The case
A 67-year-old woman with peptic ulcer disease presents to the emergency department with active large-volume hematemesis. She is tachycardic, hypotensive, and encephalopathic. Her hemoglobin is 4.6 g/dL and only increases to 6.5 g/dL after administration of 4 units of packed red blood cells (PRBCs). She remains hemodynamically unstable and is now mildly hypothermic; repeat studies reveal a venous pH of 7.14 and an ionized calcium of 2.9 mg/dL. While awaiting emergent esophagogastroduodenoscopy, she is started on vasopressors and receives 2 L of crystalloid and 4 additional units of PRBCs. Despite these interventions, she continues to decompensate.
Hemorrhagic shock and the lethal diamond
Hypovolemic shock, most often secondary to hemorrhage, accounts for one-third of shock presentations to the emergency department.1 Hemorrhagic shock is a major cause of mortality, particularly in young patients; leading causes in the United States include trauma, ruptured abdominal aortic aneurysm, and peptic ulcer disease.2 In the absence of overt bleeding, suspicion for occult hemorrhage should arise with progressive hypotension, narrow pulse pressure, and pale, cool extremities.
Appropriate resuscitation of hemorrhagic shock requires meticulous attention to detail, as suboptimal management can precipitate dilutional coagulopathy, acidemia, hypothermia, and hypocalcemia—collectively termed the lethal diamond (Figure 1)—which synergistically worsen shock.2-4 These abnormalities may be present despite hemodynamic stability.
Figure 1.
The “lethal diamond” framework highlights 4 compounding drivers of coagulopathy in hemorrhagic shock. Rapid recognition and correction of each element is essential to effective resuscitation and survival.
The solution
Effective resuscitation of hemorrhagic shock requires synchronous correction or avoidance of all components of the lethal diamond (Figure 1).
Dilutional coagulopathy results from consumption of platelets and factors, which are not repleted by crystalloid- and PRBC-predominant resuscitation. Balanced transfusion strategies—administration of even ratios of PRBCs, fresh frozen plasma, and platelets—prevent this. In trauma, such protocols reduce deaths from exsanguination.5 Viscoelastic testing (eg, thromboelastography, rotational thromboelastometry) is recommended to guide resuscitation, as studies in hemorrhagic-shock populations demonstrate comparable outcomes with reduced blood product use compared with conventional transfusion strategies.2
Acidemia, which can occur due to hypovolemia and impaired oxygen delivery, further impairs platelet and coagulation factor function; it warrants prompt resuscitation and hemorrhage control. It may develop even in normotensive patients due to reduced oxygen-carrying capacity. Pharma-cologic adjuncts like vasopressors or sodium bicarbonate allow temporization while definitive correction of hemorrhage is ongoing.
Hypothermia commonly accompanies large-volume resuscitation because of environmental exposure and room-temperature infusions; aggressive maintenance of euthermia through passive and active rewarming is essential.
Hypocalcemia is a predictable consequence of transfusion with citrate-containing blood products. Serial monitoring during resuscitation is prudent; many clinicians administer empiric calcium (eg, 1 g of calcium gluconate or calcium chloride after every 4 units of product) to mitigate coagulopathy and myocardial dysfunction from hypocalcemia.
Conclusion
Hemorrhagic shock can rapidly worsen when compounded by the lethal diamond: dilutional coagulopathy, acidemia, hypothermia, and hypocalcemia. Proactive recognition and correction through balanced transfusions, aggressive reversal of acidemia, maintenance of euthermia, and prompt calcium replacement can prevent deterioration and maximize survival.
Author contributions
J.J.P. and H.H.P. jointly contributed to the conceptualization, literature review, writing, and editing of this review.
Supplementary material
Supplementary material is available at ATS Scholar online.
Supplementary Material
Contributor Information
John J Popovich, Email: Jjp8pc@uvahealth.org, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Virginia Health, Charlottesville, VA, United States.
Hitesh H Patel, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Virginia Health, Charlottesville, VA, United States.
Conflicts of interest
Please see the ICMJE disclosure forms, which have been provided as supplementary material.
Artificial intelligence disclaimer
We used Napkin to assist with early brainstorming of formatting for the figure.
References
- 1. Gitz Holler J, Jensen HK, Henriksen DP, et al. Etiology of shock in the emergency department: a 12-year population-based cohort study. Shock. 2019;51:60-67. 10.1097/SHK.0000000000000816 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Cannon JW. Hemorrhagic shock. N Engl J Med. 2018;378:370-379. 10.1056/NEJMra1705649 [DOI] [PubMed] [Google Scholar]
- 3. Sihler KC, Napolitano LM. Complications of massive transfusion. Chest. 2010;137:209-220. 10.1378/chest.09-0252 [DOI] [PubMed] [Google Scholar]
- 4. Ditzel RMJ, Anderson JL, Eisenhart WJ, et al. A review of transfusion- and trauma-induced hypocalcemia: is it time to change the lethal triad to the lethal diamond? J Trauma Acute Care Surg. 2020;88:434-439. 10.1097/TA.0000000000002570 [DOI] [PubMed] [Google Scholar]
- 5. Holcomb JB, Tilley BC, Baraniuk S, et al. ; PROPPR Study Group. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313:471-482. 10.1001/jama.2015.12 [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.