Tag Archives: critical care

Australasian ED Airway Registry

Managing the emergency airway is one of the most important and risky things we do. We have a responsibility to record, monitor, report and improve our performance.
In the US, the National Emergency Airway Registry has been running for over a decade and has significantly contributed to our airway knowledge base.
In the UK, the NAP4 audit provided fascinating and scary insight into complications of emergency airway management.
Pre-hospital registries have been developed, like Minh Le Cong’s Flying Doctor Emergency Airway Registry; and many of us are now contributing to the Airway Management Study in Physician Manned Helicopter Emergency Medical Services (AIRPORT) study.
Now there is an opportunity for Australasian emergency departments to contribute to a national audit.
Dr Toby Fogg FACEM, emergency physician at Royal North Shore Hospital in Sydney, who began the registry, explained in a recent Life in The Fast Lane response:


I have been running an airway registry in the ED at The Royal North Shore Hospital in Sydney for the last 2 years.

I presented the first 18 months of data at the ASM in Sydney last year and I must admit, they showed room for improvement!.

One of the many things we have subsequently done is introduced a Pre Intubation Checklist which I have published, along with our preliminary findings, at www.airwayregistry.org.au.

I am happy for people to download the file and use it as is, or with appropriate modifications.

Furthermore I would love to hear from anyone keen to undertake an Airway Registry in their own ED — a PDF of the data collection form we use is also on the website.

As the authors of the NAP4 study conclude, it is essential we all audit our practice of this potentially high risk procedure.

Dr Toby Fogg uses his C-MAC video laryngoscope to demonstrate the audit form


Background: Successful airway management is one of the cornerstones of care for critically ill or injured patients in the Emergency Department (ED). The risks of intubation are known to be higher in this environment than in the operating theatre (OT) yet there are no published data on airway management in an Australian ED.

Objectives: To describe the practice of intubation in the ED of a tertiary hospital in Australia, with particular emphasis on the number of attempts, adjuncts used, the seniority of staff involved and the rate of complications.

Methods: A prospective, observational study.

Results: Over the 18-month study period, 295 episodes of intubation occurred with a total of 345 attempts. Consultant supervision occurred in 69.8% of cases, registrars made the first attempt at intubation in 57.5% and SRMOs in 31.0% of the patients. 83.7% of the patients were intubated at the first pass with a further 13.0% intubated one the second attempt. This leaves 10 patients (3.4%) that required ≥3 attempts, 4 (1.4%) ≥4 attempts and 1 (0.4%) required a 5th attempt. Difficult laryngoscopy, as defined by Cormack and Lehane grade III or IV, occurred in 24% of the first attempts. Bougies were used in 36% of attempts, whilst a stylet in 35%. Video laryngoscopy was used in 47.5% of attempts. Complications occurred in 28%.

Discussion: The success rate within two attempts is comparable to the anaesthetic literature, and although high, the rate of complications is comparable to data from EDs overseas. The rate of difficult laryngoscopy, however, is surprisingly high. The study has prompted a significant review of airway training and management within the ED at Royal North Shore Hospital and the results of the interventions will be monitored.

The Royal North Shore Hospital Emergency Department Airway Registry. A Prospective Observational Study of Airway Management in a Tertiary Hospital Emergency Department in Sydney, Australia
Annesley N,Vassiliadis J, Kerry Hitos K, Fogg T
Emerg. Med. Australas. 24 (Suppl. 1):27-28

Study authors Toby Fogg and Nick Annesley demonstrate the 'Happiness Triad'

Ventilated patients better able to communicate pain with dexmedetomidine

A multicentre European trial on intensive care units showed dexmedetomidine was non-inferior to midazolam or propofol in achieving target sedation levels, but patients were better able to communicate pain compared with midazolam and propofol. Dexmedetomidine reduced duration of mechanical ventilation compared with midazolam, but not compared with propofol.


Context Long-term sedation with midazolam or propofol in intensive care units (ICUs) has serious adverse effects. Dexmedetomidine, an α2-agonist available for ICU sedation, may reduce the duration of mechanical ventilation and enhance patient comfort.

Objective To determine the efficacy of dexmedetomidine vs midazolam or propofol (preferred usual care) in maintaining sedation; reducing duration of mechanical ventilation; and improving patients’ interaction with nursing care.

Design, Setting, and Patients Two phase 3 multicenter, randomized, double-blind trials carried out from 2007 to 2010. The MIDEX trial compared midazolam with dexmedetomidine in ICUs of 44 centers in 9 European countries; the PRODEX trial compared propofol with dexmedetomidine in 31 centers in 6 European countries and 2 centers in Russia. Included were adult ICU patients receiving mechanical ventilation who needed light to moderate sedation for more than 24 hours (midazolam, n = 251, vs dexmedetomidine, n = 249; propofol, n = 247, vs dexmedetomidine, n = 251).

Interventions Sedation with dexmedetomidine, midazolam, or propofol; daily sedation stops; and spontaneous breathing trials.

Main Outcome Measures For each trial, we tested whether dexmedetomidine was noninferior to control with respect to proportion of time at target sedation level (measured by Richmond Agitation-Sedation Scale) and superior to control with respect to duration of mechanical ventilation. Secondary end points were patients’ ability to communicate pain (measured using a visual analogue scale [VAS]) and length of ICU stay. Time at target sedation was analyzed in per-protocol population (midazolam, n = 233, vs dexmedetomidine, n = 227; propofol, n = 214, vs dexmedetomidine, n = 223).

Results Dexmedetomidine/midazolam ratio in time at target sedation was 1.07 (95% CI, 0.97-1.18) and dexmedetomidine/propofol, 1.00 (95% CI, 0.92-1.08). Median duration of mechanical ventilation appeared shorter with dexmedetomidine (123 hours [IQR, 67-337]) vs midazolam (164 hours [IQR, 92-380]; P = .03) but not with dexmedetomidine (97 hours [IQR, 45-257]) vs propofol (118 hours [IQR, 48-327]; P = .24). Patients’ interaction (measured using VAS) was improved with dexmedetomidine (estimated score difference vs midazolam, 19.7 [95% CI, 15.2-24.2]; P < .001; and vs propofol, 11.2 [95% CI, 6.4-15.9]; P < .001). Length of ICU and hospital stay and mortality were similar. Dexmedetomidine vs midazolam patients had more hypotension (51/247 [20.6%] vs 29/250 [11.6%]; P = .007) and bradycardia (35/247 [14.2%] vs 13/250 [5.2%]; P < .001).
Conclusions Among ICU patients receiving prolonged mechanical ventilation, dexmedetomidine was not inferior to midazolam and propofol in maintaining light to moderate sedation. Dexmedetomidine reduced duration of mechanical ventilation compared with midazolam and improved patients’ ability to communicate pain compared with midazolam and propofol. More adverse effects were associated with dexmedetomidine.

Dexmedetomidine vs midazolam or propofol for sedation during prolonged mechanical ventilation: two randomized controlled trials
JAMA. 2012 Mar 21;307(11):1151-60

Spinal imaging for the adult obtunded blunt trauma patient

‘You can’t clear the cervical spine until the patient wakes up!’ How often have you heard this said about a patient with severe traumatic brain injury who may not ‘wake up’ for weeks, if at all?
A controversial area, but many institutions now allow collar removal if a neck CT scan is normal. Does this rule out injury with 100% sensitivity? No – but it probably pushes the balance of risk towards removing the collar – an intervention with no evidence for benefit and plenty of reasons why it may be harmful to ventilated ICU patients. For example, clearing the cervical spine based on MDCT was associated with less delirium and less ventilator associated pneumonia, both of which have been associated with increased mortality in critically ill patients (this is referenced in the paper below).
The UK’s Intensive Care Society has had pragmatic guidelines along these lines since 2005, which can be found here. This month’s Intensive Care Medicine publishes an updated literature review providing some further support to this approach.


PURPOSE: Controversy exists over how to ‘clear’ (we mean enable the clinician to safely remove spinal precautions based on imaging and/or clinical examination) the spine of significant unstable injury among clinically unevaluable obtunded blunt trauma patients (OBTPs). This review provides a clinically relevant update of the available evidence since our last review and practice recommendations in 2004.

METHODS: Medline, Embase. Google Scholar, BestBETs, the trip database, BMJ clinical evidence and the Cochrane library were searched. Bibliographies of relevant studies were reviewed.

RESULTS: Plain radiography has low sensitivity for detecting unstable spinal injuries in OBTPs whereas multidetector-row computerised tomography (MDCT) approaches 100%. Magnetic resonance imaging (MRI) is inferior to MDCT for detecting bony injury but superior for detecting soft tissue injury with a sensitivity approaching 100%, although 40% of such injuries may be stable and ‘false positive’. For studies comparing MDCT with MRI for OBTPs; MRI following ‘normal’ CT may detect up to 7.5% missed injuries with an operative fixation in 0.29% and prolonged collar application in 4.3%. Increasing data is available on the complications associated with prolonged spinal immobilisation among a population where a minority have an actual injury.

CONCLUSIONS: Given the variability of screening performance it remains acceptable for clinicians to clear the spine of OBTPs using MDCT alone or MDCT followed by MRI, with implications to either approach. Ongoing research is needed and suggestions are made regarding this. It is essential clinicians and institutions audit their data to determine their likely screening performances in practice.

Clinical review: spinal imaging for the adult obtunded blunt trauma patient: update from 2004
Intensive Care Med. 2012 Mar 10. [Epub ahead of print]

Awake video laryngoscopy

A nice study reminds of us the option of awake video laryngoscopy as an alternative to fibreoptic instrumentation of the airway. The study was done on healthy volunteers so we have no idea of the applicability to the patient group we would be interested in using this on – those with an anticipated difficult airway sufficiently stable to allow tolerance and preparation for this procedure. The videolaryngoscopy was performed with patients upright in a face-to-face position, with the laryngoscope inserted in the inverted handle-down (“tomahawk”) position (this is the way I remove fishbones using a direct laryngoscope and Magill’s forceps).
Visualization was faster with video laryngoscopy, and grade of view was similar in both groups. Cormack Lehane grading was used to assess view, whereas the POGO score (percentage of glottic opening) might have provided a better means of assessing which view is superior. The study did not evaluate endotracheal tube insertion.
Local anaesthesia was provided with 5 ml nebulised 4% lidocaine and weight-based doses of 4% lidocaine were then sprayed into the nose and oropharynx through a mucosal atomisation device to a maximum of 9 mg/kg. Oxymetazoline was applied nasally for the flexible fibreoptic laryngoscopy.


Study objectives: We compare laryngoscopic quality and time to highest-grade view between a face-to-face approach with the GlideScope and traditional flexible fiber-optic laryngoscopy in awake, upright volunteers.

Methods: This was a prospective, randomized, crossover study in which we performed awake laryngoscopy under local anesthesia on 23 healthy volunteers, using both a GlideScope video laryngoscopy face-to-face technique with the blade held upside down and flexible fiber-optic laryngoscopy. Operator reports of Cormack-Lehane laryngoscopic views and video-reviewed time to highest-grade view, as well as number of attempts, were recorded.

Results: Ten women and 13 men participated. A grade II or better view was obtained with GlideScope video laryngoscopy in 22 of 23 (95.6%) participants and in 23 of 23 (100%) participants with flexible fiber-optic laryngoscopy (relative risk GlideScope video laryngoscopy versus flexible fiber-optic laryngoscopy 0.96; 95% confidence interval 0.88 to 1.04). Median time to highest-grade view for GlideScope video laryngoscopy was 16 seconds (interquartile range 9 to 34) versus 51 seconds (interquartile range 35 to 96) for flexible fiber-optic laryngoscopy. A distribution of interindividual differences demonstrated that GlideScope video laryngoscopy was, on average, 39 seconds faster than flexible fiber-optic laryngoscopy (95% confidence interval 0.2 to 76.9 seconds).

Conclusion: GlideScope video laryngoscopy can be used to obtain a Cormack-Lehane grade II or better view in the majority of awake, healthy volunteers when an upright face-to-face approach is used and was slightly faster than traditional flexible fiber-optic laryngoscopy. However, flexible fiber-optic laryngoscopy may be more reliable
at obtaining high-grade views of the larynx. Awake, face-to-face GlideScope use may offer an alternative approach to the difficulty airway, particularly among providers uncomfortable with flexible fiber-optic laryngoscopy.

GlideScope Versus Flexible Fiber Optic for Awake Upright Laryngoscopy
Ann Emerg Med. 2012 Mar;59(3):159-64

Phentolamine for neurogenic pulmonary oedema

A single case report might not be practice changing, but it’s helpful to know about this option:
A patient with acute intracerebral haemorrhage developed hyoxaemia due to neurogenic pulmonary oedema, accompanied by a labile blood pressure and elevated catecholamine levels.
Nicardipine and other antihypertensive agents including metoprolol, hydralazine, and labetalol were tried without benefit, and the patient continued to deteriorate.
Phentolamine was tried. The introduction, withdrawal, and reintroduction of phentolamine and the clinical status of the patient is described convincingly:


a phentolamine infusion was started at 0.17 mg/min and titrated for BP control. Over 6 h, the FIO2 requirements dropped precipitously, gas exchange improved, and the chest radiograph showed improvement of pulmonary edema. When the hospital supply of phentolamine was exhausted, the clinical status deteriorated rapidly. Within just 15 h of the discontinuation of phentolamine, the PaO2 fell from 166 mm Hg to 66 mm Hg, and FIO2 requirements rose from 60% to 100%. When the phentolamine supply was replenished and the infusion restarted, the same rapid improvement was observed and BP stabilized.

Phentolamine is a potent competitive antagonist at both alpha 1 and alpha 2 receptors . Phentolamine causes a reduction in peripheral resistance through blockade of alpha 1 receptors and possibly alpha 2 receptors on vascular smooth muscle.


Abstract
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.

Neurogenic Pulmonary Edema: Successful Treatment With IV Phentolamine
Chest March 2012 vol. 141 no. 3 793-795

Dobutamine for severe heart failure – more harm than good?

A systematic review and meta-analysis of randomised controlled trials showed dobutamine is not associated with improved mortality in heart failure patients and in the case of severe heart failure there is some suggestion of increased mortality, although this did not reach statistical significance.
The authors do point out that the quality of the reports of the trials reviewed was suboptimal. However, they state:
It should be noted that the results of this study are in accord with large observational studies that have also suggested harm associated with use of dobutamine in patients with severe heart failure. Taken together, this evidence should cause clinicians to reconsider their use of dobutamine in patients with heart failure, particularly those most at risk of the adverse effects, those with underlying ischaemic heart disease.

PURPOSE: Dobutamine is recommended for patients with severe heart failure; however uncertainty exists as to its effect on mortality. This study aims to critically review the literature to evaluate whether dobutamine, compared with placebo or standard care, is associated with lower mortality and a range of secondary outcomes, in patients with severe heart failure.
METHODS: A systematic review and meta-analysis of randomised controlled trials was performed. PubMed, EMBASE, the Cochrane Central Trials Registry, the metaRegister of Controlled Trials and bibliographies of retrieved articles were searched. Randomised trials comparing dobutamine with placebo or standard care, in human, adult patients with severe heart failure, were included if they reported at least one outcome of interest. Data regarding trial validity, methodological processes and clinical outcomes were extracted, and a meta-analysis was performed.
RESULTS: Fourteen studies, with 673 participants, met the inclusion criteria and were included; 13 studies reported mortality. There was minimal heterogeneity (I (2) = 4.5%). The estimate of the odds ratio for mortality for patients with severe heart failure treated with dobutamine compared with standard care or placebo was 1.47 (95% confidence interval 0.98-2.21, p = 0.06).
CONCLUSIONS: This meta-analysis showed that dobutamine is not associated with improved mortality in patients with heart failure, and there is a suggestion of increased mortality associated with its use, although this did not reach the conventional level of statistical significance. Further research to define the role of dobutamine in treatment of severe heart failure should be a priority.

Dobutamine for patients with severe heart failure- a systematic review and meta-analysis of randomised controlled trials
Intensive Care Med. 2012 Mar;38(3):359-67

Colloid volume therapy for critically ill patients

The European Society of Intensive Care Medicine has produced a consensus statement on colloid volume therapy for critically ill patients, published in this month’s Intensive Care Medicine.
Curiously, the full text document is not yet availablle on ESICM’s website, but I found this presentation summarising the work by one the authors (Richard Beale):


PURPOSE: Colloids are administered to more patients than crystalloids, although recent evidence suggests that colloids may possibly be harmful in some patients. The European Society of Intensive Care Medicine therefore assembled a task force to compile consensus recommendations based on the current best evidence for the safety and efficacy of the currently most frequently used colloids-hydroxyethyl starches (HES), gelatins and human albumin.

METHODS: Meta-analyses, systematic reviews and clinical studies of colloid use were evaluated for the treatment of volume depletion in mixed intensive care unit (ICU), cardiac surgery, head injury, sepsis and organ donor patients. Clinical endpoints included mortality, kidney function and bleeding. The relevance of concentration and dosage was also assessed. Publications from 1960 until May 2011 were included. The quality of available evidence and strength of recommendations were based on the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach.

RECOMMENDATIONS AND CONCLUSIONS: We recommend not to use HES with molecular weight ≥200 kDa and/or degree of substitution >0.4 in patients with severe sepsis or risk of acute kidney injury and suggest not to use 6% HES 130/0.4 or gelatin in these populations. We recommend not to use colloids in patients with head injury and not to administer gelatins and HES in organ donors. We suggest not to use hyperoncotic solutions for fluid resuscitation. We conclude and recommend that any new colloid should be introduced into clinical practice only after its patient-important safety parameters are established.

Consensus statement of the ESICM task force on colloid volume therapy in critically ill patients
Intensive Care Med. 2012 Mar;38(3):368-83
Update September 2012:
An RCT showed patients with severe sepsis assigned to fluid resuscitation with HES 130/0.42 had an increased risk of death at day 90 and were more likely to require renal-replacement therapy, as compared with those receiving Ringer’s acetate. Read more about the trial here
Hydroxyethyl Starch 130/0.42 versus Ringer’s Acetate in Severe Sepsis
N Engl J Med. 2012 Jul 12;367(2):124-34
Australian intensivist John Myburgh gives a great summary of Fluid Therapy in critical care here

Body temperature in anaesthetised HEMS patients

This study raises an important issue – how do we keep patients with major trauma warm on the way to hospital? The authors from HEMS London identified mean temperatures in hospital of 35°C in patients who had been anaesthetised in the field, although only 38% of their patients had a temperature recorded on admission!
I emailed the author Audun Langhelle for practical information on the thermal protection package they use, who was most helpful in supplying the following information. Clicking on the link will take you to online supplements to the paper describing and illustrating their technique of prehospital rewarming.

Hi Cliff,

Thank you for your request and interest in our paper. Now fully repatriated to Norway, we’re currently using the medium sized UniqueResc warming blanket (Geratherm, Germany) at my base, together with the bubble wrap. In Norway, Garatherm is the only company which has been able to provide us with the necessary paper work showing that their product complies with the rather strict pan European rules and regulations, the EN 13718-1: Requirements for medical devices used in air ambulances in particular.
Working as HEMS doc with LAA 2008-2009, we played with and introduced the policy using Diemme’s (Italy)DM EMG >> http://emj.bmj.com/content/early/2010/10/19/emj.2009.086967/suppl/DC1, but I’m not sure what blanket they currently use.

Kind regards,

Audun

We reviewed this article in one of our Sydney HEMS Clinical Governance Days last year. One of our team presented a critical appraisal and if you’re interested the deadly PowerPoint slides are here:


Background Hypothermia at hospital admission has been found to independently predict increased mortality in trauma patients.

Objectives To establish if patients anaesthetised in the prehospital phase of care had a higher rate of hypothermia than non-anaesthetised patients on admission to hospital.

Methods Retrospective review of admission body temperature in 1292 consecutive prehospital trauma patients attended by a physician-led prehospital trauma service admitted to The Royal London Hospital between 1 July 2005 and 31 December 2008.

Results 38% had a temperature recorded on admission. There was a significant difference in body temperature between the anaesthetised group (N=207) and the non-anaesthetised group (N=287): mean (SD) 35.0 (2.1) vs 36.2 (1.0)°C, respectively (p <0.001). No significant seasonal body temperature variation was demonstrated.
Conclusion This study confirmed that patients anaesthetised in the prehospital phase of care had a significantly lower admission body temperature. This has led to a change in the author’s prehospital practice. Anaesthetised patients are now actively surface heated and have whole body insulation to prevent further heat loss in an attempt to conserve body temperature and improve outcome. This is an example of best in-hospital anaesthetic practice being carried out in the prehospital phase.

Body temperature of trauma patients on admission to hospital: a comparison of anaesthetised and non-anaesthetised patients
Emerg Med J. 2012 Mar;29(3):239-42
Full text link

The REAL Shocked Patient

I promised to put some summary notes on the site for those who attended my talk on ‘The REAL Shocked Patient’ for the Australian College of Ambulance Professionals on Tuesday 21st February 2012, so here they are:

Shocked patients are important – they comprise most of the ‘talk and die’ caseload that preoccupies pub conversations between emergency physicians
It’s easy to mistake these patients as less sick than, say, hypoxic ones, but oxygen delivery to the tissues doesn’t just depend on oxygen!

Here’s a dead wombat – someone in the audience knew a worrying amount about wombat anuses.

The 4 Hs and 4 Ts aren’t a very cognitively practical mnemonic for the causes of PEA arrest (which is an extreme form of hypotension)

I prefer the ‘3 plus 3’ rule, which breaks down the causes into three – volume, pump, and obstruction. Obstruction is further broken down into three causes, being tension pneumothorax, cardiac tamponade, and pulmonary embolism:

Let’s look at some cases of shock caused by volume deficit, pump falure, or one of the three causes of obstruction to the circulation:
 
Case 1: The hypotensive motorcyclist
His low back pain suggested pelvic fracture
Think of ‘blood on the floor and four more’ (chest, abdomen, pelvis/retroperitoneum, long bones) and consider non-bleeding causes such as neurogenic (spinal injury), tension pneumothorax, cardiac tamponade, and finally medical causes/iatrogenic (drug) causes.
Don’t underestimate the importance of pelvis and limb splinting as a haemorrhage control technique in blunt trauma
Ultrasound in flight made thoracic or abdominal bleeding very unlikely, and ruled out tamponade and pneumothorax
Although he was hypotensive, no fluids were given, as he was mentating normally and peripherally well perfused, with a radial pulse. If we gave fluid, we would titrate to the presence of a radial pulse (in blunt trauma) but we don’t want to ‘pop the clot’ by elevating the BP, or make him less able to form effective clots by diluting his blood with crystalloid.
Mortality in trauma sharply rises with systolic BP below 105-110, so recalibrate your definition of hypotension in terms of when you might be concerned, and which patients may benefit from triage to a trauma centre.
 
Case 2: The child crushed by a wall
Caution regarding lower limb infusions in patients with abdominal / pelvic injuries – the fluid may not get to the heart.

The classification of shock into four classes is crap. Never let the absence of a tachycardia reassure you.


Intraosseous is awesome, and EZ-IO has the best track record by far.
 
Case 3: The boy stabbed in the upper thigh
In penetrating limb trauma, prehospital options include pressure, elevation, tourniquet, and haemostatic dressings. Foley catheters have been used successfully in transition zones such as the neck or groin.
 
Case 4: Haematemesis
Should we apply the same principles of permissive hypotension to patients with ‘medical’ bleeding?
The Trendelenburg position doesn’t make a lot of sense – no need to head down the patient, although the act of elevating the legs may ‘autoinfuse’ a bolus of blood to the core circulation, and is recommended by some bodies as a first aid manoeuvre for hypotensive patients in the field prior to iv fluids.
 
Case 5: The overdose patient with a low blood pressure but otherwise fine.
When don’t I Worry about hypotension? When the patient is:

  • With it
  • Warm peripherally
  • Weeing
  • and (in hospital) Without a raised lactate


Case 6: Two cases of pump failure: STEMI and complete heart block
Adrenaline infusions can be simply made with a 1mg 1:10000 minijet diluted in a litre of saline and dripped through a peripheral line titrated to BP / HR / mentation / pulses.
In complete heart block (or other bradycardias) with hypotension, percussion pacing is an option of you don’t have access to transcutaneous or transvenous pacing. If you get capture, it’s as effective in terms of stroke volume as a pacing wire.
 
Case 7: Obstructive shock – tamponade cases
…with resolution of hypotension after drainage by emergency physicians who identified the tamponade on ultrasound, even though they didn’t suspect it clinically. It can be a surprise!
 
Case 8: Obstructive shock – tension pneumothorax
Patients are often agitated and won’t lie flat. They may complain of ‘tight’ breathing. Crackles and/or wheezes may be heard. The classic description of deviated trachea, absent breath sounds, and hyperresonance are the exception, not the rule. Be suspicious and always palpate for subcutaneous emphysema.
Don’t assume a needle decompression will work – there is debate about the best site but in some adults a standard needle won’t reach the pleural space. If you need to place more than one needle, go for it. As physicians, we do thoracostomies to ensure we’ve hit the spot.
 
Case 9: Obstructive shock – pulmonary embolism
A tough one prehospital, as the hypotensive ones need fibrinolysis. Fluid may help the hypotension but too much can overdistend the right ventricle which can then impair left ventricular filling, and worsen the patient’s circulatory state. Once again, ultrasound may be invaluable in highlighting PE as a possible cause for shock.
 
Case 10: Penetrating trauma to the ‘box’ – chest and upper abdomen.
If these patients arrest due to tamponade, early (< 10 minutes) clamshell thoracotomy can be life saving, which means it may need to be done pre-hospital by a HEMS physician to provide a chance of survival. Be on the look out for these and if in doubt activate a medical team (in New South Wales). Like with tension pneumothorax, these patients may be extremely agitated as a manifestation of their shock.
 
Case 11: Confused elderly male with pyrexia and smelly urine who appears ostensibly ‘normotensive’
…but how many 82 year olds do you know with a BP of 110/57? His acute confusion may be a manifestation of shock and he needs aggressive evaluation in hospital including a lactate measurement. Don’t be afraid to give this guy fluids in the field – you can make a big difference here.
Here are five of the myths I promised to expose:

So…shocked patients can talk and die. Don’t let that happen. Shocked patients can be normotensive, and hypotensive patients might not be shocked. Have a plan for how you might evaluate the 3+3 causes in your setting and what you can use from your medication and equipment list to manage volume, pump, and obstruction issues. You will save many lives if you become a serious shock detective.

Severe Traumatic Brain Injury in Children

The Brain Trauma Foundation has released updated guidelines on traumatic brain injury in children.
Most of the recommendations are Grade C and therefore based on limited evidence.

Indications for ICP monitoring

Use of intracranial pressure (ICP) monitoring may be considered in infants and children with severe traumatic brain injury (TBI) (Grade C).
Four lines of evidence support the use of ICP monitoring in children with severe TBI:

  • a frequently reported high incidence of intracranial hypertension in children with severe TBI
  • a widely reported association of intracranial hypertension and poor neurologic outcome
  • the concordance of protocol-based intracranial hypertension therapy and best-reported clinical outcomes
  • and improved outcomes associated with successful ICP-lowering therapies.

Threshold for treatment of intracranial hypertension
Treatment of intracranial pressure (ICP) may be considered at a threshold of 20 mm Hg (Grade C).
Sustained elevations in ICP (>20 mm Hg) are associated with poor outcome in children after severe TBI.
Normal values of blood pressure and ICP are age-dependent (lower at younger ages), so it is anticipated that the optimal ICP treatment threshold may be age-dependent.
Cerebral perfusion pressure thresholds
A CPP threshold 40–50 mm Hg may be considered. There may be age-specific thresholds with infants at the lower end and adolescents at the upper end of this range (Grade C).
Survivors of severe pediatric TBI undergoing ICP monitoring consistently have higher CPP values vs. nonsurvivors, but no study demonstrates that active maintenance of CPP above any target threshold in pediatric TBI reduces mortality or morbidity.
CPP should be determined in a standard fashion with ICP zeroed to the tragus (as an indicator of the foramen of Monro and midventricular level) and MAP zeroed to the right atrium with the head of the bed elevated 30°.
Advanced neuromonitoring
If brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen (PbtO2) >10 mm Hg may be considered.
Neuroimaging
In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a routine repeat computed tomography (CT) scan >24 hrs after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention (Grade C).
Hyperosmolar therapy
Hypertonic saline should be considered for the treatment of severe pediatric traumatic brain injury (TBI) associated with intracranial hypertension. Effective doses for acute use range between 6.5 and 10 mL/kg (of 3%) (Grade B).
Hypertonic saline should be considered for the treatment of severe pediatric TBI associated with intracranial hypertension. Effective doses as a continuous infusion of 3% saline range between 0.1 and 1.0 mL/kg of body weight per hour administered on a sliding scale. The minimum dose needed to maintain intracranial pressure (ICP)
Temperature control
Moderate hypothermia (32–33°C) beginning early after severe traumatic brain injury (TBI) for only 24 hrs’ duration should be avoided.
Moderate hypothermia (32–33°C) be- ginning within 8 hrs after severe TBI for up to 48 hrs’ duration should be considered to reduce intracranial hypertension.
If hypothermia is induced for any indication, rewarming at a rate of >0.5°C/hr should be avoided (Grade B).
Moderate hypothermia (32–33°C) be- ginning early after severe TBI for 48 hrs, duration may be considered (Grade C).
Note: after completion of these guidelines, the committee became aware that the Cool Kids trial of hypothermia in pediatric TBI was stopped because of futility. The implications of this development on the recommendations in this section may need to be considered by the treating physician when details of the study are published.
Cerebrospinal fluid drainage
Cerebrospinal fluid (CSF) drainage through an external ventricular drain may be considered in the management of increased intracranial pressure (ICP) in children with severe traumatic brain injury (TBI).
The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drain, open basal cis- terns, and no evidence of a mass lesion or shift on imaging studies (Grade C).
Barbiturates
High-dose barbiturate therapy may be considered in hemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management.
When high-dose barbiturate therapy is used to treat refractory intracranial hy- pertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required (Grade C).
Decompressive craniectomy for the treatment of intracranial hypertension
Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for pediatric patients with traumatic brain injury (TBI) who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment (Grade C).
Hyperventilation
Avoidance of prophylactic severe hyperventilation to a PaCO2 If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring for evaluation of cerebral ischemia may be considered (Grade C).
Corticosteroids
The use of corticosteroids is not recommended to improve outcome or reduce intracranial pressure (ICP) for children with severe traumatic brain injury (TBI) (Grade B).
Analgesics, sedatives, and neuromuscular blockade
Etomidate may be considered to control severe intracranial hypertension; however, the risks resulting from adrenal suppression must be considered.
Thiopental may be considered to control intracranial hypertension.
In the absence of outcome data, the specific indications, choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used in the management of infants and children with severe traumatic brain injury (TBI) should be left to the treating physician.
*As stated by the Food and Drug Administration, continuous infusion of propofol for either sedation or the management of refractory intracranial hypertension in infants and children with severe TBI is not recommended (Grade C).
The availability of other sedatives and analgesics that do not suppress adrenal function, small sample size and single-dose administration in the study discussed previously, and limited safety profile in pediatric TBI limit the ability to endorse the general use of etomidate as a sedative other than as an option for single-dose administration in the setting of raised ICP.
Glucose and nutrition
The evidence does not support the use of an immune-modulating diet for the treatment of severe traumatic brain injury (TBI) to improve outcome (Grade B).
In the absence of outcome data, the specific approach to glycemic control in the management of infants and children with severe TBI should be left to the treating physician (Grade C).
Antiseizure prophylaxis
Prophylactic treatment with phenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in pediatric patients with severe traumatic brain injury (TBI) (Grade C).
The incidence of early PTS in pediatric patients with TBI is approximately 10% given the limitations of the available data. Based on a single class III study (4), prophylactic anticonvulsant therapy with phenytoin may be considered to reduce the incidence of early posttraumatic seizures in pediatric patients with severe TBI. Concomitant monitoring of drug levels is appropriate given the potential alterations in drug metabolism described in the context of TBI. Stronger class II evidence is available supporting the use of prophylactic anticonvulsant treatment to reduce the risk of early PTS in adults. There are no compelling data in the pediatric TBI literature to show that such treatment reduces the long-term risk of PTS or improves long-term neurologic outcome.
Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents-Second Edition
Pediatr Crit Care Med 2012 Vol. 13, No. 1 (Suppl.)
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