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Woke up paralysed—without injury or stroke
| Content Provider | Semantic Scholar |
|---|---|
| Author | Bawaskar, Himmatrao Saluba Bawaskar, Pramodini Himmatrao |
| Copyright Year | 2008 |
| Abstract | At 0930 h on April 1, 2004, a 35-year-old man was brought to our emergency department by autorickshaw. He usually worked in the city, but had spent a pleasant day’s holiday working in the paddy fi elds—until waking up, at 0230 h, unable to move his limbs. He had felt perfectly well, retiring to bed at 2200 h. He had no medical history of note. His bladder and bowels were working normally. His heart rate was 125 per min; his pulse was regular, and good in volume; his blood pressure was 160/110 mm Hg. The patient was taking 24 breaths per min, but maintaining arterial oxygen saturations of 97%. He had fl accid paralysis of all four limbs (power 0/5 throughout—hence, refl exes could not be elicited); however, sensory examination gave normal fi ndings. So did examination of the cranial nerves—except that the facial muscles were weak throughout, giving the patient a myasthenic look (fi gure). We observed alopecia areata. An electrocardiogram (ECG) showed a sinus tachycardia, prominent U waves, and a long corrected QT interval (QTc) of 560 ms (normal range 380–420 ms). Blood tests showed mild normocytic anaemia (haemoglobin concentration 119 g/L)—and a potassium concentration of only 2·0 mmol/L. A second ECG showed a QTc of 599 ms. We administered potassium intravenously; after 60 mmoles had been given, the serum potassium concentration was 4·2 mmol/L. 24 h after he arrived, the patient was able to move his limbs normally. Limb refl exes, including the plantar refl ex, were normal. The QTc was only 400 ms, and the heart rate only 93 beats per min. The face no longer looked myasthenic—in fact, the patient had lid retraction, exophthalmos, and lid lag, indicating Graves’ disease. We prescribed propranolol— as well as spironolactone, a potassium-sparing diuretic, for hypertension. Thyroid function tests confi rmed the diagnosis: serum concentrations of tri-iodothyronine (T3), thyroxine (T4), and thyrotropin were 4·0 nmol/L, 309 nmol/L, and 0·036 mIU/L respectively (normal ranges 0·9–2·6 nmol/L, 60–175 nmol/L, and 0·2–5·0 mIU/L, respectively). We prescribed carbimazole, in addition to propranolol. The patient felt his limbs increase in strength, and gained 4 kg in 20 days. After discharge, the patient was followed up elsewhere, but attended our clinic for review in February, 2008. The patient reported that he had been well since discharge, and was now taking only 5 mg carbimazole a day, and 40 mg propranolol twice daily. Blood tests indicated persisting thyrotoxicosis: concentrations of T3, T4, and thyrotropin were 3·4 nmol/L, 186 nmol/L, and 0·008 mIU/L, respectively. However, the patient’s heart rate was only 82 beats per min, and the QTc 375 ms. In hypokalaemic periodic paralysis (HPP), the patient has acute, severe muscle weakness, caused by hypokalaemia. HPP can be familial or, more commonly, caused by thyrotoxicosis. Attacks of thyrotoxic HPP are likely to occur when the patient is at rest, and nearly always happen in the early morning or late evening; physical exertion or a high-carbohydrate meal, before the period of rest, make an attack more likely still (in western Maharashtra, agricultural labour is the commonest occupation, and rice is the staple food). Episodes resolve spontaneously, within 96 h; some patients learn to terminate an attack by becoming active when they notice early symptoms. Bulbar, respiratory, and eye muscles are usually spared. Although thyrotoxicosis is far more common in women than in men, around 95% of patients with thyrotoxic HPP are men. Thyrotoxic HPP is far commoner in Asian than in white or black patients: around 2% of Asians with hyperthyroidism develop thyrotoxic HPP. The mechanism by which thyro toxi cosis causes HPP is unknown, but is thought to inc lude increased activity of sodium-potassium ATPase. β blockers reduce the risk of paralysis. Consequences of hypokalaemia, other than paralysis, can include hypertension and, rarely, ventricular fi brillation. |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/S0140-6736(08)60385-2 |
| PubMed reference number | 18328933 |
| Journal | Medline |
| Volume Number | 371 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0140673608603852 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0140673608603852?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/S0140-6736%2808%2960385-2 |
| Journal | The Lancet |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
