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Brain Oriented Resuscitation In The First Hour – Strategies



Article By


Somashekhar M Nimbalkar

Satvik C Bansal



Global cerebral ischemia occurs commonly in patients who have a variety of clinical conditions including cardiac arrest (CA), shock, and asphyxia. Unfortunately, survival with neurologic sequelae is common for adult and pediatric victims of cardiac arrest. Neurologic sequelae from brain injury are varied and constitute a spectrum that includes coma, seizures, ischemic stroke, delirium, and neurocognitive impairment. Most of the damage in the first hour is due to reperfusion injury leading to release of inflammatory mediators and reactive oxygen radicals. In the first hour of resuscitation of the child who has had a cardiac arrest, the mainstay of therapy is supportive management which include maintaining near normal pH, permissive hypercapnia, reduction of cerebral edema, maintaining normothermia and euglycemia, maintaining blood pressure within normal limits, and maintaining nutrition. Therapeutic hypothermia, a novel intervention, shows promise but is not yet recommended widely outside of a research setting or a protocol based hospital environment.




Brain Oriented Resuscitation in the First Hour- Strategies

Cerebral Ischemia is defined as diminution of cerebral blood flow (CBF) to a critical threshold that   propagates   brain   damage  involving  the entire brain or a selective region. Global cerebral ischemia  occurs  commonly   in   patients   who have a  variety of clinical conditions  including cardiac arrest (CA), shock, and asphyxia. In addition to injury to other organs from systemic hypoperfusion,  neurologic sequelae from  brain injury  are  varied  and  constitute   a  spectrum that  includes coma, seizures, ischemic stroke, delirium, and neurocognitive impairment.


Post-resuscitation neurologic management:

Meaningful   neurologic   survival   represents the most clinically relevant outcome measure for cardiopulmonary resuscitation (CPR). Unfortunately, survival with neurologic sequelae is common for both adult and pediatric victims of cardiac arrest.


a. Supportive care

Following  resuscitation   from   cardiac   arrest, there is a period of increased sensitivity of the brain to secondary injury. The precipitants of secondary injury include hypotension, hypoxia, hyperglycemia, and hyperthermia.

Early post-resuscitative supportive  care should focus on avoiding these causes of secondary injury[1].

  • Avoid hypotension
  • Maintain normoxia   (avoid   hypoxia   and prolonged hyperoxia)
  • Maintain euglycemia
  • Avoid hyperventilation
  • Avoid hyperthermia[2]



Watch out for iatrogenic hyperventilation.

  • Hyperventilation causes hypocapnia leading to vasoconstriction and decreased cerebral blood flow in children following traumatic brain injury[1,3]     and  in  adults  recovering from   cardiac   arrest.   Decreased  cerebral blood flow has been associated with poor outcomes in children with traumatic  brain injury and severe hypocapnia (PaCo2<30) is associated with increased mortality[1].
  • Hyperventilation can  also  decrease  cerebral blood   flow  by   increasing   intra-thoracic pressure causing a decrease in cardiac output and cerebral venous return.
  • In addition, respiratory alkalosis shifts the oxygen hemoglobin  dissociation  curve  to the left reducing oxygen delivery to tissue.


b. Management of Cerebral edema:

Hypoxic-ischemic encephalopathy following resuscitation from cardiac arrest is characterized by cytotoxic cerebral edema. Progressive edema results in intracranial hypertension that can contribute   to   secondary   ischemic  injury   by further reducing cerebral perfusion pressure.


  1.  Standard treatment includes
  • Promotion of   venous   drainage   by elevation of the head at 30 degrees[4].
  • Maintenance of midline head position
  • Use of isotonic fluids

2.  Hyperosmolar fluids  (mannitol   and hypertonic  saline) can be used in cases of raised   intracranial    pressure.   Supportive care management  is aimed  at maintaining normal blood pressure, pH, temperature and glucose.


c. Seizure management:

Early    post-traumatic     seizures    (EPTS)    are those that  occur within the first week of head injury. In less severe traumatic brain injury, the occurrence of EPTS is < 5 %[1]. Seizures markedly increase cerebral blood flow, glucose and oxygen consumption,  and intracranial pressure, placing the brain at risk for secondary injury. Aggressive treatment  of post-arrest seizures is indicated to prevent progression to status epilepticus[5].


Benzodiazepines  are  indicated  for  the  initial acute treatment of post-resuscitation seizures. Longer-acting antiepileptic drugs  are indicated if benzodiazepines are ineffective or if seizures rapidly recur.


  • Barbiturates such   as   phenobarbital   have the added advantage of decreasing cerebral metabolic rate[6] while controlling  seizures but may reduce cerebral perfusion pressure by causing systemic hypotension.
  • Fosphenytoin is an alternative but it should be administered cautiously because of the risk of hypotension.
  • Refractory Seizures  may   necessitate induction  of a pharmacologic coma with a long-acting barbiturate such as pentobarbital. Pentobarbital  is titrated  in doses of 1 to 5 milligram  per  kilogram  body  weight (1-5 mg/kg)  until  cessation of clinical seizures occurs and is then followed by a continuous infusion. Hemodynamic consequences of pentobarbital include myocardial depression and  vasodilation, and  concomitant  use of vasoactive infusions  is typically necessary. Electroencephalographic (EEG) monitoring is indicated to ensure that electrical seizures are resolved.


d. Blood glucose control:

It has been seen that pediatric survivors of cardiac arrest  demonstrated   the  occurrence  of  post- arrest  hyperglycemia with mean  blood glucose concentrations> 150 milligram per deciliter (mg/ dL) or >8.3 millimoles per liter (mmol/L). In an observational study of 101 children <14 years of age who  underwent  craniotomy  for  traumatic brain injury, perioperative hyperglycemia (serum glucose level >200 mg/dL) was found in 45% of children and is also significantly associated with a Glasgow coma scale <8[1].

Hypoglycemia as well as hyperglycemia have detrimental  effects on  the  growing  brain  and hence strict control is to be maintained  on the glucose levels for  a  better  prognosis.  This  is achieved by close monitoring  of glucose intake and insulin if necessary.


Is Therapeutic Hypothermia the future?

Measurement    and    control    of    temperature following   cardiac    arrest    is    an    important part   of   patient    management.    After   arrest, children  commonly  have  an  initial  period  of spontaneous hypothermia followed by a delayed (approximately 24 hours  later) development  of fever. These  temperature  changes  are  relevant because    hypothermia     is     neuro-protective, whereas   hyperthermia   can   exacerbate   brain injury.

Hence,   routine   warming   of  patients   during initial hypothermia  is no longer recommended. Rewarming can negate the neuro-protective effects  of   hypothermia   and   may   cause   an ‘‘overshoot’’   of   temperature   that   contributes to    subsequent    fever.   Intentional    induction or maintenance of hypothermia (therapeutic hypothermia) has recently been shown to be beneficial in adults recovering from cardiac arrest and is also recommended in newborns with birth asphyxia[9].

Thus, consideration should be given to actively cooling children who remain comatose following resuscitation from cardiac arrest. In addition, temperature  should  be  monitored  closely and fever should be treated aggressively.

American Heart Association currently recommends that ‘Therapeutic Hypothermia’ (32°C to34°C) may be beneficial for adolescents who   remain   comatose  following  resuscitation from a sudden, witnessed, out-of-hospital VF(ventricular  fibrillation)  cardiac  arrest.  It may also be considered for infants and children who   remain   comatose  following  resuscitation from  cardiac arrest[7].  The  use  of  therapeutic hypothermia is increasing, however, currently only about 3.3 % of intensive-care specialists in the United States are using this protocol[8].


Pointers on Therapeutic Hypothermia

Induction of hypothermia after cardiac arrest is a time-sensitive intervention and most clinical trials allow a window of only six hours after resuscitation. Target temperatures  are achieved most  effectively with  an  endovascular  cooling device, but external cooling methods have been used widely.

Although therapeutic hypothermia remains an unproven therapy in children after cardiac arrest, it is a well-accepted fact that hyperthermia exacerbates neurologic  injury  after  a  hypoxic- ischemic event.

Children  who are successfully resuscitated frequently  demonstrate  temperature  instability in the first 24 hours with a period of spontaneous hypothermia followed by rapid onset of hyperthermia.    Clinicians    should    anticipate the  possibility of  fever and  be  prepared  with interventions to restore normothermia as soon as possible.


Key Messages:

  1. In the first hour of resuscitation of a child who has had a cardiac arrest, the mainstay of therapy is supportive management.
  2. Supportive management includes  near normal pH maintenance, permissive hypercapnia,  reduction   of  cerebral edema,  maintaining  blood  pressure  and acid base balance within normal limits, normothermia, normoglycemia, and maintaining nutrition.
  3. Therapeutic hypothermia is of promise but is not yet widely recommended outside of a research setting or a protocol based hospital environment with obtained consent from family or guardian.
  4. Most of the damage in the first hour is due to reperfusion  injury  leading  to  release of inflammatory mediators and reactive oxygen species.



Dr. Amee Amin for the editing of the manuscript.


TC- Apr 2016 - 020 - Writers Art pg 30




  1. Hu CF, Fan HC, Chang CF, Chen  SJ. Current approaches to the treatment  of head injury in children.PediatrNeonatol.  2013 Apr;54 (2):73-81.   doi:   10.1016/j.pedneo.2012.12.011. Epub 2013 Jan 21.
  1. Natale JE, Joseph JG, Helfaer MA, Shaffner DH. Early hyperthermia after traumatic brain injury in children: risk factors, influence on length of stay, and effect on short-term neurologicstatus. Crit Care Med 2000; 28:2608-15.
  2. Mansfield RT. Severe traumatic Brain Injury in Children. Clin Ped EmergMed.2007.8(3): 156-64.
  3. Ng I, Lim J, Wong HB. Effects of head posture on cerebral   hemodynamics:   its   influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. Neurosurgery 2004;54: 593-7.
  4. Lumba-Brown A1, Pineda J.Evidence-based assessment    of    severe    pediatric    traumatic brain injury and emergent neurocritical care. SeminPediatr Neurol. 2014 Dec;21(4):275-83. doi: 10.1016/j.spen.2014.11.001. Epub 2014 Nov 24.
  5. Piatt JH, Schiff SJ. High dose barbiturate therapy in neurosurgery and intensive care. Neurosurgery 1984; 15:427-44.
  6. The International Liaison  Committee   on Resuscitation (ILCOR) consensus on science with treatment  recommendations  for pediatric and neonatal patients: pediatric basic and advanced  life  support.  Pediatrics.  2006; 117: 955–77.
  7. Mikkelsen ME1, Christie JD, Abella BS, Kerlin MP, Fuchs BD, Schweickert WD, Berg RA, Mosesso VN, Shofer FS, Gaieski DF; American Heart Association’s Get with the Guidelines- Resuscitation Investigators.Use of therapeutic hypothermia after in-hospital cardiac arrest.Crit Care Med. 2013 Jun;41(6):1385-95.
  8. Wyckoff MH, Aziz K, Escobedo MB, Kapadia VS, Kattwinkel J, Perlman JM, et al. Part 13: Neonatal Resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132: S543-60