Article

Impact of prehospital airway management on combat mortality

prehospital airway management “>American Journal of Emergency Medicine 37 (2019) 349-373

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Correspondence

Airway management in a Prehospital combat setting

To the Editor,

In a retrospective review of US Army medical evacuation patient care records, Hardy et al. [1] compared outcomes of US military injured that received prehospital advanced airway interventions. The authors con- clude that patients who received a supraglottic airway devices (SAD) had higher morbidity demonstrated by fewer ventilator, hospital, and ICU free days than those receiving cricothyrotomy or mask ventilation. We would like to add several appreciations. The authors do not spec- ify the SADs used. This data is essential to make an accurate analysis of the data. It is well known that Second-generation SADs, although they do not completely protect the airway from aspiration, provides better efficacy and safety compared with first-generation devices [2]. The first-generation SADs (e.g. the classic laryngeal mask airway) have sev- eral limitations, fundamentally providing only a moderate pharyngeal seal that may be associated with inadequate ventilation, gastric infla- tion, regurgitation and pulmonary aspiration. The design of second- generation Supraglottic airways allows for greater pharyngeal seal pres- sures and they contain an oesophageal port which provides functional separation of the respiratory and gastrointestinal tracts and allows for the draining or aspiration of gastric contents. Second-generation SGAs are also more likely to enable oxygenation and ventilation [3]. Thus, only second-generation SADs are recommended in the recent guide- lines [3-5]. Likewise, each second-generation SAD has specific attributes as the time of placement, seal pressure, type of separation of gastroin- testinal and respiratory tracts and use as a conduit for endotracheal in-

tubation (blind or fibre-optically guided tracheal intubation).

The competence and experience of the operator with the device also play a relevant role since they influence the success of insertion and cor- rect placement. Different studies indicate a low failure rate in the clinical use, although the consequences of failure included an increase in hospi- tal admission and ICU admission [6].

All of this justifies the need to specify the kind of SAD since they con- stitute a heterogeneous group of non-equated devices. Therefore, it is necessary to take all these data into account. Otherwise, the conclusions of this interesting work could be misleading.

Manuel Angel Gomez-Rios* Department of Anesthesia and Perioperative Medicine, Complejo Hospitalario Universitario de A Coruna, A Coruna, Galicia, Spain Anesthesiology and Pain Management Research Group, Institute for Biomedical Research of A Coruna (INIBIC), A Coruna, Spain

Spanish Difficult Airway Group (GEVAD)

*Corresponding author at: Department of Anesthesia and Perioperative Medicine, Complejo Hospitalario Universitario de A Coruna, Xubias de

Arriba, 84, A Coruna 15008, Spain

E-mail address: [email protected]

Jose Maria Calvo-Vecino Department of Anesthesia, Complejo Asistencial Universitario de Salamanca, Universidad de Salamanca (CAUSA), Salamanca, Spain

6 June 2018

https://doi.org/10.1016/j.ajem.2018.06.050

References

  1. Hardy GB, Maddry JK, Ng PC, et al. Impact of prehospital airway management on com- bat mortality. Am J Emerg Med 2018;36(6):1032-5.
  2. Gomez-Rios MA, Gaitini L, Matter I, Somri M. Guidelines and algorithms for managing the difficult airway. Rev Esp Anestesiol Reanim 2018;65(1):41-8.
  3. Higgs A, McGrath BA, Goddard C, et al. Guidelines for the management of tracheal in- tubation in critically ill adults. Br J Anaesth 2018;120(2):323-52.
  4. Rehn M, Hyldmo PK, Magnusson V, et al. Scandinavian SSAI clinical practice guideline on pre-hospital airway management. Acta Anaesthesiol Scand 2016;60(7):852-64.
  5. Frerk C, Mitchell VS, McNarry AF, et al. Difficult Airway Society 2015 guidelines for man-

    agement of unanticipated difficult intubation in adults. Br J Anaesth 2015;115(6):827-48.

    Cook TM, MacDougall-Davis SR. Complications and failure of airway management. Br J Anaesth 2012;109(Suppl 1):i68-85.

    Impact of prehospital airway management on combat mortality

    Response to Letter to Editor,

    We appreciate the inquiry regarding our publication and thank you for the letter. We were unable to determine the type or generation of supraglottic airway devices used in the prehospital combat setting from the MEDEVAC documentation. An additional consideration affect- ing patient outcomes regarding supraglottic airway devices in the prehospital combat setting is the difference in the combat environment versus the hospital environment. As mentioned in our discussion sec- tion, combat medics do not carry paralytics, the patients are not fasting, and the environment is considerably different than that of the hospital. Furthermore, the primary causes of injury in our patient population are improvised Explosive devices and high velocity rifles which result in in- juries significantly different from those in the US civilian setting. This is in addition to the differing types of supraglottic airway and varying competence of the operator that you mentioned. Regardless, further re- search comparing the different supraglottic airway devices is necessary to draw more definitive conclusions.

    Funding source

    Defense Joint Program Committee — 6.

    Garrett Hardy, MD, MC, US Army

    Department of Emergency Medicine, San Antonio Military Medical Center,

    JBSA Ft. Sam Houston, TX, United States

    0735-6757/(C) 2018

    350 Correspondence / American Journal of Emergency Medicine 37 (2019) 349373

    Joseph K. Maddry, MD, MC, USAF US Air Force En route Care Research Center 59th MDW/ST, Chief Scientist’s Office, US Army Institute of Surgical Research, JBSA Ft. Sam Houston, TX,

    United States

    Department of Emergency Medicine, San Antonio Military Medical Center,

    JBSA Ft. Sam Houston, TX, United States

    Patrick C. Ng, MD, MC, USAF

    Rocky Mountain Poison and Drug Center, Denver, CO, United States

    Shelia C. Savell, PhD, RN US Air Force En route Care Research Center 59th MDW/ST, Chief Scientist’s Office, US Army Institute of Surgical Research, JBSA Ft. Sam Houston, TX,

    United States

    Corresponding author at: USAF En route Care Research Center, 3698 Chambers Pass Bldg 3611, Fort Sam Houston, TX 78234, United States.

    E-mail address: [email protected].

    Allyson A. Arana, PhD Avery Kester, BS

    US Air Force En route Care Research Center 59th MDW/ST, Chief Scientist’s Office, US Army Institute of Surgical Research, JBSA Ft. Sam Houston, TX,

    United States

    Vikhyat S. Bebarta, MD, MC, USAF

    Department of Emergency Medicine, University of Colorado School of

    Medicine, Aurora, CO, United States Colorado Air National Guard, Buckley AFB, CO, United States

    21 June 2018

    https://doi.org/10.1016/j.ajem.2018.06.052

    Other aspects of Nitrous oxide-related neuromyelopathy

    The point is well made that the “work-up” of suspected nitrous oxide (NO2) myelopathy should include, not only serum vitamin B12 (i.e., cobalamin) measurement, but also documentation of serum homo- cysteine, Methylmalonic acid (MMA), and folate levels [1]. The rationale is that some patients in whom cobalamin derangements are implicated in the aetiopathogenesis of NO2-related neurotoxicity may, nevertheless, have serum cobalamin levels within the normal range [2]. In one such pa- tient (case 1) NO2-related neuropathy was initially mistaken for Guillain- Barre syndrome, arguably because there was no concurrent spinal cord demyelination and, hence, no abnormality detected on magnetic reso- nance imaging (MRI) of the entire spinal cord. On the basis of the provi- sional diagnosis of Guillain-Barre syndrome that patient was prescribed a 5 days course of intravenous immunoglobulin. The correct diagnosis was made only after eliciting a history of NO2 recreational use, and also after documentation of a serum MMA level of 29,653 mmol/l (normal b 280 mmol/l). He gradually improved after he was prescribed vitamin B12 injections [2]. In the same series there was a patient (case 3), with NO2-related myelopathy, in whom a normal serum vitamin B12 level coexisted with an elevated serum homocysteine level [2]. That patient ex- perienced a Complete recovery after a course of vitamin B12 injections [2]. NO2-related neuropathy in the absence of abnormalities on MRI imag- ing of the spinal cord has been documented in anecdotal reports [2-4] and also in a retrospective study of 33 patients evaluated in one institution over a period of 10 years [5]. In the latter study the coexistence of myelopathy was confirmed using clinical manifestations or T2 hyperintensity on spinal cord MRI. Fifteen patients were evaluated by spinal cord MRI, among whom seven had T2 hyperintensity of the posterior columns. Overall 20

    patients exhibited clinical features or MRI abnormalities suggestive of my- elopathy [5]. A pseudo Guillain-Barre presentation similar to the one in case 2 [2] was documented in one anecdotal case report of NO2 neurotox- icity [6]. This was a patient who initially experienced flaccid bilateral foot drop and sensory deficits in a stocking distribution. MRI of the lumbar spine was normal. The cerebrospinal fluid showeda protein concentration of 72 mg/dl and no pleocytosis. Within 24-48 h paresthesiae ascended to the nipple line, and he experienced clumsiness of fine finger movements. MRI of the cervical spine was then performed, and this showed focal nonenhancing posterior T2 lesion at C2-C6. He experienced significant im- provement after a course of vitamin B12 injections [6].

    The normal levels of serum vitamin B12 documented in cases 1 and 3 [2], and in other anecdotal reports [3,4] exemplify so-called “functional” Cobalamin deficiency, the latter characterised by coexistence of normal serum cobalamin levels and accumulation of substrates of the reactions catalysed by cobalamin, namely, MMA and homocysteine [2-4]. In all subtypes of cobalamin deficiency the toxicity of NO2 is mediated by the inactivation of vitamin B12 as a result of oxidation by NO2. This leads to a reduction in the conversion of homocysteine to methionine [3], the latter a precursor of S-adenosylmethionine, which is necessary for mye- lin production in the central and in the Peripheral nervous system [7,8]. Patients at risk of NO2-related myelopathy are, reportedly, also those in whom NO2 is administered as a general anaesthetic in the presence of Predisposing factors for cobalamin deficiency, such as old age, inflam- matory bowel disease, and vegetarianism [1]. Previous Bariatric surgery should also be included in that list, given the fact that it, too, is a risk fac-

    tor for cobalamin deficiency [9].

    When NO2 is administered as a general anaesthetic NO2-related neurotoxicity may also occur in the presence of 5,10- methlenetetrahydrofolate reductase (MTHFR) deficiency [10]. This oc- curred in a 3 month old child who had good physical status prior to ad- ministration of NO2 as a general anaesthetic, the latter for the purpose of enabling resection of a mass in the left leg. On the 25th postoperative day he experienced seizures, and was found to be hypotonic and arreflexive. The plasma homocysteine level was elevated at 0.6 mg/decilitre (normal value b 0.01) an the vitamin B12 level was normal. Genomic DNA- sequence analysis revealed that MTHFR deficiency was caused by a novel MTHFR mutation which changes the conserved methionine at po- sition 581 of the enzyme to isoleucine. The consequence was that NO2– related inactivation of methionine synthetase was superimposed on MTHFR deficiency, the combined derangements giving rise to an exces- sive accumulation of homocysteine [10], which, in turn, has well docu- mented neurotoxic potential in its own right [11,12].

    Misgivings that anesthesiologists have about using NO2 as an anaes- thetic agent have been articulated in a recent review which concluded that it was incumbent upon anesthesiologists to evaluate their patients for risk factors that might predispose them to NO2-related myelopathy, and to avoid NO2 if such risk factors are present [13].

    Oscar M.P. Jolobe

    Manchester Medical Society, Simon Building, Brunswick Street, Manchester

    M13 9PL, United Kingdom E-mail address: [email protected].

    29 May 2018

    https://doi.org/10.1016/j.ajem.2018.05.076

    References

    Egan W, Steinberg E, Rose J. Vitamin B12 deficiency-induced neuropathy secondary to prolonged recreational use of nitrous oxide. American Journal of Emergency Med- icine May 2018. https://doi.org/10.1016/j.ajem.2018.05.029.

  6. Thompson AG, Leite MI, Lunn MP, Bennett DL. Whippits, nitrous oxide and the dan- gers of legal highs. Pract Neurol 2015;15:207-9.
  7. Hirjiova J, Joutsa J, Wahlsten P, Korpela J. Recurrent paraparesis and death of a pa-

    tient with “whippet” abuse. Oxford Medical Case Reports 2016;3:41-3.

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