The Book of Lazarus
Lewis Pleasants, MD
Lazarus Syndrome is a rare phenomenon which entails the return of spontaneous circulation (ROSC) in a delayed fashion, usually after the cessation of cardiopulmonary resuscitation efforts. These cases are largely believed to be under-reported and based on a comprehensive review by Adhiyaman et al in 2007, there have been only 38 cases published in medical literature since 1982.
Our patient is an 82 year old male with a past medial history significant for HFpEF (EF 65%) secondary to AL Amyloidosis, atrial fibrillation complicated by embolic CVA’s, stage 3 CKD, hypertension and dementia. He presented from a nursing facility with a chief complaint of chest pain and shortness of breath. Of note, the patient had been admitted one month prior and was treated for a heart failure exacerbation. Initial evaluation was notable for relative hypotension, edema of the lower extremities and imaging showing bilateral pleural effusions. The patient’s troponin’s, BNP and creatinine were all elevated and he was admitted with a diagnosis of heart failure exacerbation with concomitant acute kidney injury in the setting of cardio-renal syndrome. Patient was initiated on treatment with an IV Lasix infusion. The patient unfortunately continued to have worsening renal function despite diuresis and became increasingly delirious from his multiple medical issues and extended hospital stay. Cardiology was consulted on admission and per their assessment, given multiple recent admissions, patient was likely within the end-stages of his disease. They recommended the involvement of palliative care to further discuss prognosis and goals of care and the patient was confirmed to be DNI/DNR.
Several days later, as the patient continued treatment, a code blue was called to the patient’s room after he was found to be non-responsive and pulseless with agonal pattern breathing. CPR was terminated shortly after it was initiated given the patient’s documented code status. Of note, the patient was not connected to telemetry at the time of the event. He was assessed at the bedside and found to be non-responsive to verbal or tactile stimuli (sternal rub, nail bed pressure). No heart sounds were auscultated over a 30 second period and patient displayed agonal breathing pattern which ceased after the first minute of evaluation. No carotid/radial pulses were palpable. Bilateral pupils were fixed and dilated and patient was pronounced deceased.
About 10 minutes later, the patient’s primary team was paged that the patient had resumed agonal respirations and had regained a faint pulse. A set of vitals were obtained shortly thereafter that showed a BP 107/66, O2 sat of 97%, HR 105 and RR of 12. ECG showed diffuse ST elevations. Cardiology was consulted to interrogate patient’s pacemaker which was functioning normally and showed no arrhythmias. Patient soon regained his baseline mentation (delirious but alert and responsive). Lab work obtained post-event notable for a troponin of 0.704, an anion gap of 21, a lactate of 8, VBG 7.45/39/27 and a Cr 5.2. Electrolytes were largely within normal limits and CBC showed a mildly elevated white count as compared to prior. Patient’s family was made aware of the situation and decision was made to make the patient comfort measures only. Less than 24 hours later, the patient again developed an agonal breathing pattern and became pulseless. Telemetry at the time showed an 100% paced rhythm at 45 bpm (lower limit set on patient’s pacemaker) and no organic beats were identified. He was pronounced decreased shortly thereafter.
There are several proposed mechanisms to describe the Lazarus phenomenon. One being the potential for delayed action of drugs (epinephrine, amiodarone etc.) that may be administered during resuscitation. It is thought that improved venous return after cessation of CPR allows for better delivery of medications. Another idea is that rapid manual ventilation during CPR does not allow adequate time for exhalation which in turns lead to increased end –expiratory pressure, reduced venous return and lower cardiac output. After this is stopped, as above, venous return improves. For our patient, one possible mechanism is myocardial stunning in the setting of prolonged myocardial dysfunction and ischemia (as afore mentioned, patient with ST elevations on post-event EKG and history of end stage AL Amyloidosis).
Overall, this case illustrates the curiosity that is autoresuscitation and highlights the importance of thorough and algorithmic death examinations. Recognition and more consistent reporting of this phenomenon can help us better identify and analyze the mechanisms involved.
References:
- Vedamurthy Adhiyaman, Sonja Adhiyaman, Radha Sundaram
J R Soc Med. 2007 Dec; 100(12): 552–557.
- David J Sprenkeler, Gerardus P J van Hout, Steven A J Chamuleau
Eur Heart J Case Rep. 2019 Sep; 3(3): ytz134. Published online 2019 Aug 7.
- Les Gordon, Mathieu Pasquier, Hermann Brugger, Peter Paal
Scand J Trauma Resusc Emerg Med. 2020; 28: 14. Published online 2020 Feb 26
- Kjartan Eskjaer Hannig, Rasmus Wulff Hauritz, Erik Lerkevang Grove
Case Rep Med. 2015; 2015: 724174. Published online 2015 Jun 8