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Thyroid surgery is one of the most common endocrine procedures worldwide, and anesthetic management is often considered routine. However, when the thyroid gland is enlarged, nodular, or extends retrosternally, thyroidectomy becomes a high-stakes anesthetic challenge. For anesthesiologists, the implications go beyond surgical removal of a gland — the bulk, extension, and anatomical relationships of the thyroid determine airway safety, cardiopulmonary stability, and postoperative outcomes.
Computed tomography (CT) of the thorax and neck has become indispensable in such cases, not only for surgical planning but also for perioperative risk stratification. The CT findings allow anesthesiologists to predict airway compression, mediastinal involvement, tracheomalacia, vascular displacement, and pulmonary compromise. In other words, a CT report is not just radiology — it is a roadmap for anesthetic decision-making.
The case under consideration involves a 54-year-old female with hypertension, on telmisartan (40 mg OD) and amlodipine (5 mg HS), presenting with a bulky left thyroid gland. Multiple TIRADS 3/4 nodules were noted, with the inferior pole extending retrosternally. CT thorax demonstrated a 5.2 × 3.7 × 6.8 cm lesion with peripheral calcification, pulmonary congestion, and atelectatic changes, but no gross vascular or tracheal encasement. Thyroid function was normal.
For newly joined residents, this case highlights how to translate CT findings into clinical anesthesia planning, while for senior anesthesiologists it emphasizes anticipating rare but catastrophic complications such as airway collapse, major vessel injury, or postoperative tracheomalacia.
This chapter will systematically analyze the CT findings and integrate them with respiratory physiology, cardiovascular pharmacology, airway pathophysiology, and perioperative strategies. Along the way, mnemonics, analogies, and “what if?” case drills will reinforce concepts for teaching and clinical application.
ReferencesEach CT finding in this patient has a specific anesthetic implication:
Analogies for learners help conceptualize these risks: the trachea in this patient is like a garden hose lying under a heavy stone — it looks patent until pressure dynamics change. The congested lungs are like a sponge already soaked with water — they cannot accept much more without losing elasticity.
ReferencesGeneral anesthesia reduces functional residual capacity by about 15–20%. When this falls below closing capacity, dependent airways collapse and shunt physiology develops. Atelectatic bands seen on CT are markers of these vulnerable areas that will worsen once anesthesia begins. Surfactant impairment, diaphragm displacement, and absorption atelectasis (particularly with high FiO₂) all combine to worsen gas exchange.
Pulmonary congestion is another significant finding. It is common in patients with long-standing hypertension or diastolic dysfunction. Congested lungs are stiff, poorly compliant, and prone to desaturation with even brief periods of apnea.
For anesthesia management, this means preoxygenation must be prolonged, preferably with PEEP. High oxygen concentrations should be avoided for long periods because they promote absorption atelectasis. Ventilation should follow lung-protective strategies with low tidal volumes and moderate PEEP. Fluid overload must be avoided, and some patients may benefit from diuretics preoperatively.
ReferencesThis patient’s antihypertensive therapy adds important layers to anesthetic planning.
Telmisartan, an angiotensin receptor blocker, prevents angiotensin II–mediated vasoconstriction and aldosterone release. Under anesthesia, this translates into a greater risk of refractory hypotension. Because catecholamine responsiveness may be impaired, hypotension may respond better to vasopressin.
Amlodipine, a long-acting dihydropyridine calcium channel blocker, maintains arteriolar vasodilation for many hours. This predisposes to exaggerated hypotension at induction when combined with anesthetic agents.
The key strategies are careful titration of induction drugs, preferring agents such as etomidate or low-dose propofol. Ketamine is a useful option in patients with suspected airway compression because it maintains sympathetic tone. Vasopressors such as norepinephrine, phenylephrine, and vasopressin must be prepared in advance.
ReferencesMallampati grading alone is inadequate for retrosternal goiters. CT provides objective tracheal diameters that help stratify risk. A diameter greater than 8 mm usually implies mild compression; between 5 and 8 mm indicates moderate risk; less than 5 mm suggests severe compression with high collapse risk.
Awake fiberoptic intubation is the safest approach for moderate or severe compression. Videolaryngoscopy may be sufficient when CT shows a central trachea without narrowing. Rigid bronchoscopy and surgical tracheostomy should be on standby.
A “what if” scenario illustrates the importance of preparation. If induction leads to sudden airway collapse, repositioning the patient may temporarily relieve obstruction. If this fails, rigid bronchoscopy is the next option. In extreme cases, a surgical airway or even ECMO may be required.
ReferencesInduction agents must be chosen carefully. Propofol is widely used but carries significant hypotension risk. Ketamine preserves blood pressure and airway tone but increases secretions. Sevoflurane inhalational induction can allow preservation of spontaneous ventilation, which may be safer in cases of airway compression.
Muscle relaxants should not be given until airway security is confirmed. Rocuronium can be administered once safe ventilation and intubation are ensured.
Invasive monitoring is essential. An arterial line provides beat-to-beat blood pressure monitoring. Large-bore intravenous access is needed to prepare for major bleeding. A central venous catheter is indicated if sternotomy is anticipated.
Ventilation should be lung-protective with low tidal volumes and moderate PEEP. Recruitment maneuvers should be used cautiously. Excess fluid administration must be avoided.
A practical scenario: if the innominate vein is injured during dissection, torrential blood loss can occur. Anesthesiologists must be prepared for rapid activation of the massive transfusion protocol, with balanced replacement of red cells, plasma, and platelets, along with vasopressor support and close coordination with surgeons.
ReferencesThe risks do not end with extubation.
Extubation should be staged, often over a tube exchanger, with postoperative observation in ICU or HDU.
ReferencesThe mnemonic GOITER captures the anesthetic implications:
The CT thorax in thyroidectomy patients is a perioperative blueprint. Each finding directly maps to physiology, pharmacology, and anesthetic planning.
For residents, the principle is systematic: CT finding → physiological effect → anesthetic implication → clinical action.
For senior practitioners, the key is anticipating rare but catastrophic complications such as airway collapse, vascular injury, and postoperative tracheomalacia.
Ultimately, safe anesthesia in such patients depends on anticipation, preparation, and seamless teamwork with the surgical team.
By RENNY CHACKOThyroid surgery is one of the most common endocrine procedures worldwide, and anesthetic management is often considered routine. However, when the thyroid gland is enlarged, nodular, or extends retrosternally, thyroidectomy becomes a high-stakes anesthetic challenge. For anesthesiologists, the implications go beyond surgical removal of a gland — the bulk, extension, and anatomical relationships of the thyroid determine airway safety, cardiopulmonary stability, and postoperative outcomes.
Computed tomography (CT) of the thorax and neck has become indispensable in such cases, not only for surgical planning but also for perioperative risk stratification. The CT findings allow anesthesiologists to predict airway compression, mediastinal involvement, tracheomalacia, vascular displacement, and pulmonary compromise. In other words, a CT report is not just radiology — it is a roadmap for anesthetic decision-making.
The case under consideration involves a 54-year-old female with hypertension, on telmisartan (40 mg OD) and amlodipine (5 mg HS), presenting with a bulky left thyroid gland. Multiple TIRADS 3/4 nodules were noted, with the inferior pole extending retrosternally. CT thorax demonstrated a 5.2 × 3.7 × 6.8 cm lesion with peripheral calcification, pulmonary congestion, and atelectatic changes, but no gross vascular or tracheal encasement. Thyroid function was normal.
For newly joined residents, this case highlights how to translate CT findings into clinical anesthesia planning, while for senior anesthesiologists it emphasizes anticipating rare but catastrophic complications such as airway collapse, major vessel injury, or postoperative tracheomalacia.
This chapter will systematically analyze the CT findings and integrate them with respiratory physiology, cardiovascular pharmacology, airway pathophysiology, and perioperative strategies. Along the way, mnemonics, analogies, and “what if?” case drills will reinforce concepts for teaching and clinical application.
ReferencesEach CT finding in this patient has a specific anesthetic implication:
Analogies for learners help conceptualize these risks: the trachea in this patient is like a garden hose lying under a heavy stone — it looks patent until pressure dynamics change. The congested lungs are like a sponge already soaked with water — they cannot accept much more without losing elasticity.
ReferencesGeneral anesthesia reduces functional residual capacity by about 15–20%. When this falls below closing capacity, dependent airways collapse and shunt physiology develops. Atelectatic bands seen on CT are markers of these vulnerable areas that will worsen once anesthesia begins. Surfactant impairment, diaphragm displacement, and absorption atelectasis (particularly with high FiO₂) all combine to worsen gas exchange.
Pulmonary congestion is another significant finding. It is common in patients with long-standing hypertension or diastolic dysfunction. Congested lungs are stiff, poorly compliant, and prone to desaturation with even brief periods of apnea.
For anesthesia management, this means preoxygenation must be prolonged, preferably with PEEP. High oxygen concentrations should be avoided for long periods because they promote absorption atelectasis. Ventilation should follow lung-protective strategies with low tidal volumes and moderate PEEP. Fluid overload must be avoided, and some patients may benefit from diuretics preoperatively.
ReferencesThis patient’s antihypertensive therapy adds important layers to anesthetic planning.
Telmisartan, an angiotensin receptor blocker, prevents angiotensin II–mediated vasoconstriction and aldosterone release. Under anesthesia, this translates into a greater risk of refractory hypotension. Because catecholamine responsiveness may be impaired, hypotension may respond better to vasopressin.
Amlodipine, a long-acting dihydropyridine calcium channel blocker, maintains arteriolar vasodilation for many hours. This predisposes to exaggerated hypotension at induction when combined with anesthetic agents.
The key strategies are careful titration of induction drugs, preferring agents such as etomidate or low-dose propofol. Ketamine is a useful option in patients with suspected airway compression because it maintains sympathetic tone. Vasopressors such as norepinephrine, phenylephrine, and vasopressin must be prepared in advance.
ReferencesMallampati grading alone is inadequate for retrosternal goiters. CT provides objective tracheal diameters that help stratify risk. A diameter greater than 8 mm usually implies mild compression; between 5 and 8 mm indicates moderate risk; less than 5 mm suggests severe compression with high collapse risk.
Awake fiberoptic intubation is the safest approach for moderate or severe compression. Videolaryngoscopy may be sufficient when CT shows a central trachea without narrowing. Rigid bronchoscopy and surgical tracheostomy should be on standby.
A “what if” scenario illustrates the importance of preparation. If induction leads to sudden airway collapse, repositioning the patient may temporarily relieve obstruction. If this fails, rigid bronchoscopy is the next option. In extreme cases, a surgical airway or even ECMO may be required.
ReferencesInduction agents must be chosen carefully. Propofol is widely used but carries significant hypotension risk. Ketamine preserves blood pressure and airway tone but increases secretions. Sevoflurane inhalational induction can allow preservation of spontaneous ventilation, which may be safer in cases of airway compression.
Muscle relaxants should not be given until airway security is confirmed. Rocuronium can be administered once safe ventilation and intubation are ensured.
Invasive monitoring is essential. An arterial line provides beat-to-beat blood pressure monitoring. Large-bore intravenous access is needed to prepare for major bleeding. A central venous catheter is indicated if sternotomy is anticipated.
Ventilation should be lung-protective with low tidal volumes and moderate PEEP. Recruitment maneuvers should be used cautiously. Excess fluid administration must be avoided.
A practical scenario: if the innominate vein is injured during dissection, torrential blood loss can occur. Anesthesiologists must be prepared for rapid activation of the massive transfusion protocol, with balanced replacement of red cells, plasma, and platelets, along with vasopressor support and close coordination with surgeons.
ReferencesThe risks do not end with extubation.
Extubation should be staged, often over a tube exchanger, with postoperative observation in ICU or HDU.
ReferencesThe mnemonic GOITER captures the anesthetic implications:
The CT thorax in thyroidectomy patients is a perioperative blueprint. Each finding directly maps to physiology, pharmacology, and anesthetic planning.
For residents, the principle is systematic: CT finding → physiological effect → anesthetic implication → clinical action.
For senior practitioners, the key is anticipating rare but catastrophic complications such as airway collapse, vascular injury, and postoperative tracheomalacia.
Ultimately, safe anesthesia in such patients depends on anticipation, preparation, and seamless teamwork with the surgical team.