Dear Editor,

A taser is a weapon used by police in order to provide a safe means of subduing an uncooperative person via an “electric shock”. This handheld device features two small barbed darts designed to puncture the skin. These darts are connected via copper wires to a main unit which delivers an electric current to the individual causing neuromuscular incapacitation by disrupting the voluntary control of muscles(1). A number of studies have raised concern over the health risks of tasers, including ventricular arrhythmias and cardiac arrest(2). Something I have come across during my training was a case of complete heart block provoked by a taser discharge. This phenomenon is not frequently described in the literature.

The patient in question had cardiac arrest immediately after receiving a discharge from a taser during an altercation with police. Thankfully, he was given bystander CPR and had return of spontaneous circulation after 3 minutes. On presentation to the Emergency Department the patient was found to be in complete heart block. He was admitted acutely to the coronary care unit for monitoring and had a permanent pacemaker inserted three days later.

The taser is considered a non-lethal weapon but can it truly be considered such?

Since it is not thought of as a firearm, taser use is not regulated by the Bureau of Alcohol, Tobacco, Firearms and Explosives. The main objective of this article is not to comment on the propriety of tasers, since it is the law enforcement authorities who must make a judgement call on that. However, I do believe that authorities should be judicious in its application. It is my opinion that a taser should be given equal consideration to a firearm since the consequences of discharging a taser can indeed be lethal.

References-

1. Ideker RE, Dosdall DJ. Can the direct cardiac effects of the electric pulses generated by the TASER X26 cause immediate or delayed sudden cardiac arrest in normal adults?. The American journal of forensic medicine and pathology. 2007 Sep 1;28(3):195-201.
2. Zipes DP. Sudden cardiac arrest and death following application of shocks from a TASER electronic control device. Circulation. 2012 May 22;125(20):2417-22.

Thank you very much for your letter on our published case report of a pregnant woman that was diagnosed with a left parietal glioma in the 28^th gestational week after a first generalised seizure, and for your opinion and thorough review of the literature.

In our patient we performed a two-stage approach with first a tumour resection under general anaesthesia and preservation of the pregnancy and after caesarean section performed in the 37^th gestational week an awake craniotomy for resection of residual tumour under neuropsychological monitoring and mapping.

We decided to do a two-stage approach after a round table where obstetricians, neurosurgeons, anesthetists, neonatologists, and midwives were involved and after several long conversations with the patient and her husband. For the patient clearly the health of her unborn child was the most important aspect of her treatment and therefore she wanted to prolong the pregnancy until term. The tumor of our patient was located with a broad base to the surface and seemed to have a plane to the underlying white matter. There was no, in this location possible eloquent, unaffected cortex overlying the tumor. Moreover, our patient was already in the 28^th gestational week of her pregnancy, the uterine fundus was high and the abdomen extended. The use of cortical or subcortical electric stimulation does increase the seizure risk^1-4. Because of all these reasons we decided against an awake craniotomy and an operation under general anesthesia was performed. During the first procedure we did not use electrophysiological monitoring or functional mapping at all to keep the seizure risk as low as possible.

We acknowledge that there are reports in the literature emerging that awake craniotomy during pregnancy seem to be a safe and feasible option and the authors of this letter provide a well-managed example from their own experience⁵. However, their patient was having a glioma with clear high-grade features present, leaving less time for multi staged procedures as these are aggressive tumors with limited prognosis. The tumor of our patient did radiologically not have high grade features, although preoperative imaging was obtained without administration of contrast. Histology of the tumor did show diffuse IDH-mutant astrocytoma classified between WHO grade II and III. The tumor exhibited methylation of the O-6 methylguanine DNA methyltransferase (MGMT) promotor and no complete deletion of cyclin-dependent kinase inhibitor 2a/b (CDKN2a/b) that are both positive prognostic and IDH mutation is a positive predictive marker. Morphologically it did show some anaplastic features and that is why it was finally treated like an anaplastic tumor.

5-aminolevulenic acid (5-ALA) in glioma surgery permits the intraoperative visualization of malignant glioma tissue and supports the neurosurgeon to reach a complete resection of the contrast-enhancing tumor. Some studies show a potential risk for the fetus if 5-ALA has been given together with irradiation in the first trimester⁶. To this date, there is no evidence about a possible teratogenic effect of 5-ALA in the third trimester^7-9. 

In our clinic we do not use the drug Gliolan® but a pharmaceutic product containing 5-ALA that is completely manufactured by our hospital pharmacy. Before application of this drug in our pregnant patient we had extensive consultation with our clinical pharmacologists and pharmacists. This counseling did not identify a risk to the pregnancy of our patient who was in the third trimester and therefore application was officially allowed. Before application of this medication we had a shared decision making conversation with the patient, where we informed her openly about studies showing possible risks for the fetus in the first trimester⁶ but that there was no evidence for risk to her pregnancy in the current stage. She then agreed to the use of 5-ALA for her surgery.

In the retrospect, we agree that administration of 5-ALA may not have been necessary since we considered a possible second operation already initially.

The authors of the e-letter took the statement that propofol would not be appropriate from two cases described from Sethuraman et al. where after very long procedures (11 and 10 hours respectively) the use propofol caused maternal mild metabolic acidosis¹⁰.

As our procedure did not last that long, the use of propofol during pregnancy in this case was reasonable as also confirmed by Wang et al. ¹¹      

Furthermore, during surgery we regularly performed ABGs in order to monitor the pH and avoid acidosis.

It will remain challenging to define standards of care for glioma patients in pregnancy. However, we agree with the authors of this letter that the single-stage strategy with awake craniotomy is a considerable alternative to our proposed strategy and that multidisciplinary discussion and careful perioperative planning are of upmost importance for these patients.                                                                                                  

1.           Jasper H. Electrocorticography. In. Boston: Little Brown1954:p. 692 - 738.

2.           Blume WT, Jones DC, Pathak P. Properties of after-discharges from cortical electrical stimulation in focal epilepsies. Clin Neurophysiol. 2004;115(4):982-989.

3.           Karakis I, Leeman-Markowski BA, Leveroni CL, et al. Intra-stimulation discharges: an overlooked cortical electrographic entity triggered by direct electrical stimulation. Clin Neurophysiol. 2015;126(5):882-888.

4.           PINSKY C, BURNS BD. Production of epileptiform afterdischarges in cat's cerebral cortex. J Neurophysiol. 1962;25:359-379.

5.           Kamata K, Fukushima R, Nomura M, Ozaki M. A case of left frontal high-grade glioma diagnosed during pregnancy. JA Clin Rep. 2017;3(1):18.

6.           Stummer W, Pichlmeier U, Meinel T, et al. Fluorescence-guided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase III trial. Lancet Oncol. 2006;7(5):392-401.

7.           Hadjipanayis CG, Widhalm G, Stummer W. What is the Surgical Benefit of Utilizing 5-Aminolevulinic Acid for Fluorescence-Guided Surgery of Malignant Gliomas? Neurosurgery. 2015;77(5):663-673.

8.           Yang JZ, Van Vugt DA, Melchior MF, Hahn PM, Reid RL. Photodynamic ablation of early pregnancy in the rat with 5-aminolevulinic acid: a potential new therapy for tubal ectopic pregnancy in the human. Fertil Steril. 1994;62(5):1060-1065.

9.           Olzowy B, Hundt CS, Stocker S, Bise K, Reulen HJ, Stummer W. Photoirradiation therapy of experimental malignant glioma with 5-aminolevulinic acid. J Neurosurg. 2002;97(4):970-976.

10.        Sethuraman M, Neema PK, Rathod RC. Prolonged propofol infusion in pregnant neurosurgical patients. J Neurosurg Anesthesiol. 2007;19:67-8.

11.        Wang, Lars Peter MD (Cph), FANZCA*; Paech, Michael James MBBS, DRCOG, FRCA, FANZCA, FFPMANZCA, FRANZCOG (Hon), DM† Neuroanesthesia for the Pregnant Woman, Anesthesia & Analgesia: July 2008 - Volume 107 - Issue 1 - p 193-200

We read the article published by Jaikaran O. et al on ‘Portomesenteric thrombosis after robotic sleeve gastrectomy’ with great interest. The reported about a morbid obese patient having porto-mesentric thrombosis after robotic sleeve gastrectomy due to obesity and mutation in methylenetetrahydrofolate reductase (MTHFR) mutation. However, we have few factors to report on this aspect.

Firstly, MTHFR enzyme dysfunction leads to hyperhomocysteinemia which leads to hypercoagulation state. Yet, the magnitude of this state is affected via degree of enzyme deficiency/dysfunction which is dependent on presence of heterogeneous/ homogenous mutation in enzyme gene. So, the authors must assess for the presence of hyperhomocysteinemia along with assessment of mutation.[1,2] Also the genetic homogeneity of the mutation must be assessed as heterogeneous mutation will have less effect on blood homocysteine levels.[3]

Next, the importance of folic acid for management of thrombotic state due to hyperhomocysteinemia must be considered. The patient has undergone sleeve gastrectomy which may further aggravate her vitamin and micronutrient deficiency. The administration of folic acid (instead of aspirin) will decrease the blood homocysteine levels and reduce the risk of hypercoagulation.[4]

References:
1. Friso S, Girelli D, Trabetti E, Stranieri C, Olivieri O, Tinazzi E, Martinelli N, Faccini G, Pignatti PF, Corrocher R. A1298C methylenetetrahydrofolate reductase mutation and coronary artery disease: relationships with C677T polymorphism and homocysteine/folate metabolism. Clin Exp Med. 2002 May;2(1):7-12.
2. McQuillan BM, Beilby JP, Nidorf M, Thompson PL, Hung J. Hyperhomocysteinemia but not the C677T mutation of methylenetetrahydrofolate reductase is an independent risk determinant of carotid wall thickening. The Perth Carotid Ultrasound Disease Assessment Study (CUDAS). Circulation. 1999 May 11;99(18):2383-8.
3. Zetterberg H, Regland B, Palmér M, Ricksten A, Palmqvist L, Rymo L, Arvanitis DA, Spandidos DA, Blennow K. Increased frequency of combined methylenetetrahydrofolate reductase C677T and A1298C mutated alleles in spontaneously aborted embryos. Eur J Hum Genet. 2002 Feb;10(2):113-8.
4. Serapinas D, Boreikaite E, Bartkeviciute A, Bandzeviciene R, Silkunas M, Bartkeviciene D. The importance of folate, vitamins B6 and B12 for the lowering of homocysteine concentrations for patients with recurrent pregnancy loss and MTHFR mutations. Reprod Toxicol. 2017 Sep;72:159-163.

The authors implicate caffeine as the causative agent of the cardiomyopathy in this case, caffeine being the main active ingredient within energy drinks. They ask that we enquire about energy drinks within our social histories; consumption of caffeinated products indeed not part of a standard cardiovascular history (1).

It is therefore conspicuous that within the article there are no calls to enquire about other, more widely used caffeine containing products, specifically tea and coffee. Dare I say, we would be unlikely to baulk at the idea of a patient drinking three or four coffees in a day. In fact, on the wards we offer patients tea or coffee eight times a day, yet think little of the caffeine burden we are imposing upon them. This almost tacit caffeine consumption is unlikely to make it into the medical notes, yet these patients would potentially be consuming levels of caffeine far in excess of the quantity consumed in this case report.

We seem to apply different value judgements to different drinks, assuming those drinking excess caffeine from expensive coffee machines are doing so knowingly, and as part of a healthy lifestyle. Yet we don’t afford those choosing to consume energy drinks with the same level of ability to make an informed choice. We medicalise the consumption of such drinks, assuming those using them must be doing so for sinister reasons.

We should treat all caffeinated products equally, given there is no pharmacological difference between them. Indeed, the caffeine found in energy drinks is extracted from coffee; a by-product of decaffeinated coffee production.

Further, I feel it unfair to suggest manufactures should provide warnings on cans, given that they already do – displaying both caffeine content, and warnings about its excessive consumption in certain groups. Indeed, these warnings and caffeine contents are absent from the sides of tea and coffee packaging, therein further preventing us from quantifying caffeine consumption.

That said, it is undeniable that the caffeine content of these drinks has increased over time, and it is not an unreasonable assumption that caffeine is to blame for the symptoms described in this case. Twenty years ago, the humble initial offerings of these drinks were a 250ml can with 75mg of caffeine. Today the bar has shifted to 200mg of caffeine in one can, and the market trend of increasing caffeine shows no signs of abating. This could be problematic, and lead to unwitting excess consumption as in this case report.

Direct regulation of these markets is often a wise solution. Rather than posting unheeded warnings of sugar content on the side of cans, the tax on sugar forced the hand of the market to adapt and reduce the sugar content within energy drinks, often to nil, and therein obviating the detrimental effects of sugar outright (2).

The same could be done for caffeine content; a cap of 20mg/100ml, or an overall cap of 100mg in any one drink would seem appropriate, though admittedly little can be done to stop people drinking multiple cans as in this case.

Like them or loathe them, these products do at least appeal to an ideal of activity, which should be celebrated in our overly sedentary society.

(1) Innes, J.A. et al., 2018. Macleod's Clinical Examination, Elsevier, pp.39-74
(2) Pell, D., Mytton, O., Penney, T.L., Briggs, A., Cummins, S., Penn-Jones, C., Rayner, M., Rutter, H., Scarborough, P., Sharp, S.J., Smith, R.D., White, M., Adams, J., 2021. Changes in soft drinks purchased by British households associated with the UK soft drinks industry levy: Controlled interrupted time series analysis. The BMJ 372. https://doi.org/10.1136/bmj.n254