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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.

A knee dislocation is a very serious injury which involves dislocation of the tibiofemoral joint and disruption of all the ligamentous structures. Posterior dislocations occur when with high velocity direct trauma to a flexed knee, such as a dashboard impact in a motor vehicle crash. The most serious consequence of knee dislocation is a popliteal artery injury. The popliteal artery runs in the popliteal fossa and its relative immobility makes it susceptible to disruption when dislocation occurs. A popliteal artery injury is a true emergency. When repair is delayed for more than 8 hours, the amputation rate is greater than 90%. Hard signs of vascular injury include absent pulses, limb ischemia (e.g. a cool, mottled foot), rapidly expanding hematoma, palpable thrill or audible bruit, or history of pulsatile bleeding (in the case of penetrating trauma or open injury). Though not considered a hard sign, paresthesias also raise concern for injury to popliteal structures. The workup-up for ruling out popliteal injury includes serial physical exams, ankle-brachial indices (ABI), CT angiography, conventional angiography, and duplex ultrasonography. Patients with vascular injury require emergent surgical repair.

Carpal tunnel syndrome is a median mononeuropathy and the most common mononeuropathy in the body. Classic symptoms include pain and paresthesias on the volar side of the first, second, and third fingers and radial half of the fourth finger with symptoms most notable at night. Fourth finger sensory dysfunction on the radial aspect of the finger only is very specific for the diagnosis of carpal tunnel syndrome. Extension and flexion at the wrist commonly exacerbate the condition and can aid in diagnosis. Using the Phalen test, by holding the wrists in maximum flexion for at least 1 minute, reproduction of the symptoms helps to point toward this diagnosis. A positive Tinel sign yields tingling after tapping on the wrist where the median nerve passes through the carpal tunnel between the carpal bones and the flexor retinaculum. Both of these tests have poor sensitivity, and if negative, do not effectively rule out the diagnosis. A more specific finding is divided sensation of the fourth finger, with dysfunction on the radial aspect only. Treatment for carpal tunnel syndrome includes a splint on the wrist and NSAIDs. Recurrent symptoms sometimes warrant steroid injections by a hand surgeon and possibly surgical decompression.

WHY THE OTHER ANSWERS ARE WRONG

Some patients have weakness in the muscles of the hand, a condition known as Guyon canal syndrome or handlebar palsy. It is an ulnar mononeuropathy rather than a median neuropathy as with carpal tunnel syndrome. In this rare syndrome, there is compression of the ulnar nerve at the wrist that causes weakness of the intrinsic muscles of the hand. What often happens is that the sensory function of the ulnar nerve is spared or involves only the palmar aspect of the fifth finger and half of the fourth. Carpal tunnel can cause weakness in the thenar eminence, but not the traditional intrinsic muscles of the hand.

Carpal tunnel syndrome is caused by compression of the medal nerve in the inflamed carpal tunnel between the flexor retinaculum and carpal bones, not at the medial epicondyle. Compression here causes cubital tunnel syndrome, and patients have numbness and tingling in the fifth and lateral fourth digits.

Carpal tunnel syndrome is the most common mononeuropathy in the body and involves the median nerve, not the ulnar nerve. The most common ulnar nerve mononeuropathy is cubital tunnel syndrome. Patients typically have paresthesias of the fifth and lateral fourth fingers. Ultimately, weakness of the intrinsic muscles can ensue.

The correct answer is inability to fully extend the knee. The remaining answer choices are all components of the Ottawa Knee Rules, which include: Age over 55 years old, isolated patella tenderness, tenderness at head of fibula, inability to flex knee 90 degrees, and inability to bear weight (4 steps) immediately after injury or in the ED.

Compartment syndrome is diagnosed by a compartment pressure greater than 30 or a ∆ measurement (diastolic BP – compartment pressure) <30. This patient's pressure difference is 25 which is strongly suggestive of compartment syndrome. The femur is in a large compartment and it is typically difficult to sustain compartment syndrome. More concerning areas are the anterior tibial compartment and the forearm.

A. Anterior talofibular ligament
The correct answer is anterior talofibular ligament (ATFL) injury. The anterior-posterior and oblique x-ray views of the right ankle demonstrate a normal mortise and no fractures. There is, however, right lateral ankle soft tissue swelling. Typically, the mechanism of injury helps determine the location of ligamentous injury. The most common mechanism is inversion of the plantar-flexed foot, leading to lateral ankle sprains due to injury of the anterior talofibular ligament (ATFL), the calcaneofibular ligament, and posterior talofibular ligament. Of the three ligaments, the ATFL is the most commonly injured.

B. Calcaneofibular ligament
This patient is presenting with an ankle sprain and with lateral ankle sprains, the most common ligament injured is the anterior talofibular ligament. The calcaneofibular ligament may also be injured, but isolated calcaneofibular ligament injury is uncommon.

C. Deltoid ligament
This patient is presenting with a lateral ankle sprain and the deltoid ligament is on the medial side of the ankle, is much stronger, and is much less prone to injury.

D. Tibiofibular syndesmosis
Injury to the tibiofibular syndesmosis is an uncommon, but significant, injury. Injury to this structure characterizes a “high” ankle sprain. However, the squeeze test of the tibia-fibula is reported negative, making this diagnosis less likely. The squeeze test involves compression of the fibula against the tibia at the mid-calf level, trying to reproduce pain while attempting to widen the syndesmosis between the distal tibiofibular space.

The X-ray demonstrates an anterior knee dislocation. It is important to differentiate between a knee dislocation (tibiofemoral) and patellar dislocation. The patellar dislocation is less severe and typically without other associated injuries. A knee dislocation may not always be present on arrival to the ED as spontaneous reduction can occur prior to arrival. However, even with spontaneous reduction, significant pain and soft tissue swelling remains. In an anterior knee dislocation surrounding vascular and nerve structures are at risk. The dislocation results in significant ligamentous injury. The neurovascular bundle running behind the knee is at risk. The life threatening injury is laceration of the popliteal artery within this bundle. In addition to lacerations of the vascular structure, dissection is also possible from the shear injury occurring during the trauma. The popliteal vein is the other vascular structure within the bundle. The common peroneal nerve is located within the bundle and the neurologic injury associated with an anterior dislocation. This dislocation is associated with an injury to the common peroneal nerve in 20 to 40% of patients. The common peroneal nerve arises from the L4-S2 nerve roots and branches into the deep and superficial peroneal nerves. These nerves supply sensation to most of the dorsum of the foot sparing the lateral most portion of the foot. The motor function of the common peroneal is dorsiflexion of the ankle.

Metatarsal fractures are responsible for one third of foot fractures. Fractures at the base of the metatarsal are uncommon in the first through fourth metatarsals. The isolated fracture at the base of the fifth metatarsal is common and management depends on which form of the two fractures occurs. The Jones fracture is a transverse fracture occurring in the diaphysis of the bone at least 1.5 cm distal to the end of the bone. The Jones fracture tends to displace with further weight bearing. With improper immobilization there is a higher percentage of nonunion of the fracture fragments. Therefore, patients should be immobilized in a posterior splint and given crutches for non-weight bearing ambulation. The pseudo-Jones fracture is an avulsion fracture of the tuberosity at the base of the fifth metatarsal. The injury often occurs as a result of a lateral ankle strain with tension at the attachment of the peroneus brevis tendon. These patients are treated with a compression dressing and weight bearing as tolerated. Providers may elect to give the patients a hard sole shoe.

The lateral radiograph shows a perilunate dislocation in which the lunate remains aligned with the distal radius, however the remaining carpal bones are dorsally displaced. There is significant ligamentous injury. The mechanism of injury is generally a fall on an outstretched hand (FOOSH). Patients complain of wrist pain and swelling, and tenderness is noted over the carpal bones on exam. If untreated, the patient is at risk for developing median nerve compression, avascular necrosis, compartment syndrome and long-term disability. A hand surgeon should promptly evaluate the patient with a plan for urgent open dislocation reduction.

Anterior shoulder dislocations are the most common type of shoulder dislocation. The axillary nerve is the neurologic structure most at risk for injury during a shoulder dislocation. Sensation over the deltoid muscle is the way in which axillary nerve function is tested on physical examination. Additionally, distal nerve function of the median, radial and ulnar nerves should be evaluated as part of the complete evaluation of the shoulder joint. It is important to document all findings of the neurovascular examination prior to any attempts as a baseline. Posterior dislocations are associated with significant injury 30% of the time to intrathoracic and mediastinal structures. These complications include: injury to the great vessels, tracheoesophageal fistula, pneumothorax and brachial plexus injuries.

This case describes a patient with an ankle syndesmosis injury which if not properly treated leads to chronic ankle instability and pain. The image shows widening of the tibio-fibular joint as well as a widened ankle mortise. This ankle requires non-weight bearing an urgent othopedic consultation for possible operative fixation.

It is difficult to identify cardiac tamponade by visual inspection only. Thus the first step should be opening the pericardium. Direct cardiac massage should be done after pericardium is opened and if no tamponade is found. Cross clamping of the aorta should be the next step if the patient still has no cardiac activity.

This clinical scenario depicts a patient with a tension pneumothorax. He has decreased blood pressure, decreased breath sounds, and, most important, an increased resistance to ventilation, which is the earliest sign of the development of a tension pneumothorax. Immediate decompression with a large-bore needle is the correct initial management in this condition.

Elevation of the right mainstem bronchus is suggestive of acute traumatic aortic disruption. Traumatic aortic disruption can result in immediate death if the degree of injury is severe, such as a complete transection. However, with less severe disruptions, the patient may survive and present to the ED. Prompt diagnosis and early intervention, can lead to a functional recovery.

Deviation of the trachea to the right (B), not the left suggests aortic injury. Deviation of the esophagus to the right (A), not the left suggests aortic injury. A left-sided hemothorax (D) suggests aortic injury, not a right hemothorax.

Two most common sites of aortic injury with blunt trauma are: Aortic isthmus and ascending aorta just proximal to the origin of the brachiocepahic vessels.

This patient has signs and symptoms of blunt cardiac injury. The most common chamber injured is the right ventricle as it lies most anterior in the thorax, immediately behind the sternum. Blunt cardiac injury results in myocardial contusion and “stunning” of the heart muscle. This can lead to dysrhythmias and heart failure. Cardiac contusion is most frequently caused by high-speed motor vehicle collisions or severe crush injuries. The most common etiology is a depressed sternal fracture. Symptoms of cardiac contusion include chest pain, shortness of breath, and palpitations. There is often external evidence of chest trauma including obvious depressed fractures of the sternum and steering wheel imprints. The diagnosis of significant blunt cardiac injury is made by electrocardiogram abnormalities (e.g. T wave inversions and frequent PVCs) and a serum troponin level. If either of these studies is abnormal, the patient should be admitted for telemetry monitoring.

This xray shows a Jefferson fracture, or a C1 burst fracture. These fractures occur with axial loading with vertical compression, an injury pattern that is common when a football player spears another player. When looking at the odontoid view of a c-spine film, the lateral masses of C1 shoulder align with the lateral parts of the C2 vertebral body. A Hangman’s fracture, or bilateral C2 pedicle fracture is best seen on a lateral view and shows C2 displaced anteriorly on C3. Odontoid fractures involve the odontoid process and are graded type I through type III depending on position.  Type II and III are both unstable fractures. Bilateral facet dislocation fractures are seen on lateral xrays of the c-spine and is characterized by anterior displacement greater than 50% diameter of vertebral body.

The correct answer is that this injury is associated with anterior cord syndrome. This patient has a flexion teardrop injury at C5 (note the wedge shaped fracture at the base of the vertebral body).  This is generally caused by extreme flexion and axial load, classically a diving injury. There is failure of the anterior column, often middle column, and disruption of the posterior ligamentous complex and the significant potential for cord injury from retropulsion of a fragment as a result.

Odontoid (dens) fractures are classified as Type I, II and III. Type I fractures are stable avulsion injuries to the tip of the odontoid. This patient has a Type II fracture, which is a fracture at the junction of the odontoid and body of C2. A Type III fracture is a fracture at the base of the the dens. Both Type II and III fractures are unstable because of ligamentous attachments. A bilateral C2 pedicle fracture is also known as a Hangman’s fracture and is seen on lateral xray as C2 being displaced anteriorly on C3. A teardrop fracture is an avulsion fracture of the anteroinferior portion of the vertebral body. Both of the former fractures patterns are unstable c-spine injuries.

A Clay-shoveler’s fracture, which is an avulsion of the spinous process of C6 or C7, is considered a stable cervical spine fracture. Other stable injuries include a unilateral facet dislocation and a type I odontoid fracture in which the tip of the odontoid is broken off is usually a stable cervical spine injury. This injury got its name from clay shovelers who were shoveling heavy clay that caused them to abruptly flex their neck while contracting their lower neck muscles. Now, most cases are due to direct trauma to the posterior neck.

Midline posterior bony cervical-spine tenderness is present if the patient reports pain on palpation of the posterior midline neck from the nuchal ridge to the prominence of the first thoracic vertebra, or if pain can be elicited with direct palpation of any cervical spinal process. Patients are considered intoxicated if any of the following is present: a recent history provided by the patient or an observer of intoxication or ingestion of an intoxicating substance, evidence of intoxication on physical exam (e.g., slurred speech, ataxia, dysmetria, or other cerebellar findings), or any behavior consistent with intoxication. Patients may also be considered intoxicated if tests of bodily fluids are positive for alcohol or drugs that affect the level of alertness. An altered level of consciousness can include any of the following: a GCS of 14 or less; disorientation to person, place, time, or events; an inability to remember three objects at five minutes; or a delayed or inappropriate response to external stimuli. A focal neurologic deficit is defined by any neurologic finding on motor or sensory exam. No precise definition of painful or distracting injury is possible. Determination of this is left to the treating clinician.Therefore, only the 64-year-old man with no posterior midline cervical spine tenderness nor pain when he turns his head to the left can be clinically cleared.

A 22-year-old man with no posterior midline cervical spine tenderness and the odor of alcohol on his breath (A), a 32-year-old man with no posterior midline cervical spine tenderness with a GCS of 14 (B) and an 18-year-old woman with no posterior midline cervical spine tenderness and mild numbness to her right arm (D) do not meet NEXUS criteria and require imaging.

What 3 components of the Canadian cervical spine rules are not present in the NEXUS cervical spine rules? Age, mechanism, neck rotational

A pulmonary contusion occurs most commonly from blunt trauma and is the result of a direct bruise to the lung parenchyma followed by alveolar edema and hemorrhage. Although the initial radiographic findings (patchy, irregular to dense pulmonary infiltrates over the injured area) may be non-diagnostic and initial measurements of gaseous exchange may be normal, pulmonary function may be compromised over the ensuing few hours. Subsequent radiographs taken over several hours may demonstrate irregular opacification of the pulmonary parenchyma in a non-lobular pattern. Chest CT scans may demonstrate a contusion. Uncomplicated pulmonary contusions typically develop over the first 24 hours and resolve in approximately one week. Patients with severe pulmonary contusions experience difficulty breathing and hypoxia. Repeat chest radiographs show an increasing opacity in the affected lung fields. The condition is exacerbated if extensive crystalloid fluid resuscitation has been performed. Blood gas evaluation reveals an increased a-A gradient. Treatment is initially supplemental oxygen administration to reverse hypoxia; however, subsequent intubation and ventilation with positive end-expiratory pressure may be required. Other adjunctive therapies include pulmonary toilet and analgesia.

Lung Contusion

Air within the pleural cavity (A), or pneumothorax, is part of the differential diagnosis for this patient but is less likely to occur than a pulmonary contusion with a blunt trauma mechanism. Pulmonary contusions tend to worsen over time (B) and the patient’s initial presentation can change rapidly as there is an increase in alveolar edema and hemorrhage. Lung involvement is usually localized to a segment or a lobe (D). Adult respiratory distress syndrome (ARDS) is associated with diffuse lung involvement.

This xray shows a Jefferson fracture, or a C1 burst fracture. These fractures occur with axial loading with vertical compression, an injury pattern that is common when a football player spears another player. When looking at the odontoid view of a c-spine film, the lateral masses of C1 shoulder align with the lateral parts of the C2 vertebral body. A Hangman’s fracture, or bilateral C2 pedicle fracture is best seen on a lateral view and shows C2 displaced anteriorly on C3. Odontoid fractures involve the odontoid process and are graded type I through type III depending on position.  Type II and III are both unstable fractures. Bilateral facet dislocation fractures are seen on lateral xrays of the c-spine and is characterized by anterior displacement greater than 50% diameter of vertebral body.

The correct answer is that this injury is associated with anterior cord syndrome. This patient has a flexion teardrop injury at C5 (note the wedge shaped fracture at the base of the vertebral body).  This is generally caused by extreme flexion and axial load, classically a diving injury. There is failure of the anterior column, often middle column, and disruption of the posterior ligamentous complex and the significant potential for cord injury from retropulsion of a fragment as a result.

The patient has an epidural hematoma. Epidural hematomas result from blunt trauma to the temporal or temporoparietal area with skull fracture and disruption of the middle meningeal artery. Blood pools in the potential space between the skull and dura mater, leading to a classic biconvex-appearing hematoma. Patients classically present with an initial loss of consciousness followed by a “lucid interval” and subsequent rapid neurologic decline as mass effect and herniation develops. Treatment is surgical evacuation of the hematoma.

The patient presents with minor head trauma and complaints consistent with a concussion and should have neurology follow up arranged. A concussion is a minor traumatic brain injury (TBI) that is often seen in MVCs and collision sports (football, hockey). It is typically caused by a rotational injury or an acceleration-deceleration injury. Patients will present with a number of non-specific symptoms including headaches, dizziness, confusion, amnesia, difficulty concentrating, and blurry vision but do not have focal neurologic findings. Despite the absence of severe intracranial injury, patients can have chronic and debilitating symptoms from concussions. Neurology referral is recommended, as patients should have functional testing and tracking of their symptoms for resolution. It is vital to council patients to avoid contact sports or activities that increased the risk of recurrent injury as these patients are at risk for more severe injury with second impact.

Odontoid (dens) fractures are classified as Type I, II and III. Type I fractures are stable avulsion injuries to the tip of the odontoid. This patient has a Type II fracture, which is a fracture at the junction of the odontoid and body of C2. A Type III fracture is a fracture at the base of the the dens. Both Type II and III fractures are unstable because of ligamentous attachments. A bilateral C2 pedicle fracture is also known as a Hangman’s fracture and is seen on lateral xray as C2 being displaced anteriorly on C3. A teardrop fracture is an avulsion fracture of the anteroinferior portion of the vertebral body. Both of the former fractures patterns are unstable c-spine injuries.

This patient has sustained a Zone II neck injury. He is demonstrating signs of impending airway obstruction with an expanding anterior neck hematoma, dysphagia, and dysphonia. The primary focus in the care of this patient and any other patient presenting following a traumatic injury should be the ABCs. This particular patient should be intubated right away: he is at risk for rapid deterioration and respiratory failure. Indications for establishing a definitive airway in the setting of penetrating neck trauma include respiratory distress, altered mental status, bloody secretions in the oropharynx, subcutaneous emphysema, expanding hematoma, and tracheal shift. Other signs of potential airway compromise include dysphagia and dysphonia. Orotracheal intubation is preferred in penetrating neck injury, but backup airway techniques should be available. If quickly available, awake fiberoptic intubation may be considered.

The patient’s presentation is critical. As soon as the airway is established, he should be transported immediately to the OR. Performing angiography would inappropriately delay management. All symptomatic patients with penetrating injuries to Zone II require surgical exploration.

Again, sending the patient for a CT scan would delay appropriate management. Additionally, CT is more appropriate in the evaluation of blunt trauma.

Cricothyrotomy should be avoided when an anterior neck hematoma is present. If the patient were more stable on arrival, intubation could be delayed until the patient reached the OR.

The treatment and amelioration of increased intracranial pressure (ICP) is one of the most important steps in the management of the multiple trauma patient. Mannitol is very effective, with a slightly delayed effect on the oncotic forces at work within the cranial cavity. Indicated in patients with impending herniation or evidence of increased ICP from trauma, mannitol is given as a bolus to lower ICP via osmotic diuresis and increase plasma expansion. A continuous mannitol drip can increase the chance of hypovolemia and is thus not recommended.

Hyperventilation after intubation has been used as a rapid intervention to lower ICP. It can be used for impending herniation or as a lifesaving therapeutic measure. But more recent studies indicate that patients with traumatic brain injury have a worse prognosis if hyperventilation is used in any prolonged manner, and that it should be avoided especially in the first 24 hours.

Neuromuscular paralysis is part of the process of rapid sequence intubation, but it does not in itself contribute to reduction of ICP. Successful intubation to manually control the patient’s respiratory rate and ventilation volume is made more successful with the use of neuromuscular blockers. Complete paralysis allows mechanical hyperventilation while the patient is on the ventilator.

The value of steroids in the care of patients with increased ICP from other processes, including cancer, is debatable. Several large studies have shown that steroids are not effective in treating patients with traumatic brain injury.

A. Admission to the hospital
This patient is presenting with a basilar skull fracture, evidenced by the CSF fluid coming from his ear. Recommendations are that all of these patients should be admitted to the hospital for monitoring. A recent cochrane review found no evidence that routine antibiotics were indicated for CSF leaks in these patients however. Source: Ratilal BO, Costa J, Pappamikail L, Sampaio C, Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures. Cochrane Database Syst Rev. 2015;4:CD004884. PMID: 25918919

B. Admission and systemic antibiotic therapy
While this patient should be admitted for his basilar skull fracture, antibiotics are not indicated. A recent cochrane review found no evidence that routine antibiotics were indicated for CSF leaks in these patients however. Source: Ratilal BO, Costa J, Pappamikail L, Sampaio C, Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures. Cochrane Database Syst Rev. 2015;4:CD004884. PMID: 25918919

C. Admission and systemic steroids
While this patient should be admitted for his basilar skull fracture, steroids are not indicated

D. Discharge with oral antibiotics
This has a basilar skull fracture and CSF leak, and should be admitted for monitoring.

Complex facial fractures may be classified into the Le Fort system of fracture patterns. Three types exist. Type I Le Fort fractures are transverse fractures through the base of the maxilla and often involve the roots of the teeth. It may be unilateral and bilateral. The upper teeth may be grasped and rocked independent of the midface, indicating discontinuity with the maxilla. Type II Le Fort fractures are often bilateral and are characterized by pyramidal fractures that extend through the body of maxilla, orbital floor, nasal bones, hard palate, and lacrimal bones. The nasal unit and maxilla may be grasped and move as a unit relative to the orbital complexes and lower face. Type III Le Fort fractures are considered complete craniofacial disjunction as the fracture extends from the nasal bridge traveling posteriorly along the ethmoid bone, which comprises the medial orbital wall, and continues through the inferior and lateral orbital walls and frontozygomatic suture. The sphenoid bone is often involved with type III fractures, and cerebrospinal fluid (CSF) leak may occur. CSF may also leak from involvement of the cribriform plate of the ethmoid bones. Le Fort fractures are best seen with computed tomography. Depending on the extent of the injury, Le Fort fractures often require management of a multidisciplinary team and may necessitate consultation to otolaryngology, plastic and reconstructive surgery, dentistry and neurosurgery if a CSF leak is present.

A type II Le Fort fracture involves the central maxilla (A), nasal bridge, lacrimal bones, hard palate (C), and orbital floor. It often occurs bilaterally and in a pyramidal pattern. Fractures of the mandibular condyle (D) are not included in the Le Fort classification of midface fractures.

Bedside intraocular ultrasound performed by an emergency physician is a very useful tool for rapidly diagnosing many intraocular conditions. Dislocated lens, foreign body, and detached retina can be identified by ultrasound. It has not been demonstrated as useful in the diagnosis of orbital compartment syndrome caused by a retrobulbar hemorrhage.

Heat emergencies represent a continuum of disorders that range in severity from heat cramps to heat exhaustion to life-threatening heat stroke. In most circumstances, heat emergencies can be avoided through common sense, public education, and prevention. People most at risk for heat injuries include athletes, military personnel, and laborers who work outdoors in the heat. Classic heat injury, as is the case with this patient, usually occurs during periods of high environmental heat stress. Physical exertion is not required if environmental temperatures and humidity create a situation where heat gain overwhelms native heat losses. Exertional heat injury usually affects individuals who are participating in athletic events in conditions of high heat stress. Clinical features are what determine the severity of heat illness. This patient is presenting with symptoms characteristic of heat exhaustion. Other symptoms can include muscle cramps, headache, and vomiting. On physical examination of patients with heat exhaustion, the temperature may be normal or elevated. However, patients with heat exhaustion will not have mental status changes. Mental status changes are a sign of heat stroke which can be life-threatening.

Dry skin, or anhidrosis (A), can classically be found in patients with heat stroke but this is not a requirement for the diagnosis since patients with severe heat illness can also present with diaphoresis. Heat exhaustion is characterized by the inability to maintain adequate cardiac output due to strenuous exercise and environmental heat stress. Acute dehydration may be present. Athletes with heat exhaustion have difficulty continuing with exercise. Other signs of heat exhaustion include hypotension (B), syncope, and tachycardia (D). The presence of these factors does not necessarily portend severe complications from the illness. Severe heat illness, heat stroke, presents with neurological symptoms such as hallucinations, seizure, mental status changes, or coma.

The class Arachnida contains the largest number of venomous species known, but most are not harmful to humans. Humans fear spiders and scorpions, but of this class of species ticks probably cause the greatest morbidity. One of the more venomous spiders known is the black widow spider or Latrodectus species. They are found throughout the United States, except Alaska. Symptoms of a black widow spider bite include a pinprick sensation followed by local redness and swelling, but sometimes the bite is not felt. Over the next hour, patients develop dull cramping in the area of the bite that eventually spreads to the entire body. Pain is centered in the chest in patients who suffer an upper extremity bite, and pain is centered in the abdomen in patients who suffer a lower extremity bite. The abdomen may become boardlike and can mimic pancreatitis, appendicitis, or a perforated peptic ulcer. Signs and symptoms usually abate within a few hours and definitely resolve in two to three days. Management is supportive with benzodiazepine treatment for muscle spasms.

Symptoms of a brown recluse spider (B) bite include local burning pain at the site of the bite. After a few hours, a bleb forms in the center of the bite with a surrounding erythematous ring. The area can look like a target sign or a bull’s eye. Over the next few days, the bleb darkens and begins to necrose with eventual involvement of the underlying subcutaneous fat along with the skin. Systemic symptoms such as fever, malaise, vomiting, and rash can develop and lead to shock in severe cases, although fatalities are rare. This patient does not have a bite characteristic of a brown recluse spider. A scorpion (C) sting is characterized by immediate pain at the site of the sting. Over some time, patients can develop numbness and weakness locally and will have heightened sensitivity in the sting area. Systemic symptoms such as restlessness, vomiting, muscle spasms, nystagmus, and myoclonus can develop in severe cases but are more rare. Scorpion sting symptoms can mimic those found in patients with black widow spider bites but are much less common. Most tarantulas (D) are nontoxic. They are unusual in that their abdominal hairs can be thrown and embedded in human skin, leading to allergic reactions. There is not a toxic bite. The patient in this question is not presenting with allergic reaction symptoms.

Decompression sickness occurs due to the liberation of gas bubbles associated with a decrease in ambient pressure. This can occur in divers breathing compressed air as well as high altitude pilots or astronauts. The gas bubbles likely obstruct blood flow, leading to direct tissue ischemia. They also activate a variety of inflammatory processes, leading to thrombosis and capillary leaking. Symptoms of decompression sickness typically occur minutes to hours after surfacing. Decompression sickness can include pain syndromes involving the joints (“the bends”) as well as more serious manifestations including pulmonary (“the chokes”), cardiovascular, and neurologic symptoms (“the staggers”). Treatment of decompression sickness is similar to the treatment of an arterial air embolism and includes administration of oxygen, increasing tissue perfusion with intravenous fluids, and rapid decompression with hyperbaric oxygen.

Arterial air embolism (A) is an example of a barotrauma of ascent and results from entry of air into the arterial system with resultant embolization. The brain is the most commonly affected organ. Arterial air embolism should be suspected in any diver with loss of consciousness upon surfacing. Inner ear barotrauma (C) is an example of barotrauma of rapid descent or ascent and results from rupture of the round window or tearing of the vestibular membrane due to a forceful Valsalva maneuver done during descent to clear the ears. Symptoms include vertigo (as seen in the patient above) but this condition is easily differentiated from decompression sickness due to the onset of symptoms during descent rather than after surfacing. Nitrogen narcosis (D) occurs with deep dives and includes symptoms such as loss of fine motor skills and higher-order brain functions, resulting in bizarre and dangerous behavior. Presentation is similar to alcohol intoxication.

Atrial fibrillation in hypothermia tends to be relatively benign and resolves spontaneously with rewarming. Persistent atrial fibrillation after complete rewarming is unlikely to be due to hypothermia and may suggest an underlying medical pathology. Cardioversion increases the risk of ventricular fibrillation and is contraindicated unless the patient is unstable. Anticoagulation for temporary atrial fibrillation is not indicated and could worsen the coagulopathy already present in hypothermia.

This patient presents with rhabdomyolysis after an electrical injury and should be treated with aggressive intravenous hydration. Electrical injuries are common and are the cause of about 5% of burn unit admissions and 6% of occupational fatalities. The extent of the injury is related to the type of circuit (alternating current (AC) versus direct current (DC)), the resistance, amperage, duration of contact and voltage. The initial exposure to electricity can cause severe burns spreading from the point of impact. Additionally, the energy from the shock is transmitted into the body and can cause significant muscle breakdown. Breakdown is increased if the patient experiences tetany or prolonged exposure to the electrical source. The classic finding of rhabdomyolysis is a urine dip that is positive for blood with only scant or no RBCs on microscopy. The urine dipstick falsely reports myoglobin as hemoglobin in this case. A serum creatinine kinase level should be obtained. Initial treatment is with aggressive fluid resuscitation to maintain urinary output as myoglobin accumulation can lead to renal failure. Electrolyte abnormalities (specifically hyperkalemia from cellular breakdown) should be closely monitored and treated as well.

A CT scan of the abdomen (A) is not necessary to look for a bleeding source. Intravenous antibiotics (B) are not necessary as this urinalysis does not indicate the presence of infection. Packed red blood cells (D) are not needed at this time as the patient does not exhibit signs of bleeding.

The partial pressure of oxygen decreases as barometric pressure decreases at altitude. At 8,000 feet or greater above sea level, the environment becomes hypoxic and high-altitude syndromes can occur due to hypoxia. These include acute mountain sickness (AMS), high-altitude pulmonary edema, high-altitude cerebral edema, retinopathy, and certain neurologic syndromes. High-altitude cerebral edema (HACE) is the most severe form of acute mountain sickness. At altitude, cerebral vasodilation occurs and leads to increased blood flow and blood volume. This is due to a leaky blood-brain barrier either from lack of autonomic autoregulation or increased vascular permeability, or a combination of the two. HACE is characterized by progressive global cerebral dysfunction and causes confusion, altered mental status, and ataxia. Ataxia is a cardinal and early sign of HACE, and all patients with acute mountain sickness should be monitored for ataxia. Other features, such as headache, nausea, or vomiting, may be absent. Retinal hemorrhages are also common, and cranial nerve palsies of the third and sixth cranial nerves may occur due to increased intracranial pressure. Concomitant pulmonary edema is common. Death from HACE is due to brainstem herniation, so early identification and management are critical. The highest priority is descent. If this is not possible, temporizing measures (though often unavailable) include supplemental oxygen, corticosteroids, and use of a portable hyperbaric oxygen chamber. Computed tomography of the head may demonstrate white matter hyperattenuation more than gray matter with effacement of the sulci and flattening of the gyri.

This patient presents with signs and symptoms consistent with a left middle cerebral artery stroke as well as subcutaneous emphysema that developed during ascent from diving. Any focal neurologic deficit that results during ascent or immediately thereafter should be considered a cerebral arterial air embolism until proven otherwise. Rapid uncontrolled ascent against a closed glottis causes the volume of gas in the lungs to expand according to Boyle’s law (pressure and volume of a gas are inversely related at a constant temperature). As this gas expands, it can lead to pulmonary barotrauma, including pneumothorax, pneumomediastinum, (as indicated by this patient’s subcutaneous emphysema on exam), and alveolar rupture. Alveolar rupture leads to gas leakage into the pulmonary veins, which can then move into the systemic circulation and lodge in distal arterioles as arterial gas emboli. Cerebral gas embolism presents with typical stroke symptoms and is one of the most serious complications of pulmonary barotrauma. Air embolization can be prevented by exhaling during ascent, which prevents the rapid expansion of volume within the lungs as pressure decreases. Treatment includes fluid resuscitation and rapid recompression with 100% hyperbaric oxygen. Hyperbaric oxygen works by decreasing the size of the air embolism as well as easing washout of other gases by increasing the diffusion gradient for nitrogen from the air embolism to plasma.

Barotitis (B), or ear barotrauma, is the most common diving disorder and results from unequalized increasing pressure on the tympanic membrane on descent. Symptoms include unilateral ear pain and fullness, as well as vertigo and disorientation from rupture of the tympanic membrane and uneven caloric stimulation of the middle ear. Treatment is conservative. Decompression syndrome (C), or “the bends,” usually occurs within six hours after ascent. It results from the expansion of inert gas that dissolved in tissues during descent. As the pressure of these inert gases exceeds atmospheric pressure, it can exit tissue in the form of bubbles, which often lodge in veins, leading to localized venous obstruction and inflammatory cascades. Patients either present with significant pain (type I) or ascending paresthesias or paralysis (type II). Treatment is the same as for arterial gas embolization. Nitrogen narcosis (D) results from the increased partial pressure of nitrogen in CNS tissue and therefore occurs at significant depth. Symptoms are similar to alcohol intoxication and include altered coordination and impaired judgment.

The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc.

Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (C) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

Hepatic injury, as denoted by aspartate aminotransferase 2100 U/L, alanine aminotransferase 1900 U/L, is so extremely common in heat stroke that its absence should push one to reconsider the diagnosis. The hallmarks of heat stroke include severe hyperthermia (> 40.5oC) and neurologic dysfunction. Neurologic dysfunction occurs due to a progressive increase in heat stores because of the body’s decreasing ability to perfuse the distal extremities. As the heat stores increase, intracranial pressure increases with a subsequent decrease in cerebral blood flow. There are two types of heat stroke, each with their own patient population and clinical presentation. Classic heatstroke is due to exogenous heat production, while exertional heatstroke is due to endogenous heat production. Patients with classic heat stroke are commonly elderly with chronic diseases or those with limited access to shelter against the heat or oral hydration that present with symptoms usually in the setting of a prolonged, severe heat wave. Patients with exertional heat stroke are commonly young, athletes, or military personnel that present with symptoms after strenuous exercise in the heat. Classic heat stroke patients are usually anhidrotic, while those with exertional heat stroke tend to present diaphoretic. Diagnosis is primarily clinical, though laboratory testing should always be performed, as end-organ damage is common and can help further differentiate the types of heat stroke. Classic heat stroke tends to cause respiratory alkalosis, mild coagulopathies, mild creatinine kinase elevations, and elevated troponin. It is more common to see lactic acidosis, disseminated intravascular coagulation, rhabdomyolysis, and hypoglycemia in those with exertional heat stroke. With a mortality rate of 21–63%, treatment must be immediate and aggressive. Cooling is the mainstay of treatment with the primary goal to maximize evaporative cooling and prevent heat-generating shivering. Antipyretics are not useful in cooling, as they counteract hypothalamic-mediated hyperthermia and not environmental hyperthermia. Alongside cooling, immediate supportive treatment with intravenous fluids, supplemental oxygen, and reversal of coagulopathies should be started.

Acute kidney injury, as denoted by blood urea nitrogen 30 mg/dL, creatinine 1.5 mg/dL (B), and elevated troponin 0.8 ng/mL (D) can occur in classic heat stroke but are rare in exertional heat stroke. Rhabdomyolysis, as denoted by creatinine kinase 2500 U/L (C), is common in exertional heat stroke and less so in classic heat stroke. While each of these laboratory findings is possible in heat stroke, hepatic damage is still the most common finding.