Israel Medical Association Journal

Background: Uninterrupted antithrombotic treatment (ATT) during cardiac implantable electronic device (CIED) implantation increases bleeding and device-related infections (DRI) risk. The wide-awake-local-anesthesia-no-tourniquet (WALANT) technique, using large-volume local anesthesia and adrenaline, is successful in hand surgeries but its potential to mitigate bleeding risk in CIED implantations remains unknown.

Objectives: To investigate whether WALANT protocol for CIED implantations reduces clinically significant pocket hematoma in patients with a high bleeding risk or is a contraindication for interrupting ATT.

Methods: We conducted a prospective, double-blind, randomized controlled trial with CIED surgery patients on uninterrupted ATT. They received WALANT protocol (lidocaine 1% with adrenaline 1:100,000) or standard protocol (lidocaine 1%). Following implantation, patients were blindly monitored in the ward and pacemaker clinic. Patients were monitored for bleeding outcomes post-implantation.

Results: Forty-six consecutive patients (73.6 ± 9 years, 72% male) were enrolled. In the WALANT group (n=24) no intra-pocket pro-hemostatic agents were needed, compared to 45% in the control group (P = 0.0002). Postoperative pressure dressings were used in 12.5% vs. 68% (P = 0.0002). WALANT patients had smaller hematoma areas (median 3.7 cm² IQR [1–39] vs. 46 cm² [IQR 24–76], P = 0.0004) 1-day postoperative. ATT interruption occurred in 12.5% vs. 18% (P = 0.7). Superficial skin infection rates were 4% vs. 9% (P = 0.6). No DRI occurred. No WALANT-related side effects were observed.

Conclusions: WALANT protocol in CIED implantation with uninterrupted ATT reduced pro-hemostatic agents, pressure-dressing need, and hematoma size. Larger studies are needed to assess its impact on infection rates.

We presented the emergent development of pulmonary hypertension and right ventricular impairment in a 64-year-old woman with metastatic breast cancer undergoing carboplatin–gemcitabine combination therapy. The patient's acute decompensation, characterized by dyspnea and desaturation, occurred 2 days after chemotherapy initiation. Clinical assessments revealed right ventricular dilation and systolic dysfunction, a rare manifestation not previously associated with the administered drugs, but which may be associated with cardiopulmonary toxicity of gemcitabine therapy. Prompt discontinuation of chemotherapy and initiation of diuretic therapy resulted in clinical improvement and resolution of the right ventricular dysfunction within several weeks. While a definitive causal link to gemcitabine remains inconclusive, this report highlights a potential and under-reported side effect, emphasizing the need for increased awareness and further investigation into the cardiopulmonary effects of gemcitabine.

The Nazi regime occupying Europe during World War II built a series of concentration camps for those opposing the regime, political and criminal adversaries, and eventually victims of the racial, Aryan policy. It was the suggestion of Germany's elite physician to the Schutzstaffel (SS), Reichfuehrer H.H. (Heinrich Luitpold Himmler), to use the available workforce in the camps, before their eventual liquidation [2,3]. What was the outcome?

The SS medical services in the Auschwitz concentration camp functioned based on two mutually exclusive principles. On the one hand, medical care was provided for the SS staff, and on the other hand, prisoners with contagious diseases or in the terminal stages of exhaustion were eliminated.

Gaucher disease (GD) is an inherited autosomal recessive genetic disorder caused by mutations in the glucocerebroside (GBA1) gene [1]. These variants result in decreased activity of the lysosomal enzyme β-glucocerebrosidase (GCase), which is essential for breaking down glucocerebroside into glucose and ceramide. Consequently, activated macrophages, known as Gaucher cells, accumulate undegraded glucocerebroside. The phagocytic role and naturally high-level GCase activity of macrophages may partly explain why these cells are particularly affected in GD. The accumulation of glucocerebroside in macrophages causes an expansion in the population of these cells, leading to symptoms like hepatosplenomegaly, thrombocytopenia, anemia, bleeding tendency, growth retardation, and bone issues. Bone marrow infiltration may result in bone infarction, episodes of bone crises, and osteonecrosis, mainly of large joints and less commonly as pathological fractures. These latter skeletal complications are the most critical irreversible consequence of untreated GD, significantly impacting the quality of life of patients, and hence should be avoided by early administration of specific therapy. The accumulation of glucocerebroside in lysosomes has been linked to a pro-inflammatory state [2]. In addition, the misfolding and retention of mutant GCase within the endoplasmic reticulum (ER) has been associated with ER stress and activation of the unfolded protein response, contributing to GD phenotypic heterogeneity, inflammation, and immune dysregulation [3].

On 9 August 1938, prisoners from Dachau concentration camp near Munich were sent to the town of Mauthausen in Austria to begin building a new camp. The site was chosen because of the nearby granite quarry and its proximity to Linz [1,2].

Mauthausen initially served as a prison camp for common criminals, prostitutes, and other categories of incorrigible law offenders. However, on 8 May 1939, it was converted to a labor camp. Later, Mauthausen KL became a Nazi concentration camp on a hill above the market town of Mauthausen, approximately 20 kilometers from Linz. It was complemented with dozens of subcamps in the surrounding areas.

Reversible cerebral vasoconstriction syndrome (RCVS) comprises a group of conditions characterized by reversible vasoconstrictions of cerebral arteries. Clinical manifestations include sudden-onset severe headaches with or without additional neurologic signs and symptoms [1].

The incidence of RCVS is 2.7 cases per million adults. It predominantly affects women, and about 9% of all RCVS cases occur during the postpartum period [2,3]. Other possible precipitating factors, such as subarachnoid hemorrhage, ischemic stroke, intracranial hemorrhage, and exposure to vasoactive drugs, have also been reported in association with RCVS [2]. The exact pathophysiology of RCVS is not well understood, although hormonal influences have been suggested as possible contributing factors.

Alkalosis-induced cerebral vasoconstriction is described but not well understood. Hyperventilation is commonly used in neurologic patients to decrease intracranial pressure and cerebral blood flow. Hyperventilation causes cerebral vasoconstriction directly by hypocapnia and may indirectly affect through alkalosis.

We present a case of RCVS in a postpartum patient admitted to the intensive care unit (ICU) with severe metabolic alkalosis necessitating hemodialysis.

Among patients admitted with acute decompensated heart failure (ADHF), deterioration of renal function with resulting acute kidney injury (AKI) is reported in up to 70% of patients with cardiogenic shock. Twenty percent of heart failure patients with AKI progress to dialysis (AKI-D). Optimal timing for initiation of renal replacement therapies (RRT) has been researched; however, minimal studies discuss guidelines for weaning from RRT [1]. Electronic monitoring of urine output (UO) may serve as a tool to aid in withdrawal from RRT. We present a case of ADHF with severe AKI requiring continuous renal replacement therapy (CRRT) where real-time electronic monitoring of UO was implemented for the first time to guide de-escalation therapy from CRRT until successful withdrawal.

Since 1980 dermatologists have been interested in the exceptional healing reported by patients who underwent treatments at the Dead Sea. Tens of thousands of patients have visited this area and more than 10,000 cases have been the subject of clinical and laboratory studies since this natural therapeutic option was discovered for psoriasis management. Through evaluation of the published articles on climatotherapy, we tried to reach a global assessment of the usefulness of this approach and to discover whether this treatment still can be recommended in the era of biologic treatments. I conducted a review of the available literature on clinical trials through PubMed, Medline, and Google Scholar using the terms psoriasis and Dead Sea. I found 26 studies published between 1982 and 2021. Assessment of patients showed major improvement through several selected parameters. Length of the stay and medical supervision positively influenced the major outcomes observed. Duration of improvement and possible long-term side effects of this natural treatment still need to be more precisely determined. Exposure to the unique climatic factors of the region, essentially the sun and the sea, induces fast and significant results with high clearance rates of psoriasis plaques. Dead Sea climatotherapy still has its place for the control of psoriasis symptoms.

A dramatic portrait bust of the physician Gabriele da Fonseca (1586? to 1668) at prayer is considered by art historians to be one of the finest late works of Gian Lorenzo Bernini (1598–1680), the preeminent sculptor of 17th century Rome. This statue is of medical as well as artistic interest. First, Fonseca is shown wearing his physician’s robe, thus celebrating his successful career as a leading medical figure in Rome, holding both Papal and university appointments at the highest level. In addition, the positioning of the statue in a special chapel designed by Bernini highlights Fonseca’s role as an influential participant in the introduction of quinine into Europe as a cure for malaria. Last, an examination of the statue’s hands identifies a number of pathologies and anatomical anomalies that raise interesting questions, regrettably unanswerable given the information presently available, concerning Fonseca’s illnesses and cause of death.

Higher potency bisphosphonates, typically intravenous formulations, are given at lower doses for postmenopausal women. The treatment has improved compliance compared to daily oral therapy. Since bisphosphonates are exclusively excreted via the kidneys, intravenous formulation has been associated with deterioration of renal function, specifically in the setting of preexisting renal disease or concomitant use of nephrotoxic agents [1].

Anti-tumor necrosis factor-alpha (anti-TNFα) medications are the most frequently used biologicals to treat inflammatory bowel disease (IBD). Little is known about the ocular side effects of this drug category. We present a case series of six young patients with Crohn disease (CD) and no previous ophthalmologic manifestations who developed blepharitis after commencing treatment with anti-TNFα therapy. Six otherwise healthy patients with CD, with no history of allergies or prior ocular complaints, developed blepharitis at a median of 7.5 months after the initiation of anti-TNFα therapy. All ophthalmic findings were treated topically. The ocular symptoms of two of the patients resolved shortly after discontinuation of the anti-TNFα treatment. The other four presented with relapsing-remitting symptoms. Blepharitis is a common ocular disease in the general population and an extra-intestinal manifestation in patients with IBD. It may be an adverse effect of anti-TNFα therapy in this patient population.

Uveal melanoma (UM) affects approximately six individuals per million per year in the United States, with similar rates in Mediterranean countries. Although it appears to have a low prevalence, it is the most common primary intraocular malignancy in adults. Clinically, it presents in most patients as a painless loss or distortion of vision, although it may also be accidentally discovered at routine ophthalmic examination. Associated risk factors include fair skin tone, light eye color, presence of a choroidal nevus, oculodermal melanocytosis (nevus of ota), dysplastic nevus syndrome, and germline BRCA-associated protein 1 mutations (BAP1 mutations) [1].

Biological therapies with monoclonal antibodies have revolutionized the management of many inflammatory and autoimmune diseases. Combining biological treatments is very rarely indicated and may theoretically result in severe adverse effects, specifically, an increased tendency toward infectious diseases. We present the case of a woman in whom combination therapy with canakinumab for familial Mediterranean fever (FMF) and mepolizumab for chronic eosinophilic pneumonia was successfully employed.

A review of the literature on the effect of immune modulation on the skeleton shows disappointing results.

The prevalence of choroidal nevi associated with choroidal neovascular membrane (CNV) is estimated to range between 0.58% and 8.6% [1]. The pathogenesis of CNV is not completely understood. Researchers have suggested that damage caused to the choroid capillaries above the nevi affects the overlying retinal pigment epithelium and triggers production of angiogenic factors that, in turn, cause the development of CNV [2,3]. Hypoxia and inflammation may be involved in the process. Data have been inconsistent with both theories [4].