Unveiling the Uncommon: A Case Report of Anaphylaxis with Rare Presentation

INTRODUCTION

Anaphylaxis represents a highly acute systemic hypersensitivity response, manifesting with swift onset and posing severe threats to the airway, respiration, and/or circulation. Typically, it is accompanied by observable alterations in the skin and mucosal tissues.¹

The clinical presentation of anaphylaxis varies based on the affected organ systems. Cutaneous manifestations are the most frequently observed symptoms.² But it's important to note that anaphylaxis can occur without visible skin involvement. Cardiovascular and respiratory symptoms are the most critical and potentially life-threatening features of anaphylaxis.² The gastrointestinal system can also be involved. Cardiovascular manifestations of anaphylaxis include hypotension and shock, cardiac arrhythmias, ventricular dysfunction, and cardiac arrest.³ In people with existing hypertension, a reduction of more than 30% from their baseline systolic blood pressure indicates potential cardiovascular issues.⁴ The presence of hypertension as a symptom of anaphylaxis is rarely mentioned in the literature.⁵

In this report, we present a case of anaphylaxis presenting with hypertension. Even if hypertension is noted in a patient with anaphylaxis, we should not hesitate to give epinephrine. The possibility of hypertensive anaphylaxis should always be considered.

CASE REPORT

A 68-year-old female with a previous history of coronary artery disease on antiplatelet, arrived at the emergency room with complaints of hoarseness of voice and breathing difficulty an hour after being stung by a wasp. She had no previous history of allergy to any food or drug. A few minutes after being stung, she felt an irritation at the back of her throat. Moments later, she developed breathing difficulty and hoarseness of voice.

Upon arrival at the emergency department, the patient was alert and oriented. Her pulse was 110 beats per minute, and her blood pressure measured 180/100 mmHg while she was in a semi-recumbent position. She had a respiratory rate of 24 breaths per minute and an oxygen saturation (SpO2) of 89% on room air. Hoarseness of voice was present. Examination revealed a swollen tongue occluding the oropharyngeal view. Auscultation of the chest revealed bilateral rhonchi. The rest of the systemic examination was normal. There was oedema surrounding the site of the wasp sting.

She was given oxygen support via a face mask. Intramuscular (IM) adrenaline 0.5mg, intravenous hydrocortisone 200mg, intravenous (IV) pheniramine 22.5mg. Since the patient was not showing significant improvement even after 3rd dose of IM adrenaline, she was given adrenaline 1ml of 1:10000 slow IV. Nebulised adrenaline 0.2mg with 3ml saline and salbutamol nebulisations were also given. Preparations for emergency cricothyroidotomy were also made, but were not done as the patient showed improvement in her symptoms. Oral antihistamines were not given as she had significant oropharyngeal oedema. Her vital parameters were monitored continuously. Her blood pressure remained high. As the patient was not showing significant improvement, IM adrenaline was repeated twice at 5-minute intervals. After the IV dose of adrenaline, the patient showed improvement in her symptoms. Her chest started to clear up, and her hoarseness reduced significantly. At that point, her blood pressure was recorded to have come down to 160/80mmHg. She was subsequently moved to the Intensive Care Unit (ICU) for careful observation and haemodynamic monitoring. Notably, her blood pressure readings following adrenaline treatment were lower than those at admission [Figure 1], and her symptoms improved significantly. There were no episodes of hypotension. As the clinical criteria for anaphylaxis were met, serum tryptase was not measured. On day two of admission, upon discharge, her blood pressure was recorded at 130/70 mmHg. During her hospital stay, there were no further hypertensive episodes noted.

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Figure 1:

Blood pressure monitoring in the initial 6 hours of hospital admission.

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DISCUSSION

The initial management of anaphylaxis includes a swift evaluation of the patient's circulation and respiratory status, promptly followed by the administration of epinephrine. Epinephrine is considered the primary treatment for anaphylaxis and should be administered promptly to anyone suspected of experiencing an anaphylactic reaction.⁶ Epinephrine is a sympathomimetic agent that promotes bronchodilatation and vasoconstriction. It also reduces oedema of the mucosa. It functions by reducing the release of histamine from mast cells and other inflammatory mediators. For anaphylaxis, the recommended dosage is 0.01 mg/kg (up to a maximum of 0.5 mg), administered intramuscularly every 5 to 15 minutes as needed.⁷

While cutaneous manifestations are common in anaphylaxis, the reaction can occur without any visible skin changes. The most concerning aspects of anaphylaxis are the respiratory and cardiovascular symptoms, which can be life-threatening.

The diagnosis of anaphylaxis during an acute episode relies on the presence of specific clinical signs and symptoms. In 2006, a multidisciplinary panel of experts established diagnostic criteria for anaphylaxis, which are outlined in [Table 1].⁸

During an anaphylactic reaction, basophils and mast cells promptly release various mediators, including histamines, leukotrienes, prostaglandins, thromboxanes, and bradykinins. These mediators induce heightened mucous membrane secretions, elevated capillary permeability resulting in leakage, notable relaxation of smooth muscle tone in bronchioles and blood vessels (vasodilation), and bronchospasm.⁹ Internal compensatory vasopressor responses, including the secretion of catecholamines, activation of the angiotensin system, and the production of the potent vasoconstrictor peptide endothelin-1, can lead to erratic responses during anaphylaxis. In certain patients, peripheral resistance can increase to unusually high levels during these episodes. Additionally, serotonin plays a significant role in the mechanisms of anaphylaxis and through its interactions with serotonin receptors (serotonin I and serotonin II), serotonin may contribute to systemic hypertension.¹⁰ It is possible that an early compensatory vasopressor response predominates, leading to anaphylactic reactions that present as hypertensive episodes.

In this patient, the blood pressure was recorded to be high upon admission to the emergency department. She was given adrenaline and other supportive care for anaphylaxis under close monitoring. Her blood pressure came down with the regression of her symptoms. Anaphylaxis-induced high blood pressure is a rare possibility.⁵ Thus, her elevated blood pressure upon admission suggests the potential for hypertension induced by anaphylaxis.

Hypertensive anaphylaxis has been documented in prior reports, including one by Solmazgul et al.⁵ Within minutes of the onset of anaphylaxis, the internal compensatory vasopressor mechanisms are activated, causing the release of endogenous vasoactive substances such as epinephrine and norepinephrine, as well as the production of angiotensin II.¹ Solmazgul et al. proposed that in some patients, these initial compensatory mechanisms might be predominant, leading to hypertension.⁵ This hypothesis was derived from a case review involving 62 patients with anaphylaxis, where 8 were noted to have elevated blood pressure upon presentation.

In the study by Solmazgul et al., two of these eight patients with hypertensive anaphylaxis received intramuscular (IM) adrenaline. Their systolic blood pressure before treatment was 150 mmHg, and both the anaphylaxis and hypertension fully resolved without any adverse effects after the administration of IM adrenaline. The remaining patients recovered without the need for IM adrenaline.⁵

Another case of anaphylaxis presenting with severe hypertension was reported by Govindapala et al.¹¹ The case emphasised severe supine hypertension and orthostatic intolerance in a patient who presented with anaphylaxis. The study found that orthostatic intolerance was alleviated following the administration of intramuscular adrenaline. The researchers concluded that the presence of postural symptoms alongside elevated blood pressure should serve as a warning sign to clinicians regarding potential cardiovascular implications. Early treatment with adrenaline should be approached with extreme caution in these patients.¹¹ The presence of cardiovascular disease does not preclude the use of adrenaline in anaphylaxis, as no other medications provide the same life-saving effects in this critical situation.¹²

Parenteral administration of glucagon may be used in patients with anaphylaxis with no optimal response to epinephrine (adrenaline) in patients taking beta-blockers, despite very limited evidence.¹³ Glucagon exerts positive inotropic and chronotropic effects by directly activating adenylyl cyclase and bypassing β-adrenergic receptor blockade.¹⁴

CONCLUSION

In conclusion, we could use epinephrine under strict haemodynamic monitoring in patients presenting with high blood pressure concurrently with anaphylaxis. Always keep an open mind to the possibility of hypertensive anaphylaxis. Epinephrine should be administered without delay during potentially life-threatening signs of anaphylaxis, such as upper airway obstruction. Epinephrine injection could effectively address both anaphylaxis and associated hypertension when necessary.