Anaphylaxis is characterized as a systemic, immediate hypersensitivity reaction primarily mediated by immunoglobulin E, leading to the release of mediators from mast cells and basophils [1,2]. Anaphylaxis, a critical and potentially fatal manifestation of this hypersensitivity, demands prompt medical intervention to mitigate life-threatening consequences. Patients with such severe reactions often require management in an intensive care unit (ICU) setting.

Epinephrine stands as the primary, first-line treatment for anaphylaxis, with its adrenergic agonistic properties promoting bronchodilation and vasoconstriction, reversing the symptoms of anaphylaxis [2]. Although additional therapeutic agents may be considered after post-epinephrine administration and upon initiation of supportive care, there is insufficient evidence supporting epinephrine use [3].

Shock, emanating from the cardiovascular system’s failure to maintain adequate tissue perfusion, presents through a variety of clinical syndromes. Lactic acidosis, marked by an elevation in blood lactic acid, signals tissue hypoperfusion and a shift toward anaerobic metabolism [4]. However, increased lactic acid levels may not exclusively indicate tissue hypoxia and can mirror an adaptive response to severe infections or therapeutic interventions [5]. The occurrence of lactic acidosis in the context of anaphylactic shock, especially after epinephrine administration, introduces a complex clinical dilemma, prompting a reassessment of our understanding of the interplay among adrenergic stimulation, tissue perfusion, and metabolic pathways during acute anaphylactic reactions.

Although case reports of epinephrine-induced lactic acidosis are relatively common, instances where it complicates clinical decisions during treatment of anaphylaxis are rare. This case report aims to highlight a significant episode of lactic acidosis that developed during the management of anaphylactic shock with epinephrine.

We present the case of a 57-year-old male patient, previously diagnosed with distal common bile duct cancer following an abnormal liver function test during a health screening 2 years prior, who underwent a pylorus-preserving pancreaticoduodenectomy. At the time of the initial computed tomography (CT) scan with contrast, no anaphylactic reactions were reported. After surgery, the patient was regularly monitored every 6 months with contrast-enhanced abdominal CT scans. During these follow-up sessions, he experienced symptoms of anaphylaxis, including rash and dizziness, which were preemptively treated with antihistamines and hydrocortisone before proceeding with CT scans.

During his most recent CT scan with contrast, despite pre-treatment, the patient developed a rash, itching, altered consciousness, and significant hypotension (53/46 mmHg), leading to transfer to the emergency room (ER) following an intramuscular injection into the anterolateral aspect of the thigh of 0.5 mg epinephrine in the CT suite. Upon presentation to the ER, his vital signs were temperature 36.3 °C, heart rate 98 beats/min, blood pressure 83/46 mmHg, respiratory rate 24 breaths/min, and oxygen saturation 99% with room air. Physical examination revealed a skin rash on the trunk and extremities. Arterial blood gas analysis displayed an elevated lactate level of 3.6 mmol/L, while electrocardiogram revealed sinus tachycardia. The patient was administered a third dose of intramuscular epinephrine and H1 and H2 blockers in the ER, accompanied by 1.5 L of intravenous fluids. Despite these interventions, his blood pressure remained low at 76/39 mmHg, leading to his admission to the ICU for norepinephrine and epinephrine infusions.

No abnormalities were observed in the chest x-ray and electrocardiogram after ICU admission (Fig. 1). Throughout the ICU stay, even though the patient’s blood pressure recovered to 101/45 mmHg, his lactate level continued to climb, reaching a peak of 13.5 mmol/L (Table 1). Utilizing bedside point-of-care ultrasound evaluation, it was possible to exclude the presence of cardiogenic shock. Additionally, the capillary refill time was observed to be within 2 seconds. After excluding other possible causes for lactate elevation, epinephrine-induced lactic acidosis was suspected. Consequently, epinephrine administration was halted, decreasing lactate level to 2.5 mmol/L (Fig. 2). The patient’s condition eventually stabilized, allowing discontinuation of the concurrent norepinephrine and his subsequent discharge from the ICU.

This case report highlights the rare yet critical incidence of significant lactic acidosis following the administration of epinephrine in treating anaphylaxis. The treatment involved multiple doses of epinephrine, fluid resuscitation, and vasopressor support in the ICU, reflecting the complex management of severe anaphylaxis. The observed severe lactic acidosis, which markedly improved upon cessation of epinephrine, suggests that epinephrine may directly impact the development of this complication.

Anaphylaxis is a critical, life-threatening systemic hypersensitivity reaction characterized by rapid symptom onset across multiple organ systems. The immediate administration of epinephrine is essential, aiming to prevent potentially fatal delays [6–8]. Epinephrine activates adrenergic receptors, promoting vasoconstriction, improved cardiac output, and bronchodilation [9].

In cases of severe anaphylaxis with persistent hypotension, continuous epinephrine infusions may be necessary [10]. However, this can induce lactic acidosis through mechanisms such as increased glycolysis, Na/K-ATPase activation, excessive vasoconstriction, and increased metabolic demand, elevating lactate production and causing tissue hypoxia [11,12].

Lactic acidosis, characterized by lactate level >5 mmol/L and pH <7.35, is categorized into type A or B [13]. Type A occurs in response to hypoxia or hypoperfusion, inhibiting pyruvate dehydrogenase, which prevents pyruvate conversion to acetyl-CoA, forcing anaerobic metabolism to lactate. Type B occurs in the absence of hypoxia or hypoperfusion, where pyruvate converts to lactate through aerobic glycolysis, commonly caused by diseases, drugs, or metabolic errors [14]. The patient in this case, who had not received other drugs known to cause lactic acidosis and exhibited normal liver and kidney functions without evidence of global hypoxia or hypoperfusion, experienced lactic acidosis resolution hours after stopping the epinephrine infusion.

Managing lactic acidosis in anaphylaxis contexts requires balancing the treatment of hypersensitivity reactions and mitigating acidosis effects. Persistent epinephrine-induced lactic acidosis, despite clinical recovery, may necessitate reducing or stopping the infusions and considering alternative vasopressors [6]. The decision to continue or discontinue epinephrine depends on the shock status. With clinical improvement but worsening lactic acidosis, discontinuing epinephrine should be considered.

This case underlines the importance of vigilance concerning lactic acidosis during anaphylaxis treatment with epinephrine, especially in scenarios requiring prolonged infusions. The interrelation between anaphylaxis-induced tissue hypoperfusion and the metabolic effect of epinephrine necessitates meticulous monitoring and strategic management, including potential need for alternative treatments in the face of persistent, severe lactic acidosis.