Hydrofluoric acid is a chemical known to cause chemical burns. It is commonly used in glass etching. Common hydrofluoric acid burns include dermal exposures, inhalation exposures, gastrointestinal exposures, and ophthalmic exposures. The higher the concentration of hydrofluoric acid and the body surface area and exposure all determine the cause of toxicity, which can be life-threatening. When hydrofluoric acid is exposed to tissue it will dissociate and bind to calcium and magnesium, leading to hypocalcemia, hypomagnesemia, and hyperkalemia, which can in turn cause cardiotoxicity manifesting with dysrhythmias, including VFib, VTach, or torsades de pointes (polymorphic VTach). Treatment depends on the types of exposure and includes calcium gluconate gel or intradermal calcium gluconate injection (dermal injuries) or intraarterial calcium gluconate (dermal injuries), NG tube drainage and oral or NG tube calcium and magnesium (GI exposures), nebulized calcium gluconate (inhalation), and eye irrigation with calcium eye drops (ophthalmic exposures).

This chapter covers the diverse immunophenotype associated with AML with KMT2A rearrangement. Immunophenotypic shift and lineage switch are relatively common in this subtype of AML. For differential diagnosis, the distinction between cases with an APL (acute promyelocytic leukemia)-like immunophenotype and APL cases is highlighted.

This is a case of HUS in a child following an episode of diarrhea. It highlights the recognition, management, and likely good outcome of HUS in children.

This emergency medicine case explores the evaluation and management of a patient presenting with the chief complaint of dizziness with the background of relying on an implanted pacemaker.

The chapter describes a case of a 25-year-old female with abdominal pain and vaginal bleeding. The patient is anxious and uncomfortable due to pain and has soaked through five pads since this morning. She has a history of bilateral tubal ligation and has been sexually active with her husband without using any protection. The primary survey shows pale and cool skin and normal capillary refill. The patient undergoes several tests, including CBC, BMP, PT/PTT, type and screen, and UA, and receives a crystalloid 1 L bolus IV. The transvaginal US confirms the diagnosis of a ruptured ectopic pregnancy, and the patient is taken to the OR for laparotomy. The chapter highlights the importance of early actions, including confirmatory pregnancy testing with beta hCG, resuscitation of hypotensive patients with crystalloid or blood products, and early consultation of obstetrics in patients with a high pre-test probability of ectopic pregnancy or any abnormal findings on bedside examination. It also provides several pearls related to ectopic pregnancy diagnosis and management.

This chapter describes a case of a 59-year-old obese male with sudden-onset chest pressure radiating down his left arm, associated nausea, and diaphoresis. The patient was diagnosed with anterolateral myocardial infarction and was treated with aspirin, nitroglycerin, and morphine for pain control. The chapter emphasizes the importance of recognizing the symptoms of a heart attack and activating the cardiac catheterization lab as rapidly as possible to open the blocked artery. The chapter also provides guidelines for diagnostic tests and highlights the significance of the circumflex artery in lateral wall ischemia. The chapter concludes by emphasizing the use of thrombolytic therapy in hospitals without ready access to coronary angioplasty.

Spinal cord injuries can result from various traumas, including diving accidents. Neurogenic shock, as a sequelae of spinal cord injuries, requires rapid recognition and intervention to prevent further deterioration and organ injury. High cervical spine injuries can affect respiration. This case reflects a patient found after a diving accident with cervical spine fracture and spinal cord injury. The case progresses with the need for rapid assessment of various causes of shock in trauma and appropriate treatment of neurogenic shock once other causes have been assessed and deemed unlikely. The case also considers high cervical spine injuries affecting diaphragm and respiration, requiring definitely airway management and intubation.

This chapter provides guidance on how to effectively use the book as a case-based approach to learning emergency medicine, particularly in preparation for the certifying exam. It emphasizes the importance of active learning and offers strategies for working with a partner or alone to engage with the cases. The section on certifying exam preparation highlights the value of practicing cases with a partner, such as an emergency physician, and provides examiner instructions for guiding candidates through the cases. The chapter also encourages readers to supplement their learning by referencing standard emergency medicine texts and engaging in further discussions with colleagues and mentors. A sample case script is provided to demonstrate how the book can be utilized in a practical exam setting.

Carotid artery dissection is caused by tearing of the wall of the internal carotid artery that leads to transient ischemic attack (TIA) or stroke symptoms. Cervical artery dissection (carotid artery and vertebral artery) is rare overall, but a common cause (10−25% of cases) of stroke in patients under 50 years old. Dissection can occur spontaneously or secondary to neck trauma. Patients with internal carotid artery dissection often present with unilateral headache, face pain, or neck pain hours to days before developing neurologic deficits. Neurologic signs and symptoms of carotid artery dissection can include transient monocular blindness, cranial nerve palsies, or partial Horner syndrome. Vertebral artery dissection often presents with occipital headache and posterior neck pain preceding neurologic symptoms consistent with brainstem TIA or stroke. If not treated, carotid artery dissection can progress to MCA territory stroke. Vertebral artery dissection can progress to a posterior circulation stroke. If the dissection is extracranial, then treatment involves anticoagulation to prevent thrombolic events. Do not start anticoagulation if the dissection is intracranial as this can lead to a subarachnoid hemorrhage. In that case, an antiplatelet agent should be started. Subarachnoid hemorrhage must be ruled out prior to starting anticoagulation.

This is a case of a ventricular tachycardia, likely from myocardial ischemia or infarction. Ventricular tachycardia is a life-threatening irregularity of the heart’s conduction system, which is often caused by reduced blood flow to the heart. The patient’s symptoms of palpitations, nausea, and dizziness occurred spontaneously, awaking him from sleep. Important early actions include obtaining a 12-lead EKG and administering an antiarrhythmic medication. This patient’s ventricular tachycardia is refractory to drug therapy and will persist regardless of treatment. Eventually, the patient becomes unstable, with chest pain, altered mental status, and hypotension. Without synchronized cardioversion at this point, the patient will become pulseless. After cardioversion, the patient will convert into normal sinus rhythm with a 12-lead EKG concerning for myocardial ischemia.