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.
Pharmaceutical company Eli Lilly has announced the withdrawal of its severe sepsis drug activated protein C, or drotrecogin alfa (proprietary name Xigris). This is because the PROWESS-SHOCK study, now complete, showed no benefit in its primary endpoint of 28 day mortality when compared with placebo in septic shock patients. There was also no benefit in a subgroup of patients with protein C deficiency, and no significant increased risk of severe bleeding.
Patients with severe sepsis and an elevated lactate who appear to be normotensive had a mortality similar to those presenting with hypotension. This is demonstrated in a new study on patients who were recruited to a study I have reported before.
The so-called ‘cryptic shock’ group was defined by a systolic BP of at least 90 mmHg, suggesting to me not so much that normotension and hypotension are prognostically equivalent, but that we should perhaps redefine hypotension in sepsis, as we should probably be doing in trauma. Alternatively (and preferably), the BP should be interpreted in the context of what is known to be or likely to be normal for that patient. For example, a systolic BP of 105 mmHg in a 75 year old male would be be ringing serious alarm bells for me in a febrile patient, and I would be working them up for severe sepsis from the start. Interestingly in this study, the cryptic shock group had a higher proportion of patients with diabetes and/or end stage renal disease – diagnoses one would expect to be associated with hypertension – and the median (and IQR) systolic BP in this group was 108 (92, 126). So, although this shock may have been ‘cryptic’ as opposed to ‘overt’ by the definition applied in the paper (a cut off of 90 mmHg), it is likely that some of the patients in the cryptic group were hypotensive compared with their usual blood pressure.
These observations do not detract from a key message the authors include in their discussion, with which I wholeheartedly agree:
“These data highlight the need to screen patients for signs of occult hypoperfusion, and given the high mortality rate associated with an elevated serum lactate, also suggest that patients with biochemical evidence of inadequate oxygen delivery despite normal blood pressure should be included in early sepsis resuscitation pathways.”
This paper makes an important contribution to the sepsis literature by warning against the dismissal of an elevated serum lactate in the setting of apparent haemodynamic stability as being a less acutely ill patient than one presenting with overt hypotension. It provides a reminder to check the lactate in patients with infection and signs of systemic inflammatory response, since this may provide the only early evidence of hypoperfusion.
Introduction We sought to compare the outcomes of patients with cryptic versus overt shock treated with an emergency department (ED) based early sepsis resuscitation protocol.
Methods Pre-planned secondary analysis of a large, multicenter ED-based randomized controlled trial of early sepsis resuscitation. All subjects were treated with a quantitative resuscitation protocol in the ED targeting 3 physiological variables: central venous pressure, mean arterial pressure and either central venous oxygen saturation or lactate clearance. The study protocol was continued until all endpoints were achieved or a maximum of 6 h. Outcomes data of patients who were enrolled with a lactate ≥4 mmol/L and normotension (cryptic shock) were compared to those enrolled with sustained hypotension after fluid challenge (overt shock). The primary outcome was in-hospital mortality.
Results A total of 300 subjects were enrolled, 53 in the cryptic shock group and 247 in the overt shock group. The demographics and baseline characteristics were similar between the groups. The primary endpoint of in-hospital mortality was observed in 11/53 (20%, 95% CI 11–34) in the cryptic shock group and 48/247 (19%, 95% CI 15–25) in the overt shock group, difference of 1% (95% CI −10 to 14; log rank test p = 0.81).
Conclusion Severe sepsis with cryptic shock carries a mortality rate not significantly different from that of overt septic shock. These data suggest the need for early aggressive screening for and treatment of patients with an elevated serum lactate in the absence of hypotension.
I would like to share with you a message I received via email from a fellow EM/critical care doctor, the poetry of which touched me. I have Dr Lynch’s permission to reproduce it here (hyperlinks added by me). If you’re a doctor, paramedic, nurse, military medic, or any other hard-working link in the chain of resuscitation, I hope you are as inspired as I am by Dr Lynch’s reflections:
Hello there Dr Reid,
My name is Doug Lynch.
I’m an advanced trainee of too many Australasian generalist medical colleges (ACRRM, ACEM, CICM) and a perpetual student. (a bit like Chris Nickson without the intellect or talent)
I’ve completed a M.P.H.&T.M. (JCU), GC Emergency Health (Aeromedical Retrieval) (Monash) and a PGC Disaster Management & Refugee Health (JCU).
I work at present in Anaesthetics in outer metropolitan Melbourne (Getting a JCCA qualification) and as a locum with Adult Retrieval Victoria having been their first registrar a few years back.
Im not writing to ask you for a job! I’m off to work with Minh Le Cong et al in Cairns next year.
I’ve been benefitting from your website and I really wanted to say THANK YOU.
A trial by the ARDS Clinical Trials Network of pharmaconutrition for acute lung injury1 was stopped early for futility – outcomes were worse in the intervention group that received the enteral supplementation of n-3 fatty acids, γ-linolenic acid, and antioxidants. It had been hypothesised that the immunomodulatory effects of these supplements would provide clinical benefit in acute lung injury.
An accompanying editorial2 reports benefits of pharmaconutrition in other areas of critical care:
arginine-supplemented diets are associated with reduced infections and lengths of hospital stay in patients undergoing elective operations
glutamine-supplemented parenteral nutrition is associated with reduced infection and mortality in critically ill patients
antioxidant supplementation is associated with reduced mortality among critically ill patients with systemic inflammation.
Context The omega-3 (n-3) fatty acids docosahexaenoic acid and eicosapentaenoic acid, along with γ-linolenic acid and antioxidants, may modulate systemic inflammatory response and improve oxygenation and outcomes in patients with acute lung injury.
Objective To determine if dietary supplementation of these substances to patients with acute lung injury would increase ventilator-free days to study day 28.
Design, Setting, and Participants The OMEGA study, a randomized, double-blind, placebo-controlled, multicenter trial conducted from January 2, 2008, through February 21, 2009. Participants were 272 adults within 48 hours of developing acute lung injury requiring mechanical ventilation whose physicians intended to start enteral nutrition at 44 hospitals in the National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. All participants had complete follow-up.
Interventions Twice-daily enteral supplementation of n-3 fatty acids, γ-linolenic acid, and antioxidants compared with an isocaloric control. Enteral nutrition, directed by a protocol, was delivered separately from the study supplement.
Main Outcome Measure Ventilator-free days to study day 28.
Results The study was stopped early for futility after 143 and 129 patients were enrolled in the n-3 and control groups. Despite an 8-fold increase in plasma eicosapentaenoic acid levels, patients receiving the n-3 supplement had fewer ventilator-free days (14.0 vs 17.2; P = .02) (difference, −3.2 [95% CI, −5.8 to −0.7]) and intensive care unit–free days (14.0 vs 16.7; P = .04). Patients in the n-3 group also had fewer nonpulmonary organ failure–free days (12.3 vs 15.5; P = .02). Sixty-day hospital mortality was 26.6% in the n-3 group vs 16.3% in the control group (P = .054), and adjusted 60-day mortality was 25.1% and 17.6% in the n-3 and control groups, respectively (P = .11). Use of the n-3 supplement resulted in more days with diarrhea (29% vs 21%; P = .001).
Conclusions Twice-daily enteral supplementation of n-3 fatty acids, γ-linolenic acid, and antioxidants did not improve the primary end point of ventilator-free days or other clinical outcomes in patients with acute lung injury and may be harmful.
1. Enteral Omega-3 Fatty Acid, γ-Linolenic Acid, and Antioxidant Supplementation in Acute Lung Injury JAMA. 2011; 306:1574-1581
A newly published study examines pre-hospital hypertonic saline during CPR. A randomised trial compared 7.2% hypertonic saline / hydroxyethyl starch with hydroxyethyl starch alone in over 200 adult patients with non-traumatic out-of-hospital cardiac arrest. The volume infused was 2 ml /kg over 10 mins. All patients were resuscitated by the physicians of the Emergency Medical System (EMS) in Bonn, Germany.
There were no differences in survival to admission or discharge. There was a barely statistically significant increase in those survivors with higher cerebral performance categories (1 or 2) in the hypertonic saline group, inviting further study. The study was conducted from 2001 to 2004 (according to the 2000 CPR-Guidelines), so took an interestingly long time to see print.
Aim of the study Animal models of hypertonic saline infusion during cardiopulmonary resuscitation (CPR) improve survival, as well as myocardial and cerebral perfusion during CPR. We studied the effect of hypertonic saline infusion during CPR (Guidelines 2000) on survival to hospital admission and hospital discharge, and neurological outcome on hospital discharge.
Methods The study was performed by the EMS of Bonn, Germany, with ethical committee approval. Study inclusion criteria were non-traumatic out-of-hospital cardiac arrest, aged 18–80 years, and given of adrenaline (epinephrine) during CPR. Patients were randomly infused 2 ml kg−1 HHS (7.2% NaCl with 6% hydroxyethyl starch 200,000/0.5 [HES]) or HES over 10 min.
Results 203 patients were randomised between May 2001 and June 2004. After HHS infusion, plasma sodium concentration increased significantly to 162 ± 36 mmol l−1 at 10 min after infusion and decreased to near normal (144 ± 6 mmol l−1) at hospital admission. Survival to hospital admission and hospital discharge was similar in both groups (50/100 HHS vs. 49/103 HES for hospital admission, 23/100 HHS vs. 22/103 HES for hospital discharge). There was a small improvement in neurological outcome in survivors on discharge (cerebral performance category 1 or 2) in the HHS group compared to the HES group (13/100 HHS vs. 5/100 HES, p < 0.05, odds-ratio 2.9, 95% confidence interval 1.004–8.5).
Conclusion Hypertonic saline infusion during CPR using Guidelines 2000 did not improve survival to hospital admission or hospital discharge. There was a small improvement with hypertonic saline in the secondary endpoint of neurological outcome on discharge in survivors. Further adequately powered studies using current guidelines are needed.
We know that subarachnoid haemorrhage (SAH) can cause cardiac arrest. Some questions we may have about this are:
What proportion of out-of-hospital cardiac arrests (OOHCA) who achieve return of spontaneous circulation (ROSC) are caused by SAH?
What is the usual presenting arrest rhythm – VT/VF or non-shockable rhythms?
What is the outcome of these patients – do any survive?
Do they have other characteristic cardiac features, such as ECG or echo abnormalities?
Should we do a head CT on all survivors of out-of-hospital cardiac arrest of uncertain aetiology?
A recent Japanese article in Resuscitation1 is the third from that country to be published on the topic in three years, the other two2,3 coming from different centres and all demonstrating some consistent answers, as do papers published in recent years from Europe4 and North America5:
Rates of SAH in OOHCA patients who achieve ROSC and make it to CT range from 4-16% (even higher if other sources of intracranial haemorrhage are included).
Studies consistently demonstrate VT/VF to be very rare – PEA and asystole are by far the commonest presenting arrest rhythms.
Almost no patients with this presentation due to SAH survive to hospital discharge.
In the most recent study, all patients who survived long enough to get a 12 lead showed ST-T abnormalities and/or QT prolongation, although echocardiograms were mostly normal.
Rates of SAH in OOHCA patients who achieve ROSC seem to be sufficiently high to seriously consider head CT in these patients if there is no obvious alternate explanation for the arrest.
Background Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear.
Methods and results We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n = 2/8) or presumed cardiovascular aetiologies (22%, n = 23/101) (p < 0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities.
Conclusions The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.
Objectives. The clinical course and outcome of out-of-hospital cardiopulmonary arrest (OHCPA) due to subarachnoid hemorrhage (SAH) is unclear. The objective of this study is to clarify them.
Study design. Single- center, observational study. Setting. We usually perform a brain computed tomography (CT) in OHCPA patients who present without a clear etiology (42% of all OHCPA), such as trauma, to determine the cause of OHCPA and to guide treatment.
Patients. The study included OHCPA patients without a clear etiology, who were transferred to our center and who underwent a brain CT during resuscitation.
Methods of measurement. Patients’ records were reviewed; initial cardiac rhythm, existence of a witness and bystander cardiopulmonary resuscitation efforts (CPR) were compared with patients’ outcomes.
Results. Sixty-six patients were enrolled. 72.7% achieved return of spontaneous circulation (ROSC), 71.2% were admitted, 30.3% survived more than 7 days, and 9.1. survived-to-discharge. In 41 witnessed OHCPA, 87.8% obtained ROSC, 85.4% were admitted, and 14.6% survived-to-discharge. All survivors were witnessed. In 25 non-witnessed OHCPA, 48% obtained ROSC and were admitted, and no patients were discharged. Initial cardiac rhythm was ventricular fibrillation (VF), pulseless electrical activity (PEA) and asystole in 3.0%, 39.4%, and 47.0%. In 2 VF patients 50.0% survived-to- discharge, and there was no survivor with PEA or asystole.
Conclusion. This study shows a high rate of ROSC and admission in OHCPA patients with a SAH, and also reveals their very poor neurological outcome. We conclude that the detection of a SAH in OHCPA patients is important to determine the accurate frequency of SAH in this patient group and to guide appropriate treatment of all OHCPA patients.
Aim Aneurysmal subarachnoid haemorrhage (SAH) is a relatively common cause of out-of-hospital cardiac arrest (OHCA). Early identification of SAH-induced OHCA with the use of brain computed tomography (CT) scan obtained immediately after resuscitation may help emergency physicians make therapeutic decision as quickly as they can.
Methods During the 4-year observation period, brain CT scan was obtained prospectively in 142 witnessed non-traumatic OHCA survivors who remained haemodynamically stable after resuscitation. Demographics and clinical characteristics of SAH-induced OHCA survivors were compared with those with “negative” CT finding.
Results Brain CT scan was feasible with an average door-to-CT time of 40.0min. SAH was found in 16.2% of the 142 OHCA survivors. Compared with 116 survivors who were negative for SAH, SAH-induced OHCA survivors were significantly more likely to be female, to have experienced a sudden headache, and trended to have achieved return of spontaneous circulation (ROSC) prior to arrival in the emergency department less frequently. Ventricular fibrillation (VF) was significantly less likely to be seen in SAH-induced than SAH-negative OHCA (OR, 0.06; 95% CI, 0.01–0.46). Similarly, Cardiac Trop-T assay was significantly less likely to be positive in SAH-induced OHCA (OR, 0.08; 95% CI, 0.01–0.61).
Conclusion Aneurysmal SAH causes OHCA more frequently than had been believed. Immediate brain CT scan may particularly be useful in excluding SAH-induced OHCA from thrombolytic trial enrollment, for whom the use of thrombolytics is contraindicated. The low VF incidence suggests that VF by itself may not be a common cause of SAH-induced OHCA.
Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest.
Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features.
Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome.
Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.
Introduction The incidence of out-of-hospital and in-hospital cardiorespiratory arrest from all causes in the United States occurs not infrequently. Postresuscitation care should include the identification of the inciting arrest event as well as therapy tailored to support the patient and treat the primary cause of the decompensation. The application of one particular testing modality, cranial computed tomography (CT) of the head, has not yet been determined. We undertook an evaluation of the use of head CT in patients who were resuscitated from cardiac arrest.
Methods Prehospital (emergency medical services), ED, and hospital records were reviewed for patients of all ages with cardiorespiratory arrest over a 4-year period (July 1996-June 2000). Information regarding diagnosis, management, and outcome was recorded. The results of cranial CT, if performed, and any apparent resulting therapeutic changes were recorded. Patients with a known traumatic mechanism for the cardiorespiratory arrest were excluded.
Results A total of 454 patients (mean age 58.3 years with 60% male) with cardiorespiratory arrest were entered in the study with 98 (22%) individuals (mean age 58.5 years with 53% male) undergoing cranial CT. Arrest location was as follows: emergency medical services, 41 (42%); ED, 11 (11%); and hospital, 46 (47%). Seventy-eight (79%) patients demonstrated 111 CT abnormalities: edema, 35 (32%); atrophy, 24 (22%); extra-axial hemorrhage, 14 (13%); old infarct, 12 (11%); new infarct, 11 (10%); intraparenchymal hemorrhage, 6 (5%); skull fracture, 5 (4%); mass, 3 (2%); and foreign body, 1 (1%). Therapeutic and diagnostic alterations in care were made in 38 (39%) patients—35 abnormal and 3 normal CTs. The following alterations occurred: medication administration, 26; withdrawal of life support, 7; additional diagnostic study, 6; neurologic consultation, 6; and intracranial pressure monitoring. 4. No patient survived to discharge.
Conclusion In this subset of resuscitated patients with cardiac arrest, abnormalities on the head CT were not uncommon. Alterations in management did occur in those patients with abnormalities. The indications and impact of head CT in the population of resuscitated patients with cardiac arrest remain unknown, warranting further investigation.
A small study on normal volunteers examined reversal of the new oral anticoagulants, Rivaroxaban and Dabigatran.
Rivaroxaban is a Factor Xa inhibitor and Dabigatran is a direct thrombin inhibitor.
We should note that this was a study on the reversal of effects on various coagulation tests, not on reversal of bleeding, which is what we would be interested in for our ED/critical care patients.
Nevertheless, it’s helpful to note that prothrombin complex concentrate appeared to reverse the effects of Rivaroxaban, but not of Dabigatran.
Background Rivaroxaban and dabigatran are new oral anticoagulants that specifically inhibit factor Xa and thrombin, respectively. Clinical studies on the prevention and treatment of venous and arterial thromboembolism show promising results. A major disadvantage of these anticoagulants is the absence of an antidote in case of serious bleeding or when an emergency intervention needs immediate correction of coagulation. This study evaluated the potential of prothrombin complex concentrate (PCC) to reverse the anticoagulant effect of these drugs.
Methods and Results In a randomized, double-blind, placebo-controlled study, 12 healthy male volunteers received rivaroxaban 20 mg twice daily (n=6) or dabigatran 150 mg twice daily (n=6) for 2½ days, followed by either a single bolus of 50 IU/kg PCC (Cofact) or a similar volume of saline. After a washout period, this procedure was repeated with the other anticoagulant treatment. Rivaroxaban induced a significant prolongation of the prothrombin time (15.8±1.3 versus 12.3±0.7 seconds at baseline; P<0.001) that was immediately and completely reversed by PCC (12.8±1.0; P<0.001). The endogenous thrombin potential was inhibited by rivaroxaban (51±22%; baseline, 92±22%; P=0.002) and normalized with PCC (114±26%; P<0.001), whereas saline had no effect. Dabigatran increased the activated partial thromboplastin time, ecarin clotting time (ECT), and thrombin time. Administration of PCC did not restore these coagulation tests.
Conclusion Prothrombin complex concentrate immediately and completely reverses the anticoagulant effect of rivaroxaban in healthy subjects but has no influence on the anticoagulant action of dabigatran at the PCC dose used in this study.
In comatose survivors of cardiac arrest, myoclonus is considered a grave prognostic sign. The American Academy of Neurology stated in 20061 that:
After cardiac arrest, the following clinical findings accurately predict poor outcome;
myoclonus status epilepticus within the first 24 hours in patients with primary circulatory arrest
absence of pupillary responses within days 1 to 3 after CPR
absent corneal reflexes within days 1 to 3 after CPR
and absent or extensor motor responses after 3 days.
However in the age of targeted temperature management the presence and/or timing of these signs needs to be re-evaluated. It has been suggested that therapeutic hypothermia and sedation required for induced cooling might delay recovery of motor reactions up to 5–6 days after cardiac arrest. Now a series of three survivors of cardiac arrest who had massive myoclonus in the first four hours after return of spontaneous circulation (ROSC) is reported2, all of whom were treated with TTM and experienced good neurologic outcomes.
Early myoclonus in comatose survivors of cardiac arrest, even when it is not myoclonic status epilepticus (MSE), is considered a sign of severe global brain ischemia and has been associated with high rates of mortality and poor neurologic outcomes. We report on three survivors of primary circulatory cardiac arrests who had good neurologic outcomes (two patients with a CPC score=1 and one patient with a CPC score=2) after mild therapeutic hypothermia, despite exhibiting massive myoclonus within the first four hours after return of spontaneous circulation. The concept that early myoclonus heralds a uniformly poor prognosis may need to be reconsidered in the era of post-cardiac arrest mild therapeutic hypothermia.
1. Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology Neurology. 2006 Jul 25;67(2):203-10 Full Text