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AN UNUSUAL PRESENTATION OF THYROTOXICOSIS
Authors
Dr:K.B.Rojith* , Dr.D.K Sivakumar* . Dr.T.Geetha MD**, Dr.S.Avudiappan M D
Dr .Veerakesari .MD***, Dr. Nedumaran . MD .DM ***, Dr.S.Usha.M D.***
* Junior resident
** Assistant professor
***Professor
Department of Medicine ,Coimbatore Medical College.
.
ABSTRACT
Thyrotoxic periodic paralysis (TPP) is a rare complication of thyrotoxicosis, that
constitutes an endocrine emergency. Periodic paralysis without a familial history in a
patient with hyperthyroidism is a strong clinical clue to the diagnosis, especially when
accompanied by concomitant hypokalemia1.We present a case of 28 year old male
admitted with recurrent history of weakness of all four limbs with hypokalemia which
turned out to be a thyrotoxicosis induced hypokalemic periodic paralysis.
KEY WORDS
Periodic paralysis,Thyrotoxicosis,Hypokalemia
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CASE HISTORY
28 year old male admitted with history of weakness of all four limbs of one day
duration.He noticed weakness, while getting up from bed in the morning,associated with
retention of urine .History of muscle cramps was present in the previous night .No
history suggestive of cranial nerves , sensory or cerebellar involvement
There was no preceding history of trauma,fever,or recent vaccination .He had similar
two episodes in the recent past which recovered spontaneously within a day .No history
of similar illness in the family.
On examination there was flaccid quadriparesis with predominant proximal musle
involvement, power was 2/5 in both upper and lower limbs.
Deep tendon reflexes were diminished , plantar was flexor response .
Proceeded with provisional diagnosis of periodic paralysis.Routine blood investigations
were within normal limits .Serum electrolytes report was K+ -2.3 meq/l, Na -134meq/l
,serum calcium was 8.2mg/dl . So diagnosis of hypokalemic periodic paralysis
probably of secondary causes was made.
Next step was to find out the cause of hypokalemia.From the history, gastro intestinal
loss and chronic diuretic use was ruled out .Urine electrolytes were done to rule out
renal tubular acidosis ,which came as normal. Ultrasound abdomen ,Chext xray were
within normal limit ,ECG showed sinus tachycardia.
Even though there were clinically no features of thyrotoxicosis except for tachycardia we
proceeded with a thyroid function test which shown TSH of 0.02 µIU/L , total T4
68µg/L, total T3 700ng/L. So diagnosis of hypokalemic periodic paralysis secondary to
thyrotoxicosis was made.
Patient was treated with oral potassium about 60 meq over 24 hrs and recovered very
well next day without residual paralysis.and on discharge serum k+ was 3.8 meq/l.He
was started on carbimazole 10 mg tds and propranolol 20 mg bd for the thyrotoxicosis .
DISCUSSION
Periodic paralysis associated with the thyrotoxic state is a rare and peculiar disorder
that affects only skeletal muscles. The degree of paralysis varies from one attack to
another. Severe episodes can cause paralysis of all skeletal muscles, including those
controlling respiration. Smooth muscles are seldom affected, and cardiovascular
dysfunction is not observed in this disorder. The cardinal feature of a typical attack is
muscle weakness, usually symmetrical paralysis beginning in the proximal muscles of
the legs.1 Hypokalemia (potassium level <3.0 mmol/L) associated with hyperthyroidism
is also common.1
A typical attack of thyrotoxic periodic paralysis lasts from a few hours to several days.
Most attacks occur in the morning or evening.1 In our patient , the first two attacks
lasted for about few hours each and weakness recovered spontaneously but the
current attack lasted about 24 hours and recovered with oral potassium treatment. All
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the three attacks occurred in the early morning hours.In contrast to familial periodic
paralysis, in which the first attack occurs before the age of 10 years, patients with
thyrotoxic periodic paralysis are usually aged 20 to 40 years.1
Asians are disproportionately affected by this condition, with one study showing Asians
were at 159-fold higher risk compared with white Europeans.2 There is an overwhelming
male predominance, with a male-to-female ratio of 77:20.3 The condition has been
reported worldwide, including in the United Kingdom, the United States (in whites and
African Americans), and South America.4-6 A low serum potassium level has been noted
in the majority of patients with thyrotoxic periodic paralysis. Thyrotoxicosis is associated
with normal regulation of body sodium, potassium, and cell volume. Administration of
thyroid hormone has been shown to increase the fractional excretion of potassium. 7
Compared with other body tissues, human renal tissue contains a higher concentration
of messenger RNA for the thyroid receptors alpha-1, alpha-2, and beta. An alteration of
thyroid-receptor expression may be an important mechanism that controls the tissue
effects of the hormone, as the thyroid hormone levels in the serum increase. 8 Asian and
Hispanic patients with thyrotoxicosis are particularly susceptible to periodic paralysis. It
is also important to remember that although hypokalemia is common during the acute
paralytic episode, between attacks plasma potassium and total body potassium stores
remain within normal limits.9 Precipitating factors of hypokalemic thyrotoxic periodic
paralysis include strenuous exercise followed by rest, excessive ingestion of
carbohydrate-rich food, administration of insulin or epinephrine, trauma, exposure to
cold temperatures, infection, menstruation, and emotional stress.1
Definitive treatment of thyrotoxic periodic paralysis consists of the management of
thyrotoxicosis, medical therapy, surgery or radioactive iodine therapy. Treatment for an
acute attack is potassium administration, but excessive doses of potassium can lead to
hyperkalemia once potassium shifts to the extracellular space.10No correlation between
potassium dose administered and recovery time was observed. To prevent attacks until
euthyroid state is achieved, a useful therapy is the administration of a β-adrenergic
blocker like propranolol. Other preventive measures that may be effective include a lowcarbohydrate diet and potassium-sparing diuretics.11Use of potassium supplements is
not useful for prophylaxis against further paralytic attacks, and it should not be given to
patients between episodes.12
SUMMARY
Thyrotoxic periodic paralysis is a rare complication of thyrotoxicosis that must be
regarded as an endocrine emergency. Clinical clues to this condition include a
presentation of periodic paralysis without a family history, along with a history of
hyperthyroidism. Episodes of periodic paralysis usually precede the diagnosis of thyroid
dysfunction and do not recur once euthyroidism is achieved. Therefore, it is necessary
that an early diagnosis of TPP is made to administer definitive treatment and prevent
morbidity and mortality, mainly due to fatal arrhythmias. The presence of acute
paralysis, especially with hypokalemia, should prompt the clinician to consider TPP as a
cause and evaluate thyroid function.
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