Tag Archives: haematology


Central lines in coagulopathic patients

If a patient needs a central line, he/she needs one. Often low platelets or a deranged coagulation profile are cited as reasons for omitting or delaying the procedure, but this is not based on evidence of increased complications. A recent Best Evidence Topic Review concludes:

…insertion of CVC lines do not require correction of haemostatic abnormalities prior to intervention. Rates of haemorrhage are low in patients with elevated PT, APTT or low thrombocyte count and appear to be closely related to the level of experience of the physician … rather than the defects of haemostasis.

Links to the abstracts of a couple of relevant articles reviewed are included below.

Central line insertion in deranged clotting
Emerg Med J. 2011 Jun;28(6):536-7 Full text

Low levels of prothrombin time (INR) and platelets do not increase the risk of significant bleeding when placing central venous catheters.
Med Klin (Munich). 2009 May 15;104(5):331-5

US-guided placement of central vein catheters in patients with disorders of hemostasis
Eur J Radiol. 2008 Feb;65(2):253-6

Erythropoietin for STEMI

In STEMI patients, intravenous erythropoietin within 4 hours of PCI did not reduce infarct size and was associated with higher rates of adverse cardiovascular events

Context Acute ST-segment elevation myocardial infarction (STEMI) is a leading cause of morbidity and mortality. In experimental models of MI, erythropoietin reduces infarct size and improves left ventricular (LV) function.


Objective To evaluate the safety and efficacy of a single intravenous bolus of epoetin alfa in patients with STEMI.


Design, Setting, and Patients A prospective, randomized, double-blind, placebo-controlled trial with a dose-escalation safety phase and a single dose (60 000 U of epoetin alfa) efficacy phase; the Reduction of Infarct Expansion and Ventricular Remodeling With Erythropoietin After Large Myocardial Infarction (REVEAL) trial was conducted at 28 US sites between October 2006 and February 2010, and included 222 patients with STEMI who underwent successful percutaneous coronary intervention (PCI) as a primary or rescue reperfusion strategy.


Intervention Participants were randomly assigned to treatment with intravenous epoetin alfa or matching saline placebo administered within 4 hours of reperfusion.


Main Outcome Measure Infarct size, expressed as percentage of LV mass, assessed by cardiac magnetic resonance (CMR) imaging performed 2 to 6 days after study medication administration (first CMR) and again 12 ± 2 weeks later (second CMR).


Results In the efficacy cohort, the infarct size did not differ between groups on either the first CMR scan (n = 136; 15.8% LV mass [95% confidence interval {CI}, 13.3-18.2% LV mass] for the epoetin alfa group vs 15.0% LV mass [95% CI, 12.6-17.3% LV mass] for the placebo group; P = .67) or on the second CMR scan (n = 124; 10.6% LV mass [95% CI, 8.4-12.8% LV mass] vs 10.4% LV mass [95% CI, 8.5-12.3% LV mass], respectively; P = .89). In a prespecified analysis of patients aged 70 years or older (n = 21), the mean infarct size within the first week (first CMR) was larger in the epoetin alfa group (19.9% LV mass; 95% CI, 14.0-25.7% LV mass) than in the placebo group (11.7% LV mass; 95% CI, 7.2-16.1% LV mass) (P = .03). In the safety cohort, of the 125 patients who received epoetin alfa, the composite outcome of death, MI, stroke, or stent thrombosis occurred in 5 (4.0%; 95% CI, 1.31%-9.09%) but in none of the 97 who received placebo (P = .04).


Conclusions In patients with STEMI who had successful reperfusion with primary or rescue PCI, a single intravenous bolus of epoetin alfa within 4 hours of PCI did not reduce infarct size and was associated with higher rates of adverse cardiovascular events. Subgroup analyses raised concerns about an increase in infarct size among older patients.

Intravenous Erythropoietin in Patients With ST-Segment Elevation Myocardial Infarction
JAMA. 2011 May 11;305(18):1863-72

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)

Thrombolysis for PE after limb surgery

A patient develops shock and dyspnoea on the orthopaedic ward after a total knee replacement and massive pulmonary embolism is confirmed radiologically. Would you give a fibrinolytic or is it contraindicated? Harry Wright and colleagues did, but before giving 50 mg of intravenous rtPA they applied a tourniquet (Cryocuff) to the limb to limit the proportion of the systemic thrombolytic agent that would reach the site of the surgery. The tourniquet was inflated just before the infusion and was left on for one hour. There was some oozing of blood from the postoperative wound, which settled with bandage compression. The authors state that the inflation time of one hour was sufficient for the thrombolytic agent to be largely eliminated from the circulation, since alteplase has a plasma half-life of less than five minutes, although some plasminogen activator activity does persist for up to four hours.

The patient was well at three month follow up. They suggest:

Given the success in this case, we believe that major limb surgery no longer represents a contraindication to thrombolysis.

Thrombolysis for postoperative pulmonary embolism: limiting the risk of haemorrhage
Thorax. 2011 May;66(5):452

Balloon catheters for haemorrhage control

Something I keep up my sleeve (not literally) for managing some life-threatening vascular wounds prior to surgery is the use of a balloon catheter like a foley to tamponade haemorrhage. This paper looks at series of such attempts although they state: “Except for the base of the skull (naso/oropharynx), all catheters were de- ployed in the operating room.“, so not exactly emergency medicine / pre-hospital practice, but a useful reminder that this is an option when going immediately to the operating room isn’t:

BACKGROUND: : Balloon catheter tamponade is a valuable technique for arresting exsanguinating hemorrhage. Indications include (1) inaccessible major vascular injuries, (2) large cardiac injuries, and (3) deep solid organ parenchymal bleeding. Published literature is limited to small case series. The primary goal was to review a recent experience with balloon catheter use for emergency tamponade in a civilian trauma population.

METHODS: : All patients requiring emergency use of a balloon catheter to tamponade exsanguinating hemorrhage (1998-2009) were included. Patient demographics, injury characteristics, technique, and outcomes were analyzed.

RESULTS: : Of the 44 severely injured patients (82% presented with hemodynamic instability; mean base deficit = -20.4) who required balloon catheter tamponade, 23 of the balloons (52%) remained indwelling for more than 6 hours. Overall mortality depended on the site of injury/catheter placement and indwelling time (81% if <6 hours; 52% if ≥6 hours; p < 0.05). Physiologic exhaustion was responsible for 76% of deaths in patients with short-term balloons. Mortality among patients with prolonged balloon catheter placement was 11%, 50%, and 88% for liver, abdominal vascular, and facial/pharyngeal injuries, respectively. Mean indwelling times for iliac, liver, and carotid injuries were 31 hours, 53 hours, and 78 hours, respectively. Overall survival rates were 67% (liver), 67% (extremity vascular), 50% (abdominal vascular), 38% (cardiac), and 8% (face). Techniques included Foley, Fogarty, Blakemore, and/or Penrose drains with concurrent red rubber Robinson catheters. Initial tamponade of bleeding structures was successful in 93% of patients.

CONCLUSIONS: : Balloon catheter tamponade can be used in multiple anatomic regions and for variable patterns of injury to arrest ongoing hemorrhage. Placement for central hepatic gunshot wounds is particularly useful. This technique remains a valuable tool in a surgeon’s armamentarium.

A Decade’s Experience With Balloon Catheter Tamponade for the Emergency Control of Hemorrhage
J Trauma. 2011 Feb;70(2):330-3

Fibrinogen concentrate

A case report of massive obstetric haemorrhage due to placental abruption describes the successful management of haemorrhage associated with a low fibrinogen level with blood products that included fibrinogen concentrate.

Fibrinogen concentrate can be available more quickly than other clotting products as it is rapidly solubilised from an ampoule in 50 ml water and given as a bolus. To raise the plasma fibrinogen concentration by 1 g/l in a 70-kg person, 1000 ml fresh frozen plasma (6 standard UK units), or 260 ml cryoprecipitate (10 standard UK units) will be required. Administration of adequate doses of fresh frozen plasma or cryoprecipitate to treat hypofibrinogenaemia during obstetric haemorrhage will therefore take a substantial amount of time, even with an efficient blood bank and portering system.

Fibrinogen concentrate use during major obstetric haemorrhage
Anaesthesia 2010;65(12):1229–1230

A previous retrospective study showed its use in a series of surgical and obstetric haemorrhage cases may have been associated with a subsequent decreased need for other blood products.

Fibrinogen concentrate substitution therapy in patients with massive haemorrhage and low plasma fibrinogen concentrations
Br. J. Anaesth. (2008) 101 (6): 769-773 (Full text)

rFVIIa did not reduce trauma mortality

An industry sponsored placebo-controlled multicentre randomised controlled trial has shown no mortality reduction from recombinant activated Factor VII (rFVIIa) in patients with trauma.

rFVIIa acts physiologically by enhancing clot formation in the presence of tissue factor expressed on injured or ischemic vascular subendothelium. It also acts pharmacologically, binding directly to activated platelets, increasing thrombin burst, and promoting the formation of a stable hemostatic plug.

Blunt and/or penetrating trauma patients aged 18 years to 70 years were eligible if they had continuing torso and/or proximal lower extremity bleeding after receiving 4 units of RBCs despite standard hemostatic interventions. There was no 30 day mortality reduction, although fewer blood products were transfused from dosing to 24 hours in the rFVIIa group.

No significant difference was seen in the safety profile of rFVIIa compared with placebo.

The CONTROL trial was terminated early (573 of 1502 patients) after an interim analysis suggested a high likelihood of futility in demonstrating the primary endpoint in the blunt trauma population.

Results of the CONTROL Trial: Efficacy and Safety of Recombinant Activated Factor VII in the Management of Refractory Traumatic Hemorrhage
Journal of Trauma-Injury Infection & Critical Care September 2010 69(3):489-500

European Trauma Bleeding Guidelines updated

 


Update 2013: since this post was written in 2010, new guidelines have been written entitled: “Management of bleeding and coagulopathy following major trauma: an updated European guideline” which are available here

 

The 2007 guidelines on management of bleeding in trauma have been updated in the light of new evidence and modern practice. The guideline group summarises their recommendations as:

  1. We recommend that the time elapsed between injury and operation be minimised for patients in need of urgent surgical bleeding control. (Grade 1A).
  2. We recommend adjunct tourniquet use to stop life-threatening bleeding from open extremity injuries in the pre-surgical setting. (Grade 1C).
  3. We recommend that the physician clinically assess the extent of traumatic haemorrhage using a combination of mechanism of injury, patient physiology, anatomical injury pattern and the patient’s response to initial resuscitation. (Grade 1C).
  4. We recommend initial normoventilation of trauma patients if there are no signs of imminent cerebral herniation. (Grade 1C).
  5. We recommend that patients presenting with haemorrhagic shock and an identified source of bleeding undergo an immediate bleeding control procedure unless initial resuscitation measures are successful. (Grade 1B).
  6. We recommend that patients presenting with haemorrhagic shock and an unidentified source of bleeding undergo immediate further investigation. (Grade 1B).
  7. We recommend early imaging (FAST or CT) for the detection of free fluid in patients with suspected torso trauma. (Grade 1B).
  8. We recommend that patients with significant free intraabdominal fluid and haemodynamic instability undergo urgent intervention. (Grade 1A).
  9. We recommend further assessment using computed tomography for haemodynamically stable patients who are either suspected of having torso bleeding or have a high risk mechanism of injury. (Grade 1B).
  10. We do not recommend the use of single haematocrit measurements as an isolated laboratory marker for bleeding. (Grade 1B).
  11. We recommend both serum lactate and base deficit measurements as sensitive tests to estimate and monitor the extent of bleeding and shock. (Grade 1B).
  12. We recommend that routine practice to detect post-traumatic coagulopathy include the measurement of international normalised ratio (INR), activated partial thromboplastin time (APTT), fibrinogen and platelets. INR and APTT alone should not be used to guide haemostatic therapy. (Grade 1C) We suggest that thrombelastometry also be performed to assist in characterising the coagulopathy and in guiding haemostatic therapy. (Grade 2C).
  13. We recommend that patients with pelvic ring disruption in haemorrhagic shock undergo immediate pelvic ring closure and stabilisation. (Grade 1B).
  14. We recommend that patients with ongoing haemodynamic instability despite adequate pelvic ring stabilisation receive early preperitoneal packing, angiographic embolisation and/or surgical bleeding control. (Grade 1B).
  15. We recommend that early bleeding control of the abdomen be achieved using packing, direct surgical bleeding control and the use of local haemostatic procedures. In the exsanguinating patient, aortic cross-clamping may be employed as an adjunct. (Grade 1C).
  16. We recommend that damage control surgery be employed in the severely injured patient presenting with deep hemorrhagic shock, signs of ongoing bleeding and coagulopathy. Additional factors that should trigger a damage control approach are hypothermia, acidosis, inaccessible major anatomic injury, a need for time-consuming procedures or concomitant major injury outside the abdomen. (Grade 1C).
  17. We recommend the use of topical haemostatic agents in combination with other surgical measures or with packing for venous or moderate arterial bleeding associated with parenchymal injuries. (Grade 1B).
  18. We recommend a target systolic blood pressure of 80-100 mmHg until major bleeding has been stopped in the initial phase following trauma without brain injury. (Grade 1C).
  19. We recommend that crystalloids be applied initially to treat the bleeding trauma patient. (Grade 1B) We suggest that hypertonic solutions also be considered during initial treatment. (Grade 2B) We suggest that the addition of colloids be considered within the prescribed limits for each solution in haemodynamically unstable patients. (Grade 2C).
  20. We recommend early application of measures to reduce heat loss and warm the hypothermic patient in order to achieve and maintain normothermia. (Grade 1C).
  21. We recommend a target haemoglobin (Hb) of 7-9 g/dl. (Grade 1C).
  22. We recommend that monitoring and measures to support coagulation be initiated as early as possible. (Grade 1C).
  23. We recommend that ionised calcium levels be monitored during massive transfusion. (Grade 1C) We suggest that calcium chloride be administered during massive transfusion if ionised calcium levels are low or electrocardiographic changes suggest hypocalcaemia. (Grade 2C).
  24. We recommend early treatment with thawed fresh frozen plasma in patients with massive bleeding. (Grade 1B) The initial recommended dose is 10-15 ml/kg. Further doses will depend on coagulation monitoring and the amount of other blood products administered. (Grade 1C).
  25. We recommend that platelets be administered to maintain a platelet count above 50 × 109/l. (Grade 1C) We suggest maintenance of a platelet count above 100 × 109/l in patients with multiple trauma who are severely bleeding or have traumatic brain injury. (Grade 2C) We suggest an initial dose of 4-8 platelet concentrates or one aphaeresis pack. (Grade 2C).
  26. We recommend treatment with fibrinogen concentrate or cryoprecipitate if significant bleeding is accompanied by thrombelastometric signs of a functional fibrinogen deficit or a plasma fibrinogen level of less than 1.5-2.0 g/l. (Grade 1C) We suggest an initial fibrinogen concentrate dose of 3- 4 g or 50 mg/kg of cryoprecipitate, which is approximately equivalent to 15-20 units in a 70 kg adult. Repeat doses may be guided by thrombelastometric monitoring and laboratory assessment of fibrinogen levels. (Grade 2C).
  27. We suggest that antifibrinolytic agents be considered in the bleeding trauma patient. (Grade 2C) We recommend monitoring of fibrinolysis in all patients and administration of antifibrinolytic agents in patients with established hyperfibrinolysis. (Grade 1B) Suggested dosages are tranexamic acid 10-15 mg/kg followed by an infusion of 1-5 mg/kg per hour or ε-aminocaproic acid 100-150 mg/kg followed by 15 mg/kg/h. Antifibrinolytic therapy should be guided by thrombelastometric monitoring if possible and stopped once bleeding has been adequately controlled. (Grade 2C).
  28. We suggest that the use of recombinant recombinant activated coagulation factor VII (rFVIIa) be considered if major bleeding in blunt trauma persists despite standard attempts to control bleeding and best-practice use of blood components. (Grade 2C).
  29. We recommend the use of prothrombin complex concentrate for the emergency reversal of vitamin K-dependent oral anticoagulants. (Grade 1B).
  30. We do not suggest that desmopressin (DDAVP) be used routinely in the bleeding trauma patient. (Grade 2C) We suggest that desmopressin be considered in refractory microvascular bleeding if the patient has been treated with platelet-inhibiting drugs such as aspirin. (Grade 2C).
  31. We do not recommend the use of antithrombin concentrates in the treatment of the bleeding trauma patient. (Grade 1C).

Management of bleeding following major trauma: an updated European guideline.
Crit Care. 2010 Apr 6;14(2):R52 (Pub Med abstract)
Full Text Link

Battlefield resuscitation

An excellent review of the current British military practice to prevent and treat the acute coagulopathy of trauma shock (ACoTS) describes pathophysiology and treatment options and offers an algorithm for management. Key components of the system (when indicated according to their algorithm) outlined include:

  • Pre-hospital damage control shock resuscitation by a forward medical team, consisting of RSI with reduced dose thio or ketamine with suxamethonium or rocuronium, large bore sublclavian access, and early use of warmed blood products
  • 1:1:1 packed red cells, fresh frozen plasma, and platelets,
  • Cryoprecipitate
  • Tranexamic acid
  • Recombinant activated factor VII
  • Permissive hypotension aiming for a systolic BP of 90 mmHg, using blood products and avoiding vasopressors according to a ‘flow rather than pressure’ philosophy
  • Avoiding hypothermia by giving warmed blood products and employing active patient warming methods
  • Buffering acidosis using Tris-hydroxymethyl aminomethane (THAM), which may be superior to bicarbonate by not affecting minute ventilation or coagulation, and maintaining its efficacy in hypothermic conditions
  • Minimising hypoperfusion with an anaesthetic strategy that provides effective analgesia and vasodilation, using high dose fentanyl and a low concentration volatile agent
  • Using fresh whole blood for resistant coagulopathy

Battlefield resuscitation
Curr Opin Crit Care. 2009 Dec;15(6):527-35

Extreme white cell counts

Febrile children aged three months to three years with a white cell count over 25000/mm3 and fever were compared with controls whose leucoytosis was less extreme (15000-24999). The ‘extreme’ group had serious bacterial infection (SBI) in 39% compared with 15.4% controls. Pneumonia was the commonest SBI.

The authors conclude that in febrile children aged 3–36 months, the presence of extreme leucocytosis is associated with a 39% risk of having SBIs. The increased risk for SBI is mainly due to a higher risk for pneumonia. I conclude that leucocytosis is like fever: the cause may be benign, but the higher the number the less likely that is, even though the majority still won’t have SBI.

Extreme leucocytosis and the risk of serious bacterial infections in febrile children
Arch Dis Child. 2010 Mar;95(3):209-12