C A S E

R E P O R T

JIACM 2014; 15(3-4): 222-3

Thyroid storm: An unusual presentation

NS Neki*

Abstract
A 23-year-old female patient was hospitalised with complaints of fever, diarrhoea, altered sensorium for 3 days with a rapidly
declining mental status. Before admission to the hospital, her relatives gave history of her being restless, markedly irritable with
generalised tonic-clonic seizures and a positive history of palpitations. Suspecting the diagnosis of thyroid storm clinically, she
was started on aggressive antithyroid treatment following which she showed marked clinical improvement. Thyroid storm is a
rare endocrine emergency with increased mortality risk in this otherwise fatal entity. The aim of reporting this case is to make the
physicians aware of this fatal medical disease necessitating prompt intervention. A case of thyroid storm presenting with
predominant neurological manifestations is being presented here for its rarity.
Key words: Thyroid storm, unusual presentation.

Introduction
Thyroid storm (accelerated hyperthyroidism) is a rare
manifestation of thyrotoxicosis with a wide spectrum of
clinical presentations involving multiple systems. It
generally occurs in females from the third to the sixth
decade of life, especially with Graves disease. It is usually
a life-threatening medical emergency and is fatal if left
untreated. The classic clinical presentation includes fever,
tachycardia, hypertension, tremors, nausea, vomiting,
diarrhoea, dehydration, arrhythmias, delirium, and coma1.
It usually develops in an undiagnosed hyperthyroid
patient who has a major stress or continues without
antithyroid treatment in addition to other precipitating
factors like surgery, radio-iodine therapy, trauma, acute
infection toxaemia of pregnancy, labour, excessive
palpation of the thyroid gland in hyperthyroid patients,
pulmonary thromboembolism, severe drug reactions, or
myocardial infarction, etc 2. Its early recognition and
treatment is essential in reducing the morbidity and
mortality rate in this potentially fatal disease. Only 1 - 2%
of hyperthyroid cases manifest as thyroid storm and the
mortality ranges between 20 - 30% despite treatment3.

Case report
A 23-year-old unmarried female was brought to the
hospital with complaints of fever, diarrhoea, light
headedness, altered sensorium for 3 days with a rapidly
declining mental status. Before admission, she was
reported to be restless, markedly irritable with generalised
tonic clonic seizures as well as positive history of
palpitations as narrated by relatives.
There was no history of previous illness or hospital
admission, major surgery, or antipsychotic drugs intake. On

examination, she was febrile (temp 101F), pulse rate 126/

min and regular, BP 110/70 mmHg, respiratory rate 29
breaths/mm, oxygen saturation 98% on 3L. Her pupils were
slightly dilated, mucous membranes were moist and the
she had an abrasion on the tongue consistent with biting.
JVP was normal; there was no lymphadenopathy.
Examination of the neck revealed bilateral thyroid
enlargement with diffuse toxic goitre with systolic bruit
heard over it. She had a stare with a typical anxious look.
There were no signs of meningeal irritation. Fundus
examination was normal. On neurological examination, she
responded to painful stimuli, with brisk deep tendon
reflexes and plantar flexor response. CVS examination
revealed tachycardia with regular rhythm but no murmurs.
Respiratory system and abdominal examination was
unremarkable. ECG showed sinus tachycardia. Her
laboratory results showed no abnormality of haemogram,
blood glucose levels, CSF, serum electrolytes, renal and liver
function tests. X-ray chest showed no active disease. CT
brain was normal. Blood cultures were negative. EEG
revealed bilateral frontal slow waves. Technetium scan of
thyroid showed hyperfunctioning gland with diffuse tracer
uptake (36% at 20 minutes). The constellation of signs and
symptoms suggested that this could be a case of thyroid
storm. Based on the diagnostic criteria of Burch and
Wartofsky4, she had a total score of 60, which was strongly
suggestive of thyroid storm (a score > 25 is suggestive of
thyroid storm). The patient was put on antithyroid drugs
awaiting thyroid function tests T3, T4, and TSH. She was
started on propylthiouracil 400 mg tid and propranolol 40
mg tid, IV fluids, hydrocortisone IV (later changed to oral
steroids). Her thyroid profile revealed TSH 0.02 mIU/ml, T4
28 g/dl (N 4 - 14 g/dl); T3 40 ng/dl (N = 0.8 - 2 ng/dl).
Thyroid peroxidase autoantibody was negative. Based on

*Professor of Medicine, Government Medical College, Amritsar, Punjab, and Trained Endocrinologist, Department of
Endocrinology, PGIMER, Chandigarh; and President, Geriatric Society of India.

clinical presentation and later on confirmed by results,

Lugols iodine 8 drops 8 hourly was given for 3 days. The
fever subsided, diarrhoea improved, and agitation
decreased. After considerable improvement in her
condition in about 8 days time, she was discharged in an
euthyroid state, conscious, well oriented, without tremors
and fever, and advised to continue on propylthiouracil and
propranolol. On follow-up at 3 months, she was carrying
our all routine activities with a positive frame of mind.

Discussion
Thyroid storm a dramatic exacerbation of existing
hyperthyroidism, of sudden onset associated with fever,
tachycardia, and CNS symptomatology remains a lifethreatening medical emergency if left untreated. Being a
rare endocrine emergency, all clinicians must be aware of
its clinical features and treatment so that morbidity and
mortality can be avoided. About 1 - 2% of patients with
hyperthyroidism progress to thyroid storm and the 100%
mortality reported earlier has now come down to 20 - 30%
with better recognition and treatment. It might be difficult
to distinguish between thyroid storm and infection in
thyrotoxic patients as tachycardia and fever might be
present in both. On account of an overlapping of the
symptoms, precipitating conditions and complications, a
clinical diagnosis is not easy and is often made too late.The
definitive criteria of thyroid storm laid down by Burch and
Wartotsky4 are useful. The triggering factors for thyroid
storm include surgery, major stress, noncompliance to
antithyroid drugs, infection, radio-iodine, etc2. Treatment
of thyroid storm should not be delayed if there is a high
index of suspicion, and empirical treatment should be
started on clinical grounds awaiting laboratory reports,
which was evident in our case5. Urgent thyroid function tests
is a confirmatory diagnosis. Hyperglycaemia,
hypercalcaemia, leucocytosis may co-exist. Deranged liver
functions mainly alkaline phosphatase may occur due to
increased osteoblastic activity in response to high bone
resorption. Serum thyroid hormone levels would typically
show hyperthyroidism, but due to an abrupt rise of thryoid
hormone secondary to triggering factors, the patient can
no longer adapt to the sudden metabolic stress6. An acute
elevation of FT3 or FT4 in thyrotoxic patients may produce
acute decompensation. However, no absolute levels of
serum T3 or T4 exist above which thyroid storm develops
inevitably.7 Earlier, cases of thyroid storm have been well
reported where treatment of thyroid storm was started
immediately awaiting thyroid function tests8,9. T4 may rarely
be normal or even decreasing because of co-existing
nonthyroidal illness10.
In our case, the patient presented with altered sensorium
without signs of raised intracranial tension and focal
neurological deficit. Differential diagnosis includes

Journal, Indian Academy of Clinical Medicine

neuroleptic malignant syndrome, anticholinergic poisoning,

sympathomimetic toxicity, alcohol withdrawal syndrome,
toxic/metabolic encephalopathy, hypertensive
encephalopathy, meningitis, etc. But the clinical features of
our patient in the form of hypermetabolic state made
thyroid storm a definitive diagnosis; and possibly the
triggering factor for thyroid storm in this case could be
febrile illness. Predominant neurological manifestation in
the form of altered mental status and history of tonic clonic
generalised seizures was an unusual feature in our case.
Treatment of thyroid storm includes correction of severe
thyrotoxicosis, precipitating illness, and associated active
thyroid eye disease. Patients should be monitored in the
intensive care units in the early phase. Diuretics may be
given for congestive cardiac failure (CHF). Drugs like
thionamides block hormone synthesis; iodine solution
blocks the release of thyroid hormone, beta-blockers
control adrenergic symptoms, and steroids reduce T4 to T3
conversion. Beta-blockers should be used cautiously in the
presence of CHF. Among thionamides, propylthiouracil is
preferred over methionazole as it blocks peripheral T4 to
T3 conversion. Iodinated radiocontrast iopanoic acid,
cholestyramine can also be used. Peritoneal dialysis and
plasmaphresis are used to reduce the high levels of
circulating T4 and T3 in a thyroid storm5,9,10.

Conclusion
Diagnosis may be missed on account of variable
presentation. Treatment should never be delayed. A high
index of suspicion is required for prompt recognition and
effective management of unusual presentation of thyroid
storm in order to reduce the morbidity and mortality of
this life-threatening medical disorder.

References
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Vol. 15, No. 3 & 4

July-December, 2014

223