Category Archives: Resus

Life-saving medicine

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

Simple emergency haemorrhage control

I had the honour of attending trauma rounds with leading South African trauma surgeons today at Groote Schuur Hospital in Cape Town. This was the first day of an intense week-long trauma education tour that I have organised for myself and three of my Sydney HEMS colleagues.
A technique for haemorrhage control in penetrating trauma is to place a Foley catheter (FC) in the wound and inflate the balloon to try to achieve compression of bleeding vascular structures. This has been life-saving in many cases and buys time to get the patient to a trauma or vascular surgeon or in some cases an interventional radiologist.

Catheter is knotted (black arrow) to occlude lumen. The wound is sutured around the catheter (white arrow).

First described by Gilroy and colleagues from Baragwanath Hospital in Johannesburg1, another, larger case series was subsequently reported by Cape Town’s Navsaria2, the Professor who conducted today’s trauma round I attended. In his paper he describes:


An 18- or 20-G FC was introduced into the bleeding neck wound. An attempt was made to follow the wound tract. The balloon was inflated with 5 ml of water or until resistance was felt. The FC was either clamped or knotted on itself to prevent bleeding through the lumen. The neck wound was sutured in two layers around the catheter. Continued bleeding around the catheter was an indication to proceed to surgery.

There were no deaths attributable to the use of FC balloon tamponade.
Prof. Navsaria describes the following algorithm for the subsequent investigation and management of these patients:

 I’ve been teaching this technique as an option in penetrating trauma for a few years but have never actually done it for real. Nice to finally see examples of its successful implementation by people who do this all the time. I’ve seen four patients with Foleys sticking out of their necks in the first 24 hours of being here.
1. Control of life-threatening haemorrhage from the neck: a new indication for balloon tamponade.
Injury. 1992;23(8):557-9
[EXPAND Click to read abstract]


We report the use of a Foley catheter, placed through the wound, to provide balloon tamponade of major bleeding from the neck and supraclavicular fossae. In 10 consecutive explorations for exsanguinating injury in these regions balloon tamponade was used eight times, and was judged to be fully effective in four patients, partly effective in one, and ineffective in three patients.

[/EXPAND]
2. Foley catheter balloon tamponade for life-threatening hemorrhage in penetrating neck trauma
World J Surg. 2006 Jul;30(7):1265-8
[EXPAND Click to read abstract]


BACKGROUND: Foley catheter (FC) balloon tamponade is a well-recognized technique employed to arrest hemorrhage from penetrating wounds. The aim of this study was to review our experience with this technique in penetrating neck wounds and to propose a management algorithm for patients with successful FC tamponade.

METHODS: A retrospective chart review (July 2004-June 2005 inclusive) was performed of patients identified from a prospectively collected penetrating neck injury computer database in whom FC balloon tamponade was used. The units’ policy for penetrating neck injuries is one of selective nonoperative management. All patients with successful FC tamponade underwent angiography. A venous injury was diagnosed if angiography was normal. Ancillary tests were performed as indicated. Removal of the FC was performed in the OR.

RESULTS: During the study period, 220 patients with penetrating neck injuries were admitted to our unit. Foley catheter balloon tamponade was used in 18 patients and was successful in 17 patients. Angiography was positive in 3 patients, all of whom underwent surgery. The FC was successfully removed in 13 patients at a mean of 72 (range 48-96) hours. One patient bled after removal of the catheter, mandating emergency surgery.

CONCLUSION: Foley catheter balloon tamponade remains a useful adjunct in the management of selective patients with penetrating, bleeding neck wounds.

[/EXPAND]

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

Clotbusting wisdom on tap – your questions answered

The prevention and management of venous thromboembolic disease is a huge topic, which generates questions for emergency, critical care, and acute physicians during many shifts:

  • How long should someone requiring cardioversion for atrial fibrillation be anticoagulated for?
  • How should I provide thromboprophylaxis for this intubated patient?
  • This patient with submassive pulmonary embolism isn’t hypotensive yet. Can I thrombolyse them? Can I?
  • There’s a large superficial vein thrombosis in that limb – is anticoagulation indicated?
  • This asymptomatic patient on warfarin has an INR of 9.0 – should I reverse them?
  • Do I need to add Vitamin K if I’ve reversed warfarin with prothrombin complex concentrate?

The answers to these – and many, many more – questions are provided in one of the most comprehensive guidelines I’ve ever come across. I can see myself clicking on the link below in future when on duty in the ED.
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines
Chest. 2012 Feb;141(2 Suppl) Full Text

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

Epinephrine in cardiac arrest reanalysed

A post hoc reanalysis was performed on a 2009 JAMA paper comparing patients randomised to receive or not receive prehospital drugs and iv access for cardiac arrest.
This was done to evaulate the effect of adrenaline/epinephrine. The reason for the reanalysis was that in the original intention-to-treat analysis, some of the following issues may have influenced the results:

  • Some patients randomised to adrenaline never received it as they had ROSC before the drug could be given, thus yielding a selection bias with the most easily resuscitated patients in the post hoc no-adrenaline group
  • At least 1 of 5 patients randomised to receive IV access and drugs did not receive adrenaline as it was regarded futile or it was impossible to gain intravenous access
  • 1 of 10 patients randomised to not receive drugs received adrenaline after they had regained spontaneous circulation for > 5 min.

The purpose of this post hoc analysis on the RCT data was to compare outcomes for patients actually receiving adrenaline to those not receiving adrenaline.
The actual use of adrenaline was associated with increased short-term survival, but with 48% less survival to hospital discharge. The improved survival to hospital admission is consistent with the results of a recent Australia study, and the negative association with longer term survival is similar to a multivariate analysis of observational Swedish registry data where patients receiving adrenaline were 57% less likely to be alive after one month.
Yet more evidence that we haven’t found any drugs proven to improve survival in cardiac arrest. At least not until the human studies on sodium nitroprusside come out?
I bet some of you are still going to be giving the epi exactly every four minutes though.
**Update: see Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest – more prospective data from Japan, this time showing epinephrine improves prehospital ROSC, but decreases chance of survival and good functional outcomes 1 month after the event.**


PURPOSE OF THE STUDY: IV line insertion and drugs did not affect long-term survival in an out-of-hospital cardiac arrest (OHCA) randomized clinical trial (RCT). In a previous large registry study adrenaline was negatively associated with survival from OHCA. The present post hoc analysis on the RCT data compares outcomes for patients actually receiving adrenaline to those not receiving adrenaline.

MATERIALS AND METHODS: : Patients from a RCT performed May 2003 to April 2008 were included. Three patients from the original intention-to-treat analysis were excluded due to insufficient documentation of adrenaline administration. Quality of cardiopulmonary resuscitation (CPR) and clinical outcomes were compared.

RESULTS: Clinical characteristics were similar and CPR quality comparable and within guideline recommendations for 367 patients receiving adrenaline and 481 patients not receiving adrenaline. Odds ratio (OR) for being admitted to hospital, being discharged from hospital and surviving with favourable neurological outcome for the adrenaline vs. no-adrenaline group was 2.5 (CI 1.9, 3.4), 0.5 (CI 0.3, 0.8) and 0.4 (CI 0.2, 0.7), respectively. Ventricular fibrillation, response interval, witnessed arrest, gender, age and endotracheal intubation were confounders in multivariate logistic regression analysis. OR for survival for adrenaline vs. no-adrenaline adjusted for confounders was 0.52 (95% CI: 0.29, 0.92).

CONCLUSION: Receiving adrenaline was associated with improved short-term survival, but decreased survival to hospital discharge and survival with favourable neurological outcome after OHCA. This post hoc survival analysis is in contrast to the previous intention-to-treat analysis of the same data, but agrees with previous non-randomized registry data. This shows limitations of non-randomized or non-intention-to-treat analyses.

Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial
Resuscitation. 2012 Mar;83(3):327-32

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.)
Read online
Download PDF (617k)
Other Brain Trauma Foundation Guidelines

Posterior pericardiocentesis

Dr Emanuele Catena and colleagues report a case of an adult male who presented 7 days post cardiac surgery with simultaneous pleural and pericardial effucions causing dyspnoea, tachycardia and hypotension.

Old skool pericardiocentesis

His pericardial effusion was posterior which usually requires surgical drainage, but the adjacent left pleural effusion was associated with pulmonary atelectasis and displacement of the lung, allowing them to insert a needle using sonographic guidance first into the pleural space then the pericardial space.
They inserted through the fourth intercostal space 4 cm medially to the left posterior axillary line (with the patient positioned in the semireclining position). They used agitated saline bubbles to confirm first the pleural then the pericardial location of the needle tip. A 30-cm-long catheter was introduced into the posterior pericardium using the Seldinger technique, and serous-haemorrhagic fluid was drained. The catheter was then retracted allowing drainage of the pleural effusion.
The procedure resulted in haemodynamic and respiratory improvement.
The authors summarise:


This case reports the technique of a “back pericardiocentesis” performed under echographic guidance as a valid alternative to surgery in the peculiar situation characterized by the simultaneous presence of a large left pleural effusion. In the presence of a large left pleural effusion, pulmonary atelectasis and displacement of air-filled pulmonary tissue allows ultrasound transmission from a patient’s back to the heart through a liquid interface and needle insertion “from back” to reach the pericardial space.

 
Pericardiocentesis From Back Under Echographic Guidance An Approach for Posterior Pericardial Effusions
Circulation. 2011 Dec 13;124(24):e835-6