Cushing’s reflex secondary to neck haematoma following thyroidectomy

Abstract

Neck haematoma following thyroid surgery can present with respiratory distress which is generally attributed to airway obstruction. We recently had a 63-year-old female patient who underwent total thyroidectomy for toxic nodular goitre. However, within 4 hours of surgery, she developed sudden respiratory distress which was managed by prompt evacuation of the neck haematoma. Just before the haematoma evacuation, the patient had hypertension and bradycardia along with the distress. The arterial blood gas analysis sampled at that time was normal. Intraoperatively, the tracheal framework was found rigid and non-pliable. Considering the various clinical–biochemical findings observed, we think that the cause of the respiratory distress in the index case was transiently elevated intracranial pressure, secondary to bilateral internal jugular veins' compression. We hypothesise that in many patients with immediate postoperative neck haematoma, the Cushing’s reflex would at least contribute partly, if not solely to the respiratory distress.

Background

The data from the USA’s ‘National Surgical Quality Improvement Program’ reported the neck re-exploration rate of 3.4% following thyroid surgeries, 75% of which were to evacuate the neck haematoma.¹ Most of the patients with post-thyroidectomy neck haematoma manifest as respiratory distress which is thought to be due to the mechanical compression of the trachea or the mucosal oedema of supraglottic larynx and pharynx.² We present a case of postoperative neck haematoma following thyroidectomy, in which, we suggest an alternative cause for respiratory distress. Along with the discussion on some of the features supporting our hypothesis, we have included the relevant literature review.

Case presentation

A 63-year-old female patient was referred to the department of otorhinolaryngology and head and neck surgery for the surgical management of toxic nodular goitre. She was euthyroid at the time of admission. She was recently diagnosed to have diabetes mellitus and had controlled blood sugar with dietary management, without any active antidiabetic medications. However, she was taking cilnidipine 10 mg once daily for controlling her hypertension. She was also on propranolol 40 mg once daily along with carbimazole 30 mg once daily for hyperthyroidism. On examination, she had a normal body mass index, pulse of 70 beats per minute, blood pressure of 136/80 mm Hg and a WHO grade II goitre.

Investigations

Her thyroid hormones were within normal limits at the time of surgery.

Treatment

After a detailed discussion with the endocrinologist, the patient and the patient’s attendants, it was decided to perform a total thyroidectomy. The patient had taken her antihypertensive medication on the morning of the surgery and had a pulse of 74 beats per minute with a blood pressure of 140/86 mm Hg before the surgery, as shown in figure 1. Under general anaesthesia, both the lobes of thyroid were removed along with the isthmus. However, the bilateral inferior parathyroid glands, as well as both the recurrent laryngeal nerves, were identified and preserved. Her intraoperative pulse rate was around 60 beats per minute, and the blood pressure was 110/70 mm Hg. Just after the extubation, normal mobility of both the vocal cords was confirmed, and the blood pressure was also within normal limits as shown in figure 1. At around the 4th hour after surgery, the patient felt sudden uneasiness and tightness of the neck in the anaesthesia recovery room. Her recorded blood pressure was 180/110 mm Hg, and heart rate was between 35 and 40. While the surgical resident was summoned for evaluation, the patient became restless rapidly. Her respiratory pattern changed within a few moments, her eyeballs rolled upwards and she had a near cardiac arrest. The anaesthetist on duty immediately intubated the patient and assisted the ventilation, while the surgical resident released the neck wound. The arterial blood gas analysis showed a pH of 7.32, pO₂ of 112 mm Hg, pCO₂ of 36.9 mm Hg and sO₂ of 98.3%. The patient was shifted to the operating room, and the haematoma of around 200–250 mL evacuated from the surgical bed. The tracheal framework was found to be healthy, rigid and non-pliable. The primary source of bleeding was the anterior jugular vein which was ligated again. The patient had temporary inotrope support for few hours on the day of re-exploration for low blood pressure. She was electively kept on respiratory support overnight and was extubated on the next day.

Figure 1.

Blood pressure chart of the index case during the hospital stay.

Outcome and follow-up

She had transient hypocalcaemia for 3 days, however, remained asymptomatic. She further had an uneventful postoperative recovery and was discharged after 4 days. She is on thyroxine supplementation therapy.

Discussion

The incidence of neck haematoma following thyroidectomy range from 1.36% to 2.57%.^2–4 The largest study to have analysed the retrospective data of inpatients undergoing thyroidectomy has reported the neck haematoma requiring intervention in 1.25% of 150 012 thyroidectomy procedures.⁵ Patients undergoing thyroidectomy in older age are more prone to develop postoperative neck haematoma.^{2 5–8} Also, those with previous hyperthyroidism^{6 7} and those getting the removal of both the lobes of the thyroid^{2 8} are at higher risk of having neck haematoma. Though the index patient had these risk factors, in general, women^{2 4–8} and non-obese individuals^{5 6} are less likely to encounter this complication after thyroidectomy.

Most of the symptomatic neck haematomas after thyroidectomy which require re-exploration present within the first 6 hours of surgery and often inside the anaesthesia recovery room itself.^{2 3 8} Haematomas developing later in the course are relatively indolent and can be managed by non-emergent procedures.⁹ Contrary to these late-onset cases, the acute postoperative haematomas often present with respiratory distress¹⁰ which is thought to be due to tracheal compression by the neck haematoma.¹¹ However, experimental studies have shown that even with the maximal possible pressure that could be exerted by the neck haematoma, the compression of the tracheal cartilaginous framework is not significant.¹² Some authors attribute this respiratory distress to supraglottic lymphovenous oedema, secondary to the internal jugular vein (IJV) obstruction.^{2 12} However, it takes hours for this oedema to set in, to the extent of being symptomatic,¹³ making this an unlikely cause for acute distress seen in immediate postoperative haematomas. Besides, in many reported cases of respiratory distress secondary to postoperative neck haematoma, comprising both thyroid and non-thyroid surgeries, the airway could be successfully secured by emergency endotracheal intubation.^13–15 These raise the question about the relevance of laryngopharyngeal mucosal oedema in these cases. At times, the haemodynamics may not even improve despite secured airway in neck haematoma case but may improve immediately after relieving the compression of the IJV.¹³

We think that the respiratory distress seen in our case is a manifestation of the raised intracranial pressure secondary to simultaneous compression of both the IJVs by neck haematoma. The sudden obstruction of bilateral venous outflow from the cranium, along with the continued carotid perfusion would have led to the elevated intracranial pressure and subsequent respiratory disturbance in the index case. As discussed in the subsequent paragraphs, we substantiate our hypothesis by the clinic biochemical findings observed in our case and by reviewing the relevant literature.

First of all, considerably less pressure is required to compress the IJV than the trachea. The normal pressure inside the IJV is 20 times less than the pressure needed to compress the cadaveric pig trachea.¹² Postmortem studies in humans also have shown that the IJV can be compressed even without any damage to the framework of the airway during strangulation.¹⁶ Because both the IJVs and the trachea are enclosed in a closed compartment surrounded by investing layer of deep cervical fascia, it is probable that the evolving neck haematoma compresses the IJVs quite earlier than the trachea.

Second, both experimental and clinical studies have shown that the compression of IJV significantly increases the intracranial pressure.^{17 18} Animal studies have shown that this elevation takes place within seconds of compression of the IJV.¹⁹ This can explain the rapidity with which the patient manifests in a case of immediate onset neck haematoma following surgery. The manifestations of the rapidly elevated intracranial pressure include an increase in systolic blood pressure, a decrease in heart rate and respiratory irregularities, popularly known as Cushing’s reflex or Cushing’s phenomenon.²⁰ All of these clinical findings were observed in our case just before the haematoma evacuation and were utterly normalised after haematoma evacuation.

Third, some authors have identified the ‘elevated postoperative blood pressure’ as an independent risk factor for the early onset neck haematoma following thyroidectomy.^{3 4 21} However, only the isolated recording of highest blood pressure has been taken into account in these studies. They have neither reported the continuous blood pressure monitoring in the postoperative period nor have they established a time relation between the recording of elevated systolic blood pressure and the development of neck haematoma. It is entirely possible that the elevated systolic blood pressure in these studies could actually be a manifestation of the raised intracranial pressure secondary to acute compression of the IJVs. Interestingly, in the largest retrospective study on neck haematoma after thyroidectomy, the association of hypertension in patients with neck haematoma was statistically significant compared with those without haematoma. However, further analysis of the same data revealed that hypertension did not increase or decrease the risk of neck haematoma formation in these cases.⁵

Lastly, we ruled out laryngopharyngeal mucosal oedema in our case considering the rapid onset of symptoms and the ease with which the reintubation was done even before the haematoma evacuation. Finding the normal and rigid trachea on re-exploration makes the tracheal compression also less likely. Moreover, the arterial blood gas analysis showing the normal PaO₂ of oxygen and carbon-dioxide without any respiratory acidosis or hypoxaemia suggested that the respiratory distress in our case was not attributable to airway obstruction. All of these findings indicated an alternative cause for respiratory distress in the index case. The features of Cushing’s reflex during the immediate postoperative haematoma and their disappearance after the evacuation of haematoma support our hypothesis of raised intracranial tension secondary to bilateral IJV compression. We recommend early evacuation of the neck haematoma to prevent the rapid rise in intracranial tension and its morbid consequences.

Learning points.

• Respiratory distress seen in acute neck haematoma following thyroidectomy is less likely to be due to airway compression or oedema.

• Neck haematoma can cause compression of bilateral internal jugular veins rapidly which may elevate the intracranial tension and lead to Cushing’s reflex.

• We recommend early evacuation of the neck haematoma to prevent the rapid rise in intracranial tension and its morbid consequences including respiratory suppression.