Tag Archives: Guidelines

Drugs in cardiac arrest – guess what works?

Just like epinephrine (adrenaline), amiodarone does not increase survival to hospital discharge in cardiac arrest patients. I doubt his will deter the people in the resuscitation room with their stopwatches from handing me these drugs and telling me I ought to be giving them though.

Amiodarone - a load of balls

 

AIMS: In adult cardiac arrest, antiarrhythmic drugs are frequently utilized in acute management and legions of medical providers have memorized the dosage and timing of administration. However, data supporting their use is limited and is the focus of this comprehensive review.

METHODS: Databases including PubMed, Cochrane Library (including Cochrane database for systematic reviews and Cochrane Central Register of Controlled Trials), Embase, and AHA EndNote Master Library were systematically searched. Further references were gathered from cross-references from articles and reviews as well as forward search using SCOPUS and Google scholar. The inclusion criteria for this review included human studies of adult cardiac arrest and anti-arrhythmic agents, peer-review. Excluded were review articles, case series and case reports.

RESULTS: Of 185 articles found, only 25 studies met the inclusion criteria for further review. Of these, 9 were randomised controlled trials. Nearly all trials solely evaluated Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF), and excluded Pulseless Electrical Activity (PEA) and asystole. In VT/VF patients, amiodarone improved survival to hospital admission, but not to hospital discharge when compared to lidocaine in two randomized controlled trials.

CONCLUSION: Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.

The use of antiarrhythmic drugs for adult cardiac arrest: A systematic review
Resuscitation. 2011 Jun;82(6):665-70

Thrombolysis in submassive PE – still equipoise?

The AHA has produced a comprehensive guideline on venous thromboembolic disease. Here are some excerpts pertaining to resuscitation room decision making, particularly: ‘should I thrombolyse this patient?’

Definition for massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).
Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.
RV dysfunction means the presence of at least 1 of the following:

  • RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
  • RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
  • Elevation of BNP (>90 pg/mL)
  • Elevation of N-terminal pro-BNP (>500 pg/mL); or
  • Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Myocardial necrosis is defined as either of the following:

  • Elevation of troponin I (>0.4 ng/mL) or
    Elevation of troponin T (>0.1 ng/mL)

Odds ratio for short-term mortality for RV dysfunction on echocardiography = 2.53 (95% CI 1.17 to 5.50).
Troponin elevations had an odds ratio for mortality of 5.90 (95% CI 2.68 to 12.95).
Definition for low risk PE: those with normal RV function and no elevations in biomarkers with short-term mortality rates approaching ≈ 1%

Recommendations for Initial Anticoagulation for Acute PE

  • Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
  • Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C).

 
Patients treated with a fibrinolytic agent have faster restoration of lung perfusion. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. However, by 7 days, blood flow improves similarly (≈65% to 70% reduction in total defect).
Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
When Wan et al restricted their analysis to those trials with massive PE, they identified a significant reduction in recurrent PE or death from 19.0% with heparin alone to 9.4% with fibrinolysis (odds ratio 0.45, 95% CI 0.22 to 0.90).
Data from registries indicate that the short-term mortality rate directly attributable to submassive PE treated with heparin anticoagulation is probably < 3.0%. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment.
Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. Patients with low-risk PE have an unfavorable risk-benefit ratio with fibrinolysis. Patients with PE that causes hypotension probably do benefit from fibrinolysis. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment.

An algorithm is proposed:

Two criteria can be used to assist in determining whether a patient is more likely to benefit from fibrinolysis: (1) Evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.
Evidence of circulatory failure includes any episode of hypotension or a persistent shock index (heart rate in beats per minute divided by systolic blood pressure in millimeters of mercury) >1
The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).
Evidence of moderate to severe RV injury may be derived from Doppler echocardiography that demonstrates any degree of RV hypokinesis, McConnell’s sign (a distinct regional pattern of RV dysfunction with akinesis of the mid free wall but normal motion at the apex), interventricular septal shift or bowing, or an estimated RVSP > 40 mm Hg.
Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides.
Two trials are currently ongoing that aim to assess effect of thrombolysis on patients with submassive PE: PEITHO and TOPCOAT

Recommendations for Fibrinolysis for Acute PE

  • Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
  • Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
  • Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
  • Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).

Recommendations for Catheter Embolectomy and Fragmentation

  • Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
  • Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
  • For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C).
  • Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
  • Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C).

 
Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension
Circulation. 2011 Apr 26;123(16):1788-1830 (Free Full Text)

It's a bit quiet in here

Blogging has slowed a bit as I’ve been travelling to the UK and am running courses here all week.
Just in case you’re desperate to read something useful, I came across a guideline on The Management of Diabetic Ketoacidosis in Adults by the Joint British Diabetes Societies Inpatient Care Group
The guideline contain the following approaches:

  • Measurement of blood ketones, venous (not arterial) pH and bicarbonate and their use as treatment markers
  • Monitoring of ketones and glucose using bedside meters when available and operating within their quality assurance range
  • Replacing ‘sliding scale’ insulin with weight-based fixed rate intravenous insulin infusion (IVII)
  • Use of venous blood rather than arterial blood in blood gas analysers
  • Monitoring of electrolytes on the blood gas analyser with intermittent laboratory confirmation
  • Continuation of long acting insulin analogues (Lantus® or Levemir®) as normal
  • Involvement diabetes specialist team as soon as possible

There is also a section on ‘Controversial Areas’, discussing such issues as bicarbonate therapy, rate of fluid therapy, and even 0.9% saline versus Hartmann’s (Ringer’s Lactate) solution, although this part was desperately disappointing, with the following bizarre excuse given for not recommending the latter:
In theory replacement with glucose and compound sodium lactate (Hartmann’s solution) with potassium, would prevent hyperchloraemic metabolic acidosis, as well as allow appropriate potassium replacement. However, at present this is not readily available as a licensed infusion fluid.
Apart from that, this appears to be an interesting and potentially useful document.
The Management of Diabetic Ketoacidosis in Adults
Joint British Diabetes Societies Inpatient Care Group

STEMI criteria vary with age and sex

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

  1. 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.
  2. 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).
  3. 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.
  4. 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.
  5. For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
  6. 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

Military trauma care meets standards

Recent recommendations were made regarding trauma care in the UK by the National Confidential Enquiry into Patient Outcome and Death (NCEPOD).
British military physicians at the UK military field hospital, Camp Bastion, Helmand Province, Afghanistan, evaluated their trauma cases against these standards. It is apparent that the trauma care provided to some people in Afghanistan outclasses that delivered within much of the UK.

Military medical teams

Background The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) report on trauma management, published in 2007, defined standards for United Kingdom (UK) hospitals dealing with trauma. This study compared the NCEPOD standards with the performance of a UK military field hospital in Afghanistan. Setting UK military field hospital, Camp Bastion, Helmand Province, Afghanistan.
Materials and methods Data were collected prospectively for all patients fulfilling the trauma team activation criteria during the 3 months of Operation Herrick IXa (from mid October 2008 to mid January 2009) and combined with a retrospective review of prehospital documentation, trauma resuscitation notes, operations notes and transfer notes for these patients.
Results During the study period, there were 226 trauma team activations. Of those patients brought to the medical facility at Camp Bastion by UK assets, 93.7% were accompanied by a doctor with advanced airway skills, although only 6.2% of the patients required such an intervention. Consultants in emergency medicine and anaesthesia were present in 100% of cases and were directly involved (in either leading the team or performing airway management) in 63.5% and 77.6% of cases respectively. Of those patients requiring operative intervention, 98.1% had this performed by a consultant surgeon. Of those patients requiring CT, 93.6% of cases had this performed within 1 h of arrival.
Conclusions Trauma patients presenting to the medical facility at Camp Bastion during Operation Herrick IXa, irrespective of their nationality or background, received a high standard of medical care when compared with the NCEPOD standards

National Confidential Enquiry into Patient Outcome and Death recommendations
Pre-hospital care
All agencies involved in trauma management, including emergency medical services, should be integrated into the clinical governance programmes of a regional trauma service. Airway management in trauma patients is often challenging, and the pre-hospital response for these patients should include someone with the skill to secure the airway, (including the use of rapid sequence intubation), and maintain adequate ventilation.
Hospital reception
A trauma team should be available 24 h a day, 7 days a week. This is an essential part of an organised trauma response system. A consultant must be the team leader for the management of the severely injured patient.
Airway and breathing
The current structure of prehospital management is insufficient. There is a high incidence of failed intubation and a high incidence of patients arriving at hospital with a partially or completely obstructed airway. Change is urgently required to provide a system that reliably provides a clear airway with good oxygenation and control of ventilation. This may be through the provision of personnel with the ability to provide anaesthesia and intubation in the prehospital phase or through the use of alternative airway devices.
Circulation
Trauma laparotomy is extremely challenging and requires consultant presence within the operating theatre. If CT is to be performed, all necessary images should be obtained at the same time, and routine use of head-to-toe scanning is recommended in the adult trauma patient if no indication for immediate intervention exists.
Head injuries
Patients with severe head injury should have a CT of the head performed as soon as possible after admission and within 1 hour of arrival at the hospital. All patients with severe head injury should be transferred to a neurosurgical critical care centre irrespective of the requirement for surgical intervention.
Transfers
There should be standardised transfer documentation of patient details, injuries, results of investigations and management, with records kept at the dispatching and receiving hospitals.
A comparison of civilian (National Confidential Enquiry into Patient Outcome and Death) trauma standards with current practice in a deployed field hospital in Afghanistan.
Emerg Med J 2011;28:310-312

Suspension syncope

Loss of consciousness can occur when a patient is suspended in a harness – ‘suspension syncope’, probably due to factors that include venous pooling in the lower limbs. An evidence based review of this entity was carried out:

The possibility of a fall into rope protection and subsequent suspension exists in some industrial situations. The action to take for the first aid management of rescued victims has not been clear, with some authors advising against standard first aid practices. To clarify the medical evidence relating to harness suspension the UK Health and Safety Executive commissioned an evidence-based review and guideline. Four key questions were posed relating to the incidence, circumstances, recognition and first aid management of the medical effects of harness suspension. A comprehensive literature search returned 60 potential papers with 29 papers being reviewed. The Scottish Intercollegiate Guideline Network (SIGN) methodology was used to critically review the selected papers and develop a guideline. A stakeholders’ workshop was held to review the evidence and draft recommendations. Nine papers formed the basis of the guideline recommendations. No data on the incidence of harness suspension syncope were found. Presyncopal symptoms or syncope are thought to occur with motionless suspension as a consequence of orthostasis leading to hypotension. There was no evidence of any other pathology, despite this being hypothesised by others. No evidence was found that showed the efficacy or safety of positioning a victim in a semirecumbent position. In any case of harness suspension, the standard UK first aid guidance for recovery of a semiconscious or unconscious person in a horizontal position should be followed. Other recommendations included areas for further research and proposals for standard data collection on falls into rope protection.

Harness suspension and first aid management: development of an evidence-based guideline
Emerg Med J 2011;28:265-268

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

ILCOR neonatal cooling guideline

On the basis of the published data to date the Neonatal Task Force of the International Liaison Committee on Resuscitation (ILCOR) made the following recommendation on February 2010 with regard to therapeutic hypothermia:

  • Newly born infants born at term or near-term with evolving moderate to severe hypoxic-ischemic encephalopathy should be offered therapeutic hypothermia.
  • Whole-body cooling and selective head cooling are both appropriate strategies.
  • Cooling should be initiated and conducted in neonatal intensive care facilities using protocols consistent with those used in the randomized clinical trials i.e. commence within 6 h, continue for 72 h and rewarm over at least 4 h.
  • Carefully monitor for known adverse effects of cooling – thrombocytopenia and hypotension.
  • All treated infants should be followed longitudinally.

Therapeutic hypothermia following intrapartum hypoxia-ischemia. An advisory statement from the Neonatal Task Force of the International Liaison Committee on Resuscitation
Resuscitation 2010;81(11):1459-1461

2J or 4J/kg in Paediatric Defibrillation?

Should we shock with 2J/kg or 4J/kg in Paediatric Defibrillation? The answer seems to be ‘we still don’t know’. Don’t worry – just follow the guidelines (reproduced for you at the bottom)
OBJECTIVE To examine the effectiveness of initial defibrillation attempts. We hypothesized that (1) an initial shock dose of 2 ± 10 J/kg would be less effective for terminating fibrillation than suggested in published historical data and (2) a 4 J/kg shock dose would be more effective.
PATIENTS AND METHODS This was a National Registry of Cardiopulmonary Resuscitation prospective, multisite, observational study of in-hospital pediatric (aged 18 years) ventricular fibrillation or pulseless ventricular tachycardia cardiac arrests from 2000–2008. Termination of ventricular fibrillation or pulseless ventricular tachycardia and event survival after initial shocks of 2 J/kg were compared with historic controls and a 4 J/kg shock dose.

RESULTS Of 266 children with 285 events, 173 of 285 (61%) survived the event and 61 of 266 (23%) survived to discharge. Termination of fibrillation after initial shock was achieved for 152 of 285 (53%) events. Termination of fibrillation with 2 ± 10 J/kg was much less frequent than that seen among historic control subjects (56% vs 91%; P < .001), but not different than 4 J/kg. Compared with 2 J/kg, an initial shock dose of 4 J/kg was associated with lower rates of return of spontaneous circulation (odds ratio: 0.41 [95% confidence interval: 0.21–0.81]) and event survival (odds ratio: 0.42 [95% confidence interval: 0.18–0.98]).
CONCLUSIONS The currently recommended 2 J/kg initial shock dose for in-hospital cardiac arrest was substantially less effective than previously published. A higher initial shock dose (4 J/kg) was not associated with superior termination of ventricular fibrillation or pulseless ventricular tachycardia or improved survival rates. The optimal pediatric defibrillation dose remains unknown.
Effect of defibrillation energy dose during in-hospital pediatric cardiac arrest
Pediatrics. 2011 Jan;127(1):e16-23
Here’s what the guidelines say:
Many AEDs have high specificity in recognizing pediatric shockable rhythms, and some are equipped to decrease (or attenuate) the delivered energy to make them suitable for infants and children <8 years of age. For infants a manual defibrillator is preferred when a shockable rhythm is identified by a trained healthcare provider (Class IIb, LOE C). The recommended first energy dose for defibrillation is 2 J/kg. If a second dose is required, it should be doubled to 4 J/kg. If a manual defibrillator is not available, an AED equipped with a pediatric attenuator is preferred for infants. An AED with a pediatric attenuator is also preferred for children <8 year of age. If neither is available, an AED without a dose attenuator may be used (Class IIb, LOE C). AEDs that deliver relatively high energy doses have been successfully used in infants with minimal myocardial damage and good neurological outcomes
Pediatric Basic Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Full text document

UK children sedation guideline

Despite the huge number of articles in the literature on paediatric sedation, one still encounters acrimonious debates about the appropriateness of non-anaesthetists doing it. How refreshing then, to see that the UK’s National Institute for Health & Clinical Excellence (“NICE”) has tackled this subject and come up with some reasonable recommendations. I’ve as yet only read the summary, but some of the good things are:

  • No unachievable ‘two doctors present’ rule: ‘Two trained healthcare professionals should be available during sedation
  • Differentiating painless imaging from painful procedures
  • Monitoring standards that are appropriate for the age of child and depth of sedation (no mandatory blood pressure or ECG monitoring unless deep sedation; end-tidal capnography in deep sedation).
  • Acknowledgement of the special features of ketamine: ‘Ketamine is a dissociative agent: the state of dissociative sedation cannot be readily categorised as either moderate or deep sedation; the drug is considered to have a wide margin of safety.’
  • Recognition that specialists other than anaesthetists may have specialist sedation and airway skills

There are some rather conservative recommendations on fasting, although the wording of the guideline in my interpretation allows some flexibility if ketamine is used for an emergency procedure.
Sedation in children and young people
National Institute for Health & Clinical Excellence