Targeted ICP reduction in TBI

A South American randomised controlled trial has demonstrated no improvement in mortality when traumatic brain injured patients had therapy targeted at keeping intracranial pressure below or equal to 20 mmHg as measured by an intraparenchymal monitor. The control group’s management was guided by neurologic examination and serial CT imaging(1).

Editorialist Dr Ropper summarises what we should do with this information well(2):

“[The authors]…do not advocate abandoning the treatment of elevated intracranial pressure any more than the authors of studies on wedge pressure reject the administration of fluid boluses in the treatment of shock”

BACKGROUND

Intracranial-pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently, but the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed.

METHODS
We conducted a multicenter, controlled trial in which 324 patients 13 years of age or older who had severe traumatic brain injury and were being treated in intensive care units (ICUs) in Bolivia or Ecuador were randomly assigned to one of two specific protocols: guidelines-based management in which a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring group) or a protocol in which treatment was based on imaging and clinical examination (imaging–clinical examination group). The primary outcome was a composite of survival time, impaired consciousness, and functional status at 3 months and 6 months and neuropsychological status at 6 months; neuropsychological status was assessed by an examiner who was unaware of protocol assignment. This composite measure was based on performance across 21 measures of functional and cognitive status and calculated as a percentile (with 0 indicating the worst performance, and 100 the best performance).

RESULTS
There was no significant between-group difference in the primary outcome, a composite measure based on percentile performance across 21 measures of functional and cognitive status (score, 56 in the pressure-monitoring group vs. 53 in the imaging–clinical examination group; P=0.49). Six-month mortality was 39% in the pressure-monitoring group and 41% in the imaging–clinical examination group (P=0.60). The median length of stay in the ICU was similar in the two groups (12 days in the pressure-monitoring group and 9 days in the imaging–clinical examination group; P=0.25), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging–clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P=0.002). The distribution of serious adverse events was similar in the two groups.

CONCLUSIONS
For patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination

1. A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury
N Eng J Med 367;26:2471-2381 Full Text

2. Brain in a Box
N Eng J Med DOI: 10.1056/NEJMe1212289 Full Text

Magnesium doesn’t improve SAH outcome

A multicentre RCT showed intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.
Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial
Lancet 2012 July 7; 380(9836): 44–49 Free full text
Click to read abstract

Hypothermia after long down times

You receive a patient resuscitated from cardiac arrest to a perfusing rhythm in your emergency department. History suggests a long ‘down time’: There was a ten minute duration of ‘no-flow’ (time from collapse to the start of resuscitation attempts).

Would this make you more likely or less likely to initiate targeted temperature management (TTM) and cool the patient to the recommended 32-34 degrees?

A recent study supports the suggestion that a longer no-flow time is associated with greater odds of survival with TTM compared with no TTM, than patients with shorter no-flow times. In other words, cooling the patient is more likely to make a difference in the ‘long down time’ patient, even though the overall survival in that group is obviously less.

Aim Mild therapeutic hypothermia has shown to improve long-time survival as well as favorable functional outcome after cardiac arrest. Animal models suggest that ischemic durations beyond 8 min results in progressively worse neurologic deficits. Based on these considerations, it would be obvious that cardiac arrest survivors would benefit most from mild therapeutic hypothermia if they have reached a complete circulatory standstill of more than 8 min.

Methods In this retrospective cohort study we included cardiac arrest survivors of 18 years of age or older suffering a witnessed out-of-hospital cardiac arrest, which remain comatose after restoration of spontaneous circulation. Data were collected from 1992 to 2010. We investigated the interaction of ‘no-flow’ time on the association between post arrest mild therapeutic hypothermia and good neurological outcome. ‘No-flow’ time was categorized into time quartiles (0, 1–2, 3–8, >8 min).

Results One thousand-two-hundred patients were analyzed. Hypothermia was induced in 598 patients. In spite of showing a statistically significant improvement in favorable neurologic outcome in all patients treated with mild therapeutic hypothermia (odds ratio [OR]: 1.49; 95% confidence interval [CI]: 1.14–1.93) this effect varies with ‘no-flow’ time. The effect is significant in patients with ‘no-flow’ times of more than 2 min (OR: 2.72; CI: 1.35–5.48) with the maximum benefit in those with ‘no-flow’ times beyond 8 min (OR: 6.15; CI: 2.23–16.99).

Conclusion The beneficial effect of mild therapeutic hypothermia increases with cumulative time of complete circulatory standstill in patients with witnessed out-of-hospital cardiac arrest.

The beneficial effect of mild therapeutic hypothermia depends on the time of complete circulatory standstill in patients with cardiac arrest
Resuscitation. 2012 May;83(5):596-601

Hyperosmolar therapy

A great review article from the New England Journal of Medicine summaries the current knowledge base regarding the use of hypertonic saline and mannitol for raised intracranial pressure.

Hyperosmolar Therapy for Raised Intracranial Pressure 
N Engl J Med. 2012 Aug 23;367(8):746-52

Full text access is only available to New England Journal subscribers, but I’ve summarised some of the interesting bits in a short quiz you can take to test your knowledge. Just 13 True/False questions.

If you liked the quiz and want to use it at your local teaching sessions, here’s a Keynote Version and a PowerPoint Version

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

Is there nothing ketamine can’t do?

As well as the benefits of cardiovascular stability, maintenance of cerebral perfusion pressure, possibly lowering ICP and providing other neuroprotective benefits, ketamine may have other advantages. These are reviewed in a British Journal of Anaesthesia article from which I’ve selected those benefits of interest to practitioners of emergency medicine and critical care.

 

 

Additional Beneficial Effects of Ketamine

• the dysphoric, or ‘emergence’ reactions associated with ketamine may be reduced by pre-administration or co-administration of sedatives, such as benzodiazepines, propofol, dexmedetomidine, or droperidol.
• ketamine potentiates opioid analgesia in multiple settings, reducing opioid total dose and in some groups of patients reducing postoperative desaturation
• ketamine has possible anti-inflammatory effects demonstrated in some types of surgical patients
• ketamine may prevent awareness, recall, or both during general anaesthesia

Ketamine: new uses for an old drug?
Br J Anaesth. 2011 Aug;107(2):123-6

CRASH-2 and head injury

The overall effect of the antifibrinolytic drug tranexamic acid on outcome from major trauma was assessed in the CRASH-2 trial, reported here and here. Its effect on a nested cohort of 270 patients from the trial who had traumatic brain injury has now been published¹.

Previous evaluation in nontraumatic subarachnoid haemorrhage patients showed tranexamic acid to be associated with cerebral ischaemia, whereas in CRASH-2 (in which a lower dose of tranexamic acid was used) there was a trend to fewer ischaemic lesions as well as smaller haematoma growth and decreased mortality. None of these outcomes were statistically significant so further research is warranted.

An accompanying editorial² states:

…the CRASH-2 study also justifies a re-evaluation of the possible benefit of low dose short term TXA in patients with other types of intracranial haemorrhage. Many patients with aneurysmal subarachnoid haemorrhage still have to wait for one or two days before the aneurysm is occluded. In addition, at least 30% of patients with spontaneous intracerebral haemorrhage experience substantial haematoma growth in the first 24 hours after the onset of the haemorrhage. As well as the CRASH-2 trial we therefore need new trials investigating short course low dose TXA in patients with aneurysmal subarachnoid haemorrhage and intracerebral haemorrhage.

It looks like considerable enthusiasm for this drug will be around for a while. I look forward to more outcome data, particularly in regard to this challenging group of patients with traumatic and non-traumatic intracranial bleeding.

OBJECTIVE: To assess the effect of tranexamic acid (which reduces bleeding in surgical patients and reduces mortality due to bleeding in trauma patients) on intracranial haemorrhage in patients with traumatic brain injury.

METHODS: A nested, randomised, placebo controlled trial. All investigators were masked to treatment allocation. All analyses were by intention to treat. Patients 270 adult trauma patients with, or at risk of, significant extracranial bleeding within 8 hours of injury, who also had traumatic brain injury.

INTERVENTIONS: Patients randomly allocated to tranexamic acid (loading dose 1 g over 10 minutes, then infusion of 1 g over 8 hours) or matching placebo.

MAIN OUTCOME MEASURES: Intracranial haemorrhage growth (measured by computed tomography) between hospital admission and then 24-48 hours later, with adjustment for Glasgow coma score, age, time from injury to the scans, and initial haemorrhage volume.

RESULTS: Of the 133 patients allocated to tranexamic acid and 137 allocated to placebo, 123 (92%) and 126 (92%) respectively provided information on the primary outcome. All patients provided information on clinical outcomes. The mean total haemorrhage growth was 5.9 ml (SD 26.8) and 8.1 mL (SD 29.2) in the tranexamic acid and placebo groups respectively (adjusted difference -3.8 mL (95% confidence interval -11.5 to 3.9)). New focal cerebral ischaemic lesions occurred in 6 (5%) patients in the tranexamic acid group versus 12 (9%) in the placebo group (adjusted odds ratio 0.51 (95% confidence interval 0.18 to 1.44)). There were 14 (11%) deaths in the tranexamic acid group and 24 (18%) in the placebo group (adjusted odds ratio 0.47 (0.21 to 1.04)).

CONCLUSIONS: This trial shows that neither moderate benefits nor moderate harmful effects of tranexamic acid in patients with traumatic brain injury can be excluded. However, the analysis provides grounds for further clinical trials evaluating the effect of tranexamic acid in this population

1. Effect of tranexamic acid in traumatic brain injury: a nested randomised, placebo controlled trial (CRASH-2 Intracranial Bleeding Study)
BMJ. 2011 Jul 1;343:d379 (free text available)

2. Tranexamic acid for traumatic brain injury
BMJ. 2011 Jul 1;343:d3958

How much oxygen after ROSC?

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%

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

Targeted temperature management guidelines

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

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