Category Archives: Acute Med

Acute care of the medically sick adult

Don't ignore the diastolic

Most of us are pretty good at spotting hypotension and activating help or initiating therapy.
But ‘hypotension’ in many practitioners’ minds refers to a low systolic blood pressure. Who pays serious attention to the diastolic blood pressure? A low diastolic in a sick patient to me is a warning sign that their mean arterial pressure (MAP) is – or will be – low. After all, we spend about twice as long in diastole as in systole, so the diastolic pressure contributes more to the MAP than does the systolic.
A recent study showed that a low diastolic BP was one of several factors predictive of cardiac arrest on hospital wards: the most accurate predictors were maximum respiratory rate, heart rate, pulse pressure index, and minimum diastolic BP. These factors were more predictive than some of the variables included in the commonly used Early Warning Scores that trigger an emergency review.
The ‘pulse pressure index’ examined in the study is the pulse pressure divided by the systolic blood pressure (ie. [SBP-DBP]/SBP) which of course will be higher with lower diastolic blood pressures.
Importantly, the authors point out:


“In addition, our findings suggest that for many patients there is ample time prior to cardiac arrest to provide potentially life-saving interventions.”

…suggesting that there is still room for improvement in the identification and management of patients at risk for cardiac arrest, as the NCEPOD report ‘Cardiac Arrest Procedures: Time to Intervene?’ also showed.
They also recommend:


“…although systolic BP is commonly used in rapid response team activation criteria, incorporation of pulse pressure, pulse pressure index, or diastolic BP in place of systolic BP into the predictive model may be superior.”

Perhaps this may remind all of us to keep an eye on the diastolic as well as systolic BP when patients first present to us, and to include the importance of recognising diastolic hypotension in the teaching we provide our medical, paramedical and nursing students.

Predicting Cardiac Arrest on the Wards: A Nested Case-Control Study
Chest. 2012 May;141(5):1170-6 Free Full Text here
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Background: Current rapid response team activation criteria were not statistically derived using ward vital signs, and the best vital sign predictors of cardiac arrest (CA) have not been determined. In addition, it is unknown when vital signs begin to accurately detect this event prior to CA.

Methods: We conducted a nested case-control study of 88 patients experiencing CA on the wards of a university hospital between November 2008 and January 2011, matched 1:4 to 352 control subjects residing on the same ward at the same time as the case CA. Vital signs and Modified Early Warning Scores (MEWS) were compared on admission and during the 48 h preceding CA.

Results: Case patients were older (64 ± 16 years vs 58 ± 18 years; P = .002) and more likely to have had a prior ICU admission than control subjects (41% vs 24%; P = .001), but had similar admission MEWS (2.2 ± 1.3 vs 2.0 ± 1.3; P = .28). In the 48 h preceding CA, maximum MEWS was the best predictor (area under the receiver operating characteristic curve [AUC] 0.77; 95% CI, 0.71-0.82), followed by maximum respiratory rate (AUC 0.72; 95% CI, 0.65-0.78), maximum heart rate (AUC 0.68; 95% CI, 0.61-0.74), maximum pulse pressure index (AUC 0.61; 95% CI, 0.54-0.68), and minimum diastolic BP (AUC 0.60; 95% CI, 0.53-0.67). By 48 h prior to CA, the MEWS was higher in cases (P = .005), with increasing disparity leading up to the event.

Conclusions: The MEWS was significantly different between patients experiencing CA and control patients by 48 h prior to the event, but includes poor predictors of CA such as temperature and omits significant predictors such as diastolic BP and pulse pressure index.

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COPD and heart disease interactions

Ischaemic heart disease (IHD) and chronic obstructive pulmonary disease (COPD) often affect the same patient; in fact, more than one-third of patients with angiography-proven IHD also have COPD on spirometry(1).
A recent study suggests COPD exacerbations in patients with IHD were associated with longer (5 more days) recovery times and suffered more severe breathlessness between exacerbations(2).
An accompanying editorial highlights some important points:

  • Patients admitted with COPD exacerbations are more susceptible to myocardial infarction during the admission.
  • Infective COPD exacerbations may contribute to heart failure through systemic inflammation, autonomic activation, and increased fluid in the lung. Lung infection can increase ventilation/perfusion mismatch and increased work of breathing, further straining the heart.
  • Heart failure can be very difficult to diagnose during a COPD exacerbation because cough, dyspnoea and wheeze are common to both disorders. Physical examination may not be discriminatory, and chest radiography is insensitive to milder degrees of heart failure.

The authors recommed a high index of suspicion combined with consideration of biomarkers (BNP or pro-BNP) and imaging such as echocardiography or even nuclear medicine scans, cardiac MRI, and cardiac catheterisation.
So, next time you’re managing a COPD exacerbation, ask yourself:

  • Could there be concomitant heart failure contributing to symptoms?
  • If not, is the patient at risk of cardiac events during this admission, for which we need to be vigilant?
  • Do I need to consider additional laboratory (BNP) or imaging (echo) investigations? Remember BNP may be elevated in pneumonia and other non-cardiac critical illness, although a normal BNP rules out heart failure.
  • Should I add empiric anti-failure therapy to the acute treatment regimen?
  • If there is combined COPD exacerbation and heart failure, are there any conflicting priorities in therapy (eg. the pros and cons of beta-agonists, anticholinergics, and steroids)?

1. The complex relationship between ischemic heart disease and COPD exacerbations
Chest. 2012 Apr;141(4):837-8
2. The impact of ischemic heart disease on symptoms, health status, and exacerbations in patients with COPD
Chest. 2012 Apr;141(4):851-7
[EXPAND Click to read abstract]


BACKGROUND: Comorbid ischemic heart disease (IHD) is a common and important cause of morbidity and mortality in patients with COPD. The impact of IHD on COPD in terms of a patient’s health status, exercise capacity, and symptoms is not well understood.

METHODS: We analyzed stable-state data of 386 patients from the London COPD cohort between 1995 and 2009 and prospectively collected exacerbation data in those who had completed symptom diaries for ≥ 1 year.

RESULTS: Sixty-four patients (16.6%) with IHD had significantly worse health status as measured by the St. George Respiratory Questionnaire (56.9 ± 18.5 vs 49.1 ± 19.0, P = .003), and a larger proportion of this group reported more severe breathlessness in the stable state, with a Medical Research Council dyspnea score of ≥ 4 (50.9% vs 35.1%, P = .029). In subsets of the sample, stable patients with COPD with IHD had a higher median (interquartile range [IQR]) serum N-terminal pro-brain natriuretic peptide concentration than those without IHD (38 [15, 107] pg/mL vs 12 [6, 21] pg/mL, P = .004) and a lower exercise capacity (6-min walk distance, 225 ± 89 m vs 317 ± 85 m; P = .002). COPD exacerbations were not more frequent in patients with IHD (median, 1.95 [IQR, 1.20, 3.12] vs 1.86 (IQR, 0.75, 3.96) per year; P = .294), but the median symptom recovery time was 5 days longer (17.0 [IQR, 9.8, 24.2] vs 12.0 [IQR, 8.0, 18.0]; P = .009), resulting in significantly more days per year reporting exacerbation symptoms (median, 35.4 [IQR, 13.4, 60.7] vs 22.2 [IQR, 5.7, 42.6]; P = .028). These findings were replicated in multivariate analyses allowing for age, sex, FEV(1), and exacerbation frequency where applicable.

CONCLUSIONS: Comorbid IHD is associated with worse health status, lower exercise capacity, and more dyspnea in stable patients with COPD as well as with longer exacerbations but not with an increased exacerbation frequency.

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Life, limb and sight-saving procedures

The challenge of competence in the face of rarity

by Dr Cliff Reid FCEM, and Dr Mike Clancy FCEM
This article is to be published in Emergency Medicine Journal (EMJ), and is reproduced here with permission of the BMJ Group.
Emergency physicians require competence in procedures which are required to preserve life, limb viability, or sight, and whose urgency cannot await referral to another specialist.
Some procedures that fit this description, such as tracheal intubation after neuromuscular blockade in a hypoxaemic patient with trismus, or placement of an intercostal catheter in a patient with a tension pneumothorax, are required sufficiently frequently in elective clinical practice that competence can be acquired simply by training in emergency department, intensive care, or operating room environments.
Other procedures, such as resuscitative thoracotomy, may be required so infrequently that the first time a clinician encounters a patient requiring such an intervention may be after the completion of specialist training, or in the absence of colleagues with prior experience in the technique.
Some techniques that might be considered limb or life saving may be too technically complex to acquire outside specialist surgical training programs. Examples are damage control laparotomy and limb fasciotomy. One could however argue that these are rarely too urgent to await arrival of the appropriate specialist.
The procedures which might fit the description of a time­‐critical life, limb, or sight saving procedure in which it is technically feasible to acquire competence within or alongside an emergency medicine residency, and that cannot await another specialist, include:

  • limb amputation for the entrapped casualty with life-­threatening injuries;
  • escharotomy for a burns patient with compromised ventilation or limb perfusion;

 
Defining competence for emergency physicians
A major challenge is the acquisition of competence in the face of such clinical rarity. One medical definition of competence is ‘the knowledge, skill, attitude or combination of these, that enables one to effectively perform the activities of a particular occupation or role to the standards expected’[1]; in essence the ability to perform to a standard, but where are these standards defined?
If we look to the curricula which are used to assess specialist emergency physicians in several English-­speaking nations, all the procedures in the short list above are included, although no one single nation’s curriculum includes the entire list (Table 1).

 
So an emergency physician is expected to be able to conduct these procedures, and a competent emergency physician effectively performs them to the ‘standards’ expected. It appears then that the question is not whether emergency physicians should perform them, but to what standard should they be trained? Only then can the optimal approach to training be decided.
There are convincing arguments that even after minimal training the performance of these procedures by emergency physicians is justifiable:

  • All the abovementioned interventions could be considered to carry 100% morbidity or mortality if not performed, with some chance of benefit whose magnitude depends on the timeliness of intervention. In some cases that risk is quantifiable: cardiac arrest due to penetrating thoracic trauma has 100% mortality if untreated, but an 18% survival to discharge rate, with a high rate of neurologically intact survivors, if performed by prehospital emergency medicine doctors in the field according to defined indications[2] and using a simple operative procedure[3]. In this extreme clinical example, no further harm to the patient can result from the procedure but a chance of supreme benefit exists. Thus, the ethical requirements of beneficence and non-­maleficence are both met even in the circumstance of very limited training for the procedure. It is hard to conceive of many other circumstances in medicine where the benefit:harm ratio approaches infinity.
  • The procedures in question are technically straightforward and can be executed without specialist equipment in non-­operating room environments. These factors appear to be underappreciated by non-­emergency specialist opponents of emergency physician-­provided thoracotomy whose practice and experience is likely to be predominantly operating room-­based[4].
  • Some of the procedures are recommended or mandated by official guidelines[5], raising the possibility of medicolegal consequences of failure to perform them.
  • The procedures are time-­critical and cannot await the arrival of an alternative specialist not already present. Simple pragmatism dictates that emergency physicians be trained to provide the necessary interventions.

 
The challenge of training
So how does one best train for these procedures? High volume trauma experience provided by a registrar term with the London Helicopter Emergency Medical Service or at a South African trauma centre will be an option for a very limited subset of trainees. Alternative training can be provided using simulation, animal labs, and cadaver labs, without risk to patients or requiring dedicated surgical specialty attachments.
Simulation manikins are not yet available for all the procedures mentioned, and lack realistic operable tissue. Human cadaver labs and live animal training bring administrative, legal, ethical and financial challenges that may be prohibitive to time and cash‐limited training schemes, or be less available to the ‘already trained’ providers in existing consultant posts. Even excellent focused cadaver-­based courses such as the Royal College of Surgeons’ Definitive Surgical Trauma Skills course[6] may not be appropriate for the emergency medicine environment: on such a course one of the authors (CR) was publicly castigated by a cardiothoracic surgeon instructor for inexpert suture technique during the resuscitative thoracotomy workshop, despite the former having successfully performed the procedure on several occasions ‘in the field’ without need of elaborate needlework.
An additional training challenge is that of metacompetence: the decision and ability to apply the competence at the right time. In the light of the relative technical simplicity of the practical procedures under discussion, this may indeed be the greatest challenge. Both authors can recount sad tales of colleagues failing to provide indicated life-­saving interventions despite being technically capable of intervening. Reasons for reticence include ‘I haven’t been properly trained’, and ‘I wouldn’t feel supported if it went wrong’.
 
Where do we go from here?
We have presented clinical, ethical, practical, and medicolegal arguments in favour of emergency physicians providing these procedures. Collectively, the emergency medicine curricula of English-­speaking nations mandate competence in them. The relative technical simplicity and overwhelming benefit:harm equation obviate the need to match the competence of a surgical subspecialist; these factors suggest training can be limited in time and cost as long as the metacompetences of ‘decision to act and knowing when to act’ are taught, simulated, and tested.
While we should capitalise on the technical expertise of surgical colleagues in the training situation, it is imperative that emergency physicians appreciative of the emergency department environment and equipment are directly involved in translating this training to emergency medicine practice. The rarity of the situations requiring these procedures requires that training should be revisited on a regular basis, preferably in the context of local departmental simulation in order to optimise equipment and teamwork preparation.
Finally, the College of Emergency Medicine needs to make it clear to its members and fellows that these procedures lie unquestionably within the domain of emergency medicine, and that emergency physicians are supported in performing them to the best of their abilities with limited training when circumstances dictate that this in the best interests of preserving a patient’s life, limb, or sight.
 
 
References
1. British Medical Association. Competency-­based assessment discussion paper for consultants, May 2008. http://www.bma.org.uk/employmentandcontracts/doctors_performance/1_app raisal/CompetencyBasedAssessment.jsp Accessed 22nd March 2012
2. Davies GE, Lockey DJ. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician‐Performed Resuscitation Procedure That Can Yield Good Results. J Trauma. 2011;70(5):E75-­8
3. Wise D, Davies G, Coats T, et al. Emergency thoracotomy: “how to do it”. Emerg Med J. 2005; 22(1):22–24 Free full text
4. Civil I. Emergency room thoracotomy: has availability triumphed over advisability in the care of trauma patients in Australasia? Emerg Med Australas. 2010;22(4):257­‐9
5. Soar J, Perkins GD, Abbas G, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation. 2010;81(10):1400-­33 Full text
6. Definitive Surgical Trauma Skills course. http://www.rcseng.ac.uk/courses/course-search/dsts.html Accessed 22nd March 2012
7. http://www.collemergencymed.ac.uk/Training-Exams/Curriculum/Curriculum%20from%20August%202010/ Accessed 22nd March 2012
8. http://www.eusem.org/cms/assets/1/pdf/european_curriculum_for_em-aug09-djw.pdf accessed 17 May 2012
9. The Model of the Clinical Practice of Emergency Medicine http://www.abem.org/PUBLIC/portal/alias__Rainbow/lang__en-%C2%AD%20US/tabID__4223/DesktopDefault.aspx Accessed 22nd March 2012
10. http://rcpsc.medical.org/residency/certification/objectives/emergmed_e.pdf Accessed 22nd March 2012
11. http://www.acem.org.au/media/publications/15_Fellowship_Curriculum.pdf accessed 17 May 2012
12. http://www.collegemedsa.ac.za/Documents/doc_173.pdf accessed 17 May 2012
Life, limb and sight-saving procedures-the challenge of competence in the face of rarity
Emerg Med J. 2012 Jul 16. [Epub ahead of print]

Unknown unknowns and pleural effusions

There are plenty of unknowns when it comes to management of pleural effusions on the ICU, which led to a paper with an eye-catching title1.
Mechanically ventilated patients frequently have pleural effusions detected by radiological investigations. Whether to drain them is a common conundrum for intensivists. A systematic review of the literature showed that drainage often improves oxygenation and has a low complication rate2.
While it may have the added advantage of assisting diagnosis and guiding therapy, there is a paucity of literature demonstrating improved patient-orientated outcomes with the routine drainage of pleural effusions in ventilated patients.
 
1. A pseudo-Rumsfeldian approach to pleural effusions in mechanically ventilated patients.
Crit Care. 2011 Mar 11;15(2):132 Free Full Text
2. Utility and safety of draining pleural effusions in mechanically ventilated patients: a systematic review and meta-analysis.
Crit Care. 2011;15(1):R46 Free Full Text
[EXPAND Click to read abstract]

INTRODUCTION: Pleural effusions are frequently drained in mechanically ventilated patients but the benefits and risks of this procedure are not well established.

METHODS: We performed a literature search of multiple databases (MEDLINE, EMBASE, HEALTHSTAR, CINAHL) up to April 2010 to identify studies reporting clinical or physiological outcomes of mechanically ventilated critically ill patients who underwent drainage of pleural effusions. Studies were adjudicated for inclusion independently and in duplicate. Data on duration of ventilation and other clinical outcomes, oxygenation and lung mechanics, and adverse events were abstracted in duplicate independently.

RESULTS: Nineteen observational studies (N = 1,124) met selection criteria. The mean PaO2:FiO2 ratio improved by 18% (95% confidence interval (CI) 5% to 33%, I2 = 53.7%, five studies including 118 patients) after effusion drainage. Reported complication rates were low for pneumothorax (20 events in 14 studies including 965 patients; pooled mean 3.4%, 95% CI 1.7 to 6.5%, I2 = 52.5%) and hemothorax (4 events in 10 studies including 721 patients; pooled mean 1.6%, 95% CI 0.8 to 3.3%, I2 = 0%). The use of ultrasound guidance (either real-time or for site marking) was not associated with a statistically significant reduction in the risk of pneumothorax (OR = 0.32; 95% CI 0.08 to 1.19). Studies did not report duration of ventilation, length of stay in the intensive care unit or hospital, or mortality.

CONCLUSIONS: Drainage of pleural effusions in mechanically ventilated patients appears to improve oxygenation and is safe. We found no data to either support or refute claims of beneficial effects on clinically important outcomes such as duration of ventilation or length of stay.

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Upper GI bleeding guideline update

The UK’s National Institute for Health and Clinical Excellence has issued updated guidance on the management of acute upper gastrointestinal bleeding.
The initial resuscitation section recommends haemostatic blood product resuscitation for unstable patients in line with massive transfusion practice in trauma.
A risk assessment is recommended using the Blatchford score pre-endoscopy at first assessment, and the full Rockall score after endoscopy.
Consider early discharge for patients with a pre-endoscopy Blatchford score of 0.
In non-varicesal haemorrhage, acid-suppression drugs (proton pump inhibitors or H2-receptor antagonists) before endoscopy are not recommended.
Terlipressin should be given to patients with suspected variceal bleeding at presentation and continued until definitive haemostasis has been achieved, or after 5 days, unless there is another indication for its use.
Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding.

Click image to go to interactive pathway on NICE website

National Institute for Health and Clinical Excellence: CG141 Acute upper GI bleeding: NICE guideline
http://guidance.nice.org.uk/CG141/NICEGuidance/pdf/English

Confidential stuff – in hospital cardiac arrests

A new report describes room for improvement in the care of cardiac arrest patients in hospital1.
The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) aimed to describe variability and identify remediable factors in the process of care of adult patients who receive resuscitation in hospital, including factors which may affect the decision to initiate the resuscitation attempt, the outcome and the quality of care following the resuscitation attempt, and antecedents in the preceding 48 hours that may have offered opportunities for intervention to prevent cardiac arrest.
Data were captured over a 14 day study period in late 2010 from UK hospitals, and were reviewed by an expert panel.
The summary is available here. I have picked out some findings of interest:

  • An adequate history was not recorded in 70/489 cases (14%) and clinical examination was incomplete at first contact in 117/479 cases (24%).
  • Appreciation of the severity of the situation was lacking in 74/416 (18%).
  • Timely escalation to more senior doctors was lacking in 61/347 (18%).
  • Decisions about CPR status were documented in the admission notes in 44/435 cases (10%). This is despite the high incidence of chronic disease and almost one in four cases being expected to be rapidly fatal on admission.
  • Where time to first consultant review could be identified it was more than 12 hours in 95/198 cases (48%).
  • Appreciation of urgency, supervision of junior doctors and the seeking of advice from senior doctors were rated ‘poor’ by Advisors.
  • Physiological instability was noted in 322/444 (73%) of patients who subsequently had a cardiac arrest.
  • Advisors considered that warning signs for cardiac arrest were present in 344/462 (75%) of cases. These warning signs were recognised poorly, acted on infrequently, and escalated to more senior doctors infrequently.
  • There was no evidence of escalation to more senior staff in patients who had multiple reviews.
  • Advisors considered that the cardiac arrest was predictable in 289/454 (64%) and potentially avoidable in 156/413 (38%) of cases.
  • The Advisors reported problems during the resuscitation attempt in 91/526 cases (17%). Of these, 36/91 were associated with airway management.
  • Survival to discharge after in-hospital cardiac arrest was 14.6% (85/581).
  • Only 9/165 (5.5%) patients who had an arrest in asystole survived to hospital discharge.
  • Survival to discharge after a cardiac arrest at night was much lower than after a cardiac arrest during the day time (13/176; 7.4% v 44/218; 20.1%).

 
In the opinion of the treating clinicians, earlier treatment of the problem and better monitoring may have improved outcome:

Compare these findings with a smaller scale confidential enquiry into the care of patients who ended up in intensive care units, published exactly 14 years ago by McQuillan et al2:
“The main causes of suboptimal care were failure of organisation, lack of knowledge, failure to appreciate clinical urgency, lack of supervision, and failure to seek advice.”
One of the co-authors of the McQuillan study, Professor Gary Smith , has spent years improving training in and awareness of the importance of recognition of critical illness, and pioneered the “ALERT” Course TM: Acute Life-threatening Emergencies, Recognition, and Treatment. Professor Smith provides commentary on the NCEPOD report and the slides are available here, including a reminder of the ‘Chain of Prevention’3.

It’s a shame these issues remain a problem but it is heartening to see NCEPOD tackle this important topic and provide recommendations that UK hospitals will have to act upon. It is further credit to the vision of Pete McQuillan, Gary Smith and their colleague Bruce Taylor (another co-author of the 1998 confidential inquiry). These guys opened my eyes to the world of critical care and trained me for 18 months on their ICU, which remains a beacon site for critical care expertise and training. Without their inspiration, I may not have ended up in emergency medicine-critical care and I doubt very much that Resus.ME would exist.

1. Cardiac Arrest Procedures: Time to Intervene? (2012)
National Confidential Enquiry into Patient Outcome and Death (NCEPOD)
2. Confidential inquiry into quality of care before admission to intensive care
BMJ 1998 Jun 20;316(7148):1853-8 Free Full Text
[EXPAND Click to read abstract]


OBJECTIVE: To examine the prevalence, nature, causes, and consequences of suboptimal care before admission to intensive care units, and to suggest possible solutions.

DESIGN: Prospective confidential inquiry on the basis of structured interviews and questionnaires.

SETTING: A large district general hospital and a teaching hospital.

SUBJECTS: A cohort of 100 consecutive adult emergency admissions, 50 in each centre.

MAIN OUTCOME MEASURES: Opinions of two external assessors on quality of care especially recognition, investigation, monitoring, and management of abnormalities of airway, breathing, and circulation, and oxygen therapy and monitoring.

RESULTS: Assessors agreed that 20 patients were well managed (group 1) and 54 patients received suboptimal care (group 2). Assessors disagreed on quality of management of 26 patients (group 3). The casemix and severity of illness, defined by the acute physiology and chronic health evaluation (APACHE II) score, were similar between centres and the three groups. In groups 1, 2, and 3 intensive care mortalities were 5 (25%), 26 (48%), and 6 (23%) respectively (P=0.04) (group 1 versus group 2, P=0.07). Hospital mortalities were 7 (35%), 30 (56%), and 8 (31%) (P=0.07) and standardised hospital mortality ratios (95% confidence intervals) were 1.23 (0.49 to 2.54), 1.4 (0.94 to 2.0), and 1.26 (0.54 to 2.48) respectively. Admission to intensive care was considered late in 37 (69%) patients in group 2. Overall, a minimum of 4.5% and a maximum of 41% of admissions were considered potentially avoidable. Suboptimal care contributed to morbidity or mortality in most instances. The main causes of suboptimal care were failure of organisation, lack of knowledge, failure to appreciate clinical urgency, lack of supervision, and failure to seek advice.

CONCLUSIONS: The management of airway, breathing, and circulation, and oxygen therapy and monitoring in severely ill patients before admissionto intensive care units may frequently be suboptimal. Major consequences may include increased morbidity and mortality and requirement forintensive care. Possible solutions include improved teaching, establishment of medical emergency teams, and widespread debate on the structure and process of acute care.

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3. In-hospital cardiac arrest: is it time for an in-hospital ‘chain of prevention’?
Resuscitation. 2010 Sep;81(9):1209-11
[EXPAND Click to read abstract]


The ‘chain of survival’ has been a useful tool for improving the understanding of, and the quality of the response to, cardiac arrest for many years. In the 2005 European Resuscitation Council Guidelines the importance of recognising critical illness and preventing cardiac arrest was highlighted by their inclusion as the first link in a new four-ring ‘chain of survival’. However, recognising critical illness and preventing cardiac arrest are complex tasks, each requiring the presence of several essential steps to ensure clinical success. This article proposes the adoption of an additional chain for in-hospital settings–a ‘chain of prevention’–to assist hospitals in structuring their care processes to prevent and detect patient deterioration and cardiac arrest. The five rings of the chain represent ‘staff education’, ‘monitoring’, ‘recognition’, the ‘call for help’ and the ‘response’. It is believed that a ‘chain of prevention’ has the potential to be understood well by hospital clinical staff of all grades, disciplines and specialties, patients, and their families and friends. The chain provides a structure for research to identify the importance of each of the various components of rapid response systems.

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Is diastolic worse than systolic dysfunction in sepsis?

Septic myocardial dysfunction is a well recognised contributor to shock in sepsis but for many of us we assume this to be gross systolic impairment. Interestingly a recent study highlights that patients with severe sepsis and septic shock frequently have diastolic dysfunction1. They found that diastolic dysfunction was the strongest independent predictor of early mortality, even after adjusting for the APACHE-II score and other predictors of mortality.
In this study, 9.1% of severe sepsis/septic shock patients had isolated systolic dysfunction, 14.1% had combined systolic and diastolic dysfunction, and 38% had isolated diastolic dysfunction.
Importantly, the authors point out that although diastolic dysfunction is associated with age, hypertension, diabetes mellitus, and ischaemic heart disease, diastolic dysfunction is a stronger independent predictor of mortality than age and the other co-morbidities. However, a limitation of the study acknowledged by the authors is that it did not include follow-up echocardiography examinations, so we do not know whether sepsis was responsible for a transient diastolic dysfunction or whether the observed diastolic dysfunction was a pre-existing condition.
Both troponin and NT-ProBNP elevations also predicted mortality.
Want to know how to measure diastolic dysfunction? These authors measured mitral annular early-diastolic peak velocity, or the e’-wave (called ‘e prime’). It is a way of seeing how fast myocardial tissue relaxes in diastole, and if its peak velocity is slow (in this case < 8cm/s) there is diastolic dysfunction. We measure speed using Doppler, and in this case we’re looking at the speed of heart tissue (as opposed to the blood cells within the heart chambers) so we do ‘Tissue Doppler Imaging’, or TDI. You need an echo machine with pulsed-wave Doppler, and you need to be able to get an apical view. This is explained really nicely here2 but if you don’t have the time or the echopassion to read a whole article on TDI watch this one minute video (BY emergency physicians FOR emergency physicians!) on diastology, where TDI measurement of e’ is shown from 45 seconds into the video.
For reference, there is some more detail on diastolic function measurements at the Echobasics site.

If you think you can cope with any more of this level of awesomeness and want these geniuses to talk to you from your smartphone in the ED then get the free One Minute Ultrasound app for Android or Apple devices.


AIMS: Systolic dysfunction in septic shock is well recognized and, paradoxically, predicts better outcome. In contrast, diastolic dysfunction is often ignored and its role in determining early mortality from sepsis has not been adequately investigated.

METHODS AND RESULTS: A cohort of 262 intensive care unit patients with severe sepsis or septic shock underwent two echocardiography examinations early in the course of their disease. All clinical, laboratory, and survival data were prospectively collected. Ninety-five (36%) patients died in the hospital. Reduced mitral annular e’-wave was the strongest predictor of mortality, even after adjusting for the APACHE-II score, low urine output, low left ventricular stroke volume index, and lowest oxygen saturation, the other independent predictors of mortality (Cox’s proportional hazards: Wald = 21.5, 16.3, 9.91, 7.0 and 6.6, P< 0.0001, <0.0001, 0.002, 0.008, and 0.010, respectively). Patients with systolic dysfunction only (left ventricular ejection fraction ≤50%), diastolic dysfunction only (e’-wave <8 cm/s), or combined systolic and diastolic dysfunction (9.1, 40.4, and 14.1% of the patients, respectively) had higher mortality than those with no diastolic or systolic dysfunction (hazard ratio = 2.9, 6.0, 6.2, P= 0.035, <0.0001, <0.0001, respectively) and had significantly higher serum levels of high-sensitivity troponin-T and N-terminal pro-B-type natriuretic peptide (NT-proBNP). High-sensitivity troponin-T was only minimally elevated, whereas serum levels of NT-proBNP were markedly elevated [median (inter-quartile range): 0.07 (0.02-0.17) ng/mL and 5762 (1001-15 962) pg/mL, respectively], though both predicted mortality even after adjusting for highest creatinine levels (Wald = 5.8, 21.4 and 2.3, P= 0.015, <0.001 and 0.13).

CONCLUSION: Diastolic dysfunction is common and is a major predictor of mortality in severe sepsis and septic shock.

1. Diastolic dysfunction and mortality in severe sepsis and septic shock
Eur Heart J. 2012 Apr;33(7):895-903
2. A clinician’s guide to tissue Doppler imaging
Circulation. 2006 Mar 14;113(10):e396-8 Free Full Text

Thrombolytic Therapy in Unstable Patients with PE

Most of us would give strong consideration to giving thrombolytics to patients with massive pulmonary embolism (PE), which is in keeping with many guidelines. Some physicians remain reluctant to do so, often citing the lack of good evidence. It is true that large scale RCTs have not been done in this population. The authors of this recent retrospective study state:


There are no definitive trials that prove the value of thrombolytic therapy in unstable patients with pulmonary embolism. It is extremely remote that a randomized controlled trial will be performed in the future. We therefore analyzed the database of the Nationwide Inpatient Sample to test the hypothesis that thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism.

They demonstrate a striking difference in mortality when thrombolysis is given to unstable patients with PE, which is further reduced with the addition of a vena cava filter. ‘Unstable’ was defined as having a listed code for shock or ventilator dependence.

Associated comorbid conditions were more often present in those who did not receive thrombolytic therapy than in those who did. However in their discussion the authors add:


Although unstable patients who received thrombolytic therapy had fewer comorbid conditions than those who did not, this would not explain the difference in case fatality rate because unstable patients with a primary diagnosis of pulmonary embolism and none of the comorbid conditions…also showed a lower case fatality rate with thrombolytic therapy. Therefore, differences in comorbid conditions in this group were eliminated as a possible cause of the lower case fatality rate in unstable patients who received thrombolytic therapy.

They round off their conclusion with:


Despite the marked reduction of case fatality rate with thrombolytic therapy in unstable patients, only 30% of unstable patients received it, and the proportion receiving thrombolytic therapy is diminishing. On the basis of these data, thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Many thanks to Dr Daniel Horner for highlighting this paper.


BACKGROUND: Data are sparse and inconsistent regarding whether thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism. We tested the hypothesis that thrombolytic therapy reduces case fatality rate in such patients.

METHODS: In-hospital all-cause case fatality rate according to treatment was determined in unstable patients with pulmonary embolism who were discharged from short-stay hospitals throughout the United States from 1999 to 2008 by using data from the Nationwide Inpatient Sample. Unstable patients were in shock or ventilator dependent.

RESULTS: Among unstable patients with pulmonary embolism, 21,390 of 72,230 (30%) received thrombolytic therapy. In-hospital all-cause case fatality rate in unstable patients with thrombolytic therapy was 3105 of 21,390 (15%) versus 23,820 of 50,840 (47%) without thrombolytic therapy (P< .0001). All-cause case fatality rate in unstable patients with thrombolytic therapy plus a vena cava filter was 505 of 6630 (7.6%) versus 4260 of 12,850 (33%) with a filter alone (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients was 820 of 9810 (8.4%) with thrombolytic therapy versus 1080 of 2600 (42%) with no thrombolytic therapy (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients with thrombolytic therapy plus vena cava filter was 70 of 2590 (2.7%) versus 160 of 600 (27%) with a filter alone (P<.0001).
CONCLUSION: In-hospital all-cause case fatality rate and case fatality rate attributable to pulmonary embolism in unstable patients was lower in those who received thrombolytic therapy. Thrombolytic therapy resulted in a lower case fatality rate than using vena cava filters alone, and the combination resulted in an even lower case fatality rate. Thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Thrombolytic Therapy in Unstable Patients with Acute Pulmonary Embolism: Saves Lives but Underused
Am J Med. 2012 May;125(5):465-70

T waves in V1-V3 were not associated with badness

This long term follow up study showed that T-wave inversions in right precordial leads are not associated with adverse outcome.

No worries, mate

Yikes!


Background-: T-wave inversion in right precordial leads V1 to V3 is a relatively common finding in a 12-lead ECG of children and adolescents and is infrequently found also in healthy adults. However, this ECG pattern can also be the first presentation of arrhythmogenic right ventricular cardiomyopathy. The prevalence and prognostic significance of T-wave inversions in the middle-aged general population are not well known.

Methods and Results-: We evaluated 12-lead ECGs of 10 899 Finnish middle-aged subjects (52% men, mean age 44+/-8.5 years) recorded between 1966 and 1972 for the presence of inverted T waves and followed the subjects for 30+/-11 years. Primary end points were all-cause mortality, cardiac mortality, and arrhythmic death. T-wave inversions in right precordial leads V1 to V3 were present in 54 (0.5%) of the subjects. In addition, 76 (0.7%) of the subjects had inverted T waves present only in leads other than V1 to V3. Right precordial T-wave inversions did not predict increased mortality (not significant for all end points). However, inverted T waves in leads other than V1 to V3 were associated with an increased risk of cardiac and arrhythmic death (P<0.001 for both).

Conclusions-: T-wave inversions in right precordial leads are relatively rare in the general population, and are not associated with adverse outcome. Increased mortality risk associated with inverted T waves in other leads may reflect the presence of an underlying structural heart disease.

Prevalence and prognostic significance of T-wave inversions in right precordial leads of a 12-lead electrocardiogram in the middle-aged subjects
Circulation. 2012 May 29;125(21):2572-7

Nonshockable arrest survival improves with uninterrupted compressions

A study of nonshockable out of hospital cardiac arrest survival showed significant improvement in short- and long-term survival and neurological outcome after implementation of a protocol consistent with CPR guidelines that prioritised chest compressions. These improvements were especially evident among arrests attributable to a cardiac cause, although there was no evidence of harm among arrests attributable to a noncardiac cause.
This was not a randomised trial so unrecognised factors may have contributed to the improved outcome in addition to the change in CPR protocol. However, it is interesting as it provides up to date survival rates from a large population sample: Non shockable out of hospital cardiac arrests achieve return of spontaneous circulation in 34%, 6.8% are discharged from hospital (5.1% with a favourable neurological outcome), and 4.9% survived one year.
The breakdown between PEA and asystole is of course telling, and unsurprising, with 12.8% versus 1.1% being discharged with a favourable neurological outcome, respectively. I would imagine then that some of the PEA patients had beating hearts with hypotension extreme enough to cause pulselessness (pseudo-electromechanical dissociation) – clinically a ‘cardiac arrest’ but really nothing of the sort, and the reason we use cardiac ultrasound to prognosticate.


BACKGROUND: Out-of-hospital cardiac arrest (OHCA) claims millions of lives worldwide each year. OHCA survival from shockable arrhythmias (ventricular fibrillation/ tachycardia) improved in several communities after implementation of American Heart Association resuscitation guidelines that eliminated “stacked” shocks and emphasized chest compressions. “Nonshockable” rhythms are now the predominant presentation of OHCA; the benefit of such treatments on nonshockable rhythms is uncertain.

METHODS AND RESULTS: We studied 3960 patients with nontraumatic OHCA from nonshockable initial rhythms treated by prehospital providers in King County, Washington, over a 10-year period. Outcomes during a 5-year intervention period after adoption of new resuscitation guidelines were compared with the previous 5-year historical control period. The primary outcome was 1-year survival. Patient demographics and resuscitation characteristics were similar between the control (n=1774) and intervention (n=2186) groups, among whom 471 of 1774 patients (27%) versus 742 of 2186 patients (34%), respectively, achieved return of spontaneous circulation; 82 (4.6%) versus 149 (6.8%) were discharged from hospital, 60 (3.4%) versus 112 (5.1%) with favorable neurological outcome; 73 (4.1%) versus 135 (6.2%) survived 1 month; and 48 (2.7%) versus 106 patients (4.9%) survived 1 year (all P≤0.005). After adjustment for potential confounders, the intervention period was associated with an improved odds of 1.50 (95% confidence interval, 1.29-1.74) for return of spontaneous circulation, 1.53 (95% confidence interval, 1.14-2.05) for hospital survival, 1.56 (95% confidence interval, 1.11-2.18) for favorable neurological status, 1.54 (95% confidence interval, 1.14-2.10) for 1-month survival, and 1.85 (95% confidence interval, 1.29-2.66) for 1-year survival.

CONCLUSION: Outcomes from OHCA resulting from nonshockable rhythms, although poor by comparison with shockable rhythm presentations, improved significantly after implementation of resuscitation guideline changes, suggesting their potential to benefit all presentations of OHCA.

Impact of changes in resuscitation practice on survival and neurological outcome after out-of-hospital cardiac arrest resulting from nonshockable arrhythmia
Circulation. 2012 Apr 10;125(14):1787-94