Monday, February 26, 2018

Airway and Sedation, “Answers” by emlyceum

Question #1: Do you reach for video laryngoscopy or direct laryngoscopy first for intubations?

Tracheal intubation is a fundamental skill for EM providers to master. Historically, direct laryngoscopy (DL) has been the modality of choice for endotracheal intubation, with a proven high success rate in the ED. However, video laryngoscopy (VL) devices have become increasingly popular and present. These devices havenumber of potential advantages including improved laryngeal exposure and visualization as well as allowing more experienced practitioners to observe the procedure during training. (Levitan, 2011). As VL devices are gaining wider use, some have made calls for their establishment as standard care. It is important to note that not all VL devices are equivalent. Some devices use standard geometry blades (which allow both direct and video laryngoscopy) while others have hyperangulated geometry blades which do not allow for direct laryngoscopy. Many devices interchangeably accept standard and hyperangulated blades.A full description of all of these devices is beyond the scope of this post.
Much of the early literature comparing VL to DL comes from observational studies. One prospective study at a level 1 trauma center enrolled all adult patients intubated in the ED over an 18-month span (Platts-Mills, 2009). Data collected included intubation indication, device used, and resident post-graduation year. The authors found no statistically significant difference in the primary outcome of first attempt success, but noted that VL intubation required significantly more time to complete (42 vs 30s). Another prospective study evaluating all ED intubations over a 2-year period found a statistically significant increase in first-attempt success for VL (78% vs 68%, adjusted OR 2.2), a result found more pronounced in a patient subgroup with pre-defined difficult airway predictors (OR 3.07) (Mosier, 2011).
Randomized controlled trial data is sparse. In 2013, Yeatts et al published an RCT among trauma patients at a single level 1 trauma center (Yeatts 2013). Patients requiring emergent intubation were randomized to DL or VL performed by an emergency medicine or anesthesia resident with at least one year of intubation experience. The authors found no significant difference in mortality, the primary outcome, but did observe an increased median duration of intubation in VL vs DL (56s vs 40s) with an associated increased incidence of hypoxia (50% vs 24%). The study had a number of inherent flaws including the fact that providers could selectively exclude patients at their discretion. Larger systematic reviews and meta-analyses have been limited by significant heterogeneity, and provided similarly murky results but suggest that VL may be the superior modality. One meta-analysis including only studies examining ICU intubations found that VL reduced the risk of difficult intubation, Cormack-Lehane 3 and 4 grade views, and esophageal intubations, and increased the likelihood of first-attempt success (De Jong, 2014).
Another meta-analysis included 17 trials and 1,998 patients to compare outcomes from VL vs DL (Griesdale, 2012). The authors found no significant difference in successful first-attempt intubation or time to intubation based on the use of Glidescope ® and DL. Interestingly, they did note that successful first-attempt intubation and time to intubation were improved using Glidescope ® in two studies specifically examining “non-expert” intubators, suggesting a valuable role for VL in less-experienced hands.
Further examining the potential increased efficacy of VL for less-experienced intubators, a prospective randomized control trial examined 40 fresh PGY-1s across varying disciplines (Ambrosio, 2014). All of the soon-to-be residents had not yet begun clinical duties and had individually performed no more than 5 live intubations in their training. After receiving training in both DL and VL, the participants were divided into groups and observed while intubating a difficult-airway manikin. The group using DL had significantly less successful intubations within 2 minutes (47% vs 100%) and increased overall mean time to intubation (69 vs 23s).
The skills required to use standard geometry blades with video are close to traditional direct laryngoscopy, whereas the more hyperangulated the blade, the easier is glottic visualization but the more challenging is tube delivery. Using hyperangulated blades is a somewhat different procedure, requiring a different skillset, than direct laryngoscopy or video laryngoscopy with a standard geometry blade. Many other forms of VL exist, and ultimately experience with one device does not guarantee to translate to another. (Sakles & Brown, 2012). For training purposes, a number of experts including Richard Levitan and Reuben Strayer support the use of standard geometry blades with video as they offer the benefits of video laryngoscopy while allowing training in direct laryngoscopy.
Bottom Line: Evidence suggests VL provides superior visualization in comparison to DL but improved outcomes have yet to be shown. The vast majority of airway experts support extensive training with both modalities.
Question #2: Do you use cricoid pressure during induction and paralysis?
Cricoid pressure (CP) refers to the application of firm pressure to the cricoid ring after positioning the patient’s neck in the fully extended position. It’s important to note that CP is different from external laryngeal manipulation, which acts to improve the laryngeal view during direct laryngoscopy. The pressure required to occlude the esophageal lumen is 30-44 Newtons (Wraight 1993). The goal of CP is to occlude the esophageal lumen in order to prevent regurgitation and gastric insufflation during intubation and particularly during bag mask ventilation. This maneuver is widely embraced in the anesthesiology world as standard care during induction. However, practice of routine CP has been questioned for over a decade and application in the Emergency Department setting is variable.
Although CP may have been used as far back as the 1770’s, the first published descriptions are from Sellick in 1961. Sellick applied CP during induction of anesthesia in 26 patients that were considered to be high risk for aspiration. In 3 of the patients, regurgitation occurred immediately after CP was removed (Sellick 1961). Sellick published a second article recounting a single case of a patient with CP applied who had the esophagus distended with saline solution via an esophageal tube. This patient did not regurgitate after distension (Sellick 1962). This report also contained Sellick’s personal account of 100 high-risk cases without regurgitation when CP was applied but six patients who regurgitated after CP was removed. These studies are severely flawed as there were no comparison groups, the technique’s proponent (Sellick) was the sole studied physician and it is unclear which patients had BMV prior to induction and intubation. Despite these shortcomings, CP was widely adopted after publication of Sellick’s studies.
Over the intervening decades, a significant amount of literature has emerged challenging the routine use of CP. There are four major issues with CP that should be addressed:
1) CP doesn’t occlude the esophagus as purported.
2) CP reduces airway patency.
3) CP obstructs the view of the airway.
4) CP has never been shown to prevent aspiration.
Let’s tackle each of these issues.
1) CP does not occlude the esophagus. This is the physiologic underpinning for the application of CP but was only demonstrated by Sellick in a select few cases. Subsequent literature has called this concept into question. MRI of healthy volunteers was performed with CP applied in order to better visualize the relationships of the cricoid cartilage and the esophagus (Smith 2003Boet 2012). Both of these studies demonstrated that in many people the esophagus naturally lies lateral to the cricoid cartilage. Additionally, even those in whom the esophagus is not lateral, CP does not occlude the esophagus but rather displaces it laterally. Rice and colleagues, however, concluded that the location and movement of the esophagus was irrelevant to the efficacy of CP. They argue that the hypopharynx and cricoid move as a unit and that the esophagus becomes compressed against the longus colli muscle. Even if this is true, compression against a muscle is more likely to be overcome by the increased pressure that occurs during vomiting. In their MRI study of 24 healthy volunteers, they state that 35% of patients had obliteration of the esophageal lumen when CP was applied (Rice 2009). However, they show no data to support his claim.
Finally, ultrasound has been used in children to demonstrate that the anatomical effect of CP makes it’s utility questionable. Ultrasound was applied to 55 pediatric patients with and without application of CP. At baseline, the esophagus was lateral to the airway in 61% of patients and upon application of CP, all patients had displacement of the esophagus (Tsung 2012).
It is also important to note that the application of CP reduces esophageal sphincter tone allowing for gastric insufflation. This helps to explain why Sellick witnessed regurgitation after removal of CP. Overall, CP does not appear to cause compression of the esophagus but rather lateral displacement.
2) CP reduces airway patency and 3) CP obstructs the view of the airway. Anesthesia studies in the operating room have demonstrated the effect of CP on airway patency. Allman took 50 patients mechanically ventilated in the OR and measured expired tidal volume and peak inspiratory pressure (PIP) before and after application of CP. He found that after CP, both measures were significantly reduced reflecting increased airway obstruction (Allman 1995). Palmer and Ball went a step further. They endoscopically assessed 30 anesthetized patients for airway patency with and without variable forces applied to the cricoid cartilage. They found that as force increased, there was greater cricoid deformation, increasing likelihood of vocal cord closure and increasing likelihood of difficult ventilation (MacG Palmer 1999). At the recommended 44 N of pressure, 86% of men and 100% of women experienced difficulty with ventilation. Additionally, at this force, 26.6% of men and 78.5% of women had 100% cricoid deformation. CP additionally worsens laryngoscopic view and compromises ideal intubating conditions (Haslam 2005). In a study of 33 OR patients, full vocal cord visualization was reduced from 91% to 67% with application of CP (Smith 2002) and CP compressed 27% of patients vocal cords and impeded tracheal tube placement in 15% (Smith 2002). Finally, CP has also been shown to result in worse glottic view during video laryngoscopy (Oh 2013). Overall, CP interferes with “all aspects of airway management.” (Priebe 2012).
4) CP has never been shown to prevent aspiration. There are numerous cases reported in the literature of patients with CP in place who have aspirated. Perhaps the best literature on this comes from a retrospective, observational study in 2009 out of Africa. This study looked at 5000 patients undergoing C-sections. 61% of these patients had CP applied and 24 vomited during induction. Overall, there were 11 deaths attributed to aspiration with 10 of these coming from the CP group (Fenton 2009).
CP doesn’t do what it’s supposed to. It doesn’t occlude the esophagus to prevent aspiration but rather simply displaces the esophagus laterally. Application makes ventilation more difficult because it collapses the airway and the view of the cords is compromised. Intubating conditions are worsened by CP. Some have suggested application of CP initially and if the laryngoscopic view is poor or BMV is difficult, the CP can be removed. However, lower esophageal sphincter relaxation and gastric insuffulation during CP application increases the risk for regurgitation after removal of CP as witnessed by Sellick.
Bottom Line: In spite of over 50 years of application, there is minimal evidence to either the pathophysiologic basis or clinical utility of CP.. CP also appears to decrease the likelihood for 1st pass success. CP should not be performed routinely. External laryngeal manipulation, either by the operator or an assistant, may improve an otherwise suboptimal laryngeal view.
Question #3: How long do you keep patients NPO prior to procedural sedation?
Procedural sedation (PS) describes the use of a sedative or dissociative anesthetic to elicit a depressed level of consciousness that allows an unpleasant medical procedure to be performed with minimal patient reaction or memory. Unlike general anesthesia, PS agents and doses are chosen to maintain cardiorespiratory function and avoid endotracheal tube placement.or other advanced airway adjuncts. (Tintanelli, 2011). As the airway is not definitively protected, aspiration, or the inhalation of gastric contents into the respiratory tract, during the procedure is a potential adverse outcome with significant associated morbidity. Guidance on how to reduce aspiration risk has centered on pre-procedural fasting, though the optimal prescribed fasting times differs. Many Emergency Physicians question whether pre-procedural fasting actually provides any increased protection (Strayer, 2014).
Additionally, there are significant harms to procedural delay for fasting. Fractures and dislocations put increased risk on the neurovascular supply. Procedures may become more difficult to perform. Finally, prolonged fasting times increase ED length of stay. While fasting’s potential harms have been less studied than its efficacy, they should be kept in mind as the literature is examined (Godwin, 2014).
Much of the historical evidence regarding inter-procedural aspiration has come from the Anesthesia and Surgery literature (Green, 2002). One of the earliest reported potential cases of gastric contents as a complication of general aspiration comes from 1848, in a case in which a 15-year-old girl died 2 minutes after beginning to inhale chloroform while preparing for the removal of a toenail. This patient was sitting upright in an operating chair and was not observed vomiting, but as the autopsy revealed a food-distended stomach it was surmised that aspiration was a potential cause of death. (Maltby, 1990). Later, animal experiments involving the direct introduction of gastric aspirate into tracheas (Mendelson, 1946) suggested the danger of aspiration, and the concept of pre-procedural fasting gained acceptance.
Recent Anesthesia guidelines for preoperative fasting recommend a minimum fasting period of 2 hours following ingestion of clear liquids, 4 hours following breast milk, and 6 hours following infant formula or a light meal. (Apfelbaum, 2011). This recommendation is noted to apply to healthy patients undergoing elective procedures. It is important to note that adhering to the recommended fasting times does not guarantee the presence of an empty stomach. Underlying co-morbid conditions, pain and a number of other factors are associated with gastric emptying. As procedural sedation has become a common occurrence in the Emergency Department (ED), the question has arisen of how to translate anesthesia guidelines into Emergency Medicine practice.
Recent Emergency Medicine recommendations prescribed that maximal sedation depth be based on risk stratification of the type of liquid or food intake, the urgency of the procedure, and risk of aspiration. (Green, 2007). These authors acknowledged that their consensus recommendations stemmed in part from the general anesthesia literature. General anesthesia practice involves scenarios at higher risk for aspiration than ED PS but aspiration incidence remains low. Previously, Green et al suggested several reasons why ED PS is potentially safer than general anesthesia, including 1) not routinely placing an endotracheal tube, 2) maintenance of protective airway reflexes, 3) not using pro-emetic inhalation anesthetics. In their 2007 recommendations they suggest responsible consideration of risks/benefits of aspiration risk prior to pre-procedural fasting, though they ultimately note a paucity of literature suggesting more than a theoretical aspiration risk in ED PS.
Multiple studies in the Emergency Medicine literature have not supported the relationship between fasting state and procedural sedation-related aspiration. Agraway et al conducted a prospective case series enrolling all consecutive patients in a children’s hospital ED who underwent PS and recorded pre-procedural fasting state and adverse events (Agraway, 2003). Of the 905 patients with available data, 509 (56%) did not meet established fasting guidelines. 35 (6.9%) of these 509 patients had minor adverse effects as compared to 32 (8.1%) of the 396 patients who did meet fasting guidelines. No significant difference was found in median fasting duration between the two patient groups.
Three trials involving pediatric patients (Roback, 2004Treston, 2004Babi, 2005) undergoing procedural sedation with varying sedation agents examined fasting time & adverse effects. No statistically significant relationship was found between incidence of emesis or adverse effects and fasting time (Roback, Treston) or whether fasting guidelines were met (Babi). No episodes of aspiration were reported in any of the three studies.
Bell et al conducted a prospective observational series of 400 adult and pediatric patients undergoing procedural sedation with propofol and measured the percentage of patients whom met ASA fasting guidelines and looked at adverse outcomes (Bell, 2007). They found that 70.5% of those enrolled did not meet ASA fasting guidelines. There was no identified statistically significant difference between fasting status and adverse events (emesis, respiratory interventions). Additionally, there were no aspiration events in either group.
In 2014 an ACEP Clinical Policy committee reviewed these studies and ultimately questioned the utility of pre-procedural sedation fasting (Godwin, 2014). In a Level B evidence-based recommendation, they advised against delaying procedural sedation in the ED based on fasting time, as “preprocedural fasting for any duration has not demonstrated a reduction in the risk of emesis or aspiration when administering procedural sedation and analgesia.” The conclusions of the Clinical Policy recognized a dearth of study on the potential harms of delayed procedural sedation including pediatric hypoglycemia and worsening pathology.
Bottom Line: There is no evidence supporting delay of procedural sedation and analgesia based on fasting state in order to reduce the risk of vomiting and aspiration.The potential risk of aspiration involves multiple patient factors and should be considered on a case-by-case basis, and weighed against the harms associated withdelaying the sedation and procedure.
Question #4: When using ketamine for procedural sedation do you pretreat with benzodiazepines or anticholinergics?
Ketamine is a dissociative sedative-analgesic commonly used for painful or emotionally stressful procedures. When used at its dissociative dose of 1-2mg/kg IV (or 3-4 mg/kg IM), it is thought to exert its effects by effectively disconnecting the limbic and thalamocortical systems, leaving patients unaware of and unresponsive to external stimuli. Unlike other procedural sedation medications, respiratory status is maintained, making it a critical medication in the pediatric and adult Emergency Department. (Green, 2011)
As with any medication, Ketamine is not without its potential complications. Increased salivation and post-procedure emergence reactions are two concerning potential adverse outcomes, and anticholinergics and benzodiazepines, respectively, have been used as pre-treatment to blunt or prevent these effects (Haas, 1992Strayer, 2008). Though the pharmacologic reasoning is sound for each medication and has been shown to work as treatment once patients become symptomatic, their common utility as pre-treatment is questionable.
Atropine and glycopyrrolate have commonly been administered to prevent hypersalivation and resulting adverse airway events, though their use by physicians has proven inconsistent. One prospective observational study (Brown, 2008) in a pediatric ER tracked the frequency of atropine pre-treatment and associated hypersalivation in 1,080 ketamine sedations over a 3-year period. Most (87%) of the patients in the study were not pretreated with an anticholinergic. Of the patients who received no pre-treatment, 92% were described as having no excess salivation. The authors concluded that atropine was not routinely required for prophylaxis.
A secondary analysis (Green, 2010) seemed to confirm these findings. Examining 8,282 ED ketamine sedations in pediatric patients from 32 previous series, this study found no statistically significant reduction in the number of adverse respiratory or airway events based on whether patients received atropine versus no anticholinergic drug. Interestingly, patients who received glycopyrrolate were actually found to have a significantly increased number of airway and respiratory events as defined by authors of the original studies. Taking these and other studies into account, a recent ACEP Clinical Policy on ketamine did not recommend the routine use of anticholinergics as pretreatment in adults or children. (Green, 2011)
Benzodiazepine pretreatment for the prevention of emergence reactions has been commonly recommended but erratically applied. A meta-analysis of 32 ED studies involving ketamine in pediatric patients (Green, 2009) was conducted to determine which clinical variables prevent recovery agitation. The authors found that 7.6% of patients experienced an emergency reaction though only 1.4% were judged to have “clinically significant” agitation. No apparent benefit or harm from pre-administrated benzodiazepines was found.
It has been suggested that emergence reactions are more frequent in adults than in children, and thus pre-treatment with benzodiazipines would prove more useful in this population. A double-blind randomized control trial pretreated 182 adult subjects receiving varying doses of ketamine with 0.03mg/kg IV midazoloam vs placebo (Sener, 2011).
Though the authors did not specify the intensity of the reaction that was experienced, they did find a significant decrease in recovery agitation with midazolam. An alternative to benzodiazepine prophylaxis is either pre-emergency or PRN benzodiazepine use (Strayer 2008). The current ACEP Clinical Policy recommends against the routine use of benzodiazepines in children but leaves the recommendation ambiguous for adults.
Bottom Line: Anticholinergics are not routinely needed for premedication in ketamine sedations. Benzodiazepines can be administered to adults but are not recommended routinely for children. Both medications should be available to use as PRN treatment.
Originally Posted on 

References
Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961; 404-6.
Sellick BA. The prevention of regurgitation during induction of anaesthesia. First Eur Congress Anaesthesiol. 1962;89:1-4.
Smith et al. Cricoid pressure displaces the esophagus: an observational study using magnetic resonance imaging. Anes 2003; 99(1): 60-4.
Boet S et al. Cricoid pressure provides incomplete esopogeal occlusion associated with lateral deviation: a MRI study. JEM 2012; 42(5): 606-11.
Rice et al. Cricoid pressure results in compression of the postcricoid hypopharynx: the esophageal position is irrelevant Anesth Analg 2009 109(5) 1546-52.
Tsung WJ et al. Dynamic anatomic relationship of the esophagus and trachea on sonography: Implications for endotracheal tube confirmation in children. J Ultrasound Med 2012; 31: 1365-70.
Allman KG. The effect of cricoid pressure application on airway patency. J Clin Anes 1995; 7: 197-9.
Palmer JH, Ball DR. The effect of cricoid pressure on the cricoid cartilage and vocal cords: an endoscopic study in anaesthetized patients. Anaesthesia 2000;55:253–8
Haslam N, Parker L, Duggan JE. Effect of cricoid pressure on the view at laryngoscopy. Anaesthesia 2005;60:41e7.
Smith CE, Boyer D. Cricoid pressure decreases ease of tracheal intubation using fiberoptic laryngoscopy. Can J Anesth 2002; 49(6): 614-9.
Oh J et al. Videographic analysis of glottic view with increasing cricoid pressure. Ann of EM 2013; 61: 407-13.
Priebe HJ. Use of cricoid pressure during rapid sequence induction: Facts and fiction. Tends in Anes Crit Care 2012: 123-7.
Fenton PM, Renolds F. Life-saving or ineffective? An observational study of the use of cricoid pressure and maternal outcome in an African setting. Int J Obstet Anes 2009; 18: 106-110
Agraway D., Manzi S.F., Gupta R, Krauss B. Preprocedural Fasting State and Adverse Events in Children Undergoing Procedural Sedation and Analgesia in a Pediatric Emergency Department. Annals of Emergency Medicine. 2003; 42 (5), 636-646
Apfelbaum, J.I., Caplan, R.A., Connis, R.T. et al. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. An updated report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Anesthesiology. 2011; 114: 495–511
Babl FE, Puspitadewi A, Barnett P, et al. Preprocedural fasting state and adverse events in children receiving nitrous oxide for procedural sedation and analgesia. Pediatr Emerg Care. 2005;21:736-743.
Bell A, Treston G, McNabb C, et al. Profiling adverse respiratory events and vomiting when using propofol for emergency department procedural sedation. Emerg Med Australas. 2007;19:405-410.
Godwin SA, Burton JH, Gerardo CJ, et al: Clinical policy: procedural sedation and analgesia in the emergency department. Ann Emerg Med 2014 Feb; 63(2): 247-58
Green SM, Krauss Baruch. Pulmonary aspiration risk during emergency department procedural sedation–an examination of the role of fasting and sedation depth. Acad Emerg Med. 2002 Jan;9(1):35–42
Green SM, Roback MG, Miner JR, et al: Fasting and emergency department procedural sedation and analgesia: A consensus-based clinical practice advisory. Ann Emerg Med 49: 454, 2007
Maltby JR. Early reports of pulmonary aspiration during general anesthesia [letter]. Anesthesiology. 1990; 73:792–3.
Mendelson CL. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol. 1946; 52:191 – 204.
Miner JR. Chapter 41. Procedural Sedation and Analgesia. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011
Roback MG, Bajaj L, Wathen JE, et al. Preprocedural fasting and adverse events in procedural sedation and analgesia in a pediatric emergency department: are they related? Ann Emerg Med. 2004;44:454-459.
Strayer, Reuben. “The Harms of Fasting.” EM Updates. 16 May 2014. <http://emupdates.com/2014/05/16/the-harms-of-fasting/&gt;
Treston G. Prolonged pre-procedure fasting time is unnecessary when using titrated intravenous ketamine for paediatric procedural sedation. Emerg Med Australas. 2004;16:145-150.
Brown L, Christian-Kopp S, Sherwin TS, et al. Adjunctive atropine is unnecessary during ketamine sedation in children. Acad Emerg Med. 2008;15:314-318.
Green SM, Roback MG, Krauss B, et al. Predictors of emesis and recovery agitation with emergency department ketamine sedation: an individual-patient data meta-analysis of 8,282 children. Ann Emerg Med. 2009;54:171-180
Green SM, Roback MG, Krauss B. Anticholinergics and ketamine sedation in children: a secondary analysis of atropine versus glycopyrrolate. Acad Emerg Med. 2010;17:157-162.
Green SM, Roback MG, Kennedy RM, Krauss B (2011) Clinical practice guideline for emergency department ketamine dissociative sedation: 2011 update. Ann Emerg Med 57: 449–461
Haas DA, Harper DG. Ketamine: a review of its pharmacologic pro- perties and use in ambulatory anesthesia. Anesth Prog 1992;39:61-8.
Sener S, Eken C, Schultz CH, et al. Ketamine with and without midazolam for emergency department sedation in adults: a randomized controlled trial. Ann Emerg Med. 2011;57:109-114.
Strayer RJ, Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. AM J Emerg Med. 2008;26(9):985–1028

Monday, February 19, 2018

New Onset Seizures in ED

Seizure is an episode caused by inappropriate electrical discharge from neurone due to imbalance between glutaminergic (excitatory) and γ-aminobutyric acid (inhibitory) activity whereas Epilepsy implies a fixed, more excitatory condition of the brain with a lower seizure threshold. The term epileptic does not refer to an individual a known or reversible cause of seizures.

Types of seizures:

Generalised Seizures: Generally caused by simultaneous activation of the entire cerebral cortex, or originating from a focus and then leading to secondary generalisation. 

Generalized tonic-clonic seizures (grand mal) are the most dramatic type of the generalised seizures where the patient suddenly becomes rigid (tonic phase), trunk and extremities are extended, and the patient falls to the ground. This is followed by rhythmic (clonic) jerking of the trunk and extremities. Patients may appear cyanotic when seizing due to apnea. There is often h/o bowel or bladder incontinence. Following the attack, patient remain in an unconscious state for few minutes. Consciousness returns gradually, and postictal confusion, myal- gias, and fatigue may persist for several hours or more.



Absence seizures (petit man): Classic absence seizures occur in school-age children and are often attributed by parents or teachers to daydreaming or inattention. Brief, generally lasting only a few seconds. Patients suddenly develop altered consciousness but no change in postural tone. They appear confused, detached, or withdrawn, and current activity ceases. They may stare or have twitching of the eyelids. They may not respond to voice or to other stimulation and may exhibit involuntary movements or lose continence. The attack ceases abruptly, and the patients typically resume previous activity without post-ictal symptoms. Similar attacks in adults are more likely to be minor complex partial seizures and should not be termed absence. 


Focal Seizures are more likely to be secondary to a localized structural lesion of the brain. The electrical discharges begin in a localized region of the cerebral cortex and then get secondarily generalised. In simple partial focal seizures, the seizure remains localized, and consciousness and mentation are not affected. In contrast, in complex partial seizures consciousness is affected. Focal seizures are regarded as focal seizures from treatment standpoint. 


Consider developing common protocols between ED and Neurology to expedite management in this subset of patients. 




Key Questions:
  • Differentiate between seizure or syncope (Get collateral history if possible) 
  • Preceding aura? Sudden v/s Gradual onset ? 
  • Focal, Generalised, Focal with secondary generalisation
  • Duration, Post ictal confusion, Aura, Any h/o Trauma 
  • Past h/o fits (Ask frequency, last follow up, medications, compliance, changes in dose or stressors - sleep deprivation, strenuous activity; infection; electrolyte disturbances; and alcohol or substance use or withdrawal)
  • Co-morbidities 
  • Medications, Recreational Drug use

Examination:
  • Blood Glucose
  • Tongue Bite
  • Look for other injuries (Head/Spine Injury, Shoulder dislocation)
  • Focused Neurological Examination - transient focal deficit following a focal seizure may be seen (Todd’s paralysis)

Investigations
  • Known seizure disorder presenting with a single unprovoked seizure -> blood glucose level and AED levels
  • New onset seizures -> Blood Glucose, Metabolic profile, Ca, Mg, pregnancy test, and urine tox screen. Seizure driven lactate abnormalities usually clear within 30 minutes 
  • LP - in cases of fever, immunocompromised, suspected SAH 
  • Obtain imaging (Non-Contrast CT Head) in cases of new onset seizures OR a change in seizure pattern, persistent deficits, fever, recurrent episodes. Because many pathologies may not be evident on initial CT, a follow-up MRI with EEG is frequently done as outpatients 
  • Do radiographs or imaging of Spine/Shoulder or other relevant injuries as indicated 

Treatment
  • Read more on Status Epilepticus and active seizure management here
  • Give Loading dose if already on AEDs and there is h/o being non-compliant
  • Adjustment of medication should always be made after discussing with a Neurologist
  • Outpatient treatment with AEDs in new onset fits should always be started in liaison with Neurologist 
  • Arrange timely follow up and Safety Net (Instruct discharged patients not to to take precautions to minimize the risks for injury from further seizures. Swim, drive, work with hazardous tools or machines, and working at heights)

Patients with provoked (secondary) seizures due to an identifiable underlying condition often require admission and should generally be treated to minimize seizure recurrence


Take Home:

  • Differentiate between seizure and other similar pathologies (Migraine, Pseudofits, Syncope)
  • Arranging follow up and safety netting is crucial
  • Change in AEDs to starting new AEDs should always be done in liaison with Neurologist 

Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic

  


Monday, February 12, 2018

HypoAdrenal Shock

HypoAdrenal Shock is life-threatening exacerbation of adrenal insufficiency (AI) when an increased hormone demand fails to increase the supply. AI is specifically deficiency of adrenal gland hormone production in the cortex

Physiology
The adrenal gland is made up of the cortex and medulla producing steroid hormones and catecholamines respectively. The adrenal cortex produces three categories of steroids: 



  • Glucocorticoids (cortisol) from zone fasciculate (Under Hypothalamus/Pitiutary control)
  • Mineralocorticoids (aldosterone) from zona glomerulosa (Under control of RAAS)
  • Gonadocorticoids (sex hormones) from zone reticular (Under Hypothalamus/Pitiutary control)
  • Catecholamines (adrenaline, noradrenaline and dopamine) from adrenal medulla 
Functions of steroid hormones:
GlucocorticoidsCortisol secretion is under control of hypothalmaic-pitiutary axis. Daily cortisol requirement is about 20 mg of hydrocortisone.  Cortisol facilitates (Permissive action of glucocorticoids) the stress response by affecting the heart, vascular bed, water excretion, electrolyte balance, potentiation of catecholamine action, and control of water distribution. It affects metabolism by stimulating glycogenolysis and glyconeogenesis. It is also involved in immunologic/inflammatory responses. 


Mineralocorticoids : Aldosterone secretion is controlled primarily by the renin-angio- tensin system (unlike cortisol) and serum potassium concentration. Aldosterone maintains sodium and potassium plasma concentrations. It regulates extracellular volume and controls sodium and water balance.

Gonadocorticoids: Promote the development of sex characteristics such as axillary and pubic hair and libido.





There are two types of Adrenal deficiency syndromes:

Primary AI (Addison’s disease) i.e. intrinsic adrenal gland dysfunction that results in decreased Glucocorticoids (cortisol), Mineralocorticoids (aldosterone), and sex hormones production. Fortunately, primary AI is a rare disease. Approximately 90% of the gland must be destroyed to manifest symptoms. Autoimmune disorders and infections such as tuberculosis are responsible for most cases of primary adrenal insufficiency. Infiltrative diseases such as amyloidosis, hemosiderosis, Thrombosis and/or haemorrhage (anticoagulation therapy, sepsis, DIC, meningococcemia i.e. Waterhouse-Friderichsen syndrome, APLA) and bilateral metastasis from cancer may also cause primary AI.  


Secondary AI occurs as a result of depressed adrenocorticotropic hormone (ACTH) secretion leading to diminished cortisol production. Aldosterone levels remain normal because of preserved stimulation by both the renin-angiotensin axis and potassium.  Secondary AI results in cortisol deficiency only. Adrenal sex hormone production is also preserved. Intracranial disorders such as brain tumor, pituitary disease, postpartum pituitary necrosis, or major head trauma may affect the hypothalamic-pituitary function may lead to secondary AI. However, the most common cause of secondary adrenal insufficiency is long-term therapy with pharmacologic doses of glucocorticoids. 


Clinical Features 
Primary adrenal insufficiency presents with symptoms of diminished cortisol, aldosterone, and gonadocorticoids, and elevated ACTH, which causes skin hyper pigmentation. Aldosterone deficiency symptoms include dehydration, syncope, salt craving, and hypotension. Gonadocorticoid deficiency symptoms are decreased axillary and pubic hair and decreased libido. Typical Primary AI presents with HypoNa, HyperK, Hypoglycemia, Hypotension.

Secondary adrenal insufficiency presents with symptoms of diminished cortisol (weight loss, lethargy, weakness, confusion, anorexia, GI distress, abdominal pain). Typically secondary AI presents as Hypoglycemia, Hypo/HyperNa, Hypokalemia, Hypotension.

In both primary and secondary AI, cortisol deficiency are seen

Initial set of bloods should include CBC, Basic metabolic panel, renal function and blood cultures. Serum Cortisol sample can also be drawn before administering steroids.  

Serum cortisol >18 mcg/dL generally rules out adrenal insufficiency. 
Serum adrenocorticotropic hormone (ACTH) level measurement also helps differentiate between primary and secondary adrenal insufficiency. A high ACTH level is seen in primary adrenal insufficiency, but ACTH is low in secondary adrenal insufficiency.


Treatment 
  • ABCs
  • IV Fluid Resuscitation (May need dextrose if hypoglycaemic)
  • IV Steroids once circulation is filled (Hydrocortisone 100mg IV)
  • Vasopressors
  • Manage Electrolytes (HyperK, Hypo/HyperNa)
  • Find and treat the underlying ethology
For primary AI, abdominal CT scan may be performed to evaluate the adrenal glands and CXR to assess for lower respiratory tract infections. For secondary adrenal insufficiency, a head CT or MRI, as well as blood tests of pituitary hormones, may be required for further evaluation. 


Take Home:
  • Consider adrenal crisis in situations of unexplained hypotension, especially in patients with a history of glucocorticoid therapy.
  • For a minor illness or injury, triple the daily glucocorticoid dose for 24 to 48 hours until symptoms improve.

Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic