Kounis syndrome is an understudied but clinically important condition wherein an allergic or hypersensitivity response leads to coronary vasospasm or potentially myocardial infarction. First described by Kounis and Zavras in 1991, this syndrome can be classified into three variants based on the underlying cardiac pathology: vasospastic angina pectoris, type I acute myocardial infarction and stent thrombosis
In this case report, we describe a 53-year-old man who experienced Kounis syndrome following jellyfish envenomation. Jellyfish sting can cause pain and skin rash at the site of contact or may cause slight allergic reaction systemic involvement, cardiac involvement is rare
A 53-year-old man, being a regular swimmer and with no significant past medical history except an allergic reaction following a jellyfish sting a few years prior to the current presentation, lost consciousness while swimming and was brought to the Emergency Department (ED) following malaise. A jellyfish stung the patient on his right arm during swimming but he swam for further 5 - 10 min after stinging as a result of which he developed weak feeling and went onshore. The patient was found collapsed on the shore of the River with head injury and multiple bruises on his legs and arms by the fire fighters after he was rescued. After waking up, the patient could not recall all the incidents that have occurred at all during the operation or while unconscious.
When the emergency medical services arrived, no signs of chest pains or rash were observed, the man only complained of minor breathing problems and possible aspiration of seawater. The patient also reported a specific episode of diarrhea saying that this was quite like another incident after he had been stung by jellyfish. The initial assessment on the scene revealed that he had a blood pressure of 120/80 mmHg, GCSR of 14, oxygen saturation of 92% and respiratory rate of 15 breaths per minute. Oxygen was then given through the face mask 6LPM which was later decreased to 2 LPM. There had been a similar episode of fatigue and syncope in the earlier years after stinging by a jellyfish with the same complaint of diarrhea. Since the two episodes were almost similar, the patient was transferred to the ED for further assessment.
On presentation in the ED the patient was fully awake, responding appropriately to questions and able to locate him or herself in time and place. His clinical features only on admission to the hospital were: His blood pressure was 92/51 mmHg, a pulse of 61 beats per minute, a respiratory rate of 15 breaths per minute and an oxygen saturation of 97%. The physical examination revealed the following findings: The physical examination revealed the following findings:
Cardiovascular examination: The phenomenon in question will consist of occasional, normal, regular noises of the heart without murmurs. Peripheral pulses were feasible; no swelling or tenderness in the calves; no oedema in the lower limbs.
Pulmonary examination: There was no wheezing, crackles/rale any where there were bilateral vesicular breath sounds audible. Patient was fully coordinated, Alert, Oriented and spontaneous and not dyspnoeic, even at rest, comfortable in the room air.
Neurological examination: There were no signs of focal motor and sensory abnormalities. Cranial nerves were normal, and both pupils were equal and reactive to light. Compliant to this, there was no observed nystagmus or tremor in the patient besides no neck stiffness as would be expected in this condition.
Gastrointestinal examination: Abdomen was hypoactive, there were no signs of tenderness and distension and the sounds from the gut were also normal.
Trauma assessment: The patient had a simple, neat, longitudinal incision of about 4 cm on the forehead and therefore was amenable to suturing. He also had other scrapped areas at the front of his lower legs, around his left abdominal area and the right arm. There was no evidence of pain or erythema when assessing the spine, thorax or pelvis and no definite motor or sensory impairment was elicited.
The patient underwent an electrocardiogram (ECG), which revealed sinus rhythm with fine QRS complexes and no evidence of repolarization abnormalities. His heart rate at the time of the ECG was 66 beats per minute. Laboratory tests were performed upon arrival, including a complete blood count (CBC), electrolyte levels, and cardiac biomarkers as shown in (
CBC: Hemoglobin 15 g/dL, platelets 324,000 cells/µL.
Electrolytes: Sodium 144 mmol/L, potassium 4.77 mmol/L, bicarbonate 16 mmol/L.
Inflammatory markers: White blood cell count 11,000 cells/µL without elevated C-reactive protein (CRP).
Cardiac markers: Troponin I was elevated at 121 ng/L on arrival.
Arterial blood gas (ABG): pH 7.35, pCO2 30 mmHg, pO2 69.9 mmHg, HCO3 17 mmol/L, lactate 4 mmol/L.
Test |
Result |
Reference Range |
Hemoglobin |
15 g/dL |
13.5 - 17.5 g/dL |
Platelets |
324,000 cells/µL |
150,000 - 450,000 cells/µL |
Sodium |
144 mmol/L |
135 - 145 mmol/L |
Potassium |
4.77 mmol/L |
3.5 - 5.1 mmol/L |
Bicarbonate |
16 mmol/L |
22 - 28 mmol/L |
Troponin I (on arrival) |
121 ng/L |
<14 ng/L |
White Blood Cell Count |
11,000 cells/µL |
4500 - 11,000 cells/µL |
Lactate |
4 mmol/L |
0.5 - 2.2 mmol/L |
The patient developed a transient hypotensive episode in the ED’s resuscitation room with an MAP of 60 mmHg while under observation. Due to the patient's history of Jellyfish stings and anaphylactic reactions, the medical team began with the process of intravenous normal saline infusion. Kounis syndrome, a kind of allergic angina precipitated by the sting of jellyfish, was considered as the hypothesis. Patient received one dose of Solu-Medrol (methylprednisolone) 90 mg and remained on intravenous fluids. The rest of the lab investigations included serum tryptase, troponin and lactate as a follow up test to the suspected anaphylactic reaction.
Two hours after the initial assessment, the patient’s troponin levels had increased to 428 ng/L, and his lactate had decreased to 2.75 mmol/L, indicating partial improvement. Hemodynamically, the patient stabilized, with a blood pressure of 103/63 mmHg, a heart rate of 69 beats per minute, and oxygen saturation of 99% on room air.
Test |
Time of Measurement |
Result |
Reference Range |
Troponin I |
2 hours post-arrival |
428 ng/L |
<14 ng/L |
Lactate |
2 hours post-arrival |
2.75 mmol/L |
0.5 - 2.2 mmol/L |
Sodium |
2 hours post-arrival |
144 mmol/L |
135 - 145 mmol/L |
Potassium |
2 hours post-arrival |
4.77 mmol/L |
3.5 - 5.1 mmol/L |
The cardiology team was consulted and advised that a troponin test should be repeated three hours after the first result is obtained. The next troponin level was also higher at 968 ng/L. This was especially likely because the patient subsequently had a significant increase in the troponin level with no apparent unequivocal changes on ECG, features that formed part of the Kounis syndrome (
In the cardiology ICU, a transthoracic echocardiogram was performed, revealing the following findings:
Left ventricular ejection fraction (LVEF): 60%, with no segmental wall motion abnormalities.
Left ventricular hypertrophy (LVH): Septal wall thickness of 14.6 mm.
Normal right ventricular function: Tricuspid annular plane systolic excursion (TAPSE) of 19 mm.
Normal aortic dimensions: Ascending aorta measured 30 mm.
No significant mitral or aortic valve disease.
Inferior vena cava (IVC): Thin and collapsible, with >50% modulation.
A coronary angiogram was also conducted to evaluate the possibility of CAD or Coronary Artery Disease. According to the angiography results, the patient had no angiographically relevant stenosis meaning the patient did not have coronary artery disease. Having examined and discussed the case of our patient, the diagnosis of Kounis syndrome (Type I) was made with coronary vasospasm being more probable than others as causing the elevations in the patient’s troponin level and clinical manifestations.
The patient’s troponin levels started to decrease the day after the coronary angiogram and serum tryptase level was relatively high at 75 ng /ml. Pharmacological treatment was not complemented, as no coronary disease was underlying No additional pharmacological treatment was introduced. The patient was discharged with advice to contact an allergist to determine his predisposition to anaphylactic reactions and tips on how to avoid them.
Kounis syndrome: an allergic coronary artery disorder provoked by the release of inflammatory mediators during anaphylaxis and resulting in coronary spasm, myocardial damage or myocardial infarction
In this case, the patient was diagnosed with type I Kounis syndrome which is caused by an allergic reaction to jellyfish sting leading to histamine, serotonin and tryptase; the isolated mediators that cause spasm of coronary arteries and myocardial damage
In 2021, Abdelghany et al.
In this particular case, the absence of CAD on angiography, the high serum tryptase and the rising troponin levels after the allergic reaction confirmed the diagnosis of Kounis syndrome. New research on Type I Kounis syndrome has also pointed to the fact that this variant is difficult to distinguish from other causes of myocardial damage, primarily myocarditis, or stress cardiomyopathy
In the management of Kounis syndrome, both the allergic reaction and the cardiac injury are treated. Another recent study by Brown and
In this case the patient was given corticosteroids and aspirin to bring his condition to normal. In this particular case, the increase in troponin level was moderate, and based on the coronary angiography the patient had no life threatening myocardial infarction.
There is a case of Kounis syndrome associated with bee sting which was discussed by Zhao et al. in their 2022 study; cardiac biomarkers were elevated and not CAD was significant
In the similar manner Wang et al., in a case report in 2023 described a patient who had Kounis syndrome after contact with a marine allergen, like the present case, the patient had elevated troponin levels but who did not have angiographically significant coronary artery disease
Kounis syndrome is a rare but possibly lethal form of an allergic reaction that causes coronary artery spasm and myocardial injury. For the present case, a 53-year-old male patient developed Kounis syndrome after a jellyfish envenomation with symptoms of hypotension, increased troponin levels, and without evidence of significant CAD. Because the patient received prompt diagnosis and management strategies such as corticosteroids and antiplatelet agents, the produced outcome was positive. This case report also raises awareness of Kounis syndrome in patients with allergic reactions and cardiac complications, especially after exposure to marine agents such as jellyfish envenoming. More study is required to clarify the underlying molecular mechanisms, as well as the of care strategy for Kounis syndrome, particularly among patients with propensity for recurrent allergic reactions.