Insect venoms commonly cause immunoglobulin E-mediated anaphylactic reactions. Increased vascular permeability may lead to urticaria, dyspnoea and hypotension. In severe cases, anaphylaxis can be life threatening due to airway and cardiovascular compromise. Gastrointestinal symptoms are rarely reported and seldom detected, although mucosal damage in anaphylactic reactions is well recognised.1
Prior to submission of this case report, the patient consented for the publication. The husband of a 57-year-old female patient in respiratory distress following a hornet sting in the right eyelid called the local emergency medical service for help. He had performed vigorous mouth-to-mouth ventilation to his still conscious wife before the arrival of emergency medical service; he subsequently stated that it had been difficult to get air into his wife's lungs. The emergency physician diagnosed anaphylaxis with obstructed upper airways. The patient immediately received intravenous corticosteroid and antihistamine, as well as nebulised epinephrine. The patient's condition improved; she was spontaneously breathing and able to communicate that she felt much better.
During the transfer, still some minutes away from the emergency department, the situation worsened again with increased respiratory rate and effort, in addition to decreasing oxygen saturations. As a result, intravenous ketamine was administered.
Upon arrival in our emergency department we observed a slim and athletic patient who was restless, moaning and whimpering. The patient's face was red, the lips and eyelids were swollen, and there was a small red insect bite mark at the right upper eyelid. No stinger was seen that could be removed. The patient was rubbing both her neck and abdominal region. She was drowsy and complained of difficulty phonating due to ‘a lump in the throat’. On auscultation there was bilateral wheeze that was greatest on expiration. The abdomen appeared distended, with diffuse pain on palpation. After several minutes the patient complained of progressive ‘narrowing’ with obvious respiratory distress. By this stage she was only able to speak in single words. The percutaneous oxygen saturation was 86% with 8 l min−1 oxygen by mask, blood pressure was 205/88 mmHg and heart rate 152 min−1.
At this stage the patient's trachea was intubated. During the laryngoscopy a considerably swollen pharyngeal and laryngeal region was observed and a cuffed endotracheal tube (internal diameter 7.5 mm) was inserted. After tracheal intubation, mechanical ventilation was started resulting in normalisation of oxygen saturation and blood pressure.
The patient was admitted to the ICU where chest and abdominal radiographs showed free air in the abdomen. An emergency laparotomy was performed and a perforation of the lesser curvature of the stomach was found and subsequently sutured. No signs of chronic lesions were seen at time of surgery, with the injury found in gastric mucosa of otherwise normal appearance. Histology examination showed Helicobacter pylori activity in a mild form of chronic gastritis. Eradication therapy for H. pylori was subsequently initiated. The patient remained in the ICU for 8 days and was discharged 15 days after admission.
Only four cases of gastric rupture have been described following mouth-to-mouth ventilation without chest compression.2–5 Gastric rupture can occur with pressures of more than 120 mmHg which equates to a gastric volume of approximately 4 l. However, during cardiopulmonary resuscitation high pressures can reached at lower intragastric volumes.2 Patients are especially at risk for gastric rupture following oesophageal intubation, bag mask ventilation, Heimlich manoeuvre and bystander provision of basic life support with chest compression.6,7 In our case there was no chest compression, but the strength of the mouth-to-mouth ventilation by the patient's husband might have caused the gastric perforation. This theory is supported by the fact that the perforation was in the lesser curvature of the stomach, which is the part of the stomach that has the least elasticity.
The incidence of gastric perforation with mouth-to-mouth ventilation or in the context of cardiopulmonary resuscitation is unknown. Therefore, any register including patients undergoing cardiopulmonary resuscitation should contain the adverse event of ‘gastric rupture’. Furthermore, in patients who are not successfully resuscitated, gastric rupture should be actively searched for in post mortem examinations, to try and better determine the incidence of gastric rupture in this setting.
In our patient, gastric rupture in relation with mouth-to-mouth ventilation occurred in association with an anaphylactic reaction and a mild chronic gastritis. It is possible that bradykinin and immunoglobulin E-mediated reactions played a role in the gastric injury. The histology showed helicobacter activity, which might also have contributed to the gastric rupture. This may have predisposed the patient to a more severe effect of immunoglobulin E-mediated mast cell degradation, resulting in weakening of the stomach wall.
In summary, we have presented a case of gastric rupture after mouth-to-mouth ventilation. The suspected mechanism of perforation was gastric overdistension in combination with an acute immunoglobulin E-mediated anaphylactic alteration of the gastric wall mucosa.
Acknowledgements relating to this article
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