Tag Archives: dogmalysis

Out-of hospital traumatic paediatric cardiac arrest

This small study on traumatic arrests in children1 refutes the “100% mortality from traumatic arrest” dogma that people still spout and gives information on the mechanisms associated with survival: drowning and strangulation were associated with greater rates of survival to hospital admission compared with blunt, penetrating, and other traumas. Overall, drowning had the greatest rate of survival to discharge (19.1%).
I would like to know the injuries sustained in non-survivors, to determine whether they were potentially treatable. Strikingly, in the list of prehospital procedures performed, there were NO attempts at pleural decompression, something that is standard in traumatic arrest protocols in prehospital services were I have worked.
It is interesting to compare these results with those of the London HEMS team2, who for traumatic paediatric arrest achieved 19/80 (23.8%) survival to discharged from the emergency department and 7/80 (8.75%) survival to hospital discharge. They also noted a large proportion of the survivors suffered hypoxic or asphyxial injuries, whereas those patients with hypovolaemic cardiac arrest did not survive.


OBJECTIVE:To determine the epidemiology and survival of pediatric out-of-hospital cardiac arrest (OHCA) secondary to trauma.

METHODS:The CanAm Pediatric Cardiac Arrest Study Group is a collaboration of researchers in the United States and Canada sharing a common goal to improve survival outcomes for pediatric cardiac arrest. This was a prospective, multicenter, observational study. Twelve months of consecutive data were collected from emergency medical services (EMS), fire, and inpatient records from 2000 to 2003 for all OHCAs secondary to trauma in patients aged ≤18 years in 36 urban and suburban communities supporting advanced life support (ALS) programs. Eligible patients were apneic and pulseless and received chest compressions in the field. The primary outcome was survival to discharge. Secondary measures included return of spontaneous circulation (ROSC), survival to hospital admission, and 24-hour survival.

RESULTS:The study included 123 patients. The median patient age was 7.3 years (interquartile range [IQR] 6.0-17.0). The patient population was 78.1% male and 59.0% African American, 20.5% Hispanic, and 15.7% white. Most cardiac arrests occurred in residential (47.1%) or street/highway (37.2%) locations. Initial recorded rhythms were asystole (59.3%), pulseless electrical activity (29.1%), and ventricular fibrillation/tachycardia (3.5%). The majority of cardiac arrests were unwitnessed (49.5%), and less than 20% of patients received chest compressions by bystanders. The median (IQR) call-to-arrival interval was 4.9 (3.1-6.5) minutes and the on-scene interval was 12.3 (8.4-18.3) minutes. Blunt and penetrating traumas were the most common mechanisms (34.2% and 25.2%, respectively) and were associated with poor survival to discharge (2.4% and 6.5%, respectively). For all OHCA patients, 19.5% experienced ROSC in the field, 9.8% survived the first 24 hours, and 5.7% survived to discharge. Survivors had triple the rate of bystander cardiopulmonary resuscitation (CPR) than nonsurvivors (42.9% vs. 15.2%). Unlike patients sustaining blunt trauma or strangulation/hanging, most post-cardiac arrest patients who survived the first 24 hours after penetrating trauma or drowning were discharged alive. Drowning (17.1% of cardiac arrests) had the highest survival-to-discharge rate (19.1%).

CONCLUSIONS:The overall survival rate for OHCA in children after trauma was low, but some trauma mechanisms are associated with better survival rates than others. Most OHCA in children is preventable, and education and prevention strategies should focus on those overrepresented populations and high-risk mechanisms to improve mortality.

1. Epidemiology of out-of hospital pediatric cardiac arrest due to trauma
Prehosp Emerg Care, 2012 vol. 16 (2) pp. 230-236
2. Outcome from paediatric cardiac arrest associated with trauma
Resuscitation. 2007 Oct;75(1):29-34

咽反射是沒用的 – just as we thought

The painful dogma of “GCS ≤8 = intubate” is nicely challenged by the A&E Academic Unit at Prince of Wales Hospital in Hong Kong, who provide some further evidence that patients with a higher GCS may have absent airway protective reflexes, and patients with a lower GCS may have intact reflexes.


AIM: To describe the relationship of gag and cough reflexes to Glasgow coma score (GCS) in Chinese adults requiring critical care.

METHOD: Prospective observational study of adult patients requiring treatment in the trauma or resuscitation rooms of the Emergency Department, Prince of Wales Hospital, Hong Kong. A long cotton bud to stimulate the posterior pharyngeal wall (gag reflex) and a soft tracheal suction catheter were introduced through the mouth to stimulate the laryngopharynx and elicit the cough reflex. Reflexes were classified as normal, attenuated or absent.

RESULTS: A total of 208 patients were recruited. Reduced gag and cough reflexes were found to be significantly related to reduced GCS (p=0.014 and 0.002, respectively). Of 33 patients with a GCS≤8, 12 (36.4%) had normal gag reflexes and 8 (24.2%) had normal cough reflexes. 23/62 (37.1%) patients with a GCS of 9-14 had absent gag reflexes, and 27 (43.5%) had absent cough reflexes. In patients with a normal GCS, 22.1% (25/113) had absent gag reflexes and 25.7% (29) had absent cough reflexes.

CONCLUSIONS: Our study has shown that in a Chinese population with a wide range of critical illness (but little trauma or intoxication), reduced GCS is significantly related to gag and cough reflexes. However, a considerable proportion of patients with a GCS≤8 have intact airway reflexes and may be capable of maintaining their own airway, whilst many patients with a GCS>8 have impaired airway reflexes and may be at risk of aspiration. This has important implications for airway management decisions.

What is the relationship between the Glasgow coma scale and airway protective reflexes in the Chinese population?
Resuscitation. 2011 Jul 23. [Epub ahead of print]
Related post: Do all comatose patients need intubation?

Oxygen therapy for asthma can elevate CO2

Patients with acute exacerbations of asthma randomised to receive high concentration oxygen therapy showed a greater rise in CO2 than those who received titrated oxygen to keep SpO2 > 93%.
This study has a few weaknesses but raises an interesting challenge to the dogma of high flow oxygen (and oxygen driven nebulisers) for all acute asthma exacerbations.
The suggested main mechanism for the elevation in CO2 is worsening ventilation/perfusion mismatching as a result of the release of hypoxic pulmonary vasoconstriction and a consequent increase in physiological dead space. The authors remind us that this has been demonstrated in other studies on asthma and acute COPD exacerbations. The authors infer that high concentration oxygen therapy may therefore potentially increase the PaCO2 across a range of respiratory conditions with abnormal gas exchange due to ventilation/perfusion mismatching
Some of the weaknesses include lack of blinding, recruiting fewer patients than planned, and changing their primary outcome variable after commencing the study (which the authors are honest about) from absolute CO2 to increase in CO2 (since it was apparent on preliminary analysis of the first few patients that presenting CO2 was the primary determinant of subsequent CO2). Furthermore, the CO2 was measured from a transcutaneous device as opposed to the true ‘gold standard’ of arterial blood gas analysis, although good reasons are given for this.
Despite some of these drawbacks this study provides us with a further reminder that oxygen is a drug with some unwanted effects and therefore its dose needs to be individualised for the patient.


Background The effect on Paco(2) of high concentration oxygen therapy when administered to patients with severe exacerbations of asthma is uncertain.

Methods 106 patients with severe exacerbations of asthma presenting to the Emergency Department were randomised to high concentration oxygen (8 l/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93% and 95%) for 60 min. Patients with chronic obstructive pulmonary disease or disorders associated with hypercapnic respiratory failure were excluded. The transcutaneous partial pressure of carbon dioxide (Ptco(2)) was measured at 0, 20, 40 and 60 min. The primary outcome variable was the proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min.

Results The proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min was significantly higher in the high concentration oxygen group, 22/50 (44%) vs 10/53 (19%), RR 2.3 (95% CI 1.2 to 4.4, p<0.006). The high concentration group had a higher proportion of patients with a rise in Ptco(2) ≥8 mm Hg, 11/50 (22%) vs 3/53 (6%), RR 3.9 (95% CI 1.2 to 13.1, p=0.016). All 10 patients with a final Ptco(2) ≥45 mm Hg received high concentration oxygen therapy, and in five there was an increase in Ptco(2) ≥10 mm Hg.
Conclusion High concentration oxygen therapy causes a clinically significant increase in Ptco(2) in patients presenting with severe exacerbations of asthma. A titrated oxygen regime is recommended in the treatment of severe asthma, in which oxygen is administered only to patients with hypoxaemia, in a dose that relieves hypoxaemia without causing hyperoxaemia.

Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma
Thorax. 2011 Nov;66(11):937-41

Offensive medicine: CT before LP

I’m getting worn down by clinicians – often other specialists – who insist that CT imaging of the brain is mandatory prior to lumbar puncture in all patients. There is surely a subgroup of patients (especially young ones) in whom the benefit:harm balance of CT comes out in favour of NOT doing the imaging. In these cases, getting the scan is not ‘defensive medicine’ but ‘offensive medicine’ – offending the principle of primum non nocere. During ED shifts I have recently had to perform online searches in order to furnish colleagues and patients’ medically qualified relatives with printouts of the literature on this. This page is here to save me having to repeat those searches. Regarding the practice of performing a routine head CT prior to lumbar puncture to rule out risk of herniation:

  • Mass effect on CT does not predict herniation
  • Lack of mass effect on CT does not rule out raised ICP or herniation
  • Herniation has occurred in patients who did not undergoing lumbar puncture because of CT findings
  • Clinical predictors of raised ICP are more reliable than CT findings
  • CT may delay diagnosis and treatment of meningitis
  • Even in patients in whom LP may be considered contraindicated (cerebral abscess, mass effect on CT), complications from LP were rare in several studies

Best practice, it would seem, is the following

  • If you think CT will show a cause for the headache, do a CT
  • If a CT is indicated for other reasons (depressed conscious level, focal neurology), do a CT
  • If a GCS 15 patient is to undergo LP for suspected (or to rule out) meningitis, and they have a normal neurological exam (including fundi), and are not elderly or immunosuppressed, there is no need to do a CT first.
  • If you’re seriously worried about meningitis and are intent on getting a CT prior to LP, don’t let the imaging delay antimicrobial therapy.

Here are some useful references:

1. The CT doesn’t help

CT head before lumbar puncture in suspected meningitis BestBET evidence summary: In cases of suspected meningitis it is very unlikely that patients without clinical risk factors (immunocompromise/ history of CNS disease/seizures) or positive neurological findings will have a contraindication to lumbar puncture on their CT scan If CT scan is deemed to be necessary, administration of antibiotics should not be delayed. BestBETS website

Computed Tomography of the Head before Lumbar Puncture in Adults with Suspected Meningitis Much cited NEJM paper from 2001 which concludes: “In adults with suspected meningitis, clinical features can be used to identify those who are unlikely to have abnormal findings on CT of the headN Engl J Med. 2001 Dec 13;345(24):1727-33 Full Text

Cranial CT before Lumbar Puncture in Suspected Meningitis Correspondence in 2002 NEJM including study of 75 patients with pneumococcal meningitis: CT cannot rule out risk of herniation Cranial CT before Lumbar Puncture in Suspected Meningitis N Engl J Med. 2002 Apr 18;346(16):1248-51 Full Text

2. The CT may harm

Cancer risk from CT Paucis verbis card, from the wonderful Academic Life in EM

3. Guidelines say CT is not always needed

National (UK) guidelines on meningitis (community acquired meningitis in the immunocompetent host) available from meningitis.org. , including this box:

Practice Guidelines for the Management of Bacterial Meningitis These 2004 guidelines from the Infectious Diseases Society of America provide the following table listing the recommended criteria for adult patients with suspected bacterial meningitis who should undergo CT prior to lumbar puncture:

Clin Infect Dis. (2004) 39 (9): 1267-1284 Full text

4. This is potentially even more of an issue with paediatric patients

Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma

An excellent summary of the above mentioned issues presented in a paediatric context, including the following:

On initial consideration a cranial CT would seem to be an appropriate and potentially useful diagnostic study for confirming the diagnosis of cerebral herniataion. The fallacy in this assessment has been emphasized by the finding that no clinically significant CT abnormalities are found that are not suspected on clinical assessments. Further, as previously noted, a normal CT examination may be found at about the time of a fatal herniation. Thus, the practical usefulness of a cranial CT in the majority of pediatric patients is limited to those rare patients whose increased ICP is secondary to mass lesions, not in the initial approach to acute meningitis.

Pediatrics. 2003 Sep;112(3 Pt 1):e174-6 Full Text

The last words should go to Dr Brad Spellberg, who in response to the IDSA’s guidelines wrote an excellent letter summarising much of the evidence at the time, confessed:

Why do we persist in using the CT scan for this purpose, despite the lack of supportive data? I am as guilty of this practice as anyone else, and the reason is simple: I am a chicken.

Clin Infect Dis. (2005) 40 (7): 1061 Full Text

Lateral trauma position

Image from sjtrem.com - click for original

The tradition of transporting trauma patients to hospital in a supine position may not be the safest approach in obtunded patients with unprotected airways. The ‘solution’ of having them on an extrication board (backboard / long spine board) to enable rolling them to one side in the event of vomiting may not be practicable for limited crew numbers.
The Norwegians have been including the option of the lateral trauma position in their pre-hospital trauma life support training for some years now.
A questionnaire study demonstrates that this method has successfully been adopted by Norwegian EMS systems.
The method of application is described as:

  • Check airways (look, listen, feel).
  • Apply chin lift/jaw thrust, suction if needed.
  • Apply stiff neck collar.
  • If the patient is unresponsive, but has spontaneous respiration: Roll patient to lateral/recovery position while maintaining head/neck position.
  • Roll to side that leaves the patient facing outwards in ambulance coupé.
  • Transfer to ambulance stretcher (Scoop-stretcher, log-roll onto stretcher mattress, or use multiple helpers, lifting by patient’s clothing).
  • Support head, secure with three belts (across legs, over hip, over shoulder)
  • Manual support of head, supply oxygen, observation, suction, BVM (big valve mask) ventilation when needed.

Different options for supporting the head in the lateral position, according to questionnaire responders, include:

  • putting padding under the head, such as a pillow or similar item (81%)
  • a combination of padding and putting the head on the lower arm (7%)
  • rest the head on the lower arm alone (10%)
  • rest the head on the ground (<1%)

 


BACKGROUND: Trauma patients are customarily transported in the supine position to protect the spine. The Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) principles clearly give priority to airways. In Norway, the lateral trauma position (LTP) was introduced in 2005. We investigated the implementation and current use of LTP in Norwegian Emergency Medical Services (EMS).

METHODS: All ground and air EMS bases in Norway were included. Interviews were performed with ground and air EMS supervisors. Questionnaires were distributed to ground EMS personnel.

RESULTS: Of 206 ground EMS supervisors, 201 answered; 75% reported that LTP is used. In services using LTP, written protocols were present in 67% and 73% had provided training in LTP use. Questionnaires were distributed to 3,025 ground EMS personnel. We received 1,395 (46%) valid questionnaires. LTP was known to 89% of respondents, but only 59% stated that they use it. Of the respondents using LTP, 77% reported access to written protocols. Flexing of the top knee was reported by 78%, 20% flexed the bottom knee, 81% used under head padding. Of 24 air EMS supervisors, 23 participated. LTP is used by 52% of the services, one of these has a written protocol and three arrange training.

CONCLUSIONS: LTP is implemented and used in the majority of Norwegian EMS, despite little evidence as to its possible benefits and harms. How the patient is positioned in the LTP differs. More research on LTP is needed to confirm that its use is based on evidence that it is safe and effective.

The lateral trauma position: What do we know about it and how do we use it? A cross-sectional survey of all Norwegian emergency medical services
Scand J Trauma Resusc Emerg Med. 2011 Aug 4;19:45
Open Access Full Text

Why I don't give vasopressors in sepsis

It’s become popular to use the term ‘vasopressors’ or just ‘pressors’ when noradrenaline/norepinephrine or even (in some places still) dopamine are given. I have resisted this trend and continue to use the term ‘vasoactive’ drugs, on the basis that the effects they produce (and that we may desire) are not limited to a pure alpha adrenergic effect on vascular tone, but they have effects on heart rate and contractility too (as well as preload through venous effects). If you don’t believe me about noradrenaline/norepinephrine, then check out one of my favourite critical care papers of all time: the CAT study.
There are of course real pressors out there – phenylephrine acts on alpha receptors, as does methoxamine. Metaraminol predominantly acts on alpha receptors but does also cause some release of noradrenaline/norepinephrine.
Why is this important? All these drugs will fix hypotension, right? Yes, they should. However should blood pressure be our main treatment goal? What we’re really interested in is organ perfusion, which depends on regional blood flow to vital organs. It’s possible that a drug could fix the measured blood pressure and give a nice ‘macroscopic’ number, while at the same time reducing cardiac output and adversely affecting regional blood flow to organs through local vasoconstrictive effects. My view is that this is more likely with pure ‘pressors’ (like phenylephrine), which is why I avoid them in septic shock and opt for catecholamine infusions (noradrenaline/norepinephrine).
This is important in my practice setting of retrieval medicine, where, prior to interfacility transport, physicians might sometimes be tempted to ‘push pressors’ peripherally rather than insert a central venous catheter and commence a catecholamine infusion. While the former approach might be more expeditious and make the vital signs chart look pretty, one wonders about what effect this is having on tissue oxygen delivery.
A fascinating review of papers on pressor physiology1 suggests these agents have the following effects:

  • conflicting data on changes in myocardial perfusion
  • increase both left and right heart afterload
  • decrease venous compliance with the potential to increase venous return although the impact of this on cardiac output is controversial
  • controversial effect on cerebral bloodflow
  • decrease bloodflow to the kidneys
  • adverse affects on gastrointestinal tract bloodflow


abstract1
Phenylephrine and methoxamine are direct-acting, predominantly α(1) adrenergic receptor (AR) agonists. To better understand their physiologic effects, we screened 463 articles on the basis of PubMed searches of “methoxamine” and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Both methoxamine and phenylephrine increase cardiac afterload via several mechanisms, including increased vascular resistance, decreased vascular compliance, and disadvantageous alterations in the pressure waveforms produced by the pulsatile heart. Although pure α(1) agonists increase arterial blood pressure, neither animal nor human studies have ever shown pure α(1)-agonism to produce a favorable change in myocardial energetics because of the resultant increase in myocardial workload. Furthermore, the cost of increased blood pressure after pure α(1)-agonism is almost invariably decreased cardiac output, likely due to increases in venous resistance. The venous system contains α(1) ARs, and though stimulation of α(1) ARs decreases capacitance and may transiently increase venous return, this gain may be offset by changes in afterload, venous compliance, and venous resistance. Data on the effects of α(1) stimulation in the central nervous system show conflicting changes, while experimental animal data suggest that renal blood flow is reduced by α(1)-agonists, and both animal and human data suggest that gastrointestinal perfusion may be reduced by α(1) tone.

A review of clinical articles2 reveals few evidence-based indications for true pressors. Possible situations where they may be of benefit include intraoperative hypotension, aortic stenosis, during cyanotic episodes in Tetralogy of Fallot, and some obstetric situations. In the setting of sepis, phenylephrine has been compared with noradrenaline in which an initial pilot study found a statistically significant reduction in creatinine clearance and increase in arterial lactate after initiating the phenylephrine infusion. However a subsequent randomised controlled comparison of phenylephrine with noradrenaline/norepinephrine did not show differences in cardiopulmonary performance, global oxygen transport, or regional hemodynamics, although there were only 16 patients in each group3.


abstract2
Phenylephrine is a direct-acting, predominantly α(1) adrenergic receptor agonist used by anesthesiologists and intensivists to treat hypotension. A variety of physiologic studies suggest that α-agonists increase cardiac afterload, reduce venous compliance, and reduce renal bloodflow. The effects on gastrointestinal and cerebral perfusion are controversial. To better understand the effects of phenylephrine in a variety of clinical settings, we screened 463 articles on the basis of PubMed searches of “methoxamine,” a long-acting α agonist, and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Phenylephrine has been studied as an antihypotensive drug in patients with severe aortic stenosis, as a treatment for decompensated tetralogy of Fallot and hypoxemia during 1-lung ventilation, as well as for the treatment of septic shock, traumatic brain injury, vasospasm status-postsubarachnoid hemorrhage, and hypotension during cesarean delivery. In specific instances (critical aortic stenosis, tetralogy of Fallot, hypotension during cesarean delivery) in which the regional effects of phenylephrine (e.g., decreased heart rate, favorable alterations in Q(p):Q(s) ratio, improved fetal oxygen supply:demand ratio) outweigh its global effects (e.g., decreased cardiac output), phenylephrine may be a rational pharmacologic choice. In pathophysiologic states in which no regional advantages are gained by using an α(1) agonist, alternative vasopressors should be sought.

These review articles reinforce my own bias against the use of pure pressors in septic shock, although clearly more clinical research is needed. I am inclined to agree with the reviewers’ concluding statement:
…in all clinical settings, phenylephrine reduces cardiac output, and in most clinical settings has been shown to significantly increase LV afterload. Thus, only in instances in which its regional effects are thought to outweigh its global effects should phenylephrine be used for the treatment of hypotension.
1. The physiologic implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):284-96
2. The clinical implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):297-304
3. Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial
Crit Care. 2008;12(6):R143
Full Text available here

Normal heart and respiratory rates in children


A large review has established normal ranges of heart rate and respiratory rate in children from birth to 18 years of age. Some of the results differed markedly from some existing ranges quoted, such as in the Advanced Paediatric Life Support Course.

BACKGROUND: Although heart rate and respiratory rate in children are measured routinely in acute settings, current reference ranges are not based on evidence. We aimed to derive new centile charts for these vital signs and to compare these centiles with existing international ranges.

METHODS: We searched Medline, Embase, CINAHL, and reference lists for studies that reported heart rate or respiratory rate of healthy children between birth and 18 years of age. We used non-parametric kernel regression to create centile charts for heart rate and respiratory rate in relation to age. We compared existing reference ranges with those derived from our centile charts.

FINDINGS: We identified 69 studies with heart rate data for 143,346 children and respiratory rate data for 3881 children. Our centile charts show decline in respiratory rate from birth to early adolescence, with the steepest fall apparent in infants under 2 years of age; decreasing from a median of 44 breaths per min at birth to 26 breaths per min at 2 years. Heart rate shows a small peak at age 1 month. Median heart rate increases from 127 beats per min at birth to a maximum of 145 beats per min at about 1 month, before decreasing to 113 beats per min by 2 years of age. Comparison of our centile charts with existing published reference ranges for heart rate and respiratory rate show striking disagreement, with limits from published ranges frequently exceeding the 99th and 1st centiles, or crossing the median.

INTERPRETATION: Our evidence-based centile charts for children from birth to 18 years should help clinicians to update clinical and resuscitation guidelines.

Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies
Lancet. 2011 Mar 19;377(9770):1011-8

Central lines in coagulopathic patients

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

Tympanic monitoring for targeted temperature management

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

Hyperkalaemia dogmalysis


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: