tracheal coin on X-ray based on orientation. Coins will appear “en face” on anteroposterior X-ray if they are in the esophagus.
Removal under direct laryngoscopy (A) is not recommended as the coin is too deep to be reached this way. Removal with a Foley catheter (C) may be effective in esophageal foreign bodies. If the coin remains in the esophagus, it should be removed and not observed for passage (D).

This patient presents with a perforated peptic ulcer requiring evaluation for emergent surgery. Perforation is one of the serious complications of peptic ulcer disease in addition to hemorrhage and gastric outlet obstruction. Up to 10% of patients with ulcers can develop perforation and it most commonly occurs in the anterior wall of the duodenum. Perforation typically presents with an acute onset of severe abdominal pain and should be preceded by symptoms consistent with peptic ulcer disease (burning or gnawing pain). The acute pain often radiates to the back and the patient may experience referred pain to the shoulder as a result of air sitting under the diaphragm. Upright chest X-ray and abdominal X-ray with decubitus views will often, but not always, show pneumoperitoneum. This finding should prompt immediate surgical consultation as the patient will require operative management.

Clarithromycin, amoxicillin and a proton-pump inhibitor (A) can be used to treat H. pylori. A CT scan of the abdomen and pelvis (B) is helpful in a patient with symptoms suggestive of perforation and negative plain radiographs. Ultrasound of the right upper quadrant (D) is useful in the diagnosis of biliary pathology.

Esophageal varices are dilated veins in the esophagus that result from increased pressure in the portal system usually secondary to liver cirrhosis. They are diagnosed with esophagogastroduodenoscopy and have an increased risk of bleeding. Variceal rupture can cause massive hemorrhaging and be acutely life threatening. The immediate treatment of acute variceal hemorrhage is volume resuscitation, intubation for airway protection if needed, and correction of any underlying coagulopathy. Beyond the immediate resuscitation, there are several pharmacologic treatments for variceal bleeding. However, ceftriaxone and IV antibiotics have shown to decrease mortality by reducing the infectious complications. It is common for patients with variceal bleeding to have concomitant bacterial infections from translocation of gut bacteria. Common antibiotics used are third generation cephalosporins or fluoroquinolones. This should be given as soon as possible and ideally before endoscopy.

Octreotide (C) is an analog of somatostatin that is used to reduce blood flow through the gastric mucosa and cause splanchnic vasoconstriction. The literature shows that octreotide will help achieve hemostasis and prevent rebleeding; however, it has no clear benefit in mortality. Pantoprazole (D) and other proton pump inhibitors are frequently used in undifferentiated upper gastrointestinal bleeding, but benefits are typically seen in patients with peptic ulcer bleeding. Erythromycin (B) is a promotility agent that is used to enhance endoscopic visualization but is not recommended for routine use. All variceal bleeding will need early endoscopy for definitive treatment with ligation or sclerotherapy.

Mallory-Weiss syndrome is characterized by longitudinal mucosal lacerations in the distal esophagus and proximal stomach, commonly associated with violent or repeated vomiting. The lacerations lead to bleeding from submucosal arteries. Mallory-Weiss syndrome is common, representing 8–15% of upper gastrointestinal (GI) bleeding. Symptoms include dysphagia, odynophagia, and upper GI bleeding. Bleeding is usually mild to moderate, often resolving spontaneously. Risk factors include alcoholism, hiatal hernia, and gastritis or esophagitis. The diagnostic study of choice in patients with continued bleeding is endoscopy. All patients with Mallory-Weiss syndrome should be treated with proton pump inhibitors for acid suppression and antiemetics. For patients with actively bleeding, endoscopic therapy (thermal coagulation, hemoclips, or endoscopic band ligation) is indicated.

Boerhaave’s syndrome (A) is a full-thickness esophageal perforation and a surgical emergency. Patients typically present with severe chest pain that begins acutely after vomiting. The patient in this question does not have any pain and is feeling better, making this an unlikely diagnosis. Diverticulosis (B) is a common cause of lower gastrointestinal bleeding but does not cause hematemesis. Peptic ulcer disease (D) is mostly commonly the result of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug usage. Patients will present with vague epigastric pain that may radiate to the back.

Swallowed foreign bodies most commonly obstruct at the level of C6, the cricopharyngeus muscle, one of the four natural areas of luminal narrowing in the esophagus. The cricopharyngeus is the muscle of the upper esophageal sphincter (UES). Depending on the type of material, a plain radiograph may not reveal the object, particularly with food bolus obstructions. Pediatric patients often swallow objects like coins, and it may be difficult to ascertain whether a coin is in the trachea or esophagus. On a soft tissue X-ray, a coin located in the esophagus appears in the coronal plane, “en face,” as opposed to appearing sagitally when in the trachea. Most foreign bodies less than 2 cm x 5 cm will pass spontaneously through the GI tract. If the patient is without severe symptoms, foreign bodies less than this size are observed for 24 hours as only 10-20% require endoscopic removal. Fewer than 1% will require surgical removal. Pediatric patients account for more than 75% of esophageal foreign bodies. Other at risk patients include edentulous persons, those with psychiatric disease and prisoners, and those with underlying structural abnormalities of the esophagus (rings, strictures, diverticula, malignancy).

The aortic arch (A) at the level of T4 is the second most common location for foreign body obstruction in the esophagus. The gastroesophageal junction (C) at T11 is third most common. The tracheal bifurcation (D) at T6 is the fourth most common site, particularly as the left mainstem bronchus pushes against the esophagus. The thoracic inlet at T1 is the least common location for obstruction.

This patient is presenting with peptic ulcer disease secondary to Helicobacter pylori infection. It is estimated that 30%–40% of the US population is infected with H. pylori, although many will never develop peptic ulcer disease. It is usually acquired through the fecal-oral route, typically in childhood. It is estimated that the majority of patients with duodenal and gastric ulcers are infected with H. pylori. Its presence causes mucosal inflammation and disrupts the normal defense mechanism of the stomach lining, leading to ulceration. Methods of testing include urea breath test, urea blood test, blood antibody testing, stool antigen testing, and biopsy during endoscopy. Triple therapy withclarithromycin 500 mg BID, amoxicillin 1 g BID (metronidazole 500 mg BID if allergic to penicillin), and a proton pump inhibitor (such as lansoprazole 30 mg BID) for 10–14 days is currently recommended for all patients with confirmed H. pylori infection.

Amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (A) is incorrect as you need the addition of clarithromycin; clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID for 10–14 days (C) is incorrect as you have not used a PPI; and clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (D) is incorrect as you have treated the patient with too many medications.

Esophageal varices occur in patients with cirrhotic liver disease and portal hypertension. Over time, varices develop in the lower portion of the esophagus and may acutely bleed leading to massive upper GI bleeding. Octreotide is a somatostatin analog which causes splanchnic vasoconstriction when administered intravenously. As a result of splanchnic vasoconstriction, hypertension of the portal system may decrease leading to decreased bleeding. In an acute GI bleed from varices, a bolus of 50 to 100 micrograms is administered followed by a continuous infusion of 50 micrograms/hour.

The placement of a nasogastric tube (A) will not have a therapeutic outcome in the management of upper GI bleeding due to esophageal varices. Nasogastric tubes may be placed to help prevent vomiting in patients with ongoing bleeding. Additionally, in cases where the presence of bleeding is unclear, a tube may be inserted diagnostically although the sensitivity of this limits its usefulness. Some argue that caution must be taken in the presence of variceal bleeding for fear of worsening bleeding from the trauma of tube insertion. Propranolol (C) is a beta-blocker used prophylactically in patients with known esophageal varices in order to maintain blood pressure and heart rate control. The medication has no role in the acute management of a variceal bleeding. Ranitidine (D) is an H2-antagonist used in the suppression of acid production. The pathophysiology of variceal bleeding is not due to increased acid production nor worsened by the presence of acid and these agents are not indicated. In upper GI bleeding due to peptic ulcer disease, proton pump inhibitors may have some benefit in preventing re-bleeding after the initial episode and are often part of the management of those patients.

Gastroesophageal reflux disease (GERD) is caused by damage to the mucosa of the esophagus from reflux of gastric acid. It is further subdivided into erosive and non-erosive GERD based on endoscopic identification of visible esophageal damage. GERD typically manifests as heartburn that occurs after eating and is worse in the supine position. However, it may also present with epigastric pain, indigestion, nausea, and eructation. Reflux may even extend to the oral cavity and lungs, causing sore throat, cough, and wheezing. While GERD can be diagnosed clinically, pharmaceutically refractory cases and those patients in whom alternative diagnoses are a consideration warrant further objective evaluation. Esophageal pH monitoring is appropriate for patients without alarm symptoms. The presence of dysphagia, odynophagia, or other alarming symptoms should be evaluated by endoscopy. Lifestyle changes including weight loss, elevating the head of the bed, and avoiding food triggers (e.g., caffeine, alcohol, and acidic foods) are all important interventions. Mild, intermittent disease can be treated with antacids as needed, whereas patients with more severe disease require treatment with either an H2 blocker or a proton pump inhibitor (PPI). Erosive GERD should be treated with a PPI (e.g., omeprazole and lansoprazole), whereas non-erosive disease can be treated with either an H2 blocker or a PPI. However, studies have shown the use of PPI results in better response as well as faster healing and resolution of symptoms compared to H2 blockers. Accordingly, PPIs are recommended as first-line for gastroesophageal reflux disease where financial issues are not a factor. H. pylori infection is a consideration in patients with peptic ulcer disease, but patients with GERD and a positive H. pylori test should also be treated. Initial triple therapy with lansoprazole, amoxicillin, and clarithromycin for 10 days is one treatment option.

Bismuth subsalicylate, metronidazole, and doxycycline (A) is not a treatment for H. pylori. The substitution of tetracycline for doxycycline would make it appropriate. Continuing famotidine and adding sucralfate (B) is not appropriate as the patient has tested positive for H. pylori. Triple therapy should be offered even in the absence of peptic ulcer disease. Additionally, sucralfate is not recommended for GERD treatment in the non-pregnant patient. Stopping famotidine and starting omeprazole (D) would be appropriate for a patient with objectively diagnosed GERD and a negative H. pylori result.

This patient presents with infectious esophagitis secondary to a candidal infection and can be treated with fluconazole. Esophagitis is defined as inflammation of the esophagus and can be caused by a number of mechanisms including infection, allergy related (eosinophillic) or pills. Infectious esophagitis typically occurs in patients that are immunocompromised (diabetes, HIV/AIDS, chronic steroids etc.). Esophageal candidiasis is common in the HIV/AIDS population and is considered an AIDS-defining illness. In addition to candida, it can be caused by HSV1 and CMV. Patients with infectious esophagitis present with severe odynophagia that may be to solids, liquids or both. They may also have chest pain, nausea and dyspepsia. Dehydration is common secondary to pain. Diagnosis can be made based on clinical presentation but an endoscopy can be performed to confirm the diagnosis. In immunocompromised patients with candidal esophagitis, treatment should be with fluconazole for 14 to 21 days. If they are unable to tolerate oral medications, intravenous fluconazole can be given.

Acylovir (A) is used in the treatment of herpes esophagitis. Clotrimazole troches (B) can be used in the treatment of mild oropharyngeal candidiasis in immunocompetent patients. CT scan of the neck (C) is unnecessary and is unlikely to show the pathology in the esophagus.

Pulmonary emboli most commonly result from deep venous thrombi in the legs that move and pass through the right ventricle into the pulmonary vasculature. The emboli can lodge anywhere across the pulmonary circulation including the main pulmonary arteries or at the smallest subsegmental levels. Traditional chest radiography rarely provides information helpful in identifying pulmonary embolism as the definitive cause of a patient’s symptoms but may suggest alternative causes. Westermark’s sign is a rare finding on chest X-ray representing oligemia of the pulmonary vasculature visualized distal to the site of embolism.

The pulmonary embolism rule-out criteria (PERC) is a decision rule applied to patients with a low pretest probability (< 15%). If none of the criteria are present, the patient’s pretest probability is decreased to < 2% and further diagnostic testing is not recommended.

Well’s Clinical Prediction Criteria is a clinical prediction and risk stratification tool used to quantify a patients pre-test probability of pulmonary embolism (PE). The criteria should be applied only after a history and physical suggests that venous thromboembolism is a diagnostic possibility. It should not be applied to all patients with chest pain or dyspnea or to all patients with leg pain or swelling. While there have been modified versions since its first publication in 2000, the original scoring systems involves 7 risk factors. These factors include: (1) Clinical signs and symptoms of deep vein thrombosis (DVT); (2) An alternative diagnosis is less likely than PE; (3) HR > 100; (4) Immobilization at least 3 days or surgery in the previous 4 weeks, previous;  (5) Objectively diagnosed PE or DVT; (6) Hemoptysis; and (7) Malignancy with treatment within 6 months or palliative. The patient in the above clinical scenario only has a heart rate greater than 100 beats per minute which constitutes a Well’s score of 1.5. She has no further risk factors according to Well’s Criteria. This risk stratification tool has been validated in several studies since its publication and is widely used for stratifying patients who may need further evaluation for PE with a d-dimer or CT angiogram. It is important to note that Well’s criteria have not been validated for use in pregnant females or patients less than eighteen years of age. The scoring system stratifies patients into low risk (1.3% chance of PE), moderate risk (16.2% chance of PE), and high risk (40.6% risk of PE).

This patient presents with a low-risk story for pulmonary embolism but one that cannot be ruled out by history and physical alone. Clinicians can determine low, moderate and high risk based on clinical gestalt or using a scoring system like the Wells’ Criteria seen below.

In patients who are low risk either by clinical gestalt or Wells’ criteria, the PERC rule, seen below, can be applied.

Since the patient takes oral contraceptives so she does not meet the PERC rule criteria. However, since she is low risk according to the Wells’ criteria, a d-Dimer should be obtained.

The correct answer is pulmonary embolism. CXR shows a Hampton’s hump, suggestive of a large infarction due to pulmonary embolism. Further, patients with pulmonary hypertension are at extremely high risk for PE.

Needle thoracostomy and decompression of the tension pneumothorax is indicated prior to any other interventions. COPD increases the prevalence of spontaneous pneumothoraces secondary to ruptured blebs and deformed lung parenchyma. Intubation may be required for the pulseless arrest described, but the most likely cause of this COPD patient’s sudden decompensation is a spontaneous tension pneumothorax which necessitates release via needle thoracostomy

This clinical scenario demonstrates acute pulmonary embolus. With the history of Factor V Leiden disease, this patient is predisposed to thrombotic events. With the acute onset of dyspnea, the presence of DVT in her right leg, tachypnea, and tachycardia, one must suspect PE. The treatment of PE largely depends on the clinical scenario and how stable the patient is. In this case, the patient has hemodynamic instability with evidence of altered mental status. IV thrombolytics should be given immediately. Plasmophoresis is not an indicated treatment in PE.

The correct answer is admission and heparin infusion. This patient has a pulmonary embolism but no right sided heart strain.  Emergent thrombolytic therapy is not indicated, but mortality is significant enough to warrant admission and monitoring. Patients with massive acute pulmonary embolism who have failed thrombolytics or have contraindications to thrombolytics may be considered for embolectomy. However, this patient is hemodynamically stable so embolectomy is not indicated emergently at this time. Thrombolytics are controversial in that limited studies have shown improved hemodynamics but no mortality benefit. That being said, in patients with massive acute pulmonary embolism and persistent and/or worsening hemodynamic instability, many guidelines suggest considering administration of thrombolytics. This patient is stable and so the risk of thrombolytics is too great.

The sensitivity of a single scan is 95%. Thus, 5% are missed.

In moderate- to high-risk patients with an elevated D-dimer level, a single ultrasound examination may be insufficient. A repeated study in 2 to 7 days is often sufficient to confirm the diagnosis. The lack of pulmonary symptoms precludes the need for lung and embolus evaluation at this time. During pregnancy, there is a progressive rise in baseline D-dimer concentration; thus, a “normal” value is useful, but an elevated level is of no discriminatory value.

Aortic dissection is caused by a tear in the inner layer of the aorta, which allows blood to enter the wall and travel in a “false lumen”. Chest x-ray findings consistent with aortic dissection include a widened mediastinum, obscuration of aortic knob, presence of apical cap, lateral displacement of the trachea and depression of the left mainstem bronchus. ECG findings are variable and may depict an ST-Elevation myocardial infarction (MI) if a proximal dissection dissects into the coronary arteries. This is a rare entity that usually involves the right coronary artery, causing an inferior or posterior MI. This particular case is concerning for an ascending thoracic aortic dissection, whose treatment is surgical. However, while waiting for cardiothoracic surgical consult and radiographic imaging studies, acute control of the heart rate and blood pressure is imperative to minimize aortic wall stress and shearing. Initial acute treatment consists of an intravenous beta blocker to reduce the heart rate below 60 beats/min – while propranolol, labetalol, and esmolol can be used, esmolol has the advantage of a short half-life and use in patients with relative contraindications to beta-blockers (asthma, CHF). If systolic blood pressure remains >100mmHg despite beta-blockade, nitroprusside is classically recommended, although several other anti-hypertensive intravenous medications may be used.

The patient in the question stem has exertional syncope related to his severe aortic stenosis, characterized by his narrow pulse pressure, harsh systolic murmur, and findings of left bundle branch block on EKG. Syncope is a poor prognostic indicator for patients with aortic stenosis, and they require urgent surgical management. Patients with severe aortic stenosis causing syncope have a mortality rate approached 50% within 3 years if left untreated; therefore surgical consultation is neccessary prior to discharge. Although the patient is presenting with new left bundle branch block potentially representing acute coronary syndrome, he has absence of chest pain and thus would not be the best answer choice.

This patient is presenting with symptoms concerning for acute aortic dissection.  Patients with aortic dissection (specifically type A) can show ST elevations most commonly in the inferior leads due to involvement of the right coronary artery. In addition to cardiothoracic surgery consult, treatment of aortic dissection usually involves esmolol and nitroprusside; however, labetolol can be used in isolation. The most important treatment principle is to reduce the heart rate and then lower the blood pressure. Rate reduction is important in order to reduce shear stress on the aortic wall. As a beta blocker esmolol is effective in reducing the heart rate as it is easily titratable secondary to a short half-life. Nitroprusside is preferred to nitroglycerin as it is a more potent reducer of blood pressure, and it decreases afterload. Nitroprusside should not be used in isolation as it may increase the rate of rise of aortic wall pressure by increasing shearing forces. Reflex tachycardia may also result secondary to peripheral vasodilation increasing cardiac output.

Aortic dissection is commonly seen in patients with long-term hypertension and connective tissue disorders, but can also be seen in pregnancy, coarctation of the aorta and a bicuspid aortic valve. Ascending aortic dissection is most common in the 50- to 60-year age range, whereas descending dissections occur more commonly in older individuals. Anatomic classification of aortic dissection is important for diagnosis and treatment. The Stanford classification system divides dissections into two types: A and B. Type A dissections involve the ascending aorta and Type B dissections involve the descending aorta. Type A dissections are more lethal, more common and require prompt surgical intervention. Commonly, Type A dissections often present with normotensive or hypotensive vitals, while Type B are hypertensive. The hypotension in Type A is usually due to cardiac tamponade, aortic rupture, or heart failure associated with severe aortic regurgitation. Pulse deficits are present only in 19% of Type A dissection and 9% of Type B dissection. Aortic regurgitation murmurs are present in 44% of Type A dissections and 12% of Type B dissections, according to the IRAAD registry (International Registry of Acute Aortic Dissection). While Type B dissections are typically treated medically, acute Type A ascending aortic dissections should be treated as a surgical emergency, given that these patients are at high risk for a life-threatening complications (e.g. aortic regurgitation, tamponade, and myocardial infarction) and high mortality rates for delayed repairs.

All of the answer choices are sites that aortic aneurysms may rupture into, but aortic aneurysms most commonly rupture into the retroperitoneum. The most rapidly fatal location is the intraperitoneum. Less common sites of rupture include the gastrointestinal tract and the inferior vena cava.

The most common factor predicting the risk of rupture is the size of the aneurysm. Aneurysms occur when a segment of the aorta is weakened, and the larger the aneurysm, the greater tension exerted on the wall. Most ruptured aneurysms are greater than 5cm. There is a high incidence of aneurysms in patients with atherosclerotic disease and men older than 65 years of age. Other risk factors include history of smoking, hypertension, and family history of abdominal aortic aneurysm.

Nicardipine and nitroprusside are effective parenteral drugs for acutely lowering blood pressure. They both reliably and quickly decrease blood pressure. The main disadvantage for nitroprusside is the cyanide byproduct, while for nicardipine is its longer half-life (more difficult to rapidly titrate).

This patient presents with asymptomatic hypertension in the setting of medical non-compliance and should berestarted on his medications and scheduled for follow up with a primary care physician. Accelerated hypertension is defined as markedly elevated blood pressure in the absence of symptoms. This is in contrast with hypertensive emergency where the patient has symptoms or evidence of end organ system dysfunction or both as a result of elevated blood pressure. Accelerated hypertension has a poor long-term prognosis if not controlled but does not pose an immediate threat. As such, it should not be aggressively treated with parenteral medications. Rapid lowering of blood pressure in patients with chronic elevated blood pressure can cause organ hypoperfusion, particularly brain hypoperfusion, and lead to serious sequelae. These patients should be restarted on their medications (if appropriate) and sent for follow up with a primary care physician to monitor and treat the elevated blood pressure.

The most common forms of end-organ damage in hypertensive emergencies, in order of decreasing frequency, are (1) cerebral infarction or hemorrhage; (2) acute pulmonary edema; (3) hypertensive encephalopathy; (3) acute CHF; and (4) aortic dissection. Preeclampsia is another hypertensive state associated with very high BP, but unique goals and treatment options are associated with this condition.

Hypertensive encephalopathy describes reversible cerebral disorders associated with high BP in the absence of cerebral thrombosis or hemorrhage. The theoretical mechanism of hypertensive encephalopathy is a rapid rise in BP that overwhelms the autoregulatory mechanisms of the brain and leads to blood-brain barrier permeability and brain edema. The symptoms of hypertensive encephalopathy can include headache, seizures, visual disturbances, nausea, and vomiting. The diagnosis must be made only after other potential hypertensive emergencies are excluded. A PubMed search for clinical trials, meta-analyses, and randomized controlled trials of hypertensive encephalopathy yielded 22 articles. None of the trials dealt directly with treatment or prognosis, and no studies suggested which agent is best for short-term reduction of BP in hypertensive encephalopathy. However, nitroprusside should be avoided in patients with this disorder, as the drug has been shown to decrease systemic pressure while preserving intracranial perfusion pressures. In the absence of data, the consensus goal of treatment is often stated as a 20% to 25% reduction in mean arterial pressure or a DBP of 100 to 110 mg Hg.

Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic primary cardiomyopathy that is the second most common cause of sudden cardiac death in adolescents. It is the leading cause of sudden cardiac death in athletes. It involves asymmetric interventricular septal hypertrophy that causes reduced filling of the left ventricle and diastolic dysfunction. The most frequent initial complaint is dyspnea on exertion, but other symptoms include chest pain, palpitations, and syncope. Syncope usually occurs during or immediately after exercise. Exam findings include an S4 heart sound and a systolic ejection murmur that is intensified with standing up and performing a Valsalva maneuver. Maneuvers that decreased the murmur include hand grip, passive leg raise, and squatting. Diagnosis is ultimately made with echocardiography or cardiac MRI, along with genetic testing. Hospitalization is indicated for patients presenting for syncope who are suspected to have HOCM, as these patients are at significant risk for sudden cardiac death. Beta-blockers are the treatment of choice in patients with HOCM who have chest pain.

The optimal rate for chest compressions is at least 100 compressions/minute. In order to have return of spontaneous circulation (ROSC), patients must have high-quality CPR started early and early defibrillation when indicated. High-quality CPR historically was underappreciated but recent research has brought it to the forefront of care. In addition to an appropriate compression rate of 100 per minute, compression depth of > 5 cm and minimum pauses for CPR must be maintained. Additionally, hyperventilation and resultant hypocarbia is detrimental. A ratio of 30 compressions to 2 ventilations is currently recommended. Compressions should not be held during attempted intubation. Epinephrine should be administered every 3-5 minutes. Rhythm checks should not be performed after shock delivery.

A number of viruses cause myocarditis including adenoviruses, parvovirus 19 and human herpesvirus 6. Cytomegalovirus (CMV) is a common cause in patients with cardiac transplant. Myocarditis occurs via three pathophysiological processes: necrosis from direct invasion of an infectious agent, destruction of myocytes from infiltration of components from the host immune response, and toxic effects of exogenous or endogenous chemicals produced by a pathogen. The pathophysiological process depends on the etiologic agent. In patients with cardiac transplants, CMV and toxoplasmosis gondii are common agents. Patients with myocarditis present with nonspecific symptoms including fever, fatigue, malaise and diarrhea. Dyspnea is the most common presenting complaint in children and is frequently seen in adults as well. Tachycardia out of proportion to temperature elevation should raise concerns for myocarditis. Diagnostically, ECG can have a number of changes including sinus tachycardia, wide QRS complex, prolonged QT interval or ST elevations. Definitive diagnosis is made by endocardial biopsy (MRI is slowly replacing biopsy as the disease can be patchy and biopsy can fail to make the diagnosis).

When fluid accumulates in the pericardial space rapidly (e.g., within minutes), hemodynamic compromise usually occurs. Patients experience hypotension, tachycardia, and shortness of breath. This is pericardial tamponade. Normally the pericardial elasticity can accommodate slow accumulations of fluid from conditions such as pericarditis, radiation therapy, uremia, or malignancy. When the elasticity of the pericardium is overwhelmed due to rapid fluid accumulation within the pericardial space, the right atrium and ventricles begin to be compressed. This leads to decreased end diastolic volumes in the right heart and ultimately hypotension. The decreased preload creates proximal venous engorgement and is demonstrated clinically as jugular venous distension. Patients may also have distended facial or scalp veins. Other clinical findings of pericardial tamponade include muffled heart sounds, a narrow pulse pressure, pulsus paradoxus (decreased systolic blood pressure with inspiration due to increased intrathoracic pressure causing decreased venous return), and respiratory distress. Electrocardiographic findings may include low voltage or electrical alternans (alternating high and low QRS voltage due to the heart swinging in the pericardium full of fluid). Bedside ultrasound is diagnostic and demonstrates anechoic (black) fluid between the hyperechoic pericardium and the myocardium. Right atrial or right ventricular collapse during diastole, leftward septal shifting during inspiration, and a swinging heart may be seen on ultrasound. Pericardiocentesis is the management of choice for pericardial tamponade.

The treatment of pulseless electrical activity (PEA) begins with initiation of advanced cardiac life support (ACLS). Common causes of PEA can be remembered by the Hs and Ts. This patient recently underwent an operative procedure and is at increased risk for developing a pulmonary embolism (PE). Therefore, lytic therapy with tissue plasminogen activator (t-PA) should be administered.

This patient presents with findings concerning for septic emboli secondary to endocarditis. Although rare, intravenous drug users are at the highest risk for endocarditis secondary to Pseudomonas species. They are also more likely to have right-sided endocarditis with tricuspid valve involvement. Patients should be treated with tobramycin and an extended spectrum beta-lactam antibiotic such as piperacillin-tazobactam, cefepime, or ceftazidime. Medical therapy with antibiotics can be attempted, but valve replacement is often needed for complete eradication of the underlying infection.
Ceftriaxone and vancomycin (B) do not cover Pseudomonas aeruginosa and therefore would be ineffective. The combination of gentamicin and nafcillin (C) or gentamicin and vancomycin (D) is not recommended. Although gentamicin does cover Pseudomonas species, a regimen with double coverage is more likely to be effective. Nafcillin has great coverage against non-methicillin resistant Staphylococcus aureus, and vancomycin is the treatment of choice for methicillin-resistant Staphylococcus aureus.

Myocarditis can be due to an infectious or non-infectious process, with most infectious etiologies caused by a viral infection, most commonly parvovirus B19, adenovirus, coxsackie B virus, and Echovirus. Trypanasoma cruzi (Chagas disease) is the most common etiology worldwide. Myocardial necrosis occurs likely as a result of direct invasion of the offending organism as well cytotoxic effects of the host’s immune system. Individuals develop flulike symptoms and in adults chest pain and shortness of breath. One of the hallmark signs of myocarditis is tachycardia out of proportion to fever. Depending on the time of presentation, patients may have symptoms of heart failure as the left ventricular ejection fraction is impaired as a result of the myocarditis. Troponin is often elevated as the disease progresses. The gold standard for diagnosis is endomyocardial biopsy. Management is supportive. ACE inhibitors help reduce myocardial inflammation.

Although most patients with infective endocarditis will exhibit a mumur at some point in their disease course, murmurs are often not present on initial presentation. Infective endocarditis often affects patients with underlying valvular abnormalities including rheumatic heart disease, calcific degenerative disease and patients with congenital heart defects. The incidence of infective endocarditis among intravenous drug users is particularly high. Symptoms of endocarditis are nonspecific. Most patients will report intermittent fevers (85%) and malaise (80%). Early in the disease, patients often will not have murmurs but one will almost always develop during the course of illness. Among intravenous drug users, less than 35% will present with a murmur. In patients with a moderate or high suspicion of endocarditis, an echocardiogram should be performed to establish the diagnosis.
Noninvasive cardiac monitors have been used in the ED to measure cardiac output, though they have yet to be proven to change measured clinical outcomes. A recent meta-analysis of 8 studies found that passive leg raise predicted fluid responsiveness as measured by an increase in descending aortic blood flow. The assessment was performed by transesophageal Doppler imaging in critically ill patients with a global area under the receiver operating characteristic curve of 0.95, indicating excellent sensitivity and specicity of these maneuvers in realtime clinical practice in the ED.

Ultrasonographic monitoring (transthoracic or esophageal), and arterial and venous pulse oximetry/plethysmography variation. While potentially promising as noninvasive means of monitoring cardiac output and providing information regarding the nature of a patient’s shock, further studies with clinical outcome data are needed to guide the use of these monitoring devices in the diagnosis and management of patients with shock.

Naloxone can safely be given to a pediatric patient in cardiac arrest via the endotracheal tube (ETT) if intravenous or interosseous access is not available. Endotracheal drug administration is infrequently used but has the potential to be therapeutic in patients without access. A number of medications can be given via ETT including atropine, naloxone, lidocaine and epinephrine.

This patient presents with symptoms of acute decompensated heart failure and should be started on nitroglycerintherapy immediately. Patients present with shortness of breath, increased work of breathing, tachycardia, hypoxia, crackles on lung examination and jugular venous distension. These patients experience acute worsening of left ventricular function and output secondary to a number of mechanisms including increased systemic vascular resistance. Therapy focuses on reduction of preload to decrease the flow of blood into the lungs and afterload reduction to increased the effectiveness of the left ventricle. Both of these goals can be accomplished through the administration of nitroglycerin. At lower doses, nitroglycerin acts as a peripheral vasodilator and increases venous capacitance leading to decreased preload. At higher doses, nitroglycerin causes arterial vasodilation leading to decreased afterload. Because of its rapid onset of action, nitroglycerin is the first line medication in patients with ADHF.

Furosemide (A) may be useful in patients with volume overload and ADHF but this represents less than half of patients with ADHF. Additionally, the effects are delayed. Heparin (B) can be given in cases of ischemia induced ADHF but will not yield any immediate benefits. Morphine (C) was historically used as a preload reducer but has been associated with increased morbidity in patients with ADHF and is no longer recommended.

Endpoints of death, nonfatal reinfarction, and stroke have been used in comparisons of thrombolytics and PCI. Each of these measured parameters is less in the PCI comparison group. Cumulatively endpoints were present for 8% of PCI patients versus 14% for the thrombolytic group. These groups were broken down into less short-term mortality at 30 days (4.4% vs. 6.5%), less nonfatal reinfarction (3% vs. 7%), and less hemorrhagic stroke (0.1% vs. 1.1%). PCI is especially indicated in patients that have cardiogenic shock, severe congestive heart failure and/or pulmonary edema, and hemodynamically compromising ventricular arrhythmias. These patients should proceed to primary PCI as the reperfusion strategy of choice. The addition of both thrombolytic therapy and PCI as a primary reperfusion strategy has been investigated as a therapy for STEMI. Full-dose fibrinolytic therapy followed by immediate PCI may be harmful and should not be utilized. Facilitated PCI, the term for this strategy, has been shown to have higher mortality rates as well as bleeding rates. These patients also had higher rates of recurrent infarction and needs for subsequent PCI. Rescue PCI has resulted in higher rates of early infarct arterial patency, improved regional infarct-zone wall motion, and greater freedom from adverse in-hospital events than with a deferred PCI strategy or medical therapy.

Preload and afterload reduction is your first priority in this patient. The patient’s sudden decompensation, profound hypertension, and relative lack of peripheral edema suggest this patient has acute decompensated heart failure from the “vascular pathway”. In these patients, rapid preload and afterload reduction will dramatically decrease the symptoms of acute decompensated heart failure by decreasing venous return and lowering the systolic blood pressure. The lower systolic blood pressure allows the left ventricle to empty its contents more easily. Diuresis should be delayed until afterload is reduced or not done at all. Diuresis is reserved for patients with gradual fluid accumulation and significant peripheral edema. Agents to increase inotropy are used for hypotensive patients and patients resistant to first-line therapies. Morphine is no longer a first-line agent for acute decompensated heart failure and is associated with increased rates of intubation.

Noninvasive ventilation is a useful and powerful tool in treating acute decompensated heart failure. It has been shown to simultaneously decrease preload and afterload and therefore ameliorate the symptoms of heart failure. It also improves lung mechanics by recruiting atelectatic alveoli, increasing intrathoracic pressure, improving pulmonary compliance, and reducing the work of breathing. Noninvasive ventilation has also been shown to decrease endotracheal intubation rates, decrease the need for ICU admissions, and decrease mortality.

Furosemide exerts its positive effects in treating acute decompensated heart failure by decreasing total body water and therefore preload. Furosemide does activate the renin–angiotensin system; however this is a deleterious effect as this often leads to increased blood pressure. There is no convincing evidence that furosemide has significant venous vasodilatory effects or causes afterload reduction.

See AHA recommendations (http://www.heart.org/HEARTORG/Professional/MissionLifelineHomePage/EMS/Recommendations-for-Criteria-for-STEMI-Systems-of-Care_UCM_312070_Article.jsp).

Transfer if door-to-balloon is <90 (total, including transfer). Typically need rapid transfer protocol set up.

These are deWinters complexes, indicative of LAD occlusion and generally regarded as a cath lab activating EKG. Classically depressions in V2-4 with acute t waves. Don’t need ST elevation here.

Sgarbossa criteria here met in V2 and V5, V6. Use Sgarbossa because of LBBB.

Takotsubo cardiomyopathy is also known as left apical ballooning or broken heart syndrome. Most commonly, patients are postmenopausal women who have just experienced significant emotional distress although there are numerous case reports from myriad other causes. It is unclear exactly why this occurs, but a sudden weakness in the myocardium develops after emotional distress possibly related to stress hormones, vascular spasm, focal myocarditis or other cellular changes. Patients develop symptoms consistent with acute coronary ischemia which most commonly include chest pain and dyspnea on exertion. The ECG is abnormal with ST segment elevations or deep T wave inversions usually on the anterior wall. Cardiac biomarkers are often positive. On cardiac catheterization, the coronary arteries do not have obstructive disease. If ventriculography or echocardiography is performed, the apex of the left ventricle is seen ballooning with an impaired ejection fraction. Prognosis is typically very good with recovery to normal wall motion and ejection fraction within a month.

Beta-blockers (A) do not change mortality in this condition. Almost all patients with takotsubo regain completely normal ejection fraction with no long term effects of the episode. Although beta-blockers and angiotensin converting enzyme inhibitors are considered mainstay therapy they do not impact mortality in these patients. Cardiac catheterization (B) is mandatory in this patient who has symptoms consistent with myocardial ischemia and an ECG suggestive of an anterior wall myocardial infarction. As noted above, the catheterization is unlikely to reveal an acute thrombus, but the emergency physician and cardiologist must exclude an acute myocardial infarction as the etiology of the signs and symptoms. Nitroglycerin (D) is not contraindicated in this patient. Nitroglycerin is unlikely to have any effect given the absence of coronary obstruction. In patients with hypertrophic cardiomyopathy and preload dependence for ventricular filling, agents that decrease preload like nitroglycerin should be avoided.

This patient has an ECG concerning for a right ventricular infarct. In this situation, the patient becomes preload dependent (essentially the right ventricle is impaired to there is “passive” flow into the left ventricle). When these patients become hypotensive, the immediate treatment is intravenous hydration to increase preload. Right ventricular infarction is represented on an ECG by noting ST elevation in right-sided leads (V3R and V4R). Because the right coronary artery often supplies the right side of the heart and the inferior wall of the heart, any ECG with ST elevations in leads II, III, and aVF (inferior leads) should have another ECG performed with right-sided lead placement. Aggressive volume loading with normal saline boluses is used to restore blood flow to the right ventricle and inotropic support is indicated if hypotension persists. Early percutaneous coronary intervention or thrombolytic therapy should be initiated as soon as possible. In general, patients’ with right ventricular myocardial infarction are treated in a manner similar to those with acute ST-elevation myocardial infarction. This includes the early use of dual antiplatelet therapy, statin therapy, and an anticoagulant.

Medications that lower preload such as nitroglycerin (C) and morphine (B) or drugs that slow heart rate such as beta blockers (A) should be avoided or used with extreme caution.

Brief (usually less than 10 seconds) tonic–clonic seizure activity can accompany syncope of any etiology. This activity is not accompanied by postictal disorientation, and it does not represent true seizure activity. For cerebrovascular disease to cause a loss of consciousness, either both cerebral hemispheres or the brainstem must be deprived of blood flow. Therefore transient ischemic attacks and stroke are rarely the cause of syncope. Screening laboratory studies have been shown to add little to establishing a cause of syncope. In most cases, hypoglycemia is clinically suspected and abnormal electrolytes rarely account for a loss of consciousness. Anemia from bleeding is usually clinically evident. Tilt-table testing reveals abnormalities in 20% to 70% of patients whose emergency department evaluation leaves them without a diagnosis.

Although the definition of abnormal ECG varies among the many studies examining their role in the diagnosis of syncope, particular attention should be paid to any nonsinus rhythm, signs of ischemia, or conduction abnormalities.

Syncope is defined as an interruption in cerebral perfusion causing a transient loss of consciousness. Syncopal events should last less than 5 minutes and patients should return immediately to their baseline mental status as cerebral perfusion is restored. Lateral tongue biting is more commonly associated with seizure, and the most specific sign for a seizure, while anterior tongue biting can be seen with syncope. Urinary incontinence is frequently seen in seizure patients, but would be unusual following syncope.

A is incorrect, because the R-R interval classically shortens as the PR interval lengthens. B describes a first-degree AV block, not a second-degree AV block. C is correct. D is incorrect, because Mobitz type II blocks more commonly feature a prolonged QRS complex than Mobitz type I AV blocks.

The sinoatrial (SA) node is innervated by both the sympathetic and parasympathetic nerves, which alter its discharge rate. The SA node is the normal pacemaker of the heart with an inherent rate of 60 to 100 beats per minute. The arterial supply for the SA node is either the right coronary artery (55%) or the circumflex artery (45%). The atrioventricular (AV) node is usually supplied by the right coronary artery 90% of the time with the remaining 10% originating from the circumflex. The inherent rate of the AV node is 30 to 40 beats per minute, which is primarily used as an escape rhythm if the primary pacemaker of the heart, the SA node, fails.

Lidocaine, which may abolish the ventricular rhythm completely, is contraindicated because it may cause cardiac standstill. Atropine, due to its vagolytic properties, enhances sinus node automaticity and AV nodal conduction. Isoproterenol, a beta-adrenergic agonist, has both inotropic and chronotropic effects. Isoproterenol increases myocardial oxygen demand and should be used with caution in ischemic myocardium. Glucagon has been shown to be useful in the treatment of bradyarrhythmias secondary to beta-adrenergic blocking agents and calcium antagonists. Glucagon stimulates the SA node directly giving some mild increase in heart rate. Glucagon also increases cardiac contractility.

In wide-complex atrial fibrillation, any drug that slows conduction through the AV node can cause ventricular fibrillation from rapidly conducted impulses via the accessory pathway. Adenosine, calcium channel blockers, and beta blockers are all contraindicated in this setting. Though procainamide is considered first-line pharmacotherapy in the stable patient with wide-complex atrial fibrillation, electrical cardioversion is more effective. Amiodarone is also less effective and carries the risk of slowing AV conduction.

As per the 2010 AHA guidelines, CPR should only take place until the defibrillator is ready, and defibrillation at 200 J should be performed as soon as possible in VF arrest. Escalating doses of 50–100–150 J are no longer recommended and 200 J should be used for biphasic defibrillators. Though epinephrine is recommended as part of ACLS, it should not take precedence over defibrillation and has not shown long-term benefit in the treatment of cardiac arrest.

This patient represents stable atrial fibrillation (AF) with a rapid ventricular rate. For patients presenting with AF and a rapid ventricular response, treatment is directed at slowing the ventricular rate. Calcium channel blockers, in particular diltiazem, slow ventricular response within the first few minutes of IV administration. Beta blockers such as atenolol or metoprolol are about as effective as calcium channel blockers for rate control, but are seldom used because of a higher incidence of hypotension. Neither calcium channel blockers nor beta blockers are particularly effective at producing cardioversion to sinus rhythm. Digoxin is no better than placebo in the first few hours of rate control for rapid atrial fibrillation. Stable patients do not need cardioversion in the ED. This patient has an unknown time period since the atrial fibrillation has manifested. Anticoagulation is an important management issue for patients with AF. Not only are patients with AF that lasts more than several days at risk for systemic embolization, but recent evidence suggests that even shorter periods of AF may carry a risk of embolization, particularly following conversion to sinus rhythm. Patients should be considered for anticoagulation prior to cardioversion for all presentations of atrial fibrillation that is stable. Amiodarone slows ventricular rate and increases the frequency of conversion to sinus rhythm after greater than 24 hours. There is no difference between placebo and amiodarone in the first 8 hours. Amiodarone thus has little utility in the new-onset stable patient with AF and a rapid rate.

Placement of a magnet over a pacemaker will cause synchronous pacing at model-specific rates.

This patient is presenting with ovarian torsion. This patient’s cyst is greater than 5cm, putting her at risk for ovarian torsion. Her history of episodes of sudden onset pain is concerning for stuttering, intermittent torsion leading up to this event. Although ultrasound demonstrates intact arterial blood flow, the most frequent ultrasonographic abnormality in ovarian torsion is either decreased or absence of venous flow in the presence of intact arterial flow. Laparoscopy is the gold standard for diagnosis and management.

Trichomonas vaginalis, a protozoa, is the causative agent of trichomoniasis. It is the most common non-viral sexually transmitted infection worldwide. Patients typically complain of yellow-green, frothy and malodorous vaginal discharge, with protozoa seen on wet mount. “Strawberry cervix”, or punctate hemorrhage around cervix, is seen on exam. Vaginal pH becomes more alkalotic, and is generally greater than 4.5. Treatment of trichomonas vaginitis is metronidazole. Clue cell is seen in bacterial vaginosis. Recent antibiotics use is a common risk factor for candidal vaginitis.

The most common causes of postmenopausal vaginal bleeding is vaginal/endometrial atrophy 60%) and endometrial polyps (12%). However, endometrial cancer comprises about 10% of incidence. Given the stability of the patient, no further emergent imaging is indicated at this time, and urgent outpatient gynecology referral for further workup, including, but not limited to, endometrial biopsy, cervical cytology, and/or transvaginal ultraosund.

First line treatment of symptomatic atrophic vaginitis is vaginal moisturizing agents and lubricants. If that fails, and there is no contraindication for hormonal therapy (such as estrogen-based tumors like breast cancer), then low dose vaginal estrogen is the next step. In this question, the patient is stable and first-line therapy is nonhormonal moisturizing/lubricating agents and outpatient gynecology referral for endometrial biopsy, cervical cytology, and/or ultrasound to exclude endometrial cancer first.  The biopsy should be obtained BEFORE starting any treatment. While the workup for vaginal bleeding may include serum testing, there is no indication with this clinically stable and otherwise normal patient to emergently order blood tests. These tests, along with other imaging or biopsy/cytology testing, may be performed on an outpatient basis.

An ultrasound exam is usually the initial diagnostic study in the workup for ovarian torsion. The most common ultrasound finding in ovarian torsion is enlargement of the ovary. Enlargement develops due to impaired venous and lymphatic drainage, in addition to edema and hemorrhage that may occur. Less common findings include identification of a twisted pedicle (whirlpool sign), free pelvic fluid, and identification of an ovarian mass. RISK FACTORS: ovarian mass >5mm, reproductive age, pregnancy, ovulation induction, prior torsion. CLINICAL: adnexal pain/mass, vomiting, fever, vaginal bleeding
Free pelvic and intraperitoneal fluid (B) may surround the twisted ovary. This is usually the result of interstitial fluid that weeps off an affected ovary rather than true rupture of the capsule. Many cases of surgically proven ovarian torsion will have documented blood flow (C) on Doppler exam because the ovary has a dual blood supply from both the ovarian and uterine arteries. In addition, torsion is often intermittent, so findings may vary, depending on the time of the exam. Identification of an ovarian mass or cyst (>4 cm) (D) may suggest the diagnosis of ovarian torsion, but it is not the most common finding on ultrasound.

This patient presents with a Bartholin’s abscess and should have incision and drainage (I+D) performed with the incision on the mucosal surface. Bartholin’s abscesses are infections located in the Bartholin’s glands which lie inferiorly to the vaginal opening. Patients develop cysts of the gland that become secondarily infected. These abscesses typically are caused by normally occurring aerobic and anaerobic bacteria in the vagina but may also be caused by sexually transmitted infections. Patients present with swelling and pain near the labium. Examination revels a tender, fluctuant mass along the posterolateral margin of the vaginal vestibule. Treatment focuses on incision and drainage with insertion of a Word catheter. The Word catheter has a small balloon at the end that is inflated after insertion and remains in place for 6 to 8 weeks. Because of this duration, the incision should be made on the mucosal surface so that the Word catheter can be tucked into the vaginal opening for patient comfort. Incision and drainage is usually adequate but patients with overlying cellulitis may require antibiotics. After discharge, patients should perform sitz baths to aid with drainage. Recurrence is common.

This patient has a clinical presentation consistent with pelvic inflammatory disease (PID). PID is an ascending infection that begins in the vagina or cervix. In the sexually active female, the most common responsible organisms are Chlamydia trachomatis and Neisseria gonorrhoeae. Frequently, the infection is polymicrobial. The most common presenting symptom is lower abdominal pain. Patients may also develop fever, vaginal discharge, dyspareunia or abnormal bleeding. On physical examination, the patient typically has a fever and is tender on pelvic examination either in the lower abdomen over the uterus, on cervical motion or in the adnexa. The absence of cervical motion tenderness does not rule out PID and the CDC recommends empiric treatment for sexually active women presenting with lower abdominal pain and one of the following if no other cause is identified: cervical motion tenderness, adnexal tenderness or uterine tenderness. For outpatient management, patients are treated with ceftriaxone 250 mg IM followed by a two-week course of doxycycline. Metronidazole is sometimes added to the regimen at the judgment of the clinician.

The correct answer is IV estrogens. High-dose estrogen is thought to promote rapid regrowth of endometrium and stabilize uterine bleeding within the first five hours of administration. In hemodynamically unstable patients, IV estrogen is recommended, while oral estrogen is appropriate for hemodynamically stable patients. Oxytocin and methylergonovine can be used in post-partum bleeding.

Carbaprost tromethamine is a prostaglandin analog used in postpartum bleeding that stimulates uterine contractility, promoting hemostasis at the placental site. Methylergonovine is used in post-partum uterine bleeding, by increasing uterine smooth muscle contractions to reduce blood loss. Recombinant factor VIIa has been FDA-approved for use in bleeding in patients with hemophilia A/B, factor VII deficiency, or acquired hemophilia. Off-label, recombinant factor VIIa has been used as a general hemostatic agent – in this patient, IV estrogen should be first utilized before moving onto more controversial, last-ditch efforts.

This patient likely has ovarian cancer and the biomarker likely to support this diagnosis is CA-125. AFP is elevated in certain germ cell tumors as well as in Hepatocellular CA. CEA is elevated in colorectal CA. CA 19-9 is elevated in pancreatic and some types of colorectal CA.

Fitz-Hugh-Curtis syndrome is a condition that occurs in the setting of pelvic inflammatory disease (PID) and results in inflammation of the capsule surrounding the liver and the peritoneal surface of the anterior abdominal wall. It occurs in about 10% of patients with PID. Although it can be caused by any organisms responsible for pelvic inflammatory disease, Chlamydia trachomatis is most often implicated. Patients present with right upper quadrant pleuritic pain and tenderness. They may also have symptoms of PID, such as pelvic pain and vaginal discharge although these symptoms may be mild or lacking. Treatment regimens are similar to those for PID.
nfection with Gardnerella vaginalis (B) results in symptoms of vaginitis, but does not play a role in the development of Fitz-Hugh-Curtis syndrome. Hepatitis C virus (C) causes hepatitis, but is also not involved in the development of Fitz-Hugh-Curtis syndrome. Neisseria gonorrhoeae (D) can cause Fitz-Hugh-Curtis syndrome although it is more likely to be due to a C. trachomatis.

Vaginal foreign bodies can manifest as vaginal discharge. The discharge associated with a foreign body is often malodorous and bloody or dark brown in color and occurs daily. Potential foreign bodies include small pieces of toilet paper and small objects or toys. In this case, the child recently started attending school and is likely toileting by herself. As a result, she may be at risk of poor hygiene and potentially may have a small piece of toilet paper stuck within the vagina. Attempted manual removal can be performed on cooperative children over 7 years of age through irrigation with normal saline. Vaginoscopy under anesthesia in the operating room may be necessary in younger children.