MANAGEMENT OF GRAVES’ THYROTOXICOSIS IN A PATIENT WITH NECK ABSCESS
ABSTRACT
The simultaneous occurrence of acute sepsis from a neck abscess and new-onset symptomatic Graves’ thyrotoxicosis is uncommon and presents significant management challenges. This case highlights an individualised approach to treatment in such an acute scenario, emphasising the importance of careful perioperative planning. Clinicians must remain vigilant to the heightened risk of thyroid storm in patients undergoing surgical intervention in this context.
Keywords: Graves’ thyrotoxicosis, neck abscess, thyroid storm, sepsis
CASE PRESENTATION
A woman in her forties was referred to the ENT team via the two-week-wait pathway with a one-week history of a painful, enlarging lump on the left side of her neck.
She denied voice change or dysphagia but reported longstanding anxiety, occasional palpitations for more than six months, and unquantified weight loss over the preceding year. She also noted lighter-than-usual menstrual cycles for the past two months. Her past medical history was unremarkable, but she smoked approximately 10 cigarettes daily.
On examination, she was febrile with a fluctuant, tender, erythematous mass in the left upper neck, measuring approximately 5 × 5 cm. There were no clinical signs of thyroid eye disease. Flexible nasoendoscopy demonstrated pooling of secretions.
A neck ultrasound (figure 3.1) revealed suppurative lymphadenitis with evolving abscess formation (cystic changes), as well as diffuse thyroid enlargement with increased vascularity. Ultrasound-guided fine-needle aspiration yielded frank pus and thick echogenic fluid consistent with infection.
She was admitted for intravenous antibiotics and urgent incision and drainage, as oral antibiotics had provided minimal improvement. Pre-operative ECG showed sinus tachycardia, prompting thyroid function tests (TFTs) alongside baseline bloods (table 3.1). This revealed an incidental finding of biochemical thyrotoxicosis (September 2021). The TSH receptor antibody (TRAb) result was not available.
Table 3.1
Parameters 09/21 Normal range
TSH <0.05 0.3-4.5="" mu/l="" ft4="" 49.9="" 10-22="" pmol/l="" ft3="" 32.9="" 3.1-6.8="" pmol/l="" tpo="" antibody="" 327="" 0-34="" kunits/l="" crp="" 58="" wbc="" 17.9="" question:="" what="" should="" be="" the="" immediate="" plan="" of="" action?="" 1.="" start="" carbimazole,="" lugol’s="" iodine="" and="" proceed="" with="" surgery="" immediately="" 2.="" start="" carbimazole,="" lugol’s="" iodine,="" colesevelam="" and="" proceed="" with="" surgery,="" but="" only="" after="" a="" few="" days="" 3.="" proceed="" with="" incision="" &="" drainage="" (i&d)="" and="" perform="" thyroidectomy="" at="" the="" same="" time="" 4.="" none="" of="" the="" above="" endocrine="" team="" recommendations="" the="" case="" was="" discussed="" with="" the="" endocrine="" team,="" who="" suspected="" graves’="" thyrotoxicosis="" given="" the="" markedly="" elevated="" ft3="" level="" and="" a="" ft4/ft3="" ratio="">0.05><3.0. to="" minimise="" the="" risk="" of="" thyroid="" storm,="" they="" advised="" delaying="" incision="" and="" drainage="" for="" 2–3="" days="" to="" allow="" partial="" biochemical="" control.="" the="" following="" management="" plan="" was="" initiated:="" •="" carbimazole="" 40="" mg="" once="" daily="" •="" colesevelam="" 625="" mg="" twice="" daily="" (first="" dose="" given="" immediately),="" to="" bind="" thyroid="" hormones="" in="" the="" gut="" and="" reduce="" enterohepatic="" recycling="" •="" contrast-enhanced="" ct="" scan="" of="" the="" neck="" to="" aid="" surgical="" planning="" and,="" importantly,="" to="" provide="" a="" large="" iodine="" load,="" thereby="" inducing="" the="" wolff–chaikoff="" effect="" (1)="" the="" ct="" scan="" of="" the="" neck="" (figure="" 3.2)="" showed="" evidence="" of="" left="" cervical="" suppurative="" lymphadenitis="" with="" abscess="" formation.="" the="" arrow="" mark="" shows="" the="" large="" fluid="" collection="" of="" around="" 5.5="" cm.="" following="" implementation,="" thyroid="" function="" improved="" significantly="" (table="" 3.2),="" and="" the="" patient="" subsequently="" underwent="" safe="" surgical="" incision="" and="" drainage="" without="" complications.="" later="" the="" tsh="" receptor="" antibody="" returned="" markedly="" elevated="" at="" 40.9="" iu/l="" confirming="" severe="" graves’="" thyrotoxicosis.="" table="" 3.2="" parameters="" 09/09/21="" 15/09/21="" 28/09/21="" normal="" range="" tsh="">3.0.><0.05>0.05><0.05>0.05><0.05 0.3-4.5="" mu/l="" ft4="" 49.9="" 39.7="" 7.6="" 10-22="" pmol/l="" ft3="" 32.9="" 11.3="" 5.5="" 3.1-6.8="" pmol/l="" tpo="" antibody="" 327="" 0-34="" kunits/l="" trab="" 40.9="">0.05><1.0 iu/l
crp 58
wbc 17.9
further endocrine review
it was considered likely that the patient had been suffering from undiagnosed graves’ disease for some time, which only came to light during her hospital admission with a neck abscess. she was discharged home once clinically stable, on carbimazole 40 mg once daily and a beta-blocker as required.
at endocrine follow-up, she reported having experienced tremulousness for several months and marked weight loss, dropping from clothing size 18 to size 8 over the preceding year. on examination, she had a small diffuse goitre.
discussion
it is uncommon to encounter a patient who presents with sepsis and an acute neck abscess alongside a new diagnosis of thyrotoxicosis. the most important priority in such scenarios is to recognise the risk of thyroid storm and to implement strategies that reduce this risk. management options aim to:
• inhibit thyroid hormone synthesis (e.g. antithyroid drugs such as carbimazole).
• block thyroid hormone release (e.g. high-dose iodine to induce the wolff–chaikoff effect).
• inhibit peripheral conversion of thyroxine (t4) to triiodothyronine (t3) (e.g. glucocorticoids).
• interrupt enterohepatic circulation of thyroid hormones (e.g. bile acid sequestrants such as colesevelam).
learning points
• this case illustrates the importance of prompt and effective management of thyrotoxicosis in the acute setting when urgent surgical intervention is required. the key aim is to achieve rapid biochemical and clinical stabilisation prior to surgery.
• treatment strategies in such circumstances may include:
o high-dose carbimazole to inhibit thyroid hormone synthesis.
o bile acid sequestrants (e.g. colesevelam, cholestyramine) to enhance faecal excretion of thyroid hormones via interruption of enterohepatic circulation.
o high-dose glucocorticoids to provide haemodynamic stability and reduce peripheral conversion of t4 to t3.
• lugol’s iodine (or potassium iodide) may be used to inhibit the release of pre-formed thyroid hormone. its therapeutic effect typically begins after 24–48 hours, but the benefit is transient due to the escape phenomenon; therefore, it should never be used as a stand-alone treatment and must be given only after antithyroid drugs have been initiatedalthough contrast-enhanced ct scanning is not routinely used as a therapeutic intervention in thyrotoxicosis, in this case it was employed after multidisciplinary team (mdt) discussion because of its dual diagnostic and therapeutic benefits. iu/l="" crp="" 58="" wbc="" 17.9="" further="" endocrine="" review="" it="" was="" considered="" likely="" that="" the="" patient="" had="" been="" suffering="" from="" undiagnosed="" graves’="" disease="" for="" some="" time,="" which="" only="" came="" to="" light="" during="" her="" hospital="" admission="" with="" a="" neck="" abscess.="" she="" was="" discharged="" home="" once="" clinically="" stable,="" on="" carbimazole="" 40="" mg="" once="" daily="" and="" a="" beta-blocker="" as="" required.="" at="" endocrine="" follow-up,="" she="" reported="" having="" experienced="" tremulousness="" for="" several="" months="" and="" marked="" weight="" loss,="" dropping="" from="" clothing="" size="" 18="" to="" size="" 8="" over="" the="" preceding="" year.="" on="" examination,="" she="" had="" a="" small="" diffuse="" goitre.="" discussion="" it="" is="" uncommon="" to="" encounter="" a="" patient="" who="" presents="" with="" sepsis="" and="" an="" acute="" neck="" abscess="" alongside="" a="" new="" diagnosis="" of="" thyrotoxicosis.="" the="" most="" important="" priority="" in="" such="" scenarios="" is="" to="" recognise="" the="" risk="" of="" thyroid="" storm="" and="" to="" implement="" strategies="" that="" reduce="" this="" risk.="" management="" options="" aim="" to:="" •="" inhibit="" thyroid="" hormone="" synthesis="" (e.g.="" antithyroid="" drugs="" such="" as="" carbimazole).="" •="" block="" thyroid="" hormone="" release="" (e.g.="" high-dose="" iodine="" to="" induce="" the="" wolff–chaikoff="" effect).="" •="" inhibit="" peripheral="" conversion="" of="" thyroxine="" (t4)="" to="" triiodothyronine="" (t3)="" (e.g.="" glucocorticoids).="" •="" interrupt="" enterohepatic="" circulation="" of="" thyroid="" hormones="" (e.g.="" bile="" acid="" sequestrants="" such="" as="" colesevelam).="" learning="" points="" •="" this="" case="" illustrates="" the="" importance="" of="" prompt="" and="" effective="" management="" of="" thyrotoxicosis="" in="" the="" acute="" setting="" when="" urgent="" surgical="" intervention="" is="" required.="" the="" key="" aim="" is="" to="" achieve="" rapid="" biochemical="" and="" clinical="" stabilisation="" prior="" to="" surgery.="" •="" treatment="" strategies="" in="" such="" circumstances="" may="" include:="" o="" high-dose="" carbimazole="" to="" inhibit="" thyroid="" hormone="" synthesis.="" o="" bile="" acid="" sequestrants="" (e.g.="" colesevelam,="" cholestyramine)="" to="" enhance="" faecal="" excretion="" of="" thyroid="" hormones="" via="" interruption="" of="" enterohepatic="" circulation.="" o="" high-dose="" glucocorticoids="" to="" provide="" haemodynamic="" stability="" and="" reduce="" peripheral="" conversion="" of="" t4="" to="" t3.="" •="" lugol’s="" iodine="" (or="" potassium="" iodide)="" may="" be="" used="" to="" inhibit="" the="" release="" of="" pre-formed="" thyroid="" hormone.="" its="" therapeutic="" effect="" typically="" begins="" after="" 24–48="" hours,="" but="" the="" benefit="" is="" transient="" due="" to="" the="" escape="" phenomenon;="" therefore,="" it="" should="" never="" be="" used="" as="" a="" stand-alone="" treatment="" and="" must="" be="" given="" only="" after="" antithyroid="" drugs="" have="" been="" initiatedalthough="" contrast-enhanced="" ct="" scanning="" is="" not="" routinely="" used="" as="" a="" therapeutic="" intervention="" in="" thyrotoxicosis,="" in="" this="" case="" it="" was="" employed="" after="" multidisciplinary="" team="" (mdt)="" discussion="" because="" of="" its="" dual="" diagnostic="" and="" therapeutic="">1.0 iu/l
crp 58
wbc 17.9
further endocrine review
it was considered likely that the patient had been suffering from undiagnosed graves’ disease for some time, which only came to light during her hospital admission with a neck abscess. she was discharged home once clinically stable, on carbimazole 40 mg once daily and a beta-blocker as required.
at endocrine follow-up, she reported having experienced tremulousness for several months and marked weight loss, dropping from clothing size 18 to size 8 over the preceding year. on examination, she had a small diffuse goitre.
discussion
it is uncommon to encounter a patient who presents with sepsis and an acute neck abscess alongside a new diagnosis of thyrotoxicosis. the most important priority in such scenarios is to recognise the risk of thyroid storm and to implement strategies that reduce this risk. management options aim to:
• inhibit thyroid hormone synthesis (e.g. antithyroid drugs such as carbimazole).
• block thyroid hormone release (e.g. high-dose iodine to induce the wolff–chaikoff effect).
• inhibit peripheral conversion of thyroxine (t4) to triiodothyronine (t3) (e.g. glucocorticoids).
• interrupt enterohepatic circulation of thyroid hormones (e.g. bile acid sequestrants such as colesevelam).
learning points
• this case illustrates the importance of prompt and effective management of thyrotoxicosis in the acute setting when urgent surgical intervention is required. the key aim is to achieve rapid biochemical and clinical stabilisation prior to surgery.
• treatment strategies in such circumstances may include:
o high-dose carbimazole to inhibit thyroid hormone synthesis.
o bile acid sequestrants (e.g. colesevelam, cholestyramine) to enhance faecal excretion of thyroid hormones via interruption of enterohepatic circulation.
o high-dose glucocorticoids to provide haemodynamic stability and reduce peripheral conversion of t4 to t3.
• lugol’s iodine (or potassium iodide) may be used to inhibit the release of pre-formed thyroid hormone. its therapeutic effect typically begins after 24–48 hours, but the benefit is transient due to the escape phenomenon; therefore, it should never be used as a stand-alone treatment and must be given only after antithyroid drugs have been initiatedalthough contrast-enhanced ct scanning is not routinely used as a therapeutic intervention in thyrotoxicosis, in this case it was employed after multidisciplinary team (mdt) discussion because of its dual diagnostic and therapeutic benefits.>