Salt Wastage, Plasma Volume Contraction and Hypokalemic Paralysis in Self-Induced Water Intoxication

Tanneau, Ronan S.; Pennec, Y; Morin, Josée; Codet, J. P.; Bourbigot, B.; Cañadas-Garre, Marisa; Menn, Gwenaëlle Le

doi:10.1159/000187402

Cited by 6 publications

(5 citation statements)

References 13 publications

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“…Secondary hypokalaemic paralysis has been recognized in patients suffering from diabetes, renal tubular acidosis, thyrotoxicosis and self-induced water intoxication [1,3,5,7,10]. Our patient proved to have normal kidney and thyroid function as well as unremarkable blood sugar serum levels.…”

Section: Discussionmentioning

confidence: 56%

A surprising cause of paresis following scoliosis correction

Kluba

Giehl

2001

Eur Spine J

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IntroductionThe most feared complication in spinal surgery is paraplegia. In a large reported series the risk of a cord lesion in spinal deformity surgery has been found to be 0.5-1.7%. Risk signs noted are congenital deformity, kyphosis, postradiation deformity and larger (more than 100º) curves. The lesions are caused by cord stretching in instrumented patients or direct trauma [12].We report an unusual metabolic complication which caused transient paresis of the proximal leg muscles after scoliosis surgery. Case reportA 15-year-old Turkish girl (B.U., 162 cm, 42 kg) was admitted for surgical correction of severe thoracic scoliosis. The patient presented with a marfanoid habitus and a thoracic curve of 116º (Cobb). Preoperative neurological examination was unremarkable and the MRI of the spinal cord revealed no cord abnormalities. Halogravity traction and anterior release, followed by further traction and finally posterior instrumentation were scheduled. After a 5-week period of traction, anterior release Th4-L1 was performed uneventfully in controlled hypotension. The right segmental arteries Th5-Th12 were ligated. Autologous iliac bone and rib grafts were placed in the disc spaces on the concave side of the curve. The cell saver technique was used (400 ml autotransfusion), central venous pressure was monitored (6-11 mm H 2 O) and fluid intake was adjusted accordingly. The Stagnara wake-up test and postoperative function were normal, with forceful dorsi-and plantarflexion bilaterally.During the following day the patient developed symmetrical paresis of the hip and knee flexors and extensors (0/5). The dorsiand plantarflexion of the feet were still forceful (4/5) and sensibility was not disturbed in either leg. Patellar tendon jerks and Achilles tendon reflexes were absent. There were no evident pyramidal signs. Rectal tone was normal, as was examination of the upper extremities. The neurologist additionally disclosed a decreased T5-10 sensibility on the right hemithorax and suspected a traumatic cord lesion. A CT scan of the thoracic spine was performed, and intraspinal haematoma and dislocation of intersomatic rib grafts were ruled out. A psychological exploration of the patient revealed no suspicion of simulation. At that time a routine blood check showed decreased potassium (2.8 mmol/l) and haemoglobin (8.4 mg/%) levels. Other parameters including serum pH (7.36) and sodium (138 mmol/l) were within normal limits. There were no electrocardiographic changes present.Intravenous potassium substitution (20 mEq/h) was started under continuous ECG monitoring. Red blood cells (2 units, 350 ml) were transfused to correct anaemia. A 24-h urine measurement and electromyography were initiated to determine the aetiology of the hypokalaemia, but the paresis resolved before the evaluations were finished. Secondary hypokalaemia caused by a transcellular shift due to metabolic acidosis was ruled out by arterial blood gases (serum pH 7.36). Since the patient was normothermic, increased Abstract Paralysis following scoliosis...

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Section: Discussionmentioning

confidence: 56%

A surprising cause of paresis following scoliosis correction

Kluba

Giehl

2001

Eur Spine J

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“…Electromyography result is often normal, specifically between the weakness episodes when patient is asymptomatic but it can reveal some abnormalities in some patients. This disorder can be present in patients with thyrotoxicosis, barium poisoning, renal disorders like proximal, and distal renal tubular acidosis, 3 water intoxication, syndrome of inappropriate antidiuretic hormone (ADH) secreation (SIADH), 13 nephrotic syndrome, 14 barter's syndrome, 15 diuretic phase of acute tubular acidosis, 16 treatment phase of diabetic ketoacidosis, 17,18 chlorothiazide-associated hypokalemia, 19 hypokalemia following rectosigmoidiscopy, 20,21 gastro-intestinal losses due to coeliac disease, 22 tropical sprue, 23 acute gastroenteritis, 24 malabsorption syndromes, 25 endocrinopathies like primary hyperaldosteronism 26 and pseudohyperaldosteronism induced by licorice (glycyrrhizic acid) ingestion. 27 The management of HPP includes both therapeutic agents and avoiding precipitating triggers through dietary as well as lifestyle changes, having small frequent meal for avoiding high carbohydrate load, low sodium diet and avoidance of hyperosmolar state such as dehydration and hyperglycemia, decrease the number of attacks.…”

Section: Discussionmentioning

confidence: 99%

Hypokalemic periodic paralysis in a teenage boy after an intense period of exercise: A rare case report

Noor,

Rasooly,

Alikozai

et al. 2023

Clinical Case Reports

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Key Clinical Messages Diagnosis of rare even can be missed due to less familiarity with the disorder. In patients with muscle weakness, infectious causes are prioritized. Electrolyte profile not only identifies the problem, but also prevents unnecessary workup. AbstractIn underdeveloped countries, diagnosis of rare disorders is usually delayed due to less familiarity of the clinicians to such disorders. As a result, infectious and inflammatory causes for an ailment are prioritized as compared to non‐infectious etiologies. Hypokalemic periodic paralysis (PP) is a rare disorder, characterized by episodic muscle weakness that can rarely be associated with life‐threatening cardiac arrhythmia. A teenage Afghan boy presented to the emergency department with an acute flaccid paralysis, that started 1 h after intense exercise The weakness involved both, the upper and lower extremities. Laboratory investigations, led to the impression of hypokalemic PP, precipitated by intense exercise. Accordingly, intravenous potassium chloride infusion diluted with normal saline led to the complete resolution of paralysis as well as correction of electrocardiographic changes. The list of differential diagnosis for flaccid muscle paralysis is wide, which generally requires a extensive investigations, but in hypokalemic PP, a cardinal electrolytes profile can lead towards early diagnosis. High degree of clinical suspicion with appropriate history taking and physical examination helps with the immediate identification and management of this disorder.

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“…La intoxicación acuosa aguda es frecuente en pacientes con patología psiquiátrica grave (como la esquizofrenia) con polidipsia crónica y osmolalidades en el límite bajo, con supresión permanente de ADH, que hacen hiponatremia aguda por otro factor de riesgo imprescindible: la ingestión masiva de agua en un momento determinado. Existen numerosas observaciones clínicas de este tipo de casos (5)(6)(7)(8). La intoxicación acuosa aguda en adultos sin patología psiquiátrica ni administración parenteral excesiva de líquidos hipotónicos es excepcional.…”

Section: Discussionunclassified