Large Benign Goiters: Special Considerations for Management

Yitzhak Etan Weinstock, MD
Assistant Professor

 

The term “goiter” simply refers to an abnormal enlargement of the thyroid gland.  There are multiple causes of goiters and their presence does not necessarily indicate that the thyroid gland is malfunctioning on a hormonal level.  However its presence indicates that there is a condition causing the thyroid gland to grow abnormally.  These massive thyroid glands may be benign or malignant in nature.  In this review, I am focusing on benign goiters.

Worldwide, iodine deficiency is the leading cause of goiter formation.  This is no longer a frequent cause in the United Stated because of iodization of table salt.  Still, giant goiters still present on occasion.  These patients have usually allowed the thyroid gland to grow to enormous size with many years of neglect, but occasionally growth can be rapid.  Rapid growth is a concerning sign because it may be a harbinger of malignant pathology, or may represent hemorrhage into the gland.

On a basic level, surgical management of giant goiters is the same as routine thyroid goiters, but there are multiple unique issues that must be attended to.  Euthyroid state and endocrinologic optimization prior to these cases is imperative when they are performed electively.  In some scenarios, emergency surgery is required due to the multiple effects of large thyroid goiters.  When this is the case, the patient should be optimized as best possible prior to operative intervention.

Large goiters cause multiple airway issues that may complicate surgery. First, the trachea may be deviated by the large gland making intubation challenging.  Generally, fiberoptic intubation is readily accomplished in these patients, but an airway management plan must be discussed with the anesthesiologist in advance of any attempts.  Another problem with the airway is that these patients cannot be easily tracheotomized if the patient develops respiratory compromise because the thyroid typically covers the trachea along the entire cervical portion.

Longstanding airway compression from goiters may also lead to tracheomalacia.  This can be a serious, even life threatening, issue in the postoperative patient.  Ideally, we should identify which patients have tracheomalacia as a result of longstanding compression prior to undertaking any thyroid surgery because pre-operative discussion and surgical plan will be affected by this comorbidity.  The gold standard for diagnosis is tracheoscopy while the patient is spontaneously breathing.  This dynamic evaluation would exhibit either inspiratory or expiratory collapse of the airway depending on whether the segment is extra or intra-thoracic respectively.   This can be performed prior to any neck surgery and can also be done as the first step in the thyroidectomy procedure.  However, the symptoms and findings may not manifest until after the thyroid gland is removed.  This is because fibrous attachments from the thyroid gland to the trachea may help maintain airway patency during the breathing cycle.  This external scaffolding is lost with thyroidectomy allowing the trachea to collapse.  If pre-operative diagnosis is inconclusive or impossible, intraoperative detection is the second best option.  It may be difficult to detect whether tracheomalacia exists intraoperatively because the cartilage may seem rigid when palpated after removal of the goiter.  It is usually after thyroidectomy and extubation that these patients may develop stridor from dynamic collapse of the weakened trachea.  Intraoperative tracheoscopy is not ideal because adequate evaluation requires removal of the endotracheal tube which may be stenting the trachea.  Identification should be made prior to closing the neck wound so that surgical management can be performed if necessary; however,  switching to bronchoscopy during the surgery exposes the patient to potential wound contamination.  One way that this can be accomplished safely is by having the anesthesiologist place a flexible bronchoscope through the endotracheal tube and withdrawing the tube to the level of the vocal cords.  We can then watch on the monitor to determine if there is any collapse and what degree of airway obstruction this causes.  It is imperative to discuss this with the anesthesiologist well in advance so that the anesthetic management will have the patient spontaneously breathing at the appropriate time.

Addressing this tracheomalacia presents some other interesting challenges.    Some authors suggest that sutures placed through the weakened trachea and secured to rigid fixation points such as the sternum or implanted rigid prosthesis such as an aortic endovascular stent are adequate to withstand the collapsing force.  Others recommend tracheal resection and anastomosis.  This may not be readily possible in patients with enormous goiters because the length of the segment may be too long for simple primary anastomosis and would require more extensive procedures.  Tracheotomy should allow for the patient to breathe freely despite the tracheomalacia, but this, too poses a challenge.  If the weak segment is above the thoracic inlet, tracheostomy distal to this will allow inspiratory airflow without airway collapse.  If the tracheomalacia segment is thoracic, an extended length tracheostomy tube will stent the airway open during expiration.  Both types of tracheostomy, though will be placed through the surgical incision and will thus prevent neat linear wound healing as well as expose the entire wound and neck contents to unsterile tracheal secretions, increasing risk of infections.  Maturing the tracheostoma to the skin may help alleviate some of this risk, but that in turn leads to higher incidences of tracheocutaneous fistula formation and secondary surgery if the patient ever manages to be decannulated.

There are multiple hemodynamic changes that occur with giant goiters.  Usually these occur when there is substantial substernal extension because the gland and all upper mediastinal structures are compressed between the rigid sternal bone and the spine in a finite space.    The gland may thus cause compression of the neck and upper mediastinal vessels causing venous outflow obstruction and superior vena cava syndrome.  One way to assess this pre-operatively is by having the patient elevate their arms above their head.  As venous return to the vena cava increases, outflow obstruction will cause flushing in the face and dyspnea known as Pemberton’s sign.  Another ramification of this venous congestion is that there can potentially be “downhill varices” of the upper esophagus which can lead to hematemesis.  These engorged feeding vessels should be recognized intraoperatively and appropriately ligated to help prevent bleeding.  Superior vena cava syndrome may also cause thrombosis in the vena cava.  Dyspnea may be caused by decompensated right sided congestive heart failure, pleural effusion and pulmonary hypoperfusion caused by compression of the pulmonary arteries.  There have even been numerous reports of cerebrovascular insufficiency and stroke from goiters either by direct compression of the carotid arteries or by “thyrocervical steal” caused by increased thyroid blood flow.  In these cases, thyroidectomy was curative of the ischemic events.

Incidences of intraoperative complications are higher in patients with large goiters when compared to patients with smaller thyroid glands.  These complications include higher rates of transient and permanent vocal cord paralyses as well as temporary and permanent hypocalcemia from parathyroid gland injury.

Neurologic injury from benign thyroid disease has been reported in cases of large benign goiter as well.  These include phrenic nerve palsies, Horner’s syndrome and recurrent laryngeal nerve palsies.   In these rare reports, the nerves may return to function following thyroidectomy.

Another consideration that must be made in patients with giant goiters is their proclivity towards poor nutritional status.  The thyroid in these patients may either be compressing the esophagus directly via posterior extension or indirectly via crico-tracheal compression posteriorly.  Often, it is the resultant dysphagia which leads patients to presentation.  Poorly coordinated swallow may result and may persist beyond thyroidectomy and thus the operating surgeon should be mindful of the possibility of persistent dysphagia following surgery.  The operating surgeon should also be mindful of the patient’s nutritional status pre-operatively as this may lead to poor wound healing.  This malnutrition can have multiple effects on the endocrine function of the thyroid gland.  Additionally, malnutrition can lead to low protein states causing multiple endocrine abnormalities including decreased levels of thyroid hormone and even increased thyroid size.

Overall, the technical aspects of surgical management of large goiters are similar to those of the more common smaller goiter variety; however there are many unique issues that arise as a result of the glands size.  Surgeons who undertake these cases should be mindful of all of the potential pitfalls and special considerations that confound these interesting cases.  The surgeon should also be skilled routine thyroid surgery as well as procedures which may be required based on operative findings.