Vasovagal asystole during spinal anaesthesia

A patient in whom vasovagal asystole was induced by the performance of a spinal anaesthetic in the upright position is described. This illustrates the importance of routine monitoring of the electrocardiograph during regional anaesthesia. The risk of vasovagal syncope may be increased by the use of the sitting position and by the omission of anxiolytic premedication.     

Vasovagal syncope and anaesthetic practice

We surveyed anaesthetists working in North-West England and in North Wales concerning episodes of vasovagal syncope encountered in their practice. Eighty-eight anaesthetists described 109 such events occurring in either patients or their relatives and the estimated frequency of syncope was 1 in 5000 anaesthetic episodes. The patient syncopal episodes were triggered by venous cannulation in 16 instances and regional or local techniques in 20 instances. Thirty-three of the 53 patients were in the upright position when syncope occurred. Thirty-nine of the 56 relatives were male partners of female patients and four of these partners suffered some morbidity. The results of the survey are consistent with our current knowledge of the pathophysiology of vasovagal syncope, which is summarized, and also highlight the common anaesthetic scenarios where fainting is most likely to occur. Given this information anaesthetists will be in a better position to avoid such potentially harmful episodes in the future.     

A profound case of neurally mediated syncope with asystole after septoplasty

Vasovagal syncope (VVS) is an alarming yet benign condition that may present postoperatively for the first time in otherwise healthy patients. Although VVS is associated anecdotally with nasal manipulation, no data have been found to quantify this incidence with otolaryngology surgeries. We present a case of profound, recurrent syncope and documented asystole with an initial diagnosis of glossopharyngeal neuralgia. We conclude with a discussion of neurally mediated syncope particular to the perioperative setting. It is essential to recognize neurocardiogenic etiology to differentiate it from other more concerning causes of syncope and asystole.     

Non-drug related asystole associated with anaesthetic induction

A patient is presented where routine venepuncture associated with anaesthetic induction resulted in bradycardia and asystole. The case highlights the need for special caution with, and ECG monitoring throughout induction for, patients with a history of syncope. It also demonstrates the need for caution when attributing cardiovascular events during induction to the effect of the induction agents used.     

Swallow syncope associated with paroxysmal atrial fibrillation.

Swallow or deglutition syncope is a very unusual potentially lethal but treatable disorder. We report the case of a 26-year-old woman, who presented with a history of recurrent, multiple fainting episodes precipitated by swallowing. Twenty-four-hour manometry and pH recording together with continuous 24-h ECG monitoring revealed multiple episodes of symptomatic and asymptomatic paroxysmal atrial fibrillation, and significant gastro-oesophageal reflux associated with swallowing. Oesophageal function tests and continuous electrocardiographic evaluation is important in the diagnosis of this rare condition.     

Vasovagal syncope and severe bradycardia following intranasal dexmedetomidine for pediatric procedural sedation

We report syncope and bradycardia in an 11‐year‐old girl following administration of intranasal dexmedetomidine for sedation for a voiding cystourethrogram. Following successful completion of VCUG and a 60‐min recovery period, the patient's level of consciousness and vital signs returned to presedation levels. Upon leaving the sedation area, the patient collapsed, with no apparent inciting event. The patient quickly regained consciousness and no injury occurred. The primary abnormality found was persistent bradycardia, and she was admitted to the hospital for telemetric observation. The bradycardia lasted ~2 h, and further cardiac workup revealed no underlying abnormality. Unanticipated and previously unreported outcomes may be witnessed as we expand the use of certain sedatives to alternative routes of administration.     

Trigeminal neuralgia associated with seizure and syncope. Case report

A patient with trigeminal neuralgia experienced a generalized seizure and a prolonged syncopal episode. He was found to be asystolic during the syncopal episode. There was no recurrence of loss of consciousness after implantation of a pacemaker. Mechanical stimulation of the trigeminal nerve during craniotomy for microvascular decompression of the trigeminal nerve resulted in bradycardia. Since vascular decompression of the trigeminal nerve, there has been no recurrent facial pain, and no further syncope, seizures, or bradycardia. Syncope and seizures have not been previously reported in association with trigeminal neuralgia, although they are well described with glossopharyngeal neuralgia.     

Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold-Jarisch reflex

Reflex cardiovascular depression with vasodilation and bradycardiahas been variously termed vasovagal syncope, the Bezold–Jarischreflex and neurocardiogenic syncope. The circulatory responsechanges from the normal maintenance of arterial pressure, toparasympathetic activation and sympathetic inhibition, causinghypotension. This change is triggered by reduced cardiac venousreturn as well as through affective mechanisms such as painor fear. It is probably mediated in part via afferent nervesfrom the heart, but also by various non-cardiac baroreceptorswhich may become paradoxically active. This response may occurduring regional anaesthesia, haemorrhage or supine inferiorvena cava compression in pregnancy; these factors are additivewhen combined. In these circumstances hypotension may be moresevere than that caused by bradycardia alone, because of unappreciatedvasodilation. Treatment includes the restoration of venous returnand correction of absolute blood volume deficits. Ephedrineis the most logical choice of single drug to correct the changesbecause of its combined action on the heart and peripheral bloodvessels. Epinephrine must be used early in established cardiacarrest, especially after high regional anaesthesia. Br J Anaesth 2001; 86: 859–68     

Neuroendocrine carcinoma of lung associated with bradycardia and episodic cardiac asystole

A neuroendocrine carcinoma of the lung associated with bradycardia and episodic cardiac asystole is reported. Cardiac dysfunction may have been caused by a hormonal factor produced by a carcinoma developing in the pulmonary neuroepithelial bodies because the bradycardia and periods of asystole disappeared after pneumonectomy, only to return months later when pleural metastatic tumor developed. No neoplastic involvement of the heart was present. Implications of a cholinesterase isoenzyme involvement in the cardiac dysfunction are discussed.     

Thrombocytopenia associated with intravenous desferrioxamine

Desferrioxamine (DFO) was administered intravenously to a 63-year-old chronic hemodialysis patient with osteomalacia believed secondary to aluminum intoxication. Thrombocytopenia was noted after five doses of DFO. Platelet counts normalized after DFO was withheld. Thrombocytopenia recurred upon two rechallenges with this drug. It is suggested that platelet counts be monitored in hemodialysis patients receiving intravenous DFO.     

Failed intravenous access in children

Securing intravenous access in children can, on occasion, be difficult, time-consuming and frustrating. Unhurried preoperative examination for possible cannulation sites, avoidance of long starvation times and the use of adjuncts including topical local anaesthetic creams and oral sedatives improve success rates. Despite these measures, failure of peripheral cannulation will still occur. A range of alternative methods to access the circulation including intraosseous needles and central venous cannulation are described in outline. The role of each alternative technique in a range of clinical situations is discussed along with their advantages and disadvantages.     

Hypersensitivity reactions and deaths associated with intravenous iron preparations.

BACKGROUND: Parenteral iron therapy is an accepted adjunctive management of anaemia in kidney disease. Newer agents may have fewer severe hypersensitivity adverse events (AE) compared with iron dextrans (ID). The rate of type 1 AE to iron sucrose (IS) and sodium ferric gluconate (SFG) relative to ID is unclear. We used the US Food and Drug Administration's Freedom of Information (FOI) surveillance database to compare the type 1 AE profiles for the three intravenous iron preparations available in the United States. METHODS: We tabulated reports received by the FOI database between January 1997 and September 2002, and calculated 100 mg dose equivalents for the treated population for each agent. We developed four clinical categories describing hypersensitivity AE (anaphylaxis, anaphylactoid reaction, urticaria and angioedema) and an algorithm describing anaphylaxis, for specific analyses. RESULTS: All-event reporting rates were 29.2, 10.5 and 4.2 reports/million 100 mg dose equivalents, while all-fatal-event reporting rates were 1.4, 0.6 and 0.0 reports/million 100 mg dose equivalents for ID, SFG and IS, respectively. ID had the highest reporting rates in all four clinical categories and the anaphylaxis algorithm. SFG had intermediate reporting rates for urticaria, anaphylactoid reaction and the anaphylaxis algorithm, and a zero reporting rate for the anaphylaxis clinical category. IS had either the lowest or a zero reporting rate in all clinical categories/algorithm. CONCLUSIONS: These findings confirm a higher risk for AE, especially serious type 1 reactions, with ID therapy than with newer intravenous iron products and also suggest that IS carries the lowest risk for hypersensitivity reactions.