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Emergencies and ICU

Jump to:

  • Trauma, including Burns

Resuscitation

Official guidelines available as PDFs from the Resus Council. Training is offered by the Advanced Life Support Group. My abbreviated APLS Guidelines are here.

IntraOsseous- bretylium is the only contraindicated drug! Feel calf for extravasation. Aspiration not always possible, doesn't mean you're in the wrong place. Warn labs if marrow samples sent (it blocks up their machines).

Changes to Paediatric Resuscitation guidelines (Resuscitation Council UK 2005):

  • Avoid ETT drugs (least satisfactory route, use 100mcg/kg adrenaline)
  • 1 shock only! 4J/kg for everyone.
  • 15:2 compressions for everyone, 100 per min, once intubated then uninterrupted, ventilate at 10 per min. Maximizes coronary perfusion, myocardial viability hence chance of successful defibrillation/outcome.
  • Automated External Defibrillator (AED) can be used for 8yrs plus, below that use paediatric/infant pads or appropriate program. If none available you can use the standard one for over 1 yr old but below that insufficient evidence.
  • Adrenaline dose is 10mcg/kg at all times.
  • After return of spontaneous circulation speed up ventilation to 12-20 per min.
  • Reversible causes are H's and T's: hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia; tension pneumo, tamponade, toxic/therapeutic, thromboembolism.

2005 changes to AHA resuscitation guidelines:

  • Dangers of endotracheal tubes (ETTs) emphasised. Laryngeal masks are acceptable in skilled hands.
  • Use exhaled carbon dioxide (CO2) for confirming ETT position.
  • With an advanced airway in place, no need to perform cycles of CPR. Instead, perform chest compressions continuously at 100/minute without pauses for ventilation. Deliver 8 to 10 breaths per minute (1 breath approximately every 6-8 seconds).
  • Routine use of high-dose epinephrine is not recommended.
  • Induced hypothermia (32-34 degrees C for 12-24 hours) may be considered if the child remains comatose after resuscitation.
  • Intact survival has been reported following prolonged resuscitation and 2 doses of epinephrine.
  • For neonates it is reasonable to begin resuscitation with an oxygen concentration of less than 100% or to start with room air - supplementary oxygen should be available if there is no appreciable improvement within 90 seconds after birth.
  • Current recommendations no longer advise routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born to mothers with meconium staining of amniotic fluid.
  • Infants without signs of life (no heartbeat and no respiratory effort) after 10 minutes of resuscitation show either a high mortality rate or severe neurodevelopmental disability.

Scores

The PIM is a predictive score, the second version (PIM2) has been validated in 20,787 children from ICUs in Australia, New Zealand, and the United Kingdom. Includes ten variables that are measured at entry into the PICU:

  • systolic blood pressure
  • pupillary reaction
  • Pao2
  • base excess
  • mechanical ventilation
  • elective admission to the ICU
  • recovering from surgery or procedure
  • admission after cardiac bypass
  • high-risk diagnosis
  • low-risk diagnosis

The discrimination value of the PIM-2 is 0.90. Similar, if not better, than the PRISM III score. PIM scores avoid problems of early treatment bias because it includes only data at entry into the PICU. General scales like PRISM and PIM scores may not be applicable to children with a specific disease, eg cancer, purpura fulminans but actually PRISM2 seems to work better than any of the 25+ scores developed for meningococcus!

Pediatric Logistic Organ Dysfunction (PELOD) score - 12 variables across 6 organ systems. Not a predictive score so much as a descriptive score although multiorgan dysfunction is associated with mortality.

Crash teams

Despite the resuscitation tools and drugs available, research suggests that time-to-treatment also has a significant impact on patient outcome. Identifying which patients may need intervention is perhaps not too difficult - there are almost always deteriorating basic observations eg respiratory rate, heart rate, blood pressure and sats; additionally, subjective factors eg work of breathing, nurse concern have also been associated with cardiac arrest. Furthermore, many of the pre-arrest clinical conditions have been deemed preventable eg arrests were more likely to occur in non–ICU settings; in inpatient units without adequate clinical expertise; under the care of trainees; handover times.

Having clear activation criteria for the medical emergency team is important. There may also be a role for a Rover Team that is made aware of patients at risk for deterioration - such a proactive approach helps by creating a shared mental model of clinical status and possible complications.

Such interventions have significantly reduced arrests, deaths and post-arrest ICU stays Clinical Pediatric Emergency Medicine Volume 7, Issue 4 , December 2006, Pages 241-247

Intubation check list

  • IV access
  • NGT
  • etCO2 and other monitoring (etCO2 may not be valid if poor cardiac output)
  • Oro/nasoph airways
  • Laryngeal mask, just in case
  • Yankauer
  • Tiltable bed
  • (Volume, inotropes if unstable patient)

Contraindications to nasal intubation - basal skull fracture,coagulopathy, cleft palate, age over 10 yrs

Rapid Sequence Induction (RSI)

For nonfasted, GI obstruction - but not if scary airway (gaseous?)

  • Preoxygenate (NOT same as sats 100%) - you want a residual volume of pure oxygen. But gentle bagging at most.
  • Empty stomach
  • Cricoid pressure from injection until position confirmed (so warn assistant)
  • To confirm position - see the tube go in! Else chest wall movement, breath sounds, moisture in tube, PEEP on T piece - but none 100% reliable
  • Suxamethonium (2-3mg/kg) - fastest onset/wear off (3mins), fasciculation is a useful clue, tachy or brady esp 2nd dose, hyperkalaemia (so contraindicated in burns after 36hr; also contraindicated in neuromuscular disease, family history of malignant hypertension)
  • Atracurium for renal failure (Hoffman degrad)

Failed intubation

Get help, oxygenate, is intubation really necessary eg laryngeal mask?, change equip!/approach, cricoid.

Fail through nose- trim suction catheter, use as guide wire.

Fail at cords- rotate to avoid tip getting wedged in vallecula.

Agents

  • Ketamine (1-2mg/kg) maintains/increases bp so good for sepsis, but contraindicated in RICP. Also bronchodilates so good for asthma. Can cause fits, hallucinations (give with benzodiazepine if >4yr), secretions (give with atropine or glycopyrrholate). Action: 15 minutes.
  • Thiopentone (2-5mg/kg) causes myocardial depression, bronchospasm. But good for RICP, fits. Action: 5 mins.
  • Propofol (3-4mg/kg) v fast.
  • Etomidate gives stable CVS
  • Sevoflurane non irritant, rapid (reversal too)

Induction takes longer if low cardiac output.

Postop cardiac

  • Blood/cxr forms
  • Cefuroxime 48hrs
  • Filter on test lung
  • What were anatomy/procedure, complics, times on bypass/crossclamp
  • What was Postop echo
  • What does surgeon want for bp/filling pressure
  • When does surgeon want to wake?
  • Fluids post bypass d1 50ml/kg, d2 75
  • Drains 2-5ml/kg/hr ok - above 2 definitely replace with HAS (depending on surgeon). Abrupt drop in output with rising CVP is emergency - impending tamponade.
  • Vasodilation post bypass usually leads to falling blood pressure. Small boluses ie 5ml/kg if needed
  • Beware high BP (risk of bursting sutures on left side) eg systolic over 100. GTN has short half life so easy to turn on and off but exhibits tachyphylaxis ie progressively less effective with time.
  • Low diastolic BP seen in run off through duct etc
  • Ionized calcium should be over 1.1, potassium should be kept high/normal
  • Ventriculotomy - causes RV bruising/bleeding. RBBB, JET(junctional ectopic tachycardia, ie rate 200-230). ?Poor compliance so need low cardiac demands and tend to develop pleural effusions.  Manage with inotropes (but not pressors), diuretics, nitric, ?milrinone.

Monitor cardiac output by:

  • BP
  • urine output
  • lactate (anything over 5, but less than plus rising too)
  • narrow pulse pressure (suggests vasoconstriction)
  • falling venous saturation (normal 65-75%, but less if cyanotic heart disease, misleadingly normal in hyperdynamic states)
  • drain losses, falling etCO2 (compensation), hepatomegaly

Pulmonary hypertension (clinically low sats, low BP, tachycardia, hepatomegaly; seen in previously high pulmonary flow eg VSD, Truncus):

  • bag with 100% O2 - high O2 and low CO2 as pulmonary vasodilators
  • sedate/paralyse
  • normalize CO2
  • Nitric Oxide - portable cylinders available
  • fluid bolus
  • avoid excessive suction

Heart rate:

  • in tachycardia, beware arrhythmia - 20% drop in CO if non-sinus rhythm
  • Tachycardia is expected in baby (main way of increasing cardiac output) so if not tachycardic and inadequate cardiac output then pace.
  • Isoprenaline for brady
  • Cooling for tachy

High Frequency Oscillatory Ventilation - HFOV

  • Mean airway pressure (MAP) determines oxygenation (recruitment of alveoli); delta P (=amplitude) and frequency determine ventilation (CO2 clearance). Increasing amplitude and decreasing frequency increase CO2 clearance.
  • Start with MAP at mean airway pressure of conventional ventilation, but often requires 5-10cm more. MAP attenuates down ETT esp narrow so don't worry too much about how high the pressure seems to be.
  • Over 25kg start hfov @5-8Hz, else 10Hz. Increase amplitude until reasonable visible oscillation in chest (should spread to thighs!).
  • Difficult to transfer once oscillated so transfer first if necessary
  • CXR less helpful cf neonates in judging recruitment (expansion)
  • Paralyse all
  • Anticipate drop in BP - preload with fluid, ?inotropes if borderline already
  • Care with suction - closed circuit system, else clamp tube, bag afterwards, increase MAP 5cm H2O for 10-30 minutes afterwards.
  • Consider weaning to conventional @MAP 20, sats 90, FiO2 0.6
  • Sensormedics - needs at least 15 l/min flow, press reset to pressurize, then start. Ignore MAP limit & %insp time. Piston centering according to wave. Delta P changes with compliance.

ECMO

Extracorporeal Membrane Oxygenation. Minimum 1.2kg, 32/40 corrected age. Not more than 7/7 high pressure ventilation. Unresponsive to conventional ie Oxygen Index >40 or pCO2>90mmHg.

OI = Paw (mean airway pressure)/PaO2 X FiO2 x 100, all in mmHg

  • Highest pressure in circuit found after the pump, before the membrane oxygenator. High post membrane pressure risks haemolysis or burst - kink, clot, cannula tip against wall.
  • VV double lumen catheter placed in right atrium. 2 catheters used in larger children. Depends on intrinsic cardiac function, needs high circuit flow.
  • VA double lumen catheter offers cardiac support but carotid ligation & risk of embolism, stun. Cardiac stun often seen after VA (not VV) - pulse lost although mean pressure maintained. Inotropes not helpful; resolves in 24-36 hrs.
  • Flow 100-120ml/kg/min for VA, 120-150ml/kg/min for VV.
  • Change in pulse character tends to raise renin level, hence high K losses, low Na losses.
  • Haematocrit must be kept over 0.4 to maximize oxygen delivery.
  • Venous sats usually 80%, less suggests increased utilization. High suggests recirculation (so reduce flow).
  • Flow limited by venous return ie size of catheter, position, height of bed.
  • O2 transfer is unaffected by gas flow because high gradient - too high can cause air embolism. Adjust bood flow or change membrane.
  • CO2 is unaffected by blood flow, adjust sweep gas flow across membrane.
  • Water condensing in membrane acts like pulmonary oedema - so increase gas flow.
  • Monitor Activated Clotting Time (ACT): normal 90-150. If surgery needed, aim at 150-170, with platlets >200, fibrinogen >2. Aprotinin for v high risk (1ml/kg bolus then per hour) or active bleeding. Novo7.
  • Inflammatory cascade triggered by contact with circuit so beware leaky capillaries esp in pre-existing inflamed lungs eg infection.

Shock

Reversal of shock before the transport team arrived at the patient's bedside was associated with 96% survival and >9-fold increased odds of survival. Each additional hour of persistent shock was associated with >2-fold increased odds of mortality. When resuscitation practice was in agreement with ACCM-PALS guideline, a lower mortality was observed (8% vs 38%). Pediatrics. 2003 Oct;112(4):793-9 Han YY

Similarly, early aggressive fluid resuscitation in septic shock improves survival (see Sepsis below). Children who receive larger volumes of intravenous isotonic fluid in the initial hour after presentation in septic shock have lower mortality, esp those who receive >40 mL/kg. Furthermore, when groups receiving smaller versus larger volumes of intravenous fluids are compared, there is no increase in acute respiratory distress syndrome or noncardiogenic pulmonary edema. The London experience with meningococcal sepsis is of improved survival when increased fluid resuscitation was instituted as part of early resuscitation therapy.

Initial Resuscitation

Crystalloid vs Colloid - 2001 meta-analysis showed no difference. But will need more crystalloid to achieve same end point (larger volume of distribution). SAFE study in adults confirmed, slight benefit in sepsis for albumin.

Intubation may required to secure airway. Since young infants have such low functional residual capacity ventilation should be considered early.

Give fluid boluses up to 60 ml/kg. Correct hypoglycaemia and hypocalcaemia.

Thyroid replacement beneficial in post-bypass patients but not yet studied in sepsis. Consider in trisomy 21 and pituitary disease.

Consider thyroid replacement.

At 15 mins

For peripheral infusion, make up dopamine as 3x wt =mg in 50ml 5% dex, 10ml/hr = 10mcg/kg/min

Dopamine action requires stores, often reduced in young infants. Some people like to use Dobutamine & noradrenaline because synergistic.

If fluid refractory, begin dopamine and establish arterial line.

If dopamine refractory then titrate epinephrine for cold shock (suggesting myocardial depression), norepinephrine for warm shock (ie vasodilatation).

There is evidence that adrenal insufficiency common in sepsis but poor evidence that steroid therapy is of any benefit (see below). High dose is definitely of no value in sepsis. Physiological dose would be hydrocortisone 1-2 mg/kg 6 hrly.

If catecholamine refractory, give hydrocortisone if at risk of adrenal insufficiency (pituitary disease, steroid dependent, purpura fulminans [adrenal haemorrhage=Waterhouse Friedrichsen syndrome]); consider insufficiency if random cortisol <500nmol/L) or rise <250nmol/l after ACTH).

At 60 mins

Milrinone is type 3 phosphodiesterase inhibitor, inotrope, vasodilator, faster ventricular relaxation. No increase in myocardial O2 consumption. In neonates less inotrope effect. SE hypotension. Long half life (6 hours) so loading is pharmacokinetically appropriate - but danger of overshoot hypotension.

If cold shock with normal blood pressure, add vasodilator (nitroprusside) or type 3 phosphodiesterase inhibitor (milrinone - use amrinone if renal impairment) with volume.

If other shock - titrate volume and inotropes, aim for normal MAP-CVP difference for age and CI>3.3 and <6 l/min/m2 (if pulm catheter). Consider ECMO.

Vasopressin acts on V1 receptor on vascular smooth muscle. Enhances catecholamine sensitivity, vasoconstrictor without heart effects (but differential depending on dose eg GI tract, kidneys, brain). No large trials, no dose regimens...

Consider Vasopressin - (0.01-0.04u/min in adults) does not use alpha receptor so may be useful in norepinephrine refractory shock.

Neonates

In neonates, consider prostaglandin (dinoprostone=PgE2) for duct dependent lesion, start with dopamine and dobutamine, add epinephrine if resistant. Consider NO and ECMO.

A neuroblastoma should be considered in newborn infants presenting with a shock-like condition together with systemic hypertension.

Clinical practice parameters for hemodynamic support of pediatric and neonatal patients in septic shock. Crit Care Med2002; 30 :1365 -1378

Ventilation

Reduces afterload because negative intrathoracic pressure during normal respiration detracts from systolic peak! So good for cardiac output. Equally, paralysis may reduce tissue oxygen consumption.

Monitoring

Monitor CVP (myocardial dysfunction more common in kids): 8-12cm H2O, more if ventilated or increased intrabdominal pressure. Acidosis, lactate, pulse pressure, venous pO2/sats, PiCCO (new device for measuring cardiac output, suitable for 10+ kg). Arterial-venous oxygen content difference is a better marker than venous sats if cyanotic heart disease or severe pulmonary disease.

Little evidence for benefit of PA catheter (=mixed venous sats). Doppler technique in adults.

Inotropes

Alpha receptors constrict blood vessels, but also found in heart (contractility mostly). Beta receptors on the other hand relax blood vessels, relax bronchial smooth muscle (beta-2), increase heart rate and force (beta-1). But there are many subtypes, and most inotropes have combined effects. Lots of controversy! Different actions at low/high dose, in sepsis vs non-sepsis, different amounts of tolerance... Coronary perfusion is also important: occurs during diastole (perfusion pressure = mean arterial pressure - central venous pressure), so impaired if excessive tachycardia, and related to wall stress (ie degree of relaxation). So excess volume beyond Starling curve will impair.

  • Dopamine - has its own receptors which mediate renal, coronary and mesenteric arterial vasodilatation (besides vomiting)but is also a precursor of adrenaline so mixed alpha and beta (1 mostly, for some reason) effect. Tends to increase cardiac output without doing much to SVR in sepsis. Low dose renal protection is a myth (metanalysis did not support). (
  • Dobutamine - mostly beta 1, hence a vasodilator, but often used for myocardial dysfunction because of secondary effects on heart (increased SV and CO). BP may rise esp neonates, fall or stay the same.
  • Adrenaline - mixed alpha and beta (both 1 and 2). Low dose mostly heart, high dose more SVR (cardiac output can actually fall). Potential problems are tachycardia and impaired splanchnic perfusion.
  • Noradrenaline - again mixed, except little beta 2. Weaker than adrenaline. Increases afterload (diastolic BP), so less effect overall on cardiac output. Less oxygen demand, tachycardia cf Adrenaline.
  • Milrinone - increases contractility! But vasodilates so tends to drop BP. Long half life, so 6hrs before reaches steady state unless a loading dose given. No effect on myocardial O2 consumption.

Respiratory Support

  • Tidal volume (VT) = 6-8ml/kg, but 12 ok if normal lungs eg cardiac patient
  • Minute volume (MV) = VT x Resp rate
  • pH 7.2+ ok, below that suboptimal enzyme function. Permissive hypercapnoea good for neonates but less important for older babies, in fact bad news if impaired respiratory drive as reduced sensitivity.
  • Volutrauma more likely if PIP >30 (suggests uneven compliance).
  • 100% FiO2 encourages alveolar collapse (lack of Nitrogen splinting) - probably not a significant problem below 70% FiO2
  • For non-resp disease IPPV achieves better cardiac output (increases gradient between left ventricle and body) plus reduces energy hence oxygen demands.
  • What is the optimal PEEP? Probably makes sense to increase as FiO2 rises.
  • Consider Prone position, to improve mechanics and V/Q matching.
  • Consider HFOV.
  • Sildenafil (iv form available) is phosphodiesterase inhibitor so prolongs Nitric Oxide (NO) action - good for pulmonary hypertension.

Ventilator modes

  • Volume control best for RICP where CO2 must be kept constant to keep cerebral blood flow steady.
  • Pressure support has trigger and terminator eg 30% of peak flow (beware leak - will lead to self triggering, no termination...)
  • Bipap is ventilation that allows spont expiration (ie no minimum duration of inspiration)
  • Babylog - beware low flow affecting performance (10L needed for 6kg babies)
  • Draeger Evita 4 - bipap good, ASB is assisted spont breathing=SIMV (whereas ippv has vol component)
  • Servo - pressure control does trigger but may cause problems if very active patient; PRVC autoregulates pressure to achieve set volume.

Sepsis

Septic states

Four septic states have been defined in critically ill patients:

  • systemic inflammatory response syndrome (SIRS) - 2 out of pyrexia/hypothermia, tachycardia (brady in infants), tachypnoea, abnormal leukocyte count.
  • sepsis - plus suspected or proven infection
  • severe sepsis - ARDS or 2 other organ dysfunctions
  • septic shock - cardiovascular dysfunction

Rivers (Detroit) did RCT of early (ie first 6 hours in ER) goal-directed therapy in adults (n=263, no immunosuppressed).

  • A 500-ml bolus of crystalloid was given every 30 minutes to achieve a CVP of 8-12 mmHg.
  • If the MAP was less than 65 mm Hg, vasopressors were given until achieved.
  • If the MAP was greater than 90 mmHg, vasodilators were given until achieved.
  • If the central venous oxygen saturation was less than 70%, red cells were transfused to achieve a hematocrit of at least 30%.
  • After the CVP, MAP and hematocrit were optimized, if the central venous oxygen saturation was less than 70%, dobutamine was started at 2.5 mcg/kg/min and increased by 2.5 every 30 minutes (max 20) until the central venous oxygen saturation was 70%.
  • Patients in whom hemodynamic optimization could not be achieved received mechanical ventilation and sedatives to decrease oxygen consumption.

Mortality was reduced from 46% to 30% (58%). Overall, same amounts of fluid, blood and inotropes used, but earlier in intervention group. Benefit potentially even greater for patients with normal BP but other markers of SIRS with lactate >4. N Engl J Med, Volume 345(19).November 8, 2001.1368-1377.

Delphi systematic review became Surviving Sepsis Campaign. Funded heavily by Lilly, manufacturers of rhAPC, does not include latest concerns about that drug.

  • Grade E evidence for starting and stopping antibiotics.

Critical Care Medicine. 32:858, 2004.

Systematic review of steroids in sepsis (adults) found no benefit regardless of dose or duration (possibly even harm at high doses). Possibly benefit if actually adrenal insufficient. However, with long courses of low doses, mortality at 28 days was reduced! (BMJ329:480) Adrenal insufficiency in sepsis defined as random cortisol less than 496nmol/l or Syncathen test giving rise less than 248. Variable dose recommendations for steroids, because RCTs in Dengue gave conflicting results for high doses.

Anti TNF-[alpha] receptor proteins showed reduced mortality in one study of adults with sepsis but increased mortality at highest doses in another. Recombinant interleukin-1 receptor antagonists demonstrated no benefit. But many of these cytokines are found to be at their highest levels at the time of admission and are presumably most active before symptoms appear.

Controlled studies of hemofiltration have shown no benefit. A small randomized trial of plasmapheresis in adults with septic shock showed a reduction in some inflammatory markers and less organ failure but no effect on survival. Can these techniques hope to remove cytokines in the tissues? Plasma or whole blood exchange can be of some benefit by replenishing immunomodulating compounds and anticoagulants.

Recombinant human activated protein C (rhAPC, or drotrecogin alfa) is the only adjuvant therapy licensed for adult patients with sepsis. Protein C has anticoagulant, fibrinolytic and anti-inflammatory properties, tends to drop in sepsis. A large RCT in adults with sepsis (PROWESS) showed a reduction in all cause mortality at 28 days (25% vs 31%, P = 0.003). Earlier administration increases effectiveness of rhAPC. The most important adverse event associated with rhAPC is a low but increased risk of serious bleeding including intracranial hemorrhage. Several uncontrolled case series suggest protein C therapy may be effective in reducing sequelae and mortality caused by meningococcemia among children when given within 12-18 hours after hospitalization. RESOLVE (paed study) failed to show any benefit except possibly in those with the worst coagulation defects. It also confirmed haemorrhage as side effect although almost exclusively in babies under 60 days of age. The first patient in a unit to receive it always seems to do badly... (first patient effect) Lancet, Volume 369, March 2007, 836-843 See note on Surviving Sepsis campaign above.

Anti BPI - FDA refused license despite benefit vs amputation/functional outcome. European license application ongoing. Needs to be used early, at presentation which makes it tricky.

Procalcitonin - more specific than CRP.

GM-CSF: better outcome in septic neonates with neutrophils <1.5 when given for 7 days.

Intravenous immunoglobulin - small trials only. INIS trial disappeared without a trace...

t-PA (tissue plasminogen activity) retrospectively had a 8% risk of ICH (with 47% mortality) so will never get to RCT.

Meningococcal Septicaemia

See Meningitis Research Foundation for guidelines.

Note the potential for deactivation of ceftriaxone if administered within 48 h of calcium-containing solutions, including parenteral nutrition (calcium chelation). Hence Cefotaxime should be used as the first line antibiotic in meningococcal sepsis due to the high incidence of calcium replacement requirement in severe disease. However, ceftriaxone may still be considered as first line therapy in children with clinical meningitis, and for continuation of sepsis therapy after the acute phase when calcium infusions are no longer required.

Study of clinical presentation (n=448) suggests that classic rash, meningisim, impaired consciousness late compared to other features of sepsis: leg pains (eg refusal to walk), cold hands/feet, abnormal skin colour (seen in 72%, median time 8 hours, usually before hospital admission). Thirst also a feature in older children. Most children had non specific symptoms for 4-6 hours, critically ill within 24 hours. Hence recognising sepsis features more important than specific meningococcal features. If unwell for longer than 24 hours, unlikely to be meningococcal septicaemia, on the other hand if there is concern about non-specific findings alone with a short history, review should be done within 6 hours rather than next day. The Lancet 2006; 367:397-403

Transport 

Referring hospital may be best placed to do transfer esp head injury. Scoop & run never proven for kids. First contact should provide advice even if no beds. Remember paramedics esp air paramedics. Team not strictly there for HDU patients.

  • www.picuretrieval.co.uk for tips incl directions to RHSC for parents.
  • Anticipate problems 
  • Monitoring
  • Move to A&E or theatre if better facilities 2 secure lines ?suture 
  • Don't dilate central line if in doubt about whether it's venous or arterial. 
  • Dilute inotropes to give peripherally - 3mg/kg in 50 ml gives 1ml=1mcg/kg/min
  • EtCO2 & NIBP consume propaq battery power!
  • Peter mixes ketamine 10/kg & midaz 0.2/kg in a 50ml saline @10ml/hr, for easily titratable sedation

Other ICU Measures

Enteral feeding while shock persists is controversial.

Glucose control - NEJM adult ICU (all conditions) benefits in mortality & morbidity! Relevant to PICU?

Renal failure - Theophylline maintains diuresis. ? timing of replacement ie maintenance or rescue.

ECM0

Transfusion levels - moving down? 7g/dl in adults (after early goal-directed therapy).

Selective digestive decontamination? May reduce ventilator associated pneumonia.

Empirical antibiotic cycling to discourage resistance.

Novoseven is factor VIIa initiates coagulation esp X.

Anticoagulants - some studies suggest that heparin reduces the severity of distal necrosis in meningococcal sepsis, but no effect on survival has been demonstrated in animal models or small clinical trials. One review of recombinant tissue plasminogen activator (rTPA) for meningococcal sepsis in children described improved distal perfusion that may minimize amputations, but 5 (8%) of 62 patients developed significant intracranial hemorrhages. Serine proteases are important in activation of complement and fibrinolytic systems, serine protease inhibitors (serpins, including antithrombin III and C1-inhibitor) are theoretically promising but few data. Fresh frozen plasma, containing both serpins and anticoagulant factors, has been suggested as an adjuvant therapy, providing both fluid resuscitation and immunomodulation.

Good adult evidence for hypothermia post arrest. Negative evidence for near drowned kids...

ARDS definition (consensus 1994) - acute, bilat infiltrates, wedge pressure differentiates acute lung injury. Fibrosis occurs within 2/52. Meduri (JAMA 1998) RCT of methylpred in unresolving ARDS (adults) - zero mortality in Rx group cf 5 of 8! 2mg/kg/d starting dose. Stopped early (too early?).

Ventilator-associated pneumonia

VAP = nosocomial pneumonia in ventilated patients that develops at least 48 hr after initiation of mechanical ventilation. Main bugs isolated are:

  • Pseudomonas aeruginosa
  • enteric Gram-negative bacilli
  • Staphylococcus aureus

Associated with extra 3.7 days of mechanical ventilation after adjusting for other factors (retrospective study of pediatric cardiothoracic surgery patients). Mortality and cost?

Diagnosis: clinical criteria from National Nosocomial Infection Surveillance System (NNIS).

  1. At least 2 serial CXRs with new or progressive and persistent focal infiltrate, consolidation or cavitation occurring 48+ hr after initiation of ventilation
    • or pneumatoceles in infants under 1 year
  2. Plus clinical criteria (differ by age):
    • fever > 38.4degC (38 in older children) without other recognized cause
    • leukopenia <4000 white blood cells or leukocytosis >12,000 WBC/mm3
    • New purulent sputum
    • Apnoea, tachypnoea, nasal flaring or grunting
    • Wheezing, rales or rhonchi
    • Cough
    • Worsening gas exchange, increased oxygen/ventilatory requirements
    • Bradycardia (under 100bpm) or tachycardia (over 170bpm)
  3. Lab criteria may be substituted for 1 clinical criterion:
    • positive blood or pleural fluid or quantitative bronchoalveolar lavage (BAL) culture (>=104 CFU/ml) or >=5% BAL-obtained cells with intracellular bacteria on Gram stain or histopathology.

The sensitivity and specificity of any of these clinical or radiographic findings alone is poor compared with histopathology.

Pathogenesis: aspiration, inhalation of aerosols containing bacteria, hematogenous spread and bacterial translocation from the GI tract. Risk factors include immunosuppressants, immunodeficiency, neuromuscular blockade, neuromuscular disorder, and reintubation.

Multiple preventive interventions assessed in adults, few in kids.

  • Selective digestive decontamination (SDD) with oral colistin, tobramycin and nystatin was protective in metanalysis.
  • Topical polymyxin E and tobramycin to tracheostomy sites for the first 14 postoperative days was effective cf historical controls.
  • Sucralfate is controversial, with some but not all studies showing protection. A retrospective PICU study found no difference in VAP among children receiving ranitidine (6/54), sucralfate (4/53) or no stress ulcer prophylaxis (3/48).
  • In adults perioperative oral chlorhexidine 0.12% rinse was effective in preventing VAP in cardiac surgery patients, presumably by decreasing oral Gram-negative colonization.
  • Bolus enteral feeding is associated with lower gastric pH and lower risk of VAP cf continuous.
  • Measures to decrease aspiration eg elevation of the head of the bed to 30-45 degrees, continuous subglottic suctioning and noninvasive positive pressure ventilation.
  • Glutamine-enriched enteral feeding is associated with lower rates of VAP and bloodstream infection in trauma patients (glutamine deficiency may increase intestinal permeability and decrease lymphocyte function).

Draft guidelines for prevention proposed by the Hospital Infection Prevention Committee (2002) include:

  1. the use of orotracheal rather than nasotracheal tubes;
  2. continuous supraglottic suctioning;
  3. routine use of sucralfate and H2 blockers in critically ill patients;
  4. use of a heat-moisture exchanger;
  5. change of ventilator circuits only when they malfunction or are visibly contaminated.

Routine ET aspirates seem to predict antibiotic sensitivities in ventilator associated pneumonia (as diagnosed on BAL).

Oral antiseptics reduce rate of ventilator assoc pneumonia in adults. No impact on mortality or length of stay. Less risk of selecting out resistant organisms cf use of antibiotics. But needs to be part of package including semirecumbent positioning, care of circuit, closed suction systems.

Poisoning

Paracetamol

Paracetamol - unless risk factors, under 150ml/kg don't need bloods. So a whole bottle of weak (120mg/5ml) can be taken by a 4yr old (12kg)?

Alcohol

Drink drive limit is 80 mg/dl alcohol in blood (different limits for urine/breath).

Triage

Manchester triage system for A&E: ascribes a time by which ideally a patient should be seen and where they should wait (resus vs elsewhere). Patient is allocated to 1 of 52 pathways (6 paediatric); subsequent questions delineate risk. Good inter-rater agreement. But requires experienced triage clinician. Not much evidence about how well it works; could be combined with early warning scores, although these are aimed at in-patients.

Trauma

See also Head injury.

Blast injury to the abdominal viscera is uncommon, affecting around 1% of casualties with primary blast injuries. However:

  • If the bowel is ruptured, peritonism is likely but may take hours to develop.
  • Even then it may be difficult to detect, especially if the patient has required paralysis and sedation in order to manage other injuries
  • Free gas will be detectable long before rupture is clinically evident
  • In the less dramatic forms of blast injury to the bowel, the damage may not cause immediate rupture. Small haemorrhages form in the wall of the intestine, which may eventually result in rupture some time down the line.
  • Blast injury to solid organs can occur but reflects exposure to a much stronger blast, and is uncommon.

Shock

Shock in trauma should be treated to achieve adequate perfusion, not normal BP (although debated) - ?exacerbate blood loss, exacerbate shock lung.

Burns

The fluid regime for burns is based on the percentage of body surface area burned. Only areas of partial or full thickness burns are counted. First treat shock if it is present and look for its causes.

For maintenance fluids the standard formula (Parkland formula) is:

  • Give 2-4 mls of cystalloid per kilogram bodyweight per percent burns
  • Give half over the first eight hours since the time of the burn, and half over the next 16 hours
  • The amount of fluid given should be adjusted based on the patient’s response, e.g. general condition, urinary output.

Inhalation

The effects of smoke inhalation may be delayed by 12-36 hours. There is no doubt that patients exposed to smoke who have respiratory symptoms or signs, abnormal blood gases (including lactate and carboxyhaemoglobin), or abnormal chest films, should be admitted for treatment and observation. Patients with a significant smoke exposure, and who are asymptomatic, consider observation at home with advice.

Symptoms of mild carbon monoxide poisoning include weakness, headache, nausea and dizziness. Features of severe carbon monoxide poisoning include:

  • Coma
  • Confusion
  • Myocardial ischaemia
  • Dysrhythmias
  • Hypotension
  • Metabolic acidosis

Cyanide poisoning can be difficult to diagnose. Symptoms and signs of cyanide poisoning include:

  • Headache
  • Seizures
  • Altered consciousness
  • Tachycardia or bradycardia
  • Hypertension or hypotension
  • Dyspnoea, Tachypnoea

There may be a metabolic acidosis, with an elevated lactate. A high plasma lactate (greater than 10 mmol/L) in the absence of severe burns or hypotension is suggestive of smoke inhalation.

Near-drowning

Invasive aspergillosis has been described in immunocompetent child after near-drowning.

Head Injury

See Neuro.

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