A Rare Case of Intraoperative Hypotension in Neurosurgical Setting: Diagnosis and Management of Transfusion-Associated Hypotension

Abstract

Transfusion-associated hypotension (TAH) is a rare but potentially serious complication characterized by a sudden onset of hypotension during or shortly after the initiation of a blood transfusion. Once other causes have been excluded, the hypotension resolves upon cessation of the transfusion. We report the case of a 49-year-old female scheduled for excision of a central neurocytoma via an interhemispheric approach. Intraoperatively, the patient developed unexplained hypotension unresponsive to inotropic support during tumor resection. After systematic exclusion of other differential diagnoses, TAH was considered as the most likely cause. Discontinuation of the transfusion led to the resolution of hypotension, confirming the diagnosis. This case highlights the importance of considering TAH as a differential diagnosis for intraoperative hypotension, particularly when unresponsive to standard management and temporally associated with transfusion. Prompt recognition and appropriate management are crucial to avoid unnecessary interventions and improve patient outcomes.

 

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Keywords

intraoperative hypotension - blood transfusion - transfusion-associated hypotension

Introduction

Transfusion-associated hypotension (TAH) is a rare but clinically significant reaction characterized by the sudden onset of hypotension shortly after the initiation of a blood transfusion, which typically resolves upon discontinuation of the transfusion once other potential causes have been excluded.[1] Due to its nonspecific presentation and overlap with other intraoperative events, TAH often poses a diagnostic challenge, particularly in the surgical setting. In this case report, we present a patient undergoing resection of an invasive central neurocytoma who developed intraoperative hypotension unresponsive to standard resuscitative measures. The diagnosis of TAH was established following a systematic evaluation and was managed successfully. This case aims to enhance awareness of perioperative TAH and to provide valuable insights into its recognition and management.

 

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Case Report

A 49-year-old female with a 5-year history of type 2 diabetes mellitus, managed with glimepiride and metformin, was diagnosed with an intraventricular tumor, confirmed by biopsy as invasive central neurocytoma. She had previously undergone a tumor biopsy in November 2020 and a right medium-pressure ventriculoperitoneal shunt placement in December 2021 for hydrocephalus. She was scheduled for a re-exploratory interhemispheric transcallosal craniotomy for tumor excision. Preoperative evaluation revealed a hemoglobin (Hb) level of 10 g/dL, blood type B-positive, and normal systemic examination findings.

On the day of surgery, general anesthesia was induced and maintained with sevoflurane (0.8–1.0 MAC), fentanyl infusion (2 µg/kg/h), and atracurium infusion (0.01 mg/kg/min). The patient was placed in a semi-sitting position for peri-coronal parasagittal craniotomy and an interhemispheric approach. Intraoperatively, the patient experienced ongoing blood loss from the tumor, necessitating transfusion of 5 units of packed red blood cells (PRBCs), 2 units of random donor platelets (RDPs), and 2 units of fresh frozen plasma (FFP), all of which were non-leukoreduced. Thirty minutes into the PRBC transfusion, she developed acute hypotension (blood pressure [BP]: 79/35 mm Hg), which was unresponsive to fluid boluses and escalating doses of vasopressors, including phenylephrine and norepinephrine (up to 1 µg/kg/min). Despite correction of acidosis and hypocalcemia, hypotension persisted. No ongoing bleeding, electrocardiogram (ECG) changes, hypoxia, increased airway pressures, drop in end-tidal carbon dioxide (EtCO₂) or skin signs of anaphylaxis were observed.

Given the temporal association with transfusion and exclusion of other causes, a transfusion reaction was suspected. Epinephrine boluses (10 µg) followed by an infusion (0.02 µg/kg/min, increased to 1 µg/kg/min) achieved transient hemodynamic stability. Blood products were returned for hemovigilance testing, which showed no incompatibility. The surgery was aborted, and the patient was transferred to the intensive care unit (ICU). After cessation of transfusion, hypotension resolved within 1 hour, and epinephrine was tapered.

Subsequent investigations in the ICU, including ECG, two-dimensional echocardiography, medication allergy tests, and hemoglobinuria screening, were unremarkable. Coagulation studies revealed a mildly elevated international normalized ratio (1.83), prompting FFP transfusion. Within 15 minutes of starting FFP, the patient again developed severe hypotension (BP: 60/34 mm Hg), which reversed upon stopping the transfusion and reinitiating epinephrine infusion (0.5–0.75 µg/kg/min). Hemovigilance testing for this episode was also negative for immunologic reactions. She was eventually stabilized, tracheostomized due to low Glasgow Coma Scale (GCS: 7), weaned from mechanical ventilation, and discharged after 10 days.

Based on the exclusion of alternative causes and recurrence of hypotension temporally linked to transfusions, a diagnosis of TAH was made. The event was reported to the Hemovigilance Program of India as a severe-grade TAH with probable imputability.

 

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Discussion

TAH is a rare but clinically significant transfusion reaction, with an overall incidence of 0.003 per 10,000 transfused units reported in India.[1] Component-specific rates have been reported as 0.019% for RDPs, 0.015% for PRBCs, and 0.006% for FFP.[2] TAH is typically characterized by a sudden drop in systolic blood pressure—≥30 mm Hg to ≤80 mm Hg—within 15 minutes of initiating a transfusion, resolving promptly upon cessation once other causes of hypotension are excluded.[1] [2] Due to its nonspecific presentation and overlap with other intraoperative complications, TAH often remains under-recognized, especially in high-risk surgical settings. This case represents the first documented instance of TAH at our institution.

In patients undergoing intracranial tumor resection, particularly for highly vascular lesions such as central neurocytomas, substantial intraoperative blood loss is anticipated.[3] Accordingly, our patient received multiple transfusions guided by goal-directed therapy. Hemodynamic management included crystalloids (20–30 mL/kg), phenylephrine boluses, and norepinephrine infusions to maintain a mean arterial pressure >70 mm Hg and cerebral perfusion. Despite achieving intraoperative hemoglobin targets and maintaining a pulse pressure variation below 12%, the patient developed acute, transfusion-temporal hypotension that was unresponsive to fluid resuscitation and vasopressors, raising suspicion for TAH.

Serial arterial blood gases indicated increasing hemoglobin concentrations, rising lactate, and evidence of metabolic acidosis, consistent with tissue hypoperfusion and vasoplegia, rather than ongoing hemorrhage.[4] Hypocalcemia, a known consequence of massive transfusion due to citrate toxicity, was also detected and corrected.[5] In the absence of ECG changes, elevated cardiac biomarkers (Trop I, Pro-BNP), or echocardiographic abnormalities, major cardiac events including myocardial infarction and stress cardiomyopathy were excluded.[6] Additionally, there were no signs of intraoperative pneumothorax, pulmonary embolism, or air embolism—confirmed through auscultation, chest radiography, and echocardiography, as evidenced by no increase in peak airway pressures or acute drop in EtCO₂.[7] [8]

Anaphylaxis and drug hypersensitivity were also considered. The patient received hydrocortisone and pheniramine empirically, and the postoperative allergy panel was negative. Moreover, direct antiglobulin testing, antibody screens, and hemovigilance investigations of all returned blood products were negative, ruling out hemolytic transfusion reactions.[9] [10] Similarly, other common transfusion reactions, including transfusion-associated circulatory overload, transfusion-related acute lung injury (TRALI), febrile nonhemolytic, and allergic reactions, were excluded based on clinical and radiological findings.[10]

Hemolysis was ruled out through the absence of hematuria, normal lactate dehydrogenase levels, and stable platelet counts.[10] The patient exhibited no evidence of TRALI, given normal oxygenation and absence of pulmonary infiltrates. Importantly, repeated hypotensive episodes occurred with two separate transfusion events—PRBCs intraoperatively and FFP postoperatively—both resolving promptly after cessation of transfusion and administration of epinephrine. This pattern further supported the diagnosis of TAH.[1] [10]

The precise pathophysiology of TAH remains incompletely understood. It is hypothesized to involve bradykinin accumulation due to activation of factor XII or inhibition of its degradation, particularly in patients on angiotensin-converting enzyme (ACE) inhibitors.[11] [12] However, our patient was not receiving any ACE inhibitors or antihypertensives, suggesting an ACE-independent pathway.

Notably, improper recognition of TAH can delay appropriate management. The primary approach to managing patients with acute hemolytic transfusion reactions involves stopping the transfusion and providing supportive care. Hypotension typically resolves after the transfusion is discontinued.[12] Pollard et al have illustrated the consequences of delayed diagnosis, often misattributed to anaphylaxis or surgical complications. In our case, early cessation of transfusion and initiation of vasopressor support—particularly epinephrine—proved critical in stabilizing the patient.[12]

Preventive strategies, including the use of leuco-reduced or washed red blood cells, minimizing platelet and FFP transfusions, and implementing blood conservation techniques (e.g., preoperative erythropoietin, iron therapy, antifibrinolytics), may help reduce the risk of recurrence in susceptible individuals.[12] When a patient with suspected or prior TAH presents for surgery, comprehensive preoperative planning, including hematologic consultation and blood product selection, is essential.

Hemovigilance testing for perioperative transfusion-related hypotension involves a comprehensive approach that includes clinical assessment, laboratory investigations, and systematic reporting to ensure safe and effective blood transfusion practices.[1] [2] These measures are designed to detect and manage potential adverse reactions, particularly hypotension, by monitoring various stages of the transfusion process. Pretransfusion evaluation includes a thorough review of the patient's medical history, current medications—especially ACE inhibitors—and overall clinical status. During the transfusion, continuous monitoring of vital signs such as blood pressure, heart rate, and oxygen saturation is essential.[1] [2] Medical staff must be trained to recognize and respond promptly to signs of hypotension, which may manifest as a significant drop in systolic blood pressure (≥30 mm Hg in adults or >25% in children) or an absolute systolic pressure of ≤80 mm Hg. If a transfusion reaction is suspected, posttransfusion blood samples may be analyzed for indicators of hemolysis, including free hemoglobin and bilirubin. The Direct Coombs test may also be performed to detect antibodies bound to red blood cells, suggesting a hemolytic reaction. Hemovigilance systems play a critical role by collecting and analyzing data on transfusion-related adverse events, including hypotension, thereby helping to identify underlying causes and inform strategies for prevention and improved patient safety.[1] [2]

 

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Conclusion

This case underscores the importance of maintaining a high index of suspicion for TAH in perioperative settings, particularly when hypotension occurs temporally with transfusion and is refractory to standard hemodynamic support. TAH can occur independently of ACE inhibitor therapy and may present with recurrent episodes across different transfused blood products. Early recognition, exclusion of alternative causes, and prompt cessation of transfusion remain the cornerstone of effective management.

 

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Conflict of Interest

None declared.

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Publication History

Article published online:
17 July 2025