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Case reports are always fascinating and lively, they tell stories – “les histoires de chasse”, as the French call it – much appreciated by clinically working physicians. All experienced doctors carry a wealth of them, they remind us of our own personal experiences, successes and failures, of “blood, sweat and tears” and of decision making, where guidelines are in conflict with each other and we rely on opinions, eminence and instincts. More often than not, these tough decisions concern difficult and under-studied patient populations, which are systematically and carefully excluded from controlled clinical trials and current guidelines. Case reports are therefore of particular value in teaching and research, since they often inspire a discussion on how to handle certain diseases and on how to generate new hypotheses. They are valued for illustrating clinical decision making at its best. We might call them the “icebreakers of modern medicine” and, in accordance with this view, Laura Massobrio and colleagues [1] have to be congratulated on breaking new ground. The downside is the potential risk, which our patient (and not the “pioneer doctor”!) has to take with these new icebreaker routes. Therefore, it is our obligation to perform particularly careful risk assessment and decision making, in the spirit of “primum nihil nocere” (Hypocrates) and “the least autistic thinking” [2]. In the case of Massobrio, the reader essentially partakes in three difficult decisions with new oral anticoagulants (NOACs). The case follows up a 79-year-old woman with atrial fibrillation, who suffered from a chronic sub-dural haematoma (cSDH) while on warfarin; after the evacuation she was on low molecular weight heparin (LMWH) for 1 month, after “local reactions/intolerance to all LMWHs and fondaparinux” (which occurs rarely, and it is unknown to the reader whether this was a prophylactic or therapeutic regimen). She was then (a) put on a reduced dose of apixaban (2 x 2.5 mg); (b) after 1 month, she underwent electroconversion, and eventually (c) electrophysiological ablation and pacemaker implantation with typical bridging (48 h preand 12 h post-) without further complications. She is doing well 7 months after the initial observation. This case is instructive for three general reasons and it is paradigmatic for decision making: (1.) Lack of baseline information of the case, which is important for an adequate decision. For example, the reader would like to know whether the cSDH was spontaneous or traumatic, because this has prognostic implications [3–6]. We know neither the kidney function nor her weight (<60 kg?). Which LMWHs were tested in which dose? Was there any other bleeding history? What were the significant laboratory findings (platelet count, haemoglobin)? She was on warfarin before, how was her time in therapeutic range (TTR)? Was she bleeding with an INR >4 or while in the therapeutic range? The patient did not fulfil any of the three criteria for the lower dosing regimen of 2 x 2.5 mg apixaban, but it was still chosen. This decision may expose her to the therapeutic bleeding risk, potentially without protection from thromboembolic events. (2.) Critical review and implementation of the literature. The ARISTOTLE study found an encouraging reduction of intracranial bleeds in the apixaban group and this was found with all NOACs compared with VKA [8]. Can this finding be applied to patients after ICB/SDH and if yes, after what time period? Would it be 30 days, as in this case? With or without the challenge with LMWH? In prophylactic or therapeutic dosing? Or sequentially prophylactic and then therapeutic? Should such cases be monitored by trough plasma levels [8]? Would a well-controlled VKA therapy (INR 2–2.5) at a TTR >80% be equivalent? These are all questions that are not studied and may never be studied adequately in the future. However by approximation, we do know that this patient was at high risk for thromboembolism and stroke with a CHA2DS2Vasc score of 8,

Investigators of studies of n = 1: Pioneers or kamikazes?