CVT guideline

Thanks to neuro-icu.com for highlighting this one: The American Heart Association and American Stroke Association have produced guidelines for the diagnosis and management of cerebral venous thrombosis. Here is a summary of their recommendations. The full text of the guidelines is available via the link at the bottom.

Routine Blood Work

  • In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed (Class I; Level of Evidence C).
  • Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment (specific recommendations for testing for thrombophilia are found in the long-term management section of this document) (Class I; Level of Evidence C).
  • A normal D-dimer level according to a sensitive immunoassay or rapid enzyme-linked immunosorbent assay (ELISA) may be considered to help identify patients with low probability of CVT (Class IIb; Level of Evidence B). If there is a strong clinical suspicion of CVT, a normal D-dimer level should not preclude further evaluation.

Common Pitfalls in the Diagnosis of CVT

  • In patients with lobar ICH of otherwise unclear origin or with cerebral infarction that crosses typical arterial boundaries, imaging of the cerebral venous system should be performed (Class I; Level of Evidence C).
  • In patients with the clinical features of idiopathic intracranial hypertension, imaging of the cerebral venous system is recommended to exclude CVT (Class I; Level of Evidence C).
  • In patients with headache associated with atypical features, imaging of the cerebral venous system is reasonable to exclude CVT (Class IIa; Level of Evidence C).

Imaging in the Diagnosis of CVT

  • Although a plain CT or MRI is useful in the initial evaluation of patients with suspected CVT, a negative plain CT or MRI does not rule out CVT. A venographic study (either CTV or MRV) should be performed in suspected CVT if the plain CT or MRI is negative or to define the extent of CVT if the plain CT or MRI suggests CVT (Class I; Level of Evidence C).
  • An early follow-up CTV or MRV is recommended in CVT patients with persistent or evolving symptoms despite medical treatment or with symptoms suggestive of propagation of thrombus (Class I; Level of Evidence C).
  • In patients with previous CVT who present with recurrent symptoms suggestive of CVT, repeat CTV or MRV is recommended (Class I; Level of Evidence C).
  • Gradient echo T2 susceptibility-weighted images combined with magnetic resonance can be useful to improve the accuracy of CVT diagnosis (Class IIa; Level of Evidence B).
  • Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high (Class IIa; Level of Evidence C).
  • A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients (Class IIa; Level of Evidence C).

Management and Treatment

  • Patients with CVT and a suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (Class I; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, monitoring for progressive visual loss is recommended, and when this is observed, increased intracranial pressure should be treated urgently (Class I; Level of Evidence C).
  • In patients with CVT and a single seizure with parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is recommended to prevent further seizures (Class I; Level of Evidence B).
  • In patients with CVT and a single seizure without parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is probably recommended to prevent further seizures (Class IIa; Level of Evidence C).
  • In the absence of seizures, the routine use of antiepileptic drugs in patients with CVT is not recommended (Class III; Level of Evidence C).
  • For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH (Class IIa; Level of Evidence B).
  • Admission to a stroke unit is reasonable for treatment and for prevention of clinical complications of patients with CVT (Class IIa; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, it is reasonable to initiate treatment with acetazolamide. Other therapies (lumbar puncture, optic nerve decompression, or shunts) can be effective if there is progressive visual loss. (Class IIa; Level of Evidence C).
  • Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C). In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered (Class IIb; Level of Evidence C).
  • For patients with CVT, steroid medications are not recommended, even in the presence of parenchymal brain lesions on CT/MRI, unless needed for another underlying disease (Class III; Level of Evidence B).

Long-Term Management and Recurrence of CVT

  • Testing for prothrombotic conditions, including protein C, protein S, antithrombin deficiency, antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden, can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2 to 4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. (Class IIa; Level of Evidence B).
  • In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3 to 6 months, with a target INR of 2.0 to 3.0 (Table 3) (Class IIb; Level of Evidence C).
  • In patients with unprovoked CVT, vitamin K antagonists may be continued for 6 to 12 months, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • For patients with recurrent CVT, VTE after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • Consultation with a physician with expertise in thrombosis may be considered to assist in the pro- thrombotic testing and care of patients with CVT (Class IIb; Level of Evidence C).

Management of Late Complications (Other Than Recurrent VTE)

  • In patients with a history of CVT who complain of new, persisting, or severe headache, evaluation for CVT recurrence and intracranial hypertension should be considered (Class I; Level of Evidence C)

CVT in pregnancy

  • For women with CVT during pregnancy, LMWH in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) (Class I; Level of Evidence C).
  • It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal fetal medicine specialist are reasonable. (Class IIa; Level of Evidence B).
  • It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH (Class IIa; Level of Evidence C).
  • For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended (Class IIa; Level of Evidence C).

Children

  • Supportive measures for children with CVT should include appropriate hydration, control of epileptic seizures, and treatment of elevated intracranial pressure (Class I; Level of Evidence C).
  • Given the potential for visual loss owing to severe or long-standing increased intracranial pressure in children with CVT, periodic assessments of the visual fields and visual acuity should be performed, and appropriate measures to control elevated intracranial pressure and its complications should be instituted (Class I; Level of Evidence C).
  • In all pediatric patients, if initial anticoagulation treatment is withheld, repeat neuroimaging including venous imaging in the first week after diagnosis is recommended to monitor for propagation of the initial thrombus or new infarcts or hemorrhage (Class I; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to treat with full-dose LMWH even in the presence of intracra- nial hemorrhage (Class IIa; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to continue LMWH or oral vitamin K antagonists for 3 to 6 months (Class IIa; Level of Evidence C).
  • In all pediatric patients with acute CVT, if initial anticoagulation is started, it is reasonable to perform a head CT or MRI scan in the initial week after treatment to monitor for additional hemor- rhage (Class IIa; Level of Evidence C).
  • Children with CVT may benefit from thrombophilia testing to identify underlying coagulation defects, some of which could affect the risk of subsequent rethromboses and influence therapeutic decisions (Class IIb; Level of Evidence B).
  • Children with CVT may benefit from investigation for underlying infections with blood cultures and sinus radiographs (Class IIb; Level of Evidence B).
  • In neonates with acute CVT, treatment with LMWH or UFH may be considered (Class IIb; Level of Evidence B).
  • Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C).
  • In neonates with acute CVT, continuation of LMWH for 6 weeks to 3 months may be considered (Class IIb; Level of Evidence C).
  • The usefulness and safety of endovascular intervention are uncertain in pediatric patients, and its use may only be considered in carefully selected patients with progressive neurological deterioration despite intensive and therapeutic levels of anticoagulant treatment (Class IIb; Level of Evidence C).

Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association
Stroke. 2011 Feb 3. [Epub ahead of print] Full Text

Which cardiac arrest survivors have a positive angio?

A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.

OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors.

METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site.

RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6).

CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.

Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients
Eur J Emerg Med. 2011 Apr;18(2):73-6

An easily missed cause of shock

A potentially reversible cause of haemodynamic shock in critically ill patients is left ventricular outflow tract obstruction (LVOTO). We are familiar with this phenomenon in conditions such as hypertrophic cardiomyopathy (HCM), but LVOTO can occur in the absence of HCM and result in hypotension that may be refractory to catecholamines. In fact, vasoactive drugs are often the precipitant.

A case is reported of an intubated elderly man with pneumonia and COPD who upon starting dopamine and furosemide for hypotension and anuria developed severe haemodynamic deterioration1. Echo revealed a hyperkinetic left ventricle with mild concentric hypertrophy, septal wall thickness of 12 mm (normal range up to 10mm), and a reduced end-diastolic diameter. Systolic anterior motion (SAM) of the anterior mitral leaflet causing a significant left ventricular outflow tract obstruction (LVOTO), with a peak gradient of 100 mmHg, was detected. The patient improved with discontinuation of vasoactive drugs and fluid loading. A follow up cardiac MR showed a structurally normal LV.

The authors describe the factors that combine to produce this syndrome:

  • Anatomical substrate – Left ventricular hypertrophy due to hypertension, mitral valve repair, previous aortic valve replacement, abnormalities of the mitral subvalvular apparatus, sigmoid septum and a steep aortic root angle.
  •  
  • Precipitating factors – Drug therapies such as catecholamine infusion or diuretics, which respectively enhance the contractility of the basal segments and reduce the left ventricular cavity, emotional stress (like described in the apical ballooning syndrome), hypovolaemia, dehydration, sepsis, and myocardial infarction; hypovolaemia and mechanical ventilation further exacerbate underfilling of the LV and dynamic LVOTO.

In a review article on the topic, Dr Chockalingam and colleagues describe structural and functional factors in this finely crafted explanation2:

The asymmetrically hypertrophied septum, progressive narrowing of the LVOT during systole, and direction of the bloodstream cause drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of ventricular outflow. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOTO gradients and MR.

Although classically described with hypertrophic cardiomyopathy, SAM and LVOTO can independently result from various clinical settings such as LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities (redundant, long anterior leaflet), and hypercontractility (stress, anxiety, or inotropic agents). Dynamic LVOTO may occur with acute coronary syndrome and often presents with shock and a new systolic murmur3. The presence of a new murmur in a shocked ACS patient should therefore prompt consideration of the following diagnoses:

  • Acute mitral valve dysfunction
  • Ventricular septal defect
  • Free wall rupture
  • Dynamic LVOTO

Treatment is aimed at alleviating the causes and should be individualised. Options include coronary revascularisation, volume therapy, beta blockade, removing afterload reduction (vasodilators and balloon pumps can exacerbate LVOTO), and alpha agonists such as phenylephrine.

 

In summary, dynamic LVOTO:
  • is a potentially reversible cause of haemodynamic shock in critically ill patients
  • should be considered in critically ill patients whose shock fails to improve or worsen with inotropic medication
  • should be considered in patients with ACS, shock, and a new systolic murmur
  • can result from combinations of LV hypertrophy, reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents)
  • is yet another reason why the haemodynamic monitor of choice in shocked patients should be echocardiography!

Echo showing systolic anterior motion of the mitral valve

1. Pathophysiology of Dynamic Left Ventricular Outflow Tract Obstruction in a Critically Ill Patient Echocardiography. 2010 Nov;27(10):E122-4

2. Dynamic Left Ventricular Outflow Tract Obstruction in Acute Myocardial Infarction With Shock Circulation. 2007 Jul 31;116(5):e110-3 Free Full Text 3. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock Mayo Clin Proc. 1999 Sep;74(9):901-6

Pre-hospital physician triage

A Swiss study examined the on site triage decision making of pre-hospital emergency physicians. Dispatch of the physicians was coordinated by trained nurses or paramedics.

OBJECTIVE: Accurate identification of major trauma patients in the prehospital setting positively affects survival and resource utilization. Triage algorithms using predictive criteria of injury severity have been identified in paramedic-based prehospital systems. Our rescue system is based on prehospital paramedics and emergency physicians. The aim of this study was to evaluate the accuracy of the prehospital triage performed by physicians and to identify the predictive factors leading to errors of triage.

METHODS: Retrospective study of trauma patients triaged by physicians. Prehospital triage was analyzed using criteria defining major trauma victims (MTVs, Injury Severity Score >15, admission to ICU, need for immediate surgery and death within 48 h). Adequate triage was defined as MTVs oriented to the trauma centre or non-MTV (NMTV) oriented to regional hospitals.

RESULTS: One thousand six hundred and eighti-five patients (blunt trauma 96%) were included (558 MTV and 1127 NMTV). Triage was adequate in 1455 patients (86.4%). Overtriage occurred in 171 cases (10.1%) and undertriage in 59 cases (3.5%). Sensitivity and specificity was 90 and 85%, respectively, whereas positive predictive value and negative predictive value were 75 and 94%, respectively. Using logistic regression analysis, significant (P<0.05) predictors of undertriage were head or thorax injuries (odds ratio >2.5). Predictors of overtriage were paediatric age group, pedestrian or 2 wheel-vehicle road traffic accidents (odds ratio >2.0).

CONCLUSION: Physicians using clinical judgement provide effective prehospital triage of trauma patients. Only a few factors predicting errors in triage process were identified in this study.

Accuracy of prehospital triage of trauma patients by emergency physicians: a retrospective study in western Switzerland
Eur J Emerg Med. 2011 Apr;18(2):86-93

Supplemental oxygen decreases LV perfusion in volunteers

Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.

 

OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals.

METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass.

RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content.

CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.

Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI
European Journal of Emergency Medicine 2011, 18:25–30

Pull that tongue

A way of improving glottic visualisation when attempting fibreoptic intubation is for an assistant to perform a jaw thrust manoeuvre. This is nicely demonstrated in a video on the New England Journal website. However my retrieval medicine colleague and anaesthetist Dr Anthony Lewis pointed out the following situation and its solution:

What if they are a ‘difficult airway’ and you the jaw can’t move? Get your Magills forceps, grab the tongue and pull the tongue out. Very nice!

Furosemide infusion in acute decompensated heart failure

A randomised controlled trial of 308 patients with acute decompensated heart failure compared continuous furosemide infusion with ‘low’ dose (equal to their total daily oral loop diuretic dose in furosemide equivalents) or high dose furosemide boluses. There was no outcome difference between infusion and bolus, although the high dose (2.5 times previous oral diuretic dose 12 hourly for 48 hours) improved patients’ symptoms while causing transient elevations in serum creatinine. Editorialist Dr G Fonarow states:

‘..these findings should change current practice. Since a high-dose regimen may relieve dyspnea more quickly without adverse effects on renal function, that regimen is preferable to a low-dose regimen. Administration of boluses may be more convenient than continuous infusion and equally effective.’

 

BACKGROUND: Loop diuretics are an essential component of therapy for patients with acute decompensated heart failure, but there are few prospective data to guide their use.

METHODS: In a prospective, double-blind, randomized trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high dose (2.5 times the previous oral dose). The protocol allowed specified dose adjustments after 48 hours. The coprimary end points were patients’ global assessment of symptoms, quantified as the area under the curve (AUC) of the score on a visual-analogue scale over the course of 72 hours, and the change in the serum creatinine level from baseline to 72 hours.

RESULTS: In the comparison of bolus with continuous infusion, there was no significant difference in patients’ global assessment of symptoms (mean AUC, 4236±1440 and 4373±1404, respectively; P=0.47) or in the mean change in the creatinine level (0.05±0.3 mg per deciliter [4.4±26.5 μmol per liter] and 0.07±0.3 mg per deciliter [6.2±26.5 μmol per liter], respectively; P=0.45). In the comparison of the high-dose strategy with the low-dose strategy, there was a nonsignificant trend toward greater improvement in patients’ global assessment of symptoms in the high-dose group (mean AUC, 4430±1401 vs. 4171±1436; P=0.06). There was no significant difference between these groups in the mean change in the creatinine level (0.08±0.3 mg per deciliter [7.1±26.5 μmol per liter] with the high-dose strategy and 0.04±0.3 mg per deciliter [3.5±26.5 μmol per liter] with the low-dose strategy, P=0.21). The high-dose strategy was associated with greater diuresis and more favorable outcomes in some secondary measures but also with transient worsening of renal function.

CONCLUSIONS: Among patients with acute decompensated heart failure, there were no significant differences in patients’ global assessment of symptoms or in the change in renal function when diuretic therapy was administered by bolus as compared with continuous infusion or at a high dose as compared with a low dose. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00577135.).

Diuretic strategies in patients with acute decompensated heart failure
N Engl J Med. 2011 Mar 3;364(9):797-805

African study on cricoid pressure

The inventor of cricoid pressure. Possibly.

A colleague told me about a cricoid pressure paper I would otherwise have missed, since I don’t normally check out the International Journal of Obstetric Anaesthesia. This was a multicentre observational study in Malawi, in which 30 women (of 4891 general anaesthetics) vomited or regurgitated during induction of anaesthesia, in 24 of whom cricoid pressure was applied. 11 of the 77 deaths that occurred were associated with regurgitation, in 10 of which regurgitation contributed to the death. Nine of these 11 mothers who died had had cricoid pressure applied. The incidence of regurgitation was lower, but not significantly so, among those who did not have cricoid pressure applied. Not sure why it took nine years to publish this work.

 

BACKGROUND: Cricoid pressure is a routine part of rapid-sequence induction of general anaesthesia in obstetrics, but its efficacy in saving life is difficult to ascertain.

METHODS: As part of a prospective observational study of caesarean sections performed between January 1998 and June 2000 in 27 hospitals in Malawi, the anaesthetist recorded whether cricoid pressure was applied, the method of anaesthesia, the use of endotracheal intubation, the occurrence and timing of regurgitation and any other pre- or intra-operative complications. Logistic regression was used to assess the effect of cricoid pressure, type of anaesthetic and pre-operative complications on vomiting/regurgitation and death.

RESULTS: Data were collected for 4891 general anaesthetics that involved intubation. Cricoid pressure was applied in 61%; 139 women vomited or regurgitated, but only 30 on induction of anaesthesia, in 24 of whom cricoid pressure was applied. There were 77 deaths, 11 of which were associated with regurgitation, in 10 of which regurgitation contributed to the death. Nine of the 11 mothers had cricoid pressure applied. Only one died on the table, the rest postoperatively. All those who died had preoperative complications.

CONCLUSION: This study does not provide any evidence for a protective effect of cricoid pressure as used in this context, in preventing regurgitation or death. Preoperative gastric emptying may be a more effective measure to prevent aspiration of gastric contents.

Life-saving or ineffective? An observational study of the use of cricoid pressure and maternal outcome in an African setting
Int J Obstet Anesth. 2009 Apr;18(2):106-10

Weight formula validation

Further validation of the UK-derived Luscombe weight formula has been made in the Australian setting. The nice simple formula for estimating the weight of a child based on age is:

Weight (kg) = 3 x age(years) + 7

It was compared with other formulae including the Best Guess formula, which is a bit more difficult to apply as the formula varies according to age range. This is reported in a previous post.

The authors provide the following cautionary advice:

“Whereas age-based formulae are, in the main, easy to calculate, the evidence suggests that ethnicity and body habitus pose serious challenges to their accuracy. In comparative studies, age-based formulae were found to be less accurate than the Broselow tape and parental estimate, with parental estimate being the most accurate weight estimation method. In light of this evidence, age-based formulae should only be used when these more accurate methods are not available.”

OBJECTIVE: Several paediatric weight estimation methods have been described for use when direct weight measurement is not possible. A new age-based weight estimation method has recently been proposed. The Luscombe formula, applicable to children aged 1-10 years, is calculated as (3 × age in years) + 7. Our objective was to externally validate this formula using an existing database.

METHOD: Secondary analysis of a prospective observational cohort study. Data collected included height, age, ethnicity and measured weight. The outcome of interest was agreement between estimated weight using the Luscombe formula and measured weight. Secondary outcome was comparison with performance of Argall, APLS and Best Guess formulae. Accuracy of weight estimation methods was compared using mean difference (bias), 95% limits of agreement, root mean square error and proportion with agreement within 10%.

RESULTS: Four hundred and ten children were studied. Median age was 4 years; 54.4% were boys. Mean body mass index was 17 kg/m(2) and mean measured weight was 21.2 kg. The Luscombe formula had a mean difference of 0.66 kg (95% limits of agreement -9.9 to +11.3 kg; root mean square error of 5.44 kg). 45.4% of estimates were within 10% of measured weight. The Best Guess and Luscombe formulae performed better than Argall or APLS formulae.

CONCLUSION: The Luscombe formula is among the more accurate age-based weight estimation formulae. When more accurate methods (e.g. parental estimation or the Broselow tape) are not available, it is an acceptable option for estimating children’s weight.

Validation of the Luscombe weight formula for estimating children’s weight
Emerg Med Australas 2011 Feb;23(1):59-62

Performance measures for HEMS services

A recent study highlights the need for uniform standards of outcome data collection in Helicopter Emergency Medical Services (HEMS) in Great Britain and aero-medical retrieval services in Australia. Suggested patient outcome measurements by Britsh and Australian air medical respondents to the survey included:

  1. Mortality versus TRISS predicted mortality
  2. APACHE/ TRISS predicted mortality versus actual mortality.
  3. Use of national audit tools (eg, TARN)
  4. Nationally agreed Key Performance Indicators (KPIs)
  5. Clinical outcomes benchmarked against other services
  6. In-mission clinical indicators (eg, unanticipated procedures, adverse events)
  7. Physiological scoring linked to outcome measures
  8. ISS versus survival/disability
  9. KPIs from a national body. Mortality in isolation is not a useful marker of quality
  10. Clinical KPIs provided there is a reliable method of data collection
  11. Long-term outcome
  12. Interventions performed by doctors that contribute to patient mortality/morbidity.

Background Performance outcome measures are an essential component of health service improvement. Whereas hospital critical care services have established performance measures, prehospital care services have less well-established outcome measures and this has been identified as a key issue for development. Individual studies examining long-term survival and functional outcome measures have previously been used to evaluate prehospital care delivery. There is no set of standardised patient outcome measures for Helicopter Emergency Medical Services (HEMS) in the UK or Air Medical Services (AMS) in Australia. The aim of this study is to document the patient outcome measures currently in use within British HEMS and Australian AMS.

Methods This is an observational study analysing point prevalence of practice as of November 2009. A structured questionnaire was designed to assess the method of routine patient follow-up, and the timing and nature of applied patient outcome measures.

Results Full responses were received from 17/21 (81%) British services and 6/7 (86%) Australian services. The overall response rate was 82%.

Conclusions HEMS in Britain and Australian aeromedical retrieval services do not have uniform patient outcome measures. Services tend not to follow-up patients beyond 24 h post transfer. Patient outcome data are rarely presented to an external organisation and there is no formal data comparison between surveyed services. Services are not satisfied that the data currently being collected reflects the quality of their service.

Performance measurement in British Helicopter Emergency Medical Services and Australian Air Medical Services
Emerg Med J. 2011 Feb 3. [Epub ahead of print]