Ascaris: An unusual cause of airway obstruction during general anesthesia with ProSeal laryngeal mask airway.

Sir,

Airway obstruction is a potential life-threatening event that requires expeditious intervention. Identification of the cause of obstruction can be very perplexing. We describe a case of airway obstruction by a nematode in a young girl undergoing surgery under general anesthesia with ProSeal laryngeal mask airway (PLMA).

A 20-year-old, 32 kg, 142 cm female was scheduled for right elbow arthroplasty. Preanesthetic assessment was normal. Preoperative heart rate (HR) was 70/minute, blood pressure (BP) 120/70 mmHg. Anesthesia was induced with fentanyl and propofol, and PLMA size 3 placement was facilitated with vecuronium and maintained with isoflurane 0.6% in oxygen (O2) and nitrous oxide (N2O). Surgery commenced after tourniquet inflation. The patient was stable with HR 79/minute, BP 100/50 (67) mmHg, hemoglobin oxygen saturation (SpO2) 98%, end-tidal carbon dioxide (EtCO2) 34 mmHg, and airway pressure (Paw) 13 cm H2O. One hour later, SpO2 decreased to 93%. Fraction of inspired oxygen (FiO2) was increased to 0.5, but as the SpO2 further dropped to 90%, FiO2 was maximized to 1.0. Manual bag ventilation was instituted, and PLMA position was adjusted. Bag compliance was very poor, and auscultation of the chest revealed markedly decreased air entry in the left chest. Normal EtCO2 waveform was present. SpO2 further decreased to 84% with loss of EtCO2 waveform. The PLMA was immediately removed, and manual face mask ventilation was attempted. Mask ventilation was not possible, and SpO2 was 56%. The trachea was intubated orally with a 6.5 mm cuffed tracheal tube. Bag compliance continued to be poor, Paw was 28 cm H2O, and markedly decreased air entry on left chest persisted. At this stage, HR was 98-100/minute, BP: 135-126/81-74 mmHg, SpO2: 98%-99% with FiO2 1.0 and isoflurane 0.8%-1%. Paw varied between 15 and 36 cm H2O. Twenty minutes later, frank crepitations were evident bilaterally with bloody secretions in the tracheal tube (pulmonary edema). Furosemide 15 mg and morphine 3 mg were administered intravenously (IV). HR was 83/minute, BP: 139/79 (95) mmHg, SpO2: 98%, and Paw: 23-24 cm H2O, and multiple atrial ectopics were evident on electrocardiography (ECG). The bladder was catheterized, and the tourniquet was deflated (tourniquet time: 1 hour 53 minutes). Six minutes later, SpO2 decreased to 81% despite an FiO2 of 1.0. Isoflurane was discontinued, and furosemide 10 mg and morphine 1.5 mg were repeated. Total urine output was 300 mL over 3 hours. Cardiologist evaluation ruled out a cardiac-related cause. Positive end-expiratory pressure (PEEP) 5 cm H2O was instituted as SpO2 ranged between 85% and 94% with FiO2 1.0. The patient was transferred to the intensive care unit (ICU) on controlled ventilation, FiO2 1.0, SpO2 96%-98%, paralyzed and sedated.

In the ICU, the patient was on controlled ventilation (PEEP: 5 cm H2O). Over the next six hours, saturation improved (> 95%, FiO2: 0.4) and Paw decreased (46 to 28 cm H2O). Arterial blood gas (ABG) revealed respiratory acidosis. Chest X-ray was suggestive of left lower lung zone collapse [Figure 1]. Air entry continued to be markedly decreased on the left side on day 2. Echocardiogram was normal. On day 3, muscle paralysis was discontinued. The patient was put on synchronized intermittent mandatory ventilation (SIMV) mode (PEEP: 5 cm H2O). Fiberoptic bronchoscopic (FOB) suction was done. No other abnormality was detected. Day 4 was characterized by marked tachycardia and varying Paw. On day 5, the patient again developed pulmonary edema that responded to treatment. On day 6, an elongated material was spotted in the tracheal tube. An ascaris worm of length 16 cm was suctioned out [Figure 2]. Albendazole 400 mg was administered. Over the next two days, air entry became bilaterally equal. On day 10, the trachea was extubated. Patient maintained well on ventimask (FiO2: 0.4).

Figure 1

Chest X-ray showing collapse of the left middle and lower lung zones

Figure 2

Ascaris worm suctioned out of the tracheal tube

Airway obstruction (including fatal and near-fatal cases) due to ascaris worm has been reported previously.[123] In the present case, we believe that the ascaris worm traveled retrograde through the esophagus into the mask of the PLMA and thence into the trachea and the left main bronchus. Review of the data on the monitor in retrospect revealed a rise in airway pressure to 43 cm H2O that went unnoticed. This probably occurred due to the presence of the worm in the trachea on its way to the left bronchus. Obstruction of the left main bronchus resulted in decreased air entry into the left chest and fall in SpO2 to 84%. Migration back into the trachea resulted in the inability to ventilate the lungs via the PLMA with loss of EtCO2 trace. This was further confirmed by the inability to manually ventilate the lungs by face mask after removal of the PLMA and drop of SpO2 to 56%. Intubation of the trachea probably pushed the worm back into the left bronchus.

Worm migration may be triggered by anesthetic agents, fever, sepsis, debilitating illness, subtherapeutic antihelminthic therapy, or by use of certain antihelminthics (pyrantel pamoate).[3] In the present case, worm migration was facilitated by lower esophageal sphincter incompetence due to anesthesia and the presence of the gastric tube. Pulmonary edema could be the result of re-expansion of the lungs following removal of the obstruction (worm migration).[4] Re-expansion pulmonary edema usually manifests following lung collapse of more than three days. However, a more acute form of re-expansion pulmonary edema, only two hours after atelectasis, during thoracic stage of esophagectomy has been reported.[5] Ravin et al.[6] reported unilateral pulmonary edema, after re-expansion of an atelectatic lung of a short duration, due to accidental placement of the tracheal tube in the right main bronchus. Alternatively, it could be because of the release of chemicals by the adult worm in the lungs that caused a reactive allergic response in the pulmonary tissue.

Though rare, there should be a high index of suspicion of ascaris worm as a cause of airway obstruction especially in patients living in areas of endemic parasitic infestation. In a ventilated patient, any suspicion of a foreign body should be evaluated early by flexible fiberoptic bronchoscopy, and therapeutic rigid bronchoscopy may be necessary.