15 A 71‐year‐old patient has acute, non‐perforated appendicitis. His BMI is 27 and otherwise healthy. Intra‐operatively you begin with Veress needle insertion into the abdomen and begin to establish pneumoperitoneum with high flow rates. Your anesthesiologist immediately notes a marked decrease in the patient’s end‐tidal carbon dioxide and oxygen saturations as well as new onset tachycardia. You halt insufflation but the patient quickly becomes hemodynamically unstable. What is your best step to address the underlying pathology?Convert to open.Place the patient in steep Trendelenburg and place a central line for therapeutic intervention.Administer fluid bolus.Start vasopressors.Abort the procedure and transfer the patient to the ICU.This patient is demonstrating evidence of possible air embolism secondary to intravascular insufflation. The primary goal in this case is to prevent further gas entry into the venous system and reduce the amount of gas trapped in the heart. Placing the patient in Trendelenburg position maximizes blood flow to the brain and theoretically relieves right‐sided heart airlock as well as prevent gas entry into the pulmonary artery. In a patient who is hemodynamically unstable secondary to an air embolism, a central line should be placed into the right atrium and attempts made to withdraw air from the right side of the heart. Converting to open would not address the underlying issue (choice A). Initiating fluids or vasopressors would briefly temporize the patient but would not address the underlying pathology (choices C, D). Aborting the procedure and taking a hemodynamically unstable patient to the ICU would not be correct as the underlying pathology should be addressed prior to leaving the operating room (choice E).Answer: BSandadi S, Johannigman JA, Wong VL et al. Recognition and management of major vessel injury during laparoscopy. J Minim Invasive Gynecol. 2010; 17 (6): 692–702. doi: https://doi.org/10.1016/j.jmig.2010.06.005. Epub 2010 Jul 24. PMID: 20656569.
16 A 32‐year‐old healthy man was passed out in a workplace fire but had minimal burns to the right hand. Given suspected inhalation injury, you take care to establish a definitive airway and transfer the patient to the ICU for additional monitoring. The patient is initially tachycardic and hypertensive but shortly thereafter develops bradycardia, hypotension, and cardiac dysrhythmias. On physical examination, his skin appears flushed with a cherry‐red color. Labwork reveals a marked metabolic acidosis on arterial blood gas and serum lactate is 9 mmol/L. His carboxyhemoglobin level is normal. Which of the following would be most effective in addressing his underlying pathology? Aggressive fluid resuscitationAdministration of hydroxocobalaminVasopressor supportDiuresisContinue supportive careThis patient is showing evidence of possible cyanide poisoning with evidence of cardiovascular instability, marked metabolic acidosis, and classic “cherry‐red” skin color. Although present in only a minority of patients, this finding is a result of impaired tissue oxygen utilization, resulting in high venous oxyhemoglobin concentration, and bright red appearance of the blood. Hydroxocobalamin is a precursor of Vitamin B12 that directly binds to intra‐cellular cyanide, forming cyanocobalamin. This molecule is then readily excreted in the urine. This treatment acts rapidly, does not affect tissue oxygenation, and is relatively safe, making it a first‐line agent for cyanide poisoning. The other answer questions do not address what is driving the patient’s underlying pathology.Answer: BHendry‐Hofer TB, Ng PC, Witeof AE et al. A review on ingested cyanide: risks, clinical presentation, diagnostics, and treatment challenges. J Med Toxicol. 2019; 15: 128.
17 A 37‐year‐old patient is admitted to the floor after suffering a femur fracture during a MVC. While he is stable over the next 24 hours, he shortly thereafter develops a new petechial rash on the non‐dependent portions of his body, becomes hypotensive, confused, tachypneic, and is hypoxic on pulse oximetry. A chest x‐ray is obtained but appears normal. A CT angiogram of the chest does not demonstrate any evidence of pulmonary thromboembolism. What would be the next step in management?Supportive care with fluid resuscitation and oxygenationIntravascular tPA lytic therapyBroad‐spectrum antibioticsVasopressorsECMOThis patient is showing evidence of possible fat‐embolism syndrome. This is a rare entity that can be encountered in patients 24–72 hours after an initial insult (long bone fracture in this patient). The triad of hypoxemia, neurologic abnormalities, and petechial rash is classic for fat‐embolism syndrome, though non‐specific. Fat embolism can also present with thrombocytopenia and this may help make a diagnosis. However, it remains a diagnosis of exclusion, primarily made clinically. Initial assessment is performed to exclude alternative diagnoses such as pulmonary embolism. There is no definitive treatment and therapy is primarily supportive while awaiting resolution. There is no role for intravascular lytic therapy or broad‐spectrum antibiotics (choices B, C). While vasopressors and invasive ventilator support such as ECMO may be necessary in patients with refractory shock, they are not the initial step in management (choices D, E).Answer: AStein PD, Yaekoub AY, Matta F et al. Fat embolism syndrome. Am J Med Sci. 2008; 336: 472.
18 A 54‐year‐old patient with a history of diabetes mellitus on home metformin presents to your emergency department with shortness of breath, productive cough, and fever. On imaging, he is found to have a right lower lobe opacity consistent with pneumonia. He is hemodynamically stable but blood work is noted to have a lactic acidemia of 4 and his glucose is elevated to 300. His CBC is within normal limits and an EKG is normal. He is mentating well, making appropriate urine without evidence of tissue hypoperfusion. What best describes the patient’s lactic academia?Type A lactic acidosisType B lactic acidosisSeptic shockHemorrhagic shockCardiac failureThis patient is showing evidence of lactic acidosis in the absence of systemic hypoperfusion. Type A lactic acidosis is typically related to hypoperfusion secondary to hypovolemia, cardiac failure, sepsis, or cardiopulmonary arrest. Type B lactic acidosis occurs when there is no evidence of systemic hypoperfusion and may be related to impaired cellular metabolism (choice B). Both metformin use and diabetes mellitus have been implicated as associated with Type B lactic acidosis. This patient is showing no signs of septic, hemorrhagic, or cardiogenic shock (choices C, D, E).Answer: B
3 ECMO
Mauer Biscotti III, MD1, Matthew A. Goldshore, MD, PhD, MPH2, and Jeremy W. Cannon, MD, SM3,4
1 Division of General Surgery, Department of Surgery, San Antonio Military Medical Center, San Antonio, TX, USA
2 Department of Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA
3 Division of Traumatology, Surgical Critical Care & Emergency Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA
4 Department of Surgery, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
1 A 45‐year‐old previously healthy man was a pedestrian struck by a motor vehicle resulting in multiple injuries including traumatic brain injury with a subarachnoid hemorrhage (SAH), multiple rib fractures, pulmonary contusion, hemothorax, splenic laceration, and a pelvic fracture. On postinjury day 5, he developed severe hypoxemic respiratory failure (PaO2:FiO2 ratio of 70 on FiO2 of 1) and was diagnosed with an MRSA pneumonia. Workup for other causes of respiratory failure or sepsis was negative, and there was no evidence of SAH progression or torso hemorrhage on his most recent imaging. Which