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Therapeutic Hypothermia After Cardiac Arrest in a Patient With Systemic Sclerosis and Raynaud PhenomenonTherapeutic Hypothermia Systemic Sclerosis FREE TO VIEW

Keren Bakal, MD; Mauricio Danckers, MD; Joshua L. Denson, MD; Harald Sauthoff, MD
Author and Funding Information

From the Department of Medicine (Drs Bakal, Danckers, Denson, and Sauthoff), NYU School of Medicine; and VA NY Harbor Healthcare System (Dr Sauthoff), US Department of Veterans Affairs, New York, NY.

CORRESPONDENCE TO: Harald Sauthoff, MD, Department of Medicine, NYU School of Medicine, 423 E 23rd St, New York, NY 10010; e-mail: Harald.sauthoff@nyumc.org


Part of this article has been presented and published in abstract form at CHEST 2012, October 22, 2012, Atlanta, GA (Bakal K, Danckers-Degregori M, Felner K, Sauthoff H. Chest. 2012;142[4_MeetingAbstracts]:289A).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(2):e27-e30. doi:10.1378/chest.14-1184
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Therapeutic hypothermia favorably impacts neurologic outcomes in patients after cardiopulmonary arrest, although the appropriate target temperature is less clear. Its safety profile in patients with systemic sclerosis (SSc) and Raynaud phenomenon (RP), who may be at increased risk for ischemic complications, has not been addressed in the literature, to our knowledge. Digital lesions are commonly seen in patients with SSc, and cold-induced myocardial ischemia has also been reported. We describe a case of a man with SSc, RP, and digital ulcers who underwent therapeutic hypothermia after cardiopulmonary arrest. He regained full neurologic function, and except for digital necrosis, no hypothermia-associated adverse events were observed. Other risk factors for ischemia, such as cocaine use, may have contributed to the development of the digital necrosis. However, clinicians should be aware of the risk for ischemic complications in patients with SSc and RP when considering the appropriate target temperature after cardiopulmonary arrest.

Figures in this Article

Therapeutic hypothermia in patients with cardiopulmonary arrest favorably impacts neurologic outcomes.1,2 Its safety profile and outcomes in systemic sclerosis (SSc) and Raynaud phenomenon (RP) have not been previously described, to our knowledge.

A 52-year-old man with SSc, RP, ischemic cardiomyopathy, and recent cocaine use developed cardiopulmonary arrest with ventricular fibrillation. Cardiopulmonary resuscitation was administered with return of spontaneous circulation within 20 min. Postarrest, he showed no eye or verbal response, but was withdrawing to pain, corresponding to a Glasgow Coma Scale of 6. He was hemodynamically stable with minimal use of pressors. Chronic superficial digital ulcers were present on all fingertips. Laboratory tests revealed an elevated troponin level and leukocytosis. ECG and transthoracic echocardiogram showed no evidence of acute ischemia. Therapeutic hypothermia was induced via surface cooling to a temperature of 33°C for 24 h, followed by gradual rewarming. During the cooling phase, nonblanching erythema developed on the dorsum of the feet, ankles, wrists, and tibial surfaces (Figs 1A, 1B). Dusky necrosis developed on the left fourth digit 72 h later (Fig 1C). Nifedipine was administered. He regained full neurologic function. Cardiac catheterization revealed nonobstructive coronary artery disease. An automatic implantable cardioverter defibrillator was implanted. Skin findings, except for the fingertip necrosis (Fig 2), had substantially improved by hospital discharge to home.

Figure Jump LinkFigure 1 –  A-C, Photographs of (A) the left hand and (B) both feet and ankles during the cooling phase show nonblanching erythema on the dorsum of the hand, feet, and ankles. C, Seventy-two hours later, necrosis at the tip of the left fourth digit had developed. (The patient provided written consent for the use of this photograph.)Grahic Jump Location
Figure Jump LinkFigure 2 –  The necrosis of the tip of the fourth digit was well demarcated at time of discharge. (The patient provided written consent for the use of this photograph.)Grahic Jump Location

Therapeutic hypothermia improves neurologic outcome and survival in patients who have been resuscitated after cardiopulmonary arrest,1,2 although the most appropriate temperature target is uncertain after the publication of the Targeted Temperature Management (TTM) Trial.3 TTM is recommended for comatose patients after out-of-hospital cardiac arrest due to ventricular fibrillation and may be considered in patients with nonventricular fibrillation and in-hospital arrest.4 However, the risk for side effects may be increased in certain populations, such as patients with SSc and RP.

Digital lesions are common in SSc and are frequently localized on the second and third finger, usually affecting the fingertips.5 The risk of digital ischemia in patients with SSc and RP undergoing therapeutic hypothermia has not been described. However, even in healthy subjects, mild accidental hypothermia is associated with an increased risk of local cold injuries.6

Digital ulcers may be attributable to underlying vasculopathy from SSc, as well as persistent vasospasm associated with RP.7 Intraluminal platelet activation with clot formation and thromboxane release has been proposed as another mechanism for digital ulcers in patients with SSc and RP, who are believed to have underlying endothelial dysfunction.8,9

Ischemic injury during therapeutic hypothermia could be related to an increased vasoconstrictor response to cold, which is further aggravated by an impaired “hunting reaction.”10 This reaction is described as cold-induced vasodilatation characterized by alternation of vasodilatation and vasoconstriction, which reduces the risk of local cold injuries.10 Patients with Raynaud disease may show a less pronounced hunting reaction.11

Although therapeutic hypothermia may have been an important contributor to the development of this patient’s digital necrosis, other risk factors for ischemia may have played a role. Cocaine is well known to cause ischemic complications, and ischemic finger necrosis due to cocaine has been described.12 Furthermore, profound shock, disseminated intravascular coagulation, norepinephrine, and vasopressin can all cause ischemic complications and skin necrosis. This patient was a regular user of cocaine and received epinephrine and vasopressin during resuscitation, but he was hemodynamically stable after return of spontaneous circulation and only received low-dose norepinephrine for a short time. He did not have findings consistent with disseminated intravascular coagulation.

A more serious complication, cold-induced myocardial ischemia (“myocardial RP”), is proposed to occur in patients with SSc, but the mechanism is not well understood and probably differs from peripheral RP.13 Cold exposure severe enough to induce RP was reported in one study of patients with SSc to cause increased left ventricular dysfunction without a decrease in ejection fraction.14 Another study, which followed patients with SSc for 7 years, revealed that a subset of patients with severe myocardial RP developed long-term systolic left ventricular dysfunction.15 There have been mixed results in additional studies, and further investigation is required.16 This patient tolerated therapeutic hypothermia without evidence of myocardial injury, based on serial troponins, ECGs, and echocardiography.

Overall, we did not observe unacceptable complications of therapeutic hypothermia in a patient with SSc and RP. However, clinicians should be aware of the risk of digital ischemia and necrosis in similar patients. In view of the results of the published TTM trial,3 which showed comparable outcome with a target temperature of 33°C or 36°C, controlling the temperature to 36°C may be preferable in patients with similar predisposition for ischemic complications.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

RP

Raynaud phenomenon

SSc

systemic sclerosis

TTM

Targeted Temperature Management

Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest [published correction appears inN Engl J Med. 2002;346(22):1756]. N Engl J Med. 2002;346(8):549-556. [CrossRef] [PubMed]
 
Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557-563. [CrossRef] [PubMed]
 
Nielsen N, Wetterslev J, Cronberg T, et al; TTM Trial Investigators. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197-2206. [CrossRef] [PubMed]
 
Peberdy MA, Callaway CW, Neumar RW, et al; American Heart Association. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care [published correction appears inCirculation. 2011;123(6):e237]. Circulation. 2010;122(18)(suppl 3):S768-S786. [CrossRef] [PubMed]
 
Galluccio F, Matucci-Cerinic M. Two faces of the same coin: Raynaud phenomenon and digital ulcers in systemic sclerosis. Autoimmun Rev. 2011;10(5):241-243. [CrossRef] [PubMed]
 
Moran DS, Heled Y, Shani Y, Epstein Y. Hypothermia and local cold injuries in combat and non-combat situations—the Israeli experience. Aviat Space Environ Med. 2003;74(3):281-284. [PubMed]
 
Guiducci S, Giacomelli R, Cerinic MM. Vascular complications of scleroderma. Autoimmun Rev. 2007;6(8):520-523. [CrossRef] [PubMed]
 
Lau CS, McLaren M, Saniabadi A, Belch JJ. Increased whole blood platelet aggregation in patients with Raynaud’s phenomenon with or without systemic sclerosis. Scand J Rheumatol. 1993;22(3):97-101. [CrossRef] [PubMed]
 
Chung L, Fiorentino D. Digital ulcers in patients with systemic sclerosis. Autoimmun Rev. 2006;5(2):125-128. [CrossRef] [PubMed]
 
Daanen HA. Finger cold-induced vasodilation: a review. Eur J Appl Physiol. 2003;89(5):411-426. [CrossRef] [PubMed]
 
Jobe JB, Goldman RF, Beetham WP Jr. Comparison of the hunting reaction in normals and individuals with Raynaud’s disease. Aviat Space Environ Med. 1985;56(6):568-571. [PubMed]
 
Balbir-Gurman A, Braun-Moscovici Y, Nahir AM. Cocaine-induced Raynaud’s phenomenon and ischaemic finger necrosis. Clin Rheumatol. 2001;20(5):376-378. [CrossRef] [PubMed]
 
Champion HC. The heart in scleroderma. Rheum Dis Clin North Am. 2008;34(1):181-190. [CrossRef] [PubMed]
 
Ellis WW, Baer AN, Robertson RM, Pincus T, Kronenberg MW. Left ventricular dysfunction induced by cold exposure in patients with systemic sclerosis. Am J Med. 1986;80(3):385-392. [CrossRef] [PubMed]
 
Mizuno R, Fujimoto S, Saito Y, Nakamura S. Cardiac Raynaud’s phenomenon induced by cold provocation as a predictor of long-term left ventricular dysfunction and remodelling in systemic sclerosis: 7-year follow-up study. Eur J Heart Fail. 2010;12(3):268-275. [CrossRef] [PubMed]
 
Steen V. The heart in systemic sclerosis. Curr Rheumatol Rep. 2004;6(2):137-140. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  A-C, Photographs of (A) the left hand and (B) both feet and ankles during the cooling phase show nonblanching erythema on the dorsum of the hand, feet, and ankles. C, Seventy-two hours later, necrosis at the tip of the left fourth digit had developed. (The patient provided written consent for the use of this photograph.)Grahic Jump Location
Figure Jump LinkFigure 2 –  The necrosis of the tip of the fourth digit was well demarcated at time of discharge. (The patient provided written consent for the use of this photograph.)Grahic Jump Location

Tables

References

Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest [published correction appears inN Engl J Med. 2002;346(22):1756]. N Engl J Med. 2002;346(8):549-556. [CrossRef] [PubMed]
 
Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557-563. [CrossRef] [PubMed]
 
Nielsen N, Wetterslev J, Cronberg T, et al; TTM Trial Investigators. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197-2206. [CrossRef] [PubMed]
 
Peberdy MA, Callaway CW, Neumar RW, et al; American Heart Association. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care [published correction appears inCirculation. 2011;123(6):e237]. Circulation. 2010;122(18)(suppl 3):S768-S786. [CrossRef] [PubMed]
 
Galluccio F, Matucci-Cerinic M. Two faces of the same coin: Raynaud phenomenon and digital ulcers in systemic sclerosis. Autoimmun Rev. 2011;10(5):241-243. [CrossRef] [PubMed]
 
Moran DS, Heled Y, Shani Y, Epstein Y. Hypothermia and local cold injuries in combat and non-combat situations—the Israeli experience. Aviat Space Environ Med. 2003;74(3):281-284. [PubMed]
 
Guiducci S, Giacomelli R, Cerinic MM. Vascular complications of scleroderma. Autoimmun Rev. 2007;6(8):520-523. [CrossRef] [PubMed]
 
Lau CS, McLaren M, Saniabadi A, Belch JJ. Increased whole blood platelet aggregation in patients with Raynaud’s phenomenon with or without systemic sclerosis. Scand J Rheumatol. 1993;22(3):97-101. [CrossRef] [PubMed]
 
Chung L, Fiorentino D. Digital ulcers in patients with systemic sclerosis. Autoimmun Rev. 2006;5(2):125-128. [CrossRef] [PubMed]
 
Daanen HA. Finger cold-induced vasodilation: a review. Eur J Appl Physiol. 2003;89(5):411-426. [CrossRef] [PubMed]
 
Jobe JB, Goldman RF, Beetham WP Jr. Comparison of the hunting reaction in normals and individuals with Raynaud’s disease. Aviat Space Environ Med. 1985;56(6):568-571. [PubMed]
 
Balbir-Gurman A, Braun-Moscovici Y, Nahir AM. Cocaine-induced Raynaud’s phenomenon and ischaemic finger necrosis. Clin Rheumatol. 2001;20(5):376-378. [CrossRef] [PubMed]
 
Champion HC. The heart in scleroderma. Rheum Dis Clin North Am. 2008;34(1):181-190. [CrossRef] [PubMed]
 
Ellis WW, Baer AN, Robertson RM, Pincus T, Kronenberg MW. Left ventricular dysfunction induced by cold exposure in patients with systemic sclerosis. Am J Med. 1986;80(3):385-392. [CrossRef] [PubMed]
 
Mizuno R, Fujimoto S, Saito Y, Nakamura S. Cardiac Raynaud’s phenomenon induced by cold provocation as a predictor of long-term left ventricular dysfunction and remodelling in systemic sclerosis: 7-year follow-up study. Eur J Heart Fail. 2010;12(3):268-275. [CrossRef] [PubMed]
 
Steen V. The heart in systemic sclerosis. Curr Rheumatol Rep. 2004;6(2):137-140. [CrossRef] [PubMed]
 
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