Life-saving medicine
The British Thoracic Society / SIGN Guidelines on asthma have been updated for 2011. There don’t seem to be any modificiations to the sections on acute severe asthma which were updated in 2009 and blogged here, although the treatment algorithms seem to be presented in a slightly different format and therefore are reproduced here:
Management of acute severe asthma in adults in hospital
Management of acute asthma in children in hospital
This paper is an excellent review article citing the cogent relevant evidence for optimal preoxygenation prior to RSI in the critically ill patient. The evidence has been interpreted with pertinent recommendations by two of the world’s heavy hitters in emergency medicine – Scott Weingart and Rich Levitan. If you can get a full text copy of the paper, laminate Figure 3 (‘Sequence of Preoxygenation and Prevention of Desaturation‘) and stick it to the wall in your resus bay!
The points covered include:
Preoxygenation and Prevention of Desaturation During Emergency Airway Management
Ann Emerg Med. 2011 Nov 1. [Epub ahead of print]
[EXPAND Abstract]
Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lung pathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airway against aspiration. Tracheal intubation is often required before the complete information needed to assess the risk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chest radiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk of critical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniques reviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, and passive apneic oxygenation.
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Being female or having atypical pain is associated with delays to diagnosis of aortic dissection. This recent study also shows that arrival in a non-tertiary hospital is another factor associated with delayed diagnosis. Patients may present with fever, abdominal pain, or heart failure (due to acute aortic insufficiency) that lead the clinician down alternative diagnostic algorithms. The strongest factors associated with operative delay were prolonged time from presentation to diagnosis, race other than white, and history of coronary artery bypass surgery.
Worth remembering at this point that in 2010 the AHA published Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease
Background- In acute aortic dissection, delays exist between presentation and diagnosis and, once diagnosed, definitive treatment. This study aimed to define the variables associated with these delays.
Methods and Results- Acute aortic dissection patients enrolled in the International Registry of Acute Aortic Dissection (IRAD) between 1996 and January 2007 were evaluated for factors contributing to delays in presentation to diagnosis and in diagnosis to surgery. Multiple linear regression was performed to determine relative delay time ratios (DTRs) for individual correlates. The median time from arrival at the emergency department to diagnosis was 4.3 hours (quartile 1-3, 1.5-24 hours; n=894 patients) and from diagnosis to surgery was 4.3 hours (quartile 1-3, 2.4-24 hours; n=751). Delays in acute aortic dissection diagnosis occurred in female patients; those with atypical symptoms that were not abrupt or did not include chest, back, or any pain; patients with an absence of pulse deficit or hypotension; or those who initially presented to a nontertiary care hospital (all P<0.05). The largest relative DTRs were for fever (DTR=5.11; P<0.001) and transfer from nontertiary hospital (DTR=3.34; P<0.001). Delay in time from diagnosis to surgery was associated with a history of previous cardiac surgery, presentation without abrupt or any pain, and initial presentation to a nontertiary care hospital (all P<0.001). The strongest factors associated with operative delay were prolonged time from presentation to diagnosis (DTR=1.35; P<0.001), race other than white (DTR=2.25; P<0.001), and history of coronary artery bypass surgery (DTR=2.81; P<0.001).
Conclusions- Improved physician awareness of atypical presentations and prompt transport of acute aortic dissection patients could reduce crucial time variables.
Correlates of Delayed Recognition and Treatment of Acute Type A Aortic Dissection: The International Registry of Acute Aortic Dissection (IRAD)
Circulation. 2011 Nov 1;124(18):1911-1918
In short, an ICU team decided to reduce and where possible eliminate the use of high chloride fluids including 0.9% saline and Gelofusine and replace with lower chloride fluids, mainly Ringer’s Lactate (Hartmann’s solution).
It is known that saline causes a metabolic acidosis by elevating chloride and reducing the strong ion difference. This results in a normal anion gap, hyperchloraemic acidosis. The clinical significance of this is uncertain, but the iatrogenic acidosis is often confused by clinicians as a sign of severe illness, especially those clinicians that don’t look at the chloride or anion gap.
Not surprisingly, changing the fluid policy resulted in less acidosis (and also less hypernatraemia). There was however an increase in severe alkalaemia. The study was not designed to look at patient oriented outcomes.
My observations are:
The authors point to an additional finding:
Furthermore, our results suggest that routine use of lactate fluids such as Hartmann’s or Ringer’s lactate is associated with a detectable iatrogenic increase in lactate in the first 48 hrs after ICU admission, when, presumably, lactate clearance is less effective.
While this is interesting, the mean [SD] lactate values in the two groups were 1.79 [1.57] and 2.05 [1.61] so while statistically significant I suspect this is clinically irrelevant. And as we know, the cause of a raised lactate is more of a concern than the fact of a raised lactate
A significant benefit of the change in fluid policy was a signficant cost saving, largely due to the omission of Gelofusine.
For me, this study reassures me that my current practice of preferring Ringer’s Lactate to Saline in the resuscitation setting is likely to minimise iatrogenic acidosis without significantly elevating the lactate, in a population rarely afflicted by significant alkalaemia.
The biochemical effects of restricting chloride-rich fluids in intensive care
Crit Care Med. 2011 Nov;39(11):2419-2424
[EXPAND Abstract]
Objective: To determine the biochemical effects of restricting the use of chloride-rich intravenous fluids in critically ill patients.
Design: Prospective, open-label, before-and-after study.
Setting: University-affiliated intensive care unit.
Patients: A cohort of 828 consecutive patients admitted over 6 months from February 2008 and cohort of 816 consecutive patients admitted over 6 months from February 2009.
Interventions: We collected biochemical and fluid use data during standard practice without clinician awareness. After a 6-month period of education and preparation, we restricted the use of chloride-rich fluids (0.9% saline [Baxter, Sydney, Australia], Gelofusine [BBraun, Melsungen, Germany], and Albumex 4 [CSL Bioplasma, Melbourne, Australia]) in the intensive care unit and made them available only on specific intensive care unit specialist prescription.
Measurements and Main Results: Saline prescription decreased from 2411 L in the control group to 52 L in the intervention group (p < .001), Gelofusine from 538 to 0 L (p < .001), and Albumex 4 from 269 to 80 L (p < .001). As expected, Hartmann’s lactated solution prescription increased from 469 to 3205 L (p < .001), Plasma-Lyte from 65 to 160 L (p < .05), and chloride-poor Albumex 20 from 87 to 268 L (p < .001). After intervention, the incidence of severe metabolic acidosis (standard base excess5 mEq/L) and alkalemia (pH >7.5) with an increase from 25.4% to 32.8% and 10.5% to 14.7%, respectively (p < .001). The time-weighted mean chloride level decreased from 104.9 ± 4.9 to 102.5 ± 4.6 mmol/L (p < .001), whereas the time-weighted mean standard base excess increased from 0.5 ± 4.5 to 1.8 ± 4.7 mmol/L (p < .001), mean bicarbonate from 25.3 ± 4.0 to 26.4 ± 4.1 mmol/L (p < .001) and mean pH from 7.40 ± 0.06 to 7.42 ± 0.06 (p < .001). Overall fluid costs decreased from $15,077 (U.S.) to $3,915.
Conclusions: In a tertiary intensive care unit in Australia, restricting the use of chloride-rich fluids significantly affected electrolyte and acid-base status. The choice of fluids significantly modulates acid-base status in critically ill patients.
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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?
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
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.
The European Medicines Agency’s Instructions are:
At this stage physicians should not initiate treatment with Xigris in new patients and should stop ongoing treatment
The US Food and Drug Administration’s Instructions are:
Xigris treatment should not be started in new patients. Xigris treatment should be stopped in patients being treated with Xigris.
All remaining Xigris product should be returned to the supplier from whom it was purchased.
The UK Intensive Care Society’s Announcement contains a link to Eli Lilly’s press release.
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.
Outcomes of patients undergoing early sepsis resuscitation for cryptic shock compared with overt shock
Resuscitation. 2011 Oct;82(10):1289-1293
[EXPAND Click to read abstract]
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.
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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.
Randomised study of hypertonic saline infusion during resuscitation from out-of-hospital cardiac arrest
Resuscitation. 2011 Sep 19. [Epub ahead of print]
[EXPAND Click to read abstract]
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.
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We know that subarachnoid haemorrhage (SAH) can cause cardiac arrest. Some questions we may have about this are:
Questions
- 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:
Answers
- 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.
1. Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest
Resuscitation. 2011 Oct;82(10):1294-7
[EXPAND Abstract]
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.
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2. Assessing outcome of out-of-hospital cardiac arrest due to subarachnoid hemorrhage using brain CT during or immediately after resuscitation
Signa Vitae 2010; 5(2): 21 – 24 Full Text
[EXPAND Abstract]
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.
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3. Subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest: A prospective computed tomography study
Resuscitation. 2009 Sep;80(9):977-80
[EXPAND Abstract]
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.
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4. Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest
Resuscitation. 2001 Oct;51(1):27-32
[EXPAND Abstract]
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.
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5. Cranial computed tomography in the resuscitated patient with cardiac arrest
Am J Emerg Med. 2009 Jan;27(1):63-7
[EXPAND Abstract]
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.
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