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A Dyspnoeic
Lady
Author
Dr Tang Chung Leung
Dec 2013
Case
▪ Triaged as Cat. 3
▪ A 37 years old female
▪ C/O: dizziness and chest discomfort 1 day ago, severe back pain
today, unable to walk
▪ BP 107/86 pulse 156/min
▪ Temperature and SaO2 not documented
History of Present Illness
▪ Sudden onset of back pain and limb
pain in MTR for one day
▪ SOB for 2 weeks
▪ No chest pain
▪ No fever
▪ No cough Add your first bullet point here
▪ Add your second bullet point here
▪ Add your third bullet point here
Past Medical History
• Tourist guide
• FU OLMH for thyroid problem
• Not taking any medication
Physical Examinations
▪ General conditions fair
▪ No pallor, jaundice, no LN palpable
▪ No neck mass noted
▪ Ankle edema noted
▪ No sweating
▪ Temperature not documented
Respiratory:
 Respiratory rate not documented
 Bilateral basal crepitations
CVS:
 BP 107/86 mmHg, HR 156/min.
 Distended neck veins
 Heart sound normal, no murmur
noted
Abdomen:
 soft
Investigations
▪ ECG – fast AF Rate ~ 150/min
▪ CXR: cardiomegaly, right pleural effusion
▪ Blood send for CBP, L/RFT, cardiac enzyme, thyroid function.
Summary of Clinical Findings
▪ Low back pain
▪ Fast AF
▪ Neck mass
▪ Borderline blood pressure reading
▪ Cardiomegaly/pleural effusion
Differential diagnoses
Provisional diagnoses
▪ ?Sepsis
▪ Thyroid storm
▪ ?Heart failure/pericardial effusion/
tamponade
▪ Atrial fibrillation
▪ ?Surgical emergency (Boerhaave’s Sx)
▪ ?Orthopaedics emergency
▪ ?Endocrine emergency (thyroid crisis)
▪ Heart failure
Treatment
▪ High flow O2
▪ Lasix 40mg ivi x2
▪ Betaloc 5mg ivi x2
▪ Carbimazole 20mg po
▪ Iodine (not available in AED)
▪ After treatment,
▪ BP 119/91 pulse 145/min
▪ She was admitted into medical ward.
▪ ? ICU
Progress
▪ D1 admission 21:20
▪ ? Cord compression
▪ On call medical MO,
▪ ? Rupture esophagus
▪ Found generalized hypotonia esp. lower
limbs (grade 4/5)
▪ Right pleural effusion and back pain
▪ ? Aortic dissection
▪ ? Any more
Progress
▪ Urgent CT thorax and x-ray LS spine ordered
▪ No aortic dissection, right pleural effusion
▪ X-ray LS spine were normal (assessed by orthopaedics
colleagues)
▪ Orthopaedic opinion:
▪ Unlikely to be cord compression.
▪ Surgeon opinion:
▪ Unlikely ruptured esophagus (because patient was not in severe
chest pain and not very septic)
▪ (? Sequence of events for Boerhaave’ syndrome)
Progress
▪ D1 admission 23:10
Blood Results
▪ WBC 12.3
▪ Urgent echocardiogram:
▪ Impaired LVEF (45%), functional MR and TR
▪ D2 admission 14:15
▪ Chest drain inserted with 1.5 litre pleural
fluid drained. (transudative)
▪ Hb = 10.9
▪ Free T4 > 100
▪ TSH < 0.01
▪ ESR 1
▪ CRP <1
▪ CK. Troponin T - normal
▪ PTU 200mg QID added
Progress
▪ D3 admission 13:00
▪ Patient developed shock
▪
▪
▪
▪
BP 68/24 pulse 66 SaO2 91
Drowsy, shallow breathing and cold extremities
GCS 3/15
No active bleeding and PR showed no malaena
▪ Intubated and transferred to ICU
Progress
▪ Persistent hypotension
▪ Multiple doses of volume expander and inotrope started
▪ Developed DIC
▪ INR up to 4.03
▪ Multiple doses of FFP, platelet concentrate given
▪ Developed multiple organ failure and treated conservatively.
▪ D8 admission
▪ Persistent coma
▪ Bedside EEG showed depressed EEG activities
▪ D10 admission
▪ CT brain
▪ SAH, cerebral edema
▪ NS opinion: not for surgical intervention
Causes of death
▪ D17 admission: succumbed
Causes
▪ Thyroid storm
▪ Septicemia
▪ Multiple organ failure
▪ Intracerebral hemorrhage
DISCUSSIONS
Terminology
▪ Hyperthyroidism:
▪ thyroid gland hyperfunction
▪ Increased thyroid hormone synthesis and release
▪ Thyrotoxicosis
▪ Increased metabolic and sympathetic nervous state as a result
of elevated serum free thyroid hormone
▪ Thyroid storm
▪ Emergent multisystem disorder
▪ Extreme manifestation of thyrotoxicosis
Thyroid storm
▪ Thyroid storm is a rare complication( 1- 2 % hyperthyroidism
patients)
▪ Precipitated by a physiologically stressful events such as
trauma, myocardial infarction, pulmonary embolism, diabetic
ketoacidosis, sepsis, partuition, surgery, excessive ingestion of
iodine, and incorrect discontinuation of antithyroid drugs
Thyroid physiology
▪ Thyroid function is controlled by negative feedback loop that is regulated by
circulating TSH and thyroid hormones (T4 and T3)
▪ Thyroid gland mainly produces T4 and smaller amount of T3
▪ ≈80% of T3 is formed by conversion of T4 to T3 in periphery
▪ Over 99.5% of T4 and T3 are protein bound
▪ Bound hormone is metabolically inactive
▪ Serum free T3 (FT3) and T4(FT4) provide more valuable clinical information
▪ In thyrotoxicosis/ thyroid storm states, TSH concentration is very depressed with
elevations of FT4 and FT3
Pathogenesis
▪ FT4 and FT3 are taken into the cells
whereas T4 is converted into its active
form
▪ Increase in amount of free thyroid
hormone
▪ Conversion of T4 to T3 is accomplished by
deiodination in the outer ring of T4
▪ Increase in target cell betaadrenergic receptor density
▪ Normally deiodination of T4 to T3 provides
only 20% to 30% of T3
▪ In thyrotoxic state, it can provide more
than 50%
▪ Increase post receptor
modifications in signaling
pathways
Causes of Hyperthyroidism
▪ Circulating thyroid stimulators
▪ Graves’ disease
▪ Pituitary adenoma
▪ Choriocarcinoma
▪ Hyperemesis gravidarum
▪ Thyroid autonomy
▪ Toxic nodular goitre
▪ Toxic solitary adenoma
▪ Iodine-induced hyperthyroidism
▪ Exogenous thyroid hormone
▪ Excess ingestion of thyroid hormone
▪ Destruction of thyroid follicles
(thyroiditis)
▪ Subacute thyroiditis
▪ postpartum
▪ Amiodarone induced
▪ Infectious
▪ Ectopic thyroid tissue
▪ Struma ovarii
▪ Metastatic follicular thyroid cancer
Symptoms
▪ CNS
▪ Emotional lability
▪ Anxiety
▪ Confusion
▪ GI
▪ Diarrhoea
▪ CVS
▪ Palpitations
▪ Chest pain
▪ Dyspnoea
▪ Ophthalmologic
▪ Diplopia
▪ Reproductive
▪ Oligomenorrhoea
▪ Loss of libido
▪ Dermatologic
▪ Hair loss
▪ Thyroid gland
▪ Neck fullness
Laboratory
▪ free T4 is elevated and TSH is
decreased
▪ diagnosis must be made on
the basis of the clinical
examination
Thyroid storm- diagnostic criteria
Diagnostic parameters
Scoring points
Thermoregulatory dysfunction
Temperature
99-99.9
100-100.9
101-101.9
102-102.9
103-103.9
≥ 104
5
10
15
20
25
30
CNS effects
Absent
Mild (agitation)
Moderate (delirium, psychosis, extreme lethargy)
Severe (seizure, coma)
0
10
20
30
GI-hepatic dysfunction
Absent
Moderate (diarrhoea, nausea/ vomiting, abdominal pain)
Severe (unexplained jaundice)
0
10
20
Cardiovascular dysfunction
Tachycardia
90-109
110-119
120-129
≥ 140
Congestive heart failure
Absent
Mild (pedal edema)
Moderate (bibasilar rales)
Severe (pulmonary edema)
Atrial fibrillation
Absent
Present
Precipitating event
Absent
present
5
10
15
25
0
5
10
15
0
10
0
10
SCORE: ≥ 45: HIGHLY SUGGESTIVE OF THYROID STORM; 25-44: SUGGESTIVE OF IMPENDING STORM; BELOW 25: UNLIKELY TO REPRESENT THYROID STORM
BURCH HB, WARTOFSKY L. LIFE-THREATENING THYROTOXICOSIS. THYROID STORM ENDOCRINOL META CLIN NORTH AM 1993;22(2):263-77
Management
If untreated, thyroid storm may be fatal
Thyroid storm often must be recognized and
treated on clinical grounds
Management
▪ Multiple targets
▪ Inhibition of new hormone synthesis within thyroid
gland
▪ Inhibition of thyroid hormone release
▪ Preventing conversion of T4 to T3
▪ Controlling the adrenergic symptoms
▪ Supportive therapy
▪ Deal with underlying precipitants
Management
▪ Inhibition of new hormone production
▪ Propylthiouracil (extra effect of decreases T4 to T3 conversion)
▪ Carbimazole
▪ Inhibition of thyroid hormone release
▪ Lugol’s solution
▪ Potassium iodide/ SSKI
▪ (administer at least 1 hour after anti-thyroid medication)
Management
▪ Beta-adrenergic blockade
▪ Propranolol (extra effect of decrease T4 to T3 conversion)
▪ Atenolol (cardioselective)
▪ Metoprolol (cardioselective)
▪ Esmolol (intravenous)
▪ Supportive
▪ Acetaminophen (for hyperthermia)
▪ Glucocorticoids, e.g. hydrocortisone/ dexamethasone (decreases
T4 to T3 conversion)
▪ External cooling: ice packs, cooling blankets
▪ IV fluid
Management
▪ Alternative therapies
▪ Lithium carbonate
▪ when anti-thyroid drugs or iodide therapy is contraindicated
▪ Decrease thyroid hormone secretion directly
▪ Potassium perchlorate
▪ in combination of anti-thyroid medication in treatment of Amiodarone
induced thyrotoxicosis
Thank you