Cardiac arrest causes cessation of cerebral blood flow and if prolonged can lead to permanent neurological injury. The only effective treatment in both the laboratory and clinical setting to limit the extent of this neurological injury is therapeutic hypothermia.1 This has been shown to be effective in out-of-hospital cardiac arrests.2 We describe a case of successful neurological and functional outcome after in-hospital pulseless electrical activity (PEA) arrest secondary to exsanguination from an internal carotid artery rupture. Patient consent was obtained for publication.
A 63-year-old man with a history of clival chordoma debulking with postoperative radiation 5 years prior presented for evaluation of recurrent profuse epistaxis requiring hospital admission. Nasal endoscopic examination by ear, nose, and throat surgeons revealed exposure of the petrous portion of the right internal carotid artery (RICA) with no visible bleeding. A preoperative computed tomography angiogram had been negative for a bleeding source or an aneurysm. Interventional Neurosurgery was consulted and they placed a stent across the exposed portion of the RICA via right femoral artery access. Recurrent epistaxis at completion of this procedure required placement of a 30-mL Foley balloon intranasally to achieve control of bleeding. The patient was kept intubated and admitted to the Neurological Intensive Care Unit (ICU).
The patient remained intubated in the ICU with systolic blood pressure control <140 mm Hg. Ear, nose, and throat physicians removed the nasal packing on the fifth postoperative day, performed a bedside nasal endoscopy, and identified no bleeding. The patient was subsequently weaned from mechanical ventilation and the trachea was extubated. On postoperative day 7, the patient had sudden and profound nasopharyngeal bleeding that progressed rapidly to PEA. Bag-mask ventilation and nurse-administered chest compressions were initiated immediately, but without administration of vasopressor/inotropes given the concern for uncontrolled carotid bleeding. The large amount of blood in his nasopharynx made bag-mask ventilation ineffective and blind oral intubation was successful on the first attempt. Endotracheal tube position was confirmed clinically because the large amount of blood coming up the endotracheal tube made our colorimetric CO2 detector uninterpretable. A large-bore (9.0F) femoral venous catheter was inserted emergently, the hospital exsanguination protocol3 was activated, and blood products were administered using a rapid infusion system. Once bilateral nasal Foley catheters had been placed to tamponade the bleeding, 1 mg epinephrine was given with return of spontaneous circulation (ROSC). The total time without a palpable pulse was determined to be 15 minutes by retrospective review of the telemonitoring data. The patient was taken emergently to the operating room where his RICA was killed using coils and onyx liquid embolization. A postprocedure angiogram demonstrated brisk left to right cross filling via the anterior communicating complex. His total resuscitation comprised 3.5 L crystalloid, 14 U packed red blood cells, 6 U fresh frozen plasma, and 1 U of single donor platelets. The patient was in the operating room for 3 hours and during this time his temperature was managed passively in a range of 35.8°C to 36°C because of concern for coagulopathy.
Postoperatively, given ventilatory and oxygenation difficulties secondary to aspiration of blood, the patient was sedated and chemical paralysis was instituted. We were therefore unable to assess the patient's neurological status and the decision was made to initiate the hypothermia protocol by actively controlling the patient's body temperature to 34°C to 35°C for 24 hours. This temperature range was chosen to provide metabolic benefit with minimal effects on coagulation. We started cooling 4 hours after his ROSC using the Arctic Sun Temperature Management System (Medivance Inc., Louisville, CO) and achieved our temperature goal within 30 minutes. After 24 hours of cooling, the surface cooling was discontinued, the patient was allowed to passively rewarm, and his temperature increased to 36°C within 8 hours. The rate of rewarming was <0.25°C per hour, which is consistent with published guidelines.4 His first neurological examination after rewarming revealed eye opening to voice and localization with his right side; he did not demonstrate left-sided movement.
The patient's postoperative course was significant for prolonged mechanical ventilation that required a tracheostomy and percutaneous gastrostomy placement for nutritional support. Postarrest day 28 he was discharged from the ICU to a rehabilitation facility and from there discharged to home on postarrest day 40. On discharge from the rehabilitation facility, his cognition was close to baseline, he had some minimal residual left-sided weakness but was able to walk, his tracheostomy was decannulated, and he was receiving full nutritional intake orally.
Induced therapeutic hypothermia has been shown to be effective in out-of-hospital cardiac arrest2 and is the only intervention to improve neurological outcomes after ventricular fibrillation (VF) cardiac arrest.5 Current recommendations are to institute therapeutic hypothermia in patients after ROSC from VF cardiac arrest in the range of 32°C to 34°C for 24 hours.5 The etiology of in-hospital cardiac arrest is different,1 and induced hypothermia should be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm.5
In this case, we successfully used mild therapeutic hypothermia in a post-PEA arrest patient secondary to exsanguination with excellent neurological outcome. Ideally, neurological assessment of our patient would have been performed after resuscitation to assess whether therapeutic hypothermia was indicated, but we considered it unsafe to wean sedation given his severe ventilatory failure and hypoxia. We induced therapeutic hypothermia with a goal of 34°C to 35°C to minimize the risk of further bleeding given there are limited data to support hypothermia use for cardiac arrest secondary to hemorrhage.
Hemorrhage as a cause of cardiac arrest is common in trauma patients6,7 and is associated with hypothermia; however, in this group of patients, hypothermia represents cellular hypoxia8,9 and is an indicator of the severity of injury. It is considered detrimental because it may affect platelet function,10,11 the coagulation cascade,11,12 and has been associated with worse outcomes.11,13 We believe our patient had many reasons that distinguish him from a hemorrhaging trauma patient; he had an isolated bleeding source with no other injuries, his core temperature was maintained during resuscitation because of use of the rapid infuser, and mild hypothermia was initiated after restoration of his circulating blood volume. This latter point is important because he did not require vasopressor support in the ICU, not compromising his peripheral perfusion, allowing for an increased efficiency of surface cooling.
There are many postulated mechanisms by which hypothermia exerts a protective effect: reduction of the cerebral metabolic rate (decreases between 6% and 10% for each 1°C decrease), interruption of the apoptotic pathways, decreased release of proinflammatory cytokines, and decreased free radical production.14 Many of these previously mentioned processes can contribute to fever, which is both a frequent occurrence14 and independently associated with poor outcome after neurological injury.15,16 The recent cardiac arrest guidelines include a recommendation that providers actively intervene to prevent hyperthermia5 and some of the benefit in our patient may be attributed to the acute prevention of fever.
The guidelines further state that there is inadequate evidence supporting the optimal timing for administration of vasopressor therapy,17 and we initially withheld vasopressors during our patient's resuscitation because of concern that centralization of blood volume would increase the rate of blood loss and further impair the efforts to restore the circulating volume. We acknowledge that withholding vasopressor therapy before balloon tamponade may have contributed to a prolonged resuscitation time, especially given the rapid return of a palpable pulse after the first dose of epinephrine.
This case report demonstrates a temporal, not causal, association of therapeutic hypothermia with good neurological outcome in a PEA arrest patient. We did not institute cooling therapy until the patient returned from the operating room where his temperature was passively managed, did not cool to <34°C per cardiac arrest guidelines, and did not assess neurological status before cooling. There were many important factors that contributed to the successful patient outcome: the patient's location within a critical care unit, the successful blind intubation, the rapidity of gaining large-bore IV access, and the availability of the rapid transfuser combined with our hospital's exsanguination protocol.3
Therapeutic hypothermia after in-hospital cardiac arrests may improve outcome. We expect the application of therapeutic hypothermia will continue to be researched further in non-VF arrest.
Name: Stuart McGrane, MBChB.
Contribution: This author helped write the manuscript and provided patient care.
Attestation: Stuart McGrane approved the final manuscript.
Name: Jennifer Maziad, MD.
Contribution: This author helped write the manuscript, co-wrote the manuscript, and provided patient care.
Attestation: Jennifer Maziad approved the final manuscript.
Name: James L. Netterville, MD.
Contribution: This author helped write the manuscript, reviewed and edited the manuscript, and provided patient care.
Attestation: James L. Netterville approved the final manuscript.
Name: Nahel N. Saied, MBBCh.
Contribution: This author helped write the manuscript, co-wrote and edited the manuscript, and provided patient care.
Attestation: Nahel Saied approved the final manuscript.
This manuscript was handled by: Steven L. Shafer, MD.
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