A case of recurrent course of acute obstructive laryngitis with severe relapses in a 6-month-old baby

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Introduction

Acute obstructive laryngitis (croup, AOL) is one of the pressing problems in pediatrics. It is considered a life-threatening condition, and requires immediate emergency care [1]. According to data from 2023, the Perm Emergency Medical Service recorded 2 cases of severe AOL among 456 calls regarding children [2].

In most cases, respiratory infections, most commonly parainfluenza virus, trigger the development of AOL in pediatric practice. Due to anatomical and physiological characteristics, croup occurs predominantly in infants and young children. [1]. The first symptoms of the disease are signs of laryngitis: voice hoarseness, dry rough cough. As the inflammatory process in the larynx progresses, hoarseness may increase, the cough becomes barking, noisy breathing or noisy inhalation (stridor) appears [3].

The diagnosis is clinical and is based on medical history and typical symptoms. As a rule, with timely initiation of adequate therapy, the disease is resolved within 1–2 days and has a favorable outcome [4]. At the prehospital stage, the drugs of choice are inhaled glucocorticosteroids (GCS) [5].

More than 30 % of cases of croup in children recur within 2 years after the first episode of obstruction [6]. Possible causes of recurrent AOL include allergic predisposition, gastroesophageal reflux, abnormalities in the structure of the larynx (cysts and tracheobronchomalacia), changes in the microbiota of the upper respiratory tract with the presence of streptococcus, chlamydia, and mycoplasma [7; 8].

The aim of the study is to analyze a clinical case of severe AOL with recurrent course complicated by grade III respiratory failure (RF) in a young child.

Clinical Case

A 6-month-old girl, M., was admitted to the emergency room of the city pediatric hospital with complaints of cough, severe shortness of breath, hoarseness, runny nose, fever, and loss of appetite.

The medical history shows that the first symptoms of the disease appeared in the child three days before hospitalization, when she complained of a fever of 37.7°C, “noisy breathing”, and difficulty breathing through the nose at night. The mother called an ambulance. The doctor prescribed budesonide inhalation at a dose of 250 mcg, but due to the child's severe anxiety, the treatment was not completed in full. The parents refused to hospitalize the child.

The next morning, the dry cough persisted, but her body temperature did not rise. The patient was examined by an emergency doctor: her condition was moderate, with retraction of the jugular fossa, flaring of the nostrils, tachypnea up to 32 breaths per minute, tachycardia up to 132 beats per minute, and oxygen saturation of 95 %. Hard breathing and dry rales were heard above the surface of the lungs. Rapid tests for influenza A and B and coronavirus infection were negative. Diagnosis was as follows: acute bronchitis with obstructive syndrome, RF – 0–I degree. Due to the worsening of respiratory symptoms, hospitalization was recommended again, which the mother refused once more. In the evening of the same day, the emergency doctor conducted an audio check of the patient and determined that the treatment had not been effective. Amoxicillin with clavulanic acid was prescribed remotely in an age-appropriate dosage (taken once). The child received two doses of interferon alpha (150,000 MU) in suppositories, two inhalations with ipratropium bromide and fenoterol (9 drops), and a single dose of 500 mcg of budesonide using an ultrasonic nebulizer.

The next day, during an active visit by the emergency doctor, it was established that the child's condition had deteriorated: there was a single episode of vomiting, refusal to eat and drink, mixed dyspnea, cough, runny nose against a background of low-grade fever. The condition was severe, with a significant deterioration in well-being, a negative reaction to examination, pale skin, and a sunken fontanelle. The respiratory rate increased to 40 per minute, and the heart rate rose to 142 per minute. Hard breathing with dry rales and prolonged exhalation was heard over the entire surface of the lungs. The auxiliary muscles were involved in breathing – retraction of the epigastric region and intercostal spaces was noted during inspiration, indicating increasing respiratory failure (RF) to grade I–II. Due to the severity of the condition, a resuscitation team was called. Oxygen therapy could not be administered at the prehospital stage due to the child's severe agitation.

Medical history: the mother's pregnancy was complicated by arterial hypertension and preeclampsia. The child was born prematurely with low birth weight (1860 g) by emergency cesarean section; from the 3rd to the 10th day, she was on artificial ventilation (AV). At discharge, the diagnosis was: prematurity at 33–34 weeks, respiratory distress syndrome, RF grade III, transient hypoxic-ischemic encephalopathy, patent foramen ovale (2.7 mm), patent ductus arteriosus (1.5 mm). During the first six months of life, she received treatment for atopic dermatitis and herpes infection. She had not previously suffered from respiratory infections.

The child was admitted to the emergency room of the city pediatric hospital on the third day after the onset of the disease with the following diagnosis: AOL, grade II laryngeal stenosis complicated by broncho-obstructive syndrome (BOS), grade II RF; toxicosis with grade I–II exicosis. Against a background of moderate catarrhal symptoms, hoarseness, and sunken fontanelle, the respiratory rate increased to 60 per minute, the heart rate to 165 beats per minute, and oxygen saturation decreased to 90–94 %. Due to the severity of his condition and indications for oxygen therapy, the child was admitted to the intensive care and resuscitation unit. She was given oxygen, a single inhalation with adrenaline, and received GCS and cefoperazone with sulbactam parenterally. A few hours later, the child was diagnosed with sopor (13 points on the Glasgow Coma Scale), and RF reached grade III. Spontaneous breathing was ineffective, and inhalation therapy and systemic glucocorticosteroids had no effect. Direct laryngoscopy revealed swelling of the vocal cords and narrowing of the lumen due to edema. Due to vital indications, orotracheal intubation of the trachea with a No. 3 tube to a depth of 13 cm was performed, and the child was transferred to artificial lung ventilation. Blood gases showed signs of respiratory acidosis (pH – 7.29, PCO₂ –50.9 mmHg, pO₂ –142 mmHg). In clinical blood tests there was leukopenia up to 4.3·10⁹/L. Biochemical blood test: total protein 55 g/L, albumin 36 g/L, AST 51 U/L, ALT 28 U/L. In the general urine test: ketones (1.5 mmol/L) as a manifestation of toxicosis.

With respiratory support, respiratory acidosis was compensated. By evening, the child's condition had stabilized: body temperature, heart rate, and oxygen saturation were within normal limits.

Further examination of the chest X-ray revealed no focal shadows or areas of infiltration. The electrocardiogram showed bradycardia and QT prolongation. An ultrasound examination of the heart revealed signs of a patent foramen ovale (2.5 mm in the CDI) with left-to-right shunting and an additional chord in the left ventricle. Serological testing revealed IgG antibodies (positivity coefficient – 8.0) and IgM antibodies (avidity – 11.3) to cytomegalovirus infection, and Streptococcus milleri was detected in sputum (10³). According to the neurologist's examination, there are signs of perinatal transient hypoxic-ischemic encephalopathy; according to the otolaryngologist's consultation, there are signs of acute rhinitis. In a repeat clinical blood test, hemoglobin was 107 g/L and lymphocytes were 84%. In the general urine analysis, there was phosphaturia (++).

The treatment provided a positive effect, the child was extubated, and the signs of toxicosis with exicosis were relieved. Final diagnosis at discharge: AOL complicated by BOS, RF III degree, toxicosis with exicosis I–II degree.

After this hospitalization, the child had three more episodes of AOL within six months, one of which required hospitalization in the intensive care unit. Due to the repeated severe episode of AOL, the child was referred for magnetic resonance imaging: a round cystic inclusion was found under the larynx in the tracheal lumen, covering 2/3 of the lumen, which probably caused the severity and recurrent nature of the disease. Laryngoscopy was performed with removal of the subglottic space cyst, after which, to date (within 8 months), no repeated episodes of AOL have been recorded. Histological examination of the surgical material confirmed the benign nature of the cyst.

Results and Discussion

When providing emergency care for croup in AOL, it is important to administer high-dose, short-term glucocorticosteroid therapy in a timely manner. It is recommended to use budesonide suspension in inhalations at a dose of 1 mg twice at 30-minute intervals, or 2 mg once via a compressor or mesh nebulizer (spraying GCS in an ultrasonic inhaler may negatively affect the therapeutic properties of the medication) [9]. Intramuscular administration of dexamethasone at a dose of 0.15–0.6 mg/kg could be used for a young child with increased anxiety and agitation during a croup attack, as recommended by current clinical guidelines in the presented clinical case [9]. According to Bykov et al. (2024), a single parenteral administration of 0.5 mg/kg of dexamethasone at the prehospital stage in children with AOL reduces the severity of symptoms within 6 hours, prevents repeat visits, and is no less effective than inhalation administration of adequate doses of budesonide [10].

The main cause of recurrent AOL in the child described in this clinical case was probably a laryngeal cyst against a background of an atopic phenotype, perinatal damage to the nervous system, and a history of prematurity. The attending physician's decision to refer the child for an in-depth examination due to repeated severe episodes was justified. With regard to the identification of anatomical formation of the subglottic space, it should be noted that organic causes play an important role in the genesis of recurrent AOL, making the anatomically narrow subglottic space of young children even narrower and often detected in premature babies with a history of intubation and mechanical ventilation [1].

In the case presented, when it was necessary to refer the patient to a specialized level of medical care, there were difficulties in obtaining timely consent from legal representatives for hospitalization, especially during the first episode of AOL. It should be noted that in young children, the severity of AOL can increase quite rapidly with an increase in RF, which worsens the prognosis of the disease. Effective communication between healthcare professionals and legal representatives of pediatric patients regarding treatment decisions is particularly important in cases of emergency care for young children.

According to data from the city ambulance station, in 2023, the second of two severe cases of AOL was in a 9-year-old child (Westley score at the height of croup – 11 points) [11]. In this case, timely and adequate emergency treatment led to the relief of the main symptoms within 1 hour (a decrease in severity on the Westley scale from 11 to 3 points) and the resolution of the disease without recurrence.

Conclusions

This clinical case highlights the importance of timely assessment of the course of the disease, when, during repeated severe episodes of AOL, additional examination of the patient was prescribed and an anatomical formation in the subdiaphragmatic space was identified; its removal led to the cessation of disease recurrence. It is important to follow current AOL treatment protocols in terms of dosages and routes of administration of drugs used to relieve acute symptoms in young patients.

Given the rarity of severe forms of croup in AOL, it is necessary to keep pediatricians informed about the main factors that can alter the course of the pathological process, increasing its severity or causing relapses.

About the authors

O. V. Gulyaeva

Ye.A. Vagner Perm State Medical University

Author for correspondence.
Email: oxanag@hotmail.com
ORCID iD: 0009-0002-6594-5673

PhD (Medicine), Associate Professor of the Department of Pediatrics with a Course in Polyclinic Pediatrics, Pediatrician

Russian Federation, Perm

A. S. Tretyakova

Ye.A. Vagner Perm State Medical University

Email: oxanag@hotmail.com
ORCID iD: 0009-0006-5452-7555

Resident of the Department of Pediatrics with a Course in Polyclinic Pediatrics, Pediatrician

Russian Federation, Perm

N. V. Minaeva

Ye.A. Vagner Perm State Medical University

Email: oxanag@hotmail.com
ORCID iD: 0000-0002-2573-9173

DSc (Medicine), Professor, Head of the Department of Pediatrics with a Course in Polyclinic Pediatrics, Pediatrician

Russian Federation, Perm

References

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