Tetania severa por uso de enemas fosfatados, reporte de caso / Tetany secondary to phosphate enema toxicity, case report

Los enemas fosfatados son utilizados frecuentemente en el tratamiento de la constipación. Errores en la posología pueden producir complicaciones graves. Objetivo: Reportar un caso de toxicidad grave por enema fosfatado en un pre escolar sin factores de riesgo. Caso clínico: Paciente de 2 años con constipación funcional, evaluada en servicio de urgencia por dolor abdominal a quién se le diagnosticó un fecaloma impactado. Recibió 2 dosis de enema de fosfato, “medio frasco” de Fleet® adulto (Synthon, Chile) por vez, sin resolución de su fecaloma, decidiéndose hospitalización para proctoclisis. Posterior al ingreso presentó un cuadro clínico de tetania. Ingresó a la Unidad de Paciente Crítico donde se confirmó una hiperfosfemia e hipocalcemia secundaria. Se realizó corrección electrolítica progresiva, retiro de enema fosfatado residual del recto e hiperhidratación forzando diuresis. La tetania cedió 2 horas después del ingreso sin otras complicaciones. Se realizó proctoclisis y fue dada de alta a los 3 días. Conclusión: Los enemas fosfatados pueden presentar complicaciones graves en niños sin factores de riesgo. Errores en la posología son la causa más frecuente de toxicidad en este grupo, pero esta puede estar favorecida también por una administración y eliminación inadecuadas. Pediatras y personal de salud que atiende a niños deben conocer factores de riesgo, signos y síntomas de intoxicación por enemas fosfatados.

Phosphate enemas are frequently used in the treatment of constipation. Errors in dosage and administration can lead to severe complications. Objective: To report a case of severe toxicity of phosphate enemas in a child with no risk factors. Case: 2 years old female, with functional constipation, was brought to emergency department because abdominal pain. She was diagnosed with fecal impaction and received half a bottle of Fleet Adult® (Laboratorio Synthon, Chile) two times, with no clinical resolution, deciding to start proctoclisis in pediatric ward. Soon after admission, she presented painful tetany, but alert and oriented. Patient was transferred to PICU where severe hyperphosphatemia and secondary hypocalcemia were confirmed. Her treatment included electrolyte correction; removal of residual phosphate enema and hyperhydration. Tetany resolved over 2 hours after admission and no other complications. Proctoclisis was performed and patient was discharged three days after admission with pharmacological management of constipation. Conclusion: Phosphate enemas may cause serious complications in children with no risk factors. Errors in dosage, administration and removal of the enema are causes of toxicity in this group. Pediatricians and health personnel must be aware of risks and signs of toxicity of phosphate enema.

Tetany: Possible adverse effect of bevacizumab.

Background: Bevacizumab a recombinant humanized monoclonal antibody was approved in 2004 by US FDA for metastatic colorectal cancer. It is reported to cause potentially serious toxicities including severe hypertension, proteinuria, and congestive heart failure. Aim: To correlate adverse event tetany with the use of bevacizumab. Materials and Methods : World Health Organization's Uppsala Monitoring Centre, Sweden, for reporting of adverse drug reactions from all over the world, identified 7 cases with tetany-related symptoms to bevacizumab from four different countries. These 7 patients reported to UMC database developed adverse events described as musculoskeletal stiffness (1), muscle spasm (1), muscle cramps (1), lock jaw or jaw stiffness (4), and hypertonia (1), with hypocalcaemia. Results: After detailed study of the possible mechanism of actions of bevacizumab and factors causing tetany, it is proposed that there is a possibility of tetany by bevacizumab, which may occur by interfering with calcium metabolism. Resorption of bone through osteoclasts by affecting VEGF may interfere with calcium metabolism. Another possibility of tetany may be due to associated hypomagnesaemia, hypokalemia, or hyponatremia. Conclusions: Tetany should be considered as a one of the signs. Patient on bevacizumab should carefully watch for tetany-related symptoms and calcium and magnesium levels for their safety.

Tetany in kala azar patients treated with paromomycin.

Paromomycin, an aminoglycoside, is known to cause several side effects like nephrotoxicity and ototoxicity like other aminoglycosides but tetany has not been reported. Three cases of tetany were detected in the patients of kala-azar treated with paromomycin. They were promptly treated with intravenous 10 per cent calcium gluconate and tetany was relieved immediately and treatment with paromomycin continued with oral calcium supplement. After completion of 21 days treatment with paromomycin patients' splenic aspirates were free of parasites. Paromomycin may cause temporary tubular damage leading to calcium wasting in urine and hypocalcaemia resulting in tetany. Prompt detection of symptoms and intravenous calcium gluconate treatment promptly reverse the situation.

Reversal by methylene blue of tetanic fade induced in cats by nitric oxide

Previous data from our laboratory have indicated that nitric oxide (NO) acting at the presynaptic level increases the amplitude of muscular contraction (AMC) of the phrenic-diaphragm preparations isolated from indirectly stimulated rats, but, by acting at the postsynaptic level, it reduces the AMC when the preparations are directly stimulated. In the present study we investigated the effects induced by NO when tetanic frequencies of stimulation were applied to in vivo preparations (sciatic nerve-anterior tibial muscle of the cat). Intra-arterial injection of NO (0.75-1.5 mg/kg) induced a dose-dependent increase in the Wedensky inhibition produced by high frequencies of stimulation applied to the motor nerve. Intra-arterial administration of 7.2 mug/Kg methylene blue did not produce any change in AMC at low frequencies of nerve stimulation (0.22 Hz), but antagonized the NO-induced Wedensky inhibition. The experimental data suggest that NO-induced Wedensky inhibition may be mediated by the guanylate cyclase-cGMP pathway.