Drowning is one of the leading causes of accidental death in children. Some apparent drownings may be related to sudden cardiac death, in particular to unidentified channelopathies, which are known to precipitate fatal arrhythmias during swimming-related events.
The majority of cases of sudden cardiac death in children and adolescents are secondary to either hypertrophic or right ventricular cardiomyopathy with coronary artery abnormalities also prevalent, and reports have demonstrated these cardiac abnormalities on autopsy following sudden swimming-related deaths.
However, the majority of autopsies in swimming-related sudden deaths are normal suggesting causation at molecular level, in particular ion channel defects such as type 1 long-QT syndrome (LQT1) and catecholaminergic polymorphic ventricular tachycardia (CPVT). The gene deletion in LQT1 (KCNQ1) leads to a reduction in the repolarising potassium current (IKs) and prolongation of repolarisation. This lengthens the QT interval (which may be lengthened further by facial immersion in cold water). A premature ventricular contraction (PVC) again which may be initiated by swimming occurring during the vulnerable part of repolarisation leads to establishment of polymorphic ventricular tachycardia (torsades de pointes). The ryanodine receptor gene mutation (RyR2) in catecholaminergic polymorphic ventricular tachycardia leads to defective closure of the receptor on the surface of the sarcoplasmic reticulum during diastole. This leads to increased calcium (Ca2+) leakage from the sarcoplasmic reticulum and increased potential for delayed afterdepolarisations and subsequent ventricular tachycardia.
Some recommendations are made in an article in Archives of Disease in Childhood: Proposed implementations to improve detection and appropriate management of apparent drownings secondary to cardiac channelopathies
Improving awareness in the coronial service of the possibility of a cardiac cause for poorly explained drownings.
Education of lifeguards and provision of automated defibrillators in swimming pools.
Molecular autopsy for non-survivors to look for potential channelopathies.
Screening for survivors and family members of non-survivors to identify those with a channelopathy.
Proper counselling for those identified to have a channelopathy on family screening.
A study of out-of-hospital paediatric arrests in Melbourne gives some useful outcome data: overall, paediatric victims of out-of-hospital cardiac arrest survived to leave hospital in 7.7% of cases, which is similar to adult survival in the same emergency system (8%). Survival was very rare (<1%) unless there was return of spontaneous circulation prior to hospital arrival. Sixteen of the 193 cases studied had trauma, but the survival in this subgroup was not specifically documented.
Epidemiology of paediatric out-of-hospital cardiac arrest in Melbourne, Australia Resuscitation. 2010 Sep;81(9):1095-100
Aeromedical retrieval specialists in Scotland developed a simple, cheap, effective in-flight cooling protocol using intravenous (IV) cold Hartmann’s solution and chemical cooling packs. Fluids cooled in a fridge (4°C) were transported in an insulated cool box; the patient was sedated, paralysed and intubated, and controlled ventilation started. The patient was then cooled by IV infusion of 30 ml/kg of cold Hartmann’s. Chemical ice packs were activated and placed in the axillae and groin. The time interval between successful resuscitation and the patient being retrieved and flown to an Intensive Care Unit (ICU) was at least 3.5 h. Cooled patients had a mean decrease in body temperature during retrieval compared to patients not cooled (−1.6 °C vs. +0.9 °C, p = 0.005) and a lower body temperature on ICU arrival (34.1 °C vs. 36.4 °C, p = 0.05). Two of the 5 cooled patients achieved target temperature (<34 °C) before ICU arrival. No complications of in-flight cooling were reported. Not the only way to cool down in Scotland In-flight cooling after out-of-hospital cardiac arrest Resuscitation. 2010 Aug;81(8):1041-2
Emergency physicians in Cambridge and Ipswich in the UK prospectively documented their echo use in cardiac arrest. Images were easily acquired, were quickly obtained, and influenced management. In keeping with previous studies, absence of ventricular wall motion predicted lack of return of spontaneous circulation, with a negative predictive value of 97%. An evaluation of echo in life support (ELS): is it feasible? What does it add? Emerg Med J. 2010 Oct 4. [Epub ahead of print]
An Australian randomised controlled trial assessed the effect of pre-hospital cooling (using 2 litres ice cold Hartmann’s) of post-cardiac arrest patients on functional status at hospital discharge. The intervention group were marginally cooler on arrival but did not have improved outcomes.
The authors conclude: In adults who have been resuscitated from out-of-hospital cardiac arrest with an initial cardiac rhythm of ventricular fibrillation, paramedic cooling with a rapid infusion of large-volume, ice-cold intravenous fluid decreased core temperature at hospital arrival but was not shown to improve outcome at hospital discharge compared with cooling commenced in the hospital. Induction of Therapeutic Hypothermia by Paramedics After Resuscitation From Out-of-Hospital Ventricular Fibrillation Cardiac Arrest Circulation. 2010 Aug 17;122(7):737-42 Free Full Text
One issue from this study was that relatively short urban pre-hospital transport times meant some patients did not get the full two litres, and some had already received room temperature fluids during the cardiac arrest resuscitation. The authors suggest further study should involved initiating cooling during the arrest. In fact a European study has done just that, using a device call a RhinoChill (a portable transnasal cooling device) to lower temperature during arrest in a randomised controlled trial. This trial showed pre-hospital intra-arrest transnasal cooling is safe and feasible and is associated with a significant improvement in the time intervals required to cool patients.
Intra-arrest transnasal evaporative cooling: a randomized, prehospital, multicenter study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness) Circulation. 2010 Aug 17;122(7):729-36
One for the ‘hardly surprising’ category….
A study of end-tidal CO2 during out-of-hospital adult and child cardiac arrest resuscitation showed a sudden rise in CO2 was associated with return of spontaneous circulation (ROSC), suggesting that witnessing this would be a good time for a pulse check. Data from the 59 patients who achieved ROSC are shown below, time zero being time of ROSC. There was no such observed rise in the 49 patients who did not achieve ROSC. A Sudden Increase in Partial Pressure End-Tidal Carbon Dioxide (PETCO2) at the Moment of Return of Spontaneous Circulation The Journal of Emergency Medicine, Vol. 38, No. 5, pp. 614–621, 2010
Military doctors in Afghanistan reviewed their experience of thoracotomy done within 24 hours of admission to their hospital. The ballistic nature of thoracic penetrating trauma (mainly Afghan civilians without body armour) differs from the typical knife-wound related injury seen in survivors of thoracotomy reported in the pre-hospital literature.
Six of the patients presented in cardiac arrest – four PEA and two asystole. One of the PEA patients survived; this patient had sustained a thoracoabdominal GSW and had arrested 8 minutes from hospital. Following emergency thoracotomy, aortic control, and concomitant massive transfusion, return of spontaneous circulation (ROSC) was achieved and damage control surgery undertaken in both chest and abdomen.
The two patients in asystole had sustained substantial pulmonary and hilar injuries, and ROSC was never achieved. The patients in PEA all had arrested as a consequence of hypovolaemia from solid intra-abdominal visceral haemorrhage. All patients in PEA had ROSC achieved, albeit temporarily.
Following thoracotomy, patients required surgical manoeuvres such as pulmonary hilar clamping, packing and temporary aortic occlusion; hypovolaemia was the leading underlying cause of the cardiac arrest. These factors lead the authors to conclude that although isolated cardiac wounds do feature in war, they are unusual and the injury pattern of casualties in conflict zones are often complex and multifactorial. Is pre-hospital thoracotomy necessary in the military environment? Injury. 2010 Jul;41(7):1008-12
Okay so it’s a small case series – but the results warrant further investigation: 10-20 mcg/kg terlipressin was given to five infants and children who arrested in the paediatric intensive care unit and who had not responded to several doses of adrenaline (epinephrine)1. Sustained return of spontaneous circulation (ROSC) was achieved in four, and two survived to be discharged home without sequelae and with good neurologic status at 6 and 12 month follow up. Interestingly, the four patients who had ROSC all had septic shock as the cause of their arrest. The two survivors had severe bradycardia and severe bradycarda-asystole as the arrest rhythms, and both received 20 mcg/kg terlipressin.
Terlipressin is a synthetic arginine vasopressin analog with a significantly longer duration of effect, which previously showed positive effects when administered to a small group of children unresponsive to prolonged resuscitative efforts2. 1. Pediatric cardiac arrest refractory to advanced life support: Is there a role for terlipressin? Pediatr Crit Care Med. 2010 Jan;11(1):139-41 2. Beneficial effects of terlipressin in prolonged pediatric cardiopulmonary resuscitation: A case series. Crit Care Med. 2007 Apr;35(4):1161-4
How much oxygen should we give patients after successful cardiac arrest resuscitation? Too little oxygen may potentiate anoxic injury. Too much oxygen may increase oxygen free radical production, possibly triggering cellular injury and apoptosis. A multicentre ICU database of over 6300 post-arrest patients was analysed and demonstrated an association between ‘hyperoxia’ and in-hospital mortality.
Adult patients who sustained nontraumatic cardiac arrest and were admitted to the ICU at a participating center between 2001 and 2005 were included. Specifically, inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival.
The cohort was divided into 3 exposure groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg (39.5 kPa) or greater; hypoxia, PaO2 of less than 60 mm Hg (7.9 kPa) (or ratio of PaO2 to fraction of inspired oxygen [FIO2] <300); and normoxia, cases not classified as hyperoxia or hypoxia.
Exposure to hyperoxia was found to be a significant predictor of in-hospital death (OR, 1.8 [95% CI, 1.5-2.2]; this was an independent effect that persisted after adjusting for all other significant risk factors
The authors acknowledge that association does not necessarily imply causation, but add that these data support the hypothesis that high oxygen delivery in the postcardiac arrest setting may have adverse effects. Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality JAMA. 2010;303(21):2165-2171
Percutaneous coronary intervention did not increase the risk of dysrhythmia, infection, coagulopathy, or hypotension associated with therapeutic hypothermia after cardiac arrest. Intensivists and cardiologists should perhaps agree that this adds to existing evidence that the two therapies are not mutually exclusive. Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest Resuscitation. 2010 Apr;81(4):398-403
