Guidelines for managing septic shock
These guidelines are derived from the ACCM guidelines.
Sepsis is one of the most common causes for PICU admission, and the emphasis is on aggressive early treatment.
Treatment in the first hour (Pre-ICU)
Therapeutic endpoints:
- CRT ≤ 2secs
- normal peripheral and central pulses
- warm extremities
- >1ml/kg/hr urine output
- normal mental status
- normal bp
- normal glucose
- normal ionised calcium
Monitoring
- pulse oximeter
- continuous ECG
- BP (NIBP fine if pulses palpable)
- Temperature
- Urine output
- Glucose
- Ionised calcium
Antibiotics
Cefotaxime or ceftriaxone (see here for ceftriaxone caution)
Full antibiotic guideline
Airway and Breathing
Oxygen
Clinical assessment is determinant of need for ventilation, but need for 60ml/kg fluid in first hour is indication forintubation.
40% of cardiac output is used to power work of breathing – intubation and ventilation can reverse shock.
Ketamine plus NMJ blocker recommended for intubation.
Other induction agents may cause a fall in BP (Propofol, sevoflurane, thiopentone)
Pre-load with volume.
Consider concomitant IV inotropes peripherally to cover intubation
Circulation
- IO access if IV access is not obtained within minutes
- Fluid bolus (09% saline or 4.5% albumin) 20ml/kg immediately if no hepatomegaly or lung creps. If hepatomegaly or creps, give fluid bolus more cautiously, and consider other diagnoses (heart disease, metabolic disease, pneumonia)
- Repeat fluid bolus to achieve normal CRT and BP. 60ml/kg or more is often required in paediatric sepsis in the first hour.
- If Fluid Refractory Shock star inotrope peripherally (low dose dopamine or adrenaline) while establishing circulatory access. Patient will already have been intubated and ventilated at this point.
- peripheral inotrope can be stopped when haemodynamic effect of central inotrope is seen.
- Fluid and dopamine refractory shock – add adrenaline (cold shock) or noradrenaline (warm shock)
- Start hydrocortisone ( also see below) in divided doses after obtainng random cortisol if there is clinical suspicion of adrenal suppression, or if shock is adrenaline/noradrenaline refractory.
Beyond the first hour (PICU)
Goals and therapeutic endpoints
- CRT ≤ 2secs
- Threshold heart rates
- Normal perfusion pressure (MAP-CVP)
- SVC sats >70%
- CI 3.3 – 6 L/min/m2
- Urine > 1ml/kg/hr
- Normal anion gap
- Normal INR
Monitoring
- Pulse oximetry
- ECG
- Invasive BP – pay attention to pulse pressure (wide in warm shock, narrow in cold shock)
- Core temperature
- Urine output
- CVP
- Lactate, glucose, coags
Fluids
- Requirement for boluses may be required for days – direct against endpoints
- Crystalloid (normal saline, Hartmann’s)
- If Hb < 10g/dL, give blood
- If coags abnormal give FFP – but not as a push bolus
Once resuscitated from shock, consider diuretics or CVVH if >10% fluid overloaded and not maintaining losses adequate to achieve a negative balance.
Cold normotensive shock
Normal BP, high SVR, low CI
Milrinone or glyceryl trinitrate or nitroprusside
Noradrenaline may become necessary as vasodilation occurs
Volume requirement may also increase
Warm shock
Low BP, low SVR, low CI
Noraderenaline
Vasopressin 2nd line
Refractory cold shock
Consider additional diagnoses:
| Problem | Treatment |
Pericardial effusion |
Drain |
Pneumothorax |
Drain |
Hypoadrenalism |
Hydrocortisone |
Hypothyroidism |
Thyroxine |
Ongoing fluid losses |
Replace losses |
Increased intra-abdominal pressure |
Drain |
Necrotic tissue |
Surgery |
Immune compromise |
Consider GCSF, Immunoglbulin |
ECMO may be considered if all else failing – chance of survival 50% or less.
Thresholds
Age |
Heart rate bpm |
Perfusion pressure (mean arterial pressure – CVP) mmHg |
Term newborn |
120-180 |
55 |
Up to 1y |
120-180 |
60 |
Up to 2y |
120-160 |
65 |
Up to 7y |
100-140 |
65 |
Up to 15y |
90-140 |
65 |
Controversies
FEAST study
This study published in 2011 appears to demonstrate an increase in mortality in setic shock in patients receiving aggressive fluid resuscitation. However, the population studied was very different form that encountered in the UK, and the provision for PICU was extremely limited, so no firm conclusions can be drawn. There is no recommendation that current practice should change.
Maitland K, Kiguli S, Opoka RO et al. Mortality after Fluid Bolus in African Children with Severe Infection. N Engl J Med 2011. DOI: 10.1056/NEJMoa1101549
Fever management
There are theoretical reasons why fever may be helpful in fighting infections – not least because it has evolved as a response to infection. There is evidence that viral replication may be impaired by higher temperatures. On the other hand, control of high temperatures may have metabolic advantages in reducing oxygen consumption. An observational study in adults in 2012 demonstrated an association between paracetamol use and mortality, but other studies have produced conflicting results. As yet, there is no compelling reason to stop antipyretic treatment in sepsis in children.
Evidence form adults has suggested that treatment with hydrocortisone may be benificial, but there is no clear consensus in children. Below is the policy for our PICU.
-
To be considered as a rescue therapy by the PICU Consultant in patients with:
- Septic shock and
- Ongoing fluid requirement and
- Increased inotropic support
- Perform a random Cortisol level prior to commencing steroids
- Hydrocortisone (HC) should be used rather than Dexamethasone
- There are no indications for high dose steroids in sepsis
- Stress doses should be used: HC 30 mg/m2/day IV divided 6 hourly
- Stop steroids if Cortisol level >500nmol/l
- Steroids should be weaned once patient has improved and off inotropes
- Involve endocrinology if any suspicion of adrenal insufficiency as an underlying diagnosis.
A normal stress response in meningococcal disease is a CORTISOL VALUE ON ADMISSION > 950 NMOL/L.
RELATIVE ADRENAL INSUFFICIENCY IS DEFINED AS A RANDOM CORTISOL LEVEL < 500 NMOL/L
Links
Allan Wardhaugh September 2012