Surgical Critical Care and Emergency Surgery. Группа авторов
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15 A 26‐year‐old man is admitted to the surgical intensive care unit after an automobile struck his motorcycle. He is hemodynamically stable and found to have a grade 3 splenic laceration with no active extravasation and a left, displaced, mid‐shaft fracture of the humerus. The fracture was reduced and leg placed in traction while he is being observed for his splenic laceration. Suddenly he becomes confused with progressive shortness of breath and hypoxia requiring intubation. A chest X‐ray demonstrates diffuse bilateral infiltrates. Labs reveal a platelet count is 75 000/mm 3 , prothrombin time of 19 second, partial thromboplastin time of 50 second, oozing is noted from intravenous access sites, and blood is suctioned from his endotracheal tube. Which of the following test results would be consistent with the diagnosis of disseminated intravascular coagulation?Increased antithrombin levelElevated fibrin degradation productsDecreased bleeding timeElevated fibrinogen levelDecreased D‐dimerDisseminated intravascular coagulation (DIC) is characterized by widespread microvascular thrombosis with activation of the coagulation system and impaired protein synthesis, leading to exhaustion of clotting factors and platelets. The end result is organ failure and profuse bleeding from various sites. DIC is always associated with an underlying condition that triggers diffuse activation of coagulation, most commonly sepsis, trauma with soft tissue injury, head injury, fat embolism, cancer, amniotic fluid embolism, toxins, immunologic disorders, or transfusion reaction. In this case, the patient appears to meet criteria for fat embolism syndrome which likely triggered his DIC. There is no single laboratory test that can confirm or rule out a diagnosis of DIC. A combination of tests in a patient with an appropriate clinical condition can be used to make the diagnosis. Low platelet count, elevated fibrin degradation products or D‐dimer, prolonged prothrombin time, and low fibrinogen level are all consistent with a diagnosis of DIC.Answer: BLevi, M . (2007) Disseminated intravascular coagulation. Crit Care Med , 35 (9), 2191–2195.
16 A 61‐year‐old man is admitted to the surgical intensive care unit with a diagnosis of ischemic colitis. Subcutaneous injection of unfractionated heparin was started for venous thromboembolism prophylaxis, and he is monitored closely with serial abdominal examinations. On hospital day five, he noted acute onset of left lower extremity pain and is found to have absent pedal pulses in the affected limb. His platelet count is noted to have dropped from 250 000/mm 3 to 90 000/mm 3 , and his creatinine has increased from 1.2 mg/dL to 2.8 mg/dL. He is taken to the operating room where he underwent thrombectomy of a white appearing clot in the right superficial femoral artery. He is diagnosed with Heparin Induced Thrombocytopenia (HIT) and started on argatroban postoperatively. What is the mechanism of action of argatroban?Direct factor Xa inhibitorDirect factor IIa inhibitorIndirect factor IIa inhibitorBinds antithrombin IIIIndirect factor Xa inhibitorHIT is a life‐threatening disorder that occurs after exposure to unfractionated, or less commonly, low‐molecular‐weight heparin. HIT usually occurs after 5–10 days of heparin therapy and is caused by antibodies against the heparin‐platelet factor 4 complex. Thrombotic complications occur in 20–50% of patients. The thrombus associated with HIT has been described as “white clot” with predominantly fibrin platelet aggregates and few red blood cells. Thrombocytopenia is common in the critically ill, and diagnosis of HIT can be difficult. Delays in obtaining test results often mean that management decisions must be made on the basis of clinical suspicion. Clinical findings that imply a diagnosis HIT are:Platelet fall of more than 50% from baseline, with platelet nadir > 20 000. Profound thrombocytopenia suggests a cause other than HIT.Onset on day 5–10 of heparin exposure.Thrombosis, skin necrosis, or an anaphylactoid reaction after heparin bolus.No other cause for the thrombocytopenia is present.Treatment of HIT includes discontinuation of all sources of heparin and if anticoagulation is clinically warranted, use of a direct thrombin (factor IIa) inhibitor such as argatroban is recommended.Answer: BGreinacher, A. (2015) Heparin‐induced thrombocytopenia. N Eng J Med , 373 (3), 252–261.17
17 An 18‐year‐old man is undergoing an exploratory laparotomy and right groin exploration for a gunshot wound to the right hip. Injuries to the right common femoral vein, bladder, and sigmoid colon are noted. Massive blood loss was reported at the scene and the patient was found to be in hemorrhagic shock on arrival. He has received 12 units of packed red blood cells, 12 units of fresh frozen plasma, and 2 units of apheresis platelets while in the operating room. His vital signs are: blood pressure 100/60 mm Hg, heart rate 120 beats/min, temperature 34.8 °C. Laboratory studies: hemoglobin 8.5 g/dL, platelets 100 000/mm 3 , prothrombin time 14 second, partial thromboplastin time 40 second. pH 7.1. His femoral vein has been ligated, bladder injuries were repaired, and sigmoid colon was resected. What is the next most appropriate treatment for his ongoing bleeding?Transfuse platelets, create a stoma, and close the abdomen.Transfuse fresh frozen plasma, perform primary anastomosis, and close the abdomen.No transfusion required, create stoma, and close the abdomen.External warming, primary anastomosis, and close the abdomen.Leave in discontinuity, place temporary abdominal closure device, and admit to surgical intensive care unit for external rewarming.This patient is severely hypothermic and acidotic. Following surgical control of bleeding and massive resuscitation, ongoing aggressive resuscitation is required to reverse the “lethal triad” of coagulopathy, acidosis, and hypothermia. Damage control operation should be performed with prompt admission to surgical intensive care unit for resuscitation and rewarming. Clotting factor and platelet deficiencies have been addressed during this resuscitation by maintaining 1:1 component replacement. Hypothermia < 35 °C is a strong independent risk factor for mortality in trauma patients, with more severe hypothermia conveying greater risk of mortality. Hypothermia contributes to coagulopathy through platelet and clotting factor dysfunction. Recommended measures for rewarming a patient with low body temperature include forced air warming, infusion of warmed fluids, under‐body heating pads, radiant warmers, and humidified ventilation. If bleeding continues after aggressive warming and correction of clotting abnormalities, the patient must return to the operating room without further delay.Answer: EInaba, K., Teixeira, P., Rhee, P., et al. (2009) Mortality impact of hypothermia after cavitary explorations in trauma. World J Surg , 33 (4), 864–869.Perlman, R., Callum, J., Laflamme, C., et al. (2016) A recommended early goal‐directed management guideline for the prevention of hypothermia‐related transfusion, morbidity, and mortality in severely injured trauma patients. Crit Care , 20 (1), 1–11.
18 A 22‐year‐old man was involved in a drive by shooting. He is noted to have multiple gunshot wounds to his back, abdomen, and extremities. He has a distended abdomen that is diffusely tender. His blood pressure is 80/60 mm Hg. What fluid should be administered while preparing for emergent laparotomy?Lactated ringersHypertonic salinepositive bloodType‐specific bloodCrossmatched bloodThe described physical exam findings are consistent with hemoperitoneum resulting in hemorrhagic shock; therefore, the patient requires emergent resuscitation and operative hemorrhage control to avoid mortality. Crystalloid solution should be minimized and resuscitation with blood products should be initiated without delay. Type O positive blood is readily available in most centers and can be used for emergent transfusion of male patients and women beyond childbearing age. If uncrossmatched blood resources are limited, type O negative blood may be used but is typically reserved for women of childbearing age to avoid the risk of Rh isoimmunization. Type O positive blood has been shown to be safe for transfusion in hemorrhaging trauma patients, with a very low rate of transfusion reaction. Advantages of using uncrossmatched type O blood include immediate availability before type‐specific blood becomes available and avoidance of errors in multi‐casualty situations. The safety of type O blood has been improved by prescreening donor blood for anti‐A and anti‐B antibodies, which can lead to hemolysis of native red blood cells.Answer: CBall, C.G., Salomone, J.P., Shaz, B., et al. (2010) Uncrossmatched blood transfusions for trauma patients in the emergency department: incidence, outcomes and recommendations. Can J Surg , 54 (2), 111–115.Dutton, R., Shih, D., Edelman, B., et al. (2005) Safety of uncrossmatched type‐O red cells for resuscitation from hemorrhagic