Secondary Logo

Journal Logo

Case Report

Chondronecrosis of the cricoid cartilage after intubation. Two case reports

Wiel, E.; Vilette, B.; Solanet, C.; Darras, J. A.; Scherpereel, P.

Author Information
European Journal of Anaesthesiology: July 1997 - Volume 14 - Issue 4 - p 461-463



Between January 1991 and June 1995, we saw two cases of necrosis of the cricoid cartilage from a total of 12 children with subglottic stenosis. All the children were looked after and intubated in a paediatric intensive care unit (ICU).

Case reports

Patient no. 1

An 8-month-old girl, weighing 8 kg, who had been delivered at 36 weeks of gestation by Caesarean section under general anaesthesia, developed recurrent upper respiratory infections. A diagnosis of myelomonocytic leukaemia was made. The patient had hyperleukocytosis with abnormal blasts.

She needed general anaesthesia for placement of a central venous catheter. A 4.0 mm uncuffed tracheal tube was placed orally. Anaesthesia lasted 1 h. Bronchospasm developed just after extubation and she needed re-intubation of her trachea. Mechanical ventilation continued for 2 days. Ten days later she developed dyspnoea with stridor. Direct laryngoscopy showed laryngeal oedema, with a whitish exudate of the vocal cords. Her trachea was intubated with a 3.5 mm uncuffed tube; her lungs were ventilated with a Servo 900B ventilator and she was sedated with midazolam (0.15 mg kg−1). She was given methylprednisolone (1.5 mg kg−1). Three days later, direct laryngoscopy showed persisting laryngeal oedema and extubation was not possible. Her trachea was reintubated with a 4.0 mm uncuffed tube, without a leak test. Eight days after this, there was an accidental extubation. At direct laryngoscopy under general anaesthesia, we saw lysis of the upper and posterior borders of the cartilage of the cricoid ring, with mucosal denudation. There was subglottic stenosis with granulation tissue. A 3.5 mm tracheal tube was left in place for 6 days. By then the patient was 9 months old and weighed 9 kg. Eleven days after extubation, she again became acutely dyspnoeic, and direct laryngoscopy showed subglottic stenosis. There was oedema of the false cord and a necrotic mass with scar tissue obstructing the whole subglottic region. She was treated with CO2 laser and a 3.5 mm uncuffed tracheal tube was placed. One week later, she was given a tracheostomy (No. 2 cannula). At direct laryngoscopy, there was a stenotic cricoid ring and a fixed scarred right hemilarynx. The trachea was normal. She is now 1 year old and still requires a cannula.

Patient no. 2

A healthy 4-year-old girl, weighing 20 kg, became comatose after accidental ingestion of an anti-histamine (alimemazine, 50 mg). Her trachea was intubated orally with a 5.0 mm uncuffed tube as an emergency, without a leak test. She developed short-lasting seizures and aspiration pneumonia. Two days after intubation, she was transferred to the paediatric ICU. She was extubated 8 h later but immediately developed laryngeal dyspnoea. The dyspnoea resolved with local and systemic steroids but 4 days later she developed acute laryngitis. An endoscopic investigation under local anaesthesia showed cricoid stenosis with friable granulomata. Further examination under general anaesthesia confirmed that the degree of stenosis was severe owing to inflammation. There was necrosis of the anterior cartilage of the cricoid ring with mucosal denudation. The trachea was intact. The stenotic airway was dilated, and local steroids were applied. Extubation was successful. Two days later, laryngoscopy still showed necrosis of the cricoid cartilage but the stenosis had resolved. She continued to receive intravenous (i.v.) antibiotic (amoxycillin, 50 mg kg−1 day−1) and steroids (methylprednisolone, 1.5 mg kg−1 day−1), later altered to oral steroids which were then gradually withdrawn. She made an uneventful recovery.


Chondronecrosis of the cricoid cartilage is a recognized but rare complication of tracheal intubation in infants and children [1].

The first description was in 1971: a 3-year-old girl developed chondronecrosis after intubation for toxic coma [2]. In 1980, having seen four cases of partial chondronecrosis of the cricoid out of 36 cases of laryngotracheal stenoses, Gehanno et al. reviewed the literature, and found five similar cases [3]. In 1989, Hannion et al. reported two cases out of 45 cases of laryngotracheal stenoses after intubation collected during a 10-year period [4].

The importance of causative factors in chondronecrosis of the cricoid have been emphasized by Desnos et al.[5]. Coma is a risk factor because of decreased capillary perfusion pressure, which makes ischaemic necrosis secondary to compression more likely [6]. We think this was a factor in our second case. Depression of the immune system, which was present for our first case, is a risk factor because then infection of damaged areas is more likely, and may delay wound healing. We believe our first case was caused by pressure of the tracheal tube on the cricoid ring, and our second case by the trauma of the emergency intubation. Ideally, intubation should be atraumatic [7], and the first intubation seems to be important in the development of laryngeal lesions. The route of intubation is less important, it is multiple intubations that should be avoided [8–10], and sedation is advised to reduce laryngotracheal damage during ventilation.

The size of the tracheal tube is important. There are three selection methods. Huault's tables [11] correlate age, weight and diameter of tubes, direct comparison with the width of the fifth fingernail, and estimation using a formula ([age (year) + 16]/4). In a recent study, a more accurate estimate was made with the agebased formula, but when the child's age is unknown or when calculation is impossible, an acceptable estimate can be made using the width of the fifth fingernail [12]. We based our tube sizes on age and weight.

When in doubt, it is better to use a smaller tracheal tube [13,14]. When a laryngeal lesion is diagnosed, a half size smaller tube has to be used, as we did for our first patient. In this way, the pressure exerted by the tube does not exceed the capillary perfusion pressure of the laryngotracheal mucosa, which is 18 to 25 mmHg [15]. It avoids ischaemic necrosis and exposure with partial erosion of the underlying cartilage.

We did not perform a leak test, which some authors suggest as a way of assessing tightness of fit [16], because we usually use Huault's tables to find the size that balances the risks of pressure-induced tracheal injury and aspiration, and we confirm the size of the tracheal lumen by direct laryngoscopy. If a leak test is used, an increasing leak, or a decreasing leak pressure, is a sign that the size of the tracheal lumen has increased and that extubation may be safely accomplished [17].

The clinical sign that alerted us was dyspnoea occurring just after extubation, which we suggest is an indication for direct laryngoscopy. The supraglottic and glottic regions should be examined under local anaesthesia (without prior glottic suction, which could cause reflex laryngospasm). Examination under general anaesthesia can be carried out later to examine the subglottic region. Friable granulomata may indicate underlying necrosis of the cartilage [3].

Medical treatment is steroids given by aerosol and systemically, plus broad spectrum antibiotics [18]. Intubation can prevent progression of the oedema (as in our first patient). The condition should be re-evaluated by laryngoscopy at 8 and 10 days. Massive chondronecrosis requires surgery, from laryngotracheoplasty with stent to resection of the necrosis with laryngotracheal anastomosis.

Prevention is better than later treatment and reconstruction: gentle intubation, sedation during intubation, fixation of the tracheal tube to prevent displacement, good nursing care to avoid infection, antibiotics, steroids (though this is controversial) and regular check-up.

Cricoid cartilage necrosis is rare. It is a serious complication although the cricoid cartilage is highly vascular [19]. Treatment is hazardous, lengthy and poorly tolerated. Prevention will reduce the incidence and the economic cost of the treatment.


The authors wish to thank Nam Nguyen, MD, from the department of radiation oncology, Beth Israel Hospital, New York, USA, for his help.


1 Quiney RE, Gould SJ. Subglottic stenosis: a clinicopathological study. Clin Otolaryngol 1985; 10: 315–327.
2 Gross CW, Gros JC. Rare complications after prolonged translaryngotracheal intubation. Ann Otol Rhinol Laryngol 1971; 80: 582–584.
3 Gehanno P, Leowski Y, Lallemant Y, Crepin A. Les chondronécroses du cricoïde après intubation prolongée. A propos de 4 observations. Ann Oto-Laryngol (Paris) 1980; 97: 711–724.
4 Hannion X, Legros M, Schmidt P, Le Tarnec A. Chondronécrose du cricoïde après intubation. A propos de 2 cas. J Fr Oto-Rhino-Laryngol 1989; 38: 328–331.
5 Desnos J, Pornhauser X, Dubin J. Les risques ary-cricoïdiens de I'intubation difficile. J Fr Oto-Rhino-Laryngol 1976; 25: 381–384.
6 Narcy Ph, Contencin Ph, Fligny I, Francois M. Surgical treatment for laryngotracheal stenosis in the pediatric patient. Arch Otolaryngol Head Neck Surg 1990; 116: 1047–1050.
7 Gould SJ, Graham J. Long term pathological sequelae of neonatal endotracheal intubation. J Laryngol Otol 1989; 103: 622–625.
8 Laing IA, Cowan DL, Ballantine GM, Hume R. Prevention of subglottic stenosis in neonatal ventilation. Int J Pediatr Otorhinolaryngol 1986; 11: 61–66.
9 Nicklaus PJ, Crysdale WS, Conley S, White AK, Sendi K, Forte V. Evaluation of neonatal subglottic stenosis: a 3-year prospective study. Laryngoscope 1990; 100: 1185–1190.
10 Hawkins DB. Pathogenesis of subglottic stenosis from endotracheal intubation. Ann Otol Rhinol Laryngol 1987; 96: 116–117.
11 Huault G, Labrune B. Tailles des sondes d'intubation en fonction de I'age et du poids. Pédiatrie d'urgence. In: Flammarion Médecine-Science 1981: 1099.
12 King BR, Baker MD, Braitman LE, Seidi-Freidman J, Schreiner MS. Endotracheal tube selection in children: a comparison of four methods. Ann Emerg Med 1993; 22: 530–534.
13 Weymuller EA, Bishop MJ, Fink BR, Hibbard AW, Spelman FA. Quantification of intralaryngeal pressure exerted by endotracheal tube. Ann Otol Rhinol Laryngol 1983; 92: 444–447.
14 Stamm D, Floret D, Stamm C, Cochat P, Truy E, Morgon A. Sténoses sous-glottiques séquellaires d'intubation chez l'enfant. Arch Fr Pediatr 1993; 50: 21–25.
15 Nordin U, Lindholm CE, Wolgast M. Blood flow in the rabbit tracheal mucosa under normal conditions and the influence of tracheal intubation. Acta Anaesthesiol Scand 1977; 21: 81–94.
16 Finholt DA, Henry DB, Raphaely RC. Factors affecting leak around tracheal tubes in children. Can Anaesth Soc J 1985; 32: 326–329.
17 Finholt DA, Audenart SM, Stirt JA et al. Endotracheal tube leak pressure and tracheal lumen in swine. Anesth Analg 1986; 65: 667–671.
18 Sasaki CT, Horivchi M, Koss N. Tracheotomy related subglottic stenosis: bacteriological pathogenesis. Laryngoscope 1979; 89: 857–865.
19 Guerrier Y, Andrea M. Microvascularisation de la muqueuse laryngée et trachéale. Ann Otolaryngol Chir Cervicofac (Paris) 1980; 97: 409–421.

Complications, cricoid chondronecrosis; Intubation; Children

© 1997 European Academy of Anaesthesiology