1/8. Fatal hyperkalemia during rapid and massive blood transfusion in a child undergoing hip surgery--a case report.We report a girl who developed severe and fatal hyperkalemia following rapid and massive blood transfusion during surgery. She was 7-year-old, 20-kg in weight, and received wide resection of the femoral bone with custom prosthesis implant because of malignant femoral osteosarcoma. During the procedure, bleeding was active and profuse and amounted to about 3,000 mL in 4 h, eventuating in shock. Despite rapid transfusion with 15 units of packed red blood cells (RBC) still she remained hypotensive and hypovolemic. When we switched to give her whole blood, actually 100 mL having been given, widening of QRS complex followed immediately by cardiac arrest developed. cardiopulmonary resuscitation although started at once was unsuccessful. At this juncture, arterial blood gas analysis showed acidosis and severe hyperkalemia (10.3 mmol/L), possibly resulting from transfusion of blood of older storage. The case reminded us once again the importance and necessity of the use of potassium-low blood component (fresh, saline-washed RBCs) in case of massive and rapid blood transfusion especially in pediatric patients with hypovolemia and low cardiac output.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/8. Hyperosmolar diabetic non-ketotic coma, hyperkalaemia and an unusual near death experience.Generally, cardiac arrest due to pulseless electrical activity has a poor outcome, except when reversible factors such as acute hyperkalaemia are identified and managed early. Hyperosmolar diabetic non-ketotic coma may lead to acute hyperkalaemia. Hyperosmolar diabetic non-ketotic coma is a metabolic emergency usually seen in elderly non-insulin dependent diabetics, characterized by severe hyperglycaemia, volume depletion, altered consciousness, confusion and less frequently neurological deficit. Cerebrovascular accident or transient ischaemic attack may be mistakenly diagnosed, particularly if the patient has no history of diabetes mellitus. Delays in diagnosis and management of glycaemic emergencies presenting as a constellation of neurological abnormalities can be avoided by routine early measurement of blood glucose. Hyperosmolar diabetic non-ketotic coma should be considered in any patient with altered consciousness or neurologic deficit in conjunction with hyperglycaemia. As hyperosmolar diabetic non-ketotic coma results in severe fluid depletion, electrolyte disturbance, profound hyperglycaemia and an altered mental state, the guiding principles of therapy include aggressive rehydration, insulin therapy, correction of electrolyte abnormalities and treatment of any underlying illnesses. Treatment of acute hyperkalaemia includes calcium ions, insulin with dextrose, salbutamol and haemodialysis.- - - - - - - - - - ranking = 8keywords = coma (Clic here for more details about this article) |
3/8. Fatal hyperkalemia related to combined therapy with a COX-2 inhibitor, ACE inhibitor and potassium rich diet.We describe the case of a 77-year old mildly hypertensive woman with no underlying renal disease who was admitted to the Emergency Department (ED) in a comatose state with fever. The patient had been on low dose enalapril and a potassium rich diet. Five days before admission, rofecoxib, a new selective COX-2 inhibitor nonsteroidal anti-inflammatory drug (NSAID), was added for leg pain. She was found to have severe hyperkalemia and died 90 min after her arrival. We cannot absolutely determine whether the COX-2 inhibitor was the dominant contributor to the development of hyperkalemia or the combination itself, with an intercurrent infection and some degree of dehydration. physicians should be aware of this possible complication and only prescribe NSAIDs, including the new COX-2 drugs, to the elderly under close monitoring of kidney function and electrolyte tests.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/8. life-threatening hyperkalaemia following therapeutic barbiturate coma.OBJECTIVE: To report the occurrence of life-threatening hyperkalaemia following treatment with therapeutic thiopentone coma. SETTING: The neurosurgical intensive care units of Royal North Shore Hospital and Liverpool Hospital, Sydney, australia. patients: Three patients treated with theraputic thiopentone coma. One patient with raised intracranial pressure secondary to a severe traumatic brain injury and two patients with refractory vasospasm secondary to subarachnoid haemorrhage. Two of the three patients developed hypokalaemia on starting thiopentone, which was resistant to potassium supplementation. All three patients developed severe hyperkalaemia during the recovery phase of coma. This was life-threatening in all three patients and fatal in one. CONCLUSIONS: Severe hypokalaemia refractory to potassium therapy may occur during therapeutic thiopentone coma. Severe rebound hyperkalaemia may occur after cessation of thiopentone infusion. Protocols for the management of patients with therapeutic barbiturate coma should recognise this potentially serious complication.- - - - - - - - - - ranking = 9keywords = coma (Clic here for more details about this article) |
5/8. Hypernatraemia induced by sodium polystyrene sulphonate (Kayexalate) in two extremely low birth weight newborns.Hyperkalaemia is a life-threatening electrolyte disorder that can occur in the first week of life in almost 50% of preterm infants with a birth weight less than 1000 g [extremely low birth weight (ELBW)]. serum potassium values higher than 7 mmol x l-1 are associated with cardiac arrhythmias and an increased incidence of intraventricular haemorrhage and periventricular leucomalacia. Therapeutic options to treat this dangerous imbalance comprise calcium gluconate, insulin plus glucose, albuterol/salbutamol inhalation. Administration of cation-exchange resin such as sodium polystyrene sulphonate (Kayexalate) is effective in lowering plasma potassium, although complications following oral or rectal administration are reported in newborns. We describe two ELBW infants affected by hyperkalaemia, treated with Kayexalate, who developed serious hypernatraemia, that has never been reported before in preterm infants.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/8. Hyperkalaemia induced by carbonic anhydrase inhibitor.An 81-year-old man developed hyperkalaemic and hyperchloraemic metabolic acidosis following treatment with a carbonic anhydrase inhibitor for his glaucoma. He had mild renal failure and selective aldosterone deficiency was confirmed. In this case the treatment did not lead to hypokalaemia because of the limited potassium secretory capacity in the renal tubules from selective aldosterone deficiency; rather, it may have led to hyperkalaemia because metabolic acidosis induced by the carbonic anhydrase inhibitor caused transcellular movement of potassium.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/8. Severe hyperkalemia as a complication of timolol, a topically applied beta-adrenergic antagonist.Severe hyperkalemia occurred in a patient with radiation pneumonitis and glaucoma shortly after beginning prednisone therapy. There was no evidence of renal failure, diabetes, acidosis, increased potassium intake, or significant tissue trauma. Medications having adverse effects on potassium metabolism were considered, and the patient's use of timolol maleate eyedrops was discontinued. His serum potassium level normalized despite continuation of the prednisone therapy. He became hyperkalemic on rechallenge with timolol and normokalemic following its withdrawal. This case indicates that the potential for beta-blocker-induced hyperkalemia exists even with topical appreciation.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/8. Hazards of succinylcholine administration during electrotherapy.We describe prolonged apnea following electrotherapy in a patient who was also being treated with a topical organophosphate anticholinesterase, ecothiophate iodide (phospholine iodide), for glaucoma. The increased duration of action of succinylcholine resulted from low levels of serum cholinesterase that had been caused by the organophosphate. attention is called to other drugs that directly or indirectly (by lowering serum cholinesterase) interact with succinylcholine chloride resulting in prolonged apnea. Other potential hazards of succinylcholine administration, such as hyperkalemia and cardiac arrhythmias, are also discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |