J Neurosurg Anesthesiol



Volume 27, Number 3, July 2015

REFERENCES 1. Dagres N, Hindricks G. Risk stratification after myocardial infarction. Is left ventricular ejection fraction enough to prevent sudden cardiac death. Eur Heart J. 2013;34:1964–1971. 2. Chassot PG, Delabays A, Spahn DR. Preoperative evaluation of patients with, or at risk of, coronary artery disease undergoing non-cardiac surgery. Br J Anaesth. 2002;89:747–759. 3. Chen H, Tsai C, Chao S, et al. Endoscopic discectomy of L5-S1 disc herniation via an interlaminar approach: Prospective controlled study under local and general anesthesia. Surg Neurol Int. 2011;2:93. 4. Richardson J, Lonnqvist PA, Naja Z. Bilateral thoracic paravertebral block: potential and practice. Br J Anaesth. 2011;106:164–171.

Cardiovascular Collapse After Induction To JNA Readers: An 89-year-old African American woman was admitted, semiconscious, from a nursing home. Very limited history was available. Diagnosed with normal pressure hydrocephalus, she was urgently scheduled for insertion of a ventriculo-peritoneal shunt. Monitors were placed and, using a previously established intravenous route, propofol 40 mg was injected. Within 5 minutes blood pressure and pulse were unobtainable. Fearing herniation, the neurosurgeon prepared for immediate placement of a burr hole. However, pupillary examination showed normal reactivity. A partial label on the fluid bag indicated that cephazolin 2 g had been added. The site of insertion of the needle was at the elbow. During induction, the arm, which had been bent, was straightened, allowing the fluid to flow freely. The patient’s airway was immediately secured and suspecting anaphylaxis, we replaced the fluid with lactated Ringer solution and gave epinephrine 1 mg and diphenhydramine 50 mg. Response was immediate with restoration of blood pressure and pulse. Hypotension is not uncommon after induction of general anesthesia. However, when the hypotension is The authors have no funding or conflicts of interest to disclose.

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severe especially in patients who may be dehydrated or have unknown comorbidities such as coronary artery or neurological disease, identification of the cause can be difficult. Anaphylactic/anaphylactoid reactions are rare intraoperatively. Anaphylaxis is an immediate hypersensitivity, or type 1, reaction mediated by the interaction of an antigen with IgE causing activation and degranulation of mast cells and basophils. Anaphylactoid reactions are IgEindependent reactions caused by direct activation of mast cells and basophils by allergens. Vasoactive mediators such as histamine, prostaglandins, kinins, leukotrienes, and tryptase are released. These substances cause the clinical manifestations associated with anaphylactic shock such as severe hypotension, bronchospasm, laryngeal edema, and cardiovascular collapse. Clinically, anaphylaxis and anaphylactoid reactions are indistinguishable. Muscle relaxants, antibiotics, and intravenous anesthetics have been identified as allergens.1–3 Transesophageal echocardiography can distinguish between anaphylaxis and cardiogenic shock. In anaphylaxis, stroke volume and ejection fraction are increased secondary to hyperdynamic left ventricular function.4 However, this monitor was not available to us at that time and we had to resort to a basic eye examination. Also, her dark skin made appreciation of a rash difficult. The Surgical Care Improvement Program requires preoperative administration of antibiotics to almost all surgical patients. In emergency situations, especially in comatose patients, a previous history of allergy may not be obtained. By this case we wish to emphasize that hypotension after induction may have many causes. Because anaphylaxis is readily treatable, it should be included in the diagnosis. The case also underscores the need for better practitioner vigilance and awareness of the contents of the infusing fluid in the intravenous line used for induction. Himani V. Bhatt, DO, MPA Elizabeth A.M. Frost, MD Icahn School of Medicine at Mount Sinai, NY

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REFERENCES 1. Mertes PM, Laxenaire MC. Allergic reactions occurring during anaesthesia. Eur J Anaesthesiol. 2002;19:240–262. 2. Soetens FM. Anaphylaxis during anaesthesia: diagnosis and treatment. Acta Anaesthesiol Belg. 2004;55:229–237. 3. Mertes P, Laxenaire M. Allergy and anaphylaxis in anaesthesia. Minerva Anestesiol. 2004;70:285–291. 4. Vitarelli A, Gheorghiade M. Transthoracic and transesophageal echocardiography in the hemodynamic assessment of patients with congestive heart failure. Am J Cardiol. 2000;86:36G–40G.

Near-Infrared Spectroscopy Changes During Embolization of a Vein of Galen Malformation To JNA Readers: A 10-month-old infant presented with progressive prominence of right eye and swelling of right eyelid since 4 months of age and regression of milestones. Magnetic resonance imaging of the brain showed vein of Galen malformation (VOGM). Cerebral angiography confirmed VOGM. (Fig. 1A) During embolization of the VOGM under general anesthesia, in addition to standard monitoring, near-infrared spectroscopy (NIRS) was used for monitoring changes in regional cerebral oxygen saturation (rSo2). The baseline readings before anesthesia showed a higher value on right side (81%—channel II) compared with the left (70%—channel I). Coiling of VOGM was uneventful till third hour when an abrupt and persistent decrease in the right rSo2 to 50% to 60% was noted (Fig. 1B). Checking angiogram did not reveal occlusion or hemorrhage. Elective ventilation was done for 12 hours to facilitate adaptation of the vulnerable intracranial vasculature to the new flow dynamics. NIRS is used to monitor rSo2.1 Acute and persistent reduction in the cerebral oxygen saturation is associated The authors have no funding or conflicts of interest to disclose.

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