Severe Acquired Hypokalemic Paralysis in a Bodybuilder After Self-Medication With Triamterene/Hydrochlorothiazide.

BACKGROUND: Severe hypokalemia with severe neurological impairment and electrocardiogram (ECG) abnormalities due to the misuse of triamterene/hydrochlorothiazide (HCTZ) in a bodybuilder has not yet been reported. CASE REPORT: A 22-year-old bodybuilder developed acute generalized muscle cramps, sensory disturbance of the distal lower and upper limbs, quadriparesis, and urinary retention. These abnormalities were attributed to severe hypokalemia of 1.8 mmol/L (normal range 3.4-4.5 mmol/L) due to misuse of triamterene/HCTZ together with fluid restriction. He was cardiologically asymptomatic, but ECG revealed a corrected QT (QTc) interval of 625 ms. On intravenous application of fluids along with intravenous and oral substitution of potassium, his condition rapidly improved, such that the sensory disturbances, quadriparesis, and bladder dysfunction completely resolved within 2 days after admission. CONCLUSIONS: Self-medication with diuretics along with fluid restriction may result in severe hypokalemia, paralysis, and ECG abnormalities. Those responsible for the management of bodybuilding studios and competitions must be aware of the potential severe health threats caused by self-medication with diuretics and anabolic steroids. Although triamterene is potassium-sparing, it may enhance the potassium-lowering effect of HCTZ.

Imaging appearance of myelopathy secondary to nitrous oxide abuse: a case report and review of the literature.

Purpose The abuse of nitrous oxide (N2O) can induce Vitamin B12 deficiency that subsequently leads to central nervous demyelination, myelopathy and peripheral neuropathy. Although myelopathy has been reported in the past, the specific locations and prognosis of the disease are still unclear. MATERIALS AND METHODS: We report the case of a 22-year-old male who presented with quadriplegia that began after a 3-month history of inhalation of N2O. We summarized the clinical data of this entity and performed a comprehensive literature review of various presentations and MRI features of myelopathy secondary to N2O abuse. RESULTS: In combination with previous reports of 14 cases, we found that the onset of the disease was usually subacute, and the majority of patients (92.85%) were young men. There was no definite relationship between myelopathy and the amount or duration of N2O inhalation. The most common clinical manifestation was sensory ataxia, and the cervical spinal cord was the most frequently impaired area of the whole spinal cord. The spinal cord lesions had a high signal intensity on T2-weighted MRI and usually involved more than three spinal segments and impaired the posterior column more significantly. Most patients recovered well after vitamin B12 supplementation. CONCLUSIONS: Myelopathy secondary to N2O abuse is generally seen in young men. The clinical diagnosis mainly depends on a history of N2O inhalation and the characteristic imaging changes in the posterior cervical spinal cord. Early diagnosis and intervention are important for a satisfactory prognosis.

'Gym Tonic' and Quadriparesis.

We report a case of acute onset quadriparesis which occurred after consumption of some drugs which were illicitly prescribed to our young patient by his gym instructor. The deadly concoction of so-called gym-tonic (Cyproheptadine and dexamethasone) led to hypokalaemic paralysis in our patient.

Catastrophic relapses following initiation of dimethyl fumarate in two patients with neuromyelitis optica spectrum disorder.

We report two cases of neuromyelitis optica spectrum disorder (NMOSD) who were misdiagnosed as multiple sclerosis (MS) and developed catastrophic relapses following initiation of dimethyl fumarate. Both patients developed a severe myelitis extending from the cervical cord to the medulla with significant cord swelling, resulting in complete quadriplegia and respiratory difficulties, in addition to severe bilateral visual loss in one patient. It is of note that both catastrophic relapses occurred 2 and 3 months following initiation of dimethyl fumarate.

Acute transient spinal paralysis and cardiac symptoms following an accidental epidural potassium infusion - a case report.

BACKGROUND: To describe a case of an accidental epidural potassium infusion leading to an acute transient spinal paralysis and cardiac symptoms and review the literature on that topic. CASE PRESENTATION: We report the case of an accidental infusion of 900 mg potassium chloride 7.45% (KCl) into the epidural space, which occurred during epidural analgesia in a 74-year-old patient suffering from immobilization due to lumbar back pain as well as from a paralytic Ileus. The event was resulting in vegetative symptoms, such as tachycardia and hypertension accompanied by a motor complete tetraplegia (AIS B) sub C2 with respiratory depression. The endotracheal intubation was necessary. The patient was treated with 40 mg dexamethasone intravenously, as well an epidural lavage with sodium chloride solution 0.9% (NaCl) through the epidural catheter. The neurologic symptoms completely resolved within five days. An elevation of troponin-T values and a reduced left ventricular ejection fraction (LVEF) of 40% accompanied by transient pectanginous pain were documented. An exertional dyspnea remained. CONCLUSIONS: A symptom complex with elevated sympathetic nervous system activity up to a stress cardiomyopathy is possible following epidural potassium infusion. Additionally, generalized pain and muscle spasticity evolve and a progressive acute spinal cord injury syndrome can occur within minutes, accompanied by respiratory depression. Treatment consists of early intensive care and the symptomatic therapy of the associated symptoms, leading in most of the reported cases to a good clinical outcome.

Pesticide-induced quadriplegia in a 55-year-old woman.

Acephate is a commercial organophosphate pesticide formerly used in households and now used primarily for agriculture. Poisoning symptoms include salivation, lacrimation, urination, defecation, gastrointestinal illness, and emesis. In addition to these classic symptoms, neurodegeneration can result from increased and continued exposure of organophosphates. This 55-year-old woman presented with organophosphate-induced delayed neuropathy in the form of quadriplegia due to the commonly used pesticide acephate. She was exposed to this pesticide through multiple sprayings in her work office with underrecognized poisoning symptoms. She presented to her primary care physician with neuropathic pain and paralysis in her arm following the sprayings and eventual complete paralysis. The patient lived for 2 years following her toxic exposure and quadriplegia. A complete autopsy after her death confirmed a transverse myelitis in her spinal cord. We conclude that in susceptible individuals, acephate in excessive amounts can produce severe delayed neurotoxicity as demonstrated in animal studies.

[A wing clipping beverage]. / Une boisson qui coupe les ailes.

Chronic consumption of soda energizing caffeine has known a growing success. Its deleterious effects, however, are often ignored. We report a case of tetraparesis associated with chronic excessive consumption of cola. The development of muscle weakness is variable, resulting from a hyperpolarization of excitable membranes. The outcome is most often favorable after potassium supplementation and interruption of the offending beverage consumption. The mechanisms involved are multiple and involve both a leakage of fecal and urinary potassium and a potassium entry into the intracellular compartment. Other mechanisms related to caffeine are also involved. It therefore appears mandatory to assess the consumption of such beverages in the presence of hypokalemia and muscle weakness.

Prolonged ventilatory failure and flaccid quadriparesis after ingestion of poison hemlock.

INTRODUCTION: A 28-year-old man presented with acute flaccid paralysis and respiratory failure that persisted for 2 weeks after suicidal ingestion of unknown substances. METHODS: Extensive clinical, nerve, laboratory, and neuroimaging testing excluded alternative causes of this neuromuscular syndrome. Prompted by clues provided by family members, liquid chromatography time-of-flight mass spectrometry was used to investigate for the presence of poison hemlock. RESULTS: Testing of the residue in a jar used for the ingestion of a poisonous concoction confirmed the presence of the nicotinic alkaloid coniine. Analysis of patient serum suggested the presence of conhydrine. Concentrations of amitriptyline and diazepam were also found to be supratherapeutic, but only through the first few days of hospitalization. CONCLUSIONS: Herein we describe a case of reversible coma, flaccid quadriparesis, and neuromuscular respiratory failure caused by intentional ingestion of poison hemlock.

[Rare consciousness disturbances in toxicological practice: akinetic mutism, somnambulism, locked-in syndrome, and psychogenic coma]. / Rzadkie zaburzenia swiadomosci w praktyce toksykologicznej: mutyzm akinetyczny, somnambulizm, zespól zamkniecia i spiaczka psychogenna.

The toxicity of xenobiotics can result inrare disorders of consciousness, such as akinetic mutism and somnambulism as well as syndromes mimicking consciousness disturbances, such as locked-in syndrome and psychogenic coma. Akinetic mutism is a condition characterized by a lack of spontaneous movements and little or no vocalization. Somnambulism include performing of complex motor activity in an automatic manner during deep sleep, without any awareness of its execution. The locked-in syndrome is a state with quadriplegia coexisting with cranial nerves palsies and mutism, but with fully preserved consciousness. Psychogenic coma is a condition in which the patient has preserved level of consciousness and awareness, but does not communicate with theenvironment and does not exhibit the external manifestations of consciousness. This paper presents the etiology, clinical characteristics, as well as diagnostic and therapeutic issues for the above syndromes.

An unusual complication of quadriparesis after trigger point injection: a case report.

ABSTRACT: Quadriparesis after intramuscular trigger point injections for myofascial pain syndrome has been rarely reported in the literature. A 37-year-old male patient presented with myofascial pain syndrome and was given trigger point injections in trapezius muscles under ultrasound guidance. The patient noticed weakness in all the 4 limbs at approximately 12 hours after the procedure, which gradually progressed to functional quadriplegia at the time of presentation to the emergency department. On examination, he had quadriparesis with no sensory involvement and superficial reflexes were normal. MRI screening of the whole spine was unremarkable, and MRI brain suggested an incidental granuloma, which could not explain his symptoms. Blood tests revealed severe hypokalemia (2.2 mEq/L) and deranged thyroid function tests. Immediate potassium correction with intravenous and oral potassium chloride was initiated, and the patient showed improvement within 6 hours of initiating correction. Stress of the procedure, use of steroids with mineralocorticoid effects such as methylprednisolone, or deranged thyroid function tests may have acted as triggers to precipitate hypokalemic paralysis in the patient. Knowledge of this complication is essential as prompt diagnosis and timely management of hypokalemia can result in complete resolution of the symptoms.

Spastic quadriplegia following intradermal use of hydrogen peroxide in the tardive curettage procedure for the treatment of a giant congenital nevus.

The possible transformation of a giant congenital melanocytic nevi (GCMN) in malignant melanoma estimated from 0.05% to 40% depend on the size of the lesions. Many are the surgical procedures proposed, including: full or partial-thickness excisions, dermabrasion, curettage in the first weeks of life and laser treatment. The curettage technique has been proposed in the literature for the treatment of GCMN in the first few weeks of life and defined as a relatively atraumatic surgery procedure without general complications. The authors report the first case in the literature of embolization due to use of subcutaneous peroxide infiltration before a tardive curettage procedure in a newborn case of GCMN resulting in spastic quadriplegia with dystonic reaction. Consequently, a lawsuit, due to this medical malpractice, has been opened.

An unusual complication of immunosuppression in myasthenia gravis: progressive multifocal leukoencephalopathy.

We present a 44-year-old female patient with generalised myasthenia gravis who developed progressive multifocal leukoencephalopathy. She was receiving high dose corticosteroids, azathioprine 200mg daily and high dose intravenous immunoglobulin during relapses. Two months after thymectomy she presented with progressive cognitive decline, asymmetric quadriparesis and ataxia. Two months later she was bedridden. Cranial MRI showed large asymmetric T2 and FLAIR hyperintense lesions in cortical and subcortical structures. Positive CSF PCR of JC virus confirmed the diagnosis. The patient survives with severe sequela which confirms slow progression as typical in nonAIDS cases. This is the second case of progressive multifocal leukoencephalopathy in a myasthenic patient.

Rodenticide poisoning as a cause of quadriparesis: a rare entity.

Acute flaccid paralysis with its wide repertoire of causes presents a challenge to the clinician. We present a case of barium carbonate poisoning, a rare yet easily treatable cause of acute quadriparesis. Barium acts by redistribution of potassium from the extra- to intravascular compartment causing hypokalemia. Early recognition and prompt potassium supplementation under cardiac monitoring yield gratifying results.

[Ethylene glycol intoxication. Important differential diagnosis in comatose patients with metabolic acidosis]. / Athylenglykolintoxikation. Wichtige Differenzialdiagnose beim komatösen Patienten mit metabolischer Acidose.

Ethylene glycol is an alcohol, which is mainly used as antifreeze. Intoxication with ethylene glycol can cause neurological and cardiopulmonary symptoms, metabolic acidosis and acute renal failure. Therapeutic options include reversal of metabolic acidosis, inhibition of alcohol dehydrogenase and early hemodialysis. In survivors of the acute phase, lasting damage is rare. The case of a 49-year-old patient with ethylene glycol intoxication is reported which was characterized by progressive impairment of consciousness, tetraparesis, hyperventilation and metabolic acidosis.

Ethanol poisoning as a differential diagnosis in a hunter's dog with tetraplegia.

A 4.5-month-old German pointer was presented with tetraplegia. Based on the physical examination, a tentative diagnosis of idiopathic polyneuropathy or synaptic disorder was made. Later that day additional information from the owner revealed that the dog might have ingested sloe berries that had been used to make sloe gin. Ethanol poisoning was added to the differential diagnosis. The dog's locomotion recovered in the course of 24 hours. Faecal analysis revealed that the animal had ingested at least 127 gin-saturated sloe berries and it was estimated that the blood ethanol concentration would have been at least 0.75 per thousand. The aetiology, diagnosis, and treatment of ethanol poisoning in dogs is reviewed.

Permanent lesion to the corticospinal tract after therapy with capecitabine.

Capecitabine is an oral fluoropyrimidine used to treat solid tumours such as colorectal and breast cancer. A rare but severe side effect is capecitabine-induced leukoencephalopathy, including bilateral lesion to the corticospinal tract. However, neurological symptoms due to capecitabine treatment are usually reported to be reversible after discontinuation of capecitabine. Here, we present the case of a patient with bilateral degeneration of the corticospinal tract and progressive spastic tetraplegia after chemotherapy with capecitabine mimicking primary lateral sclerosis. Although therapy with capecitabine was ended, symptoms substantially worsened over the following years and the patient finally died from aspiration pneumonia almost 3 years after the application of capecitabine.

Levofloxacin-associated hypoglycaemia complicated by pontine myelinolysis and quadriplegia.

BACKGROUND: Central pontine myelinolysis (CPM) usually presents in chronic alcoholics and in patients in whom hyponatraemia has been corrected rapidly. However, CPM may occur in other clinical circumstances, including patients with severe hypoglycaemia. We describe the occurrence of CPM and quadriplegia in a patient who experienced fluoroquinolone-associated severe hypoglycaemia. CASE REPORT: A 63-year-old man with Type 2 diabetes mellitus was admitted to hospital for resection of a large liposarcoma. Renal-dose levofloxacin was utilized as part of an antimicrobial regimen to treat post-operative peritonitis. On days 6-8 of levofloxacin therapy, the patient experienced recurrent hypoglycaemia despite total parenteral nutrition, 10% dextrose containing fluids and cessation of insulin therapy 3 days prior to the first hypoglycaemic episode. Hypoglycaemia resolved within 24 h of stopping levofloxacin. After a final and severe hypoglycaemic event, the patient developed quadriplegia and tonic left deviation of gaze. Magnetic resonance imaging revealed a high-intensity lesion in the central pons consistent with CPM. CONCLUSIONS: Fluoroquinolones should be considered as a potential cause of hypoglycaemia. Severe hypoglycaemia has the potential to cause white matter lesions in the pons. Putative mechanisms include failure of membrane ion channels, oligodendrocyte apoptosis and oxidative stress of glucose reperfusion. Fluoroquinolone-associated hypoglycaemia and hypoglycaemia-induced quadriplegia are both rare and we believe this is the first case report linking the two events.

Quadriplegia due to lead-contaminated opium--case report.

PURPOSE: Utilization of lead-contaminated opium may lead to severe motor neuron impairment and quadriplegia. CASE REPORT: Forty years oriented old male, opium addict, was admitted to the ICU, with headache, nausea and abdominal pain, and weakness in his lower and upper extremities without definitive diagnosis. The past medical and occupational history was negative. Laboratory investigation showed; anemia (Hb 7.7 g/dl), slightly elevated liver function tests, elevated total bilirubin, and ESR. Abdominal sonography and brain CT scan were normal. EMG and NCV results and neurologic examination were suggestive for Guillain-Barre. He underwent five sessions of plasmapheresis. Blood lead level was > 200 microg/dl. He received dimercaprol (BAL) and calcium disodium edetate (CaEDTA) for two five days session. Upon discharge from ICU all laboratory tests were normal and blood lead level was reduced, but he was quadriplegic. CONCLUSION: The delayed treatment of lead poisoning may lead to irreversible motor neuron defect.

Transient Hypokalemic Quadriplegia After a Lumbar Transforaminal Epidural Dexamethasone Injection: A Case Report.

A 30-year-old man with no significant medical history presented with hypokalemic quadriplegia 4 hours after he received a lumbar transforaminal epidural steroid injection (ESI) containing dexamethasone and lidocaine. A comprehensive workup ruled out acquired and hereditary causes of hypokalemic paralysis. Symptoms gradually resolved within hours after potassium restoration with no residual neurologic deficits. Paralysis after transforaminal ESI is uncommon but has been associated with particulate steroids that can coalesce into aggregates and occlude vessels. To our knowledge, there have been no case reports of paralysis after ESI with dexamethasone, a nonparticulate steroid. This transient paralysis is possibly caused by the effects of glucocorticoids on Na-K channels and insulin resistance resulting in hyperglycemia and subsequent hypokalemia. We reviewed the differential diagnosis of transient paralysis after epidural steroid injection in this report. LEVEL OF EVIDENCE: IV.

[Skeletal fluorosis: a case report]. / Fluorose osseuse: à propos d'un cas.

The authors report a case of skeletal fluorosis described in a 60 years old man living in south-west Tunisian. The main clinical sign is a severe functional legs disability. Radiographic examination has shown a diffused osteocondensation, with cervical spine degenerative discopathy, a pelvis bilateral osteoarthritis and an interosseous membrane ossification of forearms and legs. The skeletal fluorosis diagnosis has been confirmed by high serum and urinary fluoride levels.