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Anaphylactic Shock Complicated with Hematuria and Deep Venous Thrombosis: A Case Report
Wu Yali1*
1Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China
Corresponding Author: Wu Yali
Address: Department of Anaesthesiology, West China Hospital, Sichuan University, 37 Guo Xue St, Chengdu, Sichuan 610041, China.
Received date: 07 July 2025; Accepted date: 22 July 2025; Published date: 29 July 2025
Citation: Yali W. Anaphylactic Shock Complicated with Hematuria and Deep Venous Thrombosis: A Case Report. Asp Biomed Clin Case Rep. 2025 Jul 29;8(2):168-72.
Copyright © 2025 Yali W. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited.
Keywords: Anaphylactic Shock, Deep Vein Thrombosis, Hematuria, Tryptase, Systemic Inflammation
Abstract
Background: Anaphylactic shock is a common clinical emergency that shares mediators involved in the coagulation cascade and can also damage multiple systems, such as the kidneys, resulting in deep venous thrombosis and hematuria. To date, only one case of venous thrombotic events following anaphylaxis has been reported. Herein, we describe the first case of hematuria and deep venous thrombosis occurring in close temporal relation to an anaphylactic event.
Case Presentation: A 74-year-old female (153 cm, 51.5 kg) was diagnosed with, 1. Cervical spinal stenosis; 2. Cervical disc herniation at levels C3/4, C4/5, C5/6, and C6/7; 3. Spinal cord and nerve compression; 4. Chronic inflammation of both lungs; 5. Lacunar cerebral infarction; 6. Brain atrophy. She was scheduled to undergo posterior C3–7 single open-door spinal canal enlargement, laminoplasty, and mini-plate screw fixation. After anesthesia induction, the patient experienced increased airway pressure and urticaria on the anterior chest, followed by anaphylactic shock. After fluid resuscitation, corticosteroids, calcium, and adrenaline administration, the patient developed hematuria. Subsequently, 250 mL of 5% sodium bicarbonate was administered to alkalinize the urine, and blood pressure was continuously maintained. The surgery was suspended after consultation with the chief surgeon and the patient's family. Once vital signs stabilized, the endotracheal tube was removed, and the patient was safely returned to the ward. On the third postoperative day, vascular color Doppler ultrasound revealed multiple thrombi throughout the body.
Conclusion: Anaphylactic shock causes decreased renal perfusion, ischemia of the renal cortex, and damage to renal tubular epithelial cells. Immune complex deposition can lead to complement activation and subsequent intravascular injury, resulting in hematuria. The coagulation cascade shares many inflammatory mediators with conditions such as sepsis, shock, asthma, allergy, and anaphylaxis. While all these conditions, except anaphylaxis, have been linked to an increased risk of thrombosis and blood clot formation, our findings suggest that anaphylaxis may also be a contributing factor to deep vein thrombosis.