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Malaysian Journal of Medical Sciences
School of Medical Sciences, Universiti Sains Malaysia
ISSN: 1394-195X
Vol. 11, Num. 1, 2004, pp. 90-91
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Malaysian Journal of Medical Sciences, Vol. 11, No. 1, January 2004,
pp. 90-91
CASE REPORT
A Case of Thyrotoxic Hypokalemic Paralysis
Saurabh Mehrotra, Ashu Arora, Premashish Kar, Subramaniam
Anuradha
Department of Medicine Maulana Azad Medical College and Associated
LN Hospitals, Bahadurshah Zafar Marg, New Delhi-110002 India
Correspondence : Dr. Saurabh Mehrotra 8051 B-XI Vasant Kunj New Delhi-110070
India Email: rsav252002@yahoo.co.in
Submitted-4.12.2003
Accepted-31.12.2003
Code Number: mj04012
An Indian male patient with acute quadriplegia with hypokalemia
as a rare initial presentation of thyrotoxicosis is presented in this case
report.
Key words : thyrotoxicosis, quadriplegia,
hypokalemia
Introduction
Thyrotoxic hypokalemic paralysis (THP) is an unusual complication
of a fairly common disease, hyperthyroidism - it is most commonly a complication
of Graves' disease but can occur with any etiology of thyrotoxicosis (1).
THP is characterized by transient, recurrent episodes of
flaccid paralysis affecting proximal muscles more severely than the distal
muscles. During the episodes of weakness,hypokalemia is invariably present
and the severity of weakness correlates with the degree of hypokalemia. It
is most commonly seen in patients between the third and fifth decade and is
more frequently observed in males than in females (2). Manifestations of thyrotoxicosis
vary from subtle to quite obvious and usually precede or coincide with onset
of the paralytic attack.
We describe a case of a male who presented with acute onset
quadriplegia with hypokalemia as the initial presenting feature of thyrotoxicosis.
Case report
A 40 year old male patient presented with complaints of sudden
onset weakness in all four limbs, for 3 days duration. The weakness occurred
simultaneously in all limbs and reached a peak 4 hours prior to admission.
There was no proximal\distal predilection, sensory loss, bladder or bowel involvement.
There was no past history or family history of similar episodes. The patient
also had complaints of palpitations and diarrhoea-off and
on for 1 month prior to the onset of weakness.
There was no history of trauma, chest pain,
dyspnoea, swelling over body, perception of missed
beats, weight loss or change of appetite. On
examination the patient was afebrile, well built, oriented in
time, place and person with a pulse of 150/min,
regular, bounding and BP 180/90mmHg. On
neurological examination higher mental functions and
cranial nerves were normal. The muscle bulk and tone
was normal in all four limbs. The power was 0/5 in
all four limbs. The deep tendon reflex (DTR) in
upper limb and lower limb were exaggerated. There
was no clonus. Sensory and posterior column examination was normal. Bilateral
plantar response was flexor. Rest of the general physical
examination and systemic examination including spine
was normal. There were no eye or skin signs
suggestive of thyrotoxicosis.
All the routine biochemical investigations including liver
and renal functions were normal. Serum potassium was 1.9meq/L and creatine
phosphokinase was 88U/L. The ECG revealed sinus tachycardia . In view of hypokalemia
associated with' quadriplegia and brisk DTR with a past history of' palpitations
and diarrhea a possibility of THP was thought and thyroid function was assessed.
The thyroid function revealed T3 = 250 ng/dl, T4 20mg/dl, serum TSH .01 /mU/L,
confirming the diagnosis of thyrotoxicosis and associated THP. The patient
was given treatment for hypokalemia and neomercazole 10mg tid along with propranolol
20 bid. was administered. There was a dramatic clinical improvement in patient's
motor power in the ensuing
24 hours and complete neurological recovery
was achieved in the next 2 days. Further
investigations into the cause of thyrotoxicosis revealed the
presence of a multinodular goiter on ultrasound of neck.
On follow up after 3 months, the repeat T3
180mg/dl, T4 12mg/dl and TSH 0.1 mU/L were obtained.
Discussion
Periodic paralysis is a condition characterized by episodic
weakness of the muscles and may be hypo, normo or hyperkalemic type. The commonest
of these is hypokalemic periodic paralysis. The mechanisms of periodic paralysis
is believed to be an inability of the muscle membrane to propagate an action
potential (3). Periodic paralysis could be primary or secondary when associated
with thyroid, renal or gastrointestinal disease leading to potassium loss or
retention.
In the presence of hyperthyroidism, periodic paralysis is
invariably of the hypokalemic variety (4). The incidence of periodic paralysis
with thyrotoxicosis is very low in the Western population but is particularly
high in oriental races where it occurs in 8-16% of thyrotoxic males and 0.2-0.45%
of females (4). From India, reports of THP are scanty (5). The precipitating
factors include high carbohydrate diet, stress and episodes of heavy physical
activity. Attacks occur usually at rest or at night and are seen more frequently
during the warmer months (6).
The clinical features of thyrotoxic periodic paralysis are
similar to that of primary hypokalemic periodic paralysis with most patients
presenting with acute flaccid paralysis with depressed/absent DTRs. In a minority
of patients, the DTRS may be brisk and may provide the clue to the underlying
throtoxcicosis. Thyroid hormones increase the activity of sodium pump resulting
in increased intracellular potassium. This may be a reason why periodic paralysis
seen with thyrotoxicosis is typically hypokalemic (7).
The treatment of THP has two components, Immediate correction
of hypokalemia is required to improve muscle weakness. Close attention should
be given with parenteral potassium replacement since the hypokalemia is due
to an intracellular shift and hyperkalemia can result quickly with restoration
of normal sympathies. The other component is effective treatment of thyrotoxicosis
because paralytic episodes cease after the euthyroid state is achieved. Initial
management with beta blockers and antithyroid medication work well, but recurrence
of
hyperthyroidism and paralytic episodes can
occur after discontinuing antithyroid medications. Propranolol has been used
for prophylaxis and reduces the incidence of spontaneous episodes of THP (3,
8). Acetazolamide which is effective in
the prophylactic treatment for familial periodic paralysis, however provides
no protection for
THP and may worsen an attack (3, 8).
To summarise, the possibility of THP should always be kept
in any patient who presents with hypokalemic paralysis especially with brisk/exaggerated
tendon reflexes. The clinical signs of thyrotoxicosis may vary from subtle
to quite obvious and a high index of suspicion is required to establish the
diagnosis.
References:
- Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses
: a review of the etiologies, pathophysiology, presentation and therapy. Am
J Emerg Med 1992; 10: 143-6.
- Chen KW, Hung TP, Lin TY. Periodic paralysis in Taiwan.
Clinical study of 28 cases. Arch Neurol 1965; 12: 165-71.
- Conway MJ, Seibel JA, Baton RP. Thyrotoxicosis and periodic
paralysis. Improvement with beta blockade. Ann Intern Med 1974; 81: 332-36.
- Woolery W, Gharib H. Thyrotoxic hypokalemic periodic paralysis
in a white man. South Med J 81991; 84: 1399-401.
- Plat G, Cranford R. Anderson D, Hubbad J. Thyrotoxic periodic
paralysis with upper motor neuron findings. JAMA 1978; 240: 2465-2466.
- Shishiba Y, Shimuzu T, Saito I, Shizume K. Elevated immunoreactive
insulin concentration during spontaneous attacks in thyrotoxic periodic
paralysis. Metabolism,
1972; 21: 285-90.
- Berwigar J. Sudden profound weakness and thyrotoxicosis. J
Tenn Med Assoc 1990; 83: 352.
- Ober KP. Thyrotoxic periodic paralysis in the United States.
Medicine; 1992; 71: 109-20.
Copyright 2004 - Malaysian Journal of Medical Sciences
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