Chapter 31 – Endocrine Emergencies in Pregnancy




Abstract




Thyroid StormThyroid Storm





Chapter 31 Endocrine Emergencies in Pregnancy


Madhushree Ghosh and Manilka Sumanatilleke



Thyroid Storm



Key Facts




  • Thyroid storm is a true obstetric emergency with significant fetal and maternal morbidity and mortality.



  • Incidence: 1%–2 % of women with hyperthyroidism receiving thionamide treatment



  • Characterised by severe hypermetabolic state precipitated by high levels of endogenous thyroid hormones (Table 31.1).



  • Rates of fatality vary in different series from 10% to 30%.



Precipitating Factors



  • Exact trigger unknown



  • Grave’s disease or the presence of thyroid stimulating antibodies



  • Infection, surgery, trauma, venous thromboembolism



  • Other endocrinopathies such as diabetic ketoacidosis




Table 31.1 Symptoms of signs of a ‘thyroid storm’
































Symptoms Signs
Palpitations, chest pain, tremors Tachycardia, tachypnoea, hyperpyrexia
Nausea, vomiting, loss of appetite, weight loss Exophthalmos, ophthalmoplegia, changes in visual acuity and colour vision
Confusion, agitation, muscle weakness Pretibial myxoedema
Increased urinary frequency Hypertension, atrial fibrillation
Thyroid acropachy (clubbing)
Goitre, bruit over thyroid gland
Reduced fetal movements Fetal tachycardia


Key Diagnosis


Symptoms of mild hyperthyroidism may mimic symptoms of normal pregnancy:




  • Fatigue



  • Palpitations



  • Tachycardia



  • Vomiting



  • Increased appetite



  • Heat intolerance



  • Increased urinary frequency



  • Insomnia



  • Emotional lability


More specific symptoms and signs described in the text that follows should increase the suspicion of thyrotoxicosis, which warrants close clinical evaluation and biochemical testing:




  • Tremor



  • Nervousness



  • Frequent passage of stools – formed or loose



  • Muscle weakness – especially proximal muscle weakness



  • Brisk reflexes



  • Excessive sweating



  • Weight loss



  • Hypertension



  • Goitre (normal pregnancy can cause up to 15% increase in size of thyroid gland)



  • Bruit over the thyroid


Diagnostic signs:




  • Graves’ ophthalmopathy – exophthalmos, ophthalmoplegia, changes in visual acuity and colour vision



  • Thyroid acropachy (clubbing)



  • Dermopathy (pretibial myxoedema)


Accurate diagnosis of the ‘thyroid storm’ requires prompt intervention by a multidisciplinary team including obstetricians, midwives, endocrinologists, anaesthetists and maternal medicine and critical care specialists.


A scoring system has been proposed to aid diagnosis of a thyroid storm and this considers a combination of thermoregulatory, neurological, cardiovascular, gastrointestinal and hepatic dysfunctions (Table 31.2). The presence of a recognised precipitating factor should also be considered while making a diagnosis.



Key Investigations



Biochemistry

Impact of pregnancy on the thyroid:




  • Alpha subunit of the thyroid-stimulating hormone (TSH) molecule is common to those found on luteinising hormone (LH) and human chorionic gonadotropin (hCG), and high levels of these hormones will stimulate the TSH receptors in the thyroid gland to produce thyroid hormones. Gestational transient thyrotoxicosis is typically associated with hyperemesis gravidarum and molar pregnancies.



  • By 20 weeks’ gestation plasma thyroxine binding globulin (TBG) levels increase 2.5-fold due to reduced hepatic clearance and oestrogen-induced change in the structure of TBG, prolonging its half-life [1].



  • There is a 25%–40% increase in serum total thyroxine (TT4) and 30% rise in total T3 in the first trimester and 50%–60% rise later [2].



  • Monitoring free T4 and TSH is recommended, and close liaison with the laboratory is essential to obtain the trimester-specific values for the type of assay used.



Laboratory Tests



  • High free T4 and suppressed TSH; leukocytosis



  • Occasionally elevated liver enzymes




    • Mild hypercalcaemia




Key Management



Principles of Management




  • Reduce the synthesis and release of thyroid hormone.



  • Iodides: Inhibit proteolysis of thyroglobulin and block the release of stored thyroid hormones.



  • Ideally started at least 1 hour after the loading dose of propylthiouracil but should not be delayed if it is the only preparation available immediately.



  • Block the peripheral actions of thyroid hormones/decrease sympathetic outflow. Block the peripheral conversion of T4 to more active triiodothyronine (T3).



  • Identify and treat any precipitating factors such as infection.



  • Identify and treat complications.



Supportive Care




  • Patient best managed in an obstetric intensive care unit (ICU) or an ICU where continuous fetal monitoring and an emergency delivery could be handled.



  • IV fluids and correct electrolyte imbalances. Cardiac monitoring and consider central haemodynamic monitoring to guide beta-blocker therapy if there is cardiac failure due to hyperdynamic circulation.



  • Cooling measures to control the hyperpyrexia:




    • Sponge bath



    • Acetaminophen (avoid aspirin)



    • Chlorpromazine 50–100 mg IM (inhibits central thermoregulation, useful in severe agitation)




  • Oxygen therapy.



  • Nasogastric tube if indicated (useful to administer medication, especially propylthiouracil, which is not available in IV form).



  • Medication.



  • Propylthiouracil orally or via nasogastric tube, 300–800 mg loading dose followed by 150–300 mg 6-hourly.




    • Inhibits iodination of tyrosine and thyroid hormone production.



    • Blocks peripheral conversion of T4 to T3.



    • Lower incidence of aplasia cutis in newborns compared with carbimazole.




  • Routine biochemistry for any acutely ill patient should be done.



  • Most patients would benefit from an intensive care setting and consideration to continuous fetal monitoring should be given if the fetus has reached viability. Every effort should be made to resuscitate the mother first before considering delivery for fetal indications.




Table 31.2 Diagnosis of a thyroid storm




















































































































Diagnostic parameters Scoring points
Thermoregulatory dysfunction
Temperature °F (°C)
99–99.9 (37.2–37.7) 5
100–100.9 (37.8–38.2) 10
101–101.9 (38.3–38.8) 15
102–102.9 (38.9–39.4) 20
103–103.9 (39.5–39.9) 25
≥104.0 (40) 30
Central nervous system effects
Absent 0
Mild (agitation) 10
Moderate (delirium, psychosis, extreme lethargy) 20
Severe (seizures, coma) 30
Gastrointestinal–hepatic dysfunction
Absent 0
Moderate (diarrhoea, nausea/vomiting, abdominal 10
pain)
Severe (unexplained jaundice) 20
Cardiovascular dysfunction
Tachycardia (beats/minute)
90–109 5
110–119 10
120–129 15
≥140 25
Congestive heart failure
Absent 0
Mild (pedal oedema) 5
Moderate (bibasilar rales) 10
Severe (pulmonary oedema) 15
Atrial fibrillation
Absent 0
Present 10
Precipitating event
Absent 0
Present 10




Scoring system: A score of 45 or greater is highly suggestive of thyroid storm; a score of 25–44 is suggestive of impending storm; a score below 25 is unlikely to represent thyroid storm.


Adapted from Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am 1993; 22.


Key Management: Maternal




  • Adequate IV access and fluid resuscitation



  • Monitor oxygenation and consider nasogastric tube



  • Cooling blanket and acetaminophen 500 mg PO 4–6 hourly



  • Propranolol 40–60 mg PO or via nasogastric tube every 6 hours or IV 1 mg/minute every 5 minutes × 6 doses



  • Cardiac monitoring and consider central haemodynamic monitoring to guide beta blocker therapy if there is cardiac failure due to hyperdynamic circulation



Anti-thyroid Treatment


Propylthiouracil 300 mg PO or via the nasogastric tube every 6 hours; wait 30 to 60 minutes.




  • Inhibits iodination of tyrosine and thyroid hormone production.



  • Blocks peripheral conversion of T4 to T3.



  • Lower incidence of aplasia cutis in newborns compared with carbimazole.


Iodides: Inhibit proteolysis of thyroglobulin and block the release of stored thyroid hormones. Ideally started at least 1 hour after the loading dose of propylthiouracil but should not be delayed if it is the only preparation available immediately.




  • Potassium iodide 60 mg PO or via nasogastric tube every 8 hours or IV



  • Lugol’s iodine 6–8 drops 6-hourly


Beta-blockers: Control of autonomic symptoms especially tachycardia. Some inhibition of peripheral conversion of T4 to T3. Propranolol, labetalol and esmolol have been used in pregnancy [3].




  • Propranolol 160–480 mg per day in divided doses (4–6 hourly) or an infusion at a rate of 2–5 mg/hour with an aim to reduce the heart rate to <90 beats per minute.



  • Esmolol: 250–500 mcg/kg of body weight loading dose followed by an infusion of 50–100 mcg/kg per minute.



  • High-dose glucocorticoids: Blocks peripheral conversion of T4 to T3 and release of stored thyroid hormones. Will supplement adrenal function and prevents adrenal insufficiency.



  • Hydrocortisone – 100 mg IM 6-hourly.



  • Prednisolone – 60 mg PO daily.



  • Dexamethasone – 8 mg PO daily.



  • Glucocorticoids and iodides can be discontinued after initial clinical management and when the clinical status is stable. Safer to continue for at least 24–48 hours.



  • Dexamethasone 1–2 mg IV every 6 hours or hydrocortisone 100 mg IV every 8 hours.

Only gold members can continue reading. Log In or Register to continue

May 9, 2021 | Posted by in OBSTETRICS | Comments Off on Chapter 31 – Endocrine Emergencies in Pregnancy
Premium Wordpress Themes by UFO Themes