Size matters

$\bf Purpose$ Acute lung injury is a life threatening condition often requiring mechanical ventilation. Lung-protective ventilation with tidal volumes of 6 mL/kg predicted body weight (PBW, calculated on the basis of a patient’s sex and height), is part of current recommended ventilation strategy. Hence, an exact height is necessary to provide optimal mechanical ventilation. However, it is a common practice to visually estimate the body height of mechanically ventilated patients and use these estimates as a reference size for ventilator settings. We aimed to determine if the common practice of estimating visual height to define tidal volume reduces the possibility of receiving lung-protective ventilation. $\bf Methods$ In this prospective observational study, 28 mechanically ventilated patients had their heights visually estimated by 20 nurses and 20 physicians. All medical professionals calculated the PBW and a corresponding tidal volume with 6 ml/kg/PBW on the basis of their visual estimation. The patients' true heights were measured and the true PBW with a corresponding tidal volume was calculated. Finally, estimates and measurements were compared. $\bf Results$ 1033 estimations were undertaken by 153 medical professionals. The majority of the estimates were imprecise and resulting data comprised taller body heights, higher PBW and higher tidal volumes (all p$\leq$0.01). When estimates of patients' heights are used as a reference for tidal-volume definition, patients are exposed to mean tidal volumes of 6.5 $\pm$ 0.4 ml/kg/PBW. 526 estimation-based tidal volumes (51.1%) did not provide lung-protective ventilation. Shorter subjects (<175cm) were a specific risk group with an increased risk of not receiving lung protective ventilation (OR 6.6; 95%CI 1.2–35.4; p = 0.02), while taller subjects had a smaller risk of being exposed to inadequately high tidal volumes (OR 0.15; 95%CI 0.02–0.8; p = 0.02). Furthermore, we found an increased risk of overestimating if the assessor was a female (OR 1.74; 95%CI 1.14–2.65; p = 0.01). $\bf Conclusion$ The common practice of visually estimating body height and using these estimates for ventilator settings is imprecise and potentially harmful because it reduces the chance of receiving lung-protective ventilation. Avoiding this practice increases the patient safety. Instead, height should be measured as a standard procedure

A valuable cardiac magnetic resonance investigation after MINOCA/takotsubo Syndrome

Myocardial infarction with non‐obstructive coronary arteries is a working diagnosis that includes takotsubo cardiomyopathy/syndrome (TTS). Cardiac magnetic resonance (CMR) is useful for establishing the underlying aetiology of myocardial infarction with non‐obstructive coronary arteries during the acute phase, but its role in follow‐up is less well established. A 35‐year‐old man with several cardiac risk factors presented 3 days after his sister's death with biochemical and clinical features of acute myocardial infarction without coronary artery obstruction on angiography but with diagnostic features of TTS on CMR, including oedema but no late gadolinium enhancement. Subsequent CMR 3 months later revealed left ventricular late gadolinium enhancement suggesting previous acute myocardial infarction. Although the initial diagnosis of TTS was robust according to established criteria, it remained uncertain whether the later ischaemic injury was related to an ischaemic event at presentation or occurred in the intervening period. Nevertheless, CMR may have an extended role in the follow‐up of these patients and may reveal additional, actionable pathology

Dickkopf-3 in the prediction of contrast media induced acute kidney injury

$\bf Background$ Dickkopf-3 (DKK3) has recently been discovered as a urinary biomarker for the prediction of acute kidney injury (AKI) after cardiac surgery. This finding needs to be confirmed for AKI in other clinical settings. The present study investigates whether DKK3 can predict contrast-induced AKI (CI-AKI). $\bf Methods$ We performed a prospective study in 490 patients undergoing coronary angiography. Primary endpoint was an increase in serum creatinine concentration $\geq$ 0.3 mg/dl within 72 h after the procedure. DKK3 was assessed < 24 h before coronary angiography. Predictive accuracy was assessed by receiver operating characteristic (ROC) curves. $\bf Results$ CI-AKI was observed in 30 (6.1%) patients, of whom 27 corresponded to stage I and 3 to stage II according to the Acute Kidney Injury Network (AKIN) criteria. Subjects who developed CI-AKI had a 3.8-fold higher urinary DKK3/creatinine ratio than those without CI-AKI (7.5 pg/mg [interquartile range [IQR] 1.2–1392.0] vs. 2.0 pg/mg [IQR 0.9–174.0]; $\it p$ = 0.047). ROC analysis revealed an area under the curve (AUC) of 0.61. Among subjects without clinically overt chronic kidney disease (estimated glomerular filtration rate [eGFR] > 60 ml/min, urinary albumin creatinine ratio < 30 mg/g), the DKK3/creatinine ratio was 5.4-fold higher in those with subsequent CI-AKI (7.5 pg/mg [IQR 0.9–590.1] vs. 1.38 pg/mg [IQR 0.8–51.0]; $\it p$ = 0.007; AUC 0.62). Coronary angiography was associated with a 43 times increase in the urinary DKK3/creatinine ratio. $\bf Conclusions$ Urinary DKK3 is an independent predictor of CI-AKI even in the absence of overt chronic kidney disease (CKD). The study thereby expands the findings on DKK3 in the prediction of postoperative loss of kidney function to other entities of AKI

Blue toe syndrome caused by emboli from anomalous left atrial septal pouch thrombus

$\bf Background$ Left atrial septal pouches (LASPs) are a relatively newly described but common anatomical cardiac variant thought to be associated with atrial fibrillation (AF) and cardio-embolic stroke. Blue toe syndrome (BTS) describes ischemic changes in the toes due to microembolisation of the digital arteries. Establishing the etiology of BTS is vital so that the underlying cause can be treated. Here we describe the first case of BTS arising due to emboli from LASP thrombus arising on a background of new-onset AF. $\bf Case presentation$ A 65-year-old man presented with a two-day history of progressive painful swelling and bluish-purple discoloration of the second and fourth toes of his left foot and new-onset AF. Tests for hypercoagulability disorders were negative. Duplex ultrasound and CT angiography excluded deep venous thrombosis and an absence of embolus, thrombus, or occlusion in the arterial tree in the lower extremities bilaterally, so BTS was diagnosed. While transthoracic echocardiography and chest CT initially showed no cardiac abnormalities or mural thrombus, subsequent transesophageal echocardiography revealed a LASP with an associated pedunculated thrombus. The affected toes were amputated due to wet gangrene, but the patient recovered well with thrombus resolution after anticoagulation. $\bf Conclusion$ The presence of a LASP in the absence of any other identifiable cause of BTS should trigger careful investigation of the interatrial septum, preferably using a multimodality imaging approach. The possibility that LASPs may not merely be an innocent bystander but a causative mechanism for peripheral ischemia must be considered

Feasibility of non-invasive measurement of central blood pressure and arterial stiffness in shock

$\bf Background$ Patients in haemodynamic shock are in need for an intensive care treatment. Invasive haemodynamic monitoring is state of the art for these patients. However, evolved, non-invasive blood pressure monitoring devices offer advanced functions like the assessment of central blood pressure and arterial stiffness. We analysed the feasibility of two oscillometric blood pressure devices in patients with shock. $\bf Methods$ We performed a monocentre prospective study, enrolling 57 patients admitted to the intensive care unit (ICU), due to septic and/or cardiogenic shock. We assessed invasive and non-invasive peripheral and central blood pressure <24 hours and 48 hours after admission on the ICU. Additional haemodynamic parameters such as pulse wave velocity (PWV), augmentation pressure and augmentation index were obtained through Mobil-o-Graph PWA (IEM) and SphygmoCor XCEL (AtCor Medical). $\bf Results$ A complete haemodynamic assessment was successful in all patients (48) with the Mobil-o-Graph 24 hours PWA and in 29 patients with the SphygmoCor XCEL ($\it P$ = .001), when cases of death or device malfunction were excluded. Reasons for failure were severe peripheral artery disease, haemodynamic instability, oedema and agitation. Invasive blood pressure showed a sufficient correlation with both devices; however, large differences between invasive and non-invasive techniques were recorded in Bland-Altmann analysis ($\it P$ < .05 for all parameters). PWV differed between the two devices. $\bf Conclusion$ Non-invasive peripheral blood pressure measurement remains a rescue technique. However, non-invasive assessment of arterial stiffness and central blood pressure is possible in patients with septic or cardiogenic shock. Further studies are required to assess their clinical significance for patients in shock

Biomarkers in the prediction of contrast media induced nephropathy

$\bf Background$ Subjects with chronic kidney disease are at increased risk for contrast-induced acute kidney injury (CI-AKI). Risk stratification is traditionally based on glomerular filtration rate (GFR) and proteinuria. The present trial examines, whether tubular and inflammatory biomarkers are able to identify subjects at increased risk as well. $\bf Methods$ We performed a prospective study in 490 patients undergoing coronary angiography. An increase of serum creatinine concentration $\geq$ 0.3 mg/dl from baseline to day 2–3 was defined as primary endpoint (CI-AKI). Urinary neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and calprotectin were assessed < 24h before coronary angiography. Prognostic accuracy was assessed by receiver operating characteristics (ROC) calculations. $\bf Results$ 30 (6.1%) patients suffered from CI-AKI (27 AKIN stage I, 3 AKIN stage II, 0 AKIN stage III). Those subjects who developed CI-AKI had 3.1 fold higher baseline urinary NGAL/creatinine ratios than those without CI-AKI (60.8 [IQR 18.7–93.1] $\mu$g/mg vs. 19.9 [IQR 12.3–38.9] $\mu$g/mg, p = 0.001). In those subjects without clinically overt CKD (eGFR > 60 ml/min, urinary albumin creatinine ratio 0.05 each). ROC analyses revealed an area under the curve (AUC) of 0.68 (95% CI 0.60–0.81) for NGAL/creatinine. An NGAL/creatinine ratio < 56.4 $\mu$g/mg has a negative predictive value of 96.5%. $\bf Conclusions$ The present study is the largest investigation on the use of urinary biomarkers for CI-AKI risk stratification so far. It shows that NGAL provides prognostic information beyond the glomerular biomarkers eGFR and proteinuria