Article, Neurology

Good neurologic recovery after cardiac arrest using hypothermia through continuous renal replacement therapy

Unlabelled image

Neurologic recovery after cardiac a”>Case Report

Contents lists available at ScienceDirect

American Journal of Emergency Medicine

journal homepage: locate/ ajem

American Journal of Emergency Medicine 31 (2013) 1720.e1-1720.e3

Good neurologic recovery after cardiac arrest using hypothermia through continuous renal replacement therapy?,??

Abstract

Therapeutic hypothermia is becoming a standard of care to mitigate neurologic injury in cardiac arrest survivors. Several cooling methods are available for use in TH. For maintaining a target temperature, intravascular cooling is superior to, more efficacious than, and safer than Surface cooling methods. The use of an intravenous cooling catheter is independently associated with a higher odds ratio for survival. However, many techniques use commercially developed equipment that is expensive to purchase and use. The application and popularization of the intravascular cooling method have been difficult. In patients with pulmonary edema or cardiac insufficiency, liquid is restricted, so intravascular cooling systems cannot be used. Studies have shown abnormalities mimicking the immunologic and coagulation disorders observed in severe sepsis. Continuous renal replacement therapy has been widely used in the intensive care unit to improve clinical parameters and survival in patients with multiple-organ dysfunction of septic origin. Continuous renal replacement therapy can also be used as another type of core cooling method. We used continuous renal replacement therapy as a cooling method to induce TH in a patient who had a cardiac arrest, and the patient regained consciousness 52 hours later.

A 60-year-old man was transferred from the burn unit with a second-degree burn on the toes of the left foot caused by boiling water, uncontrolled diabetes, a urinary tract infection, hypertension, ischemic heart disease, chronic renal failure, anemia, a lung infection, and a large amount of seroperitoneum and hydrothorax with generalized systemic and pulmonary edema. After high-resolution Computed tomography imaging of the lung, the nurse found that the patient was not breathing and had no pulse. The first recorded cardiac rhythm was ventricular fibrillation. Advanced cardiac life support measures, including intubation, administration of 2 mg of epineph- rine, and 6 defibrillation attempts, Restored spontaneous circulation 22 minutes after the onset of the event. Upon arrival at the intensive care unit, the patient was hemodynamically stable and did not require vasopressor support. A 12-lead electrocardiogram showed sinus tachycardia with nonspecific ST changes in the inferior leads. An initial neurologic examination in the intensive care unit revealed

? The manuscript, as submitted or its essence in another version, is not under consideration for publication elsewhere and will not be published elsewhere while under consideration by the American Journal of Emergency Medicine.

?? There was no any financial support for the study.

coma (Glasgow Coma Scale score, 5) with decorticate posturing. At hour 1, the patient had no eye opening, no response to painful stimuli, absent corneal reflexes, nonreactive 2-mm pupils, and multifocal myoclonic movements that were most pronounced in the facial muscles. The patient’s temperature was 35.8?C, determined via a rectal thermometer; blood pressure was 97/52 mm Hg; pulse was 121 beats/min; respiratory rate was 16 breaths/min with assisted ventilation; and oxygen saturation was 96%, whereas 100% inspired oxygen was delivered. A blood chemistry analysis revealed blood urea at 126 mg%, serum creatinine at 3.7 mg%, serum sodium at 127 mEq/L, and serum potassium at 4.96 mEq/L. A diagnosis of post-cardiac arrest syndrome (PCAS) with coma was made. Attempts to induce Therapeutic hypothermia for neural protection were initiated at hour 2 with a surface cooling device and continuous renal replace- ment therapy (CRRT). Therapeutic hypothermia had not been attempted earlier because the patient was initially hypothermic (35.8?C) upon arrival at the intensive care unit but then rapidly became febrile.

Right femoral venous access was obtained with an 11F double-

lumen catheter, which was connected to a Dilpact (B. Braun, Melsungen, Germany), and the blood temperature was maintained

Table 1

Summary of observations made during CRRT

Pulse rate 78-88/min

BP 105-123 mm Hg systolic and55-82 mm Hg diastolic

Pulse oximeter 99%-100% saturation

CVP 10-13 cm of water

Blood sugar 332-130 mg%

Urine output 0 mL/h (without diuretics) Stomach aspirate was “coffee grounds”

once for 32 h CVVHDF data

Blood flow rate 150 mL/min

Replacement fluid used 3.428 L in 3 h

Dialysate used 4.38 L in 3 h

Ultrafiltrate drained 3.393 L in 3 h

Citric acid dose 180-220 mL/h, to maintain apt between 45 and 72 s

Weight gain -1500 mL, with 300 mL as feed

Total blood filtered 27 L in 3 h Blood chemistry after 5 h CVVHDF

Blood urea 89 mg%

Serum creatinine 2.89 mg%

Serum sodium 127 mE/L

Serum potassium 4.12 mEq/L

0735-6757/$ – see front matter (C) 2013

1720.e2 Y. Ma et al. / American Journal of Emergency Medicine 31 (2013) 1720.e11720.e3

Table 2

Timing and description of important events

Hours

0 Return of spontaneous circulation

1 Initial neurologic examination in the intensive care unit revealed coma (Glasgow Coma Scale score, 5) with decorticate posturing; at hour 1, the patient had no eye opening, no response to painful stimuli, absent corneal reflexes, nonreactive 2-mm pupils, and multifocal myoclonic movements most pronounced in the facial muscles.

2 TH initiated with surface cooling and CVVHD

15 Neurologic responses changed from decerebrate to flexor.

25 Responded to verbal commands; flexor responses were seen

30 Well enough to be disconnected from the ventilator Rewarming initiated and propofol and fentanyl infusion stopped. Examination: no eye opening, no response to pain, sluggishly reactive 4-mm pupils, no corneal reflexes, intact cough reflex and gag reflex, spontaneous respirations present

50 Rewarming initiated and propofol and fentanyl infusion stopped

52 The patient can speak and move freely, but still no urine

72 CVVHDF was stopped.

at 33.0?C for 24 hours. Heparin was used as an anticoagulant. Before hypothermia is induced, sedation and analgesia should be initiated to prevent shivering and to minimize the patient’s discomfort. The patient received no Neuromuscular blocking agents or other medica- tions with significant central nervous system depressant effects. No naloxone or other reversal agents were administered. The patient’s prothrombin time and partial thromboplastin time were within normal limits. After 24 hours of hypothermia, controlled rewarming was performed (0.5?C per hour) to a core temperature of 36.5?C. Sedation was subsequently discontinued. We have summarized the observations made during CRRT in Table 1.

The patient’s neurologic responses changed from decerebrate to flexor after 15 hours. The patient responded to verbal commands after another 10 hours. The patient was well enough to be disconnected from the ventilator after 30 hours and regained fully consciousness after 52 hours. Continuous venovenous hemodiafiltration (CVVHDF) was stopped when the filter clotted after 72 hours (Tables 2 and 3).

Therapeutic hypothermia is the only therapy in the PCAS phase that is proven to limit neurologic injury. Furthermore, TH is an integral component of bundled care for PCAS [1-3].

The global systemic ischemia/reperfusion response in PCAS is the ultimate representation of shock and is characterized by a systemic inflammatory immune response, impaired vasoregulation, increased coagulation, Adrenal suppression, impaired oxygen delivery and use, and immunosuppression. Inflammatory cascades cause immunosuppression, endothelial dysfunction, and activation of coagulation pathways within the microcirculation [4,5].

Alterations in the inflammatory response can cause endothelial activation, leukocyte infiltration, and further tissue injury [6]. Other contributing factors including hypotension, hypoxemia, impaired Cerebrovascular autoregulation, and Brain edema can further impede the delivery of oxygen to the brain. We observed that CVVHDF appears to have accelerated recovery and attempted to hypothesize the possible mechanism owing to a lack of any objective laboratory data. There was no clear explanation for the good neurologic recovery after CA by using hypothermia through CRRT. Potential explanations are as follows.

Interruption of the sepsis process

Studies have shown abnormalities mimicking the immunologic and Coagulation disorders observed in severe sepsis [7]. These findings suggest that the recent therapeutic approaches that have been successfully used in sepsis should be investigated in patients who are successfully resuscitated after CA. Animal experiments have demon- strated that hemofiltration can rapidly eliminate the toxic products of ischemia and reperfusion after CA, improving cerebral resuscitation. Studies of sepsis have shown that inflammatory and anti-inflammatory cytokines are maximally removed within the first hour by CRRT, mainly by adsorption. However, after CA, the release of cytokines may not be continuous compared with the release in a septic state.

Targeted temperature management

Core cooling can be achieved with the use of intravascular cooling catheters (made of metal or containing balloons filled with cold saline) or the intravenous infusion of cold fluids. These techniques often use commercially developed equipment that is specifically designed for the purpose of target temperature management. Continuous renal replacement therapy is another potential cooling method for achieving a target temperature and also offers the chance to manipulate temperature, as hypothermia or rewarming is possible.

Amelioration of microcirculatory impairment

The heparinization necessary for CRRT is useful in a situation in which fibrinolytic activation has been shown to improve survival. The No-reflow phenomenon may be switched off because of certain changes caused by CRRT. Coronary perfusion during cardiopulmonary resuscitation is not adequate, and support for other organs is paramount.

The described CRRT cooling method is a useful method for reaching and maintaining a target temperature. The method is especially suitable for intensive care units that use CRRT on a daily basis for patients with acute renal failure. Further studies in patients with reasonable chances of recovery would be worthwhile. Theoretically, this procedure seems to satisfy every need of the post-CA situation.

Table 3

Timing and details of Neurologic examinations

Hours

Eye opening

Motor responses

Pupillary responses

Corneal reflex

Cough/ Gag

Spontaneous respirations

Myoclonic movements

1

6 mm, NR

+

2

6 mm, sluggish

+

15

4 mm, sluggish

+

20

4 mm, sluggish

25

3 mm, sensitive

+

30

+

3 mm, sensitive

+

+

+

50

+

+

3 mm, sensitive

+

+

+

52

+

+

3 mm, sensitive

+

+

+

Y. Ma et al. / American Journal of Emergency Medicine 31 (2013) 1720.e11720.e3 1720.e3

Yu-jie Ma MD Bo Ning Medical Master

Intensive Care Unit, Air Force General Hospital People’s Liberation Army (PLA), Beijing, China E-mail address: [email protected]

Wei-hong Cao MD Department of Burn, Air Force General Hospital, People’s Liberation Army (PLA), Beijing, China

Tao Liu MBBS Lei Liu MBBS

Intensive Care Unit, Air Force General Hospital,

People’s Liberation Army (PLA), Beijing, China

http://dx.doi.org/10.1016/j.ajem.2013.07.012

References

  1. Sunde K, Pytte M, Jacobsen D, et al. Implementation of a standardized treatment protocol for post resuscitation care after out-of-hospital cardiac arrest. Resuscita- tion 2007;73:29-39.
  2. Oddo M, Schaller MD, Feihl F, et al. From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med 2006;34:1865-73.
  3. Soar J, Nolan JP. Mild hypothermia for post cardiac arrest syndrome. BMJ 2007;335: 459-60.
  4. Adrie C, Monchi M, Laurent I, et al. Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest: implication of the protein C anticoagulant pathway. J Am Coll Cardiol 2005;46:21-8.
  5. Adrie C, Adib-Conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a “sepsis-like” syndrome. Circulation 2002;106:562-8.
  6. Wong CHY, Crack PJ. Modulation of neuro-inflammation and vascular response by oxidative stress following cerebral Ischemia-reperfusion injury. Curr Med Chem 2008;15:1-14.
  7. Fischer M, Butiger BW, Popov-Cenic S, Hossmann KA. Thrombolysis using plasminogen activator and heparin reduces cerebral no-reflow after resuscitation from cardiac arrest: an experimental study in the cat. Intensive Care Med 1996;22: 1214-23.