Tag Archives: critical care

All Updates, ICU, Resus, Ultrasound

Ultrasound-Guided Radial Artery Catheterization

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In case you needed some evidence – a systematic review supports ultrasound guidance as a means of improving insertion success of radial artery catheters


BACKGROUND: Ultrasound guidance commonly is used for the placement of central venous catheters (CVCs). The Agency for Healthcare Research and Quality recommends the use of ultrasound for CVC placement as one of its 11 practices to improve patient care. Despite increased access to portable ultrasound machines and comfort with ultrasound-guided CVC access, fewer clinicians are familiar with ultrasound-guided techniques of arterial catheterization. The goal of this systematic review and meta-analysis was to determine the utility of real-time two-dimensional ultrasound guidance for radial artery catheterization.

METHODS: A comprehensive literature search of Medline, Excerpta Medica Database, and the Cochrane Central Register of Controlled Trials by two independent reviewers identified prospective, randomized controlled trials comparing ultrasound guidance with traditional palpation techniques of radial artery catheterization. Data were extracted on study design, study size, operator and patient characteristics, and the rate of first-attempt success. A meta-analysis was constructed to analyze the data.

RESULTS: Four trials with a total of 311 subjects were included in the review, with 152 subjects included in the palpation group and 159 in the ultrasound-guided group. Compared with the palpation method, ultrasound guidance for arterial catheterization was associated with a 71% improvement in the likelihood of first-attempt success (relative risk, 1.71; 95% CI, 1.25-2.32).

CONCLUSIONS: The use of real-time two-dimensional ultrasound guidance for radial artery catheterization improved first-pass success rate.

Ultrasound-Guided Catheterization of the Radial Artery
Chest. 2011 Mar;139(3):524-9

All Updates, Resus

It's up to you….

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Sometimes you have nothing to lose by doing a procedure that you may never have done before, if the patient is going to die or deteriorate without it.
In today’s competency-based-training-and-accreditation climate (a good thing), how does one achieve competence in a procedure that may be too rare to have even been seen, let alone practiced under supervision and formally assessed?
I spend a lot of time and energy trying to convince colleagues and trainees that there are situations where the benefit-harm equation is in favour of acting, despite reservations they may have about inadequate experience or training. These situations often require ‘surgical’ procedures. What they have in common is that they are all relatively simple to perform, but may save a life, a limb, or sight which otherwise may almost certainly be lost.
How best to train for these procedures, some of which may be too rare even for ‘see one, do one, teach one’ in an entire residency program? Simulators? Animal labs? Cadavers?

Slide from 'Making Things Happen' Course

In my view, the answer is to use the most high fidelity simulator in the universe – the human brain. It is those professionals who mentally rehearse the scenario and visualise the procedure over and over who are most likely to act when the patient needs it most. Several colleagues of mine over the years can recount incidents in which the indications for a thoracotomy or hysterotomy were present but they failed to act, talking themselves out of doing the procedure with a range of excuses from ‘I hadn’t had enough training’ to ‘No-one in the room wanted to do it’. Don’t be one of those! Get simulating now – you have all the equipment you need!

Ten steps to making it happen – be prepared
1. Pick a procedure (eg. thoracotomy)
2. Be ABSOLUTELY CLEAR on the indications – this helps remove any doubt when the time comes
3. Learn how to do it (talk to colleagues, read a book)
4. Know where the required equipment is kept
5. Start practicing in your mind – visualise seeing the patient, what you will say to your staff, where you will locate your equipment, what you will do procedurally step-by-step
6. Visualise possible outcomes and what your next steps would be (tamponade plus cardiac wound in a beating heart, tamponade plus wound plus VF, return of spontaneous circulation with bleeding from internal mammary arteries)
7. Read more and talk to more colleagues based on questions arising from your ‘simulations’
8. Travel, go on a course, get access to animal or cadaver labs if that’s an option in your setting
9. Speak to people who have done it in YOUR context (eg. for a resus room thoracotomy, talk to emergency physicians who have done it there, rather than a cardiothoracic surgeon who has only ever done them in the operating room)
10. Find an excuse on shift to talk about it to colleagues and rehearse the steps, locate the equipment, and so on. Remember: REPETITION IS THE MOTHER OF SKILL!

What’s on your list of life/limb/sight-saving procedures that can’t wait for someone else to do? Did I miss any? Should skull trephination be there? Comments welcome!

All Updates, PHARM, Resus, Trauma

Effect of physician specialty on pre-hospital intubation success

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Researchers from the London Helicopter Emergency Medical Service describe the success of pre-hospital laryngoscopy according to the grade and specialty of the HEMS physician…

There is conflicting evidence concerning the role and safety of prehospital intubation, and which providers should deliver it. Success rates for physician-performed rapid sequence induction are reported to be 97-100%, with limited evidence of improved survival in some patient groups. However, there is also evidence that prehospital intubation and ventilation can do harm. Prospective data were recorded on the success of intubation, the quality of the laryngeal view obtained and the number of attempts at intubation. These data were then analysed by the grade of intubating doctor and whether the intubating doctor had a background in anaesthesia or emergency medicine. All groups had a similar success rate after two attempts at intubation. Doctors with a background in anaesthesia and consultant emergency physicians had a significantly better first-pass intubation rate than emergency medicine trainees. The quality of laryngeal view was significantly better in doctors with an anaesthetics background.

Success in physician prehospital rapid sequence intubation: what is the effect of base speciality and length of anaesthetic training?
Emerg Med J. 2011 Mar;28(3):225-9

All Updates, ICU, Resus

Crike rate 1 in 500 in Scottish ED

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A review of over 2500 intubation attempts in the emergency department1, (of which 1671 were rapid sequence intubation attempts) revealed five cricothyroidotomies, giving a crike rate of 0.2% which is much lower than in some other ED based registries. In four patients, predictors of difficult airway were identified before the endotracheal intubation attempt, and formal preparation for rescue surgical airway was performed. Three of the surgical airways were performed by emergency medicine trainees, one by an emergency medicine specialist and one by an ear, nose and throat specialist. There was a 100% success rate for placement of all surgical airways on the first attempt.

Four surgical airways were done in trauma patients: laryngeal fracture, facial burns, Le Fort II facial fracture and penetrating neck injury.
This study is of interest to UK emergency physicians who may be interested in Edinburgh Royal Infirmary’s collaborative approach to emergency airway management by the Departments of Emergency Medicine, Anaesthesia and Critical Care.
It is not possible to tell from this paper whether there were patients in whom surgical airway was indicated but not performed, and therefore in my view the ostensibly ‘good’ low rate of 0.2% should be viewed with interest rather than awe. Having said that, this figure is more in keeping with my own experience and expectation from UK/Australasian practice; it has been highlighted in the UK EM literature before2, including by myself3, that in our patient group good training and supervision should result in lower surgical airway rates than the ~1% often quoted.


OBJECTIVES: To determine the frequency of and primary indication for surgical airway during emergency department intubation.

METHODS: Prospectively collected data from all intubations performed in the emergency department from January 1999 to July 2007 were analysed to ascertain the frequency of surgical airway access. Original data were collected on a structured proforma, entered into a regional database and analysed. Patient records were then reviewed to determine the primary indication for a surgical airway.

RESULTS: Emergency department intubation was undertaken in 2524 patients. Of these, only five patients (0.2%) required a surgical airway. The most common indication for a surgical airway was trauma in four of the five patients. Two patients had attempted rapid sequence induction before surgical airway. Two patients had gaseous inductions and one patient received no drugs. In all five patients, surgical airway was performed secondary to failed endotracheal intubation attempt(s) and was never the primary technique used.

CONCLUSION: In our emergency department, surgical airway is an uncommon procedure. The rate of 0.2% is significantly lower than rates quoted in other studies. The most common indication for surgical airway was severe facial or neck trauma. Our emergency department has a joint protocol for emergency intubation agreed by the Departments of Emergency Medicine, Anaesthesia and Critical Care at the Edinburgh Royal Infirmary. We believe that the low surgical airway rate is secondary to this collaborative approach. The identified low rate of emergency department surgical airway has implications for training and maintenance of skills for emergency medicine trainees and physicians.

1. Surgical airway in emergency department intubation
Eur J Emerg Med. 2011 Jun;18(3):168-71
2. Rapid sequence induction in the emergency department: a strategy for failure.
Emerg Med J. 2002 Mar;19(2):109-13
3. RSI by non-anaesthetists in the UK – lower incidence of cricothyrotomy than in the US
EMJ e-letters 2002; 3 April

Acute Med, All Updates, ICU, PHARM, Resus

How much oxygen after ROSC?

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I reported a previous JAMA publication demonstrating an association between hyperoxia and mortality in patients resuscitated post-cardiac arrest. The same authors have published furthur data to better define the relationship between supranormal oxygen tension and outcome in postresuscitation patients. They hypothesised that a linear dose-dependent relationship would be present in the association between supranormal oxygen tension and in-hospital mortality.

Background– Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.

Methods and Results– This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 [95% confidence interval 1.18 to 1.31]. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.

Conclusion– In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.

Relationship Between Supranormal Oxygen Tension and Outcome After Resuscitation From Cardiac Arrest
Circulation. 2011 Jun 14;123(23):2717-2722
Australasian investigators provided the following critique of the original JAMA study:

Unfortunately, these investigators used only the first set of arterial blood gases in the ICU to assess oxygenation, excluded close to 30% of patients because of lack of arterial blood gas data and did not adjust for standard illness severity scores. Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. Thus, their results are of uncertain significance and require confirmation.
They undertook their own study of 12,108 patients:

INTRODUCTION: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients.
METHODS: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined ‘hyperoxia’ as PaO2 of 300 mmHg or greater, ‘hypoxia/poor O2 transfer’ as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, ‘normoxia’ as any value between hypoxia and hyperoxia and ‘isolated hypoxemia’ as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.

RESULTS: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).

CONCLUSIONS: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
Crit Care. 2011 Mar 8;15(2):R90. [Epub ahead of print]
Open Access Full Text
What’s the best approach in the light of these differing results? My approach is to avoid hypoxia, since that’s probably bad, and to actively avoid overoxygenating as part of my general neuroprotection checklist in a post-cardiac arrest patient. It would seem prudent to follow the recommendations of ILCOR, summarised by the European Resuscitation Council guidelines as:

Recognition of the potential harm caused by hyperoxaemia after ROSC is achieved: once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry and/or arterial blood gas analysis), inspired oxygen is titrated to achieve a SaO2 of 94–98%

Acute Med, All Updates, Guidelines, ICU, Kids, Resus, Trauma, Ultrasound

Central lines in coagulopathic patients

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If a patient needs a central line, he/she needs one. Often low platelets or a deranged coagulation profile are cited as reasons for omitting or delaying the procedure, but this is not based on evidence of increased complications. A recent Best Evidence Topic Review concludes:

“…insertion of CVC lines do not require correction of haemostatic abnormalities prior to intervention. Rates of haemorrhage are low in patients with elevated PT, APTT or low thrombocyte count and appear to be closely related to the level of experience of the physician … rather than the defects of haemostasis. “

Links to the abstracts of a couple of relevant articles reviewed are included below.
Central line insertion in deranged clotting
Emerg Med J. 2011 Jun;28(6):536-7 Full text
Low levels of prothrombin time (INR) and platelets do not increase the risk of significant bleeding when placing central venous catheters.
Med Klin (Munich). 2009 May 15;104(5):331-5
US-guided placement of central vein catheters in patients with disorders of hemostasis
Eur J Radiol. 2008 Feb;65(2):253-6

All Updates, ICU, PHARM, Resus

Tympanic monitoring for targeted temperature management

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As the authors of this study point out, the reliability of tympanic temperature monitoring is still under debate. Since invasive measures of core temperature employed in the ICU may not be practicable in the pre-hospital setting, it would be helpful to employ a simpler method in the field, particular if we are implementing targeted temperature management post-cardiac arrest. In this small study of ten patients (with 558 temperature measurements) there was a high degree of correlation between tympanic and oesophageal temperature (r=0.95, p<0.0001, 95% CI 0.93 to 0.96) and also between tympanic and bladder temperature (r=0.96, p<0.0001, 95% CI 0.95 to 0.97). This finding is apparently in keeping with results obtained from patients undergoing cardiac surgery.

Objective Prehospital induction of therapeutic hypothermia after cardiac arrest may require temperature monitoring in the field. Tympanic temperature is non-invasive and frequently used in clinical practice. Nevertheless, it has not yet been evaluated in patients undergoing mild therapeutic hypothermia (MTH). Therefore, a prospective observational study was conducted comparing three different sites of temperature monitoring during therapeutic hypothermia.
Methods Ten consecutive patients admitted to our medical intensive care unit after out-of-hospital cardiac arrest were included in this study. During MTH, tympanic temperature was measured using a digital thermometer. Simultaneously, oesophageal and bladder temperatures were recorded in a total of 558 single measurements.
Results Compared with oesophageal temperature, bladder temperature had a bias of 0.019°C (limits of agreement ±0.61°C (2SD)), and tympanic measurement had a bias of 0.021°C (±0.80°C). Correlation analysis revealed a high relationship for tympanic versus oesophageal temperature (r=0.95, p<0.0001) and also for tympanic versus bladder temperature (r=0.96, p<0.0001).
Conclusions That tympanic temperature accurately indicates both oesophageal and bladder temperatures with a very small discrepancy in patients undergoing MTH after cardiac arrest is demonstrated in this study. Although our results were obtained in the hospital setting, these findings may be relevant for the prehospital application of therapeutic hypothermia as well. In this case, tympanic temperature may provide an easy and non-invasive method for temperature monitoring.

Tympanic temperature during therapeutic hypothermia
Emerg Med J. 2011 Jun;28(6):483-5

Acute Med, All Updates, ICU, Kids, Resus

Hyperkalaemia dogmalysis

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One of the things I enjoy most is the dismantling of medical dogma. In his brilliant blog Precious Bodily Fluids, nephrologist Joel Topf reviewed some of the hyperkalaemia literature and offers some of the following pearls:

  • The ECG is insensitive and non-specific as a means of diagnosing (and in particular ruling out) hyperkalaemia (sensitivity of ‘strict’ criteria of symmetrical peaked T waves that resolve on follow up: 18%; sensitivity of any ECG change: 52%).
  • The dangers of calcium treatment for digoxin toxicity-associated hyperkalaemia may be exaggerated and are supported by very weak evidence
  • Sodium bicarbonate does not effectively lower potassium but does lower ionised calcium which can increase the risk of hyperkalaemia-associated dysrhythmia

Read the full blog post here
View Dr Topf’s presentation below:

All Updates, Guidelines, ICU, Resus

Targeted temperature management guidelines

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Okay – rather than ‘therapeutic hypothermia’, the recommended phrase now is ‘targeted temperature management’. Several critical care authorities got together to produce clinical recommendations on this topic. Here are a few interesting points from the document:
On coagulation:
Hypothermia affects platelet function and prolongs the prothrombin time and partial thromboplastin time. These effects are masked when laboratory analysis is performed at 37°C, suggesting that any risk will be mitigated by rewarming.
Although not mentioned in the abstract, the authors examined the role of TTM in raised intracranial pressure (ICP):
Sufficient evidence exists to conclude that TTM does decrease ICP compared to unstructured temperature management. However, there is no sufficient evidence to make a recommendation regarding the use of targeted hypothermia to control elevated ICP to improve patent-important outcomes in TBI. The jury makes NO RECOMMENDATION regarding the use of TTM as an ICP control strategy to improve outcomes in brain injuries regardless of cause (trauma, hemorrhage, or ischemic stroke).
Regarding acute liver failure with severe cerebral edema:
there are currently no RCTs. There is a case series suggesting a strongly favorable effect. This is a powerful argument for support of an RCT evaluating TTM alone or in combination with hepatic dialysis strategies

OBJECTIVE: Representatives of five international critical care societies convened topic specialists and a nonexpert jury to review, assess, and report on studies of targeted temperature management and to provide clinical recommendations.
DATA SOURCES: Questions were allocated to experts who reviewed their areas, made formal presentations, and responded to questions. Jurors also performed independent searches. Sources used for consensus derived exclusively from peer-reviewed reports of human and animal studies.
STUDY SELECTION: Question-specific studies were selected from literature searches; jurors independently determined the relevance of each study included in the synthesis.
CONCLUSIONS AND RECOMMENDATIONS:

  1. The jury opines that the term “targeted temperature management” replace “therapeutic hypothermia.”
  2. The jury opines that descriptors (e.g., “mild”) be replaced with explicit targeted temperature management profiles.
  3. The jury opines that each report of a targeted temperature management trial enumerate the physiologic effects anticipated by the investigators and actually observed and/or measured in subjects in each arm of the trial as a strategy for increasing knowledge of the dose/duration/response characteristics of temperature management. This enumeration should be kept separate from the body of the report, be organized by body systems, and be made without assertions about the impact of any specific effect on the clinical outcome.
  4. The jury STRONGLY RECOMMENDS targeted temperature management to a target of 32°C-34°C as the preferred treatment (vs. unstructured temperature management) of out-of-hospital adult cardiac arrest victims with a first registered electrocardiography rhythm of ventricular fibrillation or pulseless ventricular tachycardia and still unconscious after restoration of spontaneous circulation (strong recommendation, moderate quality of evidence).
  5. The jury WEAKLY RECOMMENDS the use of targeted temperature management to 33°C-35.5°C (vs. less structured management) in the treatment of term newborns who sustained asphyxia and exhibit acidosis and/or encephalopathy (weak recommendation, moderate quality of evidence).

Targeted temperature management in critical care: A report and recommendations from five professional societies
Crit Care Med. 2011 May;39(5):1113-1125

All Updates, ICU, Kids, Resus

Steroids for sepsis in kids

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A small retrospective study suggests adrenal insufficiency is common in kids with septic shock, and that steroid administration in these children was associated with a decrease in vasoactive drug requirements.

INTRODUCTION: Adrenal insufficiency may be common in adults and children with vasopressor-resistant shock. We developed a protocolized approach to low-dose adrenocorticotropin testing and empirical low-dose glucocorticoid/mineralocorticoid supplementation in children with systemic inflammatory response syndrome and persistent hypotension following fluid resuscitation and vasopressor infusion.
HYPOTHESIS: We hypothesized that absolute and relative adrenal insufficiency was common in children with systemic inflammatory response syndrome requiring vasopressor support and that steroid administration would be associated with decreased vasopressor need.
METHODS: Retrospective review of pediatric patients with systemic inflammatory response syndrome and vasopressor-dependent shock receiving protocol-based adrenocorticotropin testing and low-dose steroid supplementation. The incidence of absolute and relative adrenal insufficiency was determined using several definitions. Vasopressor dose requirements were evaluated before, and following, initiation of corticosteroids.
RESULTS: Seventy-eight patients met inclusion criteria for systemic inflammatory response syndrome and shock; 40 had septic shock. Median age was 84 months (range, 0.5-295). By adrenocorticotropin testing, 44 (56%) had absolute adrenal insufficiency, 39 (50%) had relative adrenal insufficiency, and 69 (88%) had either form of adrenal insufficiency. Adrenal insufficiency incidence was significantly higher in children >2 yrs (p = .0209). Therapeutic interventions included median 80-mL/kg fluid resuscitation; 65% of patients required dopamine, 58% norepinephrine, and 49% dopamine plus norepinephrine. With steroid supplementation, median dopamine dose decreased from 10 to 4 μg/kg/min at 4 hrs (p = .0001), and median dose of norepinephrine decreased from 0.175 μg/kg/min to 0.05 μg/kg/min at 4 hrs (p = .039).
CONCLUSIONS: Absolute and relative adrenal insufficiency was prevalent in this cohort of children with systemic inflammatory response syndrome and vasopressor-dependent shock and increased with age. Introduction of steroids produced a significant reduction in vasopressor duration and dosage. Use of low-dose adrenocorticotropin testing may help further delineate populations who require steroid supplementation.

Incidence of adrenal insufficiency and impact of corticosteroid supplementation in critically ill children with systemic inflammatory syndrome and vasopressor-dependent shock
Crit Care Med. 2011 May;39(5):1145-50