DRH-EM Education

The anterior nasal septum is the common location of bleeding in epistaxis. Within the anterior septum is Kiesselbach’s plexus, a watershed area and the most common source of anterior bleeding. Most anterior nosebleeds resolve easily with treatment. The initial step in the evaluation of a nosebleed is to have the patient blow the nose and expel any clots. Inspection of the nose is facilitated using a nasal speculum and adequate light source. If ongoing bleeding is present, the vasoconstricting oxymetazoline spray (Afrin) is helpful in stopping active bleeding. Most episodes of venous anterior bleeding will resolve with the potent vasoconstrictor. If bleeding continues, packing may be used to tamponade the site of bleeding. There are many commercially available devices. Silver nitrate cautery is not useful when applied to a site of active bleeding, it is usually used after bleeding has stopped to prevent recurrence. Foley insertion is used in cases of posterior bleeds. Finally, direct pressure for 15-30 min is a first line maneuver, but it is NOT useful when applied to the BRIDGE of the nose… this is a common error amongst patients who try and prevent bleeding at home.

Acute sinusitis is defined as inflammation of the nasal cavity and paranasal sinuses lasting <4 weeks. The most common etiology of sinusitis is a viral infection with acute bacterial sinusitis responsible for only 0.5 to 2 percent of episodes. The most predictive signs of acute sinusitis are purulent rhinorrhea, nasal congestion and facial pain. Viral sinusitis and bacterial sinusitis are indistinguishable clinically and expert consensus recommends considering a bacterial cause once symptoms last more than 7 to 10 days. Treatment of sinusitis is aimed at symptomatic control. Once symptoms persist for more than 7 to 10 days, a bacterial etiology is possible and antibiotics should be considered. The use of topical glucocorticoids may confer some benefit although data are mixed in trials. Oral decongestant therapy also does not have significant evidence in support of their generalized use. In cases where eustachian tube dysfunction contributes to the development of sinusitis, oral decongestants appear to have benefits. The use of non-steroidal anti-inflammatory medication like ibuprofen does provide pain relief and should be prescribed to the patient.

One potential complication following a tracheostomy is fistula formation between the trachea and the first aortic arch branch, the innominate (or brachiocephalic) artery. A tracheoinnominate artery fistula is a feared complication following tracheostomy because it can lead to rapid exsanguination if not managed properly in a timely fashion. Fistula formation results from either direct vessel erosion from the tip of the tracheostomy cannula or from an overinflated cuff. It usually develops within the first four weeks after tracheostomy, with most patients presenting within the first two weeks. Patients may present with a transient sentinel bleed or with massive hemoptysis. The initial action of the provider should be to hyperinflate the tracheostomy balloon in an effort to tamponade the bleeding vessel. If this is unsuccessful, the provider should orotracheally intubate the patient. It is important to pass the endotracheal tube past the site of bleeding and inflate the cuff distal to this site. At the same time, the tracheostomy should be removed and a gloved finger should be inserted into the stoma, flexed down toward the innominate artery, and traction pulled against the sternum to digitally tamponade bleeding. This digital technique is called the Utley maneuver and is used to control stomal hemorrhage. These are temporizing measures, and otolaryngology or thoracic surgery should be consulted immediately as tracheobronchoscopy and operative repair are indicated.

The most common cause of otitis externa is infection due to Pseudomonas aeruginosa and Staphylococcus aureus. The pain from otitis externa is caused by inflammation and edema of the ear canal skin, which is normally adherent to the bone and cartilage of the auditory canal. The inflammatory reaction can be caused by bacteria, fungi, or contact dermatitis. Cerumen protects the canal by forming an acidic coat that helps prevent infection. Factors that predispose to otitis externa include absence of cerumen, often from excessive cleaning by the patient, water that macerates the skin of the auditory canal and raises the pH, and trauma to the skin of the auditory canal from foreign bodies or use of cotton swabs. Treatment includes suction and gentle warm irrigation of the canal. 2% acetic acid solution or an alternative drying medication can be administered. A topical antibiotic drop with steroid is first-line therapy (neomycin/polymyxin/hydrocortisone). Use the suspension rather than the solution if the tympanic membrane is ruptured.

The patient is complaining of symptoms consistent with iatrogenic tympanic membrane perforation that occurred during disimpaction. Tympanic membrane perforations (TMPs) can result from a complication of infection (acute otitis media, myringitis); blast injury (explosion, slap, lightening); barometric pressure changes (flying in airplane, scuba diving); and improper attempts at wax removal or ear cleaning. The pars tensa is the most common area of the TM to perforate because it is the most anterior and thinnest portion. Patients typically experience decreased or complete hearing loss, pain, and bleeding. In the setting of tympanic membrane perforation, the goal is to keep the ear dry, provide analgesics, and arrange for follow-up with an ENT. Most heal within a few months.

The patient does not require admission (A) to the hospital. ENT care can be arranged for as an outpatient. Traumatic tympanic membrane perforations do not require otic antibiotics (B) unless the ear was contaminated such as from diving in seawater or the rupture is secondary to infection. The patient should receive more than a cotton ball (D) in her ear. Her management should include analgesia and ENT follow-up because complications of tympanic membrane rupture include facial nerve palsy, vertigo, and hearing loss.

This patient has Ménière’s disease. This disorder is associated with increased endolymph within the cochlea and labyrinth. The common triad is tinnitus, vertigo, and unilateral hearing loss (sensorineural). A key finding in Ménière’s disease is fluctuating hearing loss. Episodes are abrupt in onset and associated with nausea and vomiting. There are often long, symptom-free intervals between attacks.

Benign paroxysmal positional vertigo (A) is sudden in onset, short-lived, and positional in nature. It is not associated with tinnitus or hearing loss. Salicylate (aspirin) toxicity (C) is associated with tinnitus and reversible hearing loss. The patient has a history of osteoarthritis and may be using aspirin for her pain; however, salicylate toxicity is usually associated with bilateral hearing loss. Symptoms of vertigo are also uncommon in such patients. Vestibular neuronitis (D) manifests with severe vertigo positional in nature but not associated with hearing loss. It is usually preceded by a viral upper respiratory infection.

This patient is exhibiting signs and symptoms of posterior epistaxis. Posterior epistaxis is less common than anterior epistaxis and is most commonly due to bleeding from the sphenopalatine artery, located at the posterior aspect of the middle nasal turbinate. Patients with posterior epistaxis typically complain of bleeding from both nostrils. Inspection of the posterior pharynx may reveal profuse bleeding. In treating epistaxis, start by having the patient gently blow his nose or suction out the blood. If the bleeding is profuse, apply cotton balls soaked in a topical anesthetic and vasoconstrictor for at least five minutes. A good option is 1% tetracaine plus 0.05% oxymetazoline solution. In posterior epistaxis, this may not achieve hemostasis or allow visualization of the location of bleeding. Management of posterior epistaxis should be with either a Foley catheter or dual balloon pack. A 10 to 14 French Foley catheter with a 30 cc inflatable balloon may be inserted past the site of the bleeding and inflated with 5 to 7 cc of air or saline. It should then be pulled back onto the site of the posterior bleed and inflated until it is snug. An anterior nasal pack should then be placed in both nares. A dual balloon pack is placed by anesthetizing the nare and advancing the pack past the site of the bleeding. The posterior balloon is inflated with 5 to 7 cc of saline or air and pulled back onto the site of bleeding. It is the further inflated until it is snug. The anterior balloon is then inflated. The opposite nare should be packed as well. Complications of posterior epistaxis packing include aspiration, hypoxia, hypercarbia, and symptomatic bradycardia. Antibiotics should be administered after all packing; however, there is significant controversy regarding whether prescribing antibiotics actually prevents toxic shock syndrome as there is no evidence to support this. All patients with posterior packing should be admitted to a telemetry bed for further monitoring while the packing is in place.

The facial artery (A) may be injured during oncologic surgery of the parotid gland or in severe facial trauma. Kiesselbach plexus (B) is the most common source of anterior bleeding. Given that this patient has profuse bleeding that appears bilateral, the source is most likely to be posterior. The labial artery (C) is most commonly injured in children who suffer electrical burns of the commissure of the lip while chewing on electrical cords.

In this case, the patient has symptoms concerning for mastoiditis. Mastoiditis is most common in children between 1 and 3 years old. It is a complication of acute otitis media with extension of the infection into the mastoid bone. Patients typically present with ear proptosis, fever, an injected tympanic membrane on the infected side, and postauricular erythema. Organisms involved in this infection are similar to those in otitis media, including Streptococcus pyogenes, Staphylococcus aureus, and Pseudomonas aeruginosa. Diagnosis is confirmed by CT, and consultation with ENT is indicated. If the patient has not taken antibiotics before, the initial treatment is with oral antibiotics if the disease is mild and close follow-up can be ensured. If a patient develops mastoiditis after an appropriate course of oral antibiotics, then admission, ENT consultation, and intravenous antibiotic therapy are warranted. Antibiotics with good gram-positive coverage like ampicillin-sulbactam or third-generation cephalosporins are the first-line choice.

B. This patient has already completed one course of antibiotic therapy, so starting her on a different oral antibiotic is not appropriate. Admission is warranted for more aggressive management.

C. Discharging the patient with instructions for supportive care is not the right course of action, again, because initial antimicrobial treatment failed. Admission and additional antibiotics are needed to treat the acute infection process.

D. At this point in the patient’s care, intravenous antibiotic therapy is the next step. Mastoidectomy should be considered only if intravenous antibiotic therapy fails and the infection spreads beyond the mastoid.

The patient has symptoms consistent with acute otitis media. He is a candidate for a “wait-and-see” prescription for an antibiotic if his symptoms do not improve in 48 to 72 hours. He meets the criteria for “wait and see” including age ≥ to 2 years old, unilateral infection, symptoms for fewer than 48 hours, and temperature is less than 39⁰C. Assuming there are no contraindications, amoxicillin (90 mg/kg/day PO for 5-10 days) is the first-line treatment. Amoxicillin-clavulanate is appropriate if the patient has failed a course of amoxicillin. Cephalosporins like cefdinir or cefuroxime or clindamycin are appropriate in penicillin-allergic patients. Streptococcus pneumoniae is the most common bacterial organism, although most cases are viral.

A. Given the tympanic membrane visualized, antipyretics alone are not sufficient if there is no improvement within 48 to 72 hours. Complications from untreated bacterial otitis media include mastoiditis and hearing complications.

B. If the wait-and-see approach fails, the patient should complete a course of antibiotics. Referral to an ENT for possible tympanostomy should only occur after repeated episodes of otitis media.

C. Immediate use of antibiotics has been shown not to improve outcomes when using these criteria. In addition, there is an increased risk of diarrhea and antibiotic resistance for those who take antibiotics.

This patient presents with peripheral vertigo most consistent with benign paroxysmal peripheral vertigo (BPPV) and should be treated with an Epley maneuver. Vertigo is defined as the sensation of disorientation in space combined with a sensation of motion. Patients typically describe a room-spinning sensation or the feeling of sea sickness. Vertigo can be divided into two types: central and peripheral. Central vertigo are those disorders arising from the central nervous system and include ischemic stroke, vertebrobasilar insufficiency and infectious causes (meningitis, mastoiditis, syphilis). Central vertigo is characterized by longer duration of symptoms, minimal change with position, gradual onset and multidirectional nystagmus. Peripheral vertigo includes BPPV, Menieres disease, Labyrinthitis and vestibular neuritis. Peripheral vertigo may have intermittent symptoms (BPPV) or continuous symptoms but should not be associated with other neurologic deficits or changes and should have unidirectional nystagmus. The symptoms in BPPV are elicited by specific movements of the head and relieved by returning the head to a neutral position. The symptoms should be acute in onset and of a short duration. In BPPV, the symptoms are caused by the presence of an otolith in one of the semicircular canals. Although pharmacologic intervention may be necessary in the acute setting with meclizine or benzodiazepines, the best treatment for BPPV is the Epley maneuver. The Epley maneuver is a series of positions that the clinician takes the patient through that leads to expulsion of the otolith from the semicircular canal and relief of symptoms. The Dix-Hallpike test is a DIAGNOSTIC test, not a treatment

The patient has thrombotic thrombocytopenic purpura (TTP). The classic pentad of TTP includes CNS abnormalities, renal pathology, fever, microangiopathic hemolytic anemia, and thrombocytopenia. However, diagnostic criteria have recently been simplified to include all adults with microangiopathic or microvascular hemolytic anemia and thrombocytopenia with no other explanation for these findings. TTP shares many clinical and laboratory features of HELLP syndrome. HELLP syndrome is less common before 24 weeks gestation. The derangements in hemoglobin and platelet levels are more severe in TTP. The mainstay of treatment for TTP is plasmapheresis (plasma exchange), which can achieve remission of disease in 80% of patients. If plasmapheresis cannot be immediately performed, fresh frozen plasma (FFP) should be administered until apheresis can be performed.

DDAVP stimulates the release of VWF, Factor VIII, and tissue factor. It may be used in bleeding episodes with mild Hemophilia A and von Willebrand disease. It does not affect Factor IX and so would not help in Hemophilia B. DDAVP does have beneficial effects on platelet function but would not help in the setting of thrombocytopenia.

D-dimer has an NPV of 99% in the diagnosis of DIC. If this test is negative, the clinician can be nearly certain the patient does not have DIC.

This patient most likely has tumor lysis syndrome, characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. The tetany (chvostek’s sign of tapping on facial nerve causing muscle twitching) and hyper-reflexia are likely secondary to the hypocalcemia. A uric acid level is the most important test to aid in this diagnosis. Treatment is generally supportive with fluids and correction of electrolyte abnormalities. While hypoparathyroidism can cause low calcium, it will not cause the renal insufficiency seen in tumor lysis syndrome. Neither a CBC nor a peripheral smear are likely to aid in this diagnosis.

The patient in this question has hemolytic uremic syndrome, of which the acute renal failure is the leading cause of morbidity and mortality. If anuric, these patients require plasma exchange therapy, dialysis, and/or monoclonal antibody treatment.

This patient is most likely suffering from leukostasis secondary to blast crisis. The most important treatment in this case is immediate induction chemotherapy. If induction chemotherapy is unavailable, leukaphoresis and hydroxyurea may be used as temporizing measures but the definitive treatment is induction chemotherapy. IV rasburicase is the treatment for severe tumor lysis syndrome.

This patient most likely has AML, which can present with the above gingival findings due to infiltration by tumor cells. Of note, the CBC can vary in patients with AML. Normocytic anemia and thrombocytopenia are common, however the white blood cell count may be low, normal, or elevated. Lymphadenopathy is rare in AML, in contrast to ALL in which it is a common presenting symptom. Definitive diagnosis of AML is by bone marrow biopsy.

Hypercalcemia is generally a product of another underlying disorder and not a primary process in itself. Causes are grouped into four categories: malignancy (primary hematologic, metastases to the bone, or parathyroid producing tumor), hyperparathyroidism, increased intake (milk-alkali syndrome, vitamin D or A toxicity), and increased bone breakdown (immobilization, Paget disease). Clinically, patients experience lethargy, weakness, myalgias, constipation, and anorexia. The clinical presentation is often remembered by the mnemonic “bones, stones, groans and psychiatric overtones.” The first step in treatment is aggressive hydration. The addition of intravenous bisphosphonates (e.g. zoledronic acid) inhibits calcium release from bone. It is usually reserved for hypercalcemia associated with malignancy.

Plasma exchange is the treatment for patients presenting with thrombotic thrombocytopenic purpura (TTP). Patients with this diagnosis have high mortality and should be treated as soon as possible. In a patient with altered mental status, severe thrombocytopenia, and neurologic symptoms, thrombotic thrombocytopenic purpura should be suspected. Patients commonly present with weakness, gastrointestinal symptoms, or neurologic symptoms. Neurologic manifestations may include transient neurologic deficits, confusion, coma, and headache. The classic presentation of fever, renal failure, anemia, thrombocytopenia, and severe neurologic symptoms only occurs in a small percentage of patients. The pathophysiology of TTP involves abnormal platelet aggregation secondary to an abnormality in ADAMTS13, which leads to microangiopathic hemolytic anemia, characterized by schistocytes on blood smear, thrombocytopenia, and end-organ damage.

IV immunoglobulin (A) is the treatment for patients presenting with immune thrombocytopenia (ITP). Patients with ITP will have thrombocytopenia without any clear etiology and therefore should be a diagnosis of exclusion. Patients with ITP will not have evidence of microangiopathic hemolytic anemia or signs of end-organ damage. A lumbar puncture (B) is indicated in a patient suspected to have a CNS infection. In a patient with a normal white blood cell count and no fever, a CNS infection is less likely. Also, the chances of an epidural hematoma would be higher in a patient who has a platelet count of 15 x 109/L. The risks of a lumbar puncture outweigh the benefits in a patient with severe thrombocytopenia and low clinical suspicion for infection. A platelet transfusion (D) is unnecessary in a patient with significant thrombocytopenia unless there is evidence of active bleeding or a procedure is indicated and there is a risk of significant bleeding during the intervention. There is also a potential risk with platelet administration in patients with TTP, since platelet aggregation may worsen as the result of transfusion.

Severe neutropenia is defined as having an absolute neutrophil count less than 500 cells/microL which increases the risk of spontaneous serious bacterial infection. Neutropenia can be inherited or more usually acquired while on chemotherapy. Viral infections can cause transient neutropenia and if discovered incidentally further workup may be indicated. Patients with known severe neutropenia such as a patient with a neutrophil count less than 500 cells/microL in the last week who presents to the emergency department with a fever should be immediately evaluated and started on broad–spectrum antibiotics, even if well appearing. A delay of more than 60 minutes in antibiotic administration to patients with severe neutropenia is associated with an increase in morbidity, mortality, and length of stay.

This patient with sickle cell disease (SCD) presents with acute chest syndrome requiring broad-spectrum antibioticsand intensive care unit (ICU) admission. SCD is a genetically determined disease due to an abnormal allele for hemoglobin beta chains. The end result of this abnormality is a sickled cell that is less deformable and can cause increased viscosity and sludging of the blood. Additionally, cells are sequestered in the spleen and the liver leading to destruction. Patients experience chronic hemolysis, vaso-occlusive events, thrombosis and ultimately, end organ injury. Splenic autoinfarction occurs early in life and makes patients more susceptible to encapsulated organisms such asStreptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitides. Acute chest syndrome is the leading cause of death in SCD and is defined as fever, chest pain, and the presence of new pulmonary infiltrates. Management consists of supportive care, supplemental oxygen if needed, broad spectrum antibiotics, andadmission to the ICU.

The patient in the question stem is suffering from vasoocculsive crisis, or pain crisis of the bones. In adults, this is the most common in the chest, long bones, and back. The mainstay of treatment is narcotics and IV fluids.

Acute cerebrovascular accident is a complication in sickle cell patients due to intravascular sickling and vasoocclusion. It typically manifests as ischemic changes of large intracranial arteries. However, in older patients, hemorrhagic changes can be seen as arterial walls have been weakened from prior infarcts. The ideal treatment is exchange transfusion; it is the most effective method to reduce the percentage of sickled hemoglobin and to reduce intravascular sickling and vasoocclusion. Exchange transfusion also helps minimize the risk of transfusion-associated circulatory overload and associated pulmonary edema, in addition to reduced risk of stroke recurrence. Unfortunately, there are no published evidence regarding the safety and efficacy of thrombolytics in sickle cell patients with acute ischemic strokes. If exchange transfusion is available, this option should be pursued first.

This patient is likely suffering a vasoocclusive pain episode, triggered by a likely viral upper respiratory infection. The provided information does not suggest any life-threatening complications (acute stroke, acute chest syndrome, acute bacterial infection, aplastic crisis, symptomatic anemia) that would require further blood tests or imaging at this time.

For patients who are hypovolemic, IV normal saline resuscitation would be indicated. However, there is no indication in this patient that he is dehydrated. If pain is not adequately controlled with initial PO/IM, then IV pain medication may be attempted.

Acute chest syndrome is the leading cause of death in adult sickle cell patients. It is a syndrome that includes pneumonia, pulmonary infarction, pulmonary embolism, bone marrow infarction, and fat emboli. To make the diagnosis, patient must have consolidation or infiltrate on CXR, and at least 1 of the following symptoms: fever >38.5°C, chest pain, tachypnea, cough, wheezing, or PaO2 <60mmHg. Treatment includes pain control, fluid hydration, antibiotics to cover for both typical and atypical organisms, and oxygen. Bronchodilators may be used, especially if patients already have underlying reactive airway diseases. Glucocorticoids should be avoided as studies have shown rebound vasoocclusion and pain crises following the cessation of steroids.

Although there is limited evidence regarding transfusion therapy in acute chest syndrome, transfusion is considered a mainstay therapy for acute chest syndrome. Some guidelines suggest simple blood transfusion in mild-moderate acute chest syndrome cases, while recommending exchange transfusion in moderate-severe cases.

Mild acute chest syndrome criteria include: O2Sat >90% on room air; segmental/lobar infiltrates involving no more than 1 lobe on CXR; and response to simple transfusion of no more than 2units RBC.

Moderate acute chest syndrome criteria include: O2Sat at least 85% on room air; segmental/lobar infiltrates involving no more than 2 lobes on CXR; and response to transfusion of 3 or more units RBC.

Severe acute chest syndrome criteria include: respiratory failure requiring mechanical ventilation; O2Sat <85% on room air; segmental/lobar infiltrates involving at least 3 lobes on CXR.

Very severe acute chest syndrome criteria include: presence of ARDS or life-threatening lung failure.

Given the initial transcutaneous oxygen saturation 88% on room air, this patient is classified as moderate acute chest syndrome. Hematology should be consulted for transfusion therapy.

Acute dactylitis is the most common presenting symptom for patients with sickle cell disease. It most common occurs in patients 6-18 months of age, and represents bone infarction. It is not an infection.

The genotype HbSC is associated with a higher level of total hemoglobin and a less-severe course; however, these patients are at greater risk for avascular joint necrosis. In patients with HbS beta thalassemia, the severity of disease is determined by the severity of the thalassemia mutation. Patients with mild HbS beta+ thalassemia will have near-normal lives, whereas the natural history of HbS beta0 thalassemia is similar to HbSS.

This patient is most likely suffering from transfusion-related acute lung injury (TRALI), one of the leading causes of transfusion-related mortality. It is most closely associated with platelet and fresh frozen plasma transfusions, though cases have been reported with packed red blood cells since there is some residual plasma in the packed cells. Symptoms begin abruptly during transfusion or within six hours and resemble adult respiratory distress syndrome with noncardiogenic pulmonary edema, dyspnea, hypoxemia, and bilateral infiltrates on chest radiograph. It is thought to be caused by granulocyte recruitment and degranulation. As with all transfusion-associated complications, the transfusion should be stopped immediately and supportive care instituted. Most cases resolve spontaneously.

ABO incompatibility (A) causes intravascular hemolysis of transfused red blood cells, producing hemoglobinemia and hemoglobinuria. The onset is immediate. Symptoms include fever, chills, headache, nausea, vomiting, a sensation of chest restriction, and severe joint pain. ABO incompatibility is most often due to human error. An allergic transfusion reaction (B) can vary in severity from simple pruritus with urticaria to anaphylaxis with wheezing and bronchospasm. This patient’s respiratory symptoms are not bronchospastic in nature. Although TRALI can be confused with acute transfusion-associated circulatory overload (TACO) (C), TRALI is associated with hypotension, whereas TACO is associated with a rapid rise in blood pressure.

Pancytopenia (a reduction in all blood cell lines: erythrocytes, leukocytes, and platelets) with a low reticulocyte count is suggestive of aplastic anemia. The use of medications known to cause bone marrow suppression further suggests drug-induced aplastic anemia. Bone marrow generates pluripotent stem cells that differentiate into red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes). Immature red blood cells are called reticulocytes. When red blood cell production is increased, the erythrocyte count becomes elevated. If this level is reduced, concern is raised about the integrity of bone marrow stem cell production. When red blood cell counts are low (anemia), the hormone erythropoietin is released to accelerate red cell production. Aplastic anemia is a rare type of anemia that is caused by drugs or chemicals in 50% of cases. Drugs that suppress bone marrow production include chloramphenicol, anticonvulsants (e.g., carbamazepine), insecticides, sulfonamides, and gold. Medical conditions associated with aplastic anemia include viral hepatitis, radiation, pregnancy, and autoimmune diseases. Aplasia may affect a single cell line (e.g., pure red cell aplasia) or all cell lines. Symptoms of aplastic anemia may include fatigue, malaise, infection (from neutropenia), or mucosal bleeding (from thrombocytopenia). Bone marrow analysis is needed for definitive diagnosis.

Disseminated bacteremia (A) with certain organisms (e.g., Streptococcus pneumoniae, Neisseria gonorrhoeae) may present with purpura or petechiae. However, these patients are septic with fever, hypotension, lactic acidosis, and usually normal or elevated white blood cell counts and normal red blood cell counts. Disseminated intravascular coagulation (B) is a consumptive coagulopathy with multiple etiologies (e.g., sepsis, trauma, pregnancy, cancer) that can also present with excessive bleeding and petechiae. Thrombocytopenia and schistocytes are characteristic, as well as abnormal coagulation tests. Red blood cell and white blood cell lines are typically unaffected. A type I hypersensitivity reaction (D) is an immunoglobulin E (IgE)-mediated process that results in a massive, abrupt immune response affecting multiple organ systems (e.g., skin, respiratory, circulatory). Anaphylaxis is an example.

Up to 30% of meningococcemia patients will present with this picture and no immediate evidence of meningitis or sepsis.

Antibiotics should not be held while waiting for a lumbar puncture. There have been multiple studies looking at antibiotics effects of lumbar puncture results.  Here is a link to 3 articles looking at this.

Dexamethasone should also be started as it decreases neurological complications from step pneumoniae meningitis.

Botulism presents as a descending paralysis/anticholinergic syndrome. Autonomic dysfunction with orthostatic hypotension is common. Ileus and urinary retention may occur. Antitoxin, intensive care unit admission, and early intubation are often indicated.

Localized tetanus reflects a local neuromuscular process with pain and spasm. It is likely due to a partial immunity. Immune globulin is indicated. Although mortality is lower, it can progress to generalized tetanus, and admission is warranted.

HTIG prophylaxis (250 units IM) is recommended for unimmunized and underimmunized patients with wounds at high risk for tetanus (>6 hours old, >1 cm deep, contaminated, stellate, denervated, ischemic, infected).²⁷ When tetanus toxoid and HTIG are given concurrently, separate injection sites should be used. The only contraindication to tetanus and diphtheria toxoids is a history of a neurologic or severe hypersensitivity reaction to a previous dose. Adverse reactions to tetanus toxoid and tetanus-diphtheria toxoids occur commonly and may be the result of the preservative thimerosal. The most common side effects are minor: local swelling, pain, erythema, pruritus, fever, nausea, vomiting, malaise, and nonspecific rash.

The surgical dressing must be removed to ensure there is no nasal packing or other foreign body present that could serve as a precipitant of toxic shock syndrome (fever, hypotension, diffuse erythroderma, multisystem organ dysfunction). Toxic shock syndrome is commonly associated with postsurgical dressings as well as vaginal foreign bodies (classically, extended-use tampons). Toxic shock syndrome toxin-1 (TSST-1) producing strains of S. aureuscause the infection, with the toxin serving as a superantigen that leads to overstimulation of T-lymphocytes and subsequent massive, unregulated cytokine release. Patients often report a prodrome of flu-like symptoms including headache, myalgias, vomiting, and diarrhea.

Antibiotics (A) prevent recurrence but do not affect the outcome of the acute illness. However, starting an antistaphylococcal antibiotic early is standard practice. There is evidence that the addition of clindamycin or linezolid offers an additional benefit of decreasing production of TSST-1. A wound culture (C) has limited utility in this scenario. A blood culture may be useful but should be obtained after the nidus of infection is removed. All diagnostic testing, including imaging (B), should be performed after searching for and removing the likely source of toxin.

The two most important ancillary tests in the evaluation of fever in the adult patient, and especially in elder patients who frequently have atypical presentations, are urinalysis and chest radiography. Chest radiographs are often helpful in the diagnosis of pulmonary infection but may be difficult to interpret in the patient with chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), or other chronic lung disease. The urinalysis, although not foolproof, is highly accurate for urinary tract infection, especially in men. Although the white blood cell count is almost universally used in the evaluation of febrile patients, it lacks sensitivity and specificity to be of discriminatory value. Cultures are ordered in selected patients; however, the delay in obtaining results precludes any influence in emergency evaluation and treatment. Other tests that have relevance in select patients with fever include Gram’s stain, cerebrospinal fluid (CSF) analysis, thyroid function studies, ultrasonography, and computed tomography (CT) of the abdomen or head.

Most cases of necrotizing fasciitis are caused by polymicrobial infection with gram-negative, gram-positive, andanaerobic bacteria. Commonly identified organisms include S. aureus, beta-hemolytic streptococci, enterococci, enterobacteria, and anerobes such as Bacteroides and Clostridium species. Necrotizing fasciitis is characterized by deep tissue infection involving subcutaneous fat, fascia, and muscle layers, as opposed to cellulitis, where infection does not extend past the dermal layer. Infection may begin by direct bacterial invasion of subcutaneous tissue via breaks in the skin from an abscess or wound, or via spread from a perforated viscous such as colon, rectum, or anus. The hallmark of necrotizing fasciitis is pain out of proportion to physical exam. Early recognition is critical as necrotizing fasciitis is rapidly progressive and has a high mortality rate. General surgery should be consulted as soon as necrotizing fasciitis is suspected. It is treated with surgical debridement, intravenous broad-spectrum antibiotics, and hemodynamic support.

Necrotizing fasciitis of the perineal, perianal, or scrotal is called Fournier’s gangrene.

Sepsis affects both myocardial function and peripheral vascular tone. The systemic vascular resistance is usually markedly depressed. Cardiac output is generally increased because of a compensatory tachycardia that can at least partially overcome the ventricular dilation and depressed ejection fraction. The myocardial effects are typically reversible.

The febrile neonate is a child 28 days and younger who presents with a fever. These children are at very high risk of serious bacterial infections including urinary tract infection, pneumonia, meningitis, and bacteremia. Risk factors for serious bacterial infection in a neonate include prematurity, low birth weight, premature or prolonged rupture of membranes, meconium aspiration, or maternal group B streptococcus infection. The evaluation of a neonate with a fever includes CBC, urinalysis, blood culture, urine culture, and a lumbar puncture in order to obtain CSF for cell count, gram stain, and culture. If the child has respiratory symptoms, a chest X-ray should be performed. If the child has diarrhea, stool testing should also be performed. The most common pathogens involved in serious bacterial infections, including meningitis and bacteremia, in neonates are Listeria monocytogenes, Group B streptococcus, and Escherichia coli. These children can become critically ill very rapidly; therefore, initial management should include a fluid bolus of 20 mL/kg and broad-spectrum antibiotics to cover for the most common pathogens in this age group. The most appropriate antibiotics to use in neonates with a fever are ampicillin and cefotaxime. Ampicillin will cover Listeria monocytogenes while cefotaxime will cover Group B streptococcus and Escherichia coli. If there is a history of maternal infection with herpes simplex virus, acyclovir should be added to the empiric broad-spectrum treatment. These patients universally need to be admitted to the hospital for IV antibiotics and observation until all cultures have returned.

Most cases of necrotizing fasciitis are caused by polymicrobial infection with gram-negative, gram-positive, andanaerobic bacteria. Commonly identified organisms include S. aureus, beta-hemolytic streptococci, enterococci, enterobacteria, and anerobes such as Bacteroides and Clostridium species. Necrotizing fasciitis is characterized by deep tissue infection involving subcutaneous fat, fascia, and muscle layers, as opposed to cellulitis, where infection does not extend past the dermal layer. Infection may begin by direct bacterial invasion of subcutaneous tissue via breaks in the skin from an abscess or wound, or via spread from a perforated viscous such as colon, rectum, or anus. The hallmark of necrotizing fasciitis is pain out of proportion to physical exam. Early recognition is critical as necrotizing fasciitis is rapidly progressive and has a high mortality rate. General surgery should be consulted as soon as necrotizing fasciitis is suspected. It is treated with surgical debridement, intravenous broad-spectrum antibiotics, and hemodynamic support.

Necrotizing fasciitis of the perineal, perianal, or scrotal is called Fournier’s gangrene.

That’s correct!

Sepsis is defined as meeting systemic inflammatory response criteria (SIRS) plus a suspected infection. Severe sepsis is sepsis plus organ dysfunction. Septic shock is sepsis plus hypotension not responsive to a fluid challenge. This patient has SIRS (elevated heart rate and elevated temperature), renal dysfunction (new creatinine elevation), but a normal blood pressure; thus, he meets the definition for severe sepsis.

This patient is exhibiting signs and symptoms of Lyme disease. Lyme disease is the most common vector-borne disease in the United States. It is endemic to New England, the mid-Atlantic states, and the upper Midwest. It is caused by the spirochete Borrelia burgdorferi and transmitted by the Ixodes dammini tick, more commonly known as the deer tick. The tick must be attached for more than 48 hours for transmission to occur. There are three stages of clinical Lyme disease. Early Lyme disease is characterized by erythema migrans, an erythematous blanching patch that may have central clearing and classically has a “bull’s eye” appearance. Hematogenous spread leads to diffuse erythema migrans, which spares the palms and soles. Acute disseminated Lyme disease occurs approximately 4 weeks after initial infection and can include meningoencephalitis, Bell’s palsy (which may be bilateral), or carditis which often manifests with variable AV block. This AV blockade may be high-grade and require temporary transcutaneous or transvenous pacing; however, it nearly universally resolves gradually with IV antibiotics and has a favorable prognosis with no need for permanent pacemaker placement. Late Lyme disease develops greater than 1 year after initial infection and includes chronic arthritis with or without chronic subtle encephalopathy. Only 50% of patients remember a tick bite; thus, diagnosis may be difficult. Erythema migrans is diagnostic; however, not all patients present with this finding. Initial screening involves ELISA testing with Western Blot and PCR to confirm the diagnosis. If the diagnosis is suspected, empiric treatment should be administered. Treatment for early Lyme disease and mild acute disseminated Lyme disease is doxycycline for 3-4 weeks. In pregnant women or children under the age of 8 years, amoxicillin should be substituted. Patients with neurologic or cardiac manifestations should be admitted and treated with IV ceftriaxone.

Rocky Mountain spotted fever (RMSF) is a tick-borne illness caused by Rickettsia rickettsii and transmitted to humans through the dog tick or Rocky Mountain wood tick. The disease is endemic in all 48 states, but most commonly occurs in the southeastern United States. After infection, the organism invades and replicates inside of vascular endothelial cells. The most common victims of RMSF are children. After a mean incubation period of 7 days, patients develop classic symptoms including fever, headache, myalgias, nausea and vomiting. Fever is usually the first symptom and may be the only symptom for up to one week. The rash is classically small red macules that are sometimes pruritic. The rash begins only on the ankles and feet and then spreads to the palms and soles. Thereafter, it moves centrally to the rest of the arms, legs and torso. After several days, the rash becomes papular and deeper red. In the early stage the rash blanches with direct palpation and enhances with warm compresses. In later stages, the rash becomes petechial and application of proximal pressure causes additional lesions to appear distally (Rumpel-Leede phenomenon). The cardiovascular system is affected with myocarditis and an impaired ejection fraction in some patients. Neurologically, the most common symptom is headache but may include seizures and an eosinophilic meningitis. Diagnosis is made through the identification of serum antibodies present 5 to 7 days after the infection begins. Treatment is with doxycycline

Babesiosis (A) is a tick-borne illnesses transmitted by the Ixodes tick in the northeastern part of the United States. The clinical symptoms are similar to malaria as the organism infects red blood cells causing fevers, myalgias headache and significant sweats. Approximately 20% of patients with babesiosis are co-infected with Lyme disease. Leptospirosis (B)is most commonly transmitted to humans through the urine of rodents. In most cases, patients have a flu-like illness with fever, myalgia and severe headache. Ten percent of patients develop severe leptospirosis with liver and renal failure.Lyme disease (C) is the most common vector-borne disease in the United States. The Ixodes ticks transmit the organism Borrelia burgdorferi. The initial manifestation of Lyme disease is the classic rash erythema migrans described as an erythematous macule with central clearing. With time patients develop fever, arthralgias, adenopathy and ultimately arthritis. Neurologically patients may develop unilateral or bilateral Bell’s palsy, aseptic meningitis and a neuritis causing similar pain symptoms to post-herpetic neuralgia.

Isospora and coccidial organisms may cause an almost cholera-like diarrheal illness. Eradication is very difficult.

Malaria and invasive amebiasis are not considered opportunistic infections.

AIDS patients have much more severe allergic manifestations to the antiparasitics.

Schistosomiasis enhances HIV pathogenesis.

The fish tapeworm is associated with pernicious anemia. Hookworm and whipworm are associated with gastrointestinal iron loss and microcytic anemia. Malaria causes hemolytic anemia.

Onchocerciasis is a major cause of blindness worldwide. Ninety-five percent of cases occur in Africa. The biting flies are found near rivers, and humans are the only host for the parasite. It occupies the skin, resulting in pruritus, edema, and later atrophy with redundant skin folds. The following are other causes of parasite-induced visual loss: Toxoplasma can cause retinal hemorrhages, Toxocara can cause inflammatory retinal granulomas, and Acanthamoeba may cause a keratitis in contact lens wearers.

This patient has clinical and radiographic evidence for pneumonia. Community-acquired pneumonia caused by Streptococcus pneumoniae is the most common cause of pneumonia in HIV-infected patients. Therefore, he should receive ceftriaxone and azithromycin. Additionally, his low CD4 count puts him at risk of opportunistic infections, such as Pneumocystis jiroveci pneumonia (PJP), formerly known as Pneumocystis carinii pneumonia (PCP). PJP is the most common opportunistic infection among AIDS patients. Signs and symptoms of PJP pneumonia include fatigue, fever, cough, and hypoxia. Chest radiographs typically show diffuse interstitial infiltrates, though negative radiographs are not unusual in PJP. Serum lactate dehydrogenase levels are often elevated. Initial therapy for PJP includes trimethoprim/sulfamethoxazole. In severe cases, corticosteroids are also given. The indications for corticosteroid use include an arterial oxygen partial pressure of < 70 mm Hg (equivalent to an oxygen saturation of <~93%) and an alveolar-arterial gradient > 35 mm Hg. Prophylaxis with oral trimethoprim-sulfamethoxazole is recommended for all HIV-positive patients with CD4 counts less than 200 cells/mm3 to prevent PJP pneumonia.

Amphotericin B (A) is used in the treatment of disseminated fungal infections, such as Aspergillus fumigatus and Cryptococcus neoformans. These infections are typically seen at a higher degree of immunosuppression. Azithromycin and ceftriaxone (B) treat most community-acquired pathogens, but do not cover opportunistic infections like PJP. Trimethoprim/sulfamethoxazole and prednisone (D) is incorrect because the patient should also receive treatment for community-acquired pneumonia.

In the United States, an estimated 1.2 million individuals are HIV positive, with approximately 50,000 people newly diagnosed each year. The clinical presentation of acute HIV infection, also known as acute retroviral syndrome, is variable both in type and severity of symptoms. The classic presentation is abrupt onset of a viral-like illness, which develops 10–14 days following exposure to the virus. Symptoms may include fever, malaise, sore throat, headache, arthralgias, anorexia, nausea, vomiting, and rash. Physical examination findings vary and may include generalized lymphadenopathy, nonexudative pharyngitis, mild hepatosplenomegaly, mucocutaneous ulcers, and oral thrush. A maculopapular rash on the thorax, face, and limbs may also be present. Due to the nonspecific and self-limited nature of symptoms, many affected individuals do not seek care and thus the true incidence of acute HIV is unknown. However, experts estimate that 60–90% of individuals who contract HIV develop an acute illness. Identification of acute HIV has tremendous public health implications, as acute infection represents the peak infectivity of the disease, characterized by high levels of viral shedding. Routine HIV tests used in most emergency departments measure anti-HIV antibodies, which are often falsely negative during acute infection. Therefore, when acute HIV is suspected, nucleic acid amplification tests, which directly measure viral RNA in the patient’s blood, should be utilized.

The tongue lesions seen in the image are characteristic for oral hairy leukoplakia (OHL). This is a disease of the lingual squamous epithelium and is thought to be caused by the Epstein-Barr virus (EBV). It is highly specific for concomitant HIV infection and rarely seen in other immunocompromised states. OHL is often confused with oral candidiasis (thrush). However, unlike the lesions of thrush, OHL cannot be scraped off the tongue.

OHL most commonly develops on the lateral portions of the tongue, not the posterior oropharynx (A). The disease is caused by the Epstein-Barr virus, unlike oral thrush, which is caused by the yeast (C) Candida albicans. The plaques are painless (D), and most patients are asymptomatic.

Aplastic crisis is defined as having a reticulocyte count of less than 1%. Patients with sickle cell disease who are infected with Parvovirus B19 are at risk for developing an aplastic crisis. Parvovirus B19 is the causative agent of Fifth disease and can lead to an aplastic crisis by causing a temporary arrest of red blood cell production. This is characterized by a sudden decrease in hemoglobin production by bone marrow resulting in severe anemia. Patients may present with pallor, lethargy, and shock. Treatment includes hemodynamic support and blood transfusion.

Labs that should be sent include type and cross, CBC, and reticulocyte count.  This is usually self-limited disease and resolves once the viral syndrome resolves.  Blood transfusions to support the patient through the anemia is the treatment along with other supportive measures.

Infectious mononucleosis is caused by the Epstein-Barr virus. While young children with the disease typically have minimal, if any, symptoms related to the infection, adolescents and young adults usually have a more pronounced course. It is uncommonly seen in adults as most are immune due to a previous exposure. Patients may have a prodrome of low-grade fever, headache, and malaise. There is pharyngeal erythema and tonsillar exudates that may appear white, gray-green, or necrotic. Palatal petechiae can also be seen, but may be present in streptococcal pharyngitis as well. Severe fatigue is common and often the symptom that persists the longest. The lymphadenopathy is usually mildly tender, symmetric and involves the posterior cervical chain. Hepatosplenomegaly can be noted on examination. A generalized maculopapular rash almost always occurs following administration of amoxicillin or ampicillin although the mechanism of this is unclear. Diagnosis is made based on history and physical and can be confirmed with a positive heterophile antibody test (monospot test). Treatment is supportive. Symptoms generally resolve in 1-3 weeks although the fatigue may persist for months. Patients should refrain from contact sports for four weeks post-infection.

The patient has a penetrating abdominal injury with evisceration of abdominal contents. Indications for the OR in penetrating abdominal injury include unstable vital signs, peritonitis w/ a +FAST examination, evisceration, and transabdominal GSW.

Patients with fractures of the bony pelvis are at high risk for hemorrhage due to the close proximity of the vascular structures to the pelvic bones. The internal iliac arteries and their subsequent branches provide most of the blood supply to the pelvic region. Most traumatic pelvic bleeding is venous, but in unstable patients an arterial source is suggested. In this patient with fractures and persistent hemodynamic instability without hemoperitoneum, the source of bleeding is likely the pelvis. After initial attempted stabilization with an external pelvic binder (either a sheet or commercial device), the patient needs angiography and embolization in interventional radiology. Angiography has very high success rates at controlling pelvic hemorrhage.

The correct answer is retrograde urethrogram to evaluate for urethral injury. Posterior urethral injuries can occur with pelvic fractures. A bladder fracture is also a possibility and a retrograde cystogram should be performed after the urethrogram to assess for bladder injury given the open book pelvic fracture on x-ray. A foley catheter is contraindicated until urethral injury has been excluded. IVP is rarely performed currently as CT scan can evaluate for renal injury reliably. Retrograde cystogram should be done as well but after a retrograde urethrogram. Intravenous pyelography may be done if suspect kidney injury but blood at the urethral meatus in the context of a pelvic fracture is more suggestive of a urethral or bladder injury. Placement of a foley catheter is contraindicated

The presence of gross hematuria in the setting of trauma signifies a urologic injury until proven otherwise. Gross hematuria suggests either a lower or upper urinary tract injury. Bladder injury (e.g. rupture) is suggested by lower abdominal pain and tenderness or a positive FAST examination on evaluation of the pelvis. Urethral injuries may present with blood at the meatus in which case a retrograde urethrogram is indicated. Blunt trauma accounts for approximately 90% of renal injuries and 1-5% of hospitalized trauma patients have a renal injury. In most cases, clinically significant renal injuries are associated with gross hematuria. Rarely, a significant injury is found with microscopic hematuria but also hemodynamic instability. Therefore, if renal injury is suspected, gross hematuria in the hemodynamically stable patient dictates further imaging evaluation.

The spleen is the most common organ injured in adults in blunt abdominal trauma. Most blunt abdominal trauma results from motor vehicle collisions. Many splenic injuries, including high-grade lacerations, may be managed conservatively in the hemodynamically stable patient without other significant intraabdominal injuries.

The correct answer is between the spleen and the diaphragm. Fluid is rarely seen between the spleen and kidney. Most commonly it is between the spleen and diaphragm, or simply around the spleen.

When a patient presents after suffering blunt abdominal trauma and has a concerning abdominal examination but a negative workup, decisions about appropriate management can be challenging. In this particular patient, the negative CT scan and FAST results are reassuring in terms of solid organ injury, but there is potential for other serious injuries, such as hollow viscus injury or pancreatic injury. The seatbelt sign (ecchymosis on the abdomen) suggests that the patient could have these injuries, so a period of observation in the hospital is warranted. Discharging the patient without a period of observation either in the hospital or in the emergency department creates the potential for the patient to suffer significant complications from undiagnosed intraabdominal injury. Diagnostic peritoneal lavage would be helpful in this patient if grossly positive but might not otherwise definitively determine the indication for surgical management. The formal abdominal ultrasound examination done in the radiology department is no more accurate than a FAST examination done by an experienced provider for identifying hollow viscus injury or acute pancreatic injury.

The patient is suffering from an acute traumatic uterine rupture a rare complication following blunt and penetrating abdominal trauma. The classic signs include maternal shock, abdominal pain, peritoneal signs, abnormal fetal lie, easily palpable fetal anatomy and fetal demise. The use of a lap belt alone increases the risk of developing uterine rupture and placental abruption. The patient should be aggressively resuscitated and emergent surgical and obstetric consultation is necessary for operative repair.

CT imaging is excellent in detecting solid organ injury (e.g. kidney, liver, spleen, pancreas) but not good at detecting mesenteric hematoma/tears or hollow viscus injury.

Gross hematuria is the most common sign of bladder injury and occurs in more than 95% of the cases. Bladder injury most commonly results from blunt motor vehicle trauma and 80% are associated with fracture of the bony pelvis. Bladder injuries include contusions, intraperitoneal and extraperitoneal ruptures and combination ruptures. Other signs of bladder rupture include suprapubic and lower abdominal pain, inability to urinate, pelvic fracture, and blood at the urethral meatus. Blood at the urethral meatus is a sign of underlying urethral or bladder injury, although is not the most common sign for bladder injury. A high-riding prostate is a sign of urethral injury, not bladder injury. An inability to urinate is a sign of bladder injury, however is not the most common sign.