Brief History of Therapeutic Hypothermia - Annotated Bibliography Example

Therapeutic Hypothermia Number Introduction, Brief History and Selected Statistics The art of hypothermia has been in use in the field of medicine since time immemorial. Hippocrates, the Greek physician, championed for packing of hurt soldiers in snow and ice. Napoleonic surgeon, Baron Dominique Jean Larrey observed that wounded soldiers kept closer to the fireplace survived less often that those less catered for. 1945 saw to the publishing of the first hypothermia related medical article (Alzaga, Cerdan & Varon, 2006). Research indicates that up to 300,000 people in the U.S. alone and approximately the same number in Europe suffer out-of-hospital cardiac arrests annually, with very low survival rates. However, application of therapeutic hypothermia has been credited to the great enhancement of survival rates from such sudden cardiac arrests with a huge influence on the long-term neurologically intact survival too. Further research and animal tests also point, importantly, that the earlier the hypothermia is induced, the better and higher the patient’s outcome and survival rates (Bader, 2011). Therapeutic Hypothermia Therapeutic hypothermia, also termed protective hypothermia, is a medical procedure involving reduction of a patient’s body temperature so as to help lower the chances of ischemic injury to tissues after a term of insufficient blood flow and can significantly improve the rates of long-term neurologically intact survival. This insufficient blood flow can be a result of several factors such as in the circumstance of a stroke, occlusion of an artery by an embolism, or cardiac arrest. However, in the case of cardiac arrests, the essence of use maybe debated since temperatures of 36˚C (97˚F) basically have similar effects as at the hypothermal 33˚C (91˚F) (Alzaga, Cerdan & Varon, 2006). Therapeutic hypothermia can be incited either through invasive methods or non-invasive methods. Induction by the non-invasive methods involve surface cooling with ice packs, surface cooling helmets, cool caps, application of a cold water blanket or/ and clothing directly to the patient’s skin surface. Invasive means on the other hand employ the use of a catheter placed in the inferior vena cava through the femoral vein, internal cooling methods through the infusion of cold fluids or trans-nasal evaporative cooling (Brooks, 2010). There exist five major medical conditions that therapeutic hypothermia treats effectively. These include cardiac arrest, neonatal encephalopathy, ischemic stroke, neurogenic fever (after brain trauma) and a spinal cord injury without damage. Patients who benefit more from therapeutic hypothermia include those in a coma at the time of cooling, those who can sustain a systolic blood pressure above 90mmHg [with or without pressors after CPR] and intubated patients with treatment started within 6 hours after cardiac arrest. However, this procedure may increase risk in patients such as those in coma from causes such as drug intoxication and previously present coma before arrest, those with systemic infection or sepsis, those with unknown bleeding diathesis or with an active on-going bleeding as the procedure may retard the clotting system. Also, induced hypothermia is not recommended for patients from a major surgery. This is because, in the last 14 days as hypothermia enhances the chances of infection and further blood loss, those with a valid do not resuscitate in order (DNR) (Bader, 2011). General Procedure for Conducting Therapeutic Hypothermia The aim of the process is to attain the desired temperature as fast as can be achieved, mostly within 3-4 hours of starting the cooling then followed by a period of re-warming 24 hours, from the time the procedure was commenced. It is highly required of the medical practitioner to first and foremost determine and ascertain the eligibility of the patient to undergo therapeutic hypothermia. If this has been done and the patient cleared, the medical practitioner goes on to assemble all the materials required for the procedure (Nunnally, 2010). This includes two cooling blankets (each blanket must have a sheet covering to protect the patient’s skin) and cables to put around the patient or alternatively, according to the manufacturer’s recommendations. The medical practitioner should put heat exchanger pads on the patient. This step is then followed by packing the patient’s body, for instance in the groins, chest, axillae and sides of the neck, in ice to lower temperatures of the body to between 32-34˚C. However, it is unadvisable to pack the chest with ice since it will impair the chest wall motion (Brooks, 2010). The medical practitioner should place the patient on a continual cardiac monitor and observe keenly the arrhythmia detection and hypotension while also checking the patient’s vital signs and oxygen levels. Once the desired temperature [temperature below 34˚C] has been obtained, the medical practitioner should remove the ice bags and use the cooling blankets or heat exchange device to keep the patient’s temperature stable at the desired level between 32-34˚C. During the procedure, other supportive therapies such as practicing standard neuro-protective strategies like inclining the head of bed at 38˚, applying norepinephrine from 0.01 mcg/kg/min titrated to a MAP greater than 80mmHg, checking the skin regularly (2-6 hours) for thermal damage, disallowing patient nutrition during the process and regular temperature check with a secondary temperature monitoring device (Dietrich, 2011). A medical practitioner can halt the procedure midway and re-warm the patient in cases of hemodynamic instability, bleeding and a dangerous dysrhythmia. However, a heart rate below 40 BPM during the process is normal like in presence of an ECGOs Bourne or camel wave. Therefore, there is no cause for worry especially when there are no signs of hemodynamic instability (Vincent, 2009). 24 hours after initiation of the cooling, the medical practitioner begins re-warming the patient. This takes roughly 8 hours and is carried out slowly at a rate of 0.3-0.5˚C for every hour to avoid harmful spikes in the intracranial pressure. This warming can be done by setting the water temperature in the cooling equipment to 35˚C, and then inducing an additional 0.5˚C every 1-2 hours until a stable body temperature of 36˚C is achieved. The medical practitioner should remove the blankets and ice. Until the temperature of the patient clocks 35˚C, the medical practitioner should do not get rid of the paralytic agent and sedation. He should also halt the potassium infusions while checking the patient for hypotension. Avoidance of hyperthermia during re-warming is also paramount. In addition, hemodynamically stable patients with spontaneous mild hypothermia [above 33˚C], following resuscitation from cardiac arrest are not recommended for active warming. Most deaths caused by therapeutic hypothermia result from the re-warming stage of the procedure. These deaths are easily avoidable through slow and precise re-warming (re-warming for at least 24 hours from 33˚C to 37˚C) (Loftus, 2008). Pathophysiology Hypothermia focuses on the slowing of cellular metabolism amongst other mechanism resulting to a reduction in the excitatory amino acids, attenuation of the production of free oxygen radicals and lipid peroxidation, restoration of protein synthesis and gene formation, attenuation of CSF platelet-activating factors, inhibition of cytoskeletal breakdown, inhibition of the action of deleterious products of inflammation such as cytokine and interleukins, restoration of the normal body intracellular signaling mechanisms, attenuation and/ or reversal of ischemic depolarization of the central nervous system causing normalization of intracellular water concentration and pH electrolyte redistribution and membrane stabilization. Hypothermia also reduces cerebral metabolism by about 6-8% for every 1˚C decrease (Lundbye, 2012). Hypothermia works on ischemia and its effects by decreasing the body’s need for oxygen, and during such periods, even the slightest drop in temperature would increase cell membrane stability preventing influx of unwanted ions during ischemia. It also reduces the reperfusion injury when blood supply is restored to a tissue after ischemia (Laycock, 2012). Cardiac arrest and return of spontaneous circulation (ROSC) results in progressive cell damage, neural apoptosis, multi-organ dysfunction and eventual death. These processes are majorly temperature-sensitive and therefore, hypothermia plays its function in the protection of the brain and the heart. In the heart alone, hypothermia may act to preserve intracellular high energy phosphate stores, minimize area of injury/ damage, reduce myocardial metabolic demand and promote epicardial reflow (Cribb, 2010). Negative Effects of Use and Controversies Surrounding Therapeutic Hypothermia Therapeutic hypothermia, however much useful in the field of medicine as already discussed above is surrounded with a few controversies and certain grey areas (Vincent, 2008). It is also an area where little research has been conducted on, and little information confirmed thus far. Much about this concept of treatment is yet to be discovered and applied effectively with parameters such as temperature of hypothermia, re-warming rate, duration of hypothermia, eligibility for hypothermia, re-warming time for instance still unclear/ undefined leaving room for life threatening and irreversible errors in the field of medicine (Indriðason, 2010). Therapeutic hypothermia may come with some negative effects. These effects, among others include shivering, cardiac arrhythmia, sepsis, coagulopathy, electrolyte and metabolic disturbances, as well as significantly increasing the risk of pneumonia and such related respiratory disorders. For shivering, there are alternatives for drug control during and after hypothermia. Some of the drugs most commonly used to prevent shivering in therapeutic hypothermia are desfluvane and pethidine and meperidine, also called Demerol (Clifton, Valadka, Aisuku & Okonkwo, 2010). References Alzaga, A. G., Cerdan, M., & Varon, J. (2006). Therapeutic Hypothermia. Resuscitation, 70 (3), 369-380. Bader, M. K. (2011). Clinical Q & A: Translating Therapeutic Temperature Management from Theory to Practice. Therapeutic Hypothermia and Temperature Management, 7. Brooks, V. (2010). Hypothermia. London: Josef Weinberger Plays. Clifton, G. L., Valadka, A. B., Aisuku, I. P., & Okonkwo, D. O. (2010). Future of Re-warming In Therapeutic Hypothermia for Traumatic Brain Injury: A Personalized Plan. Therapeutic Hypothermia and Temperature Management, 3, 110306234553023. Cribb, V. (2010). Hypothermia. New York: Minotaur Books. Dietrich, W. D. (2011). New Therapeutic Strategies Emerge. Therapeutic Hypothermia and Temperature Management, 18. Indriðason, A. (2010). Hypothermia. New York: Minotaur Books. Laycock, A. K. (2012). Cardiac Arrest and the Need for Therapeutic Hypothermia. n/a Loftus, C. M. (2008). Neurosurgical Emergencies (2nd Ed.). New York: Thieme. Lundbye, J. B. (2012). Therapeutic Hypothermia after Cardiac Arrest Clinical Application and Management. London: Springer. Nunnally, M. E. (2010). Therapeutic Hypothermia in the ICU. Mount Prospect, IL: Society of Critical Care Medicine. Vincent, J. L. (2008). Intensive Care Medicine Annual Update 2008. New York: Springer. Vincent, J. (2009). Intensive Care Medicine Annual Update 2009. New York, NY: Springer- Verlag New York. 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