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All Updates, Guidelines, ICU, Kids, Resus, Trauma

UK Radiology guidelines for trauma

June 19, 2011 Cliff 1 Comment

The Royal College of Radiologists in the UK has published a guideline document to set standards related to diagnostic and interventional radiology for use by major trauma centres (MTCs) and trauma units (TUs). The standards are:

The trauma team leader is in overall charge in acute care

Protocol-driven imaging and intervention must be available and delivered by experienced staff. Acute care for SIPs must be consultant delivered

MDCT should be adjacent to, or in, the emergency room

Digital radiography must be available in the emergency room

If there is an early decision to request MDCT, FAST and DR should not cause any delay

MRI must be available with safe access for the SIP

A CT request in the trauma setting should comply with the Ionising Radiation (Medical Exposure) Regulations 2000 (IR(ME)R) justification regulations like any other request for imaging involving ionising radiation

There should be clear written protocols for MDCT preparation and transfer to the scan room

Whole-body contrast-enhanced MDCT is the default imaging procedure of choice in the SIP. Imaging protocols should be clearly defined and uniform across a regional trauma network

Future planning and design of emergency rooms should concentrate on increasing the numbers of SIPs stable enough for MDCT and intervention

The primary survey report should be issued immediately to the trauma team leader

On-call consultant radiologists should provide the final report on the SIP within one hour of MDCT image acquisition

On-call consultant radiologists must have teleradiology facilities at home that allow accurate reports to be issued within one hour of MDCT image acquisition

IR facilities should be co-located to the emergency department

Angiographic facilities and endovascular theatres in MTCs should be safe environments for SIPs and should be of theatre standard

Agreed written transfer protocols between the emergency department and imaging/interventional facilities internally or externally must be available

IR trauma teams should be in place within 60 minutes of the patient’s admission or 30 minutes of referral

Any deficiency in consumable equipment should be reported at the debriefing and be the subject of an incident report

Some interesting snippets include:
IV access
Right antecubital access is preferred for contrast administration (left-sided injections compromise interpretation of mediastinal vasculature). However, if arm vein access is not possible and a central line is in situ, it should be of a type that can accept 4 ml contrast/ second via a power injector. This might require local negotiation with emergency department doctors beforehand

Pelvic fracture
If a pelvic fracture is suspected, a temporary pelvic stabilisation (wrap, binder and so on) should be applied before MDCT.
Limb fractures
Rapid immobilisation such as air splints. Only immediately limb conserving manipulations/splinting should be performed prior to CT.
Urinary catheter
All significantly injured patients without obvious contraindications should be catheterised unless this would delay transfer to CT. The catheter should be clamped prior to MDCT.
Standards of practice and guidance for trauma radiology in severely injured patients
Royal College of Radiologists – Full Text Link

All Updates, Kids, Resus, Trauma, Ultrasound

FAST in kids has low sensitivity

June 8, 2011 Cliff Leave a comment

The abstract says it all – don’t use FAST to rule out significant abdominal free fluid in kids with blunt abdominal trauma. Fine as a rule-in test (for free fluid) though.

Objectives: Focused assessment of sonography in trauma (FAST) has been shown useful to detect clinically significant hemoperitoneum in adults, but not in children. The objectives were to determine test characteristics for clinically important intraperitoneal free fluid (FF) in pediatric blunt abdominal trauma (BAT) using computed tomography (CT) or surgery as criterion reference and, second, to determine the test characteristics of FAST to detect any amount of intraperitoneal FF as detected by CT.

Methods: This was a prospective observational study of consecutive children (0–17 years) who required trauma team activation for BAT and received either CT or laparotomy between 2004 and 2007. Experienced physicians performed and interpreted FAST. Clinically important FF was defined as moderate or greater amount of intraperitoneal FF per the radiologist CT report or surgery.

Results: The study enrolled 431 patients, excluded 74, and analyzed data on 357. For the first objective, 23 patients had significant hemoperitoneum (22 on CT and one at surgery). Twelve of the 23 had true-positive FAST (sensitivity = 52%; 95% confidence interval [CI] = 31% to 73%). FAST was true negative in 321 of 334 (specificity = 96%; 95% CI = 93% to 98%). Twelve of 25 patients with positive FAST had significant FF on CT (positive predictive value [PPV] = 48%; 95% CI = 28% to 69%). Of 332 patients with negative FAST, 321 had no significant fluid on CT (negative predictive value [NPV] = 97%; 95% CI = 94% to 98%). Positive likelihood ratio (LR) for FF was 13.4 (95% CI = 6.9 to 26.0) while the negative LR was 0.50 (95% CI = 0.32 to 0.76). Accuracy was 93% (333 of 357, 95% CI = 90% to 96%). For the second objective, test characteristics were as follows: sensitivity = 20% (95% CI = 13% to 30%), specificity = 98% (95% CI = 95% to 99%), PPV = 76% (95% CI = 54% to 90%), NPV = 78% (95% CI = 73% to 82%), positive LR = 9.0 (95% CI = 3.7 to 21.8), negative LR = 0.81 (95% CI = 0.7 to 0.9), and accuracy = 78% (277 of 357, 95% CI = 73% to 82%).

Conclusion: In this population of children with BAT, FAST has a low sensitivity for clinically important FF but has high specificity. A positive FAST suggests hemoperitoneum and abdominal injury, while a negative FAST aids little in decision-making

Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma
Acad Emerg Med. 2011 May;18(5):477-82

Acute Med, All Updates, Guidelines, ICU, PHARM, Resus

STEMI criteria vary with age and sex

May 3, 2011 Cliff Leave a comment

On reading through the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 10: Acute Coronary Syndromes, I found a reminder that the ECG criteria for diagnosing ST-elevation myocardial infarction (STEMI) vary according to age and sex. From the original article in the Journal of the American College of Cardiology:

The threshold values of ST-segment elevation of 0.2 mV (2 mm) in some leads and 0.1 mV (1 mm) in others results from recognition that some elevation of the junction of the QRS complex and the ST segment (the J point) in most chest leads is normal. Recent studies have revealed that the threshold values are dependent on gender, age, and ECG lead ([8], [9], [10], [11] and [12]). In healthy individuals, the amplitude of the ST junction is generally highest in leads V2 and V3 and is greater in men than in women.
Recommendations

For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.

For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).

For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.

For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.

For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).

For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.

What does establishment of abnormal J-point mean for STEMI diagnosis? The AHA/ECC guidelines state the following:

ST-segment elevation… is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are:

J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old);

J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old);

J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).

So, in summary:

Older men – 2mm in V2/V3 and 1mm everywhere else
Younger men – 2.5 mm in V2/V3 and 1mm everywhere else
Women – 1.5 mm in V2/V3 and 1mm everywhere else

Shouldn’t be too difficult to remember.
Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010 Nov 2;122(18 Suppl 3):S787-817
AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.
J Am Coll Cardiol. 2009 Mar 17;53(11):1003-11

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'Sensitive' troponin assays do not rule out at ED presentation

May 2, 2011 Cliff Leave a comment

An assessment of new ‘sensitive’ troponin assays at presentation of chest pain patients in a real-world ED setting showed that a single troponin I assay at ED presentation has insufficient sensitivity for clinical use to rule out MI. Author Anne-Maree Kelly discusses the current requirement for a minimum interval after an episode of chest pain to ensure adequate sensitivity: Currently in Australia the recommended minimum interval is 8 h after symptom onset. New evidence suggests that a shorter interval might be appropriate with the sensitive assays. Keller et al. reported 100% sensitivity at 3 h after ED presentation. Macrae et al. suggested that an assay 6 h from pain onset or serial assays 3 h apart with one at least 6 h from pain onset has high diagnostic accuracy. Although further research in an ED chest pain cohort is needed, the weight of evidence suggests a reduction in the minimum interval from pain onset to 6 h might be appropriate.

Aim: Troponin assays have high diagnostic value for myocardial infarction (MI), but sensitivity has been weak early after chest pain onset. New, so-called ‘sensitive’ troponin assays have recently been introduced. Two studies report high sensitivity for assays taken at ED presentation, but studied selected populations. Our aim was to evaluate the diagnostic performance for MI of a sensitive troponin assay measured at ED presentation in an unselected chest pain population without ECG evidence of ischaemia.
Methods: This is a sub-study of a prospective cohort study of adult patients with potentially cardiac chest pain who underwent evaluation for acute coronary syndrome. Patients with clear ECG evidence of acute ischaemia or an alternative diagnosis were excluded. Data collected included demographic, clinical, ECG, biomarker and outcome data. A ‘positive’ troponin was defined as >99th percentile of the assay used. MI diagnosis was as judged by the treating cardiologist. The outcomes of interest were sensitivity, specificity and likelihood ratios (LR) for positive troponin assay taken at ED presentation. Data were analysed by clinical performance analysis.
Results: Totally 952 were studied. Median age was 61 years; 56.4% were male and median TIMI score was 2. There were 129 MI (13.6, 95% CI 11.5-15.9). Sensitivity of TnI at ED presentation was 76.7% (95% CI 68.5-83.7%), specificity 93.6% (95% CI 91.7-95.1%), with LR positive 11.92 and LR negative 0.25.
Conclusion: Sensitive TnI assay at ED presentation has insufficient diagnostic accuracy for detection of MI. Serial biomarker assays in patients with negative initial TnI are required.

Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.
Emerg Med Australas. 2011 Apr;23(2):181-5

Acute Med, All Updates, Resus

Triple marker panel for AMI

April 30, 2011 Cliff Leave a comment

A large Asian/Australasian study examined a 2hr triple-marker test in patients presenting with chest pain.

BACKGROUND: Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome.
METHODS: This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279.
FINDINGS: 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11.8%) patients had a major adverse cardiac event. The ADP classified 352 (9.8%) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0.9%) of these patients, giving the ADP a sensitivity of 99.3% (95% CI 97.9-99.8), a negative predictive value of 99.1% (97.3-99.8), and a specificity of 11.0% (10.0-12.2).
INTERPRETATION: This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide.

A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study.
Lancet. 2011 Mar 26;377(9771):1077-84
Full text link available at time of writing
In an accompanying editorial, nicely entitled ‘Acute MI: triple-markers resurrected or Bayesian dice?’ Dr Rick Body notes that the point-of-care triple-marker test has a relatively low sensitivity, at just 82.9%, when used alone, and the sensitivity only increased to 99.3% in the current study because it was used in an already-selected low-risk population. He writes: “Most people will probably consider this net risk to be statistically acceptable. However, if properly informed, low-risk patients might feel differently about the relative merits of waiting for definitive six-hour laboratory-based troponin testing or going home after two hours on the basis of results from a test that correctly identifies serious coronary disease, when present, in just over eight of 10 occasions.”
Dr Body has a new blog at The Bodsblog where we’re likely to be informed other data relevant to emergency cardiology as they emerge.
Point-of-care panel assessment using a similar triple-marker test at presentation and 90 minutes was also examined in the RATPAC study, in which it increased successful discharge home and reduced median length of stay, but did not alter overall hospital bed use.

All Updates, ICU, PHARM, Resus, Trauma, Ultrasound

Pre-hospital transcranial Doppler

April 1, 2011 Cliff Leave a comment

The SAMU (Service d’aide médicale urgente) guys have had a run of interesting pre-hospital publications lately. In this study, one of their ultrasound-wielding physicians travelled in a car to meet comatose head injured patients in a large semi-rural territory area with up to a 120–160-min transport time to a hospital with emergency neurosurgical capability. Pre-hospital transcranial Doppler was done, the results of which appear to have influenced treatment decisions, including the pre-hospital administration of noradrenaline (norepinephrine). I think this study has answered the ‘can it be done?’ question, but further work is needed to determine whether it really makes a difference to outcome.

Background: Investigation of the feasibility and usefulness of pre-hospital transcranial Doppler (TCD) to guide early goal-directed therapy following severe traumatic brain injury (TBI).
Methods: Prospective, observational study of 18 severe TBI patients during pre-hospital medical care. TCD was performed to estimate cerebral perfusion in the field and upon arrival at the Level 1 trauma centre. Specific therapy (mannitol, noradrenaline) aimed at improving cerebral perfusion was initiated if the initial TCD was abnormal (defined by a pulsatility index >1.4 and low diastolic velocity).
Results: Nine patients had a normal initial TCD and nine an abnormal one, without a significant difference between groups in terms of the Glasgow Coma Scale or the mean arterial pressure. Among patients with an abnormal TCD, four presented with an initial areactive bilateral mydriasis. Therapy normalized TCD in five patients, with reversal of the initial mydriasis in two cases. Among these five patients for whom TCD was corrected, only two died within the first 48 h. All four patients for whom the TCD could not be corrected during transport died within 48 h. Only patients with an initial abnormal TCD required emergent neurosurgery (3/9). Mortality at 48 h was significantly higher for patients with an initial abnormal TCD.
Conclusions: Our preliminary study suggests that TCD could be used in pre-hospital care to detect patients whose cerebral perfusion may be impaired.

Pre-hospital transcranial Doppler in severe traumatic brain injury: a pilot study
Acta Anaesthesiol Scand. 2011 Apr;55(4):422-8

Acute Med, All Updates, Guidelines, ICU, Resus

CVT guideline

March 23, 2011 Cliff Leave a comment

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

All Updates, ICU, Resus, Ultrasound

An easily missed cause of shock

March 23, 2011 Cliff Leave a comment

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

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IVC collapse depends on breathing pattern

March 13, 2011 Cliff Leave a comment

A high degree of sonographically-visualised collapse of the inferior vena cava (IVC) during inspiration suggests a volume-responsive cardiac output. This inspiratory collapse is said to be due to a fall in intra-thoracic pressure. However, the IVC traverses the abdominal compartment and is therefore under the influences of hepatic weight, intra-abdominal pressure, and venous return of pooled splanchnic and lower extremity blood.
Diaphragmatic descent, which increases intra-abdominal pressure, may contribute to the respiratory change in IVC diameter. This was borne out in a volunteer study in which diaphragmatic breathing was compared with chest wall breathing. With diaphragmatic breathing there was a trend for a larger IVC collapse index (median 0.80, range 0.48–1.00 vs. 0.57, range 0.13–1.00, P = 0.053). The authors state:
“These findings suggest that during inspiration the IVC, in addition to responding to falling intra-thoracic pressure, may also be compressed with diaphragmatic descent and have implications regarding the use of IVC diameters to estimate the central venous pressure without knowing the manner of breathing, intra-abdominal pressure, or magnitude of diaphragmatic excursion.”
The take home message for me is that there is probably a more complex mechanism of IVC behaviour during respiration than is often taught, and that breathing pattern and abdominal issues may influence the IVC diameter and degree of collapse seen on ultrasound. This might not however negate the correlation between a high degree of collapse and fluid-responsiveness, which is what I’m looking for in my patients with shock or hypotension.
Incidentally the first author of this study is Bruce Kimura, a pioneer of focused echo in the emergency setting and author of a fantastic little book all about the parasternal long axis approach, which seems to be impossible to source on the web at the moment.

AIMS: Although the inspiratory ‘collapse’ of the inferior vena cava (IVC) has been used to signify normal central venous pressure, the effect of the manner of breathing IVC size is incompletely understood. As intra-abdominal pressure rises during descent of the diaphragm, we hypothesized that inspiration through diaphragmatic excursion may have a compressive effect on the IVC.
METHODS AND RESULTS: We measured minimal and maximal intrahepatic IVC diameter on echocardiography and popliteal venous return by spectral Doppler during isovolemic inspiratory efforts in 19 healthy non-obese volunteers who were instructed to inhale using either diaphragmatic or chest wall expansion. During inspiration, the maximal diaphragmatic excursion and popliteal vein flow were compared between breathing methods. The IVC ‘collapsibility index,’ IVCCI, was calculated as (IVC(max)-IVC(min))/IVC(max). The difference in diaphragmatic excursion between diaphragmatic and chest wall breaths in each subject was correlated with the corresponding change in IVCCI. Diaphragmatic breathing resulted in more diaphragmatic excursion than chest wall breathing (median 3.4 cm, range 1.7-5.8 vs. 2.2 cm, range 1.0-5.2, P= 0.0003), and was universally associated with decreased popliteal venous return (19/19 vs. 9/19 subjects, P< 0.004). The difference in diaphragmatic excursion correlated with the difference in IVCCI (Spearman’s rho = 0.53, P= 0.024).
CONCLUSION: During inspiration of equivalent tidal volumes, the reduction in IVC diameter and lower extremity venous return was related to diaphragmatic excursion, suggesting that the IVC may be compressed through descent of the diaphragm.

The effect of breathing manner on inferior vena caval diameter
Eur J Echocardiogr. 2011 Feb;12(2):120-3

Acute Med, All Updates, ICU

H1N1 or CAP?

March 5, 2011 Cliff Leave a comment

A scoring system composed of clinical, radiological, and laboratory variables purports to distinguish H1N1 influenza virus infection from community acquired pneumonia¹. An accompanying editorial² suggests that while further validation is required, the most useful application of the score might be in those with a score of 0 or 1 (out of 5), in whom the the high negative predictive value might safely avoid inpatient isolation and neuraminidase inhibitor treatment in the under-65s.

Background Early identification of patients with H1N1 influenza-related pneumonia is desirable for the early instigation of antiviral agents. A study was undertaken to investigate whether adults admitted to hospital with H1N1 influenza-related pneumonia could be distinguished clinically from patients with non-H1N1 community-acquired pneumonia (CAP).
Methods Between May 2009 and January 2010, clinical and epidemiological data of patients with confirmed H1N1 influenza infection admitted to 75 hospitals in the UK were collected by the Influenza Clinical Information Network (FLU-CIN). Adults with H1N1 influenza-related pneumonia were identified and compared with a prospective study cohort of adults with CAP hospitalised between September 2008 and June 2010, excluding those admitted during the period of the pandemic.
Results Of 1046 adults with confirmed H1N1 influenza infection in the FLU-CIN cohort, 254 (25%) had H1N1 influenza-related pneumonia on admission to hospital. In-hospital mortality of these patients was 11.4% compared with 14.0% in patients with inter-pandemic CAP (n=648). A multivariate logistic regression model was generated by assigning one point for each of five clinical criteria: age ≤65 years, mental orientation, temperature ≥38°C, leucocyte count ≤12×10(9)/l and bilateral radiographic consolidation. A score of 4 or 5 predicted H1N1 influenza-related pneumonia with a positive likelihood ratio of 9.0. A score of 0 or 1 had a positive likelihood ratio of 75.7 for excluding it.
Conclusion There are substantial clinical differences between H1N1 influenza-related pneumonia and inter-pandemic CAP. A model based on five simple clinical criteria enables the early identification of adults admitted with H1N1 influenza-related pneumonia.

1. Clinical and laboratory features distinguishing pandemic H1N1 influenza-related pneumonia from interpandemic community-acquired pneumonia in adults
Thorax. 2011 March; 66(3): 247–252 Free Full Text
2. Predicting the unpredictable: is it possible clinically to separate H1N1 from non-H1N1 community-acquired pneumonia?
Thorax. 2011 Mar;66(3):187-8

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