Hyperthermia after cardiac arrest

In morning report today, we discussed the brain death exam and the apnea test. A theoretical case was discussed, noting the occurrence of pyrexia after arrest and its relation to neurologic sequelae. Research indicates that hyperthermia after arrest portends a poor prognosis, independent of infection. According to the 2010 AHA CPR guidelines, this may be due to the elevation of inflammatory cytokines, similar to sepsis (1). Early trials indicate that hyperthermia after cardiac arrest may be associated with the outcome of brain death (2), possibly due to dysregulation of temperature control centers.

Takino et. al. “analyzed the hyperthermia (above 38°C) occurring in the initial 48 h after resuscitation. After resuscitation, most patients showed a rapid rise in body temperature. Patients with later brain death showed significantly earlier appearance of hyperthermia (6.2 h after cardiac resuscitation; median) and a higher peak temperature (39.8°C; median) compared with patients showing prolonged coma (12.7 h and 38.3°C, respectively). Hyperthermia above 39°C was associated with subsequent brain death. The incidence of factors influencing body temperature did not differ between the brain death and prolonged coma groups. Patients achieving full recovery did not show hyperthermia. [They] analyzed the hyperthermia (above 38°C) occurring in the initial 48 h after resuscitation. After resuscitation, most patients showed a rapid rise in body temperature. Patients with later brain death showed significantly earlier appearance of hyperthermia (6.2 h after cardiac resuscitation; median) and a higher peak temperature (39.8°C; median) compared with patients showing prolonged coma (12.7 h and 38.3°C, respectively). Hyperthermia above 39°C was associated with subsequent brain death. The incidence of factors influencing body temperature did not differ between the brain death and prolonged coma groups. Patients achieving full recovery did not show hyperthermia (3).”

Additionally, as patients become hyperthermic, the difference between brain and core temperature increases, which may indicate that the true incidence of febrile episodes in the brain is even higher than that reported in large observational studies that measured only core body temperature (4). Hyperthermia causes the release of excitatory amino acids and free radicals, aggravates blood-brain barrier breakdown, amplifies cytoskeletal proteolysis, promotes acidosis, and increases cerebral metabolic rate (4, 5). In conclusion, hyperthermia is an early indicator of brain damage after resuscitation (3).

1. Circulation. 2010; 122: S768-S786

2. Resuscitation. 2001 Jun;49(3):273-7.

3. Intensive Care Med. 1991;17(7):419-20.

4. Anesthesiology Research and Practice. Volume 2012 (2012), Article ID 989487, 13 pages.

5. Critical Care 2012, 16(Suppl 2):A2

Acute COPD Exacerbation – Can pulmonary embolism be the trigger?

This week at morning report we discussed triggers for acute COPD exacerbation which include infectious and environmental pollution. Researchers have studied pulmonary embolism as another trigger. Previously on the blog we posted a nice clinical pearl about patients with COPD exacerbation and PE. In 2005, a study was published in CHEST from Northern California Kaiser Permanente Medical Care Program that suggests patients with COPD have twice the risk of venous thromboembolism than patients without COPD. A 2009 study published in CHEST did a systematic literature review of English and French articles and obtained their results from 5 articles. Based on these studies, the overall prevalence of pulmonary embolism was 19.9% (CI 6.7-33%). In the four studies that included hospitalized COPD patients, the prevalence increased to 24.7%. Interestingly, prevalence of DVT was lower in the same patient population than pulmonary embolism. Check out the 2009 study from CHEST by clicking on the link below!

Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD: A Systematic Review and Metaanalysis