Therapeutic_Cooling_Flashcards
What is therapeutic cooling?
Therapeutic cooling, or therapeutic hypothermia, is the deliberate lowering of a patient’s body temperature to cool the brain and prevent brain damage.
What are some uses of therapeutic cooling?
Uses include neuroprotection during surgeries, after ventricular fibrillation arrest, for trauma head injuries, acute ischemic strokes, and in neonates with moderate to severe hypoxic ischemic encephalopathy (HIE).
What is the proven efficacy of therapeutic cooling?
The efficacy of therapeutic cooling has been consistently proven only in neonates with moderate to severe HIE, where it reduces mortality and improves neurological outcomes.
What are the criteria for using therapeutic cooling in neonates?
Criteria include a gestational age ≥36 weeks, birth weight >1800g, evidence of perinatal hypoxia, severe metabolic acidosis, and moderate-severe HIE.
How is therapeutic cooling administered?
Cooling methods include whole-body cooling using a cooling blanket or mattress, and selective head cooling using a cap. Treatment should start within 6 hours of birth and continue for 72 hours.
What are the target temperatures for therapeutic cooling?
Target temperatures are 33°C to 34°C for whole-body cooling and 34°C to 35°C for selective head cooling.
What complications are associated with therapeutic cooling?
Complications can include arrhythmias, hypotension, renal and liver toxicity, metabolic imbalances, and neurological issues like seizures and increased intracranial pressure.
What are the indications to stop therapeutic cooling?
Indications include unresponsive hypotension, persistent pulmonary hypertension despite treatment, and clinically significant coagulopathy.
What is the procedure for rewarming after therapeutic cooling?
Rewarming should be carried out slowly, at a rate of 0.5°C every 1 to 2 hours, to minimize the risk of complications like metabolic disturbances and seizures.
summarise
Therapeutic cooling
Therapeutic cooling (otherwise known as therapeutic hypothermia) is the deliberate lowering of a patient’s body temperature. The intention of this is to cool the brain, and subsequently prevent brain damage.
Several therapeutic uses for cooling have been proposed. These include:
As neuroprotection during open-heart and neurosurgical procedures
In patients following a return of spontaneous circulation post- ventricular fibrillation arrest
In patients with trauma head injuries
In patients who have suffered acute ischaemic stroke
In neonates with moderate to severe hypoxic ischaemic encephalopathy (HIE)
Of these, the only use whose efficacy (in regard to reduction in mortality and neurological morbidity) has been consistently proven in existing literature is the use of therapeutic cooling in neonates.
The use of therapeutic cooling in the treatment of carefully selected term neonates with moderate to severe HIE has been recommended as standard care by the National Institute for Health and Care Excellence (NICE). It has been shown in studies to decrease mortality and improve the neurological and neurodevelopmental outcomes of treated neonates.
Hypoxic perinatal brain injury is caused by a decrease in the amount of oxygen supplied to an infant’s brain just prior to, or during the process of, labour. Neonates who survive a hypoxic brain injury can develop HIE. HIE occurs in an estimated 2.5/1000 term births in developed countries, and 26/1000 term births in the developing world.
An estimated 10% - 60% of infants with HIE die during the neonatal period, and an estimated 25% of those who survive suffer from long-term neurological impairment including epilepsy, mental retardation or cerebral palsy.
Therapeutic cooling remains the only intervention shown to reduce neuronal damage caused by perinatal hypoxia. However, research into pharmacological agents that may be effective is ongoing.
Pathophysiology of hypoxic brain injuries
Magnetic resonance spectroscopy studies in term infants with evidence of intrapartum hypoxia and moderate to severe encephalopathy have supported a biphasic model of neuronal death.
Primary neuronal death occurs at the time of severe ischaemic insult.
Secondary neuronal death (resulting in irreversible failure of mitochondrial function) occurs after a period of at least six hours post ischaemic insult.
This model of neuronal death suggests there is a latent period between the successful resuscitation and reperfusion post primary neuronal death, and secondary neuronal death. This period of approximately 1-6 hours provides a therapeutic window for neuroprotective intervention.
Therapeutic Cooling is thought to influence the extent of secondary neuronal death in a multifactorial manner. The exact way in which it achieves this is not fully understood.
Existing studies suggest it is related to:
The reduction of cerebral oxygen consumption
An increase in haemoglobin oxygen-binding affinity
Inhibition of the synthesis, release, and/or reuptake of neurotransmitters and neuromodulators, including glutamate, glycine, GABA, dopamine, norepinephrine, serotonin, and adenosine.
The reduction of nitric oxide, and other toxic free radicals.
Criteria for the use of therapeutic cooling in neonates:
Neonates with a gestational age ≥36 weeks and birth weight >1800g
History of acute perinatal event during delivery associated with period of hypoxia, and/or an Apgar score ≤5 at 10 minutes or at least 10 minutes of €epositive-pressure ventilation €e
Severe metabolic acidosis on cord gas, or blood gas taken within 1hr of birth
Evidence of moderate-severe HIE - demonstrated by onset of seizures, and/or on the basis of clinical assessment of consciousness level, spontaneous activity, posture, tone, primitive reflexes, and autonomic systems.
Electroencephalogram (EEG) is useful in determining eligibility (by detection of abnormal neuronal function and/or seizures).
Treatment must be initiated within 6 hours of birth and continued for a period of 72 hours.
Target Temperatures (rectal or oesophageal):
33°C to 34°C (for whole body cooling)
34°C to 35°C (for selective head cooling)
Following cooling rewarming should be carried out slowly (0.5°C every 1 to 2 hours) over a period of 6-12 hours.
Therapeutic cooling should not be offered to:
Moribund infants
Infants with major congenital/genetic abnormalities where aggressive treatment is deemed inappropriate
Infants with evidence of severe head trauma/intracranial bleeding
Management
Therapeutic cooling can only be performed in level 3 or 4 Neonatal units with Neonatologists experienced in its use as a therapeutic modality. Centres providing the treatment must have access to ultrasound, CT and MRI, and EEG.
Methods of Cooling:
Whole-body cooling- placing the infant on a cooling blanket or mattress circulated with coolant fluid.
Selective head cooling- circulating cold water in a cap fitted around the head.
Whole-body cooling is most often used. It is reported to be easier to set up, less expensive, and provides easier access to perform EEG. Existing studies however suggest that both methods of cooling are appropriate and equivalent in regard to neonatal outcomes.
Temperature is continuously monitored throughout the treatment using either a rectal or nasopharyngeal thermometer.
Complications
Close surveillance of infants during the cooling process is required given the risk for complications of both HIE, and the process of cooling itself.
Serious adverse effects are reported as rare. Existing studies suggest that the benefits of cooling on survival and neurodevelopment outweigh the (usually) short€term adverse effects.
Reported complications include the following:
Cardiac and Pulmonary:
Arrhythmias (most commonly Sinus Bradycardia, but Ventricular Arrhythmias also reported).
Prolonged QT interval
Reduced Cardiac Output and Hypotension
Reduced Surfactant production
Increased Pulmonary vascular resistance (which can lead to
Persistent Pulmonary Hypertension)
For these reasons neonates undergoing therapeutic cooling require continuous cardiorespiratory monitoring, and ventilator support during their treatment.
Haematological:
Anaemia
Coagulopathy secondary to thrombocytopaenia
Leucopaenia
Some neonates require correction of these abnormalities using blood components. Monitoring for signs of sepsis, due to increased susceptibility, are also required.
Renal and Liver Toxicity:
Renal impairment (association with urinary retention)
Impaired liver function (most commonly hyperbilirubinemia)
Metabolic:
Metabolic and lactic acidosis
Hypokalaemia
Hypoglycaemia
Hypocalcaemia
Neurological:
Seizures
Raised intracranial pressure
EEG monitoring is important during the cooling process. Sedation is required for patient comfort and to reduce the patient’s metabolic rate to increase the efficacy of the cooling procedure.
Skin:
Skin breakdown
Local skin haemorrhage
Subcutaneous fat necrosis
The risk of skin complications developing can be reduced by regular skin inspections, and repositioning of neonates undergoing treatment.
Indications to stop hypothermia and rewarm the infant include:
Hypotension (unresponsive to inotropes)
Persistent pulmonary hypertension with associated hypoxemia (despite treatment)
Clinically significant coagulopathy (despite treatment)
It is uncommon to stop cooling due to complications. Existing studies suggest this occurs in <10% of cases.
Rewarming must be carried out slowly to reduce the risk of complications (most commonly metabolic disturbances, and seizures) occurring.
Conclusion
Therapeutic cooling is being successfully used as a treatment modality for neonates with moderate-severe HIE. There is currently a lack of evidence for using therapeutic cooling in neonates with less severe hypoxic brain injury, and those with a gestational age less than 35 weeks.
Other uses for therapeutic cooling have been suggested- but their efficacy has not been proven by existing studies. More research is needed to understand how therapeutic cooling might be effectively used in other patient groups with alternative conditions.
A baby is born at full term following a vaginal delivery complicated by a shoulder dystocia. The baby is born in very poor condition and accordingly, the neonatal team resuscitate and intubate the baby. The baby is profoundly acidotic and demonstrates global hypotonia with abnormal neonatal reflexes; the neonatal team decide on the most appropriate step in management as they are concerned about hypoxic brain injury.
Which intervention is most important for this baby?
A sodium bicarbonate correction
Blood transfusion
Skin to skin contact with mum
Therapeutic cooling
Vitamin K administration
Therapeutic cooling
Therapeutic cooling at 33-35 degrees attempts to reduce the chances of severe brain damage in neonates with hypoxic injury
Important for meLess important
Therapeutic cooling is the correct answer. This case describes a baby with poor apgar scores following a traumatic delivery; with acidosis and persisting poor neurological status the baby is likely to meet the TOBY criteria for therapeutic cooling and is the most important intervention in term babies for reducing the likelihood of significant hypoxic-ischaemic brain injury.
A sodium bicarbonate correction is incorrect. Although its use may be considered in severe acidosis, administration is not essential and would not be protective against hypoxic-ischaemic brain injury.
Blood transfusion is incorrect. There is no suggestion of blood loss from either baby or mother.
Skin to skin contact with mum is incorrect. It is important for both maternal and neonatal wellbeing, however not essential. The priority is stabilisation and management of the baby’s hypoxic injury.
Vitamin K is incorrect. Although all babies should receive vitamin K at birth to prevent haemorrhagic disease of the newborn, it will not reduce brain damage from hypoxic injury.
