Question 10

College answer

Syllabus topic/section:

2.1.9 Endocrine Intensive Care: Acute thyroid crises: L1

Discussion: 

Good answers to part a) included a well organised list of clinical features including the presence of a high fever with neurological, cardiac and abdominal symptoms discussed in some detail. Good answers also noted the possibility of longer standing hyperthyroidism and it's features with possible triggers of storm.

Candidates mostly did well in part b) and were able to mention the expected T3, T4 and TSH result (of note thyroid storm is almost never due to secondary hyperthyroidism). Good answers also included some of the other likely laboratory abnormalities and that these are not specific. Some candidates wrote about non- laboratory-based tests such as ECHO and CT which did not score marks as the question specifically asked for laboratory ones.
Part c) of the question was less well answered by candidates. Candidates who did well were able to discuss the resuscitative and supportive measures as well as outlining the specific treatments and their rationale (the glossary headings for management). Supportive treatments needed to be targeted to the condition and good candidates linked the clinical presentation features from part a to their management plan.
Good answers discussed the timing of specific treatments (e.g. iodide after PTU and the rationale), included looking for a precipitant, and mentioned rescue therapies (PLEX, thyroidectomy). Excellent answers demonstrated superior subject grasp by discussion of areas of uncertainty or controversy - e.g. using beta blockers in patients at risk of decompensating shock or the use of amiodarone.

Discussion

Clinical features and laboratory findings of thyroid storm (there is no possible way you would write this much in 5 minutes, but the ABCDE structure is probably reasonable, just to prevent you from forgetting a key feature like fever which might be missed in a systems-based approach)

1. Goitre: possible airway compromise)
2. Tachypnoea due to increased CO2 production;
   Increased O₂ER (increased metabolic fuel use)
3. Tachycardia,
   Atrial fibrillation and ventricular arrhythmias
   Heart failure
   Hypertension (early), hypotension (late)
4. Tremor;
   Agitation, progressing to encephalopathy, coma and seizures.
   There is the phenomenon of "apathetic thyrotoxicosis" which presents with weakness
5. Low potassium and magnesium (particularly in "apathetic thyrotoxicosis")
   Serum cortisol should be elevated. If it is not, one might consider a relative adrenal insufficiency, and supplement some hydrocortisone.
   Also, obviously, TFTs:
   • Raised T3 and T4
   • Low TSH
   • Deranged LFTs
6. Rhabdomyolysis may be present; CK may be elevated. This is "thyrotoxic myopathy"
7. Diarrhoea, nausea and vomiting
   Increased metabolic rate; increased demand for metabolic substrate.
   Nutritional requirements are increased
   Hyperglycaemia may be apparent in the non-diabetic patient
   Jaundice may develop
8. Leukocytosis; a left shift
9. Fever: in fact, may go up to 41°C. This is apparently the most characteristic feature.

Management

• Look for a precipitant (eg. autoimmune thyroiditis, 
• Main goals are:
• Prevent synthesis of T3 and T4:
  • Thiouracils: propylthiouracil - blocks synthesis of T3 and T4 as well as peripheral T4-T3 conversion
  • Imidazoles: carbimazole - block synthesis of T3 and T4
• Prevent T3 and T4 release:
  • Inorganic iodine therapy, eg. potassium iodide (given after synthesis is blocked)
  • Lithium is an alternative
• Block peripheral T3 and T4 activity:
  • β-blockade: propanolol (which also decreases T4-T3 conversion)
  • Corticosteroids: also decrease T4-T3 conversion
• Add corticosteroids: there is always some relative adrenal insufficiency.
• Add cholestyramine to block reabsorption of thyroid hormone which is excreted with the bile
• Severe refractory disease may call for extracorporal clearance of thyroid hormone by plasma exchange or charcoal haemoperfusion.
• Thyroidectomy is a last resort